FN Thomson Reuters Web of Science™ VR 1.0 PT J AU GLEICH, O AF GLEICH, O TI THE DISTRIBUTION OF N-ACETYLGALACTOSAMINE IN THE COCHLEAR NUCLEUS OF THE GERBIL REVEALED BY LECTIN-BINDING WITH SOYBEAN AGGLUTININ SO HEARING RESEARCH LA English DT Article DE GERBIL; BRAIN STEM; COCHLEAR NUCLEUS; LECTIN; N-ACETYLGALACTOSAMINE; GLYCOCONJUGATE ID MONGOLIAN GERBIL; GABAERGIC NEURONS; OLFACTORY SYSTEM; CEREBRAL-CORTEX; BRAIN-STEM; PARVALBUMIN; RAT; IMMUNOREACTIVITY; GLYCOCONJUGATE; POPULATIONS AB A horseradish peroxidase conjugated lectin from Glycine max (soy bean agglutinin; SBA) was used to characterise the distribution of N-acetylgalactosamine in the cochlear nucleus of the mongolian gerbil. SBA bound differentially to a variety of structures within the cochlear nucleus. Specific SBA labelling was associated with large non-granule neurones of variable size and shape throughout the cochlear nucleus. Compared to adjacent Nissl-stained sections 80% of the non-granule cells in the dorsal cochlear nucleus (DCN) and more than 90% of the non-granule cells in the ventral cochlear nucleus (VCN) bound SBA. The variation in location, size and shape as well as the high percentage of the labelled neurones suggest that cells of several, if not all, non-granule cell types, which have been described for the cochlear nucleus according to the usual Nissl schemes, are SBA positive. Granule cells did not bind SBA because all SBA-labelled cells had diameters above 10 mu m. Diffuse labelling, not systematically associated with cells or fibres, was high in the molecular and fusiform cell layers of the DCN and that part of the granule cell area located close to the surface of the VCN. Darkly labelled granules (up to 2 mu m diameter) were prominent in the area of the VIIIth nerve root. After long SBA incubations, they were also present in VCN and to a lesser degree in DCN. The results are discussed with respect to findings in other brain areas and the possible co-localisation of gamma aminobutyric acid (GABA), parvalbumin and N-acetylgalactosamine. RP GLEICH, O (reprint author), UNIV REGENSBURG,DEP ENT,D-93042 REGENSBURG,GERMANY. CR ALROY J, 1988, ADV IMMUNOHISTOCHEMI, P93 AOKI E, 1990, BRAIN RES, V525, P140, DOI 10.1016/0006-8993(90)91329-F ARJIMAND E, 1988, HEARING RES, V32, P93 BRAUN K, 1991, NEUROSCIENCE, V40, P853, DOI 10.1016/0306-4522(91)90017-I Cant NB, 1992, MAMMALIAN AUDITORY P, P66 CZIBULKA A, 1991, HEARING RES, V52, P43, DOI 10.1016/0378-5955(91)90186-D CZIBULKA A, 1993, HEARING RES, V67, P1, DOI 10.1016/0378-5955(93)90226-Q DAMJANOV I, 1987, LAB INVEST, V57, P5 FADDIS BT, 1993, EXP NEUROL, V120, P160, DOI 10.1006/exnr.1993.1051 Fleckeisen C E, 1991, Acta Otolaryngol Suppl, V489, P12 FRANCESCHINI V, 1991, CELL MOL BIOL, V37, P61 GABIUS HJ, 1991, NEOGLYCOPROTEINS TOO, P32 Godfrey DA, 1988, AUDITORY PATHWAY, P107 HARRIS DM, 1990, HEARING RES, V50, P1, DOI 10.1016/0378-5955(90)90029-O HOFMANN MH, 1991, BRAIN RES, V564, P344, DOI 10.1016/0006-8993(91)91475-G Holthofer H, 1987, J HISTOCHEM CYTOCHEM, V35, P33 KEY B, 1986, NEUROSCIENCE, V18, P507, DOI 10.1016/0306-4522(86)90171-5 KOLSTON J, 1992, ANAT EMBRYOL, V186, P443 KOSAKA T, 1989, BRAIN RES, V483, P158, DOI 10.1016/0006-8993(89)90048-6 Moore J.K., 1988, AUDITORY PATHWAY STR, P123 MOORE JK, 1986, NEUROBIOLOGY HEARING, P283 MOREST DK, 1990, J COMP NEUROL, V300, P230, DOI 10.1002/cne.903000207 NAKAGAWA F, 1986, J COMP NEUROL, V243, P280, DOI 10.1002/cne.902430210 NAKAGAWA F, 1987, DEV NEUROSCI-BASEL, V9, P53, DOI 10.1159/000111608 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 PFENNINGER KH, 1981, J CELL BIOL, V89, P536, DOI 10.1083/jcb.89.3.536 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SETOOHSHIMA A, 1990, HISTOCHEMISTRY, V94, P579 SOLBACH S, 1991, ANAT EMBRYOL, V184, P103, DOI 10.1007/BF00942742 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V WEBSTER DB, 1982, AM J ANAT, V163, P103, DOI 10.1002/aja.1001630202 Wenthold RJ, 1991, NEUROBIOLOGY HEARING, P121 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 NR 36 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 1994 VL 78 IS 1 BP 49 EP 57 DI 10.1016/0378-5955(94)90043-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800006 PM 7961177 ER PT J AU KITANO, I DOI, K MORI, N UMEMOTO, M SAKAGAMI, M FUKAZAWA, K MATSUNAGA, T AF KITANO, I DOI, K MORI, N UMEMOTO, M SAKAGAMI, M FUKAZAWA, K MATSUNAGA, T TI FAILURE OF FORSKOLIN TO ELEVATE THE ENDOCOCHLEAR POTENTIAL IN KANAMYCIN-POISONED ANIMALS SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; IONIC ACTIVITY; FORSKOLIN; ADENYLATE CYCLASE; KANAMYCIN ID ADENYLATE-CYCLASE MODULATION; GUINEA-PIG; PERMEABILITY; MECHANISM; POTASSIUM AB The effect of forskolin (FSK) on the endocochlear potential (EP), K+ activity (A(K)), Na+ activity (A(Na)) and Cl- activity (A(Cl)) in scala media (SM) was compared between normal and kanamycin (KM)-poisoned guinea pigs by means of double-barrelled ion-selective microelectrodes. The perfusion of the scala vestibuli (SV) with FSK (200 mu M) produced EP elevation in normal animals whereas FSK failed to do it in KM-poisoned animals. FSK increased A(Cl) of SM with no significant change in A(k), and A(Na) of SM in both groups of animals. Histological examination of KM-poisoned animals showed damaged outer and inner hair cells with an intact appearance of the stria vascularis. The mechanism underlying the failure of FSK to elevate the EP in KM-poisoned animals is discussed. C1 OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,OSAKA 565,JAPAN. KAGAWA MED SCH,DEPT OTOLARYNGOL,KAGAWA 76107,JAPAN. RP KITANO, I (reprint author), NARA MED UNIV,DEPT OTOLARYNGOL,NARA 634,JAPAN. CR AMMANN D, 1975, HELV CHIM ACTA, V58, P1535, DOI 10.1002/hlca.19750580605 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 KITANO I, 1993, HEARING RES, V71, P23, DOI 10.1016/0378-5955(93)90017-U KITANO I, 1992, ABSTR ASS RES OT, V15, P105 KOLESNIKOV SS, 1991, FEBS LETT, V290, P167, DOI 10.1016/0014-5793(91)81251-3 KOMUNE S, 1993, HEARING RES, V70, P197, DOI 10.1016/0378-5955(93)90158-W KOMUNE S, 1983, OTOLARYNG HEAD NECK, V91, P427 KONISHI T, 1980, EXP BRAIN RES, V40, P457 KONISHI T, 1979, ACTA OTO-LARYNGOL, V87, P506, DOI 10.3109/00016487909126459 MARCUS DC, 1984, AM J PHYSIOL, V247, pC240 Robinson R. A., 1970, ELECTROLYTE SOLUTION NR 13 TC 5 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 1994 VL 78 IS 1 BP 58 EP 64 DI 10.1016/0378-5955(94)90044-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800007 PM 7961178 ER PT J AU SCHULTE, BA STEEL, KP AF SCHULTE, BA STEEL, KP TI EXPRESSION OF ALPHA-SUBUNIT AND BETA-SUBUNIT ISOFORMS OF NA,K-ATPASE IN THE MOUSE INNER-EAR AND CHANGES WITH MUTATIONS AT THE W-V OR SL(D) LOCI SO HEARING RESEARCH LA English DT Article DE COCHLEA; INNER EAR; NA,K-ATPASE; STRIA VASCULARIS; ION TRANSPORT; ENDOCOCHLEAR POTENTIAL; IMMUNOHISTOCHEMISTRY; MOUSE MUTANT ID CENTRAL-NERVOUS-SYSTEM; ENDOCOCHLEAR POTENTIAL GENERATION; STRIA VASCULARIS; ETHACRYNIC-ACID; POTASSIUM-FREE; COCHLEAR DUCT; LATERAL WALL; RAT-BRAIN; NA+,K+-ATPASE; ABNORMALITIES AB Mice homozygous for mutations at the viable dominant spotting (W-v) and Steel-dickie (Sl(d)) loci exhibit a similar phenotype which includes deafness. The auditory dysfunction derives from failure of the stria vascularis to develop normally and to generate a high positive endocochlear potential (EP). Because strial function is driven by Na,K-ATPase its expression was investigated in inner ears of W-v/W-v and Sl(d)/Sl(d) mice and their wild-type littermates by immunostaining with antisera against four of the enzyme's subunit isoforms. Wild-type mice from two different genetic backgrounds showed an identical distribution of subunit isoforms among inner ear transport cells. Several epithelial cell types coexpressed the alpha 1 and beta 1 subunits. Vestibular dark cells showed no reactivity for beta 1 but expressed abundant beta 2, whereas, strial marginal cells stained strongly for both beta isoforms. The only qualitative difference between mutant and wild-type mice was the absence of beta 1 subunit in marginal cells of the mutant's stria. However, it is unlikely that this difference accounts for failure of mutants to generate a high EP because the beta 1 subunit is not present in the stria vascularis of either rats or gerbils with normal EP values. Strong immunostaining for Na,K-ATPase in lateral wall fibrocytes of normal mice along with diminished immunoreactivity in the mutants supports the concept that these strategically located transport fibrocytes actively resorb K+ leaked across Reissner's membrane into scala vestibuli or effluxed from hair cells and nerves into scala tympani. It is further speculated that the resorbed K+ normally is siphoned down its concentration gradient into the intrastrial space through gap junctions between fibrocytes and strial basal and intermediate cells where it is recycled back to endolymph via marginal cells. Thus, failure of mutants to generate a positive EP could be explained by the absence of intermediate cells which may form the final link in the conduit for moving K+ from perilymph to the intrastrial compartment. C1 UNIV NOTTINGHAM,MRC,INST HEARING RES,NOTTINGHAM NG7 2RD,ENGLAND. RP SCHULTE, BA (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR BOSHER SK, 1965, PROC R SOC SER B-BIO, V162, P147, DOI 10.1098/rspb.1965.0030 CABLE J, 1992, HEARING RES, V64, P6, DOI 10.1016/0378-5955(92)90164-I CABLE J, UNPUB MUTATIONS W LO CARLISLE L, 1990, CELL TISSUE RES, V262, P329, DOI 10.1007/BF00309888 COVELL WP, 1957, LARYNGOSCOPE, V66, P118 DEOL MS, 1990, J EMBRYOL EXP MORPH, V23, P773 FORGE A, 1987, HEARING RES, V31, P253, DOI 10.1016/0378-5955(87)90195-X FORGE A, 1984, HEARING RES, V13, P189, DOI 10.1016/0378-5955(84)90108-4 HIEBER V, 1991, CELL MOL NEUROBIOL, V11, P253, DOI 10.1007/BF00769038 HILDING DA, 1967, ANN OTO RHINOL LARYN, V76, P647 HSU YM, 1989, BIOCHEMISTRY-US, V28, P569, DOI 10.1021/bi00428a023 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 JOHNSON DC, 1985, AM J PHYSIOL, V248, pR621 Johnsson LG, 1973, VASCULAR DISORDERS H, P249 KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUIJPERS W, 1967, SCIENCE, V157, P949, DOI 10.1126/science.157.3791.949 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MARCUS DC, 1981, HEARING RES, V4, P149, DOI 10.1016/0378-5955(81)90002-2 MCGUIRT JP, 1994, J HISTOCHEM CYTOCHEM, V42, P843 PIKE DA, 1980, HEARING RES, V3, P79, DOI 10.1016/0378-5955(80)90009-X QUICK CA, 1970, LARYNGOSCOPE, V80, P954, DOI 10.1288/00005537-197006000-00009 REALE E, 1975, J ULTRA MOL STRUCT R, V53, P284, DOI 10.1016/S0022-5320(75)80030-X RYAN A F, 1991, Molecular and Cellular Neuroscience, V2, P179, DOI 10.1016/1044-7431(91)90011-C SALT AN, 1987, LARYNGOSCOPE, V97, P984 SALT AN, 1988, PHYSL EAR, P341 SANTI PA, 1983, HEARING RES, V12, P151, DOI 10.1016/0378-5955(83)90103-X SCHNEIDER BG, 1990, EXP EYE RES, V51, P553, DOI 10.1016/0014-4835(90)90086-A SCHROTT A, 1990, HEARING RES, V46, P1, DOI 10.1016/0378-5955(90)90134-B SCHROTT A, 1987, ACTA OTO-LARYNGOL, V103, P451 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SHYJAN AW, 1990, P NATL ACAD SCI USA, V87, P1178, DOI 10.1073/pnas.87.3.1178 SOMJEN GG, 1979, ANNU REV PHYSIOL, V41, P159, DOI 10.1146/annurev.ph.41.030179.001111 SPICER SS, 1990, HEARING RES, V43, P205, DOI 10.1016/0378-5955(90)90229-I STEEL KP, 1992, DEVELOPMENT, V115, P1111 STEEL KP, 1987, HEARING RES, V27, P11, DOI 10.1016/0378-5955(87)90022-0 STEEL KP, 1989, DEVELOPMENT, V107, P453 STEEL KP, 1983, ARCH OTOLARYNGOL, V109, P22 SWEADNER KJ, 1989, BIOCHIM BIOPHYS ACTA, V988, P185, DOI 10.1016/0304-4157(89)90019-1 TAKAHASH.T, 1971, ANN OTO RHINOL LARYN, V80, P721 URAYAMA O, 1989, J BIOL CHEM, V264, P8271 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 WATTS AG, 1991, P NATL ACAD SCI USA, V88, P7425, DOI 10.1073/pnas.88.16.7425 NR 45 TC 99 Z9 102 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 1994 VL 78 IS 1 BP 65 EP 76 DI 10.1016/0378-5955(94)90045-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800008 PM 7961179 ER PT J AU HE, DZZ EVANS, BN DALLOS, P AF HE, DZZ EVANS, BN DALLOS, P TI FIRST APPEARANCE AND DEVELOPMENT OF ELECTROMOTILITY IN NEONATAL GERBIL OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE NEWBORN GERBILS; OUTER HAIR CELLS; ONSET OF MOTILITY; DEVELOPMENT; COCHLEAR MECHANICS ID GUINEA-PIG COCHLEA; MONGOLIAN GERBIL; OTOACOUSTIC EMISSIONS; INTRACELLULAR-RECORDINGS; CHARACTERISTIC FREQUENCY; MECHANICAL RESPONSES; AUDITORY FUNCTION; PLACE PRINCIPLE; SHAPE CHANGES; THRESHOLD AB With the purpose of pinpointing the time of onset of electromotility, outer hair cells (OHCs) from apical and basal turns of the cochleae of postnatal gerbils, ranging in age from 6 to 19 days, were isolated and drawn into a glass microchamber. Length changes evoked by transcellular electrical stimulation were detected and measured with a photodiode detector. Motile responses first appeared in 3 out of 14 basal turn OHCs at 7 days after birth (DAB). At 8 DAB, 3 out of 13 apical turn cells also responded to the electrical stimulation. By 12 DAB, all the OHCs from both turns showed motile responses. Input-output functions relating applied stimulus and change in cell length revealed that the motile response threshold improved from 7 DAB to 12 DAB and the response amplitude kept increasing from 7 DAB until 13-14 DAB, when mature amplitudes were reached. Measurements of OHC length revealed only minor changes in basal turn hair cell length while apical hair cells continued to elongate until approximately 16 DAB. Since the onset of auditory function in gerbils occurs around 12 DAB and fine tuning develops between 14 and 17 DAB, our results suggest that the onset of OHC motility occurs earlier than that of auditory function and the maturation of the motility amplitude occurred earlier than the development of fine tuning. The maturation of OHC motility and the development of otoacoustic emissions are also compared and discussed. RP HE, DZZ (reprint author), NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL & COMMUN SCI & DISORDERS,HUGH KNOWLES CTR,EVANSTON,IL 60208, USA. CR Anggard L., 1965, ACTA OTOLARYNGOLOGIC, V203, P1 ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 ARJMAND E, 1989, DEV NONLINEARITIES D, P348 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 ASHMORE JF, 1992, SENSORY TRANSDUCTION, P396 Bekesy G., 1960, EXPT HEARING Brownell W. E., 1983, MECH HEARING, P5 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CLARK BA, 1990, PFLUG ARCH EUR J PHY, V415, P490, DOI 10.1007/BF00373629 DALLOS P, 1988, FUNCTIONS AUDITORY S, P153 DALLOS P, 1992, J NEUROSCI, V12, P4575 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1993, J NEUROPHYSIOL, V70, P299 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DALLOS P, 1993, BIOPHYSICS HAIR CELL, P107 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 ECHTELER SM, 1993, STRUCTURAL ALTERATIO, P25 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 FORGE A, 1991, CELL TISS RES FOSS I, 1974, ACTA OTO-LARYNGOL, V77, P202, DOI 10.3109/00016487409124618 HALLWORTH R, 1993, J NEUROPHYSIOL, V70, P549 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 KALINEC F, 1992, P NATL ACAD SCI USA, V89, P8671, DOI 10.1073/pnas.89.18.8671 KEMP DT, 1988, MEAS HEAR BALANCE BA, P27 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 KING AJ, 1991, TRENDS NEUROSCI, V14, P31, DOI 10.1016/0166-2236(91)90181-S LIBERMAN MC, 1984, HEARING RES, V16, P33, DOI 10.1016/0378-5955(84)90023-6 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 NORTON SJ, 1989, DEV OTOACOUSTIC EMIS, P226 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PUJOL R, 1973, ACTA OTO-LARYNGOL, V76, P1, DOI 10.3109/00016487309121476 PUJOL R, 1991, HEARING RES, V57, P129, DOI 10.1016/0378-5955(91)90082-K PUJOL R, 1991, AUDITORY PHYSL PERCE, V83, P45 ROMAND R, 1983, DEV AUDITORY VESTIBU ROMAND R, 1971, J PHYSIOL-PARIS, V63, P763 ROMAND R, 1983, NEUROSCI LETT, V35, P271, DOI 10.1016/0304-3940(83)90329-4 ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 RYAN AF, 1982, EXP BRAIN RES, V47, P428 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 WEAVER SP, 1993, DEV SUBSURFACE CISTE, P24 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 61 TC 97 Z9 99 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 1994 VL 78 IS 1 BP 77 EP 90 DI 10.1016/0378-5955(94)90046-9 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800009 PM 7961180 ER PT J AU VASAMA, JP MAKELA, JP PARKKONEN, L HARI, R AF VASAMA, JP MAKELA, JP PARKKONEN, L HARI, R TI AUDITORY CORTICAL RESPONSES IN HUMANS WITH CONGENITAL UNILATERAL CONDUCTIVE HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED FIELDS; AUDITORY CORTEX; HEARING DISORDER; MEATAL ATRESIA; INTERSTIMULUS INTERVAL; PLASTICITY; HUMAN ID BINAURAL INTERACTION; INFERIOR COLLICULUS; COCHLEAR ABLATION; CORTEX; PLASTICITY; DEPRIVATION; MAPS AB We recorded auditory evoked magnetic fields from 6 patients with congenital unilateral conductive hearing disorder with a 122-channel whole-head neuromagnetometer. The stimuli were 50-ms 1-kHz tones delivered to the better ear at interstimulus intervals (ISIs) of 2 and 8 s at two different intensities (50 and 70 dB HL). As in normal-hearing subjects, the amplitudes of N100m, the 100-ms response, were larger in 5 patients and the latencies were shorter in 3 patients over the hemisphere contralateral to stimulation. However, in one patient N100m peaked already at 61 ms over the contralateral hemisphere and amplitudes were larger over the ipsilateral hemisphere, possibly reflecting reorganization of the auditory pathways. In 3 patients the latencies were shorter over the ipsilateral hemisphere. The effects of ISI and intensity were similar over both hemispheres and did not differ from those in controls. It seems that congenital unilateral conductive hearing loss does not necessarily lead to any gross disturbances in the human auditory cortex. RP VASAMA, JP (reprint author), HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. RI Parkkonen, Lauri/G-6755-2012; Hari, Riitta/J-1880-2012 OI Parkkonen, Lauri/0000-0002-0130-0801; Hari, Riitta/0000-0002-3142-2703 CR AHONEN AI, 1993, PHYS SCRIPTA, VT49A, P198, DOI 10.1088/0031-8949/1993/T49A/033 BRUGGE JF, 1985, HEARING RES, V20, P257 CHINO YM, 1992, VISION RES, V32, P789, DOI 10.1016/0042-6989(92)90021-A COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 Hari R, 1990, ADV AUDIOL, V6, P222 HUBEL DH, 1977, PROC R SOC SER B-BIO, V198, P1, DOI 10.1098/rspb.1977.0085 HUMES LE, 1980, AUDIOLOGY, V19, P508 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 KAUKORANTA E, 1986, EXP BRAIN RES, V63, P60 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 Makela J. P., 1993, Human Brain Mapping, V1, P48, DOI 10.1002/hbm.460010106 MCMULLEN NT, 1988, EXP BRAIN RES, V72, P195, DOI 10.1007/BF00248516 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 PAETAU R, 1994, IN PRESS J CLIN NEUR PELIZZONE M, 1986, NEUROSCI LETT, V68, P192, DOI 10.1016/0304-3940(86)90140-0 REALE RA, 1987, DEV BRAIN RES, V34, P281, DOI 10.1016/0165-3806(87)90215-X SAMS M, 1993, J COGNITIVE NEUROSCI, V5, P363, DOI 10.1162/jocn.1993.5.3.363 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 VASAMA JP, 1994, UNPUB EFFECTS INTENS NR 21 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 1994 VL 78 IS 1 BP 91 EP 97 DI 10.1016/0378-5955(94)90047-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800010 PM 7961181 ER PT J AU BRAUN, M AF BRAUN, M TI TUNED HAIR-CELLS FOR HEARING, BUT TUNED BASILAR-MEMBRANE FOR OVERLOAD PROTECTION - EVIDENCE FROM DOLPHINS, BATS, AND DESERT RODENTS SO HEARING RESEARCH LA English DT Article DE COCHLEA; BASILAR MEMBRANE; TUNING; RESONANT ABSORPTION; OVERLOAD PROTECTION ID RHINOLOPHUS-FERRUMEQUINUM; PTERONOTUS-PARNELLII; MUSTACHE BAT; INNER-EAR; COCHLEA; MECHANICS; SHIFT; MAP AB A cochlear model is presented suggesting that the organ of Corti (OC) and the basilar membrane (BM) are both tuned resonant systems, but have different functions. The OC provides frequency filtering and amplification by means of tuned outer hair cells. The BM provides resonant absorption of excessive vibrational energy as an overload protection for vulnerable elements in the OC. Evidence supporting this model is demonstrated in dolphins, bats, and desert rodents. Specialized auditory capabilities correlate with cochlear deviations, some of them dramatically changing BM compliance. In characteristic regions along the cochlea there are BM thickenings and, on both sides of the OC, hypertrophied supporting cells. Structures of striking similarity have evolved independently across orders or families, revealing multiple events of convergent evolution. In all cases, the locations of deviating structures rule out a BM function in auditory frequency selectivity but support one in resonant absorption. Cochlear microphonics and BM responses demonstrate strongest high-level absorption in the frequency bands most vital for the tested species. The assumed cause is increased internal damping in the enlarged structures during BM motion. Species with intermediate specializations supply further evidence that resonant absorption is universally the genuine function of BM mechanics in mammals, providing complementary high-level protection of low-level sensitivity. RP BRAUN, M (reprint author), PHYSIOL MUS RES,ADICKESSTR 42,D-22607 HAMBURG,GERMANY. CR BRUNDIN L, 1993, BIOPHYSICS HAIR CELL, P182 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 BRUNS V, 1976, J COMP PHYSIOL, V106, P87 BRUNS V, 1976, J COMP PHYSIOL, V106, P77 DANCER A, 1987, REV ACOUST, V81, P3 DANCER A, 1992, AUDIOLOGY, V31, P301 EHRET G, 1977, J COMP PHYSIOL, V122, P65 EVANS EF, 1975, SCIENCE, V190, P1218, DOI 10.1126/science.1198110 FAY RR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P229 GOLDSTEIN JL, 1992, J ACOUST SOC AM, V92, P2407, DOI 10.1121/1.404717 GOLDSTEIN JL, 1993, BIOPHYSICS HAIR CELL, P315 GRINNELL AD, 1958, BIOL BULL, V114, P10, DOI 10.2307/1538961 HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 HENSON JR O. W., 1961, U KANSAS SCI B, V52, P151 HENSON OW, 1965, J PHYSIOL-LONDON, V180, P871 HENSON MM, 1978, AM J ANAT, V153, P143, DOI 10.1002/aja.1001530109 HENSON OW, 1985, J COMP PHYSIOL A, V157, P587, DOI 10.1007/BF01351353 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 KEIDEL WD, 1985, PHYSL MENSCHEN KETTEN DR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P717 KHANNA SM, 1988, COCHLEAR MECH STRUCT, P387 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KOPPL C, 1993, J COMP PHYSIOL A, V171, P695, DOI 10.1007/BF00213066 KOPPL C, 1993, BIOPHYSICS HAIR CELL, P216 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KOSSL M, 1990, J COMP PHYSIOL A, V166, P711 LEGOUIX JP, 1955, ACUSTICA, V5, P208 LIBERMAN MC, 1984, HEARING RES, V16, P33, DOI 10.1016/0378-5955(84)90023-6 MANLEY GA, 1993, BIOPHYSICS HAIR CELL, P33 MANLEY GA, 1986, AUDITORY FREQUENCY S, P63 Morimoto RI, 1990, STRESS PROTEINS BIOL MOUNTAIN DC, 1993, BIOPHYSICS HAIR CELL, P361 NUTTALL AL, 1993, BIOPHYSICS HAIR CELL, P288 PLASSMANN W, 1987, BRAIN BEHAV EVOLUT, V30, P82, DOI 10.1159/000118639 POLLAK GD, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P751 PUJOL R, 1992, AUDITORY PHYSL PERCE, P45 PYE A, 1965, J ANAT, V99, P161 PYE JD, 1968, HEARING MECHANISMS V, P66 ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 ROEDERER JG, 1975, INTRO PHYSICS PSYCHO RUGGERO MA, 1993, BIOPHYSICS HAIR CELL, P258 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SALOMON G, 1963, ACTA NEUROL SCAND, V39, P161 SCHNITZLER HU, 1976, J COMP PHYSIOL, V106, P99 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 Vater M., 1988, ANIMAL SONAR, P225 WEBSTER DB, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P633 WEBSTER DB, 1961, AM J ANAT, V108, P123, DOI 10.1002/aja.1001080202 WEISS TF, 1978, EVOKED ELECTRICAL AC, P91 WEVER EG, 1971, P NATL ACAD SCI USA, V68, P2708, DOI 10.1073/pnas.68.11.2708 WEVER EG, 1972, P NATL ACAD SCI USA, V69, P657, DOI 10.1073/pnas.69.3.657 WEVER EG, 1961, J AUD RES, V2, P158 WEVER EG, 1971, P NATL ACAD SCI USA, V68, P2381, DOI 10.1073/pnas.68.10.2381 WEVER EG, 1961, ANN OTO RHINOL LARYN, V70, P5 WILSON JP, 1983, HEARING RES, V10, P15, DOI 10.1016/0378-5955(83)90016-3 NR 57 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 JUL PY 1994 VL 78 IS 1 BP 98 EP 114 DI 10.1016/0378-5955(94)90048-5 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800011 PM 7961182 ER PT J AU CASTOR, X VEUILLET, E MORGON, A COLLET, L AF CASTOR, X VEUILLET, E MORGON, A COLLET, L TI INFLUENCE OF AGING ON ACTIVE COCHLEAR MICROMECHANICAL PROPERTIES AND ON THE MEDIAL OLIVOCOCHLEAR SYSTEM IN HUMANS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; DISTORTION PRODUCT EMISSIONS; EFFERENT OLIVOCOCHLEAR SYSTEM; AGING; OUTER HAIR CELLS; MICROMECHANICAL PROPERTIES ID EVOKED OTOACOUSTIC EMISSIONS; CONTRALATERAL ACOUSTIC STIMULATION; OUTER HAIR-CELLS; RESPONSES; AGE; EAR AB Transiently evoked otoacoustic emissions (TEOAEs) without and with contralateral acoustic stimulation (CAS), as well as distortion product otoacoustic emissions (DPOAEs), were recorded on 60 subjects divided into 2 groups, the first constituted by 38 normally hearing young subjects and the second by 22 subjects aged from 70 to 88 years and with normal hearing levels in view of their age. TEOAEs and DPOAE 'audiograms' were recorded in a third group constituted by 15 subjects with ages ranging from 6 to 57 years and with hearing levels not significantly different from those of the second group for frequencies above 500 Hz. TEOAEs were present in 100% of the subjects in the first group and in 91% in the second group, although with smaller amplitude. The fall in TEOAE amplitude under CAS was smaller in the second group. Concerning DPOAE audiograms, in the first group, a response was found in 71 to 95% of cases for frequencies ranging from 1 to 6.35 kHz, and in 7 to 37% of cases in the second group. Mean amplitudes were significantly lower in the second group for frequencies ranging from 2.83 to 5.04 kHz. Mean 'thresholds' ranged from 38.55 to 43.57 dB SPL for frequencies ranging from 1 to 6 kHz in the first group and from 50 to 58 dB SPL in the second group. No significant difference was found between the second and third groups concerning the amplitude and spectrum of the TEOAEs and DPOAE audiograms. Thus, age influences TEOAEs, DPOAEs and the effect of CAS on TEOAEs. However, the alterations found in TEOAEs and DPOAEs seem to be essentially related to age linked hearing-loss. C1 HOP EDOUARD HERRIOT,CNRS,URA 1447,F-69437 LYON 03,FRANCE. HOP JEAN MINJOZ,SERV ORL & CHIRURG CERVICOFACIALE,F-25000 BESANCON,FRANCE. CR BONFILS P, 1988, ARCH OTO-RHINO-LARYN, V245, P53, DOI 10.1007/BF00463550 BONFILS P, 1988, AUDIOLOGY, V27, P27 BRAY P, 1989, THESIS U COLLEGE MID, P201 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1990, ANN OTO RHINOL LARYN, V99, P993 COLLET L, 1992, INT J NEUROSCI, V62, P113 COLLET L, 1992, AUDIOLOGY, V31, P1 GOETZINGER CP, 1961, ARCHIV OTOLARYNGOL, V73, P662 HARBERT F, 1966, J AUD RES, V6, P297 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 KEMP DT, 1990, EAR HEARING, V11, P93 LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P3 MARTIN GK, 1987, HEARING RES, V13, P29 PESTALOZZA G, 1955, Laryngoscope, V65, P1136 PROBST R, 1990, ADV AUDIOL, V7, P117 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 1990, ISO1999 INT STAND OR NR 24 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 1 EP 8 DI 10.1016/0378-5955(94)90248-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500001 PM 7928721 ER PT J AU VANBENTHEM, PPG KLIS, SFL ALBERS, FWJ DEWILDT, DJ VELDMAN, JE HUIZING, EH SMOORENBURG, GF AF VANBENTHEM, PPG KLIS, SFL ALBERS, FWJ DEWILDT, DJ VELDMAN, JE HUIZING, EH SMOORENBURG, GF TI THE EFFECT OF NIMODIPINE ON COCHLEAR POTENTIALS AND NA+/K+-ATPASE ACTIVITY IN NORMAL AND HYDROPIC COCHLEAS OF THE ALBINO GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE EXPERIMENTAL ENDOLYMPHATIC HYDROPS; ELECTROCOCHLEOGRAPHY; NA+/K+-ATPASE; NIMODIPINE ID EXPERIMENTAL ENDOLYMPHATIC HYDROPS; DEPENDENT P-NITROPHENYLPHOSPHATASE; INNER-EAR; CYTOCHEMICAL-LOCALIZATION; OUABAIN; THRESHOLDS; MEMBRANE AB In experimental endolymphatic hydrops (EEH) a decrease in the endocochlear potential (EP) has been reported and is thought to be due to decreased activity of the enzyme Na+/K+-ATPase in the stria vascularis. By stimulating Na+/K+-ATPase, the EP, and thereby cochlear function as a whole, might be restored. On the other hand, stimulation of stria vascularis Na+/K+-ATPase might result in excessive production of endolymph and thus produce or augment hydrops. In this study we have investigated the effect of intraperitoneaIly applied nimodipine on cochlear potentials and on Na+/K+-ATPase activity in the stria vascularis, both in normal cochleas (control) and in cochleas with EEH. Nimodipine is an L-type Ca2+-channel blocking agent with Na+/K+-ATPase stimulating properties at concentrations as low as 1.5 mM. The compound action potential (CAP), evoked by 2, 4 and 8 kHz tone bursts was found to be depressed in the EEH ears with and without nimodipine treatment, and in the nimodipine treated control ears. Statistical analysis (ANOVA) showed that the effects of EEH and nimodipine on the CAP were additive. The negative summating potential (SP), measured extracochlearly at the apex, in response to 4 and 8 kHz tone bursts was significantly enhanced in the EEH ears. Nimodipine treatment did not affect the SP, neither in the control, nor in the EEH ears. Cytochemically, Na+/K+-ATPase activity appeared to be decreased in the oedematous stria vascularis of hydropic cochleas. No effect of nimodipine on Na+/K+-ATPase activity could be established ultracytochemically, neither in the controls nor in the EEH ears. In the lower turns of some of the nimodipine treated control cochleas a mild hydrops was seen during light-microscopic evaluation. Although it was not possible to prove a stimulatory effect of nimodipine on the enzyme Na+/K+-ATPase cytochemically, the finding of mild endolymphatic hydrops in nimodipine treated control ears suggests (a history of) increased endolymph production. This hydrops might be responsible for the depression of the CAP in the nimodipine treated ears. C1 UNIV GRONINGEN HOSP,DEPT OTORHINOLARYNGOL,GRONINGEN,NETHERLANDS. UNIV UTRECHT,RUDOLF MAGNUS INST,DEPT MED PHARMACOL,UTRECHT,NETHERLANDS. RP VANBENTHEM, PPG (reprint author), UNIV UTRECHT HOSP,DEPT OTORHINOLARYNGOL,HEIDELBERGLAAN 100,3584 CX UTRECHT,NETHERLANDS. CR ALBERS FWJ, 1988, ACTA OTO-LARYNGOL, V105, P281, DOI 10.3109/00016488809097009 ALBERS FWJ, 1991, ACTA OTO-LARYNGOL, V111, P885, DOI 10.3109/00016489109138426 ALBERS FWJ, 1987, ACTA OTO-LARYNGOL, V104, P202, DOI 10.3109/00016488709107319 ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 BOBBIN RP, 1991, HEARING RES, V56, P101, DOI 10.1016/0378-5955(91)90159-7 BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 COHEN J, 1984, ACTA OTO-LARYNGOL, V98, P398, DOI 10.3109/00016488409107580 COLEMAN JKM, 1991, OTOLARYNG HEAD NECK, V105, P840 DOI K, 1990, HEARING RES, V45, P157, DOI 10.1016/0378-5955(90)90192-R FELDMAN AM, 1973, P NAT ACAD SCI, P1761 GODFRAIND T, 1986, PHARMACOL REV, V38, P321 HARRISON RV, 1984, HEARING RES, V14, P85, DOI 10.1016/0378-5955(84)90071-6 HORNER KC, 1990, HEARING RES, V45, P145, DOI 10.1016/0378-5955(90)90190-Z HORNER KC, 1988, HEARING RES, V32, P41, DOI 10.1016/0378-5955(88)90145-1 HORNER KC, 1987, HEARING RES, V26, P319, DOI 10.1016/0378-5955(87)90067-0 JASTREBOFF PJ, 1988, ANN NY ACAD SCI, V52, P716 KIMURA RS, 1967, ANN OTO RHINOL LARYN, V76, P664 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KLIS JFL, 1988, HEARING RES, V32, P175, DOI 10.1016/0378-5955(88)90089-5 KONISHI S, 1975, J LARYNGOL OTOL, V89, P577, DOI 10.1017/S0022215100080786 KONISHI T, 1976, ELECTROCOCHLEOGRAPHY, P295 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, 1983, ORL J OTO-RHINO-LARY, V45, P143 MAYAHARA H, 1980, HISTOCHEMISTRY, V67, P125, DOI 10.1007/BF00493231 MORIZONO T, 1985, ANN OTO RHINOL LARYN, V94, P191 PAN M, 1984, BIOCHEM PHARMACOL, V33, P787, DOI 10.1016/0006-2952(84)90463-5 PFFNER FF, 1987, HEARING RES, V29, P17 Rämsch K D, 1985, Neurochirurgia (Stuttg), V28 Suppl 1, P74 RUDING PRJW, 1987, ARCH OTO-RHINO-LARYN, V244, P174, DOI 10.1007/BF00464263 SZIKLAI I, 1989, ACTA OTO-LARYNGOL, V107, P371, DOI 10.3109/00016488909127524 THEOPOLD HM, 1985, LARYNGO RHINO OTOL, V64, P609, DOI 10.1055/s-2007-1008218 VANDEELEN GW, 1986, ACTA OTO-LARYNGOL, V101, P207, DOI 10.3109/00016488609132829 VANDEELEN GW, 1987, ARCH OTO-RHINO-LARYN, V244, P167 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 NR 36 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 9 EP 18 DI 10.1016/0378-5955(94)90249-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500002 PM 7928742 ER PT J AU DECRAEMER, WF KHANNA, SM FUNNELL, WRJ AF DECRAEMER, WF KHANNA, SM FUNNELL, WRJ TI A METHOD FOR DETERMINING 3-DIMENSIONAL VIBRATION IN THE EAR SO HEARING RESEARCH LA English DT Article DE 5-DIMENSIONAL; VIBRATION; INTERFEROMETRY; MALLEUS; CAT ID TYMPANIC MEMBRANE VIBRATIONS; CAT; FREQUENCY; MANUBRIUM; MECHANICS; MALLEUS AB In the classical concept of the middle ear function the malleus rotates around a fixed axis which implies that at small amplitudes of vibration its displacement is essentially one dimensional. As a consequence malleus vibrations have been measured previously along a single viewing axis. As a first step in the study of the complete malleus motion we determined the three dimensional components at a single point (umbo) of the manubrium. To define 3-D motion it is in principle necessary to measure the vibrations from widely different observation angles. The viewing angles are limited however in our case by the ear canal geometry to about +/-15 degrees. In order to resolve the 3-D components under these conditions it is necessary to measure the vibration components with high accuracy. Amplitude and phase of the umbo vibrations were measured with a heterodyne interferometer over a wide frequency range (100 Hz to 20 kHz). The system included a two axis goniometer with the axes of rotation positioned at the focal plane of the interferometer objective lens. It was therefore possible to change the viewing angle in small increments around two orthogonal axes while keeping the same point in focus. From a redundant set of measurements the three orthogonal components of vibration were calculated by least squares fitting. The vector sum of the three components gives the three dimensional motion of the observed point. The vibration of the point on the umbo was found not to follow a straight line but an elliptical path instead. The shape of the ellipse and the inclination of the plane of the ellips with respect to the stationary malleus position changed with frequency. These observations are consistent with our earlier findings that the mode of malleus vibration changes with frequency [Decraemer et al. (1991) Hear. Res. 54, 305-318]. C1 COLUMBIA UNIV,COLL PHYSICIANS & SURGEONS,DEPT OTOLARYNGOL,NEW YORK,NY 10032. MCGILL UNIV,DEPT BIOMED ENGN,MONTREAL H3A 2B4,PQ,CANADA. MCGILL UNIV,DEPT OTOLARYNGOL,MONTREAL H3A 2B4,PQ,CANADA. RP DECRAEMER, WF (reprint author), UNIV ANTWERP,RIJKSUNIV CENTRUM,BIOMED PHYS LAB,GROENENBORGERLAAN 171,B-2020 ANTWERP,BELGIUM. RI Funnell, Robert/B-4488-2013 CR BARANY E, 1938, ACTA OTOLARYNGOL S S, V26 BONBEKESY G, 1960, EXPT HEARING BRENKMAN CJ, 1986, THESIS LEIDEN NETHER BRENKMAN CJ, 1985, PERIPHERAL AUDITORY, P56 BUUNEA TJF, 1981, HALS NASEN ORHRENHEI, V58, P223 DECRAEMER WF, 1989, HEARING RES, V38, P1, DOI 10.1016/0378-5955(89)90123-8 DECRAEMER WF, 1990, HEARING RES, V47, P205, DOI 10.1016/0378-5955(90)90152-F DECRAEMER WF, 1994, HEARING RES, V72, P1, DOI 10.1016/0378-5955(94)90199-6 DECRAEMER WF, 1991, HEARING RES, V54, P305, DOI 10.1016/0378-5955(91)90124-R DECREAMER WF, 1994, ABSTR ASS RES OT FUNNELL WRJ, 1992, J ACOUST SOC AM, V91, P2082, DOI 10.1121/1.403694 GILAD P, 1966, J ACOUST SOC AM, V41, P1232 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 GUMMER AW, 1989, HEARING RES, V39, P1, DOI 10.1016/0378-5955(89)90077-4 HELMHOLTZ H, 1886, PFLUGERS ARCH GESAMT, V1, P1 KHANNA SM, 1972, J ACOUST SOC AM, V51, P1904, DOI 10.1121/1.1913050 KHANNA SM, 1970, HOLOGRAPHIC STUDY TY Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P51 Press W. H., 1989, NUMERICAL RECIPES AR RELKIN EM, 1980, ACTA OTO-LARYNGOL, V90, P6, DOI 10.3109/00016488009131692 RUGGERO MA, 1990, J ACOUST SOC AM, V87, P1612, DOI 10.1121/1.399409 RUTTEN WLC, 1982, CRYOGENICS, V22, P457, DOI 10.1016/0011-2275(82)90129-1 SAUNDERS JC, 1982, J COMP PHYSIOL, V146, P517 Wever EG, 1954, PHYSL ACOUSTICS Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 NR 25 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 19 EP 37 DI 10.1016/0378-5955(94)90250-X PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500003 PM 7928731 ER PT J AU BRECHTELSBAUER, PB NUTTALL, AL MILLER, JM AF BRECHTELSBAUER, PB NUTTALL, AL MILLER, JM TI BASAL NITRIC-OXIDE PRODUCTION IN REGULATION OF COCHLEAR BLOOD-FLOW SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; NG-NITRO-L-ARGININE; L-ARGININE; COMPOUND ACTION POTENTIAL ID GUINEA-PIG; ENDOTHELIAL-CELLS; STIMULATION; GANGLION; AUTOREGULATION; ACETYLCHOLINE; PRESSURE; RELEASE; INVIVO; ARTERY AB Nitric oxide (NO), recently identified as endothelium-derived relaxing factor, has been shown to influence both vascular and neural function. In blood vessels, NO is produced by endothelial and smooth muscle cells and may play a role in regulation of cochlear blood flow. In the central nervous system, NO functions as a neurotransmitter involved in long term potentiation. The principle hypothesis tested in this study was that basal NO production in the cochlear blood vessels contributes to regulation of CBF. Since NO is a vasodilator, diminished NO synthesis may decrease the level of CBF. Application of a competitive inhibitor of NO synthase either intravenously or to the round window membrane caused a reduction in CBF. The application to the round window membrane did not affect compound action potential thresholds. With intravenous adminstration, the effect on CBF was dose-related and could be reversed with the physiologic substrate, L-arginine. These data indicate that NO is produced in the cochlear blood vessels and contributes to the regulation of CBF. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR AISAKA K, 1989, BIOCHEM BIOPH RES CO, V160, P881, DOI 10.1016/0006-291X(89)92517-5 AMEZCUA JL, 1988, BRIT J PHARMACOL, V95, P830 Atkinson M, 1944, ARCHIV OTOLARYNGOL, V40, P101 BEAUSANGLINDER M, 1980, ACTA PHYSIOL SCAND, V109, P433, DOI 10.1111/j.1748-1716.1980.tb06617.x BOBBIN RP, 1978, FED PROC, V37, P613 BROWN JN, 1993, MYOGENIC REGULATION DOHI Y, 1990, HYPERTENSION, V16, P170 EHRENBERGER K, 1991, HEARING RES, V52, P73, DOI 10.1016/0378-5955(91)90188-F FARACI FM, 1990, AM J PHYSIOL, V259, pH1216 FURCHGOTT RF, 1980, NATURE, V288, P373, DOI 10.1038/288373a0 GARTHWAITE G, 1988, NEUROSCIENCE, V26, P321, DOI 10.1016/0306-4522(88)90148-0 HULTCRANTZ E, 1988, AM J OTOLARYNG, V9, P317, DOI 10.1016/S0196-0709(88)80039-5 IGNARRO LJ, 1987, P NATL ACAD SCI USA, V84, P9265, DOI 10.1073/pnas.84.24.9265 JUHN SK, 1988, ACTA OTOLARYNGOL S S, V457, P43 LARSEN HC, 1982, ARCH OTO-RHINO-LARYN, V234, P145, DOI 10.1007/BF00453621 LAURIKAINEN EA, 1993, HEARING RES, V64, P199, DOI 10.1016/0378-5955(93)90006-M MEVIO E, 1985, RICERCA CLIN LABO S1, V15, P547 Miller J M, 1986, Scand Audiol Suppl, V26, P11 MILLER JM, 1988, AM J OTOLARYNG, V9, P302, DOI 10.1016/S0196-0709(88)80038-3 MILLER JM, 1984, ARCH OTOLARYNGOL, V110, P305 MONCADA S, 1991, PHARMACOL REV, V43, P109 MYERS PR, 1989, AM J PHYSIOL, V256, pH1030 NAKASHIMA T, 1991, ANN OTO RHINOL LARYN, V100, P394 NUTTALL AL, 1982, HEARING RES, V6, P207, DOI 10.1016/0378-5955(82)90055-7 ODELL TJ, 1982, HYPERTENSION, V4, P19 REN TY, 1993, ACTA OTO-LARYNGOL, V113, P146, DOI 10.3109/00016489309135783 REN TY, 1993, ANN OTO RHINOL LARYN, V102, P378 RUTH G, 1976, ANN OTOL, V85, P94 SJOBERG A, 1964, ACTA OTOLARYNGOL S S, V58, P139, DOI 10.3109/00016486409134640 UEEDA M, 1992, CIRC RES, V70, P1296 VO PA, 1991, EUR J PHARMACOL, V195, P291 YAMAMOTO K, 1991, ACTA OTO-LARYNGOL, V111, P312, DOI 10.3109/00016489109137393 NR 32 TC 84 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 38 EP 42 DI 10.1016/0378-5955(94)90251-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500004 PM 7928737 ER PT J AU RHODE, WS AF RHODE, WS TI TEMPORAL CODING OF 200-PERCENT AMPLITUDE-MODULATED SIGNALS IN THE VENTRAL COCHLEAR NUCLEUS OF CAT SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS; TEMPORAL PROPERTIES; ONSET UNITS; AMPLITUDE MODULATION ID AUDITORY-NERVE FIBERS; RESPONSE PROPERTIES; CELLS; NEURONS; TONES; CLASSIFICATION; REGULARITY; INTENSITY; STIMULI; HEARING AB The quasiperiodicity in the acoustic waveform in speech and music is a pervasive feature in our acoustic environment. The use of 200% amplitude modulated (AM) signals allows the study of rate and temporal envelope coding using three equal amplitude components, a situation that is frequently approximated in natural vocalizations. The recordings reported here were made in the ventral cochlear nucleus of the cat, a site of auditory signal feature enhancement and the origin of several ascending auditory pathways. The discharge rate vs modulation frequency relation was nearly always all-pass in shape for all unit types indicating that discharge rate is not a code for modulation frequency. Onset cells, especially onset-choppers and onset-I units, exhibited remarkable phase locking to the signal envelope, nearly to the exclusion of phase locking to the AM components. They exhibited lowpass temporal modulation transfer functions (tMTF) that occasionally had corner frequencies greater than 1 kHz. Primary-like, primary-like with notch, and onset-L units all exhibited considerable variability in their coding properties with tMTFs that varied from lowpass to bandpass in shape. The bandpass shape became more frequent with increasing stimulus levels. A common feature in cochlear nucleus units was less sensitivity to the level of the AM stimulus than is present in the auditory nerve. Phase locking to the envelope persisted over a wider range of stimulus levels than rate changes in a subset of the units studied. The tMTFs for a 100% sinusoidally modulated, spectrally-flat noise was similar in amplitude and bandwidth to those obtained for AM stimuli. The tMTF was relatively insensitive to carrier frequencies different than the unit characteristic frequency. AM synchrony vs level curves exhibited systematic shifts that equaled or exceeded dynamic rate shifts that occur with increasing levels of a noise masker. Phase locking to the envelope was robust under a wide variety of signal conditions in all unit types. The ordering of response types based on the maximum of the tMTF is onset-I = onset-chop > choppers = primarylike-with-notch = onset-L > primarylike. RP RHODE, WS (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,1300 UNIV AVE,MADISON,WI 53706, USA. CR ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 BLACKSTAD TW, 1984, NEUROSCIENCE, V13, P827, DOI 10.1016/0306-4522(84)90099-X BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 BURNS EM, 1976, J ACOUST SOC AM, V60, P863, DOI 10.1121/1.381166 BUUNEN TJF, 1978, J ACOUST SOC AM, V64, P772, DOI 10.1121/1.382042 COOPER NP, 1993, J NEUROPHYSIOL, V70, P370 EVANS EF, 1978, AUDIOLOGY, V17, P367 FORMBY C, 1985, J ACOUST SOC AM, V78, P70, DOI 10.1121/1.392456 FRISINA RD, 1985, EXP BRAIN RES, V60, P417 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 GIBSON DJ, 1985, J NEUROPHYSIOL, V53, P940 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 Greenberg S, 1987, AUDITORY PROCESSING, P225 GREENWOO.DD, 1971, J ACOUST SOC AM, V50, P502, DOI 10.1121/1.1912668 JAVEL E, 1980, J ACOUST SOC AM, V68, P113 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 KANE EC, 1973, INT J NEUROSCI, V5, P251, DOI 10.3109/00207457309149485 KAY RH, 1982, PHYSIOL REV, V62, P894 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KIM DO, 1986, AUDITORY FREQUENCY S, P281 MARDIA KV, 1972, STATISTICS DIRECTION MOLLER AR, 1976, ACTA PHYIOL SCAND, V98, P268 MOLLER AR, 1974, ACUSTICA, V31, P292 PALMER AR, 1982, HEARING RES, V7, P305, DOI 10.1016/0378-5955(82)90042-9 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 RHODE WS, 1994, J NEUROPHYSIOL, V71, P493 RHODE WS, 1994, J NEUROPHYSIOL, V71 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 ROSE JE, 1969, J NEUROPHYSIOL, V32, P402 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 ROUILLER EM, 1984, J COMP NEUROL, V225, P167, DOI 10.1002/cne.902250203 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SENTO S, 1989, J COMP NEUROL, V280, P553, DOI 10.1002/cne.902800406 SMITH PH, 1993, MAMMALIAN COCHLEAR N, P349 SMITH PH, 1989, J COMP NEUROL, V282, P595, DOI 10.1002/cne.902820410 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 SMITH RL, 1980, HEARING RES, V2, P123, DOI 10.1016/0378-5955(80)90034-9 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 NR 43 TC 46 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 43 EP 68 DI 10.1016/0378-5955(94)90252-6 PG 26 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500005 PM 7928738 ER PT J AU TORIHARA, K SUGANUMA, T IDE, S MORIMITSU, T AF TORIHARA, K SUGANUMA, T IDE, S MORIMITSU, T TI ANIONIC SITES IN BLOOD CAPILLARIES OF THE MOUSE COCHLEAR DUCT SO HEARING RESEARCH LA English DT Article DE POLY-L-LYSINE CONJUGATED COLLOIDAL GOLD; CATION; CHARGE BARRIER; ELECTRON MICROSCOPY; LOWICRYL K4M ID CYTO-CHEMISTRY; LOWICRYL K4M; GUINEA-PIG; GOLD; MEMBRANE; SECTIONS; MARKER; TISSUE AB The blood-cochlear barrier, which consists of the molecular size and ionic charge barriers, is known to play an important role in production and absorption of inner ear fluids. In this study, we employed poly-L-lysine colloidal gold conjugates (PL-CG) in combination with Lowicryl K4M resin to demonstrate anionic sites in blood capillaries of the cochlear duct. Male ICR mice weighing 30-40 g with a positive Preyer's reflex were used. The basement membranes of blood capillaries of the stria vascularis and the spiral ligament were successfully labeled with PLCG pH 2.5. The luminal surface of capillaries in the stria vascularis and the spiral ligament intensely reacted with PGCG pH 2.5. However, PL-CG pH 1.0 stained only the basement membrane of the spiral ligament. Predigestion with several glycosidases nearly eliminated PGCG labeling. Anionic charge located on the luminal surface of the endothelial cell was mainly caused by the presence of sialic acid. On the contrary, anionic charge of the basement membrane was caused in a substantial degree by chondroitin and heparan sulfate-rich glycosaminoglycans. We obtained histochemical evidence that blood capillaries of the stria vascularis differ from those of the spiral ligament. C1 MIYAZAKI MED COLL,DEPT ANAT,MIYAZAKI 88916,JAPAN. RP TORIHARA, K (reprint author), MIYAZAKI MED COLL,DEPT OTORHINOLARYNGOL,MIYAZAKI 88916,JAPAN. CR ARIMA T, 1985, ACTA OTO-LARYNGOL, V100, P194, DOI 10.3109/00016488509104781 ARMBRUSTER BL, 1983, J HISTOCHEM CYTOCHEM, V31, P1380 CHALEMALM E, 1982, J MICROSC, V126, P123 CHAN FL, 1993, ANAT REC, V235, P191, DOI 10.1002/ar.1092350203 GOODE NP, 1992, HISTOCHEMISTRY, V98, P67, DOI 10.1007/BF00716938 HOZAWA K, 1993, GLYCOBIOLOGY, V3, P47, DOI 10.1093/glycob/3.1.47 KAWAMATA S, 1993, HEARING RES, V67, P75, DOI 10.1016/0378-5955(93)90234-R OHYAMA S, 1982, JAP J OTOL TOKYO, V85, P1482 ROTH J, 1989, METHOD CELL BIOL, V31, P513, DOI 10.1016/S0091-679X(08)61625-8 ROTH J, 1981, J HISTOCHEM CYTOCHEM, V29, P663 SAKAGAMI M, 1987, ACTA OTO-LARYNGOL, V103, P189, DOI 10.3109/00016488709107783 SLOT JW, 1985, EUR J CELL BIOL, V38, P87 SUGANUMA T, 1985, HISTOCHEMISTRY, V83, P489, DOI 10.1007/BF00492449 Suzuki M, 1991, Acta Otolaryngol Suppl, V481, P112 THIERY JP, 1979, BIOL CELLULAIRE, V36, P281 TOMODA K, 1988, ARCH OTO-RHINO-LARYN, V245, P307, DOI 10.1007/BF00464638 VORBRODT AW, 1989, J NEUROCYTOL, V18, P359, DOI 10.1007/BF01190839 NR 17 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 69 EP 74 DI 10.1016/0378-5955(94)90253-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500006 PM 7523356 ER PT J AU GARETZ, SL RHEE, DJ SCHACHT, J AF GARETZ, SL RHEE, DJ SCHACHT, J TI SULFHYDRYL COMPOUNDS AND ANTIOXIDANTS INHIBIT CYTOTOXICITY TO OUTER HAIR-CELLS OF A GENTAMICIN METABOLITE IN-VITRO SO HEARING RESEARCH LA English DT Article DE AMINOGLYCOSIDES; OTOTOXICITY; PROTECTION; GLUTATHIONE; FREE RADICALS; SCAVENGERS ID GLUTATHIONE-S-TRANSFERASES; AMINOGLYCOSIDE ANTIBIOTICS; OTOTOXICITY AB Aminoglycoside antibiotics such as gentamicin have long been known to destroy cochlear and vestibular hair cells in vivo. In the cochlea outer hair cells are preferentially affected. In contrast, gentamicin will not damage outer hair cells in vitro unless it has been enzymatically converted to a cytotoxic metabolite. Several potential inhibitors of this enzymatic reaction were tested in an in vitro assay against outer hair cells isolated from the guinea pig cochlea. Viability of hair cells (viable cells as per cent of total number of cells observed) averaged about 70% under control conditions. Addition of metabolized gentamicin significantly reduced viability to less than 50% in one hour. Sulfhydryl compounds (glutathione, dithioerythritol) and antioxidants (vitamin C, phenylene diamine, trolox) prevented the cytotoxic actions of the gentamicin metabolite. Inhibitors of amine oxidases and compounds reportedly protective against renal and acute lethal toxicity of aminoglycosides (poly-L-aspartate and pyridoxal phosphate, respectively) were ineffective as protectants. The results reinforce the hypothesis that gentamicin is enzymatically converted to a cytotoxin and imply the participation of sulfhydryl-sensitive groups or free radicals in this reaction. Alternatively or additionally, sulfhydryl compounds or antioxidants may participate in detoxification reactions. RP GARETZ, SL (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,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 CRANN SA, 1992, BIOCHEM PHARMACOL, V43, P1835, DOI 10.1016/0006-2952(92)90718-X DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FEDERSPIL P, 1979, ANTIBIOTIKASCHADEN O, P86 GARETZ S, 1994, HEAR RES, V77 GARETZ S, 1992, ASS RES OTOLARYNGOL, V15, P110 GARETZ S, 1993, ASS RES OTOLARYNGOL, V16, P141 GARETZ SL, 1994, HDB AUDITORY RES, V6 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HOFFMAN DW, 1987, HEARING RES, V31, P217, DOI 10.1016/0378-5955(87)90190-0 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 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 Jakoby W B, 1978, Adv Enzymol Relat Areas Mol Biol, V46, P383 JONES MM, 1992, FUND APPL TOXICOL, V18, P181, DOI 10.1016/0272-0590(92)90044-I KENNISTON RC, 1987, TOXICOL APLL PHARM, V88, P433 KISHORE BK, 1992, J PHARMACOL EXP THER, V262, P424 LISTOWSKY I, 1988, DRUG METAB REV, V19, P305, DOI 10.3109/03602538808994138 MEISTER A, 1991, PHARMACOL THERAPEUT, V51, P155, DOI 10.1016/0163-7258(91)90076-X PIERSON MG, 1981, HEARING RES, V4, P79, DOI 10.1016/0378-5955(81)90037-X PREZANT TR, 1993, NAT GENET, V4, P289, DOI 10.1038/ng0793-289 SCHACHT J, 1993, IN PRESS BIOCH BASIS SCHENTAG JJ, 1977, CLIN PHARMACOL THER, V22, P364 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 25 TC 82 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 75 EP 80 DI 10.1016/0378-5955(94)90254-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500007 PM 7928739 ER PT J AU GARETZ, SL ALTSCHULER, RA SCHACHT, J AF GARETZ, SL ALTSCHULER, RA SCHACHT, J TI ATTENUATION OF GENTAMICIN OTOTOXICITY BY GLUTATHIONE IN THE GUINEA-PIG IN-VIVO SO HEARING RESEARCH LA English DT Article DE AMINOGLYCOSIDES; OTOTOXICITY; PROTECTION; GLUTATHIONE; FREE RADICALS; SCAVENGERS ID REDUCED GLUTATHIONE; S-TRANSFERASES; METABOLITE; PLASMA AB The effect of glutathione co-therapy on the expression of gentamicin ototoxicity was tested in pigmented guinea pigs. The first group of animals was injected with gentamicin (100 mg/kg body weight/day) for two weeks followed by 10 weeks of rest. A second group received glutathione by gastric gavage immediately prior to each gentamicin injection. Two groups of controls were treated either with saline injections or glutathione gavage alone. Auditory brainstem responses, taken at 2-week intervals, revealed a progressive gentamicin-induced hearing loss reaching a 30 to 40 dB threshold shift at 2 kHz, approximately 60 dB at 8 kHz and 80 dB at 18 kHz. Glutathione co-therapy slowed the progression of hearing loss and significantly attenuated the final threshold shifts by 20 to 40 dB. Morphological evaluation confirmed hair cell loss after gentamicin treatment and protection by glutathione. Drug serum levels were assayed at 2 and 7 days of treatment. There were no differences between the gentamicin (mean = 183 mu g/ml; range, 90 to 300) and the gentamicin/glutathione group (mean = 164 mu g/ml; range, 80 to 320). Antimicrobial activity of gentamicin was tested against Staphylococcus aureus and Pseudomonas aeruginosa. A 30-fold molar excess of glutathione did not influence the efficacy of gentamicin. These studies suggest that glutathione protects against ototoxicity by interfering with the cytotoxic mechanism. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. CR CAVALLETTI E, 1986, CANCER LETT, V32, P1, DOI 10.1016/0304-3835(86)90032-7 CRANN SA, 1992, BIOCHEM PHARMACOL, V43, P1835, DOI 10.1016/0006-2952(92)90718-X DARROUZET J, 1967, REV LARYNGOL, V3, P187 FEDERSPIL P, 1979, ANTIBIOTIKASCHADEN O, P86 Fee Jr WE, 1980, LARYNGOSCOPE S, V90, P1 GARETZ S, 1992, ASS RES OTOLARYNGOL, V15, P110 GARETZ S, 1993, ASS RES OTOLARYNGOL, V16, P141 GARETZ S, 1994, IN PRESS HDB AUDITOR, V6 GARETZ SL, 1994, IN PRESS HEAR RES HAGEN TM, 1990, AM J PHYSIOL, V259, pG524 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HOFFMAN DW, 1987, HEARING RES, V31, P217, DOI 10.1016/0378-5955(87)90190-0 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 HUANG MY, 1990, BIOCHEM PHARMACOL, V40, pR11, DOI 10.1016/0006-2952(90)90077-X Jakoby W B, 1978, Adv Enzymol Relat Areas Mol Biol, V46, P383 LAUTERMANN J, 1994, ASS RES OT, V17, P64 LISTOWSKY I, 1988, DRUG METAB REV, V19, P305, DOI 10.3109/03602538808994138 MATZ GJ, 1986, AM J OTOLARYNG, V7, P117, DOI 10.1016/S0196-0709(86)80040-0 MEISTER A, 1991, PHARMACOL THERAPEUT, V51, P155, DOI 10.1016/0163-7258(91)90076-X ORIANA S, 1987, TUMORI, V73, P337 PRAZMA J, 1983, ANN OTO RHINOL LARYN, V92, P178 RICEEVANS CA, 1993, FREE RADICAL BIO MED, V15, P77, DOI 10.1016/0891-5849(93)90127-G SHAFER RW, 1991, AIDS, V5, P399, DOI 10.1097/00002030-199104000-00007 WENDEL A, 1981, BIOCHEM PHARMACOL, V31, P3607 WENDEL A, 1980, FEBS LETT, V120, P209, DOI 10.1016/0014-5793(80)80299-7 NR 25 TC 116 Z9 120 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 15 PY 1994 VL 77 IS 1-2 BP 81 EP 87 DI 10.1016/0378-5955(94)90255-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500008 PM 7928740 ER PT J AU WERNER, LA FOLSOM, RC MANCL, LR AF WERNER, LA FOLSOM, RC MANCL, LR TI THE RELATIONSHIP BETWEEN AUDITORY BRAIN-STEM RESPONSE LATENCIES AND BEHAVIORAL THRESHOLDS IN NORMAL-HEARING INFANTS AND ADULTS SO HEARING RESEARCH LA English DT Article DE HEARING; DEVELOPMENT; HUMAN; EVOKED POTENTIALS; PSYCHOPHYSICS ID STEM RESPONSES; DEVELOPMENTAL-CHANGES; SENSITIVITY; COCHLEA; MASKING AB The relationship between behavioral thresholds and auditory brainstem response (ABR) latencies for 4 and 8 kHz tone pips were examined in normal-hearing 3-month-olds, 6-month-olds and adults. The latencies of waves I and V and the I-V interval of the ABR were analyzed. A linear latency-intensity function was also fit to each subject's latencies for each wave at several levels. The y-intercept of the latency-intensity function was used as a summary measure of latency to examine behavior-ABR correlations. The pattern of age-related change in behavioral threshold was not closely matched by age-related latency reduction. for Wave I, Wave V or the I-V interval. However, 3-month-olds with higher behavioral thresholds had longer Wave V latencies and longer I-V intervals than 3-month-olds with lower behavioral thresholds. There was no significant difference in latency between 6-month-olds or adults with higher thresholds and 6-month-olds or adults with lower thresholds. There was also a significant correlation between the Wave V - Wave I latency-intensity intercept difference and behavioral threshold at both 4 and 8 kHz among 3-month-olds. The correlation was not significant among 6-month-olds or adults. These findings suggest that one of the factors responsible for immature behavioral thresholds at 3 months is related to transmission through the auditory brainstem. Because variability in hearing threshold among normal-hearing adults is low, it is not surprising that behavioral threshold is unrelated to ABR latency in this group. However, the lack of such a relationship among 6-month-olds implies that structures central to the auditory brainstem, either sensory or nonsensory, or both, must be responsible for immature behavioral thresholds after 6 months of age. RP WERNER, LA (reprint author), UNIV WASHINGTON,CTR CHILD DEV & MENTAL RETARDAT,DEPT SPEECH & HEARING SCI,WJ-10,BOX 47,SEATTLE,WA 98195, USA. CR BANKS MS, 1992, DEV PSYCHOACOUSTICS, P229, DOI 10.1037/10119-009 BARGONES JY, 1988, J ACOUST SOC AM, V83, P1809, DOI 10.1121/1.396515 BARGONES JY, 1992, THESIS U WASHINGTON BERG KM, 1983, J EXP CHILD PSYCHOL, V35, P409, DOI 10.1016/0022-0965(83)90017-6 BRUGGE JF, 1988, AUDITORY FUNCTION NE, P113 EGGERMONT JJ, 1991, ACTA OTO-LARYNGOL, V111, P220, DOI 10.3109/00016489109137378 EGGERMONT JJ, 1985, AUDITORY DEV INFANCY, P21 FABIANI M, 1979, ELECTROEN CLIN NEURO, V47, P483, DOI 10.1016/0013-4694(79)90164-0 FOLSOM RC, 1987, AUDIOLOGY, V26, P117 FOLSOM RC, 1985, J ACOUST SOC AM, V78, P555, DOI 10.1121/1.392422 FONTON CW, 1992, J ACOUST SOC AM, V91, P1576 GORGA MP, 1988, J SPEECH HEAR RES, V31, P87 Gottlieb G., 1971, BIOPSYCHOLOGY DEV, P67 Hall J, 1992, HDB AUDITORY EVOKED HENDLER T, 1990, EAR HEARING, V11, P403, DOI 10.1097/00003446-199012000-00002 KEEFE DH, 1994, J ACOUST SOC AM, V95, P355, DOI 10.1121/1.408380 KEEFE DH, 1993, J ACOUST SOC AM, V94, P2617, DOI 10.1121/1.407347 KLEIN AJ, 1978, J ACOUST SOC AM, V63, P1887, DOI 10.1121/1.381930 NOZZA RJ, 1984, J SPEECH HEAR RES, V27, P613 Okabe K., 1988, Journal of the Acoustical Society of Japan (E), V9 OLSHO L W, 1988, Journal of the Acoustical Society of America, V84, P1316, DOI 10.1121/1.396630 OLSHO LW, 1987, DEV PSYCHOL, V23, P627, DOI 10.1037/0012-1649.23.5.627 PERAZZO LM, 1991, ONTOGENY HUMAN BRAIN PERAZZO LM, 1992, ONTOGENY HUMAN BRAIN PONTON CW, 1994, RELATION AUDITORY BR PUJOL R, 1992, ACTA OTO-LARYNGOL, V112, P259 SANES DH, 1993, J NEUROSCI, V13, P2627 SANES DH, 1992, DEV PSYCHOACOUSTICS, P257, DOI 10.1037/10119-010 Schneider B. A., 1992, DEV PSYCHOACOUSTICS, P3, DOI 10.1037/10119-001 SCHNEIDER BA, 1986, J ACOUST SOC AM, V79, P447, DOI 10.1121/1.393532 SCHNEIDER BA, 1989, J ACOUST SOC AM, V86, P1733, DOI 10.1121/1.398604 TEAS DC, 1982, HEARING RES, V7, P19, DOI 10.1016/0378-5955(82)90080-6 TREHUB SE, 1980, J EXP CHILD PSYCHOL, V29, P282, DOI 10.1016/0022-0965(80)90020-X TREHUB SE, 1988, J EXP CHILD PSYCHOL, V46, P273, DOI 10.1016/0022-0965(88)90060-4 Werner L. A., 1992, DEV PSYCHOACOUSTICS, P47, DOI 10.1037/10119-002 WERNER LA, 1993, HEARING RES, V68, P131, DOI 10.1016/0378-5955(93)90071-8 WERNER LA, 1991, PERCEPT PSYCHOPHYS, V50, P405, DOI 10.3758/BF03205057 WIGHTMAN P, 1992, DEV PSYCHOACOUSTICS, P47 WILCOX RR, 1987, NEW STATISTICAL PROC Yakovlev P. I., 1967, REGIONAL DEV BRAIN E, P3 NR 40 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 88 EP 98 DI 10.1016/0378-5955(94)90256-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500009 PM 7928741 ER PT J AU BRUNSOBECHTOLD, JK LINVILLE, MC HENKEL, CK AF BRUNSOBECHTOLD, JK LINVILLE, MC HENKEL, CK TI TERMINAL TYPES ON IPSILATERALLY AND CONTRALATERALLY PROJECTING LATERAL SUPERIOR OLIVE CELLS SO HEARING RESEARCH LA English DT Article DE LATERAL SUPERIOR OLIVE; LATERALITY; SYNAPSE; FERRET; ULTRASTRUCTURE; AUDITORY PATHWAY ID NUCLEUS; FERRET; ADULT; CAT AB The lateral superior olive (LSO) in ferret contains two distinct populations of principal cells, one population projecting to the ipsilateral and the other projecting to the contralateral inferior colliculus. In addition, these populations have been shown to be distinct from each other on the basis of tonotopic and isofrequency distribution within LSO, of dendritic morphology, and of neurotransmitter within the somata. The present study compared the two populations on the basis of the type of synaptic input. Laterality of projection was established using horseradish peroxidase histochemistry. Synaptic terminals contacting LSO somata identified as projecting ipsilaterally or contralaterally were quantified as round (R) or nonround (NR), representing presumptive excitatory and inhibitory input, respectively. Results indicate that the vast majority of somatic terminals contacting both projection populations are NR and, furthermore, that R terminals are significantly more likely to contact ipsilaterally than contralaterally projecting LSO cells. There is no significant difference in number of NR terminals or total number of terminals between ipsilaterally and contralaterally projecting LSO cells. These findings provide additional support to the notion that the LSO is comprised of two distinct cell populations. Moreover, they indicate a difference in the balance of somatic inhibition and excitation which may have an impact on the nature of the response properties of the two populations. C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT OTOLARYNGOL,WINSTON SALEM,NC 27157. