FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Wysocki, J AF Wysocki, J TI Dimensions of the vestibular and tympanic scalae of the cochlea in selected mammals SO HEARING RESEARCH LA English DT Article DE cochlear scalae; measurement; comparative anatomy; mammal ID GUINEA-PIG; CAT AB The spiral shaped organ of hearing occurs only in mammals. This shape creates good conditions for the acoustic wave inside the cochlea. There are various forms of the cochlea in different species of mammal: the number of turns ranges from 1.5 to 4.5, a fact for which there seems no obvious explanation. In order to become more familiar with the geometry of the cochlear scalae in animals, a microanatomical study was carried out on 40 temporal bones, obtained from four common species of mammal: cat, dog, cattle and macaca. The bones were dissected with the aid of an operation microscope using standard otosurgical equipment, in which their perilymphatic spaces were filled with latex and further prepared in a formalin stain. Each of the rubber molds was removed from the osseous matrix and subsequently manually cut into I mm segments. The results, presented in diagrams, indicate that the vestibular and tympanic scalae present alternate dominance in their width and height, as was previously found in a study of humans. The change of this alternation domination appears two to five times on their entire length. The dimensions of the cochlear scalae are to a certain extent proportional to the weight of the animals the largest were found in cattle and the smallest in the macaca. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Warsaw Univ, Dept Normal Anat, Sch Med, PL-02004 Warsaw, Poland. Inst Lekow, Drug Inst, Ctr Confocal Microscopy, PL-00725 Warsaw, Poland. RP Wysocki, J (reprint author), Warsaw Univ, Dept Normal Anat, Sch Med, 5 Chalubinskiego St, PL-02004 Warsaw, Poland. CR BURDA H, 1988, J MORPHOL, V198, P269, DOI 10.1002/jmor.1051980303 Counter SA, 1999, NEUROREPORT, V10, P473, DOI 10.1097/00001756-199902250-00006 Edge RM, 1998, HEARING RES, V124, P1, DOI 10.1016/S0378-5955(98)00090-2 HADZISELIMOVIC H., 1964, ANAT ANZ, V114, P389 HARRIS DM, 1990, HEARING RES, V50, P1, DOI 10.1016/0378-5955(90)90029-O HATSUSHIKA S, 1990, ANN OTO RHINOL LARYN, V99, P871 IGARASHI M, 1968, J SPEECH HEAR RES, V11, P229 IGARASHI M, 1976, ARCH OTOLARYNGOL, V102, P428 Ketten D R, 1998, Ann Otol Rhinol Laryngol Suppl, V175, P1 Khanna SM, 1999, HEARING RES, V135, P89, DOI 10.1016/S0378-5955(99)00095-7 Koizuka I, 1997, NMR BIOMED, V10, P31, DOI 10.1002/(SICI)1099-1492(199701)10:1<31::AID-NBM446>3.0.CO;2-U SALT AN, 1988, PHYSL EAR, P341 Thorne M, 1999, LARYNGOSCOPE, V109, P1661, DOI 10.1097/00005537-199910000-00021 UFFENDAHL M, 1997, PROG NEUROBIOL, V53, P331 URLET HM, 1967, HDB VERGLEICHENDEN A, P1293 Wysocki J, 1999, HEARING RES, V135, P39, DOI 10.1016/S0378-5955(99)00088-X ZWISLOCKI-MOCIKI JOZEF, 1948, ACTA OTO LARYNGOL [STOCKHOLM], V72, P1 NR 17 TC 8 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 1 EP + DI 10.1016/S0378-5955(01)00314-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100001 PM 11744275 ER PT J AU Meyer, J Mack, AF Gummer, AW AF Meyer, J Mack, AF Gummer, AW TI Pronounced infracuticular endocytosis in mammalian outer hair cells SO HEARING RESEARCH LA English DT Article DE outer hair cell; apical endocytosis; FM 1-43; Hensen's body; protein turnover ID SUBSURFACE CISTERNAE; GUINEA-PIG; AMINOGLYCOSIDE ANTIBIOTICS; ENDOPLASMIC-RETICULUM; OPTICAL-DETECTION; LIVING CELLS; MEMBRANE; ORGAN; CORTI; MICROTUBULES AB Endocytosis in cochlear hair cells was investigated by staining with the vital fluorescent dye FM 1-43, that partitions reversibly into membranes and is trapped in vesicles during endocytosis. The temporal development and spatial distribution of FM 1-43 induced fluorescence was investigated using confocal laser-scanning microscopy. FM 1-43 rapidly and intensely stained cochlear hair cells, leaving the supporting cells unstained. For short application (0.2-30 s). only the infracuticular region of outer hair cells (OHCs) was labeled, whereas for long application (30-60 s), the OHCs were also labeled in the infranuclear zone and along a central strand extending from the infracuticular zone down to the nucleus. as well as along the entire cell membrane. Except for the cell membrane. the infracuticular zone. directly below the cuticular plate, showed the most rapid and intense staining, and in most cases staining was spherically shaped with a diameter of 3-7 mum. Localization and size of this infracuticular staining coincided with Hensen's body, a specialized variant of the endoplasmic reticulum. In contrast to the OHCs. apical fluorescence of inner hair cells presented a homozeneous distribution. When OHCs were incubated in FM 1-43 for longer than 1 min, many points of contact between the central strand, the infracuticular zone and the lateral cell membrane were observed. Since Hensen's bodies are a specialty of OHCs and the fluorescent staining pattern of these cells was unique., it is proposed that Hensen's body is involved in the turnover of OHC-specific proteins, such as those involved in the molecular machinery of the motor action of the plasma membrane. (C) 2001 Elsevier Science BN. All rights reserved. C1 Univ Tubingen, Dept Otolaryngol, Sect Physiol Acoust & Commun, D-72076 Tubingen, Germany. Univ Tubingen, Inst Anat, Dept Cellular Neurobiol, D-72074 Tubingen, Germany. RP Gummer, AW (reprint author), Univ Tubingen, Dept Otolaryngol, Sect Physiol Acoust & Commun, Silcherstr 5, D-72076 Tubingen, Germany. CR BOHNE BA, 1973, J ACOUST SOC AM, V53, P292, DOI 10.1121/1.1982166 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Cochilla AJ, 1999, ANNU REV NEUROSCI, V22, P1, DOI 10.1146/annurev.neuro.22.1.1 ENGSTROM H, 1960, Acta Otolaryngol Suppl, V158, P219 ENGSTROM H, 1953, ACTA OTOLARYNGOL STO, V44, P490 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 FORGE A, 1993, HEARING RES, V64, P175, DOI 10.1016/0378-5955(93)90003-J Fulton A., 1984, CYTOSKELETON CELLULA FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 HARADA Y, 1987, ACTA OTO-LARYNGOL, V103, P458 Hashino E, 1995, BRAIN RES, V704, P135, DOI 10.1016/0006-8993(95)01198-6 Hensen V., 1863, Z WISS ZOOL, V13, P481 HOLLEY MC, 1992, J CELL SCI, V102, P569 IKEDA K, 1993, HEARING RES, V66, P169, DOI 10.1016/0378-5955(93)90138-Q Kachar B, 1997, HEARING RES, V107, P102, DOI 10.1016/S0378-5955(97)00027-0 KIMITSUKI T, 1993, BRAIN RES, V624, P143, DOI 10.1016/0006-8993(93)90072-U KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LEE C, 1988, CELL, V54, P37, DOI 10.1016/0092-8674(88)90177-8 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MACDONALD RB, 2001, 24 ANN MIDW M ASS RE, P759 Mammano F, 1999, J NEUROSCI, V19, P6918 Meyer J, 1998, J NEUROSCI, V18, P6748 MEYERS JR, 2001, 24 ANN MIDW M ASS RE, P862 Moser T, 2000, P NATL ACAD SCI USA, V97, P883, DOI 10.1073/pnas.97.2.883 Mukherjee S, 1997, PHYSIOL REV, V77, P759 Murthy VN, 1999, CURR OPIN NEUROBIOL, V9, P314, DOI 10.1016/S0959-4388(99)80046-4 Musil LS, 2000, J BIOL CHEM, V275, P25207, DOI 10.1074/jbc.275.33.25207 Ryan TA, 1997, NATURE, V388, P478, DOI 10.1038/41335 SAITO K, 1983, CELL TISSUE RES, V229, P467 Santos-Sacchi J, 1998, NEUROSCI LETT, V256, P155, DOI 10.1016/S0304-3940(98)00788-5 Seiler C, 1999, J NEUROBIOL, V41, P424, DOI 10.1002/(SICI)1097-4695(19991115)41:3<424::AID-NEU10>3.0.CO;2-G SLEPECKY NB, 1990, J ELECTRON MICR TECH, V15, P280, DOI 10.1002/jemt.1060150307 SLOEPECKY N, 1981, ARCH OTORHINOLARYNGO, V230, P273 Sousa C, 1996, PHOTOCHEM PHOTOBIOL, V63, P601, DOI 10.1111/j.1751-1097.1996.tb05662.x Spicer SS, 1998, ANAT REC, V251, P97, DOI 10.1002/(SICI)1097-0185(199805)251:1<97::AID-AR15>3.0.CO;2-6 STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 TERASAKI M, 1986, J CELL BIOL, V103, P1557, DOI 10.1083/jcb.103.4.1557 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 Vogel SS, 1999, P NATL ACAD SCI USA, V96, P5019, DOI 10.1073/pnas.96.9.5019 ZAJIC G, 1993, HEARING RES, V66, P53, DOI 10.1016/0378-5955(93)90259-4 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 Zheng J, 2000, NATURE, V405, P149, DOI 10.1038/35012009 NR 42 TC 19 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 10 EP 22 DI 10.1016/S0378-5955(01)00338-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100002 PM 11744276 ER PT J AU Brandle, U Frohnmayer, S Krieger, T Zenner, HP Ruppersberg, JP Maassen, MM AF Brandle, U Frohnmayer, S Krieger, T Zenner, HP Ruppersberg, JP Maassen, MM TI Expression of Ca2+-activated K+ channel subunits and splice variants in the rat cochlea SO HEARING RESEARCH LA English DT Article DE auditory system; K+ channel; cochlea; maxi-K channel; subunit expression; reverse transcription polymerase chain reaction; Slo ID ACTIVATED POTASSIUM CHANNELS; HAIR-CELLS; CONDUCTANCE; MEMBRANE; SLOWPOKE; MSLO; HSLO AB The recently manifested important role of the Ca2+-activated K+ channels, especially of the Slo gene-coded channels, for the cochlea function of the chicken raised the question of homolog expression in mammalian inner ear tissue. Molecular biological methods were used to demonstrate the expression of Ca2+-activated K channel subunits and splice variants of the Slo gene in the rat organ of Corti. RT-PCR experiments for the detection of rat Slo alpha subunit mRNA revealed the presence of several already known splice variants including variants which appeared to be typical for the organ of Corti (+58 aa) and for the brain (+61 aa). To detect the accessory beta subunit we used Southern blot hybridization. Our data Support the hypothesis that Ca2+-activated K+ channel subunits (i.e. Slo variants) are also involved in the hearing of mammals in the organ of Corti. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tubingen, Dept Otolaryngol, Sect Sensory Biophys, D-72076 Tubingen, Germany. Univ Tubingen, Inst Physiol 2, D-72076 Tubingen, Germany. RP Maassen, MM (reprint author), Univ Tubingen, Dept Otolaryngol, Sect Sensory Biophys, Silcherstr 5, D-72076 Tubingen, Germany. CR ADELMAN JP, 1992, NEURON, V9, P209, DOI 10.1016/0896-6273(92)90160-F ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 ATKINSON NS, 1991, SCIENCE, V253, P551, DOI 10.1126/science.1857984 BUTLER A, 1993, SCIENCE, V261, P221, DOI 10.1126/science.7687074 Dworetzky SI, 1996, J NEUROSCI, V16, P4543 Fettiplace R, 1999, ANNU REV PHYSIOL, V61, P809, DOI 10.1146/annurev.physiol.61.1.809 GITTER AH, 1992, HEARING RES, V60, P13, DOI 10.1016/0378-5955(92)90053-P Jiang GJ, 1997, P ROY SOC B-BIOL SCI, V264, P731 KNAUS HG, 1994, J BIOL CHEM, V269, P3921 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 LAGRUTTA A, 1994, J BIOL CHEM, V269, P20347 LATORRE R, 1989, ANNU REV PHYSIOL, V51, P385 MCMANUS OB, 1995, NEURON, V14, P545 Meera P, 1996, FEBS LETT, V382, P84, DOI 10.1016/0014-5793(96)00151-2 Navaratnam DS, 1997, NEURON, V19, P1077, DOI 10.1016/S0896-6273(00)80398-0 Ramanathan K, 2000, J NEUROSCI, V20, P1675 ROSE ML, 1997, CARDIOVASC ENG, V2, P19 Saito M, 1997, J BIOL CHEM, V272, P11710, DOI 10.1074/jbc.272.18.11710 SANGER F, 1977, P NATL ACAD SCI USA, V74, P5463, DOI 10.1073/pnas.74.12.5463 TSENGCRANK J, 1994, NEURON, V13, P1315, DOI 10.1016/0896-6273(94)90418-9 NR 20 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 23 EP 28 DI 10.1016/S0378-5955(01)00323-9 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100003 PM 11744277 ER PT J AU Li, XQ Sun, JH Yu, N Sun, YR Tan, ZL Jiang, SC Li, N Zhou, CX AF Li, XQ Sun, JH Yu, N Sun, YR Tan, ZL Jiang, SC Li, N Zhou, CX TI Glutamate induced modulation of free Ca2+ in isolated inner hair cells of the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE glutamate; inner hair cell; cochlea; intracellular free calcium; guinea pig ID AMPA RECEPTOR SUBUNITS; RAT ORGAN; LOCALIZATION; SYNAPSES; CALCIUM; CORTI AB To explore the possible involvement of glutamate (Glu) in modulation of inner hair cell (IHC) functions, the glutamate (Glu) induced changes in intracellular free Ca2+ ([Ca2+](i)) concentration in isolated IHCs and outer hair cells (OHCs) of the guinea pig cochlea were investigated with fluo-3. a fluorescent probe for intracellular Ca2+. Their unique flask shape identified the IHCs with a distinct neck and spherical base with a large spherical nucleus. Normal cell shapes could be maintained for about 2 h. Fluorescence of fluo-3 was distributed in the whole isolated IHC with brighter staining nuclei. Static [Ca2+](i) remained constant within the observation period in the absence of Glu. In the presence of a low concentration of Glu (3.85 muM), there was an increase of [Ca2+](i) in IHCs, whereas no obvious [Ca2+](i) change was found in OHCs. The increase of the fluorescence in IHCs reached peak level at 180 s and then gradually reduced at 400 s after the administration of Glu. The increases of [Ca2+](i), were observed in nine of 10 IHCs. but one IHC did not show any change. For 10 of the observed OHCs, seven showed no [Ca2+](i) change, and three showed minor reduction of [Ca2+](i). The increase of the Glu concentration resulted in a corresponding change of [Ca2+](i) in the IHCs after three times administration of Glu. These results suggest that Glu acts on the IHCs presynaptic autoreceptor in a positive feedback manner. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Chinese Peoples Liberat Army Gen Hosp, Inst Otolaryngol, Beijing 100853, Peoples R China. RP Li, XQ (reprint author), Chinese Peoples Liberat Army Gen Hosp, Inst Otolaryngol, Beijing 100853, Peoples R China. CR ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 COLTON CK, 1975, COMP BIOCHEM PHYS C, V51, P275, DOI 10.1016/0306-4492(75)90074-X COTMAN CW, 1986, J PHYSIOL-LONDON, V378, P403 DEVAU G, 1993, EUR J NEUROSCI, V5, P1210, DOI 10.1111/j.1460-9568.1993.tb00975.x DOI T, 1993, HEARING RES, V67, P179, DOI 10.1016/0378-5955(93)90245-V DULON D, 1990, J NEUROSCI, V10, P1388 ENRENBERGERR K, 1991, HEARING RES, V52, P73 FELIX D, 1990, EUR ARCH OTO-RHINO-L, V248, P1, DOI 10.1007/BF00634769 GLAUM SR, 1990, P NATL ACAD SCI USA, V87, P3454, DOI 10.1073/pnas.87.9.3454 GLEICH O, 1990, HEARING RES, V45, P295, DOI 10.1016/0378-5955(90)90128-C Matsubara A, 1999, BRAIN RES, V819, P58, DOI 10.1016/S0006-8993(98)01345-6 Matsubara A, 1996, J NEUROSCI, V16, P4457 PRIGIONI I, 1990, HEARING RES, V46, P253, DOI 10.1016/0378-5955(90)90006-B Pujol R, 1990, Acta Otolaryngol Suppl, V476, P32 STARR PA, 1990, SOC NEUR ABSTR, V14, P331 THIEFFRY M, 1978, BRAIN RES, V156, P402, DOI 10.1016/0006-8993(78)90528-0 USAMI S, 1992, EXP BRAIN RES, V91, P1 USHERWOO.PN, 1966, NATURE, V210, P634, DOI 10.1038/210634a0 VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X NR 21 TC 6 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 29 EP 34 DI 10.1016/S0378-5955(01)00330-6 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100004 PM 11744278 ER PT J AU Moraes, MFD Garcia-Cairasco, N AF Moraes, MFD Garcia-Cairasco, N TI Real time mapping of rat midbrain neural circuitry using auditory evoked potentials SO HEARING RESEARCH LA English DT Article DE electric field vector; auditory evoked potential; neural circuitry; functional mapping ID INFERIOR COLLICULUS LESIONS; LOCALIZATION; BRAIN; RECORDINGS; RESPONSES; CAT AB Auditory evoked potentials were recorded in 360 homogeneously spaced sites, in a volume encapsulating the lateral lemniscus-inferior colliculus transition of anaesthetized rats, in order to calculate the electric field vector distribution with each moment in time referenced to the onset of sound presentation. Software. to conduct calculations and graphical representation, and hardware, to minimize neural damage upon recording, were developed in our laboratory. Our results indicate a smooth transition of both amplitude and direction of vectors, suggestive of sequentially activated sites with outward and inward ionic currents coherent with what is known of this part of the primary auditory pathway. That is, anatomical sites (neural generators) and latency for activation matches previous research of the auditory pathway. while adding a real time perspective to the anatomical substrates recruited during the auditory evoked response. An algorithm for calculating the divergent of the vector field, an estimate of the current source density inside the three-dimensional control volume, was used to infer the possible current sinks and sources generating the field potentials. This technique allowed a clear visualization of two distinct discharges arising from the lateral lemniscus towards the inferior colliculus, thus recording signal propagation, as a movie file, with 0.06 ms time resolution. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Fed Minas Gerais, Dept Physiol & Biophys, Inst Biol Sci, Belo Horizonte, MG, Brazil. Univ Sao Paulo, Neurophysiol & Expt Neuroethol Lab, Dept Physiol, Ribeirao Preto Sch Med, BR-14049900 Ribeirao Preto, SP, Brazil. RP Garcia-Cairasco, N (reprint author), Univ Fed Minas Gerais, Dept Physiol & Biophys, Inst Biol Sci, Belo Horizonte, MG, Brazil. RI Moraes, Marcio/D-5285-2014 OI Moraes, Marcio/0000-0002-2034-1836 CR Adrian ED, 1934, BRAIN, V57, P355, DOI 10.1093/brain/57.4.355 Berger H, 1929, ARCH PSYCHIAT NERVEN, V87, P527, DOI 10.1007/BF01797193 Biacabe B, 2001, AURIS NASUS LARYNX, V28, P85, DOI 10.1016/S0385-8146(00)00080-8 CAIRD D, 1985, ELECTROEN CLIN NEURO, V61, P50, DOI 10.1016/0013-4694(85)91072-7 CAIRD DM, 1987, ELECTROEN CLIN NEURO, V68, P237, DOI 10.1016/0168-5597(87)90034-7 CUFFIN BN, 1995, IEEE T BIO-MED ENG, V42, P68, DOI 10.1109/10.362917 Darcey T M, 1980, Prog Brain Res, V54, P128, DOI 10.1016/S0079-6123(08)61617-9 DASILVA FLL, 1993, BIOPHYSICAL ASPECTS, P78 Davis H, 1939, J NEUROPHYSIOL, V2, P500 DAWSON GD, 1951, J PHYSIOL-LONDON, V115, pP2 DAWSON GD, 1954, ELECTROEN CLIN NEURO, V6, P65, DOI 10.1016/0013-4694(54)90007-3 DURRANT JD, 1994, HEARING RES, V72, P99, DOI 10.1016/0378-5955(94)90210-0 EHRET G, 1985, J COMP PHYSIOL A, V156, P619, DOI 10.1007/BF00619111 FUNAI H, 1983, AUDIOLOGY, V22, P9 HELMHOLTZ H, 1853, ANN PHYS CHEM, V29, P211 HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 HUFFMAN RF, 1990, BRAIN RES REV, V15, P295, DOI 10.1016/0165-0173(90)90005-9 IMONIEMI RJ, 1993, BRAIN TOPOGR, V5, P331 JAYAKAR P, 1991, J CLIN NEUROPHYSIOL, V8, P414, DOI 10.1097/00004691-199110000-00006 JEFFERYS JGR, 1995, PHYSIOL REV, V75, P689 Kandel A, 1997, J NEUROSCI, V17, P6783 KAVANAGH RN, 1978, IEEE T BIO-MED ENG, V25, P421, DOI 10.1109/TBME.1978.326339 LEGATT AD, 1986, ELECTROEN CLIN NEURO, V64, P53, DOI 10.1016/0013-4694(86)90043-X LESSER RP, 1985, J CLIN NEUROPHYSIOL, V2, P45, DOI 10.1097/00004691-198501000-00003 LIEGOISCHAUVEL C, 1987, FUNDAMENTAL MECH HUM, P39 MAGNUS O, 1961, ELECTRENCEPHALOGR S, V13, P1 MITZDORF U, 1985, PHYSIOL REV, V65, P37 Moraes MFD, 2000, NEUROSCI LETT, V284, P13, DOI 10.1016/S0304-3940(00)00978-2 Moraes MFD, 1997, BRAZ J MED BIOL RES, V30, P1319 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 Nicolelis MAL, 1997, NEURON, V18, P529, DOI 10.1016/S0896-6273(00)80295-0 Niedermayer E., 1993, ELECTROENCEPHALOGRAP Nunez P. L., 1981, ELECT FIELDS BRAIN Paxinos G, 1997, RAT BRAIN STEREOTAXI SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SPENCER SS, 1982, ANN NEUROL, V12, P248, DOI 10.1002/ana.410120306 WILSON FN, 1950, CIRCULATION, V1, P84 WITWER JG, 1972, IEEE T BIO-MED ENG, VBM19, P352, DOI 10.1109/TBME.1972.324138 WOOD CC, 1982, ANN NY ACAD SCI, V388, P139, DOI 10.1111/j.1749-6632.1982.tb50789.x NR 39 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 35 EP 44 DI 10.1016/S0378-5955(01)00341-0 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100005 PM 11744279 ER PT J AU Suryadevara, AC Schulte, BA Schmiedt, RA Slepecky, NB AF Suryadevara, AC Schulte, BA Schmiedt, RA Slepecky, NB TI Auditory nerve fibers in young and quiet-aged gerbils: morphometric correlations with endocochlear potential SO HEARING RESEARCH LA English DT Article DE gerbil; auditory nerve; hearing; presbyacusis; aging; cochlea; endocochlear potential ID STRIA VASCULARIS; QUANTITATIVE-EVALUATION; SPATIAL-ORGANIZATION; MONGOLIAN GERBIL; GUINEA-PIG; COCHLEA; THRESHOLDS; DENSITY; NEURONS; HUMANS AB The number, size and distribution of myelinated nerve Fibers were analyzed in the osseous spiral lamina (OSL) of young and old gerbils raised in a quiet environment. Because decreased endocochlear potentials (EPs) play a significant role in age-related hearing loss in the gerbil, we correlated morphometric and topographical data for nerve Fibers with EP measurements in the same ear. Fibers were analyzed at the 2 and 10 kHz locations. The number of fibers at the 2 kHz location ranged from 12 to 47% greater than at the 10 kHz place in both young and aged specimens. No significant correlation was found between the number of fibers and the EP. Nerve fibers in gerbil tend to be distributed vertically by size within the OSL [Slepecky et al. (2000) Hear. Res. 144, 124-134], a result also found in cats and guinea pigs. Smaller fibers are more often found towards the scala vestibuli side of the OSL, whereas larger fibers are concentrated towards the scala tympani. The present data confirmed this distribution in young gerbils; however. in aged cars the distribution often became more uniform. Moreover. fiber distribution and ganglion cell size were highly correlated with EP. As EP declined. the fiber size distribution in the OSL became more uniform and the mean cross-sectional area of spiral ganglion cells and fiber diameter decreased. Thus, for whatever reason, certain indices of auditory nerve fiber morphometrics appear to be associated with the EP. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Med Univ S Carolina, Dept Otolaryngol & Head & Neck Surg, Charleston, SC 29425 USA. Syracuse Univ, Dept Bioengn & Neurosci, Syracuse, NY 13244 USA. Syracuse Univ, Inst Sensory Res, Syracuse, NY 13244 USA. Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. RP Schmiedt, RA (reprint author), Med Univ S Carolina, Dept Otolaryngol & Head & Neck Surg, 39 Sabin St,Rm 608,POB 250150, Charleston, SC 29425 USA. CR Adams JC, 1997, HEARING RES, V104, P101, DOI 10.1016/S0378-5955(96)00184-0 BOHNE BA, 1982, J ACOUST SOC AM, V72, P102, DOI 10.1121/1.387994 Felder E, 1997, HEARING RES, V105, P183, DOI 10.1016/S0378-5955(96)00209-2 Felder E, 1995, HEARING RES, V91, P19, DOI 10.1016/0378-5955(95)00158-1 GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S GRATTON MA, 1995, HEARING RES, V82, P44 Gratton MA, 1997, HEARING RES, V114, P1, DOI 10.1016/S0378-5955(97)00025-7 Gratton MA, 1996, HEARING RES, V94, P116, DOI 10.1016/0378-5955(96)00011-1 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N Hequembourg S, 2001, JARO, V2, P118 KAWASE T, 1992, J COMP NEUROL, V319, P312, DOI 10.1002/cne.903190210 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KIANG NYS, 1965, MONOGRAPH MIT, V35 LEAKE PA, 1993, J COMP NEUROL, V333, P257, DOI 10.1002/cne.903330211 LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 OHLEMILLER KK, 1990, J COMP PHYSIOL A, V167, P329 OHLEMILLER KK, 1991, J ACOUST SOC AM, V90, P274, DOI 10.1121/1.401298 ROBERTSON D, 1991, HEARING RES, V51, P29, DOI 10.1016/0378-5955(91)90004-S Sakaguchi N, 1998, HEARING RES, V118, P114, DOI 10.1016/S0378-5955(98)00022-7 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 Schmiedt RA, 1996, HEARING RES, V102, P125, DOI 10.1016/S0378-5955(96)00154-2 SCHMIEDT RA, 2000, ASS RES OT ABSTR, V23, P80 Schmiedt R.A, 1993, SENSORY RES MULTIMOD Schmiedt RA, 1996, J NEUROPHYSIOL, V76, P2799 Schuknecht H. F., 1974, PATHOLOGY EAR SCHULTE B, 1996, ABSWTR ASS RES OT, V19, P640 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SCHULTE BA, 2001, UNPUB ALTERATIONS SP SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 Slepecky NB, 2000, HEARING RES, V144, P124, DOI 10.1016/S0378-5955(00)00055-1 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 Thomopoulos GN, 1997, HEARING RES, V111, P31, DOI 10.1016/S0378-5955(97)00080-4 Tsuji J, 1997, J COMP NEUROL, V381, P188 NR 37 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 45 EP 53 DI 10.1016/S0378-5955(01)00340-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100006 PM 11744280 ER PT J AU Chen, L Sun, W Salvi, RJ AF Chen, L Sun, W Salvi, RJ TI Electrically evoked otoacoustic emissions from the chicken ear SO HEARING RESEARCH LA English DT Article DE electrically evoked otoacoustic emission; chicken; hair cell; kanamycin; distortion product otoacoustic emission; cochlear microphonic ID HAIR CELL LOSS; COCHLEAR GANGLION NEURONS; BASILAR-MEMBRANE MOTION; ADULT CHICKENS; KANAMYCIN OTOTOXICITY; GENTAMICIN TREATMENT; PREFERRED INTERVALS; DISCHARGE PATTERNS; INNER; REGENERATION AB The outer hair cell electromotile response is believed to underlie the sharp tuning and exquisite sensitivity of the mammalian inner ear. and contribute to the production of electrically evoked otoacoustic emissions (EEOAEs) and sound-evoked otoacoustic emissions (OAFs). Avian cars are also sharply tuned. extremely sensitive and generate spontaneous and sound-evoked OAEs, but avian hair cells do not exhibit somatic electro motility. However., stereocilia bundle movements have been observed in avian and amphibian hair cells suggesting that EEOAEs might arise from electrically evoked bundle movements. Here, we demonstrate for the first time that AC current applied to the round window of the chicken evokes EEOAE of up to 18 dB SPL. The EEOAE produces a bandpass response with maximum amplitude in the 1000-3000 Hz range, the response drops off rapidly above 4000 Hz and below 500 Hz. The impulse response to current pulses is characterized by a large peak sometimes followed by a damped oscillation with a frequency around 2000 Hz. EEOAEs decreased significantly after anoxia and paraformaldehyde damage of the cochlea. Kanamycin-induced hair cell loss also caused a significant reduction in EEOAE and distortion product OAE; these emissions showed only a small recovery at long recovery times. when most hair cells should have regenerated. These results suggest that the EEOAE has a biological origin in the cochlea. which could presumably involve electrically evoked stereocilia bundle movements. (C) 2001 Published by Elsevier Science B.V. C1 SUNY Buffalo, Hearing Res Labs, Dept Communicat Disorders & Sci, Buffalo, NY 14214 USA. RP Salvi, RJ (reprint author), SUNY Buffalo, Hearing Res Labs, Dept Communicat Disorders & Sci, 215 Parker Hall,South Campus, Buffalo, NY 14214 USA. EM salvi@buffalo.edu RI Chen, Lin/N-8327-2013 OI Chen, Lin/0000-0002-5847-2989 CR BRIX J, 1994, HEARING RES, V76, P147, DOI 10.1016/0378-5955(94)90096-5 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Burkard R, 1996, Audiol Neurootol, V1, P197 CHEN L, 1995, HEARING RES, V89, P28, DOI 10.1016/0378-5955(95)00119-5 Chen L, 1996, HEARING RES, V98, P152, DOI 10.1016/0378-5955(96)00086-X Chen L, 1996, J ACOUST SOC AM, V100, P442, DOI 10.1121/1.415959 CHEN L, 1994, HEARING RES, V81, P130, DOI 10.1016/0378-5955(94)90160-0 CHEN L, 1993, HEARING RES, V69, P15, DOI 10.1016/0378-5955(93)90089-J CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DUCKERT LG, 1993, J COMP NEUROL, V331, P75, DOI 10.1002/cne.903310105 FROYMOVICH O, 1995, J ACOUST SOC AM, V97, P3021, DOI 10.1121/1.411867 HASHINO E, 1995, HEARING RES, V88, P156, DOI 10.1016/0378-5955(95)00109-H HE D, 2001, ASS RES OTOLARYNGOL, V24, P159 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 Hofstetter P, 1997, AUDIOLOGY, V36, P301 KETTEMBEIL S, 1995, HEARING RES, V86, P47, DOI 10.1016/0378-5955(95)00053-7 KLINKE R, 1994, HEARING RES, V74, P238, DOI 10.1016/0378-5955(94)90192-9 MANLEY GA, 1994, HEARING RES, V72, P171, DOI 10.1016/0378-5955(94)90216-X Manley GA, 1997, J ACOUST SOC AM, V102, P1049, DOI 10.1121/1.419858 Manley GA, 2001, P NATL ACAD SCI USA, V98, P2826, DOI 10.1073/pnas.041604998 MANLEY GA, 1984, NATURWISSENSCHAFTEN, V71, P592, DOI 10.1007/BF01189191 Martin P, 1999, P NATL ACAD SCI USA, V96, P14306, DOI 10.1073/pnas.96.25.14306 Nakajima HH, 1998, HEARING RES, V122, P109, DOI 10.1016/S0378-5955(98)00094-X NAKAJIMA HH, 1991, PROCEEDINGS OF THE 1991 IEEE SEVENTEENTH ANNUAL NORTHEAST BIOENGINEERING CONFERENCE, P213, DOI 10.1109/NEBC.1991.154650 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 Nuttall AL, 1999, HEARING RES, V131, P39, DOI 10.1016/S0378-5955(99)00009-X Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 POWERS NL, 1995, NATURE, V375, P585, DOI 10.1038/375585a0 Ren TY, 1995, HEARING RES, V92, P178, DOI 10.1016/0378-5955(95)00217-0 Ren TY, 1998, HEARING RES, V120, P7, DOI 10.1016/S0378-5955(98)00045-8 Reyes S, 2001, HEARING RES, V158, P139, DOI 10.1016/S0378-5955(01)00309-4 REYES SA, 1999, ABSTR ASS RES OT, V22, P95 Ricci AJ, 2000, J NEUROSCI, V20, P7131 RUBEL EW, 1992, NOISE INDUCED HEARIN, P204 SALVI RJ, 1992, J COMP PHYSIOL A, V170, P227 SALVI RJ, 1994, J COMP PHYSIOL A, V174, P351 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 SAUNDERS SS, 1993, J ACOUST SOC AM, V94, P83, DOI 10.1121/1.406945 Sun W, 2000, HEARING RES, V150, P137, DOI 10.1016/S0378-5955(00)00195-7 Trautwein P, 1996, HEARING RES, V96, P71, DOI 10.1016/0378-5955(96)00040-8 Trautwein P, 1996, Audiol Neurootol, V1, P86 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 XUE SW, 1995, J ACOUST SOC AM, V97, P3030, DOI 10.1121/1.413103 NR 45 TC 11 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 54 EP 64 DI 10.1016/S0378-5955(01)00353-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100007 PM 11744281 ER PT J AU Coppens, AG Kiss, R Heizmann, CW Deltenre, P Poncelet, L AF Coppens, AG Kiss, R Heizmann, CW Deltenre, P Poncelet, L TI An original inner ear neuroepithelial degeneration in a deaf Rottweiler puppy SO HEARING RESEARCH LA English DT Article DE puppy; deafness; neuroepithelial degeneration; neuron; immunohistochemistry ID CALCIUM-BINDING PROTEINS; DALMATIAN DOG AB Histopathological investigation was conducted on both inner cars from a 4.5-month-old Rottweiler puppy with electrophysiologically confirmed bilateral deafness. The lesions were restricted to the organ of Corti and spiral ganglion that both displayed severe degenerative changes. The outer hair cells were less affected than the inner hair cells. The number of spiral ganglion neurons was reduced, and remaining neurons were altered. The basal and middle cochlear turns were more affected than the apical one. The vestibules were normal. Immunostaining with calbindin, calretinin, S100A1 and S100A6 polyclonal antisera was helpful in identifying different cell-types in the degenerated cochlea. The early and severe spiral ganglion cell degeneration is an uncommon finding no matter the species. Such lesions bear significance within the frame of cochlear implants technology for deaf infants. (C) 2001 Published by Elsevier Science B.V. C1 Free Univ Brussels, Fac Med, Dept Anat & Embryol, Lab Vet Anat, B-1070 Brussels, Belgium. Free Univ Brussels, Fac Med, Lab Histopathol, B-1070 Brussels, Belgium. Free Univ Brussels, Hop Univ Brugmann, B-1020 Brussels, Belgium. Univ Zurich, Dept Pediat, Div Clin Chem, Zurich, Switzerland. RP Coppens, AG (reprint author), Free Univ Brussels, Fac Med, Dept Anat & Embryol, Lab Vet Anat, 808 Lennik St, B-1070 Brussels, Belgium. CR ADAMS EW, 1956, J AM VET MED ASSOC, V15, P302 ALTMANN LD, 1950, ARCH OTOLARYNGOL, V51, P852 ANDRESSEN C, 1993, CELL TISSUE RES, V271, P181, DOI 10.1007/BF00318606 ANNIKO M, 1980, ACTA PATH MICRO IM A, V88, P19 ANNIKO M, 1977, OTORHINOLARYNGOL, V218, P1 BRANIS M, 1985, J COMP PATHOL, V95, P295, DOI 10.1016/0021-9975(85)90016-7 Coppens AG, 2000, HEARING RES, V145, P101, DOI 10.1016/S0378-5955(00)00077-0 Coppens AG, 2000, J COMP PATHOL, V122, P223, DOI 10.1053/jcpa.1999.0360 Coppens AG, 2001, DEV BRAIN RES, V126, P191, DOI 10.1016/S0165-3806(00)00153-X ERNFORS P, 1995, NEURON, V14, P1153, DOI 10.1016/0896-6273(95)90263-5 FAMULA T, 2000, AM J VET RES, V5, P550 Famula TR, 1996, MAMM GENOME, V7, P650, DOI 10.1007/s003359900199 FOSS I, 1968, J ULTRA MOL STRUCT R, V25, P162 Fraser J S, 1924, Proc R Soc Med, V17, P29 GWIN M, 1981, J AM ANIM HOSP ASSOC, V17, P402 Heizmann CW, 1998, BIOMETALS, V11, P383, DOI 10.1023/A:1009212521172 HIRAIDE F, 1988, Auris Nasus Larynx, V15, P97 IGARASHI M, 1972, ANN OTO RHINOL LARYN, V81, P249 Ilg EC, 1996, INT J CANCER, V68, P325, DOI 10.1002/(SICI)1097-0215(19961104)68:3<325::AID-IJC10>3.0.CO;2-7 JOHNSSON LG, 1972, VASCULAR DISORDERS H, P249 LURIE MH, 1948, LARYNGOSCOPE, V58, P279, DOI 10.1288/00005537-194804000-00001 MAIR IWS, 1976, ARCH OTO-RHINO-LARYN, V212, P1, DOI 10.1007/BF00456358 MOTOHASHI H, 1994, HEARING RES, V80, P10, DOI 10.1016/0378-5955(94)90003-5 NIPARKO JK, 1993, ANN OTO RHINOL LARYN, V102, P447 Poncelet L, 1999, ANN MED VET, V143, P41 Poncelet LC, 2000, AM J VET RES, V61, P1343, DOI 10.2460/ajvr.2000.61.1343 Rawitz B., 1896, MORPHOL ARBEIT, V6, P545 SCHIMMANG T, 1995, DEVELOPMENT, V121, P3381 STEEL KP, 1983, ARCH OTOLARYNGOL, V109, P22 Strain GM, 1996, BRIT VET J, V152, P17, DOI 10.1016/S0007-1935(96)80083-2 SUGA F, 1970, LARYNGOSCOPE, V80, P80, DOI 10.1288/00005537-197001000-00007 TANDLER J, 1905, ARCH OHRENHEILKD, V66, P161 WILKES MK, 1992, J SMALL ANIM PRACT, V33, P218, DOI 10.1111/j.1748-5827.1992.tb01120.x NR 33 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 65 EP 71 DI 10.1016/S0378-5955(01)00354-9 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100008 PM 11744282 ER PT J AU Tan, CT Hsu, CJ Lee, SY Liu, SH Lin-Shiau, SY AF Tan, CT Hsu, CJ Lee, SY Liu, SH Lin-Shiau, SY TI Potentiation of noise-induced hearing loss by amikacin in guinea pigs SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; noise; amikacin; outer hair cell; guinea pig ID OUTER HAIR-CELLS; AMINOGLYCOSIDE-INDUCED OTOTOXICITY; STIMULATED ACOUSTIC EMISSIONS; PRODUCT OTOACOUSTIC EMISSIONS; POLYAMINE-LIKE ACTIONS; FREE-RADICAL FORMATION; D-ASPARTATE RECEPTORS; NEUROTROPHIC FACTOR; AUDITORY NEURONS; THRESHOLD SHIFTS AB Noise and aminoglycosides initially attack cochlear outer hair cells (OHCs). Distortion product otoacoustic emissions (DPOAEs) are used for the early diagnosis of damage to OHCs. The effects of sub-damaging doses of amikacin, an aminoglycoside antibiotic agent, on noise-induced hearing loss (NIHL) were examined in guinea pigs. Animals were grouped by gender and exposed to broadband noise at 105 dB SPL for 12 It and/or injected i.m. with either amikacin (100 mg/kg/day) or saline for 10 days. Auditory brainstem response (ABR) thresholds, along with DPOAE amplitudes, were measured serially before and after noise exposure. DPOAE amplitudes decreased and ABR thresholds elevated immediately after noise exposure and then gradually recovered. At all frequencies, the emission amplitudes recovered completely to pre-exposure baseline values by 4 days after noise exposure. There was no effect of amikacin on either the ABR threshold or DPOAE amplitudes, in animals treated with amikacin only. However, amikacin significantly prolonged the effect of noise exposure on DPOAE amplitude but not on the noise-induced temporary threshold shift (TTS) of the ABR. In animals treated with a combination of noise and amikacin, significant changes in DPOAE amplitudes were still observed at 4 weeks after cessation of noise exposure. No gender difference in the responses to noise and/or amikacin could be demonstrated. The present findings indicate that even sub-damaging dosages of amikacin might impair recovery from NIHL in guinea pigs. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Natl Taiwan Univ, Coll Med, Inst Toxicol, Sect 1, Taipei 10043, Taiwan. Natl Taiwan Univ Hosp, Dept Otolaryngol, Taipei, Taiwan. Natl Taiwan Univ, Coll Med, Inst Pharmacol, Taipei, Taiwan. RP Lin-Shiau, SY (reprint author), Natl Taiwan Univ, Coll Med, Inst Toxicol, Sect 1, 1 Jenai Rd, Taipei 10043, Taiwan. CR AGERMAN K, 1999, COCHLEAR PHARM NOISE, P75 Attias J, 1996, J Basic Clin Physiol Pharmacol, V7, P221 Basile AS, 1996, NAT MED, V2, P1338, DOI 10.1038/nm1296-1338 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN JJ, 1978, ACTA OTO-LARYNGOL, V86, P394, DOI 10.3109/00016487809107518 Brown R D, 1985, Arch Toxicol Suppl, V8, P240 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUMMETT RE, 1992, ARCH OTOLARYNGOL, V118, P498 CANLON B, 1995, HEARING RES, V84, P112, DOI 10.1016/0378-5955(95)00020-5 Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 CODY AR, 1982, HEARING RES, V6, P199, DOI 10.1016/0378-5955(82)90054-5 CORRADO AP, 1989, ACTA PHYSIOL PHARM L, V39, P419 Duan ML, 2000, P NATL ACAD SCI USA, V97, P7597, DOI 10.1073/pnas.97.13.7597 Eddins AC, 1999, HEARING RES, V127, P119 Ernfors P, 1996, NAT MED, V2, P463, DOI 10.1038/nm0496-463 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 FECHTER LD, 1988, HEARING RES, V34, P339 GOVAERTS PJ, 1990, TOXICOL LETT, V52, P227, DOI 10.1016/0378-4274(90)90033-I Hall AJ, 1999, AUDIOLOGY, V38, P277 Harvey SC, 1999, J PHARMACOL EXP THER, V291, P285 Hester TO, 1998, OTOLARYNG HEAD NECK, V119, P581, DOI 10.1016/S0194-5998(98)70015-4 Hirose K, 1997, HEARING RES, V104, P1, DOI 10.1016/S0378-5955(96)00169-4 Hsu CJ, 2000, HEARING RES, V142, P203, DOI 10.1016/S0378-5955(00)00020-4 Huizing E H, 1987, Acta Otolaryngol Suppl, V436, P117 Jager W, 2000, EXP BRAIN RES, V134, P426, DOI 10.1007/s002210000470 JAUHIAIN.T, 1972, ACTA OTO-LARYNGOL, V73, P387, DOI 10.3109/00016487209138956 JOHNSON AC, 1990, ACTA OTO-LARYNGOL, V109, P34, DOI 10.3109/00016489009107412 JOHNSON AC, 1988, ACTA OTO-LARYNGOL, V105, P56, DOI 10.3109/00016488809119446 Kakigi A, 1998, AUDIOL NEURO-OTOL, V3, P361, DOI 10.1159/000013806 Keithley EM, 1998, NEUROREPORT, V9, P2183, DOI 10.1097/00001756-199807130-00007 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Lataye R, 1997, NEUROTOXICOL TERATOL, V19, P373, DOI 10.1016/S0892-0362(97)00049-4 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 LIU Z, 1992, CHIN J OTORHINOLARYN, V27, P24 Lopez-Gonzalez MA, 1999, HEARING RES, V136, P165, DOI 10.1016/S0378-5955(99)00122-7 Masuko T, 1999, J PHARMACOL EXP THER, V290, P1026 MAURER J, 1993, ORL J OTO-RHINO-LARY, V55, P7 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 Mills CD, 1999, HEARING RES, V128, P75, DOI 10.1016/S0378-5955(98)00190-7 MORATA TC, 1993, SCAND J WORK ENV HEA, V19, P245 Ohinata Y, 2000, HEARING RES, V146, P28, DOI 10.1016/S0378-5955(00)00096-4 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 PUEL JL, 1988, HEARING RES, V37, P65, DOI 10.1016/0378-5955(88)90078-0 QUIRK WS, 1994, HEARING RES, V74, P217, DOI 10.1016/0378-5955(94)90189-9 Ruan RS, 1999, NEUROREPORT, V10, P2067, DOI 10.1097/00001756-199907130-00014 SCHACHT J, 1993, OTOLARYNG CLIN N AM, V26, P845 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 Segal JA, 1999, BRAIN RES, V815, P270, DOI 10.1016/S0006-8993(98)01123-8 Segal JA, 1998, EUR J PHARMACOL, V347, P311, DOI 10.1016/S0014-2999(98)00108-3 Sha SH, 1999, HEARING RES, V128, P112, DOI 10.1016/S0378-5955(98)00200-7 Sha SH, 2000, HEARING RES, V142, P34, DOI 10.1016/S0378-5955(00)00003-4 Shi Yong-Bing, 1997, Journal of Basic and Clinical Physiology and Pharmacology, V8, P141 Shoji F, 2000, HEARING RES, V146, P134, DOI 10.1016/S0378-5955(00)00106-4 Shoji F, 2000, HEARING RES, V142, P41, DOI 10.1016/S0378-5955(00)00007-1 SMITH DW, 1994, BRAIN RES, V652, P243, DOI 10.1016/0006-8993(94)90233-X Staecker H, 1996, NEUROREPORT, V7, P889, DOI 10.1097/00001756-199603220-00011 SUTTON LA, 1994, HEARING RES, V75, P161, DOI 10.1016/0378-5955(94)90067-1 Tan CT, 2001, HEARING RES, V154, P81, DOI 10.1016/S0378-5955(01)00222-2 Wang ZM, 2000, NEUROREPORT, V11, P1389, DOI 10.1097/00001756-200005150-00008 Yagi M, 1999, HUM GENE THER, V10, P813, DOI 10.1089/10430349950018562 Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 YOUNG JS, 1987, HEARING RES, V26, P37, DOI 10.1016/0378-5955(87)90034-7 NR 64 TC 14 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 72 EP 80 DI 10.1016/S0378-5955(01)00359-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100009 PM 11744283 ER PT J AU Poth, EA Boettcher, FA Mills, JH Dubno, JR AF Poth, EA Boettcher, FA Mills, JH Dubno, JR TI Auditory brainstem responses in younger and older adults for broadband noises separated by a silent gap SO HEARING RESEARCH LA English DT Article DE aging; presbyacusis; evoked potential; auditory brainstem response; gap detection ID SENSORINEURAL HEARING-LOSS; LISTENERS; DISCRIMINATION; FREQUENCY; DURATION; RECOVERY; MASKING; MOUSE AB Wave V of the auditory brainstem response was measured to two 50-ms broadband noise bursts separated by silent gaps of varied duration (4, 8. 32, or 64 ms) for younger and older adults with normal hearing. All subjects had measurable wave V responses to the first noise burst. However, for the second noise burst. three of eight older adults did not have responses with gap durations of 4 and 8 ms. and one of eight younger adults did not have a measurable response with a gap duration of 4 ins. When responses were present for older adults, latencies were similar to those of younger subjects but amplitudes were smaller. These results suggest age-related deficits in gap detection at the level of the brainstem in a group of aged subjects with no threshold elevation. Results are similar to those of Boettcher et al. (1996) using an identical paradigm in young and aged Mongolian gerbils. (C) 2001 Elsevier Science BN. All rights reserved. C1 Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Charleston, SC 29425 USA. RP Poth, EA (reprint author), Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, 39 Sabin St,POB 250150, Charleston, SC 29425 USA. CR American National Standards Institute, 1996, S361996 ANSI Boettcher FA, 1996, HEARING RES, V102, P167, DOI 10.1016/S0378-5955(96)90016-7 DUBNO JR, 2001, UNPUB J ACOUST SOC A FITZGIBBONS PJ, 1994, J SPEECH HEAR RES, V37, P662 FITZGIBBONS PJ, 1982, J ACOUST SOC AM, V72, P761, DOI 10.1121/1.388256 FITZGIBBONS PJ, 1987, J ACOUST SOC AM, V81, P133, DOI 10.1121/1.395022 FLORENTINE M, 1984, J SPEECH HEAR RES, V27, P449 GLASBERG BR, 1987, J ACOUST SOC AM, V81, P1546, DOI 10.1121/1.394507 He NJ, 1999, J ACOUST SOC AM, V106, P966, DOI 10.1121/1.427109 He NJ, 1998, J ACOUST SOC AM, V103, P553, DOI 10.1121/1.421127 LUTMAN ME, 1991, ACTA OTOLARYNGOLOG S, V476, P120 MOORE BCJ, 1992, J ACOUST SOC AM, V92, P1923, DOI 10.1121/1.405240 Phillips S L, 1994, J Am Acad Audiol, V5, P210 Schneider BA, 1999, J ACOUST SOC AM, V106, P371, DOI 10.1121/1.427062 SCHNEIDER BA, 1994, J ACOUST SOC AM, V95, P980, DOI 10.1121/1.408403 Snell KB, 1997, J ACOUST SOC AM, V101, P2214, DOI 10.1121/1.418205 Strouse A, 1998, J ACOUST SOC AM, V104, P2385, DOI 10.1121/1.423748 Walton J, 1999, HEARING RES, V127, P86, DOI 10.1016/S0378-5955(98)00175-0 WALTON JP, 1995, HEARING RES, V88, P19, DOI 10.1016/0378-5955(95)00093-J Walton JP, 1998, J NEUROSCI, V18, P2764 NR 20 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 81 EP 86 DI 10.1016/S0378-5955(01)00352-5 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100010 PM 11744284 ER PT J AU Hansen, MR Vijapurkar, U Koland, JG Green, SH AF Hansen, MR Vijapurkar, U Koland, JG Green, SH TI Reciprocal signaling between spiral ganglion neurons and Schwann cells involves neuregulin and neurotrophins SO HEARING RESEARCH LA English DT Article DE Schwann cell; cell survival; spiral ganglion neuron; cell proliferation; neuregulin; neurotrophin ID NERVE GROWTH-FACTOR; NEU DIFFERENTIATION FACTOR; MESSENGER-RNA EXPRESSION; ACTIVATED PROTEIN-KINASE; PERIPHERAL-NERVE; FACTOR-BETA; TRANSFORMING GROWTH-FACTOR-BETA-1; PHOSPHATIDYLINOSITOL 3-KINASE; HIPPOCAMPAL-NEURONS; CARDIAC DEVELOPMENT AB To investigate the role of neuron-glial cell interactions in the auditory nerve, we asked whether spiral ganglion neurons (SGNs) express neuregulin and whether neuregulin regulates proliferation and/or neurotrophin expression in spiral ganglion Schwann cells (SGSCs). Using immunocytochemistry we found that type I and type II SGNs express neuregulin in vivo and in vitro. Cultured SGSCs express the neuregulin receptors ErbB2 and ErbB3, but not ErbB4, Neuregulin activates ErbB2 and ErbB3 in cultured SGSCs, evidenced by increased tyrosine phosphorylation of the receptors following neuregulin treatment. Neuregulin treatment increased the proliferation rate of cultured SGSCs by 2.5-fold. Fibroblast growth factor-2 (FGF-22) and transforming growth factor beta (TGF-beta) also increased SGSC proliferation. The mitogenic effect of neuregulin and FGF-2 was blocked by inhibition of mitogen-activated protein kinase signaling but not by inhibition of phosphatidylinositol-3'-OH kinase. Using RT-PCR, we found that cultured SGSCs express neurotrophins. including brain-derived neurotrophic factor and neurotrophin-3 (NT-3), raising the possibility that SGSCs contribute to the trophic support of SGNs. Treatment with neither neuregulin nor TGF-P increased neurotrophin expression in cultured SGSCs, as had been observed in developing sympathetic ganglia, but appeared to negatively regulate NT-3 expression. Thus, neuregulin and neurotrophins may mediate reciprocal neuron-glial interactions in the auditory nerve. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Iowa, Dept Otolaryngol Head & Neck Surg, Iowa City, IA 52242 USA. Univ Iowa, Dept Pharmacol, Iowa City, IA 52242 USA. Univ Iowa, Dept Sci Biol, Iowa City, IA 52242 USA. RP Green, SH (reprint author), Univ Iowa, Dept Otolaryngol Head & Neck Surg, Iowa City, IA 52242 USA. CR Adlkofer K, 2000, GLIA, V29, P104, DOI 10.1002/(SICI)1098-1136(20000115)29:2<104::AID-GLIA2>3.0.CO;2-2 ARCARO A, 1993, BIOCHEM J, V296, P297 AVILA MA, 1993, DEV BIOL, V159, P266, DOI 10.1006/dbio.1993.1239 BICHLER E, 1983, ARCH OTO-RHINO-LARYN, V237, P201, DOI 10.1007/BF00453725 Black IB, 1999, J NEUROBIOL, V41, P108, DOI 10.1002/(SICI)1097-4695(199910)41:1<108::AID-NEU14>3.0.CO;2-U BLOCHL A, 1995, EUR J NEUROSCI, V7, P1220, DOI 10.1111/j.1460-9568.1995.tb01112.x BROCKES JP, 1986, ANN NEUROL, V20, P317, DOI 10.1002/ana.410200308 Burden S, 1997, NEURON, V18, P847, DOI 10.1016/S0896-6273(00)80324-4 Busfield SJ, 1997, MOL CELL BIOL, V17, P4007 Cai F, 1999, MOL BRAIN RES, V71, P256, DOI 10.1016/S0169-328X(99)00200-4 Carraway KL, 1997, NATURE, V387, P512, DOI 10.1038/387512a0 Chang H, 1997, NATURE, V387, P509, DOI 10.1038/387509a0 CHEN JK, 1991, J NEUROSCI RES, V30, P321, DOI 10.1002/jnr.490300207 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 Davies AM, 1998, CURR BIOL, V8, pR15, DOI 10.1016/S0960-9822(98)70009-0 DAVIES AM, 1995, CURR BIOL, V5, P723, DOI 10.1016/S0960-9822(95)00144-8 DONG Z, 1995, NEURON, V15, P585, DOI 10.1016/0896-6273(95)90147-7 ECCLESTON PA, 1989, J NEUROSCI RES, V24, P524, DOI 10.1002/jnr.490240410 EINHEBER S, 1995, J CELL BIOL, V129, P443, DOI 10.1083/jcb.129.2.443 Erickson SL, 1997, DEVELOPMENT, V124, P4999 ERNFORS P, 1995, NEURON, V14, P1153, DOI 10.1016/0896-6273(95)90263-5 FARINAS I, 1994, NATURE, V369, P658, DOI 10.1038/369658a0 FAWCETT JW, 1990, ANNU REV NEUROSCI, V13, P43, DOI 10.1146/annurev.neuro.13.1.43 Fischbach GD, 1997, ANNU REV NEUROSCI, V20, P429, DOI 10.1146/annurev.neuro.20.1.429 Fritzsch B, 1997, TRENDS NEUROSCI, V20, P159, DOI 10.1016/S0166-2236(96)01007-7 Fritzsch B, 1997, J NEUROSCI, V17, P6213 Grinspan JB, 1996, J NEUROSCI, V16, P6107 GUENARD V, 1992, J NEUROSCI, V12, P3310 HALL SM, 1978, NEUROPATH APPL NEURO, V4, P117, DOI 10.1111/j.1365-2990.1978.tb00552.x Hansen MR, 2001, J NEUROSCI, V21, P2256 Harari D, 1999, ONCOGENE, V18, P2681, DOI 10.1038/sj.onc.1202631 Hegarty JL, 1997, J NEUROSCI, V17, P1959 KIM HH, 1994, J BIOL CHEM, V269, P24747 KOITCHEV K, 1982, ACTA OTO-LARYNGOL, V94, P431, DOI 10.3109/00016488209128931 Kramer R, 1996, P NATL ACAD SCI USA, V93, P4833, DOI 10.1073/pnas.93.10.4833 KRASNOSELSKY A, 1994, J NEUROSCI, V14, P7284 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEE KF, 1995, NATURE, V378, P394, DOI 10.1038/378394a0 LEFEBVRE PP, 1992, NEUROREPORT, V3, P295, DOI 10.1097/00001756-199204000-00001 LEINGARTNER A, 1994, EUR J NEUROSCI, V6, P1149, DOI 10.1111/j.1460-9568.1994.tb00613.x Lemke G, 1996, MOL CELL NEUROSCI, V7, P247, DOI 10.1006/mcne.1996.0019 LEVI ADO, 1995, J NEUROSCI, V15, P1329 Lewin GR, 1996, ANNU REV NEUROSCI, V19, P289, DOI 10.1146/annurev.ne.19.030196.001445 Loeb JA, 1998, MOL CELL NEUROSCI, V11, P77, DOI 10.1006/mcne.1998.0676 MAISONPIERRE PC, 1991, GENOMICS, V10, P558, DOI 10.1016/0888-7543(91)90436-I MARCHIONNI MA, 1993, NATURE, V362, P312, DOI 10.1038/362312a0 Maurel P, 2000, J NEUROSCI, V20, P4635 MEWS M, 1993, GLIA, V8, P208, DOI 10.1002/glia.440080308 MEYER D, 1995, NATURE, V378, P386, DOI 10.1038/378386a0 Mirsky R, 1996, CURR OPIN NEUROBIOL, V6, P89, DOI 10.1016/S0959-4388(96)80013-4 MORGAN L, 1994, DEVELOPMENT, V120, P1399 Morris JK, 1999, NEURON, V23, P273, DOI 10.1016/S0896-6273(00)80779-5 NADIM W, 1990, NEUROPATH APPL NEURO, V16, P411, DOI 10.1111/j.1365-2990.1990.tb01277.x Oka N, 2000, NEUROREPORT, V11, P3673, DOI 10.1097/00001756-200011270-00017 PANG L, 1995, J BIOL CHEM, V270, P13585 PAWSON T, 1995, NATURE, V373, P573, DOI 10.1038/373573a0 PELLEGRINO RG, 1986, J NEUROCYTOL, V15, P17, DOI 10.1007/BF02057901 PinkasKramarski R, 1996, J BIOL CHEM, V271, P19029 PIRVOLA U, 1994, HEARING RES, V75, P131, DOI 10.1016/0378-5955(94)90064-7 Rameh LE, 1999, J BIOL CHEM, V274, P8347, DOI 10.1074/jbc.274.13.8347 Riethmacher D, 1997, NATURE, V389, P725, DOI 10.1038/39593 ROGISTER B, 1993, J NEUROSCI RES, V34, P32, DOI 10.1002/jnr.490340105 ROMAND R, 1985, HEARING RES, V18, P111, DOI 10.1016/0378-5955(85)90002-4 SCHERER SS, 1993, GLIA, V8, P265, DOI 10.1002/glia.440080407 Schlessinger J, 2000, CELL, V103, P211, DOI 10.1016/S0092-8674(00)00114-8 SHAH NM, 1994, CELL, V77, P349, DOI 10.1016/0092-8674(94)90150-3 SKETELJ J, 1989, J NEUROSCI RES, V24, P153, DOI 10.1002/jnr.490240205 SLIWKOWSKI MX, 1994, J BIOL CHEM, V269, P14661 SPOENDLIN H, 1985, AM J OTOLARYNG, V6, P453, DOI 10.1016/S0196-0709(85)80026-0 Svenningsen AF, 1996, GLIA, V18, P68, DOI 10.1002/(SICI)1098-1136(199609)18:1<68::AID-GLIA7>3.0.CO;2-# Syroid DE, 1996, P NATL ACAD SCI USA, V93, P9229, DOI 10.1073/pnas.93.17.9229 Timmusk T, 1999, J BIOL CHEM, V274, P1078 TIMMUSK T, 1995, J CELL BIOL, V128, P185, DOI 10.1083/jcb.128.1.185 TIMMUSK T, 1993, NEURON, V10, P475, DOI 10.1016/0896-6273(93)90335-O Trachtenberg JT, 1996, NATURE, V379, P174, DOI 10.1038/379174a0 Vartanian T, 1997, J CELL BIOL, V137, P211, DOI 10.1083/jcb.137.1.211 VAYSSE PJJ, 1990, NEURON, V5, P227, DOI 10.1016/0896-6273(90)90160-H VAZQUEZ E, 1994, ANAT EMBRYOL, V189, P157 Verdi JM, 1996, NEURON, V16, P515, DOI 10.1016/S0896-6273(00)80071-9 Vijapurkar U, 1998, J BIOL CHEM, V273, P20996, DOI 10.1074/jbc.273.33.20996 VLAHOS CJ, 1994, J BIOL CHEM, V269, P5241 WATABE K, 1994, J NEUROSCI RES, V39, P525, DOI 10.1002/jnr.490390504 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 Widmann C, 1999, PHYSIOL REV, V79, P143 Wiechers B, 1999, J NEUROSCI, V19, P3033 Woldeyesus MT, 1999, GENE DEV, V13, P2538, DOI 10.1101/gad.13.19.2538 Wolpowitz D, 2000, NEURON, V25, P79, DOI 10.1016/S0896-6273(00)80873-9 YAO RJ, 1995, SCIENCE, V267, P2003, DOI 10.1126/science.7701324 Zha XM, 2001, HEARING RES, V156, P53, DOI 10.1016/S0378-5955(01)00267-2 Zhang DX, 1997, P NATL ACAD SCI USA, V94, P9562, DOI 10.1073/pnas.94.18.9562 Zheng JL, 1999, J NEUROCYTOL, V28, P901, DOI 10.1023/A:1007078307638 ZHENG JL, 1995, J NEUROSCI, V15, P5079 Zhu Y, 2000, BRAIN RES, V866, P286, DOI 10.1016/S0006-8993(00)02240-X NR 93 TC 54 Z9 56 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 87 EP 98 DI 10.1016/S0378-5955(01)00360-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100011 PM 11744285 ER PT J AU Kirk, DL AF Kirk, DL TI Effects of 4-aminopyridine on electrically evoked cochlear emissions and mechano-transduction in guinea pig outer hair cells SO HEARING RESEARCH LA English DT Article DE oto-acoustic emission; 4-aminopyridine; mechano-receptor; electro-motility ID LOW-FREQUENCY TONES; BASILAR-MEMBRANE MOTION; OTOACOUSTIC EMISSIONS; ACOUSTIC ENHANCEMENT; SCALA MEDIA; MECHANOELECTRICAL TRANSDUCTION; MECHANICAL RESPONSES; MOTOR PROTEIN; POTENTIALS; ATP AB Stimulation of the cochlea with alternating current produces sound in the ear canal. These electrically evoked oto-acoustic emissions (EEOAEs) are attributed to elect ro-motility of outer hair cells (OHCs). Earlier work suggested EEOAEs were sensitive to the open probability of OHC mechano-electrical transduction (MET) channels. They were attenuated by 4-aminopyridine (4-AP) and amplitude-modulated by low frequency sound, consistent with current gaining access to a motility source via the MET conductance, However, inconsistencies in the behaviour as well as physical considerations argued against this simple interpretation. In this study the behaviour of EEOAEs in the presence of 4-AP in scala media was examined along with OHC transfer functions derived from low frequency cochlear microphonic (CM) waveforms. Both the level and the modulation of the EEOAEs were reduced by 4-AP. but disproportionately more so than the 4-AP-induced loss of CM. In addition, the modulation as well as the level of the EEOAEs recovered more rapidly than the CM. Both these results indicated that 4-AP modified the process of EEOAE generation independently of its effect on the gross receptor current through the MET conductance. Changes in the derived OHC transfer functions, specifically shifts in the estimated operating bias of the MET channels. indicated the effects or 4-AP applied to the endolymphatic surface of OHCs were complex. It is suggested that both direct and indirect consequences of a 4-AP blockade may have contributed. 4-AP was ineffective A hen applied to scala tympani. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6097, Australia. RP Kirk, DL (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6097, Australia. EM dlkirk@cyllene.uwa.edu.au CR ALBERT AE, 1993, PHYSICAL METHODS HET, V1, P2 Bian L, 2001, J ACOUST SOC AM, V109, P671, DOI 10.1121/1.1340644 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Cole K. S., 1940, Cold Spring Harbor Symposia on Quantitative Biology, V8, P110 DALLOS P, 1992, J NEUROSCI, V12, P4575 Dallos P, 1997, J NEUROSCI, V17, P2212 DALLOS P, 1995, SCIENCE, V267, P2006, DOI 10.1126/science.7701325 DENK W, 1992, J NEUROPHYSIOL, V68, P927 Frolenkov GI, 2000, J NEUROSCI, V20, P5940 Glowatzki E, 1997, NEUROPHARMACOLOGY, V36, P1269, DOI 10.1016/S0028-3908(97)00108-1 HIRSH IJ, 1952, J ACOUST SOC AM, V24, P131, DOI 10.1121/1.1906867 HOLTON T, 1986, J PHYSIOL-LONDON, V375, P195 HOUSLEY GD, 1995, ACTIVE HEARING, P221 Housley GD, 1999, J NEUROSCI, V19, P8377 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 HUBBARD AE, 1990, LECT NOTES BIOMATH, V87, P186 HUBBARD AE, 1990, HEARING RES, V43, P269, DOI 10.1016/0378-5955(90)90234-G Hudspeth AJ, 1997, CURR OPIN NEUROBIOL, V7, P480, DOI 10.1016/S0959-4388(97)80026-8 KAKEHATA S, 1995, BIOPHYS J, V68, P2190 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 Kirk DL, 1997, HEARING RES, V112, P69, DOI 10.1016/S0378-5955(97)00104-4 Kirk DL, 1998, NEUROSCI LETT, V250, P149, DOI 10.1016/S0304-3940(98)00460-1 Kirk DL, 1996, J ACOUST SOC AM, V100, P3714, DOI 10.1121/1.417335 Kirk DL, 1998, AUDIOL NEURO-OTOL, V3, P21, DOI 10.1159/000013776 Kirk DL, 1998, J ACOUST SOC AM, V104, P1544, DOI 10.1121/1.424365 Kirk DL, 1997, HEARING RES, V112, P49, DOI 10.1016/S0378-5955(97)00105-6 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 Manley GA, 1997, J ACOUST SOC AM, V102, P1049, DOI 10.1121/1.419858 Manley GA, 2001, P NATL ACAD SCI USA, V98, P2826, DOI 10.1073/pnas.041604998 Martin P, 1999, P NATL ACAD SCI USA, V96, P14306, DOI 10.1073/pnas.96.25.14306 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 Mountain DC, 1983, MECHANICS HEARING, P119 MUNOZ DJB, 1995, HEARING RES, V90, P106, DOI 10.1016/0378-5955(95)00152-3 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I NAKAJIMA HH, 1994, J ACOUST SOC AM, V96, P786, DOI 10.1121/1.410316 Nakajima HH, 1996, AUDIT NEUROSCI, V3, P79 Nakajima HH, 2000, J ACOUST SOC AM, V107, P2603, DOI 10.1121/1.428647 Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 Oliver D, 2001, SCIENCE, V292, P2340, DOI 10.1126/science.1060939 OZDAMAR O, 1976, J ACOUST SOC AM, V59, P143 Patuzzi R, 1998, HEARING RES, V125, P1, DOI 10.1016/S0378-5955(98)00125-7 PATUZZI R, 1990, HEARING RES, V45, P15, DOI 10.1016/0378-5955(90)90179-S PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PATUZZI RB, 1995, ACTIVE HEARING, P141 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 Raybould NP, 1997, J PHYSIOL-LONDON, V498, P717 RODDY J, 1994, HEARING RES, V73, P148, DOI 10.1016/0378-5955(94)90229-1 RUGGERO MA, 1986, J ACOUST SOC AM, V80, P1375, DOI 10.1121/1.394390 RUSSELL IJ, 1992, P ROY SOC B-BIOL SCI, V250, P217, DOI 10.1098/rspb.1992.0152 SALT AN, 1992, EUR ARCH OTO-RHINO-L, V249, P157 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SURPRENANT A, 1995, TRENDS NEUROSCI, V18, P224, DOI 10.1016/0166-2236(95)93907-F Thorne M, 1999, LARYNGOSCOPE, V109, P1661, DOI 10.1097/00005537-199910000-00021 Thorne PR, 1996, SEMIN NEUROSCI, V8, P233, DOI 10.1006/smns.1996.0030 vanEmst MG, 1996, HEARING RES, V102, P70, DOI 10.1016/S0378-5955(96)00149-9 WANG J, 1993, HEARING RES, V68, P152 WEISS TF, 1982, HEARING RES, V7, P353, DOI 10.1016/0378-5955(82)90045-4 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 XUE SW, 1995, J ACOUST SOC AM, V97, P3030, DOI 10.1121/1.413103 XUE SW, 1993, HEARING RES, V70, P121, DOI 10.1016/0378-5955(93)90056-7 Yates GK, 1998, J NEUROSCI, V18, P1996 ZHANG M, 1997, ABSTR ASS RES OT, V20, P64 Zheng J, 2000, NATURE, V405, P149, DOI 10.1038/35012009 NR 64 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 99 EP 112 DI 10.1016/S0378-5955(01)00363-X PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100012 PM 11744286 ER PT J AU Rao, DB Moore, DR Reinke, LA Fechter, LD AF Rao, DB Moore, DR Reinke, LA Fechter, LD TI Free radical generation in the cochlea during combined exposure to noise and carbon monoxide: an electrophysiological and an EPR study SO HEARING RESEARCH LA English DT Article DE free radical; cochlea; auditory; electron paramagnetic resonance spectroscopy; alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone; spin-trap ID INDUCED HEARING-LOSS; OUTER HAIR CELL; PIG IN-VIVO; GUINEA-PIG; SUPEROXIDE-DISMUTASE; GENTAMICIN OTOTOXICITY; THRESHOLD SHIFTS; ANTIOXIDANTS; DAMAGE; POTENTIATION AB Ototoxicity following combined exposure to noise and carbon monoxide (CO) is known to result in more severe permanent threshold shifts than exposure to noise alone. We have previously demonstrated that such potentiation of noise-induced auditory impairment by CO can be prevented by the administration of a nitrone spin-trapping agent. Although such protection implicates injury via free radical pathways, drug-induced protection does not provide direct evidence for the presence of free radicals in the cochlea. The objective of this study was to demonstrate the actual presence of nitrone spin adducts in the cochlea following simultaneous exposure to noise and CO. Using electrophysiological end-points. the protective effects of the nitrone spin-trapping agent alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN) were assessed following combined exposure of adult male Long Evans hooded rats to noise and CO. In addition, an ex-vivo evaluation of POBN spin adducts was done by electron paramagnetic resonance spectroscopy (EPR). The noise used was octave band noise with center frequency 13.6 kHz at 100 dB(Lin) for a duration of 2 h. The level of CO used was 1200 ppm. Electro physiological results demonstrate that POBN protects against combined exposure to noise plus CO. The EPR study demonstrates POBN spin adducts in the cochleae of animals exposed to noise plus CO. Therefore, this study provides evidence to the hypothesis that ototoxicity due to noise plus CO exposure is mediated via free radicals. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Ctr Toxicol, Oklahoma City, OK 73190 USA. RP Rao, DB (reprint author), Univ Oklahoma, Hlth Sci Ctr, 1110 N Stonewall, Oklahoma City, OK 73117 USA. CR BUETTNER GR, 1987, FREE RADICAL BIO MED, V3, P259, DOI 10.1016/S0891-5849(87)80033-3 BURGESS WA, 1977, AM IND HYG ASSOC J, V38, P184, DOI 10.1080/0002889778507935 Chaudiere J, 1999, FOOD CHEM TOXICOL, V37, P949, DOI 10.1016/S0278-6915(99)00090-3 CHEN G, 1990, FREE RADICAL BIO MED, V8, P93 Chen GD, 1999, HEARING RES, V138, P181, DOI 10.1016/S0378-5955(99)00157-4 Chen GD, 1999, HEARING RES, V132, P149, DOI 10.1016/S0378-5955(99)00044-1 Clerici WJ, 1996, TOXICOL APPL PHARM, V136, P236, DOI 10.1006/taap.1996.0030 CLERICI WJ, 1995, HEARING RES, V84, P30, DOI 10.1016/0378-5955(95)00010-2 Conlon BJ, 1998, HEARING RES, V115, P1, DOI 10.1016/S0378-5955(97)00171-8 EATON DL, 1996, CASARETT DOULLS TOXI, P18 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 FECHTER LD, 1988, HEARING RES, V34, P39, DOI 10.1016/0378-5955(88)90049-4 Fechter LD, 2000, TOXICOL SCI, V58, P315, DOI 10.1093/toxsci/58.2.315 Floyd RA, 1999, P SOC EXP BIOL MED, V222, P236, DOI 10.1046/j.1525-1373.1999.d01-140.x Floyd RA, 1992, ANN NEUROL, V32, pS22 GARETZ SL, 1994, HEARING RES, V77, P81, DOI 10.1016/0378-5955(94)90255-0 HALLIWELL B, 1994, ENVIRON HEALTH PERSP, V102, P5, DOI 10.2307/3432205 Halliwell B, 1996, ANNU REV NUTR, V16, P33, DOI 10.1146/annurev.nutr.16.1.33 HALLIWELL B, 1984, BIOCHEM J, V219, P1 Hara A, 2000, HEARING RES, V143, P110, DOI 10.1016/S0378-5955(00)00029-0 HARA A, 1995, HEARING RES, V90, P228, DOI 10.1016/0378-5955(95)00166-3 Hester TO, 1998, OTOLARYNG HEAD NECK, V119, P581, DOI 10.1016/S0194-5998(98)70015-4 IKEDA K, 1993, ACTA OTO-LARYNGOL, V113, P137, DOI 10.3109/00016489309135781 JANKOVIC J, 1991, ANN OCCUP HYG, V35, P581, DOI 10.1093/annhyg/35.6.581 JANZEN EG, 1971, ACCOUNTS CHEM RES, V4, P31, DOI 10.1021/ar50037a005 KAYS SE, 1991, J NUTR, V121, P1869 KIRSCH JR, 1987, FASEB J, V46, P799 Knight JA, 2000, ANN CLIN LAB SCI, V30, P145 Kopke RD, 1997, AM J OTOL, V18, P559 LAI EK, 1986, ARCH BIOCHEM BIOPHYS, V244, P156, DOI 10.1016/0003-9861(86)90104-9 LANGE D G, 1990, Free Radical Biology and Medicine, V9, P97 LEVIN BC, 1987, FUND APPL TOXICOL, V9, P236, DOI 10.1016/0272-0590(87)90046-7 Liu KJ, 1999, FREE RADICAL BIO MED, V27, P82, DOI 10.1016/S0891-5849(99)00042-8 MOORE DR, 1995, MOL PHARMACOL, V47, P1224 Ohinata Y, 2000, BRAIN RES, V878, P163, DOI 10.1016/S0006-8993(00)02733-5 Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P229, DOI 10.1159/000013846 POYER JL, 1980, BIOCHEM BIOPH RES CO, V94, P1154, DOI 10.1016/0006-291X(80)90540-9 PRYOR WA, 1986, ANNU REV PHYSIOL, V48, P657 Rao D, 2000, TOXICOL APPL PHARM, V167, P125, DOI 10.1006/taap.2000.8995 REISCHL U, 1979, AM IND HYG ASSOC J, V40, P482, DOI 10.1080/15298667991429868 RYBAK LP, 1995, FUND APPL TOXICOL, V26, P293, DOI 10.1006/faat.1995.1100 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P457 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 Sha SH, 2001, HEARING RES, V155, P1, DOI 10.1016/S0378-5955(01)00224-6 Song BB, 1997, J PHARMACOL EXP THER, V282, P369 TREITMAN RD, 1980, AM IND HYG ASSOC J, V41, P796, DOI 10.1080/15298668091425662 Morley J C, 1999, Appl Occup Environ Hyg, V14, P645 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 YOUNG JS, 1987, HEARING RES, V26, P37, DOI 10.1016/0378-5955(87)90034-7 NR 50 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2001 VL 161 IS 1-2 BP 113 EP 122 DI 10.1016/S0378-5955(01)00366-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 490ZT UT WOS:000172084100013 PM 11744287 ER PT J AU Sage, CL Marcus, DC AF Sage, CL Marcus, DC TI Immunolocalization of CIC-K chloride channel in strial marginal cells and vestibular dark cells SO HEARING RESEARCH LA English DT Article DE chloride channel; Kir4.1 potassium channel; immunoblot; immunohistochemistry; stria vascularis; vestibular dark cell ID ION-TRANSPORT MECHANISMS; GERBIL INNER-EAR; RAT COCHLEA; TRANSEPITHELIAL VOLTAGE; BASOLATERAL MEMBRANE; CL COTRANSPORTER; MICE LACKING; KIDNEY; VASCULARIS; FAMILY AB Secretion of K+ into endolymph depends on a particular constellation of ion transport proteins in the apical and basolateral membranes of strial marginal cells and vestibular dark cells. One fundamental component is the large chloride conductance of the basolateral membrane, which recycles chloride taken up by the Na+-K+-Cl- cotransporter in the same membrane. Evidence has been reported recently that supports ClC-K, a channel subunit previously thought to be specific to the kidney, as being the molecular entity underlying this conductance. We have isolated protein from the gerbil kidney, stria vascularis and vestibular labyrinth and found by Western blot analysis a 60 kDa band, a 48 kDa band and 54 and 70 kDa bands, respectively, specifically labeled by ClC-K antibody. Subsequent immunohistochemical observations of the inner car tissues with a confocal microscope on fluorescently labeled tissue sections showed the staining to be restricted to the basolateral region of strial marginal cells and vestibular dark cells. The cochlear staining was distinct from the distribution of the Kir4.1 (KCNJ10) K+ channel, known to be present only in strial intermediate cells. These findings support the contention that CIC-K is an important component of the basolateral Cl- conductance that participates in K+ secretion by these epithelia. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA. RP Marcus, DC (reprint author), Kansas State Univ, Dept Anat & Physiol, 1600 Denison Ave, Manhattan, KS 66506 USA. CR Ando M, 2000, NEUROSCI LETT, V284, P171, DOI 10.1016/S0304-3940(00)01021-1 Ando M, 1999, CELL TISSUE RES, V298, P179, DOI 10.1007/s004419900066 Crouch JJ, 1997, J HISTOCHEM CYTOCHEM, V45, P773 GREFRATH SP, 1974, P NATL ACAD SCI USA, V71, P3913, DOI 10.1073/pnas.71.10.3913 Jentsch TJ, 1999, PFLUG ARCH EUR J PHY, V437, P783, DOI 10.1007/s004240050847 Kawasaki E, 2000, NEUROSCI LETT, V290, P76, DOI 10.1016/S0304-3940(00)01310-0 KIEFERLE S, 1994, P NATL ACAD SCI USA, V91, P6943, DOI 10.1073/pnas.91.15.6943 Lorenz Claudius, 1996, Proceedings of the National Academy of Sciences of the United States of America, V93, P13362, DOI 10.1073/pnas.93.23.13362 MARCUS DC, 1993, HEARING RES, V69, P124, DOI 10.1016/0378-5955(93)90100-F MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 1994, HEARING RES, V73, P101, DOI 10.1016/0378-5955(94)90287-9 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 Matsumura Y, 1999, NAT GENET, V21, P95, DOI 10.1038/5036 MCGUIRT JP, 1994, J HISTOCHEM CYTOCHEM, V42, P843 Oshima T, 1997, HEARING RES, V103, P63, DOI 10.1016/S0378-5955(96)00164-5 SASAKI S, 1994, JPN J PHYSIOL, V44, pS3 Simon DB, 1997, NAT GENET, V17, P171, DOI 10.1038/ng1097-171 Takeuchi S, 1997, HEARING RES, V113, P99, DOI 10.1016/S0378-5955(97)00134-2 TAKEUCHI S, 1995, HEARING RES, V83, P89, DOI 10.1016/0378-5955(94)00191-R Takeuchi S, 1996, J MEMBRANE BIOL, V150, P47, DOI 10.1007/s002329900029 THORNHILL WB, 1987, BIOCHEMISTRY-US, V26, P4381, DOI 10.1021/bi00388a029 Uchida S, 2000, EXP NEPHROL, V8, P361 UCHIDA S, 1993, J BIOL CHEM, V268, P3821 UCHIDA S, 1995, J CLIN INVEST, V95, P104, DOI 10.1172/JCI117626 Uchida S, 2000, AM J PHYSIOL-RENAL, V279, pF802 Vandewalle A, 1997, AM J PHYSIOL-RENAL, V272, pF678 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WANGEMANN P, 1992, HEARING RES, V62, P149, DOI 10.1016/0378-5955(92)90180-U WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 NR 29 TC 35 Z9 36 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 1 EP 9 DI 10.1016/S0378-5955(01)00308-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500001 PM 11591484 ER PT J AU Jia, XQ Nakashima, T Kadomatsu, K Muramatsu, T AF Jia, XQ Nakashima, T Kadomatsu, K Muramatsu, T TI Expression of midkine in the cochlea SO HEARING RESEARCH LA English DT Article DE midkine; cochlea; neurotrophic factor; development ID ACID-RESPONSIVE GENE; GROWTH-DIFFERENTIATION FACTOR; NEUROTROPHIC FACTOR; TERATOCARCINOMA SYSTEM; MOUSE EMBRYOGENESIS; FACTOR FAMILY; HB-GAM; PLEIOTROPHIN; MK; PRODUCT AB Midkine (MK) is one of a new family of heparin-binding growth factors involved in the regulation of growth and differentiation. We have analyzed expression of MK in the cochlea using ICR mice within 1 day from birth. The expression of MK in the cochlea was confirmed by Western blotting and immunohistochemistry. Anti-MK immunoreactivity was observed in the stria vascularis, spiral prominence, spiral ganglion, and ganglion nerve fibers. These findings suggest that MK plays a role in the development of the cochlea. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Nagoya Univ, Sch Med, Dept Otorhinolaryngol, Showa Ku, Nagoya, Aichi 4668550, Japan. Nagoya Univ, Sch Med, Dept Biochem, Showa Ku, Nagoya, Aichi 4668550, Japan. RP Nakashima, T (reprint author), Nagoya Univ, Sch Med, Dept Otorhinolaryngol, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan. RI Nakashima, Tsutomu/B-8259-2012; Kadomatsu, Kenji/G-8083-2012 OI Nakashima, Tsutomu/0000-0003-3930-9120; CR ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 ARIDOME K, 1995, JPN J CANCER RES, V86, P655 BARDE YA, 1982, EMBO J, V1, P549 BERKEMEIER LR, 1991, NEURON, V7, P875 GARVER RI, 1994, CANCER, V74, P1584, DOI 10.1002/1097-0142(19940901)74:5<1584::AID-CNCR2820740514>3.0.CO;2-V GARVER RI, 1993, AM J RESP CELL MOL, V9, P463 HALLBOOK F, 1991, NEURON, V6, P845, DOI 10.1016/0896-6273(91)90180-8 HOHN A, 1990, NATURE, V344, P339, DOI 10.1038/344339a0 IWAGAKI T, 2000, HEARING RES, V145, P78 KADOMATSU K, 1988, BIOCHEM BIOPH RES CO, V151, P1312, DOI 10.1016/S0006-291X(88)80505-9 KADOMATSU K, 1990, J CELL BIOL, V110, P607, DOI 10.1083/jcb.110.3.607 Kaneda N, 1996, J BIOCHEM-TOKYO, V119, P1150 Kojima S, 1997, J BIOL CHEM, V272, P9410 KOJIMA S, 1995, J BIOL CHEM, V270, P9590 LEVIMONTALCINI R, 1987, SCIENCE, V237, P149 LIM DJ, 1985, ACTA OTOLARYNGOL S, V422, P3 MATSUMOTO K, 1994, DEV BRAIN RES, V79, P229, DOI 10.1016/0165-3806(94)90127-9 MICHIKAWA M, 1993, J NEUROSCI RES, V35, P530, DOI 10.1002/jnr.490350509 MITSIADIS TA, 1995, DEVELOPMENT, V121, P37 Miyashiro M, 1998, CURR EYE RES, V17, P9, DOI 10.1076/ceyr.17.1.9.5257 Moriguchi M, 1991, Acta Otolaryngol Suppl, V486, P32 MURAMATSU H, 1993, DEV BIOL, V159, P392, DOI 10.1006/dbio.1993.1250 MURAMATSU T, 1993, INT J DEV BIOL, V37, P183 NAKAGAWARA A, 1995, CANCER RES, V55, P1792 OBrien T, 1996, CANCER RES, V56, P2515 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 SWANSON GJ, 1990, DEV BIOL, V137, P243, DOI 10.1016/0012-1606(90)90251-D TAKE M, 1994, J BIOCHEM-TOKYO, V116, P1063 TOMOMURA M, 1990, BIOCHEM BIOPH RES CO, V171, P603, DOI 10.1016/0006-291X(90)91189-Y TOMOMURA M, 1990, J BIOL CHEM, V265, P10765 Unoki Kazuhiko, 1995, Nippon Ganka Gakkai Zasshi, V99, P636 VANDEWATER TR, 1984, ANN OTO RHINOL LARYN, V95, P558 YASUHARA O, 1993, BIOCHEM BIOPH RES CO, V192, P246, DOI 10.1006/bbrc.1993.1406 YOSHIDA Y, 1995, DEV BRAIN RES, V85, P25, DOI 10.1016/0165-3806(94)00183-Z NR 34 TC 3 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 10 EP 14 DI 10.1016/S0378-5955(01)00313-6 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500002 PM 11591485 ER PT J AU Kammen-Jolly, K Ichiki, H Scholtz, AW Gsenger, M Kreczy, A Schrott-Fischer, A AF Kammen-Jolly, K Ichiki, H Scholtz, AW Gsenger, M Kreczy, A Schrott-Fischer, A TI Connexin 26 in human fetal development of the inner ear SO HEARING RESEARCH LA English DT Article DE gap junction; connexin 26; human development; inner ear; immunocytochemistry ID GAP-JUNCTION PROTEINS; RAT COCHLEA; ULTRASTRUCTURAL ANALYSIS; POTASSIUM-FREE; 26 MUTATIONS; EXPRESSION; CELLS; PERFUSION; DEAFNESS; TISSUES AB Specialized for intercellular communication, gap junctions have been theorized to provide a means (the epithelial and connective tissue gap junction systems) by which fluid and ions might be transported for maintenance of high levels of endolymphatic K+ [Kikuchi et al., 1994. Acta Otolaryngol. 114, 520-528] in the inner ear. A primary constituent of these gap junctions is connexin 26 (Cx26), a protein encoded by the gene GJB2 and found in both epithelial and connective tissue cells. It has been shown that a mutation in Cx26 accounts for 50% of patients with autosomal recessive nonsyndromic hearing loss. In the present study, we document the emergence and distribution features of Cx26 through various stages (weeks 11-31) of gestation in human, fetal cochleae. Comparative patterns of Cx26 distribution are also presented in the mature rat. The cochleae were fixed in 4% paraformaldehyde within 2 h postmortem. Immunohistochemical studies were performed using a rabbit polyclonal antibody raised against synthetic peptide and corresponding with amino acids 108-122. Specimens were mounted into paraffin sections. Results show that Cx26-like immuno reactivity is evident at a prenatal age of 11 weeks and maintains a high intensity of reactivity through 31 weeks of gestation. The appearance of this reactivity seemed to modulate in parallel with the onset of development and histological maturation as well as provide functional maintenance. In the human fetal cochlea, Cx26-like immunoreactivity distribution resembled adult patterns by fetal week 20. At the completion of morphological development by week 31, reactivity appeared to achieve an adult profile of distribution. Descriptions and discussion of Cx26 distribution patterns are presented in detail. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Innsbruck, Dept Otolaryngol, A-6020 Innsbruck, Austria. Univ Innsbruck, Dept Pathol, A-6020 Innsbruck, Austria. Univ Innsbruck, Dept Psychiat, A-6020 Innsbruck, Austria. Self Def Forces Cent Hosp, Tokyo, Japan. RP Schrott-Fischer, A (reprint author), Univ Innsbruck, Dept Otolaryngol, Anichstr 35, A-6020 Innsbruck, Austria. EM annelies.schrott@uibk.ac.at CR BUTTERWECK A, 1994, J MEMBRANE BIOL, V141, P247 Carrasquillo MM, 1997, HUM MOL GENET, V6, P2163, DOI 10.1093/hmg/6.12.2163 COCAPRADOS M, 1992, CURR EYE RES, V11, P113, DOI 10.3109/02713689209000061 DERMIETZEL R, 1990, ANAT EMBRYOL, V182, P517 DERMIETZEL R, 1989, P NATL ACAD SCI USA, V86, P10148, DOI 10.1073/pnas.86.24.10148 Forge A, 1999, NOVART FDN SYMP, V219, P134 GOLIGER JA, 1994, DEV DYNAM, V200, P1 GULLEY RL, 1976, J NEUROCYTOL, V5, P479, DOI 10.1007/BF01181652 Jahnke K, 1975, Acta Otolaryngol Suppl, V336, P1 Jun AI, 2000, LARYNGOSCOPE, V110, P269, DOI 10.1097/00005537-200002010-00016 Kelsell DP, 1997, NATURE, V387, P80, DOI 10.1038/387080a0 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KIKUCHI T, 1994, ACTA OTO-LARYNGOL, V114, P520, DOI 10.3109/00016489409126097 KONISHI T, 1976, ACTA OTO-LARYNGOL, V476, P410 Kumar N M, 1992, Semin Cell Biol, V3, P3 Lautermann J, 1999, DEV GENET, V25, P306, DOI 10.1002/(SICI)1520-6408(1999)25:4<306::AID-DVG4>3.0.CO;2-R Lautermann J, 1998, CELL TISSUE RES, V294, P415, DOI 10.1007/s004410051192 MARCUS DC, 1981, HEARING RES, V4, P149, DOI 10.1016/0378-5955(81)90002-2 PUJOL R, 1995, INT J PEDIATR OTORHI, V32, pS177, DOI 10.1016/0165-5876(94)01156-R PUJOL R, 1990, SEMIN PERINATOL, V14, P275 RISEK B, 1992, DEVELOPMENT, V116, P639 SANTOS-SACCHI J, 1983, HEARING RES, V9, P317, DOI 10.1016/0378-5955(83)90034-5 STEINBERG TH, 1994, EMBO J, V13, P744 TRAUB O, 1994, EUR J CELL BIOL, V64, P101 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 Xia AP, 1999, BRAIN RES, V846, P106, DOI 10.1016/S0006-8993(99)01996-4 ZIDANIC M, 1990, BIOPHYS J, V57, P1253 NR 27 TC 16 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 15 EP 21 DI 10.1016/S0378-5955(01)00310-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500003 PM 11591486 ER PT J AU Werner, YL Igic, PG Saunders, JC AF Werner, YL Igic, PG Saunders, JC TI Effects of surgery and other experimental factors on the evaluation of middle ear function in gekkonoid lizards SO HEARING RESEARCH LA English DT Article DE lizard; gecko; middle ear function; method; posture; surgery ID GECKO; SIZE AB This study examines three artificial factors likely to cause variation between results from different investigations of auditory function, at least in lizards. Controlled tests were performed on gecko lizards, by external laser interferometry of the middle ear transfer function at the tympanic membrane (TM). In conclusion, studies of middle ear function should examine motion both at the insertion of the columella-extracolumella shaft onto the TM, and at the tip of the extracolumellar pars inferior, because the internal proportions and function of the extracolumellar lever vary among species. At least in scansorial geckos, auditory experiments may be conducted with the animal on its back, as this posture introduces no acoustic artifacts. Positioning the subject on its belly, with the throat resting on the substrate, imposes small but significant artifacts on middle ear function. Similar artifacts occur with the belly up but the throat loaded with a modeling clay plate. The surgical fenestration of the ventral throat wall, common in auditory studies on lizards, causes (at least in Eublepharis) artificial enhancement of sensitivity at low frequencies and erratic responses at high frequencies. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Penn, Dept Otolaryngol Head & Neck Surg, Philadelphia, PA 19104 USA. Univ Chicago, Pritzker Sch Med, Chicago, IL 60637 USA. RP Werner, YL (reprint author), Hebrew Univ Jerusalem, Dept Evolut Systemat & Ecol, IL-91904 Jerusalem, Israel. CR Bauer A. M., 1998, ENCY REPTILES AMPHIB, P126 Bigelow DC, 1996, LARYNGOSCOPE, V106, P71, DOI 10.1097/00005537-199601000-00014 CAMPBELL HW, 1969, PHYSIOL ZOOL, V42, P183 Cogger H. G., 1992, REPTILES AMPHIBIANS, V4th COHEN YE, 1992, HEARING RES, V58, P1, DOI 10.1016/0378-5955(92)90002-5 Dooling R. J., 2000, COMP HEARING BIRDS R EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 KOPPL C, 1990, J COMP PHYSIOL A, V167, P139 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1972, J COMP PHYSIOL, V81, P239, DOI 10.1007/BF00693629 MANLEY GA, 1972, J EXP ZOOL, V181, P159, DOI 10.1002/jez.1401810203 MANLEY GA, 1972, J COMP PHYSIOL, V81, P251, DOI 10.1007/BF00693630 POSNER RB, 1966, COPEIA, P520 Relkin EM, 1988, PHYSL EAR, P103 ROSLER H, 1995, GECKOS WELT GATTUNGE ROSOWSKI JJ, 1984, HEARING RES, V16, P205, DOI 10.1016/0378-5955(84)90110-2 ROSOWSKI JJ, 1988, ASS RES OTOLARYNGOL, V11, P32 Saunders J. C., 2000, COMP HEARING BIRDS R, P13 SAUNDERS JC, 1972, ACTA OTO-LARYNGOL, V73, P353, DOI 10.3109/00016487209138952 SAUNDERS JC, 1985, HEARING RES, V18, P253, DOI 10.1016/0378-5955(85)90042-5 Sedgwick C J, 1986, Semin Vet Med Surg (Small Anim), V1, P215 SEDGWICK JC, 1986, COMP HEARING, V1, P215 SMIRNOV SV, 1979, ZOOL ZH, V58, P1425 SMIRNOV S V, 1981, Zhurnal Evolyutsionnoi Biokhimii i Fiziologii, V17, P395 STORR GM, 1990, LIZARDS W AUSTR 3 WERNER YI, 1976, J EXP ZOOL, V195, P319, DOI 10.1002/jez.1401950302 WERNER YL, 1972, J EXP ZOOL, V179, P1, DOI 10.1002/jez.1401790102 WERNER YL, 1971, SYST ZOOL, V20, P249, DOI 10.2307/2412063 WERNER Y L, 1972, Journal of Herpetology, V6, P147, DOI 10.2307/1562767 WERNER YL, 1983, HEARING OTHER SENSES, P149 Werner YL, 1998, J EXP BIOL, V201, P487 WEVER EG, 1978, REPTILE EAR WEVER EG, 1974, J MORPHOL, V143, P121, DOI 10.1002/jmor.1051430202 WEVER EG, 1970, J EXP ZOOL, V175, P327, DOI 10.1002/jez.1401750307 NR 34 TC 4 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 22 EP 30 DI 10.1016/S0378-5955(01)00331-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500004 PM 11591487 ER PT J AU Tabuchi, K Tsuji, S Asaka, Y Hara, A Kusakari, J AF Tabuchi, K Tsuji, S Asaka, Y Hara, A Kusakari, J TI Ischemia-reperfusion injury of the cochlea: effects of an iron chelator and nitric oxide synthase inhibitors SO HEARING RESEARCH LA English DT Article DE cochlea; ischemia; iron chelator; nitric oxide synthase ID TRANSIENT LOCAL ANOXIA; GUINEA-PIG; SELECTIVE-INHIBITION; CEREBRAL-ISCHEMIA; AMINOGUANIDINE; EXPRESSION; PROTECT; DAMAGE; DOGS AB Release of free iron from cellular stores and activation of nitric oxide synthase (NOS) has been implicated in a wide variety of cochlear injuries. In order to evaluate the effects of deferoxamine (a iron chelator), 3-bromo-7-nitroindazole (a relatively selective neuronal NOS (nNOS) inhibitor) or aminoguanidine (a relatively selective inducible NOS (iNOS) inhibitor) on the post-ischemic cochlear dysfunction, albino guinea pigs were subjected to 30 min ischemia, and the threshold shifts of the compound action potential (CAP) from pre-ischemic values were compared with those of control animals 4 h after the onset of reperfusion. A statistically significant reduction in the post-ischemic CAP threshold shift was observed in the animals treated with deferoxamine or 3-bromo-7-nitroindazole. However, aminoguanidine did not affect the post-ischemic CAP threshold shift. These results suggest that free iron and nNOS play deleterious roles in the cochlear injury induced by transient ischemia. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. RP Kusakari, J (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR Arkovitz MS, 1996, J PEDIATR SURG, V31, P1009, DOI 10.1016/S0022-3468(96)90075-5 Bland-Ward P. A., 1995, LIFE SCI, V57, P131 Bowman MA, 1996, J PHARMACOL EXP THER, V279, P790 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 Davis S, 1997, STROKE, V28, P198 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 GEYER O, 1995, FEBS LETT, V374, P399, DOI 10.1016/0014-5793(95)01147-7 Gosepath K, 1997, BRAIN RES, V747, P26, DOI 10.1016/S0006-8993(96)01149-3 Hara A, 2000, HEARING RES, V143, P110, DOI 10.1016/S0378-5955(00)00029-0 HURN PD, 1995, STROKE, V26, P688 Iadecola C, 1996, STROKE, V27, P1373 Johnson KL, 1998, ACTA OTO-LARYNGOL, V118, P660 Kusakari J, 1981, Auris Nasus Larynx, V8, P55 MISKO TP, 1993, EUR J PHARMACOL, V233, P119, DOI 10.1016/0014-2999(93)90357-N Popa R, 2000, ACTA OTO-LARYNGOL, V120, P350, DOI 10.1080/000164800750000559 SAMOKYSZYN VM, 1990, CLIN ISCHEMIC SYNDRO, P159 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P457 Song BB, 1998, FREE RADICAL BIO MED, V25, P189, DOI 10.1016/S0891-5849(98)00037-9 Tabuchi K, 1999, ACTA OTO-LARYNGOL, V119, P179 Tabuchi K, 1998, HEARING RES, V126, P28, DOI 10.1016/S0378-5955(98)00142-7 Tabuchi K, 2000, HEARING RES, V144, P1, DOI 10.1016/S0378-5955(00)00038-1 Tabuchi K, 2000, ANN OTO RHINOL LARYN, V109, P715 Takumida M, 2000, HEARING RES, V140, P91, DOI 10.1016/S0378-5955(99)00188-4 Watanabe K, 2000, ANTI-CANCER DRUG, V11, P401, DOI 10.1097/00001813-200006000-00011 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 NR 25 TC 17 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 31 EP 36 DI 10.1016/S0378-5955(01)00315-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500005 PM 11591488 ER PT J AU Erichsen, S Berger, S Schmid, W Stierna, P Hultcrantz, M AF Erichsen, S Berger, S Schmid, W Stierna, P Hultcrantz, M TI Na,K-ATPase expression in the mouse cochlea is not dependent on the mineralocorticoid receptor SO HEARING RESEARCH LA English DT Article DE inner ear; adrenal steroid; immunohistochemistry; development; knockout mouse ID MAMMALIAN INNER-EAR; STRIA VASCULARIS; MARGINAL CELLS; GERBIL COCHLEA; RAT COCHLEA; GUINEA-PIG; NA+,K+-ATPASE; SITES; ADRENOCORTICOSTEROIDS; CORTICOSTEROIDS AB This study was performed in order to test the hypothesis that the mineralocorticoid hormone stimulates the expression of Na,K-ATPase in the cochlea of the mouse. Immunohistochemistry was used to investigate the distribution of the mineralocorticoid receptor (MR) in the cochlea of the C57Bl/J6 mouse at different ages between gestational day 19 and postnatal day 30, and the occurrence and distribution of Na,K-ATPase in the inner ear of a mouse with a null mutation of the MR. Adult patterns of staining for MR were found as early as on gestational day 19 in the cochlea, with small changes thereafter. MR was detected in the same structures in the cochlea as Na,K-ATPase in earlier studies, where the amount of Na,K-ATPase increased after postnatal day 4. Thus there is latency between the increase of MR and the increase of Na,K-ATPase. In the cochlea of the MR deficient mouse, antibody labelling of Na,K-ATPase showed no significant difference as compared to the control wild type mouse. The hypothesis that mineralocorticoid hormone alone via MR stimulates the formation of Na,K-ATPase in the inner ear could not be confirmed by this study, and other regulating mechanisms must be considered. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. German Canc Res Ctr, Div Mol Biol Cell 1, D-69120 Heidelberg, Germany. Huddinge Univ Hosp, Dept Otorhinolaryngol, S-14186 Huddinge, Sweden. RP Hultcrantz, M (reprint author), Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. CR ANNIKO M, 1986, HEARING RES, V22, P279, DOI 10.1016/0378-5955(86)90104-8 Berger S, 1998, P NATL ACAD SCI USA, V95, P9424, DOI 10.1073/pnas.95.16.9424 BLOTCHABAUD M, 1990, J BIOL CHEM, V265, P11676 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 COUNTRY N, 1994, AM J PHYSIOL, V266, pC1342 COUNTRY N, 1992, AM J PHYSIOL, V263, pC61 CURTIS LM, 1993, EUR ARCH OTO-RHINO-L, V250, P265 DECOLLOGNE S, 1993, J CARDIOVASC PHARM, V22, P96 Erichsen S, 1996, HEARING RES, V100, P143, DOI 10.1016/0378-5955(96)00105-0 Erichsen S, 1998, HEARING RES, V124, P146, DOI 10.1016/S0378-5955(98)00117-8 Erichsen S, 1996, ACTA OTO-LARYNGOL, V116, P721, DOI 10.3109/00016489609137913 Garty H, 1997, PHYSIOL REV, V77, P359 IWASA KH, 1994, NEUROSCI LETT, V172, P163, DOI 10.1016/0304-3940(94)90687-4 Lippincott L, 1997, EUR ARCH OTO-RHINO-L, V254, P413, DOI 10.1007/BF02439970 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 Mikaelian D, 1965, ACTA OTO-LARYNGOL, V59, P451, DOI DOI 10.3109/00016486509124579 NAKAZAWA K, 1995, J HISTOCHEM CYTOCHEM, V43, P981 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PITOVSKI DZ, 1993, BRAIN RES, V601, P273, DOI 10.1016/0006-8993(93)91720-D PITOVSKI DZ, 1993, HEARING RES, V69, P10, DOI 10.1016/0378-5955(93)90088-I RAREY KE, 1991, LARYNGOSCOPE, V101, P1081 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 ROSE AM, 1994, CLIN CHEM, V40, P1674 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 TENCATE WJF, 1991, ARCH OTOLARYNGOL, V117, P96 YAO XF, 1994, HEARING RES, V80, P31, DOI 10.1016/0378-5955(94)90006-X ZUO J, 1995, ACTA OTO-LARYNGOL, V115, P497, DOI 10.3109/00016489509139355 NR 28 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 37 EP 46 DI 10.1016/S0378-5955(01)00317-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500006 PM 11591489 ER PT J AU Orduna, I Mercado, E Gluck, MA Merzenich, MM AF Orduna, I Mercado, E Gluck, MA Merzenich, MM TI Spectrotemporal sensitivities in rat auditory cortical neurons SO HEARING RESEARCH LA English DT Article DE cortex; directionality; electrophysiology; receptive field; sound; tuning; time-varying ID FREQUENCY-MODULATED STIMULI; MONGOLIAN GERBIL; RECEPTIVE-FIELDS; CORTEX; CAT; RESPONSES; TONES; REPRESENTATION; ORGANIZATION; AMPLITUDE AB Studies in several mammalian species have demonstrated that auditory cortical neurons respond strongly to single frequency-modulated (FM) sweeps, and that most responses are selective for sweep direction and/or rate. In the present study, we used extracellular recordings to examine how neurons in the auditory cortices of anesthetized rats respond to continuous, periodic trains of FM sweeps (described previously by deCharms et al., Science 280 (1998) pp. 1439-1444, as moving auditory gratings). Consistent with previous observations in owl monkeys, we found that the majority of cortical neurons responded selectively to trains of either up-sweeps or down-sweeps; selectivity for down-sweeps was most common. Periodic responses were typically evoked only by sweep trains with repetition rates less than 12 sweeps per second. Directional differences in responses were dependent on repetition rate. Our results support the proposal that a combination of both spectral and temporal acoustic features determines the responses of auditory cortical neurons to sound, and add to the growing body of evidence indicating that the traditional view of the auditory cortex as a frequency analyzer is not sufficient to explain how the mammalian brain represents complex sounds. (C) 2001 Published by Elsevier Science B.V. C1 Rutgers State Univ, Ctr Mol & Behav Neurosci, Newark, NJ 07102 USA. Univ Calif San Francisco, Keck Ctr Integrat Neurosci, San Francisco, CA 94143 USA. RP Orduna, I (reprint author), Rutgers State Univ, Ctr Mol & Behav Neurosci, 197 Univ Ave, Newark, NJ 07102 USA. CR Brosch M, 1999, J NEUROPHYSIOL, V82, P1542 Brosch M, 2000, CEREB CORTEX, V10, P1155, DOI 10.1093/cercor/10.12.1155 CALFORD MB, 1995, J NEUROPHYSIOL, V73, P1876 Cotillon N, 2000, HEARING RES, V142, P113, DOI 10.1016/S0378-5955(00)00016-2 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 deCharms RC, 1998, SCIENCE, V280, P1439, DOI 10.1126/science.280.5368.1439 Depireux DA, 2001, J NEUROPHYSIOL, V85, P1220 DEPIREUX DA, 1998, COMMENTS THEOR BIOL, V5, P89 EGGERMONT JJ, 1992, HEARING RES, V61, P1, DOI 10.1016/0378-5955(92)90029-M GAESE BH, 1995, EUR J NEUROSCI, V7, P438, DOI 10.1111/j.1460-9568.1995.tb00340.x HEIL P, 1992, J COMP PHYSIOL A, V171, P583 HEIL P, 1992, HEARING RES, V63, P135, DOI 10.1016/0378-5955(92)90081-W HEIL P, 1992, HEARING RES, V63, P108, DOI 10.1016/0378-5955(92)90080-7 Horikawa J, 1997, J COMP PHYSIOL A, V181, P677, DOI 10.1007/s003590050149 Kenmochi M, 1997, NEUROREPORT, V8, P1589, DOI 10.1097/00001756-199705060-00008 Kilgard MP, 1999, HEARING RES, V134, P16, DOI 10.1016/S0378-5955(99)00061-1 Klein DJ, 2000, J COMPUT NEUROSCI, V9, P85, DOI 10.1023/A:1008990412183 KOWALSKI N, 1995, J NEUROPHYSIOL, V73, P1513 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F MENDELSON JR, 1985, BRAIN RES, V327, P331, DOI 10.1016/0006-8993(85)91530-6 MENDELSON JR, 1992, EXP BRAIN RES, V91, P435 MENDELSON JR, 1993, EXP BRAIN RES, V94, P65 Nelken I, 2000, EUR J NEUROSCI, V12, P549, DOI 10.1046/j.1460-9568.2000.00935.x NELKEN I, 1994, HEARING RES, V72, P237, DOI 10.1016/0378-5955(94)90222-4 Ohl FW, 1999, LEARN MEMORY, V6, P347 PHILLIPS DP, 1985, EXP BRAIN RES, V58, P443 SALLY SL, 1988, J NEUROPHYSIOL, V59, P1627 SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 Schreiner CE, 2000, ANNU REV NEUROSCI, V23, P501, DOI 10.1146/annurev.neuro.23.1.501 Schulze H, 1997, J COMP PHYSIOL A, V181, P573, DOI 10.1007/s003590050141 Schulze H, 1999, J COMP PHYSIOL A, V185, P493, DOI 10.1007/s003590050410 SUGA N, 1965, J PHYSIOL-LONDON, V181, P671 Theunissen FE, 2000, J NEUROSCI, V20, P2315 WANG K, 1995, IEEE ENG MED BIOL, V14, P186, DOI 10.1109/51.376758 Wang XQ, 2000, P NATL ACAD SCI USA, V97, P11843, DOI 10.1073/pnas.97.22.11843 Wang XQ, 1995, J NEUROPHYSIOL, V74, P2685 WETSEL W, 1998, NEUROSCI LETT, V252, P115 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 NR 38 TC 23 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 47 EP 57 DI 10.1016/S0378-5955(01)00339-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500007 PM 11591490 ER PT J AU Sheykholeslami, K Kermany, MH Kaga, K AF Sheykholeslami, K Kermany, MH Kaga, K TI Frequency sensitivity range of the saccule to bone-conducted stimuli measured by vestibular evoked myogenic potentials SO HEARING RESEARCH LA English DT Article DE vestibular; vestibular evoked myogenic potential; myogenic potential; bone conduction; frequency sensitivity range; saccule; repetition rate ID SQUIRREL-MONKEY; RESPONSES; NEURONS; SOUND; VIBRATION; NERVE AB Vestibular evoked myogenic potentials (VEMPs) occurring in cervical muscles after intense sound stimulation conducted by air or bone are thought to be a polysynaptic response of otolith-vestibular nerve origin. We report the results of an experiment to investigate whether acoustic stimulation of the saccule by bone conduction produces VEMPs in which response amplitudes are somewhat sensitive to stimulus frequency, as appears, to be the case with air-conducted stimuli. Prior to this we investigated the effect of stimulation repetition rate on bone-conducted VEMPs (B-VEMPs) at stimulus frequencies of 200 and 400 Hz with five different repetition rates (5, 10, 20, 40, and 80 Hz). B-VEMPs were recorded from 12 normal hearing subjects in response to bone-conducted 70 dB (normal hearing level), 10-ms tone bursts (rise/fall time = 1 ms and plateau time = 8 ms) at frequencies of 100, 200, 400, 800, 1600 and 3200 Hz. Our study showed that B-VEMP amplitudes were highest at 10 Hz but decreased as the repetition rate increased. B-VEMP response amplitudes were found to be maximal for stimulus frequencies from 200 to 400 Hz. This response may contribute to the perception of loud sounds. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tokyo, Fac Med, Dept Otolaryngol, Bunkyo Ku, Tokyo 1130033, Japan. RP Sheykholeslami, K (reprint author), NE Ohio Univ, Coll Med, Dept Neurobiol & Pharmacol, 4209 State Route 44, Rootstown, OH 44272 USA. CR BOCCA E, 1960, Acta Otolaryngol, V51, P260, DOI 10.3109/00016486009124496 CAZALS Y, 1983, HEARING RES, V10, P263, DOI 10.1016/0378-5955(83)90091-6 COLEBATCH JG, 1994, J NEUROL NEUROSUR PS, V57, P190, DOI 10.1136/jnnp.57.2.190 COLEBATCH JG, 1992, NEUROLOGY, V42, P1935 FERNANDEZ C, 1976, J NEUROPHYSIOL, V39, P970 FLUUR E, 1970, LARYNGOSCOPE, V80, P1713, DOI 10.1288/00005537-197011000-00006 GOLDBERG JM, 1975, ANNU REV PHYSIOL, V37, P129, DOI 10.1146/annurev.ph.37.030175.001021 Igarashi M, 1975, Acta Otolaryngol Suppl, V330, P91 LACKNER JR, 1974, AEROSPACE MED, V45, P1267 Lorente de No R., 1933, LARYNGOSCOPE, V43, P1 LOWENSTEIN O, 1951, J PHYSIOL-LONDON, V114, P471 MACCUE MP, 1995, J NEUROPHYSIOL, V47, P1563 MOFFAT AJM, 1976, J COMP PHYSIOL, V105, P1 MUROFUSHI T, 1995, EXP BRAIN RES, V103, P174 PARKER DE, 1975, EFFECTS SOUND VESTIB, P75 POPPER AN, 1973, J ACOUST SOC AM, V53, P1515, DOI 10.1121/1.1913496 RIBARIC K, 1984, AUDIOLOGY, V23, P388 Sheykholeslami K, 2000, ACTA OTO-LARYNGOL, V120, P731 Sheykholeslami K, 2001, AURIS NASUS LARYNX, V28, P41, DOI 10.1016/S0385-8146(00)00091-2 Todd NPM, 2000, HEARING RES, V141, P180, DOI 10.1016/S0378-5955(99)00222-1 TOWNSEND GL, 1971, ANN OTO RHINOL LARYN, V80, P121 VERSTEEGH C, 1927, ACTA OTO-LARYNGOL, V11, P393, DOI 10.3109/00016482709120092 von Bekesy G, 1935, ARCH GES PHYSL, V236, P59 WIT HP, 1984, J ACOUST SOC AM, V75, P202, DOI 10.1121/1.390396 Wu CH, 1999, ACTA OTO-LARYNGOL, V119, P29 YOUNG ED, 1977, ACTA OTO-LARYNGOL, V84, P352, DOI 10.3109/00016487709123977 NR 26 TC 34 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 58 EP 62 DI 10.1016/S0378-5955(01)00333-1 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500008 PM 11591491 ER PT J AU Sugawara, M Wada, H AF Sugawara, M Wada, H TI Analysis of elastic properties of outer hair cell wall using shell theory SO HEARING RESEARCH LA English DT Article DE outer hair cell; shell model; elastic property; numerical analysis ID ELECTROKINETIC SHAPE CHANGES; ACTIVE FORCE GENERATION; STIFFNESS; MOTILITY; MEMBRANE; RESPONSES; MODULI; MODEL AB In this study, the mechanical properties of the lateral wall of the outer hair cell (OHC) are determined theoretically. First, the cell is modeled as a cylindrical two-layer shell consisting of the plasma membrane and the cortical lattice. When the stiffness of the plasma membrane is set to be 1.0 mN/m based on the estimated value of Tolomeo et al. [Biophys. J. 71 (1996) 421-429], and Poisson's ratio of the plasma membrane is assumed to be 0.90, the relationships between the stiffness, Poisson's ratio and the orthotropism of the cortical lattice are obtained by comparing the measurement results of cell inflation by Iwasa and Chadwick [J. Acoust. Soc. Am. 92 (1992) 3169-3173] with the numerical ones obtained with our model. Next, the obtained relationships between these mechanical properties of the cell are applied to the model, and the result of the cell length change due to the axial compression measured by Hallworth [J. Neurophysiol. 74 (1995) 2319-2329] is compared with that obtained from our numerical analysis. As a result, the axial and circumferential stiffnesses of the cortical lattice are evaluated to be 4.6 mN/m and 13 mN/m, respectively. Then, the contribution of the cortical lattice to the stiffness of the OHC lateral wall is examined. When the stiffness of the plasma membrane is less than 1.0 mN/m, the mechanical properties of the cortical lattice obtained from the two-layer shell model are nearly the same as those of the cell lateral wall obtained from the one-layer orthotropic shell model. Therefore, it is concluded that the stiffness of the cortical lattice is responsible for that of the whole lateral wall of the OHC. Moreover, the mechanical properties of the OHC obtained in this study are compared with those reported previously, and it is suggested that the one-layer orthotropic shell model is sufficient for further analyses of the motility and force production of the OHC. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Tohoku Univ, Dept Mech Engn, Sendai, Miyagi 9808579, Japan. RP Sugawara, M (reprint author), Tohoku Univ, Dept Mech Engn, Aoba Yama 01, Sendai, Miyagi 9808579, Japan. CR Adachi M, 1997, BIOPHYS J, V73, P2809 Alberts B., 1994, MOL BIOL CELL ARIMA T, 1991, CELL TISSUE RES, V263, P91, DOI 10.1007/BF00318403 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Brush D. O., 1975, BUCKLING BARS PLATES, Vfirst DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 Hallworth R, 1995, J NEUROPHYSIOL, V74, P2319 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 HUANG GJ, 1994, P NATL ACAD SCI USA, V91, P12268, DOI 10.1073/pnas.91.25.12268 IWASA KH, 1994, J ACOUST SOC AM, V96, P2216, DOI 10.1121/1.410094 IWASA KH, 1992, J ACOUST SOC AM, V92, P3169, DOI 10.1121/1.404194 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KALINEC F, 1992, P NATL ACAD SCI USA, V89, P8671, DOI 10.1073/pnas.89.18.8671 Oghalai JS, 1998, J NEUROSCI, V18, P48 Ratnanather JT, 1996, J ACOUST SOC AM, V99, P1025, DOI 10.1121/1.414631 RUSSELL IJ, 1995, AUDIT NEUROSCI, V1, P309 SAITO K, 1983, CELL TISSUE RES, V229, P467 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 SANTOS-SACCHI J, 1993, BIOPHYS J, V65, P2217 SANTOSSACCHI J, 1988, J ACOUST SOC AM, V92, P3169 Spector AA, 1998, ANN BIOMED ENG, V26, P157, DOI 10.1114/1.87 Spector AA, 1998, J ACOUST SOC AM, V103, P1007, DOI 10.1121/1.421217 Spector AA, 1998, J ACOUST SOC AM, V103, P1001, DOI 10.1121/1.421216 Spector AA, 1996, ANN BIOMED ENG, V24, P241, DOI 10.1007/BF02667353 Tolomeo JA, 1996, BIOPHYS J, V71, P421 TOLOMEO JA, 1995, J ACOUST SOC AM, V97, P3006, DOI 10.1121/1.411865 Ulfendahl M, 1998, PFLUG ARCH EUR J PHY, V436, P9, DOI 10.1007/s004240050598 ZENNER HP, 1992, ACTA OTO-LARYNGOL, V112, P248 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 Zheng J, 2000, NATURE, V405, P149, DOI 10.1038/35012009 NR 33 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 63 EP 72 DI 10.1016/S0378-5955(01)00343-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500009 PM 11591492 ER PT J AU Harkrider, AW Champlin, CA McFadden, D AF Harkrider, AW Champlin, CA McFadden, D TI Acute effect of nicotine on non-smokers: I. OAEs and ABRs SO HEARING RESEARCH LA English DT Article DE cholinergic; transdermal nicotine; otoacoustic; emissions; auditory evoked potential; auditory brainstem response; exogenous; afferent/efferent transmission ID EVOKED OTOACOUSTIC EMISSIONS; BRAIN-STEM RESPONSES; OUTER HAIR-CELLS; CIGARETTE-SMOKING; TRANSDERMAL NICOTINE; CONTRALATERAL SOUND; TOBACCO SMOKING; AUDITORY-SYSTEM; TRAPEZOID BODY; BLINK REFLEX AB This paper is the first in a series of three investigating the role of cholinergic mechanisms in the auditory system by assessing the acute effects of nicotine, an acetylcholinomimetic drug, on aggregate responses within the auditory pathway. In a single-blind procedure, auditory responses were obtained from 20 normal-hearing, non-smokers (10 male) under two conditions (nicotine, placebo). After the drug session, plasma tests revealed a subject's nicotine concentration. The effects of nicotine on early, exogenous responses of the auditory system (otoacoustic emissions and auditory brainstem potentials) are described in this first paper. Results indicated that transdermal administration of nicotine to non-smokers does not significantly affect cochlear activity but does acutely affect the neural transmission of acoustic information. Overall, otoacoustic emissions were unaffected by transdermal nicotine while wave I of the auditory brainstem response was significantly increased in latency and decreased in amplitude. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tennessee, Dept Speech Pathol & Audiol, Knoxville, TN 37996 USA. Univ Texas, Dept Commun Sci & Disorders, Austin, TX 78712 USA. Univ Texas, Inst Neurosci, Austin, TX 78712 USA. Univ Texas, Dept Psychol, Austin, TX 78712 USA. RP Harkrider, AW (reprint author), Univ Tennessee, Dept Speech Pathol & Audiol, 457 S Stadium Hall, Knoxville, TN 37996 USA. CR ADES HW, 1975, HDB SENSORY PHYSL, V5, P125 ADLER LE, 1992, BIOL PSYCHIAT, V32, P607, DOI 10.1016/0006-3223(92)90073-9 *ANSI, 1996, S3221987 ANSI ASHMORE JF, 1994, EXP PHYSIOL, V79, P113 BENOWITZ NL, 1993, DRUGS, V45, P151 Benowitz NL, 1997, BRIT J CLIN PHARMACO, V43, P259, DOI 10.1111/j.1365-2125.1997.00566.x BENOWITZ NL, 1988, CLIN PHARMACOL THER, V44, P23 BENOWITZ NL, 1988, NEW ENGL J MED, V319, P1318 BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BHARGAVA V, 1981, PHARMACOL BIOCHEM BE, V15, P587, DOI 10.1016/0091-3057(81)90214-8 BHARGAVA VK, 1978, NEUROPHARMACOLOGY, V17, P1009, DOI 10.1016/0028-3908(78)90026-6 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 COHEN AJ, 1981, 4 TOB ADV COUNC DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DENGERINK HA, 1985, HEARING RES, V20, P31, DOI 10.1016/0378-5955(85)90056-5 DESMEDT JE, 1975, HDB SENSORY PHYSIO 2, V5, P219 EDWARDS JA, 1985, ADDICT BEHAV, V10, P113, DOI 10.1016/0306-4603(85)90017-6 EDWARDS JA, 1983, PHARMACOL THERAPEUT, V19, P147 Ehlers CL, 1997, PHARMACOL BIOCHEM BE, V58, P713, DOI 10.1016/S0091-3057(97)90011-3 ELBERLING C, 1987, SCAND AUDIOL, V16, P49, DOI 10.3109/01050398709042155 ELKINDHIRSCH KE, 1992, HEARING RES, V60, P143, DOI 10.1016/0378-5955(92)90016-G ENGSTROM H, 1972, ULTRASTRUCTURE ANIMA, P83 EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EVINGER C, 1988, EXP BRAIN RES, V73, P477, DOI 10.1007/BF00406604 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 Foulds J, 1996, PSYCHOPHARMACOLOGY, V127, P31, DOI 10.1007/BF02805972 FRIEDMAN J, 1980, CLIN EXP PHARMACOL P, V7, P609, DOI 10.1111/j.1440-1681.1980.tb00119.x FRIEDMAN J, 1974, CLIN EXP PHARMACOL P, V1, P249, DOI 10.1111/j.1440-1681.1974.tb00547.x FUCHS PA, 1992, BRAIN RES, V159, P440 GOLDING JF, 1988, PHARMACOL BIOCHEM BE, V29, P23, DOI 10.1016/0091-3057(88)90268-7 Goldstein R., 1999, EVOKED POTENTIAL AUD GORGA MP, 1985, EAR HEARING, V6, P105, DOI 10.1097/00003446-198503000-00008 GORSLINE J, 1991, PHARMACOL RES S, V10, pS299 GROLLMAN A, 1970, PHARM THERAPEUTICS GUHA D, 1976, NEUROPHARMACOLOGY, V15, P225, DOI 10.1016/0028-3908(76)90068-X HALL RA, 1973, SCIENCE, V180, P212, DOI 10.1126/science.180.4082.212 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 Jamner LD, 1998, EXP CLIN PSYCHOPHARM, V6, P96, DOI 10.1037/1064-1297.6.1.96 Jasper H. H., 1958, ELECTROENCEPHALOGRAP, V10, P371, DOI DOI 10.1016/0013-4694(58)90053-1 JEWETT DL, 1971, BRAIN, V94, P681, DOI 10.1093/brain/94.4.681 KEITH WJ, 1987, EAR HEARING, V8, P49, DOI 10.1097/00003446-198702000-00009 Knott V., 1989, SMOKING HUMAN BEHAV, P93 Knott V, 1999, PHARMACOL BIOCHEM BE, V63, P253, DOI 10.1016/S0091-3057(99)00006-4 KNOTT VJ, 1985, NEUROPSYCHOBIOLOGY, V13, P136, DOI 10.1159/000118176 KNOTT VJ, 1989, NEUROPSYCHOBIOLOGY, V21, P216, DOI 10.1159/000118580 KNOTT VJ, 1987, ADDICT BEHAV, V12, P375, DOI 10.1016/0306-4603(87)90053-0 KNOTT VJ, 1978, PSYCHOPHYSIOLOGY, V15, P186, DOI 10.1111/j.1469-8986.1978.tb01360.x KNOTT VJ, 1985, NEUROPSYCHOBIOLOGY, V13, P74, DOI 10.1159/000118166 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 KUJAWA SG, 1993, HEARING RES, V68, P97, DOI 10.1016/0378-5955(93)90068-C Kumar Vijay, 1996, Indian Journal of Physiology and Pharmacology, V40, P381 LAWOKO G, 1995, NEUROSCI LETT, V195, P44 LeonS FE, 1997, J CLIN NEUROPHYSIOL, V14, P144, DOI 10.1097/00004691-199703000-00007 LEVIN ED, 1992, PSYCHOPHARMACOLOGY, V108, P417, DOI 10.1007/BF02247415 Levin ED, 1996, PSYCHOPHARMACOLOGY, V123, P55, DOI 10.1007/BF02246281 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 McFadden D, 1996, HEARING RES, V97, P102 McFadden D, 1999, J ACOUST SOC AM, V105, P2403, DOI 10.1121/1.426845 McFadden D, 1998, DEV NEUROPSYCHOL, V14, P261 McFadden D, 1998, P NATL ACAD SCI USA, V95, P2709, DOI 10.1073/pnas.95.5.2709 McFadden D, 2000, JARO, V1, P89, DOI 10.1007/s101620010008 MOLLER AR, 1982, ELECTROEN CLIN NEURO, V53, P612, DOI 10.1016/0013-4694(82)90137-7 MOUSA SA, 1988, PHARMACOL BIOCHEM BE, V31, P265, DOI 10.1016/0091-3057(88)90344-9 MOLLER AR, 1981, EXP NEUROL, V74, P862, DOI 10.1016/0014-4886(81)90259-4 PALMER KJ, 1992, DRUGS, V44, P498, DOI 10.2165/00003495-199244030-00011 Pasanen EG, 2000, J ACOUST SOC AM, V108, P1105, DOI 10.1121/1.1287026 PERLMAN H B, 1959, Laryngoscope, V69, P591 Pickles JO, 1988, INTRO PHYSL HEARING PICTON TW, 1980, TECHNIQUES PSYCHOPHY, P357 PILLSBURY HC, 1986, LARYNGOSCOPE, V96, P1112 POMERLEAU OF, 1986, PSYCHOPHARMACOL BULL, V22, P865 PRIEVE BA, 1993, J ACOUST SOC AM, V93, P3308, DOI 10.1121/1.405715 RUSSELL MAH, 1975, BRIT MED J, V2, P414 Sahley TL, 1997, EFFERENT AUDITORY SY SCHERG M, 1985, EEG CLIN NUEROL, V62, P235 SCHWARTZ D, 1991, DIAGNOSTIC AUDIOLOGY Schwartz D. M., 1994, PRINCIPLES APPL AUDI, P123 Souter M, 1995, HEARING RES, V91, P167, DOI 10.1016/0378-5955(95)00187-5 SRIVASTAVA ED, 1991, PSYCHOPHARMACOLOGY, V105, P63, DOI 10.1007/BF02316865 Stevens KE, 1997, PHARMACOL BIOCHEM BE, V57, P869, DOI 10.1016/S0091-3057(96)00466-2 STEVENS KE, 1995, PSYCHOPHARMACOLOGY, V119, P163, DOI 10.1007/BF02246157 TRAMMER RM, 1992, ACTA PAEDIATR, V81, P962, DOI 10.1111/j.1651-2227.1992.tb12154.x RENNARD S, 1991, JAMA-J AM MED ASSOC, V266, P3133 VAZQUEZ AJ, 1967, ANN NY ACAD SCI, V142, P201, DOI 10.1111/j.1749-6632.1967.tb13725.x Veuillet E, 1996, HEARING RES, V93, P128, DOI 10.1016/0378-5955(95)00212-X VOGEL W, 1977, J COMP PHYSIOL PSYCH, V91, P418, DOI 10.1037/h0077333 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P326, DOI 10.1016/0013-4694(83)90259-6 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P340, DOI 10.1016/0013-4694(83)90260-2 WARBURTON DM, 1981, BRIT MED BULL, V37, P121 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WESNES K, 1983, PHARMACOL THERAPEUT, V21, P189, DOI 10.1016/0163-7258(83)90072-4 WILLIAMS DM, 1995, J ACOUST SOC AM, V97, P1130, DOI 10.1121/1.412226 WOODSON PP, 1982, PHARMACOL BIOCHEM BE, V17, P915, DOI 10.1016/0091-3057(82)90472-5 YAMADA O, 1979, Scandinavian Audiology, V8, P67, DOI 10.3109/01050397909076303 YOSHIDA K, 1979, BRAIN RES, V172, P453, DOI 10.1016/0006-8993(79)90578-X ZELMAN S, 1973, JAMA-J AM MED ASSOC, V223, P920 NR 97 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 73 EP 88 DI 10.1016/S0378-5955(01)00345-8 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500010 PM 11591493 ER PT J AU Ashley, WH Champlin, CA AF Ashley, WH Champlin, CA TI Acute effect of nicotine on non-smokers: II. MLRs and 40-Hz responses SO HEARING RESEARCH LA English DT Article DE cholinergic receptor; transdermal nicotine; auditory evoked potential; middle latency response; 40-Hz response; mesogenous ID AUDITORY EVOKED-RESPONSES; SPONTANEOUS OTOACOUSTIC EMISSIONS; MIDDLE LATENCY RESPONSE; POTENTIALS; HEARING; SLEEP; CHILDREN; SYSTEMS; LESIONS; HETEROSEXUALS AB This paper is the second in a series of three investigating the role of cholinergic mechanisms in the auditory system by assessing the acute effects of nicotine, an acetylcholinomimetic drug, on aggregate responses within the auditory pathway. In a single-blind procedure, auditory responses were obtained from 20 normal-hearing, non-smokers (10 male) under two conditions (nicotine, placebo). The effects of nicotine on central, mesogenous responses of the auditory system (middle latency and 40-Hz responses) are described in this second paper. Results indicated that transdermal administration of nicotine to non-smokers does significantly affect the central, neural transmission of acoustic information. Na-Pa amplitude and Nb latency of the middle latency response and latency measures of the 40-Hz response were acutely altered by the presence of nicotine. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tennessee, Dept Speech Pathol & Audiol, Knoxville, TN 37996 USA. Univ Texas, Dept Commun Sci & Disorders, Austin, TX 78712 USA. Univ Texas, Inst Neurosci, Austin, TX 78712 USA. RP Ashley, WH (reprint author), Univ Tennessee, Dept Speech Pathol & Audiol, 457 S Stadium Hall, Knoxville, TN 37996 USA. CR BARBIERI RL, 1986, FERTIL STERIL, V46, P232 Benowitz N L, 1997, NIDA Res Monogr, V173, P48 BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 BORDA RP, 1984, BRAIN DYNAMICS, P339 BRESSLER SL, 1980, ELECTROEN CLIN NEURO, V50, P19, DOI 10.1016/0013-4694(80)90319-3 BUCHWALD JS, 1991, ELECTROEN CLIN NEURO, V80, P303, DOI 10.1016/0168-5597(91)90114-D BUCHWALD JS, 1992, ELECTROEN CLIN NEURO, V84, P164, DOI 10.1016/0168-5597(92)90021-3 BUCHWALD JS, 1989, ELECTROEN CLIN NEURO, V74, P378, DOI 10.1016/0168-5597(89)90005-1 BUCHWALD JS, 1981, BRAIN RES, V205, P91, DOI 10.1016/0006-8993(81)90722-8 CELESIA GG, 1970, EEG CLIN NEUROL, V31, P603 CHUNG DY, 1983, J ACOUST SOC AM, V73, P1277, DOI 10.1121/1.389276 COLLET L, 1988, BRAIN DEV-JPN, V10, P169 ERWIN R, 1986, ELECTROEN CLIN NEURO, V65, P383, DOI 10.1016/0168-5597(86)90017-1 FIRSCHING R, 1987, ELECTROEN CLIN NEURO, V67, P213, DOI 10.1016/0013-4694(87)90018-6 Freeman W.J., 1975, MASS ACTION NERVOUS FRIEDMAN J, 1980, CLIN EXP PHARMACOL P, V7, P609, DOI 10.1111/j.1440-1681.1980.tb00119.x GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GALAMBOS R, 1982, ANN NY ACAD SCI, V388, P722, DOI 10.1111/j.1749-6632.1982.tb50841.x Galambos R, 1992, INDUCED RHYTHMS BRAI, P201 GAULT FP, 1963, ELECTROEN CLIN NEURO, V15, P299, DOI 10.1016/0013-4694(63)90099-3 GOLDSTEIN L, 1967, ANN NY ACAD SCI, V562, P170 GROLLMAN A, 1970, PHARM THERAPEUTICS GUHA D, 1976, NEUROPHARMACOLOGY, V15, P225, DOI 10.1016/0028-3908(76)90068-X HALL RA, 1973, SCIENCE, V180, P212, DOI 10.1126/science.180.4082.212 HASHIMOTO I, 1982, ELECTROEN CLIN NEURO, V53, P652, DOI 10.1016/0013-4694(82)90141-9 Hirata K, 1996, Rinsho Shinkeigaku, V36, P1318 HOGAN K, 1987, Anesthesiology (Hagerstown), V67, pA402, DOI 10.1097/00000542-198709001-00402 JACOBSON GP, 1990, ELECTROEN CLIN NEURO, V75, P230, DOI 10.1016/0013-4694(90)90176-K JACOBSON GP, 1994, PRINCIPLES APPL AUDI JERGER J, 1986, EAR HEARING, V7, P240, DOI 10.1097/00003446-198608000-00004 JOHNSON B W, 1988, Brain Topography, V1, P117, DOI 10.1007/BF01129176 JUDD BW, 1987, BRAIN DYNAMICS, P339 KILENY P, 1987, ELECTROEN CLIN NEURO, V66, P108, DOI 10.1016/0013-4694(87)90180-5 KNAPP DE, 1962, INT J NEUROPHARMACOL, V1, P333 KOYLU EO, 1997, LIFE SCI, V64, P191 KRAUS N, 1992, BRAIN RES, V587, P186, DOI 10.1016/0006-8993(92)90996-M KRAUS N, 1993, ELECTROEN CLIN NEURO, V88, P123, DOI 10.1016/0168-5597(93)90063-U KRAUS N, 1985, ELECTROEN CLIN NEURO, V62, P343, DOI 10.1016/0168-5597(85)90043-7 Kraus N., 1994, PRINCIPLES APPL AUDI, P155 KRAUS N, 1988, EAR HEARING, V9, P451 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 KULAWIEC JT, 1995, EAR HEARING, V16, P515 LEVINE RA, 1988, NEUROPSYCHOLOGIA, V26, P603, DOI 10.1016/0028-3932(88)90116-9 LINDEN RD, 1985, EAR HEARING, V6, P167, DOI 10.1097/00003446-198505000-00008 MACMAHON B, 1982, NEW ENGL J MED, V307, P1062, DOI 10.1056/NEJM198210213071707 MAKELA JP, 1987, ELECTROEN CLIN NEURO, V66, P539, DOI 10.1016/0013-4694(87)90101-5 MAY P, 1994, NEUROREPORT, V5, P1918, DOI 10.1097/00001756-199410000-00019 McFadden D, 1996, HEARING RES, V97, P102 McFadden D, 1999, J ACOUST SOC AM, V105, P2403, DOI 10.1121/1.426845 McFadden D, 1998, P NATL ACAD SCI USA, V95, P2709, DOI 10.1073/pnas.95.5.2709 McFadden D, 2000, JARO, V1, P89, DOI 10.1007/s101620010008 McFadden D, 1998, J ACOUST SOC AM, V104, P1555, DOI 10.1121/1.424366 MCFADDEN D, 1993, HEARING RES, V71, P208, DOI 10.1016/0378-5955(93)90036-Z McFadden D, 2000, HEARING RES, V142, P23, DOI 10.1016/S0378-5955(00)00002-2 MCGEE T, 1992, HEARING RES, V61, P147, DOI 10.1016/0378-5955(92)90045-O MENDEL MI, 1980, AUDIOLOGY, V19, P1 NAMEROW NS, 1974, ELECTROEN CLIN NEURO, V37, P11, DOI 10.1016/0013-4694(74)90241-7 OSTERHAMMEL PA, 1985, SCAND AUDIOL, V14, P47, DOI 10.3109/01050398509045921 PINKERTON F, 1989, DEV MED CHILD NEUROL, V31, P569 PLOURDE G, 1990, ANESTH ANALG, V71, P460 REGAN D, 1968, ELECTROEN CLIN NEURO, V25, P231, DOI 10.1016/0013-4694(68)90020-5 ROCHE AF, 1978, J ACOUST SOC AM, V64, P1593, DOI 10.1121/1.382143 ROMANI GL, 1982, EXP BRAIN RES, V47, P381 ROYSTER LH, 1980, J ACOUST SOC AM, V68, P551, DOI 10.1121/1.384769 Scherg M, 1989, J Cogn Neurosci, V1, P336, DOI 10.1162/jocn.1989.1.4.336 Sheer D.E., 1989, BRAIN DYNAMICS, P339 SHUTE CCD, 1967, ANN NY ACAD SCI, V562, P497 SPYDELL JD, 1985, ELECTROEN CLIN NEURO, V62, P193, DOI 10.1016/0168-5597(85)90014-0 TEAS DC, 1964, EXP NEUROL, V10, P90 TIITINEN H, 1993, NATURE, V364, P59, DOI 10.1038/364059a0 TIITINEN H, 1994, NEUROREPORT, V6, P190, DOI 10.1097/00001756-199412300-00048 VALERA S, 1992, P NATL ACAD SCI USA, V89, P9949, DOI 10.1073/pnas.89.20.9949 WOODS DL, 1987, ELECTROEN CLIN NEURO, V68, P132, DOI 10.1016/0168-5597(87)90040-2 WOODSON PP, 1982, PHARMACOL BIOCHEM BE, V17, P915, DOI 10.1016/0091-3057(82)90472-5 YOSHIDA K, 1979, BRAIN RES, V172, P453, DOI 10.1016/0006-8993(79)90578-X NR 75 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 89 EP 98 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500011 ER PT J AU Harkrider, AW Champlin, CA AF Harkrider, AW Champlin, CA TI Acute effect of nicotine on non-smokers: III. LLRs and EEGs SO HEARING RESEARCH LA English DT Article DE cholinergic receptor; transdermal nicotine; auditory evoked potential; endogenous; electroencephalogram; long-latency response; afferent/efferent transmission ID AUDITORY-EVOKED-RESPONSES; EVENT-RELATED POTENTIALS; MIDDLE LATENCY RESPONSE; CIGARETTE-SMOKING; BRAIN-STEM; ALZHEIMERS-DISEASE; TOBACCO SMOKING; SEX-DIFFERENCES; NORMALIZATION; ATTENTION AB This paper is the last in a series of three investigating the role of cholinergic mechanisms in the auditory system by assessing the acute effects of nicotine, an acetylcholinomimetic drug, on aggregate responses within the auditory pathway. In a single-blind procedure, auditory responses were obtained from 20 normal-hearing, non-smokers (10 male) under two conditions (nicotine, placebo). The effects of nicotine on long-latency responses of the auditory system and on electroencephalograms are described in this paper. Results indicated that transdermal administration of nicotine to non-smokers significantly affects the afferent and efferent transmission of acoustic information, as well as enhancing cortical activation. Long-latency response amplitudes and electroencephalogram activity (dominant power and frequencies) were altered by acute doses of transdermal nicotine. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tennessee, Dept Speech Pathol & Audiol, Knoxville, TN 37996 USA. Univ Texas, Dept Commun Sci & Disorders, Austin, TX 78712 USA. Univ Texas, Inst Neurosci, Austin, TX 78712 USA. RP Harkrider, AW (reprint author), Univ Tennessee, Dept Speech Pathol & Audiol, 457 S Stadium Hall, Knoxville, TN 37996 USA. CR ADLER LE, 1992, BIOL PSYCHIAT, V32, P607, DOI 10.1016/0006-3223(92)90073-9 ADLER LE, 1993, AM J PSYCHIAT, V150, P1856 ALLISON T, 1977, EEG CLIN NEUROL, V48, P174 ARMITAGE AK, 1969, BRIT J PHARMACOL, V35, P152 BELL C, 1964, J NEUROPHYSIOL, V24, P101 BHARGAVA VK, 1978, NEUROPHARMACOLOGY, V17, P1009, DOI 10.1016/0028-3908(78)90026-6 BIRD BL, 1978, BIOFEEDBACK SELF-REG, V3, P1, DOI 10.1007/BF00998559 BROWN BA, 1967, ANN NY ACAD SCI, V562, P190 BUCHSBAUM MS, 1977, SCHIZOPHRENIA BULL, V3, P93 BUCHWALD JS, 1991, ELECTROEN CLIN NEURO, V80, P303, DOI 10.1016/0168-5597(91)90114-D BUCHWALD JS, 1992, ELECTROEN CLIN NEURO, V84, P164, DOI 10.1016/0168-5597(92)90021-3 BUCHWALD JS, 1989, ELECTROEN CLIN NEURO, V74, P378, DOI 10.1016/0168-5597(89)90005-1 BUCHWALD JS, 1981, BRAIN RES, V205, P91, DOI 10.1016/0006-8993(81)90722-8 Davis PA, 1939, J NEUROPHYSIOL, V2, P494 DICKERSON LW, 1991, EXP NEUROL, V112, P229, DOI 10.1016/0014-4886(91)90074-M DOMINO EF, 1967, ANN NY ACAD SCI, V562, P216 DONCHIN E, 1979, EVOKED BRAIN POTENTI EDWARDS JA, 1983, PHARMACOL THERAPEUT, V19, P147 ERWIN R, 1986, ELECTROEN CLIN NEURO, V65, P383, DOI 10.1016/0168-5597(86)90017-1 ERWIN R, 1988, ABSTR NEUR, V14, P339 Erwin R J, 1987, Electroencephalogr Clin Neurophysiol Suppl, V40, P461 FRIEDMAN J, 1974, NATURE, V248, P455, DOI 10.1038/248455a0 FRIEDMAN J, 1980, CLIN EXP PHARMACOL P, V7, P609, DOI 10.1111/j.1440-1681.1980.tb00119.x FRIEDMAN J, 1974, CLIN EXP PHARMACOL P, V1, P249, DOI 10.1111/j.1440-1681.1974.tb00547.x GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 Galambos R, 1992, INDUCED RHYTHMS BRAI, P201 GILBERT DG, 1979, PSYCHOL BULL, V86, P643, DOI 10.1037//0033-2909.86.4.643 GOLDING JF, 1988, PHARMACOL BIOCHEM BE, V29, P23, DOI 10.1016/0091-3057(88)90268-7 GOLDSTEIN L, 1967, ANN NY ACAD SCI, V562, P170 GUHA D, 1976, NEUROPHARMACOLOGY, V15, P225, DOI 10.1016/0028-3908(76)90068-X HALL RA, 1973, SCIENCE, V180, P212, DOI 10.1126/science.180.4082.212 HASHIMOTO I, 1982, ELECTROEN CLIN NEURO, V53, P652, DOI 10.1016/0013-4694(82)90141-9 HINMAN CL, 1983, BRAIN RES, V264, P57, DOI 10.1016/0006-8993(83)91120-4 Hirata K, 1996, Rinsho Shinkeigaku, V36, P1318 HYDE ML, 1994, PRINCIPLES APPL AUDI, P47 JACOBSON GP, 1990, ELECTROEN CLIN NEURO, V75, P230, DOI 10.1016/0013-4694(90)90176-K Jacobson J. T., 1994, PRINCIPLES APPL AUDI Jamner LD, 1998, EXP CLIN PSYCHOPHARM, V6, P96, DOI 10.1037/1064-1297.6.1.96 JONES R T, 1970, Biological Psychiatry, V2, P291 JONES GMM, 1992, PSYCHOPHARMACOLOGY, V108, P485, DOI 10.1007/BF02247426 KILENY P, 1987, ELECTROEN CLIN NEURO, V66, P108, DOI 10.1016/0013-4694(87)90180-5 KNAPP DE, 1962, INT J NEUROPHARMACOL, V1, P333 Knott V, 1999, PHARMACOL BIOCHEM BE, V63, P253, DOI 10.1016/S0091-3057(99)00006-4 KNOTT VJ, 1989, NEUROPSYCHOBIOLOGY, V21, P216, DOI 10.1159/000118580 KNOTT VJ, 1984, ADDICT BEHAV, V9, P79, DOI 10.1016/0306-4603(84)90009-1 KNOTT VJ, 1986, ADDICT BEHAV, V11, P219, DOI 10.1016/0306-4603(86)90050-X KNOTT VJ, 1988, NEUROPSYCHOBIOLOGY, V19, P54, DOI 10.1159/000118434 Knott VJ, 1996, NEUROPSYCHOBIOLOGY, V33, P210, DOI 10.1159/000119279 KNOTT VJ, 1978, PSYCHOPHYSIOLOGY, V15, P186, DOI 10.1111/j.1469-8986.1978.tb01360.x KNOTT VJ, 1984, ADDICT BEHAV, V9, P195, DOI 10.1016/0306-4603(84)90057-1 KNOTT VJ, 1985, NEUROPSYCHOBIOLOGY, V13, P74, DOI 10.1159/000118166 KNOTT VJ, 1977, PSYCHOPHYSIOLOGY, V14, P150, DOI 10.1111/j.1469-8986.1977.tb03367.x KOZELKA JW, 1990, J CLIN NEUROPHYSIOL, V7, P191, DOI 10.1097/00004691-199004000-00004 KRAUS N, 1992, BRAIN RES, V587, P186, DOI 10.1016/0006-8993(92)90996-M Kupfermann I, 1991, PRINCIPLES NEURAL SC, P735 LONGO VG, 1967, ANN NY ACAD SCI, V562, P159 Martin J. H., 1991, PRINCIPLES NEURAL SC, P777 McFadden D, 2000, JARO, V1, P89, DOI 10.1007/s101620010008 MCGEE T, 1992, HEARING RES, V61, P147, DOI 10.1016/0378-5955(92)90045-O MURPHREE HB, 1968, FED PROC, V27, P220 MURPHREE HB, 1967, ANN NY ACAD SCI, V142, P245, DOI 10.1111/j.1749-6632.1967.tb13727.x Naatanen R., 1992, ATTENTION BRAIN FUNC, P102 NAGATA K, 1995, BRAIN IMAGING NICOTI, P95 NELSEN JM, 1975, PHARMACOL BIOCHEM BE, V3, P749, DOI 10.1016/0091-3057(75)90101-X NEWHOUSE PA, 1992, PSYCHOPHARMACOLOGY, V108, P480, DOI 10.1007/BF02247425 NEWHOUSE PA, 1987, INTRAVENOUS NICOTINE, V95, P171 NORTON R, 1992, PSYCHOPHARMACOLOGY, V108, P473, DOI 10.1007/BF02247424 PANTEV C, 1991, P NATL ACAD SCI USA, V88, P389 PERRY EK, 1987, J NEUROL NEUROSUR PS, V50, P806, DOI 10.1136/jnnp.50.6.806 PFEFFERBAUM A, 1980, BIOL PSYCHIAT, V15, P209 PHILIPS C, 1971, PSYCHOPHYSIOLOGY, V8, P64, DOI 10.1111/j.1469-8986.1971.tb00437.x PICKWORTH WB, 1986, PHARMACOL BIOCHEM BE, V25, P879, DOI 10.1016/0091-3057(86)90401-6 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P191, DOI 10.1016/0013-4694(74)90156-4 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 ROTH WT, 1980, ELECTROEN CLIN NEURO, V48, P127, DOI 10.1016/0013-4694(80)90299-0 SAHAKIAN BJ, 1991, EFFECTS NICOTINE BIO, P223 SCHAEPPI U, 1967, ANN NY ACAD SCI, V562, P40 Scherg M, 1989, J Cogn Neurosci, V1, P336, DOI 10.1162/jocn.1989.1.4.336 Schurmann M, 1997, NEUROREPORT, V8, P1793 SHAGASS C, 1978, PSYCHOPHARMACOLOGY G, VS, P699 SHEER DE, 1989, BRAIN DYNAMICS, P399 Sheer D.E., 1976, NEUROPSYCHOLOGY LEAR, P71 SHUTE CCD, 1967, ANN NY ACAD SCI, V562, P497 STEVENS KE, 1995, PSYCHOPHARMACOLOGY, V119, P163, DOI 10.1007/BF02246157 STUMPF C, 1967, ANN NY ACAD SCI, V142, P143, DOI 10.1111/j.1749-6632.1967.tb13720.x TEAS DC, 1964, EXP NEUROL, V10, P90 TIITINEN H, 1993, NATURE, V364, P59, DOI 10.1038/364059a0 TIITINEN H, 1994, NEUROREPORT, V6, P190, DOI 10.1097/00001756-199412300-00048 VAZQUEZ AJ, 1967, ANN NY ACAD SCI, V142, P201, DOI 10.1111/j.1749-6632.1967.tb13725.x VINAGRODAVA OS, 1975, HIPPOCAMPUS NEUROPHY, V2, P3 VOGEL W, 1977, J COMP PHYSIOL PSYCH, V91, P418, DOI 10.1037/h0077333 WESNES K, 1983, PHARMACOL THERAPEUT, V21, P189, DOI 10.1016/0163-7258(83)90072-4 WILLIAMSON PC, 1990, ARCH NEUROL-CHICAGO, V47, P1185 WILSON CL, 1984, EXP NEUROL, V84, P74, DOI 10.1016/0014-4886(84)90007-4 WONNACOTT S, 1990, TRENDS PHARMACOL SCI, V11, P216, DOI 10.1016/0165-6147(90)90242-Z WOODSON PP, 1982, PHARMACOL BIOCHEM BE, V17, P915, DOI 10.1016/0091-3057(82)90472-5 WOOLF NJ, 1990, BRAIN RES, V520, P55, DOI 10.1016/0006-8993(90)91691-9 NR 97 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 99 EP 110 DI 10.1016/S0378-5955(01)00347-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500012 PM 11591495 ER PT J AU Sohmer, H Freeman, S AF Sohmer, H Freeman, S TI The latency of auditory nerve brainstem evoked responses to air- and bone-conducted stimuli SO HEARING RESEARCH LA English DT Article DE auditory brainstem response; bone conduction; latency; fluid ID STEM RESPONSE; INFANTS; ADULTS AB The auditory nerve brainstem evoked responses (ABRs) to bone conduction (BQ stimuli are longer in latency than those to air conduction (AC). In order to study the mechanism of this difference, ABR wave I was recorded in experimental animals in response to low intensity (0-20 dB above their threshold) logon stimuli delivered by BC and by using the same bone vibrator to generate the air-conducted stimulus. The BC stimuli were delivered to skull bone, and directly to the contents of the cranial cavity (brain and cerebrospinal fluid) through a craniotomy. ABR wave I in response to BC stimuli delivered to skull bone was significantly longer in latency than that to BC delivered on the brain, while there was no latency difference between AC stimuli and BC to the brain. Furthermore, the vibration (measured with an accelerometer) recorded on the brain during BC stimulation of skull bone was always delayed compared to that measured on the skull. Thus there is a delay in the transfer of vibratory energy from the skull bone to the underlying contents of the cranial cavity. From there, the delayed vibrations of the contents of the cranial cavity are transmitted to the inner ear. This is probably the mechanism of the longer latency BC response compared to the AC response. (C) 2001 Published by Elsevier Science B.V. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, IL-91010 Jerusalem, Israel. RP Sohmer, H (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, POB 12272, IL-91010 Jerusalem, Israel. CR BOEZEMAN EHJF, 1983, ELECTROEN CLIN NEURO, V56, P244, DOI 10.1016/0013-4694(83)90078-0 BURKARD R, 1984, AUDIOLOGY, V23, P85 CORNACCHIA L, 1983, AUDIOLOGY, V22, P430 Durrant J D, 1993, J Am Acad Audiol, V4, P213 DURRANT JD, 1993, AUDIOLOGY, V32, P175 Eggermont J J, 1974, Acta Otolaryngol Suppl, V316, P39 EGGERMON.JJ, 1973, AUDIOLOGY, V12, P193 Freeman S, 2000, HEARING RES, V146, P72, DOI 10.1016/S0378-5955(00)00098-8 GORGA MP, 1993, EAR HEARING, V14, P85, DOI 10.1097/00003446-199304000-00003 GORGA MP, 1989, EAR HEARING, V10, P217, DOI 10.1097/00003446-198908000-00002 Litovsky RY, 1999, J ACOUST SOC AM, V106, P1633, DOI 10.1121/1.427914 MAULDIN L, 1979, ARCH OTOLARYNGOL, V105, P656 MUCHNIK C, 1995, SCAND AUDIOL, V24, P185, DOI 10.3109/01050399509047533 Sohmer H, 2000, HEARING RES, V146, P81, DOI 10.1016/S0378-5955(00)00099-X SORENSEN H, 1959, Acta Otolaryngol, V50, P438, DOI 10.3109/00016485909129217 VONBEKESY G, 1960, EXPT HEARING, P163 Watson NA, 1944, J ACOUST SOC AM, V15, P153, DOI 10.1121/1.1916246 WEBER BA, 1983, SEMIN HEAR, V4, P343, DOI 10.1055/s-0028-1094196 YANG EY, 1987, EAR HEARING, V8, P244, DOI 10.1097/00003446-198708000-00009 NR 19 TC 7 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2001 VL 160 IS 1-2 BP 111 EP 113 DI 10.1016/S0378-5955(01)00337-9 PG 3 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 481GX UT WOS:000171512500013 PM 11591496 ER PT J AU Xu, LJ Jen, PHS AF Xu, LJ Jen, PHS TI The effect of monaural middle ear destruction on postnatal development of auditory response properties of mouse inferior collicular neurons SO HEARING RESEARCH LA English DT Article DE frequency tuning curve; inferior colliculus; middle ear destruction; ossicular chain; tonotopic organization ID SENSORINEURAL HEARING-LOSS; ANTEROVENTRAL COCHLEAR NUCLEUS; SINGLE-UNIT RESPONSES; BRAIN-STEM; BINAURAL INTERACTION; SOUND DEPRIVATION; ECHOLOCATING BATS; ADULT GERBIL; RAT; PROJECTIONS AB This study examined the effect of monaural middle ear destruction on postnatal development of auditory response properties of inferior collicular (IC) neurons of the laboratory mouse, Mus musculus. Monaural middle ear destruction was performed on juvenile and adult mice and the auditory response properties of neurons in both ICs were examined 4 weeks thereafter. IC neurons of control mice typically had lower minimum thresholds, larger dynamic ranges and greater QID values than IC neurons of experimental juvenile and adult mice. In experimental mice, neurons in the ipsilateral IC (relative to the intact ear) typically had longer latencies, higher minimum thresholds, and smaller dynamic ranges than neurons in the contralateral IC. In experimental adult mice, neurons in the ipsilateral IC had sharper frequency tuning curves than neurons in the contralateral IC. Clear tonotopic organization was only observed in the IC of control mice and experimental adult mice. However, the correlation of increasing minimum threshold with best frequency was observed for IC neurons in control mice but not in experimental juvenile and adult mice. Possible mechanisms for these different response properties are discussed. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA. RP Jen, PHS (reprint author), Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA. CR BATKIN S, 1970, ELECTROEN CLIN NEURO, V28, P351, DOI 10.1016/0013-4694(70)90227-0 BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 Cain D, 1999, CHINESE J PHYSIOL, V42, P1 CLOPTON BM, 1977, J NEUROPHYSIOL, V40, P1275 CLOPTON BM, 1978, EXP BRAIN RES, V32, P39 CLOPTON BM, 1976, J NEUROPHYSIOL, V39, P1081 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 ERULKAR SD, 1972, PHYSIOL REV, V52, P237 FENG AS, 1980, BRAIN RES, V189, P530, DOI 10.1016/0006-8993(80)90112-2 Hardie NA, 1999, HEARING RES, V128, P147, DOI 10.1016/S0378-5955(98)00209-3 Hardie NA, 1998, NEUROREPORT, V9, P2019, DOI 10.1097/00001756-199806220-00020 HASHISAKI GT, 1989, J COMP NEUROL, V283, P45 Jen P H, 1990, Chin J Physiol, V33, P231 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 McAlpine D, 1997, J NEUROPHYSIOL, V78, P767 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MOORE DR, 1986, BRAIN RES, V373, P268, DOI 10.1016/0006-8993(86)90341-0 MOORE DR, 1992, NEUROREPORT, V3, P269, DOI 10.1097/00001756-199203000-00014 Nishiyama N, 2000, HEARING RES, V140, P18, DOI 10.1016/S0378-5955(99)00185-9 NORDEEN KW, 1983, J COMP NEUROL, V214, P131, DOI 10.1002/cne.902140203 PASIC TR, 1994, J COMP NEUROL, V348, P111, DOI 10.1002/cne.903480106 POON PWF, 1990, BRAIN RES, V524, P327, DOI 10.1016/0006-8993(90)90710-S POON PWF, 1992, BRAIN RES, V585, P391, DOI 10.1016/0006-8993(92)91243-8 POWELL TPS, 1962, J ANAT, V96, P249 SANES DH, 1985, J NEUROSCI, V5, P1152 SANES DH, 1993, EUR J NEUROSCI, V5, P570, DOI 10.1111/j.1460-9568.1993.tb00522.x SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 SUGA N, 1972, SCIENCE, V177, P82, DOI 10.1126/science.177.4043.82 SUGA N, 1975, J EXP BIOL, V62, P277 TONNDORF J, 1976, ACTA OTO-LARYNGOL, V81, P330, DOI 10.3109/00016487609119970 TONNDORF J, 1970, ANN OTO RHINOL LARYN, V79, P743 TRUNE DR, 1982, J COMP NEUROL, V209, P425, DOI 10.1002/cne.902090411 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 ZHUANG L, 1997, NEUR ABSTR, V23, P184 NR 41 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 1 EP 13 DI 10.1016/S0378-5955(01)00304-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700001 PM 11520630 ER PT J AU Husain, K Whitworth, C Somani, SM Rybak, LP AF Husain, K Whitworth, C Somani, SM Rybak, LP TI Carboplatin-induced oxidative stress in rat cochlea SO HEARING RESEARCH LA English DT Article DE carboplatin; oxidative stress; cochlear antioxidant; lipid peroxidation; nitric oxide ID CISPLATIN-INDUCED OTOTOXICITY; OVARIAN-CANCER; NITRIC-OXIDE; ANTIOXIDANT SYSTEM; GUINEA-PIGS; GLUTATHIONE-PEROXIDASE; SUPEROXIDE-DISMUTASE; SODIUM THIOSULFATE; LIPOIC ACID; PROTECTION AB Carboplatin is currently being used in the clinic against a variety of human cancers. However, high dose carboplatin chemotherapy resulted in ototoxicity in cancer patients. This is the first study to show carboplatin-induccd oxidative stress response in the cochlea of rat, Male Wistar rats were divided into two groups of six animals each and treated as follows: (1) control (normal saline, i.p.) and (2) carboplatin (256 mg/kg, i.p.). Animals in both groups; were sedated with ketamine/xylazine and auditory brainstem-evoked responses were recorded before and 4 days after treatments. The animals were sacrificed on the fourth day and cochleae were harvested and analyzed. A significant elevation of the hearing threshold shifts was noted at clicks, 8, 16, and 32 kHz tone burst stimuli following carboplatin administration. Carboplatin significantly increased nitric oxide and malondialdehyde levels, xanthine oxidase and manganese-superoxide dismutase activities in the cochlea indicating enhanced flux of free radicals. Cochlear glutathione levels, antioxidant enzyme activities such as copper zinc-superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione S-transferase and enzyme protein levels were significantly depleted 4 days after carboplatin treatment. The data suggest that carboplatin induced free radical generation and antioxidant depletion, and caused oxidative injury in the cochleae of rats. (C) 2001 Published by Elsevier Science B.V. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. So Illinois Univ, Sch Med, Dept Surg, Springfield, IL 62794 USA. RP Husain, K (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, 801 N Rutledge, Springfield, IL 62794 USA. CR AEBI H, 1984, METHOD ENZYMOL, V105, P121 ALBERTS DS, 1995, SEMIN ONCOL, V22, P88 ANDERSON ME, 1990, FASEB J, V4, P3251 BAUER FP, 1992, LARYNGO RHINO OTOL, V71, P412, DOI 10.1055/s-2007-997325 Bishop J F, 1992, Semin Oncol, V19, P150 Blommaert FA, 1996, CANCER CHEMOTH PHARM, V38, P273, DOI 10.1007/s002800050482 Bohm S, 1999, ONCOLOGY-BASEL, V57, P115, DOI 10.1159/000012017 Bolis G, 2001, GYNECOL ONCOL, V80, P13, DOI 10.1006/gyno.2000.5995 CARLBERG I, 1985, METHOD ENZYMOL, V113, P484 Cavaletti G, 1998, ANTICANCER RES, V18, P3797 CHURCH MW, 1995, HEARING RES, V86, P195, DOI 10.1016/0378-5955(95)00066-D Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 CLERICI WJ, 1995, HEARING RES, V84, P30, DOI 10.1016/0378-5955(95)00010-2 Conlon BJ, 1999, HEARING RES, V128, P40, DOI 10.1016/S0378-5955(98)00195-6 De Lauretis A, 1999, SCAND AUDIOL, V28, P139 DELEVE LD, 1990, SEMIN LIVER DIS, V10, P251, DOI 10.1055/s-2008-1040481 DEWOSKIN RS, 1992, TOXICOL APPL PHARM, V112, P182, DOI 10.1016/0041-008X(92)90186-V EDKINS RD, 1992, BIOCHEM PHARMACOL, V43, P911, DOI 10.1016/0006-2952(92)90263-I Ettinger DS, 1998, ONCOLOGY-NY, V12, P36 FARISS MW, 1987, METHOD ENZYMOL, V143, P101 FARMS WB, 1993, HEARING RES, V67, P45, DOI 10.1016/0378-5955(93)90230-X FLOHE L, 1984, METHOD ENZYMOL, V105, P114 Gridelli C, 2001, BRIT J CANCER, V84, P38, DOI 10.1054/bjoc.2000.1541 HABIG WH, 1974, J BIOL CHEM, V249, P7130 HAMERS FPT, 1993, CANCER RES, V53, P544 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 Hofstetter P, 2000, HEARING RES, V150, P132, DOI 10.1016/S0378-5955(00)00201-X Hu BH, 1999, HEARING RES, V128, P125, DOI 10.1016/S0378-5955(98)00210-X Husain K, 2001, HEARING RES, V151, P71, DOI 10.1016/S0300-2977(00)00081-4 Husain K, 1998, MOL CELL BIOCHEM, V178, P127, DOI 10.1023/A:1006889427520 IKEDA K, 1993, ACTA OTO-LARYNGOL, V113, P137, DOI 10.3109/00016489309135781 ISHIKAWA T, 1992, TRENDS BIOCHEM SCI, V17, P463, DOI 10.1016/0968-0004(92)90489-V KENNEDY ICS, 1990, CANCER CHEMOTH PHARM, V26, P232, DOI 10.1007/BF02897206 Lautermann J, 1997, HEARING RES, V114, P75, DOI 10.1016/S0378-5955(97)00154-8 MACDONALD MR, 1994, J OTOLARYNGOL, V23, P151 MALDOON LL, 2000, CLIN CANCER RES, V6, P309 Meyer WH, 2001, J CLIN ONCOL, V19, P171 MISRA HP, 1972, J BIOL CHEM, V247, P3170 Mount R J, 1995, Acta Otolaryngol Suppl, V519, P60 Neuwelt EA, 1998, J PHARMACOL EXP THER, V286, P77 NONCLERCQ D, 1989, EXP MOL PATHOL, V51, P123, DOI 10.1016/0014-4800(89)90013-0 Obermair A, 1998, INT J ONCOL, V13, P1023 OHKAWA H, 1979, ANAL BIOCHEM, V95, P351, DOI 10.1016/0003-2697(79)90738-3 PIERSON MG, 1982, HEARING RES, V6, P141, DOI 10.1016/0378-5955(82)90050-8 PIGEOLET E, 1990, MECH AGEING DEV, V51, P283, DOI 10.1016/0047-6374(90)90078-T Pivot X, 2001, ONCOLOGY-BASEL, V60, P66, DOI 10.1159/000055299 Ranjan P, 1998, ANTI-CANCER DRUG, V9, P333, DOI 10.1097/00001813-199804000-00007 RAVI R, 1995, PHARMACOL TOXICOL, V76, P386 READ SM, 1981, ANAL BIOCHEM, V116, P53, DOI 10.1016/0003-2697(81)90321-3 Rybak LP, 1999, TOXICOL SCI, V47, P195, DOI 10.1093/toxsci/47.2.195 RYBAK LP, 1995, FUND APPL TOXICOL, V26, P293, DOI 10.1006/faat.1995.1100 SINGH NM, 1987, CLIN CHIM ACTA, V162, P29 SMITH VC, 1989, GLUTATHIONE CHEM BIO, P141 Song BB, 1996, HEARING RES, V94, P87, DOI 10.1016/0378-5955(96)00003-2 Srivastava RC, 1996, BIOMETALS, V9, P139 TAUDY M, 1992, AUDIOLOGY, V31, P293 Teranishi M, 2001, HEARING RES, V151, P61, DOI 10.1016/S0300-2977(00)00080-2 Wandt H, 1999, BONE MARROW TRANSPL, V23, P763, DOI 10.1038/sj.bmt.1701659 Watanabe K, 2000, ANTI-CANCER DRUG, V11, P401, DOI 10.1097/00001813-200006000-00011 Watanabe K, 2000, ANTI-CANCER DRUG, V11, P731, DOI 10.1097/00001813-200010000-00010 Wink DA, 1997, NITRIC OXIDE-BIOL CH, V1, P88, DOI 10.1006/niox.1996.0108 YOUNES M, 1981, CHEM-BIOL INTERACT, V34, P257, DOI 10.1016/0009-2797(81)90098-3 NR 62 TC 22 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 14 EP 22 DI 10.1016/S0378-5955(01)00306-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700002 PM 11520631 ER PT J AU Osofsky, MR Moore, CM Leake, PA AF Osofsky, MR Moore, CM Leake, PA TI Does exogenous GM1 ganglioside enhance the effects of electrical stimulation in ameliorating degeneration after neonatal deafness? SO HEARING RESEARCH LA English DT Article DE auditory system development; cochlear implant; cochlear nucleus; electrical stimulation; GM1 ganglioside; neonatal deafness; neurotrophins ID STEM AUDITORY NUCLEI; ANTEROVENTRAL COCHLEAR NUCLEUS; CONDUCTIVE HEARING-LOSS; ACUTE ISCHEMIC STROKE; INFERIOR COLLICULUS; DEAFENED CATS; CELL-SIZE; SOUND DEPRIVATION; RAPID CHANGES; SURVIVAL AB This study examined the combined effects of administration of exogenous GM1 ganglioside and electrical stimulation on the cochlear nucleus (CN) of cats deafened neonatally by ototoxic drugs. Five normal hearing adult cats served as controls. Another 12 cats were deafened bilaterally by daily injections of neomycin sulfate (60 mg/kg) for 17-21 days after birth until auditory brainstem testing demonstrated profound hearing loss. Six of the deaf animals comprised the GM1 group, which received daily injections of GM1 ganglioside (30 mg/kg) for 28 38 days during the period after profound deafness was confirmed, and prior to receiving a cochlear implant. The non-GM1 group (n=6) received no treatment during this interim period. All the deafened animals underwent unilateral cochlear implantation at 6 -9 weeks postnatal and received several months (mean duration, 32 weeks) of chronic electrical stimulation (4 h/day, 5 days/week). Stimulation was delivered by intracochlear bipolar electrodes, using electrical signals that were designed to be temporally challenging to the central auditory system. Results showed that in the neonatally deafened animals, both the GM1 and non-GM1 groups, the volume of the CN was markedly reduced (to 76% of normal), but there was no difference between the animals that received GM1 and those that did not. The cross sectional areas of spherical cell somata in both GM1 and non-GM1 groups also showed a highly significant reduction in size, to less than or equal to 75% of normal after neonatal deafening. Moreover, in both the GM1 and non-GM1 groups, the spherical cells in the CN ipsilateral to the implanted cochlea were significantly larger (6%) than cells in the control, unstimulated CN. Again, however, there was no significant difference between the GM1 group and the non-GM1 group in spherical cell size. These results contrast sharply with previous reports that exogenous GM1 prevents CN degeneration after neonatal conductive hearing loss and partially prevents spiral ganglion cell degeneration when administered immediately after ototoxic drug deafening in adult animals. Taken together, findings to date suggest that GM1 may be effective in preventing degeneration only if the GM1 is administered immediately at the time hearing loss occurs. (C)) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Francisco, Dept Otolaryngol, Epstein Labs, HNS, San Francisco, CA 94143 USA. RP Leake, PA (reprint author), Univ Calif San Francisco, Dept Otolaryngol, Epstein Labs, HNS, 533 Parnassus Ave,Room U-490, San Francisco, CA 94143 USA. CR Alter M, 1998, ANN NY ACAD SCI, V845, P391, DOI 10.1111/j.1749-6632.1998.tb09691.x ANNIKO M, 1989, ARCH OTO-RHINO-LARYN, V246, P43, DOI 10.1007/BF00454133 Araki S, 1998, LARYNGOSCOPE, V108, P687, DOI 10.1097/00005537-199805000-00012 ARGENTINO C, 1989, STROKE, V20, P1143 BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 Dobrowsky RT, 1998, ANN NY ACAD SCI, V845, P32, DOI 10.1111/j.1749-6632.1998.tb09660.x Eggermont J.J., 1986, ACTA OTOLARYNGOL S, V429, P1 FERRARI G, 1995, J BIOL CHEM, V270, P3074 Fleckeisen C E, 1991, Acta Otolaryngol Suppl, V489, P23 Fritzsch B, 1997, TRENDS NEUROSCI, V20, P159, DOI 10.1016/S0166-2236(96)01007-7 GEISLER FH, 1993, ANN EMERG MED, V22, P1041, DOI 10.1016/S0196-0644(05)82748-9 HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 KIANG NYS, 1975, J COMP NEUROL, V162, P221, DOI 10.1002/cne.901620205 Kitzes L, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P256 Leake PA, 1999, J COMP NEUROL, V412, P543, DOI 10.1002/(SICI)1096-9861(19991004)412:4<543::AID-CNE1>3.0.CO;2-3 LEAKE PA, 1992, HEARING RES, V64, P99, DOI 10.1016/0378-5955(92)90172-J LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X Leake PA, 2000, HEARING RES, V147, P221, DOI 10.1016/S0378-5955(00)00133-7 LEAKE PA, 1994, INT INTERSCIENCE SEM, P50 Leake PA, 1997, HEARING RES, V113, P117, DOI 10.1016/S0378-5955(97)00133-0 LEAKE PA, 1995, HEARING RES, V82, P65 LEAKE PA, 2000, COCHLEAR IMPLANTS, P31 Leong CK, 2000, READ WRIT, V12, P277, DOI 10.1023/A:1008168902922 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 LUSTIG LR, 1994, HEARING RES, V74, P29, DOI 10.1016/0378-5955(94)90173-2 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 Miller J M, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P57 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 MOORE DR, 1986, BRAIN RES, V373, P268, DOI 10.1016/0006-8993(86)90341-0 MOORE JK, 1994, AM J OTOL, V15, P588 Moore JK, 1997, ANN OTO RHINOL LARYN, V106, P385 Niparko JK, 1997, OTOLARYNG HEAD NECK, V117, P229, DOI 10.1016/S0194-5998(97)70179-7 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 PARKINS CW, 1999, ASS RES OT ABS, V22, P167 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 Roland JT, 2000, COCHLEAR IMPLANTS, P171 RUBEN RJ, 1980, ANN OTO RHINOL LARYN, V89, P303 Saada AA, 1996, BRAIN RES, V736, P315, DOI 10.1016/0006-8993(96)00719-6 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S SPOERRI PE, 1988, NEUROSCI LETT, V90, P21, DOI 10.1016/0304-3940(88)90780-X SVENNERHOLM L, 1994, LIFE SCI, V55, P2125, DOI 10.1016/0024-3205(94)00393-9 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 Vollmer M, 1999, J NEUROPHYSIOL, V82, P2883 Walsh Edward J., 1992, P161 WALSH ME, 1994, HEARING RES, V75, P54, DOI 10.1016/0378-5955(94)90055-8 Waltzman S B, 1999, Trends Amplif, V4, P143, DOI 10.1177/108471389900400402 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WEBSTER DB, 1983, HEARING RES, V12, P145, DOI 10.1016/0378-5955(83)90123-5 ZHENG JL, 1995, J NEUROSCI, V15, P5079 NR 56 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 23 EP 35 DI 10.1016/S0378-5955(01)00311-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700003 PM 11520632 ER PT J AU Neuert, V Pressnitzer, D Patterson, RD Winter, IM AF Neuert, V Pressnitzer, D Patterson, RD Winter, IM TI The responses of single units in the inferior colliculus of the guinea pig to damped and ramped sinusoids SO HEARING RESEARCH LA English DT Article DE temporal asymmetry; brainstem; onset unit; amplitude modulation ID COCHLEAR NUCLEUS; TEMPORAL ASYMMETRY; COMPUTER-MODEL; NEURAL REPRESENTATIONS; AMPLITUDE-MODULATION; AUDITORY PERIPHERY; PHASE SENSITIVITY; QUANTAL ANALYSIS; VIRTUAL PITCH; NEURONS AB Temporal asymmetry can have a pronounced effect on the perception of a sinusoid. For instance, if a sinusoid is amplitude modulated by a decaying exponential that restarts every 50 ms, (a damped sinusoid) listeners report a two-component percept: a tonal component corresponding to the carrier and a drumming component corresponding to the envelope modulation period. When the amplitude modulation is reversed in time (a ramped sinusoid) the perception changes markedly, the tonal component increases while the drumming component decreases. The long-term Fourier energy spectra are identical for damped and ramped sinusoids with the same exponential half-life. Modelling studies suggest that this perceptual asymmetry must occur central to the peripheral stages of auditory processing (Patterson and Irino, 1998). To test this hypothesis, we have recorded the responses of single units in the inferior colliculus of the anaesthetised guinea pig. We divided single units into three groups: onset, on-sustained and sustained, based on their temporal adaptation properties to suprathreshold tone bursts at the unit's best frequency. The asymmetry observed in the neural responses of single units was quantified in two ways: a simple total spike count measure and a ratio of the tallest bin of the modulation period histogram to the total number of spikes. Responses were more diverse than those observed with similar stimuli in a previous study in the ventral cochlear nucleus (Pressnitzer et al., 2000). The main results were: (1) The shape of the responses of on-sustained units to ramped sinusoids resembled the shape of the responses to damped sinusoids. This is in contrast to the response shapes in the VCN, which were always similar to the stimulating sinusoid. (2) Units classified as onsets often responded only to the damped stimuli. (3) All units display significant asymmetry in discharge rate for at least one of the half-lives tested and 20% showed significant response asymmetry over all of the half-lives tested. (4) A summary population measure of temporal asymmetry based on total spike count reveals the same pattern of results as that obtained psycho physically using the same stimuli (Patterson, 1994a). (C) 2001 Elsevier Science BN. All rights reserved. C1 Univ Cambridge, Physiol Lab, Ctr Neural Basis Hearing, Cambridge CB2 3EG, England. CNRS, Ircam, UMR 9912, F-75004 Paris, France. RP Winter, IM (reprint author), Univ Cambridge, Physiol Lab, Ctr Neural Basis Hearing, Downing St, Cambridge CB2 3EG, England. EM imw107@cam.ac.uk RI Pressnitzer, Daniel/F-6092-2012 CR Akeroyd MA, 1997, J ACOUST SOC AM, V101, P430, DOI 10.1121/1.417988 AKEROYD MA, 1995, J ACOUST SOC AM, V98, P2466, DOI 10.1121/1.414462 DAVIS KA, 1999, ABSTR SOC NEUROSCI, V25, P687 Fay RR, 1996, AUDIT NEUROSCI, V2, P377 Ferguson G. A., 1976, STAT ANAL PSYCHOL ED FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 FURUKAWA T, 1982, J PHYSIOL-LONDON, V322, P181 HEWITT MJ, 1994, J ACOUST SOC AM, V95, P2145, DOI 10.1121/1.408676 Irino T, 1996, J ACOUST SOC AM, V99, P2316, DOI 10.1121/1.415419 LeBeau FEN, 1996, J NEUROPHYSIOL, V75, P902 Lu T, 2001, J NEUROPHYSIOL, V85, P2364 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2883, DOI 10.1121/1.400726 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2866, DOI 10.1121/1.400725 MERRILL EG, 1972, MED BIOL ENG, V10, P662, DOI 10.1007/BF02476084 Nuding SC, 1999, HEARING RES, V131, P89, DOI 10.1016/S0378-5955(99)00023-4 Patterson RD, 1998, J ACOUST SOC AM, V104, P2967, DOI 10.1121/1.423879 PATTERSON RD, 1992, ADV BIOSCI, V83, P429 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1409, DOI 10.1121/1.410285 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1419, DOI 10.1121/1.410286 Pressnitzer D, 2000, HEARING RES, V149, P155, DOI 10.1016/S0378-5955(00)00175-1 Rees A, 1997, J NEUROPHYSIOL, V77, P2945 RHODE WS, 1987, J NEUROPHYSIOL, V57, P414 WINTER IM, 1990, HEARING RES, V44, P161, DOI 10.1016/0378-5955(90)90078-4 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 NR 24 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 36 EP 52 DI 10.1016/S0378-5955(01)00318-5 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700004 PM 11520633 ER PT J AU Tykocinski, M Duan, Y Tabor, B Cowan, RS AF Tykocinski, M Duan, Y Tabor, B Cowan, RS TI Chronic electrical stimulation of the auditory nerve using high surface area (HiQ) platinum electrodes SO HEARING RESEARCH LA English DT Article DE cochlear implant; high surface area electrode; electrical stimulation; electrode impedance; cochlear histopathology; auditory brainstem response; electrically evoked auditory brainstem response ID CHARGE INJECTION LIMITS; BALANCED STIMULI; NEURAL DAMAGE; PULSES AB High surface area cochlear implant electrodes with much smaller geometric surface areas than current designs might be used in the future to increase the number of stimulating electrodes along the carrier. Potential problems with an increase in charge density for a common stimulus resulting from decreasing the geometric surface area would be reduced by the enlarged real surface area of such electrodes. Electrochemically modified (HiQ) platinum (Pt) electrodes, with a real surface area similar to 75 times greater than the current standard Pt electrodes of the same geometric size, had shown in vitro a low polarization (Z(pol)) and electrode impedance (Z(e)), as well as a low residual direct current (DC). In this study we examined the chronic performance of HiQ electrodes in cats, which were bilaterally implanted with a two-channel HiQ or standard Pt scala tympani electrode array and unilaterally stimulated for periods of up to 2390 h. Stimuli consisted of 50 mus/phasc charge-balanced biphasic current pulses presented at 2000 pulses/s/channel with a 50%, duty cycle. Electrode impedance (Z(e)), access resistance (R-a) and polarization impedance (Z(pol)) were calculated from current and voltage measurements obtained periodically throughout the implantation period. Immediately following implantation HiQ electrodes showed a significantly smaller Z(pol), resulting in a reduced Z(e) (P < 0.0001) compared to standard electrodes, while there was no significant difference between R-a of both electrode designs (P = 0.91). Subsequently, Z(e) generally increased mainly due to a rise in R-a, which dominated Z(e) and obliterated the effect of a lower Z(pol) on Z(e) in HiQ electrodes. Peak R-a levels correlated closely (r = 0.85) with the amount of intracochlear Fibrous tissue found adjacent to the array. Following explantation of the array, voltage waveforms for both electrode designs recorded in saline were again very similar to those recorded immediately after implantation. Mean DC levels were consistently lower for HiQ electrodes compared with standard electrodes (22.45 nA vs 134.7 nA). Histopathological examination of corresponding cochlear sections comparing the stimulated test side with the unstimulated control side showed no significant difference (P > 0.05) for either animals implanted with HiQ electrodes (n = 6) or standard electrodes (n = 2). Nor were there any significant differences between the spiral ganglion cell density of the basal turn implanted with HiQ or standard electrodes for both the stimulated test (P = 0.31) and the unstimulated control side (P = 0.84). Although these findings are based on a small group of animals implanted with standard electrodes (n = 2), and those negative statistical results could potentially be due to the small sample size, similar spiral ganglion cell survival was found in a previous study of a larger group of animals using standard electrodes stimulated with the same stimulus paradigm as in the present study [Xu et al. (1997) Hear. Res. 105, 1-29]. Our data indicate that while some initial advantages of HiQ electrodes are lost during chronic implantation due to intracochlear fibrous tissue growth, low DC levels and the high surface area appear to be maintained, suggesting that HiQ electrodes may have important clinical applications. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Cooperat Res Ctr Cochlear Implant & Hearing Aid I, Melbourne, Vic 3002, Australia. Univ Melbourne, Dept Otolaryngol, Parkville, Vic 3052, Australia. Cochlear Ltd, Lane Cove, NSW 2066, Australia. RP Tykocinski, M (reprint author), Cooperat Res Ctr Cochlear Implant & Hearing Aid I, 384-388 Albert St, Melbourne, Vic 3002, Australia. RI Tabor, Bruce/C-8902-2009; 颜, 志波/G-1367-2011 OI Tabor, Bruce/0000-0002-2028-8318; CR AGNEW WF, 1983, EXP NEUROL, V79, P347 BEEBE X, 1988, IEEE T BIO-MED ENG, V35, P494, DOI 10.1109/10.2122 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BOLZAN AE, 1988, ELECTROCHIM ACTA, V33, P1743, DOI 10.1016/0013-4686(88)85009-6 BROWN WJ, 1977, J NEUROSURG, V47, P366, DOI 10.3171/jns.1977.47.3.0366 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P440, DOI 10.1109/TBME.1977.326179 BUSBY PA, 2000, P 5 EUR S PAED COCHL, P151 Clark G M, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P40 COTE KR, 1987, ANN BIOMED ENG, V15, P419, DOI 10.1007/BF02363562 DONALDSO.PE, 1974, MED BIOL ENG, V12, P131, DOI 10.1007/BF02629846 FOX WC, 1993, J BIOMED MATER RES, V27, P763 Frumkin A. N., 1963, ADVANCES ELECTROCHEM, V3, P287 Gilman S., 1967, ELECTROANALYTICAL CH, V2, P111 Huang CQ, 1999, IEEE T BIO-MED ENG, V46, P461, DOI 10.1109/10.752943 HUANHG C, 2000, HEARING RES, V3478, P1 JOHNSON PF, 1977, J BIOMED MATER RES, V11, P637, DOI 10.1002/jbm.820110502 LINAHAN L, 1998, P AUSTR NEUR SOC, P163 Loeb GE, 1995, J NEUROSCI METH, V63, P175, DOI 10.1016/0165-0270(95)00107-7 LOEB GE, 1977, J BIOMED MATER RES, V11, P195, DOI 10.1002/jbm.820110206 MCCREERY DB, 1988, ANN BIOMED ENG, V16, P463, DOI 10.1007/BF02368010 MCCREERY DB, 1990, IEEE T BIO-MED ENG, V37, P996, DOI 10.1109/10.102812 MILLER JM, 1986, AM J OTOLARYNG, V7, P239, DOI 10.1016/S0196-0709(86)80045-X Mitchell A, 1997, HEARING RES, V105, P30, DOI 10.1016/S0378-5955(96)00202-X NI D, 1992, HEARING RES, V62, P62 OTTEN JM, 1994, Patent No. 5326448 Patrick J., 1990, COCHLEAR PROSTHESES, p99 PUDENZ RH, 1977, FUNCTIONAL ELECT STI REUTER G, 1999, P 1999 C IMPL AUD PR, P68 ROSE TL, 1990, IEEE T BIO-MED ENG, V37, P1118, DOI 10.1109/10.61038 SHEPHERD RK, 1987, ANN OTO RHINOL LARYN, V96, P50 SHEPHERD RK, 1994, HEARING RES, V81, P150, DOI 10.1016/0378-5955(94)90162-7 SHEPHERD RK, 1990, 13 NIH PROGR REP U M Shepherd RK, 1990, COCHLEAR PROSTHESES, P69 Shepherd R K, 1983, Acta Otolaryngol Suppl, V399, P19 SHEPHERD RK, 1995, AM J OTOL, V16, P186 Shepherd RK, 1999, ACTA OTO-LARYNGOL, V119, P674, DOI 10.1080/00016489950180621 SHEPHERD RK, 1991, ACTA OTO-LARYNGOL, V111, P848, DOI 10.3109/00016489109138421 TABOR B, 2000, Patent No. 56116413 TYKOCINSKI M, 1999, P 19 AUST NEUR SOC, V10, P181 TYKOCINSKI M, 2000, P 4 EUR C OT HEAD NE, P327 TYKOCINSKI M, 2000, P 5 EUR S PAED COCHL, P47 Tykocinski M., 1995, Annals of Otology Rhinology and Laryngology, V104, P68 Xu J, 1997, HEARING RES, V105, P1, DOI 10.1016/S0378-5955(96)00193-1 YUEN TGH, 1981, NEUROSURGERY, V9, P292 NR 44 TC 29 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 53 EP 68 DI 10.1016/S0378-5955(01)00320-3 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700005 PM 11520634 ER PT J AU Santos-Sacchi, J Wu, M Kakehata, S AF Santos-Sacchi, J Wu, M Kakehata, S TI Furosemide alters nonlinear capacitance in isolated outer hair cells SO HEARING RESEARCH LA English DT Article DE outer hair cell; motility; nonlinear capacitance; basilar membrane tuning ID GUINEA-PIG COCHLEA; MECHANICAL RESPONSES; VOLTAGE-DEPENDENCE; BASILAR-MEMBRANE; ETHACRYNIC-ACID; GATING CHARGE; MOTILITY; SERUM; SALICYLATE; PERILYMPH AB The outer hair cell (OHC) from the organ of Corti plays a crucial role in hearing through its unique voltage-depen dent mechanical responses. Furosemide, one of the loop diuretics, disrupts normal cochlear function. Here we report on direct effects of furosemide on OHC motility-related, voltage-dependent capacitance using the whole-cell patch-clamp technique. Extracellularly applied furosemide reversibly shifted the voltage at peak capacitance (V-pkCm) to positive levels. The shift, whose maximum approached 90 mV, evidenced a Hill coefficient of 1.5 and K-1/2 of 10 MM. Changes in the magnitude of nonlinear capacitance were not fully reversible. While it is clear that the overwhelming effect of furosemide on hearing results via its effects on the endolymphatic potential, the present results indicate that furosemide directly alters OHC motility and may, in part, contribute to sensory dysfunction. (C) 2001 Published by Elsevier Science B.V. C1 Yale Univ, Sch Med, Dept Surg Otolaryngol, Otolaryngol Sect, New Haven, CT 06510 USA. Yale Univ, Sch Med, Dept Surg Otolaryngol, Neurobiol Sect, New Haven, CT 06510 USA. RP Santos-Sacchi, J (reprint author), Yale Univ, Sch Med, Dept Surg Otolaryngol, Otolaryngol Sect, BML 244,333 Cedar St, New Haven, CT 06510 USA. CR Ashmore J. F., 1990, NEUROSCI RES S, V12, pS39 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWN RD, 1972, TOXICOL APPL PHARM, V22, P589 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 COMIS SD, 1990, ACTA OTO-LARYNGOL, V109, P49, DOI 10.3109/00016489009107414 DALLOS P, 1993, J NEUROPHYSIOL, V70, P299 Dolan DF, 1997, J ACOUST SOC AM, V102, P3587, DOI 10.1121/1.421008 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P409 EVANS MG, 1986, PFLUG ARCH EUR J PHY, V406, P65, DOI 10.1007/BF00582955 Forge A, 1982, Br J Audiol, V16, P109, DOI 10.3109/03005368209081455 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 HUANG GJ, 1993, BIOPHYS J, V65, P2228 JASTREBOFF PJ, 1986, ARCH OTOLARYNGOL, V112, P1050 Kakehata S, 1996, J NEUROSCI, V16, P4881 KAKEHATA S, 1995, BIOPHYS J, V68, P2190 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 Mills CD, 1997, J CHROMATOGR B, V701, P65, DOI 10.1016/S0378-4347(97)00341-1 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 NICOLL RA, 1978, J PHYSIOL-LONDON, V283, P121 Ohnishi S, 1993, Acta Otolaryngol Suppl, V500, P42 PEARCE RA, 1993, NEURON, V10, P189, DOI 10.1016/0896-6273(93)90310-N RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RYBAK LP, 1979, ACTA OTO-LARYNGOL, V88, P382, DOI 10.3109/00016487909137182 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 Santos-Sacchi J, 2001, J PHYSIOL-LONDON, V531, P661, DOI 10.1111/j.1469-7793.2001.0661h.x SANTOS-SACCHI J, 1993, BIOPHYS J, V65, P2217 Santos-Sacchi J, 1998, J PHYSIOL-LONDON, V510, P225, DOI 10.1111/j.1469-7793.1998.225bz.x SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 WOLPAW EW, 1986, BIOCHIM BIOPHYS ACTA, V855, P302, DOI 10.1016/0005-2736(86)90178-1 Wu M, 1998, J MEMBRANE BIOL, V166, P111, DOI 10.1007/s002329900453 Zheng J, 2000, NATURE, V405, P149, DOI 10.1038/35012009 NR 34 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 69 EP 73 DI 10.1016/S0378-5955(01)00321-5 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700006 PM 11520635 ER PT J AU Baer, T Moore, BCJ Marriage, J AF Baer, T Moore, BCJ Marriage, J TI Detection and intensity discrimination of brief tones as a function of duration by hearing-impaired listeners SO HEARING RESEARCH LA English DT Article DE intensity discrimination; hearing impairment; basilar membrane compression ID BASILAR-MEMBRANE NONLINEARITY; AUDITORY FILTER SHAPES; INPUT-OUTPUT FUNCTIONS; TEMPORAL INTEGRATION; CHINCHILLA COCHLEA; FREQUENCY; RESPONSES; MECHANICS; MASKING; BASE AB For normal listeners, difference limens for intensity (DLs) for Gaussian-shaped tone pulses are largest at medium Pulse durations (corresponding to about five cycles of the tonal carrier) when the pedestals are 10 dB above threshold, either in quiet or in a pink noise background. One explanation for this is that worst performance occurs when the internal representation of the tone pulses is most compact in time and frequency, affording minimial opportunity for 'multiple looks' (Van Schijndel et al., J. Acoust. Soc. Am. 105 (1999) 3425-3435). However, the mid-duration worsening is largest for medium overall levels, suggesting an involvement of compression on the basilar membrane (BM), which is also greatest at medium levels (Baer ct al., J. Acoust. Soc. Am. 106 (1999) 1907-1916). If this is so, the mid-duration worsening should be reduced when BM compression is reduced by outer hair cell damage. To test this, subjects with sensorineural hearing losses were tested using 1-kHz or 4-kHz Gaussian-shaped tone pulses, in quiet or in pink noise that raised thresholds by 10-20 dB. For subjects with mild losses, poorest performance was sometimes found for medium durations. For more severe losses, intensity DLs tended to improve monotonically or remain roughly constant with increasing duration. Performance overall tended to be better for subjects with greater hearing losses. The results are more consistent with ail explanation based on BM compression than with an explanation based on multiple looks. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Baer, T (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. RI Moore, Brian/I-5541-2012 CR Baer T, 1999, J ACOUST SOC AM, V106, P1907, DOI 10.1121/1.427939 Buus S, 1999, J ACOUST SOC AM, V105, P3464, DOI 10.1121/1.424673 CARLYON RP, 1990, J ACOUST SOC AM, V87, P260, DOI 10.1121/1.399293 CHUNG DY, 1981, J SPEECH HEAR RES, V24, P514 COOPER NP, 1994, HEARING RES, V78, P221, DOI 10.1016/0378-5955(94)90028-0 Eddins David A., 1995, P207, DOI 10.1016/B978-012505626-7/50008-X ELLIOTT LL, 1975, AUDIOLOGY, V14, P336 FLORENTINE M, 1986, J ACOUST SOC AM, V79, P792, DOI 10.1121/1.393469 FLORENTINE M, 1988, J ACOUST SOC AM, V84, P195, DOI 10.1121/1.396964 GARNER WR, 1947, J EXP PSYCHOL, V37, P293, DOI 10.1037/h0055734 GENGEL RW, 1971, J SPEECH HEAR DISORD, V36, P213 GLASBERG BR, 1986, J ACOUST SOC AM, V79, P1020, DOI 10.1121/1.393374 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T HALL JW, 1983, J ACOUST SOC AM, V74, P1172, DOI 10.1121/1.390040 Hicks ML, 1999, J ACOUST SOC AM, V105, P326, DOI 10.1121/1.424526 HUGHES JW, 1946, PROC R SOC SER B-BIO, V133, P486, DOI 10.1098/rspb.1946.0026 Moore B., 1998, COCHLEAR HEARING LOS Moore BCJ, 1997, AUDIT NEUROSCI, V3, P289 Moore B C, 2001, Trends Amplif, V5, P1, DOI 10.1177/108471380100500102 Moore BCJ, 1998, PSYCHOL REV, V105, P108, DOI 10.1037/0033-295X.105.1.108 MOORE BCJ, 2001, IN PRESS EAR HEAR Moore BCJ, 2000, BRIT J AUDIOL, V34, P205 Moore BCJ, 1999, J ACOUST SOC AM, V106, P2761, DOI 10.1121/1.428133 Oxenham AJ, 1997, J ACOUST SOC AM, V101, P3676, DOI 10.1121/1.418328 Oxenham AJ, 1997, J ACOUST SOC AM, V101, P3666, DOI 10.1121/1.418327 PEDERSEN CB, 1973, ACTA OTO-LARYNGOL, V75, P32, DOI 10.3109/00016487309139635 Pick G., 1977, PSYCHOPHYSICS PHYSL, P273 Plack CJ, 2000, J ACOUST SOC AM, V107, P501, DOI 10.1121/1.428318 PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 Recio A, 1998, J ACOUST SOC AM, V103, P1972, DOI 10.1121/1.421377 Rhode WS, 1996, AUDIT NEUROSCI, V3, P101 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 Ruggero MA, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P23 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 Tyler R. S., 1986, FREQUENCY SELECTIVIT, P309 van Schijndel NH, 1999, J ACOUST SOC AM, V105, P3425, DOI 10.1121/1.424683 VIEMEISTER NF, 1991, J ACOUST SOC AM, V90, P858, DOI 10.1121/1.401953 VONKLITZING R, 1994, J ACOUST SOC AM, V95, P2192, DOI 10.1121/1.408679 Yates Graeme K., 1995, P41, DOI 10.1016/B978-012505626-7/50004-2 NR 41 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 74 EP 84 DI 10.1016/S0378-5955(01)00324-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700007 PM 11520636 ER PT J AU FitzGerald, JV Burkitt, AN Clark, GM Paolini, AG AF FitzGerald, JV Burkitt, AN Clark, GM Paolini, AG TI Delay analysis in the auditory brainstem of the rat: comparison with click latency SO HEARING RESEARCH LA English DT Article DE auditory brainstem; click latency; delay analysis; temporal processing ID MEDIAL SUPERIOR OLIVE; COCHLEAR NERVE; PHASE-LOCKING; HUMAN ADULTS; RESPONSES; STEM; FIBERS; DISCHARGES; FREQUENCY; INTENSITY AB Many cells in the auditory brainstem 'phase lock' to tone stimuli. From the changing phase relationship between the stimulus and the neural response in phase-locking cells, the delay between them can be estimated. This delay, however, is consistently greater than the latency measured in response to click stimuli, an important discrepancy. In this paper the different measures of delay, namely phase delay, group delay and signal-front delay are re-examined. An improved method for computing the average group delay is presented, which accounts for the cyclical nature of the phase data. Data were collected from units in successive processing sites of auditory pathway: the auditory nerve, the cochlear nucleus, the trapezoid body and the medial nucleus of the trapezoid body. Low-characteristic frequency (CF) units gave multimodal post-stimulus-time histograms in response to clicks, and showed stepwise decreases in latency with increasing intensity, with the appearance of earlier peaks in the response, rather than shifts in the timing of the peaks. The separation of peaks corresponded to the inverse of the unit's CF. High-CF units also showed a decline in click latency with intensity, but to a lesser degree than low CF units. We present an analysis which explains the difference between click latency and delay, and which in contrast to previous accounts is experimentally testable. We demonstrate that this new framework accounts for the discrepancy between the two measures of delay, and in addition accounts for the observed stepwise shifts in click latency for low-CF units. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Royal Victorian Eye & Ear Hosp, Dept Otolaryngol, Melbourne, Vic 3002, Australia. Bion Ear Inst, Melbourne, Vic 3002, Australia. RP Paolini, AG (reprint author), Univ Melbourne, Royal Victorian Eye & Ear Hosp, Dept Otolaryngol, 32 Gisborne St, Melbourne, Vic 3002, Australia. RI Burkitt, Anthony/N-9077-2013 OI Burkitt, Anthony/0000-0001-5672-2772 CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 ANDERSON DJ, 1973, J ACOUST SOC AM, V54, P361, DOI 10.1121/1.1913585 Bowman DM, 1998, HEARING RES, V119, P14, DOI 10.1016/S0378-5955(98)00041-0 Bowman DM, 1997, J ACOUST SOC AM, V101, P1550, DOI 10.1121/1.418129 CARR CE, 1988, P NATL ACAD SCI USA, V85, P8311, DOI 10.1073/pnas.85.21.8311 GEISLER CD, 1983, J ACOUST SOC AM, V73, P1671, DOI 10.1121/1.389388 GIBSON MM, 1977, PSYCHOPHYSICS PHYSL GLEICH O, 1988, HEARING RES, V32, P81, DOI 10.1016/0378-5955(88)90148-7 GOBLICK TJ, 1969, J ACOUST SOC AM, V46, P924, DOI 10.1121/1.1911812 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GOLDSTEIN JL, 1971, PHYSL AUDITORY SYSTE Grothe B, 2000, PROG NEUROBIOL, V61, P581, DOI 10.1016/S0301-0082(99)00068-4 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 Joris PX, 1996, J NEUROPHYSIOL, V76, P2137 Joris PX, 1998, NEURON, V21, P1235, DOI 10.1016/S0896-6273(00)80643-1 Kiang N. Y., 1965, MIT RES MONOGR, V35 Kiang NYS, 1965, ACTA OTOLARYNG STOCK, V59, P186, DOI 10.3109/00016486509124552 KIMBERLEY BP, 1993, J ACOUST SOC AM, V94, P1343, DOI 10.1121/1.408162 Koppl C, 1997, J NEUROSCI, V17, P3312 Mardia K. V., 1972, STAT DIRECTIONAL DAT NEELY ST, 1988, J ACOUST SOC AM, V83, P652, DOI 10.1121/1.396542 Oertel D, 1999, ANNU REV PHYSIOL, V61, P497, DOI 10.1146/annurev.physiol.61.1.497 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X Paolini AG, 2001, HEARING RES, V159, P101, DOI 10.1016/S0378-5955(01)00327-6 Parham K, 1998, HEARING RES, V125, P131, DOI 10.1016/S0378-5955(98)00140-3 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd PFEIFFER RR, 1972, J ACOUST SOC AM, V52, P1669, DOI 10.1121/1.1913301 Rhodes CH, 1997, DIAGN MOL PATHOL, V6, P49, DOI 10.1097/00019606-199702000-00008 RUGGERO MA, 1980, J ACOUST SOC AM, V67, P707, DOI 10.1121/1.383900 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SMOLDERS JWT, 1986, HEARING RES, V24, P89, DOI 10.1016/0378-5955(86)90052-3 YIN TCT, 1996, BNAURAL SPATIAL HEAR, P427 NR 32 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 85 EP 100 DI 10.1016/S0378-5955(01)00325-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700008 PM 11520637 ER PT J AU Paolini, AG FitzGerald, JV Burkitt, AN Clark, GM AF Paolini, AG FitzGerald, JV Burkitt, AN Clark, GM TI Temporal processing from the auditory nerve to the medial nucleus of the trapezoid body in the rat SO HEARING RESEARCH LA English DT Article DE auditory nerve; cochlear nucleus; medial nucleus of the trapezoid body; temporal processing ID ANTEROVENTRAL COCHLEAR NUCLEUS; BUSHY CELLS; INTRACELLULAR RESPONSES; NEURAL SYNCHRONIZATION; COINCIDENCE DETECTION; AMPLITUDE-MODULATION; PRINCIPAL CELLS; SUPERIOR OLIVE; PHASE-LOCKING; FIRE NEURONS AB This investigation examines temporal processing through successive sites in the rat auditory pathway: auditory nerve (AN), anteroventral cochlear nucleus (AVCN) and the medial nucleus of the trapezoid body (MNTB). The degree of phase-locking, measured as vector strength, varied with intensity relative to the cell's threshold, and saturated at a value that depended upon stimulus frequency. A typical pattern showed decline in the saturated vector strength from approximately 0.8 at 400 Hz to about 0.3 at 2000 Hz, with similar profiles in units with a range of characteristic frequencies (480-32000 Hz). A new expression for temporal dispersion indicates that this variation corresponds to a limiting degree of temporal imprecision, which is relatively consistent between different cells. From AN to AVCN, an increase in vector strength was seen for frequencies below 1000 Hz. At higher frequencies, a decrease in vector strength was observed. From AVCN to MNTB a tendency for temporal coding to be improved below 800 Hz and degraded further above 1500 Hz was seen. This change in temporal processing ability could be attributed to units classified as primary-like with notch (PLN). PLN MNTB units showed a similar vector strength distribution to PLN AVCN units. Our results suggest that AVCN PLN units, representing globular bushy cells, are specialised for enhancing the temporal code at low frequencies and relaying this information to principal cells of the MNTB. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Royal Victorian Eye & Ear Hosp, Dept Otolaryngol, Melbourne, Vic 3002, Australia. Bion Ear Inst, Melbourne, Vic 3002, Australia. RP Paolini, AG (reprint author), Univ Melbourne, Royal Victorian Eye & Ear Hosp, Dept Otolaryngol, 32 Gisborne St, Melbourne, Vic 3002, Australia. RI Burkitt, Anthony/N-9077-2013 OI Burkitt, Anthony/0000-0001-5672-2772 CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 ANDERSON DJ, 1973, J ACOUST SOC AM, V54, P361, DOI 10.1121/1.1913585 BANKS MI, 1992, J NEUROSCI, V12, P2819 Borst JGG, 1995, J PHYSIOL-LONDON, V489, P825 Burkitt AN, 2000, NEURAL COMPUT, V12, P1789, DOI 10.1162/089976600300015141 Burkitt AN, 1999, NEURAL COMPUT, V11, P871, DOI 10.1162/089976699300016485 Cai YD, 1996, HEARING RES, V96, P83, DOI 10.1016/0378-5955(96)00033-0 CANT NB, 1979, NEUROSCIENCE, V4, P1925, DOI 10.1016/0306-4522(79)90066-6 CARNEY LH, 1990, J NEUROPHYSIOL, V64, P437 COLBURN HS, 1990, HEARING RES, V49, P335 FENG JJ, 1994, J COMP NEUROL, V346, P1, DOI 10.1002/cne.903460102 FORSYTHE ID, 1994, J PHYSIOL-LONDON, V479, P381 FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y GEISLER CD, 1974, J NEUROPHYSIOL, V37, P1156 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HARRISON RV, 1979, ARCH OTO-RHINO-LARYN, V224, P71, DOI 10.1007/BF00455226 HILL KG, 1989, HEARING RES, V39, P63, DOI 10.1016/0378-5955(89)90082-8 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 JORIS PX, 1994, J NEUROPHYSIOL, V71, P1022 JORIS PX, 1994, J NEUROPHYSIOL, V71, P1037 Joris PX, 1998, NEURON, V21, P1235, DOI 10.1016/S0896-6273(00)80643-1 Kempter R, 1998, NEURAL COMPUT, V10, P1987, DOI 10.1162/089976698300016945 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KIANG NYS, 1965, ANN OTO RHINOL LARYN, V74, P463 Koppl C, 1997, J NEUROSCI, V17, P3312 LENN NJ, 1966, AM J ANAT, V118, P375, DOI 10.1002/aja.1001180205 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MANIS PB, 1991, J NEUROSCI, V11, P2865 Mardia K. V., 1972, STAT DIRECTIONAL DAT MOLLER AR, 1976, J PHYSIOL-LONDON, V259, P63 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x MOLLER AR, 1976, ACTA PHYSIOL SCAND, V98, P157, DOI 10.1111/j.1748-1716.1976.tb00235.x MOREST D. KENT, 1968, BRAIN RES, V9, P288, DOI 10.1016/0006-8993(68)90235-7 Oertel D, 1999, ANNU REV PHYSIOL, V61, P497, DOI 10.1146/annurev.physiol.61.1.497 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X Paolini AG, 1997, NEUROSCIENCE, V78, P229, DOI 10.1016/S0306-4522(96)00566-0 Paolini AG, 1998, BRAIN RES BULL, V46, P317, DOI 10.1016/S0361-9230(98)00017-3 Paolini AG, 1998, BRAIN RES, V785, P309, DOI 10.1016/S0006-8993(97)01404-2 Paolini AG, 1997, NEUROREPORT, V8, P3415, DOI 10.1097/00001756-199710200-00044 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd RHODE WS, 1994, J NEUROPHYSIOL, V71, P1797 ROSE JE, 1959, B JOHNS HOPKINS HOSP, V104, P211 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 Rothman JS, 1996, AUDIT NEUROSCI, V2, P47 ROTHMAN JS, 1993, J NEUROPHYSIOL, V70, P2562 SMITH PH, 1987, J COMP NEUROL, V266, P360, DOI 10.1002/cne.902660305 Smith PH, 1998, J NEUROPHYSIOL, V79, P3127 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 SPANGLER KM, 1985, J COMP NEUROL, V238, P249, DOI 10.1002/cne.902380302 TASAKI I, 1954, J NEUROPHYSIOL, V17, P97 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3053, DOI 10.1016/0306-4522(82)90229-9 WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X WOOLF NK, 1981, HEARING RES, V4, P335, DOI 10.1016/0378-5955(81)90017-4 WU SH, 1993, HEARING RES, V68, P189 WU SH, 1991, J NEUROPHYSIOL, V65, P230 NR 57 TC 66 Z9 66 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 101 EP 116 DI 10.1016/S0378-5955(01)00327-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700009 PM 11520638 ER PT J AU Sheykholeslami, K Kaga, K Mizutani, M AF Sheykholeslami, K Kaga, K Mizutani, M TI Auditory nerve fiber differences in the normal and neurofilament deficient Japanese quail SO HEARING RESEARCH LA English DT Article DE neurofilament deficiency; axonal hypotrophy; conduction velocity; morphology ID NEURONAL INTERMEDIATE FILAMENTS; MYELINATED FIBERS; CONDUCTION-VELOCITY; PERIPHERAL-NERVE; MOLECULAR-BIOLOGY; AXONAL CALIBER; SCIATIC-NERVE; TRANSPORT; ATROPHY; SIZE AB A primary axonal disease affecting the central and peripheral nervous system was discovered in a mutant strain of the Japanese quail, named quiver (Quv), We have previously demonstrated altered auditory evoked potentials in the neurofilament (NF) deficient quail. In this current study we attempt to find relationships between the auditory evoked potential results and the histo-pathological abnormalities of the auditory neurons. No abnormalities in the external auditory meatus and tympanic cavity were observed in either Quv or control quails and the ganglion cell bodies and their nuclei appeared normal by light microscopy. The myelin staining pattern was found to be similar in both strains with hematoxylin and eosin and Kluver-Barrera staining. The frequency histograms of fiber and axonal diameters of myelinated fibers showed an unimodal pattern in both strains. In Quv quails myelinated fibers and their axoplasm were smaller in diameter than in controls resulting in smaller neural tissue mass. In electron microscopic observation the axons of the Quv quail were composed of mitochondria and microtubules and smooth endoplasmic reticuli. In Quv quail electron micrographs of cochlear nerve myelinated fibers NFs were not seen in the axons and the neuronal cell bodies. Our current findings indicate that the previously reported reduction of conduction velocity of auditory evoked potentials may be due to smaller fiber and/or axonal diameter. The g-ratio, myelin thickness and fiber circularity were found to be the same for both strains. In conclusion, loss of axonal cytoskeletal elements (NFs) correlates well with our electrophysiological findings. Reduced conduction velocity and severely distorted auditory evoked potentials in NF deficient quails seem to be primarily due to axonal hypotrophy. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tokyo, Dept Otolaryngol, Bunkyo Ku, Tokyo 1130033, Japan. Nippon Inst Biol Sci, Yamanashi, Japan. RP Sheykholeslami, K (reprint author), NE Ohio Univ, Coll Med, Dept Neurobiol & Pharmacol, 4209 State Route 44, Rootstown, OH 44272 USA. CR ALBERS K, 1992, INT REV CYTOL, V134, P243 Alberts B., 1994, MOL BIOL CELL ARBUTHNOTT ER, 1980, J PHYSIOL-LONDON, V308, P125 ARBUTHNOTT ER, 1980, J PHYSIOL-LONDON, V308, P99 Berthold C. H., 1978, PHYSL PATHOBIOLOGY A, P3 BRILL MH, 1977, J NEUROL NEUROSUR PS, V40, P769, DOI 10.1136/jnnp.40.8.769 COPPIN CML, 1973, THESIS U OXFORD OXFO CORK LC, 1989, LAB INVEST, V61, P333 DYCK PJ, 1984, PERIPHERAL NEUROPATH, P666 EYER J, 1994, NEURON, V12, P389, DOI 10.1016/0896-6273(94)90280-1 FLIEGNER KH, 1991, INT REV CYTOL, V131, P109 FRIEDE RL, 1986, ACTA NEUROPATHOL, V72, P74 FRIEDE RL, 1970, ANAT REC, V167, P379, DOI 10.1002/ar.1091670402 HOFFMAN PN, 1985, J CELL BIOL, V101, P1332, DOI 10.1083/jcb.101.4.1332 HOFFMAN PN, 1984, AXONAL TRANSPORT NEU, P243 HOFFMAN PN, 1984, J CELL BIOL, V99, P705, DOI 10.1083/jcb.99.2.705 HOFFMAN PN, 1987, P NATL ACAD SCI USA, V84, P3472, DOI 10.1073/pnas.84.10.3472 Hursh JB, 1939, AM J PHYSIOL, V127, P131 JACK JJB, 1976, PERIPHERAL NERVE, P775 LASEK RJ, 1981, BASIC NEUROCHEMISTRY, P403 Liem RKH, 1993, CURR OPIN CELL BIOL, V5, P12, DOI 10.1016/S0955-0674(05)80003-1 MIZUTANI M, 1992, J HERED, V84, P234 MOORE JW, 1978, BIOPHYS J, V21, P147 MORRIS JR, 1982, J CELL BIOL, V92, P192, DOI 10.1083/jcb.92.1.192 ONEILL JH, 1987, ACTA NEUROPATHOL, V74, P62 PAINTAL AS, 1987, PHYSL PATHOBIOLOGY A, P131 PETERS A, 1967, J CELL BIOL, V32, P113, DOI 10.1083/jcb.32.1.113 SAKAGUCHI T, 1993, NEUROSCI LETT, V153, P65, DOI 10.1016/0304-3940(93)90078-Y Sheykholeslami K, 2001, HEARING RES, V153, P115, DOI 10.1016/S0378-5955(00)00262-8 STUART DG, 1983, CLIN NEUROSCIENCES, V5, P471 WAXMAN SG, 1972, NATURE-NEW BIOL, V238, P217 WEISS PA, 1971, P NATL ACAD SCI USA, V68, P846, DOI 10.1073/pnas.68.4.846 Xu Zuoshang, 1994, Current Opinion in Neurobiology, V4, P655, DOI 10.1016/0959-4388(94)90006-X YAGIHASHI S, 1990, AM J PATHOL, V136, P1365 YAMASAKI H, 1991, ACTA NEUROPATHOL, V82, P427 ZENKER W, 1972, EXPERIENTIA, V29, P77 ZHU Q, 1997, GENE DEV, V1, P699 NR 37 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 117 EP 124 DI 10.1016/S0378-5955(01)00326-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700010 PM 11520639 ER PT J AU Zajic, G Henley, C Louis, JC Nicolson, M Magal, E AF Zajic, G Henley, C Louis, JC Nicolson, M Magal, E TI Distribution of immunophilin FKBP-12 protein and mRNA within the mammalian cochlea and cochlear nucleus SO HEARING RESEARCH LA English DT Article DE FK binding protein-12; calcium; cochlea; dorsal cochlear nucleus; immunophilin; ryanodine; inositol 1,4,5-trisphosphate ID OUTER HAIR-CELLS; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; CHANNEL RYANODINE RECEPTOR; NERVE REGENERATION; RELEASE; FK506; CALCINEURIN; EXPRESSION; SYSTEM AB Immunophilin FK binding protein-12 (FKBP-12), the soluble receptor for the immunosuppressant drug FK506, is involved in a number of neuronal activities including increased nerve regeneration in the peripheral nervous system and enhanced recovery in animal models of nc uro degenerative diseases. In addition, FKBP-12 is tightly bound to the calcium release channel ryanodine receptor and physiologically interacts with the inositol 1,4,5-trisphosphate receptor. In nearly all cell types, release of intracellular Ca (2+) and subsequent second messenger signaling involves activation of these ion channels. We determined the distribution of FKBP-12 within the mammalian cochlea and dorsal cochlear nucleus (DCN) in order to gain insight into Ca 2+ regulation within the cochlea and to possibly identify potential cellular targets for neuroimmunophilin ligands that may prove useful in protection and recovery following ototoxic insult. FKBP-12 protein and mRNA were found to be abundant throughout rat and guinea pig cochlea and DCN. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Amgen Inc, Dept Neurosci, Thousand Oaks, CA 91320 USA. Amgen Inc, Dept Mammalian Cell Biol, Thousand Oaks, CA 91320 USA. RP Zajic, G (reprint author), Amgen Inc, Dept Neurosci, MS 29-2-B,1 Amgen Ctr Dr, Thousand Oaks, CA 91320 USA. CR BRILLANTES AMB, 1994, CELL, V77, P513, DOI 10.1016/0092-8674(94)90214-3 Cameron AM, 1997, J BIOL CHEM, V272, P27582, DOI 10.1074/jbc.272.44.27582 CAMERON AM, 1995, P NATL ACAD SCI USA, V92, P1784, DOI 10.1073/pnas.92.5.1784 Chavis P, 1996, NATURE, V382, P719, DOI 10.1038/382719a0 CURRAN EJ, 1995, J COMP NEUROL, V361, P57, DOI 10.1002/cne.903610106 FRUMAN DA, 1994, FASEB J, V8, P391 Gold BG, 1997, EXP NEUROL, V147, P269, DOI 10.1006/exnr.1997.6630 GOLD BG, 1994, RESTOR NEUROL NEUROS, V6, P287, DOI 10.3233/RNN-1994-6404 Gold BG, 1997, MOL NEUROBIOL, V15, P285, DOI 10.1007/BF02740664 Hamilton GS, 1997, CURR PHARM DESIGN, V3, P405 JAYARAMAN T, 1992, J BIOL CHEM, V267, P9474 LYONS WE, 1995, J NEUROSCI, V15, P2985 Mammano F, 1999, J NEUROSCI, V19, P6918 Marks AR, 1996, PHYSIOL REV, V76, P631 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SNYDER SH, 1995, NAT MED, V1, P32, DOI 10.1038/nm0195-32 STEINER JP, 1992, NATURE, V358, P584, DOI 10.1038/358584a0 TIAN F, 1999, MIDW M ASS RES OT WANG TW, 1994, SCIENCE, V265, P674, DOI 10.1126/science.7518616 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X NR 21 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 125 EP 131 DI 10.1016/S0378-5955(01)00319-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700011 PM 11520640 ER PT J AU Derleth, RP Dau, T Kollmeier, B AF Derleth, RP Dau, T Kollmeier, B TI Modeling temporal and compressive properties of the normal and impaired auditory system SO HEARING RESEARCH LA English DT Article DE cochlear nonlinearity; recruitment; forward masking; modulation processing ID BASILAR-MEMBRANE NONLINEARITY; MODULATION TRANSFER-FUNCTIONS; AMPLITUDE-MODULATION; FREQUENCY-SELECTIVITY; CHINCHILLA COCHLEA; ENVELOPE FLUCTUATIONS; MOSSBAUER TECHNIQUE; QUANTITATIVE MODEL; COMBINATION TONES; MASKER DURATION AB Three modifications of a psychoacoustically and physiologically motivated processing model [Dan et al., J. Acoust. Soc. Am. 102 (1997a) 2892-2905] are presented and tested. The modifications aim at simulating senisorineural hearing loss and incorporate a level-dependent peripheral compression whose properties are affected by hearing impairment. Model I realizes this difference by introducing for impaired listeners an instantaneous level-dependent expansion prior to the adaptation stage of the model. Model 2 and Model 3 realize a level-dependent compression with time constants of 5 and 15 ins, respectively, for normal hearing and a reduced compression for impaired hearing. In Model 2, the compression occurs after the envelope extraction stage, while in Model 3, envelope extraction follows compression. All models account to a similar extent for the recruitment phenomenon measured with narrow-band stimuli and for forward-masking data of normal-hearing and hearing-impaired subjects using a 20-ms, 2-kHz tone signal and a 1-kHz-wide bandpass noise masker centered at 2 kHz. A clear difference between the different models occurs for the processing of temporally fluctuating stimuli. A modulation-rate-independent increase in modulation-response level for simulating impaired hearing is only predicted by Model I while the other two models realize a modulation-rate-dependent increase. Hence, the predictions of Model 2 and Model 3 are in conflict with the results of modulation-matching experiments reported in the literature. It is concluded that key properties of sensorineural hearing loss (altered loudness perception, reduced dynamic range, normal temporal properties but prolonged forward-masking effects) can effectively be modeled by incorporating a fast-acting expansion within the current processing model prior to the nonlinear adaptation stage. Based on these findings, a model of both normal and impaired hearing is proposed which incorporates a fast-acting compressive nonlinearity, representing the cochlear nonlinearity (which is reduced in impaired listeners), followed by an instantaneous expansion and the nonlinear adaptation stage which represent aspects of the retro-cochlear information processing in the auditory system. (C) 2001 Published by Elsevier Science B.V. C1 Univ Oldenburg, Gra Kolleg Psychoakust, D-26111 Oldenburg, Germany. RP Kollmeier, B (reprint author), Univ Oldenburg, Gra Kolleg Psychoakust, D-26111 Oldenburg, Germany. CR BACON SP, 1992, J SPEECH HEAR RES, V35, P642 BACON SP, 1985, AUDIOLOGY, V24, P117 BLAUERT J, 2001, PHYSL PSYCHOPHYSICAL, P24 Brugge JF, 1992, MAMMALIAN AUDITORY P, P1 Carlyon RP, 1997, J ACOUST SOC AM, V101, P3636, DOI 10.1121/1.418324 CARNEY LH, 1993, J ACOUST SOC AM, V93, P401, DOI 10.1121/1.405620 Dau T, 1996, J ACOUST SOC AM, V99, P3615, DOI 10.1121/1.414959 Dau T, 1997, J ACOUST SOC AM, V102, P2906, DOI 10.1121/1.420345 Dau T, 1996, J ACOUST SOC AM, V99, P3623, DOI 10.1121/1.414960 Dau T, 1997, J ACOUST SOC AM, V102, P2892, DOI 10.1121/1.420344 Derleth RP, 2000, J ACOUST SOC AM, V108, P285, DOI 10.1121/1.429464 DERLETH RP, 1996, J ACOUST SOC AM, V100, P2632 DERLETH RP, 1999, THESIS U OLDENBURG O Ewert SD, 2000, J ACOUST SOC AM, V108, P1181, DOI 10.1121/1.1288665 FASTL H, 1997, AUDIOLOGY, P63 FLORENTINE M, 1980, J SPEECH HEAR RES, V23, P646 FORMBY C, 1982, THESIS WASHINGTON U GLASBERG BR, 1987, J ACOUST SOC AM, V81, P1546, DOI 10.1121/1.394507 GLASBERG BR, 1992, HEARING RES, V64, P81, DOI 10.1016/0378-5955(92)90170-R GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 GREENWOO.DD, 1971, J ACOUST SOC AM, V50, P502, DOI 10.1121/1.1912668 HELLER O, 1985, PSYCHOL BEITR, V27, P478 HOHMANN V, 1993, DYNHAMIKKOMPRESSION Holube I, 1996, J ACOUST SOC AM, V100, P1703, DOI 10.1121/1.417354 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KIDD G, 1982, J ACOUST SOC AM, V72, P1384, DOI 10.1121/1.388443 KOLLMEIER B, 1997, PSYCHOPHYSICAL PHYSL, P482 KOLLMEIER B, 2001, PHYSL PSYCHOPHYSICAL, P17 Launer S, 1997, MODELING SENSORINEURAL HEARING LOSS, P175 MEDDIS R, 1999, PSYCHOPHYSICS PHYSL, P131 Moore BCJ, 1998, J ACOUST SOC AM, V104, P1023, DOI 10.1121/1.423321 MOORE BCJ, 1983, J ACOUST SOC AM, V73, P1249, DOI 10.1121/1.389273 Moore B.C.J., 1995, PERCEPTUAL CONSEQUEN Moore BCJ, 2000, J ACOUST SOC AM, V108, P2337, DOI 10.1121/1.1312362 MOORE BCJ, 1997, 7 OLD S PSYCH AC OLD, P565 Moore BCJ, 1996, J ACOUST SOC AM, V100, P481, DOI 10.1121/1.415861 MOORE BCJ, 1987, HEARING RES, V28, P209, DOI 10.1016/0378-5955(87)90050-5 MOORE BCJ, 1992, BRIT J AUDIOL, V26, P229, DOI 10.3109/03005369209076641 Moore BCJ, 1999, J ACOUST SOC AM, V106, P2761, DOI 10.1121/1.428133 Oxenham AJ, 2000, HEARING RES, V150, P258, DOI 10.1016/S0378-5955(00)00206-9 Oxenham AJ, 1997, MODELING SENSORINEURAL HEARING LOSS, P273 OXENHAM AJ, 1995, J ACOUST SOC AM, V98, P1921, DOI 10.1121/1.413376 OXENHAM AJ, 1994, HEARING RES, V80, P105, DOI 10.1016/0378-5955(94)90014-0 Pascoe D. P., 1978, HEAR INSTRUM, V29, P12 PATTERSON RD, 1987, M IOC SPEECH GROUP A Patterson RD, 1986, FREQUENCY SELECTIVIT, P123 Plack CJ, 1998, J ACOUST SOC AM, V103, P1598, DOI 10.1121/1.421294 Puschel D., 1988, THESIS U GOTTINGEN G Recio A, 1998, J ACOUST SOC AM, V103, P1972, DOI 10.1121/1.421377 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 ROSEN S, 1994, HEARING RES, V73, P231, DOI 10.1016/0378-5955(94)90239-9 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P603, DOI 10.1121/1.1913151 Strickland EA, 1996, J ACOUST SOC AM, V99, P3638, DOI 10.1121/1.414962 van Hengel P. W. J., 1996, THESIS U GRONINGEN G Verhey JL, 1999, J ACOUST SOC AM, V106, P2733, DOI 10.1121/1.428101 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1354 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M Zeng FG, 1999, NEUROREPORT, V10, P1931, DOI 10.1097/00001756-199906230-00025 ZENG FG, 1997, PSYCHOPHYSICAL PHYSL, P473 ZENG FG, 1994, SCIENCE, V264, P564, DOI 10.1126/science.8160013 ZWICKER E, 1984, J ACOUST SOC AM, V75, P219, DOI 10.1121/1.390398 NR 65 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2001 VL 159 IS 1-2 BP 132 EP 149 DI 10.1016/S0378-5955(01)00322-7 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 467XU UT WOS:000170729700012 PM 11520641 ER PT J AU Sinex, DG Lopez, DE Warr, WB AF Sinex, DG Lopez, DE Warr, WB TI Electrophysiological responses of cochlear root neurons SO HEARING RESEARCH LA English DT Article DE cochlear root neuron; acoustic startle response; single unit response ID ACOUSTIC STARTLE CIRCUIT; AUDITORY-SENSITIVITY; RETICULAR-FORMATION; GIANT-NEURONS; RAT; NUCLEUS; CAT; NERVE; ORGANIZATION; FREQUENCY AB Cochlear root neurons (CRNs) are second-order neurons interspersed among the fibers of the cochlear nerve in certain rodents. They project. among other nuclei, mainly to the pontine reticular nucleus. and participate in the acoustic startle response (ASR), a short-latency motor reflex initiated by sudden intense sounds, The sound-evoked activity of CRNs has not previously been described. Here we describe extracellular responses of CRNs located in the infranuclear portion of the cochlear nerve root. CRNs exhibited secure responses to tone bursts, with first-spike latencies of approximately 2.2 ms. The characteristic frequencies of the recorded CRNs were about 30 kHz. and the best-characterized CRN had a threshold of 10 dB sound pressure level and sharpness of tuning similar to that of cochlear nerve fibers. The peristimulus time histograms were primary-like with notch. The observed response properties were consistent with the suggestion that CRNs provide the short-latency acoustic input to the reticular formation that leads to an ASR. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Arizona State Univ, Dept Speech & Hearing Sci, Tempe, AZ 85287 USA. INCYL, Dept Biol Celular & Patol, Lab Neurobiol Audic, Salamanca 37007, Spain. Boys Town Natl Res Hosp, Omaha, NE 68131 USA. RP Sinex, DG (reprint author), Arizona State Univ, Dept Speech & Hearing Sci, POB 871908, Tempe, AZ 85287 USA. EM sinex@asu.edu RI Lopez, Dolores/A-2762-2009 OI Lopez, Dolores/0000-0002-1450-7246 CR ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 Bourk TR, 1976, THESIS MIT CAMBRIDGE BOURK TR, 1981, HEARING RES, V4, P215, DOI 10.1016/0378-5955(81)90008-3 DAVIS M, 1982, J NEUROSCI, V2, P791 EVANS EF, 1978, AUDIOLOGY, V17, P369 HARRISON JM, 1962, SCIENCE, V138, P893, DOI 10.1126/science.138.3543.893 ISON JR, 1973, PHYSIOL BEHAV, V10, P1035, DOI 10.1016/0031-9384(73)90185-6 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 Kiang NY-s, 1965, DISCHARGE PATTERNS S Koch M, 1999, PROG NEUROBIOL, V59, P107, DOI 10.1016/S0301-0082(98)00098-7 Lee YL, 1996, J NEUROSCI, V16, P3775 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LINGENHOHL K, 1992, J COMP NEUROL, V325, P473, DOI 10.1002/cne.903250403 LINGENHOHL K, 1994, J NEUROSCI, V14, P1176 Lopez DE, 1999, J COMP NEUROL, V415, P160 LOPEZ DE, 1993, NATO ADV SCI INST SE, V239, P291 MERCHAN MA, 1988, J NEUROCYTOL, V17, P711, DOI 10.1007/BF01260998 NODAL FR, 1997, ABSTR ASS RES OT, V20, P161 OSEN KK, 1991, J NEUROCYTOL, V20, P17, DOI 10.1007/BF01187131 Paolini AG, 1997, NEUROREPORT, V8, P3415, DOI 10.1097/00001756-199710200-00044 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd PERRY DR, 1981, J COMP NEUROL, V197, P623, DOI 10.1002/cne.901970406 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 ROSE JE, 1959, B JOHNS HOPKINS HOSP, V104, P211 Sando I, 1965, ACTA OTOLARYNG STOCK, V59, P417, DOI 10.3109/00016486509124577 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 WANG XQ, 1994, J NEUROPHYSIOL, V71, P59 Yeomans JS, 1995, BRAIN RES REV, V21, P301, DOI 10.1016/0165-0173(96)00004-5 ZHENG CM, 1992, JPN J PHYSIOL, V42, P459, DOI 10.2170/jjphysiol.42.459 NR 31 TC 17 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 28 EP 38 DI 10.1016/S0378-5955(01)00293-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900002 PM 11506934 ER PT J AU Rodgers, KD Barritt, L Miner, JH Cosgrove, D AF Rodgers, KD Barritt, L Miner, JH Cosgrove, D TI The laminins in the murine inner ear: developmental transitions and expression in cochlear basement membranes SO HEARING RESEARCH LA English DT Article DE basement membrane; cochlea; laminin; development ID MEDIATES CELL-ADHESION; IMMUNOHISTOCHEMICAL LOCALIZATION; BETA-1 INTEGRINS; IV COLLAGEN; NEUROMUSCULAR-JUNCTION; POSTNATAL-DEVELOPMENT; EPITHELIAL-CELLS; ALPHA-5 CHAIN; MICE LACKING; S-LAMININ AB The laminins are a family of heterotrimeric extracellular matrix molecules that form suprastructural networks in basement membranes and elsewhere. They interact with integrin receptors, playing key roles in modulating programs of cytodifferentiation and maintaining tissue homeostasis in animals. Earlier studies have demonstrated an extensive laminin network in both the developing and adult cochlea, primarily associated with the basement membranes. These studies, however, did not address the laminin chain composition of these networks. In this study, we used antibodies specific for the known laminin chains to examine the composition of laminins in both the developing and adult murine cochlea. The results illustrate a complex and dynamic postnatal developmental regulation pattern for most of these chains, and suggest that an unusually large number of laminin heterotrimers are present in both the developing and adult cochlea. The laminin composition at postnatal day 2 is relatively simple. By postnatal day 7, however, activation of several laminin chains results in a very complex laminin composition. In the basement membrane underlying the region of the basilar membrane under the developing organ of Corti, eight of the I I known basement membrane laminins are possible by co-localization inference. Dynamic changes in expression continue through day 14, but simplify by adulthood. Thus, the most dynamic period for laminin expression in the mouse cochlea coincides with terminal cytodifferentiation of the cochlear epithelial structures. Considering the well established role of laminins in regulating both embryonic and organ development in other systems, these data suggest a closer look at the role of the laminins in cochlear development and function may be warranted. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Boys Town Natl Res Hosp, Dept Genet, Omaha, NE 68131 USA. Creighton Univ, Sch Dent, Omaha, NE 68178 USA. Washington Univ, Sch Med, Dept Internal Med, Div Renal, St Louis, MO 63110 USA. RP Cosgrove, D (reprint author), Boys Town Natl Res Hosp, Dept Genet, 555 30th St, Omaha, NE 68131 USA. CR ABRAHAMSON DR, 1989, J CELL BIOL, V109, P2477 Arnold W, 1984, Ann Otol Rhinol Laryngol Suppl, V112, P119 Aumailley M, 1998, J ANAT, V193, P1, DOI 10.1046/j.1469-7580.1998.19310001.x Buttery PC, 1999, MOL CELL NEUROSCI, V14, P199, DOI 10.1006/mcne.1999.0781 CARBONETTO S, 1995, CURR OPIN NEUROBIOL, V5, P596, DOI 10.1016/0959-4388(95)80064-6 Colognato H, 1997, J BIOL CHEM, V272, P29330, DOI 10.1074/jbc.272.46.29330 Colognato H, 1999, J CELL BIOL, V145, P619, DOI 10.1083/jcb.145.3.619 Cosgrove D, 1996, HEARING RES, V97, P54 Cosgrove D, 1996, HEARING RES, V100, P21, DOI 10.1016/0378-5955(96)00114-1 Cosgrove D, 2000, AM J PATHOL, V157, P1649, DOI 10.1016/S0002-9440(10)64802-X Cosgrove D, 1997, HEARING RES, V105, P159, DOI 10.1016/S0378-5955(96)00203-1 Cosgrove D, 1998, HEARING RES, V121, P84, DOI 10.1016/S0378-5955(98)00069-0 DESIMONE DW, 1994, CURR OPIN CELL BIOL, V6, P747, DOI 10.1016/0955-0674(94)90103-1 Durbeej M, 1996, MATRIX BIOL, V15, P397, DOI 10.1016/S0945-053X(96)90159-6 Ehret G, 1976, J Am Audiol Soc, V1, P179 Ekblom M, 1998, ANN NY ACAD SCI, V857, P194, DOI 10.1111/j.1749-6632.1998.tb10117.x HYNES RO, 1992, CELL, V69, P11, DOI 10.1016/0092-8674(92)90115-S Iglesias M, 1995, J NEUROCYTOL, V24, P903, DOI 10.1007/BF01215641 ITO M, 1995, HEARING RES, V88, P107, DOI 10.1016/0378-5955(95)00106-E Kikkawa Y, 1998, J BIOL CHEM, V273, P15854, DOI 10.1074/jbc.273.25.15854 Koch M, 1999, J CELL BIOL, V145, P605, DOI 10.1083/jcb.145.3.605 Lefebvre O, 1999, DEV BIOL, V210, P135, DOI 10.1006/dbio.1999.9270 Libby RT, 2000, J NEUROSCI, V20, P6517 Libby RT, 1996, INVEST OPHTH VIS SCI, V37, P1651 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 Lim D, 1992, DEV AUDITORY VESTIBU, P33 MARINKOVICH MP, 1992, J CELL BIOL, V119, P695, DOI 10.1083/jcb.119.3.695 Miner JH, 2000, DEV BIOL, V217, P278, DOI 10.1006/dbio.1999.9546 Miner JH, 1997, J CELL BIOL, V137, P685, DOI 10.1083/jcb.137.3.685 Miner JH, 1998, J CELL BIOL, V143, P1713, DOI 10.1083/jcb.143.6.1713 Muller U, 1999, J CELL SCI, V112, P3855 Muschler J, 1999, MOL BIOL CELL, V10, P2817 NOAKES PG, 1995, NAT GENET, V10, P400, DOI 10.1038/ng0895-400 Patton BL, 1997, J CELL BIOL, V139, P1507, DOI 10.1083/jcb.139.6.1507 Perris R, 1996, INT J DEV NEUROSCI, V14, P297, DOI 10.1016/0736-5748(96)00015-9 Powell SK, 1998, J NEUROSCI RES, V54, P233, DOI 10.1002/(SICI)1097-4547(19981015)54:2<233::AID-JNR11>3.0.CO;2-5 Raabe EH, 1997, DEV BRAIN RES, V101, P187, DOI 10.1016/S0165-3806(97)00064-3 ROUSSELLE P, 1991, J CELL BIOL, V114, P567, DOI 10.1083/jcb.114.3.567 Ryan MC, 1999, J CELL BIOL, V145, P1309, DOI 10.1083/jcb.145.6.1309 SANES JR, 1990, J CELL BIOL, V111, P1685, DOI 10.1083/jcb.111.4.1685 SANTI PA, 1989, HEARING RES, V39, P91, DOI 10.1016/0378-5955(89)90084-1 SANTI PA, 1989, 2 INT S MEN DIS CAMB, P177 Sasaki T, 1998, EXP CELL RES, V238, P70, DOI 10.1006/excr.1997.3837 Satoh H, 1998, EUR ARCH OTO-RHINO-L, V255, P285, DOI 10.1007/s004050050060 Schuger L, 1997, EXP LUNG RES, V23, P119, DOI 10.3109/01902149709074025 Schuger L, 1997, J CELL BIOL, V139, P553, DOI 10.1083/jcb.139.2.553 Simon-Assmann P, 1998, ANN NY ACAD SCI, V859, P46, DOI 10.1111/j.1749-6632.1998.tb11110.x Smyth N, 1998, ANN NY ACAD SCI, V857, P283, DOI 10.1111/j.1749-6632.1998.tb10133.x Sorokin LM, 1997, DEV BIOL, V189, P285, DOI 10.1006/dbio.1997.8668 STEEL KP, 1989, DEVELOPMENT, V107, P453 STEPHENS LE, 1995, GENE DEV, V9, P1883, DOI 10.1101/gad.9.15.1883 TAKAHASHI M, 1992, ANN OTO RHINOL LARYN, V101, P58 TIMPL R, 1989, EUR J BIOCHEM, V180, P487, DOI 10.1111/j.1432-1033.1989.tb14673.x Tomatis D, 1999, EXP CELL RES, V246, P421, DOI 10.1006/excr.1998.4315 UTANI A, 1995, LAB INVEST, V72, P300 Vachon PH, 1996, J CELL BIOL, V134, P1483, DOI 10.1083/jcb.134.6.1483 WEINBERGER DG, 1999, LARYNGOSCOPE, V109, P201 WOOLF NK, 1992, DEV BRAIN RES, V65, P21, DOI 10.1016/0165-3806(92)90004-G Yoshiba K, 1998, DEV DYNAM, V211, P164 YURCHENCO PD, 1992, J CELL BIOL, V117, P1119, DOI 10.1083/jcb.117.5.1119 YURCHENCO PD, 1990, FASEB J, V4, P1577 NR 61 TC 19 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 39 EP 50 DI 10.1016/S0378-5955(01)00283-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900003 PM 11506935 ER PT J AU Minami, S Kobayashi, H Yamashita, A Yanagita, T Uezono, Y Yokoo, H Shiraishi, S Saitoh, T Asada, Y Komune, S Wada, A AF Minami, S Kobayashi, H Yamashita, A Yanagita, T Uezono, Y Yokoo, H Shiraishi, S Saitoh, T Asada, Y Komune, S Wada, A TI Selective expression of aquaporin 1, 4 and 5 in the rat middle ear SO HEARING RESEARCH LA English DT Article DE aquaporin; middle ear; reverse transcription-polymerase chain reaction; immunoblot; immunohistochemistry; water homeostasis ID WATER CHANNEL; CLONING; LUNG AB The middle ear cavity is an air-filled space that must be maintained for effective sound transmission to the inner ear. To examine the mechanisms of water homeostasis in the middle ear, we investigated whether aquaporins (AQPs), a family of water-permeable channels, were expressed in the middle car. Reverse transcription-polymerase chain reaction and immunoblot analyses revealed that mRNAs encoding AQP1, 4 and 5 (but not 2 or 3) subtypes were expressed in rat middle ear epithelium, AQP1, 4 and 5 were detected as 28-, 30- and 30-kDa proteins. respectively. Immunohistochemical analysis showed that AQP1 was localized at capillary endothelial cells and fibroblasts in lamina propria mucosae.. AQP4 was present solely at the basolateral membrane of ciliated cells, whereas AQP5 was on the apical surface of ciliated cells as well as of flat and columnar epithelial cells. The characteristic different localizations of AQP1, 4 and 5 subtypes in the middle ear suggest that middle ear water homeostasis requires the coordinated operation of these AQPs. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Miyazaki Med Coll, Dept Pharmacol, Miyazaki 8891692, Japan. Miyazaki Med Coll, Dept Otolaryngol, Miyazaki 8891692, Japan. Miyazaki Med Coll, Dept Pathol 1, Miyazaki 8891692, Japan. RP Kobayashi, H (reprint author), Miyazaki Med Coll, Dept Pharmacol, 5200 Kihara, Miyazaki 8891692, Japan. RI Uezono, Yasuhito/C-2347-2011 CR Brooks HL, 2000, MOL PHARMACOL, V57, P1021 Deen PMT, 1998, CURR OPIN CELL BIOL, V10, P435, DOI 10.1016/S0955-0674(98)80055-0 Furukawa M, 1997, AM J PHYSIOL-CELL PH, V272, pC827 FUSHIMI K, 1993, NATURE, V361, P549, DOI 10.1038/361549a0 HASEGAWA H, 1994, J BIOL CHEM, V269, P5497 HERMAN P, 1998, KIDNEY INT, V65, P94 HERMAN P, 1993, J CELL PHYSIOL, V154, P615, DOI 10.1002/jcp.1041540321 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 MA TH, 1994, J BIOL CHEM, V269, P21845 RAINA S, 1995, J BIOL CHEM, V270, P1908 Ruddy MK, 1998, AM J PHYSIOL-LUNG C, V274, pL1066 STAKOVIC KM, 1995, AM J PHYSIOL, V269, pC1450 TOS M, 1984, ARCH OTOLARYNGOL, V110, P281 Towne JE, 2000, AM J RESP CELL MOL, V22, P34 Yasui M, 1997, J PHYSIOL-LONDON, V505, P3, DOI 10.1111/j.1469-7793.1997.003bc.x NR 15 TC 10 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 51 EP 56 DI 10.1016/S0378-5955(01)00284-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900004 PM 11506936 ER PT J AU Borgmann, C Ross, B Draganova, R Pantev, C AF Borgmann, C Ross, B Draganova, R Pantev, C TI Human auditory middle latency responses: influence of stimulus type and intensity SO HEARING RESEARCH LA English DT Article DE middle latency response; human auditory cortex; evoked magnetic field; amplitude; latency; intensity ID EVOKED MAGNETIC-FIELDS; SOURCE LOCALIZATION; TONE-PIPS; COMPONENTS; CORTEX; ORGANIZATION; POTENTIALS; FREQUENCY; NEURONS AB Human auditory middle latency responses (MLR) to click and tone pip stimuli of different intensities were recorded by means of magnetoencephalography (MEG) and electroencephalography (EEG). Clicks elicited larger responses with significantly shorter latencies than the tone pips at the same intensity in dB sensation level (SL). Most MLR amplitudes increased and their latencies decreased with increasing stimulus intensity for both types of stimulation. Pa and Nb amplitudes saturated at intensities of 60 dB SL in the case of click stimulation. The shorter latencies of MLR evoked by the click were explained by its short rise time and the high frequency content of its spectrum. MEG source analysis yielded MLR sources which were clearly different from those of the slow cortical wave N1. They seem to be located in primary auditory areas along Heschl's gyrus. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Munster, Inst Expt Audiol, Ctr Biomagnetism, D-48129 Munster, Germany. RP Pantev, C (reprint author), Univ Munster, Inst Expt Audiol, Ctr Biomagnetism, Kardinal von Galen Ring 10, D-48129 Munster, Germany. CR EGGERMONT JJ, 1979, J ACOUST SOC AM, V65, P463, DOI 10.1121/1.382345 ERWIN R, 1986, ELECTROEN CLIN NEURO, V65, P383, DOI 10.1016/0168-5597(86)90017-1 Hari R, 1983, Rev Laryngol Otol Rhinol (Bord), V104, P143 HASHIMOTO I, 1995, EVOKED POTENTIAL, V96, P348, DOI 10.1016/0168-5597(95)00004-C Heil P, 1998, BEHAV BRAIN RES, V95, P233, DOI 10.1016/S0166-4328(98)00044-8 KITZES LM, 1978, J NEUROPHYSIOL, V41, P1165 Kuriki S, 1995, HEARING RES, V92, P47, DOI 10.1016/0378-5955(95)00195-6 LIEGEOISCHAUVEL C, 1994, ELECTROEN CLIN NEURO, V92, P204, DOI 10.1016/0168-5597(94)90064-7 Lutkenhoner B, 1998, AUDIOL NEURO-OTOL, V3, P191, DOI 10.1159/000013790 MADELL JR, 1972, J SPEECH HEAR RES, V15, P134 MAURIZI M, 1984, AUDIOLOGY, V23, P569 MCFARLAND WH, 1977, J SPEECH HEAR RES, V20, P781 MENDEL MI, 1980, AUDIOLOGY, V19, P1 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 Onitsuka T, 2000, CLIN NEUROPHYSIOL, V111, P237, DOI 10.1016/S1388-2457(99)00241-2 OZDAMAR O, 1983, AUDIOLOGY, V22, P34 PANTEV C, 1995, ELECTROEN CLIN NEURO, V94, P26, DOI 10.1016/0013-4694(94)00209-4 PANTEV C, 1988, ELECTROEN CLIN NEURO, V69, P160, DOI 10.1016/0013-4694(88)90211-8 PANTEV C, 1990, ELECTROEN CLIN NEURO, V75, P173, DOI 10.1016/0013-4694(90)90171-F PELIZZONE M, 1987, NEUROSCI LETT, V82, P303, DOI 10.1016/0304-3940(87)90273-4 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 REITE M, 1988, ELECTROEN CLIN NEURO, V70, P490, DOI 10.1016/0013-4694(88)90147-2 Scherg M., 1989, ADV BIOMAGNETISM, P97 THORNTON AR, 1977, J SPEECH HEAR RES, V20, P81 Yoshiura T, 1995, BRAIN RES, V703, P139, DOI 10.1016/0006-8993(95)01075-0 Yoshiura T, 1996, BRAIN TOPOGR, V8, P291, DOI 10.1007/BF01184787 NR 26 TC 25 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 57 EP 64 DI 10.1016/S0378-5955(01)00292-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900005 PM 11506937 ER PT J AU Regan, MP Regan, D AF Regan, MP Regan, D TI Simulated hair cell transduction of quasi-frequency-modulated and amplitude-modulated tones SO HEARING RESEARCH LA English DT Article DE simulation; hair cell transduction; quasi-frequency-modulated tones; amplitude-modulated tones ID MIXED MODULATION; ADAPTATION AB This paper describes a method for calculating the effect of simulated hair cell transduction on (i) a quasi-frequency-modulated (quasi-FM) tone and on (ii) an amplitude-modulated (AM) tone. The main finding is that the effect of the transduction on AM and quasi-FM (which have the same power spectra but whose phase spectra differ), is to produce different power spectra. (C) 2001 Elsevier Science B.V. All rights reserved. C1 York Univ, Dept Psychol, BSB, N York, ON M3J 1P3, Canada. RP Regan, D (reprint author), York Univ, Dept Psychol, BSB, 4700 Keele St, N York, ON M3J 1P3, Canada. CR ASSAD JA, 1992, J NEUROSCI, V12, P3291 CONINX F, 1977, ACUSTICA, V39, P138 CONINX F, 1977, ACUSTICA, V39, P151 COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DEMANY L, 1986, ACUSTICA, V61, P243 FETH LL, 1972, ACUSTICA, V26, P67 Fletcher H, 1940, REV MOD PHYS, V12, P0047, DOI 10.1103/RevModPhys.12.47 HARTMANN WM, 1982, ACUSTICA, V50, P297 HOBSON EW, 1926, THEORY FUNCTIONS REA HUDSPETH AJ, 1983, TRENDS NEUROSCI, V6, P366, DOI 10.1016/0166-2236(83)90166-2 KAY RH, 1972, J PHYSL, V225, P656 MAIWALD D, 1967, ACUSTICA, V18, P193 MAIWALD D, 1967, ACUSTICA, V18, P81 MOORE B J, 1982, INTRO PSYCHOL HEARIN MOORE BCJ, 1983, HEARING RES, V28, P750 OZIMEK E, 1987, J ACOUST SOC AM, V82, P1598, DOI 10.1121/1.395149 PATTERSON RD, 1982, J ACOUST SOC AM, V72, P1788, DOI 10.1121/1.388652 Plomp R, 1976, ASPECTS TONE SENSATI REGAN D, 1979, J ACOUST SOC AM, V65, P1249, DOI 10.1121/1.382792 Regan D., 1989, HUMAN BRAIN ELECTROP REGAN MP, 1994, APPL MATH COMPUT, V62, P61, DOI 10.1016/0096-3003(94)90133-3 RUSSELL IJ, 1986, NATURE, V321, P517, DOI 10.1038/321517a0 TANSLEY BW, 1979, SENS PROCESS, V3, P132 Walker J.S., 1988, FOURIER ANAL Zwicker E., 1970, FREQUENCY ANAL PERIO, P376 Zwicker E., 1956, ACUSTICA, V6, P356 NR 27 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 65 EP 70 DI 10.1016/S0378-5955(01)00297-0 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900006 PM 11506938 ER PT J AU Uppenkamp, S Fobel, S Patterson, RD AF Uppenkamp, S Fobel, S Patterson, RD TI The effects of temporal asymmetry on the detection and perception of short chirps SO HEARING RESEARCH LA English DT Article DE chirp signal; cochlear phase delay; temporal integration; auditory image ID MASKING PERIOD PATTERNS; AUDITORY PERIPHERY; INNER-EAR; MODEL; DISPERSION; RESPONSES; POTENTIALS; SIGNALS; CLICK; SOUND AB There is an intriguing contrast between the physiological response to short frequency sweeps in the brainstem and the perception produced by these sounds. Dau et al. (2000) demonstrated that optimised chirps with increasing instantaneous frequency (up-chirps), designed to compensate for spatial dispersion along the cochlea, enhance wave V of the auditory brainstem response (ABR), by synchronising excitation of all frequency channels across the basilar membrane. Down-chirps, that is up-chirps reversed in time, increase cochlear phase delays and therefore result in a poor ABR wave V. In this study, a set of psychoacoustical experiments with up-chirps and down-chirps has been performed to investigate how these phase changes affect what we hear. The perceptual contrast is different from what was reported at the brainstem level. It is the down-chirp that sounds more compact. despite the poor synchronisation across channels and phase delays up to 20 ms. The perceived 'compactness' of a sound is apparently more determined by the fine structure of excitation within each peripheral channel than by between-channel phase differences. This suggests an additional temporal integration mechanism at a higher stage of auditory processing. which effectively removes phase differences between channels. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Cambridge, Dept Physiol, Ctr Neural Basis Hearing, Cambridge CB2 3EG, England. Carl von Ossietzky Univ Oldenburg, Fachbereich Phys, AG Med Phys, D-26111 Oldenburg, Germany. RP Uppenkamp, S (reprint author), Univ Cambridge, Dept Physiol, Ctr Neural Basis Hearing, Downing St, Cambridge CB2 3EG, England. EM stefan.uppenkamp@mrc-cbu.cam.ac.uk CR Carney LH, 1999, J ACOUST SOC AM, V105, P2384, DOI 10.1121/1.426843 Dau T, 2000, J ACOUST SOC AM, V107, P1530, DOI 10.1121/1.428438 David HA, 1988, METHOD PAIRED COMP DEBOER E, 1980, PHYS REP, V62, P87, DOI 10.1016/0370-1573(80)90100-3 DON M, 1994, J ACOUST SOC AM, V96, P3476, DOI 10.1121/1.410608 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 GIGUERE C, 1994, J ACOUST SOC AM, V95, P331 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 Helmholtz von Hermann, 1870, LEHRE TONEMPFINDUNGE JOHNSTONE JR, 1981, HEARING RES, V4, P347, DOI 10.1016/0378-5955(81)90018-6 KOHLRAUSCH A, 1995, J ACOUST SOC AM, V97, P1817, DOI 10.1121/1.413097 MATHES RC, 1947, J ACOUST SOC AM, V19, P780, DOI 10.1121/1.1916623 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2883, DOI 10.1121/1.400726 MEDDIS R, 1988, J ACOUST SOC AM, V83, P1056, DOI 10.1121/1.396050 OHM GS, 1843, ANN PHYS CHEM, V59, P512 PATTERSON RD, 1992, ADV BIOSCI, V83, P429 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1409, DOI 10.1121/1.410285 PATTERSON RD, 1987, J ACOUST SOC AM, V82, P1560, DOI 10.1121/1.395146 PATTERSON RD, 1995, J ACOUST SOC AM, V98, P1890, DOI 10.1121/1.414456 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1419, DOI 10.1121/1.410286 SCHROEDE.MR, 1970, IEEE T INFORM THEORY, V16, P85, DOI 10.1109/TIT.1970.1054411 SHORE SE, 1987, J ACOUST SOC AM, V82, P471, DOI 10.1121/1.395448 SHORE SE, 1985, J ACOUST SOC AM, V78, P1286, DOI 10.1121/1.392898 SMITH BK, 1986, J ACOUST SOC AM, V80, P1631, DOI 10.1121/1.394327 STRUBE HW, 1985, ACUSTICA, V58, P207 UPPENKAMP S, 1999, PSYCHOPHYSICS PHYSL, P235 UPPENKAMP S, 2001, PHYSL PSYCHOPHYSICAL, P343 VIEMEISTER NF, 1991, J ACOUST SOC AM, V90, P858, DOI 10.1121/1.401953 WEGNER O, 1997, 7 OLD S PSYCH BIS OL, P83 ZWICKER E, 1976, J ACOUST SOC AM, V60, P429, DOI 10.1121/1.381100 NR 31 TC 23 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 71 EP 83 DI 10.1016/S0378-5955(01)00299-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900007 PM 11506939 ER PT J AU Mendelson, JR Ricketts, C AF Mendelson, JR Ricketts, C TI Age-related temporal processing speed deterioration in auditory cortex SO HEARING RESEARCH LA English DT Article DE aging; frequency-modulated sweep; auditory cortex ID INFERIOR COLLICULUS; FUNCTIONAL TOPOGRAPHY; RESPONSE PROPERTIES; EVOKED POTENTIALS; RHESUS-MONKEY; NEURONS; RAT; SWEEPS; YOUNG; TIME AB A common problem among the elderly is a difficulty in discriminating speech sounds. One factor that may contribute to this is a deterioration in the ability to process dynamic aspects of speech such as formant transitions. For the aging auditory system, this deterioration in temporal processing speed may be manifest as a deficit in encoding time-varying sounds that contain rapidly changing frequencies such as formant transitions. The primary goal of this study was to explore the neural basis of the effects of aging on temporal processing speed. To this end, single units were recorded from the auditory cortex of young and aged rats in response to frequency-modulated (FM) sweeps that changed from trial to trial in both direction and speed. Results showed that the majority of cells recorded from young rats responded most vigorously to fast and medium speeds. By contrast, the majority of units recorded from aged animals responded best to slow speeds. For preferred direction of FM sweep, similar results were observed for both age groups, namely, approximately half of the units exhibited a direction-selective response. The results of the present study demonstrate an age-related decrease in the rate of change of frequency that can be processed by the auditory cortex. (C) 2001 Published by Elsevier Science B.V. C1 Univ Toronto, Fac Med, Dept Speech Language Pathol, Toronto, ON M5S 3H2, Canada. RP Mendelson, JR (reprint author), Univ Toronto, Fac Med, Dept Speech Language Pathol, Tanz Neurosci Bldg,6 Queens Pk Cres W, Toronto, ON M5S 3H2, Canada. CR BACKOFF PM, 1994, HEARING RES, V73, P163, DOI 10.1016/0378-5955(94)90231-3 BAIMBRIDGE KG, 1992, TRENDS NEUROSCI, V15, P303, DOI 10.1016/0166-2236(92)90081-I BIRREN JE, 1980, AGING 1980S PSYCHOL Boettcher FA, 1996, HEARING RES, V102, P167, DOI 10.1016/S0378-5955(96)90016-7 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CELESIA GG, 1977, ARCH NEUROL-CHICAGO, V34, P403 Cha CI, 1997, BRAIN RES, V753, P235, DOI 10.1016/S0006-8993(97)00009-7 CONTESTABILE MT, 1995, ACTA OPHTHALMOL SCAN, V73, P308 CREMER R, 1987, J GERONTOL, V42, P515 Double KL, 1996, NEUROBIOL AGING, V17, P513 FELDMAN ML, 1979, SPECIAL SENSES AGING, P143 FINLAYSON PG, 1993, NEUROBIOL AGING, V14, P127, DOI 10.1016/0197-4580(93)90088-S FOOTE SL, 1975, BRAIN RES, V86, P229, DOI 10.1016/0006-8993(75)90699-X FUZESSERY ZM, 1994, J NEUROPHYSIOL, V72, P1061 GRASSE KL, 1990, VISUAL NEUROSCI, V6, P604 Hugon J, 1996, BRAIN RES, V707, P288, DOI 10.1016/0006-8993(95)01393-8 Jucker M, 1997, BEHAV BRAIN RES, V85, P1, DOI 10.1016/S0166-4328(96)02243-7 KALTWASSER MT, 1990, J COMP PSYCHOL, V104, P227, DOI 10.1037/0735-7036.104.3.227 KELLY JB, 1988, J NEUROPHYSIOL, V59, P1756 KHATCHATURIAN Z, 1982, HDB STUDIES PSYCHIAT, P139 KONKLE DF, 1977, J SPEECH HEAR RES, V20, P108 MENDELSON JR, 1992, EXP BRAIN RES, V91, P435 MENDELSON JR, 1993, EXP BRAIN RES, V94, P65 Mendelson JR, 1999, BRAIN COGNITION, V39, P55 Pakkenberg B, 1997, J COMP NEUROL, V384, P312, DOI 10.1002/(SICI)1096-9861(19970728)384:2<312::AID-CNE10>3.0.CO;2-K Palombi PS, 1996, J NEUROPHYSIOL, V76, P3114 PETERS A, 1994, CEREB CORTEX, V4, P621, DOI 10.1093/cercor/4.6.621 Peters A, 1997, NEUROBIOL AGING, V18, P29, DOI 10.1016/S0197-4580(96)00208-4 PETERS A, 1981, AGING CELL STRUCTURE, P1 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 Ricketts C, 1998, HEARING RES, V123, P27, DOI 10.1016/S0378-5955(98)00086-0 Salthouse T. A., 1985, HDB PSYCHOL AGING, P400 SALTHOUSE TA, 1990, HDB PSYCHOL AGING SCHNEIDER BA, 1994, J ACOUST SOC AM, V95, P980, DOI 10.1121/1.408403 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 SHINBA T, 1992, BRAIN RES BULL, V28, P463, DOI 10.1016/0361-9230(92)90048-3 SHORE SE, 1985, J ACOUST SOC AM, V78, P1286, DOI 10.1121/1.392898 SINEX DG, 1981, HEARING RES, V4, P127, DOI 10.1016/0378-5955(81)90001-0 SUGA N, 1965, J PHYSIOL-LONDON, V181, P671 Walton JP, 1998, J NEUROSCI, V18, P2764 Wang XJ, 1998, J NEUROPHYSIOL, V79, P1549 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 WILLOTT JF, 1988, HEARING RES, V37, P1, DOI 10.1016/0378-5955(88)90073-1 Willott J. F., 1991, AGING AUDITORY SYSTE WINGFIELD A, 1985, J GERONTOL, V40, P579 Zettel ML, 1997, J COMP NEUROL, V386, P92, DOI 10.1002/(SICI)1096-9861(19970915)386:1<92::AID-CNE9>3.0.CO;2-8 NR 46 TC 46 Z9 51 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 84 EP 94 DI 10.1016/S0378-5955(01)00294-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900008 PM 11506940 ER PT J AU Dietrich, V Nieschalk, M Stoll, W Rajan, R Pantev, C AF Dietrich, V Nieschalk, M Stoll, W Rajan, R Pantev, C TI Cortical reorganization in patients with high frequency cochlear hearing loss SO HEARING RESEARCH LA English DT Article DE cortical plasticity; magnetoencephalography; auditory cortex; auditory evoked field ID PRIMARY AUDITORY-CORTEX; TONOTOPIC ORGANIZATION; PLASTICITY; REPRESENTATION; MONKEY; INJURY; FIELDS; DAMAGE; PAIN; MAP AB Animal research has shown that tonotopic representation in the auditory cortex is not statically fixed in the adult organism but can be altered after deafferentation. The present study examines the plasticity of the human auditory cortex in patients with high frequency cochlear hearing loss by means of magnetoencephalographic measurements. The data show that the cortical map can reorganize such that cortical neurons deprived of their usual most sensitive afferent input now respond to tone frequencies adjacent to the frequency range of the partial hearing loss. The results suggest that deafferentation due to cochlear damage in adults may lead to functional reorganization of auditory cortical structures. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Munster, Dept Otorhinolaryngol, D-48129 Munster, Germany. Univ Munster, Inst Expt Audiol, Ctr Biomagnetism, D-48129 Munster, Germany. Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia. Univ Toronto, Rotman Res Inst Neurosci, Toronto, ON M6A 2E1, Canada. RP Nieschalk, M (reprint author), Univ Munster, Dept Otorhinolaryngol, Kardinal von Galen Ring 10, D-48129 Munster, Germany. RI Rajan, Ramesh/A-5945-2008 CR ANNETT M, 1979, ANN HUM GENET, V42, P479, DOI 10.1111/j.1469-1809.1979.tb00681.x DARIANSMITH C, 1995, J NEUROSCI, V15, P1631 DIAMOND ME, 1993, P NATL ACAD SCI USA, V90, P2082, DOI 10.1073/pnas.90.5.2082 ELBERT T, 1995, SCIENCE, V270, P305, DOI 10.1126/science.270.5234.305 FLOR H, 1995, NATURE, V375, P482, DOI 10.1038/375482a0 GARRAGHTY PE, 1991, NEUROREPORT, V2, P747, DOI 10.1097/00001756-199112000-00004 Goebel G, 1998, TINNITUS FRAGEBOGEN ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 Irvine DRF, 2000, HEARING RES, V147, P188, DOI 10.1016/S0378-5955(00)00131-3 JACOBS KM, 1991, SCIENCE, V251, P944, DOI 10.1126/science.2000496 KRUBITZER LA, 1989, BRAIN RES, V478, P161, DOI 10.1016/0006-8993(89)91490-X MERZENIC.MM, 1973, BRAIN RES, V63, P343, DOI 10.1016/0006-8993(73)90101-7 MERZENICH MM, 1976, J COMP NEUROL, V166, P387, DOI 10.1002/cne.901660402 Moller AR, 1997, AM J OTOL, V18, P577 PANTEV C, 1988, ELECTROEN CLIN NEURO, V69, P160, DOI 10.1016/0013-4694(88)90211-8 Pantev C, 1998, NATURE, V392, P811, DOI 10.1038/33918 Rajan R, 1998, NAT NEUROSCI, V1, P138, DOI 10.1038/388 Rajan R, 1998, AUDIOL NEURO-OTOL, V3, P123, DOI 10.1159/000013786 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 RECANZONE GH, 1993, J NEUROSCI, V13, P87 Salvi RJ, 2000, HEARING RES, V147, P261, DOI 10.1016/S0378-5955(00)00136-2 Syka J, 2000, HEARING RES, V139, P59, DOI 10.1016/S0378-5955(99)00175-6 WILLIAMSON SJ, 1990, AUDITORY EVOKED MAGN, P1 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 NR 25 TC 77 Z9 78 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 95 EP 101 DI 10.1016/S0378-5955(01)00282-9 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900009 PM 11506941 ER PT J AU Idrizbegovic, E Canlon, B Bross, LS Willott, JF Bogdanovic, N AF Idrizbegovic, E Canlon, B Bross, LS Willott, JF Bogdanovic, N TI The total number of neurons and calcium binding protein positive neurons during aging in the cochlear nucleus of CBA/CaJ mice: a quantitative study SO HEARING RESEARCH LA English DT Article DE auditory; calbindin; parvalbumin; calretinin; stereology; optical fractionator ID AUDITORY BRAIN-STEM; ELECTRON-MICROSCOPIC IMMUNOCYTOCHEMISTRY; RAT HIPPOCAMPUS; CALBINDIN D-28K; MESSENGER-RNA; GUINEA-PIG; INFERIOR COLLICULUS; CEREBELLAR CORTEX; SENSORY NEURONS; ZEBRA FINCH AB The quantitative stereological method, the optical fractionator, was used for determining the total number of neurons and the total number of neurons immunostained with parvalbumin, calbindin-D28k (calbindin), and calretinin in the dorsal and posteroventral cochlear nucleus (DCN and PVCN) in CBA/CaJ (CBA) mice during aging (1-39 months old). CBA mice have only a modest sensorineural pathology late in life. An age-related decrease of the total number of neurons was demonstrated in the DCN (r = -0.54, P < 0.03), while the total number of neurons in the PVCN did not show any significant age-related differences (r = 0.16, P = 0.57). In the DCN 5.5% of neurons were parvalbumin positive in the very old (30 39 months) mice, vs. 2.2% in the 1 month old mice. In the DCN 3% of the neurons were calbindin immunopositive in the 30-39 months mice compared to 1.9% in the I month old group. In the PVCN. 20% of the neurons in the very old mice were parvalbumin immunopositive. compared to 12% in the young mice. Calbindin did not show any significant age-related differences in the PVCN. The total number of calretinin immunopositive neurons both in the DCN and PVCN did not show any significant change with increasing age. In conclusion. the total neuronal number in the DCN and PVCN was age-related and region-specific. While the neuronal number in the DCN and PVCN was decreased or unchanged, respectively, the calcium binding protein positive neuronal number showed a graded increase during aging in a region-specific and protein-specific manner. (C) 2001 Published by Elsevier Science B.V. C1 Huddinge Univ Hosp, Dept Audiol, S-14186 Huddinge, Sweden. Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden. No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. Karolinska Inst, NEUROTEC, Geriatr Sect, Stockholm, Sweden. RP Idrizbegovic, E (reprint author), Huddinge Univ Hosp, Dept Audiol, S-14186 Huddinge, Sweden. CR ARAI R, 1991, J COMP NEUROL, V310, P21, DOI 10.1002/cne.903100105 BAIMBRIDGE KG, 1992, TRENDS NEUROSCI, V15, P303, DOI 10.1016/0166-2236(92)90081-I BATINI C, 1993, NEUROREPORT, V4, P927, DOI 10.1097/00001756-199307000-00022 BRAUN K, 1985, CELL TISSUE RES, V240, P117, DOI 10.1007/BF00217564 BRAUN K, 1991, NEUROSCIENCE, V40, P853, DOI 10.1016/0306-4522(91)90017-I Caicedo A, 1997, J COMP NEUROL, V378, P1, DOI 10.1002/(SICI)1096-9861(19970203)378:1<1::AID-CNE1>3.0.CO;2-8 Caicedo A, 1996, ANAT EMBRYOL, V194, P465 CELIO MR, 1986, NATURE, V323, P715, DOI 10.1038/323715a0 CHARD PS, 1993, J PHYSIOL-LONDON, V472, P341 Chen K, 1999, NEUROSCIENCE, V90, P1043, DOI 10.1016/S0306-4522(98)00503-X CHENG B, 1991, NEURON, V7, P1031, DOI 10.1016/0896-6273(91)90347-3 COLLAZO D, 1992, NEURON, V9, P643, DOI 10.1016/0896-6273(92)90028-C DEVENECIA RK, 1995, J COMP NEUROL, V359, P595, DOI 10.1002/cne.903590407 FLORIS A, 1994, ANAT EMBRYOL, V189, P495 Forster CR, 2000, J COMP NEUROL, V416, P173, DOI 10.1002/(SICI)1096-9861(20000110)416:2<173::AID-CNE4>3.0.CO;2-V FRIAUF E, 1994, J COMP NEUROL, V349, P193, DOI 10.1002/cne.903490204 FRISINA RD, 1995, HEARING RES, V85, P53, DOI 10.1016/0378-5955(95)00029-4 GAILLY P, 1993, FEBS LETT, V326, P272, DOI 10.1016/0014-5793(93)81806-B GHOSH A, 1995, SCIENCE, V268, P239, DOI 10.1126/science.7716515 GOLDFREY DA, 1975, J COMP NEUROL, V162, P247 GUNDERSEN HJG, 1987, J MICROSC-OXFORD, V147, P229 Gundersen HJG, 1999, J MICROSC-OXFORD, V193, P199, DOI 10.1046/j.1365-2818.1999.00457.x GUNDERSEN HJG, 1986, J MICROSC-OXFORD, V143, P3 GUNDERSEN HJG, 1988, APMIS, V96, P857 Heizmann CW, 1995, CALCIUM REGULATION C HEIZMANN CW, 1992, GEN PHYSIOL BIOPHYS, V11, P411 HENRY KR, 1980, AUDIOLOGY, V19, P369 HOU TY, 1993, SIAM J SCI COMPUT, V14, P1, DOI 10.1137/0914001 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 IACOPINO A, 1992, MOL BRAIN RES, V13, P251, DOI 10.1016/0169-328X(92)90033-8 Idrizbegovic E, 1999, NEUROSCI LETT, V259, P49, DOI 10.1016/S0304-3940(98)00911-2 Idrizbegovic E, 1998, BRAIN RES, V800, P86, DOI 10.1016/S0006-8993(98)00504-6 KAWAGUCHI Y, 1987, BRAIN RES, V416, P369, DOI 10.1016/0006-8993(87)90921-8 KELLEY PE, 1992, J COMP NEUROL, V319, P196 Khachaturian Z S, 1989, Aging (Milano), V1, P17 Korada S, 2000, HEARING RES, V140, P23, DOI 10.1016/S0378-5955(99)00182-3 LANDFIELD PW, 1987, NEUROBIOL AGING, V8, P346, DOI 10.1016/0197-4580(87)90074-1 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 Lohmann C, 1996, J COMP NEUROL, V367, P90, DOI 10.1002/(SICI)1096-9861(19960325)367:1<90::AID-CNE7>3.0.CO;2-E LOWENSTEIN DH, 1994, MOL BRAIN RES, V22, P299, DOI 10.1016/0169-328X(94)90058-2 LOWENSTEIN DH, 1991, NEURON, V6, P627, DOI 10.1016/0896-6273(91)90065-8 MARTIN MR, 1981, J COMP NEUROL, V197, P141, DOI 10.1002/cne.901970111 MATTSON MP, 1995, J NEUROSCI RES, V42, P357, DOI 10.1002/jnr.490420310 MCMULLEN NT, 1994, J COMP NEUROL, V349, P493, DOI 10.1002/cne.903490402 MOLINARI M, 1995, J COMP NEUROL, V362, P171, DOI 10.1002/cne.903620203 MUGNAINI E, 1980, J COMP NEUROL, V191, P581, DOI 10.1002/cne.901910406 MUGNAINI E, 1987, ARCH ITAL BIOL, V126, P41 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 NITSCH C, 1989, NEUROSCI LETT, V105, P263, DOI 10.1016/0304-3940(89)90631-9 ORRENIUS S, 1994, J NEURAL TRANSM-SUPP, P1 Parks TN, 1997, J COMP NEUROL, V383, P112 PARMENTIER M, 1991, EUR J BIOCHEM, V196, P79, DOI 10.1111/j.1432-1033.1991.tb15788.x RESIBOIS A, 1992, NEUROSCIENCE, V46, P101, DOI 10.1016/0306-4522(92)90012-Q RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 ROGERS JH, 1987, J CELL BIOL, V105, P1343, DOI 10.1083/jcb.105.3.1343 ROGERS JH, 1989, NEUROSCIENCE, V31, P697, DOI 10.1016/0306-4522(89)90434-X RYUGO DK, 1985, J COMP NEUROL, V242, P381, DOI 10.1002/cne.902420307 Spatz WB, 1997, HEARING RES, V107, P136, DOI 10.1016/S0378-5955(97)00029-4 TORTOSA A, 1993, NEUROSCIENCE, V55, P33, DOI 10.1016/0306-4522(93)90452-L VATER M, 1994, J COMP NEUROL, V341, P534, DOI 10.1002/cne.903410409 Verkhratsky A, 1998, TRENDS NEUROSCI, V21, P2, DOI 10.1016/S0166-2236(97)01156-9 WEBSTER DB, 1982, AM J ANAT, V163, P103, DOI 10.1002/aja.1001630202 WEBSTER WR, 1990, NEUROSCI LETT, V111, P252, DOI 10.1016/0304-3940(90)90270-J WEST MJ, 1991, ANAT REC, V231, P482, DOI 10.1002/ar.1092310411 Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 Williams M J, 1996, Tech Urol, V2, P179 Willott J. F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1992, J COMP NEUROL, V321, P666, DOI 10.1002/cne.903210412 WILLOTT JF, 1990, J COMP NEUROL, V300, P61, DOI 10.1002/cne.903000106 WILLOTT JF, 1994, HEARING RES, V74, P1, DOI 10.1016/0378-5955(94)90171-6 WINSKY L, 1995, J COMP NEUROL, V354, P564, DOI 10.1002/cne.903540407 ZETTEL ML, 1991, J COMP NEUROL, V313, P1, DOI 10.1002/cne.903130102 NR 72 TC 25 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 102 EP 115 DI 10.1016/S0378-5955(01)00295-7 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900010 PM 11506942 ER PT J AU Watanabe, K Jinnouchi, K Hess, A Michel, O Yagi, T AF Watanabe, K Jinnouchi, K Hess, A Michel, O Yagi, T TI Detection of apoptotic change in the lipopolysaccharide (LPS)-treated cochlea of guinea pigs SO HEARING RESEARCH LA English DT Article DE immunohistochemistry; single-stranded DNA; caspase 3; apoptosis; endotoxin (lipopolysaccharide); cochlear damage ID SINGLE-STRANDED-DNA; SENSORINEURAL HEARING-LOSS; ROUND WINDOW MEMBRANE; ACUTE OTITIS-MEDIA; NITRIC-OXIDE; CELL-DEATH; MIDDLE-EAR; ENDOTOXIN; ANTIBODY; EXPRESSION AB This study was undertaken to examine. electrophysiologically and immunohistochemically, the effect of endotoxin on the guinea pig cochlea. A bacterial endotoxin (lipopolysaccharide. LPS, 5 mg/ml, 0.2 ml) was injected into the middle ear trans-tympanically. The electrocochleograms were continuously recorded from before to 48 h after the injection with an electrode inserted into the facial canal. Then. the animals were sacrificed by intracardiac perfusion of a fixative, temporal bones were removed and immunohistochemically stained for single-stranded DNA (ssDNA) and caspase 3 (CPP32). ssDNA was detected at 48 h in the stria vascularis and spiral ligament. CPP32 was observed in the stria vascularis. the spiral ligament and the organ of Corti. The threshold of the compound action potential increased significantly at 48 h in the LPS group. These results suggest that the activation of CPP32 and fragmentation of DNA are involved in the dysfunction of the cochlea observed under inflammatory conditions. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Nippon Med Coll, Dept Otorhinolaryngol, Bunkyo Ku, Tokyo 1138603, Japan. Univ Cologne, Dept Otorhinolaryngol, D-50924 Cologne, Germany. RP Watanabe, K (reprint author), Nippon Med Coll, Dept Otorhinolaryngol, Bunkyo Ku, 1-1-5 Sendagi, Tokyo 1138603, Japan. CR Alam SA, 2000, HEARING RES, V141, P28, DOI 10.1016/S0378-5955(99)00211-7 ANSARI B, 1993, J PATHOL, V170, P1, DOI 10.1002/path.1711700102 BERNSTEIN JM, 1980, CAN J MICROBIOL, V26, P546 BURSCH W, 1990, BIOCHEM CELL BIOL, V68, P1071 DEFRE M, 1996, CYTOKINE YB, P219 DEMARIA TF, 1984, J CLIN MICROBIOL, V20, P15 ENGEL F, 1995, INFECT IMMUN, V63, P1305 Forge A, 2000, HEARING RES, V139, P97, DOI 10.1016/S0378-5955(99)00177-X HILDESHEIMER M, 1979, ACTA OTO-LARYNGOL, V88, P37, DOI 10.3109/00016487909137137 Hsu HL, 1996, CELL, V84, P299, DOI 10.1016/S0092-8674(00)80984-8 Kawarada Y, 1998, J BIOCHEM-TOKYO, V123, P492 KIM CS, 1995, OTOLARYNG HEAD NECK, V112, P557, DOI 10.1177/019459989511200409 MARGOLIS RH, 1993, ARCH OTOLARYNGOL, V119, P682 Miller LJ, 1998, SCIENCE, V281, P1301, DOI 10.1126/science.281.5381.1301 MONCADA S, 1991, PHARMACOL REV, V43, P109 MORIZONO T, 1990, EUR ARCH OTO-RHINO-L, V247, P40 NARUSE I, 1994, HISTOCHEMISTRY, V101, P73, DOI 10.1007/BF00315834 Patel T, 1996, FASEB J, V10, P587 RAHKO T, 1989, ACTA OTO-LARYNGOL, V108, P107, DOI 10.3109/00016488909107400 SPANDOW O, 1990, LARYNGOSCOPE, V100, P995 SPANDOW O, 1989, ACTA OTO-LARYNGOL, V107, P90, DOI 10.3109/00016488909127484 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 Takumida M, 1998, EUR ARCH OTO-RHINO-L, V255, P184, DOI 10.1007/s004050050040 Thornberry NA, 1998, SCIENCE, V281, P1312, DOI 10.1126/science.281.5381.1312 Watanabe I, 1999, JPN J CANCER RES, V90, P188 Watanabe K, 2000, HEARING RES, V145, P149, DOI 10.1016/S0378-5955(00)00086-1 Watanabe K, 2000, ANTI-CANCER DRUG, V11, P731, DOI 10.1097/00001813-200010000-00010 Watanabe K, 2000, NEUROSCI LETT, V293, P57, DOI 10.1016/S0304-3940(00)01494-4 YAMAGUCHI J, 1992, OTOL JPN, V2, P259 NR 29 TC 16 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 116 EP 122 DI 10.1016/S0378-5955(01)00291-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900011 PM 11506943 ER PT J AU Lee, JH Marcus, DC AF Lee, JH Marcus, DC TI Estrogen acutely inhibits ion transport by isolated stria vascularis SO HEARING RESEARCH LA English DT Article DE voltage-sensitive vibrating probe; strial marginal cell; cochlea; gerbil; estrogen; progesterone ID INCREASES K+ SECRETION; DARK CELL EPITHELIUM; MARGINAL CELLS; ISK/KVLQT1 CHANNELS; APICAL MEMBRANE; INNER-EAR; RECEPTOR; MECHANISM; WOMEN; RAT AB We investigated the nongenomic effects of female sex steroid hormones on the short circuit current (I-sc.probe) across gerbil stria vascularis using the voltage-sensitive vibrating probe. The strial marginal cell epithelial laver produces I-sc.probe by secreting K+ via I-Ks channels in the apical membrane. Application of 17 beta -estradiol (E-2) caused a decrease of I-sc.probe in a dose-dependent manner (10 nM-10 pM) within seconds. Tamoxifen, a competitive inhibitor of the intracellular estrogen receptor, did not change the inhibitory effect of E-2. Activation Of IK, channels by 4.4 ' -diisothiocyanatostilbene-2.2 ' -disulfonic acid in the presence and absence of E-2 was used to test the mechanism of action. The results were consistent with a direct inhibitory effect of E-2 on the I-Ks channels. By contrast, progesterone caused a transient increase Of I-sc.probe. These results suggest that E2 decreases secretion of K+ by inhibition Of I-Ks channels via a nongenomic mechanism at concentrations near those occurring under some physiologic conditions while progesterone caused only transient effects on I-sc.probe. (C) 2001 Published by Elsevier Science B.V. C1 Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA. RP Marcus, DC (reprint author), Kansas State Univ, Dept Anat & Physiol, 126 Coles Hall,1600 Denison Ave, Manhattan, KS 66506 USA. CR ANDERSCH B, 1978, BRIT J OBSTET GYNAEC, V85, P546 ANDREWS JC, 1992, ARCH OTOLARYNGOL, V118, P74 BUCKLER HM, 1995, CLIN ENDOCRINOL, V42, P445, DOI 10.1111/j.1365-2265.1995.tb02660.x Busch AE, 1997, BRIT J PHARMACOL, V122, P187, DOI 10.1038/sj.bjp.0701434 CARSONJURICA MA, 1990, ENDOCR REV, V11, P201 COX JR, 1980, EAR HEARING, V1, P219, DOI 10.1097/00003446-198007000-00008 EDWARDSO.JA, 1974, NATURE, V251, P425, DOI 10.1038/251425a0 Ettinger B, 1999, MENOPAUSE, V6, P273, DOI 10.1097/00042192-199906030-00015 Gerdes D, 1998, BIOL CHEM, V379, P907 HANNA GS, 1986, J LARYNGOL OTOL, V100, P701, DOI 10.1017/S0022215100099928 HERMENS WAJJ, 1991, EUR J OBSTET GYN R B, V40, P35, DOI 10.1016/0028-2243(91)90042-J JORDAN VC, 1977, MOL CELL ENDOCRINOL, V7, P177, DOI 10.1016/0303-7207(77)90066-1 Li ZY, 2000, J CARDIOVASC PHARM, V35, P506, DOI 10.1097/00005344-200003000-00023 MAJEWSKA MD, 1986, SCIENCE, V232, P1004, DOI 10.1126/science.2422758 Marcus Daniel C., 1996, Keio Journal of Medicine, V45, P301 MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 2001, CELL PHYSL SOURCE BO, P775, DOI 10.1016/B978-012656976-6/50138-4 MATEI GL, 1965, INTERN AUDIOL, V4, P43 MILLER M H, 1967, Journal of Auditory Research, V7, P373 Nakajima T, 1999, BRIT J PHARMACOL, V127, P429, DOI 10.1038/sj.bjp.0702576 Nathan CAO, 1999, ACTA OTO-LARYNGOL, V119, P853 Norman AW, 1997, HORMONES, P361, DOI 10.1016/B978-012521441-4/50014-6 Norman AW, 1997, HORMONES, 2ND EDITION, P1, DOI 10.1016/B978-012521441-4/50002-X NORMAN AW, 1997, HORMONES, P387, DOI 10.1016/B978-012521441-4/50015-8 ORIMO A, 1993, BIOCHEM BIOPH RES CO, V195, P730, DOI 10.1006/bbrc.1993.2106 PAABY P, 1989, ACTA ENDOCRINOL-COP, V120, P636 PAUL SM, 1992, FASEB J, V6, P2311 PIETRAS RJ, 1975, NATURE, V253, P357, DOI 10.1038/253357a0 RASMUSSEN H, 1982, FED PROC, V41, P72 Selye H, 1942, ENDOCRINOLOGY, V30, P437 SHEN Z, 1995, J MEMBRANE BIOL, V146, P283 Shen ZJ, 1997, AUDIT NEUROSCI, V3, P215 Shen ZJ, 1998, HEARING RES, V123, P157, DOI 10.1016/S0378-5955(98)00110-5 SNEDECOR GW, 1954, STAT METHODS SPACH C, 1964, J CLIN INVEST, V43, P217, DOI 10.1172/JCI104906 Stenberg AE, 1999, HEARING RES, V136, P29, DOI 10.1016/S0378-5955(99)00098-2 SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 Sunose H, 1997, HEARING RES, V114, P107, DOI 10.1016/S0378-5955(97)00152-4 SWANSON SJ, 1988, J SPEECH HEAR RES, V31, P569 TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P Vetter DE, 1996, NEURON, V17, P1251, DOI 10.1016/S0896-6273(00)80255-X Waldegger S, 1996, N-S ARCH PHARMACOL, V354, P698, DOI 10.1007/BF00166894 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S Wehling M, 1997, ANNU REV PHYSIOL, V59, P365, DOI 10.1146/annurev.physiol.59.1.365 ZHANG JJ, 1994, J CLIN INVEST, V94, P1690, DOI 10.1172/JCI117514 NR 45 TC 28 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 123 EP 130 DI 10.1016/S0378-5955(01)00316-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900012 PM 11506944 ER PT J AU Zettel, ML O'Neill, WE Trang, TT Frisina, RD AF Zettel, ML O'Neill, WE Trang, TT Frisina, RD TI Early bilateral deafening prevents calretinin up-regulation in the dorsal cortex of the inferior colliculus of aged CBA/CaJ mice SO HEARING RESEARCH LA English DT Article DE calcium binding protein; presbycusis; auditory midbrain; neural plasticity ID AUDITORY BRAIN-STEM; COCHLEAR NUCLEUS; CALBINDIN D-28K; IN-VITRO; INTRACELLULAR CALCIUM; HIPPOCAMPAL-NEURONS; CORTICAL-NEURONS; MESSENGER-RNA; CBA MOUSE; RAT AB This study was conducted to test the hypothesis that age-related calretinin (CR) up-regulation seen in the dorsal cortex of the inferior colliculus (ICdc) of old hearing CBA mice is dependent upon neural activity within the auditory pathway. We tested this hypothesis by bilaterally deafening young CBA/CaJ mice with kanamycin, and then aging them until 24 months. This manipulation mimics the lack of sound-evoked auditory activity experienced by old C57BL/6J mice, who are deaf and do not show CR upregulation with age. Cell counts revealed that the density of CR+ cells in the lCdc of old hearing CBA mice was statistically different from old deafened CBA mice raised under identical conditions. Old hearing CBAs possessed an average of 27.54 more CR+ cells/100 mum(2) than old deafened CBAs. When old deafened CBAs were compared to young hearing CBAs, young hearing C57s, and old deaf C57s, there was no significant difference in mean CR+ cell density in ICdc. Thus, only the old normal hearing CBAs showed an increase in CR+ cells with age, Supporting the hypothesis that CR up-regulation depends upon sound-evoked activity. Moreover, these results demonstrate that up-regulation of CR expression was not simply due to a mouse strain difference. (C) 2001 Published by Elsevier Science B.V. C1 Univ Rochester, Sch Med & Dent, Dept Surg, Div Otolaryngol, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Neurobiol & Anat, Rochester, NY 14642 USA. Univ Hosp Cleveland, Dept Surg, Cleveland, OH 44106 USA. RP Zettel, ML (reprint author), Univ Rochester, Sch Med & Dent, Dept Surg, Div Otolaryngol, 601 Elmwood Ave, Rochester, NY 14642 USA. CR ANDERSEN RA, 1980, J COMP NEUROL, V191, P479, DOI 10.1002/cne.901910310 BATINI C, 1993, NEUROREPORT, V4, P927, DOI 10.1097/00001756-199307000-00022 Billing-Marczak K, 1999, POL J PHARMACOL, V51, P173 BRAUN AK, 1990, ASS RES OTOLARYNGOL, V13, P388 Caicedo A, 1997, J COMP NEUROL, V378, P1, DOI 10.1002/(SICI)1096-9861(19970203)378:1<1::AID-CNE1>3.0.CO;2-8 CHOI DW, 1988, TRENDS NEUROSCI, V11, P465, DOI 10.1016/0166-2236(88)90200-7 CHOI DW, 1988, NEURON, V1, P623, DOI 10.1016/0896-6273(88)90162-6 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 DIAMOND IT, 1969, BRAIN RES, V15, P305, DOI 10.1016/0006-8993(69)90160-7 DURHAM D, 1993, HEARING RES, V70, P151, DOI 10.1016/0378-5955(93)90153-R DUTAR P, 1991, EUR J NEUROSCI, V3, P839, DOI 10.1111/j.1460-9568.1991.tb00095.x Forster CR, 2000, J COMP NEUROL, V416, P173, DOI 10.1002/(SICI)1096-9861(20000110)416:2<173::AID-CNE4>3.0.CO;2-V FRANDSEN A, 1993, J NEUROCHEM, V60, P1202, DOI 10.1111/j.1471-4159.1993.tb03278.x FRISINA DR, 2001, FUNCTIONAL NEUROBIOL FRISINA RD, 2001, FUNCTIONAL NEUROBIOL GARCIA MM, 1993, NEUROREPORT, V5, P65, DOI 10.1097/00001756-199310000-00016 GERMAN DC, 1992, ANN NY ACAD SCI, V648, P42, DOI 10.1111/j.1749-6632.1992.tb24523.x Hack N.J., 2000, J NEUROSCI, V20, P1 HARTLEY DM, 1993, J NEUROSCI, V13, P1993 HUANG Q, 1995, NEUROSCIENCE, V65, P397, DOI 10.1016/0306-4522(94)00494-P HUFFMAN RF, 1990, BRAIN RES REV, V15, P295, DOI 10.1016/0165-0173(90)90005-9 Hugon J, 1996, BRAIN RES, V707, P288, DOI 10.1016/0006-8993(95)01393-8 IACOPINO A, 1992, MOL BRAIN RES, V13, P251, DOI 10.1016/0169-328X(92)90033-8 IACOPINO AM, 1990, P NATL ACAD SCI USA, V87, P4078, DOI 10.1073/pnas.87.11.4078 Jen PHS, 1998, J COMP PHYSIOL A, V183, P683, DOI 10.1007/s003590050291 KASS GEN, 1988, ARCH BIOCHEM BIOPHYS, V260, P789, DOI 10.1016/0003-9861(88)90509-7 KAZEE AM, 1995, HEARING RES, V89, P109, DOI 10.1016/0378-5955(95)00128-6 Kazee AM, 1999, HEARING RES, V133, P98, DOI 10.1016/S0378-5955(99)00058-1 Khachaturian Z.S., 1984, HDB STUDIES PSYCHIAT, P7 KUROBE N, 1992, J NEUROCHEM, V58, P128, DOI 10.1111/j.1471-4159.1992.tb09287.x LOWENSTEIN DH, 1991, NEURON, V6, P627, DOI 10.1016/0896-6273(91)90065-8 LUKAS W, 1994, NEUROSCIENCE, V61, P307, DOI 10.1016/0306-4522(94)90233-X MATTSON MP, 1991, NEURON, V6, P41, DOI 10.1016/0896-6273(91)90120-O Murchison D, 1998, J NEUROPHYSIOL, V80, P350 ONeill WE, 1997, HEARING RES, V112, P158, DOI 10.1016/S0378-5955(97)00116-0 RANDALL RD, 1992, J NEUROSCI, V12, P1882 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 SANS N, 1995, MOL BRAIN RES, V30, P177, DOI 10.1016/0169-328X(95)00025-N SEFTEL MA, 1986, ASS RES OTOLARYNGOL, V9, P8 Suga N, 2000, P NATL ACAD SCI USA, V97, P11807, DOI 10.1073/pnas.97.22.11807 SUN X, 1989, BRAIN RES, V495, P1, DOI 10.1016/0006-8993(89)91212-2 Walton JP, 1998, J NEUROSCI, V18, P2764 Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 WILLOTT JF, 1994, HEARING RES, V74, P1, DOI 10.1016/0378-5955(94)90171-6 WINSKY L, 1995, J COMP NEUROL, V354, P564, DOI 10.1002/cne.903540407 ZETTEL ML, 2001, ASS RES OTOLARYNGOL, V24, P284 Zettel ML, 1997, J COMP NEUROL, V386, P92, DOI 10.1002/(SICI)1096-9861(19970915)386:1<92::AID-CNE9>3.0.CO;2-8 Zhang YF, 1997, NATURE, V387, P900 Zhang YF, 1997, J NEUROPHYSIOL, V78, P3489 ZIRPEL L, 1995, J NEUROPHYSIOL, V74, P1355 NR 50 TC 26 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 131 EP 138 DI 10.1016/S0378-5955(01)00305-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900013 PM 11506945 ER PT J AU Reyes, S Ding, DL Sun, W Salvi, R AF Reyes, S Ding, DL Sun, W Salvi, R TI Effect of inner and outer hair cell lesions on electrically evoked otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE outer hair cell; inner hair cell; electrically evoked otoacoustic emission; distortion product otoacoustic emission; carboplatin; chinchilla ID BASILAR-MEMBRANE MOTION; DISTORTION-PRODUCT; NOISE EXPOSURE; CARBOPLATIN; FREQUENCY; STIMULATION; CHINCHILLA; ELECTROMOTILITY; THRESHOLDS; REDUCTION AB When the cochlea is stimulated by a sinusoidal current, the inner ear emits an acoustic signal at the stimulus frequency, termed the electrically evoked otoacoustic emission (EEOAE). Recent studies have found EEOAEs in birds lacking outer hair cells (OHCs), raising the possibility that other types of hair cells, including inner hair cells (IHCs), may generate EEOAEs. To determine the relative contribution of IHCs and OHCs to the generation of the EEOAE, we measured the amplitude of EEOAEs, distortion product otoacoustic emissions (DPOAEs), the cochlear microphonic (CM) and the compound action potential (CAP) in normal chinchillas and chinchillas with IHC lesions or IHC plus OHC lesions induced by carboplatin. Selective IHC loss had little or no effect on CM amplitude and caused a slight reduction in mean DPOAE amplitude. However, IHC loss resulted in a massive reduction in CAP amplitude. Importantly, selective I]HC lesions did not reduce EEOAE amplitude. but instead, EEOAE amplitude increased at high frequencies. When both IHCs and OHCs were destroyed, the amplitude of the CM, DPOAE and EEOAE all decreased. The increase in EEOAE amplitude seen with IHC loss may be due to (1) loss of tonic efferent activity to the OHCs, (2) change in the mechanical properties of the cochlea or (3) elimination of EEOAEs produced by IHCs in phase opposition to those from OHCs. (C) 2001 Published by Elsevier Science B.V. C1 SUNY Buffalo, Hearing Res Lab, Buffalo, NY 14214 USA. RP Reyes, S (reprint author), SUNY Buffalo, Hearing Res Lab, 215 Parker Hall, Buffalo, NY 14214 USA. EM sareyes@buffalo.edu CR BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T BRIX J, 1994, HEARING RES, V76, P147, DOI 10.1016/0378-5955(94)90096-5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Burkard R, 1996, Audiol Neurootol, V1, P197 CHEN L, 1997, ABSTR ASS RES OTOLAR, V20, P487 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 Ding DL, 1999, ANN NY ACAD SCI, V884, P152, DOI 10.1111/j.1749-6632.1999.tb08640.x Eddins AC, 1999, HEARING RES, V127, P119 FROYMOVICH O, 1995, J ACOUST SOC AM, V97, P3021, DOI 10.1121/1.411867 GRATTON MA, 1990, HEARING RES, V50, P211, DOI 10.1016/0378-5955(90)90046-R GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HE D, 2001, ASS RES OTOLARYNGOL, V24, P159 HE DZZ, 1994, HEARING RES, V78, P77, DOI 10.1016/0378-5955(94)90046-9 Hofstetter P, 2000, HEARING RES, V150, P132, DOI 10.1016/S0378-5955(00)00201-X Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 Hofstetter P, 1997, AUDIOLOGY, V36, P301 HUANG GJ, 1994, P NATL ACAD SCI USA, V91, P12268, DOI 10.1073/pnas.91.25.12268 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 JARAMILLO F, 1993, NATURE, V364, P527, DOI 10.1038/364527a0 Jock BM, 1996, HEARING RES, V96, P179, DOI 10.1016/0378-5955(96)00058-5 KETTEMBEIL S, 1995, HEARING RES, V86, P47, DOI 10.1016/0378-5955(95)00053-7 Manley GA, 1997, J ACOUST SOC AM, V102, P1049, DOI 10.1121/1.419858 Manley GA, 2001, P NATL ACAD SCI USA, V98, P2826, DOI 10.1073/pnas.041604998 Manley GA, 1999, HEARING RES, V138, P1, DOI 10.1016/S0378-5955(99)00126-4 Manley GA, 1996, J ACOUST SOC AM, V99, P1588, DOI 10.1121/1.414680 NAKAJIMA HH, 1991, PROCEEDINGS OF THE 1991 IEEE SEVENTEENTH ANNUAL NORTHEAST BIOENGINEERING CONFERENCE, P213, DOI 10.1109/NEBC.1991.154650 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 Nuttall AL, 1999, HEARING RES, V131, P39, DOI 10.1016/S0378-5955(99)00009-X Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 OLSON ES, 1994, J ACOUST SOC AM, V95, P395, DOI 10.1121/1.408331 Ota Y, 2000, HEARING RES, V148, P124, DOI 10.1016/S0378-5955(00)00150-7 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 POWERS NL, 1995, NATURE, V375, P585, DOI 10.1038/375585a0 Ren TY, 1995, HEARING RES, V92, P178, DOI 10.1016/0378-5955(95)00217-0 Ricci AJ, 2000, J NEUROSCI, V20, P7131 SIEGEL JH, 1982, NEW PERSPECTIVES NOI, P137 Spicer SS, 1999, HEARING RES, V136, P139, DOI 10.1016/S0378-5955(99)00118-5 Stewart CE, 2000, P NATL ACAD SCI USA, V97, P454, DOI 10.1073/pnas.97.1.454 Sun W, 2000, HEARING RES, V150, P137, DOI 10.1016/S0378-5955(00)00195-7 TAKENO S, 1994, HEARING RES, V75, P93, DOI 10.1016/0378-5955(94)90060-4 Taschenberger G, 1995, HEARING RES, V91, P87, DOI 10.1016/0378-5955(95)00174-3 Trautwein P, 1996, HEARING RES, V96, P71, DOI 10.1016/0378-5955(96)00040-8 Trautwein P, 1996, Audiol Neurootol, V1, P86 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 Wake M, 1996, ACTA OTO-LARYNGOL, V116, P374, DOI 10.3109/00016489609137860 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 WIT HP, 1989, HEARING RES, V41, P199, DOI 10.1016/0378-5955(89)90011-7 ZHENG H, 1999, ASS RES OTOLARYNGOL, V22, P385 NR 48 TC 16 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 139 EP 150 DI 10.1016/S0378-5955(01)00309-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900014 PM 11506946 ER PT J AU El-Amraoui, A Cohen-Salmon, M Petit, C Simmler, MC AF El-Amraoui, A Cohen-Salmon, M Petit, C Simmler, MC TI Spatiotemporal expression of otogelin in the developing and adult mouse inner ear SO HEARING RESEARCH LA English DT Article DE otogelin; inner ear; acellular structure; myosin VIIA ID TECTORIAL MEMBRANE; ACELLULAR MEMBRANES; MOLECULAR-CLONING; DEAFNESS DFNB18; ALPHA-TECTORIN; MYOSIN-VIIA; V COLLAGEN; LOCALIZATION; MATRIX; ULTRASTRUCTURE AB Using a PCR-based subtractive method on cDNA from 2-day-old mouse cochlea, we identified a gene encoding otogelin, Otog, an inner ear specific glycoprotein expressed in all acellular structures. Here, we provide evidence that otogelin is detected as early as embryonic day 10 in the otic vesicle. At this stage, otogelin is detected in the epithelial cells which do not overlap with the myosin VIIA-expressing cells, namely the precursors of the hair cells, thus arguing for an early commitment of the two cell populations. Analysis of otogelin spatiotemporal cell distribution allows a molecular tracing for the contribution of the cochlear and vestibular inner ear supporting cells to the formation of the acellular structures. Throughout embryonic and adult lire, the expression of the otogelin gene as monitored by LacZ inserted into Otog, and the abundance of the protein are greater in the vestibule than in the cochlea. In adult, otogelin is still produced by the vestibular supporting cells, which argues for a continuous process of otogelin renewal in the otoconial membranes and cupulae. In contrast, in the tectorial membrane, otogelin should be a long-lasting protein since both the otogelin gene and protein were almost undetectable in adult cochlear cells. The data are consistent with the requirement for otogelin in the attachment of the otoconial membranes and cupulae to their corresponding sensory epithelia as revealed in Otog -/- mice. (C) 2001 Elsevier Science BN. All rights reserved. C1 Inst Pasteur, CNRS URA 1968, Unite Genet Deficits Sensoriels, F-75724 Paris 15, France. Ecole Natl Vet, UMR 955 INRA Genet Mol, F-94704 Maisons Alfort, France. RP Petit, C (reprint author), Inst Pasteur, CNRS URA 1968, Unite Genet Deficits Sensoriels, 25 Rue Dr Roux, F-75724 Paris 15, France. CR Cohen-Salmon M, 1997, P NATL ACAD SCI USA, V94, P14450, DOI 10.1073/pnas.94.26.14450 Cohen-Salmon M, 1999, MAMM GENOME, V10, P520, DOI 10.1007/s003359901033 Coutinho P, 1999, HEARING RES, V130, P62, DOI 10.1016/S0378-5955(98)00213-5 ElAmraoui A, 1996, HUM MOL GENET, V5, P1171, DOI 10.1093/hmg/5.8.1171 GOODYEAR R, 1994, HEARING RES, V80, P93, DOI 10.1016/0378-5955(94)90013-2 GOODYEAR R, 1994, J COMP NEUROL, V345, P267, DOI 10.1002/cne.903450208 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 Jain PK, 1998, GENOMICS, V50, P290, DOI 10.1006/geno.1998.5320 KILLICK R, 1995, J CELL BIOL, V129, P535, DOI 10.1083/jcb.129.2.535 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 Legan PK, 1997, J BIOL CHEM, V272, P8791 Legan PK, 2000, NEURON, V28, P273, DOI 10.1016/S0896-6273(00)00102-1 LIM DJ, 1990, ACTA OTO-LARYNGOL, V110, P224, DOI 10.3109/00016489009122541 MUNYER PD, 1994, HEARING RES, V79, P83, DOI 10.1016/0378-5955(94)90129-5 Nakai Y, 1996, ORL J OTO-RHINO-LARY, V58, P9 PRIETO JJ, 1990, HEARING RES, V45, P283, DOI 10.1016/0378-5955(90)90127-B Rau A, 1999, J COMP NEUROL, V405, P271 RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 Sahly I, 1997, ANAT EMBRYOL, V196, P159, DOI 10.1007/s004290050088 SANTI PA, 1990, J ELECTRON MICR TECH, V15, P293, DOI 10.1002/jemt.1060150308 Simmler MC, 2000, MAMM GENOME, V11, P961, DOI 10.1007/s003350010197 Simmler MC, 2000, NAT GENET, V24, P139, DOI 10.1038/72793 SLEPECKY NB, 1992, CELL TISSUE RES, V267, P413, DOI 10.1007/BF00319363 SLEPECKY NB, 1992, ACTA OTO-LARYNGOL, V112, P611, DOI 10.3109/00016489209137449 STEEL KP, 1986, NEUROBIOLOGY HEARING, P139 Verpy E, 1999, P NATL ACAD SCI USA, V96, P529, DOI 10.1073/pnas.96.2.529 Wang YX, 1998, P NATL ACAD SCI USA, V95, P15345, DOI 10.1073/pnas.95.26.15345 NR 27 TC 27 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 151 EP 159 DI 10.1016/S0378-5955(01)00312-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900015 PM 11506947 ER PT J AU Hesselmann, V Wedekind, C Kugel, H Schulte, O Krug, B Klug, N Lackner, KJ AF Hesselmann, V Wedekind, C Kugel, H Schulte, O Krug, B Klug, N Lackner, KJ TI Functional magnetic resonance imaging of human pontine auditory pathway SO HEARING RESEARCH LA English DT Article DE functional imaging; magnetic resonance tomography; auditory system; brainstem ID ACTIVATION; CORTEX; DISCRIMINATION AB The purpose of this study is to visualize brainstem auditory pathways by functional magnetic resonance imaging (fMRI). Eighteen healthy volunteers (age 28 to 42 years) with normal hearing function underwent fMRI examination on a 1.5 Tesla imaging system (Philips, Best, The Netherlands) with periodic click stimulation. Blood oxygen level dependent images were obtained using a three-dimensional EPI sequence with shifted echo technique (principles of echo shifting with a train of observations). Control scans without click stimulation were obtained in the identical setting. Cross correlation activation maps were calculated using a postprocessing tool (Philips). They were matched with anatomic slices of identical orientation and thickness. Five of 18 subjects were excluded because of motion artifacts. In 4/13 significant activation was observed at the root entry zone of the ipsilateral acoustic nerve corresponding to the cochlear nuclei. In I 1/ 13 subjects, signif icant activation was found in the same slice contralaterally close to the floor of the 4th ventricle. corresponding to the expected region of the superior olivary nucleus. Activation of the rostral parts of the auditory pathway (inferior colliculus. medial geniculate body) was not found. In the absence of the stimulus no activation occurred in these structures. It was concluded that activation of the brainstem auditory pathways by click stimuli can be visualized by fMRI. (C) 2001 Published by Elsevier Science B.V. C1 Univ Cologne, Dept Neurosurg, D-50924 Cologne, Germany. Univ Cologne, Dept Radiol, D-50924 Cologne, Germany. RP Wedekind, C (reprint author), Univ Cologne, Dept Neurosurg, D-50924 Cologne, Germany. RI Kugel, Harald/A-4963-2013 OI Kugel, Harald/0000-0002-4349-1984 CR BANDETTINI PA, 1992, MAGNET RESON MED, V25, P390, DOI 10.1002/mrm.1910250220 Binder JR, 1997, J NEUROSCI, V17, P353 BINDER JR, 1994, ANN NEUROL, V35, P662, DOI 10.1002/ana.410350606 Guimaraes AR, 1998, HUM BRAIN MAPP, V6, P33, DOI 10.1002/(SICI)1097-0193(1998)6:1<33::AID-HBM3>3.0.CO;2-M KWONG KK, 1992, P NATL ACAD SCI USA, V89, P5675, DOI 10.1073/pnas.89.12.5675 LOCKWOOD AH, 1999, CEREB CORTEX, V65, P1047 MELCHER JR, 1999, FUNCTIONAL MRI, P393 Melcher JR, 2000, J NEUROPHYSIOL, V83, P1058 PICKLES JO, 1989, INTRO PHYSL HEARING SCHERG M, 1985, ELECTROEN CLIN NEURO, V62, P290, DOI 10.1016/0168-5597(85)90006-1 Shah NJ, 1999, JMRI-J MAGN RESON IM, V9, P19, DOI 10.1002/(SICI)1522-2586(199901)9:1<19::AID-JMRI3>3.0.CO;2-K Strainer JC, 1997, AM J NEURORADIOL, V18, P601 VLAARDINGERBROE.MT, 1996, MAGNETIC RESONANCE NR 13 TC 16 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 160 EP 164 DI 10.1016/S0378-5955(01)00307-0 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900016 PM 11506948 ER PT J AU Wu, WJ Sha, SH McLaren, JD Kawamoto, K Raphael, Y Schacht, J AF Wu, WJ Sha, SH McLaren, JD Kawamoto, K Raphael, Y Schacht, J TI Aminoglycoside ototoxicity in adult CBA, C57BL and BALB mice and the Sprague-Dawley rat SO HEARING RESEARCH LA English DT Article DE gentamicin; kanamycin; 2,3-dihydroxybenzoate; protection; pigmentation; reactive oxygen species ID INDUCED HEARING-LOSS; PRODUCT OTOACOUSTIC EMISSIONS; FREE-RADICAL FORMATION; PIG IN-VIVO; GENTAMICIN OTOTOXICITY; GUINEA-PIG; IRON CHELATORS; F1-HYBRID STRAINS; SENSITIVE PERIOD; MOUSE AB The availability of genetic information, transgenic and knock-out animals make the mouse a primary model in biomedical research. Aminoglycoside ototoxicity, however, has rarely been studied in mature mice because they are considered highly resistant to the drugs. This study presents models for kanamycin ototoxicity in adult CBA/J, C57BL/6 and BALB/c mouse strains and a comparison to Sprague-Dawley rats. Five-week-old mice were injected subcutaneously twice daily with 400-900 mg kanamycin base/ kg body weight for 15 days. Kanamycin induced dose-dependent auditory threshold shifts of up to 70 dB at 24 kHz as measured by auditory brain stem-evoked responses. Vestibular function was also affected in all strains. The functional deficits were accompanied by hair cell loss in both cochlear and vestibular neurosensory epithelia. Concomitant administration of the antioxidant 2,3-dihydroxybenzoate significantly attenuated the kanamycin-induced threshold shifts. In adult male Sprague-Dawley rats, doses of 1 X 500 mg or 2 X 300 mg kanamycin base/kg body weight/day X 14 days induced threshold shifts of approximately 50 dB at 20 kHz. These were accompanied by loss of outer hair cells. The order of susceptibility, BALB > CBA > C57, was not due to differences in the pharmacokinetics of kanamycin. It also did not correlate with the presence of AhllAhl2 genes which predispose C57 and BALB strains, respectively, to accelerated age-related hearing loss. Pigmentation, however, paralleled this rank order suggesting an influence of melanin on cochlear antioxidant status. (C) 2001 Published by Elsevier Science B.V. C1 Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. China Cent So Univ, Xiangya Med Sch, Dept Otolaryngol, Changsha, Peoples R China. Kansai Med Univ, Dept Otolaryngol, Osaka, Japan. RP Schacht, J (reprint author), Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR ASTBURY PJ, 1982, ARCH TOXICOL, V50, P267, DOI 10.1007/BF00310859 Brummett RE, 1982, AMINOGLYCOSIDES MICR, P419 CARLIER E, 1980, ARCH OTO-RHINO-LARYN, V226, P129, DOI 10.1007/BF00455127 CAUSSE R, 1949, CR SOC BIOL, V143, P619 CHEN CS, 1983, ARCH OTO-RHINO-LARYN, V238, P217, DOI 10.1007/BF00453932 CONLEE JW, 1989, HEARING RES, V41, P43, DOI 10.1016/0378-5955(89)90177-9 Conlon BJ, 1999, HEARING RES, V128, P40, DOI 10.1016/S0378-5955(98)00195-6 EDWARDS J, 1997, THESIS U COLL LONDON ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X Forge A, 2000, AUDIOL NEURO-OTOL, V5, P3, DOI 10.1159/000013861 FORGE A, 1999, 10 INT S AUD MED MAN FRIEDMAN RA, 1992, OTOLARYNG CLIN N AM, V25, P1017 HALSEY K, 2000, ASS RES OTOLARYNGOL, V23, P206 Henley CM, 1996, HEARING RES, V99, P85, DOI 10.1016/S0378-5955(96)00094-9 Henley CM, 1996, HEARING RES, V98, P93, DOI 10.1016/0378-5955(96)00077-9 HENRY KR, 1981, ARCH OTOLARYNGOL, V107, P92 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 Jimenez AM, 1999, HEARING RES, V138, P91, DOI 10.1016/S0378-5955(99)00154-9 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 LAUTERMANN J, 1995, HEARING RES, V86, P15, DOI 10.1016/0378-5955(95)00049-A LINDEMAN HH, 1969, ACTA OTO-LARYNGOL, V67, P177, DOI 10.3109/00016486909125441 Malakoff D, 2000, SCIENCE, V288, P248, DOI 10.1126/science.288.5464.248 Nakai Y, 1983, Acta Otolaryngol Suppl, V393, P1 Ohlemiller KK, 2000, HEARING RES, V149, P239, DOI 10.1016/S0378-5955(00)00191-X Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P237, DOI 10.1159/000013847 PRIEVE BA, 1984, ACTA OTO-LARYNGOL, V98, P428, DOI 10.3109/00016488409107584 Priuska EM, 1995, BIOCHEM PHARMACOL, V50, P1749, DOI 10.1016/0006-2952(95)02160-4 Probst FJ, 1999, HEARING RES, V130, P1, DOI 10.1016/S0378-5955(98)00231-7 RUCKENSTEIN MJ, 1993, ACTA OTO-LARYNGOL, V113, P160, DOI 10.3109/00016489309135785 SANDE MA, 1990, PHARMACOL BASIS THER, P1098 SCALIA M, 1990, PIGM CELL RES, V3, P115, DOI 10.1111/j.1600-0749.1990.tb00330.x Sha SH, 1999, HEARING RES, V128, P112, DOI 10.1016/S0378-5955(98)00200-7 Sha SH, 1999, FREE RADICAL BIO MED, V26, P341, DOI 10.1016/S0891-5849(98)00207-X SHA SH, 2001, IN PRESS AUDIOL NEUR Sha SH, 1999, LAB INVEST, V79, P807 Sha SH, 2000, HEARING RES, V142, P34, DOI 10.1016/S0378-5955(00)00003-4 Sha SH, 2001, HEARING RES, V155, P1, DOI 10.1016/S0378-5955(01)00224-6 SICHEL G, 1991, FREE RADIC BIOL MED, V2, P1 Sinswat P, 2000, KIDNEY INT, V58, P2525, DOI 10.1046/j.1523-1755.2000.00437.x Song BB, 1997, J PHARMACOL EXP THER, V282, P369 Song BB, 1998, FREE RADICAL BIO MED, V25, P189, DOI 10.1016/S0891-5849(98)00037-9 Song BB, 1996, HEARING RES, V94, P87, DOI 10.1016/0378-5955(96)00003-2 Stead DA, 1996, J CHROMATOGR B, V675, P295, DOI 10.1016/0378-4347(95)00355-X SULLIVAN MJ, 1987, HEARING RES, V31, P161, DOI 10.1016/0378-5955(87)90122-5 WERSALL J, 1969, J INFECT DIS, V119, P410 Wersäll J, 1973, Adv Otorhinolaryngol, V20, P14 Whitlon DS, 1999, HEARING RES, V137, P43, DOI 10.1016/S0378-5955(99)00136-7 Willott JF, 1998, HEARING RES, V115, P162, DOI 10.1016/S0378-5955(97)00189-5 NR 50 TC 105 Z9 121 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2001 VL 158 IS 1-2 BP 165 EP 178 DI 10.1016/S0378-5955(01)00303-3 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 463YY UT WOS:000170505900017 PM 11506949 ER PT J AU Agrup, C Berggren, PO Bagger-Sjoback, D AF Agrup, C Berggren, PO Bagger-Sjoback, D TI Morphological and functional characteristics of cells cultured from the endolymphatic sac SO HEARING RESEARCH LA English DT Article DE inner ear; endolymph; fura-2 method; guinea pig ID GUINEA-PIG; EPITHELIAL-CELLS; FREE CA-2+; CALCIUM; MOBILIZATION; MICROSCOPY; FILAMENTS; RELEASE; DUCT AB The endolymphatic sac is a part of the homeostasis-regulating system of the membranous labyrinth of the inner ear. Disturbances in the function of the endolymphatic sac are believed to be involved in the genesis of different inner ear disorders, such as endolymphatic hydrops and Meniere's disease. To make studies of the ion- and fluid-regulating mechanisms of the sac possible, a method to culture the tissue in vitro was developed. Epithelial cells and fibroblasts were morphologically characterised in the cell cultures with light and electron microscopy as well as immunohistochemically using antibodies against cytokeratin and vimentin. Since mesenchymal cells have been shown to express vimentin and epithelial cells cytokeratin, the antibodies against these two intermediate filament proteins were used to further confirm the morphological identification. In addition, some functional characteristics of the cultured cells from the endolymphatic sac were studied. ATP and K+ were added to the cell cultures and changes in cytoplasmic free Ca2+ concentration ([Ca2+](i)) were determined with the fura-2 method. A rapid and transient increase in [Ca2+](i), could be seen in both epithelial cells and fibroblasts after applying ATP (200 muM) extracellularly. However, when K+ was added in concentrations of 50 mM and 100 mM, no changes in [Ca2+](i) could be seen in either the epithelial cells or the fibroblasts. The results show that the cultured endolymphatic sac cells preserve their morphological characteristics and maintain a high viability. Accordingly, this method provides a tool for further studies of ion transport mechanisms and fluid homeostasis in the endolymphatic sac. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Karolinska Hosp, Karolinska Inst, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. Karolinska Hosp, Karolinska Inst, Dept Mol Med, Rolf Luft Ctr Diabet Res, S-17176 Stockholm, Sweden. RP Agrup, C (reprint author), Karolinska Hosp, Karolinska Inst, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. CR Agrup C, 1996, HEARING RES, V102, P155, DOI 10.1016/S0378-5955(96)00156-6 ALTERMATT HJ, 1990, ORL J OTO-RHINO-LARY, V52, P113 AMANO H, 1983, ARCH OTO-RHINO-LARYN, V237, P273, DOI 10.1007/BF00453732 Arishige S, 1998, ORL J OTO-RHINO-LARY, V60, P73, DOI 10.1159/000027568 ARKHAMMAR P, 1990, BIOCHEM J, V265, P203 BAGGERSJOBACK D, 1986, ARCH OTOLARYNGOL, V112, P398 BAGGERSJOBACK D, 1994, MENIERE'S DISEASE, P399 BAUWENS LJJM, 1991, EUR ARCH OTO-RHINO-L, V248, P495, DOI 10.1007/BF00627642 BERRIDGE M, 1985, TRIANGLE, V24, P79 BOYD AE, 1986, J CLIN INVEST, V77, P774, DOI 10.1172/JCI112374 Couloigner V, 1998, LARYNGOSCOPE, V108, P592, DOI 10.1097/00005537-199804000-00024 DUBYAK GR, 1986, ARCH BIOCHEM BIOPHYS, V245, P84, DOI 10.1016/0003-9861(86)90192-X Efendic S, 1991, J Intern Med Suppl, V735, P9 ERWALL C, 1988, HEARING RES, V36, P277, DOI 10.1016/0378-5955(88)90068-8 FRANKE WW, 1978, P NATL ACAD SCI USA, V75, P5034, DOI 10.1073/pnas.75.10.5034 FRIBERG U, 1984, ARCH OTOLARYNGOL, V110, P421 FUKAZAWA K, 1990, Japanese Journal of Clinical Electron Microscopy, V23, P135 GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440 Guild SR, 1927, AM J ANAT, V39, P57, DOI 10.1002/aja.1000390103 Hallpike C. S., 1938, J LARYNG, V53, P625, DOI 10.1017/S0022215100003947 HULTCRANTZ M, 1990, ACTA OTO-LARYNGOL, V109, P245, DOI 10.3109/00016489009107440 KIMURA RS, 1981, MENIERES DIS, P15 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 LAWRENCE M, 1961, ANN OTO RHINOL LARYN, V70, P753 LUNDQUIST PG, 1976, ARCH OTO-RHINO-LARYN, V212, P231, DOI 10.1007/BF00453671 LUNDQUIST PG, 1965, ACTA OTOLARYNGOL S S, V201, P1 Meissner HP, 1981, MECHANISM GATED CALC, P157 MIZUKOSHI F, 1988, ACTA OTO-LARYNGOL, V105, P202, DOI 10.3109/00016488809096999 MORI N, 1987, ARCH OTO-RHINO-LARYN, V244, P61, DOI 10.1007/BF00453493 Mori N, 1996, PFLUG ARCH EUR J PHY, V433, P58, DOI 10.1007/s004240050248 NAFTALIN L, 1958, J Laryngol Otol, V72, P118, DOI 10.1017/S0022215100053731 RASKANDERSEN H, 1979, ORL J OTO-RHINO-LARY, V41, P177 Salt AN, 1989, MENIERES DIS, P69 STERKERS O, 1988, PHYSIOL REV, V68, P1083 TAKUMIDA M, 1991, ORL J OTO-RHINO-LARY, V53, P10 TAKUMIDA M, 1988, ACTA OTO-LARYNGOL, V106, P226, DOI 10.3109/00016488809106430 TENCATE WJF, 1994, ORL J OTO-RHINO-LARY, V56, P257 TOMIYAMA S, 1986, LARYNGOSCOPE, V96, P685 TSIEN RY, 1985, CELL CALCIUM, V6, P145, DOI 10.1016/0143-4160(85)90041-7 WOLLHEIM CB, 1981, PHYSIOL REV, V61, P914 Wu DZ, 1998, PFLUG ARCH EUR J PHY, V436, P182, DOI 10.1007/s004240050621 YAMAKAWA K, 1938, P 42 M JAP OT SOC, P2310 NR 42 TC 1 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 43 EP 51 DI 10.1016/S0378-5955(01)00258-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900002 PM 11470184 ER PT J AU Gerken, GM Hesse, PS Wiorkowski, JJ AF Gerken, GM Hesse, PS Wiorkowski, JJ TI Auditory evoked responses in control subjects and in patients with problem-tinnitus SO HEARING RESEARCH LA English DT Article DE tinnitus; auditory brainstem response; middle latency response; hearing loss; elderly; evoked potential ID EVENT-RELATED POTENTIALS; MIDDLE LATENCY RESPONSE; NOISE-INDUCED TINNITUS; INFERIOR COLLICULUS; HEARING; CORTEX; ENHANCEMENT; ACTIVATION; EXPOSURE; NERVE AB Auditory brainstem responses (ABRs) and middle latency responses (MLRs) recorded from problem-tinnitus patients were compared with responses from normal hearing, hearing loss, and elderly subjects. Ten stimulus frequencies were presented in counterbalanced sequence and all frequencies were presented before any given frequency was presented again. The variables of importance were problem-tinnitus, hearing loss, subject age and stimulus frequency. Repeated measures analysis of variance showed a significant difference only in the latency of ABR wave 7. The intrinsically high variability in the problem-tinnitus and elderly groups rendered standard statistical analyses ineffective with the sample sizes used. Alternative analyses were employed in which the MLR waves of the normal hearing subjects were taken as the standard against which the other groups were compared. Very large MLR waves occurred in some, but not all, of the subjects in the problem-tinnitus and elderly groups. Different MLR waves were large in different subjects without correspondingly large ABR potentials. These results suggest: (1) selective alteration of MLR generators in different forms of tinnitus; and (2) differing effects of age on auditory physiology. Stimulus frequency and hearing loss contributed to this multivariate picture. Another variable, the average sound pressure level or the long-term acoustic environment, may also be important. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Texas, Callier Ctr Commun Disorders, Dallas, TX 75235 USA. Univ Texas, Program Math Sci, Richardson, TX 75083 USA. RP Gerken, GM (reprint author), Univ Texas, Callier Ctr Commun Disorders, 1966 Inwood Rd, Dallas, TX 75235 USA. CR Arnold W, 1996, ORL J OTO-RHINO-LARY, V58, P195 Attias J, 1996, AUDIOLOGY, V35, P259 Attias J, 1996, EAR HEARING, V17, P327, DOI 10.1097/00003446-199608000-00004 ATTIAS J, 1993, HEARING RES, V71, P106, DOI 10.1016/0378-5955(93)90026-W BARNEA G, 1990, AUDIOLOGY, V29, P36 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 CHAMBERS RD, 1991, HEARING RES, V51, P1, DOI 10.1016/0378-5955(91)90002-Q CHAMBERS RD, 1992, HEARING RES, V58, P123, DOI 10.1016/0378-5955(92)90122-4 CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O DEIBER MP, 1988, ELECTROEN CLIN NEURO, V71, P187, DOI 10.1016/0168-5597(88)90004-4 GERKEN G, 1986, BASIC APPL ASPECTS N, P195 Gerken GM, 1996, HEARING RES, V97, P75 Giraud AL, 1999, NEUROREPORT, V10, P1, DOI 10.1097/00001756-199901180-00001 HESSE PAS, 2000, THESIS U TEXAS DALLA HOKE M, 1991, ACTA OTOLARYNGOL S S, V491, P182 IKNER CL, 1990, EAR HEARING, V11, P16, DOI 10.1097/00003446-199002000-00005 Jacobson G P, 1997, Adv Otorhinolaryngol, V53, P46 JASTREBOFF PJ, 1993, BRIT J AUDIOL, V27, P7, DOI 10.3109/03005369309077884 JASTREBOFF PJ, 1990, NEUROSCI RES, V8, P221, DOI 10.1016/0168-0102(90)90031-9 Lockwood AH, 1998, NEUROLOGY, V50, P114 MAKELA JP, 1994, ELECTROEN CLIN NEURO, V92, P414, DOI 10.1016/0168-5597(94)90018-3 Melcher JR, 2000, J NEUROPHYSIOL, V83, P1058 Mirz F, 1999, HEARING RES, V134, P133, DOI 10.1016/S0378-5955(99)00075-1 MOLLER AR, 1992, LARYNGOSCOPE, V102, P1165 MOLLER AR, 1992, LARYNGOSCOPE, V102, P187 Muhlnickel W, 1998, P NATL ACAD SCI USA, V95, P10340, DOI 10.1073/pnas.95.17.10340 PENNER MJ, 1980, J SPEECH HEAR RES, V23, P779 PENNER MJ, 1989, J SPEECH HEAR RES, V32, P458 ROSENHALL U, 1995, SCAND AUDIOL, V24, P97, DOI 10.3109/01050399509047521 SALVI RJ, 1992, EFFECTS NOISE AUDITO, P156 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U Syka J, 2000, HEARING RES, V139, P59, DOI 10.1016/S0378-5955(99)00175-6 SYKA J, 1994, HEARING RES, V78, P158, DOI 10.1016/0378-5955(94)90021-3 NR 33 TC 25 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 52 EP 64 DI 10.1016/S0378-5955(01)00277-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900003 PM 11470185 ER PT J AU Tsuprun, V Santi, P AF Tsuprun, V Santi, P TI Proteoglycan arrays in the cochlear basement membrane SO HEARING RESEARCH LA English DT Article DE cochlea; basement membrane; immunohistochemistry; electron microscopy; proteoglycan ID HEPARAN-SULFATE PROTEOGLYCANS; EXTRACELLULAR-MATRIX; STRIA VASCULARIS; ANIONIC SITES; TECTORIAL MEMBRANE; IV COLLAGEN; INNER-EAR; ULTRASTRUCTURAL-LOCALIZATION; POSTNATAL-DEVELOPMENT; REISSNERS MEMBRANE AB Indirect immunofluorescence and transmission electron microscopy were used to investigate the composition and assembly of proteoglycans in the basement membranes of the spiral limbus, basilar membrane, spiral ligament, Reissner's membrane, myelinated nerve fibers, and blood capillaries of the spiral ligament and stria vascularis in the chinchilla cochlea. Four types of basement membrane components: laminin, entactin/nidogen, type IV collagen and heparan sulfate proteoglycans were immunolocalized in all basement membranes in association with heparan sulfate proteoglycans. beta 1 and alpha 1 integrin subunits were also detected along these basement membranes. The concentration of the basement membrane-associated proteins and integrin subunits differed according to the adjacent cell type. Electron microscopy showed that all basement membranes, with exception of those of stria vascularis, consist of two layers: lamina lucida and lamina densa. In the stria vascularis only a homogeneous lamina densa was observed. Cuprolinic blue treatment revealed heterogeneity in the ultrastructure and arrangement of proteoglycans in the cochlear basement membranes. Proteoglycans of the subepithelial basement membrane in the spiral limbus and spiral ligament formed quasi-regular, linear arrays within the lamina lucida, or were located at both sides of the lamina densa in the basilar membrane and Reissner's membrane. In the basement membranes of nerve fibers, and capillaries in the spiral ligament and stria vascularis, proteoglycans were scattered throughout these basement membranes, but showed different concentration and ultrastructural appearance, which may be related to different filtration and mechanical properties. In the basilar membrane, PGs were located above and below the lamina densa. An additional layer of PGs below the lamina densa may function as increased mechanical support of organ of Corti by its interaction with underlying fibrillar collagen layer. In the stria vascularis capillaries, PGs were stained considerably less with Cuprolinic blue and were scattered through the lamina densa of the basement membrane compared to capillaries of spiral ligament. This observation is compatible with a higher permeability of the strial capillaries. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Minnesota, Dept Otolaryngol, Minneapolis, MN 55455 USA. RP Tsuprun, V (reprint author), Univ Minnesota, Dept Otolaryngol, Lions Res Bldg,2001 6th St SE, Minneapolis, MN 55455 USA. CR AKIOKA K, 1990, J OTORHINOLARYNGOL S, V93, P1250 ARIMA T, 1985, ACTA OTO-LARYNGOL, V100, P194, DOI 10.3109/00016488509104781 BOSMAN FT, 1989, HISTOCHEM J, V21, P629, DOI 10.1007/BF01002481 Brakebusch C, 1997, J CELL SCI, V110, P2895 CAREY DJ, 1986, J CELL BIOL, V102, P2254, DOI 10.1083/jcb.102.6.2254 COLE G, 1997, PERSPECT DEV NEUROBI, V3, P359 Cosgrove D, 1996, HEARING RES, V97, P54 Cosgrove D, 1996, HEARING RES, V100, P21, DOI 10.1016/0378-5955(96)00114-1 Cosgrove D, 1997, HEARING RES, V105, P159, DOI 10.1016/S0378-5955(96)00203-1 Cosgrove D, 1998, HEARING RES, V121, P84, DOI 10.1016/S0378-5955(98)00069-0 ENGEL J, 1987, METHOD ENZYMOL, V145, P3 ENGEL J, 1992, BIOCHEMISTRY-US, V31, P10643, DOI 10.1021/bi00159a001 ENGVALL E, 1993, KIDNEY INT, V43, P2, DOI 10.1038/ki.1993.2 FARQUHAR M.G, 1991, CELL BIOL EXTRACELLU, P365 Fu SY, 1997, MOL NEUROBIOL, V14, P67, DOI 10.1007/BF02740621 FUJIWARA S, 1984, EUR J BIOCHEM, V143, P145, DOI 10.1111/j.1432-1033.1984.tb08353.x Galić M, 1989, Acta Otolaryngol Suppl, V461, P1 HAGEN SG, 1993, J BIOL CHEM, V268, P7261 Hayat M A, 1989, PRINCIPLES TECHNIQUE HYNES RO, 1992, CELL, V69, P11, DOI 10.1016/0092-8674(92)90115-S INOUE S, 1989, INT REV CYTOL, V117, P57, DOI 10.1016/S0074-7696(08)61334-0 ISHII K, 1992, EUR ARCH OTO-RHINO-L, V249, P224 Kalluri R, 2000, J BIOL CHEM, V275, P12719, DOI 10.1074/jbc.275.17.12719 Kashtan CE, 1999, MEDICINE, V78, P338, DOI 10.1097/00005792-199909000-00005 KATZ A, 1991, KIDNEY INT, V40, P643, DOI 10.1038/ki.1991.256 KUHN K, 1995, MATRIX BIOL, V14, P439, DOI 10.1016/0945-053X(95)90001-2 LAURIE GW, 1986, J MOL BIOL, V189, P205, DOI 10.1016/0022-2836(86)90391-8 McQueen CT, 1999, J LARYNGOL OTOL, V113, P13 MERCURIO AM, 1991, BIOESSAYS, V13, P469, DOI 10.1002/bies.950130907 MERKER HJ, 1994, MICROSC RES TECHNIQ, V28, P95, DOI 10.1002/jemt.1070280203 PAULSSON M, 1992, CRIT REV BIOCHEM MOL, V27, P93 Ruoslahti E., 1991, CELL BIOL EXTRACELLU, P343 Ryan MC, 1996, MATRIX BIOL, V15, P369, DOI 10.1016/S0945-053X(96)90157-2 SAKAGAMI M, 1987, ACTA OTO-LARYNGOL, V103, P189, DOI 10.3109/00016488709107783 Sakaguchi N, 1997, HEARING RES, V105, P44, DOI 10.1016/S0378-5955(96)00180-3 SANTI PA, 1986, HEARING RES, V24, P179, DOI 10.1016/0378-5955(86)90017-1 SANTI PA, 1990, J ELECTRON MICR TECH, V15, P293, DOI 10.1002/jemt.1060150308 SANTI PA, 1989, 2 INT S MEN DIS CAMB, P177 SATOH H, 1988, EUR ARCH OTO-RHINO-L, V255, P285 SCOTT JE, 1985, COLLAGEN REL RES, V5, P541 SONE M, 1995, HEARING RES, V83, P26, DOI 10.1016/0378-5955(94)00189-W Suzuki M, 1991, Acta Otolaryngol Suppl, V481, P112 Suzuki M, 1996, EUR ARCH OTO-RHINO-L, V253, P351 TAKAHASHI M, 1992, ANN OTO RHINOL LARYN, V101, P58 TAKUMIDA M, 1988, ARCH OTO-RHINO-LARYN, V245, P266, DOI 10.1007/BF00464628 Thomopoulos GN, 1997, HEARING RES, V111, P31, DOI 10.1016/S0378-5955(97)00080-4 TIMPL R, 1989, EUR J BIOCHEM, V180, P487, DOI 10.1111/j.1432-1033.1989.tb14673.x Timpl R, 1996, BIOESSAYS, V18, P123, DOI 10.1002/bies.950180208 Timpl R, 1994, EXS, V70, P123 TIMPL R, 1994, MATRIX BIOL, V14, P275, DOI 10.1016/0945-053X(94)90192-9 TOMODA K, 1988, ARCH OTO-RHINO-LARYN, V245, P307, DOI 10.1007/BF00464638 Tomoda K, 1992, Ann Otol Rhinol Laryngol Suppl, V157, P63 TORIHARA K, 1994, HEARING RES, V77, P69, DOI 10.1016/0378-5955(94)90253-4 TORIHARA K, 1995, J HISTOCHEM CYTOCHEM, V43, P299 Tryggvason K, 1993, CURR OPIN CELL BIOL, V5, P877, DOI 10.1016/0955-0674(93)90038-R Tsuprun V, 1999, HEARING RES, V129, P35, DOI 10.1016/S0378-5955(98)00219-6 Tsuprun V, 1997, HEARING RES, V110, P107, DOI 10.1016/S0378-5955(97)00068-3 Tsuprun V, 1996, MATRIX BIOL, V15, P31, DOI 10.1016/S0945-053X(96)90124-9 VANKUPPEVELT THMSM, 1994, MICROSC RES TECHNIQ, V28, P125, DOI 10.1002/jemt.1070280204 VANKUPPEVELT THMSM, 1984, HISTOCHEM J, V16, P657 Yamasoba T, 1996, HEARING RES, V102, P116, DOI 10.1016/S0378-5955(96)00159-1 YURCHENCO PD, 1986, J HISTOCHEM CYTOCHEM, V34, P93 YURCHENCO PD, 1994, METHOD ENZYMOL, V245, P489 YURCHENCO PD, 1990, FASEB J, V4, P1577 NR 64 TC 15 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 65 EP 76 DI 10.1016/S0378-5955(01)00278-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900004 PM 11470186 ER PT J AU Scholtz, AW Kammen-Jolly, K Felder, E Hussl, B Rask-Andersen, H Schrott-Fischer, A AF Scholtz, AW Kammen-Jolly, K Felder, E Hussl, B Rask-Andersen, H Schrott-Fischer, A TI Selective aspects of human pathology in high-tone hearing loss of the aging inner ear SO HEARING RESEARCH LA English DT Article DE high-tone hearing loss; aging; cochlea; human; ultrastructure; cuticular plate ID COCHLEAR HAIR CELL; MENIERES-DISEASE; ULTRASTRUCTURAL FINDINGS; ENDOLYMPHATIC HYDROPS; INFERIOR COLLICULUS; ELECTRON-MICROSCOPY; STRIA VASCULARIS; ACOUSTIC TRAUMA; AGED GERBILS; NERVE-FIBERS AB Accompanied with aging, the thresholds for high frequency sounds may elevate and result in a progressive hearing loss described as presbycusis. Based on correlations between audiometric measures of aged patients and histologic findings garnered from postmortem examinations, four types of presbycusis have been characterized: sensory-neural, neural, strial, and conductive [Schuknecht, H.F., Gacek, M.R., 1993. Ann. Otol. Rhinol. Laryngol. 102, 1-16]. Otopathologic changes to the inner ear as a direct function of age, however, remain controversial. The focus of this investigation involves the pathological impact on remaining sensory structures in patients having sensory-neural degeneration. The current study presents seven human temporal bones extracted from patients aged 53-67 years with high-tone hearing loss and with no known history of extraordinary environmental events involving head or noise trauma, acoustic overstimulation, or ototoxicity. In previously published findings of these specimens, all but one temporal bone failed to demonstrate a meaningful correlation between audiometric measurements and loss of functional hair cell populations with secondary retrograde degeneration of nerve fibers. Using the block surface method, electron microscopic micrographs demonstrate ultrastructural changes in the cuticular plate, stereocilia, pillar cells, stria vascularis, and the spiral ligament. In all pathological specimens, the greatest incidence of degeneration was seen at the cuticular plate. Conclusively, our findings present three implications in the aging human cochlea: firstly, audiometric measures that represent a high-tone hearing loss may take various forms with respect to ultrastructural patterns of degeneration and surviving structures; secondly, the incidence of lipofuscin and lysosome granules does not correlate with the degree of hearing loss and; thirdly, as shown only in guinea pigs [Anniko, M., 1988. Scanning Microsc. 2, 1035-1041], high-tone hearing loss can be associated with deformation of the cuticular plate. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Innsbruck, Dept Otolaryngol, A-6020 Innsbruck, Austria. Univ Uppsala Hosp, Dept Otolaryngol, S-75185 Uppsala, Sweden. RP Schrott-Fischer, A (reprint author), Univ Innsbruck, Dept Otolaryngol, Anichstr 35, A-6020 Innsbruck, Austria. EM annelies.schrott@uibk.ac.at CR ANNIKO M, 1988, SCANNING MICROSCOPY, V2, P1035 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 DAYAL VS, 1986, ANN OTO RHINOL LARYN, V95, P510 DULON D, 1992, AM J OTOL, V13, P108 ENGSTROM B, 1987, ACTA OTO-LARYNGOL, P110 Felder E, 1995, HEARING RES, V91, P19, DOI 10.1016/0378-5955(95)00158-1 FELIX H, 1992, ACTA OTO-LARYNGOL, V112, P284 GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 GLEESON M, 1987, ACTA OTO-LARYNGOL, P103 Gratton MA, 1997, HEARING RES, V114, P1, DOI 10.1016/S0378-5955(97)00025-7 HammPauler M, 1997, PROGRESS IN HUMAN AUDITORY AND VESTIBULAR HISTOPATHOLOGY, P63 HOUSLEY GD, 1995, ACTIVE HEARING, P221 Ingham NJ, 1999, ACTA OTO-LARYNGOL, V119, P42 ISHII K, 1994, EUR ARCH OTO-RHINO-L, V251, P357 JOHNSSON LG, 1990, ACTA OTO-LARYNGOL, P88 Kazee AM, 1999, HEARING RES, V133, P98, DOI 10.1016/S0378-5955(99)00058-1 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KIMURA RS, 1976, ANN OTO RHINOL LARYN, V85, P791 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 LIM DJ, 1971, ARCHIV OTOLARYNGOL, V94, P294 McFadden SL, 1998, HEARING RES, V117, P81, DOI 10.1016/S0378-5955(98)00013-6 Miller JM, 1998, SCAND AUDIOL, V27, P53 MIZUTA K, 1993, SCANNING MICROSCOPY, V7, P889 NADOL JB, 1995, ACTA OTO-LARYNGOL, P47 NADOL JB, 1987, ANN OTO RHINOL LARYN, V96, P449 NADOL JB, 1988, ACTA OTO-LARYNGOL, V105, P411, DOI 10.3109/00016488809119494 NADOL JB, 1979, OTOLARYNG HEAD NECK, V87, P818 NOMURA Y, 1979, ARCH OHREN NASEN KEH, V222, P181, DOI 10.1007/BF00456314 PAULER M, 1988, LARYNGOSCOPE, V98, P754 ROSEN S, 1970, ACTA OTO-LARYNGOL, V70, P242 SCHACHT J, 1995, ACTIVE HEARING, P209 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 SOUCEK S, 1987, ACTA OTO-LARYNGOL, P93 SPOENDLIN H, 1970, ULTRASTURCTURE PERIP, P1 SPOENDLIN H, 1987, ACTA OTO-LARYNGOL, P25 SUGA F, 1976, ANN OTO RHINOL LARYN, V85, P169 SUN JC, 1994, LARYNGOSCOPE, V104, P1251 Vasama JP, 1999, ACTA OTO-LARYNGOL, V119, P297 Willot J. F., 1991, AGING AUDITORY SYSTE WRIGHT A, 1987, ACTA OTO-LARYNGOL, P1 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 NR 43 TC 15 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 77 EP 86 DI 10.1016/S0378-5955(01)00279-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900005 PM 11470187 ER PT J AU Stenberg, AE Wang, H Fish, J Schrott-Fisher, A Sahlin, L Hultcrantz, M AF Stenberg, AE Wang, H Fish, J Schrott-Fisher, A Sahlin, L Hultcrantz, M TI Estrogen receptors in the normal adult and developing human inner ear and in Turner's syndrome SO HEARING RESEARCH LA English DT Article DE estrogen receptor; inner ear; human; fetus; hearing; Turner's syndrome; gender ID BRAIN-STEM RESPONSE; MESSENGER-RNA; BETA; RAT; EXPRESSION; MOUSE; WOMEN; ALPHA; AGE; SEX AB The influence of estrogens, the female sex hormone, on the ear and hearing is yet not fully investigated, though some studies have suggested that estrogens may influence hearing functions. The presence of estrogen receptors alpha and beta has earlier been shown in the inner ear of mice and rats. The aim of this study was to map possible estrogen receptors in the human inner ear. Inner ear tissue from human adults, aborted human normal fetuses and fetuses with Turner's syndrome were collected. Paraffin embedded sections of adult and fetal inner ears were immunostained with antibodies against estrogen receptors alpha and beta. Estrogen receptor alpha containing cells were found in the adult human inner ear only in the spiral ganglion, and estrogen receptor beta in the stria vascularis solely. The human fetal inner ear tissue from both normal and Turner fetuses showed a very weak staining of estrogen receptor alpha in the spiral ganglion cells, but no specific labeling of the Kolliker's organ of Corti at 13, 14 and 18 weeks of age. No staining of estrogen receptor beta was seen in the fetal inner ear. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. Karolinska Hosp, Dept Woman & Child Hlth, Div Reprod Endocrinol, S-17176 Stockholm, Sweden. Univ Clin, Dept Otolaryngol, Innsbruck, Austria. RP Hultcrantz, M (reprint author), Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. CR ANDREWS JC, 1992, ARCH OTOLARYNGOL, V118, P74 BARRENAS M, 2000, HEARING RES, V14, P21 COLEMAN JR, 1994, HEARING RES, V80, P209, DOI 10.1016/0378-5955(94)90112-0 Enmark E, 1997, J CLIN ENDOCR METAB, V82, P4258, DOI 10.1210/jc.82.12.4258 Erichsen S, 1996, ACTA OTO-LARYNGOL, V116, P721, DOI 10.3109/00016489609137913 Goldfien A, 1991, BASIC CLIN ENDOCRINO, P447 HORNER KC, 1991, HEARING RES, V52, P147, DOI 10.1016/0378-5955(91)90194-E HULTCRANTZ M, 1994, HEARING RES, V76, P127, DOI 10.1016/0378-5955(94)90094-9 JERGER J, 1980, ARCH OTOLARYNGOL, V106, P387 Jonsson R, 1998, SCAND AUDIOL, V27, P81, DOI 10.1080/010503998420324 Kuiper GGJM, 1998, FRONT NEUROENDOCRIN, V19, P253, DOI 10.1006/frne.1998.0170 KUMAGAMI H, 1994, ACTA OTO-LARYNGOL, V114, P48, DOI 10.3109/00016489409126015 LOSORDO DW, 1994, CIRCULATION, V89, P1501 Mosselman S, 1996, FEBS LETT, V392, P49, DOI 10.1016/0014-5793(96)00782-X Nathan CAO, 1999, ACTA OTO-LARYNGOL, V119, P853 Raab H, 1999, NEUROSCI LETT, V275, P21, DOI 10.1016/S0304-3940(99)00723-5 Stenberg AE, 1999, HEARING RES, V136, P29, DOI 10.1016/S0378-5955(99)00098-2 Stenberg AE, 1998, HEARING RES, V124, P85, DOI 10.1016/S0378-5955(98)00113-0 SWANSON SJ, 1988, J SPEECH HEAR RES, V31, P569 Taylor AH, 2000, J MOL ENDOCRINOL, V24, P145, DOI 10.1677/jme.0.0240145 TURNER RT, 1994, ENDOCR REV, V15, P275, DOI 10.1210/er.15.3.275 Wang H, 2001, MOL HUM REPROD, V7, P293, DOI 10.1093/molehr/7.3.293 WANG L, 2001, NEUROBIOLOGY, V98, P2792 WHARTON JA, 1990, AUDIOLOGY, V29, P196 NR 24 TC 58 Z9 61 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 87 EP 92 DI 10.1016/S0378-5955(01)00280-5 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900006 PM 11470188 ER PT J AU Keithley, EM Harris, B Desai, K Linthicum, F Fischel-Ghodsian, N AF Keithley, EM Harris, B Desai, K Linthicum, F Fischel-Ghodsian, N TI Mitochondrial cytochrome oxidase immunolabeling in aged human temporal bones SO HEARING RESEARCH LA English DT Article DE aging; mitochondrion; presbycusis; spiral ganglion neuron ID ALZHEIMERS-DISEASE; DNA DELETIONS; GRADED SERIES; RAT COCHLEAS; CELL COUNTS; BRAIN; IMPAIRMENT; MUTATIONS; MUSCLE AB Presbycusis, an age-related hearing loss, is accompanied by histopathological cochlear changes including variable amounts of degeneration of the auditory receptors, neurons and the stria vascularis. The causes of degeneration are unknown, although acoustic trauma and exposure to ototoxic agents are certainly contributors to the cellular degeneration. Acquired mitochondrial DNA defects are postulated as important determinants of aging in neuromuscular tissues. The cochlear neurons are highly metabolic and are, therefore, likely to be affected by mitochondrial DNA defects. Sequence analysis has demonstrated a significant number of acquired mutations in the cytochrome oxidase gene in the neurons from aged human cochleas. The current study used immunohistochemical labeling of cytochrome oxidase in the neuronal cell bodies in archival celloidin sections to evaluate relationships among label density, hearing loss, number of neurons and mitochondrial DNA changes within individual cochleas. Label density was less in many aged temporal bones, but not all. There was no relationship among any other variables. It is concluded that while there may be a decrease in the amount of cytochrome oxidase expression in aged spiral ganglion cell bodies, there are many other factors that contribute to hearing loss and cellular degeneration. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Diego, Dept Surg, Div Otolaryngol Head & Neck Surg, La Jolla, CA 92093 USA. House Ear Inst, Los Angeles, CA 90057 USA. Cedars Sinai Res Inst, Ctr Med Genet Birth Defects, Steven Spielberg Pediat Res Ctr, Ahmanson Dept Pediat, Los Angeles, CA 90048 USA. Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90048 USA. RP Keithley, EM (reprint author), Univ Calif San Diego, Dept Surg, Div Otolaryngol Head & Neck Surg, La Jolla, CA 92093 USA. CR Adams JC, 1997, HEARING RES, V104, P101, DOI 10.1016/S0378-5955(96)00184-0 Bonilla E, 1999, BBA-BIOENERGETICS, V1410, P171, DOI 10.1016/S0005-2728(98)00165-0 BOWLING AC, 1993, J NEUROCHEM, V60, P1964, DOI 10.1111/j.1471-4159.1993.tb13430.x Brierley EJ, 1998, ANN NEUROL, V43, P217, DOI 10.1002/ana.410430212 BYRNE E, 1991, MECH AGEING DEV, V60, P295, DOI 10.1016/0047-6374(91)90042-X CORRALDEBRINSKI M, 1992, NAT GENET, V2, P324, DOI 10.1038/ng1292-324 Cortopassi GA, 1999, BBA-BIOENERGETICS, V1410, P183, DOI 10.1016/S0005-2728(98)00166-2 DAVIS AC, 1989, INT J EPIDEMIOL, V18, P911, DOI 10.1093/ije/18.4.911 DAWSON DA, 1987, CURRENT ESTIMATES HL FischelGhodsian N, 1997, HEARING RES, V110, P147, DOI 10.1016/S0378-5955(97)00077-4 Gratton MA, 1997, HEARING RES, V114, P1, DOI 10.1016/S0378-5955(97)00025-7 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1995, ANN OTO RHINOL LARYN, V104, P858 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 Koehler CM, 1999, P NATL ACAD SCI USA, V96, P2141, DOI 10.1073/pnas.96.5.2141 MERCHANT SN, 2000, ARO ABSTR, V23, P29 MUTISYA EM, 1994, J NEUROCHEM, V63, P2179 Oshima T, 1996, LARYNGOSCOPE, V106, P43, DOI 10.1097/00005537-199601000-00009 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PARKER WD, 1995, NEUROLOGY, V45, P482 RYAN A F, 1991, Molecular and Cellular Neuroscience, V2, P179, DOI 10.1016/1044-7431(91)90011-C SCHEFFLER I, 1999, MITOCHONDRIA, P297 SCHUKNECHT HF, 1993, PATHOLOGY EAR, P416 Seidman MD, 1996, LARYNGOSCOPE, V106, P777, DOI 10.1097/00005537-199606000-00021 Tian Q, 1999, ANN OTO RHINOL LARYN, V108, P47 Tian LQ, 1998, FREE RADICAL BIO MED, V24, P1477, DOI 10.1016/S0891-5849(98)00025-2 WALLACE DC, 1992, SCIENCE, V256, P628, DOI 10.1126/science.1533953 Willott J. F., 1991, AGING AUDITORY SYSTE NR 28 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 93 EP 99 DI 10.1016/S0378-5955(01)00281-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900007 PM 11470189 ER PT J AU Henzl, MT O'Neal, J Killick, R Thalmann, I Thalmann, R AF Henzl, MT O'Neal, J Killick, R Thalmann, I Thalmann, R TI OCP1, an F-box protein, co-localizes with OCP2/SKP1 in the cochlear epithelial gap junction region SO HEARING RESEARCH LA English DT Article DE organ of Corti; gap junction; proteasome; F-box protein; ubiquitin; connexin ID UBIQUITIN-LIGASE COMPLEX; AMINO-ACID-SEQUENCES; CELL-CYCLE; SUBSTRATE RECOGNITION; GERBIL COCHLEA; RAT COCHLEA; SCF; ORGAN; CORTI; PROTEOLYSIS AB Immunohistochemical data indicate that OCP1 co-localizes exactly with OCP2 in the epithelial gap junction region or the guinea pig organ of Corti (OC). Despite the abundance of OCP1 in the OC, gaining access to its coding sequence - and, in particular, the 5' end of the coding sequence - proved unexpectedly challenging. The putative full-length OCP1 cDNA - 1180 nucleotides in length - includes a 67 nucleotide 5' leader sequence, 300 codons (including initiation and termination signals), and a 216 nucleotide 3' untranslated region. The cDNA encodes a protein having a predicted molecular weight of 33 700. The inferred amino acid sequence harbors an F-box motif spanning residues 52-91, consistent with a role for OCP1 and OCP2 in the proteasome-mediated degradation of select OC proteins. Although OCP1 displays extensive homology to an F-box protein recently cloned from rat brain (NFB42), clustered sequence non-identities indicate that the two proteins are transcribed from distinct genes. The presumptive human OCP1 gene was identified in the human genome databank. Located on chromosome 1p35. the inferred translation product exhibits 94% identity with the guinea pig OCP1 coding sequence. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Missouri, Dept Biochem, Columbia, MO 65211 USA. Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. Inst Psychiat, Dept Neurosci, London SE5 8AF, England. RP Henzl, MT (reprint author), Univ Missouri, Dept Biochem, Columbia, MO 65211 USA. CR Bai C, 1996, CELL, V86, P263, DOI 10.1016/S0092-8674(00)80098-7 Bochtler M, 1999, ANNU REV BIOPH BIOM, V28, P295, DOI 10.1146/annurev.biophys.28.1.295 Callis J, 2000, CURR OPIN PLANT BIOL, V3, P381, DOI 10.1016/S1369-5266(00)00100-X Cenciarelli C, 1999, CURR BIOL, V9, P1177, DOI 10.1016/S0960-9822(00)80020-2 CHEN H, 1995, GENOMICS, V27, P389, DOI 10.1006/geno.1995.1068 Connelly C, 1996, CELL, V86, P275, DOI 10.1016/S0092-8674(00)80099-9 DeMartino GN, 1999, J BIOL CHEM, V274, P22123, DOI 10.1074/jbc.274.32.22123 EDWARDS J, 2001, ANN MIDW RES M ASS R, V24, P150 Erhardt JA, 1998, J BIOL CHEM, V273, P35222, DOI 10.1074/jbc.273.52.35222 Fechner FP, 1998, J COMP NEUROL, V400, P299, DOI 10.1002/(SICI)1096-9861(19981026)400:3<299::AID-CNE1>3.0.CO;2-3 Galan JM, 1999, P NATL ACAD SCI USA, V96, P9124, DOI 10.1073/pnas.96.16.9124 Hapak RC, 1996, EXP CELL RES, V222, P234, DOI 10.1006/excr.1996.0029 Henzl MT, 1998, HEARING RES, V126, P37, DOI 10.1016/S0378-5955(98)00148-8 Jackson PK, 2000, TRENDS CELL BIOL, V10, P429, DOI 10.1016/S0962-8924(00)01834-1 Kamura T, 1999, GENE DEV, V13, P2928, DOI 10.1101/gad.13.22.2928 Kamura T, 1999, SCIENCE, V284, P657, DOI 10.1126/science.284.5414.657 Kelley PM, 2000, BRAIN RES REV, V32, P184, DOI 10.1016/S0165-0173(99)00080-6 Kelsell DP, 1997, NATURE, V387, P80, DOI 10.1038/387080a0 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 Kikuchi T, 2000, BRAIN RES REV, V32, P163, DOI 10.1016/S0165-0173(99)00076-4 King RW, 1996, SCIENCE, V274, P1652, DOI 10.1126/science.274.5293.1652 Kominami K, 1998, GENES CELLS, V3, P721, DOI 10.1046/j.1365-2443.1998.00225.x Krek W, 1998, CURR OPIN GENET DEV, V8, P36, DOI 10.1016/S0959-437X(98)80059-2 Lautermann J, 1998, CELL TISSUE RES, V294, P415, DOI 10.1007/s004410051192 Liang Y, 1997, GENE, V184, P163, DOI 10.1016/S0378-1119(96)00590-2 Lyapina SA, 1998, P NATL ACAD SCI USA, V95, P7451, DOI 10.1073/pnas.95.13.7451 Maniatis T, 1982, MOL CLONING LAB MANU Patton EE, 1998, GENE DEV, V12, P692, DOI 10.1101/gad.12.5.692 Peters JM, 1998, CURR OPIN CELL BIOL, V10, P759, DOI 10.1016/S0955-0674(98)80119-1 ROGERS S, 1986, SCIENCE, V234, P364, DOI 10.1126/science.2876518 Saffitz JE, 2000, CIRC RES, V86, P723 Skowyra D, 1999, SCIENCE, V284, P662, DOI 10.1126/science.284.5414.662 Skowyra D, 1997, CELL, V91, P209, DOI 10.1016/S0092-8674(00)80403-1 SPICER SS, 1994, HEARING RES, V79, P161, DOI 10.1016/0378-5955(94)90137-6 Steel KP, 1999, SCIENCE, V285, P1363, DOI 10.1126/science.285.5432.1363 Suzuki H, 2000, J BIOL CHEM, V275, P2877, DOI 10.1074/jbc.275.4.2877 THALMANN I, 1980, ARCH OTO-RHINO-LARYN, V226, P123, DOI 10.1007/BF00455126 THALMANN I, 1990, LARYNGOSCOPE, V100, P99 THALMANN I, 1993, HEARING RES, V64, P191, DOI 10.1016/0378-5955(93)90005-L THALMANN R, 1976, HDB AUDITORY VESTIBU, P359 Thalmann R, 1997, ACTA OTO-LARYNGOL, V117, P265, DOI 10.3109/00016489709117784 TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350 Tyers M, 1999, SCIENCE, V284, P601, DOI 10.1126/science.284.5414.601 Voges D, 1999, ANNU REV BIOCHEM, V68, P1015, DOI 10.1146/annurev.biochem.68.1.1015 WILCOX ER, 1992, HEARING RES, V62, P124, DOI 10.1016/0378-5955(92)90208-5 Winston JT, 1999, CURR BIOL, V9, P1180, DOI 10.1016/S0960-9822(00)80021-4 Wolf DA, 1999, CURR BIOL, V9, P373, DOI 10.1016/S0960-9822(99)80165-1 Yoho ER, 1997, HEARING RES, V104, P47, DOI 10.1016/S0378-5955(96)00183-9 Yu ZK, 1998, P NATL ACAD SCI USA, V95, P11324, DOI 10.1073/pnas.95.19.11324 Zhou PB, 1998, MOL CELL, V2, P571, DOI 10.1016/S1097-2765(00)80156-2 NR 50 TC 23 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 100 EP 111 DI 10.1016/S0378-5955(01)00285-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900008 PM 11470190 ER PT J AU Liu, GB Mark, RF AF Liu, GB Mark, RF TI Functional development of the inferior colliculus (IQ and its relationship with the auditory brainstem response (ABR) in the tammar wallaby (Macropus eugenii) SO HEARING RESEARCH LA English DT Article DE auditory brainstem response; tammar wallaby; inferior colliculus; development ID EVOKED-POTENTIALS; CENTRAL NUCLEUS; STEM RESPONSES; TONOTOPIC ORGANIZATION; NEURONAL ORGANIZATION; POSTNATAL MATURATION; DASYURUS-HALLUCATUS; COCHLEAR NUCLEUS; SPIRAL GANGLION; RHESUS-MONKEY AB To discover the developmental relationship between the auditory brainstem response (ABR) and the focal inferior colliculus (IC) response, 32 young tammar wallabies were used, by the application of simultaneous ABR and focal brainstem recordings, in response to acoustic clicks and tone bursts of seven frequencies. The ic or the tammar wallaby undergoes a rapid functional development from postnatal day (PND) 114 to 160. The earliest (PND 114) auditory evoked response was recorded from the rostral IC. With development, more caudal parts of the IC became functional until age about PND 127, when all parts of the IC were responsive to sound. Along a dorsoventral direction, the duration of the IC response decreased, the peak latency shortened, while the amplitude increased, reaching a maximum value at the central IC, then decreased. After PND 160, the best frequency (BF) of the ventral IC was the highest, with values between 12.5 and 16 kHz, the BF of the dorsal IC was the lowest, varying between 3.2 and 6.4 kHz, while the BF of the central IC was between 6.4 and 12.5 kHz. Between PND 114 and 125, the IC response did not have temporal correlation with the ABR. Between PND 140 and 160, only the early components of the responses from the ventral and central IC correlated with the P4 waves of the ABR. After PND 160, responses recorded from different depths of the IC had a temporal correlation with the ABR. (C) 2001 Published by Elsevier Science B.V. C1 Univ Queensland, Vis Touch & Hearing Res Ctr, St Lucia, Qld 4067, Australia. Australian Natl Univ, Res Sch Biol Sci, Dev Neurobiol Grp, Canberra, ACT 2601, Australia. RP Liu, GB (reprint author), Univ Queensland, Vis Touch & Hearing Res Ctr, St Lucia, Qld 4067, Australia. CR ACHOR LJ, 1980, ELECTROEN CLIN NEURO, V48, P174, DOI 10.1016/0013-4694(80)90302-8 ACHOR LJ, 1980, ELECTROEN CLIN NEURO, V48, P154, DOI 10.1016/0013-4694(80)90301-6 ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 AITKIN L, 1991, J COMP NEUROL, V309, P250, DOI 10.1002/cne.903090206 AITKIN L, 1986, AUDITORY MIDBRAIN, P1 AITKIN L, 1994, J COMP NEUROL, V343, P532, DOI 10.1002/cne.903430404 AITKIN L, 1995, HEARING RES, V82, P257, DOI 10.1016/0378-5955(94)00182-P AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1208 ALTMAN J, 1981, EXP BRAIN RES, V42, P411 ANNIKO M, 1983, ACTA OTO-LARYNGOL, V95, P263, DOI 10.3109/00016488309130943 ANNIKO M, 1983, ANAT EMBRYOL, V166, P355, DOI 10.1007/BF00305923 BRUGGE JF, 1978, J NEUROPHYSIOL, V41, P1557 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 CAIRD DM, 1987, ELECTROEN CLIN NEURO, V68, P237, DOI 10.1016/0168-5597(87)90034-7 ConeWesson BK, 1997, HEARING RES, V105, P119, DOI 10.1016/S0378-5955(96)00199-2 COOPER ML, 1981, J COMP NEUROL, V202, P309 EGGERMONT JJ, 1982, ANN NY ACAD SCI, V388, P471, DOI 10.1111/j.1749-6632.1982.tb50810.x EHRET G, 1992, DEV BRAIN RES, V67, P317, DOI 10.1016/0165-3806(92)90233-M EHRET G, 1994, EUR J NEUROSCI, V6, P1589, DOI 10.1111/j.1460-9568.1994.tb00549.x FULLERTON BC, 1990, HEARING RES, V49, P363, DOI 10.1016/0378-5955(90)90114-5 Geniec P, 1971, Acta Otolaryngol Suppl, V295, P1 HARRISON RV, 1984, SCAND AUDIOL, V13, P275, DOI 10.3109/01050398409042136 Kikuchi K, 1965, Acta Otolaryngol, V60, P207, DOI 10.3109/00016486509127003 Hill KG, 1998, HEARING RES, V117, P97, DOI 10.1016/S0378-5955(97)00211-6 HUANG C, 1986, EXP BRAIN RES, V61, P506 JEWETT DL, 1970, ELECTROEN CLIN NEURO, V28, P609, DOI 10.1016/0013-4694(70)90203-8 Larsell O, 1944, ARCHIV OTOLARYNGOL, V40, P233 LENOIR M, 1980, ANAT EMBRYOL, V160, P253, DOI 10.1007/BF00305106 LEV A, 1972, ARCH KLIN EXP OHR, V201, P79, DOI 10.1007/BF00341066 LIU GB, 1994, P 1 AS PAC C NEUR SI, P146 MARK RF, 1995, P AUST NEUROSCI SOC, V6, P190 Melcher JR, 1996, HEARING RES, V93, P28, DOI 10.1016/0378-5955(95)00179-4 MENINGER V, 1986, NEUROSCIENCE, V17, P1159 Mikaelian D, 1965, ACTA OTO-LARYNGOL, V59, P451, DOI DOI 10.3109/00016486509124579 MOLLER AR, 1986, ELECTROEN CLIN NEURO, V65, P361, DOI 10.1016/0168-5597(86)90015-8 MOLLER AR, 1982, EXP NEUROL, V78, P144, DOI 10.1016/0014-4886(82)90196-0 Moller AR, 1985, AUDITORY BRAINSTEM R, P13 MOLLER AR, 1982, ELECTROEN CLIN NEURO, V53, P612, DOI 10.1016/0013-4694(82)90137-7 MOORE DR, 1980, EXP BRAIN RES, V38, P103 MOORE DR, 1981, EXP BRAIN RES, V41, P301 MOORE DR, 1989, J NEUROSCI, V9, P1213 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 MOORE JK, 1987, HEARING RES, V29, P1, DOI 10.1016/0378-5955(87)90202-4 MOORE JK, 1987, HEARING RES, V29, P33, DOI 10.1016/0378-5955(87)90203-6 MOREST DK, 1964, ANAT REC, V148, P314 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 MOREST DK, 1966, ANAT REC, V154, P389 MOREST DK, 1969, Z ANAT ENTWICKLUNGS, V128, P290, DOI 10.1007/BF00522529 MULLERPREUSS P, 1984, HEARING RES, V16, P133, DOI 10.1016/0378-5955(84)90003-0 PERKINS RE, 1975, J COMP NEUROL, V163, P129, DOI 10.1002/cne.901630202 PIERSON M, 1994, BRAIN RES, V636, P55, DOI 10.1016/0006-8993(94)90175-9 POON PWF, 1990, EXP BRAIN RES, V79, P83 PUJOL R, 1970, J COMP NEUROL, V139, P115, DOI 10.1002/cne.901390108 ROCKEL AJ, 1973, J COMP NEUROL, V149, P301, DOI 10.1002/cne.901490303 ROCKEL AJ, 1973, J COMP NEUROL, V147, P11, DOI 10.1002/cne.901470103 Romand R., 1983, DEV AUDITORY VESTIBU, P47 ROMAND R, 1976, J COMP NEUROL, V170, P1, DOI 10.1002/cne.901700102 ROMAND R, 1982, J COMP NEUROL, V204, P1, DOI 10.1002/cne.902040102 ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 ROMAND R, 1990, DEV BRAIN RES, V54, P221, DOI 10.1016/0165-3806(90)90145-O ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 RUBEL EW, 1984, ANNU REV PHYSIOL, V46, P213 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEN RJ, 1967, ACTA OTOLARYNGOL S, V220, P5 RUBSAMEN R, 1992, J COMP PHYSIOL A, V170, P129 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SEMPLE MN, 1979, J NEUROPHYSIOL, V42, P1626 STIEBLER I, 1986, NEUROSCI LETT, V65, P336, DOI 10.1016/0304-3940(86)90285-5 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P352, DOI 10.1016/0013-4694(83)90261-4 WEBSTER WR, 1991, HEARING RES, V55, P70, DOI 10.1016/0378-5955(91)90093-O NR 71 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 112 EP 123 DI 10.1016/S0378-5955(01)00289-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900009 PM 11470191 ER PT J AU Dirckx, JJJ Decraemer, WF AF Dirckx, JJJ Decraemer, WF TI Effect of middle ear components on eardrum quasi-static deformation SO HEARING RESEARCH LA English DT Article DE tympanic membrane; middle ear; pressure; ossicle ID TYMPANIC MEMBRANE; DISPLACEMENT PATTERNS; VOLUME DISPLACEMENT; EUSTACHIAN-TUBE; PRESSURE; GERBIL; SHAPE AB Eardrum deformation induced by quasi-static middle ear pressure was studied at progressive stages of dissection of gerbil temporal bones. With our high resolution moire interferometer we recorded the shape and deformation of the eardrum along a line perpendicular to the manubrium and through the umbo, at different middle ear pressures. The deformation was measured from the medial side, after serially removing the cochlea, removing the stapes, cutting the tensor tympani. exposing the incudo-mallear joint, and cutting the anterior bony process which connects the malleus to the tympanic bone. The mean displacement as a function of pressure was also determined at all stages of dissection. Removing the cochlea and stapes, and cutting tensor tympani has no effect on static eardrum deformation. Exposing the incudo-mallear joint increases eardrum movement, and cutting the anterior bony connection between malleus and temporal bone strongly changes eardrum rest position and further increases its displacement. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Antwerp, RUCA, Lab Biomed Phys, B-2020 Antwerp, Belgium. RP Dirckx, JJJ (reprint author), Univ Antwerp, RUCA, Lab Biomed Phys, Groenenborgerlaan 171, B-2020 Antwerp, Belgium. CR BUCKINGH.RA, 1973, LARYNGOSCOPE, V83, P1585, DOI 10.1288/00005537-197310000-00002 Bylander A, 1985, ANN OTOL RHINOL LA S, V120, P33 DECRAEMER WF, 1980, J BIOMECH, V13, P559, DOI 10.1016/0021-9290(80)90056-1 Dirckx J J, 1997, J Biomed Opt, V2, P176, DOI 10.1117/12.268966 DIRCKX JJJ, 1992, HEARING RES, V62, P99, DOI 10.1016/0378-5955(92)90206-3 Dirckx JJJ, 1998, HEARING RES, V118, P35, DOI 10.1016/S0378-5955(98)00025-2 Dirckx JJJ, 2000, LASER MED SCI, V15, P131, DOI 10.1007/s101030050058 ELNER A, 1971, Acta Oto-Laryngologica, V72, P397, DOI 10.3109/00016487109122499 FELDING JU, 1995, ACTA OTO-LARYNGOL, V115, P408, DOI 10.3109/00016489509139339 FLISBERG K, 1961, ACTA OTOLARYNGOL S S, V182 Gaihede M, 1999, AUDIOL NEURO-OTOL, V4, P137, DOI 10.1159/000013832 GAIHEDE M, 1996, HEAR TRES, V2, P28 GRONTVED A, 1989, ACTA OTO-LARYNGOL, V108, P101, DOI 10.3109/00016488909107399 HERGILS L, 1985, ARCH OTOLARYNGOL, V111, P86 HERGILS LG, 1990, SCAND AUDIOL, V19, P183, DOI 10.3109/01050399009070770 KNIGHT LC, 1991, CLIN OTOLARYNGOL, V16, P543, DOI 10.1111/j.1365-2273.1991.tb00969.x LADAK HM, 1997, THESIS Lee CY, 2001, HEARING RES, V153, P146, DOI 10.1016/S0378-5955(00)00269-0 Rosowski JJ, 1999, AUDIOL NEURO-OTOL, V4, P129, DOI 10.1159/000013831 TAKAHASHI H, 1987, ARCH OTO-RHINO-LARYN, V243, P378, DOI 10.1007/BF00464646 Tideholm B, 1996, ACTA OTO-LARYNGOL, V116, P581, DOI 10.3109/00016489609137893 VONUNGE M, 1995, HEARING RES, V82, P184, DOI 10.1016/0378-5955(94)00017-K von Unge M, 1999, HEARING RES, V128, P1, DOI 10.1016/S0378-5955(98)00183-X Vorwerk U, 1999, AUDIOL NEURO-OTOL, V4, P150, DOI 10.1159/000013834 NR 24 TC 33 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 124 EP 137 DI 10.1016/S0378-5955(01)00290-8 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900010 PM 11470192 ER PT J AU Heffner, RS Koay, G Heffner, HE AF Heffner, RS Koay, G Heffner, HE TI Audiograms of five species of rodents: implications for the evolution of hearing and the perception of pitch SO HEARING RESEARCH LA English DT Article DE audiogram; evolution; frequency coding; groundhog; chipmunk; leaf-eared mouse; hamster; spiny mouse ID BAT ROUSETTUS-AEGYPTIACUS; SOUND LOCALIZATION; CUES; CHINCHILLAS; MECHANISMS; MAMMALS; NERVE; MAP; RAT; EAR AB Behavioral audiograms were determined for five species of rodents: groundhog (Marmota monax), Chipmunk (Tamias striatus), Darwin's leaf-cared mouse (Phyllotis darwinii), golden hamster (Mesocricetus auratus), and Egyptian spiny mouse (Acomys cahirinus). The high-frequency hearing of these animals was found to vary inversely with interaural distance, a typical mammalian pattern. With regard to low-frequency hearing, the animals fell into two groups: those with extended low-frequency hearing (chipmunks, groundhogs, and hamsters hear below 100 Hz) and those with restricted low-frequency hearing (spiny and leaf-eared mice do not hear appreciably below 1 kHz). An analysis of mammalian hearing reveals that the distribution of low-frequency hearing limits is bimodal with the two distributions separated by a gap from 125 to 500 Hz. The correspondence of this dichotomy with studies of temporal coding raises the possibility that mammals that do not hear below 500 Hz do not use temporal encoding for the perception of pitch. (C) 2001 Published by Elsevier Science B.V. C1 Univ Toledo, Dept Psychol, Toledo, OH 43606 USA. RP Heffner, HE (reprint author), Univ Toledo, Dept Psychol, Toledo, OH 43606 USA. CR BITTER KS, 2001, ARO ABSTR, V24, P63 BROWN AM, 1970, NATURE, V228, P576, DOI 10.1038/228576a0 Brown CH, 1994, COMP HEARING MAMMALS, P57 Butler RA, 1999, PERSPECT BIOL MED, V42, P157 BUTLER RA, 1975, HDB PHYSL AUDITORY S, V5, P247 FLANAGAN JL, 1960, J ACOUST SOC AM, V32, P1308, DOI 10.1121/1.1907900 Fleischer G., 1978, Advances in Anatomy Embryology and Cell Biology, V55, P1 FLOODY OR, 1979, AM ZOOL, V19, P443 Greenwood DD, 1996, HEARING RES, V94, P157, DOI 10.1016/0378-5955(95)00229-4 HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 Heffner H. E., 1998, COMP PSYCHOL HDB, P290 Heffner H. E., 1995, METHODS COMP PSYCHOA, P73 HEFFNER HE, 1994, HEARING RES, V73, P244, DOI 10.1016/0378-5955(94)90240-2 HEFFNER RS, 1992, HEARING RES, V62, P206, DOI 10.1016/0378-5955(92)90188-S HEFFNER RS, 1993, J COMP NEUROL, V331, P418, DOI 10.1002/cne.903310311 HEFFNER RS, 2000, J ACOUST SOC AM, V109, P412 Heffner RS, 1999, J COMP PSYCHOL, V113, P297, DOI 10.1037//0735-7036.113.3.297 HEFFNER RS, 1990, HEARING RES, V46, P239, DOI 10.1016/0378-5955(90)90005-A HEFFNER RS, 1995, HEARING RES, V88, P190, DOI 10.1016/0378-5955(95)00112-H Heffner RS, 1996, HEARING RES, V99, P13, DOI 10.1016/S0378-5955(96)00074-3 HEFFNER RS, 1985, J MAMMAL, V66, P745, DOI 10.2307/1380801 HEMILA S, 1995, HEARING RES, V85, P31, DOI 10.1016/0378-5955(95)00031-X Koay G, 1998, J COMP PSYCHOL, V112, P371, DOI 10.1037/0735-7036.112.4.371 Manley GA, 2000, P NATL ACAD SCI USA, V97, P11736, DOI 10.1073/pnas.97.22.11736 MARTIN GR, 1984, BEHAV PROCESS, V9, P205, DOI 10.1016/0376-6357(84)90041-X MASTERTO.B, 1969, J ACOUST SOC AM, V45, P966, DOI 10.1121/1.1911574 Moller A.R., 2000, HEARING Moore B. C. J., 1993, HUMAN PSYCHOPHYSICS, P56 Moore BCJ, 1997, INTRO PSYCHOL HEARIN Muller M, 1996, HEARING RES, V94, P148, DOI 10.1016/0378-5955(95)00230-8 MUSICANT AD, 1984, J ACOUST SOC AM, V75, P1195, DOI 10.1121/1.390770 NUMMELA S, 1999, THESIS U HELSINKI HE PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X Pepper J.W., 1991, P243 ROFFLER SK, 1968, J ACOUST SOC AM, V43, P1255, DOI 10.1121/1.1910976 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 ROSOWSKI JJ, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P615 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHAW EAC, 1974, HDB SENSORY PHYSL, V5, P450 Steinschneider M, 1998, J ACOUST SOC AM, V104, P2935, DOI 10.1121/1.423877 WEAVER EG, 1949, THEORY HEARING Wegel RL, 1924, PHYS REV, V23, P266, DOI 10.1103/PhysRev.23.266 WEST CD, 1985, J ACOUST SOC AM, V77, P1091, DOI 10.1121/1.392227 WOTTON JM, 1995, J ACOUST SOC AM, V98, P1423, DOI 10.1121/1.413410 NR 44 TC 56 Z9 56 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2001 VL 157 IS 1-2 BP 138 EP 152 DI 10.1016/S0378-5955(01)00298-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 456TT UT WOS:000170098900011 PM 11470193 ER PT J AU Simon, P Decaestecker, C Choufani, G Delbrouck, C Danguy, A Salmon, I Zick, Y Kaltner, H Hassid, S Gabius, HJ Kiss, R Darro, F AF Simon, P Decaestecker, C Choufani, G Delbrouck, C Danguy, A Salmon, I Zick, Y Kaltner, H Hassid, S Gabius, HJ Kiss, R Darro, F TI The levels of retinoid RAR beta receptors correlate with galectin-1,-3 and-8 expression in human cholesteatomas SO HEARING RESEARCH LA English DT Article DE cholesteatoma; recurrence; apoptosis; galectin; retinoic acid receptor ID MIDDLE-EAR CHOLESTEATOMA; NORMAL HUMAN SKIN; ANIMAL LECTINS; CELL-ADHESION; EMBRYONAL CARCINOMA; BINDING; DIFFERENTIATION; ACID; KERATINOCYTES; PROLIFERATION AB Cholesteatoma is a benign disease characterized by the presence of an unrestrained growth and the accumulation of keratin debris in the middle ear cavity. This often recurs, even when surgical resection is thought to be complete. In a previous study we showed that cholesteatomas with the highest apoptotic indices recurred more rapidly and also exhibited a high level of p53 immunopositive cells. In view of their relevance to the characterization of the cell differentiation status, the present study focuses on the expression of retinoid acid receptors (RARs) and galectins in human cholesteatomas. Retinoids control the differentiation processes in keratinocytes while galectins play strikingly modulatory roles at apoptosis and cell adhesion levels in a wide variety of tissue (embryonic, normal and neoplastic). To clarify the expression of these two protein families in human cholesteatomas we examined and quantified the levels of immunohistochemical expression of RAR alpha, beta and gamma, and also galectin-1, -3 and -8 in a series of 70 human cholesteatomas. Our data show clearly that predominantly RAR beta and galectin-1 were expressed. The RAR gamma concentration was significantly lower than that of the RAR alpha; this was also observed for the galectin-8 concentration in comparison with the galectin-3 one. Furthermore, the level of RAR beta expression correlated highly (P = 0.00001) with the level of galectin-8 expression, which also correlated significantly with the level of RAR alpha and RAR gamma expression. In addition, this parameter also correlated with the level of galectin-1 and galectin-3 expression. These data suggest that cholesteatomas may originate in an undifferentiated population of keratinocytes, and that a relation may exist between retinoid activity and galectins. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Free Univ Brussels, Fac Med, Lab Histopathol, B-1070 Brussels, Belgium. Hop Erasme, Clin Unv Bruxelles, Dept Otolaryngol Head & Neck Surg, Brussels, Belgium. Hop Erasme, Clin Unv Bruxelles, Dept Pathol, Brussels, Belgium. Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel. Univ Munich, Inst Physiol Chem, Munich, Germany. Lab Louis Lafon, Maisons Alfort, France. RP Kiss, R (reprint author), Free Univ Brussels, Fac Med, Lab Histopathol, 808 Route Lennik, B-1070 Brussels, Belgium. CR AGRWAL N, 1993, J BIOL CHEM, V268, P14932 AKIMOTO Y, 1992, EXP CELL RES, V199, P297, DOI 10.1016/0014-4827(92)90438-E AKIMOTO Y, 1995, CELL TISSUE RES, V280, P1 Albino AP, 1998, AM J OTOL, V19, P30 BARDOSI A, 1989, J HISTOCHEM CYTOCHEM, V37, P989 BARONDES SH, 1994, J BIOL CHEM, V269, P20807 Bernerd F, 1999, P NATL ACAD SCI USA, V96, P11329, DOI 10.1073/pnas.96.20.11329 Choufani G, 1999, LARYNGOSCOPE, V109, P1825, DOI 10.1097/00005537-199911000-00019 Choufani G, 1999, CANCER, V86, P2353, DOI 10.1002/(SICI)1097-0142(19991201)86:11<2353::AID-CNCR25>3.0.CO;2-A Fisher GJ, 1996, FASEB J, V10, P1002 Fisher GJ, 1998, J INVEST DERMATOL, V110, P297, DOI 10.1046/j.1523-1747.1998.00112.x GABIUS HJ, 1986, CANCER J, V1, P19 GABIUS HJ, 1990, ANAL BIOCHEM, V189, P91, DOI 10.1016/0003-2697(90)90050-J Gabius HJ, 2000, NATURWISSENSCHAFTEN, V87, P108, DOI 10.1007/s001140050687 Gabius HJ, 1997, EUR J BIOCHEM, V243, P543, DOI 10.1111/j.1432-1033.1997.t01-1-00543.x GABIUS S, 1990, ANTICANCER RES, V10, P1005 Haake AR, 1997, EXP CELL RES, V231, P83, DOI 10.1006/excr.1996.3441 Hadari YR, 1997, TRENDS GLYCOSCI GLYC, V9, P103 Hadari YR, 2000, J CELL SCI, V113, P2385 Kaltner H, 1998, ACTA ANAT, V161, P162 Kaltner H, 1997, HISTOL HISTOPATHOL, V12, P945 Kojima H, 1998, ARCH OTOLARYNGOL, V124, P261 Kopitz J, 1998, J BIOL CHEM, V273, P11205, DOI 10.1074/jbc.273.18.11205 LOTAN R, 1989, CANCER RES, V49, P1261 Lu Y, 2000, BBA-GENE STRUCT EXPR, V1491, P13, DOI 10.1016/S0167-4781(00)00055-5 Lu Y, 1998, BIOL CHEM, V379, P1323, DOI 10.1515/bchm.1998.379.11.1323 Magnaldo T, 1998, DIFFERENTIATION, V63, P159, DOI 10.1046/j.1432-0436.1998.6330159.x Magnan A, 1995, ANAE, V7, P168 Perillo NL, 1998, J MOL MED, V76, P402, DOI 10.1007/s001090050232 Rabinovich GA, 1999, CELL DEATH DIFFER, V6, P711, DOI 10.1038/sj.cdd.4400535 Reichrath J, 1997, HISTOCHEM J, V29, P127, DOI 10.1023/A:1026481205135 SHINODA H, 1995, LARYNGOSCOPE, V105, P1232, DOI 10.1288/00005537-199511000-00018 Siebert HC, 1997, EUR J BIOCHEM, V249, P27, DOI 10.1111/j.1432-1033.1997.00027.x SPANDAU DF, 1994, ONCOGENE, V9, P1861 WOLLENBERG A, 1993, J EXP MED, V178, P777, DOI 10.1084/jem.178.3.777 NR 35 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 1 EP 9 DI 10.1016/S0378-5955(01)00230-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900001 PM 11377877 ER PT J AU Bobbin, RP AF Bobbin, RP TI PPADS, an ATP antagonist, attenuates the effects of a moderately intense sound on cochlear mechanics SO HEARING RESEARCH LA English DT Article DE pyridoxal-phosphate-6-azophenyl-2 ',4 '-disulphonic acid; distortion product; intense tone; noise; ototoxicity ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; PHARMACOLOGICAL EVIDENCE; DISTORTION PRODUCTS; THRESHOLD SHIFT; ACOUSTIC INJURY; INNER-EAR; RECEPTOR; NOISE; TRANSMISSION AB Increasing attention is being given to the role of neurotransmitters and other signaling substances in the damage induced by intense sound to the cochlea. Adenosine triphosphate (ATP) is one example of a putative neurotransmitter that may alter cochlear mechanics during sound exposure. The purpose of the present study was to test the hypothesis that endogenous extracellular ATP has a role in the generation of the changes in cochlear mechanics induced by moderate intense sound exposure. Guinea pigs were exposed to either: (1) a perilymphatic administration of pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 1 mM), an ATP antagonist; (2) a moderately intense sound (6 kHz tone, 95 dB SPL, 15 min); or (3) a combination of the PPADS and the sound. The effects on the cubic distortion product otoacoustic emissions (DPOAEs; 2f(1)-f(2)) were monitored using three sets of equal level primaries (f(1) = 9.25 kHz, f(2) = 10.8 kHz, 2f(1)-f(2) = 7.7 kHz; f(1) = 7.2 kHz, f(2) = 8.4 kHz, 2f(1)-f(2) = 6 kHz; f(1) = 5.55 kHz, f(2) = 6.5 kHz, 2f(1)-f(2) = 4.6 kHz). PPADS alone had no effect on the cubic DPOAEs monitored. The intense sound alone suppressed all three cubic DPOAEs. The combination of PPADS with the intense sound induced a suppression of the cubic DPOAEs that was equal to or greater than induced by the intense sound alone at f(2) = 10.8 kHz but was equal to or less than induced by the intense sound at f(2) = 8.4 and 6.5 kHz. After washing the PPADS out of the cochlea with artificial perilymph, all three cubic DPOAEs were suppressed less in the PPADS with intense sound treatment group than in the intense sound alone group. The PPADS appeared to provide protection from the intense sound. Results are consistent with the hypothesis that extracellular ATP is involved in the changes in cochlear mechanics induced by moderately intense sound exposure. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Louisiana State Univ, Med Ctr, Dept Otohinolaryngol & Biocommun, Kresge Hearing Res Lab, New Orleans, LA 70112 USA. RP Bobbin, RP (reprint author), Louisiana State Univ, Med Ctr, Dept Otohinolaryngol & Biocommun, Kresge Hearing Res Lab, 533 Bolivar St,5th Floor, New Orleans, LA 70112 USA. EM rbobbi@lsuhsc.edu CR Altschuler R. A., 1999, COCHLEAR PHARM NOISE, P98 BOBBIN RP, 2000, HAIR CELL MICROMECHA, P129 Bobbin RP, 1997, HEARING RES, V113, P155, DOI 10.1016/S0378-5955(97)00140-8 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 2000, GENETICS HEARING LOS, P87 BOBBIN RP, 1998, RECENT ADV BASIC CLI, P61 BOBBIN RP, 1996, HAIR CELLS HEARING A, P29 BOBBIN RP, 1992, NOISE INDUCED HEARIN Charlton SJ, 1996, BRIT J PHARMACOL, V118, P704 Chen C, 2000, J NEUROPHYSIOL, V83, P1502 Chen C, 1998, BRIT J PHARMACOL, V124, P337, DOI 10.1038/sj.bjp.0701848 CHEN C, 1995, HEARING RES, V88, P215, DOI 10.1016/0378-5955(95)00115-K Chen C, 1998, HEARING RES, V118, P47, DOI 10.1016/S0378-5955(98)00019-7 DEATHERAGE BH, 1959, J ACOUST SOC AM, V31, P479, DOI 10.1121/1.1907739 Fechner FP, 1998, J COMP NEUROL, V400, P299, DOI 10.1002/(SICI)1096-9861(19981026)400:3<299::AID-CNE1>3.0.CO;2-3 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 Housley GD, 1998, MOL NEUROBIOL, V16, P21, DOI 10.1007/BF02740601 Housley GD, 1999, J NEUROSCI, V19, P8377 Keithley EM, 1998, NEUROREPORT, V9, P2183, DOI 10.1097/00001756-199807130-00007 Kemp DT, 1998, OTOACOUSTIC EMISSION, P1 KUJAWA SG, 1992, HEARING RES, V64, P73, DOI 10.1016/0378-5955(92)90169-N KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 LeBlanc C, 1999, HEARING RES, V138, P192, DOI 10.1016/S0378-5955(99)00164-1 Liberman MC, 1999, SING AUDIOL TEXTBK, P1 LIM DJ, 1971, ARCHIV OTOLARYNGOL, V94, P294 MILLS DM, 1998, OTOACOUSTIC EMISSION, P85 Nordmann AS, 2000, HEARING RES, V139, P13, DOI 10.1016/S0378-5955(99)00163-X Parker MS, 1998, HEARING RES, V121, P62, DOI 10.1016/S0378-5955(98)00065-3 Puel JL, 1998, NEUROREPORT, V9, P2109, DOI 10.1097/00001756-199806220-00037 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1995, ACTA ACUST, V3, P75 Puel JL, 1995, PROG NEUROBIOL, V47, P449, DOI 10.1016/0301-0082(95)00028-3 Ruel J, 1999, J PHYSIOL-LONDON, V518, P667, DOI 10.1111/j.1469-7793.1999.0667p.x Ruel J, 2000, NEUROPHARMACOLOGY, V39, P1959, DOI 10.1016/S0028-3908(00)00069-1 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 Skellett RA, 1997, HEARING RES, V111, P42, DOI 10.1016/S0378-5955(97)00093-2 SLEPECKY N, 1986, HEARING RES, V22, P307, DOI 10.1016/0378-5955(86)90107-3 WATSON GM, 2000, HAIR CELL MICROMECHA, P27 Yoshida N, 1999, J NEUROSCI, V19, P10116 ZIGANSHIN AU, 1995, PFLUG ARCH EUR J PHY, V429, P412, DOI 10.1007/BF00374157 NR 41 TC 5 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 10 EP 16 DI 10.1016/S0378-5955(01)00261-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900002 PM 11377878 ER PT J AU Pace, AJ Madden, VJ Henson, OW Koller, BH Henson, MM AF Pace, AJ Madden, VJ Henson, OW Koller, BH Henson, MM TI Ultrastructure of the inner ear of NKCC1-deficient mice SO HEARING RESEARCH LA English DT Article DE NKCC1; ion transport; Reissner's membrane; inner ear; knockout mouse ID K-CL COTRANSPORTER; ION-TRANSPORT MECHANISMS; BETA-SUBUNIT ISOFORMS; STRIA-VASCULARIS; GERBIL COCHLEA; MARGINAL CELLS; GUINEA-PIG; ALPHA-SUBUNIT; RAT COCHLEA; NA-K-2CL COTRANSPORTER AB The transduction of the auditory signal is dependent on the flow of ions within the inner ear. We have generated mice deficient in NKCC1, an ion cotransporter that is thought to be involved in the secretion of K+ by the strial marginal cells. Inner ear histology revealed partial to almost total absence of the scala media and collapse of Reissner's membrane. Ultrastructural analysis showed that Reissner's membrane consists of 3-4 cell layers instead of the usual two, and a substance of unknown composition is present between Reissner's membrane and underlying structures. Within the tunnel of Corti, hair cells and supporting cells were difficult to identify. The location of the tectorial membrane was altered, and a precipitate was observed surrounding it. Severe structural defects were noted in the interdental cells and Boettcher cells, and mild defects were observed in the stria vascularis and in type II and type IV fibrocytes. The finding that major defects occur predominantly in cells that are not known to express NKCC1 suggests that loss of NKCC1 results in functional defects in cells expressing NKCC1 and a morphological effect on cell populations downstream in the proposed K+ recycling pathway. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ N Carolina, Div Otolaryngol Head & Neck Surg, Chapel Hill, NC 27599 USA. RP Henson, MM (reprint author), Univ N Carolina, Div Otolaryngol Head & Neck Surg, Chapel Hill, NC 27599 USA. CR BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P40, DOI 10.3109/00016488009131696 Crouch JJ, 1997, J HISTOCHEM CYTOCHEM, V45, P773 Delpire E, 1999, NAT GENET, V22, P192, DOI 10.1038/9713 Dixon MJ, 1999, HUM MOL GENET, V8, P1579, DOI 10.1093/hmg/8.8.1579 DUVALL AJ, 1970, BIOCH MECH HEARING D, P149 Evans RL, 2000, J BIOL CHEM, V275, P26720 Flagella M, 1999, J BIOL CHEM, V274, P26946, DOI 10.1074/jbc.274.38.26946 FORGE A, 1976, CLIN OTOLARYNGOL, V1, P211, DOI 10.1111/j.1365-2273.1976.tb00879.x Goto S, 1997, BRAIN RES, V765, P324, DOI 10.1016/S0006-8993(97)00679-3 Grubb BR, 2000, AM J PHYSIOL-GASTR L, V279, pG707 Haas M, 2000, ANNU REV PHYSIOL, V62, P515, DOI 10.1146/annurev.physiol.62.1.515 HENSON MM, 1982, HEARING RES, V7, P91, DOI 10.1016/0378-5955(82)90083-1 Hidaka H, 1996, BIOCHEM BIOPH RES CO, V220, P425, DOI 10.1006/bbrc.1996.0421 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 Ishii T, 1966, Acta Otolaryngol, V62, P185, DOI 10.3109/00016486609119563 ISHIYAMA E, 1970, ANN OTO RHINOL LARYN, V79, P54 IURATO S, 1976, ACTA OTO-LARYNGOL, V82, P57, DOI 10.3109/00016487609120863 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 Kikuchi T, 2000, BRAIN RES REV, V32, P163, DOI 10.1016/S0165-0173(99)00076-4 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 KUSAKARI J, 1978, ACTA OTO-LARYNGOL, V86, P336, DOI 10.3109/00016487809107512 Madden VJ, 1997, HEARING RES, V111, P76, DOI 10.1016/S0378-5955(97)00107-X MARCUS DC, 1981, HEARING RES, V4, P149, DOI 10.1016/0378-5955(81)90002-2 MARCUS DC, 1994, J GEN PHYSIOL, V104, pA16 MCGUIRT JP, 1994, J HISTOCHEM CYTOCHEM, V42, P843 MIZUTA K, 1995, HEARING RES, V88, P199, DOI 10.1016/0378-5955(95)00113-I Mizuta K, 1997, HEARING RES, V106, P154, DOI 10.1016/S0378-5955(97)00010-5 MORI N, 1993, EUR ARCH OTO-RHINO-L, V250, P186 NADOL JB, 1978, ANN OTO RHINOL LARYN, V87, P70 NAKAZAWA K, 1995, J HISTOCHEM CYTOCHEM, V43, P981 Pace AJ, 2000, J CLIN INVEST, V105, P441, DOI 10.1172/JCI8553 PIKE DA, 1980, HEARING RES, V3, P79, DOI 10.1016/0378-5955(80)90009-X QVORTRUP K, 1990, CELL TISSUE RES, V261, P287, DOI 10.1007/BF00318670 QVORTRUP K, 1990, EUR ARCH OTO-RHINO-L, V248, P57, DOI 10.1007/BF00634783 RAMPRASHAD F, 1983, ANAT REC, V207, P653, DOI 10.1002/ar.1092070414 Russell J. M., 2000, PHYSIOL REV, V80, P212 RUSSELL LD, 1978, TISSUE CELL, V9, P99 RYBAK LP, 1986, ACTA OTO-LARYNGOL, V101, P59, DOI 10.3109/00016488609108608 Sakaguchi N, 1998, HEARING RES, V118, P114, DOI 10.1016/S0378-5955(98)00022-7 SANTI PA, 1983, HEARING RES, V12, P151, DOI 10.1016/0378-5955(83)90103-X SANTI PA, 1979, ACTA OTO-LARYNGOL, V88, P1, DOI 10.3109/00016487909137133 SANTOS-SACCHI J, 1983, HEARING RES, V9, P317, DOI 10.1016/0378-5955(83)90034-5 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 SELLICK P M, 1975, Progress in Neurobiology (Oxford), V5, P337, DOI 10.1016/0301-0082(75)90015-5 SHER AE, 1971, ACTA OTOLARYNGOL S, V285, P5 SHINDO M, 1992, JPN J PHYSIOL, V42, P617, DOI 10.2170/jjphysiol.42.617 Slepecky N. B., 1996, COCHLEA, P44 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 Spicer SA, 2000, HEARING RES, V143, P147, DOI 10.1016/S0378-5955(00)00037-X SPICER SS, 1994, HEARING RES, V79, P161, DOI 10.1016/0378-5955(94)90137-6 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z Spicer SS, 1998, HEARING RES, V118, P1, DOI 10.1016/S0378-5955(98)00006-9 Spicer SS, 1997, ANAT REC, V249, P117 Suko T, 2000, HEARING RES, V140, P137, DOI 10.1016/S0378-5955(99)00191-4 SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 Takeuchi S, 1997, HEARING RES, V113, P99, DOI 10.1016/S0378-5955(97)00134-2 TAKEUCHI S, 1995, HEARING RES, V83, P89, DOI 10.1016/0378-5955(94)00191-R TENCATE WJF, 1994, HEARING RES, V75, P151 TRANBAHUY P, 1989, MENIERES DIS PATHOGE, P241 Vetter DE, 1996, NEURON, V17, P1251, DOI 10.1016/S0896-6273(00)80255-X WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 Yeh TH, 1998, AM J PHYSIOL-CELL PH, V274, pC566 ZWISLOCKI JJ, 1992, HEARING RES, V57, P175, DOI 10.1016/0378-5955(92)90150-L NR 72 TC 25 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 17 EP 30 DI 10.1016/S0378-5955(01)00263-5 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900003 PM 11377879 ER PT J AU Vazquez, AE Luebke, AE Martin, GK Lonsbury-Martin, BL AF Vazquez, AE Luebke, AE Martin, GK Lonsbury-Martin, BL TI Temporary and permanent noise-induced changes in distortion product otoacoustic emissions in CBA/CaJ mice SO HEARING RESEARCH LA English DT Article DE noise damage; cochlea; distortion product otoacoustic emission; mouse; acetylcholinesterase; efferent innervation ID INDUCED HEARING-LOSS; AGE-RELATED LOSS; ACOUSTIC INJURY; THRESHOLD SHIFT; MOUSE COCHLEA; EXPOSURE; EAR; PROTECTION; TRAUMA; EFFERENT AB A number of studies have shown that the ear can be protected from sound over-exposure, either by activating the cochlear efferent system, or by sound 'conditioning' in which the role of the efferent system is less certain. To study more definitively the molecular basis of deliberately induced cochlear protection from excessive sounds, it is advantageous to determine, for an inbred mouse strain, a range of noise exposure parameters that effectively alter cochlear function. As an initial step towards this goal, young CBA/CaJ mice were exposed to a 105-dB SPL octave-band noise (OBN), centered at 10 kHz, for Various lengths of time consisting of 10 min, or 0.5, 1, 3, or 6 h. Distortion product otoacoustic emissions (DPOAEs) at the 2f(1)-f(2) frequency, in response to equilevel primary tones of low to moderate levels, were used to quantify the damaging effects of these sound over-exposures on cochlear function. In addition, staining for acetylcholinesterase (AChE) activity to assess for noise-induced changes in the pattern of efferent-nerve innervation to the cochlea was also performed in a subset of mice that were exposed to the longest-lasting 6-h OBN. The 10-min OBN resulted in only temporary reductions in DPOAE levels, which recovered to pre-exposure Values within 5 days. Increasing the exposure to 0.5 h resulted in permanent DPOAE losses that, for low primary-tone levels: were still present at 31 days post-exposure. Additionally, the l-h and longer exposures caused permanent reductions in DPOAEs for all test levels, which were measurable at 31 days following exposure. Light-microscopic observations restricted to the 11-18-kHz frequency region of the organ of Corti, for a subset of mice exposed to the 6-h OBN, uncovered a significant loss of outer hair cells (OHCs). However: despite the OHC loss in this region, the AChE activity associated with the related pattern of efferent innervation remained largely intact. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Miami, Dept Otolaryngol, Miami, FL 33101 USA. Univ Miami, Sch Med, Neurosci Program, Miami, FL 33152 USA. RP Vazquez, AE (reprint author), Univ Miami, Dept Otolaryngol, M805,POB 016960, Miami, FL 33101 USA. CR BOHNE BA, 1972, LARYNGOSCOPE, V82, P1 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 CODY AR, 1982, HEARING RES, V6, P199, DOI 10.1016/0378-5955(82)90054-5 Davis RR, 1999, HEARING RES, V134, P9, DOI 10.1016/S0378-5955(99)00060-X EHRET G, 1974, NATURWISSENSCHAFTEN, V61, P506 FOWLER T, 1995, HEARING RES, V88, P1, DOI 10.1016/0378-5955(95)00062-9 FRANKLIN DJ, 1991, HEARING RES, V58, P57 HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 HENRY KR, 1982, HEARING RES, V8, P285, DOI 10.1016/0378-5955(82)90020-X Jimenez AM, 1999, HEARING RES, V138, P91, DOI 10.1016/S0378-5955(99)00154-9 JIMENEZ AM, 2001, IN PRESS J ASS RES O JIMENEZ AM, 1999, ASS RES OTOLARYNGOL, V22, P96 KARNOVSKY MJ, 1964, J HISTOCHEM CYTOCHEM, V12, P219 KOKKOCUNNINGHAM A, 1976, ACTA OTO-LARYNGOL, V81, P48, DOI 10.3109/00016487609107476 Kujawa SG, 1997, J NEUROPHYSIOL, V78, P3095 Li H S, 1992, Scand Audiol Suppl, V36, P1 LI HS, 1993, AUDIOLOGY, V32, P195 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 LUEBKE AE, 2000, ASS RES OTOLARYNGOL, V23, P282 Maison SF, 2000, J NEUROSCI, V20, P4701 MIYAKITA T, 1992, HEARING RES, V60, P149, DOI 10.1016/0378-5955(92)90017-H Nordmann AS, 2000, HEARING RES, V139, P13, DOI 10.1016/S0378-5955(99)00163-X Ou HC, 2000, HEARING RES, V145, P111, DOI 10.1016/S0378-5955(00)00081-2 Ou HC, 2000, HEARING RES, V145, P123, DOI 10.1016/S0378-5955(00)00082-4 Pukkila M, 1997, Acta Otolaryngol Suppl, V529, P59 Puria S, 1996, J ACOUST SOC AM, V99, P500, DOI 10.1121/1.414508 ROSSI G, 1965, ACTA OTOLARYNGOL, V61, P488 RYAN AF, 1994, HEARING RES, V72, P23, DOI 10.1016/0378-5955(94)90201-1 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 Strominger RN, 1995, HEARING RES, V92, P52, DOI 10.1016/0378-5955(95)00196-4 SUBRAMANIAM M, 1992, HEARING RES, V58, P57, DOI 10.1016/0378-5955(92)90008-B Sun XM, 1999, J ACOUST SOC AM, V105, P3399, DOI 10.1121/1.424668 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 Yamasoba T, 1998, HEARING RES, V120, P143, DOI 10.1016/S0378-5955(98)00054-9 YOSHIDA N, 2000, ASS RES OTOLARYNGOL, V163, P79 Yoshida N, 2000, HEARING RES, V141, P97, DOI 10.1016/S0378-5955(99)00210-5 Yoshida N, 1999, J NEUROSCI, V19, P10116 NR 40 TC 6 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 31 EP 43 DI 10.1016/S0378-5955(01)00265-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900004 PM 11377880 ER PT J AU Ngan, EM May, BJ AF Ngan, EM May, BJ TI Relationship between the auditory brainstem response and auditory nerve thresholds in cats with hearing loss SO HEARING RESEARCH LA English DT Article DE sensorineural hearing loss; auditory brainstem response; auditory nerve fiber; off-frequency listening ID PSYCHOPHYSICAL TUNING CURVES; ACOUSTIC TRAUMA; STEM RESPONSES; 2000-4000 HZ; COCHLEAR; REPRESENTATION; MASKING; SENSITIVITY; ADULTS; FIBERS AB This study explored the relationship between the auditory brainstem response (ABR) and auditory serve sensitivity in cats with normal hearing and with noise-induced permanent threshold shifts. A statistically significant linear correlation was found between each cat's ABR thresholds and the most sensitive single neuron thresholds at the same frequency. ABR thresholds were approximately 25 dB higher than the thresholds of the most sensitive neural responses in cats with normal hearing. The two measures produced equivalent thresholds at impaired frequencies in subjects with sensorineural hearing loss. Two factors may have contributed to this convergence of ABR and neural thresholds. First, our results suggest that the elevation of the most sensitive neural responses led to a compressed threshold distribution. Consequently, only a narrow range of sound levels separated stimulus conditions that activated relatively few fibers from those that were sufficient to evoke a robust population response. In addition, the threshold responses of impaired auditory nerve fibers may have been augmented by activity in the more sensitive 'off-frequency' regions that surrounded a discrete cochlear lesion. Across varying degrees of hearing loss, the ABR maintained a systematic relationship to auditory nerve fiber thresholds, and therefore has the potential to be used as a functional assay of cochlear pathology, (C) 2001 Elsevier Science B.V. All rights reserved. C1 Johns Hopkins Univ, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21205 USA. RP May, BJ (reprint author), Johns Hopkins Univ, Dept Otolaryngol Head & Neck Surg, 505 Traylor Res Bldg,720 Rutland Ave, Baltimore, MD 21205 USA. CR ABDALA C, 1995, J ACOUST SOC AM, V97, P2394, DOI 10.1121/1.411961 BAUCH CD, 1986, EAR HEARING, V7, P314, DOI 10.1097/00003446-198610000-00004 BAUCH CD, 1988, AUDIOLOGY, V27, P156 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Byrne D, 2001, J Am Acad Audiol, V12, P37 COATS AC, 1978, ARCH OTOLARYNGOL, V104, P709 FOWLER CG, 1994, PRINCIPLES APPL AUDI, P237 GRIFFITHS SK, 1989, EAR HEARING, V10, P299, DOI 10.1097/00003446-198910000-00005 Kiang NYS, 1976, ELECTROCOCHLEOGRAPHY, P95 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 Miller RL, 1999, J ACOUST SOC AM, V105, P311, DOI 10.1121/1.424552 Miller RL, 1999, J ACOUST SOC AM, V106, P2693, DOI 10.1121/1.428135 Miller RL, 1997, J ACOUST SOC AM, V101, P3602, DOI 10.1121/1.418321 Moore BCJ, 2000, BRIT J AUDIOL, V34, P205 MUNNERLEY GM, 1991, AUDIOLOGY, V30, P25 NELSON DA, 1991, J SPEECH HEAR RES, V34, P374 Oates P, 1997, J ACOUST SOC AM, V102, P3597, DOI 10.1121/1.420148 Ohtsuka Y, 1996, Nihon Jibiinkoka Gakkai Kaiho, V99, P1764 PICKLES JO, 1988, INTRO PHYSL HEARING, P84 PICTON TW, 1977, J OTOLARYNGOL, V6, P90 RICE JJ, 1992, HEARING RES, V58, P132, DOI 10.1016/0378-5955(92)90123-5 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 ROSENHALL U, 1986, SCAND AUDIOL, V15, P179, DOI 10.3109/01050398609042141 Schilling JR, 1998, HEARING RES, V117, P57, DOI 10.1016/S0378-5955(98)00003-3 THORNTON AR, 1980, J ACOUST SOC AM, V67, P638, DOI 10.1121/1.383888 NR 28 TC 24 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 44 EP 52 DI 10.1016/S0378-5955(01)00264-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900005 PM 11377881 ER PT J AU Zha, XM Bishop, JF Hansen, MR Victoria, L Abbas, PJ Mouradian, MM Green, SH AF Zha, XM Bishop, JF Hansen, MR Victoria, L Abbas, PJ Mouradian, MM Green, SH TI BDNF synthesis in spiral ganglion neurons is constitutive and CREB-dependent SO HEARING RESEARCH LA English DT Article DE promoter region; brain-derived neurotrophic factor; cell survival; spiral ganglion neuron; gene expression regulation; Ca2+/cyclic AMP response element binding protein; Ca2+/calmodulin-dependent protein kinase; autocrine mechanism ID MESSENGER-RNA EXPRESSION; NEUROTROPHIC FACTOR BDNF; INNER-EAR INNERVATION; IMMEDIATE-EARLY GENE; SENSORY NEURONS; IN-VIVO; HIPPOCAMPAL-NEURONS; TRANSGENIC MICE; HAIR-CELLS; RAT BDNF AB Brain-derived neurotrophic factor (BDNF), which supports spiral ganglion neuron (SGN) survival in vivo and in vitro, is synthesized by SGNs. The BDNF gene generates multiple different transcripts, each from its own promoter region. Using reverse transcriptase-polymerase chain reaction (RT-PCR), we find that SGNs express only the downstream transcripts III and IV in vivo and in vitro. Using RT-PCR assays of BDNF transcripts and transfection of BDNF promoter-reporter constructs, we tested the hypothesis, originally derived from studies of cortical neurons, that depolarization induces BDNF expression via a signaling pathway that includes Ca2+/calmodulin-dependent kinases (CaMKs) and the transcription factor, Ca2+/cyclic AMP response element binding protein (CREB). In contrast, we found that in SGNs in vivo BDNF expression is constitutive and is not increased by electrical activation. Similarly, BDNF expression in vitro is not increased by stimuli that activate CREB, including depolarization, cAMP, or transfection of activated CaMK mutants. However, transfection of dominant-negative CREB mutants did abrogate gene expression driven by BDNF promoters III and IV, indicating that CREB is necessary for constitutive BDNF expression. Thus, BDNF synthesis within SGNs makes possible an autocrine or paracrine mechanism that can contribute to support SGN survival but SGNs are distinctive in that this mechanism is constitutive and not activity-regulated. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Iowa, Dept Sci Biol, Iowa City, IA 52242 USA. Univ Iowa, Dept Otolaryngol, Iowa City, IA 52242 USA. NINDS, Genet Pharmacol Unit, Expt Therapeut Branch, Bethesda, MD 20892 USA. Univ Iowa, Dept Speech, Iowa City, IA 52242 USA. Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA. Univ Iowa, Dept Otolaryngol, Iowa City, IA 52242 USA. RP Green, SH (reprint author), Univ Iowa, Dept Sci Biol, 138 Biol Bldg, Iowa City, IA 52242 USA. CR AVILA MA, 1993, DEV BIOL, V159, P266, DOI 10.1006/dbio.1993.1239 BICHLER E, 1983, ARCH OTO-RHINO-LARYN, V237, P201, DOI 10.1007/BF00453725 Bishop JF, 1997, MOL BRAIN RES, V50, P154, DOI 10.1016/S0169-328X(97)00180-0 BISHOP JF, 1994, MOL BRAIN RES, V26, P225, DOI 10.1016/0169-328X(94)90094-9 BOSHART M, 1985, CELL, V41, P521, DOI 10.1016/S0092-8674(85)80025-8 CHAO MV, 1992, NEURON, V9, P583, DOI 10.1016/0896-6273(92)90023-7 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 Conner JM, 1997, J NEUROSCI, V17, P2295 CONOVER JC, 1995, NATURE, V375, P235, DOI 10.1038/375235a0 Davies AM, 1996, NEUROCHEM RES, V21, P749, DOI 10.1007/BF02532296 ELLIOTT RC, 1994, MOL BRAIN RES, V26, P81, DOI 10.1016/0169-328X(94)90077-9 ERNFORS P, 1995, NEURON, V14, P1153, DOI 10.1016/0896-6273(95)90263-5 ERNFORS P, 1991, NEURON, V7, P165, DOI 10.1016/0896-6273(91)90084-D ERNFORS P, 1994, NATURE, V368, P147, DOI 10.1038/368147a0 Farinas I, 1998, NEURON, V21, P325, DOI 10.1016/S0896-6273(00)80542-5 Fritzsch B, 1997, TRENDS NEUROSCI, V20, P159, DOI 10.1016/S0166-2236(96)01007-7 Fritzsch B, 1997, SEMIN CELL DEV BIOL, V8, P277, DOI 10.1006/scdb.1997.0144 GABELLINI N, 1992, J CELL BIOL, V118, P131, DOI 10.1083/jcb.118.1.131 GALL CM, 1992, TRENDS PHARMACOL SCI, V13, P401, DOI 10.1016/0165-6147(92)90123-N Geschwind MD, 1996, HUM GENE THER, V7, P173, DOI 10.1089/hum.1996.7.2-173 GHOSH A, 1994, SCIENCE, V263, P1618, DOI 10.1126/science.7907431 Hansen MR, 2001, J NEUROSCI, V21, P2256 Hegarty JL, 1997, J NEUROSCI, V17, P1959 HOESCHE C, 1995, BBA-GENE STRUCT EXPR, V1261, P249, DOI 10.1016/0167-4781(95)00014-8 ISACKSON PJ, 1991, NEURON, V6, P937, DOI 10.1016/0896-6273(91)90234-Q JONES KR, 1994, CELL, V76, P989, DOI 10.1016/0092-8674(94)90377-8 Knipper M, 1996, CELL TISSUE RES, V283, P339, DOI 10.1007/s004410050545 KOITCHEV K, 1982, ACTA OTO-LARYNGOL, V94, P431, DOI 10.3109/00016488209128931 LARMET Y, 1992, NEURON, V9, P563, DOI 10.1016/0896-6273(92)90193-H Lauterborn JC, 1996, J NEUROSCI, V16, P7428 LEFEBVRE PP, 1994, NEUROREPORT, V5, P865, DOI 10.1097/00001756-199404000-00003 Lewin GR, 1996, ANNU REV NEUROSCI, V19, P289, DOI 10.1146/annurev.ne.19.030196.001445 LINDHOLM D, 1994, J NEUROBIOL, V25, P1362, DOI 10.1002/neu.480251105 LIU X, 1995, NATURE, V375, P238, DOI 10.1038/375238a0 MATTHEWS RP, 1994, MOL CELL BIOL, V14, P6107 MILLER CA, 1993, HEARING RES, V69, P35, DOI 10.1016/0378-5955(93)90091-E Miller J. M., 1995, Annals of Otology Rhinology and Laryngology, V104, P57 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 MONTMINY MR, 1990, TRENDS NEUROSCI, V13, P184, DOI 10.1016/0166-2236(90)90045-C Mou K, 1997, J COMP NEUROL, V386, P529 PIRVOLA U, 1994, HEARING RES, V75, P131, DOI 10.1016/0378-5955(94)90064-7 Robinson M, 1996, MOL CELL NEUROSCI, V7, P143, DOI 10.1006/mcne.1996.0011 Rubsamen R., 1998, DEV AUDITORY SYSTEM, P193 SCHECTERSON LC, 1994, HEARING RES, V73, P92, DOI 10.1016/0378-5955(94)90286-0 Shaywitz AJ, 1999, ANNU REV BIOCHEM, V68, P821, DOI 10.1146/annurev.biochem.68.1.821 Shieh PB, 1998, NEURON, V20, P727, DOI 10.1016/S0896-6273(00)81011-9 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 Staecker H, 1996, NEUROREPORT, V7, P889, DOI 10.1097/00001756-199603220-00011 STRUTHERS RS, 1991, NATURE, V350, P622, DOI 10.1038/350622a0 SUCHER NJ, 1993, J BIOL CHEM, V268, P22299 SUN PQ, 1994, GENE DEV, V8, P2527, DOI 10.1101/gad.8.21.2527 Tao X, 1998, NEURON, V20, P709, DOI 10.1016/S0896-6273(00)81010-7 THOENEN H, 1995, SCIENCE, V270, P593, DOI 10.1126/science.270.5236.593 Timmusk T, 1999, J BIOL CHEM, V274, P1078 TIMMUSK T, 1995, J CELL BIOL, V128, P185, DOI 10.1083/jcb.128.1.185 TIMMUSK T, 1993, NEURON, V10, P475, DOI 10.1016/0896-6273(93)90335-O VAZQUEZ E, 1994, ANAT EMBRYOL, V189, P157 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 Wiechers B, 1999, J NEUROSCI, V19, P3033 WOLOSHIN PI, 1992, MOL ENDOCRINOL, V6, P1725, DOI 10.1210/me.6.10.1725 ZAFRA F, 1990, EMBO J, V9, P3545 ZAFRA F, 1992, J NEUROSCI, V12, P4793 ZHENG JL, 1995, J NEUROSCI, V15, P5079 NR 63 TC 47 Z9 48 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 53 EP 68 DI 10.1016/S0378-5955(01)00267-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900006 PM 11377882 ER PT J AU Zum Gottesberge, AMM Felix, H Reuter, A Weiher, H AF Zum Gottesberge, AMM Felix, H Reuter, A Weiher, H TI Ultrastructural and physiological defects in the cochlea of the Mpv17 mouse strain - A comparison between young and old adult animals SO HEARING RESEARCH LA English DT Article DE kidney-inner ear relationship; peroxisome; stria vascularis; hair cell; intermediate cell; basement membrane; Alport syndrome; spiral ganglion ID GLOMERULOSCLEROSIS GENE MPV17; SENSORINEURAL HEARING-LOSS; AUTOSOMAL ALPORT-SYNDROME; INNER-EAR; STRIA VASCULARIS; BASEMENT-MEMBRANE; MODEL; MICE; KIDNEY; IDENTIFICATION AB Ultrastructural investigations were performed in young (approximately 2 months) and old (7 months) Mpv17-negative and wildtype mice. The onset, the severity and the pattern of the degeneration significantly differed between both mice strains. In the wild type mouse strain the degenerative changes of the cochlear structures were similar to the aging pattern described for other species. In contrast, the Mpv17 mutants showed degenerative changes of the cochlear structures already at the age of 2 months. The degenerative changes were patchy arranged throughout the entire length of the cochlea and involved the organ of Corti as well as the stria vascularis epithelia with alterations of the basement membrane of the capillaries. The severe sensorineural hearing loss and degenerative changes of the cochlear structures indicate that cochlear structures, especially the outer hair cells and the intermediate cells of the stria vascularis, are vulnerable to the missing Mpv17 gene product. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Dusseldorf, Dept Otorhinolaryngol, Res Lab, D-40225 Dusseldorf, Germany. Univ Zurich Hosp, Dept Otorhinolaryngol, CH-8091 Zurich, Switzerland. Univ Ulm, Ulm, Germany. Diabet Res Inst, Munich, Germany. RP Zum Gottesberge, AMM (reprint author), Univ Dusseldorf, Dept Otorhinolaryngol, Res Lab, Moorenstr 5, D-40225 Dusseldorf, Germany. EM gottesbe@uni-duesseldorf.de CR ARNOLD W, 1976, ARCH OTO-RHINO-LARYN, V212, P99, DOI 10.1007/BF00454270 ARNOLD W, 1984, ANN OTO RHINOL LARYN, V93, P119 BARKER DF, 1990, SCIENCE, V248, P1224, DOI 10.1126/science.2349482 Binder CJ, 1999, AM J PATHOL, V154, P1067, DOI 10.1016/S0002-9440(10)65359-X Chaib H, 1996, HUM MOL GENET, V5, P155, DOI 10.1093/hmg/5.1.155 Cosgrove D, 1996, GENE DEV, V10, P2981, DOI 10.1101/gad.10.23.2981 Cosgrove D, 1996, HEARING RES, V97, P54 Cosgrove D, 1998, HEARING RES, V121, P84, DOI 10.1016/S0378-5955(98)00069-0 FRIEDMANN I, 1992, PATHOLOGY INNER EAR Holme RH, 1999, CURR OPIN GENET DEV, V9, P309, DOI 10.1016/S0959-437X(99)80046-X Hoshino T, 2000, HEARING RES, V140, P145, DOI 10.1016/S0378-5955(99)00192-6 JOHNSON RJ, 1994, KIDNEY INT, V45, P352, DOI 10.1038/ki.1994.45 KARASAWA M, 1993, HUM MOL GENET, V2, P1829, DOI 10.1093/hmg/2.11.1829 KUSAKARI C, 1992, ANN OTO RHINOL LARYN, V101, P82 zumGottesberge AMM, 1996, EUR ARCH OTO-RHINO-L, V253, P470 Miner JH, 1996, J CELL BIOL, V135, P1403, DOI 10.1083/jcb.135.5.1403 MOCHIZUKI T, 1994, NAT GENET, V8, P77, DOI 10.1038/ng0994-77 Muller M, 1997, HEARING RES, V114, P259, DOI 10.1016/S0378-5955(97)00175-5 Priuska EM, 1995, BIOCHEM PHARMACOL, V50, P1749, DOI 10.1016/0006-2952(95)02160-4 QUICK CA, 1973, LARYNGOSCOPE, V83, P1469, DOI 10.1288/00005537-197309000-00007 Reuter A, 1998, MOL BIOL CELL, V9, P1675 Ruckenstein MJ, 1999, HEARING RES, V131, P22, DOI 10.1016/S0378-5955(99)00018-0 Sakaguchi N, 1997, HEARING RES, V109, P83, DOI 10.1016/S0378-5955(97)00048-8 SCHENKEL J, 1995, KIDNEY INT, V48, P80, DOI 10.1038/ki.1995.270 Schuknecht H. F., 1974, PATHOLOGY EAR SONE M, 1995, HEARING RES, V83, P26, DOI 10.1016/0378-5955(94)00189-W SPECTOR GJ, 1979, LARYNGOSCOPE, V89, P1, DOI 10.1288/00005537-197906001-00001 TAGO C, 1992, ANN OTO RHINOL LARYN, V101, P87 Thomopoulos GN, 1997, HEARING RES, V111, P31, DOI 10.1016/S0378-5955(97)00080-4 TOKAHASHI M, 1992, ANN OTO RHINOL LARYN, V191, P58 VANCAMP G, 2000, HEREDITARY HEARING L WANDERS RJA, 1995, J NEUROPATH EXP NEUR, V54, P726, DOI 10.1097/00005072-199509000-00016 Weidauer H, 1976, Laryngol Rhinol Otol (Stuttg), V55, P6 WEIHER H, 1990, CELL, V62, P425, DOI 10.1016/0092-8674(90)90008-3 Willott JF, 1998, HEARING RES, V115, P162, DOI 10.1016/S0378-5955(97)00189-5 Zhao LY, 1998, GENOMICS, V50, P23, DOI 10.1006/geno.1998.5292 Zheng QY, 1999, HEARING RES, V130, P94, DOI 10.1016/S0378-5955(99)00003-9 ZUMGOTTESBERGE AMM, IN PRESS ADV OTOL RH ZUMGOTTESBERGE AMM, 1998, MOL BASE OTOPATHOLOG, P171 ZUMGOTTESBERGE M, 2001, DEGENERATION COCHLEA, P102 ZWACKA RM, 1994, EMBO J, V13, P5129 NR 41 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 EI 1878-5891 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 69 EP 80 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900007 ER PT J AU Pantelias, AA Monsivais, P Rubel, EW AF Pantelias, AA Monsivais, P Rubel, EW TI Tonotopic map of potassium currents in chick auditory hair cells using an intact basilar papilla SO HEARING RESEARCH LA English DT Article DE potassium current; basilar papilla; hair cell physiology; patch clamp ID INNER-EAR; DEPENDENT CONDUCTANCES; TETRAETHYLAMMONIUM ION; COCHLEA; PATTERNS; CALCIUM; ORGANIZATION; INNERVATION; RESONANCE; RESPONSES AB The avian basilar papilla is tonotopically organized such that hair cells along the sensory epithelium respond best to acoustic stimulation at differing frequencies. This specificity arises due to the mechanics of the cochlea itself and intrinsic electrical properties of the hair cells. Tall hair cells show membrane voltage oscillations in response to step current injection that may allow cells to act as electrical resonators, boosting the response at the resonant frequency. These oscillations and the underlying currents have been studied in enzymatically isolated cells. This study uses a whole chick (Gallus domesticus) basilar papilla preparation where the entire epithelium and its afferent connections are intact. With this preparation, a map of changes in potassium currents of tail hair cells was produced. All cells recorded from expressed two K+ currents, a calcium-activated K+ current, I-K(Ca), and a voltage-activated K+ current, I-K. Also, apical cells expressed an inward rectifier K+ current, IIR The amplitude of total outward current increases in a gradient along the tonotopic axis. pharmacological blockers were used to separate the outward K+ currents. These experiments showed that both currents individually increase in magnitude along a gradient from apex to base. Finally, measurements of oscillation frequency in response to current steps suggest a discontinuous change in the electrical resonances at about 33% from the apex. This study demonstrates a new preparation to study the electrical properties of hair cells in more detail along the tonotopic axis of the chick basilar papilla. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Washington, Virginia Merrill Bloedel Hearing Res Ctr, Seattle, WA 98195 USA. Univ Washington, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98195 USA. RP Rubel, EW (reprint author), Univ Washington, Virginia Merrill Bloedel Hearing Res Ctr, POB 357923,CHDD CD 176, Seattle, WA 98195 USA. CR Armstrong CE, 1998, J NEUROSCI, V18, P2962 ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 ART JJ, 1993, J PHYSIOL-LONDON, V470, P109 Bekesy G., 1960, EXPT HEARING CHEN L, 1994, HEARING RES, V81, P130, DOI 10.1016/0378-5955(94)90160-0 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 EISEN MD, 1998, ASS RES OTOLARYNGOL, V21 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R FUCHS PA, 1990, J PHYSIOL-LONDON, V429, P553 FUCHS PA, 1988, J NEUROSCI, V8, P2460 FUCHS PA, 1988, J COMP PHYSIOL A, V164, P151, DOI 10.1007/BF00603947 FUCHS PA, 1990, P ROY SOC B-BIOL SCI, V241, P122, DOI 10.1098/rspb.1990.0075 FUCHS PA, 1990, J PHYSIOL-LONDON, V429, P529 Goodman MB, 1996, BIOPHYS J, V71, P430 Goodman MB, 1996, J PHYSIOL-LONDON, V497, P395 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HILLE B, 1992, IONIC CHANNELS EXCIT, P74 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 JOHNSTON D, 1995, FDN CELLULAR NEUROPH, P198 JONES SM, 1995, HEARING RES, V82, P149, DOI 10.1016/0378-5955(94)00173-N LAVIGNEREBILLARD M, 1985, J COMP NEUROL, V238, P340, DOI 10.1002/cne.902380308 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 MANLEY GA, 1979, NATURWISSENSCHAFTEN, V66, P582, DOI 10.1007/BF00368823 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MartinezDunst C, 1997, J NEUROSCI, V17, P9133 Navaratnam DS, 1997, NEURON, V19, P1077, DOI 10.1016/S0896-6273(00)80398-0 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 PANTELIAS AA, 1998, ASS RES OTOLARYNGOL, V20, P21 PITCHFORD S, 1987, HEARING RES, V27, P75, DOI 10.1016/0378-5955(87)90027-X REBILLARD G, 1981, BRAIN RES, V229, P15, DOI 10.1016/0006-8993(81)90741-1 ROSE ML, 1997, CARDIOVASC ENG, V2, P19 RUBEL EW, 1975, J COMP NEUROL, V164, P411, DOI 10.1002/cne.901640403 RYALS BM, 1985, HEARING RES, V19, P135, DOI 10.1016/0378-5955(85)90117-0 RYALS BM, 1982, ACTA OTO-LARYNGOL, V93, P205, DOI 10.3109/00016488209130873 RYALS BM, 1985, HEARING RES, V19, P73, DOI 10.1016/0378-5955(85)90099-1 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 STANFIEL.PR, 1970, J PHYSIOL-LONDON, V209, P209 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 TASAKI I, 1957, J GEN PHYSIOL, V40, P859, DOI 10.1085/jgp.40.6.859 TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WONG BS, 1980, BIOPHYS J, V32, P1037 NR 46 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 81 EP 94 DI 10.1016/S0378-5955(01)00269-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900008 PM 11377884 ER PT J AU Hsu, CJ Tan, CT Shau, WY Chen, YS Yeh, TH Lin-Shiau, SY AF Hsu, CJ Tan, CT Shau, WY Chen, YS Yeh, TH Lin-Shiau, SY TI Na+,K+-ATPase and Ca2+-ATPase activities in the cochlear lateral wall following surgical induction of hydrops SO HEARING RESEARCH LA English DT Article DE Ca2+-ATPase; Na+,K+-ATPase; microcolorimetric assay; endolymphatic hydrops ID EXPERIMENTAL ENDOLYMPHATIC HYDROPS; PIG INNER-EAR; QUIET-AGED GERBILS; NA-K-ATPASE; GUINEA-PIG; STRIA-VASCULARIS; CYTOCHEMICAL-LOCALIZATION; MORPHOLOGICAL-CHANGES; NA,K-ATPASE ACTIVITY; CEREBROSPINAL-FLUID AB Na+,K+-ATPase and Ca2+-ATPase activities have not been studied quantitatively in the cochlea affected by endolymphatic hydrops. The present study was designed to measure quantitatively the Na+,K+-ATPase and Ca2+-ATPase activities in the cochlear lateral wall and the threshold of auditory brainstem response (ABR) for guinea pigs in the early stages (=2 months) of experimentally induced endolymphatic hydrops. A significant negative association was demonstrated between Ca2+-ATPase activity and the change in ABR threshold for hydropic cochleae (P=0.014), but not for control cochleae (P=0.123), although no such significant association was revealed between Na+,K+-ATPase activity and any change in ABR threshold for both hydropic cochleae (P=0.751) and control cochleae (P=0.352). A significant increase in Ca2+-ATPase activity in the cochlear lateral wall was observed for the hydropic ear, in which normal ABR thresholds were maintained, as compared to the control ear. On the contrary, a mild decrease in Ca2+-ATPase activity in the cochlear lateral wall was observed for the hydropic ear, in which ABR thresholds increased significantly. The present findings suggest that alterations of Ca2+-ATPase activity in the cochlear lateral wall may implicate disturbed calcium-homeostasis in the inner ear, resulting in hearing dysfunction in the early stages of experimentally induced endolymphatic hydrops. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Natl Taiwan Univ Hosp, Dept Otolaryngol, Taipei, Taiwan. Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol, Taipei, Taiwan. Natl Taiwan Univ, Coll Med, Inst Pharmacol, Taipei, Taiwan. RP Hsu, CJ (reprint author), Natl Taiwan Univ Hosp, Dept Otolaryngol, 7 Chung Shan S Rd, Taipei, Taiwan. CR Agrup C, 1999, ACTA OTO-LARYNGOL, V119, P437 ALBERS FWJ, 1991, ACTA OTO-LARYNGOL, V111, P885, DOI 10.3109/00016489109138426 ALBERS FWJ, 1987, ANN OTO RHINOL LARYN, V96, P282 ALBERS FWJ, 1987, ACTA OTO-LARYNGOL, V104, P202, DOI 10.3109/00016488709107319 ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 BOHMER A, 1990, ANN OTO RHINOL LARYN, V99, P470 COHEN J, 1984, ACTA OTO-LARYNGOL, V98, P398, DOI 10.3109/00016488409107580 Curtis LM, 1997, ACTA OTO-LARYNGOL, V117, P553, DOI 10.3109/00016489709113436 FRIEDMAN PA, 1995, PHYSIOL REV, V75, P429 Gill SS, 1997, HEARING RES, V113, P191, DOI 10.1016/S0378-5955(97)00141-X Gratton MA, 1997, HEARING RES, V108, P9, DOI 10.1016/S0378-5955(97)00034-8 GRATTON MA, 1995, HEARING RES, V83, P43, DOI 10.1016/0378-5955(94)00188-V HORNER KC, 1991, HEARING RES, V52, P147, DOI 10.1016/0378-5955(91)90194-E HORNER KC, 1986, HEARING RES, V26, P319 Hsu CJ, 2000, HEARING RES, V142, P203, DOI 10.1016/S0378-5955(00)00020-4 Hsu Chuan Jen, 1993, Journal of the Formosan Medical Association, V92, P558 ICHIMIYA I, 1994, ANN OTO RHINOL LARYN, V103, P457 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 IKEDA K, 1987, HEARING RES, V26, P117, DOI 10.1016/0378-5955(87)90040-2 IKEDA K, 1988, HEARING RES, V34, P307, DOI 10.1016/0378-5955(88)90010-X IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 KEITHLEY EM, 1995, ANN OTO RHINOL LARYN, V104, P858 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KIMURA RS, 1967, ANN OTO RHINOL LARYN, V76, P664 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KLIS SFL, 1990, ANN OTO RHINOL LARYN, V99, P566 Konishi T, 1981, MENIERES DIS PATHOGE, P47 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 KUMAGAMI H, 1981, ORL J OTO-RHINO-LARY, V43, P314 KUMAGAMI H, 1983, ORL J OTO-RHINO-LARY, V45, P143 Kusakari J, 1987, Acta Otolaryngol Suppl, V435, P27 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 Nadol J B Jr, 1995, Acta Otolaryngol Suppl, V519, P47 NISHIYAMA S, 1994, HISTOL HISTOPATHOL, V9, P205 RUDING PRJW, 1987, ARCH OTO-RHINO-LARYN, V244, P174, DOI 10.1007/BF00464263 SAKAGAMI M, 1995, ANN OTO RHINOL LARYN, V104, P210 SALT AN, 1994, HEARING RES, V74, P165, DOI 10.1016/0378-5955(94)90184-8 SALT AN, 1994, HEARING RES, V74, P115, DOI 10.1016/0378-5955(94)90180-5 SALT AN, 1989, AM J OTOLARYNG, V10, P371, DOI 10.1016/0196-0709(89)90030-6 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SILVERSTEIN H, 1977, ANN OTO RHINOL LARYN, V86, P493 SZIKLAI I, 1989, ACTA OTO-LARYNGOL, V107, P371, DOI 10.3109/00016488909127524 SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 VANBENTHEM PPG, 1994, HEARING RES, V77, P9, DOI 10.1016/0378-5955(94)90249-6 WALSTED A, 1994, J LARYNGOL OTOL, V108, P637 WALSTED A, 1991, ACTA OTO-LARYNGOL, V111, P468, DOI 10.3109/00016489109138371 WANG Q, 1994, CHIN J OTORHINOLARYN, V29, P263 YAZAWA Y, 1990, MENIERES DIS, P57 YOSHIHARA T, 1987, ARCH OTO-RHINO-LARYN, V243, P395, DOI 10.1007/BF00464650 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 ZHANG S, 1995, CHIN J OTORHINOLARYN, V30, P276 ZUMGOTTESBERGE AMM, 1987, AVIAT SPACE ENVIR MD, V58, pA240 ZUMGOTTESBERGE AMM, 1988, ACTA OTOLARYNGOL S S, V460, P18 ZUMGOTTESBERGEORSULAKOVA AMM, 1986, ACTA OTO-LARYNGOL, V102, P93 NR 54 TC 0 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 95 EP 103 DI 10.1016/S0378-5955(01)00270-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900009 PM 11377885 ER PT J AU Hine, JE Ho, CT Slaven, A Thornton, ARD AF Hine, JE Ho, CT Slaven, A Thornton, ARD TI Comparison of transient evoked otoacoustic emission thresholds recorded conventionally and using maximum length sequences SO HEARING RESEARCH LA English DT Article DE evoked otoacoustic emission; maximum length sequence; detection threshold ID STIMULUS RATE; CONTRALATERAL SUPPRESSION; ACOUSTIC EMISSIONS; HEARING IMPAIRMENT; NEWBORNS; EAR AB Presenting clicks according to maximum length sequences (MLSs) enables transient evoked otoacoustic emissions (TEOAEs) to be recorded at very high stimulation rates. Despite a decrease in TEOAE amplitude, the very large number of responses obtainable at high rates means that both signal to noise ratio (SNR) and detection sensitivity increase as the click rate increases. This study characterises conventional and MLS TEOAEs near threshold for a group of normally hearing adults. Stimulus presentation rates of 40 clicks/s (conventional) and 5000 clicks/s (MLS) were used. Compared to conventional recordings, the MLS technique enabled smaller responses to be detected, when averaged for the same time and to the same SNR. TEOAE amplitude recorded at detection threshold for MLS responses was 13 dB lower than that recorded conventionally. For each individual, MLS recording also produced clear, repeatable responses at stimulus levels below the detection threshold for conventional TEOAEs. The click level at TEOAE threshold was 12 dB lower for MLS compared to conventional emissions. These results suggest that TEOAE thresholds are not absolute but strongly related to the detection sensitivity of the recording system and physiological noise. The initial growth rates and the shape of input/output functions were found to be similar for the two recording techniques. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Royal S Hants Hosp, MRC, Heart Res Inst, Southampton SO14 OYG, Hants, England. Univ Southampton, Hearing & Balance Ctr, Inst Sound & Vibrat Res, Southampton, Hants, England. RP Hine, JE (reprint author), Royal S Hants Hosp, MRC, Heart Res Inst, Southampton SO14 OYG, Hants, England. CR BONFILS P, 1989, ANN OTO RHINOL LARYN, V98, P326 BONFILS P, 1988, ARCH OTO-RHINO-LARYN, V245, P53, DOI 10.1007/BF00463550 Cope Y., 1988, PAEDIATRIC AUDIOLOGY, P221 Doyle KJ, 1997, INT J PEDIATR OTORHI, V41, P111, DOI 10.1016/S0165-5876(97)00066-9 Fitzgerald TS, 1997, J SPEECH LANG HEAR R, V40, P1164 GRANDORI F, 1990, COCHLEAR MECH OTOACO, V7, P99 GRANDORI F, 1993, BRIT J AUDIOL, V27, P97, DOI 10.3109/03005369309077898 GRANDORI F, 1994, ADV OTOACOUSTIC EMIS, V1, P46 Hine JE, 1997, EAR HEARING, V18, P121, DOI 10.1097/00003446-199704000-00004 HUNTER MF, 1994, BRIT J AUDIOL, V28, P47, DOI 10.3109/03005369409077912 Johannesen PT, 1998, SCAND AUDIOL, V27, P37, DOI 10.1080/010503998419687 JOHNSEN NJ, 1993, SCAND AUDIOL, V22, P87, DOI 10.3109/01050399309046023 Kemp David T., 1993, Seminars in Hearing, V14, P30, DOI 10.1055/s-0028-1085103 KOK MR, 1993, AUDIOLOGY, V32, P213 LinaGranade G, 1997, HEARING RES, V107, P83, DOI 10.1016/S0378-5955(97)00021-X LUTMAN ME, 1993, BRIT J AUDIOL, V27, P103, DOI 10.3109/03005369309077899 PICTON TW, 1993, EAR HEARING, V14, P299, DOI 10.1097/00003446-199310000-00001 Probst R, 1997, Adv Otorhinolaryngol, V53, P182 Rasmussen AN, 1998, BRIT J AUDIOL, V32, P355, DOI 10.3109/03005364000000087 SALOMON G, 1993, BRIT J AUDIOL, V27, P139, DOI 10.3109/03005369309077904 Slaven A, 1998, EAR HEARING, V19, P103, DOI 10.1097/00003446-199804000-00002 THORNTON ARD, 1993, BRIT J AUDIOL, V27, P109, DOI 10.3109/03005369309077900 THORNTON ARD, 1999, SERIES AUDIOLOGY OTO, V1, P21 THORNTON ARD, 1995, SCAND AUDIOL, V24, P83, DOI 10.3109/01050399509047519 THORNTON ARD, 1993, BRIT J AUDIOL, V27, P319, DOI 10.3109/03005369309076710 THORNTON ARD, 1994, SCAND AUDIOL, V23, P225, DOI 10.3109/01050399409047512 THORNTON ARD, 1993, J ACOUST SOC AM, V94, P132, DOI 10.1121/1.407090 NR 27 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 104 EP 114 DI 10.1016/S0378-5955(01)00271-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900010 PM 11377886 ER PT J AU Cheung, SW Nagarajan, SS Bedenbaugh, PH Schreiner, CE Wang, XQ Wong, A AF Cheung, SW Nagarajan, SS Bedenbaugh, PH Schreiner, CE Wang, XQ Wong, A TI Auditory cortical neuron response differences under isoflurane versus pentobarbital anesthesia SO HEARING RESEARCH LA English DT Article DE auditory cortex; isoflurane; pentobarbital; anesthesia; frequency tuning curve; cat ID SINGLE-UNIT ACTIVITY; FUNCTIONAL TOPOGRAPHY; TONE INTENSITY; COMPLEX SOUNDS; VISUAL-CORTEX; TUNING CURVES; CAT; REPRESENTATION; POTENTIALS; RECORDINGS AB Response properties of the middle layers of feline primary auditory cortex neurons to simple sounds were compared for isoflurane versus pentobarbital anesthesia in a within subject study control design. Initial microelectrode recordings were made under isoflurane anesthesia. After a several hour washout period, recordings were repeated at spatially matched locations in the same animal under pentobarbital. The median spatial separation between matched recording locations was 50 microns. Excitatory frequency tuning curves (n = 71 pairs) to tone bursts and entrainment to click train sequences (n = 64 pairs) ranging from 2 to 38 Hz were measured. Characteristic frequency and BW10 and BW30 were not different under either anesthetic. The spontaneous rate was slightly decreased (P < 0.05) for isoflurane (median 4.2 spikes/s) compared to pentobarbital (median 5.8 spikes/s). Minimum median threshold and latency were elevated by 12 dB and 2 ms, respectively, under isoflurane. Entrainment to click sequences assumed a lowpass filter profile under both anesthetics, but was markedly impoverished under isoflurane. Responses to click sequences under isoflurane were phasic to the first click but had very poor following to subsequent elements. Compared to pentobarbital, isoflurane appears to have a profound impact on response sensitivity and temporal response properties of auditory cortical neurons. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Francisco, Coleman Mem Lab, San Francisco, CA 94143 USA. Univ Calif San Francisco, WM Keck Ctr Integrat Neurosci, San Francisco, CA 94143 USA. Univ Utah, Dept Bioengn, Salt Lake City, UT 84112 USA. Univ Florida, Inst Brain, Dept Neurosci, Gainesville, FL 32610 USA. Univ Florida, Inst Brain, Dept Otolaryngol, Gainesville, FL 32610 USA. Johns Hopkins Sch Med, Dept Biomed Engn, Baltimore, MD 21205 USA. Johns Hopkins Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. Western Univ Hlth Sci, Coll Osteopath Med Pacific, Pomona, CA 91766 USA. RP Cheung, SW (reprint author), Div Otol Neurol & Skull Base Surg, Box 0342 A730,400 Parnassus Ave, San Francisco, CA 94143 USA. CR Bieser A, 1996, EXP BRAIN RES, V108, P273 BOBBIN RP, 1979, ARCH OTOLARYNGOL, V105, P467 CHURCH MW, 1987, BRAIN RES, V403, P72, DOI 10.1016/0006-8993(87)90124-7 COHEN MS, 1982, ANESTH ANALG, V61, P338 deCharms RC, 1998, SCIENCE, V280, P1439, DOI 10.1126/science.280.5368.1439 DODD F, 1992, HEARING RES, V62, P173, DOI 10.1016/0378-5955(92)90183-N EGER EI, 1981, ANESTHESIOLOGY, V55, P559, DOI 10.1097/00000542-198111000-00014 EGGERMONT JJ, 1995, J NEUROPHYSIOL, V73, P227 HARVEY SC, 1980, GOODMAN GILMANS PHAR, P350 Heil P, 1997, J NEUROPHYSIOL, V77, P2616 HEIL P, 1994, HEARING RES, V76, P188, DOI 10.1016/0378-5955(94)90099-X Issa NP, 1999, J NEUROSCI, V19, P6965 Issa NP, 2000, J NEUROSCI, V20, P8504 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X KRNJEVIC K, 1992, GEN PHARMACOL, V23, P965, DOI 10.1016/0306-3623(92)90274-N KUWADA S, 1989, J NEUROPHYSIOL, V61, P269 Lisberger SG, 1999, J NEUROSCI, V19, P2224 Mendelson JR, 1997, J COMP PHYSIOL A, V181, P615, DOI 10.1007/s003590050145 Nelken I, 1999, NATURE, V397, P154, DOI 10.1038/16456 NELKEN I, 1994, HEARING RES, V72, P206, DOI 10.1016/0378-5955(94)90220-8 PIATT JH, 1984, NEUROSURGERY, V15, P427 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 RECANZONE GH, 1992, J NEUROPHYSIOL, V67, P1071 Ries CR, 1999, J NEUROPHYSIOL, V81, P1802 RIES CR, 1999, J NEUROPHYSIOL, V81, P1797 Schreiner CE, 1998, AUDIOL NEURO-OTOL, V3, P104, DOI 10.1159/000013785 SCHREINER CE, 1992, J NEUROPHYSIOL, V68, P1487 SCHREINER CE, 1992, EXP BRAIN RES, V92, P105 Schreiner CE, 2000, ANNU REV NEUROSCI, V23, P501, DOI 10.1146/annurev.neuro.23.1.501 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 STRYKER MP, 1987, J COMP NEUROL, V258, P297, DOI 10.1002/cne.902580209 SUTTER ML, 1995, J NEUROPHYSIOL, V73, P190 Sutter ML, 2000, J NEUROPHYSIOL, V84, P1012 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 Tennigkeit F, 1997, J NEUROPHYSIOL, V78, P591 TIGWELL DA, 1992, EXP BRAIN RES, V88, P224, DOI 10.1007/BF02259146 WANG X, 1999, ASS RES OTOLARYNGOL, V22, P136 WANG XQ, 1995, NATURE, V378, P71, DOI 10.1038/378071a0 ZURITA P, 1994, NEUROSCI RES, V19, P303, DOI 10.1016/0168-0102(94)90043-4 NR 39 TC 51 Z9 53 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 115 EP 127 DI 10.1016/S0378-5955(01)00272-6 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900011 PM 11377887 ER PT J AU Kemmer, M Vater, M AF Kemmer, M Vater, M TI Cellular and subcellular distribution of AMPA-type glutamate receptor subunits and metabotropic glutamate receptor 1 alpha in the cochlear nucleus of the horseshoe bat (Rhinolophus rouxi) SO HEARING RESEARCH LA English DT Article DE excitatory amino acid; immunocytochemistry; ultrastructure; electron microscopy; echolocation; auditory ID AUDITORY BRAIN-STEM; FUNCTIONAL-ORGANIZATION; GUINEA-PIG; RAT-BRAIN; IMMUNOCYTOCHEMICAL LOCALIZATION; CA2+ PERMEABILITY; ANTIBODY SHOWS; BARN OWL; NEURONS; CELLS AB Ionotropic alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) selective glutamate receptors (GluRs) are the main mediators of fast excitatory neurotransmission and composed of a variable combination of four different subunits (GluR1-4). The metabotropic glutamate receptor 1 alpha (mGluR1 alpha) is involved in plastic synaptic events, Since horseshoe bats strongly depend on temporal cues for acoustic imaging by echolocation and exhibit prominent species specific specializations of the cochlear nucleus (CN), the subunit distribution of AMPA selective GluRs and the distribution of mGluR1 alpha was studied at the light and electron microscopic level with preembedding immunocytochemistry. Immunoreactivity to GluR1 was low throughout the CN. All types of projection neurons of the ventral CN expressed distinct GluR2/3 and GluR4 immunoreactivity with GluR4-labeling especially prominent in multipolar and octopus cell-like neurons of the posteroventral CN. The AMPA and metabotropic receptor inventory of the laminated ventral subdivision of the dorsal CN (DCNv) agreed with that reported in other mammals, whereas the specialized dorsal non-laminated subdivision of DCN (DCNd) lacked the prominent labeling for GluR2/3 and mGluR1 alpha that characterizes cartwheel cells of DCNv. Distinct GluR2/3 and GluR4 immunoreactivity combined with low expression of mGluR1 alpha immunoreactivity was characteristic for fusiform cells of DCNv and DCNd. Tuberculoventral cells of both the deep DCNv and the DCNd exhibited light to moderate GluR2/3 and GluR4 immunoreactivity. The staining patterns in DCNd thus indicate a loss of cerebellar-like microcircuits and a conservation of frequency specific circuitry of the deep and fusiform cell layers of the mammalian DCN. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Inst Biochem & Biol, D-14471 Potsdam, Germany. RP Vater, M (reprint author), Inst Biochem & Biol, Lennestr 7A, D-14471 Potsdam, Germany. CR ADAMS JC, 1986, ARCH OTOLARYNGOL, V112, P1253 BARNESDAVIES M, 1995, J PHYSIOL-LONDON, V488, P387 BERREBI AS, 1991, ANAT EMBRYOL, V183, P427 BETTLER B, 1995, NEUROPHARMACOLOGY, V34, P123, DOI 10.1016/0028-3908(94)00141-E Bilak SR, 1998, SYNAPSE, V28, P251 Caicedo A, 1999, EUR J NEUROSCI, V11, P51, DOI 10.1046/j.1460-9568.1999.00410.x Covey E, 1999, ANNU REV PHYSIOL, V61, P457, DOI 10.1146/annurev.physiol.61.1.457 Covey Ellen, 1995, Springer Handbook of Auditory Research, V5, P235 DUNN ME, 1996, ADV SP HEAR A&B, V3, P63 FARB CR, 1995, J COMP NEUROL, V362, P86, DOI 10.1002/cne.903620106 FENG AS, 1985, J COMP NEUROL, V235, P529, DOI 10.1002/cne.902350410 GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 GOLDING NL, 1995, J NEUROSCI, V15, P3138 HOLLMANN M, 1991, SCIENCE, V252, P851, DOI 10.1126/science.1709304 HUNTER C, 1993, J NEUROSCI, V13, P1932 ITOH K, 1987, BRAIN RES, V400, P145, DOI 10.1016/0006-8993(87)90662-7 JORIS PX, 1994, J NEUROPHYSIOL, V71, P1037 Kato BM, 1996, J NEUROPHYSIOL, V76, P646 KEMMER M, IN PRESS ANAT EMBRYO Kossl Manfred, 1995, Springer Handbook of Auditory Research, V5, P191 Kubke MF, 1998, MICROSC RES TECHNIQ, V41, P176 LACHICA EA, 1995, J NEUROSCI, V15, P1724 Levin MD, 1997, J COMP NEUROL, V378, P239, DOI 10.1002/(SICI)1096-9861(19970210)378:2<239::AID-CNE7>3.0.CO;2-4 LOMELI H, 1994, SCIENCE, V266, P1709, DOI 10.1126/science.7992055 MANIS PB, 1994, J COMP NEUROL, V348, P261, DOI 10.1002/cne.903480208 MARTIN LJ, 1993, NEUROSCIENCE, V53, P327, DOI 10.1016/0306-4522(93)90199-P Molitor SC, 1997, J NEUROPHYSIOL, V77, P1889 MOORE JK, 1979, AM J ANAT, V154, P393, DOI 10.1002/aja.1001540306 MOSBACHER J, 1994, SCIENCE, V266, P1059, DOI 10.1126/science.7973663 MUGNAINI E, 1980, J NEUROCYTOL, V9, P537, DOI 10.1007/BF01204841 NELKEN I, 1994, J NEUROPHYSIOL, V71, P2446 NEUWEILER G, 1990, PHYSIOL REV, V70, P615 Oertel D, 1997, NEURON, V19, P959, DOI 10.1016/S0896-6273(00)80388-8 Oertel D, 1999, ANNU REV PHYSIOL, V61, P497, DOI 10.1146/annurev.physiol.61.1.497 OSEN KK, 1995, J COMP NEUROL, V357, P482, DOI 10.1002/cne.903570311 OSEN KK, 1996, ADV SP HEAR A&B, V3, P111 Parks TN, 2000, HEARING RES, V147, P77, DOI 10.1016/S0378-5955(00)00122-2 Petralia RS, 1997, J COMP NEUROL, V385, P456, DOI 10.1002/(SICI)1096-9861(19970901)385:3<456::AID-CNE9>3.0.CO;2-2 Petralia RS, 1997, J CHEM NEUROANAT, V13, P77, DOI 10.1016/S0891-0618(97)00023-9 PETRALIA RS, 1992, J COMP NEUROL, V318, P329, DOI 10.1002/cne.903180309 Petralia RS, 1996, J COMP NEUROL, V372, P356 Popratiloff A, 1996, J NEUROSCI, V16, P3363 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 Rubio ME, 1997, NEURON, V18, P939, DOI 10.1016/S0896-6273(00)80333-5 Takahashi T, 1996, SCIENCE, V274, P594, DOI 10.1126/science.274.5287.594 Trussell LO, 1997, CURR OPIN NEUROBIOL, V7, P487, DOI 10.1016/S0959-4388(97)80027-X Trussell LO, 1999, ANNU REV PHYSIOL, V61, P477, DOI 10.1146/annurev.physiol.61.1.477 VATER M, 1990, J COMP NEUROL, V292, P373, DOI 10.1002/cne.902920305 VATER M, 1992, J COMP NEUROL, V325, P183, DOI 10.1002/cne.903250205 VATER M, 1996, ADV SP HEAR A&B, V3, P129 vonGersdorff H, 1997, J NEUROSCI, V17, P8137 Wang LY, 1998, NATURE, V394, P384, DOI 10.1038/28645 Wang YX, 1998, J NEUROSCI, V18, P1148 Washburn MS, 1997, J NEUROSCI, V17, P9393 WEINBERG RJ, 1987, NEUROSCIENCE, V20, P209, DOI 10.1016/0306-4522(87)90013-3 WENTHOLD RJ, 1992, J BIOL CHEM, V267, P501 WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 Wright DD, 1996, J COMP NEUROL, V364, P729, DOI 10.1002/(SICI)1096-9861(19960122)364:4<729::AID-CNE10>3.0.CO;2-K ZHANG S, 1994, J NEUROPHYSIOL, V71, P914 Zirpel L, 1998, J NEUROPHYSIOL, V79, P2288 Zirpel L, 1996, J NEUROPHYSIOL, V76, P4127 NR 62 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2001 VL 156 IS 1-2 BP 128 EP 142 DI 10.1016/S0378-5955(01)00266-0 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 442GB UT WOS:000169275900012 PM 11377888 ER PT J AU Sha, SH Taylor, R Forge, A Schacht, J AF Sha, SH Taylor, R Forge, A Schacht, J TI Differential vulnerability of basal and apical hair cells is based on intrinsic susceptibility to free radicals SO HEARING RESEARCH LA English DT Article DE cochlea; reactive oxygen species; free radical; antioxidant; ototoxicity ID PIG IN-VIVO; GENTAMICIN OTOTOXICITY; IRON CHELATORS; INNER-EAR; 4-METHYLTHIOBENZOIC ACID; LIPID-PEROXIDATION; COCHLEAR CULTURES; ANTIOXIDANT; NOISE; GLUTATHIONE AB The base of the cochlea is more vulnerable to trauma than the apex as seen in the pattern of hair cell damage by cisplatin or aminoglycosides. The differential vulnerability is maintained in organotypic cultures exposed directly to these drugs, suggesting there may be an intrinsic difference in sensitivity to damage along the cochlear spiral. We therefore investigated the survival capacity of isolated outer hair cells and strips dissected from different turns of the guinea pig organ of Corti in short-term culture. Cells were stained with fluorescent indicators of viable or dead cells, calcein-AM and ethidium homodimer. After 5 h at room temperature, up to 90% of outer hair cells from the apex survived, but less than 30% from the base. In contrast, basal inner hair cells remained viable, and supporting cells survived for at least 20 h. The difference in survival capacity between basal and apical outer hair cells coincided with a significantly lower level of the antioxidant glutathione in basal outer hair cells compared with apical outer hair cells. This suggested that basal outer hair cells may be more vulnerable to free-radical damage than epical outer hair cells. The survival of basal outer hair cells was significantly improved by addition of the radical scavengers,I-acetyl cysteine, p-phenylenediamine, glutathione, mannitol or salicylate. The protection by antioxidants implies that the accelerated death of basal outer hair cells is due to free-radical damage. The results support an intrinsic susceptibility to free radicals that differs among cochlear cell populations. This differential provides a rational explanation for base-to-apex gradients observed in various forms of cochlear pathology. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. UCL, Inst Laryngol & Otol, London WC1X 8EE, England. RP Schacht, J (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. EM schatch@umich.edu CR CONLEE JW, 1989, HEARING RES, V41, P43, DOI 10.1016/0378-5955(89)90177-9 Forge A, 2000, AUDIOL NEURO-OTOL, V5, P3, DOI 10.1159/000013861 Forge A, 2000, HEARING RES, V139, P97, DOI 10.1016/S0378-5955(99)00177-X FORGE A, 1993, J NEUROCYTOL, V22, P854, DOI 10.1007/BF01186357 GARETZ SL, 1994, HEARING RES, V77, P81, DOI 10.1016/0378-5955(94)90255-0 GUTTERIDGE JMC, 1987, FEBS LETT, V214, P362, DOI 10.1016/0014-5793(87)80088-1 HANNEMANN J, 1988, TOXICOLOGY, V51, P119 HOCKENBERY DM, 1993, CELL, V75, P241, DOI 10.1016/0092-8674(93)80066-N Husain K, 1996, FUND APPL TOXICOL, V32, P278, DOI 10.1006/faat.1996.0131 Kamimura T, 1999, HEARING RES, V131, P117, DOI 10.1016/S0378-5955(99)00017-9 Kopke RD, 1997, AM J OTOL, V18, P559 Lautermann J, 1997, HEARING RES, V114, P75, DOI 10.1016/S0378-5955(97)00154-8 Ohinata Y, 2000, BRAIN RES, V878, P163, DOI 10.1016/S0006-8993(00)02733-5 Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P229, DOI 10.1159/000013846 Pirvola U, 2000, J NEUROSCI, V20, P43 Priuska EM, 1998, INORG CHIM ACTA, V273, P85, DOI 10.1016/S0020-1693(97)05942-2 Priuska EM, 1995, BIOCHEM PHARMACOL, V50, P1749, DOI 10.1016/0006-2952(95)02160-4 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E Sha SH, 1999, FREE RADICAL BIO MED, V26, P341, DOI 10.1016/S0891-5849(98)00207-X Sha SH, 1999, LAB INVEST, V79, P807 Sha SH, 2000, HEARING RES, V142, P34, DOI 10.1016/S0378-5955(00)00003-4 Song BB, 1997, J PHARMACOL EXP THER, V282, P369 Song BB, 1998, FREE RADICAL BIO MED, V25, P189, DOI 10.1016/S0891-5849(98)00037-9 Song BB, 1996, HEARING RES, V94, P87, DOI 10.1016/0378-5955(96)00003-2 Tan SL, 1998, J CELL BIOL, V141, P1423, DOI 10.1083/jcb.141.6.1423 Torchinsky C, 1999, J NEUROCYTOL, V28, P913, DOI 10.1023/A:1007082424477 Usami S, 1996, BRAIN RES, V743, P337, DOI 10.1016/S0006-8993(96)01090-6 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 30 TC 162 Z9 181 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 1 EP 8 DI 10.1016/S0378-5955(01)00224-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100001 PM 11335071 ER PT J AU Trune, DR Kempton, JB AF Trune, DR Kempton, JB TI Aldosterone and prednisolone control of cochlear function in MRL/MpJ-Fas(lpr) autoimmune mice SO HEARING RESEARCH LA English DT Article DE autoimmune hearing loss; MRL/MpJ-Fas(lpr); autoimmune mouse; aldosterone; prednisolone; systemic lupus erythematosus ID SENSORINEURAL HEARING-LOSS; RECEPTOR MESSENGER-RNAS; SENSITIVE NA+ CHANNEL; RAT INNER-EAR; STRIA VASCULARIS; MRL-FAS(LPR) MOUSE; NATRIURETIC-PEPTIDE; STEROID TREATMENT; MENIERES-DISEASE; GUINEA-PIG AB Recently this laboratory showed aldosterone, a mineralocorticoid that only enhances sodium transport, was as effective as the glucocorticoid prednisolone in restoring cochlear function in autoimmune mice. To further test this relationship between sodium transport and autoimmune hearing loss, dosage comparisons were made of prednisolone and aldosterone control of the auditory dysfunction in autoimmune MRL/MpJ-Fas(lpr) mice. Mice were tested at 2 months of age to establish baseline auditory brainstem response (ABR) thresholds, hematocrit, serum immune complexes, and anti-nuclear antibodies. Mice were then given different doses of prednisolone or aldosterone in their drinking water for 2 months. After the treatment period, most untreated water controls showed elevation of ABR thresholds due to the ongoing autoimmune disease. However, the steroid groups had significantly more mice with improved or unchanged thresholds. Both steroids improved stria vascularis morphology, although aldosterone appeared to be more effective. The immune suppressive prednisolone caused a dose-related improvement in levels of serum immune complexes and hematocrit, hallmarks of systemic autoimmune disease. Aldosterone, which has no immune suppressive function, did not alter systemic disease. The comparable efficacy of prednisolone and aldosterone in restoring auditory function suggests steroid reversal of autoimmune hearing loss in mice is due to increasing stria vascularis sodium transport and not suppression of systemic autoimmune reactions. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, Portland, OR 97201 USA. RP Trune, DR (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, Mail Code NRC04,3181 SW Sam Jackson Rd, Portland, OR 97201 USA. CR BRENNER BM, 1990, PHYSIOL REV, V70, P665 BRUMMETT R, 1977, ACTA OTO-LARYNGOL, V83, P98, DOI 10.3109/00016487709128819 BYL FM, 1984, LARYNGOSCOPE, V94, P647 CHAMPIGNY G, 1994, EMBO J, V13, P2177 DICKINS JRE, 1990, AM J OTOL, V11, P51 GARTY H, 1994, FASEB J, V8, P522 HARRIS JP, 1995, OTOLARYNG HEAD NECK, V112, P639, DOI 10.1016/S0194-5998(95)70170-2 HAUSLER A, 1992, J STEROID BIOCHEM, V41, P785, DOI 10.1016/0960-0760(92)90425-I Haynes R, 1985, PHARMACOL BASIS THER, P1459 HORISBERGER JD, 1992, HYPERTENSION, V19, P221 HUGHES GB, 1993, HEAD NECK SURG OTOLA, P1833 HUGHES GB, 1983, LARYNGOSCOPE, V93, P410 HUNNEYBALL IM, 1986, AGENTS ACTIONS, V18, P384, DOI 10.1007/BF01965002 JACKSON EK, 1995, GOODMAN GILMANS PHAR, P685 KAYLIE DM, 2000, AAO ARO RES FOR WASH Kitano H, 1997, NEUROREPORT, V8, P2289, DOI 10.1097/00001756-199707070-00038 Kumagami H, 1998, PFLUG ARCH EUR J PHY, V436, P970, DOI 10.1007/s004240050731 LARAGH JH, 1985, NEW ENGL J MED, V313, P1330 Lin DW, 1997, OTOLARYNG HEAD NECK, V117, P530, DOI 10.1016/S0194-5998(97)70026-3 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 MCCABE BF, 1979, ANN OTO RHINOL LARYN, V88, P585 Mitchell C, 1996, HEARING RES, V99, P38, DOI 10.1016/S0378-5955(96)00081-0 MORI N, 1986, ACTA OTO-LARYNGOL, V101, P217, DOI 10.3109/00016488609132830 MOSCICKI RA, 1994, JAMA-J AM MED ASSOC, V272, P611, DOI 10.1001/jama.272.8.611 MOSKOWITZ D, 1984, LARYNGOSCOPE, V94, P664 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 O-Uchi Toshiaki, 1993, Auris Nasus Larynx, V20, P79 PARNES LS, 1999, LARYNGOSCOPE S, V91, P1 PITOVSKI DZ, 1993, BRAIN RES, V601, P273, DOI 10.1016/0006-8993(93)91720-D RAREY KE, 1991, LARYNGOSCOPE, V101, P1081 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 RENARD S, 1995, PFLUG ARCH EUR J PHY, V430, P299, DOI 10.1007/BF00373903 Ruckenstein MJ, 1999, HEARING RES, V131, P22, DOI 10.1016/S0378-5955(99)00018-0 Ruckenstein MJ, 1999, OTOLARYNG HEAD NECK, V121, P452, DOI 10.1016/S0194-5998(99)70236-6 Ruckenstein MJ, 1999, HEARING RES, V127, P137, DOI 10.1016/S0378-5955(98)00189-0 Ruckenstein MJ, 1999, LARYNGOSCOPE, V109, P626, DOI 10.1097/00005537-199904000-00020 RUPPRECHT R, 1993, EUR J PHARM-MOLEC PH, V247, P145, DOI 10.1016/0922-4106(93)90072-H RYBAK LP, 1986, NEUROBIOLOGY HEARING, P441 SALT AN, 1986, NEUROBIOLOGY HEARING, P109 Sismanis A, 1997, OTOLARYNG HEAD NECK, V116, P146, DOI 10.1016/S0194-5998(97)70316-4 Suzuki M, 1998, MOL BRAIN RES, V55, P165, DOI 10.1016/S0169-328X(98)00016-3 Takeda T, 1995, Acta Otolaryngol Suppl, V519, P219 TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 Trune DR, 1997, OTOLARYNG HEAD NECK, V117, P504, DOI 10.1016/S0194-5998(97)70022-6 Trune DR, 1999, HEARING RES, V137, P160, DOI 10.1016/S0378-5955(99)00147-1 Trune DR, 2000, LARYNGOSCOPE, V110, P1902, DOI 10.1097/00005537-200011000-00025 Trune DR, 1999, HEARING RES, V137, P167, DOI 10.1016/S0378-5955(99)00148-3 Trune DR, 1997, HEARING RES, V105, P57, DOI 10.1016/S0378-5955(96)00191-8 Trune DR, 1996, HEARING RES, V95, P57, DOI 10.1016/0378-5955(96)00018-4 TRUNE DR, 1989, HEARING RES, V38, P57, DOI 10.1016/0378-5955(89)90128-7 VANDERKRAAN PM, 1993, ANN RHEUM DIS, V52, P734, DOI 10.1136/ard.52.10.734 WADE JB, 1990, AM J PHYSIOL, V259, pF88 Whitlon DS, 2001, BRAIN RES PROTOC, V6, P159, DOI 10.1016/S1385-299X(00)00048-9 WILLIAMS GH, 1998, HARRISONS PRINCIPLES, P2035 WILSON WR, 1980, ARCH OTOLARYNGOL, V106, P772 Wobig RJ, 1999, OTOLARYNG HEAD NECK, V121, P344, DOI 10.1016/S0194-5998(99)70218-4 YOON YJ, 1994, ORL J OTO-RHINO-LARY, V56, P73 ZHOU NN, 1994, INT J IMMUNOPHARMACO, V16, P845 NR 59 TC 18 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 9 EP 20 DI 10.1016/S0378-5955(01)00240-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100002 PM 11335072 ER PT J AU Schneider, S Schoonhoven, R Prijs, VF AF Schneider, S Schoonhoven, R Prijs, VF TI Amplitude of distortion product otoacoustic emissions in the guinea pig in f(1)- and f(2)-sweep paradigms SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission amplitude; f(2)/f(1) ratio; guinea pig; f(1)-sweep; f(2)-sweep ID FINE-STRUCTURE; GROUP DELAYS; HUMANS; MECHANISMS; GENERATION; DPOAE; EAR; SUPPRESSION; DEPENDENCE; 2F(1)-F(2) AB The amplitude versus frequency relations of distortion product otoacoustic emissions (DPOAEs) were studied in the guinea pig, using both the f(1-) and the f(2)-sweep paradigms to vary the primary frequency separation. The amplitude of the DPOAEs 2f(1)-f(2), 3f(1)-2f(2), 4f(1)-3f(2), and 2f(2)-f(1), plotted as a function of DP frequency, exhibited a bandpass structure. The separation of the primaries for which the DPOAE level is maximum is referred to as the optimum ratio f(2)/f(1). For the lower sideband DPOAEs (f(dp) < f(1), f(2)), the optimum ratio varies non-monotonically with the primary frequency region. At an f(2) around 4.4 kHz, the optimum ratio for 2f(1) -f(2) reaches a maximum of about 1.46 while elsewhere it is in the more commonly found 1.2 1.3 range. The width of the amplitude profiles was studied by determining their Q(10dB). The f(2)-sweep yielded significantly larger Q(10dB) than f(1)-sweep, for the lower sideband DPOAEs. The amplitude versus frequency functions of the lower sideband DPOAEs approximately line up. Upon closer inspection, however, with fi-sweep the 2f(1)-f(2) DPOAE has its maximum at a slightly smaller DP frequency than the higher order DPOAEs. With f(2)-sweep, on the contrary, the 2f(1)-f(2) tends to peak at a higher DP frequency than the other lower sideband distortion products. When the amplitude is considered as a function of the ratio between f(dp) and f(2), the difference between f(1)- and f(2)-sweep with respect to the width and the alignment of the amplitude functions disappears. The amplitude profiles of the lower sideband DPOAEs are a function of the DPOAE frequency f(dp) relative to f(2). (C) 2001 Elsevier Science B.V. All rights reserved. C1 Leiden Univ, Med Ctr, Dept ENT Audiol, NL-2300 RC Leiden, Netherlands. RP Schneider, S (reprint author), Leiden Univ, Med Ctr, Dept ENT Audiol, POB 9600, NL-2300 RC Leiden, Netherlands. EM sandra_schnei@hotmail.com CR ALLEN JB, 1993, J ACOUST SOC AM, V94, P809, DOI 10.1121/1.408182 Bowman DM, 2000, HEARING RES, V142, P1, DOI 10.1016/S0378-5955(99)00212-9 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWN AM, 1993, BIOPHYSICS HAIR CELL, P72 BROWN AM, 1990, LECT NOTES BIOMATH, V87, P164 FAHEY PF, 1986, PERIPHERAL AUDITORY, P314 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 Heitmann J, 1998, J ACOUST SOC AM, V103, P1527, DOI 10.1121/1.421290 Kanis LJ, 1997, J ACOUST SOC AM, V101, P1527, DOI 10.1121/1.418173 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 Knight RD, 2000, J ACOUST SOC AM, V107, P457, DOI 10.1121/1.428351 LASKY RE, 1995, HEARING RES, V89, P35, DOI 10.1016/0378-5955(95)00120-1 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 Martin GK, 1998, J ACOUST SOC AM, V103, P1957, DOI 10.1121/1.421347 MATTHEWS JW, 1986, PERIPHERAL AUDITORY, P258 Moulin A, 1996, J ACOUST SOC AM, V100, P1640, DOI 10.1121/1.416064 Moulin A, 2000, J ACOUST SOC AM, V107, P1471, DOI 10.1121/1.428434 NEELY ST, 1997, DIVERSITY AUDITORY M, P434 Prijs VF, 2000, J ACOUST SOC AM, V107, P3298, DOI 10.1121/1.429402 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 Schneider S, 1999, J ACOUST SOC AM, V105, P2722, DOI 10.1121/1.426890 Shera CA, 1999, J ACOUST SOC AM, V105, P782, DOI 10.1121/1.426948 SMOORENBURG GF, 1976, J ACOUST SOC AM, V59, P945, DOI 10.1121/1.380954 Stover LJ, 1999, J ACOUST SOC AM, V106, P2669, DOI 10.1121/1.428097 Talmadge CL, 1999, J ACOUST SOC AM, V105, P275, DOI 10.1121/1.424584 Talmadge CL, 1998, J ACOUST SOC AM, V104, P1517, DOI 10.1121/1.424364 Taschenberger G, 1995, HEARING RES, V91, P87, DOI 10.1016/0378-5955(95)00174-3 TUBIS A, 2000, ABSTR ASS RES OT, V23, P139 VERSNEL H, 1990, HEARING RES, V46, P147, DOI 10.1016/0378-5955(90)90145-F WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 Wilson J., 1980, Proceedings of the Eighth Annual Canadian Conference on Information Science ZWICKER E, 1980, PSYCHOPHYSICAL PHYSL, P268 NR 34 TC 4 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 21 EP 31 DI 10.1016/S0378-5955(01)00239-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100003 PM 11335073 ER PT J AU Rybalko, N Syka, J AF Rybalko, N Syka, J TI Susceptibility to noise exposure during postnatal development in rats SO HEARING RESEARCH LA English DT Article DE noise exposure; young rat; evoked response; threshold shift; enhancement ID AUDITORY EVOKED-RESPONSES; AWAKE GUINEA-PIGS; INFERIOR COLLICULUS; ACOUSTIC TRAUMA; AUDIOGENIC-SEIZURE; OTOTOXICITY; STEREOCILIA; ENHANCEMENT; ENZYMES; HEARING AB Susceptibility to noise-induced hearing loss was studied during maturation in 70 female pigmented rats (strain Long Evans). Young rats, 3, 4, 5 and 6-7 weeks old, were exposed for 1 h to a broad-band noise with an intensity of 120 dB SPL. The thresholds and amplitudes of middle latency responses (MLR) recorded from electrodes implanted on the surface of the auditory cortex were analyzed before and after noise exposure. The results were compared with data from our previous study, in which the effects of broad-band noise exposure on MLR were investigated in adult rats [Syka, J. and Rybalko. N. (2000) Hear. Res. 139. 59-68]. The hearing thresholds of 3-7 week old rats before noise exposure M were within the normal adult range. Noise exposure in young rats produced an adult-like pattern with an elevation of hearing thresholds. One two weeks post-exposure a recovery of MLR thresholds was observed, though full recovery only occurred in the low frequency range. Recovery of hearing thresholds in the high. frequency range depended on the age of the animal at the time of exposure. In all animals aged less that 6-7 weeks. exposure resulted in a permanent threshold shift in the range of 4-32 kHz. The mean values of permanent threshold shifts :It 16 kHz (the frequency of maximal hearing loss) were 53.0 +/- 4.5, 47.6 +/- 9.6, 37.5 +/- 7.5 and 27 +/- 10 dB for rats exposed at 3, 4, 5 and 6-7 weeks of age, respectively. Similar to adult rats, young rats exposed to noise exhibited an enhancement of MLR amplitudes. This amplitude enhancement was more pronounced in the high frequency range. In several rats exposed at 35 weeks of age. the recovery period to normal amplitudes was substantially prolonged and lasted 4-8 weeks in comparison with 1 3 weeks in adult rats. These results demonstrate a greater susceptibility to noise exposure in rats during the first 5 postnatal weeks. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Acad Sci Czech Republ, Inst Expt Med, Prague 14220 4, Czech Republic. RP Rybalko, N (reprint author), Acad Sci Czech Republ, Inst Expt Med, Videnska 1083, Prague 14220 4, Czech Republic. RI Rybalko, Natalia/H-2629-2014; Syka, Josef/H-3103-2014 CR AGHAJANIAN G. K., 1967, BRAIN RES, V6, P716, DOI 10.1016/0006-8993(67)90128-X BILGER A, 1991, INT J DEV NEUROSCI, V9, P545, DOI 10.1016/0736-5748(91)90015-E BIRNHOLZ JC, 1983, SCIENCE, V222, P516, DOI 10.1126/science.6623091 Blatchley B J, 1987, Brain Res, V429, P75 BOCK GR, 1977, SCIENCE, V197, P396, DOI 10.1126/science.877565 CHEN CS, 1983, AUDITORY PSYCHOBIOLO, P426 CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O COLEMAN J W, 1976, Scandinavian Audiology, V5, P63, DOI 10.3109/01050397609043096 COYLE JT, 1976, BRAIN RES, V118, P429, DOI 10.1016/0006-8993(76)90310-3 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 FAINGOLD CL, 1986, ELECTROEN CLIN NEURO, V63, P296, DOI 10.1016/0013-4694(86)90097-0 FALK SA, 1974, LARYNGOSCOPE, V84, P444, DOI 10.1288/00005537-197403000-00008 Freeman S, 1999, AUDIOL NEURO-OTOL, V4, P207, DOI 10.1159/000013844 HENLEY CM, 1995, BRAIN RES REV, V20, P68, DOI 10.1016/0165-0173(94)00006-B HENRY KR, 1967, SCIENCE, V158, P938, DOI 10.1126/science.158.3803.938-a HUNTERDUVAR IM, 1977, SCANNING ELECT MICRO, V2, P421 IWASA H, 1982, OTOLARYNG HEAD NECK, V90, P95 JOHANSSON B, 1992, ACTA OBSTET GYN SCAN, V71, P610, DOI 10.3109/00016349209006229 Kriegstein A R, 1987, Brain Res, V431, P161 LALANDE NM, 1986, AM J IND MED, V10, P427, DOI 10.1002/ajim.4700100410 LENOIR M, 1980, ANAT EMBRYOL, V160, P253, DOI 10.1007/BF00305106 LENOIR M, 1979, J PHYSIOL-PARIS, V75, P521 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 MCCORMICK DA, 1987, J PHYSIOL-LONDON, V393, P743 MOUREK JINDRICK, 1967, BRAIN RES, V6, P241, DOI 10.1016/0006-8993(67)90194-1 MU MY, 1992, ACTA OTO-LARYNGOL, V112, P618, DOI 10.3109/00016489209137450 PICKLES JO, 1987, HEARING RES, V25, P177 PIERSON M, 1994, BRAIN RES, V636, P55, DOI 10.1016/0006-8993(94)90175-9 PIERSON MG, 1991, EPILEPSIA, V32, P1, DOI 10.1111/j.1528-1157.1991.tb05602.x POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 PRICE GR, 1976, J ACOUST SOC AM, V60, P886, DOI 10.1121/1.381169 PUEL JL, 1999, COCHLEAR PHARM NOISE, P1 Ross KC, 1999, DEV PSYCHOBIOL, V34, P303, DOI 10.1002/(SICI)1098-2302(199905)34:2<303::AID-DEV6>3.0.CO;2-X ROTH B, 1992, ANAT EMBRYOL, V185, P571, DOI 10.1007/BF00185616 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 SALVI RJ, 1999, NOISE HLTH, V2, P28 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SAUNDERS JC, 1972, EXP NEUROL, V37, P388, DOI 10.1016/0014-4886(72)90082-9 Syka J, 2000, HEARING RES, V139, P59, DOI 10.1016/S0378-5955(99)00175-6 Syka J, 1989, PROGR SENSORY PHYSL, V9, P97 SYKA J, 1994, HEARING RES, V78, P158, DOI 10.1016/0378-5955(94)90021-3 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 UZIEL A, 1981, AUDIOLOGY, V20, P89 Whitlon DS, 1999, HEARING RES, V137, P43, DOI 10.1016/S0378-5955(99)00136-7 WILLOTT JF, 1974, J COMP PHYSIOL PSYCH, V86, P1, DOI 10.1037/h0035922 Yamasoba T, 1998, BRAIN RES, V784, P82, DOI 10.1016/S0006-8993(97)01156-6 ZELCK U, 1993, EUR ARCH OTO-RHINO-L, V250, P218 NR 49 TC 21 Z9 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 32 EP 40 DI 10.1016/S0378-5955(01)00245-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100004 PM 11335074 ER PT J AU Glasberg, BR Moore, BCJ Peters, RW AF Glasberg, BR Moore, BCJ Peters, RW TI The influence of external and internal noise on the detection of increments and decrements in the level of sinusoids SO HEARING RESEARCH LA English DT Article DE increment detection; decrement detection; noise ID GAP DETECTION; FREQUENCY-MODULATION; UNRESOLVED HARMONICS; AMPLITUDE-MODULATION; INTENSITY DISCRIMINATION; PSYCHOMETRIC FUNCTIONS; CARRIER FREQUENCY; SIGNAL FREQUENCY; TEMPORAL WINDOW; AUDITORY-NERVE AB This paper examines the influence of external and internal noise on the detection of increments and decrements in the level of sinusoidal pedestals. In experiment 1, the pedestals were presented either 18 dB above the masked threshold in broadband noise (condition 18-Masked) or 18 dB above the absolute threshold (condition 18-Abs). Pedestal frequencies were 250. 1000 or 4000 Hz, and increment/decrement durations ranged from 5 to 200 ms. For condition 18-Masked, thresholds decreased with increasing pedestal frequency, while for condition 18-Abs, thresholds did not change significantly with pedestal frequency. These results are consistent with the idea that, in condition 18-Masked, thresholds were influenced by the inherent fluctuations produced by the background noise at the output of the auditory filter centred at the pedestal frequency. These fluctuations would decrease in rate with decreasing centre frequency, and this might hac e a greater deleterious effect on performance. In contrast, the characteristics of the internal noise that presumably limited performance in condition Is-Abs do not appear to vary with pedestal frequency. In experiment 2, a 4000 Hz pedestal was used. It was presented either in quiet or in the presence of narrow band noise centred at 4000, or 7000 Hz, or both. The noise bandwidth ranged from 50 to 400 Hz. The increment/decrement duration ranged from 5 to 100 ms. The noise centred at 7000 Hz produced only a small deterioration in performance relative to that measured in quiet. The noise centred at 4000 Hz had a larger effect, and the effect increased with decreasing noise bandwidth. This is consistent with the idea that slow fluctuations at the output of the auditory filter impair increment and decrement detection more than rapid fluctuations, A model is proposed to account for the results, based on a simulated auditory filter, a compressive non-linearity, a sliding temporal integrator, a logarithmic transform and a template mechanism. Analysis using the model suggests that the effect of centre frequency observed in experiment 1, when background noise was present, cannot be explained entirely in terms of the fluctuations produced by the background noise at the output of the auditory filter centred at the pedestal frequency. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ N Carolina, Sch Med, Dept Med Allied Hlth Profess, Div Speech & Hearing Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA. RP Moore, BCJ (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. RI Moore, Brian/I-5541-2012 CR BACON SP, 1986, HEARING RES, V23, P257, DOI 10.1016/0378-5955(86)90114-0 BACON SP, 1985, J ACOUST SOC AM, V78, P1220, DOI 10.1121/1.392890 BACON SP, 1985, J ACOUST SOC AM, V78, P1231, DOI 10.1121/1.392891 BUUS S, 1991, J ACOUST SOC AM, V90, P1371, DOI 10.1121/1.401928 CARLYON RP, 1994, J ACOUST SOC AM, V95, P3541, DOI 10.1121/1.409971 CARLYON RP, 1986, J ACOUST SOC AM, V79, P453, DOI 10.1121/1.393759 Dau T, 1996, J ACOUST SOC AM, V99, P3615, DOI 10.1121/1.414959 de Boer E., 1986, AUDITORY FREQUENCY S, P429 Eddins David A., 1995, P207, DOI 10.1016/B978-012505626-7/50008-X EDDINS DA, 1992, J ACOUST SOC AM, V91, P1069, DOI 10.1121/1.402633 FITZGIBBONS PJ, 1983, J ACOUST SOC AM, V74, P67, DOI 10.1121/1.389619 FLORENTINE M, 1981, J ACOUST SOC AM, V70, P1646, DOI 10.1121/1.387219 FORREST TG, 1987, J ACOUST SOC AM, V82, P1933, DOI 10.1121/1.395689 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T GLASBERG BR, 1992, HEARING RES, V64, P81, DOI 10.1016/0378-5955(92)90170-R Gockel H, 2001, J ACOUST SOC AM, V109, P701, DOI 10.1121/1.1342073 GREEN DM, 1979, J ACOUST SOC AM, V66, P1051, DOI 10.1121/1.383324 GROSE JH, 1989, J ACOUST SOC AM, V86, P1747, DOI 10.1121/1.398606 JEFFRESS LA, 1975, J ACOUST SOC AM, V58, P399, DOI 10.1121/1.380683 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 LAWSON JL, 1950, RAD LAB SERIES, V25 LESHOWIT.B, 1967, J ACOUST SOC AM, V41, P489, DOI 10.1121/1.1910359 MOORE BCJ, 1994, J ACOUST SOC AM, V96, P741, DOI 10.1121/1.410312 Moore BCJ, 1996, J ACOUST SOC AM, V100, P2320, DOI 10.1121/1.417941 Moore BCJ, 1996, J ACOUST SOC AM, V99, P3669, DOI 10.1121/1.414964 MOORE BCJ, 1993, J ACOUST SOC AM, V94, P3190, DOI 10.1121/1.407224 Moore BCJ, 1997, J ACOUST SOC AM, V102, P2954, DOI 10.1121/1.420350 Moore BCJ, 1999, J ACOUST SOC AM, V106, P3539, DOI 10.1121/1.428207 MOORE BCJ, 1988, J ACOUST SOC AM, V83, P1102, DOI 10.1121/1.396055 MOORE BCJ, 1995, J ACOUST SOC AM, V97, P2468, DOI 10.1121/1.411967 Nelson DA, 1996, J ACOUST SOC AM, V100, P2266, DOI 10.1121/1.417936 Oxenham AJ, 1997, J ACOUST SOC AM, V102, P1779, DOI 10.1121/1.420086 OXENHAM AJ, 1994, HEARING RES, V80, P105, DOI 10.1016/0378-5955(94)90014-0 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X PATTERSON RD, 1995, J ACOUST SOC AM, V98, P1890, DOI 10.1121/1.414456 PETERS RW, 1995, J ACOUST SOC AM, V97, P3791, DOI 10.1121/1.412394 PLACK CJ, 1990, J ACOUST SOC AM, V87, P2178, DOI 10.1121/1.399185 PLACK CJ, 1995, J ACOUST SOC AM, V98, P1355, DOI 10.1121/1.413471 PLACK CJ, 1991, J ACOUST SOC AM, V90, P3069, DOI 10.1121/1.401781 Rice S. O., 1954, SELECTED PAPERS NOIS, P133 SCHWARTZ M, 1970, INFORMATION TRANSMIS Sek A, 1999, J ACOUST SOC AM, V106, P351, DOI 10.1121/1.427061 Sek A, 2000, J ACOUST SOC AM, V107, P1598, DOI 10.1121/1.428444 SHACKLETON TM, 1994, J ACOUST SOC AM, V95, P3529, DOI 10.1121/1.409970 SHAILER MJ, 1983, J ACOUST SOC AM, V74, P467, DOI 10.1121/1.389812 SHAILER MJ, 1985, J ACOUST SOC AM, V77, P635, DOI 10.1121/1.391881 Snedecor G. W., 1967, STAT METHODS SNELL KB, 1994, J ACOUST SOC AM, V96, P1458, DOI 10.1121/1.410288 YOST WA, 1989, J ACOUST SOC AM, V86, P2138, DOI 10.1121/1.398474 YOST WA, 1989, J ACOUST SOC AM, V85, P848, DOI 10.1121/1.397556 Zeng FG, 1999, NEUROREPORT, V10, P1931, DOI 10.1097/00001756-199906230-00025 Zeng FG, 1998, NEUROREPORT, V9, P1845, DOI 10.1097/00001756-199806010-00033 Zwicker E., 1952, ACUSTICA S3, V2, P125 NR 53 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 41 EP 53 DI 10.1016/S0378-5955(01)00244-1 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100005 PM 11335075 ER PT J AU Pickles, JO AF Pickles, JO TI The expression of fibroblast growth factors and their receptors in the embryonic and neonatal mouse inner ear SO HEARING RESEARCH LA English DT Article DE fibroblast growth factor; fibroblast growth factor receptor; FGF3; FGF8; cochlea; development; mouse; otocyst ID RAT COCHLEA; CHICK COCHLEA; HAIR-CELLS; REGENERATION; GENE; REGIONS; PATTERN; FAMILY; FGF-3; MICE AB Four different fibroblast growth factor receptors (FGFR) are known, three of which have splice variants (known as the b and c variants) in the FGF-binding domain, to give different patterns of sensitivity to the different FGFs. The expression of the b and c variants of the FGF receptors. together with the expression of the ligands FGF1. FGF2, FGF3, FGF7, FGF8b and FGF8c, was determined by quantitative reverse transcription-polymerase chain reaction in developing whole mouse inner ears, and in dissected components of the postnatal mouse inner ear. At embryonic age (E)10.5 days, when the otocyst is a simple closed sac, the receptor most heavily expressed was FGFR2b, relative to the postnatal day 0 level. Over the period E10.5-E12.5. during which the structures of the inner ear start to form, the expression of the different FGF receptors increased 10(2)-10(4) fold per unit of tissue, and there was a gradual switch towards expression of the 'c' splice variants of FGFR2 and FGFR3 rather than the 'b' variants. At E10.5, the ligands most heavily expressed, relative to the postnatal day 0 level, were FGF3, FGF8b and FGF8c. In the postnatal inner eat. the patterns of expression of receptors and ligands tended to be correlated, such that receptor variants were expressed in the same regions as the ligands that are known to activate them effectively. The neural/sensory region expressed high levels of FGFR3c, and high levels of the ligand FGF8b. The same area also expressed high levels of FGFR1b and FGFR2b, and high levels of FGF3. The lateral wall of the cochlea (including the stria vascularis and the spiral ligament) expressed high levels of FGFR1c and FGF1. 11 is suggested that the different FGF receptors and ligands are expressed in a spatially coordinated pattern to selectively program cochlear development. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. RP Pickles, JO (reprint author), Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. CR Baird Andrew, 1994, Current Opinion in Neurobiology, V4, P78, DOI 10.1016/0959-4388(94)90035-3 BERMINGHAMMCDON.O, 1998, ASS RES OT ABSTR, V21, P167 Colvin JS, 1996, NAT GENET, V12, P390, DOI 10.1038/ng0496-390 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 CROSSLEY PH, 1995, DEVELOPMENT, V121, P439 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 KINOSHITA T, 1992, ANAL BIOCHEM, V206, P231, DOI 10.1016/0003-2697(92)90358-E Lee KH, 1996, HEARING RES, V94, P1, DOI 10.1016/0378-5955(95)00220-0 LUO L, 1993, HEARING RES, V69, P182 MACARTHUR CA, 1995, DEVELOPMENT, V121, P3603 MANSOUR SL, 1994, MOL REPROD DEV, V39, P62, DOI 10.1002/mrd.1080390111 McKay IJ, 1996, DEV BIOL, V174, P370, DOI 10.1006/dbio.1996.0081 Nagler JJ, 2000, J MOL ENDOCRINOL, V25, P243, DOI 10.1677/jme.0.0250243 Oesterle EC, 2000, J COMP NEUROL, V424, P307, DOI 10.1002/1096-9861(20000821)424:2<307::AID-CNE9>3.0.CO;2-M Ornitz DM, 1996, J BIOL CHEM, V271, P15292 ORRURTREGER A, 1993, DEV BIOL, V158, P475, DOI 10.1006/dbio.1993.1205 PETERS K, 1993, DEV BIOL, V155, P423, DOI 10.1006/dbio.1993.1040 Pickles JO, 1997, DEV NEUROSCI-BASEL, V19, P476, DOI 10.1159/000111245 Pickles JO, 1998, NEUROREPORT, V9, P4093, DOI 10.1097/00001756-199812210-00016 PIRVOLA U, 1995, P NATL ACAD SCI USA, V92, P9269, DOI 10.1073/pnas.92.20.9269 PIRVOLA U, 1998, ASS RES OT ABSTR, V21, P665 Pirvola U, 2000, J NEUROSCI, V20, P6125 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 WILKINSON DG, 1989, DEVELOPMENT, V105, P131 NR 24 TC 26 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 54 EP 62 DI 10.1016/S0378-5955(01)00247-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100006 PM 11335076 ER PT J AU Cohen, LT Saunders, E Clark, GM AF Cohen, LT Saunders, E Clark, GM TI Psychophysics of a prototype peri-modiolar cochlear implant electrode array SO HEARING RESEARCH LA English DT Article DE cochlear implant; peri-modiolar electrode array; spread of neural excitation; electrode discrimination; forward masking; loudness growth ID ELECTRICALLY STIMULATED COCHLEA; NORMAL-HEARING LISTENERS; AUDITORY-NERVE; SPEECH RECOGNITION; INTENSITY DISCRIMINATION; EXCITATION PATTERNS; NEURAL EXCITATION; PITCH PERCEPTION; INSERTION TRAUMA; MODEL AB Psychophysical measurements were performed in three hearing-impaired adult subjects: implanted with a CI22 cochlear prosthesis (Cochlear Ltd.) fitted with a developmental peri-modiolar electrode array. The array was manufactured with a curvature approximating that of the inner wall of the scala tympani but, after straightening and insertion, lay on average about half way between the inner and outer walls of the scala. All subjects were tested with bipolar stimulation; two were also tested with monopolar, employing the must basal electrode as the return. Maximum comfortable level and threshold reduced with decreasing distance of electrode from the modiolus, whereas dynamic range increased. The linearity of the loudness growth function did not vary significantly with electrode position but the function was more non-linear for lower maximum comfortable levels. Current level discrimination, normalized with respect to dynamic range, improved with decreasing distance of electrode from the modiolus in two subjects. Pitch varied regularly with insertion depth of the stimulated electrode for bipolar stimulation in two subjects and also for monopolar stimulation in one subject. Electrode discrimination was enhanced by closeness to the modiolus. Whereas the forward masking patterns for bipolar stimulation of electrodes close to the modiolus had a sharp double-peaked structure, those for monopolar stimulation were flatter and had a single peak. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Dept Otolaryngol, Cooperat Res Ctr Cochlear Implant & Hearing Aid I, Melbourne, Vic 3002, Australia. RP Cohen, LT (reprint author), Univ Melbourne, Dept Otolaryngol, Cooperat Res Ctr Cochlear Implant & Hearing Aid I, 384-388 Albert St, Melbourne, Vic 3002, Australia. EM l.cohen@medoto.unimelb.edu.au CR BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 Blamey P. J., 1995, Annals of Otology Rhinology and Laryngology, V104, P220 BROWN M, 1992, HEARING RES, V59, P224, DOI 10.1016/0378-5955(92)90119-8 Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P617, DOI 10.1109/10.764938 BUSBY PA, 1994, J ACOUST SOC AM, V95, P2658, DOI 10.1121/1.409835 CARHART R, 1959, J SPEECH HEAR DISORD, V24, P330 Chatterjee M, 1999, J ACOUST SOC AM, V105, P850, DOI 10.1121/1.426274 Cohen L T, 1996, Audiol Neurootol, V1, P278 COHEN LT, 1994, INT COCHL IMPL SPEEC, P60 Cohen LT, 1996, AM J OTOL, V17, P859 Cohen L T, 1996, Audiol Neurootol, V1, P265 COHEN LT, 1999, C IMPL AUD PROTH ASL Donaldson GS, 1997, J ACOUST SOC AM, V101, P3706, DOI 10.1121/1.418330 DONNELLY MJ, 1995, ANN OTOL RHINOL S166, V1084, P409 Dorman M., 1997, AM J OTOL, V18, P113 DORMAN MF, 1990, EAR HEARING, V11, P310, DOI 10.1097/00003446-199008000-00010 Dorman MF, 1998, J ACOUST SOC AM, V104, P3583, DOI 10.1121/1.423940 EDDINGTON DK, 1980, J ACOUST SOC AM, V68, P885, DOI 10.1121/1.384827 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FINLEY CC, 1991, C IMPL AUD PROTH PAC Fishman KE, 1997, J SPEECH LANG HEAR R, V40, P1201 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q Frijns JHM, 1996, HEARING RES, V95, P33, DOI 10.1016/0378-5955(96)00004-4 Fu QJ, 1998, J ACOUST SOC AM, V104, P3586, DOI 10.1121/1.423941 Fu QJ, 1998, J ACOUST SOC AM, V104, P2570, DOI 10.1121/1.423912 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HARTMANN R, 1987, ANN OTO RHINOL LARYN, V96, P30 Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HINOJOSA R, 1983, ANN NY ACAD SCI, V405, P459, DOI 10.1111/j.1749-6632.1983.tb31662.x HINOJOSA R, 1980, ARCH OTOLARYNGOL, V106, P193 Huang CQ, 1999, IEEE T BIO-MED ENG, V46, P461, DOI 10.1109/10.752943 Kawano A, 1998, ACTA OTO-LARYNGOL, V118, P313 KENNEDY DW, 1987, LARYNGOSCOPE, V97, P42 LEAKE PA, 1998, 4 EUR S PAED COCHL I LEAKE PA, 1993, 16 ANN MIDW RES M AS Liang DH, 1999, IEEE T BIO-MED ENG, V46, P35, DOI 10.1109/10.736751 LIM HH, 1989, J ACOUST SOC AM, V86, P971, DOI 10.1121/1.398732 LUSTED HS, 1980, THESIS STANFORD U ST MARSH MA, 1993, AM J OTOL, V14, P386 MERZENICH MM, 1977, FUNCTIONAL ELECT STI, P321 NADOL JB, 1979, OTOLARYNG HEAD NECK, V87, P818 Nelson DA, 1996, J ACOUST SOC AM, V100, P2393, DOI 10.1121/1.417949 PFINGST BE, 1983, J ACOUST SOC AM, V73, P1283, DOI 10.1121/1.389277 Pfingst BE, 1997, HEARING RES, V112, P247, DOI 10.1016/S0378-5955(97)00122-6 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L SAPOZHNIKOV A, 1990, THESIS U MELBOURNE A SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHEPHERD R, 1997, COCHLEAR IMPLANTS, P205 SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 SHEPHERD RK, 1990, NEUROL NEUR, V56, P281 SHEPHERD RK, 1985, ANN OTO RHINOL LARYN, V94, P55 Stevens S. S., 1940, AM J PSYCHOL, V53, P329, DOI 10.2307/1417526 STEVENS SS, 1957, J EXP PSYCHOL, V54, P377, DOI 10.1037/h0043680 TAYLOR MM, 1967, J ACOUST SOC AM, V41, P782, DOI 10.1121/1.1910407 TOWNSHEND B, 1987, J ACOUST SOC AM, V82, P106, DOI 10.1121/1.395554 Treaba C. G., 1995, Annals of Otology Rhinology and Laryngology, V104, P438 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VONWALLENBERG EL, 1994, ADV COCHLEAR IMPLANT, P186 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 Xu J, 2000, AM J OTOL, V21, P49, DOI 10.1016/S0196-0709(00)80112-X XU SA, 1993, AUST J OTOLARYNGOL, V1, P276 ZENG FG, 1992, HEARING RES, V60, P213 NR 62 TC 61 Z9 63 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 63 EP 81 DI 10.1016/S0378-5955(01)00248-9 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100007 PM 11335077 ER PT J AU Davis, RR Newlander, JK Ling, XB Cortopassi, GA Krieg, EF Erway, LC AF Davis, RR Newlander, JK Ling, XB Cortopassi, GA Krieg, EF Erway, LC TI Genetic basis for susceptibility to noise-induced hearing loss in mice SO HEARING RESEARCH LA English DT Article DE mouse; noise-induced; age-related; hearing loss; genetic ID INBRED STRAINS; DEAFNESS AB The C57BL/6J (B6) and DBA/2J (D2) inbred strains of mice exhibit an age-related hearing loss (AHL) due to a recessive gene (Ahl) that maps to Chromosome 10. The Ahl gene is also implicated in the susceptibility to noise-induced hearing loss (NIHL). The B6 mice (AhllAhl) are more susceptible to NIHL than the CBA/CaJ (CB) mice (+(Ahl)). The B6 x D2.F-1 hybrid mice (AhllAhl) are more susceptible to NIHL than the CB x B6.F-1 mice (+/Ahl) [Erway et al., 1996. Hear. Res. 93, 181-187]. These genetic effects implicate the Ahl gene as contributing to NIHL susceptibility. The present study demonstrates segregation for the putative Ahl gene and mapping of such a gene to Chromosome 10, consistent with other independent mapping of. Ahl for AHL in 10 strains of mice [Johnson et al., 2000. Genomics 70, 171-180]. The present study was based on a conventional cross between two inbred strains, CB x B6.F-1 backcrossed to B6 with segregation for the putative +/Ahl:AhllAhl. These backcross progeny were exposed to 110 dB SPL noise for 8 h. All of the progeny were tested for auditory evoked brainstem responses and analyzed for any significant permanent threshold shift of NIHL. Cluster analyses were used to distinguish the two putative genotypes, the. least affected with NIHL (+/Ahl) and most affected with PTS (AhllAhl). Approximately 1/2 of the backcross progeny exhibited PTS, particularly at 16 kHz. These mice were genotyped for two D10Mit markers. Quantitative trait loci analyses (log of the odds = 15) indicated association of the genetic factor within a few centiMorgan of the best evidence for Ahl [Johnson ct al., 2000. Genomics 70, 171-180], All of the available evidence supports a role for the Ahl gene in both AHL and NIHL among these strains of mice. (C) 2001 Elsevier Science B.V. All rights reserved. C1 NIOSH, Hearing Loss Prevent Sec, Engn & Phys Hazards Branch, Div Appl Res & Technol,Ctr Dis Control & Prevent, Cincinnati, OH 45226 USA. NIOSH, Monitoring Res & Stat Act, Div Appl Res & Technol, Ctr Dis Control & Prevent, Cincinnati, OH 45226 USA. Univ Cincinnati, Dept Biol Sci, Cincinnati, OH 45221 USA. Univ So Calif, Sch Med, Dept Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA. Univ Calif Davis, Dept Mol Biosci, Davis, CA 95616 USA. RP Davis, RR (reprint author), NIOSH, Hearing Loss Prevent Sec, Engn & Phys Hazards Branch, Div Appl Res & Technol,Ctr Dis Control & Prevent, Mailstop C-27,4676 Columbia Pkwy, Cincinnati, OH 45226 USA. RI Davis, Rickie/A-3186-2008 CR BLIN N, 1976, NUCLEIC ACIDS RES, V3, P2303 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X Davis RR, 1999, HEARING RES, V134, P9, DOI 10.1016/S0378-5955(99)00060-X DAVIS RR, 1989, J ACOUST SOC AM, V58, P963 DAVIS RR, 2001, HDB MOUSE AUDITORY R Di Palma F, 2001, NAT GENET, V27, P103 ERWAY LC, 1993, HEARING RES, V65, P123 Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X Fay R. R., 1988, HEARING VERTEBRATES Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X Johnson KR, 2000, GENOMICS, V70, P171, DOI 10.1006/geno.2000.6377 KOZEL PJ, 2001, 24 MIDW M ASS RES OT LING XB, 1995, ASS RES OT MIDW M NEWLANDER JK, 1995, ASS RES OT MIDW M NobenTrauth K, 1997, GENOMICS, V44, P266, DOI 10.1006/geno.1997.4869 Simpson EM, 1997, NAT GENET, V16, P19, DOI 10.1038/ng0597-19 Street VA, 1998, NAT GENET, V19, P390 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 Threadgill DW, 1997, MAMM GENOME, V8, P390, DOI 10.1007/s003359900453 Yoshida N, 2000, HEARING RES, V141, P97, DOI 10.1016/S0378-5955(99)00210-5 Zheng QY, 1999, HEARING RES, V130, P94, DOI 10.1016/S0378-5955(99)00003-9 NR 21 TC 71 Z9 83 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 82 EP 90 DI 10.1016/S0378-5955(01)00250-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100008 PM 11335078 ER PT J AU Henry, KR Lewis, ER AF Henry, KR Lewis, ER TI Cochlear nerve acoustic envelope response detection is improved by the addition of random-phased tonal stimuli SO HEARING RESEARCH LA English DT Article DE stochastic resonance; phase locking; dithering; Ac response; Dc response ID STOCHASTIC RESONANCE; TUNING CURVES; SIGNAL-TRANSDUCTION; MONGOLIAN GERBIL; NOISE; SUPPRESSION; INFORMATION; MECHANORECEPTORS; TRANSMISSION; ENHANCEMENT AB We test Lowenstein's de bias hypothesis as an alternative mechanism for the phenomenon sometimes called 'stochastic resonance'. Probe stimuli consisting of paired phase-locked tones at frequencies f(1) and f(2) (where f(2)-f(1) = 800 Hz, f(1) > 4.5 kHz) and at equal intensity were used to generate synchronous 800 Hz cochlear nerve activity (envelope responses). When a background tone of the same intensity, with a frequency halfway between f(1) and f(2), is presented simultaneously with the probe stimulus, the envelope response amplitude typically decreases. Consistent with Lowenstein's hypothesis, however, when the intensities of the probe and background tone are near the detection threshold of the envelope response (approximately 0-20 dB sound pressure level), the simultaneous presence of the background tone often increases the amplitude of the envelope response. At these same intensity levels, when the background tone precedes the probe stimulus, it decreases the amplitude of the response to the probe stimulus. The effects of simultaneous presentation of the probe and the background tone are frequency-dependent. becoming less pronounced or reversing as the frequency of the background tone departs from those of the probe stimuli. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif Davis, Dept Psychol, Davis, CA 95616 USA. Univ Calif Berkeley, Dept Elect Engn & Comp Sci, Berkeley, CA 94720 USA. RP Henry, KR (reprint author), Univ Calif Davis, Dept Psychol, Davis, CA 95616 USA. CR AGIN D, 1964, NATURE, V201, P625, DOI 10.1038/201625a0 BRAUN HA, 1994, NATURE, V367, P270, DOI 10.1038/367270a0 Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P1393, DOI 10.1109/10.804567 CHIALVO DR, 1993, J STAT PHYS, V70, P375, DOI 10.1007/BF01053974 Collins JJ, 1996, J NEUROPHYSIOL, V76, P642 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DALLOS P, 1977, J ACOUST SOC AM, V62, P1048, DOI 10.1121/1.381598 DEBOER E, 1978, J ACOUST SOC AM, V63, P115, DOI 10.1121/1.381704 DOUGLASS JK, 1993, NATURE, V365, P337, DOI 10.1038/365337a0 Ehrenberger K, 1999, ACTA OTO-LARYNGOL, V119, P166 FAUVE S, 1983, PHYS LETT A, V97, P5, DOI 10.1016/0375-9601(83)90086-5 FRENCH AS, 1970, IEEE T BIO-MED ENG, VBM17, P248, DOI 10.1109/TBME.1970.4502739 GOLDBERG JM, 1971, J NEUROPHYSIOL, V34, P635 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 GREENWOOD DD, 1986, J ACOUST SOC AM, V79, P1857, DOI 10.1121/1.393194 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 Henry KR, 1999, J COMP PHYSIOL A, V184, P577, DOI 10.1007/s003590050357 Henry KR, 1996, HEARING RES, V99, P151, DOI 10.1016/S0378-5955(96)00096-2 HENRY KR, 1995, HEARING RES, V90, P176, DOI 10.1016/0378-5955(95)00162-6 HENRY KR, 1992, HEARING RES, V63, P1, DOI 10.1016/0378-5955(92)90066-V Henry KR, 1996, HEARING RES, V99, P160, DOI 10.1016/S0378-5955(96)00097-4 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 Jaramillo F, 1998, NAT NEUROSCI, V1, P384, DOI 10.1038/1597 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 Kiang NY-s, 1965, DISCHARGE PATTERNS S Lewis ER, 1995, HEARING RES, V92, P1, DOI 10.1016/0378-5955(95)00189-1 LEWIS ER, 2001, ANN MIDW M ASS RES O, V24, P102 LONGTIN A, 1991, PHYS REV LETT, V67, P656, DOI 10.1103/PhysRevLett.67.656 LOWENSTEIN O, 1956, BRIT MED BULL, V12, P114 MADDOX J, 1991, NATURE, V352, P469 Morse RP, 1996, NAT MED, V2, P928, DOI 10.1038/nm0896-928 Morse RP, 1999, HEARING RES, V133, P107, DOI 10.1016/S0378-5955(99)00062-3 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RUBENSTEIN JT, 1999, HEARING RES, V127, P108 RUSSELL IJ, 1978, J PHYSL, V338, P176 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 Simonotto E, 1997, PHYS REV LETT, V78, P1186, DOI 10.1103/PhysRevLett.78.1186 STEIN RB, 1967, PROC R SOC SER B-BIO, V167, P64, DOI 10.1098/rspb.1967.0013 Stein RB, 1970, NEUROSCIENCES, P597 STEIN RB, 1972, BIOPHYS J, V12, P295 VANDERKOOY J, 1984, J AUDIO ENG SOC, V32, P106 Weisenfeld K., 1995, NATURE, V373, P33 WOLODKIN G, 1996, DIVERSITY AUDITORY M, P104 Yamada WM, 1999, HEARING RES, V130, P155, DOI 10.1016/S0378-5955(99)00005-2 YAMADA WM, 1996, DIVERSITY AUDITORY M, P111 YU XL, 1989, IEEE T BIO-MED ENG, V36, P36, DOI 10.1109/10.16447 ZENNER HP, 1993, BRIT J AUDIOL, V27, P73, DOI 10.3109/03005369309077894 NR 47 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 91 EP 102 DI 10.1016/S0378-5955(01)00251-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100009 PM 11335079 ER PT J AU Takeuchi, S Ando, M Sato, T Kakigi, A AF Takeuchi, S Ando, M Sato, T Kakigi, A TI Three-dimensional and ultrastructural relationships between intermediate cells and capillaries in the gerbil stria vascularis SO HEARING RESEARCH LA English DT Article DE melanocyte; confocal laser microscopy; electron microscopy; gap junction; K+ channel; spatial K+ buffering ID ION-TRANSPORT; INNER-EAR; COCHLEA; MELANOCYTES; POTASSIUM; PIGMENTATION; MECHANISMS; PERFUSION; CLEARANCE; MOUSE AB Structural relationships between intermediate cells and capillaries in the stria vascularis of gerbils were examined by confocal laser microscopy and electron microscopy. Immunustaining for an inward rectifier K+ channel (Kir4.1), which was localized to intermediate cells, was used to determine the three-dimensional distribution of intermediate cells. These cells constituted a honeycomb-like network, and their dendritic processes surrounded not only capillaries but also the basolateral surface of epithelial marginal cells. On the basis of the above finding and the large K+ conductance in intermediate cells, M e propose that the network composed of intermediate cells has a spatial K+ buffering function. Transmission electron microscopy revealed the absence of the basal lamina in some regions and the presence of a gap junction-like membrane association between intermediate cells and pericytes: and/or endothelial cells. This: result supported our previous finding that intermediate cells were dye-coupled with pericytes and endothelial cells. The presence of gap junctions between intermediate cells and pericytes and/or endothelial cells suggests that endothelial cells and pericytes may play roles other than forming a structural route for blood circulation. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Kochi Med Sch, Dept Physiol, Nankoku, Kochi 7838505, Japan. Kochi Med Sch, Dept Otolaryngol, Nankoku, Kochi 7838505, Japan. RP Takeuchi, S (reprint author), Kochi Med Sch, Dept Physiol, Nankoku, Kochi 7838505, Japan. CR Ando M, 1998, HEARING RES, V123, P148, DOI 10.1016/S0378-5955(98)00109-9 Ando M, 1999, CELL TISSUE RES, V298, P179, DOI 10.1007/s004419900066 CABLE J, 1994, PIGM CELL RES, V7, P17, DOI 10.1111/j.1600-0749.1994.tb00015.x Fawcett D. W., 1994, TXB HISTOLOGY Hashimoto H, 1997, CONNECT TISSUE RES, V36, P63, DOI 10.3109/03008209709160214 HILDING DA, 1977, ACTA OTO-LARYNGOL, V84, P24, DOI 10.3109/00016487709123939 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KIMURA RS, 1970, ACTA OTO-LARYNGOL, V69, P415, DOI 10.3109/00016487009123387 KIMURA RS, 1974, ACTA OTO-LARYNGOL, V77, P231 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 MARCUS DC, 1985, HEARING RES, V17, P79, DOI 10.1016/0378-5955(85)90133-9 MARCUS DC, 1981, HEARING RES, V4, P149, DOI 10.1016/0378-5955(81)90002-2 ORKAND RK, 1966, J NEUROPHYSIOL, V29, P788 REICHENBACH A, 1991, ANN NY ACAD SCI, V633, P272 SALT AN, 1987, LARYNGOSCOPE, V97, P984 Slepecky N. B., 1996, COCHLEA, P44 STEEL KP, 1989, DEVELOPMENT, V107, P453 Takeuchi S, 1998, NEUROSCI LETT, V247, P175, DOI 10.1016/S0304-3940(98)00318-8 Takeuchi S, 1996, HEARING RES, V101, P181, DOI 10.1016/S0378-5955(96)00151-7 Takeuchi S, 2000, BIOPHYS J, V79, P2572 Takeuchi S, 1999, AM J PHYSIOL-CELL PH, V277, pC91 Takeuchi S, 1998, CELL TISSUE RES, V293, P271, DOI 10.1007/s004410051118 Walz W, 2000, NEUROCHEM INT, V36, P291, DOI 10.1016/S0197-0186(99)00137-0 Wangemann P., 1996, COCHLEA, P130 NR 25 TC 24 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 103 EP 112 DI 10.1016/S0378-5955(01)00252-0 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100010 PM 11335080 ER PT J AU Cetas, JS Price, RO Velenovsky, DS Sinex, DG McMullen, NT AF Cetas, JS Price, RO Velenovsky, DS Sinex, DG McMullen, NT TI Frequency organization and cellular lamination in the medial geniculate body of the rabbit SO HEARING RESEARCH LA English DT Article DE hearing; thalamus; inferior colliculus; pitch coding; tonotopicity ID PRIMARY AUDITORY-CORTEX; INFERIOR COLLICULUS; FUNCTIONAL-ORGANIZATION; RESPONSE PROPERTIES; TONOTOPIC ORGANIZATION; MOUSTACHED BAT; SINGLE UNITS; GUINEA-PIG; CAT; THALAMUS AB Cellular laminae within the tonotopically organized ventral division of the medial geniculate body (MGV) of the cat have been proposed as the anatomical substrate for physiologically defined isofrequency contours. In most species, the laminae are not visible with routine Nissl stains, but are defined by the dendritic fields of principal cells and the terminal arbors of afferents arising from the inferior colliculus. In the present study, we have used the rabbit to directly examine the relationship between the laminar and tonotopic organization of the MGV. Best frequency maps, of the MGV in anesthetized adult New Zealand white rabbits were generated from cluster responses recorded at 30 100 mum intervals to randomly presented tone bursts. Parallel vertical penetrations, roughly perpendicular to the laminae, revealed a low-to-high frequency gradient within the MGV. Non-laminated regions of the ventral division, generally found at the rostral or caudal poles, did not demonstrate a systematic frequency gradient. Tn contrast to a predicted smooth gradient, beat frequencies shifted in discrete steps across the axis of the laminae. A similar step-wise frequency gradient has been shown in the central nucleus of the inferior colliculus of the cat. It is proposed that the central laminated core of the MGV represents an efficient architecture for creating narrow frequency filters involved in fine spectral analysis. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Arizona, Coll Med, Dept Cell Biol & Anat, Tucson, AZ 85724 USA. Arizona State Univ, Dept Speech & Hearing Sci, Tempe, AZ 85287 USA. RP McMullen, NT (reprint author), Univ Arizona, Coll Med, Dept Cell Biol & Anat, Tucson, AZ 85724 USA. CR AITKIN LM, 1973, J NEUROPHYSIOL, V36, P275 CABALLEROBLEDA M, 1991, J CHEM NEUROANAT, V4, P271, DOI 10.1016/0891-0618(91)90018-8 CAJAL SRY, 1995, HISTOLOGY NERVOUS SY, V2, P232 CALFORD MB, 1983, J NEUROSCI, V3, P2350 CALFORD MB, 1983, J NEUROSCI, V3, P2365 CALFORD MB, 1981, J NEUROPHYSIOL, V45, P1013 CETAS JS, 1999, ANN M ASS RES OT FEB Cetas J. S., 1999, Society for Neuroscience Abstracts, V25, P1420 CETAS JS, 2000, ANN M ASS RES OT FEB CLAREY JC, 1994, J NEUROPHYSIOL, V72, P2383 CLERICI WJ, 1990, J COMP NEUROL, V297, P14, DOI 10.1002/cne.902970103 DERIBAUPIERRE F, 1995, CENTRAL AUDITORY SYS, P317 DEVENECIA RK, 1995, J COMP NEUROL, V359, P595, DOI 10.1002/cne.903590407 Edeline JM, 1999, HEARING RES, V131, P135, DOI 10.1016/S0378-5955(99)00026-X Ehret G, 1997, J COMP PHYSIOL A, V181, P635, DOI 10.1007/s003590050146 GROSS NB, 1974, BRAIN RES, V65, P323, DOI 10.1016/0006-8993(74)90044-4 HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 IMIG TJ, 1985, J NEUROPHYSIOL, V53, P309 JONES EG, 1971, Z ZELLFORSCH MIK ANA, V113, P44, DOI 10.1007/BF00331201 Mendelson JR, 1997, J COMP PHYSIOL A, V181, P615, DOI 10.1007/s003590050145 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MIDDLEBROOKS JC, 1983, J NEUROSCI, V3, P203 MOREST DK, 1965, J ANAT, V99, P143 MOREST DK, 1964, J ANAT, V98, P611 Nuding SC, 1999, HEARING RES, V131, P89, DOI 10.1016/S0378-5955(99)00023-4 OLIVER DL, 1978, J COMP NEUROL, V182, P423, DOI 10.1002/cne.901820305 PHILLIPS DP, 1994, EXP BRAIN RES, V102, P210 REDIES H, 1989, J COMP NEUROL, V282, P489, DOI 10.1002/cne.902820403 REDIES H, 1991, EXP BRAIN RES, V86, P384 RODRIGUESDAGAEFF C, 1989, HEARING RES, V39, P103, DOI 10.1016/0378-5955(89)90085-3 ROSE M, 1935, MEM ACAD SCI CRACO B, V8, P53 Schreiner CE, 1997, NATURE, V388, P383, DOI 10.1038/41106 SCHREINER CE, 1992, EXP BRAIN RES, V92, P105 Schreiner CE, 2000, ANNU REV NEUROSCI, V23, P501, DOI 10.1146/annurev.neuro.23.1.501 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 STEIBLER I, 1986, NEUROSCI LETTT, V65, P336 STEIBLER I, 1985, J COMP NEUROL, V238, P65 Suga N, 1997, J NEUROPHYSIOL, V77, P2098 WHITFIELD I C, 1972, Brain Behavior and Evolution, V6, P311, DOI 10.1159/000123718 Winer JA, 1999, HEARING RES, V130, P19, DOI 10.1016/S0378-5955(98)00216-0 Winer JA, 1992, MAMMALIAN AUDITORY P, P222 WINER JA, 1988, J COMP NEUROL, V274, P422, DOI 10.1002/cne.902740310 WINER JA, 1994, J COMP NEUROL, V346, P161, DOI 10.1002/cne.903460202 NR 44 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 113 EP 123 DI 10.1016/S0378-5955(01)00257-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100011 PM 11335081 ER PT J AU Tucci, DL Cant, NB Durham, D AF Tucci, DL Cant, NB Durham, D TI Effects of conductive hearing loss on gerbil central auditory system activity in silence SO HEARING RESEARCH LA English DT Article DE conductive hearing loss; deprivation; 2-deoxyglucose; plasticity ID ANTEROVENTRAL COCHLEAR NUCLEUS; BRAIN-STEM; INFERIOR COLLICULUS; AFFERENT INFLUENCES; ACOUSTIC DEPRIVATION; PROTEIN-SYNTHESIS; MONGOLIAN GERBIL; DEHYDROGENASE ACTIVITY; MERIONES-UNGUICULATUS; SOUND DEPRIVATION AB Animal models of conductive hearing loss (CHL) show altered structure and function in the central :auditory system (CAS), particularly following unilateral deprivation. Assessment of neuronal activity as measured by 7-deoxyglucose (2-DG) uptake following CHL has been reported by two groups of investigators, with different findings. Woolf and colleagues [Brain Res. 774 (1983) 119] found that 2-DG uptake increased in the cochlear nucleus ipsilateral to the CHL. while Tucci ct al. [Laryngoscope 109 (1999) 1359] found a decrease in 2-DG uptake in the ipsilateral cochlear nucleus. One significant difference between the protocols in the two studies was that, in the first study, animals were maintained in silence following 2-DG injection, whereas in the Tucci et al. study, animals were exposed to sound. The current study was designed to replicate the protocol used by Woolf ct al. Young adult gerbils underwent unilateral malleus removal with bilateral canal ligation (n = 6) or a sham procedure (n = 7) 48 h prior to 2-DG administration and sacrifice. Optical density measurements were made from CAS nuclei. 2-DG uptake decreased in the ipsilateral cochlear nucleus and contralateral inferior colliculus, and in nuclei of the superior olivary complex bilaterally, supporting the finding that CHL is associated with a decrease in CAS neuronal activity. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Duke Univ, Med Ctr, Dept Surg, Div Otolaryngol Head & Neck Surg, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA. Univ Kansas, Med Ctr, Dept Otolaryngol Head & Neck Surg, Kansas City, KS 66160 USA. RP Tucci, DL (reprint author), Duke Univ, Med Ctr, Dept Surg, Div Otolaryngol Head & Neck Surg, BOx 3805, Durham, NC 27710 USA. CR BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 BORN DE, 1991, BRAIN RES, V557, P37, DOI 10.1016/0006-8993(91)90113-A BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 BORN DE, 1988, J NEUROSCI, V8, P901 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 CONLEE JW, 1981, J COMP NEUROL, V202, P373, DOI 10.1002/cne.902020307 DUPONT J, 1992, TINNITUS 91, P195 DUPONT J, 1994, ASS RES OT ABSTR, V41 DURHAM D, 1985, J COMP NEUROL, V231, P446, DOI 10.1002/cne.902310404 DURHAM D, 1989, HEARING RES, V43, P39, DOI 10.1016/0378-5955(89)90057-9 DURHAM D, 1993, HEARING RES, V70, P151, DOI 10.1016/0378-5955(93)90153-R FENG AS, 1980, BRAIN RES, V189, P530, DOI 10.1016/0006-8993(80)90112-2 GRAY L, 1982, BRAIN RES, V244, P360, DOI 10.1016/0006-8993(82)90098-1 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HEIL P, 1986, J COMP NEUROL, V252, P279, DOI 10.1002/cne.902520302 HYDE GE, 1990, J COMP NEUROL, V297, P329, DOI 10.1002/cne.902970302 HYSON RL, 1989, J NEUROSCI, V9, P2835 KENNEDY C, 1975, SCIENCE, V187, P850, DOI 10.1126/science.1114332 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1499 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 McAlpine D, 1997, J NEUROPHYSIOL, V78, P767 MOORE DR, 1991, NEUROBIOLOGY HEARING, P461 MOORE DR, 1989, J NEUROSCI, V9, P1213 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 NORDEEN KW, 1983, J COMP NEUROL, V214, P131, DOI 10.1002/cne.902140203 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 OLIVER DL, 1987, J COMP NEUROL, V264, P24, DOI 10.1002/cne.902640104 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 POWELL TPS, 1962, J ANAT, V96, P249 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 Salvi RJ, 2000, HEARING RES, V147, P261, DOI 10.1016/S0378-5955(00)00136-2 SANES DH, 1992, BRAIN RES, V64, P47 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 SMITH ZDJ, 1983, J COMP NEUROL, V220, P199, DOI 10.1002/cne.902200207 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x Stuermer IW, 2000, HEARING RES, V146, P185, DOI 10.1016/S0378-5955(00)00113-1 THEURICH M, 1984, BRAIN RES, V322, P157, DOI 10.1016/0006-8993(84)91197-1 Tierney TS, 1997, J COMP NEUROL, V378, P295, DOI 10.1002/(SICI)1096-9861(19970210)378:2<295::AID-CNE11>3.0.CO;2-R TONNDORF J, 1972, F MODERN AUDITORY TH, V2, P197 TRUNE DR, 1988, DEV BRAIN RES, V42, P304, DOI 10.1016/0165-3806(88)90249-0 TRUNE DR, 1988, HEARING RES, V35, P259, DOI 10.1016/0378-5955(88)90122-0 TRUNE DR, 1982, J COMP NEUROL, V209, P425, DOI 10.1002/cne.902090411 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 Tucci DL, 1999, LARYNGOSCOPE, V109, P1359, DOI 10.1097/00005537-199909000-00001 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 WEBSTER DB, 1986, ASS RES OT ABSTR, V178 WEBSTER DB, 1983, INT J PEDIATR OTORHI, V6, P107 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WEBSTER DB, 1983, HEARING RES, V12, P145, DOI 10.1016/0378-5955(83)90123-5 Werner L. A., 1992, ADV INFANCY RES, V7, P103 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 WOOLF NK, 1983, BRAIN RES, V274, P119, DOI 10.1016/0006-8993(83)90526-7 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 NR 62 TC 19 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 124 EP 132 DI 10.1016/S0378-5955(01)00256-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100012 PM 11335082 ER PT J AU Phillips, DP Hall, SE Guo, Y Burkard, R AF Phillips, DP Hall, SE Guo, Y Burkard, R TI Sensitivity of unanesthetized chinchilla auditory system to noise burst onset, and the effects of carboplatin SO HEARING RESEARCH LA English DT Article DE evoked response; auditory nerve; inferior colliculus; noise onset; carboplatin ID HAIR CELL LOSS; EVOKED-RESPONSE; RISE-TIME; CORTEX NEURONS; LEVEL; INNER; REPRESENTATION; OTOTOXICITY; AMPLITUDE; MASKING AB The gross near-field responses of the auditory nerve and inferior colliculus to noise burst stimuli were recorded through intracranially implanted electrodes in six unanesthetized chinchillas. Responses were studied as a function of stimulus plateau amplitude and rise time, both before and after a systemic dose of 75 mg/kg of carbaplatin. Both recording sites showed sensitivity to stimulus level and rise time. Increases in stimulus level and decreases in stimulus rise time each produced increases in the response magnitude, and decreases in response latency. When the stimuli were re-specified as rate of pressure change at sound onset (Pa/s), the amplitude and latency of responses at each site were found to be a direct function of rate of sound pressure change. These data provide the first confirmation in unanesthetized animals of previous single unit observations: in barbiturate-anesthetized cats. Carboplatin treatment resulted in a 20-80% loss of inner hair cells, a modest threshold elevation, and a 50 75'%, reduction in peak response amplitudes. The general patterns of sensitivity to stimulus level and rise time were not markedly affected by carboplatin, nor was the fashion in which response parameters (amplitude and latency) were ruled by rate of pressure change at sound onset. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Dalhousie Univ, Dept Psychol, Hearing Res Lab, Halifax, NS B3H 4J1, Canada. SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA. RP Phillips, DP (reprint author), Dalhousie Univ, Dept Psychol, Hearing Res Lab, Halifax, NS B3H 4J1, Canada. RI Phillips, Dennis/A-6496-2011 CR BARTH CD, 1993, AUDIOLOGY, V32, P225 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 Burkard R, 1997, J ACOUST SOC AM, V102, P3620, DOI 10.1121/1.420149 BURKARD R, 1991, AUDIOLOGY, V30, P47 DALLOS P, 1992, J NEUROSCI, V12, P4575 EGGERMONT JJ, 1991, HEARING RES, V56, P153, DOI 10.1016/0378-5955(91)90165-6 EGGERMONT JJ, 1992, HEARING RES, V61, P1, DOI 10.1016/0378-5955(92)90029-M HECOX K, 1983, J ACOUST SOC AM, V73, P2109, DOI 10.1121/1.389578 Heil P, 1996, NEUROREPORT, V7, P3073, DOI 10.1097/00001756-199611250-00056 Heil P, 1997, J NEUROPHYSIOL, V77, P2616 Heil P, 1997, J NEUROPHYSIOL, V77, P2642 Heil P, 1997, J NEUROPHYSIOL, V78, P2438 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 Liberman MC, 1997, AUDIT NEUROSCI, V3, P255 PHILLIPS DP, 1985, HEARING RES, V19, P253, DOI 10.1016/0378-5955(85)90145-5 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1995, J NEUROPHYSIOL, V73, P674 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1990, J ACOUST SOC AM, V88, P1403, DOI 10.1121/1.399718 Phillips DP, 1999, J ACOUST SOC AM, V105, P2731, DOI 10.1121/1.426891 Phillips DP, 1998, BEHAV BRAIN RES, V93, P33, DOI 10.1016/S0166-4328(97)00139-3 Qiu CX, 2000, HEARING RES, V139, P153, DOI 10.1016/S0378-5955(99)00171-9 RAGGIO MW, 1994, J NEUROPHYSIOL, V72, P2334 SUGA N, 1971, J PHYSIOL-LONDON, V217, P159 SYNDER D, 1994, LAB ANIMAL, V23, P42 WAKE M, 1993, J LARYNGOL OTOL, V107, P585, DOI 10.1017/S0022215100123771 WAKE M, 1994, LARYNGOSCOPE, V104, P488 NR 27 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 133 EP 142 DI 10.1016/S0378-5955(01)00249-0 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100013 PM 11335083 ER PT J AU Stover, T Nam, YJ Gong, TWL Lomax, MI Altschuler, RA AF Stover, T Nam, YJ Gong, TWL Lomax, MI Altschuler, RA TI Glial cell line-derived neurotrophic factor (GDNF) and its receptor complex are expressed in the auditory nerve of the mature rat cochlea SO HEARING RESEARCH LA English DT Article DE auditory nerve; glial cell line-derived neurotrophic factor; Ret; GDNF-family receptor alpha 1; reverse transcription-polymerase chain reaction; Western blot; immunocytochemistry ID GROWTH-FACTOR-BETA; MICE LACKING GDNF; NEURONS IN-VIVO; DOPAMINERGIC-NEURONS; TYROSINE KINASE; MESSENGER-RNA; RET; ACTIVATION; BRAIN; NEURTURIN AB Glial cell line-derived neurotrophic factor (GDNF) is a survival factor for many neuronal cell types which signals through a heterodimer receptor consisting of GDNF-family receptor alpha 1 (GFR alpha -1) and Ret (rearranged during transformation). GDNF expression has previously been reported in the inner hair cells of the rat cochlea, with expression of GFR alpha -1 but not Ret in the cell bodies of the auditory nerve (spiral ganglion cells), using in situ hybridization. The present study used reverse transcription-polymerase chain reaction (RT-PCR), and immunocytochemistry to examine GDNF, GFR alpha -1 and Ret in the adult rat auditory nerve. Semi-quantitative RT-PCR showed expression of GDNF and the two receptor components, GFR alpha -1 and Ret, in the modiolar subfraction of the cochlea containing spiral ganglion cells. A shorter mRNA splice variant for GDNF was also detected. Immunocytochemistry showed immunostaining in the modiolus for GDNF, GFR alpha -1 and Ret that was confined to spiral ganglion cells. When RT-PCR expression levels were compared to the expression in the substantia nigra, GFR alpha -1 expression levels were similar, Ret mRNA was lower in the modiolus and GDNF expression was higher in the modiolus. However, when GDNF was further assessed using Western blot, while GDNF protein was found in the modiolus it was at lowe cr levels than in substantia nigra tissue. These results demonstrate that GDNF and both of its receptor components are found in spiral ganglion cells of the adult rat cochlea. Along with the previous report of GDNF in inner hair cells, these new results provide a basis for the role of GDNF as a survival factor for the auditory nerve, as suggested by previous studies. (C) 2001 Published by Elsevier Science B.V. C1 Univ Michigan, Sch Med, Dept Otolaryngol Head & Neck Surg, Kresge Hearing Res Inst 6040, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Dept Anat & Cell Biol, Ann Arbor, MI 48109 USA. Med Univ Hannover, Dept Otolaryngol, D-30625 Hannover, Germany. RP Altschuler, RA (reprint author), Univ Michigan, Sch Med, Dept Otolaryngol Head & Neck Surg, Kresge Hearing Res Inst 6040, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR Altschuler RA, 1999, ANN NY ACAD SCI, V884, P305, DOI 10.1111/j.1749-6632.1999.tb08650.x Arenas E, 1995, NEURON, V15, P1465, DOI 10.1016/0896-6273(95)90024-1 Baloh RH, 1997, NEURON, V18, P793, DOI 10.1016/S0896-6273(00)80318-9 Cass WA, 1996, J NEUROSCI, V16, P8132 CHAN YL, 1990, FEBS LETT, V263, P85, DOI 10.1016/0014-5793(90)80711-Q CRISTINA N, 1995, MOL BRAIN RES, V32, P354, DOI 10.1016/0169-328X(95)00103-Y Durbec P, 1996, NATURE, V381, P789, DOI 10.1038/381789a0 Engele J, 1996, CELL TISSUE RES, V286, P235, DOI 10.1007/s004410050692 Feng L, 1999, NEUROSCIENCE, V93, P265, DOI 10.1016/S0306-4522(99)00129-3 FOLEY KP, 1993, TRENDS GENET, V9, P380, DOI 10.1016/0168-9525(93)90137-7 Glazner GW, 1998, J COMP NEUROL, V391, P42, DOI 10.1002/(SICI)1096-9861(19980202)391:1<42::AID-CNE4>3.0.CO;2-R Golden JP, 1998, J COMP NEUROL, V398, P139, DOI 10.1002/(SICI)1096-9861(19980817)398:1<139::AID-CNE9>3.0.CO;2-2 Hegarty JL, 1997, J NEUROSCI, V17, P1959 HENDERSON CE, 1994, SCIENCE, V266, P1062, DOI 10.1126/science.7973664 Hiwasa T, 1997, NEUROSCI LETT, V238, P115, DOI 10.1016/S0304-3940(97)00861-6 Hou JGG, 1996, J NEUROCHEM, V66, P74 Jing SQ, 1996, CELL, V85, P1113, DOI 10.1016/S0092-8674(00)81311-2 Krieglstein K, 1998, J NEUROSCI, V18, P9822 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 Lenhard T, 1998, NEUROREPORT, V9, P2927, DOI 10.1097/00001756-199809140-00002 LIN LFH, 1993, SCIENCE, V260, P1130, DOI 10.1126/science.8493557 LIN LFH, 1994, J NEUROCHEM, V63, P758 Moore MW, 1996, NATURE, V382, P76, DOI 10.1038/382076a0 Moreau E, 1998, AM J PHYSIOL-RENAL, V275, pF938 Murakami H, 1999, ONCOGENE, V18, P1975, DOI 10.1038/sj.onc.1202514 Nosrat CA, 1996, CELL TISSUE RES, V286, P191, DOI 10.1007/s004410050688 Nosrat CA, 1997, EXP BRAIN RES, V115, P410, DOI 10.1007/PL00005711 OPPENHEIM RW, 1995, NATURE, V373, P344, DOI 10.1038/373344a0 Pichel JG, 1996, NATURE, V382, P73, DOI 10.1038/382073a0 Pong K, 1998, J NEUROCHEM, V71, P1912 Sanicola M, 1997, P NATL ACAD SCI USA, V94, P6238, DOI 10.1073/pnas.94.12.6238 Schober A, 1999, J NEUROSCI, V19, P2008 SCHUCHARDT A, 1994, NATURE, V367, P380, DOI 10.1038/367380a0 SMITH PK, 1985, ANAL BIOCHEM, V150, P70 TAKAHASHI M, 1987, MOL CELL BIOL, V7, P1378 TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350 Treanor JJS, 1996, NATURE, V382, P80, DOI 10.1038/382080a0 Trupp M, 1998, MOL CELL NEUROSCI, V11, P47, DOI 10.1006/mcne.1998.0667 TRUPP M, 1995, J CELL BIOL, V130, P137, DOI 10.1083/jcb.130.1.137 Trupp M, 1999, J BIOL CHEM, V274, P20885, DOI 10.1074/jbc.274.30.20885 Williams LR, 1996, J PHARMACOL EXP THER, V277, P1140 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 NR 42 TC 30 Z9 32 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 143 EP 151 DI 10.1016/S0378-5955(01)00227-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100014 PM 11335084 ER PT J AU Qiu, JH Steyger, PS Trune, DR Nuttall, AL AF Qiu, JH Steyger, PS Trune, DR Nuttall, AL TI Co-existence of tyrosine hydroxylase and calcitonin gene-related peptide in cochlear spiral modiolar artery of guinea pigs SO HEARING RESEARCH LA English DT Article DE spiral modiolar artery; tyrosine hydroxylase; calcitonin gene-related peptide; immunofluorescence; cochlea ID SUPERIOR CERVICAL-GANGLION; BLOOD-FLOW; TRIGEMINAL GANGLION; IN-VITRO; RAT; INNERVATION; VASOCONSTRICTION; VASODILATOR; CELLS; ELECTROPHYSIOLOGY AB The distribution of tyrosine hydroxylase (TH) and calcitonin gene-related peptide (CGRP) on the cochlear spiral modiolar artery (SMA) was investigated in the guinea pig. The SMA was dissected from the modiolus so that the entire length of the vessel and many of its branches could be observed. Immunohistochemical labeling and double immunofluorescence were employed to localize each compound and to determine whether the TH and CGRP co-exist in neurons of the SMA. Microscopic examination of whole vessel preparations revealed numerous TH- and CGRP-positive neural networks innervating the SMA and its branches. The labeled neurons showed distinct arborization, varicosities and overlap, and were of different diameters. Confocal immunoflorescence microscopy of double-labeled TH and CGRP neurons showed that a number of the TH- and CGRP-positive neurons were colabeled. Thus, TH and CGRP partially co-exist within the neuronal innervation of SMA. These findings support;I hypothesis that specific neuropeptide and adrenergic neurons regulate cochlear blood now. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, Portland, OR 97201 USA. Fourth Mil Med Univ, Xijing Hosp, Xian 710032, Peoples R China. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Nuttall, AL (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR ARBAB MAR, 1986, NEUROSCIENCE, V19, P695, DOI 10.1016/0306-4522(86)90293-9 BAFFI J, 1992, BRAIN RES, V570, P272, DOI 10.1016/0006-8993(92)90591-V BRAIN SD, 1985, NATURE, V313, P54, DOI 10.1038/313054a0 BRECHTELSBAUER PB, 1990, OTOLARYNG HEAD NECK, V103, P566 BURNSTOCK G, 1985, J CARDIOVASC PHARM, V7, pS137, DOI 10.1097/00005344-198500073-00016 CARLISLE L, 1990, HEARING RES, V43, P107, DOI 10.1016/0378-5955(90)90219-F COLEMAN J, 2000, MIDW M ASS RES OT ST DAGERLIND A, 1994, NEUROREPORT, V5, P909 DENGERINK HA, 1988, PHYSL EAR, P327 GRACE GC, 1987, BRIT J PHARMACOL, V91, P729 Gruber DD, 1998, HEARING RES, V119, P113, DOI 10.1016/S0378-5955(98)00036-7 HULTCRANTZ E, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P271 Jiang ZG, 1999, HEARING RES, V138, P171, DOI 10.1016/S0378-5955(99)00166-5 JONES N, 1987, HEARING RES, V30, P33, DOI 10.1016/0378-5955(87)90180-8 Krimer LS, 1998, NAT NEUROSCI, V1, P286 KURJIAKA DT, 1995, CIRC RES, V76, P885 LEE Y, 1985, BRAIN RES, V330, P194, DOI 10.1016/0006-8993(85)90027-7 LINDH B, 1989, CELL TISSUE RES, V256, P259 Mannan MM, 1995, EUR RESPIR J, V8, P2029, DOI 10.1183/09031936.95.08122029 MCLAREN GM, 1993, HEARING RES, V71, P183, DOI 10.1016/0378-5955(93)90033-W MILLER JM, 1988, AM J OTOLARYNG, V9, P302, DOI 10.1016/S0196-0709(88)80038-3 OCONNOR TP, 1988, J NEUROSCI, V8, P2468 OLESEN IJ, 1995, PEPTIDES, V16, P275 Pawley J., 1995, HDB CONFOCAL MICROSC QIU JH, 1993, J CLIN OTOLARYNGOL, V7, P195 QUIRK WS, 1994, AM J OTOL, V15, P56 REN TY, 1993, ANN OTO RHINOL LARYN, V102, P378 REUSS S, 1993, J CHEM NEUROANAT, V6, P343, DOI 10.1016/0891-0618(93)90009-S Riemann R, 1999, NEUROREPORT, V10, P2641, DOI 10.1097/00001756-199908200-00037 Schmitt M, 1988, J Chem Neuroanat, V1, P287 SHIBAMORI Y, 1994, BRAIN RES, V646, P223, DOI 10.1016/0006-8993(94)90082-5 Spoendlin H, 1967, Arch Klin Exp Ohren Nasen Kehlkopfheilkd, V189, P346, DOI 10.1007/BF00440938 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 Tajti J, 1999, J AUTONOM NERV SYST, V76, P176, DOI 10.1016/S0165-1838(99)00024-7 Takenaga M, 1999, EUR J PHARMACOL, V367, P239, DOI 10.1016/S0014-2999(98)00949-2 Usami S, 1988, Acta Otolaryngol Suppl, V447, P36 VASS Z, 1994, ACTA OTO-LARYNGOL, V114, P156, DOI 10.3109/00016489409126035 VASS Z, 1995, HEARING RES, V89, P86, DOI 10.1016/0378-5955(95)00127-4 Vass Z, 1998, EXP NEUROL, V151, P241, DOI 10.1006/exnr.1998.6813 Vass Z, 1996, HEARING RES, V100, P114, DOI 10.1016/0378-5955(96)00102-5 VILLARREAL D, 1988, P SOC EXP BIOL MED, V188, P316 Wangemann P, 1998, HEARING RES, V115, P113, DOI 10.1016/S0378-5955(97)00184-6 NR 42 TC 8 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 152 EP 160 DI 10.1016/S0378-5955(01)00231-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100015 PM 11335085 ER PT J AU Mothe, AJ Brown, IR AF Mothe, AJ Brown, IR TI Expression of mRNA encoding extracellular matrix glycoproteins SPARC and SC1 is temporally and spatially regulated in the developing cochlea of the rat inner ear SO HEARING RESEARCH LA English DT Article DE extracellular matrix; calcium-binding glycoprotein; in situ hybridization; organ of corti; Deiters cell; spiral ganglion neuron ID MESSENGER-RNA EXPRESSION; CALCIUM-BINDING PROTEINS; IN-SITU HYBRIDIZATION; OUTER HAIR-CELLS; POSTNATAL-DEVELOPMENT; INSITU HYBRIDIZATION; CATARACT FORMATION; SPIRAL LIGAMENT; II COLLAGEN; BM-40 SPARC AB SPARC is a multifunctional extracellular matrix (ECM) glycoprotein that shares partial sequence homology with SCl/hevin. These ECM molecules exhibit calcium-binding properties and modulate cellular interactions. This study examines the expression of SCl and SPARC mRNA in the developing cochlea of the rat inner ear prior to and after the onset of hearing. At all ages examined, SCl mRNA is highly expressed in neurons of the spiral ganglion. In contrast, SPARC transcripts are not detected in the spiral ganglion but are enriched in the temporal bone and cartilaginous otic capsule surrounding the cochlea. Both SCl and SPARC mRNA are expressed in connective tissue elements involved in maintaining ionic homeostasis of cochlear fluids. SCI mRNA is localized to type III fibrocytes of the spiral ligament (slg) anti marginal cells of the stria vascularis, while SPARC mRNA is apparent in the spiral limbus and type I fibrocytes of the sig. At postnatal day 10, SPARC mRNA shows a dramatic change in expression. High levels of SPARC transcripts are induced in Deiters cells (dc) of the organ of Corti. Interestingly, this induction of SPARC mRNA correlates with the onset of hearing. This suggests that SPARC may play a role in calcium regulation in de when functional maturation of the cochlea is attained and rapid changes in calcium levels are required, (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Toronto, Dept Zool, Toronto, ON M1C 1A4, Canada. RP Brown, IR (reprint author), Univ Toronto, Dept Zool, 25 Harbord St, Toronto, ON M1C 1A4, Canada. CR Bassuk JA, 1999, EXP EYE RES, V68, P321, DOI 10.1006/exer.1998.0608 Corwin JT, 1998, P NATL ACAD SCI USA, V95, P12080, DOI 10.1073/pnas.95.21.12080 Cosgrove D, 1997, HEARING RES, V105, P159, DOI 10.1016/S0378-5955(96)00203-1 Cremers FPM, 1998, CURR OPIN NEUROL, V11, P11, DOI 10.1097/00019052-199802000-00003 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DECHESNE CJ, 1993, HEARING RES, V69, P91, DOI 10.1016/0378-5955(93)90096-J Gilmour DT, 1998, EMBO J, V17, P1860, DOI 10.1093/emboj/17.7.1860 Girard JP, 1996, J BIOL CHEM, V271, P4511 GIRARD JP, 1995, IMMUNITY, V2, P113, DOI 10.1016/1074-7613(95)90083-7 HOLLAND PWH, 1987, J CELL BIOL, V105, P473, DOI 10.1083/jcb.105.1.473 Jacob ANK, 1997, SOMAT CELL MOLEC GEN, V23, P83, DOI 10.1007/BF02679968 JOHNSTON IG, 1990, NEURON, V2, P165 Khetarpal U, 1998, ACTA OTO-LARYNGOL, V118, P177 KHETARPAL U, 1994, HEARING RES, V79, P59, DOI 10.1016/0378-5955(94)90127-9 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 Kuijpers W, 1986, Acta Otolaryngol Suppl, V429, P35 LANE TF, 1994, FASEB J, V8, P163 Lecain E, 1999, HEARING RES, V133, P133, DOI 10.1016/S0378-5955(99)00068-4 Legan PK, 1997, SEMIN CELL DEV BIOL, V8, P217, DOI 10.1006/scdb.1997.0145 Lim D, 1992, DEV AUDITORY VESTIBU, P33 LOPEZ CA, 1995, HEARING RES, V85, P210, DOI 10.1016/0378-5955(95)00046-7 MASON IJ, 1986, EMBO J, V5, P1465 MAURER P, 1992, EUR J BIOCHEM, V205, P233, DOI 10.1111/j.1432-1033.1992.tb16773.x McGuirt WT, 1999, NAT GENET, V23, P413 McKinnon PJ, 2000, MOL CELL BIOL, V20, P656, DOI 10.1128/MCB.20.2.656-660.2000 Motamed K, 1999, INT J BIOCHEM CELL B, V31, P1363, DOI 10.1016/S1357-2725(99)00090-4 Mothe AJ, 2000, MOL BRAIN RES, V76, P73, DOI 10.1016/S0169-328X(99)00336-8 Mustapha M, 1999, HUM MOL GENET, V8, P409, DOI 10.1093/hmg/8.3.409 Norose K, 1998, INVEST OPHTH VIS SCI, V39, P2674 Pack AK, 1995, HEARING RES, V91, P119 Petit C, 1996, NAT GENET, V14, P385, DOI 10.1038/ng1296-385 POTTGIESSER J, 1994, J MOL BIOL, V238, P563, DOI 10.1006/jmbi.1994.1315 Rau A, 1999, J COMP NEUROL, V405, P271 Raz Y, 1999, DEV BIOL, V213, P180, DOI 10.1006/dbio.1999.9364 ROBERTSON NG, 1994, GENOMICS, V23, P42, DOI 10.1006/geno.1994.1457 ROTH B, 1992, ANAT EMBRYOL, V185, P571, DOI 10.1007/BF00185616 RYAN AF, 1991, HEARING RES, V56, P148, DOI 10.1016/0378-5955(91)90164-5 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 SAGE H, 1989, J CELL BIOL, V109, P341, DOI 10.1083/jcb.109.1.341 Sakaguchi N, 1998, J HISTOCHEM CYTOCHEM, V46, P29 Schwartz A. M, 1986, NEUROBIOLOGY HEARING, P271 Skvorak AB, 1999, HUM MOL GENET, V8, P439, DOI 10.1093/hmg/8.3.439 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 Sobkowicz HM, 1992, DEV AUDITORY VESTIBU, V2, P59 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z Spoendlin H, 1986, Scand Audiol Suppl, V25, P27 Steel KP, 1999, TRENDS GENET, V15, P207, DOI 10.1016/S0168-9525(99)01753-9 UZIEL A, 1981, AUDIOLOGY, V20, P89 Whitlon DS, 1999, J COMP NEUROL, V406, P361, DOI 10.1002/(SICI)1096-9861(19990412)406:3<361::AID-CNE5>3.0.CO;2-O WOOLF NK, 1992, DEV BRAIN RES, V65, P21, DOI 10.1016/0165-3806(92)90004-G Yan Q, 1999, J HISTOCHEM CYTOCHEM, V47, P1495 NR 52 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 161 EP 174 DI 10.1016/S0378-5955(01)00246-5 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100016 PM 11335086 ER PT J AU Michel, O Hess, A Bloch, W Schmidt, A Stennert, E Addicks, K AF Michel, O Hess, A Bloch, W Schmidt, A Stennert, E Addicks, K TI Immunohistochemical detection of vascular endothelial growth factor (VEGF) and VEGF receptors Flt-1 and KDR/Flk-1 in the cochlea of guinea pigs SO HEARING RESEARCH LA English DT Article DE vascular endothelial growth factor; vascular endothelial growth factor receptor; nitric oxide/cGMP pathway; cochlea ID NITRIC-OXIDE SYNTHASE; CELL PROLIFERATION; EXPRESSION; PATHWAY; ACTIVATION; FLK-1/KDR; SYSTEM; SIGNAL AB Vascular endothelial growth factor (VEGF) is known as an endothelial cell-specific mitogen. There are no reports concerning the presence of VEGF in the inner ear. To gain information, immunohistochemical analysis using specific antibodies to VEGF and to both known VEGF receptors Flt-1 and KDR/Flk-1 was performed on paraffin-sectioned temporal bones from five guinea pigs. Immunoreactivity of VEGF, Flt-1 and KDR/Flk-1 was detectable in spiral ganglion cells. VEGF could also be found in the endothelium of blood vessels, in the spiral ligament and ill the organ of Corti. Flt-1 was found in the limbus epithelium, in all supporting cells of the organ of Corti, in Claudius cells, cells of the sulcus and in the spiral ligament. Flk-1 could be detected in some supporting cells of the organ of Corti (inner pillar cells and Deiters' cells). Immunoreactivity to Flk-1 was also found in endothelium of blood vessels and in the spiral ligament. Hair cells showed VEGF immunostaining, but did not contain staining to Flt-1 nor Flk-1. In the stria vascularis any immunoreactivity to all used VEGF and VEGF receptor antibodies could not be detected. The findings were supported by Western blot analysis on inner ear tissues and ovaries from guinea pigs. We may conclude that the growth factor EGF and both receptors participate in cochlear physiology. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Cologne, Dept Otorhinolaryngol, D-50924 Cologne, Germany. Univ Cologne, Dept Anat, D-50924 Cologne, Germany. RP Michel, O (reprint author), Univ Cologne, Dept Otorhinolaryngol, Joseph Stelzmann Str 9, D-50924 Cologne, Germany. RI Michel, Olaf/B-3673-2012 OI Michel, Olaf/0000-0003-4289-5693 CR Ahmed A, 1997, LAB INVEST, V76, P779 Bouloumie A, 1999, CARDIOVASC RES, V41, P773, DOI 10.1016/S0008-6363(98)00228-4 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 Feng YY, 1999, BIOCHEM BIOPH RES CO, V256, P192, DOI 10.1006/bbrc.1998.9790 FERRARA N, 1992, ENDOCR REV, V13, P18, DOI 10.1210/er.13.1.18 Fessenden JD, 1998, HEARING RES, V118, P168, DOI 10.1016/S0378-5955(98)00027-6 Friedman J M, 1997, Eur J Med Res, V2, P7 Hess A, 1998, BRAIN RES, V813, P97, DOI 10.1016/S0006-8993(98)00997-4 Hess A, 1999, BRAIN RES, V830, P113, DOI 10.1016/S0006-8993(99)01433-X Hess A, 2000, NEUROSCI LETT, V289, P72, DOI 10.1016/S0304-3940(00)01266-0 Hess A, 2000, NEUROSCI LETT, V280, P147, DOI 10.1016/S0304-3940(00)00774-6 Hood JD, 1998, AM J PHYSIOL, V274, P1054 KECK PJ, 1989, SCIENCE, V246, P1309, DOI 10.1126/science.2479987 Kim I, 1999, INVEST OPHTH VIS SCI, V40, P2115 Kroll J, 1998, BIOCHEM BIOPH RES CO, V252, P743, DOI 10.1006/bbrc.1998.9719 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 Malavaud B, 1997, CARDIOVASC RES, V36, P276, DOI 10.1016/S0008-6363(97)00177-6 Michel O, 1999, HEARING RES, V133, P1, DOI 10.1016/S0378-5955(99)00049-0 Morbidelli L, 1996, AM J PHYSIOL, V170, P411 Parenti A, 1998, J BIOL CHEM, V273, P4220, DOI 10.1074/jbc.273.7.4220 Shen BQ, 1999, J BIOL CHEM, V274, P33057, DOI 10.1074/jbc.274.46.33057 Sondell M, 1999, J NEUROSCI, V19, P5731 Tilton RG, 1999, INVEST OPHTH VIS SCI, V40, P689 WU HM, 1999, AM J PHYSIOL, V276, P535 Wu LW, 2000, J BIOL CHEM, V275, P5096, DOI 10.1074/jbc.275.7.5096 NR 25 TC 15 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2001 VL 155 IS 1-2 BP 175 EP 180 DI 10.1016/S0378-5955(01)00262-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 434CT UT WOS:000168798100017 PM 11335087 ER PT J AU Kondrachuk, AV AF Kondrachuk, AV TI Mathematical model of the evolution of statoconia SO HEARING RESEARCH LA English DT Article DE model; statoconia; statocyst; snail; statoconia growth; rate of growth ID BIOMPHALARIA-GLABRATA PULMONATA; STATOCYST; BASOMMATOPHORA AB A mathematical model of the evolution of statoconia in statocysts of freshwater snails based on the analysis of experimental data [Wiederhold et al., 1990: Pedrozo et al., 1996; Gao et al., 1997; Gao and Wiederhold, 1997: Wiederhold et al., 1999] is proposed. The growth of statoconia is considered as the process of solution crystallization. The model proposed assumes that two main processes determine the evolution of statoconia in developing snails: the generation of new statoconia and the linear growth of statoconia sizes. The analytical solution of the model and qualitative comparison of theoretical results with the experimental data show: (1) there are at least three periods of statoconia evolution; (2) the generation of new statoconia mainly determines the first period of evolution when the shell diameter of snails D < 4 mm, (3) when D > 6 mm the size distribution of statoconia is determined by the growth of their sizes with a constant rate; (4) on the interval DeltaD = 4-6 mm the transformation of size distribution with selective dissolution of statoconia takes place. The model agrees well with the experimental data and makes it possible to estimate some parameters of the statoconia kinetics. Additional experiments, which are necessary for further development of the model, and quantitative estimates of the mechanisms of statoconia evolution are formulated. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Natl Acad Sci Ukraine, Inst Phys, Dept Theoret Phys, UA-03028 Kiev 28, Ukraine. RP Kondrachuk, AV (reprint author), Natl Acad Sci Ukraine, Inst Phys, Dept Theoret Phys, Prospekt Nauki 46, UA-03028 Kiev 28, Ukraine. CR Gao WY, 1997, HEARING RES, V109, P109, DOI 10.1016/S0378-5955(97)00058-0 Gao WY, 1997, HEARING RES, V109, P125, DOI 10.1016/S0378-5955(97)00059-2 Pedrozo HA, 1996, CONNECT TISSUE RES, V35, P317, DOI 10.3109/03008209609029206 POLUECTOV PA, 1974, DYNAMICHESKAYA TEORI, P456 TODES OM, 1984, CHIMIYA LEINGRAD, P232 WIEDERHOLD ML, 1999, SPACE UTILIZATION RE, V15, P89 WIEDERHOLD ML, 1990, HEARING RES, V49, P63, DOI 10.1016/0378-5955(90)90095-7 NR 7 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 1 EP 11 DI 10.1016/S0378-5955(00)00185-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600001 PM 11423210 ER PT J AU Horowitz, SS Chapman, JA Kaya, U Simmons, AM AF Horowitz, SS Chapman, JA Kaya, U Simmons, AM TI Metamorphic development of the bronchial columella of the larval bullfrog (Rana catesbeiana) SO HEARING RESEARCH LA English DT Article DE anuran; tadpole; metamorphosis; development; auditory; bronchial columella ID XENOPUS-LAEVIS; FROG; SENSITIVITY; MIDBRAIN; COLLAGEN; TADPOLE; MUSCLE; SIZE; FISH; EAR AB Histological and immunohistochemical analyses of head and respiratory structures in bullfrog (Rana catesbeiana) tadpoles were undertaken to address the hypothesis that the bronchial columella (BC) is the primary sound conduction pathway in these larval anurans. In postembryonic tadpoles, the BC is composed of fibroblasts surrounded by a Type I collagen matrix, with Type II collagen located in basement membranes at the distal ends. It provides a highly flexible tendon-like attachment between the round window and the membranous sac of the primary bronchus of the ipsilateral lung. As the animals approach metamorphic climax stages, the fibroblasts decrease in number and the BC becomes almost exclusively collagenous. During metamorphic climax, the BC degenerates and is completely resorbed by the time the animal becomes a postmetamorphic froglet. At all larval stages examined, the BC is structurally and immunohistochemically different from both the opercularis muscle of tadpoles and the tympanic columella (stapes homolog) of postmetamorphic animals. These observations suggest that the BC may not be rigid enough to provide an effective coupling between the lungs and the round window. An alternative hypothesis for the function of the BC, based on its structure, is presented. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Brown Univ, Dept Neurosci, Providence, RI 02912 USA. Brown Univ, Dept Psychol, Providence, RI 02912 USA. Ege Univ, Fac Sci, Dept Biol, Sect Zool, Bornova Izmir, Turkey. RP Horowitz, SS (reprint author), Brown Univ, Dept Neurosci, Box 1953, Providence, RI 02912 USA. CR Beck CW, 1997, OECOLOGIA, V112, P187, DOI 10.1007/s004420050299 Boatright-Horowitz SS, 1997, P NATL ACAD SCI USA, V94, P14877, DOI 10.1073/pnas.94.26.14877 BURGGREN WW, 1982, RESP PHYSIOL, V47, P151, DOI 10.1016/0034-5687(82)90108-6 BURGGREN WW, 1994, AM ZOOL, V34, P238 Cannatella D, 1999, TADPOLES, P52 CAPRANICA RR, 1976, FROG NEUROBIOLOGY, P443 CORSE WA, 1980, J HERPETOL, V14, P231, DOI 10.2307/1563544 CORWIN JT, 1977, J MORPHOL, V152, P341, DOI 10.1002/jmor.1051520306 CRUMP ML, 1989, COPEIA, P794, DOI 10.2307/1445521 De Beer G. R., 1937, DEV VERTEBRATE SKULL Diaz ME, 1995, HEARING RES, V91, P33, DOI 10.1016/0378-5955(95)00159-X FRITZSCH B, 1984, J COMP NEUROL, V229, P451, DOI 10.1002/cne.902290312 FRITZSCH B, 1990, J NEUROBIOL, V21, P1011, DOI 10.1002/neu.480210707 FUNG YC, 1981, BIOMECHANICS MECH PR, P200 Boatright-Horowitz SS, 1999, J COMP PHYSIOL A, V184, P219, DOI 10.1007/s003590050320 Gosner K. L., 1960, Herpetologica, V16, P183 HANKEN J, 1988, J MORPHOL, V195, P247, DOI 10.1002/jmor.1051950303 HETHERINGTON TE, 1985, J EXP ZOOL, V235, P27, DOI 10.1002/jez.1402350105 HETHERINGTON TE, 1987, ZOOMORPHOLOGY, V106, P289, DOI 10.1007/BF00312003 Hetherington TE, 1999, J COMP PHYSIOL A, V184, P395, DOI 10.1007/s003590050338 JACOBY J, 1983, J COMP NEUROL, V216, P152, DOI 10.1002/cne.902160204 Kitamura K, 1991, Acta Otolaryngol Suppl, V481, P121 Kumaresan V, 1998, BRAIN BEHAV EVOLUT, V52, P111, DOI 10.1159/000006556 Lannoo MJ, 1999, TADPOLES, P149 Larsell O, 1934, J COMP NEUROL, V60, P473, DOI 10.1002/cne.900600306 LEWIS ER, 1974, SCANNING ELECTRON MI, P791 McDiarmid RW, 1999, TADPOLES, P7 Morris JB, 1997, MUTAT RES-FUND MOL M, V380, P113, DOI 10.1016/S0027-5107(97)00130-9 NARINS PM, 1988, P NATL ACAD SCI USA, V85, P1508, DOI 10.1073/pnas.85.5.1508 NEWMAN RA, 1989, ECOLOGY, V70, P1775, DOI 10.2307/1938111 POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 PUTT FA, 1972, MANUAL HISTOLOGICAL Rogers MJC, 1999, MAMM GENOME, V10, P513, DOI 10.1007/s003359901032 SEUFERT DW, 1994, ANAT EMBRYOL, V189, P81 BOATRIGHTHOROWITZ SS, 1995, J COMP PHYSIOL A, V177, P577 Smirnov Sergey V., 1993, Zoologische Jahrbuecher Abteilung fuer Anatomie und Ontogenie der Tiere, V123, P273 SOKOL OM, 1981, J MORPHOL, V169, P161, DOI 10.1002/jmor.1051690204 TELFORD IR, 1995, INTRO FUNCTIONAL HIS TRUNE DR, 1983, AM J OTOLARYNG, V4, P261, DOI 10.1016/S0196-0709(83)80070-2 VANBERGEIJK WA, 1959, J ACOUST SOC AM, V31, P1340, DOI 10.1121/1.1907632 Velleman SG, 1996, CONNECT TISSUE RES, V34, P175, DOI 10.3109/03008209609000697 WASSERSUG RJ, 1990, NATURWISSENSCHAFTEN, V77, P443, DOI 10.1007/BF01135948 WEISZ PB, 1945, J MORPHOL, V77, P163, DOI 10.1002/jmor.1050770204 WITSCHI EMIL, 1955, J MORPH, V96, P497, DOI 10.1002/jmor.1050960305 Witschi E., 1956, DEV VERTEBRATES WITSCHI E, 1949, Z NATURFORSCH B, V4, P230 Yonezawa S, 1999, HEARING RES, V134, P116, DOI 10.1016/S0378-5955(99)00080-5 NR 47 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 12 EP 25 DI 10.1016/S0378-5955(00)00266-5 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600002 PM 11423211 ER PT J AU Ohashi, T Ochi, K Kinoshita, H Kenmochi, M Kikuchi, H Nishino, H Taguchi, Y AF Ohashi, T Ochi, K Kinoshita, H Kenmochi, M Kikuchi, H Nishino, H Taguchi, Y TI Electrocochleogram after transection of vestibulo-cochlear nerve in a patient with a large acoustic neurinoma SO HEARING RESEARCH LA English DT Article DE vestibulo-cochlear nerve transection; paired click stimulation; compound action potential recovery; compound action potential adaptation; efferent nerve system ID POTENTIALS; SURGERY; NEUROMA; CAT AB This study reports pre- and post-operative compound action potentials (CAPs) that were recorded from a 27-year-old woman with an acoustic neurinoma. During surgery it was necessary to totally sever her vrstibulo-cochlear nerve to excise a large tumor. A pure tone audiogram changed to the scale-out pattern immediately after operation. However, CAP, the waveform of which was broadened. has been recorded 3 years post-operatively with a threshold elevation of 10 dB over the pre-operative threshold. This phenomenon suggests that CAP may originate from the extreme periphery of the auditory nerve within the cochlea. The broadening of the CAP was assumed to result from enhancement of the negative summating potential included in the CAP. We studied the effect of preceding stimulus on CAP using paired click stimuli pre- and post-operatively. A reduction of CAP amplitude in response to the second click of paired clicks was markedly suppressed in the inter-click interval between 3 and 80 ms post-operatively. We speculate that depletion of adaptation induced the abnormal CAP recovery described above and that the lateral efferent nerve system was involved in abnormal CAP adaptation with transection of the vestibulo-cochlear nerve in this case, (C) 2001 Elsevier Science B.V. All rights reserved. C1 St Marianna Univ, Yokohama City Seibu Hosp, Sch Med, Dept Otorhinolaryngol,Ashi Ku, Yokohama, Kanagawa 2410811, Japan. St Marianna Univ, Yokohama City Seibu Hosp, Sch Med, Dept Neurosurg,Ashi Ku, Yokohama, Kanagawa 2410811, Japan. RP Ohashi, T (reprint author), St Marianna Univ, Yokohama City Seibu Hosp, Sch Med, Dept Otorhinolaryngol,Ashi Ku, 1197-1 Yasashi Cho, Yokohama, Kanagawa 2410811, Japan. CR Colletti V, 1998, AUDIOLOGY, V37, P27 DAUMAN R, 1988, CLIN OTOLARYNGOL, V13, P107, DOI 10.1111/j.1365-2273.1988.tb00750.x EGGERMON.JJ, 1974, AUDIOLOGY, V13, P1 GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 LEVINE RA, 1984, ANN OTO RHINOL LARYN, V93, P116 Maison S, 1997, HEARING RES, V113, P89, DOI 10.1016/S0378-5955(97)00136-6 OHASHI T, 1993, ECOG, OAE AND INTRAOPERATIVE MONITORING, P79 OHASHI T, 1996, ACTA OTOLARYNGOL S S, V52, P17 OHASHI T, 1996, ACTA OTOLARYNGOL S S, V52, P11 OHASHI T, 1989, ORL J OTO-RHINO-LARY, V51, P235 Parham K, 1996, J NEUROPHYSIOL, V76, P17 SABIN HI, 1987, SCAND AUDIOL, V16, P109, DOI 10.3109/01050398709042164 SIEGEL JH, 1987, HEARING RES, V29, P169, DOI 10.1016/0378-5955(87)90165-1 TAKEDA T, 1992, ORL J OTO-RHINO-LARY, V54, P15 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 NR 16 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 26 EP 31 DI 10.1016/S0378-5955(00)00267-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600003 PM 11423212 ER PT J AU Ponton, CW Vasama, JP Tremblay, K Khosla, D Kwong, B Don, M AF Ponton, CW Vasama, JP Tremblay, K Khosla, D Kwong, B Don, M TI Plasticity in the adult human central auditory system: evidence from late-onset profound unilateral deafness SO HEARING RESEARCH LA English DT Article DE plasticity; auditory evoked potential; unilateral; deafness; human ID SENSORINEURAL HEARING-LOSS; INFERIOR COLLICULUS; CORTICAL RESPONSES; EVOKED-POTENTIALS; COCHLEAR NUCLEUS; MAGNETIC-FIELDS; CORTEX; LESIONS; SOUND; ORGANIZATION AB Experience-related changes in central nervous system (CNS) activity have been observed in the adult brain of many mammalian species, including humans. In humans, late-onset profound unilateral deafness creates an opportunity to study plasticity in the adult CNS consequent to monaural auditory deprivation. CNS activity was assessed by measuring long-latency auditory evoked potentials (AEPs) recorded from teens and adults with late-onset (post-childhood) profound unilateral deafness. Compared to monaurally stimulated normal-hearing subjects, the AEPs recorded from central electrode sites located over auditory cortical areas showed significant increases in inter-hemispheric waveform cross-correlation coefficients. and in inter-hemispheric AEP peak amplitude correlations. These increases provide evidence of substantial changes from the normal pattern of asymmetrical (contralateral > ipsilateral amplitude) and asynchronous (contralateral earlier than ipsilateral) central auditory system activation in the normal-hearing population to a much more symmetrical and synchronous activation in the unilaterally deaf These cross-sectional analyses of AEP data recorded from the unilaterally deaf also suggest that the changes in cortical activity occur gradually and continue for at least 2 years after the onset of hearing loss. Analyses of peak amplitude correlations suggest that the increased inter-hemispheric symmetry may be a consequence of changes in the generators producing the N-1 (approximately 100 ms peak latency) potential. These experience-related changes in central auditory system activity following late-onset profound unilateral deafness thus provide evidence of the presence and the time course of auditory system plasticity in the adult brain. (C) 2001 Elsevier Science B.V. All rights reserved. C1 House Ear Res Inst, Electrophysiol Lab, Los Angeles, CA 90057 USA. Univ Helsinki, Cent Hosp, Dept Otolaryngol, Helsinki 00290, Finland. Univ Washington, Dept Speech & Hearing Sci, Seattle, WA 98105 USA. HRI Labs LLC, Malibu, CA 90265 USA. RP Ponton, CW (reprint author), Neurosoft Inc, 5700 Cromo Dr,Suite 100, El Paso, TX 79912 USA. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 BESS FH, 1986, EAR HEARING, V7, P20, DOI 10.1097/00003446-198602000-00005 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 COLLETTI V, 1988, British Journal of Audiology, V22, P113, DOI 10.3109/03005368809077805 Donoghue JP, 1995, CURR OPIN NEUROBIOL, V5, P749, DOI 10.1016/0959-4388(95)80102-2 ELBERLING C, 1981, SCAND AUDIOL, V10, P203, DOI 10.3109/01050398109076182 FUJUKI N, 1998, NEUROREPORT, V9, P3129 GREENOUGH WT, 1975, AM SCI, V63, P37 HARRISON RV, 1993, ACTA OTO-LARYNGOL, V113, P296, DOI 10.3109/00016489309135812 HENDRY SH, 1988, NEURON, V8, P701 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JONGKEES L B, 1957, Acta Otolaryngol, V48, P465, DOI 10.3109/00016485709126908 KALTENBACH JA, 1992, HEARING RES, V59, P213, DOI 10.1016/0378-5955(92)90118-7 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 Kitzes L, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P256 KNIGHT RT, 1980, ELECTROEN CLIN NEURO, V50, P112, DOI 10.1016/0013-4694(80)90328-4 KNIGHT RT, 1988, ELECTROEN CLIN NEURO, V70, P499, DOI 10.1016/0013-4694(88)90148-4 LIEGEOISCHAUVEL C, 1994, ELECTROEN CLIN NEURO, V92, P204, DOI 10.1016/0168-5597(94)90064-7 MAKELA JP, 1992, NEUROREPORT, V3, P94 Makela JP, 1996, EXP BRAIN RES, V110, P446 NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x PANTEV C, 1986, AUDIOLOGY, V25, P54 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 Reale R A, 1987, Brain Res, V431, P281 REITE M, 1988, ELECTROEN CLIN NEURO, V70, P490, DOI 10.1016/0013-4694(88)90147-2 RIF J, 1991, ELECTROEN CLIN NEURO, V79, P464, DOI 10.1016/0013-4694(91)90166-2 Scheffler K, 1998, CEREB CORTEX, V8, P156, DOI 10.1093/cercor/8.2.156 Scherg M., 1990, ADV AUDIOL, V6, P40 SCHWABER MK, 1993, AM J OTOL, V14, P252 SKINNER JE, 1977, ATTENTION VOLUNTARY, P60 SLATTERY WH, 1994, HEARING RES, V75, P38, DOI 10.1016/0378-5955(94)90053-1 VASAMA JP, 1995, HEARING RES, V87, P132, DOI 10.1016/0378-5955(95)00086-J VASAMA JP, 1994, HEARING RES, V78, P91, DOI 10.1016/0378-5955(94)90047-7 VAUGHAN HG, 1970, ELECTROEN CLIN NEURO, V28, P360, DOI 10.1016/0013-4694(70)90228-2 WILLIS RD, 1984, J VAC SCI TECHNOL A, V2, P57, DOI 10.1116/1.572625 WILLOTT JF, 1991, HEARING RES, V53, P78, DOI 10.1016/0378-5955(91)90215-U WOODS DL, 1993, COGNITIVE BRAIN RES, V1, P227, DOI 10.1016/0926-6410(93)90007-R Yingling C. D., 1977, ATTENTION VOLUNTARY, P70 NR 41 TC 61 Z9 63 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 32 EP 44 DI 10.1016/S0378-5955(01)00214-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600004 PM 11423213 ER PT J AU Zheng, QY Johnson, KR AF Zheng, QY Johnson, KR TI Hearing loss associated with the modifier of deaf waddler (mdfw) locus corresponds with age-related hearing loss in 12 inbred strains of mice SO HEARING RESEARCH LA English DT Article DE hearing loss; mouse; inbred strain; age-related hearing loss; noise-induced hearing loss ID C57BL/6J MICE; MOUSE; GENE; SUSCEPTIBILITY; CHROMOSOME-10; PRESBYCUSIS; IMPAIRMENT AB The modifier of deaf waddler (mdfw) and age-related hearing loss (Ahl) loci were both discovered as inbred strain polymorphisms that affect hearing loss in mice. Both loci map to the same position on chromosome (Chr) 10. The mdfw locus interacts epistatically with the deaf waddler (dfw) mutation on Chr 6, and the Ahl locus is a major contributor to AHL in several inbred strains. To investigate the possibility of allelism, we examined the correspondence of mdfw and Ahl phenotypes among 12 inbred mouse strains. The effects of strain-specific mdfw alleles on hearing loss were assessed in dfw(2J)/+ F1 hybrids produced from mating BALB-dfw(2J)/+ mice with mice from each of 12 inbred strains. F1 hybrids were then assessed for hearing by auditory-evoked brainstem response threshold analysis and classified as dfw(2J)/+ or +/+ by polymerase chain reaction typing. Heterozygosity for dfw(2J) accelerated hearing Loss in F1 hybrids derived from all strains tested, except those produced with the B6.CAST + (Ahl) congenic strain. dfw-(2J)/+ F1 hybrids derived from parental strains 129P1/ReJ, A/J, BUB/BnJ, C57BR/cdJ, DBA/2J, NOD/LtJ and SKH2/J exhibited a severe hearing loss by 12 weeks of age. Those derived from strains 129T2/SvEmsJ, C3H/HeJ, CBA/CaJ and NON/LtJ exhibited only a slight to intermediate hearing loss at that age. The hearing loss associated with these strain-specific mdfw alleles corresponds with previously determined Ahl allele effects, providing additional evidence that mdfw and Ahl are manifestations of the same gene. A functional relationship therefore may exist between the Ca2+ transporting activity of the dfw gene (Atp2h2) and AHL. (C) 2001 published by Elsevier Science B.V. C1 Jackson Lab, Bar Harbor, ME 04609 USA. RP Johnson, KR (reprint author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA. RI Zheng, Qing/C-1731-2012 CR Bryda EC, 1997, MAMM GENOME, V8, P1, DOI 10.1007/s003359900336 Chaib H, 1996, HUM MOL GENET, V5, P1061, DOI 10.1093/hmg/5.7.1061 DEOL MS, 1956, PROC R SOC SER B-BIO, V145, P206, DOI 10.1098/rspb.1956.0028 Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X Fridberger A, 1998, P NATL ACAD SCI USA, V95, P7127, DOI 10.1073/pnas.95.12.7127 GORLIN RJ, 1995, HEREDITARY HEARING L, V28 HENRY KR, 1980, AUDIOLOGY, V19, P369 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X Johnson KR, 2000, GENOMICS, V70, P171, DOI 10.1006/geno.2000.6377 LI HS, 1993, AUDIOLOGY, V32, P195 Mikaelian D.O., 1979, LARYNGOSCOPE, V34, P1 MORTON NE, 1991, ANN NY ACAD SCI, V630, P16, DOI 10.1111/j.1749-6632.1991.tb19572.x NobenTrauth K, 1997, GENOMICS, V44, P266, DOI 10.1006/geno.1997.4869 Parham K, 1999, HEARING RES, V134, P29, DOI 10.1016/S0378-5955(99)00059-3 Simpson EM, 1997, NAT GENET, V16, P19, DOI 10.1038/ng0597-19 STEEL KP, 1991, ANN NY ACAD SCI, V630, P68, DOI 10.1111/j.1749-6632.1991.tb19576.x Street VA, 1998, NAT GENET, V19, P390 WardBailey PF, 1996, MAMM GENOME, V7, P793, DOI 10.1007/s003359900239 Wayne S, 1996, HUM MOL GENET, V5, P1689, DOI 10.1093/hmg/5.10.1689 WILLOTT JF, 1984, HEARING RES, V16, P161, DOI 10.1016/0378-5955(84)90005-4 Yoshida N, 2000, HEARING RES, V141, P97, DOI 10.1016/S0378-5955(99)00210-5 Zheng QY, 1999, HEARING RES, V130, P94, DOI 10.1016/S0378-5955(99)00003-9 NR 23 TC 43 Z9 51 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 45 EP 53 DI 10.1016/S0378-5955(01)00215-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600005 PM 11423214 ER PT J AU Jones, SM Jones, TA Bell, PL Taylor, MJ AF Jones, SM Jones, TA Bell, PL Taylor, MJ TI Compound gravity receptor polarization vectors evidenced by linear vestibular evoked potentials SO HEARING RESEARCH LA English DT Article DE otolith; bird; chicken; utricle; saccule; vestibular function ID INNERVATING OTOLITH ORGANS; SQUIRREL-MONKEY; RESPONSE PROPERTIES; STATIC TILTS; ACCELERATION; AFFERENTS; NERVE; PHYSIOLOGY; CHICK; FORCE AB The utricle and saccule are gravity receptor organs of the vestibular system. These receptors rely on a high-density otoconial membrane to detect linear acceleration and the position of the cranium relative to Earth's gravitational vector. The linear vestibular evoked potential (VsEP) has been shown to be an effective non-invasive functional test specifically for otoconial gravity receptors (Jones et al.. 1999). Moreover. there is some evidence that the VsEP can be used to independently test utricular and saccular function (Taylor et al.. 1997: Jones et al., 1998). Here we characterize compound macular polarization vectors for the utricle and saccule in hatchling chickens. Pulsed linear acceleration stimuli were presented in two axes. the dorsoventral (DV. +/-Z axis) to isolate the saccule. and the interaural (IA, +/- Y axis) to isolate the utricle. Traditional signal averaging was used to resolve responses recorded from the surface of the skull. Latency and amplitude of eighth nerve components of the linear VsEP were measured. Gravity receptor responses exhibited clear preferences for one stimulus direction in each axis. With respect to each utricular macula, lateral translation in the IA axis produced maximum ipsilateral response amplitudes with substantially greater amplitude-intensity (AI) slopes than medially directed movement. Downward caudal motions in the DV axis produced substantially larger response amplitudes and AI slopes. The results show that the macula lagena does not contribute to the VsEP compound polarization vectors of the sacculus and utricle. The findings suggest further that preferred compound vectors for the utricle depend on the pars externa (i.e. lateral hair cell field) whereas for the saccule they depend on pars interna (i.e. superior hair cell fields). These data provide evidence that maculae saccule and utricle can be selectively evaluated using the linear VsEP. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Missouri, Sch Med, Dept Surg, Div Otolaryngol, Columbia, MO 65212 USA. Univ Missouri, Sch Med, Columbia, MO 65212 USA. RP Jones, SM (reprint author), Univ Missouri, Sch Med, Dept Surg ENT, Rm 205,Allton Bldg,DC375-00,301 Business Loop 70W, Columbia, MO 65212 USA. CR Angelaki DE, 2000, J NEUROPHYSIOL, V83, P3005 BREUER J, 1891, ARCH GES PHYSL, V48, P195 BURKARD R, 1994, J ACOUST SOC AM, V95, P2136, DOI 10.1121/1.408675 Curthoys I S, 1991, Acta Otolaryngol Suppl, V481, P5 DeVRIES H., 1950, ACTA OTO LARYNGOL, V38, P262, DOI 10.3109/00016485009118384 DICKMAN JD, 1991, BRAIN RES, V556, P303 Fermin CD, 1998, HISTOL HISTOPATHOL, V13, P1103 FERNANDE.C, 1972, J NEUROPHYSIOL, V35, P978 FERNANDEZ C, 1976, J NEUROPHYSIOL, V39, P970 FERNANDEZ C, 1976, J NEUROPHYSIOL, V39, P985 FLOCK A, 1964, J CELL BIOL, V22, P413, DOI 10.1083/jcb.22.2.413 FLOCK AKE, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1351, DOI 10.1121/1.1918345 GOLDBERG JM, 1990, J NEUROPHYSIOL, V63, P781 Halmagyi G M, 1991, Acta Otolaryngol Suppl, V481, P47 Jones SM, 1997, J COMP PHYSIOL A, V180, P631, DOI 10.1007/s003590050079 Jones SM, 1998, HEARING RES, V121, P161, DOI 10.1016/S0378-5955(98)00074-4 Jones SM, 1999, HEARING RES, V135, P56, DOI 10.1016/S0378-5955(99)00090-8 JONES TA, 1992, ELECTROEN CLIN NEURO, V82, P377, DOI 10.1016/0013-4694(92)90007-5 Jones TA, 1998, J VESTIBUL RES-EQUIL, V8, P253 JONES TA, 1989, AM J OTOLARYNG, V10, P327, DOI 10.1016/0196-0709(89)90108-7 Jones TA, 1999, HEARING RES, V136, P75, DOI 10.1016/S0378-5955(99)00110-0 KUSAKARI J, 1970, TOHOKU J EXP MED, V100, P315 Lempert T, 1998, EXP BRAIN RES, V118, P533, DOI 10.1007/s002210050309 LINDEMAN HH, 1969, ACTA OTO-LARYNGOL, V67, P177, DOI 10.3109/00016486909125441 LOE PR, 1973, J PHYSIOL-LONDON, V230, P29 LOWENSTEIN O, 1959, NATURE, V184, P1807, DOI 10.1038/1841807a0 Nazareth AM, 1998, J VESTIBUL RES-EQUIL, V8, P233 ROSENHAL.U, 1970, ARCH KLIN EXP OHR, V197, P154, DOI 10.1007/BF00306164 Si XH, 1997, EXP BRAIN RES, V117, P242, DOI 10.1007/s002210050219 TAYLOR MJ, 1997, ASS RES OTOLARYNGOL, V37 TOMKO DL, 1981, EXP BRAIN RES, V41, P216 WEISLEDER P, 1990, ELECTROEN CLIN NEURO, V76, P362, DOI 10.1016/0013-4694(90)90037-K WERSALL J, 1965, COLD SPRING HARB SYM, V30, P115 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 NR 34 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 54 EP 61 DI 10.1016/S0378-5955(01)00216-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600006 PM 11423215 ER PT J AU Ladich, F Popper, AN AF Ladich, F Popper, AN TI Comparison of the inner ear ultrastructure between teleost fishes using different channels for communication SO HEARING RESEARCH LA English DT Article DE sound production; acoustic communication; hearing specialist; hair cell; anabantoid; evolution ID AUDITORY-SENSITIVITY; AGONISTIC BEHAVIOR; SOUND PRODUCTION; SIGNALS; ANABANTOIDEI; VOCALIZATION; MECHANISMS; SACCULUS; LAGENA; TONES AB The anatomy and ultrastructure of the inner ear of three species of gouramis which differ widely in acoustic behavior were studied using scanning electron microscopy. Of the three species, Trichopsis possess a pectoral sound-producing mechanism while Macropodus and Betta lack sonic organs. The general structure of the inner ear and the shapes of the sensory epithelia are very similar, although they do differ on the posterior part of the saccular macula which is more S-shaped in Trichopsis and Macropodus than in Betta. The maculae on the three species do not differ either in ciliary bundle type (cells with long kinocilia on the periphery of the maculae and cells with short kinocilia in the central region) or in hair cell orientation pattern. Quantitative measurements of hair cell densities and the size of the sensory epithelia of the saccule did not show significant differences between species. Data presented correlate with physiological results from other investigators showing similar auditory sensitivity in Trichopsis and Macropodus. The similarity in structure and function of the inner ears of gouramis on one hand, and the occurrence of sound generating organs in just one genus, suggests that hearing evolved prior to vocalization and thus acoustic communication in this taxon. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Vienna, Inst Zool, A-1090 Vienna, Austria. Univ Maryland, Dept Biol, College Pk, MD 20742 USA. RP Ladich, F (reprint author), Univ Vienna, Inst Zool, Althanstr 14, A-1090 Vienna, Austria. CR Bischof C, 1996, AGGRESSIVE BEHAV, V22, P447, DOI 10.1002/(SICI)1098-2337(1996)22:6<447::AID-AB5>3.0.CO;2-E Bregman AS., 1990, AUDITORY SCENE ANAL CLARKE NL, 1975, BIOPHYS J, V15, P307 COHEN MJ, 1967, J EXP ZOOL, V165, P355, DOI 10.1002/jez.1401650305 Crawford JD, 1999, J EXP BIOL, V202, P1417 CRAWFORD JD, 1997, J ACOUST SOC AM, V102, P1 HAGEDORN M, 1985, ANIM BEHAV, V33, P254, DOI 10.1016/S0003-3472(85)80139-1 Hawkins A.D., 1983, P347 HAWKINS AD, 1978, J MAR BIOL ASSOC UK, V58, P891 JOHNSTON CE, 2000, COPEIA, P657 KRATOCHVIL H, 1978, ZOOMORPHOLOGIE, V91, P91, DOI 10.1007/BF00994156 KRATOCHVIL H, 1985, ZOOL JAHRB ALLG ZOOL, V89, P203 Ladich F, 1998, BRAIN BEHAV EVOLUT, V51, P315, DOI 10.1159/000006545 Ladich F, 1998, J COMP PHYSIOL A, V182, P737, DOI 10.1007/s003590050218 Ladich F, 1999, BRAIN BEHAV EVOLUT, V53, P288, DOI 10.1159/000006600 Ladich F, 1997, MAR FRESHW BEHAV PHY, V29, P87 Ladich F., 1992, Bioacoustics, V4, P131 LADICH F, 1988, J FISH BIOL, V32, P707, DOI 10.1111/j.1095-8649.1988.tb05411.x LUNDBERG JG, 1993, BIOLOGICAL RELATIONSHIPS BETWEEN AFRICA AND SOUTH AMERICA, P156 Mann DA, 1998, J ACOUST SOC AM, V104, P562, DOI 10.1121/1.423255 Mann DA, 1997, NATURE, V389, P341, DOI 10.1038/38636 McKibben JR, 1999, J COMP PHYSIOL A, V184, P563, DOI 10.1007/s003590050356 Myrberg A.A, 1981, HEARING SOUND COMMUN, P395 MYRBERG AA, 1980, J COMP PHYSIOL, V140, P135 NELISSEN MHJ, 1978, BEHAVIOUR, V64, P137, DOI 10.1163/156853978X00477 Platt C., 1981, HEARING SOUND COMMUN, P3 PLATT C, 1984, SCANNING ELECT MICRO, V4, P1915 POPPER AN, 1981, J COMP NEUROL, V200, P357, DOI 10.1002/cne.902000306 POPPER AN, 1977, J MORPHOL, V153, P397, DOI 10.1002/jmor.1051530306 POPPER AN, 1981, HEARING RES, V5, P245, DOI 10.1016/0378-5955(81)90049-6 POPPER AN, 1980, AM J ANAT, V157, P115, DOI 10.1002/aja.1001570202 Popper A.N., 1999, COMP HEARING FISH AM, P43 POPPER AN, 1971, J AUD RES, V11, P239 POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 POPPER AN, 1982, AM ZOOL, V22, P311 POPPER AN, 1974, J EXP BIOL, V60, P295 RETZIUS G, 1881, GEHORORGAN WIRBELTTH, V1 Rogers P.H., 1988, P131 SAIDEL WM, 1987, COMP BIOCHEM PHYS A, V88, P37, DOI 10.1016/0300-9629(87)90095-8 SAND O, 1973, J EXP BIOL, V59, P405 SAND O, 1973, BASIC MECHANISMS HEA, P893 SATOU M, 1994, J COMP PHYSIOL A, V174, P539 SCHELLART NAM, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P295 Schneider Hiltrude, 1941, ZEITSCHR VERGLEICH PHYSIOL, V29, P172 Schuster S., 1986, ZOOL BEITR, V29, P295 SIMPSON M J A, 1968, Animal Behavior Monographs, V1, P1 SORENSEN PW, 1989, HORM BEHAV, V23, P317, DOI 10.1016/0018-506X(89)90046-9 STABENTHEINER A, 1988, J COMP PHYSIOL A, V162, P67, DOI 10.1007/BF01342704 STIPETIC E., 1939, ZEITSCHR VERGLEICH PHYSIOL, V26, P740, DOI 10.1007/BF00341099 WERNER CL. F., 1933, ZEITSCHR GES ANAT ABT I ZEITSCHR ANAT U ENTWICK LUNGSGESCH, V99, P696, DOI 10.1007/BF02118586 WINN HE, 1960, SCIENCE, V132, P222, DOI 10.1126/science.132.3421.222 Yan HY, 1998, J COMP PHYSIOL A, V183, P325, DOI 10.1007/s003590050259 Zelick R, 1999, COMP HEARING FISH AM, P363 NR 53 TC 9 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 62 EP 72 DI 10.1016/S0378-5955(01)00217-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600007 PM 11423216 ER PT J AU Bai, UM Seidman, MD AF Bai, UM Seidman, MD TI A specific mitochondrial DNA deletion (mtDNA(4977)) is identified in a pedigree of a family with hearing loss SO HEARING RESEARCH LA English DT Article DE specific mtDNA deletion; MtDNA(4977); family pedigree; hearing loss ID AUTOSOMAL RECESSIVE DEAFNESS; KEARNS-SAYRE SYNDROME; SENSORINEURAL DEAFNESS; CONNEXIN-26 MUTATIONS; TEMPORAL BONE; GENE; AGE; PRESBYCUSIS; IMPAIRMENT; DISEASES AB This paper presents a family pedigree of sensorineural hearing loss in patients with a mitochondrial DNA (mtDNA) deletion. Genomic DNA screenings including myo 15 and connexin 26 were normal. MtDNA deletions are associated with many pathophysiologic conditions, including neurological disorders, sensorineural hearing loss, ischemia, cardiomyopathies and aging. Several mitochondrial disorders secondary to mutations or deletions in mtDNA have been identified in association with deafness. The present study describes a pedigree of five individuals with hearing loss who harbor a 4977 bp common aging deletion, in their mtDNA. Chromosomal analysis was normal in all affected individuals. Audiologic and molecular biologic findings of these patients suggest that the common aging deletion of mtDNA may be a predisposing factor in sensorineural hearing loss in this family. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Henry Ford Hlth Syst, Dept Otolaryngol HNS, Detroit, MI 48322 USA. RP Seidman, MD (reprint author), Henry Ford Hlth Syst, Dept Otolaryngol HNS, 6777 W Maple Rd W, Detroit, MI 48322 USA. CR AMES BN, 1983, SCIENCE, V221, P1256, DOI 10.1126/science.6351251 Bai U, 1997, AM J OTOL, V18, P449 CORRALDEBRINSKI M, 1992, NAT GENET, V2, P324, DOI 10.1038/ng1292-324 Ensink RJH, 1998, ARCH OTOLARYNGOL, V124, P886 Esposito LA, 1999, P NATL ACAD SCI USA, V96, P4820, DOI 10.1073/pnas.96.9.4820 Estivill X, 1998, LANCET, V351, P394, DOI 10.1016/S0140-6736(97)11124-2 FischelGhodsian N, 1997, HEARING RES, V110, P147, DOI 10.1016/S0378-5955(97)00077-4 GOLD M, 1991, ANN NY ACAD SCI, V630, P301, DOI 10.1111/j.1749-6632.1991.tb19613.x HATTORI K, 1991, AM HEART J, V122, P866, DOI 10.1016/0002-8703(91)90542-P HEDDI A, 1993, J BIOL CHEM, V268, P12156 Kelsell DP, 1997, NATURE, V387, P80, DOI 10.1038/387080a0 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 Kopsidas G, 1998, MUTAT RES-FUND MOL M, V421, P27, DOI 10.1016/S0027-5107(98)00150-X Kopsidas G, 2000, ANN NY ACAD SCI, V908, P226 Lench N, 1998, LANCET, V351, P415, DOI 10.1016/S0140-6736(98)24006-2 MCCABE PC, 1990, GUIDE METHODS APPL P, P76 MORTON NE, 1991, ANN NY ACAD SCI, V630, P16, DOI 10.1111/j.1749-6632.1991.tb19572.x NUTTALL AL, 1979, ARCH OTOLARYNGOL, V105, P574 PREZANT TR, 1993, NAT GENET, V4, P289, DOI 10.1038/ng0793-289 Reardon W, 1998, LANCET, V351, P383, DOI 10.1016/S0140-6736(05)78347-1 Sawada S, 1997, AM J OTOL, V18, P332 SCHON EA, 1989, SCIENCE, V244, P346, DOI 10.1126/science.2711184 Seidman MD, 1997, ARCH OTOLARYNGOL, V123, P1039 Seidman MD, 2000, AM J OTOL, V21, P161, DOI 10.1016/S0196-0709(00)80003-4 SHANSKE S, 1990, NEUROLOGY, V40, P24 Soong N W, 1996, Methods Enzymol, V264, P421, DOI 10.1016/S0076-6879(96)64038-5 SWIFT AC, 1988, J LARYNGOL OTOL, V102, P626, DOI 10.1017/S0022215100105912 TASSABEHJI M, 1993, NAT GENET, V3, P26, DOI 10.1038/ng0193-26 TASSABEHJI M, 1992, NATURE, V355, P635, DOI 10.1038/355635a0 THALMANN I, 1970, ANN OTO RHINOL LARYN, V79, P12 Tiranti V, 1998, ANN NEUROL, V43, P98, DOI 10.1002/ana.410430116 TROUNCE I, 1989, LANCET, V1, P637 Ueda N, 1998, LARYNGOSCOPE, V108, P580, DOI 10.1097/00005537-199804000-00022 VANDENOUWELAND JMW, 1992, NAT GENET, V1, P368, DOI 10.1038/ng0892-368 VERNHAM GA, 1994, CLIN OTOLARYNGOL, V19, P314, DOI 10.1111/j.1365-2273.1994.tb01238.x WALLACE DC, 1992, ANNU REV BIOCHEM, V61, P1175, DOI 10.1146/annurev.bi.61.070192.005523 WALLACE DC, 1988, CELL, V55, P601, DOI 10.1016/0092-8674(88)90218-8 Wang AH, 1998, SCIENCE, V280, P1447, DOI 10.1126/science.280.5368.1447 Weil D, 1995, Nature, V374, P60 Zelante L, 1997, HUM MOL GENET, V6, P1605, DOI 10.1093/hmg/6.9.1605 NR 40 TC 10 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 73 EP 80 DI 10.1016/S0378-5955(01)00221-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600008 PM 11423217 ER PT J AU Tan, CT Lee, SY Yao, CJ Liu, SH Lin-Shiau, SY AF Tan, CT Lee, SY Yao, CJ Liu, SH Lin-Shiau, SY TI Effects of gentamicin and pH on [Ca2+](i) in apical and basal outer hair cells from guinea pigs SO HEARING RESEARCH LA English DT Article DE outer hair cell; gentamicin; intracellular calcium concentration; fura-2; extracellular pH ID CALCIUM-CHANNEL CURRENTS; AMINOGLYCOSIDE-INDUCED OTOTOXICITY; INTRACELLULAR CALCIUM; EXTERNAL PH; ANTIBIOTICS; MOTILITY; NEURONS; MECHANISMS; NEOMYCIN; COCHLEA AB Aminoglycosides are widely used antibiotics and frequently produce acute ototoxicity. In this study we attempted to comparatively investigate the effects of gentamicin on Ca2+ influx of apical and basal outer hair cells (OHCs) isolated from guineapig cochlea. Since the solution of gentamicin sulfate salt is acidic (pH 3.1 3.3), we also explored the effect of external acidification on Ca2+ influx. By means of fura-2 microspectrofluorimetry, we measured the intracellular calcium concentration ([Ca2+](i)) of OHCs bathed in Hanks' balanced salt solution (pH 7.40) during either a resting state or high K+-induced depolarization. Our results show that at the resting state, the baseline [Ca2+](i) in apical OHCs (94 +/- 2.0 nM) was slightly lower than that in basal OHCs (101.1 +/- 2.4 nM). By contrast, the increase in [Ca2+](i) evoked by high K+ depolarization in apical OHCs was about two-fold greater than that in basal OHCs. Nifedipine (30 muM) abolished the increased [Ca2+](i) in both types of OHCs, suggesting that Ca2+ influx was mainly through L-type Ca2+ channels of OHCs. While gentamicin and extracellular acidification (pH 7.14) can separately attenuate this increase in [Ca2+](i) in both types of OHCs, their suppressive effects are additive in basal OHCs, but not in apical OHCs. The implications of these findings are that: (1) apical and basal OHCs behave differently in response to depolarization-increased [Ca2+](i), and (2) basal OHCs are more vulnerable to the impairment of Ca2+ entry during depolarization by a combination of gentamicin and extracellular acidification, which is correlated with the clinical observation that ototoxicity of aminoglycosides at the basal coil of OHCs is more severe than that at the apical coils. Moreover, the possibility that extracellular acidification may enhance the acute ototoxic effects of aminoglycosides should be considered especially in topical applications. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Natl Taiwan Univ, Coll Med, Inst Toxicol, Taipei 10043, Taiwan. Natl Taiwan Univ Hosp, Dept Otolaryngol, Taipei 10043, Taiwan. RP Lin-Shiau, SY (reprint author), Natl Taiwan Univ, Coll Med, Inst Toxicol, 1 Sect,1 Jen Ai Rd, Taipei 10043, Taiwan. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWN GC, 1990, ARCH OPHTHALMOL-CHIC, V108, P1740 CHEN C, 1995, HEARING RES, V86, P25, DOI 10.1016/0378-5955(95)00050-E CORRADO AP, 1989, ACTA PHYSIOL PHARM L, V39, P419 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1992, AM J OTOL, V13, P108 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GARRIDO B, 1990, J PHYSIOL-LONDON, V428, P615 GOVAERTS PJ, 1990, TOXICOL LETT, V52, P227, DOI 10.1016/0378-4274(90)90033-I GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3450 GUO JQ, 1995, J PHYSIOL-LONDON, V483, P1 HARADA T, 1986, ANN OTO RHINOL LARYN, V95, P404 Haws CM, 1996, J GEN PHYSIOL, V107, P421, DOI 10.1085/jgp.107.3.421 HUDSPETH AJ, 1986, HEARING RES, V22, P21, DOI 10.1016/0378-5955(86)90070-5 Huizing E H, 1987, Acta Otolaryngol Suppl, V436, P117 IKEDA K, 1991, AM J PHYSIOL, V261, pC231 IKEDA K, 1989, AM J OTOLARYNG, V10, P382, DOI 10.1016/0196-0709(89)90032-X Jagger DJ, 1999, PFLUG ARCH EUR J PHY, V437, P409, DOI 10.1007/s004240050795 KROESE ABA, 1982, HEARING RES, V6, P183, DOI 10.1016/0378-5955(82)90053-3 Liu Y, 1997, HEARING RES, V112, P134, DOI 10.1016/S0378-5955(97)00110-X LLOYD KCK, 1988, AM J VET RES, V49, P650 NAKAGAWA T, 1992, BRAIN RES, V580, P345, DOI 10.1016/0006-8993(92)90966-D NAME CF, 1989, J PHARM PHARMACOL, V41, P188 Nenov AP, 1997, HEARING RES, V105, P146, DOI 10.1016/S0378-5955(96)00207-9 NILLES R, 1994, HEARING RES, V73, P27, DOI 10.1016/0378-5955(94)90279-8 REDMAN RS, 1994, BRIT J PHARMACOL, V113, P375 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 Sitges M, 1998, NEUROCHEM RES, V23, P477, DOI 10.1023/A:1022470215566 SPANDOW O, 1988, AM J OTOLARYNG, V9, P327, DOI 10.1016/S0196-0709(88)80041-3 SUAREZKURTZ G, 1987, PFLUG ARCH EUR J PHY, V410, P517, DOI 10.1007/BF00586535 TAKADA A, 1982, HEARING RES, V8, P179, DOI 10.1016/0378-5955(82)90073-9 TANGE RA, 1982, ARCH OTO-RHINO-LARYN, V236, P173, DOI 10.1007/BF00454037 Tombaugh GC, 1996, J PHYSIOL-LONDON, V493, P719 Watanabe Y, 1998, LIFE SCI, V62, P1671, DOI 10.1016/S0024-3205(98)00126-X WINKLER BS, 1992, OPHTHALMIC SURG LAS, V23, P622 Yao CJ, 1999, J NEUROCHEM, V73, P457, DOI 10.1046/j.1471-4159.1999.0730457.x ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 Zhou W, 1996, BIOPHYS J, V70, P1326 NR 40 TC 18 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 81 EP 87 DI 10.1016/S0378-5955(01)00222-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600009 PM 11423218 ER PT J AU Salt, AN Ma, YL AF Salt, AN Ma, YL TI Quantification of solute entry into cochlear perilymph through the round window membrane SO HEARING RESEARCH LA English DT Article DE cochlea; perilymph; round window membrane ID SUSTAINED-RELEASE VEHICLE; GUINEA-PIG COCHLEA; INNER-EAR; RADIAL COMMUNICATION; GENTAMICIN; INJECTION; SCALAE; TRACER; SPACE; FLOW AB The administration of drugs to the inner ear via the round window membrane is becoming more widely used for both clinical and experimental purposes. The actual drug levels achieved in different regions of the inner ear by this method have not been established. The present study has made use of simulations of solute movements in the cochlear fluids to describe the distribution of a marker solute in the guinea pig cochlear fluid spaces. Simulation parameters were derived from experimental measurements using a marker ion. trimethylphenylammonium (TMPA). The distribution of this ion in the cochlea was monitored without volume disturbance using TMPA-selective microelectrodes sealed into the first and second turns of scala tympani (ST). TMPA was applied to perilymph by irrigation of the intact round window membrane with 2 mM solution. At the end of a 90 min application period, TMPA in the first turn, 1.4 mm from the base of ST, reached an average concentration of 330 muM (standard deviation (S.D.) 147 muM, n = 8). TMPA in the second turn. 7.5 mm from the base of ST reached a concentration of 15 muM (S.D. 33 muM, n = 5). The measured time courses of TMPA concentration change were interpreted using the Washington University Cochlear Fluids Simulator (V 1.4), a public-domain program available on the internet at http://oto.wustl.edu/cochlea/. Simulations with parameters producing concentration time courses comparable to those measured were: (1) round window permeability: 1.9X10(-8) cm/s; (2) ST clearance half-time: 60 min: (3) longitudinal perilymph flow rate: 4.4 nl/min, directed from base to apex. Solute concentrations in apical regions of the cochlea were found to be determined primarily by the rate at which the solute diffuses, balanced by the rate of clearance of the solute from perilymph. Longitudinal perilymph now was not an important factor in solute distribution unless the bony otic capsule was perforated. which rapidly caused substantial changes to solute distribution. This study demonstrates the basic processes by which substances are distributed in the cochlea and provides a foundation to understand how other applied substances will be distributed in the ear. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. RP Salt, AN (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, Box 8115,660 S Euclid Ave, St Louis, MO 63110 USA. CR Balough BJ, 1998, OTOLARYNG HEAD NECK, V119, P427, DOI 10.1016/S0194-5998(98)70097-X Blakley BW, 1997, AM J OTOL, V18, P520 BRUMMETT RE, 1976, LARYNGOSCOPE, V86, P1177, DOI 10.1288/00005537-197608000-00009 COLES RRA, 1992, CLIN OTOLARYNGOL, V17, P240, DOI 10.1111/j.1365-2273.1992.tb01835.x GHIZ A, 2000, ASS RES OTOLARYNGOL, V23, P124 Hoffer ME, 1999, OTOLARYNG HEAD NECK, V120, P643, DOI 10.1053/hn.1999.v120.a91762 KOPKE R, 1995, ACTA OTOLARYNGOL STO, V116, P248 Lehner R, 1997, Ear Nose Throat J, V76, P567 MOSCOVITCH DH, 1973, ANN OTO RHINOL LARYN, V82, P198 SAIJO S, 1984, ACTA OTO-LARYNGOL, V97, P593, DOI 10.3109/00016488409132937 SALT AN, 1979, ACTA OTO-LARYNGOL, V88, P198, DOI 10.3109/00016487909137160 SALT AN, 1995, HEARING RES, V88, P79, DOI 10.1016/0378-5955(95)00103-B SALT AN, 1991, ACTA OTO-LARYNGOL, V111, P899, DOI 10.3109/00016489109138428 SALT AN, 1991, HEARING RES, V56, P37, DOI 10.1016/0378-5955(91)90151-X SALT AN, 1991, J NEUROSCI METH, V38, P233, DOI 10.1016/0165-0270(91)90173-W SALT AN, 1991, HEARING RES, V56, P29, DOI 10.1016/0378-5955(91)90150-8 Seidman MD, 1998, INT TINNITUS J, V4, P148 Silverstein H, 1999, Ear Nose Throat J, V78, P595 Stover T, 1999, HEARING RES, V136, P124, DOI 10.1016/S0378-5955(99)00115-X Thorne M, 1999, LARYNGOSCOPE, V109, P1661, DOI 10.1097/00005537-199910000-00021 YAGE M, 1999, HUM GENE THER, V10, P813 NR 21 TC 99 Z9 107 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 88 EP 97 DI 10.1016/S0378-5955(01)00223-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600010 PM 11423219 ER PT J AU Repass, JJ Watson, GM AF Repass, JJ Watson, GM TI Anemone repair proteins as a potential therapeutic agent for vertebrate hair cells: facilitated recovery of the lateral line of blind cave fish SO HEARING RESEARCH LA English DT Article DE mechanoreceptor; hair bundle; stereocilium; hair cell repair ID ANOPTICHTHYS-JORDANI CHARACIDAE; ANGELFISH PTEROPHYLLUM-EIMEKEI; FLOW FIELD ANALYSIS; MATHEMATICAL-DESCRIPTION; PLANE SURFACE; SEA-ANEMONES; SYSTEM; TRANSDUCTION; REGENERATION; PERFORMANCE AB Blind cave fish use the lateral line sensory system to detect nearby objects. The fish responds to sudden perturbations in the water column by initiating startle responses in which they swim more rapidly. Normal startle responses disappear after trauma caused by a single 15 s immersion in calcium free water, but return within 5 days if the traumatized fish are treated with 'repair proteins' isolated from sea anemones. Polyclonal antibodies raised to fraction beta, a specific chromatographic fraction of repair proteins, bind to hair cells within superficial neuromasts. Likewise, biotinylated fraction beta binds to hair cells in neuromasts. Neuromast hair cells exposed to calcium free water followed by repair proteins have more compact hair bundles than do hair cells exposed only to calcium free water. We propose that anemone repair proteins replace linkages between stereocilia destroyed by exposure to calcium free water. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ SW Louisiana, Dept Biol, Lafayette, LA 70504 USA. RP Watson, GM (reprint author), Univ SW Louisiana, Dept Biol, Box 42451, Lafayette, LA 70504 USA. CR ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X Conley RA, 1998, J COMP PHYSIOL A, V183, P335, DOI 10.1007/s003590050260 Coombs S., 1988, P553 Coombs S, 1996, J COMP PHYSIOL A, V178, P359 Corwin JT, 1997, NEURON, V19, P951, DOI 10.1016/S0896-6273(00)80386-4 Cotanche DA, 1999, AUDIOL NEURO-OTOL, V4, P271, DOI 10.1159/000013852 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 DOMENICI P, 1993, J EXP BIOL, V177, P253 DOMENICI P, 1993, CAN J ZOOL, V71, P2319, DOI 10.1139/z93-325 Eaton R.C., 1984, P213 Godin Jean-Guy J., 1997, P191 HASSAN ES, 1992, J COMP PHYSIOL A, V171, P413 HASSAN ES, 1985, BIOL CYBERN, V52, P23, DOI 10.1007/BF00336932 HASSAN ES, 1992, BIOL CYBERN, V66, P453, DOI 10.1007/BF00197726 HASSAN ES, 1992, BIOL CYBERN, V66, P443, DOI 10.1007/BF00197725 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 Kalmijn A.J., 1988, P83 MINASIAN LL, 1979, BIOL BULL, V157, P478, DOI 10.2307/1541032 Munday PL, 1997, J FISH BIOL, V51, P931, DOI 10.1006/jfbi.1997.0498 PICKLES JO, 1991, SCANNING MICROSCOPY, V5, P1115 Pitcher TJ, 1993, BEHAV TELEOST FISHES, P363 Roberts B.L., 1992, Reviews in Fish Biology and Fisheries, V2, P243, DOI 10.1007/BF00045039 Staecker H, 1998, CURR OPIN NEUROBIOL, V8, P480, DOI 10.1016/S0959-4388(98)80035-4 TEYKE T, 1990, BRAIN BEHAV EVOLUT, V35, P23, DOI 10.1159/000115853 TEYKE T, 1985, J COMP PHYSIOL A, V157, P837, DOI 10.1007/BF01350081 VONCAMPENHAUSEN C, 1981, J COMP PHYSIOL, V143, P369 Watson GM, 2000, HEARING RES, V146, P35, DOI 10.1016/S0378-5955(00)00095-2 Watson GM, 1997, HEARING RES, V107, P53, DOI 10.1016/S0378-5955(97)00022-1 Watson GM, 1998, HEARING RES, V115, P119, DOI 10.1016/S0378-5955(97)00185-8 WEBB PW, 1976, J EXP BIOL, V65, P157 WEBB PW, 1986, CAN J FISH AQUAT SCI, V43, P763 WEITZMAN S H, 1983, Bulletin of the Museum of Comparative Zoology, V150, P339 ZHAO Y, 1996, P NATL ACAD SCI USA, V94, P15469 NR 34 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 98 EP 107 DI 10.1016/S0378-5955(01)00226-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600011 PM 11423220 ER PT J AU Chen, GD Kong, J Reinhard, K Fechter, LD AF Chen, GD Kong, J Reinhard, K Fechter, LD TI NMDA receptor blockage protects against permanent noise-induced hearing loss but not its potentiation by carbon monoxide SO HEARING RESEARCH LA English DT Article DE NMDA receptor antagonist; MK-801-stereo isomers; noise-induced hearing loss; carbon monoxide ototoxicity; rat ID GUINEA-PIG COCHLEA; METHYL-D-ASPARTATE; POTASSIUM-INDUCED RELEASE; ISCHEMIC BRAIN-DAMAGE; OUTER HAIR CELL; ACOUSTIC OVERSTIMULATION; GLUTAMATE NEUROTOXICITY; INNER-EAR; PATHO-PHYSIOLOGY; MK-801 PROTECTS AB While a clear role has been proposed for glutamate as a putative neurotransmitter at the inner hair cell type I spiral ganglion cell synapse, the possible role of excessive glutamate release in cochlear impairment and of NMDA receptors in such a process is uncertain. The present study compares the protective effects of (+)-MK-801, an NMDA receptor antagonist, and the relatively inactive isomer (-)-MK-801 against permanent noise-induced hearing loss (NIHL). The study also asks whether (+)-MK-801 can protect against the NIHL potentiation by carbon monoxide (CO). Rats (n = 6) were exposed to 100-dB, 13.6-kHz octave-band noise for 2 h after receiving injection of (+)-MK-801 hydrogen maleate (1 mg/kg), (-)-MK-801 hydrogen maleate (1 mg/kg), or saline. Other groups of animals were exposed to the combination of noise and CO (1200 ppm) after receiving (+)-MK-801 or saline. Additional subjects received (+)-MK-801. saline or CO exposure alone. Compound action potential (CAP) threshold sensitivities were compared 4 weeks after the exposures. The results show significant protection by (+)-MK-801 against the permanent CAP threshold elevation induced bq noise alone. but no protective effect of (-)-MK-801. (+)-MK-801 produced limited protection against threshold shifts induced by the combination of noise and CO. Outer hair cell (OHC) loss was not protected by (+)-MK-801 administration. The data suggest that NMDA receptor stimulation may play a role in NIHL resulting from fairly mild noise exposure. The data do not support a role for NMDA receptor stimulation in the potentiation of NIHL that results from simultaneous exposure to CO and noise. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Oklahoma City, OK 73190 USA. RP Chen, GD (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, 1110 N Stonewall, Oklahoma City, OK 73190 USA. CR ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 Basile AS, 1996, NAT MED, V2, P1338, DOI 10.1038/nm1296-1338 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1990, HEARING RES, V46, P83, DOI 10.1016/0378-5955(90)90141-B BOBBIN RP, 1979, EXP BRAIN RES, V34, P389 BOBBIN RP, 1987, HEARING RES, V25, P77, DOI 10.1016/0378-5955(87)90081-5 BORG E, 1989, J ACOUST SOC AM, V86, P1776, DOI 10.1121/1.398609 Chen GD, 1999, HEARING RES, V138, P181, DOI 10.1016/S0378-5955(99)00157-4 Chen GD, 2000, HEARING RES, V145, P101 Chen GD, 1999, HEARING RES, V132, P149, DOI 10.1016/S0378-5955(99)00044-1 CHOI DW, 1988, NEURON, V1, P623, DOI 10.1016/0896-6273(88)90162-6 CHOI DW, 1990, ANNU REV NEUROSCI, V13, P171, DOI 10.1146/annurev.ne.13.030190.001131 Clark JA, 1996, HEARING RES, V99, P119, DOI 10.1016/S0378-5955(96)00092-5 Duan ML, 2000, P NATL ACAD SCI USA, V97, P7597, DOI 10.1073/pnas.97.13.7597 Engström B, 1983, Acta Otolaryngol Suppl, V402, P5 Engström B, 1983, Scand Audiol Suppl, V19, P1 Fechter LD, 1997, TOXICOL APPL PHARM, V142, P47, DOI 10.1006/taap.1996.8027 FECHTER LD, 1988, HEARING RES, V34, P39, DOI 10.1016/0378-5955(88)90049-4 Fridberger A, 1998, P NATL ACAD SCI USA, V95, P7127, DOI 10.1073/pnas.95.12.7127 GILL R, 1987, J NEUROSCI, V7, P3343 Griesbach GS, 1998, P NATL ACAD SCI USA, V95, P11435, DOI 10.1073/pnas.95.19.11435 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HENDERSON D, 1994, HEARING RES, V76, P101, DOI 10.1016/0378-5955(94)90092-2 Hu BH, 1997, HEARING RES, V110, P209, DOI 10.1016/S0378-5955(97)00075-0 HUCKER HB, 1983, DRUG METAB DISPOS, V11, P54 Hunter-Duvar I M, 1975, Can J Otolaryngol, V4, P152 Jacono AA, 1998, HEARING RES, V117, P31, DOI 10.1016/S0378-5955(97)00214-1 JANSSEN R, 1992, BRAIN RES, V590, P201, DOI 10.1016/0006-8993(92)91096-W JENISON GL, 1986, COMP BIOCHEM PHYS C, V84, P385, DOI 10.1016/0742-8413(86)90110-6 JENISON GL, 1985, HEARING RES, V20, P261, DOI 10.1016/0378-5955(85)90030-9 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x Kleinlogel S, 1999, NEUROREPORT, V10, P1879, DOI 10.1097/00001756-199906230-00015 Knipper M, 1997, CELL TISSUE RES, V287, P23 Lataye R, 2000, HEARING RES, V139, P86, DOI 10.1016/S0378-5955(99)00174-4 Levine S, 1998, Scand Audiol Suppl, V48, P27 LIM HH, 1993, HEARING RES, V69, P146 LITTMAN T, 1989, HEARING RES, V40, P45, DOI 10.1016/0378-5955(89)90098-1 LIU Y, 1995, TOXICOL APPL PHARM, V132, P196, DOI 10.1006/taap.1995.1099 LIU Z, 1992, CHIN J OTORHINOLARYN, V27, P24 LURIE MH, 1937, LARYNGOSCOPE, V48, P418 Matsubara A, 1996, J NEUROSCI, V16, P4457 MELDRUM B, 1985, TRENDS NEUROSCI, V8, P47, DOI 10.1016/0166-2236(85)90024-4 Niedzielski AS, 1997, AUDIOL NEURO-OTOL, V2, P79 NIEDZIELSKI AS, 1995, J NEUROSCI, V15, P2338 Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P229, DOI 10.1159/000013846 Puel JL, 1998, NEUROREPORT, V9, P2109, DOI 10.1097/00001756-199806220-00037 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 RAICHLE ME, 1983, ANN NEUROL, V13, P2, DOI 10.1002/ana.410130103 Rao D, 2000, TOXICOL APPL PHARM, V167, P125, DOI 10.1006/taap.2000.8995 ROTHMAN SM, 1986, ANN NEUROL, V19, P105, DOI 10.1002/ana.410190202 Ruel J, 1999, J PHYSIOL-LONDON, V518, P667, DOI 10.1111/j.1469-7793.1999.0667p.x RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 RYAN AF, 1991, NEUROREPORT, V2, P643, DOI 10.1097/00001756-199111000-00002 RYAN AF, 1984, BRAIN RES, V290, P376, DOI 10.1016/0006-8993(84)90960-0 SAFIEDDINE S, 1992, NEUROREPORT, V3, P1145, DOI 10.1097/00001756-199212000-00029 Safieddine S, 1997, J NEUROSCI, V17, P7523 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 Stebbins W C, 1979, Am J Otolaryngol, V1, P15, DOI 10.1016/S0196-0709(79)80004-6 USAMI S, 1995, NEUROREPORT, V6, P1161, DOI 10.1097/00001756-199505300-00022 VERTES D, 1982, ACTA OTO-LARYNGOL, V94, P403, DOI 10.3109/00016488209128928 Wang J A, 1990, Hear Res, V44, P143, DOI 10.1016/0378-5955(90)90076-2 WARD WD, 1981, ANN OTO RHINOL LARYN, V90, P584 Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 NR 65 TC 23 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 108 EP 115 DI 10.1016/S0378-5955(01)00228-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600012 PM 11423221 ER PT J AU Bartels, S Ito, S Trune, DR Nuttall, AL AF Bartels, S Ito, S Trune, DR Nuttall, AL TI Noise-induced hearing loss: the effect of melanin in the stria vascularis SO HEARING RESEARCH LA English DT Article DE melanin; sensorineural; stria vascularis; pigment ID PIGMENTED GUINEA-PIGS; INNER-EAR; LIQUID-CHROMATOGRAPHY; MELANOCYTES; ALBINO; EUMELANIN; HAIR; PHEOMELANIN; AGE; PROLIFERATION AB Conflicting investigations regarding the potential protective effect of melanin against noise-induced sensorineural hearing loss have suggested that eumelanin and pheomelanin may have differing effects within the stria vascularis. Three strains of C57BL/6J mice, (+/+, a/a) wild-types (dark coats/black eyes), (c2j/c2j, a/a), albinos (white coats/pink eyes), and (+/+, Ay/Ay) yellow mice (yellow coats/black eyes), were subjected to five consecutive days of broad band noise exposure at 112 dB(A) SPL for 3 h/day. Cochlear function was evaluated with auditory brainstem response audiometry to pure tones immediately pre-exposure, 5-6 h post exposure, and 14 days post-exposure. No significant difference in the degree of sensorineural hearing loss induced in the three strains of mice was identified. The eumelanin and pheomelanin content of each stria vascularis and amount of protein per stria for both mouse and guinea pig (2/NCR) were determined via high performance liquid chromatography. No pheomelanin was found in the stria of yellow mice, suggesting that coat color is not an accurate predictor of strial melanin content. The melanin content per mg of strial protein was higher in mice than in guinea pigs. A species-specific difference in melanin content does not explain the absence of a protective effect in mice. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Oregon Hearing Res Ctr, Dept Otolaryngol Head & Neck Surg, Portland, OR 97201 USA. Fujita Hlth Univ, Sch Hlth Sci, Toyoake, Aichi 4701192, Japan. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Nuttall, AL (reprint author), Oregon Hlth Sci Univ, Oregon Hearing Res Ctr, Dept Otolaryngol Head & Neck Surg, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR BARRENAS M-L, 1991, British Journal of Audiology, V25, P303, DOI 10.3109/03005369109076602 BARRENAS ML, 1992, ACTA OTO-LARYNGOL, V112, P50, DOI 10.3109/00016489209100782 BARRENAS ML, 1996, EAR HEARING, V17, P58 Barrenas ML, 1997, AUDIOLOGY, V36, P187 BARTELS S, 2000, MIDW M ASS RES OT ST Bonaccorsi P, 1965, Ann Laringol Otol Rinol Faringol, V64, P725 CONLEE JW, 1986, HEARING RES, V23, P81, DOI 10.1016/0378-5955(86)90177-2 CONLEE JW, 1994, HEARING RES, V79, P115, DOI 10.1016/0378-5955(94)90133-3 CRIFO S, 1973, ACTA OTO-LARYNGOL, V75, P38, DOI 10.3109/00016487309139636 DUM N, 1983, Z SAUGETIERKD, V48, P95 GARBER SR, 1982, EAR HEARING, V3, P207, DOI 10.1097/00003446-198207000-00004 GRENNER J, 1990, ACTA OTO-LARYNGOL, V109, P41, DOI 10.3109/00016489009107413 HENRY KR, 1982, BEHAV GENET, V12, P563, DOI 10.1007/BF01070410 Hirobe T, 1998, EUR J CELL BIOL, V75, P184 HOEFFDING V, 1991, HEARING RES, V54, P39, DOI 10.1016/0378-5955(91)90134-U ITO S, 1993, J INVEST DERMATOL, V100, pS166, DOI 10.1038/jid.1993.8 ITO S, 1985, ANAL BIOCHEM, V144, P527, DOI 10.1016/0003-2697(85)90150-2 ITO S, 1994, PIGM CELL RES, V7, P141, DOI 10.1111/j.1600-0749.1994.tb00041.x ITO S, 1983, J INVEST DERMATOL, V80, P268, DOI 10.1111/1523-1747.ep12534616 ITO S, 1998, ADV CHEM ANAL MELAMI, pCH31 JIMBOW K, 1983, J INVEST DERMATOL, V81, P506, DOI 10.1111/1523-1747.ep12522838 MILLAR SE, 1995, DEVELOPMENT, V121, P3223 Mitchell C, 1996, HEARING RES, V99, P38, DOI 10.1016/S0378-5955(96)00081-0 MOTOHASHI H, 1994, HEARING RES, V80, P10, DOI 10.1016/0378-5955(94)90003-5 Parham K, 1997, HEARING RES, V112, P216, DOI 10.1016/S0378-5955(97)00124-X PETERS TA, 1995, HEARING RES, V85, P169, DOI 10.1016/0378-5955(95)00043-4 PYE A, 1987, ARCH OTO-RHINO-LARYN, V243, P411, DOI 10.1007/BF00464654 SCHROTT A, 1990, HEARING RES, V46, P1, DOI 10.1016/0378-5955(90)90134-B SCHROTT A, 1987, ACTA OTO-LARYNGOL, V103, P451 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 STEEL KP, 1989, DEVELOPMENT, V107, P453 Tota G, 1967, Riv Otoneurooftalmol, V43, P183 WAARDENBURG PJ, 1951, AM J HUM GENET, V3, P195 Witkop Jr CJ, 1983, METABOLIC BASIS INHE, P301 YANZ JL, 1985, AUDIOLOGY, V24, P260 NR 35 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 116 EP 123 DI 10.1016/S0378-5955(01)00213-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600013 PM 11423222 ER PT J AU Zheng, JF Ren, TY Parthasarathi, A Nuttall, AL AF Zheng, JF Ren, TY Parthasarathi, A Nuttall, AL TI Quinine-induced alterations of electrically evoked otoacoustic emissions and cochlear potentials in guinea pigs SO HEARING RESEARCH LA English DT Article DE guinea pig; quinine; ototoxicity; outer hair cell; electromotility; otoacoustic emission; cochlear potential ID OUTER HAIR-CELLS; HEARING IMPAIRMENT; SOMATIC STIFFNESS; CHANNEL BLOCKERS; ACETYLCHOLINE; SALICYLATE; CURRENTS; MULTICOMPONENTS; ELECTROMOTILITY; MECHANICS AB Quinine is a well-known ototoxic drug which may affect portions of the auditory system with different biochemical effects, causing reversible hearing loss and tinnitus. Recent investigations indicate that quinine at high concentrations can act directly on cochlear outer hair cells to affect their motility and the mechanical response of the basilar membrane. This study aimed to investigate the effect of quinine on the electromotility of outer hair cells in vivo by means of measuring the electrically evoked otoacoustic emissions (EEOAEs), and the relationship between EEOAE and hearing sensitivity alterations in guinea pigs. Quinine was infused into the scala tympani with concentrations between 0.05 and 5 mM. An alternating current (35 muA RMS) swept from 400 Hz to 40 kHz was applied to the round window to evoke the EEOAE. The compound action potential (CAP), cochlear microphonic (CM) and summating potential (SP) were also measured. Results show that quinine affects the EEOAE in a dose-dependent manner and that its effects are reversible. Two aspects of the EEOAE were affected by quinine, depending on concentration: (1) the 'fine structure' only for concentrations below 0.1 mM and (2) the overall amplitude and the 'fine structure' for concentrations above 0.1 mM. At 5 mM the fine structure was completely absent and the mean amplitude of the EEOAE greatly decreased. Multiple component analysis shows the short delay component of the EEOAE is related to the mean value of the amplitude spectrum while the long delay component is related to the fine structure. The alterations of the EEOAE are roughly comparable to that of the cochlear potentials. A 'threshold concentration' for quinine's effects was found at 25 muM. CAP was significantly affected at 25 muM while EEOAE, CM and SP were not. E.nhancement of the EEOAE amplitude was noticed in five out of 20 animals in the current study. The enhancement appears only related to the EEOAE mean level or short delay component. The results suggest that quinine can affect in vivo electromotility of outer hair cells at low concentration and therefore change the cochlear amplifier performance via an effect on electro-mechanical transduction. Its effects on the cochlear spiral ganglion neurons and/or their presynaptic process are also suggested, and these are speculated to be the primary sites for quinine's effects on the auditory system. (C) 2001 Published by Elsevier Science B.V. C1 Oregon Hlth & Sci Univ, Oregon Hearing Res Ctr, Dept Otolaryngol Head & Neck Surg, Portland, OR 97201 USA. Chinese Peoples Liberat Army Gen Hosp, Dept Otolaryngol, Beijing 100853, Peoples R China. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Nuttall, AL (reprint author), Oregon Hlth & Sci Univ, Oregon Hearing Res Ctr, Dept Otolaryngol Head & Neck Surg, 3181 SW Sam Jackson Pk Rd,NRC04, Portland, OR 97201 USA. EM nuttall@ohsu.edu CR ALLEN JB, 1990, LECT NOTES BIOMATH, V87, P324 ALVAN G, 1991, BRIT J CLIN PHARMACO, V31, P409 ALVAN G, 1989, LIFE SCI, V45, P751, DOI 10.1016/0024-3205(89)90095-7 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BERNINGER E, 1995, SCAND AUDIOL, V24, P27, DOI 10.3109/01050399509042206 Berninger E, 1998, ACTA OTO-LARYNGOL, V118, P46 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DAIGNEAU.EA, 1970, TOXICOL APPL PHARM, V17, P223, DOI 10.1016/0041-008X(70)90146-8 DALLOS P, 1992, J NEUROSCI, V12, P4575 Dallos P, 1997, J NEUROSCI, V17, P2212 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 HAWKINS JE, 1972, LARYNGOSCOPE, V82, P1091, DOI 10.1288/00005537-197207000-00001 He DZZ, 2000, JARO-J ASSOC RES OTO, V1, P64, DOI 10.1007/s101620010006 He DZZ, 1999, P NATL ACAD SCI USA, V96, P8223, DOI 10.1073/pnas.96.14.8223 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 Jarboe JK, 1999, HEARING RES, V132, P43, DOI 10.1016/S0378-5955(99)00031-3 JUNG TTK, 1993, OTOLARYNG CLIN N AM, V26, P791 KARLSSON KK, 1990, NEUROSCI LETT, V116, P101, DOI 10.1016/0304-3940(90)90393-N KARLSSON KK, 1991, ACTA OTO-LARYNGOL, V111, P500, DOI 10.3109/00016489109138375 KARLSSON KK, 1991, HEARING RES, V53, P95, DOI 10.1016/0378-5955(91)90216-V Kenmochi M, 1997, HEARING RES, V113, P110, DOI 10.1016/S0378-5955(97)00137-8 Kirk DL, 1996, J ACOUST SOC AM, V100, P3714, DOI 10.1121/1.417335 Lin X, 1998, J NEUROPHYSIOL, V79, P2503 LIN X, 1995, HEARING RES, V88, P36, DOI 10.1016/0378-5955(95)00096-M MCFADDEN D, 1994, J ACOUST SOC AM, V95, P3460, DOI 10.1121/1.410022 Mulheran M, 1999, HEARING RES, V134, P145, DOI 10.1016/S0378-5955(99)00076-3 PAINTAUD G, 1994, CLIN PHARMACOL THER, V55, P317 Parthasarathi A.A, 2000, THESIS U MICHIGAN PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 Ren T, 2000, J NEUROSCI METH, V96, P97, DOI 10.1016/S0165-0270(99)00187-9 Ren TY, 1995, HEARING RES, V92, P178, DOI 10.1016/0378-5955(95)00217-0 Ren TY, 2000, HEARING RES, V143, P58, DOI 10.1016/S0378-5955(00)00027-7 ROCHE RJ, 1990, BRIT J CLIN PHARMACO, V29, P780 Ruggero MA, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P23 RYBAK LP, 1988, AM J OTOLARYNG, V9, P238, DOI 10.1016/S0196-0709(88)80033-4 STYPULKOWSKI PH, 1991, ASS RES OT MIDW RES Takeuchi S, 1998, NEUROSCI LETT, V247, P175, DOI 10.1016/S0304-3940(98)00318-8 Takeuchi S, 1996, HEARING RES, V101, P181, DOI 10.1016/S0378-5955(96)00151-7 Yamamoto T, 1997, NEUROSCI LETT, V236, P79, DOI 10.1016/S0304-3940(97)00749-0 ZHENG J, 2000, ASS RES OTOLARYNGOL NR 40 TC 14 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 124 EP 134 DI 10.1016/S0378-5955(01)00229-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600014 PM 11423223 ER PT J AU O'Leary, SJ Klis, SFL de Groot, JCMJ Hamers, FPT Smoorenburg, GF AF O'Leary, SJ Klis, SFL de Groot, JCMJ Hamers, FPT Smoorenburg, GF TI Perilymphatic application of cisplatin over several days in albino guinea pigs: dose-dependency of electrophysiological and morphological effects SO HEARING RESEARCH LA English DT Article DE cisplatin; osmotic pump; guinea pig; compound action potential; endocochlear potential; outer hair cell ID NEUROTROPHIC ACTH((4-9)) ANALOG; INDUCED OTOTOXICITY; STRIA VASCULARIS; SPONTANEOUS-RECOVERY; SODIUM THIOSULFATE; HEARING-LOSS; RAT; DIETHYLDITHIOCARBAMATE; PROTECTION; CALCIUM AB Cisplatin, at 0, 3, 30 or 300 mug/ml in saline, was applied to the scala tympani of the cochlea of guinea pigs via osmotic mini-pumps, operating at a pump rate of 0.5 mul/h. Electrocochleographic recordings were made from an implanted round window electrode. When an electrocochleographic criterion of ototoxicity was reached (40 dB loss in compound action potential (CAP) threshold at 8 kHz), or after 1 week if this criterion was not reached, the animals were sacrificed for light microscopy. A subgroup of animals had endocochlear potentials (EPs) measured prior to sacrifice. Hearing remained stable in the 0 mug/ml control group, but a sudden drop of auditory sensitivity across the whole frequency range was observed in all other groups. It took 15 days before the drop occurred, dependent on cisplatin concentration. CAP and cochlear microphonics were lost simultaneously. The EP was severely depressed in the affected animals, suggesting that cisplatin effects on the EP are primary. However. histology revealed an accompanying loss of outer hair cells, primarily in the basal turn. It is concluded that if cisplatin is given until ototoxicity becomes apparent electrophysiologically, then the cochlear pathology from intrascalar cisplatin administration resembles that from daily parenteral administration at 1.5-2.0 mg/kg. The cochlear pathology from the parenteral treatment was greater than that observed with 30 mug/ml pumps, and less than that From 300 mug/ml pumps. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Med Ctr, Hearing Res Labs, NL-3584 CX Utrecht, Netherlands. RP Klis, SFL (reprint author), Univ Utrecht, Med Ctr, Hearing Res Labs, Room G-02-531,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. CR ARAN JM, 1979, AUDITORY INVESTIGATI, P233 BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T Campbell KCM, 1996, HEARING RES, V102, P90, DOI 10.1016/S0378-5955(96)00152-9 Campbell KCM, 1999, HEARING RES, V138, P13, DOI 10.1016/S0378-5955(99)00142-2 CHURCH MW, 1995, HEARING RES, V86, P195, DOI 10.1016/0378-5955(95)00066-D deGroot JCMJ, 1997, HEARING RES, V106, P9, DOI 10.1016/S0378-5955(96)00213-4 DEOLIVIERA JAA, 1989, AUDIOVESTIBULAR TOXI, V2 GANDARA DR, 1990, CRIT REV ONCOL HEMAT, V10, P353, DOI 10.1016/1040-8428(90)90010-P Gill SS, 1997, HEARING RES, V113, P191, DOI 10.1016/S0378-5955(97)00141-X HAMERS FPT, 1994, EUR ARCH OTO-RHINO-L, V251, P23 Heijmen PS, 1999, HEARING RES, V128, P27, DOI 10.1016/S0378-5955(98)00194-4 Kamimura T, 1999, HEARING RES, V131, P117, DOI 10.1016/S0378-5955(99)00017-9 Klis SFL, 2000, NEUROREPORT, V11, P623, DOI 10.1097/00001756-200002280-00037 KOHN S, 1991, LARYNGOSCOPE, V101, P709 KOMUNE S, 1995, ANN OTO RHINOL LARYN, V104, P149 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 LAURELL G, 1990, LARYNGOSCOPE, V100, P724 LAURELL G, 1989, HEARING RES, V38, P19, DOI 10.1016/0378-5955(89)90124-X MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E Meech RP, 1998, HEARING RES, V124, P44, DOI 10.1016/S0378-5955(98)00116-6 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 OTTO WC, 1988, HEARING RES, V35, P79, DOI 10.1016/0378-5955(88)90042-1 SAITO T, 1991, HEARING RES, V56, P143, DOI 10.1016/0378-5955(91)90163-4 SCHWEITZER VG, 1993, LARYNGOSCOPE, V103, P1, DOI 10.1288/00005537-199304000-00001 Smoorenburg GF, 1999, ANN NY ACAD SCI, V884, P192, DOI 10.1111/j.1749-6632.1999.tb08642.x Stengs CHM, 1998, HEARING RES, V124, P99, DOI 10.1016/S0378-5955(98)00129-4 Stengs CHM, 1998, HEARING RES, V124, P108, DOI 10.1016/S0378-5955(98)00130-0 Stengs CHM, 1997, HEARING RES, V111, P103, DOI 10.1016/S0378-5955(97)00095-6 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 vanEmst MG, 1997, HEARING RES, V114, P93, DOI 10.1016/S0378-5955(97)00156-1 NR 30 TC 10 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 135 EP 145 DI 10.1016/S0378-5955(01)00232-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600015 PM 11423224 ER PT J AU Valentine, PA Eggermont, JJ AF Valentine, PA Eggermont, JJ TI Spontaneous burst-firing in three auditory cortical fields: its relation to local field potentials and its effect on inter-area cross-correlations SO HEARING RESEARCH LA English DT Article DE cat; auditory cortex; single unit; burst-firing; local field potential; cross-correlation ID SINGLE NEURONS; ELECTROPHYSIOLOGICAL PROPERTIES; NEOCORTICAL NEURONS; NEURAL INTERACTION; PAIR CORRELOGRAMS; CEREBRAL-CORTEX; POSTERIOR FIELD; VISUAL-CORTEX; CAT; OSCILLATIONS AB Burst-firing refers to epochs of sharply elevated neural discharge. It has been suggested that correlated firing in different cortical areas in anesthetized animals results from spontaneous burst-firing related to electroencephalogram spindling activity and state of drowsiness. To investigate this, simultaneous recordings of spontaneous firings of neurons in the primary (AI), secondary (AII) and anterior (AAF) fields of the auditory cortex in the lightly anaesthetized cat were obtained. This allowed a study of bursting behavior in the three cortical areas under exactly the same anesthetic state. Burst occurrences were detected using the Poisson-surprise method, and were typically highly synchronized with local field potentials (LFPs) and with burst-firing of other neurons recorded on the same electrode. Burst-firing occurred in 85%, of 371 units studied. and in 48 (15%) thereof there were at least 100 bursts per 15 min. Neurons in AI were bursting at a significantly higher rate, but with fewer spikes per burst, than units in AII. The average percentage of the time that a spontaneously firing neuron is in the bursting state is only about 3% (range 0.004, 29%). The average peak cross-correlation coefficients between spikes and LFP triggers were largest for burst-onset spikes, followed by those between all burst spikes and LFP triggers, and smallest when all spikes of the single unit were used in the correlation. This was the case for within- and between-area conditions. Burst-onset times in different auditory fields were not correlated. Thus, the major cause of the observed correlation of spontaneous firing in different cortical areas is not synchronous burst-firing. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Physiol & Biophys, Neurosci Res Grp, Calgary, AB T2N 1N4, Canada. RP Eggermont, JJ (reprint author), Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. CR BAIR W, 1994, J NEUROSCI, V14, P2870 BOWMAN DM, 1995, J NEUROPHYSIOL, V74, P1841 CHAGNACAMITAI Y, 1989, J NEUROPHYSIOL, V62, P1149 CONNORS BW, 1990, TRENDS NEUROSCI, V13, P99, DOI 10.1016/0166-2236(90)90185-D ECKHORN R, 1993, EXP BRAIN RES, V95, P177 Eggermont JJ, 2000, J NEUROPHYSIOL, V83, P2708 EGGERMONT JJ, 1993, CONCEPTS NEUROSCI, V2, P105 EGGERMONT JJ, 1995, NEUROREPORT, V6, P2121, DOI 10.1097/00001756-199511000-00006 Eggermont JJ, 1996, EXP BRAIN RES, V110, P379 EGGERMONT JJ, 1993, J NEUROPHYSIOL, V69, P1292 Eggermont JJ, 1998, J NEUROPHYSIOL, V80, P2743 EGGERMONT JJ, 1992, J NEUROPHYSIOL, V68, P1216 Eggermont JJ, 1998, HEARING RES, V117, P149, DOI 10.1016/S0378-5955(98)00008-2 Eggermont JJ, 1999, J NEUROPHYSIOL, V81, P2570 EGGERMONT JJ, 1995, NEUROREPORT, V6, P2125, DOI 10.1097/00001756-199511000-00007 EGGERMONT JJ, 1995, J NEUROPHYSIOL, V73, P227 FRIEDMAN A, 1987, NEUROSCI LETT, V81, P117, DOI 10.1016/0304-3940(87)90350-8 Gray CM, 1996, SCIENCE, V274, P109, DOI 10.1126/science.274.5284.109 JAHNSEN H, 1984, J PHYSIOL-LONDON, V349, P205 Kimura M, 1999, HEARING RES, V135, P146, DOI 10.1016/S0378-5955(99)00104-5 KOBAYASHI T, 1993, NEUROREPORT, V4, P735, DOI 10.1097/00001756-199306000-00034 LEGENDY CR, 1985, J NEUROPHYSIOL, V53, P926 LLINAS RR, 1988, SCIENCE, V242, P1654, DOI 10.1126/science.3059497 MCCORMICK DA, 1990, NEUROSCIENCE, V39, P103, DOI 10.1016/0306-4522(90)90225-S MITZDORF U, 1985, PHYSIOL REV, V65, P37 MOREL A, 1987, J COMP NEUROL, V265, P119, DOI 10.1002/cne.902650109 MORIN D, 1981, BRAIN RES, V205, P49, DOI 10.1016/0006-8993(81)90719-8 PHILLIPS DP, 1995, J NEUROPHYSIOL, V73, P674 PHILLIPS DP, 1984, J NEUROPHYSIOL, V51, P147 SANSEVERINO E R, 1973, Brain Research, V54, P225 Sherman SM, 1996, VISUAL NEUROSCI, V13, P205 Steriade M, 1990, THALAMIC OSCILLATION Steriade M, 1997, CEREB CORTEX, V7, P583, DOI 10.1093/cercor/7.6.583 WALLACE MN, 1991, EXP BRAIN RES, V86, P527 Winer JA, 1992, MAMMALIAN AUDITORY P, P222 NR 35 TC 12 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 146 EP 157 DI 10.1016/S0378-5955(01)00241-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600016 PM 11423225 ER PT J AU Wada, H Koike, T Yuasa, Y Kawase, T Fujii, H AF Wada, H Koike, T Yuasa, Y Kawase, T Fujii, H TI Measurement of stapes mobility in guinea pigs and rabbits SO HEARING RESEARCH LA English DT Article DE stapes; mobility; stiffness; sensor; measurement ID HUMAN TEMPORAL BONES; MIDDLE-EAR; INPUT IMPEDANCE; COCHLEA; OTOSCLEROSIS; DIAGNOSIS; MECHANICS; DISORDERS; LIGAMENT; SEX AB In tympanoplasty, it is essential to know the condition of the stapes. However, it has been difficult to evaluate stapes mobility in routine measurement. With the eve on improving future clinical practice, in this study we developed a new, easy system of measuring stapes mobility quantitatively and, as a first step, applied it to measurement of the relationship between the load and displacement of the stapes in guinea pigs and rabbits. The stapes displacement increased linearly with an increase in load in the small displacement region, and increased nonlinearly in the large displacement region. The slope of the regression line of this stiffness curve in the small displacement region was used as an index of the stapes mobility. The values in the guinea pigs and rabbits were 16 +/- 7 N/m and 115 +/- 25 N/m. respectively. A significant difference between the two species was observed. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Tohoku Univ, Dept Mech Engn, Sendai, Miyagi 9808579, Japan. Tohoku Univ, Sch Med, Dept Otolaryngol, Sendai, Miyagi 9800872, Japan. RP Wada, H (reprint author), Tohoku Univ, Dept Mech Engn, Aoba Yama 01, Sendai, Miyagi 9808579, Japan. CR BEL J, 1975, AUDIOLOGY, V14, P118 BROWNING GG, 1985, J LARYNGOL OTOL, V99, P545, DOI 10.1017/S002221510009722X GERSDORFF M, 1985, AUDIOLOGY, V24, P167 GUMMER AW, 1989, HEARING RES, V39, P1, DOI 10.1016/0378-5955(89)90077-4 GYO K, 1993, J OTO RHINO LARYNGOL, V96, P1246 GYO K, 1987, ACTA OTO-LARYNGOL, V103, P87, DOI 10.3109/00016488709134702 HOFMANN H, 1999, 2 INT S MIDDL EAR ME, P64 HUTTENBRINK KB, 1993, LARYNGOSCOPE, V103, P668 JERGER J, 1974, ARCH OTOLARYNGOL, V99, P165 Kirikae I., 1960, STRUCTURE FUNCTION M KUROKAWA H, 1995, OTOLARYNG HEAD NECK, V113, P349, DOI 10.1016/S0194-5998(95)70067-6 LYNCH TJ, 1982, J ACOUST SOC AM, V72, P108, DOI 10.1121/1.387995 Merchant SN, 1996, HEARING RES, V97, P30 ONCHI Y, 1961, J ACOUST SOC AM, V33, P794, DOI 10.1121/1.1908801 RUGGERO MA, 1990, J ACOUST SOC AM, V87, P1612, DOI 10.1121/1.399409 Schon F, 1999, AUDIOL NEURO-OTOL, V4, P142, DOI 10.1159/000013833 SHIBUYA K, 1995, J JUZEN MED SOC, V104, P175 STASCHE N, 1994, ACTA OTO-LARYNGOL, V114, P59, DOI 10.3109/00016489409126017 TIPTON CM, 1978, J BONE JOINT SURG AM, V60, P230 WADA H, 1994, J OTOLARYNGOL JPN, V97, P898 Wada H, 1998, EAR HEARING, V19, P240, DOI 10.1097/00003446-199806000-00007 WOO SLY, 1990, MECH AGEING DEV, V56, P129, DOI 10.1016/0047-6374(90)90004-Y YAMANE A, 1990, Gerodontology, V9, P9, DOI 10.1111/j.1741-2358.1990.tb00252.x NR 23 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 158 EP 164 DI 10.1016/S0378-5955(01)00242-8 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600017 PM 11423226 ER PT J AU Griffiths, TD Dean, JL Woods, W Rees, A Green, GGR AF Griffiths, TD Dean, JL Woods, W Rees, A Green, GGR TI The Newcastle Auditory Battery (NAB) - A temporal and spatial test battery for use on adult naive subjects SO HEARING RESEARCH LA English DT Article DE human; psychophysics; lesion; test battery ID TONES; RESPONSES; HEARING AB A battery of tests for assessing the perception of temporal and spatial acoustic cues is described, together with a software platform for implementing the battery. The software runs on a personal computer tither with a sound card or with widely used laboratory hardware. The battery is intended for use with neurologically impaired and other naive subjects, to allow inference at the single-subject level for any given subtest. The aim is to allow a systematic psychoacoustic evaluation of complex sound processing in single patients. Normal values are given for the threshold data for 30 of the battery are allowed by modular software architecture. naive control subjects aged from 20 to 60 years. Future modifications (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Newcastle, Sch Med, Dept Physiol Sci, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. RP Griffiths, TD (reprint author), Univ Newcastle, Sch Med, Dept Physiol Sci, Framlington Pl, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. RI Rees, Adrian/H-2200-2012; Green, Gary/D-3543-2009 CR ANNETT M, 1970, BRIT J PSYCHOL, V61, P303 Ellis A. W., 1988, HUMAN COGNITIVE NEUR GREEN GGR, 1976, J PHYSL, V260 Griffiths TD, 1997, BRAIN, V120, P785, DOI 10.1093/brain/120.5.785 Griffiths TD, 1996, NATURE, V383, P425, DOI 10.1038/383425a0 GRIFFITHS TD, IN PRESS BIOL FDN MU GRIFFITHS TD, 1998, NAT NEUROSCI, V1, P421 Griffiths TD, 1997, J NEUROL NEUROSUR PS, V62, P522, DOI 10.1136/jnnp.62.5.522 Griffiths TD, 1998, NEUROREPORT, V9, P3383, DOI 10.1097/00001756-199810260-00009 HARMS MP, 1998, NEUROIMAGE, V7, pS365 KAY RH, 1982, PHYSIOL REV, V62, P894 MOLLER AR, 1974, EXP NEUROL, V45, P104, DOI 10.1016/0014-4886(74)90104-6 Patterson RD, 1996, J ACOUST SOC AM, V100, P3286, DOI 10.1121/1.417212 Phillips DP, 1997, J ACOUST SOC AM, V101, P3694, DOI 10.1121/1.419376 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 Witton C, 1998, CURR BIOL, V8, P791, DOI 10.1016/S0960-9822(98)70320-3 ZATORRE RJ, 1988, J ACOUST SOC AM, V84, P566, DOI 10.1121/1.396834 Zwicker E., 1952, ACUSTICA S3, V2, P125 NR 18 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 165 EP 169 DI 10.1016/S0378-5955(01)00243-X PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600018 PM 11423227 ER PT J AU Campo, P Lataye, R Loquet, G Bonnet, P AF Campo, P Lataye, R Loquet, G Bonnet, P TI Styrene-induced hearing loss: a membrane insult SO HEARING RESEARCH LA English DT Article DE styrene; solvent; ototoxicity; membrane; rat ID RAT COCHLEA; EXPOSURE; TOLUENE; NOISE; TRICHLOROETHYLENE; OTOTOXICITY; SOLVENTS; ORGAN; CORTI; CELLS AB Styrene is an aromatic solvent widely used as a precursor for polystyrene plastics in many factories which produce glass-reinforced plastic. This solvent has been shown to disrupt the auditory system in both humans and animals. In order to study the sequence of events which could explain the cochlear impairments. a time course experiment was carried out with 6-month-old rats. Male LongEvans rats were exposed to 1000 ppm styrene for 6 h/day, 5 days/week, for either 1, 2, 3, or 4 consecutive weeks. Auditory function was tested by recording the near field evoked potentials from the inferior colliculus, and histological analyses of the cochleae were performed with light and transmission electron microscopy. The electrophysiological results support a toxic mid-frequency process which keeps worsening even after the end of the exposure. The histological findings demonstrate that supporting cells are the first targets of the solvent. Then. the outer hair cells of the third row (OHC3) are disrupted, followed successively by OHC2 and OHC1 from the basal (20 kHz) to the upper turn (4 kHz) of the cochlea. Basically, the disorganization of the membranous structures could be the starting point for the cochlear injury induced by styrene. This paper presents a hypothesis that the accumulation of K+ in the spaces of Nuel underlies the toxic effects of styrene. (C) 2001 published by Elsevier Science B.V. C1 Inst Natl Rech & Secur, Lab Neurotoxicite, F-54501 Vandoeuvre Nancy, France. RP Campo, P (reprint author), Inst Natl Rech & Secur, Lab Neurotoxicite, POB 27, F-54501 Vandoeuvre Nancy, France. CR BASTIDE JC, 2000, TRAV SECUR, V582, P39 CALEBRESE G, 1996, INT ARCH OCC ENV HEA, V68, P219 Campo P, 1997, NEUROTOXICOL TERATOL, V19, P129, DOI 10.1016/S0892-0362(96)00214-0 Campo P, 1999, NEUROTOXICOL TERATOL, V21, P427, DOI 10.1016/S0892-0362(99)00010-0 CROFTON KM, 1994, HEARING RES, V80, P25, DOI 10.1016/0378-5955(94)90005-1 Crofton KM, 1997, FUND APPL TOXICOL, V38, P101, DOI 10.1006/faat.1997.2327 JACOBSEN P, 1993, OCCUP MED-OXFORD, V43, P180, DOI 10.1093/occmed/43.4.180 Lataye R, 1997, NEUROTOXICOL TERATOL, V19, P373, DOI 10.1016/S0892-0362(97)00049-4 Lataye R, 2000, HEARING RES, V139, P86, DOI 10.1016/S0378-5955(99)00174-4 LEENA A, 1999, ANN OCCUP HYG, V43, P99 Loquet G, 1999, NEUROTOXICOL TERATOL, V21, P689, DOI 10.1016/S0892-0362(99)00030-6 MERCHAN MA, 1980, J ANAT, V131, P519 MILLER RR, 1994, CRIT REV TOXICOL, V24, pS1, DOI 10.3109/10408449409020137 MOLLER C, 1990, SCAND J WORK ENV HEA, V16, P189 MORATA TC, 1994, ARCH ENVIRON HEALTH, V49, P359 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 PRYOR GT, 1987, J APPL TOXICOL, V7, P55, DOI 10.1002/jat.2550070110 RAPHAEL Y, 1991, HEARING RES, V51, P173, DOI 10.1016/0378-5955(91)90034-7 RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x REBERT CS, 1993, INT J PSYCHOPHYSIOL, V14, P49, DOI 10.1016/0167-8760(93)90083-2 SANTOS-SACCHI J, 1986, CELL TISSUE RES, V245, P525 SANTOS-SACCHI J, 1991, HEARING RES, V52, P89, DOI 10.1016/0378-5955(91)90190-K Sass-Kortsak Andrea M., 1995, Annals of Epidemiology, V5, P15, DOI 10.1016/1047-2797(94)00036-S Spicer SS, 1998, HEARING RES, V118, P1, DOI 10.1016/S0378-5955(98)00006-9 YANO BL, 1992, TOXICOL PATHOL, V20, P1 NR 25 TC 33 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2001 VL 154 IS 1-2 BP 170 EP 180 DI 10.1016/S0378-5955(01)00218-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 416FX UT WOS:000167770600019 PM 11423228 ER PT J AU Tabuchi, K Tsuji, S Ito, Z Hara, A Kusakari, J AF Tabuchi, K Tsuji, S Ito, Z Hara, A Kusakari, J TI Does xanthine oxidase contribute to the hydroxyl radical generation in ischemia and reperfusion of the cochlea? SO HEARING RESEARCH LA English DT Article DE cochlea; compound action potential; ischemia; hydroxyl radical; xanthine oxidase ID BLOOD-FLOW; ALLOPURINOL; MANNITOL; PROTECTION; DAMAGE AB We investigated the effect of a hydroxyl radical scavenger, 1,3-dimethyl-2-thiourea (dimethylthiourea), and two xanthine oxidase inhibitors, oxypurinol and allopurinol, on the threshold shift of the compound action potential (CAP) after transient ischemia of the cochlea. Transient ischemia of 30 min duration was induced in albino guinea pigs via a skull base approach. The animals were treated with perilymphatic perfusion of dimethylthiourea, oxypurinol or allopurinol from 10 min before the onset of ischemia to 4 h after the termination of ischemia. Dimethylthiourea ameliorated the CAP threshold shifts at 4 h after the onset of reperfusion in a dose-dependent manner. However, oxypurinol and allopurinol did not affect the post-ischemic cochlear dysfunction. These results imply that the hydroxyl radical plays an important role in generation of cochlear dysfunction induced by ischemia-reperfusion and that xanthine oxidase may not be the primary source of this radical. (c) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. RP Kusakari, J (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR ANDREWS RJ, 1993, SURG NEUROL, V39, P218, DOI 10.1016/0090-3019(93)90186-5 Bobbin R.P., 1974, ACTA OTO-LARYNGOL, V77, P55 Fechter LD, 1997, TOXICOL APPL PHARM, V142, P47, DOI 10.1006/taap.1996.8027 GODIN DV, 1987, BIOCHEM PHARMACOL, V36, P2101, DOI 10.1016/0006-2952(87)90137-7 GRANGER DN, 1981, GASTROENTEROLOGY, V81, P22 Kusakari J, 1981, Auris Nasus Larynx, V8, P55 MOORHOUSE CP, 1987, FEBS LETT, V213, P23 Parks D A, 1986, Acta Physiol Scand Suppl, V548, P87 QUIRK WS, 1990, ACTA OTO-LARYNGOL, V109, P383, DOI 10.3109/00016489009125159 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P457 Sohmer H, 1967, Acta Otolaryngol, V64, P55, DOI 10.3109/00016486709139092 Tabuchi K, 1998, HEARING RES, V126, P28, DOI 10.1016/S0378-5955(98)00142-7 TAYLOR MD, 1985, BRAIN RES, V347, P268, DOI 10.1016/0006-8993(85)90186-6 WAKIZONO S, 1990, EUR ARCH OTO-RHINO-L, V247, P97 Weiss S J, 1986, Acta Physiol Scand Suppl, V548, P9 ZIMMERMAN BJ, 1988, AM J PHYSIOL, V255, pH202 NR 16 TC 18 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 1 EP 6 DI 10.1016/S0378-5955(00)00247-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700001 PM 11223291 ER PT J AU Nagura, M Iwasaki, S Mizuta, K Mineta, H Umemura, K Hoshino, T AF Nagura, M Iwasaki, S Mizuta, K Mineta, H Umemura, K Hoshino, T TI Role of nitric oxide in focal microcirculation disorder of guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE nitric oxide; cochlear blood flow; microcirculation disorder; photochemical reaction; reactive oxygen species; endothelial cell ID BLOOD-FLOW; CEREBRAL-ISCHEMIA; SODIUM-NITROPRUSSIDE; ION-TRANSPORT; SYNTHASE; LOCALIZATION; REPERFUSION; POTENTIALS; FLOWMETER; ACYLATION AB This study was designed to evaluate the role of endogenous nitric oxide (NO) in focal microcirculation disorder of the guinea pig cochlea. Focal microcirculation disorder was induced by a photochemical reaction at the lateral wall of the second cochlear turn. Saline or No-nitro-L-arginine methyl ester (L-NAME) was administered before the onset of photochemical reaction. Cochlear blood flow (CBF) was measured at the focal lesion (ischemic core), 1 mm from the lesion in the apical and basal direction (ischemic border zone) by using a novel non-contact laser blood flowmeter. NO synthase activities were measured by radioenzymeassay. In the saline pretreatment group, CBF was significantly decreased to 58.8 +/- 4.4% of the baseline at the ischemic core 30 min after the onset of photochemical reaction (P < 0.01), while CBF showed no significant change at the ischemic border zone. In the L-NAME pretreatment group, CBF was significantly decreased not only at the focal lesion (48.3 +/- 6.5%, P < 0.01), but also at the ischemic border zone (apical, 49.3 +/- 2.3%, P < 0.05; basal, 58.7 +/- 7.1%, P < 0.05, respectively). NO synthase III activity of cochlea was increased significantly (P < 0.01) 15 min after microcirculation disorder. These findings suggest that formation of endogenous NO plays a key role in the maintenance of CBF in acute focal cochlear microcirculation disorder. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Hamamatsu Univ Sch Med, Dept Otolaryngol, Hamamatsu, Shizuoka 4313192, Japan. Hamamatsu Univ Sch Med, Dept Pharmacol, Hamamatsu, Shizuoka 4313192, Japan. RP Nagura, M (reprint author), Hamamatsu Univ Sch Med, Dept Otolaryngol, 3600 Handa Cho, Hamamatsu, Shizuoka 4313192, Japan. EM mnagura@hei.org CR ASAI Y, 1993, EUR ARCH OTO-RHINO-L, V250, P292 Belhassen L, 1997, J BIOL CHEM, V272, P11198 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 BREDT DS, 1990, P NATL ACAD SCI USA, V87, P682, DOI 10.1073/pnas.87.2.682 BROWN MC, 1983, HEARING RES, V9, P131, DOI 10.1016/0378-5955(83)90023-0 CARLISLE L, 1990, HEARING RES, V43, P107, DOI 10.1016/0378-5955(90)90219-F CHEN C, 1995, HEARING RES, V87, P1, DOI 10.1016/0378-5955(95)00071-B CRISTOL JP, 1993, BRIT J PHARMACOL, V109, P188 Dais CGD, 1996, HEARING RES, V99, P1 DUVALL AJ, 1980, ANN OTO RHINOL LARYN, V89, P335 EYBALIN M, 1983, ACTA OTO-LARYNGOL, V96, P69, DOI 10.3109/00016488309132876 Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 Gao J, 1998, MICROSC RES TECHNIQ, V41, P323, DOI 10.1002/(SICI)1097-0029(19980515)41:4<323::AID-JEMT5>3.0.CO;2-R HIRATA K, 1988, EUR J APPL PHYSIOL O, V57, P616, DOI 10.1007/BF00418472 Iwasaki S, 1997, HEARING RES, V108, P55, DOI 10.1016/S0378-5955(97)00045-2 Iwasaki S, 1998, ACTA OTO-LARYNGOL, V118, P666 KASHIMA S, 1994, OPT LASER TECHNOL, V26, P169, DOI 10.1016/0030-3992(94)90039-6 Kong WJ, 1996, HEARING RES, V99, P22, DOI 10.1016/S0378-5955(96)00076-7 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 LAURIKAINEN EA, 1994, J PHYSIOL-LONDON, V480, P563 LAWRENCE M, 1975, ANN OTO RHINOL LARYN, V84, P499 LEE PCC, 1987, PHOTOCHEM PHOTOBIOL, V45, P79, DOI 10.1111/j.1751-1097.1987.tb08407.x Margaill I, 1997, BRIT J PHARMACOL, V120, P160, DOI 10.1038/sj.bjp.0700889 Michel O, 1999, HEARING RES, V133, P1, DOI 10.1016/S0378-5955(99)00049-0 MICHEL T, 1993, P NATL ACAD SCI USA, V90, P6252, DOI 10.1073/pnas.90.13.6252 MILLER JM, 1984, ARCH OTOLARYNGOL, V110, P305 Miyashita H, 1998, MICROSC RES TECHNIQ, V41, P334 NAGAFUJI T, 1995, NEUROREPORT, V6, P1541 NAGAFUJI T, 1995, MOL CHEM NEUROPATHOL, V26, P107 Nagura M, 1999, EUR J PHARMACOL, V366, P47, DOI 10.1016/S0014-2999(98)00881-4 PRAZMA J, 1981, ACTA OTO-LARYNGOL, V92, P459, DOI 10.3109/00016488109133284 RICHARD V, 1995, BRIT J PHARMACOL, V115, P1532 ROBINSON LJ, 1995, P NATL ACAD SCI USA, V92, P11776, DOI 10.1073/pnas.92.25.11776 Shaul PW, 1996, J BIOL CHEM, V271, P6518 SHORT SO, 1985, OTOLARYNG HEAD NECK, V93, P786 Spoendlin H, 1966, Acta Otolaryngol, V61, P423 TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 USAMI SI, 1988, ACTA OTO-LARYNGOL, P36 WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 WATSON BD, 1985, ANN NEUROL, V17, P497, DOI 10.1002/ana.410170513 Wink DA, 1998, FREE RADICAL BIO MED, V25, P434, DOI 10.1016/S0891-5849(98)00092-6 Yamane H, 1997, HEARING RES, V108, P65, DOI 10.1016/S0378-5955(97)00041-5 ZAJTCHUK JT, 1979, OTOLARYNG HEAD NECK, V87, P268 NR 45 TC 8 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 7 EP 13 DI 10.1016/S0378-5955(00)00250-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700002 PM 11223292 ER PT J AU van Dijk, P Manley, GA AF van Dijk, P Manley, GA TI Distortion product otoacoustic emissions in the tree frog Hyla cinerea SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; amphibia; frog ID AUDITORY HAIR-CELLS; ACOUSTIC DISTORTION; BASILAR-MEMBRANE; INNER-EAR; AMPHIBIAN PAPILLA; MECHANOELECTRICAL TRANSDUCTION; GENERAL-CHARACTERISTICS; TEMPERATURE-DEPENDENCE; 2-TONE DISTORTION; RANA-ESCULENTA AB The frog inner ear contains two hearing organs: the amphibian and the basilar papilla. The amphibian papilla is sensitive to low- mid-frequency stimuli (0.1-0.5 and 0.5-1.3 kHz, respectively, in Hyla cinerea), while the basilar papilla is sensitive to high-frequency stimuli (2.8-3.9 kHz in H. cinerea). Distortion product otoacoustic emissions (DPOAE) were recorded from the ear of the tree frog H. cinerea. In each of six ears investigated, a cubic distortion product (DP) at 2f(1)-f(2) was present when the primary frequencies f(1) and f(2) and the DP frequency were close to either the mid- or the high-frequency range; At frequencies between the sensitive ranges of both papillae, no emissions were observed. For the basilar papilla, the dependence of DP level on the primary tone frequency ratio f(2)/f(1) showed a pattern characteristic of the response of a single nonlinear resonator. Thus, in agreement with neural data, DPOAE from the basilar papilla reflect the contribution of a single auditory filter to emission generation. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Hosp Maastricht, Dept Otorhinolaryngol & Head & Neck Surg, NL-6202 AZ Maastricht, Netherlands. Tech Univ Munich, Inst Zool, D-85748 Garching, Germany. RP van Dijk, P (reprint author), Univ Hosp Maastricht, Dept Otorhinolaryngol & Head & Neck Surg, POB 5800, NL-6202 AZ Maastricht, Netherlands. EM p.van.dijk@kno.azm.nl RI Van Dijk, Pim/E-8019-2010 OI Van Dijk, Pim/0000-0002-8023-7571 CR Baker R. J., 1989, COCHLEAR MECHANISMS, P349 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 Capranica R. R., 1983, ADV VERTEBRATE NEURO, P701 Duffing G, 1918, ERZWUNGENE SCHWINGUN EHRET G, 1980, J COMP PHYSIOL, V141, P1 Flannery B. P., 1992, NUMERICAL RECIPES C FRISHKOP.LS, 1974, ACTA OTO-LARYNGOL, V77, P176, DOI 10.3109/00016487409124615 GIBIAN GL, 1982, HEARING RES, V6, P35, DOI 10.1016/0378-5955(82)90006-5 GOLDSTEI.JL, 1968, PR INST ELECTR ELECT, V56, P981, DOI 10.1109/PROC.1968.6449 GUCKENHEIMER J, 1983, NONLINEAR OSCILLATIO, P82 HILLERY CM, 1984, SCIENCE, V225, P1037, DOI 10.1126/science.6474164 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 JARAMILLO F, 1993, NATURE, V364, P527, DOI 10.1038/364527a0 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KETTEMBEIL S, 1995, HEARING RES, V86, P47, DOI 10.1016/0378-5955(95)00053-7 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 Koppl C, 1995, ADV HEARING RES, P207 KOPPL C, 1993, J ACOUST SOC AM, V93, P2834 LEWIS ER, 1982, SCIENCE, V215, P1641, DOI 10.1126/science.6978525 LEWIS ER, 1982, J COMP PHYSIOL, V145, P437 Long GR, 1996, HEARING RES, V98, P22, DOI 10.1016/0378-5955(96)00057-3 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MANLEY GA, 1992, ADV BIOSCI, V83, P151 MANLEY GA, 1990, LECT NOTES BIOMATH, V87, P210 Manley GA, 1997, DIVERSITY AUDITORY M, P32 Manley GA, 1999, HEARING RES, V138, P1, DOI 10.1016/S0378-5955(99)00126-4 MANLEY GA, 1993, J ACOUST SOC AM, V93, P2820, DOI 10.1121/1.405803 MARKIN VS, 1995, ANNU REV BIOPH BIOM, V24, P59 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 NUTTALL AL, 1990, J ACOUST SOC AM, V87, P782, DOI 10.1121/1.398890 PITCHFORD S, 1987, HEARING RES, V27, P75, DOI 10.1016/0378-5955(87)90027-X PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 RHODE WS, 1993, HEARING RES, V66, P31, DOI 10.1016/0378-5955(93)90257-2 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 RONKEN DA, 1991, J ACOUST SOC AM, V90, P2428, DOI 10.1121/1.402047 RONKEN DA, 1990, HEARING RES, V47, P63, DOI 10.1016/0378-5955(90)90167-N ROSOWSKI JJ, 1984, HEARING RES, V13, P141, DOI 10.1016/0378-5955(84)90105-9 RUSSELL IJ, 1992, P ROY SOC B-BIOL SCI, V250, P217, DOI 10.1098/rspb.1992.0152 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P615, DOI 10.1121/1.1913152 Smotherman MS, 1999, HEARING RES, V132, P117, DOI 10.1016/S0378-5955(99)00047-7 Smotherman MS, 1999, J NEUROSCI, V19, P5275 Taschenberger G, 1998, HEARING RES, V123, P183, DOI 10.1016/S0378-5955(98)00120-8 Taschenberger G, 1995, HEARING RES, V91, P87, DOI 10.1016/0378-5955(95)00174-3 vanDijk P, 1997, HEARING RES, V114, P229, DOI 10.1016/S0378-5955(97)00168-8 vanDijk P, 1996, HEARING RES, V101, P102 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 WILSON JP, 1990, ADV AUDIOL, V7, P47 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 NR 52 TC 29 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 14 EP 22 DI 10.1016/S0378-5955(00)00251-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700003 PM 11223293 ER PT J AU Shi, XR Ren, TY Nuttall, AL AF Shi, XR Ren, TY Nuttall, AL TI Nitric oxide distribution and production in the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE 4,5-diaminofluorescein diacetate; nitric oxide; N-G-nitro-L-arginine methyl ester HCl; N-G-monomethyl-L-arginine monoacetate; L-arginine; outer hair cell; endothelial cell ID LIPOPOLYSACCHARIDE-INDUCED EXPRESSION; GUANYLATE-CYCLASE ACTIVITY; SYNTHASE INOS/NOS-II; AUDITORY BRAIN-STEM; NADPH-DIAPHORASE; BLOOD-FLOW; VESTIBULAR SYSTEM; HAIR-CELLS; RAT; LOCALIZATION AB Production sites and distribution of nitric oxide (NO) were detected in cochlear lateral wall tissue, the organ of Corti and in isolated outer hair cells (OHCs) from the guinea pig using the fluorescent dye, 4,5-diaminofluorescein diacetate. Fluorescent signal, indicating the presence of NO, was found in the afferent nerves and their putative endings near inner hair cells (IHCs) and putative efferent nerve endings near OHCs, the IHCs and OHCs, the endothelial cells of blood vessels of the spiral ligament, the stria vascularis, and the spiral blood vessels of the basilar membrane. An increased NO signal was observed following exposure to the substrate for NO, L-arginine, while exposure to NO synthase inhibitors resulted in a decrease in NO signal. Observation of OHCs at the subcellular level revealed differentially strong fluorescent signals at the locations of cuticular plate, the subcuticular plate region, the infranuclear region, and the region adjacent to the lateral wall. The findings indicate the presence of NO in the cochlea and suggest that NO may play an important role in both regulating vascular tone and mediating neurotransmission in guinea pig cochlea. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr NRC04, Portland, OR 97201 USA. Chinese Peoples Armed Police Army, Gen Hosp, Dept Otolaryngol, Beijing 100039, Peoples R China. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Nuttall, AL (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr NRC04, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR ARNHOLD S, 1999, EUR J NEUROSCI, V11, P187 Barone P, 2000, CEREB CORTEX, V10, P160, DOI 10.1093/cercor/10.2.160 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 Brown GC, 2000, ACTA PHYSIOL SCAND, V168, P667, DOI 10.1046/j.1365-201x.2000.00718.x Brown GC, 1999, BBA-BIOENERGETICS, V1411, P351, DOI 10.1016/S0005-2728(99)00025-0 Fessenden JD, 1998, HEARING RES, V118, P168, DOI 10.1016/S0378-5955(98)00027-6 Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 Fessenden JD, 1999, J COMP NEUROL, V404, P52 FESSENDEN JD, 1994, BRAIN RES, V668, P9, DOI 10.1016/0006-8993(94)90505-3 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 GARTHWAITE J, 1991, TRENDS NEUROSCI, V14, P60, DOI 10.1016/0166-2236(91)90022-M Gosepath K, 1997, BRAIN RES, V747, P26, DOI 10.1016/S0006-8993(96)01149-3 HARPER A, 1994, OTOLARYNG HEAD NECK, V111, P430 Heinrich UR, 1998, EUR ARCH OTO-RHINO-L, V255, P483, DOI 10.1007/s004050050104 Hess A, 1998, BRAIN RES, V813, P97, DOI 10.1016/S0006-8993(98)00997-4 Hess A, 1999, BRAIN RES, V830, P113, DOI 10.1016/S0006-8993(99)01433-X Hess A, 1999, NEUROSCI LETT, V264, P145, DOI 10.1016/S0304-3940(99)00195-0 Huh Y, 2000, NEUROSCI LETT, V281, P49, DOI 10.1016/S0304-3940(00)00800-4 IKEDA K, 1993, HEARING RES, V66, P169, DOI 10.1016/0378-5955(93)90138-Q Kojima H, 1998, NEUROREPORT, V9, P3345, DOI 10.1097/00001756-199810260-00001 Konishi K, 1998, Acta Otolaryngol Suppl, V538, P40 Michel O, 1999, HEARING RES, V133, P1, DOI 10.1016/S0378-5955(99)00049-0 Reuss S, 2000, MECH AGEING DEV, V112, P125, DOI 10.1016/S0047-6374(99)00082-2 Reuss S, 1998, NEUROREPORT, V9, P3643 Riemann R, 1999, HEARING RES, V135, P181, DOI 10.1016/S0378-5955(99)00113-6 RODRIGO J, 1994, PHILOS T ROY SOC B, V345, P175, DOI 10.1098/rstb.1994.0096 Ruan RS, 1997, J BRAIN RES, V38, P433 SHI XR, 2000, SOC NEUR 2000 M NEW Takumida M, 2000, ACTA OTO-LARYNGOL, V120, P34 Takumida M, 2000, ACTA OTO-LARYNGOL, V120, P28, DOI 10.1080/000164800760370792 Takumida M, 1998, EUR ARCH OTO-RHINO-L, V255, P184, DOI 10.1007/s004050050040 Takumida M, 2000, HEARING RES, V140, P91, DOI 10.1016/S0378-5955(99)00188-4 Tian F, 1999, HEARING RES, V131, P63, DOI 10.1016/S0378-5955(99)00015-5 Usunoff KG, 1999, ANAT EMBRYOL, V200, P265, DOI 10.1007/s004290050278 Vass Z, 1996, HEARING RES, V100, P114, DOI 10.1016/0378-5955(96)00102-5 Watanabe K, 2000, ANTI-CANCER DRUG, V11, P29, DOI 10.1097/00001813-200001000-00005 Watanabe KI, 2000, FREE RADICAL RES, V32, P363, DOI 10.1080/10715760000300361 WU MD, 1999, BRAIN RES, V830, P113 Wu Men-Dar, 1997, Okajimas Folia Anatomica Japonica, V74, P155 Yamane H, 1997, HEARING RES, V108, P65, DOI 10.1016/S0378-5955(97)00041-5 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZDANSKI CJ, 1994, HEARING RES, V79, P39, DOI 10.1016/0378-5955(94)90125-2 ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 44 TC 34 Z9 36 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 23 EP 31 DI 10.1016/S0378-5955(00)00254-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700004 PM 11223294 ER PT J AU Boettcher, FA Poth, EA Mills, JH Dubno, JR AF Boettcher, FA Poth, EA Mills, JH Dubno, JR TI The amplitude-modulation following response in young and aged human subjects SO HEARING RESEARCH LA English DT Article DE aging; age-related hearing loss; amplitude-modulation following response; presbyacusis ID AUDITORY-EVOKED POTENTIALS; STEADY-STATE RESPONSES; INFERIOR COLLICULUS; INTENSITY DISCRIMINATION; COCHLEAR NUCLEUS; NORMAL-HEARING; GERBILS; TONES; FREQUENCY; THRESHOLDS AB The amplitude-modulation following response (AMFR) is a steady-state auditory response which map be an objective measure of intensity discrimination. Aged subjects with normal hearing have poorer intensity discrimination for low-frequency tones measured behaviorally, which would predict poorer AMFRs for low-frequency carriers. Experiment 1 was designed to assess age-related differences in AMFR characteristics. Response amplitudes were not significantly different among the young and aged groups for either carrier frequency (520 or 4000 Hz) or modulation depth (0-100%). Response phase did not vary systematically among groups. These results suggest that the AMFR may not be directly comparable to behavioral measures of intensity discrimination in aged subjects with normal hearing. To assess the contribution of high-frequency hearing loss on the AMFR in aged subjects, Experiment 2 compared AMFR amplitudes in aged subjects and in young subjects under the condition ofhigh-pass masking. The amplitude of the AMFR was reduced at 520 Hz for both aged subjects and masked young subjects compared to unmasked young subjects, suggesting that reduced amplitudes in aged subjects with high-frequency hearing loss were associated with threshold elevations. Furthermore, the results suggest that the base of the cochlea contributes to the AMFR for low carrier frequencies. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Charleston, SC 29425 USA. RP Boettcher, FA (reprint author), Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, 39 Sabin St,POB 250150, Charleston, SC 29425 USA. CR American National Standards Institute (ANSI), 1996, S361996 ANSI BACKOFF PA, 1994, HEARING RES, V73, P162 BANAYSCHWARTZ M, 1993, NEUROCHEM RES, V18, P417, DOI 10.1007/BF00967245 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z Boettcher FA, 1996, HEARING RES, V102, P167, DOI 10.1016/S0378-5955(96)90016-7 BOETTCHER FA, 1990, HEARING RES, V48, P125, DOI 10.1016/0378-5955(90)90203-2 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 CASPARY DM, 1990, J NEUROSCI, V10, P2363 COHEN LT, 1991, J ACOUST SOC AM, V90, P2467, DOI 10.1121/1.402050 Dobie RA, 1998, J ACOUST SOC AM, V104, P3482, DOI 10.1121/1.423931 DUBNO JR, 1995, J ACOUST SOC AM, V97, P1165, DOI 10.1121/1.413057 Felder E, 1997, HEARING RES, V105, P183, DOI 10.1016/S0378-5955(96)00209-2 Felix H, 1990, Acta Otolaryngol Suppl, V470, P71 FLORENTINE M, 1993, J ACOUST SOC AM, V94, P2575, DOI 10.1121/1.407369 FOWLER CG, 1992, J SPEECH HEAR RES, V35, P216 FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GRATTON MA, 1995, HEARING RES, V82, P44 GRIFFITHS SK, 1991, EAR HEARING, V12, P235, DOI 10.1097/00003446-199108000-00002 GUITERREZ A, 1994, J NEUROSCI, V14, P7469 He NJ, 1998, J ACOUST SOC AM, V103, P553, DOI 10.1121/1.421127 Helfert RH, 1999, J COMP NEUROL, V406, P285 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N Humes L E, 1996, J Am Acad Audiol, V7, P161 John MS, 2000, HEARING RES, V141, P57, DOI 10.1016/S0378-5955(99)00209-9 JOHNSON B W, 1988, Brain Topography, V1, P117, DOI 10.1007/BF01129176 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KUWADA S, 1986, HEARING RES, V21, P179, DOI 10.1016/0378-5955(86)90038-9 LEVI EC, 1993, HEARING RES, V68, P42, DOI 10.1016/0378-5955(93)90063-7 LINS OG, 1995, J ACOUST SOC AM, V97, P3051, DOI 10.1121/1.411869 McGeer E.G., 1975, NEUROBIOL AGING, P287 MILLS JH, 1990, HEARING RES, V46, P301 PFEIFFER E, 1975, J AM GERIATR SOC, V23, P433 PICTON TW, 1987, J ACOUST SOC AM, V82, P165, DOI 10.1121/1.395560 RANCE G, 1995, EAR HEARING, V16, P499, DOI 10.1097/00003446-199510000-00006 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 REES A, 1986, HEARING RES, V23, P123, DOI 10.1016/0378-5955(86)90009-2 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 ROSS B, 2000, J ACOUST SOC AM, V108, P579 SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K STAPELLS DR, 1984, EAR HEARING, V5, P105 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 Walton J, 1999, HEARING RES, V127, P86, DOI 10.1016/S0378-5955(98)00175-0 Walton JP, 1998, J NEUROSCI, V18, P2764 Wojtczak M, 1999, J ACOUST SOC AM, V106, P1917, DOI 10.1121/1.427940 Zettel ML, 1997, J COMP NEUROL, V386, P92, DOI 10.1002/(SICI)1096-9861(19970915)386:1<92::AID-CNE9>3.0.CO;2-8 NR 49 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 32 EP 42 DI 10.1016/S0378-5955(00)00255-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700005 PM 11223295 ER PT J AU Rattay, F Lutter, P Felix, H AF Rattay, F Lutter, P Felix, H TI A model of the electrically excited human cochlear neuron I. Contribution of neural substructures to the generation and propagation of spikes SO HEARING RESEARCH LA English DT Article DE human cochlear neuron; electrical stimulation; activating function; computer simulation; auditory nerve; compartment model; unmyelinated spiral ganglion cell ID AUDITORY-NERVE FIBERS; ACTION-POTENTIALS; EXCITATION PATTERNS; MEMBRANE CURRENTS; MYELINATED NERVE; STIMULATION; CAT; RANVIER; NODE; DEGENERATION AB Differences in neural geometry and the fact that the soma of the human cochlear neuron typically is not myelinated are reasons for disagreements between single fiber recordings in animals and the neural code evoked in cochlear implant patients. We introduce a compartment model of the human cochlear neuron to study the excitation and propagation process of action potentials. The model can be used to predict (i) the points of spike generation, (ii) the time difference between stimulation and the arrival of a spike at the proximal end of the central axon, (iii) the vanishing of peripherally evoked spikes at the soma region under specific conditions, (iv) the influence of electrode positions on spiking behavior, and (v) consequences of the loss of the peripheral axon. Every subunit of the cochlear neuron is separately modeled. Ion channel dynamics are described by a modified Hodgkin-Huxley model. Influence of membrane noise is taken into account. Additionally, the generalized activating function is introduced as a tool to give an envision of the origin of spikes in the peripheral and in the central axon without any knowledge of the gating processes in the active membranes. Comparing the reactions of a human and cat cochlear neuron, we find differences in spiking behavior, e.g, peripherally and centrally evoked spikes arrive with a time difference of about 400 mus in man and 200 mus in cat. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Vienna Univ Technol, TU Biomed, A-1040 Vienna, Austria. Univ Zurich Hosp, ENT Dept, CH-8091 Zurich, Switzerland. RP Rattay, F (reprint author), Vienna Univ Technol, TU Biomed, Wiedner Hauptstr 18-10-1145, A-1040 Vienna, Austria. RI Rattay, Frank/A-2231-2015 OI Rattay, Frank/0000-0002-2819-8827 CR ARBUTHNOTT ER, 1980, J PHYSIOL-LONDON, V308, P125 ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BROWN CJ, 1990, J ACOUST SOC AM, V88, P1385, DOI 10.1121/1.399716 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 CHIU SY, 1979, J PHYSIOL-LONDON, V292, P149 COBURN B, 1989, CRIT REV BIOMED ENG, V17, P133 COHEN LT, UNPUB AUDIOL NEUROOT COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DeFelice L. J., 1981, INTRO MEMBRANE NOISE DILLIER N, 1997, 1 EXPERIENCES NEURAL FELIX H, 1992, ACTA OTO-LARYNGOL, V112, P284 Felix H, 1997, PROGRESS IN HUMAN AUDITORY AND VESTIBULAR HISTOPATHOLOGY, P73 Felix H, 1990, Acta Otolaryngol Suppl, V470, P71 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FitzHugh R, 1969, BIOL ENG, P1 FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q GARNHAM CW, 1995, J MED ENG TECHNOL, V19, P57, DOI 10.3109/03091909509030275 GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HINOJOSA R, 1980, ARCH OTOLARYNGOL, V106, P193 HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 Holden A. V., 1976, MODELS STOCHASTIC AC Javel E, 2000, HEARING RES, V140, P45, DOI 10.1016/S0378-5955(99)00186-0 Jayel E., 1990, COCHLEAR IMPLANTS MO, P247 Knipper M, 1998, DEVELOPMENT, V125, P3709 Lai WK, 2000, AUDIOL NEURO-OTOL, V5, P333, DOI 10.1159/000013899 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 Miller CA, 1999, HEARING RES, V130, P197, DOI 10.1016/S0378-5955(99)00012-X MOTZ H, 1986, NEUROSCIENCE, V18, P699, DOI 10.1016/0306-4522(86)90064-3 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 NATTAY F, 1990, ELECT NERVE STIMULAT OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PERNKOPF E, 1960, TOPOGRAPHISCHE ANATO, V4, P599 Pollak A, 1987, Acta Otolaryngol Suppl, V436, P37 RATTAY F, 1998, BRAIN MODELLING, P7 Rattay F, 1995, PHYS ALIVE, V3, P60 Rattay F, 2001, HEARING RES, V153, P64, DOI 10.1016/S0378-5955(00)00257-4 RATTAY F, 1986, IEEE T BIO-MED ENG, V33, P974, DOI 10.1109/TBME.1986.325670 Rattay F, 1998, IEEE T BIO-MED ENG, V45, P766, DOI 10.1109/10.678611 Rattay F, 1999, NEUROSCIENCE, V89, P335, DOI 10.1016/S0306-4522(98)00330-3 Rattay F, 2000, CHAOS SOLITON FRACT, V11, P1875, DOI 10.1016/S0960-0779(99)00124-1 REILLY JP, 1985, IEEE T BIO-MED ENG, V32, P1001, DOI 10.1109/TBME.1985.325509 Romeis B, 1968, MIKROSKOPISCHE TECHN, V16th RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 Rubinstein JT, 1999, HEARING RES, V127, P108, DOI 10.1016/S0378-5955(98)00185-3 SCHWARZ JR, 1987, PFLUG ARCH EUR J PHY, V409, P569, DOI 10.1007/BF00584655 SCHWARZ JR, 1995, PFLUG ARCH EUR J PHY, V430, P283, DOI 10.1007/BF00374660 Shepherd RK, 1997, HEARING RES, V108, P112, DOI 10.1016/S0378-5955(97)00046-4 SIGWORTH FJ, 1980, J PHYSIOL-LONDON, V307, P97 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 Sweeney J. D., 1987, P 9 INT C IEEE EMBS, V9, P1577 VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VERVEEN AA, 1968, PR INST ELECTR ELECT, V56, P906, DOI 10.1109/PROC.1968.6443 Wesselink W. A., 1999, Medical and Biological Engineering and Computing, V37, P228, DOI 10.1007/BF02513291 ZHOU RZ, 1995, HEARING RES, V88, P98, DOI 10.1016/0378-5955(95)00105-D NR 60 TC 60 Z9 60 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 43 EP 63 DI 10.1016/S0378-5955(00)00256-2 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700006 PM 11223296 ER PT J AU Rattay, F Leao, RN Felix, H AF Rattay, F Leao, RN Felix, H TI A model of the electrically excited human cochlear neuron. II. Influence of the three-dimensional cochlear structure on neural excitability SO HEARING RESEARCH LA English DT Article DE cochlear neuron; electrical stimulation; activating function; computer simulation; auditory nerve; finite element ID ROTATIONALLY SYMMETRICAL MODEL; STIMULATED COCHLEA; EXCITATION AB ii simplified spiraled model of the human cochlea is developed from a cross sectional photograph. The potential distribution within this model cochlea is calculated with the finite element technique for an active scale tympani implant. The method in the companion article [Rattay et al., 2001] allows for simulation of the excitation process of selected elements of the cochlear nerve. The bony boundary has an insulating influence along every nerve fiber which shifts the stimulation condition from that of a homogeneous extracellular medium towards constant field stimulation: for a target neuron which is stimulated by a ring electrode positioned just below the peripheral end of the fiber the extracellular voltage profile is rather linear. About half of the cochlear neurons of a completely innervated cochlea are excited with monopolar stimulation at three-fold threshold intensity, whereas bipolar and especially quadrupolar stimulation focuses the excited region even for stronger stimuli. In contrast to single fiber experiments with cats, the long peripheral processes in human cochlear neurons cause first excitation in the periphery and, consequently, neurons with lost dendrite need higher stimuli. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Vienna Univ Technol, TU Biomed, A-1040 Vienna, Austria. Univ Zurich Hosp, ENT Dept, CH-8091 Zurich, Switzerland. Med Sch Uberlandia, Uberlandia, MG, Brazil. RP Rattay, F (reprint author), Vienna Univ Technol, TU Biomed, Wiedner Hauptstr 8-10-1145, A-1040 Vienna, Austria. RI Rattay, Frank/A-2231-2015 OI Rattay, Frank/0000-0002-2819-8827 CR BLACK RC, 1981, IEEE T BIO-MED ENG, V28, P721, DOI 10.1109/TBME.1981.324668 Felix H, 1997, PROGRESS IN HUMAN AUDITORY AND VESTIBULAR HISTOPATHOLOGY, P73 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q Frijns JHM, 1996, HEARING RES, V95, P33, DOI 10.1016/0378-5955(96)00004-4 Ghitza O, 1994, IEEE T SPEECH AUDI P, V2, P115, DOI 10.1109/89.260357 JOHNSON CR, 1995, BIOMEDICAL ENG HDB, P162 Jolly CN, 1996, IEEE T BIO-MED ENG, V43, P857, DOI 10.1109/10.508549 KOSTERICH JD, 1983, IEEE T BIO-MED ENG, V30, P81, DOI 10.1109/TBME.1983.325201 Kral A, 1998, HEARING RES, V121, P11, DOI 10.1016/S0378-5955(98)00061-6 LOEB GE, 1983, ANN NY ACAD SCI, V405, P123, DOI 10.1111/j.1749-6632.1983.tb31625.x Miller CA, 1999, HEARING RES, V130, P197, DOI 10.1016/S0378-5955(99)00012-X RATTAY F, 1997, Z ANGEW MATH MECH, V12, P935 Rattay F, 1990, ELECT NERVE STIMULAT RATTAY F, 1986, IEEE T BIO-MED ENG, V33, P974, DOI 10.1109/TBME.1986.325670 Rattay F, 2001, HEARING RES, V153, P43, DOI 10.1016/S0378-5955(00)00256-2 SCHMIDT R, 1998, FEM WORKSHOP, V5 SPELMAN FA, 1980, ANN OTO RHINOL LARYN, V89, P8 STRELIOF.D, 1973, J ACOUST SOC AM, V54, P620, DOI 10.1121/1.1913642 SUESSERMAN MF, 1993, IEEE T BIO-MED ENG, V40, P237, DOI 10.1109/10.216407 VONBEKESY G, 1951, J ACOUST SOC AM, V23, P18 NR 21 TC 44 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 64 EP 79 DI 10.1016/S0378-5955(00)00257-4 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700007 PM 11223297 ER PT J AU Ibsch, M Anken, RH Vohringer, P Rahmann, H AF Ibsch, M Anken, RH Vohringer, P Rahmann, H TI Vesicular bodies in fish maculae are artifacts not contributing to otolith growth SO HEARING RESEARCH LA English DT Article DE otolith growth; artifact; blister; utricle; saccule; fish; inner ear ID MYKISS INNER-EAR; OREOCHROMIS-NILOTICUS; SACCULAR EPITHELIUM; ONCORHYNCHUS-MYKISS; RAINBOW-TROUT; CICHLID FISH; ELECTRON-MICROSCOPY; CELLS; ULTRASTRUCTURE; TELEOSTEI AB The presence, morphology and possible origin of vesicle-like bodies (VBs) within the inner ear macular otolithic membrane of developmental stages of cichlid fish Oreochromis mossambicus and neonate (i.e. functionally fully developed except the reproductive organs) swordtail fish Xiphophorus helleri were analyzed by means of transmission and scanning electron microscopy (TEM and SEM, respectively) employing various fixation procedures. Some authors believe that these VBs are involved in the formation of the organic phase of inner ear otoliths (or statoliths in birds and mammals). Decreasing the osmolarity of the fixation medium from a value rather close to that of native fresh water fish tissue (i.e. 250 mOsm and 290-300 mOsm, respectively) to a value of fixatives mostly employed in TEM studies (ca. 190 mOsm), the amount of VBs increased and the components of sensory inner ear tissue increasingly dilated. Whilst a conventional prefixation with aldehydes followed by osmium tetroxide postfixation yielded numerous VBs, only few of them were observed when the tissue was fixed with aldehydes and osmium tetroxide simultaneously. Therefore, the results demonstrate that inner ear sensory epithelia are extremely sensitive to altering fixation media. On this background it must be concluded that VBs are fixative (i.e. glutaraldehyde) induced artificial structures, so-called membrane blisters. Thus, the protein matrix of otoliths (and possibly that of statoliths in higher vertebrates) is rather provided by secretion processes than by the release of vesicles. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Stuttgart Hohenheim, Inst Zool, D-70593 Stuttgart, Germany. RP Rahmann, H (reprint author), Univ Stuttgart Hohenheim, Inst Zool, Garbenstr 30, D-70593 Stuttgart, Germany. CR Adler HJ, 1997, INT J DEV NEUROSCI, V15, P375, DOI 10.1016/S0736-5748(96)00098-6 ANKEN R, 1999, P 2 EUR S UT INT SPA, P425 Anken RH, 1998, HEARING RES, V121, P77, DOI 10.1016/S0378-5955(98)00067-7 ANKEN RH, 1993, ZOOL ANZ, V231, P1 Anken RH, 1998, ACTA OTO-LARYNGOL, V118, P534, DOI 10.1080/00016489850154685 Anniko M, 1980, Am J Otolaryngol, V1, P400, DOI 10.1016/S0196-0709(80)80021-4 BECERRA M, 1993, J ANAT, V183, P463 BOWERS B, 1988, ARTIFACTS BIOL ELECT, P10 BUCKLEY IK, 1973, LAB INVEST, V29, P398 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X Couloigner V, 1999, ACTA OTO-LARYNGOL, V119, P200 Crenshaw MA, 1982, BIOL MINERALIZATION, P243 DOI K, 1992, ACTA OTO-LARYNGOL, V112, P667, DOI 10.3109/00016489209137457 DUNKELBERGER DG, 1980, J MORPHOL, V163, P367, DOI 10.1002/jmor.1051630309 Endo S, 1991, Acta Otolaryngol Suppl, V481, P116 FERMIN CD, 1990, ACTA ANAT, V138, P75 GAULDIE RW, 1988, COMP BIOCHEM PHYS A, V90, P501, DOI 10.1016/0300-9629(88)90227-7 HAY ED, 1979, FREEZE FRACTURE METH, P59 Hayat M. A., 1974, PRINCIPLES TECHNIQUE Hayat M A, 1989, PRINCIPLES TECHNIQUE HERTWIG I, 1986, ZOOMORPHOLOGY, V106, P137, DOI 10.1007/BF00312202 HOPWOOD D, 1967, J ANAT, V101, P83 IBSCH M, 1998, P 26 GOTT NEUR C, P43 Kaltenbach JA, 1997, INT J DEV NEUROSCI, V15, P509, DOI 10.1016/S0736-5748(96)00107-4 LOWENSTEIN O, 1949, J PHYSIOL-LONDON, V110, P392 MATHIEU O, 1978, J ULTRA MOL STRUCT R, V63, P20, DOI 10.1016/S0022-5320(78)80041-0 MUGIYA Y, 1984, COMP BIOCHEM PHYS A, V78, P289 Panella G, 1971, Science, V173, P1124 Pisam M, 1998, CELL TISSUE RES, V294, P261, DOI 10.1007/s004410051176 Platt C., 1983, P89 POPPER A, 1995, MAR FRESHW BEHAV PHY, V27, P95 Popper A.N., 1988, P687 Popper A.N., 1999, COMP HEARING FISH AM, P43 PRESSON JC, 1992, BRAIN BEHAV EVOLUT, V39, P197, DOI 10.1159/000114117 REIMER L, 1992, ULTRAMICROSCOPY, V46, P335, DOI 10.1016/0304-3991(92)90023-D Riley BB, 1997, DEV BIOL, V191, P191, DOI 10.1006/dbio.1997.8736 Schellart NAM, 1992, COMP EVOLUTIONARY BI, P295 Shelton E., 1979, FREEZE FRACTURE METH, P67 SLEPECKY N, 1988, J SUBMICR CYTOL PATH, V20, P37 Sobkowicz HM, 1997, INT J DEV NEUROSCI, V15, P463, DOI 10.1016/S0736-5748(96)00104-9 Steyger PS, 1995, HEARING RES, V92, P184, DOI 10.1016/0378-5955(95)00221-9 Takagi Y, 1997, ANAT REC, V248, P483, DOI 10.1002/(SICI)1097-0185(199708)248:4<483::AID-AR1>3.0.CO;2-N Takagi Y, 1999, ANAT REC, V254, P322 Tavolga W. N., 1949, Bulletin of the American Museum of Natural History, V94, P163 YAN HY, 1993, J COMP PHYSIOL A, V173, P347, DOI 10.1007/BF00212699 ZHANG Z, 1992, J ZOOL, V227, P465 ZHANG Z, 1992, J MORPHOL, V211, P213, DOI 10.1002/jmor.1052110210 ZHANG Z, 1992, J MORPHOL, V212, P99, DOI 10.1002/jmor.1052120202 NR 48 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 80 EP 90 DI 10.1016/S0378-5955(00)00258-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700008 PM 11223298 ER PT J AU Sugihara, I AF Sugihara, I TI Efferent innervation in the goldfish saccule examined by acetylcholinesterase histochemistry SO HEARING RESEARCH LA English DT Article DE hearing; inner ear; hair cell; acetylcholine; electron microscopy; synapse ID POST-SYNAPTIC POTENTIALS; OUTER HAIR-CELLS; CARASSIUS-AURATUS; NERVE-FIBERS; INNER-EAR; FISH EAR; SEMICIRCULAR CANALS; OPSANUS-TAU; AFFERENT; SYNAPSES AB In contrast to the abundance of information available regarding the anatomy and physiology of afferents within the goldfish saccule, the efferent system of this auditory endorgan has been scarcely studied morphologically. In this study, acetylcholinesterase histochemistry with diaminobenzidine enhancement was used to describe the morphology of efferents. Under light microscopy, labeled fibers appeared in the distal portion of the saccular nerve, penetrated the basement membrane and formed a horizontal meshlike plexus near the base of hair cells. Many vertical branchlets with terminal swellings protruded upward toward hair cells from the plexus. Under electron microscopy, dense extracellular labeling was present around efferent terminals, which often formed clusters on hair cells. Labeling was also present around unmyelinated fibers of passage within the sensory epithelium and the distal saccular nerve. These fibers contained coarse microtubules and small vesicles, and often ran in a bundle with other similar fibers. Based on their position within the epithelium, histochemistry and ultrastructural characteristics, these fibers were concluded to be efferents. These fibers became myelinated and unlabeled in the proximal saccular nerve. These results suggest that acetylcholinesterase can be a marker of entire distal unmyelinated portions of efferent fibers and demonstrated abundant efferent innervation in the goldfish saccule. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Tokyo Med & Dent Univ, Grad Sch Med, Dept Syst Neurophysiol, Bunkyo Ku, Tokyo 1138519, Japan. RP Sugihara, I (reprint author), Tokyo Med & Dent Univ, Grad Sch Med, Dept Syst Neurophysiol, Bunkyo Ku, 1-5-45 Yushima, Tokyo 1138519, Japan. CR BELL CC, 1981, J COMP NEUROL, V195, P391, DOI 10.1002/cne.901950303 Brichta AM, 2000, J NEUROPHYSIOL, V83, P1224 BROWN MC, 1983, SCIENCE, V222, P69, DOI 10.1126/science.6623058 CHANG JSY, 1992, J COMP NEUROL, V324, P621, DOI 10.1002/cne.903240413 CLAAS B, 1980, BRAIN RES, V193, P249, DOI 10.1016/0006-8993(80)90961-0 COHEN GM, 1987, HEARING RES, V28, P57, DOI 10.1016/0378-5955(87)90153-5 COOMBS S, 1985, HEARING RES, V19, P57, DOI 10.1016/0378-5955(85)90098-X Edds-Walton PL, 2000, HEARING RES, V141, P229, DOI 10.1016/S0378-5955(99)00207-5 ENGSTROM H, 1958, Acta Otolaryngol, V49, P109, DOI 10.3109/00016485809134734 FAY R, 1969, J AUD RES, V9, P112 FAY RR, 1986, J ACOUST SOC AM, V79, P1883, DOI 10.1121/1.393196 FRITZSCH B, 1989, NEUROSCI LETT, V96, P241, DOI 10.1016/0304-3940(89)90385-6 FUCHS PA, 1992, J NEUROSCI, V12, P800 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P193 FURUKAWA T, 1978, J COMP NEUROL, V180, P807, DOI 10.1002/cne.901800411 FURUKAWA T, 1986, JPN J PHYSIOL, V36, P1059, DOI 10.2170/jjphysiol.36.1059 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 FURUKAWA T, 1981, J PHYSIOL-LONDON, V315, P203 HAMA K, 1969, Z ZELLFORSCH MIK ANA, V94, P155, DOI 10.1007/BF00339353 HIGHSTEIN SM, 1986, J COMP NEUROL, V243, P309, DOI 10.1002/cne.902430303 Holt JC, 2000, HEARING RES, V146, P17, DOI 10.1016/S0378-5955(00)00092-7 ITO J, 1983, BRAIN RES, V259, P293, DOI 10.1016/0006-8993(83)91261-1 ITOH K, 1979, BRAIN RES, V175, P341, DOI 10.1016/0006-8993(79)91013-8 Iurato S, 1971, Acta Otolaryngol Suppl, V279, P1 JACOBS DW, 1967, ANIM BEHAV, V15, P324, DOI 10.1016/0003-3472(67)90019-X KARNOVSKY MJ, 1964, J HISTOCHEM CYTOCHEM, V12, P219 KHAN KM, 1991, NEUROSCI LETT, V131, P109, DOI 10.1016/0304-3940(91)90348-W KHAN KM, 1993, ANAT REC, V237, P141, DOI 10.1002/ar.1092370113 KIMURA R, 1962, Acta Otolaryngol, V55, P11, DOI 10.3109/00016486209127336 KUNO M, 1983, J NEUROPHYSIOL, V50, P573 Lanford PJ, 2000, HEARING RES, V143, P1, DOI 10.1016/S0378-5955(00)00015-0 LIBERMAN MC, 1980, HEARING RES, V3, P189, DOI 10.1016/0378-5955(80)90046-5 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 MCCORMICK CA, 1994, BRAIN BEHAV EVOLUT, V43, P189, DOI 10.1159/000113634 MEREDITH GE, 1986, NEUROSCIENCE, V17, P225, DOI 10.1016/0306-4522(86)90238-1 MILLER MR, 1985, J COMP NEUROL, V232, P1, DOI 10.1002/cne.902320102 NAKAI Y, 1972, LARYNGOSCOPE, V82, P177, DOI 10.1288/00005537-197202000-00004 NAKAJIMA Y, 1974, J COMP NEUROL, V156, P403, DOI 10.1002/cne.901560403 Nenov AP, 1996, HEARING RES, V101, P149, DOI 10.1016/S0378-5955(96)00143-8 NOMURA Y, 1965, ANN OTO RHINOL LARYN, V74, P289 PERKINS RE, 1975, J COMP NEUROL, V163, P129, DOI 10.1002/cne.901630202 PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 POPPER AN, 1990, HEARING RES, V46, P211, DOI 10.1016/0378-5955(90)90003-8 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 Presson JC, 1996, HEARING RES, V100, P10, DOI 10.1016/0378-5955(96)00109-8 ROSSI ML, 1994, J PHYSIOL-LONDON, V478, P17 Saidel WM, 1995, BRAIN BEHAV EVOLUT, V46, P362, DOI 10.1159/000113286 SANS A, 1984, BRAIN RES, V308, P191, DOI 10.1016/0006-8993(84)90936-3 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 SEWELL WF, 1991, J NEUROPHYSIOL, V65, P1158 SOBKOWICZ HM, 1989, J NEUROCYTOL, V18, P209, DOI 10.1007/BF01206663 STARR PA, 1991, HEARING RES, V52, P23, DOI 10.1016/0378-5955(91)90185-C SUGAI T, 1991, JPN J PHYSIOL, V41, P217, DOI 10.2170/jjphysiol.41.217 Sugihara I, 1996, J PHYSIOL-LONDON, V495, P665 Sugihara I, 1995, J PHYSIOL-LONDON, V489, P443 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 Sugihara I, 1996, NEUROREPORT, V7, P2341, DOI 10.1097/00001756-199610020-00013 TAGO H, 1986, J HISTOCHEM CYTOCHEM, V34, P1431 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 NR 61 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 91 EP 99 DI 10.1016/S0378-5955(00)00259-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700009 PM 11223299 ER PT J AU Makiishi-Shimobayashi, C Tsujimura, T Sugihara, A Iwasaki, T Yamada, N Terada, N Sakagami, M AF Makiishi-Shimobayashi, C Tsujimura, T Sugihara, A Iwasaki, T Yamada, N Terada, N Sakagami, M TI Expression of osteopontin by exudate macrophages in inflammatory tissues of the middle ear: a possible association with development of tympanosclerosis SO HEARING RESEARCH LA English DT Article DE tympanosclerosis; osteopontin; calcification; macrophage; chronic otitis media ID HUMAN ATHEROSCLEROTIC PLAQUES; BONE SIALOPROTEIN; MESSENGER-RNA; CALCIFICATION; PROTEIN; CLONING; INHIBITION; MOLECULE; GROMMET AB Tympanosclerosis is a condition leading to a calcification process in the middle ear, and often develops after chronic inflammation of the middle ear. Since osteopontin (OPN) has been shown to participate in the pathological calcification, we here investigated whether OPN is involved in the process of calcification in tympanosclerosis. The tympanic membrane and middle ear mucose, obtained from patients of tympanosclerosis and chronic otitis media, were histologically classified depending on the calcification degree. In hyalinized tissues with macroscopic calcification and fibrous tissues with microscopic calcification, OPN was immunohistochemically found in the calcification sites. In inflammatory tissues with microscopic calcification, OPN was also found in the calcifying foci, and many OPN mRNA-expressing cells, determined by in situ hybridization, located around their foci. Moreover, immunohistochemical double staining of OPN and CD68 showed that the OPN-expressing cells were CD68-positive, indicating these cells were macrophages. In inflammatory tissues without calcification, immunohistochemistry of CD68 and in situ hybridization of OPN mRNA revealed that most OPN mRNA-expressing cells were CD68-positive. The expression of OPN mRNA in inflammatory tissues was also shown by reverse transcriptase polymerase chain reaction. These results suggest that OPN secreted by exudate macrophages might be an important regulator in the calcification of tympanosclerosis. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Hyogo Coll Med, Dept Pathol, Nishinomiya, Hyogo 6638501, Japan. Hyogo Coll Med, Dept Otolaryngol, Nishinomiya, Hyogo 6638501, Japan. RP Tsujimura, T (reprint author), Hyogo Coll Med, Dept Pathol, 1-1 Mukogawa Cho, Nishinomiya, Hyogo 6638501, Japan. CR BROWN LF, 1994, AM J PATHOL, V145, P610 Butler William T., 1996, P167 CHEN Y, 1992, J BIOL CHEM, V267, P24871 DACOSTA SS, 1992, LARYNGOSCOPE, V102, P1229, DOI 10.1288/00005537-199211000-00005 FALINI B, 1993, AM J PATHOL, V142, P1359 GIACHELLI CM, 1993, J CLIN INVEST, V92, P1686, DOI 10.1172/JCI116755 HAMPAL S, 1991, J LARYNGOL OTOL, V105, P161, DOI 10.1017/S0022215100115269 HIROTA S, 1993, AM J PATHOL, V143, P1003 HIROTA S, 1995, LAB INVEST, V72, P64 HUNTER GK, 1994, BIOCHEM J, V300, P723 HUSSL B, 1984, RECENT ADV OTITIS ME, P348 Jono S, 2000, J BIOL CHEM, V275, P20197, DOI 10.1074/jbc.M909174199 KATAGIRI Y, 1995, ANN NY ACAD SCI, V760, P371, DOI 10.1111/j.1749-6632.1995.tb44660.x KOHRI K, 1992, BIOCHEM BIOPH RES CO, V184, P859, DOI 10.1016/0006-291X(92)90669-C MCKEE GJ, 1989, CLIN OTOLARYNGOL, V14, P11, DOI 10.1111/j.1365-2273.1989.tb00330.x Mohler ER, 1997, ARTERIOSCL THROM VAS, V17, P547 NOMURA S, 1988, J CELL BIOL, V106, P441, DOI 10.1083/jcb.106.2.441 OBRIEN KD, 1995, CIRCULATION, V92, P2163 OLDBERG A, 1986, P NATL ACAD SCI USA, V83, P8819, DOI 10.1073/pnas.83.23.8819 OTTO CM, 1994, CIRCULATION, V90, P844 PARKER AJ, 1990, CLIN OTOLARYNGOL, V15, P203, DOI 10.1111/j.1365-2273.1990.tb00776.x Proudfoot D, 1998, ARTERIOSCL THROM VAS, V18, P379 ROSS FP, 1993, J BIOL CHEM, V268, P9901 SHANAHAN CM, 1994, J CLIN INVEST, V93, P2393, DOI 10.1172/JCI117246 SHEEHY JL, 1962, ARCHIV OTOLARYNGOL, V76, P151 SORENSEN H, 1971, ACTA OTOLARYNGOL, V73, P18 TOS M, 1989, ARCH OTOLARYNGOL, V115, P931 WONG H, 1994, ANAL BIOCHEM, V223, P251, DOI 10.1006/abio.1994.1581 YOUNG MF, 1990, GENOMICS, V7, P491, DOI 10.1016/0888-7543(90)90191-V ZOLLNER F, 1956, J Laryngol Otol, V70, P77 NR 30 TC 7 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 100 EP 107 DI 10.1016/S0378-5955(00)00260-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700010 PM 11223300 ER PT J AU Sussman, E Ceponiene, R Shestakova, A Naatanen, R Winkler, I AF Sussman, E Ceponiene, R Shestakova, A Naatanen, R Winkler, I TI Auditory stream segregation processes operate similarly in school-aged children and adults SO HEARING RESEARCH LA English DT Article DE auditory stream segregation; school-aged children; event-related potential; mismatch negativity ID EVENT-RELATED POTENTIALS; MISMATCH NEGATIVITY SYSTEM; DEVELOPMENTAL-CHANGES; SENSORY MEMORY; INFANTS; BRAIN; MATURATION; DISCRIMINATION; SENSITIVITY; THRESHOLDS AB Our previous research with adults suggests that pre-attentive (bottom-up) brain processes govern auditory stream segregation [Sussman et al., 1998. Brain Res. 789, 130-138; Sussman et al., 1999. Psychophysiology 36, 22-34; Winkler et al., submitted for publication]. We investigated whether the pre-attentive mechanisms underlying auditory stream segregation operate similarly in school-aged (7-10 years of age) children and adults. We used an electrophysiological index of auditory change detection that does not require the experimental participant to focus on the sounds to be evoked. In Experiment 1, children were presented with mixtures of high and low frequency tones in different conditions and were instructed to watch a silent video and ignore the sounds. In Experiment 2, children were asked to listen to the same sets of sounds as presented in Experiment 1 and tell whether they heard one or two auditory streams. The pre-attentive processing of the mixture of sounds as one or two auditory streams (Experiment 1), matched with the perception of the sounds as one or two distinct streams (Experiment 2). Our results demonstrate that the mechanisms for auditory stream segregation operate similarly in school-aged children and adults when frequency proximity is the cue for segregation. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Yeshiva Univ Albert Einstein Coll Med, Dept Otolaryngol, Bronx, NY 10461 USA. CUNY, Grad Ctr, Dept Speech & Hearing Sci, New York, NY USA. Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, SF-00100 Helsinki, Finland. Hungarian Acad Sci, Inst Psychol, Budapest, Hungary. RP Sussman, E (reprint author), Yeshiva Univ Albert Einstein Coll Med, Dept Otolaryngol, 1410 Pelham Pkwy S, Bronx, NY 10461 USA. RI Winkler, Istvan/A-7659-2008; Shestakova, Anna/H-3329-2013 OI Winkler, Istvan/0000-0002-3344-6151; Shestakova, Anna/0000-0001-8323-7270 CR ALHO K, 1990, ELECTROEN CLIN NEURO, V77, P151, DOI 10.1016/0168-5597(90)90031-8 Bregman AS., 1990, AUDITORY SCENE ANAL Ceponiene R, 1998, EVOKED POTENTIAL, V108, P345, DOI 10.1016/S0168-5597(97)00081-6 Cheour M, 2000, CLIN NEUROPHYSIOL, V111, P4, DOI 10.1016/S1388-2457(99)00191-1 Cheour M, 1998, INT J PSYCHOPHYSIOL, V29, P217, DOI 10.1016/S0167-8760(98)00017-8 CheourLuhtanen M, 1996, PSYCHOPHYSIOLOGY, V33, P478, DOI 10.1111/j.1469-8986.1996.tb01074.x CLIFTON RK, 1981, CHILD DEV, V52, P833, DOI 10.1111/j.1467-8624.1981.tb03121.x CSEPE V, 1995, EAR HEARING, V16, P91 DEMANY L, 1982, INFANT BEHAV DEV, V5, P261, DOI 10.1016/S0163-6383(82)80036-2 Gomes H, 1999, DEV PSYCHOL, V35, P294, DOI 10.1037//0012-1649.35.1.294 KRAUS N, 1992, EAR HEARING, V13, P158, DOI 10.1097/00003446-199206000-00004 MCADAMS S, 1997, J COUST SOC AM MORR ML, UNPUB MATURATION MIS MORRONGIELLO BA, 1987, J EXP CHILD PSYCHOL, V44, P413, DOI 10.1016/0022-0965(87)90043-9 MUIR D, 1979, CHILD DEV, V50, P31 Naatanen R., 1992, ATTENTION BRAIN FUNC NAATANEN R, 1990, BEHAV BRAIN SCI, V13, P201 Naatanen R, 1999, PSYCHOL BULL, V125, P826, DOI 10.1037/0033-2909.125.6.826 NOZZA RJ, 1984, J SPEECH HEAR RES, V27, P613 PAETAU R, 1995, J CLIN NEUROPHYSIOL, V12, P177, DOI 10.1097/00004691-199503000-00008 Ponton CW, 2000, CLIN NEUROPHYSIOL, V111, P220, DOI 10.1016/S1388-2457(99)00236-9 Ritter W, 2000, NEUROREPORT, V11, P61, DOI 10.1097/00001756-200001170-00012 RITTER W, 1995, EAR HEARING, V16, P52, DOI 10.1097/00003446-199502000-00005 RUBEN RJ, 1992, ACTA OTO-LARYNGOL, V112, P192 Schroger E, 1997, PSYCHOPHYSIOLOGY, V34, P245, DOI 10.1111/j.1469-8986.1997.tb02395.x Shafer VL, 2000, EAR HEARING, V21, P242, DOI 10.1097/00003446-200006000-00008 Sharma A, 1997, EVOKED POTENTIAL, V104, P540, DOI 10.1016/S0168-5597(97)00050-6 SINNOTT JM, 1983, INFANT BEHAV DEV, V6, P3, DOI 10.1016/S0163-6383(83)80003-4 Sussman E, 1998, BRAIN RES, V789, P130, DOI 10.1016/S0006-8993(97)01443-1 Sussman E, 1999, PSYCHOPHYSIOLOGY, V36, P22, DOI 10.1017/S0048577299971056 Thompson NC, 1999, J SPEECH LANG HEAR R, V42, P1061 TREHUB SE, 1980, J EXP CHILD PSYCHOL, V29, P282, DOI 10.1016/0022-0965(80)90020-X VANNOORDEN LPAS, 1977, J ACOUST SOC AM, V61, P1041, DOI 10.1121/1.381388 WERNER LA, 1992, CHILD DEV, V63, P260, DOI 10.1111/j.1467-8624.1992.tb01625.x WHIGHTMAN F, 1989, CHILD DEV, V60, P611 WINKLER I, UNPUB PREATTENTIVE A NR 36 TC 34 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 108 EP 114 DI 10.1016/S0378-5955(00)00261-6 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700011 PM 11223301 ER PT J AU Sheykholeslami, K Kaga, K Tsuzuku, T Mizutani, M AF Sheykholeslami, K Kaga, K Tsuzuku, T Mizutani, M TI Electrophysiological measures of auditory function in the neurofilament-deficient mutant quail (Quv) SO HEARING RESEARCH LA English DT Article DE quail; bird; auditory evoked brainstem response; middle latency response; neurofilament deficiency; conduction velocity ID WHITE LEGHORN CHICK; MYELINATED FIBERS; EVOKED-POTENTIALS; RESPONSES; PHOSPHORYLATION; CONDUCTION AB Auditory pathway electrophysiological studies were performed on the mutant quail 'Quv'. This mutation is known to result in neurofilament deficiencies of both the peripheral and central nervous systems. Auditory evoked brainstem responses (ABRs), electrocochleograms (EcochGs) and middle latency responses (MLRs) were evaluated. ABRs in Quv quails demonstrated markedly altered waveforms exhibiting longer latencies, absence of the later peaks and lower amplitudes. The EcochG showed normal cochlear microphonics with no obvious abnormalities in amplitude or latency and normal latencies for peak N1. Quv quails had a mild threshold elevation with a normal latency for the first peak of the ABR (P1). The Quv MLRs showed no significant differences in amplitude but they revealed a latency prolongation for peaks NO, Pa and Na relative to the controls. We have discovered abnormal findings of auditory evoked potentials in the neurofilament-deficient quail (Quv). We suggest that the smaller axonal size and axonal hypotrophy due to altered neurofilament expression underlies these abnormal auditory evoked potential responses. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tokyo, Dept Otolaryngol, Bunkyo Ku, Tokyo 1130033, Japan. Teikyo Univ, Dept Otolaryngol, Itabashi Ku, Tokyo 173, Japan. Nippon Inst Biol Sci, Yamanashi, Japan. RP Sheykholeslami, K (reprint author), Univ Tokyo, Dept Otolaryngol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. EM kianoush@m.u-tokyo.ac.jp CR ALLEN AR, 1978, ELECTROEN CLIN NEURO, V45, P53, DOI 10.1016/0013-4694(78)90341-3 BECK MM, 1987, BRAIN RES, V406, P93, DOI 10.1016/0006-8993(87)90772-4 BIEDERMAN-THORSON M, 1970, Brain Research, V24, P235, DOI 10.1016/0006-8993(70)90103-4 BOORD RL, 1969, ANN NY ACAD SCI, V167, P186, DOI 10.1111/j.1749-6632.1969.tb20444.x BROWNBORG HM, 1987, COMP BIOCHEM PHYS A, V88, P391, DOI 10.1016/0300-9629(87)90052-1 DALLOS P, 1972, ACTA OTO-LARYNGOL, P1 DAUBE JR, 1980, NERVE CONDUCTION STU, P229 GEISLER CD, 1958, SCIENCE, V128, P1210, DOI 10.1126/science.128.3333.1210 HARMAN AL, 1967, EXP NEUROL, V18, P276, DOI 10.1016/0014-4886(67)90048-9 HOFFMAN PN, 1987, P NATL ACAD SCI USA, V84, P3472, DOI 10.1073/pnas.84.10.3472 JONES TA, 1987, HEARING RES, V27, P67, DOI 10.1016/0378-5955(87)90026-8 Kimura J., 1989, ELECTRODIAGNOSIS DIS, P332 MATUS A, 1988, TRENDS NEUROSCI, V11, P291, DOI 10.1016/0166-2236(88)90086-0 MIZUTANI M, 1992, J HERED, V84, P234 MOORE JW, 1978, BIOPHYS J, V21, P147 NIXON RA, 1991, TRENDS NEUROSCI, V14, P501, DOI 10.1016/0166-2236(91)90062-Y NOMOTO M, 1985, HEARING RES, V17, P13, DOI 10.1016/0378-5955(85)90125-X PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 SAKAGUCHI T, 1993, NEUROSCI LETT, V153, P65, DOI 10.1016/0304-3940(93)90078-Y TIMOTHY A, 1987, HEARING RES, V27, P67 YAMASAKI H, 1991, ACTA NEUROPATHOL, V82, P427 NR 21 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 115 EP 122 DI 10.1016/S0378-5955(00)00262-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700012 PM 11223302 ER PT J AU Apoux, F Crouzet, O Lorenzi, C AF Apoux, F Crouzet, O Lorenzi, C TI Temporal envelope expansion of speech in noise for normal-hearing and hearing-impaired listeners: effects on identification performance and response times SO HEARING RESEARCH LA English DT Article DE temporal envelope expansion; background noise; speech identification; response time; sensorineural hearing loss ID GAP DETECTION; CONSONANT RECOGNITION; INTELLIGIBILITY; QUALITY; CUES; ENHANCEMENT; COMPRESSION AB The effects of expanding the temporal envelope of speech sounds on speech identification in noise were investigated in normal-hearing and hearing-impaired listeners. Expansion was performed by applying a power-law transformation to the low-frequency temporal modulations (< 500 Hz) of vowel-consonant-vowel logatomes presented against a background noise. Stimuli were spectrally degraded, allowing a direct examination of the perceptual effects induced by the modification of the temporal envelope alone on speech reception. This study extended a previous study conducted by Lorenzi et al. [1999. Hear. Res. 136, 131-138] by measuring the effects of envelope expansion on both identification performance and response times in normal-hearing and hearing-impaired listeners. Overall, the results show that temporal expansion yields only small improvements in identification scores ( 5%) in normal-hearing listeners. No effect of expansion on identification scores was observed in hearing-impaired listeners. On the other hand, the results show that expansion led to a significant decrease in response times in both normal-hearing and hearing-impaired listeners. The average benefit from expansion was about 65 ms in both groups. These results suggest that expanding the temporal envelope of speech sounds presented in noise may improve 'ease of listening' in both normal-hearing and hearing-impaired listeners. (C) 2001 Published by Elsevier Science B.V. C1 Univ Paris 05, Expt Psychol Lab, Inst Psychol, CNRS,UMR 8581, F-92774 Boulogne, France. Intrason France, F-94607 Choisy Le Roi, France. RP Apoux, F (reprint author), Univ Paris 05, Expt Psychol Lab, Inst Psychol, CNRS,UMR 8581, 71 Av Vaillant, F-92774 Boulogne, France. RI Apoux, Frederic/C-4991-2009; Lorenzi, Christian/F-5310-2012 CR BAER T, 1993, J REHABIL RES DEV, V30, P49 CLARKSON PM, 1991, J ACOUST SOC AM, V89, P1378, DOI 10.1121/1.400538 DRULLMAN R, 1994, J ACOUST SOC AM, V95, P1053, DOI 10.1121/1.408467 EGER TE, 1984, P IEEE ICASSP Fitzgibbons PJ, 1995, J ACOUST SOC AM, V98, P3140, DOI 10.1121/1.413803 FRISINA DR, 1997, HEARING RES, V22, P1822 Fu QJ, 1998, J ACOUST SOC AM, V104, P2570, DOI 10.1121/1.423912 GATEHOUSE S J G, 1990, British Journal of Audiology, V24, P63, DOI 10.3109/03005369009077843 GLASBERG BR, 1992, HEARING RES, V64, P81, DOI 10.1016/0378-5955(92)90170-R HOUTGAST T, 1985, J ACOUST SOC AM, V77, P1069, DOI 10.1121/1.392224 Lorenzi C, 1999, HEARING RES, V136, P131, DOI 10.1016/S0378-5955(99)00117-3 MILLER GA, 1955, J ACOUST SOC AM, V27, P338, DOI 10.1121/1.1907526 MOORE BCJ, 1988, J ACOUST SOC AM, V83, P1093, DOI 10.1121/1.396054 MOORE BCJ, 1992, BRIT J AUDIOL, V26, P229, DOI 10.3109/03005369209076641 Noordhoek IM, 1997, J ACOUST SOC AM, V101, P498, DOI 10.1121/1.417993 PLOMP R, 1988, J ACOUST SOC AM, V83, P2322, DOI 10.1121/1.396363 SCHNEIDER BA, 1994, J ACOUST SOC AM, V95, P980, DOI 10.1121/1.408403 SHANNON RV, 1995, SCIENCE, V270, P303, DOI 10.1126/science.270.5234.303 Simpson A M, 1990, Acta Otolaryngol Suppl, V469, P101 Snell KB, 1997, J ACOUST SOC AM, V101, P2214, DOI 10.1121/1.418205 Snell KB, 2000, J ACOUST SOC AM, V107, P1615, DOI 10.1121/1.428446 STEENEKEN HJM, 1980, J ACOUST SOC AM, V67, P318, DOI 10.1121/1.384464 STONE MA, 1992, J REHABIL RES DEV, V29, P39, DOI 10.1682/JRRD.1992.04.0039 SUMMERFIELD Q, 1985, SPEECH COMMUN, V4, P213, DOI 10.1016/0167-6393(85)90048-2 TURNER CW, 1995, J ACOUST SOC AM, V97, P2568, DOI 10.1121/1.411911 Turner CW, 1999, J SPEECH LANG HEAR R, V42, P773 VANTASSELL DJ, 1992, J ACOUST SOC AM, V92, P1247, DOI 10.1121/1.403920 van Buuren RA, 1999, J ACOUST SOC AM, V105, P2903, DOI 10.1121/1.426943 van der Horst R, 1999, J ACOUST SOC AM, V105, P1801, DOI 10.1121/1.426718 VANTASELL DJ, 1987, J ACOUST SOC AM, V757, P1069 NR 30 TC 15 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 123 EP 131 DI 10.1016/S0378-5955(00)00265-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700013 PM 11223303 ER PT J AU Nicolas, MT Dememes, D Martin, A Kupershmidt, S Barhanin, J AF Nicolas, MT Dememes, D Martin, A Kupershmidt, S Barhanin, J TI KCNQ1/KCNE1 potassium channels in mammalian vestibular dark cells SO HEARING RESEARCH LA English DT Article DE KCNQ1/KCNE1 (KvLQT1/Isk); knock-out mouse; immunocytochemistry; in situ hybridization; electron microscopy ID LANGE-NIELSEN-SYNDROME; STRIAL MARGINAL CELLS; I-SK CHANNEL; INNER-EAR; K+ SECRETION; CELLULAR-LOCALIZATION; CARDIAC-ARRHYTHMIAS; CAUSE JERVELL; ISK; GENE AB The high [K+] in the inner ear endolymph is essential for mechanosensory transduction in hearing and balance. Several ion channels, including a slowly activating, voltage-dependent, outwardly conducting K+ channel composed of the KCNQ1 (KvLQT1) and KCNE1 (IsK/minK) subunits, are expressed at the apical surface of vestibular dark cells. We investigated the underlying molecular mechanisms of this conductance using in situ hybridization, RT-PCR, and immunocytochemistry and by tracking the ultrastructural changes of vestibular structures in kcne1(-/-) mice. In the wild type mice, the KCNE1 and KCNQ1 proteins are expressed specifically at the epical membrane of dark cells, as early as gestational day (GD) 17 for KCNE1 while KCNQ1 mRNAs can be detected at GD 18. This is the first demonstration that the two protein components of this potassium channel co-localize in a polarized fashion at the cellular level. Although the vestibular end-organs are normal at birth in kcne1(-/-) mice, they begin to show modifications during postnatal development: we observed an increase in the height of the dark cells, in their number of mitochondria, and in basolateral membrane infoldings. Subsequently, the epithelium degenerates and the endolymphatic space collapses. Similar changes are known to occur in the cardio-auditory Jervell-Lange-Nielsen syndrome which is caused by mutations in the same channel. (C) 2001 Published by Elsevier Science B.V. C1 Univ Montpellier 2, INSERM, U432, F-34095 Montpellier 05, France. Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37235 USA. CNRS, Inst Pharmacol Mol & Cellulaire, F-06560 Valbonne, France. RP Nicolas, MT (reprint author), Univ Montpellier 2, INSERM, U432, POB 089, F-34095 Montpellier 05, France. CR ANNIKO M, 1979, ARCH OTO-RHINO-LARYN, V225, P161, DOI 10.1007/BF00455250 Barhanin J, 1996, NATURE, V384, P78, DOI 10.1038/384078a0 Barhanin J, 1998, TRENDS CARDIOVAS MED, V8, P207, DOI 10.1016/S1050-1738(98)00013-9 Barhanin J, 1999, CURR TOP MEMBR, V46, P67 Chouabe C, 1997, EMBO J, V16, P5472, DOI 10.1093/emboj/16.17.5472 Cooper EC, 1999, P NATL ACAD SCI USA, V96, P4759, DOI 10.1073/pnas.96.9.4759 DEAL KK, 1994, J NEUROSCI, V14, P1666 DECHESNE CJ, 1994, J COMP NEUROL, V346, P517, DOI 10.1002/cne.903460405 Dememes D, 1998, DEV BRAIN RES, V108, P59, DOI 10.1016/S0165-3806(98)00030-3 DESMADRYL G, 1986, DEV BRAIN RES, V25, P133, DOI 10.1016/0165-3806(86)90160-4 DIEFFENBACH CW, 1995, PCR PRIMER LAB MANUA, P1 Drici MD, 1998, CIRC RES, V83, P95 FERRARY E, 1989, AM J PHYSIOL, V257, pF182 FERRARY E, 1998, KIDNEY INT, V53, pS98 Friedmann I, 1966, J Laryngol Otol, V80, P451, DOI 10.1017/S002221510006552X Guicheney P, 1998, M S-MED SCI, V14, P1025 Issa A, 1997, BRIT J AUDIOL, V31, P80 JERVELL A, 1957, AM HEART J, V54, P59, DOI 10.1016/0002-8703(57)90079-0 KAWAMATA S, 1986, ACTA OTO-LARYNGOL, V102, P168, DOI 10.3109/00016488609108662 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 LESAGE F, 1993, RECEPTOR CHANNEL, V1, P143 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 1994, AM J PHYSIOL, V267, pC857 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MBIENE JP, 1988, ANAT EMBRYOL, V177, P331, DOI 10.1007/BF00315841 MORI N, 1993, EUR ARCH OTO-RHINO-L, V250, P186 Neyroud N, 1997, NAT GENET, V15, P186, DOI 10.1038/ng0297-186 SAKAGAMI M, 1991, HEARING RES, V56, P168, DOI 10.1016/0378-5955(91)90166-7 Sanguinetti MC, 1996, NATURE, V384, P80, DOI 10.1038/384080a0 SANS A, 1994, VERTIGES, V93, P91 SCARFONE E, 1988, J NEUROSCI, V8, P4640 SchulzeBahr E, 1997, NAT GENET, V17, P267, DOI 10.1038/ng1197-267 Shen ZJ, 1997, AUDIT NEUROSCI, V3, P215 Shen ZJ, 1998, HEARING RES, V123, P157, DOI 10.1016/S0378-5955(98)00110-5 SOBIN A, 1981, ACTA OTO-LARYNGOL, V91, P247, DOI 10.3109/00016488109138505 Splawski I, 1997, NAT GENET, V17, P338, DOI 10.1038/ng1197-338 Steel KP, 1999, TRENDS GENET, V15, P207, DOI 10.1016/S0168-9525(99)01753-9 STERKERS O, 1988, PHYSIOL REV, V68, P1083 Suessbrich H, 1999, Rev Physiol Biochem Pharmacol, V137, P191 Sunose H, 1997, J MEMBRANE BIOL, V156, P25, DOI 10.1007/s002329900184 SUNOSE H, 1995, P SEND S, V5, P73 TAKEUCHI S, 1992, AM J PHYSIOL, V267, pC857 TAKUMI T, 1988, SCIENCE, V242, P1042, DOI 10.1126/science.3194754 Tyson J, 1997, HUM MOL GENET, V6, P2179, DOI 10.1093/hmg/6.12.2179 Vetter DE, 1996, NEURON, V17, P1251, DOI 10.1016/S0896-6273(00)80255-X Wang Q, 1996, NAT GENET, V12, P17, DOI 10.1038/ng0196-17 WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 Wangemann P, 1996, HEARING RES, V100, P201, DOI 10.1016/0378-5955(96)00127-X ZAJIC G, 1983, HEARING RES, V10, P249, DOI 10.1016/0378-5955(83)90090-4 NR 50 TC 58 Z9 60 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 132 EP 145 DI 10.1016/S0378-5955(00)00268-9 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700014 PM 11223304 ER PT J AU Lee, CY Rosowski, JJ AF Lee, CY Rosowski, JJ TI Effects of middle-ear static pressure on pars tensa and pars flaccida of gerbil ears SO HEARING RESEARCH LA English DT Article DE tympanic membrane; tympanometry; laser Doppler velocimetry ID SOUND-POWER COLLECTION; TYMPANIC MEMBRANE; MONGOLIAN GERBIL; MERIONES-UNGUICULATUS; AUDITORY PERIPHERY; MECHANICS; TYMPANOMETRY; VOLUME; IMPEDANCE AB It has long been known that static pressure affects middle-ear function and conventional tympanometry uses variations in static pressure for clinical assessment of the middle ear. However, conventional tympanometry treats the entire tympanic membrane as a uniform interface between the external and middle ear and does not differentiate the behavior of the two components of the tympanic membrane, pars tensa and pars flaccida. To analyze separately the different acoustic behavior of these two tympanic membrane components, laser Doppler velocimetry is used to determine the motion of each of these two structures. The velocities of points near the center of p. tensa and p. flaccida in response to the external-ear sound pressure at different middle-ear static pressures were measured in nine gerbil ears. The effect of middle-ear static pressure on the acoustic response of both structures is similar in that nan-zero middle-ear static pressures generally reduce the velocity magnitude of the two membrane components in response to sound stimuli. Middle-ear under-pressures tend to reduce the velocity magnitude more than do middle-ear over-pressures. The acoustic stiffness and inertance of both p. tensa and p. flaccida are altered by static pressure, as shown in our results as changes of transferfunction phase angle. Compared to p. tense, p. flaccida showed larger reductions in the velocity magnitude to small over- and under-pressures near the ambient middle-ear pressure. This higher pressure sensitivity of p. flaccida has been found in all ears and may link the previously proposed middle-ear pressure regulating and the acoustic shunting functions of p. flaccida. We also describe, in both p. tensa and p. flaccida, a frequency dependence of the velocity measurements, hysteresis of velocity magnitude between different directions of pressure sweep and asymmetrical effects of over- and under-pressure on the point velocity. (C) 2001 Published by Elsevier Science B.V. C1 Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA. Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA. Natl Taiwan Univ Hosp, Dept Otorhinolaryngol, Taipei, Taiwan. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. MIT, Harvard MIT Div Hlth Sci & Technol, Speech & Hearing Sci Program, Cambridge, MA 02139 USA. RP Rosowski, JJ (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA. CR ARITOMO H, 1988, OTOLARYNG HEAD NECK, V98, P310 CRETEN WL, 1974, SCAND AUDIOL, V3, P39, DOI 10.3109/01050397409044963 DECRAEMER WF, 1989, HEARING RES, V38, P1, DOI 10.1016/0378-5955(89)90123-8 Dirckx JJJ, 1998, HEARING RES, V118, P35, DOI 10.1016/S0378-5955(98)00025-2 FUNNELL WRJ, 1982, ORL J OTO-RHINO-LARY, V44, P181 Gaihede M, 1999, Auris Nasus Larynx, V26, P383, DOI 10.1016/S0385-8146(99)00018-8 GAIHEDE M, 1995, ACTA OTO-LARYNGOL, V115, P414, DOI 10.3109/00016489509139340 HELLSTROM S, 1983, ACTA PHYSIOL SCAND, V118, P337, DOI 10.1111/j.1748-1716.1983.tb07280.x HUTTENBRINK KB, 1988, ACTA OTOLARYNGOL S11, V68, P614 KOHLLOFFEL LUE, 1984, HEARING RES, V13, P83, DOI 10.1016/0378-5955(84)90098-4 LIDEN G, 1970, ARCHIV OTOLARYNGOL, V92, P248 LILLY DJ, 1984, EAR HEARING, V5, P300, DOI 10.1097/00003446-198409000-00007 LIM DJ, 1970, ACTA OTO-LARYNGOL, V70, P176 Lim D. J., 1995, Acta Oto-Rhino-Laryngologica Belgica, V49, P101 Lim D J, 1968, Acta Otolaryngol, V66, P515, DOI 10.3109/00016486809126316 Lim D J, 1968, Acta Otolaryngol, V66, P181, DOI 10.3109/00016486809126286 LYNCH TJ, 1981, THESIS MIT CAMBRIDGE Margolis RH, 1985, HDB CLIN AUDIOLOGY, P438 MARGOLIS RH, 1985, AUDIOLOGY, V24, P44 MARGOLIS RH, 1977, J SPEECH HEAR RES, V20, P437 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MUNDIE R, 1963, US ARMY MED RES REP, V576, P63 Murakami S, 1997, ACTA OTO-LARYNGOL, V117, P390, DOI 10.3109/00016489709113411 Ravicz ME, 1997, J ACOUST SOC AM, V101, P2135, DOI 10.1121/1.418275 RAVICZ ME, 1992, J ACOUST SOC AM, V92, P157, DOI 10.1121/1.404280 Ravicz ME, 1996, J ACOUST SOC AM, V99, P3044, DOI 10.1121/1.414793 Rosowski JJ, 1997, DIVERSITY AUDITORY M, P129 SHANKS JE, 1986, J SPEECH HEAR RES, V29, P11 SHANKS JE, 1981, J SPEECH HEAR RES, V24, P557 Shrapnell HJ, 1832, LONDON MED GAZ, V10, P120 STENFORS LE, 1979, ACTA OTO-LARYNGOL, V88, P395, DOI 10.3109/00016487909137184 Teoh SW, 1997, HEARING RES, V106, P39, DOI 10.1016/S0378-5955(97)00002-6 TONNDORF J, 1970, ANN OTO RHINOL LARYN, V79, P743 Vanhuyse VJ, 1975, SCAND AUDIOL, V4, P45, DOI 10.3109/01050397509075014 VONUNGE M, 1991, AM J OTOL, V12, P407 VONUNGE M, 1994, AM J OTOL, V15, P663 Wever EG, 1954, PHYSL ACOUSTICS ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 NR 38 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 146 EP 163 DI 10.1016/S0378-5955(00)00269-0 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700015 PM 11223305 ER PT J AU Lyon, MJ Jensen, RC AF Lyon, MJ Jensen, RC TI Quantitative analysis of rat inner ear blood flow using the iodo[C-14]antipyrine technique SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 21st Midwinter Research Meeting of the Association-for-Research-in-Otolaryngology CY FEB 15-19, 1998 CL ST PETERSBURG BEACH, FLORIDA SP Assoc Res Otolaryngol DE vestibule; cochlea; blood flow; microcirculation; quantitative; iodoantipyrine ID LASER DOPPLER FLOWMETER; GUINEA-PIG COCHLEA; VASCULAR MECHANISMS; C-14 IODOANTIPYRINE; GLUCOSE-UTILIZATION; MICROSPHERE METHOD; VESTIBULAR SYSTEM; MENIERES-DISEASE; SMOOTH-MUSCLE; CONTRACTION AB A number of different qualitative and quantitative techniques have been used to measure inner ear blood flow and all have required that the animal be anesthetized. It is well known that anesthesia can cause a variety of circulatory as well as other systemic changes. In this study, we have employed a technique commonly used for quantifying brain blood flow, the iodo[C-14]antipyrine technique ([C-14]IAP). Unlike other techniques, [C-14]IAP can be used in unanesthetized animals under conditions that are nearly normal, it is non-invasive, it can be used reliably in regions of low local blood flow, and data can be acquired from both the periphery and central nervous system. Results show that blood flow to the lateral wall of the basal turn of the cochlea (387 +/- 19 mul/g/min) is significantly higher (P < 0.001) than that of the utricular macula (189 +/- 23 l/g/min), horizontal (186 +/- 22 mul/g/min), superior (185 +/- 22 mul/g/min), or posterior canal crista (185 +/- 25 mul/g/min). Surprisingly, blood flow to all of the vestibular end-organs is remarkably similar. The use of this technique should allow pharmacological experimentation on inner ear blood flaw without the unknown complications of anesthesia or invasive procedures. (C) 2001 Published by Elsevier Science B.V. C1 SUNY Upstate Med Univ, Dept Otolaryngol & Commun Sci, Syracuse, NY 13210 USA. SUNY Upstate Med Univ, Dept Cell & Dev Biol, Syracuse, NY 13210 USA. RP Lyon, MJ (reprint author), SUNY Upstate Med Univ, Dept Otolaryngol & Commun Sci, 750 E Adams St, Syracuse, NY 13210 USA. CR ANDERSON KM, 1991, CIRC RES, V69, P174 ANGELBORG C, 1985, ANN OTO RHINOL LARYN, V94, P181 ANGELBORG C, 1977, ACTA OTO-LARYNGOL, V83, P92, DOI 10.3109/00016487709128818 ANGELBORG C, 1985, J OTOLARYNGOL, V14, P41 ANGELBORG C, 1987, VESTIBULAR SYSTEM NE, P157 ANGELBORG C, 1987, HEARING RES, V27, P265, DOI 10.1016/0378-5955(87)90008-6 BONNER RF, 1987, J OPT SOC AM A, V4, P423, DOI 10.1364/JOSAA.4.000423 BROWN JN, 1989, LAB ANIM SCI, V39, P142 DENGERINK HA, 1987, ACTA OTO-LARYNGOL, V104, P113, DOI 10.3109/00016488709109055 DODD F, 1992, HEARING RES, V62, P173, DOI 10.1016/0378-5955(92)90183-N GRAD A, 1989, ARCH NEUROL-CHICAGO, V46, P281 GROSS PM, 1987, J CEREBR BLOOD F MET, V7, P154 GUSSEN R, 1983, OTOLARYNG HEAD NECK, V91, P68 GUSSEN R, 1982, ARCH OTOLARYNGOL, V108, P544 HATAKEYAMA T, 1992, J CEREBR BLOOD F MET, V12, P296 HILLERDAL M, 1987, ACTA PHYSIOL SCAND, V130, P229, DOI 10.1111/j.1748-1716.1987.tb08132.x HILLERDAL M, 1987, HEARING RES, V27, P27, DOI 10.1016/0378-5955(87)90023-2 HULTCRANTZ E, 1988, AM J OTOLARYNG, V9, P317, DOI 10.1016/S0196-0709(88)80039-5 JAY TM, 1988, J CEREBR BLOOD F MET, V8, P121 Kety S. S., 1960, METHOD MED RES, V8, P228 KETY SS, 1951, PHARMACOL REV, V3, P1 KIMURA RS, 1972, VSCULAR DISORDERS HE, P205 LANCASTER JF, 1987, J ROY SOC MED, V80, P729 LAROUERE MJ, 1989, OTOLARYNG HEAD NECK, V101, P375 LAURIKAINEN EA, 1994, J PHYSIOL-LONDON, V480, P563 LAWRENCE M, 1977, ACTA OTO-LARYNGOL, V83, P146, DOI 10.3109/00016487709128825 LYON MJ, 1993, HEARING RES, V67, P157, DOI 10.1016/0378-5955(93)90243-T Lyon MJ, 2000, HEARING RES, V141, P189, DOI 10.1016/S0378-5955(00)00004-6 MAASS B, 1984, ARCH OTO-RHINO-LARYN, V240, P295 MCGILLIVRAYANDERSON KM, 1990, CIRC RES, V66, P1643 MILES FP, 1988, HEARING RES, V33, P191, DOI 10.1016/0378-5955(88)90032-9 MILLER JM, 1991, ANN OTO RHINOL LARYN, V100, P44 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 NAKASHIMA T, 1991, ACTA OTO-LARYNGOL, V111, P738, DOI 10.3109/00016489109138406 NILSSON GE, 1980, IEEE T BIO-MED ENG, V27, P597, DOI 10.1109/TBME.1980.326582 NOTZLI HP, 1989, J ORTHOPAED RES, V7, P413, DOI 10.1002/jor.1100070314 NUTTALL AL, 1988, HEARING RES, V34, P215, DOI 10.1016/0378-5955(88)90001-9 NUTTALL AL, 1988, AM J OTOLARYNG, V9, P291, DOI 10.1016/S0196-0709(88)80037-1 Olds MJ, 1997, ANN OTO RHINOL LARYN, V106, P145 PAYMAN R, 1993, ANN OTO RHINOL LARYN, V102, P893 PERLMAN H B, 1955, Ann Otol Rhinol Laryngol, V64, P1176 PRAZMA J, 1983, ARCH OTOLARYNGOL, V109, P611 RYAN AF, 1988, ACTA OTO-LARYNGOL, V105, P232, DOI 10.3109/00016488809097003 SAKURADA O, 1978, AM J PHYSIOL, V234, P59 SANDOR P, 1983, ACTA PHYSIOL HUNG, V61, P217 SCHEIBE F, 1990, EUR ARCH OTO-RHINO-L, V247, P20 Schmidt J T, 1992, Acta Otolaryngol Suppl, V497, P1 Schuknecht H. F., 1974, PATHOLOGY EAR SHADDOCK LC, 1985, HEARING RES, V20, P109, DOI 10.1016/0378-5955(85)90162-5 SMITH C, 1972, VOLUNTARY ASS PERSPE, P1 SNOW JB, 1973, ARCH OTOLARYNGOL, V97, P365 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x SOKOLOFF L, 1981, FED PROC, V40, P2311 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 TATEISHI J, 1995, CIRC RES, V76, P53 THORNE PR, 1987, HEARING RES, V31, P229, DOI 10.1016/0378-5955(87)90192-4 WALL KM, 1990, BRAIN RES, V521, P333, DOI 10.1016/0006-8993(90)91562-U NR 57 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 164 EP 173 DI 10.1016/S0378-5955(00)00270-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700016 PM 11223306 ER PT J AU Palombi, PS Backoff, PM Caspary, DM AF Palombi, PS Backoff, PM Caspary, DM TI Responses of young and aged rat inferior colliculus neurons to sinusoidally amplitude modulated stimuli SO HEARING RESEARCH LA English DT Article DE rat; aging; inferior colliculus; amplitude modulation; inhibition ID CONTRALATERAL MONAURAL STIMULI; AUDITORY-SYSTEM; BROWN BAT; SIGNALS; INHIBITION; SOUNDS; CAT; SUBDIVISIONS; PHYSIOLOGY; MIDBRAIN AB The inferior colliculus (IC) is a processing center for monaural and binaural auditory signals. Many units in the central nucleus of the inferior colliculus (CIC) respond to amplitude and frequency modulated tones, features found in communication signals. The present study examined potential effects of age on responses to sinusoidally amplitude modulated (SAM) tones in CIC and external cortex of the inferior colliculus (ECIC) units in young and aged F344 rats. Extracellular recordings from 154 localized single units of aged (24 month) rats were compared to recordings from 135 TC units from young adult (3 month) animals. SAM tones were presented at 30 dB above threshold. Comparisons were made between CIC and ECIC regarding the percentage of units responding to SAM stimuli, the relationship between SAM responsiveness and temporal response patterns, maximum discharge rates and maximum modulation gains, shapes of rate transfer functions and synchronization modulation transfer functions (MTFs) in response to SAM tones. Sixty percent of units in young and aged rat IC were selectively responsive to SAM stimuli. Eighty-one percent of units classified as onset temporal response patterns were not tonically responsive to SAM stimuli. Median maximum discharge rate in response to SAM tones was 17.6/s in young F344 rats; median maximum modulation gain was 3.85 dB. These measurements did not change significantly with age. Thirty-seven percent of young rat units displayed bandpass MTFs and 53%, had lowpass MTFs. There was a significant age-related shift in the distribution of MTF shapes in both the CIC and ECIC. Aged animals showed a lower percentage of bandpass functions and a higher percentage of lowpass functions. Age-related changes observed in SAM coding may reflect an altered balance between excitatory/inhibitory neurotransmitter efficacy in the aged rat IC, and/or possibly a change in the functional dynamic range of IC neurons. (C) 2001 published by Elsevier Science B.V. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. RP Caspary, DM (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, 801 N Rutledge,POB 19629, Springfield, IL 62794 USA. EM dcaspary@siumed.edu CR AITKIN L, 1994, EXP BRAIN RES, V98, P53 AITKIN LM, 1981, J COMP NEUROL, V196, P25, DOI 10.1002/cne.901960104 AITKIN LM, 1985, AUDITORY MIDBRAIN ST BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 Burger RM, 1998, J NEUROPHYSIOL, V80, P1686 Caspary DM, 1999, NEUROSCIENCE, V93, P307, DOI 10.1016/S0306-4522(99)00121-9 CASPARY DM, 1997, ASS RES OT ABSTR, V20, P189 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 CIARD D, 1991, NEUROBIOLOGY HEARING, P253 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 CONDON CJ, 1994, J NEUROPHYSIOL, V71, P768 Condon CJ, 1996, J COMP PHYSIOL A, V178, P147 COOLEY BC, 1992, THROMB RES, V67, P1, DOI 10.1016/0049-3848(92)90252-6 EPPING WJM, 1986, HEARING RES, V24, P55, DOI 10.1016/0378-5955(86)90005-5 FRISINA RD, 1993, SENSORY RESEARCH MULTIMODAL PERSPECTIVES, P151 GROTHE B, 1997, ASS RES OT ABSTR, V20, P90 GUTIERREZ A, 1994, J NEUROSCI, V14, P7469 HALL JC, 1994, AM ZOOL, V34, P670 Irvine D. R. F., 1992, MAMMALIAN AUDITORY P, P153 Koch U, 1998, J NEUROPHYSIOL, V80, P71 Krishna BS, 2000, J NEUROPHYSIOL, V84, P255 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 Lu Y, 1998, J NEUROPHYSIOL, V79, P2303 Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F MOLLER AR, 1986, HEARING RES, V24, P203, DOI 10.1016/0378-5955(86)90019-5 MOLLER AR, 1972, Q REV BIOPHYS, V5, P59 MULLERPREUSS P, 1994, HEARING RES, V80, P197, DOI 10.1016/0378-5955(94)90111-2 Oliver D. L., 1991, NEUROBIOLOGY HEARING, P195 Oliver DL, 1992, MAMMALIAN AUDITORY P, P168 Palombi PS, 1996, HEARING RES, V100, P41, DOI 10.1016/0378-5955(96)00115-3 Palombi PS, 1996, J NEUROPHYSIOL, V76, P3114 POON PWF, 1992, EXP BRAIN RES, V91, P94 REES A, 1987, HEARING RES, V27, P129, DOI 10.1016/0378-5955(87)90014-1 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SYKA J, 1983, HEARING PHYSL BASES, P224 Xu J, 1996, J COMP PHYSIOL A, V178, P435 Yang LC, 1997, J NEUROPHYSIOL, V77, P324 NR 40 TC 36 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 EI 1878-5891 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 174 EP 180 DI 10.1016/S0378-5955(00)00264-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700017 ER PT J AU Woolley, SMN Wissman, AM Rubel, EW AF Woolley, SMN Wissman, AM Rubel, EW TI Hair cell regeneration and recovery of auditory thresholds following aminoglycoside ototoxicity in Bengalese finches SO HEARING RESEARCH LA English DT Article DE amikacin; hearing; bird; basilar papilla; cochlea; stereocilia ID STARLING STURNUS-VULGARIS; SEVERE ACOUSTIC TRAUMA; BASILAR PAPILLA; CHICK COCHLEA; INNER-EAR; FUNCTIONAL RECOVERY; STEREOCILIARY BUNDLES; ADULT CHICKENS; AVIAN COCHLEA; GENTAMICIN AB Birds regenerate auditory hair cells when original hair cells are lost. Regenerated hair cells become innervated and restore hearing function. Functional recovery during hair cell regeneration is particularly interesting in animals that depend on hearing for vocal communication. Bengalese finches are songbirds that depend on auditory feedback for normal song learning and maintenance. We examined the structural and functional recovery of the Bengalese finch basilar papilla after aminoglycoside ototoxicity. Birds were treated with the ototoxic aminoglycoside, amikacin, daily for 1 week. Treatment resulted in hair cell loss across the basal half of the basilar papilla and corresponding high frequency hearing loss. Hair cell regeneration and recovery of auditory brainstem responses were compared in the same animals. Survival times following treatment were between 1 day and 12 weeks. Analysis of structural recovery at weekly intervals indicated that hair cells in the Bengalese finch papilla require a maximum of 1 week to regenerate and appear with immature morphology at the epithelial surface. An additional 6 days are required for adult-like morphology to develop. Repopulation of the damaged region was complete by 8 weeks. Recovery of auditory thresholds began 1 week after treatment and reached asymptote by 4 weeks. Slight residual threshold shifts at 2.0 kHz and above were observed up to 12 weeks after treatment. Direct comparison of structural and functional recovery indicates that auditory thresholds recover maximally before a full complement of hair cells has regenerated. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Washington, Dept Otolaryngol Head & Neck Surg, Neurobiol & Behav Program, Seattle, WA 98195 USA. Univ Washington, Virginia Merrill Bloedel Hearing Res Ctr, Seattle, WA 98195 USA. RP Rubel, EW (reprint author), Univ Washington, Dept Otolaryngol Head & Neck Surg, Neurobiol & Behav Program, POB 357923, Seattle, WA 98195 USA. CR ADLER HJ, 1993, HEARING RES, V71, P214, DOI 10.1016/0378-5955(93)90037-2 BEAUBIEN AR, 1995, HEARING RES, V83, P62, DOI 10.1016/0378-5955(94)00192-S CLAYTON NS, 1987, ETHOLOGY, V76, P247 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 Cotanche DA, 1999, AUDIOL NEURO-OTOL, V4, P271, DOI 10.1159/000013852 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DIETRICH K, 1980, Z TIERPSYCHOL, V52, P57 Dooling RJ, 1997, P NATL ACAD SCI USA, V94, P14206, DOI 10.1073/pnas.94.25.14206 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 DUCKERT LG, 1993, J COMP NEUROL, V331, P75, DOI 10.1002/cne.903310105 FISCHER FP, 1994, SCANNING MICROSCOPY, V8, P351 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 GLEICH O, 1994, J MORPHOL, V221, P1, DOI 10.1002/jmor.1052210102 HASHINO E, 1992, HEARING RES, V59, P46, DOI 10.1016/0378-5955(92)90101-R HASHINO E, 1991, HEARING RES, V52, P356, DOI 10.1016/0378-5955(91)90025-5 HASHINO E, 1995, HEARING RES, V88, P156, DOI 10.1016/0378-5955(95)00109-H HASHINO E, 1989, J ACOUST SOC AM, V85, P289, DOI 10.1121/1.397736 Hennig AK, 1998, J NEUROSCI, V18, P3282 Immelmann K., 1969, P61 Janas JD, 1995, HEARING RES, V92, P17, DOI 10.1016/0378-5955(95)00190-5 KITASATO I, 1990, CHEMOTHERAPY, V36, P155 LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 Marean GC, 1998, J ACOUST SOC AM, V103, P3567, DOI 10.1121/1.423085 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y Muller M, 1996, HEARING RES, V102, P133, DOI 10.1016/S0378-5955(96)00155-4 Muller M, 1998, HEARING RES, V120, P25, DOI 10.1016/S0378-5955(98)00049-5 NIEMIEC AJ, 1994, HEARING RES, V75, P209, DOI 10.1016/0378-5955(94)90072-8 Okanoya K, 1997, J NEUROBIOL, V33, P343 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 Ryals BM, 1999, HEARING RES, V131, P71, DOI 10.1016/S0378-5955(99)00022-2 SALVI RJ, 1994, J COMP PHYSIOL A, V174, P351 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SAUNDERS SS, 1995, J ACOUST SOC AM, V98, P1365, DOI 10.1121/1.413472 SAUNDERS SS, 1995, J ACOUST SOC AM, V97, P1150, DOI 10.1121/1.412228 Smolders JWT, 1999, AUDIOL NEURO-OTOL, V4, P286, DOI 10.1159/000013853 Smolders JWT, 1995, HEARING RES, V92, P151, DOI 10.1016/0378-5955(95)00214-6 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 UMEMOTO M, 1993, ORL J OTO-RHINO-LARY, V55, P325 Vago P, 1998, NEUROREPORT, V9, P431, DOI 10.1097/00001756-199802160-00014 Wang Y, 1996, HEARING RES, V97, P11, DOI 10.1016/S0378-5955(96)80003-7 Woolley SMN, 1997, J NEUROSCI, V17, P6380 WOOLLEY SMN, 1999, ANN M SOC NEUR MIAM Woolley SMN, 1999, J NEUROSCI, V19, P358 NR 50 TC 25 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2001 VL 153 IS 1-2 BP 181 EP 195 DI 10.1016/S0378-5955(00)00217-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 408XR UT WOS:000167352700018 PM 11223308 ER PT J AU Wuyts, FL Van de Heyning, PH Van Spaendonck, M Van der Stappen, A D'Haese, P Erre, JP de Sauvage, RC Aran, JM AF Wuyts, FL Van de Heyning, PH Van Spaendonck, M Van der Stappen, A D'Haese, P Erre, JP de Sauvage, RC Aran, JM TI Rate influences on tone burst summating potential amplitude in electrocochleography: clinical and experimental data SO HEARING RESEARCH LA English DT Article DE electrocochleography; tone bursts stimulation; repetition rate; hydrops; Meniere disease; human; guinea pig ID VERTEBRATE HAIR-CELLS; MENIERES-DISEASE; BASILAR-MEMBRANE; TRANSTYMPANIC ELECTROCOCHLEOGRAPHY; TYMPANIC ELECTROCOCHLEOGRAPHY; ENDOLYMPHATIC HYDROPS; COCHLEAR POTENTIALS; SENSITIVITY; DIAGNOSIS; INNER AB Electrocochleographic recordings of action and summating potentials are widely used in the electrophysiological assessment of endolymphatic hydrops (ELH). Increased amplitudes of the summating potential (SP) in response to tone burst stimuli are indicative of positive ELH. This study reports the effect of repetition rate of tone burst stimulation on the SP amplitude. Using transtympanic electrocochleography (ECochG), the SP in response to 1 kHz tone bursts was recorded in both a Meniere and a non-Meniere population. Absolute values of the SP were systematically higher in the Meniere group. Moreover, in the Meniere and non-Meniere groups, the response amplitudes of the SP at a repetition rate of 8.4 tone bursts/s were only 66 and 32%, respectively, of the maximal response amplitude which was obtained at the rate of 37.4 tone bursts/s. Additionally, in normal guinea pigs chronically implanted with a round window electrode, the SP was recorded to 0.5-16 kHz tone burst stimulations presented at 100 dB SPL with the same different repetition rates. Similar enhancement of the SP amplitude was observed from 8.4 to 37.4 stimuli/s, whatever the frequency. This effect is interpreted as an increased asymmetry of vibration of the cochlear partition, whose mechanical operating point would not return to the normal resting position at high repetition rates, since it is permanently shifted in ELH. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Antwerp, Univ Antwerp Hosp, Dept Otolaryngol Head & Neck Surg, B-2650 Antwerp, Belgium. Univ Bordeaux 2, Hosp Pellegrin, F-33076 Bordeaux, France. INSERM, EMI 99 27, F-33076 Bordeaux, France. RP Wuyts, FL (reprint author), Univ Antwerp, Univ Antwerp Hosp, Dept Otolaryngol Head & Neck Surg, Wilrijkstr 10, B-2650 Antwerp, Belgium. CR ARAN JM, 1999, MENIERES DIS, P219 ARAN JM, 1979, OXFORD MED ENG SERIE, P233 Arenberg I K, 1993, Acta Otolaryngol Suppl, V504, P58 ARENBERG IK, 1993, ECOG, OAE AND INTRAOPERATIVE MONITORING, P115 ASSAD JA, 1992, J NEUROSCI, V12, P3291 ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X Braun M, 1996, HEARING RES, V97, P1 COATS AC, 1981, ARCH OTOLARYNGOL, V107, P199 *COM HEAR EQ, 1995, OTOLARYNGOL HEAD NEC, V113, P181 DAUMAN R, 1986, ANN OTO RHINOL LARYN, V95, P389 DAUMAN R, 1988, AM J OTOL, V9, P31 DORNHOFFER JL, 1993, AM J OTOL, V14, P161 Durrant JD, 1998, J ACOUST SOC AM, V104, P370, DOI 10.1121/1.423293 Eggermont J J, 1974, Acta Otolaryngol Suppl, V316, P39 EGGERMONT JJ, 1976, ELECTROCOCHLEOGRAPHY, P67 Eggermont J J, 1974, Acta Otolaryngol Suppl, V316, P7 FERRARO JA, 1985, ARCH OTOLARYNGOL, V111, P71 GIBSON WP, 1991, SURG INNER EAR, P281 GIBSON WPR, 1983, ANN OTO RHINOL LARYN, V92, P155 GIBSON WPR, 1977, AUDIOLOGY, V16, P389 GOIN DW, 1982, LARYNGOSCOPE, V92, P1383 Hohmann D, 1990, SURG INNER EAR, P249 KLIS SFL, 1994, HEARING RES, V75, P114, DOI 10.1016/0378-5955(94)90062-0 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P126, DOI 10.1121/1.395556 LEVINE SC, 1992, LARYNGOSCOPE, V102, P614, DOI 10.1288/00005537-199206000-00005 MARGOLIS RH, 1992, AUDIOLOGY, V31, P8 MARGOLIS RH, 1995, ARCH OTOLARYNGOL, V121, P44 Meyer zum Gottesberge A M, 1987, Aviat Space Environ Med, V58, pA240 MOFFAT DA, 1978, ACTA OTO-LARYNGOL, V85, P158, DOI 10.3109/00016487809111922 Nageris B, 1996, AM J OTOL, V17, P245 ODENTHAL DW, 1976, ELECTROCOHLEOGRAPHY, P331 OHASHI T, 1989, ORL J OTO-RHINO-LARY, V51, P235 ORCHIK DJ, 1993, AM J OTOL, V14, P290 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H Recio A, 1998, J ACOUST SOC AM, V103, P1972, DOI 10.1121/1.421377 RUGGERO MA, 1991, HEARING RES, V51, P215, DOI 10.1016/0378-5955(91)90038-B SALT AN, 1994, HEARING RES, V74, P115, DOI 10.1016/0378-5955(94)90180-5 Sass K, 1998, ACTA OTO-LARYNGOL, V118, P17 Sass K, 1998, ACTA OTO-LARYNGOL, V118, P150, DOI 10.1080/00016489850154838 Stephens S D, 1974, Rev Laryngol Otol Rhinol (Bord), V95, P129 Tanaka M, 1997, Acta Otolaryngol Suppl, V528, P30 TEAS D, 1962, J ACOUST SOC AM, V32, P1438 vanEmst MG, 1997, HEARING RES, V114, P93, DOI 10.1016/S0378-5955(97)00156-1 Wuyts F L, 1997, Acta Otolaryngol Suppl, V526, P14 YOSHIE N, 1973, AUDIOLOGY, V12, P504 NR 46 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 1 EP 9 DI 10.1016/S0378-5955(00)00207-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700001 PM 11223276 ER PT J AU Boulassel, MR Gueit, JM Denison, S de Tourtchaninoff, M Wenderickx, L Botterman, N Deggouj, N Gersdorff, M Tomasi, JP AF Boulassel, MR Gueit, JM Denison, S de Tourtchaninoff, M Wenderickx, L Botterman, N Deggouj, N Gersdorff, M Tomasi, JP TI No evidence of auditory dysfunction in guinea pigs immunized with myelin P0 protein SO HEARING RESEARCH LA English DT Article DE myelin P0; inner ear; immune; audition; guinea pig ID AUTOIMMUNE-RESPONSE; HEARING-LOSS; PO PROTEIN; STRAIN; MODEL; SERUM AB Recent data have focused on the peripheral nerve myelin glycoprotein PO as a putative autoantigen involved in the autoimmune etiology of some cases of Meniere's disease, idiopathic sensorineural hearing loss and sudden deafness. To determine whether antibodies to myelin PO can alter cochlear function, 13 healthy guinea pigs were immunized with purified porcine myelin PO while 10 controls were injected with saline water. The animals were then evaluated for evidence of evolving inner ear disease using immunological, electrophysiological and morphological methods. Twenty-six experimental ears were rested weekly with a brainstem auditory evoked potential technique for a period of 4 months and were compared to 20 control ears. Uniformly, all PO-sensitized guinea pigs showed antibodies to myelin protein PO as evidenced by ELISA. Clinical signs of inflammatory demyelination were not discernible in PO-sensitized guinea pigs and all the animals were qualitatively normal. No significant increase of evoked potential thresholds was found in the PO-sensitized animals when compared to controls (P > 0.05). Peak latencies of waves I, II, III, IV and V and inter-peak latencies in PO-sensitized guinea pigs did not significantly differ from those of controls (P > 0.05). Histological sections of inner ear and peripheral nerves were free of disease in both groups. These findings indicate that the sole presence of antibodies to myelin PO in the sera of guinea pigs or patients suspected of having autoimmune inner ear diseases is unlikely to elicit auditory abnormalities and that additional factors are necessary for the pathogenic development of these disorders. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Catholique Louvain, Sch Med, Dept Microbiol, Lab Autoimmun, B-1200 Brussels, Belgium. Univ Catholique Louvain, Sch Med, Dept Neurophysiol, B-1200 Brussels, Belgium. Univ Catholique Louvain, Sch Med, Dept Anat & Histol, B-1200 Brussels, Belgium. Univ Catholique Louvain, Sch Med, Dept Otorhinolaryngol, B-1200 Brussels, Belgium. RP Boulassel, MR (reprint author), Univ Catholique Louvain, Sch Med, Dept Microbiol, Lab Autoimmun, UCL 5490,Ave Hippocrate 54, B-1200 Brussels, Belgium. CR ADELMANN M, 1992, NEUROCHEM RES, V17, P887, DOI 10.1007/BF00993264 BENJELLOUNDELLAGI S, 1992, ANN NEUROL, V32, P700 Cao MY, 1996, LARYNGOSCOPE, V106, P207, DOI 10.1097/00005537-199602000-00019 Cao MY, 1996, FASEB J, V10, P1635 CAO MY, 1995, MOL CELL BIOCHEM, V2, P157 FILBIN MT, 1990, NATURE, V344, P871, DOI 10.1038/344871a0 FUCHS S, 1976, NATURE, V263, P329, DOI 10.1038/263329a0 GERSDORFF M, 1994, REV LARYNGOLOGIE OTO, V115, P163 Hahn AF, 1996, REV NEUROL, V152, P328 HARRIS JP, 1986, ANN OTO RHINOL LARYN, V95, P176 HARRIS JP, 1987, LARYNGOSCOPE, V97, P63 HERNICKX C, 1995, ACTA OTORHINOLARYNGO, V49, P63 JOLIAT T, 1992, ANN OTO RHINOL LARYN, V101, P1000 LININGTON C, 1992, EUR J IMMUNOL, V22, P1813, DOI 10.1002/eji.1830220721 Matsuoka H, 1999, ANN OTO RHINOL LARYN, V108, P255 NORTON WT, 1973, J NEUROCHEM, V21, P749, DOI 10.1111/j.1471-4159.1973.tb07519.x PENHALE WJ, 1975, CLIN EXP IMMUNOL, V21, P362 Schulz P, 1999, J NEUROL NEUROSUR PS, V66, P672, DOI 10.1136/jnnp.66.5.672 UYEMURA K, 1991, COMP BIOCHEM PHYS C, V98, P63 Warner LE, 1996, NEURON, V17, P451, DOI 10.1016/S0896-6273(00)80177-4 Yoo T J, 1984, Ann Otol Rhinol Laryngol Suppl, V113, P3 Yoo T J, 1984, Ann Otol Rhinol Laryngol Suppl, V113, P1 NR 22 TC 6 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 10 EP 16 DI 10.1016/S0378-5955(00)00212-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700002 PM 11223277 ER PT J AU Scholik, AR Yan, HY AF Scholik, AR Yan, HY TI Effects of underwater noise on auditory sensitivity of a cyprinid fish SO HEARING RESEARCH LA English DT Article DE auditory brainstem response; noise induced hearing loss; temporary threshold shift; fathead minnow ID SENSORY HAIR-CELLS; EAR; SOUND; HETEROGENEITY; GASBLADDER AB The ability of a fish to interpret acoustic information in its environment is crucial for its survival. Thus, it is important to understand how underwater noise affects fish hearing. In this study, the fathead minnow (Pimephales promelas) was used to examine: (1) the immediate effects of white noise exposure (0.3-4.0 kHz, 142 dB re: 1 mu Pa) on auditory thresholds and (2) recovery after exposure. Audiograms were measured using the auditory brainstem response protocol and compared to baseline audiograms of fathead minnows not exposed to noise. Immediately after exposure to 24 h of white noise, five out of the eight frequencies tested showed a significantly higher threshold compared to the baseline fish. Recovery was found to depend on both duration of noise exposure and auditory frequency. These results support the hypothesis that the auditory threshold of the fathead minnow can be altered by white noise, especially in its most sensitive hearing range (0.8-2.0 kHz), and provide evidence that these effects call be long term (>14 days). (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Kentucky, Sch Biol Sci, Mechanosensory Physiol Lab, Lexington, KY 40506 USA. RP Scholik, AR (reprint author), Univ Kentucky, Sch Biol Sci, Mechanosensory Physiol Lab, Lexington, KY 40506 USA. CR Canlon B, 1988, Scand Audiol Suppl, V27, P1 Chan E, 1998, NEUROSCIENCE, V83, P961, DOI 10.1016/S0306-4522(97)00446-6 CHANG JSY, 1992, J COMP NEUROL, V324, P621, DOI 10.1002/cne.903240413 Enger PS, 1981, HEARING SOUND COMMUN, P243 von Frisch K, 1938, NATURE, V141, P8, DOI 10.1038/141008a0 Hastings MC, 1996, J ACOUST SOC AM, V99, P1759, DOI 10.1121/1.414699 Husbands JM, 1999, HEARING RES, V135, P135, DOI 10.1016/S0378-5955(99)00101-X JOHNSON DL, 1975, CP171 AGARD NATO Kenyon TN, 1998, J COMP PHYSIOL A, V182, P307, DOI 10.1007/s003590050181 Ladich F, 1998, J COMP PHYSIOL A, V182, P737, DOI 10.1007/s003590050218 LOMBARTE A, 1993, HEARING RES, V64, P166, DOI 10.1016/0378-5955(93)90002-I Myrberg A.A. Jr, 1978, P169 Platt C., 1981, HEARING SOUND COMMUN, P3 Popper A.N., 1999, COMP HEARING FISH AM, P43 POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 POPPER AN, 1976, COMP BIOCHEM PHYS A, V53, P11, DOI 10.1016/S0300-9629(76)80003-5 RICE WR, 1989, EVOLUTION, V43, P223, DOI 10.2307/2409177 Richardson WJ, 1997, MAR FRESHW BEHAV PHY, V29, P183 Saidel WM, 1995, BRAIN BEHAV EVOLUT, V46, P362, DOI 10.1159/000113286 SAUNDERS JC, 1991, J ACOUST SOC AM, V90, P136, DOI 10.1121/1.401307 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 Trautman M.B., 1981, FISHES OHIO Yan HY, 2000, J COMP PHYSIOL A, V186, P435, DOI 10.1007/s003590050443 Yan HY, 2000, J COMP PHYSIOL A, V186, P595, DOI 10.1007/s003590000114 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 Yan HY, 1998, J COMP PHYSIOL A, V183, P325, DOI 10.1007/s003590050259 Yost W. A., 1994, FUNDAMENTALS HEARING ZHAO Y, 1996, P NATL ACAD SCI USA, V94, P15469 NR 28 TC 57 Z9 62 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 17 EP 24 DI 10.1016/S0378-5955(00)00213-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700003 PM 11223278 ER PT J AU Holt, JC Lioudyno, M Athas, G Garcia, MM Perin, P Guth, PS AF Holt, JC Lioudyno, M Athas, G Garcia, MM Perin, P Guth, PS TI The effect of proteolytic enzymes on the alpha 9-nicotinic receptor-mediated response in isolated frog vestibular hair cells SO HEARING RESEARCH LA English DT Article DE acetylcholine; alpha 9-nicotinic receptor; papain; protease; hair cells; patch clamp ID GUINEA-PIG COCHLEA; ACTIVATED POTASSIUM CHANNELS; ACETYLCHOLINE-RECEPTOR; CHOLINERGIC RECEPTOR; OUTWARD CURRENTS; MESSENGER-RNA; RAT; NEURONS; EXPRESSION; INHIBITION AB In frog vestibular organs, efferent neurons exclusively innervate type II hair cells. Acetylcholine, the predominant efferent transmitter, acting on acetylcholine receptors of these hair cells ultimately inhibits and/or facilitates vestibular afferent firing. A coupling between alpha9-nicotinic acetylcholine receptors (alpha 9nAChR) and apamin-sensitive, small-conductance, calcium-dependent potassium channels (SK) is thought to drive the inhibition by hyperpolarizing hair cells thereby decreasing their release of transmitter onto afferents. The presence of a9nAChR in these cells was demonstrated using pharmacological,immunocytochemical, and molecular biological techniques. However, fewer than 10% of saccular hair cells dissociated using protease VIII, protease XXIV, or papain responded to acetylcholine during perforated-patch clamp recordings. When present, these responses were invariably transient, small in amplitude, and difficult to characterize. In contrast, the majority of saccular hair cells (similar to 90%) dissociated using trypsin consistently responded to acetylcholine with an increase in outward current and concomitant hyperpolarization, In agreement with alpha 9nAChR pharmacology obtained in other hair cells, the acetylcholine response in saccular hair cells was reversibly antagonized by strychnine, curare, tetraethylammonium, and apamin. Brief perfusions with either protease or papain permanently abolished the alpha9-nicotinic response in isolated saccular hair cells. These enzymes when inactivated became completely ineffective at abolishing the a9-nicotinic response, suggesting an enzymatic interaction with the alpha 9nAChR and/or downstream effector. The mechanism by which these enzymes render saccular hair cells unresponsive to acetylcholine remains unknown, but it most likely involves proteolysis of alpha 9nAChR, SK, or both. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Tulane Univ, Sch Med, Dept Pharmacol, New Orleans, LA 70112 USA. Tulane Univ, Sch Med, Dept Otolaryngol, New Orleans, LA 70112 USA. Univ Pavia, Dept Mol & Cell Physiol & Pharmacol, I-27100 Pavia, Italy. RP Guth, PS (reprint author), Tulane Univ, Sch Med, Dept Pharmacol, 1430 Tulane Ave, New Orleans, LA 70112 USA. CR AKAIKE N, 1994, JPN J PHYSIOL, V44, P433, DOI 10.2170/jjphysiol.44.433 AKAIKE N, 1988, NEUROSCI LETT, V87, P75, DOI 10.1016/0304-3940(88)90148-6 ALBUQUER.EX, 1968, EUR J PHARMACOL, V4, P40, DOI 10.1016/0014-2999(68)90007-1 Anderson AD, 1997, BRAIN RES, V778, P409, DOI 10.1016/S0006-8993(97)01121-9 ARMSTRONG CE, 1999, BIOPH SOC 43 ANN M F, V76, pA45 Armstrong CE, 1998, J NEUROSCI, V18, P2962 ART JJ, 1985, J PHYSIOL-LONDON, V360, P397 Art JJ, 1996, ANN NY ACAD SCI, V781, P103, DOI 10.1111/j.1749-6632.1996.tb15696.x ART JJ, 1984, J PHYSIOL-LONDON, V356, P525 ATHAS GB, 1997, ASS RES OTOLARYNGOL, V20, P37 ATHAS GB, 1997, ASS RES OTOLARYNGOL, V20, P17 BETZ W, 1971, NATURE-NEW BIOL, V232, P94 BETZ W, 1973, J PHYSIOL-LONDON, V230, P673 Bond CT, 1999, ANN NY ACAD SCI, V868, P370, DOI 10.1111/j.1749-6632.1999.tb11298.x BURGER MM, 1969, P NATL ACAD SCI USA, V62, P994, DOI 10.1073/pnas.62.3.994 BURGER MM, 1970, NATURE, V227, P170, DOI 10.1038/227170a0 Chabbert CH, 1997, PFLUG ARCH EUR J PHY, V435, P82, DOI 10.1007/s004240050486 Chen C, 1996, HEARING RES, V98, P9, DOI 10.1016/0378-5955(96)00049-4 CHURCHILL J. A., 1956, LARYNGOSCOPE, V66, P1 CONTITRONCONI BM, 1982, BIOCHEMISTRY-US, V2, P893 CUNNINGHAM CD, 2000, HEARING RES, V143, P269 DOHLMAN G, 1958, J Laryngol Otol, V72, P984, DOI 10.1017/S0022215100054797 Dulon D, 1998, EUR J NEUROSCI, V10, P907, DOI 10.1046/j.1460-9568.1998.00098.x EBERWINE J, 1992, METHOD ENZYMOL, V216, P80 ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EYBALIN M, 1993, PHYSIOL REV, V73, P309 Freshney RI, 1994, CULTURE ANIMAL CELLS, V3rd FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 FUCHS PA, 1992, J NEUROSCI, V12, P800 Goodyear R, 1999, J NEUROSCI, V19, P3761 GUPTA AK, 1997, ASS RES OT ABSTR, V20, P215 GUTH PS, 1986, ACTA OTO-LARYNGOL, V102, P194, DOI 10.3109/00016488609108666 Guth PS, 1998, PROG NEUROBIOL, V54, P193, DOI 10.1016/S0301-0082(97)00068-3 GUTH PS, 1994, HEARING RES, V75, P225, DOI 10.1016/0378-5955(94)90073-6 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 Hiel H, 1996, BRAIN RES, V738, P347, DOI 10.1016/S0006-8993(96)01046-3 HIGHSTEIN SM, 1991, NEUROSCI RES, V12, P12 Hirschberg B, 1999, BIOPHYS J, V77, P1905 HOLT JC, 1999, ARO ABSTR, V22, P188 HOLT JR, 1995, J NEUROPHYSIOL, V73, P1484 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 HOUSLEY GD, 1990, HEARING RES, V43, P121, DOI 10.1016/0378-5955(90)90221-A Ishii TM, 1997, J BIOL CHEM, V272, P23195, DOI 10.1074/jbc.272.37.23195 Kehoe J, 1998, J NEUROSCI, V18, P8198 LEE KS, 1977, NATURE, V265, P751, DOI 10.1038/265751a0 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 LINDSTROM J, 1980, BIOCHEMISTRY-US, V19, P4791, DOI 10.1021/bi00562a012 LUSTIG LR, 2000, SYN FUNCT HEAR BAL S, P56 Lysakowski A, 1996, ANN NY ACAD SCI, V781, P164, DOI 10.1111/j.1749-6632.1996.tb15700.x McNiven AI, 1996, AUDIT NEUROSCI, V2, P63 MURROW B W, 1990, Society for Neuroscience Abstracts, V16, P1079 NARAHASHI T, 1964, J PHYSL, V207, P1441 NARAHASH.T, 1974, PHYSIOL REV, V54, P813 Nenov AP, 1996, HEARING RES, V101, P149, DOI 10.1016/S0378-5955(96)00143-8 Nenov AP, 1998, HEARING RES, V123, P168, DOI 10.1016/S0378-5955(98)00121-X Nenov AP, 1996, HEARING RES, V101, P132, DOI 10.1016/S0378-5955(96)00142-6 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 OSBORNE MP, 1990, ACTA OTO-LARYNGOL, V110, P37, DOI 10.3109/00016489009122513 Ottesen M., 1970, METHOD ENZYMOL, V19, P199 OYAMA Y, 1990, CELL MOL NEUROBIOL, V10, P193, DOI 10.1007/BF00734573 Park HJ, 1997, HEARING RES, V112, P95, DOI 10.1016/S0378-5955(97)00111-1 PERILLO MA, 1998, RRD LIP RES 2, V2, P275 PERLMAN GE, 1970, METHODS ENZYMOLOGY, V19 PRECHT W, 1976, FROG NEUROBIOLOGY, P452 RODBELL M, 1970, J BIOL CHEM, V245, P718 Sambrook J., 1989, MOL CLONING LAB MANU SEFTON BM, 1970, NATURE, V227, P843, DOI 10.1038/227843a0 SHAO H, 1998, ASS RES OTOLARYNGOL, V21, P20 SHIGEMOTO T, 1991, J PHYSIOL-LONDON, V442, P669 Sinclair B, 1999, SCIENTIST, V13, P19 STEINBERG EL, 1988, J PEDIATR ORTHOPED, V8, P35 STRULOVICI B, 1984, J BIOL CHEM, V10, P4389 SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M Sugasawa M, 1996, AM J PHYSIOL-CELL PH, V271, pC1817 TAKUMIDA M, 1993, ORL J OTO-RHINO-LARY, V55, P77 VANGELDER RN, 1990, P NATL ACAD SCI USA, V87, P1663 VETTER D, 2000, S SPONS J HOPK CTR H, P54 WALSH KA, 1970, METHOD ENZYMOL, V19, P64 WEIS LS, 1969, J BIOL CHEM, V244, P3084 YOSHIDA N, 1994, BRAIN RES, V644, P90, DOI 10.1016/0006-8993(94)90351-4 NR 81 TC 30 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 25 EP 42 DI 10.1016/S0378-5955(00)00225-2 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700004 PM 11223279 ER PT J AU Sahley, TL Nodar, RH AF Sahley, TL Nodar, RH TI A biochemical model of peripheral tinnitus SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Conference on Tinnitus: New Perspective on Diagnosis and Management CY AUG 13-14, 1999 CL LEBANON, NEW HAMPSHIRE SP Dartmouth Hitchcock Med Ctr DE dynorphin; lateral efferent olivocochlear system; N-methyl-D-aspartate receptors; glutamate; stress; tinnitus ID AUDITORY EVOKED-POTENTIALS; GUINEA-PIG COCHLEA; EXCITATORY AMINO-ACIDS; LONG-LASTING ALLODYNIA; KAPPA-OPIOID RECEPTOR; D-ASPARTATE; DYNORPHIN-A; PAIN HYPERSENSITIVITY; CENTRAL SENSITIZATION; STEREOCILIA DAMAGE AB Subjective tinnitus may be defined as the perceptual correlate of altered spontaneous neural activity occurring in the absence of an externally evoking auditory stimulus. Tinnitus can be caused or exacerbated by one or more of five forms of stress. We propose and provide evidence supporting a model that explains, but is not limited to, peripheral (cochlear) tinnitus. In this model, naturally occurring opioid dynorphins are released from lateral efferent axons into the synaptic region beneath the cochlear inner hair cells during stressful episodes. In the presence of dynorphins, the excitatory neurotransmitter glutamate, released by inner hair cells in response to stimuli or (spontaneously) in silence, is enhanced at cochlear N-methyl-D-aspartate (NMDA) receptors. This results in altered neural excitability and/or an altered discharge spectrum in (modiolar-oriented) type I neurons normally characterized by low rates of spontaneous discharge and relatively poor thresholds. It is also possible that chronic exposure to dynorphins leads to auditory neural excitotoxicity via the same receptor mechanism. Finally, the proposed excitatory interactions of dynorphins and glutamate at NMDA receptors need not be restricted to the auditory periphery. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Cleveland State Univ, Dept Speech & Hearing, Cleveland, OH 44115 USA. Cleveland Clin Fdn, Dept Otolaryngol & Commun Disorders, Cleveland, OH 44195 USA. RP Sahley, TL (reprint author), Cleveland State Univ, Dept Speech & Hearing, Main Classroom Bldg,Room 431,1899 E 22nd St, Cleveland, OH 44115 USA. CR ABOUMADI L, 1987, HEARING RES, V30, P135, DOI 10.1016/0378-5955(87)90131-6 AKIL H, 1986, ANN NY ACAD SCI, V467, P140, DOI 10.1111/j.1749-6632.1986.tb14625.x AKIL H, 1984, ANNU REV NEUROSCI, V7, P223, DOI 10.1146/annurev.ne.07.030184.001255 ALTSCHULER RA, 1988, J HISTOCHEM CYTOCHEM, V36, P797 Aran JM, 1992, NOISE INDUCED HEARIN, P188 Arcaya JL, 1999, EUR J PHARMACOL, V366, P27, DOI 10.1016/S0014-2999(98)00897-8 Basbaum AI, 2000, PRINCIPLES NEURAL SC, P472 BROWNELL WE, 1996, HAIR CELLS HEARING A, P3 BURKI C, 1993, ORL J OTO-RHINO-LARY, V55, P3 CAUDLE RM, 1988, BRAIN RES, V443, P329, DOI 10.1016/0006-8993(88)91628-9 CAUDLE RM, 1987, BRAIN RES, V435, P1, DOI 10.1016/0006-8993(87)91579-4 CHEN C, 1997, 20 ASS RES OT MIDW M, V20, P150 CHENG CY, 1992, J MED CHEM, V35, P2243, DOI 10.1021/jm00090a015 CODERRE TJ, 1993, PAIN, V52, P259, DOI 10.1016/0304-3959(93)90161-H COMIS SD, 1979, EXP BRAIN RES, V36, P119 Crain SM, 1996, NEUROCHEM RES, V21, P1347, DOI 10.1007/BF02532375 Crain SM, 1998, ANN NY ACAD SCI, V845, P106, DOI 10.1111/j.1749-6632.1998.tb09665.x DAY RO, 1989, BRIT J CLIN PHARMACO, V28, P695 Denk DM, 1997, ACTA OTO-LARYNGOL, V117, P825, DOI 10.3109/00016489709114208 Denk D.-M., 1998, TINNITUS TREATMENT R, P60 Dingledine Raymond, 1999, P315 Dobie R.A., 1998, TINNITUS TREATMENT R, P43 Dobie R.A., 1997, INT TINNITUS J, V3, P33 DOLAN DF, 1990, J ACOUST SOC AM, V87, P2621, DOI 10.1121/1.399054 DRESCHER DG, 1985, AUDITORY BIOCH, P50 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x DUBNER R, 1992, PAIN, V48, P3, DOI 10.1016/0304-3959(92)90124-T DUBNER R, 1992, TRENDS NEUROSCI, V15, P96, DOI 10.1016/0166-2236(92)90019-5 EGGERMONT JJ, 1990, HEARING RES, V48, P111, DOI 10.1016/0378-5955(90)90202-Z Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 Evans E F, 1981, Ciba Found Symp, V85, P108 EYBALIN M, 1987, BRAIN RES, V421, P336, DOI 10.1016/0006-8993(87)91303-5 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FELIX D, 1989, INNER EAR BIOL, V26, P19 FELIX D, 1991, EUR ARCH OTO-RHINO-L, V248, P429, DOI 10.1007/BF00627627 FELIX D, 1990, EUR ARCH OTO-RHINO-L, V248, P1, DOI 10.1007/BF00634769 Fontana F, 1997, PEPTIDES, V18, P169, DOI 10.1016/S0196-9781(96)00319-1 Gabriels P., 1996, P 5 INT TINN SEM 199, P46 Gerken GM, 1996, HEARING RES, V97, P75 GOLDSTEIN B, 1996, P 5 INT TINN SEM 199, P142 GUBLER U, 1982, NATURE, V295, P206, DOI 10.1038/295206a0 Guth PS, 1998, TINNITUS TREATMENT R, P52 HALFORD JBS, 1991, J PSYCHOSOM RES, V35, P383, DOI 10.1016/0022-3999(91)90033-K HARRIS GG, 1968, J ACOUST SOC AM, V44, P176, DOI 10.1121/1.1911052 Hazell JWP, 1995, MECH TINNITUS, P57 Insel P. A., 1996, GOODMAN GILMANS PHAR, P617 JAFFE J H, 1990, P485 Jastreboff P. J., 1995, MECH TINNITUS, P73 Jastreboff P. J., 1998, TINNITUS TREATMENT R, P201 JASTREBOFF PJ, 1986, J ACOUST SOC AM, V80, P1384, DOI 10.1121/1.394391 JASTREBOFF PJ, 1996, P 5 INT TINN SEM POR, P114 Jastreboff P.J., 1996, P 5 INT TINN SEM 199, P58 Jessell TM, 1991, PRINCIPLES NEURAL SC, P385 KAKIDANI H, 1982, NATURE, V298, P245, DOI 10.1038/298245a0 Kaltenbach JA, 1998, HEARING RES, V124, P78, DOI 10.1016/S0378-5955(98)00119-1 KANDEL ER, 1991, PRINCIPLES NEURAL SC, P153 KATOH A, 1990, J PHARMACOL EXP THER, V253, P600 LAIRD JMA, 1989, J NEUROPHYSIOL, V62, P854 Laughlin TM, 1997, PAIN, V72, P253, DOI 10.1016/S0304-3959(97)00046-8 Lenarz T., 1995, MECH TINNITUS, P101 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LIBERMAN MC, 1980, HEARING RES, V3, P189, DOI 10.1016/0378-5955(80)90046-5 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 LIBERMAN MC, 1990, HEARING RES, V49, P209, DOI 10.1016/0378-5955(90)90105-X LIN X, 2000, UNPUB BRAIN RES LIN X, 1998, 21 ASS RES OT MIDW M, V21, P112 LIPTON SA, 1994, NEW ENGL J MED, V330, P613 MAINS RE, 1999, BASIC NEUROCHEMISTRY, P263 Mansour A, 1996, NEUROSCIENCE, V71, P671, DOI 10.1016/0306-4522(95)00464-5 MANSOUR A, 1994, J COMP NEUROL, V350, P412, DOI 10.1002/cne.903500307 MARTIN CR, 1995, DICT ENDOCRINOLOGY R, P684 Martin W.H., 1995, MECH TINNITUS, P163 Martin W.H., 1996, P 5 INT TINN SEM 199, P127 MASSARDIER D, 1989, EUR J PHARMACOL, V170, P125, DOI 10.1016/0014-2999(89)90149-0 McKenna L., 1998, TINNITUS TREATMENT R, P140 MENDELL LM, 1966, EXP NEUROL, V16, P316, DOI 10.1016/0014-4886(66)90068-9 MILLAN MJ, 1990, NEUROSCI LETT, V113, P50, DOI 10.1016/0304-3940(90)90493-S Mills CD, 1999, HEARING RES, V128, P75, DOI 10.1016/S0378-5955(98)00190-7 Moller AR, 1997, AM J OTOL, V18, P577 MUCHNIK C, 1992, HEARING RES, V58, P101, DOI 10.1016/0378-5955(92)90013-D Narita M, 1998, JPN J PHARMACOL, V76, P233, DOI 10.1254/jjp.76.233 Niedzielski AS, 1997, AUDIOL NEURO-OTOL, V2, P79 Nodar RH, 1996, INT TINNITUS J, V2, P111 Patuzzi R. B., 1992, NOISE INDUCED HEARIN, P45 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 Puel JL, 1995, PROG NEUROBIOL, V47, P449, DOI 10.1016/0301-0082(95)00028-3 PUJOL R, 1993, ACTA OTO-LARYNGOL, V113, P330, DOI 10.3109/00016489309135819 PUJOL R, 1992, NEUROREPORT, V3, P299, DOI 10.1097/00001756-199204000-00002 Reisine T., 1996, GOODMAN GILMANS PHAR, P521 REISINE T, 1993, TRENDS NEUROSCI, V16, P506, DOI 10.1016/0166-2236(93)90194-Q RUDA MA, 1988, P NATL ACAD SCI USA, V85, P622, DOI 10.1073/pnas.85.2.622 SAFIEDDINE S, 1992, NEUROREPORT, V3, P1145, DOI 10.1097/00001756-199212000-00029 SAHLEY TL, 1991, HEARING RES, V55, P133, DOI 10.1016/0378-5955(91)90099-U Sahley TL, 1996, EAR HEARING, V17, P552, DOI 10.1097/00003446-199612000-00011 Sahley TL, 1996, EAR HEARING, V17, P341, DOI 10.1097/00003446-199608000-00006 Sahley T.L., 1997, EFFERENT OLIVOCOCHLE SAHLEY TL, 1995, 18 ASS RES OT MIDW M, V18, P170 SAHLEY TL, 1994, EAR HEARING, V15, P422, DOI 10.1097/00003446-199412000-00003 SAHLEY TL, 1999, 22 ASS RES OT MIDW M, V22, P209 SALVI RJ, 1983, J SPEECH HEAR RES, V26, P626 SAMRA SK, 1984, ANESTHESIOLOGY, V61, P261, DOI 10.1097/00000542-198409000-00005 SAMRA SK, 1985, ANESTHESIOLOGY, V62, P437, DOI 10.1097/00000542-198504000-00011 Schleuning A., 1998, TINNITUS TREATMENT R, P20 Scholtz AW, 1998, HEARING RES, V118, P123, DOI 10.1016/S0378-5955(98)00023-9 SCHREINER CE, 1987, P 3 INT TINN SEM HAR, P100 Sewell W. F., 1996, COCHLEA, P503 SHEA JJ, 1978, LARYNGOSCOPE, V88, P1477 SHEN KF, 1990, NEUROPHARMACOLOGY, V29, P343, DOI 10.1016/0028-3908(90)90092-6 SHUKLA VK, 1993, EUR J PHARMACOL, V231, P293, DOI 10.1016/0014-2999(93)90463-R SHUKLA VK, 1994, TRENDS PHARMACOL SCI, V15, P420, DOI 10.1016/0165-6147(94)90091-4 Shulman A, 1997, INT TINNITUS J, V3, P77 Simon Eric J., 1994, P321 SKILLING SR, 1992, BRAIN RES, V575, P272, DOI 10.1016/0006-8993(92)90090-V Standaert D. G., 1996, GOODMAN GILMANS PHAR, P503 STEFANO GB, 1994, ADV NEUROIMMUNOL, V4, P57, DOI 10.1016/S0960-5428(05)80001-4 Stracher A, 1997, INT TINNITUS J, V3, P71 Strangman NM, 1999, J NEUROPHYSIOL, V82, P472 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E SUNEJA SK, 1995, J NEUROCHEM, V64, P161 SUNEJA SK, 1995, J NEUROCHEM, V64, P147 SZEKELY JI, 1994, OPIOID PEPTIDES SUBS, P35 SZEKELY JI, 1994, OPIOID PEPTIDES SUBS, P177 TONNDORF J, 1995, MECH TINNITUS, P231 Vanderah TW, 1996, PAIN, V68, P275, DOI 10.1016/S0304-3959(96)03225-3 VELASCO M, 1984, NEUROPHARMACOLOGY, V23, P359, DOI 10.1016/0028-3908(84)90199-0 VERNON J, 1909, TINNITUS TREATMENT R, P223 Walsh EJ, 1998, J NEUROSCI, V18, P3859 Warr WB, 1997, HEARING RES, V108, P89, DOI 10.1016/S0378-5955(97)00044-0 WOOLF CJ, 1991, PAIN, V44, P293, DOI 10.1016/0304-3959(91)90100-C Woolf CJ, 1996, PAIN, V66, P105 WOOLF CJ, 1983, NATURE, V306, P686, DOI 10.1038/306686a0 YATES GK, 1991, HEARING RES, V57, P57, DOI 10.1016/0378-5955(91)90074-J Zheng XY, 1996, HEARING RES, V95, P161, DOI 10.1016/0378-5955(96)00047-0 NR 136 TC 27 Z9 32 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 43 EP 54 DI 10.1016/S0378-5955(00)00235-5 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700005 PM 11223280 ER PT J AU Miller, AL Arenberg, JG Middlebrooks, JC Pfingst, BE AF Miller, AL Arenberg, JG Middlebrooks, JC Pfingst, BE TI Cochlear implant thresholds: comparison of middle latency responses with psychophysical and cortical-spike-activity thresholds SO HEARING RESEARCH LA English DT Article DE cochlear implant; auditory cortex; electrically evoked middle latency response; psychophysics; threshold; phase duration; electrode configuration ID AUDITORY BRAIN-STEM; STRENGTH-DURATION FUNCTIONS; ELECTRICAL-STIMULATION; GUINEA-PIGS; ELECTRODE CONFIGURATION; NERVE; POTENTIALS; USERS; TIME; SUBDIVISIONS AB The electrically evoked middle latency response (EMLR) is a potentially useful measure of activation of the auditory system by a cochlear prosthesis. The present study compared cochlear prosthesis thresholds determined using EMLR with thresholds determined for psychophysical detection and for spike activity in cortical neurons. In systemically deafened guinea pigs, the difference between EMLR and psychophysical threshold level varied, with differences ranging from -4.6 dB (EMLR threshold more sensitive) to +10.7 dB (psychophysical threshold more sensitive) across animals and phase durations. Threshold differences between EMLR and auditory cortex neural spike responses were similar in magnitude and range (-6 to +15 dB) to those seen for EMLR vs. psychophysical thresholds. These ranges are comparable to the behavioral operating range for a given condition. In 3 of 12 subjects, the EMLR was absent for some or all electrode configurations tested, even at levels well above the threshold for psychophysical detection or cortical neuronal response. These results suggest that neither the EMLR thresholds nor cortical neuronal spike thresholds are an adequate substitute for psychophysical measures of threshold. While not sufficient for use in place of psychophysical measures, EMLR threshold level is strongly correlated with psychophysical threshold level across subjects (R-2 = 0.82). Interestingly, plots of thresholds vs. phase duration were roughly parallel for psychophysical and EMLR thresholds, in contrast to the divergence of psychophysical and more peripheral (e.g., electrically evoked auditory brainstem response) evoked neural threshold vs. phase duration functions. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Michigan Hlth Sys, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Pfingst, BE (reprint author), Univ Michigan Hlth Sys, Dept Otolaryngol, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR ABBAS PJ, 1991, HEARING RES, V51, P139, DOI 10.1016/0378-5955(91)90012-X ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W ARENBERG JG, 1999, 1999 C IMPL AUD PROS ARENBERG JG, 2000, 23 MIDW M ASS RES OT Arenberg JG, 2000, JARO, V1, P183, DOI 10.1007/sl01620010036 Beitel RE, 2000, J NEUROPHYSIOL, V83, P2145 BROWN CJ, 1995, EAR HEARING, V16, P439, DOI 10.1097/00003446-199510000-00001 Brown CJ, 1996, J SPEECH HEAR RES, V39, P453 BROWN CJ, 1994, EAR HEARING, V15, P168, DOI 10.1097/00003446-199404000-00006 BURTON MJ, 1989, ARCH OTOLARYNGOL, V115, P59 CROWTHER J, 1989, OTOLARYNG HEAD NECK, V101, P51 CROWTHER JA, 1990, HEARING RES, V43, P115, DOI 10.1016/0378-5955(90)90220-J HELLWEG FC, 1977, EXP BRAIN RES, V29, P467 KAGA K, 1980, ELECTROEN CLIN NEURO, V50, P254, DOI 10.1016/0013-4694(80)90153-4 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KILENY PR, 1987, ARCH OTOLARYNGOL, V113, P1072 MASON SM, 1994, ADV COCHLEAR IMPLANT, P44 MCGEE T, 1991, BRAIN RES, V544, P211, DOI 10.1016/0006-8993(91)90056-2 MCGEE T, 1992, HEARING RES, V61, P147, DOI 10.1016/0378-5955(92)90045-O MCGEE TJ, 1983, AM J OTOLARYNG, V4, P116, DOI 10.1016/S0196-0709(83)80013-1 Miller AL, 2000, HEARING RES, V144, P175, DOI 10.1016/S0378-5955(00)00066-6 MILLER AL, 2000, THESIS U MICHIGAN MI MILLER AL, 2000, 23 MIDW M ASS RES OT Miller CA, 1995, HEARING RES, V92, P100, DOI 10.1016/0378-5955(95)00205-7 Miller CA, 1995, HEARING RES, V92, P85, DOI 10.1016/0378-5955(95)00204-9 Mitchell A, 1997, HEARING RES, V105, P30, DOI 10.1016/S0378-5955(96)00202-X MIYAMOTO RT, 1986, LARYNGOSCOPE, V96, P178 MONTNEY LM, 23 MIDW M ASS RES OT MUSIEK FE, 1981, ANN OTO RHINOL LARYN, V90, P236 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PFINGST BE, 1990, HEARING RES, V50, P225, DOI 10.1016/0378-5955(90)90047-S PFINGST BE, 1995, HEARING RES, V85, P76, DOI 10.1016/0378-5955(95)00037-5 Pfingst B E, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P127 POPELAR J, 1993, HEARING RES, V67, P69, DOI 10.1016/0378-5955(93)90233-Q REDIES H, 1989, J COMP NEUROL, V282, P473, DOI 10.1002/cne.902820402 SHALLOP JK, 1990, EAR HEARING, V11, P5, DOI 10.1097/00003446-199002000-00004 Smith DW, 1997, J ACOUST SOC AM, V102, P2228, DOI 10.1121/1.419636 SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMITH DW, 1994, ADV COCHLEAR IMPLANT, P8 SPELMAN FA, 1978, BIOM S SAN DIEG CA VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 NR 42 TC 6 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 55 EP 66 DI 10.1016/S0378-5955(00)00236-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700006 PM 11223281 ER PT J AU Perin, P Masetto, S Martini, M Rossi, ML Rubbini, G Rispoli, G Guth, P Zucca, G Valli, P AF Perin, P Masetto, S Martini, M Rossi, ML Rubbini, G Rispoli, G Guth, P Zucca, G Valli, P TI Regional distribution of calcium currents in frog semicircular canal hair cells SO HEARING RESEARCH LA English DT Article DE frog; vestibular; hair cell; semicircular canal; Ca current; patch-clamp; nimodipine ID CRISTA-AMPULLARIS; ELECTRICAL-PROPERTIES; POTASSIUM CURRENTS; CHANNELS; CHICK; LOCALIZATION; EXPRESSION; COCHLEA; RELEASE AB In the present work we studied the regional expression of voltage-dependent Ca channels in hair cells from the frog semicircular canals, employing whole-cell patch-clamp on isolated and in situ hair cells. Although Ca channels are thought to play a major role in afferent transmission, up to now no data were available regarding their distribution in vestibular organs. The problem appears of interest, especially in the light of recent results showing the presence of multiple Ca current components in semicircular canal hair cells. Our data suggest the presence, in all regions of the crista ampullaris, of two classes of cells, one displaying an inactivating Ca current (RI) and one lacking it. In the former cells, Ca current amplitude decreased from the central to the peripheral zone (the maximal currents being observed in the intermediate zone). Only L-type and R2 current components displayed regional differences in expression, whereas the size and properties of R1, although variable among cells, were not regionalized. However, in cells lacking RI, Ca current amplitudes were similar regardless of cell shape and location. The possible contributions of this Ca current distribution to afferent discharge properties are discussed. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Pavia, Sect Gen Physiol & Cell Biophys, Dept Cell & Mol Physiol & Pharmacol Sci, I-27100 Pavia, Italy. Univ Ferrara, Sect Physiol & Biophys, Dept Biol, INFM, I-44100 Ferrara, Italy. Tulane Univ, Dept Pharmacol, New Orleans, LA 70118 USA. RP Perin, P (reprint author), Univ Pavia, Sect Gen Physiol & Cell Biophys, Dept Cell & Mol Physiol & Pharmacol Sci, Viale Forlanini 6, I-27100 Pavia, Italy. RI Rossi, Maria Lisa/D-4251-2011 CR Armstrong CE, 1998, J NEUROSCI, V18, P2962 Cortopassi KA, 1996, J VESTIBUL RES-EQUIL, V6, P105 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 FUCHS PA, 1990, J PHYSIOL-LONDON, V429, P553 GUTH PS, 1998, PROG NEUROBIOL, V54, P9193 GUTH PS, 1994, HEARING RES, V73, P109, DOI 10.1016/0378-5955(94)90288-7 HONRUBIA V, 1989, J NEUROPHYSIOL, V61, P688 HORN R, 1988, J GEN PHYSIOL, V92, P145, DOI 10.1085/jgp.92.2.145 Lenzi D, 1999, J NEUROSCI, V19, P119 Lewis ER, 1999, COMP HEARING FISH AM, P101 Lysakowski A, 1996, ANN NY ACAD SCI, V781, P164, DOI 10.1111/j.1749-6632.1996.tb15700.x Marcotti W, 1999, NEUROREPORT, V10, P601, DOI 10.1097/00001756-199902250-00029 MartinezDunst C, 1997, J NEUROSCI, V17, P9133 Martini M, 2000, BIOPHYS J, V78, P1240 Masetto S, 2000, J NEUROPHYSIOL, V83, P2740 MASETTO S, 1994, J NEUROPHYSIOL, V72, P443 Perin P, 2000, NEUROREPORT, V11, P417, DOI 10.1097/00001756-200002070-00039 Prigioni I, 1996, NEUROREPORT, V7, P1841, DOI 10.1097/00001756-199607290-00031 Prigioni I, 1992, J Vestib Res, V2, P31 Ricci AJ, 2000, J PHYSIOL-LONDON, V524, P423, DOI 10.1111/j.1469-7793.2000.00423.x ROBERTS WM, 1994, J NEUROSCI, V14, P3246 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 Smotherman MS, 1999, J NEUROSCI, V19, P5275 Wu LG, 1999, J NEUROSCI, V19, P726 ZIDANIC M, 1995, BIOPHYS J, V68, P1323 NR 25 TC 14 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 67 EP 76 DI 10.1016/S0378-5955(00)00237-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700007 PM 11223282 ER PT J AU Nuttall, AL Zheng, JF Ren, TY de Boer, E AF Nuttall, AL Zheng, JF Ren, TY de Boer, E TI Electrically evoked otoacoustic emissions from apical and basal perilymphatic electrode positions in the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE guinea pig; fine structure; traveling wave; outer hair cell; electromotility; otoacoustic emission ID ACOUSTIC DISTORTION-PRODUCT; OUTER HAIR-CELLS; FINE-STRUCTURE; ENHANCEMENT; MOTILITY; MODEL; THRESHOLDS; AMPLIFIER; GERBIL AB Stimulation of the cochlea with sinusoidal current results in the production of an otoacoustic emission at the primary frequency of the stimulus current. In this study we test the hypothesis that the wide frequency response from round window (RW) stimulation is due to the involvement of a relatively large spatial segment of the organ of Corti. Tonotopically organized group delays would be evident from perilymphatic electrode locations that restrict the spatial extent of hair cell stimulation. Monopolar and bipolar-paired stimulus electrodes were placed in perilymphatic areas of the first or third cochlear turns and the electrically evoked otoacoustic emissions (EEOAE) produced by these electrodes were compared to that from the RW monopolar electrode in the anesthetized guinea pig. Current stimuli of 35 muA RMS were swept across the frequency range between 60 Hz and 100 kHz. The EEOAE was measured using a microphone coupled to the ear canal. It was found that the bandwidth of EEOAEs from RW stimulation extended to at least 40 kHz and was a relatively insensitive to electrode location on the RW. The group delay of the EEOAE from stimulation at the RW membrane (corrected to stapes motion) was about 53 mus. First and third turn stimulations from electrode placements in perilymph near the bony wall of cochlea yielded narrower band EEOAE magnitude spectra but which had the same short group delays as for RW stimulation. A confined current (from a bipolar electrode pair) applied close to the basilar membrane (BM) in the first turn produced the narrowest frequency-band magnitude emissions and a mean corrected group delay of 176 mus for a location approximately 3 mm from the high frequency end of the BM (corresponding to about the 18 kHz best frequency location). Bipolar electrodes in the third turn scala tympani produced low pass EEOAE magnitude functions with corrected group delays ranging between approximately 0.3 and I ms. The average phase slopes did not change with altered cochlear sensitivity and postmortem. These data indicate that the EEOAE from RW stimulation is the summed response from a wide tonotopic distribution of outer hair cells. A preliminary model study indicates that short time delayed emissions are the result of a large spatial distribution of current applied to perilymphatic locations possibly giving rise to 'wave-fixed' emissions. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, Portland, OR 97201 USA. Chinese PLA Gen Hosp, Dept Otolaryngol, Beijing 100853, Peoples R China. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands. RP Nuttall, AL (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, 3181 SW Sam Jackson Pk Rd,NRC04, Portland, OR 97201 USA. CR ASHMORE JF, 1995, MICROSECOND RESOLUTI, P77 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CANNON MW, 1976, THESIS SYRACUSE U DALLOS P, 1992, J NEUROSCI, V12, P4575 DALLOS P, 1995, SCIENCE, V268, P1420, DOI 10.1126/science.7770765 DALLOS P, 1995, SCIENCE, V267, P2006, DOI 10.1126/science.7701325 DEBOER E, 2001, ASS RES OT MIDW M ST FRANK GWH, 1999, P NATL ACAD SCI USA, V96, P4410 Frolenkov GI, 1998, MOL BIOL CELL, V9, P1961 Gale JE, 1997, NATURE, V389, P63, DOI 10.1038/37968 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 HARRIS FP, 1994, BRIT J AUDIOL, V29, P66 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HE NJ, 1993, J ACOUST SOC AM, V94, P2659, DOI 10.1121/1.407350 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 Kirk DL, 1996, J ACOUST SOC AM, V100, P3714, DOI 10.1121/1.417335 LONG GR, 1984, HEARING RES, V15, P73, DOI 10.1016/0378-5955(84)90227-2 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I NAKAJIMA HH, 1994, J ACOUST SOC AM, V96, P786, DOI 10.1121/1.410316 NUTTALL A, 2000, ASS RES OT MIDW M ST Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 Ren TY, 1995, HEARING RES, V92, P178, DOI 10.1016/0378-5955(95)00217-0 Ren TY, 2000, HEARING RES, V143, P58, DOI 10.1016/S0378-5955(00)00027-7 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SUN XM, 1994, J ACOUST SOC AM, V96, P2166, DOI 10.1121/1.410158 SUN XM, 1994, J ACOUST SOC AM, V96, P2175, DOI 10.1121/1.410159 von Bekesy G., 1960, EXPT HEARING, P485 XUE S, 1997, INT S DIV AUD MECH R, V1, P386 Xue SW, 1995, HEARING RES, V91, P93, DOI 10.1016/0378-5955(95)00175-1 XUE SW, 1993, HEARING RES, V70, P121, DOI 10.1016/0378-5955(93)90056-7 Yates GK, 1998, J NEUROSCI, V18, P1996 NR 33 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 77 EP 89 DI 10.1016/S0378-5955(00)00238-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700008 PM 11223283 ER PT J AU Lin, X Hant, J AF Lin, X Hant, J TI Computer-simulation studies on roles of potassium currents in neurotransmission of the auditory nerve SO HEARING RESEARCH LA English DT Article DE spiral ganglion neuron; auditory coding; action potential width; synaptic modeling; voltage-gated potassium current; accumulative inactivation ID VOLTAGE-DEPENDENT CURRENTS; APLYSIA SENSORY NEURONS; SPIRAL GANGLION NEURONS; AVIAN COCHLEAR NUCLEUS; GUINEA-PIG; TRANSMITTER RELEASE; ACTION-POTENTIALS; GLUTAMATE; CALCIUM; FACILITATION AB Our previous work showed that action potentials (APs) fired in spiral ganglion (SG) neurons broaden gradually as a result of cumulative inactivation of the potassium current (I-K), or with the application of a tinnitus-inducing drug (quinine). These results led us to speculate that AP width could affect neurotransmission of the auditory nerve under both normal and pathological conditions. This study used both experimental and theoretical approaches to test this hypothesis. We first measured the effect of AP broadening on Ca2+ entry into SG neurons. The effect of pre-synaptic AP broadening on post-synaptic responses was then assessed using computer-simulations. Results showed that wider presynaptic APs augmented responses of all types of postsynaptic glutamatergic receptors mainly by amplifying responses of postsynaptic receptors whose locations were not well aligned with the presynaptic release sites. A cumulative inactivation of I-K in SG neurons significantly enhanced the responses of kainate receptors at all spike rates, while the augmentations for the alpha -amino-3-hydroxy-5-methylisoxazole-4 acid and N-methyl-D-aspartic acid receptors were most prominent below 100 spikes/s. These modeling results suggest that, in addition to the AP firing rate and timing, the width of APs could affect the neurotransmission of the auditory nerve under both normal and pathological conditions. (C) 2001 Elsevier Science B.V. All rights reserved. C1 House Ear Inst, Dept Cell & Mol Biol, Neurobiol Sect, Los Angeles, CA 90057 USA. RP Lin, X (reprint author), House Ear Inst, Dept Cell & Mol Biol, Neurobiol Sect, 210 W 3rd St, Los Angeles, CA 90057 USA. CR ALDRICH RW, 1981, BIOPHYS J, V36, P519 AUGUSTINE GJ, 1990, J PHYSIOL-LONDON, V431, P343 BLUMENFELD H, 1990, NEURON, V5, P487, DOI 10.1016/0896-6273(90)90088-W BRAHA O, 1990, P NATL ACAD SCI USA, V87, P2040, DOI 10.1073/pnas.87.5.2040 DELANEY K, 1991, J NEUROSCI, V11, P2631 Destexhe A, 1994, J Comput Neurosci, V1, P195, DOI 10.1007/BF00961734 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 Evans E F, 1981, Ciba Found Symp, V85, P108 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HANT J, 1999, 22 MIDW M ASS RES OT, P210 Hines ML, 1997, NEURAL COMPUT, V9, P1179, DOI 10.1162/neco.1997.9.6.1179 IRWIN RJ, 1971, PERCEPT PSYCHOPHYS, V10, P189, DOI 10.3758/BF03205785 ISACOFF EY, 1990, NATURE, V345, P530, DOI 10.1038/345530a0 JACKSON MB, 1991, P NATL ACAD SCI USA, V88, P380, DOI 10.1073/pnas.88.2.380 JAHR CE, 1990, J NEUROSCI, V10, P1830 KATZ B, 1967, NATURE, V215, P651, DOI 10.1038/215651a0 Kiang NY-s, 1965, DISCHARGE PATTERNS S LESTER RAJ, 1992, J NEUROSCI, V12, P635 Lin X, 1998, J NEUROPHYSIOL, V79, P2503 Lin X, 1997, HEARING RES, V108, P157, DOI 10.1016/S0378-5955(97)00050-6 Mulheran M, 1999, HEARING RES, V134, P145, DOI 10.1016/S0378-5955(99)00076-3 NAKAGAWA T, 1991, J NEUROPHYSIOL, V65, P715 RAMAN IM, 1992, NEURON, V9, P173, DOI 10.1016/0896-6273(92)90232-3 Raman IM, 1995, BIOPHYS J, V69, P1868 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 Ruel J, 1999, J PHYSIOL-LONDON, V518, P667, DOI 10.1111/j.1469-7793.1999.0667p.x RUGGERO MA, 1992, SPRINGER HDB AUDITOR, V2, P34 Salvi RJ, 2000, HEARING RES, V147, P261, DOI 10.1016/S0378-5955(00)00136-2 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E Xie XP, 1997, P NATL ACAD SCI USA, V94, P6983, DOI 10.1073/pnas.94.13.6983 ZENG FG, 1994, J ACOUST SOC AM, V96, P2127, DOI 10.1121/1.410154 ZHANG S, 1994, J PHYSIOL-LONDON, V480, P123 NR 32 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 90 EP 99 DI 10.1016/S0378-5955(00)00239-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700009 PM 11223284 ER PT J AU Aibara, R Welsh, JT Puria, S Goode, RL AF Aibara, R Welsh, JT Puria, S Goode, RL TI Human middle-ear sound transfer function and cochlear input impedance SO HEARING RESEARCH LA English DT Article DE middle-ear sound transmission; middle-ear sound pressure gain; cochlear input impedance; scala vestibuli sound pressure; stapes footplate velocity ID HUMAN TEMPORAL BONES; PRESSURE MEASUREMENTS; MECHANICS; STAPES; MODEL AB The middle-ear pressure gain, defined as the ear canal sound pressure to cochlear vestibule pressure gain, GME, and the ear canal sound pressure to stapes footplate velocity transfer function, SVTF, simultaneously measured in 12 fresh human temporal bones for the 0.05 to 10 kHz frequency range are reported. The mean GME magnitude reached 73.5 dB at 1.2 kHz with a slope of approximately 6 dB/octave from 0.1 to 1.2 kHz and -6 dB/octave above 1.2 kHz. From 0.1 to 0.5 kHz, the mean GME phase angle was 51 degrees, rolling off at -78 degrees /octave above this frequency. The mean SVTF magnitude reached a maximum of 0.33 mm s(-1)/Pa at 1.0 kHz with nearly the same shape in magnitude and phase angle as the mean GME. The ratio of GME and SVTF provide the first direct measurements of Z(c) in human ears. The mean Z(c) was virtually flat with a value of 21.1 acoustic G Omega MKS between 0.1 and 5.0 kHz. Above 5 kHz, the mean Z(c), increased to a maximum value of 49.9 G Omega at 6.7 kHz. The mean Z(c) angle was near 0 degrees from 0.5 to 5.0 kHz decreasing below 0.5 kHz and above 5 kHz with peaks and valleys. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Dept Vet Affairs Med Ctr, Palo Alto, CA 94304 USA. Stanford Univ, Sch Med, Div Otolaryngol Head & Neck Surg, Stanford, CA 94305 USA. Stanford Univ, Dept Mech Engn, Stanford, CA 94305 USA. RP Goode, RL (reprint author), Dept Vet Affairs Med Ctr, 3801 Miranda Ave,MC 112-B1, Palo Alto, CA 94304 USA. CR BEKESY G, 1960, EXPT HEARING, P745 BRENKMAN CJ, 1987, J ACOUST SOC AM, V82, P1646, DOI 10.1121/1.395156 DALLOS P, 1973, AUDITORY PERIPHERY B, P98 DANCER A, 1980, HEARING RES, V2, P191, DOI 10.1016/0378-5955(80)90057-X Davis A, 1995, HEARING ADULTS FISHLER H, 1965, J ACOUST SOC AM, V41, P1220 Fletcher H., 1995, SPEECH HEARING COMMU GOODE RL, 1987, J ACOUST SOC AM, V82, P1646 GOODE RL, 1994, AM J OTOL, V15, P145 Gundersen T, 1971, PROSTHESES OSSICULAR GYO K, 1987, ACTA OTO-LARYNGOL, V103, P87, DOI 10.3109/00016488709134702 Heiland KE, 1999, AM J OTOL, V20, P81 HUTTENBRINK KB, 1994, HNO, V42, P49 Kohllöffel L U, 1971, Acta Otolaryngol Suppl, V288, P1 KRINGLEBOTN M, 1988, SCAND AUDIOL, V17, P75, DOI 10.3109/01050398809070695 KRINGLEBOTN M, 1985, J ACOUST SOC AM, V77, P159, DOI 10.1121/1.392280 KUROKAWA H, 1995, OTOLARYNG HEAD NECK, V113, P349, DOI 10.1016/S0194-5998(95)70067-6 LYNCH TJ, 1994, J ACOUST SOC AM, V96, P2184, DOI 10.1121/1.410160 Merchant SN, 1996, HEARING RES, V97, P30 ONCHI Y, 1961, J ACOUST SOC AM, V33, P794, DOI 10.1121/1.1908801 PURIA S, 1993, J ACOUST SOC AM, V93, P2556 Puria S, 1997, J ACOUST SOC AM, V101, P2754, DOI 10.1121/1.418563 PURIA S, 1992, J ACOUST SOC AM, V92, P2469, DOI 10.1121/1.404474 RUBENSTEIN M, 1964, J ACOUST SOC AM, V40, P1420 RUGGERO MA, 1990, J ACOUST SOC AM, V87, P1612, DOI 10.1121/1.399409 VLAMING MSMG, 1986, CLIN OTOLARYNGOL, V11, P353, DOI 10.1111/j.1365-2273.1986.tb00137.x Zwislocki J, 1965, HDB MATH PHYSL, P3 ZWISLOCKI JJ, 1975, NERVOUS SYSTEM, V3, P44 NR 28 TC 140 Z9 155 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 100 EP 109 DI 10.1016/S0378-5955(00)00240-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700010 PM 11223285 ER PT J AU Rotman, Y Bar-Yosef, O Nelken, I AF Rotman, Y Bar-Yosef, O Nelken, I TI Relating cluster and population responses to natural sounds and tonal stimuli in cat primary auditory cortex SO HEARING RESEARCH LA English DT Article DE cat; primary auditory cortex; natural sound; population coding; rate profile; Volterra kernel ID NONLINEAR SPECTRAL INTEGRATION; SPECIES-SPECIFIC VOCALIZATIONS; FREQUENCY-MODULATED SWEEPS; STEADY-STATE VOWELS; TONOTOPIC ORGANIZATION; FUNCTIONAL TOPOGRAPHY; MULTIFREQUENCY SOUNDS; COCHLEAR NUCLEUS; TUNING CURVES; IV NEURONS AB Most information about neuronal properties in primary auditory cortex (AI) has been gathered using simple artificial sounds such as purl tones and broad-band noise. These sounds are very different from the natural sounds that are processed by the auditory system in real world situations. In an attempt to bridge this gap, simple tonal stimuli and a standard set of six natural sounds were used to create models relating the responses of neuronal clusters in AI of barbiturate-anesthetized cats to the two classes of stimuli. A significant correlation was often found between the response to the separate frequency components of the natural sounds and the response to the natural sound itself. At the population level, this correlation resulted in a rate profile that represented robustly the spectral profiles of the natural sounds. There was however a significant scatter in the responses to the natural sound around the predictions based on the responses to tonal stimuli, Going the other way, in order to understand better the non-linearities in the responses to natural sounds, responses of neuronal clusters were characterized using second order Volterra kernel analysis of their responses to natural sounds. This characterization predicted reasonably well the amplitude of the response to other natural sounds, but could not reproduce the responses to tonal stimuli. Thus, second order non-linear characterizations, at least those using the Volterra kernel model, do not interpolate well between responses to tones and to natural sounds in auditory cortex. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, IL-91120 Jerusalem, Israel. Hebrew Univ Jerusalem, Interdisciplinary Ctr Neural Computat, IL-91120 Jerusalem, Israel. RP Nelken, I (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, POB 12272, IL-91120 Jerusalem, Israel. RI Nelken, Israel/B-7753-2011 OI Nelken, Israel/0000-0002-6645-107X CR ABELES M, 1970, J NEUROPHYSIOL, V33, P172 AERTSEN AMH, 1981, SPECRO TERMPORAL CHA AERTSEN AMHJ, 1979, BIOL CYBERN, V32, P175, DOI 10.1007/BF00337394 BLACKBURN CC, 1990, J NEUROPHYSIOL, V63, P1191 EGGERMONT JJ, 1990, J ACOUST SOC AM, V87, P246, DOI 10.1121/1.399291 HEIL P, 1992, HEARING RES, V63, P135, DOI 10.1016/0378-5955(92)90081-W IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 KIM PJ, 1994, J ACOUST SOC AM, V95, P410, DOI 10.1121/1.408335 Korenberg MJ, 1996, ANN BIOMED ENG, V24, P250, DOI 10.1007/BF02667354 Marmarelis PZ, 1978, ANAL PHYSL SYSTEMS MATSUBARA JA, 1988, J COMP NEUROL, V268, P38, DOI 10.1002/cne.902680105 MENDELSON JR, 1993, EXP BRAIN RES, V94, P65 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MIDDLEBROOKS JC, 1980, BRAIN RES, V181, P31, DOI 10.1016/0006-8993(80)91257-3 Nelken I, 2000, EUR J NEUROSCI, V12, P549, DOI 10.1046/j.1460-9568.2000.00935.x Nelken I, 1997, J NEUROPHYSIOL, V78, P790 NELKEN I, 1994, HEARING RES, V72, P223, DOI 10.1016/0378-5955(94)90221-6 Nelken I, 1999, NATURE, V397, P154, DOI 10.1038/16456 Nelken I, 1997, J NEUROPHYSIOL, V78, P800 NELKEN I, 1994, HEARING RES, V72, P206, DOI 10.1016/0378-5955(94)90220-8 Rauschecker JP, 1998, CURR OPIN NEUROBIOL, V8, P516, DOI 10.1016/S0959-4388(98)80040-8 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 SACHS MB, 1979, J ACOUST SOC AM, V66, P470, DOI 10.1121/1.383098 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 Seidemann E, 1996, J NEUROSCI, V16, P752 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P449 SHAMMA SA, 1993, J NEUROPHYSIOL, V69, P367 SMOLDERS JWT, 1979, BIOL CYBERN, V35, P11, DOI 10.1007/BF01845840 SOVIJARVI ARA, 1975, ACTA PHYSIOL SCAND, V93, P318, DOI 10.1111/j.1748-1716.1975.tb05821.x STEINSCHNEIDER M, 1995, BRAIN RES, V674, P147, DOI 10.1016/0006-8993(95)00008-E SUGA N, 1992, PHILOS T ROY SOC B, V336, P423, DOI 10.1098/rstb.1992.0078 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 Versnel H, 1998, J ACOUST SOC AM, V103, P2502, DOI 10.1121/1.422771 Wang XQ, 1995, J NEUROPHYSIOL, V74, P2685 WOLLBERG Z, 1972, SCIENCE, V175, P212, DOI 10.1126/science.175.4018.212 Woolsey CN, 1942, B JOHNS HOPKINS HOSP, V71, P315 YESHURUN Y, 1985, BIOL CYBERN, V51, P383, DOI 10.1007/BF00350778 ZURITA P, 1994, NEUROSCI RES, V19, P303, DOI 10.1016/0168-0102(94)90043-4 NR 39 TC 25 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 110 EP 127 DI 10.1016/S0378-5955(00)00243-4 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700011 PM 11223286 ER PT J AU Popelar, J Erre, JP Syka, J Aran, JM AF Popelar, J Erre, JP Syka, J Aran, JM TI Effects of contralateral acoustical stimulation on three measures of cochlear function in the guinea pig SO HEARING RESEARCH LA English DT Article DE transient otoacoustic emissions; auditory nerve; compound action potential; ensemble background activity; contralateral suppression; guinea pig ID EVOKED OTOACOUSTIC EMISSIONS; AUDITORY-NERVE FIBERS; EFFERENT OLIVOCOCHLEAR NEURONS; OUTER HAIR-CELLS; ELECTRICAL-STIMULATION; ROUND-WINDOW; SOUND STIMULATION; UNIT RESPONSE; SUPPRESSION; GENTAMICIN AB The magnitudes of suppression of the click-evoked compound action potential of the auditory nerve (CAP), transient click-evoked otoacoustic emissions (TEOAEs) and ensemble background activity of the auditory nerve (EBA), elicited by contralateral acoustical stimulation, were compared in awake or lightly sedated guinea pigs. The contralateral ear was stimulated either by continuous broad-band noise or by low-pass or high-pass noise (intensity 41-62 dB SPL) with cut-off frequencies of 2, 8 and 12 kHz. The maximal suppression of TEOAEs was achieved by contralateral noise containing mainly low frequencies, whereas for suppression of the CAP it was necessary for middle frequencies to be present in the contralateral noise (less than 8 kHz). in contrast to this, EBA was suppressed mainly by high-frequency noise (higher than 8 kHz) whereas low- and middle-frequency noise was ineffective in suppressing EBA. Evaluation of the root mean square voltage of the EBA (filtered in frequency range 0.75-1.25 kHz) enabled the evaluation of fast and slow components of olivocochlear activation. Both fast and dow effects were proportionally suppressed by individual types of contralateral stimulation. The mechanisms of TEOAEs and CAP generation has been confirmed in many earlier studies, but the origin of EBA has yet to be fully elucidated. The obtained data support the hypothesis that a large part of EBA is formed by spontaneous activity of high-frequency-tuned auditory nerve fibres. Suppression of the EBA magnitude during contralateral stimulation may be caused either by a reduced spontaneous firing rate or by a decrease in possible synchronised neuronal firing. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Acad Sci Czech Republ, Inst Expt Med, Prague 14220 4, Czech Republic. Univ Bordeaux 2, Hop Pellegrin, INSERM, Equipe Mixte 99 27, F-33076 Bordeaux, France. RP Popelar, J (reprint author), Acad Sci Czech Republ, Inst Expt Med, Videnska 1083, Prague 14220 4, Czech Republic. RI Popelar, Jiri/H-2558-2014; Syka, Josef/H-3103-2014 CR ARAN JM, 1994, BRIT J AUDIOL, V28, P267, DOI 10.3109/03005369409086576 Avan P, 1996, EXP BRAIN RES, V109, P9 BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BROWN SE, 1990, ABSTR ASS RES OT, V13, P230 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BUNO W, 1978, EXP NEUROL, V59, P62, DOI 10.1016/0014-4886(78)90201-7 Cazals Y, 1996, HEARING RES, V101, P81, DOI 10.1016/S0378-5955(96)00135-9 CHERYCROZE S, 1993, HEARING RES, V68, P53, DOI 10.1016/0378-5955(93)90064-8 daCosta DL, 1997, EXP BRAIN RES, V116, P259, DOI 10.1007/PL00005754 daCosta DL, 1997, J NEUROPHYSIOL, V78, P1826 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DOLAN DF, 1990, J ACOUST SOC AM, V87, P2621, DOI 10.1121/1.399054 EVANS EF, 1987, BRIT J AUDIOL, V21, P103 FEX J, 1967, J ACOUST SOC AM, V41, P666, DOI 10.1121/1.1910395 FEX J, 1959, Acta Otolaryngol, V50, P540, DOI 10.3109/00016485909129230 FUCHS PA, 1992, J NEUROSCI, V12, P800 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 GUINAN JJ, 1988, HEARING RES, V37, P29, DOI 10.1016/0378-5955(88)90075-5 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 JOHNSON DH, 1976, BIOPHYS J, V16, P719 Khvoles R, 1996, HEARING RES, V97, P120 Kiang NYS, 1976, ELECTROCOCHLEOGRAPHY, P95 KLINKE R, 1969, J ACOUST SOC AM, V45, P788, DOI 10.1121/1.1911473 LEWIS ER, 1992, HEARING RES, V63, P7, DOI 10.1016/0378-5955(92)90067-W LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORMAN M, 1993, BRIT J AUDIOL, V27, P281, DOI 10.3109/03005369309076705 POPELAR J, 1996, AUDIT NEUROSCI, V3, P425 Popelar J, 1999, HEARING RES, V135, P61, DOI 10.1016/S0378-5955(99)00091-X PRIJS VF, 1986, HEARING RES, V21, P127, DOI 10.1016/0378-5955(86)90034-1 PUEL JL, 1990, J ACOUST SOC AM, V76, P1713 SCHREINER CE, 1987, P 3 INT TINN SEM HAR, P100 SCHREINER CE, 1986, HEARING RES, V21, P213, DOI 10.1016/0378-5955(86)90220-0 SEWELL WF, 1984, J PHYSIOL-LONDON, V347, P685 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SININGER YS, 1992, TINNITUS 91, P341 SMITH DW, 1994, BRAIN RES, V652, P243, DOI 10.1016/0006-8993(94)90233-X Sridhar TS, 1997, J NEUROSCI, V17, P428 SRIDHAR TS, 1995, J NEUROSCI, V15, P3667 UEDA H, 1992, HEARING RES, V62, P199, DOI 10.1016/0378-5955(92)90187-R VELLUTI RA, 1994, HEARING RES, V72, P19, DOI 10.1016/0378-5955(94)90200-3 VERSNEL H, 1992, HEARING RES, V59, P157, DOI 10.1016/0378-5955(92)90112-Z VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 YOSHIDA N, 2000, 23 ARO M Yoshida N, 1999, J NEUROPHYSIOL, V82, P3168 ZENNER HP, 1990, ADV AUDIOL, V7, P35 NR 51 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 128 EP 138 DI 10.1016/S0378-5955(00)00244-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700012 PM 11223287 ER PT J AU Preyer, S Baisch, A Bless, D Gummer, AW AF Preyer, S Baisch, A Bless, D Gummer, AW TI Distortion product otoacoustic emissions in human hypercholesterolemia SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; growth function of DPOAE; hearing threshold; speech audiometry; familial hypercholesterolemia ID FREQUENCY HEARING-LOSS; BASILAR-MEMBRANE; GROWTH-BEHAVIOR; COCHLEAR; RESPONSES; 2F1-F2; HYPERLIPIDEMIA; SUPPRESSION; CHINCHILLA; NOISE AB Epidemiological and experimental studies suggest that hypercholesterolemia promotes the development of sensorineural hearing loss; however, the underlying cellular pathomechanism remains obscure. In the present study, 20 healthy subjects and 20 patients with familial hypercholesterolemia were compared with respect to their hearing function. None of the 40 persons reported any history of hearing disorder. In accordance with this subjective impression, mean hearing thresholds were within the normal, age-dependent ranges in both groups. Tn contrast, the single-generator distortion product otoacoustic emissions (sgDPOAE) were reduced at and above 4 kHz. Input-output functions of DPOAE could be subdivided into three groups: (i) normal, with unity slope at low intensities and slope less than unity (0.24 +/- 0.07 dB/dB at higher intensities; (ii) pathologic, described by a single straight line; (iii) ill-defined, with data usually indistinguishable from the background noise level. The ill-defined DPOAE behavior was only found in patients with hypercholesterolemia; namely, for 25% of patients at f(2) =1.5 kHz and for 50% at f(2) = 4 kHz. Patients belonging to the pathologic and ill-defined DPOAE groups had significantly (P < 0.05) higher total serum cholesterol and LDL;cholesterol levels compared with subjects from the normal DPOAE group. While hearing thresholds of patients with ill-defined growth functions were not statistically different from those of normal subjects, speech scores were significantly reduced in these cases. The data imply that nonlinear mechanical processes in the cochlea are compromised in hypercholesterolemic patients. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tubingen, Sect Physiol Acoust & Commun, Dept Otolaryngol, D-72076 Tubingen, Germany. RP Preyer, S (reprint author), Univ Tubingen, Sect Physiol Acoust & Commun, Dept Otolaryngol, Silcherstr 5, D-72076 Tubingen, Germany. CR Abdala C, 1998, HEARING RES, V121, P125, DOI 10.1016/S0378-5955(98)00073-2 Abdala C, 2000, J ACOUST SOC AM, V107, P446, DOI 10.1121/1.428315 ALLEN JB, 1992, J ACOUST SOC AM, V92, P178, DOI 10.1121/1.404281 American National Standards Institute (ANSI), 1996, S361996 ANSI AXELSSON A, 1985, ACTA OTO-LARYNGOL, V100, P379, DOI 10.3109/00016488509126561 BONFILS P, 1992, ARCH OTOLARYNGOL, V118, P1069 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CUNNINGH.DR, 1974, AUDIOLOGY, V13, P470 DALLOS P, 1992, J NEUROSCI, V12, P4575 Dorn Patricia A., 1998, Journal of the Acoustical Society of America, V104, P964, DOI 10.1121/1.423339 FELDMANN H, 1988, LARYNGO RHINO OTOL, V67, P319, DOI 10.1055/s-2007-998509 GRATTON MA, 1992, HEARING RES, V61, P97, DOI 10.1016/0378-5955(92)90040-T Hahlbrock K.H., 1957, SPRACHAUDIOMETRIE GR HAUSER R, 1991, J ACOUST SOC AM, V89, P280, DOI 10.1121/1.400511 Heitmann J, 1998, J ACOUST SOC AM, V103, P1527, DOI 10.1121/1.421290 Janssen T, 1998, J ACOUST SOC AM, V103, P3418, DOI 10.1121/1.423053 JANSSEN T, 1995, OTO RHINO LARYN NOVA, V5, P34 KELLER F, 1977, 45621 DIN, V22, P292 Kummer P, 1998, J ACOUST SOC AM, V103, P3431, DOI 10.1121/1.423054 Lonsbury-Martin B L, 1990, Ann Otol Rhinol Laryngol Suppl, V147, P3 LOWRY LD, 1978, ANN OTO RHINOL LARYN, V87, P404 Lowry L D, 1975, Trans Pa Acad Ophthalmol Otolaryngol, V28, P56 MARTIN GK, 1990, ANN OTO RHINOL LARYN, V99, P30 MCCORMIC.JG, 1972, J ACOUST SOC AM, V52, P143, DOI 10.1121/1.1981905 MORIZONO T, 1978, ANN OTO RHINOL LARYN, V87, P804 MORIZONO T, 1982, ARCH OTOLARYNGOL, V108, P210 MORIZONO T, 1985, ACTA OTO-LARYNGOL, V99, P516 Nguyen TVN, 1998, OTOLARYNG HEAD NECK, V119, P14, DOI 10.1016/S0194-5998(98)70167-6 Nieschalk M, 1998, AUDIOLOGY, V37, P83 Nuttall AL, 1996, J ACOUST SOC AM, V99, P1556, DOI 10.1121/1.414732 PATUZZI R, 1993, BRIT J AUDIOL, V27, P91, DOI 10.3109/03005369309077897 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 ROSEN S, 1962, ANN OTO RHINOL LARYN, V71, P727 ROSEN S, 1970, ACTA OTO-LARYNGOL, V70, P242 ROSEN S, 1964, Trans Am Acad Ophthalmol Otolaryngol, V68, P433 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 SPENCER JT, 1973, LARYNGOSCOPE, V83, P639, DOI 10.1288/00005537-197305000-00002 Spoor A, 1967, INT AUDIOL, V6, P48, DOI 10.3109/05384916709074230 TSAI MT, 1989, HEAD NECK SURG, V101, P200 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2359, DOI 10.1121/1.411960 Withnell RH, 1998, HEARING RES, V123, P87, DOI 10.1016/S0378-5955(98)00100-2 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 NR 43 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 139 EP 151 DI 10.1016/S0378-5955(00)00245-8 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700013 PM 11223288 ER PT J AU Harada, T Ogawa, K Inoue, Y Kanzaki, J AF Harada, T Ogawa, K Inoue, Y Kanzaki, J TI Effects of changes in stimulus level on phases of distortion product otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE distortion product; otoacoustic emission; phase; cochlear mechanics; basilar membrane vibration ID ACOUSTIC DISTORTION; GUINEA-PIG; HUMAN EARS; SUPPRESSION; COCHLEA; 2F1-F2; RESPONSES; INNER AB Effect of changes in stimulus levels of both leger (f(1)) and higher (f(2)) stimulus tones on phases of 2f(1) -f(2) component of the distortion product otoacoustic emission (DPOAE) was examined in five normal hearing adults. The f(2) was fixed at 4004 Hz in all of the measurements, and the stimulus frequency ratio (f(2)/f(1)) was varied from 1.15 to 1.3. Change of the level of lower stimulus tone (L-1) and the level of higher stimulus tone (L-2) showed different effects on the DPOAE phases. The phase lags increased with increasing Lr, when f(2)/f(1) was above 1.22, whereas the phase gains increased with increasing L-1, when f(2)/f(1) was below 1.22. On the other hand, the difference in L-2 minimally affected DPOAE phase at most f(1)s. The previous studies about basilar membrane vibration revealed that phase lags increase with increasing stimulus level, when the stimulus frequency is below the best frequency, while phase gains increase with increasing stimulus level, when the stimulus frequency is above the best frequency, and the effect of phase change in stimulus level diminished, when the stimulus frequency was far above the best frequency. Based on the comparison between the results of the present study and the previous findings of others concerning basilar membrane vibration, the DPOAE generation site is assumed to be located at apical of the peak of the f(2) traveling wave. (C) 2001 Published by Elsevier Science B.V. C1 Tokai Univ, Sch Med, Dept Otorhinolaryngol, Tokai, Ibaraki, Japan. Keio Univ, Sch Med, Dept Otorhinolaryngol, Keio, Japan. RP Harada, T (reprint author), Bohseidai, Isehara, Kanagawa, Japan. CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 Brown AM, 1996, J ACOUST SOC AM, V100, P3260, DOI 10.1121/1.417209 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X Engdahl B, 1996, J ACOUST SOC AM, V99, P1573, DOI 10.1121/1.414733 Fahey PF, 1997, J ACOUST SOC AM, V102, P2880, DOI 10.1121/1.420343 FURST M, 1988, J ACOUST SOC AM, V84, P215, DOI 10.1121/1.396968 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GEISLER CD, 1982, J ACOUST SOC AM, V71, P1201, DOI 10.1121/1.387768 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HALL JL, 1975, J ACOUST SOC AM, V58, P1046, DOI 10.1121/1.380763 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 Heitmann J, 1998, J ACOUST SOC AM, V103, P1527, DOI 10.1121/1.421290 Kemp D. T., 1983, MECH HEARING, P75 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KIMBERLEY BP, 1993, J ACOUST SOC AM, V94, P1343, DOI 10.1121/1.408162 KUMMER P, 1995, J ACOUST SOC AM, V98, P197, DOI 10.1121/1.413747 MAHONEY CFO, 1995, J ACOUST SOC AM, V97, P3721 Moulin A, 1996, J ACOUST SOC AM, V100, P1617, DOI 10.1121/1.416063 NUTTALL AL, 1993, J ACOUST SOC AM, V93, P390, DOI 10.1121/1.405619 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 Shera CA, 1999, J ACOUST SOC AM, V105, P782, DOI 10.1121/1.426948 Talmadge CL, 1998, J ACOUST SOC AM, V104, P1517, DOI 10.1121/1.424364 ZWICKER E, 1981, J ACOUST SOC AM, V70, P1277, DOI 10.1121/1.387141 ZWICKER E, 1990, J ACOUST SOC AM, V87, P2583, DOI 10.1121/1.399051 NR 26 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 152 EP 158 DI 10.1016/S0378-5955(00)00246-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700014 PM 11223289 ER PT J AU Dooling, RJ Dent, ML Leek, MR Gleich, O AF Dooling, RJ Dent, ML Leek, MR Gleich, O TI Masking by harmonic complexes in birds: behavioral thresholds and cochlear responses SO HEARING RESEARCH LA English DT Article DE masking; bird; harmonic complex; cochlear microphonics ID BUDGERIGARS MELOPSITTACUS-UNDULATUS; PRIMARY AUDITORY AFFERENTS; SCHROEDER-PHASE COMPLEXES; INNER-EAR; TAENIOPYGIA-GUTTATA; STURNUS-VULGARIS; PERIOD PATTERNS; ZEBRA FINCHES; FREQUENCY; DISPERSION AB Thresholds for pure tones embedded in harmonic complexes were measured behaviorally and physiologically for three species of birds, and physiologically in gerbils. The harmonic maskers were generated using the Schroeder-phase algorithm, characterized by monotonically increasing or decreasing phase across frequency. Previous work has shown that these stimuli produce large differences in masking in humans but not budgerigars. In this study, we show that for two additional species of birds, the patterns of masking were similar to those shown for budgerigars, with masking differing only slightly for the two Schroeder-phase waveforms, and in the opposite direction from that demonstrated in humans. Amounts of masking among species corresponded qualitatively to differences in their critical ratios. Evoked potential measurements in birds and gerbils indicated responses that were consistent with the behaviorally measured thresholds in birds and humans. Results are interpreted in light of differences in frequency selectivity and cochlear temporal processing across species. (C) 2001 Elsevier Science B.V. Al rights reserved. C1 Univ Maryland, Dept Psychol, College Pk, MD 20742 USA. Walter Reed Army Med Ctr, Army Audiol & Speech Ctr, Washington, DC 20307 USA. Univ Regensburg, ENT Dept, D-93042 Regensburg, Germany. RP Dooling, RJ (reprint author), Univ Maryland, Dept Psychol, College Pk, MD 20742 USA. CR Bekesy G., 1960, EXPT HEARING BUUS S, 1995, J ACOUST SOC AM, V98, P112, DOI 10.1121/1.414466 Carlyon RP, 1997, J ACOUST SOC AM, V101, P3636, DOI 10.1121/1.418324 Carlyon RP, 1997, J ACOUST SOC AM, V101, P3648, DOI 10.1121/1.418325 Carney LH, 1999, J ACOUST SOC AM, V105, P2384, DOI 10.1121/1.426843 Carr C. E., 2000, COMP HEARING BIRDS R, P197, DOI 10.1007/978-1-4612-1182-2_5 CYNX J, 1990, J COMP PSYCHOL, V104, P303 Dau T, 2000, J ACOUST SOC AM, V107, P1530, DOI 10.1121/1.428438 Dooling R. J., 1995, METHODS COMP PSYCHOA, P161 Dooling R. J., 2000, COMP HEARING BIRDS R, P308 Fay R. R., 1988, HEARING VERTEBRATES Gescheider G. A., 1985, PSYCHOPHYSICS METHOD GLEICH O, 1988, HEARING RES, V32, P81, DOI 10.1016/0378-5955(88)90148-7 GLEICH O, 1994, J ACOUST SOC AM, V95, P401, DOI 10.1121/1.408333 GLEICH O, 2000, COMP HEARING BIRDS R, P70 GLEICH O, 1994, HEARING RES, V79, P123, DOI 10.1016/0378-5955(94)90134-1 Green D. M., 1988, PROFILE ANAL AUDITOR GREENWOOD D, 1961, J ACOUST SOC AM, V33, P484, DOI 10.1121/1.1908699 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 HAWKINS JE, 1950, J ACOUST SOC AM, V22, P6, DOI 10.1121/1.1906581 KEMP S, 1982, ACUSTICA, V50, P63 KOHLRAUSCH A, 1995, J ACOUST SOC AM, V97, P1817, DOI 10.1121/1.413097 Leek MR, 2000, J ACOUST SOC AM, V107, P1737, DOI 10.1121/1.428455 Lohr B, 1998, J COMP PSYCHOL, V112, P36, DOI 10.1037/0735-7036.112.1.36 LOHR B, 1999, HEARING RED BILLED F MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1993, J MORPHOL, V218, P153, DOI 10.1002/jmor.1052180205 MCGUIRT JP, 1995, HEARING RES, V84, P52, DOI 10.1016/0378-5955(95)00015-V MOORE BCJ, 1978, J ACOUST SOC AM, V63, P524, DOI 10.1121/1.381752 Muller M, 1996, HEARING RES, V94, P148, DOI 10.1016/0378-5955(95)00230-8 OKANOYA K, 1987, J COMP PSYCHOL, V101, P7, DOI 10.1037//0735-7036.101.1.7 Ruggero M. A., 1992, MAMMALIAN AUDITORY P, P34 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SAUNDERS JC, 1980, J EXP BIOL, V87, P331 SCHROEDE.MR, 1970, IEEE T INFORM THEORY, V16, P85, DOI 10.1109/TIT.1970.1054411 SMITH BK, 1986, J ACOUST SOC AM, V80, P1631, DOI 10.1121/1.394327 SMOORENBURG GF, 1980, HEARING RES, V3, P301, DOI 10.1016/0378-5955(80)90025-8 Summers V, 1998, HEARING RES, V118, P139, DOI 10.1016/S0378-5955(98)00030-6 Uno H, 1997, BEHAV BRAIN RES, V89, P225, DOI 10.1016/S0166-4328(97)00064-8 NR 41 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2001 VL 152 IS 1-2 BP 159 EP 172 DI 10.1016/S0378-5955(00)00249-5 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 407ZU UT WOS:000167302700015 PM 11223290 ER PT J AU Misawa, H Suga, N AF Misawa, H Suga, N TI Multiple combination-sensitive neurons in the auditory cortex of the mustached bat SO HEARING RESEARCH LA English DT Article DE combination-sensitive neuron; delay tuning; facilitation; frequency-vs.-frequency coordinate; hearing ID MEDIAL GENICULATE-BODY; TARGET RANGE; MOUSTACHED BAT; BIOSONAR SIGNALS; INFORMATION; REPRESENTATION; ECHOLOCATION; RESPONSES; SINGLE; INPUTS AB The mustached bat, Pteronotus parnellii, emits biosonar pulses consisting of four constant-frequency (CF1-4) and four frequency-modulated (FM1-4) components. The FM-FM area of its auditory cortex consists of three subdivisions, containing either FM1-FM2, FM1-FM3 or FM1-FM4 combination-sensitive neurons. The FM-FM area also contains 'multiple combination-sensitive' neurons: FM1-FM2,3, FM1-FM3,4, FM1-FM2,4, and FM1-FM2,3,4 neurons. All FM-FM neurons are tuned to a time delay (echo delay) of FM, (n = 2-4) from FM1. In the present study, we made the following four major findings. (1) Multiple combination-sensitive neurons show the strongest response to a combination of more than two signal elements. (2) Multiple combination-sensitive neurons are located in about 100 mum wide bands at the boundaries between two adjacent subdivisions of the FM-FM area. (3) Iso-best-delay contour lines across the three single combination-sensitive subdivisions are not interrupted by multiple combination-sensitive bands. (4) Each subdivision of the FM-FM area has frequency-vs.-frequency coordinates in terms of best FM1 and best FM, frequencies for facilitation, although such coordinates were not obtained with single tone bursts. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Dept Biol, St Louis, MO 63130 USA. RP Misawa, H (reprint author), Nagoya Univ, Grad Sch Med, Dept Otorhinolaryngol, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan. CR Doupe AJ, 1997, J NEUROSCI, V17, P1147 FUZESSERY ZM, 1983, J COMP PHYSIOL, V150, P333 GRIFFIN DR, 1971, ANIM BEHAV, V19, P55, DOI 10.1016/S0003-3472(71)80134-3 MARGOLIASH D, 1983, J NEUROSCI, V3, P1039 MUDRY KM, 1977, J COMP PHYSIOL, V114, P1 Ohlemiller KK, 1996, NEUROREPORT, V7, P1749, DOI 10.1097/00001756-199607290-00011 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1275 ONEILL WE, 1979, SCIENCE, V203, P69, DOI 10.1126/science.758681 ONEILL WE, 1982, J NEUROSCI, V2, P17 Razak KA, 1999, J NEUROPHYSIOL, V81, P1438 SALES G, 1974, ULTRASONIC COMMUNICA, P23 SIMMONS JA, 1975, AM SCI, V63, P204 SUGA N, 1986, J NEUROPHYSIOL, V55, P776 SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUGA N, 1979, SCIENCE, V206, P351, DOI 10.1126/science.482944 SUGA N, 1976, SCIENCE, V194, P542, DOI 10.1126/science.973140 SUGA N, 1978, SCIENCE, V200, P778, DOI 10.1126/science.644320 SUGA N, 1983, J NEUROPHYSIOL, V49, P1573 WENSTRUP JJ, 1995, J NEUROSCI, V15, P4693 Wenstrup JJ, 1999, J COMP NEUROL, V409, P509, DOI 10.1002/(SICI)1096-9861(19990712)409:4<509::AID-CNE1>3.0.CO;2-S Yan J, 1999, J NEUROPHYSIOL, V81, P817 Yan J, 1996, SCIENCE, V273, P1100, DOI 10.1126/science.273.5278.1100 NR 22 TC 16 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 15 EP 29 DI 10.1016/S0300-2977(00)00079-6 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600002 PM 11124448 ER PT J AU Dazert, S Aletsee, C Brors, D Gravel, C Sendtner, M Ryan, A AF Dazert, S Aletsee, C Brors, D Gravel, C Sendtner, M Ryan, A TI In vivo adenoviral transduction of the neonatal rat cochlea and middle ear SO HEARING RESEARCH LA English DT Article DE adenovirus vector; gene transfer; cochlea; middle ear; neonatal rat ID MEDIATED GENE-TRANSFER; CILIARY NEUROTROPHIC FACTOR; CELLS IN-VITRO; GROWTH-FACTOR; GUINEA-PIG; HAIR-CELLS; TRANSGENE EXPRESSION; MOTOR-NEURONS; THERAPY; VECTORS AB Virally mediated gene transfer to the adult mammalian ear appears to be a powerful strategy to investigate gene function in the auditory system and to develop new therapeutic treatment for hearing impaired patients. However, there has been little work done in the neonatal middle and inner ear. In this study, a recombinant adenoviral (AdV) vector was used for gene transfer of a beta -galactosidase (beta -gal) reporter gene to the neonatal middle ear and cochlea of 5 day old rats. For transduction of middle ear, AdV was injected through the tympanic membrane into the tympanic cavity. Three and 7 days later, strong expression of P-gal was observed in epithelial cells of the mucosal but not in the underlying stroma or mesenchyme. There was little or no infiltration of leukocytes. No expression of P-gal was detected inside the cochlea or vestibular system. When AdV was injected into the basal turn of the cochlea, high levels of P-gal expression were observed in cells lining the perilymphatic space and in parts of the spiral ligament 3, 7 and 21 days later. Spiral ganglion cells did not express P-gal. However, virally mediated gene transfer was observed in some cells of the organ of Corti. A moderate infiltration of leukocytes into the labyrinth was observed, but no vestibular or auditory dysfunction. These results demonstrate that neonatal middle ear and cochlear cells can be successfully transduced with an AdV vector in vivo, without obvious morphological signs of inflammation or cellular damage. AdV vectors provide a tool for investigation of the role of genes in influencing the development of middle and inner ear structures. Virally mediated expression of protective genes could also be used to rescue hair cells or spiral ganglion cells from congenital degeneration or damage. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Diego, Sch Med, Dept Surg Otolaryngol, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Vet Affairs Med Ctr, La Jolla, CA 92093 USA. Univ Wurzburg, Dept Neurol, D-97080 Wurzburg, Germany. Univ Laval Robert Giffard, Ctr Rech, Lab Transfert Genes, Beauport, PQ, Canada. RP Ryan, A (reprint author), Univ Calif San Diego, Sch Med, Dept Surg Otolaryngol, 9500 Gilman Dr, La Jolla, CA 92093 USA. RI Sendtner, Michael/M-8137-2014 OI Sendtner, Michael/0000-0002-4737-2974 CR DARMSTADT GL, 1990, ANN OTO RHINOL LARYN, V99, P960 Dazert S, 1998, J CELL PHYSIOL, V177, P123, DOI 10.1002/(SICI)1097-4652(199810)177:1<123::AID-JCP13>3.0.CO;2-E Dazert S, 1997, INT J DEV NEUROSCI, V15, P595, DOI 10.1016/S0736-5748(96)00114-1 Dazert S, 2000, LARYNGO RHINO OTOL, V79, P26 Derby ML, 1999, HEARING RES, V134, P1, DOI 10.1016/S0378-5955(99)00045-3 DRAGHIA R, 1995, GENE THER, V2, P418 EASTHAM JA, 1995, CANCER RES, V55, P5151 Garrido JJ, 1998, J NEUROCHEM, V70, P2336 Graham F L, 1991, Methods Mol Biol, V7, P109, DOI 10.1385/0-89603-178-0:109 Gravel C, 1997, NAT MED, V3, P765, DOI 10.1038/nm0797-765 Haase G, 1997, NAT MED, V3, P429, DOI 10.1038/nm0497-429 Holt JR, 1999, J NEUROPHYSIOL, V81, P1881 Homburger SA, 1996, DEV DYNAM, V206, P112, DOI 10.1002/(SICI)1097-0177(199605)206:1<112::AID-AJA10>3.0.CO;2-7 KANEKO S, 1995, CANCER RES, V55, P5283 Kiernan AE, 1997, AUDIOL NEURO-OTOL, V2, P12 Lalwani AK, 1996, GENE THER, V3, P588 Low W, 1996, J CELL PHYSIOL, V167, P443, DOI 10.1002/(SICI)1097-4652(199606)167:3<443::AID-JCP8>3.0.CO;2-P Mondain M, 1998, HUM GENE THER, V9, P1217, DOI 10.1089/hum.1998.9.8-1217 PHILLIPS.JM, 1972, CELL IMMUNOL, V4, P116, DOI 10.1016/0008-8749(72)90011-1 Raphael Y, 1996, NEUROSCI LETT, V207, P137, DOI 10.1016/0304-3940(96)12499-X RIOS CD, 1995, ARTERIOSCL THROM VAS, V15, P2241 SENDTNER M, 1990, NATURE, V345, P440, DOI 10.1038/345440a0 Staecker H, 1997, INT J DEV NEUROSCI, V15, P553, DOI 10.1016/S0736-5748(96)00110-4 Staecker H, 1998, OTOLARYNG HEAD NECK, V119, P7, DOI 10.1016/S0194-5998(98)70194-9 Stover T, 2000, GENE THER, V7, P377, DOI 10.1038/sj.gt.3301108 TANI K, 1995, LEUK S, V1, P64 VILQUIN JT, 1995, HUM GENE THER, V6, P1391, DOI 10.1089/hum.1995.6.11-1391 Wareing M, 1999, HEARING RES, V128, P61, DOI 10.1016/S0378-5955(98)00196-8 Yamasoba T, 1999, HUM GENE THER, V10, P769, DOI 10.1089/10430349950018526 Yang J, 1995, CANCER LETT, V98, P9, DOI 10.1016/S0304-3835(06)80004-2 Zheng JL, 1998, HEARING RES, V117, P13, DOI 10.1016/S0378-5955(97)00205-0 NR 31 TC 25 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 30 EP 40 DI 10.1016/S0378-5955(00)00189-1 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600003 PM 11124449 ER PT J AU Ulfendahl, M Flock, A Scarfone, E AF Ulfendahl, M Flock, A Scarfone, E TI Structural relationships of the unfixed tectorial membrane SO HEARING RESEARCH LA English DT Article DE cochlea; confocal; extracellular; Hensen's stripe; tectorial membrane ID HEARING ORGAN; COCHLEA; MORPHOLOGY; CORTI AB Although the tectorial membrane has a key role in the function of the organ of Corti, its structural relationship within the cochlear partition is still not fully characterised. Being an acellular structure, the tectorial membrane is not readily stained with dyes and is thus difficult to visualise. We present here detailed observations of the unfixed tectorial membrane in an in vitro preparation of the guinea pig cochlea using confocal microscopy. By perfusing the fluid compartments within the cochlear partition with fluorochrome-conjugated dextran solutions, the tectorial membrane stood out against the bright background. The tectorial membrane was seen as a relatively loose structure as indicated by the dextran molecules being able to diffuse within its entire volume. There were, however, regions showing much less staining, demonstrating a heterogeneous organisation of the membrane. Especially Hensen's stripe and regions facing the outer hair cell bundles appeared more condensed. Whereas no connections between Hensen's stripe and the inner hair cell bundles could be observed, then was clearly a contact zone between the stripe and the reticular lamina inside of the inner hair cell. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden. Karolinska Inst, Inst Hearing & Commun Res, Stockholm, Sweden. Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden. Univ Montpellier 2, INSERM, U432, Montpellier, France. RP Ulfendahl, M (reprint author), Karolinska Hosp, M1-00-ENT, SE-17176 Stockholm, Sweden. CR Bekesy G., 1960, EXPT HEARING BORGHESA.C, 1969, PRACT-OTO-RHINO-LARY, V31, P129 DAVIS H, 1958, Ann Otol Rhinol Laryngol, V67, P789 Edge RM, 1998, HEARING RES, V124, P1, DOI 10.1016/S0378-5955(98)00090-2 Flock A, 1999, J NEUROSCI, V19, P4498 Flock A, 1998, NEUROSCIENCE, V83, P215, DOI 10.1016/S0306-4522(97)00335-7 Fridberger A, 1997, ACTA PHYSIOL SCAND, V161, P239, DOI 10.1046/j.1365-201X.1997.00214.x HUNTERDUVAR IM, 1977, SCANNING ELECT MICRO, V2, P421 IURATO S, 1962, Z ZELLFORSCH MIK ANA, V56, P40, DOI 10.1007/BF00326848 Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 Kronester-Frei A, 1978, SCANNING ELECT MICRO, V2, P943 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 RUGGERO MA, 1995, ACTIVE HEARING, P321 SHAH DM, 1995, HEARING RES, V87, P187, DOI 10.1016/0378-5955(95)00089-M Slepecky N. B., 1996, COCHLEA, P44 SPOENDLIN H, 1957, Pract Otorhinolaryngol (Basel), V19, P192 ter Kuile E., 1900, PFLUGERS ARCH GES PH, V79, P146 Ulfendahl M, 2000, NEUROIMAGE, V12, P307, DOI 10.1006/nimg.2000.0617 ULFENDAHL M, 1995, NEUROREPORT, V6, P1157, DOI 10.1097/00001756-199505300-00021 Ulfendahl M, 1997, PROG NEUROBIOL, V53, P331, DOI 10.1016/S0301-0082(97)00040-3 Voldrich L, 1967, Acta Otolaryngol, V63, P503 ZUMGOTTESBERGE AMM, 1993, EUR ARCH OTO-RHINO-L, V250, P88 ZWISLOCKI JJ, 1989, HEARING RES, V42, P211, DOI 10.1016/0378-5955(89)90146-9 NR 26 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 41 EP 47 DI 10.1016/S0378-5955(00)00208-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600004 PM 11124450 ER PT J AU Ren, TY Nuttall, AL AF Ren, TY Nuttall, AL TI Basilar membrane vibration in the basal turn of the sensitive gerbil cochlea SO HEARING RESEARCH LA English DT Article DE gerbil; cochlea; basilar membrane; laser interferometer; vibration ID GUINEA-PIG COCHLEA; INNER-EAR; OTOACOUSTIC EMISSIONS; NONLINEAR MECHANICS; MOSSBAUER TECHNIQUE; CHINCHILLA COCHLEA; MAMMALIAN COCHLEA; HOOK REGION; CAT COCHLEA; HAIR-CELLS AB The basal membrane (BM) velocity responses to pure tones were measured using a newly developed laser interferometer microscope that does not require placing a reflecting object on the BM. It was demonstrated that the instrument is able to measure sub-nanometer vibration from the cochlear partition in the basal turn of the gerbil. The overall shape of the amplitude spectra shows typical tuning features. The 'best frequencies (BFs) for the BR I locations studied were between 14 kHz and 77 kHz, depending on the longitudinal position. For a given BM location, tuning sharpness was input level dependent, indicated by the Q(10dB), which varied from approximately 3 at low stimulus levers to near 1.5 at high input levels, At frequencies below BF, parallel amplitude/frequency curves across stimulus levels indicate a linear growth function. However, at frequencies near BF, the velocity increased linearly at low levels (<40 dB SPL) and became compressed between 40 and 50 dB SPL, Although the velocity gain for the frequency range below BF was a function of frequency, for a given frequency the gains were approximately constant across different levels. At frequencies near BF, the velocity gain at low sound pressure level was greater than that at a high sound pressure level, indicating a nonlinear negative relationship to stimulus level. The data also showed that the BF shifts toward the low frequencies with stimulus intensity increase. The phase spectra showed two important features: (1) at frequencies about half octave below the BF, phase slope is very small, indicating an extremely short delay; (2) the greatest phase lag occurs at frequencies near the BF, indicating a significant delay near this frequency range. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol & Head & Neck Surg, Oregon Hearing Res Ctr NRC04, Portland, OR 97201 USA. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Ren, TY (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol & Head & Neck Surg, Oregon Hearing Res Ctr NRC04, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 Bekesy G., 1960, EXPT HEARING COOPER N, 2000, 23 MIDW RES M ASS RE, P20 COOPER NP, 1992, HEARING RES, V63, P191, DOI 10.1016/0378-5955(92)90084-Z COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X Cooper NP, 1999, J NEUROSCI METH, V88, P93, DOI 10.1016/S0165-0270(99)00017-5 Gummer AW, 1996, P NATL ACAD SCI USA, V93, P8727, DOI 10.1073/pnas.93.16.8727 JOHNSTON.BM, 1967, SCIENCE, V158, P389, DOI 10.1126/science.158.3799.389 Khanna SM, 1998, HEARING RES, V116, P71, DOI 10.1016/S0378-5955(97)00200-1 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P69 Khanna SM, 1999, HEARING RES, V135, P89, DOI 10.1016/S0378-5955(99)00095-7 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KLIAUGA P, 1983, PHYS MED BIOL, V28, P359, DOI 10.1088/0031-9155/28/4/004 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P155, DOI 10.1121/1.395559 MAMMANO F, 1993, NATURE, V365, P838, DOI 10.1038/365838a0 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 Murugasu E, 1996, J NEUROSCI, V16, P325 Nuttall AL, 1999, HEARING RES, V131, P39, DOI 10.1016/S0378-5955(99)00009-X Nuttall AL, 1996, J ACOUST SOC AM, V99, P1556, DOI 10.1121/1.414732 NUTTALL AL, 1991, HEARING RES, V51, P203, DOI 10.1016/0378-5955(91)90037-A Olson ES, 1999, NATURE, V402, P526, DOI 10.1038/990092 OVERSTREET EH, 1998, 21 MIDW RES M ASS RE PATUZZI R, 1983, J ACOUST SOC AM, V74, P1734, DOI 10.1121/1.390282 Ren TY, 1995, HEARING RES, V92, P30, DOI 10.1016/0378-5955(95)00192-1 Ren TY, 1996, NEUROSCI LETT, V207, P167, DOI 10.1016/0304-3940(96)12524-6 RHODE WS, 1993, HEARING RES, V66, P31, DOI 10.1016/0378-5955(93)90257-2 Rhode WS, 1996, AUDIT NEUROSCI, V3, P101 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBERTSO.D, 1974, SCIENCE, V186, P153, DOI 10.1126/science.186.4159.153 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RUGGERO MA, 1991, HEARING RES, V51, P215, DOI 10.1016/0378-5955(91)90038-B Russell IJ, 1997, P NATL ACAD SCI USA, V94, P2660, DOI 10.1073/pnas.94.6.2660 SELLICK PM, 1983, HEARING RES, V10, P101, DOI 10.1016/0378-5955(83)90020-5 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SELLICK PM, 1983, HEARING RES, V10, P93, DOI 10.1016/0378-5955(83)90019-9 TONNDORF J, 1977, ACTA OTO-LARYNGOL, V83, P113, DOI 10.3109/00016487709128820 WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 WILSON JP, 1973, J SOUND VIB, V30, P483, DOI 10.1016/S0022-460X(73)80169-5 XUE SW, 1995, J ACOUST SOC AM, V97, P3030, DOI 10.1121/1.413103 Xue SW, 1996, AUDIT NEUROSCI, V2, P301 NR 42 TC 59 Z9 60 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 48 EP 60 DI 10.1016/S0378-5955(00)00211-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600005 PM 11124451 ER PT J AU Teranishi, M Nakashima, T Wakabayaski, T AF Teranishi, M Nakashima, T Wakabayaski, T TI Effects of alpha-tocopherol on cisplatin-induced ototoxicity in guinea pigs SO HEARING RESEARCH LA English DT Article DE alpha-tocopherol; cisplatin; guinea pig; ototoxicity; free radical ID HIGH-DOSE CISPLATIN; AUDITORY HAIR-CELLS; VITAMIN-E; SODIUM THIOSULFATE; ANTIOXIDANT SYSTEM; HYDROGEN-PEROXIDE; INDUCED DAMAGE; INNER-EAR; 4-METHYLTHIOBENZOIC ACID; ADENOSINE RECEPTORS AB Cisplatin (CDDP), an antitumor agent widely used in the treatment of head and neck cancers, has dose-limiting side effects such as ototoxicity and nephrotoxicity. Recently, evidence has been accumulated to demonstrate that these side effects are closely related to oxidative stress. In the present study, we attempted to suppress CDDP-induced ototoxicity and nephrotoxicity in guinea pigs by administering a-tocopherol, a naturally occurring antioxidant. Hartley albino guinea pigs (250 similar to 300 g) were treated with CDDP (4 mg/kg intraperitoneally (I.P.)) for 3 days in the presence and absence of alpha -tocopherol (50 mg/kg I.P.) injection for 6 days. The combined treatment of animals with alpha -tocopherol distinctly improved the CDDP-induced side effects. These were: loss of Preyer's reflex at high frequencies; distinct elevation of auditory brain stem response threshold at 16 kHz; increased lipid peroxidation in the cochlea determined by the malondialdehyde-thiobarbituric acid method; substantial losses of outer hair cells in the basal and second turns of the cochlea; fragmentation of nuclear DNA detected by the TUNEL method in cochlear hair cells and cells in the stria vascularis; and increases in serum BUN and Cr. These results strongly suggest that alpha -tocopherol suppresses CDDP-induced ototoxicity and nephrotoxicity via the suppression of the increased production of reactive oxygen species. (C) 2001 Elsevier Science B.V. Pill rights reserved. C1 Nagoya Univ, Sch Med, Dept Otorhinolaryngol, Showa Ku, Nagoya, Aichi 4668550, Japan. Nagoya Univ, Sch Med, Dept Cell Biol & Mol Pathol, Showa Ku, Nagoya, Aichi 4668550, Japan. RP Teranishi, M (reprint author), Nagoya Univ, Sch Med, Dept Otorhinolaryngol, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan. RI Nakashima, Tsutomu/B-8259-2012; Teranishi, Masaaki/I-1956-2012 OI Nakashima, Tsutomu/0000-0003-3930-9120; CR Alam SA, 2000, HEARING RES, V141, P28, DOI 10.1016/S0378-5955(99)00211-7 Appenroth D, 1997, ARCH TOXICOL, V71, P677, DOI 10.1007/s002040050444 ATTANASIO G, 1994, HEARING RES, V81, P199, DOI 10.1016/0378-5955(94)90165-1 BARRON SE, 1987, HEARING RES, V26, P131, DOI 10.1016/0378-5955(87)90104-3 BOVERIS A, 1972, BIOCHEM J, V128, P617 BURTON GW, 1983, ARCH BIOCHEM BIOPHYS, V221, P281, DOI 10.1016/0003-9861(83)90145-5 CADENAS E, 1977, ARCH BIOCHEM BIOPHYS, V180, P248, DOI 10.1016/0003-9861(77)90035-2 Campbell KCM, 1996, HEARING RES, V102, P90, DOI 10.1016/S0378-5955(96)00152-9 Campbell KCM, 1999, HEARING RES, V138, P13, DOI 10.1016/S0378-5955(99)00142-2 Chow CK, 1999, FREE RADICAL BIO MED, V27, P580, DOI 10.1016/S0891-5849(99)00121-5 CHURCH MW, 1995, HEARING RES, V86, P195, DOI 10.1016/0378-5955(95)00066-D Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 deGroot JCMJ, 1997, HEARING RES, V106, P9, DOI 10.1016/S0378-5955(96)00213-4 DIRE F, 1993, ANN ONCOL, V4, P55 FERNANDEZCERVILLA F, 1993, ORL J OTO-RHINO-LARY, V55, P337 FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 Ford MS, 1997, HEARING RES, V111, P143, DOI 10.1016/S0378-5955(97)00103-2 Ford MS, 1997, HEARING RES, V105, P130, DOI 10.1016/S0378-5955(96)00204-3 Fritzsch B, 1997, TRENDS NEUROSCI, V20, P159, DOI 10.1016/S0166-2236(96)01007-7 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 GANDARA DR, 1990, CRIT REV ONCOL HEMAT, V10, P353, DOI 10.1016/1040-8428(90)90010-P GAVRIELI Y, 1992, J CELL BIOL, V119, P493, DOI 10.1083/jcb.119.3.493 Heijmen PS, 1999, HEARING RES, V128, P27, DOI 10.1016/S0378-5955(98)00194-4 HOEVE LJ, 1987, ARCH OTORHINOLARYNGO, V245, P98 Kaltenbach JA, 1997, OTOLARYNG HEAD NECK, V117, P493, DOI 10.1016/S0194-5998(97)70020-2 Kamimura T, 1999, HEARING RES, V131, P117, DOI 10.1016/S0378-5955(99)00017-9 Kopke RD, 1997, AM J OTOL, V18, P559 Lautermann J, 1997, HEARING RES, V114, P75, DOI 10.1016/S0378-5955(97)00154-8 LEMPERS ELM, 1990, INORG CHEM, V29, P217, DOI 10.1021/ic00327a014 LOWRY OH, 1951, J BIOL CHEM, V193, P265 MARUBAYASHI S, 1986, SURGERY, V99, P184 MATSURA T, 1992, BIOCHIM BIOPHYS ACTA, V1127, P277, DOI 10.1016/0005-2760(92)90232-K MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 Nair TS, 1999, HEARING RES, V129, P50, DOI 10.1016/S0378-5955(98)00220-2 NAKASHIMA T, 1988, ANN OTO RHINOL LARYN, V97, P146 OHKAWA H, 1978, J LIPID RES, V19, P1053 OTTO WC, 1988, HEARING RES, V35, P79, DOI 10.1016/0378-5955(88)90042-1 OZOLS RF, 1985, SEMIN ONCOL, V12, P21 PIEL IJ, 1974, CANCER CHEMOTH REP 1, V58, P871 Pryor WA, 2000, FREE RADICAL BIO MED, V28, P141, DOI 10.1016/S0891-5849(99)00224-5 RAPHAEL Y, 1994, HEARING RES, V76, P173, DOI 10.1016/0378-5955(94)90098-1 RAVI R, 1995, PHARMACOL TOXICOL, V76, P386 RUBIN JS, 1995, J LARYNGOL OTOL, V109, P744 Rybak LP, 1999, TOXICOL SCI, V47, P195, DOI 10.1093/toxsci/47.2.195 Rybak LP, 1997, PHARMACOL TOXICOL, V81, P173 Rybak LP, 1999, LARYNGOSCOPE, V109, P1740, DOI 10.1097/00005537-199911000-00003 RYBAK LP, 1995, FUND APPL TOXICOL, V26, P293, DOI 10.1006/faat.1995.1100 SADZUKA Y, 1992, TOXICOL LETT, V62, P293 SAITO T, 1995, SCANNING MICROSCOPY, V9, P271 Saito T, 1997, EUR ARCH OTO-RHINO-L, V254, P281, DOI 10.1007/BF02905989 SAKTHISEKARAN D, 1993, MED SCI RES, V21, P35 SCHWEITZER VG, 1987, LARYNGOSCOPE, V10, P517 SCHWEITZER VG, 1986, LARYNGOSCOPE, V96, P948 STEWART DJ, 1987, AM J CLIN ONCOL-CANC, V10, P517, DOI 10.1097/00000421-198712000-00012 STOTER G, 1989, J CLIN ONCOL, V7, P1099 SUGIHARA K, 1986, JPN J PHARMACOL, V40, P353, DOI 10.1254/jjp.40.353 SUGIHARA K, 1987, JPN J PHARMACOL, V43, P247, DOI 10.1254/jjp.43.247 TURRENS JF, 1980, BIOCHEM J, V191, P421 WALKER EM, 1994, ANN CLIN LAB SCI, V24, P121 NR 60 TC 52 Z9 55 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 61 EP 70 DI 10.1016/S0300-2977(00)00080-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600006 PM 11124452 ER PT J AU Husain, K Scott, RB Whitworth, C Somani, SM Rybak, LP AF Husain, K Scott, RB Whitworth, C Somani, SM Rybak, LP TI Dose response of carboplatin-induced hearing loss in rats: antioxidant defense system SO HEARING RESEARCH LA English DT Article DE carboplatin; hearing loss; cochlear antioxidant; lipid peroxidation; rat ID CISPLATIN-INDUCED OTOTOXICITY; OVARIAN-CANCER; GLUTATHIONE PROTECTION; SUPEROXIDE-DISMUTASE; SODIUM THIOSULFATE; LIPOIC ACID; TOXICITY; DIETHYLDITHIOCARBAMATE; NEPHROTOXICITY; CARCINOMA AB Carboplatin, a platinum-containing anticancer drug, is currently being used against a variety of cancers. However, a single high dose of carboplatin is ototoxic in cancer patients. This is the first study to show carboplatin-induced hearing loss in a rat model. Male Wistar rats were divided into five groups and treated as follows: (I) control (saline, intraperitoneally (i.p.)); (2) carboplatin (64 mg/kg, i.p.); (3) carboplatin (128 mg/kg i.p.); (4) carboplatin (192 mg/kg, i.p.) and (5) carboplatin (256 mg/kg, i.p.). Animals in all groups were sedated with ketamine/xylazine and auditory brain-evoked responses (ABRs) were recorded before and 4 days after treatments. The animals were sacrificed on the fourth day and cochleae were harvested and analyzed. Carboplatin dose-dependently decreased body weight. However, at higher doses of carboplatin (192 and 256 mg/kg), there was a significant elevation of hearing threshold shifts at clicks, 4, 8, 16 and 32 kHz tone burst stimuli. The higher doses of carboplatin (192 and 256 mg/kg) significantly increased cochlear lipid peroxidation (132 and 146% of control) and depleted cochlear glutathione levels (66 and 63% of control), respectively. The antioxidant enzyme activities such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase (GST) depressed significantly at higher doses of carboplatin. The data suggest that higher doses of carboplatin (above 128 mg/kg) induce hearing loss as evidenced by significant changes in ABRs, lipid peroxidation and antioxidants in the cochlea of rats. (C) 2001 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. So Illinois Univ, Sch Med, Dept Surg, Springfield, IL 62794 USA. RP Husain, K (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, 801 N Rutledge, Springfield, IL 62794 USA. CR AEBI H, 1984, METHOD ENZYMOL, V105, P121 ALBERTS DS, 1995, SEMIN ONCOL, V22, P88 ANDERSON ME, 1990, FASEB J, V4, P3251 BAUER FP, 1992, LARYNGO RHINO OTOL, V71, P412, DOI 10.1055/s-2007-997325 Bishop J F, 1992, Semin Oncol, V19, P150 Blommaert FA, 1996, CANCER CHEMOTH PHARM, V38, P273, DOI 10.1007/s002800050482 Bohm S, 1999, ONCOLOGY-BASEL, V57, P115, DOI 10.1159/000012017 CARLBERG I, 1985, METHOD ENZYMOL, V113, P484 Cavaletti G, 1998, ANTICANCER RES, V18, P3797 CHURCH MW, 1995, HEARING RES, V86, P195, DOI 10.1016/0378-5955(95)00066-D CLERICI WJ, 1995, HEARING RES, V84, P30, DOI 10.1016/0378-5955(95)00010-2 Conlon BJ, 1999, HEARING RES, V128, P40, DOI 10.1016/S0378-5955(98)00195-6 De Lauretis A, 1999, SCAND AUDIOL, V28, P139 DELEVE LD, 1990, SEMIN LIVER DIS, V10, P251, DOI 10.1055/s-2008-1040481 DEWOSKIN RS, 1992, TOXICOL APPL PHARM, V112, P182, DOI 10.1016/0041-008X(92)90186-V Ettinger DS, 1998, ONCOLOGY-NY, V12, P36 FARISS MW, 1987, METHOD ENZYMOL, V143, P101 FLOHE L, 1984, METHOD ENZYMOL, V105, P114 FONTANELLI R, 1992, ANN ONCOL, V3, P117 HAMERS FPT, 1993, CANCER RES, V53, P544 HAMILTON TC, 1985, BIOCHEM PHARMACOL, V34, P2583, DOI 10.1016/0006-2952(85)90551-9 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 Hu BH, 1999, HEARING RES, V128, P125, DOI 10.1016/S0378-5955(98)00210-X Husain K, 1998, MOL CELL BIOCHEM, V178, P127, DOI 10.1023/A:1006889427520 IKEDA K, 1993, ACTA OTO-LARYNGOL, V113, P137, DOI 10.3109/00016489309135781 ISHIKAWA T, 1992, TRENDS BIOCHEM SCI, V17, P463, DOI 10.1016/0968-0004(92)90489-V KENNEDY ICS, 1990, CANCER CHEMOTH PHARM, V26, P232, DOI 10.1007/BF02897206 MACDONALD MR, 1994, J OTOLARYNGOL, V23, P151 MALDOON LL, 2000, CLIN CANCER RES, V6, P309 MISRA HP, 1972, J BIOL CHEM, V247, P3170 Mount R J, 1995, Acta Otolaryngol Suppl, V519, P60 Neuwelt EA, 1998, J PHARMACOL EXP THER, V286, P77 NONCLERCQ D, 1989, EXP MOL PATHOL, V51, P123, DOI 10.1016/0014-4800(89)90013-0 Obermair A, 1998, INT J ONCOL, V13, P1023 OHKAWA H, 1979, ANAL BIOCHEM, V95, P351, DOI 10.1016/0003-2697(79)90738-3 PIGEOLET E, 1990, MECH AGEING DEV, V51, P283, DOI 10.1016/0047-6374(90)90078-T RAVI R, 1995, PHARMACOL TOXICOL, V76, P386 READ SM, 1981, ANAL BIOCHEM, V116, P53, DOI 10.1016/0003-2697(81)90321-3 Rybak LP, 1999, TOXICOL SCI, V47, P195, DOI 10.1093/toxsci/47.2.195 RYBAK LP, 1981, J LARYNGOL OTOL, V95, P745, DOI 10.1017/S0022215100091374 RYBAK LP, 1995, FUND APPL TOXICOL, V26, P293, DOI 10.1006/faat.1995.1100 SIDDIK ZH, 1987, BRIT J CANCER, V55, P375, DOI 10.1038/bjc.1987.75 SMITH VC, 1989, GLUTATHIONE CHEM BIO, P141 Song BB, 1996, HEARING RES, V94, P87, DOI 10.1016/0378-5955(96)00003-2 TAUDY M, 1992, AUDIOLOGY, V31, P293 VANDERHULST RJAM, 1988, ANN OTO RHINOL LARYN, V97, P133 WAKE M, 1994, LARYNGOSCOPE, V104, P488 Wandt H, 1999, BONE MARROW TRANSPL, V23, P763, DOI 10.1038/sj.bmt.1701659 WOLFGANG GHI, 1994, FUND APPL TOXICOL, V22, P73, DOI 10.1006/faat.1994.1010 YOUNES M, 1981, CHEM-BIOL INTERACT, V34, P257, DOI 10.1016/0009-2797(81)90098-3 NR 50 TC 24 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 71 EP 78 DI 10.1016/S0300-2977(00)00081-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600007 PM 11124453 ER PT J AU Miller, CA Robinson, BK Rubinstein, JT Abbas, PJ Runge-Samuelson, CL AF Miller, CA Robinson, BK Rubinstein, JT Abbas, PJ Runge-Samuelson, CL TI Auditory nerve responses to monophasic and biphasic electric stimuli SO HEARING RESEARCH LA English DT Article DE auditory prosthesis; electric stimulation; cochlear nerve; evoked potential; auditory nerve fiber; cat; guinea pig; monophasic; biphasic ID PSYCHOPHYSICAL DETECTION THRESHOLDS; ACTION-POTENTIALS; MYELINATED NERVE; ETHACRYNIC-ACID; GUINEA-PIGS; DURATION; FIBER; COCHLEA; MODEL; CAT AB Charge-balanced, biphasic stimulus pulses are commonly used in implantable cochlear prostheses as they can be safely delivered to living tissue. However, monophasic stimuli are more efficient (i.e. producing lower thresholds) and likely provide more spatially selective excitation of nerve fibers. We examined the neural responses to monophasic, 'pseudomonophasic', and biphasic stimuli to better understand the inherent tradeoffs of these stimuli. Using guinea pig and cat animal models, we compared the auditory nerve responses to both 40 mus monophasic and 30 mus/phase biphasic stimuli using both electrically evoked compound action potential and single-fiber recordings. We also made comparisons using a computational model of the feline auditory nerve fiber. In all cases, our stimuli were cathodic monophasic and cathodic-first biphasic pulses. As expected, monophasic stimuli provided lower thresholds relative to biphasic stimuli. They also evoked responses with relatively longer latencies. We also examined responses to charge-balanced biphasic pulses composed of two phases of differing duration (i.e. pseudomonophasic stimuli). The first phase was fixed at 40 mus, while the second phase was systematically varied from 40 to 4000 Irs. With a relatively long second phase, we hypothesized that these stimuli would provide some of the beneficial features of monophasic stimuli. Both the gross-potential and single-fiber data confirmed this and indicate that the largest incremental effects of changing the second-phase duration occur for durations less than 500 mus. Consideration of single-fiber data and computer simulations suggest that these results are consistent with the neural membrane acting as a leaky integrator. The computer simulations also suggest that the integrative properties at least partially account for the difference between our monophasic-biphasic results and previously published data. Our results apply to cathodic-leading stimuli; due to differing patterns of membrane depolarization, they may not be applicable to situations using anodic-leading stimuli. Finally, we observed differences between the guinea pig and cat response patterns. Compared to cats, guinea pigs produced smaller monophasic vs. biphasic threshold differences. This interspecies disparity may be due to differences in cochlear anatomy. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Iowa Hosp & Clin, Dept Otolaryngol Head & Neck Surg, Iowa City, IA 52242 USA. Univ Iowa, Dept Speech Pathol & Audiol, Iowa City, IA 52242 USA. Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52242 USA. RP Miller, CA (reprint author), Univ Iowa Hosp & Clin, Dept Otolaryngol Head & Neck Surg, 21201 PFP,200 Hawkins Dr, Iowa City, IA 52242 USA. CR ABBAS PJ, 1991, HEARING RES, V51, P139, DOI 10.1016/0378-5955(91)90012-X BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P59 BRUMMER SB, 1983, ANN NY ACAD SCI, V405, P159, DOI 10.1111/j.1749-6632.1983.tb31628.x Coste RL, 1996, J ACOUST SOC AM, V99, P3099, DOI 10.1121/1.414796 Frijns JHM, 1996, HEARING RES, V95, P33, DOI 10.1016/0378-5955(96)00004-4 Kandel E. R., 2000, PRINCIPLES NEURAL SC McIntyre CC, 2000, ANN BIOMED ENG, V28, P219, DOI 10.1114/1.262 Miller CA, 1998, HEARING RES, V119, P142, DOI 10.1016/S0378-5955(98)00046-X Miller CA, 1995, HEARING RES, V92, P85, DOI 10.1016/0378-5955(95)00204-9 Miller CA, 1999, HEARING RES, V135, P1, DOI 10.1016/S0378-5955(99)00081-7 Miller CA, 1999, HEARING RES, V130, P197, DOI 10.1016/S0378-5955(99)00012-X Miller CA, 2000, EAR HEARING, V21, P280, DOI 10.1097/00003446-200008000-00003 MINO H, 2000, NO1DC92106 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 RATTAY F, 1986, IEEE T BIO-MED ENG, V33, P974, DOI 10.1109/TBME.1986.325670 RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 Shepherd RK, 1999, HEARING RES, V130, P171, DOI 10.1016/S0378-5955(99)00011-8 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VANDENHONERT C, 1979, ANN BIOMED ENG, V7, P117 Verveen A. A., 1961, FLUCTUATION EXCITABI WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 White JA, 2000, TRENDS NEUROSCI, V23, P131, DOI 10.1016/S0166-2236(99)01521-0 XU SA, 1993, HEARING RES, V70, P205, DOI 10.1016/0378-5955(93)90159-X NR 23 TC 34 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 79 EP 94 DI 10.1016/S0300-2977(00)00082-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600008 PM 11124454 ER PT J AU Portfors, CV Wenstrup, JJ AF Portfors, CV Wenstrup, JJ TI Topographical distribution of delay-tuned responses in the mustached bat inferior colliculus SO HEARING RESEARCH LA English DT Article DE delay-tuned; combination-sensitive; inferior colliculus; mustached bat; spectral integration ID COMBINATION-SENSITIVE NEURONS; MEDIAL GENICULATE-BODY; AUDITORY-CORTEX; MOUSTACHED BAT; TARGET RANGE; COMPLEX SOUNDS; REPRESENTATION; ORGANIZATION; LATENCY; INFORMATION AB In the mustached bat, delay-tuned neurons respond best to specific delays between the first harmonic frequency modulated (FM) component (FM1; 24-29 kHz) of the emitted biosonar pulse and a higher harmonic FM component in returning echoes (e.g. FM3, 72-89 kHz). These delay-tuned, combinatorial responses predominate in the inferior colliculus (IC) of the mustached bat. This study examined the topographical distribution of delay-tuned neurons in the 72-89 kHz frequency representation of the IC. We recorded and histologically localized 163 single units. Ninety units were facilitated and 41 were inhibited by the combination of two frequencies in the 24-29 kHz and 72-89 kHz ranges. The facilitatory responses were selective for delays up to 20 ms between the two signals. To determine if delay-tuned neurons were topographically organized: we plotted the dorsomedio-ventrolateral and caudorostral positions of each unit versus its best delay. Best delay was not correlated with either location. Response latency to best frequency tones was topographically organized, but was not correlated with best delay. This indicates that the latency axis in the IC is unrelated to the delay tuning of these combinatorial neurons. Because delay-tuned neurons are not topographically organized in the IC but are in the auditory cortex, our findings suggest that the creation and organization of delay-tuned neurons occur at different stages in the ascending auditory system. (C) 2001 Elsevier Science B.V. All rights reserved. C1 NE Ohio Univ, Coll Med, Dept Neurobiol & Pharmacol, Rootstown, OH 44272 USA. RP Portfors, CV (reprint author), NE Ohio Univ, Coll Med, Dept Neurobiol & Pharmacol, 4209 State Route 44,POB 95, Rootstown, OH 44272 USA. CR Brosch M, 1999, J NEUROPHYSIOL, V82, P1542 Doupe AJ, 1997, J NEUROSCI, V17, P1147 EDAMATSU H, 1993, J NEUROPHYSIOL, V69, P1700 Fitzpatrick DC, 1998, J COMP NEUROL, V391, P353 FITZPATRICK DC, 1993, J NEUROSCI, V13, P931 Fitzpatrick DC, 1998, J COMP NEUROL, V391, P366 FRITZ J, 2000, ASS RES OT ABSTR, V86, P301 FUZESSERY ZM, 1983, J COMP PHYSIOL, V150, P333 Hattori T, 1997, J COMP PHYSIOL A, V180, P271, DOI 10.1007/s003590050047 LANGNER G, 1987, HEARING RES, V31, P197, DOI 10.1016/0378-5955(87)90127-4 LEROY SA, 1999, ASS RES OT ABSTR, V22, P219 MARGOLIASH D, 1992, J NEUROSCI, V12, P4309 MITTMANN DH, 1995, HEARING RES, V90, P185, DOI 10.1016/0378-5955(95)00164-X Ohlemiller KK, 1996, NEUROREPORT, V7, P1749, DOI 10.1097/00001756-199607290-00011 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1275 ONEILL WE, 1979, SCIENCE, V203, P69, DOI 10.1126/science.758681 ONEILL WE, 1982, J NEUROSCI, V2, P17 PARK TJ, 1993, J NEUROSCI, V13, P5172 PORTFORS CV, 1999, ABSTR SOC NEUROSCI, V25, P396 Portfors CV, 1999, J NEUROPHYSIOL, V82, P1326 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 Rauschecker JP, 1997, J COMP NEUROL, V382, P89 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SCHULLER G, 1991, EUR J NEUROSCI, V3, P1165, DOI 10.1111/j.1460-9568.1991.tb00051.x SIMMONS JA, 1973, J ACOUST SOC AM, V54, P157, DOI 10.1121/1.1913559 SUGA N, 1986, J NEUROPHYSIOL, V55, P776 SUGA N, 1990, COLD SH Q B, V55, P585 SUGA N, 1979, SCIENCE, V206, P351, DOI 10.1126/science.482944 SUGA N, 1979, SCIENCE, V203, P270, DOI 10.1126/science.760193 SUGA N, 1983, J NEUROPHYSIOL, V49, P1573 WENSTRUP JJ, 1995, J NEUROSCI, V15, P4693 WENSTRUP JJ, 1994, J COMP NEUROL, V346, P207, DOI 10.1002/cne.903460204 WENSTRUP JJ, 2000, ECHOLOCATION BATS DO Wenstrup JJ, 1999, J NEUROPHYSIOL, V82, P2528 Wenstrup JJ, 1999, J COMP NEUROL, V409, P509, DOI 10.1002/(SICI)1096-9861(19990712)409:4<509::AID-CNE1>3.0.CO;2-S Yan J, 1996, HEARING RES, V93, P102, DOI 10.1016/0378-5955(95)00209-X ZOOK JM, 1985, J COMP NEUROL, V231, P530, DOI 10.1002/cne.902310410 NR 37 TC 28 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 95 EP 105 DI 10.1016/S0378-5955(00)00214-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600009 PM 11124455 ER PT J AU Jero, J Tseng, CJ Mhatre, AN Lalwani, AK AF Jero, J Tseng, CJ Mhatre, AN Lalwani, AK TI A surgical approach appropriate for targeted cochlear gene therapy in the mouse SO HEARING RESEARCH LA English DT Article DE mouse; inner ear; surgical anatomy; gene therapy ID RAT MIDDLE-EAR; STAPEDIAL ARTERY; OTITIS-MEDIA; ANATOMY; MEMBRANE AB Therapeutic manipulations of the mammalian cochlea, including cochlear gene transfer, have been predominantly studied using the guinea pig as the experimental model. With the significant developments in mouse genomics and the availability of mutant strains of mice with well-characterized hearing loss, the mouse justifiably will be the preferred animal model for therapeutic manipulations. However, the potential advantages of the mouse model have not been fully realized due to the surgical difficulty of accessing its small cochlea. This study describes a ventral approach, instead of the routinely;sed postauricular approach in other rodents, for accessing the mouse middle and inner ear, and its application in cochlear gene transfer. This ventral approach enabled rapid and direct delivery of liposome-transgene complex to the mouse inner ear while avoiding blood loss, facial nerve morbidity, and mortality. Transgene expression at 3 days was detected in Reissner's membrane, spiral limbus, spiral ligament, and spiral ganglion cells, in a pattern similar to that previously described in the guinea pig. The successful access and delivery of material to the mouse cochlea and the replication of gene expression seen in the guinea pig demonstrated in this study should promote the use of the mouse in future studies investigating targeted cochlear therapy. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, Epstein Labs, Lab Mol Otol, San Francisco, CA 94143 USA. Univ Helsinki, Cent Hosp, Dept Otolaryngol, FIN-00029 Huch, Finland. RP Lalwani, AK (reprint author), Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, Epstein Labs, Lab Mol Otol, 533 Parnassus Ave,U 490A, San Francisco, CA 94143 USA. CR ALBIIN N, 1985, ANAT REC, V212, P17, DOI 10.1002/ar.1092120103 ALBIIN N, 1983, ACTA ANAT, V115, P134 Alzamil KS, 2000, ANN OTO RHINOL LARYN, V109, P30 Anson B. J., 1967, SURG ANATOMY TEMPORA ASARCH R, 1975, ANN OTO RHINOL LARYN, V84, P250 BUGGE J, 1970, ACTA ANAT, V76, P313 Flotte TR, 1997, PEDIATR CLIN N AM, V44, P153, DOI 10.1016/S0031-3955(05)70468-5 HELLSTROM S, 1982, ACTA ANAT, V112, P346 Hellstrom SOM, 1998, OTOLARYNG HEAD NECK, V119, P556 JOHANSSON U, 1993, ANN OTO RHINOL LARYN, V102, P227 Judkins RF, 1997, OTOLARYNG HEAD NECK, V117, P438, DOI 10.1016/S0194-5998(97)70011-1 KUCUK B, 1989, ARCH HISTOL CYTOL, V52, P173 SEHITOGLU M I, 1990, Ear Nose and Throat Journal, V69, P91 Steel KP, 1999, TRENDS GENET, V15, P207, DOI 10.1016/S0168-9525(99)01753-9 Steel KP, 1995, ANNU REV GENET, V29, P675 Wareing M, 1999, HEARING RES, V128, P61, DOI 10.1016/S0378-5955(98)00196-8 NR 16 TC 52 Z9 56 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 106 EP 114 DI 10.1016/S0378-5955(00)00216-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600010 PM 11124456 ER PT J AU Alegre, M Gurtubay, IG Iriarte, J Ciordia, E Manrique, M Artieda, J AF Alegre, M Gurtubay, IG Iriarte, J Ciordia, E Manrique, M Artieda, J TI Brainstem auditory evoked potentials (BAEPs) in the cynomolgus macaque monkey - Equivalence with human BAEPs and proposal of a new nomenclature SO HEARING RESEARCH LA English DT Article DE brain-stem auditory evoked potential (BAEP); monkey; inter-peak interval; intensity ID STEM RESPONSE; MACACA-MULATTA; RHESUS-MONKEY; MATURATION; GENERATORS AB Several groups have studied brainstem auditory evoked potentials (BAEPs) in non-human primates. However, the nomenclature of the waves elicited and their correspondence with human waves I-V differ among authors. BAEPs were recorded from six anaesthetised young cynomolgus macaques (Macaca fascicularis), using different. sound stimuli parameters. A constant pattern of four main waveforms was present in all the animals with stimulus intensities over 60 dB SPL, although up to four smaller waveforms were observed in some of the individuals. Latency values increased with decreasing stimulus intensities and with increasing repetition rates. These results were similar to the BAEPs observed in other species of macaques. Although an approximate equivalence between human and monkey BAEPs is possible, some discrepancies suggest that there may be generators which contribute to different waves in both species. This is the reason for our proposal of a new nomenclature for BAEP waveforms in monkeys, following a descriptive order with arabic numerals preceded by the letter M. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Navarra Clin, Dept Neurol, Expt Neurophysiol Unit, E-31008 Pamplona, Spain. Univ Navarra, Fac Med, E-31008 Pamplona, Spain. Univ Navarra Clin, Dept Ear Nose & Throat, E-31008 Pamplona, Spain. RP Artieda, J (reprint author), Univ Navarra Clin, Dept Neurol, Expt Neurophysiol Unit, Ave Pio XII,36, E-31008 Pamplona, Spain. RI Alegre, Manuel/F-5379-2011; Artieda, Julio/L-4704-2014 OI Alegre, Manuel/0000-0003-4985-9724; Artieda, Julio/0000-0003-0987-0873 CR ALLEN AR, 1978, ELECTROEN CLIN NEURO, V45, P53, DOI 10.1016/0013-4694(78)90341-3 BULLOCK TH, 1979, J COMP PHYSIOL, V129, P223 DOYLE WJ, 1985, ELECTROEN CLIN NEURO, V60, P258, DOI 10.1016/0013-4694(85)90040-9 DOYLE WJ, 1983, ELECTROEN CLIN NEURO, V56, P210, DOI 10.1016/0013-4694(83)90075-5 FULLERTON BC, 1987, ELECTROEN CLIN NEURO, V66, P547, DOI 10.1016/0013-4694(87)90102-7 HUANG C, 1980, BRAIN RES, V184, P215, DOI 10.1016/0006-8993(80)90601-0 Insausti AM, 1999, J COMP NEUROL, V414, P485 JEWETT DL, 1971, BRAIN, V94, P681, DOI 10.1093/brain/94.4.681 KAMADA T, 1991, J MED PRIMATOL, V20, P284 LASKY RE, 1995, HEARING RES, V89, P212, DOI 10.1016/0378-5955(95)00140-7 LEGATT AD, 1986, ELECTROEN CLIN NEURO, V64, P53, DOI 10.1016/0013-4694(86)90043-X LEGATT AD, 1986, ELECTROEN CLIN NEURO, V64, P41, DOI 10.1016/0013-4694(86)90042-8 LINDBURG DG, 1980, NOSTRAND REINHOLD PR Manrique M, 2000, ANN OTO RHINOL LARYN, V109, P163 MOLLER AR, 1986, ELECTROEN CLIN NEURO, V65, P361, DOI 10.1016/0168-5597(86)90015-8 Moore JK, 1996, EAR HEARING, V17, P411, DOI 10.1097/00003446-199610000-00007 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 PINEDA JA, 1989, ELECTROEN CLIN NEURO, V73, P532, DOI 10.1016/0013-4694(89)90262-9 Ponton CW, 1996, EAR HEARING, V17, P402, DOI 10.1097/00003446-199610000-00006 Rosenblum L. A., 1968, SQUIRREL MONKEY STRAIN GM, 1986, ELECTROENCEPHALOGR C, V67, P68 VELASCO M, 1984, INT J NEUROSCI, V22, P235, DOI 10.3109/00207458408990681 VELASCO M, 1982, INT J NEUROSCI, V17, P199 NR 23 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 115 EP 120 DI 10.1016/S0378-5955(00)00215-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600011 PM 11124457 ER PT J AU Terunuma, T Hara, A Senarita, M Motohashi, H Kusakari, J AF Terunuma, T Hara, A Senarita, M Motohashi, H Kusakari, J TI Effect of acoustic overstimulation on regulation of glucocorticoid receptor mRNA in the cochlea of the guinea pig SO HEARING RESEARCH LA English DT Article DE glucocorticoid receptor; mRNA; acoustic overstimulation ID INNER-EAR; TRAUMA AB Semi-quantitative reverse transcription polymerase chain reaction was performed to determine the distribution of mRNA levels of glucocorticoid receptor (GR) within the guinea pig cochlea and to examine the change in their expression after acoustic overstimulation. Using an original PCR primer for the guinea pig, the highest GR mRNA level was revealed in the modiolus and lowest in the medial portion including the organ of Corti. Total RNA was extracted from the whole cochlea of the guinea pig 0, 2, 6 and 24 h after exposure to a 2 kHz pure tone of 110, 120 or 130 dB SPL for 10 min. The level of GR mRNA significantly decreased immediately and 2 h after exposure to the sound of 120 dB SPL, and 2 and 6 h after exposure to that of 130 dB SPL. These results suggest the presence of a down-regulation of GR mRNA induced by acoustic overstimulation, although the exact mechanism of this phenomenon remains unsolved. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. Univ Tsukuba, Inst Basic Med Sci, Tsukuba, Ibaraki 3058575, Japan. Univ Tsukuba, Ctr Tsukuba Adv Res Alliance, Tsukuba, Ibaraki 3058575, Japan. RP Hara, A (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR KEIGHTLEY MC, 1994, MOL ENDOCRINOL, V8, P431, DOI 10.1210/me.8.4.431 MULLER M, 1991, BIOCHIM BIOPHYS ACTA, V1088, P171, DOI 10.1016/0167-4781(91)90052-N Rarey KE, 1996, OTOLARYNG HEAD NECK, V115, P38, DOI 10.1016/S0194-5998(96)70133-X RAREY KE, 1993, HEARING RES, V64, P205, DOI 10.1016/0378-5955(93)90007-N RAREY KE, 1995, HEARING RES, V82, P135, DOI 10.1016/0378-5955(94)00171-L ROSEWICZ S, 1988, J BIOL CHEM, V263, P2581 SPOENDLI.H, 1973, ACTA OTO-LARYNGOL, V75, P220, DOI 10.3109/00016487309139699 Takahashi K, 1996, ACTA OTO-LARYNGOL, V116, P209, DOI 10.3109/00016489609137825 TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 Tsuiki T., 1981, J OTOLARYNGOL JPN, V84, P740 NR 10 TC 15 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 121 EP 124 DI 10.1016/S0378-5955(00)00218-5 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600012 PM 11124458 ER PT J AU Sekiya, T Shimamura, N Suzuki, S Hatayama, T AF Sekiya, T Shimamura, N Suzuki, S Hatayama, T TI Methylprednisolone ameliorates cochlear nerve degeneration following mechanical injury SO HEARING RESEARCH LA English DT Article DE animal experimental model; cochlear nerve; inflammation; macrophage; methylprednisolone; nerve degeneration ID SPINAL-CORD INJURY; CONTROLLED TRIAL; HISTOPATHOLOGY; INFLAMMATION; MACROPHAGES; INHIBITION; NALOXONE; NEURONS; AXONS; RAT AB We investigated whether methylprednisolone sodium succinate can ameliorate cochlear nerve degeneration following compression injury on the cerebellopontine angle portion of the cochlear nerve, using a quantitative animal experimental model that we have developed recently. In this model, cochlear nerve degeneration after compression could be quantitatively evaluated, while cochlear ischemia induced by the compression carefully maintained below the critical limit that causes irreversible damage to the cochlea. Eleven rats were treated with methylprednisolone during the pre- and post-compression period. Two weeks after compression, the numbers of SGC were compared between the rats that received the compression without and with methylprednisolone treatment. Methylprednisolone treatment improved the survival of SGC following cochlear nerve injury statistically highly significantly in the basal turn where the traumatic stress had been less than in the other cochlear turns in our experimental setting. Although it was not statistically significant, greater survival was also observed in the other cochlear turns. The results of this experimental study indicated that at least a portion of injured cochlear nerve had been potentially treatable, and that methylprednisolone might prevent such cochlear neurons from entering into the Vicious process of irreversible damaging process. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Hirosaki Univ, Sch Med, Dept Neurosurg, Hirosaki, Aomori 0368216, Japan. RP Sekiya, T (reprint author), Hirosaki Univ, Sch Med, Dept Neurosurg, 5 Zaifu Cho, Hirosaki, Aomori 0368216, Japan. CR Amar AP, 1999, NEUROSURGERY, V44, P1027, DOI 10.1097/00006123-199905000-00052 BARTHOLDI D, 1995, BRAIN RES, V672, P177, DOI 10.1016/0006-8993(94)01410-J Berthold C H, 1977, Acta Physiol Scand Suppl, V446, P23 BLIGHT AR, 1983, NEUROSCIENCE, V10, P521, DOI 10.1016/0306-4522(83)90150-1 Blight A R, 1985, Cent Nerv Syst Trauma, V2, P299 BRACKEN MB, 1992, J NEUROSURG, V76, P23, DOI 10.3171/jns.1992.76.1.0023 Bracken MB, 1997, JAMA-J AM MED ASSOC, V277, P1597, DOI 10.1001/jama.277.20.1597 BRACKEN MB, 1990, NEW ENGL J MED, V322, P1405, DOI 10.1056/NEJM199005173222001 Carlson SL, 1998, EXP NEUROL, V151, P77, DOI 10.1006/exnr.1998.6785 Clark G M, 1988, Acta Otolaryngol Suppl, V448, P1 DUSART I, 1994, EUR J NEUROSCI, V6, P712, DOI 10.1111/j.1460-9568.1994.tb00983.x ELDRIDGE R, 1992, ACOUSTIC NEUROMA, P989 FEHLINGS MG, 1995, EXP NEUROL, V132, P220, DOI 10.1016/0014-4886(95)90027-6 GIULIAN D, 1990, ANN NEUROL, V27, P33, DOI 10.1002/ana.410270107 Hall E.D., 1997, PRIMER CEREBROVASCUL, P200 HIRSCHBERG DL, 1994, J NEUROIMMUNOL, V50, P9, DOI 10.1016/0165-5728(94)90209-7 HSU C Y, 1990, Journal of Neurotrauma, V7, P115, DOI 10.1089/neu.1990.7.115 LINTHICUM FH, 1991, AM J OTOL, V12, P245 MORGAN WE, 1994, LARYNGOSCOPE, V104, P426 Oudega M, 1999, EUR J NEUROSCI, V11, P2453, DOI 10.1046/j.1460-9568.1999.00666.x PERRY VH, 1993, TRENDS NEUROSCI, V16, P268, DOI 10.1016/0166-2236(93)90180-T SCHUKNECHT HF, 1953, LARYNGOSCOPE, V63, P441 Sekiya T, 2000, EXP NEUROL, V161, P490, DOI 10.1006/exnr.1999.7280 SEKIYA T, 1987, J NEUROSURG, V67, P244, DOI 10.3171/jns.1987.67.2.0244 Sekiya T, 2000, J NEUROSURG, V93, P90, DOI 10.3171/jns.2000.93.1.0090 SPOENDLIN H, 1987, EVOKED ELECT ACTIVIT, P21 TATOR CH, 1991, J NEUROSURG, V75, P15, DOI 10.3171/jns.1991.75.1.0015 THERY C, 1991, EUR J NEUROSCI, V3, P1155, DOI 10.1111/j.1460-9568.1991.tb00050.x Xu J, 1998, MOL BRAIN RES, V59, P135, DOI 10.1016/S0169-328X(98)00142-9 NR 29 TC 24 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 125 EP 132 DI 10.1016/S0378-5955(00)00219-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600013 PM 11124459 ER PT J AU Nakazawa, K AF Nakazawa, K TI Ultrastructural localization of calmodulin in gerbil cochlea by immunogold electron microscopy SO HEARING RESEARCH LA English DT Article DE calmodulin; Ca2+ binding protein; cochlea; immunohistochemistry; immunoelectron microscopy; Boettcher cell ID CALCIUM-BINDING PROTEINS; OUTER HAIR-CELLS; INNER-EAR; IMMUNOHISTOCHEMICAL LOCALIZATION; ORGAN; CORTI; IMMUNOLOCALIZATION; NA,K-ATPASE; ATPASE; NERVE AB Localization of calmodulin, a calcium binding protein, was identified in adult gerbil cochleas using paraffin section immunohistochemistry and immunogold electron microscopy with monoclonal antibody against bovine calmodulin. Immunoreactive calmodulin was abundant in inner hair cells (IHCs), outer hair cells (OHCs) and Boettcher cells of the cochleas. Other cell types containing calmodulin were marginal cells and basal cells of the stria vascularis, fibrocytes in the spiral ligament, spiral ganglion neurons and Vascular smooth muscle cells. Immunogold labeling for calmodulin was observed in cuticular plate, stereocilia, and within cytoplasm of IHCs and OHCs. In OHCs the labeling was mostly observed in the region underlying lateral wall corresponding to subsurface cisterna. In IHCs the staining was diffuse in the cytoplasm and denser than that in OHCs. Boettcher cells showed dense staining along the microvillous projections facing to the intercellular spaces between Boettcher cells and Claudius cells and between the neighboring Boettcher cells. These distributions of calmodulin in the hair cells consist with the assumption that IHCs act as a true neurotransducer and OHCs as an active bi-directional mechanotransducer. The rich presence of calmodulin in Boettcher cells suggests that the cells may involve in mediating Ca2+ regulation and play a distinctive active role in ion transport. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Shinshu Univ, Sch Med, Dept Pathol, Matsumoto, Nagano 3908621, Japan. RP Nakazawa, K (reprint author), Shinshu Univ, Sch Med, Dept Pathol, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan. CR ANDRESSEN C, 1993, CELL TISSUE RES, V271, P181, DOI 10.1007/BF00318606 AUGUSTINE GJ, 1987, ANNU REV NEUROSCI, V10, P633 BABU YS, 1985, NATURE, V315, P37, DOI 10.1038/315037a0 BAIMBRIDGE KG, 1982, BRAIN RES, V239, P519, DOI 10.1016/0006-8993(82)90526-1 CARAFOLI E, 1987, ANNU REV BIOCHEM, V56, P395, DOI 10.1146/annurev.biochem.56.1.395 CORWIN JT, 1991, ANNU REV NEUROSCI, V14, P301, DOI 10.1146/annurev.neuro.14.1.301 DALLOS P, 1992, J NEUROSCI, V12, P4575 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 HENSON MM, 1982, HEARING RES, V7, P91, DOI 10.1016/0378-5955(82)90083-1 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 Imamura SI, 1996, ANAT EMBRYOL, V194, P407 IQBAL Z, 1978, J NEUROCHEM, V31, P409, DOI 10.1111/j.1471-4159.1978.tb02656.x KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X Koyama M, 1999, J HISTOCHEM CYTOCHEM, V47, P7 Kretsinger R H, 1979, Adv Cyclic Nucleotide Res, V11, P1 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MEANS AR, 1980, NATURE, V285, P73, DOI 10.1038/285073a0 MEANS AR, 1982, PHYSIOL REV, V62, P1 MEPHAM BL, 1979, HISTOCHEM J, V11, P345, DOI 10.1007/BF01005033 Nakazawa K, 1996, HEARING RES, V96, P13, DOI 10.1016/0378-5955(96)00010-X NAKAZAWA K, 1995, J HISTOCHEM CYTOCHEM, V43, P981 ORDONEZ NG, 1988, AM J SURG PATHOL, V12, P121 RASMUSSEN H, 1984, PHYSIOL REV, V64, P938 SACKS DB, 1991, ANAL BIOCHEM, V194, P369, DOI 10.1016/0003-2697(91)90243-M Schulman H, 1993, CURR OPIN CELL BIOL, V5, P247, DOI 10.1016/0955-0674(93)90111-3 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 SCHULTE BA, 1993, HEARING RES, V65, P262, DOI 10.1016/0378-5955(93)90219-Q SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 SPICER SS, 1994, HEARING RES, V79, P161, DOI 10.1016/0378-5955(94)90137-6 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 NR 31 TC 13 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 133 EP 140 DI 10.1016/S0378-5955(00)00220-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600014 PM 11124460 ER PT J AU Gleich, O Dooling, RJ Ryals, BM AF Gleich, O Dooling, RJ Ryals, BM TI A quantitative analysis of the nerve fibers in the VIIIth nerve of Belgian Waterslager canaries with a hereditary sensorineural hearing loss SO HEARING RESEARCH LA English DT Article DE bird; cochlea; basilar papilla; hair cell; pathology; axon diameter ID BASILAR PAPILLA; SERINUS-CANARIUS; GUINEA-PIG; AUDITORY-THRESHOLDS; BARN OWL; INNERVATION; COCHLEAR; CHICKEN; DEGENERATION; MORPHOLOGY AB The number of auditory nerve fibers was determined for non-Belgian Waterslager canaries (non-BWS) and Belgian Waterslager canaries (BWS) that are affected by a sensorineural high frequency hearing loss and a 30% reduction in the number of auditory hair cells. Counts were obtained from semithin cross sections of the Durcupan-embedded auditory nerve at the level of the internal auditory meatus. In addition, the number of lagenar fibers was determined from cross sections near the apical end of the cochlear duct in order to separate them from the total number of auditory nerve fibers. The mean number of auditory nerve fibers was 6076 in non-BWS and 5363 in BWS canaries, representing a 12% reduction in BWS. This small reduction in the number of auditory nerve fibers? as compared to the larger reduction in hair cell number, might be explained by a predominant loss of abneural hair cells in BWS, since it has been shown for other species that a large proportion of abneural hair cells are devoid of afferent innervation. In addition, we observed that despite the prominent hair cell pathologies documented for BWS canaries, the mean diameter of auditory nerve fibers from non-BWS canaries (2.22 +/- 0.81 mum) did not differ from those of BWS canaries (2.21 +/- 0.96 mum). (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Regensburg, ENT Dept, D-93042 Regensburg, Germany. Univ Maryland, Dept Psychol, College Pk, MD 20742 USA. James Madison Univ, Dept Commun Sci & Disorders, Harrisonburg, VA 22807 USA. RP Gleich, O (reprint author), Univ Regensburg, ENT Dept, Franz Josef Strauss Allee 11, D-93042 Regensburg, Germany. CR ANNIKO M, 1988, SCANNING MICROSCOPY, V2, P1035 CHANDLER JP, 1984, J COMP NEUROL, V222, P506, DOI 10.1002/cne.902220405 COLE KS, 1990, EXP BRAIN RES, V82, P585 Dooling R.J., 1998, PSYCHOPHYSICAL PHYSL, P145 DUPONT J, 1993, HEARING RES, V68, P217, DOI 10.1016/0378-5955(93)90125-K FISCHER FP, 1994, SCANNING MICROSCOPY, V8, P351 Fischer FP, 1998, HEARING RES, V121, P112, DOI 10.1016/S0378-5955(98)00072-0 FISCHER FP, 1994, J MORPHOL, V220, P71, DOI 10.1002/jmor.1052200107 FISCHER FP, 1992, J MORPHOL, V213, P225, DOI 10.1002/jmor.1052130207 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S Gleich O, 2000, HEARING RES, V142, P56, DOI 10.1016/S0378-5955(00)00006-X Gleich O, 1997, J COMP NEUROL, V377, P5, DOI 10.1002/(SICI)1096-9861(19970106)377:1<5::AID-CNE2>3.0.CO;2-8 GLEICH O, 1995, HEARING RES, V82, P100 GLEICH O, 1994, NATURWISSENSCHAFTEN, V81, P320, DOI 10.1007/BF01131950 GLEICH O, 2000, COMP HEARING BIRDS R, P70 GLEICH O, 1994, HEARING RES, V79, P123, DOI 10.1016/0378-5955(94)90134-1 GLEICH O, 1994, J MORPHOL, V221, P1, DOI 10.1002/jmor.1052210102 Hyman BT, 1998, J NEUROPATH EXP NEUR, V57, P305, DOI 10.1097/00005072-199804000-00001 Kim JN, 1997, HEARING RES, V103, P169, DOI 10.1016/S0378-5955(96)00173-6 Koppl C, 2000, HEARING RES, V139, P123, DOI 10.1016/S0378-5955(99)00178-1 KOPPL C, 1993, J COMP PHYSIOL A, V171, P695, DOI 10.1007/BF00213066 Koppl C, 1997, AUDIT NEUROSCI, V3, P313 KUBKE MF, 1997, 20 ARO MIDW RES M, P142 MANLEY GA, 1993, J MORPHOL, V218, P153, DOI 10.1002/jmor.1052180205 OKANOYA K, 1987, J COMP PSYCHOL, V101, P213, DOI 10.1037/0735-7036.101.2.213 OKANOYA K, 1990, HEARING RES, V46, P271, DOI 10.1016/0378-5955(90)90008-D OKANOYA K, 1985, J ACOUST SOC AM, V78, P1170, DOI 10.1121/1.392885 RYALS BM, 1992, EXP NEUROL, V115, P18, DOI 10.1016/0014-4886(92)90214-B RYALS BM, 1999, 22 ARO MIDW RES M, P131 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 STRUTZ J, 1982, ACTA OTO-LARYNGOL, V94, P45, DOI 10.3109/00016488209128888 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 VONDURING M, 1985, FORTS ZOOL, V30, P681 Weisleder P, 1996, J COMP NEUROL, V369, P292, DOI 10.1002/(SICI)1096-9861(19960527)369:2<292::AID-CNE9>3.0.CO;2-Z WEISLEDER P, 1994, HEARING RES, V80, P64, DOI 10.1016/0378-5955(94)90009-4 Winter P., 1963, Zeitschrift fuer Morphologie und Oekologie der Tiere, V52, P365, DOI 10.1007/BF00408568 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 NR 38 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 141 EP 148 DI 10.1016/S0378-5955(00)00221-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600015 PM 11124461 ER PT J AU Armour, G Mhaskar, Y Rybak, L Dunaway, G AF Armour, G Mhaskar, Y Rybak, L Dunaway, G TI Alteration of 6-phosphofructo-1-kinase subunits during neonatal maturation of the rat cochlear cells SO HEARING RESEARCH LA English DT Article DE phosphofructokinase; glycolysis; energy metabolism; cochlea maturation; stria vascularis; organ of Corti; spiral ligament; development of hearing ID MESSENGER-RNA; BRAIN-DEVELOPMENT; STRIA VASCULARIS; ISOZYME POOLS; HAIR-CELLS; ENDOCOCHLEAR; EXPRESSION; PROTEIN AB During postnatal development of rat cochlear cells and the onset of hearing (10-23 days), the increasing endocochlear potential and energy requirements are largely provided by increased glucose utilization. It is well established that the ability of maturing rat tissues to use glucose is directly related to alteration of 6-phosphofructo-1-kinase (PFR) subunits. To gain insight into the alteration of PFK subunit levels in the cochlea from 6 to 60 days of age, PFK subunit types were measured in sections of paraffin-embedded temporal bone using IgG specific for each type of PFK subunit and quantified by computer image analysis. Although the L-type and C-type subunits did not exhibit statistically significant changes in the cochlear structures during maturation, the levels of M-type subunit in the stria vascularis cells, spiral ligament cell types I, II, and III, outer hair cells, inner hair cells, and support cells significantly increased. Also, the type TV and V spiral ligament fibrocytes during this period did not exhibit significant alterations of the M-type subunit. These data suggest that during neonatal development of the cochleam, the elevated levels of the M-type subunit are associated with increased glucose utilization and the onset of hearing. (C) 2001 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Div Otolaryngol, Springfield, IL 62794 USA. So Illinois Univ, Sch Med, Dept Surg, Div Otolaryngol, Springfield, IL 62794 USA. RP Dunaway, G (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, Div Otolaryngol, POB 10629, Springfield, IL 62794 USA. CR Anniko M, 1985, Acta Otolaryngol Suppl, V421, P10 BOSHER SK, 1972, ACTA OTO-LARYNGOL, V73, P203, DOI 10.3109/00016487209138931 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 CANLON B, 1983, HEARING RES, V10, P217, DOI 10.1016/0378-5955(83)90055-2 CANLON B, 1987, ARCH OTO-RHINO-LARYN, V244, P273, DOI 10.1007/BF00468635 CHOU JTH, 1964, BIOCH HORORGANS, P446 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 DAVIS H, 1965, COLD SPRING HARB SYM, V30, P181 DUNAWAY GA, 1983, MOL CELL BIOCHEM, V52, P75 DUNAWAY GA, 1987, J BIOL CHEM, V261, P17170 DUNAWAY GA, 1989, MOL CELL BIOCHEM, V87, P71, DOI 10.1007/BF00421084 DUNAWAY GA, 1988, BRAIN RES, V456, P310, DOI 10.1016/0006-8993(88)90233-8 DUNAWAY GA, 1986, MECH AGEING DEV, V36, P13, DOI 10.1016/0047-6374(86)90135-1 KAMBAYASHI J, 1982, HEARING RES, V6, P223, DOI 10.1016/0378-5955(82)90056-9 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 MHASKAR Y, 1995, DEV BRAIN RES, V85, P54, DOI 10.1016/0165-3806(94)00190-B Mhaskar Y, 1996, MECH AGEING DEV, V86, P161, DOI 10.1016/0047-6374(95)01690-2 Pujol R, 1985, Acta Otolaryngol Suppl, V421, P5 Puschner B, 1997, HEARING RES, V114, P102, DOI 10.1016/S0378-5955(97)00163-9 Romand R., 1983, DEV AUDITORY VESTIBU, P47 RYBAK LP, 1991, ORL J OTO-RHINO-LARY, V53, P72 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 Sakaguchi N, 1998, HEARING RES, V118, P114, DOI 10.1016/S0378-5955(98)00022-7 SCHACHT J, 1985, AUDITORY BIOCH, P389 Souter M, 1998, HEARING RES, V119, P81, DOI 10.1016/S0378-5955(98)00042-2 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 Spicer SS, 1998, HEARING RES, V118, P1, DOI 10.1016/S0378-5955(98)00006-9 Steel KP, 1999, SCIENCE, V285, P1363, DOI 10.1126/science.285.5432.1363 UZIEL A, 1981, AUDIOLOGY, V20, P89 Wada T., 1923, American Anatomical Memoir, Vno. 10, P1 WOOLF NK, 1986, AM J PHYSIOL, V250, pR493 YAO XF, 1994, HEARING RES, V80, P31, DOI 10.1016/0378-5955(94)90006-X NR 32 TC 4 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 149 EP 156 DI 10.1016/S0378-5955(00)00222-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600016 PM 11124462 ER PT J AU Supin, AY Popov, VV Milekhina, ON Tarakanov, MB AF Supin, AY Popov, VV Milekhina, ON Tarakanov, MB TI The effect of masking noise on rippled-spectrum resolution SO HEARING RESEARCH LA English DT Article DE spectrum-pattern resolution; rippled spectrum; masking; lateral suppression; human ID AUDITORY-NERVE FIBERS; FREQUENCY-SELECTIVITY; HEARING; LEVEL; EXCITATION; THRESHOLD; PATTERNS; STRENGTH AB Ripple-density resolution in a rippled sound spectrum (probe band) under the effect of another band (masker) was studied in normal listeners. The resolvable ripple density in the probe band was measured using a phase-reversal test. The principle of the test was to find the highest ripple density at which an interchange of mutual peak and valley position (the ripple phase reversal) was detectable. Probe bands were 0.5 octave (oct) wide with center frequencies of 1, 2, and 4 kHz. When a masker band was below the probe one (a low-frequency masker), it markedly reduced the ripple-density resolution. The effect of the low-frequency masker enhanced (ripple-density resolution decreased) with decreasing the stop-band (frequency spacing) between the probe and masker bands. The strongest masker effect was observed at zero spacing between the probe and masker bands. However, when the probe band overlapped the masker one so that no masker power was below the probe band, the masker effect diminished (ripple-density resolution partially released). Increase of the masker bandwidth above 0.5 oct by shifting its lower boundary downwards did not enhance the masker effect. Masker bands above the probe one (high-frequency maskers) did not influence the ripple-density resolution. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Russian Acad Sci, Inst Ecol & Evolut, Moscow 117071, Russia. RP Supin, AY (reprint author), Russian Acad Sci, Inst Ecol & Evolut, 33 Leninsky Prosp, Moscow 117071, Russia. CR DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 EVANS EF, 1992, PHILOS T ROY SOC B, V336, P295, DOI 10.1098/rstb.1992.0062 Fastl H, 1980, PSYCHOPHYSICAL PHYSL, P334 Hicks ML, 1999, J ACOUST SOC AM, V105, P326, DOI 10.1121/1.424526 HOUTGAST T, 1977, J ACOUST SOC AM, V62, P409, DOI 10.1121/1.381541 Houtgast T., 1974, FACTS MODELS HEARING, P258 KOHLRAUSCH A, 1992, PHILOS T ROY SOC B, V336, P375, DOI 10.1098/rstb.1992.0071 KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 MOORE BCJ, 1987, HEARING RES, V28, P209, DOI 10.1016/0378-5955(87)90050-5 Moore BCJ, 1997, J ACOUST SOC AM, V102, P2284, DOI 10.1121/1.419638 PATTERSON RD, 1976, J ACOUST SOC AM, V59, P640, DOI 10.1121/1.380914 PATTERSON RD, 1982, J ACOUST SOC AM, V72, P1788, DOI 10.1121/1.388652 Patterson RD, 1996, J ACOUST SOC AM, V100, P3286, DOI 10.1121/1.417212 Pick G., 1977, PSYCHOPHYSICS PHYSL, P273 PICK GF, 1980, J ACOUST SOC AM, V68, P1085, DOI 10.1121/1.384979 ROSEN S, 1992, J ACOUST SOC AM, V92, P773, DOI 10.1121/1.403946 SMALL AM, 1967, J ACOUST SOC AM, V41, P506, DOI 10.1121/1.1910361 SUMMERS V, 1994, J ACOUST SOC AM, V95, P3518, DOI 10.1121/1.409969 SUPIN AY, 1994, HEARING RES, V78, P31, DOI 10.1016/0378-5955(94)90041-8 Supin AY, 1997, HEARING RES, V108, P17, DOI 10.1016/S0378-5955(97)00035-X Supin AY, 1998, J ACOUST SOC AM, V103, P2042, DOI 10.1121/1.421351 WILSON JP, 1971, 7 INT C AC, V3, P397 Yost WA, 1996, J ACOUST SOC AM, V99, P1066, DOI 10.1121/1.414593 Zwicker E., 1974, FACTS MODELS HEARING, P132 ZWICKER E, 1982, PSYCHOACUSTIC NR 25 TC 6 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 157 EP 166 DI 10.1016/S0378-5955(00)00223-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600017 PM 11124463 ER PT J AU Fishman, YI Reser, DH Arezzo, JC Steinschneider, M AF Fishman, YI Reser, DH Arezzo, JC Steinschneider, M TI Neural correlates of auditory stream segregation in primary auditory cortex of the awake monkey SO HEARING RESEARCH LA English DT Article DE auditory cortex; stream segregation; current source density; multiunit activity; monkey ID SUPERIOR TEMPORAL CORTEX; ANURAN CEREBELLUM; TONE SEQUENCES; COMPLEX SOUNDS; TUNING CURVES; CAT; FREQUENCY; PERCEPTION; RESPONSES; MASKING AB An important feature of auditory scene analysis is the perceptual organization of sequential sound components, or 'auditory stream segregation'. Auditory stream segregation can be demonstrated by presenting a sequence of high and low frequency tones in an alternating pattern, ABAB. When the tone presentation rate (PR) is slow or the frequency separation (DeltaF) between the tents is small(< 10%), a connected alternating sequence ABAB is perceived. When the PR is fast or the F is large, however, the alternating sequence perceptually splits into two parallel auditory streams, one composed of interrupted 'A' tones, and the other of interrupted 'B' tones. The neurophysiological basis of this perceptual phenomenon is unknown. Neural correlates of auditory stream segregation were examined in Al of the awake monkey using neuronal ensemble techniques (multiunit activity and current source density). Responses evoked by alternating frequency sequences of tones, ABAB, were studied as a function of PR (5, 10, 20 and 40 Hz). 'A' tones corresponded to the best frequency (BF) of the cortical site, while 'B' tones were situated away from the BF by an amount DeltaF. At slow PRs, 'A' and 'B' tones evoked responses that generated an overall pattern of activity at the stimulus PR. In contrast, at fast PRs,'B' tone responses were differentially suppressed, resulting in a pattern of activity consisting predominantly of 'A' tone responses at half the PR. The magnitude of 'B' tone response suppression increased with DeltaF. Differential suppression of BF and non-BF tone responses at high PRs can be explained by physiological principles of forward masking. The effect of DeltaF is explained by the hypothesis that responses to tones distant from the BF are more susceptible to suppression by BF tones than responses to tones near the BF. These results parallel human psychoacoustics of auditory stream segregation and suggest a cortical basis for the perceptual phenomenon. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Rose F Kennedy Ctr, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, Rose F Kennedy Ctr, Bronx, NY 10461 USA. RP Fishman, YI (reprint author), Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Rose F Kennedy Ctr, Room 322,1300 Morris Pk Ave, Bronx, NY 10461 USA. CR ALAIN C, 1994, PERCEPT PSYCHOPHYS, V56, P501, DOI 10.3758/BF03206947 ANSTIS S, 1985, J EXP PSYCHOL HUMAN, V11, P257, DOI 10.1037/0096-1523.11.3.257 Arezzo JC, 1986, EVOKED POTENTIALS FR, P174 BARNA JS, 1981, ELECTROEN CLIN NEURO, V52, P494, DOI 10.1016/0013-4694(81)90035-3 BEAUVOIS MW, 1991, Q J EXP PSYCHOL-A, V43, P517 Beauvois MW, 1996, J ACOUST SOC AM, V99, P2270, DOI 10.1121/1.415414 BEAUVOIS MW, 1985, PERCEPT PSYCHOPHYS, V60, P852 Botte MC, 1997, PERCEPT PSYCHOPHYS, V59, P419, DOI 10.3758/BF03211908 BREGMAN AS, 1971, J EXP PSYCHOL, V89, P244, DOI 10.1037/h0031163 Bregman AS., 1990, AUDITORY SCENE ANAL Brosch M, 1997, J NEUROPHYSIOL, V77, P923 Brosch M, 1999, J NEUROPHYSIOL, V82, P1542 Brosch M, 1997, CEREB CORTEX, V7, P70, DOI 10.1093/cercor/7.1.70 CALFORD MB, 1995, J NEUROPHYSIOL, V73, P1876 Colombo M, 1996, J NEUROSCI, V16, P4501 COWEY A, 1976, NEUROPSYCHOLOGIA, V14, P1, DOI 10.1016/0028-3932(76)90002-6 COX CL, 1992, BRAIN RES BULL, V28, P401, DOI 10.1016/0361-9230(92)90039-Z CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 DAI HP, 1991, J ACOUST SOC AM, V89, P2837, DOI 10.1121/1.400721 De Ribaupierre F, 1972, Brain Res, V48, P205, DOI 10.1016/0006-8993(72)90179-5 deCharms RC, 1996, NATURE, V381, P610, DOI 10.1038/381610a0 EGGERMONT JJ, 1994, J NEUROPHYSIOL, V71, P246 Fay RR, 1998, HEARING RES, V120, P69, DOI 10.1016/S0378-5955(98)00058-6 Fishman Y., 1999, Society for Neuroscience Abstracts, V25, P395 Fishman YI, 2000, J ACOUST SOC AM, V108, P235, DOI 10.1121/1.429460 FREEMAN JA, 1975, J NEUROPHYSIOL, V38, P369 GALABURDA A, 1980, J COMP NEUROL, V190, P597, DOI 10.1002/cne.901900312 GOUREVITCH G, 1970, ANIMAL PSYCHOPHYSICS, P67 Griffiths TD, 1997, BRAIN, V120, P785, DOI 10.1093/brain/120.5.785 Helenius P, 1999, BRAIN, V122, P907, DOI 10.1093/brain/122.5.907 JERISON HJ, 1953, FED PROC, V12, P73 JESTEADT W, 1982, J ACOUST SOC AM, V71, P950, DOI 10.1121/1.387576 Kaas JH, 1998, AUDIOL NEURO-OTOL, V3, P73, DOI 10.1159/000013783 Kelly JB, 1996, BEHAV NEUROSCI, V110, P542 Liegeois-Chauvel Catherine, 1998, Brain, V121, P1853, DOI 10.1093/brain/121.10.1853 Lisman JE, 1997, TRENDS NEUROSCI, V20, P38, DOI 10.1016/S0166-2236(96)10070-9 Locke RE, 1997, J NEUROPHYSIOL, V78, P2309 MacDougall-Shackleton SA, 1998, J ACOUST SOC AM, V103, P3581, DOI 10.1121/1.423063 McCabe SL, 1997, J ACOUST SOC AM, V101, P1611, DOI 10.1121/1.418176 METHERATE R, 1994, J PHYSIOL-LONDON, V481, P331 METHERATE R, 1995, EXP BRAIN RES, V107, P59 MILLER GA, 1950, J ACOUST SOC AM, V22, P637, DOI 10.1121/1.1906663 MONDOR TA, 1994, PERCEPT PSYCHOPHYS, V56, P268, DOI 10.3758/BF03209761 MOODY DB, 1994, J ACOUST SOC AM, V95, P3499, DOI 10.1121/1.409967 MOORE BCJ, 1978, J ACOUST SOC AM, V63, P524, DOI 10.1121/1.381752 MOREL A, 1993, J COMP NEUROL, V335, P437, DOI 10.1002/cne.903350312 NELKEN I, 1994, HEARING RES, V72, P206, DOI 10.1016/0378-5955(94)90220-8 NICHOLSON C, 1975, J NEUROPHYSIOL, V38, P356 PFINGST BE, 1993, J ACOUST SOC AM, V93, P2124, DOI 10.1121/1.406673 PHILLIPS DP, 1995, AM J OTOL, V16, P338 PHILLIPS DP, 1989, J ACOUST SOC AM, V85, P2537, DOI 10.1121/1.397748 PHILLIPS DP, 1993, J EXP PSYCHOL HUMAN, V19, P203, DOI 10.1037//0096-1523.19.1.203 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 Rauschecker JP, 1998, CURR OPIN NEUROBIOL, V8, P516, DOI 10.1016/S0959-4388(98)80040-8 ROUILLER EM, 1991, EXP BRAIN RES, V86, P483 SHAMMA SA, 1985, HEARING RES, V19, P1, DOI 10.1016/0378-5955(85)90094-2 SPAIN WJ, 1991, J PHYSIOL-LONDON, V434, P591 STEINSCHNEIDER M, 1994, ELECTROEN CLIN NEURO, V92, P30, DOI 10.1016/0168-5597(94)90005-1 STEINSCHNEIDER M, 1992, ELECTROEN CLIN NEURO, V84, P196, DOI 10.1016/0168-5597(92)90026-8 Steinschneider M, 1998, J ACOUST SOC AM, V104, P2935, DOI 10.1121/1.423877 van Noorden L. P. A. S., 1975, THESIS TH EINDHOVEN Vaughan H. G., 1988, HDB ELECTROENCEPHALO, P45 WALLACE MN, 1991, EXP BRAIN RES, V86, P518 YOST WA, 1991, HEARING RES, V56, P8, DOI 10.1016/0378-5955(91)90148-3 NR 64 TC 137 Z9 141 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 167 EP 187 DI 10.1016/S0378-5955(00)00224-0 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600018 PM 11124464 ER PT J AU Hanekom, JJ Kruger, JJ AF Hanekom, JJ Kruger, JJ TI A model of frequency discrimination with optimal processing of auditory nerve spike intervals SO HEARING RESEARCH LA English DT Article DE frequency discrimination; phase-locking; inter-spike interval; optimal estimation; Kalman filter; volley theory ID HEARING-IMPAIRED LISTENERS; ELECTRICAL-STIMULATION; COCHLEAR NERVE; PHASE-LOCKING; GAP DETECTION; TONES; SYSTEM; PLACE; MODULATION; MECHANISM AB This paper investigates phase-lock coding of frequency in the auditory system. One objective with. the current model was to construct an optimal central estimation mechanism able to extract frequency directly from spike trains, The model bases estimates of the stimulus frequency on inter-spike intervals of spike trains phase-locked to a pure tone stimulus, phase-locking is the tendency of spikes to cluster around multiples of the stimulus period. It is assumed that these clusters have Gaussian distributions with variance that depends on the amount of phase-locking, Inter-spike intervals are then noisy measurements of the actual period of the stimulus waveform. The problem of estimating frequency from inter-spike intervals can be solved optimally with a Kalman tilter. It is shown that the number of inter-spike intervals observed in the stimulus interval determines frequency discrimination at low frequencies, while the variance of spike clusters dominates at higher frequencies. Tinting information in spike intervals is sufficient to account for human frequency discrimination performance up to 5000 Hz. When spikes are available on each stimulus cycle, the model can accurately predict frequency discrimination thresholds as a function of frequency, intensity and duration, (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Pretoria, Dept Elect Elect & Comp Engn, ZA-0002 Pretoria, South Africa. RP Hanekom, JJ (reprint author), Univ Pretoria, Dept Elect Elect & Comp Engn, ZA-0002 Pretoria, South Africa. CR Aidley D. J., 1998, PHYSL EXCITABLE CELL BACON SP, 1985, AUDIOLOGY, V24, P117 Bruce IC, 1998, INFORM SCIENCES, V111, P303, DOI 10.1016/S0020-0255(98)10010-5 Brugge JF, 1992, MAMMALIAN AUDITORY P, P1 COLBURN HS, 1973, J ACOUST SOC AM, V54, P1458, DOI 10.1121/1.1914445 Cook EP, 1999, J NEUROPHYSIOL, V81, P535 Delgutte B., 1997, HDB PHONETIC SCI, P507 Delgutte B., 1996, AUDITORY COMPUTATION, P157 Deutsch S., 1993, UNDERSTANDING NERVOU DYE RH, 1980, J ACOUST SOC AM, V67, P1746, DOI 10.1121/1.384301 Eddins David A., 1995, P207, DOI 10.1016/B978-012505626-7/50008-X ERELL A, 1988, J ACOUST SOC AM, V84, P204, DOI 10.1121/1.396966 Forrest TG, 1996, AUDIT NEUROSCI, V3, P21 Gabbiani F, 1996, NEURAL COMPUT, V8, P44, DOI 10.1162/neco.1996.8.1.44 GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 Goldstein J.L., 1977, PSYCHOPHYSICS PHYSL, P337 Green D.M., 1973, BASIC MECHANISMS HEA, P829 HIENZ RD, 1993, J ACOUST SOC AM, V93, P462, DOI 10.1121/1.405626 JAVEL E, 1988, HEARING RES, V34, P275, DOI 10.1016/0378-5955(88)90008-1 Jayel E., 1990, COCHLEAR IMPLANTS MO, P247 Johnson DH, 1996, J COMPUT NEUROSCI, V3, P275, DOI 10.1007/BF00161089 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 Johnston D, 1995, FDN CELLULAR NEUROPH Kalman R. E., 1960, T ASME D, V82, P35, DOI DOI 10.1115/1.3662552 Kay S. M., 1993, FUNDAMENTALS STAT SI KIM DO, 1991, HEARING RES, V52, P167, DOI 10.1016/0378-5955(91)90196-G KOCH C, 1982, PHILOS T ROY SOC B, V298, P227, DOI 10.1098/rstb.1982.0084 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F LEWIS ER, 1996, AUDITORY COMPUTATION, P469 Loizou PC, 1999, IEEE ENG MED BIOL, V18, P34 MARON ME, 1965, CYBERNETICS NERVOUS, P118 McKinney MF, 1999, J ACOUST SOC AM, V106, P2679, DOI 10.1121/1.428098 MCLAREN I, 1989, COMP NEUR S, P160 Mendel JM, 1995, LESSONS ESTIMATION T Moller AR, 1999, ACTA OTO-LARYNGOL, V119, P424, DOI 10.1080/00016489950180946 MOORE BCJ, 1973, J ACOUST SOC AM, V54, P610, DOI 10.1121/1.1913640 Moore B. C. J., 1993, HUMAN PSYCHOPHYSICS, P56 Moore BCJ, 1996, J ACOUST SOC AM, V100, P2320, DOI 10.1121/1.417941 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X POLLACK I, 1967, J ACOUST SOC AM, V40, P895 PROSEN CA, 1990, J ACOUST SOC AM, V88, P2152, DOI 10.1121/1.400112 RATTAY F, 1990, THEORY EXPT APPL Rattay F, 1999, NEUROSCIENCE, V89, P335, DOI 10.1016/S0306-4522(98)00330-3 Rhode WS, 1992, MAMMALIAN AUDITORY P, P94 ROSE JE, 1968, HEARING MECH VERTEBR, P144 Ruggero M.A., 1989, COCHLEAR MECH STRUCT, P259 SCHROEDE.MR, 1968, J ACOUST SOC AM, V43, P829, DOI 10.1121/1.1910902 SEK A, 1995, J ACOUST SOC AM, V97, P2479, DOI 10.1121/1.411968 SHAILER MJ, 1987, J ACOUST SOC AM, V81, P1110, DOI 10.1121/1.394631 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHANNON RV, 1990, HEARING RES, V47, P159, DOI 10.1016/0378-5955(90)90173-M SIEBERT WM, 1970, PR INST ELECTR ELECT, V58, P723, DOI 10.1109/PROC.1970.7727 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 Stevens KN, 1967, MODELS PERCEPTION SP, P88 Todd NPM, 1999, J NEW MUSIC RES, V28, P5 TOMLINSON RWW, 1998, P NATO ADV STUD I CO, P123 WAKEFIELD GH, 1985, J ACOUST SOC AM, V77, P613, DOI 10.1121/1.391879 Wever E. G., 1949, THEORY HEARING WIEGREDE L, 2000, PHYSL PSYCHOPHYSICAL, P106 WIER CC, 1977, J ACOUST SOC AM, V61, P178, DOI 10.1121/1.381251 WOLPERT DM, 1995, SCIENCE, V269, P1880, DOI 10.1126/science.7569931 ZHANG W, 1990, HEARING RES, V46, P181, DOI 10.1016/0378-5955(90)90001-6 NR 62 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 188 EP 204 DI 10.1016/S0378-5955(00)00227-6 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600019 PM 11124465 ER PT J AU Konrad-Martin, D Norton, SJ Mascher, KE Tempel, BL AF Konrad-Martin, D Norton, SJ Mascher, KE Tempel, BL TI Effects of PMCA2 mutation on DPOAE amplitudes and latencies in deafwaddler mice SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 21st Midwinter Meeting of the Association-for-Research-in-Otolaryngology CY FEB 15-19, 1998 CL ST PETERSBURG, FLORIDA SP Assoc Res Otolaryngol DE mutant mouse; distortion product otoacoustic emission; furosemide ID PRODUCT OTOACOUSTIC EMISSIONS; ACOUSTIC-DISTORTION PRODUCTS; HAIR CELL ELECTROMOTILITY; COCHLEAR ORIGIN; 2F1-F2; EAR; RESPONSES; DEAFNESS; GERBIL; MODEL AB The deafwaddler (dfw) mouse mutant is caused by a spontaneous mutation in the gene that encodes a plasma membrane Ca2+ ATPase (type 2), PMCA2 (Street et al., 1998. Nat. Genet. 19, 390-394), which is expressed in cochlear and vestibular hair cells. Distortion product otoacoustic emission (DPOAE) amplitudes and latencies were examined in control mice, deafwaddler mutants: and controls treated with the drug furosemide, Furosemide causes a transient reduction of DPOAEs (Mills et al., 1993. J. Acoust. Sec. Am. 94, 2108-2122). We wanted to determine whether DPOAEs obtained in furosemide-treated mice were similar or different from results obtained in +/dfw mice. DPOAE amplitude and phase were measured as a function of f(2)/f(1) ratio. These data were converted into waveforms using inverse fast Fourier transform, and their average latency was used to estimate DPOAE group delay. Homozygous deafwaddlers did not produce DPOAEs. Heterozygous deafwaddlers (+/dfw) had increased DPOAE thresholds and reduced amplitudes at high frequencies, compared to controls. To the extent that DPOAEs depend on functional outer hair cells (OHCs), abnormal DPOAEs in +/dfw mice suggest that PMCA2 is important for OI-IC function at high frequencies. Similar to the effects of furosemide, the mutation reduced DPOAEs for low-level stimuli; in contrast to furosemide, the mutation altered DPOAEs elicited by high levels. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Washington, Dept Speech & Hearing Sci, Seattle, WA 98195 USA. Univ Washington, Dept Otolaryngol & Head & Neck Surg, Seattle, WA 98195 USA. Univ Washington, Virginia Merrill Bloedel Hearing Res Ctr, Seattle, WA 98195 USA. Childrens Hosp & Reg Med Ctr, Seattle, WA 98105 USA. RP Konrad-Martin, D (reprint author), Boys Town Natl Res Hosp, 555 N 30th St, Omaha, NE 68131 USA. CR ALLEN JB, 1993, J ACOUST SOC AM, V94, P809, DOI 10.1121/1.408182 ANDERSON SD, 1979, ARCH OTO-RHINO-LARYN, V224, P47, DOI 10.1007/BF00455223 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWN AM, 1992, P ROY SOC B-BIOL SCI, V250, P29, DOI 10.1098/rspb.1992.0126 BROWN AM, 1993, J ACOUST SOC AM, V93, P3291, DOI 10.1121/1.405713 BROWN AM, 1993, J ACOUST SOC AM, V93, P3298, DOI 10.1121/1.405714 Brown A.M., 1975, Advances comp Physiol Biochem, V6, P1 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 CODY AR, 1981, J ACOUST SOC AM, V70, P707, DOI 10.1121/1.386906 Engdahl B, 1996, J ACOUST SOC AM, V99, P1573, DOI 10.1121/1.414733 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P409 Frolenkov GI, 1998, HEARING RES, V126, P67, DOI 10.1016/S0378-5955(98)00150-6 FURST M, 1988, J ACOUST SOC AM, V84, P222, DOI 10.1121/1.396969 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 Gaskill SA, 1996, J ACOUST SOC AM, V100, P3268, DOI 10.1121/1.417210 GREGER R, 1987, RENAL PHYSIOL BIOCH, V10, P174 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HEITMANN J, 1997, MIDW M ASS RES OT, V83, P21 Kanis LJ, 1997, J ACOUST SOC AM, V101, P1527, DOI 10.1121/1.418173 KEMP, 1983, HEARING PHYSL BASES, P82 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KEMP DT, 1999, MIDW M ASS RES OT, V22, P99 KIM DO, 1980, HEARING RES, V2, P297, DOI 10.1016/0378-5955(80)90064-7 KIMBERLEY BP, 1993, J ACOUST SOC AM, V94, P1343, DOI 10.1121/1.408162 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 Mills DM, 1997, J ACOUST SOC AM, V101, P395, DOI 10.1121/1.417985 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 NEELY ST, 1988, J ACOUST SOC AM, V83, P652, DOI 10.1121/1.396542 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W NORTON SJ, 1996, MIDW M ASS RES OT, V19, P82 OHLMS LA, 1991, OTOLARYNG HEAD NECK, V104, P159 Petit C, 1996, NAT GENET, V14, P385, DOI 10.1038/ng1296-385 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 PUJOL R, 1997, MIDW M ASS RES OT, V442, P111 Rattay F, 1998, J ACOUST SOC AM, V103, P1558, DOI 10.1121/1.421291 Ruggero M. A., 1992, MAMMALIAN AUDITORY P, P34 SCHROTT A, 1991, HEARING RES, V52, P245, DOI 10.1016/0378-5955(91)90204-M SIEGEL JH, 1982, J NEUROPHYSIOL, V47, P303 Steel KP, 1996, CURR OPIN NEUROBIOL, V6, P520, DOI 10.1016/S0959-4388(96)80059-6 Stover LJ, 1999, J ACOUST SOC AM, V106, P2669, DOI 10.1121/1.428097 Stover LJ, 1996, J ACOUST SOC AM, V99, P1016, DOI 10.1121/1.414630 Street VA, 1998, NAT GENET, V19, P390 WHITEHEAD M L, 1992, Seminars in Hearing, V13, P81, DOI 10.1055/s-0028-1085143 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X Yamoah EN, 1998, J NEUROSCI, V18, P610 ZWICKER E, 1990, J ACOUST SOC AM, V87, P2583, DOI 10.1121/1.399051 NR 50 TC 12 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 205 EP 220 DI 10.1016/S0378-5955(00)00228-8 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600020 PM 11124466 ER PT J AU Hemila, S Nummela, S Reuter, T AF Hemila, S Nummela, S Reuter, T TI Modeling whale audiograms: effects of bone mass on high-frequency hearing SO HEARING RESEARCH LA English DT Article DE middle ear; high-frequency hearing; isometry; audiogram; mass inertia; killer whale; odontocete hearing ID MIDDLE-EAR; ORCINUS-ORCA; IMPEDANCE AB In a previous paper (Hemila et al., Hear. Res. 133 (1999) 82-97) we have presented a mechanical model, based on species-specific anatomical data, for the toothed whale middle ear. For five odontocete species of six we found that the model quite well predicted published behavioral audiograms. Here we report that new published data indicate that the audiogram of the sixth and deviating species, the killer whale Orcinus orca, was from a specimen with deficient high-frequency hearing. A new published killer whale audiogram is similar to other odontocete audiograms and does fit our four-bone model. With certain general conditions, a model with isometric (middle) ears results in uniform audiograms for different species, when presented in a log-log plot; with larger ears the audiogram curves are just moved towards lower frequencies. The audiograms coincide in case all frequencies are scaled by a Factor 1/3 rootm, where m is the mass of the ear ossicles. Odontocete ears are isometric enough to show that the corresponding audiograms are indeed similar after such mass scaling. Specifically, this scaling factor can be used to predict the high-frequency hearing limits of all odontocete species. Our anatomical data and models support the notion that ossicular mass is a crucial factor limiting high-frequency hearing in both terrestrial mammals and toothed whales. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Helsinki, Dept Systemat & Ecol, Zool Lab, FIN-00014 Helsinki, Finland. Helsinki Univ Technol, Phys Lab, FIN-02150 Espoo, Finland. RP Nummela, S (reprint author), Univ Helsinki, Dept Systemat & Ecol, Zool Lab, POB 17, FIN-00014 Helsinki, Finland. CR ANDERSEN S, 1971, INVESTIGATIONS CETAC, V3, P255 EHRET G, 1974, NATURWISSENSCHAFTEN, V61, P506 HALL JD, 1972, J ACOUST SOC AM, V51, P515, DOI 10.1121/1.1912871 HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 Hemila S, 1999, HEARING RES, V133, P82, DOI 10.1016/S0378-5955(99)00055-6 HEMILA S, 1995, HEARING RES, V85, P31, DOI 10.1016/0378-5955(95)00031-X Henson Jr O. W., 1974, HDB SENSORY PHYSIOLO, P39 JACOBS DW, 1972, J ACOUST SOC AM, V51, P530, DOI 10.1121/1.1912874 JEFFERSON TA, 1993, FAO SPECIES IDENTIFI, P121 JOHNSON C. SCOTT, 1967, MAR BIO ACOUSTICS, V2, P247 KRINGLEBOTN M, 1988, SCAND AUDIOL, V17, P75, DOI 10.3109/01050398809070695 LYNCH TJ, 1982, J ACOUST SOC AM, V72, P108, DOI 10.1121/1.387995 NUMMELA S, 1995, HEARING RES, V85, P18, DOI 10.1016/0378-5955(95)00030-8 Nummela S, 1999, HEARING RES, V133, P71, DOI 10.1016/S0378-5955(99)00054-4 Nummela S, 1999, HEARING RES, V133, P61, DOI 10.1016/S0378-5955(99)00053-2 Nummela Sirpa, 1997, Comments on Theoretical Biology, V4, P387 Szymanski MD, 1999, J ACOUST SOC AM, V106, P1134, DOI 10.1121/1.427121 THOMAS J, 1988, J ACOUST SOC AM, V84, P936, DOI 10.1121/1.396662 WHITE MJ, 1978, 78109 HUBBS SEA WORL ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 NR 20 TC 17 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 221 EP 226 DI 10.1016/S0378-5955(00)00232-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600021 PM 11124467 ER PT J AU Mosnier, I Teixeira, M Loiseau, A Fernandes, I Sterkers, O Amiel, C Ferrary, E AF Mosnier, I Teixeira, M Loiseau, A Fernandes, I Sterkers, O Amiel, C Ferrary, E TI Effects of acute and chronic hypertension on the labyrinthine barriers in rat SO HEARING RESEARCH LA English DT Article DE cochlea; endolymph; perilymph; mannitol; urea ID COCHLEAR BLOOD-FLOW; BRAIN-BARRIER; AUTO-REGULATION; HEARING-LOSS; PRESSURE; PERMEABILITY; PERILYMPH; RECEPTORS; ENTRY; FLUID AB Hearing loss. vertigo, and tinnitus have been related to arterial hypertension. The aim of the present work was to study the permeability of the blood-perilymph and of the labyrinthine barrier, between endolymph and perilymph, to small molecules during chronic and acute hypertension. Experiments were performed in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acute hypertension was induced by phenylephrine. Perilymph was sampled from the first turn of the scala vestibuli and the Na, K, urea, and radioactive concentrations (C-14-urea and H-3-mannitol) were measured. In another experimental set, the endocochlear potential was recorded from the basal turn of scala media, before and after phenylephrine injection. The composition of the perilymph and the kinetic constants for C-14-urea and 3H-mannitol were similar in WKY and SHR, and not modified after acute hypertension. In endolymph, the endocochlear potential in SHR (+80 +/- 2.7 mV, n = 24) was lower (P < 0.001) than in WKY (+98 +/- 1.5 mV, n = 29). The endocochlear potential was decreased by 40 mV during acute hypertensive peak in seven out of 19 WKY but not in SHR rats (n = 13). In conclusion, chronic or acute hypertension did not severely alter the permeability to small molecules of the blood-perilymph barrier. The relationship between the low endocochlear potential and hypertension in SHR remains to be evaluated. After acute hypertensive peak, the presence of vascular protective mechanisms in the cochlea could account for the stable endocochlear potential recorded in SHR and 60% of normotensive rats. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Paris 07, Fac Xavier Bichat, INSERM, U426, F-75870 Paris 18, France. Univ Paris 07, Fac Xavier, IFR 2, F-75870 Paris, France. Hop Beaujon, Serv ORL, AP HP, Clichy, France. RP Ferrary, E (reprint author), Univ Paris 07, Fac Xavier Bichat, INSERM, U426, F-75870 Paris 18, France. CR AXELSSON A, 1983, ACTA OTO-LARYNGOL, V96, P215, DOI 10.3109/00016488309132894 BARZO P, 1993, NEUROSURGERY, V32, P611 BORG E, 1982, HEARING RES, V8, P101, DOI 10.1016/0378-5955(82)90069-7 BORG E, 1982, HEARING RES, V8, P117, DOI 10.1016/0378-5955(82)90070-3 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 CANESTRARI F, 1994, CLIN CHIM ACTA, V224, P167, DOI 10.1016/0009-8981(94)90183-X Degoute CS, 1997, EUR J APPL PHYSIOL O, V75, P326, DOI 10.1007/s004210050168 FERRARY E, 1987, AM J PHYSIOL, V253, pF59 GARG LC, 1985, AM J PHYSIOL, V249, pF863 GATES GA, 1993, ARCH OTOLARYNGOL, V119, P156 Gruber DD, 1998, HEARING RES, V119, P113, DOI 10.1016/S0378-5955(98)00036-7 HARPER SL, 1984, AM J PHYSIOL, V246, pH17 HILLERDAL M, 1987, ACTA OTO-LARYNGOL, V104, P243, DOI 10.3109/00016488709107324 INAMURA N, 1992, HEARING RES, V61, P12, DOI 10.1016/0378-5955(92)90030-Q Jahnke K, 1975, Acta Otolaryngol Suppl, V336, P1 LAURIKAINEN EA, 1994, J PHYSIOL-LONDON, V480, P563 Lippincott L, 1997, EUR ARCH OTO-RHINO-L, V254, P413, DOI 10.1007/BF02439970 Liu SY, 1996, ACTA OTO-LARYNGOL, V116, P710, DOI 10.3109/00016489609137911 MAYHAN WG, 1985, AM J PHYSIOL, V248, pH712 MAYHAN WG, 1987, HYPERTENSION, V9, P101 MOREL F, 1967, J PHYSIOL-PARIS, V59, P460 PICKAR JG, 1991, CLIN EXP HYPERTENS A, V13, P645, DOI 10.3109/10641969109042067 PORSTI I, 1984, ACTA PHYSIOL SCAND, V120, P387, DOI 10.1111/j.1748-1716.1984.tb07399.x QUIRK WS, 1989, HEARING RES, V41, P53, DOI 10.1016/0378-5955(89)90178-0 QUIRK WS, 1990, ACTA OTO-LARYNGOL, V109, P383, DOI 10.3109/00016489009125159 Rarey KE, 1996, HEARING RES, V102, P63, DOI 10.1016/S0378-5955(96)00148-7 ROSEN S, 1962, ANN OTO RHINOL LARYN, V71, P727 SAKAGAMI M, 1984, ACTA OTO-LARYNGOL, V97, P53, DOI 10.3109/00016488409130964 STERKERS O, 1987, AM J PHYSIOL, V253, pF50 STERKERS O, 1982, AM J PHYSIOL, V243, pF173 TACHIBANA M, 1984, ACTA OTO-LARYNGOL, V97, P257, DOI 10.3109/00016488409130987 TACHIBANA M, 1981, ARCH OTO-RHINO-LARYN, V232, P11, DOI 10.1007/BF00660999 TRIPPODO NC, 1981, CIRC RES, V48, P309 WERBER AH, 1990, BRAIN RES, V515, P235, DOI 10.1016/0006-8993(90)90601-7 ZIYLAN Z, 1984, EXP NEUROL, V84, P18 NR 35 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 227 EP 236 DI 10.1016/S0378-5955(00)00229-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600022 PM 11124468 ER PT J AU Raphael, Y Kobayashi, KN Dootz, GA Beyer, LA Dolan, DF Burmeister, M AF Raphael, Y Kobayashi, KN Dootz, GA Beyer, LA Dolan, DF Burmeister, M TI Severe vestibular and auditory impairment in three alleles of Ames waltzer (av) mice SO HEARING RESEARCH LA English DT Article DE mouse; Ames waltzer; hereditary deafness; organ of Corti ID PROGRAMMED CELL-DEATH; INNER-EAR; DEAFNESS; GENE; MOUSE; DEGENERATION AB The genetic and physiological characterization of circling, hearing-impaired mouse mutants has greatly facilitated our understanding of non-syndromic sensorineural deafness, the most common form of hereditary human hearing loss. Here we report the first phenotypic characterization of three alleles of Ames waltzer (av). Neither electrical potentials (auditory brainstem response) nor behavioral responses to sound could be evoked in any of the three alleles at any age or frequency. However, the endocochlear potential was found to be normal, indicating that the primary pathology is not in the stria vascularis. To determine the earliest changes and help identify the primary causes of deafness in av, we performed morphological studies in 15-16 day old mutants, just prior to the maturation of the cochlea. Although av(2J) is slightly more affected than the other two alleles, our studies show a high similarity between all three alleles. The first detectable changes are observed in the stereocilia and cytoplasm of hair cells, and in the cellular shape and microvilli of supporting cells. These changes are followed by degeneration of the cochlear and vestibular neuroepithelium. (C) 2001 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Sch Med, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Psychiat, Mental Hlth Res Inst, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Human Genet, Mental Hlth Res Inst, Ann Arbor, MI 48109 USA. RP Raphael, Y (reprint author), Univ Michigan, Sch Med, Dept Otolaryngol, Kresge Hearing Res Inst, MSRB 3,Room 9303,1150 W Med Ctr Dr, Ann Arbor, MI 48109 USA. CR Beyer LA, 2000, J NEUROCYTOL, V29, P227, DOI 10.1023/A:1026515619443 Burek MJ, 1996, BRAIN PATHOL, V6, P427, DOI 10.1111/j.1750-3639.1996.tb00874.x Chaib H, 1996, HUM MOL GENET, V5, P1061, DOI 10.1093/hmg/5.7.1061 Cohn ES, 1999, AM J MED GENET, V89, P130, DOI 10.1002/(SICI)1096-8628(19990924)89:3<130::AID-AJMG3>3.3.CO;2-D COOK S, 1993, MOUSE GENOME, V91, P554 Deloukas P, 1998, SCIENCE, V282, P744, DOI 10.1126/science.282.5389.744 GIBSON F, 1995, NATURE, V374, P62, DOI 10.1038/374062a0 Hasson T, 1996, GENOMICS, V36, P431, DOI 10.1006/geno.1996.0488 Holme RH, 1999, CURR OPIN GENET DEV, V9, P309, DOI 10.1016/S0959-437X(99)80046-X Jacobson MD, 1997, CELL, V88, P347, DOI 10.1016/S0092-8674(00)81873-5 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X Leonova EV, 1997, HEARING RES, V113, P14, DOI 10.1016/S0378-5955(97)00130-5 LI HS, 1993, HEARING RES, V68, P19, DOI 10.1016/0378-5955(93)90060-E Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 OSAKO S, 1971, ACTA OTO-LARYNGOL, V71, P365, DOI 10.3109/00016487109125376 Probst FJ, 1998, SCIENCE, V280, P1444, DOI 10.1126/science.280.5368.1444 RAFF MC, 1992, NATURE, V356, P397, DOI 10.1038/356397a0 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 Rau A, 1999, J COMP NEUROL, V405, P271 SCHAIBLE RH, 1956, MOUSE NEWS LETT, V15, P29 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 STEEL KP, 1989, DEVELOPMENT, V107, P453 Steel KP, 1995, ANNU REV GENET, V29, P675 WELL D, 1995, NATURE, V374, P60, DOI 10.1038/374060a0 Zobeley E, 1998, GENOMICS, V50, P260, DOI 10.1006/geno.1998.5298 NR 25 TC 34 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 237 EP 249 DI 10.1016/S0378-5955(00)00233-1 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600023 PM 11124469 ER PT J AU Popov, VV Supin, AY AF Popov, VV Supin, AY TI Contribution of various frequency bands to ABR in dolphins SO HEARING RESEARCH LA English DT Article DE auditory brainstem response; frequency band contribution; travelling wave velocity; Dolphin ID BRAIN-STEM RESPONSE; TRAVELING-WAVE VELOCITY; NOISE; POTENTIALS; HEARING AB Auditory brainstem responses (ABR) to clicks and noise bursts of various frequency bands and intensities were recorded in two bottlenosed dolphins, Tursiops truncatus. The purpose was to assess contributions of various parts of the cochlear partition to ABR and travelling wave velocity in the cochlea. At band-pass filtered stimuli (1-0.25 oct wide), ABR amplitude increased with increasing stimulus frequency, thus indicating higher contribution of basal cochlear parts. At high-pass and low-pass filtered stimuli, ABR amplitude increased with passband widening. However, the sum of all narrow-band contributions was a waveform of higher amplitude than the real ABR evoked by the wide-band stimulus. Applying a correction based on an assumption that the 'internal spectrum' is about 0.4 oct wider than the nominal stimulus spectrum resulted in the sum of narrow-band contributions equal to the wide-band ABR. The travelling wave velocity was computed based on ABR latencies and assigned a frequency of 128 kHz to the basal end of the cochlea. The computation gave values from 38.2 oct/ms at the proximal end of the basilar membrane to 4.0 oct/ms at a distance of 3.25 oct (13.5 kHz). (C) 2001 Elsevier Science B.V. All rights reserved. C1 Russian Acad Sci, Inst Ecol & Evolut, Moscow 117071, Russia. RP Supin, AY (reprint author), Russian Acad Sci, Inst Ecol & Evolut, 33 Leninsky Prosp, Moscow 117071, Russia. CR BURKARD R, 1983, J ACOUST SOC AM, V74, P1214, DOI 10.1121/1.390025 DAVIS H, 1976, AUDIOLOGY, V15, P181 DON M, 1994, J ACOUST SOC AM, V96, P3476, DOI 10.1121/1.410608 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 DONALDSON GS, 1993, J ACOUST SOC AM, V93, P940, DOI 10.1121/1.405454 EGGERMONT JJ, 1976, HDB SENSORY PHYSL, V5, P625 EGGERMONT JJ, 1979, J ACOUST SOC AM, V65, P463, DOI 10.1121/1.382345 ELBERLING C, 1974, SCAND AUDIOL, V3, P3 GOULD HJ, 1992, EAR HEARING, V13, P96, DOI 10.1097/00003446-199204000-00005 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 PARKER D J, 1978, Scandinavian Audiology, V7, P53, DOI 10.3109/01050397809043132 PARKER D J, 1978, Scandinavian Audiology, V7, P67, DOI 10.3109/01050397809043134 PICTON TW, 1979, J OTOLARYNGOL, V8, P289 POPOV VV, 1990, J COMP PHYSIOL A, V166, P385 TEAS DC, 1962, J ACOUST SOC AM, V34, P1428 WEVER EG, 1971, P NATL ACAD SCI USA, V68, P2708, DOI 10.1073/pnas.68.11.2708 NR 16 TC 11 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2001 VL 151 IS 1-2 BP 250 EP 260 DI 10.1016/S0378-5955(00)00234-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 393HR UT WOS:000166463600024 PM 11124470 ER PT J AU Marianowski, R Liao, WH Van Den Abbeele, T Fillit, P Herman, P Frachet, B Huy, PTB AF Marianowski, R Liao, WH Van Den Abbeele, T Fillit, P Herman, P Frachet, B Huy, PTB TI Expression of NMDA, AMPA and GABAA receptor subunit mRNAs in the rat auditory brainstem. I. Influence of early auditory deprivation SO HEARING RESEARCH LA English DT Article DE N-methyl-D-aspartate; alpha-amino-3-hydroxy-5-methyl-4-isoxazole; gamma-aminobutyric acid type A; auditory deprivation; synaptic plasticity; cochlear nucleus; inferior colliculus ID UNILATERAL COCHLEAR ABLATION; GLUTAMATE-OPERATED CHANNELS; CENTRAL-NERVOUS-SYSTEM; INFERIOR COLLICULUS; AFFERENT INFLUENCES; SOUND DEPRIVATION; PROTEIN-SYNTHESIS; NUCLEUS; REMOVAL; PROJECTIONS AB Impact of early post-natal deafening on auditory pathways was investigated in newborn rats deafened by daily amikacin injections from P7 to P16 inducing a complete destruction of the organ of Corti. The expression of mRNAs encoding N-methyl-D-aspartate (NMDA), alpha -amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) and gamma -aminobutyric acid type A (GABA(A)) receptor subunits was then studied by in situ hybridization in the dorsal and ventral cochlear nucleus and in the central nucleus of the inferior colliculus (CNIC). Early post-natal deafening decreased bilaterally the expression of mRNAs encoding NR1, NR2a, NR2b and flop isoforms of AMPA receptors. On the contrary, it increased the expression of mRNAs encoding some GABA(A) subunits (alpha1, beta1, gamma2) and flip isoforms of AMPA receptors. These changes were more pronounced in cochlear nuclei than in CNIC. They suggest that auditory sensation is essential in the normal development of central auditory pathways. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hop Lariboisiere, Serv Otorhinolaryngol, F-75010 Paris, France. Fac Lariboisiere St Louis, CNRS, UPRESA 7060, F-75010 Paris, France. Vet Gen Hosp, Dept Otorhinolaryngol, Taipei, Taiwan. Hop Avicenne, Dept Otorhinolaryngol, F-93009 Bobigny, France. Hop Necker Enfants Malad, Dept Otorhinolaryngol, Paris, France. RP Huy, PTB (reprint author), Hop Lariboisiere, Serv Otorhinolaryngol, 10 Ave Verdun, F-75010 Paris, France. CR Anderson H, 1968, ACTA OTO-LARYNGOL, P1 ANGELOTTI TP, 1993, J NEUROSCI, V13, P1429 BATKIN S, 1970, ELECTROEN CLIN NEURO, V28, P351, DOI 10.1016/0013-4694(70)90227-0 BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 COLLINGRIDGE GL, 1989, PHARMACOL REV, V41, P143 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 DURHAM D, 1985, J COMP NEUROL, V231, P446, DOI 10.1002/cne.902310404 EYBALIN M, 1990, SCIENCE, V269, P1734 Forster CR, 1998, NEUROREPORT, V9, P3531 Gaza WC, 1997, BRAIN RES, V774, P175, DOI 10.1016/S0006-8993(97)81701-5 Hashisaki G T, 1989, J Comp Neurol, V283, P5 HYSON RL, 1989, J NEUROSCI, V9, P2835 Illing RB, 1997, J COMP NEUROL, V382, P116, DOI 10.1002/(SICI)1096-9861(19970526)382:1<116::AID-CNE8>3.0.CO;2-4 ISHII T, 1993, J BIOL CHEM, V268, P2836 KHRESTCHATISKY M, 1991, J NEUROCHEM, V56, P1717, DOI 10.1111/j.1471-4159.1991.tb02072.x KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 LOLAIT SJ, 1989, FEBS LETT, V246, P145, DOI 10.1016/0014-5793(89)80271-6 LOLAIT SJ, 1989, FEBS LETT, V258, P17, DOI 10.1016/0014-5793(89)81605-9 Luo L, 1999, J COMP NEUROL, V404, P271, DOI 10.1002/(SICI)1096-9861(19990208)404:2<271::AID-CNE10>3.0.CO;2-4 Mair I W, 1973, Acta Otolaryngol Suppl, V314, P1 MAROT M, 1980, HEARING RES, V2, P111, DOI 10.1016/0378-5955(80)90032-5 MCDONALD JW, 1990, BRAIN RES REV, V15, P41, DOI 10.1016/0165-0173(90)90011-C Micheva KD, 1996, J COMP NEUROL, V373, P340, DOI 10.1002/(SICI)1096-9861(19960923)373:3<340::AID-CNE3>3.0.CO;2-2 MONYER H, 1992, SCIENCE, V256, P1217, DOI 10.1126/science.256.5060.1217 MONYER H, 1991, NEURON, V6, P799, DOI 10.1016/0896-6273(91)90176-Z MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MORIYOSHI K, 1991, NATURE, V354, P31, DOI 10.1038/354031a0 NIEDZIELSKI AS, 1995, J NEUROSCI, V15, P2338 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 Oliver D. L., 1991, NEUROBIOLOGY HEARING, P195 PARKS TN, 1979, J COMP NEUROL, V183, P665, DOI 10.1002/cne.901830313 PETRALIA RS, 1994, J NEUROSCI, V14, P667 Petralia RS, 1996, J COMP NEUROL, V372, P356 REBILLARD G, 1976, ACTA OTO-LARYNGOL, V82, P48, DOI 10.3109/00016487609120862 RIVA MA, 1994, MOL BRAIN RES, V25, P209, DOI 10.1016/0169-328X(94)90155-4 SCHUETTE WH, 1983, CELL TISSUE KINET, V16, P221 SHIVERS BD, 1989, NEURON, V3, P327, DOI 10.1016/0896-6273(89)90257-2 SILVILOTTI L, 1991, PROG NEUROBIOL, V36, P35 SMOLEN AJ, 1983, IN SITU HYBRIDIZATIO, P175 SOMMER B, 1990, SCIENCE, V249, P1580, DOI 10.1126/science.1699275 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 STEPHENSON FA, 1988, BIOCHEM J, V249, P21 STEWARD O, 1985, J COMP NEUROL, V231, P385, DOI 10.1002/cne.902310308 TRUNE DR, 1988, HEARING RES, V35, P259, DOI 10.1016/0378-5955(88)90122-0 TRUNE DR, 1983, DEV BRAIN RES, V9, P1, DOI 10.1016/0165-3806(83)90103-7 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 WARD PH, 1961, ANN OTO RHINOL LARYN, V70, P132 WATANABE M, 1992, NEUROREPORT, V3, P1138, DOI 10.1097/00001756-199212000-00027 WATANABE M, 1994, J COMP NEUROL, V343, P520, DOI 10.1002/cne.903430403 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 WENTHOLD RJ, 1978, BRAIN RES, V143, P544, DOI 10.1016/0006-8993(78)90365-7 Wynne B, 1995, J CHEM NEUROANAT, V9, P289, DOI 10.1016/0891-0618(95)00095-X YMER S, 1990, EMBO J, V9, P3261 YMER S, 1989, EMBO J, V8, P1665 ZHOU N, 1993, BRAIN RES, V628, P149, DOI 10.1016/0006-8993(93)90950-R NR 60 TC 28 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 1 EP 11 DI 10.1016/S0378-5955(00)00166-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400001 PM 11077189 ER PT J AU Liao, WH Van Den Abbeele, T Herman, P Frachet, B Huy, PTB Lecain, E Marianowski, R AF Liao, WH Van Den Abbeele, T Herman, P Frachet, B Huy, PTB Lecain, E Marianowski, R TI Expression of NMDA, AMPA and GABA(A) receptor subunit mRNAs in the rat auditory brainstem. II. Influence of intracochlear electrical stimulation SO HEARING RESEARCH LA English DT Article DE N-methyl-D-aspartate; alpha-amino-3-hydroxy-5-methyl-4-isoxazole; gamma-aminobutyric acid type A; synaptic plasticity; cochlear nucleus; cochlear implant; inferior colliculus ID GLUTAMATE-OPERATED CHANNELS; NEONATALLY DEAFENED CATS; NORMAL-HEARING KITTENS; COCHLEAR NUCLEUS; GUINEA-PIG; STEM; RESPONSES; NEURONS; CELLS; NERVE AB We investigated the effects of intracochlear electrical stimulation (ICES) on auditory pathways of neonatal rat deafened by daily amikacin injections. Expression of mRNAs encoding ionotropic glutamate receptor subunits such as alpha -amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) and N-methyl-D-aspartate (NMDA), and gamma -aminobutyric acid type A (GABA(A)) receptor subunits was assessed hi in situ hybridization in the dorsal (DCM) and the ventral cochlear nucleus (VCN) and in the central nucleus of the inferior colliculus (CNIC). After 15 days of daily unilateral ICES, the expressions of NR1, NR2b and NR2c subunits of NMDA receptor, that of GluRA. B, C, D flop isoforms of AMPA receptor. and that of some GABAA subunits (alpha1, beta1, gamma1, gamma2) were increased bilaterally in the DCN, VCN and the CNIC. These changes last over a week after stimulation for only NR1 and NR2c. These modifications might be I elated to long lasting synaptic plasticity of brainstem auditory pathways. As far as analogy to deaf children can be made, early electrical stimulation might be of interest to maintain neuronal networks. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hop Lariboisiere, Serv Otorhinolaryngol, F-75010 Paris, France. Fac Lariboisiere St Louis, CNRS, UPRESA 7060, F-75010 Paris, France. Vet Gen Hosp, Dept Otorhinolaryngol, Taipei, Taiwan. Hop Avicenne, Dept Otorhinolaryngol, F-93009 Bobigny, France. Hop Necker Enfants Malad, Dept Otorhinolaryngol, Paris, France. RP Huy, PTB (reprint author), Hop Lariboisiere, Serv Otorhinolaryngol, 10 Ave Verdun, F-75010 Paris, France. CR BARNARD EA, 1987, TRENDS NEUROSCI, V10, P502, DOI 10.1016/0166-2236(87)90130-5 Caicedo A, 1999, EUR J NEUROSCI, V11, P51, DOI 10.1046/j.1460-9568.1999.00410.x Caicedo A, 1998, EUR J NEUROSCI, V10, P941, DOI 10.1046/j.1460-9568.1998.00104.x Chew LJ, 1997, J NEUROSCI, V17, P227 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 EBERT U, 1995, EXP BRAIN RES, V104, P310 FRANKLIN SO, 1993, MOL BRAIN RES, V19, P93, DOI 10.1016/0169-328X(93)90153-G GODDARD GV, 1969, EXP NEUROL, V25, P295, DOI 10.1016/0014-4886(69)90128-9 Gu JG, 1996, NATURE, V381, P793, DOI 10.1038/381793a0 HALL RD, 1990, HEARING RES, V49, P155, DOI 10.1016/0378-5955(90)90102-U HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 ISHII T, 1993, J BIOL CHEM, V268, P2836 JUIZ JM, 1994, BRAIN RES, V639, P193, DOI 10.1016/0006-8993(94)91730-2 KANDLER K, 1995, J NEUROSCI, V15, P6890 KHRESTCHATISKY M, 1991, J NEUROCHEM, V56, P1717, DOI 10.1111/j.1471-4159.1991.tb02072.x LEAKE PA, 1992, HEARING RES, V64, P99, DOI 10.1016/0378-5955(92)90172-J LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LOLAIT SJ, 1989, FEBS LETT, V246, P145, DOI 10.1016/0014-5793(89)80271-6 LOLAIT SJ, 1989, FEBS LETT, V258, P17, DOI 10.1016/0014-5793(89)81605-9 MODY I, 1993, BRAIN PATHOL, V3, P395, DOI 10.1111/j.1750-3639.1993.tb00767.x MONYER H, 1992, SCIENCE, V256, P1217, DOI 10.1126/science.256.5060.1217 MONYER H, 1991, NEURON, V6, P799, DOI 10.1016/0896-6273(91)90176-Z NI DF, 1992, HEARING RES, V62, P63, DOI 10.1016/0378-5955(92)90203-Y NI DF, 1993, ACTA OTO-LARYNGOL, V113, P489, DOI 10.3109/00016489309135851 Oliver D. L., 1991, NEUROBIOLOGY HEARING, P195 PELLEGRINIGIAMPIETRO DE, 1991, P NATL ACAD SCI USA, V88, P4157, DOI 10.1073/pnas.88.10.4157 POLLARD H, 1993, NEUROREPORT, V4, P411, DOI 10.1097/00001756-199304000-00018 ROMAND R, 1971, J PHYSIOL-PARIS, V63, P763 SCHUETTE WH, 1983, CELL TISSUE KINET, V16, P221 SHEPHERD RK, 1994, HEARING RES, V81, P150, DOI 10.1016/0378-5955(94)90162-7 SHIVERS BD, 1989, NEURON, V3, P327, DOI 10.1016/0896-6273(89)90257-2 SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMOLER AJ, 1993, IN SITU HYBRIDIZATIO, P175 SOMMER B, 1990, SCIENCE, V249, P1580, DOI 10.1126/science.1699275 STEEL KP, 1984, HEARING RES, V15, P59, DOI 10.1016/0378-5955(84)90225-9 WISDEN W, 1992, J NEUROSCI, V12, P1040 YMER S, 1990, EMBO J, V9, P3261 YMER S, 1989, EMBO J, V8, P1665 NR 38 TC 13 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 12 EP 26 DI 10.1016/S0378-5955(00)00167-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400002 PM 11077190 ER PT J AU Gehr, DD Komiya, H Eggermont, JJ AF Gehr, DD Komiya, H Eggermont, JJ TI Neuronal responses in cat primary auditory cortex to natural and altered species-specific calls SO HEARING RESEARCH LA English DT Article DE cat; communication sound; primary auditory cortex; multi-unit recording; neural synchrony ID REPRESENTATION; VOCALIZATION; INFORMATION AB We investigated how natural and morphed cat vocalizations are represented in primary auditory cortex (AI). About 40% Of the neurons showed time-locked responses to major peaks in the vocalization envelope, 60% only responded at the onset. Simultaneously recorded multi-unit (MU) activity of these peak-tracking neurons on separate electrodes was significantly more synchronous during stimulation than under silence. Thus, the representation of the vocalizations is likely synchronously distributed across the cortex. The sum of the responses to the low and high frequency part of the meow. with the boundary at 2.5 kHz, was larger than the neuronal response to the natural meow itself, suggesting that strong lateral inhibition is shaping the response to the natural meow. In this sense, the neurons are combination-sensitive. The frequency-tuning properties and the response to amplitude-modulated tones of the MU recordings can explain the responses to natural, and temporally and spectrally altered vocalizations. Analysis of the mutual information in the firing rate suggests that the activity of at least 95 recording sites in Al would be needed to reliably distinguish between the nine different vocalizations. This suggests that a distributed representation based on temporal stimulus aspects may be more efficient than one based on firing rate. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Neurosci Res Grp, Dept Physiol & Biophys, Calgary, AB T2N 1N4, Canada. Univ Calgary, Neurosci Res Grp, Dept Psychol, Calgary, AB T2N 1N4, Canada. RP Eggermont, JJ (reprint author), Univ Calgary, Neurosci Res Grp, Dept Physiol & Biophys, Calgary, AB T2N 1N4, Canada. CR Borst A, 1999, NAT NEUROSCI, V2, P947, DOI 10.1038/14731 BOUDREAU JC, 1973, SENSORY NEUROPHYSIOL BROWN KA, 1978, DEV PSYCHOBIOL, V11, P559, DOI 10.1002/dev.420110605 Buracas GT, 1999, TRENDS NEUROSCI, V22, P303, DOI 10.1016/S0166-2236(98)01376-9 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 Eggermont JJ, 2000, HEARING RES, V142, P89, DOI 10.1016/S0378-5955(00)00024-1 Eggermont JJ, 2000, J NEUROPHYSIOL, V83, P2708 Eggermont JJ, 1998, J NEUROPHYSIOL, V80, P2743 EGGERMONT JJ, 1996, AUDIT NEUROSCI, V2, P76 Ehret G, 1997, J COMP PHYSIOL A, V181, P547, DOI 10.1007/s003590050139 Hauser M.D., 1997, EVOLUTION COMMUNICAT Kilgard MP, 1999, HEARING RES, V134, P16, DOI 10.1016/S0378-5955(99)00061-1 LEPPELSACK HJ, 1978, FED PROC, V37, P2336 Moelk M, 1944, AM J PSYCHOL, V57, P184, DOI 10.2307/1416947 NEWMAN JD, 1973, BRAIN RES, V54, P287, DOI 10.1016/0006-8993(73)90050-4 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 Rauschecker JP, 1998, AUDIOL NEURO-OTOL, V3, P86, DOI 10.1159/000013784 ROMAND R, 1984, DEV PSYCHOBIOL, V17, P629, DOI 10.1002/dev.420170606 SOVIJARVI ARA, 1975, ACTA PHYSIOL SCAND, V93, P318, DOI 10.1111/j.1748-1716.1975.tb05821.x STEIN RB, 1965, BIOPHYS J, V5, P173 Sutter ML, 1999, J NEUROPHYSIOL, V82, P2358 Wang XQ, 1995, J NEUROPHYSIOL, V74, P2685 WERNER G, 1965, J NEUROPHYSIOL, V28, P359 WINTER P, 1973, EXP BRAIN RES, V18, P489 NR 24 TC 58 Z9 58 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 27 EP 42 DI 10.1016/S0378-5955(00)00170-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400003 PM 11077191 ER PT J AU Voss, SE Rosowski, JJ Merchant, SN Peake, WT AF Voss, SE Rosowski, JJ Merchant, SN Peake, WT TI Acoustic responses of the human middle ear SO HEARING RESEARCH LA English DT Article DE middle-ear mechanics; middle-ear model; temporal-bone measurements ID HUMAN TEMPORAL BONES; INPUT IMPEDANCE; RECONSTRUCTED EARS; MEASURING SYSTEM; UMBO VIBRATION; MECHANICS; CAT; STAPES AB Measurements on human cadaver ears are reported that describe sound transmission through the middle ear. Four response variables were measured with acoustic stimulation at the tympanic membrane: stapes velocity, middle-ear cavity sound pressure, acoustic impedance at the tympanic membrane and acoustic impedance of the middle-ear cavity. Measurements of stapes velocity at different locations on the stapes suggest that stapes motion is predominantly 'piston-like', for frequencies up to at least 2000 Hz. The measurements are generally consistent with constraints of existing models. The measurements are used (1) to show how the cavity pressure and the impedance at the tympanic membrane are related, (2) to develop a measurement-based middle-ear cavity model, which shows that the middle-ear cavity has only small effects on the motion of the tympanic membrane and stapes in the normal earl although it may play a more prominent role in pathological ears, and (3) to show that inter-ear variations in the impedance at the tympanic membrane and the stapes velocity are not well correlated. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, Boston, MA 02114 USA. Harvard Univ, MIT, Div Hlth Sci & Technol, Speech & Hearing Sci Program, Cambridge, MA 02139 USA. MIT, Elect Res Lab, Cambridge, MA 02139 USA. Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Cambridge, MA 02139 USA. MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA. RP Voss, SE (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, 243 Charles St, Boston, MA 02114 USA. CR Allen J. B., 1986, PERIPHERAL AUDITORY, P44 Bekesy G., 1960, EXPT HEARING Beranek L.L., 1986, ACOUSTICS DANKBAAR WA, 1970, J ACOUST SOC AM, V48, P1021, DOI 10.1121/1.1912224 Decraemer W, 1999, S REC DEV AUD MECH S DONALDSON JA, 1992, A DONALDSON SURG ANA EGOLF DP, 1977, J ACOUST SOC AM, V61, P200, DOI 10.1121/1.381256 GOODE RL, 1993, AM J OTOL, V14, P247 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 GUNDERSE.T, 1972, ARCHIV OTOLARYNGOL, V96, P416 GYO K, 1986, ARCH OTOLARYNGOL, V112, P1262 GYO K, 1987, ACTA OTO-LARYNGOL, V103, P87, DOI 10.3109/00016488709134702 Heiland KE, 1999, AM J OTOL, V20, P81 HELMHOLTZ H, 1869, PFLUG ARCH PHYSL, V3, P1 Huang GT, 1997, J ACOUST SOC AM, V101, P1532, DOI 10.1121/1.418107 KARAL FC, 1953, J ACOUST SOC AM, V25, P327, DOI 10.1121/1.1907041 Kinsler LE, 1982, FUNDAMENTALS ACOUSTI Kirikae I., 1960, STRUCTURE FUNCTION M KRINGLEBOTN M, 1988, SCAND AUDIOL, V17, P75, DOI 10.3109/01050398809070695 KRINGLEBOTN M, 1985, J ACOUST SOC AM, V77, P159, DOI 10.1121/1.392280 KUROKAWA H, 1995, OTOLARYNG HEAD NECK, V113, P349, DOI 10.1016/S0194-5998(95)70067-6 LYNCH TJ, 1981, THESIS MIT MA LYNCH TJ, 1994, J ACOUST SOC AM, V96, P2184, DOI 10.1121/1.410160 MACH E, 1874, SITZ BER AKAD WISS M, V69, P221 Merchant SN, 1997, ANN OTO RHINOL LARYN, V106, P49 Merchant SN, 1996, HEARING RES, V97, P30 Merchant SN, 1998, J LARYNGOL OTOL, V112, P715 Merchant SN, 1997, AM J OTOL, V18, P139 MOLLER AR, 1961, J ACOUST SOC AM, V33, P168, DOI 10.1121/1.1908610 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MOLVAER OI, 1978, ACTA OTO-LARYNGOL, V85, P24, DOI 10.3109/00016487809121419 NISHIHARA S, 1993, OTOLARYNG HEAD NECK, V109, P899 ONCHI Y, 1961, J ACOUST SOC AM, V33, P794, DOI 10.1121/1.1908801 PEAKE WT, 1992, HEARING RES, V57, P245, DOI 10.1016/0378-5955(92)90155-G RABINOWITZ WM, 1981, J ACOUST SOC AM, V70, P1025, DOI 10.1121/1.386953 RAVICZ ME, 1992, J ACOUST SOC AM, V92, P157, DOI 10.1121/1.404280 Rosowski J. J., 1986, PERIPHERAL AUDITORY, P3 ROSOWSKI JJ, 1990, ANN OTO RHINOL LARYN, V99, P403 SADE J, 1982, P 2 INT C CHOL MAST, P1 SCHULNECHT H, 1968, Archives of Otolaryngology, V87, P129 Shambaugh GE, 1980, SURG EAR SHERA CA, 1992, J ACOUST SOC AM, V92, P1356, DOI 10.1121/1.403929 VLAMING MSMG, 1986, CLIN OTOLARYNGOL, V11, P353, DOI 10.1111/j.1365-2273.1986.tb00137.x VONBEKESY G, 1936, AKUST Z, V1, P13 VOSS SE, 1998, THESIS MIT MA WEISS TF, 1972, J ACOUST SOC AM, V52, P1729, DOI 10.1121/1.1913308 Wever EG, 1954, PHYSL ACOUSTICS Whittemore KR, 1998, OTOLARYNG HEAD NECK, V118, P751, DOI 10.1016/S0194-5998(98)70264-5 Zwislocki J J, 1970, ASHA Monogr, V15, P1 ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 NR 50 TC 106 Z9 110 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 43 EP 69 DI 10.1016/S0378-5955(00)00177-5 PG 27 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400004 PM 11077192 ER PT J AU Sage, C Venteo, S Jeromin, A Roder, J Dechesne, CJ AF Sage, C Venteo, S Jeromin, A Roder, J Dechesne, CJ TI Distribution of frequenin in the mouse inner ear during development, comparison with other calcium-binding proteins and synaptophysin SO HEARING RESEARCH LA English DT Article DE vestibule; cochlea; calretinin; calbindin; immunocytochemistry ID VESTIBULAR END-ORGANS; NERVOUS-SYSTEM; CALRETININ IMMUNOREACTIVITY; EFFERENT INNERVATION; HAIR-CELLS; RAT; SYNAPSES; COCHLEA; HOMOLOG; COMPLEX AB Frequenin is a calcium-binding protein previously implicated in the regulation of neurotransmission. We report its immunocytochemical detection in the mouse inner ear, in the adult, and during embryonic (E) and postnatal (P) development. The distribution of frequenin was compared with those of other calcium-binding proteins (calbindin, calretinin, parvalbumin) and synaptophysin. In the adult mouse inner ear, frequenin immunostaining was observed in the afferent neuronal systems (vestibular and cochlear neurons. their processes and endings) and in the vestibular and cochlear efferent nerve terminals. Frequenin colocalized with synaptophysin in well characterized presynaptic compartments, such as the vestibular and cochlear efferent endings, and in putative presynaptic compartments, such as the apical parr of the vestibular calyces. Frequenin was not Found in vestibular hair cells and in cochlear inner and outer hair cells. During development. frequenin immunoreactivity was first detected on El I in rile neurons of the statoacoustic ganglion. On E14, frequenin was detected in the efferent neurites innervating the vestibular sensory epithelium, along with synaptophysin. On E16. frequenin was detected in the afferent neurites below the inner hair cells in the organ of Corti. The timing of frequenin detection in vestibular and cochlear afferent neurites was consistent with their sequences of maturation, and was earlier than synaptogenesis. Thus ill the inner ear, frequenin is a very early marker of differentiated and growing neurons and is present in presynaptic and postsynaptic compartments. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Montpellier 2, INSERM, U 432, F-34095 Montpellier 5, France. Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada. RP Dechesne, CJ (reprint author), Univ Montpellier 2, INSERM, U 432, CC 89,Pl Bataillon, F-34095 Montpellier 5, France. RI Roder, John/G-6468-2013 CR BERGLUND AM, 1987, J COMP NEUROL, V255, P560, DOI 10.1002/cne.902550408 Braunewell KH, 1999, CELL TISSUE RES, V295, P1, DOI 10.1007/s004410051207 CHIMENTO TC, 1994, J NEUROPHYSIOL, V71, P1883 COLE KS, 1992, BRAIN RES, V575, P223 DECAMILLI P, 1995, NATURE, V375, P450, DOI 10.1038/375450a0 Dechesne CJ, 1997, DEV BRAIN RES, V99, P103, DOI 10.1016/S0165-3806(96)00216-7 DECHESNE CJ, 1994, J COMP NEUROL, V346, P517, DOI 10.1002/cne.903460405 DECHESNE CJ, 1988, DEV BRAIN RES, V40, P233, DOI 10.1016/0165-3806(88)90135-6 DEMEMES D, 1993, CELL TISSUE RES, V274, P487, DOI 10.1007/BF00314545 DESMADRYL G, 1992, EXP BRAIN RES, V89, P105 DESMADRYL G, 1992, DEV AUDITORY VESTIBU, V2, P461 GILLOYZAGA P, 1988, INT J DEV NEUROSCI, V6, P155, DOI 10.1016/0736-5748(88)90040-8 Hendricks KB, 1999, NAT CELL BIOL, V1, P234, DOI 10.1038/12058 Iurato S, 1972, Prog Brain Res, V37, P429, DOI 10.1016/S0079-6123(08)63917-5 KNIPPER M, 1995, DEV BRAIN RES, V89, P73, DOI 10.1016/0165-3806(95)00113-R LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LIBERMAN MC, 1990, J COMP NEUROL, V301, P442 Ludger J, 1998, EUR J NEUROSCI, V10, P415 Martone ME, 1999, CELL TISSUE RES, V295, P395, DOI 10.1007/s004410051246 MBIENE JP, 1988, ANAT EMBRYOL, V177, P331, DOI 10.1007/BF00315841 McFerran BW, 1998, J BIOL CHEM, V273, P22768, DOI 10.1074/jbc.273.35.22768 Olafsson P, 1997, MOL BRAIN RES, V44, P73, DOI 10.1016/S0169-328X(96)00188-X OLAFSSON P, 1995, P NATL ACAD SCI USA, V92, P8001, DOI 10.1073/pnas.92.17.8001 PONGS O, 1993, NEURON, V11, P15, DOI 10.1016/0896-6273(93)90267-U PUJOL R, 1986, ADV NEURAL BEHAV DEV, V2, P1 Pujol R., 1986, NEUROBIOLOGY HEARING, P161 RIVOSECCHI R, 1994, J PHYSIOL-LONDON, V474, P223 ROSS MD, 1986, ACTA OTO-LARYNGOL, V102, P75, DOI 10.3109/00016488609108649 Ruben R. J., 1967, ACTA OTO-LARYNGOL, V220, P1 Safieddine S, 1999, EUR J NEUROSCI, V11, P803, DOI 10.1046/j.1460-9568.1999.00487.x SCARFONE E, 1988, J NEUROSCI, V8, P4640 SCHELLER RH, 1995, NEURON, V14, P893 Shnerson A, 1983, AUDITORY PSYCHOBIOLO, P395 SUDHOF TC, 1995, NATURE, V375, P645, DOI 10.1038/375645a0 Warr WB, 1997, HEARING RES, V108, P89, DOI 10.1016/S0378-5955(97)00044-0 WERIE MJ, 2000, NEUROSCI LETT, V284, P33 Wersall J., 1974, P123 NR 37 TC 24 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 70 EP 82 DI 10.1016/S0378-5955(00)00183-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400005 PM 11077193 ER PT J AU Dolgobrodov, SG Lukashkin, AN Russell, IJ AF Dolgobrodov, SG Lukashkin, AN Russell, IJ TI Electrostatic interaction between stereocilia: I. Its role in supporting the structure of the hair bundle SO HEARING RESEARCH LA English DT Article DE cochlear non-linearity; glycocalyx; hair cell; electrostatic interaction ID GUINEA-PIG COCHLEA; INNER-EAR; CELL-SURFACE; TRANSDUCTION CHANNELS; CROSS-LINKS; MEMBRANE; FUSION; ORGAN; CORTI; COAT AB This paper provides theoretical estimates for the forces of electrostatic interaction between adjacent stereocilia in auditory and vestibular hair cells. Estimates are given for parameters within the measured physiological range using constraints appropriate for the known geometry of the hair bundle. Stereocilia are assumed to possess an extended, negatively charged surface coat, the glycocalyx. Different charge distribution profiles within the glycocalyx are analysed. II is shown that charged glycocalices on the apical surface of the hair cells can support spatial separation between adjacent stereocilia in the hair bundles through electrostatic repulsion between stereocilia. The charge density profile within the glycocalyx is a crucial parameter. In fact, attraction instead of repulsion between adjacent stereocilia will be observed if the charge of the glycocalyx is concentrated near the membrane of the stereocilia, thereby making this type of charge distribution unlikely. The forces of electrostatic interaction between stereocilia may influence the mechanical properties of the hair bundle and, being strongly non-linear, contribute to the non-linear phenomena that have been recorded from the periphery of the auditory and vestibular systems. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Sussex, Sch Biol Sci, Brighton BN1 9QG, E Sussex, England. IP Pavlov Physiol Inst, St Petersburg 199034, Russia. RP Lukashkin, AN (reprint author), Univ Sussex, Sch Biol Sci, Brighton BN1 9QG, E Sussex, England. CR ABRAHAM M, 1932, THEORIE ELEKTRIZITAE ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 BOSHER SK, 1978, NATURE, V273, P377, DOI 10.1038/273377a0 CEVC G, 1990, BIOCHIM BIOPHYS ACTA, V1031, P311, DOI 10.1016/0304-4157(90)90015-5 CHERNOMORDIK LV, 1987, BIOCHIM BIOPHYS ACTA, V906, P309, DOI 10.1016/0304-4157(87)90016-5 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X COURANT R, 1993, METHODEN MATH PHYSIK Derjaguin B, 1940, T FARADAY SOC, V36, P203 Dolgobrodov SG, 2000, HEARING RES, V150, P94, DOI 10.1016/S0378-5955(00)00196-9 DONATH E, 1983, J THEOR BIOL, V101, P569, DOI 10.1016/0022-5193(83)90016-4 DONATH E, 1988, COLLOID POLYM SCI, V266, P1024, DOI 10.1007/BF01428812 Donath E, 1996, LANGMUIR, V12, P4832, DOI 10.1021/la960204m DONATH E, 1980, J ELECTROANAL CHEM, V116, P41, DOI 10.1016/S0022-0728(80)80219-1 DONATH E, 1986, J COLLOID INTERF SCI, V109, P122, DOI 10.1016/0021-9797(86)90288-2 Duncan RK, 1999, HEARING RES, V127, P22, DOI 10.1016/S0378-5955(98)00168-3 Eisen MD, 1999, HEARING RES, V127, P14, DOI 10.1016/S0378-5955(98)00167-1 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 FURNESS DN, 1985, HEARING RES, V18, P177, DOI 10.1016/0378-5955(85)90010-3 Furness DN, 1997, P ROY SOC B-BIOL SCI, V264, P45 GOODYEAR R, 1992, J COMP NEUROL, V325, P243, DOI 10.1002/cne.903250208 Goodyear R, 1999, J NEUROSCI, V19, P3761 GOODYEAR R, 1994, J COMP NEUROL, V345, P267, DOI 10.1002/cne.903450208 HACOHEN N, 1989, J NEUROSCI, V9, P3988 HEINRICH R, 1982, J THEOR BIOL, V96, P211, DOI 10.1016/0022-5193(82)90222-3 HELM CA, 1992, BIOCHEMISTRY-US, V31, P1794, DOI 10.1021/bi00121a030 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 HOWARD J, 1986, HEARING RES, V23, P93, DOI 10.1016/0378-5955(86)90178-4 MARKIN VS, 1984, GEN PHYSIOL BIOPHYS, V3, P361 MCDANIEL RV, 1986, BIOPHYS J, V49, P741 MCDANIEL RV, 1986, BIOPHYS J, V49, P94 MCLAUGHLIN S, 1977, CURR TOP MEMBR TRANS, V9, P71, DOI 10.1016/S0070-2161(08)60677-2 MCLAUGHLIN S, 1989, ANNU REV BIOPHYS BIO, V18, P113, DOI 10.1146/annurev.biophys.18.1.113 NEUGEBAUER DC, 1987, CELL TISSUE RES, V249, P199, DOI 10.1007/BF00215434 OSBORNE MP, 1984, CELL TISSUE RES, V237, P43 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PRIETO JJ, 1986, HEARING RES, V24, P237, DOI 10.1016/0378-5955(86)90022-5 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SANTI PA, 1987, HEARING RES, V27, P47, DOI 10.1016/0378-5955(87)90025-6 SLEPECKY N, 1985, HEARING RES, V17, P281, DOI 10.1016/0378-5955(85)90072-3 TAKUMIDA M, 1989, J LARYNGOL OTOL, V103, P1125, DOI 10.1017/S002221510011117X Takumida M, 1988, Acta Otolaryngol Suppl, V458, P84 VANBENTHEM PPG, 1992, ACTA OTO-LARYNGOL, V112, P976, DOI 10.3109/00016489209137498 VOIGT A, 1982, J THEOR BIOL, V98, P262 WEISS TF, 1996, CELLULAR BIOPHYSICS, V1 NR 44 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 83 EP 93 DI 10.1016/S0378-5955(00)00184-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400006 PM 11077194 ER PT J AU Dolgobrodov, SG Lukashkin, AN Russell, IJ AF Dolgobrodov, SG Lukashkin, AN Russell, IJ TI Electrostatic interaction between stereocilia: II. Influence on the mechanical properties of the hair bundle SO HEARING RESEARCH LA English DT Article DE cochlear non-linearity; glycocalyx; hair cell; electrostatic interaction ID MECHANOELECTRICAL TRANSDUCTION; CELL-SURFACE; INTERNAL EAR; LATERAL-LINE; TIP LINKS; INNER-EAR; STIFFNESS; ADAPTATION; INTEGRITY; MEMBRANE AB This paper is based on our model [Dolgrobrodov et al., 2000. Hear. Res., submitted for publication] in which we examine the significance of the polyanionic surface layers of stereocilia for electrostatic interaction between them. We analyse how electrostatic forces modify the mechanical properties of the sensory hair bundle. Different charge distribution profiles within the glycocalyx are considered. When modelling a typical experiment on bundle stiffness measurements. applying an external force to the tallest row of stereocilia shows that the asymptotic stiffness of the hair bundle for negative displacements is always larger than the asymptotic stiffness for positive displacements. This increase in stiffness is monotonic for even charge distribution and shows local minima when the negative charge is concentrated in a thinner layer within the cell coat. The minima can also originate from the co-operative effect of electrostatic repulsion and inter-ciliary links with non-linear mechanical properties. Existing experimental observations are compared with the predictions of the model. We conclude that the forces of electrostatic interaction between stereocilia may influence the mechanical properties of the hair bundle and, being strongly non-linear, contribute to the non-linear phenomena, which have been recorded from the auditory periphery. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Sussex, Sch Biol Sci, Brighton BN1 9QG, E Sussex, England. IP Pavlov Physiol Inst, St Petersburg 199034, Russia. RP Lukashkin, AN (reprint author), Univ Sussex, Sch Biol Sci, Brighton BN1 9QG, E Sussex, England. CR ASSAD JA, 1992, J NEUROSCI, V12, P3291 ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X BOSHER SK, 1978, NATURE, V273, P377, DOI 10.1038/273377a0 CEVC G, 1990, BIOCHIM BIOPHYS ACTA, V1031, P311, DOI 10.1016/0304-4157(90)90015-5 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DENK W, 1989, P NATL ACAD SCI USA, V86, P5371, DOI 10.1073/pnas.86.14.5371 DENK W, 1992, J NEUROPHYSIOL, V68, P927 Dolgobrodov SG, 2000, HEARING RES, V150, P83, DOI 10.1016/S0378-5955(00)00184-2 DONATH E, 1983, J THEOR BIOL, V101, P569, DOI 10.1016/0022-5193(83)90016-4 Duncan RK, 1998, HEARING RES, V124, P69, DOI 10.1016/S0378-5955(98)00118-X Eisen MD, 1999, HEARING RES, V127, P14, DOI 10.1016/S0378-5955(98)00167-1 FORGE A, 1989, HEARING RES, V37, P129, DOI 10.1016/0378-5955(89)90035-X GOODYEAR R, 1992, J COMP NEUROL, V325, P243, DOI 10.1002/cne.903250208 Goodyear R, 1999, J NEUROSCI, V19, P3761 GOODYEAR R, 1994, J COMP NEUROL, V345, P267, DOI 10.1002/cne.903450208 HOWARD J, 1987, P NATL ACAD SCI USA, V84, P3064, DOI 10.1073/pnas.84.9.3064 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 HOWARD J, 1986, HEARING RES, V23, P93, DOI 10.1016/0378-5955(86)90178-4 HUDSPETH AJ, 1994, NEURON, V12, P1, DOI 10.1016/0896-6273(94)90147-3 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 JACOBS RA, 1990, COLD SH Q B, V55, P547 KOSSL M, 1990, HEARING RES, V44, P217, DOI 10.1016/0378-5955(90)90082-Z KROESE ABA, 1982, HEARING RES, V6, P183, DOI 10.1016/0378-5955(82)90053-3 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MARKIN VS, 1995, ANNU REV BIOPH BIOM, V24, P59 Marquis RE, 1997, P NATL ACAD SCI USA, V94, P11923, DOI 10.1073/pnas.94.22.11923 NELDER JA, 1965, COMPUT J, V7, P308 NEUGEBAUER DC, 1987, CELL TISSUE RES, V249, P199, DOI 10.1007/BF00215434 PAE SS, 1994, P NATL ACAD SCI USA, V91, P1153, DOI 10.1073/pnas.91.3.1153 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PICKLES JO, 1993, HEARING RES, V68, P159, DOI 10.1016/0378-5955(93)90120-P RUSSELL IJ, 1992, P ROY SOC B-BIOL SCI, V250, P217, DOI 10.1098/rspb.1992.0152 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SAND O, 1975, J COMP PHYSIOL, V102, P27 STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 SZYMKO YM, 1992, HEARING RES, V59, P241, DOI 10.1016/0378-5955(92)90120-C TAKUMIDA M, 1989, HEARING RES, V37, P163, DOI 10.1016/0378-5955(89)90037-3 VANNETTEN SM, 1994, P NATL ACAD SCI USA, V91, P1549, DOI 10.1073/pnas.91.4.1549 WANG BM, 1984, BIOCHEM PHARMACOL, V33, P3257, DOI 10.1016/0006-2952(84)90087-X Wersäll J, 1973, Adv Otorhinolaryngol, V20, P14 NR 40 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 94 EP 103 DI 10.1016/S0378-5955(00)00196-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400007 PM 11077195 ER PT J AU Recanzone, GH AF Recanzone, GH TI Response profiles of auditory cortical neurons to tones and noise in behaving macaque monkeys SO HEARING RESEARCH LA English DT Article DE macaque monkey; auditory cortex; physiology; primary auditory cortex; caudomedial field ID SINGLE-UNIT-ACTIVITY; POSTEROVENTRAL COCHLEAR NUCLEUS; INFERIOR COLLICULUS; RHESUS-MONKEY; TONOTOPIC ORGANIZATION; CORTEX; CAT; DORSAL; FIELDS; DEPENDENCY AB The primate auditory cortex is anatomically divided into several areas, but little is known about the functional differences between these areas. Similarly, although neurons in sub-cortical auditory areas of other species have been classified into distinct categories. these criteria have not been applied in primates. This study measured the responses of single neurons in the primary auditory cortex (AI) and the caudomedial field (CM) to tones and noise. Most neurons could be qualitatively classified as Onset, sustained,or sustained-onset, but never as primary (VIII nerve)-like or chopper. Quantitative analysis showed a continuum of response types, from having only onset responses to responding throughout the stimulus period. AI neurons had higher firing rates that CM neurons, but CM neurons had higher firing rates to noise stimuli compared to tone stimuli, and a greater percentage of CM neurons had excitatory responses after stimulus offset. There were no differences in the percentage of neurons that had tonic or inhibitory responses. These results indicate that the responses of neurons in the primate auditory cortex are better described as a continuum rather than as discrete classes, and provide further evidence that auditory information is processed in series between Al and CM in the primate. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calif Davis, Ctr Neurosci, Davis, CA 95616 USA. Univ Calif Davis, Sect Neurobiol Physiol & Behav, Davis, CA 95616 USA. RP Recanzone, GH (reprint author), Univ Calif Davis, Ctr Neurosci, 1544 Newton Ct, Davis, CA 95616 USA. CR AITKIN LM, 1972, BRAIN RES, V47, P77, DOI 10.1016/0006-8993(72)90253-3 BENSON DA, 1981, BRAIN RES, V219, P249, DOI 10.1016/0006-8993(81)90290-0 Bushara KO, 1999, NAT NEUROSCI, V2, P759 CRIST CF, 1988, J NEUROSCI METH, V26, P117, DOI 10.1016/0165-0270(88)90160-4 EHRET G, 1985, J COMP PHYSIOL A, V156, P619, DOI 10.1007/BF00619111 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 HEIMANPATTERSON TD, 1985, J MORPHOL, V186, P289, DOI 10.1002/jmor.1051860306 Kaas JH, 1999, CURR OPIN NEUROBIOL, V9, P164, DOI 10.1016/S0959-4388(99)80022-1 Kaas JH, 1998, AUDIOL NEURO-OTOL, V3, P73, DOI 10.1159/000013783 KIANG NYS, 1965, ANN OTO RHINOL LARYN, V74, P463 Kosaki H, 1997, J COMP NEUROL, V386, P304 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 MERZENIC.MM, 1973, BRAIN RES, V50, P275, DOI 10.1016/0006-8993(73)90731-2 MILLER JM, 1972, SCIENCE, V177, P449, DOI 10.1126/science.177.4047.449 MOORE JK, 1980, J COMP NEUROL, V193, P609 MOREL A, 1993, J COMP NEUROL, V335, P437, DOI 10.1002/cne.903350312 Nuding SC, 1999, HEARING RES, V131, P89, DOI 10.1016/S0378-5955(99)00023-4 PFINGST BE, 1981, J NEUROPHYSIOL, V45, P16 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 Rauschecker JP, 1997, J COMP NEUROL, V382, P89 Rauschecker JP, 1998, AUDIOL NEURO-OTOL, V3, P86, DOI 10.1159/000013784 Recanzone GH, 2000, J NEUROPHYSIOL, V83, P2315 Recanzone GH, 2000, J NEUROPHYSIOL, V83, P2723 RHODE WS, 1987, J NEUROPHYSIOL, V57, P414 Rhode WS, 1991, NEUROBIOLOGY HEARING, P47 Romanski LM, 1999, NAT NEUROSCI, V2, P1131, DOI 10.1038/16056 RYAN A, 1978, EXP BRAIN RES, V32, P389 RYAN A, 1977, J NEUROPHYSIOL, V40, P943 SACHS MB, 1991, NEUROBIOLOGY HEARING, P79 Sutter ML, 1999, J NEUROPHYSIOL, V82, P2358 VOLKOV I O, 1985, Neirofiziologiya, V17, P500 VOLKOV I O, 1985, Neirofiziologiya, V17, P728 VOLKOV I O, 1989, Neirofiziologiya, V21, P498 Weeks RA, 1999, NEUROSCI LETT, V262, P155, DOI 10.1016/S0304-3940(99)00062-2 Young E.D, 1984, HEARING SCI, P423 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 NR 38 TC 85 Z9 85 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 104 EP 118 DI 10.1016/S0378-5955(00)00194-5 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400008 PM 11077196 ER PT J AU Thiers, FA Burgess, BJ Nadol, JB AF Thiers, FA Burgess, BJ Nadol, JB TI Prevalence and ultrastructural morphology of axosomatic synapses on spiral ganglion cells in humans of different ages SO HEARING RESEARCH LA English DT Article DE spiral ganglion; synapse; efferent; maturation; degeneration ID OUTER HAIR-CELLS; ELECTRON-MICROSCOPIC OBSERVATIONS; ANTEROVENTRAL COCHLEAR NUCLEUS; MEDIAL OLIVOCOCHLEAR SYSTEM; CAT; NERVE; INNERVATION; MATURATION; NEURONS; DEGENERATION AB Axosomatic synapses were found on human spiral ganglion cells (HSGCs). Ultrastructural characterization and calculation of the prevalence of these synapses were performed by electron microscopic semi-serial sections of both type I and type II HSGCs, in specimens from subjects of ages 1 day, 14 days, 21 years and 51 years. Synapses on type I HSGCs were extremely rare. In contrast, axosomatic synapses were present on approximately 50% of type II HSGCs of a young adult. This prevalence seemed to vary by age. Thus, no synapses were found in a I-day old neonate, few in a 14-day old, and on approximately 15% of the type II SGCs from a 51-year old specimen. The origin of the nerve fibers synapsing on the type II HSGCs could not be determined. In view of the fact that some of the fibers projected from the intraganglionic spiral bundle, which is known to contain olivocochlear efferents, these fibers may represent an efferent pathway to the spiral ganglion. However, since there was morphological evidence of more than one type of nerve fiber synapsing on type II HSGCs, other neural origins must be considered. Although the physiological function of these synapses is unknown, they may mediate pre-synaptic neural modulation of the type II HSGCs at the level of the spiral ganglion. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA. RP Nadol, JB (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA. CR Abdala C, 1999, J ACOUST SOC AM, V105, P2392, DOI 10.1121/1.426844 ADAMO NJ, 1973, J NEUROCYTOL, V2, P91, DOI 10.1007/BF01099211 ARNOLD WJ, 1982, AM J OTOL, V3, P266 BERLUND AM, 1996, HEARING RES, V93, P31 BODIAN D, 1978, P NATL ACAD SCI USA, V75, P4582, DOI 10.1073/pnas.75.9.4582 CANT NB, 1979, NEUROSCIENCE, V4, P1925, DOI 10.1016/0306-4522(79)90066-6 CASTOR X, 1994, HEARING RES, V77, P1, DOI 10.1016/0378-5955(94)90248-8 CHIONG CM, 1993, HEARING RES, V67, P211, DOI 10.1016/0378-5955(93)90249-Z FRANCIS HW, 1993, HEARING RES, V64, P184, DOI 10.1016/0378-5955(93)90004-K GINZBERG RD, 1984, HEARING RES, V14, P109, DOI 10.1016/0378-5955(84)90011-X GRAY EG, 1963, J ANAT, V97, P101 HINOJOSA R, 1995, AM J OTOL, V16, P731 IVANOV E, 1992, ACTA OTO-LARYNGOL, V112, P985, DOI 10.3109/00016489209137499 KIM DO, 1984, RECENT ADV HEARING S, P241 KIMURA RS, 1986, P 33 M JAP SOC EAR R, P5 Kimura R S, 1987, Acta Otolaryngol Suppl, V438, P1 KIMURA RS, 1979, ANN OTOL RHINOL LA S, V88, P2 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 MORLET T, 1993, ACTA OTO-LARYNGOL, V113, P271, DOI 10.3109/00016489309135808 NADOL JB, 1990, HEARING RES, V49, P141, DOI 10.1016/0378-5955(90)90101-T NADOL JB, 1990, J ELECTRON MICR TECH, V15, P187, DOI 10.1002/jemt.1060150210 NADOL JB, 1977, ANN OTO RHINOL LARYN, V86, P507 NADOL JB, 1990, ANN OTO RHINOL LARYN, V99, P340 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 Rask-Andersen H, 2000, HEARING RES, V141, P1, DOI 10.1016/S0378-5955(99)00179-3 Rask-Andersen Helge, 1997, Auris Nasus Larynx, V24, P1, DOI 10.1016/S0385-8146(96)00039-9 ROMAND MR, 1987, ACTA OTO-LARYNGOL, V104, P29, DOI 10.3109/00016488709109044 ROMAND R, 1983, BRAIN RES, V229, P15 ROMAND R, 1986, HEARING RES, V21, P161, DOI 10.1016/0378-5955(86)90036-5 ROSENBLUTH J, 1962, J CELL BIOL, V12, P329, DOI 10.1083/jcb.12.2.329 RUGGERO MA, 1982, HEARING RES, V8, P339, DOI 10.1016/0378-5955(82)90023-5 Sato M, 1997, HEARING RES, V108, P46, DOI 10.1016/S0378-5955(97)00049-X SCHUKNECHT HF, 1993, PATHOLOGY EAR, P273 Spirou GA, 1998, J COMP NEUROL, V398, P257, DOI 10.1002/(SICI)1096-9861(19980824)398:2<257::AID-CNE7>3.0.CO;2-# SPOENDLIN H, 1988, ACTA OTO-LARYNGOL, V105, P403, DOI 10.3109/00016488809119493 THOMSEN E, 1967, ACTA OTOLARYNGOL S, V224, P442 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3053, DOI 10.1016/0306-4522(82)90229-9 UZIEL A, 1981, AUDIOLOGY, V20, P89 ZIMMERMANN CE, 1995, HEARING RES, V90, P192, DOI 10.1016/0378-5955(95)00165-1 NR 40 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 119 EP 131 DI 10.1016/S0378-5955(00)00193-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400009 PM 11077197 ER PT J AU Hofstetter, P Ding, DL Salvi, R AF Hofstetter, P Ding, DL Salvi, R TI Induction of spontaneous otoacoustic emissions in chinchillas from carboplatin-induced inner hair cell loss SO HEARING RESEARCH LA English DT Article DE spontaneous otoacoustic emission; chinchilla; hair cell; carboplatin ID FROG RANA-ESCULENTA; TEMPERATURE-DEPENDENCE; BUNDLE MOVEMENTS; EXTERNAL TONES; BOBTAIL LIZARD; COCHLEA; MAGNITUDE; CHANNELS; PATTERN; EARS AB Fifteen chinchillas were evaluated for spontaneous otoacoustic emissions (SOAEs) before and after administering carboplatin (126-200 mg/kg), an anti-neoplastic drug that selectively destroys inner hair cells (IHCs) in this species. SOAEs were absent from all animals prior to carboplatin treatment, but at 1 week post-treatment, 47% of the animals and 30% of the ears had developed SOAEs. SOAE frequencies were clustered between 5 and 10 kHz and SOAE intensity ranged from 10 to 32 dB SPL. All of the ears with SOAEs had THC lesions exceeding 60% throughout most of the cochlea and two ears had outer hair cell lesions of 25-60% at a cochlear place associated with the frequency of the SOAE. Thus, high doses of carboplatin that cause IHC loss can be used to create an animal model with. SOAEs. (C) 2000 Elsevier Science B.V. Ail rights reserved. C1 SUNY Buffalo, Hearing Res Lab, Buffalo, NY 14214 USA. RP Salvi, R (reprint author), SUNY Buffalo, Hearing Res Lab, 215 Parker Hall, Buffalo, NY 14214 USA. CR ASHMORE J, 1986, J PHYSIOL-LONDON, V376, P49 Benser ME, 1996, J NEUROSCI, V16, P5629 BRIX J, 1994, HEARING RES, V76, P147, DOI 10.1016/0378-5955(94)90096-5 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Burkard R, 1996, Audiol Neurootol, V1, P197 CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 DENK W, 1989, P NATL ACAD SCI USA, V86, P5371, DOI 10.1073/pnas.86.14.5371 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 Hofstetter P, 1997, AUDIOLOGY, V36, P301 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KEMP DT, 1982, NEW PERSPECTIVES NOI, P189 KOPPL C, 1994, HEARING RES, V72, P159, DOI 10.1016/0378-5955(94)90215-1 LONG GR, 1986, PERIPHERAL AUDITORY Long GR, 1996, HEARING RES, V98, P22, DOI 10.1016/0378-5955(96)00057-3 MAMMANO F, 1993, NATURE, V365, P838, DOI 10.1038/365838a0 MANLEY GA, 1994, HEARING RES, V72, P171, DOI 10.1016/0378-5955(94)90216-X Martin P, 1999, P NATL ACAD SCI USA, V96, P14306, DOI 10.1073/pnas.96.25.14306 Nuttall AL, 1999, HEARING RES, V131, P39, DOI 10.1016/S0378-5955(99)00009-X POWERS NL, 1995, NATURE, V375, P585, DOI 10.1038/375585a0 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 PROBST R, 1990, NEW ASPECTS COCHLEAR, P1 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 SNYDER DL, 1994, LAB ANIMAL, V23, P42 Stewart CE, 2000, P NATL ACAD SCI USA, V97, P454, DOI 10.1073/pnas.97.1.454 Trautwein P, 1996, HEARING RES, V96, P71, DOI 10.1016/0378-5955(96)00040-8 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 ZUREK PM, 1981, J ACOUST SOC AM, V70, P446, DOI 10.1121/1.386787 NR 34 TC 9 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 132 EP 136 DI 10.1016/S0378-5955(00)00201-X PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400010 PM 11077198 ER PT J AU Sun, W Ding, DL Reyes, S Salvi, RJ AF Sun, W Ding, DL Reyes, S Salvi, RJ TI Effects of AC and DC stimulation on chinchilla SOAE amplitude and frequency SO HEARING RESEARCH LA English DT Article DE spontaneous otoacoustic emission; electrical stimulation; chinchilla; distortion product otoacoustic emission; inner hair cell; outer hair cell ID OUTER HAIR-CELLS; SPONTANEOUS OTOACOUSTIC EMISSIONS; GUINEA-PIG; MECHANICAL RESPONSES; COCHLEAR AMPLIFIER; NONHUMAN PRIMATE; INNER; CARBOPLATIN; BUNDLES; CHICKEN AB The effects of AC and DC current on spontaneous otoacoustic emissions (SOAEs) were studied in normal chinchillas and chinchillas with selective inner hair cell(IHC) loss. Electrical stimulation was delivered through an electrode on the round window or through an electrode in scala media. SOAE frequencies ranged from 4 to 11 kHz and amplitudes ranged from 13 to 51 dB SPL. AC simulation suppressed SOAE amplitude. The suppression contours had a narrowly tuned, low-threshold tip located above the frequency of the SOAE. AC suppression contours were similar to acoustic suppression contours except that the AC suppression contours lacked a high-threshold, low frequency tail. The lowest threshold of the AC suppression contour was 3.9 muA rms whereas the lowest acoustic suppression threshold was 19 dB SPL. AC stimulation, which induced an electrically evoked otoacoustic emission, interacted with the SOAE to generate distortion product otoacoustic emissions (DPOAEs) of up to 26 dB SPL at 2f(S)-f(AC) (f(S) = SOAE). DPOAE amplitude increased with AC current, but saturated at high levels. DC current steps affected both SOAE frequency and amplitude. Positive current at the round window decreased SOAE amplitude and frequency whereas negative current increased SOAE frequency, but had little effect on amplitude. The effects of AC and DC current on SOAEs in animals with IHC loss were similar to those in normal chinchillas. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Buffalo, Hearing Res Lab, Buffalo, NY 14214 USA. PLA Gen Hosp, Otolaryngol Inst, Beijing 100853, Peoples R China. RP Salvi, RJ (reprint author), SUNY Buffalo, Hearing Res Lab, 215 Parker Hall, Buffalo, NY 14214 USA. CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BRIX J, 1994, HEARING RES, V76, P147, DOI 10.1016/0378-5955(94)90096-5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Burkard R, 1996, Audiol Neurootol, V1, P197 CHEN L, 1998, PSYCHOPHYSICAL PHYSL, P130 CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DALLOS P, 1993, J NEUROPHYSIOL, V70, P299 Ding DL, 1999, AUDIOL NEURO-OTOL, V4, P55, DOI 10.1159/000013822 Frank G, 1999, P NATL ACAD SCI USA, V96, P4420, DOI 10.1073/pnas.96.8.4420 FROYMOVICH O, 1995, J ACOUST SOC AM, V97, P3021, DOI 10.1121/1.411867 Gale JE, 1997, NATURE, V389, P63, DOI 10.1038/37968 GITTER AH, 1988, BASIC ISSUES HEARING, P32 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 He DZZ, 1999, P NATL ACAD SCI USA, V96, P8223, DOI 10.1073/pnas.96.14.8223 Hofstetter P, 2000, HEARING RES, V150, P132, DOI 10.1016/S0378-5955(00)00201-X Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KETTEMBEIL S, 1995, HEARING RES, V86, P47, DOI 10.1016/0378-5955(95)00053-7 KIRK DL, 1994, HEARING RES, V74, P38, DOI 10.1016/0378-5955(94)90174-0 MARTIN GK, 1988, HEARING RES, V33, P49, DOI 10.1016/0378-5955(88)90020-2 MARTIN GK, 1985, HEARING RES, V20, P91, DOI 10.1016/0378-5955(85)90062-0 MURPHY WJ, 1999, ABSTR ASS RES OT, V22, P94 NORTON ST, 1990, MECH BIOPHYSICS HEAR NUTTALL AL, 1985, J ACOUST SOC AM, V77, P165, DOI 10.1121/1.392282 NUTTALL AL, 1995, ACTIVE HEARING, P283 Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 PENNER MJ, 1993, HEARING RES, V68, P229, DOI 10.1016/0378-5955(93)90126-L POWERS NL, 1995, NATURE, V375, P585, DOI 10.1038/375585a0 PROBST R, 1990, NEW ASPECTS COCHLEAR, P1 Ren TY, 1996, HEARING RES, V102, P43, DOI 10.1016/S0378-5955(96)00145-1 REYES SA, 1999, ABSTR ASS RES OT, V22, P95 RUGGERO MA, 1984, HEARING RES, V13, P293, DOI 10.1016/0378-5955(84)90083-2 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 Trautwein P, 1996, HEARING RES, V96, P71, DOI 10.1016/0378-5955(96)00040-8 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 WAKE M, 1994, LARYNGOSCOPE, V104, P488 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 WILSON JP, 1980, HEARING RES, V2, P527, DOI 10.1016/0378-5955(80)90090-8 WIT HP, 1989, HEARING RES, V41, P199, DOI 10.1016/0378-5955(89)90011-7 Zhao HB, 1999, NATURE, V399, P359 Zheng J, 2000, NATURE, V405, P149, DOI 10.1038/35012009 ZIMMERMANN U, 1989, DYNAMICS PLASTICITY, P286 ZUREK PM, 1981, J ACOUST SOC AM, V70, P446, DOI 10.1121/1.386787 NR 47 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 137 EP 148 DI 10.1016/S0378-5955(00)00195-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400011 PM 11077199 ER PT J AU Barsz, K Wilson, WW Walton, JP AF Barsz, K Wilson, WW Walton, JP TI Background noise differentially effects temporal coding by tonic units in the mouse inferior colliculus SO HEARING RESEARCH LA English DT Article DE inferior colliculus; CBA mouse; temporal processing; background noise; tonic unit ID AUDITORY-NERVE FIBERS; GAP DETECTION; HEARING-LOSS; CBA MOUSE; NEURONS; RESPONSES; REPRESENTATION; CHINCHILLA; MODULATION; SINUSOIDS AB In natural environments, temporally complex signals often occur in a background of noise. The neural mechanisms underlying the preservation of temporal sensitivity in background noise are poorly understood. In the present study, we examined the ability of inferior colliculus (IC) units with primary-like and sustained response patterns ('tonic units') to encode silent gaps in quiet and in background noise, Minimum gap thresholds (MGTs), the shortest silent gap in a noise burst evoking a neural response, were measured in quiet and background noise for 34 IC units. Units were classified as background noise resistant (BNR; MGT did not change in background noise) or background noise sensitive (BNS; MGTs became elevated in background noise). In quiet, the MGTs of BNR and BNS units were comparable and both types of units encoded the gap by a cessation of activity during the gap. The addition of background noise had little effect on the response rate of BNR units either during or after the gap stimulus. In contrast, for BNS units, background noise reduced the response rate during the gap stimulus while increasing the response rate after the gap stimulus. Background noise also altered the first spike latency of BNS units. For BNS units, the mean first spike latency was no longer inversely related to BF, but this relationship was maintained in BNR units. These results suggest that the response of BNS units to background noise obliterates their response to the gap stimulus. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Rochester, Sch Med & Dent, Dept Surg, Otolaryngol Div, Rochester, NY 14642 USA. RP Walton, JP (reprint author), Univ Rochester, Sch Med & Dent, Dept Surg, Otolaryngol Div, POB 629, Rochester, NY 14642 USA. CR Barsz K, 1998, HEARING RES, V115, P13, DOI 10.1016/S0378-5955(97)00173-1 BUCHFELLNER E, 1989, J COMP PHYSIOL A, V164, P539, DOI 10.1007/BF00610447 Chen GD, 1998, HEARING RES, V122, P142, DOI 10.1016/S0378-5955(98)00103-8 COSTALUPES JA, 1984, J NEUROPHYSIOL, V51, P1326 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 EHRET G, 1984, HEARING RES, V14, P45, DOI 10.1016/0378-5955(84)90068-6 ERLICH D, 1997, J NEUROPHYSIOL, V77, P2360 FENG AS, 1994, J COMP PHYSIOL A, V175, P531 FORREST TG, 1987, J ACOUST SOC AM, V82, P1933, DOI 10.1121/1.395689 GELFAND SA, 1988, J ACOUST SOC AM, V83, P248, DOI 10.1121/1.396426 GIBSON DJ, 1985, J NEUROPHYSIOL, V53, P940 GREEN DM, 1989, J ACOUST SOC AM, V86, P961, DOI 10.1121/1.398731 HAPLEA S, 1994, J COMP PHYSIOL A, V174, P671 LeBeau FEN, 1996, J NEUROPHYSIOL, V75, P902 MCFADDEN SL, 1994, HEARING RES, V78, P132, DOI 10.1016/0378-5955(94)90019-1 PHILLIPS DP, 1987, J ACOUST SOC AM, V82, P1, DOI 10.1121/1.395547 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1990, J ACOUST SOC AM, V88, P1403, DOI 10.1121/1.399718 PHILLIPS DP, 1985, HEARING RES, V18, P87, DOI 10.1016/0378-5955(85)90112-1 Pickles JO, 1988, INTRO PHYSL HEARING REES A, 1988, J ACOUST SOC AM, V83, P1488, DOI 10.1121/1.395904 REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 Walton J. P., 1997, Society for Neuroscience Abstracts, V23, P2069 Walton JP, 1998, J NEUROSCI, V18, P2764 Walton JP, 1997, J COMP PHYSIOL A, V181, P161, DOI 10.1007/s003590050103 WILLOTT JF, 1978, J COMP PHYSIOL, V127, P175 Yan W, 1998, NAT NEUROSCI, V1, P54, DOI 10.1038/255 ZHANG W, 1990, HEARING RES, V46, P181, DOI 10.1016/0378-5955(90)90001-6 NR 28 TC 3 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 149 EP 160 DI 10.1016/S0378-5955(00)00186-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400012 PM 11077200 ER PT J AU Chen, QC Jen, PHS AF Chen, QC Jen, PHS TI Bicuculline application affects discharge patterns, rate-intensity functions, and frequency tuning characteristics of bat auditory cortical neurons SO HEARING RESEARCH LA English DT Article DE auditory cortex; bat; bicuculline; intensity function; frequency tuning curve ID INFERIOR COLLICULUS NEURONS; AMPLITUDE-SPECTRUM REPRESENTATION; SINGLE UNIT RESPONSES; BIG BROWN BAT; EPTESICUS-FUSCUS; TOPOGRAPHIC ORGANIZATION; SPACE REPRESENTATION; LATERAL LEMNISCUS; GABAERGIC NEURONS; COCHLEAR NUCLEUS AB This study examined the effect of bicuculline application on the auditory response properties in the auditory cortex of the big brown bat, Eptesicus fuscus. All auditory cortical neurons studied discharged either 1-2 or 3-7 impulses to 4 ms sound stimuli. Cortical neurons with high best frequencies tended to have high minimum thresholds. Bicuculline application increased the number of impulses and shortened the response latencies of all cortical neurons as well as changing the discharge patterns of half of the cortical neurons studied. Bicuculline application raised the rate-intensity functions but lowered the latency-intensity functions to varying degrees. Threshold-frequency tuning curves (FTCs) were either V-shaped, upper threshold or double-peaked. Threshold-FTCs and impulse-FTCs were mirror-images of each other. Bicuculline application expanded and raised the impulse-FTCs but lowered the threshold-FTCs, resulting in significantly decreased Q(n) values. Threshold-FTCs of cortical neurons determined within an orthogonally inserted electrode were very similar and expanded FTCs during bicuculline application were also very similar. Possible mechanisms for the contribution of GABAergic inhibition to shaping these response properties of cortical neurons are discussed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA. RP Jen, PHS (reprint author), Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA. CR AITKIN LM, 1974, J NEUROPHYSIOL, V37, P512 ASANUMA A, 1983, J NEUROPHYSIOL, V50, P1182 BORMANN J, 1988, TRENDS NEUROSCI, V11, P112, DOI 10.1016/0166-2236(88)90156-7 CASSEDAY JH, 1995, NEURAL REPRESENTATIO, P25 Casseday JH, 1996, BRAIN BEHAV EVOLUT, V47, P311, DOI 10.1159/000113249 CHEN QC, 1995, NEUR ABSTR, V21, P667 Cooper J. R., 1982, BIOMEDICAL BASIS NEU DEAR SP, 1993, J NEUROPHYSIOL, V70, P1988 deRibaupierre F, 1997, CENTRAL AUDITORY SYS, P317 Ebert U, 1995, HEARING RES, V91, P160, DOI 10.1016/0378-5955(96)83100-5 EHRET G, 1985, J COMP PHYSIOL A, V156, P619, DOI 10.1007/BF00619111 FAINGOLD CL, 1991, HEARING RES, V52, P201, DOI 10.1016/0378-5955(91)90200-S FAINGOLD CL, 1989, BRAIN RES, V500, P302, DOI 10.1016/0006-8993(89)90326-0 Fuzessery ZM, 1996, J NEUROPHYSIOL, V76, P1059 FUZESSERY ZM, 1982, J COMP PHYSIOL, V146, P471 GRINNELL AD, 1963, J PHYSIOL-LONDON, V167, P38 Hou T, 1992, Chin J Physiol, V35, P259 HUBEL DH, 1974, J COMP NEUROL, V158, P267, DOI 10.1002/cne.901580304 HUBEL DH, 1963, J PHYSIOL-LONDON, V165, P559 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 JEN PHS, 1989, J COMP PHYSIOL A, V165, P1, DOI 10.1007/BF00613794 Jen P H, 1997, Acta Otolaryngol Suppl, V532, P61 JEN PHS, 1987, BRAIN RES, V419, P7, DOI 10.1016/0006-8993(87)90563-4 JOHNSON BR, 1993, THESIS DUKE U DURHAM KUWADA S, 1989, J NEUROPHYSIOL, V61, P269 Lu Y, 1997, J COMP PHYSIOL A, V181, P331, DOI 10.1007/s003590050119 Lu Y, 1998, J NEUROPHYSIOL, V79, P2303 MERZENIC.MM, 1973, BRAIN RES, V50, P275, DOI 10.1016/0006-8993(73)90731-2 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 METZNER W, 1987, J COMP PHYSIOL A, V160, P395, DOI 10.1007/BF00613029 MICHAEL CR, 1981, J NEUROPHYSIOL, V46, P587 MITANI A, 1985, J COMP NEUROL, V235, P430, DOI 10.1002/cne.902350403 MITANI A, 1985, J COMP NEUROL, V235, P417, DOI 10.1002/cne.902350402 MOUNTCASTLE VB, 1957, J NEUROPHYSIOL, V20, P408 NELSON PG, 1963, J NEUROPHYSIOL, V26, P908 Palombi PS, 1996, J NEUROPHYSIOL, V75, P2211 PALOMBI PS, 1992, J NEUROPHYSIOL, V67, P738 PARK TJ, 1993, J NEUROSCI, V13, P2050 PARK TJ, 1993, J NEUROSCI, V13, P5172 PRIETO JJ, 1994, J COMP NEUROL, V344, P349, DOI 10.1002/cne.903440304 PRIETO JJ, 1994, J COMP NEUROL, V344, P383, DOI 10.1002/cne.903440305 SCHREINER CE, 1992, J NEUROPHYSIOL, V68, P1487 Shen JX, 1997, J COMP PHYSIOL A, V181, P591, DOI 10.1007/s003590050142 SUGA N, 1971, J PHYSIOL-LONDON, V217, P159 SUGA N, 1982, J NEUROPHYSIOL, V47, P225 SUGA N, 1976, SCIENCE, V194, P542, DOI 10.1126/science.973140 SUGA N, 1977, SCIENCE, V196, P64, DOI 10.1126/science.190681 SUGA N, 1964, J PHYSIOL-LONDON, V175, P50 TANIGUCHI I, 1988, NEUROSCI LETT, V88, P17, DOI 10.1016/0304-3940(88)90308-4 VANESSEN DC, 1978, J PHYSIOL-LONDON, V277, P193 VATER M, 1992, J COMP PHYSIOL A, V171, P541 WINER JA, 1992, MAMMALIAN AUDITORY P, P223 WINER JA, 1989, NEUROSCIENCE, V33, P499, DOI 10.1016/0306-4522(89)90402-8 YANG LC, 1994, J NEUROPHYSIOL, V71, P2014 YANG LC, 1992, J NEUROPHYSIOL, V68, P1760 NR 55 TC 51 Z9 57 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 161 EP 174 DI 10.1016/S0378-5955(00)00197-0 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400013 PM 11077201 ER PT J AU Flock, A Flock, B AF Flock, A Flock, B TI Hydrops in the cochlea can be induced by sound as well as by static pressure SO HEARING RESEARCH LA English DT Article DE hydrops; hearing loss; Reissners's membrane; noise trauma; Meniere's disease ID GUINEA-PIG COCHLEA; TEMPORAL BONE PREPARATION; HEARING ORGAN; ENDOLYMPHATIC HYDROPS; CONFOCAL MICROSCOPY; POTENTIALS; VIBRATIONS; MEMBRANE; CELLS AB The Reissner's membrane (RM) was visualised by confocal microscopy in the isolated temporal bone of the guinea pig. The function of the organ was followed by measuring its physiological response. Static pressure applied in the basal coil caused a distention of the RM in the apical coil into the scala vestibuli. The sensitivity to a test tone was reduced. When the pressure was relieved, the RM returned to its original position and the response recovered. If the increased pressure was maintained, the RM would bulge further. The RM could then be reversibly stretched and return gradually, with a delay, to its original position. Alternatively, it could be over-stretched and return with an over-shoot past its original position toward the organ of Corti. In response to repetitive tone pulses of above 80 dB, hydrops of the RM also developed. This was accompanied by a reduced sensitivity. A slow recovery to the original position, or over-shoot, and return of responsiveness could be seen. Above 106 dB sustained loss was generally seen. It is concluded that the RM can accommodate increased scala media pressure by distention. This will relieve the organ of Corti from part of the pressure and may protect the organ from trauma. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Karolinska Inst, Div Physiol 2, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden. RP Flock, A (reprint author), Karolinska Inst, Div Physiol 2, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden. CR ATKINSON M, 1961, ACTA OTO-LARYNGOL, V162, P1 Bouman H, 1998, HEARING RES, V117, P119, DOI 10.1016/S0378-5955(97)00216-5 BRUNDIN L, 1992, HEARING RES, V58, P175, DOI 10.1016/0378-5955(92)90126-8 COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X Counter SA, 1999, NEUROREPORT, V10, P473, DOI 10.1097/00001756-199902250-00006 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 Flock A, 1997, HEARING RES, V106, P29 Flock A, 1999, J NEUROSCI, V19, P4498 Flock A, 1998, J NEUROCYTOL, V27, P507, DOI 10.1023/A:1006999725663 Flock A, 1998, NEUROSCIENCE, V83, P215, DOI 10.1016/S0306-4522(97)00335-7 Fridberger A, 1998, P NATL ACAD SCI USA, V95, P7127, DOI 10.1073/pnas.95.12.7127 Fridberger A, 1997, ACTA PHYSIOL SCAND, V161, P239, DOI 10.1046/j.1365-201X.1997.00214.x Hallpike C. S., 1938, J LARYNG, V53, P625, DOI 10.1017/S0022215100003947 Hemmert W, 2000, HEARING RES, V142, P184, DOI 10.1016/S0378-5955(00)00017-4 HONRUBIA V, 1968, J ACOUST SOC AM, V45, P1443 HORNER KC, 1995, OTOLARYNG HEAD NECK, V112, P84, DOI 10.1016/S0194-5998(95)70306-3 Khanna SM, 1999, HEARING RES, V132, P15, DOI 10.1016/S0378-5955(99)00027-1 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KLIS JFL, 1988, HEARING RES, V32, P175, DOI 10.1016/0378-5955(88)90089-5 Meniere P, 1861, GAZ MED PARIS, V16, P597 Morioka I, 1995, ORL J OTO-RHINO-LARY, V57, P299 NADOL JB, 1986, P 2 INT C IMM OT RHI Rask-Andersen H, 1999, HEARING RES, V138, P81, DOI 10.1016/S0378-5955(99)00153-7 REISSNER E, 1851, AURIS INTERNAE FORMA RUTH RA, 1988, AM J OTOL, V9, P1 SALT AN, 1995, HEARING RES, V88, P79, DOI 10.1016/0378-5955(95)00103-B Ulfendahl M, 1996, ACTA PHYSIOL SCAND, V158, P275, DOI 10.1046/j.1365-201X.1996.563313000.x ULFENDAHL M, 1991, HEARING RES, V57, P31, DOI 10.1016/0378-5955(91)90071-G ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 Ulfendahl M, 1998, CURR OPIN NEUROBIOL, V8, P475, DOI 10.1016/S0959-4388(98)80034-2 Ulfendahl M, 1996, J NEUROPHYSIOL, V76, P3850 VONBEKESY G, 1960, EXPT HEARING, P3 NR 32 TC 13 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 175 EP 188 DI 10.1016/S0378-5955(00)00198-2 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400014 PM 11077202 ER PT J AU Rao, DB Fechter, LD AF Rao, DB Fechter, LD TI Increased noise severity limits potentiation of noise induced hearing loss by carbon monoxide SO HEARING RESEARCH LA English DT Article DE noise; carbon monoxide; hearing loss; compound action potential; rat; equal energy ID ACOUSTIC TRAUMA; GUINEA-PIG; THRESHOLD SHIFTS; AIR CONTAMINANTS; COCHLEAR DAMAGE; TIP LINKS; INNER-EAR; EXPOSURE; STEREOCILIA; OVERSTIMULATION AB This study evaluates the influence of noise intensity and duration on auditory dysfunction due to simultaneous exposure to noise and carbon monoxide (CO). Previous studies have demonstrated that CO potentiates noise induced hearing loss (NIHL). It is not known whether auditory dysfunction due to combined exposure parallels impairment due to noise alone. Based on the 5 dB exchange rate between noise intensify and exposure doubling time; equivalent noise exposure conditions were used. Long Evans hooded rats were divided into groups that received noise alone (95, 100 and 105 dB SPL), and noise plus CO (1200 ppm), for durations of 4. 2 and 1 h, respectively. Controls were exposed to sir or CO alone. Thresholds were evaluated 4 weeks later using an electrophysiological endpoint, the compound action potential threshold. Results demonstrate that the 5 dB exchange rate is not conserved under the conditions and subjects used. Moreover, dysfunction due to combined exposure did not parallel dysfunction due to noise alone. Further, although an increase in exposure duration results in increased auditory dysfunction, no further potentiation of NIHL by CO is observed. This suggests that at increasing noise severity, dysfunction due to combined exposure is limited by impairment due to noise alone. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Ctr Toxicol, Oklahoma City, OK 73117 USA. RP Rao, DB (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Ctr Toxicol, Oklahoma City, OK 73117 USA. CR BOCK GR, 1984, HEARING RES, V13, P201, DOI 10.1016/0378-5955(84)90109-6 BURGESS WA, 1977, AM IND HYG ASSOC J, V38, P184, DOI 10.1080/0002889778507935 CANLON B, 1987, HEARING RES, V30, P127, DOI 10.1016/0378-5955(87)90130-4 Canlon B, 1988, Scand Audiol Suppl, V27, P1 Cary R, 1997, ANN OCCUP HYG, V41, P455 Chen GD, 1999, HEARING RES, V138, P181, DOI 10.1016/S0378-5955(99)00157-4 Chen GD, 1999, HEARING RES, V132, P149, DOI 10.1016/S0378-5955(99)00044-1 Clark JA, 1996, HEARING RES, V99, P119, DOI 10.1016/S0378-5955(96)00092-5 EATON DL, 1996, CASARETT DOULLS TOXI, P18 Eldred KM, 1955, 55355 WADC US AIR FO Fechter L, 1989, ARCH COMPLEX ENV STU, V1, P23 FECHTER LD, 1995, OCCUP MED, V10, P609 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 FECHTER LD, 1988, HEARING RES, V34, P39, DOI 10.1016/0378-5955(88)90049-4 FECHTER LD, 2000, IN PRESS TOXICOL SCI Franks JR, 1996, PREVENTING OCCUPATIO GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 GLEASON MN, 1969, CLIN TOXICOLOGY COMM, P60 GOLD A, 1978, AM IND HYG ASSOC J, V39, P534, DOI 10.1080/0002889778507805 HENSELMAN LW, 1994, HEARING RES, V78, P1, DOI 10.1016/0378-5955(94)90038-8 *INT COMM, 1970, J OCCUP MED, V12, P276 JOHNSON AC, 1995, OCCUP MED, V10, P623 KRYTER KD, 1970, ARCH ENVIRON HEALTH, V20, P624 LEVIN BC, 1987, FUND APPL TOXICOL, V9, P236, DOI 10.1016/0272-0590(87)90046-7 MORATA TC, 1994, ARCH ENVIRON HEALTH, V49, P359 Morata T C, 1998, Scand Audiol Suppl, V48, P111 *NIOSH USDHHS, 1996, NAT OCC RES AG Nordmann AS, 2000, HEARING RES, V139, P13, DOI 10.1016/S0378-5955(99)00163-X Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P229, DOI 10.1159/000013846 OSTERGAARD PB, 1986, NOISE HEARING CONSER PICKLES JO, 1987, HEARING RES, V25, P173, DOI 10.1016/0378-5955(87)90089-X PRICE GR, 1981, J ACOUST SOC AM, V69, P171, DOI 10.1121/1.385361 PRIJS VF, 1993, HEARING RES, V71, P190, DOI 10.1016/0378-5955(93)90034-X RAO D, 2000, IN PRESS TOXICOL APP REISCHL U, 1979, AM IND HYG ASSOC J, V40, P482, DOI 10.1080/15298667991429868 ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 RYBAK LP, 1992, OTOLARYNG HEAD NECK, V106, P677 SATALOFF J, 1969, ARCH ENVIRON HEALTH, V18, P972 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 SPOENDLI.H, 1973, ACTA OTO-LARYNGOL, V75, P220, DOI 10.3109/00016487309139699 SPOENDLIN H, 1976, MONOGRAPH, P69 TREITMAN RD, 1980, AM IND HYG ASSOC J, V41, P796, DOI 10.1080/15298668091425662 Morley J C, 1999, Appl Occup Environ Hyg, V14, P645 WARD WD, 1971, OCCUPATIONAL HEARING, P225 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 YOUNG JS, 1987, HEARING RES, V26, P37, DOI 10.1016/0378-5955(87)90034-7 NR 47 TC 11 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 206 EP 214 DI 10.1016/S0378-5955(00)00202-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400016 PM 11077204 ER PT J AU Ravicz, ME Merchant, SN Rosowski, JJ AF Ravicz, ME Merchant, SN Rosowski, JJ TI Effect of freezing and thawing on stapes-cochlear input impedance in human temporal bones SO HEARING RESEARCH LA English DT Article DE cochlear impedance; stapes impedance; middle-ear mechanics; freezing and thawing; temporal bone; human ID HUMAN MIDDLE-EAR AB The use of thawed frozen temporal bones offers advantages over fresh bones in the study of middle-ear and inner-ear mechanical function. We show, however, that freezing and thawing can cause a reduction in the magnitude of the input impedance of the stapes and cochlea Z(SC) in unfixed temporal bones from human cadavers of as much as a factor of 3-10 over the frequency range 25 Hz-7 kHz. Z(SC) is considered to be the sum of the impedances of the annular ligament Z(S) and the cochlea Z(C) and has been shown to be controlled by Z(S) below 1 kHz and by Z(C) at higher frequencies [Merchant et al., 1996. Hear. Res. 97; 30-45]. Experiments in which the inner ear was opened, drained, and refilled identified two mechanisms by which freezing and thawing can cause a reduction in the magnitude of Z(SC) (\Z(SC)\) Freezing can allow air to enter the inner ear, with the result that \Z(C)\ is reduced above about 1 kHz; and freezing can reduce \Z(S)\, which causes a reduction in \Z(SC)\ below 1 kHz. Changes in the phase angle of Z(SC) induced by freezing were small and were consistent with changes in \Z(SC)\. Removing air from the inner ear returned Z(C) to near its value in fresh bones, but \Z(SC)\ remained lower in some thawed bones by a factor of 2-3. Investigations of middle-ear function for which Z(SC) is critical should use fresh temporal bones only or should allow for the possible reduction in \Z(SC)\ in thawed frozen bones. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA. MIT, Elect Res Lab, Cambridge, MA 02139 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA. Harvard Univ, MIT, Div Hlth Sci & Technol, Speech & Hearing Sci Program, Cambridge, MA 02139 USA. RP Ravicz, ME (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA. CR Huber A., 2000, RECENT DEV AUDITORY, P10, DOI 10.1142/9789812793980_0002 KRINGLEBOTN M, 1988, SCAND AUDIOL, V17, P75, DOI 10.3109/01050398809070695 KUROKAWA H, 1995, OTOLARYNG HEAD NECK, V113, P349, DOI 10.1016/S0194-5998(95)70067-6 Merchant SN, 1996, HEARING RES, V97, P30 NAKAMURA K, 1992, TRANSPLANTS IMPLANTS, P227 ONCHI Y, 1961, J ACOUST SOC AM, V33, P794, DOI 10.1121/1.1908801 PEAKE WT, 1992, HEARING RES, V57, P245, DOI 10.1016/0378-5955(92)90155-G Puria S, 1997, J ACOUST SOC AM, V101, P2754, DOI 10.1121/1.418563 ROSOWSKI JJ, 1990, ANN OTO RHINOL LARYN, V99, P403 ROSOWSKI JJ, 1995, AM J OTOL, V16, P486 Schuknecht HF, 1993, PATHOLOGY EAR Wever EG, 1954, PHYSL ACOUSTICS ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 Zwislocki J. J., 1975, NERVOUS SYSTEM, P45 NR 14 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 215 EP 224 DI 10.1016/S0378-5955(00)00200-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400017 PM 11077205 ER PT J AU Talavage, TM Ledden, PJ Benson, RR Rosen, BR Melcher, JR AF Talavage, TM Ledden, PJ Benson, RR Rosen, BR Melcher, JR TI Frequency-dependent responses exhibited by multiple regions in human auditory cortex SO HEARING RESEARCH LA English DT Article DE auditory cortex; functional magnetic resonance imaging; tonotopy; human ID TONOTOPIC ORGANIZATION; HUMAN-BRAIN; MAGNETIC-FIELDS; ARCHITECTONIC FIELDS; CORTICAL ACTIVATION; SENSORY STIMULATION; STIMULUS FREQUENCY; NEURONAL-ACTIVITY; MACAQUE MONKEYS; FUNCTIONAL MRI AB Recordings in experimental animals have detailed the tonotopic organization of auditory cortex, including the presence of multiple tonotopic maps. In contrast, relatively little is known about tonotopy within human auditory cortex, for which even the number and location of tonotopic maps remains unclear. The present study begins to develop a more complete picture of cortical tonotopic organization in humans using functional magnetic resonance imaging, a technique that enables the non-invasive localization of neural activity in the brain. Subjects were imaged while listening to lower- (below 660 Hz) and higher- (above 2490 Hz) frequency stimuli presented alternately and at moderate intensity. Multiple regions on the superior temporal lobe exhibited responses that depended upon stimulus spectral content. Eight of these 'frequency-dependent response regions' (FDRRs) were identified repeatedly across subjects. Four of the FDRRs exhibited a greater response to higher frequencies, and four exhibited a greater response to lower frequencies. Based upon the location of the eight FDRRs, a correspondence is proposed between FDRRs and anatomically defined cortical areas on the human superior temporal lobe. Our findings suggest that a larger number of tonotopically organized areas exist (i.e., four or more) in the human auditory cortex than was previously recognized. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Harvard Mit Div Hlth Sci & Technol, Speech & Hearing Sci Program, Cambridge, MA USA. Massachusetts Gen Hosp, Dept Radiol, MGH NMR Ctr, Boston, MA 02129 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Dept Otolaryngol, Boston, MA 02114 USA. RP Talavage, TM (reprint author), Purdue Univ, Sch Elect & Comp Engn, W Lafayette, IN 47907 USA. CR ARLINGER S, 1982, ELECTROEN CLIN NEURO, V54, P642, DOI 10.1016/0013-4694(82)90118-3 Bandettini PA, 1998, MAGNET RESON MED, V39, P410, DOI 10.1002/mrm.1910390311 BANDETTINI PA, 1992, MAGNET RESON MED, V25, P390, DOI 10.1002/mrm.1910250220 BANDETTINI PA, 1993, MAGNET RESON MED, V30, P161, DOI 10.1002/mrm.1910300204 Bertrand O, 1991, Acta Otolaryngol Suppl, V491, P116 Bilecen D, 1998, HEARING RES, V126, P19, DOI 10.1016/S0378-5955(98)00139-7 BINDER JR, 1994, ANN NEUROL, V35, P662, DOI 10.1002/ana.410350606 Buckner RL, 1996, P NATL ACAD SCI USA, V93, P14878, DOI 10.1073/pnas.93.25.14878 Buxton RB, 1998, MAGNET RESON MED, V39, P855, DOI 10.1002/mrm.1910390602 CANSINO S, 1994, BRAIN RES, V663, P38, DOI 10.1016/0006-8993(94)90460-X CELESIA GG, 1976, BRAIN, V99, P403, DOI 10.1093/brain/99.3.403 Diesch E, 1997, PSYCHOPHYSIOLOGY, V34, P501, DOI 10.1111/j.1469-8986.1997.tb01736.x EDMISTER WB, 1999, HUM BRAIN MAPP, V7, P88 ELBERLING C, 1982, SCAND AUDIOL, V11, P61, DOI 10.3109/01050398209076201 FOX PT, 1986, P NATL ACAD SCI USA, V83, P1140, DOI 10.1073/pnas.83.4.1140 FOX PT, 1988, SCIENCE, V241, P462, DOI 10.1126/science.3260686 FRISTON KJ, 1995, HUMAN BRAIN MAPPING, V2, P165 GALABURDA A, 1980, J COMP NEUROL, V190, P597, DOI 10.1002/cne.901900312 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 Hall DA, 1999, HUM BRAIN MAPP, V7, P213, DOI 10.1002/(SICI)1097-0193(1999)7:3<213::AID-HBM5>3.0.CO;2-N HEIL P, 1994, HEARING RES, V76, P188, DOI 10.1016/0378-5955(94)90099-X Hind JE, 1960, NEURAL MECHANISMS AU, P201 HOPPEL BE, 1993, MAGNET RESON MED, V30, P715, DOI 10.1002/mrm.1910300609 Howard MA, 2000, J COMP NEUROL, V416, P79, DOI 10.1002/(SICI)1096-9861(20000103)416:1<79::AID-CNE6>3.0.CO;2-2 Howard MA, 1996, BRAIN RES, V724, P260, DOI 10.1016/0006-8993(96)00315-0 HUOTILAINEN M, 1995, NEUROREPORT, V6, P841, DOI 10.1097/00001756-199504190-00004 IMIG TJ, 1977, J COMP NEUROL, V171, P111, DOI 10.1002/cne.901710108 IMIG TJ, 1980, J COMP NEUROL, V192, P293, DOI 10.1002/cne.901920208 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JACOBSON GP, 1992, EAR HEARING, V13, P300, DOI 10.1097/00003446-199210000-00007 Kaas JH, 1998, AUDIOL NEURO-OTOL, V3, P73, DOI 10.1159/000013783 Kosaki H, 1997, J COMP NEUROL, V386, P304 KWONG KK, 1992, P NATL ACAD SCI USA, V89, P5675, DOI 10.1073/pnas.89.12.5675 LAUTER JL, 1985, HEARING RES, V20, P199, DOI 10.1016/0378-5955(85)90024-3 LIEGEOISCHAUVEL C, 1994, ELECTROEN CLIN NEURO, V92, P204, DOI 10.1016/0168-5597(94)90064-7 LIEGEOISCHAUVEL C, 1991, BRAIN, V114, P139 Lockwood AH, 1999, CEREB CORTEX, V9, P65, DOI 10.1093/cercor/9.1.65 Lutkenhoner B, 1998, AUDIOL NEURO-OTOL, V3, P191, DOI 10.1159/000013790 Mandeville JB, 1998, MAGNET RESON MED, V39, P615, DOI 10.1002/mrm.1910390415 MCMULLEN NT, 1982, EXP NEUROL, V75, P208, DOI 10.1016/0014-4886(82)90019-X MERZENICH MM, 1976, J COMP NEUROL, V166, P387, DOI 10.1002/cne.901660402 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P321 MERZENIC.MM, 1973, BRAIN RES, V50, P275, DOI 10.1016/0006-8993(73)90731-2 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MOREL A, 1993, J COMP NEUROL, V335, P437, DOI 10.1002/cne.903350312 Muhlnickel W, 1998, P NATL ACAD SCI USA, V95, P10340, DOI 10.1073/pnas.95.17.10340 OGAWA S, 1992, P NATL ACAD SCI USA, V89, P5951, DOI 10.1073/pnas.89.13.5951 PANTEV C, 1995, ELECTROEN CLIN NEURO, V94, P26, DOI 10.1016/0013-4694(94)00209-4 PANTEV C, 1988, ELECTROEN CLIN NEURO, V69, P160, DOI 10.1016/0013-4694(88)90211-8 PANTEV C, 1994, ELECTROEN CLIN NEURO, V90, P82, DOI 10.1016/0013-4694(94)90115-5 Pantev C, 1991, Acta Otolaryngol Suppl, V491, P106 Pantev C, 1996, HEARING RES, V101, P62, DOI 10.1016/S0378-5955(96)00133-5 PANTEV C, 1990, ELECTROEN CLIN NEURO, V75, P173, DOI 10.1016/0013-4694(90)90171-F PELIZZONE M, 1985, BIOMAGNETISM APPLICA, P326 Penhune VB, 1996, CEREB CORTEX, V6, P661, DOI 10.1093/cercor/6.5.661 PHELPS ME, 1981, SCIENCE, V211, P1445, DOI 10.1126/science.6970412 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1995, J NEUROPHYSIOL, V73, P674 PHILLIPS DP, 1985, HEARING RES, V18, P73, DOI 10.1016/0378-5955(85)90111-X PHILLIPS DP, 1994, EXP BRAIN RES, V102, P210 PRICHARD J, 1991, P NATL ACAD SCI USA, V88, P5829, DOI 10.1073/pnas.88.13.5829 RADEMACHER J, 1993, CEREB CORTEX, V3, P313, DOI 10.1093/cercor/3.4.313 RAUSCHECKER JP, 1995, SCIENCE, V268, P111, DOI 10.1126/science.7701330 Rauschecker JP, 1997, J COMP NEUROL, V382, P89 RAVICZ ME, 1998, NEUROIMAGE, V7, pS556 RAVICZ ME, 2000, IN PRESS J ACOUST SO REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 Reese TG, 1995, JMRI-J MAGN RESON IM, V5, P739, DOI 10.1002/jmri.1880050621 REITE M, 1994, COGNITIVE BRAIN RES, V2, P13, DOI 10.1016/0926-6410(94)90016-7 Rivier F, 1997, NEUROIMAGE, V6, P288, DOI 10.1006/nimg.1997.0304 Roberts TPL, 1996, NEUROREPORT, V7, P1138, DOI 10.1097/00001756-199604260-00007 ROMANI GL, 1982, SCIENCE, V216, P1339, DOI 10.1126/science.7079770 ROMANI GL, 1982, EXP BRAIN RES, V47, P381 ROSE JE, 1959, B JOHNS HOPKINS HOSP, V104, P211 SALLY SL, 1988, J NEUROPHYSIOL, V59, P1627 Scheffler K, 1998, CEREB CORTEX, V8, P156, DOI 10.1093/cercor/8.2.156 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 Talairach J., 1988, COPLANAR STEREOTAXIC Talavage TM, 1999, HUM BRAIN MAPP, V7, P79, DOI 10.1002/(SICI)1097-0193(1999)7:2<79::AID-HBM1>3.0.CO;2-R TALAVAGE TM, 1997, NEUROIMAGE, V5, pS8 TIITINEN H, 1993, PSYCHOPHYSIOLOGY, V30, P537, DOI 10.1111/j.1469-8986.1993.tb02078.x Tramo M J, 1990, J Cogn Neurosci, V2, P195, DOI 10.1162/jocn.1990.2.3.195 VERKINDT C, 1995, EVOKED POTENTIAL, V96, P143, DOI 10.1016/0168-5597(94)00242-7 Wessinger CM, 1997, HUM BRAIN MAPP, V5, P18, DOI 10.1002/(SICI)1097-0193(1997)5:1<18::AID-HBM3>3.0.CO;2-Q WOOLSEY CN, 1971, PHYSL AUDITORY SYSTE, P271 YAMAMOTO T, 1988, P NATL ACAD SCI USA, V85, P8732, DOI 10.1073/pnas.85.22.8732 YAMAMOTO T, 1992, ACTA OTO-LARYNGOL, V112, P201 Yang YH, 2000, MAGNET RESON MED, V43, P185, DOI 10.1002/(SICI)1522-2594(200002)43:2<185::AID-MRM4>3.0.CO;2-3 ZATORRE RJ, 1992, SCIENCE, V256, P846, DOI 10.1126/science.1589767 NR 89 TC 110 Z9 110 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 225 EP 244 DI 10.1016/S0378-5955(00)00203-3 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400018 PM 11077206 ER PT J AU Hamernik, RP Qiu, W AF Hamernik, RP Qiu, W TI Correlations among evoked potential thresholds, distortion product otoacoustic emissions and hair cell loss following various noise exposures in the chinchilla SO HEARING RESEARCH LA English DT Article DE distortion product emission; asymptotic threshold shift; interrupted noise exposure; sensory cell loss ID BRAIN-STEM RESPONSES; ACOUSTIC DISTORTION; TUNING CURVES; AUDITORY-SYSTEM; SHIFT DYNAMICS; HEARING-LOSS; GUINEA-PIG; RESISTANCE; COCHLEA; DAMAGE AB Changes in cubic distortion product otoacoustic emissions (Delta DPOAEs), evoked potential threshold shifts (TSs) and outer hair cell (OHC) losses were measured in a population of 95 noise-exposed chinchillas. Each animal was exposed to one of 23 different noises in an asymptotic threshold shift (ATS) producing paradigm or an interrupted noise paradigm which typically produced a toughening effect. Noises were narrow band (400 Hz) impacts with center frequencies of 0.5, 1.0, 2.0, 4.0 or 8.0 kHz presented 1 impact/s at peak SPLs of 109, 115, 121 or 127 dB. The duration of the exposures was 24 h/day for 5 days (ATS paradigm) or 6 h/day for 20 days (toughening paradigm). Based on a linear regression analysis of individual subject and group mean data, correlations among the following dependent variables were made: Delta DPOAEs, ATS: toughening or TS recovery (TSr), permanent threshold shift (PTS) and OHC loss. Correlations among these metrics were generally highest for DPOAE primary frequency levels, L-1 = L-2 = 70 dB. Correlation between Delta DPOAE and TSr was typically low, while a considerably higher correlation was found between Delta DPOAE and ATS. Correlations among the permanent measures of noise-induced effects, i.e. for Delta DPOAE/PTS and Delta DPOAE/OHC loss were typically poor when there was only a small or a moderate noise-induced effect (PTS < 25 dB and DPOAE < 20 dB). However; for PTS < 25 dB the correlation between PTS and OHC loss was considerably better than the correlation between Delta DPOAE and OHC loss. For more severe noise-induced changes there was generally a good correspondence between OHC loss, PTS and Delta DPOAE metrics. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Coll Plattsburgh, Auditory Res Lab, Plattsburgh, NY 12901 USA. RP Hamernik, RP (reprint author), SUNY Coll Plattsburgh, Auditory Res Lab, 107 Beaumont Hall,101 Broad St, Plattsburgh, NY 12901 USA. CR AHROON WA, 1993, J ACOUST SOC AM, V93, P997, DOI 10.1121/1.405406 BLAKESLEE EA, 1978, J ACOUST SOC AM, V63, P876, DOI 10.1121/1.381767 Boettcher FA, 1995, J ACOUST SOC AM, V98, P3215, DOI 10.1121/1.413811 Bohne B.A., 1982, NEW PERSPECTIVES NOI, P283 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CANLON B, 1993, J ACOUST SOC AM, V94, P3232, DOI 10.1121/1.407229 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 Eddins AC, 1999, HEARING RES, V127, P119 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 Engstrom H, 1966, STRUCTURAL PATTERN O Fay R. A., 1988, HEARING VERTEBRATES, P357 Franceschini V., 1991, Theoretical and Computational Fluid Dynamics, V2, DOI 10.1007/BF00271636 GORGA MP, 1993, J ACOUST SOC AM, V93, P2050, DOI 10.1121/1.406691 Hamernik RP, 1999, HEARING RES, V132, P140, DOI 10.1016/S0378-5955(99)00039-8 Hamernik RP, 1998, J ACOUST SOC AM, V103, P3478, DOI 10.1121/1.423056 HAMERNIK RP, 1994, J ACOUST SOC AM, V95, P444, DOI 10.1121/1.408338 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 Hamernik RP, 1998, HEARING RES, V118, P73, DOI 10.1016/S0378-5955(98)00021-5 Hamernik RP, 1996, J ACOUST SOC AM, V100, P1003, DOI 10.1121/1.416285 HARGETT CE, 1986, 861 USAARL US ARM AR HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Kemp DT, 1988, ADV AUDIOL, V5, P27 Le Calvez S, 1998, HEARING RES, V120, P37, DOI 10.1016/S0378-5955(98)00050-1 LEONARD G, 1990, ADV AUDIOL, V7, P139 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LONSBURYMARTIN BL, 1990, EAR HEARING, V11, P144 McFadden SL, 1997, HEARING RES, V103, P142, DOI 10.1016/S0378-5955(96)00170-0 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 Mills J. H., 1976, EFFECTS NOISE HEARIN, P265 PUEL JL, 1995, ACTA ACUST, V3, P75 SALVI RJ, 1982, AM J OTOLARYNG, V3, P408, DOI 10.1016/S0196-0709(82)80018-5 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H SUBRAMANIAM M, 1995, EAR HEARING, V16, P372, DOI 10.1097/00003446-199508000-00004 SUBRAMANIAM M, 1994, HEARING RES, V74, P204, DOI 10.1016/0378-5955(94)90188-0 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 NR 40 TC 21 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 245 EP 257 DI 10.1016/S0378-5955(00)00204-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400019 PM 11077207 ER PT J AU Oxenham, AJ Plack, CJ AF Oxenham, AJ Plack, CJ TI Effects of masker frequency and duration in forward masking: further evidence for the influence of peripheral nonlinearity SO HEARING RESEARCH LA English DT Article DE forward masking; cochlear nonlinearity; temporal processing ID BASILAR-MEMBRANE NONLINEARITY; AUDITORY-NERVE FIBERS; TEMPORAL INTEGRATION; QUANTITATIVE MODEL; SIGNAL DELAY; HEARING; LEVEL; LISTENERS; SYSTEM; NOISE AB Forward masking has often been thought of in terms of neural adaptation, with nonlinearities in the growth and decay of forward masking being accounted for by the nonlinearities inherent in adaptation. In contrast, this study presents further evidence for the hypothesis that forward masking can be described as a linear process, once peripheral, mechanical nonlinearities are taken into account. The first experiment compares the growth of masking for on- and off-frequency maskers. Signal thresholds were measured as a function of masker level for three masker-signal intervals of 0, 10, and 30 ms. The brief 4-kHz sinusoidal signal was masked by a 200-ms sinusoidal forward masker which had a frequency of either 2.4 kHz (off-frequency) or 4 kHz (on-frequency). As in previous studies, for the on-frequency condition, the slope of the function relating signal threshold to masker level became shallower as the delay between the masker and signal was increased. In contrast, the slopes for the off-frequency condition were independent of masker-signal delay and had a value of around unity, indicating linear growth of masking for all masker-signal delays. In the second experiment, a broadband Gaussian noise forward masker was used to mask a brief 6-kHz sinusoidal signal. The spectrum level of the masker was either 0 or 40 dB (re: 20 mu Pa). The gap between the masker and signal was either 0 or 20 ms. Signal thresholds were measured for masker durations from 5 to 200 ms. The effect of masker duration was found to depend more on signal level than on gap duration or masker level. Overall, the results support the idea that forward masking call be modeled as a linear process, preceded by a static nonlinearity resembling that found on the basilar membrane. (C) 2000 Elsevier Science B.V. All rights reserved. C1 MIT, Elect Res Lab, Cambridge, MA 02139 USA. Univ Essex, Dept Psychol, Colchester CO4 3SQ, Essex, England. RP Oxenham, AJ (reprint author), MIT, Elect Res Lab, Rm 36-763, Cambridge, MA 02139 USA. CR CARLYON RP, 1988, HEARING RES, V32, P65, DOI 10.1016/0378-5955(88)90147-5 Dau T, 1996, J ACOUST SOC AM, V99, P3615, DOI 10.1121/1.414959 Dau T, 1996, J ACOUST SOC AM, V99, P3623, DOI 10.1121/1.414960 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 JESTEADT W, 1982, J ACOUST SOC AM, V71, P950, DOI 10.1121/1.387576 KIDD G, 1984, J ACOUST SOC AM, V75, P937, DOI 10.1121/1.390558 KIDD G, 1981, HEARING RES, V5, P49, DOI 10.1016/0378-5955(81)90026-5 KIDD G, 1982, J ACOUST SOC AM, V72, P1384, DOI 10.1121/1.388443 MOORE BCJ, 1983, J ACOUST SOC AM, V73, P1249, DOI 10.1121/1.389273 Moore BCJ, 1998, PSYCHOL REV, V105, P108, DOI 10.1037/0033-295X.105.1.108 MOORE BCJ, 1988, J ACOUST SOC AM, V83, P1102, DOI 10.1121/1.396055 NEFF DL, 1986, J ACOUST SOC AM, V79, P1519, DOI 10.1121/1.393678 NELSON DA, 1987, J ACOUST SOC AM, V81, P709, DOI 10.1121/1.395131 Oxenham AJ, 1997, MODELING SENSORINEURAL HEARING LOSS, P273 Oxenham AJ, 1997, J ACOUST SOC AM, V101, P3676, DOI 10.1121/1.418328 OXENHAM AJ, 1995, J ACOUST SOC AM, V98, P1921, DOI 10.1121/1.413376 Oxenham AJ, 1997, J ACOUST SOC AM, V101, P3666, DOI 10.1121/1.418327 OXENHAM AJ, 1994, HEARING RES, V80, P105, DOI 10.1016/0378-5955(94)90014-0 PENNER MJ, 1974, J ACOUST SOC AM, V56, P179, DOI 10.1121/1.1903250 PENNER MJ, 1978, J ACOUST SOC AM, V63, P195, DOI 10.1121/1.381712 PETERS RW, 1995, J ACOUST SOC AM, V97, P3791, DOI 10.1121/1.412394 Plack CJ, 2000, J ACOUST SOC AM, V107, P501, DOI 10.1121/1.428318 Plack CJ, 1998, J ACOUST SOC AM, V103, P1598, DOI 10.1121/1.421294 PLACK CJ, 1990, J ACOUST SOC AM, V87, P2178, DOI 10.1121/1.399185 PLOMP R, 1964, J ACOUST SOC AM, V36, P277, DOI 10.1121/1.1918946 RELKIN EM, 1988, J ACOUST SOC AM, V84, P584, DOI 10.1121/1.396836 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 SHANNON RV, 1990, J ACOUST SOC AM, V88, P741, DOI 10.1121/1.399777 SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 ZWICKER E, 1984, J ACOUST SOC AM, V75, P219, DOI 10.1121/1.390398 NR 31 TC 39 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2000 VL 150 IS 1-2 BP 258 EP 266 DI 10.1016/S0378-5955(00)00206-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 374WM UT WOS:000165367400020 PM 11077208 ER PT J AU Mulders, WHA Robertson, D AF Mulders, WHA Robertson, D TI Effects on cochlear responses of activation of descending pathways from the inferior colliculus SO HEARING RESEARCH LA English DT Article DE inferior colliculus; descending pathway; medial olivocochlear system; compound action potential; cochlear microphonic; distortion products; suppression ID SUPERIOR OLIVARY COMPLEX; CROSSED OLIVOCOCHLEAR BUNDLE; COMPOUND ACTION-POTENTIALS; GUINEA-PIG COCHLEA; BRAIN-STEM NUCLEI; ELECTRICAL-STIMULATION; LATERAL LEMNISCUS; ASCENDING PROJECTIONS; OTOACOUSTIC EMISSIONS; EFFERENT INNERVATION AB The inferior colliculus (IC) has been shown anatomically to make direct descending connections with medial olivocochlear (MOC) neurones in the auditory brainstem. The MOC neurones project to the outer hair cells in the cochlea and inhibit cochlear neural output. This study investigated the effect of IC stimulation on cochlear output in both guinea pigs and rats in order to determine the functional significance of the IC-to-olivocochlear system projection. Stimulation of the central nucleus and the external cortex of the IC in paralysed guinea pigs, both contra- and ipsilaterally to the test cochlea, resulted in a small increase of the cochlear microphonic amplitude and a small decrease of the compound action potential (CAP) amplitude, the latter equivalent to a 3-6 dB change in acoustic input. Effects on the CAP were maximal in the frequency range 6-10 kHz. These effects were consistent with partial activation of the MOC system. In unparalysed rats, stimulation of the inferior colliculus evoked a large, prolonged suppression ranging from 5-12 dB in the amplitude of distortion product otoacoustic emissions (2f(1) -f(2); DPOAE), as reported previously by Scates et al. (1999). However, this suppression was decreased to only 0-3 dB when the animals were paralysed, suggesting that the larger suppression in the unparalysed state was the consequence of either a general masking effect caused by animal movement, or activation of middle ear muscles by the inferior colliculus stimulation. The results indicate a small but significant excitatory effect of the inferior colliculus on the medial olivocochlear system under conditions of anaesthesia and paralysis. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. RP Robertson, D (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ALDER VA, 1978, J ACOUST SOC AM, V64, P684, DOI 10.1121/1.381993 AZEREDO W, 2000, 23 MIDW RES M ASS RE, P5679 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 BROWN MC, 1984, J PHYSIOL-LONDON, V354, P625 BUSER P, 1966, EXP BRAIN RES, V1, P102 CAICEDO A, 1993, J COMP NEUROL, V328, P377, DOI 10.1002/cne.903280305 CALFORD MB, 1983, J NEUROSCI, V3, P2365 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 Desmedt J.E., 1975, HDB SENSORY PHYSL, P219 DOLAN D F, 1988, Society for Neuroscience Abstracts, V14, P650 FAYELUND H, 1986, ANAT EMBRYOL, V175, P35, DOI 10.1007/BF00315454 FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 Feliciano M. E., 1995, AUDIT NEUROSCI, V1, P287 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 Giraud AL, 1995, BRAIN RES, V705, P15, DOI 10.1016/0006-8993(95)01091-2 Giraud AL, 1997, NEUROREPORT, V8, P1779 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 Hienz RD, 1998, HEARING RES, V116, P10, DOI 10.1016/S0378-5955(97)00197-4 JOHNSTONE BM, 1990, ADV AUDIOL, V7, P57 KAWASE T, 1993, J NEUROPHYSIOL, V70, P2519 Kelly JB, 1998, HEARING RES, V116, P43, DOI 10.1016/S0378-5955(97)00195-0 KEMP DT, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 KIRK DL, 1994, HEARING RES, V74, P38, DOI 10.1016/0378-5955(94)90174-0 KUDO M, 1980, J COMP NEUROL, V191, P545, DOI 10.1002/cne.901910403 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 Maison S, 1997, HEARING RES, V113, P89, DOI 10.1016/S0378-5955(97)00136-6 Malmierca MS, 1996, HEARING RES, V93, P167, DOI 10.1016/0378-5955(95)00227-8 MCCOWN TJ, 1991, BRAIN RES, V567, P25, DOI 10.1016/0006-8993(91)91431-Y MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Mulders WHAM, 2000, HEARING RES, V144, P65, DOI 10.1016/S0378-5955(00)00046-0 NIEDER P, 1970, EXP NEUROL, V28, P179, DOI 10.1016/0014-4886(70)90172-X OTA Y, 1999, 22 MIDW RES M ASS RE, P837 OTA Y, 2000, 23 MIDW RES M ASS RE, P5177 Puria S, 1996, J ACOUST SOC AM, V99, P500, DOI 10.1121/1.414508 RAJAN R, 1990, BRAIN RES, V506, P192, DOI 10.1016/0006-8993(90)91251-B RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 RAJAN R, 1985, ROLE EFFERENT SYSTEM ROBERTSON D, 1988, BRAIN RES, V462, P47, DOI 10.1016/0006-8993(88)90583-5 ROBERTSON D, 1987, HEARING RES, V25, P69, DOI 10.1016/0378-5955(87)90080-3 ROBERTSON D, 1989, DEV BRAIN RES, V47, P197, DOI 10.1016/0165-3806(89)90176-4 SAINTMARIE RL, 1990, BRAIN RES, V524, P244, DOI 10.1016/0006-8993(90)90698-B Scates KW, 1999, HEARING RES, V128, P51, DOI 10.1016/S0378-5955(98)00198-1 Scharf B, 1997, HEARING RES, V103, P101, DOI 10.1016/S0378-5955(96)00168-2 SCHOFIELD BR, 1992, J COMP NEUROL, V317, P438, DOI 10.1002/cne.903170409 Schofield BR, 1999, J COMP NEUROL, V409, P210, DOI 10.1002/(SICI)1096-9861(19990628)409:2<210::AID-CNE3>3.0.CO;2-A SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SUNEJA SK, 1995, J NEUROCHEM, V64, P161 SYKA J, 1971, BRAIN RES, V28, P567, DOI 10.1016/0006-8993(71)90068-0 SYKA J, 1970, EXP NEUROL, V28, P384, DOI 10.1016/0014-4886(70)90175-5 THOMPSON AM, 1991, J COMP NEUROL, V311, P495, DOI 10.1002/cne.903110405 Thompson AM, 1998, J COMP NEUROL, V390, P439, DOI 10.1002/(SICI)1096-9861(19980119)390:3<439::AID-CNE10>3.0.CO;2-J THOMPSON AM, 1993, J COMP NEUROL, V335, P402, DOI 10.1002/cne.903350309 THOMPSON AM, 1991, J COMP NEUROL, V303, P267, DOI 10.1002/cne.903030209 VETTER DE, 1993, HEARING RES, V70, P173, DOI 10.1016/0378-5955(93)90156-U VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 VETTER DE, 1992, ANAT EMBRYOL, V185, P1, DOI 10.1007/BF00213596 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 Withnell RH, 1998, J ACOUST SOC AM, V104, P350, DOI 10.1121/1.423292 NR 64 TC 30 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 11 EP 23 DI 10.1016/S0378-5955(00)00157-X PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400002 PM 11033243 ER PT J AU Norena, A Micheyl, C Chery-Croze, S AF Norena, A Micheyl, C Chery-Croze, S TI An auditory negative after-image as a human model of tinnitus SO HEARING RESEARCH LA English DT Article DE zwicker tone; auditory illusion; negative after-image; lateral inhibition; tinnitus ID LATERAL INHIBITION; COCHLEAR NUCLEUS; ENHANCEMENT; CORTEX AB The Zwicker tone (ZT) is an auditory after-image, i.e. a tonal sensation that occurs following the presentation of notched noise. In the present study, the hypothesis that neural lateral inhibition is involved in the generation of this auditory illusion was investigated in humans through differences in perceptual detection thresholds measured following broadband noise, notched noise, and low-pass noise stimulation. The detection thresholds were measured using probe tones at several frequencies, within as well as outside the suppressed frequency range of the notched noise, and below as well as above the corner frequency of the low-pass noise. Thresholds measured after broadband noise using a sequence of four 130-ms probe tones (with a 130-ms inter-burst interval) proved to be significantly smaller that those measured using the same probe tones after notched noise at frequencies falling within the notch, but larger for frequencies on the outer edges of the noise. Thresholds measured following low-pass noise using the same sequence of probe tones were found to be smaller at frequencies slightly above the corner, but larger at lower, neighboring frequencies. This pattern of results is consistent with the hypothesis that the changes in auditory sensitivity induced by stimuli containing sharp spectral contrasts reflect lateral inhibition processes in the auditory system. The potential implications of these findings for the understanding of the mechanisms underlying the generation of auditory illusions like the ZT or tinnitus are discussed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hop Edouard Herriot, CNRS, UMR 5020, Lab Neurosci & Syst Sensoriels, F-69437 Lyon 03, France. RP Micheyl, C (reprint author), Hop Edouard Herriot, CNRS, UMR 5020, Lab Neurosci & Syst Sensoriels, Pavillon U,Pl Arsonval, F-69437 Lyon 03, France. CR EVANS EF, 1993, PROG BRAIN RES, V97, P117 GABRIELS P, 1995, P 5 INT TINN SEM POR, P270 Gerken GM, 1996, HEARING RES, V97, P75 Hazell J., 1999, P 6 INT TINN SEM, P20 Henry JA, 1999, P 6 INT TINN SEM, P51 Hoke E S, 1996, Audiol Neurootol, V1, P161 Hoke ES, 1998, NEUROREPORT, V9, P3065, DOI 10.1097/00001756-199809140-00027 JASTREBOFF PJ, 1990, NEUROSCI RES, V8, P221, DOI 10.1016/0168-0102(90)90031-9 Kiang N Y, 1970, Ciba Found Symp, P241 Kimura M, 1999, HEARING RES, V135, P146, DOI 10.1016/S0378-5955(99)00104-5 Kral A, 1996, GEN PHYSIOL BIOPHYS, V15, P109 KRUMP G, 1993, THESIS MUNICH LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 MEIKLE MB, 1991, P 4 INT TINN SEM, P27 Norena A, 1999, CLIN NEUROPHYSIOL, V110, P666, DOI 10.1016/S1388-2457(98)00034-0 PALMER AR, 1995, J ACOUST SOC AM, V97, P1786, DOI 10.1121/1.412055 Pantev C, 1999, BRAIN RES, V842, P192, DOI 10.1016/S0006-8993(99)01835-1 RHODE WS, 1994, J NEUROPHYSIOL, V71, P493 ROSENBLITH WA, 1947, SCIENCE, V106, P333, DOI 10.1126/science.106.2754.333 SALVI RJ, 1995, P 5 INT TINN SEM, P455 Sirimanna T., 1996, J AUDIOL MED, V5, P38 VERNON JA, 1995, P 5 INT TINN SEM POR, P289 Wiegrebe L, 1996, HEARING RES, V100, P171, DOI 10.1016/0378-5955(96)00111-6 ZWICKER E, 1964, J ACOUST SOC AM, V36, P2413, DOI 10.1121/1.1919373 NR 24 TC 21 Z9 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 24 EP 32 DI 10.1016/S0378-5955(00)00158-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400003 PM 11033244 ER PT J AU Ahuja, TK Wu, SH AF Ahuja, TK Wu, SH TI Developmental changes in physiological properties in the rat's dorsal nucleus of the lateral lemniscus SO HEARING RESEARCH LA English DT Article DE auditory development; lateral lemniscus; brain slice; intracellular recording; action potential; synaptic potential ID CENTRAL AUDITORY-SYSTEM; VITRO BRAIN SLICE; EXCITATORY SYNAPTIC TRANSMISSION; ANTEROVENTRAL COCHLEAR NUCLEUS; BINAURAL EVOKED-RESPONSES; KAINIC ACID LESIONS; INFERIOR COLLICULUS; ASCENDING PROJECTIONS; SUPERIOR OLIVE; ALBINO-RAT AB To better understand the development of the dorsal nucleus of the lateral lemniscus (DNLL), intrinsic membrane properties and synaptic responses of DNLL neurons in brain slice preparations were examined. Intracellular recordings were taken from DNLL neurons of rat pups at postnatal days 4-8 (early group), 10-12 (intermediate group) and 16-18 (late group). In response to positive current injection, neurons in the early group displayed firing with lower frequency and a longer action potential duration in comparison to the intermediate and late groups. The action potential amplitude of DNLL neurons increased during development. Postsynaptic potentials (PSPs), with excitatory predominance, were elicited by electrical stimulation of the lateral lemniscus and commissure of Probst throughout the three age groups. Neurons showed a longer latency and rise time of the PSPs in the early group in comparison with those in the intermediate and late groups. These results suggest that the early DNLL neurons display physiological characteristics associated with immature neurons, while the other two groups tend to illustrate mature-like neuronal properties. Furthermore, it seems that the neurons at day 10-12 are in a transitional period of development, which coincides with the onset of hearing. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Carleton Univ, Life Sci Res Ctr, Inst Neurosci, Lab Sensory Neurosci, Ottawa, ON K1S 5B6, Canada. RP Wu, SH (reprint author), Carleton Univ, Life Sci Res Ctr, Inst Neurosci, Lab Sensory Neurosci, 1125 Colonel Dr, Ottawa, ON K1S 5B6, Canada. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 Altman J., 1995, ATLAS PRENATAL RAT B ALTMAN J, 1981, EXP BRAIN RES, V42, P411 Backus KH, 1998, J PHYSIOL-LONDON, V507, P783, DOI 10.1111/j.1469-7793.1998.783bs.x BAJO VM, 1993, J COMP NEUROL, V334, P241, DOI 10.1002/cne.903340207 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CARLIER E, 1979, HEARING RES, V1, P197, DOI 10.1016/0378-5955(79)90013-3 Chen L, 1999, HEARING RES, V138, P106, DOI 10.1016/S0378-5955(99)00156-2 CHURCH MW, 1984, DEV BRAIN RES, V14, P23, DOI 10.1016/0165-3806(84)90005-1 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 Ehrlich I, 1999, J PHYSIOL-LONDON, V520, P121, DOI 10.1111/j.1469-7793.1999.00121.x FAINGOLD CL, 1993, HEARING RES, V69, P98, DOI 10.1016/0378-5955(93)90097-K FORSYTHE ID, 1993, P ROY SOC B-BIOL SCI, V251, P151, DOI 10.1098/rspb.1993.0022 Foster R E, 1982, Brain Res, V255, P371 FRANSON P, 1975, NEUROBIOLOGY, V5, P8 FRIAUF E, 1990, NEUROSCI LETT, V120, P58, DOI 10.1016/0304-3940(90)90167-8 Fu XW, 1997, NEUROSCIENCE, V78, P815, DOI 10.1016/S0306-4522(96)00580-5 GEALDOR M, 1993, HEARING RES, V69, P236, DOI 10.1016/0378-5955(93)90113-F GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GLENDENNING KK, 1988, J COMP NEUROL, V275, P261 GLENDENNING KK, 1983, J NEUROSCI, V3, P1521 GLENN SL, 1992, J NEUROSCI, V12, P3688 GOLDBERG JM, 1967, J COMP NEUROL, V129, P143, DOI 10.1002/cne.901290203 GonzalezHernandez T, 1996, J COMP NEUROL, V372, P309, DOI 10.1002/(SICI)1096-9861(19960819)372:2<309::AID-CNE11>3.0.CO;2-E HACKETT JT, 1982, NEUROSCIENCE, V7, P1455, DOI 10.1016/0306-4522(82)90257-3 HUFFMAN RF, 1995, J COMP NEUROL, V357, P532, DOI 10.1002/cne.903570405 HUTSON KA, 1991, J COMP NEUROL, V312, P105, DOI 10.1002/cne.903120109 ISAACSON JS, 1995, J NEUROPHYSIOL, V73, P964 Ito M, 1996, J NEUROPHYSIOL, V76, P3493 Iwasaki S, 1998, J PHYSIOL-LONDON, V509, P419, DOI 10.1111/j.1469-7793.1998.419bn.x JACKSON H, 1982, J NEUROSCI, V2, P1736 Kakazu Y, 1999, J NEUROSCI, V19, P2843 KANDLER K, 1995, EUR J NEUROSCI, V7, P1773, DOI 10.1111/j.1460-9568.1995.tb00697.x KANDLER K, 1995, J NEUROSCI, V15, P6890 KANDLER K, 1993, J COMP NEUROL, V328, P161, DOI 10.1002/cne.903280202 KELLY JB, 1997, ACOUSTICAL SIGNAL PR, P3229 KELLY JB, 1987, J COMP PSYCHOL, V101, P60, DOI 10.1037/0735-7036.101.1.60 Kelly JB, 1996, BEHAV NEUROSCI, V110, P1445, DOI 10.1037//0735-7044.110.6.1445 Kelly JB, 1998, HEARING RES, V116, P43, DOI 10.1016/S0378-5955(97)00195-0 Kidd SA, 1996, J NEUROSCI, V16, P7390 KOESTER J, 2000, PRINCIPLES NEURAL SC, P140 KOTAK VC, 1995, J NEUROPHYSIOL, V74, P1611 Kotak VC, 1998, J NEUROSCI, V18, P4646 Kotak VC, 1996, J NEUROSCI, V16, P1836 KUDO M, 1981, BRAIN RES, V221, P57, DOI 10.1016/0006-8993(81)91063-5 LI L, 1992, J NEUROSCI, V12, P4530 METHERATE R, 1995, BRAIN RES, V699, P221, DOI 10.1016/0006-8993(95)00909-A OERTEL D, 1983, J NEUROSCI, V3, P2043 OLIVER DL, 1989, J NEUROSCI, V9, P967 Puel J L, 1987, Brain Res, V465, P179 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 SANES DH, 1993, J NEUROSCI, V13, P2627 Sanes DH, 1998, DEV AUDITORY SYSTEM, P271 Schneiderman A., 1988, J COMP NEUROL, V276, P188 SONG WJ, 1995, J PHYSIOL-LONDON, V488, P419 TANAKA K, 1985, BRAIN RES, V341, P252, DOI 10.1016/0006-8993(85)91064-9 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 UZIEL A, 1981, AUDIOLOGY, V20, P89 van Adel BA, 1999, HEARING RES, V130, P115, DOI 10.1016/S0378-5955(98)00226-3 VATER M, 1992, J COMP NEUROL, V325, P183, DOI 10.1002/cne.903250205 VATER M, 1995, J COMP NEUROL, V351, P632, DOI 10.1002/cne.903510411 Walmsley B, 1998, IMMUNOL CELL BIOL, V76, P430, DOI 10.1046/j.1440-1711.1998.00764.x WINER JA, 1995, J COMP NEUROL, V355, P317, DOI 10.1002/cne.903550302 WU SH, 1995, J NEUROPHYSIOL, V73, P794 WU SH, 1987, HEARING RES, V30, P99 WU SH, 1995, J NEUROPHYSIOL, V73, P780 WU SH, 1998, PROG NEUROBIOL, V57, P357 Wu SH, 1996, J NEUROPHYSIOL, V75, P1271 Yang LC, 1996, J COMP NEUROL, V373, P575, DOI 10.1002/(SICI)1096-9861(19960930)373:4<575::AID-CNE7>3.0.CO;2-Z Zhang DX, 1998, HEARING RES, V117, P1, DOI 10.1016/S0378-5955(97)00202-5 ZHANG S, 1994, J PHYSIOL-LONDON, V480, P123 Zine A, 1996, BRAIN RES, V721, P49, DOI 10.1016/0006-8993(96)00147-3 ZOOK JM, 1982, J COMP NEUROL, V207, P14, DOI 10.1002/cne.902070103 NR 75 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 33 EP 45 DI 10.1016/S0378-5955(00)00159-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400004 PM 11033245 ER PT J AU Salt, AN DeMott, JE AF Salt, AN DeMott, JE TI Ionic and potential changes of the endolymphatic sac induced by endolymph volume changes SO HEARING RESEARCH LA English DT Article DE cochlea; endolymphatic sac; endolymph volume; endolymphatic hydrops ID GUINEA-PIG COCHLEA; INNER-EAR; IN-VIVO; GLYCEROL; TRANSPORT; INCREASE; HYDROPS; FLOW AB The endolymphatic sac (ES) is believed to be the locus for endolymph volume regulation in the inner ear. It has recently been shown that induced endolymph volume changes in the cochlea result in anatomical changes in the ES, suggesting that function of the sac varies according to endolymph volume status. In the present study we have recorded luminal concentrations of K+ and Na+ from the ES and the endolymphatic sac potential (ESP) during cochlear endolymph volume changes. ES recordings were made by an extradural approach, thereby preserving normal cerebrospinal fluid resting pressure. Cochlear endolymph volume changes were generated by performing injections or withdrawals through a pipette inserted into endolymph by a round window approach. The pre-treatment concentrations of K+ and Na+ in the ES were found to be 5.4 mM (S.D. 3.3, n = 8) and 128.6 mM (S.D. 18.4, n = 10) respectively, and the mean ESP was 14.4 mV (S.D. 5.2, n = 18). Endolymphatic injections were found to produce a sustained increase in the K+ content of the ES by an average of 19.9 mM and to decrease Na+ by 30.7 mM measured 50 min after the start of injection. The lime for K+ increase to occur was found to correlate with the injected volume, with larger injected volumes producing a more rapid increase. Endolymphatic withdrawals were found to induce a slow decline in endolymphatic K+ by an average of 3.4 mM measured at 50 min after withdrawal, although no significant change of Na+ was detected. Volume-induced ESP changes were highly variable. Injections produced a small increase in the mean ESP and withdrawals produced a small decrease but neither change was statistically significant and some animals showed potential changes in the opposite direction. These data show that a change in cochlear endolymph volume status results in a physiologic response of the ES which is sustained for a considerable period. If the ES plays a part in the restoration of normal endolymph volume, this process appears to proceed slowly, based on the prolonged time courses of ionic changes observed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. RP Salt, AN (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, Box 8115,660 S Euclid Ave, St Louis, MO 63110 USA. CR Couloigner V, 1999, ACTA OTO-LARYNGOL, V119, P200 Couloigner V, 1998, LARYNGOSCOPE, V108, P592, DOI 10.1097/00005537-199804000-00024 ERWALL C, 1988, HEARING RES, V35, P109, DOI 10.1016/0378-5955(88)90045-7 ERWALL C, 1988, HEARING RES, V36, P277, DOI 10.1016/0378-5955(88)90068-8 FRIBERG U, 1986, ACTA OTO-LARYNGOL, V101, P172, DOI 10.3109/00016488609132825 GHIZ A, 2000, ASS RES OTOLARYNGOL, V23, P124 Guild SR, 1927, AM J ANAT, V39, P57, DOI 10.1002/aja.1000390103 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 IKEDA K, 1991, HEARING RES, V54, P118, DOI 10.1016/0378-5955(91)90141-U JANSSON B, 1993, ORL J OTO-RHINO-LARY, V55, P185 JANSSON B, 1992, ORL J OTO-RHINO-LARY, V54, P201 KIMURA RS, 1967, ANN OTO RHINOL LARYN, V76, P664 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 LUNDQUIST P, 1965, ACTA OTOLARYNGOL S, V201, P7 LUNDQUIST PG, 1964, ACTA OTOLARYNGOL S, V188, P194 MORI N, 1987, ARCH OTO-RHINO-LARYN, V244, P61, DOI 10.1007/BF00453493 MORI N, 1991, ANN OTO RHINOL LARYN, V100, P72 MORI N, 1990, EUR ARCH OTO-RHINO-L, V247, P371 Mori N, 1998, Acta Otolaryngol Suppl, V533, P12 MORI N, 1990, AM J PHYSIOL, V259, pR921 Rask-Andersen H, 1999, HEARING RES, V138, P81, DOI 10.1016/S0378-5955(99)00153-7 SALT AN, 1995, HEARING RES, V90, P122 SALT AN, 1994, HEARING RES, V74, P165, DOI 10.1016/0378-5955(94)90184-8 Salt AN, 1997, HEARING RES, V107, P29, DOI 10.1016/S0378-5955(97)00018-X SALT AN, 1992, EUR ARCH OTO-RHINO-L, V249, P157 SHINOMORI Y, 1999, ASS RES OTOLARYNGOL, V22, P76 SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 TAKEUCHI S, 1991, ANN OTO RHINOL LARYN, V100, P244 TAKUMIDA M, 1989, HEARING RES, V40, P1, DOI 10.1016/0378-5955(89)90094-4 Takumida M, 1991, Acta Otolaryngol Suppl, V481, P129 Teixeira M, 1999, HEARING RES, V128, P45, DOI 10.1016/S0378-5955(98)00197-X TSUJIKAWA S, 1992, ACTA OTO-LARYNGOL, V112, P785, DOI 10.3109/00016489209137475 Wit HP, 2000, HEARING RES, V145, P82, DOI 10.1016/S0378-5955(00)00078-2 zumGottesberge AMM, 1996, EUR ARCH OTO-RHINO-L, V253, P136 NR 35 TC 15 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 46 EP 54 DI 10.1016/S0378-5955(00)00160-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400005 PM 11033246 ER PT J AU Khanna, SM Hao, LF AF Khanna, SM Hao, LF TI Amplification in the apical turn of the cochlea with negative feedback SO HEARING RESEARCH LA English DT Article DE cochlear mechanics; guinea pig cochlea; apical turn; cellular response; amplification; negative feedback ID GUINEA-PIG COCHLEA; TEMPORAL BONE PREPARATION; OUTER HAIR-CELLS; BASILAR-MEMBRANE; HEARING ORGAN; MECHANICAL RESPONSES; NONLINEAR MECHANICS; MOSSBAUER TECHNIQUE; CHINCHILLA COCHLEA; SOUND PRESSURE AB The apical turn of the anesthetized guinea pig cochlea was opened to examine the basilar membrane optically through the intact Reissner's membrane. Vibrations of the outer Hensen's cell and the basilar membrane (BM) adjacent to and about 130 mu m below the level of the Hensen's cell were measured. Outer Hensen's cell vibration at the characteristic frequency was up to 900 times higher compared to the BM amplitude. After sacrifice BM vibration increased while Hensen's cell vibration decreased. The magnitude and sequence of change after sacrifice call best be explained by the presence of negative feedback between reticular lamina and BM. In other experiments using ototoxic drugs that damage outer hair cells, similar changes in Hensen's cell and BM vibration were observed. These results show that the apical turn behavior is different from that observed by other investigators in the basal turn. The potential benefits of the negative Feedback are discussed. The presence of negative feedback would explain the linearity at the fundamental frequency observed in the apical turn of cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Columbia Univ Coll Phys & Surg, Dept Otolaryngol & Head & Neck Surg, New York, NY 10032 USA. Univ Maryland, Sch Med, Dept Otolaryngol & Head & Neck Surg, Baltimore, MD 21201 USA. RP Khanna, SM (reprint author), Columbia Univ Coll Phys & Surg, Dept Otolaryngol & Head & Neck Surg, 630 W 168th St, New York, NY 10032 USA. EM smk3@columbia.edu CR Bode H. W., 1945, NETWORK ANAL FEEDBAC BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1992, HEARING RES, V58, P175, DOI 10.1016/0378-5955(92)90126-8 Cooper NP, 1998, J PHYSIOL-LONDON, V509, P277, DOI 10.1111/j.1469-7793.1998.277bo.x COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X Corti A., 1851, Z WISS ZOOL, V3, P109 DEBOER E, 1990, LECT NOTES BIOMATH, V87, P333 ENGSTROM B, 1972, AUDIOLOGY, V11, P6 Engstrom H, 1966, STRUCTURAL PATTERN O EVANS BN, 1993, P NATL ACAD SCI USA, V90, P8347, DOI 10.1073/pnas.90.18.8347 FRANKE R, 1992, ACUSTICA, V76, P173 Gummer A W, 1997, Ear Nose Throat J, V76, P151 GUMMER AW, 1993, BIOPHYSICS HAIR CELL, P229 Hao LF, 1996, HEARING RES, V99, P176, DOI 10.1016/S0378-5955(96)00099-8 Hao LF, 2000, HEARING RES, V148, P31, DOI 10.1016/S0378-5955(00)00112-X Hemmert W, 2000, BIOPHYS J, V78, P2285 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 *ITER, 1989, ACTA OTOLARYNGOL S, V467, P5 IURATO S, 1961, Z ZELLFORSCH MIK ANA, V53, P259, DOI 10.1007/BF00339444 JUNG HW, 2000, IN PRESS HEAR RES JUNG HW, 1999, P S REC DEV AUD MECH KHANNA SM, 1989, ACTA OTO-LARYNGOL, P195 KHANNA SM, 1998, COCHLEAR MECH STRUCT, P387 KHANNA SM, 1996, P SOC PHOTO-OPT INS, V2732, P64, DOI 10.1117/12.231687 KHANNA SM, 1989, ACTA OTO-LARYNGOL, P189 Khanna SM, 1999, HEARING RES, V132, P15, DOI 10.1016/S0378-5955(99)00027-1 KHANNA SM, 1995, ACTIVE HEARING, P257 Khanna SM, 1998, ACUSTICA, V84, P1175 KHANNA SM, 1993, BIOPHYSICS HAIRCELL, P266 Khanna SM, 1999, HEARING RES, V135, P89, DOI 10.1016/S0378-5955(99)00095-7 KHANNA SM, 1989, ACTA OTO-LARYNGOL, P183 KHANNA SM, 1989, ACTA OTO-LARYNGOL, P151 Kinsler L., 1962, FUNDAMENTALS ACOUSTI KOESTER CJ, 1990, T ROY MICR, V1, P327 KOESTER CJ, 1989, ACTA OTO-LARYNGOL, P27 KOESTER CJ, 1994, APPL OPTICS, V33, P702, DOI 10.1364/AO.33.000702 KOESTER CJ, 1980, APPL OPTICS, V19, P1749, DOI 10.1364/AO.19.001749 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LUND DT, 1989, ACTA OTO-LARYNGOL, P77 MAMMANO F, 1993, NATURE, V365, P833 PATTUZI R, 1984, HEARING RES, V13, P99 Retzius G, 1884, GEHORORGAN WIRBELTIE, pII Rhode W. S., 1973, BASIC MECHANISMS HEA, P49 RHODE WS, 1980, J ACOUST SOC AM, V67, P1696, DOI 10.1121/1.384296 Rhode WS, 1996, AUDIT NEUROSCI, V3, P101 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 RHODE WS, 1984, ANNU REV PHYSIOL, V46, P2231 ROBLES L, 1986, PERIPHERAL AUDITORY RUGGERO MA, 1992, ADV BIOSCI, V83, P85 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 Ruggero MA, 1996, AUDIT NEUROSCI, V2, P329 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 STINSON MR, 1994, J ACOUST SOC AM, V96, P170, DOI 10.1121/1.410461 TEICH MC, 1989, ACTA OTO-LARYNGOL, P265 ULFENDAHL M, 1991, HEARING RES, V57, P31, DOI 10.1016/0378-5955(91)90071-G ULFENDAHL M, 1995, NEUROREPORT, V6, P1157, DOI 10.1097/00001756-199505300-00021 ULFENDAHL M, 1993, EUR J NEUROSCI, V5, P713, DOI 10.1111/j.1460-9568.1993.tb00535.x Ulfendahl M, 1996, J NEUROPHYSIOL, V76, P3850 Ulfendahl M, 1997, PROG NEUROBIOL, V53, P331, DOI 10.1016/S0301-0082(97)00040-3 von Bekesy G., 1960, EXPT HEARING, P745 WERSALL J, 1965, COLD SPRING HARBOR S, V30 WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 WILLEMIN JF, 1989, ACTA OTO-LARYNGOL, P35 ZWICKER E, 1986, J ACOUST SOC AM, V80, P146, DOI 10.1121/1.394175 NR 67 TC 18 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 55 EP 76 DI 10.1016/S0378-5955(00)00162-3 PG 22 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400006 PM 11033247 ER PT J AU Blum, JJ Reed, MC AF Blum, JJ Reed, MC TI Model calculations of time dependent responses to binaural stimuli in the dorsal nucleus of the lateral lemniscus SO HEARING RESEARCH LA English DT Article DE binaural processing; auditory brainstem; lateral lemniscus; commissure of probst ID RATS INFERIOR COLLICULUS; AMPLITUDE-MODULATED SIGNALS; UNIT EXCITATORY RESPONSES; RATE-INTENSITY FUNCTIONS; BIG BROWN BAT; SUPERIOR OLIVE; MOUSTACHE BAT; GABAERGIC INHIBITION; EPTESICUS-FUSCUS; TONE BURSTS AB In a previous paper (Recd and Blum, 1999), we examined the connectional hypotheses put forward by Markovitz and Pollak; (1994) to explain the steady-state behavior of cells in the dorsal nucleus of the lateral lemniscus (DNLL). We found that the steady state outputs of the four major binaural types of cells found in the DNLL (El, EI/F, EE/I, and EE/FI) could be accounted for by known connectional patterns using only one or two cells per nucleus and quite simple hypotheses on cell behavior. In this study, we examine the lime course of DNLL outputs in response to constant, ongoing, monaural or binaural sounds of various intensities. The model auditory nerve fibers ramp up linearly (usually in 2 ms) to full firing and the anteroventral cochlear nucleus cells have primary-like discharge patterns. Fixed time delays of 1 ms at each synapse are included; other time delays are employed when necessary to understand and reproduce specific features of the experimental data. We find that the connectional patterns utilized in our previous study can account For the rich variety of temporal response patterns found experimentally in the DNLL. Our main findings are: (1) all of the four major binaural types of cells can arise from modifications of the basic connectional pattern that produces EI cells: (2) both excitation and inhibition from the ipsilateral lateral superior olive (LSO) are required to understand DNLL responses; (3) pauser behavior call arise either from time delayed inhibition from a DNLL interneuron or by projection from the LSO; (4) two different mechanisms can account for the ipsilaterally evoked onset response; (5) to explain completely the temporal discharge pattern and binaural interactions of EE/FI cells, a projection from the contralateral DNLL via the commissure of Probst is necessary. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Duke Univ, Med Ctr, Dept Cell Biol, Div Physiol, Durham, NC 27710 USA. Duke Univ, Dept Math, Durham, NC 27708 USA. RP Blum, JJ (reprint author), Duke Univ, Med Ctr, Dept Cell Biol, Div Physiol, Durham, NC 27710 USA. CR Bajo VM, 1999, J COMP NEUROL, V407, P349, DOI 10.1002/(SICI)1096-9861(19990510)407:3<349::AID-CNE4>3.0.CO;2-5 BLUM JJ, 1991, J ACOUST SOC AM, V90, P1968, DOI 10.1121/1.401676 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 Huffman RF, 1998, HEARING RES, V126, P161, DOI 10.1016/S0378-5955(98)00165-8 Huffman RF, 1998, HEARING RES, V126, P181, DOI 10.1016/S0378-5955(98)00166-X Irvine DR, 1986, AUDITORY BRAINSTEM Ito M, 1996, J NEUROPHYSIOL, V76, P3493 Kelly JB, 1998, HEARING RES, V122, P25, DOI 10.1016/S0378-5955(98)00082-3 Kelly JB, 1998, HEARING RES, V116, P43, DOI 10.1016/S0378-5955(97)00195-0 LI L, 1992, J NEUROSCI, V12, P4530 MARKOVITZ NS, 1994, HEARING RES, V73, P121, DOI 10.1016/0378-5955(94)90290-9 MARKOVITZ NS, 1993, HEARING RES, V71, P51, DOI 10.1016/0378-5955(93)90020-2 Oertel D, 1999, ANNU REV PHYSIOL, V61, P497, DOI 10.1146/annurev.physiol.61.1.497 Park TJ, 1997, J NEUROPHYSIOL, V77, P2863 Pollak GD, 1997, ANN OTO RHINOL LARYN, V106, P44 Reed MC, 1999, HEARING RES, V136, P13, DOI 10.1016/S0378-5955(99)00096-9 REED MC, 1990, J ACOUST SOC AM, V88, P1442, DOI 10.1121/1.399721 RUGGERO MA, 1991, MAMMALIAN AUDITORY P, P34 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SCHALK TB, 1980, J ACOUST SOC AM, V67, P903, DOI 10.1121/1.383970 SMITH RL, 1988, AUDITORY FUNCTION, V389, P264 Kelly JB, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P329, DOI 10.1007/978-1-4419-8712-9_31 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 van Adel BA, 1999, HEARING RES, V130, P115, DOI 10.1016/S0378-5955(98)00226-3 VATER M, 1995, J COMP NEUROL, V351, P632, DOI 10.1002/cne.903510411 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YANG L, 1994, AUDIT NEUROSCI, V1, P1 YANG LC, 1994, J NEUROPHYSIOL, V71, P1999 Yang LC, 1998, HEARING RES, V122, P125, DOI 10.1016/S0378-5955(98)00088-4 Yang LC, 1997, J NEUROPHYSIOL, V77, P324 YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 Zhang DX, 1998, HEARING RES, V117, P1, DOI 10.1016/S0378-5955(97)00202-5 NR 33 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 77 EP 90 DI 10.1016/S0378-5955(00)00169-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400007 PM 11033248 ER PT J AU Francis, HW Manis, PB AF Francis, HW Manis, PB TI Effects of deafferentation on the electrophysiology of ventral cochlear nucleus neurons SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 21st Midwinter Meeting of the Association-of-Research-in-Otolaryngology CY 1999 CL ST PETERSBURG, FLORIDA SP Assoc Res Otolaryngol DE deafferentation; cochlear ablation; deafness; ventral cochlear nucleus; intracellular recording; discharge pattern; brain slice ID STEM AUDITORY NUCLEI; SPINAL SENSORY NEURONS; CHANNEL MESSENGER-RNA; RAT SKELETAL-MUSCLE; EAR OSSICLE REMOVAL; DEAF WHITE CATS; BRAIN-STEM; GUINEA-PIG; CELL-SIZE; MEMBRANE-PROPERTIES AB When cochlear pathology impairs the afferent innervation of the ventral cochlear nucleus (VCN), electrical responses of the auditory brainstem are altered and changes in cell and synaptic morphology are observed. However, the impact of deafferentation on the electrical properties of cells in the VCN is unknown. We examined the electrical properties of single neurons in the anterior and posterior VCN following bilateral cochlear removal in young rats. In control animals, two populations of cells were distinguished: those with a linear subthreshold current-voltage relationship and repetitive firing of action potentials with regular interspike intervals (type II, and those with rectifying subthreshold current-voltage relationships and phasic firing of 1-3 action potentials (type II). Measures of action potential shape further distinguished these two groups. Two weeks following cochlear removal, both electrical response patterns were still seen. Type I cells showed a higher input resistance. Deafferented single-spiking type II cells were slightly more depolarized, had smaller action potentials, smaller afterhyperpolarizations and shorter membrane time constants, whereas multiple-spiking type II cells were apparently unaffected. These changes in the electrical properties of VCN neurons following cochlear injury may adversely affect central processing of sounds presented acoustically or electrically by prostheses. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21205 USA. RP Manis, PB (reprint author), Univ N Carolina, Dept Surg, Div Otolaryngol Head & Neck Surg, 610 Burnett Womack Bldg,CB 7070, Chapel Hill, NC 27599 USA. CR Aĝar E, 1996, J Basic Clin Physiol Pharmacol, V7, P179 ATTWELL D, 1979, PFLUG ARCH EUR J PHY, V379, P137, DOI 10.1007/BF00586939 Benson CG, 1997, SYNAPSE, V25, P243 BLACKBURN CC, 1990, J NEUROPHYSIOL, V63, P1191 BORN DE, 1991, BRAIN RES, V557, P37, DOI 10.1016/0006-8993(91)90113-A CAMERINO D, 1976, J NEUROBIOL, V7, P221, DOI 10.1002/neu.480070305 Cummins TR, 1997, J NEUROSCI, V17, P3503 Desai NS, 1999, NAT NEUROSCI, V2, P515 DibHajj S, 1996, P NATL ACAD SCI USA, V93, P14950, DOI 10.1073/pnas.93.25.14950 Dib-Hajj SD, 1998, P NATL ACAD SCI USA, V95, P8963, DOI 10.1073/pnas.95.15.8963 DURHAM D, 1993, HEARING RES, V70, P151, DOI 10.1016/0378-5955(93)90153-R Erisir A, 1999, J NEUROPHYSIOL, V82, P2476 Fitzakerley JL, 1997, HEARING RES, V114, P148, DOI 10.1016/S0378-5955(97)00158-5 Flannery B. P., 1992, NUMERICAL RECIPES C FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y GALLEGO R, 1987, J PHYSIOL-LONDON, V391, P39 GENTSCHE.T, 1973, BRAIN RES, V62, P37, DOI 10.1016/0006-8993(73)90618-5 GERKEN GM, 1979, J ACOUST SOC AM, V66, P721, DOI 10.1121/1.383222 GERKEN GM, 1979, J ACOUST SOC AM, V66, P728, DOI 10.1121/1.383223 GHOSHAL S, 1992, HEARING RES, V58, P153, DOI 10.1016/0378-5955(92)90124-6 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 Golowasch Jorge, 1999, Journal of Neuroscience Rapid Communications, V19, P1 GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 HARRISON JM, 1966, J COMP NEUROL, V126, P391, DOI 10.1002/cne.901260303 HARRISON JM, 1965, J COMP NEUROL, V124, P15, DOI 10.1002/cne.901240103 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 Huchton DM, 1997, OTOLARYNG HEAD NECK, V116, P286, DOI 10.1016/S0194-5998(97)70262-6 ISAACSON JS, 1995, J NEUROPHYSIOL, V73, P964 JASSAR BS, 1994, J PHYSIOL-LONDON, V479, P353 JORIS PX, 1994, J NEUROPHYSIOL, V71, P1022 KANE EC, 1974, ANAT REC, V179, P67, DOI 10.1002/ar.1091790106 Kato BM, 1999, J NEUROPHYSIOL, V81, P1587 Kiang NY, 1973, BASIC MECHANISMS HEA, P455 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 Kotak VC, 1996, J NEUROSCI, V16, P1836 Lachica EA, 1998, J NEUROBIOL, V37, P321, DOI 10.1002/(SICI)1097-4695(19981105)37:2<321::AID-NEU10>3.0.CO;2-M LESAVIO AS, 1995, LIFE SCI, V56, P249 LESPERANCE MM, 1995, HEARING RES, V86, P77, DOI 10.1016/0378-5955(95)00056-A LUPA MT, 1995, J PHYSIOL-LONDON, V483, P109 MANIS PB, 1989, J NEUROPHYSIOL, V61, P149 MANIS PB, 1990, J NEUROSCI, V10, P2338 MANIS PB, 1996, ADV SP HEAR A&B, V3, P213 MANIS PB, 1991, J NEUROSCI, V11, P2865 Mo ZL, 1997, J NEUROPHYSIOL, V77, P1294 MOORE JK, 1994, AM J OTOL, V15, P588 Morest DK, 1973, BASIC MECH HEARING, P479 Morest DK, 1997, HEARING RES, V103, P151, DOI 10.1016/S0378-5955(96)00172-4 OERTEL D, 1983, J NEUROSCI, V3, P2043 Oertel D, 1997, NEURON, V19, P959, DOI 10.1016/S0896-6273(00)80388-8 Oertel D, 1991, Curr Opin Neurobiol, V1, P221, DOI 10.1016/0959-4388(91)90082-I OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 PASIC TR, 1994, J COMP NEUROL, V348, P111, DOI 10.1002/cne.903480106 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 POTASHNER SJ, 1983, J NEUROCHEM, V41, P1094, DOI 10.1111/j.1471-4159.1983.tb09057.x Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 POWELL TPS, 1962, J ANAT, V96, P249 Rathouz M, 1998, J NEUROPHYSIOL, V80, P2824 REDFERN P, 1971, ACTA PHYSIOL SCAND, V81, P557, DOI 10.1111/j.1748-1716.1971.tb04932.x Reyes AD, 1996, J NEUROSCI, V16, P993 REYES AD, 1994, J NEUROSCI, V14, P5352 RHODE WS, 1992, MAMMALIAN AUDITORY P, V2, P94 RHODE WS, 1986, J NEUROPHYSIOL, V56, P262 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 RIZZO MA, 1995, NEUROBIOL DIS, V2, P87, DOI 10.1006/nbdi.1995.0009 ROTHMAN J, 1999, THESIS J HOPKINS U B, P247 ROTHMAN JS, 1993, J NEUROPHYSIOL, V70, P2562 ROUILLER EM, 1984, J COMP NEUROL, V225, P167, DOI 10.1002/cne.902250203 Ryugo DK, 1997, J COMP NEUROL, V385, P230, DOI 10.1002/(SICI)1096-9861(19970825)385:2<230::AID-CNE4>3.0.CO;2-2 SAH P, 1989, SCIENCE, V246, P815, DOI 10.1126/science.2573153 SASAKI CT, 1980, BRAIN RES, V194, P511, DOI 10.1016/0006-8993(80)91233-0 Schofield BR, 1996, J COMP NEUROL, V375, P128, DOI 10.1002/(SICI)1096-9861(19961104)375:1<128::AID-CNE8>3.0.CO;2-5 Schwarz DWF, 1997, HEARING RES, V114, P127, DOI 10.1016/S0378-5955(97)00162-7 SELDON HL, 1991, BRAIN RES, V551, P185, DOI 10.1016/0006-8993(91)90932-L Shofner WP, 1996, J ACOUST SOC AM, V99, P3592, DOI 10.1121/1.414957 SHOFNER WP, 1989, J ACOUST SOC AM, V86, P2172, DOI 10.1121/1.398478 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 SNYDER RL, 1991, HEARING RES, V56, P246, DOI 10.1016/0378-5955(91)90175-9 SULLIVAN WE, 1984, J NEUROSCI, V4, P1787 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 TITMUS MJ, 1990, PROG NEUROBIOL, V35, P1, DOI 10.1016/0301-0082(90)90039-J TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 Trussell LO, 1997, CURR OPIN NEUROBIOL, V7, P487, DOI 10.1016/S0959-4388(97)80027-X TUCCI DL, 1987, ANN OTO RHINOL LARYN, V96, P343 WANG XQ, 1993, J NEUROPHYSIOL, V70, P1054 WAXMAN SG, 1994, J NEUROPHYSIOL, V72, P466 WEBSTER DB, 1978, OTOLARYNG HEAD NECK, V86, P342 WENTHOLD RJ, 1978, BRAIN RES, V143, P544, DOI 10.1016/0006-8993(78)90365-7 WENTHOLD RJ, 1977, BRAIN RES, V138, P111, DOI 10.1016/0006-8993(77)90787-9 WHITE JA, 1994, J NEUROPHYSIOL, V71, P1774 WU SH, 1984, J NEUROSCI, V4, P1577 YANG JSJ, 1991, NEURON, V7, P421, DOI 10.1016/0896-6273(91)90294-A Zirpel L, 1998, J NEUROPHYSIOL, V79, P2288 Zirpel L, 1996, J NEUROPHYSIOL, V76, P4127 NR 95 TC 55 Z9 56 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 91 EP 105 DI 10.1016/S0378-5955(00)00165-9 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400008 PM 11033249 ER PT J AU Shofner, WP AF Shofner, WP TI Comparison of frequency discrimination thresholds for complex and single tones in chinchillas SO HEARING RESEARCH LA English DT Article DE frequency discrimination; harmonic tone complex; chinchilla ID ITERATED RIPPLED NOISE; PHASE SENSITIVITY; AUDITORY PERIPHERY; DIFFERENCE LIMENS; DOMINANCE REGION; PITCH PERCEPTION; COMPUTER-MODEL; VIRTUAL PITCH; RESIDUE PITCH; STRENGTH AB Frequency discrimination thresholds were measured from five chinchillas for harmonic tone complexes having a fundamental frequency of 250 Hz. Stimuli consisted of the fundamental frequency and the second through 10th harmonics with individual components added in either cosine phase or random phase. In general, thresholds were independent of overall level for sound levels between 47 and 77 dB SPL, and there was no difference in thresholds observed between cosine-phase tone complexes and random-phase tone complexes. Discrimination thresholds were also obtained for a single 250-Hz tone for comparison with complex tone thresholds. Similar to data reported in human subjects, thresholds in chinchillas for tone complexes were lower than thresholds obtained using a single tone, although chinchillas required a larger frequency difference than human listeners. The results suggest that the mechanisms of frequency discrimination of complex tones are similar between chinchillas and human listeners. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Loyola Univ, Parmly Hearing Inst, Chicago, IL 60626 USA. RP Shofner, WP (reprint author), Loyola Univ, Parmly Hearing Inst, 6525 N Sheridan Rd, Chicago, IL 60626 USA. CR CAMPBELL RA, 1963, J ACOUST SOC AM, V35, P1511, DOI 10.1121/1.1918738 Cariani PA, 1996, J NEUROPHYSIOL, V76, P1717 COHEN MA, 1995, J ACOUST SOC AM, V98, P862, DOI 10.1121/1.413512 Creelman C. D., 1991, DETECTION THEORY USE EVANS EF, 1978, AUDIOLOGY, V17, P369 FASTL H, 1981, ACUSTICA, V49, P77 FASTL H, 1978, J ACOUST SOC AM, V63, P275, DOI 10.1121/1.381725 FLANAGAN JL, 1958, J ACOUST SOC AM, V30, P435, DOI 10.1121/1.1909640 GREEN DM, 1966, SIGNAL DETECTION THE Green D.M., 1976, INTRO HEARING HEFFNER RS, 1991, HEARING RES, V52, P13, DOI 10.1016/0378-5955(91)90183-A HENNING GB, 1968, J ACOUST SOC AM, V44, P1386, DOI 10.1121/1.1911273 JESTEADT W, 1974, J ACOUST SOC AM, V55, P1266, DOI 10.1121/1.1914696 JESTEADT W, 1975, J ACOUST SOC AM, V57, P1161, DOI 10.1121/1.380574 LOFTUS GR, 1994, PSYCHON B REV, V1, P476, DOI 10.3758/BF03210951 LUNDEEN C, 1984, J ACOUST SOC AM, V75, P1578, DOI 10.1121/1.390867 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2883, DOI 10.1121/1.400726 Meddis R, 1997, J ACOUST SOC AM, V102, P1811, DOI 10.1121/1.420088 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2866, DOI 10.1121/1.400725 Moore B. C. J., 1993, HUMAN PSYCHOPHYSICS, P56 Moore B. C. J., 1988, BASIC ISSUES HEARING, P421 MOORE BCJ, 1984, J ACOUST SOC AM, V75, P550, DOI 10.1121/1.390527 MOORE BCJ, 1992, J ACOUST SOC AM, V91, P2881, DOI 10.1121/1.402925 NELSON DA, 1986, J ACOUST SOC AM, V79, P799, DOI 10.1121/1.393470 NELSON DA, 1978, J ACOUST SOC AM, V64, P114, DOI 10.1121/1.381977 NIEMIEC AJ, 1992, J ACOUST SOC AM, V92, P2636, DOI 10.1121/1.404380 PATTERSO.RD, 1973, J ACOUST SOC AM, V53, P1565, DOI 10.1121/1.1913504 PATTERSON RD, 1987, J ACOUST SOC AM, V82, P1560, DOI 10.1121/1.395146 PATTERSON RD, 1995, J ACOUST SOC AM, V98, P1890, DOI 10.1121/1.414456 PATTERSON RD, 1976, J ACOUST SOC AM, V59, P1450, DOI 10.1121/1.381034 Patterson RD, 1996, J ACOUST SOC AM, V100, P3286, DOI 10.1121/1.417212 PFINGST BE, 1993, J ACOUST SOC AM, V93, P2124, DOI 10.1121/1.406673 PROSEN CA, 1990, J ACOUST SOC AM, V88, P2152, DOI 10.1121/1.400112 Shofner W. P., 1995, AUDIT NEUROSCI, V1, P127 Shofner WP, 1997, HEARING RES, V110, P15, DOI 10.1016/S0378-5955(97)00063-4 SINNOTT JM, 1985, J ACOUST SOC AM, V78, P1977, DOI 10.1121/1.392654 SPIEGEL MF, 1984, J ACOUST SOC AM, V76, P1690, DOI 10.1121/1.391605 WIGHTMAN FL, 1973, J ACOUST SOC AM, V54, P397, DOI 10.1121/1.1913591 Yost WA, 1996, J ACOUST SOC AM, V99, P1066, DOI 10.1121/1.414593 Zar J. H., 1999, BIOSTATISTICAL ANAL, V4th NR 40 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 106 EP 114 DI 10.1016/S0378-5955(00)00171-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400009 PM 11033250 ER PT J AU Matsuoka, AJ Abbas, PJ Rubinstein, JT Miller, CA AF Matsuoka, AJ Abbas, PJ Rubinstein, JT Miller, CA TI The neuronal response to electrical constant-amplitude pulse train stimulation: evoked compound action potential recordings SO HEARING RESEARCH LA English DT Article DE pulse train; electrical stimulation; auditory nerve ID AUDITORY-NERVE FIBERS; MONOPHASIC STIMULATION; CAT; MONOPOLAR AB The purpose of this study was to gain a greater understanding of the electrically evoked compound action potential (EAP) responses to pulse train stimulation. Analysis of EAP amplitude responses suggested that an alternating pattern varied depending upon stimulus level, interpulse interval (IPI), stimulus waveform, and stimulus polarity. Stimulus level-dependent recovery was seen in the cat and the guinea pig. higher stimulus level tended to provide faster recovery. Both polarity-dependent recovery and polarity-dependent adaptation were observed in the cat and these stimulus polarity effects were less consistent in the guinea pig. The polarity-dependent recovery effect supports the hypothesis that anodal and cathodal stimuli excite different sites along auditory nerve fibers. Amplitude differences between the response to the second pulse and the steady-state response at the same IPI are significantly greater for anodal stimuli than for cathodal stimuli in all cats. These data suggest that there is a cumulative refractory effect in the auditory nerve of cats, especially in response to anodal stimuli. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Iowa, Dept Otolaryngol Head & Neck Surg, Iowa City, IA 52246 USA. Univ Iowa, Dept Speech Pathol & Audiol, Iowa City, IA 52246 USA. Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52246 USA. RP Matsuoka, AJ (reprint author), Univ Iowa, 127B SHC, Iowa City, IA 52242 USA. CR ABBAS PJ, 1997, N01DC62111 Bekesy G., 1960, EXPT HEARING BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P440, DOI 10.1109/TBME.1977.326179 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P59, DOI 10.1109/TBME.1977.326218 DYNES SBC, 1992, HEARING RES, V58, P79, DOI 10.1016/0378-5955(92)90011-B Finley C., 1997, SPEECH PROCESSORS AU Hill AV, 1936, PROC R SOC SER B-BIO, V119, P305, DOI 10.1098/rspb.1936.0012 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 MATSUOKA AJ, 1998, THESIS U IOWA IOWA C MCDERMOTT HJ, 1992, J ACOUST SOC AM, V91, P3367, DOI 10.1121/1.402826 Miller CA, 1998, HEARING RES, V119, P142, DOI 10.1016/S0378-5955(98)00046-X Miller CA, 1999, HEARING RES, V130, P197, DOI 10.1016/S0378-5955(99)00012-X Moxon E.C., 1971, THESIS MIT CAMBRIDGE OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 Rattay F, 1990, ELECT NERVE STIMULAT RETZIUS G, 1984, GEHORORGAN REPTILIEN RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 RUBINSTEIN JT, 1995, ABSTR ASS RES OT, V570 Rubinstein JT, 1999, HEARING RES, V127, P108, DOI 10.1016/S0378-5955(98)00185-3 Shepherd RK, 1999, HEARING RES, V130, P171, DOI 10.1016/S0378-5955(99)00011-8 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 WILSON BS, 1994, SPEECH PROCESSORS AU Wilson BS, 1997, AM J OTOL, V18, pS30 NR 26 TC 29 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 115 EP 128 DI 10.1016/S0378-5955(00)00172-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400010 PM 11033251 ER PT J AU Matsuoka, AJ Abbas, PJ Rubinstein, JT Miller, CA AF Matsuoka, AJ Abbas, PJ Rubinstein, JT Miller, CA TI The neuronal response to electrical constant-amplitude pulse train stimulation: additive Gaussian noise SO HEARING RESEARCH LA English DT Article DE electrical stimulation; stochastic resonance; cochlear implant ID MONOPHASIC STIMULATION; COCHLEAR IMPLANTS; ACTION-POTENTIALS; AUDITORY-NERVE; MONOPOLAR; CAT AB Experimental results from humans and animals show that electrically evoked compound action potential (EAP) responses to constant-amplitude pulse train stimulation call demonstrate an alternating pattern, due to the combined effects of highly synchronized responses to electrical stimulation and refractory effects (Wilson et al., 1994). One way to improve signal representation is to reduce the level of across-fiber synchrony and hence, the level of the amplitude alternation. To accomplish this goal, we have examined EAP responses in the presence of Gaussian noise added to the pulse train stimulus. Addition of Gaussian noise at a level approximately -30 dB relative to EAP threshold to the pulse trains decreased the amount of alternation, indicating that stochastic resonance may be induced in the auditory nerve. The use of some type of conditioning stimulus such as Gaussian noise may provide a more 'normal' neural response pattern. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Iowa, Dept Otolaryngol Head & Neck Surg, Iowa City, IA 52242 USA. Univ Iowa, Dept Speech Pathol & Audiol, Iowa City, IA 52242 USA. Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52242 USA. RP Matsuoka, AJ (reprint author), Univ Iowa, Dept Otolaryngol Head & Neck Surg, 127B SHC, Iowa City, IA 52242 USA. CR BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P440, DOI 10.1109/TBME.1977.326179 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P59, DOI 10.1109/TBME.1977.326218 ERELL A, 1988, J ACOUST SOC AM, V84, P204, DOI 10.1121/1.396966 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FRIJNS JHM, 1995, COCHLEAR IMPLANTS MO HARTMANN R, 1984, HEARING RES, V13, P46 HOCHMAIRDESOYER IJ, 1983, COCHLEAR IMPLANTS, P101 JOHNSON DH, 1976, BIOPHYS J, V16, P719 JOLLY CN, 1998, 7 S COCHL IMPL CHILD, P37 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KUZMA JA, 1998, 7 S COCHL IMPL CHILD, P22 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 Matsuoka AJ, 2000, HEARING RES, V149, P115, DOI 10.1016/S0378-5955(00)00172-6 Miller CA, 1998, HEARING RES, V119, P142, DOI 10.1016/S0378-5955(98)00046-X Miller CA, 1999, HEARING RES, V130, P197, DOI 10.1016/S0378-5955(99)00012-X MILLER CA, 1994, HEARING RES, V78, P11, DOI 10.1016/0378-5955(94)90039-6 Morse RP, 1996, NAT MED, V2, P928, DOI 10.1038/nm0896-928 SAUNDERS E, 1998, 7 S COCHL IMPL CHILD, P39 Shepherd RK, 1999, HEARING RES, V130, P171, DOI 10.1016/S0378-5955(99)00011-8 SPELMAN FA, 1997, 1997 C IMPL AUD PROS STEVENS CF, 1972, BIOPHYS J, V12, P1028 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 WIESENFELD K, 1995, NATURE, V373, P33, DOI 10.1038/373033a0 WILSON B, 1997, SPEECH PROCESSORS AU WILSON BS, 1994, SPEECH PROCESSORS AU Wilson BS, 1997, BRIT J AUDIOL, V31, P205 YOUNG ED, 1989, ABSTR ASS RES OT, V121 NR 27 TC 20 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 129 EP 137 DI 10.1016/S0378-5955(00)00173-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400011 PM 11033252 ER PT J AU Kopke, RD Weisskopf, PA Boone, JL Jackson, RL Wester, DC Hoffer, ME Lambert, DC Charon, CC Ding, DL McBride, D AF Kopke, RD Weisskopf, PA Boone, JL Jackson, RL Wester, DC Hoffer, ME Lambert, DC Charon, CC Ding, DL McBride, D TI Reduction of noise-induced hearing loss using L-NAC and salicylate in the chinchilla SO HEARING RESEARCH LA English DT Article DE antioxidant; loud noise; evoked potential; hair cell; chinchilla ID ACOUSTIC OVERSTIMULATION; GUINEA-PIG; INNER-EAR; KAPPA-B; DAMAGE; EXPOSURE; ORGAN; ASPIRIN; CORTI; MODES AB The effects of a combination of two antioxidant compounds were studied in a chinchilla model of noise-induced hearing loss. After obtaining baseline threshold using inferior colliculus evoked potentials, chinchillas were exposed for 6 h to octave band noise centered at 4 kHz (105 dB SPL). Post-noise thresholds were obtained h after the noise exposure, and then animals received either saline or salicylate and N-L-acetylcysteine combination. Another group received antioxidant treatment 1 h prior to noise. Rearing was tested at 1, 2 and 3 weeks post-noise. Subsequently, the cochleae were harvested, and cytocochleograms were prepared. There was a 20-40 dB SPL threshold shift at 3 weeks for tested controls. Permanent threshold shifts (PTS) were significantly reduced similar to the pre-treatment group at 1 and 2 kHz (0-10 dB) but was intermediate between the control and pre-treatment groups at 4 and 8 kHz (23 dB). Animals pre-treated with antioxidant had a significant reduction in hair cell loss but those post-treated with antioxidant had no protection from hair cell loss. These findings demonstrate the feasibility of reduction of noise-induced hearing loss using clinically available antioxidant compounds. (C) 2000 Elsevier Science B.V. All rights reserved. C1 USN, Med Ctr, Dept Otolaryngol, Dept Def Spatial Orientat Ctr, San Diego, CA 92134 USA. Madigan Army Med Ctr, Dept Otolaryngol, Tacoma, WA 98431 USA. Uniformed Serv Univ Hlth Sci, Dept Surg, Bethesda, MD 20814 USA. SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14260 USA. Univ Cent Florida, Dept Simulat & Training, Orlando, FL 32816 USA. RP Kopke, RD (reprint author), USN, Med Ctr, Dept Otolaryngol, Dept Def Spatial Orientat Ctr, Suite 200,34520 Bob Wilson Dr, San Diego, CA 92134 USA. CR ADES HW, 1974, ACTA OTO-LARYNGOL, V78, P192, DOI 10.3109/00016487409126345 ALBERTI P. W., 1998, NOISE HEALTH, V1, P3 ALTSCHULER RA, 1996, AUDITORY PLASTICITY ATTIAS J, 1994, AM J OTOLARYNG, V15, P26, DOI 10.1016/0196-0709(94)90036-1 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 CANLON B, 1992, NOISE INDUCED HEARIN, P489 ERLANDSSON B, 1987, ACTA OTO-LARYNGOL, V103, P204, DOI 10.3109/00016488709107785 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P81, DOI 10.3109/00016488809107374 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P373, DOI 10.3109/00016488809122260 HAMERNIK RP, 1974, ARCH OTOLARYNGOL, V99, P118 HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 HIGHT NG, 1999, MIDW M ASS RES OT ST, V22 Hu BH, 1997, HEARING RES, V113, P198, DOI 10.1016/S0378-5955(97)00143-3 Jacono AA, 1998, HEARING RES, V117, P31, DOI 10.1016/S0378-5955(97)00214-1 KEITHLEY EM, 1998, 21 MIDW RES M ASS RE KOMJATHY DA, 1998, MIDW M ASS RES OT ST KOPKE RD, 1999, ANN NY ACAD SCI, P884 Kopke RD, 1997, AM J OTOL, V18, P559 KOPP E, 1994, SCIENCE, V265, P956, DOI 10.1126/science.8052854 Lataye R, 1996, J ACOUST SOC AM, V99, P1621, DOI 10.1121/1.414885 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 LIU CC, 1999, MIDW M ASS RES OT ST, V22 LIU W, 1998, 21 MIDW RES M ASS RE MATTSON MP, 1994, J NEUROTRAUM, V11, P3, DOI 10.1089/neu.1994.11.3 Nakagawa T, 1997, ORL J OTO-RHINO-LARY, V59, P303 OHLEMILLER KK, 1998, 21 MIDW RES M ASS RE Pirvola U, 2000, J NEUROSCI, V20, P43 QUIRK WS, 1994, HEARING RES, V74, P217, DOI 10.1016/0378-5955(94)90189-9 Raffray M, 1997, PHARMACOL THERAPEUT, V75, P153, DOI 10.1016/S0163-7258(97)00037-5 ROBERTSON D, 1983, HEARING RES, V9, P263, DOI 10.1016/0378-5955(83)90031-X SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 SHOJI F, 1998, 21 MIDW RES M ASS RE SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 ULFENDAHL M, 1993, EUR J NEUROSCI, V5, P713, DOI 10.1111/j.1460-9568.1993.tb00535.x Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 Yamasoba T, 1998, BRAIN RES, V784, P82, DOI 10.1016/S0006-8993(97)01156-6 YAMASOBA T, 1998, 21 MIDW RES M ASS RE Yin MJ, 1998, NATURE, V396, P77 NR 39 TC 98 Z9 111 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 138 EP 146 DI 10.1016/S0378-5955(00)00176-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400012 PM 11033253 ER PT J AU Lecain, E Robert, JC Thomas, A Huy, PTB AF Lecain, E Robert, JC Thomas, A Huy, PTB TI Gastric proton pump is expressed in the inner ear and choroid plexus of the rat SO HEARING RESEARCH LA English DT Article DE gastric H,K-ATPase; cochlea; choroid plexus; reverse transcription-polymerase chain reaction; immunochemistry ID TISSUE-SPECIFIC EXPRESSION; H,K-ATPASE BETA-SUBUNIT; ALPHA-SUBUNIT; STRIA VASCULARIS; PLACE-FREQUENCY; DISTAL TUBULE; H+/K+-ATPASE; GUINEA-PIG; CELLS; NA,K-ATPASE AB Inner ear fluids and cerebrospinal fluid show remarkably stable ionic concentrations, particularly that of K+ and H+, but the mechanisms which control the homeostasis of these media are not well understood. We investigated a possible role of the gastric H,K-ATPase (gH,K-ATPase) pump in this control since this pump is known to be expressed in other tissues than gastric parietal cells. Here, we show by reverse transcription-polymerase chain reaction that the rat gH,K-ATPase alpha- and beta-subunits are expressed in the inner ear (lateral wall, organ of Corti and spiral ganglion cells), while only the alpha-subunit is expressed in the choroid plexus (CP). The presence of the alpha-subunit in the inner ear and CP was confirmed by immunoblotting. Immunohistochemistry localized this protein in the intermediate cells of the stria vascularis, in the spiral ligament and the spiral ganglion. gH,K-ATPase could be involved in the maintenance of H+ and K+ equilibria in cerobrospinal and labyrinthine fluids. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Fac Lariboisiere St Louis, Lab Otol Expt, UPRESA 7060, F-75010 Paris, France. Fac Med Xavier Bichat, INSERM, U410, F-75018 Paris, France. RP Huy, PTB (reprint author), Fac Lariboisiere St Louis, Lab Otol Expt, UPRESA 7060, 10 Ave Verdun, F-75010 Paris, France. CR Ahn KY, 1996, AM J PHYSIOL-RENAL, V270, pF557 AHN KY, 1995, AM J PHYSIOL-RENAL, V268, pF99 Alderuccio F, 1997, AUTOIMMUNITY, V25, P167, DOI 10.3109/08916939709008023 ARMITAGE FE, 1995, AM J PHYSIOL-RENAL, V269, pF116 BASTANI B, 1995, J AM SOC NEPHROL, V5, P1476 BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 BOSHER SK, 1968, PROC R SOC SER B-BIO, V171, P227, DOI 10.1098/rspb.1968.0066 BURNETTE WN, 1981, ANAL BIOCHEM, V112, P195, DOI 10.1016/0003-2697(81)90281-5 CABLE J, 1993, PIGM CELL RES, V6, P215, DOI 10.1111/j.1600-0749.1993.tb00605.x CAMPBELLTHOMPSON ML, 1995, AM J PHYSIOL-RENAL, V269, pF345 CANFIELD VA, 1990, J BIOL CHEM, V265, P19878 CANLON B, 1991, HEARING RES, V53, P7, DOI 10.1016/0378-5955(91)90209-R CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 FAIN GL, 1988, INVEST OPHTH VIS SCI, V29, P785 FERNANDEZ R, 1994, AM J PHYSIOL, V266, pF218 Gifford J.D., 1992, AM J PHYSIOL, V262, P692 HERVATIN F, 1989, BIOCHIM BIOPHYS ACTA, V985, P320, DOI 10.1016/0005-2736(89)90419-7 HILDING DA, 1977, ACTA OTO-LARYNGOL, V84, P24, DOI 10.3109/00016487709123939 Javaheri S, 1997, BRAIN RES, V754, P321, DOI 10.1016/S0006-8993(97)00175-3 Karet FE, 1999, NAT GENET, V21, P84, DOI 10.1038/5022 LINDVALLAXELSSON M, 1992, EXP NEUROL, V115, P394, DOI 10.1016/0014-4886(92)90204-4 MAEDA M, 1990, J BIOL CHEM, V265, P9027 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 Minowa O, 1999, SCIENCE, V285, P1408, DOI 10.1126/science.285.5432.1408 MOORADIAN AD, 1993, BRAIN RES, V629, P128, DOI 10.1016/0006-8993(93)90490-E NEWMAN PR, 1991, GENOMICS, V11, P252, DOI 10.1016/0888-7543(91)90131-W OKAMOTO CT, 1990, BIOCHIM BIOPHYS ACTA, V1037, P360, DOI 10.1016/0167-4838(90)90038-H Pestov NB, 1998, FEBS LETT, V440, P320, DOI 10.1016/S0014-5793(98)01483-5 Ponce A, 1997, J MEMBRANE BIOL, V159, P149, DOI 10.1007/s002329900278 REUBEN MA, 1990, P NATL ACAD SCI USA, V87, P6767, DOI 10.1073/pnas.87.17.6767 SACHS G, 1976, J BIOL CHEM, V251, P7690 SACHS G, 1992, J BIOENERG BIOMEMBR, V24, P301 SALT AN, 1988, PHYSL EAR, P341 SANGER F, 1977, P NATL ACAD SCI USA, V74, P5463, DOI 10.1073/pnas.74.12.5463 Scarff KL, 1999, GASTROENTEROLOGY, V117, P605, DOI 10.1016/S0016-5085(99)70453-1 SCHROTT A, 1990, HEARING RES, V46, P1, DOI 10.1016/0378-5955(90)90134-B SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 SHULL GE, 1986, J BIOL CHEM, V261, P6788 SHULL GE, 1990, J BIOL CHEM, V265, P12123 Silver RB, 1999, AM J PHYSIOL-RENAL, V276, pF799 SMITH CA, 1954, LARYNGOSCOPE, V64, P141 SMOLKA A, 1992, BIOCHIM BIOPHYS ACTA, V1108, P75, DOI 10.1016/0005-2736(92)90116-4 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 SPICER SS, 1994, HEARING RES, V79, P161, DOI 10.1016/0378-5955(94)90137-6 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z Stankovic KM, 1997, HEARING RES, V114, P21, DOI 10.1016/S0378-5955(97)00072-5 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1984, AM J PHYSIOL, V246, P47 TENCATE WJF, 1994, HEARING RES, V75, P151 WANG T, 1993, J CLIN INVEST, V91, P2776, DOI 10.1172/JCI116519 WINGO CS, 1990, KIDNEY INT, V38, P985, DOI 10.1038/ki.1990.302 NR 51 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 147 EP 154 DI 10.1016/S0378-5955(00)00174-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400013 PM 11033254 ER PT J AU Pressnitzer, D Winter, IM Patterson, RD AF Pressnitzer, D Winter, IM Patterson, RD TI The responses of single units in the ventral cochlear nucleus of the guinea pig to damped and ramped sinusoids SO HEARING RESEARCH LA English DT Article DE chopper unit; onset unit; primary-like unit; brainstem; temporal asymmetry; amplitude modulation ID AUDITORY-NERVE FIBERS; BUSHY CELL AXONS; AMPLITUDE-MODULATION; TEMPORAL ASYMMETRY; SOUND; CAT; NEURONS; SYSTEM; CLASSIFICATION; REGULARITY AB Human listeners hear an asymmetry in the perception of damped and ramped sinusoids; the partial loudness of the envelope component is greater than the partial loudness of the carrier component for damped sinusoids. Here we show that an asymmetry also occurs in the physiological responses of most units in the ventral cochlear nucleus to these same sounds. The activity elicited by damped sinusoids is mainly restricted to the beginning of each envelope period, which is not the case for ramped sinusoids. This can be quantified by computing the ratio of the tallest bin of the modulation period histogram to the total number of spikes (the peak-to-total ratio, p/t). Damped sinusoids produce a higher p/t than ramped sinusoids, which demonstrates physiological temporal asymmetry. it is also the case that ramped sinusoids typically elicit more spikes than damped sinusoids. The physiological asymmetry occurs where the perceptual asymmetry is present. It is maximal at modulation half-lives of 4 and 16 ms, greatly reduced at 1 ms and absent at 64 ms. Different unit types exhibit differing degrees of temporal asymmetry. Onset units produce the greatest p/t asymmetry, primary-like units produce the least asymmetry and chopper units are in-between. With regard to total spike count, the maximal asymmetry occurs with chopper units. If primary-like units are assumed to reflect the activity in primary auditory nerve fibres, then there is enhancement of temporal asymmetry in the ventral cochlear nucleus by both onset and chopper units. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Ctr Neural Basis Hearing, Physiol Lab, Cambridge CB2 3EG, England. RP Pressnitzer, D (reprint author), Ircam, CNRS, UMR 9912, 1 Pl Stravinsky, F-75004 Paris, France. EM pressnit@ircam.fr RI Pressnitzer, Daniel/F-6092-2012 CR BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 CARNEY LH, 1988, J NEUROPHYSIOL, V60, P1653 DEBOER E, 1978, J ACOUST SOC AM, V63, P115, DOI 10.1121/1.381704 Evans E. F., 1989, BRIT J AUDIOL, V23, P151 Fay RR, 1996, AUDIT NEUROSCI, V2, P377 FRISINA RD, 1985, EXP BRAIN RES, V60, P417 Frisina R.D., 1990, HEARING RES, V44, P90 FRISINA RD, 1990, HEARING RES, V44, P123, DOI 10.1016/0378-5955(90)90075-Z Irino T, 1996, J ACOUST SOC AM, V99, P2316, DOI 10.1121/1.415419 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KIM DO, 1986, AUDITORY FREQUENCY S, P281 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 LU T, 1999, P 22 ARO MIDW M, P35 MEDDIS R, 1986, J ACOUST SOC AM, V79, P702, DOI 10.1121/1.393460 MERRILL EG, 1972, MED BIOL ENG, V10, P662, DOI 10.1007/BF02476084 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x NEIKEN I, 1999, NATURE, V397, P154 PALMER AR, 1993, NATO ADV SCI INST SE, V239, P373 PALMER AR, 1992, ADV BIOSCI, V83, P231 Patterson RD, 1998, J ACOUST SOC AM, V104, P2967, DOI 10.1121/1.423879 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1409, DOI 10.1121/1.410285 PATTERSON RD, 1995, J ACOUST SOC AM, V98, P1890, DOI 10.1121/1.414456 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1419, DOI 10.1121/1.410286 Pressnitzer D, 1999, J ACOUST SOC AM, V105, P2773, DOI 10.1121/1.426894 RHODE WS, 1994, J NEUROPHYSIOL, V71, P1797 SALDANHA EL, 1964, J ACOUST SOC AM, V36, P2021, DOI 10.1121/1.1919317 SHANNON RV, 1995, SCIENCE, V270, P303, DOI 10.1126/science.270.5234.303 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 STABLER SE, 1996, J NEUROPHYSIOL, V76, P1677 Wang XQ, 1995, J NEUROPHYSIOL, V74, P2685 WINTER IM, 1995, J NEUROPHYSIOL, V73, P141 WINTER IM, 1990, HEARING RES, V44, P11 WINTER IM, 1998, BRIT J AUDIOL, V32, P91 Winter M, 1997, BRIT J AUDIOL, V31, P106 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 NR 37 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 155 EP 166 DI 10.1016/S0378-5955(00)00175-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400014 PM 11033255 ER PT J AU Lioudyno, MI Verbitsky, M Holt, JC Elgoyhen, AB Guth, PS AF Lioudyno, MI Verbitsky, M Holt, JC Elgoyhen, AB Guth, PS TI Morphine inhibits an alpha 9-acetylcholine nicotinic receptor-mediated response by a mechanism which does not involve opioid receptors SO HEARING RESEARCH LA English DT Article DE nACh receptor; morphine; interaction; vestibular system; efferent; hair cell ID ENKEPHALIN-LIKE IMMUNOREACTIVITY; VESTIBULAR EFFERENT NEURONS; ACETYLCHOLINE-RECEPTOR; GUINEA-PIG; CHOLINERGIC RECEPTOR; HAIR-CELLS; CHROMAFFIN CELLS; MESSENGER-RNA; CAT COCHLEA; IN-VITRO AB Nicotinic acetylcholine (nACh) receptors are known to be targets for modulation by a number of substances, including the opiates. It is known that acetylcholine (ACh) coexists with opioid peptides in cochlear efferent neurons. and such a colocalization has been proposed for the vestibular system. In the present study we test the hypothesis that morphine, an opioid receptor agonist with a broad spectrum of selectivity, modulates alpha 9nACh receptor-mediated responses in frog vestibular hair cells. Morphine dose-dependently and reversibly inhibited ACh-induced currents as recorded by the perforated patch-clamp method. In the presence of morphine the ACh dose response curve was shifted to the right in a parallel fashion, suggesting a competitive interaction. However, naloxone did not antagonize the inhibition produced by morphine. To test the hypothesis that morphine could interact with the alpha 9nACh receptor without the involvement of opioid receptors. experiments were performed using Xenopus laevis oocytes injected with the alpha 9ACh receptor cRNA. The currents activated by ACh in Xenopus oocytes, a system that lacks opioid receptors, were also dose-dependently inhibited by morphine. We conclude that morphine inhibits the alpha 9nACh receptor-mediated response in hair cells and Xenopus oocytes through a mechanism which does not involve opioid receptors but may be a direct block of the a9nACh receptor. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tulane Univ, Sch Med, Dept Pharmacol, New Orleans, LA 70112 USA. RAS, Pavlov Inst Physiol, St Petersburg, Russia. Univ Buenos Aires, CONICET, Inst Invest Ingn Genet & Biol Mol, RA-1428 Buenos Aires, DF, Argentina. RP Lioudyno, MI (reprint author), Tulane Univ, Sch Med, Dept Pharmacol, 1430 Tulane Ave, New Orleans, LA 70112 USA. CR ALTSCHULER RA, 1988, J HISTOCHEM CYTOCHEM, V36, P797 ALTSCHULER RA, 1984, J HISTOCHEM CYTOCHEM, V32, P839 ALTSCHULER RA, 1984, HEARING RES, V16, P17, DOI 10.1016/0378-5955(84)90022-4 ALTSCHULER RA, 1983, NEUROSCIENCE, V9, P621, DOI 10.1016/0306-4522(83)90178-1 Andrianov GN, 1999, NEUROSCIENCE, V93, P801, DOI 10.1016/S0306-4522(99)00159-1 Arias HR, 1998, BBA-REV BIOMEMBRANES, V1376, P173, DOI 10.1016/S0304-4157(98)00004-5 ATHAS GB, 1997, ASS RES OTOLARYNGOL, V20, P37 BOTON R, 1989, J PHYSIOL-LONDON, V408, P511 BOULTER J, 1987, P NATL ACAD SCI USA, V84, P7763, DOI 10.1073/pnas.84.21.7763 CARPENTER MB, 1987, BRAIN RES, V408, P275, DOI 10.1016/0006-8993(87)90387-8 DAVIES J, 1976, NATURE, V262, P603, DOI 10.1038/262603a0 ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 FAN P, 1995, MOL PHARMACOL, V47, P491 FEX J, 1981, P NATL ACAD SCI-BIOL, V78, P1255, DOI 10.1073/pnas.78.2.1255 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 GADDUM JH, 1957, BRIT J PHARM CHEMOTH, V12, P323 GERZANICH V, 1994, MOL PHARMACOL, V45, P212 Giniatullin R, 1999, J NEUROSCI, V19, P2945 Glowatzki E, 2000, SCIENCE, V288, P2366, DOI 10.1126/science.288.5475.2366 GUTH PS, 1976, PHARMACOL REV, V28, P95 Guth PS, 1998, PROG NEUROBIOL, V54, P193, DOI 10.1016/S0301-0082(97)00068-3 Hiel H, 1996, BRAIN RES, V738, P347, DOI 10.1016/S0006-8993(96)01046-3 HOFFMAN DW, 1984, BRAIN RES, V322, P59, DOI 10.1016/0006-8993(84)91180-6 HOFFMAN DW, 1985, HEARING RES, V17, P47, DOI 10.1016/0378-5955(85)90129-7 HOLT JC, 1999, ARO ABSTR, V22, P188 KONDO H, 1985, BRAIN RES, V335, P309, DOI 10.1016/0006-8993(85)90483-4 KUMAKURA K, 1980, NATURE, V283, P489, DOI 10.1038/283489a0 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1980, HEARING RES, V3, P189, DOI 10.1016/0378-5955(80)90046-5 LIOUDYNO MI, 1999, ARO ABSTR, V22, P114 MacMillan SJA, 1998, BRAIN RES, V794, P127, DOI 10.1016/S0006-8993(98)00223-6 Maelicke A, 1997, J RECEPT SIGNAL TR R, V17, P11, DOI 10.3109/10799899709036592 Merchan Perez A., 1994, Developmental Brain Research, V82, P29, DOI 10.1016/0165-3806(94)90145-7 MIGNAT C, 1995, LIFE SCI, V56, P793, DOI 10.1016/0024-3205(95)00010-4 MORALES MA, 1995, P NATL ACAD SCI USA, V92, P11819, DOI 10.1073/pnas.92.25.11819 Morley BJ, 1998, MOL BRAIN RES, V53, P78, DOI 10.1016/S0169-328X(97)00272-6 Oka K, 1998, PFLUG ARCH EUR J PHY, V436, P887, DOI 10.1007/s004240050719 Park HJ, 1997, HEARING RES, V112, P95, DOI 10.1016/S0378-5955(97)00111-1 PERACHIO AA, 1989, EXP BRAIN RES, V78, P315 Rothlin CV, 1999, MOL PHARMACOL, V55, P248 RYAN AF, 1991, EXP BRAIN RES, V87, P259 Scholtz AW, 1998, HEARING RES, V118, P123, DOI 10.1016/S0378-5955(98)00023-9 STALLCUP WB, 1980, P NATL ACAD SCI-BIOL, V77, P634, DOI 10.1073/pnas.77.1.634 SUAREZROCA H, 1992, EUR J PHARMACOL, V229, P1, DOI 10.1016/0014-2999(92)90278-C Vetter DE, 1999, NEURON, V23, P93, DOI 10.1016/S0896-6273(00)80756-4 Xia XM, 1998, NATURE, V395, P503 Yamakura T, 1999, ANESTHESIOLOGY, V91, P1053, DOI 10.1097/00000542-199910000-00026 ZHANG C, 1993, BRAIN RES, V622, P211, DOI 10.1016/0006-8993(93)90821-4 NR 50 TC 16 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 167 EP 177 DI 10.1016/S0378-5955(00)00180-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400015 PM 11033256 ER PT J AU Lurie, DI Durham, D AF Lurie, DI Durham, D TI Neuronal death, not axonal degeneration, results in significant gliosis within the cochlear nucleus of adult chickens SO HEARING RESEARCH LA English DT Article DE deafferentation; nucleus magnocellularis; auditory; gliosis ID STEM AUDITORY NUCLEI; AFFERENT ACTIVITY BLOCKADE; FIBRILLARY ACIDIC PROTEIN; COLONY-STIMULATING FACTOR; BRAIN-STEM; GLIAL-CELLS; RAT-BRAIN; IN-VITRO; ASTROCYTE PROLIFERATION; DEHYDROGENASE ACTIVITY AB Injury to the central nervous system initiates a series of events that leads to neuronal cell death and glial activation. Astrocytes respond to damage and disease by becoming hyperplastic and hypertrophied. This 'reaclive gliosis' is also accompanied by the upregulation of the intermediate filament protein glial fibrillary acidic protein, the release of growth factors and the formation of the glial scar. However, the signaling cascades which regulate these events, and the molecular mechanisms that give rise to this diverse response, have not been fully elucidated. For example, the role played by degenerating neurons vs. degenerating axons in the activation of astrocytes remains to be determined. To investigate the influence of neuronal cell death vs. axonal degeneration on gliosis, the current study examines the astrocyte response to cochlea removal in two different breeds of adult chickens, one of which exhibits neuronal cell death within the brainstem nucleus magnocellularis (NM) following the lesion and one which does not. Our results indicate that degeneration of NM neurons leads to large increases in both glial proliferation and hypertrophy, while eighth nerve degeneration without NM cell death results in very small increases in glial proliferation. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Montana, Dept Pharmaceut Sci, Missoula, MT 59812 USA. Univ Kansas, Med Ctr, Dept Otolaryngol, Kansas City, KS 66103 USA. Univ Kansas, Med Ctr, Smith Mental Retardat Res Ctr, Kansas City, KS 66103 USA. RP Lurie, DI (reprint author), Univ Montana, Dept Pharmaceut Sci, Skaggs Bldg 304, Missoula, MT 59812 USA. CR Aschner Michael, 1998, Toxicology Letters (Shannon), V102-103, P283, DOI 10.1016/S0378-4274(98)00324-5 BORN DE, 1991, BRAIN RES, V557, P37, DOI 10.1016/0006-8993(91)90113-A BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 Calvo CF, 1998, GLIA, V24, P180, DOI 10.1002/(SICI)1098-1136(199810)24:2<180::AID-GLIA3>3.0.CO;2-8 CANADY KS, 1994, J NEUROSCI, V14, P5973 CANADY KS, 1992, J NEUROSCI, V12, P1001 Cavanagh JFR, 1997, CEREB CORTEX, V7, P293, DOI 10.1093/cercor/7.4.293 Chao CC, 1996, GLIA, V16, P276, DOI 10.1002/(SICI)1098-1136(199603)16:3<276::AID-GLIA10>3.0.CO;2-X CHENG HW, 1994, NEUROSCIENCE, V62, P425, DOI 10.1016/0306-4522(94)90377-8 Clatterbuck RE, 1996, J COMP NEUROL, V369, P543, DOI 10.1002/(SICI)1096-9861(19960610)369:4<543::AID-CNE5>3.0.CO;2-4 DURHAM D, 1985, J COMP NEUROL, V231, P446, DOI 10.1002/cne.902310404 DURHAM D, 2000, UNPUB HEAR RES DURHAM D, 1993, HEARING RES, V70, P151, DOI 10.1016/0378-5955(93)90153-R Eclancher F, 1996, BRAIN RES, V737, P201, DOI 10.1016/0006-8993(96)00732-9 Edmonds JL, 1999, HEARING RES, V127, P62, DOI 10.1016/S0378-5955(98)00180-4 FREI K, 1992, J NEUROIMMUNOL, V40, P189, DOI 10.1016/0165-5728(92)90133-6 GALL C, 1979, J COMP NEUROL, V183, P539, DOI 10.1002/cne.901830306 GARDEN G, 1991, Society for Neuroscience Abstracts, V17, P229 GARDEN GA, 1994, J NEUROSCI, V14, P1994 GRAEBER MB, 1988, J NEUROCYTOL, V17, P209, DOI 10.1007/BF01674208 Guenard V, 1996, EXP NEUROL, V137, P175, DOI 10.1006/exnr.1996.0017 Guillemin G, 1996, GLIA, V16, P71, DOI 10.1002/(SICI)1098-1136(199601)16:1<71::AID-GLIA8>3.0.CO;2-E HEIL P, 1986, J COMP NEUROL, V252, P279, DOI 10.1002/cne.902520302 HYDE GE, 1990, J COMP NEUROL, V297, P329, DOI 10.1002/cne.902970302 HYDE GE, 1994, J NEUROSCI, V14, P291 HYDE GE, 1994, J COMP NEUROL, V339, P27, DOI 10.1002/cne.903390105 JAECKEL E, 2000, ASS RES OT ABSTR, V23, P15 Lee MY, 1997, J NEUROSCI, V17, P1137 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 LOGAN A, 1994, EUR J NEUROSCI, V6, P355, DOI 10.1111/j.1460-9568.1994.tb00278.x LURIE DI, 1999, ASS RES OT ABSTR, V22, P65 LURIE DI, 1994, J COMP NEUROL, V346, P276, DOI 10.1002/cne.903460207 Minana R, 1998, GLIA, V24, P415, DOI 10.1002/(SICI)1098-1136(199812)24:4<415::AID-GLIA7>3.0.CO;2-A MURRAY M, 1990, EXP NEUROL, V110, P248, DOI 10.1016/0014-4886(90)90036-R OTIS TS, 1995, J PHYSIOL-LONDON, V482, P309 PALACIOS G, 1995, EUR J NEUROSCI, V7, P501, DOI 10.1111/j.1460-9568.1995.tb00346.x Pasti L, 1997, J NEUROSCI, V17, P7817 PETITO CK, 1990, J CEREBR BLOOD F MET, V10, P850 Planas AM, 1998, GLIA, V23, P120, DOI 10.1002/(SICI)1098-1136(199806)23:2<120::AID-GLIA3>3.0.CO;2-A Rabchevsky AG, 1998, J NEUROSCI, V18, P10541 Reier P J, 1988, Adv Neurol, V47, P87 REIER PJ, 1983, SPINAL CORD REGENERA, P164 Reilly JF, 1998, GLIA, V22, P202, DOI 10.1002/(SICI)1098-1136(199802)22:2<202::AID-GLIA11>3.0.CO;2-1 Ridet JL, 1997, TRENDS NEUROSCI, V20, P570, DOI 10.1016/S0166-2236(97)01139-9 ROSE G, 1976, BRAIN RES BULL, V1, P87, DOI 10.1016/0361-9230(76)90052-6 RUBEL EW, 1992, J COMP NEUROL, V318, P415, DOI 10.1002/cne.903180406 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 SANDS SJ, 1999, ASS RES OT ABSTR, V22, P146 SAWADA M, 1993, NEUROSCI LETT, V160, P131, DOI 10.1016/0304-3940(93)90396-3 SIVARAMAKRISHNAN S, 1995, J NEUROSCI, V15, P6576 STEWARD O, 1993, EXP NEUROL, V124, P167, DOI 10.1006/exnr.1993.1187 STEWARD O, 1985, J COMP NEUROL, V231, P385, DOI 10.1002/cne.902310308 Steward O, 1997, J COMP NEUROL, V380, P70, DOI 10.1002/(SICI)1096-9861(19970331)380:1<70::AID-CNE5>3.0.CO;2-Q STREIT WJ, 1988, J COMP NEUROL, V268, P248, DOI 10.1002/cne.902680209 ZHOU N, 1992, HEARING RES, V60, P20, DOI 10.1016/0378-5955(92)90054-Q ZIRPEL L, 1995, J NEUROPHYSIOL, V74, P1355 NR 56 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 178 EP 188 DI 10.1016/S0378-5955(00)00181-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400016 PM 11033257 ER PT J AU Tsukasaki, N Whitworth, CA Rybak, LP AF Tsukasaki, N Whitworth, CA Rybak, LP TI Acute changes in cochlear potentials due to cisplatin SO HEARING RESEARCH LA English DT Article DE cisplatin; ototoxicity; endocochlear potential; cochlear microphonics; chinchilla ID GUINEA-PIGS; CIS-DIAMMINEDICHLOROPLATINUM; STRIA VASCULARIS; INDUCED OTOTOXICITY; HEARING-LOSS; PLATINUM; ACID; NSC-119875; MECHANISM; MODEL AB The purpose of this study was to investigate how the hair cells and stria vascularis are affected at the onset of cisplatin ototoxicity. The effects on the endocochlear potential (EP) and the cochlear microphonics (CM) were observed simultaneously in two groups of adult chinchillas receiving as follows: (1) 5 mu l of cisplatin (1 mg/ml) in normal saline, and (2) 5 mu l of normal saline on round window. The EP and the CM were recorded for 12-14 h after cisplatin application, and morphological changes were assessed using scanning electron microscopy. Both the EP and the CM amplitude demonstrated a profound reduction, and a very strong correlation was observed between these two values during this time period. Although the reduction of the EP and the CM was observed by 12-14 h, only very slight degeneration of outer hair cells was seen at that time. These data suggested that a reduction of the EP which was caused by the alteration of the stria vascularis might be primarily responsible for very early changes in cochlear function after topical cisplatin application, while later changes were the direct result of hair cell damage. (C) 2000 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Surg, Springfield, IL 62794 USA. Nagasaki Univ, Sch Med, Dept Otolaryngol, Nagasaki 8528501, Japan. RP Rybak, LP (reprint author), So Illinois Univ, Sch Med, Dept Surg, POB 19638, Springfield, IL 62794 USA. CR Alam SA, 2000, HEARING RES, V141, P28, DOI 10.1016/S0378-5955(99)00211-7 BARRON SE, 1987, HEARING RES, V26, P131, DOI 10.1016/0378-5955(87)90104-3 ESTREM SA, 1981, OTOLARYNG HEAD NECK, V89, P638 Fausti SA, 1999, EAR HEARING, V20, P497, DOI 10.1097/00003446-199912000-00005 Ford MS, 1997, HEARING RES, V111, P143, DOI 10.1016/S0378-5955(97)00103-2 HAYES DM, 1977, CANCER, V39, P1372, DOI 10.1002/1097-0142(197704)39:4<1372::AID-CNCR2820390404>3.0.CO;2-J Heijmen PS, 1999, HEARING RES, V128, P27, DOI 10.1016/S0378-5955(98)00194-4 Janning MH, 1998, OTOLARYNG HEAD NECK, V119, P574, DOI 10.1016/S0194-5998(98)70014-2 Kamimura T, 1999, HEARING RES, V131, P117, DOI 10.1016/S0378-5955(99)00017-9 KIMITSUKI T, 1993, HEARING RES, V71, P64, DOI 10.1016/0378-5955(93)90021-R KOHN S, 1988, LARYNGOSCOPE, V98, P865 KOMUNE S, 1981, OTOLARYNG HEAD NECK, V89, P275 KOMUNE S, 1985, ARCH OTO-RHINO-LARYN, V241, P149, DOI 10.1007/BF00454348 KOMUNE S, 1995, ANN OTO RHINOL LARYN, V104, P149 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E Meech RP, 1998, HEARING RES, V124, P44, DOI 10.1016/S0378-5955(98)00116-6 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 PATUZZI RB, 1987, HEARING RES, V30, P73, DOI 10.1016/0378-5955(87)90185-7 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 PIEL IJ, 1974, CANCER CHEMOTH REP 1, V58, P871 Rybak LP, 1999, TOXICOL SCI, V47, P195, DOI 10.1093/toxsci/47.2.195 RYBAK LP, 1981, J LARYNGOL OTOL, V95, P745, DOI 10.1017/S0022215100091374 SAITO T, 1994, ORL J OTO-RHINO-LARY, V56, P315 SCHWEITZER VG, 1993, LARYNGOSCOPE, V103, P1, DOI 10.1288/00005537-199304000-00001 STADNICKI SW, 1975, CANCER CHEMOTH REP 1, V59, P467 Stengs CHM, 1998, HEARING RES, V124, P99, DOI 10.1016/S0378-5955(98)00129-4 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 TAUDY M, 1992, AUDIOLOGY, V31, P293 NR 32 TC 26 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 189 EP 198 DI 10.1016/S0378-5955(00)00182-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400017 PM 11033258 ER PT J AU Shackleton, TM McAlpine, D Palmer, AR AF Shackleton, TM McAlpine, D Palmer, AR TI Modelling convergent input onto interaural-delay-sensitive inferior colliculus neurones SO HEARING RESEARCH LA English DT Article DE interaural time difference; inferior colliculus; binaural; coincidence detection; Jeffress model ID LOW-FREQUENCY NEURONS; SUPERIOR OLIVARY COMPLEX; AUDITORY-NERVE FIBERS; CENTRAL NUCLEUS; BINAURAL INTERACTION; BRAIN-STEM; RESPONSE PROPERTIES; CHANGING FREQUENCY; LATERAL LEMNISCUS; COCHLEAR NUCLEUS AB Convergent input from cells in the medial superior olive (MSO) and lateral superior olive (LSO) onto a single inferior colliculus (IC) cell explains many findings that are not compatible with a simple coincidence detector mechanism. Here this explanation is tested using a physiologically accurate computer model of the binaural pathway in which the input to the IC cell is either from two MSO cells or a MSO and a LSO cell. Auditory nerve (AN) spike trains are formed by a stochastic hair cell model following a basilar membrane simulation using a gammatone filter. In subsequent cells input spikes cause post-synaptic potentials (PSPs) which are summed causing the cell to fire when the stun crosses a threshold. The individual cells are matched to the physiology by varying the number of inputs, the magnitude and duration of the PSPs and the firing threshold. Non-linear best-phase-versus-frequency functions arise if the two IC inputs have different best frequencies and different characteristic delays. One input can be selectively suppressed by turning on an additional tone at the worst phase of that input. Non-zero characteristic phases arise if the characteristic frequencies of the AN fibres feeding into a single superior olive cell are mismatched. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Nottingham, MRC, Inst Hearing Res, Nottingham NG7 2RD, England. UCL, Dept Physiol, London WC1E 6BT, England. RP Shackleton, TM (reprint author), Univ Nottingham, MRC, Inst Hearing Res, Univ Pk, Nottingham NG7 2RD, England. EM trevor@ihr.mrc.ac.uk CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 AITKIN L, 1985, HEARING RES, V17, P87, DOI 10.1016/0378-5955(85)90134-0 Batra R, 1997, J NEUROPHYSIOL, V78, P1237 Batra R, 1997, J NEUROPHYSIOL, V78, P1222 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 Bonham BH, 1999, J ACOUST SOC AM, V106, P281, DOI 10.1121/1.427056 BRUGGE JF, 1970, J NEUROPHYSIOL, V33, P441 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CARNEY LH, 1993, J ACOUST SOC AM, V93, P401, DOI 10.1121/1.405620 Colburn HS, 1996, AUDITORY COMPUTATION, P332 ELVERLAND HH, 1978, EXP BRAIN RES, V32, P117 Evans E. F., 1975, HDB SENSORY PHYSL, V5, P1 EVANS EF, 1995, J PHYSIOL-LONDON, V485P, pP2 EVANS EF, 1980, J PHYSIOL-LONDON, V298, P6 EVANS EF, 1992, ADV BIOSCI, V83, P159 Evans EF, 1997, BRIT J AUDIOL, V31, P119 FINLAYSON PG, 1991, J NEUROPHYSIOL, V65, P598 Fitzpatrick DC, 2000, J NEUROSCI, V20, P1605 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 KUWADA S, 1983, J NEUROPHYSIOL, V50, P981 KUWADA S, 1987, J NEUROPHYSIOL, V57, P1338 LIBERMAN MC, 1991, J COMP NEUROL, V313, P240, DOI 10.1002/cne.903130205 Mardia K. V., 1972, STAT DIRECTIONAL DAT MCALPINE D, 2000, ASS RES OT ABSTR, V23, P256 McAlpine D, 1996, HEARING RES, V97, P136 McAlpine D, 1998, J NEUROSCI, V18, P6026 MEDDIS R, 1990, J ACOUST SOC AM, V87, P1813, DOI 10.1121/1.399379 MOORE DR, 1988, J COMP NEUROL, V269, P342, DOI 10.1002/cne.902690303 MOUSHEGIAN G, 1971, PHYSL AUDITORY SYSTE, P245 NORDEEN KW, 1983, J COMP NEUROL, V214, P131, DOI 10.1002/cne.902140203 Palmer AR, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P353, DOI 10.1007/978-1-4419-8712-9_32 PALMER AR, 1990, HEARING RES, V50, P71, DOI 10.1016/0378-5955(90)90034-M PALMER AR, 2001, IN PRESS PSYCHOL PSY Ripley B. D., 1987, STOCHASTIC SIMULATIO ROSE JE, 1966, J NEUROPHYSIOL, V29, P288 ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 ROTHMAN JS, 1993, J NEUROPHYSIOL, V70, P2562 SCHWEIZER H, 1981, J COMP NEUROL, V201, P25, DOI 10.1002/cne.902010104 SHNEIDERMAN A, 1989, J COMP NEUROL, V286, P28, DOI 10.1002/cne.902860103 SHNEIDERMAN A, 1988, J COMP NEUROL, V276, P188, DOI 10.1002/cne.902760204 Spitzer MW, 1998, J NEUROPHYSIOL, V80, P3062 SPITZER MW, 1995, J NEUROPHYSIOL, V73, P1668 WEISS TF, 1966, KYBERNETIK, V3, P153, DOI 10.1007/BF00290252 YIN TCT, 1983, J NEUROPHYSIOL, V50, P1020 YIN TCT, 1983, J NEUROPHYSIOL, V50, P1000 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 YIN TCT, 1986, J NEUROPHYSIOL, V55, P280 YIN TCT, 1987, J NEUROPHYSIOL, V58, P562 NR 51 TC 24 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 199 EP 215 DI 10.1016/S0378-5955(00)00187-8 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400018 PM 11033259 ER PT J AU Chen, K Godfrey, DA AF Chen, K Godfrey, DA TI Sodium pentobarbital abolishes bursting spontaneous activity of dorsal cochlear nucleus in rat brain slices SO HEARING RESEARCH LA English DT Article DE single unit recording; anesthetic effect; gamma-aminobutyric acid type A receptor; gamma-aminobutyric acid type B receptor; regular firing; irregular firing; auditory ID COMPLEX-SPIKING NEURONS; GUINEA-PIG; DISCHARGE CHARACTERISTICS; RESPONSES; CARTWHEEL; CELLS; CAT; ANESTHETICS; CHANNELS; GABA(A) AB There is evidence that pentobarbital, a commonly used anesthetic, can affect neuronal activity, but its effects on particular neurons of the dorsal cochlear nucleus (DCN) are not well known. Bursting (complex spiking) spontaneous activity has been observed in the DCN in brain slice preparations and in recordings from unanesthetized decerebrate animals, but seldom in experiments with anesthetized animals. This study investigated the effects of pentobarbital on spontaneous activity in the DCN in brain slices. Most extracellularly recorded bursting neurons decreased firing rates and reversibly changed their firing to simple spiking with irregular intervals during pentobarbital. Some reversibly stopped firing after the change to an irregular pattern. Most neurons with regular spontaneous activity (simple spiking) showed decreased firing rates and more irregular intervals during pentobarbital. The results also suggest some involvement of gamma-aminobutyric acid type A receptors in the pentobarbital effects. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Med Coll Ohio, Dept Otolaryngol, Toledo, OH 43614 USA. RP Chen, K (reprint author), Med Coll Ohio, Dept Otolaryngol, 3065 Arlington Ave, Toledo, OH 43614 USA. CR Antkowiak B, 1999, ANESTHESIOLOGY, V91, P500, DOI 10.1097/00000542-199908000-00025 BERREBI AS, 1991, ANAT EMBRYOL, V183, P427 BOLANDER HG, 1984, ACTA PHARMACOL TOX, V54, P33 Chen K, 1999, BRAIN RES, V847, P85, DOI 10.1016/S0006-8993(99)02031-4 CHEN K, 1999, ABSTR SOC NEUROSCI, V25, P394 Chen K, 1999, NEUROSCIENCE, V90, P1043, DOI 10.1016/S0306-4522(98)00503-X CHEN KJ, 1994, HEARING RES, V77, P168 EVANS EF, 1973, EXP BRAIN RES, V17, P402 GODFREY DA, 1992, J NEUROSCI METH, V41, P167, DOI 10.1016/0165-0270(92)90058-L GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 Golding NL, 1996, J NEUROSCI, V16, P2208 HAAS HL, 1979, J NEUROSCI METH, V1, P323, DOI 10.1016/0165-0270(79)90021-9 HATANAKA T, 1988, J PHARMACOBIO-DYNAM, V11, P18 JUIZ JM, 1994, BRAIN RES, V639, P193, DOI 10.1016/0006-8993(94)91730-2 LILJEQUIST S, 1986, LIFE SCI, V39, P851, DOI 10.1016/0024-3205(86)90465-0 MANIS PB, 1990, J NEUROSCI, V10, P2338 MANIS PB, 1994, J COMP NEUROL, V348, P261, DOI 10.1002/cne.903480208 MATHERS DA, 1980, SCIENCE, V209, P507, DOI 10.1126/science.6248961 MUGNAINI E, 1987, ARCH ITAL BIOL, V126, P41 PARHAM K, 1995, J NEUROPHYSIOL, V73, P550 PFEIFFER RR, 1965, BIOPHYS J, V5, P301 Rehberg B, 1999, NEUROSCI LETT, V264, P81, DOI 10.1016/S0304-3940(99)00176-7 STUDY RE, 1981, P NATL ACAD SCI-BIOL, V78, P7180, DOI 10.1073/pnas.78.11.7180 WALLER HJ, 1994, J NEUROPHYSIOL, V71, P467 Waller HJ, 1996, HEARING RES, V98, P169, DOI 10.1016/0378-5955(96)00090-1 West MO, 1998, J NEUROSCI, V18, P9055 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1384 NR 28 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 216 EP 222 DI 10.1016/S0378-5955(00)00188-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400019 PM 11033260 ER PT J AU McCreery, DB Yuen, TGH Bullara, LA AF McCreery, DB Yuen, TGH Bullara, LA TI Chronic microstimulation in the feline ventral cochlear nucleus: physiologic and histologic effects SO HEARING RESEARCH LA English DT Article DE cat; ventral cochlear nucleus; auditory brainstem implant; microelectrode; chronic stimulation ID HIGH STIMULUS RATES; AUDITORY BRAIN-STEM; ELECTRICAL-STIMULATION; SPEECH RECOGNITION; IMPLANTED MICROELECTRODES; EXCITABILITY; CAT; REDUCTION; ELECTRODES AB This study was conducted to help to establish the feasibility of a multi-channel auditory prosthesis based on microstimulation within the human ventral cochlear nucleus, and to define the range of stimulus parameters that can be used safely with such a device. We chronically implanted activated iridium microelectrodes into the feline ventral cochlear nucleus and, beginning 80-250 days after implantation, they were pulsed for 7 h/day, on up to 21 successive days. The stimulus was charge-balanced pulses whose amplitude was modulated by a simulated human voice. The pulse rate (250 Hz/electrode) and the maximum pulse amplitude were selected as those that are likely to provide a patient with useful auditory percepts. The changes in neuronal responses during the multi-day stimulation regimens were partitioned into long-lasting, stimulation-induced depression of neuronal excitability (SIDNE), and short-acting neuronal refractivity (SANR). Both SIDNE and SANR were quantified from the changes in the growth functions of the evoked potentials recorded in the inferior colliculus. All of the stimulation regimens that we tested induced measurable SIDNE and SANR. The combined effect of SIDNE and the superimposed SANR is to depress the neuronal response near threshold, and thereby, to depress the population response over the entire amplitude range of the stimulus pulses. SIDNE and SANR may cause the greatest degradation of the performance of a clinical device at the low end of the amplitude range, and this may represent an inherent limitation of this type of spatially localized, high-rate neuronal stimulation. We determined sets of stimulus parameters which preserved most of the dynamic range of the neuronal response, when using either long (150 mu s/phase) or short (40 mu s/phase) stimulus pulses. increasing the amplitude of the stimulus was relatively ineffective as a means of increasing the dynamic range of neuronal response, since the greater stimulus amplitude induced more SIDNE. All of the pulsed and unpulsed electrode sites were examined histologically, and no neuronal changes attributable to the stimulation were detected. There was some aggregation of glial cells immediately adjacent to some of the electrodes that were pulsed with the short-duration pulses, and at the highest current densities. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Huntington Med Res Inst, Neurol Res Lab, Pasadena, CA 91105 USA. RP McCreery, DB (reprint author), Huntington Med Res Inst, Neurol Res Lab, 734 Fairmount Ave, Pasadena, CA 91105 USA. CR BRACKMANN DE, 1993, OTOLARYNG HEAD NECK, V108, P624 Brill SM, 1997, AM J OTOL, V18, pS104 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CANT NB, 1982, NEUROSCI LETT, V32, P141 *CCITT, 1998, P50 CCITT WORK PART Eisenberg L S, 1987, J Rehabil Res Dev, V24, P9, DOI 10.1682/JRRD.1987.07.0009 Fishman KE, 1997, J SPEECH LANG HEAR R, V40, P1201 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 HUANG CQ, 1999, HEARING RES, V1322, P60 Huang CQ, 1998, HEARING RES, V116, P55, DOI 10.1016/S0378-5955(97)00196-2 McCreery D B, 1998, IEEE Trans Rehabil Eng, V6, P391, DOI 10.1109/86.736153 MCCREERY DB, 1994, HEARING RES, V77, P105, DOI 10.1016/0378-5955(94)90258-5 MCCREERY DB, 1986, EXP NEUROL, V92, P147, DOI 10.1016/0014-4886(86)90131-7 McCreery DB, 1997, IEEE T BIO-MED ENG, V44, P931, DOI 10.1109/10.634645 MCCREERY DB, 1992, HEARING RES, V62, P42, DOI 10.1016/0378-5955(92)90201-W MOORE JK, 1987, HEARING RES, V29, P1, DOI 10.1016/0378-5955(87)90202-4 MOORE JK, 1979, AM J ANAT, V154, P393, DOI 10.1002/aja.1001540306 Otto SR, 1998, OTOLARYNG HEAD NECK, V118, P291, DOI 10.1016/S0194-5998(98)70304-3 PARKIN JL, 1985, HEAD NECK SURG, V93, P639 ROBBLEE LS, 1983, J ELECTROCHEM SOC, V130, P731, DOI 10.1149/1.2119793 SHANNON RV, 1990, HEARING RES, V47, P159, DOI 10.1016/0378-5955(90)90173-M Shannon RV, 1993, OTOLARYNGOL HEAD NEC, V108, P635 SHANNON RV, 1995, SCIENCE, V270, P303, DOI 10.1126/science.270.5234.303 SHANNON RV, 1989, HEARING RES, V40, P173, DOI 10.1016/0378-5955(89)90110-X TYKOCINSKI M, 1995, HEARING RES, V88, P124, DOI 10.1016/0378-5955(95)00108-G Tykocinski M, 1997, HEARING RES, V112, P147, DOI 10.1016/S0378-5955(97)00117-2 WARR WB, 1972, BRAIN RES, V40, P247 WILSON BS, 1995, AM J OTOL, V16, P669 NR 28 TC 42 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 223 EP 238 DI 10.1016/S0378-5955(00)00190-8 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400020 PM 11033261 ER PT J AU Ohlemiller, KK Wright, JS Heidbreder, AF AF Ohlemiller, KK Wright, JS Heidbreder, AF TI Vulnerability to noise-induced hearing loss in 'middle-aged' and young adult mice: a dose-response approach in CBA, C57BL, and BALB inbred strains SO HEARING RESEARCH LA English DT Article DE cochlea; mouse; auditory brainstem response; aging; presbycusis; hair cell; Ah1; Ahl2 ID HAIR CELL LOSS; ACOUSTIC TRAUMA; F1-HYBRID STRAINS; GUINEA-PIG; MOUSE; SUSCEPTIBILITY; EXPOSURE; COCHLEAR; OVERSTIMULATION; OTOTOXICITY AB Vulnerability of the cochlea to noise induced permanent threshold shifts (NIPTS) was examined in young adult (1-2 months) and 'middle-aged' (5-7 months) CBA/CaJ, C57BL/6J, and BALB/cJ inbred mice. For each age and strain, a dose-response paradigm was applied, whereby groups of up to 12 animals were exposed to intense broadband noise (110 dB SPL) for varying durations. Exposure durations reliably associated with < 10% and > 90% probability of a criterion amount of NIPTS (determined 2 weeks postexposure) were identified, and the minimum NIPTS exposure and the slope of the dose-response relation were then derived by numerical modeling. For all three strains, young adult mice were more susceptible to NIPTS than older adults; That is, a shorter exposure was able to cause NIPTS in the younger mice. Strain comparisons revealed that C57 mice were more susceptible than CBAs in the older age group only. At both ages examined, however, BALE mice were most susceptible to NIPTS. When animals with a similar amount of NIPTS were compared, outer hair cell loss in the cochlear base was more widespread in the younger animals. BALE mice appear particularly susceptible to noise-induced outer hair cell loss throughout life. Our data suggest that the mechanism or site of noise injury differs between young adults and older adults, and may depend on genetic background. The finding that both BALE and C57 mice, which show pronounced age-related hearing loss, are also especially vulnerable to noise supports the notion that genes associated with age-related hearing loss often act by rendering the cochlea susceptible to insults. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Cent Inst Deaf, Fay & Carl Simons Ctr Biol Hearing & Deafness, St Louis, MO 63110 USA. RP Ohlemiller, KK (reprint author), Cent Inst Deaf, Fay & Carl Simons Ctr Biol Hearing & Deafness, 818 S Euclid Av, St Louis, MO 63110 USA. CR ANNIKO M, 1983, ACTA OTO-LARYNGOL, V95, P263, DOI 10.3109/00016488309130943 Barrenas ML, 1997, AUDIOLOGY, V36, P187 BOCK GR, 1978, AUDIOLOGY, V17, P193 Bohne B.A., 1982, NEW PERSPECTIVES NOI, P283 BURDA H, 1988, J MORPHOL, V198, P269, DOI 10.1002/jmor.1051980303 Clark JA, 1996, HEARING RES, V99, P119, DOI 10.1016/S0378-5955(96)00092-5 Davis RR, 1999, HEARING RES, V134, P9, DOI 10.1016/S0378-5955(99)00060-X ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Erway LC, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P56 Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X FALK SA, 1974, LARYNGOSCOPE, V84, P444, DOI 10.1288/00005537-197403000-00008 FINNEY DJ, 1985, ARCH TOXICOL, V56, P215, DOI 10.1007/BF00295156 FOWLER T, 1995, HEARING RES, V88, P1, DOI 10.1016/0378-5955(95)00062-9 FREDELIUS L, 1987, HEARING RES, V30, P157, DOI 10.1016/0378-5955(87)90133-X Freeman S, 1999, AUDIOL NEURO-OTOL, V4, P207, DOI 10.1159/000013844 Gates GA, 1999, ARCH OTOLARYNGOL, V125, P654 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1983, AUDIOLOGY, V22, P372 HENRY KR, 1981, ARCH OTOLARYNGOL, V107, P92 HENRY KR, 1982, BEHAV GENET, V12, P563, DOI 10.1007/BF01070410 Jimenez AM, 1999, HEARING RES, V138, P91, DOI 10.1016/S0378-5955(99)00154-9 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X JOHNSON KR, 2000, UNPUB MAJOR GENE CHR KALTENBACH JA, 1992, HEARING RES, V60, P205, DOI 10.1016/0378-5955(92)90022-F KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 LENOIR M, 1980, ACTA OTO-LARYNGOL, V89, P317, DOI 10.3109/00016488009127143 Li H S, 1992, Scand Audiol Suppl, V36, P1 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 McFadden SL, 1999, J COMP NEUROL, V413, P101 Mills JH, 1997, J ACOUST SOC AM, V101, P1681, DOI 10.1121/1.418152 *NAT CTR HLTH STAT, 1994, PREV CHAR PERS HEAR NEWLANDER JK, 1995, ARO, V18, P89 OHLEMILLER KK, 2000, ARO ABSTR, V23, P219 Ohlemiller KK, 1997, AUDIOL NEURO-OTOL, V2, P175 Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P237, DOI 10.1159/000013847 Ou HC, 2000, HEARING RES, V145, P111, DOI 10.1016/S0378-5955(00)00081-2 Ou HC, 2000, HEARING RES, V145, P123, DOI 10.1016/S0378-5955(00)00082-4 Pierson LL, 1996, SEMIN PERINATOL, V20, P21, DOI 10.1016/S0146-0005(96)80054-1 PRICE GR, 1976, J ACOUST SOC AM, V60, P886, DOI 10.1121/1.381169 PRIEVE BA, 1984, ACTA OTO-LARYNGOL, V98, P428, DOI 10.3109/00016488409107584 Pujol R, 1992, NOISE INDUCED HEARIN, P196 Saunders JC, 1985, TOXICOLOGY EYE EAR O, P145 SAUNDERS JC, 1976, J COMP PHYSIOL PSYCH, V90, P212, DOI 10.1037/h0077198 Schuknecht HF, 1993, PATHOLOGY EAR SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 Sie KCY, 1999, HEARING RES, V134, P39, DOI 10.1016/S0378-5955(99)00066-0 SPOENDLI.H, 1973, ACTA OTO-LARYNGOL, V75, P220, DOI 10.3109/00016487309139699 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 Spongr VP, 1997, J ACOUST SOC AM, V101, P3546, DOI 10.1121/1.418315 Whitlon DS, 1999, HEARING RES, V137, P43, DOI 10.1016/S0378-5955(99)00136-7 Willott J. F., 1991, AGING AUDITORY SYSTE Willott JF, 1998, HEARING RES, V115, P162, DOI 10.1016/S0378-5955(97)00189-5 YANZ JL, 1985, AUDIOLOGY, V24, P260 Yoshida N, 2000, HEARING RES, V141, P97, DOI 10.1016/S0378-5955(99)00210-5 Yoshida N, 1999, J NEUROSCI, V19, P10116 NR 55 TC 52 Z9 54 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 239 EP 247 DI 10.1016/S0378-5955(00)00191-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400021 PM 11033262 ER PT J AU Kawase, T Ogura, M Kakehata, S Takasaka, T AF Kawase, T Ogura, M Kakehata, S Takasaka, T TI Measurement of stapedius contraction during vocalization effort in patients after laryngectomy or tracheostomy SO HEARING RESEARCH LA English DT Article DE acoustic reflex; vocalization; human ID MUSCLE AB The contraction of the stapedius muscle during the effort of vocalization was examined by measurement of acoustic compliance in subjects who had undergone laryngectomy or tracheostomy. No significant level of persistent compliance change was recorded in any of the subjects, indicating the absence of effective contraction of the stapedius during the vocalization effort. In two subjects who use an electrolarynx, although no significant compliance change resulted from the simple vocalization effort without the electrolarynx (no actual vocalized sound), a remarkable level of persistent compliance change was observed during the vocalization using the electrolarynx. These results seem to indicate that a simple vocalization effort without actual voice cannot elicit effective contraction of the middle ear muscles, and that sound generation during vocalization is essential for effective contraction of the middle ear muscles during vocalization, at least in some human subjects. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tohoku Univ, Grad Sch Med, Dept Otolaryngol Head & Neck Surg, Aoba Ku, Sendai, Miyagi 9808574, Japan. RP Kawase, T (reprint author), Tohoku Univ, Grad Sch Med, Dept Otolaryngol Head & Neck Surg, Aoba Ku, Seiryo Machi 1-1, Sendai, Miyagi 9808574, Japan. CR ALBERTI PWR, 1970, LARYNGOSCOPE, V80, P735, DOI 10.1288/00005537-197005000-00005 AVAN P, 1992, HEARING RES, V59, P59, DOI 10.1016/0378-5955(92)90102-S Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 Borg E., 1984, ACOUSTIC REFLEX BASI, P63 BORG E, 1975, ACTA OTO-LARYNGOL, V79, P325, DOI 10.3109/00016487509124694 BORG E, 1989, SCI AM, V261, P62 BORG E, 1974, ACTA OTO-LARYNGOL, V78, P155, DOI 10.3109/00016487409126341 CARMEL PW, 1963, J NEUROPHYSIOL, V26, P598 COUNTER SA, 1979, ACTA OTO-LARYNGOL, V88, P13, DOI 10.3109/00016487909137134 EGAN JP, 1950, J ACOUST SOC AM, V22, P622, DOI 10.1121/1.1906661 KLOCKHOFF I, 1961, Acta Otolaryngol Suppl, V164, P1 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MOORE BCJ, 1961, INTRO PSYCHOL HEARIN Pang X-D, 1986, PERIPHERAL AUDITORY, P36 Pang XD, 1997, J ACOUST SOC AM, V102, P3576, DOI 10.1121/1.420399 SIMMONS FB, 1964, INT AUDIOL, V3, P1 NR 16 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 2000 VL 149 IS 1-2 BP 248 EP 252 DI 10.1016/S0378-5955(00)00192-1 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 365DP UT WOS:000089933400022 PM 11033263 ER PT J AU Balsamo, G Avallone, B Del Genio, F Trapani, S Marmo, FR AF Balsamo, G Avallone, B Del Genio, F Trapani, S Marmo, FR TI Calcification processes in the chick otoconia and calcium binding proteins: patterns of tetracycline incorporation and calbindin-D28K distribution SO HEARING RESEARCH LA English DT Article DE otoconia; inner ear; tetracycline; calbindin; chick embryo; chick ID GUINEA-PIG; INNER-EAR; RADIOACTIVE CALCIUM; OTOLITHIC MEMBRANES; RAT; LOCALIZATION; CELLS; CABP; APPEARANCE; TURNOVER AB In order to clarify the otoconia formation and turnover, tetracycline, an antibiotic that precipitates at calcifying fronts and serves as a fluorescent marker, was injected into eggs at different stages of chick embryonic development, as well as into postnatal chicken and into adult animals. The changes in the intensity, location patterns and time course of fluorescent labelling in each examined stage in the otolithic organs was studied. The presence and distribution of calbindin (CB)-D28K, one of the calcium-binding proteins constantly found in the mammalian and chicken cochlea and also in otolithic membrane of some adult mammals, was studied. Results in embryonal stages, postnatal and adult animals allow us to postulate that otoliths are mainly produced during the embryonal phase, but they may also be produced throughout the whole life span. Results also indicate that otoconia are dynamic structures which undergo turnover. The correspondence between the patterns of CB-D28K immunoreactivity and tetracycline fluorescence may indicate that CB-D28K participates in the formation of otoconia. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Naples Federico II, Dept Genet Gen & Mol Biol, I-80134 Naples, Italy. RP Marmo, FR (reprint author), Univ Naples Federico II, Dept Genet Gen & Mol Biol, Via Mezzocannone 8, I-80134 Naples, Italy. CR Anniko M, 1980, Am J Otolaryngol, V1, P400, DOI 10.1016/S0196-0709(80)80021-4 BALLARINO J, 1982, ANAT REC, V204, P83, DOI 10.1002/ar.1092040111 BALSAMO G, 1969, J EMBRYOL EXP MORPH, V22, P327 BALSAMO G, 1969, EXPERIENTIA, V25, P292, DOI 10.1007/BF02034402 BELANGER LF, 1960, CALCIFICATION BIOL S, P151 CELIO MR, 1990, NEUROSCIENCE, V35, P375, DOI 10.1016/0306-4522(90)90091-H COHEN GM, 1993, PHYSIOLOGIST, V36, P79 CONTI G, 1964, EXPERIENTIA, V20, P110, DOI 10.1007/BF02151272 DECHESNE CJ, 1988, DEV BRAIN RES, V41, P221, DOI 10.1016/0165-3806(88)90184-8 DECHESNE CJ, 1988, DEV BRAIN RES, V40, P233, DOI 10.1016/0165-3806(88)90135-6 DECHESNE CJ, 1988, HEARING RES, V33, P273, DOI 10.1016/0378-5955(88)90157-8 DEVINCEN.M, 1968, EXPERIENTIA, V24, P818 DEVINCEN.M, 1966, J EMBRYOL EXP MORPH, V15, P349 FERMIN CD, 1985, ACTA ANAT, V123, P148 Fermin CD, 1998, HISTOL HISTOPATHOL, V13, P1103 FERMIN CD, 1985, PHYSIOLOGIST, V2, P87 FERMIN CD, 1987, HEARING RES, V28, P23, DOI 10.1016/0378-5955(87)90150-X FERMIN CD, 1986, SEM, V4, P1649 FROST HM, 1968, J PHYSL ANTHR, V29, P183 HARADA Y, 1977, ACTA OTO-LARYNGOL, V84, P65, DOI 10.3109/00016487709123943 HARADA Y, 1981, BIOMED RES-TOKYO, V2, P415 Harada Y, 1998, ACTA OTO-LARYNGOL, V118, P74 HARADA Y, 1978, EQUILIBRIUM RES, V37, P217 Ibsen K H, 1964, Clin Orthop Relat Res, V32, P143 Karita K, 1999, Acta Otolaryngol Suppl, V540, P16 KAWAMATA S, 1995, ANAT REC, V242, P259, DOI 10.1002/ar.1092420216 KAWAMATA S, 1991, ARCH HISTOL CYTOL, V54, P173, DOI 10.1679/aohc.54.173 Kido T, 1997, HEARING RES, V105, P191, DOI 10.1016/S0378-5955(96)00210-9 KLEIN L, 1976, CALC TISS RES, V20, P275, DOI 10.1007/BF02546415 LEGRAND C, 1988, DEV BRAIN RES, V38, P121, DOI 10.1016/0165-3806(88)90090-9 LILLIE FR, 1952, DEV CHICK Lim D J, 1973, Ann Otol Rhinol Laryngol, V82, P23 LYCHAKOV DV, 1995, J EVOL BIOCHEM PHYS+, V31, P90 MARMO F, 1983, Acta Embryologiae et Morphologiae Experimentalis New Series, V4, P202 MARMO F, 1992, ACTA ZOOL-STOCKHOLM, V73, P203 Marmo F., 1965, Bollettino di Zoologia, V32, P231 MECHIGIAN I, 1979, ACTA OTO-LARYNGOL, V88, P56, DOI 10.3109/00016487909137140 MILCH RA, 1958, J BONE JOINT SURG AM, V40, P897 PRESTON RE, 1975, ACTA OTO-LARYNGOL, V80, P269, DOI 10.3109/00016487509121327 RABIE A, 1983, CELL TISSUE RES, V232, P691 Ross M D, 1979, Adv Otorhinolaryngol, V25, P26 ROSS MD, 1976, ANN OTO RHINOL LARYN, V85, P310 ROSS MD, 1975, ANN OTO RHINOL LARYN, V84, P22 SALAMAT MS, 1980, ANN OTO RHINOL LARYN, V89, P229 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 Takumida M, 1997, ORL J OTO-RHINO-LARY, V59, P4 USAMI S, 1995, ORL J OTO-RHINO-LARY, V57, P94 VEENHOFF VB, 1969, AKAD WETENSCHAPPEN A, V2 Zhang DM, 1996, ACTA OTO-LARYNGOL, V116, P812, DOI 10.3109/00016489609137931 Zhang DM, 1996, ACTA OTO-LARYNGOL, V116, P732, DOI 10.3109/00016489609137915 NR 50 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 1 EP 8 DI 10.1016/S0378-5955(00)00094-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500001 PM 10978820 ER PT J AU Emmerich, E Richter, F Reinhold, U Linss, V Linss, W AF Emmerich, E Richter, F Reinhold, U Linss, V Linss, W TI Effects of industrial noise exposure on distortion product otoacoustic emissions (DPOAEs) and hair cell loss of the cochlea - long term experiments in awake guinea pigs SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; outer hair cell; continuous noise exposure; cochlear microphonics; scanning electron microscopy; hearing loss; guinea pig ID PURE-TONE EXPOSURES; BLOOD-FLOW; ACOUSTIC DISTORTION; CHINCHILLA COCHLEA; IMPULSE NOISE; HEARING-LOSS; RESPONSES; RABBIT; INNER; THRESHOLD AB Distortion product otoacoustic emissions (DPOAEs), a sensitive detector of outer hair cell (OHC) function, cochlear microphonics (CM), and hair cell loss have been monitored in 12 awake guinea pigs before and after 2 h exposure to specific, played-back industrial noise (105 dB SPL maximal intensity). All animals had stable DPOAE levels before noise exposure. In the first hours after noise exposure DPOAE levels were reduced significantly. In about 70% a partial recovery of the DPOAEs was found within 4 months after noise exposure. In 16% of the investigated ears no recovery of DPOAEs was observed. However, in a few ears increased DPOAEs were observed after noise exposure. Exposure to industrial noise caused both morphological changes in the middle turns of the cochlea and electrophysiological changes in the middle frequency range. A close correlation existed between reduced DPOAE levels, loss in CM potentials, and area of damaged or lost OHCs, but not with the numbers of damaged or lost OHCs in the cochlea. It can be concluded that continuous industrial noise causes a damage to OHCs which differs form the damage caused by impulse noise. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Jena, Dept Neurophysiol, Inst Physiol 1, D-07740 Jena, Germany. Univ Jena, Inst Anat 1, D-6900 Jena, Germany. RP Emmerich, E (reprint author), Univ Jena, Dept Neurophysiol, Inst Physiol 1, Teichgraben 8, D-07740 Jena, Germany. CR AHROON WA, 1993, J ACOUST SOC AM, V93, P997, DOI 10.1121/1.405406 Angelborg C, 1979, Adv Otorhinolaryngol, V25, P41 ANGELBORG C, 1984, ARCH OTOLARYNGOL, V110, P297 BIEDERMANN M, 1977, ACTA BIOL MED GER, V36, P1097 BORG E, 1983, ACTA OTO-LARYNGOL, V96, P361, DOI 10.3109/00016488309132721 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 CODY AR, 1988, HEARING RES, V35, P59, DOI 10.1016/0378-5955(88)90040-8 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DIEROFF HG, 1994, LARMSCHWERHORIGKEIT DOBIE RA, 1983, LARYNGOSCOPE, V93, P906 Eddins AC, 1999, HEARING RES, V127, P119 Emmerich E, 2000, EUR ARCH OTO-RHINO-L, V257, P128, DOI 10.1007/s004050050208 EMMERICH E, 1993, DEV EVENT RELATED PO, P35 EMMERICH E, 1990, ACTIV NERV SUPER, V32, P119 Frolenkov GI, 1998, HEARING RES, V126, P67, DOI 10.1016/S0378-5955(98)00150-6 GEYER G, 1978, EXPERIENTIA, V34, P363, DOI 10.1007/BF01923037 HAMERNIK RP, 1993, J ACOUST SOC AM, V93, P2088, DOI 10.1121/1.406695 Hamernik RP, 1998, HEARING RES, V118, P73, DOI 10.1016/S0378-5955(98)00021-5 Hamernik RP, 1996, J ACOUST SOC AM, V100, P1003, DOI 10.1121/1.416285 HAUSER R, 1991, LARYNGO RHINO OTOL, V70, P123, DOI 10.1055/s-2007-998003 HENDERSON D, 1986, J ACOUST SOC AM, V80, P569, DOI 10.1121/1.394052 Henderson D, 1998, Scand Audiol Suppl, V48, P63 Henley CM, 1996, HEARING RES, V98, P93, DOI 10.1016/0378-5955(96)00077-9 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 HULTCRANTZ E, 1979, ARCH OTO-RHINO-LARYN, V224, P103, DOI 10.1007/BF00455231 Kakigi A, 1998, AUDIOL NEURO-OTOL, V3, P361, DOI 10.1159/000013806 KEMP DT, 1983, HEARING PHYSL BASES, P104 Kirk DL, 1997, HEARING RES, V112, P69, DOI 10.1016/S0378-5955(97)00104-4 Lichtenstein V, 1996, HEARING RES, V98, P125, DOI 10.1016/0378-5955(96)00084-6 LINSS W, 1991, ANAT ANZ S, V186, P451 LONSBURYMARTIN BL, 1993, PROG BRAIN RES, V97, P77 MENSH BD, 1993, HEARING RES, V70, P65, DOI 10.1016/0378-5955(93)90052-3 MENSH BD, 1993, HEARING RES, V70, P50, DOI 10.1016/0378-5955(93)90051-2 MEYER C, 1985, ANAT ANZEIGER, V158, P5 POPELAR J, 1993, HEARING RES, V67, P69, DOI 10.1016/0378-5955(93)90233-Q POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 RICHTER F, 1987, ARCH OTO-RHINO-LARYN, V244, P269, DOI 10.1007/BF00468634 SHADDOCK LC, 1985, ANN OTO RHINOL LARYN, V94, P87 SUBRAMANIAM M, 1995, EAR HEARING, V16, P372, DOI 10.1097/00003446-199508000-00004 Vinck BM, 1996, AUDIOLOGY, V35, P231 Wagner W, 1999, EUR ARCH OTO-RHINO-L, V256, P177, DOI 10.1007/s004050050136 Zenner H.P., 1994, HOREN Zheng XY, 1997, HEARING RES, V107, P147, DOI 10.1016/S0378-5955(97)00031-2 Zheng YL, 1997, HEARING RES, V112, P167, DOI 10.1016/S0378-5955(97)00118-4 NR 45 TC 24 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 9 EP 17 DI 10.1016/S0378-5955(00)00101-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500002 PM 10978821 ER PT J AU Briaire, JJ Frijns, JHM AF Briaire, JJ Frijns, JHM TI Field patterns in a 3D tapered spiral model of the electrically stimulated cochlea SO HEARING RESEARCH LA English DT Article DE cochlear implant; electrical volume conduction; preferential current pathway; potential field; auditory nerve ID ROTATIONALLY SYMMETRICAL MODEL; MYELINATED NERVE-FIBERS; BOUNDARY-ELEMENT METHOD; AUDITORY-NERVE; CURRENT DISTRIBUTIONS; NEURAL EXCITATION; STOCHASTIC-MODEL; POTENTIALS; IMPLANTS; ACCURACY AB Despite the fact that cochlear implants are widely and successfully used in clinical practice, relatively little is known to date about the electric field patterns they set up in the cochlea. Based upon the available measurements and modelling results, the scala tympani is usually considered to be a preferential current pathway that acts like a leaky transmission line. Therefore, most authors assume the current thresholds to decay exponentially along the length of the scala tympani. Here we present potential distributions calculated with a fully three-dimensional, spiralling volume conduction model of the guinea pig cochlea, and try to identify its preferential current pathways. The relatively well conducting scala tympani turns out to be the main one indeed, but the exponential decay (J similar to e(-z)) of current is only a good description of the far-field behaviour. In the vicinity of the electrodes, i.e. near the fibres that are most easily excited, higher current densities are found, that are best described by a spherical spread of the current (J similar to 1/R-2) The results are compared with those obtained with a variant of our previous, rotationally symmetric, model and with measurements in the literature. The implications of the findings are discussed in the light of simulated neural responses. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Leiden Univ, Med Ctr, ENT Dept, NL-2300 RC Leiden, Netherlands. RP Frijns, JHM (reprint author), Leiden Univ, Med Ctr, ENT Dept, POB 9600, NL-2300 RC Leiden, Netherlands. RI Briaire, Jeroen/A-7972-2008; Frijns, Johan/H-6249-2011 OI Briaire, Jeroen/0000-0003-4302-817X; CR Abbas PJ, 1999, EAR HEARING, V20, P45, DOI 10.1097/00003446-199902000-00005 ASCHENDORFF A, 1999, 1999 C IMPL AUD PROS, P56 BALKANY TJ, 1986, OTOLARYNG CLIN N AM, V19, P215 Binns K.J., 1992, ANAL NUMERICAL SOLUT BLACK RC, 1983, ANN NY ACAD SCI, V405, P137, DOI 10.1111/j.1749-6632.1983.tb31626.x BREBBIA CA, 1992, BOUNDARY ELEMENTS IN Briaire JJ, 2000, SIMULAT PRACT THEORY, V8, P57, DOI 10.1016/S0928-4869(00)00007-0 BRIAIRE JJ, 1998, 4 EUR S PED COCHL IM, P88 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P617, DOI 10.1109/10.764938 Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P630, DOI 10.1109/10.764939 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 Ferguson AS, 1997, IEEE T BIO-MED ENG, V44, P1139, DOI 10.1109/10.641342 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 FINDLEY CC, 1990, COCHLEAR IMPLANTS MO, P55 FIRTSZT J, 1999, 1999 C IMPL AUD PROS, P56 FRIJNS JHM, 2000, IN PRESS IEEE T BIOM Frijns JHM, 2000, SIMULAT PRACT THEORY, V8, P75, DOI 10.1016/S0928-4869(00)00008-2 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q FRIJNS JHM, 1994, IEEE T BIO-MED ENG, V41, P556, DOI 10.1109/10.293243 Frijns JHM, 1996, HEARING RES, V95, P33, DOI 10.1016/0378-5955(96)00004-4 Girzon G., 1987, THESIS MIT GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S IFUKUBE T, 1987, IEEE T BIO-MED ENG, V34, P883, DOI 10.1109/TBME.1987.326009 Jolly CN, 1996, IEEE T BIO-MED ENG, V43, P857, DOI 10.1109/10.508549 Kral A, 1998, HEARING RES, V121, P11, DOI 10.1016/S0378-5955(98)00061-6 KUZMA JA, 1999, 1999 C IMPL AUD PROS, P60 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MEIJS JWH, 1989, IEEE T BIO-MED ENG, V36, P1038, DOI 10.1109/10.40805 National Institutes of Health, 1995, COCHLEAR IMPLANTS AD, V13, P1 NIJDAM HF, 1982, THESIS GRONINGEN U OLEARY SJ, 1985, HEARING RES, V18, P273, DOI 10.1016/0378-5955(85)90044-9 RATTAY F, 1989, IEEE T BIO-MED ENG, V36, P676, DOI 10.1109/10.32099 Rubinstein JT, 1999, HEARING RES, V127, P108, DOI 10.1016/S0378-5955(98)00185-3 SAPOZHNIKOV A, 1990, THESIS U MELBORNE SCHWARZ JR, 1987, PFLUG ARCH EUR J PHY, V409, P569, DOI 10.1007/BF00584655 SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 SPELMAN FA, 1982, ANN OTO RHINOL LARYN, V91, P3 STRELIOF.D, 1973, J ACOUST SOC AM, V54, P620, DOI 10.1121/1.1913642 SUESSERMAN MF, 1993, IEEE T BIO-MED ENG, V40, P237, DOI 10.1109/10.216407 Suesserman M.F., 1992, THESIS U WASHINGTON VONOOSTEROM A, 1991, ACTA OTOLARYNGOL S S, V491, P70 WARMAN EN, 1992, IEEE T BIO-MED ENG, V39, P1244, DOI 10.1109/10.184700 NR 43 TC 45 Z9 45 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 18 EP 30 DI 10.1016/S0378-5955(00)00104-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500003 PM 10978822 ER PT J AU Hao, LF Khanna, SM AF Hao, LF Khanna, SM TI Mechanical nonlinearity in the apical turn of the guinea pig organ of Corti SO HEARING RESEARCH LA English DT Article DE cochlea; apical turn; vibration; nonlinearity; guinea pig ID BASILAR-MEMBRANE MECHANICS; MOSSBAUER TECHNIQUE; INNER-EAR; COCHLEA; VIBRATIONS; MICROSCOPE; BASE AB Confocal microscopy was used to view the sealed apical turn of the cochlea in a living guinea pig, and to identify the cochlear structures through the intact Reissner's membrane. X, Y and Z coordinates for each point of interest were recorded. A confocal laser heterodyne interferometer measured the cellular vibration in response to acoustical signals applied to the ear. Velocity time waveforms were recorded at 32 frequencies between 25 and 2500 Kz at each point of measurement. To characterize the vibration pattern of the organ of Corti, vibrations at multiple locations along a radial track of the reticular lamina were measured before and after sacrificing the animal. Amplitude and phase tuning curves of the fundamental and the second harmonic, velocity time waveforms, and FFTs of time waveforms are compared before and after sacrifice. The results show that a sharply tuned nonlinear part of the response disappears shortly after sacrifice. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Columbia Univ Coll Phys & Surg, Dept Otolaryngol Head & Neck Surg, New York, NY 10032 USA. Univ Maryland, Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21201 USA. RP Khanna, SM (reprint author), Columbia Univ Coll Phys & Surg, Dept Otolaryngol Head & Neck Surg, 630 W 168th St, New York, NY 10032 USA. CR COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X COOPER NP, 1992, HEARING RES, V63, P163, DOI 10.1016/0378-5955(92)90083-Y Hao LF, 1996, HEARING RES, V99, P176, DOI 10.1016/S0378-5955(96)00099-8 Hao LF, 2000, HEARING RES, V148, P47, DOI 10.1016/S0378-5955(00)00145-3 KHANNA SM, 1999, IN PRESS P S REC DEV KHANNA SM, 1996, P SOC PHOTO-OPT INS, V2732, P64, DOI 10.1117/12.231687 Khanna SM, 1999, HEARING RES, V132, P15, DOI 10.1016/S0378-5955(99)00027-1 KHANNA SM, 2000, UNPUB HEAR RES Khanna SM, 1998, ACUSTICA, V84, P1175 KHANNA SM, 2000, IN PRESS J SOLIDS ST Khanna SM, 1999, HEARING RES, V135, P89, DOI 10.1016/S0378-5955(99)00095-7 KOESTER CJ, 1990, T R MICROSC SOC, V1, P3237 KOESTER CJ, 1994, APPL OPTICS, V33, P702, DOI 10.1364/AO.33.000702 Koester C J, 1989, Acta Otolaryngol Suppl, V467, P27 KOESTER CJ, 1980, APPL OPTICS, V19, P1749, DOI 10.1364/AO.19.001749 RHODE WS, 1980, J ACOUST SOC AM, V67, P1696, DOI 10.1121/1.384296 RHODE WS, 1973, BASIC MECH HEARING RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 Ruggero MA, 1996, AUDIT NEUROSCI, V2, P329 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 NR 24 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 31 EP 46 DI 10.1016/S0378-5955(00)00112-X PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500004 PM 10978823 ER PT J AU Hao, LF Khanna, SM AF Hao, LF Khanna, SM TI Vibrations of the guinea pig organ of Corti in the apical turn SO HEARING RESEARCH LA English DT Article DE guinea pig; cochlear mechanics; Reissner's membrane; reticular lamina; Claudius' cell; osseus spiral lamina ID INNER-EAR; COCHLEA; MICROSCOPE; MECHANICS AB Vibrations of the organ of Corti were measured in response to sound applied to the ear in the apical turn of a living guinea pig. Measurements were made at 29 points on the Reissner's membrane (RM) at 10 mu spacing along a radial track. Measurements also included 22 points on the reticular lamina (RL), Claudius' cells and osseous spiral lamina. Our goal was to characterize the vibration of the RM and the RL with high spatial resolution along a radial axis. The tuning and spatial patterns of the RM are compared in the radial direction with those for the RL at the fundamental frequency and at the second harmonic. The shape of the RM tuning curve changes with radial position, and differ significantly from those observed at the RL. These results support our earlier findings (Hao and Khanna, Hear; Res. 99 (1996) 176-189). (C) 2000 Elsevier Science B.V. All rights reserved. C1 Columbia Univ Coll Phys & Surg, New York, NY 10032 USA. Univ Maryland, Sch Med, Dept Otolaryngol, Baltimore, MD 21201 USA. RP Khanna, SM (reprint author), Columbia Univ Coll Phys & Surg, 630 W 168th St, New York, NY 10032 USA. CR ADES HW, 1974, HDB SENSORY PHYSL, P276 ALLEN JB, 1977, J ACOUST SOC AM, V61, P110, DOI 10.1121/1.381272 COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X DEBOER E, 1981, HEARING RES, V4, P53, DOI 10.1016/0378-5955(81)90036-8 DUVALL AJ, 1967, ARCH OTOLARYNGOL, V86, P37 Hao LF, 1996, HEARING RES, V99, P176, DOI 10.1016/S0378-5955(96)00099-8 Hao LF, 2000, HEARING RES, V148, P31, DOI 10.1016/S0378-5955(00)00112-X KHANNA SM, 1996, P SOC PHOTO-OPT INS, V2732, P64, DOI 10.1117/12.231687 Khanna SM, 1999, HEARING RES, V132, P15, DOI 10.1016/S0378-5955(99)00027-1 Khanna SM, 1999, HEARING RES, V135, P89, DOI 10.1016/S0378-5955(99)00095-7 KOESTER CJ, 1990, T ROY MICR, V1, P327 KOESTER CJ, 1994, APPL OPTICS, V33, P702, DOI 10.1364/AO.33.000702 Koester C J, 1989, Acta Otolaryngol Suppl, V467, P27 KOESTER CJ, 1980, APPL OPTICS, V19, P1749, DOI 10.1364/AO.19.001749 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 SOKOLICH WG, 1981, Patent No. 4251686 STEELE CR, 1974, J ACOUST SOC AM, V55, P148, DOI 10.1121/1.1928144 VIERGEVER MA, 1980, MECH INNER EAR MATH von Bekesy G., 1960, EXPT HEARING, P745 WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 ZWEIG G, 1991, J ACOUST SOC AM, V89, P1229, DOI 10.1121/1.400653 ZWISLOCKI J, 1953, J ACOUST SOC AM, V25, P743, DOI 10.1121/1.1907170 NR 23 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 47 EP 62 DI 10.1016/S0378-5955(00)00145-3 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500005 PM 10978824 ER PT J AU Alcantara, JI Moore, BCJ Vickers, DA AF Alcantara, JI Moore, BCJ Vickers, DA TI The relative role of beats and combination tones in determining the shapes of masking patterns at 2 kHz: I. Normal-hearing listeners SO HEARING RESEARCH LA English DT Article DE masking pattern; beat; combination tone ID AMPLITUDE-MODULATION AB Masking patterns for a 2-kHz sinusoidal masker at 45, 65 or 85 dB SPK were measured for three normal-hearing subjects, using a 3-AFC method with feedback (condition 1). The patterns showed distinct irregularities, particularly at the highest masker level. In condition 2, a lowpass noise was added to mask combination tones. The noise increased thresholds mainly for the 85 dB masker, for signal frequencies of 2.3-3.0 kHz. In condition 3, a pair of high-frequency tones ('modulation detection interference (MDI) tones') was used to introduce beats at the same rate as produced by the interaction of the masker and signal. Thresholds were higher than for condition 1, particularly for signal frequencies adjacent to the masker frequency. In condition 4, the lowpass noise was presented simultaneously with the MDI tones. Thresholds were well predicted as a combination of the effects of the lowpass noise and the MDI tones. In condition 5, a pair of low-frequency MDI tones was added to the masker. The thresholds had the same overall pattern as in condition 4. We conclude that the shapes of masking patterns measured using a 2-kHz masker are influenced by the detection of beats for masker-signal frequency separations up to at least 300 Hz and by the detection of combination tones for separations between 300 and 1000 Hz. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Moore, BCJ (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. RI Moore, Brian/I-5541-2012 CR Dau T, 1997, J ACOUST SOC AM, V102, P2892, DOI 10.1121/1.420344 DERLETH RP, 1999, PSYCHOPHYSICS PHYSL, P622 EGAN JP, 1950, J ACOUST SOC AM, V22, P622, DOI 10.1121/1.1906661 EHMER RH, 1959, J ACOUST SOC AM, V31, P1253, DOI 10.1121/1.1907853 EHMER RH, 1959, J ACOUST SOC AM, V31, P1115, DOI 10.1121/1.1907836 FASSEL R, 2000, IN PRESS J ACOUST SO GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P458, DOI 10.1121/1.1910357 GREENWOO.DD, 1971, J ACOUST SOC AM, V50, P502, DOI 10.1121/1.1912668 Hall JL, 1997, J ACOUST SOC AM, V101, P1023, DOI 10.1121/1.418027 HELLMAN RP, 1972, PERCEPT PSYCHOPHYS, V11, P241, DOI 10.3758/BF03206257 HICKS ML, 1995, J ACOUST SOC AM, V98, P2504, DOI 10.1121/1.413216 Moore BCJ, 1998, J ACOUST SOC AM, V104, P1023, DOI 10.1121/1.423321 Riesz RR, 1928, PHYS REV, V31, P0867, DOI 10.1103/PhysRev.31.867 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P603, DOI 10.1121/1.1913151 Wegel RL, 1924, PHYS REV, V23, P266, DOI 10.1103/PhysRev.23.266 YOSH WA, 1988, J ACOUST SOC AM, V83, pS35 YOST WA, 1989, J ACOUST SOC AM, V86, P2138, DOI 10.1121/1.398474 Zwicker E., 1990, PSYCHOACOUSTICS FACT ZWICKER E, 1973, ACUSTICA, V29, P336 ZWICKER E, 1981, J ACOUST SOC AM, V70, P1277, DOI 10.1121/1.387141 NR 21 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 63 EP 73 DI 10.1016/S0378-5955(00)00114-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500006 PM 10978825 ER PT J AU May, BJ AF May, BJ TI Role of the dorsal cochlear nucleus in the sound localization behavior of cats SO HEARING RESEARCH LA English DT Article DE dorsal cochlear nucleus; sound localization; orientation behavior; spatial acuity ID ACOUSTIC STRIAE; SPECTRAL CUES; HORSERADISH-PEROXIDASE; ORIENTATION BEHAVIOR; INFERIOR COLLICULUS; NARROW-BAND; HEARING; ORGANIZATION; RESPONSES; SENSITIVITY AB The role of the dorsal cochlear nucleus (DCN) in directional hearing was evaluated by measuring sound localization behaviors before and after cats received lesions of the dorsal and intermediate acoustic striac (DAS/IAS). These lesions are presumed to disrupt spectral processing in the DCN without affecting binaural time and level difference cues that exit the cochlear nucleus via the ventral acoustic stria. Prior to DAS/IAS lesions, cats made accurate head orientation responses toward sound sources in the frontal sound field. After a unilateral DAS/IAS lesion, subjects showed increased errors in the azimuth and elevation of their responses; in addition, the final orientation of head movements tended to be more variable. Largest deficits in response elevation were observed in the hemifield that was ipsilateral to the lesion. When a second lesion was placed in the opposite DAS/IAS, increased orientation errors were observed throughout the frontal field. Nonetheless, bilaterally lesioned cats showed normal discrimination of changes in sound source location when tested with a spatial acuity task. These findings support previous interpretations that the DCN contributes to sound orientation behavior, and further suggest that the identification of absolute sound source locations and the discrimination between spatial locations involve independent auditory processing mechanisms. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Johns Hopkins Univ, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21205 USA. RP May, BJ (reprint author), Johns Hopkins Univ, Dept Otolaryngol Head & Neck Surg, 505 Traylor Res Bldg,720 Rutland Ave, Baltimore, MD 21205 USA. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1976, J COMP NEUROL, V170, P97, DOI 10.1002/cne.901700107 ADAMS JC, 1976, J COMP NEUROL, V170, P107, DOI 10.1002/cne.901700108 Armitage P, 1987, STATISTICAL METHODS, V409, P10 CASSEDAY JH, 1975, J NEUROPHYSIOL, V38, P842 DAVIS M, 1982, J NEUROSCI, V2, P791 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 HEFFNER RS, 1988, HEARING RES, V36, P221, DOI 10.1016/0378-5955(88)90064-0 Huang AY, 1996, J ACOUST SOC AM, V100, P2341, DOI 10.1121/1.417943 Huang AY, 1996, J ACOUST SOC AM, V100, P1070, DOI 10.1121/1.416293 MARTIN RL, 1987, HEARING RES, V30, P239, DOI 10.1016/0378-5955(87)90140-7 MASTERTON RB, 1988, J NEUROPHYSIOL, V60, P1841 MASTERTON RB, 1994, HEARING RES, V73, P209, DOI 10.1016/0378-5955(94)90237-2 May BJ, 1997, J ACOUST SOC AM, V101, P2705, DOI 10.1121/1.418559 May BJ, 1996, J ACOUST SOC AM, V100, P1059, DOI 10.1121/1.416292 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 MIDDLEBROOKS JC, 1992, J ACOUST SOC AM, V92, P2607, DOI 10.1121/1.404400 MIDDLEBROOKS JC, 1989, J ACOUST SOC AM, V86, P89, DOI 10.1121/1.398224 NELKEN I, 1994, J NEUROPHYSIOL, V71, P2446 OSEN KK, 1972, J COMP NEUROL, V144, P355, DOI 10.1002/cne.901440307 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 RICE JJ, 1992, HEARING RES, V58, P132, DOI 10.1016/0378-5955(92)90123-5 ROUILLER EM, 1984, J COMP NEUROL, V225, P167, DOI 10.1002/cne.902250203 RYUGO DK, 1985, J COMP NEUROL, V242, P381, DOI 10.1002/cne.902420307 SPIROU GA, 1991, J NEUROPHYSIOL, V66, P1750 SPIROU GA, 1993, J COMP NEUROL, V329, P36, DOI 10.1002/cne.903290104 Sutherland DP, 1998, HEARING RES, V120, P86, DOI 10.1016/S0378-5955(98)00056-2 Sutherland DP, 1998, BEHAV BRAIN RES, V97, P1, DOI 10.1016/S0166-4328(98)00008-4 WARR WB, 1969, EXP NEUROL, V23, P140, DOI 10.1016/0014-4886(69)90040-5 Wightman FL, 1997, J ACOUST SOC AM, V101, P1050, DOI 10.1121/1.418029 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P858, DOI 10.1121/1.397557 WIGHTMAN FL, 1992, J ACOUST SOC AM, V91, P1648, DOI 10.1121/1.402445 YOUNG ED, 1992, PHILOS T ROY SOC B, V336, P407, DOI 10.1098/rstb.1992.0076 NR 33 TC 68 Z9 70 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 74 EP 87 DI 10.1016/S0378-5955(00)00142-8 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500007 PM 10978826 ER PT J AU Goverts, ST Houtgast, T van Beek, HHM AF Goverts, ST Houtgast, T van Beek, HHM TI The precedence effect for lateralization at low sensation levels SO HEARING RESEARCH LA English DT Article DE precedence effect; localization dominance; binaural hearing; auditory perception; lateralization accuracy; normal hearing ID HIGH-FREQUENCY CLICKS; INTERAURAL DIFFERENCES; INTERCLICK INTERVAL; PERCEPTION; DURATION; TRAINS; NUMBER; ONSET AB Using dichotic signals presented by headphone, stimulus onset dominance (the precedence effect) for lateralization at low sensation levels was investigated for five normal hearing subjects. Stimuli were based on 2400-Hz low pass filtered 5-ms noise bursts. We used the paradigm, as described by Aoki and Houtgast (Hear. Res., 59 (1992) 25-30) and Houtgast and Aoki (Hear. Res., 72 (1994) 29-36), in which the stimulus is divided into a leading and a lagging part with opposite lateralization cues (i.e. an interaural time delay of 0.2 ms). The occurrence of onset dominance was investigated by measuring lateral perception of the stimulus, with fixed equal duration of leading and lagging part, while decreasing absolute signal level or adding a filtered white noise with the signal level set at 65 dBA. The dominance of the leading part was quantified by measuring the perceived lateral position of the stimulus as a function of the relative duration of the leading (and thus the lagging) part. This was done at about 45 dB SL without masking noise and also at a signal-to-noise ratio resulting in a sensation level of 10 dB. The occurrence and strength of the precedence effect was found to depend on sensation level, which was decreased either by lowering the signal level or by adding noise. With the present paradigm, besides a decreased lateralization accuracy, a decrease in the precedence effect was found for sensation levels below about 30-40 dB. In daily-life conditions, with a sensation level in noise of typically 10 dB, the onset dominance was still manifest, albeit degraded to some extent. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Vrije Univ Amsterdam, Acad Ziekenhuis, Dept Otolaryngol Audiol, NL-1007 MB Amsterdam, Netherlands. RP Goverts, ST (reprint author), Vrije Univ Amsterdam, Acad Ziekenhuis, Dept Otolaryngol Audiol, POB 7057, NL-1007 MB Amsterdam, Netherlands. CR ABEL SM, 1983, J ACOUST SOC AM, V73, P955, DOI 10.1121/1.389020 AOKI S, 1992, HEARING RES, V59, P25, DOI 10.1016/0378-5955(92)90098-8 Blauert J., 1997, SPATIAL HEARING PSYC HAAS H, 1951, J AUDIOL ENG SOC, V20, P145 HAFTER ER, 1988, FUNCTIONS AUDITORY S HAFTER ER, 1983, J ACOUST SOC AM, V73, P1708, DOI 10.1121/1.389394 HAFTER ER, 1983, J ACOUST SOC AM, V73, P644, DOI 10.1121/1.388956 HOUTGAST T, 1968, J ACOUST SOC AM, V44, P807, DOI 10.1121/1.1911178 HOUTGAST T, 1994, HEARING RES, V72, P29, DOI 10.1016/0378-5955(94)90202-X Litovsky RY, 1999, J ACOUST SOC AM, V106, P1633, DOI 10.1121/1.427914 RAKERD B, 1986, J ACOUST SOC AM, V80, P1695, DOI 10.1121/1.394282 SHINNCUNNINGHAM BG, 1993, J ACOUST SOC AM, V93, P2923, DOI 10.1121/1.405812 WALLACH H, 1949, AM J PSYCHOL, V62, P315, DOI 10.2307/1418275 Zurek P. M., 1987, DIRECTIONAL HEARING, P85, DOI 10.1007/978-1-4612-4738-8_4 ZUREK PM, 1980, J ACOUST SOC AM, V67, P952, DOI 10.1121/1.383974 NR 15 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 88 EP 94 DI 10.1016/S0378-5955(00)00143-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500008 PM 10978827 ER PT J AU Yoshikawa, H Smurzynski, J Probst, R AF Yoshikawa, H Smurzynski, J Probst, R TI Suppression of tone burst evoked otoacoustic emissions in relation to frequency separation SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 21st Midwinter Meeting of the Association-for-Research-in-Otolaryngology CY FEB 15-19, 1998 CL ST PETERSBURG, FL SP Assoc Res Otolaryngol DE suppression; frequency superposition; cochlear mechanic; transiently evoked otoacoustic emission ID 2-TONE SUPPRESSION; HEARING; CLICK; EARS; RESPONSES AB Tone burst evoked otoacoustic emissions (TBEOAEs) were measured for two tone bursts presented separately and as a two-tone burst complex to examine the linearity of TBEOAE generators for different frequency separations of the stimuli. The stimuli were: (a) tone bursts of 5-ms duration and center frequencies of 1, 1.5, 2 and 3 kHz; (b) complex stimuli with the 1-kHz tone burst combined digitally with each of the other specified tone bursts. Signals were delivered at 70 dB SPL using a non-linear processing method and at 60 dB SPL using a linear method to 21 ears of normally hearing adults. Spectra of TBEOAEs obtained with single-tone bursts were superimposed (composite) and compared to those of the two-tone burst complex. A close correspondence between the composite and complex spectra was present in all ears. However, the components on the higher-frequency slope of the 1-kHz spectral peak were reduced in the complex spectra obtained with a frequency separation of 0.5 kHz when compared to the corresponding composite spectra. The reduction was greater at a stimulus level of 70 dB SPL than with 60 dB SPL. The effect was smaller for a frequency separation of 1 kHz, and almost absent for the tone burst separation of 2 kHz. Thus, suppression leads to weak non-linear frequency superposition for higher-level., closely spaced stimuli. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Basel Hosp, Kantonsspital Basel, Dept Otorhinolaryngol, NHO Univ Klin, CH-4031 Basel, Switzerland. Juntendo Univ, Sch Med, Dept Otorhinolaryngol, Bunkyo Ku, Tokyo 1130033, Japan. RP Smurzynski, J (reprint author), Univ Basel Hosp, Kantonsspital Basel, Dept Otorhinolaryngol, NHO Univ Klin, Petersgraben 4, CH-4031 Basel, Switzerland. EM jsmurzynski@uhbs.ch CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 Avan P, 1997, J ACOUST SOC AM, V101, P2771, DOI 10.1121/1.418564 AVAN P, 1993, HEARING RES, V70, P109, DOI 10.1016/0378-5955(93)90055-6 AVAN P, 1991, HEARING RES, V52, P99, DOI 10.1016/0378-5955(91)90191-B BRASS D, 1993, J ACOUST SOC AM, V93, P920, DOI 10.1121/1.405453 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 Giguere C, 1997, J ACOUST SOC AM, V102, P2821, DOI 10.1121/1.420338 HARRIS F P, 1992, Seminars in Hearing, V13, P67, DOI 10.1055/s-0028-1085142 HOUTGAST T, 1974, THESIS I PERCEPTION HOUTGAST T, 1972, J ACOUST SOC AM, V51, P1885, DOI 10.1121/1.1913048 KEMP DT, 1990, LECT NOTES BIOMATH, V87, P202 KEMP DT, 1990, EAR HEARING, V11, P93 Long G, 1998, HEARING RES, V119, P49, DOI 10.1016/S0378-5955(98)00032-X LONG GR, 1993, BIOPHYSICS HAIR CELL, P40 Moore Brian C. J., 1995, P161, DOI 10.1016/B978-012505626-7/50007-8 MURNANE O, 2000, ABSTR ASS RES OTOLAR, V23, P160 Prieve BA, 1996, J ACOUST SOC AM, V99, P3077, DOI 10.1121/1.414794 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 RUGGERO MA, 1992, PHILOS T ROY SOC B, V336, P307, DOI 10.1098/rstb.1992.0063 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SHANNON RV, 1980, J ACOUST SOC AM, V68, P825, DOI 10.1121/1.384821 SMOORENBURG GF, 1974, FACTS MODELS HEARING, P332 Smurzynski J, 1996, J ACOUST SOC AM, V100, P2555, DOI 10.1121/1.417366 Smurzynski J, 1998, HEARING RES, V115, P197, DOI 10.1016/S0378-5955(97)00193-7 Souter M, 1995, HEARING RES, V91, P167, DOI 10.1016/0378-5955(95)00187-5 STOVER L, 1993, J ACOUST SOC AM, V94, P2670, DOI 10.1121/1.407351 SUTTON GJ, 1985, ACUSTICA, V58, P57 WABLE J, 1994, HEARING RES, V80, P141, DOI 10.1016/0378-5955(94)90105-8 Withnell RH, 2000, HEARING RES, V139, P1, DOI 10.1016/S0378-5955(99)00132-X XU L, 1994, HEARING RES, V74, P173 Xu L, 1999, NATURE, V399, P688 Yates GK, 1999, HEARING RES, V136, P49, DOI 10.1016/S0378-5955(99)00108-2 NR 33 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 95 EP 106 DI 10.1016/S0378-5955(00)00144-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500009 PM 10978828 ER PT J AU Klug, A Khan, A Burger, RM Bauer, EE Hurley, LM Yang, LC Grothe, B Halvorsen, MB Park, TJ AF Klug, A Khan, A Burger, RM Bauer, EE Hurley, LM Yang, LC Grothe, B Halvorsen, MB Park, TJ TI Latency as a function of intensity in auditory neurons: influences of central processing SO HEARING RESEARCH LA English DT Article DE latency; auditory neurons; central processing; central auditory system ID BATS INFERIOR COLLICULUS; MEDIAL SUPERIOR OLIVE; COMBINATION-SENSITIVE NEURONS; FREE-TAILED BAT; LATERAL LEMNISCUS; MOUSTACHED BAT; ECHOLOCATING BAT; RESPONSE PROPERTIES; COCHLEAR NUCLEUS; DISCHARGE CHARACTERISTICS AB The response latencies of sensory neurons typically shorten with increases in stimulus intensity. In the central auditory system this phenomenon should have a significant impact on a number of auditory functions that depend critically on an integration of precisely timed neural inputs. Evidence from previous studies suggests that the auditory system not only copes with the potential problems associated with intensity-dependent latency change, but that it also modifies latency change to shape the response properties of many cells for specific functions. This observation suggests that intensity-dependent latency change may undergo functional transformations along the auditory neuraxis. The goal of our study was to explore these transformations by making a direct, quantitative comparison of intensity-dependent latency change among a number of auditory centers from the lower brainstem to the thalamus. We found two main ways in which intensity-dependent latency change transformed along the neuraxis: (1) the range of latency change increased substantially and (2) one particular type of latency change, which has been suggested to be associated with sensitivity to temporally segregated stimulus components, occurred only at the highest centers tested, the midbrain and thalamus. Additional testing in the midbrain (inferior colliculus) indicated that inhibitory inputs are involved in shaping latency change. Our findings demonstrate that the central auditory system modifies intensity-dependent latency changes. We suggest that these changes may be functionally incorporated, actively enhanced, or modified to suit specific functions of the auditory system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Illinois, Dept Biol Sci, Neurobiol Grp, Chicago, IL 60607 USA. Univ Texas, Neurobiol Sect, Austin, TX 78712 USA. Max Planck Inst Neurobiol, Martinsried, Germany. RP Park, TJ (reprint author), Univ Illinois, Dept Biol Sci, Neurobiol Grp, 845 W Taylor St,M-C 066, Chicago, IL 60607 USA. RI Grothe, Benedikt/A-7877-2010 CR AITKIN LM, 1968, J NEUROPHYSIOL, V31, P44 AITKIN LM, 1970, J NEUROPHYSIOL, V33, P421 ANTOLICANDELA JF, 1978, EVOKED ELECT ACTIVIT, P165 Batra R, 1999, J NEUROPHYSIOL, V82, P1097 Bauer EE, 2000, HEARING RES, V141, P80, DOI 10.1016/S0378-5955(99)00206-3 BERKOWITZ A, 1989, HEARING RES, V41, P255, DOI 10.1016/0378-5955(89)90017-8 BODENHAMER RD, 1981, HEARING RES, V5, P317, DOI 10.1016/0378-5955(81)90055-1 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 Burger RM, 1998, J NEUROPHYSIOL, V80, P1686 CARNEY T, 1989, VISION RES, V29, P155, DOI 10.1016/0042-6989(89)90121-1 CASSEDAY JH, 1994, SCIENCE, V264, P847, DOI 10.1126/science.8171341 Covey E, 1999, ANNU REV PHYSIOL, V61, P457, DOI 10.1146/annurev.physiol.61.1.457 COVEY E, 1991, J NEUROPHYSIOL, V66, P1080 COVEY E, 1991, J NEUROSCI, V11, P3456 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 DEATHERAGE BH, 1959, J ACOUST SOC AM, V31, P479, DOI 10.1121/1.1907739 Eccles JC, 1964, PHYSL SYNAPSES ERULKAR SD, 1972, PHYSIOL REV, V52, P237 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GOLDBERG JM, 1973, BRAIN RES, V64, P35, DOI 10.1016/0006-8993(73)90169-8 GROTHE B, 1994, J NEUROPHYSIOL, V71, P706 GROTHE B, 1994, J COMP NEUROL, V343, P630, DOI 10.1002/cne.903430412 GROTHE B, 1992, P NATL ACAD SCI USA, V89, P5108, DOI 10.1073/pnas.89.11.5108 Grothe B, 1998, J NEUROSCI, V18, P6608 HALL J, 1986, NEUROSCI LETT, V63, P215, DOI 10.1016/0304-3940(86)90358-7 HAPLEA S, 1994, J COMP PHYSIOL A, V174, P671 HAVEY DC, 1980, ELECTROEN CLIN NEURO, V48, P249, DOI 10.1016/0013-4694(80)90313-2 Heil P, 1996, NEUROREPORT, V7, P3073, DOI 10.1097/00001756-199611250-00056 Heil P, 1998, CEREB CORTEX, V8, P125, DOI 10.1093/cercor/8.2.125 Heil P, 1997, J NEUROPHYSIOL, V77, P2616 Heil P, 1998, BEHAV BRAIN RES, V95, P233, DOI 10.1016/S0166-4328(98)00044-8 Heil P, 1997, J NEUROPHYSIOL, V77, P2642 Heil P, 1997, J NEUROPHYSIOL, V78, P2438 HIND JE, 1963, J NEUROPHYSIOL, V26, P321 IRVINE DRF, 1995, HEARING RES, V85, P127, DOI 10.1016/0378-5955(95)00040-B IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 KITZES LM, 1978, J NEUROPHYSIOL, V41, P1165 Klug A, 1999, J NEUROPHYSIOL, V82, P593 KOLEHMAINEN K, 1974, SCAND J PSYCHOL, V15, P320, DOI 10.1111/j.1467-9450.1974.tb00595.x LeBeau FEN, 1996, J NEUROPHYSIOL, V75, P902 LIT A, 1949, AM J PSYCHOL, V62, P159, DOI 10.2307/1418457 MARGOLIASH D, 1983, J NEUROSCI, V3, P1039 MOLLER AR, 1975, J NEUROPHYSIOL, V38, P812 MOUNTCASTLE VB, 1957, J NEUROPHYSIOL, V20, P374 Oertel D, 1999, ANNU REV PHYSIOL, V61, P497, DOI 10.1146/annurev.physiol.61.1.497 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1275 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1254 Oswald JP, 1999, J NEUROSCI, V19, P1149 PARK TJ, 1993, J NEUROSCI, V13, P2050 Park TJ, 1997, J NEUROPHYSIOL, V77, P2863 PARK TJ, 1993, J NEUROSCI, V13, P5172 Park TJ, 1998, J NEUROPHYSIOL, V79, P2416 Park TJ, 1996, J NEUROSCI, V16, P6554 POLLAK GD, 1993, HEARING RES, V65, P99, DOI 10.1016/0378-5955(93)90205-F POLLAK GD, 1988, HEARING RES, V36, P107, DOI 10.1016/0378-5955(88)90054-8 Pulfrich C, 1922, NATURWISSENSCHAFTEN, V10, P553 RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 ROSE JE, 1959, B JOHNS HOPKINS HOSP, V104, P211 ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 SANES DH, 1988, J NEUROSCI, V8, P682 SCHULLER G, 1986, J NEUROSCI METH, V18, P339, DOI 10.1016/0165-0270(86)90022-1 Suga N, 1988, AUDITORY FUNCTION NE, P679 SUGA N, 1970, SCIENCE, V170, P449, DOI 10.1126/science.170.3956.449 SULLIVAN WE, 1982, J NEUROPHYSIOL, V48, P1033 VATER M, 1992, J COMP PHYSIOL A, V171, P541 YANG L, 1994, AUDIT NEUROSCI, V1, P1 YANG LC, 1994, J NEUROPHYSIOL, V71, P1999 YIN TCT, 1985, J NEUROPHYSIOL, V53, P746 NR 70 TC 47 Z9 48 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 107 EP 123 DI 10.1016/S0378-5955(00)00146-5 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500010 PM 10978829 ER PT J AU Ota, Y Dolan, DF AF Ota, Y Dolan, DF TI The effects of efferent activation on the acoustically and electrically evoked otoacoustic emission SO HEARING RESEARCH LA English DT Article DE otoacoustic emissions; olivocochlear system; guinea pig; cochlea ID OUTER HAIR-CELLS; OLIVOCOCHLEAR BUNDLE STIMULATION; PERIPHERAL AUDITORY-SYSTEM; GUINEA-PIG; CONTRALATERAL SOUND; COCHLEAR MECHANICS; RESPONSES; RECEPTOR; CALCIUM AB The effects of efferent activation on the otoacoustic emission were measured in anesthetized guinea pigs. The otoacoustic emission (2F(1)-F(2)) was evoked by the conventional method of presenting either two continuous tones or a sinusoidal current to the round window (RW) of the cochlea. The efferent effects on the acoustically evoked emission are greatest at low stimulus levels and least for high levels. The efferent effects on the electrically evoked emission (EEOAE) are relatively constant across current levels. In each case, efferent activation resulted in an initial large reduction in the emission amplitude followed by a smaller and more constant reduction. Strychnine eliminated the efferent effects independent of the method of emission activation. Strychnine had no effect on the EEOAE, suggesting that the RW current did not evoke a local efferent effect. Slow versus fast efferent effects were observed in the recovery of the emission amplitude at the termination of efferent activation. Only a fast recovery in the emission amplitude was observed for stimuli below 10 kHz while the amplitude recovery had fast and slow components for stimuli presented above 10 kHz. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Inst, Ann Arbor, MI 48109 USA. Toho Univ, Dept Otolaryngol, Ota Ku, Tokyo 145, Japan. RP Dolan, DF (reprint author), Univ Michigan, Kresge Hearing Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. EM ddolan@umich.edu CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BARTOLAMI S, 1993, BRAIN RES, V626, P200, DOI 10.1016/0006-8993(93)90580-G BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BROWN MC, 1984, J PHYSIOL-LONDON, V354, P625 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DALLOS P, 1992, J NEUROSCI, V12, P4575 Dallos P, 1997, J NEUROSCI, V17, P2212 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DECOSTA DL, 1997, J NEUROPHYSIOL, V78, P1826 DOLAN DF, 1994, 17 ASS RES OT ST PET Dolan DF, 1997, J ACOUST SOC AM, V102, P3587, DOI 10.1121/1.421008 DOLAN DF, 1990, J ACOUST SOC AM, V87, P2621, DOI 10.1121/1.399054 DULON D, 1990, J NEUROSCI, V10, P1388 ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FEX J, 1959, Acta Otolaryngol, V50, P540, DOI 10.3109/00016485909129230 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 GUINAN JJ, 1988, HEARING RES, V37, P29, DOI 10.1016/0378-5955(88)90075-5 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 GUTH PS, 1976, PHARMACOL REV, V28, P95 Guth PS, 1996, HEARING RES, V98, P1, DOI 10.1016/0378-5955(96)00031-7 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 HUBBARD AE, 1990, LECT NOTES BIOMATH, V87, P186 KUJAWA SG, 1994, HEARING RES, V74, P122, DOI 10.1016/0378-5955(94)90181-3 KUJAWA SG, 1992, HEARING RES, V61, P106, DOI 10.1016/0378-5955(92)90041-K KUJAWA SG, 1993, HEARING RES, V68, P97, DOI 10.1016/0378-5955(93)90068-C LONG GR, 1989, MODIFICATION FREQUEN MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I Murugasu E, 1996, J NEUROSCI, V16, P325 NAKAJIMA HH, 1991, P 1991 IEEE 17 ANN N, P2513 Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 REITER ER, 1995, J NEUROPHYSIOL, V73, P506 Ren TY, 1995, HEARING RES, V92, P178, DOI 10.1016/0378-5955(95)00217-0 Ren TY, 1996, HEARING RES, V102, P43, DOI 10.1016/S0378-5955(96)00145-1 Safieddine S, 1996, MOL BRAIN RES, V40, P127 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 Sridhar TS, 1997, J NEUROSCI, V17, P428 SRIDHAR TS, 1995, J NEUROSCI, V15, P3667 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V XUE SW, 1995, J ACOUST SOC AM, V97, P3030, DOI 10.1121/1.413103 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 47 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 124 EP 136 DI 10.1016/S0378-5955(00)00150-7 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500011 PM 10978830 ER PT J AU Engelien, A Schulz, M Ross, B Arolt, V Pantev, C AF Engelien, A Schulz, M Ross, B Arolt, V Pantev, C TI A combined functional in vivo measure for primary and secondary auditory cortices SO HEARING RESEARCH LA English DT Article DE auditory evoked field; central auditory deficit; steady-state response; auditory cortex; magnetoencephalography ID MIDDLE-LATENCY RESPONSES; EVOKED MAGNETIC-FIELDS; STEADY-STATE RESPONSES; CORTEX; LESIONS; SCHIZOPHRENIA; ORGANIZATION; STIMULATION; POTENTIALS; ORIGIN AB Auditory evoked magnetic fields are reliable physiological in vivo markers of activity generated in auditory cortices. In recent years, several components of auditory evoked fields have been demonstrated with specific topographies within the auditory cortex in man. Their differential elicitation and analyses has rendered the discrimination of neural activities in primary vs. secondary auditory cortical fields possible. This in vivo measure may be of interest in a number of (neuro)psychiatric and neuropsychological disorders with central auditory deficits, in which in vivo anatomical measures do not allow a clear distinction of primary vs. secondary auditory cortex involvement. To help better understand the pathophysiology of such disorders, we developed and introduce a combined measure of steady-state field (SSR) and the N1 component of the transient evoked field. The acoustic stimulus for this paradigm consists of a 500-ms tone burst with 39-Hz amplitude modulation of the carrier frequency. This combined stimulation allows assessment of both auditory cortex components in one brief examination to be well tolerated by patients. We examined the source locations of SSR and N1 component with separate classical stimulation and combined stimulation within-session in healthy volunteer subjects. We demonstrate here that the distinct sources of steady-state (primary auditory cortex) and N1 (secondary auditory cortex) responses can be reliably measured without significant spatial distortion with this combined stimulation paradigm. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Munster, Inst Expt Audiol, Biomagnetism Ctr, D-48129 Munster, Germany. Univ Munster, Dept Neurol, D-48129 Munster, Germany. Cornell Univ, Weill Med Coll, Dept Psychiat, Funct Neuroimaging Lab, New York, NY 10021 USA. Univ Munster, Dept Psychiat, D-48129 Munster, Germany. RP Pantev, C (reprint author), Univ Munster, Inst Expt Audiol, Biomagnetism Ctr, D-48129 Munster, Germany. CR Binder JR, 1996, BRAIN, V119, P1239, DOI 10.1093/brain/119.4.1239 Blumenfeld LD, 1999, NEUROREPORT, V10, P2587, DOI 10.1097/00001756-199908200-00027 Eggermont JJ, 1997, NEUROREPORT, V8, P2709, DOI 10.1097/00001756-199708180-00014 ENGELIEN A, 2000, IN PRESS CENTRAL AUD Engelien A, 2000, BRAIN, V123, P532, DOI 10.1093/brain/123.3.532 ERNE SN, 1987, INT J NEUROSCI, V37, P115, DOI 10.3109/00207458708987142 FORSS N, 1993, HEARING RES, V68, P89, DOI 10.1016/0378-5955(93)90067-B FRANOWICZ MN, 1995, J NEUROPHYSIOL, V74, P96 GALABURDA A, 1980, J COMP NEUROL, V190, P597, DOI 10.1002/cne.901900312 Griffiths TD, 1999, NEUROCASE, V5, P365, DOI 10.1080/13554799908402733 Gutschalk A, 1999, CLIN NEUROPHYSIOL, V110, P856, DOI 10.1016/S1388-2457(99)00019-X HARI R, 1980, EXP BRAIN RES, V40, P237 HARI R, 1987, AUDIOLOGY, V26, P31 Hari R., 1990, AUDITORY EVOKED MAGN, P222 HARI R, 1989, J ACOUST SOC AM, V86, P1033, DOI 10.1121/1.398093 Hyde M, 1997, AUDIOL NEURO-OTOL, V2, P281 IBANEZ V, 1989, ARCH NEUROL-CHICAGO, V46, P1325 Johnsrude IS, 1997, NEUROREPORT, V8, P1761 KARMOS G, 1993, NEW DEVELOPMENTS IN EVENT-RELATED POTENTIALS, P87 KASEDA Y, 1991, J NEUROL, V238, P427, DOI 10.1007/BF00314648 KILENY P, 1987, ELECTROEN CLIN NEURO, V66, P108, DOI 10.1016/0013-4694(87)90180-5 KRAUS N, 1982, ELECTROEN CLIN NEURO, V54, P275, DOI 10.1016/0013-4694(82)90177-8 Kuriki S, 1995, HEARING RES, V92, P47, DOI 10.1016/0378-5955(95)00195-6 Kwon JS, 1999, ARCH GEN PSYCHIAT, V56, P1001, DOI 10.1001/archpsyc.56.11.1001 LIEGEOISCHAUVEL C, 1994, ELECTROEN CLIN NEURO, V92, P204, DOI 10.1016/0168-5597(94)90064-7 LUTKENHONER B, 2000, IN PRESS NEUROREPORT Lutkenhoner B, 1998, AUDIOL NEURO-OTOL, V3, P191, DOI 10.1159/000013790 MAKELA JP, 1987, ELECTROEN CLIN NEURO, V66, P539, DOI 10.1016/0013-4694(87)90101-5 MAKELA JP, 1994, ELECTROEN CLIN NEURO, V92, P414, DOI 10.1016/0168-5597(94)90018-3 MOLLER AR, 1999, CLIN NEUROPHYSIOL, V49, P27 O'Donnell BF, 1999, PSYCHOPHYSIOLOGY, V36, P388, DOI 10.1017/S0048577299971688 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 PANTEV C, 1995, ELECTROEN CLIN NEURO, V94, P26, DOI 10.1016/0013-4694(94)00209-4 PANTEV C, 1993, ELECTROEN CLIN NEURO, V88, P389, DOI 10.1016/0168-5597(93)90015-H PANTEV C, 1994, ELECTROEN CLIN NEURO, V90, P82, DOI 10.1016/0013-4694(94)90115-5 PANTEV C, 1991, P NATL ACAD SCI USA, V88, P8996, DOI 10.1073/pnas.88.20.8996 Pantev C, 1996, HEARING RES, V101, P62, DOI 10.1016/S0378-5955(96)00133-5 PARVING A, 1980, SCAND AUDIOL, V9, P161, DOI 10.3109/01050398009076350 PELIZZONE M, 1987, NEUROSCI LETT, V82, P303, DOI 10.1016/0304-3940(87)90273-4 PERONNET F, 1977, PROGR CLIN NEUROPHYS, V2, P130 REITE M, 1978, ELECTROEN CLIN NEURO, V45, P114, DOI 10.1016/0013-4694(78)90349-8 Rivier F, 1997, NEUROIMAGE, V6, P288, DOI 10.1006/nimg.1997.0304 Rockstroh B, 1998, NEUROREPORT, V9, P3819, DOI 10.1097/00001756-199812010-00010 TIIHONEN J, 1989, AUDIOLOGY, V28, P37 Weisbrod M, 2000, BIOL PSYCHIAT, V47, P51, DOI 10.1016/S0006-3223(99)00218-8 NR 45 TC 57 Z9 59 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 153 EP 160 DI 10.1016/S0378-5955(00)00148-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500013 PM 10978832 ER PT J AU Hallworth, R Luduena, RF AF Hallworth, R Luduena, RF TI Differential expression of beta tubulin isotypes in the adult gerbil cochlea SO HEARING RESEARCH LA English DT Article DE beta tubulin isotype; organ of Corti; hair cell; pillar cell; Deiters cell; multi-tubulin hypothesis ID MONOCLONAL-ANTIBODY; HAIR-CELLS; EPITHELIAL-CELLS; SUPPORTING CELLS; BOVINE BRAIN; F-ACTIN; MICROTUBULES; ORGAN; CORTI; GENE AB Tubulin, the principal component of microtubules, exists as two polypeptides, termed alpha and beta. Seven isotypes of beta tubulin are known to exist in mammals. The distributions of four beta tubulin isotypes, beta(I), beta(II), beta(III) and beta(IV), have been examined in the adult cochlea by indirect immunofluorescence using isotype-specific antibodies. In the organ of Corti, outer hair cells contained only beta(I) and beta(IV) while inner hair cells contained only beta(I) and beta(II). Inner and outer pillar cells contained beta(II) and beta(IV), but Deiters cells contained those isotypes plus beta(I). Fine fibers in the inner spiral bundle, tunnel crossing fibers, and outer spiral fibers, probably efferent in character, contained beta(I), beta(II), and beta(III), but not beta(IV). In the spiral ganglion, the somas and axons of neurons contained all four isotypes, and the myelination of ganglion cells also contained beta(I). Fibers of the intraganglionic spiral bundle contained beta(I), beta(II), and beta(III). No antibody labeled the dendritic processes of spiral ganglion neurons. The differences in isotype distribution in organ of Corti and neurons described here are consistent with and support the multi tubulin hypothesis, which states that tubulin isotypes are expressed specifically in different cell types and may therefore have different functions. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Texas, Hlth Sci Ctr, Dept Otolaryngol Head & Neck Surg, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Dept Biochem, San Antonio, TX 78229 USA. RP Hallworth, R (reprint author), Univ Texas, Hlth Sci Ctr, Dept Otolaryngol Head & Neck Surg, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA. CR AHMAD S, 1991, BIOCHIM BIOPHYS ACTA, V1090, P252, DOI 10.1016/0167-4781(91)90112-Y Angelborg C, 1972, Acta Otolaryngol Suppl, V301, P49 BANERJEE A, 1992, J BIOL CHEM, V267, P5625 BANERJEE A, 1988, J BIOL CHEM, V263, P3029 BANERJEE A, 1990, J BIOL CHEM, V265, P1794 BURGOYNE RD, 1988, EMBO J, V7, P2311 Chu BY, 1998, PLANT MOL BIOL, V37, P785, DOI 10.1023/A:1006047129410 Fulton C, 1976, CELL MOTILITY, V3, P987 FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 Guinan Jr J.J., 1996, COCHLEA, P435 Gundersen GG, 1998, BIOL BULL, V194, P358, DOI 10.2307/1543112 Hallworth R, 1998, MOL BIOL CELL, V9, p151A HALLWORTH RJ, 2000, HEARING RES, V1369, P31 Hoffman PN, 1996, BRAIN RES, V742, P329, DOI 10.1016/S0006-8993(96)00980-8 Iurato S, 1967, SUBMICROSCOPIC STRUC JOSHI HC, 1989, J CELL BIOL, V109, P663, DOI 10.1083/jcb.109.2.663 Joshi HC, 1998, CURR OPIN CELL BIOL, V10, P35, DOI 10.1016/S0955-0674(98)80084-7 KELLY RB, 1990, CELL, V61, P5, DOI 10.1016/0092-8674(90)90206-T KIKUCHI T, 1991, ACTA OTO-LARYNGOL, V111, P286, DOI 10.3109/00016489109137389 KUHN B, 1995, HEARING RES, V84, P139, DOI 10.1016/0378-5955(95)00021-U LEE MK, 1990, CELL MOTIL CYTOSKEL, V17, P118, DOI 10.1002/cm.970170207 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LOPATA MA, 1987, J CELL BIOL, V105, P1707, DOI 10.1083/jcb.105.4.1707 Lu Q, 1998, ADV STR BIO, V5, P203 Luduena RF, 1998, INT REV CYTOL, V178, P207 MENEZES JRL, 1994, J NEUROSCI, V14, P5399 MOODY SA, 1989, J COMP NEUROL, V279, P567, DOI 10.1002/cne.902790406 MOSKOWITZ PF, 1993, J NEUROSCI RES, V34, P129, DOI 10.1002/jnr.490340113 NADOL JB, 1994, HEARING RES, V81, P49, DOI 10.1016/0378-5955(94)90152-X NAGLE BW, 1986, INVEST OPHTH VIS SCI, V27, P689 RAPHAEL Y, 1994, HEARING RES, V76, P173, DOI 10.1016/0378-5955(94)90098-1 RENTHAL R, 1993, CELL MOTIL CYTOSKEL, V25, P19, DOI 10.1002/cm.970250104 Roach MC, 1998, CELL MOTIL CYTOSKEL, V39, P273 SAITO K, 1982, J ELECT MICROSC, V311, P278 SAVAGE C, 1989, GENE DEV, V3, P870, DOI 10.1101/gad.3.6.870 SLEPECKY N, 1983, HEARING RES, V10, P359, DOI 10.1016/0378-5955(83)90098-9 Slepecky N. B., 1996, COCHLEA, P44 Slepecky NB, 1995, HEARING RES, V91, P136, DOI 10.1016/0378-5955(95)00184-0 STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 Stone JS, 1996, J NEUROSCI, V16, P6157 SULLIVAN KF, 1986, MOL CELL BIOL, V6, P4409 TUCKER JB, 1993, CELL MOTIL CYTOSKEL, V25, P49, DOI 10.1002/cm.970250107 TUCKER JB, 1992, J CELL SCI, V102, P215 Walss C, 1998, MOL BIOL CELL, V9, p409A WANG D, 1986, J CELL BIOL, V103, P1903, DOI 10.1083/jcb.103.5.1903 Wilson PG, 1997, BIOESSAYS, V19, P451, DOI 10.1002/bies.950190603 WOLFE J, 1998, J ANTI-AGING MED, V1, P9, DOI 10.1089/rej.1.1998.1.9 NR 47 TC 27 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 161 EP 172 DI 10.1016/S0378-5955(00)00149-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500014 PM 10978833 ER PT J AU Loquet, G Campo, P Lataye, R Cossec, B Bonnet, P AF Loquet, G Campo, P Lataye, R Cossec, B Bonnet, P TI Combined effects of exposure to styrene and ethanol on the auditory function in the rat SO HEARING RESEARCH LA English DT Article DE styrene; ethanol; ototoxicity; potentiation; rat ID CHLORINATED HYDROCARBONS; ALCOHOL; TOLUENE; NEUROTOXICITY; METABOLISM; EXCRETION; RESPONSES; TOXICITY; COCHLEA; SYSTEM AB In order to study the auditory effects of a metabolic interaction between ethanol and styrene, a first group of rats was gavaged once a day with ethanol (4 g/kg), a second group was exposed to 750 ppm styrene by inhalation, and a third group was exposed to both ethanol and styrene (5 days/week, 4 weeks). Auditory function was tested by recording brainstem (inferior colliculus) auditory evoked potentials, and cochlear hair cell loss was estimated by light microscopy. Cytochrome P450 2E1 and the main urinary styrene metabolites, namely mandelic, phenylglyoxylic and hippuric acids, were measured by high-performance liquid chromatography to check the effects of ethanol on styrene metabolism. In our experimental conditions, ethanol alone did not have any effect on auditory sensitivity, whereas styrene alone caused permanent threshold shifts and outer hair cell damage. Hearing and outer hair cell losses were larger after the exposure to both ethanol and styrene than those induced by styrene alone, indicating a clear potentiation of styrene ototoxicity by ethanol. As expected, metabolic data showed that ethanol alters styrene metabolism and can therefore be considered a modifying factor of styrene toxicokinetics. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Inst Natl Rech & Secur, Lab Neurotox & Immunotox, F-54501 Vandoeuvre Nancy, France. RP Campo, P (reprint author), Inst Natl Rech & Secur, Lab Neurotox & Immunotox, Ave Bourgogne,POB 27, F-54501 Vandoeuvre Nancy, France. CR BERODE M, 1986, APPL IND HYG, V1, P25 BOND JA, 1989, CRIT REV TOXICOL, V19, P227, DOI 10.3109/10408448909037472 Brondeau MT, 1999, HUM EXP TOXICOL, V18, P322, DOI 10.1191/096032799678840147 CALEBRESE G, 1996, INT ARCH OCC ENV HEA, V68, P219 Campo P, 1999, NEUROTOXICOL TERATOL, V21, P427, DOI 10.1016/S0892-0362(99)00010-0 Campo P, 1998, NEUROTOXICOL TERATOL, V20, P321, DOI 10.1016/S0892-0362(97)00093-7 CERNY S, 1990, INT ARCH OCC ENV HEA, V62, P243, DOI 10.1007/BF00379441 CHAKRABARTI S, 1991, ARCH TOXICOL, V65, P366, DOI 10.1007/BF02284258 Coccini T, 1996, ARCH TOXICOL, V70, P736, DOI 10.1007/s002040050334 CROFTON KM, 1994, HEARING RES, V80, P25, DOI 10.1016/0378-5955(94)90005-1 Engelke M, 1996, TOXICOL IN VITRO, V10, P111, DOI 10.1016/0887-2333(95)00103-4 FECHTER LD, 1995, OCCUP MED, V10, P609 GUILLEMIN MP, 1988, AM IND HYG ASSOC J, V49, P497, DOI 10.1080/15298668891380123 HUNGUND BL, 1993, ALCOHOL CLIN EXP RES, V17, P329, DOI 10.1111/j.1530-0277.1993.tb00771.x KATBAMNA B, 1993, BIOL PSYCHIAT, V33, P750, DOI 10.1016/0006-3223(93)90127-Y KOHN J, 1995, TOXICOL LETT, V75, P29, DOI 10.1016/0378-4274(94)03153-X Loquet G, 1999, NEUROTOXICOL TERATOL, V21, P689, DOI 10.1016/S0892-0362(99)00030-6 LOWRY OH, 1951, J BIOL CHEM, V193, P265 LUKAS SE, 1990, ALCOHOL, V7, P471, DOI 10.1016/0741-8329(90)90034-A MILLER RR, 1994, CRIT REV TOXICOL, V24, pS1, DOI 10.3109/10408449409020137 MOLLER C, 1990, SCAND J WORK ENV HEA, V16, P189 MORGAN DL, 1993, FUND APPL TOXICOL, V20, P325, DOI 10.1006/faat.1993.1042 MUIJSER H, 1988, TOXICOLOGY, V49, P331, DOI 10.1016/0300-483X(88)90016-9 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 NAKAJIMA T, 1994, BIOCHEM PHARMACOL, V48, P637 NAKAJIMA T, 1993, IARC SCI PUBL, V127, P101 NYLEN P, 1994, ARBETE HALSA, V3, P1 NYLEN P, 1995, PHARMACOL TOXICOL, V76, P107 Peoples RW, 1996, ANNU REV PHARMACOL, V36, P185 ROSENGREN LE, 1989, BRIT J IND MED, V46, P316 SATO A, 1980, BRIT J IND MED, V37, P382 SATO A, 1981, TOXICOL APPL PHARM, V60, P8, DOI 10.1016/0041-008X(81)90129-0 SIKKEMA J, 1995, MICROBIOL REV, V59, P201 SQUIRES KC, 1978, SCIENCE, V201, P174, DOI 10.1126/science.208148 Sumner S.J., 1994, CRIT REV TOXICOL, V24, P11, DOI 10.3109/10408449409020138 WILSON HK, 1983, BRIT J IND MED, V40, P75 YANO BL, 1992, TOXICOL PATHOL, V20, P1 NR 37 TC 17 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 173 EP 180 DI 10.1016/S0378-5955(00)00151-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500015 PM 10978834 ER PT J AU Alagramam, KN Zahorsky-Reeves, J Wright, CG Pawlowski, KS Erway, LC Stubbs, L Woychik, RP AF Alagramam, KN Zahorsky-Reeves, J Wright, CG Pawlowski, KS Erway, LC Stubbs, L Woychik, RP TI Neuroepithelial defects of the inner ear in a new allele of the mouse mutation Ames waltzer SO HEARING RESEARCH LA English DT Article DE inner ear; mouse mutant; Ames waltzer ID HEREDITARY HEARING-LOSS; COCHLEAR HAIR-CELLS; INSERTIONAL MUTATION; MICE; DEAFNESS; GENES; MOUSE-CHROMOSOME-10; STRAINS AB This report presents new findings regarding a recessive insertional mutation in the transgenic line TgN2742Rpw that causes deafness and circling behavior in mice homozygous for the mutation. The mutant locus was mapped to a region on mouse chromosome 10 close to three spontaneous recessive mutations causing deafness: Ames waltzer (av), Waltzer (v), and Jackson circler (jc) Complementation testing revealed that the TgN2742Rpw mutation is allelic with av. Histological and auditory brainstem response (ABR) evaluation of animals that have the new allele balanced with the av(J) allele (called compound heterozygotes, TgN2742Rpw/av(J)) supports our genetic analysis. ABR evaluation shows complete absence of auditory response throughout the life span of TgN2742Rpw/av(J) compound heterozygotes. Scanning electron microscopy revealed abnormalities of inner and outer hair cell stereocilia in the cochleae of TgN2742Rpw mutants at 10 days after bi;th (DAB). The organ of Corti subsequently undergoes degeneration, leading to nearly complete loss of the cochlear neuroepithelium in older mutants by about 50 DAB. The vestibular neuroepithelia remain morphologically normal until at least 30 DAB. However, by 50 days, degenerative changes are evident in the saccular macula, which progresses to total loss of the saccular neuroepithelium in older animals. The new allele of av reported here will be designated av(TgN2742Rpw). (C) 2000 Elsevier Science B.V. All rights reserved. C1 Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA. Univ Tennessee, Dept Pathol, Knoxville, TN 37996 USA. Univ Texas, SW Med Ctr, Dept Otorhinolaryngol, Dallas, TX 75235 USA. Univ Cincinnati, Dept Biol Sci, Cincinnati, OH 45221 USA. Univ Calif Lawrence Livermore Natl Lab, Ctr Human Genome, Livermore, CA 94550 USA. RP Woychik, RP (reprint author), Pfizer Global Res & Dev, Alameda Labs, 1501 Harbor Bay Pkwy, Alameda, CA 94502 USA. CR Alagramam KN, 1999, GENETICS, V152, P1691 Avraham KB, 1998, NAT MED, V4, P1238, DOI 10.1038/3215 Burmeister M, 1998, MAMM GENOME, V8, pS200, DOI 10.1007/s003359900655 Chaib H, 1996, HUM MOL GENET, V5, P1061, DOI 10.1093/hmg/5.7.1061 COOK S, 1993, MOUSE GENOME, V91, P554 Deol M S, 1968, J Med Genet, V5, P137, DOI 10.1136/jmg.5.2.137 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Kalatzis V, 1998, HUM MOL GENET, V7, P1589, DOI 10.1093/hmg/7.10.1589 KITAMURA K, 1992, ACTA OTO-LARYNGOL, V112, P622, DOI 10.3109/00016489209137451 KITAMURA K, 1991, ACTA OTO-LARYNGOL, V111, P61, DOI 10.3109/00016489109137355 MEISLER MH, 1992, TRENDS GENET, V8, P341, DOI 10.1016/0168-9525(92)90278-C OSAKO S, 1971, ACTA OTO-LARYNGOL, V71, P365, DOI 10.3109/00016487109125376 PALMITER RD, 1986, ANNU REV GENET, V20, P465 Petit C, 1996, NAT GENET, V14, P385, DOI 10.1038/ng1296-385 Probst FJ, 1999, HEARING RES, V130, P1, DOI 10.1016/S0378-5955(98)00231-7 RAPHAEL Y, 1999, 22 MIDW ARO M SCHAIBLE RH, 1961, MOUSE NEWS LETT, V24, P38 SCHAIBLE RH, 1956, MOUSE NEWS LETT, V15, P29 SCHUKNECHT HF, 1993, PATHOLOGY EAR, P115 Self T, 1999, DEV BIOL, V214, P331, DOI 10.1006/dbio.1999.9424 Self T, 1998, DEVELOPMENT, V125, P557 SJOSTROM B, 1994, ORL J OTO-RHINO-LARY, V56, P119 Steel KP, 1995, ANNU REV GENET, V29, P675 Taylor BA, 1996, MAMM GENOME, V6, pS190 WAYNE S, 1996, HUM MOL GENET, V10, P1689 WAYNE S, 1997, AM J HUM GENET S, V61, P300 Zheng QY, 1999, HEARING RES, V130, P94, DOI 10.1016/S0378-5955(99)00003-9 Zobeley E, 1998, GENOMICS, V50, P260, DOI 10.1006/geno.1998.5298 NR 28 TC 35 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 181 EP 191 DI 10.1016/S0378-5955(00)00152-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500016 PM 10978835 ER PT J AU Keithley, EM Truong, T Chandronait, B Billings, PB AF Keithley, EM Truong, T Chandronait, B Billings, PB TI Immunohistochemistry and microwave decalcification of human temporal bones SO HEARING RESEARCH LA English DT Article DE auditory neuron; peripherin; cochlea; neurofilament ID SPIRAL GANGLION; RAPID DECALCIFICATION; PERIPHERIN; IMMUNOREACTIVITY; PROTEINS; SECTIONS; COCHLEA; TISSUES; RAT AB Processing of human temporal bones is a long, expensive process and the resulting celloidin sections are difficult to use for immunohistochemistry. We tested the ability of immunohistochemical assays to work in human temporal bones that were decalcified using a microwave oven. Tissue was trimmed to an approximate cube (1.5-2 cm/side) containing only the cochlea and immersed in fresh EDTA with paraformaldehyde every 6 h. This sized block required 190-400 h to decalcify. The decalcified tissue was embedded in paraffin and sectioned. Sections were immunoassayed with anti-cytochrome c oxidase, anti-neurofilament or anti-peripherin. All three antibodies labeled the appropriate structures. This procedure may stimulate advancement in the understanding of human inner ear pathology. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Diego, Dept Surg, Div Otolaryngol Head & Neck Surg, La Jolla, CA 92093 USA. RP Keithley, EM (reprint author), Univ Calif San Diego, Dept Surg, Div Otolaryngol Head & Neck Surg, 9500 Gilman Dr, La Jolla, CA 92093 USA. CR BERGLUND AM, 1991, J COMP NEUROL, V306, P393, DOI 10.1002/cne.903060304 BOON ME, 1988, MICROWAVE COOKBOOK P DESPRES G, 1994, ACTA OTO-LARYNGOL, V114, P377, DOI 10.3109/00016489409126073 Hafidi A, 1998, BRAIN RES, V805, P181, DOI 10.1016/S0006-8993(98)00448-X Hellström S, 1992, Acta Otolaryngol Suppl, V493, P15 Kaneko M, 1999, BIOTECH HISTOCHEM, V74, P49, DOI 10.3109/10520299909066477 Kovacs L, 1996, J PATHOL, V180, P106 KUIJPERS W, 1991, HEARING RES, V52, P133, DOI 10.1016/0378-5955(91)90193-D LEONG ASY, 1990, J PATHOL, V161, P327, DOI 10.1002/path.1711610409 Lysakowski A, 1999, HEARING RES, V133, P149, DOI 10.1016/S0378-5955(99)00065-9 Madden VJ, 1997, HEARING RES, V111, P76, DOI 10.1016/S0378-5955(97)00107-X NG KH, 1992, EUR J MORPHOL, V30, P150 ROMAND R, 1988, BRAIN RES, V462, P167, DOI 10.1016/0006-8993(88)90601-4 ROMAND R, 1990, HEARING RES, V49, P119, DOI 10.1016/0378-5955(90)90099-B Schuknecht HF, 1993, PATHOLOGY EAR, p[7, 417] Shiurba RA, 1998, BRAIN RES PROTOC, V2, P109, DOI 10.1016/S1385-299X(97)00029-9 Tian Q, 1999, ANN OTO RHINOL LARYN, V108, P47 Ylikoski J, 1993, Acta Otolaryngol Suppl, V503, P121 NR 18 TC 12 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 192 EP 196 DI 10.1016/S0378-5955(00)00153-2 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500017 PM 10978836 ER PT J AU Sliwinska-Kowalska, M Rzadzinska, A Jedlinska, U Rajkowska, E AF Sliwinska-Kowalska, M Rzadzinska, A Jedlinska, U Rajkowska, E TI Hair cell regeneration in the chick basilar papilla after exposure to wide-band noise: evidence for ganglion cell involvement SO HEARING RESEARCH LA English DT Article DE regeneration; hair cell; ganglion cell; wide-band noise; chick ID LIGHT-MICROSCOPIC EVIDENCE; AVIAN INNER-EAR; ACOUSTIC TRAUMA; INTENSE SOUND; TECTORIAL MEMBRANE; DNA-REPLICATION; COCHLEA; GENTAMICIN; RECOVERY; DAMAGE AB Tt has been demonstrated that the auditory epithelium in the chick basilar papilla may regenerate after acoustic or ototoxic damage. Both types of damage may elicit the appearance of new cells that may develop in to the sensory cells. Factors inducing this process and the role of ganglion cells, the first neuron cells in the auditory pathway, are still unknown. The pattern of auditory damage and regeneration, after octave-band and pure-tone noise exposure, has been well established in research studies on chicks, but there are scarce data on wide-band noise effects. The aim of this study was to investigate the effect of wide-band noise, with different exposure levels applied, on the chick basilar papilla and supporting cells. Further, it was also aimed to determine whether the proliferation of ganglion cells, after wide-band noise exposure, occurs. The morphological changes were assessed with fluorescent, light, and transmission electron microscopy. Cell proliferation was studied based on immunoreactivity assays of proliferating cell nuclear antigen (PCNA). The exposure to wide-hand noise at 120 dB SPL for 72 h produced stripe-like lesion of tall hair cells along the neural edge of the basilar papilla, mainly in the middle and, at the lesser extend, in its proximal part. There was no patch-like damage to the region of short hair cells, commonly observed after the exposure to the octave-band or pure-tone noise. The lesion extend depended on the level of exposure. The lower equivalent levels of noise (120 dB SPL for 40 h intermittent exposure) produced proportionally less damage. No morphological changes at light and fluorescent microscopy (apart from tectorial membrane exfoliation) were observed at 110 dB SPL in case of 20 h intermittent exposure. The elimination of dying hair cells took place either by pulling a damaged cell down to the basilar membrane or by extruding the cell to the subtectorial space. New hair cells reappeared at the sensory epithelium on the fifth day after the end of exposure. Cell proliferation started prior to hair cell loss. PCNA-like immunoreactivity was observed after the exposure at all levels in both the damaged and intact areas. PCNA appeared not only in the supporting cells, as indicated in previous studies, but also in the ganglion cells, suggesting ganglion cell involvement in the process of regeneration. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Nofer Inst Occupat Med, Dept Phys Hazards, PL-90950 Lodz, Poland. Nofer Inst Occupat Med, Dept Pathomorphol, PL-90950 Lodz, Poland. RP Sliwinska-Kowalska, M (reprint author), Nofer Inst Occupat Med, Dept Phys Hazards, Teresy St 8, PL-90950 Lodz, Poland. RI Sliwinska-Kowalska, Mariola/F-6119-2010 OI Sliwinska-Kowalska, Mariola/0000-0001-7569-3882 CR Adler HJ, 1996, NEUROSCI LETT, V205, P17, DOI 10.1016/0304-3940(96)12367-3 BHAVE SA, 1995, J NEUROSCI, V15, P4618 BRAVO R, 1987, J CELL BIOL, V105, P1549, DOI 10.1083/jcb.105.4.1549 CHEN L, 1994, HEARING RES, V81, P130, DOI 10.1016/0378-5955(94)90160-0 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1992, EXP NEUROL, V115, P7, DOI 10.1016/0014-4886(92)90212-9 COTANCHE DA, 1987, HEARING RES, V30, P197, DOI 10.1016/0378-5955(87)90136-5 COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 COTANCHE DA, 1992, EXP NEUROL, V115, P23, DOI 10.1016/0014-4886(92)90215-C Cotanche DA, 1997, ANN OTO RHINOL LARYN, V106, P9 COTANCHE DA, 1990, HEARING RES, V46, P29, DOI 10.1016/0378-5955(90)90137-E CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 FAIRMAN MP, 1990, J CELL SCI, V95, P1 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 HASHINO E, 1993, J CELL SCI, V105, P23 HASHINO E, 1992, P SENDAI S, V2, P63 Janas JD, 1995, HEARING RES, V92, P17, DOI 10.1016/0378-5955(95)00190-5 KIJAKAWA H, 1997, J NEUROCYTOL, V26, P501 Lee KH, 1996, HEARING RES, V94, P1, DOI 10.1016/0378-5955(95)00220-0 MARSH RR, 1990, HEARING RES, V46, P229, DOI 10.1016/0378-5955(90)90004-9 OESTERLE EC, 1993, HEARING RES, V66, P213, DOI 10.1016/0378-5955(93)90141-M PUGLIANO FA, 1993, NEUROSCI LETT, V151, P214, DOI 10.1016/0304-3940(93)90023-E RAPHAEL Y, 1993, J COMP NEUROL, V330, P521, DOI 10.1002/cne.903300408 RAPHAEL Y, 1991, HEARING RES, V53, P173, DOI 10.1016/0378-5955(91)90052-B RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 Roberson DW, 1996, AUDIT NEUROSCI, V2, P195 RUBEL EW, 1982, ACTA OTO-LARYNGOL, V93, P31, DOI 10.3109/00016488209130849 RYALS BM, 1985, HEARING RES, V19, P135, DOI 10.1016/0378-5955(85)90117-0 RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N Ryals BM, 1999, HEARING RES, V131, P71, DOI 10.1016/S0378-5955(99)00022-2 RYALS BM, 1994, HEARING RES, V72, P81, DOI 10.1016/0378-5955(94)90208-9 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A STONE JS, 1994, J COMP NEUROL, V341, P50, DOI 10.1002/cne.903410106 STONE JS, 1992, J CELL SCI, V102, P671 TSUE TT, 1994, P NATL ACAD SCI USA, V91, P1584, DOI 10.1073/pnas.91.4.1584 UMEMOTO M, 1995, CELL TISSUE RES, V281, P435, DOI 10.1007/s004410050440 NR 36 TC 6 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 197 EP 212 DI 10.1016/S0378-5955(00)00154-4 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500018 PM 10978837 ER PT J AU Yoshida, N Liberman, MC AF Yoshida, N Liberman, MC TI Sound conditioning reduces noise-induced permanent threshold shift in mice SO HEARING RESEARCH LA English DT Article DE sound conditioning; acoustic trauma; noise-induced hearing loss; protection ID INDUCED HEARING-LOSS; ACOUSTIC INJURY; ACQUIRED-RESISTANCE; TRAUMATIC EXPOSURE; PROTECTION; STIMULUS AB The phenomenon of conditioning-related protection, whereby prior exposure to moderate-level, non-traumatic, sound protects the ear from subsequent traumatic exposure, has been documented in a number of mammalian species. To probe the molecular mechanisms underlying this effect, the mouse would be a useful model; however, a previous study reported no conditioning effects in this species (Fowler et al., 1995). In our study, mice (CBA/CaJ) were exposed to a traumatic octave-band noise (8-16 kHz at 100 dB SPL for 2 h) with, or without, prior exposure to a sound-conditioning protocol consisting of exposure to the same noise band at lower sound pressure levels. Two conditioning protocols were investigated: one (81 dB SPL for 1 week) was analogous to those used in other conditioning studies in mammals; the second was significantly shorter (89 dB SPL for 15 min). Noise-induced permanent threshold shift (PTS) was assessed in a terminal experiment, after the traumatic exposure, via compound action potentials. Neither conditioning protocol elevated threshold, indeed both protocols increased amplitudes of distortion product otoacoustic emissions when animals were conditioned but not traumatized. Both conditioning exposures significantly reduced PTS from the subsequent traumatic exposure, compared to groups exposed without prior conditioning. Protective effects of 15-min conditioning were maximal when the condition-trauma interval was 24 h; protection disappeared when the traumatic exposure was presented 48 h after conditioning. These data are consistent with the view that protein synthesis is required for expression of the protective effect. The enhancement of distortion products in the condition-only state suggests that conditioning changes outer hair cell function. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA. Tohoku Univ, Sch Med, Dept Otolaryngol, Sendai, Miyagi 9808574, Japan. RP Liberman, MC (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA. CR Bobbin R P, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P299 CAMPO P, 1991, HEARING RES, V55, P195, DOI 10.1016/0378-5955(91)90104-H CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 Canlon B, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P118 CANLON B, 1991, PHYSL MORPHOLOGIC AS CANLON B, 1993, NEUROSCI LETT, V150, P103, DOI 10.1016/0304-3940(93)90118-5 FOWLER T, 1995, HEARING RES, V88, P1, DOI 10.1016/0378-5955(95)00062-9 Kujawa SG, 1997, J NEUROPHYSIOL, V78, P3095 KUJAWA SG, 1996, ABSTR ASS RES OT, V19, P34 LINDQUIST S, 1994, BIOL HEAT SHOCK PROT Morimoto R. I, 1994, BIOL HEAT SHOCK PROT Pukkila M, 1997, Acta Otolaryngol Suppl, V529, P59 RYAN AF, 1994, HEARING RES, V72, P23, DOI 10.1016/0378-5955(94)90201-1 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 Subramaniam M, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P128 SUBRAMANIAM M, 1992, HEARING RES, V58, P57, DOI 10.1016/0378-5955(92)90008-B Yamasoba T, 1999, HEARING RES, V127, P31, DOI 10.1016/S0378-5955(98)00178-6 Yoshida N, 2000, HEARING RES, V141, P97, DOI 10.1016/S0378-5955(99)00210-5 Yoshida N, 1999, J NEUROSCI, V19, P10116 Zheng XY, 1997, HEARING RES, V104, P191, DOI 10.1016/S0378-5955(96)00187-6 NR 20 TC 45 Z9 51 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 2000 VL 148 IS 1-2 BP 213 EP 219 DI 10.1016/S0378-5955(00)00161-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 354DX UT WOS:000089315500019 PM 10978838 ER PT J AU Kubke, MF Carr, CE AF Kubke, MF Carr, CE TI Development of the auditory brainstem of birds: comparison between barn owls and chickens SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE bird; cochlear nucleus; nucleus laminaris; magnocellularis; angularis ID AVIAN COCHLEAR NUCLEUS; INTERAURAL TIME DIFFERENCES; SELECTIVE GLUTAMATE RECEPTORS; SUPERIOR OLIVARY NUCLEUS; D-ASPARTATE RECEPTORS; SYNAPTIC TRANSMISSION; COINCIDENCE DETECTION; INFERIOR COLLICULUS; N-LAMINARIS; AMPA RECEPTORS AB Birds have proved to be extremely useful models for the study of hearing function. In particular, chickens and barn owls have been widely used by a number of researchers to study diverse aspects of auditory function. These studies have benefited from the advantages offered by each of these two species, including differences of auditory specialization. Direct comparisons between chickens and barn owls become complicated when the degree of auditory specialization and their modes of development are brought into consideration. In this article we review the available literature on the development of the auditory brainstem of chickens and barn owls in the context of such differences. In addition, we present a time line constructed on the basis of common stages of structural differentiation, rather than chronological time. We suggest that such a time line should be considered when discussing comparative data between these two species. Such an approach should facilitate the interpretation of similarities and differences observed in the developmental processes of the auditory system of chickens and barn owls. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Maryland, Dept Biol, College Pk, MD 20742 USA. RP Kubke, MF (reprint author), Univ Maryland, Dept Biol, College Pk, MD 20742 USA. RI Kubke, Maria Fabiana/E-2472-2011; Kubke, M Fabiana/H-3320-2012 CR Agmon-Snir H, 1998, NATURE, V393, P268 Aleksandrov L I, 1992, Neurosci Behav Physiol, V22, P132, DOI 10.1007/BF01192385 Ariens Kappers CU, 1967, COMP ANATOMY NERVOUS BENNETT PM, 1985, J ZOOL, V207, P491 BENNETT PM, 1985, J ZOOL, V207, P151 BOOK KJ, 1990, J COMP NEUROL, V297, P55, DOI 10.1002/cne.902970105 BOORD RL, 1969, ANN NY ACAD SCI, V167, P186, DOI 10.1111/j.1749-6632.1969.tb20444.x BRAINARD MS, 1993, J NEUROSCI, V13, P4589 BUCKLEY K, 1985, J CELL BIOL, V100, P1284, DOI 10.1083/jcb.100.4.1284 Caicedo A, 1997, J COMP NEUROL, V378, P1, DOI 10.1002/(SICI)1096-9861(19970203)378:1<1::AID-CNE1>3.0.CO;2-8 CAJAL CRY, 1999, TEXTURA SISTEMA NERV, V1, P566 CALFORD MB, 1988, J COMP PHYSIOL A, V162, P503, DOI 10.1007/BF00612515 CARR C, 2000, COMP HEARING BIRDS R CARR CE, 1994, 10 INT S HEAR Carr CE, 1996, J COMP NEUROL, V373, P467, DOI 10.1002/(SICI)1096-9861(19960930)373:4<467::AID-CNE1>3.0.CO;2-# CARR CE, 1989, J COMP NEUROL, V286, P190, DOI 10.1002/cne.902860205 CARR CE, 1993, J COMP NEUROL, V334, P337, DOI 10.1002/cne.903340302 CARR CE, 1991, J COMP NEUROL, V314, P306, DOI 10.1002/cne.903140208 CARR CE, 1996, P 24 GOTT NEUR C CARR CE, 1990, J NEUROSCI, V10, P3227 CARR CE, 1988, P NATL ACAD SCI USA, V85, P8311, DOI 10.1073/pnas.85.21.8311 CARR CE, 1998, PSYCHOPHYSICAL PHYSL, P344 CONLEE JW, 1983, J COMP NEUROL, V217, P216, DOI 10.1002/cne.902170208 CONLEE JW, 1986, BRAIN RES, V367, P96, DOI 10.1016/0006-8993(86)91583-0 Craigie EH, 1930, J COMP NEUROL, V49, P223, DOI 10.1002/cne.900490202 Craigie EH, 1928, J COMP NEUROL, V45, P377, DOI 10.1002/cne.900450203 Fay R. R., 1988, HEARING VERTEBRATES Fay R.R., 1987, P179 Feldman DE, 1996, SCIENCE, V271, P525, DOI 10.1126/science.271.5248.525 FELDMAN DE, 1994, J NEUROSCI, V14, P5939 FINLAY BL, 1995, SCIENCE, V268, P1578, DOI 10.1126/science.7777856 GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 GILLAND E, 1993, ACTA ANAT, V148, P110 GILLAND EH, 1992, THESIS HARVARD U HACK NJ, 2000, J NEUROSCI HAMBURGER V, 1951, J MORPHOL, V88, P49, DOI 10.1002/jmor.1050880104 HARESIGN T, 1988, AUK, V105, P699 HARKMARK W, 1954, J COMP NEUROL, V100, P115, DOI 10.1002/cne.901000107 HYSON RL, 1994, HEARING RES, V81, P109, DOI 10.1016/0378-5955(94)90158-9 JACKSON H, 1985, NEUROSCIENCE, V16, P171, DOI 10.1016/0306-4522(85)90054-5 JACKSON H, 1988, J COMP NEUROL, V271, P106, DOI 10.1002/cne.902710111 JACKSON H, 1982, J NEUROSCI, V2, P1736 JACKSON H, 1982, J COMP NEUROL, V210, P80, DOI 10.1002/cne.902100109 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 JHAVERI S, 1982, NEUROSCIENCE, V7, P837, DOI 10.1016/0306-4522(82)90046-X JHAVERI S, 1982, NEUROSCIENCE, V7, P855, DOI 10.1016/0306-4522(82)90047-1 JHAVERI S, 1982, NEUROSCIENCE, V7, P809, DOI 10.1016/0306-4522(82)90045-8 JOSEPH AW, 1993, J NEUROPHYSIOL, V69, P1197 KNOWLTON VY, 1967, J MORPHOL, V121, P179, DOI 10.1002/jmor.1051210302 KNUDSEN EI, 1983, J COMP NEUROL, V218, P174, DOI 10.1002/cne.902180205 KNUDSEN EI, 1984, J NEUROSCI, V4, P1001 KNUDSEN EI, 1983, SCIENCE, V222, P939, DOI 10.1126/science.6635667 KNUDSEN EI, 1995, ANNU REV NEUROSCI, V18, P19, DOI 10.1146/annurev.neuro.18.1.19 KNUDSEN EI, 1978, SCIENCE, V200, P795, DOI 10.1126/science.644324 KONISHI M, 1985, ANNU REV NEUROSCI, V8, P125 KONISHI M, 1970, Z VERGL PHYSIOL, V66, P257, DOI 10.1007/BF00297829 KONISHI M, 1999, NEURAL CODES DISTRIB, P1 KONISHI M, 1973, AM SCI, V61, P414 KOPPL C, 1994, J COMP NEUROL, V339, P438, DOI 10.1002/cne.903390310 Koppl C, 1997, J COMP NEUROL, V378, P265 Kubke MF, 1998, BIOL BULL, V195, P218, DOI 10.2307/1542848 Kubke MF, 1998, MICROSC RES TECHNIQ, V41, P176 Kubke MF, 1999, J COMP NEUROL, V415, P189, DOI 10.1002/(SICI)1096-9861(19991213)415:2<189::AID-CNE4>3.0.CO;2-E LACHICA EA, 1994, J COMP NEUROL, V348, P403, DOI 10.1002/cne.903480307 LARSEN ON, 1997, DIVERSITY AUDITORY M, P253 LEVIMONTALCINI R, 1949, J COMP NEUROL, V91, P209, DOI 10.1002/cne.900910204 Levin MD, 1997, J COMP NEUROL, V378, P239, DOI 10.1002/(SICI)1096-9861(19970210)378:2<239::AID-CNE7>3.0.CO;2-4 LEWIS B, 1980, TRENDS NEUROSCI, V5, P102 LUMSDEN A, 1989, NATURE, V337, P424, DOI 10.1038/337424a0 MARIN F, 1995, EUR J NEUROSCI, V7, P1714, DOI 10.1111/j.1460-9568.1995.tb00693.x MASSOGLIA D, 1997, THESIS U MARYLAND MASTERTON B, 1975, J COMP PHYSIOL PSYCH, V89, P379, DOI 10.1037/h0077034 Meyer SU, 1995, ZOOL-ANAL COMPLEX SY, V99, P103 MOISEFF A, 1983, J NEUROSCI, V3, P2553 MOISEFF A, 1981, J COMP PHYSIOL, V144, P299 MOSBACHER J, 1994, SCIENCE, V266, P1059, DOI 10.1126/science.7973663 NAKANISHI S, 1992, SCIENCE, V258, P597, DOI 10.1126/science.1329206 NEMETH EF, 1983, NEUROSCI LETT, V40, P39, DOI 10.1016/0304-3940(83)90089-7 NEMETH EF, 1985, NEUROSCI LETT, V59, P297, DOI 10.1016/0304-3940(85)90148-X NORBERG R A, 1977, Philosophical Transactions of the Royal Society of London B Biological Sciences, V280, P375, DOI 10.1098/rstb.1977.0116 NORBERG RA, 1966, ARKIV ZOOLOGIE, V20, P181 OTIS TS, 1995, J PHYSIOL-LONDON, V482, P309 OVERHOLT EM, 1992, J NEUROSCI, V12, P1698 PARKS TN, 1975, J COMP NEUROL, V164, P435, DOI 10.1002/cne.901640404 PARKS TN, 1995, MOL BIOL HEAR DEAFN, V2, P124 Parks TN, 1997, J COMP NEUROL, V383, P112 PARKS TN, 1987, J COMP NEUROL, V260, P312, DOI 10.1002/cne.902600211 PARKS TN, 1978, J COMP NEUROL, V180, P435 PARKS TN, 1981, J COMP NEUROL, V202, P47, DOI 10.1002/cne.902020105 PARKS TN, 1984, J COMP NEUROL, V227, P459, DOI 10.1002/cne.902270315 PAYNE RS, 1971, J EXP BIOL, V54, P535 Pena JL, 1996, J NEUROSCI, V16, P7046 PLATT JB, 1889, B MUS COMP ZOOL HARV, V17, P171 PUELLES L, 1994, J COMP NEUROL, V340, P98, DOI 10.1002/cne.903400108 RAMAN IM, 1992, NEURON, V9, P173, DOI 10.1016/0896-6273(92)90232-3 RAMAN IM, 1994, J NEUROSCI, V14, P4998 Ramon y Cajal S, 1908, TRAB LAB INVEST BIOL, V6, P195 RAVINDRANATHAN A, 1996, ARO ABSTR, V19, P88 Ravindranathan A, 1997, MOL BRAIN RES, V50, P143, DOI 10.1016/S0169-328X(97)00179-4 Ravindranathan A, 1996, NEUROREPORT, V7, P2707, DOI 10.1097/00001756-199611040-00060 ROSOWSKI JJ, 1980, J COMP PHYSIOL, V136, P183 Rubel EW, 1988, BRAIN FUNCTION, P3 RUBEL EW, 1975, J COMP NEUROL, V164, P411, DOI 10.1002/cne.901640403 RUBEL EW, 1976, J COMP NEUROL, V166, P469, DOI 10.1002/cne.901660408 RYUGO DK, 1982, J COMP NEUROL, V210, P239, DOI 10.1002/cne.902100304 Sanders EB, 1929, J COMP NEUROL, V49, P155, DOI 10.1002/cne.900490104 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SAUNDERS JC, 1974, MIN OTO, V24, P221 Schwab M.E., 1979, BIOL REPTILIA, V10, P201 SMITH DJ, 1979, J COMP NEUROL, V186, P213, DOI 10.1002/cne.901860207 SMITH ZDJ, 1981, J COMP NEUROL, V203, P309, DOI 10.1002/cne.902030302 Starck J.M., 1993, Current Ornithology, V10, P275 SULLIVAN WE, 1984, J NEUROSCI, V4, P1787 SULLIVAN WE, 1986, P NATL ACAD SCI USA, V83, P8400, DOI 10.1073/pnas.83.21.8400 TAKAHASHI T, 1984, J NEUROSCI, V4, P1781 TAKAHASHI TT, 1987, J NEUROSCI, V7, P1843 TAKAHASHI TT, 1988, J COMP NEUROL, V274, P190, DOI 10.1002/cne.902740206 TAKAHASHI TT, 1988, J COMP NEUROL, V274, P212, DOI 10.1002/cne.902740207 Tello J. F., 1923, Travaux du Laboratoire de Recherches Biologiques Universite de Madrid, V21, P1 Viete S, 1997, J NEUROSCI, V17, P1815 VOLMAN SF, 1990, BRAIN BEHAV EVOLUT, V36, P154, DOI 10.1159/000115304 WARCHOL ME, 1990, J COMP PHYSIOL A, V166, P721 WEINBERGER NM, 1969, EXPERIENTIA, V26, P46 WESTERBERG BD, 1995, J OTOLARYNGOL, V24, P20 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 WINSKY L, 1995, J COMP NEUROL, V354, P564, DOI 10.1002/cne.903540407 WINTER P, 1961, EXPERIENTIA, V17, P515, DOI 10.1007/BF02158630 Yang LC, 1999, J NEUROSCI, V19, P2313 YOUNG SR, 1983, J NEUROSCI, V3, P1373 ZHANG S, 1994, J NEUROPHYSIOL, V72, P705 Zhou N, 1995, NEUROREPORT, V6, P2273, DOI 10.1097/00001756-199511270-00002 ZHOU N, 1991, HEARING RES, V52, P195, DOI 10.1016/0378-5955(91)90199-J NR 132 TC 41 Z9 41 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 1 EP 20 DI 10.1016/S0378-5955(00)00116-7 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200002 PM 10962169 ER PT J AU Richardson, FC Kaczmarek, LK AF Richardson, FC Kaczmarek, LK TI Modification of delayed rectifier potassium currents by the Kv9.1 potassium channel subunit SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE inferior colliculus; shaker; potassium channel; Kv2.1 ID ALPHA-SUBUNITS; K+ CHANNEL; RAT-BRAIN; SHAB; SUBFAMILY AB Within auditory pathways, the intrinsic electrical properties of neurons, and in particular their complement of potassium channels, play a key role in shaping the timing and pattern of action potentials produced by sound stimuli. The Kv9.1 gene encodes a potassium channel alpha subunit that is expressed in a variety of neurons, including those of the inferior colliculus. When cRNA encoding this subunit is injected into Xenopus oocytes, no functional channels are expressed. When, however, Kv9.1 is co-expressed with certain other alpha potassium channel subunits, it changes the characteristics of the currents produced by these functional channel proteins. We have found that Kv9.1 isolated from a rat brain cDNA library alters the kinetics and the Voltage-dependence of activation and inactivation of Kv2.1, a channel subunit that generates slowly inactivating delayed rectifier potassium currents. The rate of activation of Kv2.1 is slowed by co-expression with Kv9.1. With Kv2.1 alone, the amplitude of evoked currents increases monotonically with increasing command potentials. In contrast, when Kv2.1 is co-expressed with Kv9.1, the amplitude of currents increases with increasing depolarization up to potentials of only similar to+60 mV, after which increasing depolarization results in a decrease in current amplitude. Currents produced by Kv2.1 alone and by Kv2.1/Kv9.1 are both sensitive to the potassium channel blocker tetraethyl ammonium ions (TEA), but higher concentrations of TEA (20 mM) eliminate the biphasic voltage-dependence of the Kv2.1/Kv9.1 currents. Co-expression with Kv9.1 also produces an apparent negative shift in the voltage-dependence of inactivation and activation. Computer simulations of model neurons suggest that co-expression of Kv9.1 with Kv2.1 may have different effects in neurons depending on whether their firing pattern is limited by the inactivation of inward currents. In excitable cells in which the inward currents do not inactivate, co-expression with Kv9.1 could produce an inhibition of firing during sustained depolarization. In contrast, in model neurons with rapidly inactivating inward current, the change in the voltage-dependence of activation produced by Kv9.1 may allow the cells to follow high frequency stimulation more effectively. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06520 USA. RP Kaczmarek, LK (reprint author), Yale Univ, Sch Med, Dept Pharmacol, 333 Cedar St, New Haven, CT 06520 USA. CR BECKH S, 1990, EMBO J, V9, P777 BOYLE MB, 1991, METHODS NEUROSCIENCE, V4, P157 Chandy K, 1995, HDB RECEPTORS CHANNE, P1 Doyle DA, 1998, SCIENCE, V280, P69, DOI 10.1126/science.280.5360.69 HEGINBOTHAM L, 1994, BIOPHYS J, V66, P1061 Hille B., 1992, IONIC CHANNELS EXCIT, V2nd Hugnot JP, 1996, EMBO J, V15, P3322 HWANG PM, 1993, J NEUROSCI, V13, P1569 ISACOFF EY, 1990, NATURE, V345, P530, DOI 10.1038/345530a0 Joiner WJ, 1998, NAT NEUROSCI, V1, P462, DOI 10.1038/2176 Levitan I.B., 1991, NEURON CELL MOL BIOL Liu SQJ, 1998, J NEUROSCI, V18, P8758 MACKINNON R, 1991, NATURE, V350, P232, DOI 10.1038/350232a0 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 Oliver D. L., 1991, NEUROBIOLOGY HEARING, P195 Patel AJ, 1997, EMBO J, V16, P6615, DOI 10.1093/emboj/16.22.6615 PERNEY TM, 1992, J NEUROPHYSIOL, V68, P756 Perney TM, 1997, J COMP NEUROL, V386, P178 Peruzzi D., 1994, Society for Neuroscience Abstracts, V20, P321 Richardson F. C., 1997, Society for Neuroscience Abstracts, V23, P1478 RUPPERSBERG JP, 1990, NATURE, V345, P535, DOI 10.1038/345535a0 Salinas M, 1997, J BIOL CHEM, V272, P24371, DOI 10.1074/jbc.272.39.24371 Salinas M, 1997, J BIOL CHEM, V272, P8774 Stocker M, 1999, J NEUROCHEM, V72, P1725, DOI 10.1046/j.1471-4159.1999.721725.x Stocker M, 1998, BIOCHEM BIOPH RES CO, V248, P927, DOI 10.1006/bbrc.1998.9072 Wang YL, 1998, FOLD DES, V3, P1, DOI 10.1016/S1359-0278(98)00003-0 WISGIRDA ME, 1996, SOC NEUR ABSTR, V22, P889 NR 27 TC 26 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 21 EP 30 DI 10.1016/S0378-5955(00)00117-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200003 PM 10962170 ER PT J AU Fitzakerley, JL Star, KV Rinn, JL Elmquist, BJ AF Fitzakerley, JL Star, KV Rinn, JL Elmquist, BJ TI Expression of Shal potassium channel subunits in the adult and developing cochlear nucleus of the mouse SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE auditory brainstem; development; ion channel; transient K+ channel; in situ hybridization; reverse transcription polymerase chain reaction ID GATED K+ CHANNELS; DEVELOPING RAT-BRAIN; A-TYPE; BETA-SUBUNIT; DEVELOPMENTAL EXPRESSION; FUNCTIONAL-CHARACTERIZATION; HETEROMULTIMERIC CHANNELS; SUBTHRESHOLD POTENTIALS; XENOPUS-OOCYTES; PYRAMIDAL CELLS AB The pattern of expression of potassium (K+) channel subunits is thought to contribute to the establishment of the unique discharge characteristics exhibited by cochlear nucleus (CN) neurons. This study describes the developmental distribution of mRNA for the three Shal channel subunits Kv4.1, Kv4.2 and Kv4.3 within the mouse CN. as assessed with in situ hybridization and RT-PCR techniques. Kv4.1 was not present in CN at any age. Kv4.2 mRNA was detectable as early as postnatal day 2 (P2) in all CN subdivisions, and continued to be constitutively expressed throughout development. Kv4.2 was abundantly expressed in a variety of CN cell types, including all of the major projection neuron classes (i.e., octopus, bushy, stellate, fusiform, and giant cells). In contrast, Kv4.3 was expressed at lower levels and by fewer cell types. Kv4.3-labeled cells were more prevalent in ventral subdivisions than in the dorsal CN. Kv4.3 expression was significantly delayed developmentally in comparison to Kv4.2, as it was detectable only after P14. Although the techniques employed in this study detect mRNA and not protein, it can be inferred from the differential distribution of Kv4 transcripts that CN neurons selectively regulate the expression of Shal K+ channels among individual neurons throughout development. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Minnesota, Sch Med, Dept Pharmacol, Duluth, MN 55812 USA. Univ Minnesota, Sch Med, Dept Med & Mol Physiol, Duluth, MN 55812 USA. RP Fitzakerley, JL (reprint author), Univ Minnesota, Sch Med, Dept Pharmacol, Duluth, MN 55812 USA. CR An WF, 2000, NATURE, V403, P553, DOI 10.1038/35000592 ATTALI B, 1993, J BIOL CHEM, V268, P24283 BALDWIN TJ, 1992, COLD SPRING HARB SYM, V57, P491 BALDWIN TJ, 1991, NEURON, V7, P471, DOI 10.1016/0896-6273(91)90299-F Baro DJ, 1997, J NEUROSCI, V17, P6597 BOSMA MM, 1993, J NEUROSCI, V13, P5242 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 Burger C, 1996, J NEUROSCI, V16, P1412 CANT NB, 1984, HEARING SCI RECENT A, P371 CASTELLINO RC, 1995, AM J PHYSIOL-HEART C, V269, pH385 CHABALA LD, 1993, J GEN PHYSIOL, V102, P713, DOI 10.1085/jgp.102.4.713 Chandy K, 1995, HDB RECEPTORS CHANNE, P1 CHANDY KG, 1991, NATURE, V352, P26, DOI 10.1038/352026b0 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 CHRISTIE MJ, 1990, NEURON, V4, P405, DOI 10.1016/0896-6273(90)90052-H CRITZ SD, 1993, J NEUROCHEM, V60, P1175, DOI 10.1111/j.1471-4159.1993.tb03273.x DECAMILLI P, 1984, NEUROSCIENCE, V11, P819, DOI 10.1016/0306-4522(84)90194-5 Du J, 1996, J NEUROSCI, V16, P506 Eder C, 1996, NEUROREPORT, V7, P1565, DOI 10.1097/00001756-199607080-00006 ENGLAND SK, 1995, P NATL ACAD SCI USA, V92, P6309, DOI 10.1073/pnas.92.14.6309 FITZAKERLEY JL, 1998, ARO ABSTR, V21, P213 Grigg JJ, 2000, HEARING RES, V140, P77, DOI 10.1016/S0378-5955(99)00187-2 GRISSMER S, 1994, MOL PHARMACOL, V45, P1227 Hallows JL, 1998, J NEUROSCI, V18, P5682 HEINEMANN S, 1994, J PHYSIOLOGY-PARIS, V88, P173, DOI 10.1016/0928-4257(94)90003-5 Heinemann SH, 1996, J PHYSIOL-LONDON, V493, P625 ISACOFF EY, 1990, NATURE, V345, P530, DOI 10.1038/345530a0 Kanold PO, 1999, J NEUROSCI, V19, P2195 LESAGE F, 1992, FEBS LETT, V310, P162, DOI 10.1016/0014-5793(92)81320-L LUNEAU CJ, 1991, P NATL ACAD SCI USA, V88, P3932, DOI 10.1073/pnas.88.9.3932 MAJUMDER K, 1995, FEBS LETT, V361, P13, DOI 10.1016/0014-5793(95)00120-X MALETICSAVATIC M, 1995, J NEUROSCI, V15, P3840 MANIS PB, 1990, J NEUROSCI, V10, P2338 MANIS PB, 1991, J NEUROSCI, V11, P2865 MATSUBARA H, 1991, J BIOL CHEM, V266, P13324 MCCORMACK K, 1990, BIOCHEM BIOPH RES CO, V171, P1361, DOI 10.1016/0006-291X(90)90836-C Oertel D, 1991, Curr Opin Neurobiol, V1, P221, DOI 10.1016/0959-4388(91)90082-I OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 PAK MD, 1991, P NATL ACAD SCI USA, V88, P4386, DOI 10.1073/pnas.88.10.4386 PARDO LA, 1992, P NATL ACAD SCI USA, V89, P2466, DOI 10.1073/pnas.89.6.2466 PERNEY TM, 1992, J NEUROPHYSIOL, V68, P756 Perney TM, 1997, J COMP NEUROL, V386, P178 REHM H, 1991, FASEB J, V5, P164 RETTIG J, 1994, NATURE, V369, P289, DOI 10.1038/369289a0 Ribera A B, 1992, Ion Channels, V3, P1 RIBERA AB, 1990, NEURON, V5, P691, DOI 10.1016/0896-6273(90)90223-3 ROBERDS SL, 1991, FEBS LETT, V284, P152, DOI 10.1016/0014-5793(91)80673-Q ROTHMAN JS, 1993, J NEUROPHYSIOL, V70, P2562 RUDY B, 1988, NEUROSCIENCE, V25, P729, DOI 10.1016/0306-4522(88)90033-4 RUPPERSBERG JP, 1990, NATURE, V345, P535, DOI 10.1038/345535a0 Serodio P, 1998, J NEUROPHYSIOL, V79, P1081 Serodio P, 1996, J NEUROPHYSIOL, V75, P2174 SERODIO P, 1994, J NEUROPHYSIOL, V72, P1516 Sheng M, 1995, PROG BRAIN RES, V105, P87 SHENG M, 1993, NATURE, V365, P72, DOI 10.1038/365072a0 Song WJ, 1998, J NEUROSCI, V18, P3124 Stephens GJ, 1996, FEBS LETT, V378, P250, DOI 10.1016/0014-5793(95)01469-1 STORM JF, 1990, PROG BRAIN RES, V83, P161 SWANSON R, 1990, NEURON, V4, P929, DOI 10.1016/0896-6273(90)90146-7 Takahashi K, 1998, PHYSIOL REV, V78, P307 TANAKA H, 1999, UNPUB TRIMMER JS, 1993, FEBS LETT, V324, P205, DOI 10.1016/0014-5793(93)81394-F TSUNODA S, 1995, J NEUROSCI, V15, P1741 Vullhorst D, 1998, FEBS LETT, V421, P259, DOI 10.1016/S0014-5793(97)01577-9 WANG H, 1993, NATURE, V365, P75, DOI 10.1038/365075a0 WANG H, 1994, J NEUROSCI, V14, P4588 Wang YL, 1998, FOLD DES, V3, P1, DOI 10.1016/S1359-0278(98)00003-0 WEI A, 1990, SCIENCE, V248, P599, DOI 10.1126/science.2333511 WEISER M, 1995, J PHYSL, V509, P183 WERKMAN TR, 1992, NEUROSCIENCE, V50, P935, DOI 10.1016/0306-4522(92)90216-O WU SH, 1987, HEARING RES, V30, P99 Xu HD, 1996, J GEN PHYSIOL, V108, P405, DOI 10.1085/jgp.108.5.405 YOKOYAMA S, 1989, FEBS LETT, V259, P37, DOI 10.1016/0014-5793(89)81488-7 Young E.D, 1984, HEARING SCI, P423 NR 74 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 31 EP 45 DI 10.1016/S0378-5955(00)00118-0 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200004 PM 10962171 ER PT J AU Sanes, DH Friauf, E AF Sanes, DH Friauf, E TI Development and influence of inhibition in the lateral superior olivary nucleus SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE superior olivary complex; glycine; gamma-aminobutyric acid; neurotransmission; dendrite ID AUDITORY BRAIN-STEM; SUBUNIT MESSENGER-RNA; ELECTRICAL MEMBRANE-PROPERTIES; GLYCINE RECEPTOR DISTRIBUTION; VENTRAL COCHLEAR NUCLEUS; POSTNATAL-DEVELOPMENT; DENDRITIC ARBORS; CORTICAL-NEURONS; DEVELOPING RATS; LIGAND-BINDING AB While studies of neuronal development and plasticity have focused on excitatory pathways, the inhibitory projection from the MNTB to the LSO provides a favorable model for studies of synaptic inhibition. This review covers recent studies from our laboratories indicating that inhibitory connections are quite dynamic during development, These findings suggest that there are two phases inhibitory transmission. During an initial depolarizing phase is growth and branching of pre- and postsynaptic elements in the LSO. During a second hyperpolarizing phase there is refinement of inhibitory afferent arborizations and the LSO dendrites that they innervate. (C) 2000 Elsevier Science B.V. All rights reserved. C1 NYU, Ctr Neural Sci, New York, NY 10016 USA. Univ Kaiserslautern, FB Biol, Abt Tierphysiol, D-67653 Kaiserslautern, Germany. RP Sanes, DH (reprint author), NYU, Ctr Neural Sci, 4 Washington Pl, New York, NY 10016 USA. RI Friauf, Eckhard/D-7529-2012 OI Friauf, Eckhard/0000-0002-1833-1698 CR Aponte JE, 1996, AUDIT NEUROSCI, V2, P235 BARBIN G, 1993, NEUROSCI LETT, V152, P1150 BECKER CM, 1988, EMBO J, V7, P3717 Behar TN, 1996, J NEUROSCI, V16, P1808 Boudreau J C, 1970, Contrib Sens Physiol, V4, P143 CORNER MA, 1992, DEV BRAIN RES, V65, P57, DOI 10.1016/0165-3806(92)90008-K Craig AM, 1996, J NEUROSCI, V16, P3166 Ehrlich I, 1999, J PHYSIOL-LONDON, V520, P121, DOI 10.1111/j.1469-7793.1999.00121.x Essrich C, 1998, NAT NEUROSCI, V1, P563 Friauf E, 1999, J COMP NEUROL, V412, P17 Friauf E, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P181, DOI 10.1007/978-1-4419-8712-9_17 Friauf E, 1997, J COMP NEUROL, V385, P117, DOI 10.1002/(SICI)1096-9861(19970818)385:1<117::AID-CNE7>3.0.CO;2-5 FRIAUF E, 1993, J COMP NEUROL, V334, P59, DOI 10.1002/cne.903340105 Friauf E, 1999, CELL TISSUE RES, V297, P187, DOI 10.1007/s004410051346 FRIAUF E, 1999, SOC NEUR ABSTR, V29, P571 FRIEDER B, 1985, J NEUROCHEM, V45, P37, DOI 10.1111/j.1471-4159.1985.tb05471.x Giustetto M, 1998, J COMP NEUROL, V395, P231, DOI 10.1002/(SICI)1096-9861(19980601)395:2<231::AID-CNE7>3.0.CO;2-3 HABLITZ JJ, 1989, BRAIN RES, V501, P332, DOI 10.1016/0006-8993(89)90650-1 JOHNSTON D, 1992, ANNU REV PHYSIOL, V54, P489 Kakazu Y, 1999, J NEUROSCI, V19, P2843 KANDLER K, 1995, EUR J NEUROSCI, V7, P1773, DOI 10.1111/j.1460-9568.1995.tb00697.x KANDLER K, 1995, J NEUROSCI, V15, P6890 KANDLER K, 1993, J COMP NEUROL, V328, P161, DOI 10.1002/cne.903280202 KIL J, 1995, J COMP NEUROL, V353, P317, DOI 10.1002/cne.903530302 KIM HY, 1993, J NEUROCHEM, V61, P2334, DOI 10.1111/j.1471-4159.1993.tb07481.x KITZES LM, 1995, J COMP NEUROL, V353, P341, DOI 10.1002/cne.903530303 Koch U, 1998, MICROSC RES TECHNIQ, V41, P263, DOI 10.1002/(SICI)1097-0029(19980501)41:3<263::AID-JEMT9>3.0.CO;2-U KOTAK VC, 2000, IN PRESS J NEUROSCI Kotak VC, 1998, J NEUROSCI, V18, P4646 Kotak VC, 1996, J NEUROSCI, V16, P1836 KUHSE J, 1990, J BIOL CHEM, V265, P22317 Kullmann P. H. M., 1999, Society for Neuroscience Abstracts, V25, P394 Kungel M, 1997, DEV BRAIN RES, V101, P107, DOI 10.1016/S0165-3806(97)00053-9 KUNGEL M, 1995, ANAT EMBRYOL, V191, P425, DOI 10.1007/BF00304428 LANGOSCH D, 1988, P NATL ACAD SCI USA, V85, P7394, DOI 10.1073/pnas.85.19.7394 Liu JP, 1997, J NEUROSCI RES, V49, P645, DOI 10.1002/(SICI)1097-4547(19970901)49:5<645::AID-JNR15>3.0.CO;2-U Lohmann C, 1998, J NEUROBIOL, V34, P97, DOI 10.1002/(SICI)1097-4695(19980205)34:2<97::AID-NEU1>3.0.CO;2-6 Lohmann C, 1996, J COMP NEUROL, V367, P90, DOI 10.1002/(SICI)1096-9861(19960325)367:1<90::AID-CNE7>3.0.CO;2-E Lohrke S, 1998, J NEUROBIOL, V36, P395 Lopez-Corcuera B, 1998, J NEUROCHEM, V71, P2211 MALENKA RC, 1993, TRENDS NEUROSCI, V16, P521, DOI 10.1016/0166-2236(93)90197-T MATTSON MP, 1989, BRAIN RES, V478, P337, DOI 10.1016/0006-8993(89)91514-X MATZENBACH B, 1994, J BIOL CHEM, V269, P2607 MICHLERSTUKE A, 1987, NEUROTROPHIC ACTIVIT, P253 MONTPIED P, 1991, J BIOL CHEM, V266, P6011 PIECHOTTA K, 1999, P GOTT NEUR C, V1, P287 PIECHOTTA K, 1998, ASS RES OT ABSTR, V21, P843 Poulter MO, 1997, J NEUROCHEM, V68, P631 REDBURN DA, 1992, PROG BRAIN RES, V90, P133 Rietzel HJ, 1998, J COMP NEUROL, V390, P20 RUSSELL FA, 1995, J COMP NEUROL, V352, P607, DOI 10.1002/cne.903520409 SANES DH, 1993, J NEUROSCI, V13, P2627 SANES DH, 1997, DEV AUDITORY SYSTEM, P271 SANES DH, 1992, NEUROREPORT, V3, P323, DOI 10.1097/00001756-199204000-00008 SANES DH, 1992, J COMP NEUROL, V321, P637, DOI 10.1002/cne.903210410 SANES DH, 1988, J NEUROSCI, V8, P682 SANES DH, 1991, J NEUROBIOL, V8, P837 SANES DH, 1992, DEV BRAIN RES, V67, P47, DOI 10.1016/0165-3806(92)90024-Q SANES DH, 1993, EUR J NEUROSCI, V5, P570, DOI 10.1111/j.1460-9568.1993.tb00522.x Sanes DH, 1996, J NEUROBIOL, V31, P503, DOI 10.1002/(SICI)1097-4695(199612)31:4<503::AID-NEU9>3.0.CO;2-D SANES DH, 1987, J NEUROSCI, V7, P3803 SASSOEPOGNETTO M, 1995, J COMP NEUROL, V357, P1, DOI 10.1002/cne.903570102 Sato K, 1999, NEUROSCIENCE, V89, P839, DOI 10.1016/S0306-4522(98)00350-9 SPOERRI PE, 1988, SYNAPSE, V2, P11, DOI 10.1002/syn.890020104 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 TAKAHASHI T, 1992, NEURON, V9, P1155, DOI 10.1016/0896-6273(92)90073-M Thoss VS, 1996, DEV BRAIN RES, V97, P269 ZOOK JM, 1988, HEARING RES, V34, P141, DOI 10.1016/0378-5955(88)90101-3 NR 68 TC 67 Z9 71 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 46 EP 58 DI 10.1016/S0378-5955(00)00119-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200005 PM 10962172 ER PT J AU Petralia, RS Rubio, ME Wang, YX Wenthold, RJ AF Petralia, RS Rubio, ME Wang, YX Wenthold, RJ TI Differential distribution of glutamate receptors in the cochlear nuclei SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE AMPA; NMDA; kainate; metabotropic; endbulb; fusiform cell ID CENTRAL-NERVOUS-SYSTEM; SUBUNIT MESSENGER-RNAS; IN-SITU HYBRIDIZATION; UNIPOLAR BRUSH CELLS; D-ASPARTATE RECEPTOR; AUDITORY BRAIN-STEM; AMPA RECEPTORS; MONOCLONAL-ANTIBODY; GLIAL LOCALIZATIONS; CA2+ PERMEABILITY AB Glutamate receptors are the major excitatory neurotransmitter receptors of the mammalian central nervous system, and include AMPA. kainate, delta, NMDA, and metabotropic types. In the cochlear nucleus (CN), the AMPA receptor subunits GluR2-4 are found in major kinds of neurons, while GluR1 subunit distribution is more restricted. GluR2 is low in the anteroventral CN, suggesting that many AMPA receptors here are calcium-permeable. Delta receptors are most prevalent in cartwheel cells in the dorsal CN. Of the NMDA receptors, NR1 is widespread while the NR2 subunits show more restricted distributions. Of the metabotropic glutamate receptors, mGluR1 alpha is most prevalent in the dorsal CN, and mGluR2 is concentrated in Golgi cells and unipolar brush cells. AMPA receptors in endbulb synapses in the anteroventral CN are mainly GluR3+4 complexes: probably an adaptation for rapid auditory neurotransmission. Glutamate receptors are differentially distributed in synapses of fusiform cells of the dorsal CN; GluR4 and mGluR1 alpha are present only at basal dendrite synapses (auditory nerve), while other glutamate receptors occupy both apical and basal synapses. Analysis of cytoplasmic distribution suggests that a selective targeting mechanism may restrict movement of GluR4 and mGluR1 alpha to basal dendrites, although other targeting mechanisms may be present. (C) 2000 Elsevier Science B.V. All rights reserved. C1 NIDCD, NIH, Bethesda, MD 20892 USA. RP Petralia, RS (reprint author), NIDCD, NIH, 36-5D08,36 Convent Dr MSC 4162, Bethesda, MD 20892 USA. CR Bilak MM, 1996, NEUROSCIENCE, V75, P1075, DOI 10.1016/0306-4522(96)00197-2 Bilak SR, 1998, SYNAPSE, V28, P251 Bradley SR, 1998, J NEUROCHEM, V71, P636 CACIEDO A, 1999, EUR J NEUROSCI, V11, P51 Das S, 1998, NATURE, V393, P377 Forster CR, 1998, NEUROREPORT, V9, P3531 Gardner SM, 1999, J NEUROSCI, V19, P8721 GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 Hirokawa N, 1998, SCIENCE, V279, P519, DOI 10.1126/science.279.5350.519 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HUNTER C, 1993, J NEUROSCI, V13, P1932 Jaarsma D, 1998, J NEUROCYTOL, V27, P303, DOI 10.1023/A:1006982023657 Joelson D, 1998, MICROSC RES TECHNIQ, V41, P246, DOI 10.1002/(SICI)1097-0029(19980501)41:3<246::AID-JEMT8>3.3.CO;2-P Kinoshita G, 1998, LUPUS, V7, P7, DOI 10.1191/096120398678919606 Landsend AS, 1997, J NEUROSCI, V17, P834 Levin MD, 1997, J COMP NEUROL, V378, P239, DOI 10.1002/(SICI)1096-9861(19970210)378:2<239::AID-CNE7>3.0.CO;2-4 MAYAT E, 1995, J NEUROSCI, V15, P2533 Mermall V, 1998, SCIENCE, V279, P527, DOI 10.1126/science.279.5350.527 Molitor SC, 1997, J NEUROPHYSIOL, V77, P1889 Morales M, 1999, NEURON, V23, P431, DOI 10.1016/S0896-6273(00)80797-7 MOSBACHER J, 1994, SCIENCE, V266, P1059, DOI 10.1126/science.7973663 Mugnaini E, 1997, PROG BRAIN RES, V114, P131 Munemoto Y, 1998, NEUROSCI LETT, V251, P101, DOI 10.1016/S0304-3940(98)00509-6 OHISHI H, 1993, NEUROSCIENCE, V53, P1009, DOI 10.1016/0306-4522(93)90485-X Ohishi H, 1998, NEUROSCI RES, V30, P65, DOI 10.1016/S0168-0102(97)00120-X OHISHI H, 1993, J COMP NEUROL, V335, P252, DOI 10.1002/cne.903350209 OHISHI H, 1995, J COMP NEUROL, V360, P555, DOI 10.1002/cne.903600402 OTIS TS, 1995, J PHYSIOL-LONDON, V482, P309 Petralia R. S., 1996, EXCITATORY AMINO ACI, P55 Petralia R. S., 1997, IONOTROPIC GLUTAMATE, P219 PETRALIA RS, 1994, J NEUROSCI, V14, P667 PETRALIA RS, 1994, J COMP NEUROL, V349, P85, DOI 10.1002/cne.903490107 Petralia RS, 1996, NEUROSCIENCE, V71, P949, DOI 10.1016/0306-4522(95)00533-1 Petralia RS, 1997, J COMP NEUROL, V385, P456, DOI 10.1002/(SICI)1096-9861(19970901)385:3<456::AID-CNE9>3.0.CO;2-2 Petralia RS, 1997, J CHEM NEUROANAT, V13, P77, DOI 10.1016/S0891-0618(97)00023-9 Petralia RS, 1998, CELL BIOL INT, V22, P603, DOI 10.1006/cbir.1998.0385 Petralia R. S., 1999, V141, P143 Petralia RS, 1996, J COMP NEUROL, V372, P356 RAMAN IM, 1994, J NEUROSCI, V14, P4998 Rubio ME, 1997, NEURON, V18, P939, DOI 10.1016/S0896-6273(00)80333-5 Rubio ME, 1999, J NEUROSCI, V19, P5549 Rubio ME, 1999, J NEUROCHEM, V73, P942, DOI 10.1046/j.1471-4159.1999.0730942.x Ryugo DK, 1996, J COMP NEUROL, V365, P141, DOI 10.1002/(SICI)1096-9861(19960129)365:1<141::AID-CNE11>3.0.CO;2-T Sanes DH, 1998, J NEUROPHYSIOL, V80, P209 Sato K, 1998, MICROSC RES TECHNIQ, V41, P217 SHIGEMOTO R, 1992, J COMP NEUROL, V322, P121, DOI 10.1002/cne.903220110 Solum D, 1997, J NEUROSCI, V17, P4744 Wang YX, 1998, J NEUROSCI, V18, P1148 WATANABE M, 1994, J COMP NEUROL, V343, P520, DOI 10.1002/cne.903430403 Wenthold RJ, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P93, DOI 10.1007/978-1-4419-8712-9_10 WENTHOLD RJ, 1993, NATO ADV SCI INST SE, V239, P179 Wright DD, 1996, J COMP NEUROL, V364, P729, DOI 10.1002/(SICI)1096-9861(19960122)364:4<729::AID-CNE10>3.0.CO;2-K Zhao HM, 1997, J NEUROCHEM, V68, P1041 Zhao HM, 1998, J NEUROSCI, V18, P5517 Zhou N, 1995, NEUROREPORT, V6, P2273, DOI 10.1097/00001756-199511270-00002 Zuo J, 1997, NATURE, V388, P769 NR 56 TC 40 Z9 40 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 59 EP 69 DI 10.1016/S0378-5955(00)00120-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200006 PM 10962173 ER PT J AU Schwartz, IR Keh, A Eager, PR AF Schwartz, IR Keh, A Eager, PR TI Differential postsynaptic distribution of GluRs 1-4 on cartwheel and octopus cell somata in the gerbil cochlear nucleus SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE AMPA preferring glutamate receptors; auditory system; cochlear nucleus; cartwheel cells; octopus cells; immunocytochemistry ID GLUTAMATE-RECEPTOR SUBUNITS; CALCIUM-BINDING PROTEINS; AUDITORY BRAIN-STEM; AMPA RECEPTORS; CA2+ PERMEABILITY; GUINEA-PIG; NEURONS; RAT; INTERNEURONS; EXPRESSION AB Differences were demonstrated in the distribution of glutamate receptors (GluR) 1, 2, 2/3 and 4 postsynaptic immunoreactivity (PSIR) on the somata of cartwheel and octopus cells in the adult gerbil cochlear nucleus (CN). Montages of electron micrographs of cartwheel and octopus cells immunoreacted with antibodies to GluR 1, 2, 2/3 and 4 were prepared. The number of synaptic terminals with PSIR were counted on all cells for each antibody, normalized to the total length of somatic surface analyzed. The density of terminals apposed to PSIR on octopus cells was similar for the antibodies GluR1, 2/3 and 4, but significantly less for GluR2. On cartwheel somata the numbers of terminals apposed to immunoreactive postsynaptic specializations with GluR 1, 2, 2/3 or 4 were not significantly different from each other. The density of terminals apposed to GluR2/3 and 4 positive postsynaptic specializations was significantly less on cartwheel cells than on octopus somata. The data suggest that the decreased presence of the GluR2 subunit, which confers calcium impermeability to the assembled receptor and slower gating kinetics to receptors with a high GluR4 content, is the major difference in the AMPA receptors on the somata of these cell types. The presence on cartwheel cells of a majority of AMPA receptors which contain GluR2 may account for the fact that cartwheel cells respond to shocks to the auditory nerve with 100 ms excitatory postsynaptic potentials (EPSPs), while octopus cells, most of whose AMPA receptors lack GluR?, respond with 1 ms EPSPs. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Yale Univ, Sch Med, Otolaryngol Sect, New Haven, CT 06520 USA. RP Schwartz, IR (reprint author), Yale Univ, Sch Med, Otolaryngol Sect, POB 208041, New Haven, CT 06520 USA. CR Caicedo A, 1997, J COMP NEUROL, V378, P1, DOI 10.1002/(SICI)1096-9861(19970203)378:1<1::AID-CNE1>3.0.CO;2-8 Caicedo A, 1996, ANAT EMBRYOL, V194, P465 Gardner SM, 1999, J NEUROSCI, V19, P8721 GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 Golding NL, 1997, J NEUROPHYSIOL, V78, P248 GOLDING NL, 1995, J NEUROSCI, V15, P3138 Golding NL, 1999, J NEUROSCI, V19, P2897 GOLDMAN SA, 1995, MACH LEARN, V18, P127 HOLLMANN M, 1991, SCIENCE, V252, P851, DOI 10.1126/science.1709304 HUNTER C, 1993, J NEUROSCI, V13, P1932 KEH A, 1999, ARO MIDW M, V22, P68 Keppel G., 1991, DESIGN ANAL RESEARCH KORADA S, 1909, SOC NEUR ABSTR, V25, P1419 Korada S., 1997, Society for Neuroscience Abstracts, V23, P182 Korada S, 2000, HEARING RES, V140, P23, DOI 10.1016/S0378-5955(99)00182-3 Oertel D, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P127, DOI 10.1007/978-1-4419-8712-9_12 Rubio ME, 1997, NEURON, V18, P939, DOI 10.1016/S0896-6273(00)80333-5 Rubio ME, 1999, J NEUROSCI, V19, P5549 SCHWARTZ IR, 1995, C MOL BIOL HEAR BETH Schwartz I. R., 1992, Society for Neuroscience Abstracts, V18, P1036 Schwartz IR, 1999, HEARING RES, V137, P77, DOI 10.1016/S0378-5955(99)00140-9 SCHWARTZ IR, 1999, C MOL MECH CENTR AUD SOMMER B, 1990, SCIENCE, V249, P1580, DOI 10.1126/science.1699275 Spatz WB, 1997, HEARING RES, V107, P136, DOI 10.1016/S0378-5955(97)00029-4 Toth K, 1998, NAT NEUROSCI, V1, P572 Wang YX, 1998, J NEUROSCI, V18, P1148 Washburn MS, 1996, J PHARMACOL EXP THER, V278, P669 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 NR 28 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 70 EP 76 DI 10.1016/S0378-5955(00)00121-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200007 PM 10962174 ER PT J AU Parks, TN AF Parks, TN TI The AMPA receptors of auditory neurons SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE glutamate receptor; calcium-permeable; rapid desensitization; cochlear nucleus; nucleus magnocellularis ID D-ASPARTATE RECEPTORS; NON-NMDA RECEPTORS; SELECTIVE GLUTAMATE RECEPTORS; DORSAL COCHLEAR NUCLEUS; EXCITATORY SYNAPTIC TRANSMISSION; BRAIN-STEM; INFERIOR COLLICULUS; MESSENGER-RNAS; RAT-BRAIN; IMMUNOCYTOCHEMICAL LOCALIZATION AB The ionotropic glutamate receptor (GluR) subtype known as the AMPA receptor, which mediates rapid excitatory synaptic transmission in many regions of the nervous system, is composed of four different protein subunits, termed GluRs 1-4. The functional properties of each AMPA receptor are determined by the relative levels of GluRs 1-4 and by post-transcriptional modifications of these proteins through mRNA editing and alternative exon splicing. The present paper reviews the published evidence for (1) localization of mRNAs and immunoreactivity for GluRs 1-4 in the cochlea and subcortical central nervous system auditory pathways of mammals and birds, and (2) involvement of AMPA receptors in synaptic transmission in the auditory system. Recent biochemical and electrophysiological evidence concerning the specialized properties of AMPA receptors on brainstem auditory neurons is also reviewed, along with data concerning how these properties emerge during normal development. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Utah, Sch Med, Dept Neurobiol & Anat, Salt Lake City, UT 84132 USA. RP Parks, TN (reprint author), Univ Utah, Sch Med, Dept Neurobiol & Anat, Rm 401,Bldg 531,50 N Med Dr, Salt Lake City, UT 84132 USA. CR Angulo MC, 1997, J NEUROSCI, V17, P6685 BANKS MI, 1992, J NEUROSCI, V12, P2819 BARNESDAVIES M, 1993, P R SOC LOND B, V251, P151 BARNESDAVIES M, 1995, J PHYSIOL-LONDON, V488, P387 Borges K, 1998, PROG BRAIN RES, V116, P153, DOI 10.1016/S0079-6123(08)60436-7 Caicedo A, 1999, EUR J NEUROSCI, V11, P51, DOI 10.1046/j.1460-9568.1999.00410.x Caicedo A, 1998, EUR J NEUROSCI, V10, P941, DOI 10.1046/j.1460-9568.1998.00104.x CASPARY DM, 1989, BRAIN RES, V503, P83, DOI 10.1016/0006-8993(89)91707-1 Chittajallu R, 1999, TRENDS PHARMACOL SCI, V20, P26, DOI 10.1016/S0165-6147(98)01286-3 COLLINGRIDGE GL, 1989, PHARMACOL REV, V41, P143 DANYSZ W, 1999, AMINO ACIDS, V17, P10 Dingledine R, 1999, PHARMACOL REV, V51, P7 FELDMAN DE, 1994, J NEUROSCI, V14, P5939 Ferragamo MJ, 1998, J NEUROPHYSIOL, V79, P51 GALLO V, 1992, J NEUROSCI, V12, P1010 Gardner SM, 1999, J NEUROSCI, V19, P8721 Gaza WC, 1997, BRAIN RES, V774, P175, DOI 10.1016/S0006-8993(97)81701-5 GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 HACK MJ, 2000, J NEUROSCI RC, V20, pRC67 HACKETT JT, 1982, NEUROSCIENCE, V7, P1455, DOI 10.1016/0306-4522(82)90257-3 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HUNTER C, 1993, J NEUROSCI, V13, P1932 ISAACSON JS, 1995, J NEUROPHYSIOL, V73, P964 JACKSON H, 1985, NEUROSCIENCE, V16, P171, DOI 10.1016/0306-4522(85)90054-5 KANDLER K, 1995, J NEUROSCI, V15, P6890 Kidd FL, 1999, NATURE, V400, P569 KUBKE MF, 2000, IN PRESS HEAR RES Kubke MF, 1998, MICROSC RES TECHNIQ, V41, P176 KURIYAMA H, 1994, HEARING RES, V80, P233, DOI 10.1016/0378-5955(94)90114-7 Lawrence J. J., 1998, Society for Neuroscience Abstracts, V24, P846 Lee JC, 1998, BRAIN RES PROTOC, V3, P142, DOI 10.1016/S1385-299X(98)00035-X Levin MD, 1997, J COMP NEUROL, V378, P239, DOI 10.1002/(SICI)1096-9861(19970210)378:2<239::AID-CNE7>3.0.CO;2-4 LODGE D, 1997, IONOTROPIC GLUTAMATE, P1 LOMELI H, 1994, SCIENCE, V266, P1709, DOI 10.1126/science.7992055 LUO L, 1995, J COMP NEUROL, V361, P372, DOI 10.1002/cne.903610303 Manis PB, 1996, J NEUROPHYSIOL, V76, P1639 MARTIN MR, 1985, HEARING RES, V17, P153, DOI 10.1016/0378-5955(85)90018-8 Matsubara A, 1996, J NEUROSCI, V16, P4457 Meldrum BS, 1998, PROG BRAIN RES, V116, P441, DOI 10.1016/S0079-6123(08)60454-9 Michaelis EK, 1998, PROG NEUROBIOL, V54, P369, DOI 10.1016/S0301-0082(97)00055-5 Moore DR, 1998, J NEUROPHYSIOL, V80, P2229 MOSBACHER J, 1994, SCIENCE, V266, P1059, DOI 10.1126/science.7973663 Myers SJ, 1999, ANNU REV PHARMACOL, V39, P221, DOI 10.1146/annurev.pharmtox.39.1.221 NAKAGAWA T, 1991, J NEUROPHYSIOL, V65, P715 NEMETH EF, 1983, NEUROSCI LETT, V40, P39, DOI 10.1016/0304-3940(83)90089-7 Niedzielski AS, 1997, AUDIOL NEURO-OTOL, V2, P79 NIEDZIELSKI AS, 1995, J NEUROSCI, V15, P2338 OTIS TS, 1995, J PHYSIOL-LONDON, V482, P309 PATERNAIN AV, 1995, NEURON, V14, P185, DOI 10.1016/0896-6273(95)90253-8 Petralia R. S., 1997, IONOTROPIC GLUTAMATE, P219 Petralia RS, 1997, J COMP NEUROL, V385, P456, DOI 10.1002/(SICI)1096-9861(19970901)385:3<456::AID-CNE9>3.0.CO;2-2 PETRALIA RS, 1992, J COMP NEUROL, V318, P329, DOI 10.1002/cne.903180309 Petralia RS, 1996, J COMP NEUROL, V372, P356 PRUSS RM, 1991, NEURON, V7, P509, DOI 10.1016/0896-6273(91)90302-G Puel JL, 1995, PROG NEUROBIOL, V47, P449, DOI 10.1016/0301-0082(95)00028-3 RAMAN IM, 1994, J NEUROSCI, V14, P4998 Ravindranathan A, 2000, J PHYSIOL-LONDON, V523, P667, DOI 10.1111/j.1469-7793.2000.00667.x Ravindranathan A, 1997, MOL BRAIN RES, V50, P143, DOI 10.1016/S0169-328X(97)00179-4 Reng D, 1999, NEUROREPORT, V10, P2137, DOI 10.1097/00001756-199907130-00026 ROGERS SW, 1991, J NEUROSCI, V11, P2713 Rubel EW, 1988, AUDITORY FUNCTION NE, P3 Rubio ME, 1997, NEURON, V18, P939, DOI 10.1016/S0896-6273(00)80333-5 Ruel J, 1999, J PHYSIOL-LONDON, V518, P667, DOI 10.1111/j.1469-7793.1999.0667p.x RYAN AF, 1991, NEUROREPORT, V2, P643, DOI 10.1097/00001756-199111000-00002 SAFIEDDINE S, 1992, NEUROREPORT, V3, P1145, DOI 10.1097/00001756-199212000-00029 SATO K, 1993, NEUROSCIENCE, V52, P515, DOI 10.1016/0306-4522(93)90403-3 SEWELL WF, 1997, ENCY ACOUSTICS, P1401 SIMMONS DD, 1994, NEUROREPORT, V5, P1433, DOI 10.1097/00001756-199407000-00007 SUGDEN S, 1999, ABSTR MIDW M ASS RES, P68 Swanson GT, 1997, J NEUROSCI, V17, P58 Trussell L, 1998, PROG BRAIN RES, V116, P59, DOI 10.1016/S0079-6123(08)60430-6 Trussell LO, 1997, CURR OPIN NEUROBIOL, V7, P487, DOI 10.1016/S0959-4388(97)80027-X Trussell LO, 1999, ANNU REV PHYSIOL, V61, P477, DOI 10.1146/annurev.physiol.61.1.477 Vitten H., 1999, Society for Neuroscience Abstracts, V25, P974 Wagner T, 1996, EUR J NEUROSCI, V8, P1231, DOI 10.1111/j.1460-9568.1996.tb01291.x Waller HJ, 1996, HEARING RES, V98, P169, DOI 10.1016/0378-5955(96)00090-1 Walmsley B, 1998, TRENDS NEUROSCI, V21, P81, DOI 10.1016/S0166-2236(97)01170-3 Wang YX, 1998, J NEUROSCI, V18, P1148 Washburn MS, 1997, J NEUROSCI, V17, P9393 WATKINS JC, 1990, TRENDS PHARMACOL SCI, V11, P25, DOI 10.1016/0165-6147(90)90038-A Webber TJ, 1999, EXP BRAIN RES, V124, P295, DOI 10.1007/s002210050626 WENTHOLD RJ, 1992, J BIOL CHEM, V267, P501 Wenthold RJ, 1998, PROG BRAIN RES, V116, P133, DOI 10.1016/S0079-6123(08)60435-5 Wu SH, 1998, HEARING RES, V122, P47, DOI 10.1016/S0378-5955(98)00085-9 Wu SH, 1996, J NEUROPHYSIOL, V75, P1271 WU SH, 1992, J NEUROSCI, V12, P3084 ZHOU N, 1992, HEARING RES, V60, P20, DOI 10.1016/0378-5955(92)90054-Q Zhou N, 1995, NEUROREPORT, V6, P2273, DOI 10.1097/00001756-199511270-00002 ZHOU N, 1991, HEARING RES, V52, P195, DOI 10.1016/0378-5955(91)90199-J ZHOU N, 1993, BRAIN RES, V628, P149, DOI 10.1016/0006-8993(93)90950-R ZHOU N, 1992, DEV BRAIN RES, V67, P145, DOI 10.1016/0165-3806(92)90215-I ZHOU N, 1993, NEUROPHARMACOLOGY, V32, P767, DOI 10.1016/0028-3908(93)90185-6 NR 92 TC 52 Z9 52 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 77 EP 91 DI 10.1016/S0378-5955(00)00122-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200008 PM 10962175 ER PT J AU Zhang, Y Wu, SH AF Zhang, Y Wu, SH TI Long-term potentiation in the inferior colliculus studied in rat brain slice SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE auditory system; plasticity; brain slice; lateral lemniscus; inferior colliculus; N-methyl-D-aspartate receptor; GABA(B) receptor ID SYNAPTIC TRANSMISSION; GUINEA-PIG; LASTING POTENTIATION; GABAB AUTORECEPTORS; CEREBRAL-CORTEX; VISUAL-CORTEX; SPINAL-CORD; IN-VITRO; INPUT; HIPPOCAMPUS AB The purpose of this study is to determine whether long-term potentiation (LTP) can be induced in the central nucleus of the inferior colliculus (ICC) by electrical stimulation of the lateral lemniscus. If LTP can be induced, is it mediated by N-methyl-D-aspartate (NMDA) and/or other receptors? Brain slices of the ICC were obtained from 14-35 day old Wistar rats. The field potentials were recorded from the ICC after GABAergic and glycinergic inhibition was suppressed. Following tetanic stimulation (50 Hz, 20 s), the amplitude of the response was increased to about 146% of control response for at least 30 min. LTP was observed in about 78% of the cases tested. Induction of LTP in the ICC required activation of both NMDA and gamma-aminobutyric acid (GABA)(B) receptors. GABAergic inhibitory postsynaptic potentials (IPSPs) were blocked by the GABA(A) receptor antagonist, but not by the GABA(B) receptor antagonist. The IPSPs were decreased by the GABA(B) receptor agonist, baclofen. The intrinsic postsynaptic membrane properties were not affected by baclofen. These results suggest that GABAergic inhibition in the ICC is mediated only by GABA(A) receptors, but that it is modulated by presynaptic GABAB receptors. The GABA(B) receptors in the ICC may suppress GABAergic inhibition and promote induction of LTP. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Carleton Univ, Inst Neurosci, Life Sci Res Ctr, Lab Sensory Neurosci, Ottawa, ON K1S 5B6, Canada. RP Wu, SH (reprint author), Carleton Univ, Inst Neurosci, Life Sci Res Ctr, Lab Sensory Neurosci, 1125 Colonel Dr, Ottawa, ON K1S 5B6, Canada. CR ANDERSON RA, 1985, EUR J PHARMACOL, V118, P355, DOI 10.1016/0014-2999(85)90148-7 BARANYI A, 1987, BRAIN RES, V423, P378, DOI 10.1016/0006-8993(87)90867-5 BLISS TVP, 1973, J PHYSIOL-LONDON, V232, P331 BONANNO G, 1989, EUR J PHARM-MOLEC PH, V172, P41, DOI 10.1016/0922-4106(89)90043-6 BONANNO G, 1989, BRIT J PHARMACOL, V96, P341 CastroAlamancos MA, 1996, P NATL ACAD SCI USA, V93, P1335, DOI 10.1073/pnas.93.3.1335 CHEN W, 1994, EXP BRAIN RES, V100, P149 CHU DCM, 1990, NEUROSCIENCE, V34, P341, DOI 10.1016/0306-4522(90)90144-S COLLINGRIDGE GL, 1983, J PHYSIOL-LONDON, V334, P33 Davies CH, 1996, J PHYSIOL-LONDON, V496, P451 DAVIES CH, 1991, NATURE, V349, P609, DOI 10.1038/349609a0 DEISZ RA, 1989, J PHYSIOL-LONDON, V412, P513 Ehret G., 1997, CENTRAL AUDITORY SYS, P259 Fubara BM, 1996, J COMP NEUROL, V369, P83 GERREN RA, 1983, BRAIN RES, V265, P138, DOI 10.1016/0006-8993(83)91344-6 GIRALT MT, 1990, EUR J PHARMACOL, V175, P137, DOI 10.1016/0014-2999(90)90224-T GonzalezHernandez T, 1996, J COMP NEUROL, V372, P309, DOI 10.1002/(SICI)1096-9861(19960819)372:2<309::AID-CNE11>3.0.CO;2-E HARRISON NL, 1990, J PHYSIOL-LONDON, V422, P433 HOSOMI G, 1995, NEUROSCI LETT, P175 KIRKWOOD A, 1994, J NEUROSCI, V14, P1634 Kotak VC, 1998, J NEUROSCI, V18, P4646 KUDOH M, 1994, NEUROSCI LETT, V171, P21, DOI 10.1016/0304-3940(94)90594-0 KULESZA RJ, 1999, ARO ABSTR, V22, P70 Kuno M., 1995, SYNAPSE FUNCTION PLA McEachern JC, 1996, BRAIN RES REV, V22, P51 MIYAMOTO T, 1990, BRAIN RES, V518, P166, DOI 10.1016/0006-8993(90)90968-H Moore DR, 1998, J NEUROPHYSIOL, V80, P2229 MOTT DD, 1990, NEUROSCI LETT, V113, P222, DOI 10.1016/0304-3940(90)90307-U Mott D D, 1992, Epilepsy Res Suppl, V7, P119 MOTT DD, 1991, SCIENCE, V252, P1718, DOI 10.1126/science.1675489 OKADA Y, 1989, NEUROSCI LETT, V96, P108, DOI 10.1016/0304-3940(89)90251-6 PERKINS AT, 1988, BRAIN RES, V439, P222 PITTALUGA A, 1987, EUR J PHARMACOL, V144, P45, DOI 10.1016/0014-2999(87)90007-0 POCKETT S, 1995, NEUROSCIENCE, V67, P791, DOI 10.1016/0306-4522(95)00077-V RANDIC M, 1993, J NEUROSCI, V13, P5228 STRIPLING JS, 1988, BRAIN RES, V441, P281, DOI 10.1016/0006-8993(88)91406-0 THOMPSON SM, 1989, J NEUROPHYSIOL, V61, P524 Wagner T, 1996, EUR J NEUROSCI, V8, P1231, DOI 10.1111/j.1460-9568.1996.tb01291.x Weisskopf MG, 1999, J NEUROSCI, V19, P10512 WEISSKOPF MG, 1994, SCIENCE, V265, P1878, DOI 10.1126/science.7916482 Zhang DX, 1998, HEARING RES, V117, P1, DOI 10.1016/S0378-5955(97)00202-5 NR 41 TC 22 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 92 EP 103 DI 10.1016/S0378-5955(00)00123-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200009 PM 10962176 ER PT J AU Morley, BJ Happe, HK AF Morley, BJ Happe, HK TI Cholinergic receptors: dual roles in transduction and plasticity SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE auditory brainstem; plasticity; nicotinic acetylcholine receptor; development; calcium; synchronization ID NICOTINIC ACETYLCHOLINE-RECEPTORS; RAT COCHLEAR NUCLEUS; IN-SITU HYBRIDIZATION; SYNAPTIC TRANSMISSION; ALPHA-7 SUBUNITS; NERVOUS-SYSTEM; MESSENGER-RNA; BRAIN-STEM; DEVELOPMENTAL-CHANGES; OCTOPUS CELLS AB The regional distributions and possible functions of nicotinic acetylcholine receptors (nAChRs) in the developing and adult auditory rat brain are reviewed. The predominant nAChR in the auditory brainstem is the alpha 7 homomeric receptor. alpha 7 mRNA and protein are expressed in selected regions of the cochlear nucleus (CN), inferior colliculus (IC), medial superior olive, lateral superior olive, ventral nucleus of the lateral lemniscus and superior paraolivary nucleus. Peak expression of mRNA and protein occurs by the second postnatal week in most auditory brainstem areas. In contrast, the alpha 3 and beta 4 nicotinic subunits are expressed in the embryo and early in postnatal development in the CN and IC, but not other brainstem nuclei. Of particular interest is the octopus cell region of the posteroventral cochlear nucleus (PVCN). alpha 3 and beta 4 are down-regulated in the octopus cell region about postnatal day 10, which is the age that alpha 7 is at peak expression. NAChRs play important roles in transduction and in regulating intracellular calcium. The ability of the alpha 7 receptor to synchronize synaptic activity and stabilize synapses makes it a prime candidate as a mechanism underlying homeostatic plasticity in the auditory system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Boys Town Natl Res Hosp, Omaha, NE 68131 USA. RP Morley, BJ (reprint author), Boys Town Natl Res Hosp, Omaha, NE 68131 USA. EM morley@boystown.org CR Albuquerque EX, 1997, J PHARMACOL EXP THER, V280, P1117 Aramakis VB, 1998, J NEUROSCI, V18, P8485 ARIMATSU Y, 1981, J COMP NEUROL, V198, P603, DOI 10.1002/cne.901980405 BENNETTCLARKE CA, 1999, MOT RES, V16, P269 Blumenthal EM, 1999, J NEUROPHYSIOL, V81, P111 BonfanteCabarcas R, 1996, J PHARMACOL EXP THER, V277, P432 Burden SJ, 1998, GENE DEV, V12, P133, DOI 10.1101/gad.12.2.133 Caicedo A, 1998, EUR J NEUROSCI, V10, P941, DOI 10.1046/j.1460-9568.1998.00104.x CASPARY DM, 1983, EXP NEUROL, V82, P491, DOI 10.1016/0014-4886(83)90419-3 Chang KT, 1999, J NEUROSCI, V19, P3701 CHEN D, 1997, J BIOL CHEM, V19, P24024 CHEN KJ, 1995, HEARING RES, V89, P137, DOI 10.1016/0378-5955(95)00131-6 CONNOLLY JG, 1995, J PHYSIOL-LONDON, V484, P87 CONROY WG, 1995, J BIOL CHEM, V270, P4424 DECKER ER, 1990, J NEUROSCI, V10, P3410 DUDAI Y, 1978, BRAIN RES, V154, P167, DOI 10.1016/0006-8993(78)91066-1 Edwards JA, 1999, J NEUROPHYSIOL, V81, P895 Fenster CP, 1997, J NEUROSCI, V17, P5747 Flores CM, 1996, J NEUROSCI, V16, P7892 FORSTER I, 1995, P ROY SOC B-BIOL SCI, V260, P139, DOI 10.1098/rspb.1995.0071 Fregnac Y, 1998, NATURE, V391, P845, DOI 10.1038/35996 FROSTHOLM A, 1986, BRAIN RES BULL, V16, P189, DOI 10.1016/0361-9230(86)90033-X Fuchs PA, 1996, CURR OPIN NEUROBIOL, V6, P514, DOI 10.1016/S0959-4388(96)80058-4 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GODFREY DA, 1987, HEARING RES, V28, P237, DOI 10.1016/0378-5955(87)90052-9 GOLDING NL, 1995, J NEUROSCI, V15, P3138 Golding NL, 1999, J NEUROSCI, V19, P2897 Haghighi AP, 2000, J NEUROSCI, V20, P529 Happe HK, 1998, J COMP NEUROL, V397, P163, DOI 10.1002/(SICI)1096-9861(19980727)397:2<163::AID-CNE2>3.0.CO;2-Z HARRISON JM, 1966, J COMP NEUROL, V126, P391, DOI 10.1002/cne.901260303 Hebb D.O., 1949, ORG BEHAV NEUROPSYCH HENDERSON Z, 1991, J COMP NEUROL, V314, P147, DOI 10.1002/cne.903140114 Hiel H, 1996, BRAIN RES, V738, P347, DOI 10.1016/S0006-8993(96)01046-3 KEMP G, 1985, BRAIN RES, V18, P274 LAUTERBORN JC, 1993, MOL BRAIN RES, V17, P59, DOI 10.1016/0169-328X(93)90073-X Li XY, 1998, J NEUROSCI, V18, P1904 Lohmann C, 1998, J NEUROBIOL, V34, P97, DOI 10.1002/(SICI)1097-4695(19980205)34:2<97::AID-NEU1>3.0.CO;2-6 MANDELZYS A, 1995, J NEUROPHYSIOL, V74, P1212 MATHISEN JS, 1964, ACTA ANAT, V56, P216 MCDONALD DM, 1971, BRAIN RES, V28, P1, DOI 10.1016/0006-8993(71)90520-8 MCGEHEE DS, 1995, SCIENCE, V269, P1692, DOI 10.1126/science.7569895 MORLEY BJ, 1981, BRAIN RES REV, V3, P81, DOI 10.1016/0165-0173(81)90013-8 Morley BJ, 1998, MOL BRAIN RES, V53, P78, DOI 10.1016/S0169-328X(97)00272-6 Morley BJ, 1997, MOL BRAIN RES, V48, P407, DOI 10.1016/S0169-328X(97)00159-9 MORLEY BJ, 1977, BRAIN RES, V134, P161, DOI 10.1016/0006-8993(77)90935-0 ORRURTEGER A, 1997, J NEUROSCI, V1, P9165 OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 OSEN KK, 1969, BRAIN RES, V16, P165, DOI 10.1016/0006-8993(69)90092-4 RHODE WS, 1994, HEARING RES, V77, P43, DOI 10.1016/0378-5955(94)90252-6 RUST G, 1994, EUR J NEUROSCI, V6, P478, DOI 10.1111/j.1460-9568.1994.tb00290.x SALPETER MM, 1985, PROG NEUROBIOL, V25, P297, DOI 10.1016/0301-0082(85)90018-8 SEGAL M, 1978, BRAIN RES, V148, P105, DOI 10.1016/0006-8993(78)90381-5 SEGUELA P, 1993, J NEUROSCI, V13, P596 SHERRIFF FE, 1994, NEUROSCIENCE, V58, P627, DOI 10.1016/0306-4522(94)90086-8 Shoop RD, 1999, J NEUROSCI, V19, P692 TURRIGIANO GC, 1998, TRENDS NEUROSCI, V22, P221 VETTER DE, 1993, NATO ADV SCI INST SE, V239, P279 WinzerSerhan UH, 1997, J COMP NEUROL, V386, P540, DOI 10.1002/(SICI)1096-9861(19971006)386:4<540::AID-CNE2>3.0.CO;2-2 Yao WP, 1999, HEARING RES, V128, P97, DOI 10.1016/S0378-5955(98)00199-3 Yao WP, 1996, J COMP NEUROL, V373, P27 Yao WP, 1997, NEUROSCI LETT, V229, P21, DOI 10.1016/S0304-3940(97)00400-X Yao WP, 1999, J HISTOCHEM CYTOCHEM, V47, P83 YAO WP, 1995, HEARING RES, V89, P76, DOI 10.1016/0378-5955(95)00123-7 ZOLI M, 1995, J NEUROSCI, V15, P1912 Zucker RS, 1999, CURR OPIN NEUROBIOL, V9, P305, DOI 10.1016/S0959-4388(99)80045-2 NR 65 TC 35 Z9 39 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 104 EP 112 DI 10.1016/S0378-5955(00)00124-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200010 PM 10962177 ER PT J AU Garcia, MM Edwards, R Brennan, GB Harlan, RE AF Garcia, MM Edwards, R Brennan, GB Harlan, RE TI Deafferentation-induced changes in protein kinase C expression in the rat cochlear nucleus SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE calbindin D28k; ectopic Purkinje cell; dorsal cochlear nucleus; ventral cochlear nucleus; neural plasticity; central auditory pathway ID LONG-TERM POTENTIATION; SPIRAL GANGLION-CELLS; AUDITORY BRAIN-STEM; GAMMA-MUTANT MICE; SYNAPTIC TRANSMISSION; INFERIOR COLLICULUS; DIFFERENTIAL EXPRESSION; RECEPTOR SUBUNITS; NERVOUS-SYSTEM; TONOTOPIC MAP AB Isoforms of the signal transducing molecule, protein kinase C (PKC), may play a role in neural plasticity following sensory deafferentation. To explore the role of PKC in central auditory plasticity, we studied the effect of auditory deafferentation on the expression of PKC beta I, beta II, gamma, and delta in the rat dorsal (DCN) and ventral cochlear nucleus (VCN), using immunocytochemistry. Male rats were treated with kanamycin and furosemide to induce hair cell loss. At various intervals post-treatment, brains were perfusion-fixed and processed for immunocytochemistry. Following deafferentation, we observed a gradual increase in PKC beta I immunoreactivity (ir) in the deepest layers of the DCN, possibly representing synapses of primary afferents or parallel fibers on unlabeled neurons. Correlated with this, we observed an increase in the number of neurons in the deep DCN that showed PKC delta ir. In controls, we observed PKC gamma ir in small ovoid cells concentrated in the middle layer of the DCN. From days 4 through 14 after deafferentation, we found an increase in the intensity of staining of these cells, with a return toward control levels by day 28. Finally, Purkinje-like cells (PLC) in the VCN, which express only PKC delta in control rats, began to express PKC gamma after deafferentation, correlated with increased expression of calbindin D28k in PLC. Thus PKC isoforms are differentially regulated in the CN following deafferentation, supporting a role for PKC in auditory plasticity. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tulane Univ, Sch Med, Dept Otolaryngol, New Orleans, LA 70112 USA. Tulane Univ, Sch Med, Dept Anat, New Orleans, LA 70112 USA. Tulane Univ, Sch Med, Neurosci Program, New Orleans, LA 70112 USA. Tulane Univ, Sch Med, Mol & Cellular Biol Program, New Orleans, LA 70112 USA. RP Garcia, MM (reprint author), Tulane Univ, Sch Med, Dept Otolaryngol, 1430 Tulane Ave SL-59, New Orleans, LA 70112 USA. CR ABELIOVICH A, 1993, CELL, V75, P1263, DOI 10.1016/0092-8674(93)90614-V ABELIOVICH A, 1993, CELL, V75, P1253, DOI 10.1016/0092-8674(93)90613-U ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ALTSCHULER RA, 1995, MOL BIOL HEARING DEA, P84 ALTSCHULER RA, 1996, MOL MECH CENTRAL AUD, P8 Bilak MM, 1996, NEUROSCIENCE, V75, P1075, DOI 10.1016/0306-4522(96)00197-2 Bilak SR, 1998, SYNAPSE, V28, P251 Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 BRUMMETT RE, 1975, ACTA OTO-LARYNGOL, V80, P86, DOI 10.3109/00016487509121305 CAPOGNA M, 1995, J NEUROSCI, V15, P1249 CELIO MR, 1990, NEUROSCIENCE, V35, P375, DOI 10.1016/0306-4522(90)90091-H CLINE HT, 1990, NEURON, V4, P899, DOI 10.1016/0896-6273(90)90143-4 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 COLLEY PA, 1993, BRAIN RES REV, V18, P115, DOI 10.1016/0165-0173(93)90009-O ELKABES S, 1993, J NEUROCHEM, V60, P1835, DOI 10.1111/j.1471-4159.1993.tb13410.x FOX K, 1993, TRENDS NEUROSCI, V16, P116, DOI 10.1016/0166-2236(93)90136-A FRANCIS HW, 1995, ASS RES OTOLARYNGOL, V18, P38 GARCIA MM, 1993, NEUROREPORT, V5, P65, DOI 10.1097/00001756-199310000-00016 GARCIA MM, 1993, J COMP NEUROL, V331, P375, DOI 10.1002/cne.903310307 Garcia MM, 1997, J COMP NEUROL, V385, P26 Garcia MM, 1997, J COMP NEUROL, V385, P1 GUTIERREZ C, 1994, BRAIN RES, V651, P300, DOI 10.1016/0006-8993(94)90710-2 Hori T, 1999, J NEUROSCI, V19, P7262 HUNTER C, 1996, MOL MECH CENTRAL AUD, P9 HUNTER C, 1993, J NEUROSCI, V13, P1932 HUNTER C, 1995, MOL BIOL HEARING DEA, P122 HURD LB, 1994, HEARING RES, V72, P143, DOI 10.1016/0378-5955(94)90214-3 Idrizbegovic E, 1998, BRAIN RES, V800, P86, DOI 10.1016/S0006-8993(98)00504-6 ILLING RB, 1994, NEUROSCI LETT, V194, P9 Illing RB, 1997, J COMP NEUROL, V382, P116, DOI 10.1002/(SICI)1096-9861(19970526)382:1<116::AID-CNE8>3.0.CO;2-4 KALTENBACH JA, 1992, HEARING RES, V59, P213, DOI 10.1016/0378-5955(92)90118-7 KULLMANN DM, 1995, NEURON, V15, P997, DOI 10.1016/0896-6273(95)90089-6 LESPERANCE MM, 1995, HEARING RES, V86, P77, DOI 10.1016/0378-5955(95)00056-A MALENKA RC, 1986, NATURE, V321, P175, DOI 10.1038/321175a0 Meleca RJ, 1997, BRAIN RES, V750, P201, DOI 10.1016/S0006-8993(96)01354-6 Moore D R, 1993, J Am Acad Audiol, V4, P277 MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 MUGNAINI E, 1972, COMP ANATOMY HISTOLO, P210 PETRALIA RS, 1994, J NEUROSCI, V14, P667 PETRALIA RS, 1994, J NEUROSCI, V14, P6102 Petralia RS, 1996, J COMP NEUROL, V372, P356 PONS TP, 1991, SCIENCE, V252, P1857, DOI 10.1126/science.1843843 Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 RUSSELL NJ, 1979, ACTA OTO-LARYNGOL, V88, P369, DOI 10.3109/00016487909137181 RYAN A, 1977, ANN OTO RHINOL LARYN, V86, P176 RYAN AF, 1988, HEARING RES, V36, P181, DOI 10.1016/0378-5955(88)90060-3 RYUGO DK, 1995, J COMP NEUROL, V358, P102, DOI 10.1002/cne.903580107 SANTI PA, 1982, HEARING RES, V7, P261, DOI 10.1016/0378-5955(82)90040-5 SATO K, 1996, ABST ASS RES OT, V19, P116 SCOTT JC, 1992, ARO ABSTR, V15, P43 SHAPIRA R, 1987, NATURE, V325, P58, DOI 10.1038/325058a0 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 Sone M, 1998, HEARING RES, V115, P217, DOI 10.1016/S0378-5955(97)00191-3 Staecker H, 1998, OTOLARYNG HEAD NECK, V119, P7, DOI 10.1016/S0194-5998(98)70194-9 SWARTZ KJ, 1993, NATURE, V361, P165, DOI 10.1038/361165a0 Takeno S, 1998, AUDIOL NEURO-OTOL, V3, P281, DOI 10.1159/000013800 THOMAS KL, 1994, NEURON, V13, P737, DOI 10.1016/0896-6273(94)90040-X TOYODA Y, 1977, ACTA OTO-LARYNGOL, V84, P202, DOI 10.3109/00016487709123958 WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 WINSKY L, 1995, J COMP NEUROL, V354, P564, DOI 10.1002/cne.903540407 NR 61 TC 20 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 113 EP 124 DI 10.1016/S0378-5955(00)00125-8 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200011 PM 10962178 ER PT J AU Potashner, SJ Suneja, SK Benson, CG AF Potashner, SJ Suneja, SK Benson, CG TI Altered glycinergic synaptic activities in guinea pig brain stem auditory nuclei after unilateral cochlear ablation SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE deafness; plasticity; glycine; cochlear nucleus; superior olive ID SUPERIOR OLIVARY COMPLEX; EAR OSSICLE REMOVAL; TRAPEZOID BODY; D-ASPARTATE; MEDIAL NUCLEUS; AUTORADIOGRAPHIC LOCALIZATION; IMMUNOREACTIVE PROJECTIONS; RECEPTOR DISTRIBUTION; RETROGRADE TRANSPORT; INFERIOR COLLICULUS AB This paper reviews efforts to determine if a unilateral hearing loss altered inhibitory glycinergic synapses in the cochlear nucleus (CN) and the superior olive. In young adult guinea pigs, 2-147 days after unilateral cochlear ablation, we quantified the electrically evoked release and the high-affinity uptake of [(14)C]glycine as measures of transmitter release from glycinergic presynaptic endings and glycine removal from extracellular spaces. The specific binding of [(3)H]strychnine was quantified to measure synaptic glycine receptor activity and/or expression. Three types of post-lesion change were observed. First, several tissues exhibited changes consistent with a persistent deficiency in glycinergic inhibitory transmission. Deficient binding prevailed on the ablated side in the anterior and caudal anteroventral CN, the posteroventral CN and the lateral superior olive (LSO), while glycine release was near normal and uptake was elevated (except in the LSO). However, deficient release prevailed in the dorsal CN, bilaterally, and was accompanied by elevated uptake. Second, the LSO on the intact side exhibited changes consistent with strengthened glycinergic inhibition, as binding was elevated while release and uptake were near normal. Third, several tissues exhibited various transient changes in activity. These types of post-lesion change might contribute to altered auditory functions, which often accompany hearing loss. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Connecticut, Ctr Hlth, Dept Anat, Farmington, CT 06030 USA. RP Potashner, SJ (reprint author), Univ Connecticut, Ctr Hlth, Dept Anat, Farmington, CT 06030 USA. EM sjp@neuron.uchc.edu CR ADAMS JC, 1990, HEARING RES, V49, P281, DOI 10.1016/0378-5955(90)90109-3 ALBUS U, 1983, TOXICON, V21, P97, DOI 10.1016/0041-0101(83)90053-3 ALTSCHULER RA, 1986, BRAIN RES, V369, P316, DOI 10.1016/0006-8993(86)90542-1 AXELSSON A, 1992, NOISE INDUCED HEARIN, P267 BENSON CG, 1990, J COMP NEUROL, V296, P415, DOI 10.1002/cne.902960307 Benson CG, 1997, SYNAPSE, V25, P243 Bilak M, 1997, EXP NEUROL, V147, P256, DOI 10.1006/exnr.1997.6636 BLEDSOE SC, 1990, BRAIN RES, V517, P189, DOI 10.1016/0006-8993(90)91025-C Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 BOETTCHER FA, 1993, J ACOUST SOC AM, V94, P2123, DOI 10.1121/1.407484 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 Cant N. B., 1991, NEUROBIOLOGY HEARING, P99 CASPARY DM, 1994, J NEUROPHYSIOL, V72, P2124 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 CASPARY DM, 1987, BRAIN RES, V417, P273, DOI 10.1016/0006-8993(87)90452-5 Caspary DM, 1991, NEUROBIOLOGY HEARING, P141 DUPONT J, 1994, ASS RES OT ABSTR, V17, P11 FROSTHOLM A, 1985, BRAIN RES BULL, V15, P473, DOI 10.1016/0361-9230(85)90038-3 FROSTHOLM A, 1986, BRAIN RES BULL, V16, P189, DOI 10.1016/0361-9230(86)90033-X Fubara BM, 1996, J COMP NEUROL, V369, P83 GERKEN GM, 1979, J ACOUST SOC AM, V66, P721, DOI 10.1121/1.383222 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 Godfrey DA, 1988, AUDITORY PATHWAY, P107 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GODFREY DA, 1978, J HISTOCHEM CYTOCHEM, V26, P118 GROTHE B, 1993, J NEUROPHYSIOL, V69, P1192 GROTHE B, 1994, J NEUROSCI, V14, P1701 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 Hillyer E.V., 1997, FERRETS RABBITS RODE, P243 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 Irvine D.R.F., 1986, Progress in Sensory Physiology, V7, P1 JASTREBOFF PJ, 1990, NEUROSCI RES, V8, P221, DOI 10.1016/0168-0102(90)90031-9 JEANBAPTISTE M, 1975, J COMP NEUROL, V162, P111, DOI 10.1002/cne.901620107 Kaltenbach JA, 1996, AUDIT NEUROSCI, V3, P57 Kim JN, 1997, HEARING RES, V103, P169, DOI 10.1016/S0378-5955(96)00173-6 KUWABARA N, 1991, J COMP NEUROL, V314, P684, DOI 10.1002/cne.903140405 KUWABARA N, 1992, J COMP NEUROL, V324, P522, DOI 10.1002/cne.903240406 MCCORMICK JG, 1976, BIOL GUINEA PIG, P282 *MCID, 1995, MICR IM DEV M2 M4 OP, P13 MILBRANDT JC, 1995, NEUROSCIENCE, V67, P713, DOI 10.1016/0306-4522(95)00082-T MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 MOREST DK, 1983, HEARING RES, V9, P145, DOI 10.1016/0378-5955(83)90024-2 Morest DK, 1997, HEARING RES, V103, P151, DOI 10.1016/S0378-5955(96)00172-4 OERTEL D, 1993, NATO ADV SCI INST SE, V239, P225 OLIVER DL, 1983, J NEUROSCI, V3, P967 Ostapoff EM, 1997, J COMP NEUROL, V381, P500, DOI 10.1002/(SICI)1096-9861(19970519)381:4<500::AID-CNE9>3.0.CO;2-6 POTASHNER SJ, 1983, J NEUROCHEM, V41, P1094, DOI 10.1111/j.1471-4159.1983.tb09057.x POTASHNER SJ, 1993, NATO ADV SCI INST SE, V239, P195 Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 POTASHNER SJ, 1984, J NEUROCHEM, V42, P1135, DOI 10.1111/j.1471-4159.1984.tb12722.x POWELL TPS, 1962, J ANAT, V96, P249 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 SAINTMARIE RL, 1991, HEARING RES, V51, P11, DOI 10.1016/0378-5955(91)90003-R SALVI RJ, 1992, NOISE INDUCED HEARIN, P156 SANES DH, 1987, J NEUROSCI, V7, P3793 SANES DH, 1987, J NEUROSCI, V7, P3803 SAUNDERS JC, 1991, J ACOUST SOC AM, V90, P136, DOI 10.1121/1.401307 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 SHORE SE, 1992, HEARING RES, V62, P16, DOI 10.1016/0378-5955(92)90199-W SPANGLER KM, 1987, J COMP NEUROL, V259, P452, DOI 10.1002/cne.902590311 SPANGLER KM, 1985, J COMP NEUROL, V238, P249, DOI 10.1002/cne.902380302 STAATZBENSON C, 1987, J NEUROCHEM, V49, P128, DOI 10.1111/j.1471-4159.1987.tb03404.x STAATZBENSON C, 1988, J NEUROCHEM, V51, P370, DOI 10.1111/j.1471-4159.1988.tb01048.x SUNEJA SK, 1995, J NEUROCHEM, V64, P161 SUNEJA SK, 1997, ASS RES OT ABS, V20, P84 Suneja S. K., 1995, Society for Neuroscience Abstracts, V21, P404 SUNEJA SK, 1995, J NEUROCHEM, V64, P147 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja S. K., 1997, Society for Neuroscience Abstracts, V23, P184 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 Warr WB, 1996, HEARING RES, V93, P83, DOI 10.1016/0378-5955(95)00198-0 WENTHOLD RJ, 1987, BRAIN RES, V415, P183, DOI 10.1016/0006-8993(87)90285-X WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X WENTHOLD RJ, 1977, BRAIN RES, V138, P111, DOI 10.1016/0006-8993(77)90787-9 WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 WICKESBERG RE, 1994, J COMP NEUROL, V339, P311, DOI 10.1002/cne.903390302 WICKESBERG RE, 1991, J COMP NEUROL, V313, P457, DOI 10.1002/cne.903130306 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 WU SH, 1986, J NEUROSCI, V6, P2691 WU SH, 1994, HEARING RES, V73, P57 WU SH, 1995, J NEUROPHYSIOL, V73, P256 NR 83 TC 64 Z9 65 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 125 EP 136 DI 10.1016/S0378-5955(00)00126-X PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200012 PM 10962179 ER PT J AU Sato, K Shiraishi, S Nakagawa, H Kuriyama, H Altschuler, RA AF Sato, K Shiraishi, S Nakagawa, H Kuriyama, H Altschuler, RA TI Diversity and plasticity in amino acid receptor subunits in the rat auditory brain stem SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE plasticity; cochlear nucleus; N-methyl, D-aspartate receptor; gamma aminobutyric acid receptor; glycine receptor; glutamate receptor; deafness ID SUPERIOR OLIVARY COMPLEX; CENTRAL-NERVOUS-SYSTEM; IN-SITU HYBRIDIZATION; COCHLEAR-NUCLEUS; MESSENGER-RNA; NMDA RECEPTOR; DIFFERENTIAL DISTRIBUTION; GLUTAMATE RECEPTORS; INFERIOR COLLICULUS; GLYCINE RECEPTORS AB Glutamate, gamma aminobutyric acid (GABA) and glycine receptors have different properties depending on the specific subunit combination utilized. The subunit composition of amino acid receptors may help to shape the responses of neurons and can provide a diversity of response properties in different neuronal types and regions. This allows a synaptic fine tuning for an optimization of processing requirements and may also allow for changes in response to changes in input. This article reviews the diversity that has been found in the subunit composition of GABA, glycine, alpha amino-3-bydroxy-5-methyl-4 isoxazole propionic acid and N-Methyl, D-aspartate (NMDA) receptors in the mammalian auditory brain stem and provides new data on how the NMDAR1 glutamate receptor subunit changes as a consequence of deafness. In the latter study, quantitative in situ hybridization was used to assess NMDAR1 mRNA expression in six cell types of the rat cochlear nucleus. A unilateral cochlear ablation was performed and expression determined in the ipsilateral and contralateral cochlear nucleus 5 and 20 days later. Significantly decreased expression, compared to normal, was found 5 days following deafness, in ipsilateral spherical bushy cells, octopus cells and shell neurons, but not in fusiform cells, corn cells or granule cells. At 20 days the expression was not significantly different from normal in any of the six cell types. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Altschuler, RA (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. EM shuler@umich.edu CR Altschuler RA, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P193, DOI 10.1007/978-1-4419-8712-9_18 ARAKI T, 1992, NEUROSCIENCE, V47, P45, DOI 10.1016/0306-4522(92)90119-M ARAKI T, 1992, MOL BRAIN RES, V12, P293, DOI 10.1016/0169-328X(92)90132-U Barnard EA, 1998, PHARMACOL REV, V50, P291 Betz H, 1991, Adv Exp Med Biol, V287, P421 Bilak MM, 1996, NEUROSCIENCE, V75, P1075, DOI 10.1016/0306-4522(96)00197-2 Brenman JE, 1996, CELL, V84, P757, DOI 10.1016/S0092-8674(00)81053-3 BULLER AL, 1994, J NEUROSCI, V14, P5471 CANT NB, 1984, HEARING SCI RECENT A, P371 Caspary DM, 1999, NEUROSCIENCE, V93, P307, DOI 10.1016/S0306-4522(99)00121-9 Fessenden JD, 1999, J COMP NEUROL, V404, P52 FORSYTHE I, 1993, P R SOC LOND, V251, P51 Friauf E, 1997, J COMP NEUROL, V385, P117, DOI 10.1002/(SICI)1096-9861(19970818)385:1<117::AID-CNE7>3.0.CO;2-5 FUJITA M, 1991, BRAIN RES, V560, P23, DOI 10.1016/0006-8993(91)91210-R GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 GUITIERREZ A, 1996, J COMP NEUROL, V365, P504 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HOLLMANN M, 1991, SCIENCE, V252, P851, DOI 10.1126/science.1709304 HUME RI, 1991, SCIENCE, V253, P1028, DOI 10.1126/science.1653450 HUNTER C, 1993, J NEUROSCI, V13, P1932 HUNTER WN, 1995, MOL MED TODAY, V1, P31, DOI 10.1016/1357-4310(95)80017-4 Hurd LB, 1999, SYNAPSE, V33, P83 Hutson KA, 1996, J COMP NEUROL, V371, P397, DOI 10.1002/(SICI)1096-9861(19960729)371:3<397::AID-CNE4>3.0.CO;2-Y IM WB, 1995, J BIOL CHEM, V270, P26063 Krenning J, 1998, LARYNGOSCOPE, V108, P26, DOI 10.1097/00005537-199801000-00005 LAURIE DJ, 1994, J NEUROSCI, V14, P3180 MALOSIO ML, 1991, EMBO J, V10, P2401 McDonald RL, 1994, ANNU REV NEUROSCI, V17, P569 McKernan RM, 1996, TRENDS NEUROSCI, V19, P139, DOI 10.1016/S0166-2236(96)80023-3 Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F MISHINA M, 1993, MOL BASIS ION CHANNE, P136 MONAGHAN DT, 1989, ANNU REV PHARMACOL, V29, P365 MONYER H, 1992, SCIENCE, V256, P1217, DOI 10.1126/science.256.5060.1217 MORIYOSHI K, 1991, NATURE, V354, P31, DOI 10.1038/354031a0 MOSBACHER J, 1994, SCIENCE, V266, P1059, DOI 10.1126/science.7973663 NAKAGAWA H, 1998, ASS RES OT ABSTR, V21, P841 NAKANISHI N, 1992, P NATL ACAD SCI USA, V89, P8552, DOI 10.1073/pnas.89.18.8552 NAKANISHI S, 1992, SCIENCE, V258, P7 NAYEEM N, 1994, J NEUROCHEM, V62, P815 PETRALIA RS, 1994, J NEUROSCI, V14, P667 Petralia RS, 1997, J COMP NEUROL, V385, P456, DOI 10.1002/(SICI)1096-9861(19970901)385:3<456::AID-CNE9>3.0.CO;2-2 PETRALIA RS, 1992, J COMP NEUROL, V318, P9 Petralia RS, 1996, J COMP NEUROL, V372, P356 Potashner SJ, 2000, HEARING RES, V147, P125, DOI 10.1016/S0378-5955(00)00126-X RAMAN IM, 1992, NEURON, V9, P173, DOI 10.1016/0896-6273(92)90232-3 SATO K, 1996, ARO ABSTR, V19, P476 Sato K, 1999, NEUROSCIENCE, V89, P839, DOI 10.1016/S0306-4522(98)00350-9 Sato K, 1998, MICROSC RES TECHNIQ, V41, P217 Sato K, 1995, HEARING RES, V91, P7, DOI 10.1016/0378-5955(95)00156-5 SHIRAISHI Y, 1999, ASS RES OT ABSTR, V22, P69 SIEGHART W, 1995, PHARMACOL REV, V47, P181 SIGEL E, 1990, NEURON, V5, P703, DOI 10.1016/0896-6273(90)90224-4 SOMMER B, 1991, CELL, V67, P11, DOI 10.1016/0092-8674(91)90568-J SUGIHARA H, 1992, BIOCHEM BIOPH RES CO, V185, P826, DOI 10.1016/0006-291X(92)91701-Q Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 TRETTER V, 1997, J NEUROCHEM, V17, P2726 Trussell LO, 1999, ANNU REV PHYSIOL, V61, P477, DOI 10.1146/annurev.physiol.61.1.477 Wang YX, 1998, J NEUROSCI, V18, P1148 WATANABE M, 1994, J COMP NEUROL, V343, P520, DOI 10.1002/cne.903430403 Wenthold RJ, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P93, DOI 10.1007/978-1-4419-8712-9_10 WENTHOLD RJ, 1993, NATO ADV SCI INST SE, V239, P179 Wynne B, 1995, J CHEM NEUROANAT, V9, P289, DOI 10.1016/0891-0618(95)00095-X Zhang J H, 1991, Adv Exp Med Biol, V287, P381 NR 64 TC 26 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 137 EP 144 DI 10.1016/S0378-5955(00)00127-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200013 PM 10962180 ER PT J AU Durham, D Park, DL Girod, DA AF Durham, D Park, DL Girod, DA TI Central nervous system plasticity during hair cell loss and regeneration SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE nucleus magnocellularis; gentamicin; deafferentation; avian; auditory ID STEM AUDITORY NUCLEI; CHICK COCHLEAR NUCLEUS; AFFERENT INFLUENCES; ACOUSTIC TRAUMA; INNER-EAR; INTENSE SOUND; BASILAR PAPILLA; AMINOGLYCOSIDE OTOTOXICITY; MAGNOCELLULARIS NEURONS; TONOTOPIC ORGANIZATION AB Following cochlear ablation, auditory neurons in the central nervous system (CNS) undergo alterations in morphology and function, including neuronal cell death. The trigger for these CNS changes is the abrupt cessation of afferent input via eighth nerve fiber activity. Gentamicin can cause ototoxic damage to cochlear hair cells responsible for high frequency hearing, which seems likely to cause a frequency-specific loss of input into the CNS. In birds, these hair cells can regenerate, presumably restoring input into the CNS. This review summarizes current knowledge of how CNS auditory neurons respond to this transient: frequency-specific loss of cochlear function. A single systemic injection of a high dose of gentamicin results in the complete loss of high frequency hair cells by 5 days, followed by the regeneration of new hair cells. Both hair cell-specific functional measures and estimates of CNS afferent activity suggest that newly regenerated hair cells restore afferent input to brainstem auditory neurons. Frequency-specific neuronal cell death and shrinkage occur following gentamicin damage to hair cells, with an unexpected recovery of neuronal cell number at longer survival times. A newly-developed method for topical, unilateral gentamicin application will allow future studies to compare neuronal changes within a given animal. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Kansas, Med Ctr, Dept Otolaryngol, Kansas City, KS 66160 USA. Univ Kansas, Med Ctr, Smith Mental Retardat & Human Dev Ctr, Kansas City, KS 66160 USA. Univ Kansas, Med Ctr, Dept Speech & Hearing, Kansas City, KS 66160 USA. Vet Affairs Med Ctr, Kansas City, MO USA. RP Durham, D (reprint author), Univ Kansas, Med Ctr, Dept Otolaryngol, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 ADLER HJ, 1995, J NEUROCYTOL, V24, P111, DOI 10.1007/BF01181554 ALVAREZBUYLLA A, 1994, J COMP NEUROL, V347, P233, DOI 10.1002/cne.903470207 Bengzon J, 1997, P NATL ACAD SCI USA, V94, P10432, DOI 10.1073/pnas.94.19.10432 BORN DE, 1991, BRAIN RES, V557, P37, DOI 10.1016/0006-8993(91)90113-A BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 BORN DE, 1988, J NEUROSCI, V8, P901 CANADY KS, 1992, J NEUROSCI, V12, P1001 Chen L, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P43 CHEN L, 1993, HEARING RES, V69, P15, DOI 10.1016/0378-5955(93)90089-J CLORFENE JB, 1994, DEV BRAIN RES, V79, P93, DOI 10.1016/0165-3806(94)90052-3 CODE RA, 1989, J COMP NEUROL, V284, P504, DOI 10.1002/cne.902840403 COHEN YE, 1994, HEARING RES, V81, P11, DOI 10.1016/0378-5955(94)90148-1 Corwin JT, 1997, NEURON, V19, P951, DOI 10.1016/S0896-6273(00)80386-4 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 Dooling RJ, 1997, P NATL ACAD SCI USA, V94, P14206, DOI 10.1073/pnas.94.25.14206 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 DUCKERT LG, 1993, J COMP NEUROL, V331, P75, DOI 10.1002/cne.903310105 EPSTEIN JE, 1995, HEARING RES, V90, P31, DOI 10.1016/0378-5955(95)00141-9 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R FROYMOVICH O, 1995, J ACOUST SOC AM, V97, P3021, DOI 10.1121/1.411867 GARDEN GA, 1994, J NEUROSCI, V14, P1991 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 GIROD GD, 2000, IN PRESS AM J OTOLAR Gould E, 1997, NEUROSCIENCE, V80, P427, DOI 10.1016/S0306-4522(97)00127-9 Harzsch S, 1996, J NEUROBIOL, V29, P384, DOI 10.1002/(SICI)1097-4695(199603)29:3<384::AID-NEU9>3.0.CO;2-5 HASHINO E, 1991, HEARING RES, V52, P356, DOI 10.1016/0378-5955(91)90025-5 HASHINO E, 1989, J ACOUST SOC AM, V85, P289, DOI 10.1121/1.397736 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HENNING A, 1998, J NEUROSCI, V18, P111 Husmann KR, 1998, HEARING RES, V125, P109, DOI 10.1016/S0378-5955(98)00137-3 HYDE GE, 1990, J COMP NEUROL, V297, P329, DOI 10.1002/cne.902970302 HYDE GE, 1994, J COMP NEUROL, V339, P27, DOI 10.1002/cne.903390105 Janas JD, 1995, HEARING RES, V92, P17, DOI 10.1016/0378-5955(95)00190-5 Kempermann G, 1997, NATURE, V386, P493, DOI 10.1038/386493a0 LACHICA EA, 1994, J COMP NEUROL, V348, P403, DOI 10.1002/cne.903480307 LINDEN R, 1994, NEUROSCIENCE, V58, P671, DOI 10.1016/0306-4522(94)90447-2 Ling CY, 1997, J COMP NEUROL, V379, P300 LIPPE W, 1985, J COMP NEUROL, V237, P273, DOI 10.1002/cne.902370211 LIPPE WR, 1991, HEARING RES, V51, P193, DOI 10.1016/0378-5955(91)90036-9 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y Mattson MP, 1996, PERSPECT DEV NEUROBI, V3, P79 MORGAN AS, 1999, ARO ABSTR, V22, P96 NIEMIEC AJ, 1994, HEARING RES, V74, P209 NUCKOLS DA, 1999, ARO ABSTR, V22, P129 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 Ofsie MS, 1996, J COMP NEUROL, V370, P281 Ofsie MS, 1997, HEARING RES, V113, P207, DOI 10.1016/S0378-5955(97)00150-0 Park DL, 1999, HEARING RES, V138, P45, DOI 10.1016/S0378-5955(99)00138-0 Park DL, 1998, HEARING RES, V126, P84, DOI 10.1016/S0378-5955(98)00157-9 PARKS TN, 1981, J COMP NEUROL, V203, P425, DOI 10.1002/cne.902030307 PARKS TN, 1979, J COMP NEUROL, V183, P665, DOI 10.1002/cne.901830313 PASIC TR, 1991, OTOLARYNG HEAD NECK, V104, P6 PerezCanellas MR, 1996, DEV BRAIN RES, V93, P49, DOI 10.1016/0165-3806(96)00014-4 PUGLIANO FA, 1993, NEUROSCI LETT, V151, P214, DOI 10.1016/0304-3940(93)90023-E ROBINSON AM, 1999, ARO ABSTR, V22, P129 RUBEL E W, 1991, Brain Dysfunction, V4, P55 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 RYALS BM, 1982, ACTA OTO-LARYNGOL, V93, P205, DOI 10.3109/00016488209130873 RYALS BM, 1985, HEARING RES, V19, P73, DOI 10.1016/0378-5955(85)90099-1 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1995, HEARING RES, V83, P51, DOI 10.1016/0378-5955(94)00190-2 RYALS BM, 1994, HEARING RES, V72, P81, DOI 10.1016/0378-5955(94)90208-9 SALVI RJ, 1994, J COMP PHYSIOL A, V174, P351 Saunders JC, 1996, J NEUROPHYSIOL, V76, P770 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A Saunders JC, 1998, J COMP NEUROL, V390, P412 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x STEWARD O, 1985, J COMP NEUROL, V231, P385, DOI 10.1002/cne.902310308 Stone JS, 1998, CURR OPIN NEUROL, V11, P17, DOI 10.1097/00019052-199802000-00004 STREUBEL SO, 1998, ARO ABSTR, V21, P62 Tierney TS, 1997, J COMP NEUROL, V378, P295, DOI 10.1002/(SICI)1096-9861(19970210)378:2<295::AID-CNE11>3.0.CO;2-R TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 TSUE TT, 1994, OTOLARYNG HEAD NECK, V111, P281, DOI 10.1016/S0194-5998(94)70603-4 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WESTRUM LE, 1999, ARO ABSTR, V22, P127 WILSON CR, 1999, UNPUB J COMP NEUROL ZIRPEL L, 1995, J NEUROPHYSIOL, V74, P1355 ZUPANC GKH, 1995, J COMP NEUROL, V353, P213, DOI 10.1002/cne.903530205 NR 83 TC 16 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 145 EP 159 DI 10.1016/S0378-5955(00)00128-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200014 PM 10962181 ER PT J AU Redd, EE Pongstaporn, T Ryugo, DK AF Redd, EE Pongstaporn, T Ryugo, DK TI The effects of congenital deafness on auditory nerve synapses and globular bushy cells in cats SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE endbulb; extracellular cisterna; hearing; postsynaptic density ID ANTEROVENTRAL COCHLEAR NUCLEUS; NEURONAL ARCHITECTURE; WHITE CATS; GLUTAMATE RECEPTORS; CENTRAL PROJECTIONS; GUINEA-PIG; TIME; CHILDREN; REGION; ROOT AB It is well known that auditory deprivation affects the structure and function of the central nervous system. Congenital deafness represents one form of deprivation, and in the adult white cat, it has been shown to have a clear effect upon the synaptic interface between endbulbs of Held and spherical bushy cells. It is not known, however, whether all primary synapses are affected and/or whether they are affected in the same way and to the same extent. Thus, we studied a second neuronal circuit in the deaf white cat involving modified (small) endbulbs and globular bushy cells. Compared to normal hearing cats, modified endbulbs of congenitally deaf cats were 52.2% smaller but unchanged in structural complexity. There was also a striking loss of extracellular space between ending and cell body. The somata of postsynaptic globular bushy cells were 13.4% smaller and had enlarged postsynaptic densities. These data reveal that axosomatic synapses demonstrate abnormal structure as a consequence of deafness and that the extent of the abnormalities can vary with respect to the circuits involved. The implication of these observations is that synaptic anomalies would introduce differential delays within separate circuits, thereby desynchronizing neural activity from sound stimuli. This loss of synchronization could in turn disrupt temporal processing and compromise a host of related functions, including language comprehension. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Ctr Hearing Sci, Baltimore, MD 21205 USA. RP Ryugo, DK (reprint author), Johns Hopkins Univ, Sch Med, Ctr Hearing Sci, Traylor Res Bldg,5th Floor,720 Rutland Ave, Baltimore, MD 21205 USA. EM dryugo@bme.jhu.edu CR Bergles DE, 1999, CURR OPIN NEUROBIOL, V9, P293, DOI 10.1016/S0959-4388(99)80043-9 Bergles DE, 1997, P NATL ACAD SCI USA, V94, P14821, DOI 10.1073/pnas.94.26.14821 BERGSMA DR, 1971, J HERED, V62, P171 BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 BOSHER SK, 1965, PROC R SOC SER B-BIO, V162, P147, DOI 10.1098/rspb.1965.0030 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 Brighton P, 1991, ANN NY ACAD SCI, V630, P152 CANT NB, 1978, NEUROSCIENCE, V3, P1003, DOI 10.1016/0306-4522(78)90120-3 DEOL MS, 1970, PROC R SOC SER B-BIO, V175, P201, DOI 10.1098/rspb.1970.0019 Diamond JS, 1997, J NEUROSCI, V17, P4672 Doucet JR, 1997, J COMP NEUROL, V385, P245 FEKETE DM, 1984, J COMP NEUROL, V229, P432, DOI 10.1002/cne.902290311 Fitzpatrick DC, 1997, NATURE, V388, P871, DOI 10.1038/42246 FRYAUFBERTSCHY H, 1992, J SPEECH HEAR RES, V35, P913 GANTZ BJ, 1994, AM J OTOL, V15, P1 HACKNEY CM, 1990, ANAT EMBRYOL, V182, P123 Hackney CM, 1996, EUR J NEUROSCI, V8, P79, DOI 10.1111/j.1460-9568.1996.tb01169.x HARRISON JM, 1966, J COMP NEUROL, V126, P391, DOI 10.1002/cne.901260303 Irvine D. R. F., 1992, MAMMALIAN AUDITORY P, P153 Irvine D.R.F., 1986, AUDITORY BRAINSTEM R Klinke R, 1999, SCIENCE, V285, P1729, DOI 10.1126/science.285.5434.1729 LARSEN SA, 1992, EXP NEUROL, V115, P151, DOI 10.1016/0014-4886(92)90240-Q LENN NJ, 1966, AM J ANAT, V118, P375, DOI 10.1002/aja.1001180205 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC Mair I W, 1973, Acta Otolaryngol Suppl, V314, P1 Mandelbrot B. B., 1982, FRACTAL GEOMETRY NAT MANIS PB, 1991, J NEUROSCI, V11, P2865 MOORE JK, 1994, AM J OTOL, V15, P588 NADOL JB, 1982, LARYNGOSCOPE, V92, P1028 NUSSER Z, 1994, NEUROSCIENCE, V61, P421, DOI 10.1016/0306-4522(94)90421-9 Oertel D, 1991, Curr Opin Neurobiol, V1, P221, DOI 10.1016/0959-4388(91)90082-I OSTAPOFF EM, 1991, J COMP NEUROL, V314, P598, DOI 10.1002/cne.903140314 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 PORTER R, 1991, NEUROSCI LETT, V130, P112, DOI 10.1016/0304-3940(91)90240-T PUJOL R, 1977, ACTA OTO-LARYNGOL, V83, P59, DOI 10.3109/00016487709128813 QUITTNER AL, 1991, AM J OTOL, V12, P89 RAWITZ B, 1896, MORPHAL ARB, V6, P546 REBILLARD M, 1981, HEARING RES, V5, P179, DOI 10.1016/0378-5955(81)90044-7 ROUILLER EM, 1986, J COMP NEUROL, V249, P261, DOI 10.1002/cne.902490210 Rubio ME, 1997, NEURON, V18, P939, DOI 10.1016/S0896-6273(00)80333-5 RYUGO DK, 1981, BRAIN RES, V210, P342, DOI 10.1016/0006-8993(81)90907-0 Ryugo DK, 1997, J COMP NEUROL, V385, P230, DOI 10.1002/(SICI)1096-9861(19970825)385:2<230::AID-CNE4>3.0.CO;2-2 RYUGO DK, 1991, J COMP NEUROL, V305, P35, DOI 10.1002/cne.903050105 Ryugo DK, 1998, J COMP NEUROL, V397, P532, DOI 10.1002/(SICI)1096-9861(19980810)397:4<532::AID-CNE6>3.0.CO;2-2 Saada AA, 1996, BRAIN RES, V736, P315, DOI 10.1016/0006-8993(96)00719-6 SCHEIBE A, 1992, ARCH OTOLARYNGOL, V211, P12 Schofield BR, 1996, J COMP NEUROL, V375, P128, DOI 10.1002/(SICI)1096-9861(19961104)375:1<128::AID-CNE8>3.0.CO;2-5 SCHWARTZ IR, 1982, ACTA OTO-LARYNGOL, V93, P9, DOI 10.3109/00016488209130847 SPANGLER KM, 1987, J COMP NEUROL, V259, P452, DOI 10.1002/cne.902590311 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 Suga F, 1970, Laryngoscope, V80, P81 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3013, DOI 10.1016/0306-4522(82)90227-5 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3031, DOI 10.1016/0306-4522(82)90228-7 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3053, DOI 10.1016/0306-4522(82)90229-9 Tyler RS, 1996, EAR HEARING, V17, pS38, DOI 10.1097/00003446-199617031-00005 WAARDENBURG PJ, 1951, AM J HUM GENET, V3, P195 WALTZMAN S, 1994, ANN OTO RHINOL LARYN, V104, P15 WARR WB, 1982, CONTRIBUTIONS SENSOR, P1 WENTHOLD RJ, 1993, NATO ADV SCI INST SE, V239, P179 WEST CD, 1973, J COMP NEUROL, V151, P377, DOI 10.1002/cne.901510406 Wolff D, 1942, J HERED, V33, P39 Yin T. C. T., 1988, AUDITORY FUNCTION, P385 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 Young E. D., 1988, AUDITORY FUNCTION NE, P277 NR 65 TC 32 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 160 EP 174 DI 10.1016/S0378-5955(00)00129-5 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200015 PM 10962182 ER PT J AU Bauer, CA Brozoski, TJ Holder, TM Caspary, DM AF Bauer, CA Brozoski, TJ Holder, TM Caspary, DM TI Effects of chronic salicylate on GABAergic activity in rat inferior colliculus SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE salicylate; auditory plasticity; GABA; GAD; tinnitus; inferior colliculus; rat ID GLUTAMIC-ACID DECARBOXYLASE; GABA(A) RECEPTOR-BINDING; PRIMARY AUDITORY-CORTEX; EAR OSSICLE REMOVAL; GAD MESSENGER-RNA; GUINEA-PIG; BRAIN-STEM; FREQUENCY REPRESENTATION; COCHLEAR ABLATION; BARREL CORTEX AB It is well accepted that salicylate ototoxicity results in reversible tinnitus in humans. Salicylate-induced tinnitus may be an example of plasticity of the central auditory system and could potentially serve as a model to further understand mechanisms of tinnitus generation. This study examined levels of glutamic acid decarboxylase (GAD) and the binding characteristics of the GABA(A) receptor in auditory brainstem structures of Long-Evans rats chronically treated with salicylate. Western blotting revealed a significant 63% (P < 0.008) elevation of GAD levels in the inferior colliculus (IC) of salicylate-treated subjects. This occurred in subjects demonstrating behavioral evidence of tinnitus. Muscimol saturation analysis was indicative of a salicylate-related increase in receptor affinity. Linear regression of [H-3]muscimol saturation analysis data revealed a significant (P < 0.05) reduction in Kd values in whole IC (-48%), as well as in the central nucleus of IC (CIC, -58%) and combined external and dorsal cortex of IC (E/DCIC, -46%). The number of GABA(A) binding sites (B-max) were also significantly (P < 0.05) decreased. These changes were observed only in central auditory structures. This suggests that GAD expression and GABA(A) receptor binding characteristics may be altered with chronic exposure to sodium salicylate and these changes may represent aberrant plasticity clinically experienced as tinnitus. (C) 2000 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Div Otolaryngol, Springfield, IL 62794 USA. RP Bauer, CA (reprint author), So Illinois Univ, Sch Med, Div Otolaryngol, POB 19662, Springfield, IL 62794 USA. CR Abbott SD, 1999, NEUROSCIENCE, V93, P1375, DOI 10.1016/S0306-4522(99)00300-0 Bauer CA, 1999, OTOLARYNG HEAD NECK, V121, P457, DOI 10.1016/S0194-5998(99)70237-8 Benson CG, 1997, SYNAPSE, V25, P243 Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 Bowers G, 1998, J NEUROSCI, V18, P5938 BRUMMETT RE, 1995, MECH TINNITUS, P7 Buonomano DV, 1998, ANNU REV NEUROSCI, V21, P149, DOI 10.1146/annurev.neuro.21.1.149 Caspary DM, 1999, NEUROSCIENCE, V93, P307, DOI 10.1016/S0306-4522(99)00121-9 CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O Dalezios Y, 1998, NEUROCHEM INT, V32, P213, DOI 10.1016/S0197-0186(97)00089-2 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 EGGERMONT JJ, 1990, HEARING RES, V48, P111, DOI 10.1016/0378-5955(90)90202-Z Eggermont JJ, 1998, HEARING RES, V117, P149, DOI 10.1016/S0378-5955(98)00008-2 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 Evans E F, 1981, Ciba Found Symp, V85, P108 FAINGOLD CL, 1994, BRAIN RES, V640, P40, DOI 10.1016/0006-8993(94)91855-4 Fuchs JL, 1998, J COMP NEUROL, V395, P209 GARRAGHTY PE, 1991, SOMATOSENS MOT RES, V8, P347 GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 GUTIERREZ A, 1994, J NEUROSCI, V14, P7469 Hensch TK, 1998, SCIENCE, V282, P1504, DOI 10.1126/science.282.5393.1504 Houser CR, 1996, EPILEPSY RES, V26, P207, DOI 10.1016/S0920-1211(96)00054-X ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JASTREBOFF PJ, 1986, J ACOUST SOC AM, V80, P1384, DOI 10.1121/1.394391 JASTREBOFF PJ, 1990, NEUROSCI RES, V8, P221, DOI 10.1016/0168-0102(90)90031-9 KAUFMAN DL, 1991, J NEUROCHEM, V56, P7203 Liang F, 1996, EXP BRAIN RES, V110, P163 LITWAK J, 1990, NEUROSCI LETT, V116, P179, DOI 10.1016/0304-3940(90)90406-Y Manabe Y, 1997, HEARING RES, V103, P192, DOI 10.1016/S0378-5955(96)00181-5 MARTIN WH, 1993, LARYNGOSCOPE, V103, P600 Meikle M. B., 1995, MECH TINNITUS, P181 Melzer P, 1998, NEUROSCIENCE, V83, P27, DOI 10.1016/S0306-4522(97)00332-1 Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F Milbrandt JC, 1996, NEUROSCIENCE, V73, P449, DOI 10.1016/0306-4522(96)00050-4 Ochi K, 1996, HEARING RES, V95, P63, DOI 10.1016/0378-5955(96)00019-6 PAN HS, 1983, J NEUROSCI, V3, P1189 Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 RECANZONE GH, 1993, J NEUROSCI, V13, P87 ROBERTS RC, 1985, BRAIN RES, V361, P324, DOI 10.1016/0006-8993(85)91303-4 Scholze P, 1996, EUR J PHARMACOL, V304, P155, DOI 10.1016/0014-2999(96)00088-X SCHREINER CE, 1987, P 3 INT TINN SEM HAR, P100 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E Sugita Y, 1996, NATURE, V380, P523, DOI 10.1038/380523a0 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 SZCZEPANIAK WS, 1995, NEUROSCI LETT, V196, P77, DOI 10.1016/0304-3940(95)11851-M Vees AM, 1998, J COMP NEUROL, V400, P110 WallhausserFranke E, 1997, NEUROREPORT, V8, P725, DOI 10.1097/00001756-199702100-00029 Wang J, 1996, J NEUROPHYSIOL, V75, P171 Weinberger N M, 1993, Curr Opin Neurobiol, V3, P570, DOI 10.1016/0959-4388(93)90058-7 WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 NR 52 TC 56 Z9 72 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 175 EP 182 DI 10.1016/S0378-5955(00)00130-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200016 PM 10962183 ER PT J AU Mossop, JE Wilson, MJ Caspary, DM Moore, DR AF Mossop, JE Wilson, MJ Caspary, DM Moore, DR TI Down-regulation of inhibition following unilateral deafening SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE deafness; cochlear ablation; inferior colliculus; auditory plasticity ID STEM AUDITORY NUCLEI; INFERIOR COLLICULUS; GABAERGIC NEURONS; COCHLEAR ABLATION; BRAIN-STEM; EVOKED-POTENTIALS; PLASTIC CHANGES; VISUAL-CORTEX; GABA; GERBIL AB Physiological and neurochemical experiments described here suggest that unilateral deafening causes a reduction in inhibition in the adult gerbil inferior colliculus (IC) contralateral to the deafened ear. Multiple-unit recordings were made from single electrode penetrations in the IC prior to and directly after contralateral cochlear ablation. These recordings showed up to 60% increases in the proportion of sampled loci at which neural activity excited by ipsilateral stimulation was observed after the ablation. Novel excitatory responses were evident within minutes of the ablation. Western blotting for glutamic acid decarboxylase protein levels showed significant decreases in the IC contralateral to cochlear ablation, relative to those in the ipsilateral IC, at 24 h and 7 days survival after the ablation. Four hour or 1 year survival post-ablation did not produce significant contralateral/ipsilateral differences in relation to the control group. Taken together, these results suggest the presence of at least two, short-term mechanisms involved in the central response to cochlear removal, both of which appear to implicate a decreased inhibitory influence. One is a very rapid, stimulus-related, functional unmasking. The other is a more delayed reduction in the capacity of gamma-aminobutyric acid synthesis in the IC. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Oxford, Physiol Lab, Oxford OX1 3PT, England. So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. RP Moore, DR (reprint author), Univ Oxford, Physiol Lab, Parks Rd, Oxford OX1 3PT, England. CR Abbott SD, 1999, NEUROSCIENCE, V93, P1375, DOI 10.1016/S0306-4522(99)00300-0 Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 CASPARY DM, 1990, J NEUROSCI, V10, P2363 GARRAGHTY PE, 1991, SOMATOSENS MOT RES, V8, P347 HENDRY SHC, 1990, J NEUROSCI, V10, P2438 HENDRY SHC, 1986, NATURE, V320, P750, DOI 10.1038/320750a0 HENDRY SHC, 1988, NEURON, V1, P701, DOI 10.1016/0896-6273(88)90169-9 JONES EG, 1993, CEREB CORTEX, V3, P361, DOI 10.1093/cercor/3.5.361-a McAlpine D, 1997, J NEUROPHYSIOL, V78, P767 Milbrandt JC, 2000, HEARING RES, V147, P251, DOI 10.1016/S0378-5955(00)00135-0 Moore DR, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P489, DOI 10.1007/978-1-4419-8712-9_45 MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 Moore DR, 1998, J NEUROPHYSIOL, V80, P2229 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 REALE RA, 1987, DEV BRAIN RES, V34, P281, DOI 10.1016/0165-3806(87)90215-X ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Szczepaniak WS, 1996, EVOKED POTENTIAL, V100, P158, DOI 10.1016/0013-4694(95)00234-0 Tierney TS, 1997, J COMP NEUROL, V378, P295, DOI 10.1002/(SICI)1096-9861(19970210)378:2<295::AID-CNE11>3.0.CO;2-R WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 NR 23 TC 78 Z9 81 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 183 EP 187 DI 10.1016/S0378-5955(00)00054-X PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200017 PM 10962184 ER PT J AU Irvine, DRF Rajan, R McDermott, HJ AF Irvine, DRF Rajan, R McDermott, HJ TI Injury-induced reorganization in adult auditory cortex and its perceptual consequences SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE auditory cortex; plasticity; cochlear lesion; hearing loss; tonotopicity; frequency discrimination; growth of loudness; tinnitus ID COCHLEAR HEARING-LOSS; MASSIVE CORTICAL REORGANIZATION; PRIMARY VISUAL-CORTEX; SOMATOSENSORY CORTEX; BRAILLE READERS; PREPULSE INHIBITION; LOUDNESS PERCEPTION; NEURAL PLASTICITY; STARTLE RESPONSE; C57BL/6J MICE AB Restricted cochlear lesions in adult animals result in a reorganization of auditory cortex such that the cortical region deprived of its normal input by the lesion is occupied by expanded representations of adjacent cochlear loci, and thus of the frequencies represented at those loci. Analogous injury-induced reorganization is seen in somatosensory, visual and motor cortices Of adult animals after restricted peripheral lesions. The occurrence of such reorganization in a wide range of species (including simian primates), and across different sensory systems and forms of peripheral lesion, suggests that it would also occur in humans with similar lesions. Direct evidence in support of this suggestion is provided by a small body of functional imaging evidence in the somatosensory and auditory systems. Although such reorganization does not seem to have a compensatory function, such a profound change in the pattern of cortical activation produced by stimuli exciting peri-lesion parts of the receptor epithelium would be expected to have perceptual consequences. However, there is only limited psychophysical evidence for perceptual effects that might be attributable to injury-induced cortical reorganization, and very little direct evidence for the correlation between the perceptual phenomena and the occurrence of reorganization. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia. Monash Univ, Dept Physiol, Clayton, Vic 3168, Australia. Cooperat Res Ctr Cochlear Implant Speech & Hearin, Melbourne, Vic 3002, Australia. RP Irvine, DRF (reprint author), Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia. EM d.irvine@sci.monash.edu.au RI Rajan, Ramesh/A-5945-2008; Irvine, Dexter/F-7474-2011 CR Buss E, 1998, HEARING RES, V125, P98, DOI 10.1016/S0378-5955(98)00131-2 Carlson S, 1996, HEARING RES, V99, P168, DOI 10.1016/S0378-5955(96)00098-6 DAVIS H, 1970, HEARING DEAFNESS, P83 Doetsch GS, 1998, NEUROREPORT, V9, pR29, DOI 10.1097/00001756-199806010-00001 DOHERTY KA, 1995, J ACOUST SOC AM, V97, P3277, DOI 10.1121/1.411569 ELBERT T, 1995, SCIENCE, V270, P305, DOI 10.1126/science.270.5234.305 ELBERT T, 1994, NEUROREPORT, V5, P2593, DOI 10.1097/00001756-199412000-00047 FLOR H, 1995, NATURE, V375, P482, DOI 10.1038/375482a0 Florentine M, 1997, MODELING SENSORINEURAL HEARING LOSS, P187 Gilbert CD, 1998, PHYSIOL REV, V78, P467 GILBERT CD, 1992, NATURE, V356, P150, DOI 10.1038/356150a0 HARRISON RV, 1992, ADV BIOSCI, V83, P625 HARRISON RV, 1991, HEARING RES, V54, P11, DOI 10.1016/0378-5955(91)90131-R HELLMAN RP, 1994, J ACOUST SOC AM, V96, P2655, DOI 10.1121/1.411445 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 IRVINE DRF, 1995, ADV HEARING RES, P3 Kaas Jon H., 1995, P51 KAAS JH, 1991, ANNU REV NEUROSCI, V14, P137, DOI 10.1146/annurev.neuro.14.1.137 KAAS JH, 1990, SCIENCE, V248, P229, DOI 10.1126/science.2326637 Knecht S, 1998, BRAIN, V121, P717, DOI 10.1093/brain/121.4.717 Knecht S, 1996, BRAIN, V119, P1213, DOI 10.1093/brain/119.4.1213 McDermott HJ, 1998, J ACOUST SOC AM, V104, P2314, DOI 10.1121/1.423744 MERZENICH MM, 1984, J COMP NEUROL, V224, P591, DOI 10.1002/cne.902240408 MOGILNER A, 1993, P NATL ACAD SCI USA, V90, P3593, DOI 10.1073/pnas.90.8.3593 Moore BCJ, 1997, AUDIT NEUROSCI, V3, P289 Muhlnickel W, 1998, P NATL ACAD SCI USA, V95, P10340, DOI 10.1073/pnas.95.17.10340 Pantev C, 1998, NATURE, V392, P811, DOI 10.1038/33918 PASCUALLEONE A, 1993, BRAIN, V116, P39, DOI 10.1093/brain/116.1.39 PONS TP, 1991, SCIENCE, V252, P1857, DOI 10.1126/science.1843843 Rajan R, 1998, NAT NEUROSCI, V1, P138, DOI 10.1038/388 Rajan R, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P224 Rajan R, 1998, J COMP NEUROL, V399, P35 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 RAMACHANDRAN VS, 1993, P NATL ACAD SCI USA, V90, P10413, DOI 10.1073/pnas.90.22.10413 RAMACHANDRAN VS, 1992, SCIENCE, V258, P1159, DOI 10.1126/science.1439826 Schmid LM, 1996, CEREB CORTEX, V6, P388, DOI 10.1093/cercor/6.3.388 SCHWABER MK, 1993, AM J OTOL, V14, P252 Sterr A, 1998, NATURE, V391, P134, DOI 10.1038/34322 Sterr A, 1998, J NEUROSCI, V18, P4417 TEUBER H, 1949, FED PROC, V8, P156 Weiss T, 1998, NEUROREPORT, V9, P213, DOI 10.1097/00001756-199801260-00007 WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 Willott JF, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P297 WILLOTT JF, 1995, BEHAV NEUROSCI, V109, P396, DOI 10.1037//0735-7044.109.3.396 WILLOTT JF, 1994, BEHAV NEUROSCI, V108, P1 YANG TT, 1994, NEUROREPORT, V5, P701, DOI 10.1097/00001756-199402000-00010 NR 46 TC 36 Z9 36 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 188 EP 199 DI 10.1016/S0378-5955(00)00131-3 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200018 PM 10962185 ER PT J AU Snyder, RL Sinex, DG McGee, JD Walsh, EW AF Snyder, RL Sinex, DG McGee, JD Walsh, EW TI Acute spiral ganglion lesions change the tuning and tonotopic organization of cat inferior colliculus neurons SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE plasticity; inferior colliculus; hearing loss; tonotopic reorganization; cochlear lesion ID COCHLEAR HEARING-LOSS; RECEPTIVE-FIELD REORGANIZATION; PRIMARY SOMATOSENSORY CORTEX; LATERAL THALAMIC NUCLEUS; BAT AUDITORY-SYSTEM; ADULT FLYING-FOX; DIGIT AMPUTATION; RESTRICTED DEAFFERENTATION; TOPOGRAPHIC REORGANIZATION; PERIPHERAL DEAFFERENTATION AB Many studies have reported plastic changes in central auditory frequency organization after chronic cochlear lesions. These studies employed mechanical, acoustic or drug-induced disruptions of restricted regions of the organ of Col ti that permanently alter its tuning and sensitivity and require an extended recovery period before central effects can be measured. In this study, mechanical lesions were made to 1 mm sectors of the spiral ganglion (SG). These lesions remove a restricted portion of the cochlear output, but leave the organ of Corti and basilar membrane intact. Multiunit mapping assessed the pre- and post-lesion tonotopic organization of the inferior colliculus (IC). Immediately after SG lesions, IC neurons previously tuned to the lesion frequencies became less sensitive to those frequencies but more sensitive to lesion edge frequencies, resulting in a shift in their characteristic frequencies (CFs). Notches in the excitatory response areas at frequencies corresponding to the lesion frequencies and expansion of spatial tuning curves were also observed. CFs of neurons tuned to unlesioned frequencies were unchanged. These results suggest that 'plastic' changes similar to those observed after long survival times in previous studies require little or no experience and occur within minutes to hours following the lesion. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Francisco, Epstein Lab, San Francisco, CA 94143 USA. Arizona State Univ, Dept Speech & Hearing Sci, Tempe, AZ 85287 USA. Boys Town Natl Res Hosp, Omaha, NE 68131 USA. RP Snyder, RL (reprint author), Univ Calif San Francisco, Epstein Lab, POB 0526,U490, San Francisco, CA 94143 USA. CR BYRNE JA, 1991, BRAIN RES, V565, P218, DOI 10.1016/0006-8993(91)91652-H CALFORD MB, 1993, NEUROSCIENCE, V55, P953, DOI 10.1016/0306-4522(93)90310-C Calford MB, 1999, P ROY SOC B-BIOL SCI, V266, P499 CALFORD MB, 1991, J NEUROPHYSIOL, V65, P178 CALFORD MB, 1988, NATURE, V332, P446, DOI 10.1038/332446a0 CALFORD MB, 1991, SOMATOSENS MOT RES, V8, P249 Carson L V, 1981, Clin Neurosurg, V28, P532 CHINO YM, 1992, VISION RES, V32, P789, DOI 10.1016/0042-6989(92)90021-A CHINO YM, 1995, J NEUROSCI, V15, P2417 DARIANSMITH C, 1995, J NEUROSCI, V15, P1631 DOSTROVSKY JO, 1976, EXP NEUROL, V52, P480, DOI 10.1016/0014-4886(76)90219-3 GARRAGHTY PE, 1991, NEUROREPORT, V2, P747, DOI 10.1097/00001756-199112000-00004 GILBERT CD, 1992, NATURE, V356, P150, DOI 10.1038/356150a0 Gilbert CD, 1996, P NATL ACAD SCI USA, V93, P615, DOI 10.1073/pnas.93.2.615 HARRISION RV, 1996, AUDITORY SYSTEM PLAS, P255 Harrison R V, 1995, Acta Otolaryngol Suppl, V519, P30 HARRISON RV, 1991, HEARING RES, V54, P11, DOI 10.1016/0378-5955(91)90131-R HARRISON RV, 1993, J OTOLARYNGOL, V22, P4 HEINEN SJ, 1991, EXP BRAIN RES, V83, P670 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 IRVINE DRF, 1994, ASS RES OTOLARYNGOL, V17, P21 KAAS JH, 1990, SCIENCE, V248, P229, DOI 10.1126/science.2326637 KAAS JH, 1994, COGNITIVE NEUROSCIEN, P51 KALTENBACH JA, 1992, HEARING RES, V59, P213, DOI 10.1016/0378-5955(92)90118-7 KALTENBACH JA, 1996, AUDITORY SYSTEM PLAS, P217 KELAHAN AM, 1981, BRAIN RES, V223, P151 KELAHAN AM, 1984, SOMATOSENS RES, V2, P49 KIM DO, 1991, HEARING RES, V52, P167, DOI 10.1016/0378-5955(91)90196-G Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 MCMAHON SB, 1983, EXP NEUROL, V80, P195, DOI 10.1016/0014-4886(83)90016-X MERZENICH MM, 1983, NEUROSCIENCE, V10, P639, DOI 10.1016/0306-4522(83)90208-7 MERZENICH MM, 1983, NEUROSCIENCE, V8, P33, DOI 10.1016/0306-4522(83)90024-6 METZLER J, 1979, BRAIN RES, V177, P379, DOI 10.1016/0006-8993(79)90790-X MILLAR J, 1976, EXP NEUROL, V50, P658, DOI 10.1016/0014-4886(76)90035-2 NAKAHAMA H, 1966, PROGR BRAIN RES, V21, pA180 NICOLELIS MAL, 1993, NATURE, V361, P533, DOI 10.1038/361533a0 Northgrave SA, 1996, SOMATOSENS MOT RES, V13, P103, DOI 10.3109/08990229609051398 Pettit MJ, 1996, J NEUROPHYSIOL, V75, P1117 PETTIT MJ, 1993, SCIENCE, V262, P2054, DOI 10.1126/science.8266104 Phillips Dennis P., 1992, Cerebral Cortex, V2, P425, DOI 10.1093/cercor/2.5.425 Rajan R, 1998, NAT NEUROSCI, V1, P138, DOI 10.1038/388 Rajan R, 1998, AUDIOL NEURO-OTOL, V3, P123, DOI 10.1159/000013786 Rajan R, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P224 Rajan R, 1998, J COMP NEUROL, V399, P35 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 Rasmusson D, 1996, J COMP NEUROL, V364, P92 RASMUSSON DD, 1983, BRAIN RES, V288, P368, DOI 10.1016/0006-8993(83)90120-8 Rasmusson DD, 1996, J NEUROPHYSIOL, V75, P2441 RASMUSSON DD, 1993, SOMATOSENS MOT RES, V10, P69, DOI 10.3109/08990229309028825 Rauschecker Josef P., 1987, IMPRINTING CORTICAL ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 Salvi RJ, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P275 SCHWABER MK, 1993, AM J OTOL, V14, P252 Silva AC, 1996, J COMP NEUROL, V366, P700, DOI 10.1002/(SICI)1096-9861(19960318)366:4<700::AID-CNE9>3.0.CO;2-8 SNOW PJ, 1991, PROGR SENSORY PHYSL, V11, P1 Snyder RL, 1997, J COMP NEUROL, V384, P293, DOI 10.1002/(SICI)1096-9861(19970728)384:2<293::AID-CNE9>3.0.CO;2-X SNYDER RL, 1996, SOC NEUR ABSTR SNYDER RL, 2000, ASS RES OT 23 MIDW M SNYDER RL, 1998, SOC NEUR ABSTR SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S Snyder RL, 1997, J COMP NEUROL, V379, P133, DOI 10.1002/(SICI)1096-9861(19970303)379:1<133::AID-CNE9>3.0.CO;2-5 TURNBULL BG, 1990, SOMATOSENS MOT RES, V8, P213 WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 Willott JF, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P297 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 Yan W, 1998, NAT NEUROSCI, V1, P54, DOI 10.1038/255 Zhang YF, 1997, NATURE, V387, P900 NR 67 TC 35 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 200 EP 220 DI 10.1016/S0378-5955(00)00132-5 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200019 PM 10962186 ER PT J AU Leake, PA Snyder, RL Rebscher, SJ Moore, CM Vollmer, M AF Leake, PA Snyder, RL Rebscher, SJ Moore, CM Vollmer, M TI Plasticity in central representations in the inferior colliculus induced by chronic single- vs. two-channel electrical stimulation by a cochlear implant after neonatal deafness SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE cochlear implant; electrical stimulation; auditory system development; neonatal deafness; altered central auditory representation; plasticity ID AUDITORY BRAIN-STEM; SPIRAL GANGLION NEURONS; CONDUCTIVE HEARING-LOSS; MONOCULAR DEPRIVATION; RESPONSE PROPERTIES; DEAFENED CATS; NERVE FIBERS; ACOUSTIC DEPRIVATION; VISUAL-CORTEX; NUCLEUS AB The goal of this research is to examine the functional consequences of patterned electrical stimulation delivered by a cochlear implant in the deafened developing auditory system. In previous electrophysiological experiments conducted in the inferior colliculus (IC), we have demonstrated that the precise cochleotopic organization of the central nucleus (ICC) develops normally in neonatally deafened unstimulated cats and is unaltered despite the lack of normal auditory input during development. However, these studies also showed that chronic electrical stimulation delivered at a single intracochlear location by one bipolar channel of a cochlear implant induces significant expansion of the central representation of the stimulated cochlear sector and degrades the cochleotopic organization of the IC. This report presents additional data from a new experimental series of neonatally deafened cats that received chronic stimulation on two adjacent bipolar intracochlear channels of a cochlear implant. Results suggest that competing inputs elicited by electrical stimulation delivered by two adjacent channels can maintain the selective representations of each activated cochlear sector within the central auditory system and prevent the expansion seen after single-channel stimulation. Alternating stimulation of two channels and use of highly controlled electrical signals may be particularly effective in maintaining or even sharpening selectivity of central representations of stimulated cochlear sectors. In contrast? simultaneous stimulation using two channels of a model analog cochlear implant processor in one experimental animal failed to maintain channel selectivity and resulted in marked expansion and fusion of the central representations of the stimulated channels. This potentially important preliminary result suggests that under some conditions the central auditory system may be unable to discriminate simultaneous, overlapping inputs from adjacent cochlear implant channels as distinct. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Francisco, Epstein Lab, Dept Otolaryngol, San Francisco, CA 94143 USA. RP Leake, PA (reprint author), Univ Calif San Francisco, Epstein Lab, Dept Otolaryngol, Room U490,533 Parnassus Ave, San Francisco, CA 94143 USA. CR AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 ALTMANN L, 1987, J NEUROPHYSIOL, V58, P965 BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 BRUGGE JF, 1984, J ACOUST SOC AM, V75, P1548, DOI 10.1121/1.390826 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 COLEMAN J R, 1979, Experimental Neurology, V64, P533 CREMIEUX J, 1987, J NEUROPHYSIOL, V57, P1511 CYNADER M, 1980, J NEUROPHYSIOL, V43, P1026 Dawson PW, 1997, EAR HEARING, V18, P488, DOI 10.1097/00003446-199712000-00007 Dowell R. C., 1995, Annals of Otology Rhinology and Laryngology, V104, P324 Eggermont J.J., 1986, ACTA OTOLARYNGOL S, V429, P1 EISELE LE, 1988, J NEUROBIOL, V19, P395, DOI 10.1002/neu.480190502 EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 FENG AS, 1980, BRAIN RES, V189, P530, DOI 10.1016/0006-8993(80)90112-2 GREENWOOD DD, 1974, SENSATION MEASUREMEN, P231 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HARRISON RV, 1996, AUDITORY SYSTEM PLAS, P283 HARTMANN R, 1984, ADV AUDIOL, V1, P18 HARTMANN R, 1987, ANN OTO RHINOL LARYN, V96, P30 HARTMANN R, 1989, COCHLEAR IMPLANTS MO, P135 HUBEL DH, 1965, J NEUROPHYSIOL, V28, P1041 IRVINE DRF, 1994, 17 ANN M ASS RES OT, P21 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 JEANBAPTISTE M, 1975, J COMP NEUROL, V162, P111, DOI 10.1002/cne.901620107 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 Kirk KI, 2000, COCHLEAR IMPLANTS, P225 Kitzes L, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P256 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 Leake PA, 1999, J COMP NEUROL, V412, P543, DOI 10.1002/(SICI)1096-9861(19991004)412:4<543::AID-CNE1>3.0.CO;2-3 LEAKE PA, 1992, HEARING RES, V64, P99, DOI 10.1016/0378-5955(92)90172-J LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEAKE PA, 1987, ANN OTO RHINOL LARYN, V96, P48 Leake PA, 1997, HEARING RES, V113, P117, DOI 10.1016/S0378-5955(97)00133-0 LEAKE PA, 1995, HEARING RES, V82, P65 LEAKE PA, 2000, COCHLEAR IMPLANTS, P31 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LUSTIG LR, 1994, HEARING RES, V74, P29, DOI 10.1016/0378-5955(94)90173-2 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 Mitchell DE, 1984, HDB PHYSL 1 1, V3, P507 MOORE DR, 1989, J NEUROSCI, V9, P1213 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 MOORE DR, 1981, BRAIN RES, V208, P98 MOWER GD, 1985, J NEUROPHYSIOL, V53, P572 Moxon E. C., 1971, NEURAL MECH RESPONSE National Institutes of Health, 1995, COCHLEAR IMPLANTS AD, V13, P1 Niparko JK, 1997, OTOLARYNG HEAD NECK, V117, P229, DOI 10.1016/S0194-5998(97)70179-7 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 POWELL TPS, 1962, J ANAT, V96, P249 ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 RUBEL EW, 1984, HEARING SCI, P109 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 RUBEN RJ, 1980, ANN OTO RHINOL LARYN, V89, P303 Ruben R J, 1986, Acta Otolaryngol Suppl, V429, P61 RUSSELL FA, 1995, J COMP NEUROL, V352, P607, DOI 10.1002/cne.903520409 Sato M, 1999, HEARING RES, V127, P1, DOI 10.1016/S0378-5955(98)00143-9 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 Shepherd RK, 1997, HEARING RES, V108, P112, DOI 10.1016/S0378-5955(97)00046-4 Shepherd RK, 1999, HEARING RES, V130, P171, DOI 10.1016/S0378-5955(99)00011-8 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 SNYDER R, 1995, J NEUROPHYSIOL, V73, P449 Snyder RL, 2000, HEARING RES, V147, P200, DOI 10.1016/S0378-5955(00)00132-5 SNYDER RL, 1991, HEARING RES, V56, P246, DOI 10.1016/0378-5955(91)90175-9 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S Stryker MP, 1984, INVEST OPHTHALMOL S, V25, P278 TIEMAN DG, 1983, BRAIN RES, V280, P41, DOI 10.1016/0006-8993(83)91171-X Tieman SB, 1997, VISUAL NEUROSCI, V14, P929 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 TUMOSA N, 1980, SCIENCE, V208, P421, DOI 10.1126/science.7367872 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VANSLUYTERS RC, 1980, J NEUROPHYSIOL, V43, P686 Vollmer M, 1999, J NEUROPHYSIOL, V82, P2883 VUREK LS, 1981, ANN OTO RHINOL LARYN, V90, P21 WALSH EJ, 1986, J ACOUST SOC AM, V79, P745, DOI 10.1121/1.393463 WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 Walsh Edward J., 1992, P161 Waltzman S B, 1999, Trends Amplif, V4, P143, DOI 10.1177/108471389900400402 WALTZMAN SB, 2000, COCHLEAR IMPLANTS, P199 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WEBSTER DB, 1983, HEARING RES, V12, P145, DOI 10.1016/0378-5955(83)90123-5 Weliky M, 1997, NATURE, V386, P680, DOI 10.1038/386680a0 WIESEL TN, 1963, J NEUROPHYSIOL, V26, P978 WIESEL TN, 1965, J NEUROPHYSIOL, V28, P1029 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 XU SA, 1993, HEARING RES, V70, P205, DOI 10.1016/0378-5955(93)90159-X NR 93 TC 40 Z9 42 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 221 EP 241 DI 10.1016/S0378-5955(00)00133-7 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200020 PM 10962187 ER PT J AU Nagase, S Miller, JM Dupont, J Lim, HH Sato, K Altschuler, RA AF Nagase, S Miller, JM Dupont, J Lim, HH Sato, K Altschuler, RA TI Changes in cochlear electrical stimulation induced Fos expression in the rat inferior colliculus following deafness SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE c-fos; inferior colliculus; plasticity; cochlear implant; electrical stimulation; auditory brain stem ID STEM AUDITORY NUCLEI; BRAIN-STEM; GUINEA-PIG; RECEPTOR-BINDING; FISCHER-344 RAT; IMMUNOREACTIVITY; SYSTEM; CAT; PROJECTIONS; ABLATION AB Fos immunoreactive (IR) staining was used to examine changes in excitatory neuronal activity in the rat inferior colliculus (IC) between normal hearing and 21 day deaf rats evoked by basal or apical monopolar cochlear electrical stimulation. The location of evoked Fos IR neurons was consistent with expected tonotopic areas. The number of Fos IR cells increased as stimulation intensity increased in both normal and 21 day deaf animals. Stimulation at 1.5 x threshold evoked fewer Fos IR cells in 21 day deafened animals compared to normal hearing animals. At 5 x and above, however, significantly increased numbers of Fos IR neurons (in a larger grouping) were evoked in 21 day deafened animals compared to normal hearing animals. Another group of animals had 7 days of deafness followed by 14 days of chronic basal cochlear electrical stimulation. In this group basal monopolar stimulation at 5 x evoked not only a greater number of Fos IR neurons, compared to normal hearing animals, but the location of their grouping was slightly shifted to a more dorso-lateral region in the contralateral IC, compared to the normal hearing and 21 day deaf groups. These observations indicate that both deafness and chronic electrical stimulation may alter central auditory processing. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Dept Otolaryngol, Ann Arbor, MI 48109 USA. RP Altschuler, RA (reprint author), Univ Michigan, Kresge Hearing Res Inst, Dept Otolaryngol, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1995, J COMP NEUROL, V361, P645, DOI 10.1002/cne.903610408 ALTSCHULER RA, 1991, NOISE INDUCED HEARIN ALTSCHULER RA, 1997, ACOUSTIC SIGNAL PROC ALTSHULER RA, 1995, ACTIVE HEARING, P239 BERGMAN M, 1989, HEARING RES, V42, P283, DOI 10.1016/0378-5955(89)90152-4 Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 Bledsoe SC, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P513, DOI 10.1007/978-1-4419-8712-9_47 BROWN MC, 1995, J COMP NEUROL, V357, P85, DOI 10.1002/cne.903570109 CANADY KS, 1992, J NEUROSCI, V12, P1001 Caspary DM, 1999, NEUROSCIENCE, V93, P307, DOI 10.1016/S0306-4522(99)00121-9 DUPONT J, 1992, TINNITUS 91, P195 EHRET G, 1991, BRAIN RES, V567, P350, DOI 10.1016/0006-8993(91)90819-H FRIAUF E, 1991, SOC NEUR ABST, V17, P123 GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 Helfert RH, 1999, J COMP NEUROL, V406, P285 HULTCRANTZ M, 1991, HEARING RES, V54, P272, DOI 10.1016/0378-5955(91)90121-O Irvine DRF, 2000, HEARING RES, V147, P188, DOI 10.1016/S0378-5955(00)00131-3 JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LESPERANCE MM, 1995, HEARING RES, V86, P77, DOI 10.1016/0378-5955(95)00056-A LUSTIG LR, 1994, HEARING RES, V74, P29, DOI 10.1016/0378-5955(94)90173-2 MILBRANDT JC, 1995, NEUROSCIENCE, V67, P713, DOI 10.1016/0306-4522(95)00082-T Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F Milbrandt JC, 1996, NEUROSCIENCE, V73, P449, DOI 10.1016/0306-4522(96)00050-4 Miller JM, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P378 MILLER JM, 1991, NOISE INDUCED HEARIN MOORE DR, 1991, NEUROBIOLOGY HEARING, P461 Mossop JE, 2000, HEARING RES, V147, P183, DOI 10.1016/S0378-5955(00)00054-X OLIVER DL, 1984, J COMP NEUROL, V224, P155, DOI 10.1002/cne.902240202 OLIVER DL, 1987, J COMP NEUROL, V264, P24, DOI 10.1002/cne.902640104 OLIVER DL, 1985, J COMP NEUROL, V237, P343, DOI 10.1002/cne.902370306 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 PFINGST BE, 1995, HEARING RES, V85, P76, DOI 10.1016/0378-5955(95)00037-5 POTASHNER SJ, 1985, J NEUROCHEM, V45, P1558, DOI 10.1111/j.1471-4159.1985.tb07227.x PUJOL R, 1980, HEARING RES, V423, P30 Rajan R, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P224 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 REES S, 1985, BRAIN RES, V325, P370, DOI 10.1016/0006-8993(85)90343-9 ROUILLER EM, 1992, NEUROSCI LETT, V144, P19, DOI 10.1016/0304-3940(92)90706-D RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 Saito H, 1999, NEUROSCIENCE, V91, P139, DOI 10.1016/S0306-4522(98)00581-8 Salvi RJ, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P275 Salvi RJ, 2000, HEARING RES, V147, P261, DOI 10.1016/S0378-5955(00)00136-2 SANES DH, 1994, ASS RES OT MIDW M, V17, P10 SATO K, 1992, NEUROSCI LETT, V142, P48, DOI 10.1016/0304-3940(92)90617-G Sato K, 1993, Acta Otolaryngol Suppl, V500, P18 SCHWARTZ DR, 1993, HEARING RES, V70, P463 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 VISCHER MW, 1994, NEUROSCI RES, V19, P175, DOI 10.1016/0168-0102(94)90141-4 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 Willott JF, 1997, J COMP NEUROL, V385, P405 Willott JF, 2000, HEARING RES, V147, P275, DOI 10.1016/S0378-5955(00)00137-4 ZAPPIA JJ, 1989, HEARING RES, V40, P29, DOI 10.1016/0378-5955(89)90096-8 Zhang JS, 1996, BRAIN RES BULL, V39, P75, DOI 10.1016/0361-9230(95)02053-5 NR 58 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 242 EP 250 DI 10.1016/S0378-5955(00)00134-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200021 PM 10962188 ER PT J AU Milbrandt, JC Holder, TM Wilson, MC Salvi, RJ Caspary, DM AF Milbrandt, JC Holder, TM Wilson, MC Salvi, RJ Caspary, DM TI GAD levels and muscimol binding in rat inferior colliculus following acoustic trauma SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE inferior colliculus; glutamic acid decarboxylase; noise exposure; rat; gamma-aminobutyric acid ID GLUTAMIC-ACID DECARBOXYLASE; GABA(A) RECEPTOR-BINDING; STEM AUDITORY NUCLEI; MESSENGER-RNA LEVELS; AGE-RELATED-CHANGES; ADULT GUINEA-PIG; HAIR CELL LOSS; EVOKED-POTENTIALS; 2 FORMS; COMPARATIVE LOCALIZATION AB Pharmacological studies of the inferior colliculus (IC) suggest that the inhibitory amino acid neurotransmitter gamma-aminobutyric acid (GABA) plays an important role in shaping responses to simple and complex acoustic stimuli. Several models of auditory dysfunction, including age-related hearing loss, tinnitus, and peripheral deafferentation, suggest an alteration of normal GABA neurotransmission in central auditory pathways. The present study attempts to further characterize noise-induced changes in GABA markers in the IC. Four groups (unexposed control, 0 h post-exposure, 42 h post-exposure, and 30 days post-exposure) of 3-month-old male Fischer 344 rats were exposed to a high intensity sound (12 kHz, 106 dB) for 10 h. Observed hair cell damage was primarily confined to the basal half of the cochlea. There was a significant decrease in glutamic acid decarboxylase (GAD(65)) immunoreactivity in the IC membrane fraction compared to controls (P < 0.05) at 0 h (-41%) and 42 h (-28%) post-exposure, with complete recovery by 30 days post-exposure (P > 0.98). Observed decreases in cytosolic levels of GAD(65) were not significant. Quantitative muscimol receptor binding revealed a significant increase (+20%) in IC 30 days after sound exposure (P < 0.05). These data suggest that changes in GABA neurotransmission occur in the IC of animals exposed to intense sound. Additional studies are needed to determine whether these changes are a result of protective/compensatory mechanisms or merely peripheral differentiation, as well as whether these changes preserve or diminish central auditory system function. (C) 2000 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. RP Caspary, DM (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, 801 N Rutledge St,POB 19629, Springfield, IL 62794 USA. CR Abbott SD, 1999, NEUROSCIENCE, V93, P1375, DOI 10.1016/S0306-4522(99)00300-0 Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 BU DF, 1992, P NATL ACAD SCI USA, V89, P2115, DOI 10.1073/pnas.89.6.2115 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1996, 19 MIDW RES M ARO ST Caspary DM, 1999, NEUROSCIENCE, V93, P307, DOI 10.1016/S0306-4522(99)00121-9 Dumoulin A, 1996, EUR J NEUROSCI, V8, P2553, DOI 10.1111/j.1460-9568.1996.tb01549.x DUPONT J, 1994, 17 MIDW RES M ARO ST ERLANDER MG, 1991, NEUROCHEM RES, V16, P215, DOI 10.1007/BF00966084 ESCLAPEZ M, 1993, J COMP NEUROL, V331, P339, DOI 10.1002/cne.903310305 ESCLAPEZ M, 1994, J NEUROSCI, V14, P1834 FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 FELDBLUM S, 1993, J NEUROSCI RES, V34, P689, DOI 10.1002/jnr.490340612 Fuchs JL, 1998, J COMP NEUROL, V395, P209 GERKEN G, 1986, BASIC APPL ASPECTS N, P195 GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 GOLD BI, 1979, J NEUROCHEM, V32, P883, DOI 10.1111/j.1471-4159.1979.tb04572.x GRIFFITH WH, 1995, J NEUROSCI, V14, P7469 Hofstetter P, 1997, AUDIOLOGY, V36, P301 KAUFMAN DL, 1991, J NEUROCHEM, V56, P720, DOI 10.1111/j.1471-4159.1991.tb08211.x Krenning J, 1998, LARYNGOSCOPE, V108, P26, DOI 10.1097/00005537-199801000-00005 Liang F, 1996, EXP BRAIN RES, V110, P163 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1984, HEARING RES, V16, P45 LITWAK J, 1990, NEUROSCI LETT, V116, P179, DOI 10.1016/0304-3940(90)90406-Y LONSBURYMARTIN BL, 1981, J NEUROPHYSIOL, V46, P563 MARTIN DL, 1991, J NEUROSCI, V11, P2725 MARTIN DL, 1991, NEUROCHEM RES, V16, P243, DOI 10.1007/BF00966087 MARTIN DL, 1993, J NEUROCHEM, V60, P395, DOI 10.1111/j.1471-4159.1993.tb03165.x MERCUGLIANO M, 1992, J COMP NEUROL, V318, P245, DOI 10.1002/cne.903180302 Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F Milbrandt JC, 1996, NEUROSCIENCE, V73, P449, DOI 10.1016/0306-4522(96)00050-4 Morest DK, 1998, MICROSC RES TECHNIQ, V41, P205 Palombi PS, 1996, J NEUROPHYSIOL, V76, P3114 PAN HS, 1983, J NEUROSCI, V3, P1189 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd PINARD R, 1991, BRAIN RES, V543, P287, DOI 10.1016/0006-8993(91)90039-X POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 RAZA A, 1994, HEARING RES, V77, P221, DOI 10.1016/0378-5955(94)90270-4 RIMVALL K, 1993, J NEUROCHEM, V60, P714, DOI 10.1111/j.1471-4159.1993.tb03206.x RIMVALL K, 1994, J NEUROCHEM, V62, P1375 Salvi RJ, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P477, DOI 10.1007/978-1-4419-8712-9_44 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U Sanna E, 1998, J NEUROCHEM, V70, P2539 SIEGHART W, 1992, TRENDS PHARMACOL SCI, V13, P446, DOI 10.1016/0165-6147(92)90142-S SPOENDLIN LH, 1976, EFFECTS NOISE HEARIN, P69 Spongr VP, 1997, J ACOUST SOC AM, V101, P3546, DOI 10.1121/1.418315 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 Szczepaniak WS, 1996, EVOKED POTENTIAL, V100, P158, DOI 10.1016/0013-4694(95)00234-0 SZCZEPANIAK WS, 1995, NEUROSCI LETT, V196, P77, DOI 10.1016/0304-3940(95)11851-M WILLOTT JF, 1988, HEARING RES, V37, P1, DOI 10.1016/0378-5955(88)90073-1 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 WYBORSKI RJ, 1990, MOL BRAIN RES, V8, P193, DOI 10.1016/0169-328X(90)90016-7 ZHANG J, 1998, NEUROSCI LETT, V250, P1 NR 56 TC 90 Z9 100 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 251 EP 260 DI 10.1016/S0378-5955(00)00135-0 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200022 PM 10962189 ER PT J AU Salvi, RJ Wang, J Ding, D AF Salvi, RJ Wang, J Ding, D TI Auditory plasticity and hyperactivity following cochlear damage SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UT DE plasticity; inner hair cell; acoustic trauma; chinchilla; inhibition; inferior colliculus; auditory cortex ID HAIR CELL LOSS; EAR OSSICLE REMOVAL; ADULT GUINEA-PIG; INFERIOR COLLICULUS; BRAIN-STEM; RESPONSE PROPERTIES; ACOUSTIC TRAUMA; TUNING CURVES; GAP-43 IMMUNOREACTIVITY; UNILATERAL COCHLEAR AB This paper will review some of the functional changes that occur in the central auditory pathway after the cochlea is damaged by acoustic overstimulation or by carboplatin, an ototoxic drug that selectively destroys inner hair cells (IHCs) in the chinchilla. Acoustic trauma typically impairs the sensitivity and tuning of auditory nerve fibers and reduces the neural output of the cochlea. Surprisingly, our results show that restricted cochlear damage enhances neural activity in the central auditory pathway. Despite a reduction in the auditory-nerve compound action potential (CAP), the local field potential from the inferior colliculus (IC) increases at a faster than normal rate and its maximum amplitude is enhanced at frequencies below the region of hearing loss. To determine if this enhancement was due to loss of sideband inhibition, we recorded from single neurons in the IC and dorsal cochlear nucleus before and after presenting a traumatizing above the unit's characteristic frequency (CF). Following the exposure, some neurons showed substantial broadening of tuning below CF, less inhibition, and a significant increase in discharge rate, consistent with a model involving loss of sideband inhibition. The central auditory system of the chinchilla can be deprived of some of its cochlear inputs by selectively destroying IHCs with carboplatin. Selective IHC loss reduces the amplitude of the CAP without affecting the threshold and tuning of the remaining auditory nerve fibers. Although the output of the cochlea is reduced in proportion to the amount of IHC loss. the IC response shows only a modest amplitude reduction, and remarkably, the response of the auditory cortex is enhanced. These results suggest that the gain of the central auditory pathway can be up- or down regulated to compensate for the amount of neural activity from the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Buffalo, Hearing Res Lab, Buffalo, NY 14214 USA. RP Salvi, RJ (reprint author), SUNY Buffalo, Hearing Res Lab, 215 Parker Hall, Buffalo, NY 14214 USA. EM salvi@buffalo.edu CR Abbott SD, 1999, NEUROSCIENCE, V93, P1375, DOI 10.1016/S0306-4522(99)00300-0 ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 AREHOLE S, 1987, HEARING RES, V27, P193, DOI 10.1016/0378-5955(87)90001-3 ATHERLEY GR, 1968, J ACOUST SOC AM, V44, P1503, DOI 10.1121/1.1911288 Benson CG, 1997, SYNAPSE, V25, P243 Bilak M, 1997, EXP NEUROL, V147, P256, DOI 10.1006/exnr.1997.6636 BOETTCHER FA, 1993, J ACOUST SOC AM, V94, P2123, DOI 10.1121/1.407484 CALFORD MB, 1988, NATURE, V332, P446, DOI 10.1038/332446a0 CASPARY DM, 1984, HEARING RES, V13, P113, DOI 10.1016/0378-5955(84)90102-3 CASPARY DM, 1983, EXP NEUROL, V82, P491, DOI 10.1016/0014-4886(83)90419-3 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 Davis GW, 1998, NEURON, V20, P305, DOI 10.1016/S0896-6273(00)80458-4 DAVIS H, 1950, Acta Otolaryngol Suppl, V88, P1 Ding DL, 1999, AUDIOL NEURO-OTOL, V4, P55, DOI 10.1159/000013822 DOSTROVSKY JO, 1976, EXP NEUROL, V52, P480, DOI 10.1016/0014-4886(76)90219-3 Eldredge D H, 1973, Adv Otorhinolaryngol, V20, P64 EVANS EF, 1973, EXP BRAIN RES, V17, P402 EVANS EF, 1993, NATO ADV SCI INST SE, V239, P253 GERKEN G, 1986, BASIC APPL ASPECTS N, P195 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HALLPIKE CS, 1960, ACTA OTOLARYNGOL, V50, P472 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 Horvath M, 1997, J COMP NEUROL, V382, P104, DOI 10.1002/(SICI)1096-9861(19970526)382:1<104::AID-CNE7>3.0.CO;2-5 House J W, 1981, Ciba Found Symp, V85, P204 ILLING RB, 1995, NEUROSCI LETT, V194, P9, DOI 10.1016/0304-3940(95)11706-3 Illing RB, 1997, J COMP NEUROL, V382, P116, DOI 10.1002/(SICI)1096-9861(19970526)382:1<116::AID-CNE8>3.0.CO;2-4 JEANBAPTISTE M, 1975, J COMP NEUROL, V162, P111, DOI 10.1002/cne.901620107 KALTENBACH JA, 1996, P 5 INT TINN SEM AM, P455 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 Kim JN, 1997, HEARING RES, V103, P169, DOI 10.1016/S0378-5955(96)00173-6 LIBERMAN MC, 1986, BASIC APPL ASPECTS N, P163 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 Lockwood AH, 1998, NEUROLOGY, V50, P114 McFadden SL, 1998, HEARING RES, V120, P121, DOI 10.1016/S0378-5955(98)00052-5 MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 MOREST DK, 1983, HEARING RES, V9, P145, DOI 10.1016/0378-5955(83)90024-2 Morest DK, 1998, MICROSC RES TECHNIQ, V41, P205 MOREST DK, 1982, NEW PERSPECTIVES NOI, P87 Morest DK, 1997, HEARING RES, V103, P151, DOI 10.1016/S0378-5955(96)00172-4 OSEN KK, 1972, J COMP NEUROL, V144, P355, DOI 10.1002/cne.901440307 POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 Qiu CX, 2000, HEARING RES, V139, P153, DOI 10.1016/S0378-5955(99)00171-9 RAZA A, 1994, HEARING RES, V77, P221, DOI 10.1016/0378-5955(94)90270-4 SALVI R, 1980, HEARING RES, V2, P335, DOI 10.1016/0378-5955(80)90067-2 Salvi RJ, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P275 SALVI RJ, 1982, AM J OTOLARYNG, V3, P408, DOI 10.1016/S0196-0709(82)80018-5 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SALVI RJ, 1983, EAR HEARING, V4, P115 SALVI RJ, 1983, HEARING RES THEORY, P173 SALVI RJ, 1992, NOISE INDUCED HEARIN, P156 SALVI RJ, 1979, HEARING RES, V1, P237, DOI 10.1016/0378-5955(79)90017-0 SALVI RJ, 1997, ACOUSTICAL SIGNAL PR, P29 SASAKI CT, 1980, BRAIN RES, V194, P511, DOI 10.1016/0006-8993(80)91233-0 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SHOFNER WP, 1985, J NEUROPHYSIOL, V54, P917 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 SNYDER DL, 1994, LAB ANIMAL, V23, P42 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 Takeno S, 1998, AUDIOL NEURO-OTOL, V3, P281, DOI 10.1159/000013800 TAKENO S, 1994, HEARING RES, V75, P93, DOI 10.1016/0378-5955(94)90060-4 Trautwein P, 1996, HEARING RES, V96, P71, DOI 10.1016/0378-5955(96)00040-8 Turrigiano GG, 1998, NATURE, V391, P892, DOI 10.1038/36103 Wake M, 1996, ACTA OTO-LARYNGOL, V116, P714, DOI 10.3109/00016489609137912 WAKE M, 1993, J LARYNGOL OTOL, V107, P585, DOI 10.1017/S0022215100123771 WAKE M, 1994, LARYNGOSCOPE, V104, P488 WANG CY, 1972, J ACOUST SOC AM, V52, P1678, DOI 10.1121/1.1913302 Wang J, 1999, NEUROREPORT, V10, P811, DOI 10.1097/00001756-199903170-00027 Wang J, 1996, J NEUROPHYSIOL, V75, P171 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 WIGHTMAN FL, 1982, NEW PERSPECTIVES NOI, P375 YANG LC, 1992, J NEUROPHYSIOL, V68, P1760 YOUNG ED, 1982, HEARING RES, V6, P153, DOI 10.1016/0378-5955(82)90051-X ZENG FG, 1991, Q J EXP PSYCHOL-A, V43, P565 ZHENG FG, 1991, Q J EXP PSYCHOL-A, V43, P565 NR 77 TC 183 Z9 195 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 261 EP 274 DI 10.1016/S0378-5955(00)00136-2 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200023 PM 10962190 ER PT J AU Willott, JF Turner, JG AF Willott, JF Turner, JG TI Neural plasticity in the mouse inferior colliculus: relationship to hearing loss, augmented acoustic stimulation, and prepulse inhibition SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE hearing-loss induced plasticity; deprivation; inbred mouse; progressive hearing loss ID AUDITORY-CORTEX; STARTLE RESPONSE; COCHLEAR NUCLEUS; C57BL/6J MICE; DBA/2J MICE; NEURONS; SYSTEM; REPRESENTATION; ORGANIZATION; THRESHOLDS AB C57BL/6J (C57) and DBA/2J (DBA) mice exhibit progressive high-frequency hearing loss. Extracellular recordings of responses of neurons in the inferior colliculus (IC) evoked by 70-dB SPL tones indicated that normal tonotopic organization was greatly disrupted in both strains: still-audible lower frequencies (4-12 kHz) evoked responses in a large percentage of recording sites in ventral tonotopic regions that normally respond strongly to high frequencies only. To relate the IC responses to an auditory behavior, prepulse inhibition (PPI) was measured using 70-dB tones as prepulses. As high-frequency hearing loss progressed in C57 mice, prepulses of 4-12 kHz elicited stronger PPI, and this was significantly correlated with changes in the percentage of IC recording sites responding to 70-dB tones (the neural pathway for PPI includes the IC). The analysis was extended to DBA mice that had been exposed to an augmented acoustic environment (AAE)- a procedure that improves PPI. In these mice, a higher percentage of IC recording sites responded to 70-dB tones, and this was correlated with improved PPI. The data suggest that responses of IC neurons reflect both hearing loss-induced plasticity and changes induced by exposure to an AAE, and these neural changes are correlated with the magnitude of PPI. (C) 2000 Elsevier Science B.V. All rights reserved. C1 No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. RP Willott, JF (reprint author), No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. CR CALFORD MB, 1993, NEUROSCIENCE, V55, P953, DOI 10.1016/0306-4522(93)90310-C Carlson S, 1996, HEARING RES, V99, P168, DOI 10.1016/S0378-5955(96)00098-6 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H FOX JE, 1979, PHYSIOL BEHAV, V23, P291, DOI 10.1016/0031-9384(79)90370-6 HENRY KR, 1980, AUDIOLOGY, V19, P369 HOFFMAN HS, 1980, PSYCHOL REV, V87, P175, DOI 10.1037/0033-295X.87.2.175 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 LEITNER DS, 1985, PHYSIOL BEHAV, V34, P65, DOI 10.1016/0031-9384(85)90079-4 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 Li L, 1998, BEHAV NEUROSCI, V112, P1187, DOI 10.1037/0735-7044.112.5.1187 Li L, 1998, PHYSIOL BEHAV, V65, P133, DOI 10.1016/S0031-9384(98)00143-7 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 PARHAM K, 1997, ASS RES OT ABSTR, V20, P194 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 RALLS K, 1967, ANIM BEHAV, V15, P123, DOI 10.1016/S0003-3472(67)80022-8 SCHWABER MK, 1993, AM J OTOL, V14, P252 TURNER JG, 1999, ASS RES OT ABSTR, V22, P220 Turner JG, 1998, HEARING RES, V118, P101, DOI 10.1016/S0378-5955(98)00024-0 Willott JF, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P297 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 Willott JF, 1999, HEARING RES, V135, P78, DOI 10.1016/S0378-5955(99)00094-5 WILLOTT JF, 1995, BEHAV NEUROSCI, V109, P396, DOI 10.1037//0735-7044.109.3.396 WILLOTT JF, 1982, NEUROSCI LETT, V34, P13, DOI 10.1016/0304-3940(82)90085-4 WILLOTT JF, 1981, J NEUROPHYSIOL, V45, P35 WILLOTT JF, 1994, BEHAV NEUROSCI, V108, P703, DOI 10.1037/0735-7044.108.4.703 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 WILLOTT JF, 1995, HEARING RES, V88, P143, DOI 10.1016/0378-5955(95)00107-F NR 28 TC 23 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 275 EP 281 DI 10.1016/S0378-5955(00)00137-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200024 PM 10962191 ER PT J AU Kaltenbach, JA Zhang, JS Afman, CE AF Kaltenbach, JA Zhang, JS Afman, CE TI Plasticity of spontaneous neural activity in the dorsal cochlear nucleus after intense sound exposure SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE plasticity; spontaneous activity; hyperactivity; cochlear nucleus; noise-induced tinnitus ID STEM AUDITORY NUCLEI; RECEPTOR ANTAGONIST KETAMINE; CENTRAL-NERVOUS-SYSTEM; EAR OSSICLE REMOVAL; HAIR CELL LOSS; INFERIOR COLLICULUS; BRAIN-STEM; D-ASPARTATE; HEARING-LOSS; GUINEA-PIG AB Increases in multiunit spontaneous activity (hyperactivity) can be induced in the dorsal cochlear nucleus (DCN) by intense sound exposure. This hyperactivity has been observed in the hamster and rat following exposure to a 10 kHz tone at a level of 115-130 dB SPL for a period of 4 h. The present study demonstrates that the onset of this hyperactivity is not immediate, but develops in the DCN between 2 and 5 days after exposure. Mean rates of multiunit spontaneous activity increased sharply from below normal levels at day 2 to higher than normal levels at day 5. The mean magnitude of activity continued to increase mere gradually over the next 6 months. During this period, changes in the distribution of hyperactivity across the tonotopic array were also noted. The hyperactivity was more broadly distributed across the DCN at the early post-exposure times (5 and 14 days) than at later post-exposure recovery times (30 and 180 days), and peak activity was found at increasingly more medial positions over this rime frame. These changes over time indicate that the mechanisms leading to hyperactivity following intense sound exposure are more complex than previously realized. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Wayne State Univ, Dept Otolaryngol, Detroit, MI 48201 USA. RP Kaltenbach, JA (reprint author), Wayne State Univ, Dept Otolaryngol, 5E-UHC, Detroit, MI 48201 USA. CR Abbott SD, 1999, NEUROSCIENCE, V93, P1375, DOI 10.1016/S0306-4522(99)00300-0 ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ATHERLEY GR, 1968, J ACOUST SOC AM, V44, P1503, DOI 10.1121/1.1911288 Axelsson A., 1992, NOISE INDUCED HEARIN, P269 BAUER CA, 1999, ARO ABS, V22, P154 Bilak M, 1997, EXP NEUROL, V147, P256, DOI 10.1006/exnr.1997.6636 WallhausserFranke E, 1996, NEUROREPORT, V7, P1585, DOI 10.1097/00001756-199607080-00010 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O Chen KJ, 1998, BRAIN RES, V783, P219, DOI 10.1016/S0006-8993(97)01348-6 Choe H, 1997, ANESTH ANALG, V84, P560, DOI 10.1097/00000539-199703000-00017 EGGERMONT JJ, 1999, P 6 INT TINN SEM LON, P146 Eggermont JJ, 1998, HEARING RES, V117, P149, DOI 10.1016/S0378-5955(98)00008-2 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 Evans E F, 1981, Ciba Found Symp, V85, P108 FELDMANN H, 1971, AUDIOLOGY, V10, P138 FORSYTHE ID, 1988, J PHYSIOL-LONDON, V396, P515 GERKEN GM, 1985, HEARING RES, V20, P221, DOI 10.1016/0378-5955(85)90027-9 GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 Godfrey DA, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P139, DOI 10.1007/978-1-4419-8712-9_13 HARRISON RV, 1991, HEARING RES, V54, P11, DOI 10.1016/0378-5955(91)90131-R Hazell J., 1999, P 6 INT TINN SEM TIN, P133 HEFFNER HE, 1999, ARO ABSTR, V22, P47 Hu RQ, 1997, EXP BRAIN RES, V115, P311, DOI 10.1007/PL00005699 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 Irvine D R, 1997, Acta Otolaryngol Suppl, V532, P39 JASTREBOFF PJ, 1986, J ACOUST SOC AM, V80, P1384, DOI 10.1121/1.394391 JASTREBOFF PJ, 1988, BEHAV NEUROSCI, V102, P811, DOI 10.1037/0735-7044.102.6.811 JASTREBOFF PJ, 1988, LARYNGOSCOPE, V98, P280 JASTREBOFF PJ, 1991, ARCH OTOLARYNGOL, V117, P1162 KALTENBACH JA, 1992, HEARING RES, V59, P213, DOI 10.1016/0378-5955(92)90118-7 KALTENBACH JA, 1999, J AM ACAD AUDIOL, V11, P125 KALTENBACH JA, 1999, ASS RES OT ABSTR, V22, P47 KALTENBACH JA, 1996, P 5 INT TINN SEM AM, P34 Kaltenbach JA, 1998, HEARING RES, V124, P78, DOI 10.1016/S0378-5955(98)00119-1 Kaltenbach JA, 1996, AUDIT NEUROSCI, V3, P57 KALTENBACH JA, 1991, HEARING RES, V51, P149, DOI 10.1016/0378-5955(91)90013-Y Kenmochi M, 1997, HEARING RES, V113, P110, DOI 10.1016/S0378-5955(97)00137-8 Kim HS, 1996, LIFE SCI, V58, P1397, DOI 10.1016/0024-3205(96)00109-9 Kim JN, 1997, HEARING RES, V103, P169, DOI 10.1016/S0378-5955(96)00173-6 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 KUMAGAI M, 1992, Hokkaido Journal of Medical Science, V67, P216 LIBERMAN MC, 1978, ACTA OTOLARYNGOL S, V358, P5 LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 LOEB M, 1967, J ACOUST SOC AM, V42, P453, DOI 10.1121/1.1910600 LUMMIS RC, 1972, J ACOUST SOC AM, V51, P1930, DOI 10.1121/1.1913052 MCFADDEN D, 1982, TINNITUS FACTS THEOR, P1 MCFADDEN D, 1983, NEW PERSPECTIVES NOI, P347 McFadden SL, 1998, HEARING RES, V120, P121, DOI 10.1016/S0378-5955(98)00052-5 Meleca RJ, 1997, BRAIN RES, V750, P201, DOI 10.1016/S0006-8993(96)01354-6 MICKLEY GA, 1995, DEV BRAIN RES, V85, P119, DOI 10.1016/0165-3806(94)00202-B Morest DK, 1998, MICROSC RES TECHNIQ, V41, P205 Ochi K, 1997, HEARING RES, V105, P105, DOI 10.1016/S0378-5955(96)00201-8 Oertel D, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P127, DOI 10.1007/978-1-4419-8712-9_12 OLIVER DL, 1984, J COMP NEUROL, V224, P155, DOI 10.1002/cne.902240202 OLIVER DL, 1983, J NEUROSCI, V3, P967 OSEN KK, 1972, J COMP NEUROL, V144, P355, DOI 10.1002/cne.901440307 POTASHNER SJ, 1983, J NEUROCHEM, V41, P1094, DOI 10.1111/j.1471-4159.1983.tb09057.x Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 Reid IC, 1997, SEIZURE, V6, P351, DOI 10.1016/S1059-1311(97)80034-9 RYUGO DK, 1981, BRAIN RES, V210, P342, DOI 10.1016/0006-8993(81)90907-0 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SALVI RJ, 1976, EFFECTS NOISE HEARIN, P247 SASAKI CT, 1981, LARYNGOSCOPE, V91, P2018 SASAKI CT, 1980, BRAIN RES, V194, P511, DOI 10.1016/0006-8993(80)91233-0 Silva E, 1997, EXP BRAIN RES, V117, P379, DOI 10.1007/s002210050232 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 Takahashi H, 1998, PAIN, V75, P391, DOI 10.1016/S0304-3959(97)00189-9 WALLER HJ, 1994, J NEUROPHYSIOL, V71, P467 WallhausserFranke E, 1997, NEUROREPORT, V8, P725, DOI 10.1097/00001756-199702100-00029 Wang J, 1996, J NEUROPHYSIOL, V75, P171 Warncke T, 1997, NEUROSCI LETT, V227, P1, DOI 10.1016/S0304-3940(97)00263-2 Wenthold RJ, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P93, DOI 10.1007/978-1-4419-8712-9_10 WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 Zhang JS, 1998, NEUROSCI LETT, V250, P197, DOI 10.1016/S0304-3940(98)00482-0 NR 78 TC 101 Z9 105 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 282 EP 292 DI 10.1016/S0378-5955(00)00138-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200025 PM 10962192 ER PT J AU Lomax, MI Huang, L Cho, YS Gong, TWL Altschuler, RA AF Lomax, MI Huang, L Cho, YS Gong, TWL Altschuler, RA TI Differential display and gene arrays to examine auditory plasticity SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Molecular Mechanisms in Central Auditory Function and Plasticity CY JUN 25-27, 1999 CL PARK CITY, UTAH DE noise trauma; ubiquitin ligase; UBE3B; inferior colliculus; auditory nerve ID CHICK BASILAR PAPILLA; UBIQUITIN-PROTEIN LIGASE; EXPRESSED SEQUENCE TAGS; ARBITRARILY PRIMED PCR; COCHLEAR GENE; MESSENGER-RNA; CDNA LIBRARY; HAIR-CELLS; INNER-EAR; MICROARRAYS AB Differential gene expression forms the basis for development, differentiation, regeneration, and plasticity of tissues and organs. We describe two methods to identify differentially expressed genes. Differential display: a PCR-based approach, compares the expression of subsets of genes under two or more conditions. Gene arrays, or DNA microarrays, contain cDNAs from both known genes and novel genes spotted on a solid support (nylon membranes or glass slides). Hybridization of the arrays with RNA isolated from two different experimental conditions allows the simultaneous analysis of large numbers of genes, from hundreds to thousands to whole genomes. Using differential display to examine differential gene expression after noise trauma in the chick basilar papilla? we identified the UBE3B gene that encodes a new member of the E3 ubiquitin ligase family (UBE3B). UBE3B is highly expressed immediately after noise in the lesion, but not in the undamaged ends, of the chick basilar papilla. UBE3B is most similar to a ubiquitin ligase gene from Caenorhabditis elegans, suggesting that this gene has been conserved throughout evolution. We also describe preliminary experiments to profile gene expression in the cochlea and brain with commercially available low density gene arrays on nylon membranes and discuss potential applications of this and DNA microarray technology to the auditory system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Sch Med, Kresge Hearing Res Inst, Dept Otolaryngol Head & Neck Surg, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA. RP Lomax, MI (reprint author), Univ Michigan, Sch Med, Kresge Hearing Res Inst, Dept Otolaryngol Head & Neck Surg, 9301E Med Sci Res Bldg 3,Box 0648, Ann Arbor, MI 48109 USA. CR ADAMS MD, 1991, SCIENCE, V252, P1651, DOI 10.1126/science.2047873 Adler HJ, 1999, GENOMICS, V56, P59, DOI 10.1006/geno.1998.5672 ADLER HJ, 1995, HEARING RES, V86, P43, DOI 10.1016/0378-5955(95)00051-5 Bassett DE, 1999, NAT GENET, V21, P51, DOI 10.1038/4478 Bonaldo MDF, 1996, GENOME RES, V6, P791, DOI 10.1101/gr.6.9.791 Brown PO, 1999, NAT GENET, V21, P33, DOI 10.1038/4462 Cheung VG, 1999, NAT GENET, V21, P15, DOI 10.1038/4439 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 de Kok YJM, 1999, HUM MOL GENET, V8, P361, DOI 10.1093/hmg/8.2.361 Duggan DJ, 1999, NAT GENET, V21, P10, DOI 10.1038/4434 EBERWINE J, 1992, P NATL ACAD SCI USA, V89, P3010, DOI 10.1073/pnas.89.7.3010 Ermolaeva O, 1998, NAT GENET, V20, P19 Gerhold D, 1999, TRENDS BIOCHEM SCI, V24, P168, DOI 10.1016/S0968-0004(99)01382-1 Gong TWL, 1996, HEARING RES, V96, P20, DOI 10.1016/0378-5955(96)00013-5 Gong TWL, 1999, GENE, V239, P117, DOI 10.1016/S0378-1119(99)00370-4 Gong TWL, 1997, BBA-GENE STRUCT EXPR, V1352, P282, DOI 10.1016/S0167-4781(97)00027-4 Hershko A., 1998, UBIQUITIN BIOL CELL, P1 Hershko A, 1998, ANNU REV BIOCHEM, V67, P425, DOI 10.1146/annurev.biochem.67.1.425 Hochstrasser M, 1996, ANNU REV GENET, V30, P405, DOI 10.1146/annurev.genet.30.1.405 Hochstrasser M, 1998, UBIQUITIN BIOL CELL, P279 HUIBREGTSE JM, 1998, UBIQUITIN BIOL CELL, P323 HUIBREGTSE JM, 1991, EMBO J, V10, P4129 Iyer VR, 1999, SCIENCE, V283, P83, DOI 10.1126/science.283.5398.83 Kollmar R, 1999, CURR OPIN NEUROBIOL, V9, P394, DOI 10.1016/S0959-4388(99)80059-2 Konzok A, 1999, J CELL BIOL, V146, P453, DOI 10.1083/jcb.146.2.453 Kozel PJ, 1998, J BIOL CHEM, V273, P18693, DOI 10.1074/jbc.273.30.18693 LEE KH, 1995, HEARING RES, V87, P9, DOI 10.1016/0378-5955(95)00072-C Lennon G, 1996, GENOMICS, V33, P151, DOI 10.1006/geno.1996.0177 LIANG P, 1993, NUCLEIC ACIDS RES, V21, P3269, DOI 10.1093/nar/21.14.3269 LIANG P, 1992, SCIENCE, V257, P967, DOI 10.1126/science.1354393 Matsuura T, 1997, NAT GENET, V15, P74, DOI 10.1038/ng0197-74 MCCLELLAND M, 1995, TRENDS GENET, V11, P242, DOI 10.1016/S0168-9525(00)89058-7 RAPHAEL Y, 1993, J COMP NEUROL, V330, P521, DOI 10.1002/cne.903300408 RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E Robertson NG, 1997, GENOMICS, V46, P345, DOI 10.1006/geno.1997.5067 ROBERTSON NG, 1994, GENOMICS, V23, P42, DOI 10.1006/geno.1994.1457 Robertson NG, 1998, NAT GENET, V20, P299 Rodal AA, 1999, J CELL BIOL, V145, P1251, DOI 10.1083/jcb.145.6.1251 Scheffner M, 1998, PHARMACOL THERAPEUT, V78, P129, DOI 10.1016/S0163-7258(98)00003-5 SCHEFFNER M, 1993, CELL, V75, P495, DOI 10.1016/0092-8674(93)90384-3 Schena M, 1998, TRENDS BIOTECHNOL, V16, P301, DOI 10.1016/S0167-7799(98)01219-0 SCHENA M, 1995, SCIENCE, V270, P467, DOI 10.1126/science.270.5235.467 Schena M, 1996, P NATL ACAD SCI USA, V93, P10614, DOI 10.1073/pnas.93.20.10614 Skvorak AB, 1999, HUM MOL GENET, V8, P439, DOI 10.1093/hmg/8.3.439 Skvorak AB, 1997, GENOMICS, V46, P191, DOI 10.1006/geno.1997.5026 Soares MB, 1997, CURR OPIN BIOTECH, V8, P542, DOI 10.1016/S0958-1669(97)80026-2 SOARES MB, 1994, P NATL ACAD SCI USA, V91, P9228, DOI 10.1073/pnas.91.20.9228 Staecker H, 1998, CURR OPIN NEUROBIOL, V8, P480, DOI 10.1016/S0959-4388(98)80035-4 Stone JS, 1998, CURR OPIN NEUROL, V11, P17, DOI 10.1097/00019052-199802000-00004 Street VA, 1998, NAT GENET, V19, P390 VANGELDER RN, 1990, P NATL ACAD SCI USA, V87, P1663 WELSH J, 1992, NUCLEIC ACIDS RES, V20, P4965, DOI 10.1093/nar/20.19.4965 NR 52 TC 29 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 2000 VL 147 IS 1-2 BP 293 EP 302 DI 10.1016/S0378-5955(00)00139-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 352HV UT WOS:000089210200026 PM 10962193 ER PT J AU Nam, YJ Stover, T Hartman, SS Altschuler, RA AF Nam, YJ Stover, T Hartman, SS Altschuler, RA TI Upregulation of glial cell line-derived neurotrophic factor (GDNF) in the rat cochlea following noise SO HEARING RESEARCH LA English DT Article DE cochlea; noise; glial cell line-derived neurotrophic factor; Western blotting; stress response ID NEURONS IN-VITRO; MESSENGER-RNA; GROWTH-FACTOR; DOPAMINERGIC-NEURONS; STRIATAL NEURONS; TYROSINE KINASE; SURVIVAL FACTOR; MOTOR-NEURONS; C-RET; EXPRESSION AB There are endogenous intracellular mechanisms that provide cells with protection from stress, as well as repair from damage. These pathways often involve stress proteins and neurotrophic factors. The present study used Western blot analysis to examine changes in glial cell line-derived neurotrophic factor (GDNF) following noise overstimulation. A noise exposure was utilized which causes a temporary threshold shift and has been previously shown to upregulate heat shock protein 72 in the rat cochlea. This noise exposure also provides protection from a second noise exposure that would otherwise cause a permanent threshold shift. Experimental animals were assessed 2, 4, 8 and 12 h after cessation of noise exposure. Control animals received the same treatment except for the noise exposure and were assessed at the 8 h time point. A moderate expression of GDNF was observed in the normal cochlea. No significant change in GDNF levels was observed at 2 or 4 h following noise overstimulation. However, a significant increase was found at 8 h. At 12 h following noise overstimulation, GDNF levels were no longer significantly elevated from normal. These results suggest that GDNF is involved in the endogenous stress response in the cochlea and are consistent with the protection that exogenously applied GDNF has been shown to provide. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Sch Med, Kresge Hearing Res Inst, Dept Otolaryngol Head & Neck Surg, Ann Arbor, MI 48109 USA. Univ Michigan, Sch Med, Dept Anat & Cell Biol, Ann Arbor, MI 48109 USA. Med Univ Hannover, Dept Otolaryngol, D-30625 Hannover, Germany. RP Altschuler, RA (reprint author), Univ Michigan, Sch Med, Kresge Hearing Res Inst, Dept Otolaryngol Head & Neck Surg, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR Abe K, 1997, BRAIN RES, V776, P230, DOI 10.1016/S0006-8993(97)01041-X AGERMAN K, 1999, COCHLEAR PHARM NOISE, P75 Altschuler RA, 1999, ANN NY ACAD SCI, V884, P305, DOI 10.1111/j.1749-6632.1999.tb08650.x Altschuler R. A., 1999, COCHLEAR PHARM NOISE, P98 Appel E, 1997, NEUROREPORT, V8, P3309, DOI 10.1097/00001756-199710200-00023 Arenas E, 1995, NEURON, V15, P1465, DOI 10.1016/0896-6273(95)90024-1 BUJBELLO A, 1995, NEURON, V15, P821, DOI 10.1016/0896-6273(95)90173-6 Canlon B, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P118 CHENG B, 1993, BRAIN RES, V607, P275, DOI 10.1016/0006-8993(93)91517-V DAVIES AM, 1995, TRENDS NEUROSCI, V18, P355, DOI 10.1016/0166-2236(95)93928-Q Durbec P, 1996, NATURE, V381, P789, DOI 10.1038/381789a0 Farkas LM, 1997, J NEUROSCI RES, V50, P361 Gash DM, 1996, NATURE, V380, P252, DOI 10.1038/380252a0 Hammarberg H, 1996, NEUROREPORT, V7, P857, DOI 10.1097/00001756-199603220-00004 HENDERSON CE, 1994, SCIENCE, V266, P1062, DOI 10.1126/science.7973664 Henderson D, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P143 HENDERSON D, 1999, COCHLEAR PARM NOISE, P85 Hou JGG, 1996, J NEUROCHEM, V66, P74 Humpel C, 1996, CELL TISSUE RES, V286, P249, DOI 10.1007/s004410050694 Jing SQ, 1996, CELL, V85, P1113, DOI 10.1016/S0092-8674(00)81311-2 Keithley EM, 1998, NEUROREPORT, V9, P2183, DOI 10.1097/00001756-199807130-00007 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 Liberatore GT, 1997, NEUROREPORT, V8, P3097, DOI 10.1097/00001756-199709290-00018 Lim HH, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P43 LIM HH, 1993, HEARING RES, V69, P146 LIN LFH, 1993, SCIENCE, V260, P1130, DOI 10.1126/science.8493557 LIN LFH, 1994, J NEUROCHEM, V63, P758 MILLER JM, 1998, RECENT ADV INNER EAR OPPENHEIM RW, 1995, NATURE, V373, P344, DOI 10.1038/373344a0 PIRVOLA U, 1995, P NATL ACAD SCI USA, V92, P9269, DOI 10.1073/pnas.92.20.9269 Reeben M, 1998, NEUROSCIENCE, V83, P151, DOI 10.1016/S0306-4522(97)00361-8 Shoji F, 2000, HEARING RES, V142, P41, DOI 10.1016/S0378-5955(00)00007-1 SMITH PK, 1985, ANAL BIOCHEM, V150, P76, DOI 10.1016/0003-2697(85)90442-7 STOVER T, 2000, UNPUB HEAR RES Subramaniam M, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P128 Tang YP, 1998, J NEUROSCI RES, V53, P593 TOMAC A, 1995, NATURE, V373, P335, DOI 10.1038/373335a0 TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350 Treanor JJS, 1996, NATURE, V382, P80, DOI 10.1038/382080a0 Trupp M, 1996, NATURE, V381, P785, DOI 10.1038/381785a0 TRUPP M, 1995, J CELL BIOL, V130, P137, DOI 10.1083/jcb.130.1.137 Trupp M, 1999, J BIOL CHEM, V274, P20885, DOI 10.1074/jbc.274.30.20885 Wang Y, 1997, J NEUROSCI, V17, P4341 Williams LR, 1996, J PHARMACOL EXP THER, V277, P1140 Yagi M, 1999, HUM GENE THER, V10, P813, DOI 10.1089/10430349950018562 YAN Q, 1995, NATURE, V373, P341, DOI 10.1038/373341a0 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 NR 47 TC 21 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 1 EP 6 DI 10.1016/S0378-5955(00)00072-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500001 PM 10913878 ER PT J AU Lee, JH Kim, SJ Jung, SJ Lim, W Kim, KW Kim, J AF Lee, JH Kim, SJ Jung, SJ Lim, W Kim, KW Kim, J TI Voltage-dependent K+ currents in spiral prominence epithelial cells of rat cochlea SO HEARING RESEARCH LA English DT Article DE spiral prominence epithelial cell; K+ current; delayed rectifier; inward rectifier ID POTASSIUM CURRENTS; STRIA VASCULARIS; MARGINAL CELLS; FINE-STRUCTURE; ION-TRANSPORT; SECRETION; HEARING AB It has been suggested that spiral prominence is associated with ion transport, but the characterization of ion channels has not been explored so far. We studied the electrical properties and ion conductances of the spiral prominence epithelial cells (SPECs), which are epithelial cells covering the luminal side of spiral prominence, in the upper turn of neonatal rat cochlea using a whole-cell variant patch clamp technique. The cell capacitance was 16.3 +/- 2.1 pF (n = 33) and the resting membrane potential was -68.9 +/- 2.5 mV (n = 14) in perilymph-like bath solution. It was found that those SPECs possess a large voltage-activated, outwardly rectifying K+ current and a small inwardly rectifying K+ current. The outward K+ current was activated by depolarizing pulses more positive than -30 mV, and sensitive to tetraethylammonium chloride (20 mM), 4-aminopyridine (10 mM), but not to Ba2+ (0.5 mM). Tail current analysis revealed that it was primarily K+-selective. The time course of activation was well fitted by an exponential function raised to second power. The small inwardly rectifying K+ current was sensitive to Ba2+ (0.5 mM), and the Ba2+-senssttve current was K+-selective. In cell-attached or inside-out patch recordings, no discernible K+ channel currents were found in the apical membrane of SPECs. Based on these results, we conclude that SPECs have two types of voltage-dependent K+ currents, which are most likely located in the basolateral membrane. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Seoul Natl Univ, Coll Med, Dept Physiol & Biophys, Seoul 110799, South Korea. RP Kim, J (reprint author), Seoul Natl Univ, Coll Med, Dept Physiol & Biophys, 28 Yongon Dong, Seoul 110799, South Korea. RI Kim, Sang Jeong/J-2740-2012 CR BORGHESAN E, 1957, Laryngoscope, V67, P1266 DALLOS P, 1992, J NEUROSCI, V12, P4575 DECUORSEY TE, 1988, J PHYSIOL-LONDON, V395, P487 DECUORSEY TE, 1987, J GEN PHYSIOL, V89, P379 FENWICK EM, 1982, J PHYSIOL-LONDON, V331, P577 GEALDOR M, 1993, HEARING RES, V69, P236, DOI 10.1016/0378-5955(93)90113-F GILLESPIE PG, 1995, CURR OPIN NEUROBIOL, V5, P449, DOI 10.1016/0959-4388(95)80004-2 Hille B, 1992, IONIC CHANNELS EXCIT, P341 HINOJOSA R, 1972, ACTA OTO-LARYNGOL, V74, P1, DOI 10.3109/00016487209128416 Kim SJ, 1997, HEARING RES, V112, P186, DOI 10.1016/S0378-5955(97)00120-2 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 Kros CJ, 1998, NATURE, V394, P281, DOI 10.1038/28401 Mammano F, 1996, NEUROREPORT, V7, P537, DOI 10.1097/00001756-199601310-00039 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MARCUS DC, 1994, AM J PHYSIOL, V267, pC857 Marcus DC, 1999, HEARING RES, V134, P48, DOI 10.1016/S0378-5955(99)00074-X Nenov AP, 1998, HEARING RES, V123, P168, DOI 10.1016/S0378-5955(98)00121-X NOMURA Y, 1970, ARCH KLIN EXP OHR, V195, P266, DOI 10.1007/BF00302954 SIM DW, 1989, J LARYNGOL OTOL, V103, P1122, DOI 10.1017/S0022215100111168 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 STRAUSS O, 1993, BIOCHEM BIOPH RES CO, V191, P775, DOI 10.1006/bbrc.1993.1284 TAO Q, 1994, J MEMBRANE BIOL, V141, P123 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WEN R, 1993, J PHYSIOL-LONDON, V465, P121 Yeh TH, 1997, HEARING RES, V109, P1, DOI 10.1016/S0378-5955(97)00030-0 ZIDANIC M, 1990, BIOPHYS J, V57, P1253 NR 27 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 7 EP 16 DI 10.1016/S0378-5955(00)00074-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500002 PM 10913879 ER PT J AU Holt, JC Pantoja, AM Athas, GB Guth, PS AF Holt, JC Pantoja, AM Athas, GB Guth, PS TI A role for chloride in the hyperpolarizing effect of acetylcholine in isolated frog vestibular hair cells SO HEARING RESEARCH LA English DT Article DE acetylcholine; nicotinic; chloride; saccule; frog; hair cell ID GAMMA-AMINOBUTYRIC-ACID; POTASSIUM CURRENTS; CRISTA-AMPULLARIS; ACTIVATED CHLORIDE; CHANNEL BLOCKERS; OUTWARD CURRENTS; APLYSIA NEURONS; MUSCLE-CELLS; PORTAL-VEIN; RECEPTOR AB Acetylcholine (ACh) is the dominant transmitter released from inner ear efferent neurons. In frog vestibular organs, these efferent neurons synapse exclusively with type II hair cells. Hair cells isolated from the frog saccule hyperpolarize following the application of 50 mu M ACh, thereby demonstrating the presence of an ACh receptor. A role for Cl- in the response of hair cell-bearing organs to efferent nerve activation or ACh application was suggested some years ago. Perfusion with solutions in which mast of the Cl- was replaced by large impermeant anions decreased the cholinergic inhibition of afferent firing in the cat and turtle cochleas, and frog semicircular canal. Our previous work in the intact organ demonstrated that substitution of large impermeant anions for Cl- or use of Cl- channel blockers reduced the effect of ACh on saccular afferent firing. Using the perforated-patch clamping technique, replacement of Cl- by methanesulfonate, iodide, nitrate, or thiocyanate attenuated the hyperpolarizing response to ACh in hair cells isolated from the frog saccule. The chloride channel blockers picrotoxin and 4,4'-dinitrostilbene-2,2'-disulfonic acid were also tested and found to inhibit the ACh response. Thus, the present work demonstrates that the effects of Cl- substitutions or Cl- channel blockers on the ACh response in the intact saccule can be explained completely by effects on the hair cell. Evidence is also presented for the presence of the messenger RNA for a calcium-dependent chloride channel in all hair cells but especially saccular hair cells. This channel may be involved in the response to ACh. The precise role for chloride in this response, whether as a distinct ion current, as a transported ion, or as a permissive ion for other components, is discussed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tulane Univ, Sch Med, Dept Pharmacol, New Orleans, LA 70112 USA. Univ Valle, Dept Farmacol, Cali, Colombia. Tulane Univ, Sch Med, Dept Otolaryngol, New Orleans, LA 70112 USA. RP Guth, PS (reprint author), Tulane Univ, Sch Med, Dept Pharmacol, 1430 Tulane Ave, New Orleans, LA 70112 USA. CR ART JJ, 1984, J PHYSIOL-LONDON, V356, P525 ATHAS GB, 1997, ASS RES OTOLARYNGOL, V20, P37 BRETAG AH, 1987, PHYSIOL REV, V67, P618 BUSCH AE, 1994, MOL PHARMACOL, V46, P750 CARMELIET E, 1977, J PHYSIOL-LONDON, V265, P193 Costa E, 1979, Adv Exp Med Biol, V123, P371 DANI JA, 1983, J GEN PHYSIOL, V81, P255, DOI 10.1085/jgp.81.2.255 DESMEDT JE, 1975, J PHYSIOL-LONDON, V247, P407 EBERWINE J, 1992, P NATL ACAD SCI USA, V89, P3010, DOI 10.1073/pnas.89.7.3010 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FINDLAY I, 1985, PFLUG ARCH EUR J PHY, V403, P328, DOI 10.1007/BF00583609 FINKEL AS, 1983, J PHYSIOL-LONDON, V344, P119 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 FUCHS PA, 1992, J NEUROSCI, V12, P800 GREENWOOD IA, 1995, BRIT J PHARMACOL, V116, P2939 GREGER R, 1991, PFLUG ARCH EUR J PHY, V419, P190, DOI 10.1007/BF00373006 GUTH PS, 1986, ACTA OTO-LARYNGOL, V102, P194, DOI 10.3109/00016488609108666 Guth PS, 1998, PROG NEUROBIOL, V54, P193, DOI 10.1016/S0301-0082(97)00068-3 GUTH PS, 1994, HEARING RES, V75, P225, DOI 10.1016/0378-5955(94)90073-6 Guth PS, 1998, HEARING RES, V125, P154, DOI 10.1016/S0378-5955(98)00145-2 Guth PS, 1996, HEARING RES, V98, P1, DOI 10.1016/0378-5955(96)00031-7 GUTH PS, 1994, HEARING RES, V73, P109, DOI 10.1016/0378-5955(94)90288-7 HILLMAN DE, 1976, FROG NEUROBIOLOGY, V1, P452 HOLT JC, 2000, UNPUB NEUROSCIENCE HORN R, 1988, J GEN PHYSIOL, V92, P145, DOI 10.1085/jgp.92.2.145 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 HOUSLEY GD, 1990, HEARING RES, V43, P121, DOI 10.1016/0378-5955(90)90221-A HOUSLEY GD, 1989, HEARING RES, V38, P259, DOI 10.1016/0378-5955(89)90070-1 KEHOE J, 1972, J PHYSIOL-LONDON, V225, P115 Kehoe J, 1998, J NEUROSCI, V18, P8198 KENYON JL, 1977, J GEN PHYSIOL, V70, P635, DOI 10.1085/jgp.70.5.635 Kirkup AJ, 1996, BRIT J PHARMACOL, V117, P175 KONCZ C, 1994, AM J PHYSIOL-HEART C, V267, pH2114 Laurienti PJ, 1996, J NEUROPHYSIOL, V76, P1531 LEEBLUNDBERG F, 1980, P NATL ACAD SCI-BIOL, V77, P7468, DOI 10.1073/pnas.77.12.7468 LIU QY, 1994, MOL PHARMACOL, V46, P1197 MARVIZON JCG, 1988, EUR J PHARMACOL, V151, P157, DOI 10.1016/0014-2999(88)90709-1 MASETTO S, 1994, J NEUROPHYSIOL, V72, P443 MAYER ML, 1983, J PHYSIOL-LONDON, V340, P19 MCCANN JD, 1990, ANNU REV PHYSIOL, V52, P115 MENA EE, 1982, BRAIN RES, V243, P378, DOI 10.1016/0006-8993(82)90265-7 NAGAHAMA T, 1993, P ROY SOC B-BIOL SCI, V254, P275, DOI 10.1098/rspb.1993.0156 NORRIS CH, 1992, J NEUROPHYSIOL, V68, P1642 Pantoja AM, 1997, HEARING RES, V112, P21, DOI 10.1016/S0378-5955(97)00101-9 PAOLETTI P, 1995, NEURON, V15, P1109, DOI 10.1016/0896-6273(95)90099-3 PERILLO MA, 1998, RRD LIP RES 2, V2, P275 PERT CB, 1973, SCIENCE, V179, P1011, DOI 10.1126/science.179.4077.1011 PFEIFFERLINN C, 1989, SCIENCE, V245, P1249, DOI 10.1126/science.2476848 PIGGOTT SM, 1977, COMP BIOCHEM PHYS C, V57, P107, DOI 10.1016/0306-4492(77)90054-5 ROSSI ML, 1982, BRAIN RES, V233, P181, DOI 10.1016/0006-8993(82)90939-8 Sambrook J., 1989, MOL CLONING LAB MANU SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M SUGAI T, 1989, Japanese Journal of Physiology, V39, pS168 TAKAHASHI T, 1990, J PHYSIOL-LONDON, V423, P47 Thoreson WB, 1997, J NEUROPHYSIOL, V77, P2175 VANGELDER RN, 1990, P NATL ACAD SCI USA, V87, P1663 WELSH MJ, 1990, FASEB J, V4, P2718 WORRELL RT, 1989, AM J PHYSIOL, V256, pC1111 YAROWSKY PJ, 1978, J NEUROPHYSIOL, V41, P531 YOSHIDA N, 1994, BRAIN RES, V644, P90, DOI 10.1016/0006-8993(94)90351-4 ZUFALL F, 1989, BRAIN RES, V503, P342, DOI 10.1016/0006-8993(89)91688-0 NR 61 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 17 EP 27 DI 10.1016/S0378-5955(00)00092-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500003 PM 10913880 ER PT J AU Ohinata, Y Yamasoba, T Schacht, J Miller, JM AF Ohinata, Y Yamasoba, T Schacht, J Miller, JM TI Glutathione limits noise-induced hearing loss SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 22nd Midwinter Meeting of the Association-for-Research-in-Otolaryngology CY FEB 13-18, 1999 CL ST PETERSBURG, FLORIDA SP Assoc Res Otolaryngol DE reactive oxygen species; antioxidant; noise; hearing loss; diet; guinea pig ID COCHLEAR BLOOD-FLOW; LASER DOPPLER MEASUREMENTS; PIG INNER-EAR; GUINEA-PIG; LOUD SOUND; GENTAMICIN OTOTOXICITY; CISPLATIN OTOTOXICITY; ACOUSTIC TRAUMA; CELL VELOCITY; FREE-RADICALS AB The generation of reactive oxygen species (ROS) is thought to be part of the mechanism underlying noise-induced hearing loss (NIHL). Glutathione (GSH) is an important cellular antioxidant that limits cell damage by ROS. In this study, we investigated the effectiveness of a GSH supplement to protect GSH-deficient animals from NIHL. Pigmented guinea pigs were exposed to a 4 kHz octave band noise, 115 dB SPL, for 5 h. Group 1 had a normal diet, while groups 2, 3 and 4 were fed a 7% low protein diet (leading to lowered tissue levels of GSH) for 10 days prior to noise exposure. One hour before, immediately after and 5 h after noise exposure, subjects received either an intraperitoneal injection of 5 ml/kg body weight of 0.9% NaCl (groups 1 and 2), 0.4 M glutathione monoethyl eater (GSHE; group 3) or 0.8 M GSHE (group 4). Auditory thresholds were measured by evoked brain stem response at 2, 4, 8, 12, 16 and 20 kHz before and after noise exposure. Ten days post exposure, group 1 showed noise-induced threshold shifts of approximately 20 dB at 2, 16 and 20 kHz and 35 to 40 dB at other frequencies. Threshold shifts in group 2 were significantly greater than baseline at 2, 4, 16 and 20 kHz. GSHE supplementation in a dose-dependent fashion attenuated the threshold shifts in the low protein diet animals. Hair cell loss, as evaluated with cytocochleograms, was consistent with the auditory-evoked brainstem response results. Group 2 exhibited significantly more hair cell loss than any of the other groups; hair cell loss in group 3 was similar to that seen in group 1; group 4 showed less loss than group 1. These results indicate that GSH is a significant factor in limiting noise-induced cochlear damage. This is compatible with the notion that ROS generation plays a role in NIHL and that antioxidant treatment may be an effective prophylactic intervention. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Osaka Med Coll, Dept Otolaryngol, Osaka 5698686, Japan. Univ Tokyo, Dept Otolaryngol, Bunkyo Ku, Tokyo 1138655, Japan. RP Miller, JM (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR ANDERSON ME, 1989, ANAL BIOCHEM, V183, P16, DOI 10.1016/0003-2697(89)90164-4 AXELSSON A, 1987, HEARING RES, V31, P183, DOI 10.1016/0378-5955(87)90125-0 CANLON B, 1983, HEARING RES, V10, P217, DOI 10.1016/0378-5955(83)90055-2 DELEVE LD, 1991, PHARMACOL THERAPEUT, V52, P287, DOI 10.1016/0163-7258(91)90029-L ELBARBARY A, 1993, HEARING RES, V71, P80 GARETZ SL, 1994, HEARING RES, V77, P75, DOI 10.1016/0378-5955(94)90254-2 GARETZ SL, 1994, HEARING RES, V77, P81, DOI 10.1016/0378-5955(94)90255-0 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HOFFMAN DW, 1987, HEARING RES, V31, P217, DOI 10.1016/0378-5955(87)90190-0 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 HU BH, 1996, ASS RES OT ABSTR, V19, P802 HULTCRANTZ E, 1979, ARCH OTO-RHINO-LARYN, V224, P103, DOI 10.1007/BF00455231 HUNTERDU.IM, 1973, J ACOUST SOC AM, V54, P1179, DOI 10.1121/1.1914364 JACONO AA, 1997, ASS RES OT ABSTR, V20, P132 JULICHER RHM, 1984, ARCH TOXICOL, V56, P83, DOI 10.1007/BF00349076 Lamm K, 1996, Audiol Neurootol, V1, P148 Lautermann J, 1996, ARCH OTOLARYNGOL, V122, P837 LAUTERMANN J, 1995, HEARING RES, V88, P47, DOI 10.1016/0378-5955(95)00097-N LAUTERMANN J, 1995, HEARING RES, V86, P15, DOI 10.1016/0378-5955(95)00049-A Lautermann J, 1997, HEARING RES, V114, P75, DOI 10.1016/S0378-5955(97)00154-8 LIBERMAN MC, 1995, HEARING RES, V90, P158, DOI 10.1016/0378-5955(95)00160-2 MEISTER A, 1983, ANNU REV BIOCHEM, V52, P711, DOI 10.1146/annurev.bi.52.070183.003431 MEISTER A, 1991, PHARMACOL THERAPEUT, V51, P155, DOI 10.1016/0163-7258(91)90076-X OHINATA Y, 1999, INN EAR BIOL ABSTR, V36, pC11 OHLEMILLE RKK, 1998, ASS RES OT ABSTR, V21, P518 ORRENIUS S, 1984, TRENDS PHARMACOL SCI, V5, P432, DOI 10.1016/0165-6147(84)90495-4 Puel JL, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P36 PURI RN, 1983, P NATL ACAD SCI-BIOL, V80, P5258, DOI 10.1073/pnas.80.17.5258 QUIRK WS, 1991, HEARING RES, V52, P217, DOI 10.1016/0378-5955(91)90201-J QUIRK WS, 1994, HEARING RES, V74, P217, DOI 10.1016/0378-5955(94)90189-9 QUIRK WS, 1992, HEARING RES, V63, P102, DOI 10.1016/0378-5955(92)90079-3 QUIRK WS, 1995, AM J OTOL, V16, P322 RAPHAEL Y, 1991, HEARING RES, V51, P173, DOI 10.1016/0378-5955(91)90034-7 RAVI R, 1995, PHARMACOL TOXICOL, V76, P386 RYAN CME, 1982, BEHAV ANAL LETT, V2, P213 SCHEIBE F, 1990, EUR ARCH OTO-RHINO-L, V247, P84 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 Usami S, 1996, BRAIN RES, V743, P337, DOI 10.1016/S0006-8993(96)01090-6 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 YAMANE H, 1991, ACTA OTO-LARYNGOL, V111, P85, DOI 10.3109/00016489109137358 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 Yamasoba T, 1998, BRAIN RES, V784, P82, DOI 10.1016/S0006-8993(97)01156-6 Yamasoba T, 1998, BRAIN RES, V804, P72, DOI 10.1016/S0006-8993(98)00660-X NR 45 TC 91 Z9 103 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 28 EP 34 DI 10.1016/S0378-5955(00)00096-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500004 PM 10913881 ER PT J AU Watson, GM Venable-Thibodeaux, S AF Watson, GM Venable-Thibodeaux, S TI Immunological evidence that anemone repair proteins include replacement linkages SO HEARING RESEARCH LA English DT Article DE hair bundle; stereocilia; hair cell ID HAIR BUNDLES; SEA-ANEMONES; NEMATOCYST DISCHARGE; FREQUENCY; COMPLEXES; CELLS AB In response to damage to hair bundles caused by exposure to calcium free buffers, sea anemones secrete large protein complexes named 'repair proteins' that rapidly restore structural integrity and function to hair bundles. A specific chromatographic fraction of the repair protein mixture, named 'fraction beta', has biological activity comparable to the complete repair protein mixture (Watson et al., 1998, Hear. Res. 115, 119-128). In this study, we find that polyclonal antibodies raised against deglycosylated fraction beta specifically bind fraction beta on Western blots. Anti-fraction beta delays the normal recovery of vibration sensitivity in experimental animals (i.e., those with hair bundles damaged by calcium free buffers). Moreover, anti-fraction beta disrupts vibration sensitivity in control animals (i.e., those with healthy hair bundles). Experimentally damaged hair bundles subsequently exposed to repair protein and then processed for immunoelectron microscopy show labeled linkages interconnecting stereocilia of the hair bundle. Immunofluorescence microscopy confirms strong labeling of hair bundles treated with repair proteins and only weak labeling of tips of hair bundles from control animals. Immunofluorescence microscopy indicates stores of repair proteins in gland cells of the body column in control animals and in gland cells of the mouth in experimental animals. Repair biological activity is confirmed in column purified homogenates of these tissues. Apparently repair proteins are delivered to damaged hair bundles in mucus carried by beating cilia. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ SW Louisiana, Dept Biol, Lafayette, LA 70504 USA. RP Watson, GM (reprint author), Univ SW Louisiana, Dept Biol, Box 42451, Lafayette, LA 70504 USA. CR ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 HOLLEY MC, 1984, J EXP BIOL, V108, P151 HOLSTEIN T, 1984, SCIENCE, V223, P830, DOI 10.1126/science.6695186 Mariscal R. N., 1984, BIOL INTEGUMENT, P57 MARISCAL RN, 1974, COELENTERATE BIOL RE, P1290 Mire P, 1997, HEARING RES, V113, P224, DOI 10.1016/S0378-5955(97)00145-7 MIRETHIBODEAUX P, 1994, J EXP ZOOL, V268, P282, DOI 10.1002/jez.1402680404 OSBORNE MP, 1990, ACTA OTO-LARYNGOL, V110, P37, DOI 10.3109/00016489009122513 PETEYA DJ, 1975, TISSUE CELL, V7, P243, DOI 10.1016/0040-8166(75)90003-8 PREYER S, 1995, J PHYSL, V491, P707 SHICK JM, FUNCTIONAL BIOL SEA, P91 SKAER RJ, 1965, PHILOS T ROY SOC B, V250, P131, DOI 10.1098/rstb.1965.0022 WATSON GM, 1989, SCIENCE, V243, P1589, DOI 10.1126/science.2564698 WATSON GM, 1994, J EXP ZOOL, V268, P177, DOI 10.1002/jez.1402680302 Watson GM, 1999, HEARING RES, V136, P1, DOI 10.1016/S0378-5955(99)00087-8 WATSON GM, 1995, CELL MOTIL CYTOSKEL, V30, P208, DOI 10.1002/cm.970300305 Watson GM, 1997, HEARING RES, V107, P53, DOI 10.1016/S0378-5955(97)00022-1 Watson GM, 1998, J EXP ZOOL, V281, P582 WATSON GM, 1983, BIOL BULL, V164, P506, DOI 10.2307/1541259 Watson GM, 1998, HEARING RES, V115, P119, DOI 10.1016/S0378-5955(97)00185-8 Watson GM, 1999, CURR TOP DEV BIOL, V43, P51 WATSON GM, 1994, INT REV CYTOL, V156, P275 ZHAO Y, 1996, P NATL ACAD SCI USA, V94, P15469 NR 24 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 35 EP 46 DI 10.1016/S0378-5955(00)00095-2 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500005 PM 10913882 ER PT J AU Kummer, P Janssen, T Hulin, P Arnold, W AF Kummer, P Janssen, T Hulin, P Arnold, W TI Optimal L(1)-L(2) primary tone level separation remains independent of test frequency in humans SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; clinical application; human; basilar membrane; mechanics ID PRODUCT OTOACOUSTIC EMISSIONS; ACOUSTIC DISTORTION-PRODUCT; COCHLEAR HEARING-LOSS; 2 DISCRETE SOURCES; AUDITORY-SENSITIVITY; HUMAN EARS; GROWTH-BEHAVIOR; FINE-STRUCTURE; IMPAIRED EARS; DEPENDENCE AB Previous studies described a systematic asymmetry of the level of the 2f(1)-f(2) distortion product otoacoustic emission (DP) in the space of the primary tones levels L(1) and L(2) in normal-hearing humans. Optimal primary tone level separations L(1)-L(2), which result in maximum DP levels, were close to L(1) = L(2) at high levels, but continuously increased with decreasing stimulus level towards L(1) > L(2) (Gaskill and Brown, 1990, J. Acoust. Sec. Am. 88, 821-839). At these optimal L(1)-L(2), however, not only DP levels in normal hearing were maximal, but also trauma-induced DP reductions. A linear equation that approximates optimal L(1)-L(2) level separations thus was suggested to be optimum for use in clinical applications (Whitehead et al., 1995, J. Acoust. Sec. Am. 97, 2359-2377). It was the aim of this study to extend the generality of optimal L(1)-L(2) separations to the typical human test frequency range for f(2) frequencies between 1 and 8 kHz. DPs were measured in 22 normal-hearing human ears at 61 primary tone level combinations, with L(2) between 5 and 65 dB SPL and L(1) between 30 and 70 dB SPL (f(2)/f(1) = 1.2). It was found that the systematic dependence of the maximum DP level on the L(1)-L(2) separation is independent on frequency. Optimal L(1)-L(2) level separations may well be approximated by a linear equation L(1) = a L(2)+(1-a) b (after Whitehead et al., 1995) with parameters a = 0.4 and b = 70 dB SPL at f(2) frequencies between 1 and 8 kHz and L(2) levels between 20 and 65 dB SPL. Below L(2) = 20 dB SPL, the optimal L(1) was found to be almost constant. Following previous notions (Gaskill and Brown, 1990), an analysis of basilar membrane response data in experimental animals (after Ruggero and Rich, 1991, Hear. Res. 51, 215-230) is further presented that relates optimal L(1)-L(2) separations to frequency-selective compression of the basilar membrane. Based on the assumption that optimal conditions for the DP generation are equal primary tone responses at the f(2) place, a linear increase of the optimal L(1)-L(2) level separation is graphically demonstrated, similar to our results in human ears. (C) 2000 Published by Elsevier Science B.V. C1 Tech Univ Munich, Klinikum Rechts Isar, Hals Nasen Ohren Klin, D-81675 Munich, Germany. RP Kummer, P (reprint author), Tech Univ Munich, Klinikum Rechts Isar, Hals Nasen Ohren Klin, Ismaninger Str 22, D-81675 Munich, Germany. CR BOEGE P, 20 MIDW M ASS RES OT BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 DALLOS P, 1992, J NEUROSCI, V12, P4575 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 Dhar S, 1998, J SPEECH LANG HEAR R, V41, P1307 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 Gorga MP, 1996, J ACOUST SOC AM, V100, P968, DOI 10.1121/1.416208 HAUSER R, 1991, J ACOUST SOC AM, V89, P280, DOI 10.1121/1.400511 HE NJ, 1993, J ACOUST SOC AM, V94, P2659, DOI 10.1121/1.407350 He NJ, 1997, J ACOUST SOC AM, V101, P3554, DOI 10.1121/1.418316 HEITMANN J, 1997, 20 MIDW M ASS RES OT, P83 Janssen T, 1998, J ACOUST SOC AM, V103, P3418, DOI 10.1121/1.423053 JANSSEN T, 1995, OTO RHINO LARYN NOVA, V5, P34 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 Kemp D. T., 1983, MECH HEARING, P75 KEMP DT, 1990, LECT NOTES BIOMATH, V87, P202 KUMMER P, 1995, J ACOUST SOC AM, V98, P197, DOI 10.1121/1.413747 Kummer P, 1998, J ACOUST SOC AM, V103, P3431, DOI 10.1121/1.423054 MARTIN GK, 1990, ANN OTO RHINOL LARYN, V99, P30 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 NELSON DA, 1992, J SPEECH HEAR RES, V35, P1142 POPELKA GR, 1993, HEARING RES, V71, P12, DOI 10.1016/0378-5955(93)90016-T RASMUSSEN AN, 1993, SCAND AUDIOL, V22, P223, DOI 10.3109/01050399309047473 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 RUGGERO MA, 1991, HEARING RES, V51, P215, DOI 10.1016/0378-5955(91)90038-B Stover L, 1996, J ACOUST SOC AM, V100, P956, DOI 10.1121/1.416207 SUTTON LA, 1994, HEARING RES, V75, P161, DOI 10.1016/0378-5955(94)90067-1 WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2359, DOI 10.1121/1.411960 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2346, DOI 10.1121/1.411959 WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 NR 33 TC 83 Z9 86 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 47 EP 56 DI 10.1016/S0378-5955(00)00097-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500006 PM 10913883 ER PT J AU Huang, CQ Shepherd, RK AF Huang, CQ Shepherd, RK TI Reduction in excitability of the auditory nerve following electrical stimulation at high stimulus rates: V. Effects of electrode surface area SO HEARING RESEARCH LA English DT Article DE auditory nerve; high rate electrical stimulation; electrically evoked auditory brainstem response; cochlear implant; large surface area electrode; charge density ID DEFINED CHARGE-DENSITIES; GUINEA-PIG; EXTRACELLULAR POTASSIUM; BALANCED STIMULI; INDUCED DAMAGE; 8TH NERVE; COCHLEA; CORTEX; CAT; CEREBELLUM AB High rate intracochlear electrical stimulation at high intensities can induce significant reductions in the excitability of the auditory nerve as measured by a decrement in the amplitude of the electrically evoked auditory brainstem response (EABR). Such changes are primarily associated with stimulus induced neuronal activity, although direct current (DC) can also contribute. We examined the extent of stimulus induced change in auditory nerve excitability using large surface area platinum electrodes ('high-Q' electrodes). These electrodes have a surface area similar to 70 times greater than standard Pt electrodes of the same geometric area, resulting in lower DC and charge density (charge/electrode surface area) for a common stimulus. Guinea pigs were bilaterally implanted with either high-Q or standard Pt electrodes, and unilaterally stimulated for 2 h using stimulus intensities of 12 dB or 20-30 dB above EABR threshold (0.34 mu C/phase) at stimulus rates of 200, 400, or 1000 pulses per second (pps). EABRs were recorded before and following the acute stimulation. While there were significant reductions in EABR amplitudes and elevated EABR thresholds following stimulation at 12 dB above threshold using 400 and 1000 pps delivered to standard Pt electrodes, there were fewer or no significant changes in the post-stimulus EABR amplitude and threshold using high-Q electrodes under equivalent stimulus conditions. At a higher stimulus intensity (20-30 dB above EABR threshold), no reduction in EABR amplitude was observed at 200 pps for both stimulating electrodes. However, EABRs were reduced significantly at 400 and 1000 pps. There was significantly greater EABR recovery following stimulation using high-Q electrodes compared with standard Pt electrodes at 400 (P<0.05) and 1000 pps (P < 0.05). These data indicate that large surface area electrodes can significantly reduce stimulus induced changes in auditory nerve excitability, and may therefore have important clinical application. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Dept Otolaryngol, CRC Cochlear Implant & Hearing Aid Innovat, E Melbourne, Vic 3002, Australia. RP Shepherd, RK (reprint author), Univ Melbourne, Dept Otolaryngol, CRC Cochlear Implant & Hearing Aid Innovat, 32 Gisborne St, E Melbourne, Vic 3002, Australia. RI Shepherd, Robert/I-6276-2012 CR Agnew WF, 1990, NEURAL PROSTHESES FU, P225 Agnew W F, 1975, Surg Neurol, V4, P438 AGNEW WF, 1990, J BIOMED ENG, V12, P301, DOI 10.1016/0141-5425(90)90004-7 AGNEW WF, 1983, EXP NEUROL, V79, P397, DOI 10.1016/0014-4886(83)90221-2 AGNEW WF, 1986, EXP NEUROL, V92, P162, DOI 10.1016/0014-4886(86)90132-9 BABB TL, 1977, J NEUROSURG, V47, P353, DOI 10.3171/jns.1977.47.3.0353 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BOSTOCK H, 1994, BRAIN, V117, P913, DOI 10.1093/brain/117.5.913 BROWN WJ, 1977, J NEUROSURG, V47, P366, DOI 10.3171/jns.1977.47.3.0366 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P436, DOI 10.1109/TBME.1977.326178 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P440, DOI 10.1109/TBME.1977.326179 BURKE D, 1989, BRAIN, V112, P913, DOI 10.1093/brain/112.4.913 deSauvage RC, 1997, HEARING RES, V110, P119 Clark G M, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P40 Duckert L G, 1984, Acta Otolaryngol Suppl, V411, P28 GREATBATCH W, 1981, CRC CR REV BIOM ENG, V5, P1 Haenggeli A, 1998, AUDIOLOGY, V37, P353 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 Huang CQ, 1999, IEEE T BIO-MED ENG, V46, P461, DOI 10.1109/10.752943 Huang CQ, 1998, HEARING RES, V116, P55, DOI 10.1016/S0378-5955(97)00196-2 HUANG CQ, 1998, P 18 AUST NEUR SOC, V9, P162 Huang CQ, 1999, HEARING RES, V132, P60, DOI 10.1016/S0378-5955(99)00034-9 HUANG CQ, 2000, P 20 AUST NEUR SOC, V11, P216 HUANG CQ, 1997, P 17 AUST NEUR SOC, V8, P167 HUGHES JR, 1957, J ACOUST SOC AM, V29, P275, DOI 10.1121/1.1908854 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 KILLIAN MJP, 1994, HEARING RES, V81, P66, DOI 10.1016/0378-5955(94)90154-6 KILLIAN MJP, 1994, THESIS U UTRECHT KOCSIS JD, 1983, J PHYSIOL-LONDON, V334, P225 MCCREERY DB, 1983, EXP NEUROL, V79, P371, DOI 10.1016/0014-4886(83)90220-0 MCCREERY DB, 1992, HEARING RES, V62, P42, DOI 10.1016/0378-5955(92)90201-W MCCREERY DB, 1990, IEEE T BIO-MED ENG, V37, P996, DOI 10.1109/10.102812 MILLER CA, 1993, HEARING RES, V69, P35, DOI 10.1016/0378-5955(93)90091-E MILLER JM, 1985, COCHLEAR IMPLANTS, P35 MILLER JM, 1983, ANN OTO RHINOL LARYN, V92, P599 Mitchell A, 1997, HEARING RES, V105, P30, DOI 10.1016/S0378-5955(96)00202-X National Institutes of Health, 1995, COCHLEAR IMPLANTS AD, V13, P1 NI DF, 1992, HEARING RES, V62, P63, DOI 10.1016/0378-5955(92)90203-Y ORKAND KR, 1980, FED PROC, V39, P1514 OTTEN JM, 1994, Patent No. 5326448 PUDENZ R H, 1975, Surgical Neurology, V4, P265 Pudenz R H, 1975, Surg Neurol, V4, P389 REUTER G, 1999, 1999 C IMPL AUD PROS, P68 SHANNON RV, 1992, IEEE T BIO-MED ENG, V39, P424, DOI 10.1109/10.126616 SHEPHERD RK, 1987, ANN OTO RHINOL LARYN, V96, P50 Shepherd RK, 1997, HEARING RES, V108, P112, DOI 10.1016/S0378-5955(97)00046-4 Shepherd RK, 1990, COCHLEAR PROSTHESES, P69 Shepherd RK, 1986, THESIS U MELBOURNE Shepherd RK, 1999, ACTA OTO-LARYNGOL, V119, P674, DOI 10.1080/00016489950180621 SHEPHERD RK, 1991, BIOMATERIALS, V12, P417 SHEPHERD RK, 1991, ACTA OTO-LARYNGOL, V111, P848, DOI 10.3109/00016489109138421 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 TYKOCINSKI M, 1995, HEARING RES, V88, P124, DOI 10.1016/0378-5955(95)00108-G TYKOCINSKI M, 1999, P 19 AUST NEUR SOC, V10, P181 Tykocinski M, 1997, HEARING RES, V112, P147, DOI 10.1016/S0378-5955(97)00117-2 URBANICS R, 1978, PFLUG ARCH EUR J PHY, V378, P47, DOI 10.1007/BF00581957 Vischer M, 1997, AM J OTOL, V18, pS27 WALSH SM, 1981, ANN OTO RHINOL LARYN, V90, P27 Xu J, 1997, HEARING RES, V105, P1, DOI 10.1016/S0378-5955(96)00193-1 YUEN TGH, 1981, NEUROSURGERY, V9, P292 NR 60 TC 11 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 57 EP 71 DI 10.1016/S0378-5955(00)00100-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500007 PM 10913884 ER PT J AU Freeman, S Sichel, JY Sohmer, H AF Freeman, S Sichel, JY Sohmer, H TI Bone conduction experiments in animals - evidence for a non-osseous mechanism SO HEARING RESEARCH LA English DT Article DE bone conduction; auditory nerve-brainstem evoked response; vibrator; skull; cerebro-spinal fluid; cochlea ID COCHLEAR BLOOD-FLOW; MANNITOL; PRESSURE; GLYCEROL; AQUEDUCT; DOPPLER AB Bone conducted stimuli are used to differentiate between conductive and sensori-neural hearing loss. It has been thought that the main route for the transfer of vibratory energy from the point of application of the bone vibrator on the skull to the inner ear is completely osseous. An additional mechanism may play a prominent role. In rats, a bone vibrator was applied to the skull and also directly on the brain, after removing bone (a craniotomy), exposing the brain. Auditory nerve-brainstem evoked response (ABR) could be elicited not only with the vibrator on bone, but also with the vibrator directly on the brain. Similar results were obtained in guinea-pigs and fat sand rats. Noise masked this ABR. Extensive removal of skull bone did not alter the ABR to bone-conducted stimuli delivered to the exposed brain. Experimental elimination of the ossicular chain inertial mechanism and of the occlusion effect did not greatly alter the bone conduction response. A reduction in the fluid volume of the cranial cavity induced threshold elevations of the bone conducted ABR but not of the air conducted ABR. These findings call be interpreted as evidence that the 'classical' bone conduction mechanisms should be modified to include a major pathway for cochlear excitation which is non-osseous: when a bone vibrator is applied to the skull, the bone vibrations may induce audio-frequency sound pressures in the skull contents (brain and cerebro-spinal fluid) which are then communicated by fluid channels to the fluids of the inner ear. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, IL-91120 Jerusalem, Israel. Hadassah Univ Hosp, Dept Otolaryngol Head & Neck Surg, IL-91120 Jerusalem, Israel. RP Sohmer, H (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, POB 12272, IL-91120 Jerusalem, Israel. CR ANSON BJ, 1965, LARYNGOSCOPE, V75, P1203 BALDWIN DL, 1992, ANN OTO RHINOL LARYN, V101, P168 Barany E, 1938, ACTA OTO-LARYNGOL, V26, P1 Bekesy G., 1960, EXPT HEARING BERING EA, 1955, ARCH NEURO PSYCHIATR, V73, P165 Böhmer A, 1993, Acta Otolaryngol Suppl, V507, P3 CARLBORG B, 1982, ANN OTO RHINOL LARYN, V91, P209 DONATO T, 1994, ANESTH ANALG, V78, P58 DUNBAR HS, 1966, ARCH NEUROL-CHICAGO, V14, P624 GEALDOR M, 1993, HEARING RES, V69, P236, DOI 10.1016/0378-5955(93)90113-F GOODWIN PC, 1984, ACTA OTO-LARYNGOL, V98, P403, DOI 10.3109/00016488409107581 KIRIKAE I, 1959, Acta Otolaryngol Suppl, V145, P1 Kitahara M, 1994, Acta Otolaryngol Suppl, V510, P113 KONRADSSON KS, 1994, ACTA OTO-LARYNGOL, V114, P24, DOI 10.3109/00016489409126012 LARSEN HC, 1982, ARCH OTO-RHINO-LARYN, V234, P145, DOI 10.1007/BF00453621 MARCHBANKS R J, 1990, British Journal of Audiology, V24, P179, DOI 10.3109/03005369009076554 MARTINEZ DM, 1968, ACTA OTOLARYNGOL S S, V238, P5 PALVA T, 1979, ACTA OTO-LARYNGOL, V87, P310, DOI 10.3109/00016487909126425 SANDO I, 1971, ANN OTO RHINOL LARYN, V80, P826 SCHNEIDER W, 1959, Z Laryngol Rhinol Otol, V38, P723 Schuknecht H F, 1988, Adv Otorhinolaryngol, V39, P1 Sohmer H, 2000, HEARING RES, V146, P81, DOI 10.1016/S0378-5955(00)00099-X Stenfelt S, 2000, J ACOUST SOC AM, V107, P422, DOI 10.1121/1.428314 Tonndorf J., 1966, ACTA OTO-LARYNGOL, V213, P1 TONNDORF J, 1968, ARCH OTOLARYNGOL, V87, P595 TONNDORF J, 1962, ANN OTO RHINOL LARYN, V71, P5 Treib J, 1998, EUR NEUROL, V40, P212, DOI 10.1159/000007982 von Bekesy G, 1932, ANN PHYS-BERLIN, V13, P111 Wever EG, 1954, PHYSL ACOUSTICS YOSHIDA M, 1991, EUR ARCH OTO-RHINO-L, V248, P139 NR 30 TC 64 Z9 72 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 72 EP 80 DI 10.1016/S0378-5955(00)00098-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500008 PM 10913885 ER PT J AU Sohmer, H Freeman, S Geal-Dor, M Adelman, C Savion, I AF Sohmer, H Freeman, S Geal-Dor, M Adelman, C Savion, I TI Bone conduction experiments in humans - a fluid pathway from bone to ear SO HEARING RESEARCH LA English DT Article DE bone conduction; human; craniotomy; fontanelle; CSF; cochlea; vibration ID BRAIN-STEM RESPONSE; SKULL IN-VIVO; PLACEMENT; INFANTS AB Animal experiments in this laboratory have led to the suggestion that a major pathway in bone conduction stimulation to the inner ear is via the skull contents (brain and CSF). This hypothesis was now tested in humans. Auditory nerve brainstem evoked responses could be recorded in neonates to bone conduction stimulation over the fontanelle and audiometric responses were obtained in neurosurgical patients with the bone Vibrator on the skin over a craniotomy. There were no differences in threshold between these responses and those obtained to bone conduction stimulation over skull bone in the same subjects. Audiometric thresholds in response to bone vibrator stimulation of the eye (a 'natural craniotomy') were no different from those to bone stimulation delivered to several sites on the head. Thus there is no need to vibrate bone in order to obtain 'bone conduction' responses. Bone vibrator thresholds to stimulation at the head region with thinnest bone (temporal) were better than those to stimulation at the forehead region which has much thicker bone, implying that the vibrations penetrate the skull at the site of the vibrator. In addition, the magnitude of vibration (acceleration) measured at various sites around the head in response to bone vibrator stimulation at a fixed point on the forehead generally decreased with distance from the point of vibration. Therefore it seems that the vibrations produced by a bone vibrator at a point on the head are also able to penetrate the skull, setting up audio-frequency pressures in the CSF which spread by fluid communications to the inner ear fluids, exciting the ear. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, IL-91120 Jerusalem, Israel. Hadassah Univ Hosp, Speech & Hearing Ctr, IL-91120 Jerusalem, Israel. Hadassah Univ Hosp, Dept Maxillofacial Prosthesis, IL-91120 Jerusalem, Israel. RP Sohmer, H (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, POB 12272, IL-91120 Jerusalem, Israel. CR AASLID R, 1982, J NEUROSURG, V57, P769, DOI 10.3171/jns.1982.57.6.0769 Barany E, 1938, ACTA OTO-LARYNGOL, V26, P1 BARBER PS, 1969, AM J MENT DEF, V73, P666 Bekesy G., 1960, EXPT HEARING DUNLAP SA, 1988, HEAD NECK SURG, V99, P389 Durrant J D, 1993, J Am Acad Audiol, V4, P213 Freeman S, 2000, HEARING RES, V146, P72, DOI 10.1016/S0378-5955(00)00098-8 GARFIN SR, 1986, J PEDIATR ORTHOPED, V6, P434 Gerhardt KJ, 1996, AM J OTOLARYNG, V17, P374, DOI 10.1016/S0196-0709(96)90069-1 Hakansson B, 1996, J ACOUST SOC AM, V99, P2239 HAKANSSON B, 1994, J ACOUST SOC AM, V95, P1474 Stenfelt S, 2000, J ACOUST SOC AM, V107, P422, DOI 10.1121/1.428314 STUART A, 1990, EAR HEARING, V11, P363, DOI 10.1097/00003446-199010000-00007 Tonndorf J., 1966, ACTA OTO-LARYNGOL, V213, P1 TONNDORF J, 1968, ARCH OTOLARYNGOL, V87, P595 TONNDORF J, 1962, ANN OTO RHINOL LARYN, V71, P5 von Bekesy G, 1932, ANN PHYS-BERLIN, V13, P111 Wever EG, 1954, PHYSL ACOUSTICS YANG EY, 1987, EAR HEARING, V8, P244, DOI 10.1097/00003446-198708000-00009 NR 19 TC 67 Z9 71 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 81 EP 88 DI 10.1016/S0378-5955(00)00099-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500009 PM 10913886 ER PT J AU Kapadia, S Lutman, ME AF Kapadia, S Lutman, ME TI Nonlinear temporal interactions in click-evoked otoacoustic emissions. I. Assumed model and polarity-symmetry SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; nonlinear interaction; model; inter-click interval; cochlear mechanics; click response ID MAXIMUM LENGTH SEQUENCES; STIMULATED ACOUSTIC EMISSIONS; CONTRALATERAL SUPPRESSION; IPSILATERAL SUPPRESSION; VIBRATION; PRESSURE; RATES AB Click-evoked otoacoustic emissions (CEOAEs) are reduced in amplitude by the presentation of 'suppressor' clicks that either closely lead or follow the stimulus ('test') clicks. This suppression of the response represents nonlinear temporal interactions between the test and suppressor clicks and/or the CEOAEs they evoke. There are some discrepancies amongst previous reports of the phenomenon, and the underlying mechanisms are not understood. In particular: it is unclear whether the suppression reported simply reflects the compressive nonlinearity of the CEOAE input-output (I-O) function. This paper presents a simple model of the nonlinear interactions between CEOAEs evoked by two closely-spaced clicks. The model shows that suppression as reported may be entirely derived from CEOAE I-O nonlinearity, in combination with the extended duration of the cochlear responses to click stimuli. It is also shown experimentally that suppression is insensitive to the polarities of test and suppressor clicks, which is consistent with the model based on I-O nonlinearity. A companion paper (Kapadia and Lutman, Hear. Res. 146 (2000)) presents experimental findings from a detailed parametric study of nonlinear temporal interactions in CEOAEs in human subjects with normal hearing. The findings are compared with the pattern of results generated by the above model, in order to assess the role of I-O nonlinearity in these nonlinear interactions. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Southampton, Inst Sound & Vibrat Res, Southampton SO17 1BJ, Hants, England. RP Kapadia, S (reprint author), Univ Southampton, Inst Sound & Vibrat Res, Southampton SO17 1BJ, Hants, England. CR COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E Cope Y., 1988, PAEDIATRIC AUDIOLOGY, P221 GRANDORI F, 1993, BRIT J AUDIOL, V27, P97, DOI 10.3109/03005369309077898 HOWARD J, 1987, P NATL ACAD SCI USA, V84, P3064, DOI 10.1073/pnas.84.9.3064 Johannesen PT, 1998, SCAND AUDIOL, V27, P37, DOI 10.1080/010503998419687 Kapadia S, 1997, J ACOUST SOC AM, V101, P3566, DOI 10.1121/1.418317 Kapadia S, 2000, HEARING RES, V146, P101, DOI 10.1016/S0378-5955(00)00103-9 Keefe DH, 1998, J ACOUST SOC AM, V103, P3489, DOI 10.1121/1.423057 Keefe DH, 1998, J ACOUST SOC AM, V103, P3499, DOI 10.1121/1.423058 KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Kevanishvili Z, 1996, SCAND AUDIOL, V25, P161, DOI 10.3109/01050399609047999 LinaGranade G, 1997, HEARING RES, V107, P83, DOI 10.1016/S0378-5955(97)00021-X LINAGRANADE G, 1995, HEARING RES, V87, P55, DOI 10.1016/0378-5955(95)00078-I PICTON TW, 1993, EAR HEARING, V14, P299, DOI 10.1097/00003446-199310000-00001 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 Rasmussen AN, 1998, BRIT J AUDIOL, V32, P355, DOI 10.3109/03005364000000087 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 TAVARTKILADZE GA, 1994, BRIT J AUDIOL, V28, P193, DOI 10.3109/03005369409086568 THORNTON ARD, 1995, SCAND AUDIOL, V24, P83, DOI 10.3109/01050399509047519 THORNTON ARD, 1994, BRIT J AUDIOL, V28, P227, DOI 10.3109/03005369409086572 THORNTON ARD, 1994, SCAND AUDIOL, V23, P225, DOI 10.3109/01050399409047512 THORNTON ARD, 1993, J ACOUST SOC AM, V94, P132, DOI 10.1121/1.407090 THORNTON ARD, 1994, ADV OTOACOUSTIC EMIS, V1, P28 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X ZWICKER E, 1987, ACUSTICA, V64, P102 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 ZWICKER E, 1987, J ACOUST SOC AM, V81, P1043, DOI 10.1121/1.394676 NR 31 TC 14 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 89 EP 100 DI 10.1016/S0378-5955(00)00102-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500010 PM 10913887 ER PT J AU Kapadia, S Lutman, ME AF Kapadia, S Lutman, ME TI Nonlinear temporal interactions in click-evoked otoacoustic emissions. II. Experimental data SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; nonlinear interaction; model; inter-click interval; cochlear mechanics; click response ID COCHLEAR MICROMECHANICAL PROPERTIES; OTO-ACOUSTIC EMISSIONS; BASILAR-MEMBRANE; HAIR CELL; IPSILATERAL SUPPRESSION; STIMULUS RATE; GUINEA-PIG; PURE-TONE; HEARING; FREQUENCY AB Click-evoked otoacoustic emissions (CEOAEs) are reduced in amplitude by the presentation of 'suppressor' clicks that either closely lead or follow the stimulus ('test') clicks. A model described in a companion paper (Kapadia and Lutman, Hear. Res. 146 (2000) 89-100) shows that such nonlinear temporal interactions, as previously reported, may be explained terms of the compressive non-linearity of the CEOAE input-output (I-O) function. This paper presents the results of a detailed parametric investigation into such nonlinear interactions, studied in 12 normal adult ears over a wide range of test and suppressor click levels and inter-click intervals. The results differ from those generated by the model in a number of respects. Principally, maximum suppression is generally obtained for suppressors presented in advance of test clicks, rather than co-incident with the test clicks. The amount of advance depends systematically on the two click levels. The measured suppression can also exceed the theoretical maximum allowed by the model. It is concluded that the nonlinear temporal interactions measured do not simply reflect CEOAE I-O function non-linearity. They may, instead, arise from disturbance of the generator elements from their resting state prior to generation of the CEOAE. These results may also have general implications relating to cochlear responses to transient stimuli and indicate the potential of CEOAEs in probing aspects of cochlear mechanics. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Southampton, Inst Sound & Vibrat Res, Southampton SO17 1BJ, Hants, England. RP Kapadia, S (reprint author), Univ Southampton, Inst Sound & Vibrat Res, Southampton SO17 1BJ, Hants, England. CR Avan P, 1997, J ACOUST SOC AM, V101, P2771, DOI 10.1121/1.418564 AVAN P, 1993, HEARING RES, V70, P109, DOI 10.1016/0378-5955(93)90055-6 AVAN P, 1991, HEARING RES, V52, P99, DOI 10.1016/0378-5955(91)90191-B BERLIN CI, 1995, HEARING RES, V87, P96, DOI 10.1016/0378-5955(95)00082-F BONFILS P, 1988, AUDIOLOGY, V27, P27 CHEATHAM MA, 1994, HEARING RES, V75, P103, DOI 10.1016/0378-5955(94)90061-2 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E Cooper NP, 1996, AUDIT NEUROSCI, V2, P289 Cope Y., 1988, PAEDIATRIC AUDIOLOGY, P221 DEBOER E, 1991, PHYS REP, V203, P125, DOI 10.1016/0370-1573(91)90068-W Frank G, 1997, HEARING RES, V113, P57, DOI 10.1016/S0378-5955(97)00131-7 GOBSCH H, 1993, HEARING RES, V69, P176, DOI 10.1016/0378-5955(93)90105-A Hine JE, 1997, EAR HEARING, V18, P121, DOI 10.1097/00003446-199704000-00004 JOHNSEN NJ, 1988, SCAND AUDIOL, V17, P27, DOI 10.3109/01050398809042177 Kapadia S, 2000, HEARING RES, V146, P89, DOI 10.1016/S0378-5955(00)00102-7 Kemp D., 1997, OTOACOUSTIC EMISSION, P1 KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 Kevanishvili Z, 1996, SCAND AUDIOL, V25, P161, DOI 10.3109/01050399609047999 KULAWIEC JT, 1995, EAR HEARING, V16, P515 LinaGranade G, 1997, HEARING RES, V107, P83, DOI 10.1016/S0378-5955(97)00021-X LINAGRANADE G, 1995, HEARING RES, V87, P55, DOI 10.1016/0378-5955(95)00078-I Lukashkin AN, 1998, J ACOUST SOC AM, V103, P973, DOI 10.1121/1.421214 Patuzzi R., 1996, COCHLEA, P186 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 Prieve BA, 1996, J ACOUST SOC AM, V99, P3077, DOI 10.1121/1.414794 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 Recio A, 1998, J ACOUST SOC AM, V103, P1972, DOI 10.1121/1.421377 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O RUGGERO MA, 1994, AUDIOLOGY, V33, P131 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 SUTTON GJ, 1985, ACUSTICA, V58, P57 TAVARTKILADZE GA, 1994, BRIT J AUDIOL, V28, P193, DOI 10.3109/03005369409086568 Tavartkiladze GA, 1996, ACTA OTO-LARYNGOL, V116, P213, DOI 10.3109/00016489609137826 Ueda H, 1999, J ACOUST SOC AM, V105, P306, DOI 10.1121/1.424551 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WABLE J, 1994, HEARING RES, V80, P141, DOI 10.1016/0378-5955(94)90105-8 Withnell RH, 1998, J ACOUST SOC AM, V104, P344, DOI 10.1121/1.423243 XU L, 1994, HEARING RES, V74, P173 Yates GK, 1999, J ACOUST SOC AM, V105, P922, DOI 10.1121/1.426281 Yates GK, 1999, HEARING RES, V136, P49, DOI 10.1016/S0378-5955(99)00108-2 YATES GK, 1999, J ACOUST SOC AM, V105, P919 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 NR 43 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 101 EP 120 DI 10.1016/S0378-5955(00)00103-9 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500011 PM 10913888 ER PT J AU Surin, AM Reimann-Philipp, U Fechter, LD AF Surin, AM Reimann-Philipp, U Fechter, LD TI Simultaneous monitoring of slow cell motility and calcium signals of the guinea pig outer hair cells SO HEARING RESEARCH LA English DT Article DE calcium; outer hair cell; motility; Na+/Ca2+ exchange; guinea pig ID INTRACELLULAR CA-ATPASE; SENSORY CELLS; ION CHANNELS; RESPONSES; COCHLEA; ENTRY; DEPOLARIZATION; HOMEOSTASIS; INVOLVEMENT; MICROSCOPY AB 'Slow' motility (shape changes over seconds to minutes) of the mammalian cochlear outer hair cell (OHC) could play a protection role from intense sound pressure and is associated with elevation of the cytosolic free Ca2+ concentration ([Ca2+](i)). In the present work, a new approach was elaborated using fluorescent imaging for continuous monitoring of both [Ca2+](i) changes and slow motility of OHCs employing the Ca2+ fluorescent indicator Fura-2. Whole OHC fluorescence and that of cell segments were analyzed to discriminate between fluorescence changes caused by [Ca2+](i) rise and those related to change of the cell shape. The reliability of the method was examined by simultaneous monitoring of [Ca2+](i) and OHC length changes induced by change of buffer osmolarity or by increase of KCl concentration. The method revealed that the time course of [Ca2+](i) increase and rate of cell shortening often do not coincide. It was also observed that [Ca2+](i) increased in 70 mM KCl more slowly than the rate of KCl delivery to OHCs. The comparison of the time courses of [Ca2+](i) elevation, induced by increase of K+/Na+ ratio and by substitution of Na+ with N-methyl-D-glucamine(+), indicated that the relatively slow kinetics of [Ca2+](i) increase in the OHC is partially attributed to regulation of Ca2+ homeostasis by the Na+/Ca2+ exchanger. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Dept Pharmacol & Toxicol, Oklahoma City, OK 73190 USA. Univ Oklahoma, Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK 73190 USA. RP Surin, AM (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Dept Pharmacol & Toxicol, POB 26901, Oklahoma City, OK 73190 USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BLAUSTEIN MP, 1988, TRENDS NEUROSCI, V11, P438, DOI 10.1016/0166-2236(88)90195-6 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CATTERALL WA, 1995, ANNU REV BIOCHEM, V64, P493, DOI 10.1146/annurev.biochem.64.1.493 CECOLA RP, 1992, HEARING RES, V61, P65, DOI 10.1016/0378-5955(92)90037-N CHABBERT C, 1995, HEARING RES, V89, P101, DOI 10.1016/0378-5955(95)00126-2 CHEN C, 1995, HEARING RES, V86, P25, DOI 10.1016/0378-5955(95)00050-E Coling DE, 1998, HEARING RES, V115, P175, DOI 10.1016/S0378-5955(97)00194-9 CRIST JR, 1993, HEARING RES, V69, P194, DOI 10.1016/0378-5955(93)90107-C DING JP, 1991, HEARING RES, V56, P19, DOI 10.1016/0378-5955(91)90149-4 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1992, AM J OTOL, V13, P108 DULON D, 1990, J NEUROSCI, V10, P1388 Fettiplace R, 1999, ANNU REV PHYSIOL, V61, P809, DOI 10.1146/annurev.physiol.61.1.809 Frolenkov GI, 1998, MOL BIOL CELL, V9, P1961 Furuta H, 1998, HEARING RES, V123, P10, DOI 10.1016/S0378-5955(98)00091-4 GARCIA ML, 1990, J BIOL CHEM, V265, P3763 GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440 Hall JD, 1997, BIOPHYS J, V73, P1243 HARADA N, 1994, ACTA OTO-LARYNGOL, V114, P510, DOI 10.3109/00016489409126095 IKEDA K, 1992, PFLUG ARCH EUR J PHY, V420, P493, DOI 10.1007/BF00374624 IKEDA K, 1991, AM J PHYSIOL, V261, pC231 IKEDA K, 1993, HEARING RES, V66, P169, DOI 10.1016/0378-5955(93)90138-Q KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KEITH RA, 1992, J MOL NEUROSCI, V3, P147, DOI 10.1007/BF02919406 KLEYMAN TR, 1988, J MEMBRANE BIOL, V105, P1, DOI 10.1007/BF01871102 Liu Y, 1996, ACTA OTO-LARYNGOL, V116, P417, DOI 10.3109/00016489609137866 Liu Y, 1997, TOXICOL APPL PHARM, V142, P270, DOI 10.1006/taap.1996.8059 NAKAGAWA T, 1991, NEUROSCI LETT, V125, P81, DOI 10.1016/0304-3940(91)90136-H OHNISHI S, 1992, AM J PHYSIOL, V263, pC1088 Oshima T, 1996, AM J PHYSIOL-CELL PH, V271, pC944 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A Puschner B, 1997, HEARING RES, V110, P251, DOI 10.1016/S0378-5955(97)00086-5 SCHULTE BA, 1993, HEARING RES, V65, P262, DOI 10.1016/0378-5955(93)90219-Q Shuttleworth TJ, 1996, BIOCHEM J, V316, P819 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 Suckfull M, 1999, ACTA OTO-LARYNGOL, V119, P316 SUNOSE H, 1992, HEARING RES, V62, P237, DOI 10.1016/0378-5955(92)90190-X ULFENDAHL M, 1987, ACTA PHYSIOL SCAND, V130, P521, DOI 10.1111/j.1748-1716.1987.tb08171.x YAMASHITA T, 1990, ACTA OTO-LARYNGOL, V109, P256, DOI 10.3109/00016489009107441 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 Zine A, 1996, BRAIN RES, V721, P1, DOI 10.1016/0006-8993(95)01496-9 NR 47 TC 5 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 121 EP 133 DI 10.1016/S0378-5955(00)00105-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500012 PM 10913889 ER PT J AU Shoji, F Miller, AL Mitchell, A Yamasoba, T Altschuler, RA Miller, JM AF Shoji, F Miller, AL Mitchell, A Yamasoba, T Altschuler, RA Miller, JM TI Differential protective effects of neurotrophins in the attenuation of noise-induced hair cell loss SO HEARING RESEARCH LA English DT Article ID NERVE GROWTH-FACTOR; DEVELOPING INNER-EAR; INDUCED HEARING-LOSS; HEAT-SHOCK PROTEIN; RAT COCHLEA; GUINEA-PIG; AUDITORY NEURONS; MESSENGER-RNAS; EXPRESSION; DAMAGE AB The protective efficacy of neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF) at 1 or 10 mu g/ml was assessed in guinea pigs exposed to 4 kHz octave band noise at 115 dB SPL for 5 h. BDNF, NT-3 or artificial perilymph was delivered to the scala tympani via a mini-osmotic pump, beginning 4 days prior to noise exposure and continuing for 1 week post-exposure. Protection was assessed physiologically by the change in auditory brainstem response (ABR) threshold, and histologically by outer hair cell (OHC) survival. There was a statistically significant increase in OHC survival and a decrease in ABR threshold shift in animals receiving NT-3 at a concentration of 10 mu g/ml. In animals receiving 1 mu g/ml NT-3, there was a significant increase in OHC survival in the first row of OHC, but no significant change in ABR threshold, relative to control animals. In animals treated with BDNF, no significant functional or histological protection was observed. The protection afforded by NT-3 (10 mu g/ml) treatment was similar in magnitude to that reported previously with glial cell line-derived neurotrophic factor and suggests that several factors may be involved in the protective response. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Miller, JM (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR Baxter GT, 1997, J NEUROSCI, V17, P2683 Bhave SV, 1999, J NEUROSCI, V19, P3277 Brandoli C, 1998, J NEUROSCI, V18, P7953 DECHESNE CJ, 1992, HEARING RES, V59, P195, DOI 10.1016/0378-5955(92)90116-5 Dugan LL, 1997, P NATL ACAD SCI USA, V94, P4086, DOI 10.1073/pnas.94.8.4086 Estevez AG, 1998, J NEUROSCI, V18, P923 Fritzsch B, 1998, INT J DEV NEUROSCI, V16, P493, DOI 10.1016/S0736-5748(98)00043-4 Gabaizadeh R, 1997, MOL BRAIN RES, V50, P71, DOI 10.1016/S0169-328X(97)00173-3 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 Gestwa G, 1999, J COMP NEUROL, V414, P33, DOI 10.1002/(SICI)1096-9861(19991108)414:1<33::AID-CNE3>3.0.CO;2-M GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 Hu BH, 1997, HEARING RES, V113, P198, DOI 10.1016/S0378-5955(97)00143-3 Jacono AA, 1998, HEARING RES, V117, P31, DOI 10.1016/S0378-5955(97)00214-1 Keithley EM, 1998, NEUROREPORT, V9, P2183, DOI 10.1097/00001756-199807130-00007 Knipper M, 1996, CELL TISSUE RES, V283, P339, DOI 10.1007/s004410050545 LIM HH, 1993, HEARING RES, V69, P146 Malgrange B, 1998, NEUROCHEM RES, V23, P1133, DOI 10.1023/A:1020724506337 Mattson MP, 1996, RESTOR NEUROL NEUROS, V9, P191, DOI 10.3233/RNN-1996-9401 MITCHELL A, 1997, MIDW M ASS RES OT PE MYERS MW, 1992, LARYNGOSCOPE, V102, P981 NAKAO N, 1995, EXP NEUROL, V131, P1, DOI 10.1016/0014-4886(95)90002-0 NAM YJ, 2000, MIDW M ASS RES OT ST *NIDCD, 1999, NIH PUB Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P229, DOI 10.1159/000013846 Oppenheim R W, 1997, Adv Neurol, V72, P69 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 PIRVOLA U, 1994, HEARING RES, V75, P131, DOI 10.1016/0378-5955(94)90064-7 Prieskorn DM, 2000, HEARING RES, V140, P212, DOI 10.1016/S0378-5955(99)00193-8 Rong P, 1999, J NEUROCHEM, V72, P2294, DOI 10.1046/j.1471-4159.1999.0722294.x Ruan RS, 1999, NEUROREPORT, V10, P2067, DOI 10.1097/00001756-199907130-00014 SCHECTERSON LC, 1994, HEARING RES, V73, P92, DOI 10.1016/0378-5955(94)90286-0 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 Shoji F, 2000, HEARING RES, V142, P41, DOI 10.1016/S0378-5955(00)00007-1 SHOJI F, 1999, MIDW M ASS RES OT ST STOVER T, 2000, IN PRESS HEAR RES THOMPSON AM, 1992, OTOLARYNG HEAD NECK, V107, P769 Tremblay R, 1999, J NEUROCHEM, V72, P102, DOI 10.1046/j.1471-4159.1999.0720102.x Webb B, 1996, BRAIN RES, V729, P176, DOI 10.1016/0006-8993(96)00419-2 WHEELER EF, 1994, HEARING RES, V73, P46, DOI 10.1016/0378-5955(94)90281-X Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 Yamasoba T, 1998, BRAIN RES, V784, P82, DOI 10.1016/S0006-8993(97)01156-6 Yamasoba T, 1998, BRAIN RES, V804, P72, DOI 10.1016/S0006-8993(98)00660-X YAMASOBA T, 1998, ROLE NEUROTROPHIC FA Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C Yoshida N, 1999, J NEUROSCI, V19, P10116 NR 48 TC 53 Z9 64 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 134 EP 142 DI 10.1016/S0378-5955(00)00106-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500013 PM 10913890 ER PT J AU Cartee, LA van den Honert, C Finley, CC Miller, RL AF Cartee, LA van den Honert, C Finley, CC Miller, RL TI Evaluation of a model of the cochlear neural membrane. I. Physiological measurement of membrane characteristics in response to intrameatal electrical stimulation SO HEARING RESEARCH LA English DT Article DE auditory nerve; cat; cochlear implant; electrical stimulation; single-fiber recording ID AUDITORY-NERVE; FIBERS; RECORDINGS; PATTERNS; CELLS; CATS AB To understand the auditory neural response to electrical stimuli similar to those used in a cochlear implant, it will be necessary to understand the neural refraction and summation response kinetics. Evidence exists indicating that the cell soma may alter the auditory neural response kinetics and could be the site of conduction failure for excitation initiated on the peripheral process. There is, however, reason to believe that the excitation site in some healthy, type I neurons and in pathological, type III neurons is the central process of the cell. To characterize the neural response to activation at a controlled central process site, cat auditory neurons were stimulated with an intrameatal electrode, and the summation and refraction response kinetics were measured. This approach was used to: (1) characterize the behavior of the neural response to central process excitation; (2) make comparisons between intrameatal excitation at a known central site and scala tympani excitation at an unknown site; and (3) provide membrane characterization free from the possible alteration of membrane kinetics produced by the cell soma. The membrane kinetics measured using intrameatal stimulation differ from those recorded with scala tympani stimulation indicating that the mechanisms for scala tympani and intrameatal stimulation differ. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Res Triangle Inst, Ctr Auditory Prosthesis Res, Res Triangle Pk, NC 27709 USA. Cochlear Corp, Englewood, CO 80112 USA. Univ N Carolina, Sch Med, Chapel Hill, NC 27599 USA. Duke Univ, Med Ctr, Div Otolaryngol Head & Neck Surg, Durham, NC 27710 USA. RP Cartee, LA (reprint author), Res Triangle Inst, Ctr Auditory Prosthesis Res, POB 12194, Res Triangle Pk, NC 27709 USA. CR ADRIAN ED, 1928, BASIS SENSATION ACTI, P63 CARTEE LA, 1999, 22 MIDW RES M ASS RE Cartee LA, 2000, HEARING RES, V146, P153, DOI 10.1016/S0378-5955(00)00110-6 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 Dynes S.B.C., 1996, THESIS MIT GOLDSTEI.SS, 1974, BIOPHYS J, V14, P731 Goldstein SS, 1978, PHYSL PATHOBIOLOGY A, P227 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 Hill AV, 1936, PROC R SOC SER B-BIO, V119, P440, DOI 10.1098/rspb.1936.0015 JOYNER RW, 1978, BIOPHYS J, V22, P155 KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 KOHLLOFFEL LUE, 1974, ARCH OTORHINOLARYNGO, V209, P179 Lapicque L, 1907, J PHYSIOL-PARIS, V9, P622 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LUSTED HS, 1986, IEEE T BIO-MED ENG, V33, P800, DOI 10.1109/TBME.1986.325909 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 Plonsey R., 1988, BIOELECTRICITY QUANT RATTAY F, 1987, J THEOR BIOL, V125, P339, DOI 10.1016/S0022-5193(87)80066-8 ROBERTSON D, 1976, BRAIN RES, V109, P487, DOI 10.1016/0006-8993(76)90029-9 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 TYLER RS, 1991, COCHLEAR IMPLANTS PR, P58 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VELTINK PH, 1988, IEEE T BIO-MED ENG, V35, P69, DOI 10.1109/10.1338 Wilson B.S., 1993, COCHLEAR IMPLANTS AU, P35 NR 26 TC 34 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 143 EP 152 DI 10.1016/S0378-5955(00)00109-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500014 PM 10913891 ER PT J AU Cartee, LA AF Cartee, LA TI Evaluation of a model of the cochlear neural membrane. II: Comparison of model and physiological measures of membrane properties measured in response to intrameatal electrical stimulation SO HEARING RESEARCH LA English DT Article DE auditory neuron; cochlear implant; electrical stimulation; Hodgkin-Huxley equation; neural model ID MYELINATED NERVE-FIBERS; AUDITORY-NERVE; EXCITATION; CURRENTS; PATTERNS; CAT AB This study examines existing equation sets describing neural membrane ionic currents, such as the Hodgkin-Huxley (1952) equations, used to define the membrane currents in a numerical model of the auditory neuron and determines their adequacy for modeling the summation and refraction properties of auditory neurons in response to electrical stimulation. Specifically, the summation and refraction time constants of each equation set are compared to physiological measures of these time constants. Since previous studies have shown the cell body and peripheral process of the auditory neuron may influence the measurement of neural time constants, the physiological time constants used for comparison are those which were recorded using intrameatal electrical stimulation. The intrameatal electrode should stimulate the neuron in an area where the axon has a uniform geometry. Accordingly, the neural model used to duplicate this experiment was also of uniform geometry. Of the membrane equation sets evaluated, none was clearly superior for modeling both the refraction and summation properties of the auditory neuron, though some equation sets were capable of accurately modeling either the refraction or the summation properties, provided operating temperatures were adjusted to provide appropriate kinetics. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Res Triangle Inst, Ctr Auditory Prosthesis Res, Res Triangle Pk, NC 27709 USA. RP Cartee, LA (reprint author), Res Triangle Inst, Ctr Auditory Prosthesis Res, POB 12194, Res Triangle Pk, NC 27709 USA. CR ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 Cartee LA, 2000, HEARING RES, V146, P143, DOI 10.1016/S0378-5955(00)00109-X CARTEE LA, 1995, ANN BIOMED ENG S1, V23, pS80 CHIU SY, 1979, J PHYSIOL-LONDON, V292, P149 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 CRANK J, 1947, P CAMB PHILOS SOC, V43, P50 FITZHUGH R, 1962, BIOPHYS J, V2, P11 FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q FRIJNS JHM, 1994, IEEE T BIO-MED ENG, V41, P556, DOI 10.1109/10.293243 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 HORACKOVA M, 1968, PROC INT UNION PHYSIOL SCI, V7, P198 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MCNEAL DR, 1976, IEEE T BIO-MED ENG, V23, P329, DOI 10.1109/TBME.1976.324593 Morse RP, 1999, HEARING RES, V133, P107, DOI 10.1016/S0378-5955(99)00062-3 MOTZ H, 1986, NEUROSCIENCE, V18, P699, DOI 10.1016/0306-4522(86)90064-3 RATTAY F, 1993, IEEE T BIO-MED ENG, V40, P1201, DOI 10.1109/10.250575 Rattay F, 1990, ELECT NERVE STIMULAT Rattay F, 1997, ARTIF ORGANS, V21, P213 RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 SCHWARZ JR, 1987, PFLUG ARCH EUR J PHY, V409, P569, DOI 10.1007/BF00584655 Sweeney J. D., 1987, P 9 INT C IEEE EMBS, V9, P1577 TASAKI I, 1955, AM J PHYSIOL, V181, P639 TYLER RS, 1991, COCHLEAR IMPLANTS PR, P58 Wilson B.S., 1993, COCHLEAR IMPLANTS AU, P35 NR 26 TC 14 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 153 EP 166 DI 10.1016/S0378-5955(00)00110-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500015 PM 10913892 ER PT J AU Recio, A Rhode, WS AF Recio, A Rhode, WS TI Representation of vowel stimuli in the ventral cochlear nucleus of the chinchilla SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; speech; vowel ID SINGLE-FORMANT STIMULI; AUDITORY-NERVE FIBERS; BUSHY CELL AXONS; AMPLITUDE-MODULATION; RESPONSE PROPERTIES; DISCHARGE PATTERNS; STELLATE CELLS; CAT; STATE; NEURONS AB Responses of neurons in the ventral cochlear nucleus (VCN) of anesthetized chinchillas to six synthetic vowel sounds (\a\, \e\, \epsilon\, \i\, \o\ and \u\) were recorded at several intensity levels. Stimuli were synthesized with a fundamental frequency of 100 Hz or 181.6 Hz and had formant values at integer multiples of 100 Hz. Responses came from most neuron types in the VCN (with the exception of onset cells with an I-shaped pattern). Population studies, performed only on primary-like (PL) and chopper neurons, showed that PL neurons provide a better temporal representation than do chopper neurons. At the lowest level of stimulation, all neuron types provide an accurate rate-place representation of vowel spectra. With an increase in stimulus level, the rate-place representation of PL neurons becomes inferior to that of chopper neurons, either sustained choppers or transient choppers. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Wisconsin, Dept Physiol, Madison, WI 53706 USA. RP Recio, A (reprint author), Univ Wisconsin, Dept Physiol, 1300 Univ Ave, Madison, WI 53706 USA. EM recio@physiology.wisc.edu RI Recio-Spinoso, Alberto/F-7744-2013 CR BLACKBURN CC, 1990, J NEUROPHYSIOL, V63, P1191 BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 CANT NB, 1981, NEUROSCIENCE, V6, P2643, DOI 10.1016/0306-4522(81)90109-3 CANT NB, 1982, NEUROSCI LETT, V32, P241, DOI 10.1016/0304-3940(82)90300-7 CASPARY DM, 1977, EXP NEUROL, V54, P414, DOI 10.1016/0014-4886(77)90246-1 Delgutte B., 1997, HDB PHONETIC SCI, P507 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P866, DOI 10.1121/1.390596 EVANS EF, 1973, EXP BRAIN RES, V17, P402 Ferragamo MJ, 1998, J NEUROPHYSIOL, V79, P51 FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y FRISINA RD, 1990, HEARING RES, V44, P123, DOI 10.1016/0378-5955(90)90075-Z GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 Greenberg S, 1996, PRINCIPLES EXPT PHON, P362 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HOLLIEN H, 1972, J SPEECH HEAR RES, V15, P155 HOLLIEN H, 1969, LANG SPEECH, V12, P119 Keilson SE, 1997, J ACOUST SOC AM, V102, P1056, DOI 10.1121/1.419859 KLATT DH, 1980, J ACOUST SOC AM, V67, P971, DOI 10.1121/1.383940 LePrell G, 1996, AUDIT NEUROSCI, V2, P275 Lieberman P., 1977, SPEECH PHYSL ACOUSTI Lindblom B., 1986, EXPT PHONOLOGY, P13 Mardia K. V., 1972, STAT DIRECTIONAL DAT May BJ, 1998, J NEUROPHYSIOL, V79, P1755 MOLLER AR, 1976, ACTA PHYSIOL SCAND, V98, P157, DOI 10.1111/j.1748-1716.1976.tb00235.x MOREST DK, 1990, J COMP NEUROL, V300, P230, DOI 10.1002/cne.903000207 PALMER AR, 1986, J ACOUST SOC AM, V79, P100, DOI 10.1121/1.393633 PETERSON GE, 1952, J ACOUST SOC AM, V24, P175, DOI 10.1121/1.1906875 RALL TW, 1993, GOODMAN GILMANS PHAR, P359 RHODE WS, 1994, J NEUROPHYSIOL, V71, P493 RHODE WS, 1987, J NEUROPHYSIOL, V57, P414 Rhode WS, 1991, NEUROBIOLOGY HEARING, P47 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 Rhode WS, 1998, HEARING RES, V117, P39, DOI 10.1016/S0378-5955(98)00002-1 SACHS MB, 1979, J ACOUST SOC AM, V66, P470, DOI 10.1121/1.383098 SHOFNER WP, 1989, J ACOUST SOC AM, V86, P2172, DOI 10.1121/1.398478 SINEX DG, 1983, J ACOUST SOC AM, V73, P602, DOI 10.1121/1.389007 SMITH PH, 1989, J COMP NEUROL, V282, P595, DOI 10.1002/cne.902820410 SMITH PH, 1993, NATO ADV SCI INST SE, V239, P349 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 TEICH MC, 1989, IEEE T BIO-MED ENG, V36, P150, DOI 10.1109/10.16460 WANG XQ, 1993, J NEUROPHYSIOL, V70, P1054 WANG XQ, 1994, J NEUROPHYSIOL, V71, P59 WINTER IM, 1990, J ACOUST SOC AM, V88, P1433 WINTER IM, 1995, J NEUROPHYSIOL, V73, P141 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 NR 47 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 167 EP 184 DI 10.1016/S0378-5955(00)00111-8 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500016 PM 10913893 ER PT J AU Stuermer, IW Scheich, H AF Stuermer, IW Scheich, H TI Early unilateral auditory deprivation increases 2-deoxyglucose uptake in contralateral auditory cortex of juvenile Mongolian gerbils SO HEARING RESEARCH LA English DT Article DE conductive hearing loss; development; auditory cortex; sensory deprivation; plasticity; tonotopic map; 2-deoxyglucose ID CONDUCTIVE HEARING-LOSS; SINGLE-UNIT RESPONSES; INFERIOR COLLICULUS; MERIONES-UNGUICULATUS; COCHLEAR NUCLEUS; FUNCTIONAL-ORGANIZATION; BINAURAL INTERACTION; ORGAN DAMAGE; GUINEA-PIGS; BRAIN-STEM AB The effects of early onset, unilateral conductive hearing loss on tone-induced 2-deoxyglucose (2-DG) uptake in the auditory cortex of juvenile Mongolian gerbils (Meriones unguiculatus) were studied. Atresia of the left ear canal was induced at postnatal day 9 (P9) to achieve reversible auditory deprivation prior to onset of hearing (around P12). Atresia either persisted (ATR, n = 4) or the canal was opened 15 min before the 2-DG experiments (RE, n = 4) at P27. Control animals were either non-deprived (CON, n = 4), or their left ears were plugged acutely (PAX, it = 4). In PAX, 2-DG uptake in primary auditory cortex (AI) and anterior auditory field (AAF) was lower in right than in left AI and AAF. In contrast, in ATR and RE, uptake was significantly higher on the right side contralateral to the atresia. Hence, atresia during early development leads to plastic changes resulting in an interhemispheric imbalance of functional metabolism in favor of the auditory cortex contralateral to the manipulated ear. Distances between tone-induced 2-DG labeling in AI and AAF were increased in PAX, but smaller in ATR in the right compared to the left hemisphere, suggesting effects of atresia also on spatial relations in cortical tonotopic maps. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Leibniz Inst Neurobiol, D-39008 Magdeburg, Germany. RP Stuermer, IW (reprint author), Univ Gottingen, Dept Phoniatr & Pedaudiol, Robert Koch Str 40, D-37075 Gottingen, Germany. CR Aitkin L. M., 1990, AUDITORY CORTEX STRU BESS FH, 1984, PEDIATRICS, V74, P206 Brodmann K., 1909, VERGLEICHENDE LOKALI BROOKHOUSER PE, 1991, LARYNGOSCOPE, V101, P1264 BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T BRUGGE JF, 1985, HEARING RES, V20, P275, DOI 10.1016/0378-5955(85)90032-2 CAIRD D, 1991, J COMP PHYSIOL A, V168, P13, DOI 10.1007/BF00217100 Cant NB, 1998, SPR HDB AUD, V9, P315 CLAREY JC, 1992, SPRINGER HDB AUDITOR, V2, P232 CLAREY JC, 1991, MAMMALIAN AUDITORY P, V2, P232 CLOPTON BM, 1977, J NEUROPHYSIOL, V40, P1275 CLOPTON BM, 1978, EXP BRAIN RES, V32, P39 Clopton B M, 1980, Birth Defects Orig Artic Ser, V16, P271 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 FENG AS, 1980, BRAIN RES, V189, P530, DOI 10.1016/0006-8993(80)90112-2 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 GRAVEL JS, 1996, SPR HDB AUD, V7, P86 HARRISON RV, 1992, ADV BIOSCI, V83, P625 HEIL P, 1986, J COMP NEUROL, V252, P279, DOI 10.1002/cne.902520302 Heil P, 1995, AUDIT NEUROSCI, V1, P363 HENRY KR, 1995, HEARING RES, V90, P176, DOI 10.1016/0378-5955(95)00162-6 HUMES LE, 1980, AUDIOLOGY, V19, P508 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 KELLY JB, 1986, J COMP PSYCHOL, V100, P37 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 KNUDSEN EI, 1985, J NEUROSCI, V5, P3094 KRAUS N, 1987, HEARING RES, V27, P165, DOI 10.1016/0378-5955(87)90017-7 McAlpine D, 1997, J NEUROPHYSIOL, V78, P767 MCGINN MD, 1987, HEARING RES, V31, P235, DOI 10.1016/0378-5955(87)90193-6 MCGINN MD, 1982, THESIS U MICROFILMS MCGINN MD, 1984, ACTA OTO-LARYNGOL, V97, P297, DOI 10.3109/00016488409130992 Moore DR, 1999, J NEUROSCI, V19, P8704 MOORE DR, 1988, J COMP NEUROL, V269, P342, DOI 10.1002/cne.902690303 MOORE DR, 1998, PSYCHOPHYSICAL PHYSL, P412 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MOORE DR, 1994, J COMP NEUROL, V339, P301, DOI 10.1002/cne.903390209 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 NAGER GT, 1993, PATHOLOGY EAR TEMP0O, P1341 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 NUDO RJ, 1984, CONTRIBUTIONS SENSOR, V18, P79 OLTHOFF A, 1999, 27 GOETT NEUR C, V2, P305 OTHOFF A, 1999, 27 GOETT NEUR C THIE, V2, P305 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 Rajan R, 1998, NAT NEUROSCI, V1, P138, DOI 10.1038/388 Rajan R, 1998, AUDIOL NEURO-OTOL, V3, P123, DOI 10.1159/000013786 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 Richter K, 1999, BRAIN RES, V831, P184, DOI 10.1016/S0006-8993(99)01440-7 RUSSELL FA, 1995, J COMP NEUROL, V352, P607, DOI 10.1002/cne.903520409 RYAN AF, 1992, DEV AUDITORY VESTIBU, V2, P243 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SALVI RJ, 1996, AUDITORY SYSTEM PLAS SCHEICH H, 1993, EUR J NEUROSCI, V5, P898, DOI 10.1111/j.1460-9568.1993.tb00941.x SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x Stuermer I. W., 1994, Society for Neuroscience Abstracts, V20, P323 Stuermer I. W., 1995, Society for Neuroscience Abstracts, V21, P1177 Tharpe AM, 1999, PEDIATR CLIN N AM, V46, P65, DOI 10.1016/S0031-3955(05)70081-X THARPE AM, 1991, INT J PEDIATR OTORHI, V21, P41, DOI 10.1016/0165-5876(91)90058-J THOMAS H, 1993, EUR J NEUROSCI, V5, P882, DOI 10.1111/j.1460-9568.1993.tb00940.x Tucci DL, 1999, LARYNGOSCOPE, V109, P1359, DOI 10.1097/00005537-199909000-00001 Tyler R. S., 1986, FREQUENCY SELECTIVIT, P309 Watier-Launey C, 1998, Ann Otolaryngol Chir Cervicofac, V115, P149 WEBSTER DB, 1986, ASS RES OT ABS, P178 WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 NR 67 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 2000 VL 146 IS 1-2 BP 185 EP 199 DI 10.1016/S0378-5955(00)00113-1 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 339YY UT WOS:000088506500017 PM 10913894 ER PT J AU Fontilla, MF Peterson, EH AF Fontilla, MF Peterson, EH TI Kinocilia heights on utricular hair cells SO HEARING RESEARCH LA English DT Article DE hair cell; kinocilia; otolith organ; utricle; turtle; immunochemistry; mechanics ID MECHANOELECTRICAL TRANSDUCTION; MACULA; SUPRASTRUCTURE; ADAPTATION; FROG; EAR AB Kinocilium height is a critical determinant of any hair cell's response to head movement, but accurate measurements of kinocilia heights have been difficult to achieve. We have developed a method for measuring kinocilia heights that combines immunochemical staining with three-dimensional morphometry, and we have used this method to measure kinocilia in the utricle of a turtle, Pseudemys scripta. Our results suggest that kinocilium height varies with position on the utricular epithelium and that kinocilia in the striola are significantly shorter than kinocilia in other regions of the utricle. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Ohio Univ, Neurosci Program, Athens, OH 45701 USA. Ohio Univ, Dept Biol Sci, Athens, OH 45701 USA. RP Peterson, EH (reprint author), Ohio Univ, Neurosci Program, Athens, OH 45701 USA. CR ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 BRICHTA AM, 1994, J COMP NEUROL, V344, P481, DOI 10.1002/cne.903440402 Cleveland W, 1993, VISUALIZING DATA COTTON JR, 1998, ASS RES OT ABSTR, V21, P144 Cotton J. R., 1996, Society for Neuroscience Abstracts, V22, P1064 COTTON JR, 2000, ASS RES OT ABSTR, V23, P170 EATOCK RA, 1987, J NEUROSCI, V7, P2821 ERNSTSON S, 1986, ACTA OTO-LARYNGOL, V101, P395, DOI 10.3109/00016488609108624 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 FONTILLA MF, 1999, ASS RES OT ABSTR, V22, P191 Gillespie PG, 1997, NEURON, V19, P955, DOI 10.1016/S0896-6273(00)80387-6 Haddon C, 1996, J COMP NEUROL, V365, P113, DOI 10.1002/(SICI)1096-9861(19960129)365:1<113::AID-CNE9>3.0.CO;2-6 HILLMAN DE, 1969, BRAIN RES, V13, P407, DOI 10.1016/0006-8993(69)90301-1 HILLMAN DE, 1971, SCIENCE, V174, P416, DOI 10.1126/science.174.4007.416 Hounsgaard J., 1990, PREPARATIONS VERTEBR, P155 HUDSPETH AJ, 1983, ANNU REV NEUROSCI, V6, P187, DOI 10.1146/annurev.ne.06.030183.001155 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 Hunter-Duvar IM, 1984, ULTRASTRUCTURAL ATLA, P211 JORGENSEN JM, 1988, ACTA ZOOL-STOCKHOLM, V69, P169 JORGENSEN JM, 1989, J MORPHOL, V201, P187, DOI 10.1002/jmor.1052010208 JORGENSEN J M, 1974, Acta Zoologica (Stockholm), V55, P289 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A KELLEY MW, 1992, HEARING RES, V59, P108 Lewis ER, 1985, VERTEBRATE INNER EAR, P66 Lim DJ, 1979, SCANNING ELECTRON MI, V3, P929 OGATA Y, 1995, HEARING RES, V86, P125, DOI 10.1016/0378-5955(95)00063-A ROSS MD, 1987, ACTA OTO-LARYNGOL, V104, P56, DOI 10.3109/00016488709109047 ROSS MD, 1987, ACTA OTO-LARYNGOL, V103, P56, DOI 10.3109/00016488709134698 RUSCH A, 1990, HEARING RES, V48, P247, DOI 10.1016/0378-5955(90)90065-W SPOENDLIN HH, 1964, Z ZELLFORSCH MIK ANA, V62, P701, DOI 10.1007/BF00341855 NR 30 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 8 EP 16 DI 10.1016/S0378-5955(00)00068-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100002 PM 10867272 ER PT J AU Brown, DK Bowman, DM Kimberley, BP AF Brown, DK Bowman, DM Kimberley, BP TI The effects of maturation and stimulus parameters on the optimal f(2)/f(1) ratio of the 2f(1)-f(2) distortion product otoacoustic emission in neonates SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Annual Meeting of the Canadian-Acoustical-Association CY 1996 CL CALGARY, CANADA SP Canadian Acoust Assoc DE distortion product otoacoustic emission; optimal f(2)/f(1) ratio; human; development ID ACOUSTIC DISTORTION; FREQUENCY RATIO; HUMAN ADULTS; AMPLITUDE; COCHLEA; TONES; EAR AB Distortion product otoacoustic emission (DPOAE) measurements are becoming popular in the clinical realm because they have been shown to reflect cochlear function. The primary tones used to evoke the DPOAE are important in determining the amplitude of the emission recorded in the ear canal. This study examined the ratio of the primaries necessary to determine the maximum amplitude emission asa function of development, stimulus level and frequency. Optimum f(2)/f(1) ratios were measured utilizing the f(1)-sweep technique from 105 neonates between 30-42 weeks conceptional age (CA) and 40 adults. No significant difference for optimum ratio was shown between the neonatal and the adult groups. Primary tone frequency had a significant effect on optimum ratio for both neonates and adults. Low f(2) frequencies (<4 kHz) were associated with higher optimum ratios than high f(2) frequencies (>4 kHz). The adult group was used to investigate the effect of stimulus level on the optimum f(2)/f(1) ratio for f(2) frequencies from 1.7 to 10 kHz. Regression analysis showed significant differences across levels of the primaries at all frequencies except for f(2) = 3.4 and 7.0 kHz. These differences in f(2)/f(1) ratio across stimulus frequency and level may be attributed to the change in the shape of the excitation profiles along the basilar membrane. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Surg, Calgary, AB, Canada. Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Physiol & Biophys, Calgary, AB, Canada. RP Brown, DK (reprint author), Univ Calgary, Dept Surg, Calgary, AB, Canada. CR Abdala C, 1996, HEARING RES, V98, P38, DOI 10.1016/0378-5955(96)00056-1 Abdala C, 1996, J ACOUST SOC AM, V100, P3726, DOI 10.1121/1.417234 BONFILS P, 1991, ARCH OTOLARYNGOL, V117, P1167 Bowman DM, 2000, HEARING RES, V142, P1, DOI 10.1016/S0378-5955(99)00212-9 BROWN AM, 1990, LECT NOTES BIOMATH, V87, P164 BROWN AM, 1994, BRIT J AUDIOL, V28, P273, DOI 10.3109/03005369409086577 BROWN AM, 1995, AUDIT NEUROSCI, V1, P169 BROWN DK, 1996, ABSTR ASS RES OT, V19, P180 *CUBEDIS, 1992, US MAN CUBEDIS DIST Eggermont JJ, 1996, EAR HEARING, V17, P386, DOI 10.1097/00003446-199610000-00004 EVANS EF, 1975, AUDIOLOGY, V14, P419 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 Kemp D. T., 1983, MECH HEARING, P75 Lasky RE, 1998, J ACOUST SOC AM, V103, P981, DOI 10.1121/1.421215 NIELSEN LH, 1993, SCAND AUDIOL, V22, P159, DOI 10.3109/01050399309047462 PROBST R, 1990, ADV AUDIOL, V7, P117 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P615, DOI 10.1121/1.1913152 Wilson J., 1980, Proceedings of the Eighth Annual Canadian Conference on Information Science NR 22 TC 11 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 17 EP 24 DI 10.1016/S0378-5955(00)00064-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100003 PM 10867273 ER PT J AU Kolston, PJ AF Kolston, PJ TI The importance of phase data and model dimensionality to cochlear mechanics SO HEARING RESEARCH LA English DT Article DE cochlear mechanics; cochlear amplifier; phase response; three-dimensional model; energy injection; impedance reduction ID BASILAR-MEMBRANE MECHANICS; MOSSBAUER TECHNIQUE; CHINCHILLA COCHLEA; IN-VIVO; AMPLIFIER; BASE; CAT AB The vulnerability of the mammalian cochlear amplifier to surgical trauma hinders observations of its behaviour in vivo. This produces a greater need for realistic models to aid the interpretation of the experimental observations. The emphasis in most modelling studies has been to simulate the gain of the response of the basilar membrane. This paper argues that matching the phase behaviour of the response should be given at least equal importance. When it is, many of the models used to justify hypotheses regarding the operation of the cochlear amplifier cannot simulate the response even of the dead cochlea. This discrepancy is due to oversimplification of the mechanics of the cochlear fluids. It is argued that three-dimensional fluid behaviour should be regarded as a bare minimum in any quantitative description of cochlear mechanics. Furthermore, it is shown that a three-dimensional model is consistent with experimental data from a healthy cochlea only when the main effect of the cochlear amplifier is to inject mechanical energy into the basilar membrane. The injection of mechanical energy is fundamentally different to modifying the stiffness of the basilar membrane. This means that existing models which possess cochlear amplifiers that effect large changes on the stiffness of the basilar membrane may not be accurate representations of the real organ. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Keele, MacKay Inst Commun & Neurosci, Keele ST5 5BG, Staffs, England. RP Kolston, PJ (reprint author), Univ Keele, MacKay Inst Commun & Neurosci, Keele ST5 5BG, Staffs, England. CR BRASS D, 1993, J ACOUST SOC AM, V93, P1502, DOI 10.1121/1.406808 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CODY AR, 1992, HEARING RES, V62, P166, DOI 10.1016/0378-5955(92)90182-M COOPER NP, 1992, HEARING RES, V63, P163, DOI 10.1016/0378-5955(92)90083-Y DEBOER E, 1995, J ACOUST SOC AM, V98, P1400, DOI 10.1121/1.414407 De Boer E, 1996, SPRINGER HDB AUDITOR, P258 DEBOER E, 1983, J ACOUST SOC AM, V73, P567, DOI 10.1121/1.389002 deBoer E, 1997, J ACOUST SOC AM, V101, P2148, DOI 10.1121/1.418201 DIEPENDAAL RJ, 1987, J ACOUST SOC AM, V82, P917, DOI 10.1121/1.395290 GEISLER CD, 1995, HEARING RES, V86, P132, DOI 10.1016/0378-5955(95)00064-B Greenwood DD, 1996, HEARING RES, V94, P157, DOI 10.1016/0378-5955(95)00229-4 HUBBARD A, 1993, SCIENCE, V259, P68, DOI 10.1126/science.8418496 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 Kolston PJ, 1999, P NATL ACAD SCI USA, V96, P3676, DOI 10.1073/pnas.96.7.3676 KOLSTON PJ, 1990, J ACOUST SOC AM, V88, P1794, DOI 10.1121/1.400200 KOLSTON PJ, 1989, J ACOUST SOC AM, V86, P133, DOI 10.1121/1.398332 KOLSTON PJ, 1995, TRENDS NEUROSCI, V18, P427, DOI 10.1016/0166-2236(95)90091-8 MAMMANO F, 1993, J ACOUST SOC AM, V93, P3320, DOI 10.1121/1.405716 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 Rhode WS, 1996, AUDIT NEUROSCI, V3, P101 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 ZWEIG G, 1991, J ACOUST SOC AM, V89, P1229, DOI 10.1121/1.400653 NR 25 TC 23 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 25 EP 36 DI 10.1016/S0378-5955(00)00067-8 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100004 PM 10867274 ER PT J AU Saito, H Miller, JM Altschuler, RA AF Saito, H Miller, JM Altschuler, RA TI Cochleotopic fos immunoreactivity in cochlea and cochlear nuclei evoked by bipolar cochlear electrical stimulation SO HEARING RESEARCH LA English DT Article DE Fos-like immunoreactivity; tonotopy; spiral ganglion; cochlear nucleus; electrical stimulation; cochlear prosthesis ID AUDITORY BRAIN-STEM; SPIRAL GANGLION; RAT; RESPONSES; CAT; CELLS; NERVE; CONNECTIONS; IMPLANTS; NEURONS AB Fos-like immunoreactivity evoked by basal, second or apical turn bipolar intracochlear electrical stimulation was evaluated in the spiral ganglion and cochlear nuclei. At stimulation levels of six times the electrically evoked auditory brain stem response thresholds, immunoreactive neurons were observed at appropriate discrete cochleotopic regions relative to stimulation site. The number of neurons increased with stimulus level and closely correlated to wave I amplitude. At 10 times thresholds, some spread in fos-like immunoreactivity to adjacent cochlear turns was found. However, fos-like immunoreactivity at this high level of stimulation still clearly showed a differential distribution in density of expression. These results indicated that the restricted topographic distribution of activity evoked by high levels of electrical stimulation is initiated at first order primary neurons of the system. For the profoundly deaf with cochlear implants, this indicates that place (channel) information can be maintained in the spiral ganglion and central nervous system even at very high levels of electrical stimulation. Together with our previous studies, these results indicate that fos provides a marker which can be used for evaluation of extent and pattern of cellular activation throughout the central auditory pathways, including activation of auditory nerve cells. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Tokyo Med Coll, Dept Otolaryngol, Tokyo 160, Japan. RP Miller, JM (reprint author), Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR ADAMS JC, 1995, J COMP NEUROL, V361, P645, DOI 10.1002/cne.903610408 ASMUS SE, 1994, J NEUROBIOL, V25, P156, DOI 10.1002/neu.480250207 BOURK TR, 1981, HEARING RES, V4, P215, DOI 10.1016/0378-5955(81)90008-3 BROWN CJ, 1994, EAR HEARING, V15, P168, DOI 10.1097/00003446-199404000-00006 BROWN MC, 1995, J COMP NEUROL, V357, P85, DOI 10.1002/cne.903570109 CANT NB, 1982, J COMP NEUROL, V212, P313, DOI 10.1002/cne.902120308 EDDINGTON DK, 1983, ANN NY ACAD SCI, V405, P241, DOI 10.1111/j.1749-6632.1983.tb31637.x EHRET G, 1991, BRAIN RES, V567, P350, DOI 10.1016/0006-8993(91)90819-H Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FRIAUF E, 1992, EUR J NEUROSCI, V4, P798, DOI 10.1111/j.1460-9568.1992.tb00190.x HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 LEAKE PA, 1989, J COMP NEUROL, V281, P612, DOI 10.1002/cne.902810410 MERZENIC.MM, 1973, ANN OTO RHINOL LARYN, V82, P486 Miller CA, 1995, HEARING RES, V92, P85, DOI 10.1016/0378-5955(95)00204-9 MOORE JK, 1986, NEUROBIOLOGY HEARING, P283 Moxon E.C., 1971, THESIS MIT CAMBRIDGE NAGASE S, IN PRESS HEAR RES OLEARY SJ, 1994, HEARING RES, V74, P181, DOI 10.1016/0378-5955(94)90186-4 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 ROUILLER EM, 1984, J COMP NEUROL, V225, P167, DOI 10.1002/cne.902250203 ROUILLER EM, 1992, NEUROSCI LETT, V144, P19, DOI 10.1016/0304-3940(92)90706-D RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L Saito H, 1999, NEUROSCIENCE, V91, P139, DOI 10.1016/S0306-4522(98)00581-8 Sando I, 1965, ACTA OTOLARYNG STOCK, V59, P417, DOI 10.3109/00016486509124577 SATO K, 1992, NEUROSCI LETT, V142, P48, DOI 10.1016/0304-3940(92)90617-G Sato K, 1993, Acta Otolaryngol Suppl, V500, P18 SHANNON RV, 1985, HEARING RES, V18, P135, DOI 10.1016/0378-5955(85)90005-X SHANNON RV, 1993, J ACOUST SOC AM, V93, P1651, DOI 10.1121/1.406799 SHARP FR, 1991, J NEUROSCI, V11, P2321 SHOFNER WP, 1987, HEARING RES, V29, P45, DOI 10.1016/0378-5955(87)90204-8 SHOFNER WP, 1985, J NEUROPHYSIOL, V54, P917 SHORE SE, 1992, HEARING RES, V62, P16, DOI 10.1016/0378-5955(92)90199-W SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S SPELMAN FA, 1987, P IEEE EMBS, V4, P191 SPELMAN FA, 1982, ANN OTO RHINOL LARYN, V91, P3 Spelman F A, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P131 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 Vischer MW, 1995, ORL J OTO-RHINO-LARY, V57, P305 VISCHER MW, 1994, NEUROSCI RES, V19, P175, DOI 10.1016/0168-0102(94)90141-4 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 WOUTERLOOD FG, 1984, J NEUROCYTOL, V13, P639, DOI 10.1007/BF01148083 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 Zhang JS, 1996, BRAIN RES BULL, V39, P75, DOI 10.1016/0361-9230(95)02053-5 NR 48 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 37 EP 51 DI 10.1016/S0378-5955(00)00070-8 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100005 PM 10867275 ER PT J AU Morand, N Khalfa, S Ravazzani, P Tognola, G Grandori, F Durrant, JD Collet, L Veuillet, E AF Morand, N Khalfa, S Ravazzani, P Tognola, G Grandori, F Durrant, JD Collet, L Veuillet, E TI Frequency and temporal analysis of contralateral acoustic stimulation on evoked otoacoustic emissions in humans SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; wavelet ID COCHLEAR MICROMECHANICAL PROPERTIES; OLIVOCOCHLEAR BUNDLE; STIMULUS VARIABLES; WAVELET ANALYSIS; EFFERENT SYSTEM; SUPPRESSION; DEPENDENCE; SOUND; EAR; RESPONSES AB Previous studies have shown that the effect of contralateral acoustic stimulation (CAS) on ipsilateral evoked otoacoustic emissions (EOAE) depends somewhat upon the spectrum of the eliciting stimulus. The latency of the EOAE, however, is itself frequency-dependent. Consequently, two general ways of analyzing the effects of CAS may be considered: by frequency band or by temporal segment. In this study, we analyzed the effects of CAS both ways in the same subjects, essentially simultaneously. The frequency analysis of the EOAE derived from the wavelet transform (WT). The WT is known to provide a robust approach to the analysis of non-stationary signals and was anticipated to avoid possible time-frequency confounds of the cochlear mechanical system. For comparison, a more basic analysis - using a temporal moving window - was employed. The results largely support earlier findings and confirm that in humans the greatest suppression of EOAEs by CAS is obtained for lower frequency and/or longer latency EOAE components. Despite expectations for the WT analysis, the more basic, temporal, analysis tended to yield the clearer results. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hop Edouard Herriot, Lab Neurosci & Syst Sensoriels, CNRS, UMR 5020, F-69003 Lyon, France. Univ Lyon 1, F-69365 Lyon, France. CNR, Ctr Biomed Engn, I-20133 Milan, Italy. Polytech Milan, Dept Biomed Engn, Milan, Italy. Univ Pittsburgh, Dept Commun Sci & Disorders, Pittsburgh, PA USA. Univ Pittsburgh, Dept Otolaryngol, Pittsburgh, PA 15260 USA. RP Morand, N (reprint author), Hop Edouard Herriot, Lab Neurosci & Syst Sensoriels, CNRS, UMR 5020, 3 Pl Arsonval,Pavillon U, F-69003 Lyon, France. RI Tognola, Gabriella/B-9025-2015; Ravazzani, Paolo/B-9139-2015 OI Ravazzani, Paolo/0000-0003-0282-3329 CR BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1992, AUDIOLOGY, V31, P1 DAUBECHIES I, 1990, IEEE T INFORM THEORY, V36, P961, DOI 10.1109/18.57199 Fex J., 1962, ACTA PHYSL SCAN S189, V55, P2 FOLSOM RL, 1985, ACTA OTOLARYNGOL, V103, P262 Giraud AL, 1995, BRAIN RES, V705, P15, DOI 10.1016/0006-8993(95)01091-2 GRANDORI F, 1993, BRIT J AUDIOL, V27, P97, DOI 10.3109/03005369309077898 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 Maison S, 1997, J NEUROPHYSIOL, V77, P1759 MALLAT SG, 1989, IEEE T PATTERN ANAL, V11, P674, DOI 10.1109/34.192463 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 Ravazzani P, 1998, IEEE T BIO-MED ENG, V45, P1089, DOI 10.1109/10.709551 RAVAZZANI P, 1997, ELECTROEN CLIN NEURO, V103, P71, DOI 10.1016/S0013-4694(97)88231-8 Tognola G, 1998, IEEE T BIO-MED ENG, V45, P686, DOI 10.1109/10.678603 Tognola G, 1997, HEARING RES, V106, P112, DOI 10.1016/S0378-5955(97)00007-5 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WARREN EH, 1989, HEARING RES, V37, P105, DOI 10.1016/0378-5955(89)90033-6 WILLIAMS EA, 1993, SCAND AUDIOL, V22, P197, DOI 10.3109/01050399309047469 WILLIAMS EA, 1994, ACTA OTO-LARYNGOL, V114, P121, DOI 10.3109/00016489409126029 WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 WIT HP, 1994, HEARING RES, V73, P141, DOI 10.1016/0378-5955(94)90228-3 NR 27 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 52 EP 58 DI 10.1016/S0378-5955(00)00069-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100006 PM 10867276 ER PT J AU Tabuchi, K Tsuji, S Hara, A Kusakari, J AF Tabuchi, K Tsuji, S Hara, A Kusakari, J TI Effect of calmodulin antagonists on the compound action potential of the cochlea SO HEARING RESEARCH LA English DT Article DE cochlea; compound action potential; ischemia; calmodulin antagonist ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; CALCIUM-BINDING PROTEINS; BRAIN; TRANSDUCTION; NIMODIPINE; MOTILITY; RATS AB This study aimed to evaluate the effect of calmodulin antagonists on the threshold of the compound action potential (CAP) and the functional recovery of the cochlea after transient ischemia. When trifluoperazine and W-7 were administered to albino guinea pigs with perilymphatic perfusion, these drugs did not significantly affect the CAP thresholds. Transient cochlear ischemia of 30-min duration was obtained via a skull base approach. Although trifluoperazine significantly ameliorated the post-ischemic CAP threshold shifts 4 h after the onset of reperfusion, 1 to 50 mu M W-7 did not affect the CAP threshold shifts. These results suggest that the action antagonizing calmodulin has no effect on the CAP threshold, while the role that calmodulin plays in cochlear ischemia-reperfusion injury still remains unclear. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. RP Kusakari, J (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR Bobbin R.P., 1974, ACTA OTO-LARYNGOL, V77, P55 BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BREDT DS, 1990, P NATL ACAD SCI USA, V87, P682, DOI 10.1073/pnas.87.2.682 CLAPHAM DE, 1995, CELL, V80, P259, DOI 10.1016/0092-8674(95)90408-5 Coling DE, 1998, HEARING RES, V115, P175, DOI 10.1016/S0378-5955(97)00194-9 DULON D, 1990, J NEUROSCI, V10, P1388 Imamura SI, 1996, ANAT EMBRYOL, V194, P407 Jaramillo F, 1995, NEURON, V15, P1227, DOI 10.1016/0896-6273(95)90003-9 JOHNSON JD, 1983, BIOCHEM J, V211, P473 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 Kuroda S, 1997, STROKE, V28, P2539 Kusakari J, 1981, Auris Nasus Larynx, V8, P55 LAHTI RA, 1993, EUR J PHARMACOL, V236, P483, DOI 10.1016/0014-2999(93)90488-4 Pack AK, 1995, HEARING RES, V91, P119 Puschner B, 1997, HEARING RES, V110, P251, DOI 10.1016/S0378-5955(97)00086-5 TRZECIAK HI, 1995, EUR ARCH PSY CLIN N, V245, P179, DOI 10.1007/BF02193092 UEMATSU D, 1991, NEUROLOGY, V41, P88 Walker RG, 1996, P NATL ACAD SCI USA, V93, P2203, DOI 10.1073/pnas.93.5.2203 WANG KKW, 1989, BIOCHEM J, V262, P693 Yamoah EN, 1998, J NEUROSCI, V18, P610 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 21 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 59 EP 64 DI 10.1016/S0378-5955(00)00071-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100007 PM 10867277 ER PT J AU Pickles, JO van Heumen, WRA AF Pickles, JO van Heumen, WRA TI Lateral interactions account for the pattern of the hair cell array in the chick basilar papilla SO HEARING RESEARCH LA English DT Article DE hair cell; development; lateral inhibition; notch; delta; chick ID AVIAN INNER-EAR; RETINOIC ACID; NOTCH; EXPRESSION; DELTA; ORGAN; DIFFERENTIATION; REGENERATION; PROGENITOR; COCHLEA AB It has been suggested that lateral interactions set up the array of hair cells and supporting cells in the chick basilar papilla. The presence of a hair cell would inhibit adjacent cells from becoming hair cells, and promote the formation of supporting cells. Models of cell specification were tested, starting with a closely packed array of multipotent progenitor cells. Lateral interactions, in which emerging hair cells promoted a supporting cell phenotype in adjacent cells, and in which emerging supporting cells promoted a hair cell phenotype in adjacent cells, produced an array of cells similar to that observed experimentally in the distal and central parts of the basilar papilla. In these areas, the ratio of supporting cells to hair cells is very close to 2:1, each hair cell on average being surrounded by six supporting cells, and each supporting cell being surrounded by three hair cells and three supporting cells. Identical patterns of hair and supporting cells could be produced by models in which either of the lateral inhibitory factors was replaced by a diffusive factor, i.e. a factor which acts on all cells in the model irrespective of position. The agreement of the model with observed cell ratios supports the view that the fate of both hair cells and supporting cells in the chick basilar papilla is a product of cell interactions within the papilla. It is possible that one factor, that provides contact lateral inhibition and promotes the formation of supporting cells, is the Notch/Delta system. It is possible that the other factor is retinoic acid, a diffusive factor that promotes the formation of hair cells. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. RP Pickles, JO (reprint author), Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. CR Adam J, 1998, DEVELOPMENT, V125, P4645 Collier JR, 1996, J THEOR BIOL, V183, P429, DOI 10.1006/jtbi.1996.0233 CORWIN JT, 1991, CIBA F SYMP, V160, P103 COTANCHE DA, 1984, DEV BRAIN RES, V16, P181, DOI 10.1016/0165-3806(84)90024-5 Fekete DM, 1998, J NEUROSCI, V18, P7811 Goodyear R, 1997, J NEUROSCI, V17, P6289 GOODYEAR R, 1995, J COMP NEUROL, V351, P81, DOI 10.1002/cne.903510108 Haddon C, 1998, DEVELOPMENT, V125, P4637 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 KELLEY MW, 1993, DEVELOPMENT, V119, P1041 Lanford PJ, 1999, NAT GENET, V21, P289 Lewis AK, 1998, MECH DEVELOP, V78, P159, DOI 10.1016/S0925-4773(98)00165-8 Morrison A, 1999, MECH DEVELOP, V84, P169, DOI 10.1016/S0925-4773(99)00066-0 Raz Y, 1999, DEV BIOL, V213, P180, DOI 10.1006/dbio.1999.9364 Riley BB, 1999, DEVELOPMENT, V126, P5669 Stone JS, 1999, DEVELOPMENT, V126, P961 NR 16 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 65 EP 74 DI 10.1016/S0378-5955(00)00073-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100008 PM 10867278 ER PT J AU Iwagaki, T Suzuki, T Nakashima, T AF Iwagaki, T Suzuki, T Nakashima, T TI Development and regression of cochlear blood vessels in fetal and newborn mice SO HEARING RESEARCH LA English DT Article DE cochlear vasculature; development; mouse ID CELL-DEATH; INNER-EAR; MOUSE; RAT; ANATOMY AB Various strains of mice have been used for hearing research, but there have been few reports regarding the cochlear vasculature in mice. In this study, the development of the cochlear vasculature was investigated in C57BL/6 mice from day 15 of gestation to day 15 after birth, and mature vessels were also observed in 3-month-old mice. Both India ink injection and the resin casting method were used. On gestational day 17, spiral vessels of the basilar membrane were developing and were elaborating communicating branches that ran toward the external wall and the spiral lamina. On day 18, the spiral vessels showed the largest diameter of all vessels in the cochlea, but these vessels subsequently regressed and finally disappeared by day 14 after birth. The external wall vessels formed a single-layer capillary network at birth and subsequently divided into two layers, which became the vessels of the stria vascularis and the spiral ligament vessels. This process occurred progressively from the basal turn toward the apical turn between days 5 and 8 after birth. A general tendency for the cochlear vasculature to mature from the basal turn towards the apex was observed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Nagoya Univ, Sch Med, Dept Otorhinolaryngol, Showa Ku, Nagoya, Aichi 4668550, Japan. RP Iwagaki, T (reprint author), Nagoya Univ, Sch Med, Dept Otorhinolaryngol, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan. RI Nakashima, Tsutomu/B-8259-2012 OI Nakashima, Tsutomu/0000-0003-3930-9120 CR Ando M, 1998, HEARING RES, V123, P148, DOI 10.1016/S0378-5955(98)00109-9 ANNIKO M, 1981, ANN OTO RHINOL LARYN, V90, P25 Axelsson A., 1968, ACTA OTOLARYNGOL S S, V243, P5 AXELSSON A, 1986, ACTA OTO-LARYNGOL, V101, P75, DOI 10.3109/00016488609108610 AXELSSON A, 1988, AM J OTOLARYNG, V9, P278, DOI 10.1016/S0196-0709(88)80036-X Erichsen S, 1996, HEARING RES, V100, P143, DOI 10.1016/0378-5955(96)00105-0 Franz P, 1997, HEARING RES, V112, P33, DOI 10.1016/S0378-5955(97)00112-3 HORNSTRAND C, 1980, ACTA OTO-LARYNGOL, V89, P1, DOI 10.3109/00016488009127102 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P22 KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 LIM DJ, 1985, ACTA OTOLARYNGOL S, V422, P3 MATSUBARA K, 1979, Auris Nasus Larynx, V6, P1 Mikaelian D, 1965, ACTA OTO-LARYNGOL, V59, P451, DOI DOI 10.3109/00016486509124579 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MORIGUCHI M, 1968, ACTA OTOLARYNGOL S S, V243, P2 Moriguchi M, 1991, Acta Otolaryngol Suppl, V486, P32 Moriguchi M, 1991, Acta Otolaryngol Suppl, V486, P39 Nishizaki K, 1998, ACTA OTO-LARYNGOL, V118, P96 REPRESA JJ, 1990, ANN OTO RHINOL LARYN, V99, P482 SADANAGA M, 1995, HEARING RES, V89, P155, DOI 10.1016/0378-5955(95)00133-X Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 WOOLF NK, 1986, AM J PHYSIOL, V250, P493 NR 22 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 75 EP 81 DI 10.1016/S0378-5955(00)00075-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100009 PM 10867279 ER PT J AU Wit, HP Warmerdam, TJ Albers, FWJ AF Wit, HP Warmerdam, TJ Albers, FWJ TI Measurement of the mechanical compliance of the endolymphatic compartments in the guinea pig SO HEARING RESEARCH LA English DT Article DE cochlea; hydrops; hypertension; Meniere; basilar membrane ID PRESSURE DIFFERENCE; COCHLEA; PERILYMPH; POTENTIALS; FLOW AB During injection of artificial endolymph into scala media of the guinea pig, fluid pressure was simultaneously measured in endolymph and perilymph with micropipettes. Pressure differences in the order of 10 Pa could reproducibly be measured upon injection of 2-4 mu l of artificial endolymph with a rate of 50 nl/s. Injection of larger volumes damaged the endolymphatic system. From the results, values were derived for the compliances of the membranes surrounding scala media and the vestibular part of the endolymphatic system. The shape of the pressure-time curve during and between repetitive injections of fluid could well be described with a two-component model for the endolymphatic system, consisting of two compartments with compliant walls, connected through a flow resistance. With this model, a larger compliance was found for the second compartment (vestibular part of endolymphatic system) than for the first compartment, into which fluid was injected (scala media). (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Groningen Hosp, Dept Otorhinolaryngol, NL-9700 RB Groningen, Netherlands. RP Wit, HP (reprint author), Univ Groningen Hosp, Dept Otorhinolaryngol, POB 30-001, NL-9700 RB Groningen, Netherlands. EM h.p.wit@med.rug.nl CR ALLEN GW, 1987, AM J OTOL, V8, P319 CHAMBERLIN ME, 1989, AM J PHYSIOL, V257, P159 DECORY L, 1990, LECT NOTES BIOMATH, V87, P270 DEMOTT J, 1997, ASS RES OT ABSTR, V47, P20 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 KLIS JFL, 1985, HEARING RES, V20, P15, DOI 10.1016/0378-5955(85)90054-1 KLIS SFL, 1994, HEARING RES, V75, P114, DOI 10.1016/0378-5955(94)90062-0 KONISHI S, 1977, J LARYNGOL OTOL, V91, P1033, DOI 10.1017/S0022215100084747 LEWIS ER, 1985, VERTEBRATE INNER EAR, P75 Mrowinski D, 1996, Audiol Neurootol, V1, P125 RAUCH S, 1964, BIOCH HORORGANS, P142 RUGGERO MA, 1990, J ACOUST SOC AM, V87, P1612, DOI 10.1121/1.399409 Salt AN, 1997, HEARING RES, V107, P29, DOI 10.1016/S0378-5955(97)00018-X SALT AN, 1986, NEUROBIOLOGY HEARING, P109 TAKEDA T, 1990, ACTA OTO-LARYNGOL, V110, P68, DOI 10.3109/00016489009122516 TAKEUCHI S, 1991, ANN OTO RHINOL LARYN, V100, P244 TONNDORF J., 1957, ANN OTOL RHINOL AND LARYNGOL, V66, P766 Wit HP, 1999, HEARING RES, V132, P131, DOI 10.1016/S0378-5955(99)00048-9 WIT HP, 2000, IN PRESS P 4 INT S M Yeh TH, 1997, HEARING RES, V109, P1, DOI 10.1016/S0378-5955(97)00030-0 YOSHIDA M, 1985, AM J OTOLARYNG, V6, P297, DOI 10.1016/S0196-0709(85)80058-2 ZUCCA G, 1991, ACTA OTO-LARYNGOL, V111, P820, DOI 10.3109/00016489109138417 ZUCCA G, 1995, ACTA OTO-LARYNGOL, V115, P34, DOI 10.3109/00016489509133343 ZWICKER E, 1977, J ACOUST SOC AM, V61, P1031, DOI 10.1121/1.381387 NR 25 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 82 EP 90 DI 10.1016/S0378-5955(00)00078-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100010 PM 10867280 ER PT J AU Chen, GD McWilliams, ML Fechter, LD AF Chen, GD McWilliams, ML Fechter, LD TI Succinate dehydrogenase (SDH) activity in hair cells: a correlate for permanent threshold elevations SO HEARING RESEARCH LA English DT Article DE cochlea; succinate dehydrogenase activity; surface preparation; noise-induced hearing loss; carbon monoxide ototoxicity; rat ID INTENSE AUDITORY-STIMULATION; INDUCED HEARING-LOSS; INNER-EAR CHANGES; CARBON-MONOXIDE; SIMULTANEOUS EXPOSURE; SQUIRREL-MONKEY; GUINEA-PIGS; NOISE; TOLUENE; POTENTIATION AB Hair cell loss is often used as a histological correlate of hearing loss. However, the histological and the physiological data are not always well correlated. This paper investigates the use of succinate dehydrogenase (SDH) activity in the hair cells as a marker of cellular dysfunction and so the loss of auditory sensitivity. In our previous studies, potentiation of noise-induced auditory threshold elevation by carbon monoxide (CO) was observed [Chen and Fechter, 1999; Chen et al., 1999]. However, its histological basis is still unclear. In this study, rats were exposed to 100-dB octave-band noise (center frequency = 13.6 kHz, 2 h) or to the combination of the noise and CO (1200 ppm). Threshold elevation of compound action potential (CAP) and cochlear histological changes were assessed 4 weeks after exposure. The noise alone caused CAP threshold elevations with little if any or without hair cell loss. However, the SDH activity in the hair cells decreased after the exposure. The SDH reduction, especially in the inner hair cells, was well related to the loss of auditory sensitivity. The combined exposure to noise and CO caused more severe CAP threshold elevation and SDH activity reduction than did the noise alone and it also caused significant outer hair cell loss. However, across all the test frequencies, neither the hair cell loss nor the SDH reduction alone had good correlation to the reduction of the auditory sensitivity. Under this situation, CAP threshold elevation seemed to follow OHC loss at high frequencies and to follow SDH reductions in the IHCs at low frequencies, where no hair cell loss occurred. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Oklahoma City, OK 73190 USA. RP Chen, GD (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, POB 26901,1110 N Stonewall, Oklahoma City, OK 73190 USA. CR BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T BORG E, 1989, J ACOUST SOC AM, V86, P1776, DOI 10.1121/1.398609 Campo P, 1997, NEUROTOXICOL TERATOL, V19, P129, DOI 10.1016/S0892-0362(96)00214-0 Campo P, 1998, NEUROTOXICOL TERATOL, V20, P321, DOI 10.1016/S0892-0362(97)00093-7 Chen GD, 1999, HEARING RES, V138, P181, DOI 10.1016/S0378-5955(99)00157-4 Chen GD, 1999, HEARING RES, V132, P149, DOI 10.1016/S0378-5955(99)00044-1 Engström B, 1983, Acta Otolaryngol Suppl, V402, P5 Engström B, 1983, Scand Audiol Suppl, V19, P1 FECHTER LD, 1988, HEARING RES, V34, P39, DOI 10.1016/0378-5955(88)90049-4 HAMERNIK RP, 1994, J ACOUST SOC AM, V95, P444, DOI 10.1121/1.408338 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HENDERSO.D, 1974, J ACOUST SOC AM, V56, P1210, DOI 10.1121/1.1903410 HORN KL, 1978, ARCH OTOLARYNGOL, V104, P42 HUNTERDU.IM, 1973, J ACOUST SOC AM, V54, P1179, DOI 10.1121/1.1914364 HUNTERDU.IM, 1972, J ACOUST SOC AM, V52, P1181, DOI 10.1121/1.1913230 Lataye R, 1997, NEUROTOXICOL TERATOL, V19, P373, DOI 10.1016/S0892-0362(97)00049-4 Lataye R, 2000, HEARING RES, V139, P86, DOI 10.1016/S0378-5955(99)00174-4 LI X, 1994, CHUNG HUA REH PI YEN, V29, P74 LURIE MH, 1937, LARYNGOSCOPE, V48, P418 McFadden SL, 1998, HEARING RES, V120, P121, DOI 10.1016/S0378-5955(98)00052-5 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 SAITO T, 1989, Auris Nasus Larynx, V16, P13 SCHUKNECHT HF, 1953, ZTRANS AM ACAD OPTH, P366 Stebbins W C, 1979, Am J Otolaryngol, V1, P15, DOI 10.1016/S0196-0709(79)80004-6 SUN AH, 1990, ANN OTO RHINOL LARYN, V99, P968 Wang J A, 1990, Hear Res, V44, P143, DOI 10.1016/0378-5955(90)90076-2 YANG FS, 1991, EUR ARCH OTO-RHINO-L, V248, P195 Zhai SQ, 1998, ACTA OTO-LARYNGOL, V118, P813, DOI 10.1080/00016489850182495 NR 29 TC 19 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 91 EP 100 DI 10.1016/S0378-5955(00)00076-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100011 PM 10867281 ER PT J AU Coppens, AG Resibois, A Poncelet, L AF Coppens, AG Resibois, A Poncelet, L TI Immunolocalization of calbindin D28k and calretinin in the dog cochlea during postnatal development SO HEARING RESEARCH LA English DT Article DE dog; cochlea; postnatal development; calbindin D28k; calretinin; immunohistochemistry ID CALCIUM-BINDING PROTEINS; MOUSE INNER-EAR; NEUROFILAMENT PROTEIN; GUINEA-PIG; LOCALIZATION; RAT; PARVALBUMIN; RETINA; APPEARANCE; NEURONS AB The calbindin (CB) and the calretinin (CR) immunoreactivities were studied in the dog cochlea during its postnatal maturation from birth to the 33rd postnatal day. At birth, CB was expressed in the Kolliker's organ, in the immature inner (IHC) and outer hair cells (OHC), in neurons of the spiral ganglion, and in nerve fibers running in the basilar membrane of the apical turn. During the cochlear maturation, non-sensorineuronal structures, such as the Kolliker's organ, the rods of Corti, and the inner sulcus cells, displayed a transient CB-staining. In the adult-like dog cochlea, CB was found in the cytoplasm, the cuticular plate, and the stereocilia of the IHC and OHC. All the neurons of the spiral ganglion and some nerves fibers in the modulius were CB-positive. At birth, CR exhibited a neuronal distribution: about 75% of the spiral ganglion neurons, some nerve fibers in the modulius and nerve fibers running in the basilar membrane were CR-labeled. During the postnatal maturation, a CR-immunostaining appeared around the IHC body and CR was expressed transiently in the OHC. In the adult-like dog cochlea, a CR-positive network surrounded the unlabeled IHC. The neuronal CR-labeling remained unchanged from birth. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Free Univ Brussels, Fac Med, Lab Anat Vet, B-1070 Brussels, Belgium. Free Univ Brussels, Fac Med, Lab Chim Biol & Nutr, B-1070 Brussels, Belgium. RP Coppens, AG (reprint author), Free Univ Brussels, Fac Med, Lab Anat Vet, CP 619,808 Route Lennik, B-1070 Brussels, Belgium. CR ANDRESSEN C, 1993, CELL TISSUE RES, V271, P181, DOI 10.1007/BF00318606 CELIO MR, 1990, NEUROSCIENCE, V35, P375, DOI 10.1016/0306-4522(90)90091-H CHRISTAKOS S, 1979, ENDOCRINOLOGY, V104, P1495 DECHESNE CJ, 1993, HEARING RES, V69, P91, DOI 10.1016/0378-5955(93)90096-J DECHESNE CJ, 1991, BRAIN RES, V560, P139, DOI 10.1016/0006-8993(91)91224-O DECHESNE CJ, 1994, J COMP NEUROL, V346, P517, DOI 10.1002/cne.903460405 DECHESNE CJ, 1988, DEV BRAIN RES, V41, P221, DOI 10.1016/0165-3806(88)90184-8 DECHESNE CJ, 1988, DEV BRAIN RES, V40, P233, DOI 10.1016/0165-3806(88)90135-6 HAMANO K, 1990, J COMP NEUROL, V302, P417, DOI 10.1002/cne.903020217 Hof PR, 1996, J CHEM NEUROANAT, V11, P1, DOI 10.1016/0891-0618(96)00117-2 Hof PR, 1996, J CHEM NEUROANAT, V11, P81, DOI 10.1016/0891-0618(96)00126-3 INAMURA S, 1996, ANAT EMBRYOL BERL, V194, P407 Jeon MH, 1998, NEUROSCI RES, V32, P75, DOI 10.1016/S0168-0102(98)00070-4 JOHNSSON LG, 1972, VASCULAR DISORDERS H, P249 LEGRAND C, 1988, DEV BRAIN RES, V38, P121, DOI 10.1016/0165-3806(88)90090-9 Lim D, 1992, DEV AUDITORY VESTIBU, P33 NOMIYA S, 1998, BRAIN RES DEV BRAIN, V10, P7 Pack AK, 1995, HEARING RES, V91, P119 PASTEELS B, 1990, VISUAL NEUROSCI, V5, P1 Pochet R, 1989, Adv Exp Med Biol, V255, P435 PUJOL R, 1973, ACTA OTO-LARYNGOL, V76, P1, DOI 10.3109/00016487309121476 RESIBOIS A, 1990, ADV EXP MED BIOL, V269, P211 RESIBOIS A, 1992, NEUROSCIENCE, V46, P101, DOI 10.1016/0306-4522(92)90012-Q ROGERS JH, 1987, J CELL BIOL, V105, P1343, DOI 10.1083/jcb.105.3.1343 Schucknecht H, 1993, PATHOLOGY EAR Shimada A, 1998, J VET MED SCI, V60, P41, DOI 10.1292/jvms.60.41 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 Sobkowicz HM, 1992, DEV AUDITORY VESTIBU, V2, P59 SPATZ WB, 1995, HEARING RES, V86, P89, DOI 10.1016/0378-5955(95)00059-D STEEL KP, 1983, ARCH OTOLARYNGOL, V109, P22 Strain GM, 1996, BRIT VET J, V152, P17, DOI 10.1016/S0007-1935(96)80083-2 USAMI S, 1995, ORL J OTO-RHINO-LARY, V57, P94 WASSERMA.RH, 1966, SCIENCE, V152, P791, DOI 10.1126/science.152.3723.791 NR 33 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 101 EP 110 DI 10.1016/S0378-5955(00)00077-0 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100012 PM 10867282 ER PT J AU Ou, HC Bohne, BA Harding, GW AF Ou, HC Bohne, BA Harding, GW TI Noise damage in the C57BL/CBA mouse cochlea SO HEARING RESEARCH LA English DT Article DE mouse; noise exposure; temporary threshold shift; permanent threshold shift; auditory brainstem response; quantitative histopathology ID F1-HYBRID STRAINS; HEARING-LOSS; MICE; AGE; GENETICS; EXPOSURE AB The present study was designed to determine the response to noise of the auditory system of a genetically well-defined laboratory mouse in preparation for examining the effect of noise on mice with specific genetic mutations. The mice were C57BL/CBA F1 hybrids. Eight mice served as non-noise-exposed controls and 39 mice were exposed for 1-24 h to an octave band of noise with a center frequency of 2, 4 or 8 kHz and a sound pressure level of 100-120 dB. Auditory brainstem response thresholds were measured pre-exposure and several times post-exposure (i.e., 0-27 days) to determine the magnitude of the temporary threshold shift (TTS) and permanent threshold shift (PTS). After Fixation by cardiac perfusion, the cochleas from each mouse were embedded in plastic, dissected into quarter turns of the cochlear duct and analyzed quantitatively. Immediately post-exposure, all mice had sizable TTSs at the tested frequencies (i.e., 3-50 kHz). At this time, two mice were killed. Thresholds of the other 37 mice recovered somewhat in the first 4 days post-exposure. One mouse fully recovered from its TTS; 10 mice were left with PTSs at all frequencies; 26 mice recovered at some frequencies but not others. Most mice with PTSs for 30-50 kHz had focal losses of inner and outer hair cells in the basal 20% of the organ of Corti, often with degeneration of adjacent myelinated nerve fibers in the osseous spiral lamina. On the other hand, mice with PTSs for the lower frequencies (i.e., 3-20 kHz) had stereocilia disarray without significant hair cell losses in the second and first turns. Considerable variability was found in the magnitude of hair cell losses in those mice that received identical noise exposures, despite their genetic homogeneity. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. RP Bohne, BA (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. RI Bohne, Barbara/A-9113-2008 OI Bohne, Barbara/0000-0003-3874-7620 CR BOHNE BA, 1985, LARYNGOSCOPE, V95, P818 BOHNE BA, 2000, IN PRESS AM J OTOLAR Bohne BA, 1997, HEARING RES, V109, P34, DOI 10.1016/S0378-5955(97)00019-1 BOHNE BA, 1986, J ACOUST SOC AM, V80, P1729, DOI 10.1121/1.394285 BOHNE BA, 1976, ANN OTO RHINOL LARYN, V85, P711 Bredberg G, 1973, Adv Otorhinolaryngol, V20, P102 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 CLARK DT, 1978, CRC CRIT R SOLID ST, V1, P1 DAVIS H, 1950, Acta Otolaryngol Suppl, V88, P1 Engström B, 1983, Acta Otolaryngol Suppl, V402, P5 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X HAWKINS JE, 1943, INJURY INNER EAR PRO HENRY KR, 1984, BEHAV NEUROSCI, V98, P107, DOI 10.1037/0735-7044.98.1.107 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 Lurie MH, 1942, ANN OTO RHINOL LARYN, V51, P712 MCFADDEN D, 1982, NEW PERSPECTIVES NOI, P363 MELNICK W, 1976, EFFECTS NOISE HEARIN, P277 MIKAELIA.DO, 1974, ACTA OTO-LARYNGOL, V77, P327, DOI 10.3109/00016487409124632 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLS JH, 1970, J ACOUST SOC AM, V48, P524, DOI 10.1121/1.1912167 Nordmann AS, 2000, HEARING RES, V139, P13, DOI 10.1016/S0378-5955(99)00163-X STOCKWEL.CW, 1969, ANN OTO RHINOL LARYN, V78, P1144 SULKOWSKI W, 1973, P INT C NOIS PUBL HL, P139 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 WARD W D, 1961, Laryngoscope, V71, P1590 NR 26 TC 44 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 111 EP 122 DI 10.1016/S0378-5955(00)00081-2 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100013 PM 10867283 ER PT J AU Ou, HC Harding, GW Bohne, BA AF Ou, HC Harding, GW Bohne, BA TI An anatomically based frequency-place map for the mouse cochlea SO HEARING RESEARCH LA English DT Article DE mouse; noise exposure; permanent hearing loss; auditory brainstem response; quantitative histopathology; frequency-place map ID NOISE AB An anatomically based frequency-place map was created for the mouse using C57BL/CBA F1 hybrids by matching noise-induced lesions in the organ of Corti with permanent hearing losses as determined by auditory brainstem response (ABR) thresholds. Twenty-six mice developed 'notched' ABR threshold shifts after exposure to an octave band of noise with a center frequency of 2 kHz at 120 dB SPL for 24 h, 4 kHz at 110 dB SPL for 4 h or 8 kHz at 100 dB SPL for 1 or 2 h. ABR thresholds were determined at several intervals post-exposure until thresholds stabilized (14-27 days). Once thresholds had stabilized, the mice were killed and their cochleas were prepared for phase-contrast microscopic examination as plastic-embedded flat preparations. Hair cell loss, stereocilia damage, and myelinated nerve fiber degeneration as a function of percentage distance from the cochlear apex were determined. Frequency-position matches could be made for 22 of the 26 mice by correlating areas of hair cell loss/stereocilia damage with permanent changes in ABR thresholds. These frequency-position data were fitted with the equation: % Distance from apex = 56.6 log (f(Hz))-179.1; r(2) = 0.810. This frequency-place function agrees well with Ehret's (1975) theoretical function based on critical bands and masked auditory thresholds. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. RP Harding, GW (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, 660 S Euclid Ave,Box 8115, St Louis, MO 63110 USA. RI Bohne, Barbara/A-9113-2008 OI Bohne, Barbara/0000-0003-3874-7620 CR BOHNE BA, 1986, J ACOUST SOC AM, V80, P1729, DOI 10.1121/1.394285 BREDBERG G, 1970, SCIENCE, V170, P861, DOI 10.1126/science.170.3960.861 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 BROWN AM, 1973, J COMP PHYSIOL, V83, P393, DOI 10.1007/BF00696354 EHRET G, 1975, J COMP PHYSIOL, V103, P329 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 Engström B, 1983, Acta Otolaryngol Suppl, V402, P5 ENGSTROM B, 1981, ARCH OTO-RHINO-LARYN, V230, P279, DOI 10.1007/BF00456330 FAY RR, 1988, HEARING VERTEBRATES, P367 Fletcher H, 1940, REV MOD PHYS, V12, P0047, DOI 10.1103/RevModPhys.12.47 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 HORIKAWA K, 1988, J NEUROSCI METH, V25, P1, DOI 10.1016/0165-0270(88)90114-8 KOENIG W, 1949, BELL LAB RECORD AUG, P200 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 Nordmann AS, 2000, HEARING RES, V139, P13, DOI 10.1016/S0378-5955(99)00163-X Ou HC, 2000, HEARING RES, V145, P111, DOI 10.1016/S0378-5955(00)00081-2 RYDMARKER S, 1989, SCANNING MICROSCOPY, V3, P1253 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SCHLEIDT WM, 1952, NATURWISSENSCHAFTEN, V39, P69 SCHUKNECHT HF, 1953, AMA ARCH OTOLARYNGOL, V58, P377 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 STOPP PE, 1983, HEARING RES, V11, P55, DOI 10.1016/0378-5955(83)90045-X VONBEKESY G, 1949, J ACOUST SOC AM, V21, P233 Zheng QY, 1999, HEARING RES, V130, P94, DOI 10.1016/S0378-5955(99)00003-9 NR 25 TC 47 Z9 49 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 123 EP 129 DI 10.1016/S0378-5955(00)00082-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100014 PM 10867284 ER PT J AU Braun, M AF Braun, M TI Inferior colliculus as candidate for pitch extraction: multiple support from statistics of bilateral spontaneous otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE inferior colliculus; fibrodendritic lamina; critical bandwidth; fundamental frequency f(o); auditory lateralization; music ID CONTRALATERAL ACOUSTIC STIMULATION; FREQUENCY-FOLLOWING RESPONSES; MISSING FUNDAMENTAL STIMULI; DISTORTION-PRODUCT; AUDITORY MIDBRAIN; NON-MUSICIANS; CORTICOFUGAL REGULATION; SPECTRAL INTEGRATION; OLIVOCOCHLEAR BUNDLE; CENTRAL NUCLEUS AB The fibrodendritic laminae of the central nucleus of the inferior colliculus (ICC) constitute a frequency map in stacked sheets that are consistently related to the psychoacoustic critical bandwidth (CB) [Schreiner and Langner, 1997. Nature 388, 383-386]. The recently observed co-occurrence of the CB and the double CB (2CB) suggested an adaptation of the ICC frequency map to the extraction of the fundamental frequency f(0) [Braun, 1999. Hear. Res. 129, 71-82]. The present study examined a possible influence of this frequency map upon efferent signaling towards the cochlea. The f(0) distribution of 2890 monaural and 2604 binaural pairs of human spontaneous otoacoustic emissions was analyzed by three statistical methods and in each case showed non-random behavior in the CB-2CB range. Single results were (1) a bias of right ear f(0) (mode at 349 Hz) and left ear f(0) (mode at 162 Hz) towards different ranges of speech f(0) (P < 0.02); (2) a bias of binaural, but not monaural, f(0) towards five of 12 semitone bins, C-G-D-A-E, representing the most frequent tones in music (P < 0.003); (3) a bias of binaural, but not monaural, f(0) fine-distribution towards the exact pitch frequencies used in music, according to the international standard A4 = 440 Hz (P = 0.03). The results support a model of lamina-based f(0) extraction in the ICC and suggest a specific colliculo-cochlear feedback for f(0) enhancement. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Physiol Mus Res, D-22607 Hamburg, Germany. RP Braun, M (reprint author), Neurosci Mus, Gansbyn 14, S-67195 Klassbol, Sweden. CR Attias J, 1996, ACTA OTO-LARYNGOL, V116, P534, DOI 10.3109/00016489609137885 Biebel UW, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P263, DOI 10.1007/978-1-4419-8712-9_24 Braun M, 1998, HEARING RES, V118, P129, DOI 10.1016/S0378-5955(98)00028-8 Braun M, 1997, HEARING RES, V114, P197, DOI 10.1016/S0378-5955(97)00160-3 Braun M, 1999, HEARING RES, V129, P71, DOI 10.1016/S0378-5955(98)00223-8 Ehret G., 1997, CENTRAL AUDITORY SYS, P259 EHRET G, 1985, SCIENCE, V227, P1245, DOI 10.1126/science.3975613 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 GALBRAITH GC, 1994, ELECTROEN CLIN NEURO, V92, P321, DOI 10.1016/0168-5597(94)90100-7 Galbraith GC, 1998, NEUROREPORT, V9, P1889, DOI 10.1097/00001756-199806010-00041 GALBRAITH GC, 1995, INT J PSYCHOPHYSIOL, V19, P203, DOI 10.1016/0167-8760(95)00008-G Geniec P, 1971, Acta Otolaryngol Suppl, V295, P1 GREENBERG S, 1987, HEARING RES, V25, P91, DOI 10.1016/0378-5955(87)90083-9 Guinan Jr J.J., 1996, COCHLEA, P435 GUMMER M, 1988, HEARING RES, V36, P41, DOI 10.1016/0378-5955(88)90136-0 Jen PHS, 1998, J COMP PHYSIOL A, V183, P683, DOI 10.1007/s003590050291 Jen PHS, 1999, BRAIN RES, V841, P184, DOI 10.1016/S0006-8993(99)01786-2 KAISER A, 1994, J NEUROPHYSIOL, V72, P2966 LANGNER G, 1998, PSYCHOPHYSICAL PHYSL, P277 Liberman MC, 1996, J ACOUST SOC AM, V99, P3572, DOI 10.1121/1.414956 MALMIERCA MS, 1995, J COMP NEUROL, V357, P124, DOI 10.1002/cne.903570112 Manley GA, 1999, HEARING RES, V138, P1, DOI 10.1016/S0378-5955(99)00126-4 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 Micheyl C, 1996, J ACOUST SOC AM, V99, P1604, DOI 10.1121/1.414734 MICHEYL C, 1995, BRAIN COGNITION, V29, P127, DOI 10.1006/brcg.1995.1272 Micheyl C, 1997, NEUROREPORT, V8, P1047, DOI 10.1097/00001756-199703030-00046 MICHEYL C, 1995, ACTA OTO-LARYNGOL, V115, P178, DOI 10.3109/00016489509139286 Nieschalk M, 1997, HNO, V45, P378, DOI 10.1007/s001060050113 OLIVER DL, 1984, J COMP NEUROL, V222, P237, DOI 10.1002/cne.902220207 Palombi PS, 1996, J NEUROPHYSIOL, V75, P2211 PENNER MJ, 1993, HEARING RES, V68, P229, DOI 10.1016/0378-5955(93)90126-L Perrot X, 1999, NEUROSCI LETT, V262, P167, DOI 10.1016/S0304-3940(99)00044-0 PLINKERT PK, 1992, LARYNGO RHINO OTOL, V71, P74, DOI 10.1055/s-2007-997249 Pratt H, 1998, HEARING RES, V115, P39, DOI 10.1016/S0378-5955(97)00178-0 Scates KW, 1999, HEARING RES, V128, P51, DOI 10.1016/S0378-5955(98)00198-1 Schreiner CE, 1997, NATURE, V388, P383, DOI 10.1038/41106 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SEMPLE MN, 1979, J NEUROPHYSIOL, V42, P1626 SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 TALMADGE CL, 1993, HEARING RES, V71, P170, DOI 10.1016/0378-5955(93)90032-V van Dijk P, 1998, J ACOUST SOC AM, V104, P336, DOI 10.1121/1.423259 WEBSTER WR, 1985, J NEUROSCI, V5, P1820 Yan J, 1999, J NEUROPHYSIOL, V81, P817 Zatorre RJ, 1996, J COGNITIVE NEUROSCI, V8, P29, DOI 10.1162/jocn.1996.8.1.29 ZATORRE RJ, 1994, J NEUROSCI, V14, P1908 Zwicker E., 1990, PSYCHOACOUSTICS FACT NR 47 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 130 EP 140 DI 10.1016/S0378-5955(00)00083-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100015 PM 10867285 ER PT J AU Lord, RM Mills, RP Abel, EW AF Lord, RM Mills, RP Abel, EW TI An anatomically shaped incus prosthesis for reconstruction of the ossicular chain SO HEARING RESEARCH LA English DT Article DE middle ear; ossiculoplasty; ossicular chain; incus prosthesis; laser vibrometer ID BASILAR-MEMBRANE VIBRATION; MIDDLE-EAR; MECHANICS AB An anatomically shaped incus replica prosthesis has been designed to reconstruct the ossicular chain. A series of in vitro studies on human temporal bones evaluated the acoustic performance of this prosthesis and compared it with a Causse partial ossicular replacement prosthesis (PORP). Pure tones in the frequency range 0.125-8 kHz stimulated the tympanic membrane at sound pressure levels of 80, 90 and 100 dB. Measurements of the stapes footplate velocity were made with a laser interferometer. The acoustic function of the ossicular chain reconstructed with the incus replica prosthesis was found to be within 10 dB of that of the original intact ossicular chain, when both the upper and lower joints of the implant were rigidly fixed in place. It was shown that a rigid mechanical contact between the ossicular prosthesis and ossicles is a prerequisite for effective sound transmission. The anatomically shaped incus prosthesis gave a 15-dB improvement on the PORP at frequencies below 1.5 kHz. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Dundee, Med Engn Res Inst, Dundee DD1 4HN, Scotland. Royal Infirm, Dept Otolaryngol, Edinburgh EH3 9EN, Midlothian, Scotland. RP Abel, EW (reprint author), Univ Dundee, Med Engn Res Inst, Dundee DD1 4HN, Scotland. CR Bekesy G., 1960, EXPT HEARING BUUNEN TJF, 1981, J ACOUST SOC AM, V69, P744, DOI 10.1121/1.385574 COHEN YE, 1992, HEARING RES, V51, P1 HUTTENBRINK KB, 1997, P INT WORKSH MIDDL E, P165 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P69 Merchant SN, 1996, HEARING RES, V97, P30 Merchant SN, 1998, J LARYNGOL OTOL, V112, P715 Mills RP, 1996, CLIN OTOLARYNGOL, V21, P499, DOI 10.1111/j.1365-2273.1996.tb01099.x MISURYA VK, 1980, ARCH OTOLARYNGOL, V106, P557 MULLER J, 1997, P INT WORKSH MIDDL E, P151 NUTTALL AL, 1991, HEARING RES, V51, P203, DOI 10.1016/0378-5955(91)90037-A PAU HW, 1997, P INT WORKSH MIDDL E, P207 Puria S, 1997, J ACOUST SOC AM, V101, P2754, DOI 10.1121/1.418563 ROSOWSKI JJ, 1990, ANN OTO RHINOL LARYN, V99, P403 RUGGERO MA, 1991, HEARING RES, V51, P215, DOI 10.1016/0378-5955(91)90038-B STASCHE N, 1994, ACTA OTO-LARYNGOL, V114, P59, DOI 10.3109/00016489409126017 Tonndorf J, 1974, Acta Otorhinolaryngol Belg, V28, P425 VLAMING MSMG, 1986, CLIN OTOLARYNGOL, V11, P353, DOI 10.1111/j.1365-2273.1986.tb00137.x ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 NR 19 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 141 EP 148 DI 10.1016/S0378-5955(00)00085-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100016 PM 10867286 ER PT J AU Watanabe, K Hess, A Zumegen, C Stennert, E Bloch, W Addicks, K Michel, O AF Watanabe, K Hess, A Zumegen, C Stennert, E Bloch, W Addicks, K Michel, O TI Changes of the compound action potential (CAP) and the expression of inducible nitric oxide synthase (iNOS/NOS II) in the cochlea under the inflammatory condition SO HEARING RESEARCH LA English DT Article DE electrocochleography; immunohistochemistry; nitric oxide synthase; endotoxin; cochlear damage ID SENSORINEURAL HEARING-LOSS; ROUND WINDOW MEMBRANE; ACUTE OTITIS-MEDIA; GUINEA-PIG COCHLEA; MIDDLE-EAR; BLOOD-FLOW; IN-VIVO; ENDOTOXIN; LIPOPOLYSACCHARIDE; LOCALIZATION AB In this study, the effect of endotoxin on the guinea pig cochlea has been examined electrophysiologically and immunohistochemically. Bacterial lipopolysaccharide (LPS, 5 mg/ml, 0.2 ml) was injected into the middle ear trans-tympanically. The electrocochleograms were measured before, immediately upon, and 3, 6 and 12 h after the injection continuously with an electrode inserted into the facial canal. After each measurement, some of the animals were killed with an intracardiac perfusion of fixative, temporal bones were removed and were immunohistochemically examined for inducible nitric oxide synthase (iNOS/NOS II). On serial paraffin section, iNOS could be detected first after 3 h in the lateral wall, the supporting cells of the organ of Corti and in cells of the spiral ganglion and was observed up to 12 h. After the injection of LPS, the threshold of compound action potential became significantly worse after 12 h in the LPS group. These changes became evident first at higher frequency (8 kHz). These results suggest that iNOS-generated NO is involved in the cochlea dysfunction under inflammatory conditions. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Nippon Med Sch, Dept Otorhinolaryngol, Bunkyo Ku, Tokyo 1138603, Japan. Univ Cologne, Dept Otorhinolaryngol, D-50924 Cologne, Germany. Univ Cologne, Dept Anat, D-50924 Cologne, Germany. RP Watanabe, K (reprint author), Nippon Med Sch, Dept Otorhinolaryngol, Bunkyo Ku, 1-1-5 Sendagi, Tokyo 1138603, Japan. CR Ando N, 1998, NITRIC OXIDE-BIOL CH, V2, P481, DOI 10.1006/niox.1999.0205 Aono K, 1997, J CELL BIOCHEM, V65, P349, DOI 10.1002/(SICI)1097-4644(19970601)65:3<349::AID-JCB5>3.0.CO;2-S Arnhold S, 1997, NEUROSCI LETT, V229, P165, DOI 10.1016/S0304-3940(97)00457-6 Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424 BERNSTEIN JM, 1980, CAN J MICROBIOL, V26, P546 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 DAWSON VL, 1993, J NEUROSCI, V13, P2651 DAWSON VL, 1991, P NATL ACAD SCI USA, V88, P6368, DOI 10.1073/pnas.88.14.6368 DEMARIA TF, 1984, J CLIN MICROBIOL, V20, P15 ENGEL F, 1995, INFECT IMMUN, V63, P1305 Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 Hess A, 1998, BRAIN RES, V813, P97, DOI 10.1016/S0006-8993(98)00997-4 HILDESHEIMER M, 1979, ACTA OTO-LARYNGOL, V88, P37, DOI 10.3109/00016487909137137 KIM CS, 1995, OTOLARYNG HEAD NECK, V112, P557, DOI 10.1177/019459989511200409 Liu SF, 1997, CRIT CARE MED, V25, P512, DOI 10.1097/00003246-199703000-00022 MARGOLIS RH, 1993, ARCH OTOLARYNGOL, V119, P682 MICHEL O, 2000, IN PRESS HEAR RES MONCADA S, 1991, PHARMACOL REV, V43, P109 MORIZONO T, 1990, EUR ARCH OTO-RHINO-L, V247, P40 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 RAHKO T, 1989, ACTA OTO-LARYNGOL, V108, P107, DOI 10.3109/00016488909107400 SPANDOW O, 1990, LARYNGOSCOPE, V100, P995 SPANDOW O, 1989, ACTA OTO-LARYNGOL, V107, P90, DOI 10.3109/00016488909127484 Takumida M, 1998, EUR ARCH OTO-RHINO-L, V255, P184, DOI 10.1007/s004050050040 Takumida M, 1997, ORL J OTO-RHINO-LARY, V59, P311 WALGER M, 1985, LARYNGO RHINO OTOL, V64, P638, DOI 10.1055/s-2007-1008224 YAMAGUCHI J, 1992, OTOL JPN, V2, P259 NR 27 TC 24 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 149 EP 155 DI 10.1016/S0378-5955(00)00086-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100017 PM 10867287 ER PT J AU He, DZZ Zheng, J Edge, R Dallos, P AF He, DZZ Zheng, J Edge, R Dallos, P TI Isolation of cochlear inner hair cells SO HEARING RESEARCH LA English DT Article DE inner hair cell; outer hair cell; isolation technique; morphology; voltage-clamp; gerbil ID GUINEA-PIG COCHLEA; MECHANICAL RESPONSES; MONGOLIAN GERBIL; CURRENTS AB In order to identify hair cell specific genes, it is essential to obtain isolated hair cells in quantity. While whole-cell recordings have been made from isolated inner hair cells (IHCs) from guinea pigs, detailed methods for obtaining a fairly large amount of isolated inner hair cells have not been published. Here we describe a protocol that can yield a fairly large amount of isolated gerbil IHCs. This technique can provide sufficient numbers of solitary IHCs for either electrophysiological studies of the cell's membrane properties or identifying genes related to IHC functions using techniques of molecular biology. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Northwestern Univ, Dept Neurobiol & Physiol, Auditory Physiol Lab, Evanston, IL 60208 USA. Northwestern Univ, Dept Commun Sci & Disorders, Evanston, IL 60208 USA. RP He, DZZ (reprint author), Northwestern Univ, Dept Neurobiol & Physiol, Auditory Physiol Lab, 2299 N Campus Dr, Evanston, IL 60208 USA. CR Amsterdam A, 1978, Methods Cell Biol, V20, P361, DOI 10.1016/S0091-679X(08)62028-2 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BROWNELL WE, 1984, SCANNING ELECTRON MI, V3, P1401 Edge RM, 1998, HEARING RES, V124, P1, DOI 10.1016/S0378-5955(98)00090-2 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 GUILD STACY R., 1932, ACTA OTO LARYNGOL, V17, P207, DOI 10.3109/00016483209129041 He DZZ, 1999, J NEUROPHYSIOL, V81, P1162 Iurato S, 1967, Arch Klin Exp Ohren Nasen Kehlkopfheilkd, V189, P113, DOI 10.1007/BF00417420 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 MROZ EA, 1993, HEARING RES, V70, P9, DOI 10.1016/0378-5955(93)90048-6 Muller M, 1996, HEARING RES, V94, P148, DOI 10.1016/0378-5955(95)00230-8 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SCHUKNECHT HF, 1960, NEURAL MECHANISMS AU, P76 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 Zheng J, 2000, NATURE, V405, P149, DOI 10.1038/35012009 NR 21 TC 22 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 156 EP 160 DI 10.1016/S0378-5955(00)00084-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100018 PM 10867288 ER PT J AU Knief, A Schulte, M Bertrand, O Pantev, C AF Knief, A Schulte, M Bertrand, O Pantev, C TI The perception of coherent and non-coherent auditory objects: a signature in gamma frequency band SO HEARING RESEARCH LA English DT Article DE auditory object; perception; gamma band activity; induced; evoked; auditory cortex; independent components analysis ID COMPLEX TONES; BRAIN ACTIVITY; PITCH; RESPONSES; HUMANS; REPRESENTATION; MEMORY; TASK; EEG; MEG AB The pertinence of gamma band activity in magnetoencephalographic and electroencephalographic recordings for the performance of a gestalt recognition process is a question at issue. We investigated the functional relevance of gamma band activity for the perception of auditory objects. An auditory experiment was performed as an analog to the Kanizsa experiment in the visual modality, comprising four different coherent and non-coherent stimuli. For the first time functional differences of evoked gamma band activity due to the perception of these stimuli were demonstrated by various methods (localization of sources, wavelet analysis and independent component analysis, ICA). Responses to coherent stimuli were found to have more features in common compared to non-coherent stimuli (e.g. closer located sources and smaller number of ICA components). The results point to the existence of a pitch processor in the auditory pathway. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Munster, Inst Expt Audiol, Biomagnetism Ctr, D-48129 Munster, Germany. INSERM, U280, Unite Mental Proc & Brain Activat, F-69424 Lyon 03, France. RP Pantev, C (reprint author), Univ Munster, Inst Expt Audiol, Biomagnetism Ctr, Kardinal von Galen Ring 10, D-48129 Munster, Germany. RI Bertrand, Olivier/B-6165-2008 CR BEERENDS JG, 1989, J ACOUST SOC AM, V86, P1835, DOI 10.1121/1.398562 BELL A, 1996, NETWORK COMPUT NEURA, V7 BERTRAND O, 1999, IN PRESS ADV BIOMAGN BERTRAND O, 1998, NEUROIMAGE, V7, P370 BORSCHBACH M, 1999, P ICS 99 IASTED SANT, P143 GOLDSTEI.JL, 1973, J ACOUST SOC AM, V54, P1496, DOI 10.1121/1.1914448 GREENBERG S, 1987, HEARING RES, V25, P91, DOI 10.1016/0378-5955(87)90083-9 JOKEIT H, 1994, P NATL ACAD SCI USA, V91, P6339, DOI 10.1073/pnas.91.14.6339 Karakas S, 1998, INT J PSYCHOPHYSIOL, V31, P13, DOI 10.1016/S0167-8760(98)00030-0 Llinas R., 1992, INDUCED RHYTHMS BRAI, P147 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 Pantev Christo, 1995, Brain Topography, V7, P321, DOI 10.1007/BF01195258 Pantev C, 1996, HEARING RES, V100, P164, DOI 10.1016/0378-5955(96)00124-4 PANTEV C, 1991, P NATL ACAD SCI USA, V88, P8896 Pantev C, 1998, NATURE, V392, P811, DOI 10.1038/33918 PFURTSCHELLER G, 1994, ELECTROEN CLIN NEURO, V90, P456, DOI 10.1016/0013-4694(94)90137-6 Pulvermuller F, 1999, TRENDS COGN SCI, V3, P250, DOI 10.1016/S1364-6613(99)01344-3 Pulvermuller F, 1996, ELECTROEN CLIN NEURO, V98, P76, DOI 10.1016/0013-4694(95)00191-3 Revonsuo A, 1997, NEUROREPORT, V8, P3867, DOI 10.1097/00001756-199712220-00006 Rodriguez E, 1999, NATURE, V397, P430 Salenius S, 1996, NEUROSCI LETT, V213, P75, DOI 10.1016/0304-3940(96)12796-8 TallonBaudry C, 1997, J NEUROSCI, V17, P722 Tallon-Baudry C, 1999, TRENDS COGN SCI, V3, P151, DOI 10.1016/S1364-6613(99)01299-1 TallonBaudry C, 1996, J NEUROSCI, V16, P4240 TallonBaudry C, 1997, NEUROREPORT, V8, P1103, DOI 10.1097/00001756-199703240-00008 Tallon-Baudry C, 1998, J NEUROSCI, V18, P4244 TERHARDT E, 1974, J ACOUST SOC AM, V55, P1061, DOI 10.1121/1.1914648 TIITINEN H, 1993, NATURE, V364, P59, DOI 10.1038/364059a0 NR 28 TC 20 Z9 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 161 EP 168 DI 10.1016/S0378-5955(00)00091-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100019 PM 10867289 ER PT J AU Ison, JR Bowen, GP AF Ison, JR Bowen, GP TI Scopolamine reduces sensitivity to auditory gaps in the rat, suggesting a cholinergic contribution to temporal acuity SO HEARING RESEARCH LA English DT Article DE gap detection; temporal resolution; aged auditory system; scopolamine; cholinergic mechanism; rat ID ACOUSTIC STARTLE RESPONSE; PREPULSE INHIBITION; EVOKED-POTENTIALS; REFLEX INHIBITION; BACKGROUND-NOISE; FACILITATION; HYPOTHESIS; MECHANISMS; NUCLEUS; LEVEL AB Prior research [Caine et al., 1981] suggested that scopolamine, a central cholinergic antagonist, may increase gap thresholds in young human listeners. If confirmed, an effect of scopolamine on gap detection might help to explain why both aged humans and aged laboratory animals have less sensitive temporal acuity on gap detection tests, as they may be presumed to have less effective cholinergic mechanisms. Here we measured the effect of scopolamine on gap detection in rats (n = 8) using reflex modification audiometry, which depends on the fact that brief gaps in noise presented immediately prior to a loud noise inhibit the acoustic startle reflex. Scopolamine increased the gap threshold and reduced reflex inhibition produced by gaps that were presented at and beyond about 40 ms prior to the startle reflex, but not at shorter lead times. A peripheral antagonist had no effect at long lead times. These data indicate that central cholinergic mechanisms are involved in relatively high level perceptual processing of gaps. This conclusion is consistent with the hypothesis that temporal acuity may be compromised in the aged listener because of deficits in the efficacy of these central mechanisms. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Rochester, Dept Brain & Cognit Sci, Rochester, NY 14627 USA. RP Ison, JR (reprint author), Univ Rochester, Dept Brain & Cognit Sci, Meliora Hall, Rochester, NY 14627 USA. CR BARSZ K, 2000, ASS RES OT ABSTR, V23, P534 BARTUS RT, 1982, SCIENCE, V217, P408, DOI 10.1126/science.7046051 CAINE ED, 1981, PSYCHOPHARMACOLOGY, V74, P74, DOI 10.1007/BF00431761 CAMPBELL KA, 1995, BRAIN RES, V702, P110, DOI 10.1016/0006-8993(95)01027-4 CROFTON KM, 1990, PSYCHOBIOLOGY, V18, P467 DICKERSON LW, 1991, EXP NEUROL, V112, P229, DOI 10.1016/0014-4886(91)90074-M DRACHMAN DA, 1974, ARCH NEUROL-CHICAGO, V30, P115 Fitzgibbons P J, 1996, J Am Acad Audiol, V7, P183 GALLAGHER M, 1995, CURR OPIN NEUROBIOL, V5, P161, DOI 10.1016/0959-4388(95)80022-0 Ison JR, 1997, BEHAV NEUROSCI, V111, P1335, DOI 10.1037//0735-7044.111.6.1335 ISON JR, 1991, BEHAV NEUROSCI, V105, P33, DOI 10.1037//0735-7044.105.1.33 ISON JR, 1982, J COMP PHYSIOL PSYCH, V96, P945, DOI 10.1037/0735-7036.96.6.945 KOCH M, 1993, EXP BRAIN RES, V97, P71 Lin D. Y., 1995, Society for Neuroscience Abstracts, V21, P908 Martinez-Serrano A, 1998, P NATL ACAD SCI USA, V95, P1858, DOI 10.1073/pnas.95.4.1858 MCCROSKEY RL, 1982, EAR HEARING, V3, P124, DOI 10.1097/00003446-198205000-00005 MEADOR KJ, 1987, INT J NEUROSCI, V33, P199, DOI 10.3109/00207458708987404 METHERATE R, 1990, SYNAPSE, V6, P364, DOI 10.1002/syn.890060409 PICKLES JO, 1973, J NEUROPHYSIOL, V36, P1131 PLOMP R, 1964, J ACOUST SOC AM, V36, P244 PUTCHA L, 1989, PHARMACEUT RES, V6, P481, DOI 10.1023/A:1015916423156 QUIRION R, 1995, J NEUROSCI, V15, P1455 SAMRA SK, 1985, ANESTHESIOLOGY, V62, P437, DOI 10.1097/00000542-198504000-00011 SCHNEIDER BA, 1994, J ACOUST SOC AM, V95, P980, DOI 10.1121/1.408403 Snell KB, 1997, J ACOUST SOC AM, V101, P2214, DOI 10.1121/1.418205 WU MF, 1985, TOXICOL APPL PHARM, V79, P377, DOI 10.1016/0041-008X(85)90136-X WU MF, 1993, BEHAV NEUROSCI, V107, P306, DOI 10.1037/0735-7044.107.2.306 YOUNG JS, 1983, J ACOUST SOC AM, V73, P1686, DOI 10.1121/1.389391 NR 28 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 169 EP 176 DI 10.1016/S0378-5955(00)00088-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100020 PM 10867290 ER PT J AU Rutkowski, RG Wallace, MN Shackleton, TM Palmer, AR AF Rutkowski, RG Wallace, MN Shackleton, TM Palmer, AR TI Organisation of binaural interactions in the primary and dorsocaudal fields of the guinea pig auditory cortex SO HEARING RESEARCH LA English DT Article DE auditory cortex; interaural level difference; interaural intensity difference; binaural interaction; binaural topography ID SOUND PRESSURE LEVEL; INTERAURAL INTENSITY DIFFERENCES; CAT CEREBRAL-CORTEX; SINGLE NEURONS; RESPONSE PROPERTIES; ORGANIZATION; REPRESENTATION; SENSITIVITY; SYSTEM; TIME AB This study investigated the nature and topography of binaural interactions in the primary auditory field (AI) and dorsocaudal field (DC) of the urethane anaesthetised guinea pig auditory cortex. Single and multi-units were classified by their responses to monaural and binaural stimulation. In both AI and DC, units displayed binaural facilitation, binaural inhibition, or a level dependent mixture of facilitation and inhibition. There was a significant difference in the distribution of binaural response types between the two fields. Facilitated units predominated in DC (facilitated: 58%; inhibited: 24%; mixed: 6%; non-interacting: 12%), while inhibited units were the most common class in AI (facilitated: 15%; inhibited: 44%; mixed: 18%; non-interacting: 22%). It has previously been suggested that inhibited and facilitated units are concerned with processing different areas of space suggesting a possible separation of function between the two core fields. Topographically, the binaural response properties in AI and DC varied along isofrequency bands, with neurones displaying similar interactions aggregating in clusters. These clusters were similar in size for the two fields and often overlapped neighbouring isofrequency bands. However, their shape and position varied between different animals. This clustered organisation of binaural interactions is similar to that reported in recent studies of AI in other mammals. (C) 2000 Elsevier Science B.V. All rights reserved. C1 MRC, Inst Hearing Res, Nottingham NG7 2RD, England. RP Rutkowski, RG (reprint author), MRC, Inst Hearing Res, Univ Pk, Nottingham NG7 2RD, England. CR AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 BULLOCK DC, 1988, MED BIOL ENG COMPUT, V26, P669, DOI 10.1007/BF02447511 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HELLWEG FC, 1977, EXP BRAIN RES, V29, P467 Hosokawa Y, 1997, J COMP PHYSIOL A, V181, P607, DOI 10.1007/s003590050144 Hosokawa Y, 1999, HEARING RES, V134, P123, DOI 10.1016/S0378-5955(99)00073-8 IMIG TJ, 1978, J COMP NEUROL, V182, P637, DOI 10.1002/cne.901820406 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 IRVINE DRF, 1987, HEARING RES, V30, P169, DOI 10.1016/0378-5955(87)90134-1 Irvine DRF, 1996, J NEUROPHYSIOL, V75, P75 Irvine DRF, 1998, ZOOL-ANAL COMPLEX SY, V101, P260 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 KAYSER K, 1989, PATHOL RES PRACT, V185, P729 KELLY JB, 1988, J NEUROPHYSIOL, V59, P1756 KELLY JB, 1994, J NEUROPHYSIOL, V71, P904 Liu W, 1997, J COMP PHYSIOL A, V181, P599, DOI 10.1007/s003590050143 MIDDLEBROOKS JC, 1980, BRAIN RES, V181, P31, DOI 10.1016/0006-8993(80)91257-3 MILLS AW, 1972, FDN MODERN AUDITORY, V2 ORMAN SS, 1984, J NEUROPHYSIOL, V51, P1028 PHILLIPS DP, 1981, HEARING RES, V4, P299, DOI 10.1016/0378-5955(81)90014-9 PHILLIPS DP, 1982, BRAIN RES, V248, P237, DOI 10.1016/0006-8993(82)90581-9 PHILLIPS DP, 1983, J NEUROPHYSIOL, V49, P383 RAJAN R, 1990, J NEUROPHYSIOL, V64, P872 RALEIGH, 1907, PHILOS MAG, V13, P214 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 REDIES H, 1989, J COMP NEUROL, V282, P473, DOI 10.1002/cne.902820402 REDIES H, 1989, J COMP NEUROL, V282, P489, DOI 10.1002/cne.902820403 RUTKOWSKI RG, 1999, BRIT J AUDIOL, V33, P98 RUTKOWSKI RG, 2000, IN PRESS BR J AUDIOL SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P449 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P462 Shen JX, 1997, J COMP PHYSIOL A, V181, P591, DOI 10.1007/s003590050142 Stevens SS, 1936, AM J PSYCHOL, V48, P297, DOI 10.2307/1415748 WALLACE MN, 2000, IN PRESS EXP BRAIN R Wallace MN, 1999, NEUROREPORT, V10, P2095, DOI 10.1097/00001756-199907130-00019 NR 37 TC 44 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 177 EP 189 DI 10.1016/S0378-5955(00)00087-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100021 PM 10867291 ER PT J AU Chertoff, ME Lerner, D Amani-Taleshi, D Nagai, Y AF Chertoff, ME Lerner, D Amani-Taleshi, D Nagai, Y TI Characterizing non-linearity in the cochlear microphonic using the instantaneous frequency SO HEARING RESEARCH LA English DT Article DE cochlear microphonic; instantaneous frequency; hearing loss ID OUTER HAIR-CELLS; GUINEA-PIG; BASILAR-MEMBRANE; RESPONSES; MECHANICS; INNER AB In this paper, we examine the non-linearity of mechano-electric transduction in the cochlea by computing the instantaneous frequency (IF) of the cochlear microphonic (CM) in response to sinusoidal stimuli. In contrast to a linear system which yields a constant IF when driven with a sinusoid, the IF of the CM varied during one period of oscillation. This variation was not symmetric, but differed for positive and negative slopes of the CM. Administration of tetrodotoxin to eliminate neural activity indicated that the variation of the IF was not due to neural contamination. Moreover, comparing the IF of the stimulus to that of the CM indicated that the IF was not due to non-linearity in the acoustic signal. Signal frequency, signal level and acoustic trauma altered the IF. A cochlear model of the CM was developed to determine the influence of the saturation of hair-cell receptor currents and vector summation on the IF. Results indicated that these factors could not fully account for the variation in the IF. We conclude that the variation in IF within one period of cochlear partition vibration indicates that the mechanical and/or electrical oscillations which produce the CM differ from those of a linear system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Kansas, Med Ctr, Dept Speech & Hearing, Kansas City, KS 66160 USA. Univ Kansas, Dept Math, Kansas City, KS USA. RP Chertoff, ME (reprint author), Univ Kansas, Med Ctr, Dept Speech & Hearing, 39th & Rainbow Blvd, Kansas City, KS 66160 USA. CR Bian L, 1998, J ACOUST SOC AM, V104, P2261, DOI 10.1121/1.423739 BIAN L, 1999, ASS RES OT ABSTR, P834 BOASHASH B, 1992, P IEEE, V80, P520, DOI 10.1109/5.135376 COHEN L, 1989, P IEEE, V77, P941, DOI 10.1109/5.30749 DALLOS P, 1973, AUDITORY PERIPHERY B, pCH5 DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 DALLOS P, 1969, J ACOUST SOC AM, V45, P37, DOI 10.1121/1.1911371 de Boer E, 1975, J Acoust Soc Am, V58, P1030, DOI 10.1121/1.380762 deBoer E, 1997, J ACOUST SOC AM, V101, P3583, DOI 10.1121/1.418319 Huang NE, 1998, P ROY SOC A-MATH PHY, V454, P903 Lerner DE, 2000, HEARING RES, V145, P203, DOI 10.1016/S0378-5955(00)00089-7 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 Patuzzi R, 1998, HEARING RES, V125, P71, DOI 10.1016/S0378-5955(98)00124-5 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 PATUZZI RB, 1987, HEARING RES, V30, P73, DOI 10.1016/0378-5955(87)90185-7 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 TABACHNICK BG, 1983, USING MULTIVARIATE S, P228 NR 21 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 190 EP 202 DI 10.1016/S0378-5955(00)00090-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100022 PM 10867292 ER PT J AU Lerner, DE Chertoff, ME Amani-Taleshi, D AF Lerner, DE Chertoff, ME Amani-Taleshi, D TI Mathematical decomposition of the round window potential SO HEARING RESEARCH LA English DT Article DE cochlear microphonic; compound action potential; summating potential AB We present an algorithm called the median transform which can be used to decompose the round window auditory potential into AC and DC components. The first of these is identified with the cochlear microphonic, and the second with the combined summating and compound action potentials. Elsewhere in this volume, the algorithm is employed as an intermediate step in obtaining the instantaneous frequency of the CM. Since the algorithm is easily implemented and operates entirely in the time domain, it may prove useful to clinicians as well as researchers. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Kansas, Dept Math, Lawrence, KS 66045 USA. Univ Kansas, Med Ctr, Dept Speech & Hearing, Kansas City, KS 66160 USA. RP Lerner, DE (reprint author), Univ Kansas, Dept Math, Lawrence, KS 66045 USA. CR Chertoff ME, 2000, HEARING RES, V145, P190, DOI 10.1016/S0378-5955(00)00090-3 Dallos P., 1973, AUDITORY PERIPHERY B Huang NE, 1998, P ROY SOC A-MATH PHY, V454, P903 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 Pickles JO, 1988, INTRO PHYSL HEARING NR 5 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 2000 VL 145 IS 1-2 BP 203 EP 205 DI 10.1016/S0378-5955(00)00089-7 PG 3 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 329YB UT WOS:000087935100023 PM 10867293 ER PT J AU Tabuchi, K Ito, Z Tsuji, S Wada, T Takahashi, K Hara, A Kusakari, J AF Tabuchi, K Ito, Z Tsuji, S Wada, T Takahashi, K Hara, A Kusakari, J TI The contribution of phospholipase A2 to the cochlear dysfunction induced by transient ischemia SO HEARING RESEARCH LA English DT Article DE cochlea; compound action potential; ischemia; mepacrine; phospholipase A2 ID RAT CEREBRAL-CORTEX; GLUTAMATE NEUROTOXICITY; LOCAL ANOXIA; A(2); BRAIN; REPERFUSION; MECHANISMS; RELEASE AB The objective of the present study was to examine whether mepacrine, a commonly used phospholipase A2 inhibitor. decreases ischemic damage to the cochlea. Transient ischemia of the cochlea was induced in albino guinea pigs for 15, 30 or 60 min by pressing the labyrinthine artery at the porus acusticus internus. The animals were intraperitoneally given mepacrine or physiological saline solution (PSS) 20 min prior to ischemia. Although mepacrine failed to alleviate the post-ischemic threshold shift of compound action potential (CAP) in case of 60 min ischemia. a statistically significant reduction in the CAP threshold shift was observed in the mepacrine-treated animals after 15 acid 30 min ischemia. However, there was no statistically significant difference in the post-ischemic threshold shift of cochlear microphonic between the mepacrine-given and the PSS-given animals. Furthermore, mepacrine partially alleviated ischemia-induced swelling of radial afferent dendrites of primary auditory neurons. These results suggest that excessive activation of phospholipase A2, plays an injury-producing role at least by enhancing excitotoxicity in ischemia-reperfusion injury of the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. RP Kusakari, J (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR Bonventre JV, 1997, NATURE, V390, P622, DOI 10.1038/37635 CHOI DW, 1987, J NEUROSCI, V7, P369 Dennis EA, 1997, TRENDS BIOCHEM SCI, V22, P1, DOI 10.1016/S0968-0004(96)20031-3 EYBALIN M, 1993, PHYSIOL REV, V73, P309 Farooqui AA, 1997, J NEUROCHEM, V69, P889 Kusakari J, 1981, Auris Nasus Larynx, V8, P55 LIU Y, 1995, TOXICOL APPL PHARM, V132, P196, DOI 10.1006/taap.1995.1099 Matsuo Y, 1996, BRAIN RES, V709, P296, DOI 10.1016/0006-8993(95)01324-5 OLNEY JW, 1986, NEUROSCI LETT, V65, P65, DOI 10.1016/0304-3940(86)90121-7 ORegan MH, 1996, NEUROSCI LETT, V202, P201, DOI 10.1016/0304-3940(95)12238-9 OREGAN MH, 1995, NEUROSCI LETT, V185, P191, DOI 10.1016/0304-3940(95)11259-Y Phillis J. W., 1996, Life Sciences, V58, P97 Phillis JW, 1996, BRAIN RES, V730, P150 PUEL JL, 1994, J COMP NEUROL, V341, P241, DOI 10.1002/cne.903410209 PUJOL R, 1992, NEUROREPORT, V3, P299, DOI 10.1097/00001756-199204000-00002 RORDORF G, 1991, J NEUROSCI, V11, P1829 SMITS AJ, 1984, EXP FLUIDS, V2, P33 Tabuchi K, 1999, ACTA OTO-LARYNGOL, V119, P179 Tabuchi K, 1998, HEARING RES, V126, P28, DOI 10.1016/S0378-5955(98)00142-7 Uozumi N, 1997, NATURE, V390, P618 VADAS P, 1982, LIFE SCI, V30, P155, DOI 10.1016/0024-3205(82)90647-6 VIGO C, 1980, BIOCHEM PHARMACOL, V29, P623, DOI 10.1016/0006-2952(80)90386-X NR 22 TC 3 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 1 EP 7 DI 10.1016/S0378-5955(00)00038-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000001 PM 10831860 ER PT J AU Bailey, GP Sewell, WF AF Bailey, GP Sewell, WF TI Contribution of glutamate receptors to spontaneous and stimulus-evoked discharge in afferent fibers innervating hair cells of the Xenopus lateral line organ SO HEARING RESEARCH LA English DT Article DE glutamate; cochlea; synapse; 6-cyano-7-nitroquinoxaline-2,3-dione; lateral line ID GUINEA-PIG COCHLEA; ION-DEPENDENT CONDUCTANCES; AUDITORY-NERVE FIBERS; METHYL-D-ASPARTATE; NEUROTRANSMITTER RELEASE; CONCANAVALIN-A; QUISQUALATE RECEPTORS; SYNAPTIC TRANSMISSION; HIPPOCAMPAL-NEURONS; VESTIBULAR ORGANS AB The relative contributions of NMDA (N-methyl-D-aspartate) and non-NMDA glutamate receptors to spontaneous and stimulus-evoked transmission at the hair cell/afferent fiber synapse were determined in the Xenopus laevis lateral line organ. The non-NMDA receptor antagonist, CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) reversibly reduced both spontaneous and stimulus-evoked discharge rate with an EC50 of 0.5 mu M. NMDA receptor antagonism with the combination of chlorokynurenic acid (100 mu M) and elevated magnesium (1.1 mM), or elevated magnesium alone, blocked responses to NMDA without significantly altering spontaneous or stimulus-evoked discharge rate or the responses to kainate. All non-NMDA receptor agonists tested increased discharge rate at low concentrations and. at higher concentrations, increased, then suppressed discharge rate. The EC(50)s were: domoic acid (2.4 mu M) < quisqualic acid (6 mu M) < kainic acid (18 mu M) < AMPA (82 mu M) << glutamate (1150 mu M). NMDA and ibotenic acid also produced an increase in discharge followed by a suppression, but the suppressive phase of the response predominated and maximum increases in discharge rates were low compared to effects of the non-NMDA agonists. The EC(50)s were: NMDA (148 mu M) < ibotenic acid (463 mu M). The EC50 for the suppression of afferent discharge that followed the initial excitatory effect was similar to the EC50 for excitation. Perfusion with active concentrations of kainate, AMPA. or NMDA did not alter the threshold for electrical stimulation of these nerve fibers. We conclude that most of the postsynaptic signal normally seen in afferent fibers is mediated by non-NMDA receptors. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otolaryngol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02115 USA. Boston Univ, Dept Pathol, Boston, MA 02115 USA. RP Sewell, WF (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, 243 Charles St, Boston, MA 02114 USA. CR Andrew RD, 1996, J NEUROPHYSIOL, V76, P2707 ANNONI JM, 1984, J NEUROSCI, V4, P2106 ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 BENVENISTE M, 1991, BIOPHYS J, V59, P560 BLAKE JF, 1988, NEUROSCI LETT, V89, P182, DOI 10.1016/0304-3940(88)90378-3 BLEDSOE SC, 1982, NEUROSCI LETT, V32, P315, DOI 10.1016/0304-3940(82)90313-5 BLEDSOE S C JR, 1983, Comparative Biochemistry and Physiology C Pharmacology Toxicology and Endocrinology, V75, P199, DOI 10.1016/0742-8413(83)90180-9 BOBBIN RP, 1985, COMP BIOCHEM PHYS C, V80, P313, DOI 10.1016/0742-8413(85)90062-3 BOBBIN RP, 1979, EXP BRAIN RES, V34, P389 CLEMENTS JD, 1991, NEURON, V7, P605, DOI 10.1016/0896-6273(91)90373-8 COCHRAN SL, 1992, ANN NY ACAD SCI, V656, P580, DOI 10.1111/j.1749-6632.1992.tb25237.x COMIS SD, 1979, EXP BRAIN RES, V36, P119 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 COREY DP, 1983, J NEUROSCI, V3, P962 DEVAU G, 1993, EUR J NEUROSCI, V5, P1210, DOI 10.1111/j.1460-9568.1993.tb00975.x DRESCHER DG, 1987, LIFE SCI, V40, P1371, DOI 10.1016/0024-3205(87)90327-4 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 EDMONDS B, 1995, ANNU REV PHYSIOL, V57, P495 ELEPFANDT A, 1988, ACTA BIOL HUNG, V39, P251 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 GLEICH O, 1990, HEARING RES, V45, P295, DOI 10.1016/0378-5955(90)90128-C Guth PS, 1998, HEARING RES, V125, P154, DOI 10.1016/S0378-5955(98)00145-2 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 GUTH SL, 1990, BRAIN RES, V508, P76, DOI 10.1016/0006-8993(90)91120-6 GUTH SL, 1990, LIFE SCI, V47, P1437, DOI 10.1016/0024-3205(90)90522-S HARRIS GG, 1966, J ACOUST SOC AM, V40, P32, DOI 10.1121/1.1910060 HARRIS GERARD G., 1967, P135 HILLE B, 1998, IONIC CHANNELS EXCIT, P303 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 HUETTNER JE, 1990, NEURON, V5, P255, DOI 10.1016/0896-6273(90)90163-A ISHII Y, 1971, JPN J PHYSIOL, V21, P79 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 KEHOE JS, 1978, NATURE, V274, P866, DOI 10.1038/274866a0 KROESE ABA, 1978, PFLUG ARCH EUR J PHY, V375, P167, DOI 10.1007/BF00584240 KROGSGAARDLARSEN P, 1980, NATURE, V284, P64, DOI 10.1038/284064a0 KURIYAMA H, 1993, HEARING RES, V69, P215, DOI 10.1016/0378-5955(93)90110-M KURIYAMA H, 1994, HEARING RES, V80, P233, DOI 10.1016/0378-5955(94)90114-7 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 LITTMAN T, 1989, HEARING RES, V40, P45, DOI 10.1016/0378-5955(89)90098-1 MANLEY GA, 1976, J PHYSIOL-LONDON, V258, P323 Matsubara A, 1996, J NEUROSCI, V16, P4457 MAYER ML, 1989, P NATL ACAD SCI USA, V86, P1411, DOI 10.1073/pnas.86.4.1411 MILEDI R, 1966, NATURE, V212, P1233, DOI 10.1038/2121233a0 MOUDY AM, 1994, NEUROPHARMACOLOGY, V33, P953, DOI 10.1016/0028-3908(94)90153-8 MROZ EA, 1989, HEARING RES, V38, P141, DOI 10.1016/0378-5955(89)90136-6 MURRAY RW, 1955, Q J MICROSC SCI, V96, P351 NAKAGAWA T, 1991, J NEUROPHYSIOL, V65, P715 NIEDZIELSKI AS, 1995, J NEUROSCI, V15, P2338 Otis T, 1996, J NEUROSCI, V16, P7496 PARTIN KM, 1993, NEURON, V11, P1069, DOI 10.1016/0896-6273(93)90220-L Paternain AV, 1996, EUR J NEUROSCI, V8, P2129, DOI 10.1111/j.1460-9568.1996.tb00734.x PATNEAU DK, 1990, J NEUROSCI, V10, P2385 Pirotte B, 1998, J MED CHEM, V41, P2946, DOI 10.1021/jm970694v PRIGIONI I, 1990, HEARING RES, V46, P253, DOI 10.1016/0378-5955(90)90006-B PUEL JL, 1991, NEUROSCIENCE, V45, P63, DOI 10.1016/0306-4522(91)90103-U RAMAN IM, 1995, BIOPHYS J, V68, P137 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 Ruel J, 1999, J PHYSIOL-LONDON, V518, P667, DOI 10.1111/j.1469-7793.1999.0667p.x RUSSELL IJ, 1971, J EXP BIOL, V54, P643 RYAN AF, 1991, NEUROREPORT, V2, P643, DOI 10.1097/00001756-199111000-00002 SAFIEDDINE S, 1992, NEUROREPORT, V3, P1145, DOI 10.1097/00001756-199212000-00029 SAND O, 1975, J COMP PHYSIOL, V102, P13 SEWELL WF, 1984, J PHYSIOL-LONDON, V347, P685 SEWELL WF, 1990, HEARING RES, V44, P71, DOI 10.1016/0378-5955(90)90023-I SEWELL WF, 1987, J NEUROSCI, V17, P2465 Shero M, 1998, NEUROSCI LETT, V257, P81, DOI 10.1016/S0304-3940(98)00821-0 STARR PA, 1991, HEARING RES, V52, P23, DOI 10.1016/0378-5955(91)90185-C SUGIYAMA H, 1989, NEURON, V3, P129, DOI 10.1016/0896-6273(89)90121-9 TRUSSELL LO, 1989, NEURON, V3, P209, DOI 10.1016/0896-6273(89)90034-2 TRUSSELL LO, 1993, NEURON, V10, P1185, DOI 10.1016/0896-6273(93)90066-Z Tucker T, 1995, NEURON, V15, P1323, DOI 10.1016/0896-6273(95)90011-X VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 WEAKLY JN, 1973, J PHYSIOL-LONDON, V234, P597 YAMADA KA, 1992, J PHYSIOL-LONDON, V458, P409 ZIMMERMAN DM, 1979, NATURE, V282, P82, DOI 10.1038/282082a0 ZUCCA G, 1992, HEARING RES, V63, P52, DOI 10.1016/0378-5955(92)90073-V NR 79 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 8 EP 20 DI 10.1016/S0378-5955(00)00023-X PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000002 PM 10831861 ER PT J AU Barrenas, ML Landin-Wilhelmsen, K Hanson, C AF Barrenas, ML Landin-Wilhelmsen, K Hanson, C TI Ear and bearing in relation to genotype and growth in Turner syndrome SO HEARING RESEARCH LA English DT Article DE Turner syndrome; hearing; chromosome; insulin-like growth factor-1; body height; cell cycle delay hypothesis; Down syndrome; aneuploidy ID DOWNS-SYNDROME; OTITIS-MEDIA; INNER-EAR; EUSTACHIAN-TUBE; SHORT STATURE; HEARING-LOSS; FACTOR-I; CHILDREN; WOMEN; SKULL AB Hearing loss, auricular anomalies and middle ear infections are common findings in many genetic disorders, but the mechanisms have remained unknown. We studied ear and hearing problems in Turner's syndrome (TS) in relation to the degree of X chromosome loss (i.e, degree of mosaicism) and growth. One hundred and nineteen girls and women with TS were studied regarding audiometry, fluorescent in situ hybridisation, serum concentration of insulin-like growth factor-1 (IGF-1) and body height. It was found that sensorineural hearing loss and occurrence of auricular anomalies were significantly increased the greater the proportion of 45,X cells in a particular individual (P < 0.05 and P < 0.001, respectively). Middle ear infections and sensorineural hearing loss were negatively correlated with IGF-1 (P < 0.05 and P < 0.001. respectively). Hearing correlated positively with height (P < 0.01) and IGF-1 independently of age (P < 0.05). Height correlated positively with IGF-1 (P ( 0.001). Auricular malformations, middle ear infections and hearing impairment in TS were interpreted as due to growth disturbances during development. A new hypothesis on the pathophysiology of external, middle and inner ear disorders due to a delayed cell cycle caused by chromosomal aberrations per se and not only to the specific X chromosome deletion is presented. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Gothenburg, Sahlgrens Univ Hosp, Dept Audiol, SE-41345 Gothenburg, Sweden. Univ Gothenburg, Sahlgrens Univ Hosp, Res Ctr Endocrinol & Metab, SE-41345 Gothenburg, Sweden. Univ Gothenburg, Sahlgrens Univ Hosp, Dept Obstet & Gynaecol, SE-41345 Gothenburg, Sweden. RP Barrenas, ML (reprint author), Univ Gothenburg, Sahlgrens Univ Hosp, Dept Audiol, SE-41345 Gothenburg, Sweden. EM marie-louise.barrenas@audiology.gu.se CR AITKIN M, 1990, STAT MODELLING GLIM, P167 Anderson H., 1969, ACTA OTO-LARYNGOL, V247, P1 Barrenas ML, 1999, HEARING RES, V138, P163, DOI 10.1016/S0378-5955(99)00162-8 Benazzo M, 1997, J AUDIOL MED, V6, P147 Bilgin H, 1996, ARCH OTOLARYNGOL, V122, P271 BROWN PM, 1989, CLIN OTOLARYNGOL, V14, P241, DOI 10.1111/j.1365-2273.1989.tb00368.x Ellison JW, 1997, HUM MOL GENET, V6, P1341, DOI 10.1093/hmg/6.8.1341 Gorlin R.J., 1995, HEREDITARY HEARING L Gravholt CH, 1996, BRIT MED J, V312, P16 Hulander M, 1998, NAT GENET, V20, P374 HULTCRANTZ M, 1994, HEARING RES, V76, P127, DOI 10.1016/0378-5955(94)90094-9 Hultcrantz M, 1997, HEARING RES, V103, P69, DOI 10.1016/S0378-5955(96)00165-7 JAKOBSSON AH, 1995, J ASSIST REPROD GEN, V12, P422, DOI 10.1007/BF02211142 Jonsson R, 1998, SCAND AUDIOL, V27, P81, DOI 10.1080/010503998420324 LANDINWILHELMSEN K, 1994, CLIN ENDOCRINOL, V41, P351, DOI 10.1111/j.1365-2265.1994.tb02556.x LEHEUP B P, 1988, Journal de Genetique Humaine, V36, P315 LEON Y, 1995, ENDOCRINOLOGY, V136, P3494, DOI 10.1210/en.136.8.3494 Leonova J, 1999, HEREDITAS, V131, P87, DOI 10.1111/j.1601-5223.1999.00087.x LINDSTEN J, 1963, THESIS STOCKHOLM Ludwig M, 1997, ANN ANAT, V179, P525 MAZZONI DS, 1994, J INTELL DISABIL RES, V38, P549 MELNICK M, 1979, BIRTH DEFECTS, P9 Fernandez R, 1996, HUM GENET, V98, P29, DOI 10.1007/s004390050155 NIELSEN J, 1980, HUM GENET, V55, P357, DOI 10.1007/BF00290218 Nielsen J, 1995, INT CONGR SER, V1089, P67 PATON GR, 1974, HUMANGENETIK, V23, P173 Rao E, 1997, NAT GENET, V16, P54, DOI 10.1038/ng0597-54 ROIZEN NJ, 1994, CLIN PEDIATR, V33, P439, DOI 10.1177/000992289403300710 RUDIN R, 1987, ACTA OTO-LARYNGOL, V103, P217, DOI 10.3109/00016488709107787 SCULERATI N, 1990, ARCH OTOLARYNGOL, V116, P704 SELIKOWITZ M, 1992, J PAEDIATR CHILD H, V28, P383, DOI 10.1111/j.1440-1754.1992.tb02697.x SHIBAHARA Y, 1989, ANN OTO RHINOL LARYN, V98, P543 Shimizu T, 1997, PRENATAL DIAG, V17, P545, DOI 10.1002/(SICI)1097-0223(199706)17:6<545::AID-PD108>3.0.CO;2-3 Soderlund B, 1998, HUM REPROD, V13, P110 STEEL KP, 1994, TRENDS GENET, V10, P428, DOI 10.1016/0168-9525(94)90113-9 Stenberg AE, 1998, HEARING RES, V124, P85, DOI 10.1016/S0378-5955(98)00113-0 STENSTROM C, 1994, INT J PEDIATR OTORHI, V29, P23, DOI 10.1016/0165-5876(94)90105-8 STENSTROM C, 1991, INT J PEDIATR OTORHI, V21, P127, DOI 10.1016/0165-5876(91)90143-Y SZPUNAR J, 1968, ARCH OTOLARYNGOL, V87, P34 Torres M, 1998, MECH DEVELOP, V71, P5, DOI 10.1016/S0925-4773(97)00155-X VINTZILEOS AM, 1995, AM J OBSTET GYNECOL, V172, P837, DOI 10.1016/0002-9378(95)90008-X WATKIN PM, 1989, J LARYNGOL OTOL, V103, P731, DOI 10.1017/S0022215100109934 WINDLETAYLOR PC, 1982, CLIN OTOLARYNGOL, V7, P75, DOI 10.1111/j.1365-2273.1982.tb01566.x WRIGHT A, 1988, ACTA OTOLARYNGOL S S, V444, P1 NR 44 TC 64 Z9 64 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 21 EP 28 DI 10.1016/S0378-5955(00)00040-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000003 PM 10831862 ER PT J AU Abnet, CC Freeman, DM AF Abnet, CC Freeman, DM TI Deformations of the isolated mouse tectorial membrane produced by oscillatory forces SO HEARING RESEARCH LA English DT Article DE cochlea; tectorial membrane; magnetic bead; viscoelastic; mechanical coupling; anisotropy; micromechanics; mouse ID POLYELECTROLYTE GEL MODEL; COCHLEAR MICROMECHANICS; EQUILIBRIUM BEHAVIOR; LOCAL MEASUREMENTS; COLLAGEN; ORGAN; CORTI; GLYCOSAMINOGLYCANS; ORGANIZATION; PROTEOGLYCAN AB Mechanical properties of the isolated tectorial membrane (TM) of the mouse were measured by applying oscillatory shear forces to the TM with a magnetic bead (radius similar to 10 um). Sinusoidal forces at 10 Hz with amplitudes from 5 to 33 nN were applied tangentially to the surfaces of 11 TMs. The ratio of force to bead displacement ranged from 0.04 to 0.98 N/m (median: 0.18 N/m, interquartile range: 0.11-0.30 N/m, n = 90). Increasing frequency from 10 to 100 Hz decreased the magnitude of the displacement of the magnetic bead by 6-7.3 dB/decade. The phase of the displacement lagged that of the stimulus current by approximately 27-44 degrees across frequencies. Displacement of the adjacent tissue decreased as the distance from the magnetic bead increased. Space constants were of the order of tens of micrometers. Forces with equal amplitude and frequency were applied radially and longitudinally. Longitudinal displacements in response to longitudinal forces were 1-10 times as large as radial displacements in response to radial forces in 85% of 560 paired measurements. These results suggest that the following mechanical properties of the TM are important. (1) Viscoelasticity: The frequency dependence of TM displacement lies between that of a purely viscous and a purely elastic material, suggesting that both are important. (2) Mechanical coupling: Space constants indicate that hair bundles could interact mechanically with adjacent hair bundles via the TM. (3) Anisotropy: The mechanical impedance is greater in the radial direction than it is in the longitudinal direction. This mechanical anisotropy correlates with anatomical anisotropies, such as the radially oriented fibrillar structure of the TM. (C) 2000 Elsevier Science B.V. All rights reserved. C1 MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA. MIT, Dept Mech Engn, Cambridge, MA 02139 USA. MIT, Elect Res Lab, Cambridge, MA 02139 USA. Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, Boston, MA 02114 USA. RP Freeman, DM (reprint author), MIT, Dept Elect Engn & Comp Sci, Room 36-889,50 Vassar St, Cambridge, MA 02139 USA. CR ABNET CC, 1998, 21 MIDW RES M ST PET, P183 ABNET CC, 1997, 20 MIDW RES M ST PET, P13 ALLEN JB, 1980, J ACOUST SOC AM, V68, P1660, DOI 10.1121/1.385198 Bausch AR, 1998, BIOPHYS J, V75, P2038 Bekesy G., 1960, EXPT HEARING BILLONE M, 1973, J ACOUST SOC AM, V54, P1143, DOI 10.1121/1.1914361 COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 Davis CQ, 1998, OPT ENG, V37, P1290, DOI 10.1117/1.601966 Davis CQ, 1998, OPT ENG, V37, P1299, DOI 10.1117/1.601967 DAVIS H, 1958, Ann Otol Rhinol Laryngol, V67, P789 de Boer E., 1996, COCHLEA, P258 Freeman DM, 1997, AUDIT NEUROSCI, V3, P363 FREEMAN DM, 1986, LECT NOTES BIOMATH, V64, P147 GEISLER CD, 1986, HEARING RES, V24, P125, DOI 10.1016/0378-5955(86)90056-0 HARTOG J. P. D., 1956, MECH VIBRATIONS HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 HAYES WC, 1978, J BIOMECH, V11, P407, DOI 10.1016/0021-9290(78)90075-1 HUDSPETH AJ, 1978, AM J PHYSIOL, V234, pC56 JAMES SL, 1982, J PHYS E SCI INSTRUM, V15, P179, DOI 10.1088/0022-3735/15/2/008 JOHNSTON.JR, 1966, J ACOUST SOC AM, V40, P1405, DOI 10.1121/1.1910240 KEMPSON GE, 1973, BIOCHIM BIOPHYS ACTA, V297, P456, DOI 10.1016/0304-4165(73)90093-7 KING M, 1977, J APPL PHYSIOL, V42, P797 KOLSTON PJ, 1988, J ACOUST SOC AM, V83, P1481, DOI 10.1121/1.395903 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LUTZ RJ, 1973, RHEOLOGY BIOL SYSTEM MAMMANO F, 1993, J ACOUST SOC AM, V93, P3320, DOI 10.1121/1.405716 NAIDU RC, 1998, 21 MIDW RES M ST PET NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 Patuzzi R., 1996, COCHLEA, P186 RHODE WS, 1967, J ACOUST SOC AM, V42, P185, DOI 10.1121/1.1910547 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 Riché G., 1989, Cahiers de la Recherche-Développement, P57 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 Seifriz W, 1924, BR J EXP BIOL, V2, P1 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SHAH DM, 1995, HEARING RES, V87, P187, DOI 10.1016/0378-5955(95)00089-M STEEL KP, 1983, HEARING RES, V12, P265, DOI 10.1016/0378-5955(83)90111-9 STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 THALMANN I, 1993, ARCH BIOCHEM BIOPHYS, V307, P391, DOI 10.1006/abbi.1993.1605 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 THALMANN I, 1993, CONNECT TISSUE RES, V29, P191, DOI 10.3109/03008209309016826 Tortonese M, 1997, P SOC PHOTO-OPT INS, V3009, P53, DOI 10.1117/12.271229 Tortonese M, 1997, IEEE ENG MED BIOL, V16, P28, DOI 10.1109/51.582173 TRANSONTAY R, 1988, REV SCI INSTRUM, V59, P1399, DOI 10.1063/1.1139676 Tsuprun V, 1996, MATRIX BIOL, V15, P31, DOI 10.1016/S0945-053X(96)90124-9 WANG N, 1993, SCIENCE, V260, P1124, DOI 10.1126/science.7684161 Weiss TF, 1997, HEARING RES, V111, P55, DOI 10.1016/S0378-5955(97)00096-8 Weiss TF, 1997, AUDIT NEUROSCI, V3, P351 Yih C.-S., 1979, FLUID MECH Zahn M., 1979, ELECTROMAGNETIC FIEL ZANER KS, 1989, J CELL BIOL, V109, P2233, DOI 10.1083/jcb.109.5.2233 Zhu WB, 1996, J BIOMECH, V29, P773, DOI 10.1016/0021-9290(95)00136-0 ZIEMANN F, 1994, BIOPHYS J, V66, P2210 ZWISLOCKI JJ, 1980, HEARING RES, V2, P505, DOI 10.1016/0378-5955(80)90087-8 ZWISLOCKI JJ, 1979, ACTA OTO-LARYNGOL, V87, P267, DOI 10.3109/00016487909126419 ZWISLOCKI JJ, 1989, HEARING RES, V42, P211, DOI 10.1016/0378-5955(89)90146-9 ZWISLOCKI JJ, 1979, SCIENCE, V204, P639, DOI 10.1126/science.432671 NR 62 TC 42 Z9 42 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 29 EP 46 DI 10.1016/S0378-5955(00)00041-1 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000004 PM 10831863 ER PT J AU Sato, K Kuriyama, H Altschuler, RA AF Sato, K Kuriyama, H Altschuler, RA TI Expression of glycine receptor subunit mRNAs in the rat cochlear nucleus SO HEARING RESEARCH LA English DT Article DE glycine; in situ hybridization; auditory; brainstem ID AUDITORY BRAIN-STEM; SUPERIOR OLIVARY COMPLEX; GUINEA-PIG; MESSENGER-RNA; AUTORADIOGRAPHIC LOCALIZATION; REGIONAL DISTRIBUTION; GABAERGIC INPUTS; SPINAL-CORD; NEURONS; GABA AB The distribution of glycine receptor subunit mRNAs in the cochlear nucleus of the adult rat was examined using radioactive in situ hybridization. Expression was compared among six cell types by counting silver grains over somata. Expression of the immature alpha 2 subunit was not above the threshold for detection in any neurons. Levels of expression of mature subunits varied among different cell types. Spherical bushy, small cell cap/shell neurons and fusiform cells had high expression of glycine receptor mRNA for alpha 1, alpha 3 and beta subunits. Octopus cells and corn cells had high expression for alpha 3 and beta subunits, and only moderate expression for alpha 1 subunit. Granule cells located between the dorsal and ventral cochlear nucleus had moderate expression of alpha 3 and beta subunits and no detectable alpha 1 expression. These patterns of expression predict differences in glycinergic pharmacological properties between the cochlear nucleus neurons. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Kansai Med Univ, Dept Otolaryngol, Osaka, Japan. RP Altschuler, RA (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. EM shuler@umich.edu CR ADAMS JC, 1993, NATO ADV SCI INST SE, V239, P133 ALTSCHULER RA, 1986, BRAIN RES, V369, P316, DOI 10.1016/0006-8993(86)90542-1 ALTSCHULER RA, 1993, NATO ADV SCI INST SE, V239, P211 Backoff PM, 1997, HEARING RES, V110, P155, DOI 10.1016/S0378-5955(97)00081-6 BETZ H, 1988, NEUROCHEM INT, V13, P137, DOI 10.1016/0197-0186(88)90048-4 Betz H, 1991, Adv Exp Med Biol, V287, P421 Betz H, 1999, ANN NY ACAD SCI, V868, P667, DOI 10.1111/j.1749-6632.1999.tb11343.x CANT NB, 1984, HEARING SCI RECENT A, P371 CASPARY DM, 1985, AUDITORY BIOCH, P198 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 Caspary D.M., 1986, NEUROBIOLOGY HEARING, P303 CASPARY DM, 1993, NATO ADV SCI INST SE, V239, P239 Ehrlich I, 1998, NEUROREPORT, V9, P2785, DOI 10.1097/00001756-199808240-00019 EVANS EF, 1993, NATO ADV SCI INST SE, V239, P253 Friauf E, 1997, J COMP NEUROL, V385, P117, DOI 10.1002/(SICI)1096-9861(19970818)385:1<117::AID-CNE7>3.0.CO;2-5 FROSTHOLM A, 1985, BRAIN RES BULL, V15, P473, DOI 10.1016/0361-9230(85)90038-3 Fubara BM, 1996, J COMP NEUROL, V369, P83 FUJITA M, 1991, BRAIN RES, V560, P23, DOI 10.1016/0006-8993(91)91210-R GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 Godfrey DA, 1988, AUDITORY PATHWAY, P107 Golding NL, 1996, J NEUROSCI, V16, P2208 Harty TP, 1996, J NEUROPHYSIOL, V75, P2300 Harty TP, 1998, J NEUROPHYSIOL, V79, P1891 Hutson KA, 1996, J COMP NEUROL, V371, P397, DOI 10.1002/(SICI)1096-9861(19960729)371:3<397::AID-CNE4>3.0.CO;2-Y Juiz JM, 1996, J BRAIN RES, V37, P561 Juiz JM, 1996, J COMP NEUROL, V373, P11, DOI 10.1002/(SICI)1096-9861(19960909)373:1<11::AID-CNE2>3.0.CO;2-G KAKEHATA S, 1992, BRAIN RES, V574, P21, DOI 10.1016/0006-8993(92)90794-A KOLSTON J, 1992, ANAT EMBRYOL, V186, P443 KUHSE J, 1990, NEURON, V5, P867, DOI 10.1016/0896-6273(90)90346-H KUHSE J, 1990, J BIOL CHEM, V265, P22317 Kungel M, 1997, DEV BRAIN RES, V102, P157, DOI 10.1016/S0165-3806(97)00087-4 MALOSIO ML, 1991, EMBO J, V10, P2401 MARTIN MR, 1982, NEUROPHARMACOLOGY, V21, P201, DOI 10.1016/0028-3908(82)90188-5 MOORE JK, 1986, NEUROBIOLOGY HEARING, P283 OERTEL D, 1993, NATO ADV SCI INST SE, V239, P225 Ostapoff EM, 1997, J COMP NEUROL, V381, P500, DOI 10.1002/(SICI)1096-9861(19970519)381:4<500::AID-CNE9>3.0.CO;2-6 PFEIFFER F, 1984, P NATL ACAD SCI-BIOL, V81, P7224, DOI 10.1073/pnas.81.22.7224 POTASHNER SJ, 1993, NATO ADV SCI INST SE, V239, P195 PRIBILLA I, 1992, EMBO J, V11, P4305 RAMAN IM, 1992, NEURON, V9, P173, DOI 10.1016/0896-6273(92)90232-3 SANES DH, 1987, J NEUROSCI, V7, P3793 SATO K, 1991, NEUROSCIENCE, V43, P381, DOI 10.1016/0306-4522(91)90302-5 SATO K, 1992, BRAIN RES, V590, P95, DOI 10.1016/0006-8993(92)91085-S Sato K, 1995, HEARING RES, V91, P7, DOI 10.1016/0378-5955(95)00156-5 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 TRUSSELL LO, 1989, NEURON, V3, P209, DOI 10.1016/0896-6273(89)90034-2 Trussell LO, 1999, ANNU REV PHYSIOL, V61, P477, DOI 10.1146/annurev.physiol.61.1.477 VANDENPOL AN, 1988, J NEUROSCI, V8, P472 WENTHOLD RJ, 1990, GLYCINE NEUROTRANSMI, P391 WENTHOLD RJ, 1988, J COMP NEUROL, V276, P423, DOI 10.1002/cne.902760307 Wenthold RJ, 1991, NEUROBIOLOGY HEARING, P121 WICKESBERG RE, 1993, MAMMALIAN COCHLEAR N, P77 WU SH, 1986, J NEUROSCI, V6, P2691 ZARBIN MA, 1981, J NEUROSCI, V1, P532 NR 54 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 47 EP 52 DI 10.1016/S0378-5955(00)00044-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000005 PM 10831864 ER PT J AU Mulders, WHAM Robertson, D AF Mulders, WHAM Robertson, D TI Morphological relationships of peptidergic and noradrenergic nerve terminals to olivocochlear neurones in the rat SO HEARING RESEARCH LA English DT Article DE superior olivary complex; hearing; substance P; noradrenaline; cholecystokinin; enkephalin ID SUPERIOR OLIVARY COMPLEX; AUDITORY BRAIN-STEM; ROSTRAL PERIOLIVARY REGIONS; TEMPORARY THRESHOLD SHIFTS; IN-SITU HYBRIDIZATION; SUBSTANCE-P RECEPTOR; EFFERENT NEURONS; INFERIOR COLLICULUS; GUINEA-PIG; IMMUNOHISTOCHEMICAL LOCALIZATION AB In the rat, the outer hair cells in the cochlea receive direct synaptic input from neurones in the ventral nucleus of the trapezoid body. These so-called medial olivocochlear neurones exert an inhibitory influence on the cochlear neural output. Electrophysiological in vitro studies suggest that the activity of medial olivocochlear neurones may be affected by a variety of neuropeptides as well as noradrenaline, but anatomical confirmation of direct synaptic input is still lacking. We have investigated, at the light microscopical level, the morphological relationships between terminals containing noradrenaline, substance P, cholecystokinin and leu-enkephalin, and medial olivocochlear neurones in the rat. A retrograde tracer was injected into the cochlea to label medial olivocochlear neurones and a double labelling immunocytochemical method was used to visualise the retrograde tracer as well as the neurotransmitters within each brain section. Light microscopical analysis revealed nerve endings containing substance P, cholecystokinin and leu-enkephalin in close apposition to the dendrites of medial olivocochlear neurones, and nerve endings containing dopamine-beta-hydroxylase, a marker for noradrenaline. in close contact with the somata as well as dendrites of medial olivocochlear neurones. Although the technique cannot prove the existence of functional synaptic contacts, the results are broadly consistent with electrophysiological data and suggest a direct input to medial olivocochlear neurones from substance P, cholecystokinin, leu-enkephalin and noradrenaline-containing neural pathways. Differences in the densities and spatial distribution of the various neuropharmacological inputs suggest differences in the relative strengths and possible roles of these diverse inputs to the olivocochlear system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. RP Robertson, D (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. CR Adams J. C., 1996, Society for Neuroscience Abstracts, V22, P127 ALTSCHULER RA, 1983, NEUROSCIENCE, V9, P621, DOI 10.1016/0306-4522(83)90178-1 Brown MC, 1998, J NEUROPHYSIOL, V79, P3088 BROWN MC, 1993, J COMP NEUROL, V337, P600, DOI 10.1002/cne.903370406 CALVERLEY RKS, 1990, BRAIN RES REV, V15, P215, DOI 10.1016/0165-0173(90)90002-6 FALLON JH, 1984, NEUROSCI LETT, V45, P81, DOI 10.1016/0304-3940(84)90333-1 FINLEY JCW, 1981, J COMP NEUROL, V198, P541, DOI 10.1002/cne.901980402 Giraud AL, 1995, BRAIN RES, V705, P15, DOI 10.1016/0006-8993(95)01091-2 Giraud AL, 1997, NEUROREPORT, V8, P1779 Hienz RD, 1998, HEARING RES, V116, P10, DOI 10.1016/S0378-5955(97)00197-4 HOFFMAN DW, 1993, HEARING RES, V69, P1, DOI 10.1016/0378-5955(93)90087-H KIYAMA H, 1983, NEUROSCIENCE, V10, P1341, DOI 10.1016/0306-4522(83)90116-1 KLEPPER A, 1991, BRAIN RES, V557, P190, DOI 10.1016/0006-8993(91)90134-H KUBOTA Y, 1983, NEUROSCIENCE, V9, P587, DOI 10.1016/0306-4522(83)90176-8 LEVITT P, 1979, J COMP NEUROL, V186, P505, DOI 10.1002/cne.901860402 LIU HT, 1994, P NATL ACAD SCI USA, V91, P1009, DOI 10.1073/pnas.91.3.1009 LlewellynSmith IJ, 1997, NEUROSCIENCE, V77, P1137, DOI 10.1016/S0306-4522(96)00534-9 MAENO H, 1993, MOL BRAIN RES, V18, P43, DOI 10.1016/0169-328X(93)90172-L MAGEE JC, 1995, SCIENCE, V268, P301, DOI 10.1126/science.7716525 MARKRAM H, 1994, P NATL ACAD SCI USA, V91, P5207, DOI 10.1073/pnas.91.11.5207 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 NAKAYA Y, 1994, J COMP NEUROL, V347, P249, DOI 10.1002/cne.903470208 OSTAPOFF EM, 1991, J COMP NEUROL, V314, P598, DOI 10.1002/cne.903140314 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V RAJAN R, 1988, J NEUROPHYSIOL, V60, P569 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 Reuss S, 1999, CELL TISSUE RES, V297, P13, DOI 10.1007/s004410051329 Robertson D, 1996, AUDIT NEUROSCI, V2, P15 ROBERTSON D, 1994, BRAIN RES, V646, P37, DOI 10.1016/0006-8993(94)90055-8 ROBERTSON D, 1989, DEV BRAIN RES, V47, P197, DOI 10.1016/0165-3806(89)90176-4 RYAN AF, 1991, EXP BRAIN RES, V87, P259 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SAR M, 1978, J COMP NEUROL, V182, P17, DOI 10.1002/cne.901820103 Scharf B, 1997, HEARING RES, V103, P101, DOI 10.1016/S0378-5955(96)00168-2 SCHIFFMANN SN, 1991, J COMP NEUROL, V304, P219, DOI 10.1002/cne.903040206 THOMPSON AM, 1995, BRAIN RES, V695, P263, DOI 10.1016/0006-8993(95)00863-L VETTER DE, 1993, HEARING RES, V70, P173, DOI 10.1016/0378-5955(93)90156-U VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 VETTER DE, 1992, ANAT EMBRYOL, V185, P1, DOI 10.1007/BF00213596 Wang XY, 1997, HEARING RES, V106, P20, DOI 10.1016/S0378-5955(96)00211-0 Wang XY, 1998, J NEUROPHYSIOL, V80, P218 Wang XY, 1998, HEARING RES, V116, P86, DOI 10.1016/S0378-5955(97)00203-7 Wang XY, 1997, J NEUROPHYSIOL, V78, P1800 Warr WB, 1997, HEARING RES, V108, P89, DOI 10.1016/S0378-5955(97)00044-0 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WILLIAMS RG, 1983, NEUROSCIENCE, V9, P563, DOI 10.1016/0306-4522(83)90175-6 Woods CI, 1999, BRAIN RES, V836, P9, DOI 10.1016/S0006-8993(99)01541-3 WOUTERLOOD FG, 1985, BRAIN RES, V326, P188, DOI 10.1016/0006-8993(85)91402-7 Wynne B, 1995, J CHEM NEUROANAT, V9, P289, DOI 10.1016/0891-0618(95)00095-X Wynne B, 1997, J CHEM NEUROANAT, V12, P259, DOI 10.1016/S0891-0618(97)00219-6 Wynne B, 1996, Audiol Neurootol, V1, P54 NR 53 TC 20 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 53 EP 64 DI 10.1016/S0378-5955(00)00045-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000006 PM 10831865 ER PT J AU Mulders, WHAM Robertson, D AF Mulders, WHAM Robertson, D TI Evidence for direct cortical innervation of medial olivocochlear neurones in rats SO HEARING RESEARCH LA English DT Article DE hearing; auditory cortex; immunocytochemistry; anterograde labelling; retrograde labelling; olivocochlear efferent ID AUDITORY-NERVE FIBERS; INFERIOR COLLICULUS; COCHLEAR NUCLEUS; DESCENDING PROJECTIONS; CHOLERA-TOXIN; BRAIN-STEM; GUINEA-PIG; PHA-L; CORTEX; CONNECTIONS AB We have investigated the morphological relationship between auditory cortex efferents and medial olivocochlear neurones. Using combined retrograde and anterograde tracing we describe close contacts between medial olivocochlear neurones and corticofugal terminals in the ventral nucleus of the trapezoid body. The data indicate a possible direct action of the auditory cortex on the activity of the medial olivocochlear neurones and thus possibly the sensitivity of the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. RP Robertson, D (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. CR ARNAULT P, 1990, J COMP NEUROL, V302, P110, DOI 10.1002/cne.903020109 Benson TE, 1996, J COMP NEUROL, V365, P27 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 CAICEDO A, 1993, J COMP NEUROL, V328, P377, DOI 10.1002/cne.903280305 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 Feliciano M. E., 1995, AUDIT NEUROSCI, V1, P287 GAMES KD, 1988, HEARING RES, V34, P1, DOI 10.1016/0378-5955(88)90047-0 Ghoshal S, 1996, NEUROSCI LETT, V205, P71, DOI 10.1016/0304-3940(96)12386-7 HERBERT H, 1991, J COMP NEUROL, V304, P103, DOI 10.1002/cne.903040108 KIM DO, 1995, ACTIVE HEARING, P31 LIBERMAN MC, 1993, J COMP NEUROL, V327, P17, DOI 10.1002/cne.903270103 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 Paxinos G., 1982, RAT BRAIN STEREOTAXI ROGER M, 1989, J COMP NEUROL, V287, P339, DOI 10.1002/cne.902870306 RYAN AF, 1990, J COMP NEUROL, V300, P572, DOI 10.1002/cne.903000410 Saldana E, 1996, J COMP NEUROL, V371, P15, DOI 10.1002/(SICI)1096-9861(19960715)371:1<15::AID-CNE2>3.0.CO;2-O Swanson LW, 1992, BRAIN MAPS STRUCTURE THOMPSON AM, 1993, J COMP NEUROL, V335, P402, DOI 10.1002/cne.903350309 Tsuji J, 1997, J COMP NEUROL, V381, P188 VETTER DE, 1993, HEARING RES, V70, P173, DOI 10.1016/0378-5955(93)90156-U VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 VETTER DE, 1992, ANAT EMBRYOL, V185, P1, DOI 10.1007/BF00213596 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 Weedman DL, 1996, BRAIN RES, V706, P97, DOI 10.1016/0006-8993(95)01201-X WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WINER JA, 1987, J COMP NEUROL, V257, P282, DOI 10.1002/cne.902570212 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E WOUTERLOOD FG, 1985, BRAIN RES, V326, P188, DOI 10.1016/0006-8993(85)91402-7 NR 28 TC 66 Z9 67 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 65 EP 72 DI 10.1016/S0378-5955(00)00046-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000007 PM 10831866 ER PT J AU Spezio, ML Keller, CH Marrocco, RT Takahashi, TT AF Spezio, ML Keller, CH Marrocco, RT Takahashi, TT TI Head-related transfer functions of the Rhesus monkey SO HEARING RESEARCH LA English DT Article DE sound localization; virtual auditory space; binaural cue; spectral cue; ear canal; auditory perception ID PRIMATE SUPERIOR COLLICULUS; AUDITORY-CORTEX LESIONS; EAR TRANSFER-FUNCTIONS; SOUND LOCALIZATION; EXTERNAL-EAR; JAPANESE MACAQUES; AREA LIP; CAT; SIMULATION; PERIPHERY AB Head-related transfer functions (HRTFs) are direction-specific acoustic filters formed by the head, the pinnae and the ear canals. They can be used to assess acoustical cues available for sound localization and to construct virtual auditory environments. We measured the HRTFs of three anesthetized Rhesus monkeys (Macaca mulatta) from 591 locations in the frontal hemisphere ranging from -90 degrees (left) to 90 degrees (right) in azimuth and -60 degrees (down) to 90 degrees (up) in elevation for frequencies between 0.5 and 15 kHz. Acoustic validation of the HRTFs shows good agreement between free field and virtual sound sources. Monaural spectra exhibit deep notches at frequencies above 9 kHz, providing putative cues for elevation discrimination. Interaural level differences (ILDs) and interaural time differences (ITDs) generally vary monotonically with azimuth between 0.5 and 8 kHz, suggesting that these two cues can be used to discriminate azimuthal position. Comparison with published subsets of HRTFs from squirrel monkeys (Saimiri sciureus) shows good agreement. Comparison with published human HRTFs from the frontal hemisphere demonstrates overall similarity in the patterns of ILD and ITD, suggesting that the Rhesus monkey is a good acoustic model for these two sound localization cues in humans. Finally, the measured ITDs in the horizontal plane agree well between -40 degrees and 40 degrees in azimuth with those calculated from a spherical head model with a radius of 52 mm, one-half the interaural distance of the monkey. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Oregon, Inst Neurosci, Eugene, OR 97403 USA. RP Spezio, ML (reprint author), Univ Oregon, Inst Neurosci, Eugene, OR 97403 USA. CR Blauert J., 1997, SPATIAL HEARING BROWN CH, 1980, J ACOUST SOC AM, V68, P127, DOI 10.1121/1.384638 BROWN CH, 1978, SCIENCE, V201, P753, DOI 10.1126/science.97785 BRUGGE JF, 1994, HEARING RES, V73, P67, DOI 10.1016/0378-5955(94)90284-4 CARLILE S, 1990, J ACOUST SOC AM, V88, P2180, DOI 10.1121/1.400115 CARLILE S, 1990, J ACOUST SOC AM, V88, P2196, DOI 10.1121/1.400116 GOUREVITCH G, 1970, ANIMAL PSYCHOPHYSICS, P67 HARRISON JM, 1970, J ACOUST SOC AM, V47, P1509, DOI 10.1121/1.1912082 Hartmann W. M., 1998, SIGNALS SOUND SENSAT Hartung K, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P407, DOI 10.1007/978-1-4419-8712-9_37 Heffner H E, 1997, Acta Otolaryngol Suppl, V532, P22 HEFFNER HE, 1986, J NEUROPHYSIOL, V55, P256 HEFFNER HE, 1990, J NEUROPHYSIOL, V64, P915 HOCHERMAN S, 1976, BRAIN RES, V117, P51, DOI 10.1016/0006-8993(76)90555-2 Hofman PM, 1998, NAT NEUROSCI, V1, P417, DOI 10.1038/1633 HOUBEN D, 1979, J ACOUST SOC AM, V66, P1057, DOI 10.1121/1.383377 JAY MF, 1987, J NEUROPHYSIOL, V57, P35 JAY MF, 1984, NATURE, V309, P345, DOI 10.1038/309345a0 KELLER CH, 1998, M SOC NEUR LOS ANG C Keller CH, 1998, HEARING RES, V118, P13, DOI 10.1016/S0378-5955(98)00014-8 KUHN GF, 1977, J ACOUST SOC AM, V62, P157, DOI 10.1121/1.381498 LARSEN ON, 1996, ARO ABSTR, V19, P205 MARROCCO RT, 1987, J NEUROSCI, V7, P2756 Mazzoni P, 1996, J NEUROPHYSIOL, V75, P1233 MEHRGARDT S, 1977, J ACOUST SOC AM, V61, P1567, DOI 10.1121/1.381470 MELLERT V, 1974, J ACOUST SOC AM, V56, P1913, DOI 10.1121/1.1903534 Middlebrooks JC, 1999, J ACOUST SOC AM, V106, P1493, DOI 10.1121/1.427147 MIDDLEBROOKS JC, 1989, J ACOUST SOC AM, V86, P89, DOI 10.1121/1.398224 MIDDLEBROOKS JC, 1990, J ACOUST SOC AM, V87, P2149, DOI 10.1121/1.399183 Middlebrooks JC, 1999, J ACOUST SOC AM, V106, P1480, DOI 10.1121/1.427176 MUSICANT AD, 1990, J ACOUST SOC AM, V87, P757, DOI 10.1121/1.399545 Populin LC, 1998, J NEUROSCI, V18, P4233 Proakis J. G., 1996, DIGITAL SIGNAL PROCE Rauschecker J P, 1997, Acta Otolaryngol Suppl, V532, P34 Rauschecker JP, 1997, J COMP NEUROL, V382, P89 Rauschecker JP, 1998, AUDIOL NEURO-OTOL, V3, P86, DOI 10.1159/000013784 SHAW EAG, 1968, J ACOUST SOC AM, V44, P240, DOI 10.1121/1.1911059 Stricanne B, 1996, J NEUROPHYSIOL, V76, P2071 TERANISH.R, 1968, J ACOUST SOC AM, V44, P257, DOI 10.1121/1.1911061 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P858, DOI 10.1121/1.397557 Woodworth R. S., 1938, EXPT PSYCHOL NR 41 TC 32 Z9 32 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 73 EP 88 DI 10.1016/S0378-5955(00)00050-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000008 PM 10831867 ER PT J AU Halmos, G Gaborjan, A Lendvai, B Repassy, G Szabo, LZ Vizi, ES AF Halmos, G Gaborjan, A Lendvai, B Repassy, G Szabo, LZ Vizi, ES TI Veratridine-evoked release of dopamine from guinea pig isolated cochlea SO HEARING RESEARCH LA English DT Article DE dopamine release; glutamate receptor antagonist; in vitro superfusion method; veratridine ID EFFERENT INNERVATION; MAMMALIAN COCHLEA; STRIATAL SLICES; HAIR-CELLS; RAT; CHANNELS; MODULATION; INNER; NEUROTRANSMITTERS; PATHOPHYSIOLOGY AB Dopamine released from the lateral olivocochlear efferent system is thought to inhibit the toxic effect of the extreme glutamate outflow from the inner hair cells during ischemia or acoustic trauma. Using in vitro microvolume superfusion, we have studied the release of [H-3]dopamine from the lateral olivocochlear efferent bundle of guinea pig in response to accumulation of [Na+](i), under condition characteristics of ischemia. Veratridine, that acts only on excitable membranes as a specific activator of voltage-sensitive sodium channels, significantly increased the electrically evoked release of [H-3]dopamine, which was completely inhibited by tetrodotoxin. Dizocilpine (MK-801), a non-competitive NMDA-receptor antagonist, and GYKI-52466, a selective non-NMDA-receptor antagonist, had no effect on veratridine-induced [H-3]dopamine release. Our data provide further evidence that the cochlear release of dopamine is of neural origin and possibly independent on a local effect of glutamate. The veratridine-induced transmitter release in the cochlea will be a very useful method in studying the effect of drugs on ischemic injury. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hungarian Acad Sci, Inst Expt Med, Dept Pharmacol, H-1450 Budapest, Hungary. Semmelweis Univ, Fac Hlth Sci, Dept Otorhinolaryngol, Budapest, Hungary. Semmelweis Univ, Fac Med, Dept Otorhinolaryngol Head & Neck Surg, Budapest, Hungary. RP Vizi, ES (reprint author), Hungarian Acad Sci, Inst Expt Med, Dept Pharmacol, POB 67, H-1450 Budapest, Hungary. CR ADAMVIZI V, 1993, J PHYSIOLOGY-PARIS, V87, P43, DOI 10.1016/0928-4257(93)90023-M ADAMVIZI V, 1991, J NEUROCHEM, V56, P52, DOI 10.1111/j.1471-4159.1991.tb02561.x BERGLUND AM, 1987, J COMP NEUROL, V255, P560, DOI 10.1002/cne.902550408 BILLETT TE, 1989, HEARING RES, V41, P189, DOI 10.1016/0378-5955(89)90010-5 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 CARVALHO CM, 1995, BRAIN RES, V669, P234, DOI 10.1016/0006-8993(94)01252-D CATTERALL WA, 1980, ANNU REV PHARMACOL, V20, P15, DOI 10.1146/annurev.pa.20.040180.000311 DALDIN C, 1995, EUR ARCH OTO-RHINO-L, V252, P270 DALDIN C, 1995, HEARING RES, V90, P202, DOI 10.1016/0378-5955(95)00167-5 DALLOS P, 1985, J NEUROSCI, V5, P1597 DIAMANT S, 1987, FEBS LETT, V219, P445, DOI 10.1016/0014-5793(87)80269-7 EYBALIN M, 1993, NEUROSCIENCE, V54, P133, DOI 10.1016/0306-4522(93)90389-W EYBALIN M, 1983, NEUROSCIENCE, V9, P863, DOI 10.1016/0306-4522(83)90274-9 EYBALIN M, 1989, ARCH OTO-RHINO-LARYN, V246, P228, DOI 10.1007/BF00463561 EYBALIN M, 1993, PHYSIOL REV, V73, P309 Gaborjan A, 1999, NEUROSCIENCE, V90, P131, DOI 10.1016/S0306-4522(98)00461-8 Gaborjan A, 1999, NEUROSCI LETT, V269, P49, DOI 10.1016/S0304-3940(99)00410-3 GILLOYZAGA P, 1993, BRAIN RES, V623, P177, DOI 10.1016/0006-8993(93)90027-K GILLOYZAGA PE, 1995, ACTA OTO-LARYNGOL, V115, P222, DOI 10.3109/00016489509139296 GODFREY DA, 1976, J HISTOCHEM CYTOCHEM, V24, P468 Haruta A, 1998, Acta Otolaryngol Suppl, V539, P44 IKEDA K, 1991, AM J PHYSIOL, V261, pC231 Karadaghy AA, 1997, MOL BRAIN RES, V44, P151, DOI 10.1016/S0169-328X(96)00261-6 KISS JP, 1994, BRAIN RES, V641, P145, DOI 10.1016/0006-8993(94)91828-7 Matsubara A, 1998, Acta Otolaryngol Suppl, V539, P48 Milusheva EA, 1996, NEUROCHEM INT, V28, P501, DOI 10.1016/0197-0186(95)00129-8 Oestreicher E, 1997, HEARING RES, V107, P46, DOI 10.1016/S0378-5955(97)00023-3 Ohmori H, 1996, NEWS PHYSIOL SCI, V11, P161 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PUEL JL, 1988, HEARING RES, V37, P65, DOI 10.1016/0378-5955(88)90078-0 Puel JL, 1995, PROG NEUROBIOL, V47, P449, DOI 10.1016/0301-0082(95)00028-3 PUJOL R, 1993, ACTA OTO-LARYNGOL, V113, P330, DOI 10.3109/00016489309135819 PUJOL R, 1994, BRIT J AUDIOL, V28, P185, DOI 10.3109/03005369409086567 Pujol R, 1990, Acta Otolaryngol Suppl, V476, P32 PUJOL R, 1995, NEWS PHYSIOL SCI, V10, P178 Safieddine S, 1997, EUR J NEUROSCI, V9, P356, DOI 10.1111/j.1460-9568.1997.tb01405.x SCHOFFELMEER ANM, 1983, N-S ARCH PHARMACOL, V323, P188, DOI 10.1007/BF00497661 STYS PK, 1992, J NEUROSCI, V12, P430 Tarnawa I, 1998, RESTOR NEUROL NEUROS, V13, P41 ULBRICHT W, 1998, REV PHYSL BIOCH PHAR, V133, P4 Usami S, 1988, Acta Otolaryngol Suppl, V447, P36 Vizi E. S., 1996, CNS DRUG REV, V2, P91, DOI 10.1111/j.1527-3458.1996.tb00292.x Vizi ES, 1998, HIPPOCAMPUS, V8, P566, DOI 10.1002/(SICI)1098-1063(1998)8:6<566::AID-HIPO2>3.0.CO;2-W VIZI ES, 1985, NEUROSCIENCE, V16, P907, DOI 10.1016/0306-4522(85)90105-8 Warr WB, 1997, HEARING RES, V108, P89, DOI 10.1016/S0378-5955(97)00044-0 NR 45 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 89 EP 96 DI 10.1016/S0378-5955(00)00053-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000009 PM 10831868 ER PT J AU Jovanovic, S Jamali, Y Anft, D Schonfeld, U Scherer, H Muller, G AF Jovanovic, S Jamali, Y Anft, D Schonfeld, U Scherer, H Muller, G TI Influence of pulsed laser irradiation on the morphology and function of the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE laser stapedotomy; Er : YSGG laser; Ho : YAG laser; guinea pig cochlea; scanning electron microscopy; compound action potential ID STAPES FOOTPLATE; STAPEDOTOMY; SYSTEMS; NOISE; SUITABILITY; EXPOSURE; DAMAGE; ORGAN; CORTI; ION AB Recent experimental and clinical studies have demonstrated that several pulsed laser systems are also suitable for stapedotomy. The aim of the study was to investigate morphological and functional inner ear changes after irradiating the basal turn of the guinea pig cochlea with two pulsed laser systems of different wavelengths. The Er:YSGG (lambda = 2.78 mu m) and Ho:YAG (lambda = 2.1 mu m) lasers were used applying the laser energies necessary for perforating a human stapes footplate. The cochleas were removed 90 min, 1 day 2 weeks, or 4 weeks after laser application. Acoustic evoked potentials (compound action potentials) were measured before and after laser application and at the above times immediately before removal of the cochleas. The organ of Corti was examined by scanning electron microscopy. Application of Er:YSGG laser parameters effective for stapedotomy had no adverse effects on Corti's organ in the guinea pig cochlea. On the other hand, effective Ho:YAG laser parameters cause damage to the outer hair cells with fusion of. stereocilia and formation of giant cilia leading to partial or total cell loss. The inner hair cells and supporting cells were usually normal. These morphological data show a good correlation with the electrophysiological measurements. Our results clearly demonstrate that, besides achieving efficient bone management, the Er:YSGG laser has high application safety. On the other hand, the Ho:YAG laser is not well tolerated in our animal study. Its use in stapedotomy would be unreliable and dangerous for the inner ear. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Free Univ Berlin, Univ Med Ctr Benjamin Franklin, ENT Dept, D-12200 Berlin, Germany. Univ Halle Wittenberg, Clin Otorhinolaryngol Face & Neck Surg, Halle, Germany. Free Univ Berlin, Univ Med Ctr Benjamin Franklin, Inst Med Tech Phys & Laser Med, D-12200 Berlin, Germany. RP Jovanovic, S (reprint author), Free Univ Berlin, Univ Med Ctr Benjamin Franklin, ENT Dept, Hindenburgerdamm 30, D-12200 Berlin, Germany. CR BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 DUVALL AJ, 1967, ANN OTO RHINOL LARYN, V76, P688 GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 HAMERNIK RP, 1984, HEARING RES, V13, P229, DOI 10.1016/0378-5955(84)90077-7 JOVANOVIC S, 1999, AM J OTOL, V20, P1 JOVANOVIC S, 1995, EUR ARCH OTO-RHINO-L, V252, P422 JOVANOVIC S, 1990, ARCH OTORHINOLARYN S, V2, P73 Jovanovic S, 1998, LASER SURG MED, V23, P7, DOI 10.1002/(SICI)1096-9101(1998)23:1<7::AID-LSM2>3.0.CO;2-T Jovanovic S, 1997, LASER SURG MED, V21, P341, DOI 10.1002/(SICI)1096-9101(1997)21:4<341::AID-LSM5>3.0.CO;2-Q Jovanovic S, 1996, LASER SURG MED, V19, P424, DOI 10.1002/(SICI)1096-9101(1996)19:4<424::AID-LSM7>3.0.CO;2-U KAUTZKY M, 1991, EUR ARCH OTO-RHINO-L, V248, P449, DOI 10.1007/BF00627632 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 MCDOWELL EM, 1976, ARCH PATHOL LAB MED, V100, P405 PFALZ R, 1994, EUR ARCH OTO-RHINO-L, V2, P36 PFALZ R, 1995, LARYNGO RHINO OTOL, V74, P21, DOI 10.1055/s-2007-997680 Pfander F., 1975, KNALLTRAUMA Pratistio H, 1996, LASER SURG MED, V18, P100, DOI 10.1002/(SICI)1096-9101(1996)18:1<100::AID-LSM14>3.0.CO;2-D ROMANO V, 1993, P SOC PHOTO-OPT INS, V2077, P87 Rydmarker S, 1987, Acta Otolaryngol Suppl, V441, P3 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SCHONFELD U, 1994, EUR ARCH OTO-RHINO-L, V2, P244 SOUDIJN ER, 1976, ANN OTOL RHINOL LA S, V29, P1 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 STUBIG IM, 1993, P SOC PHOTO-OPT INS, V1876, P10, DOI 10.1117/12.147017 THOMA J, 1986, ANN OTO RHINOL LARYN, V95, P126 NR 25 TC 9 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 97 EP 108 DI 10.1016/S0378-5955(00)00058-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000010 PM 10831869 ER PT J AU Mire, P Nasse, J Venable-Thibodeaux, S AF Mire, P Nasse, J Venable-Thibodeaux, S TI Gap junctional communication in the vibration-sensitive response of sea anemones SO HEARING RESEARCH LA English DT Article DE hair cell; hair bundle; gap junction; connexin ID HAIR BUNDLES; INNER-EAR; TRANSDUCTION CHANNELS; PROTEIN CONNEXIN-43; CELLS; PHOSPHORYLATION; ULTRASTRUCTURE; LOCALIZATION; NEMATOCYSTS; COMPLEXES AB Although gap junctions occur in auditory and vestibular systems, their function is unclear. Here we present evidence for gap junctional communication in transmitting mechanosensory signals in a sea anemone model system. Hair bundles on anemone tentacles are vibration-sensitive mechanoreceptors that regulate discharge of nematocyst from effector cells. We find that vibration-dependent nematocyst discharge is selectively and reversibly blocked by the gap junction uncouplers, heptanol and arachidonic acid. Epidermal cells within excised tentacles exhibit a low level of dye coupling which is significantly enhanced upon deflection of overlying hair bundles. Dye coupling is inhibited both by gap junction uncouplers and by agents that interfere with mechanotransduction, including streptomycin and elastase. Electrophysiological data suggest gap junctional communication between cells giving rise to different hair bundles. When hair bundles are stimulated with a sweep of vibrations, individual cells show responses to five to eight frequencies. The number of responsive frequencies is reduced to one or two by heptanol and essentially abolished with streptomycin treatment. Immunoreactivity to the gap junction protein, connexin 43, is abundant in the tentacle epidermis and localized to membranes at junctions between several cell types. Small areas of close membrane apposition are observed between these cell types with intermembrane clefts of 4-7 nm. Of the several membrane proteins isolated from tentacles, immunoreactivity to connexin 43 is observed in a single band with an apparent molecular weight of approximately 46 kDa. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Louisiana, Dept Biol, Lafayette, LA 70504 USA. RP Mire, P (reprint author), Univ Louisiana, Dept Biol, Lafayette, LA 70504 USA. EM pmt9606@louisiana.edu CR Beyer E C, 1993, Int Rev Cytol, V137C, P1 DETWILER PB, 1973, J GEN PHYSIOL, V62, P618, DOI 10.1085/jgp.62.5.618 DUNN RA, 1975, P NATL ACAD SCI USA, V72, P3599, DOI 10.1073/pnas.72.9.3599 Germain G, 1996, BIOL BULL, V191, P353, DOI 10.2307/1543008 Goodenough DA, 1996, ANNU REV BIOCHEM, V65, P475, DOI 10.1146/annurev.bi.65.070196.002355 HUDSPETH AJ, 1992, SOC GEN PHY, V47, P357 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LEITCH B, 1992, ELECTRON MICROSC REV, V5, P311, DOI 10.1016/0892-0354(92)90014-H MARISCAL RN, 1978, SCANNING ELECTRON MI, V2, P959 MASUDA M, 1995, ANAT REC, V242, P267, DOI 10.1002/ar.1092420217 MILLER MR, 1990, J COMP NEUROL, V293, P223, DOI 10.1002/cne.902930206 Mire P, 1997, HEARING RES, V113, P224, DOI 10.1016/S0378-5955(97)00145-7 MIRETHIBODEAUX P, 1994, J EXP ZOOL, V270, P517, DOI 10.1002/jez.1402700605 MIRETHIBODEAUX P, 1994, J EXP ZOOL, V268, P282, DOI 10.1002/jez.1402680404 MUSIL LS, 1990, J CELL BIOL, V111, P2077, DOI 10.1083/jcb.111.5.2077 MUSIL LS, 1990, J MEMBRANE BIOL, V116, P163, DOI 10.1007/BF01868674 NADOL JB, 1976, AM J ANAT, V147, P281, DOI 10.1002/aja.1001470304 OESTERLE EC, 1992, J COMP NEUROL, V318, P64, DOI 10.1002/cne.903180105 PAUL DL, 1995, CURR OPIN CELL BIOL, V7, P665, DOI 10.1016/0955-0674(95)80108-1 PETEYA DJ, 1975, TISSUE CELL, V7, P243, DOI 10.1016/0040-8166(75)90003-8 Phelan P, 1998, TRENDS GENET, V14, P348, DOI 10.1016/S0168-9525(98)01547-9 Simon AM, 1998, TRENDS CELL BIOL, V8, P477, DOI 10.1016/S0962-8924(98)01372-5 Simon AM, 1999, TRENDS CELL BIOL, V9, P169, DOI 10.1016/S0962-8924(99)01547-0 Toyofuku T, 1998, J BIOL CHEM, V273, P12725, DOI 10.1074/jbc.273.21.12725 WARNER A, 1988, J CELL SCI, V89, P1 Watson GM, 1997, HEARING RES, V107, P53, DOI 10.1016/S0378-5955(97)00022-1 Watson GM, 1998, J EXP ZOOL, V281, P582 Watson GM, 1998, HEARING RES, V115, P119, DOI 10.1016/S0378-5955(97)00185-8 WATSON GM, 1994, INT REV CYTOL, V156, P275 WESTFALL JA, 1993, BIOL BULL, V185, P109, DOI 10.2307/1542134 Williamson Roddy, 1995, P503 WTSON GM, 1999, CURR TOP DEV BIOL, V43, P51 NR 34 TC 26 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 109 EP 123 DI 10.1016/S0378-5955(00)00047-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000011 PM 10831870 ER PT J AU Slepecky, NB Galsky, MD Swartzentruber-Martin, H Savage, J AF Slepecky, NB Galsky, MD Swartzentruber-Martin, H Savage, J TI Study of afferent nerve terminals and fibers in the gerbil cochlea: distribution by size SO HEARING RESEARCH LA English DT Article DE auditory nerve; cochlea ID AUDITORY-NERVE; SPIRAL GANGLION; GUINEA-PIG; TOPOGRAPHIC ORGANIZATION; SPATIAL-ORGANIZATION; CAT; INNERVATION; PROJECTIONS AB The purpose of the present study was to determine if the synaptic terminals and nerve fibers in thc gerbil cochlea fall into morphologically and spatially classified groups. In cats and guinea pigs, these groups. based on size, location oil inner hail cell (IHC) and stratification within the osseous spiral lamina, have been found to correlate with spontaneous rate, threshold sensitivity and projection pattern to the cochlear nucleus. Thus, there may be anatomical data to suggest mechanisms for intensity coding of different frequencies of sound. Afferent nerve terminals contacting IHCs in the gerbil cochlea were analyzed with regard to size and location. Data were obtained from serial thin sections (700 for each THC) cut perpendicular to the lung axis of eight IHCs (two apical and two basal IHCs from two cochleas), observed and photographed using a transmission election microscope. Results indicate tart the percentage of modiolar versus pillar-side terminals around each IHC varies from cell to cell. In some cases, the smallest fibers were located on the modiolar side, but a consistent distribution of the smallest fibers on this side of the cell was not characteristic. While a size-based segregation of terminals does not appear around the perimeter of the IHC, modest size-based segregation of nerve fibers is found in the osseous spiral lamina. Perimeter measurements were made from myelinated fibers cut in cross-section, obtained from semi-thin sections in the distal (near the IHCs) and proximal (near the spiral ganglion) regions of the osseous spiral lamina. Best-fit line analysis indicates there is a modest nerve fiber size/vertical organization along the scala lympani/scala vestibuli (SV) axis of the nerve bundles within the osseous spiral lamina such that more of the smaller perimeter fibers are located on the SV side and more of the larger perimeter fibers are located on the ST side. Our data for terminals at the IHC are different from those seen in the cat. our data for nerve fibers in the osseous spiral lamina support those seen in the cat and guinea pig. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Syracuse Univ, Dept Bioengn & Neurosci, Syracuse, NY 13244 USA. Syracuse Univ, Inst Sensory Res, Syracuse, NY 13244 USA. Syracuse Univ, Dept Biol, Syracuse, NY 13244 USA. RP Slepecky, NB (reprint author), Syracuse Univ, Dept Bioengn & Neurosci, Syracuse, NY 13244 USA. CR Bekesy G, 1960, EXPT HEARING GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 GINZBERG RD, 1984, HEARING RES, V14, P109, DOI 10.1016/0378-5955(84)90011-X GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S KAWASE T, 1992, J COMP NEUROL, V319, P312, DOI 10.1002/cne.903190210 LEAKE PA, 1989, J COMP NEUROL, V281, P612, DOI 10.1002/cne.902810410 LEAKE PA, 1993, J COMP NEUROL, V333, P257, DOI 10.1002/cne.903330211 LEAKE PA, 1992, J COMP NEUROL, V320, P468, DOI 10.1002/cne.903200405 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 Muller M, 1996, HEARING RES, V94, P148, DOI 10.1016/0378-5955(95)00230-8 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 Tsuji J, 1997, J COMP NEUROL, V381, P188 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E NR 17 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 124 EP 134 DI 10.1016/S0378-5955(00)00055-1 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000012 PM 10831871 ER PT J AU Cardinaal, RM de Groot, JCMJ Huizing, EH Veldman, JE Smoorenburg, GF AF Cardinaal, RM de Groot, JCMJ Huizing, EH Veldman, JE Smoorenburg, GF TI Dose-dependent effect of 8-day cisplatin administration upon the morphology of the albino guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE cisplatin; guinea pig; ototoxicity; dose dependence; outer hair cell loss ID STRIA VASCULARIS; ADENYLATE-CYCLASE; AUDITORY NEURONS; CIS-PLATINUM; HAIR-CELLS; INNER-EAR; OTOTOXICITY; DIURETICS; DAMAGE AB Numerous studies investigating cisplatin ototoxicity in animals have been performed, but it is difficult to derive a clear dose-effect relation from these studies. The degree of cisplatin-induced ototoxicity depends on a multitude of,factors. Many parameters, such as dose, mode of administration, dosage schedule and concomitant administration of protective additives, vary among the published studies. Therefore, we performed a basic dose-effect study on cisplatin ototoxicity in the guinea pig. Albino guinea pigs were treated with cisplatin at daily doses of either 0.7, 1.0, 1.25, 1.5 or 2.0 mg/kg for 8 consecutive days. Electrocochleography was performed on day 10 after which the cochleas were removed and processed for histological examination. The electrophysiological results showed a marked transition from almost no ototoxic effect to a large effect between a daily dose of 1.25 and 1.5 mg/kg (Stengs et al., 1998). Outer hair cell (OHC) counts corresponded well with the electrophysiological results. At daily doses of 0.7, 1.0 and 1.25 mg/kg no statistically significant OHC loss was observed, whereas OHC loss averaged 60% and 65% in the basal turns at daily doses of 1.5 and 2.0 mg/kg, respectively. Morphological changes in the stria vascularis were present only in cochleas from animals treated with cisplatin doses of 1.0, 1.25 and 1.5 mg/kg/day. Cochleas from animals treated with a daily cisplatin dose of 2.0 mg/kg for 8 consecutive days showed an endolymphatic hydrops. The present study shows that cisplatin, administered at a daily dose of 1.5 mg/ kg for 8 consecutive days, provides a degree of OHC loss that is well suited to study the effects of putative protective agents and possible hair cell recovery. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, NL-3508 GA Utrecht, Netherlands. RP Smoorenburg, GF (reprint author), Univ Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, Room G-02-531,POB 85-500, NL-3508 GA Utrecht, Netherlands. CR BAGGERSJOBACK D, 1980, ARCH OTO-RHINO-LARYN, V228, P217, DOI 10.1007/BF00454231 Bouman H, 1998, HEARING RES, V117, P119, DOI 10.1016/S0378-5955(97)00216-5 DEGROOT JCMJ, 1987, ACTA OTO-LARYNGOL, V104, P234, DOI 10.3109/00016488709107323 deGroot JCMJ, 1997, HEARING RES, V106, P9, DOI 10.1016/S0378-5955(96)00213-4 ESTERM SA, 1981, OTOLARYNGOL HEAD NEC, V89, P638 FERNANDEZCERVILLA F, 1993, ORL J OTO-RHINO-LARY, V55, P337 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 HOEVE LJ, 1988, ARCH OTO-RHINO-LARYN, V245, P98, DOI 10.1007/BF00481444 KOCH T, 1991, EUR ARCH OTO-RHINO-L, V248, P459, DOI 10.1007/BF00627634 KOHN S, 1988, LARYNGOSCOPE, V98, P865 KOHN S, 1991, LARYNGOSCOPE, V101, P709 KOMUNE S, 1981, OTOLARYNG HEAD NECK, V89, P275 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 LAURELL GFE, 1992, ANN OTO RHINOL LARYN, V101, P969 LAURELL G, 1991, J OTOLARYNGOL, V20, P158 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LAUTERMANN J, 1995, HEARING RES, V88, P47, DOI 10.1016/0378-5955(95)00097-N NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 RYBAK LP, 1993, OTOLARYNG CLIN N AM, V26, P829 SAITO T, 1994, ORL J OTO-RHINO-LARY, V56, P315 SCHWEITZER VG, 1993, LARYNGOSCOPE S, V103, P59 Stengs CHM, 1998, HEARING RES, V124, P99, DOI 10.1016/S0378-5955(98)00129-4 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 TANGE RA, 1982, ARCH OTO-RHINO-LARYN, V237, P17, DOI 10.1007/BF00453712 TAUDY M, 1992, AUDIOLOGY, V31, P293 WENDELL TN, 1995, J LARYNGOL OTOL, V109, P926 Zheng JL, 1996, EUR J NEUROSCI, V8, P1897, DOI 10.1111/j.1460-9568.1996.tb01333.x NR 27 TC 49 Z9 54 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 135 EP 146 DI 10.1016/S0378-5955(00)00059-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000013 PM 10831872 ER PT J AU Cardinaal, RM de Groot, JCMJ Huizing, EH Veldman, JE Smoorenburg, GF AF Cardinaal, RM de Groot, JCMJ Huizing, EH Veldman, JE Smoorenburg, GF TI Cisplatin-induced ototoxicity: Morphological evidence of spontaneous outer hair cell recovery in albino guinea pigs? SO HEARING RESEARCH LA English DT Article DE cisplatin; guinea pig; ototoxicity; outer hair cell loss; recovery ID CIS-DIAMMINEDICHLOROPLATINUM; AUDITORY NEURONS; STRIA VASCULARIS; ORGAN; CORTI; PLATINUM; REGENERATION; INTOXICATION; NEUROPATHY; THERAPY AB Cisplatin is frequently used in the treatment of various forms of malignancies. Its therapeutic efficacy, however, is limited by the occurrence of sensorineural hearing loss. Little is known about the course of hearing loss over longer time intervals after cessation of cisplatin administration. Infrequently, recovery of hearing has been described in animals and humans. Stengs et al. (1997) treated guinea pigs with cisplatin at a daily dose of 1.5 mg/kg for 8 consecutive days and subsequently studied cochlear function after survival times varying from 1 day to 16 weeks. Spontaneous improvement of the hair cell-related potentials (cochlear microphonics and summating potentials) was observed starting 2 weeks after cessation of treatment. In the present study we examined light microscopically the cochleas used in the study of Stengs et al. (1997). One day after cessation of cisplatin administration outer hair cell (OHC) loss in the basal cochlear turn averaged 66%. In the 1-week survival group, OHC counts were similar to those of the 1-day survival group. In the 4-week survival group, however, a relatively small loss of OHCs was found in the basal cochlear turn; OHC loss averaged only 15%. A similar loss was found after 8 weeks. In the 16-week survival group, OHC loss in the basal turn increased to 48%. but this was not statistically significant. Our histological observations are in line with the electrophysiological data from the same animals. Our findings suggest that OHCs recover from cisplatin-induced damage 1-4 weeks after treatment. However, the results do not allow a conclusion as to whether the observed recovery is due to the formation of new OHCs or to (self-)repair of damaged OHCs. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, NL-3508 GA Utrecht, Netherlands. RP Smoorenburg, GF (reprint author), Univ Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, Room G-02-531,POB 85-500, NL-3508 GA Utrecht, Netherlands. CR AGUILARMARKULIS NV, 1981, J SURG ONCOL, V16, P111, DOI 10.1002/jso.2930160203 BARRON SE, 1987, HEARING RES, V26, P431 BOHEIM K, 1985, ARCH OTORHINOLARYNGO, V242, P7 Cardinaal RM, 2000, HEARING RES, V144, P135, DOI 10.1016/S0378-5955(00)00059-9 CHARDIN S, 1995, SCIENCE, V267, P707, DOI 10.1126/science.7839151 DEGROOT JCMJ, 1991, ACTA OTO-LARYNGOL, V111, P273, DOI 10.3109/00016489109137387 deGroot JCMJ, 1997, HEARING RES, V106, P9, DOI 10.1016/S0378-5955(96)00213-4 ESTREM SA, 1981, OTOLARYNG HEAD NECK, V89, P638 FERNANDEZCERVILLA F, 1993, ORL J OTO-RHINO-LARY, V55, P337 FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 GRUNBERG SM, 1989, CANCER CHEMOTH PHARM, V25, P62, DOI 10.1007/BF00694340 HAMERS FPT, 1991, EUR J CANCER, V27, P372, DOI 10.1016/0277-5379(91)90549-S HAMERS FPT, 1994, EUR ARCH OTO-RHINO-L, V251, P23 KOHN S, 1988, LARYNGOSCOPE, V98, P865 KOMUNE S, 1981, OTOLARYNG HEAD NECK, V89, P275 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LAURELL G, 1991, ACTA OTO-LARYNGOL, V111, P891, DOI 10.3109/00016489109138427 LEFEBVRE PP, 1993, SCIENCE, V260, P692, DOI 10.1126/science.8480180 Lenoir M, 1997, INT J DEV NEUROSCI, V15, P487, DOI 10.1016/S0736-5748(96)00105-0 LOMONACO M, 1992, J NEUROL, V239, P199, DOI 10.1007/BF00839140 LOW M, 1992, HNO, V40, P271 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 SAITO T, 1994, ORL J OTO-RHINO-LARY, V56, P315 SCHWEITZER VG, 1993, LARYNGOSCOPE, V103, P1, DOI 10.1288/00005537-199304000-00001 Sobkowicz HM, 1996, ACTA OTO-LARYNGOL, V116, P257, DOI 10.3109/00016489609137836 SOBKOWICZ HM, 1992, EXP NEUROL, V115, P44, DOI 10.1016/0014-4886(92)90219-G STADNICKI SW, 1975, CANCER CHEMOTH REP 1, V59, P467 Stengs CHM, 1998, HEARING RES, V124, P99, DOI 10.1016/S0378-5955(98)00129-4 Stengs CHM, 1997, HEARING RES, V111, P103, DOI 10.1016/S0378-5955(97)00095-6 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 TANGE RA, 1982, ARCH OTO-RHINO-LARYN, V237, P17, DOI 10.1007/BF00453712 THOMPSON SW, 1984, CANCER, V54, P1269, DOI 10.1002/1097-0142(19841001)54:7<1269::AID-CNCR2820540707>3.0.CO;2-9 Vago P, 1998, NEUROREPORT, V9, P431, DOI 10.1097/00001756-199802160-00014 VERMORKEN JB, 1983, EUR J CANCER CLIN ON, V19, P53, DOI 10.1016/0277-5379(83)90398-X YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C Zheng JL, 1996, EUR J NEUROSCI, V8, P1897, DOI 10.1111/j.1460-9568.1996.tb01333.x Zine A, 1998, NEUROREPORT, V9, P263, DOI 10.1097/00001756-199801260-00016 NR 40 TC 31 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 147 EP 156 DI 10.1016/S0378-5955(00)00060-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000014 PM 10831873 ER PT J AU Cardinaal, RM de Groot, JCMJ Huizing, EH Veldman, JE Smoorenburg, GF AF Cardinaal, RM de Groot, JCMJ Huizing, EH Veldman, JE Smoorenburg, GF TI Histological effects of co-administration of an ACTH((4-9)) analogue, ORG 2766, on cisplatin ototoxicity in the albino guinea pig SO HEARING RESEARCH LA English DT Article DE cisplatin; guinea pig; ototoxicity; prevention; melanocortin; ORG 2766 ID ADENYLATE-CYCLASE; ELECTROPHYSIOLOGICAL EVIDENCE; CIS-DIAMMINEDICHLOROPLATINUM; INDUCED NEUROTOXICITY; SODIUM THIOSULFATE; AUDITORY NEURONS; ACTH(4-9) ANALOG; STRIA VASCULARIS; HAIR-CELLS; PROTECTION AB Cisplatin is one of the most potent antineoplastic drugs presently known, but its therapeutic efficacy is seriously limited by several side effects such as ototoxicity. Several compounds that are known for their nephroprotective effects also seem to reduce the incidence and severity of cisplatin-induced ototoxicity. Hamers et al. (1994) and De Groot et al. (1997) investigated the possibly protective effect of concomitant administration of the ACTH((4-9)) analogue ORG 2766 upon cisplatin ototoxicity in guinea pigs. Animals were treated with cisplatin at a daily dose of 2.0 mg/kg for 8 consecutive days and ORG 2766 at a daily dose of 75 mu g/kg for 9 days. Concomitant administration of cisplatin plus ORG 2766 resulted in a bimodal distribution of the electrophysiological data (compound action potential and cochlear microphonics amplitudes) and the histological data (outer hair cell (OHC) counts). It was surmised that this dichotomy might occur at a certain cisplatin dose. We investigated whether this protective effect of ORG 2766 could be enhanced by reducing the daily dose of cisplatin while maintaining the same dose of ORG 2766. Thirty-six animals were treated with daily i.p. injections of cisplatin at a dose of 1.0 mg/kg (n = 18) or 1.5 mg/kg (n = 18) for 8 consecutive days. When comparing the mean OHC counts of the different experimental groups, treatment with cisplatin at a daily dose of 1.5 mg/kg for 8 consecutive days resulted in a considerable loss of OHCs, which was significantly reduced after co-administration of ORG 2766. Co-treatment with ORG 2766 did not result in a change in the volume of the scala media. The present results are in agreement with the electrophysiological results published earlier (Stengs et al., 1998b). (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, NL-3508 GA Utrecht, Netherlands. RP Smoorenburg, GF (reprint author), Univ Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, Room G-02-531,POB 85-500, NL-3508 GA Utrecht, Netherlands. CR BAGGERSJOBACK D, 1980, ARCH OTO-RHINO-LARYN, V228, P217, DOI 10.1007/BF00454231 BODENNER DL, 1986, CANCER RES, V46, P2751 Campbell KCM, 1996, HEARING RES, V102, P90, DOI 10.1016/S0378-5955(96)00152-9 Cardinaal RM, 2000, HEARING RES, V144, P147, DOI 10.1016/S0378-5955(00)00060-5 Cardinaal RM, 2000, HEARING RES, V144, P135, DOI 10.1016/S0378-5955(00)00059-9 CAVALETTI G, 1991, INT J TISSUE REACT, V13, P151 CHARY KK, 1977, CANCER TREAT REP, V61, P367 Ciges M, 1996, ACTA OTO-LARYNGOL, V116, P263, DOI 10.3109/00016489609137837 DEKONING P, 1987, EXP NEUROL, V97, P746, DOI 10.1016/0014-4886(87)90132-4 deGroot JCMJ, 1997, HEARING RES, V106, P9, DOI 10.1016/S0378-5955(96)00213-4 DEWIED D, 1982, PHYSIOL REV, V62, P976 DUCKERS HJ, 1993, BRAIN, V116, P1059, DOI 10.1093/brain/116.5.1059 ESTREM SA, 1981, OTOLARYNG HEAD NECK, V89, P638 FERNANDEZCERVILLA F, 1993, ORL J OTO-RHINO-LARY, V55, P337 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 GANDARA DR, 1990, CRIT REV ONCOL HEMAT, V10, P353, DOI 10.1016/1040-8428(90)90010-P GISPEN WH, 1990, TRENDS PHARMACOL SCI, V11, P221, DOI 10.1016/0165-6147(90)90244-3 HAMERS FPT, 1991, EUR J CANCER, V27, P372, DOI 10.1016/0277-5379(91)90549-S HAMERS FPT, 1994, EUR ARCH OTO-RHINO-L, V251, P23 HAMERS FPT, 1997, NEUROPROTECTION CNS, P513 HASKO JA, 1990, HEARING RES, V45, P63, DOI 10.1016/0378-5955(90)90183-P Heijmen PS, 1999, HEARING RES, V128, P27, DOI 10.1016/S0378-5955(98)00194-4 HOFFMAN DW, 1987, HEARING RES, V31, P217, DOI 10.1016/0378-5955(87)90190-0 Kaltenbach JA, 1997, OTOLARYNG HEAD NECK, V117, P493, DOI 10.1016/S0194-5998(97)70020-2 KOCH T, 1991, EUR ARCH OTO-RHINO-L, V248, P459, DOI 10.1007/BF00627634 KOHN S, 1988, LARYNGOSCOPE, V98, P865 KOMUNE S, 1981, OTOLARYNG HEAD NECK, V89, P275 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LAURELL G, 1991, ACTA OTO-LARYNGOL, V111, P891, DOI 10.3109/00016489109138427 LOMONACO M, 1992, J NEUROL, V239, P199, DOI 10.1007/BF00839140 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E MOUNTJOY KG, 1992, SCIENCE, V257, P1248, DOI 10.1126/science.1325670 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 OTTO WC, 1988, HEARING RES, V35, P79, DOI 10.1016/0378-5955(88)90042-1 Saito T, 1997, EUR ARCH OTO-RHINO-L, V254, P281, DOI 10.1007/BF02905989 SAITO T, 1994, ORL J OTO-RHINO-LARY, V56, P315 SCHACHT J, 1982, AM J OTOLARYNG, V3, P328, DOI 10.1016/S0196-0709(82)80005-7 SCHWEITZER VG, 1993, LARYNGOSCOPE, V103, P1, DOI 10.1288/00005537-199304000-00001 Stengs CHM, 1998, HEARING RES, V124, P99, DOI 10.1016/S0378-5955(98)00129-4 Stengs CHM, 1998, HEARING RES, V124, P108, DOI 10.1016/S0378-5955(98)00130-0 Stengs CHM, 1997, HEARING RES, V111, P103, DOI 10.1016/S0378-5955(97)00095-6 STRAND FL, 1991, PHYSIOL REV, V71, P1017 Suzuki M, 1996, EUR ARCH OTO-RHINO-L, V253, P351 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 TANGE RA, 1982, ARCH OTO-RHINO-LARYN, V237, P17, DOI 10.1007/BF00453712 THOMPSON SW, 1984, CANCER, V54, P1269, DOI 10.1002/1097-0142(19841001)54:7<1269::AID-CNCR2820540707>3.0.CO;2-9 VANDERHOOP RG, 1994, J NEUROL SCI, V126, P109, DOI 10.1016/0022-510X(94)90259-3 VANDERHOOP RG, 1990, NEW ENGL J MED, V322, P89, DOI 10.1056/NEJM199001113220204 Zheng JL, 1996, EUR J NEUROSCI, V8, P1897, DOI 10.1111/j.1460-9568.1996.tb01333.x NR 50 TC 12 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 157 EP 167 DI 10.1016/S0378-5955(00)00061-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000015 PM 10831874 ER PT J AU Nizami, L Schneider, BA AF Nizami, L Schneider, BA TI The periodicity of forward-masked auditory pip-detection thresholds, predicted from the output power of the auditory filter during ringing SO HEARING RESEARCH LA English DT Article DE ringing; forward-masking; auditory filter ID RESPONSE PATTERNS; GAP DETECTION; NERVE FIBERS; MASKING; STIMULI; CAT AB The plot of detection thresholds vs. time for a forward-masked Gaussian-shaped 2 kHz Dip (S.D. = 0.5 ms) shows a noisy 'fine structure' that disappears with across-subject averaging. The averaging uncovers a slower threshold periodicity, that can be predicted From the output power of the auditory filter during extended ringing. (C) 2090 Elsevier Science B.V. All rights reserved. C1 Boys Town Natl Res Hosp, Omaha, NE 68131 USA. Univ Toronto, Erindale Coll, Dept Psychol, Mississauga, ON L5L 1C6, Canada. RP Nizami, L (reprint author), Boys Town Natl Res Hosp, 555 N 30th St, Omaha, NE 68131 USA. CR CARLYON RP, 1988, HEARING RES, V32, P65, DOI 10.1016/0378-5955(88)90147-5 DUIFHUIS H, 1973, J ACOUST SOC AM, V54, P1471, DOI 10.1121/1.1914446 ECHEVERRIA EL, 1983, J ACOUST SOC AM, V73, P592 Gabor D., 1946, Journal of the Institution of Electrical Engineers. III. Radio and Communication Engineering, V93 GORGA MP, 1980, J ACOUST SOC AM, V67, P1821, DOI 10.1121/1.384262 Kiang NY-s, 1965, DISCHARGE PATTERNS S NIZAMI L, 1999, AUDITORY DYNAMIC RAN Nizami L, 1999, J ACOUST SOC AM, V106, P1187, DOI 10.1121/1.427130 Nizami L., 1999, Society for Neuroscience Abstracts, V25, P132 PFEIFFER RR, 1972, J ACOUST SOC AM, V52, P1669, DOI 10.1121/1.1913301 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBINSON CE, 1973, J ACOUST SOC AM, V53, P1313, DOI 10.1121/1.1913471 SCHNEIDER BA, 1994, J ACOUST SOC AM, V95, P980, DOI 10.1121/1.408403 SHAILER MJ, 1987, J ACOUST SOC AM, V81, P1110, DOI 10.1121/1.394631 ZWICKER E, 1984, J ACOUST SOC AM, V75, P219, DOI 10.1121/1.390398 NR 15 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 168 EP 174 DI 10.1016/S0378-5955(00)00063-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000016 PM 10831875 ER PT J AU Miller, AL Morris, DJ Pfingst, BE AF Miller, AL Morris, DJ Pfingst, BE TI Effects of time after deafening and implantation on guinea pig electrical detection thresholds SO HEARING RESEARCH LA English DT Article DE guinea pig; cochlear implant; spiral ganglion cell; psychophysics; electrical detection threshold; time; aminoglycoside ID SPIRAL GANGLION NEURONS; COCHLEAR-IMPLANT; PSYCHOPHYSICAL MEASURES; AUDITORY-NERVE; 8TH NERVE; FUNCTIONAL-RESPONSES; STIMULATION; SURVIVAL; CATS; HISTOPATHOLOGY AB Changes in detection threshold level as a function of time after deafening and implantation have been described previously in macaque [Pfingst, 1990] and human [Skinner et al., 1995] cochlear implant subjects. Characterization of the mechanisms underlying these changes will contribute to our understanding of the anatomical and physiological factors affecting electrical stimulus detection. In addition. understanding the time course of early threshold changes is essential to the interpretation of acute physiological studies of cochlear implants. To better characterize time-dependent threshold changes, we monitored changes in guinea pig psychophysical electrical detection thresholds with time after deafening and cochlear implantation. Threshold levels for 100 Hz sinusoidal bursts were initially unstable over the first 30 days post-surgery (DPS), after which thresholds stabilized. At longer intervals (> 100 DPS), increases(> 10 dB) in threshold level were observed for 100 Hz sinusoids in three of 11 cases. These changes were transient in one case and long-term in two cases. The time course of threshold change, both early and late, could not be explained on the basis of changes in spiral ganglion cell survival. The guinea pig seems to be an ideal preparation for studies of this nature, because threshold changes are similar in type, but accelerated in lime course, relative to those observed in primates. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan Hlth Syst, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Pfingst, BE (reprint author), Univ Michigan Hlth Syst, Dept Otolaryngol, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR Blamey P, 1997, AM J OTOL, V18, pS11 Bledsoe SC, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P513, DOI 10.1007/978-1-4419-8712-9_47 BROWN CJ, 1995, EAR HEARING, V16, P439, DOI 10.1097/00003446-199510000-00001 Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P617, DOI 10.1109/10.764938 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 Dodson HC, 1997, J NEUROCYTOL, V26, P541, DOI 10.1023/A:1015434524040 DORMAN MF, 1992, J SPEECH HEAR RES, V35, P1126 DUCKERT LG, 1983, LARYNGOSCOPE, V93, P841 EDDINGTON DK, 1978, ANN OTOL RHINOL LA S, V53, P1 GANTZ BJ, 1993, ANN OTO RHINOL LARYN, V102, P909 HALL RD, 1990, HEARING RES, V49, P155, DOI 10.1016/0378-5955(90)90102-U HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 KOITCHEV K, 1982, ACTA OTO-LARYNGOL, V94, P431, DOI 10.3109/00016488209128931 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1992, HEARING RES, V64, P99, DOI 10.1016/0378-5955(92)90172-J LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEAKE PA, 1995, HEARING RES, V82, P65 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MARSH MA, 1992, AM J OTOL, V13, P241 MICHELSO.RP, 1971, ARCHIV OTOLARYNGOL, V93, P317 MILLER AL, 1999, ASS RES OTOLARYNGOL, V22, P654 Miller CA, 1995, HEARING RES, V92, P100, DOI 10.1016/0378-5955(95)00205-7 Miller CA, 1995, HEARING RES, V92, P85, DOI 10.1016/0378-5955(95)00204-9 MILLER CA, 1994, HEARING RES, V78, P11, DOI 10.1016/0378-5955(94)90039-6 MILLER JM, 1995, AUDITORY PLASTICITY Mitchell A, 1997, HEARING RES, V105, P30, DOI 10.1016/S0378-5955(96)00202-X PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1990, HEARING RES, V50, P225, DOI 10.1016/0378-5955(90)90047-S Skinner Margaret W., 1995, Seminars in Hearing, V16, P228, DOI 10.1055/s-0028-1083720 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 SNYDER R, 1995, J NEUROPHYSIOL, V73, P449 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S SPELMAN FA, 1978, P SAN DIEGO BIOMED S, V17, P1 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 WALTZMAN SB, 1991, OTOLARYNG HEAD NECK, V105, P797 WEBSTER DB, 1996, ASS RES OTOLARYNGOL, V19, P820 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 White M.W., 1978, THESIS U CALIFORNIA White M. W., 1987, Proceedings of the Ninth Annual Conference of the IEEE Engineering in Medicine and Biology Society (Cat. No.87CH2513-0) XUE XL, 1989, J NEUROSCI METH, V28, P189, DOI 10.1016/0165-0270(89)90035-6 NR 43 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 175 EP 186 DI 10.1016/S0378-5955(00)00066-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000017 PM 10831876 ER PT J AU Zheng, XY McFadden, SL Ding, DL Henderson, D AF Zheng, XY McFadden, SL Ding, DL Henderson, D TI Cochlear de-efferentation and impulse noise-induced acoustic trauma in the chinchilla SO HEARING RESEARCH LA English DT Article DE inner ear; cochlear efferent; impulse noise; hair cell loss; noise-induced hearing loss; olivocochlear bundle ID SINGLE OLIVOCOCHLEAR NEURONS; TEMPORARY THRESHOLD SHIFTS; INDUCED HEARING-LOSS; AUDITORY-SENSITIVITY; GUINEA-PIG; ACQUIRED-RESISTANCE; SYSTEM; BUNDLE; INNER; SUSCEPTIBILITY AB The olivocochlear bundle (OCB) has been shown to protect the ear from acoustic trauma induced by continuous noise or tones. The present study examines the OCB's role in the ear's response to impulse noise (150 dB pSPL, 100 impulses, 50 s total exposure duration). Successful section of the OCB was achieved through a posterior parafloccular fossa approach for the right ears of six out of 15 adult chinchillas. The left ears from the same animals served as efferent-innervated controls. Measurements of inferior colliculus evoked potentials (ICPs) showed that the de-efferented ears incurred similar temporary and permanent threshold shifts as the control ears. Twenty days after noise exposure, depressed ICP amplitudes had virtually recovered to pre-values in the control ears whereas those in the de-efferented ears remained significantly depressed. Greater loss of inner hair cells was seen in the deefferented ears than in the control ears. Both control and de-efferented ears incurred large loss of outer hair cells, with no statistically significant differences between groups. The current data are intriguing, yielding tentative evidence to suggest that inner hair cells of de-efferented ears are more susceptible to impulse noise than those in efferented control ears. In contrast, outer hair cell vulnerability to impulse noise appears to be unaffected by de-efferentation. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA. RP Zheng, XY (reprint author), SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA. CR Bobbin R P, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P299 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 Brown MC, 1998, J NEUROPHYSIOL, V79, P3077 Brown MC, 1998, J NEUROPHYSIOL, V79, P3088 Burkard R, 1997, J ACOUST SOC AM, V102, P3620, DOI 10.1121/1.420149 CODY AR, 1982, HEARING RES, V6, P199, DOI 10.1016/0378-5955(82)90054-5 DANIELSON R, 1991, J ACOUST SOC AM, V90, P209, DOI 10.1121/1.402361 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 GUNTHER T, 1989, AM J OTOL, V10, P36 HAMERNIK RP, 1974, ARCH OTOLARYNGOL, V99, P118 HAMERNIK RP, 1987, J ACOUST SOC AM, V81, P1118, DOI 10.1121/1.394632 HAMERNIK RP, 1984, HEARING RES, V13, P229, DOI 10.1016/0378-5955(84)90077-7 HANDROCK M, 1982, ARCH OTO-RHINO-LARYN, V234, P191, DOI 10.1007/BF00453630 Harel N, 1997, HEARING RES, V110, P25, DOI 10.1016/S0378-5955(97)00061-0 HENDERSON D, 1986, J ACOUST SOC AM, V80, P569, DOI 10.1121/1.394052 KARNOVSKY MJ, 1964, J HISTOCHEM CYTOCHEM, V12, P219 Kujawa SG, 1997, J NEUROPHYSIOL, V78, P3095 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 LIBERMAN MC, 1995, HEARING RES, V90, P158, DOI 10.1016/0378-5955(95)00160-2 LIBERMAN MC, 1992, NOISE INDUCED HEARIN, P423 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 McFadden SL, 1998, HEARING RES, V120, P121, DOI 10.1016/S0378-5955(98)00052-5 McFadden SL, 1999, EAR HEARING, V20, P164, DOI 10.1097/00003446-199904000-00007 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V PUJOL R, 1994, BRIT J AUDIOL, V28, P185, DOI 10.3109/03005369409086567 Qiu CX, 2000, HEARING RES, V139, P153, DOI 10.1016/S0378-5955(99)00171-9 RAJAN R, 1989, HEARING RES, V39, P299, DOI 10.1016/0378-5955(89)90049-X RAJAN R, 1995, J NEUROPHYSIOL, V74, P582 RAJAN R, 1983, HEARING RES, V9, P279, DOI 10.1016/0378-5955(83)90032-1 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 RAJAN R, 1995, J NEUROPHYSIOL, V74, P598 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 REITER ER, 1995, J NEUROPHYSIOL, V73, P506 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SLEPECKY N, 1982, ACTA OTO-LARYNGOL, V93, P329, DOI 10.3109/00016488209130890 SNYDER DL, 1994, LAB ANIMAL, V23, P42 TRAHIOTI.C, 1970, J ACOUST SOC AM, V47, P592, DOI 10.1121/1.1911934 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 Yamasoba T, 1998, HEARING RES, V120, P143, DOI 10.1016/S0378-5955(98)00054-9 Zheng XY, 1999, J COMP NEUROL, V406, P72 Zheng XY, 1997, HEARING RES, V107, P147, DOI 10.1016/S0378-5955(97)00031-2 Zheng XY, 1998, NEUROSCIENCE, V85, P579, DOI 10.1016/S0306-4522(97)00603-9 Zheng XY, 1997, HEARING RES, V113, P76, DOI 10.1016/S0378-5955(97)00127-5 Zheng XY, 1997, HEARING RES, V104, P191, DOI 10.1016/S0378-5955(96)00187-6 NR 47 TC 15 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 187 EP 195 DI 10.1016/S0378-5955(00)00065-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000018 PM 10831877 ER PT J AU Crofton, KM Ding, DL Padich, R Taylor, M Henderson, D AF Crofton, KM Ding, DL Padich, R Taylor, M Henderson, D TI Hearing loss following exposure during development to polychlorinated biphenyls: A cochlear site of action SO HEARING RESEARCH LA English DT Article DE polychlorinated biphenyl; ototoxicity; hair cell loss; apical hair cell ID THYROID-HORMONE CONCENTRATIONS; AUDITORY FUNCTION; CONGENITAL HYPOTHYROIDISM; POSTNATAL EXPOSURE; PCB CONGENERS; RAT; THYROXINE; AROCLOR-1254; RECEPTOR; ABNORMALITIES AB Maternal exposure to polyhalogenated hydrocarbons results in early postnatal hypothyroxenemia and a low-frequency hearing loss in adult offspring (Goldey et al., 1995a. Toxicol. Appl. Pharmacol. 135, 67-76; Herr et al., 1996. Fundam. Appl. Toxicol. 33, 120-128). The purpose of the present work was to determine whether the site-of-action of this auditory impairment was within the cochlea. Primiparous Long-Evans rats were given daily oral doses of corn oil (control) or 8 mg/kg of the commercial PCB mixture Aroclor 1254 (A1254) from gestation day (GD) 6 through postnatal day (PND) 21. Auditory thresholds for 1-, 4-, 16-, and 40-kHz tones were assessed using reflex modification audiometry in young adult offspring on postnatal days (PND) 92-110. Approximately 6 weeks after auditory assessments, a subset of animals (n=4 per group) were killed for histological assessment of the cochlea. Surface preparations of the organ of Corti were prepared from one cochlea per animal and modiolar sections were prepared from the opposite cochlea. Consistent with previous findings, auditory thresholds for 1-kHz tones were elevated by approximately 25 dB in the A1254-exposed animals. Thresholds for all higher frequencies were not different compared to controls. Surface preparations of the organ of Corti revealed a mild to moderate loss of outer hair cells in the upper-middle and apical turns. Inner hair cells were not affected. Modiolar sections failed to reveal alterations in any other cochlear structures. There was also no apparent loss of ganglion cells. These data clearly link the loss of low-frequency hearing caused by exposure during development to A1254 to a loss of outer hair cells in the organ of Corti. The mechanism that underlies this developmental ototoxicity remains to be determined. These data provide the first evidence of a structural deficit in the nervous system of adult animals exposed to PCBs during development. (C) 2000 Elsevier Science B.V. All rights reserved. C1 US EPA, Natl Hlth & Environm Effects Res Lab, Div Neurotoxicol, Res Triangle Pk, NC 27711 USA. SUNY Buffalo, Dept Communicat Disorders & Sci, Hearing Res Labs, Buffalo, NY 14260 USA. Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC USA. RP Crofton, KM (reprint author), US EPA, Natl Hlth & Environm Effects Res Lab, Div Neurotoxicol, MD-74B, Res Triangle Pk, NC 27711 USA. CR BRADLEY DJ, 1994, P NATL ACAD SCI USA, V91, P439, DOI 10.1073/pnas.91.2.439 Cheek AO, 1999, ENVIRON HEALTH PERSP, V107, P273, DOI 10.2307/3434593 CHOU T, 1999, TOXICOLOGIST, V1, P267 COLBORN T, 1993, ENVIRON HEALTH PERSP, V101, P378, DOI 10.2307/3431890 COLLINS WT, 1980, AM J PATHOL, V99, P125 Corey DA, 1996, GROWTH DEVELOP AGING, V60, P131 Crofton K. M., 1992, NEUROTOXICOLOGY, P181 CROFTON KM, 1990, TOXICOL APPL PHARM, V105, P123, DOI 10.1016/0041-008X(90)90364-Z CROFTON KM, 1994, HEARING RES, V80, P129, DOI 10.1016/0378-5955(94)90104-X CROFTON KM, 1997, 36 ANN M SOC TOX CIN, V36, P61 Darnerud PO, 1996, TOXICOLOGY, V106, P105, DOI 10.1016/0300-483X(95)03169-G DEESCOBAR GM, 1985, ENDOCRINOLOGY, V117, P1890 DEOL MS, 1976, ACTA OTO-LARYNGOL, V81, P429 DEOL MS, 1973, J MED GENET, V10, P235, DOI 10.1136/jmg.10.3.235 Eggermont J J, 1986, Acta Otolaryngol Suppl, V429, P5 FIOLET DCM, 1997, COMPOUNDS, V34, P459 Forrest D, 1996, NAT GENET, V13, P354, DOI 10.1038/ng0796-354 Frame G.M., 1996, J HIGH RES CHROMATOG, V19, P657, DOI DOI 10.1002/JHRC.1240191202 Goldey ES, 1998, TOXICOL SCI, V45, P94, DOI 10.1093/toxsci/45.1.94 GOLDEY ES, 1995, TOXICOL APPL PHARM, V135, P67, DOI 10.1006/taap.1995.1209 GOLDEY ES, 1995, TOXICOL APPL PHARM, V135, P77, DOI 10.1006/taap.1995.1210 HEBERT R, 1985, DEV BRAIN RES, V23, P161, DOI 10.1016/0165-3806(85)90037-9 Herr DW, 1996, FUND APPL TOXICOL, V33, P120, DOI 10.1006/faat.1996.0149 Ilsen A, 1996, CHEMOSPHERE, V33, P1317, DOI 10.1016/0045-6535(96)00269-X Knipper M, 1999, J NEUROBIOL, V38, P338, DOI 10.1002/(SICI)1097-4695(19990215)38:3<338::AID-NEU4>3.0.CO;2-1 KOOPMANESSEBOOM C, 1994, PEDIATR RES, V36, P468, DOI 10.1203/00006450-199410000-00009 Lautermann J, 1997, HEARING RES, V107, P23, DOI 10.1016/S0378-5955(97)00014-2 MESERVE LA, 1992, B ENVIRON CONTAM TOX, V48, P715 Meza G, 1996, INT J DEV NEUROSCI, V14, P515, DOI 10.1016/0736-5748(95)00100-X Morse DC, 1996, TOXICOL APPL PHARM, V136, P269, DOI 10.1006/taap.1996.0034 MORSE DC, 1993, TOXICOL APPL PHARM, V122, P27, DOI 10.1006/taap.1993.1168 Nagayama J, 1998, CHEMOSPHERE, V37, P1789, DOI 10.1016/S0045-6535(98)00244-6 NESS DK, 1993, TOXICOL LETT, V68, P311, DOI 10.1016/0378-4274(93)90023-Q OMALLEY BW, 1995, HEARING RES, V88, P181, DOI 10.1016/0378-5955(95)00111-G PLUIM HJ, 1993, ENVIRON HEALTH PERSP, V101, P504, DOI 10.2307/3431587 Rosiak KL, 1997, J ENVIRON SCI HEAL B, V32, P377, DOI 10.1080/03601239709373093 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 Rubel E W, 1985, Acta Otolaryngol Suppl, V421, P114 RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 SAFE SH, 1994, CRIT REV TOXICOL, V24, P87, DOI 10.3109/10408449409049308 SARNE DH, 1995, ENDOCRINOLOGY, P617 SAS INSTITUTE, 1989, SAS STAT US GUID, V2 SEO BW, 1995, TOXICOL LETT, V78, P253, DOI 10.1016/0378-4274(95)03329-J SINJARI T, 1997, THESIS UPPSALA U SWE UZIEL A, 1985, DEV BRAIN RES, V19, P111, DOI 10.1016/0165-3806(85)90236-6 Uziel A, 1986, Acta Otolaryngol Suppl, V429, P23 UZIEL A, 1981, ACTA OTO-LARYNGOL, V92, P469, DOI 10.3109/00016488109133286 UZIEL A, 1985, DEV BRAIN RES, V19, P123, DOI 10.1016/0165-3806(85)90237-8 UZIEL A, 1980, BRAIN RES, V182, P172, DOI 10.1016/0006-8993(80)90840-9 UZIEL A, 1983, HEARING RES, V11, P203, DOI 10.1016/0378-5955(83)90079-5 VINCENT J, 1983, J PHYSIOL-PARIS, V78, P729 WHO, 1993, ENV HLTH CRIT, V140 YOUNG JS, 1983, J ACOUST SOC AM, V73, P1686, DOI 10.1121/1.389391 ZOELLER R, 1998, 71 ANN M AM THYR ASS NR 54 TC 54 Z9 54 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 2000 VL 144 IS 1-2 BP 196 EP 204 DI 10.1016/S0378-5955(00)00062-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 320YK UT WOS:000087428000019 PM 10831878 ER PT J AU Lanford, PJ Platt, C Popper, AN AF Lanford, PJ Platt, C Popper, AN TI Structure and function in the saccule of the goldfish (Carassius auratus): a model of diversity in the non-amniote ear SO HEARING RESEARCH LA English DT Article DE hair cell; saccule; cellular variation; review ID POST-SYNAPTIC POTENTIALS; AUDITORY-NERVE FIBERS; SENSORY HAIR-CELLS; INNER-EAR; SYNAPSES; ORGAN; FISH; ZEBRAFISH; AFFERENT; NOTCH AB The vertebrate inner ear is comprised of a remarkable diversity of cell types, including several types of sensory hair cells. In amniotes (reptiles, birds, and mammals), the morphological and physiological characteristics that distinguish these cell types have been well documented, while cellular variation in the ears of non-amniotes (all other vertebrate groups) has remained underrecognized. Since non-amniotes have become increasingly popular models for developmental and genetic research, a more comprehensive understanding of structure and function in the inner ears of these species is warranted. This paper first reviews the large body of data describing the morphology and physiology of hair cells and afferent neurons in the inner ear of the goldfish (Carassius auratus). In particular, we examine the structure of the goldfish saccule, an endorgan that has been the subject of numerous investigations on audition. New data on the structural variation of synaptic bodies in saccular hair cells are also presented, and the functional implications of these data are discussed. Finally, we conclude that hair cell structure varies along the length of the goldfish saccule in a manner consistent with known physiological characteristics of the endorgan. The saccule provides an excellent model for investigating structure-function relationships in the vertebrate inner ear, Bs well as the development of auditory and vestibular sensory epithelia. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Maryland, Dept Biol, College Pk, MD 20742 USA. RP Lanford, PJ (reprint author), Natl Inst Deafness & Other Commun Disorders, 5 Res Ct, Rockville, MD 20850 USA. CR Adam J, 1998, DEVELOPMENT, V125, P4645 CHANG JSY, 1992, J COMP NEUROL, V324, P621, DOI 10.1002/cne.903240413 COOMBS S, 1987, J ACOUST SOC AM, V81, P1025, DOI 10.1121/1.395113 Corti A., 1851, Z WISS ZOOL, V3, P109 Davis JG, 1997, P NATL ACAD SCI USA, V94, P707, DOI 10.1073/pnas.94.2.707 DEITERS O, 1860, UNTERSUCHUNGE LAMINA Eatock RA, 1998, OTOLARYNG HEAD NECK, V119, P172, DOI 10.1016/S0194-5998(98)70052-X Echteler SM, 1994, COMP HEARING MAMMALS, P134 EDDSWALTON PL, 2000, IN PRESS HEAR RES FAY RR, 1978, J ACOUST SOC AM, V63, P136, DOI 10.1121/1.381705 FAY RR, 1986, J ACOUST SOC AM, V79, P1883, DOI 10.1121/1.393196 Fay R.R., 1985, P291 FAY RR, 1988, HEARING VERTEBRATES, P29 FLOCK A, 1964, J CELL BIOL, V22, P413, DOI 10.1083/jcb.22.2.413 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P193 FURUKAWA T, 1978, J COMP NEUROL, V180, P807, DOI 10.1002/cne.901800411 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 FURUKAWA T, 1967, JPN J PHYSIOL, V17, P572 Granato M, 1996, CURR OPIN GENET DEV, V6, P461, DOI 10.1016/S0959-437X(96)80068-2 GRAY EG, 1971, BRAIN RES, V35, P1, DOI 10.1016/0006-8993(71)90591-9 Haddon C, 1998, DEVELOPMENT, V125, P359 Haddon C, 1998, DEVELOPMENT, V125, P4637 HAMA K, 1969, Z ZELLFORSCH MIK ANA, V94, P155, DOI 10.1007/BF00339353 HOPSU VK, 1965, EXP CELL RES, V37, P484, DOI 10.1016/0014-4827(65)90196-5 HUDSPETH AJ, 1994, NEURON, V12, P1, DOI 10.1016/0896-6273(94)90147-3 KESSLER DS, 1994, SCIENCE, V266, P596, DOI 10.1126/science.7939714 KIDD M, 1962, J ANAT, V96, P179 Lanford PJ, 1996, HEARING RES, V100, P1, DOI 10.1016/0378-5955(96)00110-4 Lanford PJ, 1999, NAT GENET, V21, P289 Lenzi D, 1999, J NEUROSCI, V19, P119 LEWIS ER, 1985, VERTEBRATE EAR LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MerchanPerez A, 1996, J COMP NEUROL, V371, P208, DOI 10.1002/(SICI)1096-9861(19960722)371:2<208::AID-CNE2>3.0.CO;2-6 Morrison A, 1999, MECH DEVELOP, V84, P169, DOI 10.1016/S0925-4773(99)00066-0 NAKAJIMA Y, 1974, J COMP NEUROL, V156, P403, DOI 10.1002/cne.901560403 NUSSLEINVOLHARD C, 1994, SCIENCE, V266, P572, DOI 10.1126/science.7939708 PARSONS TD, 1994, NEURON, V13, P875, DOI 10.1016/0896-6273(94)90253-4 Peterson EH, 1996, ANN NY ACAD SCI, V781, P85, DOI 10.1111/j.1749-6632.1996.tb15695.x PIERIBONE VA, 1995, NATURE, V375, P493, DOI 10.1038/375493a0 PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 PLATT C, 1984, SCANNING ELECT MICRO, V4, P1915 POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 Presson JC, 1996, HEARING RES, V100, P10, DOI 10.1016/0378-5955(96)00109-8 PUJOL R, 1997, DEV AUDITORY SYSTEM QUICK DC, 1977, J NEUROL SCI, V31, P1, DOI 10.1016/0022-510X(77)90002-8 Retzius G, 1881, GEHORORGAN WIRBELTHI Riley BB, 1997, DEV BIOL, V191, P191, DOI 10.1006/dbio.1997.8736 SAIDEL WM, 1990, HEARING RES, V47, P139, DOI 10.1016/0378-5955(90)90171-K Saidel WM, 1995, BRAIN BEHAV EVOLUT, V46, P362, DOI 10.1159/000113286 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 Simmons D. D., 1995, AUDIT NEUROSCI, V1, P183 SIMMONS DD, 1994, HEARING RES, V80, P71, DOI 10.1016/0378-5955(94)90010-8 SJOSTRAND FS, 1953, J CELL COMPAR PHYSL, V42, P15, DOI 10.1002/jcp.1030420103 SMITH CA, 1961, J ULTRA MOL STRUCT R, V5, P184, DOI 10.1016/S0022-5320(61)90013-2 SOBKOWICZ HM, 1984, ULTRASTRUCTURAL ATLA SOBKOWICZ HM, 1986, J NEUROCYTOL, V15, P693, DOI 10.1007/BF01625188 SOKOLOWSKI BHA, 1988, J MORPHOL, V198, P49, DOI 10.1002/jmor.1051980107 SOKOLOWSKI BHA, 1987, J MORPHOL, V194, P323, DOI 10.1002/jmor.1051940311 Sugihara I, 1995, J PHYSIOL-LONDON, V489, P443 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P330 TITOVA LK, 1970, DEV RECEPTOR STRUCTU WACHTEL AW, 1966, J MORPHOL, V119, P51, DOI 10.1002/jmor.1051190106 Weber E. H., 1820, AURE AUDITU HOMINI 1 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 WERSALL J, 1960, ACTA OTO-LARYNGOL, V163, P25 WESTERMAN LA, 1988, J ACOUST SOC AM, V83, P2266, DOI 10.1121/1.396357 Zetes DE, 1997, J ACOUST SOC AM, V101, P3593, DOI 10.1121/1.418320 NR 68 TC 24 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 1 EP 13 DI 10.1016/S0378-5955(00)00015-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900001 PM 10771179 ER PT J AU Zheng, XY McFadden, SL Henderson, D Ding, DL Burkard, R AF Zheng, XY McFadden, SL Henderson, D Ding, DL Burkard, R TI Cochlear microphonics and otoacoustic emissions in chronically de-efferented chinchilla SO HEARING RESEARCH LA English DT Article DE cochlear efferent; acetylcholinesterase; non-linearity; inner ear; otoacoustic emission; cochlear microphonic ID OUTER HAIR-CELLS; CROSSED OLIVOCOCHLEAR BUNDLE; BASILAR-MEMBRANE MECHANICS; GUINEA-PIG COCHLEA; STIMULATION; ACETYLCHOLINE; CAT; AMPLIFIER; RESPONSES; RECEPTOR AB The effects of eliminating the olivocochlear bundle (OCB) on cochlear electromechanical properties were examined by measuring cochlear microphonics (CM) and distortion product otoacoustic emissions (DPOAEs) in chronically de-efferented chinchillas. The OCB fibers to the right ears were successfully sectioned in six out of 15 adult chinchillas via a posterior paraflocular fossa approach. At the end of the experiment, these ears were histologically verified as being deprived of both lateral and medial OCB fibers. The opposite (left) ears from the animals served as controls. Following de-efferentation, changes of the inter-modulation distortion components (2f(1)-f(2), f(2)-f(1), 3f(1)-2f(2), 3f(2)-2f(1)) varied, depending on the frequencies and levels of the stimuli. DPOAE amplitudes to low-level stimuli were within the 95% confidence intervals around mean DPOAE amplitudes of the control ears at all the frequencies (1-8 kHz). At high stimulus levels, DPOAE amplitudes increased by 5-20 dB at 1 and 2 kHz while remaining in the normal range at 4 and 8 kHz. In contrast, the CM input/output functions to stimuli from 1 to 8 kHz were significantly reduced by approximately 40-50% at all input levels. The results suggest that the OCB may play a role in modulating electrical properties of the outer hair cells and in reducing the magnitude of cochlear distortion to high-level stimuli. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA. RP Zheng, XY (reprint author), SUNY Buffalo, Ctr Hearing & Deafness, 215 Parker Hall, Buffalo, NY 14214 USA. CR ALTSCHULER R, 1992, NOISE INDUCED HEARIN, P60 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BONFILS P, 1987, HEARING RES, V30, P267, DOI 10.1016/0378-5955(87)90142-0 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 COOPER NP, 1992, HEARING RES, V63, P163, DOI 10.1016/0378-5955(92)90083-Y Dallos P, 1997, J NEUROSCI, V17, P2212 DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X FEX J, 1959, Acta Otolaryngol, V50, P540, DOI 10.3109/00016485909129230 GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 Harel N, 1997, HEARING RES, V110, P25, DOI 10.1016/S0378-5955(97)00061-0 IURATO S, 1978, J COMP NEUROL, V182, P57, DOI 10.1002/cne.901820105 Jock BM, 1996, HEARING RES, V96, P179, DOI 10.1016/0378-5955(96)00058-5 KARNOVSKY MJ, 1964, J HISTOCHEM CYTOCHEM, V12, P219 KATZ B, 1977, PROC R SOC SER B-BIO, V196, P59, DOI 10.1098/rspb.1977.0029 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KUJAWA SG, 1993, HEARING RES, V68, P97, DOI 10.1016/0378-5955(93)90068-C Liberman MC, 1996, J ACOUST SOC AM, V99, P3572, DOI 10.1121/1.414956 LIBERMAN MC, 1990, HEARING RES, V49, P209, DOI 10.1016/0378-5955(90)90105-X LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Murugasu E, 1996, J NEUROSCI, V16, P325 PATUZZI R, 1990, HEARING RES, V45, P15, DOI 10.1016/0378-5955(90)90179-S PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RAJAN R, 1989, HEARING RES, V39, P299, DOI 10.1016/0378-5955(89)90049-X RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SIEGEL JH, 1982, HEARING RES, V6, P245 SZIKLAI I, 1993, ACTA OTO-LARYNGOL, V113, P326, DOI 10.3109/00016489309135818 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WIEDERHO.ML, 1966, J ACOUST SOC AM, V40, P1427, DOI 10.1121/1.1910243 Zheng XY, 1999, J COMP NEUROL, V406, P72 Zheng XY, 1997, HEARING RES, V107, P147, DOI 10.1016/S0378-5955(97)00031-2 NR 37 TC 11 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 14 EP 22 DI 10.1016/S0378-5955(99)00217-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900002 PM 10771180 ER PT J AU Michel, O Hess, A Su, JP Bloch, W Stennert, E Addicks, K AF Michel, O Hess, A Su, JP Bloch, W Stennert, E Addicks, K TI Expression of inducible nitric oxide synthase (iNOS/NOS II) in the hydropic cochlea of guinea pigs SO HEARING RESEARCH LA English DT Article DE nitric oxide; ototoxicity; endolymphatic hydrops; immunohistochemistry ID EXPERIMENTAL ENDOLYMPHATIC HYDROPS; SODIUM-NITROPRUSSIDE; VESTIBULAR SYSTEM; NMDA RECEPTORS; LOCALIZATION; PHYSIOLOGY; PRESSURE; ISOFORMS; ORGAN AB Immunohistochemical investigations of the guinea pig cochlea, using a specific antibody to the inducible isoform of NO synthase (iNOS/NOS II), have been performed 3 weeks after closure of the right endolymphatic duct (n = 7). Endolymphatic hydrops, the morphological substrate of Meniere's disease, became evident by distension of the Reissner's membrane. iNOS expression could be noted in endothelium, spiral ganglion cells, in nerve fibers, in supporting cells of the organ of Corti and cells of the spiral ligament. Temporal bones of non-operated controls (n = 6) as well as of sham-operated animals (n = 3) did not show structures positive to iNOS. These findings imply that iNOS-generated NO could be involved in the pathophysiology of cochlear dysfunction in Meniere's disease. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Cologne, Dept Otorhinolaryngol, D-50924 Cologne, Germany. Univ Cologne, Dept Anat, D-50924 Cologne, Germany. Guangxi Med Univ, Dept Otolaryngol, Nanning 530021, Guangxi, Peoples R China. RP Michel, O (reprint author), Univ Cologne, Dept Otorhinolaryngol, Joseph Stelzmann Str 9, D-50924 Cologne, Germany. RI Michel, Olaf/B-3673-2012 OI Michel, Olaf/0000-0003-4289-5693 CR ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 BECKMAN JS, 1990, P NATL ACAD SCI USA, V87, P1620, DOI 10.1073/pnas.87.4.1620 BRECHTELSBAUER PB, 1995, HEARING RES, V89, P130, DOI 10.1016/0378-5955(95)00130-4 BROWN GC, 1995, NEUROSCI LETT, V193, P201, DOI 10.1016/0304-3940(95)11703-Y Chan E, 1997, ACTA PHYSIOL SCAND, V161, P533, DOI 10.1046/j.1365-201X.1997.00241.x CLEETER MWJ, 1994, FEBS LETT, V345, P50, DOI 10.1016/0014-5793(94)00424-2 Dais CGD, 1996, HEARING RES, V99, P1 DAWSON VL, 1991, P NATL ACAD SCI USA, V88, P6368, DOI 10.1073/pnas.88.14.6368 EHRENBERGER K, 1991, HEARING RES, V52, P73, DOI 10.1016/0378-5955(91)90188-F Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 FORSTERMANN U, 1991, BIOCHEM PHARMACOL, V42, P1849, DOI 10.1016/0006-2952(91)90581-O Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 Fridberger A, 1997, ACTA PHYSIOL SCAND, V161, P239, DOI 10.1046/j.1365-201X.1997.00214.x Gosepath K, 1997, BRAIN RES, V747, P26, DOI 10.1016/S0006-8993(96)01149-3 Hallpike C S, 1938, Proc R Soc Med, V31, P1317 Hess A, 1999, NEUROSCI LETT, V264, P145, DOI 10.1016/S0304-3940(99)00195-0 Hess A, 1998, NEUROSCI LETT, V251, P185, DOI 10.1016/S0304-3940(98)00532-1 Horner K C, 1989, Acta Otolaryngol Suppl, V468, P65 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 Kong WJ, 1996, HEARING RES, V99, P22, DOI 10.1016/S0378-5955(96)00076-7 KUMAGAMI H, 1983, ORL J OTO-RHINO-LARY, V45, P143 MANZONI O, 1992, NEURON, V8, P653, DOI 10.1016/0896-6273(92)90087-T Michel O, 1999, HEARING RES, V133, P1, DOI 10.1016/S0378-5955(99)00049-0 MONCADA S, 1991, PHARMACOL REV, V43, P109 NIEDZIELSKI AS, 1995, J NEUROSCI, V15, P2338 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 Takumida M, 1998, EUR ARCH OTO-RHINO-L, V255, P184, DOI 10.1007/s004050050040 VANDEELEN GW, 1988, ACTA OTO-LARYNGOL, V105, P193, DOI 10.3109/00016488809096998 YAMAKAWA K, 1938, P 42 JPN OT SOC, V44, P181 YAMAMOTO K, 1991, ACTA OTO-LARYNGOL, V111, P312, DOI 10.3109/00016489109137393 NR 30 TC 24 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 23 EP 28 DI 10.1016/S0378-5955(00)00018-6 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900003 PM 10771181 ER PT J AU Furst, M Aharonson, V Levine, RA Fullerton, BC Tadmor, R Pratt, H Polyakov, A Korczyn, AD AF Furst, M Aharonson, V Levine, RA Fullerton, BC Tadmor, R Pratt, H Polyakov, A Korczyn, AD TI Sound lateralization and interaural discrimination. Effects of brainstem infarcts and multiple sclerosis lesions SO HEARING RESEARCH LA English DT Article DE auditory pathway; brainstem magnetic resonance imaging; lateralization; multiple sclerosis; infarct ID AUDITORY-EVOKED-POTENTIALS; CLICK LATERALIZATION; PONTINE LESIONS; STEM LESIONS; HUMANS AB Subjects with brainstem lesions due to either an infarct or multiple sclerosis (MS) underwent two types of binaural testing (lateralization testing and interaural discrimination) for three types of sounds (clicks and high and low frequency narrow-band noise) with two kinds of interaural differences (level and time). Two major types of abnormalities were revealed in the lateralization performances: perception of all stimuli, regardless of interaural differences (time and/or level) in the center of the head (center-oriented), or lateralization of all stimuli to one side or the other of the head (side-oriented). Similar patterns of abnormal lateralization (center-oriented and side-oriented) occurred for MS and stroke patients. A subject's pattern of abnormal lateralization testing was the same regardless of the type of stimulus or type of interaural disparity. Lateralization testing was a more sensitive test than interaural discrimination testing for both types of subjects. Magnetic resonance image (MRI) scanning in three orthogonal planes of the brainstem was used to detect lesions. A semi-automated algorithm superimposed the auditory pathway onto each MRI section. Whenever a lesion overlapped the auditory pathway, some binaural performance was abnormal and vice versa. Given a lateralization test abnormality, whether the pattern was center-oriented or side-oriented was mainly determined by lesion site. Center-oriented performance was principally associated with caudal pontine lesions and side-oriented performance with lesions rostral to the superior olivary complex. For lesions restricted to the lateral lemniscus and/or inferior colliculus, whether unilateral or bilateral, just noticeable differences (JNDs) were nearly always abnormal, but for caudal pontine lesions JNDs could be normal or abnormal. MS subjects were more sensitive to interaural time delays than interaural level differences particularly for caudal pontine lesions, while stroke patients showed no differential sensitivity to the two kinds of interaural differences. These results suggest that neural processing of binaural stimuli is multilevel and begins with independent interaural time and level analyzers in the caudal pens. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tel Aviv Univ, Fac Engn, Dept Elect Engn Syst, IL-69978 Tel Aviv, Israel. Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Tel Aviv Univ, Sackler Fac Med, Dept Radiol, IL-69978 Tel Aviv, Israel. Technion Israel Inst Technol, Evoked Potentials Lab, IL-32000 Haifa, Israel. Tel Aviv Univ, Sackler Sch Med, Sieratzki Chair Neurol, IL-69978 Tel Aviv, Israel. RP Furst, M (reprint author), Tel Aviv Univ, Fac Engn, Dept Elect Engn Syst, IL-69978 Tel Aviv, Israel. EM mira@eng.tau.ac.il CR Aharonson V, 1998, J ACOUST SOC AM, V103, P2624, DOI 10.1121/1.422783 Bookstein F., 1978, LECT NOTES BIOMATHEM Furst M, 1995, J Basic Clin Physiol Pharmacol, V6, P149 FURST M, 1995, HEARING RES, V82, P109 FURST M, 1990, HEARING RES, V49, P347, DOI 10.1016/0378-5955(90)90113-4 FURST M, 1992, ADV BIOSCI, V83, P635 HAUSLER R, 1980, BRAIN RES, V191, P589, DOI 10.1016/0006-8993(80)91312-8 HENDLER T, 1990, EAR HEARING, V11, P403, DOI 10.1097/00003446-199012000-00002 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 LEVINE RA, 1993, HEARING RES, V68, P59, DOI 10.1016/0378-5955(93)90065-9 LEVINE RA, 1995, BRAIN, V117, P1127 LEVINE RA, 1993, HEARING RES, V68, P73, DOI 10.1016/0378-5955(93)90066-A LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 POSER CM, 1983, ANN NEUROL, V13, P227, DOI 10.1002/ana.410130302 Pratt H, 1998, EVOKED POTENTIAL, V108, P511, DOI 10.1016/S0168-5597(98)00029-X RICHTER EA, 1983, AM J ANAT, V168, P157, DOI 10.1002/aja.1001680205 TADMOR R, 1994, P 15 S NEUR, P34 TENNY R, 1994, THESIS TEL AVIV U TE NR 18 TC 25 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 29 EP 42 DI 10.1016/S0378-5955(00)00019-8 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900004 PM 10771182 ER PT J AU Lohuis, TD Fuzessery, ZM AF Lohuis, TD Fuzessery, ZM TI Neuronal sensitivity to interaural time differences in the sound envelope in the auditory cortex of the pallid bat SO HEARING RESEARCH LA English DT Article DE interaural time difference; auditory cortex; interaural intensity difference; inferior colliculus; binaural processing; sound localization ID LATERAL SUPERIOR OLIVE; AMPLITUDE-MODULATED TONES; HIGH-FREQUENCY NEURONS; INFERIOR COLLICULUS; INTENSITY DIFFERENCES; BINAURAL INTERACTION; PRESSURE LEVEL; RATTUS-NORVEGICUS; COMPLEX WAVEFORMS; SPECTRAL LOCUS AB Interaural time differences in the envelope of a sound (envelope ITDs) call potentially provide spatial information at high frequencies where interaural phase differences (IPDs) are not available. Interaural intensity differences (IIDs) also provide important spatial information at high frequencies. Both IIDs and envelope ITDs can influence spatial perception at high frequencies, but behavioral and physiological studies suggest that IIDs dominate perception. This study examines envelope ITD sensitivity in the auditory cortex of the pallid bat, a species that uses passive sound localization at the low end of its audible range to find prey. Its auditory system is entirely 'high-frequency' in that phase-locking does not occur at the low end of its audible range. If the bat uses ITDs, they must be derived from the envelope of the signal. A previous study of envelope ITD sensitivity in its inferior colliculus (IC) reported that neurons are sensitive to the small +/- 70 mu s range of available ITDs. This study extends these findings to the cortical level to assess the transformation of ITD sensitivity and the binaural response properties that underlie this sensitivity. Two measures of sensitivity were used. The dynamic ITD range measures the range of ITDs over which the maximum response of a neuron decreases by 80%. When presented with square-wave amplitude-modulated tones statically delayed in arrival time, the average dynamic ITD range in the IC is 304 mu s, but dropped to 175 mu s in auditory cortex. IC neurons average a 38% change in maximum response over the relevant ITD range, while cortical neurons average a 67% change. Also measured were time-intensity trading ratios, which index the extent to which a change in IID can cause a shift the dynamic ITD range. Average trading ratios are approximately the same in the IC and auditory cortex (17.9 mu s/dB vs. 16.7 mu s/dB, respectively). Binaural interactions changed from the IC to auditory cortex. In IC, ITD sensitivity is an inhibitory, subtractive process in which ITDs reduce the response evoked by contralateral monaural stimulation. In the auditory cortex, both binaural inhibition and facilitation occur. In the majority of cortical neurons, IID and ITD functions were remarkably similar in shape, having stepped, step-peaked or peaked functions. The binaural interactions (inhibition and/or facilitation) evoked by ITDs and IIDs were also typically similar. These results suggest that IIDs and envelope ITDs are having similar effects on output of the same binaural comparator system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Wyoming, Dept Zool & Physiol, Laramie, WY 82071 USA. RP Fuzessery, ZM (reprint author), Univ Wyoming, Dept Zool & Physiol, POB 3166, Laramie, WY 82071 USA. CR BATRA R, 1993, J NEUROPHYSIOL, V70, P64 BELL GP, 1982, BEHAV ECOL SOCIOBIOL, V10, P217, DOI 10.1007/BF00299688 BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BERNSTEIN LR, 1985, J ACOUST SOC AM, V78, P514, DOI 10.1121/1.392473 Bernstein LR, 1996, J ACOUST SOC AM, V99, P1670, DOI 10.1121/1.414689 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BRUGGE JF, 1969, J COMP PHYSL, V192, P445 CAIRD D, 1987, EXP BRAIN RES, V68, P379 DEATHERAGE BH, 1959, J ACOUST SOC AM, V31, P486, DOI 10.1121/1.1907740 Fitzpatrick DC, 1997, NATURE, V388, P871, DOI 10.1038/42246 Fuzessery ZM, 1996, HEARING RES, V95, P1, DOI 10.1016/0378-5955(95)00223-5 Fuzessery ZM, 1997, HEARING RES, V109, P46, DOI 10.1016/S0378-5955(97)00053-1 FUZESSERY ZM, 1993, J COMP PHYSIOL A, V171, P767, DOI 10.1007/BF00213073 FUZESSERY ZM, 1991, J NEUROSCI METH, V36, P45, DOI 10.1016/0165-0270(91)90136-N GROTHE B, 1995, NATURWISSENSCHAFTEN, V82, P521, DOI 10.1007/BF01134488 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 Hafter E. R., 1984, DYNAMIC ASPECTS NEOC, P425 HAFTER ER, 1983, J ACOUST SOC AM, V73, P644, DOI 10.1121/1.388956 HARNISCHFEGER G, 1985, J NEUROPHYSIOL, V53, P89 HEFFNER HE, 1985, HEARING RES, V19, P151, DOI 10.1016/0378-5955(85)90119-4 HENNING GB, 1974, J ACOUST SOC AM, V55, P84, DOI 10.1121/1.1928135 Irvine D. R. F., 1986, PROGR SENSORY PHYSL, P1 Irvine DRF, 1996, J NEUROPHYSIOL, V75, P75 IRVINE DRF, 1995, HEARING RES, V85, P127, DOI 10.1016/0378-5955(95)00040-B IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 JORIS PX, 1995, J NEUROPHYSIOL, V73, P1043 KELLY JB, 1980, J NEUROPHYSIOL, V44, P1161 KELLY JB, 1991, HEARING RES, V55, P39, DOI 10.1016/0378-5955(91)90089-R KELLY JB, 1988, J NEUROPHYSIOL, V59, P1756 Kidd SA, 1996, J NEUROSCI, V16, P7390 KITZES LM, 1980, J COMP NEUROL, V192, P455, DOI 10.1002/cne.901920306 KNUDSEN EI, 1984, DYNAMIC ASPECTS NEOC MCFADDEN D, 1976, J ACOUST SOC AM, V59, P634, DOI 10.1121/1.380913 MIDDLEBROOKS JC, 1990, J ACOUST SOC AM, V87, P2149, DOI 10.1121/1.399183 NUETZEL JM, 1976, J ACOUST SOC AM, V60, P1339, DOI 10.1121/1.381227 ORR ROBERT T., 1954, PROC CALIFORNIA ACAD SCI, V28, P165 Park TJ, 1996, J NEUROSCI, V16, P6554 PHILLIPS DP, 1981, HEARING RES, V4, P299, DOI 10.1016/0378-5955(81)90014-9 POLLAK GD, 1988, HEARING RES, V36, P107, DOI 10.1016/0378-5955(88)90054-8 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 REALE RA, 1990, J NEUROPHYSIOL, V64, P1247 ROTH GL, 1980, J ACOUST SOC AM, V68, P1643, DOI 10.1121/1.385196 SANES DH, 1990, J NEUROSCI, V10, P3494 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P449 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P462 SHEN W, 1996, THESIS U WYOMING LAR STANFORD TR, 1992, J NEUROSCI, V12, P3200 TRAHIOTIS C, 1986, J ACOUST SOC AM, V79, P1950, DOI 10.1121/1.393202 Woodworth R. S., 1938, EXPT PSYCHOL WU SH, 1992, J NEUROPHYSIOL, V68, P1151 YIN TCT, 1985, J NEUROPHYSIOL, V53, P746 YIN TCT, 1983, J NEUROPHYSIOL, V50, P1000 YIN TCT, 1986, J NEUROPHYSIOL, V55, P280 YIN TCT, 1984, J ACOUST SOC AM, V76, P1401, DOI 10.1121/1.391457 NR 55 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 43 EP 57 DI 10.1016/S0378-5955(00)00021-6 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900005 PM 10771183 ER PT J AU Ren, TY Nuttall, AL AF Ren, TY Nuttall, AL TI Fine structure and multicomponents of the electrically evoked otoacoustic emission in gerbil SO HEARING RESEARCH LA English DT Article DE electrical stimulation; cochlea; otoacoustic emission; electrically evoked otoacoustic emission; cochlear amplifier; furosemide; signal processing ID OUTER HAIR-CELLS; ACOUSTIC DISTORTION-PRODUCT; TIME-DELAY SPECTROMETRY; GUINEA-PIG; BASILAR-MEMBRANE; COCHLEA; FUROSEMIDE; MODEL; EAR AB Like the acoustically evoked distortion product otoacoustic emissions (DPOAE), the amplitude spectrum of the extracochlear electrically evoked otoacoustic emission (EEOAE) also shows peaks and valleys, which are termed the fine structure (FS) of the EEOAE. The hypothesis that the FS of the EEOAE is generated by multiple wave interactions in the cochlea is investigated by examining the relationship between the FS and the multiple-delay components of the EEOAE. The bulla of the gerbil was exposed using a ventral surgical approach. One pole of a bipolar electrode was placed in the round window niche, and the other pole on the surface of the first cochlear turn. A microphone was used to measure electrically evoked sound pressure change in the ear canal. A recently developed multicomponent analysis method was used to detect the EEOAE multiple delays. It was found that the FS is the spectral representation of the multiple-delay components. The relative power of a prominent long delay component (LDC) shows a negative relationship to the electrical stimulus level. Both the FS and the LDC were abolished by intravenous furosemide. Reconstructed signals showed that mathematical removal of the EEOAE LDC also completely eliminated the FS. These data demonstrate that the FS and the EEOAE multicomponents are properties of normal cochlear mechanics in a healthy ear and that the FS is a manifestation of the multicomponents. The findings in this study strongly indicate that the FS of the EEOAE evoked by extracochlear electrical stimulation is generated by wave interaction in the cochlea. The similarity between the EEOAE FS and the DPOAE FS suggests that they may share the same mechanism. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol & Head & Neck Surg, Oregon Hearing Res Ctr NRC04, Portland, OR 97201 USA. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Ren, TY (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol & Head & Neck Surg, Oregon Hearing Res Ctr NRC04, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Brown AM, 1996, J ACOUST SOC AM, V100, P3260, DOI 10.1121/1.417209 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 COHEN L, 1989, P IEEE, V77, P941, DOI 10.1109/5.30749 DALLOS P, 1992, J NEUROSCI, V12, P4575 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DANTONIO P, 1989, J AUDIO ENG SOC, V37, P674 DAVIS H, 1965, COLD SPRING HARB SYM, V30, P181 Fahey PF, 1997, J ACOUST SOC AM, V102, P2880, DOI 10.1121/1.420343 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HE NJ, 1993, J ACOUST SOC AM, V94, P2659, DOI 10.1121/1.407350 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 Kirk DL, 1996, J ACOUST SOC AM, V100, P3714, DOI 10.1121/1.417335 LONG GR, 1984, HEARING RES, V15, P73, DOI 10.1016/0378-5955(84)90227-2 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 POLETTI MA, 1988, J AUDIO ENG SOC, V36, P457 REN T, 1998, HEARING RES, P120 REN T, 2000, IN PRESS J NEUROSCI Ren TY, 1995, HEARING RES, V92, P178, DOI 10.1016/0378-5955(95)00217-0 Ren TY, 1996, HEARING RES, V102, P43, DOI 10.1016/S0378-5955(96)00145-1 Ren TY, 1996, NEUROSCI LETT, V207, P167, DOI 10.1016/0304-3940(96)12524-6 RONKEN DA, 1981, J ACOUST SOC AM, V70, P410, DOI 10.1121/1.386784 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RYBAK LP, 1982, OTOLARYNG HEAD NECK, V90, P808 Sakaguchi N, 1998, HEARING RES, V118, P114, DOI 10.1016/S0378-5955(98)00022-7 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 Stover LJ, 1996, J ACOUST SOC AM, V99, P1016, DOI 10.1121/1.414630 SUN XM, 1994, J ACOUST SOC AM, V96, P2166, DOI 10.1121/1.410158 Talmadge CL, 1999, J ACOUST SOC AM, V105, P275, DOI 10.1121/1.424584 Wilson J., 1980, Proceedings of the Eighth Annual Canadian Conference on Information Science ZWEIG G, 1995, J ACOUST SOC AM, V98, P2018, DOI 10.1121/1.413320 NR 39 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 58 EP 68 DI 10.1016/S0378-5955(00)00027-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900006 PM 10771184 ER PT J AU Cunningham, CD Weber, PC Spicer, SS Schulte, BA AF Cunningham, CD Weber, PC Spicer, SS Schulte, BA TI Canalicular reticulum in vestibular hair cells SO HEARING RESEARCH LA English DT Article DE inner ear; endoplasmic reticulum; ultrastructure; ion transport; synaptic vesicle; membranogenesis; gerbil ID GUINEA-PIG COCHLEA; AGE-RELATED-CHANGES; ENDOPLASMIC-RETICULUM; CURRENTS; GERBIL; TRANSDUCTION; POTENTIALS; CHANNELS AB A membrane limited system referred to as canalicular reticulum (CR) has been demonstrated in the apical cytosol of the cochlea's inner and outer hair cells. Similarities between cochlear and vestibular hair cells prompted investigation of the presence of CR in hair cells of the gerbil vestibular labyrinth. A method of fixation with glutaraldehyde followed by an osmium-ferrocyanide mixture demonstrated abundant CR in the apex of both type I and type II hair cells. The CR was closely associated with numerous Golgi zones in the apex of the vestibular hair cells, indicating its genesis from Golgi cisternae. Also preserved in upper cytosol were discrete complexes of mitochondria with granular reticulum. These complexes offered a possible site for generating the membrane in Golgi zones and CR. Single and parallel cisternae of granular reticulum were observed in the basal half of the hair cells together with numerous synaptic-like vesicles. These cisternae with their terminal blebbing and accompanying canaliculi were interpreted as novel structures mediating synaptic vesicle genesis in vestibular hair cells in a manner comparable to that postulated for cochlear inner hair cells. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. RP Cunningham, CD (reprint author), Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Walton Res Bldg,Room 608,39 Sabin St,POB 250150, Charleston, SC 29425 USA. CR Alberts B., 1994, MOL BIOL CELL ASHMORE JF, 1986, NATURE, V322, P386 BARON DA, 1984, LAB INVEST, V51, P233 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z CHANG JSY, 1992, J COMP NEUROL, V324, P621, DOI 10.1002/cne.903240413 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 DEBRUIJN WC, 1968, P 4 EUR REG C EL MIC, P65 ENGSTROM H., 1958, EXPTL CELL RES SUPPL, V5, P460 Engström H, 1972, Acta Otolaryngol Suppl, V301, P75 FAWCETT DW, 1981, CELL, P369 FLOCK A, 1964, J CELL BIOL, V22, P413, DOI 10.1083/jcb.22.2.413 FORGE A, 1982, CELL TISSUE RES, V226, P375 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 HOUSLEY GD, 1992, J PHYSIOL-LONDON, V448, P73 HUDSPETH AJ, 1983, ANNU REV NEUROSCI, V6, P187, DOI 10.1146/annurev.ne.06.030183.001155 Hunter-Duvar IM, 1984, ULTRASTRUCTURAL ATLA, P211 Iurato S, 1967, SUBMICROSCOPIC STRUC Karnosky M., 1971, P 11 M AM SOC CELL B, P146 KIMURA R, 1963, ACTA OTOLARYNGOL, V57, P517 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 Light P, 1996, BBA-REV BIOMEMBRANES, V1286, P65, DOI 10.1016/0304-4157(96)00004-4 LOWENSTEIN O, 1959, NATURE, V184, P1807, DOI 10.1038/1841807a0 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MOLLER OJ, 1983, CELL TISSUE RES, V228, P13 MOLLGARD K, 1978, J MEMBRANE BIOL, V40, P71, DOI 10.1007/BF02025999 MOLLGARD K, 1981, WATER TRANSPORT EPIT, P85 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 QVORTRUP K, 1990, CELL TISSUE RES, V261, P287, DOI 10.1007/BF00318670 ROSTGAARD J, 1980, CELL TISSUE RES, V212, P17 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 Spicer SS, 1999, J COMP NEUROL, V409, P424 Spicer SS, 1999, HEARING RES, V130, P7, DOI 10.1016/S0378-5955(98)00202-0 Spicer SS, 1998, ANAT REC, V251, P97, DOI 10.1002/(SICI)1097-0185(199805)251:1<97::AID-AR15>3.0.CO;2-6 SPOENDLIN H, 1970, ULTRASTRUCTURE PERIP, P264 Valtorta E, 1996, BIOCHEM SOC T, V24, P645 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 Wersäll J, 1972, Prog Brain Res, V37, P3, DOI 10.1016/S0079-6123(08)63890-X WILLINGHAM MC, 1984, J HISTOCHEM CYTOCHEM, V32, P455 NR 39 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 69 EP 82 DI 10.1016/S0378-5955(00)00022-8 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900007 PM 10771185 ER PT J AU Lychakov, DV Rebane, YT AF Lychakov, DV Rebane, YT TI Otolith regularities SO HEARING RESEARCH LA English DT Article DE fish; otolith; morphometry; mathematical modeling; ecomorphology ID VERTEBRATE HAIR-CELLS; MECHANOELECTRICAL TRANSDUCTION; MACULA NEGLECTA; GROWTH-RATES; LATERAL-LINE; FISH EAR; BULLFROG; SOUND; ULTRASTRUCTURE; SENSITIVITY AB The masses and the area sizes of the otoliths for the utriculus, sacculus and lagena of 15 species of the Black Sea fish are analyzed. Morphometrical otolith regularities are derived and their functional and ecomorphological explanations are suggested. The otolith regularities are summarized in four otolith rules: (1) the masses of the otoliths gradually increase with the fish growth. (2) The mass ratio of the sacculus and utriculus or the sacculus and lagena otoliths does not change with the fish growth. (3) The ratio between the otolith area s and the otolith mass m is described by the exponential equation s = alpha m(2/3). (4) The ratio between the otolith and macula sizes does not change with fish growth. Mathematical modeling of the otolith displacement responses to the acoustic and the instant force stimuli is performed. Based on the modeling the functional and ecomorphological explanations of the otolith regularities are suggested: (1) the greater the otolith mass, the higher the acoustic sensitivity at low frequencies and the sharper the frequency-response curve at its maximum. (2) The separation between maxima of the frequency-response curves for the saccular and lagenar otoliths remains virtually constant with the fish growth. (3) The bottom and littoral fish have better auditory capabilities than the pelagic fish. (4) The sensitivity to vestibular stimuli for greater otoliths is higher but the response is slower. The corresponding acceleration resolution for greater otoliths is higher and the range of accelerations in which the otolith organ can operate is narrower. (5) The relative vestibular sensitivities of the utriculus, sacculus and lagena otolith organs remain constant with fish growth. (6) The otolith organs of the bottom and littoral fish are tuned to different accelerations and possess different functional properties. The otolith organs of pelagic fish are adapted to a limited range of accelerations and are less sensitive to low accelerations as compared to the bottom and littoral fish. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Sechenov Inst, St Petersburg 194223, Russia. AF Ioffe Phys Tech Inst, St Petersburg 194021, Russia. RP Lychakov, DV (reprint author), Sechenov Inst, Thorez Pr 44, St Petersburg 194223, Russia. CR ABAKUMOV VA, 1971, ANIMAL LIFE ALEEV YG, 1963, FUNCTIONAL PRINCIPLE BENSER ME, 1993, HEARING RES, V68, P243, DOI 10.1016/0378-5955(93)90128-N BUDELMANN BU, 1990, SQUID EXPT ANIMALS BULOG B, 1989, J MORPHOL, V201, P59, DOI 10.1002/jmor.1052010106 CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 CLARKE MR, 1980, J MAR BIOL ASSOC UK, V60, P329 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 CORWIN JT, 1985, J COMP NEUROL, V239, P445, DOI 10.1002/cne.902390410 CORWIN JT, 1983, J COMP NEUROL, V217, P345, DOI 10.1002/cne.902170309 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DAVID AW, 1993, FISH B, V92, P509 DeVRIES H., 1950, ACTA OTO LARYNGOL, V38, P262, DOI 10.3109/00016485009118384 DIJKGRAAF S, 1976, SOUND RECEPTION FISH, V7, P116 Fay R.R., 1980, P3 Fermin CD, 1998, HISTOL HISTOPATHOL, V13, P1103 GAULDIE RW, 1988, COMP BIOCH PHYSL A, V91, P359 GAULDIE RW, 1993, J MORPHOL, V218, P1, DOI 10.1002/jmor.1052180102 GOLDSCHMID A, 1989, TRENDS VERTEBR MORPH, V35, P501 GOVARDOVSKII V I, 1977, Zhurnal Evolyutsionnoi Biokhimii i Fiziologii, V13, P162 GRANT W, 1987, AVIAT SPACE ENVIR MD, V58, P970 GRODINS FS, 1966, CONTROL THEORY BIOL HOFF GR, 1993, COMP BIOCHEM PHYS A, V106, P209, DOI 10.1016/0300-9629(93)90502-U Holt JR, 1997, J NEUROSCI, V17, P8739 HORN E, 1986, J COMP PHYSIOL A, V159, P869, DOI 10.1007/BF00603740 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 HUDSPETH AJ, 1979, P NATL ACAD SCI USA, V76, P1506, DOI 10.1073/pnas.76.3.1506 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 Isakovich M.A., 1973, GEN ACOUSTICS KHARKEEVICH TA, 1990, Z MIKROSK ANAT FORSC, V104, P639 KOTRSCHAL K, 1992, ENVIRON BIOL FISH, V33, P135, DOI 10.1007/BF00002560 KOTRSCHAL K, 1990, Z ZOOL SYST EVOL, V28, P166 LI CW, 1979, ANN OTO RHINOL LARYN, V88, P427 LIM DJ, 1974, BRAIN BEHAV EVOLUT, V10, P37, DOI 10.1159/000124301 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 Lindsey C. C., 1978, FISH PHYSIOL, VVII, P1, DOI DOI 10.1016/S1546-5098(08)60163-6 LYCHAKOV DV, 1995, J EVOL BIOCHEM PHYS+, V31, P90 LYCHAKOV D V, 1990, Zhurnal Evolyutsionnoi Biokhimii i Fiziologii, V26, P550 Lychakov DV, 1995, J EVOL BIOCHEM PHYS+, V31, P182 LYCHAKOV DV, IN PRESS P 2 INT S F LYCHAKOV DV, 1992, J EVOL BIOCHEM PHYS+, V28, P531 LYCHAKOV D V, 1984, Zhurnal Evolyutsionnoi Biokhimii i Fiziologii, V20, P391 Lychakov DV, 1988, ZH EVOL BIOKHIM FIZ, V24, P256 LYCHAKOV DV, 1994, J EVOL BIOCHEM PHYS, V30, P69 LYCHAKOV DV, 1988, KOSM BIOL AVIAK MED, V5, P33 Lychakov D V, 1998, Zh Evol Biokhim Fiziol, V34, P364 Lychakov DV, 1993, J EVOL BIOCHEM PHYS+, V28, P531 MATHIESEN C, 1987, J MORPHOL, V194, P129, DOI 10.1002/jmor.1051940203 MONEY KE, 1966, NASA, P91 MOSEGAARD H, 1988, CAN J FISH AQUAT SCI, V45, P1514, DOI 10.1139/f88-180 MYAGKOV N A, 1984, Arkhiv Anatomii Gistologii i Embriologii, V86, P24 OHMORI H, 1987, J PHYSIOL-LONDON, V387, P589 Platt C., 1981, HEARING SOUND COMMUN, P3 PLATT C, 1993, HEARING RES, V65, P133, DOI 10.1016/0378-5955(93)90208-I PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 PLATT C, 1973, J EXP BIOL, V59, P491 Platt C., 1983, P89 POPPER AN, 1978, J COMP NEUROL, V181, P117, DOI 10.1002/cne.901810107 Popper AN, 1998, T AM FISH SOC, V127, P673, DOI 10.1577/1548-8659(1998)127<0673:AOSAOS>2.0.CO;2 POPPER AN, 1980, AM J ANAT, V157, P115, DOI 10.1002/aja.1001570202 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1979, J MORPHOL, V161, P241, DOI 10.1002/jmor.1051610302 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 POPPER AN, 1982, AM ZOOL, V22, P311 POPPER AN, 1987, BRAIN BEHAV EVOLUT, V30, P43, DOI 10.1159/000118637 Popper Arthur N., 1993, P99 POTE KG, 1991, COMP BIOCH PHYSL B, V98, P203 PROKOFIEVA LI, 1986, DOKL AKAD NAUK SSSR+, V286, P978 PROTASOV VR, 1965, BIOACOUSTIC FISH PROTASOV VR, 1978, FISH BEHAV RADTKE RL, 1981, FISH B-NOAA, V79, P360 RADTKE RL, 1985, J EXP MAR BIOL ECOL, V90, P259, DOI 10.1016/0022-0981(85)90171-6 RADTKE RL, 1982, FISH B-NOAA, V80, P201 RESHETNIKOV YS, 1989, DICT ANIMAL NAMES 5, P1 REZNICK D, 1989, CAN J FISH AQUAT SCI, V46, P108, DOI 10.1139/f89-014 RIMAN IS, 1947, T TSAGI, V637, P1 ROGERS PH, 1988, J ACOUST SOC AM, V83, P338, DOI 10.1121/1.396444 SAMARIN GI, 1973, KOSM BIOL AVIAK MED+, V7, P37 SAMARIN GI, 1992, THESIS MOSCOW, P1 SANCHEZ DY, 1990, J NEUROSCI, V10, P361 SECOR DH, 1989, CAN J FISH AQUAT SCI, V46, P113, DOI 10.1139/f89-015 SHOFNER WP, 1984, J COMP NEUROL, V224, P141, DOI 10.1002/cne.902240113 SHOFNER WP, 1981, J EXP BIOL, V93, P181 SIREGAR YI, 1994, ACTA ZOOL-STOCKHOLM, V75, P213 SMIRNOV AN, 1959, T KARADAG BIOL STANS, V15, P31 STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 SVETOVIDOV AN, 1964, FISH BLACK SEA TAVOLGA WN, 1976, SOUND RECEPTION FISH, V7, P182 THOMAS RM, 1983, S AFRICAN J MARINE S, V1, P133 TICHOMIROVA LI, 1985, ARCH ANAT GISTOL EMB, V89, P35 TICHOMIROVA LI, 1984, ARCH ANAT GISTOL EMB, V87, P37 VANNETTEN SM, 1987, HEARING RES, V29, P55, DOI 10.1016/0378-5955(87)90205-X WIEDERHOLD ML, 1990, HEARING RES, V49, P63, DOI 10.1016/0378-5955(90)90095-7 WRIGHT PJ, 1990, J FISH BIOL, V36, P241, DOI 10.1111/j.1095-8649.1990.tb05599.x ZAUNREITER M, 1991, VISION RES, V31, P383, DOI 10.1016/0042-6989(91)90091-I NR 96 TC 41 Z9 43 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 83 EP 102 DI 10.1016/S0378-5955(00)00026-5 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900008 PM 10771186 ER PT J AU Ahroon, WA Hamernik, RP AF Ahroon, WA Hamernik, RP TI The effects of interrupted noise exposures on the noise-damaged cochlea SO HEARING RESEARCH LA English DT Article DE toughening; hearing loss; interrupted noise; asymptotic threshold ID TOUGHENED AUDITORY-SYSTEM; INDUCED HEARING-LOSS; THRESHOLD SHIFT; CONDITIONING EXPOSURES; TRAUMATIC EXPOSURE; IMPULSE NOISE; CHINCHILLA; PROTECTION AB A variety of interrupted noise exposure paradigms will produce a toughening effect in the mammalian auditory system. That is, the threshold shift will gradually become smaller with each successive daily exposure. The ability of the system to be toughened has not been explored in subjects with a pre-existing noise-induced hearing loss. Using the chinchilla as the experimental animal, evoked potential audiometry to obtain thresholds, and surface preparation histology to quantify the sensory cell population, the issue of toughening was examined in the noise-damaged auditory system. Toughening was produced by a 1.0 kHz, narrow-band impact at 115 dB peak SPL for 10 days, 6 h/day, and trauma was produced by a 1.0 kHz, narrow-band impact at 121 dB peak SPL for 5 days, 24 h/day. Four groups of animals were used. Group 1: traumatic exposure followed 30 days later by the toughening exposure. Group 2: toughening exposure followed 30 days later by the traumatic exposure. Group 3: a trauma-only control. Group 4: a toughening only control. Group 2 that received the toughening exposure 30 days prior to the traumatic exposure showed a 10 to more than 20 dB toughening effect between the 0.5 and 4.0 kHz test frequencies, while Group 1 that received the traumatic exposure followed 30 days later by the toughening exposure showed no toughening. The permanent changes in the evoked response audiograms and sensory cell populations were the same in Groups 1, 2 and 3 that were exposed to the traumatic noise, regardless of whether or not the animals were ever subjected to the toughening noise or whether the toughening noise preceded or followed the traumatic noise. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Coll Plattsburgh, Auditory Res Lab, Plattsburgh, NY 12901 USA. RP Hamernik, RP (reprint author), SUNY Coll Plattsburgh, Auditory Res Lab, 107 Beaumont Hall,101 Broad St, Plattsburgh, NY 12901 USA. CR Ahroon WA, 1996, J ACOUST SOC AM, V100, P2247, DOI 10.1121/1.417934 Ahroon WA, 1999, HEARING RES, V129, P101, DOI 10.1016/S0378-5955(98)00227-5 BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T CAMPO P, 1991, HEARING RES, V55, P195, DOI 10.1016/0378-5955(91)90104-H CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 DAVIS H, 1950, Acta Otolaryngol Suppl, V88, P1 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 Fay R. R., 1988, HEARING VERTEBRATES Hamernik RP, 1999, HEARING RES, V132, P140, DOI 10.1016/S0378-5955(99)00039-8 Hamernik RP, 1998, J ACOUST SOC AM, V103, P3478, DOI 10.1121/1.423056 HAMERNIK RP, 1994, J ACOUST SOC AM, V95, P444, DOI 10.1121/1.408338 HENDERSON D, 1979, J ACOUST SOC AM, V65, P1231, DOI 10.1121/1.382790 HENSELMAN LW, 1994, HEARING RES, V78, P1, DOI 10.1016/0378-5955(94)90038-8 McFadden SL, 1997, HEARING RES, V103, P142, DOI 10.1016/S0378-5955(96)00170-0 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLS JH, 1992, NOISE INDUCED HEARIN, P237 SAUNDERS JC, 1977, J ACOUST SOC AM, V61, P558, DOI 10.1121/1.381298 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H SUBRAMANIAM M, 1992, HEARING RES, V58, P57, DOI 10.1016/0378-5955(92)90008-B SUBRAMANIAM M, 1993, HEARING RES, V65, P234, DOI 10.1016/0378-5955(93)90216-N White DR, 1998, J ACOUST SOC AM, V103, P1566, DOI 10.1121/1.421303 NR 21 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 103 EP 109 DI 10.1016/S0378-5955(00)00030-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900009 PM 10771187 ER PT J AU Hara, A Serizawa, F Tabuchi, K Senarita, M Kusakari, J AF Hara, A Serizawa, F Tabuchi, K Senarita, M Kusakari, J TI Hydroxyl radical formation in the perilymph of asphyxic guinea pig SO HEARING RESEARCH LA English DT Article DE hydroxyl radical; asphyxia; high performance liquid chromatography; iron; free radical ID 2,3-DIHYDROXYBENZOIC ACID; LIQUID-CHROMATOGRAPHY; CEREBROSPINAL-FLUID; IN-VIVO; SALICYLATE; SUPEROXIDE; COCHLEA; ASPIRIN; METABOLITES; ISCHEMIA AB To elucidate the role of hydroxyl radical ((OH)-O-.) species in the generation mechanism of the cochlear pathology induced by transient asphyxia and subsequent re-ventilation, the concentrations of 2,3-hydroxybenzoic acid (DHBA) and 2,5-DHBA, major products arising from the attack of (OH)-O-. upon salicylate, were measured in the perilymph of the guinea pig by the high performance liquid chromatography-electrochemical/UV method. The mean value of 2,3-DHBA concentration in the perilymph significantly increased from the pre-asphyxic level (6.4 mu M) to 7.6 mu M and 8.8 mu M during asphyxia of 3 min duration and at 5 min after the onset of re-ventilation, respectively. The 2,5-DHBA concentration was 7.9 mu M before asphyxia, and also significantly increased to 11.5 mu M and 16.2 mu M during and after asphyxia, respectively. These results strongly indicated that (OH)-O-. was generated in the perilymph of the asphyxic and re-ventilated guinea pig cochlea, and the significance of this increased (OH)-O-. in generating anoxia and re-perfusion injury is discussed with respect to iron and oxygen-derived free radicals. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. RP Hara, A (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR BARRETTE WC, 1983, BIOCHEMISTRY-US, V22, P624, DOI 10.1021/bi00272a015 BECKMAN JS, 1990, P NATL ACAD SCI USA, V87, P1620, DOI 10.1073/pnas.87.4.1620 BIEMOND P, 1986, BIOCHEM J, V239, P169 CLELAND LG, 1985, J RHEUMATOL, V12, P136 ESCOUBET B, 1985, PROSTAGLANDINS, V29, P589 FLOYD RA, 1984, J BIOCHEM BIOPH METH, V10, P221, DOI 10.1016/0165-022X(84)90042-3 FLOYD R A, 1986, Journal of Free Radicals in Biology and Medicine, V2, P13, DOI 10.1016/0748-5514(86)90118-2 FRIDOVICH I, 1986, ARCH BIOCHEM BIOPHYS, V247, P1, DOI 10.1016/0003-9861(86)90526-6 GROOTVELD M, 1988, BIOCHEM PHARMACOL, V37, P271, DOI 10.1016/0006-2952(88)90729-0 GROOTVELD M, 1986, BIOCHEM J, V237, P499 HALLIWELL B, 1991, FREE RADICAL BIO MED, V10, P439, DOI 10.1016/0891-5849(91)90052-5 HALLIWELL B, 1987, FEBS LETT, V213, P9, DOI 10.1016/0014-5793(87)81455-2 HALLIWELL B, 1992, J NEUROCHEM, V59, P1609, DOI 10.1111/j.1471-4159.1992.tb10990.x HARA A, 1991, OTOL JPN, V1, P28 HARA A, 1988, GLYCOCONJUGATES MED, P333 HARA A, 1989, HEARING RES, V42, P265 HARA A, 1995, HEARING RES, V90, P228, DOI 10.1016/0378-5955(95)00166-3 INGELMANSUNDBERG M, 1991, BIOCHEM J, V276, P753 MCCABE PA, 1965, ANN OTO RHINOL LARYN, V74, P312 MOORHOUSE CP, 1985, BIOCHIM BIOPHYS ACTA, V843, P261, DOI 10.1016/0304-4165(85)90147-3 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 OCONNELL MJ, 1990, J PHARM PHARMACOL, V42, P205 Ohlemiller KK, 1999, AUDIOL NEURO-OTOL, V4, P219, DOI 10.1159/000013845 RICHMOND R, 1981, ANAL BIOCHEM, V118, P328, DOI 10.1016/0003-2697(81)90590-X RUMBLE RH, 1981, J CHROMATOGR, V225, P252, DOI 10.1016/S0378-4347(00)80270-4 SILVERST.H, 1967, ANN OTO RHINOL LARYN, V76, P118 SLOOT WN, 1995, J NEUROSCI METH, V60, P141, DOI 10.1016/0165-0270(95)00005-F Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 NR 28 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 110 EP 114 DI 10.1016/S0378-5955(00)00029-0 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900010 PM 10771188 ER PT J AU Zheng, L Godfrey, DA Waller, HJ Godfrey, TG Chen, K Kong, W AF Zheng, L Godfrey, DA Waller, HJ Godfrey, TG Chen, K Kong, W TI Metabolism of the dorsal cochlear nucleus in rat brain slices SO HEARING RESEARCH LA English DT Article DE adenosine triphosphate; choline acetyltransferase; acetylcholinesterase; amino acid; malate dehydrogenase; high performance liquid chromatography ID AMINO-ACID-CONCENTRATIONS; HIPPOCAMPAL SLICES; GUINEA-PIG; PROTEIN-SYNTHESIS; IN-VITRO; CEREBROSPINAL-FLUID; SYNAPTIC TRANSMISSION; INVITRO HIPPOCAMPUS; PREPARATIVE METHODS; GLUTAMATE RELEASE AB In vitro brain slices of the cochlear nucleus have been used for electrophysiological and pharmacological studies. More information is needed about the extent to which the slice resembles in vivo tissue, since this affects the interpretation of results obtained from slices. In this study, some chemical parameters of the dorsal cochlear nucleus (DCN) in rat brain slices were measured and compared to the in vivo state. The activities of malate dehydrogenase and lactate dehydrogenase were reduced in some DCN layers of incubated slices compared to in vivo brain tissue. The activities of choline acetyltransferase and acetylcholinesterase were increased or unchanged in DCN layers of slices. Adenosine triphosphate (ATP) concentrations for in vivo rat DCN were similar to those of cerebellar cortex. Compared with in vivo values, ATP concentrations were decreased in the DCN of brain slices, especially in the deep layer. Vibratome-cut slices had lower ATP levels than chopper-cut slices. Compared with the in vivo data, there were large losses of aspartate, glutamate, glutamine, gamma-aminobutyrate and taurine from incubated slices. These amino acid changes within the slices correlated with the patterns of release from the slices. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Med Coll Ohio, Dept Otolaryngol Head & Neck Surg, Toledo, OH 43614 USA. RP Godfrey, DA (reprint author), Med Coll Ohio, Dept Otolaryngol Head & Neck Surg, 3065 Arlington Ave, Toledo, OH 43614 USA. EM dgodfrey@mco.edu CR AITKEN PG, 1995, J NEUROSCI METH, V59, P139, DOI 10.1016/0165-0270(94)00204-T Alger B.E., 1984, BRAIN SLICES, P381 BATTAGLIOLI G, 1990, J NEUROCHEM, V54, P1179, DOI 10.1111/j.1471-4159.1990.tb01946.x BATTAGLIOLI G, 1991, NEUROCHEM RES, V16, P151, DOI 10.1007/BF00965703 BEGLEY DJ, 1994, J CHROMATOGR B, V657, P185, DOI 10.1016/0378-4347(94)80085-5 BENJAMIN AM, 1975, J NEUROCHEM, V25, P197, DOI 10.1111/j.1471-4159.1975.tb06953.x BERREBI AS, 1993, NATO ADV SCI INST SE, V239, P107 BOSLEY TM, 1983, J NEUROCHEM, V40, P189, DOI 10.1111/j.1471-4159.1983.tb12670.x BRADFORD HF, 1978, J NEUROCHEM, V30, P1453, DOI 10.1111/j.1471-4159.1978.tb10477.x BRADFORD HF, 1983, GLUTAMINE GLUTAMATE, P249 Chebib M, 1997, J NEUROCHEM, V68, P786 Chen K, 1999, NEUROSCIENCE, V90, P1043, DOI 10.1016/S0306-4522(98)00503-X Chen KJ, 1998, BRAIN RES, V783, P219, DOI 10.1016/S0006-8993(97)01348-6 CONSTANTI A, 1980, BRAIN RES, V195, P403, DOI 10.1016/0006-8993(80)90075-X COOPER JR, 1996, BIOCH BASIS NEUROPHA, P194 DAGANI F, 1987, J NEUROCHEM, V49, P1229, DOI 10.1111/j.1471-4159.1987.tb10015.x DAVIES JA, 1995, J NEUROL SCI, V13, P8 Espanol MT, 1996, ANESTHESIOLOGY, V84, P201, DOI 10.1097/00000542-199601000-00022 Fiber JM, 1997, NEUROCHEM INT, V31, P769, DOI 10.1016/S0197-0186(97)00036-3 FLORIS A, 1994, ANAT EMBRYOL, V189, P496 FOLBERGR.J, 1970, J NEUROCHEM, V17, P1155, DOI 10.1111/j.1471-4159.1970.tb03363.x FUJII T, 1991, BRAIN RES, V540, P224, DOI 10.1016/0006-8993(91)90511-S GARTHWAITE J, 1979, BRAIN RES, V173, P373, DOI 10.1016/0006-8993(79)90641-3 GATFIELD PD, 1966, J NEUROCHEM, V13, P185, DOI 10.1111/j.1471-4159.1966.tb07512.x GODFREY DA, 1983, HEARING RES, V11, P133, DOI 10.1016/0378-5955(83)90076-X GODFREY DA, 2000, NEUROCHEMISTRY VESTI, P347 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GODFREY DA, 1994, NEUROCHEM RES, V19, P693, DOI 10.1007/BF00967708 Godfrey DA, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P139, DOI 10.1007/978-1-4419-8712-9_13 GODFREY DA, 1976, J HISTOCHEM CYTOCHEM, V24, P697 GODFREY DA, 1992, J NEUROSCI METH, V41, P167, DOI 10.1016/0165-0270(92)90058-L Hackney CM, 1996, EUR J NEUROSCI, V8, P79, DOI 10.1111/j.1460-9568.1996.tb01169.x Hamberger A, 1981, Adv Biochem Psychopharmacol, V29, P509 HESSE GW, 1990, NEUROSCI LETT, V109, P186, DOI 10.1016/0304-3940(90)90560-V KAPETANOVIC IM, 1993, J NEUROCHEM, V61, P865, DOI 10.1111/j.1471-4159.1993.tb03597.x KAUPPINEN RA, 1988, NEUROSCIENCE, V27, P175, DOI 10.1016/0306-4522(88)90228-X KAWAI S, 1989, DEV BRAIN RES, V48, P11, DOI 10.1016/0165-3806(89)90089-8 KORNHUBER ME, 1986, NEUROSCI LETT, V69, P212, DOI 10.1016/0304-3940(86)90606-3 LIPTON P, 1977, J NEUROCHEM, V28, P1347, DOI 10.1111/j.1471-4159.1977.tb12330.x LIPTON P, 1979, J PHYSIOL-LONDON, V287, P427 LIPTON P, 1984, BRAIN SLICES, P113 LIPTON P, 1978, J NEUROCHEM, V31, P1299, DOI 10.1111/j.1471-4159.1978.tb06255.x LIPTON P, 1995, J NEUROSCI METH, V59, P151, DOI 10.1016/0165-0270(94)00205-U LIPTON P, 1982, J PHYSIOL-LONDON, V325, P51 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC LUPICA CR, 1991, SYNAPSE, V8, P237, DOI 10.1002/syn.890080402 LUST WD, 1981, ANAL BIOCHEM, V110, P258, DOI 10.1016/0003-2697(81)90144-5 MADL JE, 1993, J NEUROSCI, V13, P4429 MALCANGIO M, 1995, NEUROREPORT, V6, P399, DOI 10.1097/00001756-199501000-00042 Manis PB, 1996, J NEUROPHYSIOL, V76, P1639 MANIS PB, 1990, J NEUROSCI, V10, P2338 MASTERTON RB, 1990, OTOLARYNGOL HEAD NEC, V103, P189 MCDOUGAL DB, 1992, J NEUROCHEM, V59, P1915, DOI 10.1111/j.1471-4159.1992.tb11027.x MCILWAIN H, 1964, BIOCHEM J, V90, P442 MIHALY A, 1991, BRAIN RES BULL, V26, P559, DOI 10.1016/0361-9230(91)90096-3 MISGELD U, 1982, BRAIN RES B, V8, P93 NEWMAN GC, 1989, J NEUROSCI METH, V28, P23, DOI 10.1016/0165-0270(89)90006-X NICHOLLS D, 1990, TRENDS PHARMACOL SCI, V11, P462, DOI 10.1016/0165-6147(90)90129-V NISHIMURA F, 1995, BRAIN RES, V691, P217, DOI 10.1016/0006-8993(95)00719-7 Norenberg W, 1997, BRIT J PHARMACOL, V122, P71, DOI 10.1038/sj.bjp.0701347 OERTEL D, 1983, J NEUROSCI, V3, P2043 OSEN KK, 1995, J COMP NEUROL, V357, P482, DOI 10.1002/cne.903570311 Ottersen O. P., 1984, HDB CHEM NEUROANATOM, V3, P141 PASCHEN W, 1995, J NEUROCHEM, V65, P1692 Passonneau J. V., 1993, ENZYMATIC ANAL PRACT PATTERSON TA, 1995, NEUROCHEM RES, V20, P225, DOI 10.1007/BF00970548 Ross CD, 1995, NEUROCHEM RES, V20, P1483, DOI 10.1007/BF00970598 SANCHEZPRIETO J, 1988, J NEUROCHEM, V50, P1322, DOI 10.1111/j.1471-4159.1988.tb10611.x SCHIFF SJ, 1985, BRAIN RES, V343, P366, DOI 10.1016/0006-8993(85)90758-9 SHAHBAZIAN FM, 1986, INT J DEV NEUROSCI, V4, P209, DOI 10.1016/0736-5748(86)90060-2 SHANK RP, 1981, LIFE SCI, V28, P837, DOI 10.1016/0024-3205(81)90044-8 Sriram K, 1997, BRAIN RES, V749, P44, DOI 10.1016/S0006-8993(96)01271-1 SUBRAMANIAN N, 1976, EUR J PHARMACOL, V35, P203, DOI 10.1016/0014-2999(76)90316-2 SZERB JC, 1985, J NEUROCHEM, V44, P1724, DOI 10.1111/j.1471-4159.1985.tb07160.x SZERB JC, 1984, BRAIN RES, V293, P293, DOI 10.1016/0006-8993(84)91236-8 THALMANN I, 1970, ANN OTO RHINOL LARYN, V79, P12 WALLER HJ, 1994, J NEUROPHYSIOL, V71, P467 Waller HJ, 1996, HEARING RES, V98, P169, DOI 10.1016/0378-5955(96)00090-1 WANG J, 1995, J PHARMACOL EXP THER, V275, P877 WARD HK, 1983, J NEUROCHEM, V40, P855, DOI 10.1111/j.1471-4159.1983.tb08058.x WENTHOLD RJ, 1979, BRAIN RES, V162, P338, DOI 10.1016/0006-8993(79)90294-4 WHITTINGHAM TS, 1984, J NEUROCHEM, V43, P689, DOI 10.1111/j.1471-4159.1984.tb12788.x WICKESBERG RE, 1994, J COMP NEUROL, V339, P311, DOI 10.1002/cne.903390302 YUDKOFF M, 1990, NEUROCHEM RES, V15, P1191, DOI 10.1007/BF01208579 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1384 ZHENG L, 2000, IN PRESS NEUROCHEM R NR 86 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 115 EP 129 DI 10.1016/S0378-5955(00)00033-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900011 PM 10771189 ER PT J AU Kondrachuk, AV AF Kondrachuk, AV TI Computer simulation of the mechanical stimulation of the saccular membrane of bullfrog SO HEARING RESEARCH LA English DT Article DE otolith; Young's modulus; simulation; finite-element method; hair cell bundle ID OTOLITHIC-MEMBRANE; TRANSDUCTION; STIFFNESS; MACULA; FROG AB A three-dimensional computer simulation of the experiment (Benser M.E., Issa N.P., Hudspeth A.J., 1993. Hear. Res. 68, 243-252), devoted to the mechanical stimulation of the surface of saccular membrane of bullfrog with the otoconial mass removed was carried out by finite-element method. Comparison of the calculated distribution of the membrane displacements with the experimental data indicates that the gel layer of the saccular membrane is inhomogeneous. Its lower, thin (6-10 mu m) sublayer bordering the macular surface has the smaller Young's modulus which is 20 times less than the modulus of the upper part of the gel membrane (2.5 x 10(2) N/m(2) and 6.6 x 10(3) N/m(2), respectively). Possible consequences of this result and modification of the experiment are being discussed. The estimates based on the results of simulation support the conclusion that hair bundle stiffness may dominate the elastic reactance to otolithic membrane shear (Benser et al., 1993). (C) 2000 Elsevier Science B.V. All rights reserved. C1 Ukrainian Acad Sci, Inst Phys, Dept Theoret Phys, UA-252650 Kiev, Ukraine. RP Kondrachuk, AV (reprint author), Ukrainian Acad Sci, Inst Phys, Dept Theoret Phys, Prospect Nauki 46, UA-252650 Kiev, Ukraine. EM kondr@kondr.kiev.ua CR BENSER ME, 1993, HEARING RES, V68, P243, DOI 10.1016/0378-5955(93)90128-N DeVRIES H., 1950, ACTA OTO LARYNGOL, V38, P262, DOI 10.3109/00016485009118384 FERNANDEZ C, 1976, J NEUROPHYSIOL, V39, P985 Grant J W, 1990, J Vestib Res, V1, P139 HOWARD J, 1986, HEARING RES, V23, P93, DOI 10.1016/0378-5955(86)90178-4 HUDSPETH AJ, 1992, SOC GEN PHY, V47, P357 JACOBS RA, 1990, COLD SH Q B, V55, P547 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A KONDRACHUK AV, 1991, PHYSIOLOGIST S, V34, P212 KONDRACHUK AV, 1996, 12 AM SOC GRAV SPAC KONDRACHUK AV, 1987, SPACE BIOL AVIASPACE, P41 KONDRACHUK AV, 1997, 20 ANN MIDW M ASS RE LANDAU LD, 1986, THEORY ELASTICITY, P42 ROSS MD, 1987, ACTA OTO-LARYNGOL, V103, P56, DOI 10.3109/00016488709134698 SHIPOV AA, 1997, BIMECHANICS VESTIBUL, P200 TAKUMIDA M, 1992, ACTA OTO-LARYNGOL, V112, P643, DOI 10.3109/00016489209137454 TIMOSHENKO SP, 1987, THEORY ELASTICITY, P409 Trincker D, 1962, S SOC EXP BIOL, V16, P289 VILSTRUP G, 1952, ANN OTO RHINOL LARYN, V61, P189 NR 19 TC 15 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 130 EP 138 DI 10.1016/S0378-5955(00)00034-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900012 PM 10771190 ER PT J AU Naito, Y Tateya, I Fujiki, N Hirano, S Ishizu, K Nagahama, Y Fukuyama, H Kojima, H AF Naito, Y Tateya, I Fujiki, N Hirano, S Ishizu, K Nagahama, Y Fukuyama, H Kojima, H TI Increased cortical activation during hearing of speech in cochlear implant users SO HEARING RESEARCH LA English DT Article DE cochlear implant; postlingual deafness; language; neuronal network; speech activation ID POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-FLOW; SOMATOSENSORY CORTEX; SOUND STIMULATION; LOCALIZATION; REDUCTIONS; RESPONSES; BRAIN; AGE; PET AB To investigate the cortical activities while listening to noise and speech in cochlear implant (CI) users, we compared cerebral blood flow in postlingually deafened CI users with that in normal hearing subjects using positron emission tomography. While noise activation in CI users did not significantly differ from that in normal subjects, hearing speech activated more cortical areas in CI users than in normal subjects. A comparison of speech activation in these two groups revealed higher activation in CI users not only in the temporal cortices but also in Broca's area and its right hemisphere homologue, the supplementary motor area and the anterior cingulate gyrus. In postlingually deafened subjects, the hearing of speech coded by CI may be accompanied by increased activation of both the temporal and frontal cortices. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Kyoto Univ, Grad Sch Med, Dept Speech & Hearing Sci, Sakyo Ku, Kyoto 6068507, Japan. Kyoto Univ, Grad Sch Med, Dept Nucl Med, Sakyo Ku, Kyoto 6068507, Japan. Kyoto Univ, Grad Sch Med, Dept Brain Pathophysiol, Sakyo Ku, Kyoto 6068507, Japan. RP Naito, Y (reprint author), Kyoto Univ, Grad Sch Med, Dept Speech & Hearing Sci, Sakyo Ku, Kyoto 6068507, Japan. CR CHASE CH, 1995, COGNITIVE SCI INTRO Clark G.M., 1978, J OTOLARYNGOL SOC AU, V4, P208 CREUTZFELDT O, 1989, EXP BRAIN RES, V77, P451, DOI 10.1007/BF00249600 DEMONET JF, 1992, BRAIN, V115, P1753, DOI 10.1093/brain/115.6.1753 ELBERLING C, 1981, SCAND AUDIOL, V10, P203, DOI 10.3109/01050398109076182 FRIBERG L, 1991, BRAIN WORK MENTAL AC, P294 FRISTON KJ, 1991, J CEREBR BLOOD F MET, V11, P690 Friston KJ, 1994, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402 Friston KJ, 1994, HUMAN BRAIN MAPPING, V1, P214 GARRAGHTY PE, 1991, SOMATOSENS MOT RES, V8, P347 GRADY CL, 1995, SCIENCE, V269, P218, DOI 10.1126/science.7618082 Hirano S, 1997, EXP BRAIN RES, V113, P75, DOI 10.1007/BF02454143 HOUSE WF, 1973, ANN OTO RHINOL LARYN, V82, P504 HOWARD D, 1992, BRAIN, V115, P1769, DOI 10.1093/brain/115.6.1769 KAAS JH, 1991, ANNU REV NEUROSCI, V14, P137, DOI 10.1146/annurev.neuro.14.1.137 MARTIN WR, 2001, J CERERB BLOOD FLOW, V11, P684 Naito Y, 1997, ACTA OTO-LARYNGOL, V117, P490, DOI 10.3109/00016489709113426 NAITO Y, 1995, COGNITIVE BRAIN RES, V2, P207, DOI 10.1016/0926-6410(95)90009-8 NISHIZAWA Y, 1982, J NEUROPHYSIOL, V48, P458 Okazawa H, 1996, BRAIN, V119, P1297, DOI 10.1093/brain/119.4.1297 PANTANO P, 1984, STROKE, V15, P635 Penfield W, 1959, SPEECH BRAIN MECH POSNER MI, 1988, SCIENCE, V240, P1627, DOI 10.1126/science.3289116 Roland P. E., 1993, BRAIN ACTIVATION ROLAND PE, 1980, J NEUROPHYSIOL, V43, P118 Scheffler K, 1998, CEREB CORTEX, V8, P156, DOI 10.1093/cercor/8.2.156 Talairach J, 1988, COPLANAR SEREOTAXIC VASAMA JP, 1995, NEUROREPORT, V6, P961, DOI 10.1097/00001756-199505090-00003 WALL JT, 1983, SCIENCE, V221, P771, DOI 10.1126/science.6879175 WISE R, 1991, BRAIN, V114, P1803, DOI 10.1093/brain/114.4.1803 Wong D, 1999, HEARING RES, V132, P34, DOI 10.1016/S0378-5955(99)00028-3 YOSHII F, 1988, J CEREBR BLOOD F MET, V8, P654 ZATORRE RJ, 1992, SCIENCE, V256, P846, DOI 10.1126/science.1589767 NR 33 TC 27 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 139 EP 146 DI 10.1016/S0378-5955(00)00035-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900013 PM 10771191 ER PT J AU Spicer, SA Thomopoulos, GN Schulte, BA AF Spicer, SA Thomopoulos, GN Schulte, BA TI Structural evidence for ion transport and tectorial membrane maintenance in the gerbil limbus SO HEARING RESEARCH LA English DT Article DE cochlea; ultrastructure; fibrocyte; interdental cell; gerbil ID TUBULOCISTERNAL ENDOPLASMIC-RETICULUM; GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; CANALICULAR RETICULUM; PLACE-FREQUENCY; POTASSIUM; MECHANISMS; PATHWAY; SYSTEM; STRIA AB Cells medial to the tunnel of Corti were examined to assess fine structural features relevant to their proposed role in cochlear K+ homeostasis. A dense network of canaliculi referred to as canalicular reticulum (CR) resided in the foot body of inner pillar cells, where it bordered and could resorb ions released from inner radial and spiral nerv es. Lateral interdental cells (IDCs) formed columns which connected the inner sulcus epithelium with the base of the tectorial membrane's (TM) middle zone. A spout-like neck in cells at the top of lateral IDC columns housed a dense concentration of CR which resembled that characteristic of ion transporting epithelia and appeared to be located here for transporting ions and fluid toward the TM. Clustered IDCs in the center of the limbus connected underlying limbal stroma with the TM's limbal zone and appeared capable of transporting ions from stroma to TM. Abundant CR in limbal stellate fibrocytes evidenced their capacity to transport ions and fluid, presumably from inner sulcus epithelium toward central IDCs. The most medial IDCs possibly function as the terminus of an ion cycling path from scala vestibuli to endolymph. Light fibrocytes situated between supralimbal fibrocytes and medial IDCs appeared to serve as a link in this pathway. The limbal zone of the TM overlying central IDCs consisted of three distinct regions,which offered a structural basis for transformation of an amorphous matrix supplied by central IDCs into the protofibrils of the membrane's middle zone. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. Aristotelian Univ Salonika, GR-54006 Salonika, Macedonia, Greece. RP Spicer, SA (reprint author), Med Univ S Carolina, Dept Pathol & Lab Med, 165 Ashley Ave, Charleston, SC 29425 USA. CR ASHMORE JF, 1986, NATURE, V322, P371 BARON DA, 1984, LAB INVEST, V51, P233 BERGERON M, 1981, BIOL CELL, V42, P43 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 FORGE A, 1982, CELL TISSUE RES, V226, P375 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 HOUSLEY GD, 1992, ORL J OTORHINOLARYNG, V48, P68 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KIMURA RS, 1990, AM J OTOLARYNG, V11, P99, DOI 10.1016/0196-0709(90)90006-H KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 LIM D J, 1970, Journal of Laryngology and Otology, V84, P1241, DOI 10.1017/S0022215100072984 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MOLLER OJ, 1973, CELL TISSUE RES, V228, P13 MOLLGARD K, 1978, J MEMBRANE BIOL, V40, P71, DOI 10.1007/BF02025999 MOLLGARD K, 1981, WATER TRANSPORT EPIT, P85 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 PRIETO JJ, 1990, HEARING RES, V45, P51, DOI 10.1016/0378-5955(90)90182-O PRIETO JJ, 1991, HEARING RES, V54, P59, DOI 10.1016/0378-5955(91)90136-W QVORTRUP K, 1990, CELL TISSUE RES, V261, P287, DOI 10.1007/BF00318670 SALT AN, 1986, NEUROBIOLOGY HEARING, P108 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 Spicer SS, 1999, J COMP NEUROL, V409, P424 Spicer SS, 1999, HEARING RES, V130, P7, DOI 10.1016/S0378-5955(98)00202-0 SPICER SS, 1994, ANAT REC, V240, P149, DOI 10.1002/ar.1092400202 SPICER SS, 1994, HEARING RES, V79, P161, DOI 10.1016/0378-5955(94)90137-6 Spicer SS, 1999, HEARING RES, V136, P139, DOI 10.1016/S0378-5955(99)00118-5 Spicer SS, 1998, HEARING RES, V118, P1, DOI 10.1016/S0378-5955(98)00006-9 Spicer SS, 1998, ANAT REC, V251, P97, DOI 10.1002/(SICI)1097-0185(199805)251:1<97::AID-AR15>3.0.CO;2-6 Spicer SS, 1997, ANAT REC, V249, P117 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 ZIDANIC M, 1994, BIOPHYS J, V57, P1253 NR 33 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 147 EP 161 DI 10.1016/S0378-5955(00)00037-X PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900014 PM 10771192 ER PT J AU Dehne, N Lautermann, J ten Cate, WJF Rauen, U de Groot, H AF Dehne, N Lautermann, J ten Cate, WJF Rauen, U de Groot, H TI In vitro effects of hydrogen peroxide on the cochlear neurosensory epithelium of the guinea pig SO HEARING RESEARCH LA English DT Article DE organ of Corti; reactive oxygen species; calcium; iron; antioxidant ID OXYGEN SPECIES GENERATION; INDUCED HEARING-LOSS; OUTER HAIR-CELLS; FREE-RADICALS; CULTURED-HEPATOCYTES; CALCIUM HOMEOSTASIS; INNER-EAR; GENTAMICIN OTOTOXICITY; DRUG-METABOLISM; ACOUSTIC TRAUMA AB Reactive oxygen species (ROS) have been postulated to be involved in drug ototoxicity and noise-induced hearing loss. Hydrogen peroxide (H2O2)-induced cell damage in the inner ear was investigated using the neurosensory epithelium of a guinea pig cochlea. Hair cells and supporting cells of the epithelium incubated in Hanks' balanced salt solution were viable up to 6 h. After 2 h of treatment with 0.2 mM H2O2 about 85% of the outer hair cells lost their viability. in contrast inner hair cells slowly began to die after 2 h of H2O2 treatment. The Deiters cells and Hensen cells did not show any signs of damage in the presence of H2O2. Nifedipine, a calcium channel blocker, Quin-2 AM, an intracellular calcium chelator, and 2,2'-dipyridyl, a membrane-permeable iron chelator, all provided partial protection against H2O2-induced outer hair cell death. The combination of both chelators showed an additional protective effect. The antioxidants N-acetylcysteine and glutathione-monoethyl ester completely protected against H2O2 damage. These results suggest that calcium, iron, and thiol homeostasis play a crucial role in hair cell death caused by H2O2. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Essen Gesamthsch, Dept Otorhinolaryngol, D-45122 Essen, Germany. Univ Essen Gesamthsch, Dept Physiol Chem, Essen, Germany. RP Lautermann, J (reprint author), Univ Essen Gesamthsch, Dept Otorhinolaryngol, Hufelandstr 55, D-45122 Essen, Germany. RI Rauen, Ursula/N-2137-2014 CR ANDERSON ME, 1985, ARCH BIOCHEM BIOPHYS, V239, P538, DOI 10.1016/0003-9861(85)90723-4 BELLOMO G, 1985, HEPATOLOGY, V5, P876, DOI 10.1002/hep.1840050529 BELLOMO G, 1983, FEBS LETT, V163, P136, DOI 10.1016/0014-5793(83)81180-6 BHATTACHARYYA TK, 1991, ANAT REC, V230, P136, DOI 10.1002/ar.1092300114 Boettcher FA, 1996, LARYNGOSCOPE, V106, P772, DOI 10.1097/00005537-199606000-00020 BOVERIS A, 1973, BIOCHEM J, V134, P707 BUJA LM, 1993, ARCH PATHOL LAB MED, V117, P1208 CANTONI O, 1989, EUR J BIOCHEM, V182, P209, DOI 10.1111/j.1432-1033.1989.tb14819.x CARLIER E, 1980, ARCH OTO-RHINO-LARYN, V226, P129, DOI 10.1007/BF00455127 CHEN CS, 1983, ARCH OTO-RHINO-LARYN, V238, P217, DOI 10.1007/BF00453932 Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 Clerici WJ, 1996, HEARING RES, V101, P14, DOI 10.1016/S0378-5955(96)00126-8 CLERICI WJ, 1995, HEARING RES, V84, P30, DOI 10.1016/0378-5955(95)00010-2 DEGROOT H, 1994, HEPATO-GASTROENTEROL, V41, P328 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FARBER JL, 1990, LAB INVEST, V62, P670 Goldwyn BG, 1997, LARYNGOSCOPE, V107, P1112, DOI 10.1097/00005537-199708000-00019 HALLIWELL B, 1990, METHOD ENZYMOL, V186, P1 Hirose K, 1997, HEARING RES, V104, P1, DOI 10.1016/S0378-5955(96)00169-4 Hu BH, 1997, HEARING RES, V113, P198, DOI 10.1016/S0378-5955(97)00143-3 Huizing E H, 1987, Acta Otolaryngol Suppl, V436, P117 HYSLOP PA, 1986, J CELL PHYSIOL, V129, P356, DOI 10.1002/jcp.1041290314 IKEDA K, 1993, ACTA OTO-LARYNGOL, V113, P137, DOI 10.3109/00016489309135781 Ison JR, 1997, HEARING RES, V106, P179, DOI 10.1016/S0378-5955(96)00216-X Jacono AA, 1998, HEARING RES, V117, P31, DOI 10.1016/S0378-5955(97)00214-1 JEWELL SA, 1982, SCIENCE, V217, P1257, DOI 10.1126/science.7112127 KIMURA M, 1992, BRIT J PHARMACOL, V107, P488 Kopke RD, 1997, AM J OTOL, V18, P559 KVIETYS PR, 1989, AM J PHYSIOL, V257, pH1640 KYLE ME, 1989, BIOCHEM PHARMACOL, V38, P3797, DOI 10.1016/0006-2952(89)90588-1 LAUTERMANN J, 1995, HEARING RES, V88, P47, DOI 10.1016/0378-5955(95)00097-N LAUTERMANN J, 1995, HEARING RES, V86, P15, DOI 10.1016/0378-5955(95)00049-A Lautermann J, 1997, HEARING RES, V114, P75, DOI 10.1016/S0378-5955(97)00154-8 Lomonosova EE, 1998, FREE RADICAL BIO MED, V25, P493, DOI 10.1016/S0891-5849(98)00080-X MANN W, 1987, HNO, V35, P203 MEISTER A, 1983, ANNU REV BIOCHEM, V52, P711, DOI 10.1146/annurev.bi.52.070183.003431 Meneghini R, 1997, FREE RADICAL BIO MED, V23, P783, DOI 10.1016/S0891-5849(97)00016-6 NAKAGAWA T, 1991, NEUROSCI LETT, V125, P81, DOI 10.1016/0304-3940(91)90136-H ORRENIUS S, 1989, TRENDS PHARMACOL SCI, V10, P281, DOI 10.1016/0165-6147(89)90029-1 ORRENIUS S, 1984, TRENDS PHARMACOL SCI, V5, P432, DOI 10.1016/0165-6147(84)90495-4 OSAKO S, 1979, ACTA OTO-LARYNGOL, V88, P359, DOI 10.3109/00016487909137180 Oshima T, 1996, AM J PHYSIOL-CELL PH, V271, pC944 PENTZ S, 1981, MICROSC ACTA, V84, P117 PRASAD MR, 1989, FREE RADICAL RES COM, V7, P381, DOI 10.3109/10715768909087965 PRIEVE BA, 1984, ACTA OTO-LARYNGOL, V98, P428, DOI 10.3109/00016488409107584 Priuska EM, 1995, BIOCHEM PHARMACOL, V50, P1749, DOI 10.1016/0006-2952(95)02160-4 QUIRK WS, 1994, HEARING RES, V74, P217, DOI 10.1016/0378-5955(94)90189-9 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E Rimpler MM, 1999, BIOCHEM J, V340, P291, DOI 10.1042/0264-6021:3400291 RUBIN R, 1984, ARCH BIOCHEM BIOPHYS, V228, P450, DOI 10.1016/0003-9861(84)90010-9 Sha Su-Hua, 1997, Keio Journal of Medicine, V46, P115 Song BB, 1997, J PHARMACOL EXP THER, V282, P369 Song BB, 1998, FREE RADICAL BIO MED, V25, P189, DOI 10.1016/S0891-5849(98)00037-9 STARKE PE, 1985, J BIOL CHEM, V260, P99 THOR H, 1984, J BIOL CHEM, V259, P6612 Usami S, 1996, BRAIN RES, V743, P337, DOI 10.1016/S0006-8993(96)01090-6 Walker P. D., 1987, AM J PHYSIOL, V253, P495 WALKER PD, 1988, J CLIN INVEST, V81, P334, DOI 10.1172/JCI113325 Watanabe H, 1998, Nihon Jibiinkoka Gakkai Kaiho, V101, P967 Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 NR 62 TC 23 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 162 EP 170 DI 10.1016/S0378-5955(00)00036-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900015 PM 10771193 ER PT J AU Williams, JA Holder, N AF Williams, JA Holder, N TI Cell turnover in neuromasts of zebrafish larvae SO HEARING RESEARCH LA English DT Article DE zebrafish; neuromast; cell turnover ID LATERAL LINE SYSTEM; HAIR-CELL; INNER-EAR; ACOUSTIC TRAUMA; CHICK COCHLEA; AMINOGLYCOSIDE ANTIBIOTICS; EMBRYONIC ZEBRAFISH; SENSORY EPITHELIA; REGENERATION; PROLIFERATION AB The numbers and positions of cells undergoing cell death and proliferation in the neuromasts of 10 day old zebrafish larvae were assessed to investigate the ability of supporting cells to differentiate into hair cells. Evaluations of cell death and proliferation showed that a subpopulation of cells located in the centre of the neuromast undergo cell death, and a different subpopulation located at the periphery proliferate. This suggests that cell death of hair cells and proliferation of mantle supporting cells occurs as part of normal development, creating constant turnover of hair cells. We show that the caspase inhibitor zVADfmk reduces cell death while the aminoglycoside neomycin specifically induces an increased amount of cell death in the central population of cells. Both of these treatments affect the rate of proliferation of the peripheral subpopulation of cells in the neuromast suggesting that a feedback mechanism occurs regulating cell death and proliferation. We propose that the dying population of cells are hair cells and the proliferating cells are 'mantle' supporting cells, which is in agreement with previous observations suggesting that supporting cells can give rise to hair cells following hair cell death. (C) 2000 Elsevier Science B.V. All rights reserved. C1 UCL, Dept Anat & Dev Biol, London WC1E 6BT, England. RP Williams, JA (reprint author), UCL, Dept Anat & Dev Biol, Gower St, London WC1E 6BT, England. EM juliet.williams@ucl.ac.uk RI Zebrafish, UCL/A-3125-2009 CR ABRAMS JM, 1993, DEVELOPMENT, V117, P29 BALAK KJ, 1990, J NEUROSCI, V10, P2502 CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 Corwin JT, 1997, NEURON, V19, P951, DOI 10.1016/S0896-6273(00)80386-4 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1991, ANNU REV NEUROSCI, V14, P301, DOI 10.1146/annurev.neuro.14.1.301 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 Cotanche Douglas A., 1994, Current Opinion in Neurobiology, V4, P509, DOI 10.1016/0959-4388(94)90051-5 DAVIES S, 1987, J MICROSC-OXFORD, V147, P89 FORGE A, 1985, HEARING RES, V19, P171, DOI 10.1016/0378-5955(85)90121-2 Forge A, 2000, HEARING RES, V139, P97, DOI 10.1016/S0378-5955(99)00177-X FORGE A, 1993, SCIENCE, V224, P129 Haddon C, 1996, J COMP NEUROL, V365, P113, DOI 10.1002/(SICI)1096-9861(19960129)365:1<113::AID-CNE9>3.0.CO;2-6 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 Hendzel MJ, 1997, CHROMOSOMA, V106, P348, DOI 10.1007/s004120050256 Jacobson MD, 1997, CELL, V88, P347, DOI 10.1016/S0092-8674(00)81873-5 JONES JE, 1993, J NEUROSCI, V13, P1022 KATAYAMA A, 1993, J COMP NEUROL, V333, P28, DOI 10.1002/cne.903330103 KAUS S, 1987, ACTA OTO-LARYNGOL, V103, P291, DOI 10.3109/00016488709107796 Kil J, 1997, HEARING RES, V114, P117, DOI 10.1016/S0378-5955(97)00166-4 KIMMEL CB, 1995, DEV DYNAM, V203, P253 KNOWLTON VY, 1967, J MORPHOL, V121, P179, DOI 10.1002/jmor.1051210302 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 Lanford PJ, 1996, HEARING RES, V100, P1, DOI 10.1016/0378-5955(96)00110-4 LARISON KD, 1990, DEVELOPMENT, V109, P567 Li L., 1995, AUDIT NEUROSCI, V1, P111 LI L, 1995, J COMP NEUROL, V355, P405, DOI 10.1002/cne.903550307 LOMBARTE A, 1994, J COMP NEUROL, V345, P419, DOI 10.1002/cne.903450308 METCALFE WK, 1985, J COMP NEUROL, V233, P377, DOI 10.1002/cne.902330307 MULLINS MC, 1994, CURR BIOL, V4, P189, DOI 10.1016/S0960-9822(00)00048-8 OESTERLE EC, 1993, HEARING RES, V66, P213, DOI 10.1016/0378-5955(93)90141-M POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 PRESSON JC, 1994, HEARING RES, V80, P1, DOI 10.1016/0378-5955(94)90002-7 RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E RUBIN RJ, 1967, ACTA OTO-LARYNGOL, P220 STONE JS, 1994, J COMP NEUROL, V341, P50, DOI 10.1002/cne.903410106 Stone LS, 1933, J COMP NEUROL, V57, P507, DOI 10.1002/cne.900570307 Stone LS, 1937, J COMP NEUROL, V68, P83, DOI 10.1002/cne.900680105 UCHIYAMA M, 1991, J MORPHOL, V207, P157, DOI 10.1002/jmor.1052070206 WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 WEBB JF, 1989, J MORPHOL, V202, P53, DOI 10.1002/jmor.1052020105 WEI Y, 1998, TRENDS CELL BIOL, V8, P166 Weil M, 1997, CURR BIOL, V7, P281, DOI 10.1016/S0960-9822(06)00125-4 Westerfield M., 1995, ZEBRAFISH BOOK GUIDE, V3rd WILLIAMS JA, 1999, THESIS U COLLEGE LON WILSON SW, 1990, DEVELOPMENT, V108, P121 NR 48 TC 125 Z9 127 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 171 EP 181 DI 10.1016/S0378-5955(00)00039-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900016 PM 10771194 ER PT J AU Hultcrantz, M Stenberg, AE Fransson, A Canlon, B AF Hultcrantz, M Stenberg, AE Fransson, A Canlon, B TI Characterization of bearing in an X,0 'Turner mouse' SO HEARING RESEARCH LA English DT Article DE Turner's syndrome; mouse model; auditory brainstem response; hair cell; pathology; cochlea; distortion product otoacoustic emission; morphology; hearing loss ID NEWBORN CHILDREN; OTITIS-MEDIA; WOMEN; MICE; EAR; AGE AB Turner's syndrome is due to total (45,X) or partial (mosaicism) loss of one X-chromosome. The main features are short stature, ovarian dysgenesis with no estrogen production and infertility. In addition to ear and hearing disorders, middle ear problems including acute/serous otitis media and chronic middle ear disease are frequent. Sensorineural hearing loss is often seen with a dip in the mid-frequencies and also an early high frequency loss. In this study, middle-and inner-ear pathology was characterized using physiological and morphological techniques in a 'Turner mouse' that has been generated with the chromosomal aberration X,0. Otitis media was found in some of these X,0 animals, a symptom that is seldom found in control animals. The auditory brainstem responses (ABR) of the Turner mouse showed a progressive hearing loss in the high frequency region that exceeded the normal age-related hearing loss of control mice and increased latencies of the first ABR wave. Outer hair cell loss was apparent in the cochlear basal turn of Turner mice. Decreases in the amplitude of distortion product otoacoustic emissions were correlated with the loss of ABR threshold sensitivity. These results indicate that hearing problems in the Turner mouse seems to be of cochlear origin with an eighth nerve component. This Turner mouse model appears to have ear and hearing problems quite similar to humans and can therefore be used as a model to determine the auditory pathology underlying this syndrome. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden. RP Hultcrantz, M (reprint author), Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. EM mhz@ent.ks.se CR ANDERSON H, 1969, ACTA OTOLARYNGOL S S, V247 COLEMAN JR, 1994, HEARING RES, V80, P209, DOI 10.1016/0378-5955(94)90112-0 HULTCRANTZ M, 1994, HEARING RES, V76, P127, DOI 10.1016/0378-5955(94)90094-9 Hultcrantz M, 1997, HEARING RES, V103, P69, DOI 10.1016/S0378-5955(96)00165-7 Hultcrantz M, 1995, INT CONGR SER, V1089, P249 HULTCRANTZ M, 1995, ORL J OTO-RHINO-LARY, V57, P1 HULTCRANTZ M, 1993, EUR ARCH OTO-RHINO-L, V250, P257 INFANTERIVARD C, 1993, EPIDEMIOL REV, V15, P444 Jonsson R, 1998, SCAND AUDIOL, V27, P81, DOI 10.1080/010503998420324 LINDSTEN J, 1963, THESIS STOCKHOLM NIELSEN J, 1991, HUM GENET, V87, P81, DOI 10.1007/BF01213097 NIELSEN J, 1975, HUMANGENETIK, V30, P1, DOI 10.1007/BF00273626 ROSENFELD RG, 1994, ENDOCRINOLOGIST, V4, P351, DOI 10.1097/00019616-199409000-00006 SCULERATI N, 1990, ARCH OTOLARYNGOL, V116, P704 Stenberg AE, 1998, HEARING RES, V124, P85, DOI 10.1016/S0378-5955(98)00113-0 Turner HH, 1938, ENDOCRINOLOGY, V23, P566 WATKIN PM, 1989, J LARYNGOL OTOL, V103, P731, DOI 10.1017/S0022215100109934 NR 17 TC 27 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 182 EP 188 DI 10.1016/S0378-5955(00)00042-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900017 PM 10771195 ER PT J AU Lohuis, PJFM Borjesson, PKE Klis, SFL Smoorenburg, GF AF Lohuis, PJFM Borjesson, PKE Klis, SFL Smoorenburg, GF TI The rat cochlea in the absence of circulating adrenal hormones: an electrophysiological and morphological study SO HEARING RESEARCH LA English DT Article DE summating potential; aldosterone; Na+/K+-ATPase; endolymph ID MAMMALIAN INNER-EAR; LOW-FREQUENCY SOUND; GUINEA-PIG; ENDOLYMPHATIC HYDROPS; MODULATION; ADRENOCORTICOSTEROIDS; NA+,K+-ATPASE; POTENTIALS; RECEPTORS; OUABAIN AB Circulating adrenal hormones affect strial function. Removal of endogenous levels of adrenal steroids by bilateral adrenalectomy (ADX) in rats causes a decrease of Na+/K+-ATPase activity in the cochlear lateral wall [Rarey et al., 1989. Arch. Otolaryngol. Head Neck Surg. 115, 817-821] and a decrease of the volume of the marginal cells in the stria vascularis [Lohuis et al., 1990. Acta Otolaryngol. (Stockh.) 110, 348-356]. To study further the effect of absence of circulating adrenocorticosteroids on cochlear function, 18 male Long Evans rats underwent either an ADX or a SHAM operation. Electrocochleography was performed 1 week after surgery for tone bursts in a frequency range of 1-16 kHz. Thereafter, the cochleas were harvested and examined histologically. No significant changes in the amplitude growth curves of the summating potential (SP), the compound action potential (CAP) and the cochlear microphonics (CM) were detected after ADX. However, visually, there appeared to be a decrease of endolymphatic volume (tentatively called imdrops). Reissner's membrane (RM) extended less into scala vestibuli in ADX animals than in SHAM-operated animals. The ratio between the length of RM and the straight distance between the medial and lateral attachment points of RM were used as an objective measure to quantify this effect in each sub-apical half turn of the cochlea. The decrease in length of RM was statistically significant. Thus, circulating adrenal hormones appear to be necessary for normal cochlear fluid homeostasis. Absence of one or more of these hormones leads to shrinkage of the scala media (imdrops). However, the absence of adrenal hormones does not affect the gross cochlear potentials. Apparently, the cochlea is capable of compensating for the absence of circulating adrenal hormones to sustain the conditions necessary for proper cochlear transduction. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, NL-3584 CX Utrecht, Netherlands. RP Lohuis, PJFM (reprint author), Univ Utrecht, Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, Room G-02-531,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. CR BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 Bouman H, 1998, HEARING RES, V117, P119, DOI 10.1016/S0378-5955(97)00216-5 Brunschwig AS, 1997, HEARING RES, V114, P62, DOI 10.1016/S0378-5955(97)00153-6 Dallos P., 1996, COCHLEA, P1 DURRANT JD, 1974, J ACOUST SOC AM, V56, P562, DOI 10.1121/1.1903291 EWART HS, 1995, AM J PHYSIOL-CELL PH, V269, pC295 FURUTA H, 1994, HEARING RES, V78, P175, DOI 10.1016/0378-5955(94)90023-X KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KLIS JFL, 1985, HEARING RES, V20, P15, DOI 10.1016/0378-5955(85)90054-1 KLIS JFL, 1988, HEARING RES, V32, P175, DOI 10.1016/0378-5955(88)90089-5 KLIS SFL, 1999, MENIERES DIS, P27 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 PITOVSKI DZ, 1993, BRAIN RES, V601, P273, DOI 10.1016/0006-8993(93)91720-D PITOVSKI DZ, 1993, HEARING RES, V69, P10, DOI 10.1016/0378-5955(93)90088-I RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 Yao XF, 1996, ACTA OTO-LARYNGOL, V116, P493, DOI 10.3109/00016489609137879 NR 18 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 189 EP 196 DI 10.1016/S0378-5955(00)00043-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900018 PM 10771196 ER PT J AU Molenaar, DG Shaw, G Eggermont, JJ AF Molenaar, DG Shaw, G Eggermont, JJ TI Noise suppression of transient-evoked otoacoustic emissions. I. A comparison with the non-linear method SO HEARING RESEARCH LA English DT Article DE human; otoacoustic emission; noise suppression; click ID WAVELET ANALYSIS; SYSTEM; EAR AB A new method to record transient-evoked otoacoustic emissions (TEOAEs) is introduced. Click stimuli were presented both with and without a simultaneously presented wide-band noise burst. Subtraction of the recorded signal evoked by the noise burst plus click from the signal evoked by the click alone, cancelled the eardrum reflection components of the response and resulted in a measure of the emission. This was used to obtain the TEOAEs from 21 subjects for peak click stimulus levels of 48-66 dB SPL. The root-mean-square (RMS) level of the noise burst was set 10 dB higher than the peak click level, and resulted in suppression of the TEOAE by up to 20 dB. The TEOAE waveforms obtained by the new method were compared to those obtained with Kemp's nonlinear method, and were indistinguishable in 20 of the 21 subjects. On basis of the emission spectra, they were indistinguishable in 18 out of 21 subjects. The latencies of narrow-band filtered components from the TEOAEs obtained with the two methods were also similar. This suggests that this noise-suppression method produces similar results as Kemp's non-linear method with the advantage that emission components with very short latencies can be obtained. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Physiol & Biophys, Calgary, AB, Canada. RP Eggermont, JJ (reprint author), Univ Calgary, Dept Psychol, 2500 Univ Dr NW, Calgary, AB T2N 1N4, Canada. CR BERLIN CI, 1995, HEARING RES, V87, P96, DOI 10.1016/0378-5955(95)00082-F Geisler C. D., 1998, SOUND SYNAPSE PHYSL GORGA MP, 1993, J ACOUST SOC AM, V94, P2639, DOI 10.1121/1.407348 Hammershoi D, 1996, J ACOUST SOC AM, V100, P408 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Kruglov AV, 1997, ACTA OTO-LARYNGOL, V117, P174, DOI 10.3109/00016489709117763 Molenaar DG, 2000, HEARING RES, V143, P208, DOI 10.1016/S0378-5955(00)00048-4 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 Shera CA, 1999, J ACOUST SOC AM, V105, P782, DOI 10.1121/1.426948 Tavartkiladze GA, 1996, ACTA OTO-LARYNGOL, V116, P213, DOI 10.3109/00016489609137826 Tognola G, 1998, IEEE T BIO-MED ENG, V45, P686, DOI 10.1109/10.678603 WIT HP, 1994, HEARING RES, V73, P141, DOI 10.1016/0378-5955(94)90228-3 NR 12 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 197 EP 207 DI 10.1016/S0378-5955(00)00049-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900019 PM 10771197 ER PT J AU Molenaar, DG Shaw, G Eggermont, JJ AF Molenaar, DG Shaw, G Eggermont, JJ TI Noise suppression of transient-evoked otoacoustic emissions. II. Derived narrow-band contributions SO HEARING RESEARCH LA English DT Article DE derived narrow band; transient-evoked otoacoustic emission; human; high-pass noise suppression ID NORMAL-HEARING; HUMAN ADULTS; DISTORTION; CLICK; EARS; SYSTEM AB Transient-evoked otoacoustic emissions (TEOAEs) were decomposed into cochlear place specific components using high-pass noise suppression. This was performed using high-pass filtered noise with cut-off frequencies between 0.7 and 5.6 kHz in 0.5-octave steps. Subtraction of the TEOAEs obtained in the presence of two high-pass noise suppressors with 0.5-octave difference in their cutoff frequencies, f(A) and f(B), should theoretically result in TEOAE components with frequencies between f(A) and f(B). The reconstructed wide-band emission power spectrum obtained by summing the narrow-band emission power spectra, was nearly identical to the power spectrum of the original wide-band emission. This suggests that no phase-cancellation occurs and that the individual narrow-band TEOAEs are uncorrelated, and thus that their generators are potentially independent. About 66% of the derived narrow-band emissions had spectral components that extended below the cut-off frequency of the lower high-pass noise filter. These tail components were interpreted as resulting from high-frequency side suppression of the high-pass noise on the click emission and potentially distortion product components from the TEOAE. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Physiol & Biophys, Calgary, AB, Canada. RP Eggermont, JJ (reprint author), Univ Calgary, Dept Psychol, 2500 Univ Dr NW, Calgary, AB T2N 1N4, Canada. CR Bowman DM, 1998, HEARING RES, V119, P14, DOI 10.1016/S0378-5955(98)00041-0 Bowman DM, 1997, J ACOUST SOC AM, V101, P1550, DOI 10.1121/1.418129 BRASS D, 1993, J ACOUST SOC AM, V93, P920, DOI 10.1121/1.405453 BROWN D, 1994, J OTOLARYNGOL, V23, P234 Dallos P., 1973, AUDITORY PERIPHERY B DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 EGGERMONT JJ, 1976, HDB SENSORY PHYSL, P626 EGGERMONT JJ, 1983, BASES AUDITORY BRAIN, P287 ELBERLING C, 1974, SCAND AUDIOL, V3, P13, DOI 10.3109/01050397409044959 Guinan Jr J.J., 1996, COCHLEA, P435 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Kruglov AV, 1997, ACTA OTO-LARYNGOL, V117, P174, DOI 10.3109/00016489709117763 Molenaar DG, 2000, HEARING RES, V143, P197, DOI 10.1016/S0378-5955(00)00049-6 OMAHONEY CF, 1995, J ACOUST SOC AM, V97, P3721, DOI 10.1121/1.412994 PLOMP R, 1976, ASPECTS TONE SENSATI, P27 PONTON CW, 1992, SCAND AUDIOL, V21, P131, DOI 10.3109/01050399209045993 Prieve BA, 1996, J ACOUST SOC AM, V99, P3077, DOI 10.1121/1.414794 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 RUGGERO MA, 1992, MAMMALIAN AUDITORY P, P35 SHER ACA, 1999, J ACOUST SOC AM, V105, P782 Steiglitz K., 1996, DIGITAL SIGNAL PROCE Stover LJ, 1996, J ACOUST SOC AM, V99, P1016, DOI 10.1121/1.414630 Tavartkiladze GA, 1996, ACTA OTO-LARYNGOL, V116, P213, DOI 10.3109/00016489609137826 Yates GK, 1999, HEARING RES, V136, P49, DOI 10.1016/S0378-5955(99)00108-2 NR 26 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 2000 VL 143 IS 1-2 BP 208 EP 222 DI 10.1016/S0378-5955(00)00048-4 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 309AK UT WOS:000086744900020 PM 10771198 ER PT J AU Bowman, DM Brown, DK Kimberley, BP AF Bowman, DM Brown, DK Kimberley, BP TI An examination of gender differences in DPOAE phase delay measurements in normal-hearing human adults SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; distortion product; phase delay; gender difference; human ID PRODUCT OTOACOUSTIC EMISSIONS; ACOUSTIC DISTORTION-PRODUCT; BASILAR-MEMBRANE; AUDITORY-SYSTEM; HUMAN EARS; RESPONSES; AMPLITUDE; COCHLEA; SOUND; ESTROGEN AB This study examined gender differences in f(1)- and f(2)-sweep distortion product otoacoustic emission (DPOAE) phase delay measures in 60 normal-hearing human adults. Phase delay measures were obtained at six different f(2) frequencies ranging from 1.1 to 6.0 kHz (f(2)/f(1) ratios were 1.1-1.3). Primary levels for f(2) were 45 and 50 dB SPL (f(1) was 15 dB > f(2)). Gender, differences have been observed in normal-hearing human adults in both auditory brainstem response (ABR) and fi-sweep DPOAE studies. Gender differences in delay have been attributed to differences in the average length of the cochlea, where female cochleas are 13% shorter than male cochleas. Previously, the authors have proposed that the f(1)-sweep phase delay estimate is predominantly composed of a level-independent transport time to the site of DPOAE generation and a small proportion of the level and frequency-dependent filter build-up time. The f(2)-sweep delay also contains the transport time, however, it is predominantly composed of the filter build-up time. Therefore, delay differences between stimulation paradigms are equal to a proportion of the filter build-up time. In this study, mean f(1) - and f(2)-sweep delays were significantly longer in male ears than female ears at 1.1 kHz (45 and 50 dB). At 50 dB, f(1)-sweep phase delay measures were 18% longer in male ears (6.5 ms) than female ears (5.5 ms). Mean f(2)-sweep delays were 23% longer in male ears (10.0 ms) than female ears (8.1 ms). This gender difference was not observed when the isolated filter build-up time was calculated from the DPOAE phase delay difference. These observations may therefore be attributed to a gender-related anatomical difference in cochlear length. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Surg, Auditory Res Program, Calgary, AB T2N 4N1, Canada. Univ Calgary, Dept Physiol & Biophys, Calgary, AB, Canada. RP Brown, DK (reprint author), Univ Calgary, Dept Surg, Auditory Res Program, 3330 Hosp Dr NW, Calgary, AB T2N 4N1, Canada. CR Abdala C, 1996, J ACOUST SOC AM, V100, P3726, DOI 10.1121/1.417234 Bowman DM, 1998, HEARING RES, V119, P14, DOI 10.1016/S0378-5955(98)00041-0 Bowman DM, 1997, J ACOUST SOC AM, V101, P1550, DOI 10.1121/1.418129 BROWN AM, 1992, P ROY SOC B-BIOL SCI, V250, P29, DOI 10.1098/rspb.1992.0126 BROWN D, 1994, J OTOLARYNGOL, V23, P234 BROWNE R, 1995, J AM CULTURE, V18, P121 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 DON M, 1993, J ACOUST SOC AM, V94, P2135, DOI 10.1121/1.407485 ELKINDHIRSCH KE, 1992, HEARING RES, V60, P143, DOI 10.1016/0378-5955(92)90016-G GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 Kemp D. T., 1983, MECH HEARING, P75 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 KIMBERLEY BP, 1993, J ACOUST SOC AM, V94, P1343, DOI 10.1121/1.408162 MAHONEY CFO, 1995, J ACOUST SOC AM, V97, P3721 McFadden D, 1998, DEV NEUROPSYCHOL, V14, P261 McFadden D, 1998, P NATL ACAD SCI USA, V95, P2709, DOI 10.1073/pnas.95.5.2709 McFadden D, 1998, J ACOUST SOC AM, V104, P1555, DOI 10.1121/1.424366 Moulin A, 1996, J ACOUST SOC AM, V100, P1640, DOI 10.1121/1.416064 Moulin A, 1996, J ACOUST SOC AM, V100, P1617, DOI 10.1121/1.416063 NORTH GR, 1992, ENVIRONMETRICS, V3, P1, DOI 10.1002/env.3170030101 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 Recio A, 1998, J ACOUST SOC AM, V103, P1972, DOI 10.1121/1.421377 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O RUGGERO MA, 1980, J ACOUST SOC AM, V67, P707, DOI 10.1121/1.383900 SATO H, 1991, ACTA OTO-LARYNGOL, V111, P1037, DOI 10.3109/00016489109138447 Stover LJ, 1996, J ACOUST SOC AM, V99, P1016, DOI 10.1121/1.414630 Wable J, 1996, J ACOUST SOC AM, V100, P2228, DOI 10.1121/1.417932 WHITEHEAD ML, 1994, ABSTR ASS RES OT, V17, P46 Wilson J., 1980, Proceedings of the Eighth Annual Canadian Conference on Information Science NR 32 TC 27 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 1 EP 11 DI 10.1016/S0378-5955(99)00212-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400001 PM 10748323 ER PT J AU Khan, DC DeGagne, JM Trune, DR AF Khan, DC DeGagne, JM Trune, DR TI Abnormal cochlear connective tissue mineralization in the Palmerston North autoimmune mouse SO HEARING RESEARCH LA English DT Article DE autoimmune hearing loss; autoimmune disease; fibrosis; otosclerosis; osteogenesis; inner ear ID SYSTEMIC LUPUS-ERYTHEMATOSUS; SENSORINEURAL HEARING-LOSS; HUMAN TEMPORAL BONE; II COLLAGEN AUTOIMMUNITY; FIBROBLAST GROWTH-FACTOR; INNER-EAR; DEAFNESS; OTOSCLEROSIS; DISEASE; MICE AB Inner ear fibrosis and osteogenesis are common features of human autoimmune disease, although the cellular mechanisms are unknown. The Palmerston North (PN) autoimmune strain mouse has been shown to develop modiolar sclerotic lesions with progression of its systemic disease. Therefore, lesion development was studied in the cochleas of PN mice to gain insight into potential autoimmune osteogenic processes in the human ear. Cochleas from PN mice were examined with electron microscopy to characterize the cellular and extracellular matrix changes that lead to abnormal mineralization. Initially, activated fibroblasts produced extracellular- matrix fibers, ranging in size from fine fibrils to larger collagen-like fibers. These proliferating fibers appeared to 'seed' the mineralizing lesions by serving as the framework for mineral deposition. As mineralization continued, the Foci grew in size and fused to form large sclerotic masses within the connective tissue. However, the lesions never invaded nor degraded the normal modiolar bone. These observations of abnormal mineralization of cochlear connective tissue fibers show some parallels with human cochlear autoimmune osteogenesis, suggesting similar molecular processes may be involved. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Hearing Res Ctr, Portland, OR 97201 USA. RP Trune, DR (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Hearing Res Ctr, NRC04,3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR ANDONOPOULOS AP, 1995, CLIN EXP RHEUMATOL, V13, P137 Axon PR, 1998, AM J OTOL, V19, P724 BAIRD A, 1989, BRIT MED BULL, V45, P438 BLATT IM, 1961, ARCHIV OTOLARYNGOL, V73, P639 FISHER ER, 1961, ARCH PATHOL, V72, P572 GOSPODAROWICZ D, 1987, ENDOCR REV, V8, P95 GUSSEN R, 1977, ARCH OTO-RHINO-LARYN, V217, P263, DOI 10.1007/BF00465544 HARRIS JP, 1986, ANN OTO RHINOL LARYN, V95, P176 HELFGOTT SM, 1991, LANCET, V337, P387, DOI 10.1016/0140-6736(91)91165-Q HERTLER CK, 1990, OTOLARYNG HEAD NECK, V103, P713 Hoistad DL, 1998, AM J OTOLARYNG, V19, P33, DOI 10.1016/S0196-0709(98)90063-1 HONGJUN X, 1995, P SEND S, V5, P55 HOSHINO T, 1980, ACTA OTO-LARYNGOL, V90, P257, DOI 10.3109/00016488009131723 HUANG CC, 1987, AM J OTOLARYNG, V8, P332, DOI 10.1016/S0196-0709(87)80052-2 Jenkins H A, 1981, Am J Otolaryngol, V2, P99, DOI 10.1016/S0196-0709(81)80026-9 JOLIAT T, 1992, ANN OTO RHINOL LARYN, V101, P1000 JURZYK RS, 1992, CUTIS, V49, P289 Keithley EM, 1998, LARYNGOSCOPE, V108, P87, DOI 10.1097/00005537-199801000-00016 LIM DJ, 1985, HEARING LOSS DIZZINE, P43 LIM DJ, 1975, ACTA OTO-LARYNGOL, V80, P255, DOI 10.3109/00016487509121326 MARKS SC, 1988, AM J ANAT, V183, P1, DOI 10.1002/aja.1001830102 MILLER LM, 1987, DERMATOLOGY GENERAL, P1763 NADOL JB, 1991, ANN OTO RHINOL LARYN, V100, P712 NOMURA M, 1990, ARCH DERMATOL, V126, P1057, DOI 10.1001/archderm.126.8.1057 OHASHI T, 1989, ANN OTO RHINOL LARYN, V98, P556 PEDERSEN AD, 1993, HEARING RES, V66, P253, DOI 10.1016/0378-5955(93)90145-Q RAREY KE, 1986, AM J OTOLARYNG, V4, P387 REYDON JL, 1968, LARYNGOSCOPE, V78, P95, DOI 10.1288/00005537-196801000-00009 ROTHE MJ, 1990, ARCH DERMATOL, V126, P1060, DOI 10.1001/archderm.126.8.1060 Schuknecht HF, 1993, PATHOLOGY EAR SCHUKNECHT HF, 1994, LARYNGOSCOPE, V104, P1135 SIMMONS DJ, 1992, BONE OSTEOBLAST OSTE, V1, P193 SOLIMAN AM, 1990, AM J OTOL, V11, P27 Sone M, 1999, ANN OTO RHINOL LARYN, V108, P338 SORENSEN MS, 1988, ACTA OTO-LARYNGOL, V105, P242, DOI 10.3109/00016488809097004 Sperling NM, 1998, OTOLARYNG HEAD NECK, V118, P762, DOI 10.1016/S0194-5998(98)70265-7 SUGA F, 1977, ANN OTO RHINOL LARYN, V86, P17 THALMANN I, 1987, AM J OTOLARYNG, V8, P308, DOI 10.1016/S0196-0709(87)80049-2 TRAYNOR SJ, 1992, OTOLARYNG HEAD NECK, V106, P196 TRUNE DR, 1990, HEARING RES, V48, P241, DOI 10.1016/0378-5955(90)90064-V TRUNE DR, 1994, AM J OTOLARYNG, V15, P114, DOI 10.1016/0196-0709(94)90060-4 Trune DR, 1997, HEARING RES, V105, P57, DOI 10.1016/S0378-5955(96)00191-8 TRUNE DR, 1991, AM J OTOLARYNG, V12, P259, DOI 10.1016/0196-0709(91)90003-X WEINBERGER A, 1979, ANN RHEUM DIS, V38, P384, DOI 10.1136/ard.38.4.384 WOLFF D, 1965, ANN OTO RHINOL LARYN, V74, P507 YANAGITA N, 1987, LARYNGOSCOPE, V97, P345 YOO TJ, 1982, SCIENCE, V217, P1153, DOI 10.1126/science.7112122 YOO TJ, 1983, ANN OTO RHINOL LARYN, V92, P267 YOO TJ, 1984, ANN OTO RHINOL LARYN, V93, P3 YOO TJ, 1983, ANN OTO RHINOL LARYN, V92, P103 YOON TH, 1990, LARYNGOSCOPE, V100, P707 YOON TH, 1989, LARYNGOSCOPE, V99, P600 ZECHNER G, 1980, ACTA OTO-LARYNGOL, V89, P310, DOI 10.3109/00016488009127142 NR 53 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 12 EP 22 DI 10.1016/S0378-5955(99)00221-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400002 PM 10748324 ER PT J AU McFadden, D AF McFadden, D TI Masculinizing effects on otoacoustic emissions and auditory evoked potentials in women using oral contraceptives SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; auditory evoked potential; oral contraceptive; masculinization; estrogen ID BRAIN-STEM RESPONSES; MENSTRUAL-CYCLE; YOUNG-WOMEN; BLOOD-PRESSURE; ABR LATENCY; ESTROGEN; SEX; GENDER; TEMPERATURE; REPLACEMENT AB The otoacoustic emissions (OAEs) and auditory evoked potentials (AEPs) measured in two separate large scale studies were examined retrospectively for potential differences between those women using, and those not using, oral contraception (OC). Fourteen dependent variables were examined, all of which exhibited substantial sex differences. For 13 of those 14 dependent variables, the means for the users of OC were shifted away from the means of the non-users in the direction of the males. Specifically, for four different measures of OAE strength, for seven of eight measures of AEP latency or amplitude, and for two cognitive tests (mental rotation and water level), the means for the users of OC were located intermediate to those of the non-users of OC and the males. Few of these differences between users and non-users of OC achieved statistical significance, but the near universality of the direction of the difference suggests that oral contraceptives do produce a weak masculinizing effect on some auditory structures. These weak masculinizing effects appear to run contrary to the facts that the levels of both free testosterone and estradiol are lower in women using OC than in normal-cycling women. Past findings on auditory sex differences may have underestimated those sex differences. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Texas, Dept Psychol, Austin, TX 78712 USA. Univ Texas, Inst Neurosci, Austin, TX 78712 USA. RP McFadden, D (reprint author), Univ Texas, Dept Psychol, Mezes Hall 330, Austin, TX 78712 USA. CR ADAM K, 1989, EUR J APPL PHYSIOL O, V58, P471, DOI 10.1007/BF02330699 BANCROFT J, 1991, ARCH SEX BEHAV, V20, P121, DOI 10.1007/BF01541939 BELL A, 1992, HEARING RES, V58, P91, DOI 10.1016/0378-5955(92)90012-C BURNS EM, 1993, ABST ASS RES OT, V16, pA98 COHEN J, 1992, PSYCHOL BULL, V112, P155, DOI 10.1037/0033-2909.112.1.155 COLEMAN JR, 1994, HEARING RES, V80, P209, DOI 10.1016/0378-5955(94)90112-0 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DON M, 1993, J ACOUST SOC AM, V94, P2135, DOI 10.1121/1.407485 ELKINDHIRSCH KE, 1992, HEARING RES, V60, P143, DOI 10.1016/0378-5955(92)90016-G ELKINDHIRSCH KE, 1994, OTOLARYNG HEAD NECK, V110, P46, DOI 10.1016/S0194-5998(94)70791-X ELKINDHIRSCH KE, 1992, HEARING RES, V64, P93, DOI 10.1016/0378-5955(92)90171-I GASPARD UJ, 1983, CONTRACEPTION, V27, P577, DOI 10.1016/0010-7824(83)90023-9 HAGGERTY HS, 1993, HEARING RES, V70, P31, DOI 10.1016/0378-5955(93)90050-B Hall J, 1992, HDB AUDITORY EVOKED HAMPSON E, 1990, PSYCHONEUROENDOCRINO, V15, P97, DOI 10.1016/0306-4530(90)90018-5 HAMPSON E, 1990, BRAIN COGNITION, V14, P26, DOI 10.1016/0278-2626(90)90058-V Heintz B, 1996, J HYPERTENS, V14, P333, DOI 10.1097/00004872-199603000-00010 JERGER J, 1988, EAR HEARING, V9, P168, DOI 10.1097/00003446-198808000-00002 KATTAPONG KR, 1995, CHRONOBIOL INT, V12, P257, DOI 10.3109/07420529509057274 KUSSELING FS, 1995, J AM COLL HEALTH, V43, P191 McFadden D, 1996, HEARING RES, V97, P102 MCFADDEN D, 2000, UNPUB J ASS RES OTOL McFadden D, 1999, J ACOUST SOC AM, V105, P2403, DOI 10.1121/1.426845 McFadden D, 1998, DEV NEUROPSYCHOL, V14, P261 McFadden D, 1998, P NATL ACAD SCI USA, V95, P2709, DOI 10.1073/pnas.95.5.2709 McFadden D, 1998, J ACOUST SOC AM, V104, P1555, DOI 10.1121/1.424366 MCFADDEN D, 1993, P NATL ACAD SCI USA, V90, P11900, DOI 10.1073/pnas.90.24.11900 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 Reinberg AE, 1996, CHRONOBIOL INT, V13, P199, DOI 10.3109/07420529609012653 Rogers SM, 1997, EUR J APPL PHYSIOL O, V75, P34 ROSENBERG MJ, 1995, J REPROD MED, V40, P355 SAMANI F, 1987, CONTRACEPTION, V35, P41, DOI 10.1016/0010-7824(87)90049-7 Smail P.J., 1981, PEDIAT ANDROLOGY, P9 SWANSON SJ, 1988, J SPEECH HEAR RES, V31, P569 THOMAS H, 1973, SCIENCE, V181, P173, DOI 10.1126/science.181.4095.173 TRUNE DR, 1988, HEARING RES, V32, P165, DOI 10.1016/0378-5955(88)90088-3 TRUSSELL J, 1987, STUD FAMILY PLANN, V18, P237, DOI 10.2307/1966856 VANDENBERG SG, 1978, PERCEPT MOTOR SKILL, V47, P599 VERMEULEN A, 1982, CONTRACEPTION, V26, P505, DOI 10.1016/0010-7824(82)90149-4 NR 39 TC 32 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 23 EP 33 DI 10.1016/S0378-5955(00)00002-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400003 PM 10748325 ER PT J AU Sha, SH Schacht, J AF Sha, SH Schacht, J TI Antioxidants attenuate gentamicin-induced free radical formation in vitro and ototoxicity in vivo: D-methionine is a potential protectant SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 21st Annual Meeting of the Association-for-Research-in-Otolaryngology CY FEB 15-19, 1998 CL ST PETERSBURG BEACH, FLORIDA SP Assoc Res Otolaryngol DE aminoglycoside; reactive oxygen species; antioxidant therapy; histidine; methionine ID PIG IN-VIVO; RENAL CORTICAL MITOCHONDRIA; GUINEA-PIG; IRON CHELATORS; GLUTATHIONE; SULFOXIDE; TOXICITY AB We have recently suggested antioxidant therapy against aminoglycoside-induced hearing loss based on the hypothesis of a redox-active aminoglycoside-iron complex causing ototoxicity. The present study compares seven antioxidants and iron chelators for their ability to attenuate gentamicin-induced free radical generation in vitro and ototoxicity in guinea pie in vivo. Free radical formation by gentamicin was measured by chemiluminescence detection both in a non-enzymatic system in vitro and in cell culture. Deferoxamine, 2,3-dibydroxybenzoate, or salicylic acid suppressed gentamicin-induced luminescence in both tests. This indicated the usefulness of the assay as a screen For potential protectants since these agents had previously been shown to attenuate gentamicin-induced ototoxicity in vivo. Histidine and D-methionine, amino acids with chelating and antioxidant properties, also suppressed gentamicin-mediated luminosity both in vitro and in cell culture. In contrast, the metal chelators succimer (2,3-dimercaptosuccinic acid (DMSA)) and trientine (N,N'-bis[2-aminoethyl]-1,2 ethanediamine) promoted free radical formation and were excluded from further studies. Histidine and D-methionine were then administered to guinea pigs receiving concurrent treatment with gentamicin (120 mg/kg x 19 days). Threshold shifts induced by gentamicin were significantly attenuated by twice daily injections of D-methionine. Once-daily injections of histidine or D-methionine were less effective, pointing to the importance of pharmacokinetics in antioxidant protection in vivo. The study presents a simple screening system for agents with the potential to attenuate gentamicin-induced hearing loss. It also supports the hypothesis of free radical formation as an underlying cause of gentamicin ototoxicity, (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Schacht, J (reprint author), Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR BOCK GR, 1983, HEARING RES, V9, P255, DOI 10.1016/0378-5955(83)90030-8 Campbell KCM, 1996, HEARING RES, V102, P90, DOI 10.1016/S0378-5955(96)00152-9 Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 Conlon BJ, 1998, LARYNGOSCOPE, V108, P284, DOI 10.1097/00005537-199802000-00023 Conlon BJ, 1999, HEARING RES, V128, P40, DOI 10.1016/S0378-5955(98)00195-6 DAWSON RMC, 1986, DATA BIOCH RES, P409 GARETZ SL, 1994, HEARING RES, V77, P81, DOI 10.1016/0378-5955(94)90255-0 GYLLENHAMMAR H, 1987, J IMMUNOL METHODS, V97, P209, DOI 10.1016/0022-1759(87)90461-3 Hirose K, 1997, HEARING RES, V104, P1, DOI 10.1016/S0378-5955(96)00169-4 JONES MM, 1989, ANTICANCER RES, V9, P1937 KAJI H, 1987, RES COMMUN CHEM PATH, V36, P101 KIES C, 1975, J NUTR, V105, P809 LAUTERMANN J, 1995, HEARING RES, V86, P15, DOI 10.1016/0378-5955(95)00049-A Liochev SI, 1997, ARCH BIOCHEM BIOPHYS, V337, P115, DOI 10.1006/abbi.1997.9766 NEUBERT D, 1999, XENOBIOTICA S1, V18, P45 OLIN B, 1991, DRUG FACTS COMP, P2115 PIERSON MG, 1981, HEARING RES, V4, P79, DOI 10.1016/0378-5955(81)90037-X Priuska EM, 1998, INORG CHIM ACTA, V273, P85, DOI 10.1016/S0020-1693(97)05942-2 Priuska EM, 1995, BIOCHEM PHARMACOL, V50, P1749, DOI 10.1016/0006-2952(95)02160-4 RAO UM, 1989, FREE RADICAL BIO MED, V7, P513 Sha SH, 1999, HEARING RES, V128, P112, DOI 10.1016/S0378-5955(98)00200-7 Sha SH, 1999, FREE RADICAL BIO MED, V26, P341, DOI 10.1016/S0891-5849(98)00207-X Sha SH, 1999, LAB INVEST, V79, P807 SHA SH, 1998, ABS ASS RES OT, V21, P134 Song BB, 1997, J PHARMACOL EXP THER, V282, P369 Song BB, 1998, FREE RADICAL BIO MED, V25, P189, DOI 10.1016/S0891-5849(98)00037-9 Song BB, 1996, HEARING RES, V94, P87, DOI 10.1016/0378-5955(96)00003-2 STADTMAN ER, 1993, ANNU REV BIOCHEM, V62, P797, DOI 10.1146/annurev.bi.62.070193.004053 STEGINK LD, 1986, J NUTR, V116, P1185 UNNIKRISHNAN MK, 1990, AGENTS ACTIONS, V31, P110, DOI 10.1007/BF02003229 WALKER PD, 1987, AM J PHYSIOL, V253, pC495 YANG CL, 1995, RENAL FAILURE, V17, P21, DOI 10.3109/08860229509036371 NR 32 TC 135 Z9 143 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 34 EP 40 DI 10.1016/S0378-5955(00)00003-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400004 PM 10748326 ER PT J AU Shoji, F Yamasoba, T Magal, E Dolan, DF Altschuler, RA Miller, JM AF Shoji, F Yamasoba, T Magal, E Dolan, DF Altschuler, RA Miller, JM TI Glial cell line-derived neurotrophic factor has a dose dependent influence on noise-induced hearing loss in the guinea pig cochlea SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 21st Annual Meeting of the Association-for-Research-in-Otolaryngology CY FEB 15-19, 1998 CL ST PETERSBURG BEACH, FLORIDA SP Assoc Res Otolaryngol DE cochlea; HC; GDNF; neurotrophic factor; osmotic pump; noise-induced hearing loss ID RECEPTOR TYROSINE KINASE; GDNF MESSENGER-RNA; NEURONS IN-VITRO; HAIR-CELLS; INNER-EAR; AUDITORY NEURONS; GROWTH-FACTOR; DOPAMINERGIC-NEURONS; GANGLION NEURONS; FACTOR PROTECTS AB We examined the effectiveness of glial cell line-derived neurotrophic factor (GDNF) to attenuate cochlear damage from intense noise stress. Subjects were exposed to 115 dB SPL one octave band noise centered at 4 kHz for 5 h. They received artificial perilymph with or without GDNF into the left scala tympani at 0.5 mu l/h from 4 days before noise exposure through 8 days following noise exposure. Different concentrations of GDNF (1 ng/ml, 10 ng/ml, 100 ng/ml, and 1 ng/ml) were applied chronically directly into the guinea pig cochlea via a microcannula and osmotic pump.:Noise-induced hearing loss was assessed with pure tone auditory brainstem responses (at 2, 4, 8 and 20 kHz), measured, prior to surgery, 1 day before noise exposure, and 7 days following noise exposure. Subjects were killed on day 8 following exposure for histological preparation and quantitative assessment of hair cell (HC) damage. A dose-dependent protective effect of GDNF on both sensory cell preservation and hearing function was found in the treated ears. At 1 ng/ml, GDNF showed no significant protection; at 10 ng/ml, GDNF showed significant HC protection; and at 100ng/ml, it was greater and bilateral. At 1 mu g/ml, GDNF appeared to have a toxic effect under noise stress in some cochleae. These findings indicate that GDNF at certain concentrations can effectively protect the inner ear from noise-induced hearing loss. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Tohoku Univ, Sch Med, Dept Otolaryngol, Sendai, Miyagi 980, Japan. Univ Tokyo, Dept Otolaryngol, Bunkyo Ku, Tokyo 113, Japan. Amgen Inc, Dept Neurosci, Thousand Oaks, CA 91320 USA. RP Miller, JM (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR Abe K, 1997, NEUROSCI LETT, V231, P37, DOI 10.1016/S0304-3940(97)00517-X Altschuler R. A., 1997, Society for Neuroscience Abstracts, V23, P619 AVILA MA, 1993, DEV BIOL, V159, P266, DOI 10.1006/dbio.1993.1239 Baloh RH, 1997, NEURON, V18, P793, DOI 10.1016/S0896-6273(00)80318-9 BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T BujBello A, 1997, NATURE, V387, P721 CHENG B, 1993, BRAIN RES, V607, P275, DOI 10.1016/0006-8993(93)91517-V CHOI DW, 1992, J NEUROBIOL, V23, P1261, DOI 10.1002/neu.480230915 CHOILUNDBERG DL, 1995, DEV BRAIN RES, V85, P80, DOI 10.1016/0165-3806(94)00197-8 Clarkson ED, 1995, NEUROREPORT, V7, P145, DOI 10.1097/00001756-199512000-00035 DAVIES AM, 1995, TRENDS NEUROSCI, V18, P355, DOI 10.1016/0166-2236(95)93928-Q Durbec P, 1996, NATURE, V381, P789, DOI 10.1038/381789a0 EMFORS P, 1996, NAT MED, V2, P463 Farkas LM, 1997, J NEUROSCI RES, V50, P361 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 Hu BH, 1997, HEARING RES, V113, P198, DOI 10.1016/S0378-5955(97)00143-3 HUDSPETH AJ, 1994, NEURON, V12, P1, DOI 10.1016/0896-6273(94)90147-3 Jing SQ, 1997, J BIOL CHEM, V272, P33111, DOI 10.1074/jbc.272.52.33111 Jing SQ, 1996, CELL, V85, P1113, DOI 10.1016/S0092-8674(00)81311-2 JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 Kearns CM, 1997, J NEUROSCI, V17, P7111 Keithley EM, 1998, NEUROREPORT, V9, P2183, DOI 10.1097/00001756-199807130-00007 Klein RD, 1997, NATURE, V387, P717 Kotzbauer PT, 1996, NATURE, V384, P467, DOI 10.1038/384467a0 Kristian T, 1998, STROKE, V29, P705 Lalwani AK, 1997, HEARING RES, V114, P139, DOI 10.1016/S0378-5955(97)00151-2 Leclere P, 1998, NEUROSCIENCE, V82, P545 LIM DJ, 1971, ARCHIV OTOLARYNGOL, V94, P294 LIN LFH, 1993, SCIENCE, V260, P1130, DOI 10.1126/science.8493557 LIN LFH, 1996, NEURAL NOTES, V11, P3 Low W, 1996, J CELL PHYSIOL, V167, P443, DOI 10.1002/(SICI)1097-4652(199606)167:3<443::AID-JCP8>3.0.CO;2-P Magal E., 1996, Society for Neuroscience Abstracts, V22, P1621 Mattson MP, 1996, RESTOR NEUROL NEUROS, V9, P191, DOI 10.3233/RNN-1996-9401 Milbrandt J, 1998, NEURON, V20, P245, DOI 10.1016/S0896-6273(00)80453-5 MILLER JM, 1996, ABSTR ASS RES OT, V19, P106 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 NAM YJ, 2000, ASS RES OT ABSTR, P216 Nosrat CA, 1996, CELL TISSUE RES, V286, P191, DOI 10.1007/s004410050688 Nosrat CA, 1997, EXP BRAIN RES, V115, P410, DOI 10.1007/PL00005711 OHLEMILLER KK, 1998, ASS RES OT ABSTR, V21, P130 OPPENHEIM RW, 1995, NATURE, V373, P344, DOI 10.1038/373344a0 PARK GH, 1998, ASS RES OT ABSTR, V21, P61 PerezNavarro E, 1996, NEUROSCIENCE, V75, P345, DOI 10.1016/0306-4522(96)00336-3 PETTIS RM, 1998, ASS RES OT ABSTR, V673, P169 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H PIRVOLA U, 1994, HEARING RES, V75, P131, DOI 10.1016/0378-5955(94)90064-7 PUEL JL, 1999, COCHLEAR PHARM NOISE, P1 PUJOL R, 1993, ACTA OTO-LARYNGOL, V113, P330, DOI 10.3109/00016489309135819 QUIRK WS, 1994, HEARING RES, V74, P217, DOI 10.1016/0378-5955(94)90189-9 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 SALT AN, 1988, PHYSL EAR, P341 SCHEIBE F, 1992, HEARING RES, V63, P19, DOI 10.1016/0378-5955(92)90069-Y SCHINDLER RA, 1995, AM J OTOL, V16, P304 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 SLEPECKY N, 1986, HEARING RES, V22, P307, DOI 10.1016/0378-5955(86)90107-3 SPOENDLIN H, 1984, ANN OTOL RHINOL LA S, V14, P282 STAECKER H, 1995, NEUROREPORT, V6, P1533 Staecker H, 1996, NEUROREPORT, V7, P889, DOI 10.1097/00001756-199603220-00011 STOVER T, 1999, IN PRESS GENE THERAP STOVER T, 1999, UNPUB REVISION Suvanto P, 1997, HUM MOL GENET, V6, P1267, DOI 10.1093/hmg/6.8.1267 TAY H, 1998, ASS RES OT ABSTR, V538, P135 TOMAC A, 1995, NATURE, V373, P335, DOI 10.1038/373335a0 Treanor JJS, 1996, NATURE, V382, P80, DOI 10.1038/382080a0 Trupp M, 1996, NATURE, V381, P785, DOI 10.1038/381785a0 TRUPP M, 1995, J CELL BIOL, V130, P137, DOI 10.1083/jcb.130.1.137 Tsuji J, 1997, J COMP NEUROL, V381, P188 Wang Y, 1997, J NEUROSCI, V17, P4341 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 Widenfalk J, 1997, J NEUROSCI, V17, P8506 Yagi M, 1999, HUM GENE THER, V10, P813, DOI 10.1089/10430349950018562 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 Yamasoba T, 1998, BRAIN RES, V784, P82, DOI 10.1016/S0006-8993(97)01156-6 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 ZHENG JL, 1995, J NEUROBIOL, V28, P330 NR 76 TC 55 Z9 60 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 41 EP 55 DI 10.1016/S0378-5955(00)00007-1 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400005 PM 10748327 ER PT J AU Gleich, O Dooling, RJ Ryals, BM AF Gleich, O Dooling, RJ Ryals, BM TI Neither endocochlear potential nor Tegmentum vasculosum are affected in hearing impaired Belgian Waterslager canaries SO HEARING RESEARCH LA English DT Article DE inner ear; bird; cochlear pathology; hereditary hearing loss; endocochlear potential ID INNER-EAR ABNORMALITIES; SERINUS-CANARIUS; BASILAR PAPILLA; POTASSIUM CONCENTRATION; COCHLEAR POTENTIALS; AUDITORY-THRESHOLDS; ADULT CHICKENS; SINGLE-FIBER; FUROSEMIDE; CELLS AB We previously showed that the Belgian Waterslager canary strain is affected by a hereditary hearing loss that is associated with a reduced number of hair cells and hair cell pathologies in the basilar papilla. Since hair cell pathologies were also present in the sacculus, Weisleder et al. (1994) suggested that these birds are afflicted by Scheibe's like dysplasia, a cochleo-saccular defect, in mammals, cochleo-saccular defects are characterized primarily by the lack of an endocochlear potential and abnormalities in the Stria vascularis which only secondarily lead to hair cell loss (Steel and Beck, 1983; Steel, 1994; 1995). Here we report the endocochlear potential of six ears from three non-Belgian Waterslager canaries and three ears of two Belgian Waterslager canaries to decide if Waterslager canaries are affected by a cochleo-saccular or by a neuroepithelial defect. The mean endocochlear potential was 17.6 +/- 2.5 mV in the non-Waterslager canaries and 20.3 +/- 0.6 mV in Waterslager canaries. In addition, and consistent with the presence of a normal endocochlear potential, light microscopy of the tegmentum vasculosum provided no evidence for pathology. These data show that Belgian Waterslager canaries are affected by a neuroepithelial rather than a cochleo-saccular inner ear defect. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Regensburg, ENT Dept, D-93042 Regensburg, Germany. Univ Maryland, Dept Psychol, College Pk, MD 20742 USA. James Madison Univ, Dept Commun Sci & Disorders, Harrisonburg, VA 22807 USA. RP Gleich, O (reprint author), Univ Regensburg, ENT Dept, Franz Josef Str Allee 11, D-93042 Regensburg, Germany. CR VONBEKESY G, 1952, J ACOUST SOC AM, V24, P72 CHEN L, 1995, HEARING RES, V89, P28, DOI 10.1016/0378-5955(95)00119-5 COTANCHE DA, 1987, HEARING RES, V25, P125, DOI 10.1016/0378-5955(87)90086-4 Cotanche DA, 1995, HEARING RES, V91, P148, DOI 10.1016/0378-5955(95)00185-9 Gleich O, 1997, J COMP NEUROL, V377, P5, DOI 10.1002/(SICI)1096-9861(19970106)377:1<5::AID-CNE2>3.0.CO;2-8 GLEICH O, 1995, HEARING RES, V82, P100 GLEICH O, 1994, NATURWISSENSCHAFTEN, V81, P320, DOI 10.1007/BF01131950 GLEICH O, 1994, HEARING RES, V79, P123, DOI 10.1016/0378-5955(94)90134-1 Hellstrom LI, 1996, J ACOUST SOC AM, V100, P3275, DOI 10.1121/1.417211 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 Kirk DL, 1998, AUDIOL NEURO-OTOL, V3, P21, DOI 10.1159/000013776 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MCGUIRT JP, 1995, HEARING RES, V84, P52, DOI 10.1016/0378-5955(95)00015-V MILLS JH, 1996, 19 ARO MIDW RES M, P161 NECKER R, 1970, Z VERGL PHYSIOL, V69, P367, DOI 10.1007/BF00333768 OKANOYA K, 1987, J COMP PSYCHOL, V101, P213, DOI 10.1037/0735-7036.101.2.213 OKANOYA K, 1990, HEARING RES, V46, P271, DOI 10.1016/0378-5955(90)90008-D OKANOYA K, 1985, J ACOUST SOC AM, V78, P1170, DOI 10.1121/1.392885 POJE CP, 1995, HEARING RES, V82, P197, DOI 10.1016/0378-5955(94)00177-R RUNHAAR G, 1991, HEARING RES, V56, P227, DOI 10.1016/0378-5955(91)90173-7 RUNHAAR G, 1987, HEARING RES, V29, P93, DOI 10.1016/0378-5955(87)90207-3 RYALS BM, 1995, HEARING RES, V83, P51, DOI 10.1016/0378-5955(94)00190-2 SALT AN, 1979, HEARING RES, V1, P343, DOI 10.1016/0378-5955(79)90005-4 SCHERMULY L, 1990, HEARING RES, V50, P295, DOI 10.1016/0378-5955(90)90053-R SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 STEEL KP, 1987, HEARING RES, V27, P11, DOI 10.1016/0378-5955(87)90022-0 Steel KP, 1995, ANNU REV GENET, V29, P675 STEEL KP, 1994, TRENDS GENET, V10, P428, DOI 10.1016/0168-9525(94)90113-9 STEEL KP, 1983, ARCH OTOLARYNGOL, V109, P22 Trautwein PG, 1997, HEARING RES, V110, P266, DOI 10.1016/S0378-5955(97)00082-8 VOSSIECK T, 1991, HEARING RES, V56, P93, DOI 10.1016/0378-5955(91)90158-6 WANG J, 1992, HEARING RES, V59, P31, DOI 10.1016/0378-5955(92)90099-9 Weisleder P, 1996, J COMP NEUROL, V369, P292, DOI 10.1002/(SICI)1096-9861(19960527)369:2<292::AID-CNE9>3.0.CO;2-Z WEISLEDER P, 1994, HEARING RES, V80, P64, DOI 10.1016/0378-5955(94)90009-4 WHITWORTH C, 1993, HEARING RES, V71, P202, DOI 10.1016/0378-5955(93)90035-Y NR 36 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 56 EP 62 DI 10.1016/S0378-5955(00)00006-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400006 PM 10748328 ER PT J AU Kawase, T Ogura, M Hidaka, H Sasaki, N Suzuki, Y Takasaka, T AF Kawase, T Ogura, M Hidaka, H Sasaki, N Suzuki, Y Takasaka, T TI Effects of contralateral noise on measurement of the psychophysical tuning curve SO HEARING RESEARCH LA English DT Article DE contra sound; olivocochlear efferent; psychophysical tuning curve; human ID CROSSED OLIVOCOCHLEAR BUNDLE; AUDITORY-NERVE FIBERS; COCHLEAR MICROMECHANICAL PROPERTIES; COMPOUND ACTION-POTENTIALS; ELECTRICAL-STIMULATION; RESPONSE PROPERTIES; EFFERENT NEURONS; MASKED TONES; GUINEA-PIG; CAT AB The effects of the addition of contralateral noise on the psychophysical tuning curve (PTC) were examined in subjects with normal hearing. The masking threshold of the tail part of the PTC tended to decrease with the addition of contralateral noise, although the threshold reduction was usually less than 5 dB. On the other hand, the effects of contralateral noise were relatively small around the tip of the PTC contour. Focusing on the effects of contralateral noise on the masking threshold at the tail part of the PTC, the effects of changing the time between initiation of masking the tone and the presentation of the masked probe tone on the threshold reduction at the tail part of the PTC were also observed. The results indicate that the reduction of the masking threshold by the addition of contralateral noise tended to be larger when the presentation of the signal tone was delayed after the onset of the masker. Usually, when the signal tone was presented under conditions of the forward masking paradigm, the reduction of the threshold was most remarkable. Results obtained in the present study are discussed based on the known characteristics of the olivocochlear (OC)-efferent fibers activated by contralateral noise. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tohoku Univ, Grad Sch Med, Dept Otolaryngol Head & Neck Surg, Aoba Ku, Sendai, Miyagi 9808574, Japan. Tohoku Univ, Res Inst Elect Commun, Aoba Ku, Sendai, Miyagi 9808574, Japan. RP Kawase, T (reprint author), Tohoku Univ, Grad Sch Med, Dept Otolaryngol Head & Neck Surg, Aoba Ku, 1-1 Seiryo Machi, Sendai, Miyagi 9808574, Japan. CR BROWN MC, 1989, HEARING RES, V40, P93, DOI 10.1016/0378-5955(89)90103-2 BUNO W, 1978, EXP NEUROL, V59, P62, DOI 10.1016/0014-4886(78)90201-7 CODY AR, 1982, J ACOUST SOC AM, V72, P280, DOI 10.1121/1.387993 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E DOLAN DF, 1988, J ACOUST SOC AM, V83, P1081, DOI 10.1121/1.396052 Fex J., 1962, ACTA PHYSL SCAN S189, V55, P2 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 GUINAN JJ, 1988, HEARING RES, V37, P29, DOI 10.1016/0378-5955(88)90075-5 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 HALL JL, 1968, J ACOUST SOC AM, V44, P370, DOI 10.1121/1.1970490 He NJ, 1998, J ACOUST SOC AM, V103, P553, DOI 10.1121/1.421127 KAWASE T, 1993, J NEUROPHYSIOL, V70, P2519 Kawase T, 1995, HEARING RES, V91, P1, DOI 10.1016/0378-5955(95)00145-X KAWASE T, 1993, J NEUROPHYSIOL, V70, P2533 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K NIEDER P, 1970, EXP NEUROL, V28, P179, DOI 10.1016/0014-4886(70)90172-X OGURA Y, 1989, J ACOUST SOC JPN, V45, P441 SUZUKI Y, 1996, 43WG1 ISOTC VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Vogten LL, 1974, FACTS MODELS HEARING, P142 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WILLIAMS EA, 1994, ACTA OTO-LARYNGOL, V114, P121, DOI 10.3109/00016489409126029 WINSLOW RL, 1988, HEARING RES, V35, P165, DOI 10.1016/0378-5955(88)90116-5 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 Zwicker E., 1974, FACTS MODELS HEARING, P132 ZWICKER E, 1978, AUDIOLOGY, V17, P120 NR 32 TC 10 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 63 EP 70 DI 10.1016/S0378-5955(00)00010-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400007 PM 10748329 ER PT J AU Foth, HJ Farber, S Gauer, A Wagner, R AF Foth, HJ Farber, S Gauer, A Wagner, R TI Thermal damage threshold at 633 nm of tympanic membrane of pig SO HEARING RESEARCH LA English DT Article DE laser induced thermal damage; tympanic membrane; coagulation; scattering AB Doppler vibrometers are used by many research groups to monitor the motion of the tympanic membrane (TM) and of middle ear ossicles for in vivo and in vitro studies. Power densities in these applications reach 80 W/cm(2). To determine the safe limit of exposure, a cw dye laser at a wavelength of 633 nm was used to investigate the threshold of thermal damage of TM of pigs under exposure times of 60 s. To determine the applied power density accurately, the spot size of the laser beam was monitored by an objective lens and a CCD camera. Twenty-six laser exposed samples of TM were stained by haematoxylin and eosin stain and the semi-thin sections were examined microscopically. In none of the sections was any laser induced damage observed with power densities below 7.1 kW/cm(2), whereas serious damage occurred showing coagulation, carbonisation and perforation in all cases with laser powers above 8.2 kW/cm(2). The threshold for damage and the conical shape of the damage zone is explained by photon propagation and absorption in the tissue especially by the increase of the scattering factor at higher tissue temperature. The thermal damage threshold of 8 kW/cm(2) is compared to the maximum permissible exposure given in laser safety standards for skin. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Kaiserslautern, Dept Phys, D-67663 Kaiserslautern, Germany. Westpfalz Klinikum, Dept Pathol, D-67655 Kaiserslautern, Germany. RP Foth, HJ (reprint author), Univ Kaiserslautern, Dept Phys, Erwin Schrodinger Str, D-67663 Kaiserslautern, Germany. CR ANDREOLA S, 1988, LASER SURG MED, V8, P142 BECK JF, 1993, MED OPTICAL TOMOG IS, V11, P193 DECRAEMER WF, 1992, HEARING RES, V72, P1 Duck F. A., 1990, PHYSICAL PROPERTIES *EN, 1997, 60825 EN ESSENPREIS M, 1992, INDUCED CHANGES OPTI FOTH HJ, 1994, P SOC PHOTO-OPT INS, V2084, P178, DOI 10.1117/12.167300 GOODE RL, 1993, AM J OTOL, V14, P247 JAQUES SL, 1987, LASER LIFE SCI, V1, P309 KIENLE A, 1995, PHYS MED BIOL, V40, P1559, DOI 10.1088/0031-9155/40/10/001 Rodriguez Jorge J, 1997, HNO, V45, P997, DOI 10.1007/s001060050185 Roggan A, 1999, PHYS BL, V55, P25 STASCHE N, 1994, ACTA OTO-LARYNGOL, V114, P59, DOI 10.3109/00016489409126017 Vogel U, 1997, MIDDLE EAR MECH RES, P128 WAN S, 1981, PHOTOCHEM PHOTOBIOL, V34, P493, DOI 10.1111/j.1751-1097.1981.tb09391.x Welsh AJ, 1995, OPTICAL THERMAL RESP NR 16 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 71 EP 78 DI 10.1016/S0378-5955(00)00013-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400008 PM 10748330 ER PT J AU Willott, JF Turner, JG Sundin, VS AF Willott, JF Turner, JG Sundin, VS TI Effects of exposure to an augmented acoustic environment on auditory function in mice: roles of hearing loss and age during treatment SO HEARING RESEARCH LA English DT Article DE BXD mouse; CBA/CaJ mouse; BALB/cJ mouse; sensorineural hearing loss; development ID INFERIOR COLLICULUS NEURONS; PREPULSE INHIBITION; STARTLE RESPONSE; C57BL/6J MICE; COCHLEAR-PATHOLOGY; GENETICS; MOUSE; PRESBYCUSIS; PLASTICITY; THRESHOLDS AB The effects of exposure to an augmented acoustic environment (AAE) on auditory function were evaluated in mouse strains that exhibit various degrees and time courses of progressive hearing loss (BXD-22, BXD-12, BXD-16, BXD-14, BALB/cJ), and in normal-hearing CBA/CaJ mice. Beginning at age 25 days, mice were exposed 12 h every night to a 70 dB SPL broadband noise AAE. The AAE was maintained for at least 30 days in each strain. Same-strain control mice were age-matched and maintained under normal vivarium acoustic conditions. The auditory brainstem response (ABR), acoustic startle response amplitude, and prepulse inhibition (PPI) were used to assess the auditory system. Exposure to the AAE resulted in improved auditory performance (better PPI, lower ABR thresholds) when hearing impairment was present, but not when hearing was normal. The ameliorative effects occurred irrespective of a mouse's age at the onset of hearing loss, as long as initiation of AAE treatment preceded the occurrence of severe hearing loss. If AAE treatment was delayed beyond such a point, loss of threshold sensitivity progressed as usual, although PPI could still benefit. Finally, AAE treatment can slow, but not prevent, the occurrence of severe genetically determined hearing loss. (C) 2000 Elsevier Science B.V. All rights reserved. C1 No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. RP Willott, JF (reprint author), No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. CR Carlson S, 1996, HEARING RES, V99, P168, DOI 10.1016/S0378-5955(96)00098-6 Davis M., 1984, P287 Dawson M. E., 1999, STARTLE MODIFICATION ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1980, AUDIOLOGY, V19, P369 HOFFMAN HS, 1980, PSYCHOL REV, V87, P175, DOI 10.1037/0033-295X.87.2.175 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 LEITNER DS, 1985, PHYSIOL BEHAV, V34, P65, DOI 10.1016/0031-9384(85)90079-4 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 Li L, 1998, BEHAV NEUROSCI, V112, P1187, DOI 10.1037/0735-7044.112.5.1187 Li L, 1998, PHYSIOL BEHAV, V65, P133, DOI 10.1016/S0031-9384(98)00143-7 Turner JG, 1998, HEARING RES, V118, P101, DOI 10.1016/S0378-5955(98)00024-0 WILLOTT JF, 1988, HEARING RES, V37, P15, DOI 10.1016/0378-5955(88)90074-3 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 Willott JF, 1998, HEARING RES, V115, P162, DOI 10.1016/S0378-5955(97)00189-5 Willott JF, 1999, HEARING RES, V135, P78, DOI 10.1016/S0378-5955(99)00094-5 WILLOTT JF, 1995, BEHAV NEUROSCI, V109, P396, DOI 10.1037//0735-7044.109.3.396 WILLOTT JF, 1994, BEHAV NEUROSCI, V108, P703, DOI 10.1037/0735-7044.108.4.703 Willott JF, 1998, HEARING RES, V119, P27, DOI 10.1016/S0378-5955(98)00029-X WILLOTT JF, 1995, HEARING RES, V88, P143, DOI 10.1016/0378-5955(95)00107-F NR 21 TC 28 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 79 EP 88 DI 10.1016/S0378-5955(00)00014-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400009 PM 10748331 ER PT J AU Eggermont, JJ Komiya, H AF Eggermont, JJ Komiya, H TI Moderate noise trauma in juvenile cats results in profound cortical topographic map changes in adulthood SO HEARING RESEARCH LA English DT Article DE single unit; cat; primary auditory cortex; pure tone trauma; topographic map; reorganization ID PRIMARY AUDITORY-CORTEX; PARTIAL COCHLEAR LESIONS; INFERIOR COLLICULUS; NEURAL INTERACTION; HEARING-LOSS; PLASTICITY; REORGANIZATION; REPRESENTATION; INHIBITION; RESPONSES AB Cortical topographic map changes have been reported after profound drug-induced hearing loss in neonates, after progressive high-frequency hearing loss, and after mechanically induced lesions in the cochlea of adult animals. The present study demonstrates that exposure of 5-week-old kittens to a loud 6 kHz tone, producing mild to moderate high-frequency hearing loss, induces a profound reorganization of the frequency map in auditory cortex. In the reorganized cortical region, the frequency-tuning curves were of normal sharpness with near normal thresholds. Inhibitory tuning curve bandwidths were similar to those in control animals. Spontaneous activity in the reorganized part of the cortex was significantly increased. In contrast, the strength of the crosscorrelation of the spontaneous activity of units recorded on different electrodes was the same in the normal and reorganized part. Minimum first-spike latency was significantly increased in trauma cats, largely for units at the dorsal side of the sampled region. Because most other neural response properties are normal in the reorganized part of cortex, sub-cortical topographic mag changes are likely involved in producing the altered cortical topographic maps. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Physiol & Biophys, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. RP Eggermont, JJ (reprint author), Univ Calgary, Dept Physiol & Biophys, 2500 Univ Dr NW, Calgary, AB T2N 1N4, Canada. CR Buonomano DV, 1998, ANNU REV NEUROSCI, V21, P149, DOI 10.1146/annurev.neuro.21.1.149 CALFORD MB, 1995, J NEUROPHYSIOL, V73, P1876 DARIANSMITH C, 1994, NATURE, V368, P737, DOI 10.1038/368737a0 De Ribaupierre F, 1972, Brain Res, V48, P185, DOI 10.1016/0006-8993(72)90178-3 DINSE HR, 1993, NEUROREPORT, V5, P173, DOI 10.1097/00001756-199311180-00020 EGGERMONT JJ, 1994, J NEUROPHYSIOL, V71, P246 EGGERMONT JJ, 1992, J NEUROPHYSIOL, V68, P1216 EGGERMONT JJ, 1996, AUDIT NEUROSCI, V2, P76 Eggermont JJ, 1996, AUDIT NEUROSCI, V2, P309 Flor H, 1998, EXP BRAIN RES, V119, P205, DOI 10.1007/s002210050334 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 Harrison RV, 1998, EXP BRAIN RES, V123, P449, DOI 10.1007/s002210050589 HARRISON RV, 1991, HEARING RES, V54, P11, DOI 10.1016/0378-5955(91)90131-R HARRISON RV, 1993, ACTA OTO-LARYNGOL, V113, P296, DOI 10.3109/00016489309135812 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 IRVINE DRF, 1994, 17 MIDW M ASS RES OT, P82 Kaas JH, 1997, ADV NEUROL, V73, P147 Kaltenbach JA, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P317 Mendelson JR, 1997, J COMP PHYSIOL A, V181, P615, DOI 10.1007/s003590050145 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MOORE DR, 1981, EXP BRAIN RES, V41, P301 Muhlnickel W, 1998, P NATL ACAD SCI USA, V95, P10340, DOI 10.1073/pnas.95.17.10340 Ponton CW, 1996, NEUROREPORT, V8, P61, DOI 10.1097/00001756-199612200-00013 Rajan R, 1998, NAT NEUROSCI, V1, P138, DOI 10.1038/388 Rajan R, 1998, J COMP NEUROL, V399, P35 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P449 VOLKOV IO, 1991, NEUROSCIENCE, V43, P307, DOI 10.1016/0306-4522(91)90295-Y WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 WILLOTT JF, 1988, HEARING RES, V37, P15, DOI 10.1016/0378-5955(88)90074-3 NR 30 TC 92 Z9 95 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 89 EP 101 DI 10.1016/S0378-5955(00)00024-1 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400010 PM 10748332 ER PT J AU Zeng, FG Martino, KM Linthicum, FH Soli, SD AF Zeng, FG Martino, KM Linthicum, FH Soli, SD TI Auditory perception in vestibular neurectomy subjects SO HEARING RESEARCH LA English DT Article DE olivocochlear bundle; auditory efferent system; anti-masking; vestibular neurectomy; signal detection in noise; overshoot; intensity discrimination; forward masking ID CROSSED OLIVOCOCHLEAR BUNDLE; INTENSITY DISCRIMINATION; OTOACOUSTIC EMISSIONS; MASKER LEVEL; ELECTRICAL-STIMULATION; CONTRALATERAL SOUND; THRESHOLD SHIFT; NERVE RESPONSES; HEARING; OVERSHOOT AB The auditory efferent nerve is a feedback pathway that originates in the brainstem and projects to the inner ear. Although the anatomy and physiology of efferents have been rather thoroughly described, their functional roles in auditory perception are still not clear. Here, we report data in six human subjects who had undergone vestibular neurectomy, during which their efferent nerves were: also presumably severed. The surgery had alleviated these subjects' vertigo but also resulted in mild to moderate hearing loss. We designed our experiments with a focus on the possible role of efferents in anti-masking. Consistent with previous studies, we found little effects of vestibular neurectomy on pure-tone detection and discrimination in quiet. However, we noted several new findings in all subjects tested. Efferent section increased loudness sensation (one subject), reduced overshoot effect (five subjects), accentuated 'the midlevel hump' in forward masking (two subjects), and worsened intensity discrimination in noise (four subjects). Poorer speech. in noise recognition was also observed in the surgery ear than the non-surgery ear in three out of four subjects tested, bur this finding was confounded by hearing loss. The present results suggest an active role of efferents in auditory perception in noise. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Maryland, Dept Speech & Hearing Sci, College Pk, MD 20742 USA. Univ Maryland, Program Neurosci & Cognit Sci, College Pk, MD 20742 USA. House Ear Inst, Los Angeles, CA 90057 USA. RP Zeng, FG (reprint author), Univ Maryland, Dept Speech & Hearing Sci, 0100 Lefrak Hall, College Pk, MD 20742 USA. RI Zeng, Fan-Gang/G-4875-2012 CR BACON SP, 1992, J ACOUST SOC AM, V91, P2865, DOI 10.1121/1.402967 BACON SP, 1990, J ACOUST SOC AM, V88, P698, DOI 10.1121/1.399773 BORG E, 1971, EXP NEUROL, V31, P301, DOI 10.1016/0014-4886(71)90234-2 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 CARLYON RP, 1987, J ACOUST SOC AM, V82, P1078, DOI 10.1121/1.395329 CARLYON RP, 1992, J ACOUST SOC AM, V91, P1034, DOI 10.1121/1.402629 CHATTERJEE M, 1996, 19 ARO MIDW RES M, P140 CODY AR, 1982, HEARING RES, V6, P199, DOI 10.1016/0378-5955(82)90054-5 DELACRUZ A, 1984, LARYNGOSCOPE, V94, P874 DEWSON JH, 1968, J NEUROPHYSIOL, V31, P122 DOLAN DF, 1988, J ACOUST SOC AM, V83, P1081, DOI 10.1121/1.396052 Galambos R., 1960, NEURAL MECHANISMS AU, P137 Giraud AL, 1997, NEUROREPORT, V8, P1779 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 Guinan JJ, 1996, J ACOUST SOC AM, V100, P1680, DOI 10.1121/1.416066 Guinan Jr J.J., 1996, COCHLEA, P435 HANDROCK M, 1982, ARCH OTO-RHINO-LARYN, V234, P191, DOI 10.1007/BF00453630 Hienz RD, 1998, HEARING RES, V116, P10, DOI 10.1016/S0378-5955(97)00197-4 HOUSE JW, 1984, OTOLARYNG HEAD NECK, V92, P212 IGARASHI M, 1972, ACTA OTO-LARYNGOL, V73, P455, DOI 10.3109/00016487209138966 IGARASHI M, 1979, ACTA OTO-LARYNGOL, V87, P79, DOI 10.3109/00016487909126390 IGARASHI M, 1979, ACTA OTO-LARYNGOL, V87, P429, DOI 10.3109/00016487909126446 IGARASHI M, 1974, ACTA OTO-LARYNGOL, V77, P311, DOI 10.3109/00016487409124630 JESTEADT W, 1982, J ACOUST SOC AM, V71, P950, DOI 10.1121/1.387576 KAWASE T, 1993, J NEUROPHYSIOL, V70, P2519 KAWASE T, 1993, J NEUROPHYSIOL, V70, P2533 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LIBERMAN MC, 1995, HEARING RES, V90, P158, DOI 10.1016/0378-5955(95)00160-2 LIBERMAN MC, 1980, HEARING RES, V3, P189, DOI 10.1016/0378-5955(80)90046-5 Liberman MC, 1998, J COMMUN DISORD, V31, P471, DOI 10.1016/S0021-9924(98)00019-7 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 LITTMAN TA, 1992, J ACOUST SOC AM, V92, P1945, DOI 10.1121/1.405242 Maison S, 1997, HEARING RES, V113, P89, DOI 10.1016/S0378-5955(97)00136-6 May BJ, 1995, AUDIT NEUROSCI, V1, P385 MCFADDEN D, 1989, J ACOUST SOC AM, V85, P254, DOI 10.1121/1.397732 Micheyl C, 1996, J ACOUST SOC AM, V99, P1604, DOI 10.1121/1.414734 Michie PT, 1996, HEARING RES, V98, P54, DOI 10.1016/0378-5955(96)00059-7 Moulin A, 1998, NEUROREPORT, V9, P3741, DOI 10.1097/00001756-199811160-00031 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NGUYEN CD, 1992, AM J OTOL, V13, P328 NIEDER P, 1970, EXP NEUROL, V28, P179, DOI 10.1016/0014-4886(70)90172-X NILSSON M, 1994, J ACOUST SOC AM, V95, P1085, DOI 10.1121/1.408469 OATMAN LC, 1976, EXP NEUROL, V51, P41, DOI 10.1016/0014-4886(76)90052-2 PLACK CJ, 1995, J ACOUST SOC AM, V97, P1141, DOI 10.1121/1.412227 RAJAN J, 1990, INFORMATION PROCESSI, P81 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 Scharf B, 1997, HEARING RES, V103, P101, DOI 10.1016/S0378-5955(96)00168-2 SCHARF B, 1994, HEARING RES, V75, P11, DOI 10.1016/0378-5955(94)90051-5 Schlauch RS, 1999, J ACOUST SOC AM, V105, P822, DOI 10.1121/1.426271 TRAHIOTI.C, 1970, J ACOUST SOC AM, V47, P592, DOI 10.1121/1.1911934 Turner CW, 1997, MODELING SENSORINEURAL HEARING LOSS, P387 Walsh EJ, 1998, J NEUROSCI, V18, P3859 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WARREN EH, 1989, HEARING RES, V37, P105, DOI 10.1016/0378-5955(89)90033-6 WILLIAMS EA, 1994, ACTA OTO-LARYNGOL, V114, P121, DOI 10.3109/00016489409126029 WINSLOW RL, 1988, HEARING RES, V35, P165, DOI 10.1016/0378-5955(88)90116-5 Wright BA, 1997, J ACOUST SOC AM, V101, P420, DOI 10.1121/1.417987 ZENG FG, 1991, HEARING RES, V55, P223, DOI 10.1016/0378-5955(91)90107-K Zeng FG, 1998, J ACOUST SOC AM, V103, P2021, DOI 10.1121/1.421373 ZENG FG, 1995, HEARING RES, V82, P216, DOI 10.1016/0378-5955(94)00179-T Zheng XY, 1999, J COMP NEUROL, V406, P72 ZWICKER E, 1965, J ACOUST SOC AM, V37, P653, DOI 10.1121/1.1909389 ZWICKER E, 1965, J ACOUST SOC AM, V38, P132, DOI 10.1121/1.1909588 NR 66 TC 28 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 102 EP 112 DI 10.1016/S0378-5955(00)00011-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400011 PM 10748333 ER PT J AU Cotillon, N Nafati, M Edeline, JM AF Cotillon, N Nafati, M Edeline, JM TI Characteristics of reliable tone-evoked oscillations in the rat thalamo-cortical auditory system SO HEARING RESEARCH LA English DT Article DE low-frequency oscillations; stimulus-locked oscillations; auditory cortex; auditory thalamus; thalmic reticular nucleus ID CAT VISUAL-CORTEX; DEPENDENT NEURONAL OSCILLATIONS; HIGH-FREQUENCY OSCILLATIONS; IN-VITRO; SYNCHRONIZED OSCILLATIONS; THALAMOCORTICAL OSCILLATIONS; RECEPTIVE-FIELD; SYNAPTIC ORIGIN; STRIATE CORTEX; TEMPORAL POLE AB Tone-evoked oscillations were studied from simultaneous recordings collected in the auditory cortex, auditory thalamus and auditory sector of the reticular nucleus in urethane anesthetized rats. These oscillations were precisely time-locked to tone onset and were easily observed on peristimulus time histograms (PSTHs). Visual inspection of PSTHs and rasters led us to distinguish between 'reliable' oscillations (which exhibited oscillatory patterns in more than 50% of the trials) and 'labile' oscillations (which exhibited oscillations in less than 50% of the trials). Systematic quantification of oscillations based on several indices derived from power spectra confirmed this distinction. 'Reliable' stimulus-locked oscillations were observed in 51/184 (28%) of the recordings from auditory cortex, 9/55 (17%) of the recordings from auditory thalamus and 11/26 (42%) of the recordings from the auditory sector of the reticular nucleus. The frequency range of these oscillations was the same in the three structures (5-14 Hz). Within the same animal, when one electrode exhibited oscillations, there was a high probability of detecting similar oscillations from electrodes located in the same structure, but not from electrodes located in the other structures. These oscillations were observed for pure tone frequency (or for clicks) whatever the tone duration (1 s, 100 ms, 10 ms). The inter-tone interval (ITI) was found to be the critical factor controlling the occurrence of these oscillations: they were present for ITIs of 2 s or longer, but were absent for ITIs of 1 s or less. In contrast, the occurrence of the oscillations was a funct:ion neither of the strength of the 'on' evoked response nor of the animal's temperature. However, lowering the animal's temperature from 37-38 degrees C to 35-36 degrees C systematically led to a decrease in the frequency and an increase in the duration of the tone-evoked oscillations. These results suggest that, even in well defined conditions (temperature, EEG, ITI, level of anesthesia), the oscillations triggered by presentation of the same stimulus can be stable or unstable. This temporal instability of stimulus-evoked oscillations has to be taken into account before stating percentages of oscillations in a given brain structure. They also suggest that some general factors such as the animals temperature or the inter-stimulus interval can considerably affect their characteristics and/or their occurrence. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Paris 11, CNRS UMR 8620, Lab Neurobiol Apprentissage Memorie & Commun, F-91405 Orsay, France. RP Edeline, JM (reprint author), Univ Paris 11, CNRS UMR 8620, Lab Neurobiol Apprentissage Memorie & Commun, Bat 446, F-91405 Orsay, France. EM jean-marc.edeline@ibaic.u-psud.fr CR AITKIN LM, 1966, J NEUROPHYSIOL, V29, P109 BAL T, 1993, J PHYSIOL-LONDON, V468, P669 Bal T, 1996, NEURON, V17, P297, DOI 10.1016/S0896-6273(00)80161-0 BAL T, 1995, J PHYSIOL-LONDON, V483, P641 BAL T, 1995, J PHYSIOL-LONDON, V483, P665 Barrie JM, 1996, J NEUROPHYSIOL, V76, P520 Bartlett EL, 1999, J NEUROPHYSIOL, V81, P1999 BAUER R, 1995, BRAIN RES, V669, P291, DOI 10.1016/0006-8993(94)01273-K Bekisz Marek, 1993, Acta Neurobiologiae Experimentalis (Warsaw), V53, P175 BORDI F, 1994, EXP BRAIN RES, V98, P261, DOI 10.1007/BF00228414 Brett B, 1997, J NEUROPHYSIOL, V78, P573 Bringuier V, 1997, J PHYSIOL-LONDON, V500, P751 BRINGUIER V, 1992, NEUROREPORT, V3, P1065, DOI 10.1097/00001756-199212000-00008 Brosch M, 1997, CEREB CORTEX, V7, P70, DOI 10.1093/cercor/7.1.70 BROSCH M, 1995, EUR J NEUROSCI, V7, P86, DOI 10.1111/j.1460-9568.1995.tb01023.x CHATILA M, 1992, ELECTROEN CLIN NEURO, V83, P217, DOI 10.1016/0013-4694(92)90147-A CHATILA M, 1993, CR ACAD SCI III-VIE, V316, P51 COTILLON N, 1999, SOC NEUR ABSTR, V25 Dinse HR, 1997, INT J PSYCHOPHYSIOL, V26, P205, DOI 10.1016/S0167-8760(97)00765-4 ECKHORN R, 1993, EXP BRAIN RES, V95, P177 ECKHORN R, 1993, NEUROREPORT, V4, P243, DOI 10.1097/00001756-199303000-00004 ECKHORN R, 1988, BIOL CYBERN, V60, P121, DOI 10.1007/BF00202899 Edeline JM, 1995, EXP BRAIN RES, V107, P221 EGGERMONT JJ, 1992, HEARING RES, V61, P1, DOI 10.1016/0378-5955(92)90029-M EGGERMONT JJ, 1995, J NEUROPHYSIOL, V73, P227 ENGEL AK, 1990, EUR J NEUROSCI, V2, P588, DOI 10.1111/j.1460-9568.1990.tb00449.x ENGEL AK, 1991, P NATL ACAD SCI USA, V88, P6048, DOI 10.1073/pnas.88.14.6048 ENGEL AK, 1991, SCIENCE, V252, P1177, DOI 10.1126/science.252.5009.1177 ENGEL AK, 1991, P NATL ACAD SCI USA, V88, P9136, DOI 10.1073/pnas.88.20.9136 FRANOWICZ MN, 1995, J NEUROPHYSIOL, V74, P96 FREEMAN WJ, 1987, BRAIN RES, V422, P267, DOI 10.1016/0006-8993(87)90933-4 Freeman W.J., 1994, TEMPORAL CODING BRAI Fregnac Y., 1994, TEMPORAL CODING BRAI, P81 FRIEN A, 1994, NEUROREPORT, V5, P2273, DOI 10.1097/00001756-199411000-00017 GALAMBOS R, 1952, J NEUROPHYSIOL, V15, P359 GHOSE GM, 1992, J NEUROPHYSIOL, V68, P1558 GRAY CM, 1989, P NATL ACAD SCI USA, V86, P1698, DOI 10.1073/pnas.86.5.1698 GRAY CM, 1989, NATURE, V338, P334, DOI 10.1038/338334a0 GRAY CM, 1990, EUR J NEUROSCI, V2, P607, DOI 10.1111/j.1460-9568.1990.tb00450.x Gray CM, 1997, J NEUROSCI, V17, P3239 HU B, 1995, J PHYSIOL-LONDON, V483, P167 HU B, 1994, J PHYSIOL-LONDON, V479, P217 Kenmochi M, 1997, NEUROREPORT, V8, P1589, DOI 10.1097/00001756-199705060-00008 KIM U, 1995, J NEUROPHYSIOL, V74, P1301 KONIG P, 1995, P NATL ACAD SCI USA, V92, P290, DOI 10.1073/pnas.92.1.290 KREITER AK, 1992, EUR J NEUROSCI, V4, P369, DOI 10.1111/j.1460-9568.1992.tb00884.x Kruse W, 1996, P NATL ACAD SCI USA, V93, P6112, DOI 10.1073/pnas.93.12.6112 Livingstone MS, 1996, J NEUROPHYSIOL, V75, P2467 MACDONALD KD, 1995, BRAIN RES, V694, P1, DOI 10.1016/0006-8993(95)00662-A Maldonado PE, 1996, EXP BRAIN RES, V112, P420 Manunta Y, 1998, EXP BRAIN RES, V118, P361, DOI 10.1007/s002210050290 Manunta Y, 1997, EUR J NEUROSCI, V9, P833, DOI 10.1111/j.1460-9568.1997.tb01433.x McCormick DA, 1997, ANNU REV NEUROSCI, V20, P185, DOI 10.1146/annurev.neuro.20.1.185 NAKAMURA K, 1991, NEUROSCI RES, V12, P293, DOI 10.1016/0168-0102(91)90119-J NAKAMURA K, 1992, NEUROREPORT, V3, P117, DOI 10.1097/00001756-199201000-00031 ROUGEULBUSER A, 1994, NATO ADV SCI INST SE, V271, P275 RougeulBuser A, 1997, INT J PSYCHOPHYSIOL, V26, P191, DOI 10.1016/S0167-8760(97)00764-2 ROUILLER EM, 1991, HEARING RES, V56, P179, DOI 10.1016/0378-5955(91)90168-9 SALLY SL, 1988, J NEUROPHYSIOL, V59, P1627 SCHONER G, 1992, NEUROREPORT, V3, P579 SHOSAKU A, 1983, EXP BRAIN RES, V49, P432 STERIADE M, 1993, SCIENCE, V262, P679, DOI 10.1126/science.8235588 STERIADE M, 1994, TRENDS NEUROSCI, V17, P199 WROBEL A, 1994, ACTA NEUROBIOL EXP, V54, P95 WROBEL A, 1994, NATO ADV SCI INST SE, V271, P311 NR 65 TC 20 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 113 EP 130 DI 10.1016/S0378-5955(00)00016-2 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400012 PM 10748334 ER PT J AU Torre, P Fowler, CG AF Torre, P Fowler, CG TI Age-related changes in auditory function of rhesus monkeys (Macaca mulatta) SO HEARING RESEARCH LA English DT Article DE aging; auditory brainstem response; distortion product otoacoustic emission; rhesus monkey ID SPONTANEOUS OTOACOUSTIC EMISSIONS; BRAIN-STEM RESPONSE; EVOKED-POTENTIALS; NONHUMAN PRIMATE; HEARING-LOSS; LATENCY; HUMANS; GENDER; SEX AB The purpose of this study was to investigate the changes in auditory function associated with aging in rhesus monkeys (Macaca mulatta) as a model for age-related changes in humans. One advantage of using monkeys from the Wisconsin Regional Primate Research Center was that lifestyle factors such as diet and excessive noise exposure were controlled. Twenty younger (mean: 10 years, 9 months, S.D. = +/-6 months) and 20 older (mean: 25 years, 11 months, S.D. = +/-11 months) monkeys were used in this study. Cochlear function in these monkeys was measured with distortion product otoacoustic emissions (DPOAEs); neural function was measured with auditory brainstem responses (ABRs) and middle latency responses (MLRs). Older monkeys had (1) significantly smaller DPOAEs, (2) significantly smaller ABR peak amplitudes, and (3) significantly longer ABR peak latencies compared to younger monkeys. Overall, these results suggest that older monkeys have decreased cochlear and neural function to the level of the brainstem as compared to younger monkeys. The decrease in DPOAE level and the increase in age accounted for approximately 70% of the increase in peak IV latency. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Wisconsin, Dept Commun Disorders, Madison, WI 53706 USA. RP Torre, P (reprint author), Univ Wisconsin, Dept Commun Disorders, 1975 Willow Dr, Madison, WI 53706 USA. CR ALLEN AR, 1978, ELECTROEN CLIN NEURO, V45, P53, DOI 10.1016/0013-4694(78)90341-3 BENNETT CL, 1983, BEHAV NEUROSCI, V97, P602, DOI 10.1037//0735-7044.97.4.602 BONFILS P, 1988, AUDIOLOGY, V27, P27 CHAMBERS RD, 1991, HEARING RES, V51, P1, DOI 10.1016/0378-5955(91)90002-Q Cruickshanks KJ, 1998, AM J EPIDEMIOL, V148, P879 DOYLE WJ, 1983, ELECTROEN CLIN NEURO, V56, P210, DOI 10.1016/0013-4694(83)90075-5 DURRANT JD, 1990, EAR HEARING, V11, P210, DOI 10.1097/00003446-199006000-00008 HAWKINS JE, 1976, ACTA OTO-LARYNGOL, V81, P337, DOI 10.3109/00016487609119971 HAWKINS JE, 1985, BEHAV PATHOLOGY AGIN, P137 JERGER J, 1988, EAR HEARING, V9, P168, DOI 10.1097/00003446-198808000-00002 JERGER J, 1980, ARCH OTOLARYNGOL, V106, P387 KING FA, 1988, SCIENCE, V240, P1475, DOI 10.1126/science.3287624 Kirk RR, 1995, EXPT DESIGN PROCEDUR LASKY RE, 1995, HEARING RES, V89, P35, DOI 10.1016/0378-5955(95)00120-1 LASKY RE, 1995, HEARING RES, V89, P212, DOI 10.1016/0378-5955(95)00140-7 Lasky RE, 1999, HEARING RES, V136, P35, DOI 10.1016/S0378-5955(99)00100-8 Laughlin NK, 1999, DEV PSYCHOBIOL, V34, P37, DOI 10.1002/(SICI)1098-2302(199901)34:1<37::AID-DEV6>3.0.CO;2-W LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 LONSBURYMARTIN BL, 1988, HEARING RES, V34, P313, DOI 10.1016/0378-5955(88)90011-1 LONSBURYMARTIN BL, 1988, HEARING RES, V33, P69, DOI 10.1016/0378-5955(88)90021-4 MARTIN GK, 1988, HEARING RES, V33, P49, DOI 10.1016/0378-5955(88)90020-2 MARTIN GK, 1985, HEARING RES, V20, P91, DOI 10.1016/0378-5955(85)90062-0 MOLLER AR, 1986, ELECTROEN CLIN NEURO, V65, P361, DOI 10.1016/0168-5597(86)90015-8 PARK JY, 1995, HEARING RES, V86, P147, DOI 10.1016/0378-5955(95)00065-C PFINGST BE, 1978, HEARING RES, V1, P43, DOI 10.1016/0378-5955(78)90008-4 PSATTA DM, 1988, ELECTROEN CLIN NEURO, V71, P27, DOI 10.1016/0168-5597(88)90016-0 SAAD MM, 1982, ACTA ANAT, V112, P117 STEBBINS WC, 1966, SCIENCE, V153, P1646, DOI 10.1126/science.153.3744.1646-a STOVER L, 1993, J ACOUST SOC AM, V94, P2670, DOI 10.1121/1.407351 Strouse A L, 1996, J Am Acad Audiol, V7, P339 TIGGES J, 1988, AM J PRIMATOL, V15, P263, DOI 10.1002/ajp.1350150308 Watson DR, 1996, AUDIOLOGY, V35, P246 WOODS DL, 1986, ELECTROEN CLIN NEURO, V65, P297, DOI 10.1016/0168-5597(86)90008-0 NR 33 TC 26 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 131 EP 140 DI 10.1016/S0378-5955(00)00025-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400013 PM 10748335 ER PT J AU de Sauvage, RC Erre, JP Aran, JM AF de Sauvage, RC Erre, JP Aran, JM TI Discharge rate of the auditory nerve during noise revealed by electrocochlear stimulation SO HEARING RESEARCH LA English DT Article DE auditory nerve; noise stimulation; electrical stimulation; rate-intensity function ID RATE-INTENSITY FUNCTIONS; SINGLE-FIBER RESPONSES; GUINEA-PIG COCHLEA; ELECTRICAL-STIMULATION; SPIRAL GANGLION; DYNAMIC-RANGE; ROUND WINDOW; PHYSIOLOGICAL-PROPERTIES; ACTION-POTENTIALS; UNIT RESPONSE AB The purpose of this study was to evaluate the average discharge rate of all fibres in the whole auditory nerve (Ii,) when a broadband noise with steady-state effects is applied to the ear. We assessed the R-wn parameter by detecting the state of refractoriness of the nerve during noise stimulation using an electric stimulus (ES) as a probe. The technique, applied in awake pre-implanted guinea pigs (Charlet de Sauvage et al., 1994), made it possible to obtain electro-acoustic responses (EARs), from which an estimate of the R-wn parameter could be deduced. Negative current pulses of 100 mu s duration, each followed by an identical pulse of positive polarity for charge balance, were applied between round window and indifferent vertex electrodes at intervals of 160 ms. The 120 ms wide-band noise masker started 92 ms before every other negative ES. The signal on the stimulating electrodes was averaged over a 5.12 ms window in synchrony with the negative pulse. EARs were obtained by alternately subtracting recordings during noise from those during silence. The R-wn parameter was determined by comparing experimental and computed EAR patterns. For this purpose, a model of unit response incorporating changes in amplitude and conduction velocity during the relative refractory period was designed. The recovery function of the firing probability in response to ES was evaluated. Fibres were classified in different categories according to their background discharge rates. The probability of response of single fibres to ES in each category was calculated on the basis of their interval histograms during silence and noise. Individual spikes were combined accordingly to obtain the computed EAR waveform. R-wn was determined by adjusting the EAR amplitude of the model in relation to that of the experimental EAR. R-wn generally increases in a linear fashion with respect to noise intensity expressed in dB, thus following the increase in loudness perception estimated by Weber's law. At the highest noise levels, R-wn tends to saturate. The estimated saturation rate was found to be about 380 spikes/s. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Bordeaux 2, Hop Pellegrin, Lab Audiol, EMI INSERM 99 27, F-33076 Bordeaux, France. RP de Sauvage, RC (reprint author), Univ Bordeaux 2, Hop Pellegrin, Lab Audiol, EMI INSERM 99 27, Bat PQR,Entree 3, F-33076 Bordeaux, France. CR ARAN JM, 1979, TECHNICAL BASIS AUDI, P233 Aran J M, 1974, Rev Laryngol Otol Rhinol (Bord), V95, P31 AVAN P, 1992, HEARING RES, V59, P59, DOI 10.1016/0378-5955(92)90102-S BONFILS P, 1988, THESIS MONTPELLIER BROWN MC, 1994, J NEUROPHYSIOL, V71, P1835 BROWN MC, 1983, HEARING RES, V10, P345, DOI 10.1016/0378-5955(83)90097-7 Buus S, 1997, J ACOUST SOC AM, V101, P669, DOI 10.1121/1.417959 CAZALS Y, 1980, HEARING RES, V2, P95, DOI 10.1016/0378-5955(80)90031-3 deSauvage RC, 1997, HEARING RES, V110, P119 Chatterjee M, 1998, HEARING RES, V124, P170, DOI 10.1016/S0378-5955(98)00135-X COOPER NP, 1989, THESIS U KEELE daCosta DL, 1997, EXP BRAIN RES, V116, P259, DOI 10.1007/PL00005754 DESAUVAGE RC, 1985, HEARING RES, V18, P121, DOI 10.1016/0378-5955(85)90003-6 DESAUVAGE RC, 1988, INNOV TECH BIOL MED, V9, P357 DESAUVAGE RC, 1983, J ACOUST SOC AM, V73, P616 DESAUVAGE RC, 1994, ELECTROEN CLIN NEURO, V92, P462 deSauvage RC, 1996, HEARING RES, V102, P15, DOI 10.1016/S0378-5955(96)00137-2 DOLAN DF, 1990, J ACOUST SOC AM, V87, P2621, DOI 10.1121/1.399054 DOUCET JR, 1995, AUDIT NEUROSCI, V1, P151 EGGERMON.JJ, 1973, AUDIOLOGY, V12, P193 EVANS EF, 1981, NEURONAL MECHANISMS, P69 EVANS EF, 1975, HDB SENSORY PHYSL, V2 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FECHNER GT, 1884, ELEMENTE PSYCHOPHYSI FRIJNS JHM, 1994, MED BIOL ENG COMPUT, V32, P391, DOI 10.1007/BF02524690 GACEK RR, 1961, ANAT REC, V139, P455, DOI 10.1002/ar.1091390402 GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 GILBERT AG, 1980, HEARING RES, V2, P327, DOI 10.1016/0378-5955(80)90066-0 GRAY PR, 1967, BIOPHYS J, V7, P759, DOI 10.1016/S0006-3495(67)86621-9 GRAY PR, 1966, 451 MIT RES LAB EL HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 Hursh JB, 1939, AM J PHYSIOL, V127, P131 JANSSEN R, 1992, NEUROSCI BIOBEHAV R, V16, P399, DOI 10.1016/S0149-7634(05)80209-X Kiang NYS, 1965, RES MONOGRAPH, V35 LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LUSTED HS, 1988, J ACOUST SOC AM, V83, P657, DOI 10.1121/1.396160 LUTTGAU HC, 1956, EXPERIENTIA, V12, P482, DOI 10.1007/BF02162535 MANLEY GA, 1976, J PHYSIOL-LONDON, V258, P323 MATSUOKA AJ, 1999, ARO MIDW M ST PET BE, V22, P7 MILLER MI, 1985, J ACOUST SOC AM, V77, P1452, DOI 10.1121/1.392040 MORRISON D, 1975, ACTA OTO-LARYNGOL, V79, P11, DOI 10.3109/00016487509124649 MULHERAN M, 1987, BRIT J AUDIOL, V21, P309 Nizami L, 1997, MATH BIOSCI, V141, P1, DOI 10.1016/S0025-5564(96)00153-8 Nuttall AL, 1995, HEARING RES, V92, P170, DOI 10.1016/0378-5955(95)00216-2 PAINTAL AS, 1965, J PHYSIOL-LONDON, V180, P20 PAINTAL AS, 1966, J PHYSIOL-LONDON, V184, P791 PALMER AR, 1980, HEARING RES, V2, P319, DOI 10.1016/0378-5955(80)90065-9 PEAKE WT, 1962, BIOPHYS J, V2, P23 PRIJS VF, 1980, ACUSTICA, V45, P1 PRIJS VF, 1993, HEARING RES, V71, P190, DOI 10.1016/0378-5955(93)90034-X PRIJS VF, 1986, HEARING RES, V21, P127, DOI 10.1016/0378-5955(86)90034-1 ROBERTSON D, 1985, HEARING RES, V20, P93 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X RYAN AF, 1989, BRAIN RES, V483, P283, DOI 10.1016/0006-8993(89)90172-8 SACHS MB, 1969, J ACOUST SOC AM, V45, P1025, DOI 10.1121/1.1911493 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 Schoonhoven R, 1997, HEARING RES, V113, P247, DOI 10.1016/S0378-5955(97)00149-4 SCHOONHOVEN R, 1994, J ACOUST SOC AM, V95, P2104, DOI 10.1121/1.408672 SCHROEDE.MR, 1974, J ACOUST SOC AM, V55, P1055, DOI 10.1121/1.1914647 SHEPHERD RK, 1997, HEARING RES, V108, P108 STEGEMAN DF, 1983, ELECTROEN CLIN NEURO, V55, P668, DOI 10.1016/0013-4694(83)90277-8 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 TASAKI I, 1953, NERVOUS TRANSMISSION, P80 TEAS DC, 1962, J ACOUST SOC AM, V24, P1431 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VERSNEL H, 1990, HEARING RES, V46, P147, DOI 10.1016/0378-5955(90)90145-F VIEMEISTER NF, 1988, HEARING RES, V34, P267, DOI 10.1016/0378-5955(88)90007-X VIEMEISTER NF, 1988, J ACOUST SOC AM, V84, P172, DOI 10.1121/1.396961 WAXMAN SG, 1979, ELECTROEN CLIN NEURO, V47, P717, DOI 10.1016/0013-4694(79)90299-2 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E WINTER IM, 1991, J ACOUST SOC AM, V90, P1958, DOI 10.1121/1.401675 YATES GK, 1991, HEARING RES, V57, P57, DOI 10.1016/0378-5955(91)90074-J NR 73 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 141 EP 158 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400014 ER PT J AU Hemmert, W Zenner, HP Gummer, AW AF Hemmert, W Zenner, HP Gummer, AW TI Characteristics of the travelling wave in the low-frequency region of a temporal-bone preparation of the guinea-pig cochlea SO HEARING RESEARCH LA English DT Article DE laser interferometry; cochlear mechanics; basilar membrane; travelling wave ID AUDITORY-NERVE FIBERS; OUTER HAIR-CELLS; BASILAR-MEMBRANE MECHANICS; MOSSBAUER TECHNIQUE; TECTORIAL MEMBRANE; CHINCHILLA COCHLEA; RESPONSE CHARACTERISTICS; NONLINEAR MECHANICS; RECEPTOR POTENTIALS; INFERIOR COLLICULUS AB This study provides a detailed quantitative description of the acoustically evoked vibration responses in the low-frequency region of the in vitro guinea-pig cochlea. Responses of the basilar membrane, the reticular lamina and Hensen cells were measured with a laser Doppler vibrometer, without the need for introducing artificial light reflectors. The apex of the cochlea was opened, leaving the helicotrema intact. Two response components were detected: a 'fast' component, which was probably caused by the hole in the cochlea, and a 'slow' component, which shared the features of a classical travelling wave. The velocity response of the "slow" component exhibited a relatively flat low-frequency slope (15 dB/oct) and a much steeper high-frequency roll-off (third turn: -47 dB/oct; fourth turn: -35 dB/oct). The group delay was dependent on the characteristic frequency. In the fourth turn, the sharpness of the velocity tuning curves (Q(10) (dB): 1.0) was similar to those of in vivo mechanical and neural recordings, whereas in the third turn the tuning (Q(10 dB): 1.1) was much less than for in vivo recordings. The results indicate that cochlear amplification, which is responsible for the high sensitivity and sharp tuning in the basal part of the cochlea, is much less pronounced in the apical turn of the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Tubingen, Dept Otolaryngol, Sect Physiol Acoust & Commun, D-72076 Tubingen, Germany. RP Gummer, AW (reprint author), Univ Tubingen, Dept Otolaryngol, Sect Physiol Acoust & Commun, Silcherstr 5, D-72076 Tubingen, Germany. EM anthony.gummer@uni-tuebingen.de CR BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 BRUNDIN L, 1991, NEUROSCI LETT, V128, P77, DOI 10.1016/0304-3940(91)90763-J Cooper NP, 1998, J PHYSIOL-LONDON, V509, P277, DOI 10.1111/j.1469-7793.1998.277bo.x Cooper NP, 1996, AUDIT NEUROSCI, V3, P123 COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X COOPER NP, 1996, DIVERSITY COCHLEAR M, P298 COOPER NP, 1993, BIOPHYSICS HAIR CELL, P229 COOPER NP, 1992, HEARING RES, V63, P163, DOI 10.1016/0378-5955(92)90083-Y Cooper NP, 1996, AUDIT NEUROSCI, V2, P289 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1971, J ACOUST SOC AM, V49, P1140, DOI 10.1121/1.1912475 DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 DALLOS P, 1970, J ACOUST SOC AM, V48, P489, DOI 10.1121/1.1912163 DEBOER E, 1990, LECT NOTES BIOMATH, V87, P333 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 Goode RL, 1996, AM J OTOL, V17, P813 GUMMER AW, 1993, BIOPHYSICS HAIR CELL, P229 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 Gummer AW, 1996, P NATL ACAD SCI USA, V93, P8727, DOI 10.1073/pnas.93.16.8727 Hao LF, 1996, HEARING RES, V99, P176, DOI 10.1016/S0378-5955(96)00099-8 HEMMERT W, 1994, FORTSCHRITTE AKUSTIK, P1045 HEMMERT W, 1995, FORTSCHRITTE AKUSTIK, P207 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 *ITER, 1989, ACTA OTOLARYNGOL S, V467, P5 JOHNSTON.BM, 1967, SCIENCE, V158, P389, DOI 10.1126/science.158.3799.389 JOHNSTON.BM, 1974, J ACOUST SOC AM, V55, P584, DOI 10.1121/1.1914568 Jorge JR, 1997, HNO, V45, P997 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KOHLLOFF.LU, 1972, ACUSTICA, V27, P66 KOSSL M, 1992, J NEUROSCI, V12, P1575 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 Maier H, 1997, J NEUROSCI METH, V77, P31, DOI 10.1016/S0165-0270(97)00105-2 Meyer J, 1998, J NEUROSCI, V18, P6748 MORIOKA I, 1995, HEARING RES, V83, P142, DOI 10.1016/0378-5955(95)00002-L Murugasu E, 1996, J NEUROSCI, V16, P325 Narayan SS, 1998, SCIENCE, V282, P1882, DOI 10.1126/science.282.5395.1882 Nuttall AL, 1996, J ACOUST SOC AM, V99, P1556, DOI 10.1121/1.414732 NUTTALL AL, 1991, HEARING RES, V51, P203, DOI 10.1016/0378-5955(91)90037-A Preyer S, 1996, Audiol Neurootol, V1, P3 RHODE WS, 1996, DIVERSITY AUDITORY M, P318 Rhode WS, 1996, AUDIT NEUROSCI, V3, P101 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1967, J ACOUST SOC AM, V42, P185, DOI 10.1121/1.1910547 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 ROSE JE, 1971, J NEUROPHYSIOL, V34, P685 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RUGGERO MA, 1991, HEARING RES, V51, P215, DOI 10.1016/0378-5955(91)90038-B Russell IJ, 1997, P NATL ACAD SCI USA, V94, P2660, DOI 10.1073/pnas.94.6.2660 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SELLICK PM, 1980, HEARING RES, V2, P439, DOI 10.1016/0378-5955(80)90080-5 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SHAH DM, 1995, HEARING RES, V87, P187, DOI 10.1016/0378-5955(95)00089-M Tsuji J, 1997, J COMP NEUROL, V381, P188 ULFENDAHL M, 1991, HEARING RES, V57, P31, DOI 10.1016/0378-5955(91)90071-G ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 Ulfendahl M, 1996, J NEUROPHYSIOL, V76, P3850 VONBEKESY G, 1960, EXPT HERING von Bekesy G, 1928, PHYS Z, V29, P793 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 YOUNG ED, 1979, J ACOUST SOC AM, V66, P1381, DOI 10.1121/1.383532 Zinn C, 2000, HEARING RES, V142, P159, DOI 10.1016/S0378-5955(00)00012-5 Zwicker E., 1990, PSYCHOACOUSTICS ZWISLOCKI J, 1948, ACTA OTOLARYNGOL S, V72 ZWISLOCK.JJ, 1974, J ACOUST SOC AM, V55, P578, DOI 10.1121/1.1914567 NR 71 TC 15 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 184 EP 202 DI 10.1016/S0378-5955(00)00017-4 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400016 PM 10748338 ER PT J AU Hsu, CJ Shau, WY Chen, YS Liu, T Lin-Shiau, SY AF Hsu, CJ Shau, WY Chen, YS Liu, T Lin-Shiau, SY TI Activities of Na+,K+-ATPase and Ca2+-ATPase in cochlear lateral wall after acoustic trauma SO HEARING RESEARCH LA English DT Article DE Na+,K+-ATPase; Ca2+-ATPase; microcolorimetric assay; noise-induced hearing loss ID SERIAL-SECTION RECONSTRUCTION; QUIET-AGED GERBILS; GUINEA-PIG COCHLEA; INNER-EAR; STRIA VASCULARIS; ATPASE ACTIVITY; ULTRASTRUCTURAL-CHANGES; NA,K-ATPASE ACTIVITY; STEREOCILIA DAMAGE; HYPERTENSIVE RATS AB Na+,K+-ATPase and Ca2+-ATPase are well known participants in the active transport of ions in the inner ear. These two enzymes play an important role in maintaining cochlear function. Although changes in these enzymes' activities in the cochlea have been implicated in noise-induced hearing loss, no evidence of quantitative alteration of Na+,K+-ATPase or Ca2+-ATPase activities has ever been shown. The present study was undertaken to determine the quantitative alterations of their activities by microcolorimetric assay in the cochlear lateral wall after acoustic trauma. Adult albino guinea pigs were exposed to white noise at 105 +/- 2 dB A for 10 min or 40 h. The age-matched control animals were not exposed to noise. Noise exposure resulted in a significant threshold shift of the auditory brainstem response (P < 0.001). Significant decreases in activities of Na+,K+-ATPase and Ca2+-ATPase were found in the cochlear lateral wall after noise exposure (P < 0.001). Statistical analysis indicated that a good correlation held not only between the decline of these enzyme activities and noise-induced hearing loss, but also between the gradual partial recovery of these parameters during the first 10-day recovery period. The present findings suggest that metabolic damage and ionic disturbance may contribute, at least partially, to noise-induced hearing threshold shift. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Natl Taiwan Univ, Coll Med, Dept Otolaryngol, Taipei, Taiwan. Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol, Taipei 10764, Taiwan. Natl Taiwan Univ, Coll Med, Inst Pharmacol, Taipei 10764, Taiwan. RP Hsu, CJ (reprint author), Natl Taiwan Univ, Coll Med, Dept Otolaryngol, 7 Chung Shan S Rd, Taipei, Taiwan. CR Agrup C, 1999, ACTA OTO-LARYNGOL, V119, P437 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 CHEN CC, 1988, BIOCHEM PHARMACOL, V37, P1661, DOI 10.1016/0006-2952(88)90424-8 CHEN CC, 1986, EUR J PHARMACOL, V122, P311, DOI 10.1016/0014-2999(86)90411-5 CHEN L, 1991, CHIN J OTORHINOLARYN, V26, P70 Curtis LM, 1997, ACTA OTO-LARYNGOL, V117, P553, DOI 10.3109/00016489709113436 DUVALL AJ, 1987, ARCH OTOLARYNGOL, V113, P1066 Erlandsson B, 1980, Acta Otolaryngol Suppl, V367, P1 GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 Gratton MA, 1997, HEARING RES, V108, P9, DOI 10.1016/S0378-5955(97)00034-8 GRATTON MA, 1995, HEARING RES, V83, P43, DOI 10.1016/0378-5955(94)00188-V GUO YC, 1994, J LARYNGOL OTOL, V108, P310 HENDERSON D, 1994, HEARING RES, V76, P101, DOI 10.1016/0378-5955(94)90092-2 Hsu CJ, 1998, ORL J OTO-RHINO-LARY, V60, P314, DOI 10.1159/000027616 Hsu C J, 1992, J Formos Med Assoc, V91, P258 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 IKEDA K, 1988, HEARING RES, V32, P103, DOI 10.1016/0378-5955(88)90081-0 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KONISHI T, 1983, HEARING RES, V11, P219, DOI 10.1016/0378-5955(83)90080-1 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 LANZETTA PA, 1979, ANAL BIOCHEM, V100, P95, DOI 10.1016/0003-2697(79)90115-5 Li WD, 1997, CHINESE MED J-PEKING, V110, P883 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 MELICHAR I, 1980, Hearing Research, V2, P55, DOI 10.1016/0378-5955(80)90016-7 Nario K, 1998, ACTA OTO-LARYNGOL, V118, P198 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SALT AN, 1979, HEARING RES, V1, P343, DOI 10.1016/0378-5955(79)90005-4 Schuknecht HF, 1993, PATHOLOGY EAR, P289 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SLEPECKY N, 1981, ARCH OTO-RHINO-LARYN, V230, P273, DOI 10.1007/BF00456329 SMITH PK, 1985, ANAL BIOCHEM, V150, P76, DOI 10.1016/0003-2697(85)90442-7 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 VANBENTHEM PPG, 1994, HEARING RES, V77, P9, DOI 10.1016/0378-5955(94)90249-6 VASSOUT P, 1984, ACTA OTO-LARYNGOL, V98, P199, DOI 10.3109/00016488409107555 WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 WARD WD, 1981, ANN OTO RHINOL LARYN, V90, P584 YOSHIHARA T, 1987, ARCH OTO-RHINO-LARYN, V243, P395, DOI 10.1007/BF00464650 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 Zhai SQ, 1998, ACTA OTO-LARYNGOL, V118, P813, DOI 10.1080/00016489850182495 NR 46 TC 23 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 2000 VL 142 IS 1-2 BP 203 EP 211 DI 10.1016/S0378-5955(00)00020-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 302FQ UT WOS:000086355400017 PM 10748339 ER PT J AU Rask-Andersen, H Tylstedt, S Kinnefors, A Illing, RB AF Rask-Andersen, H Tylstedt, S Kinnefors, A Illing, RB TI Synapses on human spiral ganglion cells: a transmission electron microscopy and immunohistochemical study SO HEARING RESEARCH LA English DT Article DE spiral ganglion; inner ear; electron microscopy; synaptophysin; human ID COCHLEA; INHIBITION AB A transmission electron microscopy (TEM) study and synaptophysin immunoreactivity analysis of neurons in the human spiral ganglion was performed with particular emphasis on the demonstration of synapses. The study was based on surgical biopsy material obtained during transcochlear meningioma surgery. Vesiculated nerve endings of unmyelinated nerve fibers occurred frequently on the small ganglion cells at all levels. The nerve terminals exhibited abundant clear synaptic vesicles but also dense-core vesicles. Multisynaptic contact sites were also seen with fibers of the intraganglionic spiral bundle (IGSB). Complex associations of synapses could be demonstrated, including several synaptic terminals in conjunction with contact sites or an adherent type of junctions on large ganglion cells. These contact sites exhibited membrane densities which were symmetric or asymmetric, changed their polarity recurrently over their extension from one cell to the other and back and lacked clear synaptic vesicles. This suggests the existence of connections between efferents, belonging to the olivocochlear bundle, and both small and large ganglion cells. Thus, both the inner and outer hair cell system may be under the influence of efferent innervation in the human spiral ganglion. The morphology and course of synaptophysin-positive nerve fibers indicated that synaptic contacts within the spiral ganglion, as observed under the electron microscope, may be abundant. These results indicate that complex neural processing may occur at the level of the spiral ganglion in man. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Uppsala Hosp, Akad Sjukhuset, Dept Otolaryngol, S-75185 Uppsala, Sweden. Univ Freiburg, Dept Otorhinolaryngol, Neurobiol Res Lab, D-79106 Freiburg, Germany. RP Rask-Andersen, H (reprint author), Univ Uppsala Hosp, Akad Sjukhuset, Dept Otolaryngol, S-75185 Uppsala, Sweden. CR Arnold W, 1987, Acta Otolaryngol Suppl, V436, P76 ARNOLD WJ, 1982, AM J OTOL, V3, P266 BERGLUND AM, 1994, HEARING RES, V75, P121, DOI 10.1016/0378-5955(94)90063-9 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 Cajal R. Y., 1909, HISTOLOGIE SYSTEME N KIANG NYS, 1984, COMP PHYSL SENSORY S KIMURA R S, 1979, Annals of Otology Rhinology and Laryngology, V88, P1 Kimura R S, 1987, Acta Otolaryngol Suppl, V438, P1 Kral A, 1996, GEN PHYSIOL BIOPHYS, V15, P109 LEAKEJONES PA, 1982, HEARING RES, V8, P199, DOI 10.1016/0378-5955(82)90075-2 Lorente de No R., 1937, LARYNGOSCOPE, V47, P373 MAW AR, 1974, ANN OTO RHINOL LARYN, V83, P180 NADOL JB, 1993, ACTA OTO-LARYNGOL, V113, P312, DOI 10.3109/00016489309135815 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 Rask-Andersen Helge, 1997, Auris Nasus Larynx, V24, P1, DOI 10.1016/S0385-8146(96)00039-9 RETZIUS G, 1895, BIOL UNTERSUCHUNGEN, V6 RHODE WS, 1994, J NEUROPHYSIOL, V71, P493 ROSS MD, 1973, ACTA OTO-LARYNGOL, V76, P381, DOI 10.3109/00016487309121526 Ross M D, 1973, Adv Otorhinolaryngol, V20, P316 RUGGERO MA, 1982, HEARING RES, V8, P339, DOI 10.1016/0378-5955(82)90023-5 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 SPOENDLIN H, 1979, J LARYNGOL OTOL, V93, P853, DOI 10.1017/S002221510008782X Tylstedt S, 1997, ACTA OTO-LARYNGOL, V117, P505, DOI 10.3109/00016489709113429 WEVER EG, 1909, THEORY HEARING NR 25 TC 21 Z9 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 1 EP 11 DI 10.1016/S0378-5955(99)00179-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800001 PM 10713490 ER PT J AU White, JA Burgess, BJ Hall, RD Nadol, JB AF White, JA Burgess, BJ Hall, RD Nadol, JB TI Pattern of degeneration of the spiral ganglion cell and its processes in the C57BL/6J mouse SO HEARING RESEARCH LA English DT Article DE neural degeneration; spiral ganglion; C57BL/6J mouse; deafness ID HEARING-LOSS; COCHLEAR IMPLANTATION; QUANTITATIVE-EVALUATION; NEURAL DEGENERATION; F1-HYBRID STRAINS; AUDITORY-NERVE; NEURONS; MICE; GENETICS; FIBERS AB Although degeneration of spiral ganglion cells has been described as a histopathologic correlate of hearing loss both in animals and humans, the pattern and sequence of this degeneration remain controversial. Degeneration of hair cells and of spiral ganglion cells and their dendritic processes was evaluated in the C57BL/6J mouse, in which there is a genetically determined progressive sensorineural loss starling in the high frequencies that is similar to the pattern commonly seen in the human. Auditory function was evaluated by brainstem evoked responses, and degeneration of hair cells, ganglion cells and their dendrites was evaluated histologically at 3, 8, 12 and 18 months of age. Progressive loss of auditory sensitivity was correlated with the loss of outer and inner hair cells and spiral ganglion cells and their dendritic processes. In addition, dendritic counts were consistently lower at a distal location in the osseous spiral lamina (i.e. near the organ of Corti) than at a proximal location (i.e, near the spiral ganglion), and the difference between the number of distal dendrites and the number of proximal dendrites tended to be greater with advancing age. These observations suggest an age-related progressive retrograde degeneration of spiral ganglion cells. Thus, in degenerating cochleas, some remaining spiral ganglion cells may have no distal dendritic processes near the organ of Corti. This may have implications for successful stimulation of the cochlear neuron in cochlear implantation. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Lahey Clin Med Ctr, Dept Otolaryngol Head & Neck Surg, Burlington, MA 01805 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA. RP White, JA (reprint author), Lahey Clin Med Ctr, Dept Otolaryngol Head & Neck Surg, 41 Mall Rd, Burlington, MA 01805 USA. CR BICHLER E, 1983, ARCH OTO-RHINO-LARYN, V237, P201, DOI 10.1007/BF00453725 BREDBERG G, 1968, ACTA OTOLARYNGOL S S, V236, P6 CAVANAGH JB, 1964, INT REV EXP PATHOL, V3, P219 CLOPTON BM, 1980, ANN OTO RHINOL LARYN, V89, P5 COHEN GM, 1990, J ELECTRON MICR TECH, V15, P165, DOI 10.1002/jemt.1060150208 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X Felder E, 1997, HEARING RES, V105, P183, DOI 10.1016/S0378-5955(96)00209-2 Felder E, 1995, HEARING RES, V91, P19, DOI 10.1016/0378-5955(95)00158-1 Felix H, 1990, Acta Otolaryngol Suppl, V470, P71 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1980, AUDIOLOGY, V19, P369 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 Kellerhals B., 1967, ACTA OTO-LARYNGOL, V226, P1 Kerr A, 1968, Acta Otolaryngol, V65, P586, DOI 10.3109/00016486809121002 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LINDSAY JR, 1978, ANN OTO RHINOL LARYN, V87, P10 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 NADOL JB, 1990, HEARING RES, V49, P141, DOI 10.1016/0378-5955(90)90101-T NADOL JB, 1988, ORL J OTO-RHINO-LARY, V50, P363 NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 Nadol JB, 1997, OTOLARYNG HEAD NECK, V117, P220, DOI 10.1016/S0194-5998(97)70178-5 NADOL JB, 1990, AM J OTOLARYNG, V11, P112, DOI 10.1016/0196-0709(90)90007-I OTTE J, 1978, LARYNGOSCOPE, V88, P1231 Shnerson A., 1982, DEV BRAIN RES, V2, P65 Spoendlin H, 1990, Acta Otolaryngol Suppl, V470, P61 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 SPOENDLIN H, 1979, J LARYNGOL OTOL, V93, P853, DOI 10.1017/S002221510008782X Spoendlin H, 1984, Ann Otol Rhinol Laryngol Suppl, V112, P76 Suzuka Y, 1988, Acta Otolaryngol Suppl, V450, P1 Willott J. F., 1991, AGING AUDITORY SYSTE YLIKOSKI J, 1978, ARCH OTOLARYNGOL, V104, P202 YLIKOSKI J, 1981, ACTA OTO-LARYNGOL, V91, P161, DOI 10.3109/00016488109138495 ZIMMERMANN CE, 1995, HEARING RES, V90, P192, DOI 10.1016/0378-5955(95)00165-1 NR 38 TC 47 Z9 50 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 12 EP 18 DI 10.1016/S0378-5955(99)00204-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800002 PM 10713491 ER PT J AU Zine, A Nyffeler, M de Ribaupierre, F AF Zine, A Nyffeler, M de Ribaupierre, F TI Spatial expression patterns of epidermal growth factor receptor gene transcripts in the postnatal mammalian cochlea SO HEARING RESEARCH LA English DT Article DE reverse transcriptase-polymerase chain reaction; organ of Corti; epidermal growth factor receptor; in situ hybridization; rat ID IN-SITU HYBRIDIZATION; AUDITORY HAIR-CELLS; FACTOR-ALPHA; RAT-BRAIN; SENSORY EPITHELIA; MESSENGER-RNA; PROLIFERATION; FIBROBLAST; NEURONS; PROBES AB Recent in vitro studies demonstrated that members of the epidermal growth factor (EGF) family are involved in hair cell replacement in the postnatal mammalian organ of Corti (OC) after ototoxic damage. This suggests a role for the EGF receptor (EGFR) in this process. We examined the expression of EGFR mRNA within the normal postnatal day 3 (P3) and adult rat cochlear epithelium by RT-PCR and examined its cellular localization with non-radioactive in situ hybridization in P3 and adult cochleae. RT-PCR demonstrated that EGFR mRNA is expressed in P3 and adult cochlear epithelium. In situ hybridization localized high levels of EGFR transcripts in the OC, spiral ganglion, Kolliker's organ and detectable levels in the supporting cells and the stria vascularis of P3 cochlea. In the adult cochlea, EGFR transcripts were detected only in the spiral ganglion. Our results support that the EGFR is implicated in the differentiation of several cochlear cell types and in the response of OC to ototoxic damage of the P3 rat. In the adult, it may participate in the maintenance of the mature neurons and its absence in the OC may contribute to the lack of regenerative responses in the adult cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Lausanne, Inst Physiol, CH-1005 Lausanne, Switzerland. RP de Ribaupierre, F (reprint author), Univ Lausanne, Inst Physiol, 7 Rue Bugnon, CH-1005 Lausanne, Switzerland. CR COX KH, 1984, DEV BIOL, V101, P485, DOI 10.1016/0012-1606(84)90162-3 DERYNCK R, 1988, CELL, V54, P593, DOI 10.1016/S0092-8674(88)80001-1 EARP HS, 1995, BREAST CANCER RES TR, V35, P115, DOI 10.1007/BF00694752 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 JAMES R, 1984, ANNU REV BIOCHEM, V53, P259 Kornblum HI, 1997, J COMP NEUROL, V380, P243, DOI 10.1002/(SICI)1096-9861(19970407)380:2<243::AID-CNE7>3.0.CO;2-3 Kuntz AL, 1998, J COMP NEUROL, V399, P413 LAMBERT PR, 1994, LARYNGOSCOPE, V104, P701 LEE DC, 1995, PHARMACOL REV, V47, P51 LEFEBVRE PP, 1991, NEUROREPORT, V2, P305, DOI 10.1097/00001756-199106000-00001 Low W, 1996, J CELL PHYSIOL, V167, P443, DOI 10.1002/(SICI)1097-4652(199606)167:3<443::AID-JCP8>3.0.CO;2-P Malgrange B, 1998, NEUROCHEM RES, V23, P1133, DOI 10.1023/A:1020724506337 MORRISON RS, 1987, SCIENCE, V238, P72, DOI 10.1126/science.3498986 PALATASALAMAN CR, 1991, PEPTIDES, V12, P653 PETCH LA, 1990, MOL CELL BIOL, V10, P2973 PIRVOLA U, 1995, P NATL ACAD SCI USA, V92, P9269, DOI 10.1073/pnas.92.20.9269 Saffer LD, 1996, HEARING RES, V94, P14, DOI 10.1016/0378-5955(95)00228-6 SCHAERENWIEMERS N, 1993, HISTOCHEMISTRY, V100, P431, DOI 10.1007/BF00267823 SEROOGY KB, 1995, BRAIN RES, V670, P157, DOI 10.1016/0006-8993(94)01300-7 SIBON OCM, 1994, HISTOCHEMISTRY, V101, P223, DOI 10.1007/BF00269548 STAECKER H, 1995, SCIENCE, V267, P709, DOI 10.1126/science.267.5198.709 WANG SL, 1989, ENDOCRINOLOGY, V124, P240 WEICKERT CS, 1995, DEV BRAIN RES, V86, P203, DOI 10.1016/0165-3806(95)00026-A Weiss FU, 1997, CURR OPIN GENET DEV, V7, P80, DOI 10.1016/S0959-437X(97)80113-X YAMASHITA H, 1995, P NATL ACAD SCI USA, V92, P3152, DOI 10.1073/pnas.92.8.3152 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 Zheng JL, 1997, J NEUROSCI, V17, P216 Zine A, 1998, NEUROREPORT, V9, P263, DOI 10.1097/00001756-199801260-00016 Zine A, 1999, J NEUROBIOL, V38, P313, DOI 10.1002/(SICI)1097-4695(19990215)38:3<313::AID-NEU2>3.0.CO;2-O NR 29 TC 13 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 19 EP 27 DI 10.1016/S0378-5955(99)00203-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800003 PM 10713492 ER PT J AU Alam, SA Ikeda, K Oshima, T Suzuki, M Kawase, T Kikuchi, T Takasaka, T AF Alam, SA Ikeda, K Oshima, T Suzuki, M Kawase, T Kikuchi, T Takasaka, T TI Cisplatin-induced apoptotic cell death in Mongolian gerbil cochlea SO HEARING RESEARCH LA English DT Article DE TUNEL; Hoechst 33342 apoptosis; Bax; Bcl-2; distortion product otoacoustic emission; endocochlear potential ID GUINEA-PIG COCHLEA; PROXIMAL TUBULE CELLS; OUTER HAIR-CELLS; STRIA VASCULARIS; OTOTOXICITY; BCL-2; DNA; DRUG; MITOCHONDRIA; GENERATION AB Cisplatin is well known to cause cochleotoxicity. In order to determine the underlying mechanisms of cisplatin-induced cell death in the cochlea, we investigated the apoptotic changes and the expression of bcl-2 family proteins controlling apoptosis. Mongolian gerbils were administered 4 mg/kg/day cisplatin consecutively for 5 days. The cisplatin-treated animals showed a significant deterioration in the responses of both distortion product otoacoustic emissions and the endocochlear potential as compared with those of the age-matched controls, suggesting outer hair cell and stria vascularis dysfunction. The presence of DNA fragmentation revealed by a terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling method was recognized in the organ of Corti, the spiral ganglion, and the stria vascularis in the cisplatin-treated animals whereas almost negative results were obtained in the control animals. The nuclear morphology obtained by Hoechst 33342 staining revealed pyknotic and condensed nuclei, confirming the presence of the characteristic features of apoptosis. A significant increase and reduction in the number of bax- and bcl-2-positive cells, respectively, following cisplatin treatment was observed in the cells of the organ of Corti, the spiral ganglion, and the lateral wall. These findings suggest a critical role for bcl-2 family proteins in the regulation of apoptotic cell death induced by cisplatin. The underlying mechanisms of the cisplatin-induced cell death are discussed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Tohoku Univ, Sch Med, Dept Otorhinolaryngol Head & Neck Surg, Aoba Ku, Sendai, Miyagi 980, Japan. RP Ikeda, K (reprint author), Tohoku Univ, Sch Med, Dept Otorhinolaryngol Head & Neck Surg, Aoba Ku, 1-1 Seiryo Machi, Sendai, Miyagi 980, Japan. CR Alam SA, 1998, TOHOKU J EXP MED, V186, P79, DOI 10.1620/tjem.186.79 BLAKLEY BW, 1993, OTOLARYNG HEAD NECK, V109, P385 BRADY HR, 1990, AM J PHYSIOL, V258, pF1181 BRIGHT J, 1994, BIOSCIENCE REP, V14, P67 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 Cai JY, 1998, J BIOL CHEM, V273, P11401, DOI 10.1074/jbc.273.19.11401 CANON LL, 1991, ENDOCRINOLOGY, V5, P1169 CharriautMarlangue C, 1995, NEUROREPORT, V7, P61, DOI 10.1097/00001756-199512000-00014 Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 DIVE C, 1991, BRIT J CANCER, V64, P192, DOI 10.1038/bjc.1991.269 DOLE M, 1994, CANCER RES, V54, P3253 FERNANDEZCERVILLA F, 1993, ORL J OTO-RHINO-LARY, V55, P337 FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 Fukuoka K, 1998, LIFE SCI, V62, P1125, DOI 10.1016/S0024-3205(98)00036-8 GAVRIELI Y, 1992, J CELL BIOL, V119, P493, DOI 10.1083/jcb.119.3.493 GERSCHENSON LE, 1992, FASEB J, V6, P2450 HINOJOSA R, 1995, AM J OTOL, V16, P731 HOCKENBERY DM, 1993, CELL, V75, P241, DOI 10.1016/0092-8674(93)80066-N Ichimiya M, 1998, AM J PHYSIOL-CELL PH, V275, pC832 IKEDA K, 1994, PROG NEUROBIOL, V42, P703, DOI 10.1016/0301-0082(94)90024-8 IKEDA K, 1993, ACTA OTO-LARYNGOL, V113, P137, DOI 10.3109/00016489309135781 Jokay I, 1998, HEARING RES, V117, P131, DOI 10.1016/S0378-5955(97)00215-3 KHARBANDA S, 1995, NATURE, V376, P785, DOI 10.1038/376785a0 KIMITSUKI T, 1993, HEARING RES, V71, P64, DOI 10.1016/0378-5955(93)90021-R KOHN S, 1988, LARYNGOSCOPE, V98, P865 KOMUNE S, 1995, ANN OTO RHINOL LARYN, V104, P149 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LEIBBRANDT MEI, 1995, KIDNEY INT, V48, P760 LEIBERTHAL W, 1996, AM J PHYSIOL, V271, pF477 Lieberthal W, 1996, AM J PHYSIOL-RENAL, V270, pF700 Liu W, 1998, NEUROREPORT, V9, P2609, DOI 10.1097/00001756-199808030-00034 MACONKEY DJ, 1989, ARCH BIOCHEM BIOPHYS, V269, P365 Murphy AN, 1996, P NATL ACAD SCI USA, V93, P9893, DOI 10.1073/pnas.93.18.9893 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 Neame SJ, 1998, J CELL BIOL, V142, P1583, DOI 10.1083/jcb.142.6.1583 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W Pettmann B, 1998, NEURON, V20, P633, DOI 10.1016/S0896-6273(00)81004-1 RYBAK L, 1981, J LARYNGOL OTOL, V89, P275 SAITO T, 1995, SCANNING MICROSCOPY, V9, P271 SAITO T, 1991, HEARING RES, V56, P143, DOI 10.1016/0378-5955(91)90163-4 SASANO H, 1995, MODERN PATHOL, V8, P11 Satoh T, 1997, J NEUROSCI RES, V50, P413, DOI 10.1002/(SICI)1097-4547(19971101)50:3<413::AID-JNR7>3.0.CO;2-L SCHWARTZMAN RA, 1993, ENDOCR REV, V14, P133, DOI 10.1210/er.14.2.133 SCHWEITZER VG, 1993, LARYNGOSCOPE, V103, P1, DOI 10.1288/00005537-199304000-00001 Simonian PL, 1996, J BIOL CHEM, V271, P22764 SUGIYAMA S, 1989, BIOCHEM BIOPH RES CO, V159, P1121, DOI 10.1016/0006-291X(89)92225-0 Takeda M, 1997, ARCH TOXICOL, V71, P612, DOI 10.1007/s002040050434 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 YAMAMOTO T, 1994, BRAIN RES, V648, P296, DOI 10.1016/0006-8993(94)91130-4 Zheng Y, 1998, HEARING RES, V126, P11, DOI 10.1016/S0378-5955(98)00138-5 NR 50 TC 85 Z9 108 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 28 EP 38 DI 10.1016/S0378-5955(99)00211-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800004 PM 10713493 ER PT J AU Shatz, LF AF Shatz, LF TI The effect of hair bundle shape on hair bundle hydrodynamics of inner ear hair cells at low and high frequencies SO HEARING RESEARCH LA English DT Article DE cochlea; hair cell; hydrodynamics; spheroid; hair bundle ID ALLIGATOR LIZARD COCHLEA; FREESTANDING STEREOCILIA; SIGNAL TRANSMISSION; RESONANCE; FORCES; MODEL; STAGE; FLUID; FLOW AB The relationship between size and shape of the hair bundle of a hair cell in the inner ear and its sensitivity at asymptotically high and low frequencies was determined, thereby extending the results of an analysis of hair bundle hydrodynamics in two dimensions (Freeman and Weiss, 1990. Hydrodynamic analysis of a two-dimensional model for micromechanical resonance of free-standing hair bundles. Hear. Res. 48, 37-68) to three dimensions. A hemispheroid was used to represent the hair bundle. The hemispheroid had a number of advantages: it could represent shapes that range from thin, pencil-like shapes, to wide, flat, disk-like shapes. Also analytic methods could be used in the high frequency range to obtain an exact solution to the equations of motion. In the low frequency range, where an approximate solution was found using boundary element methods, the sensitivity of the responses of hair cells was mainly proportional to the cube of the heights of their hair bundles, and at high frequencies, the sensitivity of the hair cells was mainly proportional to the inverse of their heights. An excellent match was obtained between measurements of sensitivity curves in the basillar papilla of the alligator and bobtail lizards and the model's predictions. These results also suggest why hair bundles of hair cells in vestibular organs which are sensitive to low frequencies have ranges of heights that are an order of magnitude larger than the range of heights of hair bundles of hair cells found in auditory organs. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Suffolk Univ, Dept Elect & Comp Engn, Boston, MA 02114 USA. Boston Univ, Hearing Res Ctr, Boston, MA 02215 USA. RP Shatz, LF (reprint author), Suffolk Univ, Dept Elect & Comp Engn, 41 Temple St, Boston, MA 02114 USA. CR ACHESON DJ, 1964, ELEMENTARY FLUID DYN CHWANG AT, 1975, J FLUID MECH, V67, P787, DOI 10.1017/S0022112075000614 EATOCK RA, 1993, J NEUROSCI, V13, P1767 FREEMAN DM, 1990, HEARING RES, V48, P1, DOI 10.1016/0378-5955(90)90195-U FREEMAN DM, 1990, HEARING RES, V48, P31, DOI 10.1016/0378-5955(90)90197-W FREEMAN DM, 1990, HEARING RES, V48, P17, DOI 10.1016/0378-5955(90)90196-V FREEMAN DM, 1990, HEARING RES, V48, P37, DOI 10.1016/0378-5955(90)90198-X FREEMAN DM, 1988, HEARING RES, V35, P201, DOI 10.1016/0378-5955(88)90118-9 FRISHKOPF LS, 1983, HEARING RES, V12, P393, DOI 10.1016/0378-5955(83)90008-4 HOLTON T, 1983, J PHYSIOL-LONDON, V345, P205 HOLTON T, 1983, J PHYSIOL-LONDON, V345, P241 KOPPL C, 1988, HEARING RES, V35, P209, DOI 10.1016/0378-5955(88)90119-0 Landau L. D., 1959, FLUID MECH Lewis ER, 1985, VERTEBRATE INNER EAR MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MULROY MJ, 1987, HEARING RES, V25, P11, DOI 10.1016/0378-5955(87)90075-X MULROY MJ, 1974, BRAIN BEHAV EVOLUT, V10, P69, DOI 10.1159/000124303 ROSOWSKI JJ, 1985, HEARING RES, V20, P139, DOI 10.1016/0378-5955(85)90165-0 Shatz LF, 1998, INT J NUMER METH FL, V28, P961 Shatz LF, 1998, PHYS FLUIDS, V10, P2177, DOI 10.1063/1.869739 VATER M, 1992, J COMP NEUROL, V318, P367, DOI 10.1002/cne.903180403 WEISS TF, 1985, HEARING RES, V20, P157, DOI 10.1016/0378-5955(85)90166-2 Zetes DE, 1997, J ACOUST SOC AM, V101, P3593, DOI 10.1121/1.418320 NR 23 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 39 EP 50 DI 10.1016/S0378-5955(99)00205-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800005 PM 10713494 ER PT J AU Dailey, SH Wackym, PA Brichta, AM Gannon, PJ Popper, P AF Dailey, SH Wackym, PA Brichta, AM Gannon, PJ Popper, P TI Topographic distribution of nicotinic acetylcholine receptors in the cristae of a turtle SO HEARING RESEARCH LA English DT Article DE acetylcholine; efferent; nicotinic; receptor; vestibular ID VESTIBULAR END-ORGANS; COCHLEAR HAIR-CELLS; ALPHA-BUNGAROTOXIN BINDING; SUBUNIT MESSENGER-RNA; GUINEA-PIG COCHLEA; CHOLINERGIC RECEPTOR; OUTWARD CURRENTS; SCRIPTA-ELEGANS; FROG; RAT AB The neurochemical basis of cholinergic efferent modulation of afferent function in the vestibular periphery remains incompletely understood; however, there is cellular, biochemical and molecular biological evidence for both muscarinic and nicotinic acetylcholine (ACh) receptors (nAChRs) in this system. This study examined the topographic distribution of alpha-bungarotoxin (alpha-BTX) nAChRs in the cristae of a turtle species. Cristae were perfusion-fixed, cut at 20 mu m on a cryostat and incubated with alpha-BTX or polyclonal antibodies raised against Torpedo nAChR. Light microscopy showed abundant specific labeling of nAChR in the central zone of each hemicrista on the calyx-bearing afferents surrounding type I hair cells and on the base of the type II hair cells. Within the peripheral zone, dense labeling of type II hair cells near the torus and sparse or no label was observed on type II hair cells near the planum. The alpha-BTX binding showed a similar pattern within the cristae. The similarity between the topographic distribution of alpha-BTX binding nAChR and of efferent inhibition of afferents supports the notion that the inhibitory effect of afferents is mediated by nAChR. (C) 2000 Elsevier Science B.V. Ail rights reserved. C1 Med Coll Wisconsin, Dept Otolaryngol & Commun Sci, Milwaukee, WI 53226 USA. Mt Sinai Sch Med, Dept Otolaryngol, New York, NY USA. Univ Chicago, Dept Surg, Otolaryngol Sect, Chicago, IL 60637 USA. RP Wackym, PA (reprint author), Med Coll Wisconsin, Dept Otolaryngol & Commun Sci, 9200 W Wisconsin Ave, Milwaukee, WI 53226 USA. CR Anderson AD, 1997, BRAIN RES, V778, P409, DOI 10.1016/S0006-8993(97)01121-9 ART JJ, 1984, J PHYSIOL-LONDON, V356, P525 ART JJ, 1984, J PHYSIOL-LONDON, V356, P507 Brichta AM, 1996, ANN NY ACAD SCI, V781, P183, DOI 10.1111/j.1749-6632.1996.tb15701.x BRICHTA AM, 1994, J COMP NEUROL, V344, P481, DOI 10.1002/cne.903440402 DICKMAN JD, 1993, NEUROSCIENCE, V57, P1097, DOI 10.1016/0306-4522(93)90052-H ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 Fuchs PA, 1996, CURR OPIN NEUROBIOL, V6, P514, DOI 10.1016/S0959-4388(96)80058-4 GACEK RR, 1974, ACTA OTO-LARYNGOL, V77, P92, DOI 10.3109/00016487409124603 GUTH PS, 1986, ACTA OTO-LARYNGOL, V102, P194, DOI 10.3109/00016488609108666 GUTH PS, 1994, HEARING RES, V75, P225, DOI 10.1016/0378-5955(94)90073-6 Hiel H, 1996, BRAIN RES, V738, P347, DOI 10.1016/S0006-8993(96)01046-3 HILDING D, 1962, Acta Otolaryngol, V55, P205, DOI 10.3109/00016486209127354 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 HOUSLEY GD, 1990, HEARING RES, V43, P121, DOI 10.1016/0378-5955(90)90221-A ISHII T, 1967, ANN OTO RHINOL LARYN, V76, P69 ISHIYAMA A, 1994, CELL BIOL INT, V18, P979, DOI 10.1006/cbir.1994.1019 ISHIYAMA A, 1995, LARYNGOSCOPE, V105, P1167, DOI 10.1288/00005537-199511000-00005 IURATO S, 1971, ACTA OTO-LARYNGOL, V71, P147, DOI 10.3109/00016487109125343 KONG WJ, 1994, HEARING RES, V75, P191, DOI 10.1016/0378-5955(94)90070-1 LINDSTROM J, 1995, ANN NY ACAD SCI, V757, P100, DOI 10.1111/j.1749-6632.1995.tb17467.x MATSUDA Y, 1991, NEUROSCI RES S, V14, pS163, DOI 10.1016/S0921-8696(06)80477-9 MCGEHEE DS, 1995, ANNU REV PHYSIOL, V57, P521, DOI 10.1146/annurev.ph.57.030195.002513 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 OGAWA K, 1993, HEARING RES, V69, P207, DOI 10.1016/0378-5955(93)90109-E Park HJ, 1997, HEARING RES, V112, P95, DOI 10.1016/S0378-5955(97)00111-1 ROSSI ML, 1991, BRAIN RES, V555, P123, DOI 10.1016/0006-8993(91)90868-V SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M THORNHILL RA, 1991, BRAIN RES, V561, P174, DOI 10.1016/0006-8993(91)90765-N USAMI S, 1987, BRAIN RES, V418, P383, DOI 10.1016/0006-8993(87)90108-9 VALLI P, 1984, ACTA OTO-LARYNGOL, V97, P611, DOI 10.3109/00016488409132938 WACKYM PA, 1995, CELL BIOL INT, V19, P291, DOI 10.1006/cbir.1995.1071 Wackym PA, 1996, CELL BIOL INT, V20, P187, DOI 10.1006/cbir.1996.0023 Yamashita T, 1993, Acta Otolaryngol Suppl, V500, P26 YOSHIDA N, 1994, BRAIN RES, V644, P90, DOI 10.1016/0006-8993(94)90351-4 NR 37 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 51 EP 56 DI 10.1016/S0378-5955(99)00208-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800006 PM 10713495 ER PT J AU John, MS Picton, TW AF John, MS Picton, TW TI Human auditory steady-state responses to amplitude-modulated tones: phase and latency measurements SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT Meeting of the International-Electric-Response-Audiometry-Study-Group CY JUN, 1999 CL TORMSO, NORWAY SP Int Elect Response Audiometry Study Grp DE auditory evoked potential; steady-state response; apparent latency; phase; travelling wave ID BRAIN-STEM RESPONSE; PRODUCT OTOACOUSTIC EMISSIONS; TRAVELING-WAVE VELOCITY; EVOKED-POTENTIALS; INFERIOR COLLICULUS; COCHLEAR MECHANICS; MENIERES-DISEASE; SOUND INTENSITY; NOTCHED-NOISE; NERVE FIBERS AB Human auditory steady-state responses were recorded to four stimuli, with carrier frequencies VE) of 750, 1500, 3000 and 6000 Hz, presented simultaneously at 60 dB SPL. Each carrier frequency was modulated by a specific modulation frequency (f(m)) of 80.6, 85.5, 90.3 or 95.2 Hz. By using four different recording conditions we obtained responses for all permutations of f(m) and f(c). The phase delays (P) of the responses were unwrapped and converted to latency (L) using the equation: L = P/(360 x f(m)). The number of cycles of the stimulus that occurred prior to the recorded response was estimated by analyzing the effect of modulation frequency on the responses. These calculations provided latencies of 20.7, 17.7, 16.1 and 16.1 ms for carrier frequencies 750, 1500, 3000 and 6000 Hz. This latency difference of about 4.5 ms between low and high carrier frequencies remained constant over many different manipulations of the stimuli: faster modulation rates (150-190 Hz), binaural rather than monaural presentation, different intensities, stimuli presented alone or in conjunction with other stimuli, and modulation frequencies that were separated by as little as 0.24 Hz. This frequency-related delay is greater than that measured using transient evoked potentials, most likely because of differences in how transient and steady-state responses are generated and how their latencies are determined. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Toronto, Baycrest Ctr Geriatr Care, Rotman Res Inst, Toronto, ON M6A 2E1, Canada. RP Picton, TW (reprint author), Univ Toronto, Baycrest Ctr Geriatr Care, Rotman Res Inst, 3560 Bathurst St, Toronto, ON M6A 2E1, Canada. CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 AZZENA GB, 1995, HEARING RES, V83, P1, DOI 10.1016/0378-5955(94)00184-R BASAR E, 1987, INT J NEUROSCI, V33, P103 Bekesy G., 1960, EXPT HEARING Von Bekesy G., 1963, Journal of the Acoustical Society of America, V35 BIJL GK, 1985, ELECTROEN CLIN NEURO, V62, P465, DOI 10.1016/0168-5597(85)90059-0 Bowman DM, 1997, J ACOUST SOC AM, V101, P1550, DOI 10.1121/1.418129 BROWN D, 1994, J OTOLARYNGOL, V23, P234 BROWN PB, 1982, ELECT MODERN SCI CARNEY LH, 1993, J ACOUST SOC AM, V93, P401, DOI 10.1121/1.405620 CHERTOFF ME, 1990, J ACOUST SOC AM, V87, P1248, DOI 10.1121/1.398800 COHEN LT, 1991, J ACOUST SOC AM, V90, P2467, DOI 10.1121/1.402050 COREY DP, 1983, J NEUROSCI, V3, P942 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1971, J ACOUST SOC AM, V49, P1140, DOI 10.1121/1.1912475 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 DANCER A, 1992, AUDIOLOGY, V31, P301 DIAMOND AL, 1977, ELECTROEN CLIN NEURO, V42, P125 DOBIE RA, 1993, ELECTROEN CLIN NEURO, V88, P516, DOI 10.1016/0168-5597(93)90040-V Dobie RA, 1998, J ACOUST SOC AM, V104, P3482, DOI 10.1121/1.423931 Dobie RA, 1996, J ACOUST SOC AM, V100, P2236, DOI 10.1121/1.417933 DON M, 1993, J ACOUST SOC AM, V94, P2135, DOI 10.1121/1.407485 Don M, 1998, J ACOUST SOC AM, V104, P2280, DOI 10.1121/1.423741 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 Donaldson GS, 1996, J SPEECH HEAR RES, V39, P534 Eggermont J. J., 1979, SCAND AUDIOL S, V9, P129 EGGERMONT JJ, 1980, J ACOUST SOC AM, V68, P1671, DOI 10.1121/1.385199 Eggermont JJ, 1996, EAR HEARING, V17, P386, DOI 10.1097/00003446-199610000-00004 EGGERMONT JJ, 1979, J ACOUST SOC AM, V65, P463, DOI 10.1121/1.382345 EGGERMONT JJ, 1985, HEARING RES, V18, P57, DOI 10.1016/0378-5955(85)90110-8 Elberling C, 1976, Rev Laryngol Otol Rhinol (Bord), V97 Suppl, P527 Fisher N. I., 1993, STAT ANAL CIRCULAR D FRIDMAN J, 1984, AUDIOLOGY, V23, P99 GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T Goldstein JL, 1971, PHYSL AUDITORY SYSTE, P133 GUMMER AW, 1984, J ACOUST SOC AM, V76, P1388, DOI 10.1121/1.391456 Gutschalk A, 1999, CLIN NEUROPHYSIOL, V110, P856, DOI 10.1016/S1388-2457(99)00019-X HARI R, 1989, J ACOUST SOC AM, V86, P1033, DOI 10.1121/1.398093 HONRUBIA V, 1968, J ACOUST SOC AM, V44, P951, DOI 10.1121/1.1911234 John MS, 2000, COMPUT METH PROG BIO, V61, P125, DOI 10.1016/S0169-2607(99)00035-8 John MS, 1998, AUDIOLOGY, V37, P59 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 Kim Y, 1994, Acta Otolaryngol Suppl, V511, P71 KIMBERLEY BP, 1993, J ACOUST SOC AM, V94, P1343, DOI 10.1121/1.408162 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F LEVI EC, 1993, HEARING RES, V68, P42, DOI 10.1016/0378-5955(93)90063-7 LINS OG, 1995, EVOKED POTENTIAL, V96, P420, DOI 10.1016/0168-5597(95)00048-W Lins OG, 1996, EAR HEARING, V17, P81, DOI 10.1097/00003446-199604000-00001 LINS OG, 1995, J ACOUST SOC AM, V97, P3051, DOI 10.1121/1.411869 MARGOLIS RH, 1995, ARCH OTOLARYNGOL, V121, P44 MAUER G, 1999, JUN 1999 M INT EV RE MOLLER AR, 1985, HEARING RES, V17, P177, DOI 10.1016/0378-5955(85)90020-6 MOLLER AR, 1975, J NEUROPHYSIOL, V38, P812 MOLLER AR, 1989, HEARING RES, V42, P237, DOI 10.1016/0378-5955(89)90148-2 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x Moulin A, 1996, J ACOUST SOC AM, V100, P1640, DOI 10.1121/1.416064 Moulin A, 1996, J ACOUST SOC AM, V100, P1617, DOI 10.1121/1.416063 MUNRO KJ, 1995, BRIT J AUDIOL, V29, P23, DOI 10.3109/03005369509086582 NEELY ST, 1988, J ACOUST SOC AM, V83, P652, DOI 10.1121/1.396542 OMAHONEY C, 1995, J ACOUST SOC AM, V97, P1 PARKER D J, 1978, Scandinavian Audiology, V7, P67, DOI 10.3109/01050397809043134 PATTERSON RD, 1994, J ACOUST SOC AM, V96, P1409, DOI 10.1121/1.410285 PATUZZI R, 1996, SPRINGER HDB AUDITOR, V8, P187 PICTON TW, 1979, J OTOLARYNGOL, V8, P289 Plourde G, 1991, Acta Otolaryngol Suppl, V491, P153 RANCE G, 1995, EAR HEARING, V16, P499, DOI 10.1097/00003446-199510000-00006 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 REGAN D, 1966, ELECTROEN CLIN NEURO, V20, P238, DOI 10.1016/0013-4694(66)90088-5 Regan D., 1989, HUMAN BRAIN ELECTROP RICKARDS FW, 1994, BRIT J AUDIOL, V28, P327, DOI 10.3109/03005369409077316 Rickards F.W., 1984, EVOKED POTENTIAL, VII, P163 RICKMAN MD, 1991, J ACOUST SOC AM, V89, P2818, DOI 10.1121/1.400720 RODRIGUEZ R, 1986, EAR HEARING, V7, P300, DOI 10.1097/00003446-198610000-00003 RUGGERO MA, 1994, AUDIOLOGY, V33, P131 RUGGERO MA, 1992, SPRINGER HDB AUDITOR, V2, P35 SANTARELLI R, 1995, HEARING RES, V83, P9, DOI 10.1016/0378-5955(94)00185-S SATO H, 1991, ACTA OTO-LARYNGOL, V111, P1037, DOI 10.3109/00016489109138447 Schneider S, 1999, J ACOUST SOC AM, V105, P2722, DOI 10.1121/1.426890 Shera CA, 1999, J ACOUST SOC AM, V105, P782, DOI 10.1121/1.426948 Shirane M, 1991, Acta Otolaryngol Suppl, V489, P32 STAPELLS DR, 1987, ELECTROEN CLIN NEURO, V67, P260, DOI 10.1016/0013-4694(87)90024-1 STAPELLS DR, 1984, EAR HEARING, V5, P105 Sutton GJ, 1983, MECHANICS HEARING, P83 TEAS DONALD C, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1438, DOI 10.1121/1.1918366 THORNTON ARD, 1991, SCAND AUDIOL, V20, P13, DOI 10.3109/01050399109070784 Valdes JL, 1997, EAR HEARING, V18, P420, DOI 10.1097/00003446-199710000-00007 VANDERTW.LH, 1965, ELECTROEN CLIN NEURO, V18, P587, DOI 10.1016/0013-4694(65)90076-3 ZUREK PM, 1992, EAR HEARING, V13, P307, DOI 10.1097/00003446-199210000-00008 ZWISLOCKI JJ, 1991, ACTA OTO-LARYNGOL, V111, P256, DOI 10.3109/00016489109137384 NR 91 TC 75 Z9 79 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 57 EP 79 DI 10.1016/S0378-5955(99)00209-9 PG 23 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800007 PM 10713496 ER PT J AU Bauer, EE Klug, A Pollak, GD AF Bauer, EE Klug, A Pollak, GD TI Features of contralaterally evoked inhibition in the inferior colliculus SO HEARING RESEARCH LA English DT Article DE inferior colliculus; inhibition; iontophoresis; bicuculline; strychnine; glutamate ID FREE-TAILED BAT; MEDIAL SUPERIOR OLIVE; TADARIDA-BRASILIENSIS-MEXICANA; MONAURAL RESPONSE PROPERTIES; INTERAURAL TIME DIFFERENCES; CENTRAL AUDITORY-SYSTEM; CENTRAL-NERVOUS-SYSTEM; BIG BROWN BAT; MOUSTACHE BAT; LATERAL LEMNISCUS AB Cells in the central nucleus of the inferior colliculus (ICc) receive a large number of convergent inputs that are not only excitatory but inhibitory as well. While the excitatory responses of ICc cells have been studied extensively, less attention has been paid to the effects that inhibitory inputs have on auditory processing in the ICc. The purpose of this study was to examine the role of contralaterally evoked inhibition in single ICc cells in awake Mexican free-tailed bats. To study the contralaterally evoked inhibition, we created background activity by the iontophoretic application of the excitatory neurotransmitters glutamate and aspartate and visualized the inhibition as a gap in the carpet of background activity. We found that 85% of ICc cells exhibit a contralaterally evoked excitation followed by a period of inhibition. The inhibition acts primarily through GABAA receptors since the application of bicuculline eliminated or greatly reduced the inhibition in all cells. The inhibition has two parts: an early part which is coincident with the tone stimulus and a later persistent component which outlasts the tone stimulus by tells of milliseconds. The persistent inhibition typically is level-dependent, increasing in duration with increasing sound level. The persistent inhibition is also sensitive to the duration of the stimulus, with short (5 ms) tones being less effective than longer (> 20 ms) tones in generating persistent inhibition. While the early inhibition has clear roles in the shaping of excitatory response properties to a stimulus, the later persistent component of the inhibition is more enigmatic. The fact that the persistent inhibition lasts well beyond the duration of excitatory inputs to the ICc cell implies that the persistent inhibition may be important for the temporal segregation of the responses to multiple sound sources. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Texas, Dept Zool, Austin, TX 78712 USA. RP Pollak, GD (reprint author), Univ Texas, Dept Zool, Austin, TX 78712 USA. CR AITKEN L, 1985, AUDITORY MIDBRAIN ST ANDRADE R, 1986, SCIENCE, V234, P1261, DOI 10.1126/science.2430334 Backoff PM, 1997, HEARING RES, V110, P155, DOI 10.1016/S0378-5955(97)00081-6 BALCOMBE JP, 1992, ANIM BEHAV, V43, P79, DOI 10.1016/S0003-3472(05)80073-9 Banks MI, 1998, J NEUROSCI, V18, P1305 BODENHAMER RD, 1981, HEARING RES, V5, P317, DOI 10.1016/0378-5955(81)90055-1 Bregman AS., 1990, AUDITORY SCENE ANAL Burger RM, 1998, J NEUROPHYSIOL, V80, P1686 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 CASPARY DM, 1987, BRAIN RES, V417, P273, DOI 10.1016/0006-8993(87)90452-5 CASSEDAY JH, 1995, NEURAL REPRESENTATIO, P25 Casseday JH, 1997, J NEUROPHYSIOL, V77, P1595 CASSEDAY JH, 1994, SCIENCE, V264, P847, DOI 10.1126/science.8171341 CHU DCM, 1990, NEUROSCIENCE, V34, P341, DOI 10.1016/0306-4522(90)90144-S Covey E, 1996, J NEUROSCI, V16, P3009 FAINGOLD CL, 1991, HEARING RES, V52, P201, DOI 10.1016/0378-5955(91)90200-S FAINGOLD CL, 1989, HEARING RES, V40, P127, DOI 10.1016/0378-5955(89)90106-8 FAINGOLD CL, 1989, BRAIN RES, V500, P302, DOI 10.1016/0006-8993(89)90326-0 Fitzpatrick DC, 1995, J NEUROPHYSIOL, V74, P2469 FRIEND JH, 1966, J CELL PHYSIOL, V67, P319, DOI 10.1002/jcp.1040670212 Fubara BM, 1996, J COMP NEUROL, V369, P83 Fuzessery ZM, 1996, J NEUROPHYSIOL, V76, P1059 GELFAND DL, 1986, ANIM BEHAV, V34, P1078, DOI 10.1016/S0003-3472(86)80167-1 GonzalezHernandez T, 1996, J COMP NEUROL, V372, P309, DOI 10.1002/(SICI)1096-9861(19960819)372:2<309::AID-CNE11>3.0.CO;2-E GRINNELL AD, 1963, J PHYSIOL-LONDON, V167, P67 GROTHE B, 1994, J NEUROPHYSIOL, V71, P706 GROTHE B, 1994, J COMP NEUROL, V343, P630, DOI 10.1002/cne.903430412 Grothe B, 1998, J NEUROSCI, V18, P6608 Grothe B, 1997, J NEUROPHYSIOL, V77, P1553 HAVEY DC, 1980, ELECTROEN CLIN NEURO, V48, P249, DOI 10.1016/0013-4694(80)90313-2 HOLTZ GG, 1986, NATURE, V319, P670 Irvine D. R. F., 1986, PROGR SENSORY PHYSL, V7 Klug A, 1999, J NEUROPHYSIOL, V82, P593 KLUG A, 1995, J NEUROPHYSIOL, V74, P1701 Kuwada S, 1997, J NEUROSCI, V17, P7565 LeBeau FEN, 1996, J NEUROPHYSIOL, V75, P902 Lu Y, 1997, J COMP PHYSIOL A, V181, P331, DOI 10.1007/s003590050119 MCCRACKEN GF, 1984, SCIENCE, V223, P1090, DOI 10.1126/science.223.4640.1090 MOORE MJ, 1983, J NEUROSCI, V3, P237 NELSON PG, 1963, J NEUROPHYSIOL, V26, P908 OLIVER DL, 1994, J COMP NEUROL, V340, P27, DOI 10.1002/cne.903400104 Oliver DL, 1992, MAMMALIAN AUDITORY P, V1, P168 OTIS TS, 1993, J PHYSIOL-LONDON, V463, P391 Palombi PS, 1996, J NEUROPHYSIOL, V75, P2211 Pape HC, 1996, ANNU REV PHYSIOL, V58, P299, DOI 10.1146/annurev.physiol.58.1.299 Park TJ, 1998, NATURWISSENSCHAFTEN, V85, P176, DOI 10.1007/s001140050479 PARK TJ, 1993, J NEUROSCI, V13, P5172 PARK TJ, 1994, J NEUROPHYSIOL, V72, P1080 Park TJ, 1996, J NEUROSCI, V16, P6554 Pedemonte M, 1997, BRAIN RES, V759, P24, DOI 10.1016/S0006-8993(97)00123-6 PFRIEGER FW, 1994, NEURON, V12, P97, DOI 10.1016/0896-6273(94)90155-4 POLLAK G, 1977, SCIENCE, V196, P675, DOI 10.1126/science.857318 Pollak G. D., 1986, NEURAL BASIS ECHOLOC POLLAK GD, 1993, HEARING RES, V65, P99, DOI 10.1016/0378-5955(93)90205-F POLLAK GD, 1977, J COMP PHYSIOL, V120, P215 POLLAK GD, 1978, J NEUROPHYSIOL, V41, P677 POLLAK GD, 1977, J NEUROPHYSIOL, V40, P926 POLLAK GD, 1981, J NEUROPHYSIOL, V45, P208 ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 SaintMarie RL, 1997, BRAIN RES, V765, P173, DOI 10.1016/S0006-8993(97)00654-9 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SALDANA E, 1992, J COMP NEUROL, V319, P417, DOI 10.1002/cne.903190308 SCHMIDT S, 1994, HEARING RES, V77, P125, DOI 10.1016/0378-5955(94)90260-7 SCHULLER G, 1986, J NEUROSCI METH, V18, P339, DOI 10.1016/0165-0270(86)90022-1 SEMPLE MN, 1987, J NEUROPHYSIOL, V57, P1130 SHNEIDERMAN A, 1989, J COMP NEUROL, V286, P28, DOI 10.1002/cne.902860103 SHNEIDERMAN A, 1988, J COMP NEUROL, V276, P188, DOI 10.1002/cne.902760204 SIMMONS JA, 1979, SCIENCE, V203, P16, DOI 10.1126/science.758674 SIMMONS JA, 1978, J COMP PHYSIOL, V125, P291 SIVILOTTI L, 1991, PROG NEUROBIOL, V36, P35, DOI 10.1016/0301-0082(91)90036-Z SPITZER MW, 1993, J NEUROPHYSIOL, V69, P1245 Suga N, 1997, J NEUROPHYSIOL, V77, P2098 SUGA N, 1964, J PHYSIOL-LONDON, V175, P50 Torterolo P, 1995, ARCH ITAL BIOL, V134, P57 VATER M, 1992, J COMP PHYSIOL A, V171, P541 Vater M, 1995, HEARING RES, V91, P178, DOI 10.1016/0378-5955(95)00188-3 WINER JA, 1995, J COMP NEUROL, V355, P317, DOI 10.1002/cne.903550302 WU SH, 1986, J NEUROSCI, V6, P2691 YANG LC, 1994, J NEUROPHYSIOL, V71, P1999 YANG LC, 1994, J NEUROPHYSIOL, V71, P2014 YANG LC, 1992, J NEUROPHYSIOL, V68, P1760 YIN TCT, 1994, J NEUROSCI, V14, P5170 NR 82 TC 27 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 80 EP 96 DI 10.1016/S0378-5955(99)00206-3 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800008 PM 10713497 ER PT J AU Yoshida, N Hequembourg, SJ Atencio, CA Rosowski, JJ Liberman, MC AF Yoshida, N Hequembourg, SJ Atencio, CA Rosowski, JJ Liberman, MC TI Acoustic injury in mice: 129/SvEv is exceptionally resistant to noise-induced hearing loss SO HEARING RESEARCH LA English DT Article DE cochlea; age-related hearing loss; noise-induced hearing loss ID C57BL/6J MICE; MIDDLE-EAR; AGE; SUSCEPTIBILITY; EXPOSURES; DAMAGE; MOUSE AB 129/SvEv is an inbred mouse strain popular for use in genetic knockout studies. Here, we compare normal auditory function and vulnerability to acoustic injury in wild-type mice of the 129/SvEv vs. CBA/CaJ strains. Compound action potentials (CAPs) and distortion product otoacoustic emissions (DPOAEs) showed slightly higher thresholds for 129/SvEv re CBA/CaJ, especially at frequencies > 20 kHz. Middle-ear motion (i.e. umbo velocity) was similar in the two strains; although frequencies > 20 kHz could not be evaluated. Permanent threshold shift (PTS) and hair cell losses, measured 1 week after high-intensity exposure to an 8-16 kHz noise band, were smaller in 129/SvEv at all exposure levels and durations from 97 dB SPL x 2 h to 106 dB SPL x 8 h. Furthermore, PTS growth with increasing exposure energy was slower in 129/SvEv(< 2 dB/dB) than CBA/CaJ (9 dB/dB). These data suggest that the vulnerability differences lie in the inner ear, not the middle ear. Several 129/Sv substrains show age-related hearing loss (AHL): 129/SvEv has not yet been evaluated (Zheng, Q.Y., Johnson, K.R., Erway, L.C., 1999. Assessment of hearing in 80 inbred strains of mice by ABR threshold analyses. Hear. Res. 130, 94-107). Thus, although other strains with AHL, e.g. C57Bl/6J, show increased vulnerability to noise-induced hearing loss (NIHL), pairing of AHL and NIHL vulnerabilities may not be obligatory. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA. Tohoku Univ, Grad Sch Med, Dept Otol & Laryngol, Sendai, Miyagi 9808574, Japan. RP Liberman, MC (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA. CR CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DAVIS RR, 1999, IN PRESS HEAR RES Doan DE, 1996, HEARING RES, V97, P174, DOI 10.1016/0378-5955(96)00060-3 DOAN DE, 1994, J COMP PHYSIOL A, V174, P103 Ehret G, 1983, AUDITORY PSYCHOBIOLO, P169 Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X FOWLER T, 1995, HEARING RES, V88, P1, DOI 10.1016/0378-5955(95)00062-9 GOULIOS H, 1983, HEARING RES, V11, P327, DOI 10.1016/0378-5955(83)90065-5 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X LI HS, 1993, AUDIOLOGY, V32, P195 LIBERMAN MC, 1978, ACTA OTOLARYNGOL S, V358, P5 LIBERMAN MC, 1995, HEARING RES, V90, P158, DOI 10.1016/0378-5955(95)00160-2 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 RYAN A, 1978, J ACOUST SOC AM, V63, P1145, DOI 10.1121/1.381822 SAUNDERS JC, 1982, J COMP PHYSIOL, V146, P517 Vetter DE, 1999, NEURON, V23, P93, DOI 10.1016/S0896-6273(00)80756-4 Zheng QY, 1999, HEARING RES, V130, P94, DOI 10.1016/S0378-5955(99)00003-9 NR 18 TC 63 Z9 65 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 97 EP 106 DI 10.1016/S0378-5955(99)00210-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800009 PM 10713498 ER PT J AU Ehret, G Schreiner, CE AF Ehret, G Schreiner, CE TI Regional variations of noise-induced changes in operating range in cat AI SO HEARING RESEARCH LA English DT Article DE auditory cortex; dynamic range; noise masking; response mapping ID PRIMARY AUDITORY-CORTEX; MULTIPLE-NEURON RECORDINGS; DORSAL COCHLEAR NUCLEUS; FUNCTIONAL TOPOGRAPHY; TONE INTENSITY; SINGLE UNITS; FREQUENCY RESOLUTION; SPECTRAL INTEGRATION; INFERIOR COLLICULUS; CORTICAL-NEURONS AB Regional differences in spectral integration of neurons in cat primary auditory cortex (AI) suggest that regions differ in effects of background noise on operating characteristics of neurons. Therefore, tone-response threshold, best level (peak-rate intensity), dynamic range, and sharpness of tuning in quiet and in continuous broadband noise were mapped for single neurons along the isofrequency domain of AI. Neurons did not show an excitatory response to the noise. Noise invariably increased the tone-response threshold and best levels. Consequently, the dynamic ranges and receptive fields shifted to higher intensity levels without changes of average sharpness of tuning. These shifts were linearly related to noise level and showed little inter-neuronal variability for neurons in the central, mostly sharply tuned part of AI. In more dorsal and ventral parts of AI, neurons were more variable in lone-response threshold, dynamic range and best level, and no systematic relationship between increase in noise level, threshold increase and best-level increase was observed. We conclude that linear shifts in the operating range of neurons in central AI in the presence of continuous noise backgrounds do not affect other response properties and may relate to the unaltered analysis and representation of spectral components of sounds. In contrast, neurons in dorsal and ventral AI change response properties in a non-predictable way in the presence of noise in accordance with the more complex receptive field properties in those areas. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Ulm, Dept Neurobiol, D-89069 Ulm, Germany. Univ Calif San Francisco, WN Keck Ctr Integrat Neurosci, Coleman Lab, San Francisco, CA 94143 USA. RP Ehret, G (reprint author), Univ Ulm, Dept Neurobiol, D-89069 Ulm, Germany. CR Brugge JF, 1998, J NEUROPHYSIOL, V80, P2417 CLAREY JC, 1994, J NEUROPHYSIOL, V72, P2383 COSTALUPES JA, 1984, J NEUROPHYSIOL, V51, P1326 deCharms RC, 1996, NATURE, V381, P610, DOI 10.1038/381610a0 deRibaupierre F, 1997, CENTRAL AUDITORY SYS, P317 EHRET G, 1985, J COMP PHYSIOL A, V156, P619, DOI 10.1007/BF00619111 Ehret G, 1997, J COMP PHYSIOL A, V181, P635, DOI 10.1007/s003590050146 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 Ehret G, 1997, J COMP PHYSIOL A, V181, P547, DOI 10.1007/s003590050139 EHRET G, 1984, HEARING RES, V14, P45, DOI 10.1016/0378-5955(84)90068-6 FRISINA RD, 1994, EXP BRAIN RES, V102, P160 GOLDSTEI.MH, 1968, J ACOUST SOC AM, V43, P444, DOI 10.1121/1.1910851 GREENWOO.DD, 1970, J ACOUST SOC AM, V47, P1022, DOI 10.1121/1.1912002 HEIL P, 1992, HEARING RES, V63, P135, DOI 10.1016/0378-5955(92)90081-W HEIL P, 1994, HEARING RES, V76, P188, DOI 10.1016/0378-5955(94)90099-X Krauth J., 1988, DISTRIBUTION FREE ST Mendelson JR, 1997, J COMP PHYSIOL A, V181, P615, DOI 10.1007/s003590050145 PHILLIPS DP, 1985, HEARING RES, V19, P253, DOI 10.1016/0378-5955(85)90145-5 PHILLIPS DP, 1986, J ACOUST SOC AM, V80, P177, DOI 10.1121/1.394178 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1985, HEARING RES, V18, P87, DOI 10.1016/0378-5955(85)90112-1 PHILLIPS DP, 1994, EXP BRAIN RES, V102, P210 PICKLES JO, 1976, J ACOUST SOC AM, V60, P1151, DOI 10.1121/1.381217 Read H. L., 1998, Society for Neuroscience Abstracts, V24, P1878 REES A, 1988, J ACOUST SOC AM, V83, P1488, DOI 10.1121/1.395904 RHODE WS, 1978, J NEUROPHYSIOL, V41, P692 Sachs L., 1974, ANGEW STAT Schreiner CE, 1998, AUDIOL NEURO-OTOL, V3, P104, DOI 10.1159/000013785 SCHREINER CE, 2000, IN PRESS ANN REV NEU SCHREINER CE, 1992, J NEUROPHYSIOL, V68, P1487 SCHREINER CE, 1992, EXP BRAIN RES, V92, P105 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 SCHRIENER CE, 1999, LISTENING SPEECH AUD SOKOLICH WG, 1981, Patent No. 4251686 SUTTER ML, 2000, IN PRESS J NEUROPHYS SUTTER ML, 1995, J NEUROPHYSIOL, V73, P190 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 WINSLOW RL, 1988, HEARING RES, V35, P165, DOI 10.1016/0378-5955(88)90116-5 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 ZURITA P, 1994, NEUROSCI RES, V19, P303, DOI 10.1016/0168-0102(94)90043-4 NR 41 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 107 EP 116 DI 10.1016/S0378-5955(99)00213-0 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800010 PM 10713499 ER PT J AU Katz, E Verbitsky, M Rothlin, CV Vetter, DE Heinemann, SF Elgoyhen, AB AF Katz, E Verbitsky, M Rothlin, CV Vetter, DE Heinemann, SF Elgoyhen, AB TI High calcium permeability and calcium block of the alpha 9 nicotinic acetylcholine receptor SO HEARING RESEARCH LA English DT Article DE nicotinic receptor; outer hair cell; olivocochlear efferent synapse; Ca2+ permeability; voltage-dependent blockage; neurotransmitter receptor channel; ligand-gated channel ID OUTER HAIR-CELLS; RAT CENTRAL NEURONS; GUINEA-PIG COCHLEA; XENOPUS-OOCYTES; DIVALENT-CATIONS; CHLORIDE CURRENT; GATED CHANNELS; PC12 CELLS; RT-PCR; CONDUCTANCE AB At the synapse between olivocochlear efferent fibers and outer hair cells (OHCs) of the cochlea, a non-classical ionotropic cholinergic receptor allows Ca2+ entry into the hair cell, thus activating a Ca2+-sensitive K+ current which hyperpolarizes the cell's membrane. In the mammalian ear, this leads to a reduction in basilar membrane motion, altering auditory nerve fiber activity and reducing the dynamic range of hearing. The alpha 9 nicotinic acetylcholine receptor (nAChR) subunit mediates synaptic transmission between cholinergic olivocochlear fibers and OHCs. Given that Ca2+ is a key player at this inhibitory synapse, we evaluated the permeability to Ca2+ of the recombinant a9 receptor expressed in Xenopus laevis oocytes and the modulation of its activity by extracellular Ca2+. Our results show that the a9 receptor is highly permeable to Ca2+ and that this cation potently blocks monovalent currents through this channel (IC50 = 100 mu M, at -70 mV) in a voltage-dependent manner. At a Ca2+ concentration similar to that found in the perilymph bathing the base of the OHCs, approximately 90% of the Na+ current through the alpha 9 receptor is blocked, suggesting that one of the main functions of this channel could be to provide a pathway for Ca2+ influx. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Buenos Aires, Fac Ciencias Exactas & Nat, Consejo Nacl Invest Cient & Tecn, Inst Invest Ingn Genet & Biol Mol, RA-1428 Buenos Aires, DF, Argentina. Univ Buenos Aires, Fac Ciencias Exactas & Nat, Dept Biol, RA-1428 Buenos Aires, DF, Argentina. Salk Inst Biol Studies, Mol Neurobiol Lab, La Jolla, CA 92037 USA. RP Elgoyhen, AB (reprint author), Univ Buenos Aires, Fac Ciencias Exactas & Nat, Consejo Nacl Invest Cient & Tecn, Inst Invest Ingn Genet & Biol Mol, Vuelta Obligado 2490, RA-1428 Buenos Aires, DF, Argentina. CR ADAMS DJ, 1980, J GEN PHYSIOL, V75, P493, DOI 10.1085/jgp.75.5.493 ALMERS W, 1984, J PHYSIOL-LONDON, V353, P585 AMADOR M, 1995, J NEUROSCI, V15, P4525 ARELLANO RO, 1995, J PHYSIOL-LONDON, V484, P593 BARISH ME, 1983, J PHYSIOL-LONDON, V342, P309 BERTRAND D, 1990, P NATL ACAD SCI USA, V87, P1993, DOI 10.1073/pnas.87.5.1993 BERTRAND D, 1993, P NATL ACAD SCI USA, V90, P6971, DOI 10.1073/pnas.90.15.6971 Blanchet C, 1996, J NEUROSCI, V16, P2574 BOTON R, 1989, J PHYSIOL-LONDON, V408, P511 BOULTER J, 1987, P NATL ACAD SCI USA, V84, P7763, DOI 10.1073/pnas.84.21.7763 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BURNASHEV N, 1992, SCIENCE, V257, P1415, DOI 10.1126/science.1382314 Burnashev N, 1996, CURR OPIN NEUROBIOL, V6, P311, DOI 10.1016/S0959-4388(96)80113-9 Chen C, 1996, HEARING RES, V98, P9, DOI 10.1016/0378-5955(96)00049-4 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DECKER ER, 1990, J NEUROSCI, V10, P3413 DOI T, 1993, HEARING RES, V67, P179, DOI 10.1016/0378-5955(93)90245-V Dulon D, 1998, EUR J NEUROSCI, V10, P907, DOI 10.1046/j.1460-9568.1998.00098.x Ebihara L, 1996, BIOPHYS J, V71, P742 ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 Evans MG, 1996, J PHYSIOL-LONDON, V491, P563 FIEBER LA, 1991, J PHYSIOL-LONDON, V434, P215 FRINGS S, 1995, NEURON, V15, P169, DOI 10.1016/0896-6273(95)90074-8 Galzi JL, 1996, EMBO J, V15, P5824 GERZANICH V, 1994, MOL PHARMACOL, V45, P212 GLOWATZKI E, 1995, P ROY SOC B-BIOL SCI, V262, P141, DOI 10.1098/rspb.1995.0188 Guinan Jr J.J., 1996, COCHLEA, P435 Hille B., 1992, IONIC CHANNELS EXCIT, V2nd Holley M. C., 1996, COCHLEA, P386 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 IFUNE CK, 1991, J PHYSIOL-LONDON, V443, P683 JAHR CE, 1993, P NATL ACAD SCI USA, V90, P11573, DOI 10.1073/pnas.90.24.11573 Jaramillo F, 1995, NEURON, V15, P1227, DOI 10.1016/0896-6273(95)90003-9 LEWIS CA, 1979, J PHYSIOL-LONDON, V286, P417 MAYER ML, 1987, J PHYSIOL-LONDON, V394, P501 McNiven AI, 1996, AUDIT NEUROSCI, V2, P63 MILEDI R, 1984, J PHYSIOL-LONDON, V357, P173 Morley BJ, 1998, MOL BRAIN RES, V53, P78, DOI 10.1016/S0169-328X(97)00272-6 MULLE C, 1992, NEURON, V8, P937, DOI 10.1016/0896-6273(92)90208-U MULLE C, 1992, NEURON, V8, P135, DOI 10.1016/0896-6273(92)90115-T Nenov AP, 1996, HEARING RES, V101, P149, DOI 10.1016/S0378-5955(96)00143-8 Nenov AP, 1996, HEARING RES, V101, P132, DOI 10.1016/S0378-5955(96)00142-6 NUTTER TJ, 1995, J GEN PHYSIOL, V105, P701, DOI 10.1085/jgp.105.6.701 Park HJ, 1997, HEARING RES, V112, P95, DOI 10.1016/S0378-5955(97)00111-1 Ragozzino D, 1998, J PHYSIOL-LONDON, V507, P749, DOI 10.1111/j.1469-7793.1998.749bs.x RATHOUZ MM, 1994, J NEUROSCI, V14, P6935 ROGERS M, 1995, BIOPHYS J, V68, P501 Rothlin CV, 1999, MOL PHARMACOL, V55, P248 SANDS SB, 1993, BIOPHYS J, V65, P2614 SANDS SB, 1992, J PHYSIOL-LONDON, V447, P467 SANDS SB, 1991, BRAIN RES, V560, P38, DOI 10.1016/0006-8993(91)91211-I Schneggenburger R, 1996, BIOPHYS J, V70, P2165 SCHNEGGENBURGER R, 1993, NEURON, V11, P133, DOI 10.1016/0896-6273(93)90277-X SEGUELA P, 1993, J NEUROSCI, V13, P596 STEVENS CF, 1979, MEMBRANE TRANSPORT P, P133 VERNINO S, 1992, NEURON, V8, P127, DOI 10.1016/0896-6273(92)90114-S VERNINO S, 1994, J NEUROSCI, V14, P5514 Vetter DE, 1999, NEURON, V23, P93, DOI 10.1016/S0896-6273(00)80756-4 WOODHULL AM, 1973, J GEN PHYSIOL, V61, P687, DOI 10.1085/jgp.61.6.687 ZHOU Z, 1993, PFLUG ARCH EUR J PHY, V425, P511, DOI 10.1007/BF00374879 NR 61 TC 61 Z9 70 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 117 EP 128 DI 10.1016/S0378-5955(99)00214-2 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800011 PM 10713500 ER PT J AU Rask-Andersen, H Ekvall, L Scholtz, A Schrott-Fischer, A AF Rask-Andersen, H Ekvall, L Scholtz, A Schrott-Fischer, A TI Structural/audiometric correlations in a human inner ear with noise-induced hearing loss SO HEARING RESEARCH LA English DT Article DE noise; human cochlea; transmission electron microscopy; hair cell ID SERIAL-SECTION RECONSTRUCTION; HUMAN ORGAN; ACOUSTIC OVERSTIMULATION; SPIRAL GANGLION; HAIR-CELLS; CORTI; DEGENERATION; NERVE AB A morphological analysis was performed on a human cochlea removed during skull base surgery. The patient experienced a noise-induced hearing loss following 30 years of mechanical exposure. The tissue was processed according to the block surface technique and the organ of Corti, osseous spiral lamina and spiral ganglion were analyzed at different levels. There was a circumscribed lesion approx. LO mm from the round window extending to about 13 mm. At this site, the dominant pathological feature was the loss of outer hair cells that was comprehensive in the centermost area and partial in the peripheral region of the damage. The degradation of inner hair cells was less severe with signs of cell atrophy yet with limited loss. Outer pillar cells were often collapsed leading to deformation of the acoustic ridge. The Deiters cells were often present and physically interactive with remaining nerve fibers. In the reticular lamina, surgical manipulation and dissection resulted in tears which may be attributed to a reduction of intercellular strength between cells. In the damaged area, there was a 45% loss of myelinated nerve fibers measured at the osseous spiral lamina. Pathological changes could not be observed in the spiral ganglion with certainty although the type II cells innervating the outer hair cells were often difficult to discern. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Innsbruck, Dept Otolaryngol, A-6020 Innsbruck, Austria. Univ Uppsala Hosp, Dept Otolaryngol, S-75185 Uppsala, Sweden. RP Schrott-Fischer, A (reprint author), Univ Innsbruck, Dept Otolaryngol, Anichstr 35, A-6020 Innsbruck, Austria. EM annelies.schrott.@uibk.ac.at CR ARNOLD W, 1981, ACTA OTO-LARYNGOL, V91, P399, DOI 10.3109/00016488109138521 Beagley H A, 1965, Acta Otolaryngol, V60, P479, DOI 10.3109/00016486509127031 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 Felder E, 1997, HEARING RES, V105, P183, DOI 10.1016/S0378-5955(96)00209-2 FERNANDEZ C, 1960, Laryngoscope, V70, P363 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P81, DOI 10.3109/00016488809107374 HAWKINS JE, 1976, EFFECTS NOISE HEARIN, P91 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 Lurie M. H., 1944, LARYNGOSCOPE, V54, P375 NADOL JB, 1983, LARYNGOSCOPE, V93, P599 NADOL JB, 1985, J COMP NEUROL, V237, P333, DOI 10.1002/cne.902370305 NADOL JB, 1994, HEARING RES, V81, P49, DOI 10.1016/0378-5955(94)90152-X NADOL JB, 1995, ACTA OTO-LARYNGOL, P47 NADOL JB, 1988, ACTA OTO-LARYNGOL, V105, P411, DOI 10.3109/00016488809119494 RASKANDERSEN H, 1997, AURIS NASUS LARYNX, V27, P1 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 SPOENDLIN H, 1987, ACTA OTO-LARYNGOL, P25 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 STOCKWEL.CW, 1969, ANN OTO RHINOL LARYN, V78, P1144 SUZUKA Y, 1988, ACTA OTO-LARYNGOL, P1 TETI A, 1985, ACTA OTO-LARYNGOL, P15 Tylstedt S, 1997, ACTA OTO-LARYNGOL, V117, P505, DOI 10.3109/00016489709113429 Ulfendahl M, 1996, J NEUROPHYSIOL, V76, P3850 YLIKOSKI J, 1981, ACTA OTO-LARYNGOL, V91, P161, DOI 10.3109/00016488109138495 NR 26 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 129 EP 139 DI 10.1016/S0378-5955(99)00216-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800012 PM 10713501 ER PT J AU Carlyon, RP Geurts, L Wouters, J AF Carlyon, RP Geurts, L Wouters, J TI Detection of small across-channel timing differences by cochlear implantees SO HEARING RESEARCH LA English DT Article DE cochlear implant; across-channel timing; phase effect ID AUDITORY-NERVE FIBERS; MULTICHANNEL ELECTRICAL-STIMULATION; TEMPORAL RESPONSE PATTERNS; RECOGNITION; MECHANISMS; PERCEPTION; FREQUENCY; INTERVAL; NUCLEUS; TRAINS AB Five post-lingually deafened users of the LAURA cochlear implant were presented with two trains of biphasic pulses applied concurrently to two widely separated channels. They could all discriminate between stimuli where pulses on the two channels were nearly synchronous (inter-channel delay = 0.1 ms) and those where there was a longer delay applied to one channel. All showed an asymmetry, being more sensitive when the longer delay was on either the more basal or, depending on the listener, the more apical channel. For four out of the five listeners this asymmetry could be at least partly attributed to one stimulus, with a 0.1-ms delay in either the apical (three listeners) or basal tone listener) channel, sounding markedly different from all other stimuli used in the experiment. Both the overall sensitivity of listeners and the general pattern of results survived the presentation of maskers on intermediate channels, and did not vary markedly with changes in the polarity of the pulses applied to one channel. Although the results varied substantially across listeners, it is concluded that they demonstrate a genuine sensitivity to the relative timing of stimulation applied to discrete populations of auditory nerve fibers. (C) 2000 Elsevier Science B.V. All rights reserved. C1 MRC, Cognit & Brain Sci Unit, Cambridge CB2 2EF, England. Katholieke Univ Leuven, Lab Exp ORL, B-3000 Louvain, Belgium. RP Carlyon, RP (reprint author), MRC, Cognit & Brain Sci Unit, 15 Chaucer Rd, Cambridge CB2 2EF, England. RI Carlyon, Robert/A-5387-2010; Geurts, Luc/A-4855-2015; Wouters, Jan/D-1800-2015 CR CARLYON RP, 1994, J ACOUST SOC AM, V95, P3541, DOI 10.1121/1.409971 CARLYON RP, 1994, J ACOUST SOC AM, V95, P968, DOI 10.1121/1.410013 CARTEE LA, 1997, 997 C IMPL AUD PROST Chatterjee M, 1998, J ACOUST SOC AM, V103, P2565, DOI 10.1121/1.422777 DANNENBRING GL, 1978, PERCEPT PSYCHOPHYS, V24, P369, DOI 10.3758/BF03204255 Eddington D K, 1978, Ann Otol Rhinol Laryngol, V87, P1 Ferguson G. A., 1989, STAT ANAL PSYCHOL ED GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GOLDING NL, 1995, J NEUROSCI, V15, P3138 HAFTER ER, 1983, J ACOUST SOC AM, V73, P644, DOI 10.1121/1.388956 LAWSON D, 1999, SPEECH PROCESSORS AU LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 McKay CM, 1999, J ACOUST SOC AM, V106, P998, DOI 10.1121/1.428052 McKay CM, 1996, J ACOUST SOC AM, V100, P1081, DOI 10.1121/1.416294 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PIJL S, 1995, J ACOUST SOC AM, V98, P886, DOI 10.1121/1.413514 SHANNON RV, 1983, HEARING RES, V12, P1, DOI 10.1016/0378-5955(83)90115-6 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHANNON RV, 1985, COCHLEAR IMPLANTS, P323 Shepherd RK, 1997, HEARING RES, V108, P112, DOI 10.1016/S0378-5955(97)00046-4 Shepherd RK, 1999, HEARING RES, V130, P171, DOI 10.1016/S0378-5955(99)00011-8 STRICKLAND EA, 1989, J ACOUST SOC AM, V86, P2160, DOI 10.1121/1.398476 TONG YC, 1986, J ACOUST SOC AM, V79, P1958, DOI 10.1121/1.393203 TONG YC, 1983, J ACOUST SOC AM, V74, P73, DOI 10.1121/1.389620 van Noorden L. P. A. S., 1975, THESIS EINDHOVEN U T VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 vanHoesel RJM, 1997, J ACOUST SOC AM, V102, P495, DOI 10.1121/1.419611 van Wieringen A, 1999, EAR HEARING, V20, P89, DOI 10.1097/00003446-199904000-00001 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 YOST WA, 1989, J ACOUST SOC AM, V85, P848, DOI 10.1121/1.397556 YOST WA, 1974, J ACOUST SOC AM, V55, P1299, DOI 10.1121/1.1914701 NR 32 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 140 EP 154 DI 10.1016/S0378-5955(99)00215-4 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800013 PM 10713502 ER PT J AU Roberson, DW Alosi, JA Messana, EP Cotanche, DA AF Roberson, DW Alosi, JA Messana, EP Cotanche, DA TI Effect of violation of the labyrinth on the sensory epithelium in the chick cochlea SO HEARING RESEARCH LA English DT Article DE hair cell; regeneration; intralabyrinthine infusion; gentamicin; chick ID HAIR CELL REGENERATION; INNER-EAR; IN-VIVO; ROUND WINDOW; GENTAMICIN; OTOTOXICITY; HEARING; DAMAGE AB Models in which a single large systemic dose of gentamicin is used to cause near-synchronous hair cell (HC) loss in the basal end of the chick cochlea have proven increasingly useful in the study of HC regeneration. We quantified the amount of HC death, as a percentage of the length of the basilar papilla, following single doses of 200 mg/kg and 300 mg/kg of gentamicin in 23-day-old chicks. Following 200 mg/kg of gentamicin, there was total HC loss in the basal 18.0% of the sensory epithelium and partial HC loss in the basal 26.3%. Following 300 mg/kg of gentamicin, there was total HC loss in the basal 30.5% of the epithelium and partial HC loss in the basal 40.9%. The second goal of this study was to determine whether cannula implantation in the inner ear, and infusion of bromodeoxyuridine causes HC damage. We found that creation of a fistula in the labyrinth is not associated with HC damage, but that cannula implantation can cause HC death, and can also cause potentiation of gentamicin-induced HC death. Revision of the cannula and surgical technique to ensure minimal penetration into the labyrinth almost entirely eliminated these effects. We conclude that surgical technique is critical in experimental models in which the labyrinth is violated. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Boston Childrens Hosp, Dept Otolaryngol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. RP Roberson, DW (reprint author), Boston Childrens Hosp, Dept Otolaryngol, Fegan 9,300 Longwood Ave, Boston, MA 02115 USA. CR Adler HJ, 1996, NEUROSCI LETT, V205, P17, DOI 10.1016/0304-3940(96)12367-3 BALKANY T, 1994, OTOLARYNG HEAD NECK, V111, P439 BHAVE SA, 1995, J NEUROSCI, V15, P4618 BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T Carvalho GJ, 1999, AM J OTOL, V20, P87 Code RA, 1998, HEARING RES, V126, P113, DOI 10.1016/S0378-5955(98)00158-0 COTANCHE DA, 1987, HEARING RES, V30, P197, DOI 10.1016/0378-5955(87)90136-5 Cotanche D A, 1997, Ann Otol Rhinol Laryngol Suppl, V168, P9 COTANCHE DA, 1999, IN PRESS AUDIOL NEUR, V4 Cotanche D. A., 1997, Molecular Biology of the Cell, V8, p225A DAVIES E, 1994, AM J OTOL, V15, P757 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GOKLANI S, 1999, ASS RES OT ABSTR, V22, P127 Hennig AK, 1998, J NEUROSCI, V18, P3282 Hu BH, 1999, HEARING RES, V128, P125, DOI 10.1016/S0378-5955(98)00210-X Husmann KR, 1998, HEARING RES, V125, P109, DOI 10.1016/S0378-5955(98)00137-3 Janas JD, 1995, HEARING RES, V92, P17, DOI 10.1016/0378-5955(95)00190-5 Kuntz AL, 1998, J COMP NEUROL, V399, P413 Lalwani AK, 1996, GENE THER, V3, P588 LAUTERMANN J, 1995, HEARING RES, V88, P47, DOI 10.1016/0378-5955(95)00097-N LURIE DI, 1999, ASS RES OT ABSTR, V22, P65 Muller M, 1998, HEARING RES, V120, P25, DOI 10.1016/S0378-5955(98)00049-5 Roberson DW, 1996, AUDIT NEUROSCI, V2, P195 RUBEL EW, 1995, SCIENCE, V267, P701, DOI 10.1126/science.7839150 RYALS BM, 1997, ASS RES OT ABSTR, V20, P180 Stone JS, 1996, J NEUROSCI, V16, P6157 NR 26 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 155 EP 164 DI 10.1016/S0378-5955(99)00218-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800014 PM 10713503 ER PT J AU Roberson, DW Alosi, JA Messana, EP Nedder, AP Cotanche, DA AF Roberson, DW Alosi, JA Messana, EP Nedder, AP Cotanche, DA TI Endotracheal isoflurane anesthesia for chick auditory surgery SO HEARING RESEARCH LA English DT Article DE isoflurane; anesthesia; surgery; chick ID HAIR-CELLS AB Survival surgeries upon chicks are commonly used in auditory research. Appropriate anesthesia is usually obtained with intramuscular or intraperitoneal injections of systemic agents. These techniques have several drawbacks, including delayed onset of anesthesia, difficulty in adjusting the dosage to accomodate individual animals' different responses, prolonged recovery times, and in some cases substantial mortality. We present a technique of administering inhaled isoflurane via an endotracheal tube which we have used for over a year with excellent results. With this agent, onset of deep anesthesia is very rapid, dosage can be titrated readily, overdosage is survivable, complete recovery occurs within a few minutes and mortality is rare. This technique may be valuable for other auditory scientists performing survival surgery in avian species. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Boston Childrens Hosp, Dept Otolaryngol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Cambridge, MA 02138 USA. Boston VA Med Ctr, Dept Lab Anim Med, Boston, MA USA. RP Roberson, DW (reprint author), Boston Childrens Hosp, Dept Otolaryngol, Fegan 9,300 Longwood Ave, Boston, MA 02115 USA. CR Code RA, 1998, HEARING RES, V126, P113, DOI 10.1016/S0378-5955(98)00158-0 CORNICK JL, 1992, J AM VET MED ASSOC, V200, P1661 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 GREENLEES KJ, 1990, AM J VET RES, V51, P757 Husmann KR, 1998, HEARING RES, V125, P109, DOI 10.1016/S0378-5955(98)00137-3 KILANDER K, 1992, PHYSIOL BEHAV, V51, P657, DOI 10.1016/0031-9384(92)90193-6 LURIE DI, 1999, ASS RES OT ST PET FL Roberson DW, 1996, AUDIT NEUROSCI, V2, P195 NR 8 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 165 EP 168 DI 10.1016/S0378-5955(99)00219-1 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800015 PM 10713504 ER PT J AU Dammeijer, PFM van Mameren, H van Dijk, P Moorman, AFM Habets, P Manni, JJ Drukker, J AF Dammeijer, PFM van Mameren, H van Dijk, P Moorman, AFM Habets, P Manni, JJ Drukker, J TI Stapedius muscle fibre composition in the rat SO HEARING RESEARCH LA English DT Article DE stapedius muscle; myosin ATPase lability; myosin heavy chain; middle ear muscle; rat ID MYOSIN HEAVY-CHAIN; EXTENSOR DIGITORUM LONGUS; RABBIT TIBIALIS ANTERIOR; SKELETAL-MUSCLE; FIBER TYPES; SOUND-TRANSMISSION; MASSETER MUSCLE; SINGLE FIBERS; ATPASE; IDENTIFICATION AB The stapedius muscle (SM) is supposed to prevent cochlear damage by noise. Consequently functional demands are the ability of fast contraction with long endurance. This implies the presence of a large fraction of myosin type II fibres with an appreciable oxidative capacity. We determined the myosin composition of SM fibres using consecutive complete SM. cross-sections (6 week old rats) which were processed by enzyme histochemistry (EHC) to determine acid/alkali lability of myofibrillar adenosine triphosphatase (mATPase) or by immunohistochemistry (IHC) using myosin heavy chain (MyHC) antibodies. Method accuracy was determined in co-processed extensor digitorum longus (EDL). Four hundred SM and 200 EDL fibres were assigned to mATPase type I, IIA, IIB, IIX or 'miscellaneous' ('Misc') categories. Per mATPase category the fibres were attributed to groups with specific MyHC composition. In the EDL, mATPase type I and IIB fibres expressed only MyHC I and IIB respectively, whereas about 10% of the type IIA and 40% of the type IIX fibres expressed more than one MyHC. Thus IHC detects amounts of myosin isoforms which are not detected by EHC. The mATPase IIX category criterion leaves the possibility that this category contains fibres with myosin type IIA and/or IIB in larger amounts. The criteria of the mATPase categories type I, IIA or IIB preclude assignment to these categories of fibres which also contain other myosin isoforms in larger amounts. Such fibres were classified in one of the mATPase 'Misc' categories. Thus in the EDL the capability of the EHC criteria to select 'pure' fibres in terms of myosin differs per mATPase category. None of the SM fibres were assigned to the mATPase type I or IIB categories, about 25% to the type IIA, 60% to type IIX and 15% (including most fibres which expressed MyHC I) to a 'Misc' category. All SM fibres expressed two or more MyHC isoforms, MyHC IIB occurring in all fibres and substantial amounts of MyHC IIA and/or IIX in most. These findings confirm the hypothesis that such fibres have the capacity to contract fast and have the better fatigue resistance. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Maastricht, Dept Anat Embryol, NL-6200 MD Maastricht, Netherlands. Univ Hosp Maastricht, Dept Otorhinolaryngol Head & Neck Surg, Maastricht, Netherlands. Univ Amsterdam, Dept Anat Embryol, Amsterdam, Netherlands. RP van Mameren, H (reprint author), Univ Maastricht, Dept Anat Embryol, NL-6200 MD Maastricht, Netherlands. CR BORG E, 1984, ACOUSTIC REFLEX BASI, P50 BREDMAN JJ, 1991, HISTOCHEM J, V23, P160, DOI 10.1007/BF01046587 BREDMAN JJ, 1992, HISTOCHEM J, V24, P260, DOI 10.1007/BF01046840 BROOKE MH, 1970, ARCH NEUROL-CHICAGO, V23, P369 BURGENER J, 1980, ANAT EMBRYOL, V161, P65, DOI 10.1007/BF00304669 BUTLERBROWNE GS, 1988, MUSCLE NERVE, V11, P610, DOI 10.1002/mus.880110614 DJUPESLAND G, 1975, HDB CLIN IMPEDANCE A, P85 FLETCHER JL, 1960, J ACOUST SOC AM, V32, P401, DOI 10.1121/1.1908079 GORZA L, 1990, J HISTOCHEM CYTOCHEM, V38, P257 GUTH L, 1970, EXP NEUROL, V28, P365, DOI 10.1016/0014-4886(70)90244-X HILDING D A, 1961, Trans Am Acad Ophthalmol Otolaryngol, V65, P297 LARSSON L, 1993, J PHYSIOL-LONDON, V472, P595 LEFAUCHEUR L, 1995, DEV DYNAM, V203, P27 LEXELL J, 1994, J ANAT, V185, P95 LODDER MAN, 1993, J MUSCLE RES CELL M, V14, P47, DOI 10.1007/BF00132179 LYON MJ, 1982, ACTA OTO-LARYNGOL, V94, P99, DOI 10.3109/00016488209128894 MOORMAN AFM, 1984, CELL DIFFER DEV, V14, P113, DOI 10.1016/0045-6039(84)90036-8 OGILVIE RW, 1990, STAIN TECHNOL, V65, P231 PEREIRA JAAS, 1995, HISTOCHEM J, V27, P715 PETER JB, 1972, BIOCHEMISTRY-US, V11, P2627, DOI 10.1021/bi00764a013 PULLEN AH, 1977, J ANAT, V123, P467 Rivero JLL, 1998, J MUSCLE RES CELL M, V19, P733, DOI 10.1023/A:1005482816442 Sant'ana Pereira J A, 1995, J Muscle Res Cell Motil, V16, P21 SCHIAFFINO S, 1989, J MUSCLE RES CELL M, V10, P197, DOI 10.1007/BF01739810 SCHMALBRUCH H, 1985, HDB MICROSCOPIC ANAT, V2, P217 STARON RS, 1993, HISTOCHEMISTRY, V100, P149, DOI 10.1007/BF00572901 STARON RS, 1987, PFLUG ARCH EUR J PHY, V409, P67, DOI 10.1007/BF00584751 TEIG E, 1973, ACTA PHYSIOL SCAND, V88, P382, DOI 10.1111/j.1748-1716.1973.tb05467.x VANBUREN P, 1995, CIRC RES, V77, P439 VANDENBERGE H, 1990, HEARING RES, V48, P209, DOI 10.1016/0378-5955(90)90061-S VANDENBERGE H, 1989, J ANAT, V166, P157 VANDENBERGE H, 1990, J ANAT, V170, P99 VEGETTI A, 1982, J ANAT, V135, P333 WHALEN RG, 1981, NATURE, V292, P805, DOI 10.1038/292805a0 ZAKRISSON JE, 1975, ACTA OTO-LARYNGOL, V79, P1, DOI 10.3109/00016487509124648 NR 35 TC 9 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 169 EP 179 DI 10.1016/S0378-5955(99)00220-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800016 PM 10713505 ER PT J AU Todd, NPM Cody, FWJ Banks, JR AF Todd, NPM Cody, FWJ Banks, JR TI A saccular origin of frequency tuning in myogenic vestibular evoked potentials?: implications for human responses to loud sounds SO HEARING RESEARCH LA English DT Article DE sacculus; vestibule-spinal tract; sternocleidomastoid; acoustic sensitivity; frequency tuning ID INTENSITY PERCEPTION; HEARING-LOSS; GUINEA-PIG; TRAPEZIUS; COCHLEAR; NERVE; DISCRIMINATION; SENSITIVITY; SELECTIVITY; INNERVATION AB Previous research has indicated that an early component of click-evoked myogenic potentials in the sternocleidomastoid muscle is vestibularly mediated, since it can be obtained in subjects with loss of cochlear function, but is absent in subjects with loss of vestibular function (Colebatch et al., 1994). We report here the results of an experiment to investigate whether this response shows any tuning properties. In a sample of 11 subjects, we obtained acoustically evoked EMG from the sternocleidomastoid muscle in response to 110 dB SPL 10 ms tone pips with frequencies of 100 Hz, 200 Hz, 400 Hz, 800 Bz, 1600 Hz and 3200 Hz. The results of this experiment indicate that this response does indeed have a well-defined frequency tuning which may be modelled as a resonance with a maximum response at frequencies between 300-350 Hz. The possible saccular origin of the tuning response and the consequences that this may have in human responses to loud sounds is discussed. Also discussed are the consequences of particular electrode arrangements in relation to the innervation and anatomy of sternocleidomastoid. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Manchester, Dept Psychol, Manchester M13 9PT, Lancs, England. Univ Manchester, Dept Biol Sci, Manchester M13 9PT, Lancs, England. RP Todd, NPM (reprint author), Univ Manchester, Dept Psychol, Manchester M13 9PT, Lancs, England. CR Basmajian JV, 1985, MUSCLES ALIVE THEIR BICKFORD RG, 1964, ANN NY ACAD SCI, V112, P204, DOI 10.1111/j.1749-6632.1964.tb26749.x BURIAN M, 1989, ARCH OTO-RHINO-LARYN, V246, P238, DOI 10.1007/BF00463563 CAZALS Y, 1983, ACTA OTO-LARYNGOL, V95, P211, DOI 10.3109/00016488309130937 CAZALS Y, 1983, HEARING RES, V10, P263, DOI 10.1016/0378-5955(83)90091-6 CAZALS Y, 1982, BRAIN RES, V231, P197, DOI 10.1016/0006-8993(82)90019-1 COLEBATCH JG, 1994, J NEUROL NEUROSUR PS, V57, P190, DOI 10.1136/jnnp.57.2.190 DIBBLE K, 1995, J AUDIO ENG SOC, V43, P251 DILAZZARO V, 1995, EXP BRAIN RES, V102, P474 Donald John A., 1998, P407 Fant G., 1960, ACOUSTIC THEORY SPEE Fay R. R., 1988, HEARING VERTEBRATES Ferber-Viart C, 1999, ACTA OTO-LARYNGOL, V119, P6 FerberViart C, 1997, ACTA OTO-LARYNGOL, V117, P472, DOI 10.3109/00016489709113424 FITZGERALD MJT, 1982, J ANAT, V134, P471 FLORENTINE M, 1993, J ACOUST SOC AM, V94, P2575, DOI 10.1121/1.407369 HOUTSMA AJM, 1980, J ACOUST SOC AM, V68, P807, DOI 10.1121/1.384819 Kalmijn A.J., 1989, P187 KATAFUCHI T, 1987, BRAIN RES, V400, P62, DOI 10.1016/0006-8993(87)90653-6 KRAUSE HR, 1991, J CRANIO MAXILL SURG, V19, P87, DOI 10.1016/S1010-5182(05)80613-4 MCCUE MP, 1995, J NEUROPHYSIOL, V74, P1563 MOFFAT AJM, 1976, J COMP PHYSIOL, V105, P1 Moore B. C. J., 1989, INTRO PSYCHOL HEARIN PITCHER TJ, 1986, BEHAV TELEOST FISH POPPER A, 1982, TRENDS NEUROSCI AUG, P276 ROBERTSON DD, 1995, J OTOLARYNGOL, V24, P3 Schellart Nico A.M., 1998, P283 SUNDBERG R, 1992, MUSIC PERCEPT, V9, P261 Todd NPM, 2000, J ACOUST SOC AM, V107, P496, DOI 10.1121/1.428317 TODD NPM, 1993, MUSIC PERCEPT, V10, P379 TOWNSEND GL, 1971, ANN OTO RHINOL LARYN, V80, P121 Uchino Y, 1997, J NEUROPHYSIOL, V77, P3003 ULLAH M, 1986, J ANAT, V145, P97 WARD LM, 1993, J ACOUST SOC AM, V94, P2587, DOI 10.1121/1.407370 WIER CC, 1977, J ACOUST SOC AM, V61, P178, DOI 10.1121/1.381251 WILSON V, 1981, HDB PHYSL 1, V2, P677 WIT HP, 1984, J ACOUST SOC AM, V75, P202, DOI 10.1121/1.390396 Yates BJ, 1996, ANN NY ACAD SCI, V781, P458, DOI 10.1111/j.1749-6632.1996.tb15720.x YOUNG ED, 1977, ACTA OTO-LARYNGOL, V84, P352, DOI 10.3109/00016487709123977 NR 39 TC 72 Z9 75 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 180 EP 188 DI 10.1016/S0378-5955(99)00222-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800017 PM 10713506 ER PT J AU Lyon, MJ Payman, RN AF Lyon, MJ Payman, RN TI Comparison of the vascular innervation of the rat cochlea and vestibular system SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 22nd Midwinter Meeting of the Association-for-Research-in-Otolaryngology CY FEB 13-18, 1999 CL ST PETERSBURG, FL SP Assoc Res Otolaryngol DE immunohistochemistry; vestibular; cochlear; microcirculation; blood flow ID GENE-RELATED PEPTIDE; NITRIC-OXIDE SYNTHASE; SPIRAL MODIOLAR ARTERY; BLOOD-FLOW; GUINEA-PIG; SUBSTANCE-P; CEREBRAL-ARTERIES; NEUROPEPTIDE-Y; ADRENERGIC-INNERVATION; NERVE FIBERS AB In order to gain a better understanding of the neuronal and local control of inner ear blood flow, the Vascular innervation to the rat cochlea and vestibular system was examined. Specimens were removed in tote beginning at the basilar artery extending to the anterior inferior cerebellar artery, labyrinthine artery, common cochlear artery, modiolar artery and anterior vestibular artery. When possible the Vessels were dissected in continuity through the cribrose area. The vestibular endorgans were also removed. Specimens were examined using immunohistochemical techniques for the presence of vasoactive intestinal peptide, neuronal nitric oxide synthase, neuropeptide-Y, substance P and calcitonin gene related peptide. Results show that the vasculature to the cochlea and vestibular portion of the inner ear receive similar types of nonadrenergic innervation, that within the vestibular endorgans, only CGRP and SP were found in the neuroepithelium or in association with vessels, and that within the vestibular system, the majority of the vascular innervation appears to stop at or near the cribrose area. In the cochlea however, it extends to include the radiating arterioles. These findings suggest that cochlear blood flow is under finer control and that neuronally induced changes in blood flow may have a more global effect in the vestibular periphery. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Hlth Sci Ctr, Dept Otolaryngol, Syracuse, NY 13210 USA. RP Lyon, MJ (reprint author), SUNY Hlth Sci Ctr, Dept Otolaryngol, 750 E Adams St, Syracuse, NY 13210 USA. EM lyonm@hscsyr.edu CR Axelsson A, 1988, PHYSL EAR, P295 BALOH RW, 1990, CLIN NEUROPHYSIOL, P220 BECKMAN JS, 1993, BIOCHEM SOC T, V21, P330 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 BREDT DS, 1992, NEURON, V8, P3, DOI 10.1016/0896-6273(92)90104-L Burgio DL, 1997, ACTA OTO-LARYNGOL, V117, P819, DOI 10.3109/00016489709114207 BURNSTOCK G, 1987, J CARDIOVASC PHARM S, V12, pS74 BURNSTOCK G, 1990, BIOL EFFECTS EXTRACE, P1 CARLISLE L, 1990, HEARING RES, V43, P107, DOI 10.1016/0378-5955(90)90219-F CARRASCO VN, 1990, ARCH OTOLARYNGOL, V116, P411 CHANGEUX JP, 1992, ANN NY ACAD SCI, V657, P361, DOI 10.1111/j.1749-6632.1992.tb22783.x DENSERT O, 1974, ACTA OTO-LARYNGOL, V78, P345, DOI 10.3109/00016487409126365 DEVOR M, 1989, NEUROSCI LETT, V103, P203, DOI 10.1016/0304-3940(89)90576-4 DEY RD, 1993, NEUROSCIENCE, V54, P839, DOI 10.1016/0306-4522(93)90578-4 EDVINSSON L, 1990, BRIT J PHARMACOL, V100, P312 EDVINSSON L, 1984, J AUTON PHARMACOL, V4, P193, DOI 10.1111/j.1474-8673.1984.tb00096.x EDVINSSON L, 1985, ACTA PHYSIOL SCAND, V125, P33, DOI 10.1111/j.1748-1716.1985.tb07690.x EULER U. S., 1931, JOUR PHYSIOL, V72, P74 Fessenden JD, 1998, HEARING RES, V118, P168, DOI 10.1016/S0378-5955(98)00027-6 Fessenden JD, 1999, J COMP NEUROL, V404, P52 FORSSMANN WG, 1998, ANN NY ACAD SCI, V865 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 Gosepath K, 1997, BRAIN RES, V747, P26, DOI 10.1016/S0006-8993(96)01149-3 Gruber DD, 1998, HEARING RES, V119, P113, DOI 10.1016/S0378-5955(98)00036-7 GUSSEN R, 1982, ARCH OTOLARYNGOL, V108, P544 HATA R, 1993, NEUROSCIENCE, V56, P423, DOI 10.1016/0306-4522(93)90343-E Hess A, 1998, BRAIN RES, V813, P97, DOI 10.1016/S0006-8993(98)00997-4 HILLERDAL M, 1989, ACTA OTO-LARYNGOL, V108, P94, DOI 10.3109/00016488909107398 HILLERDAL M, 1991, HEARING RES, V52, P321, DOI 10.1016/0378-5955(91)90022-2 HOZAWA K, 1990, ACTA OTO-LARYNGOL, V110, P46, DOI 10.3109/00016489009122514 HOZAWA K, 1989, ACTA OTO-LARYNGOL, V107, P171, DOI 10.3109/00016488909127496 IADECOLA C, 1993, BRAIN RES, V606, P148, DOI 10.1016/0006-8993(93)91583-E JANSEN I, 1990, REGUL PEPTIDES, V31, P167, DOI 10.1016/0167-0115(90)90003-F KITAMURA Y, 1993, INVEST OPHTH VIS SCI, V34, P2859 Kitanishi T, 1998, ACTA OTO-LARYNGOL, P52 KOBARI M, 1993, BRAIN RES BULL, V31, P443, DOI 10.1016/0361-9230(93)90107-M LU SM, 1987, HEARING RES, V31, P137, DOI 10.1016/0378-5955(87)90119-5 MCCUE MP, 1994, J NEUROSCI, V14, P6058 MCLAREN GM, 1993, HEARING RES, V71, P183, DOI 10.1016/0378-5955(93)90033-W Moll-Kaufmann C, 1998, J HEPATOL, V28, P1031, DOI 10.1016/S0168-8278(98)80353-X NAKAI Y, 1990, MENIERES DIS, P35 NEW HV, 1986, NATURE, V323, P809, DOI 10.1038/323809a0 OHLSEN KA, 1991, CIRC RES, V69, P509 OHLSEN KA, 1992, HEARING RES, V58, P19, DOI 10.1016/0378-5955(92)90004-7 OTSUKA M, 1993, PHYSIOL REV, V73, P229 PAYMAN R, 1993, ANN OTO RHINOL LARYN, V102, P893 QUIRK WS, 1994, AM J OTOL, V15, P56 REN TY, 1993, ACTA OTO-LARYNGOL, V113, P146, DOI 10.3109/00016489309135783 REN TY, 1993, ANN OTO RHINOL LARYN, V102, P378 ROSS MD, 1971, ACTA OTO-LARYNGOL, P1 Scarfone E, 1996, NEUROSCIENCE, V75, P587, DOI 10.1016/0306-4522(96)00243-6 Schickinger B, 1996, ORL J OTO-RHINO-LARY, V58, P121 SHAMBOUGH GE, 1906, ARCH OTOLARYNGOL, V35, P11 SHIBAMORI Y, 1994, BRAIN RES, V646, P223, DOI 10.1016/0006-8993(94)90082-5 Spoendlin H, 1966, Acta Otolaryngol, V61, P423 TERAYAMA Y, 1973, ACTA OTO-LARYNGOL, V76, P244, DOI 10.3109/00016487309121505 TERAYAMA Y, 1966, ANN OTO RHINOL LARYN, V75, P69 TIPPINS JR, 1986, J HYPERTENS, V4, pS102 UDDMAN R, 1988, NONADRENERGIC INNERV, V2, P213 UDDMAN R, 1982, ARCH OTO-RHINO-LARYN, V236, P7, DOI 10.1007/BF00464052 UDDMAN R, 1989, Cerebrovascular and Brain Metabolism Reviews, V1, P230 USAMI SI, 1991, ACTA OTO-LARYNGOL, P166 VASS Z, 1995, HEARING RES, V89, P86, DOI 10.1016/0378-5955(95)00127-4 Vass Z, 1997, NEUROSCIENCE, V79, P605, DOI 10.1016/S0306-4522(96)00641-0 Vass Z, 1996, HEARING RES, V100, P114, DOI 10.1016/0378-5955(96)00102-5 WACKYM PA, 1991, OTOLARYNG HEAD NECK, V105, P493 WANAMAKER HH, 1990, OTOLARYNG HEAD NECK, V103, P586 WESTFALL TC, 1987, J CARDIOVASC PHARM, V10, P716, DOI 10.1097/00005344-198712000-00016 YLIKOSKI J, 1979, ARCH OTOLARYNGOL, V105, P726 NR 69 TC 8 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 189 EP 198 DI 10.1016/S0378-5955(00)00004-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800018 PM 10713507 ER PT J AU Gates, GA Schmid, P Kujawa, SG Nam, BH D'Agostino, R AF Gates, GA Schmid, P Kujawa, SG Nam, BH D'Agostino, R TI Longitudinal threshold changes in older men with audiometric notches SO HEARING RESEARCH LA English DT Article DE hearing; noise damage; aging ID HEARING-LOSS; NOISE; COHORT AB Age-related hearing loss (presbycusis) is a multifactorial process that results chiefly from the accumulating effects of noise damage and aging on the cochlea. Noise damage is typically evidenced clinically by a discrete elevation (notch) of the auditory thresholds in the 3-6 kHz region of the audiogram whereas aging affects the highest frequencies first. To determine whether the presence of such high-frequency notches influences auditory aging, we examined the 15 year change in audiometric thresholds in 203 men from the Framingham Heart Study cohort. The mean age at the first hearing test was 64 years (range 58-80). Occupational and recreational noise exposure over the 15 years was assumed to be minimal due to the age of the subjects. The presence or absence of a notch was determined using a piecewise linear/parabolic curve fitting strategy. A discrete elevation of the pure-tone thresholds of 15-34 dB in the 3-6 kHz region was deemed a small notch (N1), and elevations of 35 dB or greater were deemed large notches (N2). Absence of a notch (NO) was encoded those ears with < 15 dB elevation in the 3-6 kHz region. The presence and absence of notches correlated with the subjects' history of noise exposure. The 15 year pattern of change in age-adjusted pure-tone thresholds varied significantly by notch category. There was less change over time in the notch frequencies (3-6 kHz) and significantly greater change in the adjacent frequency of 2 kHz in the N2 group as compared to the NO and N1 groups. The adjacent frequency of 8 kHz showed a significant, but smaller, change in the N1 group as compared to the NO and N2 groups. The change at 2 kHz was independent of the starting hearing level at E15, whereas the changes at 4-8 kHz were influenced by the hearing level at E15. These data suggest that the noise-damaged ear does not 'age' at the same rate as the non-noise damaged ear. The finding of increased loss at 2 kHz suggests that the effects of noise damage may continue long after the noise exposure has stopped. The mechanism for this finding is unknown but presumably results from prior noise-induced damage to the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Washington, Sch Med, Dept Otolaryngol Head & Neck Surg, Seattle, WA USA. Univ Washington, Dept Appl Math, Seattle, WA USA. Boston Univ, Dept Math, Boston, MA 02215 USA. RP Gates, GA (reprint author), Univ Washington, Virginia Merrill Bloedel Hearing Res Ctr, Seattle, WA 98195 USA. CR ACOM (American College of Occupational Medicine), 1989, J OCCUP MED, V31, P996 HALL WH, 1990, JAMA-J AM MED ASSOC, V263, P3185 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 CLARK WW, 1978, ANN OTO RHINOL LARYN, V87, P1 Committee on Hearing Bioacoustics and Biomechanics (CHABA), 1988, J ACOUST SOC AM, V83, P859 COOPER JC, 1991, EAR HEARING, V12, P304, DOI 10.1097/00003446-199110000-00002 COOPER JC, 1976, ARCH OTOLARYNGOL, V102, P148 Cruickshanks KJ, 1998, JAMA-J AM MED ASSOC, V279, P1715, DOI 10.1001/jama.279.21.1715 Dawber TR, 1980, THE FRAMINGHAM STUDY DOBIE RA, 1992, EAR HEARING, V13, P19, DOI 10.1097/00003446-199202000-00006 GALLO R, 1964, Am Ind Hyg Assoc J, V25, P237 GATES GA, 1993, ARCH OTOLARYNGOL, P119 GATES GA, 1999, IN PRESS J OCCUP HEA GRAVENDEEL DW, 1958, ARCH OTOLARYNGOL, V69, P714 *INT ORG STAND, 1990, ISO1999 INT ORG STAN Lee FS, 1998, OTOLARYNG HEAD NECK, V118, P221, DOI 10.1016/S0194-5998(98)80020-X Mills JH, 1997, J ACOUST SOC AM, V101, P1681, DOI 10.1121/1.418152 MOSCICKI EK, 1985, EAR HEARING, V6, P184, DOI 10.1097/00003446-198507000-00003 PIERSON LL, 1994, AM J OTOLARYNG, V15, P37, DOI 10.1016/0196-0709(94)90038-8 Spicer SS, 1998, ANAT REC, V251, P97, DOI 10.1002/(SICI)1097-0185(199805)251:1<97::AID-AR15>3.0.CO;2-6 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 WARD WD, 1961, J AUD RES, V1, P325 NR 22 TC 56 Z9 67 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 220 EP 228 DI 10.1016/S0378-5955(99)00223-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800020 PM 10713509 ER PT J AU Edds-Walton, PL Popper, AN AF Edds-Walton, PL Popper, AN TI Dendritic arbors on the saccule and lagena in the ear of the goldfish, Carassius auratus SO HEARING RESEARCH LA English DT Article DE auditory; cobalt label; fish; innervation ID ASTRONOTUS-OCELLATUS; FISH EAR; CELL AB The ear of the goldfish (Carassius auratus) contains three otolithic endorgans: the saccule, lagena, and utricle. The saccule has an auditory function in most teleost fishes for whom data are available, and there is evidence that the lagena is also an auditory endorgan in the goldfish. This study was conducted to compare the innervation of the saccule and the lagena to one another and to previously published data from goldfish and other species. We placed cobaltous-lysine in saccular and lagenar nerves in vivo and permitted uptake over 18-24 h. A total of 59 saccular and 59 lagenar dendritic arbors were labeled in 10 fishes. Our data indicate that arbors on the saccule and lagena have similar morphologies, but differ in relative size. Saccular arbors tend to be smaller than lagenar arbors, with median arbor widths of 50 mu m on the saccule and 74 mu m on the lagena. Fiber diameters on the two endorgans are similar. A regional analysis of the saccule indicated that a wide range of arbor sizes are found along the rostral-caudal axis, with larger arbors more common caudally. Our data do not support the presence of two distinct categories of saccular afferents with nonoverlapping distributions. Moderate arbor widths (50-99 mu m) were most common in all regions of the lagena. Maximum arbor width and hair cell density do not appear to be correlated with one another on either the saccule or the lagena. Comparisons with published data from goldfish and oscar revealed similarities and differences that may be attributable to variations in label uptake or transport as well as potential species differences. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Maryland, Dept Biol, College Pk, MD 20742 USA. Loyola Univ, Parmly Hearing Inst, Chicago, IL 60626 USA. RP Edds-Walton, PL (reprint author), Univ Calif Riverside, Dept Biol, Riverside, CA 92521 USA. CR EDDS PL, 1990, ASS RES OT ABSTR Edds-Walton PL, 1999, J COMP NEUROL, V411, P212, DOI 10.1002/(SICI)1096-9861(19990823)411:2<212::AID-CNE4>3.0.CO;2-X FAY RR, 1984, SCIENCE, V225, P951, DOI 10.1126/science.6474161 FAY RR, 1979, COMP BIOCHEM PHYS A, V62, P377, DOI 10.1016/0300-9629(79)90074-4 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 KOPPL C, 1988, HEARING RES, V32, P111, DOI 10.1016/0378-5955(88)90082-2 MCCORMICK CA, 1994, BRAIN BEHAV EVOLUT, V43, P189, DOI 10.1159/000113634 PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 POPPER AN, 1981, J COMP NEUROL, V200, P357, DOI 10.1002/cne.902000306 POPPER AN, 1990, HEARING RES, V46, P211, DOI 10.1016/0378-5955(90)90003-8 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1993, BRAIN BEHAV EVOLUT, V41, P14, DOI 10.1159/000113821 POPPER AN, 1982, AM ZOOL, V22, P311 POPPER AN, 1983, FISH NEUROBIOLOGY BE PRESSON JC, 1993, CELL TISSUE RES, V274, P97, DOI 10.1007/BF00327990 PRESSON JC, 1992, BRAIN BEHAV EVOLUT, V39, P187 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 YAN HY, 1992, J COMP PHYSIOL A, V171, P105 NR 18 TC 6 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 2000 VL 141 IS 1-2 BP 229 EP 242 DI 10.1016/S0378-5955(99)00207-5 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 294YE UT WOS:000085937800021 PM 10713510 ER PT J AU Takeda, T Takeda, S Kitano, H Okada, T Kakigi, A AF Takeda, T Takeda, S Kitano, H Okada, T Kakigi, A TI Endolymphatic hydrops induced by chronic administration of vasopressin SO HEARING RESEARCH LA English DT Article DE vasopressin; endolymphatic hydrops; Meniere's disease ID INNER-EAR; ADENYLATE-CYCLASE; LOCALIZATION; CORTISOL; HORMONE; STRESS; MOUSE AB Recently, many lines of evidence have supported the possibilities that vasopressin (VP) is closely linked to the formation of endolymphatic hydrops in Menieres disease. In the present study, it was examined whether or not the chronic administration of VP might induce endolymphatic hydrops. For this purpose, histological studies and VP radioimmunoassay were independently performed in 20 and 40 guinea pigs, respectively. The degree of hydrops was quantitatively assessed by the increase ratio (IR) of the scala media area in the mid-modiolar sections of the cochlea. The IR was defined by the following equation: 100 x (A-B)/B (A: the cross-sectional area of the bulging scala media; B: the no-bulging scala media, enclosed by an idealized straight Reissner's membrane), VP was administered at the rates of 200 mu U/kg/min, 400 mu U/kg/min and 1000 mu U/kg/min for 1 week via the osmotic mini-pump. The IR of the total of the apical, second, third and basal turns (means +/- S.D.s) were 4.4 +/- 0.7, 10.4 +/- 1.8, 17.1 +/- 7.9 (n = 10 ears, each) in respective doses of VP. Comparing with that of the control animals (5.2 +/- 1.7, n = 10 ears), the area increased significantly in the VP dosage of 400 and 1000 mu U/kg/min (Bonferroni's method. P < 0.05). Plasma VP concentrations produced by the VP administration in these dosages were 2.2 +/- 0.4, 3.5 +/- 0.8 and 14.0 +/- 3.9 (il = 10, each) pg/ml. Although 3.5 pg/ml is the upper limit of plasma VP concentration in normal human subjects, 14.0 pg/ml was almost the same concentration as those observed in the acute phase of Meniere's disease (Takeda et al., 1995). Therefore, the formation of endolymphatic hydrops in cases of Meniere's disease might be caused by high concentrations of plasma VP. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Kochi Med Sch, Dept Otolaryngol, Kochi 7838505, Japan. Shiga Univ Med Sci, Dept Otolaryngol, Kochi, Japan. Kochi Med Sch, Dept Anat, Kochi 7838505, Japan. RP Takeda, T (reprint author), Kochi Med Sch, Dept Otolaryngol, Kochi 7838505, Japan. CR AHLSTROM P, 1975, LARYNGOSCOPE, V85, P1241, DOI 10.1288/00005537-197507000-00016 ANNIKO M, 1981, HEARING RES, V4, P11, DOI 10.1016/0378-5955(81)90033-2 Aperia A, 1996, KIDNEY INT, V49, P1743, DOI 10.1038/ki.1996.259 BAGGERSJOBACK D, 1980, ARCH OTO-RHINO-LARYN, V228, P217, DOI 10.1007/BF00454231 Beitz E, 1999, HEARING RES, V132, P76, DOI 10.1016/S0378-5955(99)00036-2 BERNARD C, 1986, J PHYSIOL-LONDON, V371, P17 DUGUE B, 1993, SCAND J CLIN LAB INV, V53, P555, DOI 10.3109/00365519309092553 Hallpike C. S., 1938, J LARYNG, V53, P625, DOI 10.1017/S0022215100003947 Kitano H, 1997, NEUROREPORT, V8, P2289, DOI 10.1097/00001756-199707070-00038 MALARKEY WB, 1995, PSYCHONEUROENDOCRINO, V20, P499, DOI 10.1016/0306-4530(94)00077-N MEES K, 1984, ARCH OTO-RHINO-LARYN, V240, P55, DOI 10.1007/BF00464345 OUDAR O, 1991, EUR ARCH OTO-RHINO-L, V248, P386, DOI 10.1007/BF01463559 Sawada S, 1997, Acta Otolaryngol Suppl, V528, P109 STERKERS O, 1988, PHYSIOL REV, V68, P1083 Takeda T, 1995, Acta Otolaryngol Suppl, V519, P219 Yamakawa K, 1938, J OTORHINOLARYNGOL S, V4, P2310 ZAJIC G, 1983, HEARING RES, V10, P249, DOI 10.1016/0378-5955(83)90090-4 ZENNER HP, 1979, ARCH OTO-RHINO-LARYN, V222, P275, DOI 10.1007/BF01261174 NR 18 TC 69 Z9 76 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 1 EP 6 DI 10.1016/S0378-5955(99)00180-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500001 PM 10675630 ER PT J AU Zhang, JS Kaltenbach, JA AF Zhang, JS Kaltenbach, JA TI Modulation of spontaneous activity by acetylcholine receptors in the rat dorsal cochlear nucleus in vivo SO HEARING RESEARCH LA English DT Article DE dorsal cochlear nucleus; spontaneous activity; carbachol; atropine; muscarinic receptors; rat; cholinergic ID COMPLEX-SPIKING NEURONS; HIGH-INTENSITY SOUND; DISCHARGE CHARACTERISTICS; FUSIFORM CELLS; CAT; EXPOSURE; PHYSIOLOGY; MORPHOLOGY; INCREASES; CARTWHEEL AB In vitro studies have implicated muscarinic acetylcholine receptors (mAChRs) in the modulation of spontaneous activity (SA) of neurons in the rat dorsal cochlear nucleus (DCN) (Chen et al., 1994,1998). Early studies suggest that cholinergic pathways also modulate SA in vivo, but these effects have not been investigated pharmacologically. The purpose of the present study was to determine whether multiunit SA can be modulated in vivo by application of cholinergic agents to the surface of the DCN. Sprague Dawley rats were used in the current experiment. The influence of cholinergic activation on SA was tested by applying carbachol (5-500 mu M) to the DCN surface while recording multiunit SA at a depth of 256 mu m. Out of a total of 32 sites tested, all but 2 (94%) showed well-defined responses to carbachol, characterized by suppression, activation or a combination of both (two-component responses). The most common responses were pure suppression and suppression accompanied by transient activation. Both the proportion of sites showing suppressive responses and the magnitude of suppression averaged across sites increased with dose. Although the proportion of sites showing pure activation in response to carbachol decreased with dose, there was no clear trend in the magnitude of activation with dose. The suppressive responses to high doses of carbachol were blocked by pre-application of atropine. These results extend previous work by suggesting that muscarinic receptors play an important role in the modulation of SA in vivo. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Wayne State Univ, Sch Med, Dept Otolaryngol, Detroit, MI 48201 USA. RP Zhang, JS (reprint author), Wayne State Univ, Sch Med, Dept Otolaryngol, 5E-UHC,4201 St Antoine, Detroit, MI 48201 USA. EM jinzhang@med.wayne.edu CR BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 CASPARY D, 1972, EXP NEUROL, V37, P131, DOI 10.1016/0014-4886(72)90231-2 CASPARY DM, 1983, EXP NEUROL, V82, P491, DOI 10.1016/0014-4886(83)90419-3 CHEN KJ, 1994, HEARING RES, V77, P168 Chen KJ, 1998, BRAIN RES, V783, P219, DOI 10.1016/S0006-8993(97)01348-6 COMIS SD, 1974, NEUROPHARMACOLOGY, V13, P633, DOI 10.1016/0028-3908(74)90053-7 Davis KA, 1996, J NEUROPHYSIOL, V76, P3012 Davis KA, 1996, J NEUROPHYSIOL, V75, P1411 Gdowski GT, 1997, HEARING RES, V105, P85, DOI 10.1016/S0378-5955(96)00196-7 GODFREY DA, 1971, THESIS HARVARD U CAM Godfrey DA, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P139, DOI 10.1007/978-1-4419-8712-9_13 GODFREY DA, 1990, HEARING RES, V49, P259, DOI 10.1016/0378-5955(90)90108-2 GODFREY DA, 1993, NATO ADV SCI INST SE, V239, P267 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 Kaltenbach JA, 1998, HEARING RES, V124, P78, DOI 10.1016/S0378-5955(98)00119-1 Kaltenbach JA, 1996, AUDIT NEUROSCI, V3, P57 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 Manis PB, 1996, J NEUROPHYSIOL, V76, P1639 MANIS PB, 1990, J NEUROSCI, V10, P2338 MANIS PB, 1994, J COMP NEUROL, V348, P261, DOI 10.1002/cne.903480208 MUGNAINI E, 1980, J NEUROCYTOL, V9, P537, DOI 10.1007/BF01204841 OERTEL D, 1989, J COMP NEUROL, V283, P228, DOI 10.1002/cne.902830206 OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 PARHAM K, 1995, J NEUROPHYSIOL, V73, P550 RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 SHERRIFF FE, 1994, NEUROSCIENCE, V58, P627, DOI 10.1016/0306-4522(94)90086-8 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 VETTER DE, 1993, NATO ADV SCI INST SE, V239, P279 WALLER HJ, 1994, J NEUROPHYSIOL, V71, P467 STARR A, 1968, J NEUROPHYSIOL, V31, P549 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 Zhang JS, 1998, NEUROSCI LETT, V250, P197, DOI 10.1016/S0304-3940(98)00482-0 ZHANG S, 1994, J NEUROPHYSIOL, V71, P914 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1384 NR 34 TC 11 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 7 EP 17 DI 10.1016/S0378-5955(99)00181-1 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500002 PM 10675631 ER PT J AU Nishiyama, N Hardie, NA Shepherd, RK AF Nishiyama, N Hardie, NA Shepherd, RK TI Neonatal sensorineural hearing loss affects neurone size in cat auditory midbrain SO HEARING RESEARCH LA English DT Article DE afferent deprivation; auditory system; inferior colliculus; neonatal deafness; soma area ID COCHLEAR NUCLEUS NEURONS; INFERIOR COLLICULUS; BRAIN-STEM; ELECTRICAL-STIMULATION; AFFERENT INFLUENCES; PROTEIN-SYNTHESIS; CELL-SIZE; REMOVAL; ABLATION; CHICKEN AB We examined the effect of a neonatal sensorineural hearing loss on the soma area of neurones in the central nucleus of the inferior colliculus (ICC) in adult cats to evaluate the role of auditory experience on neuronal atrophy within the auditory midbrain. Three groups of animals were used: bilaterally deafened, unilaterally deafened and normal hearing controls. Soma area measurements were made from the laminated central and medial divisions of the ICC of eight deafened and two normal hearing cats. A small but significant reduction in soma area was evident for bilaterally deafened animals compared with normal hearing controls (P < 0.05, Dunnett's test). In contrast, there was no significant difference in mean soma area between normal hearing and unilaterally deafened animals (P > 0.05) irrespective of whether the ICC examined was ipsi- or contralateral to the deafened ear. These results demonstrate that the reduction in soma area of auditory brainstem neurones reported following a sensorineural hearing loss is also evident at the level of the auditory midbrain. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Dept Otolaryngol, Human Commun Res Ctr, Melbourne, Vic 3002, Australia. RP Shepherd, RK (reprint author), Univ Melbourne, Dept Otolaryngol, Human Commun Res Ctr, 32 Gisborne St, Melbourne, Vic 3002, Australia. RI Shepherd, Robert/I-6276-2012 CR BORN DE, 1988, J NEUROSCI, V8, P901 DURHAM D, 1989, HEARING RES, V43, P39, DOI 10.1016/0378-5955(89)90057-9 Ehret G., 1997, CENTRAL AUDITORY SYS, P259 GARDEN GA, 1995, J COMP NEUROL, V359, P412, DOI 10.1002/cne.903590305 Hardie NA, 1999, HEARING RES, V128, P147, DOI 10.1016/S0378-5955(98)00209-3 Hardie NA, 1998, NEUROREPORT, V9, P2019, DOI 10.1097/00001756-199806220-00020 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HYDE GE, 1990, J COMP NEUROL, V297, P329, DOI 10.1002/cne.902970302 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 LUSTIG LR, 1994, HEARING RES, V74, P29, DOI 10.1016/0378-5955(94)90173-2 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 Rogers NJ, 1998, ANN OTO RHINOL LARYN, V107, P337 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 Moore JK, 1997, ANN OTO RHINOL LARYN, V106, P385 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 Oliver D. L., 1991, NEUROBIOLOGY HEARING, P195 PASIC TR, 1994, J COMP NEUROL, V348, P111, DOI 10.1002/cne.903480106 POWELL TPS, 1962, J ANAT, V96, P249 ROCKEL AJ, 1973, J COMP NEUROL, V147, P11, DOI 10.1002/cne.901470103 SELDON HL, 1991, ARCH OTOLARYNGOL, V117, P1158 Shepherd RK, 1999, J NEUROPHYSIOL, V82, P1363 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 Tierney TS, 1997, J COMP NEUROL, V378, P295, DOI 10.1002/(SICI)1096-9861(19970210)378:2<295::AID-CNE11>3.0.CO;2-R TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 WONGRILEY MTT, 1978, BRAIN RES, V141, P185, DOI 10.1016/0006-8993(78)90629-7 NR 26 TC 15 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 18 EP 22 DI 10.1016/S0378-5955(99)00185-9 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500003 PM 10675632 ER PT J AU Korada, S Schwartz, IR AF Korada, S Schwartz, IR TI Calcium binding proteins and the AMPA glutamate receptor subunits in gerbil cochlear nucleus SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; AMPA receptor; calcium binding protein; colocalization ID ELECTRON-MICROSCOPIC IMMUNOCYTOCHEMISTRY; GAMMA-AMINOBUTYRIC ACID; CA2+ PERMEABILITY; GUINEA-PIG; NERVOUS-SYSTEM; GRANULE CELLS; D-ASPARTATE; ION FLOW; NEURONS; RAT AB The alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) glutamate receptors mediate fast excitatory synaptic transmission in the central nervous system. The GluR2 subunit confers calcium impermeability to AMPA receptors. Various calcium binding proteins play a role in calcium regulation within the neurons. This study sought to identify possible relationships between calcium binding proteins and glutamate receptor subunits, especially GluR2, in gerbil cochlear nucleus neurons. Our immunohistochemical observations reveal no particular correlation between GluR2 and calbindin; all the cell types show labeling for all the antibodies studied except calretinin. There was coincidence of strong GluR4 and strong parvalbumin staining in octopus cells, although calbindin was also present in these cells. This study suggests a possible relationship between parvalbumin and predominantly GluR4 containing receptors, even when calbindin is present. The absence of a strong inverse correlation between the presence of ionotropic AMPA receptor subunit GluR2 and calbindin suggests a more significant role of non-AMPA ionotropic glutamate receptors or other voltage-gated channels in the regulation of calcium in the neurons of cochlear nucleus. Alternatively, more detailed analysis of receptor composition at particular synapses and the subcellular localization of specific calcium binding proteins may be required. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Yale Univ, Sch Med, Dept Surg Otolaryngol, New Haven, CT 06520 USA. RP Schwartz, IR (reprint author), Yale Univ, Sch Med, Dept Surg Otolaryngol, POB 208041, New Haven, CT 06520 USA. CR BAIMBRIDGE KG, 1992, TRENDS NEUROSCI, V15, P303, DOI 10.1016/0166-2236(92)90081-I BATINI C, 1990, ARCH ITAL BIOL, V128, P127 BUCHAN AM, 1991, NEUROSCI LETT, V132, P255, DOI 10.1016/0304-3940(91)90314-J BURNASHEV N, 1992, NEURON, V8, P189, DOI 10.1016/0896-6273(92)90120-3 CAICEDO A, 1995, ASS RES OT ABSTR, V18, P790 CANT NB, 1992, HDB AUDITORY RES, P67 CARDOZO BN, 1997, SOC NEUR ABSTR, V23, P1542 CELIO MR, 1986, SCIENCE, V231, P995, DOI 10.1126/science.3945815 Chen K, 1999, NEUROSCIENCE, V90, P1043, DOI 10.1016/S0306-4522(98)00503-X CZIBULKA A, 1991, HEARING RES, V52, P43, DOI 10.1016/0378-5955(91)90186-D DIEMER NH, 1992, ACTA NEUROL SCAND, V86, P45 GEIGER JRP, 1995, NEURON, V15, P193, DOI 10.1016/0896-6273(95)90076-4 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 Godfrey DA, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P139, DOI 10.1007/978-1-4419-8712-9_13 GODFREY DA, 1978, J HISTOCHEM CYTOCHEM, V26, P118 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HOLLMANN M, 1991, SCIENCE, V252, P851, DOI 10.1126/science.1709304 JONAS P, 1995, NEURON, V15, P987, DOI 10.1016/0896-6273(95)90087-X JONAS P, 1994, NEURON, V12, P1281, DOI 10.1016/0896-6273(94)90444-8 KANE EC, 1974, J COMP NEUROL, V155, P301, DOI 10.1002/cne.901550303 KEH A, 1999, ARO MIDW M, V22, P68 KOLSTON J, 1992, ANAT EMBRYOL, V186, P443 LLEWELLYNSMITH IJ, 1993, J NEUROSCI METH, V46, P27, DOI 10.1016/0165-0270(93)90138-H Lohmann C, 1996, J COMP NEUROL, V367, P90, DOI 10.1002/(SICI)1096-9861(19960325)367:1<90::AID-CNE7>3.0.CO;2-E McGinn M. D., 1992, Society for Neuroscience Abstracts, V18, P1036 MUGNAINI E, 1980, J NEUROCYTOL, V9, P537, DOI 10.1007/BF01204841 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 NICOLL RA, 1990, PHYSIOL REV, V70, P513 OLIVER DL, 1983, J NEUROSCI, V3, P455 Osen K.K., 1990, GLYCINE NEUROTRANSMI, P417 Petralia RS, 1997, J COMP NEUROL, V385, P456, DOI 10.1002/(SICI)1096-9861(19970901)385:3<456::AID-CNE9>3.0.CO;2-2 Petralia RS, 1996, J COMP NEUROL, V372, P356 POTASHNER SJ, 1983, J NEUROCHEM, V41, P1094, DOI 10.1111/j.1471-4159.1983.tb09057.x RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 ROMAND R, 1978, BRAIN RES, V148, P43, DOI 10.1016/0006-8993(78)90377-3 Rubio ME, 1997, NEURON, V18, P939, DOI 10.1016/S0896-6273(00)80333-5 RYUGO DK, 1992, HDB AUDITORY RES, P23 SCHWARTZ IR, 1992, ASS RES OT ABSTR, V15, P59 Schwartz I. R., 1992, Society for Neuroscience Abstracts, V18, P1036 SCHWARTZ I R, 1987, Society for Neuroscience Abstracts, V13, P544 Schwartz IR, 1999, HEARING RES, V137, P77, DOI 10.1016/S0378-5955(99)00140-9 SCHWARTZ IR, 1992, C MOL BIOL HEAR DEAF, P84 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 SOMMER B, 1991, CELL, V67, P11, DOI 10.1016/0092-8674(91)90568-J VATER M, 1994, J COMP NEUROL, V341, P534, DOI 10.1002/cne.903410409 VERDOORN TA, 1991, SCIENCE, V252, P1715, DOI 10.1126/science.1710829 WEBSTER WR, 1990, NEUROSCI LETT, V111, P252, DOI 10.1016/0304-3940(90)90270-J WENTHOLD RJ, 1992, J BIOL CHEM, V267, P501 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 YU SM, 1987, ASS RES OT ABSTR, V10, P213 NR 51 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 23 EP 37 DI 10.1016/S0378-5955(99)00182-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500004 PM 10675633 ER PT J AU Ekborn, A Laurell, G Andersson, A Wallin, I Eksborg, S Ehrsson, H AF Ekborn, A Laurell, G Andersson, A Wallin, I Eksborg, S Ehrsson, H TI Cisplatin-induced hearing loss: influence of the mode of drug administration in the guinea pig SO HEARING RESEARCH LA English DT Article DE cisplatin; pharmacokinetics; ototoxicity; nephrotoxicity ID 5-DAY CONTINUOUS INFUSION; MONOHYDRATED COMPLEX; UNCHANGED CISPLATIN; TESTICULAR CANCER; OVARIAN-CANCER; OTOTOXICITY; TOXICITY; DIETHYLDITHIOCARBAMATE; CIS-DIAMMINEDICHLOROPLATINUM(II); PHARMACOKINETICS AB Cisplatin (8 mg/kg) was given intravenously to guinea pigs either as a 15 s bolus injection (25 animals) or as a 1 h infusion (28 animals). To determine the influence of the mode of cisplatin administration and pharmacokinetics on the ototoxic side-effect, the concentrations of cisplatin and the biotransformation product monoaquated cisplatin were determined in blood ultrafiltrate using liquid chromatography with post-column derivatization. Ototoxic effect was evaluated as difference in pre- and 96 h post-exposure auditory brainstem response (ABR) threshold. The cisplatin peak concentration was considerably higher, 19.2 +/- 2.4 mu g/ml, in the bolus injection group than in the infusion group, 6.7+/-0.5 mu g/ml (mean+/-S.E.M.). The area under the blood ultrafiltrate concentration time curve (AUC) for cisplatin was slightly greater in the infusion group, 442+/-26 mu g/ml/min, than in the bolus injection group, 340 +/- 5 mu g/ml/min. For monoaqua cisplatin, the AUC was not different between the groups (bolus injection: 30.8 +/- 1.5 mu g/ml/min, infusion: 34.1 +/- 3.3 mu g/ml/min). A significant ototoxic effect was observed in both groups at 20 and 12.5 kHz, but there was no difference between the groups in the extent of threshold shift. The interindividual variability in susceptibility to ABR threshold shift was far greater than the variability in pharmacokinetics, suggesting that other factors are more important in determining the degree of hearing loss. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Karolinska Inst, Dept Physiol, SE-17176 Stockholm, Sweden. Karolinska Hosp, ENT Clin, SE-17176 Stockholm, Sweden. Karolinska Pharm, S-10401 Stockholm, Sweden. RP Ekborn, A (reprint author), Karolinska Inst, Dept Physiol, SE-17176 Stockholm, Sweden. CR AAMDAL S, 1987, CANCER TREAT REV, V14, P389, DOI 10.1016/0305-7372(87)90035-1 ANDERSSON A, 1994, J CHROMATOGR B, V652, P203, DOI 10.1016/0378-4347(93)E0403-D Andersson A, 1996, J PHARM SCI, V85, P824, DOI 10.1021/js960037a AXDORPH U, 1993, J INTERN MED, V233, P401 BERRY JM, 1990, J CLIN ONCOL, V8, P1585 Bokemeyer C, 1998, BRIT J CANCER, V77, P1355, DOI 10.1038/bjc.1998.226 BOXENBAU.HG, 1974, J PHARMACOKINET BIOP, V2, P123, DOI 10.1007/BF01061504 COMIS RL, 1994, SEMIN ONCOL, V21, P109 Dormans TPJ, 1996, J AM COLL CARDIOL, V28, P376, DOI 10.1016/0735-1097(96)00161-1 FINLEY RS, 1985, DRUG INTEL CLIN PHAR, V19, P362 FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 FORASTIERE AA, 1988, CANCER RES, V48, P3869 GANDARA DR, 1990, CRIT REV ONCOL HEMAT, V10, P353, DOI 10.1016/1040-8428(90)90010-P HAINSWORTH JD, 1988, ANN INTERN MED, V108, P165 HAYES DM, 1977, CANCER, V39, P1372, DOI 10.1002/1097-0142(197704)39:4<1372::AID-CNCR2820390404>3.0.CO;2-J JONES MM, 1991, CANCER CHEMOTH PHARM, V29, P29, DOI 10.1007/BF00686332 LAURELL G, 1995, CANCER CHEMOTH PHARM, V36, P83 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LOKICH JJ, 1980, CANCER TREAT REP, V64, P905 MARTY M, 1989, EUR J CANCER CLIN ON, V25, P41 MUGGIA FM, 1985, CANCER CHEMOTH PHARM, V15, P1 Nagai N, 1997, CANCER CHEMOTH PHARM, V40, P11, DOI 10.1007/s002800050618 PIEL IJ, 1974, CANCER CHEMOTH REP 1, V58, P871 REDDEL RR, 1982, CANCER TREAT REP, V66, P19 REECE PA, 1989, CANCER CHEMOTH PHARM, V24, P256 RYBAK LP, 1995, FUND APPL TOXICOL, V26, P293, DOI 10.1006/faat.1995.1100 SALEM P, 1984, CANCER, V53, P837, DOI 10.1002/1097-0142(19840215)53:4<837::AID-CNCR2820530403>3.0.CO;2-L THOMPSON SW, 1984, CANCER, V54, P1269, DOI 10.1002/1097-0142(19841001)54:7<1269::AID-CNCR2820540707>3.0.CO;2-9 VARGO DL, 1984, NONPARAMETRIC STAT Q VERMORKEN JB, 1983, EUR J CANCER CLIN ON, V19, P53, DOI 10.1016/0277-5379(83)90398-X Yachnin JR, 1998, CANCER LETT, V132, P175, DOI 10.1016/S0304-3835(98)00175-X ZUNINO F, 1989, CHEM-BIOL INTERACT, V70, P89, DOI 10.1016/0009-2797(89)90065-3 NR 32 TC 38 Z9 40 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 38 EP 44 DI 10.1016/S0378-5955(99)00190-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500005 PM 10675634 ER PT J AU Javel, E Shepherd, RK AF Javel, E Shepherd, RK TI Electrical stimulation of the auditory nerve - III. Response initiation sites and temporal fine structure SO HEARING RESEARCH LA English DT Article DE auditory nerve fiber; electrical stimulation; cochlear implant ID FIBERS; CAT; PATTERNS; COCHLEA; MODEL AB Latency, temporal dispersion and input-output characteristics of auditory nerve fiber responses to electrical pulse trains in normal and chronically deafened cat ears were classified and tentatively associated with sites where activity is initiated. Spikes occurred in one or more of four discrete time ranges whose endpoints overlapped partially. A responses had latencies < 0.44 ms, exhibited asymptotic temporal dispersion of 8-12 mu s and possessed an average dynamic range of 1.2 dB for 200 pulses/s (pps) pulse trains. They likely originated from central processes of spiral ganglion cells. B-1 and B-2 responses (0.45-0.9 ms, 25-40 mu s, 1.9 dB) likely stemmed from activity at myelinated and unmyelinated peripheral processes, respectively. C responses (0.9-1.2 ms, > 100 mu s) likely originated from direct stimulation of inner hair cells, and D responses (> 1.1 ms, > 100 mu s, >8 dB) arose from propagating traveling waves possibly caused by electrically induced motion of-outer hair cells. C and D responses were recorded only in acoustically responsive ears. Mean latencies of spikes in all time ranges usually decreased with intensity, and activity at two or even three discrete latencies was often observed in the same spike train. Latency shifts from one discrete time range to another often occurred as intensity increased, Some shifts could be attributed to responses to the opposite-polarity phase of the biphasic pulse, In these cases, temporal dispersion and dynamic range were approximately equal for activity at each latency. A second type of latency shift was also often observed, in which responses at each latency exhibited dissimilar temporal dispersion and dynamic range. This behavior was attributed to a centralward shift in the spike initiation site and it occurred for monophasic as well as biphasic signals. Several fibers exhibited dual latency activity with a 40-90 mu s time difference between response peaks. This may have stemmed from spike initiation at nodes on either side of the cell body. Increasing the Stimulus pulse rate to 800-1000 pps produced small increases in temporal dispersion and proportionate increases in asymptotic discharge rate and dynamic range, but thresholds did not improve and slopes of rate-intensity functions (in spikes/s/dB) did not change. Responses to high-rate stimuli also exhibited discrete latency increases when discharge rates exceeded 300-400 spikes/s, Spike by spike latencies in these cases depended strongly on the discharge history; Implications for high-rate speech processing strategies are discussed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Minnesota, Dept Otolaryngol, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Neurosci, Minneapolis, MN 55455 USA. Univ Melbourne, Dept Otolaryngol, Parkville, Vic 3052, Australia. RP Javel, E (reprint author), Univ Minnesota, Dept Otolaryngol, 209 Lions Res Bldg,2001 6th St SE, Minneapolis, MN 55455 USA. RI Shepherd, Robert/I-6276-2012 CR ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BRILL S, 1997, 5 INT COCHL IMPL C Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P617, DOI 10.1109/10.764938 COLUMBO J, 1987, HEARING RES, V31, P287 COOMBS JS, 1957, J PHYSIOL-LONDON, V139, P232 CRAGG BG, 1964, J NEUROL NEUROSUR PS, V27, P106, DOI 10.1136/jnnp.27.2.106 DYNES SBC, 1992, HEARING RES, V58, P79, DOI 10.1016/0378-5955(92)90011-B FINLEY CC, 1991, ABST ASS RES OT, V14, P52 FRIJNS JHM, 1995, THESIS U LEIDEN GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HARTMANN R, 1990, P135 HARTMANN R, 1984, ADV AUDIOL, V1, P18 Held H., 1926, HDB NORMALEN PATHOLO, P467 Hill AV, 1936, PROC R SOC SER B-BIO, V119, P305, DOI 10.1098/rspb.1936.0012 JAVEL E, 1997, ABST ASS RES OT, V20, P56 JAVEL E, 1991, ASS RES OT MIDW M FL, V14, P130 JAVEL E, 1990, P247 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 Javel E., 1986, NEUROBIOLOGY HEARING, P213 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KIEFER J, 1997, 5 INT COCHL IMPL C KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MCDERMOTT HJ, 1992, J ACOUST SOC AM, V91, P3367, DOI 10.1121/1.402826 MCNEAL DR, 1976, IEEE T BIO-MED ENG, V23, P329, DOI 10.1109/TBME.1976.324593 MILLER CA, 1997, NEUROPHYSIOLOGICAL E Moxon E.C., 1971, THESIS MIT NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 Nguyen BH, 1999, AM J OTOL, V20, P522 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PENDER MP, 1984, BRAIN, V107, P699, DOI 10.1093/brain/107.3.699 Press WH, 1988, NUMERICAL RECIPES C RANCK JB, 1975, BRAIN RES, V98, P417, DOI 10.1016/0006-8993(75)90364-9 RASMINSK.M, 1972, J PHYSIOL-LONDON, V227, P323 RUBINSTEIN JT, 1997, NEUROPHYSIOLOGICAL E RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 RUSHTON WAH, 1951, J PHYSIOL-LONDON, V115, P101 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 Shepherd RK, 1997, HEARING RES, V108, P112, DOI 10.1016/S0378-5955(97)00046-4 SHEPHERD RK, 1999, IN PRESS HEAR RES SHEPHERD RK, 1992, P AUST NEUROSCI SOC, V3, P129 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VERVEEN A. A., 1962, ACTA MORPHOL NEERLANDO SCAND, V5, P79 VERVEEN AA, 1968, PR INST ELECTR ELECT, V56, P906, DOI 10.1109/PROC.1968.6443 WHITE MW, 1987, IEEE 9 ANN C ENG MED, P1906 WILSON B, 1997, SPEECH PROCESSORS AU WILSON BS, 1994, SPEECH PROCESSORS AU NR 52 TC 57 Z9 59 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 45 EP 76 DI 10.1016/S0378-5955(99)00186-0 PG 32 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500006 PM 10675635 ER PT J AU Grigg, JJ Brew, HM Tempel, BL AF Grigg, JJ Brew, HM Tempel, BL TI Differential expression of voltage-gated potassium channel genes in auditory nuclei of the mouse brainstem SO HEARING RESEARCH LA English DT Article DE auditory system; Kv channel; gene expression; in situ hybridization; Shaker; Shaw ID ANTEROVENTRAL COCHLEAR NUCLEUS; HETEROMULTIMERIC K+ CHANNELS; CENTRAL-NERVOUS-SYSTEM; RAT MEDIAL NUCLEUS; TRAPEZOID BODY; NEURAL SYNCHRONIZATION; SUPERIOR OLIVE; NEURONS; CELLS; DENDROTOXIN AB Voltage-gated potassium (Kv) channels may play an important role in the encoding of auditory information, Towards understanding the roles of Shaker and Shaw-like channels in this process, we examine here the expression of Kv1.1, Kv1.2, Kv3.1, and Kv3.3 in the central auditory nuclei of the mouse using quantitative in:situ hybridization techniques. We establish rank order for each channel's expression in each region, finding that the medial nucleus of the trapezoid body shows the highest signal for each of the four channel genes. In other auditory nuclei differential expression is found among and between members of both Shaker and Shaw subfamilies. Of particular interest is the stark contrast between high level expression of Kv1.1 and very low level expression of Kv3.1 in the octopus cell area of the cochlear nucleus and in the lateral superior olivary nucleus. These unique expression patterns suggest that Kv channel gene expression is regulated to allow brainstem auditory neurons to transmit temporally patterned signals with high fidelity. In instances where specific cell types can be tentatively identified, we discuss the possible contribution made by these channel genes to the physiological properties of those neurons. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Washington, Sch Med, Virginia Merrill Bloedel Hearing Res Ctr, Seattle, WA 98195 USA. Univ Washington, Sch Med, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98195 USA. Univ Washington, Sch Med, Dept Pharmacol, Seattle, WA 98195 USA. Univ Leicester, Dept Cell Physiol & Pharmacol, Leicester LE1 9HN, Leics, England. RP Tempel, BL (reprint author), Univ Washington, Sch Med, Virginia Merrill Bloedel Hearing Res Ctr, Box 357923, Seattle, WA 98195 USA. CR BANKS MI, 1992, J NEUROSCI, V12, P2819 BOSMA MM, 1993, J NEUROSCI, V13, P5242 Brew HM, 1995, J NEUROSCI, V15, P8011 COVARRUBIAS M, 1991, NEURON, V7, P763, DOI 10.1016/0896-6273(91)90279-9 EDGAR PP, 1990, J NEUROSCI, V10, P603 FERRAGAMO MJ, 1998, ASS RES OT ABSTR, V25, P96 FORSYTHE ID, 1993, P ROY SOC B-BIOL SCI, V251, P151, DOI 10.1098/rspb.1993.0022 Fubara BM, 1996, J COMP NEUROL, V369, P83 Gan L, 1996, J BIOL CHEM, V271, P5859 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GOLDING NL, 1995, J NEUROSCI, V15, P3138 Golding NL, 1999, J NEUROSCI, V19, P2897 GRISSMER S, 1994, MOL PHARMACOL, V45, P1227 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 GUTMAN GA, 1993, SEMIN NEUROSCI, V5, P101, DOI 10.1016/S1044-5765(05)80004-1 HOPKINS WF, 1994, PFLUG ARCH EUR J PHY, V428, P382, DOI 10.1007/BF00724522 Irvine D.R.F., 1986, AUDITORY BRAINSTEM R JORIS PX, 1994, J NEUROPHYSIOL, V71, P1022 JORIS PX, 1994, J NEUROPHYSIOL, V71, P1037 LAVINE RA, 1971, J NEUROPHYSIOL, V34, P467 LOCK LF, 1994, GENOMICS, V20, P354, DOI 10.1006/geno.1994.1188 LUNEAU CJ, 1991, P NATL ACAD SCI USA, V88, P3932, DOI 10.1073/pnas.88.9.3932 MANIS PB, 1998, ASS RES OT ABSTR, V25, P163 MANIS PB, 1991, J NEUROSCI, V11, P2865 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 Navaratnam DS, 1997, NEURON, V19, P1077, DOI 10.1016/S0896-6273(00)80398-0 OERTEL D, 1985, J ACOUST SOC AM, V78, P328, DOI 10.1121/1.392494 PARAMESHWARAN S, 1998, ASS RES OT ABSTR, V25, P213 PERNEY TM, 1993, SOC NEUR ABSTR, V19 PERNEY TM, 1992, J NEUROPHYSIOL, V68, P756 Perney TM, 1997, J COMP NEUROL, V386, P178 Rosenblatt KP, 1997, NEURON, V19, P1061, DOI 10.1016/S0896-6273(00)80397-9 RUGGERO MA, 1992, SPRINGER HDB AUDITOR, V2, P34 Rusznak Z, 1997, EUR J NEUROSCI, V9, P2348, DOI 10.1111/j.1460-9568.1997.tb01652.x SCOTT VES, 1994, BIOCHEMISTRY-US, V33, P1617, DOI 10.1021/bi00173a001 SEQUIER JM, 1990, FEBS LETT, V263, P163, DOI 10.1016/0014-5793(90)80729-3 SHENG M, 1993, NATURE, V365, P72, DOI 10.1038/365072a0 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 WANG H, 1993, NATURE, V365, P75, DOI 10.1038/365075a0 WANG H, 1994, J NEUROSCI, V14, P4588 Wang LY, 1998, J PHYSIOL-LONDON, V509, P183, DOI 10.1111/j.1469-7793.1998.183bo.x WEBSTER DB, 1982, AM J ANAT, V163, P103, DOI 10.1002/aja.1001630202 WEISER M, 1994, J NEUROSCI, V14, P949 WERKMAN TR, 1992, NEUROSCIENCE, V50, P935, DOI 10.1016/0306-4522(92)90216-O Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 WU SH, 1993, HEARING RES, V68, P189 WU SH, 1991, J NEUROPHYSIOL, V65, P230 NR 47 TC 83 Z9 84 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 77 EP 90 DI 10.1016/S0378-5955(99)00187-2 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500007 PM 10675636 ER PT J AU Takumida, M Anniko, M Ropa, P Zhang, DM AF Takumida, M Anniko, M Ropa, P Zhang, DM TI Lipopolysaccharide-induced expression of inducible nitric oxide synthase in the guinea pig organ of Corti SO HEARING RESEARCH LA English DT Article DE nitric oxide; inducible nitric oxide synthase; bacterial lipopolysaccharide; organ of Corti; immunohistochemistry; guinea pig ID ACTION-POTENTIAL THRESHOLDS; SODIUM-NITROPRUSSIDE; POSSIBLE INVOLVEMENT; COCHLEA; LOCALIZATION; CELLS; INDUCTION; SYSTEM; OTOTOXICITY; PHYSIOLOGY AB The purpose of the investigation was to ascertain whether inoculation of bacterial lipopolysaccharide (LP) into the cochlea of the guinea pig could elicit formation of inducible nitric oxide synthase (iNOS). Immunohistochemical study revealed that immunoreactivity to iNOS was seen below outer hair cells representing nerve fibers and synaptic nerve endings. iNOS-staining could also be observed ill phalangeal dendrites of Deiter's cells pointing to the cuticular membrane, Hensen's cells and on stria vascularis 48 h after inoculation with LPS. Immunohistochemical investigation with a specific anti-nitrotyrosine antibody also revealed intense immunoreactivity identical to that of iNOS, suggesting formation of peroxynitrite in the organ of Corti by the reaction of NO with O-2(-). On the basis of these findings, it can be concluded that NO together with O-2(-), which form the more reactive peroxynitrite. are the most important pathogenic agents in LPS-induced damage of cochlea in the guinea pig. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hiroshima Univ, Sch Med, Dept Otolaryngol, Minami Ku, Hiroshima 7348551, Japan. Univ Uppsala Hosp, Dept Otolaryngol Head & Neck Surg, Uppsala, Sweden. RP Takumida, M (reprint author), Hiroshima Univ, Sch Med, Dept Otolaryngol, Minami Ku, 1-2-3 Kasumicho, Hiroshima 7348551, Japan. CR AMAEE FR, 1995, ACTA OTO-LARYNGOL, V115, P386, DOI 10.3109/00016489509139334 Amaee FR, 1997, ACTA OTO-LARYNGOL, V117, P329, DOI 10.3109/00016489709113403 Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424 CHAO CC, 1992, J IMMUNOL, V149, P2736 Dais CGD, 1996, HEARING RES, V99, P1 EHRENBERGER K, 1991, HEARING RES, V52, P73, DOI 10.1016/0378-5955(91)90188-F Fessenden JD, 1998, HEARING RES, V118, P168, DOI 10.1016/S0378-5955(98)00027-6 Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 FESSENDEN JD, 1994, BRAIN RES, V668, P9, DOI 10.1016/0006-8993(94)90505-3 FORSTERMANN U, 1994, HYPERTENSION, V23, P1121 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 GALEA E, 1992, P NATL ACAD SCI USA, V89, P10945, DOI 10.1073/pnas.89.22.10945 GARTHWAITE J, 1991, TRENDS NEUROSCI, V14, P60, DOI 10.1016/0166-2236(91)90022-M GUEVARAGUZMAN R, 1994, J NEUROCHEM, V62, P807 Hess A, 1998, BRAIN RES, V813, P97, DOI 10.1016/S0006-8993(98)00997-4 Hess A, 1999, BRAIN RES, V830, P113, DOI 10.1016/S0006-8993(99)01433-X Hess A, 1998, NEUROSCI LETT, V251, P185, DOI 10.1016/S0304-3940(98)00532-1 HOGG N, 1992, BIOCHEM J, V281, P419 IADECOLA C, 1995, J CEREBR BLOOD F MET, V15, P52 IADECOLA C, 1995, J CEREBR BLOOD F MET, V15, P378 Johnson KL, 1998, ACTA OTO-LARYNGOL, V118, P660 Kong WJ, 1996, HEARING RES, V99, P22, DOI 10.1016/S0378-5955(96)00076-7 LOWENSTEIN CJ, 1994, ANN INTERN MED, V120, P227 LOWENSTEIN CJ, 1992, P NATL ACAD SCI USA, V89, P6711, DOI 10.1073/pnas.89.15.6711 MOLLACE V, 1993, BIOCHEM BIOPH RES CO, V191, P327, DOI 10.1006/bbrc.1993.1221 PUEL JL, 1991, NEUROSCIENCE, V45, P63, DOI 10.1016/0306-4522(91)90103-U Ruan RS, 1997, HEARING RES, V114, P169, DOI 10.1016/S0378-5955(97)00159-7 SCHMIDT HHHW, 1994, CELL, V78, P919, DOI 10.1016/0092-8674(94)90267-4 SCHUMAN EM, 1994, ANNU REV NEUROSCI, V17, P153, DOI 10.1146/annurev.neuro.17.1.153 SIMMONS ML, 1992, J NEUROCHEM, V59, P897, DOI 10.1111/j.1471-4159.1992.tb08328.x Takumida M, 1998, ORL J OTO-RHINO-LARY, V60, P254, DOI 10.1159/000027606 Takumida M, 1998, EUR ARCH OTO-RHINO-L, V255, P184, DOI 10.1007/s004050050040 Takumida M, 1998, ORL J OTO-RHINO-LARY, V60, P67, DOI 10.1159/000027567 Takumida M, 1999, ORL J OTO-RHINO-LARY, V61, P63, DOI 10.1159/000027643 Takumida M, 1998, ORL J OTO-RHINO-LARY, V60, P246, DOI 10.1159/000027605 WATKINS JC, 1987, TRENDS NEUROSCI, V10, P265, DOI 10.1016/0166-2236(87)90171-8 ZDANSKI CJ, 1994, HEARING RES, V79, P39, DOI 10.1016/0378-5955(94)90125-2 ZIELASEK J, 1992, CELL IMMUNOL, V141, P111, DOI 10.1016/0008-8749(92)90131-8 NR 38 TC 39 Z9 43 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 91 EP 98 DI 10.1016/S0378-5955(99)00188-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500008 PM 10675637 ER PT J AU Faulstich, F Kossl, M AF Faulstich, F Kossl, M TI Evidence for multiple DPOAE components based upon group delay of the 2f(1)-f(2) distortion in the gerbil SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; cochlear amplifier; cochlear non-linearity; DPOAE ID PRODUCT OTOACOUSTIC EMISSIONS; COCHLEAR NERVE-FIBERS; ACOUSTIC DISTORTION; MONGOLIAN GERBIL; FREQUENCY MAP; TUNING CURVES; IMPAIRED EARS; GUINEA-PIG; RESPONSES; SUPPRESSION AB The cochlear delay of the 2f(1)-f(2) distortion product otoacoustic emission (DPOAE) was measured using the phase gradient method. With a constant f(2) and swept f(1), the resulting phase change of 2f(1)-f(2) was used to calculate the group delay for f(2) frequencies from 1 to 60 kHz. For f(2) frequencies between 2 and 60 kHz, the group delays were between 2.2 and 0.11 ms and continuously decreased for increasing f(2) and For increasing primary stimulus levels. For f(2) frequencies below 2 kHz, the group delay decreased to around 1 ms and was largely independent of stimulus level. The ratio curves resulting from the f(1) sweeps for high frequencies (f(2) > 16 kHz) displayed the typical mammalian shape with a peak in the level of 2f(1)-f(2) for a larger primary frequency separation (f(2)/f(1) > 1.15) and decreasing 2f(1) - f(2) level for smaller primary separation. In addition to this typical level maximum, for f(2) frequencies from about 1.8 to 16 kHz, the ratio curves displayed a second component in the form of an increase in the level of 2f(1)-f(2) for small primary separation at higher primary levels (level of f(2) > 30 dB SPL). For f(2) frequencies below 1.8 kHz, only the second component and no typical ratio peak as for higher f(2) could be observed and the associated group delay was always close to 0.8 ms. Several possible causes for this behavior are discussed, including different modes of DPOAE generation and modulation as well as changes in the nature of mechanical processing from base to apex in the gerbil cochlea. To evaluate the relative sensitivity of non-linear cochlear mechanics, an iso-distortion threshold curve was constructed from acoustical growth functions of the 2f(1)-f(2) DPOAE at optimum primary separation, by plotting the level of f(2) sufficient to evoke a distortion of -10 dB SPL as a function of f(2). This distortion audiogram resembled the neuronal and behavioral audiogram for frequencies > 2.5 kHz but failed to reflect the sensitivity for lower frequencies. This may be a consequence of more linear frequency processing in the apex. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Munich, Inst Zool, D-80333 Munich, Germany. RP Faulstich, F (reprint author), Salk Inst Biol Studies, Lab SNLD, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA. CR ALLEN JB, 1993, J ACOUST SOC AM, V94, P809, DOI 10.1121/1.408182 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWN AM, 1992, P ROY SOC B-BIOL SCI, V250, P29, DOI 10.1098/rspb.1992.0126 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 Brown AM, 1996, J ACOUST SOC AM, V100, P3260, DOI 10.1121/1.417209 COOPER NP, 1994, HEARING RES, V78, P221, DOI 10.1016/0378-5955(94)90028-0 Faulstich M, 1999, J ACOUST SOC AM, V105, P491, DOI 10.1121/1.424586 Faulstich M, 1996, HEARING RES, V94, P47, DOI 10.1016/0378-5955(95)00232-4 Frank G, 1996, HEARING RES, V98, P104, DOI 10.1016/0378-5955(96)00083-4 FRANK G, 1995, HEARING RES, V83, P151, DOI 10.1016/0378-5955(94)00197-X Gaskill SA, 1996, J ACOUST SOC AM, V100, P3268, DOI 10.1121/1.417210 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HEITMANN J, 1997, 20 MIDW M ASS RES OT, P83 KIMBERLEY BP, 1993, J ACOUST SOC AM, V94, P1343, DOI 10.1121/1.408162 KOSSL M, 1992, HEARING RES, V60, P156, DOI 10.1016/0378-5955(92)90018-I Kossl M, 1996, J COMP PHYSIOL A, V178, P427 KUMMER P, 1995, J ACOUST SOC AM, V98, P197, DOI 10.1121/1.413747 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1999, 24 MIDW RES M ASS RE, P210 MARTIN GK, 1999, 24 MIDW RES M ASS RE, P382 Mills DM, 1997, J ACOUST SOC AM, V102, P413, DOI 10.1121/1.419763 Mills DM, 1997, J ACOUST SOC AM, V101, P395, DOI 10.1121/1.417985 Muller M, 1996, HEARING RES, V94, P148, DOI 10.1016/0378-5955(95)00230-8 NEELY ST, 1997, DIVERSITY AUDITORY M, P434 OHLEMILLER KK, 1994, HEARING RES, V80, P174, DOI 10.1016/0378-5955(94)90109-0 OHLEMILLER KK, 1991, J ACOUST SOC AM, V90, P274, DOI 10.1121/1.401298 OMAHONEY CF, 1995, J ACOUST SOC AM, V97, P3721, DOI 10.1121/1.412994 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 Ravicz ME, 1996, J ACOUST SOC AM, V99, P3044, DOI 10.1121/1.414793 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SCHMIEDT RA, 1978, J ACOUST SOC AM, V64, P502, DOI 10.1121/1.382000 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 Shera CA, 1999, J ACOUST SOC AM, V105, P782, DOI 10.1121/1.426948 Stover LJ, 1996, J ACOUST SOC AM, V99, P1016, DOI 10.1121/1.414630 Talmadge CL, 1999, J ACOUST SOC AM, V105, P275, DOI 10.1121/1.424584 White S. D., 1992, Waltham International Focus, V2, P2 Whitehead M. L., 1996, CLIN ASPECTS HEARING, P199 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2359, DOI 10.1121/1.411960 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2346, DOI 10.1121/1.411959 Whitehead ML, 1996, J ACOUST SOC AM, V100, P1663, DOI 10.1121/1.416065 NR 42 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 99 EP 110 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500009 ER PT J AU Maison, S Micheyl, C Andeol, G Gallego, S Collet, L AF Maison, S Micheyl, C Andeol, G Gallego, S Collet, L TI Activation of medial olivocochlear efferent system in humans: influence of stimulus bandwidth SO HEARING RESEARCH LA English DT Article DE bandwidth; cochlea; human; medial olivocochlear efferent; noise; otoacoustic emission ID EVOKED OTOACOUSTIC EMISSIONS; COCHLEAR MICROMECHANICAL PROPERTIES; CONTRALATERAL ACOUSTIC STIMULATION; AUDITORY-NERVE FIBERS; INTENSITY DISCRIMINATION; MODULATED TONES; MASKED TONES; BUNDLE; NOISE; NEURONS AB The activity of the medial olivocochlear bundle (MOCB) can be studied in humans through variations in the level of evoked otoacoustic emissions (EOAEs) elicited by contralateral acoustic stimuli (CAS). The present study sought to investigate how the activity of the MOC system at a given frequency! as measured through the contralateral suppression of tone-pip EOAEs, depends on the bandwidth of the contralateral stimulus. EOAEs were recorded in 155 normal-hearing subjects, successively with and without contralateral stimuli whose bandwidth, center frequency and level were systematically varied. We showed a dear dependence of contralateral EOAE suppression on bandwidth demonstrating increased suppression with increased bandwidth over about two octaves around the center frequency of the noise. This effect was obtained irrespective of whether contralateral noise energy was kept constant independently of bandwidth or not, which indicates a role of bandwidth per se in contralateral EOAE suppression. Results are interpreted in terms of a simple model of MOCB activation mechanisms including peripheral bandpass filtering, within-channel compression and across-channel spatial summation by the afferent paths. Complementary experiments suggested a greater-effectiveness of increases in bandwidth on the upper than on the lower side and of frequency components akin to or remote from the test frequency than of intermediate bands. Finally; these results were complemented by detailed spectrum analyses of the EOAE level variations induced by the different noises, which revealed that whilst noise components close to or remote from the center frequency generally attenuated EOAE level, intermediate components could in some cases lead to a relative increase in EOAE level. These results can further be explained by assuming different positive and negative weights on the inputs to the spatial summation process depending on their position relative to the center frequency. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Lyon 1, Lab Neurosci & Syst Sensoriels, UPRESA CNRS 5020, F-69365 Lyon, France. RP Maison, S (reprint author), Hop Edouard Herriot, Pavillon U,3 Pl Arsonval, F-69437 Lyon 03, France. CR ALLEN JB, 1977, IEEE T ACOUST SPEECH, V25, P235, DOI 10.1109/TASSP.1977.1162950 BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E DEWSON JH, 1968, J NEUROPHYSIOL, V31, P122 Giraud AL, 1995, BRAIN RES, V705, P15, DOI 10.1016/0006-8993(95)01091-2 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T Guinan JJ, 1996, J ACOUST SOC AM, V100, P1680, DOI 10.1121/1.416066 GUMMER M, 1988, HEARING RES, V36, P41, DOI 10.1016/0378-5955(88)90136-0 Hood LJ, 1996, HEARING RES, V101, P113, DOI 10.1016/S0378-5955(96)00138-4 IGARASHI M, 1972, ACTA OTO-LARYNGOL, V73, P455, DOI 10.3109/00016487209138966 IGARASHI M, 1979, ACTA OTO-LARYNGOL, V87, P79, DOI 10.3109/00016487909126390 IGARASHI M, 1979, ACTA OTO-LARYNGOL, V87, P429, DOI 10.3109/00016487909126446 KAWASE T, 1993, J NEUROPHYSIOL, V70, P2519 Kawase T, 1995, HEARING RES, V91, P1, DOI 10.1016/0378-5955(95)00145-X KAWASE T, 1993, J NEUROPHYSIOL, V70, P2533 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 Maison S, 1999, NEUROSCIENCE, V91, P133, DOI 10.1016/S0306-4522(98)00608-3 MAISON S, 1999, SCAND AUDIOL, V28, P1 Maison S, 1997, HEARING RES, V113, P89, DOI 10.1016/S0378-5955(97)00136-6 Maison S, 1998, HEARING RES, V117, P114, DOI 10.1016/S0378-5955(97)00213-X Maison S, 1997, J NEUROPHYSIOL, V77, P1759 MAY BJ, 1995, ASS RES OT ABSTR, V18, P146 Micheyl C, 1997, BEHAV NEUROSCI, V111, P801, DOI 10.1037/0735-7044.111.4.801 Micheyl C, 1996, J ACOUST SOC AM, V99, P1604, DOI 10.1121/1.414734 Micheyl C, 1999, J ACOUST SOC AM, V105, P293, DOI 10.1121/1.424525 MICHEYL C, 1995, ACTA OTO-LARYNGOL, V115, P178, DOI 10.3109/00016489509139286 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 RYAN S, 1991, British Journal of Audiology, V25, P391, DOI 10.3109/03005369109076614 Scharf B, 1997, HEARING RES, V103, P101, DOI 10.1016/S0378-5955(96)00168-2 SCHARF B, 1994, HEARING RES, V75, P11, DOI 10.1016/0378-5955(94)90051-5 THOMPSON AM, 1991, J COMP NEUROL, V303, P267, DOI 10.1002/cne.903030209 TRAHIOTI.C, 1970, J ACOUST SOC AM, V47, P592, DOI 10.1121/1.1911934 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WILLIAMS EA, 1993, SCAND AUDIOL, V22, P197, DOI 10.3109/01050399309047469 WILLIAMS EA, 1994, ACTA OTO-LARYNGOL, V114, P121, DOI 10.3109/00016489409126029 WINSLOW RL, 1988, HEARING RES, V35, P165, DOI 10.1016/0378-5955(88)90116-5 WINTER IM, 1995, J NEUROPHYSIOL, V73, P141 YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 NR 46 TC 32 Z9 36 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 111 EP 125 DI 10.1016/S0378-5955(99)00196-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500010 PM 10675639 ER PT J AU Devau, G AF Devau, G TI Glycine induced calcium concentration changes in vestibular type I sensory cells SO HEARING RESEARCH LA English DT Article DE N-methyl-D-aspartate; glycine; calcium; vestibular sensory cell; guinea pig ID NMDA RECEPTOR-CHANNEL; SIZE-RELATED PROPERTIES; SACCULAR HAIR-CELLS; METHYL-D-ASPARTATE; GUINEA-PIG; GLUTAMATE RECEPTORS; SYNAPTIC TRANSMISSION; NEUROTRANSMITTER TRANSPORTERS; SYNAPTOPHYSIN EXPRESSION; INDUCED DEPOLARIZATION AB Glutamate is the neurotransmitter of the synapse between vestibular type I hair cells and the afferent nerve calyx. This calyx may also be involved in local feedback, which may modify sensory cell activity via N-methyl-D-aspartate (NMDA) receptors. Glycine is the co-agonist of glutamate ill NMDA receptor activation. Both agents have been detected by immunocytochemistry in the nerve calyx. Glutamate and NMDA stimulations cause changes in the intracellular calcium concentration ([Ca2+](i)) of isolated type I sensory cells. We investigated the effect of glycine stimulation on [Ca2+](i) in guinea pig type I sensory cells by spectrofluorimetry with fura-2. Glycine application to isolated type I sensory cells induced a rapid and transient increase in [Ca2+](i). The fluorescence ratio increased by 55% above the resting level. The peak was reached in 9 s and the return to basal level took about 20 s. A specific antagonist of the glycine site on NMDA receptors, 7-chlorokynurenate (10 mu M), decreased the calcium response to glycine by 60%. Glycine may activate NMDA receptors. Glycine may also activate the strychnine-sensitive glycine receptor-gated channel. Strychnine (50 mu M) decreased the calcium response to glycine by 60%. Thus, glycine probably induces calcium concentration changes in type I vestibular sensory cells via NMDA receptors and/or glycine receptors. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Montpellier 2, INSERM, U432, F-34095 Montpellier 5, France. RP Devau, G (reprint author), Univ Montpellier 2, INSERM, U432, Pl Eugene Bataillon, F-34095 Montpellier 5, France. CR ANNONI JM, 1984, J NEUROSCI, V4, P2106 ANSON LC, 1994, 1 INT S INN EAR NEUR, V1, P3 Attwell David, 1994, Current Opinion in Neurobiology, V4, P353, DOI 10.1016/0959-4388(94)90096-5 Baurle J, 1997, NEUROREPORT, V8, P2443 Boyer C, 1998, EUR J NEUROSCI, V10, P971, DOI 10.1046/j.1460-9568.1998.00107.x Breitinger HG, 1998, CURR PHARM DESIGN, V4, P315 CECOLA RP, 1992, HEARING RES, V61, P65, DOI 10.1016/0378-5955(92)90037-N Corsi M, 1996, TRENDS PHARMACOL SCI, V17, P220, DOI 10.1016/0165-6147(96)10018-3 Dechesne CJ, 1997, DEV BRAIN RES, V99, P103, DOI 10.1016/S0165-3806(96)00216-7 DEMEMES D, 1995, BRAIN RES, V671, P83, DOI 10.1016/0006-8993(94)01322-9 DEMEMES D, 1990, HEARING RES, V46, P261, DOI 10.1016/0378-5955(90)90007-C Denk W, 1995, NEURON, V15, P1311, DOI 10.1016/0896-6273(95)90010-1 DEVAU G, 1993, EUR J NEUROSCI, V5, P1210, DOI 10.1111/j.1460-9568.1993.tb00975.x DEVAU G, 1997, 3 M FRENCH NEUR SOC DRESCHER MJ, 1987, BRAIN RES, V417, P39, DOI 10.1016/0006-8993(87)90177-6 DRESCHER MJ, 1992, J NEUROCHEM, V59, P93, DOI 10.1111/j.1471-4159.1992.tb08879.x Fuchs PA, 1996, CURR OPIN NEUROBIOL, V6, P514, DOI 10.1016/S0959-4388(96)80058-4 FUJITA S, 1994, NEUROREPORT, V5, P862, DOI 10.1097/00001756-199404000-00002 GRIGUER C, 1993, NEUROSCI LETT, V149, P51, DOI 10.1016/0304-3940(93)90345-L GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440 GUTH PS, 1988, HEARING RES, V33, P223, DOI 10.1016/0378-5955(88)90152-9 Guth PS, 1998, PROG NEUROBIOL, V54, P193, DOI 10.1016/S0301-0082(97)00068-3 GUTH PS, 1994, HEARING RES, V75, P225, DOI 10.1016/0378-5955(94)90073-6 Guth PS, 1998, HEARING RES, V125, P154, DOI 10.1016/S0378-5955(98)00145-2 Guth PS, 1996, HEARING RES, V98, P1, DOI 10.1016/0378-5955(96)00031-7 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HARADA N, 1994, ACTA OTO-LARYNGOL, V114, P609, DOI 10.3109/00016489409126113 Hiel H, 1996, BRAIN RES, V738, P347, DOI 10.1016/S0006-8993(96)01046-3 HOCKBERGER PE, 1989, J NEUROSCI, V9, P2272 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 ISSA NP, 1994, P NATL ACAD SCI USA, V91, P7578, DOI 10.1073/pnas.91.16.7578 JOHNSON JW, 1987, NATURE, V325, P529, DOI 10.1038/325529a0 Jones MV, 1996, TRENDS NEUROSCI, V19, P96, DOI 10.1016/S0166-2236(96)80037-3 Kataoka Y, 1996, J NEUROPHYSIOL, V76, P1870 KEMP JA, 1988, P NATL ACAD SCI USA, V85, P6547, DOI 10.1073/pnas.85.17.6547 KEMP JA, 1993, TRENDS PHARMACOL SCI, V14, P20, DOI 10.1016/0165-6147(93)90108-V KUTSUWADA T, 1992, NATURE, V358, P36, DOI 10.1038/358036a0 LANGOSCH D, 1988, P NATL ACAD SCI USA, V85, P7394, DOI 10.1073/pnas.85.19.7394 Lenzi David, 1994, Current Opinion in Neurobiology, V4, P496, DOI 10.1016/0959-4388(94)90049-3 MARSH SJ, 1995, NEURON, V15, P729, DOI 10.1016/0896-6273(95)90160-4 MEGURO H, 1992, NATURE, V357, P70, DOI 10.1038/357070a0 MOLINOFF PB, 1994, PROG BRAIN RES, V100, P39 MORI H, 1995, NEUROPHARMACOLOGY, V34, P1219, DOI 10.1016/0028-3908(95)00109-J MORIYOSHI K, 1991, NATURE, V354, P31, DOI 10.1038/354031a0 MURPHY SN, 1988, P NATL ACAD SCI USA, V85, P8737, DOI 10.1073/pnas.85.22.8737 Nelson N, 1998, J NEUROCHEM, V71, P1785 NIEDZIELSKI AS, 1995, J NEUROSCI, V15, P2338 Olivares L, 1997, J BIOL CHEM, V272, P1211 PARSONS TD, 1994, NEURON, V13, P875, DOI 10.1016/0896-6273(94)90253-4 Paudice P, 1998, EUR J NEUROSCI, V10, P2934, DOI 10.1046/j.1460-9568.1998.00302.x PRIGIONI I, 1994, NEUROREPORT, V5, P516, DOI 10.1097/00001756-199401120-00038 PRIGIONI I, 1990, HEARING RES, V46, P253, DOI 10.1016/0378-5955(90)90006-B Rabejac D, 1997, EUR J NEUROSCI, V9, P221, DOI 10.1111/j.1460-9568.1997.tb01393.x REICHENBERGER I, 1994, J COMP NEUROL, V349, P603, DOI 10.1002/cne.903490408 Rennie KJ, 1997, AM J PHYSIOL-CELL PH, V273, pC1972 SCARFONE E, 1988, J NEUROSCI, V8, P4640 SCARFONE E, 1991, J NEUROSCI, V11, P1173 Scarfone E, 1996, NEUROSCIENCE, V75, P587, DOI 10.1016/0306-4522(96)00243-6 Sorimachi M, 1997, J NEUROCHEM, V69, P797 SOTO E, 1988, BRAIN RES, V462, P104, DOI 10.1016/0006-8993(88)90591-4 SOTO E, 1994, BRAIN RES, V633, P289, DOI 10.1016/0006-8993(94)91551-2 Straka H, 1996, NEUROSCIENCE, V70, P697, DOI 10.1016/S0306-4522(96)83008-9 Straka H, 1996, NEUROSCIENCE, V70, P685, DOI 10.1016/S0306-4522(96)83007-7 Sucher NJ, 1996, TRENDS PHARMACOL SCI, V17, P348, DOI 10.1016/S0165-6147(96)10046-8 Tucker T, 1995, NEURON, V15, P1323, DOI 10.1016/0896-6273(95)90011-X Tucker T, 1996, ANN NY ACAD SCI, V781, P123, DOI 10.1111/j.1749-6632.1996.tb15697.x VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 VANDENBERG RJ, 1992, NEURON, V9, P491, DOI 10.1016/0896-6273(92)90186-H VANDENPOL AN, 1988, J NEUROSCI, V8, P472 WANG J, 1994, EUR J NEUROSCI, V6, P1275, DOI 10.1111/j.1460-9568.1994.tb00317.x Wang YX, 1997, AM J PHYSIOL-CELL PH, V273, pC509 WATKINS JC, 1987, TRENDS NEUROSCI, V10, P265, DOI 10.1016/0166-2236(87)90171-8 Wersall J., 1974, P123 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 Zafra F, 1997, MOL NEUROBIOL, V14, P117, DOI 10.1007/BF02740653 ZUCCA G, 1992, HEARING RES, V63, P52, DOI 10.1016/0378-5955(92)90073-V ZUCCA G, 1993, NEUROREPORT, V4, P403, DOI 10.1097/00001756-199304000-00015 NR 78 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 126 EP 136 DI 10.1016/S0378-5955(99)00194-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500011 PM 10675640 ER PT J AU Suko, T Ichimiya, I Yoshida, K Suzuki, M Mogi, G AF Suko, T Ichimiya, I Yoshida, K Suzuki, M Mogi, G TI Classification and culture of spiral-ligament fibrocytes from mice SO HEARING RESEARCH LA English DT Article DE caldesmon; cochlea; immunocytochemistry; S-100 protein; Na-K-ATPase; ultrastructure ID GUINEA-PIG COCHLEA; INNER-EAR; IMMUNOHISTOCHEMICAL LOCALIZATION; MARGINAL CELLS; S-100 PROTEIN; STRIA AB In this study, we established an immunocytochemical strategy to classify the fibrocytes of the murine spiral ligament (SL), and SL cultures were characterized. Similar to those in other mammals, three different types of fibrocytes were identified. Type I fibrocytes, which are found lateral to the stria vascularis, showed positive immunoreactivity for caldesmon and S-100 protein and were not stained for sodium-potassium-adenosinetriphosphatase (Na-K-ATPase). Type II fibrocytes are located lateral to the spiral prominence epithelium and suprastrial region, and they were distinguishable by their positive staining for Na-K-ATPase. Type III fibrocytes, which are found adjacent to bone in the inferior region of the SL, contained caldesmon but not S-100 or Na-K-ATPase. Secondary cultures from the SL were positive for caldesmon and S-100 and negative for Na-K-ATPase, suggesting that these cells were type I fibrocytes. The present immunocytochemical approach was useful for the classification of murine fibrocyte cultures, and these cultures may benefit future immunological studies of the inner ear because mice have been well characterized immunologically. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Oita Med Univ, Dept Otolaryngol, Hasama, Oita 8795593, Japan. RP Mogi, G (reprint author), Oita Med Univ, Dept Otolaryngol, 1-1 Idaigaoka, Hasama, Oita 8795593, Japan. CR ACHOUCHE J, 1991, ANN OTO RHINOL LARYN, V100, P999 BOWMAN PD, 1985, CELL TISSUE RES, V241, P479 DONATO R, 1986, CELL CALCIUM, V7, P123, DOI 10.1016/0143-4160(86)90017-5 FOSTER JD, 1994, HEARING RES, V74, P67, DOI 10.1016/0378-5955(94)90176-7 Gratton MA, 1996, HEARING RES, V99, P71, DOI 10.1016/S0378-5955(96)00080-9 HAIMOTO H, 1987, LAB INVEST, V57, P489 ICHIMIYA I, 1994, ANN OTO RHINOL LARYN, V103, P457 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 Ichimiya I, 1998, LARYNGOSCOPE, V108, P585, DOI 10.1097/00005537-199804000-00023 Ichimiya I, 1999, HEARING RES, V131, P128, DOI 10.1016/S0378-5955(99)00025-8 KARNOVSK.MJ, 1965, J CELL BIOL, V27, pA137 Kelsell DP, 1997, NATURE, V387, P80, DOI 10.1038/387080a0 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 LIM D J, 1970, Journal of Laryngology and Otology, V84, P413, DOI 10.1017/S0022215100072029 MELICHAR I, 1992, ACTA OTO-LARYNGOL, V112, P762, DOI 10.3109/00016489209137471 OWADA MK, 1984, P NATL ACAD SCI-BIOL, V81, P3133, DOI 10.1073/pnas.81.10.3133 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 SHI SR, 1992, LARYNGOSCOPE, V102, P734, DOI 10.1288/00005537-199207000-00002 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TAKAHASHI T, 1970, Acta Oto-Laryngologica, V69, P46, DOI 10.3109/00016487009123335 NR 22 TC 26 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 137 EP 144 DI 10.1016/S0378-5955(99)00191-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500012 PM 10675641 ER PT J AU Hoshino, T Mizuta, K Gao, J Araki, S Araki, K Takeshita, T Wu, R Morita, H AF Hoshino, T Mizuta, K Gao, J Araki, S Araki, K Takeshita, T Wu, R Morita, H TI Cochlear findings in the white spotting (Ws) rat SO HEARING RESEARCH LA English DT Article DE cochlea; white spotting rat; stria vascularis; hair cell; melanocyte ID INNER-EAR; C-KIT; MELANOCYTES; MOUSE; LOCUS; MICE; DYSFUNCTION; MUTATIONS; GENE AB White spotting (Ws) rats possess a c-kit gene mutation at the W locus, resulting in a variety of characteristics including a lack of intermediate cells of the stria vascularis. The present study employs a light microscope (LM), scanning (SEM) and transmission electron microscopes (TEM), diaminobenzidine (DAB) staining techniques and auditory brainstem response (ABR) to investigate the structure and function of the cochlea in 26 homozygous Ws/Ws rats aged 1-6 months. A slight thinning of the stria vascularis and moderate elevation of ABR threshold were about the only defects noted in 1 month animals, while older animals displayed various defects that tended to worsen with age. At 3 months LM revealed pigment granules in the basal turn of most animals, with a loss of pigmentation in the upper turns. The stria vascularis and organ of Corti tended to be well preserved in the lower. pigmented portion, while the upper. unpigmented portion showed severe strial degeneration and some outer hair cell loss. DAB staining revealed a well developed strial capillary net throughout the pigmented portion of the cochlea. with severe degradation in the unpigmented apical portion. ABR thresholds were slightly elevated over 1 month values. At 6 months great differences in degeneration were noted between right and left ears of the same animal. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hamamatsu Univ Sch Med, Dept Otolaryngol, Hamamatsu, Shizuoka 4313192, Japan. RP Hoshino, T (reprint author), Hamamatsu Univ Sch Med, Dept Otolaryngol, 3600 Handa Cho, Hamamatsu, Shizuoka 4313192, Japan. EM thoshino@hama-med.ac.jp CR Bosher S K, 1966, J Laryngol Otol, V80, P222, DOI 10.1017/S0022215100065191 CABLE J, 1992, HEARING RES, V64, P6, DOI 10.1016/0378-5955(92)90164-I CABLE J, 1995, MECH DEVELOP, V50, P139, DOI 10.1016/0925-4773(94)00331-G CABLE J, 1994, PIGM CELL RES, V7, P17, DOI 10.1111/j.1600-0749.1994.tb00015.x DEOL MS, 1970, J EMBRYOL EXP MORPH, V23, P773 Gao J, 1998, MICROSC RES TECHNIQ, V41, P323, DOI 10.1002/(SICI)1097-0029(19980515)41:4<323::AID-JEMT5>3.0.CO;2-R GRAHAM RC, 1966, J HISTOCHEM CYTOCHEM, V14, P291 HUDSON WR, 1962, ARCHIV OTOLARYNGOL, V75, P213 KITAMURA K, 1994, ACTA OTO-LARYNGOL, V114, P177, DOI 10.3109/00016489409126038 MIZUTA K, 1990, SCANNING MICROSCOPY, V4, P967 MOTOHASHI H, 1994, HEARING RES, V80, P10, DOI 10.1016/0378-5955(94)90003-5 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 NIWA Y, 1991, BLOOD, V78, P1936 SCHROTT A, 1987, ACTA OTO-LARYNGOL, V103, P451 STEEL KP, 1989, DEVELOPMENT, V107, P453 Steel KP, 1995, ANNU REV GENET, V29, P675 TACHIBANA M, 1992, MOL CELL NEUROSCI, V3, P433 TSUJIMURA T, 1991, BLOOD, V78, P1942 NR 18 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 145 EP 156 DI 10.1016/S0378-5955(99)00192-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500013 PM 10675642 ER PT J AU Zenk, J Scheffler, D Scheffler, P Delb, W Iro, H AF Zenk, J Scheffler, D Scheffler, P Delb, W Iro, H TI The influence of noise on blood flow in the basilar artery (BA) - measurements with transcranial color-coded duplex sonography (TCCD) SO HEARING RESEARCH LA English DT Article DE cerebral blood flow; cochlear blood flow; transcranial color-coded duplex sonography; basilar artery; noise exposure ID INFERIOR CEREBELLAR ARTERY; GUINEA-PIG; COCHLEAR; SOUND; EXPOSURE; VELOCITY; SYSTEM AB Acoustic stimuli are being reported as a cause of changes in resistance in the basilar artery (BA). II was the aim of this study to investigate this effect under standardized conditions dependent upon the intensity of the evoking stimulus. Twenty healthy subjects with normal hearing (male/female 14/6; mean age 26.4 years) were exposed to 'pink noise: for periods of 2 min at 75, 85 and 95 dB(A). Parallel to this, the Doppler spectrum of the BA and both the Pourcelor resistance index and the Gosling pulsatility index were measured by means of transcranial color-coded Doppler sonography. In comparison with the base value (al rest) a significant increase in resistance was noted during noise exposure. The noise-induced resistance changes could be interpreted as a consequence of changes in activity of the various centers of the auditory pathway and cerebral function. Further animal experiments may prove the connection between BA blood flow and resistance and their changes depending on different acoustic stimuli or different hearing pathophysiology. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Saarland, Dept Otorhinolaryngol Head & Neck Surg, D-66424 Homburg, Germany. Univ Saarland, Dept Cardiol & Angiol, D-6650 Homburg, Germany. RP Zenk, J (reprint author), Univ Erlangen Nurnberg, Dept Otorhinolaryngol Head & Neck Surg, Waldstr 1, D-91054 Erlangen, Germany. CR AASLID R, 1987, STROKE, V18, P771 Algers B., 1978, ACTA VET SCAND S, V67, P1 ALLESSIO HM, 1992, SCAND AUDIOL, V21, P163 AMES DR, 1972, J ANIM SCI, V34, P994 ANGELBORG C, 1977, ACTA OTO-LARYNGOL, V83, P92, DOI 10.3109/00016487709128818 BECKER G, 1993, J ULTRAS MED, V12, P395 BORG E, 1973, FORSK FRAMSTEG, V7, P5 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 CANLON B, 1984, COMP BIOCHEM PHYS A, V78, P43, DOI 10.1016/0300-9629(84)90089-6 Coleman JKM, 1998, HEARING RES, V119, P61, DOI 10.1016/S0378-5955(98)00038-0 COOPER RAY, 1966, BRAIN RES, V3, P174, DOI 10.1016/0006-8993(66)90075-8 Cransac H, 1998, HEARING RES, V118, P151, DOI 10.1016/S0378-5955(98)00031-8 GALIN D, 1964, SCIENCE, V146, P270, DOI 10.1126/science.146.3641.270 GOMEZ SM, 1990, STROKE, V21, P1746 GOSLING RG, 1974, P ROY SOC MED, V67, P447 JENSEN MM, 1970, PHYSL EFFECTS NOISE, P57 LAURIKAINEN EA, 1993, HEARING RES, V64, P199, DOI 10.1016/0378-5955(93)90006-M Laurikainen EA, 1997, HEARING RES, V105, P141, DOI 10.1016/S0378-5955(96)00198-0 LEHMANN G, 1956, Int Z Angew Physiol, V16, P217 LIBERMAN MC, 1983, NEW PERSPECTIVES NOI, P105 LONSBURYMARTIN BL, 1981, J NEUROPHYSIOL, V46, P563 Mandal A, 1997, HEARING RES, V106, P1, DOI 10.1016/S0378-5955(96)00214-6 MILLEN SJ, 1995, LARYNGOSCOPE, V105, P1305, DOI 10.1288/00005537-199512000-00008 MILLER JM, 1988, AM J OTOLARYNG, V9, P302, DOI 10.1016/S0196-0709(88)80038-3 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 MILLER JM, 1995, OTOLARYNG HEAD NECK, V112, P101, DOI 10.1016/S0194-5998(95)70308-X MIYAZAKI M, 1971, JPN CIRCULATION J, V35, P931 Mueck-Weymann M., 1996, Vasa, V25, P327 Nakai Y, 1988, Acta Otolaryngol Suppl, V447, P23 NIEHAUS L, 1994, BILDGEBUND IMAGING, V61, P82 PALCHUN VT, 1992, VESTN OTORINOLARYNG, V5, P47 POURCELOT L, 1974, COLLOQ INSERM, V34, P213 REN TY, 1993, HEARING RES, V71, P91, DOI 10.1016/0378-5955(93)90024-U ROSEN S, 1970, PHYSL EFFECTS NOISE, P57 Roy C S, 1890, J Physiol, V11, P85 SCHWEIZER J, 1995, VASA-J VASCULAR DIS, V24, P238 Schweizer J, 1996, ULTRASCHALL MED, V17, P68, DOI 10.1055/s-2007-1003149 SILLMAN JS, 1988, ANN OTO RHINOL LARYN, V97, P1 Sturzenegger M, 1996, STROKE, V27, P2256 Suzuki T, 1998, ANN OTO RHINOL LARYN, V107, P648 THORNE PR, 1989, ACTA OTO-LARYNGOL, V107, P71, DOI 10.3109/00016488909127481 WEILLE FL, 1954, AMA ARCH OTOLARYNGOL, V59, P731 WIDDER B, 1995, TRANSCRANIELLE DOPPL, P1 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 NR 44 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 157 EP 164 DI 10.1016/S0378-5955(99)00195-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500014 PM 10675643 ER PT J AU Kaltenbach, JA Afman, CE AF Kaltenbach, JA Afman, CE TI Hyperactivity in the dorsal cochlear nucleus after intense sound exposure and its resemblance to tone-evoked activity: a physiological model for tinnitus SO HEARING RESEARCH LA English DT Article DE plasticity; spontaneous activity; tinnitus; cochlear nucleus; noise-induced hearing loss; noise-induced tinnitus ID HAIR CELL LOSS; INFERIOR COLLICULUS; TONOTOPIC MAP; SALICYLATE; MECHANISMS; INCREASES; THRESHOLD; RATS AB Intense tone exposure induces increased spontaneous activity (hyperactivity), in the dorsal cochlear nucleus (DCN) of hamsters. This increase may represent an important neural correlate of noise-induced tinnitus, a condition in which sound, typically of very high pitch, is perceived in the absence of a corresponding acoustic stimulus. Since high pitch sounds are thought to be represented in central auditory structures by the place of activation across the tonotopic array; it is therefore possible that the high pitch of noise-induced tinnitus occurs because intense sound exposure induces a tonotopic distribution of chronic hyperactivity in the DCN similar to that normally evoked only under conditions of high frequency stimulation. To investigate this possibility we compared this tone-induced hyperactivity with the activity evoked in normal animals by presentation of a tone. This comparison revealed that the activity in the DCN of animals which had been exposed to an intense 10 kHz tone 1 month previously showed a striking similarity to the activity in the DCN of normal animals during presentation of low to moderate level tonal stimuli of the same frequency. In both test conditions similar patterns were seen in the topographic distribution of the increased activity along the tonotopic axis. The magnitude of hyperactivity in exposed animals was similar to the evoked activity in the normal DCN responding to a stimulus at a level of 20 dB SL. These results suggest that the altered DCN following intense tone exposure behaves physiologically as though it is responding to a tone in the absence of a corresponding acoustic stimulus. The relevance of these findings to noise-induced tinnitus and their implications for understanding its underlying mechanisms are discussed. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Wayne State Univ, Dept Otolaryngol, Detroit, MI 48201 USA. RP Kaltenbach, JA (reprint author), Wayne State Univ, Dept Otolaryngol, 5E-UHC, Detroit, MI 48201 USA. CR WallhausserFranke E, 1996, NEUROREPORT, V7, P1585, DOI 10.1097/00001756-199607080-00010 CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O COLES RA, 1996, P 5 INT TINN SEM AM, P135 Dandy W, 1941, SURG GYNECOL OBSTET, V72, P421 EVANS EF, 1978, AUDIOLOGY, V17, P369 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 EVANS EF, 1981, NEURONAL MECHANISMS, P69 Evans E F, 1981, Ciba Found Symp, V85, P108 HEFFNER HE, 1999, ARO ABSTR, V22, P47 House J W, 1981, Ciba Found Symp, V85, P204 JASTREBOFF PJ, 1986, J ACOUST SOC AM, V80, P1384, DOI 10.1121/1.394391 JASTREBOFF PJ, 1988, BEHAV NEUROSCI, V102, P811, DOI 10.1037/0735-7044.102.6.811 JASTREBOFF PJ, 1990, NEUROSCI RES, V8, P221, DOI 10.1016/0168-0102(90)90031-9 KALTENBACH JA, 1992, HEARING RES, V59, P213, DOI 10.1016/0378-5955(92)90118-7 Kaltenbach JA, 1998, HEARING RES, V124, P78, DOI 10.1016/S0378-5955(98)00119-1 KALTENBACH JA, 1999, P 6 INT TINN SEM, V6, P133 Kaltenbach JA, 1996, AUDIT NEUROSCI, V3, P57 KALTENBACH JA, 1991, HEARING RES, V51, P149, DOI 10.1016/0378-5955(91)90013-Y KUMAGAI M, 1992, Hokkaido Journal of Medical Science, V67, P216 LIBERMAN MC, 1978, ACTA OTOLARYNGOL S, V358, P5 LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 MCFADDEN D, 1982, TINNITUS FACTS THEOR, P1 Meikle M, 1984, J Laryngol Otol Suppl, V9, P17 Meikle M. B., 1995, MECH TINNITUS, P181 Meleca RJ, 1997, BRAIN RES, V750, P201, DOI 10.1016/S0006-8993(96)01354-6 MULHERAN M, 1990, EFFECTS SYSTEMIC BLO SHEHATADIELER WE, 1994, HEARING RES, V74, P77, DOI 10.1016/0378-5955(94)90177-5 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 Zhang JS, 1998, NEUROSCI LETT, V250, P197, DOI 10.1016/S0304-3940(98)00482-0 NR 30 TC 133 Z9 138 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 165 EP 172 DI 10.1016/S0378-5955(99)00197-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500015 PM 10675644 ER PT J AU Carlyon, RP AF Carlyon, RP TI Detecting coherent and incoherent frequency modulation SO HEARING RESEARCH LA English DT Article DE frequency modulation; pitch; perceptual asymmetry ID COMPLEX TONES; FUNDAMENTAL-FREQUENCY; UNRESOLVED HARMONICS; IMPAIRED LISTENERS; PITCH PERCEPTION; DISCRIMINATION; COMPONENTS; SEGREGATION; CARRIERS; VOWELS AB Three experiments investigated whether or not the auditory system contains a neural mechanism that is sensitive to differences in the pattern of frequency modulation imposed on widely separated carriers. Experiment 1 measured the discrimination between an unmodulated two-tone complex and one in which either coherent or: incoherent frequency modulation was imposed on the two carrier frequencies. These two frequencies were either 1100+1925 Hz or 1100+2000 Hz, and the stimuli were presented against a pink-noise background. The method was based on that used in experiments by Furukawa and Moore (1996), which were previously interpreted as providing evidence in favour of a mechanism sensitive to FM coherence. Discrimination was sometimes better for coherent than for incoherent FM, as reported by Furukawa and Moore, but only for four out of the eight listeners tested. The remaining experiments excluded those subjects who had shown no effect of FM coherence in experiment 1. Experiment 2 showed that detection of a static shift on the carrier frequencies of the two components was better when the carriers were shifted in the same, compared to the opposite. direction. This difference occurred regardless of whether the carriers were modulated coherently, incoherently, or were unmodulated. The experiment also showed that performance was better when the 1100-Hz carrier was shifted down and the 1925-Hz carrier was shifted up; compared to when the 1100-Hz carrier shifted up and the 1925-Hz carrier shifted down. Experiment 3 showed that this difference also applied to dynamic changes: detection of quasi-linear frequency sweeps (0.5 cycles of sinusoidal FM) was better when the higher component glided up: and the lower component glided down than vice versa. In the former condition, performance was as good as with same-direction sweeps. It is concluded that the effects observed in experiment 1 and by Furukawa and Moore result from the processing of a global percept arising from the perceptual fusion of the two carriers, and do not represent an across-frequency mechanism sensitive to FM coherence. In addition, it is argued that experiments 2 and 3 demonstrate the existence of perceptual asymmetries in hearing. (C) 2000 Elsevier Science B.V. All rights reserved. C1 MRC, Cognit & Brain Sci Unit, Cambridge CB2 2EF, England. RP Carlyon, RP (reprint author), MRC, Cognit & Brain Sci Unit, 15 Chaucer Rd, Cambridge CB2 2EF, England. EM bob.carylon@mrc-cbu.cam.ac.uk RI Carlyon, Robert/A-5387-2010 CR ASSMANN PF, 1990, J ACOUST SOC AM, V88, P680, DOI 10.1121/1.399772 Beck J, 1982, ORG REPRESENTATION P, P285 BROKX JPL, 1982, J PHONETICS, V10, P23 BUUS S, 1994, J ACOUST SOC AM, V96, P1445, DOI 10.1121/1.411442 CARLYON RP, 1994, J ACOUST SOC AM, V95, P2622, DOI 10.1121/1.410019 CARLYON RP, 1991, J ACOUST SOC AM, V89, P329, DOI 10.1121/1.400468 CARLYON RP, 1992, PHILOS T ROY SOC B, V336, P347, DOI 10.1098/rstb.1992.0068 CARLYON RP, 1989, J ACOUST SOC AM, V85, P2563, DOI 10.1121/1.397750 CARLYON RP, 1994, J ACOUST SOC AM, V95, P949, DOI 10.1121/1.410012 CARLYON RP, 1990, J ACOUST SOC AM, V87, P260, DOI 10.1121/1.399293 Carlyon RP, 1996, J ACOUST SOC AM, V99, P525, DOI 10.1121/1.414511 CARLYON RP, 1994, J ACOUST SOC AM, V95, P968, DOI 10.1121/1.410013 CUSACK R, 1999, AUDITORY POP OUT PER DANNENBRING GL, 1978, PERCEPT PSYCHOPHYS, V24, P369, DOI 10.3758/BF03204255 DARWIN CJ, 1984, Q J EXP PSYCHOL-A, V36, P193 DEMANY L, 1991, J ACOUST SOC AM, V90, P3019, DOI 10.1121/1.401776 DUIFHUIS H, 1982, J ACOUST SOC AM, V71, P1568, DOI 10.1121/1.387811 Edwards AL, 1973, STAT METHODS ELLIOTT LL, 1992, J ACOUST SOC AM, V92, P1919, DOI 10.1121/1.405239 FURUKAWA S, 1996, CHANNEL PROCESSES MO Furukawa S, 1996, J ACOUST SOC AM, V100, P2299, DOI 10.1121/1.417939 Furukawa S, 1997, J ACOUST SOC AM, V101, P1632, DOI 10.1121/1.418147 JESTEADT W, 1975, J ACOUST SOC AM, V57, P1161, DOI 10.1121/1.380574 Lacher-Fougere S, 1998, AUDIOLOGY, V37, P109 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2866, DOI 10.1121/1.400725 Micheyl C, 1998, J ACOUST SOC AM, V104, P3006, DOI 10.1121/1.423975 Moore B. C. J., 1989, INTRO PSYCHOL HEARIN MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1853, DOI 10.1121/1.391936 MOORE BCJ, 1992, J ACOUST SOC AM, V92, P3119, DOI 10.1121/1.404208 MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1861, DOI 10.1121/1.391937 PLACK CJ, 1995, J ACOUST SOC AM, V98, P1355, DOI 10.1121/1.413471 SCHEFFERS MTM, 1983, U GRONINGEN GRONINGE SEK A, 1995, J ACOUST SOC AM, V97, P2479, DOI 10.1121/1.411968 SHACKLETON TM, 1994, J ACOUST SOC AM, V95, P3529, DOI 10.1121/1.409970 Slaney M., 1990, P IEEE INT C AC SPEE, P357 STRICKLAND EA, 1989, J ACOUST SOC AM, V86, P2160, DOI 10.1121/1.398476 SUMMERFIELD Q, 1992, PHILOS T ROY SOC B, V336, P357, DOI 10.1098/rstb.1992.0069 TREISMAN A, 1988, PSYCHOL REV, V95, P15, DOI 10.1037//0033-295X.95.1.15 YOST WA, 1987, J ACOUST SOC AM, V81, P1896, DOI 10.1121/1.394754 YOST WA, 1989, J ACOUST SOC AM, V85, P848, DOI 10.1121/1.397556 YOST WA, 1992, ADV BIOSCI, V83, P487 NR 41 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 173 EP 188 DI 10.1016/S0378-5955(99)00200-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500016 PM 10675645 ER PT J AU Avan, P Buki, B Maat, B Dordain, M Wit, HP AF Avan, P Buki, B Maat, B Dordain, M Wit, HP TI Middle ear influence on otoacoustic emissions. I: Noninvasive investigation of the human transmission apparatus and comparison with model results SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; distortion; middle ear impedance; stapedius reflex; middle ear pressure ID CONTRALATERAL ACOUSTIC STIMULATION; DISTORTION PRODUCTS; PRESSURE CHANGES; REFLEX; IMPEDANCE; ORIGIN AB Evoked otoacoustic emissions (EOAEs) are generated within the cochlea in response to external sounds, and they can be acoustically detected in the external auditory meatus after backward propagation through the middle ear. In addition to being used to probe the cochlear mechanisms, they are expected to be sensitive to minute changes in middle ear impedance. Systematic measurements of the changes in the vectorial components of EOAEs were carried out after various manipulations of the human middle ear in order to characterize the influence of stiffness and inertia of the stapes and tympanic-membrane systems. For this purpose, stapedius muscle contractions were elicited by high-level contralateral sound, controlled changes in middle ear pressure (range +/- 100 daPa) were produced and the tympanic membrane was loaded with water droplets. A computer model of the middle ear network was implemented using a standard lumped-element electric: analog of the middle ear (Zwislocki's model). Forward and backward transmission changes were simulated and model predictions were compared to experimental data. Apart from the case of positive middle ear pressures. a close qualitative correspondence was found between model and real-ear results. Each of the effects was characterized by a unique pattern of phase and magnitude changes as a function of frequency, in relation to the mechanical characteristics of the involved subsystem (i.e. stapes stiffness, tympanic-membrane stiffness or mass) and its resonance properties. Owing to their high sensitivity; EOAEs could be helpful for an accurate-individual multifrequency analysis of middle ear impedance by comparisons under rest and lest conditions. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Auvergne, Fac Med, Lab Biophys Sensorielle EA 2667, Clermont Ferrand, France. Semmelweis Univ, ENT Dept, H-1085 Budapest, Hungary. AZG, ENT & Audiol Dept, Groningen, Netherlands. RP Avan, P (reprint author), Sch Med, Biophys Lab, POB 38, F-63001 Clermont Ferrand, France. EM paul.avan@u-clermont1.fr CR ALLEN JB, 1990, CUBE DIS USER MANUAL AMEDEE RG, 1995, LARYNGOSCOPE, V105, P589, DOI 10.1288/00005537-199506000-00006 Antonelli A, 1986, Scand Audiol Suppl, V25, P97 Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 Borg E., 1984, ACOUSTIC REFLEX BASI, P63 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 Buki B, 1996, HEARING RES, V94, P125, DOI 10.1016/0378-5955(96)00015-9 Buki B, 2000, HEARING RES, V140, P202, DOI 10.1016/S0378-5955(99)00202-6 BURNS EM, 1993, HEARING RES, V67, P117, DOI 10.1016/0378-5955(93)90239-W COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E Giraud AL, 1996, HEARING RES, V94, P54, DOI 10.1016/0378-5955(96)00002-0 Guinan Jr J.J., 1996, COCHLEA, P435 HAUSER R, 1993, HEARING RES, V69, P133, DOI 10.1016/0378-5955(93)90101-6 HUTTENBRINK KB, 1988, ACTA OTO-LARYNGOL, P1 KEMP DT, 1980, HEARING RES, V2, P533, DOI 10.1016/0378-5955(80)90091-X KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 KOBLER JB, 1987, BRAIN RES, V10, P372 KRINGLEBOTN M, 1988, SCAND AUDIOL, V17, P75, DOI 10.3109/01050398809070695 LAWRENCE M, 1965, ARCHIV OTOLARYNGOL, V82, P478 LUTMAN ME, 1979, J SOUND VIB, V64, P133, DOI 10.1016/0022-460X(79)90578-9 Marchbanks RJ, 1982, HEARING AID J, V35, P14 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K Murakami S, 1997, ACTA OTO-LARYNGOL, V117, P390, DOI 10.3109/00016489709113411 NAEVE SL, 1992, J ACOUST SOC AM, V91, P2091, DOI 10.1121/1.403695 NISHIHARA S, 1993, OTOLARYNG HEAD NECK, V109, P899 OSTERHAMMEL PA, 1993, SCAND AUDIOL, V22, P111, DOI 10.3109/01050399309046026 OWENS J J, 1992, Seminars in Hearing, V13, P53, DOI 10.1055/s-0028-1085141 PANG XD, 1985, PERIPHERAL AUDITORY, P36 PLINKERT PK, 1994, EUR ARCH OTO-RHINO-L, V251, P95 Puria S, 1996, J ACOUST SOC AM, V99, P500, DOI 10.1121/1.414508 RABINOWITZ WM, 1981, J ACOUST SOC AM, V70, P1025, DOI 10.1121/1.386953 RICHTER B, 1994, ACTA OTO-LARYNGOL, V114, P278, DOI 10.3109/00016489409126056 SHERA CA, 1992, J ACOUST SOC AM, V92, P1371, DOI 10.1121/1.403930 TRINE MB, 1993, EAR HEARING, V14, P401, DOI 10.1097/00003446-199312000-00005 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L Wever EG, 1954, PHYSL ACOUSTICS WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V WIEDERHOLD ML, 1990, LECT NOTES BIOMATH, V87, P251 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X Wilson J P, 1981, Ciba Found Symp, V85, P82 Wilson R., 1984, ACOUSTIC REFLEX, P329 Zhang M, 1997, J ACOUST SOC AM, V102, P1032, DOI 10.1121/1.419856 ZWICKER E, 1990, HEARING RES, V47, P185, DOI 10.1016/0378-5955(90)90150-N ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 NR 47 TC 35 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 189 EP 201 DI 10.1016/S0378-5955(99)00201-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500017 PM 10675646 ER PT J AU Buki, B Chomicki, A Dordain, M Lemaire, JJ Wit, HP Chazal, J Avan, P AF Buki, B Chomicki, A Dordain, M Lemaire, JJ Wit, HP Chazal, J Avan, P TI Middle-ear influence on otoacoustic emissions. II: Contributions of posture and intracranial pressure SO HEARING RESEARCH LA English DT Article DE posture; intracranial pressure; otoacoustic emission; distortion; middle-ear impedance; hydrocephalus ID COCHLEAR AQUEDUCT; FLUID PRESSURE; PATENCY; REFLEX AB Although it seems likely that body till or surgically provoked variations in intracranial pressure (ICP) can result in variations of intralabyrinthine pressure, the channels for pressure transmission remain controversial and the reasons why evoked otoacoustic emissions (EOAEs) exhibit attendant modifications are unclear. The theoretical framework implemented in the companion paper [Avan et al, part I, 2000] provides sensitive and non-invasive means to identify the middle-ear mechanism(s) entailed in EOAE changes. It was thus applied to analyze the influence of posture on EOAE phases and magnitudes as a function of frequency, in a series of experiments involving body tilt from sitting to supine (0 degrees or -30 degrees). Controlled ICP variations were surgically carried out in a series of hydrocephalic patients and the resulting EOAE changes were compared to posture data and model predictions. In all cases, the EOAE changes closely resembled those due to an increase in the stiffness of the stapes' annular ligament, in keeping with the assumption that ICP gets transmitted to intralabyrinthine spaces and modifies the hydrostatic load on the stapes, thereby influencing EOAE features. A small additional contribution of middle-ear pressure to EOAE changes was identified in addition to the main stapes component. Dynamical EOAE measurements showed that sudden ICP changes were transmitted to the inner ear within 8-30 s. The high sensitivity of EOAE phases below 2 kHz to ICP changes, together with the absence of any significant confounding middle-ear effect, favors EOAEs for a reliable non-invasive monitoring of ICP and intralabyrinthine pressures. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Auvergne, Fac Med, Lab Biophys Sensorielle EA 2667, F-63001 Clermont Ferrand, France. Semmelweis Univ, ENT Dept, H-1085 Budapest, Hungary. AZG, ENT & Audiol Dept, Groningen, Netherlands. RP Avan, P (reprint author), Univ Auvergne, Fac Med, Lab Biophys Sensorielle EA 2667, POB 38, F-63001 Clermont Ferrand, France. EM paul.avan@u-clermont1.fr CR ALLEN JB, 1990, CUBE DIS USER MANUAL Antonelli A, 1986, Scand Audiol Suppl, V25, P97 Avan P, 2000, HEARING RES, V140, P189, DOI 10.1016/S0378-5955(99)00201-4 Buki B, 1996, HEARING RES, V94, P125, DOI 10.1016/0378-5955(96)00015-9 CARLBORG B, 1982, ANN OTO RHINOL LARYN, V91, P209 CASSELBRANT M, 1979, ACTA OTO-LARYNGOL, P7 CHAPMAN PH, 1990, NEUROSURGERY, V26, P181 CORSO JF, 1962, PERCEPT MOTOR SKILL, V14, P449 Davson H, 1967, PHYSL CREBROSPINAL F Gaihede Michael, 1998, Auris Nasus Larynx, V25, P255, DOI 10.1016/S0385-8146(98)00009-1 Gopen Q, 1997, HEARING RES, V107, P9, DOI 10.1016/S0378-5955(97)00017-8 HORST JW, 1983, HEARING PHYSL BASES, P89 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 LACKNER JR, 1974, ACTA OTO-LARYNGOL, V77, P19, DOI 10.3109/00016487409124593 LUTMAN ME, 1979, J SOUND VIB, V64, P133, DOI 10.1016/0022-460X(79)90578-9 MACRAE JH, 1972, J SPEECH HEAR RES, V15, P330 MARCHBANKS RJ, 1993, MMS 10 TYMPANIC DISP Marchbanks RJ, 1982, HEARING AID J, V35, P14 MARCHBANKS RJ, 1984, ACTA OTO-LARYNGOL, V98, P119, DOI 10.3109/00016488409107543 Miyake H, 1997, NEUROSURGERY, V40, P931, DOI 10.1097/00006123-199705000-00009 Moss S M, 1990, Z Kinderchir, V45 Suppl 1, P26 PHILLIPS AJ, 1992, BRIT J AUDIOL, V26, P339, DOI 10.3109/03005369209076657 PHILLIPS A J, 1989, British Journal of Audiology, V23, P279, DOI 10.3109/03005368909076515 REID A, 1990, British Journal of Audiology, V24, P123, DOI 10.3109/03005369009077853 SEO T, 1997, ASS RES OTOLARYNGOL, P157 Wable J, 1996, INTRACRANIAL AND INTRALABYRINTHINE FLUIDS, P191 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X Wilson J P, 1981, Ciba Found Symp, V85, P82 WLODYKA J, 1978, ANN OTO RHINOL LARYN, V87, P22 YOSHIDA M, 1991, EUR ARCH OTO-RHINO-L, V248, P139 ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 NR 31 TC 25 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 202 EP 211 DI 10.1016/S0378-5955(99)00202-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500018 PM 10675647 ER PT J AU Prieskorn, DM Miller, JM AF Prieskorn, DM Miller, JM TI Technical report: chronic and acute intracochlear infusion in rodents SO HEARING RESEARCH LA English DT Article DE intracochlear infusion; osmotic pump; bolus injection; hearing; rodent ID GUINEA-PIG; AUDITORY NEURONS; GROWTH-FACTOR; COCHLEA AB As a follow-up to the Brown ct al., 1993 technique, we have made several improvements to the micro-cannula, osmotic pump procedure, enabling chronic intracochlear infusions while maintaining hearing. In addition, acute bolus injection techniques are briefly described in guinea pig, rat and mouse. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Miller, JM (reprint author), Univ Michigan, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T Carvalho GJ, 1999, AM J OTOL, V20, P87 Ernfors P, 1996, NAT MED, V2, P463, DOI 10.1038/nm0496-463 KINGMA GG, 1992, J NEUROSCI METH, V45, P127, DOI 10.1016/0165-0270(92)90050-N Lalwani AK, 1996, GENE THER, V3, P588 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 Nair TS, 1997, HEARING RES, V107, P93, DOI 10.1016/S0378-5955(97)00024-5 Nair TS, 1999, HEARING RES, V129, P50, DOI 10.1016/S0378-5955(98)00220-2 PARK GH, 1998, 21 MIDW M ARO ST PET SCHINDLER RA, 1995, AM J OTOL, V16, P304 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 NR 11 TC 70 Z9 70 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 2000 VL 140 IS 1-2 BP 212 EP 215 DI 10.1016/S0378-5955(99)00193-8 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 285ZD UT WOS:000085417500019 PM 10675648 ER PT J AU Withnell, RH Yates, GK Kirk, DL AF Withnell, RH Yates, GK Kirk, DL TI Changes to low-frequency components of the TEOAE following acoustic trauma to the base of the cochlea SO HEARING RESEARCH LA English DT Article DE transient-evoked otoacoustic emission; intermodulation distortion; acoustic trauma; guinea pig ID EVOKED OTOACOUSTIC EMISSIONS; GUINEA-PIG COCHLEA; BASILAR-MEMBRANE VIBRATIONS; TRAVELING WAVES; HAIR-CELLS; HEARING; ENHANCEMENT; SENSITIVITY; FUROSEMIDE; EXPOSURES AB Several studies have shown that acoustic trauma to the base of the cochlea can result in loss of transient-evoked otoacoustic emission (TEOAE) energy at frequencies much lower than those affected in the audiogram. We have extended these studies to show that the low-frequency emission energy was substantially affected if the transient stimulus included frequencies within the range affected by the trauma, otherwise the change observed was small. In keeping with the suggestion that TEOAEs are predominantly comprised of intermodulation distortion energy (Yates and Withnell, Hear. Res. 136 (1999) 49-64), trauma to the basal region of the cochlea was found to affect emission energy across a broad Frequency range in response to a wide-band acoustic stimulus. Further, group delay measurements demonstrated that the dominant contribution to the TEOAE originated from the basal region of the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. RP Yates, GK (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. CR AVAN P, 1990, HEARING RES, V44, P151, DOI 10.1016/0378-5955(90)90077-3 Avan P, 1997, J ACOUST SOC AM, V101, P2771, DOI 10.1121/1.418564 AVAN P, 1993, HEARING RES, V70, P109, DOI 10.1016/0378-5955(93)90055-6 AVAN P, 1995, J ACOUST SOC AM, V97, P1 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DALLOS P, 1992, J NEUROSCI, V12, P4575 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 deBoer E, 1997, J ACOUST SOC AM, V102, P3810, DOI 10.1121/1.420356 DOLAN TG, 1985, J ACOUST SOC AM, V77, P1475, DOI 10.1121/1.392042 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 GEISLER CD, 1982, J ACOUST SOC AM, V71, P1201, DOI 10.1121/1.387768 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 GUELKE RW, 1985, HEARING RES, V19, P185, DOI 10.1016/0378-5955(85)90137-6 GUMMER AW, 1984, J ACOUST SOC AM, V76, P1388, DOI 10.1121/1.391456 HILGER AW, 1995, HEARING RES, V84, P1, DOI 10.1016/0378-5955(95)00007-Q Hudspeth AJ, 1997, CURR OPIN NEUROBIOL, V7, P480, DOI 10.1016/S0959-4388(97)80026-8 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 KIRK DL, 1994, HEARING RES, V74, P38, DOI 10.1016/0378-5955(94)90174-0 Kirk DL, 1996, J ACOUST SOC AM, V100, P3714, DOI 10.1121/1.417335 Kirk DL, 1998, AUDIOL NEURO-OTOL, V3, P21, DOI 10.1159/000013776 KOSHIGOE S, 1982, J ACOUST SOC AM, V71, P1194, DOI 10.1121/1.387767 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 NAKAJIMA HH, 1994, J ACOUST SOC AM, V96, P786, DOI 10.1121/1.410316 PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 Prieve BA, 1996, J ACOUST SOC AM, V99, P3077, DOI 10.1121/1.414794 REBILLARD G, 1992, HEARING RES, V62, P142, DOI 10.1016/0378-5955(92)90179-Q Ruggero MA, 1996, AUDIT NEUROSCI, V2, P329 SCHMIEDT RA, 1984, J ACOUST SOC AM, V76, P1293, DOI 10.1121/1.391446 SUBRAMANIAM M, 1994, HEARING RES, V74, P204, DOI 10.1016/0378-5955(94)90188-0 SUTTON LA, 1994, HEARING RES, V75, P161, DOI 10.1016/0378-5955(94)90067-1 UEDA H, 1992, HEARING RES, V62, P199, DOI 10.1016/0378-5955(92)90187-R Withnell RH, 1998, J ACOUST SOC AM, V104, P344, DOI 10.1121/1.423243 Withnell RH, 1998, J ACOUST SOC AM, V104, P350, DOI 10.1121/1.423292 YATES DK, 1995, HEARING, P41 Yates GK, 1999, HEARING RES, V136, P49, DOI 10.1016/S0378-5955(99)00108-2 NR 38 TC 28 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 1 EP 12 DI 10.1016/S0378-5955(99)00132-X PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800001 PM 10601708 ER PT J AU Nordmann, AS Bohne, BA Harding, GW AF Nordmann, AS Bohne, BA Harding, GW TI Histopathological differences between temporary and permanent threshold shift SO HEARING RESEARCH LA English DT Article DE noise; temporary threshold shift; permanent threshold shift; auditory brainstem response; histopathology; chinchilla ID SERIAL-SECTION RECONSTRUCTION; HIGH-FREQUENCY NOISE; INDUCED HEARING-LOSS; ACOUSTIC TRAUMA; INNER-EAR; ULTRASTRUCTURAL-CHANGES; CHINCHILLA-COCHLEA; CUTICULAR PLATES; EXPOSURE; STEREOCILIA AB The structural changes associated with noise-induced temporary threshold shift (TTS) were compared to the damage associated with permanent threshold shift (PTS). A within-animal paradigm involving survival-fixation was used to minimize problems with data interpretation from interanimal variability in response to noise. Auditory brainstem response thresholds for clicks and tone pips were determined pre- and 1-2 h post-exposure in 11 chinchillas. The animals were exposed for 24 h to an octave band of noise with a center frequency of 4 kHz and a sound pressure level of 86 dB. Three animals (0/0-day) had both cochleas terminal-fixed 2-3 h postexposure. Two animals (27/27-day) had threshold shifts determined every other day for 1 week, every week thereafter, and underwent terminal-fixation of both cochleas 27 days after exposure. Six animals (0/n-day) had threshold shifts determined in both ears upon removal from the noise their left cochlea was then survival-fixed 2-3 h post-exposure. Threshold shifts were determined in their right ear every 2-3 days until their hearing either returned to pre-exposure values or stabilized at a reduced level at which time their right cochlea was terminal-fixed (4-13 days post-exposure). All cochleas were prepared as plastic-embedded flat preparations. Missing hair cells were counted and supporting cells and nerve fibers were evaluated throughout the organ of Corti using phase-contrast microscopy. Post-exposure, all animals had moderate TTSs in their left and right ears which averaged 43 dB for 4-12 kHz. In the 0/0-day animals, the only abnormality which correlated with TTS was a buckling of the pillar bodies. In the 0/n-day animals, their left cochlea (survival-fixed 2-3 h post-exposure) had outer hair cell (OHC) stereocilia which were not embedded in the tectorial membrane in the region of the TTS whereas OHC stereocilia were embedded in the tectorial membrane throughout the cochleas of non-noise-exposed, survival-fixed controls. Three of six right cochleas (terminal-fixed 4-13 days post-exposure) from the Gin-day animals developed a PTS and two of these cochleas had focal losses of inner and outer hair cells and afferent nerve fibers at the corresponding frequency location. The other cochlea with PTS had buckled pillars in the corresponding frequency region. These results suggest that with moderate levels of noise exposure, buckling of the supporting cells results in an uncoupling of the OHC stereocilia from the tectorial membrane which results in a TTS. The mechanisms resulting in TTS appear to be distinct from those that produce permanent hair cell damage and a PTS. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. RP Bohne, BA (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, Box 8115, St Louis, MO 63110 USA. RI Bohne, Barbara/A-9113-2008 OI Bohne, Barbara/0000-0003-3874-7620 CR BAGGOT PJ, 1987, J ACOUST SOC AM, V81, P1499, DOI 10.1121/1.394502 BEAGLEY HA, 1965, ACTA OTOLARYNGOL, V60, P437, DOI 10.3109/00016486509127027 Bohne B.A., 1982, NEW PERSPECTIVES NOI, P283 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 BOHNE BA, 1987, HEARING RES, V29, P251, DOI 10.1016/0378-5955(87)90172-9 BOHNE BA, 1972, LARYNGOSCOPE, V82, P1 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 BOHNE BA, 1986, J ACOUST SOC AM, V80, P1729, DOI 10.1121/1.394285 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 BOHNE GA, 1999, HEARING RES, V134, P163 DAVIS H, 1953, J ACOUST SOC AM, V25, P1180, DOI 10.1121/1.1907260 Dunn D. E., 1979, ABSTR ASS RES OTOLAR, V2, P37 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 Flock A, 1999, J NEUROSCI, V19, P4498 GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 HARDING GW, 1992, HEARING RES, V63, P26, DOI 10.1016/0378-5955(92)90070-4 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HAYAT MA, 1978, INTRO BIOL SCANNING, P134 HUNTERDUVAR IM, 1977, SCANNING ELECT MICRO, V2, P421 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 LIM DJ, 1979, OTOLARYNG CLIN N AM, V12, P493 LIM DJ, 1971, ARCHIV OTOLARYNGOL, V94, P294 LIPSCOMB DM, 1973, LARYNGOSCOPE, V83, P259, DOI 10.1288/00005537-197302000-00008 Lurie MH, 1942, ANN OTO RHINOL LARYN, V51, P712 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLS JH, 1973, J SPEECH HEAR RES, V16, P426 MILLS JH, 1972, J SPEECH HEAR RES, V15, P624 MULROY MJ, 1982, SCANNING ELECT MICRO, V4, P1753 PACK AK, 1999, ABSTR ASS RES OT, V22, P150 PERLMAN H B, 1962, Acta Otolaryngol, V54, P99, DOI 10.3109/00016486209126927 Puel JL, 1998, NEUROREPORT, V9, P2109, DOI 10.1097/00001756-199806220-00037 PUEL JL, 1994, J COMP NEUROL, V341, P241, DOI 10.1002/cne.903410209 Pujol R, 1992, NOISE INDUCED HEARIN, P196 RICHTER CP, 1999, ABSTR ASS RES OT, V22, P211 ROBERTSON D, 1983, HEARING RES, V9, P263, DOI 10.1016/0378-5955(83)90031-X ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 ROYSTER LH, 1986, NOISE HEARING CONSER, P143 RYDMARKER S, 1989, SCANNING MICROSCOPY, V3, P1253 SLEPECKY N, 1982, ACTA OTO-LARYNGOL, V93, P329, DOI 10.3109/00016488209130890 SPOENDLI.H, 1969, PRACT-OTO-RHINO-LARY, V31, P257 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 STOPP P, 1982, NEW PERSPECTIVES NOI, P331 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 Tolomeo JA, 1997, BIOPHYS J, V73, P2241 TONNDORF J, 1980, ANN OTO RHINOL LARYN, V89, P353 Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 NR 50 TC 125 Z9 139 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 13 EP 30 DI 10.1016/S0378-5955(99)00163-X PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800002 PM 10601709 ER PT J AU Hallworth, R McCoy, M Polan-Curtain, J AF Hallworth, R McCoy, M Polan-Curtain, J TI Tubulin expression in the developing and adult gerbil organ of Corti SO HEARING RESEARCH LA English DT Article DE tubulin; microtubule; cochlea; organ of Corti; development; hair cell; pillar cell; deiters cell ID COCHLEAR EPITHELIAL-CELLS; HAIR-CELLS; F-ACTIN; MICROTUBULES; MATURATION AB In the late stages of inner ear development, the relatively undifferentiated cells of Kollicker's organ are transformed into the elaborately specialized cell types of the organ of Corti. Microtubules are prominent features of adult cells in the organ of Corti, particularly supporting cells. To test the possible role of microtubules in organ of Corti development, the microtubule organization in the organ of Corti has been examined using indirect immunofluorescence to beta-tubulin in the developing gerbil cochlea. Tubulin first appears at post-natal day 0 (P0) as filamentous asters in inner hair cells and by P2, asters are also seen in outer hair cells Tubulin appears at P3 in inner pillar cells in a tooth crown-like figure. By P6, tubulin expression is also evident in outer pillar cells and by P9, it is seen in Deiters cells. Elaboration of microtubules in pillar cells was observed to proceed from the reticular lamina towards the basilar membrane. The pattern of tubulin expression in the apical organ of Corti lags the base by about 3 days until P6, but by P9, apical and basal organ of Corti appear substantially the same. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Texas, Hlth Sci Ctr, Dept Otolaryngol Head & Neck Surg, San Antonio, TX 78284 USA. Northside Independent Sch Dist, San Antonio, TX 78240 USA. RP Hallworth, R (reprint author), Univ Texas, Hlth Sci Ctr, Dept Otolaryngol Head & Neck Surg, 7703 Floyd Curl Dr, San Antonio, TX 78284 USA. CR Angelborg C, 1972, Acta Otolaryngol Suppl, V301, P49 FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 Gundersen GG, 1998, BIOL BULL, V194, P358, DOI 10.2307/1543112 HALLWORTH R, 1998, PATTERNS TABULIN EXP HENDERSON CG, 1995, J CELL SCI, V108, P37 ITO M, 1995, HEARING RES, V88, P107, DOI 10.1016/0378-5955(95)00106-E Joshi HC, 1998, CURR OPIN CELL BIOL, V10, P35, DOI 10.1016/S0955-0674(98)80084-7 KUHN B, 1995, HEARING RES, V84, P139, DOI 10.1016/0378-5955(95)00021-U Lange BMH, 1996, TRENDS CELL BIOL, V6, P348, DOI 10.1016/0962-8924(96)10033-7 Mogensen MM, 1997, CELL MOTIL CYTOSKEL, V36, P276, DOI 10.1002/(SICI)1097-0169(1997)36:3<276::AID-CM8>3.0.CO;2-5 RAPHAEL Y, 1994, HEARING RES, V76, P173, DOI 10.1016/0378-5955(94)90098-1 Romand R., 1983, DEV AUDITORY VESTIBU, P47 RUBSAMEN R, 1997, HDB AUDITORY RES, V9, P193 Slepecky NB, 1995, HEARING RES, V91, P136, DOI 10.1016/0378-5955(95)00184-0 Souter M, 1997, J COMP NEUROL, V386, P635 STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 Tannenbaum J, 1997, CELL MOTIL CYTOSKEL, V38, P146, DOI 10.1002/(SICI)1097-0169(1997)38:2<146::AID-CM4>3.0.CO;2-5 Tucker JB, 1998, J ANAT, V192, P119, DOI 10.1046/j.1469-7580.1998.19210119.x TUCKER JB, 1993, CELL MOTIL CYTOSKEL, V25, P49, DOI 10.1002/cm.970250107 NR 19 TC 18 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 31 EP 41 DI 10.1016/S0378-5955(99)00165-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800003 PM 10601710 ER PT J AU van Heumen, WRA Claxton, C Pickles, JO AF van Heumen, WRA Claxton, C Pickles, JO TI Expression of EphA4 in developing inner ears of the mouse and guinea pig SO HEARING RESEARCH LA English DT Article DE Eph; ephrin; EphA4; ephrin-B2; ephrin-B3; development; cochlea; mouse; guinea pig ID RECEPTOR TYROSINE KINASES; LIGANDS; FAMILY; HINDBRAIN; GUIDANCE; COCHLEA; GROWTH; AXONS; NUK AB The expression of EphA4, an Eph-class receptor tyrosine kinase, was determined by immunohistochemistry in developing inner ears of the mouse and the guinea pig. In the mouse, EphA4 expression was visible in the fibroblasts of the spiral ligament and in the structures that were to become the osseous spiral lamina. Cochlear nerve ganglion cells expressed ephrin-B2, and the modiolus expressed mRNA coding for ephrin-B3, both transmembrane ligands for EphA4. In contrast, in the guinea pig, cells of the cochlear nerve ganglion expressed EphA4, as did supporting cells of the organ of Corti (Wensen's cells and inner pillar cells). There was also some expression in fibroblasts of the spiral ligament but none in the structures that were to become the osseous spiral lamina. It is suggested that in the mouse, EphA4 may help direct the cochlear innervation towards the organ of Corti by a repulsive interaction, but that this is highly species dependent. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. RP Pickles, JO (reprint author), Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. CR Bergemann AD, 1998, ONCOGENE, V16, P471, DOI 10.1038/sj.onc.1201557 Bianchi LM, 1999, ANAT REC, V254, P127 Bianchi LM, 1998, HEARING RES, V117, P161, DOI 10.1016/S0378-5955(98)00010-0 Brambilla R, 1996, MOL CELL NEUROSCI, V8, P199, DOI 10.1006/mcne.1996.0057 Brennan C, 1997, DEVELOPMENT, V124, P655 Cerretti DP, 1995, MOL IMMUNOL, V32, P1197, DOI 10.1016/0161-5890(95)00108-5 CHENG HJ, 1995, CELL, V82, P37 Dottori M, 1998, P NATL ACAD SCI USA, V95, P13248, DOI 10.1073/pnas.95.22.13248 DRESCHER U, 1995, CELL, V82, P359, DOI 10.1016/0092-8674(95)90425-5 Flanagan JG, 1998, ANNU REV NEUROSCI, V21, P309, DOI 10.1146/annurev.neuro.21.1.309 Fritzsch B, 1997, TRENDS NEUROSCI, V20, P159, DOI 10.1016/S0166-2236(96)01007-7 Gale NW, 1996, NEURON, V17, P9, DOI 10.1016/S0896-6273(00)80276-7 Gale NW, 1996, ONCOGENE, V13, P1343 GILARDIHEBENSTREIT P, 1992, ONCOGENE, V7, P2499 HENSON MM, 1988, HEARING RES, V35, P237, DOI 10.1016/0378-5955(88)90121-9 Holland SJ, 1996, NATURE, V383, P722, DOI 10.1038/383722a0 Jones TL, 1998, P NATL ACAD SCI USA, V95, P576, DOI 10.1073/pnas.95.2.576 Lee AM, 1996, DNA CELL BIOL, V15, P817, DOI 10.1089/dna.1996.15.817 Ohta K, 1996, MECH DEVELOP, V54, P59, DOI 10.1016/0925-4773(95)00461-0 Orioli D, 1996, EMBO J, V15, P6035 Pickles JO, 1997, DEV NEUROSCI-BASEL, V19, P476, DOI 10.1159/000111245 Pujol R, 1998, SPRINGER HDB AUDITOR, P146 RinkwitzBrandt S, 1996, HEARING RES, V99, P129, DOI 10.1016/S0378-5955(96)00093-7 SAJJADI FG, 1993, ONCOGENE, V8, P1807 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 SOANS CA, 1994, ONCOGENE, V89, P3353 Takahashi T, 1998, KIDNEY INT, V53, P826, DOI 10.1046/j.1523-1755.1998.00822.x Tanaka M, 1998, ONCOGENE, V17, P1509, DOI 10.1038/sj.onc.1202068 Wang HU, 1998, CELL, V93, P741, DOI 10.1016/S0092-8674(00)81436-1 NR 29 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 42 EP 50 DI 10.1016/S0378-5955(99)00158-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800004 PM 10601711 ER PT J AU Suzuki, M Kitanishi, T Kitano, H Yazawa, Y Kitajima, K Takeda, T Tokunaga, Y Maeda, T Kimura, H Tooyama, I AF Suzuki, M Kitanishi, T Kitano, H Yazawa, Y Kitajima, K Takeda, T Tokunaga, Y Maeda, T Kimura, H Tooyama, I TI C-type natriuretic peptide-like immunoreactivity in the rat inner ear SO HEARING RESEARCH LA English DT Article DE C-type natriuretic peptide; inner ear; immunohistochemistry; endolymph; perilymph; ultrastructure ID HUMAN ENDOLYMPHATIC SAC; ATRIAL; COCHLEA; RECEPTORS; ANP; SECRETION; BRAIN; EXPRESSION; CELLS; CNP AB C-type natriuretic peptide (CNP) is a member of the atrial natriuretic peptide family (ANP family). The family also includes ANP and brain natriuretic peptide (BNP). These peptides regulate the homeostasis of body fluid and blood pressure as a neuropeptide in the central nervous system as well as a cardiac hormone in the periphery. We have recently reported the expression of CNP mRNA in the inner ear. To assess the possible physiological role of CNP in the inner ear, we investigated the localization of CNP peptide in the rat inner ear by immunohistochemistry at the light and electron microscopic level. CNP-like immunoreactivity was widely distributed in the secretory and the neuronal portion of the inner ear. i.e. the spiral ligament, the dark cell region of the utriculus, the epithelium of the endolymphatic sac, the spiral ganglion cells and the vestibular ganglion cells. The results suggest that CNP may play a role in the homeostasis of the perilymph and endolymph and may also influence nerve activities in the inner ear. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Shiga Univ Med Sci, Dept Otolaryngol, Otsu, Shiga 5202192, Japan. Kouchi Med Sch, Dept Otolaryngol, Nango Ku, Kouchi, Japan. Shiga Univ Med Sci, Dept Anat, Otsu, Shiga 5202192, Japan. Shiga Univ Med Sci, Mol Neurosci Res Ctr, Otsu, Shiga 5202192, Japan. RP Suzuki, M (reprint author), Shiga Univ Med Sci, Dept Otolaryngol, Otsu, Shiga 5202192, Japan. CR ALTERMATT HJ, 1992, ORL J OTO-RHINO-LARY, V54, P173 BARTOLI E, 1989, AM J PHYSIOL, V257, pF341 BJURHOLM A, 1989, CALCIFIED TISSUE INT, V45, P227, DOI 10.1007/BF02556042 DAHLMANN A, 1995, CELL TISSUE RES, V282, P277, DOI 10.1007/s004410050479 Furuta H, 1998, HEARING RES, V117, P140, DOI 10.1016/S0378-5955(98)00009-4 Furuta H, 1995, HEARING RES, V92, P78, DOI 10.1016/0378-5955(95)00203-0 Galli SM, 1996, P SOC EXP BIOL MED, V213, P128 IMURA H, 1992, FRONT NEUROENDOCRIN, V13, P217 KOCH T, 1992, HEARING RES, V63, P197, DOI 10.1016/0378-5955(92)90085-2 KOMATSU Y, 1991, ENDOCRINOLOGY, V129, P1104 Krause G, 1997, HEARING RES, V110, P95, DOI 10.1016/S0378-5955(97)00064-6 LAMPRECHT J, 1988, ARCH OTO-RHINO-LARYN, V245, P300, DOI 10.1007/BF00464636 ZUMGOTTESBERGE AMM, 1991, HEARING RES, V56, P86 NAZARIO B, 1995, J CLIN INVEST, V95, P1151, DOI 10.1172/JCI117763 Qvortrup K, 1996, AM J PHYSIOL-RENAL, V270, pF1073 RASKANDERSEN H, 1991, ANN OTO RHINOL LARYN, V100, P148 STERKERS O, 1988, PHYSIOL REV, V68, P1083 Suzuki M, 1998, MOL BRAIN RES, V55, P165, DOI 10.1016/S0169-328X(98)00016-3 Suzuki M, 1997, NEUROREPORT, V8, P439, DOI 10.1097/00001756-199701200-00013 Yamamoto S, 1997, NEUROSCI LETT, V229, P97, DOI 10.1016/S0304-3940(97)00431-X YOON YJ, 1994, ORL J OTO-RHINO-LARY, V56, P73 YOON YJ, 1992, ACTA OTO-LARYNGOL, V112, P604, DOI 10.3109/00016489209137448 ZUMGOTTESBERGE AMM, 1989, ACTA OTO-LARYNGOL, V468, P53 ZUMGOTTESBERGE AMM, 1995, ACTA OTO-LARYNGOL, V520, P170 NR 24 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 51 EP 58 DI 10.1016/S0378-5955(99)00173-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800005 PM 10601712 ER PT J AU Syka, J Rybalko, N AF Syka, J Rybalko, N TI Threshold shifts and enhancement of cortical evoked responses after noise exposure in rats SO HEARING RESEARCH LA English DT Article DE noise exposure; threshold shift; evoked response; enhancement; rat ID DORSAL COCHLEAR NUCLEUS; INDUCED HEARING-LOSS; AWAKE GUINEA-PIGS; AUDITORY-CORTEX; INFERIOR COLLICULUS; ACOUSTIC TRAUMA; INTENSE SOUND; POTENTIALS; PLASTICITY AB The effect of exposure to various types of noise (broadband, high-frequency or low-frequency) was studied in adult pigmented rats. Thresholds and amplitudes of middle latency responses (MLR) recorded from electrodes implanted on the surface of the auditory cortex were analyzed before and after noise exposure. Exposure to noise with intensities ranging from 105 to 120 dB for 1 h produced only temporary threshold shifts (TTS). Exposure to broadband noise produced TTS throughout the whole frequency range of the rat's hearing, mostly expressed at Frequencies of maximal hearing sensitivity (16-32 kHz). Hearing loss produced by high- or low-frequency noise exposure was related to the spectral characteristics of the noise. The exposure to high-intensity noise may also result in amplitude enhancement of the MLR. This phenomenon was seen mainly after broadband noise exposure and occurred in response to both low-frequency and high-frequency test stimuli. High-frequency and low-frequency noise produced amplitude enhancement mainly at frequencies which corresponded to the maximum exposure energy. In contrast to the relatively similar values of TTS obtained in different rats under the same conditions of noise exposure, great inter-individual variability was found in the MLR amplitude enhancement. III all rats the dynamics of recovery functions for amplitude enhancement were different from those for MLR thresholds. The data indicate that whereas post-exposure TTS are related to peripheral changes, the post-exposure MLR amplitude enhancement is most probably connected with a change in the processing of auditory information in the central nervous system. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Acad Sci Czech Republ, Inst Expt Med, Prague 14220, Czech Republic. RP Syka, J (reprint author), Acad Sci Czech Republ, Inst Expt Med, Videnska 1083, Prague 14220, Czech Republic. RI Rybalko, Natalia/H-2629-2014; Syka, Josef/H-3103-2014 CR Axelsson A, 1996, SCI BASIS NOISE INDU Bock G R, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P338 BORG E, 1982, HEARING RES, V8, P117, DOI 10.1016/0378-5955(82)90070-3 CHALOUPK.Z, 1968, ACTIV NERV SUPER, V10, P207 GERKEN G, 1986, BASIC APPL ASPECTS N, P195 GERKEN GM, 1993, J ACOUST SOC AM, V93, P2038, DOI 10.1121/1.406690 GUMNIT RJ, 1961, AM J PHYSIOL, V200, P1219 HENDERSON D, 1975, J ACOUST SOC AM, V57, P53 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 Kaltenbach JA, 1998, HEARING RES, V124, P78, DOI 10.1016/S0378-5955(98)00119-1 LENOIR M, 1979, J PHYSIOL-PARIS, V75, P521 LONSBURYMARTIN BL, 1981, J NEUROPHYSIOL, V46, P563 MOLLER DR, 1990, J COMP NEUROL, V302, P810 POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 REALE RA, 1987, DEV BRAIN RES, V34, P281, DOI 10.1016/0165-3806(87)90215-X Ryan AF, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P50 SALVI RJ, 1992, EFFECTS NOISE AUDITO, P156 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U Salvi RJ, 1999, P 2 S MOL MECH CENTR, P52 SALVI RJ, 1982, SCIENCE, V216, P1331 Syka J, 1989, PROGR SENSORY PHYSL, V9, P97 SYKA J, 1994, HEARING RES, V78, P158, DOI 10.1016/0378-5955(94)90021-3 Szczepaniak WS, 1996, EVOKED POTENTIAL, V100, P158, DOI 10.1016/0013-4694(95)00234-0 TANIGUCHI I, 1978, P JPN ACAD B-PHYS, V54, P496, DOI 10.2183/pjab.54.496 URBAN GP, 1979, EXP NEUROL, V63, P229, DOI 10.1016/0014-4886(79)90120-1 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 WILLOTT JF, 1974, J COMP PHYSIOL PSYCH, V86, P1, DOI 10.1037/h0035922 Zhang JS, 1998, NEUROSCI LETT, V250, P197, DOI 10.1016/S0304-3940(98)00482-0 NR 29 TC 49 Z9 49 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 59 EP 68 DI 10.1016/S0378-5955(99)00175-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800006 PM 10601713 ER PT J AU Jiang, H Lepore, F Poirier, P Guillemot, JP AF Jiang, H Lepore, F Poirier, P Guillemot, JP TI Responses of cells to stationary and moving sound stimuli in the anterior ectosylvian cortex of cats SO HEARING RESEARCH LA English DT Article DE sound localization; free field; motion ID PRIMARY AUDITORY-CORTEX; SUPERIOR COLLICULUS; PRESSURE LEVEL; CORTICAL-NEURONS; SINGLE NEURONS; CEREBRAL-CORTEX; SOURCE LOCATION; DEEP LAYERS; ORGANIZATION; FIELD AB The azimuthal, directional and angular speed sound selectivities of single units were examined in the posterior parr of the anterior ectosylvian cortex. Broadband noise bursts and simulated moving sounds were delivered from 16 loudspeakers fixed on the horizontal plant in a quasi-anechoic sound-isolation chamber. The activity of 78 neurons was recorded and quantitatively analyzed. Most cells responded to at least the static sound. The relative strengths of their responses suggested that the cells could be classed as omnidirectional (37.2%), contralateral hemifield (29.5%), ipsilateral hemifield (2.5%) and azimuth (7.7%) selective. The remaining 23.1% could not be classified. All cells responded to a simulated moving sound displaced at five different speeds. A majority (88%) of them showed some directional preference in that they discharged at least twice as strongly for one direction as for the other for at least one speed. 14.7% displayed angular speed selectivity. Different patterns of neuronal discharges were evoked. For static sounds, most of the cells gave ON-type responses. A large proportion (60%) of the cells responded in a sustained manner to maintained stimulation. Among these, 68% also gave sustained discharges to moving sounds. The spatial tuning and the directional and angular speed selectivity of neurons in the posterior part of the AEC suggest that this area is involved in the processing of static and moving sounds. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Montreal, Dept Psychol, Grp Rech Neuropsychol Expt, Montreal, PQ H3C 3J7, Canada. Univ Quebec, Dept Kinanthropol, Montreal, PQ H3C 3P8, Canada. RP Guillemot, JP (reprint author), Univ Montreal, Dept Psychol, Grp Rech Neuropsychol Expt, CP 6128,Succ Ctr Ville, Montreal, PQ H3C 3J7, Canada. CR AHISSAR M, 1992, J NEUROPHYSIOL, V67, P203 Bronkhorst AW, 1999, NATURE, V397, P517, DOI 10.1038/17374 CLAREY JC, 1990, J COMP NEUROL, V301, P304, DOI 10.1002/cne.903010212 CLAREY JC, 1990, J COMP NEUROL, V301, P289, DOI 10.1002/cne.903010211 CLAREY JC, 1986, BRAIN RES, V386, P12, DOI 10.1016/0006-8993(86)90136-8 CLEMO HR, 1983, J NEUROPHYSIOL, V50, P910 IMIG TJ, 1990, J NEUROPHYSIOL, V63, P1448 Irvine DRF, 1996, J NEUROPHYSIOL, V75, P75 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 JIANG H, 1994, EXP BRAIN RES, V97, P404 KLUVER H, 1953, J NEUROPATH EXP NEUR, V12, P400 KORTE M, 1993, J NEUROPHYSIOL, V70, P1717 MEREDITH MA, 1989, J COMP NEUROL, V289, P687 MIDDLEBROOKS JC, 1994, SCIENCE, V264, P842, DOI 10.1126/science.8171339 Middlebrooks JC, 1998, J NEUROPHYSIOL, V80, P863 MIDDLEBROOKS JC, 1984, J NEUROSCI, V4, P2621 MINCIACCHI D, 1987, BRAIN RES, V410, P21, DOI 10.1016/S0006-8993(87)80016-1 Moore D.R., 1999, CURR BIOL, V20, P361 OLSON CR, 1987, J COMP NEUROL, V261, P277, DOI 10.1002/cne.902610209 PHILLIPS DP, 1982, BRAIN RES, V248, P237, DOI 10.1016/0006-8993(82)90581-9 PHILLIPS DP, 1981, J NEUROPHYSIOL, V45, P48 Poirier P, 1997, HEARING RES, V113, P1, DOI 10.1016/S0378-5955(97)00126-3 POIRIER P, 1994, NEUROPSYCHOLOGIA, V32, P541, DOI 10.1016/0028-3932(94)90143-0 PTITO M, 1987, EXP BRAIN RES, V66, P90 RAJAN R, 1990, J NEUROPHYSIOL, V64, P872 RAUSCHECKER JP, 1995, TRENDS NEUROSCI, V18, P36, DOI 10.1016/0166-2236(95)93948-W RAUSCHECKER JP, 1989, BRAIN RES, V490, P56, DOI 10.1016/0006-8993(89)90430-7 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 REINOSOSUAREZ F, 1985, EXP BRAIN RES, V59, P313 SCHREINER CE, 1984, J NEUROPHYSIOL, V51, P1284 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P449 SEMPLE MN, 1987, J NEUROPHYSIOL, V57, P1130 SOVIJARV.AR, 1974, BRAIN RES, V73, P455, DOI 10.1016/0006-8993(74)90669-6 STEIN BE, 1981, BRAIN BEHAV EVOLUT, V19, P180, DOI 10.1159/000121641 STUMPF E, 1992, EXP BRAIN RES, V88, P158, DOI 10.1007/BF02259137 TORONCHUK JM, 1992, EXP BRAIN RES, V88, P169, DOI 10.1007/BF02259138 WALLACE MT, 1992, EXP BRAIN RES, V91, P484 WISE LZ, 1983, J NEUROPHYSIOL, V49, P674 WISE LZ, 1985, J NEUROPHYSIOL, V54, P185 Xu L, 1998, J NEUROPHYSIOL, V80, P882 NR 41 TC 15 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 69 EP 85 DI 10.1016/S0378-5955(99)00176-8 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800007 PM 10601714 ER PT J AU Lataye, R Campo, P Loquet, G AF Lataye, R Campo, P Loquet, G TI Combined effects of noise and styrene exposure on hearing function in the rat SO HEARING RESEARCH LA English DT Article DE styrene; noise; synergism; rat ID SERIAL-SECTION RECONSTRUCTION; ACOUSTIC TRAUMA; ULTRASTRUCTURAL-CHANGES; CUTICULAR PLATES; GUINEA-PIG; STEREOCILIA; SOLVENTS; TOLUENE; COCHLEA AB Combined exposure to both noise and aromatic solvents such as styrene is common in many industries. In order to study the combined effects of simultaneous exposure to both noise and styrene on hearing, male adult Long-Evans rats were exposed either to 750 ppm styrene alone, to a 97 dB SPL octave band of noise centered at 8 ItHz, or to a combination of noise and styrene. The exposure duration was 6 h/day, 5 days/week. for 4 consecutive weeks. Auditory function was tested over a frequency range from 2 to 32 kHz by recording near field potentials From the inferior colliculus, whereas histopathological analyses of the cochleae were pel formed with conventional morphometric approaches. Whereas both noise and styrene each caused permanent threshold shifts, the mechanisms of cochlear damage were different. Noise-induced hearing loss was mainly related to injuries of the stereocilia, whereas styrene-induced hearing loss was related to outer hair cell losses. Following the combined exposure, the threshold elevations as well as the cell losses exceeded the summed loss caused by noise and by styrene alone in the range of 8-16 kHz. Therefore, these results suggest that the two ototoxicants carl cause a permanent synergistic loss of auditory sensitivity. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Inst Natl Rech & Secur, Lab Neurotoxicol & Immunotoxicol, F-54501 Vandoeuvre Nancy, France. RP Campo, P (reprint author), Inst Natl Rech & Secur, Lab Neurotoxicol & Immunotoxicol, Ave Bourgogne,POB 27, F-54501 Vandoeuvre Nancy, France. CR BARREGARD L, 1984, SCAND AUDIOL, V13, P151, DOI 10.3109/01050398409043054 BORG E, 1995, SCAND AUDIOL S40, V24 CALEBRESE G, 1996, INT ARCH OCC ENV HEA, V68, P219 Campo P, 1997, NEUROTOXICOL TERATOL, V19, P129, DOI 10.1016/S0892-0362(96)00214-0 CAMPO P, 1999, COCHLEAR PHARM NOISE, P113 Cary R, 1997, ANN OCCUP HYG, V41, P455 CROFTON KM, 1994, HEARING RES, V80, P25, DOI 10.1016/0378-5955(94)90005-1 FECHTER LD, 1995, OCCUP MED, V10, P609 FECHTER LD, 1993, NEUROTOXICOL TERATOL, V15, P151, DOI 10.1016/0892-0362(93)90010-L FILSER JG, 1993, ARCH TOXICOL, V67, P517, DOI 10.1007/BF01969264 GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 JACOBSEN P, 1993, OCCUP MED-OXFORD, V43, P180, DOI 10.1093/occmed/43.4.180 JOHNSON AC, 1988, ACTA OTO-LARYNGOL, V105, P56, DOI 10.3109/00016488809119446 JOHNSON AC, 1995, OCCUP MED, V10, P623 Lataye R, 1997, NEUROTOXICOL TERATOL, V19, P373, DOI 10.1016/S0892-0362(97)00049-4 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 MILLER RR, 1994, CRIT REV TOXICOL, V24, pS1, DOI 10.3109/10408449409020137 MOLLER C, 1990, SCAND J WORK ENV HEA, V16, P189 MORATA TC, 1994, ARCH ENVIRON HEALTH, V49, P359 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 Mulroy MJ, 1998, HEARING RES, V115, P93, DOI 10.1016/S0378-5955(97)00181-0 NYLEN P, 1994, ARBETE HALSA, V3, P1 PROSEN CA, 1991, HEARING RES, V57, P142, DOI 10.1016/0378-5955(91)90083-L ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U Sass-Kortsak Andrea M., 1995, Annals of Epidemiology, V5, P15, DOI 10.1016/1047-2797(94)00036-S YANO BL, 1992, TOXICOL PATHOL, V20, P1 NR 28 TC 60 Z9 69 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 86 EP 96 DI 10.1016/S0378-5955(99)00174-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800008 PM 10601715 ER PT J AU Forge, A Li, L AF Forge, A Li, L TI Apoptotic death of hair cells in mammalian vestibular sensory epithelia SO HEARING RESEARCH LA English DT Article DE caspase inhibitor; staurosporine; deferoxamine; gentamicin; organotypic culture; programmed cell death ID INNER-EAR; GENTAMICIN TREATMENT; COCHLEAR CULTURES; GUINEA-PIGS; MACROPHAGE; ORGAN; CORTI; DNA; REGENERATION; RECRUITMENT AB Hair cell death was examined in cultured explants of vestibular organs from mature guinea pigs and gerbils. The effects of gentamicin were compared with those of staurosporine, a membrane-permeable kinase inhibitor that induces programmed cell death in almost all cell types. Under the conditions used staurosporine killed hair cells but supporting cells appeared unaffected, and a topographic pattern of differential sensitivity to staurosporine amongst hair cells, similar to that described for aminoglycoside antibiotics, was revealed. This suggests such differential sensitivity is an inherent property of the hair cell population. Thin sectioning, and examination of whole mount preparations after application of the TUNEL procedure or after double fluorescent labelling with phalloidin and with propidium iodide, which labels nuclei, revealed that hair cells after exposure to gentamicin show features identical to those of apoptotic cells after exposure to staurosporine. Furthermore, cells showing features of apoptosis constitute a major proportion of the hair cells that are ultimately lost following exposure to gentamicin. Incubation of cultures with gentamicin in the presence of broad-spectrum inhibitors of caspases, proteases involved specifically in the cell death pathway, prevented almost all of the hair cell deaths normally triggered by gentamicin. This confirms that apoptosis is the predominant mode of hair cell death after gentamicin exposure. Hair cells exposed to gentamicin in the presence of caspase inhibitors appeared to be preserved intact. This, and the thin section observations, suggests that apoptotic death is the fate of the majority of hair cells affected by that drug and that any sub-lethal damage to hair cells exposed to gentamicin does not result in significant morphological alterations. Hair cell death was also prevented by deferoxamine which has been shown to protect cochlear hair cells in vivo from the effects of gentamicin. Explant cultures of mature vestibular organs may be, therefore, a useful model system for examining putative hair cell protecting agents. (C) 2000 Elsevier Science B.V. All rights reserved. C1 UCL, Inst Laryngol & Otol, London WC1X 8EE, England. RP Forge, A (reprint author), UCL, Inst Laryngol & Otol, 330-332 Grays Inn Rd, London WC1X 8EE, England. EM a.forge@ucl.ac.uk CR Alnemri ES, 1996, CELL, V87, P171, DOI 10.1016/S0092-8674(00)81334-3 Bhave SA, 1998, J COMP NEUROL, V398, P241, DOI 10.1002/(SICI)1096-9861(19980824)398:2<241::AID-CNE6>3.0.CO;2-0 Camp V, 1996, ANAT EMBRYOL, V194, P341 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 FORGE A, 1985, HEARING RES, V19, P171, DOI 10.1016/0378-5955(85)90121-2 FORGE A, 1993, J NEUROCYTOL, V22, P854, DOI 10.1007/BF01186357 Forge A, 1998, J COMP NEUROL, V397, P69 FORGE A, 1992, SCANNING MICROSCOPY, V6, P521 GAVRIELI Y, 1992, J CELL BIOL, V119, P493, DOI 10.1083/jcb.119.3.493 HIEL H, 1992, ACTA OTO-LARYNGOL, V112, P272 HOCKENBERY DM, 1993, CELL, V75, P241, DOI 10.1016/0092-8674(93)80066-N HOPKINSONWOOLLEY J, 1994, J CELL SCI, V107, P1159 Jacobson MD, 1997, CELL, V88, P347, DOI 10.1016/S0092-8674(00)81873-5 Jacobson MD, 1996, J CELL BIOL, V133, P1041, DOI 10.1083/jcb.133.5.1041 Jokay I, 1998, HEARING RES, V117, P131, DOI 10.1016/S0378-5955(97)00215-3 Jones JE, 1996, J NEUROSCI, V16, P649 KERR JFR, 1972, BRIT J CANCER, V26, P239, DOI 10.1038/bjc.1972.33 Krohn AJ, 1998, J NEUROSCI, V18, P8186 Leonova EV, 1997, HEARING RES, V113, P14, DOI 10.1016/S0378-5955(97)00130-5 LEWIS ME, 1993, EXP NEUROL, V124, P73, DOI 10.1006/exnr.1993.1177 Li L., 1995, AUDIT NEUROSCI, V1, P111 LI L, 1997, ASS RES OTOLARYNGOL, V20, P445 LI L, 1995, J COMP NEUROL, V355, P405, DOI 10.1002/cne.903550307 LINDEMAN HH, 1969, ACTA OTO-LARYNGOL, V67, P177, DOI 10.3109/00016486909125441 Lopez I, 1997, INT J DEV NEUROSCI, V15, P447, DOI 10.1016/S0736-5748(96)00103-7 LORENZO A, 1994, NATURE, V368, P756, DOI 10.1038/368756a0 Martinou I, 1999, J CELL BIOL, V144, P883, DOI 10.1083/jcb.144.5.883 Martins LM, 1997, TRENDS CELL BIOL, V7, P111 MEITELES LZ, 1994, HEARING RES, V79, P26, DOI 10.1016/0378-5955(94)90124-4 Nakagawa T, 1998, EUR ARCH OTO-RHINO-L, V255, P127, DOI 10.1007/s004050050027 NEIDERMEYER HP, 1997, ARO ABSTR, V20, P479 Platt N, 1998, TRENDS CELL BIOL, V8, P365, DOI 10.1016/S0962-8924(98)01329-4 RAFF MC, 1992, NATURE, V356, P397, DOI 10.1038/356397a0 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 Richardson GP, 1997, J NEUROSCI, V17, P9506 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E ROBERSON DW, 1994, AM J OTOL, V15, P28 Sobkowicz HM, 1997, INT J DEV NEUROSCI, V15, P463, DOI 10.1016/S0736-5748(96)00104-9 Song BB, 1996, HEARING RES, V94, P87, DOI 10.1016/0378-5955(96)00003-2 Staecker H, 1998, CURR OPIN NEUROBIOL, V8, P480, DOI 10.1016/S0959-4388(98)80035-4 Steyger PS, 1997, INT J DEV NEUROSCI, V15, P417, DOI 10.1016/S0736-5748(96)00101-3 Tan SL, 1998, J CELL BIOL, V141, P1423, DOI 10.1083/jcb.141.6.1423 Thornberry NA, 1998, SCIENCE, V281, P1312, DOI 10.1126/science.281.5381.1312 Usami S, 1997, BRAIN RES, V747, P147, DOI 10.1016/S0006-8993(96)01243-7 Warchol ME, 1997, J NEUROBIOL, V33, P724, DOI 10.1002/(SICI)1097-4695(19971120)33:6<724::AID-NEU2>3.0.CO;2-B WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 Weil M, 1996, J CELL BIOL, V133, P1053, DOI 10.1083/jcb.133.5.1053 Wyllie A H, 1980, Int Rev Cytol, V68, P251 Zheng JL, 1999, J NEUROSCI, V19, P2161 Zheng Y, 1998, HEARING RES, V126, P11, DOI 10.1016/S0378-5955(98)00138-5 NR 50 TC 138 Z9 146 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 97 EP 115 DI 10.1016/S0378-5955(99)00177-X PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800009 PM 10601716 ER PT J AU Ichimiya, I Suzuki, M Mogi, G AF Ichimiya, I Suzuki, M Mogi, G TI Age-related changes in the murine cochlear lateral wall SO HEARING RESEARCH LA English DT Article DE inner ear; sensorineural hearing loss; spiral ligament; connexin 26; sodium-potassium-adenosinetriphosphatase; C57BL/6 mouse ID GERBIL COCHLEA; INNER-EAR; ION; PRESBYCUSIS; FIBROCYTES; CELLS; STRIA AB Cochleas From C57BL/6 mice were investigated electrophysiologically and histochemically to evaluate the pathology of presbycusis. The average auditory brainstem response thresholds from 6-week-old mice were significantly lower than those of 6-month-old mice and those of I-year-old mice. Histologic observation revealed changes in the cochlea after age 6 months. Conventional hematoxylin and eosin (H&E) staining showed disorganization of the organ of Corti, a decrease in the number of spiral ganglion cells, and atrophy of the stria vascularis. Although H&E staining and type II collagen immunolabeling did not show obvious changes in the spiral ligament (SL), the density of connexin 26 staining was reduced in this region. Sodium-potassium-adenosinetriphosphatase immunolabeling was increased in the St., whereas its average density was not significantly altered in the stria vascularis. These results suggest that the SL could be among the regions responsible for cochlear malfunction with aging. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Oita Med Univ, Dept Otolaryngol, Hasama, Oita 8795593, Japan. RP Mogi, G (reprint author), Oita Med Univ, Dept Otolaryngol, 1-1 Idaigaoka, Hasama, Oita 8795593, Japan. CR ALLAM A F, 1970, Journal of Laryngology and Otology, V84, P765, DOI 10.1017/S0022215100072534 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 ICHIMIYA I, 1994, ANN OTO RHINOL LARYN, V103, P457 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 Ichimiya I, 1998, LARYNGOSCOPE, V108, P585, DOI 10.1097/00005537-199804000-00023 Ichimiya I, 1999, HEARING RES, V131, P128, DOI 10.1016/S0378-5955(99)00025-8 Kelsell DP, 1997, NATURE, V387, P80, DOI 10.1038/387080a0 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 MIKAELIA.DO, 1974, ACTA OTO-LARYNGOL, V77, P327, DOI 10.3109/00016487409124632 ROSEN S, 1965, B NEW YORK ACAD MED, V41, P1052 ROSEN S, 1966, T NEW YORK ACAD SCI, V29, P9 SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z Spicer SS, 1997, HEARING RES, V111, P93, DOI 10.1016/S0378-5955(97)00097-X TAKAHASHI T, 1970, Acta Oto-Laryngologica, V69, P46, DOI 10.3109/00016487009123335 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WRIGHT JL, 1972, ARCHIV OTOLARYNGOL, V96, P16 YOO TJ, 1988, LARYNGOSCOPE, V98, P1255 NR 20 TC 42 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 116 EP 122 DI 10.1016/S0378-5955(99)00170-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800010 PM 10601717 ER PT J AU Koppl, C Wegscheider, A Gleich, O Manley, GA AF Koppl, C Wegscheider, A Gleich, O Manley, GA TI A quantitative study of cochlear afferent axons in birds SO HEARING RESEARCH LA English DT Article DE auditory; basilar papilla; eighth nerve; barn owl; chicken; myelination ID STARLING STURNUS-VULGARIS; AUDITORY-NERVE FIBERS; OWL TYTO-ALBA; EMU DROMAIUS-NOVAEHOLLANDIAE; PIGEON BASILAR PAPILLA; HAIR CELL REGENERATION; BARN OWL; NUCLEUS MAGNOCELLULARIS; FREQUENCY REPRESENTATION; SOUND LOCALIZATION AB This paper is a comparative study of auditory-nerve morphology in birds. The chicken (Gallus gallus), the emu (Dromaius novaehollandiae) and the starling (Sturnus vulgaris) were chosen as unspecialised birds that have already been used in auditory research The data are discussed in comparison to a similar earlier study on the barn owl: a bird with highly specialised hearing, in an attempt to separate general avian patterns from species specialisations. Average numbers of afferent fibres from 8775 (starling) to 12406 (chicken) were counted, excluding fibres to the lagenar macula. The number of fibres representing different frequency ranges showed broad maxima in the chicken and emu, corresponding to hearing ranges of best sensitivity and/or particular behavioural relevance. Mean axon diameters were around 2 mu m in the chicken and starling and around 3 mu m in the emu. Virtually all auditory afferents were myelinated. The mean thickness of the myelin sheaths was between 0.33 mu m (starling) and 0.4 mu m (emu). There was a consistent pattern in the diameters of axons deriving from different regions. Axons from very basal, i.e. highest-frequency, parts of the basilar papilla were always the smallest. In the emu and the chicken, axons from the middle papillar regions were, in addition, larger than axons innervating apical regions, (C) 2000 Elsevier Science B.V, All rights reserved. C1 Tech Univ Munich, Inst Zool, D-85747 Garching, Germany. Univ Regensburg, HNO Klin, D-93042 Regensburg, Germany. RP Koppl, C (reprint author), Tech Univ Munich, Inst Zool, Lichtenbergstr 4, D-85747 Garching, Germany. CR ADRETHAUSBERGER M, 1988, BEHAVIOUR, V107, P138, DOI 10.1163/156853988X00322 ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BOORD RL, 1969, NY ACAD SOC, V169, P186 BOORD RL, 1963, J COMP NEUROL, V120, P463, DOI 10.1002/cne.901200305 BRUNS V, 1980, HEARING RES, V3, P27, DOI 10.1016/0378-5955(80)90006-4 CALFORD MB, 1988, J COMP PHYSIOL A, V162, P491, DOI 10.1007/BF00612514 CARR CE, 1991, J COMP NEUROL, V314, P306, DOI 10.1002/cne.903140208 CHEN L, 1994, HEARING RES, V81, P130, DOI 10.1016/0378-5955(94)90160-0 COLE KS, 1990, EXP BRAIN RES, V82, P585 DOUCET JR, 1995, AUDIT NEUROSCI, V1, P151 EISENSAMER B, 1991, THESIS TU MUNICH FERMIN CD, 1984, ACTA OTO-LARYNGOL, V98, P42, DOI 10.3109/00016488409107533 FISCHER FP, 1994, HEARING RES, V73, P1, DOI 10.1016/0378-5955(94)90277-1 FISCHER FP, 1994, SCANNING MICROSCOPY, V8, P351 Fischer FP, 1998, HEARING RES, V121, P112, DOI 10.1016/S0378-5955(98)00072-0 FISCHER FP, 1994, J MORPHOL, V220, P71, DOI 10.1002/jmor.1052200107 FISCHER FP, 1992, J MORPHOL, V213, P225, DOI 10.1002/jmor.1052130207 FISCHER FP, 1988, HEARING RES, V34, P87, DOI 10.1016/0378-5955(88)90053-6 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S GLEICH O, IN PRESS COMP HEARIN GLEICH O, 1995, HEARING RES, V82, P100 GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 GLEICH O, 1998, 21 MIDW M ARO ST PET, P198 GLEICH O, 1994, J MORPHOL, V221, P1, DOI 10.1002/jmor.1052210102 KLUMP GM, 1992, J COMP PHYSIOL A, V170, P243 KNUDSEN EI, 1979, J COMP PHYSIOL, V133, P13 Koppl C, 1997, J ACOUST SOC AM, V101, P1574, DOI 10.1121/1.418145 Koppl C, 1997, J NEUROPHYSIOL, V77, P364 KOPPL C, 1993, J COMP PHYSIOL A, V171, P695, DOI 10.1007/BF00213066 Koppl C, 1997, J NEUROSCI, V17, P3312 KOPPL C, 1994, J COMP NEUROL, V339, P438, DOI 10.1002/cne.903390310 Koppl C, 1998, HEARING RES, V126, P99, DOI 10.1016/S0378-5955(98)00156-7 Koppl C, 1997, AUDIT NEUROSCI, V3, P313 KREITHEN ML, 1979, J COMP PHYSIOL, V129, P1 LANDOLT JP, 1972, 858 DCIEM, P1 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 Manley GA, 1996, J MORPHOL, V227, P197, DOI 10.1002/(SICI)1097-4687(199602)227:2<197::AID-JMOR6>3.0.CO;2-6 MANLEY GA, 1993, J MORPHOL, V218, P153, DOI 10.1002/jmor.1052180205 MANLEY GA, 1991, HEARING RES, V56, P211, DOI 10.1016/0378-5955(91)90172-6 Manley GA, 1997, J ACOUST SOC AM, V101, P1560, DOI 10.1121/1.418273 MARCHANT S, 1990, HDB AUSTR NZ ANT BIR, V1, P47 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y Motis Anna, 1996, Bioacoustics, V7, P119 Muller M, 1996, HEARING RES, V102, P133, DOI 10.1016/S0378-5955(96)00155-4 MULLER M, 1992, J COMP PHYSIOL A, V171, P469 Ofsie MS, 1996, J COMP NEUROL, V370, P281 OKANOYA K, 1987, J COMP PSYCHOL, V101, P7, DOI 10.1037//0735-7036.101.1.7 PAINTAL AS, 1966, J PHYSIOL-LONDON, V184, P791 PAINTAL AS, 1967, J PHYSIOL-LONDON, V193, P523 PARKS TN, 1981, J COMP NEUROL, V203, P425, DOI 10.1002/cne.902030307 PAYNE RS, 1971, J EXP BIOL, V54, P535 RITCHIE JM, 1982, PROC R SOC SER B-BIO, V217, P29, DOI 10.1098/rspb.1982.0092 ROSOWSKI JJ, 1980, J COMP PHYSIOL, V136, P183 ROTH B, 1993, ANAT EMBRYOL, V187, P565, DOI 10.1007/BF00214435 RUSHTON WAH, 1951, J PHYSIOL-LONDON, V115, P101 RYALS BM, 1989, HEARING RES, V43, P81, DOI 10.1016/0378-5955(89)90061-0 Ryugo DK, 1992, MAMMALIAN AUDITORY P, P23 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SALVI RJ, 1992, J COMP PHYSIOL A, V170, P227 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SAUNDERS SS, 1993, J ACOUST SOC AM, V94, P83, DOI 10.1121/1.406945 SCHERMULY L, 1990, HEARING RES, V48, P69, DOI 10.1016/0378-5955(90)90199-Y SMITH CA, 1985, HEARING RES, V17, P237, DOI 10.1016/0378-5955(85)90068-1 SMITH RS, 1970, AM J PHYSIOL, V219, P1256 Smolders JWT, 1995, HEARING RES, V92, P151, DOI 10.1016/0378-5955(95)00214-6 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 SULLIVAN WE, 1984, J NEUROSCI, V4, P1787 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TILNEY LG, 1986, HEARING RES, V22, P55, DOI 10.1016/0378-5955(86)90077-8 VONDURING M, 1985, FORTS ZOOL, V30, P681 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 Winter P., 1963, Zeitschrift fuer Morphologie und Oekologie der Tiere, V52, P365, DOI 10.1007/BF00408568 ZOOK JM, 1989, J COMP NEUROL, V290, P243, DOI 10.1002/cne.902900206 NR 76 TC 11 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 123 EP 143 DI 10.1016/S0378-5955(99)00178-1 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800011 PM 10601718 ER PT J AU Kudo, M Sakurai, H Kurokawa, K Yamada, H AF Kudo, M Sakurai, H Kurokawa, K Yamada, H TI Neurogenesis in the superior olivary complex in the rat SO HEARING RESEARCH LA English DT Article DE auditory pathway; superior olive; inferior colliculus; fluoro-gold; bromodeoxyuridine; development; rat; thymidine analogue ID INFERIOR COLLICULUS; AUDITORY PATHWAY; COCHLEAR NUCLEUS; GUINEA-PIG; NEURONS; PROJECTIONS AB In a previous paper we provided evidence that crossed projection neurons are generated earlier than uncrossed projection neurons in the lateral superior olive. The aim of the present study was to determine if other major nuclei of the superior olivary complex (SOC), the medial superior olivary (MSO), the superior paraolivary (SPN) and the medial trapezoid (MTB) nuclei, are distinguished by their neuronal constitutions of birthdates. Pregnant rats were injected intraperitoneally with 5-bromodeoxyuridine (BrdU), the thymidine analogue, to label the neurons on one of the embryonic (E) days E11-E16. When the progeny rats reached adulthood, the brains were processed for BrdU immunohistochemistry. The MSO was mostly composed of neurons generated on E12 (95%,). The remaining neurons in the MSO completed their neurogenesis by E13. The SPN neurons were generated from E12, to E14 with a peak on E13 (80%,). Regardless of the morphological heterogeneity, the SPN consisted of a single population of neurons in terms of neurogenesis. The MTB neurons were generated from E13 to E16 with a pe ak on E14(73%). In contrast to the previous assumption, no topographical relationship existed between neurogenesis and tonotopicity within each nucleus of the SOC. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Shiga Univ Med Sci, Sch Med, Dept Anat, Otsu, Shiga 5202192, Japan. RP Kudo, M (reprint author), Shiga Univ Med Sci, Sch Med, Dept Anat, Otsu, Shiga 5202192, Japan. CR AITKIN L, 1991, J COMP NEUROL, V309, P250, DOI 10.1002/cne.903090206 ALTMAN J, 1980, J COMP NEUROL, V194, P877, DOI 10.1002/cne.901940410 ALTMAN J, 1981, EXP BRAIN RES, V42, P411 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 CARR CE, 1992, EVOLUTIONARY BIOL HE COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 COOPER ML, 1981, J COMP NEUROL, V202, P309 DRUGA R, 1984, PHYSIOL BOHEMOSLOV, V33, P31 FRAIUF E, 1993, MAMMALIAN COCHLEAR N, P19 HENKEL CK, 1991, J COMP NEUROL, V313, P259, DOI 10.1002/cne.903130206 Irvine D. R. F., 1992, MAMMALIAN AUDITORY P, P153 KITAO Y, 1993, BRAIN RES, V620, P149, DOI 10.1016/0006-8993(93)90283-S Kudo M, 1996, DEV BRAIN RES, V95, P72, DOI 10.1016/0165-3806(96)00081-8 MARTIN MR, 1981, J COMP NEUROL, V197, P169, DOI 10.1002/cne.901970113 MOREST D. KENT, 1968, BRAIN RES, V9, P288, DOI 10.1016/0006-8993(68)90235-7 MOREST D K, 1968, Zeitschrift fuer Anatomie und Entwicklungsgeschichte, V127, P201, DOI 10.1007/BF00526129 NOORDEEN KW, 1983, J COMP NEUROL, V214, P131 OBLINGER MM, 1981, J COMP NEUROL, V197, P45, DOI 10.1002/cne.901970105 SANDERSON KJ, 1990, BRAIN BEHAV EVOLUT, V35, P325, DOI 10.1159/000115878 SANES DH, 1987, J NEUROSCI, V7, P3803 SCHOFIELD BR, 1991, J COMP NEUROL, V312, P68, DOI 10.1002/cne.903120106 SCHOFIELD BR, 1992, J COMP NEUROL, V317, P438, DOI 10.1002/cne.903170409 Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 SPITZER N, 1981, TRENDS NEUROSCI, V4, P169, DOI 10.1016/0166-2236(81)90055-2 Taber-Pierce E, 1973, PROG BRAIN RES, V40, P53 NR 25 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 144 EP 152 DI 10.1016/S0378-5955(99)00172-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800012 PM 10601719 ER PT J AU Qiu, CX Salvi, R Ding, DL Burkard, R AF Qiu, CX Salvi, R Ding, DL Burkard, R TI Inner hair cell loss leads to enhanced response amplitudes in auditory cortex of unanesthetized chinchillas: evidence for increased system gain SO HEARING RESEARCH LA English DT Article DE inner hair cell loss; carboplatin; enhancement; auditory nerve; inferior colliculus; auditory cortex ID PRODUCT OTOACOUSTIC EMISSIONS; EVOKED-POTENTIAL THRESHOLDS; COCHLEAR NERVE-FIBERS; AWAKE GUINEA-PIGS; INFERIOR COLLICULUS; ACOUSTIC TRAUMA; PLASTIC CHANGES; NOISE EXPOSURE; TUNING CURVES; ANIMAL-MODEL AB Carboplatin preferentially destroys inner hair cells (IHCs) in the chinchilla inner ear, while retaining a near-normal outer hair cell (OHC) population. The present study investigated the functional consequences of IHC loss on the compound action potential (CAP), inferior colliculus potential (ICP) and auditory cortex potential (ACP) recorded from chronically implanted electrodes. IHC lass led to a reduction in CAP amplitude that was roughly proportional to IHC loss. The ICP amplitude was typically reduced by IHC loss, but the magnitude of this reduction was generally less than that observed for the CAP. In contrast to the CAP and ICP, ACP amplitudes were generally not reduced following IHC loss. In some animals, the ACP amplitude remained at pre-carboplatin values despite substantial IHC loss. However, in other animals, IHC loss led to an increase ('enhancement') of ACP amplitude. ACP enhancement was greatest at 1-2 weeks post-carboplatin, returning towards baseline amplitudes at 5 weeks post-carboplatin. In other animals, the ACP remained enhanced up to 5 weeks post-carboplatin. We interpret the transient and sustained enhancement of ACP amplitude following partial IHC loss as evidence of functional reorganization occurring at or below the level of the auditory cortex. These results suggest that the gain of the central auditory pathway increases following IHC loss to compensate for the reduced input from the cochlea. (C) 2000 Elsevier Science B.V. All rights reserved. C1 SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA. SUNY Buffalo, Dept Communicat Disorders & Sci, Buffalo, NY 14214 USA. SUNY Buffalo, Dept Otolaryngol, Buffalo, NY 14214 USA. RP Burkard, R (reprint author), SUNY Buffalo, Ctr Hearing & Deafness, 215 Parker Hall, Buffalo, NY 14214 USA. CR Abbott SD, 1999, NEUROSCIENCE, V93, P1375, DOI 10.1016/S0306-4522(99)00300-0 Bilak M, 1997, EXP NEUROL, V147, P256, DOI 10.1006/exnr.1997.6636 BROWNING GG, 1978, ANN OTO RHINOL LARYN, V87, P875 Burkard R, 1997, J ACOUST SOC AM, V102, P3620, DOI 10.1121/1.420149 DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 Durrant JD, 1998, J ACOUST SOC AM, V104, P370, DOI 10.1121/1.423293 GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 Harrison RV, 1998, EAR HEARING, V19, P355, DOI 10.1097/00003446-199810000-00002 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 ILLING RB, 1995, NEUROSCI LETT, V194, P9, DOI 10.1016/0304-3940(95)11706-3 Illing RB, 1997, J COMP NEUROL, V382, P116, DOI 10.1002/(SICI)1096-9861(19970526)382:1<116::AID-CNE8>3.0.CO;2-4 Jock BM, 1996, HEARING RES, V96, P179, DOI 10.1016/0378-5955(96)00058-5 LIBERMAN MC, 1986, BASIC APPL ASPECTS N, P163 Liberman MC, 1997, AUDIT NEUROSCI, V3, P255 McFadden SL, 1998, HEARING RES, V120, P121, DOI 10.1016/S0378-5955(98)00052-5 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 PRIETO JJ, 1994, J COMP NEUROL, V344, P383, DOI 10.1002/cne.903440305 RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SCHUKNECHT HF, 1953, LARYNGOSCOPE, V63, P441 SIEGEL JH, 1982, NEW PERSPECTIVES NOI, P137 SNYDER DL, 1994, LAB ANIMAL, V23, P42 Spoendlin H., 1978, EVOKED ELECTRICAL AC, P21 Starr A, 1996, BRAIN, V119, P741, DOI 10.1093/brain/119.3.741 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Suneja SK, 1998, EXP NEUROL, V154, P473, DOI 10.1006/exnr.1998.6946 SYKA J, 1994, HEARING RES, V78, P158, DOI 10.1016/0378-5955(94)90021-3 TAKENO S, 1994, SCANNING MICROSCOPY, V8, P97 TAKENO S, 1994, HEARING RES, V75, P93, DOI 10.1016/0378-5955(94)90060-4 Trautwein P, 1996, HEARING RES, V96, P71, DOI 10.1016/0378-5955(96)00040-8 WAKE M, 1993, J LARYNGOL OTOL, V107, P585, DOI 10.1017/S0022215100123771 WAKE M, 1994, LARYNGOSCOPE, V104, P488 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 NR 43 TC 48 Z9 51 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 2000 VL 139 IS 1-2 BP 153 EP 171 DI 10.1016/S0378-5955(99)00171-9 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 269QJ UT WOS:000084488800013 PM 10601720 ER PT J AU Manley, GA Taschenberger, G Oeckinghaus, H AF Manley, GA Taschenberger, G Oeckinghaus, H TI Influence of contralateral acoustic stimulation on distortion-product and spontaneous otoacoustic emissions in the barn owl SO HEARING RESEARCH LA English DT Article DE DPOAE; otoacoustic emission; contralateral acoustic stimulation; barn owl; bird; efferent system ID COCHLEAR HAIR-CELLS; OLIVOCOCHLEAR BUNDLE STIMULATION; EFFERENT VESTIBULAR SYSTEM; AUDITORY-NERVE; SOUND STIMULATION; BASILAR PAPILLA; GUINEA-PIG; ELECTRICAL-STIMULATION; AFFERENT ACTIVITY; CHICKS COCHLEA AB The avian auditory papilla provides an interesting object on which to study efferent influences, because whereas a significant population of hair cells in birds is not afferently innervated, all hair cells are efferently innervated (Fischer, 1992, 1994a, b). Previous studies in mammals using contralateral sound to stimulate the efferent system demonstrated a general suppressive effect on spontaneous and click-evoked, as well as on distortion-product otoacoustic emissions (DPOAE). As little is known about the effects of contralateral stimulation on hearing in birds, we studied the effect of such stimuli (broadband noise, pure tones) on the amplitude of the DPOAE 2f(1)-f(2) and on spontaneous otoacoustic emissions (SOAE) in the barn owl, Tyro alba. For the DPOAE measurements, fixed primary-tone pairs [f(1) = 8.875 kHz (ratio = 1.2), f(1) = 8.353 kHz (ratio = 1.15) and f(1) = 7.889 kHz (ratio = 1.1)] were presented and the DPOAE measured in the presence and absence of continuous contralateral stimulation. The DPOAE often declined in amplitude but in some cases we observed DPOAE enhancement. The changes in amplitude were as large as 9 dB. The influence of the contralateral noise changed over time, however, and the effects of contralateral tones were frequency-dependent. SOAE were suppressed in amplitude and shifted in frequency by contralateral broadband noise. Control measurements in animals after middle-ear muscle resection showed that these phenomena were not attributable to the acoustic middle-ear reflex. The finding of DPOAE enhancement is interesting, because a type of efferent fiber that suppressed its discharge rate during stimulation has been described in birds (Kaiser and Manley, 1994). (C) 1999 Elsevier Science B.V. All rights reserved. C1 Tech Univ Munich, Inst Zool, D-85747 Garching, Germany. RP Manley, GA (reprint author), Tech Univ Munich, Inst Zool, Lichtenbergstr 4, D-85747 Garching, Germany. EM geoffrey.manley@bio.tum.de CR ART JJ, 1984, J PHYSIOL-LONDON, V356, P525 ART JJ, 1982, PROC R SOC SER B-BIO, V216, P377, DOI 10.1098/rspb.1982.0081 BORG E, 1979, ACTA OTO-LARYNGOL, V88, P20, DOI 10.3109/00016487909137135 BROWN MC, 1989, HEARING RES, V40, P93, DOI 10.1016/0378-5955(89)90103-2 BUNO W, 1978, EXP NEUROL, V59, P62, DOI 10.1016/0014-4886(78)90201-7 CHERYCROZE S, 1993, HEARING RES, V68, P53, DOI 10.1016/0378-5955(93)90064-8 CODY AR, 1982, HEARING RES, V6, P199, DOI 10.1016/0378-5955(82)90054-5 COHEN GM, 1987, HEARING RES, V28, P57, DOI 10.1016/0378-5955(87)90153-5 COLLET L, 1992, AUDIOLOGY, V31, P1 COLLET L, 1990, ADV AUDIOL, P164 COUNTER SA, 1979, ACTA OTO-LARYNGOL, V88, P13, DOI 10.3109/00016487909137134 DESMEDT JE, 1965, EXP NEUROL, V11, P1, DOI 10.1016/0014-4886(65)90019-1 Dolan DF, 1997, J ACOUST SOC AM, V102, P3587, DOI 10.1121/1.421008 FIRBAS W, 1983, HEARING RES, V10, P109, DOI 10.1016/0378-5955(83)90021-7 FISCHER FP, 1994, HEARING RES, V73, P1, DOI 10.1016/0378-5955(94)90277-1 FISCHER FP, 1994, SCANNING MICROSCOPY, V8, P351 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R FREEMAN S, 1995, J NEUROL SCI, V131, P21, DOI 10.1016/0022-510X(95)00038-4 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 FUCHS PA, 1992, J NEUROSCI, V12, P800 GOLDBERG JM, 1980, J NEUROPHYSIOL, V43, P986 GOLUBEVA T B, 1972, Zhurnal Evolyutsionnoi Biokhimii i Fiziologii, V8, P173 GUINAN JJ, 1988, HEARING RES, V33, P115, DOI 10.1016/0378-5955(88)90024-X HARTMANN R, 1980, PFLUG ARCH EUR J PHY, V388, P123, DOI 10.1007/BF00584117 HIGHSTEIN SM, 1985, J NEUROPHYSIOL, V54, P370 KAISER A, 1994, J NEUROPHYSIOL, V72, P2966 KETTEMBEIL S, 1995, HEARING RES, V86, P47, DOI 10.1016/0378-5955(95)00053-7 KLINKE R, 1974, PHYSIOL REV, V54, P316 KOPPL C, 1996, ABSTR ASS RES OT, V19, P126 Koppl C, 1997, J NEUROPHYSIOL, V77, P364 KUMMER P, 1995, J ACOUST SOC AM, V98, P197, DOI 10.1121/1.413747 LIBERMAN MC, 1980, HEARING RES, V3, P189, DOI 10.1016/0378-5955(80)90046-5 Liberman MC, 1996, J ACOUST SOC AM, V99, P3572, DOI 10.1121/1.414956 MARKIN VS, 1995, BIOPHYS J, V69, P138 MOISEFF A, 1981, J COMP PHYSIOL, V144, P299 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K MURROW BW, 1990, P ROY SOC B-BIOL SCI, V242, P189, DOI 10.1098/rspb.1990.0123 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 OECKINGHAUS H, 1983, J COMP PHYSIOL, V150, P61 OHMORI H, 1991, ACTA OTO-LARYNGOL, P1 PAYNE RS, 1971, J EXP BIOL, V54, P535 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 ROBERTS BL, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P185 ROBERTSON D, 1985, HEARING RES, V20, P63, DOI 10.1016/0378-5955(85)90059-0 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X SHIGEMOTO T, 1991, J PHYSIOL-LONDON, V442, P669 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 Taschenberger G, 1997, HEARING RES, V110, P61, DOI 10.1016/S0378-5955(97)00070-1 Taschenberger G, 1998, HEARING RES, V123, P183, DOI 10.1016/S0378-5955(98)00120-8 ULFENDAHL M, 1995, NEUROREPORT, V6, P1157, DOI 10.1097/00001756-199505300-00021 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 NR 57 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 1 EP 12 DI 10.1016/S0378-5955(99)00126-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800001 PM 10575110 ER PT J AU Campbell, KCM Meech, RP Rybak, LP Hughes, LF AF Campbell, KCM Meech, RP Rybak, LP Hughes, LF TI D-Methionine protects against cisplatin damage to the stria vascularis SO HEARING RESEARCH LA English DT Article DE D-Methionine; cisplatin; stria vascularis; ototoxicity; semi-quantitative analysis ID AUDITORY HAIR-CELLS; GUINEA-PIG; INDUCED OTOTOXICITY; CIS-PLATINUM; RAT; DIETHYLDITHIOCARBAMATE; FOSFOMYCIN; MOLECULES; REDUCTION; PROTEINS AB D-Methionine (D-met) protects against cisplatin (CDDP)-induced hearing loss and outer hair cell loss (Campbell et al., 1996). However, D-met's protective effects on the stria vascularis has not been previously investigated. The purpose of this study was to examine, using semi-quantitative analysis, whether D-met also protects the stria vascularis. We removed a basal turn section of the stria vascularis from five groups of five male Wistar rats each: (1) a CDDP-treated control group receiving a 30 min i.p. infusion of 16 mg/kg CDDP, (2) a saline-injected control group receiving an equivalent volume of saline, and (3) three groups injected with either 75, 150, or 300 mp/kg D-methionine (D-met) i.p. 30 min prior to receiving the 16 mg/kg CDDP dosing. Using transmission electron microscopy and light microscopy, we analyzed strial volume (i.e. edema), marginal cell damage classification (bulging and/or compression), and relative optical density (ROD) ratios (i.e. depletion of marginal cell cytoplasmic organelles). All three levels of D-met provided complete protection against marginal cell bulging and/or compression but only partial protection against strial edema. At 300 mg/kg, D-met significantly reduced ROD ratio degradation in the spiral prominence and middle stria vascularis regions. In Reissner's membrane region, values from the D-met pretreated group were not significantly different from either the treated or untreated control groups suggesting only partial protection for that area. Protection of marginal cell cytoplasmic organelles was also noted. In summary, D-met partially or fully protects the stria vascularis from several types of CDDP-induced damage. (C) 1999 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Springfield, IL 62794 USA. RP Campbell, KCM (reprint author), So Illinois Univ, Sch Med, POB 19629, Springfield, IL 62794 USA. CR BRUMMETT R, 1977, ACTA OTO-LARYNGOL, V83, P98, DOI 10.3109/00016487709128819 Campbell KCM, 1996, HEARING RES, V102, P90, DOI 10.1016/S0378-5955(96)00152-9 CHURCH MW, 1995, HEARING RES, V86, P195, DOI 10.1016/0378-5955(95)00066-D FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 Gabaizadeh R, 1997, ACTA OTO-LARYNGOL, V117, P232, DOI 10.3109/00016489709117778 HINOJOSA R, 1995, AM J OTOL, V16, P731 HOEVE LJ, 1988, ARCH OTO-RHINO-LARYN, V245, P98, DOI 10.1007/BF00481444 JONES MM, 1989, ANTICANCER RES, V9, P1937 KAJI H, 1987, RES COMMUN CHEM PATH, V56, P101 KIES C, 1975, J NUTR, V105, P809 KOHN S, 1988, LARYNGOSCOPE, V98, P865 Kohn S, 1997, ULTRASTRUCT PATHOL, V21, P289 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 Kopke RD, 1997, AM J OTOL, V18, P559 KORVER KD, 1998, ASS RES OT ABSTR, V536, P135 LAURELL G, 1995, HEARING RES, V87, P16, DOI 10.1016/0378-5955(95)00074-E LEMPERS ELM, 1990, INORG CHEM, V29, P217, DOI 10.1021/ic00327a014 Meech RP, 1998, HEARING RES, V124, P44, DOI 10.1016/S0378-5955(98)00116-6 MELVIK JE, 1987, INORG CHIM A-BIOINOR, V137, P115, DOI 10.1016/S0020-1693(00)87128-5 MEYER GJ, 1985, EUR J NUCL MED, V10, P373 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 OHTANI I, 1985, ORL J OTO-RHINO-LARY, V47, P229 OLIN BR, 1991, DRUG FACTS COMP OTTO WC, 1988, HEARING RES, V35, P79, DOI 10.1016/0378-5955(88)90042-1 PRINTEN KJ, 1979, AM J CLIN NUTR, V32, P1200 RESER DH, 1998, ASS RES OT ABSTR, V203, P51 RHO MB, 1998, ASS RES OT ABSTR, V202, P51 RYBAK LP, 1992, HEARING RES, V59, P75, DOI 10.1016/0378-5955(92)90104-U SANTI PA, 1983, HEARING RES, V12, P151, DOI 10.1016/0378-5955(83)90103-X SANTI PA, 1979, ACTA OTO-LARYNGOL, V88, P1, DOI 10.3109/00016487909137133 SCHWEITZER VG, 1993, LARYNGOSCOPE, V103, P1, DOI 10.1288/00005537-199304000-00001 STEGINK LD, 1986, J NUTR, V116, P1185 Suzuki M, 1996, EUR ARCH OTO-RHINO-L, V253, P351 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 VOGT W, 1995, FREE RADICAL BIO MED, V18, P93, DOI 10.1016/0891-5849(94)00158-G NR 35 TC 56 Z9 61 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 13 EP 28 DI 10.1016/S0378-5955(99)00142-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800002 PM 10575111 ER PT J AU Chen, GD Sinex, DG AF Chen, GD Sinex, DG TI Effects of interaural time differences on the responses of chinchilla inferior colliculus neurons to consonant-vowel syllables SO HEARING RESEARCH LA English DT Article DE interaural time difference; consonant-vowel syllable; inferior colliculus; single unit; chinchilla ID VOICE-ONSET TIME; DISCHARGE RATE REPRESENTATION; PRIMARY AUDITORY-CORTEX; HIGH-FREQUENCY NEURONS; UNANESTHETIZED RABBIT; BINAURAL INTERACTION; NOISE STIMULI; DELAYS; CAT; SENSITIVITY AB The responses of 100 inferior colliculus neurons to syllables differing in voice onset time (VOT) presented binaurally were studied. As in a previous study of monaural responses (Chen et al., 1996), the responses consisted of 1-3 response 'components', referred to as release responses, VOT responses or vowel responses. The discharge rate of all response components could vary cyclically with the interaural time difference (ITD). The maximal rate often occurred at an ITD around +0.2 ms (contralateral ear leading). Response frequencies (RF) based on the periodicity of the delay curves varied with the characteristic frequency (CF) and VOT. RF also varied across response components. Overall, RF was correlated with the 'most effective frequency', the spectral component with the highest amplitude, relative to the tuning curve. VOT response latency for a given syllable could change by a few ms with ITD, but those changes were small, relative to the range of latencies observed over the entire range of VOTs. Changes in ITD produced large changes in the overall shape of the peristimulus time histogram. There was no relation between the histogram shape and perceptual consonant categories. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Arizona State Univ, Dept Speech & Hearing Sci, Tempe, AZ 85287 USA. RP Sinex, DG (reprint author), Arizona State Univ, Dept Speech & Hearing Sci, Box 871908, Tempe, AZ 85287 USA. CR AITKIN LM, 1972, BRAIN RES, V47, P91, DOI 10.1016/0006-8993(72)90254-5 BATRA R, 1993, J NEUROPHYSIOL, V70, P64 BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 CAIRD D, 1980, HEARING RES, V3, P257, DOI 10.1016/0378-5955(80)90021-0 CHAN JCK, 1987, J NEUROPHYSIOL, V58, P543 CHEN GD, 1996, ABSTR ASS RES OT, P363 Chen GD, 1996, AUDIT NEUROSCI, V3, P179 EGGERMONT JJ, 1995, J ACOUST SOC AM, V98, P911, DOI 10.1121/1.413517 GEISLER CD, 1969, J NEUROPHYSIOL, V32, P960 GIBSON DJ, 1982, HEARING RES, V7, P325, DOI 10.1016/0378-5955(82)90043-0 KUHL PK, 1981, J ACOUST SOC AM, V70, P340, DOI 10.1121/1.386782 KUWADA S, 1983, J NEUROPHYSIOL, V50, P981 KUWADA S, 1987, J NEUROPHYSIOL, V57, P1338 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 KUWADA S, 1989, J NEUROPHYSIOL, V61, P269 LISKER L, 1964, WORD, V20, P384 McGee T, 1996, J ACOUST SOC AM, V99, P3606, DOI 10.1121/1.414958 Nuding SC, 1999, HEARING RES, V131, P89, DOI 10.1016/S0378-5955(99)00023-4 PALMER AR, 1990, HEARING RES, V50, P71, DOI 10.1016/0378-5955(90)90034-M ROSE JE, 1966, J NEUROPHYSIOL, V29, P288 SINEX DG, 1991, J ACOUST SOC AM, V90, P2441, DOI 10.1121/1.402048 SINEX DG, 1989, J ACOUST SOC AM, V85, P1995, DOI 10.1121/1.397852 SINEX DG, 1988, J ACOUST SOC AM, V83, P1817, DOI 10.1121/1.396516 STANFORD TR, 1992, J NEUROSCI, V12, P3200 STEINSCHNEIDER M, 1995, BRAIN LANG, V48, P326, DOI 10.1006/brln.1995.1015 TAKAHASHI T, 1986, J NEUROSCI, V6, P3413 YIN TCT, 1986, J NEUROPHYSIOL, V55, P280 YIN TCT, 1984, J ACOUST SOC AM, V76, P1401, DOI 10.1121/1.391457 NR 28 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 29 EP 44 DI 10.1016/S0378-5955(99)00146-X PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800003 PM 10575112 ER PT J AU Park, DL Girod, DA Durham, D AF Park, DL Girod, DA Durham, D TI Tonotopic changes in 2-deoxyglucose activity in chick cochlear nucleus during hair cell loss and regeneration SO HEARING RESEARCH LA English DT Article DE nucleus magnocellularis; gentamicin; hair cell regeneration; neuronal plasticity; glucose metabolism ID STEM AUDITORY NUCLEI; SENSORINEURAL HEARING-LOSS; AFFERENT INFLUENCES; ACOUSTIC TRAUMA; INNER-EAR; BASILAR PAPILLA; AMINOGLYCOSIDE OTOTOXICITY; FUNCTIONAL RECOVERY; NEURONS; REMOVAL AB Following cochlear ablation, auditory neurons in the central nervous system (CNS) undergo alterations in morphology and function, including neuronal cell death. The trigger for these CNS changes is the abrupt cessation of eighth nerve fiber activity. Gentamicin can cause ototoxic damage to cochlear hair cells responsible for high frequency hearing. In birds, these hair cells can regenerate. Therefore, gentamicin causes a partial, yet reversible insult to the ear. It is not known how this partial hair cell damage affects excitatory input to the cochlear nucleus. We examined chick cochlear nucleus activity during hair cell loss and regeneration by measuring 2-deoxyglucose (2DG) uptake. Normal animals showed a rostral to caudal gradient of 2DG activity, with higher activity in caudal regions. When hair cells are damaged (2, 5 days), 2DG uptake is decreased in cochlear nucleus. When hair cells regenerate (9, 16, 28 days), 2DG uptake returns to control levels. This decrease and subsequent return of activity only occurs in the rostral, high frequency region of the cochlear nucleus. No changes are seen in the caudal, low frequency region. These results suggest that changes in activity of cochlear nucleus occur at a similar time course to anatomical changes in the cochlea. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Dept Otolaryngol, Kansas City, KS 66160 USA. Smith Mental Redardat & Human Dev Res Ctr, Kansas City, KS 66160 USA. Univ Kansas, Med Ctr, Dept Speech & Hearing, Kansas City, KS 66103 USA. Kansas City Vet Affairs Med Ctr, Kansas City, MO USA. RP Durham, D (reprint author), Dept Otolaryngol, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 BORN DE, 1991, BRAIN RES, V557, P37, DOI 10.1016/0006-8993(91)90113-A BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 BORN DE, 1988, J NEUROSCI, V8, P901 BROWN M, 1992, HEARING RES, V59, P224, DOI 10.1016/0378-5955(92)90119-8 Chen L, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P43 COHEN YE, 1994, HEARING RES, V81, P11, DOI 10.1016/0378-5955(94)90148-1 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 DUCKERT LG, 1993, J COMP NEUROL, V331, P75, DOI 10.1002/cne.903310105 DURHAM D, 1985, J COMP NEUROL, V231, P446, DOI 10.1002/cne.902310404 EPSTEIN JE, 1995, HEARING RES, V90, P31, DOI 10.1016/0378-5955(95)00141-9 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HEIL P, 1986, J COMP NEUROL, V252, P279, DOI 10.1002/cne.902520302 HYDE GE, 1990, J COMP NEUROL, V297, P329, DOI 10.1002/cne.902970302 HYSON RL, 1995, BRAIN RES, V672, P196, DOI 10.1016/0006-8993(94)01390-4 Janas JD, 1995, HEARING RES, V92, P17, DOI 10.1016/0378-5955(95)00190-5 KEITHLEY EM, 1994, HEARING RES, V80, P79, DOI 10.1016/0378-5955(94)90011-6 LINDEN R, 1994, NEUROSCIENCE, V58, P671, DOI 10.1016/0306-4522(94)90447-2 LIPPE W, 1985, J COMP NEUROL, V237, P273, DOI 10.1002/cne.902370211 LIPPE WR, 1991, HEARING RES, V51, P193, DOI 10.1016/0378-5955(91)90036-9 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 LIPPE WR, 1994, J NEUROSCI, V14, P1486 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y Mattson MP, 1996, PERSPECT DEV NEUROBI, V3, P79 McCasland JS, 1996, J NEUROSCI METH, V68, P113, DOI 10.1016/0165-0270(96)00063-5 MORGAN AS, 1999, ARO ABSTR, V22, P96 NIEMIEC AJ, 1994, HEARING RES, V74, P209 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 Park DL, 1998, HEARING RES, V126, P84, DOI 10.1016/S0378-5955(98)00157-9 PARKS TN, 1979, J COMP NEUROL, V183, P665, DOI 10.1002/cne.901830313 Parks TN, 1997, ANN OTO RHINOL LARYN, V106, P37 PUGLIANO FA, 1993, ACTA OTO-LARYNGOL, V113, P18, DOI 10.3109/00016489309135761 RUBEL E W, 1991, Brain Dysfunction, V4, P55 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 RUBEL EW, 1982, ACTA OTO-LARYNGOL, V93, P31, DOI 10.3109/00016488209130849 RYALS BM, 1982, ACTA OTO-LARYNGOL, V93, P205, DOI 10.3109/00016488209130873 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 Ryugo DK, 1998, J COMP NEUROL, V397, P532, DOI 10.1002/(SICI)1096-9861(19980810)397:4<532::AID-CNE6>3.0.CO;2-2 Saunders JC, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P62 Saunders JC, 1998, J COMP NEUROL, V390, P412 Stone JS, 1998, CURR OPIN NEUROL, V11, P17, DOI 10.1097/00019052-199802000-00004 Tierney TS, 1997, J COMP NEUROL, V387, P421 TSUE TT, 1994, OTOLARYNG HEAD NECK, V111, P281, DOI 10.1016/S0194-5998(94)70603-4 TUCCI DL, 1985, J COMP NEUROL, V238, P371, DOI 10.1002/cne.902380402 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 TUCCI DL, 1987, ANN OTO RHINOL LARYN, V96, P343 WESTRUM LE, 1999, ARO ABSTR, V22, P127 NR 54 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 45 EP 55 DI 10.1016/S0378-5955(99)00138-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800004 PM 10575113 ER PT J AU Munoz, DJB Thorne, PR Housley, GD AF Munoz, DJB Thorne, PR Housley, GD TI P2X receptor-mediated changes in cochlear potentials arising from exogenous adenosine 5 '-triphosphate in endolymph SO HEARING RESEARCH LA English DT Article DE adenosine triphosphate; adenosine diphosphate; cochlear function; cochlear microphonic; endocochlear potential; endolymph; P2 receptor agonist; P2 receptor antagonist; uridine triphosphate ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; MARGINAL CELLS; PHARMACOLOGICAL EVIDENCE; PURINERGIC RECEPTORS; STRIA VASCULARIS; AUDITORY-NERVE; INNER-EAR; ATP; SUBUNIT AB Our previous studies have determined the presence of adenosine 5'-triphosphate (ATP) in the cochlear fluids and shown that extracellular ATP introduced into the endolymphatic compartment of the guinea pig cochlea has a significant dose-dependent suppressive effect on both endocochlear potential (EP) and cochlear microphonic (CM), which is mediated via P2 receptors. In the present study, the influence of P2 receptor agonists and antagonists on this suppressive effect was investigated to characterise the subtypes of P2 receptor mediating the ATP-induced effect on cochlear function. Using a double-barreled pipette attached to a pressure injector, small volumes (2-10 nl) of ATP (0.01-1 mM) and P2 receptor agonists or P2 receptor antagonists in artificial endolymph were introduced into the scala media of the first (basal) and third turns of the guinea pig cochlea, while the EP and CM were monitored. ATP and P2 receptor agonists (5 x 10(-14)-1 x 10(-11) moles) reversibly decreased the magnitude of EP and CM in a dose-dependent manner, in the order: 2-methylthioATP > ATP > alpha,beta-methyleneATP much greater than adenosine 5'-diphosphate. The ATP-induced decline of EP and CM was significantly inhibited by P2 receptor antagonists in the order of potency: pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid much greater than suramin > cibacron blue. Neither adenosine nor uridine 5'-triphosphate (2 x 10(-13)-2 x 10(-11) moles) nor the P2 receptor antagonists on their own had any effect on EP and CM. The ATP effect on the potentials was greater at the third cochlear turn when compared to the first turn. These results provide evidence that in the endolymphatic compartment of the guinea pig, the extracellular ATP effect on cochlear function is likely mediated through an interaction with P2 receptors which assemble as ATP-gated ion channels. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Auckland, Dept Physiol, Fac Med & Hlth Sci, Auckland, New Zealand. RP Thorne, PR (reprint author), Univ Auckland, Dept Physiol, Fac Med & Hlth Sci, Private Bag 92019, Auckland, New Zealand. CR Brandle U, 1997, FEBS LETT, V404, P294, DOI 10.1016/S0014-5793(97)00128-2 BURNSTOCK G, 1987, BRIT J PHARMACOL, V90, P383 Chen C, 1998, BRIT J PHARMACOL, V124, P337, DOI 10.1038/sj.bjp.0701848 Chen C, 1998, HEARING RES, V118, P47, DOI 10.1016/S0378-5955(98)00019-7 Fredholm BB, 1997, TRENDS PHARMACOL SCI, V18, P79, DOI 10.1016/S0165-6147(96)01038-3 GLOWATZKI E, 1995, P ROY SOC B-BIOL SCI, V262, P141, DOI 10.1098/rspb.1995.0188 HONRUBIA V, 1969, J ACOUST SOC AM, V46, P388, DOI 10.1121/1.1911701 HOUSLEY GD, 1993, BIOPHYSICS HAIR CELL, P116 HOUSLEY GD, 1995, ACTIVE HEARING, P221 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HOUSLEY GD, 1995, BIOCHEM BIOPH RES CO, V212, P501, DOI 10.1006/bbrc.1995.1998 Housley GD, 1998, MOL NEUROBIOL, V16, P21, DOI 10.1007/BF02740601 HOUSLEY GD, 1999, IN PRESS J NEUROSCI Housley GD, 1998, HEARING RES, V119, P1, DOI 10.1016/S0378-5955(97)00206-2 Housley GD, 1998, J COMP NEUROL, V393, P403 JARLEBARK L, 1996, DRUG DEVELOP RES, V37, P184 KENNEDY C, 1995, TRENDS PHARMACOL SCI, V16, P168, DOI 10.1016/S0165-6147(00)89010-0 KHAKH BS, 1995, J PHYSIOL-LONDON, V484, P385 King M, 1998, NEUROREPORT, V9, P2467, DOI 10.1097/00001756-199808030-00008 Kirk DL, 1998, NEUROSCI LETT, V250, P149, DOI 10.1016/S0304-3940(98)00460-1 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 LIU J, 1995, AUDIT NEUROSCI, V1, P331 Marcus DC, 1998, HEARING RES, V115, P82, DOI 10.1016/S0378-5955(97)00180-9 MOCKETT BG, 1995, HEARING RES, V84, P177, DOI 10.1016/0378-5955(95)00024-X MOCKETT BG, 1994, J NEUROSCI, V14, P6992 MUNOZ DJB, 1995, HEARING RES, V90, P106, DOI 10.1016/0378-5955(95)00152-3 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 NILLES R, 1994, HEARING RES, V73, P27, DOI 10.1016/0378-5955(94)90279-8 OGAWA K, 1995, NEUROREPORT, V6, P1538 Parker MS, 1998, HEARING RES, V121, P62, DOI 10.1016/S0378-5955(98)00065-3 PIPER AS, 1995, EUR J PHARMACOL, V280, P125, DOI 10.1016/0014-2999(95)00182-K Raybould NP, 1997, J PHYSIOL-LONDON, V498, P717 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SALIH SG, 1999, IN PRESS NEUROREPORT Salih SG, 1998, NEUROREPORT, V9, P279, DOI 10.1097/00001756-199801260-00019 SALT AN, 1995, HEARING RES, V88, P79, DOI 10.1016/0378-5955(95)00103-B SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 Skellett RA, 1997, HEARING RES, V111, P42, DOI 10.1016/S0378-5955(97)00093-2 Thorne PR, 1996, SEMIN NEUROSCI, V8, P233, DOI 10.1006/smns.1996.0030 THORNE PR, 1999, ASS RES OTOLARYNGOL, V23, P482 Vlajkovic SM, 1998, NEUROREPORT, V9, P1559 Wangemann P, 1996, AUDIT NEUROSCI, V2, P187 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WHITE PN, 1995, HEARING RES, V90, P97, DOI 10.1016/0378-5955(95)00151-1 NR 45 TC 24 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 56 EP 64 DI 10.1016/S0378-5955(99)00151-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800005 PM 10575114 ER PT J AU Li, DQ Henley, CM O'Malley, BW AF Li, DQ Henley, CM O'Malley, BW TI Distortion product otoacoustic emissions and outer hair cell defects in the hyt/hyt mutant mouse SO HEARING RESEARCH LA English DT Article DE hyt/hyt; hypothyroidism; distortion product otoacoustic emission; outer hair cell ID ACOUSTIC DISTORTION; COCHLEAR MECHANICS; HYPO-THYROIDISM; HEARING-LOSS; EAR; HYPOTHYROIDISM; NONLINEARITY; RESPONSES; RECEPTOR; MUTATION AB Thyroid hormone plays an important role in hearing development. Hereditary hypothyroidism is frequently associated with sensorineural hearing loss as identified in both animal models and human patients. Building upon our original demonstration of congenital deafness and hair cell abnormality in a hyt/hyt mouse model which carries an autosomal recessive mutation causing hereditary hypothyroidism, we investigated the functional capacity of the outer hair cell (OHC) system in these animals using distortion product otoacoustic emissions (DPOAEs). In particular, the amplitude and detection features of DPOAEs were correlated with measures of the auditory brainstem response (ABR) as well as the cellular structure and ultrastructure of the organ of Corti. Input-output (I/O) functions for the 2f(2)-f(1) DPOAEs were obtained for frequencies from 2 to 18 kHz. The thresholds were significantly higher and amplitudes were significantly lower in the homozygous mice (hyt/hyt) than in both heterozygous mice (hyt/+) and wild-type controls at DPOAE frequencies recorded above 6 kHz. Hearing thresholds were significantly elevated in the mutant compared to control mice. In addition, morphological studies revealed consistent inner ear defects in hyt/hyt animals including distortion of the tectorial membrane, dysplasia of the tunnel of Corti and distinct OHC abnormalities. The most striking histopathological finding was a contiguous membrane along the apices of all of the OHC stereocilia. Such ultrastructural changes in the stereocilia of the OHC may limit the deflection of the stereocilia and therefore affect an active cochlear function that produces otoacoustic emissions as well as cause a failure to evoke the normal action potentials in the auditory nerve. From both functional and morphologic evaluations, it was concluded that the OHC system is the most susceptible to the developmental effects of congenital hypothyroidism in the hyt/hyt mouse. The normal OHCs with well-developed ciliary bundles are crucial to maintain the activity of biological mechanisms within the cochlea. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Maryland, Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21201 USA. Baylor Coll Med, Dept Otorhinolaryngol & Communicat Sci, Houston, TX 77030 USA. RP Li, DQ (reprint author), Univ Maryland, Sch Med, Dept Otolaryngol Head & Neck Surg, 436 MSTF 10 S Pine St, Baltimore, MD 21201 USA. CR Bargman G J, 1972, Adv Exp Med Biol, V30, P305 BARGMAN GJ, 1967, J CLIN INVEST, V46, P1828, DOI 10.1172/JCI105673 BATSAKIS JG, 1962, ARCHIV OTOLARYNGOL, V76, P401 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 CROSS HE, 1968, PEDIATRICS, V41, P413 DEOL MS, 1976, ACTA OTO-LARYNGOL, V81, P429 DEOL MS, 1973, J MED GENET, V10, P235, DOI 10.1136/jmg.10.3.235 FISHER DA, 1979, J PEDIATR-US, V94, P700, DOI 10.1016/S0022-3476(79)80133-X FRASER GR, 1965, ANN HUM GENET, V28, P201 GREIG WR, 1966, J CLIN ENDOCR METAB, V26, P1309 GU WX, 1995, ENDOCRINOLOGY, V136, P3146, DOI 10.1210/en.136.7.3146 HARRIS FP, 1990, J SPEECH HEAR RES, V33, P594 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 KAPLAN M, 1977, AM J DIS CHILD, V131, P1264 KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KOHONEN A, 1971, LARYNGOSCOPE, V81, P947, DOI 10.1288/00005537-197106000-00015 KULIN HE, 1967, J PEDIATR-US, V71, P714, DOI 10.1016/S0022-3476(67)80209-9 LEGRAND J, 1977, P137 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P3 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MEYERHOFF WL, 1979, LARYNGOSCOPE, V89, P1 MEYERHOFF WL, 1976, LARYNGOSCOPE, V86, P483, DOI 10.1288/00005537-197604000-00002 OHLMS LA, 1990, ANN OTO RHINOL LARYN, V99, P30 OMALLEY BW, 1995, HEARING RES, V88, P181, DOI 10.1016/0378-5955(95)00111-G ORTI E, 1971, J PEDIATR-US, V78, P675, DOI 10.1016/S0022-3476(71)80473-0 RITTER FN, 1967, LARYNGOSCOPE, V77, P1427, DOI 10.1288/00005537-196708000-00016 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SPEKTOR Z, 1991, LARYNGOSCOPE, V101, P956 STEEL KP, 1983, AUDITORY PSYCHOBIOLO, P341 STEIN SA, 1994, MOL ENDOCRINOL, V8, P129, DOI 10.1210/me.8.2.129 TROTTER WR, 1960, BRIT MED BULL, V16, P92 UZIEL A, 1981, ACTA OTO-LARYNGOL, V92, P469, DOI 10.3109/00016488109133286 WITHERS BT, 1972, LARYNGOSCOPE, V82, P779, DOI 10.1288/00005537-197205000-00003 NR 37 TC 28 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 65 EP 72 DI 10.1016/S0378-5955(99)00150-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800006 PM 10575115 ER PT J AU Marzella, PL Gillespie, LN Clark, GM Bartlett, PF Kilpatrick, TJ AF Marzella, PL Gillespie, LN Clark, GM Bartlett, PF Kilpatrick, TJ TI The neurotrophins act synergistically with LIF and members of the TGF-beta superfamily to promote the survival of spiral ganglia neurons in vitro SO HEARING RESEARCH LA English DT Article DE auditory neuron; pharmacological therapy; cytokine; neurotrophin; neuronal degeneration; neurotrophic effect ID LEUKEMIA INHIBITORY FACTOR; ADULT AUDITORY NEURONS; NERVE GROWTH-FACTOR; SENSORY NEURONS; MESSENGER-RNA; IN-VITRO; HAIR-CELLS; INNER-EAR; NT-3; BDNF AB A number of growth factor families have been implicated in normal inner ear development, auditory neuron survival and protection. Several growth factors, including transforming growth factor-beta 5 (TGF-beta 5) and TGF-beta 3, neurotrophin-3 (NT-3), brain-derived neurotrophic factor (BDNF) and leukemia inhibitory factor (LIF) were tested for their ability, individually or in combination, to promote auditory neuron survival in dissociated cell cultures of early rat post-natal spiral ganglion cells (SGCs). The results indicate that at discrete concentrations all growth factors act in an additive fashion and some in synergy when promoting neuronal survival. These findings support the hypothesis that growth factors from different families may be interdependent when sustaining neuronal integrity. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Royal Victorian Eye & Ear Hosp, Dept Otolaryngol, E Melbourne, Vic 3002, Australia. Walter & Eliza Hall Inst Med Res, Dev & Neuroimmunol Lab, Parkville, Vic 3052, Australia. RP Marzella, PL (reprint author), Univ Melbourne, Royal Victorian Eye & Ear Hosp, Dept Otolaryngol, 32 Gisborne St, E Melbourne, Vic 3002, Australia. RI Bartlett, Perry/F-3813-2012 CR Blesch A, 1999, J NEUROSCI, V19, P3556 CHALAZONITIS A, 1992, DEV BIOL, V152, P121, DOI 10.1016/0012-1606(92)90162-A ERNFORS P, 1995, NEURON, V14, P1153, DOI 10.1016/0896-6273(95)90263-5 Ernfors P., 1995, NEURON, V15, P739 FARINAS I, 1994, NATURE, V369, P658, DOI 10.1038/369658a0 FRENZ DA, 1992, DEV BIOL, V153, P324, DOI 10.1016/0012-1606(92)90117-Y Hartnick CJ, 1996, J NEUROBIOL, V30, P246, DOI 10.1002/(SICI)1097-4695(199606)30:2<246::AID-NEU6>3.0.CO;2-5 Ip NY, 1996, ANNU REV NEUROSCI, V19, P491 KAARTINEN V, 1995, NAT GENET, V11, P415, DOI 10.1038/ng1295-415 Komeda M, 1999, HEARING RES, V131, P1, DOI 10.1016/S0378-5955(99)00006-4 KONDAIAH P, 1990, J BIOL CHEM, V265, P1089 Kretzschmar M, 1998, CURR OPIN GENET DEV, V8, P103, DOI 10.1016/S0959-437X(98)80069-5 Krieglstein K, 1996, NEUROCHEM RES, V21, P843, DOI 10.1007/BF02532308 LEFEBVRE PP, 1991, NEUROREPORT, V2, P305, DOI 10.1097/00001756-199106000-00001 LEFEBVRE PP, 1992, NEUROREPORT, V3, P295, DOI 10.1097/00001756-199204000-00001 Malgrange B, 1996, NEUROREPORT, V7, P913, DOI 10.1097/00001756-199603220-00016 MANESS LM, 1994, NEUROSCI BIOBEHAV R, V18, P143, DOI 10.1016/0149-7634(94)90043-4 Marzella PL, 1998, NEUROSCI LETT, V240, P77, DOI 10.1016/S0304-3940(97)00928-2 Marzella PL, 1997, NEUROREPORT, V8, P1641, DOI 10.1097/00001756-199705060-00017 Matsuoka I, 1997, BRAIN RES, V776, P170, DOI 10.1016/S0006-8993(97)01015-9 MESSAGUE J, 1991, TRANSFORMING GROWTH, P51 MESSAGUE J, 1997, TRENDS CELL BIOL, V7, P187 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 Minichiello L, 1995, DEVELOPMENT, V121, P4067 Mou K, 1997, J COMP NEUROL, V386, P529 PELTON RW, 1991, J CELL BIOL, V115, P1091, DOI 10.1083/jcb.115.4.1091 Pirvola U, 1997, J NEUROBIOL, V33, P1019, DOI 10.1002/(SICI)1097-4695(199712)33:7<1019::AID-NEU11>3.0.CO;2-A RAJAN P, 1995, NEUROREPORT, V6, P2240, DOI 10.1097/00001756-199511000-00033 Rajan P, 1998, BRAIN RES, V802, P198, DOI 10.1016/S0006-8993(98)00611-8 SEGARINI PR, 1991, TRANSFORMING GROWTH, P29 SHAH SB, 1995, AM J OTOL, V16, P310 Staecker H, 1996, DEV BRAIN RES, V92, P49, DOI 10.1016/0165-3806(95)00198-0 STAECKER H, 1995, NEUROREPORT, V6, P1533 Staecker H, 1996, NEUROREPORT, V7, P889, DOI 10.1097/00001756-199603220-00011 THALER CD, 1994, DEV BIOL, V161, P338, DOI 10.1006/dbio.1994.1035 Van de Water T R, 1980, Birth Defects Orig Artic Ser, V16, P5 WHEELER EF, 1994, HEARING RES, V73, P46, DOI 10.1016/0378-5955(94)90281-X ZHENG JL, 1995, J NEUROBIOL, V28, P330 NR 38 TC 54 Z9 54 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 73 EP 80 DI 10.1016/S0378-5955(99)00152-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800007 PM 10575116 ER PT J AU Rask-Andersen, H DeMott, JE Bagger-Sjoback, D Salt, AN AF Rask-Andersen, H DeMott, JE Bagger-Sjoback, D Salt, AN TI Morphological changes of the endolymphatic sac induced by microinjection of artificial endolymph into the cochlea SO HEARING RESEARCH LA English DT Article DE endolymphatic sac; endolymph; injection; inner ear; volume regulation; hydrops ID GUINEA-PIG; INNER-EAR; GLYCEROL AB Morphological changes of the endolymphatic sac were analyzed in guinea pigs following microinjection of artificial endolymph into the cochlea or withdrawal of a quantity of native endolymph. Injections were performed into the second turn of scala media with a micro-pump at a rate of 60-100 nl/min, lasting for a period of 4, 7.5, 15 or 18 min. In withdrawal experiments, endolymph was aspirated from the second cochlear turn over a period of 8 min. For each procedure the contralateral (non-treated) ear served as a histological control. Following artificial endolymph injections of 7.5 min or more there was an almost total absence of the normal intraluminal homogeneous substance (HS) on the injected side. Our observations suggest that the disappearance of the HS occurs by both enzymatic and macrophagic activity, After endolymphatic withdrawals the ES was found to contain increased amounts of HS. The results could suggest that the volume of fluid in the ES, and hence the volume of the entire membranous labyrinth, may be regulated by a dynamic relationship between active secretion and enzymatic degradation of a lumen-expanding substance that is intimately related to the intraluminal macrophages. The exact mechanism governing these regulatory systems, and their relationship to ion and water movements across the epithelium of the sac, remain to be elucidated. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Uppsala Hosp, Dept Otolaryngol, Akad Sjukhuset, S-75185 Uppsala, Sweden. Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. Karolinska Hosp, Dept Otolaryngol, S-10401 Stockholm, Sweden. RP Rask-Andersen, H (reprint author), Univ Uppsala Hosp, Dept Otolaryngol, Akad Sjukhuset, S-75185 Uppsala, Sweden. CR Couloigner V, 1998, LARYNGOSCOPE, V108, P592, DOI 10.1097/00005537-199804000-00024 ERWALL C, 1989, ACTA OTO-LARYNGOL, V107, P63, DOI 10.3109/00016488909127480 ERWALL C, 1988, ACTA OTO-LARYNGOL, V105, P209, DOI 10.3109/00016488809097000 ERWALL C, 1988, HEARING RES, V35, P109, DOI 10.1016/0378-5955(88)90045-7 FRIBERG U, 1986, ACTA OTO-LARYNGOL, V101, P172, DOI 10.3109/00016488609132825 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 JANSSON B, 1993, ORL J OTO-RHINO-LARY, V55, P185 JANSSON B, 1992, ORL J OTO-RHINO-LARY, V54, P201 MIZUKOSHI F, 1988, ACTA OTO-LARYNGOL, V105, P202, DOI 10.3109/00016488809096999 RASKANDERSEN H, 1979, ORL J OTO-RHINO-LARY, V41, P177 SALT A, 1997, HEARING RES, V29, P107 TAKUMIDA M, 1989, HEARING RES, V40, P1, DOI 10.1016/0378-5955(89)90094-4 NR 12 TC 30 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 81 EP 90 DI 10.1016/S0378-5955(99)00153-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800008 PM 10575117 ER PT J AU Jimenez, AM Stagner, BB Martin, GK Lonsbury-Martin, BL AF Jimenez, AM Stagner, BB Martin, GK Lonsbury-Martin, BL TI Age-related loss of distortion product otoacoustic emissions in four mouse strains SO HEARING RESEARCH LA English DT Article DE cochlea; aging; distortion product otoacoustic emission; inbred mouse strain ID SCANNING ELECTRON-MICROSCOPY; HEARING-IMPAIRED MICE; COCHLEAR MECHANICS; MUTANT MICE; CBA/J MICE; C57BL/6J; MORPHOLOGY; RABBIT; PRESBYCUSIS; GENETICS AB Changes in cochlear function in four inbred strains of mice, CBA/CaJ (CBA), C57BL/6J (C57), BALB/cByJ (BALB), and WB/ReJ (WB), previously used to study age-related hearing loss, were evaluated serially as a function of age with 2f(1)-f(2) distortion-product otoacoustic emissions (DPOAEs). DPOAE levels in response to equilevel primary tones for geometric-mean (GM) frequencies from 5.6 to 48.5 kHz were recorded systematically as DP-grams and response/growth or input/output (I/O) functions at monthly intervals from about 2 to 15 months of age. Over the approximate 13-month measurement period, CBAs showed robust and unchanged DPOAEs far all tested frequencies, while BALBs, C57s, and WBs showed strain-specific, age-related decreases in DPOAEs that progressed systematically from the high to low frequencies. Specifically, for the youngest WBs at 2 months of age, no DPOAEs were recordable for GM frequencies greater than or equal to 32 kHz, while C57s and BALBs reached the identical stage of cochlear dysfunction by 5 and 8 months, respectively. The differential decline in DPOAE activity shown for WE, C57, and BALE mice supports the notion that they represent unique animal models of age-related changes in cochlear function. In contrast, the unchanging DPOAEs for CBAs over the same time period indicate that this strain makes an effective control for normal cochlear function in the mouse, at least, up to 15 months of age. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Miami, Sch Med, Neurosci Program, Ear Inst M805, Miami, FL 33101 USA. Univ Miami, Sch Med, Dept Otolaryngol, Miami, FL USA. RP Jimenez, AM (reprint author), Univ Miami, Sch Med, Neurosci Program, Ear Inst M805, POB 016960, Miami, FL 33101 USA. EM ajimenez@mednet.med.miami.edu CR ANDERSON SD, 1979, ARCH OTO-RHINO-LARYN, V224, P47, DOI 10.1007/BF00455223 BONFILS P, 1988, AUDIOLOGY, V27, P27 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 CABLE J, 1994, PIGM CELL RES, V7, P17, DOI 10.1111/j.1600-0749.1994.tb00015.x CASTOR X, 1994, HEARING RES, V77, P1, DOI 10.1016/0378-5955(94)90248-8 COLLET L, 1990, ANN OTO RHINOL LARYN, V99, P993 EHRET G, 1979, ACTA OTO-LARYNGOL, V87, P28, DOI 10.3109/00016487909126384 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Frisina RD, 1997, J ACOUST SOC AM, V101, P2741, DOI 10.1121/1.418562 GLANTZ SA, 1992, PRIMER BIOSTATISTICS, P67 Green MC, 1965, TRANSPLANTATION, V3, P767 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1980, AUDIOLOGY, V19, P369 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 Huang JM, 1996, HEARING RES, V98, P18, DOI 10.1016/0378-5955(96)00041-X HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 JIMENEZ AM, 1998, ASS RES OT ABSTR, V21, P79 JIMENEZ AM, 1996, ASS RES OT ABSTR, V19, P25 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 Le Calvez S, 1998, HEARING RES, V120, P51, DOI 10.1016/S0378-5955(98)00051-3 Le Calvez S, 1998, HEARING RES, V120, P37, DOI 10.1016/S0378-5955(98)00050-1 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 Martin GK, 1998, J ACOUST SOC AM, V104, P972, DOI 10.1121/1.423340 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MCGINN MD, 1992, HEARING RES, V59, P1, DOI 10.1016/0378-5955(92)90094-4 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 MILLS DM, 1998, OTOACOUSTIC EMISSION, P85 MIZUTA K, 1993, SCANNING MICROSCOPY, V7, P889 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 PARHAM K, 1995, ASS RES OT ABSTR, V18, P70 Parham K, 1997, HEARING RES, V112, P216, DOI 10.1016/S0378-5955(97)00124-X PARHAM K, 1996, ASS RES OT ABSTR, V19, P26 SCHROTT A, 1991, HEARING RES, V52, P245, DOI 10.1016/0378-5955(91)90204-M SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 Spongr VP, 1997, J ACOUST SOC AM, V101, P3546, DOI 10.1121/1.418315 STOVER L, 1993, J ACOUST SOC AM, V94, P2670, DOI 10.1121/1.407351 Strouse A L, 1996, J Am Acad Audiol, V7, P339 SUN XM, 1996, ASS RES OT ABSTR, V19, P25 SUN XM, 1997, ASS RES OT ABSTR, V20, P101 WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 WILLOTT JF, 1992, J COMP NEUROL, V321, P666, DOI 10.1002/cne.903210412 Willott JF, 1998, HEARING RES, V115, P162, DOI 10.1016/S0378-5955(97)00189-5 WILLOTT JF, 1990, J COMP NEUROL, V300, P61, DOI 10.1002/cne.903000106 Willott JF, 1998, HEARING RES, V119, P27, DOI 10.1016/S0378-5955(98)00029-X ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 NR 51 TC 43 Z9 50 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 91 EP 105 DI 10.1016/S0378-5955(99)00154-9 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800009 PM 10575118 ER PT J AU Chen, L Kelly, JB Wu, SH AF Chen, L Kelly, JB Wu, SH TI The commissure of Probst as a source of GABAergic inhibition SO HEARING RESEARCH LA English DT Article DE auditory brainstem; dorsal nucleus of the lateral lemniscus; commissure of Probst; gamma-aminobutyric acid; binaural interaction ID STEM AUDITORY NUCLEI; RATS DORSAL NUCLEUS; VITRO BRAIN SLICE; LATERAL LEMNISCUS; INFERIOR COLLICULUS; GABA-IMMUNOREACTIVITY; RESPONSE PROPERTIES; BINAURAL RESPONSES; NEURONS; LOCALIZATION AB Whole-cell patch-clamp recordings were made from neurons in the rat's dorsal nucleus of the lateral lemniscus (DNLL) in a brain slice preparation. Planes of section were chosen to preserve the integrity of fibers in the commissure of Probst (CP) and postsynaptic responses were evoked by electrical stimulation along its length. Results showed that the crossed projection to the DNLL through the CP is mainly, if not exclusively, inhibitory in the rat. Inhibitory postsynaptic responses (IPSPs) evoked by stimulation of the CP were blocked by the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline, but were unaffected by the glycine receptor antagonist strychnine, supporting the conclusion that the crossed inhibitory projection to DNLL from the contralateral DNLL is GABAergic. Stimulation of the CP close to the DNLL frequently evoked excitatory postsynaptic responses as well as IPSPs, but stimulation near the midline evoked IPSPs only. Thus, the excitatory responses probably originated from a pathway other than the projection to the DNLL from the contralateral DNLL through the CP. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Carleton Univ, Inst Neurosci, Sensory Neurosci Lab, Life Sci Res Ctr, Ottawa, ON K1S 5B6, Canada. RP Wu, SH (reprint author), Carleton Univ, Inst Neurosci, Sensory Neurosci Lab, Life Sci Res Ctr, 1125 Colonel By Dr, Ottawa, ON K1S 5B6, Canada. RI Chen, Lin/N-8327-2013 OI Chen, Lin/0000-0002-5847-2989 CR ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 FAINGOLD CL, 1993, HEARING RES, V69, P98, DOI 10.1016/0378-5955(93)90097-K GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GonzalezHernandez T, 1996, J COMP NEUROL, V372, P309, DOI 10.1002/(SICI)1096-9861(19960819)372:2<309::AID-CNE11>3.0.CO;2-E Ito M, 1996, J NEUROPHYSIOL, V76, P3493 Kelly JB, 1996, BEHAV NEUROSCI, V110, P1445, DOI 10.1037//0735-7044.110.6.1445 Kelly J. B., 1997, Society for Neuroscience Abstracts, V23, P1549 Kidd SA, 1996, J NEUROSCI, V16, P7390 LI L, 1992, J NEUROSCI, V12, P4530 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 OLIVER DL, 1989, J NEUROSCI, V9, P967 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 SHNEIDERMAN A, 1993, J NEUROCHEM, V60, P72, DOI 10.1111/j.1471-4159.1993.tb05824.x SHNEIDERMAN A, 1989, J COMP NEUROL, V286, P28, DOI 10.1002/cne.902860103 SHNEIDERMAN A, 1988, J COMP NEUROL, V276, P188, DOI 10.1002/cne.902760204 Kelly JB, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P329, DOI 10.1007/978-1-4419-8712-9_31 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 van Adel BA, 1999, HEARING RES, V130, P115, DOI 10.1016/S0378-5955(98)00226-3 VATER M, 1992, J COMP NEUROL, V325, P183, DOI 10.1002/cne.903250205 WINER JA, 1995, J COMP NEUROL, V355, P317, DOI 10.1002/cne.903550302 WU SH, 1995, J NEUROPHYSIOL, V73, P794 WU SH, 1995, J NEUROPHYSIOL, V73, P780 Wu SH, 1996, J NEUROPHYSIOL, V75, P1271 Zhang DX, 1998, HEARING RES, V117, P1, DOI 10.1016/S0378-5955(97)00202-5 NR 25 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 106 EP 114 DI 10.1016/S0378-5955(99)00156-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800010 PM 10575119 ER PT J AU O'Beirne, GA Patuzzi, RB AF O'Beirne, GA Patuzzi, RB TI Basic properties of the sound-evoked post-auricular muscle response (PAMR) SO HEARING RESEARCH LA English DT Article DE auditory-evoked potential; objective neonatal screening test; objective audiogram; pinna movement ID POTENTIALS; COMPONENTS AB One objective electrophysiological test for deafness involves presenting a brief acoustic stimulus to a subject and measuring the electrical activity evoked in the muscle located just behind the ear (the post-auricular muscle or PAM). Although this electrical response has been known for many years, it has been ignored by most clinicians and frequently misreported in the literature. This paper presents the fundamental properties of the PAM electrical response (the PAMR) and examines wars in which its measurement can be improved by altering the standard electrode position and filtering. The response consists of a simple bipolar compound action potential with a first peak latency of between 12.5 and 15 ms, depending on the stimulus intensity and PAM muscle tone. The largest recordings can be made with an active electrode over the PAM and with the reference electrode on the dorsal surface of the pinna. It can be obtained with click and tone-burst stimuli within 20 dB of the subjective detection threshold, can be evoked with tone-bursts between 500 Hz and 16 kHz and grows either linearly with the click level or approximately exponentially with the tone-burst level, reaching a maximum of as large as 250 mu V pp in some subjects. It has a frequency spectrum mostly between 25 and 200 Hz. The response is often visible in raw recordings, with as few as 20 averages required for obtaining a stable waveform. There is very little amplitude and latency difference in stimulating the ear on the same side or opposite side to the recording electrodes and the binaurally evoked response is similar to the simple arithmetic sum of the waveforms obtained with monaural stimulation. The response latency and duration are longer in very young infants, but reach adult values by 12 months of age. In a companion paper, we describe a method of enhancing the PAMR using lateral eye movement (Patuzzi and O'Beirne, 1999a). (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Nedlands, WA 6009, Australia. RP Patuzzi, RB (reprint author), Univ Western Australia, Dept Physiol, Nedlands, WA 6009, Australia. RI O'Beirne, Greg/I-3838-2012 OI O'Beirne, Greg/0000-0002-3545-4630 CR BICKFORD RG, 1964, ANN NY ACAD SCI, V112, P204, DOI 10.1111/j.1749-6632.1964.tb26749.x BOCHENEK W, 1976, ACTA OTO-LARYNGOL, V81, P264, DOI 10.3109/00016487609119961 BUFFIN JT, 1977, J LARYNGOL OTOL, V91, P1047, DOI 10.1017/S0022215100084759 CLIFFORDJONES RE, 1979, J NEUROL NEUROSUR PS, V42, P749, DOI 10.1136/jnnp.42.8.749 CODY DTR, 1969, LARYNGOSCOPE, V79, P400, DOI 10.1288/00005537-196903000-00007 COLEBATCH JG, 1994, J NEUROL NEUROSUR PS, V57, P190, DOI 10.1136/jnnp.57.2.190 DEGRANDIS D, 1980, ELECTROEN CLIN NEURO, V50, P437, DOI 10.1016/0013-4694(80)90009-7 DIDIER A, 1989, HEARING RES, V37, P123, DOI 10.1016/0378-5955(89)90034-8 DOUEK E, 1973, J LARYNGOL OTOL, P711 DOUEK E, 1974, DEV MED CHILD NEUROL, V16, P32 Eggermont J J, 1985, Acta Otolaryngol Suppl, V421, P41 FENEIS H, 1994, POCKET ATLAS HUMAN A Flood L M, 1982, Br J Audiol, V16, P211, DOI 10.3109/03005368209081464 GIBSON WPR, 1975, THESIS U LONDON LOND GOLDSTEIN PJ, 1979, AM J OBSTET GYNECOL, V135, P622 HALL JW, 1992, HDB AUDITORY EVOKED, P101 JOHNSTONE JR, 1981, HEARING RES, V4, P347, DOI 10.1016/0378-5955(81)90018-6 KATZ B, 1965, PROC R SOC SER B-BIO, V161, P453, DOI 10.1098/rspb.1965.0015 NORTON MP, 1989, FUNDAMENTALS NOISE V, P361 OudesluysMurphy AM, 1996, EUR J PEDIATR, V155, P429, DOI 10.1007/BF01955176 OZDAMAR O, 1978, BRAIN RES, V155, P169, DOI 10.1016/0006-8993(78)90320-7 Patuzzi RB, 1999, HEARING RES, V138, P147, DOI 10.1016/S0378-5955(99)00161-6 Patuzzi RB, 1999, HEARING RES, V138, P133, DOI 10.1016/S0378-5955(99)00160-4 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 ROBINSON K, 1977, BRAIN, V100, P19, DOI 10.1093/brain/100.1.19 Spehlmann R, 1985, EVOKED POTENTIAL PRI STRELETZ LJ, 1977, ELECTROEN CLIN NEURO, V43, P192, DOI 10.1016/0013-4694(77)90127-4 THORNTON ARD, 1975, CLIN NEUROPHYSIOL, V39, P195 THORNTON ARD, 1975, J LARYNGOL OTOL, V89, P997, DOI 10.1017/S0022215100081317 TOTSUKA G, 1954, ANN OTO RHINOL LARYN, V63, P939 YOSHIE N, 1969, Acta Oto-Laryngologica Supplement, V252, P89 NR 31 TC 37 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 115 EP 132 DI 10.1016/S0378-5955(99)00159-8 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800011 PM 10575120 ER PT J AU Patuzzi, RB O'Beirne, GA AF Patuzzi, RB O'Beirne, GA TI Effects of eye rotation on the sound-evoked post-auricular muscle response (PAMR) SO HEARING RESEARCH LA English DT Article DE post-auricular muscle; eye rotation; infant hearing screening ID SUPERIOR COLLICULUS; PINNA MOVEMENTS; CAT; CONNECTIONS; POTENTIALS; COMPONENTS; POSITION AB One objective electrophysiological test for deafness involves presenting a brief acoustic stimulus to a subject and measuring the electrical activity evoked in the muscle located just behind the ear (the post-auricular muscle or PAM). We describe a method for enhancing this post-auricular muscle response (PAMR) using lateral eye movement, which increases both the tonic EMG activity in the PAM and the magnitude of the PAMR, and decreases response latency. EMG activity in most subjects tested (more than 30) increased almost instantly on rotation of the eyes, and thereafter grew more slowly with maintained lateral gaze, with the largest increase occurring with eye rotation towards rather than away from the measurement electrodes over the PAM. The EMG activity returned rapidly to near pre-rotation levels when the eyes were returned to the forwards position, with full recovery taking some minutes. While there was a similar increase and return of the PAMR amplitude with eye rotation, the time-course of these changes was somewhat different, largely because the EMG activity and the PAMR amplitude were not proportional. Rather the PAMR amplitude was a saturating function of EMG level, so that the PAMR response did not fall as markedly as the EMG when the eyes were returned to a forwards gaze, and the recovery of the PAMR amplitude to pre-rotation levels appeared to take longer. We discuss the neural mechanisms that may be responsible for this PAMR potentiation with eye movement and discuss its probable role in increasing variability in early studies which did not control for eye movement. We also discuss the utility of eye rotation in potentiating and stabilising the PAMR to allow its use in screening for deafness. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Nedlands, WA 6009, Australia. RP Patuzzi, RB (reprint author), Univ Western Australia, Dept Physiol, Nedlands, WA 6009, Australia. RI O'Beirne, Greg/I-3838-2012 OI O'Beirne, Greg/0000-0002-3545-4630 CR CLIFFORDJONES RE, 1979, J NEUROL NEUROSUR PS, V42, P749, DOI 10.1136/jnnp.42.8.749 CODY DTR, 1964, ANN OTO RHINOL LARYN, V73, P763 DUS V, 1975, ELECTROEN CLIN NEURO, V39, P523, DOI 10.1016/0013-4694(75)90055-3 EDWARDS SB, 1978, J COMP NEUROL, V179, P451, DOI 10.1002/cne.901790212 FELDON SE, 1987, ADLERS PHYSL EYE, P122 Feliciano M. E., 1995, AUDIT NEUROSCI, V1, P287 GIBSON WPR, 1975, THESIS U LONDON LOND HENKEL CK, 1978, J COMP NEUROL, V182, P763, DOI 10.1002/cne.901820502 Jacobson J. L., 1964, PHYSIOLOGIST, V7, P167 JOSEPH JP, 1985, EXP BRAIN RES, V57, P286 Kiang N. Y. -S., 1963, QUARTERLY PROGRESS R, V44, P218 MIDDLEBROOKS JC, 1987, J NEUROPHYSIOL, V57, P672 O'Beirne GA, 1999, HEARING RES, V138, P115, DOI 10.1016/S0378-5955(99)00159-8 Patuzzi RB, 1999, HEARING RES, V138, P147, DOI 10.1016/S0378-5955(99)00161-6 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 Populin LC, 1998, J NEUROSCI, V18, P4233 SCHMIDT D, 1978, A GRAEF ARCH KLIN EX, V206, P227, DOI 10.1007/BF02387334 STEIN BE, 1981, BRAIN BEHAV EVOLUT, V19, P180, DOI 10.1159/000121641 STRELETZ LJ, 1977, ELECTROEN CLIN NEURO, V43, P192, DOI 10.1016/0013-4694(77)90127-4 THORNTON ARD, 1975, J LARYNGOL OTOL, V89, P997, DOI 10.1017/S0022215100081317 URBAN PP, 1993, BRAIN, V116, P727, DOI 10.1093/brain/116.3.727 Wagner A, 1984, Psychiatr Neurol Med Psychol (Leipz), V36, P527 WEYAND TG, 1993, J NEUROPHYSIOL, V69, P2258 Wilson S. A. K., 1908, REV NEUROL PSYCHIAT, V6, P331 YOSHIE N, 1969, Acta Oto-Laryngologica Supplement, V252, P89 NR 25 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 133 EP 146 DI 10.1016/S0378-5955(99)00160-4 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800012 PM 10575121 ER PT J AU Patuzzi, RB O'Beirne, GA AF Patuzzi, RB O'Beirne, GA TI A correlation method for detecting the sound-evoked post-auricular muscle response (PAMR) SO HEARING RESEARCH LA English DT Article DE auditory evoked response; objective hearing test; infant hearing screening ID SINGLE AB We have made detailed measurements of the sound-evoked post-auricular muscle response (PAMR) in four adults and two infants, in an attempt to understand the inter-relationships between sound level, potentiation of the PAMR with voluntary PAM contraction or eye rotation, electromyographic (EMG) noise, amplitude of the PAMR, and a correlation measure of the presence of the PAMR. We have found that the amplitude of the PAMR is a simple linear function of the decibel level of a monophasic click (0.1 ms duration), and that the PAMR amplitude is also a saturating power function of the level of tonic EMG. As a result, PAMR = PAM(o).SL.(EMG-EMG(noise))(2)/[(EMG-EMG(noise))(2)+beta(2) where SL is the decibel level of a click above subjective threshold, PAM, is a parameter accounting for the differing PAMR amplitude across individuals or with altered electrode placement, EMG(noise) is the component of EMG not associated with PAMR potentiation, and beta determines the initial rate of growth of PAMR at low levels of PAM activation. We have also found that the correlation measure (C) of the PAMR follows a saturating power function of the signal-to-noise ratio (SNR = PAMR/EMG), with C = SNR2/(SNR2+delta(2)), where delta determines the onset of saturation in the correlation as a function of SNR. The combination of these two relationships means that correlation is a non-monotonic function of the EMG (PAM activation): it can be large for moderate levels of EMG, but small for high levels of EMG, because the PAMR amplitude saturates but the EMG does not. The correlation is a fast, convenient means of detecting the PAMR, whether using clicks or tone-bursts, and can be used effectively in adults or infants, as long as the reflex is moderately activated. This moderate activation is most effectively produced by eye rotation towards the recording electrodes. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Nedlands, WA 6009, Australia. RP Patuzzi, RB (reprint author), Univ Western Australia, Dept Physiol, Nedlands, WA 6009, Australia. RI O'Beirne, Greg/I-3838-2012 OI O'Beirne, Greg/0000-0002-3545-4630 CR BUFFIN JT, 1977, J LARYNGOL OTOL, V91, P1047, DOI 10.1017/S0022215100084759 CLIFFORDJONES RE, 1979, J NEUROL NEUROSUR PS, V42, P749, DOI 10.1136/jnnp.42.8.749 DEGRANDIS D, 1980, ELECTROEN CLIN NEURO, V50, P437, DOI 10.1016/0013-4694(80)90009-7 GIBSON WPR, 1975, THESIS U LONDON LOND MENDELL LM, 1976, J PHYSIOL-LONDON, V255, P81 O'Beirne GA, 1999, HEARING RES, V138, P115, DOI 10.1016/S0378-5955(99)00159-8 Patuzzi RB, 1999, HEARING RES, V138, P133, DOI 10.1016/S0378-5955(99)00160-4 THORNTON ARD, 1975, J LARYNGOL OTOL, V89, P997, DOI 10.1017/S0022215100081317 YOSHIE N, 1969, Acta Oto-Laryngologica Supplement, V252, P89 NR 9 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 147 EP 162 DI 10.1016/S0378-5955(99)00161-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800013 PM 10575122 ER PT J AU Barrenas, ML Nylen, O Hanson, C AF Barrenas, ML Nylen, O Hanson, C TI The influence of karyotype on the auricle, otitis media and hearing in Turner syndrome SO HEARING RESEARCH LA English DT Article DE Turner syndrome; otitis media; hearing loss; karyotype; growth; SHOX ID WOMEN AB The study has investigated the relationship between the chromosomal aberration and ear and/or hearing disorders in 115 girls/women with Turner syndrome (TS). A dose-response relationship was found between the karyotype and hearing function. Hearing deteriorated more rapidly with increasing age in TS women lacking the whole p-arm of chromosome X (i.e. monosomy 45,X, or isochromosome cases 46,X,i(Xq)) as compared to women having a partial deletion of the p-arm (structural deletions or mosaicism cases), who, in turn, had poorer hearing than a female random population sample (46,XX) (P < 0.001). Moreover, TS subjects having total deletion of the p-arm were three times more likely to have auricular anomalies or conductive hearing loss due to otitis media than subjects with partial deletion (P < 0.05). The results support the hypothesis that lack of growth-regulating genes such as the short stature homeobox-containing gene (SHOX), which is located within the pseudo-autosomal region on the p-arm of the X chromosome, may increase the occurrence of auricular malformations and otitis media and also induce an earlier loss of hearing function. Accordingly, the ear and hearing disorders in TS may be a result of growth disturbances of the auricle, the mastoid, the Eustachian tube and the organ of Corti during development. It is suggested that karyotype may be used as a predictor for future ear and hearing problems in TS. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Gothenburg, Sahlgrens Univ Hosp, Dept Audiol, S-41345 Gothenburg, Sweden. Univ Gothenburg, Sahlgrens Univ Hosp, Dept Otorhinolaryngol, S-41345 Gothenburg, Sweden. Univ Gothenburg, Sahlgrens Univ Hosp, Dept Obstet & Gynaecol, S-41345 Gothenburg, Sweden. RP Barrenas, ML (reprint author), Univ Gothenburg, Sahlgrens Univ Hosp, Dept Audiol, S-41345 Gothenburg, Sweden. CR Aitkin M., 1990, STAT MODELLING GLIM Anderson H., 1969, ACTA OTO-LARYNGOL, V247, P1 Benazzo M, 1997, J AUDIOL MED, V6, P147 ELMQVISTSTENBER.A, 1998, HEARING RES, V124, P85 FILIPSSO.R, 1965, ACTA ENDOCRINOL-COP, V48, P91 FORD CE, 1959, LANCET, V1, P711 Gravholt CH, 1996, BRIT MED J, V312, P16 HULTCRANTZ M, 1994, HEARING RES, V76, P127, DOI 10.1016/0378-5955(94)90094-9 Hultcrantz M, 1997, HEARING RES, V103, P69, DOI 10.1016/S0378-5955(96)00165-7 LEHEUP B P, 1988, Journal de Genetique Humaine, V36, P315 LINDSTEN J, 1963, THESIS STOCKHOLM SWE LINDSTEN J, 1961, LANCET, V1, P1228 LINDSTEN J, 1965, Endokrynol Pol, V16, P141 LONBERG NC, 1977, HUM GENET, V38, P363, DOI 10.1007/BF00402166 Melnick M, 1979, Birth Defects Orig Artic Ser, V15, P155 Rao E, 1997, NAT GENET, V16, P54, DOI 10.1038/ng0597-54 RONGENWESTERLAK.C, 1992, J BIOL BUCCALE, V20, P180 RONGENWESTERLAKEN C, 1991, J PEDIATR-US, V119, P268, DOI 10.1016/S0022-3476(05)80737-1 RUDIN R, 1987, ACTA OTO-LARYNGOL, V103, P217, DOI 10.3109/00016488709107787 SCULERATI N, 1990, ARCH OTOLARYNGOL, V116, P704 Sculerati N, 1996, LARYNGOSCOPE, V106, P992, DOI 10.1097/00005537-199608000-00015 STENSTROM C, 1991, INT J PEDIATR OTORHI, V21, P127, DOI 10.1016/0165-5876(91)90143-Y SZPUNAR J, 1968, ARCH OTOLARYNGOL, V87, P34 WATKIN PM, 1989, J LARYNGOL OTOL, V103, P731, DOI 10.1017/S0022215100109934 WINDLETAYLOR PC, 1982, CLIN OTOLARYNGOL, V7, P75, DOI 10.1111/j.1365-2273.1982.tb01566.x WRIGHT A, 1988, ACTA OTOLARYNGOL S S, V444, P1 NR 26 TC 26 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 163 EP 170 DI 10.1016/S0378-5955(99)00162-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800014 PM 10575123 ER PT J AU Jiang, ZG Qiu, JH Ren, TY Nuttall, AL AF Jiang, ZG Qiu, JH Ren, TY Nuttall, AL TI Membrane properties and the excitatory junction potentials in smooth muscle cells of cochlear spiral modiolar artery in guinea pigs SO HEARING RESEARCH LA English DT Article DE spiral modiolar artery; smooth muscle cells; membrane potential; excitatory junction potential; alpha-receptor; cochlea ID MIDDLE CEREBRAL-ARTERY; MAIN PULMONARY-ARTERY; AGE-RELATED-CHANGES; BLOOD-FLOW; NEUROMUSCULAR-TRANSMISSION; NEUROEFFECTOR TRANSMISSION; SUBMUCOSAL ARTERIOLES; NORADRENALINE; STIMULATION; RECEPTORS AB Blood circulation changes in the inner ear play an important role in many physiological and pathological conditions of hearing function. The spiral modiolar artery (SMA) is the terminal artery to the cochlea. It was surrounded with nerve fibers immunostained by an antibody for tyrosine hydroxylase. By using intracellular recording techniques on the acutely isolated SMA, membrane properties of the smooth muscle cells and the neuromuscular transmission in this preparation were investigated. With minimum tension and normal extracellular K+ concentration (5 mM), the majority of muscle cells showed a resting potential near - 80 mV and an input resistance of about 8 M Omega. V/I plot showed an inward rectification in these cells. Barium (50-500 mu M) caused strong depolarization and an increase in input resistance. Transmural electrical stimulation evoked stimulation intensity-dependent depolarizations (2-31 mV) following a short latency (similar to 20 ms). The evoked potential by a low intensity stimulus was completely blocked by I CIM tetrodotoxin. The potential and a depolarization induced by norepinephrine (10 mu M) was usually partially (40-90%) blocked by a-receptor antagonists prazosin and/or idazoxan with concentrations up to 1 mu M. Action potentials were observed when the depolarization was more than -40 mV. It is concluded that SMA smooth muscle cells, similar to those in other brain small arteries, highly express inward rectifying potassium channels; the cells receive catecholaminergic innervation, and stimulation of the nerves elicited an excitatory junction potential that is partially mediated by adrenergic receptors. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Oregon Hearing Res Ctr, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97201 USA. Fourth Mil Med Univ, Xijing Hosp, Xian 710032, Peoples R China. Univ Michigan, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. RP Jiang, ZG (reprint author), Oregon Hlth Sci Univ, Oregon Hearing Res Ctr, NRC-04, Portland, OR 97201 USA. CR BROWN JN, 1995, HEARING RES, V86, P189 CARRASCO VN, 1990, ARCH OTOLARYNGOL, V116, P411 CASTEELS R, 1977, J PHYSIOL-LONDON, V271, P63 CHEUNG DW, 1982, J PHYSIOL-LONDON, V328, P461 EDWARDS FR, 1988, J PHYSIOL-LONDON, V404, P437 EDWARDS FR, 1988, J PHYSIOL-LONDON, V404, P455 FUJIWARA S, 1982, BRIT J PHARMACOL, V77, P197 Gruber DD, 1998, HEARING RES, V119, P113, DOI 10.1016/S0378-5955(98)00036-7 Hashitani H, 1997, J PHYSIOL-LONDON, V501, P319, DOI 10.1111/j.1469-7793.1997.319bn.x Hashitani H, 1998, J PHYSIOL-LONDON, V510, P209, DOI 10.1111/j.1469-7793.1998.209bz.x HILL CE, 1986, J PHYSIOL-LONDON, V371, P305 HIRST GDS, 1978, J PHYSIOL-LONDON, V280, P87 HIRST GDS, 1980, NATURE, V283, P767, DOI 10.1038/283767a0 HIRST GDS, 1977, J PHYSIOL-LONDON, V273, P263 HIRST GDS, 1986, J PHYSIOL-LONDON, V371, P289 HIRST GDS, 1982, J PHYSIOL-LONDON, V328, P351 HIRST GDS, 1982, J PHYSIOL-LONDON, V333, P53 HIRST GDS, 1989, PHYSIOL REV, V69, P546 HOLMAN ME, 1979, J PHYSIOL-LONDON, V287, P337 HULTCRANTZ E, 1988, AM J OTOLARYNG, V9, P317, DOI 10.1016/S0196-0709(88)80039-5 ITOH T, 1981, J PHYSIOL-LONDON, V321, P513 JIANG ZG, 1991, J PHYSIOL-LONDON, V443, P533 JIANG ZG, 1998, ARO MIDW M, V21, P188 JIANG ZG, 1999, ARO MIDW M, V22, P205 JIANG ZG, 1998, FASEB J, V12, pA705 KAJIWARA M, 1981, J PHYSIOL-LONDON, V315, P283 KIMURA RS, 1986, AM J OTOLARYNG, V7, P130, DOI 10.1016/S0196-0709(86)80042-4 KNOT HJ, 1995, AM J PHYSIOL-HEART C, V269, pH348 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 LAMM K, 1997, ARO MIDW M, V20, P17 MCPHERSON GA, 1995, CLIN EXP PHARMACOL P, V22, P724, DOI 10.1111/j.1440-1681.1995.tb01926.x OHLSEN KA, 1991, CIRC RES, V69, P509 Quayle JM, 1997, PHYSIOL REV, V77, P1165 REN TY, 1993, ACTA OTO-LARYNGOL, V113, P146, DOI 10.3109/00016489309135783 REN TY, 1993, ANN OTO RHINOL LARYN, V102, P378 Ren TY, 1995, HEARING RES, V92, P30, DOI 10.1016/0378-5955(95)00192-1 SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SCHUKNECHT HF, 1982, AM J OTOLARYNG, V3, P349, DOI 10.1016/S0196-0709(82)80009-4 Setoguchi M, 1997, J PHYSIOL-LONDON, V501, P343, DOI 10.1111/j.1469-7793.1997.343bn.x SOMLYO AP, 1969, FED PROC, V28, P1634 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 SUZUKI H, 1983, J PHYSIOL-LONDON, V336, P47 SUZUKI H, 1986, JPN J PHYSIOL, V36, P433, DOI 10.2170/jjphysiol.36.433 Suzuki T, 1998, ANN OTO RHINOL LARYN, V107, P648 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 NR 45 TC 10 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 171 EP 180 DI 10.1016/S0378-5955(99)00166-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800015 PM 10575124 ER PT J AU Chen, GD McWilliams, ML Fechter, LD AF Chen, GD McWilliams, ML Fechter, LD TI Intermittent noise-induced hearing loss and the influence of carbon monoxide SO HEARING RESEARCH LA English DT Article DE intermittent noise; noise-induced hearing loss; carbon monoxide; compound action potential; surface preparation; rat ID TEMPORARY THRESHOLD SHIFT; AUDITORY HAIR-CELLS; GUINEA-PIG; ACOUSTIC OVERSTIMULATION; RAT COCHLEA; EXPOSURE; CHINCHILLA; DAMAGE; OXYGEN; TRAUMA AB Intermittent noise causes less hearing loss than continuous noise of equal intensity. The reduction in damage observed with intermittent noise may be explained by the fact that the auditory system has time to recover between the noise phases. Simultaneous carbon monoxide (CO) exposure produces greater noise-induced hearing loss than does noise alone (Chen and Fechter, 1999). In the present study, intermittent noise (octave-band with a center frequency of 13.6 kHz, 100 dB) of a 2 h total duration but with a different duty cycle (% of noise during exposure) was used. The intermittent exposure that had a shorter noise duty cycle induced a less permanent threshold shift (PTS) than those that had a longer noise duty cycle (or less rest periods). This relation between the loss in compound action potential (CAP) sensitivity and the noise duty cycle (or rest period) was abolished by the presence of CO. The cochlear microphonic (CM) amplitude revealed similar results to those seen using the CAP. While intermittent noise that had a short noise duty cycle did not cause hair cell loss by itself, the combined exposure to noise and CO (1200 ppm) caused remarkable OHC loss in the basal turn. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, Oklahoma City, OK 73190 USA. RP Chen, GD (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Pharm, 1110 N Stonewall, Oklahoma City, OK 73190 USA. CR BAKER SR, 1977, ANN OTO RHINOL LARYN, V86, P323 Borg E, 1992, NOISE INDUCED HEARIN, P467 CAMPO P, 1992, NOISE INDUCED HEARIN, P456 Canlon B, 1998, NOISE HLTH, V1, P13 Chen GD, 1999, HEARING RES, V132, P149, DOI 10.1016/S0378-5955(99)00044-1 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 CLARK WW, 1992, NOISE INDUCED HEARIN, P445 DEW LA, 1993, HEARING RES, V66, P99, DOI 10.1016/0378-5955(93)90264-2 Eddins AC, 1999, HEARING RES, V127, P119 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 Fechter LD, 1997, TOXICOL APPL PHARM, V142, P47, DOI 10.1006/taap.1996.8027 FECHTER LD, 1999, IN PRESS NOISE HLTH FECHTER LD, 1988, HEARING RES, V34, P39, DOI 10.1016/0378-5955(88)90049-4 FREDELIUS L, 1992, HEARING RES, V62, P194, DOI 10.1016/0378-5955(92)90186-Q Fridberger A, 1998, P NATL ACAD SCI USA, V95, P7127, DOI 10.1073/pnas.95.12.7127 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HATCH M, 1991, HEARING RES, V56, P265, DOI 10.1016/0378-5955(91)90176-A Hu BH, 1997, HEARING RES, V110, P209, DOI 10.1016/S0378-5955(97)00075-0 Hu BH, 1997, HEARING RES, V113, P198, DOI 10.1016/S0378-5955(97)00143-3 HU ZY, 1991, AVIAT SPACE ENVIR MD, V62, P403 Jacono AA, 1998, HEARING RES, V117, P31, DOI 10.1016/S0378-5955(97)00214-1 Kowalska S, 1981, Med Pr, V32, P145 Kowalska S, 1980, Med Pr, V31, P63 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 LIM HH, 1993, HEARING RES, V69, P146 LIU Z, 1992, CHIN J OTORHINOLARYN, V27, P24 MAKISHIMA K, 1977, T AM ACAD OPHTHALMOL, V84, P452 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 MULROY MJ, 1990, HEARING RES, V49, P79, DOI 10.1016/0378-5955(90)90096-8 Mulroy MJ, 1998, HEARING RES, V115, P93, DOI 10.1016/S0378-5955(97)00181-0 Ohanian EV, 1997, FUND APPL TOXICOL, V39, P81, DOI 10.1006/faat.1997.2358 Patuzzi R, 1998, HEARING RES, V125, P17, DOI 10.1016/S0378-5955(98)00126-9 Puel JL, 1998, NEUROREPORT, V9, P2109, DOI 10.1097/00001756-199806220-00037 QUIRK WS, 1994, HEARING RES, V74, P217, DOI 10.1016/0378-5955(94)90189-9 Slikker W, 1996, FUND APPL TOXICOL, V29, P18 Wang J A, 1990, Hear Res, V44, P143, DOI 10.1016/0378-5955(90)90076-2 Yamane H, 1995, Acta Otolaryngol Suppl, V519, P87 Yamane H, 1995, EUR ARCH OTO-RHINO-L, V252, P504, DOI 10.1007/BF02114761 Yamasoba T, 1999, BRAIN RES, V815, P317, DOI 10.1016/S0006-8993(98)01100-7 YOUNG JS, 1987, HEARING RES, V26, P37, DOI 10.1016/0378-5955(87)90034-7 NR 40 TC 29 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 181 EP 191 DI 10.1016/S0378-5955(99)00157-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800016 PM 10575125 ER PT J AU LeBlanc, C Bobbin, RP AF LeBlanc, C Bobbin, RP TI An interaction between PPADS, an ATP antagonist, and a moderately intense sound in the cochlea SO HEARING RESEARCH LA English DT Article DE pyridoxal-phosphate-6-azophenyl-2 ',4 '-disulfonic acid; cochlear potential; cochlear microphonic; auditory nerve ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; NOISE EXPOSURE ALTERS; ADENOSINE 5'-TRIPHOSPHATE; PHARMACOLOGICAL EVIDENCE; OTOACOUSTIC EMISSIONS; SUPPORTING CELLS; ORGAN; RESPONSES; CORTI AB In the organ of Corti ionotropic receptors for ATP (ATPRs) on cells that are bathed by perilymph have been suggested to modulate cochlear mechanics. The purpose of the present study was to test the hypothesis that endogenous extracellular ATP acting through ATPRs is involved in modulating cochlear mechanics during moderately intense sound exposure. Guinea pigs were exposed to either: (1) a perilymphatic administration of pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 1 mM), an ATP antagonist; (2) a moderately intense sound (6.7 kHz tone, 95 dB SPL, 15 min); or (3) a combination of both the PPADS and the sound. The effects on cochlear potentials (cochlear microphonic, CM; negative summating potential, SP; compound action potential of the auditory nerve, CAP; and N-1 latency) evoked by a 10 kHz tone pip were monitored. PPADS alone reduced the CAP and the SP and increased N-1 latency. The intense sound alone reduced the CAP and SP. The combination of PPADS with the intense tone induced reversible effects on cochlear potentials that were greater than induced by either treatment alone. The effect on N-1 latency and low intensity CM was a potentiation since the effect was greater than a simple addition of the effect of either treatment alone. The effects of the combination treatment on CAP, SP and high intensity CM were not different from additive. Results are consistent with the hypothesis that ATPRs in the organ of Corti are involved in modulating cochlear mechanics during moderately intense sound exposure. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Louisiana State Univ, Med Ctr, Dept Otorhinolaryngol & Biocommun, Kresge Hearing Res Lab S, New Orleans, LA 70112 USA. RP Bobbin, RP (reprint author), Louisiana State Univ, Med Ctr, Dept Otorhinolaryngol & Biocommun, Kresge Hearing Res Lab S, 2020 Gravier St,Suite A, New Orleans, LA 70112 USA. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BLEDSOE SC, 1980, EXP BRAIN RES, V40, P97 Bobbin RP, 1997, HEARING RES, V113, P155, DOI 10.1016/S0378-5955(97)00140-8 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1981, PHARM HEARING, P19 BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BOBBIN RP, 1998, RECENT ADV BASIC CLI, P61 BOBBIN RP, 1996, HAIR CELLS HEARING A, P29 BOBBIN RP, 1992, NOIS INDUCED HEARING Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 BURNSTOCK G, 1990, ANN NY ACAD SCI, V603, P1 CHEN C, 1995, HEARING RES, V86, P25, DOI 10.1016/0378-5955(95)00050-E Chen C, 1998, BRIT J PHARMACOL, V124, P337, DOI 10.1038/sj.bjp.0701848 CHEN C, 1995, HEARING RES, V88, P215, DOI 10.1016/0378-5955(95)00115-K Chen C, 1997, HEARING RES, V110, P87, DOI 10.1016/S0378-5955(97)00069-5 Chen C, 1998, HEARING RES, V118, P47, DOI 10.1016/S0378-5955(98)00019-7 Dulon D., 1995, ACTIVE HEARING, P195 DULON D, 1994, BIOCHEM BIOPH RES CO, V201, P1263, DOI 10.1006/bbrc.1994.1841 DULON D, 1993, CELL CALCIUM, V14, P245, DOI 10.1016/0143-4160(93)90071-D GERO A, 1971, DRILLS PHARM MED, P67 HAMERNIK RP, 1982, NEW PERSPECTIVE NOIS HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HOUSLEY GD, 1997, MOL NEUROBIOL, V16, P21 Kemp DT, 1998, OTOACOUSTIC EMISSION, P1 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 LIU J, 1995, AUDIT NEUROSCI, V1, P331 Mammano F, 1999, J NEUROSCI, V19, P6918 MILLS DM, 1998, OTOACOUSTIC EMISSION, P85 MOCKETT BG, 1995, HEARING RES, V84, P177, DOI 10.1016/0378-5955(95)00024-X MUNOZ DJB, 1995, HEARING RES, V90, P106, DOI 10.1016/0378-5955(95)00152-3 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 Parker MS, 1998, HEARING RES, V121, P62, DOI 10.1016/S0378-5955(98)00065-3 Puel JL, 1998, NEUROREPORT, V9, P2109, DOI 10.1097/00001756-199806220-00037 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1995, ACTA ACUST, V3, P75 Puel JL, 1995, PROG NEUROBIOL, V47, P449, DOI 10.1016/0301-0082(95)00028-3 Skellett RA, 1998, HEARING RES, V116, P21, DOI 10.1016/S0378-5955(97)00199-8 Skellett RA, 1997, HEARING RES, V111, P42, DOI 10.1016/S0378-5955(97)00093-2 Skellett RA, 1996, HEARING RES, V98, P68, DOI 10.1016/0378-5955(96)00062-7 Spicer SS, 1999, HEARING RES, V130, P7, DOI 10.1016/S0378-5955(98)00202-0 SUZUKI M, 1995, HEARING RES, V86, P68, DOI 10.1016/0378-5955(95)00055-9 ZIGANSHIN AU, 1995, PFLUG ARCH EUR J PHY, V429, P412, DOI 10.1007/BF00374157 NR 45 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1999 VL 138 IS 1-2 BP 192 EP 200 DI 10.1016/S0378-5955(99)00164-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 260AU UT WOS:000083926800017 PM 10575126 ER PT J AU Wang, SC Bian, Q Liu, ZY Feng, Y Lian, NJ Chen, H Hu, CQ Dong, YY Cai, ZH AF Wang, SC Bian, Q Liu, ZY Feng, Y Lian, NJ Chen, H Hu, CQ Dong, YY Cai, ZH TI Capability of serum to convert streptomycin to cytotoxin in patients with aminoglycoside-induced hearing loss SO HEARING RESEARCH LA English DT Article DE hearing loss; outer hair cell; serum; protein; streptomycin; metabolite ID OUTER HAIR-CELLS; GENTAMICIN; METABOLITE; ANTIBIOTICS; OTOTOXICITY AB Individual variations in sensitivity to the ototoxic effects of aminoglycoside antibiotics are well documented. Our research demonstrates that there is an apparent difference in serum from patients who are resistant or susceptible to aminoglycoside ototoxicity. In the first study, the cytotoxicity of sera from patients with and without hearing loss after various time periods following the discontinuation of aminoglycoside treatment was assayed using the isolated outer hair cell toxicity assay. The results indicate that sera from patients with hearing loss were significantly more toxic than sera from patients with normal hearing or minimal hearing loss. This toxicity may persist for up to 1 year after discontinuation of aminoglycoside therapy. In a second study, sera were obtained from patients who had received aminoglycoside therapy several years previously. None of these sera was toxic to isolated outer hair cells in vitro. Streptomycin was then incubated with the sera or a protein fraction isolated from sera, and the incubation mixtures were tested for toxicity. The percentage of damaged outer hair cells was significantly higher when streptomycin had been treated with sera or a serum protein fraction from patients with hearing loss (58 +/- 10% and 68 +/- 9%, respectively) than with sera or a serum protein fraction from a control group (10 +/- 5% and 17 +/- 4%, respectively). In addition, several incubation mixtures were analyzed using high performance liquid chromatography. A new chromatographic peak was only found in the incubations of streptomycin with serum protein from patients with hearing loss. The results suggest that sera from individuals sensitive to aminoglycoside antibiotics may metabolize these drugs to cytotoxins. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Beijing Inst Otorhinolaryngol, Beijing, Peoples R China. Peking Union Med Coll Hosp, Beijing, Peoples R China. Natl Inst Control Pharmaceut & Biol Prod, Beijing, Peoples R China. RP Wang, SC (reprint author), Beijing Inst Otorhinolaryngol, 17 Hougou Lane Chong-Nei, Beijing, Peoples R China. CR BRUMMETT RE, 1990, ARCH OTOLARYNGOL, V116, P406 CRANN SA, 1992, BIOCHEM PHARMACOL, V43, P1835, DOI 10.1016/0006-2952(92)90718-X Crann S A, 1996, Audiol Neurootol, V1, P80 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FISCHELGHODSIAN N, 1993, AM J OTOLARYNG, V14, P399, DOI 10.1016/0196-0709(93)90113-L GARETZ SL, 1994, HEARING RES, V77, P75, DOI 10.1016/0378-5955(94)90254-2 HAUROWITZ F, 1963, CHEM FUNCTION PROTEI, P185 HUANG MY, 1990, BIOCHEM PHARMACOL, V40, pR11, DOI 10.1016/0006-2952(90)90077-X HUTCHIN T, 1993, NUCLEIC ACIDS RES, V21, P4174, DOI 10.1093/nar/21.18.4174 LANE AZ, 1977, AM J MED, V62, P911, DOI 10.1016/0002-9343(77)90660-X PRAZIC M, 1964, J Laryngol Otol, V78, P1037 PREZANT TR, 1992, AM J MED GENET, V44, P465, DOI 10.1002/ajmg.1320440416 PRIEST JH, 1977, MED CYTOGENETICS CEL, P316 SCHENTAG JJ, 1977, CLIN PHARMACOL THER, V22, P364 WHALL TJ, 1981, J CHROMATOGR, V219, P89, DOI 10.1016/S0021-9673(00)80577-4 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZHOU Y, 1990, CHIN J ANTIBIOT, V15, P175 NR 17 TC 6 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 1 EP 7 DI 10.1016/S0378-5955(99)00116-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600002 PM 10545628 ER PT J AU Zucca, G Botta, L Valli, S Giannoni, B Mira, E Perin, P Buizza, A Valli, P AF Zucca, G Botta, L Valli, S Giannoni, B Mira, E Perin, P Buizza, A Valli, P TI Effects of caloric stimuli on frog ampullar receptors SO HEARING RESEARCH LA English DT Article DE vestibular system; ampullar receptor; caloric stimulus; convective theory; temperature changes ID VESTIBULAR ORGANS; MECHANICAL MODEL; HAIR-CELLS; PRESSURE AB The observation that caloric nystagmus can be evoked even in microgravity conditions argues against Barany's convective theory. To justify this result, gravity-independent mechanisms (mainly endolymphatic volume changes and direct action of the temperature on vestibular sensors) are believed to contribute to caloric-induced activation of vestibular receptors. To define the importance of both gravity-dependent and gravity-independent mechanisms, the posterior semicircular canal of the frog was thermally stimulated by a microthermistor positioned close to the sensory organ. The stimulus produced a gravity-dependent transcupular pressure difference that, depending on the position of the heater, could result in either excitation or inhibition of ampullar receptor sensory discharge. When the heater was positioned on the ampulla, or when the canal rested on the horizontal plane, no responses could be evoked by thermal stimuli. These results suggest that, in our experimental conditions (Delta T up to 1.5 degrees C), neither a thermally induced expansion of the endolymph nor a direct action of the temperature on vestibular sensors play any major role. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Pavia, Dept Physiol & Pharmacol Sci, I-27100 Pavia, Italy. Univ Pavia, Dept Comp & Syst Sci, I-27100 Pavia, Italy. Univ Pavia, IRCCS, Policlin San Matteo, Dept Otolaryngol, I-27100 Pavia, Italy. Univ Florence, Serv Audiol, Florence, Italy. RP Valli, P (reprint author), Univ Pavia, Dept Physiol & Pharmacol Sci, Via Forlanini 6, I-27100 Pavia, Italy. CR BALOH RW, 1998, DIZZINESS HEARING LO, P31 Barany R., 1906, MSCHR OHRENHEILK, V40, P193 CAWTHORNE T, 1954, ACTA OTO-LARYNGOL, V44, P580, DOI 10.3109/00016485409127670 GENTINE A, 1991, ACTA OTO-LARYNGOL, V111, P633, DOI 10.3109/00016489109138393 GENTINE A, 1991, ACTA OTO-LARYNGOL, V111, P463, DOI 10.3109/00016489109138370 GENTINE A, 1990, ACTA OTO-LARYNGOL, V110, P328, DOI 10.3109/00016489009107451 GENTINE A, 1991, ACTA OTO-LARYNGOL, V111, P10, DOI 10.3109/00016489109137349 Guth PS, 1998, PROG NEUROBIOL, V54, P193, DOI 10.1016/S0301-0082(97)00068-3 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HARADA Y, 1987, VESTIBULAR SYSTEM NE, P107 HOOD JD, 1989, ACTA OTO-LARYNGOL, V107, P161, DOI 10.3109/00016488909127494 JACOBSON GP, 1993, HDB BALANCE FUNCTION, P192 Masetto S, 1995, NEUROREPORT, V7, P230, DOI 10.1097/00001756-199512000-00055 PARNES LS, 1990, ANN OTO RHINOL LARYN, V99, P330 Ross M D, 1993, J Vestib Res, V3, P241 Ross M D, 1994, Acta Otolaryngol Suppl, V516, P1 ROSSI ML, 1995, PRIM SENSORY NEURON, V1, P95 SHERER H, 1985, ACTA OTOLARYNGOL, V100, P328 STAHLE J, 1990, ACTA OTO-LARYNGOL, V109, P162, DOI 10.3109/00016489009107430 Suzuki M, 1998, J VESTIBUL RES-EQUIL, V8, P169 ZENNER HP, 1995, ACTA OTO-LARYNGOL, V115, P484, DOI 10.3109/00016489509139352 ZUCCA G, 1992, HEARING RES, V63, P52, DOI 10.1016/0378-5955(92)90073-V ZUCCA G, 1991, ACTA OTO-LARYNGOL, V111, P820, DOI 10.3109/00016489109138417 Zucca G, 1983, Boll Soc Ital Biol Sper, V59, P1016 Zucca G, 1983, Boll Soc Ital Biol Sper, V59, P1010 ZUCCA G, 1995, ACTA OTO-LARYNGOL, V115, P34, DOI 10.3109/00016489509133343 Zucca G, 1999, J NEUROSCI METH, V88, P141, DOI 10.1016/S0165-0270(99)00021-7 NR 27 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 8 EP 14 DI 10.1016/S0378-5955(99)00125-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600003 PM 10545629 ER PT J AU Li, Y Evans, MS Faingold, CL AF Li, Y Evans, MS Faingold, CL TI Synaptic response patterns of neurons in the cortex of rat inferior colliculus SO HEARING RESEARCH LA English DT Article DE inferior colliculus; neuron; slice; synaptic response ID STEM AUDITORY NUCLEI; EPILEPSY-PRONE RAT; AUDIOGENIC-SEIZURE SUSCEPTIBILITY; GLUTAMIC-ACID DECARBOXYLASE; EAR OSSICLE REMOVAL; GABAERGIC NEURONS; AMINO-ACIDS; GUINEA-PIG; MEDIATED INHIBITION; ACOUSTIC RESPONSES AB The present study examined synaptic potentials of neurons in inferior colliculus (IC) cortex slice and the roles of GABA and glutamate receptors in generating these potentials. Multipolar (82%) and elongated (18%) cells were observed with intracellular biocytin staining. Electrical stimulation of the IC commissure (CoIC) elicited only inhibitory postsynaptic potentials (IPSPs) (10% of cells), only excitatory postsynaptic potentials (EPSPs) (51%), or both (38%). IPSPs were elicited at lower thresholds and shorter latencies than EPSPs (mean: 1.6 +/- 1.2 ms) and IPSPs were observed in all neurons following membrane depolarization. Short-latency EPSPs were blocked by non-NMDA. receptor antagonists, and longer-latency EPSPs were blocked by NMDA antagonists. CoIC stimulation evoked short-latency IPSPs (mean: 0.55 +/- 0.33 ms) in 48% of neurons, and the IPSPs persisted despite glutamate receptor blockade, which implies monosynaptic inhibitory input. A GABA(A) antagonist blocked IPSPs and paired pulse inhibition of EPSPs, suggesting GABA(A) receptor mediation. A GABA(B) antagonist reduced paired pulse inhibition of IPSPs, suggesting GABA(B) receptor modulation. Thus, GABA-mediated inhibition plays a critical role in shaping synaptic responses of IC cortex neurons. Normal GABAergic function in IC has been shown to be important in acoustic coding, and reduced efficacy of GABA function in IC neurons is critical in IC pathophysiology in presbycusis, tinnitus and audiogenic seizures. (C) 1999 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. So Illinois Univ, Sch Med, Dept Neurol, Springfield, IL 62794 USA. RP Faingold, CL (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, POB 19629, Springfield, IL 62794 USA. CR ALBECK Y, 1995, J NEUROPHYSIOL, V74, P1689 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 BERRY MS, 1976, BRAIN RES, V105, P1, DOI 10.1016/0006-8993(76)90919-7 Bledsoe SC, 1995, NEUROREPORT, V7, P225, DOI 10.1097/00001756-199512000-00054 Browning R.A., 1994, IDIOPATHIC GEN EPILE, P399 Caicedo A, 1998, EUR J NEUROSCI, V10, P941, DOI 10.1046/j.1460-9568.1998.00104.x Caird D, 1991, NEUROBIOLOGY HEARING, P253 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 Chakravarty DN, 1997, BRAIN RES, V761, P263, DOI 10.1016/S0006-8993(97)00331-4 Chakravarty DN, 1996, EXP NEUROL, V141, P280, DOI 10.1006/exnr.1996.0162 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 Covey E, 1996, J NEUROSCI, V16, P3009 DRUGA R, 1984, PHYSIOL BOHEMOSLOV, V33, P31 FAINGOLD CL, 1986, EXP NEUROL, V93, P145, DOI 10.1016/0014-4886(86)90154-8 FAINGOLD CL, 1999, JASPERS BASIC MECHAN, P311 Faingold Carl L., 1998, Epilepsia, V39, P37 FAINGOLD CL, 1991, HEARING RES, V52, P201, DOI 10.1016/0378-5955(91)90200-S Faingold CL, 1999, BRAIN RES, V815, P250, DOI 10.1016/S0006-8993(98)01136-6 FAINGOLD CL, 1989, HEARING RES, V40, P127, DOI 10.1016/0378-5955(89)90106-8 FAINGOLD CL, 1991, EXP NEUROL, V113, P354, DOI 10.1016/0014-4886(91)90026-9 FAINGOLD CL, 1989, BRAIN RES, V500, P302, DOI 10.1016/0006-8993(89)90326-0 Faingold C.L., 1991, NEUROBIOLOGY HEARING, P223 FAINGOLD CL, 1986, ELECTROEN CLIN NEURO, V63, P296, DOI 10.1016/0013-4694(86)90097-0 FARLEY GR, 1983, HEARING RES, V11, P73, DOI 10.1016/0378-5955(83)90046-1 FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 FAYELUND H, 1985, ANAT EMBRYOL, V173, P53, DOI 10.1007/BF00707304 FELDMAN DE, 1994, J NEUROSCI, V14, P5939 FELICIANO M, 1995, J NEUROCHEM, V65, P1348 Fuzessery ZM, 1996, J NEUROPHYSIOL, V76, P1059 Gaza WC, 1997, BRAIN RES, V774, P175, DOI 10.1016/S0006-8993(97)81701-5 Gerken GM, 1996, HEARING RES, V97, P75 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GOLDSMITH JD, 1995, HEARING RES, V83, P80, DOI 10.1016/0378-5955(94)00193-T HERBERT H, 1991, J COMP NEUROL, V304, P103, DOI 10.1002/cne.903040108 Hosomi H, 1997, J NEUROPHYSIOL, V77, P994 HOSOMI H, 1995, NEUROSCI LETT, V195, P175, DOI 10.1016/0304-3940(95)11811-A IKEUCHI Y, 1995, BIOCHEM BIOPH RES CO, V214, P589, DOI 10.1006/bbrc.1995.2326 Kanter ED, 1996, J NEUROSCI, V16, P307 KLUG A, 1995, J NEUROPHYSIOL, V74, P1701 Kuwada S, 1997, J NEUROSCI, V17, P7565 LAMBERT NA, 1994, J NEUROPHYSIOL, V72, P121 LeBeau FEN, 1996, J NEUROPHYSIOL, V75, P902 LI Y, 1994, BRAIN RES, V660, P232, DOI 10.1016/0006-8993(94)91294-7 Li Y, 1998, HEARING RES, V121, P1, DOI 10.1016/S0378-5955(98)00066-5 MCCOWN TJ, 1987, EPILEPSIA, V28, P234, DOI 10.1111/j.1528-1157.1987.tb04213.x MCCOWN TJ, 1984, EXP NEUROL, V86, P527, DOI 10.1016/0014-4886(84)90087-6 Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F Milbrandt JC, 1996, NEUROSCIENCE, V73, P449, DOI 10.1016/0306-4522(96)00050-4 MILLAN MH, 1986, EXP NEUROL, V91, P634, DOI 10.1016/0014-4886(86)90059-2 Moore DR, 1998, J NEUROPHYSIOL, V80, P2229 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 Mori K, 1997, HEARING RES, V111, P22, DOI 10.1016/S0378-5955(97)00090-7 NAJLERAHIM A, 1990, MOL BRAIN RES, V7, P317, DOI 10.1016/0169-328X(90)90082-O NELSON PG, 1963, J NEUROPHYSIOL, V26, P908 NGouemo P, 1996, BRAIN RES, V724, P200, DOI 10.1016/0006-8993(96)00304-6 OLAZABAL UE, 1989, J COMP NEUROL, V282, P98, DOI 10.1002/cne.902820108 Oliver D. L., 1991, NEUROBIOLOGY HEARING, P195 Oliver DL, 1992, MAMMALIAN AUDITORY P, P168 OLIVER DL, 1994, J COMP NEUROL, V340, P27, DOI 10.1002/cne.903400104 Palombi PS, 1996, J NEUROPHYSIOL, V75, P2211 Palombi PS, 1996, HEARING RES, V100, P41, DOI 10.1016/0378-5955(96)00115-3 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd Pedemonte M, 1997, BRAIN RES, V759, P24, DOI 10.1016/S0006-8993(97)00123-6 PIERSON MG, 1989, BRAIN RES, V486, P381, DOI 10.1016/0006-8993(89)90528-3 Potashner SJ, 1997, EXP NEUROL, V148, P222, DOI 10.1006/exnr.1997.6641 Ribak C E, 1994, J Hirnforsch, V35, P303 ROBERTS RC, 1985, BRAIN RES, V361, P324, DOI 10.1016/0006-8993(85)91303-4 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 SaintMarie RL, 1996, J COMP NEUROL, V373, P255, DOI 10.1002/(SICI)1096-9861(19960916)373:2<255::AID-CNE8>3.0.CO;2-2 SALDANA E, 1992, J COMP NEUROL, V319, P417, DOI 10.1002/cne.903190308 SMITH PH, 1992, J NEUROSCI, V12, P3700 Suneja SK, 1998, EXP NEUROL, V151, P273, DOI 10.1006/exnr.1998.6812 Szczepaniak WS, 1996, HEARING RES, V97, P46 Tanabe M, 1996, BRAIN RES, V716, P101, DOI 10.1016/0006-8993(96)00051-0 Tang E, 1997, EUR J PHARMACOL, V327, P109, DOI 10.1016/S0014-2999(97)89649-5 THOMPSON SM, 1989, J NEUROPHYSIOL, V61, P524 TOKUNAGA A, 1984, J HIRNFORSCH, V25, P461 Wagner T, 1996, EUR J NEUROSCI, V8, P1231, DOI 10.1111/j.1460-9568.1996.tb01291.x WAGNER T, 1994, NEUROREPORT, V6, P89, DOI 10.1097/00001756-199412300-00024 YAMAUCHI R, 1989, NEUROSCI RES, V6, P446, DOI 10.1016/0168-0102(89)90006-0 NR 81 TC 24 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 15 EP 28 DI 10.1016/S0378-5955(99)00129-X PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600004 PM 10545630 ER PT J AU Szonyi, M He, DZZ Ribari, O Sziklai, I Dallos, P AF Szonyi, M He, DZZ Ribari, O Sziklai, I Dallos, P TI Cyclic GMP and outer hair cell electromotility SO HEARING RESEARCH LA English DT Article DE electromotility; outer hair cell; phosphorylation; cyclic guanosine monophosphate; 3 ',5 '-cyclic GMP-dependent protein kinase; 3 ',5 ''-cyclic AMP-dependent protein kinase; calcium/phospholipid-dependent protein kinase ID GUINEA-PIG COCHLEA; VASCULAR SMOOTH-MUSCLE; MECHANICAL RESPONSES; EFFERENT STIMULATION; NATRIURETIC PEPTIDE; SHAPE CHANGES; ADP-RIBOSE; INNER-EAR; ACETYLCHOLINE; PROTEIN AB The aim of this study is to examine the effect of phosphorylation pathways on the electrically evoked fast motile response of isolated outer hair cells (OHCs). Transcellular electrical stimulation was applied in the microchamber to guinea pig OHCs and motility was measured before and after drug application. Forskolin (adenylate cyclase activator), phorbol 12-myristate 13-acetate (PMA, protein kinase C activator) and dibutyryl 3',5'-cyclic guanosine monophosphate (cGMP agonist) were studied. As controls, L15 medium and dimethyl-sulfoxide (DMSO) were used. In each group, 12 cells were measured. Forskolin and PMA were dissolved in 0.1% DMSO to render them membrane permeable. DMSO by itself caused a statistically significant electromotility magnitude decrease. Forskolin and PMA could not reverse the motility decrease due to DMSO, the effects seen in their presence were the same as observed with DMSO alone. Thus, neither 3',5'-cyclic AMP-dependent protein kinase nor calcium/phospholipid-dependent protein kinase appear to have modulatory effects on electromotility. Dibutyryl cGMP (DBcGMP), in concentrations of 200 mu M, elicited a significant electromotility magnitude increase. The DBcGMP effect could be inhibited by co-application of 200 mu M DBcGMP and 100 mu M 8-Rp-pCPT-cGMPS (8-4-chlorophenylthio-guanosine 3',5'-cyclic monophosphothioate, Rp isomer, a cGMP antagonist). Our results suggest that OHC electromotility is modulated by a cGMP-dependent pathway. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Northwestern Univ, Dept Commun Sci & Disorders, Auditory Physiol Lab, Evanston, IL 60208 USA. Northwestern Univ, Dept Neurobiol & Physiol, Inst Neurosci, Evanston, IL 60208 USA. Semmelweis Univ, Sch Med, Dept Otorhinolaryngol Head & Neck Surg, H-1083 Budapest, Hungary. Debrecen Univ, Sch Med, Otorhinolaryngol Clin, Debrecen, Hungary. RP Dallos, P (reprint author), Northwestern Univ, Dept Commun Sci & Disorders, Auditory Physiol Lab, Evanston, IL 60208 USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BARTOLAMI S, 1993, BRAIN RES, V626, P200, DOI 10.1016/0006-8993(93)90580-G BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Clementi E, 1996, J BIOL CHEM, V271, P17739 Coling DE, 1998, HEARING RES, V115, P175, DOI 10.1016/S0378-5955(97)00194-9 COLING DE, 1991, HEARING RES, V57, P113, DOI 10.1016/0378-5955(91)90080-S Crawford JH, 1997, J NEUROPHYSIOL, V77, P2573 DALLOS P, 1988, FUNCTIONS AUDITORY S, P153 Dallos P, 1997, J NEUROSCI, V17, P2212 DALLOS P, 1993, J NEUROPHYSIOL, V70, P299 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DOI T, 1993, HEARING RES, V67, P179, DOI 10.1016/0378-5955(93)90245-V DULON D, 1990, J NEUROSCI, V10, P1388 ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 Evans MG, 1996, J PHYSIOL-LONDON, V491, P563 EYBALIN M, 1993, PHYSIOL REV, V73, P309 Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 FURUKAWA KI, 1991, J BIOL CHEM, V266, P12337 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 Guihard G, 1996, BIOCHEM J, V318, P849 GUTH PS, 1977, J NEUROCHEM, V28, P263, DOI 10.1111/j.1471-4159.1977.tb07741.x HAFFNER C, 1995, EMBO J, V14, P19 HALLWORTH R, 1993, J NEUROPHYSIOL, V70, P549 HE DZZ, 1994, HEARING RES, V78, P77, DOI 10.1016/0378-5955(94)90046-9 HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 Kannan MS, 1997, AM J PHYSIOL-LUNG C, V272, pL1 KUIJPERS W, 1992, HEARING RES, V62, P1, DOI 10.1016/0378-5955(92)90197-U ZUMGOTTESBERGE AMM, 1991, HEARING RES, V56, P86 MURTHY KS, 1993, AM J PHYSIOL, V264, pG967 Murugasu E, 1996, J NEUROSCI, V16, P325 MURUGASU E, 1996, AUDIT NEUROSCI, V2, P263 NIEDZIELSKI AS, 1991, HEARING RES, V57, P107, DOI 10.1016/0378-5955(91)90079-O NIEDZIELSKI AS, 1992, HEARING RES, V59, P250, DOI 10.1016/0378-5955(92)90121-3 Puschner B, 1997, HEARING RES, V110, P251, DOI 10.1016/S0378-5955(97)00086-5 REINHARD M, 1992, EMBO J, V11, P2063 SAFFIEDINE S, 1996, MOL BRAIN RES, V40, P127 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X Schuch U, 1989, NEURON, V3, P13 Siegel S., 1956, NONPARAMETRIC STAT B Sridhar TS, 1997, J NEUROSCI, V17, P428 SRIDHAR TS, 1995, J NEUROSCI, V15, P3667 Sziklai I, 1996, HEARING RES, V95, P87, DOI 10.1016/0378-5955(96)00026-3 Szonyi M, 1999, ACTA OTO-LARYNGOL, V119, P185 THALMANN R, 1979, ACTA OTO-LARYNGOL, V87, P375, DOI 10.3109/00016487909126436 TOHSE N, 1995, BRIT J PHARMACOL, V114, P1076 WILLIAMSON MP, 1994, BIOCHEM J, V297, P249 WILMOTT N, 1996, J BIOL CHEM, V271, P3699 XU X, 1994, J BIOL CHEM, V269, P12645 YOON YJ, 1994, ORL J OTO-RHINO-LARY, V56, P73 YOSHIDA Y, 1991, J BIOL CHEM, V266, P19819 NR 52 TC 26 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 29 EP 42 DI 10.1016/S0378-5955(99)00127-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600005 PM 10545631 ER PT J AU Whitlon, DS Wright, LS Nelson, SA Szakaly, R Siegel, FL AF Whitlon, DS Wright, LS Nelson, SA Szakaly, R Siegel, FL TI Maturation of cochlear glutathione-S-transferases correlates with the end of the sensitive period for ototoxicity SO HEARING RESEARCH LA English DT Article DE cochlea; glutathione-S-transferase; development; detoxification; vestibular system; ototoxicity ID ANTIOXIDANT SYSTEM; HAIR-CELLS; GENTAMICIN OTOTOXICITY; CISPLATIN OTOTOXICITY; SUPERGENE FAMILY; ACOUSTIC TRAUMA; IN-VITRO; RAT; PROTECTION; ISOENZYMES AB The developing mammalian cochlea is especially sensitive to chemical toxins. In rats, the period of increased sensitivity falls roughly between postnatal days (P) 8 and 28. One unexplored hypothesis for this 'sensitive period' is that young cochleas may have immature complements of detoxification enzymes. Glutathione-S-transferases (GSTs) are a family of detoxification enzymes which catalyze the conjugation of many xenobiotics to glutathione. Using high performance liquid chromatography (HPLC), we measured the concentrations of soluble GST isoforms in cochleas of developing Fischer 344 rats. At P1, the concentration of isoform rGSTP1 was 9 pmol/mg protein. That of the remaining isoforms studied was low, < 2 pmol/mg protein, and, except for rGSTA3, remained so throughout the period of study. At P2, immunolabelling visualized rGSTP1 in the stria vascularis, Reissner's membrane, spiral limbus and organ of Corti. From P1 to P28, rGSTP1 increased to 15 pmol/mg protein and was detected additionally in satellite cells of the spiral ganglion and in the spiral ligament. From P7 to P28, rGSTA3 increased 8-fold (3-24 pmol/mg protein), became the predominant isoform in the adult organ and localized to pillar cells, the limbus and the spiral ligament. In the vestibule, rGSTP1 predominated, although rGSTA3 increased slightly over time. These observations suggest that biochemical immaturity in detoxification enzymes in the cochlea may contribute to the increased sensitivity to ototoxins during development and that differences in detoxification enzymes between cells in the cochlea and between inner ear organs may underlie differences in susceptibility to ototoxins. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Northwestern Univ, Audiol & Hearing Sci Program, Evanston, IL 60201 USA. Northwestern Univ, Inst Neurosci, Evanston, IL USA. VA Chicago Hlth Care Syst, Lakeside Div, Chicago, IL 60611 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Whitlon, DS (reprint author), Northwestern Univ, Audiol & Hearing Sci Program, Evanston, IL 60201 USA. CR BOCK GR, 1977, SCIENCE, V197, P396, DOI 10.1126/science.877565 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 BROCK M, 1994, HEARING RES, V72, P37, DOI 10.1016/0378-5955(94)90203-8 Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 Daggett DA, 1997, TOXICOLOGY, V117, P61, DOI 10.1016/S0300-483X(96)03555-X Eggermont J J, 1986, Acta Otolaryngol Suppl, V429, P5 ELBARBARY A, 1993, HEARING RES, V71, P80 GARETZ SL, 1994, HEARING RES, V77, P75, DOI 10.1016/0378-5955(94)90254-2 GARETZ SL, 1994, HEARING RES, V77, P81, DOI 10.1016/0378-5955(94)90255-0 GILLOYZAGA P, 1990, EUR ARCH OTO-RHINO-L, V248, P40, DOI 10.1007/BF00634780 Habig W H, 1981, Methods Enzymol, V77, P398 Hayes JD, 1995, CRIT REV BIOCHEM MOL, V30, P445, DOI 10.3109/10409239509083491 HAYES JD, 1995, FREE RADICAL RES, V22, P193, DOI 10.3109/10715769509147539 HAYES JD, 1988, BIOCHEM J, V255, P913 HENLEY CM, 1987, BRAIN RES BULL, V19, P695, DOI 10.1016/0361-9230(87)90056-6 HENLEY CM, 1995, BRAIN RES REV, V20, P68, DOI 10.1016/0165-0173(94)00006-B Hirose K, 1997, HEARING RES, V104, P1, DOI 10.1016/S0378-5955(96)00169-4 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 JOHNSON JA, 1992, BIOCHEM J, V282, P279 JOHNSON JA, 1993, J NEUROSCI, V13, P2013 KETTERER B, 1990, GLUTATHIONE S-TRANSFERASES AND DRUG RESISTANCE, P97 Kopke RD, 1997, AM J OTOL, V18, P559 LAUTERMANN J, 1995, HEARING RES, V86, P15, DOI 10.1016/0378-5955(95)00049-A LENOIR M, 1980, ACTA OTO-LARYNGOL, V89, P317, DOI 10.3109/00016488009127143 LENOIR M, 1979, J PHYSIOL-PARIS, V75, P521 OBrien ML, 1996, EUR J CANCER, V32A, P967, DOI 10.1016/0959-8049(96)00051-2 PHILBERT MA, 1995, NEUROTOXICOLOGY, V16, P349 Pujol R, 1986, Acta Otolaryngol Suppl, V429, P29 RAVI R, 1995, PHARMACOL TOXICOL, V76, P386 Rybak LP, 1997, PHARMACOL TOXICOL, V81, P173 RYBAK LP, 1995, FUND APPL TOXICOL, V26, P293, DOI 10.1006/faat.1995.1100 RYBAK LP, 1991, LARYNGOSCOPE, V101, P1167 SINGHAL SS, 1994, ARCH BIOCHEM BIOPHYS, V311, P242, DOI 10.1006/abbi.1994.1233 STUPAK HD, 1998, ASS RES OT ABSTR, V21, P132 Sun QA, 1996, BIOCHEM MOL BIOL INT, V39, P343 Tanaka T, 1997, INT J ONCOL, V10, P1009 Uziel A, 1986, Acta Otolaryngol Suppl, V429, P23 Xie CS, 1998, FREE RADICAL BIO MED, V25, P979, DOI 10.1016/S0891-5849(98)00186-5 Yamasoba T, 1998, BRAIN RES, V784, P82, DOI 10.1016/S0006-8993(97)01156-6 Yao XF, 1996, HEARING RES, V96, P199, DOI 10.1016/0378-5955(96)00050-0 ZELCK U, 1993, EUR ARCH OTO-RHINO-L, V250, P218 NR 41 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 43 EP 50 DI 10.1016/S0378-5955(99)00136-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600006 PM 10545632 ER PT J AU Freeman, S Plotnik, M Elidan, J Sohmer, H AF Freeman, S Plotnik, M Elidan, J Sohmer, H TI Development of short latency vestibular evoked potentials in the neonatal rat SO HEARING RESEARCH LA English DT Article DE development; inner ear; vestibular; auditory; evoked potential; rat ID AUDITORY BRAIN-STEM; POSTNATAL-DEVELOPMENT; RECEPTOR SURFACES; HUMAN FETUSES; HAIR-CELLS; NEURONS; MOUSE; ACCELERATION; RESPONSES; MATURATION AB The development of short latency vestibular evoked potentials (VsEPs) was investigated in the neonatal rat. Using the appropriate stimulus (linear or angular acceleration impulses) and head orientation, responses elicited in various vestibular end-organs (utricle: x-VsEP; saccule: z-VsEP; lateral semi-circular canal: a-VsEP) were measured in rat pups at various ages between post-natal days (PND) 5 and 30, and compared to those recorded from adult animals. It was found that the VsEPs initially appeared on PND 6 (x-VsEPs and z-VsEPs) or 7 (a-VsEPs), and that by PND 8 the three responses could be recorded in all animals. The first wave of the responses, generated in the primary sensory nerve and reflecting end-organ activity, reached adult latencies and amplitudes by PND 10, showing rapid maturity of the responses. Auditory responses, on the other hand, develop at a later stage (from PND 11). The possible mechanisms involved in this differential maturation between vestibular and auditory activity are discussed. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, IL-91120 Jerusalem, Israel. Hadassah Univ Hosp, Dept Otolaryngol Head & Neck Surg, IL-91120 Jerusalem, Israel. RP Freeman, S (reprint author), Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Physiol, POB 12272, IL-91120 Jerusalem, Israel. CR ANNIKO M, 1983, ANAT EMBRYOL, V166, P355, DOI 10.1007/BF00305923 ANNIKO M, 1985, ORL J OTO-RHINO-LARY, V47, P57 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 CURTHOYS IS, 1979, BRAIN RES, V167, P41, DOI 10.1016/0006-8993(79)90261-0 CURTHOYS IS, 1982, EXP BRAIN RES, V47, P295 DECHESNE C, 1986, ACTA OTO-LARYNGOL, V101, P11, DOI 10.3109/00016488609108602 DECHESNE CJ, 1985, AM J OTOLARYNG, V6, P378, DOI 10.1016/S0196-0709(85)80016-8 DESMADRYL G, 1986, DEV BRAIN RES, V25, P133, DOI 10.1016/0165-3806(86)90160-4 ELDREDGE DH, 1961, ANN OTO RHINOL LARYN, V70, P1024 ELIDAN J, 1989, LARYNGOSCOPE, V99, P92 ELIDAN J, 1982, ELECTROEN CLIN NEURO, V53, P501, DOI 10.1016/0013-4694(82)90062-1 ELIDAN J, 1987, BRAIN RES, V423, P385, DOI 10.1016/0006-8993(87)90868-7 ELIDAN J, 1991, ELECTROEN CLIN NEURO, V80, P140, DOI 10.1016/0168-5597(91)90151-M FAWER CL, 1982, NEUROPEDIATRICS, V14, P88 Freeman S, 1996, HEARING RES, V97, P19 Freeman S, 1999, AM J OTOL, V20, P41 FREEMAN S, 1995, J NEUROL SCI, V128, P143, DOI 10.1016/0022-510X(94)00229-H FREEMAN S, 1993, HEARING RES, V69, P229, DOI 10.1016/0378-5955(93)90112-E Freeman S, 1999, ACTA OTO-LARYNGOL, V119, P311 GAGNON R, 1989, SEMIN PERINATOL, V13, P393 GEALDOR M, 1993, HEARING RES, V69, P236, DOI 10.1016/0378-5955(93)90113-F GOLD S, 1985, ELECTROEN CLIN NEURO, V60, P146, DOI 10.1016/0013-4694(85)90021-5 HE DZZ, 1994, HEARING RES, V78, P77, DOI 10.1016/0378-5955(94)90046-9 HENLEY CM, 1995, BRAIN RES REV, V20, P68, DOI 10.1016/0165-0173(94)00006-B HEYWOOD P, 1976, ACTA OTO-LARYNGOL, V82, P359, DOI 10.3109/00016487609120920 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X Johnston AR, 1996, NEUROSCI LETT, V219, P17, DOI 10.1016/S0304-3940(96)13152-9 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 LANNOU J, 1979, BRAIN RES, V175, P219, DOI 10.1016/0006-8993(79)91002-3 LARY S, 1985, J PEDIATR-US, V107, P593, DOI 10.1016/S0022-3476(85)80030-5 LI G, 1995, ARCH OTOLARYNGOL, V121, P34 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 Meza G, 1996, INT J DEV NEUROSCI, V14, P507, DOI 10.1016/0736-5748(95)00099-2 Moriguchi M, 1991, Acta Otolaryngol Suppl, V486, P32 NORDEMAR H, 1983, ACTA OTO-LARYNGOL, V96, P447, DOI 10.3109/00016488309132731 Plotnik M, 1997, EVOKED POTENTIAL, V104, P522, DOI 10.1016/S0168-5597(97)00062-2 Pujol R, 1991, Acta Otolaryngol Suppl, V482, P7 PUJOL R, 1980, HEARING RES, V2, P423, DOI 10.1016/0378-5955(80)90078-7 Rusch A, 1998, J NEUROSCI, V18, P7487 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 SANS A, 1982, J COMP NEUROL, V206, P1, DOI 10.1002/cne.902060102 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 Shnerson A, 1981, Brain Res, V254, P65 SOHMER H, 1989, ELECTROEN CLIN NEURO, V74, P50, DOI 10.1016/0168-5597(89)90051-8 STARR A, 1977, PEDIATRICS, V60, P831 UZIEL A, 1981, AUDIOLOGY, V20, P89 WANG Z, 1993, ANN OTO RHINOL LARYN, V102, P802 Yakovlev P. I., 1967, REGIONAL DEV BRAIN E, P3 NR 49 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 51 EP 58 DI 10.1016/S0378-5955(99)00137-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600007 PM 10545633 ER PT J AU Fukazawa, T Ishida, K Murai, Y AF Fukazawa, T Ishida, K Murai, Y TI A micromechanical model of the cochlea with radial movement of the tectorial membrane SO HEARING RESEARCH LA English DT Article DE tectorial membrane; cochlear model; micromechanics ID HAIR CELL MOTILITY; MECHANICS; ORGAN; CORTI AB The function of the tectorial membrane in the cochlear micromechanics is uncertain. In modeling approaches some models have assumed it to be a resonator that participates in the sharp tuning mechanisms of the cochlea with its mass coupled to the ciliary stiffness of outer hair cells, being driven by the shear force between the reticular lamina and itself. This paper presents a different type of micromechanical model which assumes that the tectorial membrane is driven by a lymphatic fluid flow that can be shown to have a substantial radial component. It also assumes that the reticular lamina is relatively stiff and thereby restrains the top end of outer hair cells that exert a force to the basilar membrane via Deiters cells. When combined with a three-dimensional block model, it can simulate the sharp tuning mechanisms of the cochlea well. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Kasukabe City Hosp, Dept Otolaryngol, Kasukabe, Saitama 3440067, Japan. RP Fukazawa, T (reprint author), Kasukabe City Hosp, Dept Otolaryngol, Kasukabe, Saitama 3440067, Japan. CR de Boer E., 1996, COCHLEA, P258 DEBOER E, 1995, J ACOUST SOC AM, V98, P1400, DOI 10.1121/1.414407 DEBOER E, 1981, HEARING RES, V4, P53, DOI 10.1016/0378-5955(81)90036-8 DEBOER E, 1993, J ACOUST SOC AM, V93, P2845, DOI 10.1121/1.406851 Evans E. F., 1975, HDB SENSORY PHYSL, V5, P1 Fukazawa T, 1997, HEARING RES, V113, P182, DOI 10.1016/S0378-5955(97)00138-X GEISLER CD, 1995, HEARING RES, V86, P132, DOI 10.1016/0378-5955(95)00064-B GUMMER AW, 1996, P NATL ACAD SCI USA, V93, P8728 KRONESTERFREI A, 1979, ARCH OTO-RHINO-LARYN, V224, P3, DOI 10.1007/BF00455217 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 MAMMANO F, 1993, J ACOUST SOC AM, V93, P3320, DOI 10.1121/1.405716 NEELY ST, 1981, J ACOUST SOC AM, V69, P1386, DOI 10.1121/1.385820 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NEELY ST, 1993, BIOPHYSICS HAIR CELL, P64 NEELY ST, 1993, J ACOUST SOC AM, V94, P137, DOI 10.1121/1.407091 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 Patuzzi R., 1996, COCHLEA, P186 REUTER G, 1990, HEARING RES, V43, P219, DOI 10.1016/0378-5955(90)90230-M RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 Voldrich L, 1983, MECH HEARING, P163 ZWISLOCKI JJ, 1980, HEARING RES, V2, P171, DOI 10.1016/0378-5955(80)90055-6 ZWISLOCKI JJ, 1989, COCHLEAR MECH STRUCT, P163 NR 24 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 59 EP 67 DI 10.1016/S0378-5955(99)00128-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600008 PM 10545634 ER PT J AU Langemann, U Hamann, I Friebe, A AF Langemann, U Hamann, I Friebe, A TI A behavioral test of presbycusis in the bird auditory system SO HEARING RESEARCH LA English DT Article DE bird; European starling; auditory threshold; aging; presbycusis ID HAIR-CELL REGENERATION; STARLING STURNUS-VULGARIS; CANARIES SERINUS-CANARIUS; BRAIN-STEM RESPONSES; ACOUSTIC TRAUMA; CHICK COCHLEA; INTENSE SOUND; HEARING-LOSS; AMINOGLYCOSIDE OTOTOXICITY; MONGOLIAN GERBIL AB Absolute auditory thresholds were determined behaviorally in European starlings (Sturnus vulgaris) between the age of 6 months and up to 13 years using a GO/NOGO procedure. The thresholds that we observed in individual starlings over a time period of 11 years showed no systematic increase over time. When comparing young starlings (age 6 to 12 months) with old starlings (age 8 to 13 years), we discovered no substantial age-related hearing loss. In the frequency range from 0.5 to 4 kHz, the thresholds of old subjects were on average increased by 1.5 to 3 dB. For frequencies of 6 and 8 kHz, the mean threshold increase of old subjects was 6.1 and 4.9 dB, respectively. This demonstrates excellent hearing in subjects that had lived on average more than five times the starlings' demographic life span of 22 months. This result is discussed with respect to the large threshold shift usually found in aging mammals and to differences between the bird and the mammalian auditory system. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Tech Univ Munich, Inst Zool, D-85747 Garching, Germany. RP Langemann, U (reprint author), Tech Univ Munich, Inst Zool, Lichtenbergstr 4, D-85747 Garching, Germany. CR BAUR A, 1989, THESIS TU MUNCHEN BENNETT CL, 1983, BEHAV NEUROSCI, V97, P602, DOI 10.1037//0735-7044.97.4.602 BUUS S, 1995, J ACOUST SOC AM, V98, P112, DOI 10.1121/1.414466 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F COOPER W A JR, 1986, Society for Neuroscience Abstracts, V12, P1280 Corwin JT, 1997, NEURON, V19, P951, DOI 10.1016/S0896-6273(00)80386-4 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1992, EXP NEUROL, V115, P7, DOI 10.1016/0014-4886(92)90212-9 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 Cotanche DA, 1997, ANN OTO RHINOL LARYN, V106, P9 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 COULSON JC, 1960, J ANIM ECOL, V29, P251, DOI 10.2307/2203 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DELVINGT W., 1962, GERFAUT REV BELG ORNITHOL, V52, P586 Dooling R.J., 1980, P261 Dooling R. J., 1995, METHODS COMP PSYCHOA, P161 Dooling R.J., 1998, PSYCHOPHYSICAL PHYSL, P145 DOOLING RJ, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P545 DUM N, 1983, LARYNG RHINOL OTOL V, V62, P378, DOI 10.1055/s-2007-1008456 EHRET G, 1974, NATURWISSENSCHAFTEN, V61, P506 EHRET G, 1979, ACTA OTO-LARYNGOL, V87, P28, DOI 10.3109/00016487909126384 FAY RR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P229 Forge A, 1998, J COMP NEUROL, V397, P69 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 Gleich O, 1997, J COMP NEUROL, V377, P5, DOI 10.1002/(SICI)1096-9861(19970106)377:1<5::AID-CNE2>3.0.CO;2-8 GLEICH O, 1995, HEARING RES, V82, P100 GLEICH O, 1994, NATURWISSENSCHAFTEN, V81, P320, DOI 10.1007/BF01131950 GLEICH O, 1994, HEARING RES, V79, P123, DOI 10.1016/0378-5955(94)90134-1 Gratton M A, 1996, Hear Res, V102, P181, DOI 10.1016/S0378-5955(96)90017-9 GRATTON MA, 1997, ASS RES OTOLARYNGOL, V20, P104 Gratton MA, 1997, HEARING RES, V108, P9, DOI 10.1016/S0378-5955(97)00034-8 HARRISON J, 1982, NEUROBIOL AGING, V3, P163, DOI 10.1016/0197-4580(82)90036-7 HELLSTROM LI, 1990, ASS RES OTOLARYNGOL, V13, P149 HELLSTROM LI, 1989, ASS RES OTOLARYNGOL, V12, P43 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1980, ARCH OTO-RHINO-LARYN, V228, P233, DOI 10.1007/BF00660735 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 Klump Georg M., 1996, P321 KLUMP GM, 1990, J COMP PSYCHOL, V104, P94, DOI 10.1037/0735-7036.104.1.94 KUHN A, 1982, NATURWISSENSCHAFTEN, V69, P245, DOI 10.1007/BF00398648 LANGEMANN U, 1995, HEARING RES, V84, P167, DOI 10.1016/0378-5955(95)00023-W MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 Marean GC, 1998, J ACOUST SOC AM, V103, P3567, DOI 10.1121/1.423085 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MILLS JH, 1996, ASS RES OTOLARYNGOL, V19, P161 MILLS JH, 1989, ASS RES OTOLARYNGOL, V12, P44 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 Muller M, 1999, HEARING RES, V131, P153, DOI 10.1016/S0378-5955(99)00029-5 NIEMIEC AJ, 1994, HEARING RES, V75, P125 OESTERLE EC, 1993, HEARING RES, V66, P213, DOI 10.1016/0378-5955(93)90141-M OKANOYA K, 1987, J COMP PSYCHOL, V101, P7, DOI 10.1037//0735-7036.101.1.7 Pickles JO, 1988, INTRO PHYSL HEARING PUGLIANO FA, 1993, NEUROSCI LETT, V151, P214, DOI 10.1016/0304-3940(93)90023-E RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SAUNDERS SS, 1995, J ACOUST SOC AM, V97, P1150, DOI 10.1121/1.412228 Schmiedt RA, 1996, HEARING RES, V102, P125, DOI 10.1016/S0378-5955(96)00154-2 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SCHMIEDT RA, 1989, ASS RES OTOLARYNGOL, V12, P41 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K Sinnott JM, 1997, HEARING RES, V112, P235, DOI 10.1016/S0378-5955(97)00125-1 Spoor A, 1967, INT AUDIOL, V6, P48, DOI 10.3109/05384916709074230 Svensson L, 1992, IDENTIFICATION GUIDE Swets J.A., 1964, SIGNAL DETECTION REC TRAINER JE, 1946, THESIS CORNELL U ITA TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 TURNOCK MT, 1975, J ACOUST SOC AM S1, V58, P90 VONBLOTZHEIM UNG, 1993, HDB VOGEL MITTELEURO, V13, P2025 VOSSIECK T, 1991, HEARING RES, V56, P93, DOI 10.1016/0378-5955(91)90158-6 Willott J. F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1991, ABSTR ASS RES OT, V14, P16 NR 75 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 68 EP 76 DI 10.1016/S0378-5955(99)00139-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600009 PM 10545635 ER PT J AU Schwartz, IR Eager, PR AF Schwartz, IR Eager, PR TI Glutamate receptor subunits in neuronal populations of the gerbil lateral superior olive SO HEARING RESEARCH LA English DT Article DE glutamate receptor subunits; auditory system; superior olive; AMPA-preferring; immunochemistry; light microscopy; electron microscopy ID D-ASPARTATE RECEPTOR; GENE-RELATED PEPTIDE; RAT SPINAL-CORD; COCHLEAR NUCLEUS; IMMUNOCYTOCHEMICAL LOCALIZATION; HORSERADISH-PEROXIDASE; ENDOPLASMIC-RETICULUM; OLIVOCOCHLEAR NEURONS; KAINATE RECEPTORS; GLIAL-CELLS AB The distribution of AMPA-preferring ionotropic glutamate receptors (GluR) within the gerbil lateral superior olive (LSO) was investigated immunocytochemically using antibodies to GluR1, 2, 2/3 and 4. Light microscopy showed GluR1 antibody preferentially labeling a population of small neurons located in the dorsal hilus and a population mainly at or near the margins of the LSO. GluR4 antibody strongly stained most large LSO neuronal somata and proximal dendrites including all principal cells. GluR2/3 antibody showed very modest staining and appeared in most cell types. GluR2 showed less intense neuronal staining than GluR2/3 and was observed as a punctate accumulation at the surface of some neuronal profiles. GluR1, 2, 2/3 and 4 immunoreactivity was found along dendrites of most large LSO neurons and in their somata. Postsynaptic specializations positive for GluR2 were rare on LSO somata compared to the high frequency of GluR4 and 1 specializations. Double labeling studies showed that different portions of the distal dendrites showed a preponderance of GluR1 or GluR4 subunits. Electron microscopic observations confirm similarities in the localization of immunoreactivity for the antibodies tested in the cytoplasm of somata and dendrites, but reveal differences at the plasmalemma, at synaptic appositions and appositions with glial processes. Receptor composition Varied with cell type and location on cells. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Yale Univ, Sch Med, Dept Surg Otolaryngol, New Haven, CT 06520 USA. RP Schwartz, IR (reprint author), Yale Univ, Sch Med, Dept Surg Otolaryngol, POB 20841, New Haven, CT 06520 USA. CR ADAMS JC, 1986, ABSTR ASS RES OT, V9, P5 ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 Bilak MM, 1996, NEUROSCIENCE, V75, P1075, DOI 10.1016/0306-4522(96)00197-2 BURNASHEV N, 1992, SCIENCE, V256, P1566, DOI 10.1126/science.1317970 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 CASPARY DM, 1989, BRAIN RES, V503, P83, DOI 10.1016/0006-8993(89)91707-1 CASPARY DM, 1985, AUDITORY BIOCH, P198 Caspary DM, 1991, NEUROBIOLOGY HEARING, P141 FORSAYETH JR, 1992, J CELL BIOL, V117, P841, DOI 10.1083/jcb.117.4.841 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 FRYDMAN J, 1994, NATURE, V370, P111, DOI 10.1038/370111a0 FURUYAMA T, 1993, MOL BRAIN RES, V18, P141, DOI 10.1016/0169-328X(93)90183-P GALLO V, 1992, J NEUROSCI, V12, P1010 GELMAN MS, 1995, J BIOL CHEM, V270, P15085 HAMMOND C, 1995, CURR OPIN CELL BIOL, V7, P523, DOI 10.1016/0955-0674(95)80009-3 HELFERT RH, 1992, J COMP NEUROL, V323, P305, DOI 10.1002/cne.903230302 HELFERT RH, 1988, J NEUROSCI, V8, P3111 HELFERT RH, 1987, AM J ANAT, V179, P55, DOI 10.1002/aja.1001790108 HOLLMANN M, 1994, ANNU REV NEUROSCI, V17, P31, DOI 10.1146/annurev.ne.17.030194.000335 HUNTER C, 1993, J NEUROSCI, V13, P1932 HUNTER C, 1992, MOL BIOL HEAR DEAFNE, V83 HUNTER C, 1993, ARO MIDW M, V16, P124 HURTLEY SM, 1989, ANNU REV CELL BIOL, V5, P277 Joelson D, 1998, MICROSC RES TECHNIQ, V41, P246, DOI 10.1002/(SICI)1097-0029(19980501)41:3<246::AID-JEMT8>3.3.CO;2-P KANDLER K, 1995, J NEUROSCI, V15, P6890 KEH A, 1999, ARO MIDW M, V22, P68 Korada S., 1997, Society for Neuroscience Abstracts, V23, P182 Lerea LS, 1997, CELL SIGNAL, V9, P219, DOI 10.1016/S0898-6568(96)00134-9 LERMA J, 1994, EUR J NEUROSCI, V6, P1080, DOI 10.1111/j.1460-9568.1994.tb00605.x LOPEZ T, 1994, NEUROREPORT, V5, P504, DOI 10.1097/00001756-199401120-00034 LU SM, 1987, HEARING RES, V31, P137, DOI 10.1016/0378-5955(87)90119-5 LUQUE JM, 1995, GLIA, V13, P228, DOI 10.1002/glia.440130309 Mano I, 1998, NEUROREPORT, V9, P327, DOI 10.1097/00001756-199801260-00027 MARTIN LJ, 1993, NEUROSCIENCE, V53, P327, DOI 10.1016/0306-4522(93)90199-P MARTIN LJ, 1993, J NEUROSCI, V13, P2249 MULLER T, 1992, SCIENCE, V256, P1563, DOI 10.1126/science.1317969 PETRALIA RS, 1994, J NEUROSCI, V14, P667 Petralia RS, 1997, J COMP NEUROL, V385, P456, DOI 10.1002/(SICI)1096-9861(19970901)385:3<456::AID-CNE9>3.0.CO;2-2 PETRALIA RS, 1992, J COMP NEUROL, V318, P329, DOI 10.1002/cne.903180309 PETRALIA RS, 1992, MOL BIOL HEAR DEAFNE, P106 Petralia RS, 1996, J COMP NEUROL, V372, P356 Rietzel HJ, 1998, J COMP NEUROL, V390, P20 RYAN AF, 1987, J COMP NEUROL, V255, P606, DOI 10.1002/cne.902550411 Schwartz I. R., 1996, Society for Neuroscience Abstracts, V22, P125 SCHWARTZ IR, 1997, ARO MIDW M, V20, P83 SCHWARTZ IR, 1994, CONTRIBUTIONS SENSOR, V8, P99 SCHWARTZ IR, 1994, ASS RES OTOLARYNGOL, V17, P14 SCHWARTZ IR, 1995, ARO MIDW M, V18, P39 SCHWARTZ IR, 1996, ARO MIDW M, V19, P120 SCHWARTZ IR, 1982, STAIN TECHNOL, V57, P52 SCHWEITZER L, 1985, NEUR ABSTR, V11, P1051 SIMMONS DD, 1993, J CHEM NEUROANAT, V6, P407, DOI 10.1016/0891-0618(93)90015-V SPANGLER KM, 1987, J COMP NEUROL, V259, P452, DOI 10.1002/cne.902590311 SPANGLER KM, 1985, J COMP NEUROL, V238, P249, DOI 10.1002/cne.902380302 SUNEJA SK, 1995, J NEUROCHEM, V64, P161 TACHIBANA M, 1994, J COMP NEUROL, V344, P431, DOI 10.1002/cne.903440307 WARR W B, 1989, Society for Neuroscience Abstracts, V15, P745 WENTHOLD RJ, 1992, J BIOL CHEM, V267, P501 Wenthold RJ, 1996, J NEUROSCI, V16, P1982 WU SH, 1992, J NEUROSCI, V12, P3084 Wu TY, 1996, BIOCHEM J, V319, P731 YU SM, 1989, STAIN TECHNOL, V64, P143 ZOOK JM, 1988, HEARING RES, V34, P141, DOI 10.1016/0378-5955(88)90101-3 NR 63 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 77 EP 90 DI 10.1016/S0378-5955(99)00140-9 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600010 PM 10545636 ER PT J AU Cappaert, NLM Klis, SFL Muijser, H de Groot, JCMJ Kulig, BM Smoorenburg, GF AF Cappaert, NLM Klis, SFL Muijser, H de Groot, JCMJ Kulig, BM Smoorenburg, GF TI The ototoxic effects of ethyl benzene in rats SO HEARING RESEARCH LA English DT Article DE rat; ethyl benzene; ototoxicity; reflex modification audiometry; electrocochleography; histology ID OUTER HAIR-CELLS; FREQUENCY HEARING-LOSS; GUINEA-PIG; EVOKED-POTENTIALS; TOLUENE EXPOSURE; TRICHLOROETHYLENE; STYRENE; INNER; INHALATION; SOLVENTS AB Exposure to organic solvents has been shown to be ototoxic in animals and there is evidence that these solvents can induce hearing loss in humans. In this study, the effects of inhalation of the possibly ototoxic solvent ethyl benzene on the cochlear function and morphology were evaluated using three complementary techniques: (1) reflex modification audiometry (RMA), (2) electrocochleography and (3) histological examination of the cochleas. Rats were exposed to either ethyl benzene (800 ppm, 8 h/day for 5 days) or to control conditions. The RMA threshold increased significantly by about 25 dB, 1 and 4 weeks after the exposure, irrespective of the stimulus frequency tested (4-24 kHz). Electrocochleography was performed between 8 and 11 weeks after exposure to the organic solvent. The threshold for the compound action potential increased significantly by 10-30 dB at all frequencies tested (1-24 kHz). Histological examination of the cochlea showed outer hair cell (OHC) loss, especially in the upper basal and lower middle turns (corresponding to the mid-frequency region) to an extent of 65%. We conclude that exposure to 800 ppm ethyl benzene for 8 h/day during 5 days induces hearing loss in rats due to OHC loss. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, NL-3584 CX Utrecht, Netherlands. TNO, Food & Nutr Res, Div Toxicol, NL-3704 HE Zeist, Netherlands. RP Cappaert, NLM (reprint author), Univ Utrecht, Med Ctr, Dept Otorhinolaryngol, Hearing Res Labs, Room G02-531,POB 85500,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. CR *AM CHEM SOC, 1996, PROD US CHEM IND CHE BISCALDI GP, 1983, TOXICOL EUR RES, V3, P271 Campo P, 1997, NEUROTOXICOL TERATOL, V19, P129, DOI 10.1016/S0892-0362(96)00214-0 Crofton K. M., 1992, NEUROTOXICOLOGY, P181 CROFTON KM, 1994, HEARING RES, V80, P25, DOI 10.1016/0378-5955(94)90005-1 Crofton KM, 1997, FUND APPL TOXICOL, V38, P101, DOI 10.1006/faat.1997.2327 CROFTON KM, 1993, NEUROTOXICOL TERATOL, V15, P413, DOI 10.1016/0892-0362(93)90059-W DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 DEGROOT JCMJ, 1987, ACTA OTO-LARYNGOL, V104, P234, DOI 10.3109/00016488709107323 ENGSTROM B, 1984, SCAND AUDIOL, V13, P87, DOI 10.3109/01050398409043045 FAY RR, 1988, HEARING VERTEBRATES, P363 Fechter LD, 1998, TOXICOL SCI, V42, P28 FORNAZZARI L, 1983, ACTA NEUROL SCAND, V67, P319 JASPERS RMA, 1993, NEUROTOXICOL TERATOL, V15, P407, DOI 10.1016/0892-0362(93)90058-V JOHNSON AC, 1994, HEARING RES, V75, P201, DOI 10.1016/0378-5955(94)90071-X JOHNSON AC, 1994, HEARING RES, V72, P189, DOI 10.1016/0378-5955(94)90218-6 LAZAR RB, 1983, NEUROLOGY, V33, P1337 MAKITIE A, 1997, THESIS U HELSINKI HE METRICK SA, 1982, ANN NEUROL, V12, P553, DOI 10.1002/ana.410120609 MORATA TC, 1993, SCAND J WORK ENV HEA, V19, P245 MUIJSER H, 1988, TOXICOLOGY, V49, P331, DOI 10.1016/0300-483X(88)90016-9 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PRYOR GT, 1993, NEUROTOXICOLOGY INHA PRYOR GT, 1994, PRINCIPLES NEUROTOXI, P345 PRYOR GT, 1987, J APPL TOXICOL, V7, P55, DOI 10.1002/jat.2550070110 Pryor GT, 1995, HDB NEUROTOXICOLOGY, P377 PRYOR GT, 1983, NEUROBEH TOXICOL TER, V5, P47 PRYOR GT, 1984, NEUROBEH TOXICOL TER, V6, P111 REBERT CS, 1993, INT J PSYCHOPHYSIOL, V14, P49, DOI 10.1016/0167-8760(93)90083-2 REBERT CS, 1991, NEUROTOXICOL TERATOL, V13, P83, DOI 10.1016/0892-0362(91)90031-Q REBERT CS, 1983, NEUROBEH TOXICOL TER, V5, P59 RYBAK LP, 1992, OTOLARYNG HEAD NECK, V106, P677 Sass-Kortsak Andrea M., 1995, Annals of Epidemiology, V5, P15, DOI 10.1016/1047-2797(94)00036-S SPENCER PS, 1985, SCAND J WORK ENV HEA, V11, P53 Stengs CHM, 1997, HEARING RES, V111, P103, DOI 10.1016/S0378-5955(97)00095-6 SULLIVAN MJ, 1989, NEUROTOXICOL TERATOL, V10, P525 Szulc-Kuberska J, 1976, MINERVA OTORINOLARIN, V26, P108 YANO BL, 1992, TOXICOL PATHOL, V20, P1 NR 40 TC 28 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 91 EP 102 DI 10.1016/S0378-5955(99)00141-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600011 PM 10545637 ER PT J AU Lohuis, PJFM Klis, SFL Klop, WMC van Emst, MG Smoorenburg, GF AF Lohuis, PJFM Klis, SFL Klop, WMC van Emst, MG Smoorenburg, GF TI Signs of endolymphatic hydrops after perilymphatic perfusion of the guinea pig cochlea with cholera toxin; a pharmacological model of acute endolymphatic hydrops SO HEARING RESEARCH LA English DT Article DE model; acute endolymphatic hydrops; cholera toxin; adenylate cyclase; summating potential; cochlear homeostasis ID ADENYLATE-CYCLASE MODULATION; MENIERES-DISEASE; MORPHOLOGICAL-CHANGES; INNER-EAR; POTENTIALS; ELECTROCOCHLEOGRAPHY; LOCALIZATION; FORSKOLIN; MECHANISM; MEMBRANE AB There are indications that endolymph homeostasis is controlled by intracellular cAMP levels in cells surrounding the scala media. Cholera toxin is a potent stimulator of adenylate cyclase, i.e. it increases cAMP levels. We hypothesized that perilymphatic perfusion of cholera toxin might increase endolymph volume by stimulating adenylate cyclase activity, providing us with a pharmacological model of acute endolymphatic hydrops (EH). Guinea pig cochleas were perfused with artificial perilymph (15 min), with or without cholera toxin (10 mu g/ml). The endocochlear potential (EP) was measured during and after perfusion. The summating potential (SP), evoked by 2, 4 and 8 kHz tone bursts, was measured via an apically placed electrode 0, 1, 2, 3 and 4 h after perfusion. Thereafter, the cochleas were fixed to enable measurement of the length of Reissner's membrane, reflecting EH. After perfusion the EP increased significantly over time in the cholera toxin group as compared to the controls. Also, the SP increased gradually at all frequencies in the cholera toxin group. Comparison within animals showed that the increase in SP became significant after 2 h at 4 kHz, after 3 h at 2 kHz and after 4 h at 8 kHz. In the control group the SP did not change significantly. The compound action potential (CAP) amplitude decreased monotonically over time at all frequencies in both the cholera toxin group and the control group, but it decreased faster in the cholera toxin group. Also, the cochlear microphonics amplitude decreased over time at all frequencies in both groups, but the decrease was significant only in the cholera toxin group after 3 h at 2 and 4 kHz. Quantification of the length of Reissner's membrane showed a small but insignificant enlargement in the cholera toxin treated animals compared to controls. These results are in accord with our view that EH is accompanied by an increase in SP and a decrease in CAP. Our results partially confirm previous results of Feldman and Brusilow (Proc. Natl. Acad. Sci. USA (1973) 73, 1761-1764). New aspects in relation to that study are the significantly increased EP and SP. In the classical EH model, based on obstruction of the absorptive function of the endolymphatic sac, increased SPs are accompanied by decreased EPs. In this cholera toxin model of EH, it is unlikely that the endolymphatic sac is involved. Apparently, EH can be based on mechanisms located in the cochlea itself as opposed to mechanisms located in the endolymphatic sac. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Utrecht, Dept Otorhinolaryngol, Hearing Res Labs, NL-3584 CX Utrecht, Netherlands. RP Lohuis, PJFM (reprint author), Univ Utrecht, Dept Otorhinolaryngol, Hearing Res Labs, Room G-02-531,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. CR ALBERS FWJ, 1987, ANN OTO RHINOL LARYN, V96, P282 ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 Bouman H, 1998, HEARING RES, V117, P119, DOI 10.1016/S0378-5955(97)00216-5 Brunschwig AS, 1997, HEARING RES, V114, P62, DOI 10.1016/S0378-5955(97)00153-6 COHEN J, 1984, ACTA OTO-LARYNGOL, V98, P398, DOI 10.3109/00016488409107580 DOI K, 1992, ACTA OTO-LARYNGOL, V112, P667, DOI 10.3109/00016489209137457 DOI K, 1990, HEARING RES, V45, P157, DOI 10.1016/0378-5955(90)90192-R DOI K, 1992, HEARING RES, V58, P221, DOI 10.1016/0378-5955(92)90131-6 DURRANT JD, 1974, J ACOUST SOC AM, V56, P562, DOI 10.1121/1.1903291 EWART HS, 1995, AM J PHYSIOL-CELL PH, V269, pC295 FELDMAN AM, 1976, P NATL ACAD SCI USA, V73, P1761, DOI 10.1073/pnas.73.5.1761 GIBSON WPR, 1977, AUDIOLOGY, V16, P389 GOIN DW, 1982, LARYNGOSCOPE, V92, P1383 Hallpike C. S., 1938, J LARYNG, V53, P625, DOI 10.1017/S0022215100003947 HORNER KC, 1986, HEARING RES, V26, P319 HORNER KC, 1993, SCANNING MICROSCOPY, V7, P223 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KITANO I, 1995, HEARING RES, V83, P37, DOI 10.1016/0378-5955(94)00187-U KLIS JFL, 1988, HEARING RES, V32, P175, DOI 10.1016/0378-5955(88)90089-5 KLIS SFL, 1999, MENIERES DIS, P279 KUMAGAMI H, 1983, ACTA OTOLARYNGOL STO, V97, P547 KUSAKARI J, 1986, ACTA OTO-LARYNGOL, V101, P27, DOI 10.3109/00016488609108604 MERCHANT SN, 1995, EUR ARCH OTO-RHINO-L, V252, P63 MORI N, 1987, AUDIOLOGY, V26, P103 MORIZONO T, 1985, ANN OTO RHINOL LARYN, V94, P191 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 RUDING PRJW, 1987, ARCH OTO-RHINO-LARYN, V244, P174, DOI 10.1007/BF00464263 SANTI PA, 1994, J HISTOCHEM CYTOCHEM, V42, P705 SCHACHT J, 1982, AM J OTOLARYNG, V3, P328, DOI 10.1016/S0196-0709(82)80005-7 Sunose H, 1997, HEARING RES, V114, P107, DOI 10.1016/S0378-5955(97)00152-4 THALMANN I, 1982, J ACOUST SOC AM, V71, P599 VANBENTHEM PPG, 1993, EUR ARCH OTO-RHINO-L, V250, P73 VANDEELEN GW, 1988, ACTA OTO-LARYNGOL, V105, P193, DOI 10.3109/00016488809096998 VANDEELEN GW, 1987, ARCH OTO-RHINO-LARYN, V244, P167 VANEMST MG, 1998, THESIS UTRECHT U Yamakawa K, 1938, J OTORHINOLARYNGOL S, V4, P2310 ZAJIC G, 1983, HEARING RES, V10, P249, DOI 10.1016/0378-5955(83)90090-4 NR 37 TC 6 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 103 EP 113 DI 10.1016/S0378-5955(99)00130-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600012 PM 10545638 ER PT J AU Oukda, M Bautz, A Membre, H Ghanbaja, J Francois, M Dournon, C AF Oukda, M Bautz, A Membre, H Ghanbaja, J Francois, M Dournon, C TI Appearance and evolution of calcitic and aragonitic otoconia during Pleurodeles waltl development SO HEARING RESEARCH LA English DT Article DE amphibian; inner ear; otoconium; otolith; aragonite; calcite ID RED-BELLIED NEWT; CYNOPS-PYRRHOGASTER; DIFFRACTION; MICROSCOPY; AMPHIBIANS; MEMBRANE; OTOLITH; PROTEIN AB The aim of this study is to determine the stages of appearance, morphology, crystallographic structure and chemical composition of otoconia during the inner ear development of an urodele amphibian, Pleurodeles waltl. The first otoconia are detected in the otocyst. Near hatching, calcitic otoconia are polyhedral in the saccule and cylindrical in the utricle. During the following stages, the saccular otoconia agglomerate and constitute a polyhedral calcitic otolith. At larval stage 44, aragonitic fusiform otoconia appear on the otolithic surface. At stage 52, X-ray diffraction analysis shows calcite and aragonite patterns. In adults, all the saccular otoconia are aragonitic. In contrast, the utricular otoconia do not show any modification up to adulthood. In the endolymphatic sac, otoconia appear at stage 45 and in the lagena at stage 49. They remain aragonitic up to adulthood. Energy dispersive X-ray spectroscopy (EDXS) elemental analysis of the otoconia reveals a high quantity of calcium with trace quantities of sodium, magnesium, phosphorus, sulfur, chlorine and potassium. However, magnesium and sulfur have a lower concentration in lagenar aragonitic otoconia than in utricular and saccular calcitic ones. As in adults, trace amounts of strontium are only found in aragonitic otoconia. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Henri Poincare Univ, Lab Expt Biol Immunol, UPRES EA 2401, F-54506 Vandoeuvre Nancy, France. Univ Nancy 1, Transmiss Electron Microscopy Serv, F-54506 Vandoeuvre Nancy, France. Univ Nancy 1, Lab Chem Mineral Solids, UMR 7555, F-54506 Vandoeuvre Nancy, France. RP Dournon, C (reprint author), Henri Poincare Univ, Lab Expt Biol Immunol, UPRES EA 2401, BP 239, F-54506 Vandoeuvre Nancy, France. RI FRANCOIS, Michel/B-4277-2013 CR BALLARINO J, 1985, AM J ANAT, V174, P131, DOI 10.1002/aja.1001740204 BIDWELL JP, 1986, BIOL BULL, V170, P75, DOI 10.2307/1541382 CAMPOS A, 1992, MICRON MICROSC ACTA, V23, P349, DOI 10.1016/0739-6260(92)90039-G CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 CARLSTROM D, 1953, LARYNGOSCOPE, V63, P1052, DOI 10.1288/00005537-195311000-00002 Fermin CD, 1998, HISTOL HISTOPATHOL, V13, P1103 FERMIN CD, 1993, MICROSC RES TECHNIQ, V25, P297, DOI 10.1002/jemt.1070250406 GALLIEN L., 1957, BULL BIOL FRANCE ET BELGIQUE, V91, P97 HALLWORTH R, 1995, HEARING RES, V85, P115, DOI 10.1016/0378-5955(95)00038-6 JOHANSSON KE, 1980, J PHYS E SCI INSTRUM, V13, P1289, DOI 10.1088/0022-3735/13/12/015 Kido Toshishige, 1997, Auris Nasus Larynx, V24, P125, DOI 10.1016/S0385-8146(96)00020-X LIM DJ, 1974, BRAIN BEHAV EVOLUT, V10, P37, DOI 10.1159/000124301 Lim D J, 1973, Ann Otol Rhinol Laryngol, V82, P23 LYCHAKOV DV, 1995, J EVOL BIOCHEM PHYS+, V31, P90 LYCHAKOV DV, 1994, J EVOL BIOCHEM PHYS, V30, P99 MALMROS G, 1973, ACTA CHEM SCAND, V27, P483 MARMO F, 1981, CELL TISSUE RES, V218, P265 MARMO F, 1983, ACTA ZOOL-STOCKHOLM, V64, P219 MARMO F, 1983, CELL TISSUE RES, V233, P35 NUSINOVICI J, 1994, ADV X RAY ANAL, V37, P59 Oukda M, 1999, HEARING RES, V132, P85, DOI 10.1016/S0378-5955(99)00041-6 POTE KG, 1991, COMP BIOCHEM PHYS B, V98, P287, DOI 10.1016/0305-0491(91)90181-C POTE KG, 1993, BIOCHEMISTRY-US, V32, P5017, DOI 10.1021/bi00070a007 POTE KG, 1993, HEARING RES, V67, P189, DOI 10.1016/0378-5955(93)90246-W ROSS MD, 1984, PHILOS T ROY SOC B, V304, P445, DOI 10.1098/rstb.1984.0038 ROSS MD, 1975, ANN OTO RHINOL LARYN, V84, P22 Sondag HNPM, 1998, ACTA OTO-LARYNGOL, V118, P86 Steyger PS, 1995, HEARING RES, V92, P184, DOI 10.1016/0378-5955(95)00221-9 STEYGER PS, 1995, HEARING RES, V84, P61, DOI 10.1016/0378-5955(95)00013-T Takumida M, 1997, ACTA OTO-LARYNGOL, V117, P538, DOI 10.3109/00016489709113434 Takumida M, 1997, ACTA OTO-LARYNGOL, V117, P529, DOI 10.3109/00016489709113433 Verpy E, 1999, P NATL ACAD SCI USA, V96, P529, DOI 10.1073/pnas.96.2.529 WANG DL, 1990, NEURAL COMPUT, V2, P95 WIEDERHOLD ML, 1995, HEARING RES, V84, P41, DOI 10.1016/0378-5955(95)00012-S WRIGHT CG, 1982, ANN OTO RHINOL LARYN, V91, P193 Zhang D M, 1997, Nihon Jibiinkoka Gakkai Kaiho, V100, P927 NR 36 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 114 EP 126 DI 10.1016/S0378-5955(99)00143-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600013 PM 10545639 ER PT J AU Hamernik, RP Ahroon, WA AF Hamernik, RP Ahroon, WA TI Sound-induced priming of the chinchilla auditory system SO HEARING RESEARCH LA English DT Article DE noise-induced hearing loss (NIHL); priming; conditioning; toughening; protection ID NOISE-INDUCED HEARING; INTERRUPTED NOISE; THRESHOLD SHIFTS; CELL LOSS; EXPOSURE; PROTECTION; TRAUMA; ENERGY AB Exposure of the auditory system to either continuous or interrupted nontraumatic noises, often collectively referred to as priming exposures, has been shown, in a number of experimental paradigms, to reduce the susceptibility of the auditory system to noise-induced hearing and sensory cell loss from a subsequent traumatic exposure. Using auditory evoked potentials to obtain pure-tone thresholds and cochleograms to quantify sensory cell losses, the issue of priming-induced protective effects was examined in the chinchilla. Priming was accomplished with either a continuous noise or with a continuous noise followed by an interrupted noise. Trauma was induced by exposure to high-level impacts over a 5-day period that resulted in an asymptotic threshold shift. A comparison of the two groups of primed subjects with an unprimed control group showed that there were some statistically significant reductions in the asymptotic response of the primed groups to the traumatic exposure but no differences in permanent changes in thresholds among the three groups 30 days following the traumatic exposure. There were, however, some statistically significant, frequency-specific, reductions in outer hair cell loss in the primed groups. When conditioning was followed by the interrupted exposure that produced a threshold shift toughening effect, the conditioning protocol had no effect on the response of subjects to the interrupted exposure. There were also no differences in thresholds or sensory cell loss between the two primed groups 30 days post-trauma. Priming protocols may have different effects on the development of noise-induced trauma that are dependent on the nature of the traumatic stimulus, that is, long-term high-level impact noise exposure versus acute continuous noise exposure. (C) 1999 Elsevier Science B.V. All rights reserved. C1 SUNY Coll Plattsburgh, Auditory Res Lab, Plattsburgh, NY 12901 USA. RP Hamernik, RP (reprint author), SUNY Coll Plattsburgh, Auditory Res Lab, 107 Beaumont Hall, Plattsburgh, NY 12901 USA. CR AHROON WA, 1993, J ACOUST SOC AM, V93, P997, DOI 10.1121/1.405406 Ahroon WA, 1999, HEARING RES, V129, P101, DOI 10.1016/S0378-5955(98)00227-5 BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T CAMPO P, 1991, HEARING RES, V55, P195, DOI 10.1016/0378-5955(91)90104-H CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CANLON B, 1995, HEARING RES, V84, P112, DOI 10.1016/0378-5955(95)00020-5 CANLON B, 1992, NOISE INDUCED HEARIN, P489 CANLON B, 1998, 21 MIDW RES M ASS RE, P136 Canlon B, 1999, HEARING RES, V127, P158, DOI 10.1016/S0378-5955(98)00170-1 CANLON B, 1996, AUDITORY SYSTEM PLAS, P128 Canlon B, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P172 CARDER HM, 1972, J SPEECH HEAR RES, V15, P603 Dagli S, 1997, HEARING RES, V104, P39, DOI 10.1016/S0378-5955(96)00179-7 DAVIS H, 1950, Acta Otolaryngol Suppl, V88, P1 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 Fay R. R., 1988, HEARING VERTEBRATES FOWLER T, 1995, HEARING RES, V88, P1, DOI 10.1016/0378-5955(95)00062-9 Hamernik RP, 1999, HEARING RES, V132, P140, DOI 10.1016/S0378-5955(99)00039-8 Hamernik RP, 1998, J ACOUST SOC AM, V103, P3478, DOI 10.1121/1.423056 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HUMES LE, 1984, J ACOUST SOC AM, V76, P1318, DOI 10.1121/1.391447 LIBERMAN MC, 1998, 21 MIDW RES M ASS RE, P140 McFadden SL, 1997, HEARING RES, V103, P142, DOI 10.1016/S0378-5955(96)00170-0 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLS JH, 1992, NOISE INDUCED HEARIN, P237 MILLS JH, 1973, J SPEECH HEAR RES, V16, P700 Roberto M, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P165 Skellett RA, 1998, HEARING RES, V116, P21, DOI 10.1016/S0378-5955(97)00199-8 SUBRAMANIAM M, 1993, HEARING RES, V65, P234, DOI 10.1016/0378-5955(93)90216-N White DR, 1998, J ACOUST SOC AM, V103, P1566, DOI 10.1121/1.421303 NR 30 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 127 EP 136 DI 10.1016/S0378-5955(99)00131-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600014 PM 10545640 ER PT J AU Fuzessery, ZM Hall, JC AF Fuzessery, ZM Hall, JC TI Sound duration selectivity in the pallid bat inferior colliculus SO HEARING RESEARCH LA English DT Article DE inferior colliculus; duration selectivity; pallid bat; gamma-aminobutyric acid; bicuculline; synaptic integration ID MEDIAL SUPERIOR OLIVE; BIG BROWN BAT; AUDITORY-CORTEX; REPETITION RATE; TONOTOPIC ORGANIZATION; ANTROZOUS-PALLIDUS; LATERAL LEMNISCUS; EPTESICUS-FUSCUS; MYOTIS-LUCIFUGUS; MOUSTACHED BAT AB Neurons selective for sound duration have been reported in the auditory midbrain and cortex of several specialized vertebrate species that process behaviorally relevant signals of stereotypic duration. This study examines duration selectivity in the inferior colliculus (IC) of the pallid bat to determine if this selectivity is limited to regions that serve echolocation, or if it extends to low-frequency regions that serve passive listening. It also focuses on the temporal response properties of duration-selective neurons to elucidate mechanisms that may underlie the creation of this selectivity. Of 140 neurons tested, 36% were selective for short durations of less than or equal to 7 ms, and acted as short-pass or bandpass duration filters. Sixteen percent, termed long duration neurons, differed in that they required minimum sound durations of 5-50 ms before responding, and all acted as long-pass duration filters. Short duration neurons were equally common in the high-frequency region serving echolocation and the lateral low-frequency region that serves passive listening, indicating that selectivity for short duration sounds was not associated only with the specialized function of echolocation. Long duration neurons were most common in the medial low-frequency region IC. Selectivity for short and long duration sounds was therefore not uniformly distributed across the IC. Analyses of the temporal response properties of short duration neurons, and the application of bicuculline to block gamma-aminobutyric acid-A receptors, were used to infer the synaptic interactions that underlie the creation of duration selectivity, the role of inhibition in its creation, and whether a coincidence mechanism proposed by Casseday et al. (Science 264 (1994) 847-850) is consistent with the behavior of the duration-selective neurons recorded in the pallid bat IC. Present results suggest that while some neurons do behave in a manner that is consistent with the coincidence mechanism, the behaviors of others suggest that more than one mechanism may create a selectivity for short duration sounds. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Wyoming, Dept Zool & Physiol, Laramie, WY 82001 USA. Univ Tennessee, Dept Biochem Cell & Mol Biol, Knoxville, TN 37996 USA. RP Fuzessery, ZM (reprint author), Univ Wyoming, Dept Zool & Physiol, POB 3166, Laramie, WY 82001 USA. CR AITKIN LM, 1970, J NEUROPHYSIOL, V33, P421 BELL GP, 1982, BEHAV ECOL SOCIOBIOL, V10, P217, DOI 10.1007/BF00299688 Bertrand S, 1998, J NEUROPHYSIOL, V79, P342 Bregman AS., 1990, AUDITORY SCENE ANAL BROWN P, 1976, Z TIERPSYCHOL, V41, P34 CALFORD MB, 1981, J NEUROPHYSIOL, V45, P1013 CASSEDAY JH, 1994, SCIENCE, V264, P847, DOI 10.1126/science.8171341 Casseday JH, 1996, BRAIN BEHAV EVOLUT, V47, P311, DOI 10.1159/000113249 CHERRY EC, 1953, J ACOUST SOC AM, V25, P975, DOI 10.1121/1.1907229 COOLEY BC, 1992, THROMB RES, V67, P1, DOI 10.1016/0049-3848(92)90252-6 Covey E, 1996, J NEUROSCI, V16, P3009 Ehrlich D, 1997, J NEUROPHYSIOL, V77, P2360 Fuzessery ZM, 1997, HEARING RES, V109, P46, DOI 10.1016/S0378-5955(97)00053-1 FUZESSERY ZM, 1994, J NEUROPHYSIOL, V72, P1061 FUZESSERY ZM, 1993, J COMP PHYSIOL A, V171, P767, DOI 10.1007/BF00213073 Fuzessery ZM, 1996, J NEUROPHYSIOL, V76, P1059 FUZESSERY ZM, 1995, INT C NEUR FUZESSERY ZM, 1991, J NEUROSCI METH, V36, P45, DOI 10.1016/0165-0270(91)90136-N Galazyuk AV, 1997, J COMP PHYSIOL A, V180, P301, DOI 10.1007/s003590050050 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GROTHE B, 1994, J NEUROPHYSIOL, V71, P706 HALL J, 1986, NEUROSCI LETT, V63, P215, DOI 10.1016/0304-3940(86)90358-7 HALL JC, 1988, HEARING RES, V36, P261, DOI 10.1016/0378-5955(88)90067-6 HALL JC, 1991, J NEUROPHYSIOL, V66, P955 He JF, 1997, J NEUROSCI, V17, P2615 Heil P, 1997, J NEUROPHYSIOL, V77, P2616 HIND JE, 1963, J NEUROPHYSIOL, V26, P321 Jen PHS, 1999, J COMP PHYSIOL A, V184, P185, DOI 10.1007/s003590050317 KITZES LM, 1978, J NEUROPHYSIOL, V41, P1165 KUWADA S, 1983, J NEUROPHYSIOL, V50, P981 Kuwada S, 1997, J NEUROSCI, V17, P7565 LESSER HD, 1990, EXP BRAIN RES, V82, P137 NARINS PM, 1980, BRAIN BEHAV EVOLUT, V17, P48, DOI 10.1159/000121790 PARK TJ, 1993, J NEUROSCI, V13, P5172 PINHEIRO AD, 1991, J COMP PHYSIOL A, V169, P69 POLLAK GD, 1981, J NEUROPHYSIOL, V45, P208 POTTER HD, 1965, J NEUROPHYSIOL, V28, P1155 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 Sanes DH, 1998, J NEUROSCI, V18, P794 SUGA N, 1990, SCI AM, V262, P60 SULLIVAN WE, 1982, J NEUROPHYSIOL, V48, P1011 SULLIVAN WE, 1986, P NATL ACAD SCI USA, V83, P8400, DOI 10.1073/pnas.83.21.8400 WU SH, 1995, J NEUROPHYSIOL, V73, P780 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 NR 44 TC 63 Z9 67 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 137 EP 154 DI 10.1016/S0378-5955(99)00133-1 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600015 PM 10545641 ER PT J AU Yoshida, K Ichimiya, I Suzuki, M Mogi, G AF Yoshida, K Ichimiya, I Suzuki, M Mogi, G TI Effect of proinflammatory cytokines on cultured spiral ligament fibrocytes SO HEARING RESEARCH LA English DT Article DE mouse; inner ear; interleukin-1 beta; tumor necrosis factor-alpha; chemokine; soluble intercellular adhesion molecule-1 ID INNER-EAR INFLAMMATION; CLONING; INTEGRINS; PROTEINS; ADHESION; COCHLEA AB To clarify the effect of proinflammatory cytokines on spiral ligament (SL) fibrocytes, in vitro studies were performed using secondary cell cultures. Cultures from murine SL fibrocytes were stimulated by interleukin (IL)-1 beta or tumor necrosis factor (TNF)-alpha, and secretion of various mediators was measured by enzyme-linked immunosorbent assay. After stimulation with the proinflammatory cytokines, IL-6, TNF-alpha, monocyte chemoattractant protein-1, KC, macrophage inflammatory protein-2, soluble intercellular adhesion molecule-1, and vascular endothelial growth factor levels were elevated. Secretion of these chemokines and other mediators could induce inflammatory cell movement, which would prolong the inflammatory response, leading to fibrocyte damage. Given that SL fibrocytes may play a role in cochlear fluid and ion homeostasis, such fibrocyte disruption could cause cochlear malfunction. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Oita Med Univ, Dept Otolaryngol, Oita 8795593, Japan. RP Mogi, G (reprint author), Oita Med Univ, Dept Otolaryngol, 1-1 Idaigaoka, Oita 8795593, Japan. CR COCHRAN BH, 1983, CELL, V33, P939, DOI 10.1016/0092-8674(83)90037-5 DRISCOLL KE, 1994, EXP LUNG RES, V20, P473, DOI 10.3109/01902149409031733 FONG GH, 1995, NATURE, V376, P66, DOI 10.1038/376066a0 Gratton MA, 1996, HEARING RES, V99, P71, DOI 10.1016/S0378-5955(96)00080-9 HARRIS JP, 1990, ACTA OTO-LARYNGOL, V110, P357, DOI 10.3109/00016489009107455 HYNES RO, 1992, CELL, V69, P11, DOI 10.1016/0092-8674(92)90115-S ICHIMIYA I, 1994, ANN OTO RHINOL LARYN, V103, P457 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 Ichimiya I, 1998, LARYNGOSCOPE, V108, P585, DOI 10.1097/00005537-199804000-00023 Ichimiya I, 1999, HEARING RES, V131, P128, DOI 10.1016/S0378-5955(99)00025-8 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KISHIMOTO TK, 1989, ADV IMMUNOL, V46, P149 LIM D J, 1970, Journal of Laryngology and Otology, V84, P413, DOI 10.1017/S0022215100072029 MILLAUER B, 1994, NATURE, V367, P576, DOI 10.1038/367576a0 Proost P, 1996, INT J CLIN LAB RES, V26, P211, DOI 10.1007/BF02602952 RYSECK RP, 1989, EXP CELL RES, V180, P266, DOI 10.1016/0014-4827(89)90230-9 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SHALABY F, 1995, NATURE, V376, P62, DOI 10.1038/376062a0 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z SUZUKI M, 1995, ANN OTO RHINOL LARYN, V104, P69 TEKAMPOLSON P, 1990, J EXP MED, V172, P911, DOI 10.1084/jem.172.3.911 TOMIYAMA S, 1986, LARYNGOSCOPE, V96, P685 NR 22 TC 46 Z9 47 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 155 EP 159 DI 10.1016/S0378-5955(99)00134-3 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600016 PM 10545642 ER PT J AU Trune, DR Wobig, RJ Kempton, JB Hefeneider, SH AF Trune, DR Wobig, RJ Kempton, JB Hefeneider, SH TI Steroid treatment improves cochlear function in the MRL.MpJ-Fas(lpr) autoimmune mouse SO HEARING RESEARCH LA English DT Article DE prednisolone; autoimmune disease; autoimmune mouse; Fas gene; inner ear; glucocorticoid ID SENSITIVE NA+ CHANNEL; LPR LPR MOUSE; INNER-EAR; STRIA VASCULARIS; GLUCOCORTICOID RECEPTOR; HEARING-LOSS; RAT COCHLEA; NZB/W MICE; DISEASE; MODEL AB Corticosteroid therapy is used to reverse autoimmune sensorineural hearing loss, although little is known of the mechanism by which this occurs. This has been due to the lack of a suitable animal model with spontaneous hearing loss that is steroid responsive. The present study examined the effects of prednisolone treatment on auditory thresholds in the MRL.MpJ-Fas(lpr) autoimmune mouse to determine its suitability as such a model. Autoimmune mice at 3.5-4.5 months of age were evaluated by pure-tone auditory brainstem response (ABR) to establish threshold elevations due to the disease. The steroid treatment: group was then given prednisolone in their drinking water for 2.5 months, while untreated controls were given tap water. Significantly more steroid treated mice survived to the time of post-treatment ABR evaluation. Half of the steroid treated ears demonstrated either improvement or no change in cochlear function compared to only 25% in the untreated controls. Overall, cochlear thresholds in the untreated controls increased by 14.7 dB, whereas no significant threshold increase was seen in the steroid treated group (4.3 dB) over the treatment period. No qualitative anatomical differences were seen in the ears of those mice surviving to the end of the study. These findings establish the autoimmune mouse as a model for studies of steroid responsive mechanisms within the ear. This could apply to autoimmune sensorineural hearing loss, as well as any hearing disorder for which steroid therapy is recommended. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Dept Med, Div Arthrit & Rheumat Dis, Portland, OR 97201 USA. Vet Affairs Med Ctr, Dept Immunol, Portland, OR USA. RP Trune, DR (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, NRC04,3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR CHAMPIGNY G, 1994, EMBO J, V13, P2177 GELFAND MC, 1972, ARTHRITIS RHEUM, V15, P247, DOI 10.1002/art.1780150305 GELFAND MC, 1972, ARTHRITIS RHEUM, V15, P239, DOI 10.1002/art.1780150304 HARRIS JP, 1995, OTOLARYNG HEAD NECK, V112, P639, DOI 10.1016/S0194-5998(95)70170-2 HUGHES GB, 1993, HEAD NECK SURG OTOLA, P1833 HUNNEYBALL IM, 1986, AGENTS ACTIONS, V18, P384, DOI 10.1007/BF01965002 KUSAKARI C, 1992, ANN OTO RHINOL LARYN, V101, P82 Lin DW, 1997, OTOLARYNG HEAD NECK, V117, P530, DOI 10.1016/S0194-5998(97)70026-3 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 Mitchell C, 1996, HEARING RES, V99, P38, DOI 10.1016/S0378-5955(96)00081-0 RAREY KE, 1991, LARYNGOSCOPE, V101, P1081 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1993, HEARING RES, V64, P205, DOI 10.1016/0378-5955(93)90007-N RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 RENARD S, 1995, PFLUG ARCH EUR J PHY, V430, P299, DOI 10.1007/BF00373903 RUCKENSTEIN MJ, 1993, ACTA OTO-LARYNGOL, V113, P160, DOI 10.3109/00016489309135785 Ruckenstein MJ, 1999, LARYNGOSCOPE, V109, P626, DOI 10.1097/00005537-199904000-00020 SHIMMER BP, 1996, GOODMAN GILMANS PHAR, P1459 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 Trune DR, 1997, OTOLARYNG HEAD NECK, V117, P504, DOI 10.1016/S0194-5998(97)70022-6 Trune DR, 1999, HEARING RES, V137, P167, DOI 10.1016/S0378-5955(99)00148-3 Trune DR, 1997, HEARING RES, V105, P57, DOI 10.1016/S0378-5955(96)00191-8 Trune DR, 1996, HEARING RES, V95, P57, DOI 10.1016/0378-5955(96)00018-4 TRUNE DR, 1989, HEARING RES, V38, P57, DOI 10.1016/0378-5955(89)90128-7 VANDERKRAAN PM, 1993, ANN RHEUM DIS, V52, P734, DOI 10.1136/ard.52.10.734 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WOBIG RJ, 1999, HEAD NECK SURG, V121, P344 ZHOU NN, 1994, INT J IMMUNOPHARMACO, V16, P845 ZUO J, 1995, HEARING RES, V87, P220, DOI 10.1016/0378-5955(95)00092-I NR 31 TC 21 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 160 EP 166 DI 10.1016/S0378-5955(99)00147-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600017 PM 10545643 ER PT J AU Trune, DR Wobig, RJ Kempton, JB Hefeneider, SH AF Trune, DR Wobig, RJ Kempton, JB Hefeneider, SH TI Steroid treatment in young MRL.MpJ-Fas(lpr) autoimmune mice prevents cochlear dysfunction SO HEARING RESEARCH LA English DT Article DE prednisolone; autoimmune disease; autoimmune mouse; Fas gene; inner ear; glucocorticoid ID SENSORINEURAL HEARING-LOSS; CIRCULATING IMMUNE-COMPLEXES; LPR LPR MOUSE; INNER-EAR; MENIERES-DISEASE; SERUM ANTIBODIES; STRIA VASCULARIS; NZB/W MICE; RECEPTORS; MODEL AB Corticosteroid therapy reverses clinical autoimmune sensorineural hearing loss, although little is known of how steroids restore normal auditory function. If suppression of systemic autoimmune processes underlies hearing restoration, then preventing autoimmune symptoms from developing should prevent cochlear dysfunction. MRL.MpJ-Fas(lpr) autoimmune mice were used to test this potential mechanism by initiating oral prednisolone treatment at 6 weeks of age, prior to autoimmune disease and hearing loss onset. The steroid treatment group was given prednisolone in their drinking water, while untreated controls were given tap water. Treatment continued for 7 months with periodic evaluations of cochlear function with auditory brainstem response (ABR) audiometry. Autoimmune mice given the steroid lived longer and did not develop levels of serum immune complexes seen in their untreated controls. Also, their ABR thresholds remained near normal throughout the 7 months of treatment: while untreated controls showed progressive threshold elevations typical for autoimmune disease. This correlation of suppressed systemic autoimmune activity and maintenance of normal cochlear function identifies one potential mechanism for autoimmune hearing loss and hearing restoration with steroid therapy. The autoimmune mouse should serve as a valuable model for future studies of the cochlear mechanisms responsive to steroid treatment in autoimmune hearing loss. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Vet Affairs Med Ctr, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Dept Med, Div Arthrit & Rheumat Dis, Portland, OR 97201 USA. RP Trune, DR (reprint author), Oregon Hlth Sci Univ, Dept Otolaryngol Head & Neck Surg, Oregon Hearing Res Ctr, NRC04,3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. CR ARNOLD W, 1985, ACTA OTO-LARYNGOL, V99, P437, DOI 10.3109/00016488509108935 Atlas MD, 1998, AM J OTOL, V19, P628 BERNSTEIN JM, 1987, IMMUNOLOGY EAR, P419 BLOCH DB, 1995, ARCH OTOLARYNGOL, V121, P1167 BROOKES GB, 1986, ARCH OTOLARYNGOL, V112, P536 BROOKES GB, 1985, J ROY SOC MED, V78, P47 DEREBERY MJ, 1991, LARYNGOSCOPE, V101, P225 Disher MJ, 1997, ANN NY ACAD SCI, V830, P253, DOI 10.1111/j.1749-6632.1997.tb51896.x GELFAND MC, 1972, ARTHRITIS RHEUM, V15, P247, DOI 10.1002/art.1780150305 GELFAND MC, 1972, ARTHRITIS RHEUM, V15, P239, DOI 10.1002/art.1780150304 GOTTSCHLICH S, 1995, LARYNGOSCOPE, V105, P1347, DOI 10.1288/00005537-199512000-00016 HARRIS JP, 1995, OTOLARYNG HEAD NECK, V112, P639, DOI 10.1016/S0194-5998(95)70170-2 HONGJUN X, 1995, P SEND S, V5, P55 HSU L, 1990, ANN OTO RHINOL LARYN, V99, P535 HUGHES GB, 1993, HEAD NECK SURG OTOLA, P1833 HUGHES GB, 1983, LARYNGOSCOPE, V93, P410 HUNNEYBALL IM, 1986, AGENTS ACTIONS, V18, P384, DOI 10.1007/BF01965002 KUSAKARI C, 1992, ANN OTO RHINOL LARYN, V101, P82 Lin DW, 1997, OTOLARYNG HEAD NECK, V117, P530, DOI 10.1016/S0194-5998(97)70026-3 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 Mitchell C, 1996, HEARING RES, V99, P38, DOI 10.1016/S0378-5955(96)00081-0 RAREY KE, 1991, LARYNGOSCOPE, V101, P1081 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 RAUCH SD, 1995, AM J OTOL, V16, P648 RUCKENSTEIN MJ, 1993, ACTA OTO-LARYNGOL, V113, P160, DOI 10.3109/00016489309135785 Ruckenstein MJ, 1999, HEARING RES, V127, P137, DOI 10.1016/S0378-5955(98)00189-0 Ruckenstein MJ, 1999, LARYNGOSCOPE, V109, P626, DOI 10.1097/00005537-199904000-00020 SHIMMER BP, 1996, GOODMAN GILMANS PHAR, P1459 Shin SO, 1997, LARYNGOSCOPE, V107, P222, DOI 10.1097/00005537-199702000-00015 TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 Trune DR, 1997, OTOLARYNG HEAD NECK, V117, P504, DOI 10.1016/S0194-5998(97)70022-6 Trune DR, 1999, HEARING RES, V137, P160, DOI 10.1016/S0378-5955(99)00147-1 Trune DR, 1997, HEARING RES, V105, P57, DOI 10.1016/S0378-5955(96)00191-8 Trune DR, 1996, HEARING RES, V95, P57, DOI 10.1016/0378-5955(96)00018-4 TRUNE DR, 1989, HEARING RES, V38, P57, DOI 10.1016/0378-5955(89)90128-7 VANDERKRAAN PM, 1993, ANN RHEUM DIS, V52, P734, DOI 10.1136/ard.52.10.734 VELDMAN JE, 1984, LARYNGOSCOPE, V94, P501, DOI 10.1288/00005537-198404000-00014 VELDMAN JE, 1989, AM J OTOL, V10, P183 WATANABEFUKUNAGA R, 1992, NATURE, V356, P314, DOI 10.1038/356314a0 WOBIG RJ, 1999, HEAD NECK SURG, V21, P344 XENELLIS J, 1986, J LARYNGOL OTOL, V100, P21, DOI 10.1017/S0022215100098698 ZHOU NN, 1994, INT J IMMUNOPHARMACO, V16, P845 NR 42 TC 16 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 167 EP 173 DI 10.1016/S0378-5955(99)00148-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600018 PM 10545644 ER PT J AU Shen, JX Xu, ZM Yao, YD AF Shen, JX Xu, ZM Yao, YD TI Evidence for columnar organization in the auditory cortex of the mouse SO HEARING RESEARCH LA English DT Article DE mouse; auditory cortex; columnar organization ID FREQUENCY REPRESENTATION; CAT; BAT AB Single cortical auditory neurons sequentially isolated within orthogonal electrode penetrations in the mouse were studied using tonal stimulation. They had common functional properties, such as firing pattern, best frequency, minimum threshold, sharpness of frequency tuning and onset latency. The finding suggests that there is columnar organization in the cortex. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Chinese Acad Sci, Inst Biophys, Lab Visual Informat Proc, Beijing 100101, Peoples R China. RP Shen, JX (reprint author), Chinese Acad Sci, Inst Biophys, Lab Visual Informat Proc, 13 Datun Rd,Chaoyang Dist, Beijing 100101, Peoples R China. CR ABELES M, 1970, J NEUROPHYSIOL, V33, P172 HUBEL DH, 1962, J PHYSIOL-LONDON, V160, P106 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 MOUNTCASTLE VB, 1957, J NEUROPHYSIOL, V20, P408 OONISHI S, 1965, JPN J PHYSIOL, V15, P342 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 Shen JX, 1997, J COMP PHYSIOL A, V181, P591, DOI 10.1007/s003590050142 Stiebler I, 1997, J COMP PHYSIOL A, V181, P559, DOI 10.1007/s003590050140 SUGA N, 1982, J NEUROPHYSIOL, V47, P225 SUGA N, 1976, SCIENCE, V194, P542, DOI 10.1126/science.973140 NR 10 TC 21 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1999 VL 137 IS 1-2 BP 174 EP 177 DI 10.1016/S0378-5955(99)00149-5 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 254AD UT WOS:000083588600019 PM 10545645 ER PT J AU Watson, GM Venable, S Hudson, RR Repass, JJ AF Watson, GM Venable, S Hudson, RR Repass, JJ TI ATP enhances repair of hair bundles in sea anemones SO HEARING RESEARCH LA English DT Article DE ATP; ecto-ATPase; mechanoreceptor; stereocilia ID GUINEA-PIG COCHLEA; ADENOSINE 5'-TRIPHOSPHATE; NEMATOCYST DISCHARGE; CELLS; RECEPTORS; FREQUENCY; CALCIUM AB Hair bundle mechanoreceptors of sea anemones are similar to those of the acousticolateralis system of vertebrates (Watson, Mire and Hudson, 1997, Hear. Res. 107, 53-63). Anemone hair bundles are repaired by 'repair proteins' secreted following a complete loss of structural integrity and loss of function caused by 1 h exposure to calcium free seawater. Exogenously supplied repair proteins (RP) restore structural integrity to hair bundles and restore vibration sensitivity in 7-8 mill (Watson, Mire and Hudson, 1998. Hear. Res. 115, 119-128). We here report that exogenously supplied ATP enhances the rate by which RP restore vibration sensitivity. A bimodal dose response to ATP indicates maximal enhancement at picomolar and micromolar concentrations of ATP. At these concentrations of ATP, vibration sensitivity is restored in 2 min. These data suggest that at least two ATPases exhibiting different binding affinities for ATP are involved in the repair process. Whereas the higher affinity site is specific for ATP, the lower affinity site does not discriminate between ATP and ADP. Nucleotidase cytochemistry localizes ATPase activity in isolated repair proteins. In the absence of exogenously added RP, sea anemones secrete and consume ATP during the 4 h recovery period after 1 h exposure to calcium free seawater. In the presence of exogenously added RP, ATP is secreted and then consumed within 10 min. Quinacrine cytochemistry localizes possible stores of ATP in the apical cytoplasm of sensory neurons located at the center of the hair bundle. According to our model, ATP is secreted by the sensory neuron after its hair bundle loses structural integrity. Hydrolysis of ATP by repair proteins is essential to the repair process. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ SW Louisiana, Dept Biol, Lafayette, LA 70504 USA. RP Watson, GM (reprint author), Univ SW Louisiana, Dept Biol, POB 42451, Lafayette, LA 70504 USA. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X Budelmann B.-U., 1988, P757 Housley GD, 1998, HEARING RES, V119, P1, DOI 10.1016/S0378-5955(97)00206-2 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 Lemasters JJ, 1978, METHOD ENZYMOL, V57, P36 LIN SH, 1991, BIOCHEM J, V278, P155 MIRE P, 1997, HEARING RES, V113, P234 MUNOZ DJB, 1995, HEARING RES, V90, P119, DOI 10.1016/0378-5955(95)00153-5 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 PLESNER L, 1995, INT REV CYTOL, V158, P141 PREYER S, 1995, HEARING RES, V89, P187, DOI 10.1016/0378-5955(95)00136-5 Sugasawa M, 1996, J PHYSIOL-LONDON, V491, P707 WATSON GM, 1994, J EXP ZOOL, V268, P177, DOI 10.1002/jez.1402680302 Watson GM, 1997, HEARING RES, V107, P53, DOI 10.1016/S0378-5955(97)00022-1 Watson GM, 1998, J EXP ZOOL, V281, P582 Watson GM, 1998, HEARING RES, V115, P119, DOI 10.1016/S0378-5955(97)00185-8 Watson GM, 1999, CURR TOP DEV BIOL, V43, P51 WATSON GM, 1994, INT REV CYTOL, V156, P275 WATSON GM, 1992, EXP CELL RES, V198, P8, DOI 10.1016/0014-4827(92)90142-U WHITE PN, 1995, HEARING RES, V90, P97, DOI 10.1016/0378-5955(95)00151-1 ZHAO Y, 1996, P NATL ACAD SCI USA, V94, P15469 NR 22 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 1 EP 12 DI 10.1016/S0378-5955(99)00087-8 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200001 PM 10511619 ER PT J AU Reed, MC Blum, JJ AF Reed, MC Blum, JJ TI Model calculations of steady state responses to binaural stimuli in the dorsal nucleus of the lateral lemniscus SO HEARING RESEARCH LA English DT Article DE binaural processing; auditory brainstem; lateral lemniscus ID KAINIC ACID LESIONS; AMPLITUDE-MODULATED SIGNALS; SUPERIOR OLIVARY COMPLEX; INFERIOR COLLICULUS; MOUSTACHE BAT; GABAERGIC INHIBITION; SOUND LOCALIZATION; ALBINO-RAT; SINGLE NEURONS; AUDITORY-NERVE AB Several studies have been performed in which both the time-dependent and steady state output of cells in the dorsal nucleus of the lateral lemniscus (DNLL) have been measured in response to binaural sound stimulation. In this paper, a mathematical and computational model for the steady state output of DNLL cells is formulated. The model includes ascending connections from both lateral and medial superior olives (LSO and MSG) as well connections from interneurons in the DNLL and connections from the contralateral DNLL through the commissure of Probst. Our intent is to understand how the steady state behavior arises from the cell properties in and connectional patterns from lower brainstem nuclei. In particular, we examine the connectional hypotheses put forward by Markovitz and Pollak (1994) to explain the observed behavior of EI, EI/F, EE/I and EE/FI cells. Using these connections (with minor modifications) and cells with simple input-output relations, we are able to account for the steady state behavior of these cell types. We are able to explain interesting features of the data not commented on before: for example, the initial dip in spike output for EE cells at low ipsilateral sound levels. The presence of an inhibitory interneuron in the DNLL is essential for facilitation. In addition, we examine the effects of the MSO and the commissure of Probst on DNLL output. Furthermore, we propose a simple mechanism by which the cells of the DNLL and LSO could create a topographic place map in the inferior colliculus. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Duke Univ, Dept Math, Durham, NC 27708 USA. Duke Univ, Med Ctr, Dept Cell Biol, Div Physiol, Durham, NC 27710 USA. RP Reed, MC (reprint author), Duke Univ, Dept Math, Durham, NC 27708 USA. CR AITKIN LM, 1970, J NEUROPHYSIOL, V33, P421 BLUM JJ, 1991, J ACOUST SOC AM, V90, P1968, DOI 10.1121/1.401676 Brugge JF, 1992, MAMMALIAN AUDITORY P, P1 BRUGGE JF, 1970, J NEUROPHYSIOL, V33, P441 Burger RM, 1998, J NEUROPHYSIOL, V80, P1686 CARNEY LH, 1994, HEARING RES, V76, P31, DOI 10.1016/0378-5955(94)90084-1 CARR CE, 1993, ANNU REV NEUROSCI, V16, P223, DOI 10.1146/annurev.ne.16.030193.001255 Covey E., 1995, HEARING BATS, P235 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 FUZESSERY ZM, 1990, J NEUROPHYSIOL, V63, P1128 GLENN SL, 1992, J NEUROSCI, V12, P3688 Henkel CK, 1997, J COMP NEUROL, V380, P136 Irvine D. R. F., 1992, MAMMALIAN AUDITORY P, P153 Irvine DR, 1986, AUDITORY BRAINSTEM Ito M, 1996, J NEUROPHYSIOL, V76, P3493 Kelly JB, 1998, HEARING RES, V122, P25, DOI 10.1016/S0378-5955(98)00082-3 Kelly JB, 1997, HEARING RES, V104, P112, DOI 10.1016/S0378-5955(96)00182-7 Kelly JB, 1996, BEHAV NEUROSCI, V110, P1445, DOI 10.1037//0735-7044.110.6.1445 Kidd SA, 1996, J NEUROSCI, V16, P7390 Konishi M., 1991, Neural Computation, V3, DOI 10.1162/neco.1991.3.1.1 LI L, 1992, J NEUROSCI, V12, P4530 MARKOVITZ NS, 1994, HEARING RES, V73, P121, DOI 10.1016/0378-5955(94)90290-9 MARKOVITZ NS, 1993, HEARING RES, V71, P51, DOI 10.1016/0378-5955(93)90020-2 METZNER W, 1987, J COMP PHYSIOL A, V160, P395, DOI 10.1007/BF00613029 PARK TJ, 1994, J NEUROPHYSIOL, V72, P1080 Peddicord R, 1998, HEARING RES, V123, P111, DOI 10.1016/S0378-5955(98)00102-6 Pollak G. D., 1995, HEARING BATS, P296 POLLAK GD, 1989, NEUROBIOLOGY OF SENSORY SYSTEMS, P469 Pollak GD, 1997, ANN OTO RHINOL LARYN, V106, P44 REED MC, 1990, J ACOUST SOC AM, V88, P1442, DOI 10.1121/1.399721 SACHS MB, 1979, J ACOUST SOC AM, V66, P470, DOI 10.1121/1.383098 SALLY SL, 1992, BRAIN RES, V572, P5, DOI 10.1016/0006-8993(92)90444-E Kelly JB, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P329, DOI 10.1007/978-1-4419-8712-9_31 van Adel BA, 1998, BEHAV NEUROSCI, V112, P432, DOI 10.1037/0735-7044.112.2.432 Wu SH, 1996, J NEUROPHYSIOL, V75, P1271 YANG L, 1994, AUDIT NEUROSCI, V1, P1 YANG LC, 1994, J NEUROPHYSIOL, V71, P1999 Yang LC, 1998, HEARING RES, V122, P125, DOI 10.1016/S0378-5955(98)00088-4 YANG LC, 1994, J NEUROPHYSIOL, V71, P2014 Yang LC, 1997, J NEUROPHYSIOL, V77, P324 Yang LC, 1996, J COMP NEUROL, V373, P575, DOI 10.1002/(SICI)1096-9861(19960930)373:4<575::AID-CNE7>3.0.CO;2-Z YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 NR 42 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 13 EP 28 DI 10.1016/S0378-5955(99)00096-9 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200002 PM 10511620 ER PT J AU Stenberg, AE Wang, H Sahlin, L Hultcrantz, M AF Stenberg, AE Wang, H Sahlin, L Hultcrantz, M TI Mapping of estrogen receptors alpha and beta in the inner ear of mouse and rat SO HEARING RESEARCH LA English DT Article DE estrogen receptor; inner ear; rat; mouse; hearing; presbyacusis; sex difference; Turner's syndrome ID EXPRESSION; WOMEN AB The sex hormone estrogen is classically known to influence growth, differentiation and function of peripheral tissues of both the female and male reproductive tract, mediated through the estrogen receptors alpha and beta. The influence of estrogens on the ear and hearing is yet not fully investigated, though some studies have suggested that estrogens may influence hearing functions. The aim of this study was to map eventual estrogen receptors in the inner ear in mouse and rat. Paraffin embedded sections of mouse and rat inner ear were immunostained with antibodies against estrogen receptors alpha and beta. Estrogen receptors alpha and beta containing cells were found in the inner ear, showing a unique distribution pattern, both in the auditory pathways and in the water/ion regulating areas. The presence of estrogen receptors indicates that estrogens may have an effect on the inner ear and hearing functions. (C) 1999 Elsevier Science B.V. All ri hts reserved. C1 Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. Karolinska Hosp, Dept Woman & Child Hlth, Div Reprod Endocrinol, S-17176 Stockholm, Sweden. RP Hultcrantz, M (reprint author), Karolinska Hosp, Dept Otorhinolaryngol, S-17176 Stockholm, Sweden. CR ANNIKO M, 1980, MICRON, V11, P103, DOI 10.1016/0047-7206(80)90146-6 COLEMAN JR, 1994, HEARING RES, V80, P209, DOI 10.1016/0378-5955(94)90112-0 ERICHSEN S, 1996, ACTA OTOLARYNGOL STO, V116, P92 Fridberger A, 1996, ACTA OTO-LARYNGOL, V116, P17, DOI 10.3109/00016489609137707 Goldfien A, 1991, BASIC CLIN ENDOCRINO, P447 HULTCRANTZ M, 1994, HEARING RES, V76, P127, DOI 10.1016/0378-5955(94)90094-9 HULTCRANTZ M, 1999, UNPUB HEAR RES Jonsson R, 1998, SCAND AUDIOL, V27, P81, DOI 10.1080/010503998420324 Kuiper GGJM, 1998, FRONT NEUROENDOCRIN, V19, P253, DOI 10.1006/frne.1998.0170 KUMAGAMI H, 1994, ACTA OTO-LARYNGOL, V114, P48, DOI 10.3109/00016489409126015 LAUGEL GR, 1987, HEARING RES, V31, P245, DOI 10.1016/0378-5955(87)90194-8 LOSORDO DW, 1994, CIRCULATION, V89, P1501 Saunders PTK, 1997, J ENDOCRINOL, V154, pR13, DOI 10.1677/joe.0.154R013 SWANSON SJ, 1988, J SPEECH HEAR RES, V31, P569 TURNER RT, 1994, ENDOCR REV, V15, P275, DOI 10.1210/er.15.3.275 WHARTON JA, 1990, AUDIOLOGY, V29, P196 NR 16 TC 66 Z9 69 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 29 EP 34 DI 10.1016/S0378-5955(99)00098-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200003 PM 10511621 ER PT J AU Lasky, RE Soto, AA Luck, ML Laughlin, NK AF Lasky, RE Soto, AA Luck, ML Laughlin, NK TI Otoacoustic emission, evoked potential, and behavioral auditory thresholds in the rhesus monkey (Macaca mulatta) SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; auditory brainstem evoked response; auditory threshold; rhesus monkey ID DISTORTION-PRODUCT; EARS AB Distortion product otoacoustic emission (DPOAE), auditory brainstem evoked response (ABR), and behavioral thresholds were recorded in a group of 15 adult rhesus monkeys with normal auditory function. DPOAE thresholds were recorded with stimulus parameters selected to maximize signal-to-noise ratio. Additional averaging at the lowest frequencies ensured comparable noise levels across frequencies. DPOAE thresholds decreased with increasing frequency (f(2) = 0.5-16 kHz) and at 16 kHz were close to 0 dB SPL. ABR thresholds were best from 1 through 16 kHz (32-38 dB peSPL); higher at 0.5 (45 dB peSPL), 24 (39 dB peSPL), and 30 kHz (49 dB peSPL). At all levels including threshold, the early ABR waves (II and I) were more prominent at the high frequencies while the later waves (IV and V) were more prominent at the low frequencies. The behavioral thresholds recorded were similar to those reported by other researchers although elevated by about 10 dB presumably because of the complexity of the threshold task. DPOAE and ABR thresholds can be reliably and efficiently recorded in the rhesus monkey and provide information concerning site of processing in the auditory pathway not directly available from behavioral data. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Wisconsin, Sch Med, Dept Neurol, Madison, WI 53792 USA. Univ Wisconsin, Harlow Ctr Biol Psychol, Madison, WI 53715 USA. RP Lasky, RE (reprint author), Univ Wisconsin, Sch Med, Dept Neurol, H6-528 Clin Sci Bldg,600 Highland Ave, Madison, WI 53792 USA. CR FELDMAN ML, 1995, ASS RES OTOL, V18, P537 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 *I LAB AN RES COMM, 1985, GUID CAR US LAB AN KAMADA T, 1991, J MED PRIMATOL, V20, P284 KUMMER P, 1998, IN PRESS J ACOUST SO LASKY RE, 1995, HEARING RES, V89, P35, DOI 10.1016/0378-5955(95)00120-1 LASKY RE, 1998, ASS RES OTOL, V21, P600 LASKY RE, 1995, NEUROTOXICOL TERATOL, V17, P633, DOI 10.1016/0892-0362(95)02006-3 LASKY RE, 1997, ASS RES OTOL, V20, P777 Lasky RE, 1998, J ACOUST SOC AM, V103, P992, DOI 10.1121/1.421246 Laughlin NK, 1999, DEV PSYCHOBIOL, V34, P37, DOI 10.1002/(SICI)1098-2302(199901)34:1<37::AID-DEV6>3.0.CO;2-W LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 Neely S. T., 1993, 17 BOYS TOWN NAT RES OWREN MJ, 1988, J COMP PSYCHOL, V102, P99 PARK JY, 1995, HEARING RES, V86, P147, DOI 10.1016/0378-5955(95)00065-C PFINGST BE, 1975, J ACOUST SOC AM, V57, P431, DOI 10.1121/1.380466 PFINGST BE, 1978, HEARING RES, V1, P43, DOI 10.1016/0378-5955(78)90008-4 Rhode WS, 1996, AUDIT NEUROSCI, V3, P101 Schroeder C E, 1995, Electroencephalogr Clin Neurophysiol Suppl, V44, P55 Stapells D. R., 1994, PRINCIPLES APPL AUDI, P251 STAPELLS DR, 1990, AUDIOLOGY, V29, P262 STEBBINS WC, 1966, SCIENCE, V153, P1646, DOI 10.1126/science.153.3744.1646-a WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2359, DOI 10.1121/1.411960 NR 24 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 35 EP 43 DI 10.1016/S0378-5955(99)00100-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200004 PM 10511622 ER PT J AU Naito, R Murofushi, T Mizutani, M Kaga, K AF Naito, R Murofushi, T Mizutani, M Kaga, K TI Auditory brainstem responses, electrocochleograms, and cochlear microphonics in the myelin deficient mutant hamster 'bt' SO HEARING RESEARCH LA English DT Article DE hamster; mutant; dysmyelination; ABR; compound action potential ID NERVE AB Electrophysiological studies of the auditory pathway were performed on the mutant hamster 'bt' which is known to have myelin deficiencies in the central nervous system. Auditory brainstem responses (ABRs), electrocochleograms (EcochGs), and cochlear microphonics (CMs) were recorded. ABRs in 'bt' demonstrated markedly transformed waveforms with significantly prolonged latencies. EcochG in 'bt' showed significantly prolonged NI latencies of the compound action potentials (CAPs) while 'bt' showed normal CMs. The myelin deficient mutant hamster 'bt' may have myelin deficiencies not only in the brainstem auditory pathway but also in the cochlear nerve. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Tokyo, Dept Otolaryngol, Bunkyo Ku, Tokyo, Japan. Nippon Inst Biol Sci, Yamanashi, Japan. RP Naito, R (reprint author), Sanraku Hosp, Dept Otolaryngol, Chiyoda Ku, Kandasurugadai 2-5, Tokyo 1018326, Japan. CR BRISMAR T, 1981, ACTA PHYSIOL SCAND, V113, P161, DOI 10.1111/j.1748-1716.1981.tb06877.x CRAGG BG, 1964, J NEUROL NEUROSUR PS, V27, P106, DOI 10.1136/jnnp.27.2.106 EGERMONT JJ, 1976, REV LARYNGOL S, V97, P497 KOITCHEV K, 1982, ACTA OTO-LARYNGOL, V94, P431, DOI 10.3109/00016488209128931 MIZUTANI M, 1986, EXP ANIM TOKYO, V35, P175 MOLLER AR, 1983, J NEUROSURG, V59, P493, DOI 10.3171/jns.1983.59.3.0493 NUNOYA T, 1985, ACTA NEUROPATHOL, V65, P305 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 NR 9 TC 18 Z9 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 44 EP 48 DI 10.1016/S0378-5955(99)00107-0 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200005 PM 10511623 ER PT J AU Yates, GK Withnell, RH AF Yates, GK Withnell, RH TI The role of intermodulation distortion in transient-evoked otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE click-evoked otoacoustic emission; non-linearity; intermodulation distortion ID STIMULATED ACOUSTIC EMISSIONS; BASILAR-MEMBRANE MECHANICS; GUINEA-PIG; NORMAL-HEARING; EAR; RESPONSES; COCHLEA; TONE; SUPPRESSION; GENERATOR AB Transient-evoked otoacoustic emissions (TEOAEs) are low-intensity sounds recorded in the external ear canal immediately following stimulation by a transient stimulus, typically a click. While the details of their production is unknown, there is evidence to suggest that the amplitude of each component frequency reflects the physiological condition of the corresponding region of the cochlea. Certain observations are at variance with this assumption, however, suggesting that pathology at a basal site within the cochlea might affect the production of emissions at frequencies which are not characteristic for that site. We have recorded click-evoked emissions in guinea pigs using high-pass clicks and found emissions at frequencies which are not present in the stimulus and which could not, therefore, have originated from the characteristic place for those emission frequencies. These new frequencies are, by definition, intermodulation distortion frequencies and must have been generated from combinations of frequencies in the stimulus by non-linear processes within the cochlea. Further processing of the emissions by Kemp's technique of non-linear recovery showed that the magnitude of emissions at frequencies within the stimulus frequency pass-band was approximately the same as that of frequencies not present in the stimulus. We propose that, in guinea pigs at least, most of the click-evoked emission energy is generated as intermodulation distortion, produced by non-linear intermodulation between various frequency components of the stimulus. If this result is confirmed in humans, many of the anomalies in the literature may be resolved. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. RP Yates, GK (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. CR Avan P, 1997, J ACOUST SOC AM, V101, P2771, DOI 10.1121/1.418564 AVAN P, 1993, HEARING RES, V70, P109, DOI 10.1016/0378-5955(93)90055-6 AVAN P, 1995, J ACOUST SOC AM, V97, P1 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWN AM, 1993, BIOPHYSICS HAIR CELL, P72 Brown AM, 1996, J ACOUST SOC AM, V100, P3260, DOI 10.1121/1.417209 COOPER NP, 1992, HEARING RES, V63, P163, DOI 10.1016/0378-5955(92)90083-Y ELLIOTT E, 1958, NATURE, V181, P1076, DOI 10.1038/1811076a0 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 Gaskill SA, 1996, J ACOUST SOC AM, V100, P3268, DOI 10.1121/1.417210 Heitmann J, 1998, J ACOUST SOC AM, V103, P1527, DOI 10.1121/1.421290 HILGER AW, 1995, HEARING RES, V84, P1, DOI 10.1016/0378-5955(95)00007-Q KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 Kruglov AV, 1997, ACTA OTO-LARYNGOL, V117, P174, DOI 10.3109/00016489709117763 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MANLEY GA, 1983, MECH HEARING, P2 NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 Prieve BA, 1996, J ACOUST SOC AM, V99, P3077, DOI 10.1121/1.414794 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 SHERA CA, 1993, J ACOUST SOC AM, V93, P3333, DOI 10.1121/1.405717 SOUTER M, 1995, HEARING RES, V90, P1, DOI 10.1016/0378-5955(95)00124-9 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 SUTTON GJ, 1985, ACUSTICA, V58, P57 UEDA H, 1992, HEARING RES, V62, P199, DOI 10.1016/0378-5955(92)90187-R van den Brink G, 1970, FREQUENCY ANAL PERIO, P362 WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 Withnell RH, 1998, J ACOUST SOC AM, V104, P344, DOI 10.1121/1.423243 Withnell RH, 1998, J ACOUST SOC AM, V104, P350, DOI 10.1121/1.423292 XU L, 1994, HEARING RES, V74, P173 ZUREK PM, 1985, J ACOUST SOC AM, V78, P340, DOI 10.1121/1.392496 ZWEIG G, 1995, J ACOUST SOC AM, V98, P2018, DOI 10.1121/1.413320 ZWICKER E, 1981, HEARING RES, V4, P43, DOI 10.1016/0378-5955(81)90035-6 NR 41 TC 49 Z9 51 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 49 EP 64 DI 10.1016/S0378-5955(99)00108-2 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200006 PM 10511624 ER PT J AU Mom, T Bonfils, P Gilain, L Avan, P AF Mom, T Bonfils, P Gilain, L Avan, P TI Vulnerability of the gerbil cochlea to sound exposure during reversible ischemia SO HEARING RESEARCH LA English DT Article DE noise-induced hearing loss; distortion-product otoacoustic emission; cochlear blood flow; ischemia; reperfusion ID PRODUCT OTOACOUSTIC EMISSIONS; ACOUSTIC DISTORTION PRODUCTS; LASER-DOPPLER MEASUREMENTS; GUINEA-PIG COCHLEA; FOREBRAIN ISCHEMIA; BLOOD-FLOW; TRANSIENT ISCHEMIA; NEUROMA SURGERY; THRESHOLD SHIFT; ACTIVE PROCESS AB Cochlear ischemia induces a sensorineural hearing loss, in part through a fast functional impairment of outer hair cellls. Assuming that the cochlea is rendered fragile during ischemia and reperfusion and that stimulation itself can jeopardize its functional recovery, we used a model of reversible selective cochlear ischemia in Mongolian gerbils to establish what type of sound exposure call be deleterious during and immediately after reversible ischemia. Several groups of gerbils were used, with different ischemia durations and levels of sound exposure. Control groups were only exposed to tones at 80 and 90 dB SPL during 30 min, while other groups underwent complete and fully reversible blockage of the labyrinthine artery, during 5.5 or 8 min, and were exposed to 60 or SO dB SPL tones during 30 min. The amount of ischemia and reperfusion was measured by means of laser Doppler velocimetry, whereas outer hair cells' function was continuously monitored through distortion-product otoacoustic emissions (DPOAEs). The losses of DPOAE levels after 8 min transient ischemia and 60 dB SPL exposure were as large as those induced by 80 dB SPL exposures combined with 5.5 min ischemia, or 90 dB SPL exposures without ischemia, with a maximum loss around 25-30 dB, half an octave above the stimulus frequency. These results give evidence for an extremely high cochlear vulnerability to low-level sound exposure when associated with reversible ischemia. This vulnerability may have important clinical consequences in patients with cochlear circulatory disturbances. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Auvergne, Fac Med, Lab Biophys Sensorielle, EA 2667, F-63001 Clermont Ferrand, France. UPRESA CNRS 7060, Paris, France. RP Avan, P (reprint author), Univ Auvergne, Fac Med, Lab Biophys Sensorielle, EA 2667, POB 38, F-63001 Clermont Ferrand, France. CR Allen J. B, 1990, USER MANUAL CUBDIS D AMES A, 1995, J CEREBR BLOOD F MET, V15, P433 Avan P, 1998, EUR J NEUROSCI, V10, P1764, DOI 10.1046/j.1460-9568.1998.00188.x Avan P, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P65 BILLETT TE, 1989, HEARING RES, V41, P189, DOI 10.1016/0378-5955(89)90010-5 Bonne C, 1998, GEN PHARMACOL, V30, P275, DOI 10.1016/S0306-3623(97)00357-1 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Chan PH, 1996, STROKE, V27, P1124 DAS DK, 1993, PATHOPHYSIOLOGY REPE, P149 Davies K J, 1995, Biochem Soc Symp, V61, P1 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DECORY L, 1992, NOISE INDUCED HEARIN, P73 Dowdy S., 1991, STAT RES Hakuba N, 1997, NEUROSCI LETT, V230, P69, DOI 10.1016/S0304-3940(97)00462-X HYSLOP PA, 1995, BRAIN RES, V671, P181, DOI 10.1016/0006-8993(94)01291-O KANO T, 1994, BRAIN RES, V641, P149, DOI 10.1016/0006-8993(94)91829-5 KATO H, 1995, BRAIN RES, V679, P1, DOI 10.1016/0006-8993(95)00198-Y KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KLIS JFL, 1988, HEARING RES, V36, P163, DOI 10.1016/0378-5955(88)90058-5 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 LEVINE RA, 1993, ANN OTO RHINOL LARYN, V102, P127 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MCCORD JM, 1985, NEW ENGL J MED, V312, P159 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 MILLS DM, 1994, AUDIT NEUROSCI, V1, P77 Mom T, 1997, BRAIN RES, V751, P20, DOI 10.1016/S0006-8993(96)01388-1 NAKAMURA K, 1993, BRAIN RES, V613, P181, DOI 10.1016/0006-8993(93)90898-W NUTTALL AL, 1984, HEARING RES, V16, P1, DOI 10.1016/0378-5955(84)90021-2 OHTSUKI T, 1993, BRAIN RES, V620, P305, DOI 10.1016/0006-8993(93)90171-I Patuzzi R., 1996, COCHLEA, P186 PERLMAN H B, 1959, Laryngoscope, V69, P591 Preyer S, 1996, Audiol Neurootol, V1, P3 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1995, ACTA ACUST, V3, P75 RANDOLF HB, 1990, EUR ARCH OTO-RHINO-L, V247, P226 Ren TY, 1995, HEARING RES, V92, P30, DOI 10.1016/0378-5955(95)00192-1 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 SAUNDERS JC, 1986, HEARING RES, V23, P245, DOI 10.1016/0378-5955(86)90113-9 SCHEIBE F, 1990, EUR ARCH OTO-RHINO-L, V247, P20 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 Schuknecht H. F., 1974, PATHOLOGY EAR SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P511 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P457 SEREGHY T, 1993, STROKE, V24, P1702 SORIANO MA, 1995, BRAIN RES, V670, P317, DOI 10.1016/0006-8993(94)01352-I TELISCHI FF, 1995, AM J OTOL, V16, P597 WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 WIDICK MP, 1994, OTOLARYNG HEAD NECK, V111, P407 Zweig G, 1976, Cold Spring Harb Symp Quant Biol, V40, P619 NR 53 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 65 EP 74 DI 10.1016/S0378-5955(99)00109-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200007 PM 10511625 ER PT J AU Jones, TA Jones, SM AF Jones, TA Jones, SM TI Short latency compound action potentials from mammalian gravity receptor organs SO HEARING RESEARCH LA English DT Article DE vestibular; vestibular evoked potential; linear acceleration; otolith; gerbil; mouse; rat; guinea pig; VsEP ID VESTIBULAR EVOKED-POTENTIALS; PULSED LINEAR ACCELERATION; UNANESTHETIZED ANIMALS; PERIPHERAL GENERATORS; JAPANESE-QUAIL; RESPONSES; MICROGRAVITY; CAT; WEIGHTLESSNESS; CHICKEN AB Gravity receptor function was characterized in four mammalian species using far-field vestibular evoked potentials (VsEPs). VsEPs are compound action potentials of the vestibular nerve and central relays that are elicited by linear acceleration ramps applied to the cranium. Rats, mice, guinea pigs, and gerbils were studied. In all species, response onset occurred within 1.5 ms of the stimulus onset. Responses persisted during intense (116 dBSPL) wide-band (50 to 50 000 Hz) forward masking, whereas auditory responses to intense clicks (112 dBpeSPL) were eliminated under the same conditions. VsEPs remained after cochlear extirpation but were eliminated following bilateral labyrinthectomy. Responses included a series of positive and negative peaks that occurred within 8 ms of stimulus onset (range of means at +6 dBre: 1.0 g/ms: P1 = 908 to 1062 mu s, N1 = 1342 to 1475 mu s, P2 = 1632 to 1952 mu s, N2 = 2038 to 2387 mu s) Mean response amplitudes at +6 dBre: 1.0 g/ms ranged from 0.14 to 0.99 mu V. VsEP input/output functions revealed latency slopes that varied across peaks and species ranging from -19 to -51 mu s/dB. Amplitude-intensity slopes also varied ranging from 0.04 to 0.08 mu V/dB for rats and mice. Latency Values were comparable to those of birds although amplitudes were substantially smaller in mammals. VsEP threshold values were considerably higher in mammals compared to birds and ranged from -8.1 to -10.5 dBre 1.0 g/ms across species. These results support the hypothesis that mammalian gravity receptors are less sensitive to dynamic stimuli than are those of birds. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Missouri, Sch Med, Dept Surg, Columbia, MO 65212 USA. Univ Missouri, Sch Med, Dept Physiol, Columbia, MO 65212 USA. Univ Missouri, Sch Med, Div Otolaryngol, Dept Surg, Columbia, MO 65212 USA. RP Jones, TA (reprint author), Univ Missouri, Sch Med, Dept Surg, 207 Allton Bldg,DC 375-00, Columbia, MO 65212 USA. CR Bergstrom RA, 1998, GENETICS, V150, P815 BOHMER A, 1995, AM J OTOL, V16, P498 Böhmer A, 1995, Acta Otolaryngol Suppl, V520 Pt 1, P120, DOI 10.3109/00016489509125206 Böhmer A, 1983, Adv Otorhinolaryngol, V30, P54 ELIDAN J, 1995, ACTA OTO-LARYNGOL, V115, P141, DOI 10.3109/00016489509139277 ELIDAN J, 1984, ANN OTO RHINOL LARYN, V93, P257 ELIDAN J, 1984, J OTOLARYNGOL S, V9, P111 Fermin CD, 1998, HISTOL HISTOPATHOL, V13, P1103 Fermin CD, 1996, HISTOL HISTOPATHOL, V11, P407 GURYEVA TS, 1993, ACTA VET BRNO, V62, pS25, DOI 10.2754/avb199362suppl60025 HIXSON WC, 1996, MONOGRAPH NAVAC AERO, V14, pR93 Jones SM, 1997, J COMP PHYSIOL A, V180, P631, DOI 10.1007/s003590050079 Jones SM, 1998, HEARING RES, V121, P161, DOI 10.1016/S0378-5955(98)00074-4 Jones SM, 1999, HEARING RES, V135, P56, DOI 10.1016/S0378-5955(99)00090-8 Jones SM, 1996, J VESTIBUL RES-EQUIL, V6, P71 JONES TA, 1993, ACTA VET BRNO, V62, pS35, DOI 10.2754/avb199362suppl60035 JONES TA, 1992, ELECTROEN CLIN NEURO, V82, P377, DOI 10.1016/0013-4694(92)90007-5 Jones TA, 1998, J VESTIBUL RES-EQUIL, V8, P253 JONES TA, 1995, ABSTR SOC NEUROSCI, V21, P919 JONES TA, 1983, J NEUROSCI METH, V7, P261, DOI 10.1016/0165-0270(83)90008-0 JONES TA, 1992, HEARING RES, V62, P181, DOI 10.1016/0378-5955(92)90184-O JONES TA, 1989, AM J OTOLARYNG, V10, P327, DOI 10.1016/0196-0709(89)90108-7 KOSTAL L, 1993, ACTA VET BRNO, V62, pS65 KOSTAL L, 1993, PHYSIOLOGIST, V36, P50 LANGE ME, 1988, THESIS U NEBRASKA LI LANGE ME, 1989, ASGSB B, V3, P31 LANGE ME, 1990, ASS RES OTOLARYNGOL, V390, P343 LI G, 1993, ELECTROEN CLIN NEURO, V88, P225, DOI 10.1016/0168-5597(93)90007-C LI G, 1995, ARCH OTOLARYNGOL, V121, P34 Lindeman H H, 1973, Adv Otorhinolaryngol, V20, P405 Nazareth AM, 1998, J VESTIBUL RES-EQUIL, V8, P233 ROSENHAL.U, 1970, ARCH KLIN EXP OHR, V197, P154, DOI 10.1007/BF00306164 Ross M D, 1993, J Vestib Res, V3, P241 Ross M D, 1994, Acta Otolaryngol Suppl, V516, P1 Si XH, 1997, EXP BRAIN RES, V117, P242, DOI 10.1007/s002210050219 WEISLEDER P, 1990, ELECTROEN CLIN NEURO, V76, P362, DOI 10.1016/0013-4694(90)90037-K NR 36 TC 37 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 75 EP 85 DI 10.1016/S0378-5955(99)00110-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200008 PM 10511626 ER PT J AU Tabuchi, K Ito, Z Wada, T Takahashi, K Hara, A Kusakari, J AF Tabuchi, K Ito, Z Wada, T Takahashi, K Hara, A Kusakari, J TI Effect of A1 adenosine receptor agonist upon cochlear dysfunction induced by transient ischemia SO HEARING RESEARCH LA English DT Article DE cochlea; compound action potential (CAP); transient ischemia; 2-chloro-N6-cyclopentyladenosine (CCPA); A1 adenosine receptor ID CONDUCTANCE; CHINCHILLA; ACTIVATION; NEURONS; CALCIUM; INJURY; HEART; A(1) AB The present study was undertaken to determine whether 2-chloro-N6-cyclopentyladenosine (CCPA), a highly selective Al adenosine receptor agonist, attenuated cochlear dysfunction induced by transient ischemia or not. Ischemia of different durations (15, 30 or 60 min) was induced in 46 albino guinea pigs by transiently pressing the labyrinthine artery. CCPA or physiological saline solution was intraperitoneally administered to the animals 15 min prior to ischemia. The post-ischemic CAP threshold shift from the pre-administration value was measured 4 h after the onset of reperfusion to assess post-ischemic cochlear dysfunction. A statistically significant reduction in the CAP threshold shift was seen in CCPA-given animals after 15- and 30-min ischemia, whereas there was no statistical difference after 60-min ischemia. These results suggest that Al adenosine receptor agonist exerts a protective effect on the cochlear injury induced by transient ischemia of intermediate duration. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, Tsukuba, Ibaraki 3058575, Japan. RP Kusakari, J (reprint author), Univ Tsukuba, Inst Clin Med, Dept Otolaryngol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. CR DRAGUNOW M, 1988, TRENDS PHARMACOL SCI, V9, P193, DOI 10.1016/0165-6147(88)90079-X Ford MS, 1997, HEARING RES, V105, P130, DOI 10.1016/S0378-5955(96)00204-3 Hu BH, 1997, HEARING RES, V113, P198, DOI 10.1016/S0378-5955(97)00143-3 Jordan JE, 1997, J PHARMACOL EXP THER, V280, P301 KLOTZ KN, 1989, N-S ARCH PHARMACOL, V340, P679, DOI 10.1007/BF00717744 Kusakari J, 1981, Auris Nasus Larynx, V8, P55 LOHSE MJ, 1988, N-S ARCH PHARMACOL, V337, P687 Lozza G, 1997, PHARMACOL RES, V35, P57, DOI 10.1006/phrs.1996.0120 MAGER R, 1990, BRAIN RES, V532, P58, DOI 10.1016/0006-8993(90)91741-X NARIO K, 1994, EUR ARCH OTO-RHINO-L, V251, P428 PAUL S, 1990, MOL PHARMACOL, V37, P870 RAMKUMAR V, 1994, AM J PHYSIOL, V27, pC731 Revan S, 1996, J BIOL CHEM, V271, P17114 RUDOLPHI KA, 1992, TRENDS PHARMACOL SCI, V13, P439, DOI 10.1016/0165-6147(92)90141-R SCHUBERT P, 1986, BRAIN RES, V376, P382, DOI 10.1016/0006-8993(86)90204-0 SCHUBERT P, 1988, BRAIN RES, V458, P162, DOI 10.1016/0006-8993(88)90510-0 SIMPSON RE, 1992, J NEUROCHEM, V58, P1683, DOI 10.1111/j.1471-4159.1992.tb10041.x Stambaugh K, 1997, AM J PHYSIOL-HEART C, V273, pH501 Tabuchi K, 1998, HEARING RES, V126, P28, DOI 10.1016/S0378-5955(98)00142-7 Tracey WR, 1997, CARDIOVASC RES, V33, P410, DOI 10.1016/S0008-6363(96)00240-4 TRUSSELL LO, 1985, P NATL ACAD SCI USA, V82, P4857, DOI 10.1073/pnas.82.14.4857 VonLubitz DKJE, 1996, EUR J PHARMACOL, V302, P43, DOI 10.1016/0014-2999(96)00101-X NR 22 TC 9 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 86 EP 90 DI 10.1016/S0378-5955(99)00111-2 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200009 PM 10511627 ER PT J AU Capsius, B Leppelsack, HJ AF Capsius, B Leppelsack, HJ TI Response patterns and their relationship to frequency analysis in auditory forebrain centers of a songbird SO HEARING RESEARCH LA English DT Article DE auditory cortex analogue; field L; frequency analysis; starling; mapping; telencephalon ID STARLING STURNUS-VULGARIS; FINCHES TAENOPYGIA-GUTTATA; CORTEX ANALOG; FUNCTIONAL-ORGANIZATION; FIELD-L; DISCRIMINATION; CONNECTIONS; REPRESENTATION; NEOSTRIATUM; STIMULI AB In the field L complex, the auditory part of the caudal telencephalon, multi-unit recordings were performed in seven awake, adult male starlings (Sturnus vulgaris, L). Pure tones in a frequency range between 0.5 and 6.0 kHz were used as stimuli. The field L complex of starlings consists of at least 11 functionally separated, tonotopically organized subcenters. The auditory processing of frequency information was investigated in eight of these areas. Two kinds of response patterns could be distinguished. The centers NA-L, NA2a, NA3 and NA4 showed phasic and sustained excitation, the other areas responded with phasic excitation only. All these auditory areas show strong tonotopic gradients, each of them representing the complete hearing range. The sharpest picture of the stimulus frequency is represented in the functional area NA-L. In relation to its total size, NA-L shows the smallest active area if stimulated by pure tones. In addition, in NA-L, only the excited neurons are surrounded by inhibited neurons during the response to a pure tone. This leads to an additional sharpening of frequency representation. In comparison with the other auditory areas, NA-L shows the greatest spatial extension of the tonotopic gradient. This, in combination with the smallest active size in NA-L, leads to the conclusion that in the primary projection field NA-L, the most neural space is available for the processing of a given frequency range. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Tech Univ Munich, Inst Zool, D-85747 Garching, Germany. RP Leppelsack, HJ (reprint author), Tech Univ Munich, Inst Zool, Lichtenbergstr 4, D-85747 Garching, Germany. CR AHUSLER U, 1989, THESIS TU MUNCHEN MU BONKE D, 1979, J COMP PHYSIOL, V132, P243 BOORD RL, 1969, ANN NY ACAD SCI, V167, P186, DOI 10.1111/j.1749-6632.1969.tb20444.x Capsius B, 1996, HEARING RES, V96, P59, DOI 10.1016/0378-5955(96)00038-X Ehret G, 1997, J COMP PHYSIOL A, V181, P547, DOI 10.1007/s003590050139 FORTUNE ES, 1992, J COMP NEUROL, V325, P388, DOI 10.1002/cne.903250306 Gehr DD, 1999, NEUROREPORT, V10, P375, DOI 10.1097/00001756-199902050-00030 HEIL P, 1992, J COMP PHYSIOL A, V171, P583 HEIL P, 1991, BRAIN RES, V539, P110, DOI 10.1016/0006-8993(91)90692-O IMIG TJ, 1980, J COMP NEUROL, V192, P293, DOI 10.1002/cne.901920208 KLUMP GM, 1990, J COMP PSYCHOL, V104, P94, DOI 10.1037/0735-7036.104.1.94 KUHN A, 1980, NATURWISSENSCHAFTEN, V67, P102, DOI 10.1007/BF01054703 LANGEMANN U, 1992, HEARING RES, V63, P43, DOI 10.1016/0378-5955(92)90072-U LEPPELSACK EH, 1992, THESIS TU MUNCHEN MU MAIER EH, 1990, J ACOUST SOC AM, V88, P616, DOI 10.1121/1.399765 MOREL A, 1993, J COMP NEUROL, V335, P437, DOI 10.1002/cne.903350312 MULLER CM, 1988, J NEUROPHYSIOL, V59, P1673 REHKAMPER G, 1991, CELL TISSUE RES, V263, P3, DOI 10.1007/BF00318396 ROSE M, 1914, J PSYCHOL NEUROL, V21, P278 SACHS MB, 1978, FED PROC, V37, P2329 SACHS MB, 1978, J COMP PHYSIOL, V126, P347 SAINI KD, 1981, J COMP NEUROL, V198, P209, DOI 10.1002/cne.901980203 THOMAS H, 1993, EUR J NEUROSCI, V5, P882, DOI 10.1111/j.1460-9568.1993.tb00940.x THOMPSON RF, 1960, J NEUROPHYSIOL, V23, P321 Vates GE, 1996, J COMP NEUROL, V366, P613, DOI 10.1002/(SICI)1096-9861(19960318)366:4<613::AID-CNE5>3.0.CO;2-7 WILD JM, 1993, J COMP NEUROL, V337, P32 NR 26 TC 28 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 91 EP 99 DI 10.1016/S0378-5955(99)00112-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200010 PM 10511628 ER PT J AU Pickles, JO van Heumen, WRA Claxton, C AF Pickles, JO van Heumen, WRA Claxton, C TI A tyrosine kinase screen of mouse vestibular maculae SO HEARING RESEARCH LA English DT Article DE tyrosine kinase; PCR screen; FGF receptor; IGF-1 receptor; hair cell; vestibular maculae; mouse ID FIBROBLAST GROWTH-FACTOR; HAIR CELL REGENERATION; INNER-EAR; SENSORY EPITHELIA; MESSENGER-RNA; RAT COCHLEA; EXPRESSION; FAMILY; ADULT; RECEPTORS AB Receptor tyrosine kinases allow extracellular signals to influence intracellular events, while other tyrosine kinases are involved in intracellular signalling. They may therefore be involved in the development, maintenance and repair of the sensory epithelia of the inner ear, since these are believed to be affected by inter- and intracellular signalling. In order to analyse possible tyrosine kinases expressed in sensory areas of the inner ear, a reverse transcription polymerase chain reaction screen of microdissected sensory epithelia was undertaken, using primers targeted at conserved sequences in tyrosine kinase domains. Tissue was taken from the maculae of the mouse vestibular organs, and consisted mainly of hair cells and their supporting cells. Of 80 clones sequenced, 49 coded for tyrosine kinases, and 11 for other known molecules. Further analysis of one of the sequences, for FGF receptor 4, showed a novel variant, expressed in the inner ear and elsewhere, with a variation in the intracellular domain which suggests differential activation of known signalling pathways. Other clones coded for tyrosine kinases expected to be involved in cell surface and intracellular signalling. The technique forms a powerful tool for analysing a range of the tyrosine kinases expressed, and provides a starting point for the analysis of cell-cell signalling in the inner ear. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. RP Pickles, JO (reprint author), Univ Queensland, Dept Physiol & Pharmacol, Vis Touch & Hearing Res Ctr, Brisbane, Qld 4072, Australia. CR Carter-Su C, 1998, RECENT PROG HORM RES, V53, P61 Colvin JS, 1996, NAT GENET, V12, P390, DOI 10.1038/ng0496-390 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 GILARDIHEBENSTREIT P, 1992, ONCOGENE, V7, P2499 Haigh J, 1996, CELL GROWTH DIFFER, V7, P931 HANKS SK, 1988, SCIENCE, V241, P42, DOI 10.1126/science.3291115 HANKS SK, 1992, P NATL ACAD SCI USA, V89, P8487, DOI 10.1073/pnas.89.18.8487 LAI C, 1994, ONCOGENE, V9, P2567 LAI C, 1991, NEURON, V6, P691, DOI 10.1016/0896-6273(91)90167-X Lee KH, 1996, HEARING RES, V94, P1, DOI 10.1016/0378-5955(95)00220-0 Lewis JM, 1998, J BIOL CHEM, V273, P14225, DOI 10.1074/jbc.273.23.14225 LUO L, 1993, HEARING RES, V69, P182 MOHAMMADI M, 1991, MOL CELL BIOL, V11, P5068 Moreau-Fauvarque C, 1998, MECH DEVELOP, V78, P47, DOI 10.1016/S0925-4773(98)00147-6 Ornitz DM, 1996, J BIOL CHEM, V271, P15292 Pickles JO, 1997, DEV NEUROSCI-BASEL, V19, P476, DOI 10.1159/000111245 Pickles JO, 1998, NEUROREPORT, V9, P4093, DOI 10.1097/00001756-199812210-00016 PIRVOLA U, 1995, P NATL ACAD SCI USA, V92, P9269, DOI 10.1073/pnas.92.20.9269 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 Robinson D, 1996, P NATL ACAD SCI USA, V93, P5958, DOI 10.1073/pnas.93.12.5958 Saffer LD, 1996, HEARING RES, V94, P14, DOI 10.1016/0378-5955(95)00228-6 SCHULZ NT, 1995, MOL BRAIN RES, V28, P273, DOI 10.1016/0169-328X(94)00216-2 STARK KL, 1991, DEVELOPMENT, V113, P641 UMEMOTO M, 1995, CELL TISSUE RES, V281, P435, DOI 10.1007/s004410050440 WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 NR 25 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 100 EP 104 DI 10.1016/S0378-5955(99)00114-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200011 PM 10511629 ER PT J AU Martin, GK Stagner, BB Jassir, D Telischi, FF Lonsbury-Martin, BL AF Martin, GK Stagner, BB Jassir, D Telischi, FF Lonsbury-Martin, BL TI Suppression and enhancement of distortion-product otoacoustic emissions by interference tones above f(2). I. Basic findings in rabbits SO HEARING RESEARCH LA English DT Article DE distortion-product otoacoustic emission; interference response area; suppression; enhancement ID STIMULATED ACOUSTIC EMISSIONS; HUMAN AUDITORY-SYSTEM; TUNING CHARACTERISTICS; GENERAL-CHARACTERISTICS; COCHLEAR MECHANICS; AWAKE RABBITS; IMPAIRED EARS; 2F1-F2; 2F(1)-F(2); F2-F1 AB The present study measured interference-response areas (IRAs) for distortion-product otoacoustic emissions (DPOAEs) at 2f(1)-f(2), 3f(1)-2f(2), and 2f(2)-f(1). The IRAs were obtained in either awake or anesthetized rabbits, or in anesthetized guinea pigs and mice, by sweeping the frequencies and levels of an interference tone (IT) around a set of f(1) and f(2) primary tones, at several fixed frequencies and levels, while plotting the effects of the IT on DPOAE level. An unexpected outcome was the occurrence of regions of suppression and/or enhancement of DPOAE level when the IT was at a frequency slightly less than to more than an octave above f(2). The IRA of the 2f(1)-f(2) DPOAE typically displayed a high-frequency (HF) lobe of suppression, while the 2f(2)-f(1) emission often exhibited considerable amounts of enhancement. Moreover, for the 2f(2)-f(1) DPOAE, when enhancement was absent, its IRA usually tuned to a region above f(2) Whether or not suppression/enhancement was observed depended upon primary-tone level and frequency separation, as well as on the relative levels of the two primaries. Various physiological manipulations involving anesthesia, eighth-nerve section, diuretic administration, or pure-tone overstimulation showed that these phenomena were of cochlear origin, and were not dependent upon the acoustic reflex or cochlear-efferent activity. The aftereffects of applying diuretics or over-exposures revealed that suppression/enhancement required the presence of sensitive, low-level DPOAE-generator sources. Additionally, suppression/enhancement were general effects in that, in addition to rabbits, they were also observed in mice and guinea pigs. Further, corresponding plots of DPOAE phase often revealed areas of differing phase change in the vicinity of the primary tones as compared to regions above f(2). These findings, along with the effects of tonal exposures designed to fatigue regions above f(2), and instances in which; DPOAE level was dependent upon the amount of suppression/enhancement, suggested that the interactions of two DPOAE-generator sources contributed, in some manner, to these phenomena. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Miami, Sch Med, Dept Otolaryngol M805, Miami, FL 33101 USA. RP Martin, GK (reprint author), Univ Miami, Sch Med, Dept Otolaryngol M805, POB 016960, Miami, FL 33101 USA. EM gmartin@newssun.med.miami.edu CR Abdala C, 1998, HEARING RES, V121, P125, DOI 10.1016/S0378-5955(98)00073-2 Abdala C, 1996, EAR HEARING, V17, P374, DOI 10.1097/00003446-199610000-00003 Abdala C, 1996, HEARING RES, V98, P38, DOI 10.1016/0378-5955(96)00056-1 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1988, HEARING RES, V34, P27, DOI 10.1016/0378-5955(88)90048-2 Chang KW, 1997, J ACOUST SOC AM, V102, P1719, DOI 10.1121/1.420082 Frank G, 1996, HEARING RES, V98, P104, DOI 10.1016/0378-5955(96)00083-4 FRANK G, 1995, HEARING RES, V83, P151, DOI 10.1016/0378-5955(94)00197-X GASKILL SA, 1996, J ACOUST SOC AM, V100, P3260 JASSIR D, 1996, ASS RES OT ABSTR, V19, P24 JIMENEZ AM, 1996, ASS RES OT ABSTR, V19, P25 Kemp DT, 1998, OTOACOUSTIC EMISSION, P1 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KETTEMBEIL S, 1995, HEARING RES, V86, P47, DOI 10.1016/0378-5955(95)00053-7 KIM DO, 1981, J ACOUST SOC AM, V69, pS51, DOI 10.1121/1.386198 KIRK DL, 1993, HEARING RES, V67, P20, DOI 10.1016/0378-5955(93)90228-S KOPPL C, 1993, J ACOUST SOC AM, V93, P2834 KUJAWA SG, 1995, HEARING RES, V85, P142, DOI 10.1016/0378-5955(95)00041-2 KUMMER P, 1995, J ACOUST SOC AM, V98, P197, DOI 10.1121/1.413747 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 Liberman MC, 1996, J ACOUST SOC AM, V99, P3572, DOI 10.1121/1.414956 LOWE M, 1995, HEARING RES, V83, P133, DOI 10.1016/0378-5955(94)00198-Y MARTIN G, 1995, ABSTR ASS RES OT, V18, P124 Martin GK, 1998, J ACOUST SOC AM, V104, P972, DOI 10.1121/1.423340 Martin GK, 1998, J ACOUST SOC AM, V103, P1957, DOI 10.1121/1.421347 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1999, UNPUB SUPPRESSION EN MATTHEWS JW, 1986, PERIPHERAL AUDITORY, P258 Mills DM, 1997, J ACOUST SOC AM, V102, P413, DOI 10.1121/1.419763 Mills DM, 1998, J ACOUST SOC AM, V103, P507, DOI 10.1121/1.421101 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 MILLS DM, 1998, OTOACOUSTIC EMISSION, P85 MILLS DM, 1999, ASS RES OT ABSTR, V22, P388 Moulin A, 1996, J ACOUST SOC AM, V100, P1640, DOI 10.1121/1.416064 Moulin A, 1996, J ACOUST SOC AM, V100, P1617, DOI 10.1121/1.416063 NEELY ST, 1997, DIVERSITY AUDITORY M, P351 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 SCHMIEDT RA, 1986, PERIPHERAL AUDITORY, P330 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SIEGEL JH, 1998, ABSTR ASS RES OT, V21, P87 Talmadge CL, 1999, J ACOUST SOC AM, V105, P275, DOI 10.1121/1.424584 Talmadge CL, 1998, J ACOUST SOC AM, V104, P1517, DOI 10.1121/1.424364 Taschenberger G, 1998, HEARING RES, V123, P183, DOI 10.1016/S0378-5955(98)00120-8 Wable J, 1996, J ACOUST SOC AM, V100, P2228, DOI 10.1121/1.417932 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V WHITEHEAD ML, 1991, HEARING RES, V51, P293, DOI 10.1016/0378-5955(91)90045-B WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2359, DOI 10.1121/1.411960 WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1567 WHITEHEAD ML, 1995, ASS RES OT ABSTR, V18, P124 WHITEHEAD ML, 1995, J ACOUST SOC AM, V97, P2346, DOI 10.1121/1.411959 WIDICK MP, 1994, OTOLARYNG HEAD NECK, V111, P407 NR 52 TC 35 Z9 36 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 105 EP 123 DI 10.1016/S0378-5955(99)00119-7 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200012 PM 10511630 ER PT J AU Stover, T Yagi, M Raphael, Y AF Stover, T Yagi, M Raphael, Y TI Cochlear gene transfer: round window versus cochleostomy inoculation SO HEARING RESEARCH LA English DT Article DE cochlea; gene transfer; adenovirus; guinea pig ID HAIR CELL LOSS; GUINEA-PIG; IN-VIVO; ADENOASSOCIATED VIRUS; AUDITORY NEURONS; GROWTH-FACTOR; INNER-EAR; DEGENERATION; TRANSGENE; EXPRESSION AB Two possible approaches for cochlear gene transfer have been inoculation via the round window membrane and through a cochleostomy. The aim of this study was to determine which of the two is more effective. Using both approaches, normal-hearing and deafened guinea pigs were inoculated with adenovirus carrying the reporter gene lacZ. After 5 days, the animals were killed and the cochlear tissue was stained with X-gal. The distribution and intensity of staining was estimated by a score system developed to compare gene transfer results between animals. We found that gene transfer via the cochleostomy resulted in a better distribution throughout the cochlea and in higher staining intensity, due to more efficient transfection. Auditory brainstem response (ABR) results showed that neither virus inoculation through a cochleostomy nor through the round window membrane had a significant effect on the click-ABR threshold measured on day 5 following virus injection. Gene transfer via both approaches was also found to be more effective in deafened animals than in hearing animals. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Sch Med, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Med Hsch Hannover, Dept Otolaryngol, D-30625 Hannover, Germany. Kansai Med Univ, Dept Otolaryngol, Moriguchi, Osaka 5708506, Japan. RP Raphael, Y (reprint author), Univ Michigan, Sch Med, Dept Otolaryngol, Kresge Hearing Res Inst, MSRB 3,Rm 9303,1150 W Med Ctr Dr, Ann Arbor, MI 48109 USA. CR BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T Carvalho GJ, 1999, AM J OTOL, V20, P87 DAVIDSON BL, 1993, NAT GENET, V3, P219, DOI 10.1038/ng0393-219 Ernfors P, 1996, NAT MED, V2, P463, DOI 10.1038/nm0496-463 Geschwind MD, 1996, HUM GENE THER, V7, P173, DOI 10.1089/hum.1996.7.2-173 Keithley EM, 1998, NEUROREPORT, V9, P2183, DOI 10.1097/00001756-199807130-00007 Kiernan AE, 1997, AUDIOL NEURO-OTOL, V2, P12 Komeda M, 1999, HEARING RES, V131, P1, DOI 10.1016/S0378-5955(99)00006-4 Lalwani AK, 1998, AM J OTOL, V19, P390 Lalwani AK, 1998, GENE THER, V5, P277, DOI 10.1038/sj.gt.3300573 Lalwani AK, 1997, HEARING RES, V114, P139, DOI 10.1016/S0378-5955(97)00151-2 Lalwani AK, 1996, GENE THER, V3, P588 LENARZ T, 1997, AM J OTOL S, V18, P39 Miller JM, 1997, INT J DEV NEUROSCI, V15, P631, DOI 10.1016/S0736-5748(96)00117-7 Mitchell A, 1997, HEARING RES, V105, P30, DOI 10.1016/S0378-5955(96)00202-X Mondain M, 1998, HUM GENE THER, V9, P1217, DOI 10.1089/hum.1998.9.8-1217 Probst FJ, 1998, SCIENCE, V280, P1444, DOI 10.1126/science.280.5368.1444 Raphael Y., 1998, CURR OPIN OTOLARYNGO, V6, P311, DOI 10.1097/00020840-199810000-00005 Raphael Y, 1996, NEUROSCI LETT, V207, P137, DOI 10.1016/0304-3940(96)12499-X SALT AN, 1991, ACTA OTO-LARYNGOL, V111, P899, DOI 10.3109/00016489109138428 Salt AN, 1998, HEARING RES, V123, P137, DOI 10.1016/S0378-5955(98)00106-3 SHAH SB, 1995, AM J OTOL, V16, P310 Staecker H, 1998, OTOLARYNG HEAD NECK, V119, P7, DOI 10.1016/S0194-5998(98)70194-9 Weiss MA, 1997, INT J DEV NEUROSCI, V15, P577, DOI 10.1016/S0736-5748(96)00112-8 WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 Yagi M, 1999, HUM GENE THER, V10, P813, DOI 10.1089/10430349950018562 Ylikoski J, 1998, HEARING RES, V124, P17, DOI 10.1016/S0378-5955(98)00095-1 NR 27 TC 69 Z9 82 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 124 EP 130 DI 10.1016/S0378-5955(99)00115-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200013 PM 10511631 ER PT J AU Lorenzi, C Berthommier, F Apoux, F Bacri, N AF Lorenzi, C Berthommier, F Apoux, F Bacri, N TI Effects of envelope expansion on speech recognition SO HEARING RESEARCH LA English DT Article DE temporal envelope; envelope expansion; speech recognition; background noise ID PURE WORD DEAFNESS; LOUDNESS RECRUITMENT; GAP DETECTION; FREQUENCY-SELECTIVITY; BILATERAL LESIONS; TEMPORAL CUES; INTELLIGIBILITY; NOISE; MODULATIONS; RESOLUTION AB This study investigated the effects of expanding the gross time-amplitude variations of 'speech-envelope noise' stimuli on speech recognition. The initial stimuli were VCV logatomes presented in quiet or against a steady white noise with a 0-dB signal-to-noise ratio. Their low-frequency temporal modulations (< 500 Hz) were extracted in broad frequency bands, and raised to the power 2. The resulting envelopes were then used to modulate a white noise, and combined to produce the 'speech-envelope noise' stimuli. As a consequence, listeners were forced to identify speech using primarily temporal envelope cues. The results obtained with four normal-hearing listeners show small decrements in recognition performance of 1-15% when expanding the envelope of the speech stimuli presented in quiet. The results also show a small but consistent improvement in performance of 6-14% when expanding the envelope of the speech stimuli presented in noise. These results are consistent with those obtained by Fu and Shannon (J. Acoust. Sec. Am. 104 (1998) 2570-2577) with speech presented in quiet. They also suggest that the reduction in the modulation depth of the speech envelope caused by noise or reverberation could be compensated by expanding low-frequency temporal modulations. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Paris 05, UMR CNRS 8581, Inst Psychol, Expt Psychol Lab, F-75006 Paris, France. INPG, UPRESA CNRS 5009, Inst Commun Parlee, F-38031 Grenoble, France. RP Lorenzi, C (reprint author), Univ Paris 05, UMR CNRS 8581, Inst Psychol, Expt Psychol Lab, 28 Rue Serpente, F-75006 Paris, France. RI Apoux, Frederic/C-4991-2009; Lorenzi, Christian/F-5310-2012 CR ALBERT ML, 1974, BRAIN, V97, P373, DOI 10.1093/brain/97.1.373 AUERBACH SH, 1982, BRAIN, V105, P271, DOI 10.1093/brain/105.2.271 CLARKSON PM, 1991, J ACOUST SOC AM, V89, P1378, DOI 10.1121/1.400538 DRULLMAN R, 1994, J ACOUST SOC AM, V95, P1053, DOI 10.1121/1.408467 DRULLMAN R, 1994, J ACOUST SOC AM, V95, P2670, DOI 10.1121/1.409836 DUQUESNOY AJ, 1980, J ACOUST SOC AM, V68, P537, DOI 10.1121/1.384767 EFRON R, 1985, NEUROPSYCHOLOGIA, V23, P43, DOI 10.1016/0028-3932(85)90042-9 EGER TE, 1984, P IEEE ICASSP FRISINA DR, 1997, HEARING RES, V22, P1822 Fu QJ, 1998, J ACOUST SOC AM, V104, P2570, DOI 10.1121/1.423912 GLASBERG BR, 1992, HEARING RES, V64, P81, DOI 10.1016/0378-5955(92)90170-R HOCHMAIR ES, 1984, COCHLEAR IMPLANTS, P101 HOU ZZ, 1994, J ACOUST SOC AM, V96, P1325, DOI 10.1121/1.410279 HOUTGAST T, 1985, J ACOUST SOC AM, V77, P1069, DOI 10.1121/1.392224 MILLER GA, 1955, J ACOUST SOC AM, V27, P338, DOI 10.1121/1.1907526 Moore B.C.J., 1995, PERCEPTUAL CONSEQUEN MOORE BCJ, 1995, BRIT J AUDIOL, V29, P131, DOI 10.3109/03005369509086590 Moore BCJ, 1996, J ACOUST SOC AM, V100, P481, DOI 10.1121/1.415861 Nejime Y, 1997, J ACOUST SOC AM, V102, P603, DOI 10.1121/1.419733 Noordhoek IM, 1997, J ACOUST SOC AM, V101, P498, DOI 10.1121/1.417993 SHANNON RV, 1995, SCIENCE, V270, P303, DOI 10.1126/science.270.5234.303 Snell KB, 1997, J ACOUST SOC AM, V101, P2214, DOI 10.1121/1.418205 Souza PE, 1996, J SPEECH HEAR RES, V39, P901 TALLAL P, 1993, ANN NY ACAD SCI, V682, P27, DOI 10.1111/j.1749-6632.1993.tb22957.x TANAKA Y, 1987, BRAIN, V110, P381, DOI 10.1093/brain/110.2.381 TURNER CW, 1995, J ACOUST SOC AM, V97, P2568, DOI 10.1121/1.411911 VANTASSELL DJ, 1992, J ACOUST SOC AM, V92, P1247, DOI 10.1121/1.403920 van der Horst R, 1999, J ACOUST SOC AM, V105, P1801, DOI 10.1121/1.426718 VANTASELL DJ, 1987, J ACOUST SOC AM, V77, P1069 Wright BA, 1997, NATURE, V387, P176, DOI 10.1038/387176a0 NR 30 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 131 EP 138 DI 10.1016/S0378-5955(99)00117-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200014 PM 10511632 ER PT J AU Spicer, SS Salvi, RJ Schulte, BA AF Spicer, SS Salvi, RJ Schulte, BA TI Ablation of inner hair cells by carboplatin alters cells in the medial K+ flow route and disrupts tectorial membrane SO HEARING RESEARCH LA English DT Article DE chinchilla; cochlea; interdental cell; ion transport; endolymph ID GUINEA-PIG COCHLEA; GERBIL COCHLEA; IONIC BASIS; POTASSIUM; EAR; NA+,K+-ATPASE; LOCALIZATION; OTOTOXICITY; CHINCHILLA; ENDOLYMPH AB The thesis that K+ effluxing from inner hair cells (IHCs) cycles medially back to endolymph through inner sulcus and interdental cells (IDCs) was tested by comparing control chinchilla cochleas with those in which IHCs were selectively destroyed by carboplatin. By light microscopy inner sulcus cells appeared tall and nearly empty in control ears, but 4 months after the carboplatin treatment many showed vacuolization and shrinkage. Inner pillar cells also consistently developed abnormal vacuoles after carboplatin treatment. Control cochleas exhibited lateral columns and central clusters of IDCs which at their apex possessed expanded presumably hydrated phalanges. Four months after carboplatin, the IDC epithelium enclosed empty looking spaces and the apical phalangeal compartment collapsed into a thin, apparently dehydrated layer. This alteration was accompanied by changes in the tectorial membrane (TM) whereby the membrane's limbal zone thickened progressively to form a tall hollow mound in advanced lesions. The clear spaces in the epithelium and collapse of the phalanges are thought to reflect diminished flow of ions and fluid through IDCs. The accumulation of limbal TM supports the premise that IDCs secrete macromolecules for TM turnover as well as ions and fluid for promoting lateral migration of its precursor constituents. Occurring after ablation of IHCs by carboplatin, the changes in inner pillar, inner sulcus and IDCs and limbal TM can be viewed as a secondary effect of the interrupted ion efflux from IHCs and as further evidence that this effluent follows a medial route. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. SUNY Buffalo, Hearing Res Lab, Buffalo, NY 14214 USA. RP Spicer, SS (reprint author), Med Univ S Carolina, Dept Pathol & Lab Med, 171 Ashley Ave, Charleston, SC 29425 USA. CR ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 BELANGER LF, 1953, SCIENCE, V118, P520, DOI 10.1126/science.118.3070.520 BOSHER SK, 1978, NATURE, V273, P377, DOI 10.1038/273377a0 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 Crouch JJ, 1997, J HISTOCHEM CYTOCHEM, V45, P773 DEBRUIJN WC, 1968, P 4 EUR REG C EL MIC, P65 Ding DL, 1997, AUDIOL NEURO-OTOL, V2, P155 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 Hofstetter P, 1997, HEARING RES, V112, P199, DOI 10.1016/S0378-5955(97)00123-8 Karnosky M., 1971, P 11 M AM SOC CELL B, P146 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 LIM D J, 1970, Journal of Laryngology and Otology, V84, P1241, DOI 10.1017/S0022215100072984 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 LIM DJ, 1987, HEARING RES, V28, P9 Lumpkin EA, 1997, P NATL ACAD SCI USA, V94, P10997, DOI 10.1073/pnas.94.20.10997 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MCGUIRT JP, 1994, J HISTOCHEM CYTOCHEM, V42, P843 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 PRIETO JJ, 1990, HEARING RES, V45, P51, DOI 10.1016/0378-5955(90)90182-O PRIETO JJ, 1991, HEARING RES, V54, P59, DOI 10.1016/0378-5955(91)90136-W ROSTGAARD J, 1980, CELL TISSUE RES, V212, P17 Sakaguchi N, 1998, HEARING RES, V118, P114, DOI 10.1016/S0378-5955(98)00022-7 SALT AN, 1986, NEUROBIOLOGY HEARING, P108 Sánchez Fernández J M, 1983, Acta Otolaryngol, V95, P460 SANTI PA, 1988, PHYSL EAR, P173 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 Spicer SS, 1999, HEARING RES, V130, P7, DOI 10.1016/S0378-5955(98)00202-0 Spicer SS, 1998, HEARING RES, V118, P1, DOI 10.1016/S0378-5955(98)00006-9 STERKERS O, 1984, AM J PHYSIOL, V246, pF47 Takeno S, 1998, AUDIOL NEURO-OTOL, V3, P281, DOI 10.1159/000013800 Voldrich L, 1967, Acta Otolaryngol, V63, P503 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 WAKE M, 1993, J LARYNGOL OTOL, V107, P585, DOI 10.1017/S0022215100123771 WAKE M, 1994, LARYNGOSCOPE, V104, P488 Wang J, 1997, HEARING RES, V107, P67, DOI 10.1016/S0378-5955(97)00020-8 ZIDANIC M, 1994, BIOPHYS J, V57, P1253 NR 39 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 139 EP 150 DI 10.1016/S0378-5955(99)00118-5 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200015 PM 10511633 ER PT J AU Robertson, D Sellick, PM Patuzzi, R AF Robertson, D Sellick, PM Patuzzi, R TI The continuing search for outer hair cell afferents in the guinea pig spiral ganglion SO HEARING RESEARCH LA English DT Article DE cochlea; afferent; outer hair cell; antidromic stimulation; guinea pig ID AUDITORY-NERVE FIBERS; OLIVOCOCHLEAR NEURONS; EFFERENT NEURONS; COCHLEA; PROJECTIONS; MORPHOLOGY; RESPONSES; CAT AB Antidromic stimulation of the stump of the VIIIth nerve was combined with microelectrode recording in the spiral ganglion of the guinea pig cochlea in an attempt to identify a sub-population of neurons with long-latency antidromic action potentials that might correspond to the thin unmyelinated afferent neurons emanating from the outer hair cells. The techniques used were similar but not identical to those employed in an earlier study by Brown (1994). By far the largest population of cells contacted had short antidromic latencies (0.58 +/- 0.12 ms, 76 units) and also responded to acoustic stimulation. These were assumed to be type I afferents emanating from inner hair cells. Eight cells had antidromic latencies larger than 1 ms, all but one of which had a zero spontaneous rate. All eight of these longer-latency cells were unresponsive to acoustic stimulation despite the fact that short-latency neurons in the same cochleas showed robust responses to sound before and after they were contacted. Four of these longer-latency cells had their antidromic thresholds accurately measured and two had significantly higher thresholds to electrical stimulation (0.1 ms duration) than type I cells in the same animal while two had similar electrical thresholds. Attempts to trace the eight long-latency neurons to the outer hair cells using intracellular injection of horseradish peroxidase were unsuccessful. On the basis of present evidence, we cannot conclude definitively that the long-latency neurons found in the spiral ganglion belong to the outer hair cell afferent population. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. RP Robertson, D (reprint author), Univ Western Australia, Dept Physiol, Auditory Lab, Nedlands, WA 6907, Australia. CR BROWN MC, 1994, J NEUROPHYSIOL, V71, P1835 BROWN MC, 1989, HEARING RES, V40, P93, DOI 10.1016/0378-5955(89)90103-2 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S HONRUBIA V, 1989, J NEUROPHYSIOL, V61, P688 LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 ROBERTSON D, 1988, BRAIN RES, V462, P47, DOI 10.1016/0006-8993(88)90583-5 ROBERTSON D, 1985, HEARING RES, V20, P63, DOI 10.1016/0378-5955(85)90059-0 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X SMITH CA, 1973, ACTA OTO-LARYNGOL, V75, P203, DOI 10.3109/00016487309139696 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 THOMPSON AM, 1991, J COMP NEUROL, V303, P267, DOI 10.1002/cne.903030209 Tsuji J, 1997, J COMP NEUROL, V381, P188 WALSH BT, 1972, INT J NEUROSCI, V3, P221, DOI 10.3109/00207457209147026 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 NR 16 TC 24 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 151 EP 158 DI 10.1016/S0378-5955(99)00120-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200016 PM 10511634 ER PT J AU McKay, CM O'Brien, A James, CJ AF McKay, CM O'Brien, A James, CJ TI Effect of current level on electrode discrimination in electrical stimulation SO HEARING RESEARCH LA English DT Article DE cochlear implant; electrical stimulation; electrode discrimination; current level ID HEARING-IMPAIRED LISTENERS; FREQUENCY DISCRIMINATION; COCHLEAR IMPLANT; PITCH PERCEPTION; SENSATION LEVEL; EXCITATION AB The effect of the stimulation intensity (current amplitude) on the ability to discriminate electrodes was tested in an experiment with four adult users of the Nucleus-22 cochlear implant. A total of 12 adjacent pairs of electrodes were used in the four-interval forced-choice discrimination task with random current variation. Tests were carried out at three average stimulation levels: 40 and 70% of the dynamic range and close to maximum comfortable loudness. Analysis of variance revealed a significant (P<0.0001) deterioration in electrode discrimination with a decreasing level. However, the overall effect was very small, representing a deterioration in the discrimination score of only 18% correct from the highest to lowest levels tested. The reason for the small deterioration in discriminability with a decreasing level is difficult to determine from this experiment, however, the results are consistent with the hypothesis that changes in the 'peak' or 'edge' of the excitation pattern are more important for discrimination tasks than the relative amount of non-overlap of the excitation areas from the two electrodes. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Melbourne, Dept Otolaryngol, Parkville, Vic 3052, Australia. RP McKay, CM (reprint author), Univ Melbourne, Dept Otolaryngol, 384-388 Albert St, Parkville, Vic 3052, Australia. CR CARHART R, 1959, J SPEECH HEAR DISORD, V24, P330 Chatterjee M, 1998, J ACOUST SOC AM, V103, P2565, DOI 10.1121/1.422777 FREYMAN RL, 1991, J SPEECH HEAR RES, V34, P1371 HENRY B, 1997, COCHLEAR IMPLANTS, P89 Kral A, 1998, HEARING RES, V121, P11, DOI 10.1016/S0378-5955(98)00061-6 McDermott HJ, 1997, J ACOUST SOC AM, V101, P1622, DOI 10.1121/1.418177 NELSON DA, 1983, J ACOUST SOC AM, V73, P2117, DOI 10.1121/1.389579 PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1990, HEARING RES, V50, P43, DOI 10.1016/0378-5955(90)90032-K PFINGST BE, 1994, HEARING RES, V78, P197, DOI 10.1016/0378-5955(94)90026-4 Pijl S, 1997, EAR HEARING, V18, P316, DOI 10.1097/00003446-199708000-00006 TONG YC, 1983, J ACOUST SOC AM, V74, P73, DOI 10.1121/1.389620 TOWNSHEND B, 1987, J ACOUST SOC AM, V82, P106, DOI 10.1121/1.395554 WAKEFIELD GH, 1985, J ACOUST SOC AM, V77, P613, DOI 10.1121/1.391879 WIER CC, 1977, J ACOUST SOC AM, V61, P178, DOI 10.1121/1.381251 NR 15 TC 30 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 159 EP 164 DI 10.1016/S0378-5955(99)00121-5 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200017 PM 10511635 ER PT J AU Lopez-Gonzalez, MA Delgado, F Lucas, M AF Lopez-Gonzalez, MA Delgado, F Lucas, M TI Aminoglycosides activate oxygen metabolites production in the cochlea of mature and developing rats SO HEARING RESEARCH LA English DT Article DE aminoglycoside; free radical; hearing loss; protection ID HAIR-CELLS; IN-VITRO; SPECIES GENERATION; IRON CHELATORS; FREE-RADICALS; OTOTOXICITY; GENTAMICIN; CISPLATIN; DAMAGE AB The ototoxicity of antibiotics, particularly of aminoglycosides, is a well-known undesirable side effect which may be based on a free radical mechanism. We studied the effect of different antibiotics in the production of reactive oxygen species in freshly isolated cochleas of mature and 2-10 weeks old developing rats. Phorbol myristate acetate induced the release of reactive oxygen species after a lag time close to 30 s and declined back to basal values in 10-20 min. The rate of reactive oxygen species production correlated inversely to the age in 2-10 weeks old rats. The study of a set of antibiotics showed that a very low concentration of gentamicin and streptomycin (10-100 ng/ml) enhanced the effect of phorbol myristate acetate. At the above-indicated concentrations, ciprofloxacin did not modify phorbol myristate acetate-induced activation. These results show the enhancement by aminoglycosides of reactive oxygen species production in cochlear tissues, particularly in developing rats. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Virgen Macarena Univ Hosp, Sch Med, Mol Biol Serv, E-41009 Seville, Spain. Virgen Rocio Univ Infantile Hosp, Unit Pediat Otorhinolaryngol, Seville, Spain. RP Lucas, M (reprint author), Virgen Macarena Univ Hosp, Sch Med, Mol Biol Serv, Avda Sanchez Pizjuan 4, E-41009 Seville, Spain. CR Baliga R, 1997, AM J KIDNEY DIS, V29, P465, DOI 10.1016/S0272-6386(97)90212-2 Clerici WJ, 1996, HEARING RES, V98, P116, DOI 10.1016/0378-5955(96)00075-5 Clerici WJ, 1996, HEARING RES, V101, P14, DOI 10.1016/S0378-5955(96)00126-8 CLERICI WJ, 1995, HEARING RES, V84, P30, DOI 10.1016/0378-5955(95)00010-2 Conlon BJ, 1998, LARYNGOSCOPE, V108, P284, DOI 10.1097/00005537-199802000-00023 Ford MS, 1997, HEARING RES, V111, P143, DOI 10.1016/S0378-5955(97)00103-2 GARETZ SL, 1994, HEARING RES, V77, P75, DOI 10.1016/0378-5955(94)90254-2 HALLIWEL B, 1995, TRENDS NEUROSCI, V79, P22 Henley CM, 1996, HEARING RES, V99, P85, DOI 10.1016/S0378-5955(96)00094-9 HENLEY CM, 1993, OTOLARYNG CLIN N AM, V26, P857 HENLEY CM, 1995, BRAIN RES REV, V20, P68, DOI 10.1016/0165-0173(94)00006-B Hirose K, 1997, HEARING RES, V104, P1, DOI 10.1016/S0378-5955(96)00169-4 KNIGHT JA, 1995, ANN CLIN LAB SCI, V25, P111 Kopke RD, 1997, AM J OTOL, V18, P559 LAUTERMANN J, 1995, HEARING RES, V88, P47, DOI 10.1016/0378-5955(95)00097-N Lopez-Gonzalez MA, 1998, NEUROCHEM INT, V33, P55, DOI 10.1016/S0197-0186(05)80009-9 LUCAS M, 1995, ANAL BIOCHEM, V231, P277, DOI 10.1006/abio.1995.0051 Priuska E M, 1997, Ear Nose Throat J, V76, P164 Priuska EM, 1995, BIOCHEM PHARMACOL, V50, P1749, DOI 10.1016/0006-2952(95)02160-4 SEIDMAN MD, 1993, OTOLARYNG HEAD NECK, V109, P1052 Sha SH, 1998, NEUROREPORT, V9, P3893, DOI 10.1097/00001756-199812010-00023 Sha SH, 1999, HEARING RES, V128, P112, DOI 10.1016/S0378-5955(98)00200-7 Sha SH, 1999, FREE RADICAL BIO MED, V26, P341, DOI 10.1016/S0891-5849(98)00207-X Song BB, 1997, J PHARMACOL EXP THER, V282, P369 Song BB, 1998, FREE RADICAL BIO MED, V25, P189, DOI 10.1016/S0891-5849(98)00037-9 Walker P. D., 1987, AM J PHYSIOL, V253, P495 ZELCK U, 1993, EUR ARCH OTO-RHINO-L, V250, P218 NR 27 TC 20 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1999 VL 136 IS 1-2 BP 165 EP 168 DI 10.1016/S0378-5955(99)00122-7 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 243TK UT WOS:000083013200018 PM 10511636 ER PT J AU Miller, CA Abbas, PJ Rubinstein, JT AF Miller, CA Abbas, PJ Rubinstein, JT TI An empirically based model of the electrically evoked compound action potential SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 1st International Symposium Workshop on Objective Measures in Cochlear Implantation CY 1998 CL NOTTINGHAM, ENGLAND DE cochlear implant; electrical stimulation; auditory nerve; cat; single-fiber recording; compound action potential; model; population response ID AUDITORY-NERVE; STIMULATION; EXCITATION; FLUCTUATIONS; RESPONSES; SURVIVAL; RANVIER; NODE; CAT AB The relationship between electrically evoked single-fiber action potentials and the electrically evoked compound action potential of the auditory nerve is of interest to those attempting to model such responses with computational techniques. It also relates to efforts to exploit the gross potentials that can now be recorded by some implantable cochlear prostheses. In this paper, we develop a computational model of the auditory nerve response to single, pulsatile, electrical stimuli based upon the response characteristics obtained from 230 single fibers of 13 cats. These fibers were stimulated by brief (39 mu s) monophasic cathodic stimuli delivered by a monopolar intracochlear electrode. The data were pooled to obtain an estimate of the distribution of fiber thresholds. Post-stimulus time histograms were modeled using Poisson functions and adjusted to account for empirically determined latency and jitter characteristics. The probabilistic nature of single-fiber input-output functions (i.e. Verveen's (1961) 'relative spread') was also modelled. PST histograms from 5000 modelled fibers were then summed and convolved with an estimated 'unit potential' following the method of Goldstein and Kiang (1958). This convolution produced modelled compound action potentials, which were then compared with experimentally obtained data. Manipulations of model parameters affecting threshold, jitter, and relative spread suggest that the most important determinant of the shape of the EAP amplitude-level function is the threshold distribution. A model based solely on threshold distribution produces an EAP input-output function similar to one that accounts for probabilistic single-fiber input-output functions. Discrepancies between these two models do occur if the threshold distribution function is compressed significantly, as might be the case in pathological cochleae with altered distributions or numbers of nerve fibers. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Iowa, Dept Otolaryngol Head & Neck Surg, Iowa City, IA 52242 USA. Univ Iowa, Dept Speech Pathol & Audiol, Iowa City, IA 52242 USA. Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52242 USA. RP Miller, CA (reprint author), Univ Iowa, Dept Otolaryngol Head & Neck Surg, 200 Hawkins Dr,C-21 GH, Iowa City, IA 52242 USA. CR ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BEMENT SL, 1969, EXP NEUROL, V24, P147, DOI 10.1016/0014-4886(69)90012-0 BROWN CJ, 1994, EAR HEARING, V15, P168, DOI 10.1097/00003446-199404000-00006 Bruce IC, 1999, IEEE T BIO-MED ENG, V46, P617, DOI 10.1109/10.764938 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DESAUVAGE RC, 1983, J ACOUST SOC AM, V73, P616 Doucet JR, 1997, J ACOUST SOC AM, V101, P2720, DOI 10.1121/1.418560 Finley C. C., 1990, COCHLEAR IMPLANTS MO FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 Frijns JHM, 1996, HEARING RES, V95, P33, DOI 10.1016/0378-5955(96)00004-4 GIRZON B, 1987, THESIS MIT CAMBRIDGE GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U KIANG NYS, 1976, ELECTROCOCHLEOGRAPHY LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MCNEAL DR, 1976, IEEE T BIO-MED ENG, V23, P329, DOI 10.1109/TBME.1976.324593 Miller CA, 1998, HEARING RES, V119, P142, DOI 10.1016/S0378-5955(98)00046-X Miller CA, 1999, HEARING RES, V130, P197, DOI 10.1016/S0378-5955(99)00012-X MILLER CA, 1994, HEARING RES, V78, P11, DOI 10.1016/0378-5955(94)90039-6 POUSSART DJM, 1965, THESIS MIT CAMBRIDGE Press W., 1992, NUMERICAL RECIPES FO RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 Sando I, 1965, ACTA OTOLARYNG STOCK, V59, P417, DOI 10.3109/00016486509124577 SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 SIGWORTH FJ, 1980, J PHYSIOL-LONDON, V307, P97 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 STRELIOF.D, 1973, J ACOUST SOC AM, V54, P620, DOI 10.1121/1.1913642 SUESSERMAN MF, 1993, IEEE T BIO-MED ENG, V40, P237, DOI 10.1109/10.216407 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VERVEEN AA, 1961, THESIS U AMSTERDAM WANG B, 1978, J ACOUST SOC AM, V63, pS77, DOI 10.1121/1.2016823 Wang B, 1979, THESIS MIT CAMBRIDGE WILSON BS, 1994, N01DC22401 NIH NEUR NR 33 TC 25 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 1 EP 18 DI 10.1016/S0378-5955(99)00081-7 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400001 PM 10491949 ER PT J AU Oghalai, JS Tran, TD Raphael, RM Nakagawa, T Brownell, WE AF Oghalai, JS Tran, TD Raphael, RM Nakagawa, T Brownell, WE TI Transverse and lateral mobility in outer hair cell lateral wall membranes SO HEARING RESEARCH LA English DT Article DE diffusion; cochlea; hearing; confocal microscope; fluidity; phospholipid bilayer ID GUINEA-PIG; ERYTHROCYTE-MEMBRANE; VOLTAGE-DEPENDENCE; FORCE GENERATION; MODEL MEMBRANES; GATING CHARGE; MOTILITY; DIFFUSION; CHOLESTEROL; ORGAN AB Cochlear outer hair cell (OHC) electromotility is associated with the cell's lateral wall. The lateral wall contains two distinct membranes: the plasma membrane (PM) and the subsurface cisternae (SSC). We explored biophysical characteristics of these lipid structures using membrane-specific fluorescent dyes. We have previously demonstrated that di-8-ANEPPS stains the PM while NBD-Cs-ceramide partitions to the SSC. In this report we show that NBD-cholesterol also partitions to the SSC. Transmigration of the SSC dyes across the PM was visualized under confocal microscopy, after separating the two membranes using the micropipette aspiration technique. The transverse mobility of NBD-cholesterol was faster than that of NBD-Cs-ceramide. We then measured the lateral mobility of the dyes within both the PM and the SSC using fluorescence recovery after photobleaching (FRAP). The diffusion coefficients at 12-37 degrees C and the activation energies for diffusion were found to be similar to those of other biological membranes. These data indicate that both the PM and the SSC are membranes in the fluid phase, with no evidence of temperature-dependent phase transitions. Our observations are consistent with a fluid-mosaic model of the lateral wall membranes. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Baylor Coll Med, Bobby R Alford Dept Otorhinolaryngol & Communicat, Houston, TX 77030 USA. Johns Hopkins Univ, Sch Med, Dept Biomed Engn, Baltimore, MD 21205 USA. Kyushu Univ, Fac Med, Dept Otorhinolaryngol, Fukuoka 812, Japan. RP Oghalai, JS (reprint author), Baylor Coll Med, Bobby R Alford Dept Otorhinolaryngol & Communicat, Houston, TX 77030 USA. CR ARIMA T, 1991, CELL TISSUE RES, V263, P91, DOI 10.1007/BF00318403 ASHMORE JF, 1949, SENSORY TRANSDUCTION, P396 AXELROD D, 1976, BIOPHYS J, V16, P1055 BALCOM BJ, 1993, BIOPHYS J, V65, P630 BLOOM JA, 1983, BIOPHYS J, V42, P295 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Bullen A, 1997, BIOPHYS J, V73, P477 CHATTOPADHYAY A, 1990, CHEM PHYS LIPIDS, V53, P1, DOI 10.1016/0009-3084(90)90128-E Dallos P, 1991, Curr Opin Neurobiol, V1, P215, DOI 10.1016/0959-4388(91)90081-H DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DERZKO Z, 1980, BIOCHEMISTRY-US, V19, P6050, DOI 10.1021/bi00567a016 FLUHLER E, 1985, BIOCHEMISTRY-US, V24, P5749, DOI 10.1021/bi00342a010 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 GALE JE, 1994, P ROY SOC B-BIOL SCI, V255, P243, DOI 10.1098/rspb.1994.0035 GOLAN DE, 1984, BIOCHEMISTRY-US, V23, P332, DOI 10.1021/bi00297a024 GULLEY RL, 1977, ANAT REC, V189, P109, DOI 10.1002/ar.1091890108 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 IWASA KH, 1994, J ACOUST SOC AM, V96, P2216, DOI 10.1121/1.410094 IWASA KH, 1992, J ACOUST SOC AM, V92, P3169, DOI 10.1121/1.404194 IWASA KH, 1993, BIOPHYS J, V65, P492 Kakehata S, 1996, J NEUROSCI, V16, P4881 KAKEHATA S, 1995, BIOPHYS J, V68, P2190 KALINEC F, 1992, P NATL ACAD SCI USA, V89, P8671, DOI 10.1073/pnas.89.18.8671 KAPITZA HG, 1980, BIOCHIM BIOPHYS ACTA, V595, P56, DOI 10.1016/0005-2736(80)90247-3 KORNBERG RD, 1971, BIOCHEMISTRY-US, V10, P1111 LIPSKY NG, 1985, SCIENCE, V228, P745, DOI 10.1126/science.2581316 Nguyen TVN, 1998, OTOLARYNG HEAD NECK, V119, P14, DOI 10.1016/S0194-5998(98)70167-6 Oghalai JS, 1998, J NEUROPHYSIOL, V79, P2235 Oghalai JS, 1998, J NEUROSCI, V18, P48 POLLICE PA, 1993, HEARING RES, V70, P187, DOI 10.1016/0378-5955(93)90157-V Raphael RM, 1996, BIOPHYS J, V71, P1374 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SAITO K, 1983, CELL TISSUE RES, V229, P467 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 Santos-Sacchi J, 1998, J PHYSIOL-LONDON, V510, P225, DOI 10.1111/j.1469-7793.1998.225bz.x SIEGEL JH, 1986, J NEUROCYTOL, V15, P311, DOI 10.1007/BF01611434 SINGER SJ, 1972, SCIENCE, V175, P720, DOI 10.1126/science.175.4023.720 Sit PS, 1997, BIOPHYS J, V72, P2812 THOMPSON NL, 1980, BIOCHIM BIOPHYS ACTA, V597, P155, DOI 10.1016/0005-2736(80)90159-5 TOCANNE JF, 1989, FEBS LETT, V257, P10, DOI 10.1016/0014-5793(89)81774-0 TOCANNE JF, 1994, PROG LIPID RES, V33, P203, DOI 10.1016/0163-7827(94)90027-2 VAZ WLC, 1982, MEMBRANE RECONSTITUT, P83 NR 43 TC 26 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 19 EP 28 DI 10.1016/S0378-5955(99)00077-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400002 PM 10491950 ER PT J AU Sato, M Henson, MM Henson, OW Smith, DW AF Sato, M Henson, MM Henson, OW Smith, DW TI The innervation of outer hair cells: 3D reconstruction from TEM serial sections in the Japanese macaque SO HEARING RESEARCH LA English DT Article DE outer hair cell; synapse; organ of corti; Japanese macaque; three-dimensional reconstruction; innervation ID CROSSED OLIVOCOCHLEAR BUNDLE; MEDIAL EFFERENT SYSTEM; AUDITORY-NERVE; CONTRALATERAL SOUND; ELECTRICAL-STIMULATION; HUMAN ORGAN; NEURONS; COCHLEA; NOISE; CORTI AB Transmission electron micrographs from serial sections were obtained from the neural pole of outer hair cells (OHCs) in the Japanese macaque (Macaca fuscata) and reconstructions of nerve terminals were made using computer software. Data are based on observations of six cells in the basal turn, eight in the middle turn and four in the apex. In general, the number of afferent (type II) terminals on each OHC increased from base to apex, and for a given turn, the numbers appeared unrelated to OHC row. On the other hand, the number of efferent terminals was greater in the middle turn than in other areas, and the number decreased from row 1 to row 3. Reciprocal synapses increased in frequency from the upper basal turn apicalward. The total number of terminals synapsing on an individual OHC increased from base to apex by nearly 100%. Three-dimensional reconstructions showed that nerve fibers terminating on basal and middle turn OHCs ascended directly from sub-OHC regions to synapse on the subnuclear regions of the OHC. In contrast, apical turn fibers ran horizontally at the level of the subnuclear region and the terminals appeared as en passant swellings along a single fiber. Although physiological data are wanting for the macaque, the anatomical findings suggest that functional differences may exist along the length of the cochlea. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Duke Univ, Med Ctr, Div Otolaryngol Head & Neck Surg, Hearing Res Labs, Durham, NC 27710 USA. Natl Def Med Coll, Dept Otolaryngol Head & Neck Surg, Tokorozawa, Saitama 359, Japan. Univ N Carolina, Div Otolaryngol Head & Neck Surg, Chapel Hill, NC USA. Univ N Carolina, Dept Cell Biol & Anat, Chapel Hill, NC USA. RP Smith, DW (reprint author), Duke Univ, Med Ctr, Div Otolaryngol Head & Neck Surg, Hearing Res Labs, Box 3550, Durham, NC 27710 USA. CR ADES HW, 1974, AUDITORY SYSTEM ANAT, P125 BISHOP AL, 1998, ANIMAL SONAR, P307 BREDBERG G, 1977, ACTA OTO-LARYNGOL, V83, P71, DOI 10.3109/00016487709128815 BROWN MC, 1989, HEARING RES, V40, P93, DOI 10.1016/0378-5955(89)90103-2 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E DOLAN DF, 1994, ASS RES OT ABSTR, V17, P89 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 GUINAN JJ, 1997, COCHLEA, P435 HASHIMOTO S, 1988, ACTA OTO-LARYNGOL, V105, P64, DOI 10.3109/00016488809119447 HENSON OW, 1995, HEARING RES, V86, P111, DOI 10.1016/0378-5955(95)00061-8 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NADOL JB, 1984, ANN OTO RHINOL LARYN, V93, P247 NADOL JB, 1983, LARYNGOSCOPE, V93, P780 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 NAKAI Y, 1974, ACTA OTO-LARYNGOL, V77, P393, DOI 10.3109/00016487409124641 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 Sato M, 1997, HEARING RES, V108, P46, DOI 10.1016/S0378-5955(97)00049-X SCHUKNECHT HF, 1953, AMA ARCH OTOLARYNGOL, V58, P377 SMITH CA, 1961, J ULTRASTRUCT RES, V5, P185 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 Spoendlin H., 1966, ORG COCHLEAR RECEPTO SPOENDLIN HH, 1963, ANN OTO RHINOL LARYN, V72, P660 Takasaka T, 1987, Acta Otolaryngol Suppl, V435, P7 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARREN EH, 1989, HEARING RES, V37, P105, DOI 10.1016/0378-5955(89)90033-6 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 XIE DH, 1993, HEAR RES, V44, P81 NR 32 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 29 EP 38 DI 10.1016/S0378-5955(99)00086-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400003 PM 10491951 ER PT J AU Wysocki, J AF Wysocki, J TI Dimensions of the human vestibular and tympanic scalae SO HEARING RESEARCH LA English DT Article DE cochlear scala; measurement; cochlear implant ID COCHLEAR IMPLANT-SURGERY; TEMPORAL BONE STRUCTURES; 3-DIMENSIONAL RECONSTRUCTION; CAT AB The cochlear scalae provide a practical access route for the insertion of cochlear implant electrodes. A microanatomical study was carried out on 25 human temporal bones obtained from cadavers. These bones were dissected with the aid of an operation microscope, in which their perilymphatic spaces were filled with coloured latex and further prepared in a formalin stain. Each of the rubber moulds was removed from the osseous matrix using standard otosurgical equipment, and subsequently cut into 1 mm segments. The height and width of the vestibular and tympanic scalae were measured. The results, presented in diagrams, indicate that the vestibular scala is less prominent than the tympanic scala in the basic and middle coil of the cochlea and in the upper coil, they display greater dimensions which could serve as a place for electrode insertion in cochlear implant procedures. In addition, the vestibular and tympanic scalae present alternate dominance in their width and height as corroborated by the calculated coefficients. The results obtained in this study supplement our knowledge of the anatomy of the cochlea thus far lacking a full investigation of the scalae, and could serve as a basis for other studies dealing with the physiology of the organs of hearing. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Warsaw, Sch Med, Dept Normal Anat, PL-02004 Warsaw, Poland. Inst Hearing Physiol & Pathol Warsaw, Warsaw, Poland. RP Wysocki, J (reprint author), Univ Warsaw, Sch Med, Dept Normal Anat, 5 Chalubinskiego Str, PL-02004 Warsaw, Poland. CR BURIAN K, 1979, ACTA OTO-LARYNGOL, V87, P190, DOI 10.3109/00016487909126406 CLARK GM, 1975, J LARYNGOL OTOL, V89, P787, DOI 10.1017/S0022215100081020 DIMOPOULOS P, 1990, ACTA RADIOL, V31, P439 EDDINGTON D K, 1978, Annals of Otology Rhinology and Laryngology, V87, P5 GANTZ BJ, 1988, OTOLARYNG HEAD NECK, V98, P72 GREEN JD, 1990, LARYNGOSCOPE, V100, P1 Gulya AJ, 1996, ARCH OTOLARYNGOL, V122, P130 HATSUSHIKA S, 1990, ANN OTO RHINOL LARYN, V99, P871 IGARASHI M, 1968, J SPEECH HEAR RES, V11, P229 IGARASHI M, 1976, ARCH OTOLARYNGOL, V102, P428 SKARZYNSKI H, 1996, CEEJOHNS, V1, P42 TAKAGI A, 1989, ANN OTO RHINOL LARYN, V98, P515 TAKAHASHI H, 1990, LARYNGOSCOPE, V100, P417 TESTUT L, 1905, TRAITE ANATOMIE HUMA, V3 WALBY AP, 1985, ANN OTO RHINOL LARYN, V94, P393 WEBB RL, 1991, ANN OTO RHINOL LARYN, V100, P131 Wysocki J, 1998, SURG RADIOL ANAT, V20, P267, DOI 10.1007/BF01628488 ZRUNEK M, 1981, ARCH OTO-RHINO-LARYN, V233, P99, DOI 10.1007/BF00464279 ZRUNEK M, 1980, ARCH OTO-RHINO-LARYN, V229, P159, DOI 10.1007/BF02565517 ZWISLOCKI-MOCIKI JOZEF, 1948, ACTA OTO LARYNGOL [STOCKHOLM], V72, P1 NR 20 TC 26 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 39 EP 46 DI 10.1016/S0378-5955(99)00088-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400004 PM 10491952 ER PT J AU Miller, AL Smith, DW Pfingst, BE AF Miller, AL Smith, DW Pfingst, BE TI Across-species comparisons of psychophysical detection thresholds for electrical stimulation of the cochlea: II. Strength-duration functions for single, biphasic pulses SO HEARING RESEARCH LA English DT Article DE cochlear implant; psychophysics; human; animal; single pulse; threshold; auditory prosthesis; species; strength-duration function ID AUDITORY-NERVE; SCALA TYMPANI; NEURAL EXCITATION; PHASE DURATION; GUINEA-PIGS; INNER-EAR; IMPLANTS; RESPONSES; CAT; MODEL AB This paper compares psychophysical detection threshold data (new and previously published) for pulsatile electrical stimulation of the deafened inner ear, obtained from different human and nonhuman subjects. Subjects were grouped according to species. Other variables, however, such as the electrode array type and method of deafening, varied within and across species. Detection threshold levels and slopes of threshold versus phase duration functions for presentations of single, biphasic pulsatile stimuli (strength-duration functions) were compared for humans, macaques, cats, and guinea pigs. For bipolar stimulation, statistically significant differences in threshold level were observed between human subjects and all other species. The species difference did not depend on the phase duration tested. For monopolar stimulation, only nonhuman species were tested. Effects of electrode configuration on both the level and slope of psychophysical strength-duration functions were statistically significant across nonhuman species, but there was not a statistically significant interaction between species and electrode configuration. The similarity in function shape and relative paucity of significant differences in psychophysical functions across species support the continued use of multiple species for cochlear implant research. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Med Ctr, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Duke Univ, Med Ctr, Dept Surg, Div Otolaryngol Head & Neck Surg,Hearing Res Labs, Durham, NC 27710 USA. RP Pfingst, BE (reprint author), Univ Michigan, Med Ctr, Dept Otolaryngol, Kresge Hearing Res Inst, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. CR ABBAS PJ, 1991, HEARING RES, V51, P139, DOI 10.1016/0378-5955(91)90012-X AIDLEY DJ, 1971, PHYSL EXCITABLE CELL BEITEL RE, 1995, ABSTR ASS RES OT, P181 BROWN CJ, 1994, EAR HEARING, V15, P168, DOI 10.1097/00003446-199404000-00006 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HATSUSHIKA S, 1990, ANN OTO RHINOL LARYN, V99, P871 IGARASHI M, 1976, ARCH OTOLARYNGOL, V102, P428 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 Kawano A, 1998, ACTA OTO-LARYNGOL, V118, P313 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 MARSHALL L, 1986, J SPEECH HEAR RES, V29, P82 MCNEAL DR, 1976, IEEE T BIO-MED ENG, V23, P329, DOI 10.1109/TBME.1976.324593 Miller AL, 1997, HEARING RES, V109, P21, DOI 10.1016/S0378-5955(97)00037-3 MILLER AL, 1997, 1997 AS C IMPL PROST Miller AL, 1999, HEARING RES, V134, P89, DOI 10.1016/S0378-5955(99)00072-6 Miller CA, 1995, HEARING RES, V92, P100, DOI 10.1016/0378-5955(95)00205-7 Miller CA, 1995, HEARING RES, V92, P85, DOI 10.1016/0378-5955(95)00204-9 MOON AK, 1993, HEARING RES, V67, P166, DOI 10.1016/0378-5955(93)90244-U PARKINS CW, 1994, ADV COCHLEAR IMPLANT, P54 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 Pfingst BE, 1996, HEARING RES, V98, P77, DOI 10.1016/0378-5955(96)00071-8 PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PFINGST BE, 1993, J ACOUST SOC AM, V94, P1287, DOI 10.1121/1.408155 Pfingst BE, 1997, HEARING RES, V112, P247, DOI 10.1016/S0378-5955(97)00122-6 PFINGST BE, 1988, HEARING RES, V34, P243, DOI 10.1016/0378-5955(88)90005-6 PFINGST BE, 1990, HEARING RES, V50, P225, DOI 10.1016/0378-5955(90)90047-S PFINGST BE, 1995, HEARING RES, V85, P76, DOI 10.1016/0378-5955(95)00037-5 Pfingst B E, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P127 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHANNON RV, 1985, HEARING RES, V18, P135, DOI 10.1016/0378-5955(85)90005-X SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 Skinner Margaret W., 1995, Seminars in Hearing, V16, P228, DOI 10.1055/s-0028-1083720 SMITH DW, 1995, J ACOUST SOC AM, V98, P211, DOI 10.1121/1.413755 SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMITH DW, 1997, J ACOUST SOC AM, V102, P1 SMITH DW, 1993, ADV COCHLEAR IMPLANT, P8 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 XUE XL, 1989, J NEUROSCI METH, V28, P189, DOI 10.1016/0165-0270(89)90035-6 ZWISLOCKI J, 1958, J ACOUST SOC AM, V30, P254, DOI 10.1121/1.1909559 NR 43 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 47 EP 55 DI 10.1016/S0378-5955(99)00089-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400005 PM 10491953 ER PT J AU Jones, SM Erway, LC Bergstrom, RA Schimenti, JC Jones, TA AF Jones, SM Erway, LC Bergstrom, RA Schimenti, JC Jones, TA TI Vestibular responses to linear acceleration are absent in otoconia-deficient C57BL/6JEi-het mice SO HEARING RESEARCH LA English DT Article DE vestibular evoked potential; mammal; gravity receptor; utricle; saccule ID EVOKED-POTENTIALS; SYSTEM AB Vestibular evoked potentials (VsEPs) were measured in normal mice and in mice homozygous for the head tilt mutation (hetlhet, abbr. het). The het mice lack otoconia, the inertial mass critical for natural stimulation of inner ear gravity receptors. Our findings demonstrate that vestibular neural responses to pulsed linear acceleration are absent in het mice. The results: (1) confirm that adequate sensory stimuli fail to activate gravity receptors in the het model; and (2) serve as definitive evidence that Far-field vestibular responses to pulsed linear acceleration depend critically on otolith end organs. The C57BL/6JEi-het mouse may be an excellent model of gravity receptor sensory deprivation. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Missouri, Sch Med, Dept Surg ENT, Columbia, MO 65212 USA. Univ Cincinnati, Dept Biol Sci, Cincinnati, OH 45221 USA. Jackson Lab, Bar Harbor, ME 04609 USA. Univ Missouri, Sch Med, Dept Physiol, Columbia, MO 65212 USA. RP Jones, TA (reprint author), Univ Missouri, Sch Med, Dept Surg, 207 Allton Bldg,DC37500, Columbia, MO 65212 USA. CR Bergstrom RA, 1998, GENETICS, V150, P815 BOHMER A, 1995, AM J OTOL, V16, P498 Fermin CD, 1996, HISTOL HISTOPATHOL, V11, P407 HUBEL DH, 1970, J PHYSIOL-LONDON, V206, P419 Jones SM, 1997, J COMP PHYSIOL A, V180, P631, DOI 10.1007/s003590050079 Jones SM, 1996, J VESTIBUL RES-EQUIL, V6, P71 JONES TA, 1993, ACTA VET BRNO, V62, pS35, DOI 10.2754/avb199362suppl60035 JONES TA, 1992, ELECTROEN CLIN NEURO, V82, P377, DOI 10.1016/0013-4694(92)90007-5 Jones TA, 1998, J VESTIBUL RES-EQUIL, V8, P253 JONES TA, 1992, HEARING RES, V62, P181, DOI 10.1016/0378-5955(92)90184-O JONES TA, 1999, IN PRESS HEAR RES JONES TA, 1989, AM J OTOLARYNG, V10, P327, DOI 10.1016/0196-0709(89)90108-7 LANGE ME, 1988, THESIS U NEBRASKA LI LANGE ME, 1989, ASGSB B, V3, P31 Ross M D, 1993, J Vestib Res, V3, P241 Ross M D, 1994, Acta Otolaryngol Suppl, V516, P1 Sweet H, 1980, MOUSE NEWS LETT, V63, P19 WIESEL TN, 1965, J NEUROPHYSIOL, V28, P1060 WIESEL TN, 1963, J NEUROPHYSIOL, V26, P978 WIESEL TN, 1965, J NEUROPHYSIOL, V28, P1029 NR 20 TC 50 Z9 50 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 56 EP 60 DI 10.1016/S0378-5955(99)00090-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400006 PM 10491954 ER PT J AU Popelar, J Valvoda, J Syka, J AF Popelar, J Valvoda, J Syka, J TI Acoustically and electrically evoked contralateral suppression of otoacoustic emissions in guinea pigs SO HEARING RESEARCH LA English DT Article DE evoked otoacoustic emission; contralateral suppression; acoustic stimulation; electrical stimulation; guinea pig ID EFFERENT OLIVOCOCHLEAR NEURONS; AUDITORY-NERVE FIBERS; DISTORTION PRODUCTS; COCHLEAR MECHANICS; ROUND WINDOW; STIMULATION; RESPONSES; EAR; HUMANS; NOISE AB It is generally accepted that stimulation of the efferent auditory system results in changes of cochlear activity. A simple method of activating the olivocochlear pathway by contralateral electrical stimulation of the round window (ES-RW) was used in this study with the aim of comparing the efficacy of acoustically and/or electrically evoked contralateral suppression. The suppression of transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs) was elicited by contralateral acoustic stimulation (AS) (61 dB SPL continuous white noise), and/or by electrical stimulation of an electrode implanted at the contralateral round window (monopolar rectangular pulses 0.1 ms, repetition rate 300 Hz, intensity 50-100 mu A) in 12 guinea pigs. The average value of contralateral suppression of TEOAEs amounted to 1.04 +/- 0.48 dB for acoustic stimulation and 0.97 +/- 0.53 dB for round window electrical stimulation. The simultaneous presentation of both acoustic and electrical stimulation had only a slight additive effect and resulted in 1.27+/-0.79 dB diminution of TEOAEs. The suppression of DPOAEs during contralateral acoustic and electrical stimulation was evident mainly at low and middle frequencies (1-4 kHz). In two guinea pigs the maximum DPOAE suppression was present at high frequencies. The average values of contralateral suppression measured at individual f(2) frequencies of DPOAEs were similar to those calculated from 1/4 octave power spectrum analysis of the TEOAEs in half of the animals. The results demonstrated that contralateral ES-RW had a similar suppressive effect on TEOAEs and DPOAEs as did contralateral AS and simultaneous AS+(ES-RW). The results of spectral analysis suggested that both modes of contralateral stimulation excited similar sensory cochlear elements and induce comparable suppression of both TEOAEs and DPOAEs. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Acad Sci Czech Republ, Inst Expt Med, Prague 14220 4, Czech Republic. Charles Univ, Fac Med 1, ENT Clin, Prague, Czech Republic. RP Popelar, J (reprint author), Acad Sci Czech Republ, Inst Expt Med, Videnska 1083, Prague 14220 4, Czech Republic. RI Popelar, Jiri/H-2558-2014; Syka, Josef/H-3103-2014 CR ARAN JM, 1979, TECHNICAL BASIS AUDI, P233 AVAN P, 1990, HEARING RES, V44, P151, DOI 10.1016/0378-5955(90)90077-3 AVAN P, 1995, J ACOUST SOC AM, V97, P3012, DOI 10.1121/1.411866 BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Cazals Y, 1996, HEARING RES, V101, P81, DOI 10.1016/S0378-5955(96)00135-9 CHERYCROZE S, 1993, HEARING RES, V68, P53, DOI 10.1016/0378-5955(93)90064-8 Collet L, 1989, Rev Laryngol Otol Rhinol (Bord), V110, P67 daCosta DL, 1997, EXP BRAIN RES, V116, P259, DOI 10.1007/PL00005754 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 FEX J, 1959, Acta Otolaryngol, V50, P540, DOI 10.3109/00016485909129230 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 GUINAN JJ, 1988, HEARING RES, V37, P29, DOI 10.1016/0378-5955(88)90075-5 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 Hood LJ, 1996, HEARING RES, V101, P113, DOI 10.1016/S0378-5955(96)00138-4 KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Khvoles R, 1996, HEARING RES, V97, P120 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORMAN M, 1993, BRIT J AUDIOL, V27, P281, DOI 10.3109/03005369309076705 OHYAMA K, 1991, HEARING RES, V56, P111, DOI 10.1016/0378-5955(91)90160-B POPELAR J, 1996, AUDIT NEUROSCI, V3, P425 POPELAR J, 1993, HEARING RES, V67, P69, DOI 10.1016/0378-5955(93)90233-Q POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 PRASHER D, 1994, BRIT J AUDIOL, V28, P247, DOI 10.3109/03005369409086574 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 PUEL JL, 1995, ACTA ACUST, V3, P75 PUEL JL, 1990, J ACOUST SOC AM, V76, P1713 RAJAN R, 1983, HEARING RES, V12, P405, DOI 10.1016/0378-5955(83)90009-6 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SMITH DW, 1994, BRAIN RES, V652, P243, DOI 10.1016/0006-8993(94)90233-X SYKA J, 1994, HEARING RES, V75, P1, DOI 10.1016/0378-5955(94)90050-7 UEDA H, 1992, HEARING RES, V62, P199, DOI 10.1016/0378-5955(92)90187-R VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 ZENNER HP, 1990, ADV AUDIOL, V7, P35 ZWICKER E, 1981, HEARING RES, V4, P43, DOI 10.1016/0378-5955(81)90035-6 NR 42 TC 6 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 61 EP 70 DI 10.1016/S0378-5955(99)00091-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400007 PM 10491955 ER PT J AU Kierner, AC Zelenka, I Lukas, JR Aigner, M Mayr, R AF Kierner, AC Zelenka, I Lukas, JR Aigner, M Mayr, R TI Observations on the number, distribution and morphological peculiarities of muscle spindles in the tensor tympani and stapedius muscle of man SO HEARING RESEARCH LA English DT Article DE tensor tympani muscle; stapedius muscle; muscle spindle; human anatomy AB Although the middle ear muscles have been described for the first time more than four hundred years ago their role in modulation and transmission of sound is not yet fully understood. Surprisingly very little is known about proprioceptors in these muscles, especially in man, although this seems to be the key to the understanding of their various functions. Therefore, the question for proprioceptive sensory organs in these muscles is still relevant. The tensor tympani and stapedius muscles of four women who had donated their bodies to our institute were taken. Complete serial sections of these muscles were made which were either impregnated with silver, stained with ferric oxide for acidic polysaccharides or incubated with antibodies against S-100 protein. Thereby four to eight (mean five) muscle spindles distributed along the whole muscle could be detected in the tensor tympani muscles. These spindles contain one to three intrafusal muscle fibres and their length ranges from 140 to 4270 mu m (mean 1492.8 mu m). Furthermore, in three stapedius muscles one to two (mean 1.7) muscle spindles were found. They were from 350 to 500 mu m (mean 482 mu m) long and contained only one intrafusal muscle fiber. Regarding the diameter of intrafusal muscle fibers in both, the tensor tympani as well as the stapedius muscle, no difference to extrafusal muscle fibers of these muscles could be detected. The structure of these spindles differs considerably from those found in skeletal muscles. The morphological findings presented strongly suggest that muscle spindles occur regularly in both middle ear muscles. The results presented herein are consistent with clinical findings obtained from electromyographic studies and may help to elucidate all functions the middle ear muscles might serve in man. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Vienna, Inst Anat, Dept 2, A-1090 Vienna, Austria. Univ Hosp Vienna, Dept Ophthalmol, Vienna, Austria. RP Kierner, AC (reprint author), Univ Vienna, Inst Anat, Dept 2, Waehringerstr 13-3, A-1090 Vienna, Austria. CR BLEVINS CE, 1967, ARCH OTOLARYNGOL, V86, P130 BLUMER R, 1999, IN PRESS INVEST OPHT, V40 BLUMER R, 1995, ANN ANAT S S177, V177, P214 BORG E, 1975, ACTA OTO-LARYNGOL, V79, P325, DOI 10.3109/00016487509124694 BRZEZINSKI D K, 1962, Arch Ohren Nasen Kehlkopfheilkd, V179, P550, DOI 10.1007/BF02103626 CANCURA W, 1970, M SCHR OHRENHEILK, V19, P1 CANDIOLL.L, 1965, Z ZELLFORSCH MIK ANA, V67, P34, DOI 10.1007/BF00339275 Djupesland G, 1964, ACTA OTO-LARYNGOL, V188, P287 EUSTACHIUS B, 1562, EPISTOLA AUDITUS ORG Ingelstedt S, 1966, ACTA OTO-LARYNGOL, V224, P452 KAMERER DB, 1978, OTOLARYNG HEAD NECK, V86, P416 Kato T, 1913, PFLUG ARCH GES PHYS, V150, P569, DOI 10.1007/BF01681012 LIDEN B, 1963, ACTA OTOLARYNGOL S, V188, P275 LUKAS JR, 1994, INVEST OPHTH VIS SCI, V35, P4317 POLLITZER A, 1864, OHR NAS KEHLK HK, V1, P59 RUSKELL GL, 1989, J ANAT, V167, P199 SALEN B, 1978, ACTA OTO-LARYNGOL, V85, P453, DOI 10.3109/00016487809121474 SALOMON G, 1963, ACTA NEUROL SCAND, V39, P161 SIMMONS FB, 1964, ANN OTO RHINOL LARYN, V73, P724 STEINITZ W, 1907, ARCH OHRENHEILK, V70, P45 WINCKLER G, 1982, Archives d'Anatomie d'Histologie et d'Embryologie Normales et Experimentales, V65, P49 ZUCKERLANDL E, 1884, ARCH OHRENHEILK, V20, P104 NR 22 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 71 EP 77 DI 10.1016/S0378-5955(99)00092-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400008 PM 10491956 ER PT J AU Willott, JF Turner, JG AF Willott, JF Turner, JG TI Prolonged exposure to an augmented acoustic environment ameliorates age-related auditory changes in C57BL/6J and DBA/2J mice SO HEARING RESEARCH LA English DT Article DE sensorineural hearing loss; mouse model; prepulse inhibition; auditory brainstem response; startle ID SENSORINEURAL HEARING-LOSS; INFERIOR COLLICULUS NEURONS; PREPULSE INHIBITION; STARTLE RESPONSE; ELECTRICAL-STIMULATION; COCHLEAR NUCLEUS; GUINEA-PIG; CORTEX; PLASTICITY; LESIONS AB The effects of exposure to an augmented acoustic environment (AAE) on auditory function were evaluated in mouse strains that exhibit high-frequency hearing loss beginning during young adulthood (the C57BL/6J strain [C57]) or around the time of weaning/ adolescence (the DBA/2J strain [DBA]). Beginning at age 25 days, mice were exposed 12 h every night to a 70 dB SPL broad-band noise AAE. The AAE was maintained until age 14 months in C57 mice and 9 months in DBA mice. Control mice were age-matched and maintained under normal vivarium acoustic conditions. The auditory brainstem response (ABR), acoustic startle response amplitude, and prepulse inhibition (PPI) were used to assess the auditory system. Exposure to the AAE resulted in improved auditory performance in both strains (better PPT. lower ABR thresholds, bigger startle amplitudes). (C) 1999 Elsevier Science B.V. All rights reserved. C1 No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. RP Willott, JF (reprint author), No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. CR HALL WH, 1990, JAMA-J AM MED ASSOC, V263, P3185 CALFORD MB, 1993, NEUROSCIENCE, V55, P953, DOI 10.1016/0306-4522(93)90310-C Canlon B, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P118 Carlson S, 1996, HEARING RES, V99, P168, DOI 10.1016/S0378-5955(96)00098-6 Carlson S, 1998, J NEUROPHYSIOL, V79, P2603 COTMAN CW, 1996, HDB BIOL AGING, P284 Davis M., 1984, P287 DUBLIN W, 1976, FUNDAMENTALS SENSORI ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H FOX JE, 1979, PHYSIOL BEHAV, V23, P291, DOI 10.1016/0031-9384(79)90370-6 Henderson D, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P143 HENRY KR, 1980, AUDIOLOGY, V19, P369 HOFFMAN HS, 1980, PSYCHOL REV, V87, P175, DOI 10.1037/0033-295X.87.2.175 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEITNER DS, 1985, PHYSIOL BEHAV, V34, P65, DOI 10.1016/0031-9384(85)90079-4 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 Li L, 1998, BEHAV NEUROSCI, V112, P1187, DOI 10.1037/0735-7044.112.5.1187 Li L, 1998, PHYSIOL BEHAV, V65, P133, DOI 10.1016/S0031-9384(98)00143-7 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MCFADDEN SL, 1994, HEARING RES, V78, P132, DOI 10.1016/0378-5955(94)90019-1 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 Miller JM, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P378 Northern J. L., 1991, HEARING CHILDREN PARHAM K, 1997, ASS RES OT ABSTR, V20, P194 PARHAM K, 1988, Behavioral Neuroscience, V102, P881, DOI 10.1037/0735-7044.102.6.881 PARHAM K, 1990, BEHAV NEUROSCI, V104, P831, DOI 10.1037//0735-7044.104.6.831 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 RALLS K, 1967, ANIM BEHAV, V15, P123, DOI 10.1016/S0003-3472(67)80022-8 SAUNDERS JC, 1980, BRAIN RES, V187, P69, DOI 10.1016/0006-8993(80)90495-3 Schuknecht H. F., 1974, PATHOLOGY EAR SCHWABER MK, 1993, AM J OTOL, V14, P252 SHNERSON A, 1980, J COMP PHYSIOL PSYCH, V94, P36, DOI 10.1037/h0077648 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 Subramaniam M, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P128 SWERDLOW NR, 1993, BEHAV NEUROSCI, V107, P104, DOI 10.1037//0735-7044.107.1.104 TURNER JG, 1999, ASS RES OT ABSTR, V22, P220 Turner JG, 1998, HEARING RES, V118, P101, DOI 10.1016/S0378-5955(98)00024-0 Willott JF, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P297 Willott J. F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1996, PATHOBIOLOGY AGING M, P179 WILLOTT JF, 1993, J COMP NEUROL, V329, P402, DOI 10.1002/cne.903290310 WILLOTT JF, 1978, BRAIN RES, V148, P230, DOI 10.1016/0006-8993(78)90395-5 WILLOTT JF, 1984, HEARING RES, V16, P161, DOI 10.1016/0378-5955(84)90005-4 WILLOTT JF, 1995, BEHAV NEUROSCI, V109, P396, DOI 10.1037//0735-7044.109.3.396 WILLOTT JF, 1981, J NEUROPHYSIOL, V45, P35 WILLOTT JF, 1994, BEHAV NEUROSCI, V108, P703, DOI 10.1037/0735-7044.108.4.703 WILLOTT JF, 1999, ASS RES OT ABSTR, V22, P153 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 Willott JF, 1996, DEV BRAIN RES, V91, P218, DOI 10.1016/0165-3806(95)00188-3 WILLOTT JF, 1995, HEARING RES, V88, P143, DOI 10.1016/0378-5955(95)00107-F NR 54 TC 37 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 78 EP 88 DI 10.1016/S0378-5955(99)00094-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400009 PM 10491957 ER PT J AU Khanna, SM Hao, LF AF Khanna, SM Hao, LF TI Nonlinearity in the apical turn of living guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE cochlea; mechanical response; guinea pig; heterodyne interferometry; nonlinearity; harmonic distortion; waveform distortion; tuning curves; negative feedback ID BASILAR-MEMBRANE; MOSSBAUER TECHNIQUE; HAIR BUNDLES; INNER-EAR; VIBRATION; MICROSCOPE; MECHANICS; RESPONSES; ORGAN AB Mechanical vibrations were measured at the apical turn in living guinea pig cochlea, in response to sinusoidal acoustic stimuli, using heterodyne interferometry. The cochlea was sealed and the vibrations were measured at different cellular locations along a radial track at the level of reticular lamina and one point on the osseous spiral lamina. Averaged time waveforms were recorded at each test frequency. The nonlinearity in the apical turn is demonstrated by the distortion in the time waveforms and the richness of the harmonic components in their Fourier transforms. Tuning curves and input/output curves for the fundamental and harmonics components are shown. The fundamental component is essentially linear below about 90 dB SPL while the harmonics display strong nonlinearity and saturation. Negative feedback in the apical turn of the cochlea linearizes the response at the fundamental frequency. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Columbia Univ, Coll Phys & Surg, Dept Otolaryngol & Head & Neck Surg, New York, NY 10032 USA. Univ Maryland, Sch Med, Dept Otolaryngol & Head & Neck Surg, Baltimore, MD 21201 USA. RP Khanna, SM (reprint author), Columbia Univ, Coll Phys & Surg, Dept Otolaryngol & Head & Neck Surg, New York, NY 10032 USA. CR BRUNDIN L, 1991, NEUROSCI LETT, V128, P77, DOI 10.1016/0304-3940(91)90763-J Cooper NP, 1998, J PHYSIOL-LONDON, V509, P277, DOI 10.1111/j.1469-7793.1998.277bo.x COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X COOPER NP, 1996, DIVERSITY COCHLEAR M, P298 FLOCK A, 1984, NATURE, V310, P597, DOI 10.1038/310597a0 FLOCK A, 1965, COLD SPRING HARB S Q, V30 Galambos R, 1943, J NEUROPHYSIOL, V6, P39 GUMMER AW, 1993, BIOPHYSICS HAIR CELL, P229 Hao LF, 1996, HEARING RES, V99, P176, DOI 10.1016/S0378-5955(96)00099-8 Johnstone BM, 1967, SCIENCE, V158, P390 KHANNA SM, 1996, P SOC PHOTO-OPT INS, V2732, P64, DOI 10.1117/12.231687 Khanna SM, 1999, HEARING RES, V132, P15, DOI 10.1016/S0378-5955(99)00027-1 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P205 KHANNA SM, 1993, BIOPHYSICS HAIRCELL, P266 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P195 KHANNA SM, 1998, IN PRESS ACOUSTICA, V84 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KOESTER CJ, 1990, T ROY MICR, V1, P327 KOESTER CJ, 1994, APPL OPTICS, V33, P702, DOI 10.1364/AO.33.000702 Koester C J, 1989, Acta Otolaryngol Suppl, V467, P27 KOESTER CJ, 1980, APPL OPTICS, V19, P1749, DOI 10.1364/AO.19.001749 LEONARD DGB, 1984, J ACOUST SOC AM, V2, P515 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 Ruggero MA, 1997, J ACOUST SOC AM, V101, P2151, DOI 10.1121/1.418265 RUSSELL IJ, 1992, P ROY SOC B-BIOL SCI, V250, P217, DOI 10.1098/rspb.1992.0152 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 SEIGEL JH, 1982, NEW PERSPECTIVES NOI SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SOKOLICH WG, 1981, Patent No. 4251686 Stevens S. S., 1938, HEARING ITS PSYCHOL STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 TASAKI I, 1952, J ACOUST SOC AM, V24, P502, DOI 10.1121/1.1906928 Teich M C, 1989, Acta Otolaryngol Suppl, V467, P265 WERSALL J, 1965, COLD SPRING HARB S Q, V30 WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 NR 39 TC 33 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 89 EP 104 DI 10.1016/S0378-5955(99)00095-7 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400010 PM 10491958 ER PT J AU LeBlanc, CS Fallon, M Parker, MS Skellett, R Bobbin, RP AF LeBlanc, CS Fallon, M Parker, MS Skellett, R Bobbin, RP TI Phosphorothioate oligodeoxynucleotides can selectively alter neuronal activity in the cochlea SO HEARING RESEARCH LA English DT Article DE antisense; toxicity; cochlear potential; otoacoustic emission; ATP receptor ID CONTINUOUS PRIMARY STIMULATION; F(2)-F(1) DPOAE RESPONSE; TIME-VARYING ALTERATIONS; ANTISENSE OLIGONUCLEOTIDES; PHARMACOLOGICAL EVIDENCE; GENE-EXPRESSION; RECEPTOR; MECHANISMS; TRANSMISSION; INHIBITORS AB A growing body of evidence indicates that extracellular adenosine triphosphate (ATP) may have a major role in cochlear function. Antagonists of ionotropic ATP receptors (P2X(2)) have significant effects on cochlear potentials and distortion product otoacoustic emissions (DPOAEs). We tested whether antisense oligodeoxynucleotides (ODNs) would mimic the functional deficiencies induced by the ATP antagonists through binding to P2X(2) ATP receptor mRNA and thereby reduce the number of ATP receptors expressed in the membrane of the cells. Both a phosphorothioate ODN (S-ODN) antisense and a phosphodiester ODN (P-ODN) antisense to the P2X(2) sequence and random sense ODNs containing 21 nucleotides were administered chronically (7 days) to the guinea pig cochlea via the perilymph compartment. Sound evoked cochlear potentials (cochlear microphonic; summating potential; compound action potential of the auditory nerve, CAP; latency of the first negative peak in the CAP, N1 latency) and DPOAEs were monitored to assess the effects of the ODNs. Results indicate that the phosphorothioate derivatives of both the antisense and random sense ODNs suppressed the CAP and prolonged the N1 latency with no significant effect on the other parameters. The P-ODNs had no effect. Since both the antisense and random sense S-ODNs had the same effect, we conclude that the S-ODNs affected neuronal function in a manner that did not involve binding to the ATP receptor mRNA. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Louisiana State Univ, Med Ctr, Dept Otorhinolaryngol & Biocommun, Kresge Hearing Res Lab S, New Orleans, LA 70112 USA. RP Bobbin, RP (reprint author), Louisiana State Univ, Med Ctr, Dept Otorhinolaryngol & Biocommun, Kresge Hearing Res Lab S, 2020 Gravier St,Suite A, New Orleans, LA 70112 USA. CR Bobbin RP, 1997, HEARING RES, V113, P155, DOI 10.1016/S0378-5955(97)00140-8 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1996, HAIR CELLS HEARING A, P29 BOBBIN RP, 1998, OTOACOUSTIC EMISSION, P61 BROWN JN, 1993, HEARING RES, V70, P167, DOI 10.1016/0378-5955(93)90155-T BRUSSAARD AB, 1995, NEUROSCI LETT, V191, P111, DOI 10.1016/0304-3940(95)11539-6 BURNSTOCK G, 1990, ANN NY ACAD SCI, V603, P1 Chen C, 1998, HEARING RES, V118, P47, DOI 10.1016/S0378-5955(98)00019-7 d'Aldin C, 1998, MOL BRAIN RES, V55, P151, DOI 10.1016/S0169-328X(97)00352-5 EYBALIN M, 1993, PHYSIOL REV, V73, P309 GAO WY, 1992, MOL PHARMACOL, V41, P223 Gewirtz AM, 1996, P NATL ACAD SCI USA, V93, P3161, DOI 10.1073/pnas.93.8.3161 GHOSH MK, 1992, PROG NUCLEIC ACID RE, V42, P79 HOUSLEY GD, 1997, MOL NEUROBIOL, V16, P21 Kemp DT, 1998, OTOACOUSTIC EMISSION, P1 KUJAWA SG, 1995, HEARING RES, V85, P142, DOI 10.1016/0378-5955(95)00041-2 Kujawa SG, 1996, HEARING RES, V97, P153 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 LEONETTI JP, 1993, PROG NUCLEIC ACID RE, V44, P143, DOI 10.1016/S0079-6603(08)60219-6 MILLS DM, 1998, OTOACOUSTIC EMISSION, P85 PARKER MS, 1997, ARO ABSTR, V20, P217 Parker MS, 1998, HEARING RES, V121, P62, DOI 10.1016/S0378-5955(98)00065-3 Rossi Grace, 1994, Life Sciences, V54, P375 Roush W, 1997, SCIENCE, V276, P1192, DOI 10.1126/science.276.5316.1192 Shaw DR, 1997, BIOCHEM PHARMACOL, V53, P1123, DOI 10.1016/S0006-2952(97)00091-9 Skellett RA, 1997, HEARING RES, V111, P42, DOI 10.1016/S0378-5955(97)00093-2 SLAVKIN HC, 1995, INT J DEV BIOL, V39, P123 STANDIFER KM, 1995, J NEUROCHEM, V65, P1981 WHITESELL L, 1993, P NATL ACAD SCI USA, V90, P4665, DOI 10.1073/pnas.90.10.4665 ZHANG M, 1993, NEUROSCI LETT, V161, P223, DOI 10.1016/0304-3940(93)90299-Z NR 31 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 105 EP 112 DI 10.1016/S0378-5955(99)00093-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400011 PM 10491959 ER PT J AU Marcotti, W Russo, G Prigioni, I AF Marcotti, W Russo, G Prigioni, I TI Inactivating and non-inactivating delayed rectifier K+ currents in hair cells of frog crista ampullaris SO HEARING RESEARCH LA English DT Article DE frog; semicircular canal; hair cell; potassium current; delayed rectifier ID GUINEA-PIG COCHLEA; POTASSIUM CURRENTS; SYNAPTIC TRANSMISSION; IONIC CURRENTS; CHANNELS; CAPSAICIN; NEURONS; TRANSDUCTION; CONDUCTANCE; EXPRESSION AB The possible presence of different types of delayed rectifier K+ current (IK) was studied in vestibular hair cells of frog semicircular canals. Experiments were performed in thin slice preparations of the whole crista ampullaris and recordings were made using the whole-cell patch-clamp technique. We found that an apparent homogeneous IK, isolated from the other K+ currents, could be pharmacologically separated into two complementary components: a capsaicin-sensitive current (I-K,I-c) and a barium-sensitive current (I-K,I-b) I-K,I-c was recruited at potentials more positive than -60 mV and showed a slow activation having a time constant (tau(a)) ranging on average from 12 ms at 40 mV to 32 ms at -20 mV. This current inactivated slowly with two voltage-independent time constants (tau(dl) and tau(d2) were 300 ms and 4 s respectively) and more than 80% of the channels were in an inactivated state at the cell resting potential. I-K,I-b was also recruited at potentials more positive than -60 mV, but in contrast to I-K,I-c, it activated more rapidly (tau(a), ranged on average from 1 ms at 40 mV to 4.5 ms at -20 mV and it did not exhibit any inactivation process. Current clamp experiments revealed that I-K,I-b, at variance with I-K,I-c contributes to the cell resting potential and represents the main repolarizing current when sensory cells are depolarized from rest. I-K,I-c could have a role in hair cells when they are depolarized after hyperpolarizing stimuli, a condition that removes channel inactivation. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Pavia, Ist Fisiol Gen, I-27100 Pavia, Italy. RP Prigioni, I (reprint author), Univ Pavia, Ist Fisiol Gen, Via Forlanini 6, I-27100 Pavia, Italy. CR ADAMS PR, 1982, J PHYSIOL-LONDON, V330, P537 ADAMS PR, 1982, J PHYSIOL-LONDON, V332, P223 BAKER MD, 1994, P ROY SOC B-BIOL SCI, V255, P259, DOI 10.1098/rspb.1994.0037 BLAUSTEI.MP, 1968, J GEN PHYSIOL, V51, P279, DOI 10.1085/jgp.51.3.279 DUBOIS JM, 1982, BRAIN RES, V245, P372, DOI 10.1016/0006-8993(82)90820-4 DUBOIS JM, 1983, PROG BIOPHYS MOL BIO, V42, P1, DOI 10.1016/0079-6107(83)90002-0 Fuchs PA, 1996, CURR OPIN NEUROBIOL, V6, P514, DOI 10.1016/S0959-4388(96)80058-4 FUCHS PA, 1992, PROG NEUROBIOL, V39, P493, DOI 10.1016/0301-0082(92)90003-W GRIGUER C, 1993, PFLUG ARCH EUR J PHY, V425, P344, DOI 10.1007/BF00374185 Hille B., 1992, IONIC CHANNELS EXCIT, V2nd HOUSLEY GD, 1992, J PHYSIOL-LONDON, V448, P73 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 LANG DG, 1989, J NEUROPHYSIOL, V62, P935 LO YC, 1995, EUR J PHARM-ENVIRON, V292, P321 MASETTO S, 1994, J NEUROPHYSIOL, V72, P443 MURROW BW, 1994, J PHYSIOL-LONDON, V480, P247 Oh U, 1996, J NEUROSCI, V16, P1659 Prigioni I, 1996, NEUROREPORT, V7, P1841, DOI 10.1097/00001756-199607290-00031 Prigioni I, 1992, J Vestib Res, V2, P31 RENNIE KJ, 1994, J NEUROPHYSIOL, V71, P317 Ricci AJ, 1996, PFLUG ARCH EUR J PHY, V432, P34, DOI 10.1007/s004240050102 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 ROPER J, 1989, J PHYSIOL-LONDON, V416, P93 RUDY B, 1988, NEUROSCIENCE, V25, P729, DOI 10.1016/0306-4522(88)90033-4 Rusch A, 1996, J NEUROPHYSIOL, V76, P995 Russo G, 1996, NEUROREPORT, V7, P2143, DOI 10.1097/00001756-199609020-00016 RUSSO G, 1995, NEUROREPORT, V6, P425, DOI 10.1097/00001756-199502000-00005 STEINACKER A, 1991, BRAIN RES, V556, P22, DOI 10.1016/0006-8993(91)90543-5 ZHAO B, 1994, NEURON, V13, P1205, DOI 10.1016/0896-6273(94)90058-2 NR 31 TC 7 Z9 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 113 EP 123 DI 10.1016/S0378-5955(99)00097-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400012 PM 10491960 ER PT J AU Garcia-Diaz, JF AF Garcia-Diaz, JF TI Development of a fast transient potassium current in chick cochlear ganglion neurons SO HEARING RESEARCH LA English DT Article DE chick embryo; cochlear ganglion; development; potassium current; neurotrophin ID MOUSE HIPPOCAMPAL-NEURONS; AMPHIBIAN SPINAL NEURONS; NERVE GROWTH-FACTOR; INNER-EAR; IN-VITRO; COCHLEOVESTIBULAR GANGLION; NEUROTROPHIC FACTORS; SYMPATHETIC NEURONS; CALCIUM CURRENTS; EMBRYONIC CHICK AB Neurons of the cochlear ganglion are endowed with a set of voltage-gated ion channels that enable them to encode and transmit sound information from the cochlear receptors to the brain. The temporal expression pattern of the K+ currents in chick cochlear ganglion neurons during embryonic development was analyzed using whole-cell voltage clamp techniques. In acutely isolated neurons, slowly activating delayed rectifier Kf currents appear at embryonic day 7 (E7) and increase in amplitude during development. A fast activating, fast inactivating K+ current of the A type is first expressed at E10, increasing in amplitude thereafter. To investigate the possible role of neurotrophins in the induction of these K+ channels, neurons were grown in culture in the presence or absence of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Neurons isolated at E8 and grown in culture for I day exhibit a high expression of A-current, together with the outgrowth of neurites. A-currents are not seen in acutely dissociated neurons from age-matched embryos (E9) which lack neurites, cut off by the isolation procedure. This suggests a preferential neuritic location of the channels carrying the A-current. However, the level of expression of the Kt currents was independent of BDNF or NT-3 application. Similarly, neurons isolated at E10 and grown in culture for up to 4 days maintain the amplitude of the K+ currents independently of the presence of the neurotrophins. These results indicate that BDNF and NT-3 may not directly regulate the expression of K+ channels in chick cochlear ganglion neurons. The notable expression of the fast inactivating A-current suggests that it plays a significant role-in the modulation of synaptic efficacy and the encoding of auditory stimuli. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Boston Univ, Sch Med, Dept Physiol, Boston, MA 02118 USA. RP Garcia-Diaz, JF (reprint author), Boston Univ, Sch Med, Dept Physiol, 715 Albany St, Boston, MA 02118 USA. CR Alonso G, 1997, NEUROSCIENCE, V77, P617 AVILA MA, 1993, DEV BIOL, V159, P266, DOI 10.1006/dbio.1993.1239 BARISH ME, 1986, J PHYSIOL-LONDON, V375, P229 BREWER GJ, 1993, J NEUROSCI RES, V35, P567, DOI 10.1002/jnr.490350513 CONNOR JA, 1978, FED PROC, V37, P2139 CONNOR JA, 1971, J PHYSIOL-LONDON, V213, P21 DOURADO MM, 1992, J PHYSIOL-LONDON, V449, P411 DOURADO MM, 1994, J PHYSIOL-LONDON, V474, P367 Fritzsch B, 1997, TRENDS NEUROSCI, V20, P159, DOI 10.1016/S0166-2236(96)01007-7 FUCHS PA, 1990, P ROY SOC B-BIOL SCI, V241, P122, DOI 10.1098/rspb.1990.0075 Garrido JJ, 1998, J NEUROCHEM, V70, P2336 Griguer C, 1996, J NEUROPHYSIOL, V75, P508 Hoffman DA, 1997, NATURE, V387, P869 Jimenez C, 1997, NEUROSCIENCE, V77, P673, DOI 10.1016/S0306-4522(96)00505-2 JONES SM, 1995, HEARING RES, V82, P139, DOI 10.1016/0378-5955(94)00172-M Lesser SS, 1997, MOL CELL NEUROSCI, V10, P173, DOI 10.1006/mcne.1997.0656 LEVINE ES, 1995, J NEUROSCI, V15, P3084 Lewin GR, 1996, ANNU REV NEUROSCI, V19, P289, DOI 10.1146/annurev.ne.19.030196.001445 Lin X, 1997, HEARING RES, V108, P157, DOI 10.1016/S0378-5955(97)00050-6 MALETICSAVATIC M, 1995, J NEUROSCI, V15, P3840 MANDEL G, 1988, P NATL ACAD SCI USA, V85, P924, DOI 10.1073/pnas.85.3.924 MCFARLANE S, 1993, J NEUROSCI, V13, P2591 Moore EJ, 1996, ACTA OTO-LARYNGOL, V116, P552, DOI 10.3109/00016489609137888 RAUCHER S, 1994, J PHYSIOL-LONDON, V479, P77 RIBERA AB, 1990, J NEUROSCI, V10, P1886 ROGAWSKI MA, 1985, TRENDS NEUROSCI, V8, P214, DOI 10.1016/0166-2236(85)90082-7 SANTOS-SACCHI J, 1993, J NEUROSCI, V13, P3599 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SHENG M, 1992, NEURON, V9, P271, DOI 10.1016/0896-6273(92)90166-B SHEPPARD DN, 1992, NEUROSCIENCE, V51, P631, DOI 10.1016/0306-4522(92)90302-I Sherwood NT, 1997, P NATL ACAD SCI USA, V94, P5917, DOI 10.1073/pnas.94.11.5917 Sokolowski BHA, 1997, EXP NEUROL, V145, P1, DOI 10.1006/exnr.1997.6444 SPITZER NC, 1991, J NEUROBIOL, V22, P659, DOI 10.1002/neu.480220702 VALVERDE MA, 1992, NEUROSCIENCE, V51, P621, DOI 10.1016/0306-4522(92)90301-H WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P277, DOI 10.1016/0306-4522(85)90178-2 Wu RL, 1998, J NEUROSCI, V18, P6261 WU RL, 1994, J NEUROSCI, V14, P1677 YAMAGUCHI K, 1990, J PHYSIOL-LONDON, V420, P185 NR 38 TC 8 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 124 EP 134 DI 10.1016/S0378-5955(99)00099-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400013 PM 10491961 ER PT J AU Husbands, JM Steinberg, SA Kurian, R Saunders, JC AF Husbands, JM Steinberg, SA Kurian, R Saunders, JC TI Tip-link integrity on chick tall hair cell stereocilia following intense sound exposure SO HEARING RESEARCH LA English DT Article DE auditory system; chick; hair cell; tip link; basilar papilla; acoustic injury; hearing loss; cochlear damage; recovery of function ID SEVERE ACOUSTIC TRAUMA; BASILAR PAPILLA; BIRD COCHLEA; NEONATAL CHICKS; ACTIN-FILAMENTS; MECHANOELECTRICAL TRANSDUCTION; TECTORIAL MEMBRANE; AVIAN COCHLEA; NOISE DAMAGE; REGENERATION AB Hair bundle tip links have been implicated in the process of hair cell transduction, and previous studies have shown that acoustic overstimulation or exposure to low calcium can disrupt them. Severed tip links would thus be expected to cause a loss in hair cell function. This study investigates the presence of tip links on chick tall hair cells at three exposure durations and three recovery durations. After 4, 24, or 48 h of exposure, and 24, 96, and 288 h of recovery, the basilar papilla was harvested and prepared for scanning electron microscopy. Photomicrographs of hair bundles from sound-exposed and age-matched control ears were obtained in regions of the papilla adjacent to the 'patch' lesion. The percentage of tip links present on these hair bundles was determined from the photomicrographs. After 4, 24, or 48 h of exposure, an average of 49%, 41.1% and 52% of the observed sensory hairs exhibited links. This was significantly lower than that seen in the control ears (71.2%). There also was a reliable recovery of tip links between 24 and 48 h of exposure. The recovery continued and by 24 h post exposure, tip links were present on 61.3% of the sensory hairs. At subsequent recovery intervals, the mean number of tip links on sound-exposed tall hair cells was statistically the same as seen on control cells. The results indicated a predictable loss in the number of tip links during the exposure and their restoration within a relatively short time after the exposure. This structural damage to the tall hair cell, and its recovery, could account for some of the loss and recovery of function in the auditory periphery of these sound-damaged chicks. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Penn, Sch Med, Dept Otorhinolaryngol Head & Neck Surg, Philadelphia, PA 19104 USA. Univ Penn, Sch Vet Med, Neurol Sect, Philadelphia, PA 19104 USA. RP Saunders, JC (reprint author), Auditory Res Lab, 5 Ravdin ORL,3400 Spruce St, Philadelphia, PA 19104 USA. CR ADLER HJ, 1993, HEARING RES, V86, P43 ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 ANDERSON GJ, 1989, ABSTR ASS RES OT, V12, P94 ASSAD JA, 1991, NEURON, V7, P1 Chen L, 1996, HEARING RES, V98, P152, DOI 10.1016/0378-5955(96)00086-X Clark JA, 1996, HEARING RES, V99, P119, DOI 10.1016/S0378-5955(96)00092-5 COHEN YE, 1993, EXP BRAIN RES, V95, P202 COTANCHE DA, 1987, HEARING RES, V30, P197, DOI 10.1016/0378-5955(87)90136-5 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1992, EXP NEUROL, V115, P23, DOI 10.1016/0014-4886(92)90215-C COTANCHE DA, 1983, ARCH OTO-RHINO-LARYN, V237, P191, DOI 10.1007/BF00453723 Cotanche DA, 1997, ANN OTO RHINOL LARYN, V106, P9 COTANCHE DA, 1992, ABSTR ASS RES OT, V15, P116 COTANCHE DA, 1990, HEARING RES, V46, P29, DOI 10.1016/0378-5955(90)90137-E COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 Duncan RK, 1999, HEARING RES, V127, P22, DOI 10.1016/S0378-5955(98)00168-3 Duncan RK, 1998, HEARING RES, V124, P69, DOI 10.1016/S0378-5955(98)00118-X Duncan RK, 1995, AUDIT NEUROSCI, V1, P321 EATOCK RA, 1987, J NEUROSCI, V7, P2821 Eisen MD, 1999, HEARING RES, V127, P14, DOI 10.1016/S0378-5955(98)00167-1 Erulkar J. S., 1996, Scanning Microscopy, V10, P1127 FISCHER FP, 1994, SCANNING MICROSCOPY, V8, P351 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R FURNESS DN, 1986, HEARING RES, V21, P243, DOI 10.1016/0378-5955(86)90222-4 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 MARKIN VS, 1995, ANNU REV BIOPH BIOM, V24, P59 MARSH RR, 1990, HEARING RES, V46, P229, DOI 10.1016/0378-5955(90)90004-9 MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 PICKLES JO, 1989, HEARING RES, V41, P31, DOI 10.1016/0378-5955(89)90176-7 PICKLES JO, 1987, HEARING RES, V25, P173, DOI 10.1016/0378-5955(87)90089-X PICKLES JO, 1990, HEARING RES, V50, P139, DOI 10.1016/0378-5955(90)90040-V POJE CP, 1995, HEARING RES, V82, P197, DOI 10.1016/0378-5955(94)00177-R PUGLIANO FA, 1993, ACTA OTO-LARYNGOL, V113, P18, DOI 10.3109/00016489309135761 RYALS BM, 1995, HEARING RES, V83, P51, DOI 10.1016/0378-5955(94)00190-2 Saunders JC, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P62 SAUNDERS JC, 1993, HEAR RES, V69, P23 Saunders JC, 1996, J NEUROPHYSIOL, V76, P770 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A STONE JS, 1992, J CELL SCI, V102, P671 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 TILNEY LG, 1988, J CELL BIOL, V106, P355, DOI 10.1083/jcb.106.2.355 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 Trautwein PG, 1997, HEARING RES, V110, P266, DOI 10.1016/S0378-5955(97)00082-8 VOSSIECK T, 1990, EUR ARCH OTO-RHINO-L, V248, P11, DOI 10.1007/BF00634773 VOSSIECK T, 1991, HEARING RES, V56, P93, DOI 10.1016/0378-5955(91)90158-6 ZHAO Y, 1996, P NATL ACAD SCI USA, V94, P15469 NR 47 TC 26 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 135 EP 145 DI 10.1016/S0378-5955(99)00101-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400014 PM 10491962 ER PT J AU Kimura, M Eggermont, JJ AF Kimura, M Eggermont, JJ TI Effects of acute pure tone induced hearing loss on response properties in three auditory cortical fields in cat SO HEARING RESEARCH LA English DT Article DE noise trauma; cat; auditory cortex; single unit; local field potential frequency tuning; spontaneous activity; tinnitus ID INFERIOR COLLICULUS; ELECTRICAL-STIMULATION; LATERAL INHIBITION; NEURAL ACTIVITY; CORTEX NEURONS; SALICYLATE; SOUND; PLASTICITY; TINNITUS; POTENTIALS AB In this study, we assessed the changes in spontaneous activity;and frequency tuning by simultaneous recording of multi-units and local field potentials in primary auditory cortex (AI), anterior auditory field (AAF) and secondary auditory cortex (AII) of cats before and immediately after 30 min exposure to a loud (93-123 dB SPL) pure tone. The average difference of the pure tone and the characteristic frequency (CF) was less than one octave for 70% of the recordings. We found that the mean threshold at CF increased significantly in AI and in AAF but not in AII. The mean CF for units in AI decreased significantly, whereas no significant effect uas noted in AAF and AII. The mean frequency-tuning curve bandwidth decreased significantly in AII. Spontaneous activity increased significantly in AI, did not change in AAF, and decreased significantly in AII. Inter-area neural synchrony was not affected. Multiunit response areas were usually similarly affected as local field potentials based response areas because the 'damaged area', defined as the response surface before minus the surface after the trauma, was very similar. This suggests that the damage reflects peripheral activity changes. Enhancement of frequency response areas around CF, but at least one octave below the frequency of the traumatizing tone, was found most frequently in AAF and suggests a reduction of inhibition likely as a result of the peripheral hearing loss. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada. Univ Calgary, Dept Physiol & Biophys, Calgary, AB T2N 1N4, Canada. RP Eggermont, JJ (reprint author), Univ Calgary, Dept Psychol, 2500 Univ Dr NW, Calgary, AB T2N 1N4, Canada. CR Buracas GT, 1998, NEURON, V20, P959 CALFORD MB, 1993, NEUROSCIENCE, V55, P953, DOI 10.1016/0306-4522(93)90310-C CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O COLES RRA, 1984, J LARYNGOL OTOL S, V9, P195 Eggermont JJ, 1997, NEUROREPORT, V8, P2709, DOI 10.1097/00001756-199708180-00014 Eggermont JJ, 1995, MECH TINNITUS, P21 EGGERMONT JJ, 1992, J NEUROPHYSIOL, V68, P1216 Eggermont JJ, 1998, HEARING RES, V117, P149, DOI 10.1016/S0378-5955(98)00008-2 EGGERMONT JJ, 1996, AUDIT NEUROSCI, V2, P76 EGGERMONT JJ, 1995, J NEUROPHYSIOL, V73, P227 EPPING WJM, 1985, HEARING RES, V18, P223, DOI 10.1016/0378-5955(85)90040-1 Gerken GM, 1996, HEARING RES, V97, P75 GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 GERKEN GM, 1991, HEARING RES, V53, P101, DOI 10.1016/0378-5955(91)90217-W ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 Kaltenbach JA, 1996, AUDIT NEUROSCI, V3, P57 Kral A, 1996, GEN PHYSIOL BIOPHYS, V15, P109 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LONSBURYMARTIN BL, 1981, J NEUROPHYSIOL, V46, P563 LONSBURYMARTIN BL, 1978, J NEUROPHYSIOL, V41, P787 Manabe Y, 1997, HEARING RES, V103, P192, DOI 10.1016/S0378-5955(96)00181-5 MITZDORF U, 1985, PHYSIOL REV, V65, P37 Ochi K, 1997, HEARING RES, V105, P105, DOI 10.1016/S0378-5955(96)00201-8 Ochi K, 1996, HEARING RES, V95, P63, DOI 10.1016/0378-5955(96)00019-6 Phillips Dennis P., 1992, Cerebral Cortex, V2, P425, DOI 10.1093/cercor/2.5.425 Postman L., 1949, EXPT PSYCHOL INTRO Puel JL, 1998, NEUROREPORT, V9, P2109, DOI 10.1097/00001756-199806220-00037 Rajan R, 1998, NAT NEUROSCI, V1, P138, DOI 10.1038/388 SALGANICOFF M, 1988, J NEUROSCI METH, V25, P181, DOI 10.1016/0165-0270(88)90132-X Salvi RJ, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P275 SALVI RJ, 1976, EFFECTS NOISE HEARIN, P247 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 Szczepaniak WS, 1996, HEARING RES, V97, P46 VOLKOV IO, 1991, NEUROSCIENCE, V43, P307, DOI 10.1016/0306-4522(91)90295-Y Wang J, 1996, J NEUROPHYSIOL, V75, P171 Weinberger Norman M., 1995, P1071 NR 36 TC 36 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 146 EP 162 DI 10.1016/S0378-5955(99)00104-5 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400015 PM 10491963 ER PT J AU Lue, AJC Brownell, WE AF Lue, AJC Brownell, WE TI Salicylate induced changes in outer hair cell lateral wall stiffness SO HEARING RESEARCH LA English DT Article DE outer hair cell; salicylate; subsurface cisternae; micropipette aspiration ID GUINEA-PIG COCHLEA; SUBSURFACE CISTERNAE; ACOUSTIC EMISSIONS; FINE-STRUCTURE; MEMBRANES; ELECTROMOTILITY; PERILYMPH; FREEZE; SERUM; FLUID AB Micropipette aspiration was used to study the lateral wall stiffness of isolated guinea pig outer hair cells (OHCs) perfused with a sodium salicylate solution. Salicylate treatment significantly decreased lateral wall stiffness as measured by a stiffness parameter (S) compared to cells perfused with a standard bathing solution (S= 0.68 +/- 0.26 vs. S= 1.09 +/- 0.25, P < 0.05). The effect was reversible cells treated with salicylate and then with bathing solution exhibited a lateral wall stiffness similar to control cells (S= 1.10 +/- 0.40, P=0.94). Salicylate perfusion diminishes electromotile responses in isolated OHCs and physiologic doses of salicylate produce hearing loss and tinnitus in human subjects. The OHC lateral wall, the locus of electromotility, consists of three concentric layers: (1) an outermost plasma membrane, (2) a cytoskeletal network of actin and spectrin called the cortical lattice and (3) an innermost collection of flattened membranes called the subsurface cisternae (SSC). Ultrastructural studies have shown that salicylate treatment dilates and vesiculates the lateral wall subsurface cisternae (SSC) in guinea pig OHCs. In addition, salicylate causes an outward curvature of plasma membranes in human erythrocytes. The reversible, salicylate induced increase in lateral wall compliance may result from a direct action on the SSC and/or the plasma membrane. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Baylor Coll Med, Bobby R Alford Dept Otorhinolaryngol & Communicat, Houston, TX 77030 USA. RP Lue, AJC (reprint author), Baylor Coll Med, Bobby R Alford Dept Otorhinolaryngol & Communicat, 1 Baylor Plaza, Houston, TX 77030 USA. CR ARIMA T, 1991, CELL TISSUE RES, V263, P91, DOI 10.1007/BF00318403 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BOETTCHER FA, 1990, ARCH OTOLARYNGOL, V116, P681 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CHERTOFF ME, 1994, AM J PHYSIOL, V266, pC467 DEUTICKE B, 1968, BIOCHIM BIOPHYS ACTA, V163, P494, DOI 10.1016/0005-2736(68)90078-3 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DIELER R, 1994, HEARING RES, V74, P85, DOI 10.1016/0378-5955(94)90178-3 DOUEK EE, 1983, J LARYNGOL OTOL, V93, P793 ENGSTROM KG, 1992, BLOOD CELLS, V18, P241 EVANS EA, 1973, BIOPHYS J, V13, P941 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 FORGE A, 1993, HEARING RES, V64, P175, DOI 10.1016/0378-5955(93)90003-J GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 HALLWORTH R, 1996, DIVERSITY AUDITORY M Hallworth R, 1997, HEARING RES, V114, P204, DOI 10.1016/S0378-5955(97)00167-6 HOCHMUTH RM, 1987, ANNU REV PHYSIOL, V49, P209, DOI 10.1146/annurev.ph.49.030187.001233 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 JASTREBOFF PJ, 1986, ARCH OTOLARYNGOL, V112, P1050 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 OGHALAI JS, 1999, UNPUB NANOSCALE RIPP Oghalai JS, 1998, J NEUROSCI, V18, P48 POLLICE PA, 1993, HEARING RES, V70, P187, DOI 10.1016/0378-5955(93)90157-V RUSSELL IJ, 1995, AUDIT NEUROSCI, V1, P309 SAITO K, 1983, CELL TISSUE RES, V229, P467 SATO M, 1987, J BIOMECH ENG-T ASME, V109, P27 SHEETZ MP, 1974, P NATL ACAD SCI USA, V71, P4457, DOI 10.1073/pnas.71.11.4457 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SIT SP, 1997, BIOPHYS J, V72, P2812 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E TUNSTALL MJ, 1995, J PHYSIOL-LONDON, V485, P739 NR 37 TC 37 Z9 39 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 163 EP 168 DI 10.1016/S0378-5955(99)00102-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400016 PM 10491964 ER PT J AU Mei, Y Gawai, KR Nie, ZZ Ramkumar, V Helfert, RH AF Mei, Y Gawai, KR Nie, ZZ Ramkumar, V Helfert, RH TI Age-related reductions in the activities of antioxidant enzymes in the rat inferior colliculus SO HEARING RESEARCH LA English DT Article DE inferior colliculus; aging; antioxidant enzyme; malondialdehyde; protein kinase C; mitochondrion; gamma-aminobutyric acid ID SUPEROXIDE-DISMUTASE ACTIVITY; AGING RATS; OXIDATIVE STRESS; LIPID PEROXIDES; TONAL STIMULI; NEURONS; BRAIN; YOUNG; MICE; MITOCHONDRIA AB The inferior colliculus (IC) is a major relay and processing center of auditory signals in the midbrain and receives inputs from most other auditory nuclei. A number of studies have indicated age-related declines in the GABAergic and excitatory amino acid systems in the IC, including losses in both GABA immunoreactive (+) and GABA immunonegative (-) synapses. The goal of this project was to identify potential biochemical and morphological changes in the IC that may contribute to deficits in the functions of these neurotransmitters, using three age groups of Fischer-344 rats. Homogenates obtained from the IC showed age-dependent reductions in activities of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), with a concomitant increase in lipid peroxidation. Dephosphorylation of IC homogenates with alkaline phosphatase reduced the activities of SOD and CAT in all age groups, which could be restored by protein kinase C (PKC)-dependent phosphorylation. Restoration of enzyme activity was specific to the PKC-alpha isozyme, but not to the beta(1), beta(2), delta or gamma forms. No age-dependent change in the levels of PKC isoforms (alpha, beta(1), beta(2) and gamma) was detectable in IC homogenates. Morphological analyses indicate decreases in mitochondrial density in the somata of both GABA+ and GABA- IC neurons in 19- and 28-month-old rats when compared to 3-month-olds, along with significantly higher matricial abnormalities. These data indicate age-related increases in oxidative stress in the IC, which could be partially restored by PKC. The progressive increase in oxidative stress with age may underlie changes in neuronal morphology and function of the IC. (C) 1999 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. So Illinois Univ, Sch Med, Dept Surg, Springfield, IL 62794 USA. RP Ramkumar, V (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, POB 19629, Springfield, IL 62794 USA. CR AEBI H, 1984, METHOD ENZYMOL, V105, P121 BAIRD MB, 1971, GERONTOLOGY, V17, P105 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 CARILLO MC, 1996, LIFE SCI, V59, P1047 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F Ehret G., 1997, CENTRAL AUDITORY SYS, P259 FAINGOLD CL, 1991, NEUROBIOLOGY HEARING, P233 FRIDOVICH I, 1989, J BIOL CHEM, V264, P7761 GUTIERREZ A, 1994, J NEUROSCI, V14, P7469 HAGINO N, 1988, RECENT ADV PHARM KAM, P144 HANSEN CC, 1965, ARCHIV OTOLARYNGOL, V82, P115 HAZELTON GA, 1985, MECH AGEING DEV, V29, P71, DOI 10.1016/0047-6374(85)90048-X Helfert RH, 1999, J COMP NEUROL, V406, P285 HIRAMATSU M, 1989, NEUROCHEM RES, V14, P249, DOI 10.1007/BF00971319 HOEFFDING V, 1988, J COMP NEUROL, V276, P537, DOI 10.1002/cne.902760408 Husain K, 1996, FUND APPL TOXICOL, V32, P278, DOI 10.1006/faat.1996.0131 Kantrow SP, 1997, ARCH BIOCHEM BIOPHYS, V345, P278, DOI 10.1006/abbi.1997.0264 Karbowski M, 1997, BBA-LIPID LIPID MET, V1349, P242, DOI 10.1016/S0005-2760(97)00140-9 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 MAGGIRWAR SB, 1994, BIOCHEM BIOPH RES CO, V201, P508, DOI 10.1006/bbrc.1994.1731 MATUHASHI T, 1997, FREE RADICAL BIOL ME, V23, P285 McGeer E.G., 1975, NEUROBIOL AGING, P287 MIGUEL J, 1986, FREE RADICALS AGING, P51 MILBRANDT JC, 1994, NEUROBIOL AGING, V15, P699, DOI 10.1016/0197-4580(94)90051-5 Milbrandt JC, 1997, J COMP NEUROL, V379, P455, DOI 10.1002/(SICI)1096-9861(19970317)379:3<455::AID-CNE10>3.0.CO;2-F Mishra HP, 1972, J BIOL CHEM, V247, P3170 OHKAWA H, 1979, ANAL BIOCHEM, V95, P351, DOI 10.1016/0003-2697(79)90738-3 Palombi PS, 1996, HEARING RES, V100, P59, DOI 10.1016/0378-5955(96)00113-X PIKE CJ, 1995, BRAIN RES, V671, P293, DOI 10.1016/0006-8993(94)01354-K Przedborski S, 1996, J NEUROCHEM, V67, P1383 RAMKUMAR V, 1995, TRENDS PHARMACOL SCI, V16, P283, DOI 10.1016/S0165-6147(00)89051-3 RAO G, 1990, MECH AGEING DEV, V53, P49, DOI 10.1016/0047-6374(90)90033-C REISS U, 1976, BIOCHEM BIOPH RES CO, V73, P255, DOI 10.1016/0006-291X(76)90701-4 Sastre J, 1998, FREE RADICAL BIO MED, V24, P298, DOI 10.1016/S0891-5849(97)00228-1 SCHISLER NJ, 1987, GENOME, V29, P748 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x STADEL JM, 1988, BIOCH J, V4252, P771 TURRENS JF, 1982, ARCH BIOCHEM BIOPHYS, V217, P401, DOI 10.1016/0003-9861(82)90518-5 Ueda Y, 1996, NEUROCHEM RES, V21, P909, DOI 10.1007/BF02532340 Urano S, 1997, EUR J BIOCHEM, V245, P64, DOI 10.1111/j.1432-1033.1997.00064.x VAUGHAN DW, 1979, J NEUROCYTOL, V8, P215, DOI 10.1007/BF01175562 WARNER BB, 1991, AM J PHYSIOL, V260, pL296 Watson AL, 1998, J CLIN ENDOCR METAB, V83, P1697, DOI 10.1210/jc.83.5.1697 WEIBEL ER, 1979, STEOROLOGICAL METHOD, V1 WILLOTT JF, 1988, HEARING RES, V37, P1, DOI 10.1016/0378-5955(88)90073-1 NR 48 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 169 EP 180 DI 10.1016/S0378-5955(99)00103-3 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400017 PM 10491965 ER PT J AU Riemann, R Reuss, S AF Riemann, R Reuss, S TI Nitric oxide synthase in identified olivocochlear projection neurons in rat and guinea pig SO HEARING RESEARCH LA English DT Article DE nitric oxide synthase; fluoro-gold; retrograde tracing; superior olivary complex; cochlea ID AUDITORY BRAIN-STEM; COCHLEAR BLOOD-FLOW; MICROSCOPIC LOCALIZATION; EFFERENT INNERVATION; VASODILATING AGENTS; NUCLEUS; NITROPRUSSIDE; ISOFORMS; ENZYME; ORGAN AB Nitric oxide (NO) is thought to be involved in the effects of amino acids at the level of cochlear hair cell afferents. Recently, the isoform of the NO-producing enzyme, neuronal NO synthase (nNOS), has been demonstrated in neuronal structures of the cochlea in rats and guinea pigs histochemically and immunohistochemically. To investigate the sources of cochlear NO, we injected Fluoro-Gold (FG) into the cochlea of rats and guinea pigs. Upon terminal uptake of the tracer and neuronal transport we observed FG in terminals at the base of inner (IHC) and outer hair cells (OHC) and in neurons of the spiral ganglion. Ganglion cells and terminals at the IHC were clearly nNOS-positive, while terminals at the OHC exhibited nNOS-immunoreactivity to a minor degree. The immunohistochemical investigation of the auditory brainstem showed that about one-fourth of the neurons of the superior olivary complex contained nNOS. The comparison with retrogradely labeled neurons showed that perikarya in the lateral superior olivary nucleus and, in particular, the medial nucleus of the trapezoid body were double-labeled. These results were similar in both, rat and guinea pig. Our data reveal that neurons of the superior olivary complex are likely to be additional sources of neuronal NOS in the cochlea. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Wurzburg, Dept Otorhinolaryngol, D-97080 Wurzburg, Germany. Univ Mainz, Dept Anat, D-55099 Mainz, Germany. RP Riemann, R (reprint author), Univ Wurzburg, Dept Otorhinolaryngol, Josef Schneider Str 11, D-97080 Wurzburg, Germany. CR ALM P, 1993, ACTA PHYSIOL SCAND, V148, P421, DOI 10.1111/j.1748-1716.1993.tb09578.x Amaee FR, 1997, ACTA OTO-LARYNGOL, V117, P329, DOI 10.3109/00016489709113403 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 CHEN C, 1995, HEARING RES, V87, P1, DOI 10.1016/0378-5955(95)00071-B Fessenden JD, 1998, HEARING RES, V118, P168, DOI 10.1016/S0378-5955(98)00027-6 FESSENDEN JD, 1994, BRAIN RES, V668, P9, DOI 10.1016/0006-8993(94)90505-3 FORSTERMANN U, 1995, N-S ARCH PHARMACOL, V352, P351 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 GARTHWAITE J, 1988, NATURE, V336, P385, DOI 10.1038/336385a0 Gosepath K, 1997, BRAIN RES, V747, P26, DOI 10.1016/S0006-8993(96)01149-3 Guinan Jr J.J., 1996, COCHLEA, P435 Heinrich UR, 1998, EUR ARCH OTO-RHINO-L, V255, P483, DOI 10.1007/s004050050104 Heinrich UR, 1997, EUR ARCH OTO-RHINO-L, V254, P396, DOI 10.1007/BF01642558 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 Kong WJ, 1996, HEARING RES, V99, P22, DOI 10.1016/S0378-5955(96)00076-7 MCLEAN IW, 1974, J HISTOCHEM CYTOCHEM, V22, P1077 NAKASHIMA T, 1994, HEARING RES, V80, P241, DOI 10.1016/0378-5955(94)90115-5 OHLSEN A, 1993, ACTA OTO-LARYNGOL, V113, P55, DOI 10.3109/00016489309135767 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd Puel JL, 1995, PROG NEUROBIOL, V47, P449, DOI 10.1016/0301-0082(95)00028-3 PUJOL R, 1991, ACTA OTOLARYNGOL S S, V476, P32 Reuss S, 1998, NEUROREPORT, V9, P3643 Reuss S, 1999, CELL TISSUE RES, V297, P13, DOI 10.1007/s004410051329 REUSS S, 1995, BRAIN RES, V695, P257, DOI 10.1016/0006-8993(95)00829-F Riemann R, 1998, ORL J OTO-RHINO-LARY, V60, P278, DOI 10.1159/000027610 ROBERTSON D, 1989, DEV BRAIN RES, V47, P197, DOI 10.1016/0165-3806(89)90176-4 Ruan RS, 1997, J BRAIN RES, V38, P433 Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 SPANGLER KM, 1985, J COMP NEUROL, V238, P249, DOI 10.1002/cne.902380302 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 STRUTZ J, 1984, BRAIN RES, V299, P174, DOI 10.1016/0006-8993(84)90803-5 STRUTZ J, 1981, ANN OTO RHINOL LARYN, V90, P158 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 Webster William R., 1995, P797 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 ZDANSKI CJ, 1994, HEARING RES, V79, P39, DOI 10.1016/0378-5955(94)90125-2 NR 37 TC 27 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1999 VL 135 IS 1-2 BP 181 EP 189 DI 10.1016/S0378-5955(99)00113-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 231TY UT WOS:000082327400018 PM 10491966 ER PT J AU Derby, ML Sena-Esteves, M Breakefield, XO Corey, DP AF Derby, ML Sena-Esteves, M Breakefield, XO Corey, DP TI Gene transfer into the mammalian inner ear using HSV-1 and vaccinia virus vectors SO HEARING RESEARCH LA English DT Article DE gene transfer; gene therapy; viral vector; herpes simplex virus; vaccinia virus; cochlea; inner ear ID HERPES-SIMPLEX VIRUS; GUINEA-PIG COCHLEA; IN-VIVO; RIBONUCLEOTIDE REDUCTASE; ADENOASSOCIATED VIRUS; THYMIDINE KINASE; NEUROTROPHIC FACTOR; IMMUNE-RESPONSES; MESSENGER-RNAS; NERVOUS-SYSTEM AB The introduction of foreign genes into cells has become an effective means of achieving intracellular expression of foreign proteins, both for therapeutic purposes and for experimental manipulation. Gene delivery to the nervous system has been extensively studied, primarily using viral vectors. However, to date less work has focused on gene delivery to the inner ear, and existing studies have primarily used adenovirus and adeno-associated virus. Using two recombinant viral vectors, herpes simplex type 1 (HSV-1), and vaccinia virus, bearing the Escherichia coli lacZ gene, we tested gene delivery to the guinea pig cochlea in vivo with beta-galactosidase staining as an assay. The HSV-1 and vaccinia virus vectors were both found to infect and elicit transgene expression successfully in many cells in the guinea pig cochlea, including cells in the organ of Corti. These data demonstrate the feasibility of gene delivery to the inner ear using these two viral vectors. Such techniques may facilitate study of the auditory systems, and might be used to develop gene therapy strategies for some forms of hearing loss, (C) 1999 Elsevier Science B.V. All rights reserved. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02114 USA. Howard Hughes Med Inst, Boston, MA 02114 USA. RP Corey, DP (reprint author), Massachusetts Gen Hosp, WEL414, Boston, MA 02114 USA. CR BOVIATSIS EJ, 1994, GENE THER, V1, P323 BOVIATSIS EJ, 1994, CANCER RES, V54, P5745 BREAKEFIELD XO, 1997, CNS REGNERATION BASI, V4, P1281 Brubaker JO, 1996, J IMMUNOL, V157, P1598 BULLER RML, 1985, NATURE, V317, P813, DOI 10.1038/317813a0 Chakrabarti S, 1997, BIOTECHNIQUES, V23, P1094 COHEN NL, 1993, NEW ENGL J MED, V328, P233, DOI 10.1056/NEJM199301283280403 DARMSTADT GL, 1990, ANN OTO RHINOL LARYN, V99, P960 DARROW DH, 1992, LARYNGOSCOPE, V102, P683, DOI 10.1288/00005537-199206000-00015 Dazert S, 1997, INT J DEV NEUROSCI, V15, P595, DOI 10.1016/S0736-5748(96)00114-1 DERBY ML, 1995, MOL BIOL HEAR DEAFN, V152 Earl P, 1991, CURRENT PROTOCOLS MO ERNFORS P, 1995, NEURON, V14, P1153, DOI 10.1016/0896-6273(95)90263-5 Fraefel C, 1996, J VIROL, V70, P7190 FRIEDMANN T, 1994, TRENDS GENET, V10, P210, DOI 10.1016/0168-9525(94)90258-5 Geschwind MD, 1996, HUM GENE THER, V7, P173, DOI 10.1089/hum.1996.7.2-173 GLORIOSO JC, 1995, ANNU REV MICROBIOL, V49, P675 GOLDSTEIN DJ, 1988, J VIROL, V62, P196 HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 Holt JR, 1999, J NEUROPHYSIOL, V81, P1881 KEITHLEY EM, 1989, LARYNGOSCOPE, V99, P409, DOI 10.1288/00005537-198904000-00010 Kelley MW, 1997, AUDIOL NEURO-OTOL, V2, P50 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KOBURG E, 1961, Arch Ohren Nasen Kehlkopfheilkd, V178, P150, DOI 10.1007/BF02103190 Lalwani AK, 1998, AM J OTOL, V19, P390 Lalwani AK, 1998, GENE THER, V5, P277, DOI 10.1038/sj.gt.3300573 Lalwani AK, 1996, GENE THER, V3, P588 LOW W, 1995, ASS RES OT ABSTR, V18, P797 MACKETT M, 1985, DNA CLONING PRACTICA, P191 MINETA T, 1994, CANCER RES, V54, P3963 Pettit D L, 1995, Neuron, V14, P685, DOI 10.1016/0896-6273(95)90212-0 PETTIT DL, 1994, SCIENCE, V266, P1881, DOI 10.1126/science.7997883 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 Raphael Y, 1996, NEUROSCI LETT, V207, P137, DOI 10.1016/0304-3940(96)12499-X ROBERSON DW, 1994, AM J OTOL, V15, P28 RUBEN RJ, 1967, ACTA OTOLARYNGOL S, V220, P4 SATNANIEGO LA, 1998, J VIROL, V72, P3307 SMITH F, 1995, RESTOR NEUROL NEUROS, V8, P21, DOI 10.3233/RNN-1995-81207 STAECKER H, 1995, NEUROREPORT, V6, P1533 Staecker H, 1998, OTOLARYNG HEAD NECK, V119, P7, DOI 10.1016/S0194-5998(98)70194-9 STEARNS GS, 1993, LARYNGOSCOPE, V103, P890 Steel KP, 1996, CURR OPIN NEUROBIOL, V6, P520, DOI 10.1016/S0959-4388(96)80059-6 SUHR ST, 1993, ARCH NEUROL-CHICAGO, V50, P1252 SUZUKI M, 1995, ANN OTO RHINOL LARYN, V104, P69 Weiss MA, 1997, INT J DEV NEUROSCI, V15, P577, DOI 10.1016/S0736-5748(96)00112-8 WEISZ OA, 1913, METHODS CELL BIOL WHEELER EF, 1994, HEARING RES, V73, P46, DOI 10.1016/0378-5955(94)90281-X Wood MJA, 1996, TRENDS NEUROSCI, V19, P497, DOI 10.1016/S0166-2236(96)10060-6 WU GY, 1995, NEURON, V14, P681, DOI 10.1016/0896-6273(95)90211-2 YEO SW, 1995, LARYNGOSCOPE, V105, P623, DOI 10.1288/00005537-199506000-00012 YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C ZHENG JL, 1995, J NEUROSCI, V15, P5079 NR 52 TC 65 Z9 72 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 1 EP 8 DI 10.1016/S0378-5955(99)00045-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900001 PM 10452370 ER PT J AU Davis, RR Cheever, ML Krieg, EF Erway, LC AF Davis, RR Cheever, ML Krieg, EF Erway, LC TI Quantitative measure of genetic differences in susceptibility to noise-induced hearing loss in two strains of mice SO HEARING RESEARCH LA English DT Article DE noise-induced; age-related; hearing loss; mice ID ACOUSTIC TRAUMA; C57BL/6J MICE; AGE; GENOTYPE; EXPOSURE; DAMAGE; MOUSE AB The CBA/CaJ (CB) and C57BL/6J (B6) inbred strains of mice were exposed for 1 h to noise intensities between 98 and 119 dB SPL, Previous studies indicated that the B6 mice exhibited permanent threshold shifts (PTS) after 1 h exposure to 110 dB, whereas the CB mice did not exhibit any PTS. These differences in susceptibility to noise-induced hearing loss (NIHL) appear to be due to a gene for age-related hearing loss (AHL). The current study was designed to determine dose-response curves for NIHL over the ranges of intensities of noise that would characterize the B6 and CB inbred strains of mice. Because of the considerable differences in sensitivity to NIHL, the noise exposures for the two strains overlapped only at 110 and 113 dB. Nevertheless, the two strains exhibited two different dose-response curves, offset and with different slopes. We postulate that the B6 strain of mice exhibits a more linear increase for PTS from 98-113 dB, consistent with incremental effects on some metabolic physiological mechanism(s); the abrupt transition in NIHL between 113 and 116 dB for the CB mice is consistent with an ototraumatic structural injury. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Ctr Dis Control & Prevent, Bioacoust & Occupat Vibrat Sect, Phys Agents Effects Branch, Natl Inst Occupat Safety & Hlth, Cincinnati, OH 45226 USA. Univ Cincinnati, Dept Biol Sci, Cincinnati, OH 45221 USA. Ctr Dis Control & Prevent, Div Biomed & Behav Sci, Natl Inst Occupat Safety & Hlth, Cincinnati, OH 45226 USA. RP Davis, RR (reprint author), Ctr Dis Control & Prevent, Bioacoust & Occupat Vibrat Sect, Phys Agents Effects Branch, Natl Inst Occupat Safety & Hlth, Mailstop C-27,4676 Columbia Pkwy, Cincinnati, OH 45226 USA. RI Davis, Rickie/A-3186-2008 CR Burns W., 1970, HEARING NOISE IND CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DAVIS RR, 1989, J ACOUST SOC AM, V58, P963 DUNN DE, 1991, J ACOUST SOC AM, V90, P1979, DOI 10.1121/1.401677 ERWAY LC, 1993, HEARING RES, V65, P123 Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X Goldstein A, 1974, PRINCIPLES DRUG ACTI HENDERSON D, 1982, NEW PERSPECTIVES NOI, P265 HENRY KR, 1992, ACTA OTO-LARYNGOL, V112, P599, DOI 10.3109/00016489209137447 HENRY KR, 1983, AUDIOLOGY, V22, P372 HENRY KR, 1982, BEHAV GENET, V12, P563, DOI 10.1007/BF01070410 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X Li H S, 1992, Scand Audiol Suppl, V36, P1 LI HS, 1993, AUDIOLOGY, V32, P195 LI HS, 1993, HEARING RES, V68, P19, DOI 10.1016/0378-5955(93)90060-E LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 NEWLANDER JK, 1995, ASS RES OT MIDW RES, P356 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 NR 20 TC 18 Z9 21 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 9 EP 15 DI 10.1016/S0378-5955(99)00060-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900002 PM 10452371 ER PT J AU Kilgard, MP Merzenich, MM AF Kilgard, MP Merzenich, MM TI Distributed representation of spectral and temporal information in rat primary auditory cortex SO HEARING RESEARCH LA English DT Article DE auditory cortex; cerebral cortex; tonotopic map; temporal processing; repetition rate transfer function; rat ID MEDIAL GENICULATE-BODY; TONOTOPIC ORGANIZATION; FREQUENCY REPRESENTATION; FUNCTIONAL-ORGANIZATION; NEURONAL RESPONSES; ALBINO-RAT; CAT; CONNECTIONS; MODULATION; FIELDS AB Modulations of amplitude and frequency ae common features of natural sounds, and are prominent in behaviorally important communication sounds. The mammalian auditory cortex is known to contain representations of these important stimulus parameters. This study describes the distributed representations of tone frequency and modulation rate in the rate primary auditory cortex (Al). Detailed maps of auditory cortex responses to single tones and tone trains were constructed from recordings from 50-60 microelectrode penetrations introduced into each hemisphere. Recorded data demonstrated that the cortex uses a distributed coding strategy to represent both spectral and temporal information in the rat, as in other species. Just as spectral information is encoded in the firing patterns of neurons tuned to different frequencies, temporal information appears to be encoded using a set of filters covering a range of behaviorally important repetition rates. Although the average Al repetition rate transfer function (RRTF) was low-pass with a sharp drop-off in evoked spikes per tone above 9 pules per second (pps), individual RRTFs exhibited significant structure between 4 and 10 pps, including substantial facilitation or depression to tones presented at specific rates. No organized topography of these temporal filters could be determined. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Francisco, Keck Ctr Integrat Neurosci, Coleman Lab, Dept Otolaryngol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Keck Ctr Integrat Neurosci, Dept Physiol, San Francisco, CA 94143 USA. Sci Learning Corp, Berkeley, CA 94104 USA. RP Kilgard, MP (reprint author), Univ Texas, Sch Human Dev, Neurosci Program, GR41, Richardson, TX 75083 USA. CR AITKIN LM, 1986, J COMP NEUROL, V252, P175, DOI 10.1002/cne.902520204 ARNAULT P, 1990, J COMP NEUROL, V302, P110, DOI 10.1002/cne.903020109 BATZRIIZRAELI R, 1990, BRAIN BEHAV EVOLUT, V36, P237, DOI 10.1159/000115310 Brosch M, 1997, J NEUROPHYSIOL, V77, P923 BUONOMANO DV, 1995, SCIENCE, V267, P1028, DOI 10.1126/science.7863330 Buonomano DV, 1997, P NATL ACAD SCI USA, V94, P10403, DOI 10.1073/pnas.94.19.10403 CLERICI WJ, 1990, J COMP NEUROL, V297, P14, DOI 10.1002/cne.902970103 DEAR SP, 1988, J NEUROPHYSIOL, V70, P2009 Dinse HR, 1997, INT J PSYCHOPHYSIOL, V26, P205, DOI 10.1016/S0167-8760(97)00765-4 EGGERMONT JJ, 1991, HEARING RES, V56, P153, DOI 10.1016/0378-5955(91)90165-6 Eggermont JJ, 1998, J NEUROPHYSIOL, V80, P2743 EGGERMONT JJ, 1995, J NEUROPHYSIOL, V73, P227 Ehret G, 1997, J COMP PHYSIOL A, V181, P547, DOI 10.1007/s003590050139 GAESE BH, 1995, EUR J NEUROSCI, V7, P438, DOI 10.1111/j.1460-9568.1995.tb00340.x GRIGORIEVA TI, 1981, ZH VYSSH NERV DEYAT+, V31, P284 KAYSER K, 1989, PATHOL RES PRACT, V185, P729 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KELLY JB, 1986, HEARING RES, V24, P111, DOI 10.1016/0378-5955(86)90054-7 Kenmochi M, 1997, NEUROREPORT, V8, P1589, DOI 10.1097/00001756-199705060-00008 Kilgard MP, 1998, SCIENCE, V279, P1714, DOI 10.1126/science.279.5357.1714 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F MCMULLEN NT, 1982, EXP NEUROL, V75, P208, DOI 10.1016/0014-4886(82)90019-X MERZENICH MM, 1976, J COMP NEUROL, V166, P387, DOI 10.1002/cne.901660402 MERZENIC.MM, 1973, BRAIN RES, V50, P275, DOI 10.1016/0006-8993(73)90731-2 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MIDDLEBROOKS JC, 1980, BRAIN RES, V181, P31, DOI 10.1016/0006-8993(80)91257-3 PHILLIPS DP, 1989, J ACOUST SOC AM, V85, P2537, DOI 10.1121/1.397748 PUBOLS BH, 1971, J COMP NEUROL, V141, P63, DOI 10.1002/cne.901410106 RAGGIO MW, 1994, J NEUROPHYSIOL, V72, P2334 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 REDIES H, 1989, J COMP NEUROL, V282, P473, DOI 10.1002/cne.902820402 ROGER M, 1989, J COMP NEUROL, V287, P339, DOI 10.1002/cne.902870306 ROMANI GL, 1982, SCIENCE, V216, P1339, DOI 10.1126/science.7079770 ROMANSKI LM, 1993, CEREB CORTEX, V3, P499, DOI 10.1093/cercor/3.6.499 SALLY SL, 1988, J NEUROPHYSIOL, V59, P1627 Scheich H, 1991, Curr Opin Neurobiol, V1, P236, DOI 10.1016/0959-4388(91)90084-K Schreiner C E, 1992, Curr Opin Neurobiol, V2, P516, DOI 10.1016/0959-4388(92)90190-V SCHREINER CE, 1986, AUDITORY FUNCTION, P337 SCHREINER CE, 1992, J NEUROPHYSIOL, V68, P1487 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 Schreiner C E, 1997, Acta Otolaryngol Suppl, V532, P54 SHAMMA SA, 1993, J NEUROPHYSIOL, V69, P367 Shi CJ, 1997, J COMP NEUROL, V382, P153 Stiebler I, 1997, J COMP PHYSIOL A, V181, P559, DOI 10.1007/s003590050140 SUGA N, 1976, SCIENCE, V194, P542, DOI 10.1126/science.973140 THOMAS H, 1993, EUR J NEUROSCI, V5, P882, DOI 10.1111/j.1460-9568.1993.tb00940.x TUNTURI AR, 1950, AM J PHYSIOL, V162, P489 WINER JA, 1987, J COMP NEUROL, V257, P282, DOI 10.1002/cne.902570212 NR 48 TC 96 Z9 98 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 16 EP 28 DI 10.1016/S0378-5955(99)00061-1 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900003 PM 10452372 ER PT J AU Parham, K Sun, XM Kim, DO AF Parham, K Sun, XM Kim, DO TI Distortion product otoacoustic emissions in the CBA/J mouse model of presbycusis SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; aging; mouse; hearing loss; outer hair cell ID BRAIN-STEM RESPONSE; AGE-RELATED-CHANGES; INFERIOR COLLICULUS NEURONS; HEARING-IMPAIRED MICE; 2 DISCRETE SOURCES; ACOUSTIC DISTORTION; COCHLEAR MECHANICS; PHYSIOLOGICAL VULNERABILITY; AUDITORY-SENSITIVITY; STRIA VASCULARIS AB CBA mice do not exhibit age-related loss of auditory sensitivity or cochlear pathology until relatively late in life. Therefore, this strain is believed to be an excellent animal model for the examination of the effects of age on the cochlea. To evaluate the effects of age on outer hair cell function, 2f(1)-f(2) distortion product otoacoustic emissions (DPOAEs) were measured for f(2) between 8 and 16 kHz in CBA/J mice between 1 and 25 months of age. CBA mice exhibited mild age-related changes in DPOAE level and detection threshold at 17 months of age, and changes of 20-40 dB by 25 months of age. The DPOAE level decreased and detection threshold increased with age in a frequency-dependent manner, starting at high frequencies and eventually extending to low frequencies. The range of frequencies in which notches were observed in the DPOAE input/output (I/O) functions extended toward lower frequencies by 17 months of age. Notches were absent in the I/O functions of 25-month-old mice. The present results for a frequency range of 8-16 kHz suggest that age has modest effects on outer hair cell function in CBA mice. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Connecticut, Ctr Hlth, Dept Surg, Div Otolaryngol, Farmington, CT 06030 USA. Univ Connecticut, Dept Commun Sci, Storrs, CT 06268 USA. RP Parham, K (reprint author), Univ Connecticut, Ctr Hlth, Dept Surg, Div Otolaryngol, Farmington, CT 06030 USA. EM parham@neuron.uchc.edu CR ANDERSON SD, 1979, ARCH OTO-RHINO-LARYN, V224, P47, DOI 10.1007/BF00455223 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 BONFILS P, 1988, AUDIOLOGY, V27, P27 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 BROWN AM, 1989, HEARING RES, V19, P191 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 COLLET L, 1990, ANN OTO RHINOL LARYN, V99, P993 Doan DE, 1996, HEARING RES, V97, P174, DOI 10.1016/0378-5955(96)00060-3 ENGSTROM B, 1987, ACTA OTO-LARYNGOL, P110 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H GRATTON MA, 1995, HEARING RES, V82, P44 Gratton MA, 1997, HEARING RES, V114, P1, DOI 10.1016/S0378-5955(97)00025-7 Green M.C., 1989, GENETIC VARIANTS STR, P12 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1982, HEARING RES, V8, P285, DOI 10.1016/0378-5955(82)90020-X HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 JIMENEZ AM, 1997, ASS RES OT ABSTR, V20, P101 Johnson KR, 1997, HEARING RES, V114, P83, DOI 10.1016/S0378-5955(97)00155-X JOHNSSON LG, 1979, SPECIAL SENSES AGING, P119 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KIM DO, 1980, HEARING RES, V2, P297, DOI 10.1016/0378-5955(80)90064-7 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KOSSL M, 1992, HEARING RES, V60, P156, DOI 10.1016/0378-5955(92)90018-I Le Calvez S, 1998, HEARING RES, V120, P51, DOI 10.1016/S0378-5955(98)00051-3 Le Calvez S, 1998, HEARING RES, V120, P37, DOI 10.1016/S0378-5955(98)00050-1 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LI HS, 1994, ORL J OTO-RHINO-LARY, V56, P61 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P965 Liberman MC, 1996, J ACOUST SOC AM, V99, P3572, DOI 10.1121/1.414956 LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 MILLS DM, 1994, HEARING RES, V77, P183, DOI 10.1016/0378-5955(94)90266-6 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORTON SJ, 1990, LECT NOTES BIOMATH, V87, P219 Parham K, 1997, HEARING RES, V112, P216, DOI 10.1016/S0378-5955(97)00124-X PARHAM K, 1997, ASS RES OT ABSTR, V20, P194 PARHAM K, 1988, Behavioral Neuroscience, V102, P881, DOI 10.1037/0735-7044.102.6.881 PARHAM K, 1996, ASS RES OT ABSTR, V19, P26 PATUZZI R, 1992, HEARING RES, V60, P165, DOI 10.1016/0378-5955(92)90019-J PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SCHROTT A, 1991, HEARING RES, V52, P245, DOI 10.1016/0378-5955(91)90204-M Schuknecht H. F., 1974, PATHOLOGY EAR SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SCHUKNECHT HF, 1964, ARCHIV OTOLARYNGOL, V80, P369 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K Shimada A, 1998, J VET MED SCI, V60, P41, DOI 10.1292/jvms.60.41 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SJOSTROM B, 1990, ACTA OTO-LARYNGOL, V109, P353, DOI 10.3109/00016489009125155 SMURZYNSKI J, 1992, HEARING RES, V58, P227, DOI 10.1016/0378-5955(92)90132-7 Spongr VP, 1997, J ACOUST SOC AM, V101, P3546, DOI 10.1121/1.418315 STOVER L, 1993, J ACOUST SOC AM, V94, P2670, DOI 10.1121/1.407351 SUN JC, 1994, LARYNGOSCOPE, V104, P1251 SUN XM, 1996, ASS RES OT ABSTR, V19, P25 SUN XM, 1997, ASS RES OT ABSTR, V20, P101 Walton JP, 1998, J NEUROSCI, V18, P2764 WENNGREN BI, 1988, ACTA OTO-LARYNGOL, V106, P238, DOI 10.3109/00016488809106431 WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 WILLOTT JF, 1991, HEARING RES, V53, P78, DOI 10.1016/0378-5955(91)90215-U WILLOTT JF, 1988, HEARING RES, V37, P1, DOI 10.1016/0378-5955(88)90073-1 Willott J. F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 WILLOTT JF, 1994, BEHAV NEUROSCI, V108, P703, DOI 10.1037/0735-7044.108.4.703 Willott JF, 1998, HEARING RES, V119, P27, DOI 10.1016/S0378-5955(98)00029-X ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 NR 79 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 29 EP 38 DI 10.1016/S0378-5955(99)00059-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900004 PM 10452373 ER PT J AU Sie, KCY deSerres, LM Norton, SJ AF Sie, KCY deSerres, LM Norton, SJ TI Age-related sensitivity to cisplatin ototoxicity in gerbils SO HEARING RESEARCH LA English DT Article DE cisplatin; ototoxicity; distortion product otoacoustic emission; development ID BRAIN-STEM RESPONSE; OTOACOUSTIC EMISSIONS; POSTNATAL-DEVELOPMENT; AUDITORY FUNCTION; MONGOLIAN GERBIL; CHILDREN; COCHLEA AB This study was undertaken to define the developmental period of maximal sensitivity to cisplatin ototoxicity in gerbils. Five groups were established based upon post-natal age (P) at exposure to cisplatin, P10 (n = 8), P14 (n = 8), P18 (n = 6), P22 (n = 7) and P42 (n = 7). Animals were given cisplatin, 1 mg/kg/day intraperitoneal for 4 days. In the first four groups, P10, P14, P18 and P22, distortion product otoacoustic emissions were measured at 45; days of age, when responses were expected to be developmentally stable. Distortion product grams and input-output functions were measured. There was a statistically significant difference only between P14 and P42 (P < 0.01). There was a significant interaction of age and frequency in the P14 group only (P< 0.01). A secondary analysis compared distortion product grams of P14 animals, exposed to cisplatin, and age-matched saline-treated animals (n = 6). There was a significant treatment effect. In summary, there was an effect of age on the cisplatin ototoxicity in gerbils. Also, there was an effect of the frequency on DPOAE levels in P14 gerbils. These data support the presence of a 'sensitive' period to cisplatin ototoxicity in gerbils. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Washington, Sch Med, Childrens Hosp & Reg Med Ctr, Seattle, WA 98105 USA. Univ Washington, Sch Med, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98105 USA. Columbia Univ, Babies & Childrens Hosp, New York Presbyterian Hosp, New York, NY USA. RP Sie, KCY (reprint author), Univ Washington, Sch Med, Childrens Hosp & Reg Med Ctr, 4800 Sand Point Way NE, Seattle, WA 98105 USA. CR AXELSSON A, 1986, ACTA OTO-LARYNGOL, V101, P75, DOI 10.3109/00016488609108610 BOCK GR, 1977, SCIENCE, V197, P396, DOI 10.1126/science.877565 BROCK P, 1988, MED PEDIATR ONCOL, V16, P368, DOI 10.1002/mpo.2950160517 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FAUSTI SA, 1984, CANCER, V53, P224, DOI 10.1002/1097-0142(19840115)53:2<224::AID-CNCR2820530207>3.0.CO;2-D HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HAYES DM, 1977, CANCER, V39, P1372, DOI 10.1002/1097-0142(197704)39:4<1372::AID-CNCR2820390404>3.0.CO;2-J HENLEY CM, 1993, OTOLARYNG CLIN N AM, V26, P857 HENRY KR, 1981, ARCH OTOLARYNGOL, V107, P92 KHAN AB, 1982, CANCER TREAT REP, V66, P2013 LAIRD NM, 1982, BIOMETRICS, V38, P963, DOI 10.2307/2529876 LAURELL G, 1988, SCAND AUDIOL, V17, P241, DOI 10.3109/01050398809070712 LENOIR M, 1980, ACTA OTO-LARYNGOL, V89, P317, DOI 10.3109/00016488009127143 LENOIR M, 1983, ACTA OTOLARYNGOL S, V405, P3 MAROT M, 1980, HEARING RES, V2, P111, DOI 10.1016/0378-5955(80)90032-5 MCGUIRT JP, 1995, HEARING RES, V84, P52, DOI 10.1016/0378-5955(95)00015-V Mills DM, 1996, J ACOUST SOC AM, V100, P428, DOI 10.1121/1.415857 Neter J, 1996, APPL LINEAR STAT MOD NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PASIC TR, 1991, LARYNGOSCOPE, V101, P985 PRIEVE BA, 1984, ACTA OTO-LARYNGOL, V98, P428, DOI 10.3109/00016488409107584 REDDEL RR, 1982, CANCER TREAT REP, V66, P19 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 RYBAK LP, 1991, LARYNGOSCOPE, V101, P1167 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 Sie KCY, 1997, OTOLARYNG HEAD NECK, V116, P585, DOI 10.1016/S0194-5998(97)70232-8 SMITH DI, 1987, HEARING RES, V27, P157, DOI 10.1016/0378-5955(87)90016-5 STRAUSS M, 1983, LARYNGOSCOPE, V93, P1554, DOI 10.1288/00005537-198312000-00007 WEATHERLY RA, 1991, LARYNGOSCOPE, V101, P917 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 WOOLF NK, 1986, AM J PHYSIOL, V250, P493 YANCEY C, 1985, SCIENCE, V225, P741 NR 32 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 39 EP 47 DI 10.1016/S0378-5955(99)00066-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900005 PM 10452374 ER PT J AU Marcus, DC Chiba, T AF Marcus, DC Chiba, T TI K+ and Na+ absorption by outer sulcus epithelial cells SO HEARING RESEARCH LA English DT Article DE vibrating probe; patch clamp; gerbil; cochlea; gadolinium; non-selective cation channel ID VESTIBULAR DARK CELLS; POTASSIUM SECRETION; APICAL MEMBRANE; GERBIL COCHLEA; CHANNEL; LOCALIZATION; MECHANISMS; STRIA AB Transduction of sound into nerve impulses by hair cells depends on modulation of a current carried primarily by K- into the cell across apical transduction channels that are permeable to cations. The cochlear function thus depends on active secretion of K+ accompanied by absorption of Na+ by epithelial cell enclosing the cochlear duct. The para-sensory cells which participate in the absorption of Na+ (down to the uniquely low level of 1 mM) were previously unidentified and the existence of a para-sensory pathway which actively absorbs K+ was previously unknown. A relative short circuit current (I-sc,I-probe, measured as the extracellular current density wit a vibrating electrode) was directed into the apical side of the outer sulcus epithelium, decreased by ouabain (1 mM), an inhibitor of Na+, K+-ATPase, and found to depend on bath NA(+) and K+ but on neither Ca2+ nor Cl-, I-sc,I-probe was shown to be an active current by its sensitivity to ouabain. On-cell patch clamp recordings of the apical membrane of outer sulcus cells displayed a channel activity, which carried inward currents under conditions identical to those used to measure I-sc,I-probe. Both I-sc,I-probe and non-selective cation channels (27.4 +/- 0.6 ps. n=22) in excised outside-out patches from the apical membrane were inhibited by Gd3+ (1 mM), I-sc,I-probe was also inhibited by 5 mM lidocaine, 1 mM quinine and 500 mu M amiloride but not by 10 mu M amiloride. These results demonstrate that outer sulcus epithelial cell contribute to the homeostasis of endolymph by actively absorbing Na+ and K+. An entry pathway in the apical membrane was shown to be through non-selective cation channels that were sensitive to Gd3+. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA. RP Marcus, DC (reprint author), Kansas State Univ, Dept Anat & Physiol, 1600 Denison Ave, Manhattan, KS 66506 USA. CR BONANNO JA, 1989, AM J PHYSIOL, V257, pC290 BOSHER SK, 1968, P R SOC LOND BIOL, V171, P247 Caldwell RA, 1998, AM J PHYSIOL-CELL PH, V275, pC619 CHIBA T, 1998, ASS RES OTOLARYNGOL, V21, P119 FRELIN C, 1987, KIDNEY INT, V32, P785, DOI 10.1038/ki.1987.277 IKEDA K, 1992, PFLUG ARCH EUR J PHY, V420, P493, DOI 10.1007/BF00374624 KAUFMAN AI, 1986, PFLUG ARCH EUR J PHY, V407, P596, DOI 10.1007/BF00582637 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 Marcus Daniel C., 1996, Keio Journal of Medicine, V45, P301 MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 1997, CELL PHYSL SOURCE BO, P688 MIZUTA K, 1995, HEARING RES, V88, P199, DOI 10.1016/0378-5955(95)00113-I NAKAZAWA K, 1995, J HISTOCHEM CYTOCHEM, V43, P981 NONAKA T, 1995, BBA-BIOMEMBRANES, V1233, P163, DOI 10.1016/0005-2736(94)00241-G RODRIGUEZECHAND.EL, 1965, Z ZELLFORSCH, V67, P600 SCHEFFEY C, 1991, AM J PHYSIOL, V261, pF963 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTZ SG, 1981, AM J PHYSIOL, V241, pF579 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 THALMANN R, 1973, LARYNGOSCOPE, V83, P1690, DOI 10.1288/00005537-197310000-00010 Wangemann P, 1997, HNO, V45, P205, DOI 10.1007/s001060050105 Wangemann P, 1996, HEARING RES, V94, P94, DOI 10.1016/0378-5955(96)00008-1 NR 24 TC 45 Z9 47 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 48 EP 56 DI 10.1016/S0378-5955(99)00074-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900006 PM 10452375 ER PT J AU Azeredo, WJ Kliment, ML Morley, BJ Relkin, E Slepecky, NB Sterns, A Warr, WB Weekly, JM Woods, CI AF Azeredo, WJ Kliment, ML Morley, BJ Relkin, E Slepecky, NB Sterns, A Warr, WB Weekly, JM Woods, CI TI Olivocochlear neurons in the chinchilla: a retrograde fluorescent labelling study SO HEARING RESEARCH LA English DT Article DE olivocochlear bundle; olivocochlear neuron; superior olivary complex; efferent innervation of the cochlea; chinchilla ID TENSOR TYMPANI MUSCLE; CONTRALATERAL SOUND STIMULATION; COMPOUND ACTION-POTENTIALS; SUPERIOR OLIVARY COMPLEX; COCHLEAR EFFERENT SYSTEM; GUINEA-PIG COCHLEA; BRAIN-STEM; HORSERADISH-PEROXIDASE; ACOUSTIC STIMULATION; SQUIRREL-MONKEY AB Although the chinchilla is widely used as a model for auditory research, little is known about the distribution and morphology of its olivocochlear neurons. Here, we report on the olivocochlear neurons projecting to one cochlea, as determined by single and double retrograde fluorescent tracer techniques. 10 adult chinchillas were anesthetized and given either unilateral or bilateral injections of a fluorescent tracer (either Fluoro-Gold or Fast Blue) into scala tympani or as a control, a unilateral injection into the middle ear cavity. The results indicate that there are similarities as well as significant differences between the chinchilla and other species of rodents in the distributions of their olivocochlear neurons. Based on three well-labelled cases, there was a mean total of 1168 olivocochlear neurons in the chinchilla. Of these, the majority (mean 787) were small, lateral olivocochlear neurons found almost exclusively within the ipsilateral lateral superior olivary nucleus. The next largest group consisted of a mean of 280 medial olivocochlear neurons virtually all of which were located in the dorsomedial peri-olivary nucleus. Chinchilla medial olivocochlear neurons were more predominantly crossed in their projections (4:1) than in any known species. The smallest group of olivocochlear neurons (mean 101) consisted of larger lateral olivocochlear neurons (shell neurons) which were located on the margins of the superior olivary nucleus and which projected mainly (2.2:1) ipsilaterally. Double retrograde labelling was observed only in medial olivocochlear neurons and occurred in only 1-2% of these cells. The results confirm previous findings which indicated a relative paucity of fibers belonging to the uncrossed as compared to the crossed olivocochlear bundle. This, together with the strong apical bias of the uncrossed projection reported previously, offers possible explanations for the apparent absence of efferent-mediated suppressive effects of contralateral acoustic stimulation in this species. Regarding the lateral olivocochlear system, the chinchilla is shown to possess both intrinsic and shell neurons, as in the rat. (C) 1999 Elsevier Science B.V. All rights reserved. C1 SUNY Hlth Sci Ctr, Dept Otolaryngol, Syracuse, NY 13210 USA. Syracuse Univ, Inst Sensory Res, Dept Bioengn & Neurosci, Syracuse, NY USA. Boys Town Natl Res Hosp, Omaha, NE 68131 USA. RP Woods, CI (reprint author), SUNY Hlth Sci Ctr, Dept Otolaryngol, 750 E Adams St, Syracuse, NY 13210 USA. CR ADAMS JC, 1983, J COMP NEUROL, V215, P275, DOI 10.1002/cne.902150304 ASCHOFF A, 1988, EXP BRAIN RES, V71, P252 AZEREDO WJ, 1997, ASS RES OT ABSTR, V20, P163 BISHOP AL, 1987, HEARING RES, V31, P175, DOI 10.1016/0378-5955(87)90124-9 BOHNE BA, 1982, J ACOUST SOC AM, V72, P102, DOI 10.1121/1.387994 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BROWN MC, 1993, J COMP NEUROL, V337, P600, DOI 10.1002/cne.903370406 BUNO W, 1978, EXP NEUROL, V59, P62, DOI 10.1016/0014-4886(78)90201-7 CAMPBELL JP, 1988, HEARING RES, V35, P271, DOI 10.1016/0378-5955(88)90124-4 CHERYCROZE S, 1993, HEARING RES, V68, P53, DOI 10.1016/0378-5955(93)90064-8 CONTRERAS RJ, 1980, J COMP NEUROL, V190, P373, DOI 10.1002/cne.901900211 COUNTER SA, 1993, ACTA OTO-LARYNGOL, V113, P43, DOI 10.3109/00016489309135765 daCosta DL, 1997, J NEUROPHYSIOL, V78, P1826 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 GANNON PJ, 1987, BRAIN RES, V404, P257, DOI 10.1016/0006-8993(87)91376-X GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 Guinan Jr J.J., 1996, COCHLEA, P435 GULLEY RL, 1977, J COMP NEUROL, V171, P517, DOI 10.1002/cne.901710407 HELFERT RH, 1987, AM J ANAT, V179, P55, DOI 10.1002/aja.1001790108 HIURA T, 1977, BRAIN RES, V137, P145, DOI 10.1016/0006-8993(77)91017-4 IURATO S, 1978, J COMP NEUROL, V182, P57, DOI 10.1002/cne.901820105 JOSEPH MP, 1985, J COMP NEUROL, V232, P43, DOI 10.1002/cne.902320105 KLIMENT ML, 1997, ASS RES OT ABSTR, V20, P162 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 MARCO J, 1993, ACTA OTO-LARYNGOL, V113, P229, DOI 10.3109/00016489309135798 Marco J, 1991, Acta Otorrinolaringol Esp, V42, P260 MATHISEN JS, 1964, ACTA ANAT, V56, P216 MIZUNO N, 1982, NEUROSCI LETT, V31, P205, DOI 10.1016/0304-3940(82)90020-9 MORLEY BJ, 1991, BRAIN RES, V544, P94, DOI 10.1016/0006-8993(91)90889-4 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MURATA K, 1980, NEUROSCI LETT, V18, P289, DOI 10.1016/0304-3940(80)90299-2 NOMURA S, 1981, BRAIN RES, V214, P229, DOI 10.1016/0006-8993(81)91191-4 NOMURA S, 1983, NEUROSCI LETT, V39, P11, DOI 10.1016/0304-3940(83)90157-X OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 Puria S, 1996, J ACOUST SOC AM, V99, P500, DOI 10.1121/1.414508 ROBERTSON D, 1987, EXP BRAIN RES, V66, P449, DOI 10.1007/BF00270677 ROBERTSON D, 1989, DEV BRAIN RES, V47, P197, DOI 10.1016/0165-3806(89)90176-4 SAHLEY TL, 1991, HEARING RES, V55, P133, DOI 10.1016/0378-5955(91)90099-U SANES DH, 1990, J COMP NEUROL, V294, P443, DOI 10.1002/cne.902940312 SCHMUED LC, 1986, BRAIN RES, V377, P147, DOI 10.1016/0006-8993(86)91199-6 SHAW MD, 1983, J COMP NEUROL, V216, P10, DOI 10.1002/cne.902160103 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SMITH CA, 1963, ANN OTO RHINOL LARYN, V72, P489 SOMMER I, 1993, EXP BRAIN RES, V95, P223 SPANGLER KM, 1982, NEUROSCI LETT, V32, P23, DOI 10.1016/0304-3940(82)90223-3 STRUTZ J, 1988, ARCH OTO-RHINO-LARYN, V245, P108, DOI 10.1007/BF00481446 TAKAHASHI O, 1984, NEUROSCI LETT, V49, P19, DOI 10.1016/0304-3940(84)90129-0 THOMPSON GC, 1985, J COMP NEUROL, V231, P270, DOI 10.1002/cne.902310214 THOMPSON GC, 1986, J COMP NEUROL, V254, P246, DOI 10.1002/cne.902540208 TSUCHITANI C, 1982, J NEUROPHYSIOL, V47, P479 VETTER DE, 1992, ANAT EMBRYOL, V185, P1, DOI 10.1007/BF00213596 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 Warr WB, 1997, HEARING RES, V108, P89, DOI 10.1016/S0378-5955(97)00044-0 Warr WB, 1978, EVOKED ELECTRICAL AC, P43 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 Weekly J. M., 1992, Society for Neuroscience Abstracts, V18, P1192 Zheng XY, 1997, HEARING RES, V107, P147, DOI 10.1016/S0378-5955(97)00031-2 Zheng XY, 1997, HEARING RES, V104, P191, DOI 10.1016/S0378-5955(96)00187-6 NR 62 TC 18 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 57 EP 70 DI 10.1016/S0378-5955(99)00069-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900007 PM 10452376 ER PT J AU Keithley, EM Erkman, L Bennett, T Lou, L Ryan, AF AF Keithley, EM Erkman, L Bennett, T Lou, L Ryan, AF TI Effects of a hair cell transcription factor, Brn-3.1, gene deletion on homozygous and heterozygous mouse cochleas in adulthood and aging SO HEARING RESEARCH LA English DT Article DE inner ear; genetic hearing loss; spiral ganglion ID RETINAL GANGLION-CELLS; POU; EXPRESSION; NEURONS; FAMILY; DISTINCT; SUBSETS AB The transcription factor Brn-3.1, is expressed in the inner ear hair cells throughout life and is necessary for the development of these cells. Mutant mice in which the Brn-3.1 encoding region has been deleted have no identifiable hair cells, greatly reduced numbers of spiral ganglion cells and are deaf. A mutation in the human homologue of this gene has been shown to be related to adult onset, sensorineural hearing loss (Vahava et al., 1998). The question whether haploinsufficiency in the mutant Brn-3.1 mouse with a mixed C57BL6/129Sv genetic background could affect the adult or aged cochlear was tested, therefore, by measuring the auditory brainstem responses and examining the cochlea's histologically at 2, 18 and 24 months of age. The heterozygotes had a comparable hearing to the wild-type animals and similar patterns of cochlear degeneration. Both groups showed an about 30 dB hearing loss beginning at 18 months of age, outer hair cell degeneration and loss of spiral ganglion neurons in the basal turn. There appeared to be no effect of Brn-3.1 haploinsufficiency on the mouse cochlea, implying that one intact copy of the gene is sufficient to maintain a normal cochlea. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Diego, Sch Med, Dept Otolaryngol, VAMC, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Med, VAMC, La Jolla, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Neurosci, VAMC, La Jolla, CA 92093 USA. RP Keithley, EM (reprint author), Univ Calif San Diego, Sch Med, Dept Otolaryngol, VAMC, 9500 Gilman Dr, La Jolla, CA 92093 USA. CR Erkman L, 1996, NATURE, V381, P603, DOI 10.1038/381603a0 FEDTSOVA NG, 1995, MECH DEVELOP, V53, P291, DOI 10.1016/0925-4773(95)00435-1 GERRERO MR, 1993, P NATL ACAD SCI USA, V90, P10841, DOI 10.1073/pnas.90.22.10841 Gratton MA, 1997, HEARING RES, V114, P1, DOI 10.1016/S0378-5955(97)00025-7 HE X, 1989, Nature (London), V340, P35, DOI 10.1038/340035a0 KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 KLEMM JD, 1994, CELL, V77, P21, DOI 10.1016/0092-8674(94)90231-3 LILLYCROP KA, 1992, NUCLEIC ACIDS RES, V20, P5093, DOI 10.1093/nar/20.19.5093 NINKINA NN, 1993, NUCLEIC ACIDS RES, V21, P3175, DOI 10.1093/nar/21.14.3175 Ryan AK, 1997, GENE DEV, V11, P1207, DOI 10.1101/gad.11.10.1207 TURNER EE, 1994, NEURON, V12, P205, DOI 10.1016/0896-6273(94)90164-3 Vahava O, 1998, SCIENCE, V279, P1950, DOI 10.1126/science.279.5358.1950 Xiang MQ, 1997, P NATL ACAD SCI USA, V94, P9445, DOI 10.1073/pnas.94.17.9445 XIANG MQ, 1995, J NEUROSCI, V15, P4762 XIANG MQ, 1993, NEURON, V11, P689, DOI 10.1016/0896-6273(93)90079-7 NR 15 TC 17 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 71 EP 76 DI 10.1016/S0378-5955(99)00070-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900008 PM 10452377 ER PT J AU Backoff, PM Palombi, PS Caspary, DM AF Backoff, PM Palombi, PS Caspary, DM TI gamma-Aminobutyric acidergic and glycinergic inputs shape coding of amplitude modulation in the chinchilla cochlear nucleus SO HEARING RESEARCH LA English DT Article DE chinchilla; cochlear nucleus; amplitude modulation; gamma-aminobutyric acid; glycine; inhibitory amino acid ID AUDITORY-NERVE FIBERS; SINGLE UNIT-ACTIVITY; INFERIOR COLLICULUS; FREQUENCY MODULATIONS; BACKGROUND-NOISE; GUINEA-PIG; BROWN BAT; NEURONS; CAT; RESPONSES AB Amplitude modulation is a prominent acoustic feature of biologically relevant sounds, such as speech and animal vocalizations. Enhanced temporal coding of amplitude modulation signals is found in certain dorsal and posteroventral cochlear nucleus neurons when they are compared to auditory nerve. Although mechanisms underlying this improved temporal selectivity are not known, involvement of inhibition has been suggested. gamma-Aminobutyric acid- and glycine-mediated inhibition have been shown to shape the dorsal cochlear nucleus and posteroventral cochlear nucleus response properties to other acoustic stimuli. In the present study, responses to amplitude modulation tones were obtained from chinchilla dorsal cochlear nucleus and posteroventral cochlear nucleus neurons. The amplitude modulation carrier was set to the neuron's characteristic frequency and the modulating frequency varied from 10 Hz. Rate and temporal modulation transfer functions were compared across neurons. Bandpass temporal modulation transfer functions were observed in 74% of the neurons studied. Most cochlear nucleus neurons (90%) displayed flat or lowpass rate modulation transfer functions to amplitude modulation signals presented at 25-40 dB (re: characteristic frequency threshold). The role of inhibition in shaping responses to amplitude modulation stimuli was examined using iontophoretic application of glycine or gamma-aminobutyric acid(A) receptor agonists and antagonists. Blockade of gamma-aminobutyric acid(A) or glycine receptors increased stimulus-evoked discharge rates for a majority of neurons tested. Synchronization to the envelope was reduced, particularly at low and middle modulating frequencies, with temporal modulation transfer functions becoming flattened and less bandpass in appearance. Application of glycine, gamma-aminobutyric acid or muscimol increased the modulation gain over the low- and mid-modulation frequencies and reduced the discharge rate across envelope frequencies for most neurons tested. These findings support the hypothesis that glycinergic and gamma-aminobutyric acidergic inputs onto certain dorsal cochlear nucleus and posteroventral cochlear nucleus neurons play a role in shaping responses to amplitude modulation stimuli and may be responsible for the reported preservation of amplitude modulation temporal coding in dorsal cochlear nucleus and posteroventral cochlear nucleus neurons at high stimulus intensities or in background noise. (C) 1999 Elsevier Science B.V. All rights reserved. C1 So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA. RP Caspary, DM (reprint author), So Illinois Univ, Sch Med, Dept Pharmacol, POB 19629, Springfield, IL 62794 USA. EM dcaspary@wpsmtp.siumed.edu CR Backoff PM, 1997, HEARING RES, V110, P155, DOI 10.1016/S0378-5955(97)00081-6 BACKOFF PM, 1991, THESIS U MICHIGAN CASPARY DM, 1990, GLYCINE NEUROTRANSMI, P3 CASPARY DM, 1984, HEARING RES, V13, P113, DOI 10.1016/0378-5955(84)90102-3 Caspary DM, 1997, ACOUSTICAL SIGNAL PROCESSING IN THE CENTRAL AUDITORY SYSTEM, P227, DOI 10.1007/978-1-4419-8712-9_21 CASPARY DM, 1994, J NEUROPHYSIOL, V72, P2124 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 CASPARY DM, 1987, BRAIN RES, V417, P273, DOI 10.1016/0006-8993(87)90452-5 CASPARY DM, 1993, NATO ADV SCI INST SE, V239, P239 CONDON CJ, 1994, J NEUROPHYSIOL, V71, P768 EBERT U, 1995, EXP BRAIN RES, V104, P310 EVANS EF, 1993, NATO ADV SCI INST SE, V239, P253 FENG AS, 1994, J NEUROPHYSIOL, V72, P2209 FRISINA RD, 1985, EXP BRAIN RES, V60, P417 Frisina RD, 1996, J ACOUST SOC AM, V99, P475, DOI 10.1121/1.414559 FRISINA RD, 1983, ENHANCEMENT RESPONSE FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y FRISINA RD, 1990, HEARING RES, V44, P123, DOI 10.1016/0378-5955(90)90075-Z FRISINA RD, 1994, EXP BRAIN RES, V102, P160 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 HAVEY DC, 1980, ELECTROEN CLIN NEURO, V48, P249, DOI 10.1016/0013-4694(80)90313-2 JAVEL E, 1980, J ACOUST SOC AM, V68, P133, DOI 10.1121/1.384639 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 KIANG NYS, 1965, ANN OTO RHINOL LARYN, V74, P463 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S Koch U, 1998, J NEUROPHYSIOL, V80, P71 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 MARTIN MR, 1982, NEUROPHARMACOLOGY, V21, P201, DOI 10.1016/0028-3908(82)90188-5 MOLLER AR, 1974, EXP NEUROL, V45, P104, DOI 10.1016/0014-4886(74)90104-6 MOLLER AR, 1973, BASIC MECH HEARING, P593 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x MOLLER AR, 1976, ACTA PHYSIOL SCAND, V98, P157, DOI 10.1111/j.1748-1716.1976.tb00235.x PALOMBI PS, 1992, J NEUROPHYSIOL, V67, P738 REES A, 1987, HEARING RES, V27, P129, DOI 10.1016/0378-5955(87)90014-1 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1994, HEARING RES, V77, P43, DOI 10.1016/0378-5955(94)90252-6 Rhode WS, 1992, MAMMALIAN AUDITORY P, P94 Rhode WS, 1998, HEARING RES, V117, P39, DOI 10.1016/S0378-5955(98)00002-1 RHODE WS, 1994, J NEUROPHYSIOL, V71, P1797 RHODE WS, 1995, J ACOUST SOC AM, V97, P2414, DOI 10.1121/1.411963 WANG XQ, 1992, PHILOS T ROY SOC B, V336, P399, DOI 10.1098/rstb.1992.0074 WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 ZHAO HB, 1995, HEARING RES, V82, P244, DOI 10.1016/0378-5955(94)00181-O ZHAO HB, 1994, HEARING RES, V82, P244 Zhao HB, 1997, HEARING RES, V106, P83, DOI 10.1016/S0378-5955(97)00004-X ZHAO W, 1990, BRIT J AUDIOL, V24, P193 NR 51 TC 36 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 77 EP 88 DI 10.1016/S0378-5955(99)00071-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900009 PM 10452378 ER PT J AU Miller, AL Smith, DW Pfingst, BE AF Miller, AL Smith, DW Pfingst, BE TI Across-species comparisons of psychophysical detection thresholds for electrical stimulation of the cochlea: I. Sinusoidal stimuli SO HEARING RESEARCH LA English DT Article DE cochlear implant; psychophysics; human; animal; sinusoid; threshold; auditory prosthesis; species ID BRAIN-STEM RESPONSE; AUDITORY-NERVE; SCALA TYMPANI; FUNCTIONAL-RESPONSES; SPEECH RECOGNITION; NEURAL EXCITATION; SPIRAL GANGLION; PHASE DURATION; GUINEA-PIGS; IMPLANTS AB Several species have been, and continue to be, used as subjects in studies of electrical stimulation of the cochlea. Few attempts, however, have been made to determine if data obtained from different species are quantitatively or qualitatively similar. The present work compares psychophysical absolute detection threshold vs. frequency functions for sinusoidal stimuli obtained from humans, nonhuman primates, cats, and guinea pigs. Threshold data for monopolar and bipolar electrode configurations from both previously published and unpublished studies are compared. In general, within all four species, significant intersubject variation in detection threshold level was found, but slopes of threshold vs. frequency functions were relatively well conserved within a species, under the conditions studied. With one exception (cat bipolar stimulation), threshold functions reached a minimum at or near 100 Hz across species and electrode configurations. In all cases, thresholds were significantly lower for monopolar, as compared with bipolar, configurations. Statistically, there were no significant differences in absolute threshold level across species. Threshold levels increased with frequency above 100 Hz at a rate of 3.0-7.9 dB/octave, depending on both electrode configuration and species. Slopes were steeper for monopolar than for bipolar configurations. When slopes were averaged between 200 and 2000 Hz, no statistically significant differences in overall slopes were found, nor was there a significant interaction between electrode configuration and species. There were, however, consistent species differences within more restricted regions of the function. Human functions for both monopolar and bipolar stimulation were steeper than all animal functions in the range of 100-300 Hz. Within this range, the differences between slopes for human and nonhuman subjects were statistically significant. In addition, differences were noted in the frequency at which slope decreased, with slopes for nonhuman subjects showing the decrease at higher frequencies than did those for human subjects. These differences may be true species differences, or may reflect the influence of confounding variables associated with each experimental-subject model. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Med Ctr, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Duke Univ, Med Ctr, Div Otolaryngol Head & Neck Surg, Hearing Res Labs, Durham, NC 27710 USA. RP Pfingst, BE (reprint author), Univ Michigan, Med Ctr, Dept Otolaryngol, Kresge Hearing Res Inst, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. CR AIDLEY DJ, 1971, PHYSL EXCITABLE CELL Araki S, 1997, ADV OTO-RHINO-LARYNG, V52, P39 BLACK RC, 1983, ACTA OTO-LARYNGOL, V95, P27, DOI 10.3109/00016488309130912 BROWN CJ, 1995, EAR HEARING, V16, P439, DOI 10.1097/00003446-199510000-00001 BRUCE IC, 1999, IN PRESS IEEE T BIOM Cazals Y, 1990, Acta Otolaryngol Suppl, V469, P150 CLARK GM, 1972, EXP NEUROL, V36, P350, DOI 10.1016/0014-4886(72)90029-5 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 Donnelly M J, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P409 DORMAN MF, 1992, J SPEECH HEAR RES, V35, P1126 EDDINGTON DK, 1980, J ACOUST SOC AM, V68, P885, DOI 10.1121/1.384827 Eddington D K, 1978, Ann Otol Rhinol Laryngol, V87, P1 FAY RR, 1988, HEARING RES, V34, P295, DOI 10.1016/0378-5955(88)90009-3 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FRANZ BKHG, 1987, AM J OTOL, V8, P516 FRIJNS JHM, 1995, HEARING RES, V87, P170, DOI 10.1016/0378-5955(95)00090-Q GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 GOYCOOLEA MV, 1990, LARYNGOSCOPE, V100, P19, DOI 10.1288/00005537-199002001-00002 HATSUSHIKA S, 1990, ANN OTO RHINOL LARYN, V99, P871 HAWKINS JE, 1976, ACTA OTO-LARYNGOL, V81, P337, DOI 10.3109/00016487609119971 IGARASHI M, 1976, ARCH OTOLARYNGOL, V102, P428 Kawano A, 1998, ACTA OTO-LARYNGOL, V118, P313 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LOEB GE, 1983, MED BIOL ENG COMPUT, V21, P241, DOI 10.1007/BF02478489 LOEB GE, 1983, ANN NY ACAD SCI, V405, P123, DOI 10.1111/j.1749-6632.1983.tb31625.x LONG GR, 1984, J ACOUST SOC AM, V57, P421 MILLER AL, 1995, ABSTR ASS RES OTOLAR, P180 Miller CA, 1995, HEARING RES, V92, P100, DOI 10.1016/0378-5955(95)00205-7 Miller CA, 1995, HEARING RES, V92, P85, DOI 10.1016/0378-5955(95)00204-9 MOON AK, 1993, HEARING RES, V67, P166, DOI 10.1016/0378-5955(93)90244-U NADOL JB, 1990, HEARING RES, V49, P141, DOI 10.1016/0378-5955(90)90101-T Nadol JB, 1997, OTOLARYNG HEAD NECK, V117, P220, DOI 10.1016/S0194-5998(97)70178-5 NADOL JB, 1984, LARYNGOSCOPE, V140, P299 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 NELSON DA, 1995, J ACOUST SOC AM, V98, P1987, DOI 10.1121/1.413317 NIEMIEC AJ, 1995, METHODS COMP PSYCHOA, P65 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PFINGST BE, 1993, J ACOUST SOC AM, V93, P2124, DOI 10.1121/1.406673 Pfingst BE, 1996, HEARING RES, V98, P77, DOI 10.1016/0378-5955(96)00071-8 PFINGST BE, 1993, J ACOUST SOC AM, V94, P1287, DOI 10.1121/1.408155 PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1979, ANN OTO RHINOL LARYN, V88, P613 PFINGST BE, 1989, COCHLEAR IMPLANTS MO, P161 PFINGST BE, 1988, HEARING RES, V34, P243, DOI 10.1016/0378-5955(88)90005-6 PFINGST BE, 1984, ARCH OTOLARYNGOL, V110, P140 PFINGST BE, 1990, HEARING RES, V50, P225, DOI 10.1016/0378-5955(90)90047-S PFINGST BE, 1995, HEARING RES, V85, P76, DOI 10.1016/0378-5955(95)00037-5 Pfingst B E, 1995, Ann Otol Rhinol Laryngol Suppl, V166, P127 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHANNON RV, 1986, SENSORINEURAL HEARIN, P349 SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 SHEPHERD RK, 1994, HEARING RES, V81, P150, DOI 10.1016/0378-5955(94)90162-7 Shepherd R K, 1983, Acta Otolaryngol Suppl, V399, P19 Simmons F. B., 1966, ARCH OTOLARYNGOL, V84, P24 SKINNER MW, 1994, AM J OTOL, V15, P15 Skinner Margaret W., 1995, Seminars in Hearing, V16, P228, DOI 10.1055/s-0028-1083720 SMITH DW, 1995, J ACOUST SOC AM, V98, P211, DOI 10.1121/1.413755 SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMITH DW, 1995, 18 MIDW RES M, P177 SMITH DW, 1997, J ACOUST SOC AM, V102, P1 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 SUZUKA Y, 1988, ACTA OTOLARYNGOL STO, V470, P71 TONG YC, 1982, J ACOUST SOC AM, V71, P153, DOI 10.1121/1.387342 WALLOCH RA, 1980, LARYNGOSCOPE, V90, P861 WALSH SM, 1982, HEARING RES, V7, P281, DOI 10.1016/0378-5955(82)90041-7 WALTZMAN SB, 1991, OTOLARYNG HEAD NECK, V105, P797 WEST CD, 1985, J ACOUST SOC AM, V77, P1091, DOI 10.1121/1.392227 WHITE MW, 1984, ARCH OTOLARYNGOL, V110, P493 WILLIAMS AJ, 1976, PHYSIOL PSYCHOL, V4, P23 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 XU SA, 1993, ANN OTO RHINOL LARYN, V102, P363 XUE XL, 1989, J NEUROSCI METH, V28, P189, DOI 10.1016/0165-0270(89)90035-6 ZENG FG, 1994, SCIENCE, V264, P564, DOI 10.1126/science.8160013 ZHOU RZ, 1995, HEARING RES, V88, P98, DOI 10.1016/0378-5955(95)00105-D ZHOU RZ, 1995, HEARING RES, V88, P87, DOI 10.1016/0378-5955(95)00104-C NR 78 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 89 EP 104 DI 10.1016/S0378-5955(99)00072-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900010 PM 10452379 ER PT J AU Pfingst, BE Holloway, LA Zwolan, TA Collins, LM AF Pfingst, BE Holloway, LA Zwolan, TA Collins, LM TI Effects of stimulus level on electrode-place discrimination in human subjects with cochlear implants SO HEARING RESEARCH LA English DT Article DE auditory prosthesis; cochlear implant; electrode-place discrimination; human subject; stimulus level ID MODULATION TRANSFER-FUNCTIONS; ELECTRICAL-STIMULATION; RECOGNITION ABILITY; SPEECH RECOGNITION AB Effects of stimulus level on discrimination of one stimulation site from another were examined in 15 human subjects with Nucleus-22 cochlear implant systems. Bipolar stimulation was used in all cases with electrodes in the bipolar pair separated by 1.5 mm (center to center). Subjects were first tested at a medium loudness level, using an adaptive tracking procedure, to determine the regions of the electrode array where electrode-place discrimination was best and the regions where it was poorest. Electrode-place discrimination was then tested at three regions distributed throughout the array, which included the regions of best and poorest discrimination. At each region, electrode-place discrimination was tested at three levels: 25%, 50%, and 75% of the dynamic range. For each of these nine conditions (3 sites x 3 levels), the test-electrode pairs were loudness balanced with the reference-electrode pairs. A two-interval forced-choice same-different procedure was then used to determine discriminability of the reference-electrode pair from the nearest, apical, test-electrode pair. If P(C)(max) was < 0.707 at all three levels, additional testing was done using the next, more apical, electrode pair as the test-electrode pair. A tendency toward better discrimination at more apical regions of the array was observed. Electrode pairs with poor discrimination typically had smaller dynamic ranges than those with good discrimination. There was a weak tendency toward better discrimination at higher levels of stimulation. However, effects of level on electrode-place discrimination were less pronounced and less consistent than previously observed effects of level on temporal discriminations. These results suggest interactions between current spread and the condition of the implanted cochlea as underlying mechanisms. (C) 1999 Elsevier Science B.V. Published by Elsevier Science B.V. All rights reserved. C1 Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, Ann Arbor, MI 48109 USA. Duke Univ, Dept Elect & Comp Engn, Durham, NC 27708 USA. RP Pfingst, BE (reprint author), Univ Michigan, Dept Otolaryngol, Kresge Hearing Res Inst, 1301 E Ann St, Ann Arbor, MI 48109 USA. CR Abramowitz M., 1964, HDB MATH FUNCTIONS BLAMEY PJ, 1992, ANN OTO RHINOL LARYN, V101, P342 CARBART R, 1959, J SPEECH HEAR DISORD, V24, P330 COLLINS LM, 1994, J ACOUST SOC AM, V96, P2731, DOI 10.1121/1.411279 Collins LM, 1997, J ACOUST SOC AM, V101, P440, DOI 10.1121/1.417989 GREEN DM, 1973, SIGNAL DETECTION THE Hartmann R, 1990, Acta Otolaryngol Suppl, V469, P128 HENRY B, 1997, 16 WORLD C OT HEAD N, P89 HERNDON MK, 1981, G9065 STANF U JESTEADT W, 1980, PERCEPT PSYCHOPHYS, V28, P85, DOI 10.3758/BF03204321 Kawano A, 1998, ACTA OTO-LARYNGOL, V118, P313 KUK FK, 1990, SCAND AUDIOL, V19, P139, DOI 10.3109/01050399009070765 PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1990, HEARING RES, V50, P43, DOI 10.1016/0378-5955(90)90032-K PFINGST BE, 1994, HEARING RES, V78, P197, DOI 10.1016/0378-5955(94)90026-4 RUVIAN K, 1987, COCHLEAR IMPLANT CUR, P157 Saito H, 1999, NEUROSCIENCE, V91, P139, DOI 10.1016/S0306-4522(98)00581-8 SHANNON RV, 1993, J ACOUST SOC AM, V93, P1651, DOI 10.1121/1.406799 SHANNON RV, 1989, J ACOUST SOC AM, V85, P2587, DOI 10.1121/1.397753 SHANNON RV, 1992, J ACOUST SOC AM, V91, P2156, DOI 10.1121/1.403807 SHIROMA M, 1992, ANN OTO RHINOL LARYN, V101, P32 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S TOWNSHEND B, 1987, J ACOUST SOC AM, V82, P106, DOI 10.1121/1.395554 Zwolan TA, 1997, J ACOUST SOC AM, V102, P3673, DOI 10.1121/1.420401 NR 25 TC 30 Z9 31 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 105 EP 115 DI 10.1016/S0378-5955(99)00079-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900011 PM 10452380 ER PT J AU Yonezawa, S Yoshiki, A Hanai, A Matsuzaki, T Matsushima, J Kamada, T Kusakabe, M AF Yonezawa, S Yoshiki, A Hanai, A Matsuzaki, T Matsushima, J Kamada, T Kusakabe, M TI Chromosomal localization of a gene responsible for vestibulocochlear defects of BUS/Idr mice: identification as an allele of waltzer SO HEARING RESEARCH LA English DT Article DE inner ear; mutant; waltzer; linkage map; auditory brain-stem response; the organ of Corti ID UNCONVENTIONAL MYOSINS; MOUSE; DEAFNESS; HEARING; GENOME; CELLS; MAP AB Mice of the bustling mutant strain BUS/ldr have vestibulocochlear defects, bus/bus homozygotes, but not heterozygotes, are hyperactive and display an abnormal behavior such as circling, head bobbin and head tilting. To characterize BUS mice further, the auditory brain-stem response of the mutant was examined. In +/bus heterozygotes as well as control animals, the auditory brain-stem response was developmentally first recorded as early as 11 days of age and heterozygous and normal adults showed typical auditory brain-stem responses with five peaks in a threshold of 40-45 dB SPI. In contrast, bus/bus homozygotes showed no auditory brainstem response at any age in response to stimuli up to 130 dB SPL, indicating that they are deaf throughout life. Linkage analysis revealed that the responsible gene, originally designated as bus, maps on chromosome 10, 1.09 +/- 0.9 cM distal to D10Mit127 and D10Mit59, and 0.72 +/- 0.51 proximal to three markers, D10Mit48, D10Mit112 and D10Mit258, at a site indistinguishable from that of the Albany waltzer v(Alb). The results of allelism tests between BUS and Albany waltzer indicated that bus is allelic with v(Alb). From these data, we propose here that the bus mutation could represent another allele of waltzer now designated v(bus). (C) 1999 Elsevier Science B.V. All rights reserved. C1 Inst Phys & Chem Res, RIKEN, Tsukuba Life Sci Ctr, Div Expt Anim Res, Tsukuba, Ibaraki 3050074, Japan. Aichi Human Serv Ctr, Inst Dev Res, Dept Embryol, Kasugai, Aichi 4800392, Japan. Hokkaido Univ, Sch Med, Dept Otolaryngol, Sapporo, Hokkaido 0600812, Japan. Hokkaido Univ, Sch Dent, Dept Oral Physiol, Sapporo, Hokkaido 0600812, Japan. RP Kusakabe, M (reprint author), Inst Phys & Chem Res, RIKEN, Tsukuba Life Sci Ctr, Div Expt Anim Res, Tsukuba, Ibaraki 3050074, Japan. CR AVRAHAM KB, 1995, NAT GENET, V11, P369, DOI 10.1038/ng1295-369 Bryda EC, 1997, MAMM GENOME, V8, P1, DOI 10.1007/s003359900336 Chaib H, 1996, HUM MOL GENET, V5, P1061, DOI 10.1093/hmg/5.7.1061 Dietrich WF, 1996, NATURE, V380, P149, DOI 10.1038/380149a0 DOOLITTLE DP, 1998, GENETIC VARIANTS STR, V1, P17 FLAHERTY L, 1992, P NATL ACAD SCI USA, V89, P2859, DOI 10.1073/pnas.89.7.2859 GIBSON F, 1995, NATURE, V374, P62, DOI 10.1038/374062a0 Hanai Atsuko, 1995, Congenital Anomalies, V35, P467, DOI 10.1111/j.1741-4520.1995.tb00313.x Hasson T, 1996, GENOMICS, V36, P431, DOI 10.1006/geno.1996.0488 Hasson T, 1997, J CELL BIOL, V137, P1287, DOI 10.1083/jcb.137.6.1287 MANLY KF, 1991, MAMM GENOME, V1, P123, DOI 10.1007/BF02443789 Moriyama K, 1997, ACTA OTO-LARYNGOL, V117, P20, DOI 10.3109/00016489709117985 NADEAU JH, 1991, ANN NY ACAD SCI, V630, P49, DOI 10.1111/j.1749-6632.1991.tb19575.x Otani H, 1995, Acta Otolaryngol Suppl, V519, P286 Probst FJ, 1998, SCIENCE, V280, P1444, DOI 10.1126/science.280.5368.1444 SHOJI R, 1988, MOUSE NEWS LETT, V81, P68 STEEL KP, 1983, AUDITORY PSYCHOBIOLO, P341 Steel KP, 1995, ANNU REV GENET, V29, P675 Toyoda Y., 1971, JAP J ANIM REPROD, V16, P152 Yonezawa S, 1996, ACTA OTO-LARYNGOL, V116, P409, DOI 10.3109/00016489609137865 NR 20 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 116 EP 122 DI 10.1016/S0378-5955(99)00080-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900012 PM 10452381 ER PT J AU Hosokawa, Y Horikawa, J Nasu, M Taniguchi, I AF Hosokawa, Y Horikawa, J Nasu, M Taniguchi, I TI Spatiotemporal representation of binaural difference in time and intensity of sound in the guinea pig auditory cortex SO HEARING RESEARCH LA English DT Article DE optical recording; auditory cortex; interaural time difference; interaural intensity difference; guinea pig ID UNIT AZIMUTH SENSITIVITY; PRESSURE LEVEL; SINGLE-UNIT; INTERAURAL INTENSITY; RESPONSE PROPERTIES; IN-VIVO; CAT; NEURONS; ORGANIZATION; STIMULATION AB Neural activity of the auditory cortex (AC) in response to a change of interaural intensity difference (IID) and interaural time difference (ITD) of sound stimuli was observed by optical recording with a 12X12 photodiode array and the voltage-sensitive dye, RH795. Guinea pigs (280-450 g) were anesthetized with sodium pentobarbital (30 mg/kg) and supplemental doses of neuroleptic solutions. When both ears were stimulated dichotically by tone bursts (14 kHz, 75 dB SPL), excitatory optical signals appeared in both anterior (A) and dorsocaudal (DC) fields of AC. An increase of intensity of ipsilateral stimulation from 65 to 95 dB SPL caused a decrease of neural activity of isofrequency bands in both fields. An increase of ipsilateral leads from -2.5 to 10 ms resulted in a gradual decrease of the amplitude of the excitatory responses. A strong inhibition was observed in field DC and the ventral portion of field A. These results show the different spatiotemporal representation of IID and ITD sensitivities in AC. However, the ipsilateral lead inducing a large inhibition was much longer than the time difference (80 mu s) calculated from the interaural distance of the guinea pig. This indicates that the longer binaural inhibition observed in AC would have a different functional significance from that of the neural system of ITD detection in the guinea pig. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Tokyo Med & Dent Univ, Med Res Inst, Dept Neurophysiol, Chiyoda Ku, Tokyo 1010062, Japan. RP Hosokawa, Y (reprint author), Tokyo Med & Dent Univ, Med Res Inst, Dept Neurophysiol, Chiyoda Ku, Kanda Surugadai 2-3-10, Tokyo 1010062, Japan. CR AITKIN LM, 1985, J NEUROPHYSIOL, V53, P43 BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 CLAREY JC, 1994, J NEUROPHYSIOL, V72, P2383 COHEN LB, 1986, OPTICAL METHODS CELL, P71 GRINVALD A, 1986, NATURE, V324, P361, DOI 10.1038/324361a0 Horikawa J, 1996, J PHYSIOL-LONDON, V497, P629 Hosokawa Y, 1997, J COMP PHYSIOL A, V181, P607, DOI 10.1007/s003590050144 IMIG TJ, 1990, J NEUROPHYSIOL, V63, P1448 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 Irvine DRF, 1996, J NEUROPHYSIOL, V75, P75 KELLY JB, 1988, J NEUROPHYSIOL, V59, P1756 KELLY JB, 1994, J NEUROPHYSIOL, V71, P904 KING AJ, 1983, J PHYSIOL-LONDON, V342, P361 KITZES LM, 1980, J COMP NEUROL, V192, P455, DOI 10.1002/cne.901920306 KNUDSEN EI, 1978, SCIENCE, V200, P795, DOI 10.1126/science.644324 METHERATE R, 1994, J PHYSIOL-LONDON, V481, P331 METHERATE R, 1993, J NEUROSCI, V13, P5312 MIDDLEBROOKS JC, 1981, J NEUROSCI, V1, P107 Moriyama T, 1997, Acta Otolaryngol Suppl, V532, P138 MURATA K, 1986, HEARING RES, V23, P169, DOI 10.1016/0378-5955(86)90014-6 RAJAN R, 1990, J NEUROPHYSIOL, V64, P872 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 SALZBERG BM, 1988, SPECTROSCOPIC MEMBRA, V3, P67 SAMSON FK, 1993, J NEUROPHYSIOL, V70, P492 SAMSON FK, 1994, J NEUROPHYSIOL, V71, P2194 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P449 SEMPLE MN, 1993, J NEUROPHYSIOL, V69, P462 TANIGUCHI I, 1992, NEUROSCI LETT, V146, P37, DOI 10.1016/0304-3940(92)90166-5 TANIGUCHI I, 1993, NEUROSCI LETT, V151, P178, DOI 10.1016/0304-3940(93)90015-D NR 30 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 123 EP 132 DI 10.1016/S0378-5955(99)00073-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900013 PM 10452382 ER PT J AU Mulheran, M AF Mulheran, M TI The effects of quinine on cochlear nerve fibre activity in the guinea pig SO HEARING RESEARCH LA English DT Article DE quinine ototoxicity; cochlear nerve fibre tuning curve; spontaneous activity; absolute refractory period ID OUTER HAIR-CELLS; OTOACOUSTIC EMISSIONS; HEALTHY-VOLUNTEERS; STEREOCILIA DAMAGE; TUNING CURVES; FIBERS; PATHOLOGY; CURRENTS AB The effect of quinine on single cochlear nerve fibre activity (n = 38) was measured in four pigmented guinea pigs, which were given 10-30 mg/kg of quinine intravenously. The frequency tuning curves of these fibres exhibited significant increases in the thresholds of both 'tip' and 'tails' regions of the frequency tuning curve, but these changes did not appear to be accompanied by significant changes in tuning, as measured by the Q('10'dB). In comparison with control fibres (n = 178) from 13 untreated animals, significant changes in the proportion of low:high spontaneous rates (SIR) were also seen. Using a boundary criterion of 25 sp/s, this rate changed from 26:74% to 47:53% in control and quinine-poisoned fibres, respectively. Independent of changes in the spontaneous rate, significant increases in the mean absolute refractory period from 0.85 to 1 ms were measured following quinine administration. The absence of a significant effect on fibre tuning whilst threshold was elevated indicates that quinine does not affect the integrity of the cochlear amplifier, though appears to affect cochlear sensitivity. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Leicester, Ctr Mechanisms Human Technol, MRC, Toxicol Unit, Leicester LE1 9HN, Leics, England. RP Mulheran, M (reprint author), Univ Leicester, Ctr Mechanisms Human Technol, MRC, Toxicol Unit, Leicester LE1 9HN, Leics, England. CR ALEXANDER SPH, 1997, TRENDS PHARM SCI S, P79 ALVAN G, 1991, BRIT J CLIN PHARMACO, V31, P409 ALVAN G, 1989, LIFE SCI, V45, P751, DOI 10.1016/0024-3205(89)90095-7 BERNINGER E, 1995, SCAND AUDIOL, V24, P27, DOI 10.3109/01050399509042206 BIGGER JT, 1990, PHARMACOL BASIS THER, P716 EVANS EF, 1984, BR J AUDITOL, V18, P252 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 EVANS EF, 1979, AUDITORY INVESTIGATI, P324 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 Grace AA, 1998, NEW ENGL J MED, V338, P35 HARVEY SC, 1990, PHARMACOL BASIS THER, P339 KARLSSON KK, 1991, SCAND AUDIOL, V20, P83, DOI 10.3109/01050399109070795 KIANG NYS, 1986, HEARING RES, V22, P171 KOTUN RJ, 1986, HDB CNS AGENTS LOCAL, P33 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 Lin X, 1998, J NEUROPHYSIOL, V79, P2503 LIN X, 1995, HEARING RES, V88, P36, DOI 10.1016/0378-5955(95)00096-M LUKASIEWICZ RJ, 1968, ANAL LETT, V1, P455 MARSBOOM DVM, 1971, P ASS VET ANAESTH, V2, P81 MCFADDEN D, 1994, J ACOUST SOC AM, V95, P3460, DOI 10.1121/1.410022 MULHERAN M, 1988, BRIT J AUDIOL, V21, P309 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 RYBAK LP, 1988, AM J OTOLARYNG, V9, P238, DOI 10.1016/S0196-0709(88)80033-4 SEWELL WF, 1984, J PHYSIOL-LONDON, V347, P685 SEWELL WF, 1984, HEARING RES, V15, P69, DOI 10.1016/0378-5955(84)90226-0 SOLARY E, 1992, J CLIN ONCOL, V10, P1730 WEBSTER LT, 1990, PHARMACOL BASIS THER, P1029 Yamamoto T, 1997, NEUROSCI LETT, V236, P79, DOI 10.1016/S0304-3940(97)00749-0 NR 32 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 145 EP 152 DI 10.1016/S0378-5955(99)00076-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900015 PM 10452384 ER PT J AU Morlet, T Goforth, L Hood, LJ Ferber, C Duclaux, R Berlin, CI AF Morlet, T Goforth, L Hood, LJ Ferber, C Duclaux, R Berlin, CI TI Development of human cochlear active mechanism asymmetry: involvement of the medial olivocochlear system? SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; efferent auditory pathway; neonate; maturation; auditory asymmetry ID EVOKED OTOACOUSTIC EMISSIONS; CONTRALATERAL ACOUSTIC STIMULATION; DEVELOPING RAT COCHLEA; OUTER HAIR-CELLS; PRETERM INFANTS; EFFERENT INNERVATION; MICROMECHANICAL PROPERTIES; FUNCTIONAL MATURATION; QUANTITATIVE-ANALYSIS; DISTORTION-PRODUCT AB To study the functional development of the medial oilivocochlear system, transient-evoked otoacoustic emission suppression experiments were conducted in 73 ears of 38 pre-term and 11 full-term neonates. The continuous contralateral stimulation was a broad band white noise, presented at 70 dB SPL. Efferent suppression was determined by subtracting the without-contralateral stimulation condition from the with-contralateral stimulation condition. Across this population, a mean suppression effect of contralateral stimulation on transient-evoked otoacoustic emissions was found, with most of the suppression effect observed after 8 ms. The amount of suppression is linearly, positively correlated with the conceptional age. In the subgroup of bilaterally tested neonates, the suppression of transient-evoked otoacoustic emissions is similar in the right ear and the left ear in subjects whose conceptional age is less than 36 weeks and significantly higher in the right ear than in the left ear in older neonates. This last observation was seen at frequencies where transient-evoked otoacoustic emission amplitudes became higher in the right ear than in the left ear as the conceptional age increased, a finding already reported in adults. This study shows that the functional adult pattern of the medial efferent system, probably involved in the detection of signals in noise such as speech sounds, seems to appear gradually in neonates and represents one of the several arguments in favor of functional auditory lateralization in humans, with a right ear advantage (C) 1999 Elsevier Science B.V. All rights reserved. C1 Louisiana State Univ, Med Ctr, Kresge Hearing Res Lab S, New Orleans, LA 70112 USA. Hop Debrousse, Serv Explorat Fonct Neurosensorielles, F-69005 Lyon, France. RP Morlet, T (reprint author), Louisiana State Univ, Med Ctr, Kresge Hearing Res Lab S, 2020 Gravier St, New Orleans, LA 70112 USA. CR BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 Bray P., 1989, THESIS U COLL MIDDLE BREDBERG G, 1968, ACTA OTOLARYNGOL STO, V236, P135 Brienesse P, 1997, PEDIATR RES, V42, P478, DOI 10.1203/00006450-199710000-00009 Brienesse P, 1996, AUDIOLOGY, V35, P296 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BUNO W, 1978, EXP NEUROL, V59, P62, DOI 10.1016/0014-4886(78)90201-7 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 CHANG KW, 1993, ARCH OTOLARYNGOL, V119, P276 CHI JG, 1977, ARCH NEUROL-CHICAGO, V34, P346 CHUANG SW, 1993, INT J PEDIATR OTORHI, V26, P39, DOI 10.1016/0165-5876(93)90194-8 CHUNG DY, 1983, J ACOUST SOC AM, V73, P1277, DOI 10.1121/1.389276 COLE KS, 1992, BRAIN RES, V575, P223 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E DANNHOF BJ, 1993, HEARING RES, V66, P8, DOI 10.1016/0378-5955(93)90255-Y DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DESPRES G, 1994, LIFE SCI, V54, P1291, DOI 10.1016/0024-3205(94)00506-0 Eshraghi A, 1996, INT J PEDIATR OTORHI, V37, P121, DOI 10.1016/0165-5876(96)01391-2 Giraud AL, 1997, NEUROREPORT, V8, P1779 GOFORTH L, 1997, ABST ASS RES OT, P662 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 HAMBURGER A, 1998, INT TINNITUS J, V1, P53 Hood LJ, 1996, HEARING RES, V101, P113, DOI 10.1016/S0378-5955(96)00138-4 IURATO S, 1978, J COMP NEUROL, V182, P57, DOI 10.1002/cne.901820105 JERGER J, 1972, ARCHIV OTOLARYNGOL, V96, P513 Kei J, 1997, AUDIOLOGY, V36, P61 KELLEY MW, 1993, DEVELOPMENT, V119, P1041 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Khalfa S, 1997, ACTA OTO-LARYNGOL, V117, P192, DOI 10.3109/00016489709117767 Khalfa S, 1996, NEUROREPORT, V7, P993, DOI 10.1097/00001756-199604100-00008 KOK MR, 1993, HEARING RES, V69, P115, DOI 10.1016/0378-5955(93)90099-M LAVIGNEREBILLARD M, 1988, ACTA OTO-LARYNGOL, V105, P398, DOI 10.3109/00016488809119492 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LUO L, 1993, HEARING RES, V69, P182 MCFADDEN D, 1993, HEARING RES, V68, P143, DOI 10.1016/0378-5955(93)90118-K Micheyl C, 1996, J ACOUST SOC AM, V99, P1604, DOI 10.1121/1.414734 MICHEYL C, 1995, ACTA OTO-LARYNGOL, V115, P178, DOI 10.3109/00016489509139286 Morlet T, 1996, NEUROSCI LETT, V220, P49, DOI 10.1016/S0304-3940(96)13226-2 MORLET T, 1995, HEARING RES, V90, P44, DOI 10.1016/0378-5955(95)00144-4 MORLET T, 1993, ACTA OTO-LARYNGOL, V113, P271, DOI 10.3109/00016489309135808 MORLET T, UNPUB DEV AUD ASYMM MURATA K, 1980, NEUROSCI LETT, V18, P289, DOI 10.1016/0304-3940(80)90299-2 Newmark M., 1997, Journal of Basic and Clinical Physiology and Pharmacology, V8, P133 ORMEROD F C, 1960, J Laryngol Otol, V74, P919, DOI 10.1017/S0022215100057376 PIRILA T, 1991, ACTA U OULUENSIS D, P220 PUJOL R, 1995, INT J PEDIATR OTORHI, V32, P177 Pujol R, 1985, Acta Otolaryngol Suppl, V421, P5 PUJOL R, 1992, ACTA OTO-LARYNGOL, V112, P259 PUJOL R, 1980, HEARING RES, V2, P423, DOI 10.1016/0378-5955(80)90078-7 Pujol R, 1985, Acta Otolaryngol Suppl, V423, P43 Quinonez RE, 1997, ANN OTO RHINOL LARYN, V106, P721 ROBERTSON D, 1989, DEV BRAIN RES, V47, P197, DOI 10.1016/0165-3806(89)90176-4 ROTH B, 1993, ANAT EMBRYOL, V187, P565, DOI 10.1007/BF00214435 RYAN S, 1991, British Journal of Audiology, V25, P391, DOI 10.3109/03005369109076614 RYAN S, 1994, ACTA OTO-LARYNGOL, V114, P485, DOI 10.3109/00016489409126091 Scharf B, 1997, HEARING RES, V103, P101, DOI 10.1016/S0378-5955(96)00168-2 Simmons DD, 1996, J COMP NEUROL, V370, P551, DOI 10.1002/(SICI)1096-9861(19960708)370:4<551::AID-CNE10>3.0.CO;2-M SMURZYNSKI J, 1994, EAR HEARING, V15, P210, DOI 10.1097/00003446-199406000-00002 THORNTON ARD, 1993, BRIT J AUDIOL, V27, P319, DOI 10.3109/03005369309076710 VANDEWATER TR, 1992, DEV AUDITORY VESTIBU, V2, P1 VANZANTEN BG, 1995, INT J PEDIATR OTORHI, V32, P187 Veuillet E, 1996, HEARING RES, V93, P128, DOI 10.1016/0378-5955(95)00212-X VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WADA H, 1993, AUDIOLOGY, V32, P282 Walsh EJ, 1998, J NEUROSCI, V18, P3859 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WEATHERBY LA, 1980, SCAND AUDIOL, V9, P103, DOI 10.3109/01050398009076343 WEN H, 1993, ABST ASS RES OT, P102 WHEELER EF, 1994, HEARING RES, V73, P46, DOI 10.1016/0378-5955(94)90281-X WILLIAMS EA, 1993, SCAND AUDIOL, V22, P197, DOI 10.3109/01050399309047469 NR 72 TC 30 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 153 EP 162 DI 10.1016/S0378-5955(99)00078-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900016 PM 10452385 ER PT J AU Bohne, BA Harding, GW Nordmann, AS Tseng, CJ Liang, GE Bahadori, RS AF Bohne, BA Harding, GW Nordmann, AS Tseng, CJ Liang, GE Bahadori, RS TI Survival-fixation of the cochlea: a technique for following time-dependent degeneration and repair in noise-exposed chinchillas SO HEARING RESEARCH LA English DT Article DE chinchilla; noise damage; left-right symmetry; survival surgery ID INDUCED HEARING-LOSS; ACOUSTIC INJURY; SUSCEPTIBILITY; MICE; AGE AB To minimize problems with data interpretation due to interanimal variation in susceptibility to noise, we developed a survival-fixation paradigm which involves fixing one cochlea of an experimental chinchilla at one post-exposure time and fixing the second cochlea as much as 14-24 days later. This paradigm is analytically effective because there is a high correlation in the magnitude and pattern of damage in the left and right cochleas of binaurally exposed animals. Thus, each experimental animal provides two snapshots in the degeneration and repair continua in which it call be certain that both cochleas sustained equivalent amounts of damage during the exposure. Using this technique, the time course of degeneration of different structures and cells in the organ of Corti can be determined and primary damage can be distinguished from secondary effects. The present paper discusses the issues which had to be addressed to develop this technique and provides preliminary results from chinchillas exposed to a traumatic noise. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA. Georgetown Univ, Sch Med, Dept Otolaryngol, Washington, DC USA. RP Bohne, BA (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, Box 8115, St Louis, MO 63110 USA. RI Bohne, Barbara/A-9113-2008 OI Bohne, Barbara/0000-0003-3874-7620 CR ALTSCHULER R, 1992, NOISE INDUCED HEARIN, P60 Blitzer A, 1998, LARYNGOSCOPE, V108, P1435, DOI 10.1097/00005537-199810000-00003 Bohne B.A., 1982, NEW PERSPECTIVES NOI, P283 BOHNE BA, 1985, J ACOUST SOC AM, V77, P153, DOI 10.1121/1.392279 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 BOHNE BA, 1987, HEARING RES, V29, P251, DOI 10.1016/0378-5955(87)90172-9 BOHNE BA, 1972, LARYNGOSCOPE, V82, P1 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 BOHNE BA, 1976, HEARING DAVIS ESSAYS, P85 BOHNE BA, 1986, J ACOUST SOC AM, V80, P1729, DOI 10.1121/1.394285 BOHNE BA, 1976, ANN OTO RHINOL LARYN, V85, P711 BORG E, 1995, SCAND AUDIOL S40, V24, P9 BREDBERG G, 1975, HDB SENSORY PHYSL, P261 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 Erway LC, 1996, HEARING RES, V93, P181, DOI 10.1016/0378-5955(95)00226-X FREDELIUS L, 1988, THESIS KAROLINSKA I HELLSTROM S, 1994, OTOLARYNG CLIN N AM, V27, P307 HENDERSON D, 1993, EAR HEARING, V14, P152, DOI 10.1097/00003446-199306000-00002 HENDERSON D, 1994, HEARING RES, V76, P101, DOI 10.1016/0378-5955(94)90092-2 HUMES LE, 1984, J ACOUST SOC AM, V76, P1318, DOI 10.1121/1.391447 Kitchen H, 1967, LAB ANIM DIGEST, V3, P3 KITTS WD, 1971, CAN J ZOOLOG, V49, P1079 KOHONEN A, 1965, ACTA OTOLARYNGOL S, V208 Kujawa SG, 1997, J NEUROPHYSIOL, V78, P3095 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 LIANG GE, 1997, MIDW RES M ARO, V20, P203 LIBERMAN MC, 1995, HEARING RES, V90, P158, DOI 10.1016/0378-5955(95)00160-2 NADOL JB, 1980, AGING COMMUNICATION, P63 Pack AK, 1995, HEARING RES, V91, P119 RHO MB, 1998, MIDW RES M ARO, V21, P51 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SHEA JJ, 1994, OTOLARYNG CLIN N AM, V27, P317 STOCKWEL.CW, 1969, ANN OTO RHINOL LARYN, V78, P1144 SULKOWSKI W, 1973, 550973008 EPA, P139 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 THALMANN RR, 1976, EFFECTS NOISE HEARIN, P129 VERTES D, 1976, THESIS U TENNESSEE N WARD WD, 1973, 550973008 EPA, P281 Wheeler AH, 1998, HEADACHE, V38, P468, DOI 10.1046/j.1526-4610.1998.3806468.x WLIKOSKI J, 1974, ACTA OTOLARYNGOL S, V326 ZORMEIER MM, 1998, MIDW RES M ARO, V21, P60 NR 41 TC 13 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 163 EP 178 DI 10.1016/S0378-5955(99)00082-9 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900017 PM 10452386 ER PT J AU Jager, W Khanna, SM Flock, B Flock, A AF Jager, W Khanna, SM Flock, B Flock, A TI Micromechanical effects in the cochlea of tetracaine SO HEARING RESEARCH LA English DT Article DE local anesthetic; mechanical; fundamental; second harmonic; non-linearity; summating potential ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; HEARING ORGAN; LOCAL-ANESTHETICS; INNER-EAR; OVERSTIMULATION; STIMULATION; LIGNOCAINE; RESPONSES; VIBRATION AB Local anesthetics applied in the tympanic cavity have earlier been shown to affect the gross receptor potentials in reducing the cochlear microphonics and increasing the positive summating potential. To study the effects of this drug on the mechanical responses in the cochlea, vibrations were measured using laser heterodyne interferometry in an isolated in vitro temporal bone preparation from the guinea pig. Measurements were made at a set of frequencies in the fourth cochlear turn from the Hensen's cells and the outer hair cells in response to sound applied to the ear. The tuning curves of the fundamental and the second harmonic components of the vibratory responses were plotted. When 2 mM tetracaine was applied, the high frequency slope of the second harmonic curve shifted down in frequency, this caused the frequency of the maximum of second harmonic tuning to shift down. These changes were reversible when tetracaine was washed out. Observations were also made in the temporal bone preparation in vitro with a confocal microscope. Fluorescent probes were used to label various structures in the organ of Corti. Optical sections were obtained by tilting the organ permitting a view from the side like a radial section through the organ. Images were acquired before, during and after application of tetracaine and were later analyzed with a computer program. Simultaneously, cochlear microphonics and the summating potential were obtained to monitor the electrical response of the preparation. Although the cochlear microphonics and summating potential decreased when 2 mM tetracaine was applied, structural changes were not measurable in the organ of Corti. The decrease was reversible when tetracaine was washed out. It is concluded that tetracaine affected the high frequency part of the non-linear second harmonic component, possibly by lowering the stiffness of the stereocilia bundle or the body of the outer hair cells. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden. Huddinge Univ Hosp, Dept Otolaryngol, S-14146 Huddinge, Sweden. Columbia Univ Coll Phys & Surg, Dept Otolaryngol, New York, NY 10032 USA. RP Jager, W (reprint author), Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BRUNDIN L, 1994, HEARING RES, V73, P35, DOI 10.1016/0378-5955(94)90280-1 BUTTERWORTH JF, 1990, ANESTHESIOLOGY, V72, P711, DOI 10.1097/00000542-199004000-00022 CAPUTO C, 1976, J PHYSL, V255, P192 DALLOS P, 1992, J NEUROSCI, V12, P4575 DAVIS H, 1950, P NATL ACAD SCI USA, V35, P580 ENGEBRET.AM, 1968, J ACOUST SOC AM, V44, P548, DOI 10.1121/1.1911119 Flock A, 1997, HEARING RES, V106, P29 FLOCK A, 1999, UNPUB J NEUROSCI Flock A, 1998, NEUROSCIENCE, V83, P215, DOI 10.1016/S0306-4522(97)00335-7 Fridberger A, 1998, P NATL ACAD SCI USA, V95, P7127, DOI 10.1073/pnas.95.12.7127 *ITER, 1989, ACTA OTOLARYNGOL S, V467, P7 Jager W, 1997, ACTA OTO-LARYNGOL, V117, P49, DOI 10.3109/00016489709117991 JARAMILLO F, 1993, NATURE, V364, P527, DOI 10.1038/364527a0 KHANNA SM, 1996, P SOC PHOTO-OPT INS, V2732, P64, DOI 10.1117/12.231687 Khanna SM, 1999, HEARING RES, V132, P15, DOI 10.1016/S0378-5955(99)00027-1 KHANNA SM, 1999, IN PRESS HEAR RES KHANNA SM, 1998, ACTA ACOUST, V84, P1 KOESTER CJ, 1994, APPL OPTICS, V33, P702, DOI 10.1364/AO.33.000702 KONISHI T, 1964, J ACOUST SOC AM, V43, P471 LAURIKAINEN E, 1992, ACTA OTO-LARYNGOL, V112, P800, DOI 10.3109/00016489209137477 MARTIN FW, 1980, CLIN OTOLARYNGOL, V5, P3, DOI 10.1111/j.1365-2273.1980.tb01622.x MELDING PS, 1978, J LARYNGOL OTOL, V92, P115, DOI 10.1017/S002221510008511X PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 Rhode W. S., 1973, BASIC MECHANISMS HEA, P49 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 Sakata E, 1976, AURIS NASUS LARYNX, V3, P133 SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 SAUNDERS JC, 1986, HEARING RES, V24, P217, DOI 10.1016/0378-5955(86)90020-1 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SOKOLICH WG, 1977, J ACOUST SOC AM, V56, P12 ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 Ulfendahl M, 1996, J NEUROPHYSIOL, V76, P3850 WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 XU L, 1993, J GEN PHYSIOL, V101, P207, DOI 10.1085/jgp.101.2.207 Zetes DE, 1997, J ACOUST SOC AM, V101, P3593, DOI 10.1121/1.418320 NR 38 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1999 VL 134 IS 1-2 BP 179 EP 185 DI 10.1016/S0378-5955(99)00083-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 223BY UT WOS:000081820900018 PM 10452387 ER PT J AU Michel, O Hess, A Bloch, W Stennert, E Su, JP Addicks, K AF Michel, O Hess, A Bloch, W Stennert, E Su, JP Addicks, K TI Localization of the NO/cGMP-pathway in the cochlea of guinea pigs SO HEARING RESEARCH LA English DT Article DE nitric oxide; NO synthase; cGMP; soluble guanylyl cyclase; cochlea; neurotransmission; cochlear amplifier ID NITRIC-OXIDE SYNTHASE; OUTER HAIR-CELLS; BLOOD-FLOW; SODIUM-NITROPRUSSIDE; OTOTOXICITY; PHYSIOLOGY; RESPONSES; BONE AB The presence of nitric oxide synthase (NOS) in substructures of the cochlea of guinea pigs is an issue of current focus. Moreover, information concerning the localization of cells effected by the NO/GMP-pathway are rare. Paraffin sections of guinea pig cochlea were incubated with specific antibodies to the three known NOS isoforms, soluble guanylyl cyclase (sGC) and cyclic guanosine monophosphate (cGMP), the second messenger system of NO. While detection of inducible iNOS failed in all cochlear structures, expression of endothelial eNOS was found in the spiral ligament, in the stria vascularis, in cells of the organ of Corti, in nerve fibers and in some perikaryia of the spiral ganglion. The cochlear nerve showed an accentuated affinity for immunostaining in distal, basal segments of the cochlea. Neuronal bNOS was found predominantly in the endosteum of the modiolus and cochlea and was less intensively present in all perikaryia of the spiral ganglion and in the spiral ligament. Supporting cells of the organ of Corti and cells in the limbus spiralis displayed only modest immunostaining, while bNOS was not found in outer and inner hair cells. NOS detection was accompanied by immunoreactivity to sGC and to cGMP. The presence of NOS and its second messenger system gives evidence for a possible involvement in neurotransmission, regulation of the cochlear amplifier and in homeostasis. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Cologne, Klin & Poliklin Hals Nasen & Ohrenheilkunde, Dept Otorhinolaryngol, D-50924 Cologne, Germany. Univ Cologne, Dept Anat, D-50924 Cologne, Germany. RP Michel, O (reprint author), Univ Cologne, Klin & Poliklin Hals Nasen & Ohrenheilkunde, Dept Otorhinolaryngol, Joseph Stelzmann Str 9, D-50924 Cologne, Germany. CR Arnhold S, 1997, NEUROSCI LETT, V229, P165, DOI 10.1016/S0304-3940(97)00457-6 BECKMAN JS, 1990, P NATL ACAD SCI USA, V87, P1620, DOI 10.1073/pnas.87.4.1620 Bloch W, 1997, PROSTATE, V33, P1 BRECHTELSBAUER PB, 1994, HEARING RES, V77, P38, DOI 10.1016/0378-5955(94)90251-8 CHEN C, 1995, HEARING RES, V87, P1, DOI 10.1016/0378-5955(95)00071-B CHOW JWM, 1996, J BONE MINER RES S1, V11, pS270 Dais CGD, 1996, HEARING RES, V99, P1 DAWSON VL, 1991, P NATL ACAD SCI USA, V88, P6368, DOI 10.1073/pnas.88.14.6368 DULON D, 1990, J NEUROSCI, V10, P1388 Evans DM, 1996, J BONE MINER RES, V11, P300 Fessenden JD, 1997, J HISTOCHEM CYTOCHEM, V45, P1401 FORSTERMANN U, 1994, HYPERTENSION, V23, P1121 Franz P, 1996, ACTA OTO-LARYNGOL, V116, P726, DOI 10.3109/00016489609137914 Gosepath K, 1997, BRAIN RES, V747, P26, DOI 10.1016/S0006-8993(96)01149-3 Hess A, 1998, NEUROSCI LETT, V251, P185, DOI 10.1016/S0304-3940(98)00532-1 IGNARRO LJ, 1990, HYPERTENSION, V16, P477 KALINEC F, 1993, NEUROSCI LETT, V157, P231, DOI 10.1016/0304-3940(93)90744-6 Kong WJ, 1996, HEARING RES, V99, P22, DOI 10.1016/S0378-5955(96)00076-7 MANZONI O, 1992, NEURON, V8, P653, DOI 10.1016/0896-6273(92)90087-T MONCADA S, 1991, PHARMACOL REV, V43, P109 Murad F, 1994, NEUROTRANSMISSIONS, V10, P1 Ralston SH, 1997, BRIT J RHEUMATOL, V36, P831 Ruan RS, 1997, HEARING RES, V114, P169, DOI 10.1016/S0378-5955(97)00159-7 Vass Z, 1996, HEARING RES, V100, P114, DOI 10.1016/0378-5955(96)00102-5 Yamane H, 1997, HEARING RES, V108, P65, DOI 10.1016/S0378-5955(97)00041-5 ZDANSKI CJ, 1994, HEARING RES, V79, P39, DOI 10.1016/0378-5955(94)90125-2 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 27 TC 42 Z9 46 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 1 EP 9 DI 10.1016/S0378-5955(99)00049-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600001 PM 10416859 ER PT J AU Matsuda, K Ueda, Y Doi, T Tono, T Haruta, A Toyama, K Komune, S AF Matsuda, K Ueda, Y Doi, T Tono, T Haruta, A Toyama, K Komune, S TI Increase in glutamate-aspartate transporter (GLAST) mRNA during kanamycin-induced cochlear insult in rats SO HEARING RESEARCH LA English DT Article DE glutamate-aspartate transporter; glutamate; cochlea; kanamycin; northern hybridization; neurotoxicity ID MESSENGER-RNA EXPRESSION; GUINEA-PIG COCHLEA; IMMUNOCYTOCHEMICAL LOCALIZATION; GLUTAMATE/ASPARTATE TRANSPORTER; BRAIN; ORGAN; NEUROTRANSMITTERS; HIPPOCAMPUS; RECEPTOR; ISCHEMIA AB Kanamycin (KM)-induced changes in expression of the gene for glutamate-aspartate transporter (GLAST) in the rat cochlea were analyzed by Northern blotting. With the administration of KM (600 mg/kg/day) once daily for 20 days, the expression of GLAST mRNA gradually increased and reached a peak on day 20. Although the expression of GLAST mRNA remained at a high level until 12 days after the completion of the KM treatment, it then fell to the normal level within 2 months. Such KM treatment resulted in loss of both inner and outer hair cells and a concomitant profound permanent threshold shift. The present findings suggest that during KM administration, high concentrations of extracellular glutamate released by collapsing hair cells induced GLAST mRNA expression. Increased GLAST mRNA might play an important role in the prevention of the secondary death of spiral ganglion neurons from glutamate neurotoxicity. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Miyazaki Med Coll, Dept Otorhinolaryngol, Kiyotake, Miyazaki 8891692, Japan. Miyazaki Med Coll, Dept Psychiat, Kiyotake, Miyazaki 8891692, Japan. RP Matsuda, K (reprint author), Miyazaki Med Coll, Dept Otorhinolaryngol, 5200 Kihara, Kiyotake, Miyazaki 8891692, Japan. CR ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 AMARA SG, 1992, NATURE, V360, P420, DOI 10.1038/360420d0 ARRIZA JL, 1994, J NEUROSCI, V14, P5559 Arzberger T, 1997, J NEUROPATH EXP NEUR, V56, P440, DOI 10.1097/00005072-199704000-00013 ASTBURY PJ, 1982, ARCH TOXICOL, V50, P267, DOI 10.1007/BF00310859 Basile AS, 1996, NAT MED, V2, P1338, DOI 10.1038/nm1296-1338 BENVENISTE H, 1984, J NEUROCHEM, V43, P1369, DOI 10.1111/j.1471-4159.1984.tb05396.x Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 DUCKERT LG, 1993, OTOLARYNG CLIN N AM, V26, P873 Ernfors P, 1996, NAT MED, V2, P1313, DOI 10.1038/nm1296-1313 EYBALIN M, 1991, ASS RES OT ST PET BE, P18 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FORGE A, 1985, HEARING RES, V19, P171, DOI 10.1016/0378-5955(85)90121-2 Furness DN, 1997, EUR J NEUROSCI, V9, P1961, DOI 10.1111/j.1460-9568.1997.tb00763.x GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 HAWKINS JE, 1964, ACTA OTO-LARYNGOL, V188, P100 KANAI Y, 1992, NATURE, V360, P467, DOI 10.1038/360467a0 KAPLAN BB, 1979, BIOCHEM J, V183, P181 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 KLINKE R, 1981, ACTA OTO-LARYNGOL, V91, P541, DOI 10.3109/00016488109138540 Kohonen A., 1965, ACTA OTO-LARYNGOL, V208, P1 KOITCHEV K, 1982, ACTA OTO-LARYNGOL, V94, P431, DOI 10.3109/00016488209128931 LI HS, 1994, HEARING RES, V78, P235, DOI 10.1016/0378-5955(94)90029-9 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 LIM DJ, 1976, ANN OTO RHINOL LARYN, V85, P740 MIKAELIA.DO, 1974, ACTA OTO-LARYNGOL, V77, P327, DOI 10.3109/00016487409124632 NICHOLLS D, 1990, TRENDS PHARMACOL SCI, V11, P462, DOI 10.1016/0165-6147(90)90129-V NUDEL U, 1983, NUCLEIC ACIDS RES, V11, P1759, DOI 10.1093/nar/11.6.1759 OTORI Y, 1994, MOL BRAIN RES, V27, P310, DOI 10.1016/0169-328X(94)90014-0 PINES G, 1992, NATURE, V360, P464, DOI 10.1038/360464a0 PUJOL R, 1993, ACTA OTO-LARYNGOL, V113, P330, DOI 10.3109/00016489309135819 PUJOL R, 1991, ACTA OTOLARYNGOL S S, V476, P32 PULLAN LM, 1992, J NEUROCHEM, V59, P2087 RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 RAPHAEL Y, 1991, HEARING RES, V51, P173, DOI 10.1016/0378-5955(91)90034-7 ROSSI G, 1976, ACTA OTO-LARYNGOL, V81, P270, DOI 10.3109/00016487609119962 Rothstein JD, 1996, NEURON, V16, P675, DOI 10.1016/S0896-6273(00)80086-0 ROTHSTEIN JD, 1995, ANN NEUROL, V38, P73, DOI 10.1002/ana.410380114 SANGER F, 1977, P NATL ACAD SCI USA, V74, P5463, DOI 10.1073/pnas.74.12.5463 Shibata T, 1996, NEUROREPORT, V7, P705, DOI 10.1097/00001756-199602290-00006 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 STORCK T, 1992, P NATL ACAD SCI USA, V89, P10955, DOI 10.1073/pnas.89.22.10955 SUGA F, 1976, ANN OTO RHINOL LARYN, V85, P169 Takumi Y, 1997, NEUROSCIENCE, V79, P1137, DOI 10.1016/S0306-4522(97)00025-0 TORP R, 1995, EXP BRAIN RES, V103, P51 USAMI S, 1992, EXP BRAIN RES, V91, P1 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 Yamashita T, 1996, MOL BRAIN RES, V38, P294, DOI 10.1016/0169-328X(96)00043-5 NR 48 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 10 EP 16 DI 10.1016/S0378-5955(99)00050-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600002 PM 10416860 ER PT J AU Dye, BJ Frank, TC Newlands, SD Dickman, JD AF Dye, BJ Frank, TC Newlands, SD Dickman, JD TI Distribution and time course of hair cell regeneration in the pigeon utricle SO HEARING RESEARCH LA English DT Article DE regeneration; vestibular; hair cell; ototoxicity ID AVIAN VESTIBULAR EPITHELIUM; AMINOGLYCOSIDE TOXICITY; CRISTA-AMPULLARIS; GENTAMICIN; RECOVERY; STREPTOMYCIN; BULLFROG; COCHLEA; EAR AB Vestibular and cochlear regeneration following ototoxic insult from aminoglycoside antibiotics has been well documented, particularly in birds. In the present study, intraotic application of a 2 mg streptomycin paste was used to achieve complete vestibular hair cell destruction in pigeons (Columba livia) while preserving regenerative ability. Scanning electron microscopy was used to quantify hair cell density longitudinally during regeneration in three different utricular macula locations, including the striola, central and peripheral regions. The utricular epithelium was void of stereocilia (indicating hair cell loss) at 4 days after intraotic treatment with streptomycin. At 2 weeks the stereocilia began to appear randomly and mostly in an immature form. However, when present most kinocilia were polarized toward the developing striola. Initially, regeneration occurred more rapidly in the central and peripheral regions of the utricle as compared to the striola. As regeneration proceeded from 2 to 12 weeks, hair cell density in the striola region equaled the density noted in the central and peripheral regions. At 24 weeks, hair cell density of the central and peripheral regions was equal to normal values, however the striola region had a slightly greater hair cell density than that observed for normal animals. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Mississippi, Med Ctr, Dept Surg, Div Otolaryngol, Jackson, MS 39216 USA. RP Dickman, JD (reprint author), Univ Mississippi, Med Ctr, Dept Surg, Div Otolaryngol, 2500 N State St, Jackson, MS 39216 USA. CR BAIRD RA, 1993, HEARING RES, V65, P164, DOI 10.1016/0378-5955(93)90211-I BERG K, 1951, Acta Otolaryngol Suppl, V97, P1 Carey JP, 1996, J NEUROPHYSIOL, V76, P3301 Carranza A, 1997, LARYNGOSCOPE, V107, P137, DOI 10.1097/00005537-199701000-00025 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DEY S, 1989, J MICROSC-OXFORD, V156, P259 FLOCK A, 1964, J CELL BIOL, V22, P413, DOI 10.1083/jcb.22.2.413 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 FRANK TC, 1998, IN PRESS LARYNGOSCOP JONES TA, 1992, HEARING RES, V62, P181, DOI 10.1016/0378-5955(92)90184-O JORGENSEN J M, 1973, Acta Zoologica (Stockholm), V54, P121 LINDEMAN HH, 1969, ACTA OTO-LARYNGOL, V67, P177, DOI 10.3109/00016486909125441 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 LOMBARTE A, 1993, HEARING RES, V64, P166, DOI 10.1016/0378-5955(93)90002-I Lopez I, 1997, INT J DEV NEUROSCI, V15, P447, DOI 10.1016/S0736-5748(96)00103-7 Masetto S, 1997, INT J DEV NEUROSCI, V15, P387, DOI 10.1016/S0736-5748(96)00099-8 Omura R, 1989, Acta Otolaryngol Suppl, V468, P41 WEISLEDER P, 1992, EXP NEUROL, V115, P2, DOI 10.1016/0014-4886(92)90211-8 WEISLEDER P, 1993, J COMP NEUROL, V331, P97, DOI 10.1002/cne.903310106 WERSALL J, 1962, Acta Otolaryngol, V54, P1, DOI 10.3109/00016486209126917 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 NR 21 TC 18 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 17 EP 26 DI 10.1016/S0378-5955(99)00046-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600003 PM 10416861 ER PT J AU Li, L Parkins, CW Webster, DB AF Li, L Parkins, CW Webster, DB TI Does electrical stimulation of deaf cochleae prevent spiral ganglion degeneration? SO HEARING RESEARCH LA English DT Article DE cochlear implant; electrical stimulation; auditory brainstem response; inferior colliculus electrically evoked response; cochlear histology; spiral ganglion neuron; Rosenthal's canal ID AUDITORY-NERVE; CATS; PATHOLOGY; SURVIVAL; KITTENS AB Thirty-six drug deafened guinea pigs were studied to determine how electrical stimulation of the cochlea affects spiral ganglion cell (SGC) survival. Animals were divided into two groups, extracochlear and intracochlear stimulation, and each group was further divided into four stimulus subgroups: no stimulation (implanted controls), the inferior colliculus electrically evoked potential (ICEEP) threshold-2 dB, ICEEP threshold+2 dB, and ICEEP threshold+6 dB. Stimuli consisted of 200 mu s/phase charge balanced biphasic current pulses presented at 100 pulses per second using monopolar stimulation. Animals were stimulated 5 h/day, 5 days per week, for 8 weeks. The animals were then perfused and the cochleae serially sectioned at 4 mu m saving every 8th section. We counted the number of intact SGCs, those containing a nucleus with chromatin, in each 20% segment of the cochlea and also measured SGC densities (number of neurons per mm(2) of Rosenthal's canal). The number of surviving spiral ganglion neurons was not significantly different (P > 0.05) between the implanted and the unimplanted ears in any of the experimental groups. However, the spiral ganglion neuron densities were significantly elevated in the electrically stimulated ears (P < 0.001) but not in the implanted but not chronically stimulated ears (P > 0.05). We measured the volume of Rosenthal's canal in one subgroup (ICEEP threshold+2 dB) and found a decrease in this volume in the stimulated ear compared to the unstimulated ear (P < 0.01). These findings support the hypothesis that chronic monopolar electrical intracochlear or extracochlear stimulation is not a neurotrophic factor, increasing spiral ganglion neuron survival, but instead causes a narrowing of Rosenthal's canal that accounts for the increased spiral ganglion neuronal densities seen in the stimulated cochleae. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Louisiana State Univ, Med Ctr, Kresge Hearing Res Lab S, Dept Otorhinolaryngol & Biocommun, New Orleans, LA 70112 USA. RP Li, L (reprint author), Louisiana State Univ, Med Ctr, Kresge Hearing Res Lab S, Dept Otorhinolaryngol & Biocommun, 2020 Gravier St,Suite A, New Orleans, LA 70112 USA. CR Araki S, 1998, LARYNGOSCOPE, V108, P687, DOI 10.1097/00005537-199805000-00012 BRIGHTON CT, 1975, J BONE JOINT SURG AM, VA 57, P368 FRIEDENB.ZB, 1974, ANN NY ACAD SCI, V238, P564, DOI 10.1111/j.1749-6632.1974.tb26822.x GARRATT AC, 1860, ELECTROPHYSIOLOGY EL, P657 Guild SR, 1921, ANAT REC, V22, P141 HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 Hawkins J E Jr, 1973, Adv Otorhinolaryngol, V20, P125 KLAPPER L, 1974, ANN NY ACAD SCI, V238, P530, DOI 10.1111/j.1749-6632.1974.tb26819.x LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1992, HEARING RES, V64, P99, DOI 10.1016/0378-5955(92)90172-J LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEAKE PA, 1995, HEARING RES, V82, P65 LEVY DD, 1974, ANN NY ACAD SCI, V238, P478, DOI 10.1111/j.1749-6632.1974.tb26814.x LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MATZ GJ, 1993, OTOLARYNG CLIN N AM, V26, P705 Miller JM, 1996, AUDITORY SYSTEM PLASTICITY AND REGENERATION, P378 MILLER JM, 1992, NOISE INDUCED HEARIN, P130 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PARKINS CW, 1994, ADV COCHLEAR IMPLANT, P54 SCHUKNECHT HF, 1974, PATHOLOGH EAR SHEPHERD RK, 1994, HEARING RES, V81, P150, DOI 10.1016/0378-5955(94)90162-7 SHEPHERD RK, 1991, ACTA OTO-LARYNGOL, V111, P848, DOI 10.3109/00016489109138421 SPADARO JA, 1977, CLIN ORTHOP RELAT R, P325 WALSH SM, 1982, HEARING RES, V7, P281, DOI 10.1016/0378-5955(82)90041-7 WALSH SM, 1981, ANN OTO RHINOL LARYN, V90, P27 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 NR 27 TC 34 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 27 EP 39 DI 10.1016/S0378-5955(99)00043-X PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600004 PM 10416862 ER PT J AU Mom, T Telischi, FF Martin, GK Lonsbury-Martin, BL AF Mom, T Telischi, FF Martin, GK Lonsbury-Martin, BL TI Measuring the cochlear blood flow and distortion-product otoacoustic emissions during reversible cochlear ischemia: a rabbit model SO HEARING RESEARCH LA English DT Article DE cochlear blood flow; laser-Doppler flowmetry; reversible cochlear ischemia; distortion product otoacoustic emission; rabbit ID PURE-TONE EXPOSURES; LASER-DOPPLER MEASUREMENTS; ACOUSTIC NEUROMA SURGERY; GUINEA-PIG COCHLEA; GERBIL COCHLEA; OCCLUSION AB Impairment to the cochlear blood flow likely induces many types of sensorineural hearing loss. Models using several small laboratory animals have been described in the literature that permit the simultaneous monitoring of the cochlear blood flow with laser-Doppler flowmetry and cochlear function using evoked responses. However, these models have not permitted a direct application of the resulting knowledge to the human condition, primarily due to differences in the translucence of the otic capsule between species. In the present study, to approximate conditions relevant to the human patient, the rabbit was utilized to develop a procedure in which laser-Doppler flowmetry could be used to measure the cochlear blood flow ill an animal with an opaque otic capsule. At the same time, the cochlear function was monitored non-invasively using. distortion-product otoacoustic emissions. In this manner. a laser-Doppler probe was positioned in the round window niche and the cochlear function measured using distortion-product otoacoustic emissions during a systematic series of ischemic episodes. Cochlear ischemia was produced by deliberately compressing the eighth nerve complex at the porus of the internal acoustic meatus, for periods lasting from 1-3 min, while cochlear blood flow and distortion-product otoacoustic emission measures were obtained simultaneously before, during and following the occlusion. Results demonstrated that the cochlear blood flow sharply decreased within 1 s after compression onset, whereas distortion-product otoacoustic emissions showed obstruction-induced changes after a delay of several seconds, provided that the blood flow decreased, at least, 40%. Similarly, upon release of the compression, the cochlear blood now began to recover within 1 s, whereas the recovery of the corresponding distortion-product otoacoustic emissions was slightly delayed. Although not apparent in the distortion-product otoacoustic emission recovery time course, the cochlear blood flow consistently overshot its initial baseline value during the recovery process. Thus, although cochlear ischemia produced changes in the distortion-product otoacoustic emission activity that generally followed the resulting alterations in the cochlear blood flow, the detailed relationship between the two measures was complex. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Dauvergne, Fac Med, Serv Otorhinolaryngol, F-63001 Clermont Ferrand, France. Univ Miami, Sch Med, Dept Otolaryngol, Miami, FL USA. Univ Dauvergne, Fac Med, Lab Biophys Sensorielle 2R3, F-63001 Clermont Ferrand, France. RP Mom, T (reprint author), Univ Dauvergne, Fac Med, Serv Otorhinolaryngol, BP 38, F-63001 Clermont Ferrand, France. CR ASAMI K, 1995, ORL J OTO-RHINO-LARY, V57, P239 BILLETT TE, 1989, HEARING RES, V41, P189, DOI 10.1016/0378-5955(89)90010-5 BONFILS P, 1988, AM J OTOL, V9, P412 LEVINE RA, 1993, ANN OTO RHINOL LARYN, V102, P127 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 LONSBURYMARTIN BL, 1989, 2 INT S MEN DIS PATH, P337 LOTZ P, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P233 MARTIN GK, 1989, 2ND INT S MEN DIS PA, P205 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1983, HEARING RES, V12, P65, DOI 10.1016/0378-5955(83)90119-3 MENSH BD, 1993, HEARING RES, V70, P65, DOI 10.1016/0378-5955(93)90052-3 MENSH BD, 1993, HEARING RES, V70, P50, DOI 10.1016/0378-5955(93)90051-2 MILLER JM, 1991, ANN OTO RHINOL LARYN, V100, P44 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 Mom T, 1997, BRAIN RES, V751, P20, DOI 10.1016/S0006-8993(96)01388-1 PERLMAN H B, 1959, Laryngoscope, V69, P591 RANDOLF HB, 1990, EUR ARCH OTO-RHINO-L, V247, P226 REN TY, 1994, J APPL PHYSIOL, V76, P212 Ren TY, 1995, HEARING RES, V92, P30, DOI 10.1016/0378-5955(95)00192-1 SCHEIBE F, 1990, EUR ARCH OTO-RHINO-L, V247, P20 Schuknecht HF, 1974, PATHOLOGY EAR, P303 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P457 STERN MD, 1977, AM J PHYSIOL, V232, P441 Telischi FF, 1998, LARYNGOSCOPE, V108, P837, DOI 10.1097/00005537-199806000-00011 TELISCHI FF, 1995, AM J OTOL, V16, P597 WIDICK MP, 1994, OTOLARYNG HEAD NECK, V111, P407 NR 26 TC 29 Z9 32 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 40 EP 52 DI 10.1016/S0378-5955(99)00056-8 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600005 PM 10416863 ER PT J AU Ogata, Y Slepecky, NB Takahashi, M AF Ogata, Y Slepecky, NB Takahashi, M TI Study of the gerbil utricular macula following treatment with gentamicin, by use of bromodeoxyuridine and calmodulin immunohistochemical labelling SO HEARING RESEARCH LA English DT Article DE hair cell regeneration; hair cell marker; calmodulin; bromodeoxyuridine; gentamicin ototoxicity ID HAIR CELL REGENERATION; MAMMALIAN INNER-EAR; PERIPHERAL VESTIBULAR SYSTEM; GROWTH-FACTOR-ALPHA; ACOUSTIC TRAUMA; SENSORY EPITHELIA; SUPPORTING CELL; LOCALIZATION; PROLIFERATION; MACROPHAGE AB Effects of ototoxic drugs on the gerbil vestibular sensory epithelium were probed by use of immunocytochemical labelling with antibodies to both a mitogenic marker (bromodeoxyuridine) and a hair cell specific protein (calmodulin). Nine animals had gentamicin administered once daily for 5 days, as a transtympanic injection into the right middle ear. They additionally were given a daily intraperitoneal injection of bromodeoxyuridine, starting on the same day as the gentamicin injection and continuing until the day of sacrifice. Wine other animals, serving as controls for bromodeoxyuridine incorporation, received only the intraperitoneal injections of bromodeoxyuridine. The inner ears from three gerbils were obtained at 1, 2 or 4 weeks following the last gentamicin injection and utricles from the injected ears were processed for immunohistochemical analysis. In specimens where gentamicin was administered, we found evidence of bromodeoxyuridine incorporation in 17 cells (10 single cells and 7 pairs of cells) in a total of 216 sections taken from the central regions of the 9 utricles. However, in control specimens, no bromodeoxyuridine labelling was found in any cells of the 216 sections examined. Of 10 single cells labelled with bromodeoxyuridine, two cells in the hair cell layer were labelled with antibodies against calmodulin. One had a faint labelling in the nucleus and the other in the stereocilia, but not in the cell bodies. Of 7 pairs of cells, two pairs with nuclei localized in the hair cell layer had faint labelling for calmodulin in the nuclei, but no labelling in any other part of the cell. The other 13 cells labelled with antibodies to bromodeoxyuridine were not labelled with antibodies to calmodulin. Our results suggest that the bromodeoxyuridine-labelled cells could not be positively identified as hair cells based on immunohistochemical labelling for calmodulin. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Yamaguchi Univ, Sch Med, Dept Otolaryngol, Yamaguchi 7558505, Japan. Syracuse Univ, Inst Sensory Res, Dept Bioengn & Neurosci, Syracuse, NY 13244 USA. RP Ogata, Y (reprint author), Yamaguchi Univ, Sch Med, Dept Otolaryngol, Yamaguchi 7558505, Japan. CR Bhave SA, 1998, J COMP NEUROL, V398, P241, DOI 10.1002/(SICI)1096-9861(19980824)398:2<241::AID-CNE6>3.0.CO;2-0 CHAFOULEAS JG, 1982, CELL, V28, P41, DOI 10.1016/0092-8674(82)90373-7 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DECHESNE CJ, 1991, BRAIN RES, V560, P139, DOI 10.1016/0006-8993(91)91224-O DECHESNE CJ, 1988, HEARING RES, V33, P273, DOI 10.1016/0378-5955(88)90157-8 DEMEMES D, 1993, CELL TISSUE RES, V274, P487, DOI 10.1007/BF00314545 DUPONT J, 1993, SCANNING MICROSCOPY, V7, P597 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 HOLTHAM KA, 1995, J HISTOCHEM CYTOCHEM, V43, P637 Jones JE, 1996, J NEUROSCI, V16, P649 Kil J, 1997, HEARING RES, V114, P117, DOI 10.1016/S0378-5955(97)00166-4 Kuntz AL, 1998, J COMP NEUROL, V399, P413 Li L, 1997, INT J DEV NEUROSCI, V15, P433, DOI 10.1016/S0736-5748(96)00102-5 LI X, 1995, BIOTECH HISTOCHEM, V70, P234, DOI 10.3109/10520299509108200 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MACFADDEN EA, 1989, HEARING RES, V41, P205 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y MEANS AR, 1980, NATURE, V285, P73, DOI 10.1038/285073a0 Nishizaki K, 1998, ACTA OTO-LARYNGOL, V118, P96 Ogata Y, 1998, J VESTIBUL RES-EQUIL, V8, P209 ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RUBEL EW, 1995, SCIENCE, V267, P701, DOI 10.1126/science.7839150 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SANS A, 1987, BRAIN RES, V435, P293, DOI 10.1016/0006-8993(87)91612-X SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 TANYERI H, 1995, HEARING RES, V89, P194, DOI 10.1016/0378-5955(95)00137-7 TSUE TT, 1994, J NEUROSCI, V14, P140 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 USAMI S, 1995, ORL J OTO-RHINO-LARY, V57, P94 Warchol ME, 1997, J NEUROBIOL, V33, P724, DOI 10.1002/(SICI)1097-4695(19971120)33:6<724::AID-NEU2>3.0.CO;2-B WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 WEISLEDER P, 1995, HEARING RES, V82, P125 WEISLEDER P, 1993, J COMP NEUROL, V331, P97, DOI 10.1002/cne.903310106 YAMASHITA H, 1995, P NATL ACAD SCI USA, V92, P3152, DOI 10.1073/pnas.92.8.3152 Zheng JL, 1997, J NEUROSCI, V17, P8270 NR 37 TC 23 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 53 EP 60 DI 10.1016/S0378-5955(99)00057-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600006 PM 10416864 ER PT J AU Nummela, S Reuter, T Hemila, S Holmberg, P Paukku, P AF Nummela, S Reuter, T Hemila, S Holmberg, P Paukku, P TI The anatomy of the killer whale middle ear (Orcinus orca) SO HEARING RESEARCH LA English DT Article DE computer tomography; dolphin; odontoceti; underwater hearing ID EVOLUTION AB The paper first reviews our present understanding of the functional morphology of the odontocete (toothed whale) ear. The tympano-periotic complex forming the ear region consists of a ventral bowl-shaped tympanic bone in direct contact with the surrounding soft tissues and the incident sound, and a dorsal periotic bone containing the inner ear. Apparently sound brings the tympanic bone, and especially its thin tympanic plate, into vibration. The ossicles in the air-filled middle ear cavity form a bridge from the tympanic plate to the periotic bone connecting the vibrating plate to the oval window and the inner ear. Our computer tomography (CT) sections and camera lucida drawings reveal two hitherto unknown features of the odontocete ear, both of them of potential relevance to sound reception and impedance matching. (1) It is well known that, in addition to the ossicular chain, two other bone structures connect the tympanic to the periotic bone. We show that the most delicate parts of these extra-ossicular connections consist of thin and folded bony sheets which apparently allow compliance in the tympano-periotic bone contacts and enable plate vibration in relation to the periotic bone. (2) The round head of the malleus, in combination with a fitting round depression on the periotic side, seems to form a joint. We propose that this (hypothetical) joint, together with the adjacent structures, forms a lever producing an amplification of the vibration velocity at the level of the oval window. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Helsinki, Dept Systemat & Ecol, Zool Lab, FIN-00014 Helsinki, Finland. Helsinki Univ Technol, Phys Lab, FIN-02015 Helsinki, Finland. Univ Helsinki, Dept Physiol, Inst Biomed, FIN-00014 Helsinki, Finland. Univ Helsinki, Dept Surg 4, FIN-00014 Helsinki, Finland. RP Nummela, S (reprint author), Univ Helsinki, Dept Systemat & Ecol, Zool Lab, POB 17, FIN-00014 Helsinki, Finland. CR Beauregard H, 1894, J ANAT PARIS, V1894, P366 Boenninghaus G, 1904, ZOOL JB A, V19, P189 BULLOCK TH, 1968, Z VERGL PHYSIOL, V59, P117 DEHAAN FWR, 1957, ACTA OTOLARYNGOL S, V134 DORAN AHG, 1878, T LINN SOC LOND, V1, P371 FLEISCHER G, 1975, Zeitschrift fuer Saeugetierkunde, V40, P89 Fleischer G., 1978, Advances in Anatomy Embryology and Cell Biology, V55, P1 FLEISCHER G, 1973, Saeugetierkundliche Mitteilungen, V21, P131 Fraser F. C., 1954, B BRIT MUS NAT HIST, V2, P103 FRASER F. C., 1960, BULL BRIT MUS [NAT HIST] ZOOL, V7, P1 Hemila S, 1999, HEARING RES, V133, P82, DOI 10.1016/S0378-5955(99)00055-6 HEMILA S, 1995, HEARING RES, V85, P31, DOI 10.1016/0378-5955(95)00031-X HENSON JR O. W., 1961, U KANSAS SCI B, V52, P151 HYRTL J, 1845, VERGLEICHENDANATOMIS KETTEN DR, 1990, NATO ADV SCI I A-LIF, V196, P81 Ketten D. R., 1994, P UNDERWATER ACOUST, V1, P264 Ketten Darlene R., 1997, Bioacoustics, V8, P103 KETTEN DR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P717 Lancaster W.C., 1990, Journal of Vertebrate Paleontology, V10, P117 Lillie D.G., 1910, P ZOOL SOC LOND, P769 MCCORMICK J G, 1970, Journal of the Acoustical Society of America, V48, P1418, DOI 10.1121/1.1912302 Norris K. S., 1964, P317 NOVACEK MJ, 1977, MAMMAL REV, V7, P131, DOI 10.1111/j.1365-2907.1977.tb00366.x NUMMELA S, 1995, HEARING RES, V85, P18, DOI 10.1016/0378-5955(95)00030-8 Nummela S, 1999, HEARING RES, V133, P71, DOI 10.1016/S0378-5955(99)00054-4 OELSCHLAGER HA, 1990, NATO ADV SCI I A-LIF, V196, P137 PILLERI G, 1990, ETHOL ECOL EVOL, V2, P135 STARCK D., 1979, VERGLEICHENDE ANATOM, VII WEVER EG, 1972, P NATL ACAD SCI USA, V69, P657, DOI 10.1073/pnas.69.3.657 NR 29 TC 25 Z9 32 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 61 EP 70 DI 10.1016/S0378-5955(99)00053-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600007 PM 10416865 ER PT J AU Nummela, S Wagar, T Hemila, S Reuter, T AF Nummela, S Wagar, T Hemila, S Reuter, T TI Scaling of the cetacean middle ear SO HEARING RESEARCH LA English DT Article DE hearing; bone density; isometry; allometry; tympanic bulla; ossicle; whale ID WHALES AB Functionally interesting dimensions of the tympano-periotic complex were measured and compared in 18 odontocete and six mysticete species, ranging from small porpoises to the blue whale. We determined (i) the masses of the tympanic and periotic bones (T and P) and of the ossicles malleus, incus, and stapes (M, I and S), (ii) the volume occupied by the tympanic bone (V), (iii) the areas of the tympanic plate and oval window (A(1) and A(2)), (iv) the thickness of the tympanic plate (D), and (v) the densities of the ossicles (d(M), d(I), and d(S)). In most cases, roughly isometric scaling was found in both toothed and baleen whales. P is isometric to T,and the tympanic bone is structurally isometric in all species studied, although not within mysticetes as a group, shown by the isometric relations of V to T, of T(2/3) to A(1), and of D to root A(1). The essentially isometric scaling of the tympanic bone provides a basis for the functional models described by Hemila et al. (1999). The relation of S to M+I is also isometric, but the relation of M+I+S to T is negatively allometric, as is the relation of A(2) to A(1), both with slopes close to 2/3. The possible functional implication of this allometry is unknown. The mean ossicular density is 2.64 g/cm(3) for odontocetes, and 2.35 g/cm(3) for mysticetes. The highly mineralized and convex tympanic plate provides cetaceans with a uniquely large and stiff sound collecting area. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Helsinki, Dept Systemat & Ecol, Zool Lab, FIN-00014 Helsinki, Finland. Helsinki Univ Technol, Phys Lab, FIN-02015 Helsinki, Finland. RP Nummela, S (reprint author), Univ Helsinki, Dept Systemat & Ecol, Zool Lab, POB 17, FIN-00014 Helsinki, Finland. EM sirpa.nummela@helsinki.fi CR Arnason U, 1996, MOL BIOL EVOL, V13, P407 BARNES LG, 1985, MAR MAMMAL SCI, V1, P15, DOI 10.1111/j.1748-7692.1985.tb00530.x Beauregard H, 1894, J ANAT PARIS, V1894, P366 Cato D, 1992, ACOUST AUST, V20, P76 CATO D H, 1991, Memoirs of the Queensland Museum, V30, P277 DEHAAN FWR, 1957, ACTA OTOLARYNGOL S, V134 FLEISCHER G, 1976, Saeugetierkundliche Mitteilungen, V24, P48 FLEISCHER G, 1975, Zeitschrift fuer Saeugetierkunde, V40, P89 FLEISCHER G, 1976, Z SAUGETIERKD, V41, P30 FLEISCHER G, 1976, J PALEONTOL, V50, P133 Fleischer G., 1978, Advances in Anatomy Embryology and Cell Biology, V55, P1 FLEISCHER G, 1973, Saeugetierkundliche Mitteilungen, V21, P131 FORTELIUS M, 1999, IN PRESS SINAP FORMA FRASER F. C., 1960, BULL BRIT MUS [NAT HIST] ZOOL, V7, P1 Giraud-Sauveur D., 1969, Mammalia, V33, P285, DOI 10.1515/mamm.1969.33.2.285 Hemila S, 1999, HEARING RES, V133, P82, DOI 10.1016/S0378-5955(99)00055-6 HEMILA S, 1995, HEARING RES, V85, P31, DOI 10.1016/0378-5955(95)00031-X Hyrtl J, 1845, VERGLEICHEND ANATOMI Kasuya T., 1973, Scientific Rep Whales Res Inst Tokyo, VNo. 25, P1 KETTEN DR, 1990, NATO ADV SCI I A-LIF, V196, P81 Ketten D. R., 1994, P UNDERWATER ACOUST, V1, P264 Ketten Darlene R., 1997, Bioacoustics, V8, P103 KETTEN DR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P717 KHANNA SM, 1972, J ACOUST SOC AM, V51, P1904, DOI 10.1121/1.1913050 Lancaster W.C., 1990, Journal of Vertebrate Paleontology, V10, P117 Lees S, 1996, J ACOUST SOC AM, V99, P2421, DOI 10.1121/1.415430 LEES S, 1983, J ACOUST SOC AM, V74, P28, DOI 10.1121/1.389723 MULLINS J, 1988, CAN J FISH AQUAT SCI, V45, P1736, DOI 10.1139/f88-205 Norris KS, 1968, EVOLUTION ENV, P297 Nowak R. M., 1991, WALKERS MAMMALS WORL, VII NUMMELA S, 1995, HEARING RES, V85, P18, DOI 10.1016/0378-5955(95)00030-8 Nummela S, 1999, HEARING RES, V133, P61, DOI 10.1016/S0378-5955(99)00053-2 Nummela Sirpa, 1997, Comments on Theoretical Biology, V4, P387 OELSCHLAGER HA, 1986, AM J ANAT, V177, P353, DOI 10.1002/aja.1001770306 OELSCHLAGER HA, 1990, NATO ADV SCI I A-LIF, V196, P137 Richardson W.J., 1995, MARINE MAMMALS NOISE Spector WS, 1956, HDB BIOL DATA Thewissen J. G. M., 1994, Journal of Mammalian Evolution, V2, P157, DOI 10.1007/BF01473527 Urick R. J., 1975, PRINCIPLES UNDERWATE VAN VALEN LEIGH, 1966, BULL AMER MUS NATUR HIST, V132, P1 WATKINS WA, 1987, J ACOUST SOC AM, V82, P1901, DOI 10.1121/1.395685 NR 41 TC 34 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 71 EP 81 DI 10.1016/S0378-5955(99)00054-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600008 PM 10416866 ER PT J AU Hemila, S Nummela, S Reuter, T AF Hemila, S Nummela, S Reuter, T TI A model of the odontocete middle ear SO HEARING RESEARCH LA English DT Article DE impedance matching; hearing sensitivity; audiogram; acoustics; mammal ID HEARING AB The high acoustic sensitivity of the bottlenose dolphin is physically defined and related to the anatomy of the middle car. The paper presents a conceptual and parametric analysis of the demands imposed by this high sensitivity upon the middle ear mechanisms: the head and the middle ear structures must collect sound energy from a large area and concentrate it onto the oval window. Assuming that the specific input impedance of the mammalian cochlea is relatively constant, and smaller than the characteristic acoustic impedance of water, we find that the impedance matching task of the cetacean middle car is very different from that of terrestrial mammals: instead of a large pressure amplification, cetaceans need amplification of particle velocity. Our mechanical four-bone model of the odontocete middle ear is based on the anatomy of the tympano-periotic complex and consists of four rigid bone units (tympanic bone, the malleus-incus complex, stapes, periotic bone) connected through elastic junctions. The velocity amplification is brought about by lever mechanisms and elastic couplings. The model produced velocity amplifications ranging from 7- to 23-fold when provided with middle ear parameters from the sir; odontocete species for which audiograms are available. The model reproduces the complete audiograms of these six species fairly well for frequencies up to about 100-120 kHz. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Helsinki, Dept Systemat & Ecol, Zool Lab, FIN-00014 Helsinki, Finland. Helsinki Univ Technol, Phys Lab, FIN-02015 Helsinki, Finland. RP Nummela, S (reprint author), Univ Helsinki, Dept Systemat & Ecol, Zool Lab, POB 17, FIN-00014 Helsinki, Finland. CR ANDERSEN S, 1971, INVESTIGATIONS CETAC, V3, P255 BRILL RL, 1988, MAR MAMMAL SCI, V4, P223, DOI 10.1111/j.1748-7692.1988.tb00203.x BULLOCK TH, 1968, Z VERGL PHYSIOL, V59, P117 Cato D, 1992, ACOUST AUST, V20, P76 CATO DH, 1995, P 15 INT C AC ICA 95, V1, P219 DALLAND JI, 1965, SCIENCE, V150, P1185, DOI 10.1126/science.150.3700.1185 EVANS EF, 1982, SENSES, P251 Fay R. R., 1988, HEARING VERTEBRATES Fleischer G., 1978, Advances in Anatomy Embryology and Cell Biology, V55, P1 GOODSON AD, 1990, NATO ADV SCI I A-LIF, V196, P255 HALL JD, 1972, J ACOUST SOC AM, V51, P515, DOI 10.1121/1.1912871 HEMILA S, 1996, P NORD AC M NAM 96 H, P241 HEMILA S, 1995, HEARING RES, V85, P31, DOI 10.1016/0378-5955(95)00031-X JACOBS DW, 1972, J ACOUST SOC AM, V51, P530, DOI 10.1121/1.1912874 JOHNSON C. SCOTT, 1967, MAR BIO ACOUSTICS, V2, P247 KETTEN DR, 1990, NATO ADV SCI I A-LIF, V196, P81 Ketten D. R., 1994, P UNDERWATER ACOUST, V1, P264 KETTEN DR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P717 MCCORMICK J G, 1970, Journal of the Acoustical Society of America, V48, P1418, DOI 10.1121/1.1912302 MOLLER AR, 1974, HDB SENSORY PHYSL AU, V5, P491 Norris KS, 1968, EVOLUTION ENV, P297 Norris K. S., 1964, P317 NUMMELA S, 1995, HEARING RES, V85, P18, DOI 10.1016/0378-5955(95)00030-8 Nummela S, 1999, HEARING RES, V133, P71, DOI 10.1016/S0378-5955(99)00054-4 Nummela S, 1999, HEARING RES, V133, P61, DOI 10.1016/S0378-5955(99)00053-2 Nummela Sirpa, 1997, Comments on Theoretical Biology, V4, P387 PHILLIPS DP, 1982, HEARING RES, V8, P13, DOI 10.1016/0378-5955(82)90031-4 Rosowski J. J., 1986, PERIPHERAL AUDITORY, P3 THOMAS J, 1988, J ACOUST SOC AM, V84, P936, DOI 10.1121/1.396662 von Bekesy G., 1941, AKUST Z, V6, P1 WATKINS WA, 1987, J ACOUST SOC AM, V82, P1901, DOI 10.1121/1.395685 WHITE MJ, 1978, 78109 HUBBS SEA WORL NR 32 TC 28 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 82 EP 97 DI 10.1016/S0378-5955(99)00055-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600009 PM 10416867 ER PT J AU Kazee, AM West, NR AF Kazee, AM West, NR TI Preservation of synapses on principal cells of the central nucleus of the inferior colliculus with aging in the CBA mouse SO HEARING RESEARCH LA English DT Article DE hearing; aging; presbycusis; inferior colliculus; morphometry ID SENSORINEURAL HEARING-LOSS; ANTEROVENTRAL COCHLEAR NUCLEUS; AGE-RELATED DECREASE; C57BL/6J MICE; RESPONSE PROPERTIES; AZIMUTHAL LOCATION; AUDITORY MIDBRAIN; LIFE-SPAN; NEURONS; YOUNG AB The light and electron microscopic features of principal neurons of the central nucleus of the inferior colliculus were quantitated in the CBA mouse. Three age groups of mice were examined, including young (3 months), middle-aged (8 months) and old (25 months). No changes were noted in the size of the principal neurons over the age range examined. At the ultrastructural level, synapses on the somata of the principal neurons showed no change in the number or type of synapses, the length of synaptic apposition nor the size of synaptic terminal area. These results are in contrast with the moderately severe synapse loss which we previously reported in the C57BL/6 mouse strain, a strain which has a genetic deficit producing progressive sensorineural hearing loss starting in young adulthood (Kazee et al., 1995). In contrast, hearing is quite well-preserved across the lifespan in the CBA mouse strain, making this a useful animal to study the intrinsic effects of aging in the auditory system versus the effects of sensorineural hearing loss. The preservation of synapses on principal neurons in this strain suggests that synaptic loss is not an inevitable event in aging, but may be related to the preservation of peripheral auditory function and input to the neurons. (C) 1999 Elsevier Science B.V. All rights reserved. C1 SUNY Hlth Sci Ctr, Dept Pathol, Syracuse, NY 13210 USA. RP Kazee, AM (reprint author), SUNY Hlth Sci Ctr, Dept Pathol, 750 E Adams St, Syracuse, NY 13210 USA. CR BRINER W, 1989, NEUROBIOL AGING, V10, P295, DOI 10.1016/0197-4580(89)90039-0 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 Frisina RD, 1998, HEARING RES, V115, P61, DOI 10.1016/S0378-5955(97)00176-7 GUTIERREZ A, 1994, J NEUROSCI, V14, P7469 KAZEE AM, 1995, HEARING RES, V89, P109, DOI 10.1016/0378-5955(95)00128-6 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 MCFADDEN SL, 1994, HEARING RES, V78, P132, DOI 10.1016/0378-5955(94)90019-1 MCFADDEN SL, 1994, HEARING RES, V78, P115, DOI 10.1016/0378-5955(94)90018-3 MILBRANDT JC, 1995, ASS RES OT ABSTR, V18, P33 MILBRANDT JC, 1994, NEUROBIOL AGING, V15, P699, DOI 10.1016/0197-4580(94)90051-5 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 OLIVER DL, 1984, J COMP NEUROL, V222, P237, DOI 10.1002/cne.902220207 PARHAM K, 1988, Behavioral Neuroscience, V102, P881, DOI 10.1037/0735-7044.102.6.881 ROCKEL AJ, 1973, J COMP NEUROL, V147, P61, DOI 10.1002/cne.901470104 SEMPLE MN, 1979, J NEUROPHYSIOL, V42, P1626 SHNERSON A, 1979, EXP BRAIN RES, V37, P373 Shnerson A., 1982, DEV BRAIN RES, V2, P77 Shnerson A., 1982, DEV BRAIN RES, V2, P65 Spongr VP, 1997, J ACOUST SOC AM, V101, P3546, DOI 10.1121/1.418315 STIEBLER I, 1985, J COMP NEUROL, V238, P65, DOI 10.1002/cne.902380106 SYKA J, 1981, NEURONAL MECH HEARIN, P137 Walton JP, 1998, J NEUROSCI, V18, P2764 Walton JP, 1997, J COMP PHYSIOL A, V181, P161, DOI 10.1007/s003590050103 WILLIAMSON BP, 1993, NLGI SPOKESMAN, V57, P329 WILLOTT JF, 1988, HEARING RES, V37, P15, DOI 10.1016/0378-5955(88)90074-3 WILLOTT JF, 1988, HEARING RES, V37, P1, DOI 10.1016/0378-5955(88)90073-1 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1992, J COMP NEUROL, V321, P666, DOI 10.1002/cne.903210412 WILLOTT JF, 1990, J COMP NEUROL, V300, P61, DOI 10.1002/cne.903000106 WILLOTT JF, 1978, BRAIN RES, V148, P230, DOI 10.1016/0006-8993(78)90395-5 WILLOTT JF, 1995, BEHAV NEUROSCI, V109, P396, DOI 10.1037//0735-7044.109.3.396 WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 WILLOTT JF, 1994, NEUROBIOL AGING, V15, P175, DOI 10.1016/0197-4580(94)90109-0 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 WILLOTT JF, 1985, J COMP NEUROL, V237, P545, DOI 10.1002/cne.902370410 Willott JF, 1996, DEV BRAIN RES, V91, P218, DOI 10.1016/0165-3806(95)00188-3 NR 37 TC 9 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 98 EP 106 DI 10.1016/S0378-5955(99)00058-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600010 PM 10416868 ER PT J AU Morse, RP Evans, EF AF Morse, RP Evans, EF TI Additive noise can enhance temporal coding in a computational model of analogue cochlear implant stimulation SO HEARING RESEARCH LA English DT Article DE cochlear implant; speech coding; Frankenhauser-Huxley model; stochastic resonance; temporal coding; noise ID AUDITORY-NERVE FIBERS; STOCHASTIC RESONANCE; ELECTRICAL-STIMULATION; DISCHARGE PATTERNS; MYELINATED NERVE; REPRESENTATION; PROSTHESIS; MECHANORECEPTORS; EXCITATION; PARAMETERS AB Conventional analogue multichannel cochlear implants are unlikely to convey formant information by the fine time structure of evoked discharges. Theoretically, however, the addition of noise to the channel outputs could enhance the representation of formants by time coding. In this study, the potential benefit of noise in analogue coding schemes was investigated using a computer model of cochlear implant stimulation. The cochlear nerve was modelled by the Frankenhauser-Huxley equations. For all five vowels investigated, the optimal addition of noise to the first channel of the simulated implant (200-671 Hz) caused enhancement of the first formant representation las seen in amplitude spectra of the simulated discharges). For vowels with a low-frequency second formant, clear enhancement of the second formant resulted from the optimal addition of noise to the third channel (1200-2116 Hz). On the basis of the present computational study, additive noise would be expected to enhance the coding of temporal information by the discharges of a single nerve fiber. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Keele, Sch Life Sci, MacKay Inst Commun & Neurosci, Ctr Human & Machine Percept Res, Keele ST5 5BG, Staffs, England. RP Morse, RP (reprint author), Univ Keele, Sch Life Sci, MacKay Inst Commun & Neurosci, Ctr Human & Machine Percept Res, Keele ST5 5BG, Staffs, England. CR ADRIAN ED, 1901, J PHYSL, V47, P460 ANDERSON DJ, 1973, J ACOUST SOC AM, V54, P361, DOI 10.1121/1.1913585 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P59 BOX GEP, 1958, ANN MATH STAT, V29, P610, DOI 10.1214/aoms/1177706645 Bulsara AR, 1996, PHYS TODAY, V49, P39, DOI 10.1063/1.881491 BUTIKOFER R, 1978, IEEE T BIO-MED ENG, V25, P526, DOI 10.1109/TBME.1978.326286 Chialvo DR, 1997, PHYS REV E, V55, P1798, DOI 10.1103/PhysRevE.55.1798 CLOPTON BM, 1984, HEARING RES, V14, P1, DOI 10.1016/0378-5955(84)90063-7 CLOPTON BM, 1983, ANN NY ACAD SCI, V405, P295 COLLINS JJ, 1995, NATURE, V376, P236, DOI 10.1038/376236a0 Collins JJ, 1996, J NEUROPHYSIOL, V76, P642 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 Delattre P, 1952, WORD, V8, P195 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P866, DOI 10.1121/1.390596 DODGE FA, 1958, J PHYSIOL-LONDON, V143, P76 DODGE FA, 1959, J PHYSIOL-LONDON, V148, P188 DOUGLASS JK, 1993, NATURE, V365, P337, DOI 10.1038/365337a0 DYKMAN MI, 1995, NUOVO CIMENTO D, V17, P661, DOI 10.1007/BF02451825 EDDINGTON D K, 1978, Annals of Otology Rhinology and Laryngology, V87, P5 Erlanger J, 1937, ELECT SIGNS NERVOUS EVANS EF, 1991, IEE DIGEST, V179 EVANS EF, 1978, AUDIOLOGY, V17, P369 FRANKENHAEUSER B, 1963, J PHYSIOL-LONDON, V169, P445 FRANKENHAEUSER B, 1962, J PHYSIOL-LONDON, V160, P54 FRANKENHAEUSER B, 1962, J PHYSIOL-LONDON, V160, P46 FRANKENHAEUSER B, 1963, J PHYSIOL-LONDON, V169, P431 FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 FRANKENHAEUSER B, 1959, J PHYSIOL-LONDON, V148, P671 FRANKENHAEUSER B, 1963, J PHYSIOL-LONDON, V169, P424 FRANKENHAEUSER B, 1962, J PHYSIOL-LONDON, V160, P40 FRANKENHAUSER B, 1959, J PHYSL, V151, P491 FRANKENHAEUSER B, 1963, J PHYSIOL-LONDON, V169, P438 FRIJNS JHM, 1994, MED BIOL ENG COMPUT, V32, P391, DOI 10.1007/BF02524690 FRY FB, 1979, PHYSICS SPEECH GANTZ B, 1987, ADV OTOL HEAD NECK S, V1, P171 GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 Gasser HS, 1939, AM J PHYSIOL, V127, P393 GASSER HS, 1926, AM J PHYSIOL, V86, P522 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GOLDMAN L, 1968, BIOPHYS J, V8, P596 HARDING RD, 1986, SIMPLE INTRO NUMERIC HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 Hartmann WM, 1996, J ACOUST SOC AM, V100, P3491, DOI 10.1121/1.417248 HUTCHINS.NA, 1970, J PHYSIOL-LONDON, V208, P279 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KLATT DH, 1980, J ACOUST SOC AM, V67, P971, DOI 10.1121/1.383940 KNAUTH M, 1994, HEARING RES, V74, P247, DOI 10.1016/0378-5955(94)90193-7 Levin JE, 1996, NATURE, V380, P165, DOI 10.1038/380165a0 LOEB GE, 1990, ANNU REV NEUROSCI, V13, P357, DOI 10.1146/annurev.neuro.13.1.357 MERZENICH MM, 1977, FUNCTIONAL ELECT STI, P321 MILLAR JB, 1984, J SPEECH HEAR RES, V27, P280 Miller RL, 1997, J ACOUST SOC AM, V101, P3602, DOI 10.1121/1.418321 MOORE BCJ, 1985, COCHLEAR IMPLANTS, P163 MOORE JW, 1978, BIOPHYS J, V21, P147 Morse RP, 1996, NAT MED, V2, P928, DOI 10.1038/nm0896-928 MORSE RP, 1998, BRIT J AUDIOL, V32, P111 MORSE RP, 1997, THESIS KEELE U MOTZ H, 1986, NEUROSCIENCE, V18, P699, DOI 10.1016/0306-4522(86)90064-3 PAINTAL AS, 1966, J PHYSIOL-LONDON, V184, P791 PALMER AR, 1986, J ACOUST SOC AM, V79, P100, DOI 10.1121/1.393633 PARKIN JL, 1993, LARYNGOSCOPE, V103, P835 PARKIN JL, 1987, COCHLEAR IMPLANTS CU, P429 PETERSON GE, 1960, J ACOUST SOC AM, V32, P693, DOI 10.1121/1.1908183 PFINGST BE, 1986, OTOLARYNG CLIN N AM, V19, P219 PHAN TT, 1994, ADV COCHLEAR IMPLANT, P342 PLOMP R, 1967, J ACOUST SOC AM, V41, P707, DOI 10.1121/1.1910398 POLS LCW, 1969, J ACOUST SOC AM, V46, P458, DOI 10.1121/1.1911711 Press WH, 1988, NUMERICAL RECIPES C RATTAY F, 1993, IEEE T BIO-MED ENG, V40, P1201, DOI 10.1109/10.250575 ROSEN SM, 1981, NATURE, V291, P150, DOI 10.1038/291150a0 Rosenbrock H, 1996, J PROCESS CONTR, V6, P1, DOI 10.1016/0959-1524(96)81787-2 SCHINDLER RA, 1993, AM J OTOL, V14, P263 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SIMMONS FB, 1966, ARCHIV OTOLARYNGOL, V84, P2 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 STEVENS KN, 1983, ANN NY ACAD SCI, V405, P2, DOI 10.1111/j.1749-6632.1983.tb31613.x TONG YC, 1980, J ACOUST SOC AM, V68, P1897, DOI 10.1121/1.385184 TYLER RS, 1989, AUDIOLOGY, V28, P301 VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 WIESENFELD K, 1995, NATURE, V373, P33, DOI 10.1038/373033a0 WIESENFELD K, 1993, ANN NY ACAD SCI, V706, P13, DOI 10.1111/j.1749-6632.1993.tb24678.x YOUNG ED, 1979, J ACOUST SOC AM, V66, P1381, DOI 10.1121/1.383532 NR 82 TC 31 Z9 32 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 107 EP 119 DI 10.1016/S0378-5955(99)00062-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600011 PM 10416869 ER PT J AU Morse, RP Evans, EF AF Morse, RP Evans, EF TI Preferential and non-preferential transmission of formant information by an analogue cochlear implant using noise: the role of the nerve threshold SO HEARING RESEARCH LA English DT Article DE cochlear implant; speech coding; linearization; stochastic resonance; noise ID APERIODIC STOCHASTIC RESONANCE; TEMPORAL RESPONSE PATTERNS; AUDITORY-NERVE; ELECTRICAL-STIMULATION; SYSTEMS; FIBERS; DISCRIMINATION; ENHANCEMENT; FREQUENCY; CRAYFISH AB Previous experiments have shown that, in principle. the addition of noise to any vowel coded by an analogue multichannel cochlear implant can enhance the representation of formant information by the temporal pattern of evoked nerve discharges. The optimal addition of noise to some vowel stimuli caused a largely uniform transmission of all input harmonics, including those related to a formant. But for other vowel stimuli, the optimal addition of noise caused preferential transmission of the harmonic closest to a formant compared with other input harmonics. Such preferential transmission may be useful to a cochlear implantee for formant estimation, but the basis of this transmission is unknown. In the present study, the nature of this preferential transmission was investigated with a set of parallel discriminators (or level-crossing detectors) to determine whether the inherent threshold of a nerve fiber was the main cause of the effect. An explicit threshold was found to account for some but not all of the previously observed preferential transmission. Furthermore, many discriminators were required to obtain preferential transmission. Therefore, preferential transmission of a formant-related harmonic may be best achieved by pre-processing a stimulus and using methods associated with stochastic resonance. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Keele, Sch Life Sci, MacKay Inst Commun & Neurosci, Ctr Human & Machine Percept Res, Keele ST5 5BG, Staffs, England. RP Morse, RP (reprint author), Univ Keele, Sch Life Sci, MacKay Inst Commun & Neurosci, Ctr Human & Machine Percept Res, Keele ST5 5BG, Staffs, England. CR ANDERSON DJ, 1973, J ACOUST SOC AM, V54, P361, DOI 10.1121/1.1913585 Benzi R, 1981, J PHYS A, V14, P453 BOX GEP, 1958, ANN MATH STAT, V29, P610, DOI 10.1214/aoms/1177706645 BRAZIER M, 1961, ELECT ACTIVITY NERVO Bulsara AR, 1996, PHYS TODAY, V49, P39, DOI 10.1063/1.881491 CHIALVO DR, 1993, J STAT PHYS, V70, P375, DOI 10.1007/BF01053974 Chialvo DR, 1997, PHYS REV E, V55, P1798, DOI 10.1103/PhysRevE.55.1798 CLOPTON BM, 1983, ANN NY ACAD SCI, V405, P295 COLLINS JJ, 1995, PHYS REV E, V52, pR3321 COLLINS JJ, 1995, NATURE, V376, P236, DOI 10.1038/376236a0 Collins JJ, 1996, PHYS REV E, V54, P5575, DOI 10.1103/PhysRevE.54.5575 Delattre P, 1952, WORD, V8, P195 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P866, DOI 10.1121/1.390596 DOUGLASS JK, 1993, NATURE, V365, P337, DOI 10.1038/365337a0 EDDINGTON DK, 1980, J ACOUST SOC AM, V68, P885, DOI 10.1121/1.384827 EVANS EF, 1991, IEE DIGEST, V179 GAMMAITONI L, 1995, PHYS REV E, V52, P4691, DOI 10.1103/PhysRevE.52.4691 GAMMAITONI L, 1995, PHYS REV LETT, V74, P1052, DOI 10.1103/PhysRevLett.74.1052 GERSTEIN GL, 1960, BIOPHYS J, V1, P15 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 Heneghan C, 1996, PHYS REV E, V54, pR2228 HINOJOSA R, 1983, ANN NY ACAD SCI, V405, P459, DOI 10.1111/j.1749-6632.1983.tb31662.x HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 JAVEL E, 1990, COCHLEAR IMPACTS MOD, P135 KLATT DH, 1980, J ACOUST SOC AM, V67, P971, DOI 10.1121/1.383940 KNAUTH M, 1994, HEARING RES, V74, P247, DOI 10.1016/0378-5955(94)90193-7 Levin JE, 1996, NATURE, V380, P165, DOI 10.1038/380165a0 Liberman AM, 1954, PSYCHOL MONOGR-GEN A, V68, P1 LONGTIN A, 1991, PHYS REV LETT, V67, P656, DOI 10.1103/PhysRevLett.67.656 MORSE RP, 1998, UNPUB CHAOS SOLITONS Morse RP, 1996, NAT MED, V2, P928, DOI 10.1038/nm0896-928 Morse RP, 1999, HEARING RES, V133, P107, DOI 10.1016/S0378-5955(99)00062-3 MORSE RP, 1996, BRIT J AUDIOL, V30, P97 MOSS F, 1993, ANN NY ACAD SCI, V706, P21 MOSS F, 1994, INT J BIFURCAT CHAOS, V4, P1383, DOI 10.1142/S0218127494001118 NADOL JB, 1992, ANN OTO RHINOL LARYN, V101, P988 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PARKIN JL, 1988, LARYNGOSCOPE, V98, P262 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 SCHINDLER RA, 1993, AM J OTOL, V14, P263 VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 WHITE MW, 1983, ANN NY ACAD SCI, V405, P348, DOI 10.1111/j.1749-6632.1983.tb31649.x WIESENFELD K, 1995, NATURE, V373, P33, DOI 10.1038/373033a0 ZHOU T, 1990, PHYS REV A, V41, P4255, DOI 10.1103/PhysRevA.41.4255 NR 45 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 120 EP 132 DI 10.1016/S0378-5955(99)00063-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600012 PM 10416870 ER PT J AU Lecain, E Sauvaget, E Crisanti, P Van den Abbeele, T Huy, PTB AF Lecain, E Sauvaget, E Crisanti, P Van den Abbeele, T Huy, PTB TI Potassium channel ether a go-go mRNA expression in the spiral ligament of the rat SO HEARING RESEARCH LA English DT Article DE K+ channel; ether a go-go; rat; cochlea; reverse transcription-PCR; in situ hybridization ID STRIA VASCULARIS; INNER-EAR; CARDIAC-ARRHYTHMIA; GAP-JUNCTIONS; ALPHA-SUBUNIT; MUTATIONS; VOLTAGE; NA,K-ATPASE; DROSOPHILA; CURRENTS AB Identification of the K+ transporters located in the lateral wall of the cochlea is essential for a better understanding of the mechanisms by which a positive endocochlear potential and a high K+ concentration are achieved in endolymph. In this study, we have determined the distribution of the K+ channel rat ether ri go-go (eag) mRNA in the cochlea. After reverse transcription of adult rat cochlear tissues, cDNA was amplified with primers specific to eag channel. The eag mRNA was localized in cochlear tissues by in situ hybridization using specific oligonucleotide probes tailed with digoxigenin conjugated UTP. Eag mRNA was detected in the organ of Corti but mainly in the fibrocytes of the spiral ligament but not in spiral prominence or in stria vascularis. The expression pattern of rat eag transcript in spiral ligament is complementary to the Na+,K+-ATPase distribution in the cochlear lateral wall. The localization of eag mRNA suggests that eag potassium channel may be produced in the corresponding cells. Considering the importance of the K+ gradient in the cochlea, the result reported here suggests that eag channel may play a role in the control of K+ fluxes in the spiral ligament. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Fac Lariboisiere St Louis, Lab Otol Expt, UPRESA 7060, F-75010 Paris, France. INSERM, U450, F-75016 Paris, France. RP Huy, PTB (reprint author), Fac Lariboisiere St Louis, Lab Otol Expt, UPRESA 7060, 10 Ave Verdun, F-75010 Paris, France. CR BARRIO LC, 1991, P NATL ACAD SCI USA, V88, P8410, DOI 10.1073/pnas.88.19.8410 BOSHER SK, 1968, PROC R SOC SER B-BIO, V171, P227, DOI 10.1098/rspb.1968.0066 Chen ML, 1996, NEURON, V17, P535, DOI 10.1016/S0896-6273(00)80185-3 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 Crouch JJ, 1997, J HISTOCHEM CYTOCHEM, V45, P773 CURRAN ME, 1995, CELL, V80, P795, DOI 10.1016/0092-8674(95)90358-5 Erichsen S, 1996, HEARING RES, V100, P143, DOI 10.1016/0378-5955(96)00105-0 Kelsell DP, 1997, NATURE, V387, P80, DOI 10.1038/387080a0 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 Kumar NM, 1996, CELL, V84, P381, DOI 10.1016/S0092-8674(00)81282-9 LUDWIG J, 1994, EMBO J, V13, P4451 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 MORENO AP, 1994, BIOPHYS J, V67, P113 NAKAZAWA K, 1995, J HISTOCHEM CYTOCHEM, V43, P981 Nenov AP, 1998, HEARING RES, V123, P168, DOI 10.1016/S0378-5955(98)00121-X Occhiodoro T, 1998, FEBS LETT, V434, P177, DOI 10.1016/S0014-5793(98)00973-9 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SANGER F, 1977, P NATL ACAD SCI USA, V74, P5463, DOI 10.1073/pnas.74.12.5463 SANGUINETTI MC, 1995, CELL, V81, P299, DOI 10.1016/0092-8674(95)90340-2 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 Spicer SS, 1996, HEARING RES, V100, P80, DOI 10.1016/0378-5955(96)00106-2 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TENCATE WJF, 1994, HEARING RES, V75, P151 Terlau H, 1996, PFLUG ARCH EUR J PHY, V432, P301, DOI 10.1007/s004240050137 TRUDEAU MC, 1995, SCIENCE, V269, P92, DOI 10.1126/science.7604285 WARMKE JW, 1994, P NATL ACAD SCI USA, V91, P3438, DOI 10.1073/pnas.91.8.3438 WU CF, 1983, SCIENCE, V220, P1076, DOI 10.1126/science.6302847 ZHONG Y, 1991, SCIENCE, V252, P1562, DOI 10.1126/science.2047864 NR 30 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 133 EP 138 DI 10.1016/S0378-5955(99)00068-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600013 PM 10416871 ER PT J AU Wiener-Vacher, SR Guinan, JJ Kobler, JB Norris, BE AF Wiener-Vacher, SR Guinan, JJ Kobler, JB Norris, BE TI Motoneuron axon distribution in the cat stapedius muscle SO HEARING RESEARCH LA English DT Article DE acoustic reflex; middle-ear muscle; motor control; motor unit size ID RESPONSES; NUCLEUS AB Stapedius-motoneuron cell bodies in the brainstem are spatially organized according to their acoustic response laterality, as demonstrated by intracellular labeling of physiologically identified motoneurons [Vacher et al., 1989. J. Comp. Neurol, 289, 401-415]. To determine whether a similar functional spatial segregation is present in the muscle, we traced physiologically identified, labeled axons into the stapedius muscle. Ten labeled axons were visible in the facial nerve and five could be traced to endplates within the muscle. These five axons had 39 observed branches (others may have been missed). This indicates an average innervation ratio (greater than or equal to 7.8) which is much higher than that obtained from previous estimates of the numbers of stapedius motoneurons and muscle fibers in the cat. One well-labeled stapedius motor axon innervated only a single muscle fiber. In contrast, two labeled axons had over 10 endings and innervated muscle fibers spread over wide areas in the muscle. Two of the axons branched and coursed through two primary stapedius fascicles, indicating that the muscle zones innervated by different primary fascicles are not functionally segregated. In another series of experiments, retrograde tracers were deposited in individual primary nerve fascicles. In every case, labeled stapedius-motoneuron cell bodies were found in each of the physiologically identified stapedius-motoneuron regions in the brainstem. These observations suggest there is little, if any, functional spatial segregation based on separate muscle compartments in the stapedius muscle, despite there being functional spatial segregation in the stapedius-motoneuron pool centrally. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Eaton Peabody Lab Auditory Physiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. Massachusetts Eye & Ear Infirm, Dept Otolaryngol, HP Mosher Laryngol Res Lab, Boston, MA 02114 USA. RP Guinan, JJ (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Eaton Peabody Lab Auditory Physiol, 243 Charles St, Boston, MA 02114 USA. CR ADAMS JC, 1977, NEUROSCIENCE, V2, P141, DOI 10.1016/0306-4522(77)90074-4 Aikawa Masuo, 1994, Okajimas Folia Anatomica Japonica, V70, P329 ANDERSON SD, 1976, SCI FDN OTOLARYNGOLO, P257 BLEVINS CE, 1967, ARCHIV OTOLARYNGOL, V86, P136 BLEVINS CE, 1964, ANAT REC, V149, P157, DOI 10.1002/ar.1091490114 Borg E., 1984, ACOUSTIC REFLEX BASI, P63 BORG E, 1974, ACTA OTO-LARYNGOL, V78, P155, DOI 10.3109/00016487409126341 BUCHTHAL F, 1980, PHYSIOL REV, V60, P90 Efron B., 1993, INTRO BOOTSTRAP FERNAND VSV, 1969, J PHYSIOL-LONDON, V200, P547 FULLERTON BC, 1983, SOC NEUR ABSTR, V9, P1085 GORDON DC, 1991, J COMP NEUROL, V304, P357, DOI 10.1002/cne.903040303 GORDON DC, 1990, J COMP NEUROL, V292, P424, DOI 10.1002/cne.902920308 Henneman E, 1981, HDB PHYSL NERVOUS 1, VII, P423 HENNEMAN E, 1965, J NEUROPHYSIOL, V28, P560 HESS A, 1969, J PHYSL, V200, P547 HURSH JB, 1939, AM J PHYSIOL, V27, P140 JOSEPH MP, 1985, J COMP NEUROL, V232, P43, DOI 10.1002/cne.902320105 KOBLER JB, 1987, BRAIN RES, V425, P372, DOI 10.1016/0006-8993(87)90523-3 KOBLER J B, 1987, Society for Neuroscience Abstracts, V13, P549 KOBLER JB, 1992, J NEUROPHYSIOL, V68, P807 LYON MJ, 1982, ACTA OTO-LARYNGOL, V94, P99, DOI 10.3109/00016488209128894 LYON MJ, 1979, EXP NEUROL, V66, P707, DOI 10.1016/0014-4886(79)90215-2 LYON MJ, 1978, BRAIN RES, V143, P437, DOI 10.1016/0006-8993(78)90355-4 MCCUE MP, 1988, J NEUROPHYSIOL, V60, P1160 Mesulam M., 1982, TRACING NEURAL CONNE Pang XD, 1997, J ACOUST SOC AM, V102, P3576, DOI 10.1121/1.420399 RUSHTON WAH, 1951, J PHYSIOL-LONDON, V115, P101 SHAW MD, 1983, J COMP NEUROL, V216, P10, DOI 10.1002/cne.902160103 TEIG E, 1972, HISTOCHEMISTRY, V29, P1, DOI 10.1007/BF00305695 VACHER SR, 1989, J COMP NEUROL, V289, P401, DOI 10.1002/cne.902890306 VEGETTI A, 1982, J ANAT, V135, P333 WEEKS OI, 1985, J COMP NEUROL, V235, P255, DOI 10.1002/cne.902350208 NR 33 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 139 EP 148 DI 10.1016/S0378-5955(99)00064-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600014 PM 10416872 ER PT J AU Lysakowski, A Alonto, A Jacobson, L AF Lysakowski, A Alonto, A Jacobson, L TI Peripherin immunoreactivity labels small diameter vestibular 'bouton' afferents in rodents SO HEARING RESEARCH LA English DT Article DE semicircular canal; crista ampullaris; macula; otolith; utriculus; sacculus; Scarpa's ganglion; chinchilla; mouse; rat ID INTERMEDIATE FILAMENT PROTEIN; INNERVATION PATTERNS; CRISTAE AMPULLARES; SEMICIRCULAR CANALS; UTRICULAR MACULA; SQUIRREL-MONKEY; CHINCHILLA; NERVE; PHOSPHORYLATION; NEUROFILAMENTS AB Recent morphophysiological studies have described three different subpopulations of vestibular afferents. The purpose of this study was to determine whether peripherin, a 56-kDa type III intermediate filament protein present in small sensory neurons in dorsal root ganglion and spiral ganglion cells, would also label thin vestibular afferents. Peripherin immunohistochemistry was done on vestibular sensory organs (cristae ampullares, utriculi and sacculi) of chinchillas, rats, and mice. In these sensory organs, immunoreactivity was confined to the extrastriolar region of the utriculus and the peripheral region of the crista. The labelled terminals were all boutons, except for an occasional calyx. In vestibular ganglia, immunoreactivity was restricted to small vestibular ganglion cells with thin axons. The immunoreactive central axons of vestibular ganglion cells form narrow bundles as they pass through the caudal spinal trigeminal tract. As they exit this tract, several bundles coalesce to form a single, narrow bundle passing caudally through the ventral part of the lateral vestibular nucleus. Finally, we conclude that all labelled axons and terminals were vestibular afferents rather than efferents, as no immunoreactivity in the vestibular efferent nucleus of the brainstem was observed. (C) 1999 Elsevier Science B.V. All rights reserved. C1 Univ Illinois, Dept Anat & Cell Biol, Chicago, IL 60612 USA. RP Lysakowski, A (reprint author), Univ Illinois, Dept Anat & Cell Biol, 808 S Wood St, Chicago, IL 60612 USA. RI Lysakowski, Anna/F-9534-2010 OI Lysakowski, Anna/0000-0001-6259-0294 CR Alonto A., 1997, Society for Neuroscience Abstracts, V23, P732 Angelastro JM, 1998, J NEUROCHEM, V70, P540 BAIRD RA, 1988, J NEUROPHYSIOL, V60, P182 DESMADRYL G, 1992, EXP BRAIN RES, V89, P105 DESPRES G, 1994, ACTA OTO-LARYNGOL, V114, P377, DOI 10.3109/00016489409126073 FERNANDEZ C, 1990, J NEUROPHYSIOL, V63, P767 FERNANDEZ C, 1995, J NEUROPHYSIOL, V73, P1253 FERNANDEZ C, 1988, J NEUROPHYSIOL, V60, P167 GEISLER N, 1988, EMBO J, V7, P15 GOLDBERG JM, 1990, J NEUROPHYSIOL, V63, P791 GREENE LA, 1989, TRENDS NEUROSCI, V12, P228, DOI 10.1016/0166-2236(89)90127-6 Hafidi A, 1998, BRAIN RES, V805, P181, DOI 10.1016/S0006-8993(98)00448-X Ho CL, 1998, J NEUROCHEM, V70, P1916 INAGAKI M, 1987, NATURE, V328, P649, DOI 10.1038/328649a0 JACOBSON L, 1996, ARO MIDW, P173 Kevetter G. A., 1996, Society for Neuroscience Abstracts, V22, P1831 Lysakowski A, 1997, J COMP NEUROL, V389, P419, DOI 10.1002/(SICI)1096-9861(19971222)389:3<419::AID-CNE5>3.0.CO;2-3 LYSAKOWSKI A, 1995, J NEUROPHYSIOL, V73, P1270 OBLINGER MM, 1989, J NEUROSCI, V9, P3766 PARYSEK LM, 1988, J NEUROSCI, V8, P555 PORTIER MM, 1984, DEV NEUROSCI-BASEL, V6, P335 SHARPE CR, 1989, DEVELOPMENT, V107, P701 Xu ZS, 1996, J CELL BIOL, V133, P1061, DOI 10.1083/jcb.133.5.1061 ZEH C, 1999, ARO 22 MIDW M, P186 NR 24 TC 30 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1999 VL 133 IS 1-2 BP 149 EP 154 DI 10.1016/S0378-5955(99)00065-9 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 212PN UT WOS:000081225600015 PM 10416873 ER EF