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,NEUROSCI PROGRAM,WINSTON SALEM,NC 27157. RP BRUNSOBECHTOLD, JK (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT NEUROBIOL & ANAT,300 S HAWTHORNE RD,WINSTON SALEM,NC 27157, USA. CR ADAMS JC, 1990, HEARING RES, V49, P281, DOI 10.1016/0378-5955(90)90109-3 BRUNSOBECHTOLD JK, 1990, J COMP NEUROL, V294, P389, DOI 10.1002/cne.902940308 CAMPBELL G, 1992, J NEUROSCI, V12, P1847 CANT NB, 1991, NEUROBIOLOGY HEARING, P141 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 CANT NB, 1984, J COMP NEUROL, V227, P63, DOI 10.1002/cne.902270108 HELFERT RH, 1992, J COMP NEUROL, V323, P305, DOI 10.1002/cne.903230302 HELFERT RH, 1986, J COMP NEUROL, V244, P533, DOI 10.1002/cne.902440409 HENKEL CK, 1993, J COMP NEUROL, V331, P458, DOI 10.1002/cne.903310403 HENKEL C K, 1991, Society for Neuroscience Abstracts, V17, P1484 HENKEL CK, 1994, IN PRESS J COMP NEUR Irvine D. R. F., 1992, MAMMALIAN AUDITORY P, P153 Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 TSUCHITANI C, 1991, NEUROBIOLOGY HEARING, P163 NR 14 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 99 EP 104 DI 10.1016/0378-5955(94)90257-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500010 PM 7928743 ER PT J AU MCCREERY, DB YUEN, TGH AGNEW, WF BULLARA, LA AF MCCREERY, DB YUEN, TGH AGNEW, WF BULLARA, LA TI STIMULUS PARAMETERS AFFECTING TISSUE-INJURY DURING MICROSTIMULATION IN THE COCHLEAR NUCLEUS OF THE CAT SO HEARING RESEARCH LA English DT Article DE CATS; COCHLEAR NUCLEUS; ELECTRIC STIMULATION; STIMULUS PARAMETERS; MICROELECTRODES; MICROSTIMULATION; NEURAL DAMAGE (INJURY) ID ELECTRICAL-STIMULATION; PERIPHERAL-NERVE; CHARGE INJECTION; ELECTRODES; DAMAGE; SALINE; DISSOLUTION; PLATINUM AB We investigated the effects of continuous microstimulation in the cats' posteroventral cochlear nucleus, using chronically implanted activated iridium microelectrodes. We examined 51 electrode sites (39 pulsed sites, and 12 unpulsed sites). Seven hours of continuous stimulation at 500 Hz often produced tissue injury near the tips of the pulsed microelectrodes. The damage took the form of a region of vacuolated tissue extending 200 mu m or more from the site of the electrode tip. Electron microscope studies showed the vacuoles to be severely edematous segments of myelinated axons. The statistical correlation between the amount of damaged tissue and the charge per phase was large and highly significant (P < 0.0001). When the electrodes were pulsed for 7 h at 500 Hz with charge-balanced biphasic pulse pairs, the threshold for the damage was approximately 3 nC/phase. The damage threshold was not appreciably lower when the stimulation protocol was extended to 35 h (7 h/day for 5 days). in contrast, the threshold for exciting neurons near the microelectrode is approximately 1 nC/phase, as determined by the evoked response recorded in the inferior colliculus. There was little correlation between the severity of the tissue damage and the geometric charge density at the surface of the electrodes, between the damage and amplitude of the cathodic phase of the voltage transient induced across the stimulating electrodes by the stimulus current pulses, or between the damage and the stimulus pulse duration. RP MCCREERY, DB (reprint author), HUNTINGTON MED RES INST,NEUROL RES LAB,734 FAIRMOUNT AVE,PASADENA,CA 91105, USA. CR ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W AGNEW WF, 1992, NEUROSCIENCE, V52, P45 AGNEW WF, 1990, J BIOMED ENG, V12, P301, DOI 10.1016/0141-5425(90)90004-7 AGNEW WF, 1986, EXP NEUROL, V92, P162, DOI 10.1016/0014-4886(86)90132-9 BEEBE X, 1988, IEEE T BIO-MED ENG, V35, P494, DOI 10.1109/10.2122 BLACK RC, 1979, APPL NEUROPHYSIOL, V42, P366 Bockris J., 1970, MODERN ELECTROCHEMIS BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P440, DOI 10.1109/TBME.1977.326179 BRUMMER SB, 1977, BRAIN BEHAV EVOLUT, V14, P10, DOI 10.1159/000124611 BULLARA LA, 1983, J NEUROSCI METH, V9, P15, DOI 10.1016/0165-0270(83)90104-8 DONALDSON N, 1985, MED BIOL ENG COMP EDGERTON BJ, 1982, ANN OTOL RHINOL Eisenberg L S, 1987, J Rehabil Res Dev, V24, P9, DOI 10.1682/JRRD.1987.07.0009 Gorsuch R. L., 1983, FACTOR ANAL LASSMANN H, 1984, NEUROSCIENCE, V13, P691, DOI 10.1016/0306-4522(84)90089-7 MCCREERY DB, 1988, ANN BIOMED ENG, V16, P463, DOI 10.1007/BF02368010 MCCREERY DB, 1992, MED BIOL ENG COMPUT, V30, P109, DOI 10.1007/BF02446202 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 MCHARDY J, 1980, BIOMATERIALS, V1, P129, DOI 10.1016/0142-9612(80)90034-4 OLNEY JW, 1981, NATURE, V292, P165, DOI 10.1038/292165a0 ROBBLEE LS, 1983, J ELECTROCHEM SOC, V130, P731, DOI 10.1149/1.2119793 ROBBLEE LS, 1990, 9TH Q PROGR REP Robblee LS, 1990, NEURAL PROSTHESES FU SHANNON RV, 1990, HEARING RES, V47, P159, DOI 10.1016/0378-5955(90)90173-M NR 25 TC 51 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 105 EP 115 DI 10.1016/0378-5955(94)90258-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500011 PM 7928722 ER PT J AU PREYER, S HEMMERT, W PFISTER, M ZENNER, HP GUMMER, AW AF PREYER, S HEMMERT, W PFISTER, M ZENNER, HP GUMMER, AW TI FREQUENCY-RESPONSE OF MATURE GUINEA-PIG OUTER HAIR-CELLS TO STEREOCILIARY DISPLACEMENT SO HEARING RESEARCH LA English DT Article DE GUINEA-PIG; OUTER HAIR CELL; MECHANOELECTRICAL TRANSDUCTION; RECEPTOR POTENTIAL; CELL ELECTRICAL INPUT IMPEDANCE ID ELECTRICAL CIRCUIT PROPERTIES; MOUSE COCHLEA; MECHANICAL RESPONSES; REACTIVE ELEMENTS; SHAPE CHANGES; MOTILITY; CURRENTS; ORGAN; CORTI; TRANSDUCTION AB Outer hair cells (OHC) were isolated from the apical two turns of the guinea-pig cochlea and their hair-bundle stimulated mechanically by a glass probe. In accordance with in vivo data (Dallos, 1985), the resting membrane potential was typically -64 mV (N = 200). The maximum amplitudes of the receptor potentials were between 0.4 and 5.2 mV peak-to-peak, with mean of 1.5 mV +/- 0.9 mV (N = 81). The sensitivity was 0.015 mV/nm or 2 mV/deg. The frequency response of the receptor potential followed a first order low-pass filter characteristic with a corner frequency of about 63 Hz. For frequencies up to at least 1.6 kHz, the frequency response of mechanoelectrical transduction was dominated by the electrical input impedance of the cell. The presence of a single time constant in the voltage response to stereociliary deflection implies that the frequency response of mechanoelectrical transduction far exceeds that of the electrical input impedance of the cell; its time constant must be faster than 100 mu s. Under in vivo conditions, OHC should be capable of providing a sufficiently large receptor potential to supply enough energy for electromechanical feedback. RP PREYER, S (reprint author), UNIV TUBINGEN,DEPT OTORHINOLARYNGOL,SECT PHYSIOL ACOUST & COMMUN,SLICHERSTR 5,D-72076 TUBINGEN,GERMANY. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWN MC, 1984, J PHYSL, V254, P625 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1993, J NEUROPHYSIOL, V70, P299 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DALLOS P, 1983, HEARING RES, V12, P89, DOI 10.1016/0378-5955(83)90120-X DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 DAVIS H, 1965, COLD SPRING HARB SYM, V30, P181 EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 HALLWORTH R, 1993, J NEUROPHYSIOL, V70, P549 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HOUSLEY GD, 1992, J PHYSIOL-LONDON, V448, P73 HOWARD J, 1987, P NATL ACAD SCI USA, V84, P3064, DOI 10.1073/pnas.84.9.3064 HUANG GJ, 1993, BIOPHYS J, V65, P2228 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KROS CJ, 1992, P ROY SOC B-BIOL SCI, V249, P185, DOI 10.1098/rspb.1992.0102 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 Ohmori H, 1991, Acta Otolaryngol Suppl, V481, P1 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 OHMORI H, 1987, J PHYSIOL-LONDON, V387, P589 PREYER S, 1993, HNO, V41, P471 PREYER WT, 1900, ENTIWCKLUNG MENSCHEN, P57 REUTER G, 1990, HEARING RES, V43, P219, DOI 10.1016/0378-5955(90)90230-M REUTER G, 1992, HEARING RES, V60, P236, DOI 10.1016/0378-5955(92)90025-I RUSSELL IJ, 1989, HEARING RES, V43, P55, DOI 10.1016/0378-5955(89)90059-2 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 SANTOS-SACCHI J, 1993, BIOPHYS J, V65, P2217 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 SAUNDERS JC, 1989, J ACOUST SOC AM, V86, P1797, DOI 10.1121/1.398612 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V149, P304, DOI 10.1016/0006-291X(87)91639-1 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 42 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 116 EP 124 DI 10.1016/0378-5955(94)90259-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500012 PM 7928723 ER PT J AU SCHMIDT, S THALLER, J AF SCHMIDT, S THALLER, J TI TEMPORAL AUDITORY SUMMATION IN THE ECHOLOCATING BAT, TADARIDA-BRASILIENSIS SO HEARING RESEARCH LA English DT Article DE PSYCHOPHYSICS; TEMPORAL SUMMATION; MASKED AUDITORY THRESHOLD; BAT ID INTEGRATION; HEARING AB Auditory thresholds improve with increasing signal duration within the maximum integration time of the auditory system, a phenomenon called temporal summation. The temporal summation function is a basic characteristic of particular relevance for bat sonar, as it determines the ability to detect targets with short echolocation calls. Temporal summation was studied in 6 Mexican free-tailed bats (Tadarida brasiliensis) in a forced two-choice behavioural test. Masked auditory thresholds for 40-kHz test tone pulses with durations between 2 ms and 400 ms were determined in broadband noise of two different spectrum levels (-18 dB, +17 dB). At both masker levels, thresholds decreased by considerably more than 10 dB per decade of duration. The time constants of the summation functions, which are a measure of the maximum integration time, shortened significantly with increasing masker level from 62 ms to 14 ms. The steep summation functions are only partly accounted for by spectral splatter. This suggests that the bats are capable of a neural overintegration of sound intensity. Finally, it is shown that such short time constants are typical for echolocating animals, and the implications of the found summation functions for echolocation are considered. RP SCHMIDT, S (reprint author), UNIV MUNICH,INST ZOOL,LUISENSTR 14,D-80333 MUNICH,GERMANY. CR AIRAPETJANZ ES, 1974, ECHOLOCATION NATURE CLACK TD, 1966, J ACOUST SOC AM, V40, P1140, DOI 10.1121/1.1910199 COSTALUPES JA, 1983, HEARING RES, V9, P43, DOI 10.1016/0378-5955(83)90133-8 EHRET G, 1976, J ACOUST SOC AM, V59, P1421, DOI 10.1121/1.381030 FAY RR, 1988, HEARING RES, V34, P295, DOI 10.1016/0378-5955(88)90009-3 FAY RR, 1983, HEARING RES, V10, P69, DOI 10.1016/0378-5955(83)90018-7 FAY RR, 1988, HEARING VERTEBRATES, P381 Feldtkeller R, 1956, ACUSTICA, V6, P489 FENTON MB, 1981, J MAMMAL, V62, P233, DOI 10.2307/1380701 Finney D. J., 1971, PROBIT ANAL, V3rd FLORENTINE M, 1988, J ACOUST SOC AM, V84, P195, DOI 10.1121/1.396964 GARNER WR, 1947, J ACOUST SOC AM, V19, P808, DOI 10.1121/1.1916625 GRINNELL AD, 1972, Z VERGL PHYSIOL, V76, P41, DOI 10.1007/BF00395500 HUGHES JW, 1946, PROC R SOC SER B-BIO, V133, P486, DOI 10.1098/rspb.1946.0026 JOHNSON CS, 1991, J ACOUST SOC AM, V89, P2996, DOI 10.1121/1.400736 JOHNSON CS, 1968, J ACOUST SOC AM, V43, P757, DOI 10.1121/1.1910893 KICK SA, 1982, J COMP PHYSIOL, V145, P431 KLUMP GM, 1990, J COMP PSYCHOL, V104, P94, DOI 10.1037/0735-7036.104.1.94 KONSTANTINOV AJ, 1988, ECHOLOKAZIONNAJA SEN, P67 Mohl B., 1988, ANIMAL SONAR PROCESS, P435 NEUWEILER G, 1984, NATURWISSENSCHAFTEN, V71, P446, DOI 10.1007/BF00455897 OFFUTT GC, 1967, J ACOUST SOC AM, V41, P13, DOI 10.1121/1.1910309 PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 POPPER AN, 1972, J ACOUST SOC AM, V52, P596, DOI 10.1121/1.1913150 SACHS L, 1978, STATISTISCHE AUSWERT SCHMIDT S, 1990, BRAIN PERCEPTION COG, P146 Schnitzler H. U., 1980, ANIMAL SONAR SYSTEMS, P109, DOI 10.1007/978-1-4684-7254-7_6 SIMMONS JA, 1978, J COMP PHYSIOL, V125, P291 SUTHERS RA, 1980, J COMP PHYSIOL, V136, P227 TROEST N, 1986, J COMP PHYSIOL A, V159, P559, DOI 10.1007/BF00604175 WATSON CS, 1969, J ACOUST SOC AM, V46, P989, DOI 10.1121/1.1911819 WRIGHT HN, 1968, J SPEECH HEAR RES, V11, P109 Zwicker E., 1990, PSYCHOACOUSTICS FACT ZWISLOCK.JJ, 1969, J ACOUST SOC AM, V46, P431, DOI 10.1121/1.1911708 ZWISLOCKI J, 1960, J ACOUST SOC AM, V32, P1046, DOI 10.1121/1.1908276 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 125 EP 134 DI 10.1016/0378-5955(94)90260-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500013 PM 7928724 ER PT J AU FITZAKERLEY, JL MCGEE, J WALSH, EJ AF FITZAKERLEY, JL MCGEE, J WALSH, EJ TI RESPONSES OF PERIPHERAL AUDITORY NEURONS TO 2-TONE STIMULI DURING DEVELOPMENT .1. CORRELATION WITH FREQUENCY-SELECTIVITY SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; AUDITORY NERVE; COCHLEAR NUCLEAR COMPLEX; 2-TONE SUPPRESSION ID COCHLEAR-NERVE-FIBERS; 2-TONE RATE SUPPRESSION; HAIR CELL LESIONS; GUINEA-PIG; POSTNATAL-DEVELOPMENT; MAMMALIAN COCHLEA; TUNING CURVES; CAT; INTENSITY; NUCLEUS AB The responses of peripheral auditory neurons to two-tone stimuli were used to inferentially examine the nature of cochlear processing during development. Rate suppression was not seen in the youngest animals, and was first observed at 77 gestational days, in units exhibiting adultlike frequency selectivity. Suppression was highly correlated with the degree of tuning, and neurons were segregated into three classes based on these responses. Broadly tuned neurons (type Ig) with low characteristic frequencies (CFs) did not exhibit suppression, and were observed early in postnatal life. Sharply tuned, but still immature neurons (type I,) exhibited suppression, but to a lesser degree than mature neurons (type M). One interpretation of these results is that basilar membrane mechanics are linear during the final stages of cochlear development, indicating that the immature signal transduction process is fundamentally different from that of adults. C1 CREIGHTON UNIV,DEPT PHYSIOL,OMAHA,NE 68131. BOYS TOWN NATL RES HOSP,OMAHA,NE 68131. CR CHEATHAM MA, 1992, HEARING RES, V60, P1, DOI 10.1016/0378-5955(92)90052-O DALLOS P, 1988, AUDITORY FUNCTION NE, P153 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 DELGUTTE B, 1988, BASIC ISSUES HEARING, P204 DELGUTTE B, 1990, HEARING RES, V49, P225, DOI 10.1016/0378-5955(90)90106-Y DOLAN DF, 1985, J ACOUST SOC AM, V78, P544, DOI 10.1121/1.392421 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 FITZAKERLEY J L, 1991, Society for Neuroscience Abstracts, V17, P304 FITZAKERLEY JL, 1994, HEARING RES, V77, P135, DOI 10.1016/0378-5955(94)90261-5 FITZAKERLEY JL, 1992, THESIS CREIGHTON U FITZAKERLEY JL, 1994, HEARING RES, V77, P162, DOI 10.1016/0378-5955(94)90263-1 GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 GREEN DM, 1966, SIGNAL DETECTION THE GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 GREENWOOD DD, 1976, J ACOUST SOC AM, V59, P607, DOI 10.1121/1.380906 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 HOLTON T, 1980, HEARING RES, V2, P21, DOI 10.1016/0378-5955(80)90014-3 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIM DO, 1990, J ACOUST SOC AM, V87, P1648, DOI 10.1121/1.399412 KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 Larsell O, 1944, ARCHIV OTOLARYNGOL, V40, P233 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 LIM DJ, 1977, INNER EAR BIOL, P47 LIPPE W, 1985, J COMP NEUROL, V237, P273, DOI 10.1002/cne.902370211 MILLER MI, 1987, J ACOUST SOC AM, V81, P665, DOI 10.1121/1.394835 MILLS JH, 1983, HEARING RES THEORY, V2, P233 MOTT JB, 1990, J ACOUST SOC AM, V88, P2682, DOI 10.1121/1.399987 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W OHLEMILLER KK, 1990, J COMP PHYSIOL A, V167, P329 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 PFEIFFER RR, 1966, SCIENCE, V154, P667, DOI 10.1126/science.154.3749.667 PRIJS VF, 1989, HEARING RES, V42, P73, DOI 10.1016/0378-5955(89)90118-4 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 ROBERTSON D, 1981, J ACOUST SOC AM, V69, P1096, DOI 10.1121/1.385689 ROMAND R, 1983, NEUROSCI LETT, V35, P271, DOI 10.1016/0304-3940(83)90329-4 ROSE JE, 1974, J NEUROPHYSIOL, V37, P218 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBSAMEN R, 1992, J COMP PHYSIOL A, V170, P129 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SINEX DG, 1986, J NEUROPHYSIOL, V56, P1763 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 TASAKI I, 1954, J NEUROPHYSIOL, V17, P97 TEICH MC, 1985, J ACOUST SOC AM, V77, P1110, DOI 10.1121/1.392176 VIEMEISTER NF, 1988, HEARING RES, V34, P267, DOI 10.1016/0378-5955(88)90007-X WALSH EJ, 1988, HEARING RES, V36, P97 WALSH EJ, 1990, AM J OTOLARYNG, V11, P23, DOI 10.1016/0196-0709(90)90166-S WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 Walsh Edward J., 1992, P161 WALSH EJ, 1990, J NEUROPHYSIOL, V64, P961 WEISS TF, 1978, EVOKED ELECTRICAL AC, P91 WINTER IM, 1991, J ACOUST SOC AM, V90, P1958, DOI 10.1121/1.401675 YATES GK, 1992, TRENDS NEUROSCI, V15, P57, DOI 10.1016/0166-2236(92)90027-6 YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 NR 67 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 135 EP 149 DI 10.1016/0378-5955(94)90261-5 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500014 PM 7928725 ER PT J AU FITZAKERLEY, JL MCGEE, J WALSH, EJ AF FITZAKERLEY, JL MCGEE, J WALSH, EJ TI RESPONSES OF PERIPHERAL AUDITORY NEURONS TO 2-TONE STIMULI DURING DEVELOPMENT .2. FACTORS RELATED TO NEURAL RESPONSIVENESS SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; AUDITORY NERVE; COCHLEAR NUCLEAR COMPLEX; 2-TONE SUPPRESSION ID COCHLEAR NERVE-FIBERS; 2-TONE RATE SUPPRESSION; LOW-FREQUENCY TONES; OUTER HAIR-CELLS; BASILAR-MEMBRANE NONLINEARITY; GUINEA-PIG; POSTNATAL-DEVELOPMENT; TUNING CURVES; INTENSITY FUNCTIONS; MAMMALIAN COCHLEA AB In an accompanying paper (Fitzakerley et al., 1994), it was demonstrated that there is a significant developmental correlation between the appearance of tuning and two-tone suppression. However, it was also found that some sharply tuned neurons meeting minimal adult standards did not exhibit suppression. Therefore, in order to investigate other factors that may be related to the demonstration of suppression in peripheral auditory neurons, the relationship of two-tone suppression with various parameters related to neural responsiveness was studied in perinatal kittens. A positive correlation was made between the observance of suppression and driven discharge rate, characteristic frequency (CF), and threshold, all properties which change significantly during the final stages of cochlear differentiation. In older animals, suppression was also observed in higher percentages of neurons having low spontaneous rates (< 1 spk/s). Suppression was evoked less often by test tones placed below CF than above CF in neurons recorded from younger animals, and was generally produced by a narrower range of test tone intensities than those recorded from adults. As a result, the conventional description of suppression as observed in peripheral auditory neurons in mature animals must be extended to include these factors when responses of immature neurons are considered. C1 CREIGHTON UNIV,BOYS TOWN NATL RES HOSP,DEPT PHYSIOL,OMAHA,NE 68131. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 Barbary A. E., 1991, Hearing Research, V54, DOI 10.1016/0378-5955(91)90139-Z CARLIER E, 1978, BRAIN RES, V147, P174, DOI 10.1016/0006-8993(78)90784-9 CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 CHEATHAM MA, 1992, HEARING RES, V60, P1, DOI 10.1016/0378-5955(92)90052-O COSTALUPES JA, 1987, HEARING RES, V26, P155, DOI 10.1016/0378-5955(87)90107-9 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 DELGUTTE B, 1990, HEARING RES, V49, P225, DOI 10.1016/0378-5955(90)90106-Y DOLAN DF, 1985, J ACOUST SOC AM, V78, P544, DOI 10.1121/1.392421 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 FITZAKERLEY JL, 1994, HEARING RES, V77, P135, DOI 10.1016/0378-5955(94)90261-5 FITZAKERLEY JL, 1992, THESIS CREIGHTON U GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 GREENWOOD DD, 1976, J ACOUST SOC AM, V59, P607, DOI 10.1121/1.380906 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HE ZZ, 1993, ABSTR ASS RES OT, P25 HILL KG, 1991, HEARING RES, V55, P167, DOI 10.1016/0378-5955(91)90101-E JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 KETTNER RE, 1985, J NEUROSCI, V5, P275 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 MILLS JH, 1983, HEARING RES THEORY, V2, P233 MOORE DR, 1981, EXP BRAIN RES, V41, P301 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 OHLEMILLER KK, 1990, J COMP PHYSIOL A, V167, P329 OHLEMILLER KK, 1991, J ACOUST SOC AM, V90, P274, DOI 10.1121/1.401298 PATUZZI R, 1984, HEARING RES, V13, P9, DOI 10.1016/0378-5955(84)90090-X PATUZZI R, 1984, HEARING RES, V13, P19, DOI 10.1016/0378-5955(84)90091-1 PRIJS VF, 1989, HEARING RES, V42, P73, DOI 10.1016/0378-5955(89)90118-4 PUJOL R, 1991, HEARING RES, V57, P129, DOI 10.1016/0378-5955(91)90082-K ROBERTSON D, 1991, HEARING RES, V51, P29, DOI 10.1016/0378-5955(91)90004-S ROBERTSON D, 1981, J ACOUST SOC AM, V69, P1096, DOI 10.1121/1.385689 Robles L., 1986, Lecture Notes in Biomathematics, V64, P121 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 ROMAND R, 1983, DEV AUDITORY VESTIBU ROMAND R, 1979, BRAIN RES, V173, P554, DOI 10.1016/0006-8993(79)90251-8 ROMAND R, 1983, NEUROSCI LETT, V35, P271, DOI 10.1016/0304-3940(83)90329-4 ROMAND R, 1984, EXP BRAIN RES, V56, P395 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1976, J ACOUST SOC AM, V60, P1157, DOI 10.1121/1.381218 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SINEX DG, 1986, J NEUROPHYSIOL, V56, P1763 SOKOLOWSKI BHA, 1989, HEARING RES, V41, P115, DOI 10.1016/0378-5955(89)90005-1 TEICH MC, 1985, J ACOUST SOC AM, V77, P1110, DOI 10.1121/1.392176 WALSH EJ, 1987, HEARING RES, V28, P97, DOI 10.1016/0378-5955(87)90157-2 WALSH EJ, 1990, AM J OTOLARYNG, V11, P23, DOI 10.1016/0196-0709(90)90166-S WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 WALSH E J, 1989, Society for Neuroscience Abstracts, V15, P744 Walsh Edward J., 1992, P161 WALSH EJ, 1990, J NEUROPHYSIOL, V64, P961 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M YATES GK, 1991, HEARING RES, V57, P57, DOI 10.1016/0378-5955(91)90074-J YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 NR 65 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 15 PY 1994 VL 77 IS 1-2 BP 150 EP 161 DI 10.1016/0378-5955(94)90262-3 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500015 PM 7928726 ER PT J AU FITZAKERLEY, JL MCGEE, J WALSH, EJ AF FITZAKERLEY, JL MCGEE, J WALSH, EJ TI RESPONSES OF PERIPHERAL AUDITORY NEURONS TO 2-TONE STIMULI DURING DEVELOPMENT .3. RATE FACILITATION SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; AUDITORY NERVE; COCHLEAR NUCLEAR COMPLEX; 2-TONE SUPPRESSION ID COCHLEAR INNERVATION; GOLGI METHOD; GUINEA-PIG; ENHANCEMENT; SUPPRESSION; BOUNDARIES AB Approximately 25% of peripheral auditory neurons having low characteristic frequencies (CFs) and bread tuning, and recorded from immature animals, responded to two-tone stimuli with increases in discharge rate greater than predicted by linear summation of the responses to probe tones (facilitation), in contrast to the two-tone suppression observed in adult animals and in more sharply tuned immature neurons. Facilitation was not seen after 81 gestational days and was not observed when test tones produced a substantial increase in rate when presented alone. The fact that some neural responses were facilitated under conditions of two-tone stimulation during the final stages of cochlear differentiation provides additional evidence that signal transduction is fundamentally different in neonatal kittens than in adults. A linear model of basilar membrane mechanics coupled to nonlinear neural processes is proposed which can account for the production of facilitation. C1 CREIGHTON UNIV,BOYS TOWN NATL RES HOSP,DEPT PHYSIOL,OMAHA,NE 68131. CR FITZAKERLEY J L, 1991, Society for Neuroscience Abstracts, V17, P304 FITZAKERLEY JL, 1994, HEARING RES, V77, P135, DOI 10.1016/0378-5955(94)90261-5 FITZAKERLEY JL, 1994, HEARING RES, V77, P150, DOI 10.1016/0378-5955(94)90262-3 FITZAKERLEY JL, 1992, THESIS CREIGHTON U GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 HENRY KR, 1991, HEARING RES, V56, P197, DOI 10.1016/0378-5955(91)90170-E HENRY KR, 1991, HEARING RES, V56, P239, DOI 10.1016/0378-5955(91)90174-8 MOORE TJ, 1969, J ACOUST SOC AM, V47, P534 MORRISON D, 1975, ACTA OTO-LARYNGOL, V79, P11, DOI 10.3109/00016487509124649 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W NUTTALL AL, 1991, HEARING RES, V51, P235, DOI 10.1016/0378-5955(91)90040-G PERKINS RE, 1975, J COMP NEUROL, V163, P129, DOI 10.1002/cne.901630202 PRIJS VF, 1989, HEARING RES, V42, P73, DOI 10.1016/0378-5955(89)90118-4 PUJOL R, 1985, HEARING RES, V18, P145, DOI 10.1016/0378-5955(85)90006-1 RUBIN H, 1960, J ACOUST SOC AM, V32, P670, DOI 10.1121/1.1908177 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 Spoendlin H., 1978, EVOKED ELECTRICAL AC, P21 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 WALSH EJ, 1990, AM J OTOLARYNG, V11, P23, DOI 10.1016/0196-0709(90)90166-S WALSH EJ, 1993, J NEUROPHYSIOL, V69, P201 WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 NR 23 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 162 EP 167 DI 10.1016/0378-5955(94)90263-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500016 PM 7928727 ER PT J AU CHEN, KJ WALLER, HJ GODFREY, DA AF CHEN, KJ WALLER, HJ GODFREY, DA TI CHOLINERGIC MODULATION OF SPONTANEOUS ACTIVITY IN RAT DORSAL COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE AUDITORY; BRAIN SLICE; CARBACHOL; MUSCARINE; NICOTINE; ATROPINE ID ISOLATED NERVE-TERMINALS; SINGLE UNIT-ACTIVITY; ACETYLCHOLINE-RELEASE; AUTORADIOGRAPHIC LOCALIZATION; ACETYLTRANSFERASE ACTIVITY; ALPHA-BUNGAROTOXIN; STRIATAL SLICES; GUINEA-PIG; INVITRO; RECEPTORS AB Extracellular recordings were made from brain stem slices to test the effects of bath application of cholinergic agonists and antagonists on the firing rates of spontaneously active dorsal cochlear nucleus neurons. About 90% of neurons responded to carbachol. A higher proportion responded to muscarine than to nicotine. Muscarine elicited larger responses at lower concentrations than nicotine. Responses to either carbachol or muscarine were always blocked by atropine or scopolamine. The nicotinic antagonists d-tubocurarine, hexamethonium, and mecamylamine blocked the responses to nicotine, but did not decrease the responses to carbachol. Regularly firing neurons showed only increases of firing rate during exposure to cholinergic agonists. About half of responsive bursting neurons showed increased firing; half showed increased followed by decreased firing to 10 mu M carbachol or muscarine. All phases of the responses of most bursting neurons were greatly decreased or abolished in low calcium, high magnesium medium, while responses of regular neurons were not detectably affected. Thus, cholinergic agonists appear to act directly on regularly firing neurons, while their actions on bursting neurons may require synaptic activity. The data suggest that cholinergic transmission in the dorsal cochlear nucleus is predominantly muscarinic, and that most regularly firing spontaneously active neurons have muscarinic receptors. C1 MED COLL OHIO,DEPT NEUROL SURG,TOLEDO,OH 43699. RP CHEN, KJ (reprint author), MED COLL OHIO,DEPT OTOLARYNGOL,POB 10008,TOLEDO,OH 43699, USA. CR ARIMATSU Y, 1981, J COMP NEUROL, V198, P603, DOI 10.1002/cne.901980405 AUGUSTINE GJ, 1987, ANNU REV NEUROSCI, V10, P633 BENSON DM, 1988, J PHYSIOL-LONDON, V404, P479 BLEDSOE S C JR, 1983, Comparative Biochemistry and Physiology C Pharmacology Toxicology and Endocrinology, V75, P199, DOI 10.1016/0742-8413(83)90180-9 CASPARY DM, 1983, EXP NEUROL, V82, P491, DOI 10.1016/0014-4886(83)90419-3 CHEN K, 1994, ABSTR ASS RES OT, V12 CHEN K, 1994, ABSTR ASS RES OT, V13 CHESSELET MF, 1984, NEUROSCIENCE, V12, P347, DOI 10.1016/0306-4522(84)90058-7 COMIS SD, 1968, J NEUROPHYSIOL, V31, P62 COMIS SD, 1970, J PHYSIOL-LONDON, V210, P751 CURTIS DR, 1960, J PHYSIOL-LONDON, V153, P17 DESARNO P, 1989, J NEUROSCI RES, V22, P194, DOI 10.1002/jnr.490220213 DEUTSCH SI, 1990, NEUROSCI LETT, V118, P124, DOI 10.1016/0304-3940(90)90264-A DOLEZAL V, 1990, J PHARMACOL EXP THER, V252, P739 DOLEZAL V, 1990, NEUROCHEM RES, V15, P41, DOI 10.1007/BF00969182 EDMONDS B, 1990, SCIENCE, V250, P1142, DOI 10.1126/science.2174573 FROSTHOLM A, 1986, BRAIN RES BULL, V16, P189, DOI 10.1016/0361-9230(86)90033-X GODFREY DA, 1987, HEARING RES, V28, P253, DOI 10.1016/0378-5955(87)90053-0 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 GODFREY DA, 1993, MAMMALIAN COCHLEAR N, P267 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 GONZALES RA, 1993, J PHARMACOL EXP THER, V264, P282 HAAS HL, 1979, J NEUROSCI METH, V1, P323, DOI 10.1016/0165-0270(79)90021-9 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P535 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 HUNT S, 1978, BRAIN RES, V157, P213, DOI 10.1016/0006-8993(78)90025-2 HUSSAIN S, 1991, NEUROPHARMACOLOGY, V30, P1029, DOI 10.1016/0028-3908(91)90130-4 INOKUCHI H, 1992, CAN J PHYSIOL PHARM, V70, pS92 KAUPPINEN RA, 1988, NEUROSCIENCE, V27, P175, DOI 10.1016/0306-4522(88)90228-X Kelly JS, 1985, NEUROTRANSMITTER ACT, P143 KIANG NYS, 1965, ANN OTO RHINOL LARYN, V74, P463 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 MADISON DV, 1987, J NEUROSCI, V7, P733 MANIS PB, 1993, MAMMALIAN COCHLEAR N, P361 MARTIN MR, 1979, NEUROSCIENCE, V4, P1097, DOI 10.1016/0306-4522(79)90191-X MATTHEWS JC, 1983, BIOCHEM PHARMACOL, V32, P455, DOI 10.1016/0006-2952(83)90523-3 MCDONALD DM, 1971, BRAIN RES, V28, P1, DOI 10.1016/0006-8993(71)90520-8 MORLEY BJ, 1977, BRAIN RES, V134, P161, DOI 10.1016/0006-8993(77)90935-0 NICHOLLS DG, 1989, J NEUROCHEM, V52, P331, DOI 10.1111/j.1471-4159.1989.tb09126.x NOGRADY T, 1986, COMP BIOCHEM PHYS C, V83, P339, DOI 10.1016/0742-8413(86)90133-7 NORDSTROM O, 1980, ACTA PHYSIOL SCAND, V108, P347, DOI 10.1111/j.1748-1716.1980.tb06543.x OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 OSEN KK, 1969, BRAIN RES, V16, P165, DOI 10.1016/0006-8993(69)90092-4 PICKLES JO, 1973, J NEUROPHYSIOL, V36, P1131 PONTZER NJ, 1990, J PHARMACOL EXP THER, V253, P921 POTTER LT, 1970, J PHYSIOL-LONDON, V206, P145 Rasmussen G.L., 1960, NEURAL MECHANISMS AU, P105 SCHURR A, 1989, EXPERIENTIA, V45, P684, DOI 10.1007/BF01974560 STRAHLENDORF JC, 1989, NEUROSCIENCE, V30, P117, DOI 10.1016/0306-4522(89)90358-8 SUZUKI T, 1988, NEUROSCI LETT, V84, P209, DOI 10.1016/0304-3940(88)90409-0 TAYLOR P, 1985, GOODMAN GILMANS PHAR, P222 TAYLOR P, 1985, GOODMAN GILMANS PHAR, P100 TAYLOR P, 1985, GOODMAN GILMANS PHAR, P215 VETTER DE, 1993, MAMMALIAN COCHLEAR N, P279 WALLER HJ, 1994, J NEUROPHYSIOL, V71, P467 WAMSLEY JK, 1981, J NEUROSCI, V1, P176 WEINER N, 1985, GOODMAN GILMANS PHAR, P130 WHIPPLE MR, 1984, J NEUROCHEM, V43, P192, DOI 10.1111/j.1471-4159.1984.tb06696.x ZHANG S, 1993, J NEUROPHYSIOL, V69, P1384 NR 61 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 168 EP 176 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500017 PM 7928728 ER PT J AU CAZALS, Y WU, ZY HORNER, K AF CAZALS, Y WU, ZY HORNER, K TI ALTERATIONS OF AUDITORY-NERVE RESPONSES BY HYPOXIA IN NORMAL AND HYDROPIC EARS OF AWAKE GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE POTENTIAL; HYPOXIA; COCHLEA; ENDOLYMPHATIC HYDROPS ID STRIA VASCULARIS; ENDOLYMPHATIC HYDROPS; THRESHOLD SHIFTS; CARBON-MONOXIDE; OTOTOXICITY; NOISE AB Total interruption of blood or oxygen supply to the inner ear produces very rapid and drastic effects, whereas moderate decreases can be well tolerated by normal ears. In experimental endolymphatic hydrops some moderate alterations of cochlear vasculatures have been described which might affect cochlear adaptation to moderate blood or oxygen deficiencies. In order to test this hypothesis an hypoxia at 5% oxygen was imposed for 30 min in normal and hydropic ears of awake guinea pigs and cochlear function was monitored with an electrode at the round window. Electrophysiological recordings used measures of compound action potential (CAP) amplitudes evoked by high-intensity tones, and of CAP thresholds. In normal ears hypoxia induced threshold elevations at all frequencies and decreases of CAP amplitude only for high frequencies. Hydropic ears presented similar or smaller threshold elevations but showed CAP amplitude decreases extending to lower frequencies and showed a much slower recovery both for CAP thresholds and amplitudes. The data indicate that hypoxia had different effects on auditory nerve responses evoked by high versus low intensity tones. The deleterious effects of hypoxia were increased in hydropic ears. Hypoxia-induced alterations were measured twice at one week intervals during which an anti-ischemic drug was administered to the animals; some beneficial effects of the drug treatment were observed on normal but not on hydropic ears. RP CAZALS, Y (reprint author), UNIV BORDEAUX 2,HOP PELLEGRIN,INSERM,U229,AUDIOL EXPTL LAB,F-33076 BORDEAUX,FRANCE. CR ALBERS FWJ, 1987, ACTA OTO-LARYNGOL, V104, P202, DOI 10.3109/00016488709107319 Aubert A, 1990, Ann Otolaryngol Chir Cervicofac, V107 Suppl 1, P28 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P40, DOI 10.3109/00016488009131696 CAZAIS Y, 1988, BASIC ISSUES HEARING, P457 CAZALS Y, 1992, ADV GINGKO BILOBA EX, V2, P115 CAZALS Y, 1988, HEARING RES, V36, P89, DOI 10.1016/0378-5955(88)90139-6 DENGERINK HA, 1984, ACTA OTO-LARYNGOL, V98, P81, DOI 10.3109/00016488409107537 DIDIER A, 1993, HEARING RES, V69, P199, DOI 10.1016/0378-5955(93)90108-D 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 FORGE A, 1987, HEARING RES, V31, P253, DOI 10.1016/0378-5955(87)90195-X Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HORNER KC, 1988, HEARING RES, V32, P41, DOI 10.1016/0378-5955(88)90145-1 HORNER KC, 1990, HEARING RES, V48, P281, DOI 10.1016/0378-5955(90)90068-Z HORNER KC, 1993, SCANNING MICROSCOPY, V7, P223 HORNER KC, 1993, HEARING RES, V68, P1, DOI 10.1016/0378-5955(93)90059-A HULCRANTZ E, 1982, ACTA OTOLARYNGOL, V94, P439 KIMURA RS, 1967, ANN OTO RHINOL LARYN, V76, P664 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 LABRID C, 1988, ARCH OTOLARYNG S DEC, P64 LAWRENCE M, 1977, ACTA OTO-LARYNGOL, V83, P146, DOI 10.3109/00016487709128825 MILLER JM, 1988, AM J OTOLARYNG, V9, P302, DOI 10.1016/S0196-0709(88)80038-3 MISRAHY GA, 1958, J ACOUST SOC AM, V30, P701, DOI 10.1121/1.1909734 NUTTALL AL, 1988, AM J OTOLARYNG, V9, P291, DOI 10.1016/S0196-0709(88)80037-1 PUEL LJ, 1992, ADV BIOSCI, V83, P589 YOUNG JS, 1987, HEARING RES, V26, P27 1992, SIGMASTAT PACKAGE NR 27 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 177 EP 182 DI 10.1016/0378-5955(94)90265-8 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500018 PM 7928729 ER PT J AU MILLS, DM RUBEL, EW AF MILLS, DM RUBEL, EW TI VARIATION OF DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS WITH FUROSEMIDE INJECTION SO HEARING RESEARCH LA English DT Article DE DISTORTION PRODUCT OTOACOUSTIC EMISSIONS; FUROSEMIDE; ACTIVE COCHLEAR MECHANICS; ENDOCOCHLEAR POTENTIAL; GERBIL ID 2 DISCRETE SOURCES; OUTER HAIR-CELLS; ACOUSTIC-DISTORTION; PHYSIOLOGICAL VULNERABILITY; COCHLEAR AMPLIFIER; BASILAR-MEMBRANE; MUTANT MICE; GUINEA-PIG; EAR; 2F1-F2 AB Cochlear function was monitored in adult gerbils using distortion product otoacoustic emissions (DPOAE) during intraperitoneal injection of furosemide. All stimulus parameters were varied independently over a wide range, the stimulus frequencies f(1) and f(2) from 1 to 16 kHz, and the stimulus levels L(1) and L(2) from 20 to 80 dB SPL. The observed emissions at 2f(1) - f(2) and 3f(1) - 2f(2) could be considered to be made up of two distinct components: (1) an 'active' source which depended in a complex way on the stimulus frequencies and levels, which was dominant at low and moderate stimulus levels, and which, by definition, was eliminated by sufficient furosemide intoxication; and (2) a 'passive' source which was essentially the same at all frequencies, with a level dependence given approximately by a simple power law distribution. The change from the active to the passive source was usually accompanied by an abrupt shift in emission phase angle. A simple summation model was shown to account for the observed form of this transition. The amount of the decrease in 2f(1) - f(2) emission amplitude after furosemide injection was approximately independent of frequency and consistent for the middle frequency ratios and intensity levels (f(2)/f(1) congruent to 1.3, L(1) x L(2) congruent to 55 x 50 dB SPL). It was concluded that the combination of DPOAE with furosemide injection can usefully be employed as a probe of active cochlear mechanics. C1 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,SEATTLE,WA 98195. CR ALLEN JB, 1992, J ACOUST SOC AM, V92, P178, DOI 10.1121/1.404281 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 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 AVAN P, 1992, HEARING RES, V59, P59, DOI 10.1016/0378-5955(92)90102-S 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 BROWN AM, 1990, MECH BIOPHYSICS HEAR, P164 BROWN AM, 1993, P INT S BIOPH HAIR C, P72 DALLOS P, 1992, J NEUROSCI, V12, P4575 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P409 Forge A, 1982, Br J Audiol, V16, P109, DOI 10.3109/03005368209081455 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 Henley C, 1989, HEARING RES, V43, P141 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUBBARD AE, 1990, HEARING RES, V43, P269, DOI 10.1016/0378-5955(90)90234-G JOHNSTONE BM, 1990, ADV AUDIOL, V7, P57 KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 LENOIR M, 1987, HEARING RES, V29, P265, DOI 10.1016/0378-5955(87)90173-0 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, 1990, ANN OTO RHINOL S147, V99, P3 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, 1993, 16TH MIDW M ASS RES, P79 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W NORTON SJ, 1990, MECH BIOPHYSICS HEAR, P219 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 RUBEL EW, 1991, 14TH MIDW RES M ASS, P84 RUBSAMEN R, 1994, UNPUB J NEUROPHYS RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 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 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 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, 1990, MECH BIOPHYSICS HEAR, P243 WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 NR 42 TC 97 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 183 EP 199 DI 10.1016/0378-5955(94)90266-6 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500019 PM 7928730 ER PT J AU REN, TY BRECHTELSBAUER, PB MILLER, JM NUTTALL, AL AF REN, TY BRECHTELSBAUER, PB MILLER, JM NUTTALL, AL TI COCHLEAR BLOOD-FLOW MEASURED BY AVERAGED LASER-DOPPLER FLOWMETRY (ALDF) SO HEARING RESEARCH LA English DT Article DE MICROCIRCULATION; COCHLEAR BLOOD FLOW; LASER DOPPLER FLOWMETRY; SIGNAL AVERAGING; PULSE BLOOD FLOW; PULSE BLOOD PRESSURE ID GUINEA-PIG; MICROCIRCULATION; GANGLION; VELOCIMETRY; STIMULATION; MODEL AB This report describes a new approach to estimate the hydromechanical properties of a vascular system. Averaged laser Doppler flowmetry (ALDF) was developed by averaging the flux signal of a laser Doppler flowmeter (LDF) synchronized to the heart cycle. The usefulness of this method was verified by manipulation of the cochlear microvasculature. Twelve pigmented guinea pigs under pentobarbital/fentanyl anesthesia were used. The cochlea was surgically exposed and the LDF probe placed on the bony surface of the first turn to monitor cochlear blood flow (CBF). The LDF flux signal (0.2 s time constant) was sampled by an A/D board at 2 kHz for 255 ms and averaged with synchronization to the heart bent. The mean blood flow, peak to peak amplitude, and time (phase) delay of pulsatile flow were measured from the averaged signal. According to a transmission line model of the vascular system, under a given perfusion pressure, mean flow reflects resistance while amplitude and time delay of the pulsatile flow are related to the reactance component of the impedance of the vascular system. During the formation of photochemically-induced thrombosis in the cochlear microvasculature, there was a dramatic mean flux decrease (90.1 +/- 3.4% from baseline (BL), N = 6). Additionally, a time-dependent decrease in amplitude and time delay of pulsatile flow were indicated by ALDF. These results suggest a large increase in vascular resistance and significant decrease in compliance. After application of 2% sodium nitroprusside (NP) to the round window membrane, mean flux increased by 78.3 +/- 17.6% BL; amplitude and time delay of pulsate blood flow increased by 81.0 +/- 14.6% (N = 6) and 11.5 +/- 3.2 ms (N = 6), respectively. These changes can be interpreted as lowered resistance and increased compliance consistent with vasodilatation by NP. ALDF is a new method which derives additional information from the LDF signal. The new information provided by ALDF can be of importance in assessment of basic cochlear microcirculation and interpretation of peripheral vascular diseases in the cochlea and other organs. C1 UNIV MICHIGAN,SCH MED,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. XIAN MED UNIV,DEPT OTOLARYNGOL,XIAN,PEOPLES R CHINA. CR DRUCE HM, 1984, J APPL PHYSIOL, V57, P1276 GRAAF JC, 1992, CIRCULATION, V85, P2284 HABERL RL, 1989, AM J PHYSIOL, V256, pH1247 HELLEM S, 1983, INT J ORAL MAXILLOF, V12, P165, DOI 10.1016/S0300-9785(83)80063-5 JOHNSON JM, 1984, J APPL PHYSIOL, V56, P798 LAURIKAINEN EA, 1993, HEARING RES, V64, P199, DOI 10.1016/0378-5955(93)90006-M LAURIKAINEN EA, 1993, AM J OTOL, V14, P24 LIPOWSKY HH, 1977, MICROVASC RES, V14, P345, DOI 10.1016/0026-2862(77)90030-9 MCILROY MB, 1986, CARDIOVASC RES, V20, P581, DOI 10.1093/cvr/20.8.581 MILLER JM, 1990, LASER DOPPLER FLOWME, P319 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 OHLSEN KA, 1991, CIRC RES, V69, P509 QUIRK WS, 1988, HEARING RES, V33, P129, DOI 10.1016/0378-5955(88)90025-1 REN TY, 1993, ACTA OTO-LARYNGOL, V113, P609, DOI 10.3109/00016489309135872 REN TY, 1991, J XIAN MED U, V12, P408 REN TY, 1993, ACTA OTO-LARYNGOL, V113, P146, DOI 10.3109/00016489309135783 REN TY, 1993, ANN OTO RHINOL LARYN, V102, P378 REN TY, 1993, HEARING RES, V71, P91, DOI 10.1016/0378-5955(93)90024-U RIVA CE, 1990, LASER DOPPLER BLOOD, P349 ROMAN RJ, 1986, AM J PHYSIOL, V251, pF115 SHEPHERD AP, 1982, AM J PHYSIOL, V242, pG668 SILLMAN JS, 1989, OTOLARYNG HEAD NECK, V100, P308 SUGA F, 1969, LARYNGOSCOPE, V79, P1956, DOI 10.1288/00005537-196911000-00008 TAYLOR MG, 1959, PHYS MED BIOL, V4, P3 Tyml K., 1990, LASER DOPPLER BLOOD, P215 UMEMURA K, 1990, EUR ARCH OTO-RHINO-L, V248, P105 WOMERSLEY JR, 1957, PHYS MED BIOL, V2, P178, DOI 10.1088/0031-9155/2/2/305 NR 27 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 15 PY 1994 VL 77 IS 1-2 BP 200 EP 206 DI 10.1016/0378-5955(94)90267-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500020 PM 7928732 ER PT J AU JAEGER, RG FEX, J KACHAR, B AF JAEGER, RG FEX, J KACHAR, B TI STRUCTURAL BASIS FOR MECHANICAL TRANSDUCTION IN THE FROG VESTIBULAR SENSORY APPARATUS .2. THE ROLE OF MICROTUBULES IN THE ORGANIZATION OF THE CUTICULAR PLATE SO HEARING RESEARCH LA English DT Article DE MICROTUBULES; MICROTUBULE-ASSOCIATED PROTEINS; CUTICULAR PLATE; MECHANICAL TRANSDUCTION; VESTIBULAR SENSORY MACULA; FROG VESTIBULAR SENSORY ORGAN ID COCHLEAR HAIR-CELLS; ACTIN-FILAMENTS; INNER-EAR; MECHANOELECTRICAL TRANSDUCTION; IMMUNOELECTRON MICROSCOPY; MOLECULAR-STRUCTURE; BIRD COCHLEA; STEREOCILIA; CYTOSKELETAL; MOTILITY AB The actin matrix of the cuticular plate, which supports the sensory stereocilia bundle, is coupled to the axial cytoskeleton of the hair cell through a well defined microtubule columnar framework. A collection of axial microtubules in a columnar organization penetrate deep into the dense actin matrix of the cuticular plate. Each microtubule displays at the end a 300-500 nm long fuzzy cap that enmeshes with the actin matrix of the cuticular plate. The microtubule associated proteins MAP-1A and MAP-1B were localized by confocal immunofluorescence to the point of microtubule insertion in the cuticular plate. These proteins are likely components of the microtubule capping structure and may mediate the interaction of the microtubules with the actin matrix. The structural interaction of the microtubules with the cuticular plate provides important mechanical coupling of the transduction apparatus to the axial cytoskeleton of the hair cell. C1 NIDCD,CELLULAR BIOL LAB,STRUCT CELL BIOL SECT,ROCKVILLE,MD 20850. NIDCD,MOLEC BIOL LAB,ROCKVILLE,MD 20850. RI Jaeger, Ruy/G-8230-2011 CR ALLEN RD, 1985, J CELL BIOL, V100, P1736, DOI 10.1083/jcb.100.5.1736 Bajer A. S., 1972, INT REV CYTOL S, V3, P1 BEHNKE O, 1970, J ULTRA MOL STRUCT R, V31, P61, DOI 10.1016/S0022-5320(70)90145-0 BRAY D., 1992, CELL MOVEMENTS DRENCKHAHN D, 1988, J CELL BIOL, V107, P1037, DOI 10.1083/jcb.107.3.1037 EVANS BN, 1993, P NATL ACAD SCI USA, V90, P8347, DOI 10.1073/pnas.90.18.8347 FAVRE D, 1983, ACTA OTO-LARYNGOL, V96, P15, DOI 10.3109/00016488309132870 FLOCK A, 1981, J NEUROCYTOL, V10, P133, DOI 10.1007/BF01181749 FLOCK A, 1981, ARCH OTO-RHINO-LARYN, V233, P55, DOI 10.1007/BF00464275 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FREED JJ, 1970, J CELL BIOL, V45, P334, DOI 10.1083/jcb.45.2.334 FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 GOLDSTEIN LSB, 1992, NATURE, V359, P193, DOI 10.1038/359193a0 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HUDSPETH AJ, 1983, ANNU REV NEUROSCI, V6, P187, DOI 10.1146/annurev.ne.06.030183.001155 INOUE S, 1967, J GEN PHYSIOL, V50, P259, DOI 10.1085/jgp.50.6.259 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A LEESMILLER JP, 1992, NATURE, V359, P244, DOI 10.1038/359244a0 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H RAPHAEL Y, 1986, J SUBMICR CYTOL PATH, V18, P731 SATOYOSHITAKE R, 1989, NEURON, V3, P229, DOI 10.1016/0896-6273(89)90036-6 SHIOMURA Y, 1987, J NEUROSCI, V7, P1461 SHIOMURA Y, 1987, J CELL BIOL, V104, P1575, DOI 10.1083/jcb.104.6.1575 SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 SLEPECKY NB, 1992, HEARING RES, V57, P201, DOI 10.1016/0378-5955(92)90152-D STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 TILNEY LG, 1983, J CELL BIOL, V96, P822, DOI 10.1083/jcb.96.3.822 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 TUCKER JB, 1979, MICROTUBULES, P315 VALE RD, 1985, CELL, V42, P39, DOI 10.1016/S0092-8674(85)80099-4 YATES GK, 1992, TRENDS NEUROSCI, V15, P57, DOI 10.1016/0166-2236(92)90027-6 ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1986, NEUROBIOLOGY HEARING, P1 NR 34 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 207 EP 215 DI 10.1016/0378-5955(94)90268-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500021 PM 7928733 ER PT J AU PITOVSKI, DZ DRESCHER, MJ DRESCHER, DG AF PITOVSKI, DZ DRESCHER, MJ DRESCHER, DG TI GLUCOCORTICOID RECEPTORS IN THE MAMMALIAN INNER-EAR - RU-28362 BINDING-SITES SO HEARING RESEARCH LA English DT Article DE GLUCOCORTICOID; RECEPTORS; NA,K-ATPASE; COCHLEA; VESTIBULE ID NA-K-ATPASE; ADRENOCORTICOSTEROID HORMONES; ALDOSTERONE; NA+,K+-ATPASE; MECHANISM; SEGMENTS; INVITRO; ABSENCE; CELLS AB The effects of glucocorticoid hormones are thought to be initiated by binding of the steroid to stereospecific intracellular receptor proteins in target tissues. The synthetic glucocorticoid [H-3]-RU 28362, which demonstrates negligible affinity for mineralocorticoid (Type I) receptors [Philibert et al., (1983) Endocrine Sec. Abstr. 65, 335], was employed to identify the high-affinity glucocorticoid (Type II) receptors in the inner ear. By Scatchard analysis, the K-d of the [H-3]-RU 28362-cytoplasmic receptor complex was 11.4 X 10(-9) M for the lateral wall of the basal turn of the cochlea and 11.7 x 10(-9) M for the ampullae of the semicircular canals. The concentration of binding sites, B-max, was 240 fmol/mg dry tissue for the cochlear specimen and 89 fmol/mg dry tissue for the ampullae. Time course studies indicated that the binding of [H-3]-RU 28362 by inner ear tissues reached equilibrium within 30 min of incubation at 25 degrees C. Based on the total specific binding measured with [H-3]-RU 28362, the glucocorticoid receptor concentration in the lateral wall of the basal turn of the cochlea appears to exceed that in the ampullae of the semicircular canal by a factor of 2.7. Substantial specific [H-3]-RU 28362 binding to the cochlear lateral wail and ampullar tissue suggests the presence of glucocorticoid receptors and sites of glucocorticoid action in the inner ear. C1 WAYNE STATE UNIV,SCH MED,DEPT BIOCHEM,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,BIOOTOL LAB,DETROIT,MI 48201. RP PITOVSKI, DZ (reprint author), WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,540 E CANFIELD AVE,DETROIT,MI 48201, USA. CR BALLARD PL, 1974, ENDOCRINOLOGY, V94, P998 BAXTER JD, 1979, GLUCOCORTICOID HORMO, P16 BIA MJ, 1981, AM J PHYSIOL, V240, pF257 COIRINI H, 1985, BRAIN RES, V361, P212, DOI 10.1016/0006-8993(85)91291-0 FUNDER JW, 1972, ENDOCRINOLOGY, V92, P1005 GARG LC, 1981, AM J PHYSIOL, V240, pF536 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 KUSAKARI J, 1976, LARYNGOSCOPE, V86, P132, DOI 10.1288/00005537-197601000-00025 Luttage W.G., 1983, P247 MARVER D, 1983, MINER ELECTROL METAB, V9, P1 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PHILIBERT D, 1983, P ANN M ENDOCR SOC, V65, P335 PITOVSKI DZ, 1992, ASS RES OT ABSTR, V24, P11 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, 1993, ASS RES OT ABSTR, V24, P11 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 RAYSON BM, 1982, AM J PHYSIOL, V243, pF463 ROUSSEAU G, 1972, J STEROID BIOCHEMIST, V3, P219, DOI 10.1016/0022-4731(72)90053-2 SCATCHARD G, 1949, ANN NY ACAD SCI, V51, P660, DOI 10.1111/j.1749-6632.1949.tb27297.x SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 TENCATE WJF, 1990, ACTA OTO-LARYNGOL, V110, P234 TENCATE WJF, 1991, ACTA OTOLARYNGOL S, V373, P1 NR 26 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 JUN 15 PY 1994 VL 77 IS 1-2 BP 216 EP 220 DI 10.1016/0378-5955(94)90269-0 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500022 PM 7928734 ER PT J AU RAZA, A MILBRANDT, JC ARNERIC, SP CASPARY, DM AF RAZA, A MILBRANDT, JC ARNERIC, SP CASPARY, DM TI AGE-RELATED-CHANGES IN BRAIN-STEM AUDITORY NEUROTRANSMITTERS - MEASURES OF GABA AND ACETYLCHOLINE FUNCTION SO HEARING RESEARCH LA English DT Article DE GABA; GAD; AGING; CENTRAL AUDITORY; INFERIOR COLLICULUS; COCHLEAR NUCLEUS ID INFERIOR COLLICULUS NEURONS; ANTEROVENTRAL COCHLEAR NUCLEUS; CNS STRUCTURAL ELEMENTS; GAMMA-AMINOBUTYRIC ACID; RAT MEDIAL NUCLEUS; CHOLINE-ACETYLTRANSFERASE; LATERAL LEMNISCUS; DORSAL NUCLEUS; RESPONSE PROPERTIES; GABAERGIC PROJECTION AB This study was designed to determine if there are age-related alterations in the bio-synthetic enzyme glutamic acid decarboxylase (GAD), the degradative enzyme GABA-transaminase (GABA-T), and the uptake system for GABA in the central nucleus of the inferior colliculus (CIC), the cochlear nucleus (CN), and/or nuclei of the lateral lemniscus (NLL) of Fischer-344 rats. For purposes of comparison, the cholinergic neuronal system was studied in parallel in young adult (3-7 months), mature (15-17 months) and aged (24-26 months) rats. In young adults GAD activity was highest in the CIC (219 nmol/mg protein/h; N = 5), intermediate in NLL (82 nmol/mg protein/h), and lowest in CN (34 nmol/mg protein/h). Chorine acetyltransferase (ChAT) activity was highest in NLL and CN, and approximately 35-40% lower in CIC. A more uniform pattern was observed with GABA-T activity. Reductions in GAD activity were seen in the CIC of mature (- 31%) and aged (- 30%) rats that were not graded with age when compared to young adult, P < 0.05 (N= 5). This effect was regionally selective, since the CN did not show any loss of GAD or ChAT activity. The neurotransmitter selectivity of this deficit in CIC is supported by the non-parallel changes in ChAT activity (- 22%, aged vs. mature, P < 0.05) that occurred after the changes in GAD activity. In contrast to the loss of GABAergic biosynthetic capacity in aged CIC, high affinity uptake processes (K-d and V-max) for C-14-GABA and H-3-d-aspartate were not significantly altered (P<0.05). Similar to the CIC, the NLL showed remarkable age-related deficits, but these deficits were more substantial for the cholinergic system (ChAT activity: -56% aged vs. young adult, P < 0.05; GAD activity: -35% aged vs. mature). None of the areas examined showed a significant loss of GABA-T activity with aging. These data suggest: 1) Age-related loss of GABA-mediated inhibition in the CIC of Fischer-344 rats is not;attributable to changes in uptake or degradation of GABA, but may be related loss of biosynthetic capacity (i.e. activity or quantity) of the GAD present; 2) processing centers of the central auditory pathway (i.e. CIC and NLL), but not necessarily primary (i.e. CN) integrative nuclei, demonstrate selective, age-related neurochemical deficits; and 3) age-related neurochemical changes in central auditory structures may contribute substantially to the abnormal perception of signals in noise and loss of speech discrimination observed in neural presbycusis. C1 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62702. CR ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 ADAMS JC, 1979, NEUROSCIENCE, V4, P1947, DOI 10.1016/0306-4522(79)90067-8 ARNERIC SP, 1986, BRAIN RES, V374, P153, DOI 10.1016/0006-8993(86)90404-X ARNERIC SP, 1988, BRAIN RES, V454, P11, DOI 10.1016/0006-8993(88)90799-8 BACKOFF PM, 1994, HEARING RES, V73, P163, DOI 10.1016/0378-5955(94)90231-3 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P563, DOI 10.1007/BF00964919 BENTZEN O, 1983, HEARING BALANCE ELDE, P123 Bisso G. M., 1992, Brain Dysfunction, V5, P121 BRINER W, 1989, NEUROBIOL AGING, V10, P295, DOI 10.1016/0197-4580(89)90039-0 BRISTOW DR, 1988, EUR J PHARMACOL, V148, P238 BRODY H, 1955, J COMP NEUROL, V102, P511, DOI 10.1002/cne.901020206 BROWN CH, 1984, EXP AGING RES, V10, P35 CASEY MA, 1985, J COMP NEUROL, V232, P401, DOI 10.1002/cne.902320311 CASEY M A, 1987, Society for Neuroscience Abstracts, V13, P328 CASEY MA, 1982, NEUROBIOL AGING, V3, P187, DOI 10.1016/0197-4580(82)90039-2 CASEY MA, 1990, NEUROBIOL AGING, V11, P391, DOI 10.1016/0197-4580(90)90004-J CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1985, AUDITORY BIOCH, P198 CASPARY DM, 1983, EXP NEUROL, V82, P491, DOI 10.1016/0014-4886(83)90419-3 CHU DCM, 1990, NEUROSCIENCE, V34, P341, DOI 10.1016/0306-4522(90)90144-S CLERICI WJ, 1987, NEUROBIOL AGING, V8, P171, DOI 10.1016/0197-4580(87)90028-5 COLEMAN GL, 1977, J GERONTOL, V32, P258 COMIS SD, 1966, J PHYSL, V183, P22 CONTRERAS NEIR, 1979, EXP BRAIN RES, V36, P573 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 DEBLER EA, 1987, J NEUROCHEM, V48, P1851, DOI 10.1111/j.1471-4159.1987.tb05747.x ERECINSKA M, 1987, BIOCHEM PHARMACOL, V36, P3547, DOI 10.1016/0006-2952(87)90001-3 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 FARLEY GR, 1983, HEARING RES, V11, P73, DOI 10.1016/0378-5955(83)90046-1 FINLAYSON PG, 1990, ASS RES OT ABSTR, V305, P266 FISHER SK, 1976, J NEUROCHEM, V27, P1145, DOI 10.1111/j.1471-4159.1976.tb00321.x FONNUM F, 1975, J NEUROCHEM, V24, P407, DOI 10.1111/j.1471-4159.1975.tb11895.x FONNUM F, 1977, J NEUROCHEM, V29, P221, DOI 10.1111/j.1471-4159.1977.tb09612.x GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GODFREY DA, 1981, J HISTOCHEM CYTOCHEM, V29, P720 GODFREY DA, 1978, J HISTOCHEM CYTOCHEM, V26, P118 GRAY EG, 1962, J ANAT, V96, P79 HANSEN CC, 1965, ARCHIV OTOLARYNGOL, V82, P115 HUNTER C, 1989, BRAIN RES, V482, P247, DOI 10.1016/0006-8993(89)91187-6 INGVAR MC, 1985, BRAIN, V108, P155, DOI 10.1093/brain/108.1.155 JERGER J, 1989, EAR HEARING, V10, P79, DOI 10.1097/00003446-198904000-00001 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 KENDALL DA, 1982, AGING BRAIN CELLULAR KIMURA H, 1981, J COMP NEUROL, V200, P151, DOI 10.1002/cne.902000202 KIRIKAE ICHIRO, 1964, LARYNGOSCOPE, V74, P205 LI L, 1992, J NEUROSCI, V12, P4530 LI L, 1992, HEARING RES, V61, P73, DOI 10.1016/0378-5955(92)90038-O LONDON ED, 1981, J NEUROCHEM, V37, P217, DOI 10.1111/j.1471-4159.1981.tb05311.x MARSHALL L, 1981, J SPEECH HEAR DISORD, V46, P226 McGeer E.G., 1975, NEUROBIOL AGING, P287 MHATRE MC, 1992, MOL BRAIN RES, V14, P71, DOI 10.1016/0169-328X(92)90012-Z MHATRE MC, 1992, MU, V14 MICHALEK H, 1989, NEUROBIOL AGING, V10, P143, DOI 10.1016/0197-4580(89)90023-7 MILBRANDT JC, 1994, ASS RES OT ABSTR, V17, P42 Milbrandt J. C., 1993, Society for Neuroscience Abstracts, V19, P1425 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 MORLEY BJ, 1985, AUDITORY BIOCH, P227 NAGAI T, 1985, J COMP NEUROL, V231, P260, DOI 10.1002/cne.902310213 PALOMBI PS, 1992, J NEUROPHYSIOL, V67, P738 PARK TJ, 1993, J NEUROSCI, V13, P2050 RAZA A, 1989, Society for Neuroscience Abstracts, V15, P1115 READ SM, 1981, ANAL BIOCHEM, V116, P53, DOI 10.1016/0003-2697(81)90321-3 ROBERTS RC, 1987, J NEUROCYTOL, V16, P333, DOI 10.1007/BF01611345 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 SIEGHART W, 1986, J NEUROCHEM, V47, P920 SIMPSON GV, 1985, BRAIN RES, V348, P28, DOI 10.1016/0006-8993(85)90355-5 SOLLEVELD HA, 1984, J NATL CANCER I, V72, P929 STERRI SH, 1978, EUR J BIOCHEM, V91, P215, DOI 10.1111/j.1432-1033.1978.tb20954.x VATER M, 1992, J COMP NEUROL, V325, P183, DOI 10.1002/cne.903250205 VIZI SE, 1978, BRAIN RES BULL, V3, P93, DOI 10.1016/0361-9230(78)90032-1 WAMSLEY JK, 1986, BENZODIAZEPINE GABA, P299 WATANABE T, 1973, JPN J PHYSIOL, V23, P291 WHEELER DD, 1983, EXP GERONTOL, V18, P125, DOI 10.1016/0531-5565(83)90005-0 WHEELER DD, 1982, EXP GERONTOL, V17, P71, DOI 10.1016/0531-5565(82)90010-9 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 J. F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 WILLOTT JF, 1985, J COMP NEUROL, V237, P545, DOI 10.1002/cne.902370410 NR 86 TC 62 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 15 PY 1994 VL 77 IS 1-2 BP 221 EP 230 DI 10.1016/0378-5955(94)90270-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NV015 UT WOS:A1994NV01500023 PM 7928735 ER PT J AU WEAVER, SP SCHWEITZER, L AF WEAVER, SP SCHWEITZER, L TI A RADIAL GRADIENT OF FIBRIL DENSITY IN THE GERBIL TECTORIAL MEMBRANE SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEA; COLLAGEN; GERBIL; TECTORIAL MEMBRANE ID INNER-EAR; MECHANICAL-PROPERTIES; COLLAGEN; IX; ULTRASTRUCTURE; ORGANIZATION; LOCALIZATION; MORPHOLOGY; INVIVO; CELLS AB The tectorial membrane plays a key role in the transduction of mechanical to neural energy in the inner ear. To better understand the transduction process the composition of the tectorial membrane needs to be elucidated. This study was done to determine if Type A collagen fibrils are distributed homogeneously in the tectorial membrane or if there are longitudinal or radial gradients of fibril concentrations. Our results suggest that while there is no longitudinal gradient, there is a radial gradient of fibril concentration, The concentration of fibrils in the limbal (inner) zone of the tectorial membrane exceeds that in the marginal (outer) zone in all cochlear locations examined. This gradient is most marked in the basal, high frequency coding region of the cochlea. While fibril gradients in the tectorial membrane have not been the focus of previous investigations, several findings by other authors support the proposition that the marginal zone of the tectorial membrane is more compliant than the limbal zone. This radial gradient of tectorial membrane stiffness is likely to contribute to the characteristics of movement of the cochlear partition. C1 UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. CR ARIMA T, 1990, HEARING RES, V46, P289, DOI 10.1016/0378-5955(90)90010-M Bekesy G., 1960, EXPT HEARING BROWN AM, 1992, P ROY SOC B-BIOL SCI, V250, P29, DOI 10.1098/rspb.1992.0126 ENGSTROM H., 1958, EXPTL CELL RES SUPPL, V5, P460 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 IURATO S, 1961, Z ZELLFORSCH MIK ANA, V53, P259, DOI 10.1007/BF00339444 IURATO S, 1967, SUBMICROSCOPIC STRUC, P59 JEANLOZ RW, 1976, BIOL ROLES SIALIC AC, P201 JURATO S, 1962, Z ZELLFORSCH, V56, P40 KARNOVSK.MJ, 1965, J CELL BIOL, V27, pA137 Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 LIM D J, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P47 Montes GS, 1984, ULTRASTRUCTURE CONNE, P65 RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 ROSS MD, 1974, AM J ANAT, V139, P449, DOI 10.1002/aja.1001390402 ROTH B, 1992, ANAT EMBRYOL, V185, P559, DOI 10.1007/BF00185615 RUGGERI A, 1984, ULTRASTRUCTURE CONNE, P113 SANTI PA, 1990, J ELECTRON MICR TECH, V15, P293, DOI 10.1002/jemt.1060150308 SLEPECKY NB, 1992, MATRIX, V11, P80 SLEPECKY NB, 1992, ACTA OTO-LARYNGOL, V112, P611, DOI 10.3109/00016489209137449 STEEL KP, 1986, NEUROBIOLOGY HEARING, P139 SUGIYAMA S, 1991, HEARING RES, V55, P263, DOI 10.1016/0378-5955(91)90111-L SUGIYAMA S, 1992, HEARING RES, V58, P35, DOI 10.1016/0378-5955(92)90006-9 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 VANDERREST M, 1988, J BIOL CHEM, V263, P1615 ZWISLOCKI JJ, 1989, HEARING RES, V42, P211, DOI 10.1016/0378-5955(89)90146-9 ZWISLOCKI JJ, 1988, HEARING RES, V33, P207, DOI 10.1016/0378-5955(88)90151-7 ZWISLOCKI JJ, 1988, ACTA OTO-LARYNGOL, V105, P450, DOI 10.3109/00016488809119500 NR 31 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 1 EP 6 DI 10.1016/0378-5955(94)90081-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200001 PM 7928702 ER PT J AU HAFNER, H PRATT, H BLAZER, S SUJOV, P AF HAFNER, H PRATT, H BLAZER, S SUJOV, P TI INTRAUTERINE AND EXTRAUTERINE DEVELOPMENT OF NEONATAL 3-CHANNEL LISSAJOUS TRAJECTORY OF AUDITORY BRAIN-STEM EVOKED-POTENTIALS SO HEARING RESEARCH LA English DT Article DE NEWBORN; AUDITORY BRAIN-STEM; EVOKED POTENTIALS; 3-CHANNEL LISSAJOUS TRAJECTORY; DEVELOPMENT; GESTATIONAL AGE; POSTCONCEPTIONAL AGE; INTRAUTERINE; EXTRAUTERINE ID FULL-TERM INFANTS; STEM RESPONSE; PRETERM INFANTS; PREMATURE-INFANTS; NEWBORN-INFANTS; MATURATION; AGE; ABR AB This study compared intra- and extra-uterine maturation of the auditory pathway, using auditory brainstem evoked potentials (ABEPs), recorded with three orthogonal differential electrode configurations. From the three records of each subject, 3-channel Lissajous' trajectories (3CLTs) were derived and analyzed. 107 newborns were compared at the same gestational and post-conceptional (gestational + postnatal) age, from 29 weeks (wks) up to 43 wks. In addition, we explored the effects and neurophysiological consequences of early exposure to extra-uterine life, on the peripheral and central portions of the auditory pathway. Our findings indicate that exposure of premature infants to the extra-uterine environment is associated with advanced peripheral development, but slower central conduction compared to intra-uterine development. C1 RAMBAM MED CTR,NEONATAL INTENS CARE UNIT,HAIFA,ISRAEL. CR CASHORE WJ, 1984, CLIN PERINATOL, V11, P339 Cohen B A, 1987, Electromyogr Clin Neurophysiol, V27, P469 DESPLAND PA, 1980, PEDIATR RES, V14, P154, DOI 10.1203/00006450-198002000-00018 DUBOWITZ LM, 1970, J PEDIATR-US, V77, P1, DOI 10.1016/S0022-3476(70)80038-5 EGGERMONT JJ, 1988, HEARING RES, V33, P35, DOI 10.1016/0378-5955(88)90019-6 EYRE JA, 1988, BRIT MED BULL, V44, P1076 FAWER CL, 1982, NEUROPEDIATRICS, V13, P200, DOI 10.1055/s-2008-1059623 FERRARI F, 1983, DEV MED CHILD NEUROL, V25, P450 GOLDSTEIN PJ, 1970, AM J OBSTET GYNECOL, V135, P622 HAFNER H, 1993, HEARING RES, V66, P157, DOI 10.1016/0378-5955(93)90137-P HAFNER H, 1991, HEARING RES, V51, P33, DOI 10.1016/0378-5955(91)90005-T HAKAMADA S, 1981, BRAIN DEV-JPN, V3, P339 HENDERSONSMART DJ, 1983, NEW ENGL J MED, V308, P353, DOI 10.1056/NEJM198302173080702 HITNER HM, 1977, J PEDIATR, V91, P455 ISAACSON G, 1986, ATLAS FETAL SECTIONA JEWETT DL, 1987, ELECTROEN CLIN NEURO, V68, P386, DOI 10.1016/0168-5597(87)90020-7 KAGA K, 1986, British Journal of Audiology, V20, P121, DOI 10.3109/03005368609079005 KENDROR A, 1987, ELECTROEN CLIN NEURO, V68, P209, DOI 10.1016/0168-5597(87)90028-1 KILENY P, 1985, J OTOLARYNGOL, V14, P34 KRUMHOLZ A, 1985, ELECTROEN CLIN NEURO, V62, P124, DOI 10.1016/0168-5597(85)90024-3 MARTIN WH, 1986, ELECTROEN CLIN NEURO, V63, P54, DOI 10.1016/0013-4694(86)90062-3 PAQUEREAU J, 1986, AUDIOLOGY, V25, P107 PARMELEE AH, 1975, BIOL PSYCHIAT, V10, P501 PIPER MC, 1989, DEV MED CHILD NEUROL, V31, P591 PRATT H, 1984, ELECTROEN CLIN NEURO, V58, P83, DOI 10.1016/0013-4694(84)90204-9 PRATT H, 1985, ELECTROEN CLIN NEURO, V61, P530, DOI 10.1016/0013-4694(85)90972-1 PRATT H, 1983, ELECTROEN CLIN NEURO, V56, P682, DOI 10.1016/0013-4694(83)90036-6 ROTTEVEEL JJ, 1987, HEARING RES, V26, P21, DOI 10.1016/0378-5955(87)90033-5 SALAMY A, 1984, J CLIN NEUROPHYSIOL, V1, P293, DOI 10.1097/00004691-198407000-00003 Scherg M, 1984, Rev Laryngol Otol Rhinol (Bord), V105, P163 SININGER YS, 1987, ELECTROEN CLIN NEURO, V68, P368, DOI 10.1016/0168-5597(87)90018-9 STARR A, 1977, PEDIATRICS, V60, P831 STEVEN AJ, 1984, INT MED CARE J HOSPI, P9 STEVEN AJ, 1984, INT MED CARE J HOSPI, P83 USHER R, 1969, J PEDIATR-US, V74, P901, DOI 10.1016/S0022-3476(69)80224-6 VOLPE JJ, 1981, NEUROLOGY NEWBORN WILLISTON JS, 1981, BRAIN RES, V223, P181, DOI 10.1016/0006-8993(81)90820-9 NR 37 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 7 EP 15 DI 10.1016/0378-5955(94)90082-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200002 PM 7928717 ER PT J AU SAMSDODD, F CAPRANICA, RR AF SAMSDODD, F CAPRANICA, RR TI REPRESENTATION OF ACOUSTIC-SIGNALS IN THE 8TH NERVE OF THE TOKAY-GECKO .I. PURE-TONES SO HEARING RESEARCH LA English DT Article DE INFORMATION PROCESSING; PERIPHERAL AUDITORY SYSTEM; REPTILES; SPECTRAL DOMAIN; TEMPORAL DOMAIN; TOKAY GECKO ID PERIPHERAL AUDITORY-SYSTEM; LIZARD TILIQUA-RUGOSA; FREQUENCY-SELECTIVITY; HAIR-CELLS; ALLIGATOR LIZARD; COCHLEAR-NERVE; FIBER ACTIVITY; TUNING CURVES; PHASE-LOCKING; SINGLE FIBERS AB A systematic study of the encoding properties of 146 auditory nerve fibers in the Tokay gecko (Gekko gecko, L) was conducted with respect to pure tones and two-tone rate suppression. Our aim was a comprehensive understanding of the peripheral encoding of simple tonal stimuli and their representation by temporal synchronization and spike rate codes as a prelude to subsequent studies of more complex signals. Auditory nerve fibers in the Tokay gecko have asymmetrical, V-shaped excitatory tuning curves with best excitatory frequencies that range from 200-5100 Hz and thresholds between 4-35 dB SPL. A low-frequency excitatory 'tail' extends far into the low-frequency range and two-tone suppression is present only on the high frequency side of the tuning curve. The response properties to pure tones at different loci within a tuning curve can differ greatly, due to evident interactions between the representations of temporal, spectral and intensity stimulus features. For frequencies below 1250 Hz, pure tones are encoded by both temporal synchronization and spike rate codes, whereas above this frequency a fiber's ability to encode the waveform periodicity is lost and only a rate code predominates. These complimentary representations within a tuning curve raise fundamental issues which need to be addressed in interpreting how more complex, bioacoustic communication signals are represented in the peripheral and central auditory system. And since auditory nerve fibers in the Tokay gecko exhibit tonal sensitivity, selective frequency tuning, and iso-intensity and iso-frequency contours that seem comparable to similar measures in birds and mammals, these issues likely apply to most higher vertebrates in general. The simpler wiring diagram of the reptilian auditory system, coupled with the Tokay gecko's remarkable vocalizations, make this animal a good evolutionary model in which to experimentally explore the encoding of more complex sounds of communicative significance. C1 CORNELL UNIV,NEUROBIOL & BEHAV SECT,ITHACA,NY 14853. RP SAMSDODD, F (reprint author), H LUNDBECK & CO AS,PHARMACOL RES,OTTILIAVEJ 9,DK-2500 COPENHAGEN,DENMARK. CR BATSCHELET E, 1965, STATISTICAL METHODS CAPRANICA RR, 1989, NEURAL MECHANISMS BE, P88 DODD F, 1992, HEARING RES, V62, P173, DOI 10.1016/0378-5955(92)90183-N EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 EATOCK RA, 1981, J COMP PHYSIOL, V142, P203 EVANS EF, 1978, AUDIOLOGY, V17, P369 Frankenberg E., 1984, Amphibia-Reptilia, V5, P109 FRANKENBERG E, 1974, Journal of Herpetology, V8, P59, DOI 10.2307/1563077 FRISHKOP.LS, 1968, PR INST ELECTR ELECT, V56, P969, DOI 10.1109/PROC.1968.6448 HILL KG, 1989, HEARING RES, V39, P37, DOI 10.1016/0378-5955(89)90080-4 HILL KG, 1989, HEARING RES, V39, P63, DOI 10.1016/0378-5955(89)90082-8 HILLERY CM, 1987, HEARING RES, V25, P233, DOI 10.1016/0378-5955(87)90095-5 HOLTON T, 1983, J PHYSIOL-LONDON, V345, P205 HOLTON T, 1980, HEARING RES, V2, P21, DOI 10.1016/0378-5955(80)90014-3 HOLTON T, 1983, J PHYSIOL-LONDON, V345, P241 JOHNSTON.JR, 1969, EXP NEUROL, V24, P528, DOI 10.1016/0014-4886(69)90156-3 KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 KLINKE R, 1977, PSYCHOACOUSTICS PHYS KLUGE AG, 1967, B AM MUS NAT HIST, V135, P5 MANLEY GA, 1974, BRAIN BEHAV EVOLUT, V10, P244, DOI 10.1159/000124316 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1990, J COMP PHYSIOL A, V167, P89, DOI 10.1007/BF00192409 MANLEY GA, 1977, J COMP PHYSIOL, V118, P249 MANLEY GA, 1981, PROGR SENSORY PHYSL, V2, P49 MANLEY GA, 1990, J COMP PHYSIOL A, V167, P129, DOI 10.1007/BF00192412 Marcellini D.L., 1978, P287 MEGELA AL, 1981, J NEUROPHYSIOL, V46, P465 MILLER MR, 1985, J COMP NEUROL, V232, P1, DOI 10.1002/cne.902320102 MILLER MR, 1973, Z ZELLFORSCH MIK ANA, V136, P307, DOI 10.1007/BF00307037 MOLLER AR, 1983, HEARING RES, V11, P267, DOI 10.1016/0378-5955(83)90062-X Paulsen K., 1967, PRINZIP STIMMBILDUNG PFEIFFER RR, 1973, BASIC MECHANISMS HEA, P555 PORTER KR, 1972, HERPETOLOGY, P193 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 ROSE GJ, 1985, J NEUROPHYSIOL, V53, P446 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SIEVERT LM, 1988, HERPETOLOGICA, V44, P266 SMOLDERS JWT, 1986, HEARING RES, V24, P89, DOI 10.1016/0378-5955(86)90052-3 SUGA N, 1967, SCIENCE, V157, P88, DOI 10.1126/science.157.3784.88 TURNER RG, 1987, HEARING RES, V26, P287, DOI 10.1016/0378-5955(87)90064-5 UNDERWOOD GARTH, 1954, PROC ZOOL SOC LONDON, V124, P469 VRIESLANDER JD, 1990, J ACOUST SOC AM, V87, pS25, DOI 10.1121/1.2028142 WAGNER E, 1980, REPRODUCTIVE BIOL DI, P115 WEISS TF, 1988, HEARING RES, V33, P175, DOI 10.1016/0378-5955(88)90030-5 WEISS TF, 1978, EVOKED ELECTRICAL AC, P91 WEISS TF, 1976, BRAIN RES, V115, P71, DOI 10.1016/0006-8993(76)90823-4 WERNER YI, 1976, J EXP ZOOL, V195, P319, DOI 10.1002/jez.1401950302 WESTERMAN LA, 1987, J ACOUST SOC AM, V81, P680, DOI 10.1121/1.394836 Wever EG, 1978, REPTILE EAR ITS STRU WEVER E G, 1973, Journal of Herpetology, V7, P323, DOI 10.2307/1562866 WILKINSON L, 1987, SYSYAT SYSTEM STATIS NR 51 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 16 EP 30 DI 10.1016/0378-5955(94)90083-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200003 PM 7928709 ER PT J AU CARNEY, LH AF CARNEY, LH TI SPATIOTEMPORAL ENCODING OF SOUND LEVEL - MODELS FOR NORMAL ENCODING AND RECRUITMENT OF LOUDNESS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; COMPRESSIVE NONLINEARITY; INTENSITY CODING; DYNAMIC RANGE; LOUDNESS RECRUITMENT; SPATIOTEMPORAL PATTERNS ID AUDITORY-NERVE FIBERS; ANTEROVENTRAL COCHLEAR NUCLEUS; HEARING-IMPAIRED SUBJECTS; RATE-INTENSITY FUNCTIONS; BASILAR-MEMBRANE; DYNAMIC-RANGE; GUINEA-PIG; FREQUENCY-SELECTIVITY; DISCHARGE PATTERNS; MAMMALIAN COCHLEA AB This study explores the hypothesis that sound level is encoded in the spatiotemporal response patterns of auditory nerve (AN) fibers. The temporal properties of AN fiber responses depend upon sound level due to nonlinearities in the auditory periphery. In particular, the compressive nonlinearity of the inner ear introduces systematic changes in the timing of the responses of AN fibers as a function of level. Changes in single fiber responses that depend upon both sound level and characteristic frequency (CF) result in systematic changes in the spatiotemporal response patterns across populations of AN fibers. This study investigates the changes in the spatiotemporal response patterns as a function of level using a computational model for responses of low-frequency AN fibers. A mechanism that could extract information encoded in this form is coincidence detection across AN fibers of different CFs. This study shows that this mechanism could play a role in encoding of sound level for simple and complex stimuli. The model demonstrates that this encoding scheme would be influenced by auditory pathology that affects the peripheral compressive nonlinearity in a way that is consistent with the phenomenon of recruitment of loudness, which often accompanies sensorineural hearing loss. RP CARNEY, LH (reprint author), BOSTON UNIV,DEPT BIOMED ENGN,44 CUMMINGTON ST,BOSTON,MA 02215, USA. CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 Bourk T.R., 1976, THESIS CAMBRIDGE CAIRD D, 1983, EXP BRAIN RES, V52, P385 CARNEY LH, 1992, PHILOS T ROY SOC B, V336, P403, DOI 10.1098/rstb.1992.0075 CARNEY LH, 1990, J NEUROPHYSIOL, V64, P437 CARNEY LH, 1993, J ACOUST SOC AM, V93, P401, DOI 10.1121/1.405620 CARNEY LH, 1988, J NEUROPHYSIOL, V60, P1653 COLBURN HS, 1990, HEARING RES, V49, P335 COLBURN H S, 1984, Journal of the Acoustical Society of America, V76, pS5, DOI 10.1121/1.2021931 Delgutte B, 1987, PSYCHOPHYSICS SPEECH, P333 DENG L, 1987, J ACOUST SOC AM, V82, P2001, DOI 10.1121/1.395644 DRESCHLER WA, 1986, AUDITORY FREQUENCY S, P331 DYNES SBC, 1992, HEARING RES, V58, P79, DOI 10.1016/0378-5955(92)90011-B EVANS EF, 1978, AUDIOLOGY, V17, P369 EVANS EF, 1980, EXP BRAIN RES, V40, P115 EVANS EF, 1981, NEURONAL MECHANISMS, P69 FLORENTINE M, 1981, J ACOUST SOC AM, V70, P1646, DOI 10.1121/1.387219 FOWLER EP, 1936, ARCH OTOLARYNGOL, V24, P31 Fowler EP, 1936, ARCHIV OTOLARYNGOL, V24, P731 FRISINA RD, 1990, HEARING RES, V44, P123, DOI 10.1016/0378-5955(90)90075-Z GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GUINAN JJ, 1990, HEARING RES, V49, P321, DOI 10.1016/0378-5955(90)90111-2 HELLMAN RP, 1978, J ACOUST SOC AM, V63, P1114, DOI 10.1121/1.381819 HELLMAN RP, 1974, SENSATION MEASUREMEN, P241 Hood J D, 1969, J Laryngol Otol, V83, P695, DOI 10.1017/S0022215100070857 HOOD JD, 1977, AUDIOLOGY, V16, P215 HORST JW, 1987, J ACOUST SOC AM, V82, P874, DOI 10.1121/1.395286 HORST JW, 1990, J ACOUST SOC AM, V88, P2656, DOI 10.1121/1.399986 Jerger J., 1962, ASHA, V4, P139 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 JORIS PX, 1994, IN PRESS J NEUROPHYS Kiang NY, 1970, SENSORINEURAL HEARIN, P241 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 LAI YC, 1993, ABSTR ASS RES OT, V16, P121 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIBERMAN MC, 1991, J COMP NEUROL, V313, P240, DOI 10.1002/cne.903130205 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MANIS PB, 1991, J NEUROSCI, V11, P2865 MAY BJ, 1992, J NEUROPHYSIOL, V68, P1589 Moore B. C. J., 1989, INTRO PSYCHOL HEARIN MOORE B C J, 1988, British Journal of Audiology, V22, P93, DOI 10.3109/03005368809077803 MOORE BCJ, 1987, HEARING RES, V28, P209, DOI 10.1016/0378-5955(87)90050-5 MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1505, DOI 10.1121/1.392045 OERTEL D, 1983, J NEUROSCI, V3, P2043 OSEN KK, 1970, ARCH ITAL BIOL, V108, P21 OSEN KK, 1969, ACTA OTO-LARYNGOL, V67, P352, DOI 10.3109/00016486909125462 PALMER AR, 1982, HEARING RES, V7, P305, DOI 10.1016/0378-5955(82)90042-9 PALMER AR, 1982, ARCH OTO-RHINO-LARYN, V236, P197, DOI 10.1007/BF00454039 PALMER AR, 1993, ABST MIDWINTER RES M, V16, P123 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 PETERS RW, 1992, J ACOUST SOC AM, V91, P256, DOI 10.1121/1.402769 PFEIFFER RR, 1966, SCIENCE, V154, P667, DOI 10.1126/science.154.3749.667 PICK GF, 1980, J ACOUST SOC AM, V68, P1085, DOI 10.1121/1.384979 RANKOVIC CM, 1992, J ACOUST SOC AM, V91, P354, DOI 10.1121/1.402778 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 M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O RUGGERO MA, 1993, ASS RES OT MIDW M, V16, P31 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SACHS MB, 1986, AUDITORY FREQUENCY S, P121 SHAMMA SA, 1985, J ACOUST SOC AM, V78, P1622, DOI 10.1121/1.392800 SHANNON RV, 1993, COCHLEAR IMPLANTS AU, P357 SIEBERT WM, 1965, KYBERNETIK, V2, P206, DOI 10.1007/BF00306416 SMITH PH, 1989, J COMP NEUROL, V282, P595, DOI 10.1002/cne.902820410 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 Smith R. L., 1988, AUDITORY FUNCTION NE, P243 SMITH RL, 1983, HEARING PHYSL BASES, P112 SMITH RL, 1980, BRAIN RES, V184, P499, DOI 10.1016/0006-8993(80)90817-3 SMITH RL, 1980, HEARING RES, V2, P123, DOI 10.1016/0378-5955(80)90034-9 STUTMAN ER, 1993, ABSTR ASS RES OT, V16, P121 TSUTCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 Viemeister N., 1988, AUDITORY FUNCTION NE, P213 VIEMEISTER NF, 1988, HEARING RES, V34, P267, DOI 10.1016/0378-5955(88)90007-X VIEMEISTER NF, 1983, SCIENCE, V221, P1206, DOI 10.1126/science.6612337 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WESTERMAN LA, 1988, J ACOUST SOC AM, V83, P2266, DOI 10.1121/1.396357 Winslow R. L., 1987, AUDITORY PROCESSING, P212 WINSLOW RL, 1988, HEARING RES, V35, P165, DOI 10.1016/0378-5955(88)90116-5 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, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 YIN TCT, 1987, J NEUROPHYSIOL, V58, P562 YOUNG ED, 1979, J ACOUST SOC AM, V66, P1381, DOI 10.1121/1.383532 YOUNG ED, 1993, MAMMALIAN COCHLEAR N, P395 YOUNG ED, 1989, ASS RES OT ABSTR, V12, P121 NR 94 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 31 EP 44 DI 10.1016/0378-5955(94)90084-1 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200004 PM 7928712 ER PT J AU HORIKAWA, J TANAHASHI, A SUGA, N AF HORIKAWA, J TANAHASHI, A SUGA, N TI AFTER-DISCHARGES IN THE AUDITORY-CORTEX OF THE MOUSTACHED BAT - NO OSCILLATORY DISCHARGES FOR BINDING AUDITORY INFORMATION SO HEARING RESEARCH LA English DT Article DE MOUSTACHED BAT; AUDITORY CORTEX; NEURAL OSCILLATION; AFTER-DISCHARGES; AUTOCORRELOGRAMS ID AMPLITUDE-SPECTRUM REPRESENTATION; COMBINATION-SENSITIVE NEURONS; CAT VISUAL-CORTEX; TARGET RANGE; RESPONSES; COMPLEX; SYSTEM; ORGANIZATION; SIMULATION; FREQUENCY AB Action potentials of single or multi-neurons were recorded from the DSCF, FM-FM and DF areas in the auditory cortex of the mustached bat to study stimulus-induced neural oscillation in the auditory system. Out of 125 neurons 120 recorded in these three areas showed after-discharges to a best stimulus. Durations of after-discharges of 120 neurons ranged between 4.8 and 217 ms. In the remaining 5 neurons, the duration of the discharges was shorter than that of the stimulus. The PST histograms displaying responses of these 125 neurons showed no oscillatory component locked to the stimulus. 98% of the autocorrelograms of responses (122/125) showed no sign of oscillation, but the remaining two percent showed a very weak oscillatory component that was not stimulus-locked. The duration of the after-discharges had no correlation with the best delay or cortical depth of neurons. After-discharges are common in the auditory cortex of the mustached bat, but oscillatory discharges are very rare, so that neural oscillations play no role in binding various types of biosonar information processed in the different 'specialized' areas in the auditory cortex. C1 WASHINGTON UNIV,DEPT BIOL,ST LOUIS,MO 63130. RP HORIKAWA, J (reprint author), TOKYO MED & DENT UNIV,MED RES INST,DEPT NEUROPHYSIOL,CHIYODA KU,KANDASURUGADAI 2-3-10,TOKYO 101,JAPAN. CR BUTMAN JA, 1992, THESIS WASHINGTON U ECKHORN R, 1993, NEUROREPORT, V4, P243, DOI 10.1097/00001756-199303000-00004 ECKHORN R, 1988, BIOL CYBERN, V60, P121, DOI 10.1007/BF00202899 EDAMATSU H, 1989, J NEUROPHYSIOL, V61, P202 EDAMATSU H, 1993, J NEUROPHYSIOL, V69, P1700 EGGERMONT JJ, 1992, HEARING RES, V61, P1, DOI 10.1016/0378-5955(92)90029-M ENGEL AK, 1992, TRENDS NEUROSCI, V15, P218, DOI 10.1016/0166-2236(92)90039-B ENGEL AK, 1990, SOC NEUR ABSTR, V16 FREEMAN WJ, 1987, BIOL CYBERN, V56, P139, DOI 10.1007/BF00317988 FREEMAN WJ, 1968, J NEUROPHYSIOL, V31, P337 GHOSE GM, 1992, J NEUROPHYSIOL, V68, P1558 GHOSE GM, 1990, SOC NEUR ABSTR, V16 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 Kanou M., 1992, Society for Neuroscience Abstracts, V18, P883 Kiang NY-s, 1965, DISCHARGE PATTERNS S LLINAS R, 1993, P NATL ACAD SCI USA, V90, P2078, DOI 10.1073/pnas.90.5.2078 LLINAS R, 1989, Society for Neuroscience Abstracts, V15, P660 ONEILL WE, 1979, SCIENCE, V203, P69, DOI 10.1126/science.758681 ONEILL WE, 1982, J NEUROSCI, V2, P17 PHILLIPS DP, 1991, HEARING RES, V53, P17, DOI 10.1016/0378-5955(91)90210-Z POMPEIANO O, 1978, ABNORMAL NEURONAL DI, P75 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 SALLY SL, 1988, J NEUROPHYSIOL, V59, P1627 STERIADE M, 1988, PHYSIOL REV, V68, P649 SUGA N, 1986, J NEUROPHYSIOL, V55, P776 SUGA N, 1990, COLD SH Q B, V55, P585 SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUGA N, 1982, J NEUROPHYSIOL, V47, P225 Suga N., 1984, DYNAMIC ASPECTS NEOC, P315 SUGA N, 1979, SCIENCE, V206, P351, DOI 10.1126/science.482944 SUGA N, 1977, SCIENCE, V196, P64, DOI 10.1126/science.190681 Suga N, 1988, ANIMAL SONAR, P149 SUGA N, 1983, J NEUROPHYSIOL, V49, P1573 TANAHASHI A, 1993, NMDA MEDIATED FACILI, P130 TSUCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 WILSON M, 1992, J NEUROPHYSIOL, V67, P981 YOUNG MP, 1992, J NEUROPHYSIOL, V67, P1464 NR 39 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 45 EP 52 DI 10.1016/0378-5955(94)90085-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200005 PM 7928713 ER PT J AU MUROFUSHI, T KAGA, K ASAKAGE, T AF MUROFUSHI, T KAGA, K ASAKAGE, T TI TEMPORARY LATENCY SHIFTS IN AUDITORY-EVOKED POTENTIALS BY INJECTION OF LIDOCAINE IN THE RAT SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIAL; AUDITORY BRAIN-STEM RESPONSE; MIDDLE LATENCY RESPONSE; INFERIOR COLLICULUS; LIDOCAINE; RAT ID INFERIOR COLLICULUS LESIONS; BRAIN-STEM; RESPONSES; MONKEY AB Temporary latency shifts in auditory evoked potentials by intravenous injection of lidocaine were investigated in albino rats. Auditory brainstem responses (ABR) were recorded with 4000Hz short tone bursts. There was no significant difference of latencies in wave P1 of the ABR between drug-administered group (6 mg/kg body weight of lidocaine) and control group (0.6 ml/kg of 0.9% saline). As for waves P2. P3 and P4 of ABR, the latencies of the waves were significantly prolonged after the lidocaine injection (p < 0.05. U-test). The prolongation of latency of wave P4 was the most prominent in the fast waves and dependent on the dose of lidocaine. The latencies of the slow positive wave of the evoked potentials on the inferior colliculus (wave 8) with clicks and the slow positive wave (wave P) and the negative wave following ABR (wave NA) with 4000Hz short tone bursts were also studied. The latencies of waves S. P and NA showed significant temporal prolongation (p < 0.05, U-test) after lidocaine injection. The present study revealed that a relatively small dose of lidocaine can cause temporary prolongation of latencies of auditory evoked potentials not only in the fast components but also in the slow components including wave NA which is a large slow negative wave following the ABR. The effects are considered to be caused by the action of lidocaine which reduces the excitabilities on the auditory nervous system. RP MUROFUSHI, T (reprint author), UNIV TOKYO,FAC MED,DEPT OTOLARYNGOL,BUNKYO KU,7-3-1 HONGO,TOKYO 113,JAPAN. CR BENOWITZ N, 1974, CLIN PHARMACOL THER, V16, P87 BUCHWALD JS, 1981, BRAIN RES, V205, P91, DOI 10.1016/0006-8993(81)90722-8 CAIRD DM, 1987, ELECTROEN CLIN NEURO, V68, P237, DOI 10.1016/0168-5597(87)90034-7 FUNAI H, 1984, J OTOLARYNGOL JPN, V87, P785 FUNAI H, 1983, AUDIOLOGY, V22, P9 HASHIMOTO I, 1982, ELECTROEN CLIN NEURO, V53, P652, DOI 10.1016/0013-4694(82)90141-9 HASHIMOTO I, 1981, BRAIN, V104, P841, DOI 10.1093/brain/104.4.841 HUGHES DW, 1975, AURIS NASUS LARYNX, V2, P107 JAVEL E, 1982, ARCH OTOLARYNGOL, V108, P71 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 LAURIKAINEN E, 1992, ACTA OTO-LARYNGOL, V112, P800, DOI 10.3109/00016489209137477 MCGEE T, 1991, BRAIN RES, V544, P211, DOI 10.1016/0006-8993(91)90056-2 OZDAMAR O, 1980, NEUR ABSTR, V6, P595 RITCHIE J M, 1990, P311 Suzuki M, 1983, Auris Nasus Larynx, V10, P25 TABATABAI M, 1990, CLIN PHYSIOL BIOCH, V8, P289 UNO A, 1991, Audiology Japan, V34, P47 VELASCO M, 1982, INT J NEUROSCI, V17, P199 NR 18 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 53 EP 59 DI 10.1016/0378-5955(94)90086-8 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200006 PM 7928714 ER PT J AU LOPEZESCAMEZ, JA CANIZARES, FJ CRESPO, PV BAEYENS, JM CAMPOS, A AF LOPEZESCAMEZ, JA CANIZARES, FJ CRESPO, PV BAEYENS, JM CAMPOS, A TI ELECTRON-PROBE MICROANALYSIS OF GENTAMICIN-INDUCED CHANGES ON IONIC COMPOSITION OF THE VESTIBULAR GELATINOUS MEMBRANE SO HEARING RESEARCH LA English DT Article DE VESTIBULAR SYSTEM; ELECTRON PROBE X-RAY MICROANALYSIS; UTRICLE; SACCULE; GELATINOUS MEMBRANE; OTOTOXICITY ID OUTER HAIR-CELLS; X-RAY-MICROANALYSIS; GUINEA-PIG COCHLEA; AMINOGLYCOSIDE ANTIBIOTICS; OTOLITHIC MEMBRANE; TRANSDUCTION CHANNELS; INNER-EAR; NERVE-TERMINALS; ETHACRYNIC-ACID; CALCIUM AB Gentamicin-induced changes in ionic composition in the otolithic membrane of adult OF1 mice were evaluated in the gelatinous layers of the saccule and utricle by quantitative electron probe X-ray microanalysis. The otolithic membranes were plunge-frozen and freeze-dried to prevent the redistribution of elements. Quantitative analysis was carried out with an energy dispersive detector using the peak-to-background (P/B) ratio method and different salts dissolved in dextran as standards to calibrate the P/B ratio against the concentration of the elements P, S and K in the microprobe. Gentamicin selectively decreased the concentrations of P (P < 0.001) and S (P < 0.01) in the gelatinous membrane of the saccule, and had no effect in the utricle. The concentration of K also increased in the utricular gelatinous membrane (P < 0.05). The mechanism of ototoxicity in the gelatinous membrane is unknown, but the ability of aminoglycosides to block calcium channels may induce disturbances in the ionic equilibrium of the endolymphatic fluid, and thus affect the biochemical composition of the gelatinous membrane. This technique can be useful to evaluate the distribution of ions in the process of drug-induced ototoxicity. C1 UNIV GRANADA,FAC MED,DEPT CELL BIOL & HISTOL,E-18071 GRANADA,SPAIN. UNIV GRANADA,FAC MED,DEPT PHARMACOL,E-18071 GRANADA,SPAIN. CR Aran J M, 1982, Acta Otolaryngol Suppl, V390, P1 ATCHISON WD, 1988, J PHARMACOL EXP THER, V245, P394 BAIRD RA, 1993, HEARING RES, V65, P164, DOI 10.1016/0378-5955(93)90211-I CAMPOS A, 1992, MICRON MICROSC ACTA, V23, P349, DOI 10.1016/0739-6260(92)90039-G CAMPOS A, 1990, TUMOR DIAGNOSIS ELEC, V3, P251 CAMPOS A, 1994, ACTA OTO-LARYNGOL, V114, P18, DOI 10.3109/00016489409126011 CANIZARES FJ, 1990, ADV OTO-RHINO-LARYNG, V45, P94 CRESPO PV, 1993, ACTA OTO-LARYNGOL, V113, P176, DOI 10.3109/00016489309135788 DEGROOT JCM, 1990, HEARING RES, V35, P39 DEGROOT JCMJ, 1991, ACTA OTO-LARYNGOL, V111, P273, DOI 10.3109/00016489109137387 DEGROOT JCMJ, 1988, HEARING RES, V35, P39, DOI 10.1016/0378-5955(88)90038-X DELPOZO E, 1987, EUR J PHARMACOL, V128, P49 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FAUSTI SA, 1992, J INFECT DIS, V165, P1026 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 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 HALL TA, 1973, J MICROSC-OXFORD, V99, P177 HARADA Y, 1977, ACTA OTO-LARYNGOL, V84, P65, DOI 10.3109/00016487709123943 HARPUR ES, 1979, J LARYNGOL OTOL, V93, P7, DOI 10.1017/S0022215100086679 HAYASHIDA T, 1989, ACTA OTO-LARYNGOL, V108, P404, DOI 10.3109/00016488909125546 HIEL H, 1992, HEARING RES, V57, P157, DOI 10.1016/0378-5955(92)90148-G HUDSPETH AJ, 1983, J PHYSIOL-LONDON, V345, pP66 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A KEITH RA, 1992, J MOL NEUROSCI, V3, P147, DOI 10.1007/BF02919406 KHAN KM, 1990, HEARING RES, V43, P149, DOI 10.1016/0378-5955(90)90224-D KNAUS HG, 1987, N-S ARCH PHARMACOL, V336, P583 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 Lim DJ, 1979, SCANNING ELECTRON MI, V3, P929 LINDEMAN HH, 1969, ACTA OTO-LARYNGOL, V67, P177, DOI 10.3109/00016486909125441 LOHDI S, 1976, BIOCH ET BIOPHYSICA, V426, P781 LOPEZESCAMEZ JA, 1993, HISTOL HISTOPATHOL, V8, P113 LOPEZESCAMEZ JA, 1992, SCANNING MICROSCOPY, V6, P765 LOPEZESCAMEZ JA, 1993, J MICROSC-OXFORD, V171, P215 LULLMANN H, 1982, BIOCHEM PHARMACOL, V31, P3769, DOI 10.1016/0006-2952(82)90291-X MECHIGIAN I, 1979, ACTA OTO-LARYNGOL, V88, P56, DOI 10.3109/00016487909137140 MROZ EA, 1993, HEARING RES, V70, P9, DOI 10.1016/0378-5955(93)90048-6 NAKAGAWA T, 1992, BRAIN RES, V580, P345, DOI 10.1016/0006-8993(92)90966-D ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x PARSONS TD, 1992, J GEN PHYSIOL, V99, P491, DOI 10.1085/jgp.99.4.491 ROSS MD, 1987, ACTA OTO-LARYNGOL, V103, P56, DOI 10.3109/00016488709134698 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SHARON N, 1982, MOL CELL BIOCHEM, V42, P167, DOI 10.1007/BF00238511 SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 TAKADA A, 1982, HEARING RES, V8, P179, DOI 10.1016/0378-5955(82)90073-9 TAKUMIDA M, 1989, ACTA OTO-LARYNGOL, V107, P39, DOI 10.3109/00016488909127477 HUY PTB, 1988, ACTA OTO-LARYNGOL, V105, P511, DOI 10.3109/00016488809119511 Wersall J., 1981, AMINOGLYCOSIDE OTOTO, P197 WERSALL J, 1969, J INFECT DIS, V119, P410 Wersäll J, 1973, Adv Otorhinolaryngol, V20, P14 WILLIAMS SE, 1987, BIOCHEM PHARMACOL, V36, P89, DOI 10.1016/0006-2952(87)90385-6 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 YUNG MW, 1987, ACTA OTO-LARYNGOL, V103, P73, DOI 10.3109/00016488709134700 NR 57 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 1 PY 1994 VL 76 IS 1-2 BP 60 EP 66 DI 10.1016/0378-5955(94)90087-6 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200007 PM 7928715 ER PT J AU FROST, SB MASTERTON, RB AF FROST, SB MASTERTON, RB TI HEARING IN PRIMITIVE MAMMALS - MONODELPHIS-DOMESTICA AND MARMOSA ELEGANS SO HEARING RESEARCH LA English DT Article DE MONODELPHIS; MARMOSA; DIDELPHIDAE; AUDIOGRAM; TONE-DETECTION THRESHOLD; EVOLUTION ID RAT; MOUSE AB Although opossums of the Family Didelphidae usually serve as a parsimonious starting point for tracing the otological and neurological evolution of modern mammals, audiological data for Didelphid opossums is available only for the North American opossum (Didelphis virginiana) which because of its large size, may be one of the least representative genera of the family. The present report extends the audiological data to two other species of Didelphid opossums, Monodelphis domestica, and Marmosa elegans. At 60 dB SPL, the hearing of Monodelphis extends from 3.6 kHz to 77 kHz, with a range of best sensitivity from 8 to 64 kHz while the hearing of Marmosa extends from 3.8 kHz to 80 kHz, with a range of best sensitivity from 8 to 64 kHz. Neither species was found to be particularly sensitive to tones, with the average lowest threshold near 20 dB SPL for Monodelphis and 33 dB SPL for Marmosa. These results indicate that like the North American opossum both genera are sensitive to high frequencies yet relatively insensitive to sound. Because the hearing of the three genera of Didelphids agree in several respects, it can be concluded that sensitivity to high frequencies almost certainly was present in ancient mammals, probably following quickly after the acquisition of a 3 ossicle middle ear linkage. It is not unlikely that the utility value of high frequency hearing, rather than highly sensitive hearing, may have been a primary source of selective pressure for this morphological transformation. RP FROST, SB (reprint author), FLORIDA STATE UNIV,DEPT PSYCHOL,PSYCHOBIOL & NEUROSCI PROGRAM,TALLAHASSEE,FL 32306, USA. CR EDINGER T, 1948, MEM GEOL SOC AM, V25 Fleischer G, 1978, Adv Anat Embryol Cell Biol, V55, P3 FLEISCHER G, 1973, Saeugetierkundliche Mitteilungen, V21, P131 FROST SB, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P655 GREGORY WK, 1929, OUR FACE FISH MAN HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 HEFFNER HE, 1985, J COMP PSYCHOL, V99, P275, DOI 10.1037//0735-7036.99.3.275 HEFFNER RS, 1990, HEARING RES, V48, P231, DOI 10.1016/0378-5955(90)90063-U Heffner R. S., 1990, COMP PERCEPTION, VI, P285 HEFFNER RS, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P691 HEFFNER RS, 1992, HEARING RES, V62, P206, DOI 10.1016/0378-5955(92)90188-S HEFFNER RS, 1990, HEARING RES, V46, P239, DOI 10.1016/0378-5955(90)90005-A HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KERMACK KA, 1981, ZOOL J LINN SOC-LOND, V71, P1, DOI 10.1111/j.1096-3642.1981.tb01127.x KIRSCH JAW, 1977, AM SCI, V65, P276 KUDO M, 1986, J COMP NEUROL, V245, P176, DOI 10.1002/cne.902450205 Le Gros Clark W.E., 1934, EARLY FORERUNNERS MA Loo YT, 1930, J COMP NEUROL, V51, P13, DOI 10.1002/cne.900510103 MARSHALL LG, 1979, ZOOL J LINN SOC-LOND, V66, P369, DOI 10.1111/j.1096-3642.1979.tb01914.x MASTERTO.B, 1969, J ACOUST SOC AM, V45, P966, DOI 10.1121/1.1911574 MASTERTON RB, 1988, J NEUROPHYSIOL, V60, P1841 MASTERTON RB, 1991, ASS RES OTOLARYNGOL, V14, P32 OLSON EC, 1959, EVOLUTION, V13, P344, DOI 10.2307/2406111 RAVIZZA RJ, 1969, J AUD RES, V9, P1 REIG OA, 1987, STUDIES EVOLUTION, V1, P10 ROSOWSKI JJ, 1991, ZOOL J LINN SOC-LOND, V101, P131, DOI 10.1111/j.1096-3642.1991.tb00890.x Rowe T., 1988, Journal of Vertebrate Paleontology, V8, P241 Simpson G. G., 1949, MEANING EVOLUTION SIMPSON GG, 1959, EVOLUTION, V13, P405, DOI 10.2307/2406116 Smith GE, 1910, LANCET, V1, P147 Smith GE, 1910, LANCET, V1, P1 Smith GE, 1910, LANCET, V1, P221 THOMPSON M, 1990, BEHAV RES METH INSTR, V22, P449, DOI 10.3758/BF03203193 TUMARKIN A, 1955, EVOLUTION, V9, P221, DOI 10.2307/2405646 WATSON DMS, 1953, EVOLUTION, V1, P159 NR 36 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 67 EP 72 DI 10.1016/0378-5955(94)90088-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200008 PM 7928716 ER PT J AU URBANI, L LUCERTINI, M AF URBANI, L LUCERTINI, M TI EFFECTS OF HYPOBARIC HYPOXIA ON THE HUMAN AUDITORY BRAIN-STEM RESPONSES SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIALS; HYPOXIA ID STEM EVOKED-RESPONSE; POTENTIALS; LATENCY; HYPOXEMIA; SHIFTS; RABBIT; RATS; ABR AB Auditory brainstem responses (ABRs) were recorded in six volunteers before, during and after 90-min exposure to hypobaric hypoxia (5,184 m; barometric pressure = 405 mmHg) in an altitude chamber. Waves I, III and V absolute and interpeak latencies were analysed. The main result of the experiment was a significant shortening of the brainstem transmission time (I-V interval) in the recovery from hypoxia compared with the basal condition. This finding could be explained with a slow decay of the compensatory mechanisms acting during hypoxia and/or a transient neuronal hyperexcitability at the end of the hypoxic stress. C1 ITALIAN AIR FORCE,DASRS,DEPT AEROSP MED,I-00040 ROME,ITALY. CR ATTIAS J, 1990, HEARING RES, V45, P247, DOI 10.1016/0378-5955(90)90124-8 BERNTMAN L, 1978, J NEUROCHEM, V31, P1265, DOI 10.1111/j.1471-4159.1978.tb06251.x CARLILE S, 1992, ACTA OTO-LARYNGOL, V112, P939, DOI 10.3109/00016489209137494 COLIN F, 1978, ARCH INT PHYSIOL BIO, V86, P677, DOI 10.3109/13813457809055940 DEECKE L, 1973, AEROSPACE MED OCT, P1106 FREEMAN S, 1991, ELECTROEN CLIN NEURO, V78, P284, DOI 10.1016/0013-4694(91)90182-4 HOLMSTROM FMG, 1971, AEROSPACE MED, P56 LUCERTINI M, 1993, AUDIOLOGY, V32, P356 MCPHERSON RW, 1986, STROKE, V17, P30 MOSKO SS, 1981, ELECTROEN CLIN NEURO, V51, P477, DOI 10.1016/0013-4694(81)90224-8 PIERELLI F, 1986, EXP NEUROL, V94, P479, DOI 10.1016/0014-4886(86)90231-1 SCHIFF SJ, 1987, STROKE, V18, P30 SHEFFIELD PJ, 1985, FUNDAMENTALS AEROSPA, P91 SOHMER H, 1986, ELECTROEN CLIN NEURO, V64, P334, DOI 10.1016/0013-4694(86)90157-4 SOHMER H, 1982, ELECTROEN CLIN NEURO, V53, P506, DOI 10.1016/0013-4694(82)90063-3 SOHMER H, 1986, ELECTROEN CLIN NEURO, V64, P328, DOI 10.1016/0013-4694(86)90156-2 SOHMER H, 1991, ACTA OTO-LARYNGOL, V111, P206, DOI 10.3109/00016489109137376 NR 17 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 73 EP 77 DI 10.1016/0378-5955(94)90089-2 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200009 PM 7928718 ER PT J AU LLORENS, J DEMEMES, D AF LLORENS, J DEMEMES, D TI HAIR CELL DEGENERATION RESULTING FROM 3,3'-IMINODIPROPIONITRILE TOXICITY IN THE RAT VESTIBULAR EPITHELIA SO HEARING RESEARCH LA English DT Article DE 3,3'-IMINODIPROPIONITRILE; NITRILES; VESTIBULAR RECEPTORS; SCANNING ELECTRON MICROSCOPY; TRANSMISSION ELECTRON MICROSCOPY ID ALIPHATIC NITRILES; MICE AB The present work was aimed at characterizing, using both scanning- and transmission-electron microscopy, the morphological changes occurring in the vestibular sensory epithelia of rats exposed to the synthetic nitrile 3,3'-iminodipropionitrile (IDPN), that belongs to a new class of vestibulotoxic compounds. Male Long-Evans rats were administered 0, 200, 400, 600, 800 or 1000 mg/kg of IDPN (i.p., in 2 ml/kg saline), and sacrificed at 1 day to 34 weeks post-dosing. IDPN induced a selective hair cell (HC) loss. Little evidence of HC degeneration was found after 200 mg/kg, but loss of HC was evident after 400 mg/kg. The HC degeneration was almost complete after 600 mg/kg, and complete after 1000 mg/kg of IDPN. Both intra-epitherial (central regions of the receptors > peripheral regions) and inter-epithelial (crista > utricle > saccule) differences in sensitivity were found. Type I HC were found to be more sensitive to the toxic effects of IDPN than type II HC. The degeneration process was characterized by cytoplasm vacuolization. The vacuoles likely originated from the endoplasmic reticulum. Alterations in the cell nucleus, mitochondria, and ciliary structures appeared to occur later in the degeneration process. The membrane of the degenerating HC was found to detach from the innervating terminals, and disappearance of the pre-, post-, and synaptic-cleft densities was observed. A striking preservation of both afferent and efferent terminals was observed to occur. Nerve terminals remained in place during the acute period of the IDPN toxicity and after HC loss, degenerating only after long times of deafferentation. The HC degeneration induced by IDPN occurred mostly within 8 days post-dosing, and was finished by 3 weeks post-dosing. No evidence for further degeneration nor for regeneration of the HC was found at 6, 10, or 34 weeks post-dosing. The only changes in the morphology of the vestibular receptors after 3 weeks of survival was the placement of the otoconia from the utriculi of the high-dose animals below a thin layer of cells, and a slow degeneration of the deafferented nerve endings. The present work demonstrates that IDPN has a specific toxic effect on the vestibular HC. C1 UNIV MONTPELLIER 2,SENSORY NEUROPHYSIOL LAB,INSERM,U254,F-34095 MONTPELLIER 5,FRANCE. RP LLORENS, J (reprint author), CSIC,DEPT FARMACOL & TOXICOL,JORDI GIRONA 18-26,E-08034 BARCELONA,SPAIN. RI Llorens, Jordi/A-6959-2008 OI Llorens, Jordi/0000-0002-3894-9401 CR AHMED AE, 1983, PROG DRUG METAB, V7, P229 Aran J M, 1982, Acta Otolaryngol Suppl, V390, P1 CROFTON KM, 1991, NEUROTOXICOL TERATOL, V13, P575, DOI 10.1016/0892-0362(91)90040-4 DEGROOT JCMJ, 1991, ACTA OTO-LARYNGOL, V111, P273, DOI 10.3109/00016489109137387 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 GENTER MB, 1992, J PHARMACOL EXP THER, V263, P1432 GENTSCHE.T, 1973, BRAIN RES, V62, P37, DOI 10.1016/0006-8993(73)90618-5 GOLDEY ES, 1993, HEARING RES, V69, P221, DOI 10.1016/0378-5955(93)90111-D LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LLORENS J, 1993, TOXICOL APPL PHARM, V123, P199, DOI 10.1006/taap.1993.1238 RUBIN E, 1989, PATHOLOGY, P3 SELYE H., 1957, REV CANADIENNE BIOL, V16, P1 SERA K, 1987, SCANNING MICROSCOPY, V1, P1191 SHAPI MM, 1991, J CHROMATOGR-BIOMED, V562, P681, DOI 10.1016/0378-4347(91)80618-M TAKUMIDA M, 1989, ACTA OTO-LARYNGOL, V107, P39, DOI 10.3109/00016488909127477 TANII H, 1989, NEUROTOXICOLOGY, V10, P157 TANII H, 1989, EXP NEUROL, V103, P64, DOI 10.1016/0014-4886(89)90186-6 WERSALL J, 1962, Acta Otolaryngol, V54, P1, DOI 10.3109/00016486209126917 WILLHITE CC, 1981, TOXICOL APPL PHARM, V59, P589, DOI 10.1016/0041-008X(81)90314-8 NR 19 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 78 EP 86 DI 10.1016/0378-5955(94)90090-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200010 PM 7928719 ER PT J AU KUJAWA, SG EROSTEGUI, C FALLON, M CRIST, J BOBBIN, RP AF KUJAWA, SG EROSTEGUI, C FALLON, M CRIST, J BOBBIN, RP TI EFFECTS OF ADENOSINE 5'-TRIPHOSPHATE AND RELATED AGONISTS ON COCHLEAR FUNCTION SO HEARING RESEARCH LA English DT Article DE 5'-TRIPHOSPHATE; ADENOSINE 5'-TRIPHOSPHATE ANALOGS; PURINOCEPTORS; COCHLEA ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; INTRACELLULAR CALCIUM; ATP; ACETYLCHOLINE; RESPONSES; ORGAN; CORTI; P2-PURINOCEPTORS; NUCLEOTIDES AB Several lines of evidence implicate a neurotransmitter/modulator role for ATP in the cochlea. Most of the work supporting such a notion has been accomplished using in vitro preparations of sensory hair cells or other cochlear tissues. Little is known regarding the functional consequences of ATP receptor activation in vivo. In the present experiments, we tested ATP and related agonist analogs for their effects on sound-evoked responses of the cochlea (cochlear microphonic, CM; summating potential, SP; distortion product otoacoustic emissions, DPOAE) and auditory nerve (compound action potential, CAP) in vivo and on outer hair cell (OHC) currents and cell length in vitro. In vivo, local application of these compounds was associated with concentration- and intensity-dependent response alterations. The slowly-hydrolyzable P-2y agonist, ATP-gamma-S, was clearly of greatest in vivo potency: At low to moderate stimulus intensities, micromolar concentrations of this drug reduced all responses, in particular CAP and DPOAEs, which fell to the level of the noise floor. At high intensities, response suppression was smaller and SP was increased. In vivo effects of ATP, ATP-alpha-S and 2-Me-S-ATP were qualitatively similar to, but smaller in magnitude and requiring higher concentrations than those observed for ATP-gamma-S. Adenosine was without significant effect on responses of the cochlea and auditory nerve. In vitro, effects of ATP-gamma-S and ATP were similar: both induced inward currents in OHCs held at -60 mV without producing observable (> 0.3 mu m) changes in OHC length. Results suggest that endogenous ATP influences cochlear function through receptors at several sites in the cochlea. Results suggest further that these response alterations are mediated, at least in part, by receptors of the P-2y subtype. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 AUBERT A, 1993, ATP MAY HAVE NEUROMO, V16, P114 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BOBBIN RP, 1992, NOISE INDUCED HEARIN, P38 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1991, HEARING RES, V56, P101, DOI 10.1016/0378-5955(91)90159-7 BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BOBBIN RP, 1981, HEARING RES, V5, P265, DOI 10.1016/0378-5955(81)90050-2 BOBBIN RP, 1979, SOC NEUR ABSTR, V5, P16 Brownell W. E., 1986, NEUROBIOLOGY HEARING, P91 BURNSTOCK G, 1990, ANN NY ACAD SCI, V603, P1 CRIST JR, 1993, HEARING RES, V69, P194, DOI 10.1016/0378-5955(93)90107-C DALLOS P, 1992, J NEUROSCI, V12, P4575 Dallos P., 1973, AUDITORY PERIPHERY B DULON D, 1993, CELL CALCIUM, V14, P245, DOI 10.1016/0143-4160(93)90071-D DULON D, 1991, NEUROREPORT, V2, P69, DOI 10.1097/00001756-199102000-00001 EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 IKEDA K, 1991, ORL J OTO-RHINO-LARY, V53, P78 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 KONISHI T, 1979, ACTA OTO-LARYNGOL, V87, P506, DOI 10.3109/00016487909126459 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 KUJAWA SG, 1994, IN PRESS HEAR RES KUJAWA SG, 1992, HEARING RES, V61, P106, DOI 10.1016/0378-5955(92)90041-K MROZ EA, 1989, HEARING RES, V38, P141, DOI 10.1016/0378-5955(89)90136-6 MURASE K, 1989, NEUROSCI LETT, V103, P56, DOI 10.1016/0304-3940(89)90485-0 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PEARSON JD, 1980, BIOCHEM J, V190, P421 SALT AN, 1986, NEUROBIOLOGY HEARING, P109 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 THALMANN R, 1973, LARYNGOSCOPE, V83, P1690, DOI 10.1288/00005537-197310000-00010 ULFENDAHL M, 1987, ACTA PHYSIOL SCAND, V130, P521, DOI 10.1111/j.1748-1716.1987.tb08171.x WELFORD LA, 1987, EUR J PHARMACOL, V141, P123, DOI 10.1016/0014-2999(87)90418-3 WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 Yamashita T, 1993, Acta Otolaryngol Suppl, V500, P26 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 42 TC 73 Z9 73 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 1 PY 1994 VL 76 IS 1-2 BP 87 EP 100 DI 10.1016/0378-5955(94)90091-4 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200011 PM 7928720 ER PT J AU HENDERSON, D SPONGR, V SUBRAMANIAM, M CAMPO, P AF HENDERSON, D SPONGR, V SUBRAMANIAM, M CAMPO, P TI ANATOMICAL EFFECTS OF IMPACT NOISE SO HEARING RESEARCH LA English DT Article DE IMPACT NOISE; NOISE INDUCED HEARING LOSS; COCHLEAR PATHOLOGY ID CHINCHILLA; COCHLEA; EXPOSURE; RECOVERY; DAMAGE; TRAUMA AB Four groups of binaural chinchillas were exposed to impact noise (B-duration = 200 ms) ranging from 119 dB to 137 dB peak equivalent SPL at repetition rates of 1/s or 4/s. The duration of exposure was adjusted so that each exposure consisted of equal acoustic energy. Animals were then sacrificed immediately, 24 h or 30 days after the exposure and their cochleas subjected to scanning electron microscopy. For exposures of 119 dB or greater, there appeared to be direct mechanical damage, including large clefts between the third row of outer hair cells and Deiters' cells and fracture of tight cell junctions at the reticular lamina. There was also a progressive increase in cochlear damage over the 30 days of recovery. The patterns of cochlear pathology are compared with hearing losses and cochleograms of chinchillas previously subjected to similar exposures and with results of studies using higher level impulse noise. The results are discussed in terms of 'critical level' for impact and impulse noise. C1 INST NATL RECH & SECUR,F-54501 VANDOEUVRE NANCY,FRANCE. RP HENDERSON, D (reprint author), SUNY BUFFALO,DEPT COMMUNICAT DISORDERS & SCI,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214, USA. CR BOHNE B, 1976, HEARING DAVIS ESSAYS BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 CEYPEK T, 1973, P INT C NOISE PUBLIC DANIELSON R, 1991, J ACOUST SOC AM, V90, P209, DOI 10.1121/1.402361 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 HAMERNIK RP, 1984, HEARING RES, V13, P229, DOI 10.1016/0378-5955(84)90077-7 HAMERNIK RP, 1984, HEARING RES, V16, P143, DOI 10.1016/0378-5955(84)90004-2 HAMERNIK RP, 1988, J ACOUST SOC AM, V84, P941, DOI 10.1121/1.396663 HENDERSON D, 1991, J ACOUST SOC AM, V89, P1350, DOI 10.1121/1.400658 HENDERSO.D, 1974, J ACOUST SOC AM, V56, P1210, DOI 10.1121/1.1903410 HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 HUNTERDUVAR IM, 1987, DISEASES EAR CLIN PA HUNTERDUVAR IM, 1982, NEW PERSPECTIVES NOI LUZ GA, 1971, J ACOUST SOC AM, V49, P1770, DOI 10.1121/1.1912580 MALICK LE, 1975, EVALUATION MODIFIED, P259 MARTIN A, 1976, EFFECTS NOISE HEARIN MCROBERT H, 1973, J ACOUST SOC AM, V53, P1297, DOI 10.1121/1.1913468 PASSCHIERVERMEE.W, 1983, NOISE PUBLIC HLTH PR RAPHAEL Y, 1991, HEARING RES, V53, P173, DOI 10.1016/0378-5955(91)90052-B Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 WARD WD, 1963, MODERN DEV AUDIOLOGY 1983, FED REGISTER, V48, P9738 NR 23 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 101 EP 117 DI 10.1016/0378-5955(94)90092-2 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200012 PM 7928703 ER PT J AU MATSUNAGA, T KANZAKI, J HOSODA, Y AF MATSUNAGA, T KANZAKI, J HOSODA, Y TI ULTRASTRUCTURE OF ASTROCYTES IN THE TRANSITIONAL REGION OF THE HUMAN 8TH CRANIAL NERVE SO HEARING RESEARCH LA English DT Article DE ULTRASTRUCTURE; ASTROCYTES; HUMAN 8TH CRANIAL NERVE ROOT; TRANSITIONAL REGION; GLIAL LIMITING MEMBRANE ID GLIAL LIMITING MEMBRANE; CORTEX AB The nerve root segment where the transition from central to peripheral nervous tissue occurs is referred to as the transitional region (TR). Part of the TR is a continuation of the subpial glial limiting membrane (SGLM) which covers the surface of the brain. To assess the physiological and pathophysiological roles of astrocytes in the TR of the human eighth cranial nerve, electron microscopy was performed on surgically resected specimens of the eighth cranial nerve root obtained from patients with cerebellopontine angle tumors. The astrocytic glial dome was sharply bounded by a basement membrane and was mainly composed of the bodies and processes of fibrous astrocytes. Desmosomes and gap junctions were found between these astrocytic processes. Half-desmosomes were found on the edge of the astrocytic glial dome and at the luminal surface of the perivascular glial limiting membrane. These ultrastructural features indicate that the astrocytes of. the TR might have some motility capacity that allows adjustment to changes in the pressure exerted by the vessels, the peripheral nervous tissue, and the cerebrospinal fluid. In addition, it is also suggested that lack of structures linking the central and peripheral portions of the nerve and the abrupt change of nerve composition at the TR might predispose this area to injury by tractional forces or pathologic conditions such as tumor or arterial compression. C1 KEIO UNIV,SCH MED,DEPT PATHOL,SHINJUKU KU,TOKYO 160,JAPAN. RP MATSUNAGA, T (reprint author), KEIO UNIV,SCH MED,DEPT OTOLARYNGOL,SHINJUKU KU,35 SHINANOMACHI,TOKYO 160,JAPAN. CR BENECKE JE, 1988, LARYNGOSCOPE, V98, P807 Berthold C H, 1977, Acta Physiol Scand Suppl, V446, P23 BERTHOLD CH, 1984, PERIPHERAL NEUROPATH, V2, P156 BONDAREF.W, 1973, AM J ANAT, V136, P277, DOI 10.1002/aja.1001360303 BRAAK E, 1975, CELL TISSUE RES, V157, P367 BRIGHTMA.MW, 1969, J CELL BIOL, V40, P648, DOI 10.1083/jcb.40.3.648 Ghadially FN, 1988, ULTRASTRUCTURAL PATH Janetta PJ, 1980, ANN SURG, V192, P518 JANETTA PJ, 1984, NEW ENGL J MED, V310, P1700 Kanzaki J, 1991, Acta Otolaryngol Suppl, V487, P6 Kanzaki J, 1991, Acta Otolaryngol Suppl, V487, P17 KING JS, 1968, ANAT REC, V161, P111, DOI 10.1002/ar.1091610112 KING JS, 1970, Z ZELLFORSCH MIK ANA, V106, P309, DOI 10.1007/BF00335775 KVETON JF, 1989, OTOLARYNG HEAD NECK, V100, P594 LANDIS DMD, 1981, J EXP BIOL, V95, P35 LANDIS DMD, 1982, NEUROSCIENCE, V7, P937, DOI 10.1016/0306-4522(82)90053-7 LOPES CAS, 1974, ACTA NEUROPATHOL, V28, P79 MORI S, 1969, J COMP NEUROL, V137, P197, DOI 10.1002/cne.901370206 NEMECEK S, 1969, Folia Morphologica (Prague), V17, P171 PETERS A, 1967, J CELL BIOL, V32, P113, DOI 10.1083/jcb.32.1.113 PETERS A, 1976, FINE STRUCTURE NERVO, P231 REESE TS, 1967, J CELL BIOL, V34, P207, DOI 10.1083/jcb.34.1.207 ROSS MD, 1971, AM J ANAT, V130, P73, DOI 10.1002/aja.1001300106 SASAKI H, 1989, ANAT EMBRYOL, V179, P533, DOI 10.1007/BF00315696 SEKIYA T, 1987, J NEUROSURG, V67, P244, DOI 10.3171/jns.1987.67.2.0244 SUAREZNAJERA I, 1980, J ANAT, V130, P55 Tarlov IM, 1937, ARCH NEURO PSYCHIATR, V37, P555 UEHARA M, 1988, JPN J VET SCI, V50, P115 VAUGHN JE, 1969, Z ZELLFORSCH MIK ANA, V94, P293, DOI 10.1007/BF00319179 VAUGHN JE, 1967, AM J ANAT, V121, P131, DOI 10.1002/aja.1001210109 WAGNER HJ, 1983, ANAT EMBRYOL, V166, P427, DOI 10.1007/BF00305928 NR 31 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 118 EP 126 DI 10.1016/0378-5955(94)90093-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200013 PM 7928704 ER PT J AU HULTCRANTZ, M SYLVEN, L BORG, E AF HULTCRANTZ, M SYLVEN, L BORG, E TI EAR AND HEARING PROBLEMS IN 44 MIDDLE-AGED WOMEN WITH TURNERS-SYNDROME SO HEARING RESEARCH LA English DT Article DE TURNERS SYNDROME; AGING; HEARING LOSS; KARYOTYPE ID NEWBORN CHILDREN AB The present study has investigated ear and hearing problems in 44 women with Turner's syndrome (median age 45.5 years). Social hearing problems were common after the age of 40 and 27% were fitted with hearing aids. Audiograms revealed a hearing loss > 20 dB hearing level (HL) in 91% leading to clinically significant hearing problems in 60%. A distinct dip in the 1.5 kHz frequency range, with a mean value of 46 dB was found in 30 women. The occurrence of the dip was correlated to the karyotype. All women with the karyotype 45,X and 45,X/46,X,i(Xq) demonstrated this dip while in the 45,X/46,XX group it was found in 31%. No dips were found among 45,X/46,XY and 45,X/46,XX/47,XXX women. With increasing age a progressive high frequency hearing loss was added to the dip leading to severe hearing problems earlier in the Turner women than age-matched controls. This might be due to a genetic defect leading to premature ageing of their hearing organ. These data emphasize the importance of providing early information to Turner girls of their predisposition to hearing impairment. Patient awareness of importance of audiological evaluations and the benefit of hearing aids should be stressed. C1 KAROLINSKA HOSP,DEPT OBSTET & GYNECOL,S-10401 STOCKHOLM,SWEDEN. KAROLINSKA HOSP,DEPT AUDIOL,S-10401 STOCKHOLM,SWEDEN. OREBRO MED CTR HOSP,DEPT AUDIOL,S-70185 OREBRO,SWEDEN. RP HULTCRANTZ, M (reprint author), KAROLINSKA HOSP,DEPT OTORHINOLARYNGOL,S-10401 STOCKHOLM,SWEDEN. CR ANDERSON H, 1969, ACTA OTOLARYNGOL S S, V247 Anderson H, 1968, Acta Otolaryngol, V65, P535, DOI 10.3109/00016486809120997 BERTHRAND LL, 1990, HDB HORSELMATNING BUCHANAN LH, 1990, SCAND AUDIOL, V19, P103, DOI 10.3109/01050399009070760 EVANS HJ, 1977, J MED GENET, V14, P309, DOI 10.1136/jmg.14.5.309 GARRON DC, 1977, BEHAV GENET, V7, P105, DOI 10.1007/BF01066000 Hassold T, 1990, Birth Defects Orig Artic Ser, V26, P297 HASSOLD T, 1992, HUM GENET, V89, P647 HULTCRANTZ M, 1993, EUR ARCH OTO-RHINO-L, V250, P257 LI HS, 1993, ORL, V56, P61 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 Paparella M M, 1970, Trans Am Acad Ophthalmol Otolaryngol, V74, P108 PEERHENTUPA J, 1975, ACTA PAEDIATR SC S, V256, P24 POLANI PE, 1982, HUM GENET, V60, P207, DOI 10.1007/BF00303003 SCULERATI N, 1990, ARCH OTOLARYNGOL, V116, P704 SYLVEN L, 1991, ACTA ENDOCRINOL-COP, V125, P359 Takano K, 1986, Acta Paediatr Scand Suppl, V325, P58 Turner HH, 1938, ENDOCRINOLOGY, V23, P566 WATKIN PM, 1989, J LARYNGOL OTOL, V103, P731, DOI 10.1017/S0022215100109934 ZACHMANN M, 1992, EUR J PEDIATR, V151, P167, DOI 10.1007/BF01954375 1985, ISO DOCUMENTS NR 23 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 127 EP 132 DI 10.1016/0378-5955(94)90094-9 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200014 PM 7928705 ER PT J AU STERBING, SJ SCHMIDT, U RUBSAMEN, R AF STERBING, SJ SCHMIDT, U RUBSAMEN, R TI THE POSTNATAL-DEVELOPMENT OF FREQUENCY-PLACE CODE AND TUNING CHARACTERISTICS IN THE AUDITORY MIDBRAIN OF THE PHYLLOSTOMID BAT - CAROLLIA-PERSPICILLATA SO HEARING RESEARCH LA English DT Article DE AUDITION; ONTOGENY; TONOTOPY; MIDBRAIN; BAT ID INFERIOR COLLICULUS; GERBIL COCHLEA; RAT ORGAN; TONOTOPY; MATURATION; PRINCIPLE; AUDITION; CORTI; MAP AB This report describes the postnatal development of hearing range, auditory sensitivity and tonotopy within the inferior colliculus (IC) of a mammal specialized for ultrasonic hearing. The experimental animal, Carollia perspicillata, has an adult hearing range of 7-110 kHz (characteristic frequencies) but lack any significant overrepresentation of a limited frequency band as known for rhinolophoid bats and Pteronotus, The audiogram of the newborn Carollia includes characteristic frequencies from 8 to 76 kHz, which is about 65% of the adult hearing range. As in adults, low frequencies are represented in the dorsolateral portion of the IC. However, at birth the ventromedial IC is non-responsive to acoustic stimulation up to intensities of 90 dB SPL. During development there is a progressive conversion of non-responsive IC areas into acoustically responsive slabs with characteristic frequencies above 76 kHz along the dorsolateral to ventromedial (low-to-high frequency) IC axis. This development is superimposed by a non-uniform shift of characteristic frequency: a decrease of CFs in dorsolateral regions, and an increase of CFs in ventromedial areas. The results suggest a bidirectional shift of frequency representation along the cochlear tonotopic axis. C1 UNIV BONN,INST ZOOL,D-53012 BONN,GERMANY. UNIV LEIPZIG,INST ZOOL,D-04130 LEIPZIG,GERMANY. RP STERBING, SJ (reprint author), RUHR UNIV BOCHUM,LEHRSTUHL ALLGEMEINE ZOOL & NEUROBIOL,UNIV STR 150,D-44780 BOCHUM,GERMANY. RI Sterbing-D'Angelo, Susanne/H-5899-2012 CR ARATA ANDREW A., 1967, LOZANIA ACTA ZOOL COLOMBIANA, V14, P1 ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 Brown P.E., 1980, ANIMAL SONAR SYSTEMS, P355 BRUGGE JF, 1978, J NEUROPHYSIOL, V41, P1557 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 GOULD E, 1975, J MAMMAL, V56, P15, DOI 10.2307/1379603 HUFFMAN RF, 1991, HEARING RES, V56, P79, DOI 10.1016/0378-5955(91)90156-4 KOSSL M, 1985, HEARING RES, V19, P157, DOI 10.1016/0378-5955(85)90120-0 Larsell O, 1944, ARCHIV OTOLARYNGOL, V40, P233 LARSELLO, 1944, T AM ACAD OPHTALMOL, V48, P333 Lorente de No R., 1933, LARYNGOSCOPE, V43, P1 MARIMUTHU G, 1987, J COMP PHYSIOL A, V159, P403 MCNAB BK, 1969, COMP BIOCHEM PHYSIOL, V31, P227, DOI 10.1016/0010-406X(69)91651-X MEININGER V, 1986, NEUROSCIENCE, V17, P1159, DOI 10.1016/0306-4522(86)90085-0 MOREST K, 1966, ANAT REC, V154, P389 NEUWEILER G, 1990, PHYSIOL REV, V70, P615 PUJOL R, 1970, J COMP NEUROL, V139, P115, DOI 10.1002/cne.901390108 Romand R., 1983, DEV AUDITORY VESTIBU, P47 ROMAND R, 1990, DEV BRAIN RES, V54, P221, DOI 10.1016/0165-3806(90)90145-O ROTH B, 1992, ANAT EMBRYOL, V185, P559, DOI 10.1007/BF00185615 ROTH B, 1992, ANAT EMBRYOL, V185, P571, DOI 10.1007/BF00185616 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RUBEL EW, 1984, ANN OTO RHINOL LARYN, V93, P609 RUBSAMEN R, 1989, J COMP PHYSIOL A, V165, P755, DOI 10.1007/BF00610874 RUBSAMEN R, 1990, J COMP PHYSIOL A, V167, P757 RUBSAMEN R, 1990, J COMP PHYSIOL A, V167, P771 RUBSAMEN R, 1988, J COMP PHYSIOL A, V163, P271, DOI 10.1007/BF00612436 RUBSAMEN R, 1992, J COMP PHYSIOL A, V170, P129 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 Ryan A F, 1988, Brain Res, V469, P61 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SCHAFER M, 1991, THESIS RUHR U BOCHUM SCHMIDT U, 1991, J COMP PHYSIOL A, V168, P45, DOI 10.1007/BF00217102 STERBING S, 1990, 18TH P GOTT NEUR C VATER M, 1988, COCHLEAR MECH STRUCT, P217 NR 35 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 133 EP 146 DI 10.1016/0378-5955(94)90095-7 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200015 PM 7928706 ER PT J AU BRIX, J MANLEY, GA AF BRIX, J MANLEY, GA TI MECHANICAL AND ELECTROMECHANICAL PROPERTIES OF THE STEREOVILLAR BUNDLES OF ISOLATED AND CULTURED HAIR-CELLS OF THE CHICKEN SO HEARING RESEARCH LA English DT Article DE STEREOVILLAR BUNDLES; STIMULATION; RESONANCE; MOVEMENT; ACTIVATION ID BASILAR PAPILLA; MECHANOELECTRICAL TRANSDUCTION; ADAPTATION; COCHLEA; MOVEMENTS; INNERVATION; CURRENTS; SEM AB Isolated single chicken hair cells and pieces of epithelium without the tectorial membrane, either freshly isolated or in tissue culture, were studied using water-jet stimulation of their stereovillar bundles and current injection. Responses were measured under enhanced video-microscopic observation or while using a differential photodiode technique sensitive down into the nanometer range. When stimulated with a water jet at low displacement amplitudes up to about 200 nm, the stereovillar bundle displacement was asymmetrical, indicating a lower stiffness in the excitatory direction, but the reverse was true at higher displacement amplitudes. Undamaged bundles showed no mechanical resonances below 1 kHz. In damaged bundles, however, such resonances were prominent and accompanied by splaying of the stereovilli. Hair cells in the epithelium showed small bundle movements (0.6 nm/mV) whose polarity depended on the polarity of the injected current. These movements probably resulted from activation of the bundle's adaptation motors. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. CR ASSAD JA, 1992, J NEUROSCI, V12, P3291 COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 DALLOS P, 1992, J NEUROSCI, V12, P4575 EATOCK RA, 1987, J NEUROSCI, V7, P2821 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 FUCHS PA, 1988, J NEUROSCI, V8, P2460 HOLTON T, 1986, J PHYSIOL-LONDON, V375, P195 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 KOPPL C, 1993, BIOPHYSICS HAIR CELL, P216 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1989, COCHLEAR MECH STRUCT, P143 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MURROW BW, 1990, P ROY SOC B-BIOL SCI, V242, P189, DOI 10.1098/rspb.1990.0123 PICKLES JO, 1990, HEARING RES, V50, P139, DOI 10.1016/0378-5955(90)90040-V RUSCH A, 1990, HEARING RES, V48, P247, DOI 10.1016/0378-5955(90)90065-W SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SZYMKO YM, 1992, HEARING RES, V59, P241, DOI 10.1016/0378-5955(92)90120-C 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 YATES GK, 1982, J NEUROSCI METH, V6, P103, DOI 10.1016/0165-0270(82)90020-6 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 ZWISLOCKI J, 1988, 11TH M ASS RES OT, P170 NR 29 TC 19 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 147 EP 157 DI 10.1016/0378-5955(94)90096-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200016 PM 7928707 ER PT J AU FAY, RR AF FAY, RR TI PERCEPTION OF TEMPORAL ACOUSTIC PATTERNS BY THE GOLDFISH (CARASSIUS-AURATUS) SO HEARING RESEARCH LA English DT Article DE HEARING; PERCEPTION; PITCH; TEMPORAL PATTERNS; GOLDFISH; STIMULUS GENERALIZATION ID FREQUENCY DISCRIMINATION; INTENSITY; LEVEL; TONES; PITCH AB The perception of temporal acoustic patterns was studied in the goldfish using classical respiratory conditioning in combination with a stimulus generalization paradigm. Stimuli consisted of a bandpass filtered pulse repeated in various periodic and aperiodic temporal patterns. In each of 14 experiments, animals received 40 conditioning trials to a given stimulus pattern and were then tested for generalization to eight novel stimuli differing only in temporal pattern. In experiments 1-5, animals were conditioned to a periodic pulse train with a particular interpulse interval (IPI) and then tested to novel periodic pulse trains with various IPIs. Generalization gradients were substantially symmetric and monotonic with repetition rate, suggesting a perceptual continuum in goldfish that is similar to periodicity pitch or roughness in human listeners. Several additional experiments indicated that the perceptual qualities of simple and complex temporal patterns are not primarily determined by spectral structure or pulse rate, but rather are determined by the distribution of IPIs. A model for the central analysis of IPIs was successful in accounting for the results of experiments in which animals were conditioned to simple, periodic stimuli. However, the model failed when animals were conditioned to more complex stimuli having aperiodic temporal patterns. These experiments demonstrate the potential usefulness of the stimulus generalization paradigm for investigating aspects of complex sound source perception in non-human animals. C1 LOYOLA UNIV,DEPT PSYCHOL,CHICAGO,IL 60626. LOYOLA UNIV,PARMLY HEARING INST,CHICAGO,IL 60626. CR Bregman AS., 1990, AUDITORY SCENE ANAL COOMBS S, 1989, J ACOUST SOC AM, V86, P925, DOI 10.1121/1.398727 DEBOER E, 1976, HDB SENSORY PHYSL, V5, P479 FAY RR, 1992, HEARING RES, V59, P101, DOI 10.1016/0378-5955(92)90107-X FAY RR, 1972, J ACOUST SOC AM, V52, P660, DOI 10.1121/1.1913155 Fay R. R., 1988, HEARING VERTEBRATES FAY RR, 1970, J EXP ANAL BEHAV, V14, P353, DOI 10.1901/jeab.1970.14-353 FAY R, 1969, J AUD RES, V9, P112 FAY RR, 1970, J COMP PHYSIOL PSYCH, V73, P175, DOI 10.1037/h0030245 FAY RR, 1992, J ACOUST SOC AM, V92, P189, DOI 10.1121/1.404282 FAY RR, 1989, J ACOUST SOC AM, V85, P500, DOI 10.1121/1.397704 FAY RR, 1978, J EXP BIOL, V74, P83 FAY RR, 1982, J COMP PHYSIOL, V147, P201 FAY RR, 1986, J ACOUST SOC AM, V79, P1883, DOI 10.1121/1.393196 FAY RR, 1974, J COMP PHYSIOL PSYCH, V87, P708, DOI 10.1037/h0037002 FAY RR, 1985, J ACOUST SOC AM, V78, P1296, DOI 10.1121/1.392899 FAY RR, 1989, J ACOUST SOC AM, V85, P503, DOI 10.1121/1.397705 Green D. M., 1988, PROFILE ANAL HALL JW, 1984, J ACOUST SOC AM, V76, P50, DOI 10.1121/1.391005 Hartmann W. M., 1988, AUDITORY FUNCTION, P623 HOUTSMA AJM, 1972, J ACOUST SOC AM, V51, P520, DOI 10.1121/1.1912873 JACOBS DW, 1968, ANIM BEHAV, V16, P67, DOI 10.1016/0003-3472(68)90111-5 Licklider J. C. R., 1959, PSYCHOL STUDY SCI, V1, P41 LICKLIDER JCR, 1951, EXPERIENTIA, V7, P128, DOI 10.1007/BF02156143 LU Z, 1993, J COMP PHYSIOL A, V173, P33 Malott R. W., 1970, ANIMAL PSYCHOPHYSICS, P363 STOVER LJ, 1983, J ACOUST SOC AM, V73, P1701, DOI 10.1121/1.389393 STREIDTER GF, 1991, J COMP NEUROL, V312, P311 TAVOLGA WN, 1974, J ACOUST SOC AM, V55, P1323, DOI 10.1121/1.1914704 TERHARDT E, 1974, ACUSTICA, V30, P201 YOST WA, 1989, J ACOUST SOC AM, V86, P2138, DOI 10.1121/1.398474 YOST WA, 1992, HEARING RES, V56, P8 NR 32 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 1 PY 1994 VL 76 IS 1-2 BP 158 EP 172 DI 10.1016/0378-5955(94)90097-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200017 PM 7928708 ER PT J AU RAPHAEL, Y ATHEY, BD WANG, Y LEE, MK ALTSCHULER, RA AF RAPHAEL, Y ATHEY, BD WANG, Y LEE, MK ALTSCHULER, RA TI F-ACTIN, TUBULIN AND SPECTRIN IN THE ORGAN OF CORTI - COMPARATIVE DISTRIBUTION IN DIFFERENT CELL-TYPES AND MAMMALIAN-SPECIES SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; CONFOCAL MICROSCOPY; CYTOSKELETON; MEMBRANE SKELETON; HISTOCHEMISTRY ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; INNER-EAR; PROTEINS; CYTOSKELETAL; LOCALIZATION; FODRIN; REORGANIZATION; DEGENERATION; EXPRESSION AB Laser scanning confocal microscopy was used to determine the distribution of actin, spectrin and tubulin in whole mounts of the organ of Corti of guinea pig, monkey, rat and chinchilla. Actin, spectrin and tubulin were localized in all cell types in the auditory epithelium. No specialized cytoskeletal organization of tubulin was detected in the cytoplasmic domain of hair cells. The only specialized organization of actin and spectrin in the cytoplasmic domain was the infra-cuticular network, found exclusively in apical guinea pig outer hair cells. In contrast, the lateral wall of inner and outer hair cells contained a homogenous distribution of label specific for actin and spectrin. The label intensity was similar in the base and the apex of the cochlea. These results indicate that the distribution of spectrin and actin in the auditory epithelium is similar to that in other epithelial cells, suggesting that actin and spectrin participate in the formation of cellular shape and possibly in docking molecules to the membrane. RP RAPHAEL, Y (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR ALBRECHTBUEHLER G, 1990, INT REV CYTOL, V120, P191, DOI 10.1016/S0074-7696(08)61601-0 ANGELBORG C, 1973, BASIC MECHANISMS HEA, P157 BANNIKO M, 1989, ACTA OTOLARYNGOL, V180, P385 Bannister L H, 1988, Prog Brain Res, V74, P213 BAUWENS LJJM, 1991, ANN OTO RHINOL LARYN, V100, P211 BRETSCHER A, 1991, ANNU REV CELL BIOL, V7, P337, DOI 10.1146/annurev.cb.07.110191.002005 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BURRIDGE K, 1982, J CELL BIOL, V95, P478, DOI 10.1083/jcb.95.2.478 CARLISLE L, 1988, HEARING RES, V33, P201, DOI 10.1016/0378-5955(88)90033-0 DALLOS P, 1992, J NEUROSCI, V12, P4575 ELBARBARY A, 1993, HEARING RES, V71, P80 FLOCK A, 1982, HEARING RES, V6, P75 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 HAWKINS JE, 1976, HDB AUDITORY PHYSL, V5, P723 HELD H, 1926, HDB NORMALEN PATHOLO, V2, P467 HIEL H, 1992, HEARING RES, V57, P157, DOI 10.1016/0378-5955(92)90148-G HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1992, J CELL SCI, V102, P569 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 KACHAR B, 1993, ASS RES OTOLARYNGOL, P455 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KUIJPERS W, 1991, HEARING RES, V52, P133, DOI 10.1016/0378-5955(91)90193-D KUIJPERS W, 1992, HEARING RES, V62, P1, DOI 10.1016/0378-5955(92)90197-U NISHIDA Y, 1993, HEARING RES, V65, P274, DOI 10.1016/0378-5955(93)90220-U RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 RAPHAEL Y, 1986, J SUBMICR CYTOL PATH, V18, P731 REPASKY EA, 1991, STRUCTURE BIOL MEMBR, P449 SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SLEPECKY N, 1982, CELL TISSUE RES, V224, P15, DOI 10.1007/BF00217262 SLEPECKY NB, 1992, HEARING RES, V57, P201, DOI 10.1016/0378-5955(92)90152-D STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 WEAVER SP, 1993, BRAIN RES BULL, V31, P225, DOI 10.1016/0361-9230(93)90029-B WRIGHT CG, 1973, BRAIN RES, V58, P37, DOI 10.1016/0006-8993(73)90822-6 YLIKOSKI J, 1990, HEARING RES, V43, P199, DOI 10.1016/0378-5955(90)90228-H YLIKOSKI J, 1992, HEARING RES, V60, P80, DOI 10.1016/0378-5955(92)90061-Q ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 43 TC 50 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 173 EP 187 DI 10.1016/0378-5955(94)90098-1 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200018 PM 7928710 ER PT J AU HEIL, P RAJAN, R IRVINE, DRF AF HEIL, P RAJAN, R IRVINE, DRF TI TOPOGRAPHIC REPRESENTATION OF TONE INTENSITY ALONG THE ISOFREQUENCY AXIS OF CAT PRIMARY AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE INTENSITY; INTENSITY DISCRIMINATION; LOUDNESS; TOPOGRAPHY; AUDITORY CORTEX ID SOUND PRESSURE LEVEL; FUNCTIONAL TOPOGRAPHY; INFERIOR COLLICULUS; NERVE FIBERS; NEURONS; RESPONSES; ORGANIZATION; NOISE; SENSITIVITY; AI AB The sound pressure level (SPL), henceforth termed intensity, of acoustic signals is encoded in the central auditory system by neurons with different forms of intensity sensitivity. However, knowledge about the topographic organization of neurons with these different properties and hence about the spatial representation of intensity, especially at higher levels of the auditory pathway, is limited. Here we show that in the tonotopically organized primary auditory cortex (AI) of the cat there are orderly topographic organizations, along the isofrequency axis, of several neuronal properties related to the coding of the intensity of tones, viz. minimum threshold, dynamic range, best SPL, and non-monotonicity of spike count - intensity functions to tones of characteristic frequency (CF). Minimum threshold, dynamic range, and best SPL are correlated and alter periodically along isofrequency strips. The steepness of the high-intensity descending slope of spike count - intensity functions also varies systematically, with steepest slopes occurring in the regions along an isofrequency strip where low thresholds, narrow dynamic ranges and low best SPLs are found. As a consequence, CF-tones of various intensities are represented by orderly and, for most intensities, periodic, spatial patterns of distributed neuronal activity along an isofrequency strip. For low - to -moderate intensities, the mean relative activity along the entire isofrequency strip increases rapidly with intensity, with the spatial pattern of activity remaining quite constant along the strip. At higher intensities, however, the mean relative activity along the strip remains fairly constant with changes in intensity, but the spatial patterns change markedly. As a consequence of these effects, low- and high-intensity tones are represented by complementary distributions of activity alternating along an isofrequency strip. We conclude that in AI tone intensity is represented by two complementary modes, viz. discharge rate and place. Furthermore, the magnitude of the overall changes in the representation of tone intensity in Al appears to be closely related to psychophysical measures of loudness and of intensity discrimination. C1 MONASH UNIV,DEPT PSYCHOL,CLAYTON,VIC 3168,AUSTRALIA. RP HEIL, P (reprint author), TECH UNIV DARMSTADT,INST ZOOL,SCHNITTSPAHNSTR 3,D-64287 DARMSTADT,GERMANY. RI Rajan, Ramesh/A-5945-2008; Irvine, Dexter/F-7474-2011 CR AITKIN L., 1990, AUDITORY CORTEX BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 EHRET G, 1988, HEARING RES, V35, P1, DOI 10.1016/0378-5955(88)90035-4 FAY RR, 1988, HEARING VERTEBRATES, P397 HEIL P, 1993, GENE BRAIN BEHAVIOR, pS284 HEIL P, 1992, HEARING RES, V63, P135, DOI 10.1016/0378-5955(92)90081-W HEIL P, 1993, EUR J NEUROSCI, V6, P801 HEILP, 1992, HEARING RES, V63, P108 HELLMAN RP, 1961, J ACOUST SOC AM, V33, P687, DOI 10.1121/1.1908764 IMIG TJ, 1990, J NEUROPHYSIOL, V63, P1448 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 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 OESTERRE.RE, 1971, BRAIN RES, V27, P251, DOI 10.1016/0006-8993(71)90252-6 Ojima H, 1991, CEREB CORTEX, V1, P80, DOI 10.1093/cercor/1.1.80 PFINGST BE, 1981, J NEUROPHYSIOL, V45, P16 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1985, HEARING RES, V18, P73, DOI 10.1016/0378-5955(85)90111-X PHILLIPS DP, 1981, J NEUROPHYSIOL, V45, P48 RAJAN R, 1990, J NEUROPHYSIOL, V64, P888 RAJAN R, 1991, HEARING RES, V53, P153, DOI 10.1016/0378-5955(91)90222-U RAJAN R, 1993, J COMP NEUROL, V338, P17, DOI 10.1002/cne.903380104 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SCHREINER CE, 1992, EXP BRAIN RES, V92, P105 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SHAMMA SA, 1993, J NEUROPHYSIOL, V69, P367 Smith R. L., 1988, AUDITORY FUNCTION NE, P243 Suga N., 1982, CORTICAL SENSORY ORG, P157 Suga N., 1984, DYNAMIC ASPECTS NEOC, P315 SUGA N, 1985, J NEUROPHYSIOL, V53, P1109 SUGA N, 1977, SCIENCE, V196, P64, DOI 10.1126/science.190681 THOMAS H, 1993, EUR J NEUROSCI, V5, P882, DOI 10.1111/j.1460-9568.1993.tb00940.x Viemeister N., 1988, AUDITORY FUNCTION NE, P213 VIEMEISTER NF, 1983, SCIENCE, V221, P1206, DOI 10.1126/science.6612337 WALLACE MN, 1991, EXP BRAIN RES, V86, P527 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E NR 41 TC 94 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 JUN 1 PY 1994 VL 76 IS 1-2 BP 188 EP 202 DI 10.1016/0378-5955(94)90099-X PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NR712 UT WOS:A1994NR71200019 PM 7928711 ER PT J AU SYKA, J POPELAR, J AF SYKA, J POPELAR, J TI MODULATION OF THRESHOLDS TO ACOUSTICAL AND ELECTRICAL-STIMULATION OF THE INTACT EAR IN GUINEA-PIG BY FUROSEMIDE AND NOISE SO HEARING RESEARCH LA English DT Article DE INNER EAR; ELECTRICAL STIMULATION; ELECTROPHONIC EFFECT; GUINEA PIG; MIDDLE LATENCY RESPONSES ID OUTER HAIR-CELLS; AUDITORY-NERVE; PHYSIOLOGICAL-PROPERTIES; RESPONSES; COCHLEA; POTENTIALS; RECORDINGS; CATS AB Middle latency responses (MLR) to acoustical stimulation (AS) and to electrical stimulation (ES) of the intact inner ear were recorded in guinea pigs. ES threshold curve decreased in the frequency range 2-16 kHz with a slope 5.4 dB/ octave. Immediately after 50 mg/kg intravenous injection of the furosemide, which resulted in a temporary suppression of the cochlear function, the ES thresholds increased and resembled thresholds found in gentamicin-treated animals. Whereas temporary threshold shift (TTS) at 1 kHz ES was negligible at this time, maximum TTS at 8 kHz and 20 kHz ES was limited to 27 dB and 37 dB resp. TTS to acoustical stimulation was larger than TTS to ES (in some cases exceeded 50 dB) and it was similar at all frequencies. Amplitude-intensity functions (AIF) to high-frequency ES stimuli (20 kHz) consisted of two parts - a flat part at low intensities and a steep part at high intensities of the ES. High-frequency noise exposure (third-octave band noise, centered at 16 kHz, intensity 105 dB for 1 h) reduced or abolished only the flat part of the AIF, the steep part, as well as the responses to low-frequency ES, were not substantially changed. TTS at high frequencies, elicited by the noise exposure, were similar for ES and AS. However, amplitudes of acoustically evoked MLR significantly increased after the noise exposure while MLR amplitudes to ES did not change. The results characterize the frequency-intensity domain of the electrophonic effect in the guinea pig and its changes after influencing the inner ear function by furosemide and noise. RP SYKA, J (reprint author), ACAD SCI CZECH REPUBL,INST EXPTL MED,VIDENSKA 1083,CR-14220 PRAGUE 4,CZECH REPUBLIC. RI Popelar, Jiri/H-2558-2014; Syka, Josef/H-3103-2014 CR Aran J M, 1986, Scand Audiol Suppl, V25, P63 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BURTON MJ, 1989, ARCH OTOLARYNGOL, V115, P59 DESAUVAGE RC, 1983, J ACOUST SOC AM, V73, P616 GARDI JN, 1985, COCHLEAR IMPLANTS, P351 GERSUNI GV, 1937, J EXP PSYCHOL, V19, P370 GLASS I, 1983, HEARING RES, V12, P223, DOI 10.1016/0378-5955(83)90108-9 GYO K, 1980, ACTA OTO-LARYNGOL, V90, P25, DOI 10.3109/00016488009131694 Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KAHLER K, 1931, Z HALS NASEN OHRENH, V29, P218 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 LUSTED HS, 1988, J ACOUST SOC AM, V83, P657, DOI 10.1121/1.396160 MCANALLY KI, 1993, HEARING RES, V67, P55, DOI 10.1016/0378-5955(93)90232-P MERZENIC.MM, 1973, ANN OTO RHINOL LARYN, V82, P486 MIYAMOTO RT, 1986, LARYNGOSCOPE, V96, P178 Moxon E.C., 1971, THESIS MIT CAMBRIDGE NAGEL D, 1974, ARCH OTO-RHINO-LARYN, V206, P293, DOI 10.1007/BF00460282 OLEARY SJ, 1985, HEARING RES, V18, P273, DOI 10.1016/0378-5955(85)90044-9 PIKE DA, 1980, HEARING RES, V3, P79, DOI 10.1016/0378-5955(80)90009-X 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 RYBAK LP, 1982, J OTOLARYNGOL, V11, P127 SIMMONS BF, 1972, ANN OTOL, V81, P731 SIMMONS FB, 1979, ANN OTO RHINOL LARYN, V88, P533 Stevens SS, 1939, J ACOUST SOC AM, V10, P261, DOI 10.1121/1.1915984 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 Syka J, 1981, Scand Audiol Suppl, V14 Suppl, P63 SYKA J, 1994, UNPUB HEAR RES SYKA J, 1985, HEARING RES, V20, P267, DOI 10.1016/0378-5955(85)90031-0 VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VOLTA A, 1800, T ROY SOC LOND, V90, P402 YAMANE H, 1981, OTOLARYNG HEAD NECK, V89, P117 ZENNER HP, 1990, ADV AUDIOL, V7, P35 NR 39 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 MAY PY 1994 VL 75 IS 1-2 BP 1 EP 10 DI 10.1016/0378-5955(94)90050-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400001 PM 8071135 ER PT J AU SCHARF, B MAGNAN, J COLLET, L ULMER, E CHAYS, A AF SCHARF, B MAGNAN, J COLLET, L ULMER, E CHAYS, A TI ON THE ROLE OF THE OLIVOCOCHLEAR BUNDLE IN HEARING - A CASE-STUDY SO HEARING RESEARCH LA English DT Article DE EFFERENT SYSTEM; OLIVOCOCHLEAR BUNDLE; SELECTIVE ATTENTION; SIGNAL DETECTION IN NOISE; MENIERES DISEASE ID COCHLEAR FREQUENCY-SELECTIVITY; AUDITORY-NERVE RESPONSE; ELECTRICAL-STIMULATION; CONTRALATERAL SOUND; EFFERENT TRACTS; FILTER SHAPES; NOISE; ATTENTION; NEURONS; BANDWIDTHS AB A young patient with normal pure-tone thresholds in both ears underwent a unilateral vestibular neurotomy in January 1992 to relieve severe vertigo ascribed to Meniere's disease. Evidence is provided that the whole vestibular nerve including the olivocochlear bundle (OCB) was sectioned. Just prior to the surgery, the patient was examined in several psychoacoustic tests involving mainly signal detection and selective attention. Over the next 20 months, he was reexamined in those same tests. The patient's ability to detect expected tones in the quiet (including audiograms) or in noise was the same as before the surgery. The one change was a marked improvement in the detection of unexpected signals in noise, which appears to reflect impaired selective attention. During those 20 months, new tests were also performed on discrimination, loudness, pitch, lateralization, and temporary threshold shift. On these tests, the only differences between the operated and unoperated ears concerned binaural diplacusis and loudness adaptation close to threshold, but these differences may well have been present prior to the surgery. Except with respect to what is probably selective attention, we uncovered no other clear role for the OCB in hearing. This outcome agrees with limited measurements on other patients, with their subjective reports, and with a number of published neurophysiological observations. C1 HOP NORD MARSEILLE,SERV ORL & CHIRUG CERVICOFACIALE,MARSEILLE,FRANCE. HOP EDOUARD HERRIOT,EXPLORAT FONCTIONNELLES ORL LAB,LYON,FRANCE. RP SCHARF, B (reprint author), LAB MECAN & ACOUST,CNRS,MARSEILLE,FRANCE. CR Arnesen A R, 1985, Acta Otolaryngol Suppl, V423, P81 ARNESEN AR, 1984, ACTA OTO-LARYNGOL, V98, P501, DOI 10.3109/00016488409107591 BARGONES JY, 1992, THESIS U WASHINGTON BARUCH C, 1989, 5TH P M INT SOC PSYC, P102 BODIAN D, 1980, J COMP NEUROL, V192, P785, DOI 10.1002/cne.901920411 BONFILS P, 1986, HEARING RES, V24, P277, DOI 10.1016/0378-5955(86)90026-2 BONFILS P, 1986, HEARING RES, V24, P285, DOI 10.1016/0378-5955(86)90027-4 BROOKES GB, 1993, 3RD INT S MEN DIS RO CANEVET G, 1993, ETUDE DETECTION AUDI CANEVET G, 1985, AUDIOLOGY, V24, P430 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1992, AUDIOLOGY, V31, P1 DAI HP, 1991, J ACOUST SOC AM, V89, P2837, DOI 10.1121/1.400721 FISCH U, 1970, ADV OTO-RHINO-LARYNG, V17, P203 Florentine M, 1976, J Am Audiol Soc, V1, P243 GACEK RR, 1961, ARCHIV OTOLARYNGOL, V74, P690 GIARD MH, 1994, BRAIN RES, V633, P353, DOI 10.1016/0006-8993(94)91561-X GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T GREENBER.GZ, 1968, J ACOUST SOC AM, V44, P1513, DOI 10.1121/1.1911290 GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 HAWKINS JE, 1950, J ACOUST SOC AM, V22, P6, DOI 10.1121/1.1906581 HERNANDEZPEON R, 1956, SCIENCE, V123, P331, DOI 10.1126/science.123.3191.331 KRONENBERG J, 1989, MENIERES DISEASE LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 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 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 LITTMAN TA, 1992, J ACOUST SOC AM, V92, P1945, DOI 10.1121/1.405242 MACMILLAN NA, 1975, J ACOUST SOC AM, V58, P1051, DOI 10.1121/1.380764 MAGNAN J, 1992, J FRANCAIS OTORHINOL, V41, P89 MCFADDEN D, 1989, J ACOUST SOC AM, V85, P254, DOI 10.1121/1.397732 MCQUONE SJ, 1993, 16TH MIDW M A R O, P51 MOORE BCJ, 1983, J ACOUST SOC AM, V74, P750, DOI 10.1121/1.389861 PATTERSON RD, 1976, J ACOUST SOC AM, V59, P640, DOI 10.1121/1.380914 PUEL JL, 1988, BRAIN RES, V447, P380, DOI 10.1016/0006-8993(88)91144-4 PUJOL R, 1986, ADV NEURAL BEHAVIORA, P1 PURIA S, 1993, 16TH MIDW M ASS RES, P45 Rajan R, 1992, NOISE INDUCED HEARIN, P429 Schally A V, 1983, Res Front Fertil Regul, V2, P1 SCHARF B, 1993, SENSORY RESEARCH MULTIMODAL PERSPECTIVES, P299 SCHARF B, 1994, SYSTEME EFFERENT COC Scharf B., 1978, HDB PERCEPTION, VIV, P187 SCHARF B, 1987, PERCEPT PSYCHOPHYS, V42, P215, DOI 10.3758/BF03203073 SCHARF B, 1986, HDB PERCEPTION HUMAN, V1 SCHLAUCH RS, 1991, J ACOUST SOC AM, V90, P1332, DOI 10.1121/1.401925 SCHMIDT S, 1991, J ACOUST SOC AM, V89, P1324, DOI 10.1121/1.400656 TAKEYAMA M, 1992, ACTA OTO-LARYNGOL, V112, P205 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WILLIAMS EA, 1993, SCAND AUDIOL, V22, P197, DOI 10.3109/01050399309047469 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 YAMA MF, 1982, J ACOUST SOC AM, V71, P694, DOI 10.1121/1.387546 ZWICKER E, 1965, J ACOUST SOC AM, V38, P132, DOI 10.1121/1.1909588 ZWISLOCK.JJ, 1972, J ACOUST SOC AM, V52, P644, DOI 10.1121/1.1913154 ZWISLOCKI JJ, 1967, PERCEPT PSYCHOPHYS, V2, P59 1969, ANSI S36 AM NAT STAN NR 60 TC 71 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 MAY PY 1994 VL 75 IS 1-2 BP 11 EP 26 DI 10.1016/0378-5955(94)90051-5 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400002 PM 8071137 ER PT J AU SAITOH, Y HOSOKAWA, M SHIMADA, A WATANABE, Y YASUDA, N TAKEDA, T MURAKAMI, Y AF SAITOH, Y HOSOKAWA, M SHIMADA, A WATANABE, Y YASUDA, N TAKEDA, T MURAKAMI, Y TI AGE-RELATED HEARING IMPAIRMENT IN SENESCENCE-ACCELERATED MOUSE (SAM) SO HEARING RESEARCH LA English DT Article DE SENESCENCE-ACCELERATED MOUSE, SAM; PRESBYCUSIS; AUDITORY BRAIN-STEM RESPONSE, ABR; SPIRAL GANGLION ID ANTEROVENTRAL COCHLEAR NUCLEUS; INFERIOR COLLICULUS NEURONS; BRAIN-STEM; GANGLION-CELL; MURINE MODEL; RESPONSE PROPERTIES; SENILE AMYLOIDOSIS; AUDITORY LOSS; STRAIN MOUSE; MICE AB The auditory brainstem response and histopathology of the cochlea were investigated in an accelerated senescence-prone strain, SAM-P/1 mice and a senescence-resistant strain, SAM-R/1 mice. Each strain displayed an age-related auditory loss expressed as elevated thresholds similar to human hearing loss in that high-frequency losses occurred earlier than middle- or low-frequency losses. SAM-P/1 showed a more rapid decline of hearing with age than did SAM-R/1. Interpeak intervals I-III and I-IV were prolonged with age in both strains, especially at high frequency. The prolongation was more marked in SAM-P/1 than in SAM-R/1. The decrease in amplitude of wave I observed in both strains was greater in SAM-P/1 than in SAM-R/1. The auditory function assessed by thresholds, interpeak intervals and amplitudes of wave I in SAM-P/1 at 12 months of age corresponded roughly to that in SAM-R/1 at 20 months of age. In morphological studies, there was an age-related decrease in the cell density as well as in the size of spiral ganglion neurons in both strains, but these changes were more pronounced in SAM-P/1 than in SAM-R/1. These results reveal that age-related hearing impairment associated with morphological changes in the cochlea is manifested earlier and progresses more rapidly in SAM-P/1 than in SAM-R/1. Thus, the SAM-P/1 strain should prove useful as a model of presbycusis. C1 KYOTO UNIV,CHEST DIS RES INST,DEPT SENESCENCE BIOL,SAKYO KU,KYOTO 606,JAPAN. KYOTO PREFECTURAL UNIV MED,DEPT OTOLARYNGOL,KYOTO,JAPAN. DOSHISHA UNIV,DEPT ELECTR,KYOTO 602,JAPAN. CR AKIYAMA H, 1986, ACTA NEUROPATHOL, V72, P124 ANGEVINE JB, 1975, TXB HISTOLOGY, P336 BORG E, 1982, HEARING RES, V8, P101, DOI 10.1016/0378-5955(82)90069-7 BRINER W, 1989, NEUROBIOL AGING, V10, P295, DOI 10.1016/0197-4580(89)90039-0 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 CHEN WH, 1989, AM J PATHOL, V135, P379 CHOLE RA, 1983, AUDIOLOGY, V22, P384 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F COTRAN RS, 1989, ROBBINS PATHOLOGIC B, P550 COVELL W. P., 1957, LARYNGOSCOPE, V67, P118 GUILD SR, 1921, ANAT REC, V22, P147 HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HENRY KR, 1979, ACTA OTO-LARYNGOL, V87, P61, DOI 10.3109/00016487909126387 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1992, AUDIOLOGY, V31, P181 HENRY KR, 1982, J GERONTOL, V37, P275 HENRY KR, 1980, ARCH OTO-RHINO-LARYN, V228, P233, DOI 10.1007/BF00660735 HENRY KR, 1978, ACTA OTO-LARYNGOL, V86, P366, DOI 10.3109/00016487809107515 HIGUCHI K, 1986, J BIOL CHEM, V261, P2834 HIGUCHI K, 1991, VIRCHOWS ARCH B, V60, P231, DOI 10.1007/BF02899551 HOSOKAWA M, 1984, MECH AGEING DEV, V26, P91, DOI 10.1016/0047-6374(84)90168-4 HOSOKAWA M, 1984, EXP EYE RES, V38, P105, DOI 10.1016/0014-4835(84)90095-2 Ishii T, 1967, Acta Otolaryngol, V64, P17, DOI 10.3109/00016486709139088 JORTNER BS, 1978, PATHOLOGY LABORATORY, P402 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 KELLY JB, 1989, HEARING RES, V39, P231, DOI 10.1016/0378-5955(89)90043-9 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LOHUIS PJFM, 1990, HEARING RES, V47, P95, DOI 10.1016/0378-5955(90)90169-P MANN DMA, 1974, BRAIN, V97, P481, DOI 10.1093/brain/97.1.481 MATSUSHITA M, 1986, AM J PATHOL, V125, P276 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MIYAMOTO M, 1986, PHYSIOL BEHAV, V38, P399, DOI 10.1016/0031-9384(86)90112-5 MYERS DD, 1978, GENETIC EFFECT AGING, P43 NAIKI H, 1990, LAB INVEST, V62, P768 NAIKI H, 1988, AM J PATHOL, V130, P579 ROBINSON DW, 1979, AUDIOLOGY, V18, P320 Romand R, 1984, ULTRASTRUCTURAL ATLA, P165 RYALS BM, 1988, HEARING RES, V36, P1, DOI 10.1016/0378-5955(88)90133-5 SAMORAJS.T, 1965, J CELL BIOL, V26, P779, DOI 10.1083/jcb.26.3.779 SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SCHUKNECHT HF, 1974, PATHOLOGY EA, P387 SCHUKNECHT HF, 1953, AMA ARCH OTOLARYNGOL, V58, P377 SHIMADA A, 1992, J NEUROPATH EXP NEUR, V51, P440, DOI 10.1097/00005072-199207000-00006 TAKAHASH.T, 1971, ANN OTO RHINOL LARYN, V80, P721 TAKEDA T, 1981, MECH AGEING DEV, V17, P183, DOI 10.1016/0047-6374(81)90084-1 TAKEDA T, 1991, J AM GERIATR SOC, V39, P911 TAKESHITA S, 1985, AM J PATHOL, V121, P455 TERRY RD, 1981, ANN NEUROL, V10, P184, DOI 10.1002/ana.410100209 TERRY RD, 1987, ANN NEUROL, V21, P530, DOI 10.1002/ana.410210603 TRUNE DR, 1991, AM J OTOLARYNG, V12, P259, DOI 10.1016/0196-0709(91)90003-X TRUNE DR, 1989, HEARING RES, V38, P57, DOI 10.1016/0378-5955(89)90128-7 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, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 YAGI H, 1988, BRAIN RES, V474, P86, DOI 10.1016/0006-8993(88)90671-3 YAGI H, 1989, J NEUROPATH EXP NEUR, V48, P577, DOI 10.1097/00005072-198909000-00008 NR 60 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 MAY PY 1994 VL 75 IS 1-2 BP 27 EP 37 DI 10.1016/0378-5955(94)90052-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400003 PM 8071152 ER PT J AU SLATTERY, WH MIDDLEBROOKS, JC AF SLATTERY, WH MIDDLEBROOKS, JC TI MONAURAL SOUND LOCALIZATION - ACUTE VERSUS CHRONIC UNILATERAL IMPAIRMENT SO HEARING RESEARCH LA English DT Article DE SOUND LOCALIZATION; MONAURAL HEARING; HEAD-RELATED TRANSFER FUNCTION ID BINAURAL LOCALIZATION; HUMAN LISTENERS; FREE-FIELD; CHILDREN; SPACE; PLANE AB We tested the ability of human listeners to localize broadband noise bursts in the absence of binaural localization cues. The subject population consisted of five patients, who had normal hearing in one ear and congenital deafness in the other, and seven normal controls, who were tested with both ears open and with one ear plugged. Consistent with previous reports, the introduction of an earplug unilaterally into control subjects resulted in a prominent lateral displacement in their localization judgements by an average of 30.9 degrees toward the side of the open ear. Vertical localization was less strongly impaired. The five monaural patients showed a considerable range of ability to localize sounds. Two of the patients were essentially indistinguishable from the plugged control subjects in that they showed a prominent displacement of responses toward the side of the hearing ear. The other three subjects localized significantly better than the plugged controls, in that they demonstrated little or no lateral displacement toward the hearing side and that they localized targets on the hearing and on the impaired sides about equally well. The performance of these latter patients demonstrates that monaural cues can provide useful localization information in the horizontal as well as in the vertical dimension. C1 UNIV FLORIDA,INST BRAIN,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. UNIV FLORIDA,INST BRAIN,DEPT NEUROSCI,GAINESVILLE,FL 32610. CR Angell JR, 1901, PSYCHOL REV, V8, P225, DOI 10.1037/h0073690 BUTLER RA, 1986, HEARING RES, V21, P67, DOI 10.1016/0378-5955(86)90047-X BUTLER RA, 1990, PERCEPTION, V19, P241, DOI 10.1068/p190241 BUTLER RA, 1980, PERCEPT PSYCHOPHYS, V28, P449, DOI 10.3758/BF03204889 Fisher H G, 1968, Acta Otolaryngol, V66, P213, DOI 10.3109/00016486809126288 GATEHOUSE R W, 1972, Journal of Auditory Research, V12, P179 GATEHOUSE R W, 1976, Journal of Auditory Research, V16, P265 Häusler R, 1983, Acta Otolaryngol Suppl, V400, P1 HEBRANK J, 1974, J ACOUST SOC AM, V56, P935, DOI 10.1121/1.1903351 HUMANSKI RA, 1988, J ACOUST SOC AM, V83, P2300, DOI 10.1121/1.396361 HUMES LE, 1980, AUDIOLOGY, V19, P508 JONGKEES L B, 1957, Acta Otolaryngol, V48, P465, DOI 10.3109/00016485709126908 MAKOUS JC, 1990, J ACOUST SOC AM, V87, P2188, DOI 10.1121/1.399186 MIDDLEBROOKS JC, 1992, J ACOUST SOC AM, V92, P2607, DOI 10.1121/1.404400 MIDDLEBROOKS JC, 1991, ANNU REV PSYCHOL, V42, P135, DOI 10.1146/annurev.ps.42.020191.001031 MUSICANT AD, 1985, J ACOUST SOC AM, V77, P202, DOI 10.1121/1.392259 NEWTON VE, 1981, J LARYNGOL OTOL, V95, P41, DOI 10.1017/S0022215100090381 NEWTON VE, 1983, AUDIOLOGY, V22, P189 OLDFIELD SR, 1986, PERCEPTION, V15, P67, DOI 10.1068/p150067 SHAW EAG, 1974, J ACOUST SOC AM, V56, P1848, DOI 10.1121/1.1903522 VIEHWEG R, 1960, Ann Otol Rhinol Laryngol, V69, P622 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P868, DOI 10.1121/1.397558 NR 22 TC 91 Z9 93 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 1994 VL 75 IS 1-2 BP 38 EP 46 DI 10.1016/0378-5955(94)90053-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400004 PM 8071153 ER PT J AU HOUSLEY, GD BATCHER, S KRAFT, M RYAN, AF AF HOUSLEY, GD BATCHER, S KRAFT, M RYAN, AF TI NICOTINIC ACETYLCHOLINE-RECEPTOR SUBUNITS EXPRESSED IN RAT COCHLEA DETECTED BY THE POLYMERASE CHAIN-REACTION SO HEARING RESEARCH LA English DT Article DE NICOTINIC ACETYLCHOLINE RECEPTOR; POLYMERASE CHAIN REACTION; COCHLEA; EFFERENT; CDNA; MESSENGER-RNA ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; GENE FAMILY; ENZYMATIC AMPLIFICATION; CHOLINERGIC INHIBITION; FUNCTIONAL EXPRESSION; ION CHANNEL; DNA; NEUROTRANSMISSION; LOCALIZATION AB Poly(A)(+) RNA was extracted from rat cochleae using guanidinium thiocyanate and oligo(dT)-cellulose and converted into cDNA by reverse transcriptase using an oligo(dT) primer. Oligonucleotides complementary to conserved 5' and 3' regions of alpha and beta subunits of the neuronal nicotinic acetylcholine receptor subunit (nAChR) family were then used as primers to screen the cochlear cDNA via the polymerase chain reaction (PCR) procedure. PCR products of approximately 900 bp length, purified by agarose gel electrophoresis, were nick translated to produce [P-32]-dCTP labelled probes for Southern Blot screening of nAChR cDNAs. Of the four alpha and three beta subunits screened, only alpha 5 and beta 4 nAChR cDNAs hybridized. The alpha 5 PCR product was cloned and sequenced and proved to be identical to published sequence for alpha 5. The detection of alpha 5 and beta 4 nAChR subunit expression in cochlear tissue supports previous electrophysiological and immunocytochemical evidence for nAChR-mediated centrifugal control of hearing function. C1 UNIV CALIF SAN DIEGO,DEPT OTOLARYNGOL,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. RP HOUSLEY, GD (reprint author), UNIV AUCKLAND,DEPT PHYSIOL,PRIVATE BAG 92019,AUCKLAND,NEW ZEALAND. CR ANAND R, 1993, SOC NEUR ABSTR, V19, P485 Ashmore J F, 1990, Neurosci Res Suppl, V12, pS39, DOI 10.1016/0921-8696(90)90007-P BARRON SE, 1987, TRENDS PHARMACOL SCI, V8, P204, DOI 10.1016/0165-6147(87)90059-9 BOBBIN RP, 1971, NATURE-NEW BIOL, V231, P222 BOULTER J, 1986, NATURE, V319, P368, DOI 10.1038/319368a0 BOULTER J, 1990, J BIOL CHEM, V265, P4472 BOULTER J, 1987, P NATL ACAD SCI USA, V84, P7763, DOI 10.1073/pnas.84.21.7763 BROWN AM, 1991, FASEB J, V5, P2175 BRUNDIN L, 1992, NEUROSCIENCE, V49, P607, DOI 10.1016/0306-4522(92)90230-Y CANLON B, 1989, ACTA PHYSIOL SCAND, V137, P549, DOI 10.1111/j.1748-1716.1989.tb08795.x CHANGEUX JP, 1987, TRENDS NEUROSCI, V10, P245, DOI 10.1016/0166-2236(87)90167-6 COUTURIER S, 1990, NEURON, V5, P847, DOI 10.1016/0896-6273(90)90344-F Dallos P, 1991, Curr Opin Neurobiol, V1, P215, DOI 10.1016/0959-4388(91)90081-H DENERIS ES, 1989, J BIOL CHEM, V264, P6268 DENERIS ES, 1988, NEURON, V1, P45, DOI 10.1016/0896-6273(88)90208-5 DESMEDT JE, 1963, NATURE, V200, P472, DOI 10.1038/200472b0 DRESCHER DG, 1993, J NEUROCHEM, V61, P1167, DOI 10.1111/j.1471-4159.1993.tb03638.x DRESCHER DG, 1992, J NEUROCHEM, V59, P765, DOI 10.1111/j.1471-4159.1992.tb09436.x ERLICH HA, 1991, SCIENCE, V252, P1643, DOI 10.1126/science.2047872 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FELIX D, 1992, HEARING RES, V64, P1, DOI 10.1016/0378-5955(92)90163-H FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 FEX J, 1978, BRAIN RES, V159, P440, DOI 10.1016/0006-8993(78)90555-3 FUCHS PA, 1992, J NEUROSCI, V12, P800 Giovanoni SJ, 1991, NUCL ACID TECHNIQUES, P177 GOLDMAN D, 1987, CELL, V48, P965, DOI 10.1016/0092-8674(87)90705-7 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HEINEMANN S, 1988, NATO ASI SER, V25, P173 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 HUGANIR RL, 1990, NEURON, V5, P555, DOI 10.1016/0896-6273(90)90211-W IWASA KH, 1992, J ACOUST SOC AM, V92, P3169, DOI 10.1121/1.404194 KANDEL ER, 1991, PRINCIPLES NEURAL SC, P869 KANDEL ER, 1991, PRINCIPLES NEURAL SC, P153 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 LORING RH, 1988, TRENDS NEUROSCI, V11, P73, DOI 10.1016/0166-2236(88)90168-3 MULLIS K, 1986, COLD SPRING HARB SYM, V51, P263 NORRIS CH, 1974, ACTA OTO-LARYNGOL, V77, P318, DOI 10.3109/00016487409124631 PAPKE RL, 1989, NEURON, V3, P589, DOI 10.1016/0896-6273(89)90269-9 PLINKERT PK, 1991, HEARING RES, V53, P123, DOI 10.1016/0378-5955(91)90219-Y RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 RASMUSSEN GL, 1953, J COMP NEUROL, V99, P61, DOI 10.1002/cne.900990105 SAIKI RK, 1988, SCIENCE, V239, P487, DOI 10.1126/science.2448875 Sambrook J., 1989, MOL CLONING SANGER F, 1977, P NATL ACAD SCI USA, V74, P5463, DOI 10.1073/pnas.74.12.5463 SEQUELA P, 1993, J NEUROSCI, V13, P596 SOBKOWICZ HM, 1989, J NEUROCYTOL, V18, P209, DOI 10.1007/BF01206663 THORNE PR, 1983, J ACOUST SOC AM, V76, P440 WADA K, 1988, SCIENCE, V240, P330, DOI 10.1126/science.2832952 NR 49 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 MAY PY 1994 VL 75 IS 1-2 BP 47 EP 53 DI 10.1016/0378-5955(94)90054-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400005 PM 7520901 ER PT J AU WALSH, ME WEBSTER, DB AF WALSH, ME WEBSTER, DB TI EXOGENOUS GM1 GANGLIOSIDE EFFECTS ON CONDUCTIVE AND SENSORINEURAL HEARING LOSSES SO HEARING RESEARCH LA English DT Article DE GM1 GANGLIOSIDE; SPIRAL GANGLION; COCHLEAR NUCLEI; OCTOPUS CELLS; GLOBULAR CELLS; SPHERICAL CELLS; CBA/J MICE ID ANTEROVENTRAL COCHLEAR NUCLEUS; NERVE GROWTH-FACTOR; STEM AUDITORY NUCLEI; NEURONOTROPHIC ACTIVITY; ELECTRICAL-STIMULATION; ACOUSTIC DEPRIVATION; AFFERENT INFLUENCES; WOUND CAVITY; NEURONS; RAT AB Both CBA/J mice with neonatal cochlea removals and CBA/J mice with neonatal atresias of the external auditory meatus have significantly smaller ventral cochlear nucleus volumes and significantly smaller neuronal somata of their ventral cochlear nucleus. The volume reduction of the ventral cochlear nuclei is greater in the mice with cochlea removals, but the soma area reduction is greater in the mice with external auditory meatus atresias. GM1 gangliosides were subcutaneously injected daily into a group of CBA/J mice with conductive hearing loss caused by neonatal removals of their left external auditory meatus, and into a group of CBA/J mice unilaterally deafened by left cochlea removals. In the mice with conductive hearing loss, the ganglioside treatment significantly ameliorated the atrophy of spiral ganglion neurons, ventral cochlear nucleus neurons, and ventral cochlear nucleus volume. In unilaterally deafened mice, the ganglioside treatment had no measurable effect on the atrophy of ventral cochlear nucleus neurons or of ventral cochlear nucleus volume. It is suggested that GM1 ganglioside treatment potentiates growth factors which sustain spiral ganglion integrity and that this sustained activity of the spiral ganglion in turn maintains the integrity of the cochlear nuclei. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,DEPT ANAT,NEW ORLEANS,LA 70112. CR 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 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 DIPATRE PL, 1989, EUR J PHARMACOL, V162, P43, DOI 10.1016/0014-2999(89)90602-X DIPATRE PL, 1989, BRAIN RES, V480, P219, DOI 10.1016/0006-8993(89)91585-0 DOHERTY P, 1985, J NEUROCHEM, V44, P1259, DOI 10.1111/j.1471-4159.1985.tb08752.x EDWARDS AL, 1964, EXPT DESIGN PSYCHOL, P136 GORIO A, 1981, GANGLIOSIDES NEUROLO, P259 GORIO A, 1984, GANGLIOSIDE STRUCTUR, P549 HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HYSON RL, 1989, J NEUROSCI, V9, P2835 KARPIAK SE, 1984, DEV NEUROSCI-BASEL, V6, P127 KASARSKIS EJ, 1981, DEV BRAIN RES, V1, P25, DOI 10.1016/0165-3806(81)90091-2 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEDEEN RW, 1978, J SUPRAMOL STR CELL, V8, P1, DOI 10.1002/jss.400080102 LEON A, 1984, J NEUROSCI RES, V12, P277, DOI 10.1002/jnr.490120215 LEON A, 1988, J NEUROSCI, V8, P746 LI CC, 1964, INTRO EXPT STATISTIC LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MAHADIK SP, 1986, NEUROTOXICOLOGY, V7, P161 MANTHORPE M, 1983, BRAIN RES, V267, P47, DOI 10.1016/0006-8993(83)91038-7 NIETOSAMPEDRO M, 1983, J NEUROSCI, V3, P2219 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 PEREZPOLO JR, 1990, MOL NEUROBIOL, P57 SKAPER SD, 1989, MOL NEUROBIOL, V3, P173, DOI 10.1007/BF02935630 SKAPER SD, 1985, DEV BRAIN RES, V23, P19, DOI 10.1016/0165-3806(85)90003-3 SPOERRI PE, 1988, NEUROSCI LETT, V90, P21, DOI 10.1016/0304-3940(88)90780-X TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 TUCCI DL, 1985, J COMP NEUROL, V238, P371, DOI 10.1002/cne.902380402 VANDEWATER TR, 1992, DEV AUDITORY VESTIBU, V2, P1 WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 WEBSTER DB, 1983, INT J PEDIATR OTORHI, V6, P107 WEBSTER DB, 1988, HEARING RES, V32, P193, DOI 10.1016/0378-5955(88)90091-3 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 NR 37 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 MAY PY 1994 VL 75 IS 1-2 BP 54 EP 60 DI 10.1016/0378-5955(94)90055-8 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400006 PM 8071154 ER PT J AU XIE, DH HENSON, MM HENSON, OW AF XIE, DH HENSON, MM HENSON, OW TI ACHE-STAINING OF TYPE-II GANGLION-CELLS, PROCESSES AND TERMINALS IN THE COCHLEA OF THE MOUSTACHED BAT SO HEARING RESEARCH LA English DT Article DE MOUSTACHED BAT; TYPE II GANGLION CELLS; ACETYLCHOLINESTERASE; ACHE ID CHOLINERGIC NEURONS; SPIRAL GANGLION; ACETYLCHOLINESTERASE; RETINA; LOCALIZATION AB There have been a number of reports showing that ganglion cells of sensory neurons may be stained by traditional acetylcholinesterase (AChE) histochemical techniques commonly used to demonstrate efferent nerve fibers and terminals. AChE-staining has been described for cell bodies in the vestibular and spiral ganglia; staining of peripheral and central processes, however, is rare and the presence of reaction product in afferent terminals has not been reported. The outer hair cells of mustached bats, Pteronotus parnellii, differ from those of most mammals in that they typically have a single, large efferent terminal surrounded by 5-7 small, afferent terminals. In this animal an AChE-positive reaction was found not only in efferent fibers and terminals but also in type II ganglion cells, their peripheral and central processes and in outer hair cell terminals. The stained cell bodies were smaller than the unstained type I ganglion cells and they were much fewer in number. The processes of the stained cells could be followed from the soma. The central processes were dispersed throughout the VIIIth nerve trunk. Stained peripheral processes were evident in the osseous spiral lamina, floor of the tunnel of Corti and first space of Nuel and in the outer spiral plexus along the sides of the outer phalangeal (Deiters') cells. AChE-stained afferent terminals were easy to identify after transection of the crossed olivocochlear bundle (COCB) and subsequent degeneration of large efferent terminals. These results are of interest in that assessments of efferent nerve histochemistry after COCB transection need to recognize the potential contribution of AChE reaction product in afferent terminals. The functional significance of AChE-positive sensory nerves is not known; the positive reaction of the type II neurons does not mean that they are cholinergic. C1 UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. CR APPLEYARD ME, 1992, TRENDS NEUROSCI, V15, P485, DOI 10.1016/0166-2236(92)90100-M BERGLUND AM, 1986, BRAIN RES, V383, P327, DOI 10.1016/0006-8993(86)90034-X Bishop AL, 1988, ANIMAL SONAR, P307 BRANDON C, 1987, BRAIN RES, V401, P385, DOI 10.1016/0006-8993(87)91426-0 CAUNA N, 1963, ITAL GEN REV ORL, V2, P587 FIRBAS W, 1972, Monatsschrift fuer Ohrenheilkunde und Laryngo-Rhinologie, V106, P105 HOZAWA K, 1990, ACTA OTO-LARYNGOL, V110, P46, DOI 10.3109/00016489009122514 HUTCHINS JB, 1987, BRAIN RES, V400, P300, DOI 10.1016/0006-8993(87)90629-9 ISHII T, 1967, ANN OTO RHINOL LARYN, V76, P69 IURATO S, 1974, ACTA OTO-LARYNGOL, V78, P28, DOI 10.3109/00016487409126322 IURATO SL, 1975, GOLGI CENTENIAL S P, P553 KARCZMAR AG, 1980, GEN PHARMACOL, V11, P127, DOI 10.1016/0306-3623(80)90021-X KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 MALATOVA Z, 1985, J HIRNFORSCH, V26, P683 NISHI S, 1974, PERIPHERAL NERVOUS S, P225 PALOUZIER B, 1987, NEUROSCI LETT, V80, P147, DOI 10.1016/0304-3940(87)90644-6 POURCHO RG, 1986, EXP EYE RES, V43, P585, DOI 10.1016/S0014-4835(86)80025-2 Schwartz A. M, 1986, NEUROBIOLOGY HEARING, P271 SPOENDLIN H, 1981, ACTA OTO-LARYNGOL, V91, P451, DOI 10.3109/00016488109138527 SPOENDLIN H, 1979, ACTA OTOLARYNGOL, V97, P3581 STOPP PE, 1979, ACTA OTOLARYNGOL, V223, P11 TAGO H, 1986, J HISTOCHEM CYTOCHEM, V34, P1431 WILSON JL, 1991, HEARING RES, V55, P98, DOI 10.1016/0378-5955(91)90096-R XIE DH, 1993, HEARING RES, V66, P81, DOI 10.1016/0378-5955(93)90262-Y NR 24 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 MAY PY 1994 VL 75 IS 1-2 BP 61 EP 66 DI 10.1016/0378-5955(94)90056-6 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400007 PM 7520902 ER PT J AU SAMS, M SALMELIN, R AF SAMS, M SALMELIN, R TI EVIDENCE OF SHARP FREQUENCY TUNING IN THE HUMAN AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE MAGNETOENCEPHALOGRAPHY; MEG; PITCH; EVOKED RESPONSES; MASKING; AUDITORY FILTERS; FREQUENCY SELECTIVITY ID MAGNETIC-FIELDS; HUMAN-BRAIN; NEUROMAGNETIC RESPONSES; TONOTOPIC ORGANIZATION; PATHOLOGICAL HUMAN; CURVES; CAT; LOCALIZATION; INTENSITY; TRANSIENT AB The frequency tuning of the human auditory cortex was studied by masking 100-ms tones of 1 and 2 kHz by continuous white-noise maskers with frequency notches around the tone frequencies. The subjects ignored the stimuli and concentrated on a reading task. The neuronal activity elicited by the test tones in the auditory cortex was measured with a 24-channel neuromagnetometer. The masker affected the amplitude and latency of the neuromagnetic N100m response, peaking about at 100 ms after stimulus onset, in a systematic way: the wider the notch, the shorter was the latency and the larger the amplitude. The source location of N100m in the auditory cortex did not depend on the notch width. Auditory filters at 1 and 2 kHz were modelled by a single-parameter rounded-exponential [Roex(p)] filter, based on the amplitude changes of N100m. The filters revealed sharp tuning of the auditory cortex, resembling that obtained in psychoacoustical masking studies. The results demonstrate that frequency tuning of the neurons or neuron ensembles in the human auditory cortex can be studied completely noninvasively. Moreover, since the stimuli were ignored by the subjects, the filter shape is not affected by the criterion adopted by the subject in the discrimination task. RP SAMS, M (reprint author), HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. RI Sams, Mikko/G-7060-2012; Salmelin, Riitta/I-7044-2012 CR AHONEN AI, 1991, IEEE T MAGN, V27, P2786, DOI 10.1109/20.133789 BAK CK, 1985, ELECTROEN CLIN NEURO, V61, P141, DOI 10.1016/0013-4694(85)91053-3 BURROWS DL, 1990, J ACOUST SOC AM, V88, P180, DOI 10.1121/1.399938 BUTLER RA, 1968, J ACOUST SOC AM, V44, P945, DOI 10.1121/1.1911233 Clarey J.C., 1992, MAMMALIAN AUDITORY P, P232 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DAVIS H, 1968, J ACOUST SOC AM, V43, P431, DOI 10.1121/1.1910849 EGGERMONT JJ, 1977, J ACOUST SOC AM, V62, P1247, DOI 10.1121/1.381639 ELBERLING C, 1980, SCAND AUDIOL, V9, P185, DOI 10.3109/01050398009076353 ELBERLING C, 1981, SCAND AUDIOL, V10, P203, DOI 10.3109/01050398109076182 Fletcher H, 1940, REV MOD PHYS, V12, P0047, DOI 10.1103/RevModPhys.12.47 HAMALAINEN M, 1993, REV MOD PHYS, V65, P413, DOI 10.1103/RevModPhys.65.413 HARI R, 1980, EXP BRAIN RES, V40, P237 Hari R, 1990, ADV AUDIOL, V6, P222 HARI R, 1988, EXP BRAIN RES, V71, P87 HARRISON RV, 1981, J ACOUST SOC AM, V69, P1374, DOI 10.1121/1.385819 HASHIMOTO I, 1982, ELECTROEN CLIN NEURO, V53, P652, DOI 10.1016/0013-4694(82)90141-9 Houtgast T., 1974, LATERAL SUPPRESSION JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 KAUKORANTA E, 1986, SOMATOSENS MOT RES, V3, P309 NAATANEN R, 1988, ELECTROEN CLIN NEURO, V69, P523, DOI 10.1016/0013-4694(88)90164-2 PANTEV C, 1988, ELECTROEN CLIN NEURO, V69, P160, DOI 10.1016/0013-4694(88)90211-8 PATTERSON RD, 1980, J ACOUST SOC AM, V67, P229, DOI 10.1121/1.383732 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 PHILLIPS DP, 1991, NEUROBIOLOGY HEARING, P335 PICKLES JO, 1979, J ACOUST SOC AM, V66, P1725, DOI 10.1121/1.383645 PICTON TW, 1978, ELECTROEN CLIN NEURO, V45, P198, DOI 10.1016/0013-4694(78)90004-4 ROMANI GL, 1982, SCIENCE, V216, P1339, DOI 10.1126/science.7079770 SAMS M, 1985, ELECTROEN CLIN NEURO, V61, P254, DOI 10.1016/0013-4694(85)91092-2 SCHREINER CE, 1984, J NEUROPHYSIOL, V51, P1284 Zwicker E., 1990, PSYCHOACOUSTICS FACT NR 32 TC 32 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 MAY PY 1994 VL 75 IS 1-2 BP 67 EP 74 DI 10.1016/0378-5955(94)90057-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400008 PM 8071155 ER PT J AU HENSON, MM HENSON, OW GEWALT, SL WILSON, JL JOHNSON, GA AF HENSON, MM HENSON, OW GEWALT, SL WILSON, JL JOHNSON, GA TI IMAGING THE COCHLEA BY MAGNETIC-RESONANCE MICROSCOPY SO HEARING RESEARCH LA English DT Article DE COCHLEA; MAGNETIC RESONANCE MICROSCOPY; MRI ID LIMITED RESOLUTION; DIFFUSION AB The isolated, fixed cochlea of the mustached bat was studied with three dimensional magnetic resonance (MR) microscopy. The cochlea of this animal is about 4 mm in diameter and its entire volume was imaged. With the field of view and matrix size used, the volume elements (voxels) making up the volume data set were isotropic 25 X 25 x 25 mu m cubes. Three dimensional (3D) MR microscopy based on isotropic voxels has many advantages over commonly used light microscopy: 1) it is non destructive; 2) it is much less time consuming; 3) no dehydration is required and shrinkage is minimized; 4) the data set can be used to create sections in any desired plane; 5) the proper alignment of sections is inherent in the 3D acquisition so that no reference points are required; 6) the,entire data set can be viewed from any point of view in a volume rendered image; 7) the data is digital and features can be enhanced by computer image processing; and 8) the isotropic dimensions of the voxels make the data well-suited for structural reconstructions and measurements. Good images of the osseous spiral lamina, spiral ligament, scala tympani, scala vestibuli, and nerve bundles were obtained. The vestibular (Reissner's) membrane was easily identified in the mustached bat and it appears to bulge into the scala vestibuli. The visibility of this structure suggests that MR microscopy would be well-suited for studies of endolymphatic hydrops. C1 UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. DUKE UNIV,MED CTR,DEPT RADIOL,CTR IN VIVO MICROSCOPY,DURHAM,NC 27710. RP HENSON, MM (reprint author), UNIV N CAROLINA,DIV OTOLARYNGOL HEAD & NECK SURG,CB NUMBER 7090,TAYLOR HALL,CHAPEL HILL,NC 27599, USA. CR AGUAYO JB, 1986, NATURE, V322, P190, DOI 10.1038/322190a0 AHN CB, 1989, MED PHYS, V16, P22, DOI 10.1118/1.596393 ARGIRO VJ, 1990, PIXEL, V1, P35 BANSON ML, 1992, INVEST RADIOL, V27, P157, DOI 10.1097/00004424-199202000-00013 BLACK RD, 1993, SCIENCE, V259, P793, DOI 10.1126/science.8430331 Callaghan P. T., 1991, PRINCIPLES NUCLEAR M CALLAGHAN PT, 1990, J MAGN RESON, V87, P304, DOI 10.1016/0022-2364(90)90007-V CALLAGHAN PT, 1987, J MAGN RESON, V71, P426, DOI 10.1016/0022-2364(87)90243-5 CALLAGHAN PT, 1988, J MAGN RESON, V78, P1, DOI 10.1016/0022-2364(88)90151-5 CHO ZH, 1988, MED PHYS, V15, P815, DOI 10.1118/1.596287 Drebin R. A., 1988, Computer Graphics, V22 DUVALL AJ, 1967, ARCHIV OTOLARYNGOL, V86, P143 ECCLES CD, 1986, J MAGN RESON, V68, P393, DOI 10.1016/0022-2364(86)90261-1 Hunter-Duvar I M, 1978, Acta Otolaryngol Suppl, V351, P24 HYSLOP WB, 1991, J MAGN RESON, V94, P501, DOI 10.1016/0022-2364(91)90136-H JARA H, 1993, MAGNET RESON MED, V29, P528, DOI 10.1002/mrm.1910290415 JOHNSON GA, 1986, J MAGN RESON, V68, P129, DOI 10.1016/0022-2364(86)90322-7 MCFARLAND EW, 1992, MAGN RESON IMAGING, V10, P269, DOI 10.1016/0730-725X(92)90486-J TIEDE U, 1990, IEEE COMPUT GRAPH, V10, P41, DOI 10.1109/38.50672 VOIE AH, 1993, J MICROSC-OXFORD, V170, P229 VOIE AH, 1992, ABSTR ASS RES OT, V288, P100 ZHOU XH, 1993, MAGNET RESON MED, V30, P60, DOI 10.1002/mrm.1910300110 NR 22 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 MAY PY 1994 VL 75 IS 1-2 BP 75 EP 80 DI 10.1016/0378-5955(94)90058-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400009 PM 8071156 ER PT J AU SOBKOWICZ, HM SLAPNICK, SM AF SOBKOWICZ, HM SLAPNICK, SM TI THE EFFERENTS INTERCONNECTING AUDITORY INNER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE EFFERENT ENDINGS; INNER HAIR CELLS; ORGAN OF CORTI ID GUINEA-PIG ORGAN; SENSORY EPITHELIUM; CAT COCHLEA; CORTI; SYNAPSES; MICROSCOPY; MOUSE; RECONSTRUCTION; AFFERENT AB The work describes the system of efferent terminals that interconnect inner hair cells through a chain of direct somatic synapses organized in repetitive patterns. The efferent boutons were discovered in the apical turns of 12-day-old (hearing)mice. Clusters or short rows of vesiculated boutons are located between adjoining hair cells at the lower half of the receptors, close to their modiolar side. The individual endings, about 1.2 mu m in diameter, adjoin inner hair cells and form one synapse per hair cell. On the hair cell side, the synaptic contact is apposed by a classical postsynaptic cisterna. Within a cluster of endings, some synapse simultaneously with either or both neighbouring inner hair cells. The efferent boutons also connect synaptically with each other and with other-different in type-vesiculated and nonvesiculated endings. These endings seem to derive from the climbing collaterals of the inner spiral bundle, and we believe them to be GABAergic. RP SOBKOWICZ, HM (reprint author), UNIV WISCONSIN,DEPT NEUROL,ROOM 75 MED SCI CTR,1375 UNIV AVE,MADISON,WI 53706, USA. CR ANGELBORG C, 1973, BASIC MECHANISMS HEA, P125 EHRET G, 1977, J ACOUST SOC AM, V62, P143, DOI 10.1121/1.381496 EMMERLING MR, 1990, J ELECTRON MICR TECH, V15, P123, DOI 10.1002/jemt.1060150205 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 HASHIMOTO S, 1990, ACTA OTO-LARYNGOL, V109, P228, DOI 10.3109/00016489009107438 IURATO S, 1974, HDB SENSORY PHYSL, V5, P261 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X 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 Mikaelian D, 1965, ACTA OTO-LARYNGOL, V59, P451, DOI DOI 10.3109/00016486509124579 NADOL JB, 1983, LARYNGOSCOPE, V93, P599 PUJOL R, 1980, HEARING RES, V2, P423, DOI 10.1016/0378-5955(80)90078-7 SAITO K, 1980, J ULTRA MOL STRUCT R, V71, P222, DOI 10.1016/S0022-5320(80)90108-2 SAITO K, 1990, J ELECTRON MICR TECH, V15, P173, DOI 10.1002/jemt.1060150209 Shnerson A., 1982, DEV BRAIN RES, V2, P65 Smith C A, 1973, Adv Otorhinolaryngol, V20, P296 SMITH CA, 1957, AM J ANAT, V100, P337, DOI 10.1002/aja.1001000304 SOBKOWICZ HM, 1994, ABST ASS RES OT, V17, P91 Sobkowicz HM, 1992, DEV AUDITORY VESTIBU, V2, P59 SOBKOWICZ HM, 1989, J NEUROCYTOL, V18, P209, DOI 10.1007/BF01206663 SOBKOWICZ HM, 1993, J NEUROCYTOL, V22, P979, DOI 10.1007/BF01218355 SOBKOWICZ HM, 1992, EXP NEUROL, V115, P44, DOI 10.1016/0014-4886(92)90219-G SPOENDLIN H, 1984, ULTRASTRUCTURAL ATLA, P133 Spoendlin H, 1973, BASIC MECHANISMS HEA, P185 WHITLON DS, 1989, J NEUROCYTOL, V18, P505, DOI 10.1007/BF01474546 NR 26 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 1994 VL 75 IS 1-2 BP 81 EP 92 DI 10.1016/0378-5955(94)90059-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400010 PM 8071157 ER PT J AU TAKENO, S HARRISON, RV IBRAHIM, D WAKE, M MOUNT, RJ AF TAKENO, S HARRISON, RV IBRAHIM, D WAKE, M MOUNT, RJ TI COCHLEAR FUNCTION AFTER SELECTIVE INNER HAIR CELL DEGENERATION INDUCED BY CARBOPLATIN SO HEARING RESEARCH LA English DT Article DE CARBOPLATIN; ORGAN OF CORTI; CHINCHILLA; COCHLEAR ACTION POTENTIALS; COCHLEAR MICROPHONICS ID CIS-DIAMMINEDICHLOROPLATINUM NSC-119875; GUINEA-PIG; CLINICAL-EXPERIENCE; HEARING-LOSS; OTOTOXICITY; PLATINUM; CISPLATIN; POTENTIALS; RESPONSES; ANALOGS AB The ototoxicity of carboplatin, a second generation anti-cancer agent, was examined using the chinchilla as an animal model. In animals treated with a clinical therapeutic dose (400 mg/m(2)), the dominant degenerative change is to inner hair cells (IHCs). This is in sharp contrast to most other ototoxic agents, which damage primarily the outer hair cells (OHCs). Functional changes to the cochlea have been evaluated in carboplatin treated subjects by recording cochlear action potentials (CAP) and cochlear microphonics (CM); cochlear lesions were evaluated using scanning electron microscopy. In carboplatin treated animals, CAP thresholds to tone-pip stimuli were elevated in proportion to IHC damage in corresponding cochlear regions. In contrast, CM amplitudes and 'thresholds' remained close to normal in most cases, reflecting the preservation of OHCs in the basal turn. These results indicate a high degree of independence between the inner and outer hair cell systems in the cochlear transduction mechanism. We suggest that this species-specific preparation with selective IHC loss will provide a valuable tool for studying, separately, the role of OHCs in both afferent and efferent cochlear function. C1 HIROSHIMA UNIV,DEPT OTOLARYNGOL,HIROSHIMA,JAPAN. UNIV TORONTO,DEPT PHYSIOL,TORONTO,ON,CANADA. RP TAKENO, S (reprint author), HOSP SICK CHILDREN,DEPT OTOLARYNGOL,AUDITORY SCI LAB,555 UNIV AVE,TORONTO M5G 1X8,ON,CANADA. CR ANZAI T, 1987, EAR RES JPN, V18, P122 CALVERT AH, 1982, CANCER CHEMOTH PHARM, V9, P140, DOI 10.1007/BF00257742 CANETTA R, 1986, 14TH INT CANC C BUD, V9, P19 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 DALLOS P, 1974, AUDIOLOGY, V13, P277 Dallos P, 1973, BASIC MECHANISMS HEA, P335 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 ESTREM SA, 1981, OTOLARYNG HEAD NECK, V89, P638 Evans EF, 1976, J PHYSIOL-LONDON, V256, P43 FUKUSHIMA N, 1990, HEARING RES, V50, P107, DOI 10.1016/0378-5955(90)90037-P HARRISON RV, 1982, HEARING RES, V6, P303, DOI 10.1016/0378-5955(82)90062-4 HAWKINS JE, 1976, HDB SENSORY PHYSL, V3, P707 HAYES DM, 1977, CANCER, V39, P1372, DOI 10.1002/1097-0142(197704)39:4<1372::AID-CNCR2820390404>3.0.CO;2-J JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 KENNEDY ICS, 1990, CANCER CHEMOTH PHARM, V26, P232, DOI 10.1007/BF02897206 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 Kiang N Y, 1970, Ciba Found Symp, P241 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 LIPPMAN AJ, 1973, CANCER CHEMOTH REP 1, V57, P191 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PIEL IJ, 1974, CANCER CHEMOTH REP 1, V58, P871 ROSENBER.B, 1965, NATURE, V205, P698, DOI 10.1038/205698a0 ROSENBER.B, 1969, NATURE, V222, P385, DOI 10.1038/222385a0 ROSSOF AH, 1972, CANCER, V30, P1451, DOI 10.1002/1097-0142(197212)30:6<1451::AID-CNCR2820300606>3.0.CO;2-Q RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 SAITO T, 1989, Auris Nasus Larynx, V16, P13 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SCHWEITZER VG, 1986, OTOLARYNG HEAD NECK, V94, P458 SLEPECKY N, 1985, HEARING RES, V17, P281, DOI 10.1016/0378-5955(85)90072-3 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 SPOENDLIN H, 1979, ACTA OTO-LARYNGOL, V87, P381, DOI 10.3109/00016487909126437 STADNICKI SW, 1975, CANCER CHEMOTH REP 1, V59, P467 STRAUSS M, 1983, LARYNGOSCOPE, V93, P1554, DOI 10.1288/00005537-198312000-00007 TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 VANDERHULST RJAM, 1988, ANN OTO RHINOL LARYN, V97, P133 VANHENNIK MB, 1987, CANCER RES, V47, P6297 WAKE M, 1993, J LARYNGOL OTOL, V107, P585, DOI 10.1017/S0022215100123771 YATES FE, 1986, J PHARM SCI, V75, P1019, DOI 10.1002/jps.2600751103 NR 45 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 1994 VL 75 IS 1-2 BP 93 EP 102 DI 10.1016/0378-5955(94)90060-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400011 PM 8071158 ER PT J AU CHEATHAM, MA DALLOS, P AF CHEATHAM, MA DALLOS, P TI STIMULUS BIASING - A COMPARISON BETWEEN COCHLEAR HAIR CELL AND ORGAN OF CORTI RESPONSE PATTERNS SO HEARING RESEARCH LA English DT Article DE COCHLEAR HAIR CELLS; COCHLEAR POTENTIALS; ORGAN OF CORTI; STIMULUS BIASING; 2-TONE SUPPRESSION ID BASILAR-MEMBRANE MOTION; GUINEA-PIG COCHLEA; LOW-FREQUENCY TONES; MAMMALIAN COCHLEA; INTRACELLULAR-RECORDINGS; RECEPTOR POTENTIALS; AUDITORY-NERVE; 2-TONE SUPPRESSION; SUPPORTING CELLS; ROUND WINDOW AB Responses from the organ of Corti (OC) fluid space and from individual hair cells are collected for short duration tone pips measured alone and in the presence of a 20 Hz bias tone. Because of the relatively long period of the acoustic bias signal, a probe can be selectively placed at precise locations within a single response period. Since bias effects produced during maximum basilar membrane velocity are negligible, this report documents changes associated with basilar membrane displacements to scala vestibuli and scala tympani. Hair cell response patterns are compared with those measured nearby in the OC to determine the degree to which inner (IHC) and outer hair cells (OHC) contribute to the gross cochlear potentials. It is shown that intracellular OHC and OC de responses are strongly influenced by the bias while intracellular IHC de responses are minimally affected. Although an association has been established between the cochlear microphonic and outer hair cell ac receptor potentials, the well correlated changes in the outer hair cell de receptor potential and the organ of Corti summating potential suggest that gross cochlear potentials reflect de as well as ac contributions from nearby OHCs. Since IHC responses are not influenced by the bias, they appear to contribute less than OHCs to extracellular potentials. These conclusions, however, are restricted to the moderately high input levels required to produce these effects (Durrant and Dallos, 1974) and to the central region of the cochlea where the recordings are made. Finally, the degree to which bias effects are contaminated by two-tone suppression is discussed. C1 NORTHWESTERN UNIV, HUGH KNOWLES CTR, DEPT NEUROBIOL & PHYSIOL, AUDITORY PHYSIOL LAB, EVANSTON, IL 60208 USA. RP CHEATHAM, MA (reprint author), NORTHWESTERN UNIV, HUGH KNOWLES CTR, DEPT COMMUN SCI & DISORDERS, AUDITORY PHYSIOL LAB, EVANSTON, IL 60208 USA. CR BUTLER RA, 1963, J ACOUST SOC AM, V35, P1188, DOI 10.1121/1.1918672 CHEATHAM MA, 1992, HEARING RES, V59, P39, DOI 10.1016/0378-5955(92)90100-2 CHEATHAM MA, 1993, ABS ASS RES OT, P31 CHEATHAM MA, 1993, PROG BRAIN RES, V97, P13 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DALLOS P, 1969, J ACOUST SOC AM, V45, P999, DOI 10.1121/1.1911576 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1989, J ACOUST SOC AM, V86, P1790, DOI 10.1121/1.398611 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 DALLOS P, 1972, ACTA OTO-LARYNGOL, P1 DALLOS P, 1983, MECHANISMS HEARING, P11 DALLOS P, 1992, SOC GEN PHY, V47, P371 DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 DAVIS H, 1950, P NATL ACAD SCI USA, V36, P580, DOI 10.1073/pnas.36.10.580 DAVIS H, 1958, AM J PHYSIOL, V195, P251 DEATHERAGE BH, 1957, J ACOUST SOC AM, V29, P132, DOI 10.1121/1.1908641 DURRANT JD, 1975, ACTA OTO-LARYNGOL, V80, P13, DOI 10.3109/00016487509121295 DURRANT JD, 1974, J ACOUST SOC AM, V56, P562, DOI 10.1121/1.1903291 DURRANT JD, 1972, J ACOUST SOC AM, V52, P542, DOI 10.1121/1.1913143 ENGEBRET.AM, 1968, J ACOUST SOC AM, V44, P548, DOI 10.1121/1.1911119 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 HONRUBIA VH, 1969, J ACOUST SOC AM, V45, P1443, DOI 10.1121/1.1911622 INGVARSSON K, 1981, THESIS NW U EVANSTON KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 KLIS JFL, 1985, HEARING RES, V20, P15, DOI 10.1016/0378-5955(85)90054-1 KLIS JFL, 1988, HEARING RES, V36, P163, DOI 10.1016/0378-5955(88)90058-5 KONISHI T, 1978, JPN J PHYSIOL, V28, P291 KOSSL M, 1992, J NEUROSCI, V12, P1575 LEGOUIX JP, 1973, J ACOUST SOC AM, V53, P409, DOI 10.1121/1.1913337 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 NIEDER P, 1971, J ACOUST SOC AM, V49, P478, DOI 10.1121/1.1912376 NIEDER P, 1968, J ACOUST SOC AM, V44, P1409, DOI 10.1121/1.1911276 NIEDER P, 1968, J ACOUST SOC AM, V43, P1092, DOI 10.1121/1.1910944 NUTTALL AL, 1981, BRAIN RES, V211, P171, DOI 10.1016/0006-8993(81)90078-0 OESTERLE EC, 1989, J ACOUST SOC AM, V86, P1013, DOI 10.1121/1.398092 OESTERLE EC, 1990, J NEUROPHYSIOL, V64, P617 PATUZZI R, 1984, HEARING RES, V13, P9, DOI 10.1016/0378-5955(84)90090-X PATUZZI R, 1984, HEARING RES, V13, P19, DOI 10.1016/0378-5955(84)90091-1 PATUZZI R, 1984, HEARING RES, V13, P1, DOI 10.1016/0378-5955(84)90089-3 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 RUGGERO MA, 1986, J ACOUST SOC AM, V79, P1491, DOI 10.1121/1.393763 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 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 SOKOLICH WG, 1976, J ACOUST SOC AM, V59, P963, DOI 10.1121/1.380955 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 ZWISLOCKI JJ, 1974, FACTS MODELS HEARING, P107 NR 54 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 1994 VL 75 IS 1-2 BP 103 EP 113 DI 10.1016/0378-5955(94)90061-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400012 PM 8071136 ER PT J AU KLIS, SFL SMOORENBURG, GF AF KLIS, SFL SMOORENBURG, GF TI OSMOTICALLY INDUCED PRESSURE DIFFERENCE IN THE COCHLEA AND ITS EFFECT ON COCHLEAR POTENTIALS SO HEARING RESEARCH LA English DT Article DE OSMOLALITY; SUMMATING POTENTIAL; COMPOUND ACTION POTENTIAL; COCHLEAR MICROPHONICS; HYDROPS ID EXPERIMENTAL ENDOLYMPHATIC HYDROPS; LOW-FREQUENCY SOUND; OUTER HAIR-CELLS; MODULATION; MOTILITY AB The electrophysiological effects observed during scala tympani displacements in low-frequency biasing experiments, an increase of the summating potential (SP) together with a decrease of the compound action potential (CAP), correlate well with the effects found in guinea pigs with evoked endolymphatic hydrops. This contributes to the hypothesis that displacement of the basilar membrane underlies the changes found in endolymphatic hydrops. A major difference between both experimental situations is that in low-frequency biasing the basilar membrane is continuously moving, whereas in hydrops the hypothesized displacement would be static. To evaluate the importance of this difference, experiments were performed which attempted to evoke a static displacement of the basilar membrane by perfusing the perilymphatic spaces with perfusates of various osmolalities. Perfusion with hypotonic perfusate (183 mOsm/kg) increased the SP and decreased the CAF (4 kHz stimulation) whereas perfusion with a hypertonic perfusate (397 mOsm/kg) decreased both these potentials. The cochlear microphonics were hardly affected. These data demonstrate that both experimental situations (biasing, i.e. dynamic displacement and osmotic pressure, i.e. static displacement) cause similar changes in the SP and the CAP and the data support the hypothesis that basilar membrane displacement towards scala tympani is an important contributing factor to the electrophysiologic changes in endolymphatic hydrops. RP KLIS, SFL (reprint author), UNIV UTRECHT,DEPT OTORHINOLARYNGOL,EXPTL AUDIOL LAB,ROOM G02531,HEIDELBERGLAAN 100,3584 CX UTRECHT,NETHERLANDS. CR ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 BUTLER RA, 1963, J ACOUST SOC AM, V35, P1188, DOI 10.1121/1.1918672 DAVIS H, 1958, AM J PHYSIOL, V195, P251 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 DURRANT JD, 1974, J ACOUST SOC AM, V56, P562, DOI 10.1121/1.1903291 HARRISON RV, 1984, HEARING RES, V14, P85, DOI 10.1016/0378-5955(84)90071-6 HORNER KC, 1986, HEARING RES, V26, P319 HORNER KC, 1991, ANN OTO RHINOL LARYN, V100, P496 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 KONISHI T, 1968, J ACOUST SOC AM, V43, P462, DOI 10.1121/1.1910853 KUMAGAMI H, 1983, ORL J OTO-RHINO-LARY, V45, P143 MORIZONO T, 1984, ANN OTO RHINOL LARYN, V93, P225 Rose B.D., 1984, CLIN PHYSL ACID BASE SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 TONNDORF J., 1957, ANN OTOL RHINOL AND LARYNGOL, V66, P766 VANBENTHEM PPG, 1993, UNPUB HEAR RES VANDEELEN GW, 1987, ARCH OTO-RHINO-LARYN, V244, P167 NR 19 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 MAY PY 1994 VL 75 IS 1-2 BP 114 EP 120 DI 10.1016/0378-5955(94)90062-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400013 PM 8071138 ER PT J AU BERGLUND, AM BROWN, MC AF BERGLUND, AM BROWN, MC TI CENTRAL TRAJECTORIES OF TYPE-II SPIRAL GANGLION-CELLS FROM VARIOUS COCHLEAR REGIONS IN MICE SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS; OUTER HAIR CELLS; AFFERENT ID AUDITORY-NERVE FIBERS; OUTER HAIR-CELLS; HORSERADISH-PEROXIDASE; INFERIOR COLLICULUS; ADULT CATS; INNERVATION; NUCLEUS; MOUSE; PROJECTIONS; MORPHOLOGY AB Type II spiral ganglion cells provide the afferent pathway from outer hair cells in the mammalian cochlea to neurons in the cochlear nucleus. The present study compares the projection patterns of type II fibers originating from spiral ganglion cells of apical, middle and basal cochlear regions in mice. Fibers were labeled by extracellular injections of horseradish peroxidase into the spiral ganglion. Type II fibers from all regions displayed many 'en passant' swellings (mean = 95) and had very few terminal swellings (mean = 6); fibers from the base had significantly more swellings than those from the apex. Type II fibers traveled into the cochlear nucleus together with type I fibers labeled by the same injection, and both types bifurcated in a cochleotopic manner. The bifurcations formed ascending and descending branches that traveled initially with type I branches in the magnocellular regions of the cochlear nucleus. Type II fibers differed from type I branches in that many fibers subsequently distributed collaterals and terminals to granule cell regions and to the boundaries of these regions that typically do not receive type I input. This projection into the granule cell regions depended on cochlear origin: ascending branches of type II fibers from the cochlea apex did not usually terminate in granule cell regions, whereas those from the base often ended in these regions. Descending branches of type II fibers from all regions, however, projected to the granule cell regions, particularly the granule cell lamina between ventral and dorsal cochlear nucleus. These observations suggest that afferent information from outer hair cells reaches a wide area of the magnocellular parts of the cochlear nucleus in a cochleotopic fashion, and reaches granule cell regions with a less distinct cochleotopic mapping. C1 HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. RP BERGLUND, AM (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 BENSON TE, 1990, J COMP NEUROL, V295, P52, DOI 10.1002/cne.902950106 BERGLUND AM, 1991, ABSTR ASS RES OT, V14, P139 BERGLUND A M, 1989, Society for Neuroscience Abstracts, V15, P742 BERGLUND AM, 1987, J COMP NEUROL, V255, P560, DOI 10.1002/cne.902550408 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BROWN MC, 1990, HEARING RES, V49, P105, DOI 10.1016/0378-5955(90)90098-A BROWN MC, 1988, J COMP NEUROL, V278, P581, DOI 10.1002/cne.902780409 CAJAL SR, 1909, HISTOLOGIE SYSTEME N, V1, P7 CANT NB, 1993, MAMMALIAN COCHLEAR N DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X EHRET G, 1991, BRAIN RES, V567, P350, DOI 10.1016/0006-8993(91)90819-H FEKETE DM, 1984, J COMP NEUROL, V229, P432, DOI 10.1002/cne.902290311 GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 HARRISON JM, 1962, SCIENCE, V138, P893, DOI 10.1126/science.138.3543.893 KELLERHALS B, 1967, ACTA OTOLARYNGOL S, V226, P6 KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIM DO, 1984, RECENT ADV HEARING S LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIBERMAN MC, 1993, J COMP NEUROL, V327, P17, DOI 10.1002/cne.903270103 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 Lorente de No R., 1937, LARYNGOSCOPE, V47, P373 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MUGNAINI E, 1980, J NEUROCYTOL, V9, P537, DOI 10.1007/BF01204841 OERTEL D, 1990, J COMP NEUROL, V295, P136, DOI 10.1002/cne.902950112 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 OSEN KK, 1970, ARCH ITAL BIOL, V108, P21 Peters A, 1991, FINE STRUCTURE NERVO, V3rd ROSE JE, 1959, B JOHNS HOPKINS HOSP, V104, P211 ROUILLER EM, 1992, NEUROSCI LETT, V144, P19, DOI 10.1016/0304-3940(92)90706-D RYUGO DK, 1991, J COMP NEUROL, V308, P209, DOI 10.1002/cne.903080208 Sando I, 1965, ACTA OTOLARYNG STOCK, V59, P417, DOI 10.3109/00016486509124577 SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SIMMONS DD, 1988, J COMP NEUROL, V270, P132, DOI 10.1002/cne.902700111 SPOENDLIN H, 1982, AM J OTOL, V3, P274 TSUCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 NR 40 TC 46 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 MAY PY 1994 VL 75 IS 1-2 BP 121 EP 130 DI 10.1016/0378-5955(94)90063-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400014 PM 8071139 ER PT J AU PIRVOLA, U ARUMAE, U MOSHNYAKOV, M PALGI, J SAARMA, M YLIKOSKI, J AF PIRVOLA, U ARUMAE, U MOSHNYAKOV, M PALGI, J SAARMA, M YLIKOSKI, J TI COORDINATED EXPRESSION AND FUNCTION OF NEUROTROPHINS AND THEIR RECEPTORS IN THE RAT INNER-EAR DURING TARGET INNERVATION SO HEARING RESEARCH LA English DT Article DE NEUROTROPHIC SYSTEM; NEURITOGENESIS; NEURONAL SURVIVAL; COCHLEOVESTIBULAR GANGLION; OTIC VESICLE ID NERVE GROWTH-FACTOR; COCHLEO-VESTIBULAR GANGLION; MOLECULAR-CLONING; IMMUNOHISTOCHEMICAL LOCALIZATION; COCHLEOVESTIBULAR GANGLION; MESSENGER-RNAS; FACTOR FAMILY; OTIC VESICLE; NGF RECEPTOR; TRK FAMILY AB We show that trkB and trkC mRNAS, encoding the high-affinity receptor tyrosine kinases for brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), respectively, as well as low-affinity nerve growth factor receptor (p75(LNGFR)) mRNA are expressed in the cochleovestibular ganglion (CVG) before and during innervation of the target fields. Correspondingly, from preinnervation stages onward, BDNF and NT-3, but neither nerve growth factor (NGF)nor neurotrophin-4(NT-4) mRNAs are expressed in the sensory epithelium of the otic vesicle, the peripheral target field of CVG neurons. No neurotrophin transcripts were detected by in situ hybridization in the medullary central targets. In explant cultures, neuritogenesis from both the cochlear and vestibular part of the CVG was promoted by BDNF, while NT-3 evoked neurites mainly from the cochlear neurons. Also NT-4 stimulated neurite outgrowth from the CVG in vitro. In dissociated neuron-enriched cultures, NT-3 and BDNF promoted survival of overlapping subsets of CVG neurons and, correspondingly, results from in situ hybridization showed that both trkC and trkB mrnas were expressed in most neurons of this ganglion. The negligible effect of NGF seen in the bioassays agrees well with the expression of only a few trkA transcripts, encoding the high-affinity receptor for NGF, in the CVG. Based on the spatiotemporal expression patterns and biological effects in vitro, peripherally-synthesized BDNF and NT-3 regulate the survival of CVG neurons as well as the establishment of neuron-target cell contacts in the early-developing inner ear. In addition, the expression of trkB mRNA, more specifically its truncated form, and trkC as well as p75(LNGFR) mRNAS in distinct, non-neuronal structures indicates novel roles for these molecules during development. C1 UNIV HELSINKI,INST BIOTECHNOL,HELSINKI,FINLAND. ESTONIAN ACAD SCI,INST CHEM PHYS & BIOPHYS,TALLINN,ESTONIA. UNIV KUOPIO,DEPT OTOLARYNGOL,SF-70211 KUOPIO,FINLAND. RP PIRVOLA, U (reprint author), UNIV HELSINKI,DEPT PATHOL,POB 21,SF-00014 HELSINKI,FINLAND. CR ALTMAN J, 1982, ADV ANAT EMBRYOL CEL, V74, P1 ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 ARUMAE U, 1993, J CELL BIOL, V122, P1053, DOI 10.1083/jcb.122.5.1053 BARDE YA, 1982, EMBO J, V1, P549 BARDE YA, 1989, NEURON, V2, P1525, DOI 10.1016/0896-6273(89)90040-8 BERKEMEIER LR, 1991, NEURON, V7, P857, DOI 10.1016/0896-6273(91)90287-A BERND P, 1989, DEV BIOL, V134, P11, DOI 10.1016/0012-1606(89)90073-0 BUCHMAN VL, 1993, DEVELOPMENT, V118, P989 DAMICOMARTEL A, 1982, AM J ANAT, V163, P351, DOI 10.1002/aja.1001630407 DAVIES AM, 1985, DEV BIOL, V111, P62, DOI 10.1016/0012-1606(85)90435-X DAVIES AM, 1986, J NEUROSCI, V6, P1897 DESPRES G, 1991, HEARING RES, V52, P157, DOI 10.1016/0378-5955(91)90195-F DESPRES G, 1988, NEUROSCI LETT, V85, P5, DOI 10.1016/0304-3940(88)90418-1 EBENDAL T, 1989, NERVE GROWTH FACTORS, P81 ERNFORS P, 1992, EUR J NEUROSCI, V4, P1140, DOI 10.1111/j.1460-9568.1992.tb00141.x ERNFORS P, 1990, P NATL ACAD SCI USA, V87, P5454, DOI 10.1073/pnas.87.14.5454 Glass David J., 1993, Trends in Cell Biology, V3, P262, DOI 10.1016/0962-8924(93)90054-5 GUNDERSEN RW, 1979, SCIENCE, V206, P1079, DOI 10.1126/science.493992 HALLBOOK F, 1993, EUR J NEUROSCI, V5, P1, DOI 10.1111/j.1460-9568.1993.tb00199.x HALLBOOK F, 1990, DEVELOPMENT, V108, P693 HALLBOOK F, 1991, NEURON, V6, P845, DOI 10.1016/0896-6273(91)90180-8 HAUGER SH, 1989, NEUROSCIENCE, V33, P241, DOI 10.1016/0306-4522(89)90203-0 HEMOND SG, 1992, ANAT REC, V232, P273, DOI 10.1002/ar.1092320212 HOHN A, 1990, NATURE, V344, P339, DOI 10.1038/344339a0 HOYLE GW, 1993, NEURON, V10, P1019, DOI 10.1016/0896-6273(93)90051-R IP NY, 1993, NEURON, V10, P137, DOI 10.1016/0896-6273(93)90306-C IP NY, 1992, P NATL ACAD SCI USA, V89, P3060, DOI 10.1073/pnas.89.7.3060 JULIEN JP, 1985, BIOCHIM BIOPHYS ACTA, V825, P398, DOI 10.1016/0167-4781(85)90067-3 KLEIN R, 1990, CELL, V61, P647, DOI 10.1016/0092-8674(90)90476-U LAMBALLE F, 1991, CELL, V66, P967, DOI 10.1016/0092-8674(91)90442-2 LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEFEBVRE PP, 1991, ACTA OTO-LARYNGOL, V111, P304, DOI 10.3109/00016489109137392 LEIBROCK J, 1989, NATURE, V341, P149, DOI 10.1038/341149a0 LEVIMONTALCINI R, 1987, SCIENCE, V237, P1154, DOI 10.1126/science.3306916 LUMSDEN AGS, 1983, NATURE, V306, P786, DOI 10.1038/306786a0 MAISONPIERRE PC, 1990, SCIENCE, V247, P1446, DOI 10.1126/science.2321006 MARTINZANCA D, 1989, MOL CELL BIOL, V9, P24 MERLIO JP, 1992, NEUROSCIENCE, V51, P513, DOI 10.1016/0306-4522(92)90292-A MIDDLEMAS DS, 1991, MOL CELL BIOL, V11, P143 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 RADEKE MJ, 1987, NATURE, V325, P593, DOI 10.1038/325593a0 RAIVICH G, 1987, J COMP NEUROL, V256, P229, DOI 10.1002/cne.902560204 REPRESA J, 1991, ANAT EMBRYOL, V184, P421, DOI 10.1007/BF01236048 ROMEIS B, 1948, MIKROSKOPISCHE TEKNI, P70 ROSENTHAL A, 1990, NEURON, V4, P767, DOI 10.1016/0896-6273(90)90203-R TESSAROLLO L, 1993, DEVELOPMENT, V118, P463 TESSIERLAVIGNE M, 1991, TRENDS NEUROSCI, V14, P303, DOI 10.1016/0166-2236(91)90142-H TIMMUSK T, 1993, NEURON, V10, P475, DOI 10.1016/0896-6273(93)90335-O TSOULFAS P, 1993, NEURON, V10, P1 VANDEWATER TR, 1984, ACTA OTOLARYNGOL STO, V95, P470 VOGEL KS, 1991, NEURON, V6, P649 VONBARTHELD CS, 1991, DEVELOPMENT, V113, P455 WHEELER EF, 1992, J NEUROSCI, V12, P930 WHITTEMORE SR, 1988, J NEUROSCI RES, V20, P403, DOI 10.1002/jnr.490200402 WILKINSON DG, 1990, POSTIMPLANTATION MAM, P151 YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C NR 56 TC 169 Z9 174 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 1994 VL 75 IS 1-2 BP 131 EP 144 DI 10.1016/0378-5955(94)90064-7 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400015 PM 8071140 ER PT J AU SOHMER, H GEALDOR, M WEINSTEIN, D AF SOHMER, H GEALDOR, M WEINSTEIN, D TI HUMAN FETAL AUDITORY THRESHOLD IMPROVEMENT DURING MATERNAL OXYGEN RESPIRATION SO HEARING RESEARCH LA English DT Article DE THRESHOLD; FETUS; NEONATE; OXYGEN; SENSORI-NEURAL ID HEART-RATE VARIABILITY; BRAIN-STEM RESPONSE; VIBROACOUSTIC STIMULATION; HUMAN FETUSES; SOUND ENVIRONMENT; SHEEP; INTENSITY; MOVEMENTS; PERCEPTION; POTENTIALS AB It has been suggested that the near full-term fetus in-utero has a sensori-neural hearing loss compared to the neonate due to the relative hypoxia resulting from placental oxygenation compared to pulmonary oxygenation. This hypothesis was tested by estimating the threshold of the fetus to vibro-acoustic stimulation applied to the maternal abdomen while the mother was breathing room air and again when breathing oxygen. Fetal response was assessed by maternal perception of fetal movement and by objective demonstration of movement by ultrasound. It has been shown that the fetal responses are to the acoustic component of the stimulus, that the acoustic stimulus is not overly attenuated or masked, and that maternal oxygen inhalation enhances fetal oxygenation. The results showed that the threshold was lower and/or the response was stronger when the mother was breathing oxygen compared to when she was breathing room air. Thus it is confirmed that in-utero the fetus has an hypoxia-induced sensori-neural hearing loss. At birth, with the shift to more efficient pulmonary oxygenation, there is an improvement in auditory threshold. C1 HADASSAH UNIV HOSP,CTR SPEECH & HEARING,IL-91120 JERUSALEM,ISRAEL. HADASSAH UNIV HOSP,DEPT OBSTET & GYNECOL,IL-91120 JERUSALEM,ISRAEL. RP SOHMER, H (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 1172,IL-91010 JERUSALEM,ISRAEL. CR ADELMAN C, 1990, ELECTROEN CLIN NEURO, V77, P77, DOI 10.1016/0168-5597(90)90019-A BATTAGLI.FC, 1968, J CLIN INVEST, V47, P548, DOI 10.1172/JCI105751 BIRNHOLZ JC, 1983, SCIENCE, V222, P516, DOI 10.1126/science.6623091 CARTER AM, 1989, J DEV PHYSIOL, V12, P305 FAWER CL, 1982, NEUROPEDIATRICS, V13, P200, DOI 10.1055/s-2008-1059623 GAFNI M, 1976, ACTA OTO-LARYNGOL, V82, P354, DOI 10.3109/00016487609120919 GAGNON R, 1990, AM J OBSTET GYNECOL, V163, P1894 GAGNON R, 1989, SEMIN PERINATOL, V13, P393 GAGNON R, 1992, OBSTET GYNECOL, V79, P950 GERHARDT KJ, 1989, SEMIN PERINATOL, V13, P362 GERHARDT KJ, 1992, AM J OTOLARYNG, V13, P226, DOI 10.1016/0196-0709(92)90026-P HERTOGS K, 1979, BRIT MED J, V2, P1183 HILDESHEIMER M, 1987, LARYNGOSCOPE, V97, P204 JACKSON BT, 1987, AM J PHYSIOL, V252, pR94 JOHNSTON.BM, 1972, Q REV BIOPHYS, V5, P1 LARY S, 1985, J PEDIATR-US, V107, P593, DOI 10.1016/S0022-3476(85)80030-5 LECANUET JP, 1986, EARLY HUM DEV, V13, P269, DOI 10.1016/0378-3782(86)90061-7 LECANUET JP, 1988, EARLY HUM DEV, V18, P81, DOI 10.1016/0378-3782(88)90045-X LONGO LD, 1977, J APPL PHYSIOL, V43, P885 METCALFE J, 1967, PHYSIOL REV, V47, P782 NYMAN M, 1991, OBSTET GYNECOL, V78, P803 PARKES MJ, 1991, AM J OBSTET GYNECOL, V164, P1336 RABINOWITZ R, 1983, OBSTET GYNECOL, V61, P16 RAYBURN WF, 1980, AM J OBSTET GYNECOL, V138, P210 RITCHIE K, 1980, SEMIN PERINATOL, V4, P295 RUEDICH DA, 1989, AM J OBSTET GYNECOL, V161, P189 SOHMER H, 1986, ELECTROEN CLIN NEURO, V64, P334, DOI 10.1016/0013-4694(86)90157-4 SOHMER H, 1989, HEARING RES, V40, P87, DOI 10.1016/0378-5955(89)90102-0 SOHMER H, 1994, HEARING RES, V73, P116, DOI 10.1016/0378-5955(94)90289-5 SOHMER H, 1991, HEARING RES, V55, P92, DOI 10.1016/0378-5955(91)90095-Q STARR A, 1977, PEDIATRICS, V60, P831 TALBOT WH, 1968, J NEUROPHYSIOL, V31, P301 VANVLIET MAT, 1985, EUR J OBSTET GYN R B, V20, P221, DOI 10.1016/0028-2243(85)90068-1 WESTGREN M, 1987, BRIT J OBSTET GYNAEC, V94, P523, DOI 10.1111/j.1471-0528.1987.tb03144.x YAO QW, 1990, OBSTET GYNECOL, V75, P206 NR 35 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 1994 VL 75 IS 1-2 BP 145 EP 150 DI 10.1016/0378-5955(94)90065-5 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400016 PM 8071141 ER PT J AU TENCATE, WJF CURTIS, LM RAREY, KE AF TENCATE, WJF CURTIS, LM RAREY, KE TI NA,K-ATPASE ALPHA-SUBUNIT AND BETA-SUBUNIT ISOFORM DISTRIBUTION IN THE RAT COCHLEAR AND VESTIBULAR TISSUES SO HEARING RESEARCH LA English DT Article DE ENDOLYMPH MICROHOMEOSTASIS; IMMUNOCYTOCHEMISTRY; ION TRANSPORT ID NA+-K+-ATPASE; DIFFERENTIAL EXPRESSION; FUNCTIONAL IMPLICATIONS; MESSENGER-RNAS; NA+,K+-ATPASE; BRAIN; IDENTIFICATION; LOCALIZATION; TRANSPORT; KIDNEY AB The distribution of five Na,K-ATPase subunit isoforms (alpha(1), alpha(2), alpha(3), beta(1), and beta(2)) in rat cochlear and vestibular tissues was determined by immunocytochemical techniques using subunit isoform specific polyclonal antibodies. The expression of Na,K-ATPase alpha and beta subunit isoforms varied among different cell regions of the inner ear. The alpha(1) subunit isoform was more extensively distributed in all inner ear tissues than the alpha(2) or alpha(3) subunit isoforms. The beta(1) subunit isoform was distributed primarily in spiral ligament and inner hair cells of the cochlea, and in crista ampullaris and macula of the saccule. The beta(2) subunit isoform was most abundant in the stria vascularis, dark cells of the ampullae and utricle. The alpha(1) beta(1) subunit combination of Na,K-ATPase was most commonly found in the spiral ligament, while the alpha(1) beta(2) combination was most abundant in the stria vascularis. Similarly, alpha(1) beta(2) was confined more to the dark cells of the ampullae and utricle. The alpha(3) beta(1) subunit combination of Na,K-ATPase was identified in the inner hair cells of the cochlea and the sensory regions of the vestibular end organs. These observations may reflect functional diversity of Na,K-ATPase in the individual inner ear regions and may provide insight into the differences between fluid and ion transport in the inner ear and that of other transporting tissues. Overall, the distribution pattern further indicates that the different isoform combinations have specific roles. C1 UNIV FLORIDA,COLL MED,DEPT ANAT & CELL BIOL,GAINESVILLE,FL. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL. CR ASKARI A, 1987, J BIOENERG BIOMEMBR, V19, P359, DOI 10.1007/BF00768539 AZUMA KK, 1991, AM J PHYSIOL, V260, pC958 BONTING SL, 1984, SECRETION MECHANISMS, P127 BONTING SL, 1961, ARCH BIOCHEM BIOPHYS, V95, P416, DOI 10.1016/0003-9861(61)90170-9 BRODSKY JL, 1990, AM J PHYSIOL, V258, pC803 BURNHAM JA, 1984, J NEUROCYTOL, V13, P617, DOI 10.1007/BF01148082 DEVARAJAN P, 1992, J BIOL CHEM, V267, P22435 DEWEER P, 1985, KIDNEY PHYSL PATHOPH, P31 DRESCHER D, 1985, AUDITORY BIOCH, P436 EMANUEL JR, 1989, MOL CELL BIOL, V9, P3744 FARMAN N, 1992, AM J PHYSIOL, V263, pC810 FINA M, 1993, ABSTR ASS RES OT, V76, P19 GEERING K, 1989, AM J PHYSIOL, V257, pC851 GEERING K, 1987, J CELL BIOL, V105, P2613, DOI 10.1083/jcb.105.6.2613 GHOSH S, 1991, J CELL PHYSIOL, V149, P184, DOI 10.1002/jcp.1041490203 Guild SR, 1927, AM J ANAT, V39, P1, DOI 10.1002/aja.1000390102 HERRERA VLM, 1987, J CELL BIOL, V105, P1855, DOI 10.1083/jcb.105.4.1855 HORISBERGER JD, 1989, CURRENT TOPICS MEMBR, P253 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 JORGENSEN PL, 1982, BIOCHIM BIOPHYS ACTA, V694, P27, DOI 10.1016/0304-4157(82)90013-2 JORGENSEN PL, 1986, KIDNEY INT, V29, P10, DOI 10.1038/ki.1986.3 KATZ AI, 1982, AM J PHYSIOL, V242, pF207 LUNDQUIST PG, 1984, ULTRASTRUCTURAL ATLA, P309 LUNDQUIST PG, 1963, ACTA OTOLARYNGOL STO, V188, P198 MANNI JJ, 1987, HEARING RES, V26, P229, DOI 10.1016/0378-5955(87)90059-1 MANNI JJ, 1986, ARCH OTOLARYNGOL, V112, P423 MARTINVASALLO P, 1989, J BIOL CHEM, V264, P4613 MCGRAIL KM, 1989, EUR J NEUROSCI, V2, P170 MIZUKOSHI F, 1988, ACTA OTO-LARYNGOL, V105, P202, DOI 10.3109/00016488809096999 PEDERSEN PL, 1987, TRENDS BIOCHEM SCI, V12, P146, DOI 10.1016/0968-0004(87)90071-5 RYAN A F, 1991, Molecular and Cellular Neuroscience, V2, P179, DOI 10.1016/1044-7431(91)90011-C SCHMITT CA, 1986, J BIOL CHEM, V261, P439 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SHULL GE, 1986, BIOCHEMISTRY-US, V25, P8125, DOI 10.1021/bi00373a001 SHYJAN AW, 1989, BIOCHEMISTRY-US, V28, P4531, DOI 10.1021/bi00437a002 SHYJAN AW, 1990, J BIOL CHEM, V265, P5166 SHYJAN AW, 1990, P NATL ACAD SCI USA, V87, P1178, DOI 10.1073/pnas.87.3.1178 SKOU JC, 1988, METHOD ENZYMOL, V156, P1 SPICER SS, 1990, HEARING RES, V43, P205, DOI 10.1016/0378-5955(90)90229-I VERREY F, 1989, MOL ENDOCRINOL, V3, P1369 WACKYM PA, 1988, ARCH OTO-RHINO-LARYN, V245, P221, DOI 10.1007/BF00463931 WANG ZM, 1993, PEDIATR RES, V33, P1 WATTS AG, 1991, P NATL ACAD SCI USA, V88, P7425, DOI 10.1073/pnas.88.16.7425 WIENER H, 1992, ANN NY ACAD SCI, V671, P461, DOI 10.1111/j.1749-6632.1992.tb43830.x Yamane H, 1988, Adv Otorhinolaryngol, V42, P123 NR 45 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 MAY PY 1994 VL 75 IS 1-2 BP 151 EP 160 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400017 PM 8071142 ER PT J AU SUTTON, LA LONSBURYMARTIN, BL MARTIN, GK WHITEHEAD, ML AF SUTTON, LA LONSBURYMARTIN, BL MARTIN, GK WHITEHEAD, ML TI SENSITIVITY OF DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN HUMANS TO TONAL OVER-EXPOSURE - TIME-COURSE OF RECOVERY AND EFFECTS OF LOWERING L(2) SO HEARING RESEARCH LA English DT Article DE TONAL OVER-EXPOSURE; 2F(1)-F(2) DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS; TEMPORARY-THRESHOLD SHIFT; SUSCEPTIBILITY; HUMANS ID TEMPORARY THRESHOLD SHIFT; SENSORY CELL LOSS; ACOUSTIC-DISTORTION; COCHLEAR MECHANICS; HEARING-LOSS; MUTANT MICE; 2F1-F2; STIMULATION; EAR; SIMILARITIES AB An important concern of industrial hearing-conservation programs is detecting the onset of noise-induced hearing loss. If it can be shown that otoacoustic emissions are sufficiently sensitive to reliably detect auditory fatigue and the permanent hearing loss that eventually develops, they could become an important part of the hearing-conservation test battery. The present study in humans was designed to examine the influence of overall primary-tone level and the effects of lowering the f(2) primary on the sensitivity of distortion-product otoacoustic emissions (DPOAEs) to acoustic overstimulation. One ear from each of 14 subjects with normal hearing was exposed to a 105-dB SPL pure tone at 2.8 kHz for 3 min using a protocol consisting of distinct pre-exposure, exposure, and post-exposure periods. As a quantitative index of the functional status of the outer hair cells, 2f(1)-f(2) DPOAEs were monitored systematically over time using four stimulus-test conditions consisting of either one of two levels of equilevel primary tones, or one of two levels of offset primaries, with L(2) set 25 dB lower than L(1). The overall finding was that the DPOAE protocol incorporating both the lowest level of stimulation and an f(2)-primary tone that was 25 dB below the level of the f(1) stimulus [i.e., L(1) (55 dB SPL)- L(2) (30 dB SPL)= 25 dB] was most sensitive to the exposure effects. The results establish that DPOAEs elicited with unequal, in contrast to equal-level primaries, have comparable signal-to-noise ratios, but are considerably more sensitive to reductions in emission levels induced by exposure to short-lasting, moderately intense tones. The recovery of DPOAE amplitudes over the first 15 min post-exposure appeared to be roughly linear in log time and, in many cases, could be closely approximated by fitting a logarithmic curve to the post-exposure data. From these functions, the initial amount of loss (y-intercept) and the slope of recovery were identified as potential measures of vulnerability to acoustic, exposure in that these variables appeared to be related to the susceptibility of some of the subjects, who also participated in a subsequent experiment on the behavioral effects of the exposure stimulus, Finally, compared to behaviorally measured temporary threshold shift (TTS), the time course of the recovery for DPOAEs was very similar, suggesting that, with the appropriate parameters, DPOAEs can be as sensitive to TTS as routine pure-tone audiometry. C1 UNIV MIAMI, INST EAR M805, DEPT OTOLARYNGOL, MIAMI, FL 33101 USA. UNIV HOUSTON, SCH COMMUN, COLLABORAT SCI & TECHNOL INC, HOUSTON, TX USA. UNIV HOUSTON, SCH COMMUN, PROGRAM COMMUN DISORDERS, HOUSTON, TX USA. CR 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, 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 CLARK WW, 1978, ANN OTOL RHINOL LA S, V51, P1 CODY AR, 1988, HEARING RES, V35, P59, DOI 10.1016/0378-5955(88)90040-8 CODY AR, 1992, NOISE INDUCED HEARIN, P11 DALLOS P, 1969, J ACOUST SOC AM, V46, P1437, DOI 10.1121/1.1911882 DANCER A, 1986, BASIC APPLIED ASPECT, P137 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DAVIS H, 1950, Acta Otolaryngol Suppl, V88, P1 DAVIS RI, 1989, HEARING RES, V41, P1, DOI 10.1016/0378-5955(89)90173-1 DOLAN TG, 1985, J ACOUST SOC AM, V77, P1475, DOI 10.1121/1.392042 EDWARDS AL, 1954, STATISTICAL METHODS, P128 FAHEY PF, 1986, PERIPHERAL AUDITORY, P314 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GORGA MP, 1993, J ACOUST SOC AM, V93, P2050, DOI 10.1121/1.406691 HALL JL, 1974, J ACOUST SOC AM, V56, P1818, DOI 10.1121/1.1903519 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HARRIS JD, 1955, J ACOUST SOC AM, V27, P177, DOI 10.1121/1.1907484 HAUSER R, 1991, J ACOUST SOC AM, V89, P280, DOI 10.1121/1.400511 HIRSH IJ, 1955, J ACOUST SOC AM, V27, P1186, DOI 10.1121/1.1908157 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KEMP DT, 1982, NEW PERSPECTIVES NOI, P189 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 Lonsbury-Martin B, 1992, HEARING J, V45, P47 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P3 Lonsbury-Martin B L, 1981, Am J Otolaryngol, V2, P321, DOI 10.1016/S0196-0709(81)80042-7 LONSBURYMARTIN BL, 1978, J NEUROPHYSIOL, V41, P987 LONSBURYMARTIN BL, 1993, EAR HEARING, V14, P11, DOI 10.1097/00003446-199302000-00003 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1990, ANN OTOL RHINOL S147, V99, P29 MELNICK W, 1991, J ACOUST SOC AM, V90, P147, DOI 10.1121/1.401308 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 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORTON SJ, 1989, HEARING RES, V38, P243, DOI 10.1016/0378-5955(89)90069-5 PICKLES JO, 1988, INTRO PHYSL HEARING, P47 ROSOWSKI JJ, 1984, HEARING RES, V13, P141, DOI 10.1016/0378-5955(84)90105-9 SAUNDERS JC, 1991, J ACOUST SOC AM, V90, P136, DOI 10.1121/1.401307 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 SPEKTOR Z, 1991, LARYNGOSCOPE, V101, P965 Ward W. D., 1973, MODERN DEV AUDIOLOGY, P301 WARD WD, 1973, P INT C NOIS PUBL HL, P281 WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 WHITEHEAD ML, 1990, LECT NOTES BIOMATH, V87, P243 WHITEHEAD ML, 1993, ABSTR ASS RES OTOLAR, V16, P100 WHITEHEAD ML, 1994, IN PRESS J ACOUST SO WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 YATES GK, 1983, HEARING RES, V12, P305, DOI 10.1016/0378-5955(83)90003-5 YOUNG E, 1973, J ACOUST SOC AM, V54, P1535, DOI 10.1121/1.1914451 ZWICKER E, 1983, HEARING PHYSL BASES, P104 NR 58 TC 59 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 MAY PY 1994 VL 75 IS 1-2 BP 161 EP 174 DI 10.1016/0378-5955(94)90067-1 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400018 PM 8071143 ER PT J AU PALOMBI, PS BACKOFF, PM CASPARY, DM AF PALOMBI, PS BACKOFF, PM CASPARY, DM TI PAIRED TONE FACILITATION IN DORSAL COCHLEAR NUCLEUS NEURONS - A SHORT-TERM POTENTIATION MODEL TESTABLE IN-VIVO SO HEARING RESEARCH LA English DT Article DE POTENTIATION; CHINCHILLA; DCN; FUSIFORM CELL ID UNANESTHETIZED DECEREBRATE CATS; GABA-B RECEPTORS; GUINEA-PIG; INFERIOR COLLICULUS; PULSE FACILITATION; RAT HIPPOCAMPUS; AUDITORY-NERVE; DISCHARGE CHARACTERISTICS; DESCENDING PROJECTIONS; SYNAPTIC ORGANIZATION AB It has been suggested that the dorsal cochlear nucleus (DCN) is involved in coding stimulus history or prior auditory activity [Manis (1989) J. Neurophys, 61, 149-161; Manis (1990) J. Neurosci., 10, 2338-2351]. The major output neurons of the DCN are the fusiform (pyramidal) cells which are thought to receive excitatory inputs from the descending branch of the acoustic nerve onto their basal dendrites and significant inhibitory glycinergic and GABAergic inputs to the soma and dendrites. The apical dendrites of these neurons lie within the molecular layer of the DCN and encounter parallel fibers which are thought to utilize the excitatory amino acid neurotransmitter glutamate. In this study of anesthetized chinchillas, we found that, in contrast to the responses of acoustic nerve fibers and most cochlear nucleus neurons which are masked by an appropriate preceding signal, many DCN principal cells are facilitated during the second of two identical stimuli. Facilitated DCN responses often have a reduced interspike interval and a more chopper-like temporal response pattern to the second characteristic frequency tone. This paired tone facilitation in the chinchilla DCN provides an in vivo model of short-term potentiation elicited by sensory stimulation similar to the paired-pulse facilitation observed with electrical stimulation in other models. C1 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62702. SO ILLINOIS UNIV,SCH MED,DEPT SURG,SPRINGFIELD,IL 62702. CR ADAMS JC, 1983, NEUROSCI LETT, V37, P205, DOI 10.1016/0304-3940(83)90431-7 ADAMS JC, 1987, J COMP NEUROL, V262, P375, DOI 10.1002/cne.902620305 ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ANIS NA, 1983, BRIT J PHARMACOL, V79, P565 AUSTIN KB, 1989, EXP BRAIN RES, V77, P594 BEATTIE JL, 1993, ABSTR ASS RES OT, V16, P119 BERREBI AS, 1991, ANAT EMBRYOL, V183, P427 Boettcher F.A., 1988, P141 BOETTCHER FA, 1990, HEARING RES, V48, P125, DOI 10.1016/0378-5955(90)90203-2 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 CAO F, 1991, EXP BRAIN RES, V87, P553 CASPARY DM, 1984, HEARING RES, V13, P113, DOI 10.1016/0378-5955(84)90102-3 CASPARY DM, 1994, ADV SPEECH HEARING L CASPARY DM, 1987, BRAIN RES, V417, P273, DOI 10.1016/0006-8993(87)90452-5 COHEN ES, 1972, EXP NEUROL, V35, P470, DOI 10.1016/0014-4886(72)90117-3 COLLINGRIDGE GL, 1987, TRENDS NEUROSCI, V10, P288, DOI 10.1016/0166-2236(87)90175-5 CONLEE JW, 1982, NEUROSCIENCE, V7, P161, DOI 10.1016/0306-4522(82)90158-0 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 CREAGER R, 1980, J PHYSIOL-LONDON, V299, P409 DAVIES CH, 1990, J PHYSIOL-LONDON, V424, P513 DEUPREE DL, 1993, NEUROBIOL AGING, V14, P249, DOI 10.1016/0197-4580(93)90009-Z EVANS EF, 1992, PHILOS T ROY SOC B, V336, P295, DOI 10.1098/rstb.1992.0062 EVANS EF, 1973, EXP BRAIN RES, V17, P428 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GODFREY DA, 1978, J HISTOCHEM CYTOCHEM, V26, P118 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 GONZALEZLIMA F, 1984, BRAIN RES, V299, P201, DOI 10.1016/0006-8993(84)90702-9 GRANT IS, 1981, BRIT J ANAESTH, V53, P805, DOI 10.1093/bja/53.8.805 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 Helfert RH, 1991, NEUROBIOLOGY HEARING, P1 HENRY KR, 1991, HEARING RES, V56, P197, DOI 10.1016/0378-5955(91)90170-E HERNANDEZPEON R, 1972, J NEUROPHYSIOL, V35, P864 HESS G, 1987, NEUROSCI LETT, V77, P187, DOI 10.1016/0304-3940(87)90584-2 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P535 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 ITOH K, 1987, BRAIN RES, V400, P145, DOI 10.1016/0006-8993(87)90662-7 KALTENBACH JA, 1993, HEARING RES, V67, P35, DOI 10.1016/0378-5955(93)90229-T KANE EC, 1974, J COMP NEUROL, V155, P301, DOI 10.1002/cne.901550303 KANE ES, 1977, J NEUROCYTOL, V6, P583, DOI 10.1007/BF01205221 KANE ES, 1977, NEUROSCIENCE, V2, P897, DOI 10.1016/0306-4522(77)90113-0 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KRNJEVIC K, 1981, GABA BENZODIAZEPINE, P111 Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MANIS PB, 1989, J NEUROPHYSIOL, V61, P149 MANIS PB, 1990, J NEUROSCI, V10, P2338 MANIS PB, 1983, J NEUROPHYSIOL, V50, P1156 MOORE JK, 1980, J COMP NEUROL, V193, P609 MOORE JK, 1979, AM J ANAT, V154, P393, DOI 10.1002/aja.1001540306 MOREST DK, 1990, J COMP NEUROL, V300, P230, DOI 10.1002/cne.903000207 MUGNAINI E, 1980, J COMP NEUROL, V191, P581, DOI 10.1002/cne.901910406 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 NATHAN T, 1990, BRAIN RES, V531, P55, DOI 10.1016/0006-8993(90)90757-3 Oertel D., 1988, AUDITORY FUNCTION NE, P313 OERTEL D, 1989, J COMP NEUROL, V283, P228, DOI 10.1002/cne.902830206 OLIVER DL, 1984, J COMP NEUROL, V224, P155, DOI 10.1002/cne.902240202 OLIVER DL, 1983, J NEUROSCI, V3, P455 OSEN KK, 1972, J COMP NEUROL, V144, P355, DOI 10.1002/cne.901440307 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 Osen KK, 1981, NEURONAL MECHANISMS, P119 Osen K.K., 1990, GLYCINE NEUROTRANSMI, P417 OTIS TS, 1992, J NEUROPHYSIOL, V67, P227 PARHAM K, 1992, J NEUROPHYSIOL, V67, P1247 POTASHNER SJ, 1983, J NEUROCHEM, V41, P1094, DOI 10.1111/j.1471-4159.1983.tb09057.x RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1987, J NEUROPHYSIOL, V57, P414 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 RYUGO DK, 1985, J COMP NEUROL, V242, P381, DOI 10.1002/cne.902420307 SCHWARTZ IR, 1981, EXP NEUROL, V73, P601, DOI 10.1016/0014-4886(81)90199-0 SEMPLE MN, 1980, EXP BRAIN RES, V41, P19 SHOFNER WP, 1987, HEARING RES, V29, P45, DOI 10.1016/0378-5955(87)90204-8 SHOFNER WP, 1985, J NEUROPHYSIOL, V54, P917 SHORE SE, 1991, HEARING RES, V52, P255, DOI 10.1016/0378-5955(91)90205-N SIEGEL JH, 1987, HEARING RES, V29, P169, DOI 10.1016/0378-5955(87)90165-1 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 Spangler K., 1991, NEUROBIOLOGY HEARING, P27 van Noort J, 1969, STRUCTURE CONNECTION WATANABE T, 1971, JPN J PHYSIOL, V21, P537 WEINBERG RJ, 1987, NEUROSCIENCE, V20, P209, DOI 10.1016/0306-4522(87)90013-3 YOUNG ED, 1992, PHILOS T ROY SOC B, V336, P407, DOI 10.1098/rstb.1992.0076 YOUNG ED, 1993, ASS RES OTOLARYNGOL, V16, P124 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 ZUCKER RS, 1989, ANNU REV NEUROSCI, V12, P13, DOI 10.1146/annurev.neuro.12.1.13 NR 82 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 1994 VL 75 IS 1-2 BP 175 EP 183 DI 10.1016/0378-5955(94)90068-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400019 PM 8071144 ER PT J AU FROEHLICH, P FERBER, C REMOND, J JABOULAY, JM MORGON, A DUCLAUX, R COLLET, L AF FROEHLICH, P FERBER, C REMOND, J JABOULAY, JM MORGON, A DUCLAUX, R COLLET, L TI LACK OF ASSOCIATION BETWEEN TRANSIENTLY EVOKED OTOACOUSTIC EMISSION AMPLITUDE AND EXPERIMENTATION LINKED-FACTORS (REPEATED ACOUSTIC STIMULATION, CEREBROSPINAL-FLUID PRESSURE, SUPINE AND SITTING POSITIONS, ALERTNESS LEVEL) SO HEARING RESEARCH LA English DT Article DE TRANSIENTLY EVOKED OTOACOUSTIC EMISSIONS; CIRCADIAN RHYTHM; CEREBROSPINAL FLUID PRESSURE; SLEEP; ATTENTION; TIME EFFECT ID ACTIVE MICROMECHANICAL PROPERTIES; FREQUENCY; ATTENTION; COCHLEA; TASK AB Changes in transiently evoked otoacoustic;emissions (TEOAEs) occur during sleep and during tasks requiring attention. This can be due to a central nervous system effect on the cochlea. But, an additional or dominant influence by non-controlled factors is possible. In this paper, the effect of click-stimulus repetition, lying and sitting positions, state of alertness (awake or asleep) and CSF pressure variation on TEOAE features were studied. None of these factors affected TEOAE amplitude. In 2 subjects, TEOAE amplitude increased considerably during the night while remaining stable in 7 subjects during daytime sleep. This may be due to circadian variations of TEOAE amplitude. C1 HOP EDOUARD HERRIOT,CNRS,URA 1447,F-69003 LYON,FRANCE. HOP NEUROL,U600,F-69003 LYON,FRANCE. HOP NEUROL,U800,F-69003 LYON,FRANCE. FAC MED LYON SUD,PHYSIOL SENSORIELLE LAB,F-69310 PIERRE BENITE,FRANCE. CR AVAN P, 1992, HEARING RES, V57, P269, DOI 10.1016/0378-5955(92)90156-H BELL A, 1992, HEARING RES, V58, P91, DOI 10.1016/0378-5955(92)90012-C 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 DENSERT O, 1981, ACTA OTO-LARYNGOL, V91, P55, DOI 10.3109/00016488109138482 FLOCK A, 1984, HEAD NECK SURG, V243, P83 FROEHLICH P, 1990, BRAIN RES, V508, P286, DOI 10.1016/0006-8993(90)90408-4 FROEHLICH P, 1993, HEARING RES, V66, P1, DOI 10.1016/0378-5955(93)90254-X FROEHLICH P, 1993, PHYSIOL BEHAV, V53, P679, DOI 10.1016/0031-9384(93)90173-D HERNANDEZPEON R, 1956, SCIENCE, V123, P331, DOI 10.1126/science.123.3191.331 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 MERIC C, 1992, INT J PSYCHOPHYSIOL, V12, P233, DOI 10.1016/0167-8760(92)90061-F MERIC C, IN PRESS ACTA OTOLAR Puel J.L., 1989, COCHLEAR MECHANISMS, P315 PUEL JL, 1988, BRAIN RES, V447, P380, DOI 10.1016/0006-8993(88)91144-4 Rechtschaffen A, 1968, MANUAL STANDARDIZED SORENSEN PS, 1985, REGUL PEPTIDES, V10, P115 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WHITEHEAD ML, 1991, HEARING RES, V53, P269, DOI 10.1016/0378-5955(91)90060-M WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 NR 22 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 1994 VL 75 IS 1-2 BP 184 EP 190 DI 10.1016/0378-5955(94)90069-8 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400020 PM 8071145 ER PT J AU KONG, WJ EGG, G HUSSL, B SPOENDLIN, H SCHROTTFISCHER, A AF KONG, WJ EGG, G HUSSL, B SPOENDLIN, H SCHROTTFISCHER, A TI LOCALIZATION OF CHAT-LIKE IMMUNOREACTIVITY IN THE VESTIBULAR ENDORGANS OF THE RAT SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINE (ACH); CHOLINE ACETYLTRANSFERASE (CHAT); IMMUNOCYTOCHEMISTRY; LIGHT AND ELECTRON MICROSCOPY; VESTIBULAR SENSORY PERIPHERY ID GABA-LIKE IMMUNOREACTIVITY; GENE-RELATED PEPTIDE; GUINEA-PIG COCHLEA; CHOLINE-ACETYLTRANSFERASE; EFFERENT NEURONS; END-ORGANS; IMMUNOELECTRON MICROSCOPY; SQUIRREL-MONKEY; HAIR-CELLS; INNER-EAR AB In vertebrates acetylcholine (ACh) has been generally considered as a neurotransmitter of the vestibular efferent system. The precise localization and innervation of the cholinergic nerve endings in the vestibular sensory periphery is still unknown. We examined choline acetyltransferase (ChAT)-like immunoreactivity in all five endorgans of the rat vestibule with light and electron microscopy using a modified pre-embedding immunostaining technique. The results were: (1) ChAT-like immunoreactivity was widespread in all five endorgans of the vestibule and confined to the vesiculated efferent nerve endings. (2) Two types of ChAT-like immunostained nerve endings can be identified according to their size and innervation pattern: a large nerve ending and a small - middle size one. (3) Vestibular endorgans differ in their ChAT-like immunoreactivity: staining is dense in the macula of the utricule and the three ampullary cristae, but less so in the macula of the saccule. (4) We found also a regional difference of the ChAT-like immunostaining in ampullary crista. ChAT-like immunostained nerve endings were predominant in the periphery close to the semilunar plane, and less in density in the central area. These findings demonstrate that ACh is a major neurotransmitter in the vestibular efferent system. C1 UNIV INNSBRUCK, DEPT OTOLARYNGOL, A-6020 INNSBRUCK, AUSTRIA. TONGJI MED UNIV, UNION HOSP, WUHAN, PEOPLES R CHINA. CR ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 ANNIKO M, 1991, ACTA OTO-LARYNGOL, V111, P491, DOI 10.3109/00016489109138374 BERNARD C, 1985, BRAIN RES, V338, P225, DOI 10.1016/0006-8993(85)90151-9 CARPENTER MB, 1987, BRAIN RES, V408, P275, DOI 10.1016/0006-8993(87)90387-8 COHEN GM, 1987, HEARING RES, V28, P57, DOI 10.1016/0378-5955(87)90153-5 CRISWELL MH, 1992, BRAIN RES, V577, P101, DOI 10.1016/0006-8993(92)90542-H DANNHOF BJ, 1991, CELL TISSUE RES, V266, P89, DOI 10.1007/BF00678715 DECHESNE C, 1980, ACTA OTO-LARYNGOL, V90, P82, DOI 10.3109/00016488009131701 DEMEMES D, 1983, NEUROSCIENCE, V8, P285, DOI 10.1016/0306-4522(83)90066-0 DIDIER A, 1990, CELL TISSUE RES, V260, P415, DOI 10.1007/BF00318645 ECKENSTEIN F, 1983, J NEUROSCI, V3, P2286 EYBALIN M, 1984, BRAIN RES, V305, P313, DOI 10.1016/0006-8993(84)90437-2 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 EYBALIN M, 1985, BRAIN RES, V358, P354, DOI 10.1016/0006-8993(85)90983-7 FELIX D, 1982, ACTA OTO-LARYNGOL, V93, P101, DOI 10.3109/00016488209130858 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 FIBIGER HC, 1982, BRAIN RES REV, V4, P327, DOI 10.1016/0165-0173(82)90011-X GACEK R R, 1965, Acta Otolaryngol, V59, P541, DOI 10.3109/00016486509124585 GACEK RR, 1974, ACTA OTO-LARYNGOL, V77, P92, DOI 10.3109/00016487409124603 GERMAN DC, 1985, NEUROSCI LETT, V61, P1, DOI 10.1016/0304-3940(85)90391-X GOLDBERG JM, 1980, J NEUROPHYSIOL, V43, P986 HILDING D, 1962, Acta Otolaryngol, V55, P205, DOI 10.3109/00016486209127354 HOUSER CR, 1983, BRAIN RES, V266, P97, DOI 10.1016/0006-8993(83)91312-4 Hunter-Duvar IM, 1984, ULTRASTRUCTURAL ATLA, P211 IRELAND PE, 1961, ANN OTO RHINOL LARYN, V70, P490 IURATO S, 1971, ACTA OTO-LARYNGOL, V71, P147, DOI 10.3109/00016487109125343 IURATO S, 1971, ACTA OTO-LARYNGOL, P1 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 KLINKE R, 1974, PHYSIOL REV, V54, P316 LOPEZ I, 1988, NEUROSCIENCE, V25, P13 LOPEZ I, 1990, BRAIN RES, V530, P170, DOI 10.1016/0006-8993(90)90677-4 MARCO J, 1993, ACTA OTO-LARYNGOL, V113, P229, DOI 10.3109/00016489309135798 MCLAMB WT, 1992, HEARING RES, V58, P193, DOI 10.1016/0378-5955(92)90128-A MESROBIAN RJO, 1987, ARCH OTOLARYNGOL, V113, P543 MEZA G, 1987, HEARING RES, V28, P73, DOI 10.1016/0378-5955(87)90155-9 ROSSI ML, 1980, BRAIN RES, V185, P125, DOI 10.1016/0006-8993(80)90677-0 ROTH B, 1991, ANAT EMBRYOL, V183, P483 SPOENDLIN H, 1970, ULTRASTRUCTURE PERIP, P263 TANAKA M, 1989, BRAIN RES, V504, P31, DOI 10.1016/0006-8993(89)91593-X TANAKA M, 1988, BRAIN RES, V447, P175, DOI 10.1016/0006-8993(88)90981-X USAMI S, 1987, BRAIN RES, V418, P383, DOI 10.1016/0006-8993(87)90108-9 USAMI S, 1987, BRAIN RES, V417, P367, DOI 10.1016/0006-8993(87)90466-5 USAMI S, 1988, ORL J OTO-RHINO-LARY, V50, P162 USAMI SI, 1991, ACTA OTO-LARYNGOL, P166 WACKYM PA, 1991, OTOLARYNG HEAD NECK, V105, P493 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 WHITLON DS, 1989, J NEUROCYTOL, V18, P505, DOI 10.1007/BF01474546 NR 50 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 MAY PY 1994 VL 75 IS 1-2 BP 191 EP 200 DI 10.1016/0378-5955(94)90070-1 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400021 PM 8071146 ER PT J AU JOHNSON, AC CANLON, B AF JOHNSON, AC CANLON, B TI PROGRESSIVE HAIR CELL LOSS INDUCED BY TOLUENE EXPOSURE SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEA; MORPHOLOGY; OTOTOXICITY; OUTER HAIR CELLS; PHALLOIDIN; RATS; SEM; SOLVENT ID HEARING-LOSS; INDUCED OTOTOXICITY; WEANLING RATS; COCHLEA; AGE; NOISE; DAMAGE AB Rats were exposed to toluene by inhalation (1400 ppm, 16 h/d, 8 days) and sacrificed for morphological investigations at 3 and 5 days after the start of the exposure, and 4 days and 6 weeks after the end of the exposure. The cochleae were removed and prepared for light microscopy and scanning electron microscopy. After 3 days of toluene exposure no loss of hair cells was found. A slight loss in the third row outer hair cells was observed after 5 days of exposure. Four days after the 8-day long exposure a loss of hair cells was found in all 3 rows of outer hair cells, mainly in the middle and upper turns of the cochlea. Six weeks post-exposure the damage on the hair cells had progressed towards the basal part of the cochlea, and a 50-100% loss of outer hair cells together with some loss of inner hair cells were seen. A fairly good correlation was found between the frequency regions showing loss of hair cells and the threshold shifts previously measured by auditory brainstem responses and distortion product otoacoustic emissions in the same rats at corresponding times (Johnson and Canlon, 1994). These results indicate that the outer hair cells in the middle frequency region of the cochlea, were primarily affected by toluene exposure. However, after a long post-exposure period the damage extended basally and apically and some damage to the inner hair cells was seen. C1 KAROLINSKA INST,DEPT PHYSIOL & PHARMACOL,S-17177 STOCKHOLM,SWEDEN. RP JOHNSON, AC (reprint author), NATL INST OCCUPAT HLTH,DEPT NEUROMED,S-17184 SOLNA,SWEDEN. CR Anniko M, 1985, Arch Toxicol Suppl, V8, P221 ASTBURY PJ, 1982, ARCH TOXICOL, V50, P267, DOI 10.1007/BF00310859 BARREGARD L, 1984, SCAND AUDIOL, V13, P151, DOI 10.3109/01050398409043054 BERGSTROM B, 1986, SCAND AUDIOL, V15, P227, DOI 10.3109/01050398609042148 BHATTACHARYYA TK, 1985, ANN OTO RHINOL LARYN, V94, P75 BORG E, 1987, HEARING RES, V30, P111, DOI 10.1016/0378-5955(87)90128-6 BRUMMETT RE, 1980, DRUGS, V19, P412, DOI 10.2165/00003495-198019060-00002 BURDA H, 1988, J MORPHOL, V198, P269, DOI 10.1002/jmor.1051980303 COLEMAN JW, 1976, ACTA OTO-LARYNGOL, V82, P33, DOI 10.3109/00016487609120860 CROFTON KM, 1993, NEUROTOXICOL TERATOL, V15, P413, DOI 10.1016/0892-0362(93)90059-W CROFTON KM, 1993, 32ND ANN M SOC TOX T, V13, P365 EHYAI A, 1983, J NEUROL NEUROSUR PS, V46, P349, DOI 10.1136/jnnp.46.4.349 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, 1990, ACTA OTO-LARYNGOL, V109, P34, DOI 10.3109/00016489009107412 JOHNSON AC, 1988, ACTA OTO-LARYNGOL, V105, P56, DOI 10.3109/00016488809119446 JOHNSON AC, 1992, NEUROREPORT, V3, P1141, DOI 10.1097/00001756-199212000-00028 JOHNSON AC, 1994, HEARING RES, V72, P189, DOI 10.1016/0378-5955(94)90218-6 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LAZAR RB, 1983, NEUROLOGY, V33, P1337 LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LI HS, 1992, ARCH TOXICOL, V66, P383 MORATA TC, 1993, SCAND J WORK ENV HEA, V19, P245 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 PRYOR GT, 1984, NEUROBEH TOXICOL TER, V6, P223 PRYOR GT, 1983, NEUROBEH TOXICOL TER, V5, P53 PRYOR GT, 1983, NEUROBEH TOXICOL TER, V5, P47 PRYOR GT, 1984, NEUROBEH TOXICOL TER, V6, P111 PRYOR GT, 1986, NEUROTOXICOL TERATOL, V8, P103 REBERT CS, 1983, NEUROBEH TOXICOL TER, V5, P59 RYBACK LP, 1992, OTOLARYNGOL HEAD NEC, V1006, P677 SPOENDLI.H, 1973, ACTA OTO-LARYNGOL, V75, P220, DOI 10.3109/00016487309139699 SULLIVAN MJ, 1989, NEUROTOXICOL TERATOL, V10, P525 NR 34 TC 38 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 MAY PY 1994 VL 75 IS 1-2 BP 201 EP 208 DI 10.1016/0378-5955(94)90071-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400022 PM 8071147 ER PT J AU NIEMIEC, AJ RAPHAEL, Y MOODY, DB AF NIEMIEC, AJ RAPHAEL, Y MOODY, DB TI RETURN OF AUDITORY FUNCTION FOLLOWING STRUCTURAL REGENERATION AFTER ACOUSTIC TRAUMA - BEHAVIORAL MEASURES FROM QUAIL SO HEARING RESEARCH LA English DT Article DE REGENERATION; RECOVERY; NOISE DAMAGE; HAIR CELLS; ANIMAL PSYCHOPHYSICS ID INTENSE SOUND EXPOSURE; HAIR CELL REGENERATION; AVIAN INNER-EAR; CHICK COCHLEA; STEREOCILIARY BUNDLES; THRESHOLDS; CINGULIN; RECOVERY AB After measuring baseline behavioral audiograms, three of four behaviorally trained quail and fifteen untrained cohorts were exposed to a 1.5-kHz octave-band noise at 116-dB SPL for 4 h. The trained birds were tested daily following the exposure and showed a steady recovery of absolute sensitivity with a return to normal absolute thresholds by post-exposure days 8-10. Thirteen untrained cohorts were sacrificed after various survival times to evaluate the structural condition of the ear. The cohorts all showed regeneration of sensory cells similar to that seen in chicks. The effects of repeated acoustic trauma on recovery of sensitivity were evaluated by re-exposing the three trained birds and two untrained cohorts 106 days after the first exposure. One of the trained birds was exposed a third time, 113 days following the second exposure. The findings demonstrate that, following acoustic trauma, normal sensitivity returns prior to complete structural regeneration of the sensory epithelium and that repeated acoustic trauma may increase the time course of recovery of normal hearing sensitivity. RP NIEMIEC, AJ (reprint author), UNIV MICHIGAN,SCH MED,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR ADLER HJ, 1993, HEARING RES, V71, P214, DOI 10.1016/0378-5955(93)90037-2 CITI S, 1989, J CELL SCI, V93, P107 CITI S, 1988, NATURE, V333, P272, DOI 10.1038/333272a0 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 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, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 GOERDELLEITCH A, 1984, NATURWISSENSCHAFTEN, V71, pS98 GRAY L, 1985, J ACOUST SOC AM, V77, P1162, DOI 10.1121/1.392180 HARRISON JB, 1971, J AUD RES, V11, P33 HASHINO E, 1989, J ACOUST SOC AM, V85, P289, DOI 10.1121/1.397736 HASHINO E, 1988, J ACOUST SOC AM, V83, P2450, DOI 10.1121/1.396325 HEINZ RD, 1977, J COMP PHYSIOL PSYCH, V91, P1365 HEISE GA, 1953, AM J PSYCHOL, V66, P1, DOI 10.2307/1417964 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 MAIORANA V A, 1972, Journal of Auditory Research, V12, P203 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 OKANOYA K, 1985, J ACOUST SOC AM, V78, P1170, DOI 10.1121/1.392885 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 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 RAPHAEL Y, 1994, HEARING RES, P85 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1989, HEARING RES, V43, P81, DOI 10.1016/0378-5955(89)90061-0 Stebbins WC, 1970, ANIMAL PSYCHOPHYSICS TILNEY LG, 1983, J CELL BIOL, V96, P822, DOI 10.1083/jcb.96.3.822 TRAINER JE, 1946, THESIS CORNELL U TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 NR 30 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 MAY PY 1994 VL 75 IS 1-2 BP 209 EP 224 DI 10.1016/0378-5955(94)90072-8 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400023 PM 8071148 ER PT J AU GUTH, PS DUNN, A KRONOMER, K NORRIS, CH AF GUTH, PS DUNN, A KRONOMER, K NORRIS, CH TI THE CHOLINERGIC PHARMACOLOGY OF THE FROG SACCULE SO HEARING RESEARCH LA English DT Article DE SACCULE; CHOLINERGIC; FROG; ACETYLCHOLINE; AFFERENT; EFFERENT ID SEMICIRCULAR CANAL AFFERENTS; EFFERENT STIMULATION; VESTIBULAR NERVE; OPSANUS-TAU; HAIR-CELLS; BULLFROG; RECEPTORS; TOADFISH; GOLDFISH; NEURONS AB Stimulation of the efferent nerves to the vestibular organs of the frog's inner ear produces either facilitation or inhibition of afferent firing. Similarly, application of acetylcholine (ACH), the major transmitter of the efferents, can produce both facilitation and/or inhibition as previously reported [Guth et al. (1986) Acta Otolaryngol. 102, 194-204; Norris et al. (1988) Hear, Res. 32, 197-206]. The firing rates of afferent neurons of the semicircular canal (SCC) using multiunit recordings are generally facilitated by ACH. Conversely, the firing rates of afferent units innervating the saccule are generally inhibited by ACH. This latter inhibition is antagonized by strychnine more potently than by curare, which is more potent than atropine. When inhibition is antagonized by strychnine or curare an underlying facilitation is revealed. The inhibition of saccular afferents by ACH shows desensitization requiring about 20 min to recover. The ACH-induced inhibition is mimicked by nicotine at very high concentrations but not by dimethyl phenylpiperazinium or cytisine. The fact that multiunit afferent firing from the SCC is generally facilitated while that from the saccule is generally inhibited by ACH suggests a different distribution of ACH receptors and receptor types (i.e. muscarinic or nicotinic and their subtypes) in the two organs and demonstrates the usefulness of recording from multiple units simultaneously. The difference in distribution of ACH receptors may be important for understanding the physiology of vestibular efferents. C1 TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA 70112. RP GUTH, PS (reprint author), TULANE UNIV,SCH MED,DEPT PHARMACOL,1430 TULANE AVE,NEW ORLEANS,LA 70112, USA. CR ADAMO S, 1985, FEBS LETT, V190, P161, DOI 10.1016/0014-5793(85)80449-X BAIRD RA, 1986, BRAIN RES, V369, P48, DOI 10.1016/0006-8993(86)90512-3 BARRON SE, 1987, TRENDS PHARMACOL SCI, V8, P206 BARRON SE, 1987, TRENDS PHARMACOL SCI, V8, P204, DOI 10.1016/0165-6147(87)90059-9 BARTOLAMI S, 1993, NEUROREPORT, V4, P1003 BELESLIN DB, 1974, NEUROPHARMACOLOGY, V13, P1091, DOI 10.1016/0028-3908(74)90100-2 BOBBIN EP, 1971, NATURE, V231, P221 BOYLE R, 1991, J NEUROPHYSIOL, V66, P1504 BROWN DA, 1990, ANNU REV PHYSIOL, V52, P215 CHRISTENSENDALS.J, 1993, COMP PHYSL A, P653 EROSTEGUI C, 1994, IN PRESS HEAR RES, V74 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 FURUKAWA T, 1981, J PHYSIOL-LONDON, V315, P203 GASSER HS, 1929, J PHYSL, V67, P581 GEBBER GL, 1968, J PHARMACOL EXP THER, V163, P64 GINSBORG BL, 1965, J PHARMACOL EXP THER, V150, P216 GRENNINGLOH G, 1987, NATURE, V328, P215, DOI 10.1038/328215a0 GUTH PS, 1986, ACTA OTO-LARYNGOL, V102, P194, DOI 10.3109/00016488609108666 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HARTMANN R, 1980, PFLUG ARCH EUR J PHY, V388, P123, DOI 10.1007/BF00584117 HIGHSTEIN SM, 1986, J COMP NEUROL, V243, P309, DOI 10.1002/cne.902430303 HILLMAN DE, 1969, EXP BRAIN RES, V9, P1 HONRUBIA V, 1981, INT J NEUROSCI, V15, P197, DOI 10.3109/00207458108985857 HONRUBIA V, 1985, LARYNGOSCOPE, V95, P1526 HONRUBIA V, 1989, J NEUROPHYSIOL, V61, P688 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 KRSTIC MK, 1972, EUR J PHARMACOL, V17, P87, DOI 10.1016/0014-2999(72)90273-7 KUHLMANN J, 1991, FEBS LETT, V2, P216 LLINAS R, 1969, EXP BRAIN RES, V9, P16 MILES K, 1988, MOL NEUROBIOL, V2, P9 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 PRECHT W, 1974, EXP BRAIN RES, V19, P377 ROSSI ML, 1988, BRAIN RES, V185, P125 SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M Taglietti V, 1973, Arch Sci Biol (Bologna), V57, P73 VALLI P, 1986, BRAIN RES, V362, P92, DOI 10.1016/0006-8993(86)91402-2 VOLLE RL, 1980, PHARM GANGLIONIC TRA, P281 NR 37 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 MAY PY 1994 VL 75 IS 1-2 BP 225 EP 232 DI 10.1016/0378-5955(94)90073-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400024 PM 8071149 ER PT J AU CHOLE, RA TINLING, SP AF CHOLE, RA TINLING, SP TI BONE LINING CELLS OF THE MAMMALIAN COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; BONE; BONE LINING CELLS; CALCIUM ID CALCIUM AB It is generally believed that all bone surfaces are covered by a nearly continuous layer of cells known as bone lining cells (BLC) which separate the general extracellular fluid (GECF) from bone and its fluid compartment. Within the cochlea of some mammals regions of bane matrix are exposed to extracellular fluid. Within the scalae of the cochlea, perilymph is in contact with bone matrix; there is no evidence of a lining endothelium. Within the modiolus and subjacent to the spiral ligament, bone matrix is in contact with GECF. These findings may have importance in understanding calcium homeostasis within the scalae and may relate to the pathophysiology of labyrinthitis ossificans. Additionally, since BLCs probably represent a specific phenotype, the presence of a pure population of BLCs within the scalae may provide a source for the development of a pure culture of this cell. RP CHOLE, RA (reprint author), UNIV CALIF DAVIS,SCH MED,OTOLARYNGOL RES LABS,515 NEWTON COURT,SUITE 205,DAVIS,CA 95616, USA. CR CHOLE RA, 1993, ANN OTO RHINOL LARYN, V102, P543 DOTY SB, 1972, CALCIUM PARATHYROID, P3 HOWARD JE, 1956, CIBA F S BONE STRUCT JEE WSS, 1988, CELL TISSUE BIOL TXB MARSH MA, 1992, AM J OTOL, V13, P241 MATTHEWS JL, 1971, AM J MED, V50, P589, DOI 10.1016/0002-9343(71)90114-8 PARFITT AM, 1989, BONE, V10, P87, DOI 10.1016/8756-3282(89)90003-3 SCHERFT JP, 1972, J ULTRA MOL STRUCT R, V38, P318, DOI 10.1016/S0022-5320(72)90008-1 SUGA F, 1975, ANN OTO RHINOL LARYN, V84, P37 SUGIURA S, 1967, LARYNGOSCOPE, V77, P1974, DOI 10.1288/00005537-196711000-00003 NR 10 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 1994 VL 75 IS 1-2 BP 233 EP 243 DI 10.1016/0378-5955(94)90074-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400025 PM 8071150 ER PT J AU BRIX, J FISCHER, FP MANLEY, GA AF BRIX, J FISCHER, FP MANLEY, GA TI THE CUTICULAR PLATE OF THE HAIR CELL IN RELATION TO MORPHOLOGICAL GRADIENTS OF THE CHICKEN BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE BIRD; COCHLEA; HAIR CELL; CUTICULAR PLATE ID INNER-EAR; STEREOCILIA; ACTIN; ORGANIZATION; INNERVATION; MICROTUBULES; TRANSDUCTION; TROPOMYOSIN; COCHLEA; MYOSIN AB The aim of the present study was to provide details on the diversity and morphological gradients in the anatomy of the cuticular plate of hair cells in the chicken basilar papilla. The structure of the cuticular plate, which is mainly made up of a network of actin filaments, may be related to differences in the mechanical demands on the anchorage of the stereovillar bundle. We describe the morphological gradients in the cuticular plates as seen in transverse section for four positions along the basilar papilla. Three different shapes of cuticular plate could be distinguished. In general, cuticular plates in neurally-lying hair cells have their main mass on the neural side of the cells; for abneural cells, the converse is true. The shape of the plates changes gradually across the papilla; symmetrical forms exist. The hair-cell bundle orientation (and thus the preferred direction of stimulation of the bundle), as measured using scanning EM preparations, does not correlate with the shape of the plate in transverse section. The present data confirm the notion developed from other studies that (1) there are no distinct populations of hair cells, (2) there are no linear or monotonic morphological gradients, and (3) the gradients on the papilla are species- and position-specific. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. CR BRIX J, 1992, ABSTR ASS RES OT, P15 CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 DURING MV, 1974, Z ANAT ENTWICKLUNGS, V145, P41, DOI 10.1007/BF00519125 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 FISCHER RP, 1994, HEARING RES, V73, P1 FLOCK A, 1982, HEARING RES, V6, P75 Flock A, 1971, FISH PHYSIOL, V5, P241 FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 FURNESS DN, 1990, ACTA OTO-LARYNGOL, V109, P66, DOI 10.3109/00016489009107416 GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 HUDSPETH AJ, 1979, P NATL ACAD SCI USA, V76, P1506, DOI 10.1073/pnas.76.3.1506 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 LAVIGNEREBILLARD M, 1985, J COMP NEUROL, V238, P340, DOI 10.1002/cne.902380308 LEAKE PA, 1977, SCAN ELEC MICROS, V2, P437 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P561 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MILLER MR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P463 MILLER MR, 1990, J COMP NEUROL, V293, P223, DOI 10.1002/cne.902930206 PICKLES JO, 1989, HEARING RES, V41, P31, DOI 10.1016/0378-5955(89)90176-7 REYNOLDS ES, 1963, J CELL BIOL, V17, P208, DOI 10.1083/jcb.17.1.208 RYALS BM, 1991, ABSTR ASS RES OT, V105 SANS A, 1989, HEARING RES, V40, P117, DOI 10.1016/0378-5955(89)90105-6 SLEPECKY N, 1987, CELL TISSUE RES, V248, P63, DOI 10.1007/BF01239963 SLEPECKY NB, 1990, J ELECTRON MICR TECH, V15, P280, DOI 10.1002/jemt.1060150307 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 TILNEY MS, 1987, HEARING RES, V25, P141, DOI 10.1016/0378-5955(87)90087-6 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 NR 37 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 MAY PY 1994 VL 75 IS 1-2 BP 244 EP 256 DI 10.1016/0378-5955(94)90075-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NK064 UT WOS:A1994NK06400026 PM 8071151 ER PT J AU WILLOTT, JF BROSS, LS MCFADDEN, SL AF WILLOTT, JF BROSS, LS MCFADDEN, SL TI MORPHOLOGY OF THE COCHLEAR NUCLEUS IN CBA/J MICE WITH CHRONIC, SEVERE SENSORINEURAL COCHLEAR PATHOLOGY INDUCED DURING ADULTHOOD SO HEARING RESEARCH LA English DT Article DE AUDITORY SYSTEM; INBRED MICE; SENSORINEURAL HEARING LOSS; NEURONS; AGING ID INFERIOR COLLICULUS NEURONS; CONDUCTIVE HEARING-LOSS; STEM AUDITORY NUCLEI; BRAIN-STEM; RESPONSE PROPERTIES; TRAPEZOID BODY; NOISE EXPOSURE; AGING C57BL/6J; MOUSE; YOUNG AB The effects of chronic cochlear impairment on morphological features of the adult cochlear nucleus (CN) were assessed in CBA/J mice in which severe sensorineural damage had been induced by exposure to intense noise. Sections from various CN subdivisions, stained for Nissl substance and fibers, were quantitatively evaluated in four groups of noise-exposed mice that differed with regard to the age at noise exposure (2, 6, or 11 months), age at the time the CN was evaluated (6, 11, or 24 months), and the duration (chronicity) of sensorineural impairment (4, 5, 13, or 18 months). Like-aged, non-exposed CBA mice were used as controls, so the effects of peripheral damage and aging could be compared. Cochlear damage produced significant changes in CN subdivisions thought to receive the heaviest input from cochlear afferents (anteroventral CN, octopus cell area, dorsal CN layer III). These changes included a reduction of neuropil volume, reductions in neuron size, and increases in neuronal packing density that were complementary to reduced volume in these subdivisions. Effects on neuron number were minimal in all subdivisions. Central changes in noise-exposed mice were absent or diminished in DCN layers I and II, which receive relatively less input from primary fibers. The age at onset and chronicity of damage had little to do with the severity of central effects of cochlear damage. The effects of cochlear damage were not additive with age-related changes seen in the old controls. RP WILLOTT, JF (reprint author), NO ILLINOIS UNIV,DEPT PSYCHOL,DE KALB,IL 60115, USA. CR 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 BRINER W, 1989, NEUROBIOL AGING, V10, P295, DOI 10.1016/0197-4580(89)90039-0 BROWNER RH, 1982, J COMP NEUROL, V211, P115, DOI 10.1002/cne.902110203 CANT NB, 1984, HEARING SCI RECENT A, P371 CASEY MA, 1985, J COMP NEUROL, V232, P401, DOI 10.1002/cne.902320311 CASPARY DM, 1990, J NEUROSCI, V10, P2363 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 COTMAN CW, 1988, ANNU REV NEUROSCI, V11, P61, DOI 10.1146/annurev.neuro.11.1.61 CRACE R, 1970, THESIS OHIO U DUARA R, 1985, HDB BIOL AGING, P595 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H FELDMAN ML, 1979, SPECIAL SENSES AGING, P143 GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 HALL JG, 1976, ACTA OTO-LARYNGOL, V81, P344, DOI 10.3109/00016487609119972 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1980, AUDIOLOGY, V19, P369 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 JEANBAPTISTE M, 1975, J COMP NEUROL, V162, P111, DOI 10.1002/cne.901620107 JONES DR, 1992, SYNAPSE, V10, P291, DOI 10.1002/syn.890100404 KANE EC, 1974, ANAT REC, V179, P67, DOI 10.1002/ar.1091790106 KEITHLEY EM, 1990, HEARING RES, V49, P169, DOI 10.1016/0378-5955(90)90103-V KLUVER H, 1953, J NEUROPATH EXP NEUR, V12, P400 KOITCHEV K, 1986, ACTA OTO-LARYNGOL, V102, P31, DOI 10.3109/00016488609108643 KONIGSMARK B W, 1972, Journal of Neuropathology and Experimental Neurology, V31, P304, DOI 10.1097/00005072-197204000-00006 KONIGSMA.BW, 1970, NATURE, V228, P1335, DOI 10.1038/2281335a0 LAMBERT PR, 1982, OTOLARYNG HEAD NECK, V90, P787 LIDEN G, 1973, ACTA OTO-LARYNGOL, V75, P325, DOI 10.3109/00016487309139734 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MOORE DR, 1990, J COMP NEUROL, V302, P810, DOI 10.1002/cne.903020412 MOORE JK, 1986, NEUROBIOLOGY HEARING, P251 MOREST DK, 1983, HEARING RES, V9, P145, DOI 10.1016/0378-5955(83)90024-2 MOREST DK, 1982, NEW PERSPECTIVES NOI, P87 MUGNAINI E, 1980, J COMP NEUROL, V191, P581, DOI 10.1002/cne.901910406 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 PARHAM K, 1988, BEHAV NEUROSCI, V101, P881 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 POWELL TPS, 1962, J ANAT, V96, P249 SCHEIBEL ME, 1975, EXP NEUROL, V47, P392, DOI 10.1016/0014-4886(75)90072-2 SELDON HL, 1991, BRAIN RES, V551, P185, DOI 10.1016/0006-8993(91)90932-L THEOPOLD HM, 1975, ARCH OTO-RHINO-LARYN, V209, P247, DOI 10.1007/BF00456545 URBAN GP, 1979, EXP NEUROL, V63, P229, DOI 10.1016/0014-4886(79)90120-1 VAUGHAN DW, 1977, J COMP NEUROL, V171, P501, DOI 10.1002/cne.901710406 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, 1982, AM J ANAT, V163, P103, DOI 10.1002/aja.1001630202 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WEBSTER DB, 1983, HEARING RES, V12, P145, DOI 10.1016/0378-5955(83)90123-5 Wenthold RJ, 1991, NEUROBIOLOGY HEARING, P121 Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 WILLOTT JF, 1988, HEARING RES, V37, P15, DOI 10.1016/0378-5955(88)90074-3 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, 1988, EXP NEUROL, V99, P615, DOI 10.1016/0014-4886(88)90178-1 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1991, ABSTR ASS RES OT, V14, P16 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, 1993, IN PRESS NEUROBIOL A WILLOTT JF, 1982, NEUROSCI LETT, V34, P13, DOI 10.1016/0304-3940(82)90085-4 WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 WILLOTT JF, 1978, J COMP PHYSIOL, V127, P175 WILLOTT JF, 1981, J NEUROPHYSIOL, V45, P35 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 WILLOTT JF, 1985, J COMP NEUROL, V237, P545, DOI 10.1002/cne.902370410 WILLOTT JF, 1984, EXP NEUROL, V83, P495, DOI 10.1016/0014-4886(84)90118-3 NR 68 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 APR PY 1994 VL 74 IS 1-2 BP 1 EP 21 DI 10.1016/0378-5955(94)90171-6 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500001 PM 8040081 ER PT J AU HENDERSON, D SUBRAMANIAM, M PAPAZIAN, M SPONGR, VP AF HENDERSON, D SUBRAMANIAM, M PAPAZIAN, M SPONGR, VP TI THE ROLE OF MIDDLE-EAR MUSCLES IN THE DEVELOPMENT OF RESISTANCE TO NOISE-INDUCED HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE MIDDLE EAR MUSCLES; TOUGHENING; THRESHOLD SHIFT ID EXPOSURE AB The role of middle ear muscles (MEMs) in the development of increased resistance to noise induced hearing loss (NIHL) was studied using monaural chinchillas. Animals with severed MEMs as well as those with intact MEMs were exposed to an octave band noise (OBN) centered at 0.5 kHz at 95 dB for six hours/day for ten consecutive days. Results indicated that animals with severed MEMs showed greater initial threshold shifts (TS) than the animals with intact MEMs. Both the groups showed a decrease in TS over the ten days of exposure. The subjects were given five days of recovery and then re-exposed to the same noise at 106 dB for 48 h. Permanent threshold shifts (PTS) in each group was compared against those in a control group exposed to the noise only at the higher level. Interestingly, both the 'conditioned' groups incurred substantially less PTS than the control group exposed only to the higher level. C1 MINNESOTA EAR CLIN,MINNEAPOLIS,MN 55455. RP HENDERSON, D (reprint author), SUNY BUFFALO,DEPT COMMUN SCI & DISORDERS,HEART RES LAB,215 PARKER HALL,BUFFALO,NY 14214, USA. CR BORG E, 1983, ACTA OTO-LARYNGOL, V96, P361, DOI 10.3109/00016488309132721 CANLON B, 1988, HEARING RES, V34, P194 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 GALAMBOS R, 1959, J ACOUST SOC AM, V31, P344 HENDERSON D, 1992, NOISE INDUCED HEARIN HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MOLLER AR, 1965, ACTA OTOLARYNGOL, V59, P1 RYAN A, COMMUNICATION SUBRAMANIAM M, 1991, HEARING RES, V56, P65, DOI 10.1016/0378-5955(91)90154-2 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H Zakrisson J. E., 1980, SCAND AUDIOL S, P326 NR 12 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 APR PY 1994 VL 74 IS 1-2 BP 22 EP 28 DI 10.1016/0378-5955(94)90172-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500002 PM 8040091 ER PT J AU LUSTIG, LR LEAKE, PA SNYDER, RL REBSCHER, SJ AF LUSTIG, LR LEAKE, PA SNYDER, RL REBSCHER, SJ TI CHANGES IN THE CAT COCHLEAR NUCLEUS FOLLOWING NEONATAL DEAFENING AND CHRONIC INTRACOCHLEAR ELECTRICAL-STIMULATION SO HEARING RESEARCH LA English DT Article DE AUDITORY DEPRIVATION; CHRONIC ELECTRICAL STIMULATION; COCHLEAR NUCLEUS; NEONATAL DEAFNESS; AMINOGLYCOSIDE; OTOTOXICITY ID CONDUCTIVE HEARING-LOSS; STEM AUDITORY NUCLEI; BRAIN-STEM; INFERIOR COLLICULUS; ACOUSTIC DEPRIVATION; SOUND DEPRIVATION; CELL-SIZE; NEURONS; PROJECTIONS; REMOVAL AB The effects of chronic intracochlear electrical stimulation on the cochlear nucleus (CN) were studied in eight cats that were neonatally deafened by daily intramuscular injections of neomycin. Profound hearing loss was confirmed in each animal by auditory brainstem response (ABR) and frequency following response (500 Hz) testing. Five of the kittens were implanted unilaterally with a scala tympani electrode array at ages 8-16 weeks. These kittens were stimulated daily for four hours at 2 dB above the evoked ABR threshold, over a period of three months, and subsequently euthanized for histological analysis at 26-32 weeks of age. The three remaining deaf kittens were maintained without stimulation over prolonged periods in order to study the long-term consequences of neonatal deafening, and were euthanized at 66-133 weeks of age. This study compares the CN of these deafened experimental animals and the CN of normal adult cats. Three experimental parameters were examined: CN volume, cross-sectional area of spherical cells in the rostral anteroventral cochlear nucleus (AVCN), and spherical cell density in this same region. The CN in animals that received electrical stimulation showed significant bilateral degenerative changes in all three measured parameters. Total nuclear volume was reduced by 35-36%, spherical cell size was reduced by 20-26%, and spherical cell density decreased by 36-42%, as compared to the normal cat CN. Comparisons were also made in the stimulated animals between CN ipsilateral to the stimulated cochlea and the contralateral, unstimulated CN. Although CN volume and cell density were not significantly different between the two sides, the spherical cells ipsilateral to the stimulated cochlea were on average 6% larger than cells in the contralateral, unstimulated CN. This difference was statistically significant (paired Student's t-test, P = 0.035). After neonatal long-term deafening, there was highly significant shrinkage of about 42% in total CN volume, a 38% reduction in mean spherical cell size, and a 57% decrease in spherical cell density in the AVCN, compared to the CN of the normal adult cat. From these data it is concluded that neonatal deafening induces severe reduction in CN volume and a decrease in AVCN spherical cell area and density that are progressive over many months. The spherical cell shrinkage that was induced by deafness was mitigated slightly by chronic intracochlear electrical stimulation; however the other effects of deafening were not prevented or reversed by chronic stimulation. C1 UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,EPSTEIN COLEMAN LABS,SAN FRANCISCO,CA 94143. CR BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 CHOUARD CH, 1983, ACTA OTO-LARYNGOL, V95, P639, DOI 10.3109/00016488309139456 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 CURTISS J, 1989, COCHLEAR IMPLANTS YO, P293 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HOLM VA, 1969, PEDIATRICS, V43, P833 HULTCRANTZ M, 1991, HEARING RES, V54, P272, DOI 10.1016/0378-5955(91)90121-O JEANBAPTISTE M, 1975, J COMP NEUROL, V162, P111, DOI 10.1002/cne.901620107 Larsen S A, 1984, Acta Otolaryngol Suppl, V417, P1 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, 1990, NEURAL PROSTHESES FU, P253 LOEB GE, 1990, ANNU REV NEUROSCI, V13, P357, DOI 10.1146/annurev.neuro.13.1.357 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MOORE DR, 1990, J COMP NEUROL, V302, P810, DOI 10.1002/cne.903020412 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 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 OWENS E, 1989, COCHLEAR IMPLANTS YO, P315 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 PASIC TR, 1991, OTOLARYNG HEAD NECK, V104, P6 POWELL TPS, 1962, J ANAT, V96, P249 Rebscher S. J., 1985, COCHLEAR IMPLANTS, P74 RUBEL EW, 1984, HEARING SCI, P109 Ruben R J, 1986, Acta Otolaryngol Suppl, V429, P61 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 TRUNE DR, 1988, DEV BRAIN RES, V42, P304, DOI 10.1016/0165-3806(88)90249-0 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 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 NR 37 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 APR PY 1994 VL 74 IS 1-2 BP 29 EP 37 DI 10.1016/0378-5955(94)90173-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500003 PM 8040097 ER PT J AU KIRK, DL YATES, GK AF KIRK, DL YATES, GK TI EVIDENCE FOR ELECTRICALLY-EVOKED TRAVELING WAVES IN THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE TRAVELING WAVE; CAP; ELECTRICAL STIMULATION; COCHLEA ID OUTER HAIR-CELLS; AUDITORY-NERVE FIBERS; PHYSIOLOGICAL-PROPERTIES; OTOACOUSTIC EMISSIONS; 2-TONE SUPPRESSION; BASILAR-MEMBRANE; TUNING CURVES; STIMULATION; RESPONSES; MASKING AB Electrically evoked compound action potentials (EECAP) were produced by the injection of pulsed sinusoidal current through metal electrodes into the basal turn. Plots of current threshold against frequency closely resembled conventional compound action potentials (CAP) audiograms for frequencies represented apically of the electrode location. EECAPs were masked by sound and CAPs were masked by current in a manner consistent with the generation of a propagated travelling wave, RP KIRK, DL (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR ABBAS PJ, 1981, J ACOUST SOC AM, V69, P492, DOI 10.1121/1.385477 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1986, J PHYSIOL-LONDON, V377, pP41 Bekesy G., 1960, EXPT HEARING BROWN MC, 1983, HEARING RES, V10, P345, DOI 10.1016/0378-5955(83)90097-7 Brownell W. E., 1983, MECH HEARING, P5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 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 DALLOS P, 1971, J ACOUST SOC AM, V49, P1140, DOI 10.1121/1.1912475 DAVIS H, 1957, PHYSIOL REV, V37, P1 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HARTMANN R, 1989, COCHLEAR IMPLANTS MO, P135 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 HUMES LE, 1980, HEARING RES, V2, P115, DOI 10.1016/0378-5955(80)90033-7 JOHNSTON.BM, 1966, J ACOUST SOC AM, V40, P1398, DOI 10.1121/1.1910239 Jones RC, 1940, J ACOUST SOC AM, V12, P281, DOI 10.1121/1.1916103 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 Kim D. O., 1980, PSYCHOPHYSICAL PHYSL, P7 KIM DO, 1980, HEARING RES, V2, P297, DOI 10.1016/0378-5955(80)90064-7 LEVICK WR, 1972, MED BIOL ENG, V10, P510, DOI 10.1007/BF02474199 MCANALLY KI, 1991, J ACOUST SOC AM, V90, P2231 MOLLER AR, 1985, HEARING RES, V17, P177, DOI 10.1016/0378-5955(85)90020-6 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 Mountain DC, 1983, MECHANICS HEARING, P119 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I 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 OZDAMAR O, 1976, J ACOUST SOC AM, V59, P143 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PICKLES JO, 1984, HEARING RES, V14, P245, DOI 10.1016/0378-5955(84)90053-4 RAJAN R, 1989, HEARING RES, V39, P299, DOI 10.1016/0378-5955(89)90049-X REUTER G, 1990, HEARING RES, V43, P219, DOI 10.1016/0378-5955(90)90230-M REUTER G, 1992, HEARING RES, V60, P236, DOI 10.1016/0378-5955(92)90025-I ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X ROSENBLUETH A, 1957, J CELL COMP PHYSL, V38, P321 SELLICK PM, 1980, HEARING RES, V2, P439, DOI 10.1016/0378-5955(80)90080-5 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 TASAKI I, 1954, J ACOUST SOC AM, V26, P765, DOI 10.1121/1.1907415 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 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 NR 48 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 APR PY 1994 VL 74 IS 1-2 BP 38 EP 50 DI 10.1016/0378-5955(94)90174-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500004 PM 8040098 ER PT J AU EGGERMONT, JJ AF EGGERMONT, JJ TI TEMPORAL-MODULATION TRANSFER-FUNCTIONS FOR AM AND FM STIMULI IN CAT AUDITORY-CORTEX - EFFECTS OF CARRIER TYPE, MODULATING WAVE-FORM AND INTENSITY SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; CAT; SINGLE UNIT; TEMPORAL MODULATION TRANSFER FUNCTIONS; AM; FM ID SPEECH-EVOKED ACTIVITY; INFERIOR COLLICULUS; SINGLE NEURONS; AMPLITUDE-MODULATION; DYNAMIC PROPERTIES; LEOPARD FROG; RESPONSES; REPRESENTATION; SENSITIVITY; MIDBRAIN AB For 167 single units, recorded from primary auditory cortex in 28 cats, we show that tuning to the modulation frequency (MF) of amplitude-modulated (AM) sound is strongly dependent on carrier type. In general AM noise-bursts and click-trains produce good tuning to MFs with repetition rates around 8-10 Hz. Amplitude- or frequency-modulation of tone-carriers resulted largely in low-pass temporal modulation transfer functions (tMTFs) with a best modulation frequency (BMF) around 4 Hz. Individual BMFs for noise carriers ranged from 3-26 Hz, whereas for tone carriers they were mostly below 6 Hz and rarely above 10 Hz. The sharpness of tuning for broad-band stimuli decreased with increasing duty-cycle of the modulation; it was most pronounced for clicks, next best for exponential sine-AM and broadest for sinusoidal AM. In contrast the reverse was found for tone carriers; the better modulation following was found for sinusoidal modulation and was most likely entirely due to a stronger onset response. Decreasing the modulation depth below 100% showed an increasing influence of onset transients and periodic rebounds, however, the average tMTFs for depths between 50-100% are similar. The optimal intensity level for noise carriers was usually higher than for tone carriers. Overall the modulation-sensitivity of cortical neurons regardless of carrier type and modulating waveform was in the range of modulation frequencies found in music, speech and other complex sounds. RP EGGERMONT, JJ (reprint author), UNIV CALGARY,DEPT PSYCHOL,BEHAV NEUROSCI RES GRP,2500 UNIV DR NW,CALGARY T2N 1N4,AB,CANADA. CR BATRA R, 1989, J NEUROPHYSIOL, V61, P257 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 EGGERMONT JJ, 1990, HEARING RES, V43, P181, DOI 10.1016/0378-5955(90)90227-G EGGERMONT JJ, 1991, HEARING RES, V56, P153, DOI 10.1016/0378-5955(91)90165-6 EGGERMONT JJ, 1989, HEARING RES, V40, P147, DOI 10.1016/0378-5955(89)90108-1 EGGERMONT JJ, 1992, J NEUROPHYSIOL, V68, P1216 EGGERMONT JJ, 1992, HEARING RES, V61, P1, DOI 10.1016/0378-5955(92)90029-M EGGERMONT JJ, 1993, HEARING RES, V65, P175, DOI 10.1016/0378-5955(93)90212-J EPPING WJM, 1986, HEARING RES, V24, P55, DOI 10.1016/0378-5955(86)90005-5 Fastl H., 1983, HEARING PHYSL BASES, P282 FAY RR, 1982, J COMP PHYSIOL, V147, P201 FESTEN JM, 1981, J ACOUST SOC AM, V70, P356, DOI 10.1121/1.386771 HEIL P, 1992, J COMP PHYSIOL A, V171, P583 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 MARDIA KV, 1972, STATISTICS DIRECTION MENDELSON JR, 1985, BRAIN RES, V327, P331, DOI 10.1016/0006-8993(85)91530-6 MOLLER AR, 1986, HEARING RES, V24, P203, DOI 10.1016/0378-5955(86)90019-5 MOLLER AR, 1973, BRAIN RES, V57, P443, DOI 10.1016/0006-8993(73)90148-0 Muller-Preuss P., 1988, AUDITORY PATHWAY STR, P327 MUMFORD D, 1991, BIOL CYBERN, V65, P135, DOI 10.1007/BF00202389 PHILLIPS DP, 1987, EXP BRAIN RES, V67, P479 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1989, SENSORY PROCESSING M, P172 PHILLIPS DP, 1990, BEHAV BRAIN RES, V40, P85, DOI 10.1016/0166-4328(90)90001-U Plomp R., 1983, HEARING PHYSL BASES, P270 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 ROUILLER EM, 1991, EXP BRAIN RES, V86, P483 SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SCHREINER CE, 1988, AUDITORY FUNCTION NE, P337 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 STEINSCHNEIDER M, 1980, BRAIN RES, V198, P75, DOI 10.1016/0006-8993(80)90345-5 STEINSCHNEIDER M, 1990, BRAIN RES, V519, P158, DOI 10.1016/0006-8993(90)90074-L STEINSCHNEIDER M, 1982, BRAIN RES, V252, P353, DOI 10.1016/0006-8993(82)90403-6 Steriade M, 1990, THALAMIC OSCILLATION VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 VOSS RF, 1978, J ACOUST SOC AM, V63, P258, DOI 10.1121/1.381721 WALLACE MN, 1991, EXP BRAIN RES, V86, P527 ZEKI S, 1990, SIGNAL SENSE LOCAL G, P85 NR 39 TC 116 Z9 117 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 1994 VL 74 IS 1-2 BP 51 EP 66 DI 10.1016/0378-5955(94)90175-9 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500005 PM 8040099 ER PT J AU FOSTER, JD DRESCHER, MJ HATFIELD, JS DRESCHER, DG AF FOSTER, JD DRESCHER, MJ HATFIELD, JS DRESCHER, DG TI IMMUNOHISTOCHEMICAL LOCALIZATION OF S-100 PROTEIN IN AUDITORY AND VESTIBULAR END ORGANS OF THE MOUSE AND HAMSTER SO HEARING RESEARCH LA English DT Article DE S-100 PROTEINS; CALCIUM; HAIR CELLS; COCHLEA; VESTIBULE; IMMUNOHISTOCHEMISTRY ID PERIPHERAL INNERVATION PATTERNS; CALCIUM-BINDING PROTEIN; CALBINDIN-D 28K; HAIR-CELLS; GUINEA-PIG; IMMUNOCYTOCHEMICAL DETECTION; SEMICIRCULAR CANALS; GANGLION NEURONS; UTRICULAR MACULA; XENOPUS-LAEVIS AB The distribution of S-100-like immunoreactivity in mouse and hamster auditory and vestibular end organs was determined by the use of immunohistochemistry. Within the organ of Corti, the cytoplasm of cells of Deiter and Hensen were strongly immunoreactive. Inner hair cells and the peripheral processes and cell bodies of the spiral ganglion were weakly immunoreactive for S-100, whereas the supranuclear regions of outer hair cells and cells underlying the basilar membrane were unstained. Immunoreactivity was observed near the base of outer hair cells. In the lateral wall of the cochlea, cellular components of the spiral ligament and a subpopulation of epithelial cells in the stria vascularis, identified as predominantly basal cells, were immunoreactive. For the saccule, utricle, and semicircular canals, S-100 immunoreactivity was observed in vestibular hair cells, types I, and II, and the nerve calyces surrounding type I hair cells as well as in nerve fibers underlying the sensory epithelium. Weak S-100-like immunoreactivity was associated with vestibular nerve fibers and cell bodies in the vestibular ganglion. The localization of S-100-like immunoreactivity to the sensory cells and nerve fibers of the peripheral auditory and vestibular end organs is consistent with a functional role for S-100 proteins at these sites. C1 WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL,BIOOTOL LAB,DETROIT,MI 48201. VET AFFAIRS MED CTR,LAB SERV,ALLEN PK,MI 48101. CR ALI SM, 1989, NATURE, V340, P313, DOI 10.1038/340313a0 ANNIKO M, 1990, ADV OTO-RHINO-LARYNG, V45, P1 ANNIKO M, 1984, ULTRASTRUCTURAL ATLA, P184 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BAIRD RA, 1988, J NEUROPHYSIOL, V60, P182 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, 1991, MOL BRAIN RES, V9, P153, DOI 10.1016/0169-328X(91)90141-J DEMEMES D, 1992, BRAIN RES, V582, P168, DOI 10.1016/0006-8993(92)90334-6 DESMADRYL G, 1992, EXP BRAIN RES, V89, P105 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DONATO R, 1983, FEBS LETT, V162, P310, DOI 10.1016/0014-5793(83)80778-9 DONATO R, 1991, FEBS LETT, V1, P713 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 DRUST DS, 1988, NATURE, V331, P88, DOI 10.1038/331088a0 DULON D, 1993, CELL CALCIUM, V14, P245, DOI 10.1016/0143-4160(93)90071-D ENDO T, 1983, FEBS LETT, V161, P235, DOI 10.1016/0014-5793(83)81015-1 FANO G, 1989, FEBS LETT, V255, P381, DOI 10.1016/0014-5793(89)81127-5 FERNANDEZ C, 1990, J NEUROPHYSIOL, V63, P767 FERNANDEZ C, 1988, J NEUROPHYSIOL, V60, P167 Foster J. D., 1992, Society for Neuroscience Abstracts, V18, P1400 FUJI T, 1990, J BIOCHEM-TOKYO, V107, P133 GERKE V, 1984, EMBO J, V3, P227 GOLDBERG JM, 1990, J NEUROPHYSIOL, V63, P791 KLEE CB, 1988, BIOCHEMISTRY-US, V27, P6645, DOI 10.1021/bi00418a001 MOLIN SO, 1985, J HISTOCHEM CYTOCHEM, V33, P367 MOLIN SO, 1984, J HISTOCHEM CYTOCHEM, V32, P805 PERSECHINI A, 1989, TRENDS NEUROSCI, V12, P462, DOI 10.1016/0166-2236(89)90097-0 RABIE A, 1983, CELL TISSUE RES, V232, P691 REYDON JL, 1968, LARYNGOSCOPE, V78, P95, DOI 10.1288/00005537-196801000-00009 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 ROGERS JH, 1989, NEUROSCIENCE, V31, P697, DOI 10.1016/0306-4522(89)90434-X RUSSELL IJ, 1971, J EXP BIOL, V54, P643 SAIDEL WM, 1990, HEARING RES, V47, P139, DOI 10.1016/0378-5955(90)90171-K SANS A, 1986, BRAIN RES, V364, P190, DOI 10.1016/0006-8993(86)91003-6 SCHUKNECHT HF, 1974, PAHTOLOGY EAR SHI SR, 1992, LARYNGOSCOPE, V102, P734, DOI 10.1288/00005537-199207000-00002 SIEGEL JH, 1987, HEARING RES, V28, P131, DOI 10.1016/0378-5955(87)90044-X VANELDIK LJ, 1988, J BIOL CHEM, V263, P7830 VANELDIK LJ, 1991, BRAIN RES, V542, P280, DOI 10.1016/0006-8993(91)91579-P WINNINGHAMMAJOR F, 1989, J CELL BIOL, V107, pA729 WINNINGHAMMAJOR F, 1989, J CELL BIOL, V109, P3063, DOI 10.1083/jcb.109.6.3063 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 APR PY 1994 VL 74 IS 1-2 BP 67 EP 76 DI 10.1016/0378-5955(94)90176-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500006 PM 8040100 ER PT J AU SHEHATADIELER, WE RICHTER, CP DIELER, R KLINKE, R AF SHEHATADIELER, WE RICHTER, CP DIELER, R KLINKE, R TI EFFECTS OF ENDOLYMPHATIC AND PERILYMPHATIC APPLICATION OF SALICYLATE IN THE PIGEON .1. SINGLE-FIBER ACTIVITY AND COCHLEAR POTENTIALS SO HEARING RESEARCH LA English DT Article DE BIRD; PIGEON; BASILAR PAPILLA; SALICYLATE; COCHLEAR POTENTIALS ID HAIR-CELLS; OTOACOUSTIC EMISSIONS; BASILAR PAPILLA; CHICK; ELECTROMOTILITY; INNERVATION; CURRENTS; NERVE AB The effects of salicylate on the mammalian cochlea function are well documented. However, there is a lack of reports on salicylate effects on the avian auditory periphery and it might well be that salicylate is not ototoxic at all in submammalian vertebrates. We therefore recorded single fiber activities, compound action potential (CAP) and endocochlear potential (EP) during application of salicylate (calculated final concentration of about 2-18 mmol/l) into the scala media of pigeons. We furthermore recorded CAP and EP during perilymphatic perfusion of salicylate (2-20 mmol/l). SaIicylate applied into the scala media led to an elevation of tip threshold in single fibers ranging from 5 to 35 dB. The characteristic frequencies of the fibers were not changed. This effect on auditory nerve fibers was reflected in an elevation of CAP thresholds. The mean spontaneous discharge rate was either slightly increased or remained unchanged in the majority of fibers. Perilymphatic salicylate perfusion also led to an elevation of CAP thresholds that was reversible following subsequent perfusion with artificial perilymph. The EP remained unchanged in both application modes. The effects of salicylate were dose dependent and more pronounced in the mid to high-frequency range. These results are consistent with an action of salicylate on the process (electrical or mechanical, or both) responsible for the sensitivty and frequency selectivity in the avian peripheral hearing organ. C1 UNIV FRANKFURT,ZENTRUM PHYSIOL,FRANKFURT,GERMANY. UNIV WURZBURG,DEPT OTOLARYNGOL HEAD & NECK SURG,WURZBURG,GERMANY. RI Richter, Claus-Peter/B-4641-2012 CR DAUBITZ E, 1992, RHYTHMOGENESIS NEURO, P247 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, V97, P793, DOI 10.1017/S0022215100095025 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 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, 1990, J PHYSIOL-LONDON, V429, P529 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X KUJAWA SG, 1992, HEARING RES, V64, P73, DOI 10.1016/0378-5955(92)90169-N LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 LONG GR, 1986, PERIPHERAL AUDITORY, P213 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1987, HEARING RES, V26, P257, DOI 10.1016/0378-5955(87)90062-1 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SACHS MB, 1980, COMP STUDIES HEARING, P241 SCHERMULY L, 1990, HEARING RES, V50, P295, DOI 10.1016/0378-5955(90)90053-R SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SMOLDERS JWT, 1992, ADV BIOSCI, V83, P197 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 THALMANN R, 1975, NERVOUS SYSTEM, V3, P31 VONDURING M, 1985, FORTS ZOOL, V30, P681 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 Wald A., 1947, SEQUENTIAL ANAL ZIMMERMANN U, 1989, DYNAMICS PLASTICITY, P286 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 1994 VL 74 IS 1-2 BP 77 EP 84 DI 10.1016/0378-5955(94)90177-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500007 PM 8040101 ER PT J AU DIELER, R SHEHATADIELER, WE RICHTER, CP KLINKE, R AF DIELER, R SHEHATADIELER, WE RICHTER, CP KLINKE, R TI EFFECTS OF ENDOLYMPHATIC AND PERILYMPHATIC APPLICATION OF SALICYLATE IN THE PIGEON .2. FINE-STRUCTURE OF AUDITORY HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE BIRD; PIGEON; BASILAR PAPILLA; HAIR CELLS; SALICYLATE OTOTOXICITY; FINE STRUCTURE ID OTOACOUSTIC EMISSIONS; BASILAR PAPILLA; ENDOPLASMIC-RETICULUM; SUBSURFACE CISTERNAE; COCHLEA; ORGAN; CORTI; ELECTROMOTILITY; RESPONSES; SHAPE AB Large doses of salicylate are known to cause reversible ototoxic effects including fine structural alterations of the auditory hair cells in mammals. To investigate possible fine structural correlates of salicylate effects on pigeon auditory hair cells, the basilar papillae following perilymphatic or endolymphatic application of salicylate were fixed and processed for transmission electron microscopy. The pigeon auditory hair cells possessed organelles typically described in avians. A single or multi-layered array of cisternae along the cytoplasmic side of the lateral plasma membrane, i.e. subsurface cisternae that are characteristic for mammalian outer hair cells, was not seen. The most prominent fine structural alterations of hair cells after salicylate application were an increase in the luminal width of smooth and rough endoplasmic reticulum as well as the frequent occurrence of prominent single-membrane-bound vesicles filled with electron-dense bodies. Based on the assumption that subsurface cisternae represent a specialized form of endoplasmic reticulum, the present findings indicate that the structural correlates of salicylate toxicity are similar in mammalian and avian auditory hair cells. C1 UNIV FRANKFURT,ZENTRUM PHYSIOL,FRANKFURT,GERMANY. UNIV WURZBURG,DEPT OTOLARYNGOL HEAD & NECK SURG,WURZBURG,GERMANY. RI Richter, Claus-Peter/B-4641-2012 CR ASHMORE JF, 1991, ANNU REV PHYSIOL, V53, P465, DOI 10.1146/annurev.physiol.53.1.465 BOOTH C, 1989, CELL, V59, P729, DOI 10.1016/0092-8674(89)90019-6 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BROWNELL WE, 1982, HEARING RES, V6, P335, DOI 10.1016/0378-5955(82)90064-8 CHANDLER JP, 1984, J COMP NEUROL, V222, P506, DOI 10.1002/cne.902220405 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALMARK M, 1972, J PHYSIOL-LONDON, V224, P583 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 Dooling R.J., 1980, P261 DOUEK EE, 1983, J LARYNGOL OTOL, V97, P793, DOI 10.1017/S0022215100095025 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A EVANS BN, 1993, ASS RES OTOLARYNGOL, V116 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 FALBEHANSEN J, 1941, CLIN EXPT HISTOLOGIC FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R FUCHS PA, 1988, J NEUROSCI, V8, P2460 Ghadially FN, 1988, ULTRASTRUCTURAL PATH GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 HOLGUIN JA, 1988, BIOCHEM PHARMACOL, V37, P4035, DOI 10.1016/0006-2952(88)90092-5 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X KOCH GLE, 1988, J CELL SCI, V91, P511 KUJAWA SG, 1992, HEARING RES, V64, P73, DOI 10.1016/0378-5955(92)90169-N LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1987, HEARING RES, V26, P257, DOI 10.1016/0378-5955(87)90062-1 MCFADDEN D, 1984, HEARING RES, V16, P251, DOI 10.1016/0378-5955(84)90114-X MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MOLDERINGS GJ, 1987, N-S ARCH PHARMACOL, V336, P403, DOI 10.1007/BF00164873 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 PUJOL R, 1991, HEARING RES, V57, P129, DOI 10.1016/0378-5955(91)90082-K ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X RUSSELL IJ, 1989, HEARING RES, V43, P55, DOI 10.1016/0378-5955(89)90059-2 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SAITO K, 1983, CELL TISSUE RES, V229, P467 SAMBROOK JF, 1990, CELL, V61, P197, DOI 10.1016/0092-8674(90)90798-J SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SHEHATADIELER WE, 1994, HEARING RES, V74, P77, DOI 10.1016/0378-5955(94)90177-5 SHENNAN DB, 1992, BIOCHEM PHARMACOL, V44, P645, DOI 10.1016/0006-2952(92)90398-3 SLEPECKY NB, 1990, J ELECTRON MICR TECH, V15, P280, DOI 10.1002/jemt.1060150307 SLEPECKY NB, 1992, J NEUROCYTOL, V21, P374, DOI 10.1007/BF01191705 SMOLDERS JWT, 1992, ADV BIOSCI, V83, P197 Spoendlin H, 1988, PHYSL EAR, P201 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 VONDURING M, 1985, FORTS ZOOL, V30, P681 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P457, DOI 10.3109/00016488809119501 ZIMMERMANN U, 1989, DYNAMICS PLASTICITY, P286 NR 55 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 1994 VL 74 IS 1-2 BP 85 EP 98 DI 10.1016/0378-5955(94)90178-3 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500008 PM 8040102 ER PT J AU WILMINGTON, D GRAY, L JAHRSDOERFER, R AF WILMINGTON, D GRAY, L JAHRSDOERFER, R TI BINAURAL PROCESSING AFTER CORRECTED CONGENITAL UNILATERAL CONDUCTIVE HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE BINAURAL HEARING; MASKING LEVEL DIFFERENCE; SOUND LOCALIZATION; SPEECH INTELLIGIBILITY; DEVELOPMENT ID MIDDLE-EAR SURGERY; INTERAURAL TIME; BRAIN-STEM; NOISE AB Binaural processing was measured in a series of tests in patients before and after surgery to correct congenital unilateral conductive hearing losses. Data are presented from 19 patients between the ages of 6 and 33 years that had an abnormal external and/or middle ear on one side but normal hearing in the other ear. Surgery improved thresholds an average of 36 dB HL (from 56 to 20 dB HL). Patients were tested pre- and postoperatively for interaural temporal difference limens, alternate and simultaneous loudness balances, sound localization, binaural detection thresholds, and speech perception in noise. There was statistically significant improvement after surgery in all tests, and the amount of improvement varied along a continuum that appears to be related to the simplicity of the task. For example, most postoperative patients had normal or near-normal performance in a test of interaural temporal difference limens, while almost all had difficulty localizing sounds. Neither binaural performance (before or after surgery) nor the improvement in performance was correlated with age, pure-tone thresholds, or asymmetry. Limited available data show no significant changes in performance from four weeks to over 24 weeks after surgery. In conclusion, binaural ability following corrective surgery exists in varying degrees in these tasks, suggesting different effects of abnormal early experience on different aspects of binaural hearing. C1 UNIV TEXAS,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,HOUSTON,TX 77030. CR ASHMEAD DH, 1994, IN PRESS CHILD DEV BILGER RC, 1984, J SPEECH HEAR RES, V27, P32 BRONKHORST AW, 1988, J ACOUST SOC AM, V83, P1508, DOI 10.1121/1.395906 BRUGGE JF, 1985, HEARING RES, V20, P275, DOI 10.1016/0378-5955(85)90032-2 COLBURN HS, 1992, NOISE INDUCED HEARIN, P293 Durlach N. I., 1978, HDB PERCEPTION, V4, P365 DURLACH NI, 1981, AUDIOLOGY, V20, P181 Florentine M, 1976, J Am Audiol Soc, V1, P243 Gottlieb G., 1976, NEURAL BEHAV SPECIFI, P25 HALL JW, 1986, ANN OTO RHINOL LARYN, V95, P525 HALL JW, 1990, ARCH OTOLARYNGOL, V116, P946 HALL JW, 1988, AUDIOLOGY, V27, P89 HAUSSLER R, 1983, ACTA OTO-LARYNGOL, P400 HIRSH IJ, 1950, J ACOUST SOC AM, V22, P196, DOI 10.1121/1.1906588 HUBEL DH, 1970, J PHYSIOL-LONDON, V206, P419 JAHRSDOERFER RA, 1978, LARYNGOSCOPE, V88, P1 JERGER JF, 1960, J SPEECH HEAR RES, V3, P15 JERGER S, 1980, INT J PEDIATR OTORHI, V2, P217, DOI 10.1016/0165-5876(80)90047-6 JONGKEES L B, 1957, Acta Otolaryngol, V48, P465, DOI 10.3109/00016485709126908 KNUDSEN EI, 1983, SCIENCE, V222, P939, DOI 10.1126/science.6635667 KNUDSEN EI, 1985, SCIENCE, V230, P545, DOI 10.1126/science.4048948 KOEHNKE J, 1989, AM SPEECH LANAGUAGE LEVITT H, 1988, J ACOUST SOC AM, V43, P65 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 MAGLIULO G, 1990, British Journal of Audiology, V24, P117, DOI 10.3109/03005369009077852 MOORE DR, 1989, J NEUROSCI, V9, P1213 NORDLUND B, 1964, Acta Otolaryngol, V57, P1, DOI 10.3109/00016486409136942 SEBER GAF, 1984, MULTIVARIATE TRAHIOTIS C, 1990, J ACOUST SOC AM, V87, P1359, DOI 10.1121/1.399513 TUCCI DL, 1985, J COMP NEUROL, V238, P371, DOI 10.1002/cne.902380402 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 NR 31 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 APR PY 1994 VL 74 IS 1-2 BP 99 EP 114 DI 10.1016/0378-5955(94)90179-1 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500009 PM 8040103 ER PT J AU SALT, AN DEMOTT, J AF SALT, AN DEMOTT, J TI ENDOLYMPH CALCIUM INCREASES WITH TIME AFTER SURGICAL INDUCTION OF HYDROPS IN GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE ENDOLYMPH; CALCIUM; ENDOLYMPHATIC HYDROPS; COCHLEA, MENIERES DISEASE ID OUTER HAIR-CELLS; COCHLEAR ENDOLYMPH; CA++ ACTIVITY; POTENTIALS; CHANNELS AB The ionized Ca2+ concentration in cochlear endolymph is normally extremely low. Previous studies have shown that endolymph Ca2+ levels become elevated when measured at long intervals after endolymphatic hydrops is surgically induced. The present study was designed to investigate how rapidly endolymph Ca2+ increases following endolymphatic duct ablation. Hydropic animals were tested at either 4 days, 4 weeks, 8 weeks or 16 weeks after surgery. In each animal endolymph Ca2+ and endocochlear potentials were measured in all four cochlear turns using double-barreled Ca2+-sensitive electrodes. Cochlear sensitivity was assessed using compound action potential thresholds. Our results confirm that hydropic animals show an elevation of endolymph Ca2+ and a reduction of EP which is initially small, but becomes more pronounced at longer times after surgery. At 16 weeks endolymph Ca2+ was increased by an average factor of 2.0 in the basal turn and 7.5 in the fourth turn. These findings suggest that endolymph Ca2+ changes may not be the primary factor responsible for hydrops generation, but probably contribute to cochlear dysfunction in later phases of hydrops. For some experimental groups, the elevation of AP threshold was more closely correlated with endolymph Ca2+ level than it was with endolymph volume. Endolymph Ca2+ changes must therefore be considered in order to account for dysfunction in the hydropic cochlea. RP SALT, AN (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID AVE,ST LOUIS,MO 63110, USA. CR BOBBIN RP, 1991, HEARING RES, V56, P101, DOI 10.1016/0378-5955(91)90159-7 BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BOSHER SK, 1978, NATURE, V273, P377, DOI 10.1038/273377a0 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 HACOHEN N, 1989, J NEUROSCI, V9, P3988 Haid T, 1988, Acta Otolaryngol Suppl, V460, P149 HORNER KC, 1991, HEARING RES, V52, P147, DOI 10.1016/0378-5955(91)90194-E IKEDA K, 1987, HEARING RES, V26, P117, DOI 10.1016/0378-5955(87)90040-2 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KIMURA RS, 1967, ANN OTO RHINOL LARYN, V76, P1 KLIS SFL, 1990, ANN OTO RHINOL LARYN, V99, P566 Konishi T, 1981, MENIERES DIS PATHOGE, P47 MOSCOVIT.DH, 1966, J ACOUST SOC AM, V40, P583, DOI 10.1121/1.1910122 NINOYU O, 1986, ARCH OTO-RHINO-LARYN, V243, P106, DOI 10.1007/BF00453759 NINOYU O, 1986, ARCH OTO-RHINO-LARYN, V243, P141, DOI 10.1007/BF00453767 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 SALT AN, 1986, HEARING RES, V23, P141, DOI 10.1016/0378-5955(86)90011-0 Salt AN, 1989, MENIERES DIS, P69 SALT AN, 1990, AUDIOLOGY, V29, P135 SALT AN, 1994, HEARING RES, V74, P165, DOI 10.1016/0378-5955(94)90184-8 SALT AN, 1993, ASS RES OTOLARYNGOL, P135 SALT AN, 1989, AM J OTOLARYNG, V10, P371, DOI 10.1016/0196-0709(89)90030-6 SCHULTE BA, 1993, HEARING RES, V65, P262, DOI 10.1016/0378-5955(93)90219-Q SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 Sokal RR, 1981, BIOMETRY PRINCIPLES STARR PA, 1991, HEARING RES, V52, P23, DOI 10.1016/0378-5955(91)90185-C SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 TANAKA Y, 1979, P JPN ACAD B-PHYS, V55, P31, DOI 10.2183/pjab.55.31 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 ZUMGOTTESBERGEORSULAKOVA AMM, 1986, ACTA OTO-LARYNGOL, V102, P93 NR 32 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 1994 VL 74 IS 1-2 BP 115 EP 121 DI 10.1016/0378-5955(94)90180-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500010 PM 8040082 ER PT J AU KUJAWA, SG GLATTKE, TJ FALLON, M BOBBIN, RP AF KUJAWA, SG GLATTKE, TJ FALLON, M BOBBIN, RP TI A NICOTINIC-LIKE RECEPTOR MEDIATES SUPPRESSION OF DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS BY CONTRALATERAL SOUND SO HEARING RESEARCH LA English DT Article DE CHOLINERGIC RECEPTORS; MOC EFFERENTS; OUTER HAIR CELLS ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; OLIVOCOCHLEAR BUNDLE STIMULATION; INOSITOL PHOSPHATE FORMATION; KAPPA-BUNGAROTOXIN BLOCKS; GAMMA-AMINOBUTYRIC-ACID; ACETYLCHOLINE-RECEPTOR; RAT COCHLEA; FUNCTIONAL EXPRESSION; BICUCULLINE BLOCKS AB The purpose of this investigation was to provide in vivo pharmacologic characterization of a cholinergic receptor mediating the suppressive effects of medial olivocochlear (MOC) efferent activation. MOC neurons were activated by contralateral sound and the resulting suppression of ipsilateral distortion product otoacoustic emissions (DPOAEs) was monitored before and after intracochlear perfusions of cholinergic antagonists. Results revealed a dose-dependent blockade of contralateral suppression of DPOAEs by a wide variety of nicotinic and muscarinic cholinergic receptor antagonists, as well as by non-traditional antagonists of cholinergic activity. The nicotinic antagonists, alpha-bungarotoxin, curare and k-bungarotoxin, and the glycine antagonist, strychnine, blocked contralateral suppression at nanomolar concentrations and demonstrated similar potencies. IC50 values were 2.38 x 10(-7), 2.79 x 10(-7), 3.81 x 10(-7) and 2.96 x 10(-7) M, respectively. These agents were followed in potency by the nicotinic antagonist, trimethaphan (1.75 x 10(-6) M), the M(3) muscarinic antagonist, 4-DAMP (1.88 x 10(-6) M) and the GABA(A) antagonist, bicuculline (2.39 X 10(-6) M). Increasingly greater concentrations of the muscarinic antagonists, atropine (9.52 x 10(-6) M), AF-DX 116 (2.72 x 10(-5) M) and pirenzepine (8.24 x 10(-4) M) were necessary to block contralateral suppression of DPOAEs. The in vivo pharmacology of this putative outer hair cell cholinergic receptor suggests that it may be a member of the nicotinic family of receptors. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB,NEW ORLEANS,LA 70112. UNIV ARIZONA,DEPT SPEECH & HEARING SCI,TUCSON,AZ 85721. CR ASCHER P, 1979, J PHYSIOL-LONDON, V295, P139 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BARRON SE, 1987, TRENDS PHARMACOL SCI, V8, P204, DOI 10.1016/0165-6147(87)90059-9 BARTOLAMI S, 1990, HEARING RES, V47, P229, DOI 10.1016/0378-5955(90)90154-H BARTOLAMI S, 1992, RECENT ADV CELLULAR, V3, P251 BARTOLAMI S, 1993, IN PRESS BRAIN RES BARTOLAMI S, 1993, IN PRESS NEUROREPORT BENSON JA, 1988, MOL BASIS DRUG PESTI, P193 BENSON JA, 1988, BRAIN RES, V458, P65, DOI 10.1016/0006-8993(88)90496-9 BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BOBBIN RP, 1971, NATURE-NEW BIOL, V231, P222 BOBBIN RP, 1991, HEARING RES, V56, P101, DOI 10.1016/0378-5955(91)90159-7 BREER H, 1987, J INSECT PHYSIOL, V33, P771, DOI 10.1016/0022-1910(87)90025-4 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 CANLON B, 1989, ACTA PHYSIOL SCAND, V137, P549, DOI 10.1111/j.1748-1716.1989.tb08795.x CHIAPPINELLI VA, 1991, SNAKE TOXINS, P223 CHIAPPINELLI VA, 1989, J EXP BIOL, V141, P61 CLINE HT, 1986, J NEUROSCI, V6, P2848 DRESCHER DG, 1992, J NEUROCHEM, V59, P765, DOI 10.1111/j.1471-4159.1992.tb09436.x DULON D, 1990, J NEUROSCI, V10, P1388 EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FEX J, 1978, BRAIN RES, V159, P440, DOI 10.1016/0006-8993(78)90555-3 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 GALLEY N, 1973, BRAIN RES, V64, P55, DOI 10.1016/0006-8993(73)90170-4 GITTER AH, 1992, EUR ARCH OTO-RHINO-L, V249, P62 GRENNINGLOH G, 1987, NATURE, V328, P215, DOI 10.1038/328215a0 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 JAMES WM, 1983, HEARING RES, V9, P113, DOI 10.1016/0378-5955(83)90139-9 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 KILBINGER H, 1984, TRENDS PHARM SCI MAR, P103 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 KLINKE R, 1977, EXP BRAIN RES, V28, P311 KUJAWA SG, 1992, HEARING RES, V64, P73, DOI 10.1016/0378-5955(92)90169-N 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 LENA C, 1993, TRENDS NEUROSCI, V16, P181, DOI 10.1016/0166-2236(93)90150-K LUETJE CW, 1991, J NEUROSCI, V11, P837 LUKAS RJ, 1992, INT REV NEUROBIOL, V34, P25 MARSHALL J, 1990, EMBO J, V9, P4391 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NIEDZIELSKI AS, 1992, HEARING RES, V59, P250, DOI 10.1016/0378-5955(92)90121-3 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W ONO JK, 1981, J NEUROSCI, V1, P259 OT SM, 1977, COMP BIOCH PHYSL C, V57, P107 PINNOCK RD, 1988, BRAIN RES, V458, P45, DOI 10.1016/0006-8993(88)90494-5 PLINKERT PK, 1991, HEARING RES, V53, P123, DOI 10.1016/0378-5955(91)90219-Y PLINKERT PK, 1990, HEARING RES, V44, P25, DOI 10.1016/0378-5955(90)90019-L PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 SARGENT PB, 1993, ANNU REV NEUROSCI, V16, P403, DOI 10.1146/annurev.ne.16.030193.002155 SCHMIDT J, 1992, J EXP BIOL, V171, P329 SCHOFIELD PR, 1987, NATURE, V328, P221, DOI 10.1038/328221a0 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 SHIGEMOTO T, 1991, J PHYSIOL-LONDON, V442, P669 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SLATER NT, 1984, BIOPHYS J, V45, P34 VANMEGEN YJB, 1988, BRAIN RES, V474, P185, DOI 10.1016/0006-8993(88)90682-8 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 YAROWSKY PJ, 1978, J NEUROPHYSIOL, V41, P531 ZHANG ZW, 1991, BRIT J PHARMACOL, V102, P19 NR 62 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 APR PY 1994 VL 74 IS 1-2 BP 122 EP 134 DI 10.1016/0378-5955(94)90181-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500011 PM 8040083 ER PT J AU EROSTEGUI, C NORRIS, CH BOBBIN, RP AF EROSTEGUI, C NORRIS, CH BOBBIN, RP TI IN-VITRO PHARMACOLOGICAL CHARACTERIZATION OF A CHOLINERGIC RECEPTOR ON OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELLS; ACETYLCHOLINE; RECEPTOR; NICOTINIC; MUSCARINIC ID GUINEA-PIG COCHLEA; NICOTINIC ACETYLCHOLINE-RECEPTORS; FUNCTIONAL EXPRESSION; MECHANICAL RESPONSES; CURRENTS; CHICK; ORGAN; CORTI; INHIBITION; INCREASE AB Acetylcholine (ACh) is the major neurotransmitter released from the efferent fibers in the cochlea onto the outer hair cells (OHCs). The type of ACh receptor on OHCs and the events subsequent to receptor activation are unclear. Therefore we studied the effect of agonists and antagonists of the ACh receptor on isolated OHCs from the guinea pig. OHCs were recorded from in whole cell voltage and current clamp configuration. ACh induced an increase in outward K+ current (I-ACh) which hyperpolarized the OHCs. No desensitization to ACh application was observed. Cs+ replaced K+ in carrying the I-ACh. The I-ACh is Ca2+-dependent, time and voltage sensitive, and different from the I-KCa induced by depolarization of the membrane potential. When tested at 100 alpha M, several agonists also induced outward current responses (acetylchorine > suberyldicholine greater than or equal to carbachol > DMPP) whereas nicotine, cytisine and muscarine did not. The I-ACh response to 10 mu M ACh was blocked by low concentrations of traditional and non-traditional nicotinic antagonists (strychnine > curare > bicuculline > alpha-bungarotoxin > trimethaphan) and by higher concentrations of muscarinic antagonists (atropine > 4-DAMP > AF-DX 116 > pirenzepine). Pharmacologically, the ACh receptor on OHCs is nicotinic. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB,NEW ORLEANS,LA 70112. CR ART JJ, 1985, J PHYSIOL-LONDON, V360, P397 BARTOLAMI S, 1992, RECENT ADV CELLULAR, V3, P251 BARTOLAMI S, 1993, IN PRESS BRAIN RES BARTOLAMI S, 1990, HEARING RES, V428, P109 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 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 DOI T, 1993, HEARING RES, V67, P179, DOI 10.1016/0378-5955(93)90245-V DULON D, 1990, J NEUROSCI, V10, P1388 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FREEDMAN R, 1993, J NEUROSCI, V13, P1965 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 FUCHS PA, 1992, J NEUROSCI, V12, P800 GIOVANELLI A, 1991, P NATL ACAD SCI USA, V88, P10069, DOI 10.1073/pnas.88.22.10069 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HOUSLEY GD, 1992, J PHYSIOL-LONDON, V448, P73 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, 1992, 1992 P MOL BIOL HEAR, P48 HUGANIR RL, 1990, NEURON, V5, P555, DOI 10.1016/0896-6273(90)90211-W KAKEHATA S, 1992, P SENDAI S, V2, P25 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 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 LENA C, 1993, TRENDS NEUROSCI, V16, P181, DOI 10.1016/0166-2236(93)90150-K LUETJE CW, 1991, J NEUROSCI, V11, P837 MARSHALL J, 1990, EMBO J, V9, P4391 MURASE K, 1989, NEUROSCI LETT, V103, P56, DOI 10.1016/0304-3940(89)90485-0 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 NIEDZIELSKI AS, 1992, HEARING RES, V59, P250, DOI 10.1016/0378-5955(92)90121-3 NOONEY JM, 1992, J PHYSIOL-LONDON, V455, P503 PLINKERT PK, 1990, HEARING RES, V44, P25, DOI 10.1016/0378-5955(90)90019-L PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RICCI AJ, 1993, IN PRESS COMP BIOCH SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SARGENT PB, 1993, ANNU REV NEUROSCI, V16, P403, DOI 10.1146/annurev.ne.16.030193.002155 SCHMIDT J, 1992, J EXP BIOL, V171, P329 SCHOFIELD PR, 1987, NATURE, V328, P221, DOI 10.1038/328221a0 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 SHIGEMOTO T, 1991, J PHYSIOL-LONDON, V442, P669 SLEPECKY N, 1988, HEARING RES, V34, P119, DOI 10.1016/0378-5955(88)90099-8 STEINACKER A, 1988, HEARING RES, V35, P265, DOI 10.1016/0378-5955(88)90123-2 SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M WACKYM PA, 1992, 1992 P MOL BIOL HEAR, P49 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 NR 51 TC 108 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 APR PY 1994 VL 74 IS 1-2 BP 135 EP 147 DI 10.1016/0378-5955(94)90182-1 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500012 PM 8040084 ER PT J AU MOGDANS, J KNUDSEN, EI AF MOGDANS, J KNUDSEN, EI TI REPRESENTATION OF INTERAURAL LEVEL DIFFERENCE IN THE VLVP, THE FIRST SITE OF BINAURAL COMPARISON IN THE BARN OWLS AUDITORY-SYSTEM SO HEARING RESEARCH LA English DT Article DE NUCLEUS OF THE LATERAL LEMNISCUS; LATERAL SUPERIOR OLIVE; NEURAL MAPS; SOUND LOCALIZATION ID UNIT EXCITATORY RESPONSES; SUPERIOR OLIVARY COMPLEX; LATERAL LEMNISCUS; DORSAL NUCLEUS; OPTIC TECTUM; INTENSITY DIFFERENCES; COCHLEAR NUCLEUS; TONE BURSTS; NEURAL MAP; BRAIN-STEM AB In the avian auditory system, the posterior division of the ventral nucleus of the lateral lemniscus (VLVp) is the first site where the levels of sound arriving at the two ears art compared. VLVp units are excited by sound at the contralateral ear and are inhibited by sound at the ipsilateral ear, and, as a result, are sensitive to interaural level differences (ILD). In this study, we investigate the functional properties of VLVp units and describe the topography of ILD sensitivity along the dorsoventral dimension of this nucleus. The responses of VLVp units were tested with monaural and binaural noise delivered through earphones. Excitatory and inhibitory responsiveness was quantified using several measures that assessed the effect of contra-ear stimulation and the effect of ipsi-ear stimulation on the contra-ear response. On the basis of these measures, we characterize the map of ILD sensitivity in the VLVp. The temporal pattern of unit responses were also analyzed. The discharges of VLVp units were regular and time-locked to the onset of a stimulus, a pattern of discharge reminiscent of the 'chopper pattern' observed in the lateral superior olive (LSO) of mammals. The temporal discharge patterns of a single VLVp neuron often distinguished between equivalent ILDs, resulting from different combinations of contra- and ipsi-ear levels, that were not distinguished by spike count alone. However, the temporal response pattern did not distinguish between all such combinations of contra- and ipsi-ear levels. The additional information was encoded by the pattern of activity across the entire population of VLVp neurons. This study describes similarities in the functional properties of VLVp and LSO units that suggest similar physiological mechanisms in avians and mammals for encoding similar acoustic information. C1 STANFORD UNIV,SCH MED,DEPT NEUROBIOL,STANFORD,CA 94305. CR ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 ADOLPHS R, 1993, THESIS CALTECH PASAD AITKIN LM, 1970, J NEUROPHYSIOL, V33, P412 BOUDREAU JC, 1970, CONTRIBUTIONS SENSOR, P143 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BRUGGE JF, 1970, J NEUROPHYSIOL, V33, P441 CAIRD D, 1983, EXP BRAIN RES, V52, P385 ESTERLY SD, COMMUNICATION GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 KNUDSEN EI, 1991, J NEUROSCI, V11, P1727 KNUDSEN EI, 1982, J NEUROSCI, V2, P1177 KNUDSEN EI, 1978, SCIENCE, V200, P795, DOI 10.1126/science.644324 MANLEY GA, 1988, J NEUROSCI, V8, P2665 MOGDANS J, 1992, J NEUROSCI, V12, P3473 MOISEFF A, 1983, J NEUROSCI, V3, P2553 MOISEFF A, 1981, J COMP PHYSIOL, V144, P299 OLIVER DL, 1989, J NEUROSCI, V9, P967 OLSEN JF, 1989, J NEUROSCI, V9, P2591 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 SHNEIDERMAN A, 1988, J COMP NEUROL, V276, P188, DOI 10.1002/cne.902760204 SPENCE CD, 1991, ANAL MODELING NEURAL, P297 SPENCE CD, 1990, ADV NEURAL INFORMATI, V2, P10 SULLIVAN WE, 1985, J NEUROPHYSIOL, V53, P201 SULLIVAN WE, 1984, J NEUROSCI, V4, P1787 TAKAHASHI T, 1984, J NEUROSCI, V4, P1781 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 TAKAHASHI TT, 1992, J COMP PHYSIOL A, V170, P161 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 TSUCHITANI C, 1985, J ACOUST SOC AM, V77, P1484, DOI 10.1121/1.392043 NR 31 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 APR PY 1994 VL 74 IS 1-2 BP 148 EP 164 DI 10.1016/0378-5955(94)90183-X PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500013 PM 8040085 ER PT J AU SALT, AN DEMOTT, J AF SALT, AN DEMOTT, J TI TIME-COURSE OF ENDOLYMPH VOLUME INCREASE IN EXPERIMENTAL HYDROPS MEASURED IN-VIVO WITH AN IONIC VOLUME MARKER SO HEARING RESEARCH LA English DT Article DE ENDOLYMPH; ENDOLYMPHATIC HYDROPS; ION-SELECTIVE ELECTRODES; MENIERES DISEASE ID GUINEA-PIG COCHLEA; FLOW-RATE; POTENTIALS; PERILYMPH AB A new method has been developed to measure the cross-sectional area (CSA) of scala media in the living cochlea. The method has some advantages over histological methods, in which tissues may shrink or move during processing. In the present study, scala media CSA was measured in the second turn of guinea-pig cochleas in which endolymphatic hydrops was induced surgically. The area measurement method used an iontophoretic injection of a volume marker into scala media, during which the concentration of marker in endolymph was monitored with an ion-selective microelectrode. The measured marker concentration was inversely proportional to the CSA of endolymph. The marker we used was the anion arsenic hexafluoride (AsF6-), which was almost ideal for the purpose as it was retained well in endolymph. Area was measured in normal animals and in hydropic animals at times from 4 days to 16 weeks after endolymphatic duct obstruction. The results showed that hydrops develops within days of ablation of the endolymphatic duct. The degree of hydrops was compared with electrophysiological measures of function, including the endocochlear potential, action potential thresholds and the amplitudes of the cochlear microphonic, summating potential and action potentials. In the initial stages of hydrops development, electrophysiological changes were small. In contrast, there were marked functional changes between 8 and 16 weeks, when endolymph volume was no longer increasing. These data support earlier studies which have shown that dysfunction in the hydropic cochlea does not correlate directly with the degree of endolymphatic hydrops. If the same is true for dysfunction in the ears of patients with Meniere's Disease, then it may not be possible to restore normal function simply by alleviating the hydrops. Furthermore, if dysfunction depends on factors other than the degree of hydrops, it may be possible to alleviate symptoms in ways other than by directly reducing hydrops. RP SALT, AN (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,BOX 8115,517 S EUCLID AVE,ST LOUIS,MO 63110, USA. CR COHEN J, 1984, ACTA OTO-LARYNGOL, V98, P398, DOI 10.3109/00016488409107580 DOI K, 1992, ACTA OTO-LARYNGOL, V112, P667, DOI 10.3109/00016489209137457 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 HORNER KC, 1991, HEARING RES, V52, P147, DOI 10.1016/0378-5955(91)90194-E HORNER KC, 1988, HEARING RES, V32, P41, DOI 10.1016/0378-5955(88)90145-1 HORNER KC, 1988, AUDIOLOGY, V27, P147 HORNER KC, 1988, ARCH OTO-RHINO-LARYN, V245, P103, DOI 10.1007/BF00481445 KIANG NYS, 1989, MENIERES DIS, P13 KIMURA RS, 1976, ARCH OTO-RHINO-LARYN, V212, P263, DOI 10.1007/BF00453674 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 KUSAKARI J, 1986, ACTA OTO-LARYNGOL, V101, P27, DOI 10.3109/00016488609108604 LONG CH, 1987, OTOLARYNG HEAD NECK, V96, P83 MORIZONO T, 1985, ANN OTO RHINOL LARYN, V94, P191 NICHOLSON C, 1981, J PHYSIOL-LONDON, V321, P225 NINOYU O, 1986, ARCH OTO-RHINO-LARYN, V243, P106, DOI 10.1007/BF00453759 OHYAMA K, 1988, HEARING RES, V35, P119, DOI 10.1016/0378-5955(88)90111-6 SALT AN, 1986, HEARING RES, V23, P141, DOI 10.1016/0378-5955(86)90011-0 SALT AN, 1990, AUDIOLOGY, V29, P135 SALT AN, 1991, HEARING RES, V56, P37, DOI 10.1016/0378-5955(91)90151-X SALT AN, 1992, EUR ARCH OTO-RHINO-L, V249, P157 SALT AN, 1991, J NEUROSCI METH, V38, P233, DOI 10.1016/0165-0270(91)90173-W SALT AN, 1994, HEARING RES, V74, P115, DOI 10.1016/0378-5955(94)90180-5 SALT AN, 1989, MENIERES DISEASE, P55 SHINKAWA H, 1986, ACTA OTO-LARYNGOL, V101, P43, DOI 10.3109/00016488609108606 SOKAL RR, 1981, BIOMETRY, P594 THALMANN R, 1989, 2 INT S MEN DIS, P55 ZUMGOTTESBERGEORSULAKOVA AMM, 1986, ACTA OTO-LARYNGOL, V102, P93 NR 29 TC 22 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 APR PY 1994 VL 74 IS 1-2 BP 165 EP 172 DI 10.1016/0378-5955(94)90184-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500014 PM 7518819 ER PT J AU XU, L PROBST, R HARRIS, FP ROEDE, J AF XU, L PROBST, R HARRIS, FP ROEDE, J TI PERIPHERAL ANALYSIS OF FREQUENCY IN HUMAN EARS REVEALED BY TONE BURST EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; FREQUENCY ANALYSIS; COCHLEAR MECHANICS; TRANSIENTLY EVOKED OTOACOUSTIC EMISSIONS; INNER EAR; COCHLEAR FREQUENCY SELECTIVITY ID OTO-ACOUSTIC EMISSIONS; 2-TONE SUPPRESSION; HEARING; MASKING AB Otoacoustic emissions were evoked in the same ears with single tone bursts at 1, 2 and 3 kHz and with a complex stimulus consisting of a digital addition of the three tone bursts. Stimuli were presented at 75, 59 and 37 dB SPL to 28 ears of human subjects with normal hearing. The purpose was to determine if comparisons of responses to the complex stimulus with a posthoc addition of responses from single tone bursts could delineate features of cochlear frequency analysis of short-duration signals. For processing of the data, the results from the individual tone bursts were combined offline to form a composite response. This was then compared with the response obtained with the complex stimulus. Results revealed close correspondence between the spectra of the complex and composite responses in all ears despite interindividual differences in response morphology. Correlations between the complex and composite waveforms exceeded 80% for all stimulus levels. Subtractions of the two spectra revealed that the majority of the differences occurred at frequencies on the high-frequency slopes of the 1- and 2-kHz spectral peaks. This was due to a reduction in energy for the responses obtained with the complex stimulus. There was little variation between the two response types in the peak frequencies of their spectra, in the energy at frequencies on the lower frequency sides of the spectral peaks at 1 and 2 kHz, or in the spectral components at 3 kHz. Results reveal characteristics of the analysis of frequency in the preneural stages of cochlear processing. C1 KANTONSSPITAL BASEL,DEPT OTORHINOLARYNGOL,CH-4031 BASEL,SWITZERLAND. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 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 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 Elberling C, 1985, Acta Otolaryngol Suppl, V421, P77 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 HARRIS FP, 1990, MECH BIOPHYSICS HEAR, P178 HOUTGAST T, 1972, J ACOUST SOC AM, V51, P1885, DOI 10.1121/1.1913048 KEMP DT, 1990, ADV AUDIOL, V7, P77 Kemp D. T., 1980, PSYCHOPHYSICAL PHYSL Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J COUST SOC AM, V80, P1365 SHANNON RV, 1976, J ACOUST SOC AM, V59, P1460, DOI 10.1121/1.381007 STOVER LJ, 1992, ABSTR ASS RES OT, V15, P153 SUTTON GJ, 1985, ACUSTICA, V58, P57 ZWICKER E, 1990, ACUSTICA, V70, P189 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 NR 23 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 APR PY 1994 VL 74 IS 1-2 BP 173 EP 180 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500015 PM 8040086 ER PT J AU OLEARY, SJ TONG, YC CLARK, GM AF OLEARY, SJ TONG, YC CLARK, GM TI NEURAL PROCESSES IN THE DORSAL COCHLEAR NUCLEUS OF THE ANESTHETIZED CAT INVESTIGATED FROM UNIT RESPONSES TO ELECTRICAL-STIMULATION OF THE AUDITORY-NERVE SO HEARING RESEARCH LA English DT Article DE DORSAL COCHLEAR NUCLEUS; ELECTRICAL STIMULATION; AUDITORY NERVE ID GUINEA-PIG; SLICE PREPARATIONS; MICE; NEURONS; CELLS; INVITRO; CONNECTIONS; SUPPRESSION; MORPHOLOGY; ORGANIZATION AB Extracellular responses of dorsal cochlear nucleus single units were recorded in response to biphasic, bipolar electrical stimulation of spiral ganglion cells and their peripheral processes using a banded electrode array in the scala tympani of the barbiturate anaesthetised cat. The DCN responses to this stimulus were the result of excitatory and suppressive (including inhibitory) processes. The excitatory responses from DCN units were usually within a range of 1.8-2.8 ms and these responses were probably the result of monosynaptic input from the auditory nerve. Latencies > 2.8 ms were most likely due to activation of di- and poly-synaptic pathways from auditory nerve fibres, except that latencies between 3.5-4.75 in hearing animals could have arisen from electrophonic mechanisms. Suppression of spontaneous activity was usually long acting, lasting > 70 ms following each pulse of the pulse train, but short acting suppression with a latency of 3.5-4.75 ms and a duration of < 10 ms was occasionally observed. These suppressive responses probably resulted from synaptic inhibitory input, but neural membrane properties may have contributed. In hearing animals, excitatory latencies within the range 1.8-5.2 ms were similar for units with different response area types or different PSTH patterns in response to acoustic CF tones or noise. C1 UNIV MELBOURNE,DEPT OTOLARYNGOL,PARKVILLE,VIC 3052,AUSTRALIA. CR ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BLACK RC, 1978, THESIS U MELBOURNE BLACK RC, 1979, APPL NEUROPHYSIOL, V42, P366 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BRUMMER SB, 1977, BRAIN BEHAV EVOLUT, V14, P10, DOI 10.1159/000124611 CLOPTON BM, 1982, ANN OTO RHINOL LARYN, V91, P285 COUSILLAS H, 1988, HEARING RES, V36, P21, DOI 10.1016/0378-5955(88)90135-9 DENO RL, 1981, PRIMARY ACOUSTIC NUC, P1 EVANS EF, 1973, EXP BRAIN RES, V17, P402 FENG AS, 1985, J COMP NEUROL, V235, P529, DOI 10.1002/cne.902350410 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 HARTMANN R, 1984, ADV AUDIOL, V1, P18 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P535 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 Javel E., 1990, COCHLEAR IMPLANTS MO JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KONISHI T, 1979, ACTA OTO-LARYNGOL, V88, P41, DOI 10.3109/00016487909137138 LEAKEJONES PA, 1980, SEM, V3, P427 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MAFFI CL, 1988, AUDITORY PATHWAYS ST, P149 MANIS PB, 1989, J NEUROPHYSIOL, V61, P149 MANIS PB, 1990, J NEUROSCI, V10, P2338 MANIS PB, 1983, J NEUROPHYSIOL, V50, P1156 MERZENICH MM, 1977, FUNCTIONAL ELECT STI, P321 MERZENICH MM, 1974, NERVOUS SYSTEM, V3, P539 MOXON EC, 1971, THESIS CAMBRIDGE MIT Nuttall AL, 1981, AMINOGLYCOSIDE OTOTO, P51 NUTTALL AL, 1977, ACTA OTO-LARYNGOL, V83, P393, DOI 10.3109/00016487709128863 OERTEL D, 1990, J COMP NEUROL, V295, P136, DOI 10.1002/cne.902950112 OERTEL D, 1989, J COMP NEUROL, V283, P228, DOI 10.1002/cne.902830206 OSEN KK, 1970, ARCH ITAL BIOL, V108, P21 PERKEL DH, 1970, NEUROSCIENCES 2 STUD, P587 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SCHWEITZER L, 1984, J COMP NEUROL, V225, P228, DOI 10.1002/cne.902250208 SHEPHERD RK, 1988, 5TH Q PROGR REP SHOFNER WP, 1987, HEARING RES, V29, P45, DOI 10.1016/0378-5955(87)90204-8 SHOFNER WP, 1985, J NEUROPHYSIOL, V54, P917 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 STARR A, 1970, J NEUROPHYSIOL, V33, P137 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VOIGT HF, 1988, J NEUROPHYSIOL, V59, P1014 VOIGT HF, 1980, J NEUROPHYSIOL, V44, P76 WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 WICKESBERG RE, 1988, J COMP NEUROL, V268, P389, DOI 10.1002/cne.902680308 YOUNG ED, 1982, HEARING RES, V6, P153, DOI 10.1016/0378-5955(82)90051-X YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 YOUNG ED, 1980, BRAIN RES, V200, P23, DOI 10.1016/0006-8993(80)91091-4 NR 59 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 APR PY 1994 VL 74 IS 1-2 BP 181 EP 196 DI 10.1016/0378-5955(94)90186-4 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500016 PM 8040087 ER PT J AU OGAWA, K SCHACHT, J AF OGAWA, K SCHACHT, J TI G-PROTEINS COUPLED TO PHOSPHOINOSITIDE HYDROLYSIS IN THE COCHLEAR AND VESTIBULAR SENSORY EPITHELIA OF THE RAT ARE INSENSITIVE TO CHOLERA AND PERTUSSIS TOXINS SO HEARING RESEARCH LA English DT Article DE G-PROTEIN; INOSITOL PHOSPHATE; ADP-RIBOSYLATION; COCHLEA TOXIN; PERTUSSIS TOXIN; COCHLEA; VESTIBULE; RAT ID NUCLEOTIDE BINDING-PROTEIN; ISLET-ACTIVATING PROTEIN; ADENYLATE-CYCLASE; POLYPHOSPHOINOSITIDE PHOSPHODIESTERASE; INOSITOL PHOSPHATES; SIGNAL TRANSDUCTION; PHOSPHOLIPASE-C; CALCIUM MOBILIZATION; REGULATORY COMPONENT; ADP-RIBOSYLATION AB In the cochlear (CSE) and vestibular sensory epithelia (VSE), phosphoinositides are hydrolyzed in response to stimulation of phospholipase C (PLC) by cholinergic muscarinic and purinergic P-2y agonists. Such receptor-mediated activation of PLC is expected to be coupled through guanine nucleotide-binding proteins (G-proteins). Although several classes of G-proteins have been identified in the inner ear, nothing is known about the type of G-proteins associated with the phosphoinositide second messenger system in CSE and VSE. Phosphoinositide hydrolysis was determined by the release of radiolabeled inositol phosphates (InsPs). Ten mM NaF plus 10 mu M AlCl3 increased basal InsPs accumulation 2-fold in both CSE and VSE of the rat. Release of InsPs was also enhanced by guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) in saponin-permeabilized tissues. Furthermore, release of InsPs stimulated by both carbamylcholine (CCh) and adenosine 5'-O-[3-thiotriphosphate] (ATP-gamma-S) was significantly inhibited by 100 mu M guanosine 5'-O-[2-thiodiphosphate] (GDP-beta-S). These results strongly suggest the involvement of G-proteins in the receptor-PLC coupling in CSE and VSE. ADP-ribosylation in membrane fractions of CSE and VSE in the presence of cholera toxin (CTX) or pertussis toxin (PTX) indicated the existence of G(s)- and G(i)-type G-proteins. However, neither CTX nor PTX affected basal or agonist-stimulated release of InsPs. These observations suggest that muscarinic and P-2y purinergic receptors are coupled to PLC via CTX- and PTX-insensitive G-proteins in CSE and VSE. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR BERRIDGE MJ, 1983, BIOCHEM J, V212, P473 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 CANLON B, 1991, EUR J NEUROSCI, V3, P1338, DOI 10.1111/j.1460-9568.1991.tb00066.x COCKCROFT S, 1985, NATURE, V314, P534, DOI 10.1038/314534a0 COCKCROFT S, 1987, BIOCHEM J, V241, P409 DEAN NM, 1989, ANAL BIOCHEM, V183, P199, DOI 10.1016/0003-2697(89)90468-5 DUBYAK GR, 1990, ANN NY ACAD SCI, V603, P227 DUNLOP ME, 1986, BIOCHEM J, V240, P731 FISCHER SK, 1993, J NEUROCHEM, V60, P1800 FISHMAN PH, 1982, J CELL BIOL, V93, P860, DOI 10.1083/jcb.93.3.860 FLEMING N, 1989, LIFE SCI, V44, P1027, DOI 10.1016/0024-3205(89)90554-7 GILL DM, 1988, METHOD ENZYMOL, V165, P235 GILL DM, 1978, P NATL ACAD SCI USA, V75, P3050, DOI 10.1073/pnas.75.7.3050 GILMAN AG, 1987, ANNU REV BIOCHEM, V56, P615, DOI 10.1146/annurev.biochem.56.1.615 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HAGGBLAD J, 1988, FEBS LETT, V235, P133, DOI 10.1016/0014-5793(88)81248-1 HELPER JR, 1986, BIOCHEM J, V239, P141 HEPLER JR, 1992, TRENDS BIOCHEM SCI, V17, P383, DOI 10.1016/0968-0004(92)90005-T HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 KAKEHATA S, 1992, P SENDAI S, V2, P25 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 KATADA T, 1984, J BIOL CHEM, V259, P3578 KATADA T, 1982, J BIOL CHEM, V257, P3739 KAZIRO Y, 1991, ANN REV BIOCH, V60, P344 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LITOSCH I, 1985, J BIOL CHEM, V260, P5464 MARC S, 1988, BIOCHEM J, V255, P705 MASTERS SB, 1985, BIOCHEM J, V227, P933 MEI L, 1988, Brain Research, V447, P360, DOI 10.1016/0006-8993(88)91140-7 NANOFF C, 1990, BRIT J PHARMACOL, V100, P63 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 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 OGAWA K, 1993, HEARING RES, V69, P207, DOI 10.1016/0378-5955(93)90109-E OKAJIMA F, 1989, J BIOL CHEM, V264, P13029 SASAGURI T, 1986, BIOCHEM J, V239, P567 SCHNEFEL S, 1988, FEBS LETT, V230, P125, DOI 10.1016/0014-5793(88)80655-0 STERNWEIS PC, 1982, P NATL ACAD SCI-BIOL, V79, P4888, DOI 10.1073/pnas.79.16.4888 STERNWEIS PC, 1992, TRENDS BIOCHEM SCI, V17, P502, DOI 10.1016/0968-0004(92)90340-F TACHIBANA M, 1992, HEARING RES, V62, P82, DOI 10.1016/0378-5955(92)90204-Z YAMADA M, 1992, CIRC RES, V70, P477 NR 41 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 1994 VL 74 IS 1-2 BP 197 EP 203 DI 10.1016/0378-5955(94)90187-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500017 PM 8040088 ER PT J AU SUBRAMANIAM, M SALVI, RJ SPONGR, VP HENDERSON, D POWERS, NL AF SUBRAMANIAM, M SALVI, RJ SPONGR, VP HENDERSON, D POWERS, NL TI CHANGES IN DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS AND OUTER HAIR-CELLS FOLLOWING INTERRUPTED NOISE EXPOSURES SO HEARING RESEARCH LA English DT Article DE DPOAES; TOUGHENING; SEM ID 2 DISCRETE SOURCES; ACOUSTIC-DISTORTION; HEARING-LOSS; MECHANICAL RESPONSES; PERIODIC REST; COCHLEAR; DAMAGE; SENSITIVITY; STEREOCILIA; RESISTANCE AB Changes in distortion product otoacoustic emissions (DPOAEs) were examined during and after interrupted noise exposures and compared to the condition of the outer hair cells (OHCs) and inner hair cells (IHCs) as assessed by scanning electron microscopy (SEM). Binaural, adult chinchillas were exposed to a 95 dB SPL, octave band noise centered at 0.5 kHz for 15 days using a 3 h on/9 h off schedule. DPOAEs were measured before, during and after the exposures. DPOAE amplitudes decreased significantly during the first few days of the interrupted noise exposures and then began to recover. At most frequencies, the emission amplitudes recovered completely to pre-exposure baseline values by five days after the last exposure. The results of the present study indicate that the changes in DPOAE amplitude paralleled the recovery in the amplitude and threshold of the compound action potentials as reported previously (Boettcher et al., 1992). Although the DPOAEs completely recovered, considerable OHC loss and stereocilia disarray was evident even four weeks after exposure. RP SUBRAMANIAM, M (reprint author), SUNY BUFFALO,DEPT COMMUN SCI & DISORDERS,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214, USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 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, 1992, NOISE INDUCED HEARIN, P489 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X CODY AR, 1992, NOISE INDUCED HEARIN, P11 CRANE HD, 1983, HEARING RES THEORY, V2, P126 ELDREDGE EH, 1981, J ACOUST SOC AM, V67, P1091 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 HUNTERDUVAR IM, 1977, SCANNING ELECT MICRO, V2, P421 LENOIR M, 1987, HEARING RES, V29, P265, DOI 10.1016/0378-5955(87)90173-0 LIBERMAN MC, 1986, BASIC APPL ASPECTS N, P163 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LONSBURYMARTIN BL, 1991, J SPEECH HEAR RES, V34, P964 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 NORTON SJ, 1990, MECH BIOPHYSICS HEAR, P219 OHLMS LA, 1991, OTOLARYNG HEAD NECK, V104, P159 ROSOWSKI JJ, 1984, HEARING RES, V18, P141 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SAUNDERS JC, 1982, BASIC APPLIED ASPECT, P11 SCHMIEDT RA, 1986, ABSTR ASS RES OT, V112 SIEGEL JH, 1982, NEW PERSPECTIVES NOI, P137 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 SUBRAMANIAM M, 1991, HEARING RES, V56, P65, DOI 10.1016/0378-5955(91)90154-2 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 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 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 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 38 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 APR PY 1994 VL 74 IS 1-2 BP 204 EP 216 DI 10.1016/0378-5955(94)90188-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500018 PM 8040089 ER PT J AU QUIRK, WS SHIVAPUJA, BG SCHWIMMER, CL SEIDMAN, MD AF QUIRK, WS SHIVAPUJA, BG SCHWIMMER, CL SEIDMAN, MD TI LIPID-PEROXIDATION INHIBITOR ATTENUATES NOISE-INDUCED TEMPORARY THRESHOLD SHIFTS SO HEARING RESEARCH LA English DT Article DE NOISE INDUCED HEARING LOSS; TEMPORARY THRESHOLD SHIFTS; U74389F; FREE OXYGEN RADICALS; LIPID PEROXIDATION ID BLOOD-CELL VELOCITY; U74006F; DEGRADATION; RADICALS; ISCHEMIA; COCHLEA AB The purpose of this study was to investigate the protective effects of U74389F (Upjohn Co. Kalamazoo, MI), a 21-aminosteroid/lipid peroxidation inhibitor, and a member of the lazaroid drug class, on temporary threshold shifts in animals exposed to prolonged noise stimulation. Animals treated with U74389F and exposed to noise showed attenuated cochlear action potential threshold (CAP) shifts and cochlear microphonic (CM) when compared to non-drug treated noise-exposed subjects. These data suggest that inhibition of FOR induced lipid peroxidation is an important mechanism in noise-induced asymptotic temporary threshold shifts. C1 WAYNE STATE UNIV,DEPT OTOLARYNGOL,MICROCIRCULAT LAB,DETROIT,MI 48201. HENRY FORD HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,DIV NEUROTOL SKULL BASE SURG,OTOL RES LAB,W BLOOMFIELD,MI 48322. CR ADACHI H, 1979, JPN CIRC J, V43, P395 AXELSSON A, 1981, ACTA OTO-LARYNGOL, V91, P237, DOI 10.3109/00016488109138504 BEAGLEY HA, 1965, ACTA OTOLARYNGOL, V60, P437, DOI 10.3109/00016486509127027 CHAN PH, 1984, NEUROLOGY, V34, P315 CROWELL JW, 1969, AM J PHYSIOL, V216, P944 Demopoulos H B, 1980, Acta Physiol Scand Suppl, V492, P91 DOLAN DF, 1988, J ACOUST SOC AM, V83, P1081, DOI 10.1121/1.396052 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 FISCH U, 1983, OTOLARYNG HEAD NECK, V91, P3 FLEISHAKER JC, 1993, J CLIN PHARMACOL, V33, P175 FLEISHAKER JC, 1993, J CLIN PHARMACOL, V33, P182 GRANGER DN, 1981, GASTROENTEROLOGY, V81, P22 GRUM CM, 1985, CHEST, V88, P763, DOI 10.1378/chest.88.5.763 HALL E D, 1989, Journal of Neurotrauma, V6, P169, DOI 10.1089/neu.1989.6.169 HALL ED, 1992, J NEUROTRAUM, V9, P5425 HALL ED, 1988, STROKE, V19, P997 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HENDERSON D, 1982, ASYMPTOTIC THRESHOLD, P265 HIBLER N, 1948, Monatsschr Ohrenheilkd Laryngorhinol, V82, P441 KELLERHA.B, 1971, PRACT-OTO-RHINO-LARY, V33, P260 MILLER JM, 1983, HEARING RES, V11, P69 NATALE JE, 1988, STROKE, V19, P1371 PUJOL R, 1991, ACTA OTOLARYNGOL S S, V476, P32 QUIRK WS, 1991, HEARING RES, V52, P217, DOI 10.1016/0378-5955(91)90201-J QUIRK WS, 1992, HEARING RES, V63, P102, DOI 10.1016/0378-5955(92)90079-3 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P511 SIEDMAN MD, 1994, UNPUB OTOLARYNGOL HE SILVIA R C, 1987, Society for Neuroscience Abstracts, V13, P1495 WOOLLISCROFT JO, 1986, AM J MED, V81, P472, DOI 10.1016/0002-9343(86)90302-5 NR 29 TC 65 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 APR PY 1994 VL 74 IS 1-2 BP 217 EP 220 DI 10.1016/0378-5955(94)90189-9 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500019 PM 8040090 ER PT J AU GRIFFITHS, SK PIERSON, LL GERHARDT, KJ ABRAMS, RM PETERS, AJM AF GRIFFITHS, SK PIERSON, LL GERHARDT, KJ ABRAMS, RM PETERS, AJM TI NOISE-INDUCED HEARING-LOSS IN FETAL SHEEP SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; FETAL SHEEP; FETAL HEARING; NOISE-INDUCED HEARING LOSS ID AUDITORY-EVOKED-POTENTIALS; BRAIN-STEM RESPONSE; SOUND ENVIRONMENT; STIMULATION; MOVEMENTS; VIBRATION; INUTERO; SHIFTS; FETUS; ABR AB The auditory brainstem response (ABR) was recorded in utero from chronically instrumented fetal sheep prior to and following exposure of pregnant ewes to intense broadband noise (120 dB SPL for 16 h). ABRs were elicited by clicks and tone bursts (0.5, 1, 2, and 4 kHz) delivered through a bone oscillator secured to the fetal skull. Latency-intensity functions for most of the four vertex-positive waves (labelled I-IV) were prolonged and ABR thresholds were temporarily elevated by an average of 8 dB following the noise exposure. Results show that exogenous sounds can penetrate the uterus and result in alterations of the fetal ABR. C1 UNIV FLORIDA,INST ADV STUDY COMMUN PROC,GAINESVILLE,FL 32611. UNIV FLORIDA,DEPT OBSTET & GYNAECOL,GAINESVILLE,FL 32611. UNIV FLORIDA,DEPT PEDIAT,GAINESVILLE,FL 32611. RP GRIFFITHS, SK (reprint author), UNIV FLORIDA,DEPT COMMUN PROC & DISORDERS,435 DAUER HALL,GAINESVILLE,FL 32611, USA. CR ABRAMS RM, 1989, DEV BRAIN RES, V48, P1, DOI 10.1016/0165-3806(89)90088-6 ARMITAGE SE, 1980, SCIENCE, V208, P1173, DOI 10.1126/science.7375927 ATTIAS J, 1985, AUDIOLOGY, V24, P149 ATTIAS J, 1986, AUDIOLOGY, V25, P116 ATTIAS J, 1990, HEARING RES, V45, P247, DOI 10.1016/0378-5955(90)90124-8 BALDWIN JN, 1983, PHYSL SOC, V131 BENCH J, 1968, J GENET PSYCHOL, V113, P85 COOK CJ, 1987, J DEV PHYSIOL, V9, P429 COOK RO, 1982, DEV PSYCHOBIOL, V15, P95, DOI 10.1002/dev.420150202 Dawes GS, 1968, FETAL NEONATAL PHYSL DUNN DE, 1981, ABSTR ASS RES OT, V61 GAGNON R, 1986, AM J OBSTET GYNECOL, V155, P1227 GELMAN SR, 1982, AM J OBSTET GYNECOL, V143, P484 GERHARDT KJ, 1989, SEMIN PERINATOL, V13, P362 GERHARDT KJ, 1990, AM J OBSTET GYNECOL, V162, P282 GERHARDT KJ, 1992, AM J OTOLARYNG, V13, P226, DOI 10.1016/0196-0709(92)90026-P GERHARDT KJ, 1990, SEMIN PERINATOL, V14, P299 GRIMWADE JC, 1971, AM J OBSTET GYNECOL, V109, P86 HENDERSON D, 1993, EAR HEARING, V14, P152, DOI 10.1097/00003446-199306000-00002 HORNER KC, 1987, HEARING RES, V26, P327, DOI 10.1016/0378-5955(87)90068-2 Jones CT, 1985, PHYSL DEV FETUS NEWB LACIAK J, 1968, 27 ZJASD OT POLSK W LALANDE NM, 1986, AM J IND MED, V10, P427, DOI 10.1002/ajim.4700100410 OLIVER CC, 1989, SEMIN PERINATOL, V13, P354 PATRICK J, 1989, MATERNAL FETAL MED, P268 Peters A. J. M., 1993, Journal of Low Frequency Noise & Vibration, V12 PETERS AJM, 1993, AM J OBSTET GYNECOL Querleu D., 1988, EUR J OBSTET GYN R B, V29, P191 QUERLEU D, 1981, J GYNECOL OBST BIO R, V10, P307 RICHARDS DS, 1992, OBSTET GYNECOL, V80, P186 RICHARDS DS, 1988, OBSTET GYNECOL, V71, P535 SOHMER H, 1991, ACTA OTO-LARYNGOL, V111, P206, DOI 10.3109/00016489109137376 Stapells DR, 1985, AUDITORY BRAINSTEM R, P147 VINCE MA, 1985, EARLY HUM DEV, V11, P179, DOI 10.1016/0378-3782(85)90105-7 VINCE MA, 1982, BEHAVIOUR, V81, P296, DOI 10.1163/156853982X00184 WALKER D, 1971, AM J OBSTET GYNECOL, V109, P91 WOLFSON MR, 1990, ELECTROEN CLIN NEURO, V75, P242, DOI 10.1016/0013-4694(90)90177-L WOLLACK CH, 1963, J AUD RES, V3, P121 WOODS JR, 1985, OTOLARYNG HEAD NECK, V93, P759 WOODS JR, 1983, PEDIATR RES, V18, P83 NR 40 TC 17 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 1994 VL 74 IS 1-2 BP 221 EP 230 DI 10.1016/0378-5955(94)90190-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500020 PM 8040092 ER PT J AU ROBERTS, BL MASLAM, S LOS, I VANDERJAGT, B AF ROBERTS, BL MASLAM, S LOS, I VANDERJAGT, B TI COEXISTENCE OF CALCITONIN-GENE-RELATED PEPTIDE AND CHOLINE-ACETYLTRANSFERASE IN EEL EFFERENT NEURONS SO HEARING RESEARCH LA English DT Article DE EFFERENT; CALCITONIN GENE-RELATED PEPTIDE; CHOLINE ACETYLTRANSFERASE; ACETYLCHOLINE ID NICOTINIC ACETYLCHOLINE-RECEPTOR; AFFERENT FIBER SYNAPSE; OUTER HAIR-CELLS; GUINEA-PIG ORGAN; LATERAL LINE; OLIVOCOCHLEAR NEURONS; FINE-STRUCTURE; SPINAL-CORD; END-ORGANS; RAT AB We applied choline acetyltransferase, (ChAT) and calcitonin gene-related peptide (CGRP) immunocytochemistry to the efferent neurons that innervate the lateral line and the ear of the eel. Strong immunoreactivity to the ChAT antiserum was observed in neurons located within the octavolateralis efferent nucleus that could be distinguished, on the basis of their form, location and dendritic organization, from the ChAT-immunopositive motoneurons of the adjacent facial motor nucleus. Both facial motoneurons and efferent neurons were found to be immunopositive for CGRP, although the reaction was always stronger in the motoneurons. Double labelling experiments established the presence of both ChAT and CGRP in many efferent neurons. The results are evidence that cholinergic efferent neurons supplying end organs of different modalities may also produce calcitonin gene-related peptide. C1 UNIV AMSTERDAM,CTR BIOL,DEPT EXPTL ZOOL,1098 SM AMSTERDAM,NETHERLANDS. CR ADAMS JC, 1987, BRAIN RES, V419, P347, DOI 10.1016/0006-8993(87)90606-8 ALTSCHULER RA, 1984, J HISTOCHEM CYTOCHEM, V32, P839 ANNONI JM, 1984, J NEUROSCI, V4, P2106 ART JJ, 1984, J PHYSIOL-LONDON, V356, P525 BERNARD C, 1985, BRAIN RES, V338, P225, DOI 10.1016/0006-8993(85)90151-9 BOBBIN RP, 1985, COMP BIOCHEM PHYS C, V80, P313, DOI 10.1016/0742-8413(85)90062-3 BRANTLEY RK, 1988, J COMP NEUROL, V275, P87, DOI 10.1002/cne.902750108 DANIELSON PD, 1988, BRAIN RES, V448, P158, DOI 10.1016/0006-8993(88)91112-2 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 FONTAINE B, 1986, NEUROSCI LETT, V71, P59, DOI 10.1016/0304-3940(86)90257-0 FRITZSCH B, 1993, HEARING RES, V65, P51, DOI 10.1016/0378-5955(93)90200-K FUCHS PA, 1992, J NEUROSCI, V12, P800 GONZALEZ A, 1993, J COMP NEUROL, V332, P258, DOI 10.1002/cne.903320209 GUTH PS, 1986, ACTA OTO-LARYNGOL, V102, P194, DOI 10.3109/00016488609108666 GUTH PS, 1989, P ASS RES OTOLARYNGO, P325 HIETANEN M, 1990, HISTOCHEMISTRY, V93, P473, DOI 10.1007/BF00266403 HIGHSTEIN SM, 1991, NEUROSCI RES, V12, P13, DOI 10.1016/0168-0102(91)90096-H 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 KITAJIRI M, 1985, BRAIN RES, V358, P394, DOI 10.1016/0006-8993(85)90992-8 KURIYAMA H, 1990, BRAIN RES, V517, P76, DOI 10.1016/0006-8993(90)91010-E LAUFER R, 1987, EMBO J, V6, P901 MEREDITH GE, 1986, NEUROSCI LETT, V68, P69, DOI 10.1016/0304-3940(86)90231-4 MEREDITH GE, 1987, J COMP NEUROL, V265, P494, DOI 10.1002/cne.902650404 MEREDITH GE, 1986, NEUROSCIENCE, V17, P225, DOI 10.1016/0306-4522(86)90238-1 MILES K, 1989, NEURON, V2, P1517, DOI 10.1016/0896-6273(89)90198-0 MULLE C, 1988, P NATL ACAD SCI USA, V85, P5728, DOI 10.1073/pnas.85.15.5728 NIEDZIELSKI AS, 1992, HEARING RES, V59, P250, DOI 10.1016/0378-5955(92)90121-3 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 PERACHIO AA, 1989, EXP BRAIN RES, V78, P315 ROBERTS BL, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P185 SCHWARZ DWF, 1986, EXP BRAIN RES, V64, P19 SEWELL WF, 1991, J NEUROPHYSIOL, V65, P1158 SHIGEMOTO T, 1991, J PHYSIOL-LONDON, V442, P669 SLIWINSKAKOWALSKA M, 1989, HEARING RES, V42, P83, DOI 10.1016/0378-5955(89)90119-6 STEINACKER A, 1988, HEARING RES, V35, P2654 SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M SUGAI T, 1991, JPN J PHYSIOL, V41, P217, DOI 10.2170/jjphysiol.41.217 TAKAMI K, 1985, BRAIN RES, V328, P386, DOI 10.1016/0006-8993(85)91055-8 TAKEDA N, 1987, ACTA OTO-LARYNGOL, V103, P567 TAKEDA N, 1986, EXP BRAIN RES, V61, P575 TANAKA M, 1989, BRAIN RES, V504, P31, DOI 10.1016/0006-8993(89)91593-X TOHYAMA Y, 1990, BRAIN RES, V515, P312, DOI 10.1016/0006-8993(90)90613-G VANDERJAGT B, 1990, EUR J NEUROSCI, V3, P157 VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 Warr W.B., 1992, Springer Handbook of Auditory Research, V1, P410 WHIM MD, 1990, J NEUROSCI, V10, P3313 ZOTTOLI SJ, 1987, BRAIN BEHAV EVOLUT, V30, P143, DOI 10.1159/000118643 NR 48 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 APR PY 1994 VL 74 IS 1-2 BP 231 EP 237 DI 10.1016/0378-5955(94)90191-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500021 PM 8040093 ER PT J AU KLINKE, R MULLER, M RICHTER, CP SMOLDERS, J AF KLINKE, R MULLER, M RICHTER, CP SMOLDERS, J TI PREFERRED INTERVALS IN BIRDS AND MAMMALS - A FILTER RESPONSE TO NOISE SO HEARING RESEARCH LA English DT Article DE PREFERRED INTERVALS; BIRD; MAMMAL; AUDITORY NERVE; HAIR CELL ID AUDITORY-NERVE FIBERS; HAIR-CELLS; COCHLEAR GANGLION; PHASE-LOCKING; CHARACTERISTIC FREQUENCY; DISCHARGE PATTERNS; SINGLE FIBERS; GUINEA-PIG; SPIKE RATE; NEURONS AB Quasi-periodic spontaneous activity (preferred intervals, PIs) has been reported from avian primary auditory afferents. In mammals, PIs have not been reported, as yet. As the length of PIs is close to 1/characteristic frequency, it has been suggested that this type of spontaneous activity indicates particular mechanisms in avian inner ear transduction. However, the present paper shows that pigeon auditory fibres possessing preferred intervals in their spontaneous activity always belong to the most sensitive and the most sharply-tuned fibres recorded. This leads to the assumption that preferred intervals are the response of narrow-band filters to noise. This view is supported by three additional findings: (i) Near-threshold noise provokes PIs in avian fibres that show no spontaneous PIs. (ii) Similarly, PIs can also be evoked in mammalian (gerbil) auditory afferents by low level noise. (iii) Phase-locking of auditory afferents can be achieved by sound stimuli 10-20 dB below rate threshold. It is argued that no conclusions may be drawn from the presence of PIs about the nature of the underlying filter. RP KLINKE, R (reprint author), ZENTRUM PHYSIOL,THEODOR STERN KAI 7,D-60590 FRANKFURT,GERMANY. RI Richter, Claus-Peter/B-4641-2012 CR CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 DENK W, 1992, HEARING RES, V60, P89, DOI 10.1016/0378-5955(92)90062-R EATOCK RA, 1981, J COMP PHYSIOL, V142, P203 FUCHS PA, 1988, J NEUROSCI, V8, P2460 GLEICH O, 1988, HEARING RES, V32, P81, DOI 10.1016/0378-5955(88)90148-7 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GUMMER AW, 1991, HEARING RES, V55, P143, DOI 10.1016/0378-5955(91)90100-N GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIM DO, 1979, J NEUROPHYSIOL, V42, P16 LEWIS ER, 1992, HEARING RES, V63, P7, DOI 10.1016/0378-5955(92)90067-W Manley G. A., 1990, PERIPHERAL HEARING M 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, 1984, NATURWISSENSCHAFTEN, V71, P592, DOI 10.1007/BF01189191 NARINS PM, 1989, J ACOUST SOC AM, V85, P1255, DOI 10.1121/1.397456 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X ROBERTSO.D, 1974, J COMP PHYSIOL, V91, P363, DOI 10.1007/BF00694467 RODE WS, 1978, J NEUROPHYSIOL, V41, P692 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RUGGERO MA, 1973, J NEUROPHYSIOL, V36, P569 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SALVI R, 1993, MIDWINTER RES M ARO SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SCHERMULY L, 1990, J COMP PHYSIOL A, V166, P355 SKOLICH WG, 1973, J ACOUST SOC AM, V54, P283 SMOLDERS JWT, 1993, UNPUB SMOLDERS JWT, 1992, ADV BIOSCI, V83, P197 SUGA N, 1975, J EXP BIOL, V63, P161 TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 VOSSIECK T, 1991, HEARING RES, V56, P93, DOI 10.1016/0378-5955(91)90158-6 WALSH BT, 1972, INT J NEUROSCI, V3, P227 ZWICKER E, 1984, ELEKTROAKUSTIK, P20 NR 36 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 APR PY 1994 VL 74 IS 1-2 BP 238 EP 246 DI 10.1016/0378-5955(94)90192-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500022 PM 8040094 ER PT J AU KNAUTH, M HARTMANN, R KLINKE, R AF KNAUTH, M HARTMANN, R KLINKE, R TI DISCHARGE PATTERN IN THE AUDITORY-NERVE EVOKED BY VOWEL STIMULI - A COMPARISON BETWEEN ACOUSTICAL AND ELECTRICAL-STIMULATION SO HEARING RESEARCH LA English DT Article DE ELECTRICAL STIMULATION; SPEECH; VOWEL; CAT; AUDITORY NERVE ID TEMPORAL RESPONSE PATTERNS; STEADY-STATE VOWELS; FIBERS; REPRESENTATION; SOUNDS; PERCEPTS AB Single channel cochlear implants only transmit the time structure of the electrically coded input signal. All nerve fibres show similar thresholds for monopolar round window stimulation, i.e., activation does not depend on their site of origin. To investigate the fine structure of the firing pattern elicited by stimulation with an analogue coded speech processing system (VIENNA 1-channel implant), cats were electrically stimulated with German steady-state vowels at the round window. Single fibre activity was recorded from primary auditory fibres and period histograms were calculated. The electrically evoked impulse patterns were compared with those from acoustic stimulation with the same vowels. With acoustic stimulation, the response of a fibre depends on the individual characteristic frequency (CF) with regard to the fundamental F0 and the formants F1, F2 and F3 of the vowels, the spontaneous activity of the fibre and the sound level. The evoked firing pattern was used to calculate period histograms, the frequency content of which was analysed by Fourier transformation. With electrical stimulation in the threshold range, an action potential is strongly synchronized to a cathodic peak of the current within one period of F0. With increasing current level 3-5 impulses can be locked to the same period. The timing of the short intervals is determined by the relative refractory period and current peaks (negative or positive) caused by the dominant higher formant F2 or F3. The acoustically evoked patterns art specific for the CF of the neuron and represent the spectral information of the different vowels. The electrically evoked patterns are uniform and only small differences in the short intervals between successive nerve pulses with suprathreshold stimulation may enable the implanted patient to differentiate vowels. C1 ZENTRUM PHYSIOL,D-60590 FRANKFURT,GERMANY. CR DELGUTTE B, 1984, J ACOUST SOC AM, V75, P908, DOI 10.1121/1.390537 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P897, DOI 10.1121/1.390599 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P866, DOI 10.1121/1.390596 DELGUTTE B, 1980, J ACOUST SOC AM, V68, P843, DOI 10.1121/1.384824 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P887, DOI 10.1121/1.390598 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P879, DOI 10.1121/1.390597 EDDINGTON DK, 1978, T AM SOC ART INT ORG, V24, P1 Fourcin A J, 1979, Br J Audiol, V13, P85, DOI 10.3109/03005367909078883 Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HOCHMAIR ES, 1983, ANN NY ACAD SCI, V405, P268, DOI 10.1111/j.1749-6632.1983.tb31640.x Hochmair-Desoyer I. J., 1985, COCHLEAR IMPLANTS, P291 HOCHMAIRDESOYER IJ, 1983, ANN NY ACAD SCI, V405, P295, DOI 10.1111/j.1749-6632.1983.tb31642.x Jayel E., 1990, COCHLEAR IMPLANTS MO, P247 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KIANG NYS, 1980, J ACOUST SOC AM, V68, P830, DOI 10.1121/1.384822 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KLINKE R, 1993, EUROP ARCH OTORHIN S, V2, P83 KNAUTH M, 1993, THESIS FRANKFURT AM MILLER MI, 1984, HEARING RES, V14, P257, DOI 10.1016/0378-5955(84)90054-6 Moxon E.C., 1971, THESIS MIT CAMBRIDGE MUNDIE JR, 1974, CYBERNETICS BIONICS, P292 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 PFINGST BE, 1988, HEARING RES, V34, P243, DOI 10.1016/0378-5955(88)90005-6 SACHS MB, 1979, J ACOUST SOC AM, V66, P470, DOI 10.1121/1.383098 SINEX DG, 1983, J ACOUST SOC AM, V73, P602, DOI 10.1121/1.389007 TYLER RS, 1989, AUDIOLOGY, V28, P301 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 YOUNG ED, 1979, J ACOUST SOC AM, V66, P1381, DOI 10.1121/1.383532 NR 30 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 APR PY 1994 VL 74 IS 1-2 BP 247 EP 258 DI 10.1016/0378-5955(94)90193-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500023 PM 8040095 ER PT J AU KEPPLER, C SCHERMULY, L KLINKE, R AF KEPPLER, C SCHERMULY, L KLINKE, R TI THE COURSE AND MORPHOLOGY OF EFFERENT NERVE-FIBERS IN THE PAPILLA BASILARIS OF THE PIGEON (COLUMBA-LIVIA) SO HEARING RESEARCH LA English DT Article DE PIGEON; PAPILLA BASILARIS; EFFERENT INNERVATION; HRP ID HORSERADISH-PEROXIDASE; HYALINE CELLS; COCHLEA; CHICKEN; INNERVATION; NEURONS AB This paper describes the course and morphology of efferent fibres in an avian cochlea. Horseradish peroxidase stained efferent fibres in the pigeon papilla basilaris were identified by Nomarski optics and camera lucida drawings. There are at least two types of efferent fibres: Large thick fibres take mainly a transversal course and contact short and intermediate hair cells over the free basilar membrane as well as hyaline cells. Large efferent fibres contact both hair cells and hyaline cells. Small thin fibres contact short or intermediate hair cells over the free basilar membrane or tall hair cells over the neural limbus. A physiological consequence of the findings is that efferent activity will concomitantly lead to a contraction of hyaline cells and a hyperpolarzation of hair cells. C1 ZENTRUM PHYSIOL,D-60590 FRANKFURT,GERMANY. CR ADAMS JC, 1977, NEUROSCIENCE, V2, P141, DOI 10.1016/0306-4522(77)90074-4 BOORD RL, 1961, EXP NEUROL, V3, P225, DOI 10.1016/0014-4886(61)90014-0 COLE KS, 1990, EXP BRAIN RES, V82, P585 COTANCHE DA, 1992, J COMP NEUROL, V324, P353, DOI 10.1002/cne.903240306 DRENCKHAHN D, 1991, HEARING RES, V54, P29, DOI 10.1016/0378-5955(91)90133-T EISENSAMER B, 1990, BRAIN PERCEPTION COG, P136 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 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 LEAKEJONES PA, 1982, HEARING RES, V8, P199, DOI 10.1016/0378-5955(82)90075-2 MANLEY GA, 1991, HEARING RES, V56, P211, DOI 10.1016/0378-5955(91)90172-6 SCHERMULY L, 1990, HEARING RES, V48, P69, DOI 10.1016/0378-5955(90)90199-Y SCHWARZ IE, 1981, J COMP NEUROL, V196, P1, DOI 10.1002/cne.901960102 SMOLDERS JWT, 1992, ADV BIOSCI, V83, P197 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 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 VONDURING M, 1985, FORTS ZOOL, V30, P681 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 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 APR PY 1994 VL 74 IS 1-2 BP 259 EP 264 DI 10.1016/0378-5955(94)90194-5 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NF065 UT WOS:A1994NF06500024 PM 8040096 ER PT J AU WIT, HP VANDIJK, P AVAN, P AF WIT, HP VANDIJK, P AVAN, P TI WAVELET ANALYSIS OF REAL EAR AND SYNTHESIZED CLICK-EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; WAVELETS; LATENCY; TIME-FREQUENCY MAP AB Wavelet analysis was performed to obtain time-frequency analyses of click evoked otoacoustic emissions from normal ears and one ear with a high-frequency hearing loss; mainly to introduce this relatively new method and to show its potentials for emission analysis. The same analysis was then used to obtain time-frequency decompositions of synthesized emissions. It was found that the introduction of a slightly irregular frequency to place relation for the inner ear yielded synthetic results that were remarkably similar to those obtained from real ears. C1 FAC MED CLERMONT FERRAND, BIOPHYS LAB, CLERMONT FERRAND, FRANCE. RP WIT, HP (reprint author), UNIV HOSP GRONINGEN, INST AUDIOL, POB 30001, 9700 RB GRONINGEN, NETHERLANDS. RI Van Dijk, Pim/E-8019-2010 OI Van Dijk, Pim/0000-0002-8023-7571 CR ANDERSON SD, 1980, HEARING RES, V2, P273, DOI 10.1016/0378-5955(80)90063-5 ARNEODO A, 1991, RES NOTE AP, V20, P286 BRAY PJ, 1989, THESIS U LONDON Chui C.K., 1992, INTRO WAVELETS KEMP DT, 1990, EAR HEARING, V11, P93 KOLLMEIER B, 1989, COCHLEAR MECH STRUCT, P331 MEYER Y, 1991, WAVELETS APPLICATION PATTERSON RD, 1992, ADV BIOSCI, V83, P429 SCHROEDE.MR, 1973, J ACOUST SOC AM, V53, P429, DOI 10.1121/1.1913339 SHERA CA, 1994, IN PRESS J ACOUST SO STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 SUN HW, 1993, ABSTR ASS RES OT Wit HP, 1983, MECHANICS HEARING, P101 ZWICKER E, 1990, HEARING RES, V44, P209, DOI 10.1016/0378-5955(90)90081-Y NR 14 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 MAR PY 1994 VL 73 IS 2 BP 141 EP 147 DI 10.1016/0378-5955(94)90228-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400001 PM 8188542 ER PT J AU RODDY, J HUBBARD, AE MOUNTAIN, DC XUE, S AF RODDY, J HUBBARD, AE MOUNTAIN, DC XUE, S TI EFFECTS OF ELECTRICAL BIASING ON ELECTRICALLY-EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE COCHLEA; OTOACOUSTIC EMISSIONS; HAIR CELLS; ENDOLYMPHATIC POTENTIAL; ELECTROMOTILITY; VOLTAGE-DEPENDENT CONDUCTANCES ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; RECEPTOR POTENTIALS; MEMBRANE; INNER AB Electrically-evoked otoacoustic emissions were produced using a 10 mu A, 750 Hz AC current plus a biasing DC current in the range of +/- 10 mu A. Concurrently, a 1643 Hz tonal stimulation was delivered to the eardrum. At low sound levels, negative DC current increased the emission while positive DC current reduced the emission. Such findings are reasonably explained by a negative-feedback model of cochlear function. At high sound levels, negative DC current reduces the emission, while positive current has little effect. These data can be accounted for by voltage-dependent length changes shown to occur in isolated outer hair cells, with the additional requirement that voltage-dependent K+ channels in outer hair cells reduce the effectiveness of positive DC current in changing membrane potential. C1 BOSTON UNIV, DEPT BIOMED ENGN, BOSTON, MA 02215 USA. BOSTON UNIV, DEPT OTOLARYNGOL, BOSTON, MA 02215 USA. BOSTON UNIV, DEPT ELECT COMP & SYST ENGN, BOSTON, MA 02215 USA. CR ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1992, AUDITORY PHYSL PERCE GITTER AH, 1992, HEARING RES, V60, P13, DOI 10.1016/0378-5955(92)90053-P 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 MILLS DM, 1993, 16TH MIDW M ASS RES, P79 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 MOUNTAIN DC, 1989, HEARING RES, V41, P101, DOI 10.1016/0378-5955(89)90003-8 MOUNTAIN DC, 1980, HEARING RES, V3, P231, DOI 10.1016/0378-5955(80)90049-0 MOUNTAIN DC, 1983, MECHANICS HEARING MOUNTAIN DC, 1986, NEUROBIOLOGY HEARING, P77 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 NR 17 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 MAR PY 1994 VL 73 IS 2 BP 148 EP 154 DI 10.1016/0378-5955(94)90229-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400002 PM 8188543 ER PT J AU OGAWA, K MCLAREN, J SCHACHT, J AF OGAWA, K MCLAREN, J SCHACHT, J TI EFFECT OF AGING ON MYOINOSITOL AND PHOSPHOINOSITIDE METABOLISM IN THE COCHLEAR AND VESTIBULAR SENSORY EPITHELIA OF THE RAT SO HEARING RESEARCH LA English DT Article DE AGING; INOSITOL PHOSPHATES; PHOSPHOINOSITIDES; MYOINOSITOL; 2ND MESSENGER; COCHLEA; VESTIBULE; RAT, FISCHER-344 ID AGE-RELATED IMPAIRMENT; PHOSPHATIDYLINOSITOL TURNOVER; DEPENDENT CHANGES; SENESCENT RATS; BRAIN; HYDROLYSIS; PHOSPHATES; CALCIUM; RELEASE; SYSTEM AB Neurotransmission and transmembrane signaling ari among the cellular mechanisms affected in the aging nervous system. In the inner ear, the phosphoinositide second messenger cascade is of particular interest as a target of the aging process. In both the cochlear (CSE) and vestibular sensory epithelia (VSE), the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PtdInsP(2)) to the second messenger inositol 1,4,5-trisphosphate (InsP(3)) is coupled to muscarinic cholinergic and P-2y purinergic receptors and may be linked to calcium homeostasis. The present study compared the turnover of phosphoinositides (PtdInsPs), receptor-mediated release of inositol phosphates (InsPs), and concentrations of endogenous myo-inositol in the CSE and VSE of young (3 months) and aged (24 months) Fischer-344 rats. In the aged rat, there was a significant increase in [H-3]inositol incorporation (per mass of protein) into PtdInsPs plus InsPs in both sensory epithelia while the protein content remained unchanged. In contrast, no age-dependent differences were found when pre-labeled [H-3]PtdInsPs were 'chased' with non-radiolabeled myo-inositol indicating that the turnover of these lipids was unaffected. The cholinergic receptor agonist carbamylcholine and the P-2 purinergic receptor agonist adenosine 5'-O-(3-thiotriphosphate) stimulated the release of [H-3]InsPs two- to six-fold in both organs. This agonist-stimulated release of [H-3]InsPs (per mass of protein) was significantly higher in aged animals. However, when the same stimulation was expressed as per cent of control values, there was no age-dependent difference. Finally, the concentration of endogenous myo-inositol decreased by 44% in the aged CSE and by 24% in the aged VSE. In contrast, levels of added myo-[H-3]inositol were higher in aged tissues. These results suggest that the increased labeling of PtdInsPs and InsPs in the aged CSE and VSE is a consequence of the increased specific radioactivity of the myo-[H-3]inositol precursor pool. The activity of the phosphoinositide second messenger pathway thus appears unchanged. However, a decreased myo-inositol content may contribute to age-dependent pathology in these tissues. myo-Inositol is an organic osmolyte and volume regulator. Changes in osmotic pressure or turgor of hair cells could alter micromechanical coupling on the basilar membrane and vestibular epithelium causing pathophysiological changes in sensory transduction. C1 UNIV MICHIGAN, KRESGE HEARING RES INST, ANN ARBOR, MI 48109 USA. CR BARRITT GJ, 1987, NEUROBIOL AGING, V8, P359 BASTYR EJ, 1990, AM J MED, V88, P601, DOI 10.1016/0002-9343(90)90525-I BERRIDGE MJ, 1993, NATURE, V361, P315, DOI 10.1038/361315a0 BERRIDGE MJ, 1983, BIOCHEM J, V212, P473 BONETTI AC, 1987, NEUROENDOCRINOLOGY, V45, P123, DOI 10.1159/000124714 BORST SE, 1990, MECH AGEING DEV, V56, P275, DOI 10.1016/0047-6374(90)90088-W BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1990, LECT NOTES BIOMATH, V87, P52 BURNETT DM, 1990, MOL PHARMACOL, V37, P566 BURNETT DM, 1990, J PHARMACOL EXP THER, V255, P1265 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F CREWS FT, 1986, PSYCHOPHARMACOL BULL, V22, P775 DEAN NM, 1989, ANAL BIOCHEM, V183, P199, DOI 10.1016/0003-2697(89)90468-5 DULON D, 1990, J NEUROSCI, V10, P1388 FULOP T, 1989, FEBS LETT, V245, P249, DOI 10.1016/0014-5793(89)80231-5 GARCIAPEREZ A, 1990, HYPERTENSION, V16, P595 GIBSON GE, 1987, NEUROBIOL AGING, V8, P329, DOI 10.1016/0197-4580(87)90072-8 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HENZI V, 1992, NEUROSCIENCE, V46, P251, DOI 10.1016/0306-4522(92)90049-8 HOFFMAN DW, 1988, BRAIN RES, V40, P366 IRVINE RF, 1992, FASEB J, V6, P3085 ISHIKAWA Y, 1988, BIOCHIM BIOPHYS ACTA, V968, P203, DOI 10.1016/0167-4889(88)90009-2 JOSEPH JA, 1990, BRAIN RES, V537, P40, DOI 10.1016/0006-8993(90)90337-B KARGACIN ME, 1987, J CHROMATOGR, V393, P454, DOI 10.1016/S0021-9673(01)94244-X KURIAN P, 1992, NEUROBIOL AGING, V13, P521, DOI 10.1016/0197-4580(92)90081-8 LAITINEN JT, 1992, NEUROENDOCRINOLOGY, V55, P492, DOI 10.1159/000126162 MAJERUS PW, 1992, ANNU REV BIOCHEM, V61, P225, DOI 10.1146/annurev.bi.61.070192.001301 MIYAMOTO A, 1989, GEN PHARMACOL, V20, P647, DOI 10.1016/0306-3623(89)90101-8 MOSCONAAMIR E, 1989, BIOCHEMISTRY-US, V28, P7130, DOI 10.1021/bi00443a052 MUNDY W, 1991, LIFE SCI, V49, P97 NALEPA I, 1989, NEUROSCI LETT, V107, P195, DOI 10.1016/0304-3940(89)90816-1 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 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 OGAWA K, 1993, ABST ASS RES OT, V16, P91 OGAWA K, 1993, HEARING RES, V69, P207, DOI 10.1016/0378-5955(93)90109-E OHNUKI T, 1991, JPN J PHARMACOL, V57, P483, DOI 10.1254/jjp.57.483 OOSTEVELD WF, 1983, HEARING BALANCE ELDE, P354 PAREDES A, 1992, AM J PHYSIOL, V263, pC1282 Schuknecht H., 1974, PATHOLOGY EAR, P388 SHERMAN WR, 1989, INOSITOL LIPIDS CELL, P39 SIMPSON GV, 1985, BRAIN RES, V348, P28, DOI 10.1016/0006-8993(85)90355-5 STOKES CE, 1983, BIOCHIM BIOPHYS ACTA, V753, P136, DOI 10.1016/0005-2760(83)90108-X TANDON P, 1991, PHARMACOL BIOCHEM BE, V38, P861, DOI 10.1016/0091-3057(91)90254-Y UNDIE AS, 1992, NEUROBIOL AGING, V13, P505, DOI 10.1016/0197-4580(92)90079-D WELLS WW, 1989, INOSITOL LIPIDS CELL, P207 WILLOTT JF, 1991, AGING AUDITORY SYSTE, P56 WILLSKARP M, 1991, LIFE SCI, V49, P1039, DOI 10.1016/0024-3205(91)90305-U NR 49 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 1994 VL 73 IS 2 BP 155 EP 162 DI 10.1016/0378-5955(94)90230-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400003 PM 8188544 ER PT J AU BACKOFF, PM CASPARY, DM AF BACKOFF, PM CASPARY, DM TI AGE-RELATED-CHANGES IN AUDITORY BRAIN-STEM RESPONSES IN FISCHER-344 RATS - EFFECTS OF RATE AND INTENSITY SO HEARING RESEARCH LA English DT Article DE AGING; BRAIN-STEM EVOKED POTENTIALS; AUDITORY BRAIN-STEM; RAT, FISCHER 344 ID INFERIOR COLLICULUS NEURONS; CNS STRUCTURAL ELEMENTS; PURE-TONE AUDIOGRAM; STEM RESPONSE; EVOKED-POTENTIALS; AMINO-ACIDS; GABA; GLYCINE; YOUNG; THRESHOLDS AB Age-related changes in auditory brainstem responses (ABR) observed in humans may reflect peripheral or centrally-occurring deficits. In clinical studies, high stimulus repetition rates have been used to improve the identification of central auditory pathology. In the present study, interactions between stimulus level and repetition rate were examined in the Fischer 344 rat, an animal demonstrating both peripheral hearing loss and changes in auditory brainstem neurochemistry with age. Monaural threshold and standard P;BR morphology were determined in young (3-6 months) and old (20-23 months) rats using clicks at 10/s, with intensity varied from 0-100 dB. The effects of increasing stimulus repetition rate on ABR latency and morphology were evaluated at 60-100 dB using rates of 5, 10, 20, and 40/s. Old animals demonstrated elevated ABR click thresholds, reflected by shifts in the latency-intensity curves. With increased stimulation rates, aged rats exhibited prolonged Wave 4 and 5 latencies, especially at the highest intensities, with degraded waveform morphology. Peak amplitudes were generally reduced in old rats, irrespective of rate or stimulus level. These findings suggest auditory processing is altered in aged animals, while the selective effects of rate increases on Waves 4 and 5 provide supporting evidence for possible involvement of the central auditory generators of these components. RP BACKOFF, PM (reprint author), SO ILLINOIS UNIV, SCH MED, DEPT PHARMACOL, 801 N RUTLEDGE, SPRINGFIELD, IL 62702 USA. CR BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P563, DOI 10.1007/BF00964919 Boorman G.A., 1990, PATHOLOGY FISCHER RA BURKARD R, 1990, AUDIOLOGY, V29, P146 Campbell D. G., 1992, Society for Neuroscience Abstracts, V18, P841 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 Caspary DM, 1991, NEUROBIOLOGY HEARING, P141 CASPARY DM, 1993, NATO ADV SCI INST SE, V239, P239 CHAMBERS RD, 1992, HEARING RES, V58, P123, DOI 10.1016/0378-5955(92)90122-4 CHURCH MW, 1984, ELECTROEN CLIN NEURO, V59, P328, DOI 10.1016/0168-5597(84)90050-9 CHURCH MW, 1987, ELECTROEN CLIN NEURO, V67, P570, DOI 10.1016/0013-4694(87)90060-5 COATS AC, 1977, ARCH OTOLARYNGOL, V103, P605 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 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 FINLAYSON PG, 1993, NEUROBIOL AGING, V14, P127, DOI 10.1016/0197-4580(93)90088-S FUJIKAWA SM, 1977, J AM AUDITORY SOC, V3, P147 FUNAI H, 1983, AUDIOLOGY, V22, P9 GORGA MP, 1985, EAR HEARING, V6, P105, DOI 10.1097/00003446-198503000-00008 HERMAN GE, 1977, J GERONTOL, V32, P187 HUNTER C, 1989, BRAIN RES, V482, P247, DOI 10.1016/0006-8993(89)91187-6 HYDE ML, 1985, AUDITORY BRAINSTEM R, P133 JERGER J, 1980, ARCH OTOLARYNGOL, V106, P387 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X KEITHLEY EM, 1990, HEARING RES, V49, P169, DOI 10.1016/0378-5955(90)90103-V KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 KITO S, 1990, J HISTOCHEM CYTOCHEM, V38, P1725 KONKLE DF, 1977, J SPEECH HEAR RES, V20, P108 LONDON ED, 1981, J NEUROCHEM, V37, P217, DOI 10.1111/j.1471-4159.1981.tb05311.x MAURIZI M, 1982, SCAND AUDIOL, V11, P213, DOI 10.3109/01050398209087470 McGeer E.G., 1975, NEUROBIOL AGING, P287 MILBRANDT JC, 1993, UNPUB NEUROBIOL AGIN MOORE MJ, 1983, J NEUROSCI, V3, P237 NEWTON EH, 1992, HEARING RES, V60, P73, DOI 10.1016/0378-5955(92)90060-Z POLLAK GD, 1993, HEARING RES, V65, P99, DOI 10.1016/0378-5955(93)90205-F ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 SHAW NA, 1988, PROG NEUROBIOL, V31, P19, DOI 10.1016/0301-0082(88)90021-4 SIMPSON GV, 1985, BRAIN RES, V348, P28, DOI 10.1016/0006-8993(85)90355-5 SMITH CB, 1980, BRAIN, V103, P351, DOI 10.1093/brain/103.2.351 STAPELLS DR, 1990, AUDIOLOGY, V29, P262 VANDERDRIFT JFC, 1987, AUDIOLOGY, V26, P1 VATER M, 1992, J COMP PHYSIOL A, V171, P541 Willott J. F., 1991, AGING AUDITORY SYSTE ZHAO W, 1990, BRIT J AUDIOL, V24, P193 NR 46 TC 51 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 MAR PY 1994 VL 73 IS 2 BP 163 EP 172 DI 10.1016/0378-5955(94)90231-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400004 PM 8188545 ER PT J AU KOTECHA, B RICHARDSON, GP AF KOTECHA, B RICHARDSON, GP TI OTOTOXICITY IN-VITRO - EFFECTS OF NEOMYCIN, GENTAMICIN, DIHYDROSTREPTOMYCIN, AMIKACIN, SPECTINOMYCIN, NEAMINE, SPERMINE AND POLY-L-LYSINE SO HEARING RESEARCH LA English DT Article DE EAR, INTERNAL; COCHLEA; HAIR CELLS; AMINOGLYCOSIDE ANTIBIOTICS; OTOTOXICITY ID AMINOGLYCOSIDE ANTIBIOTICS; PHOSPHOLIPASE-C; HAIR-CELLS; POLYPHOSPHOINOSITIDES; CALCIUM; METABOLISM; KANAMYCIN; CULTURES; COCHLEA; INVITRO AB The effects that the aminoglycoside-aminocyclitol antibiotics amikacin, dihydrostreptomycin, gentamicin, neomycin, and spectinomycin, the neomycin fragment neamine, and the polybasic compounds spermine and poly-L-lysine, have on outer hair cells in cochlear cultures prepared from the early post-natal mouse have been assessed using both scanning and transmission electron microscopy (SEM and TEM). The antibiotics were used at concentrations ranging from 0.25-1.0 mM, spermine from 10 mu M to 3.0 mM, and poly-L-lysine from 0.05-2 mu M. Qualitative assessment of apical surface damage allows the antibiotics to be ranked in the following order: neomycin > gentamicin > dihydrostreptomycin > amikacin > neamine > spectinomycin. At a concentration of 1 mM spectinomycin is essentially non-toxic and the effects of neamine are marginal. Poly-L-lysine and spermine also cause surface damage, with poly-L-lysine being substantially more toxic than any of the antibiotics, and spermine ranking, on the basis of SEM observations, between dihydrostreptomycin and amikacin. TEM indicates that although all toxic compounds cause damage to the apical surface of the hair cell, only neomycin, poly-L-lysine and spermine induce the formation of whorls of tightly packed membrane resembling myelin within the apical surface lesions to any great extent. Apical-surface changes induced by dihydrostreptomycin and amikacin are simply large distensions of the cell filled with cytoplasmic organelles of normal appearance. Although the effects of the aminoglycoside antibiotics are largely limited to the apical surface of the cell, poly-L-lysine induces complete necrosis of the cell, and spermine causes a dramatic increase in cytoplasmic electron density and condensation of the nuclear chromatin. C1 UNIV SUSSEX,SCH BIOL SCI,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. ROYAL SUSSEX CTY HOSP,DEPT EAR NOSE & THROAT,BRIGHTON,E SUSSEX,ENGLAND. CR BROWN RD, 1978, ANNU REV PHARMACOL, V18, P233, DOI 10.1146/annurev.pa.18.040178.001313 Brummett RE, 1982, AMINOGLYCOSIDES MICR, P419 BRUMMETT RE, 1978, J ANTIMICROB CHEMOTH, V4, P73 CARLIER E, 1980, ARCH OTO-RHINO-LARYN, V226, P129, DOI 10.1007/BF00455127 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FORGE A, 1993, J NEUROCYTOL, V22, P854, DOI 10.1007/BF01186357 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HUANG MY, 1989, MED TOXICOL ADV DRUG, V4, P452 HUANG MY, 1990, BIOCHEM PHARMACOL, V40, pR11, DOI 10.1016/0006-2952(90)90077-X KAHLMETER G, 1984, J ANTIMICROB CHEMOTH, V13, P9 KALOYANIDES GJ, 1980, KIDNEY INT, V18, P571, DOI 10.1038/ki.1980.175 KOSSL M, 1990, HEARING RES, V44, P217, DOI 10.1016/0378-5955(90)90082-Z KOTECHA B, 1993, UNPUB THESIS U SUSSE Lenoir M, 1983, Acta Otolaryngol Suppl, V405, P1 LIPSKY JJ, 1982, J PHARMACOL EXP THER, V220, P287 LODHI S, 1976, BIOCHIM BIOPHYS ACTA, V426, P781, DOI 10.1016/0005-2736(76)90147-4 LODHI S, 1980, BIOCHEM PHARMACOL, V29, P597, DOI 10.1016/0006-2952(80)90382-2 MARCHE P, 1983, J PHARMACOL EXP THER, V227, P415 ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x Pujol R, 1986, Acta Otolaryngol Suppl, V429, P29 REYNOLDS ES, 1963, J CELL BIOL, V17, P208, DOI 10.1083/jcb.17.1.208 Riché G., 1989, Cahiers de la Recherche-Développement, P57 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 RYBAK LP, 1986, ANNU REV PHARMACOL, V26, P79 RYBAK LP, 1986, NEUROBIOLOGY HEARING, P441 SCHIBECI A, 1977, BIOCHEM PHARMACOL, V26, P1769, DOI 10.1016/0006-2952(77)90344-6 SCHWERTZ DW, 1984, J PHARMACOL EXP THER, V231, P48 TAKADA A, 1982, J PHARM SCI, V71, P1410, DOI 10.1002/jps.2600711226 TRANBAHUY P, 1981, AMINOGLYCOSIDE OTOTO, P81 WANG BM, 1984, BIOCHEM PHARMACOL, V33, P3257, DOI 10.1016/0006-2952(84)90087-X YUNG MW, 1987, ANN OTO RHINOL LARYN, V96, P455 NR 32 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 MAR PY 1994 VL 73 IS 2 BP 173 EP 184 DI 10.1016/0378-5955(94)90232-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400005 PM 7514588 ER PT J AU HEFFNER, RS HEFFNER, HE CONTOS, C KEARNS, D AF HEFFNER, RS HEFFNER, HE CONTOS, C KEARNS, D TI HEARING IN PRAIRIE DOGS - TRANSITION BETWEEN SURFACE AND SUBTERRANEAN RODENTS SO HEARING RESEARCH LA English DT Article DE AUDIOGRAM; RODENT; SQUIRREL; CYNOMYS; INFRASOUND; LOCALIZATION ID MOUSE ONYCHOMYS-LEUCOGASTER; SOUND LOCALIZATION; SPALAX-EHRENBERGI; MOLE-RAT; SPECTRAL CUES AB Behavioral audiograms were determined for four black-tailed and one white-tailed prairie dogs (Cynomys ludovicianus and C. leucurus) using a conditioned avoidance procedure. The hearing of black-tailed prairie dogs ranges from 29 Hz to 26 kHz and that of the white-tailed prairie dog from 44 Hz to 26 kHz (at sound pressure levels of 60 dB). Both species have good low-frequency hearing, especially black-tailed prairie dogs which can hear as low as 4 Hz and are more sensitive than any other rodent yet tested at frequencies below 63 Hz. In contrast, prairie dogs are relatively insensitive in their midrange and have poor high-frequency hearing. It is suggested that the reduced midrange sensitivity and high-frequency hearing are related to their adaptation to an underground lifestyle with its reduced selective pressure for sound localization. In this respect they appear to be intermediate between the more exclusively subterranean rodents (such as gophers and mole rats) and surface dwellers (such as chinchillas and kangaroo rats). RP HEFFNER, RS (reprint author), UNIV TOLEDO,DEPT PSYCHOL,TOLEDO,OH 43606, USA. CR BRONCHTI G, 1989, J COMP NEUROL, V284, P253, DOI 10.1002/cne.902840209 CARLILE S, 1987, HEARING RES, V31, P111, DOI 10.1016/0378-5955(87)90117-1 FLEISCHER G, 1978, CELL BIOL, V55, P5 Hartenberger J.-L., 1985, EVOLUTIONARY RELATIO, P1 HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 HEFFNER HE, 1985, J COMP PSYCHOL, V99, P275, DOI 10.1037//0735-7036.99.3.275 HEFFNER HE, 1994, HEARING RES, V73, P244, DOI 10.1016/0378-5955(94)90240-2 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 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, 1988, J COMP PSYCHOL, V102, P66, DOI 10.1037/0735-7036.102.1.66 HEFFNER RS, 1990, HEARING RES, V46, P239, DOI 10.1016/0378-5955(90)90005-A HEFFNER RS, 1985, J MAMMAL, V66, P745, DOI 10.2307/1380801 HEFFNER RS, 1991, HEARING RES, V52, P13, DOI 10.1016/0378-5955(91)90183-A HETH G, 1986, EXPERIENTIA, V42, P1287, DOI 10.1007/BF01946426 KOAY G, 1993, ABSTR ASS RES OT, V16, P49 MUSICANT AD, 1984, J ACOUST SOC AM, V75, P1195, DOI 10.1121/1.390770 NARINS PM, 1992, J COMP PHYSIOL A, V170, P13 PETERSON EA, 1974, J AUD RES, V14, P227 RAPHAEL Y, 1991, J COMP NEUROL, V314, P367, DOI 10.1002/cne.903140211 RICE JJ, 1992, HEARING RES, V58, P132, DOI 10.1016/0378-5955(92)90123-5 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 WARING GH, 1969, AM MIDL NAT, V83, P167 Webster D.B., 1984, CONTRIBUTIONS TO SENSORY PHYSIOLOGY, V8, P161 WEBSTER DOUGLAS B., 1962, PHYSIOL ZOOL, V35, P248 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 1994 VL 73 IS 2 BP 185 EP 189 DI 10.1016/0378-5955(94)90233-X PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400006 PM 8188546 ER PT J AU PENNER, MJ BRAUTH, SE JASTREBOFF, PJ AF PENNER, MJ BRAUTH, SE JASTREBOFF, PJ TI COVARIATION OF BINAURAL, CONCURRENTLY-MEASURED SPONTANEOUS OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE BINAURAL SOAES; EFFERENT SYSTEM; MIDDLE-EAR MUSCLES ID HUMAN EARS; FREQUENCY; STIMULATION; OSCILLATORS; NEURONS AB Simultaneous recordings of binaural spontaneous otoacoustic emissions (SOAEs) were made for 2 female subjects. For SOAEs below about 3.6 kHz measured within a testing session, the frequencies of nearby monaural and binaural SOAEs tended to move in tandem, whereas widely separated SOAEs did not. Across many testing sessions spanning a menstrual cycle, all monaural and binaural SOAE frequencies shifted in tandem. Possible mechanisms consistent with these results are discussed. C1 UNIV MARYLAND, SCH MED, BALTIMORE, MD 21201 USA. RP PENNER, MJ (reprint author), UNIV MARYLAND, DEPT PSYCHOL, COLL PK, MD 20742 USA. CR BELL A, 1992, HEARING RES, V58, P91, DOI 10.1016/0378-5955(92)90012-C BIALEK W, 1984, PHYS LETT A, V104, P173, DOI 10.1016/0375-9601(84)90371-2 BURNS EM, 1984, HEARING RES, V16, P271, DOI 10.1016/0378-5955(84)90116-3 BURNS EM, 1993, HEARING RES, V67, P117, DOI 10.1016/0378-5955(93)90239-W HAGGERTY HS, 1990, ASS RES OT ABSTR, V268, P233 KEEFE DH, 1990, LECT NOTES BIOMATH, V87, P194 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 LONG GR, 1991, J ACOUST SOC AM, V89, P1201, DOI 10.1121/1.400651 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 PENNER MJ, 1994, IN PRESS ARCH OTOLAR PENNER MJ, 1993, HEARING RES, V68, P229, DOI 10.1016/0378-5955(93)90126-L TALMADGE CL, 1991, J ACOUST SOC AM, V89, P2391, DOI 10.1121/1.400958 WHITEHEAD ML, 1991, HEARING RES, V53, P269, DOI 10.1016/0378-5955(91)90060-M WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 1970, ANSI5361969 AM NAT S NR 20 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 1994 VL 73 IS 2 BP 190 EP 194 DI 10.1016/0378-5955(94)90234-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400007 PM 8188547 ER PT J AU FERMIN, CD LEE, DH MARTIN, D AF FERMIN, CD LEE, DH MARTIN, D TI POSTEMBEDDING TEM SIGNAL-TO-NOISE RATIO OF S-100 SO HEARING RESEARCH LA English DT Article DE INNER EAR; S-100; IMMONUGOLD; NERVE; EPOXY; PLASTIC ID SCHWANN-CELLS; S100 PROTEIN AB We assessed the reactivity of purified S-100 antiserum in immune-electron microscopy by counting the number of gold particles per mu m(2) over inner ear tissues embedded in different media. Sections containing predominantly Schwann's cell cytoplasm and nucleus, afferent fiber axoplasm and myelin sheath of chick cochleae were reacted with anti-S-100 IgG, an antibody to a calcium binding protein of neuronal tissues, then labeled with anti-IgG-gold conjugate. This investigation was conducted because previously published procedures, unmodified, did not yield acceptable results. Preparation of all specimens was identical. Only the medium (PolyBed 812(R), Araldite(R) or Spurr(R) epoxies; and LR White(R), LR Gold(R) or Lowicryl(R) plastics) was changed. The medium was made the changing variable because antigens available in post-embedding immune-electron microscopy are decreased by heat, either used and/or released during polymerization of the embedding medium. The results indicate that: (a) none of the embedding media above provided optimal signal-to-noise ratio for all parts of the nerve stained in the same section; (b) aggregation of gold particles over cells was highest in embedding media with high background labeling over areas devoid of tissue (noise); (c) aggregation occurred randomly throughout both cellular and acellular regions; and (d) particles aggregated less and were distributed more evenly in tissues from media yielding good ultrastructural integrity. RP FERMIN, CD (reprint author), TULANE UNIV,SCH MED,DEPT PATHOL & LAB MED,1430 TULANE AVE,RM 6720,NEW ORLEANS,LA 70112, USA. CR Beesley J. E., 1989, COLLOIDAL GOLD NEW P BENDAYAN M, 1989, COLLOIDAL GOLD PRINC, P146 BHATTACHARYYA A, 1992, J NEUROBIOL, V23, P451, DOI 10.1002/neu.480230410 DONATO R, 1989, J NEUROCHEM, V53, P566, DOI 10.1111/j.1471-4159.1989.tb07371.x ENESTROM S, 1990, STAIN TECHNOL, V65, P263 HAGEN SJ, 1990, J ELECTRON MICR TECH, V16, P37, DOI 10.1002/jemt.1060160106 HAYASHI K, 1991, ACTA NEUROPATHOL, V81, P657 Igarashi S, 1991, Acta Otolaryngol Suppl, V481, P163 JANAS MS, 1991, ANAT EMBRYOL, V184, P549, DOI 10.1007/BF00942577 KANITAKIS J, 1991, ANTICANCER RES, V11, P635 KLIGMAN D, 1988, TRENDS BIOCHEM SCI, V13, P437, DOI 10.1016/0968-0004(88)90218-6 Lewis ER, 1985, VERTEBRATE INNER EAR MARSHAK DR, 1990, PROG BRAIN RES, V86, P169 MATA M, 1990, J NEUROCYTOL, V19, P432, DOI 10.1007/BF01188409 MUTASA HCF, 1989, HISTOCHEM J, V21, P249, DOI 10.1007/BF01757177 POLAK JM, 1992, ELECTRON MICROSCOPIC ROTH J, 1986, PROTEIN AGOLD TECHNI SILVER MM, 1987, ULTRASTRUCT PATHOL, V11, P693 TAATJES DJ, 1990, J HISTOCHEM CYTOCHEM, V38, P233 TSUCHIDA T, 1991, BRAIN RES, V564, P164, DOI 10.1016/0006-8993(91)91368-B VANELDIK LJ, 1991, BRAIN RES, V542, P280, DOI 10.1016/0006-8993(91)91579-P NR 21 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 1994 VL 73 IS 2 BP 195 EP 202 DI 10.1016/0378-5955(94)90235-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400008 PM 8188548 ER PT J AU TINLING, SP CHOLE, RA AF TINLING, SP CHOLE, RA TI APICAL COCHLEAR NERVE EXPOSED TO PERILYMPH IN THE GERBIL AND RAT SO HEARING RESEARCH LA English DT Article DE COCHLEA; MODIOLUS; BONE; LINING CELLS ID GUINEA-PIG; RADIAL COMMUNICATION; CEREBROSPINAL-FLUID; SCALAE; TRACER; FLOW AB There is considerable controversy regarding the origin and composition of perilymph in the scala vestibuli and scala tympani and the barriers and transport mechanisms between them. To elucidate the anatomical separation between perilymph and the extracellular fluid which surrounds the cochlear nerve in Mongolian gerbils (Meriones unguiculatus) and Sprague Dawley rats (Rattus rattus) we examined the modiolus, osseous spiral lamina and the bone of the perilymphatic scalae using light and electron microscopy. Although the cochlear nerve, spiral ganglion and their extracellular fluid are separated from perilymph by the bone of the modiolus in the middle and basal turns, no bone separates these neural structures from perilymph in the apical turn in the two species examined. Instead, the spiral ganglion and axonal elements of the apical turn were covered by a continuation of the bone lining cell layer of the scala tympani. Gaps between lining cells appeared to provide direct communication between the perilymphatic fluid and the extracellular fluid investing the cochlear nerve. Various authors have described openings in modiolar bone in both the scala vestibuli and the scala tympani. While the bone and cellular covering of the modiolus in the basal middle turns of the cochlea is not presumed to be a complete barrier to fluid exchange between the two scalae and the modiolar canal it can be expected to impose some limitation on the rate of passive diffusion. Therefore our data indicates that in the apical turn of the Mongolian gerbil and Sprague-Dawley rat there may be a more significant communication between perilymph and the extracellular fluid and neural elements of the apical modiolar canal than previously reported. RP TINLING, SP (reprint author), UNIV CALIF DAVIS,SCH MED,DEPT OTOLARYNGOL,1515 NEWTON COURT,ROOM 209,DAVIS,CA 95616, USA. CR CHOLE RA, 1993, IN PRESS ANN OTOL RH DUCKERT LG, 1978, OTOLARYNG HEAD NECK, V86, P434 DUVALL AJ, 1972, ANN OTO RHINOL LARYN, V81, P705 HARA A, 1989, HEARING RES, V42, P265 KELLERHALS B, 1979, ACTA OTO-LARYNGOL, V87, P370, DOI 10.3109/00016487909126435 Kelly DE, 1984, BAILEYS TXB MICROSCO KUCUK B, 1991, J ELECTRON MICROSC, V40, P193 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, 1988, PHYSL EAR, P341 SALT AN, 1991, HEARING RES, V56, P29, DOI 10.1016/0378-5955(91)90150-8 SANTI PA, 1988, PHYSL EAR, P173 SCHEIBE F, 1985, HEARING RES, V17, P61, DOI 10.1016/0378-5955(85)90131-5 SCHEIBE F, 1984, ARCH OTO-RHINO-LARYN, V240, P43, DOI 10.1007/BF00464343 SCHNIEDE.EA, 1974, ANN OTO RHINOL LARYN, V83, P76 SCHUKNECHT H, 1974, PATHOLOGY EAR, P143 STERKERS O, 1988, PHYSIOL REV, V68, P1083 NR 17 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 1994 VL 73 IS 2 BP 203 EP 208 DI 10.1016/0378-5955(94)90236-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400009 PM 8188549 ER PT J AU MASTERTON, RB GRANGER, EM GLENDENNING, KK AF MASTERTON, RB GRANGER, EM GLENDENNING, KK TI ROLE OF ACOUSTIC STRIAE IN HEARING - MECHANISM FOR ENHANCEMENT OF SOUND DETECTION IN CATS SO HEARING RESEARCH LA English DT Article DE DORSAL ACOUSTIC STRIA; INTERMEDIATE ACOUSTIC STRIA; VENTRAL ACOUSTIC STRIA; TRAPEZOID BODY; COCHLEAR NUCLEUS; DESCENDING SYSTEM ID DORSAL COCHLEAR NUCLEUS; PHYSIOLOGICAL-RESPONSE PROPERTIES; LATERAL SUPERIOR OLIVE; HORSERADISH-PEROXIDASE; BRAIN-STEM; IMMUNOCYTOCHEMICAL LOCALIZATION; EFFERENT PROJECTIONS; INFERIOR COLLICULUS; GUINEA-PIG; CELLS AB We report the results of behavioral studies in cats conducted first, to demonstrate the presence of a monaural mechanism for the enhancement of signal to noise; and then to examine the necessity or sufficiency of the acoustic striae for this mechanism. The results show that cats do indeed have a monaural mechanism for enhancing the detection of tones in co-located background noise for noise levels at least as high as 60 dB SPL. The ablation-behavior results show that surgical section of the dorsal (DAS) and most of the intermediate (IAS) striae has no measurable effect on this mechanism. In sharp contrast, even partial section of the trapezoid body results in a profound and permanent deficit and this deficit is not accounted for by hearing loss alone. It is concluded that the ascending and descending fibers in the dorsal and intermediate acoustic striae are neither necessary nor sufficient for enhancing the detection of salient sounds in a noisy environment while the ascending or descending fibers in the ventral acoustic stria are sufficient and probably necessary. RP MASTERTON, RB (reprint author), FLORIDA STATE UNIV,DEPT PSYCHOL,PROGRAM PSYCHOBIOL & NEUROSCI,R-54,TALLAHASSEE,FL 32306, USA. CR ADAMS JC, 1976, J COMP NEUROL, V170, P107, DOI 10.1002/cne.901700108 ALTSCHULER RA, 1986, BRAIN RES, V369, P316, DOI 10.1016/0006-8993(86)90542-1 CANT NB, 1982, J COMP NEUROL, V212, P313, DOI 10.1002/cne.902120308 CANT NB, 1978, NEUROSCIENCE, V3, P1003, DOI 10.1016/0306-4522(78)90120-3 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 CASSEDAY JH, 1975, J NEUROPHYSIOL, V38, P842 de Olmos JS, 1981, NEUROANATOMICAL TRAC, P117 DIAMOND IT, 1969, BRAIN RES, V15, P305, DOI 10.1016/0006-8993(69)90160-7 ELVERLAND HH, 1977, EXP BRAIN RES, V27, P397 FERNANDE.C, 1967, J COMP NEUROL, V131, P371, DOI 10.1002/cne.901310307 GLENDENNING KK, 1984, ANAT REC, V208, pA62 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GLENDENNING KK, 1986, ASS RES OTOLARYNGOL, V9, P38 GLENDENNING KK, 1990, OTOLARYNGOL HEAD NEC, V103, P190 GLENDENNING KK, 1983, J NEUROSCI, V3, P1521 Godfrey DA, 1988, AUDITORY PATHWAY, P107 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GODFREY DA, 1978, J HISTOCHEM CYTOCHEM, V26, P118 GODFREY DA, 1984, J NEUROCHEM, V42, P1450, DOI 10.1111/j.1471-4159.1984.tb02808.x GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 Heffner R. S., 1990, COMP PERCEPTION, VI, P285 HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 Held H, 1893, ARCH ANAT PHYSL ANAT, V3+4, P201 JANE JA, 1965, J COMP NEUROL, V125, P165, DOI 10.1002/cne.901250203 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 KLINKE R, 1969, PFLUG ARCH EUR J PHY, V306, P165, DOI 10.1007/BF00586883 LIVINGSTON RB, 1959, HDB PHYSL NEUROPHYSI, V1, P741 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MANIS PB, 1983, J NEUROPHYSIOL, V50, P1156 MAST TE, 1973, BRAIN RES, V62, P61, DOI 10.1016/0006-8993(73)90619-7 MASTERTO.B, 1967, J NEUROPHYSIOL, V30, P341 MASTERTON RB, 1988, J NEUROPHYSIOL, V60, P1841 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 MORELANDGRANGER E, 1986, ASS RES OTOLARYNGOL, V9, P45 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 NUDO RJ, 1984, CONTRIBUTIONS SENSOR, V8, P79 OSEN KK, 1972, J COMP NEUROL, V144, P355, DOI 10.1002/cne.901440307 OSEN KK, 1980, NEURONAL MECH HEARIN, P119 OSEN KK, 1969, BRAIN RES, V16, P165, DOI 10.1016/0006-8993(69)90092-4 PALMER AR, 1982, HEARING RES, V7, P305, DOI 10.1016/0378-5955(82)90042-9 PFALZ REINHARD K. J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1472, DOI 10.1121/1.1918372 PICKLES JO, 1973, J NEUROPHYSIOL, V36, P1131 PICKLES JO, 1976, J NEUROPHYSIOL, V39, P394 Pickles JO, 1988, INTRO PHYSL HEARING RASMUSSEN GL, 1964, NEUROLOGICAL ASPECTS, P1 Rasmussen G.L., 1960, NEURAL MECHANISMS AU, P105 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 ROSE JE, 1949, ELECTROEN CLIN NEURO, V1, P391, DOI 10.1016/0013-4694(49)90212-6 RYUGO DK, 1985, J COMP NEUROL, V242, P381, DOI 10.1002/cne.902420307 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 SMITH PH, 1987, J COMP NEUROL, V266, P360, DOI 10.1002/cne.902660305 SPANGLER KM, 1987, J COMP NEUROL, V259, P452, DOI 10.1002/cne.902590311 SYKA J, 1988, AUDITORY PATHWAY STR, P279 THOMPSON AM, 1987, BRAIN RES, V421, P382, DOI 10.1016/0006-8993(87)91313-8 TOBIAS J, 1970, F MODERN AUDITORY TH, V1 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3031, DOI 10.1016/0306-4522(82)90228-7 VONMONAKOW C, 1891, NERVENKRANK, V22, P1 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 Warr W. B., 1981, NEUROANATOMICAL TRAC, P207 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WENTHOLD RJ, 1986, BRAIN RES, V380, P7, DOI 10.1016/0006-8993(86)91423-X STARR A, 1968, J NEUROPHYSIOL, V31, P549 WICKESBERG RE, 1988, J COMP NEUROL, V268, P389, DOI 10.1002/cne.902680308 YOUNG ED, 1982, HEARING RES, V6, P153, DOI 10.1016/0378-5955(82)90051-X YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 NR 68 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 MAR PY 1994 VL 73 IS 2 BP 209 EP 222 DI 10.1016/0378-5955(94)90237-2 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400010 PM 8188550 ER PT J AU VANNETTEN, SM KARLSSON, KK KHANNA, SM FLOCK, A AF VANNETTEN, SM KARLSSON, KK KHANNA, SM FLOCK, A TI EFFECTS OF QUININE ON THE MECHANICAL FREQUENCY-RESPONSE OF THE CUPULA IN THE FISH LATERAL-LINE SO HEARING RESEARCH LA English DT Article DE QUININE; HAIR CELLS; MECHANICS; CUPULAR MOTION; FISH LATERAL LINE ID OUTER HAIR-CELLS; TRANSDUCTION; EXCITATION AB Quinine induces changes in the motion of the cupula in the lateral line canal of the African knife-fish in response to sinusoidal water movements. Two different phases in the action of quinine on the cupular frequency response can be discerned. In the first phase the best frequency, i.e., the frequency at which the cupular vibratory displacement is maximal in response to constant-amplitude sinusoidal canal fluid displacement, shifts toward higher frequencies. During this phase, lasting about 70-100 min, the best frequency increases by a factor between 1.3 and 1.5. In the second phase, during roughly the following 90 min, the best frequency decreases gradually to a value 0.3-0.5 times that observed before the application of quinine. C1 HUDDINGE UNIV HOSP,DEPT AUDIOL,HUDDINGE,SWEDEN. COLUMBIA UNIV,COLL PHYS & SURG,NEW YORK,NY. KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM,SWEDEN. RP VANNETTEN, SM (reprint author), UNIV GRONINGEN,DEPT BIOPHYS,NIJENBORGH 4,GRONINGEN,NETHERLANDS. CR ALVAN G, 1991, BRIT J CLIN PHARMACO, V31, P409 ALVAN G, 1989, LIFE SCI, V45, P751, DOI 10.1016/0024-3205(89)90095-7 DENTON EJ, 1983, PROC R SOC SER B-BIO, V218, P1, DOI 10.1098/rspb.1983.0023 DIJKGRAAF S, 1963, BIOL REV, V38, P51, DOI 10.1111/j.1469-185X.1963.tb00654.x FALBEHANSEN J, 1941, THESIS HELSINKI Flock A., 1965, ACTA OTO LARYNG ST S, V199, P1 Flock A., 1971, HDB SENSORY PHYSIOLO, V1, P396 HAWKINS JE, 1976, HDB SENSORY PHYSL, V3, P707 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 KARLSSON KK, 1990, T ROY SOC TROP MED H, V84, P765, DOI 10.1016/0035-9203(90)90069-Q 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 KELLY JP, 1991, J MORPHOL, V207, P23, DOI 10.1002/jmor.1052070105 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P43 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P51 KOEGEL L, 1985, AM J OTOL, V6, P190 Koester C J, 1989, Acta Otolaryngol Suppl, V467, P27 KORESE ABA, 1989, MECHANOSENSORY LATER, P265 KOSSL M, 1990, HEARING RES, V44, P217, DOI 10.1016/0378-5955(90)90082-Z Lund D T, 1989, Acta Otolaryngol Suppl, V467, P77 MATSUURA S, 1971, JPN J PHYSIOL, V21, P579 MELIER F, 1843, MEM ACAD MED PARIS, V10, P722 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 OSWALD RL, 1978, COMP BIOCHEM PHYS C, V60, P19, DOI 10.1016/0306-4492(78)90021-7 POHLMAN AG, 1922, P SOC EXP BIOL MED, V20, P140 POWELL RD, 1972, P HELM SOC WASH, V39, P331 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 SUAREZKU.G, 1973, J PHARMACOL EXP THER, V186, P562 VANNETTEN SM, 1994, UNPUB MECHANICS CUPU VANNETTEN SM, 1991, J ACOUST SOC AM, V89, P310, DOI 10.1121/1.400512 VANNETTEN SM, 1990, 13TH MIDW RES M 1990, P341 VANNETTEN SM, 1987, HEARING RES, V29, P55, DOI 10.1016/0378-5955(87)90205-X VANNETTEN SM, 1989, COCHLEAR MECH STRUCT, P47 Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 NR 35 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 1994 VL 73 IS 2 BP 223 EP 230 DI 10.1016/0378-5955(94)90238-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400011 PM 8188551 ER PT J AU ROSEN, S BAKER, RJ AF ROSEN, S BAKER, RJ TI CHARACTERIZING AUDITORY FILTER NONLINEARITY SO HEARING RESEARCH LA English DT Article DE FREQUENCY SELECTIVITY; NOTCHED-NOISE MASKING; EXCITATION PATTERNS; AUDITORY FILTERS; AUDITORY NONLINEARITY ID BASILAR-MEMBRANE; FREQUENCY-SELECTIVITY; LEVEL; ASYMMETRY; THRESHOLD; MASKING; HEARING; GROWTH AB An important aspect of auditory nonlinearity is that psychoacoustically measured auditory filters broaden as the level at which they are measured increases. However, it is not yet clear whether the change in filter shape is controlled primarily by the level of the probe or that of the masker. We have therefore developed a new method for fitting filter shapes to notched-noise data in which filter parameters depend explicitly on signal level (either probe, or masker). By applying this technique to a set of notched-noise data in which both fixed-probe and fixed-masker paradigms have been used at a range of levels, we have been able to show that models in which filter parameters depend on probe level are considerably more successful than models in which filter parameters depend upon masker level. The results from this new procedure have enabled us to describe tl;e nonlinear changes in auditory filter shape at 2 kHz with only five parameters. Also discussed are the implications of these findings for the generation of excitation patterns and for the computational implementation of simple, yet reasonably realistic nonlinear auditory filters whose shape depends on their output. C1 UCL, DEPT PHONET & LINGUIST, LONDON NW1 2HE, ENGLAND. RI Rosen, Stuart/A-7875-2008 OI Rosen, Stuart/0000-0002-4893-8669 CR BAKER RJ, 1992, SPEECH HEARING LANGU, V6, P1 CARNEY LH, 1993, J ACOUST SOC AM, V93, P401, DOI 10.1121/1.405620 DARLING AM, 1991, SPEECH HEARING LANGU, V5, P43 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T GOLDSTEIN JL, 1988, WORKING MODELS HUMAN, P19 GOLDSTEIN JL, 1990, HEARING RES, V49, P39, DOI 10.1016/0378-5955(90)90094-6 LEEK MR, 1993, J ACOUST SOC AM, V94, P3127, DOI 10.1121/1.407218 LUTFI RA, 1984, J ACOUST SOC AM, V76, P739, DOI 10.1121/1.391260 MOORE BCJ, 1987, HEARING RES, V28, P209, DOI 10.1016/0378-5955(87)90050-5 PATTERSON RD, 1980, J ACOUST SOC AM, V67, P229, DOI 10.1121/1.383732 PATTERSON RD, 1991, 2 AUD CONN TECHN SPE PATTERSON RD, 1982, J ACOUST SOC AM, V72, P1788, DOI 10.1121/1.388652 Patterson RD, 1986, FREQUENCY SELECTIVIT, P123 PATTERSON RD, 1988, 2341 APPL PSYCH UN R 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, 1989, WORK PROGR, V3, P189 ROSEN S, 1992, J ACOUST SOC AM, V92, P773, DOI 10.1121/1.403946 ROSEN S, 1992, ADV BIOSCI, V83, P171 ROSOWSKI JJ, 1991, J ACOUST SOC AM, V90, P124, DOI 10.1121/1.401306 RUGGERO MA, 1992, ADV BIOSCI, V83, P85 SHAW EAG, 1974, J ACOUST SOC AM, V56, P1848, DOI 10.1121/1.1903522 WEBER DL, 1977, J ACOUST SOC AM, V62, P424, DOI 10.1121/1.381542 NR 23 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 MAR PY 1994 VL 73 IS 2 BP 231 EP 243 DI 10.1016/0378-5955(94)90239-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MZ714 UT WOS:A1994MZ71400012 PM 8188552 ER PT J AU FISCHER, FP AF FISCHER, FP TI QUANTITATIVE TEM ANALYSIS OF THE BARN OWL BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE BIRD; COCHLEA; HAIR CELL; INNERVATION; BARN OWL ID OUTER HAIR-CELLS; INNER-EAR; SERIAL SECTIONS; AVIAN COCHLEA; CAT COCHLEA; TYTO-ALBA; INNERVATION; ACTIN; CHICKEN; LENGTH AB The morphology of the barn owl's basilar papilla was quantitatively analyzed using TEM methods. The hair-cell (HC) parameters studied in the basal two-thirds of the papilla are remarkably constant. This large portion represents an extended high frequency area, or fovea [Koppl et al. (1993) J. Comp. Physiol. A 171, 695-704]. In the apical third of the papilla, in contrast, these parameters change regularly, as they do in other avian species. The HC in the most neural position remain morphologically more similar along the entire length of the papilla than do neighbouring cell rows. In the behaviourally most important frequency range (4-9 kHz), the afferent innervation of these neural HC is very dense and is reminiscent of the situation in mammals. Differences in HC morphology also indicate a specialization of the extreme apex of the papilla in the barn owl. Avian HC morphology is not correlated with a specific place along the basilar papilla but rather with the best frequency. Based on the body of recent quantitative morphological data on avian HC structure, a modified definition of HC types in birds is suggested (while keeping introduced terms): THC (tall hair cells) are defined as air those HC with afferent (and normally also efferent) innervation. SHC (short hair cells) are the (more specialized) HC without afferent innervation; obviously their function is restricted to the papilla itself. RP FISCHER, FP (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,D-85747 GARCHING,GERMANY. CR BOORD RL, 1969, NY ACAD SOC, V169, P186 BRIX J, 1992, ELECTRICAL MECHANOEL, P15 CHANDLER JP, 1984, J COMP NEUROL, V222, P506, DOI 10.1002/cne.902220405 DANNHOF BJ, 1993, HEARING RES, V66, P8, DOI 10.1016/0378-5955(93)90255-Y DANNHOF BJ, 1991, NATURWISSENSCHAFTEN, V78, P570, DOI 10.1007/BF01134454 FIRBAS W, 1983, HEARING RES, V10, P109, DOI 10.1016/0378-5955(83)90021-7 FISCHER FP, 1991, HEARING RES, V53, P281, DOI 10.1016/0378-5955(91)90061-D 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 FRISHKOPF LS, 1983, HEARING RES, V12, P393, DOI 10.1016/0378-5955(83)90008-4 GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLTON T, 1983, SCIENCE, V222, P508, DOI 10.1126/science.6623089 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KONISHI M, 1973, AM SCI, V61, P414 KOPPL C, 1993, J COMP PHYSIOL A, V171, P695, DOI 10.1007/BF00213066 KOPPL C, 1993, S BIOPHYSICS HAIR CE LAVIGNEREBILLARD M, 1985, J COMP NEUROL, V238, P340, DOI 10.1002/cne.902380308 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1980, HEARING RES, V3, P189, DOI 10.1016/0378-5955(80)90046-5 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1992, EVOLUTIONARY BIOL HE MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MOISEFF A, 1989, J COMP PHYSIOL A, V164, P629, DOI 10.1007/BF00614505 PARK JC, 1984, ACTA OTO-LARYNGOL, V98, P72, DOI 10.3109/00016488409107536 PAYNE RS, 1971, J EXP BIOL, V54, P435 PICARD DA, 1990, TALL HAIR CELLS CHIC, P384 PUJOL R, 1991, LENGTH OHCS CORRELAT, P125 SCHWARTZKOPFF J., 1960, BIOL ZENTRALBL, V79, P607 SMITH CA, 1985, HEARING RES, V17, P237, DOI 10.1016/0378-5955(85)90068-1 SMOLDERS JWT, 1992, ADV BIOSCI, V83, P197 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 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 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 VONDURING M, 1985, FORTS ZOOL, V30, P681 Winter P., 1963, Zeitschrift fuer Morphologie und Oekologie der Tiere, V52, P365, DOI 10.1007/BF00408568 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZIMMERMANN U, 1989, DYNAMICS PLASTICITY, P286 NR 41 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 FEB PY 1994 VL 73 IS 1 BP 1 EP 15 DI 10.1016/0378-5955(94)90277-1 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100001 PM 8157497 ER PT J AU SLEPECKY, NB SAVAGE, JE AF SLEPECKY, NB SAVAGE, JE TI EXPRESSION OF ACTIN ISOFORMS IN THE GUINEA-PIG ORGAN OF CORTI - MUSCLE ISOFORMS ARE NOT DETECTED SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; OUTER HAIR CELLS; ACTIN; ACTIN ISOFORMS ID OUTER HAIR-CELLS; INNER-EAR; SKELETAL-MUSCLE; GAMMA-ACTIN; F-ACTIN; PROTEINS; FILAMENTS; MOTILITY; IDENTIFICATION; REORGANIZATION AB The specificity of antibodies to actin was assayed by use of immunoblots and histological sections of control tissues enriched for each of six different isoforms. On immunoblots, all antibodies stained at most one band of protein in most of the control materials, with a molecular weight of approximately 43 kDa. Their pattern of staining of muscle and nonmuscle tissues indicated their isoform specificity. On tissue sections, immunocytochemical staining demonstrated cellular and subcellular localization of the different isoforms. Once characterized with regard to specificity, these antibodies were used to probe actin in the guinea pig organ of Corti. None of the four muscle isoforms of actin were found in either immunoblots or tissue sections of the organ of Corti. Both beta- and gamma-cytoplasmic isoforms of actin were present in hair cells and supporting cells. This leaves open to investigation the role which cytoplasmic actins play in these cells of the organ of Corti. RP SLEPECKY, NB (reprint author), SYRACUSE UNIV,INST SENSORY RES,DEPT BIOENGN & NEUROSCI,SYRACUSE,NY 13244, USA. CR Angelborg C, 1972, Acta Otolaryngol Suppl, V301, P49 BOHNE BA, 1976, HEARING DAVIS ESSAYS, P85 BRETSCHER A, 1991, CURR OPIN STRUCT BIO, V1, P281, DOI 10.1016/0959-440X(91)90074-4 CARLISLE L, 1988, HEARING RES, V33, P201, DOI 10.1016/0378-5955(88)90033-0 CRAIG SW, 1983, CELL MOTIL CYTOSKEL, V3, P449 DENOFRIO D, 1989, J CELL BIOL, V109, P191, DOI 10.1083/jcb.109.1.191 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1982, HEARING RES, V6, P75 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GARRELS JI, 1976, CELL, V9, P793, DOI 10.1016/0092-8674(76)90142-2 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HOLLEY MC, 1990, J CELL SCI, V96, P283 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 NIEDZIELSKI AS, 1992, HEARING RES, V59, P250, DOI 10.1016/0378-5955(92)90121-3 ORMAN S, 1983, HEARING RES, V11, P261, DOI 10.1016/0378-5955(83)90061-8 OTEY CA, 1987, J CELL BIOCHEM, V34, P113, DOI 10.1002/jcb.240340205 OTEY CA, 1988, CELL MOTIL CYTOSKEL, V9, P337, DOI 10.1002/cm.970090406 PARDO JV, 1983, CELL, V32, P1093, DOI 10.1016/0092-8674(83)90293-3 PINDER JC, 1983, J CELL BIOL, V96, P768, DOI 10.1083/jcb.96.3.768 RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 RUBENSTEIN PA, 1977, P NATL ACAD SCI USA, V74, P120, DOI 10.1073/pnas.74.1.120 RUBENSTEIN PA, 1981, ARCH BIOCHEM BIOPHYS, V210, P598, DOI 10.1016/0003-9861(81)90226-5 SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 SCHEVZOV G, 1992, J CELL BIOL, V117, P775, DOI 10.1083/jcb.117.4.775 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 SLEPECKY N, 1986, HEARING RES, V22, P307, DOI 10.1016/0378-5955(86)90107-3 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SLEPECKY N, 1983, HEARING RES, V10, P359, DOI 10.1016/0378-5955(83)90098-9 SLEPECKY N, 1982, CELL TISSUE RES, V224, P15, DOI 10.1007/BF00217262 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 SLEPECKY NB, 1990, J ELECTRON MICR TECH, V15, P280, DOI 10.1002/jemt.1060150307 SLEPECKY NB, 1992, HEARING RES, V57, P201, DOI 10.1016/0378-5955(92)90152-D STOSSEL TP, 1985, ANNU REV CELL BIOL, V1, P353 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 TILNEY LG, 1980, J CELL BIOL, V86, P244, DOI 10.1083/jcb.86.1.244 ULFENDAHL M, 1987, ACTA PHYSIOL SCAND, V130, P521, DOI 10.1111/j.1748-1716.1987.tb08171.x VANDEKERCKHOVE J, 1981, EUR J BIOCHEM, V113, P595, DOI 10.1111/j.1432-1033.1981.tb05104.x VANDEKERCKHOVE J, 1978, J MOL BIOL, V126, P783, DOI 10.1016/0022-2836(78)90020-7 WEAVER SP, 1993, BRAIN RES BULL, V31, P225, DOI 10.1016/0361-9230(93)90029-B WOLOSEWICK J, 1982, BIOL CELL, V44, P85 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 48 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 FEB PY 1994 VL 73 IS 1 BP 16 EP 26 DI 10.1016/0378-5955(94)90278-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100002 PM 8157502 ER PT J AU NILLES, R JARLEBARK, L ZENNER, HP HEILBRONN, E AF NILLES, R JARLEBARK, L ZENNER, HP HEILBRONN, E TI ATP-INDUCED CYTOPLASMIC [CA2+]] INCREASES IN ISOLATED COCHLEAR OUTER HAIR-CELLS - INVOLVED RECEPTOR AND CHANNEL MECHANISMS SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; EXTRACELLULAR ATP; ATP(4-); G-PROTEIN; P-2-PURINERGIC RECEPTOR SUBTYPES; CYTOPLASMIC [CA2+] ID GUINEA-PIG COCHLEA; CHOLINERGIC SYNAPTIC VESICLES; CULTURED CHICK MYOTUBES; EXTRACELLULAR ATP; INTRACELLULAR CALCIUM; RESPONSES; MEMBRANE; MOTILITY; HEARING; MUSCLE AB Outer hair cells (OHC) of the mammalian cochlea are thought to preprocess the sound signal by active movements, which can be induced by electrical or chemical stimulation, e.g. depolarization evoked by high [K+] or increased cytoplasmic [Ca2+]. Extracellular ATP has been found to induce cytoplasmic [Ca2+] increases in OHC but involved mechanisms have not been elucidated. Cytoplasmic [Ca2+] was measured in non-enzymatically isolated single OHC using Fura-2 microspectrometry. Results, using ATP/derivatives and other P-2-purinergic receptor (P(2)R) ligands, as well as Ca2+-channel blockers and pertussis toxin, revealed several signal transduction; pathways that increase cytoplasmic [Ca2+] in OHC: a P-2-purinergic receptor (P(2)R) G-protein - effector (phospholipase C or an ion channel) system and a voltage-dependent Ca2+ channel. Agonist potency studies denote a pattern analogous to that found in skeletal muscle, i.e. ATP-alpha-S > ATP = 2-methyl-S-ATP much greater than ADP > alpha,beta-methylene-ATP, but no activation by ADP beta F or UTP, leaving a choice of P-2y or P(2z)R subtypes. The latter possibility gained strength from calculations showing that up to 8% of ATP may have formed the P(2z)R agonist ATP(4-) in the experimental medium. Experiments in Ca2+-free medium and with pertussis toxin revealed that the main Ca2+ source was intracellular. Pertussis toxin did not affect [Ca2+] increase induced by carbachoI. Acetylcholine, administered a few seconds before ATP, did not affect total cytoplasmic [Ca2+] increases. Induced cytoplasmic [Ca2+] increases were high enough (> 500 nM at 50 mu M ATP/derivatives) to hyperpolarize the OHC membrane by opening K+-channels and decreased little with time. Artifacts may have been caused by the sustained Ca2+ levels, e.g. activation of proteases by the high cytoplasmic [Ca2+]. Similar events in vivo may have pathological consequences. C1 STOCKHOLM UNIV,DEPT NEUROCHEM & NEUROTOXICOL,S-10691 STOCKHOLM,SWEDEN. UNIV TUBINGEN,DEPT OTOLARYNGOL,HEARING RES SECT,W-7400 TUBINGEN,GERMANY. CR ABOOD LG, 1962, AM J PHYSIOL, V202, P469 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BROOKS SPJ, 1992, ANAL BIOCHEM, V201, P119, DOI 10.1016/0003-2697(92)90183-8 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BURNSTOCK G, 1983, BRIT J PHARMACOL, V79, P907 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 COCKCROFT S, 1980, BIOCHEM J, V188, P789 DOWDALL MJ, 1974, BIOCHEM J, V140, P1 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1991, NEUROREPORT, V2, P69, DOI 10.1097/00001756-199102000-00001 DULON D, 1990, J NEUROSCI, V10, P1388 EDWARDS FA, 1992, NATURE, V359, P144, DOI 10.1038/359144a0 ELMOATASSIM C, 1992, BIOCHIM BIOPHYS ACTA, V1134, P31, DOI 10.1016/0167-4889(92)90025-7 ERIKSSON H, 1989, BIOCHEM BIOPH RES CO, V159, P878, DOI 10.1016/0006-291X(89)92190-6 EVANS RJ, 1992, NATURE, V357, P503, DOI 10.1038/357503a0 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GITTER AH, 1992, HEARING RES, V60, P13, DOI 10.1016/0378-5955(92)90053-P GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 GORDON JL, 1986, BIOCHEM J, V233, P309 GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440 HAGGBLAD J, 1987, THESIS STOCKHOLM U S HAGGBLAD J, 1987, NEUROSCI LETT, V74, P199, DOI 10.1016/0304-3940(87)90149-2 HAGGBLAD J, 1988, FEBS LETT, V235, P133, DOI 10.1016/0014-5793(88)81248-1 HOURANI SMO, 1988, EUR J PHARMACOL, V147, P131, DOI 10.1016/0014-2999(88)90642-5 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HUME RI, 1988, J PHYSIOL-LONDON, V406, P503 IKEDA K, 1991, ORL J OTO-RHINO-LARY, V53, P78 ISRAEL M, 1980, J NEUROCHEM, V34, P923, DOI 10.1111/j.1471-4159.1980.tb09667.x LUSTIG KD, 1992, BIOCHEM J, V284, P733 MALIK MN, 1983, J BIOL CHEM, V258, P8955 NAKAGAWA T, 1991, NEUROSCI LETT, V125, P81, DOI 10.1016/0304-3940(91)90136-H PLINKERT PK, 1991, HEARING RES, V53, P123, DOI 10.1016/0378-5955(91)90219-Y PLINKERT PK, 1990, HEARING RES, V44, P25, DOI 10.1016/0378-5955(90)90019-L PLINKERT PK, 1989, LARYN RHINOL OTOL, V65, P450 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 SMITH CA, 1978, EVOKED ELECT ACTIVIT, P3 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 TASHIRO T, 1978, EUR J BIOCHEM, V90, P479, DOI 10.1111/j.1432-1033.1978.tb12627.x WELFORD LA, 1987, EUR J PHARMACOL, V141, P123, DOI 10.1016/0014-2999(87)90418-3 ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 ZENNER HP, 1986, HNO, V34, P133 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 ZIMMET J, 1993, NUCLEOS NUCLEOT, V12, P1, DOI 10.1080/07328319308016190 NR 50 TC 39 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 1994 VL 73 IS 1 BP 27 EP 34 DI 10.1016/0378-5955(94)90279-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100003 PM 8157503 ER PT J AU BRUNDIN, L RUSSELL, I AF BRUNDIN, L RUSSELL, I TI TUNED PHASIC AND TONIC MOTILE RESPONSES OF ISOLATED OUTER HAIR-CELLS TO DIRECT MECHANICAL STIMULATION OF THE CELL BODY SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELLS; COCHLEA; MOTILITY; MECHANOSENSITIVE; FREQUENCY TUNING ID GUINEA-PIG COCHLEA; HEARING ORGAN; DISPLACEMENT RESPONSE; MOUSE COCHLEA; ION CHANNELS; ELECTROMOTILITY; SENSITIVITY; POTENTIALS; COMPONENT; CORTI AB Guinea pig outer hair cells (OHCs) isolated from the two apical turns of the cochlea and firmly attached to a suction pipette, were subjected to the stimulus of the near-field (particle) displacements of a calibrated oscillating fluid jet aimed at the lateral cell walls. The longitudinal length changes of the OHCs in response to stimulation, in a direction orthogonal to that of the fluid jet, were recorded by a photodiode array. The response had two components; a phasic length change which followed the frequency of the particle displacement of the jet cycle by cycle, and a tonic length change which took several milliseconds to develop depending on the magnitude of the mechanical stimulus. When the hair cell changed length the lateral walls of the OHC moved in antiphase, moving apart during shortening and together during lengthening. With increased stimulus level the phasic response grew in proportion to the stimulus magnitude and began to saturate at the highest stimulus levels, while the tonic response grew in proportion to the square of the stimulus magnitude. Both the direction of the tonic length change and the phase of the phasic component could alter with the level of stimulation. Isolevel and isoresponse-frequency functions of both the tonic and phasic length changes revealed that both response types were tuned to similar resonant frequencies (RF) between 150 and 2500 Hz. The phase of the phasic length change began to lag at frequencies just below the RF, lagged by about 90 degrees at the RF and lagged by a further 90 degrees at frequencies above RF. The frequency response properties of the OHCs closely corresponded to those of a damped, forced, mechanical resonance. The tonic response disappeared and the phasic response was reduced at low-levels as a consequence of intense mechanical stimulation and with time. C1 UNIV SUSSEX,SCH BIOL SCI,BRIGHTON BN1 9QG,ENGLAND. KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM,SWEDEN. CR ART JJ, 1986, J PHYSIOL-LONDON, V371, pP18 ASHMORE JF, 1987, J PHYSIOL-LONDON, V385, P207 Bendat J., 1971, RANDOM DATA ANAL MEA 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 BROWNELL WE, 1990, MECH BIOPHYSICS HEAR, P52 BRUNDIN L, 1991, NEUROSCI LETT, V128, P77, DOI 10.1016/0304-3940(91)90763-J BRUNDIN L, 1992, NEUROSCIENCE, V49, P607, DOI 10.1016/0306-4522(92)90230-Y BRUNDIN L, 1992, HEARING RES, V58, P175, DOI 10.1016/0378-5955(92)90126-8 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V315, P317 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V315, P317 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DALMAYR C, 1985, ACUSTICA, V59, P67 DANCER A, 1980, HEARING RES, V2, P191, DOI 10.1016/0378-5955(80)90057-X DING JP, 1991, HEARING RES, V56, P19, DOI 10.1016/0378-5955(91)90149-4 DODSON HC, 1987, HEARING RES, V31, P65, DOI 10.1016/0378-5955(87)90214-0 EVANS BN, 1988, COCHLEAR MECHANISMS, P163 EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 GULLEY RL, 1977, ANAT REC, V189, P109, DOI 10.1002/ar.1091890108 HOLLEY M C, 1991, Journal of Cell Biology, V115, p345A HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 IWASA KH, 1991, NEUROSCI LETT, V133, P171, DOI 10.1016/0304-3940(91)90562-8 KALINEC F, 1992, P NATL ACAD SCI USA, V89, P8671, DOI 10.1073/pnas.89.18.8671 KEMP DT, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KOSSL M, 1992, J NEUROSCI, V12, P1575 KROS CJ, 1992, P ROY SOC B-BIOL SCI, V249, P185, DOI 10.1098/rspb.1992.0102 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X MORRIS CE, 1990, J MEMBRANE BIOL, V113, P93, DOI 10.1007/BF01872883 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PUJOL R, 1991, AUDITORY PHYSL PERCE, P44 RUSSELL IJ, 1989, HEARING RES, V43, P55, DOI 10.1016/0378-5955(89)90059-2 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1992, HEARING RES, V247, P97 SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 ZWICKER E, 1988, COCHLEAR MECH, P359 ZWISLOCKI JJ, 1988, COCHLEAR MECHANISMS, P163 NR 50 TC 33 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 1994 VL 73 IS 1 BP 35 EP 45 DI 10.1016/0378-5955(94)90280-1 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100004 PM 8157504 ER PT J AU WHEELER, EF BOTHWELL, M SCHECTERSON, LC VONBARTHELD, CS AF WHEELER, EF BOTHWELL, M SCHECTERSON, LC VONBARTHELD, CS TI EXPRESSION OF BDNF AND NT-3 MESSENGER-RNA IN HAIR-CELLS OF THE ORGAN OF CORTI - QUANTITATIVE-ANALYSIS IN DEVELOPING RATS SO HEARING RESEARCH LA English DT Article DE TROPHIC FACTOR; COCHLEA; DEVELOPMENT; IN SITU HYBRIDIZATION; NEUROTROPHIN; HAIR CELL; COCHLEAR GANGLION ID NERVE GROWTH-FACTOR; DEVELOPING INNER-EAR; AFFINITY NGF RECEPTOR; COCHLEAR INNERVATION; IMMUNOHISTOCHEMICAL LOCALIZATION; EFFERENT INNERVATION; MESSENGER-RNAS; NEURONS; EMBRYOS; BRAIN AB Brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are synthesized by inner and outer hair cells of the developing organ of Corti. This raises the possibility that the reorganization of cochlear innervation patterns that occurs postnatally may be influenced by changing levels of neurotrophin expression. To determine if differential expression of BDNF or NT-3 in the inner and outer hair cells correlates with the reorganization of afferent and efferent innervation, we used in situ hybridization techniques to quantify relative levels of transcript biosynthesis in hair cells of developing rats. BDNF transcripts decreased in inner and outer hair cells from E17 to insignificant levels at P4. NT-3 expression was high at E17 in inner and outer hair cells, decreased in outer hair cells by E21, in inner hair cells by P1, remained low during the first postnatal week and was increased in the adult, The decreases in expression of both neurotrophins at birth precede the retraction of afferent nerve terminals from outer hair cells. BDNF and NT-3 transcription decreases substantially in outer hair cells between E21 and P4 when efferent innervation begins, indicating target biosynthesis of these neurotrophins is not likely to be instrumental in efferent target selection. C1 UNIV WASHINGTON,SCH MED,DEPT PHYSIOL & BIOPHYS SI 40,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,VIRGINIA MERRILL BLOEDEL HEARING RES CTR RL 30,SEATTLE,WA 98195. CR ABE H, 1991, ACTA OTO-LARYNGOL, V111, P691, DOI 10.3109/00016489109138401 ANGERER LM, 1981, NUCLEIC ACIDS RES, V9, P2819, DOI 10.1093/nar/9.12.2819 BIANCHI LM, 1991, DEV BRAIN RES, V64, P167, DOI 10.1016/0165-3806(91)90221-4 BOTHWELL M, 1991, CELL, V65, P915, DOI 10.1016/0092-8674(91)90540-F CHANDLER CE, 1984, J BIOL CHEM, V259, P6882 COLE KS, 1992, BRAIN RES, V575, P223 COX KH, 1984, DEV BIOL, V101, P485, DOI 10.1016/0012-1606(84)90162-3 DESPRES G, 1991, HEARING RES, V52, P157, DOI 10.1016/0378-5955(91)90195-F DESPRES G, 1988, NEUROSCI LETT, V85, P5, DOI 10.1016/0304-3940(88)90418-1 ERNFORS P, 1992, EUR J NEUROSCI, V4, P1140, DOI 10.1111/j.1460-9568.1992.tb00141.x FRITZSCH B, 1993, HEARING RES, V65, P51, DOI 10.1016/0378-5955(93)90200-K GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 HAFIDI A, 1990, J COMP NEUROL, V300, P153, DOI 10.1002/cne.903000202 HEMPSTEAD BL, 1991, NATURE, V350, P678, DOI 10.1038/350678a0 HEUER JG, 1990, DEV BIOL, V137, P287, DOI 10.1016/0012-1606(90)90255-H LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEFEBVRE PP, 1992, ACTA OTO-LARYNGOL, V112, P288 LEFEBVRE PP, 1991, ACTA OTO-LARYNGOL, V111, P304, DOI 10.3109/00016489109137392 LENOIR M, 1980, ANAT EMBRYOL, V160, P253, DOI 10.1007/BF00305106 MELTON DA, 1984, NUCLEIC ACIDS RES, V12, P7035, DOI 10.1093/nar/12.18.7035 MURPHY RA, 1993, NEUROSCIENCE, V13, P2853 OPPENHEIM RW, 1991, ANNU REV NEUROSCI, V14, P453, DOI 10.1146/annurev.neuro.14.1.453 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 Pujol R., 1986, BIOL CHANGE OTOLARYN, P47 PUJOL R, 1978, J COMP NEUROL, V177, P529, DOI 10.1002/cne.901770311 PUJOL R, 1979, NEUROSCI LETT, V15, P97, DOI 10.1016/0304-3940(79)96096-8 Purves D., 1988, BODY BRAIN TROPHIC T REPRESA J, 1991, ANAT EMBRYOL, V184, P421, DOI 10.1007/BF01236048 ROBERTSON D, 1989, DEV BRAIN RES, V47, P197, DOI 10.1016/0165-3806(89)90176-4 SCHECTERSON LC, 1992, IN PRESS HEAR RES, V9, P449 STAECKER H, 1993, ASS RES OTOLARYNGOL, V16, P26 VANDEWATER TR, 1992, ASS RES OTOLARYNGOL, V15, P47 VANDEWATER TR, 1988, DEVELOPMENT, V103, P185 VONBARTHELD CS, 1991, J COMP NEUROL, V310, P103, DOI 10.1002/cne.903100110 VONBARTHELD CS, 1991, DEVELOPMENT, V113, P455 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WHEELER EF, 1992, J NEUROSCI, V12, P930 WHITEHEAD MC, 1986, NEUROBIOLOGY HEARING, P191 YAN Q, 1988, J NEUROSCI, V8, P3481 YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C ZHOU XN, 1987, ACTA OTO-LARYNGOL, V104, P90, DOI 10.3109/00016488709109052 NR 41 TC 111 Z9 113 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 1994 VL 73 IS 1 BP 46 EP 56 DI 10.1016/0378-5955(94)90281-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100005 PM 8157505 ER PT J AU WU, SH KELLY, JB AF WU, SH KELLY, JB TI PHYSIOLOGICAL EVIDENCE FOR IPSILATERAL INHIBITION IN THE LATERAL SUPERIOR OLIVE - SYNAPTIC RESPONSES IN MOUSE-BRAIN SLICE SO HEARING RESEARCH LA English DT Article DE BINAURAL INTERACTION; SOUND LOCALIZATION; TRAPEZOID BODY; SUPERIOR OLIVE ID ANTEROVENTRAL COCHLEAR NUCLEUS; UNIT EXCITATORY RESPONSES; SINGLE AUDITORY UNITS; BINAURAL TONE BURSTS; BUSHY CELL AXONS; TRAPEZOID BODY; MEDIAL NUCLEUS; GUINEA-PIG; GLYCINE IMMUNOREACTIVITY; HORSERADISH-PEROXIDASE AB The incidence of ipsilateral inhibition in the lateral superior olive (LSO) was examined in a brain slice preparation of the mouse superior olivary complex. A 400 mu m brain slice was taken in the frontal plane and maintained in a warm, oxygenated saline solution. Intracellular recordings were made from the LSO with micropipettes filled with 4 M potassium acetate. Synaptic responses were elicited by electrical stimulation of the trapezoid body in different slices at various locations between the cochlear nucleus and the ipsilateral superior olivary complex (SOC). The results show that ipsilateral stimulation can evoke inhibitory as well as excitatory postsynaptic potentials. The ipsilateral IPSPs have short latencies and are elicited by stimulation of the trapezoid body at any point along its course between cochlear nucleus and LSO. Short-latency IPSPs can also be produced by direct stimulation of the ventral cochlear nucleus itself. Ipsilateral IPSPs are blocked by low concentrations of the glycine antagonist, strychnine. In addition, bath application of sodium pentobarbital in one case eliminated ipsilateral IPSPs without eliminating EPSPs. The results suggest that there is a rapidly conducting, glycinergic pathway from cochlear nucleus through the trapezoid body to the LSO on the same side of the brain. This pathway is probably served by either a direct projection from the ventral cochlear nucleus to the LSO or an indirect one from cochlear nucleus to LSO through the lateral nucleus of the trapezoid body (LNTB). C1 CARLETON UNIV,DEPT PSYCHOL,SENSORY NEUROSCI LAB,OTTAWA K1S 5B6,ON,CANADA. CR ADAMS JC, 1990, HEARING RES, V49, P281, DOI 10.1016/0378-5955(90)90109-3 ADAMS J C, 1987, Society for Neuroscience Abstracts, V13, P1259 BANKS MI, 1992, J NEUROSCI, V12, P2819 BLEDSOE SC, 1990, BRAIN RES, V517, P189, DOI 10.1016/0006-8993(90)91025-C BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BROWNELL WE, 1979, BRAIN RES, V177, P189, DOI 10.1016/0006-8993(79)90930-2 CAIRD D, 1983, EXP BRAIN RES, V52, P385 Cant N. B., 1991, NEUROBIOLOGY HEARING, P99 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 CANT NB, 1984, J COMP NEUROL, V227, P63, DOI 10.1002/cne.902270108 CASPARY DM, 1989, BRAIN RES, V503, P83, DOI 10.1016/0006-8993(89)91707-1 FINLAYSON PG, 1989, HEARING RES, V38, P221, DOI 10.1016/0378-5955(89)90067-1 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 GLENDENNING KK, 1991, J COMP NEUROL, V310, P377, DOI 10.1002/cne.903100308 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 HARRISON JM, 1967, J COMP NEUROL, V126, P51 HARRISON JM, 1962, J COMP NEUROL, V119, P341, DOI 10.1002/cne.901190306 HELFERT RH, 1992, J COMP NEUROL, V323, P305, DOI 10.1002/cne.903230302 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 HELFERT RH, 1993, ASS RES OT ABSTR, V16, P126 KUWABARA N, 1991, J COMP NEUROL, V314, P707, DOI 10.1002/cne.903140406 KUWABARA N, 1990, NEUR ABSTR, V16, P723 KUWABARA N, 1991, J COMP NEUROL, V314, P684, DOI 10.1002/cne.903140405 KUWADA S, 1989, J NEUROPHYSIOL, V61, P269 MOORE MJ, 1983, J NEUROSCI, V3, P237 MOREST DK, 1975, J COMP NEUROL, V162, P135, DOI 10.1002/cne.901620108 OERTEL D, 1983, J NEUROSCI, V3, P2043 PEYRET D, 1987, ACTA OTO-LARYNGOL, V104, P71, DOI 10.3109/00016488709109049 SANES DH, 1990, J NEUROSCI, V10, P3494 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 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3031, DOI 10.1016/0306-4522(82)90228-7 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 TSUCHITANI C, 1969, J ACOUST SOC AM, V46, P978 TSUCHITANI C, 1985, J ACOUST SOC AM, V77, P1484, DOI 10.1121/1.392043 TSUCHITA.C, 1966, J NEUROPHYSIOL, V29, P684 TSUCHITANI C, 1982, J NEUROPHYSIOL, V47, P479 TSUCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WARR WB, 1993, ASS RES OT ABSTR, V16, P125 WARR W B, 1989, Society for Neuroscience Abstracts, V15, P745 WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X Wenthold RJ, 1991, NEUROBIOLOGY HEARING, P121 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 WU SH, 1992, J NEUROPHYSIOL, V68, P1151 WU SH, 1992, NEUROSCI LETT, V134, P257, DOI 10.1016/0304-3940(92)90529-G WU SH, 1986, J NEUROSCI, V6, P2691 WU SH, 1991, J NEUROPHYSIOL, V65, P230 WU SH, 1992, J NEUROSCI, V12, P3084 ZOOK JM, 1988, HEARING RES, V34, P141, DOI 10.1016/0378-5955(88)90101-3 NR 55 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 FEB PY 1994 VL 73 IS 1 BP 57 EP 64 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100006 PM 8157506 ER PT J AU WILCOX, ER FEX, J AF WILCOX, ER FEX, J TI CONSTRUCTION OF A CDNA LIBRARY FROM MICRODISSECTED GUINEA-PIG CRISTA-AMPULLARIS SO HEARING RESEARCH LA English DT Article DE CRISTA AMPULLARIS; GUINEA PIG; MOLECULAR BIOLOGY; CLONING ID ORGAN; CORTI AB Poly(A) RNA was isolated from microdissected guinea pig crista ampullaris epithelium and converted into cDNA with RNase H- murine leukemia virus reverse transcriptase. After size fractionation, the cDNA was directionally ligated into the vector pSPORT 1 and the plasmids electroporated into E. coli. The library was found to have 1.6 x 10(7) independent colonies with 5% of the colonies lacking an insert. Thirty randomly selected colonies were checked for inserts and the average insert size was 833 base pairs with a range of 400 to 2300 base pairs. The library was screened with a beta-actin guinea pig cDNA probe and 0.16% of the colonies contained an insert hybridizing to the probe: RP WILCOX, ER (reprint author), NIDOCD,MOLEC BIOL LAB,BLDG 36,ROOM 5D-08,BETHESDA,MD 20892, USA. CR BERNARDI G, 1988, J MOL EVOL, V28, P7, DOI 10.1007/BF02143493 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 DUGUID JR, 1988, P NATL ACAD SCI USA, V85, P5738, DOI 10.1073/pnas.85.15.5738 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H Sambrook J., 1989, MOL CLONING LABORATO SLEPECKY N, 1992, UNPUBLISHED OBSERVAT WILCOX ER, 1992, OTOLARYNG CLIN N AM, V25, P1011 WILCOX ER, 1992, HEARING RES, V62, P124, DOI 10.1016/0378-5955(92)90208-5 NR 8 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 1994 VL 73 IS 1 BP 65 EP 66 DI 10.1016/0378-5955(94)90283-6 PG 2 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100007 PM 8157507 ER PT J AU BRUGGE, JF REALE, RA HIND, JE CHAN, JCK MUSICANT, AD POON, PWF AF BRUGGE, JF REALE, RA HIND, JE CHAN, JCK MUSICANT, AD POON, PWF TI SIMULATION OF FREE-FIELD SOUND SOURCES AND ITS APPLICATION TO STUDIES OF CORTICAL MECHANISMS OF SOUND LOCALIZATION IN THE CAT SO HEARING RESEARCH LA English DT Article DE VIRTUAL ACOUSTIC SPACE; SOUND LOCALIZATION; AUDITORY CORTEX ID PRIMARY AUDITORY-CORTEX; SPATIAL RECEPTIVE-FIELDS; SPECTRAL CUES; MEDIAN PLANE; EXTERNAL EAR; AZIMUTHAL SENSITIVITY; HEADPHONE SIMULATION; INFERIOR COLLICULUS; CENTRAL NUCLEUS; SINGLE NEURONS AB We synthesized a set of signals (clicks) for earphone delivery whose waveforms and amplitude spectra, measured at the eardrum, mimic those of sounds arriving from a free-field source. The complete stimulus set represents 1816 sound-source directions, which together surround the head to form a 'virtual acoustic space' for the cat. Virtual-space stimuli were delivered via calibrated earphones sealed into the external meatus in cats under barbiturate anesthesia. Neurons recorded in Al cortex exhibited sensitivity to the direction of sound in virtual acoustic space. The aggregation of effective sound directions formed a virtual space receptive field (VSRF). At 20 dB above minimal threshold, VSRFs fell into one of several categories based on spatial dimension and location. Most VSRFs were confined to either the contralateral (59%) or ipsilateral (10%) sound hemifield. Seven percent spanned the frontal quadrants and 16% were omnidirectional. Eight percent fit into no clear category and were termed 'complex'. The size, shape, and location of VSRFs remained stable over many hours of recording. The results are in essential agreement with free-field studies. VSRFs were found to be shaped by excitatory and inhibitory interactions of activity arriving from the two ears. Some cortical neurons were found to preserve the spectral information in the free-field sound which was generated by the acoustical properties of the head and pinna, filtered by the cochlea and transmitted by auditory nerve fibers. C1 UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,MADISON,WI 53706. RP BRUGGE, JF (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,627 WAISMAN CTR,MADISON,WI 53706, USA. CR AHISSAR M, 1992, J NEUROPHYSIOL, V67, P203 ASANO F, 1990, J ACOUST SOC AM, V88, P159, DOI 10.1121/1.399963 BLAUERT J, 1969, ACUSTICA, V22, P205 Blauert J., 1983, SPATIAL HEARING BLOOM PJ, 1977, J ACOUST SOC AM, V61, P820, DOI 10.1121/1.381346 BRUGGE JF, 1991, VIRTUAL SPACE RECEPT BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 BRUGGE JF, 1992, J ACOUST SOC AM, V92, P2333, DOI 10.1121/1.404987 BRUGGE JF, 1985, CEREB CORTEX, V4, P229 BUTLER RA, 1977, J ACOUST SOC AM, V61, P1264, DOI 10.1121/1.381427 BUTLER RA, 1975, HDB SENSORY PHYSL, P247 CHAN JCK, 1990, NEUROSCIENCE, P720 CHAN JCK, 1993, J ACOUST SOC AM, V93, P1496, DOI 10.1121/1.406807 CHAN JCK, 1992, SPATIAL DISTRIBUTION EISENMAN LM, 1974, BRAIN RES, V75, P203, DOI 10.1016/0006-8993(74)90742-2 GEORGOPOULOS AP, 1993, SCIENCE, V260, P47, DOI 10.1126/science.8465199 HEBRANK J, 1974, J ACOUST SOC AM, V56, P1829, DOI 10.1121/1.1903520 IMIG TJ, 1990, J NEUROPHYSIOL, V63, P1448 IMIG TJ, 1978, J COMP NEUROL, V182, P637, DOI 10.1002/cne.901820406 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 KNUDSEN EI, 1984, DYNAMIC ASPECTS NEOC, P375 Kuhn GF, 1987, DIRECTIONAL HEARING, P3 Kuwada S., 1987, P146 MEHRGARDT S, 1977, J ACOUST SOC AM, V61, P1567, DOI 10.1121/1.381470 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MIDDLEBROOKS JC, 1992, J ACOUST SOC AM, V92, P2607, DOI 10.1121/1.404400 MIDDLEBROOKS JC, 1990, J ACOUST SOC AM, V87, P2149, DOI 10.1121/1.399183 MIDDLEBROOKS JC, 1981, J NEUROSCI, V1, P107 MOORE DR, 1984, HEARING RES, V13, P159, DOI 10.1016/0378-5955(84)90106-0 MOORE DR, 1984, HEARING RES, V13, P175, DOI 10.1016/0378-5955(84)90107-2 MUSICANT AD, 1990, J ACOUST SOC AM, V87, P757, DOI 10.1121/1.399545 MUSICANT AD, 1984, J ACOUST SOC AM, V75, P1195, DOI 10.1121/1.390770 Neff WD, 1975, HDB SENSORY PHYSL, P307 PHILLIPS DP, 1982, HEARING RES, V8, P13, DOI 10.1016/0378-5955(82)90031-4 PHILLIPS DP, 1981, J NEUROPHYSIOL, V45, P48 PLENGE G, 1974, J ACOUST SOC AM, V56, P944, DOI 10.1121/1.1903353 POON PWF, 1993, J NEUROPHYSIOL, V70, P667 POON PWF, 1993, J NEUROPHYSIOL, V70, P655 RAJAN R, 1990, J NEUROPHYSIOL, V64, P872 RAJAN R, 1990, J NEUROPHYSIOL, V64, P888 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 REALE RA, 1991, NEUROSCIENCE, P449 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 REALE RA, 1990, J NEUROPHYSIOL, V64, P1247 RHODE WS, 1976, CURRENT COMPUTER TEC, P543 RICE JJ, 1992, HEARING RES, V58, P132, DOI 10.1016/0378-5955(92)90123-5 Shaw BAG, 1974, HDB SENSORY PHYSL, VV/1, P455 SHAW EAG, 1974, J ACOUST SOC AM, V56, P1848, DOI 10.1121/1.1903522 SOVIJARV.AR, 1974, BRAIN RES, V73, P455, DOI 10.1016/0006-8993(74)90669-6 Sutherland IE, 1968, AFIPS C P, V33, P757 Sutherland IE, 1965, P IFIP C, P506 WATKINS AJ, 1978, J ACOUST SOC AM, V63, P1152, DOI 10.1121/1.381823 WENSEL EM, 1992, PRESENCE, V1, P80 WHITFIEL.IC, 1972, J NEUROPHYSIOL, V35, P718 WIGHTMAN FL, 1987, DIRECTIONAL HEARING, P27 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P858, DOI 10.1121/1.397557 WIGHTMAN FL, 1991, J ACOUST SOC AM, V89, P1995, DOI 10.1121/1.2029816 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P868, DOI 10.1121/1.397558 YIN TCT, 1984, DYNAMIC ASPECTS NEOC, P263 Yost W.A., 1987, DIRECTIONAL HEARING, P49 ZHOU B, 1992, J ACOUST SOC AM, V92, P1169, DOI 10.1121/1.404045 NR 62 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 FEB PY 1994 VL 73 IS 1 BP 67 EP 84 DI 10.1016/0378-5955(94)90284-4 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100008 PM 8157508 ER PT J AU RAPHAEL, Y WANG, Y LEE, MK AF RAPHAEL, Y WANG, Y LEE, MK TI INTERCELLULAR CONTACTS BETWEEN CHICK STEREOCILIA AFTER ACOUSTIC OVERSTIMULATION SO HEARING RESEARCH LA English DT Article DE CHICKS; NOISE; STEREOCILIA; REGENERATION; ACTIN ID GUINEA-PIG COCHLEA; HAIR CELL-DAMAGE; INNER-EAR; ACTIN-FILAMENTS; RECEPTOR CELLS; AVIAN COCHLEA; SENSORY HAIRS; TRAUMA; NOISE; REORGANIZATION AB The gear of this study was to analyze the distribution of actin and the shape of stereocilia of chick hair cells that survive acoustic trauma. Chicks were exposed to intense octave band noise for 4 h. They were killed either immediately after the exposure, after 6 or after 72 h. The basilar papillae were examined using scanning electron microscopy and fluorescence microscopy, with phalloidin as an actin-specific probe. Injured hair cells which survived the trauma displayed disorganized stereocilia bundles, elongated stereocilia, and supernumerary stereocilia bundles. Tips of stereocilia in the damaged region of the basilar papilla appeared to be in contact with tips of stereocilia of neighboring hair cells. These contacts may represent 'stress links' which appear in traumatized hair cells. These results show that substantial changes in stereocilia occur within hours of exposure to intense noise. We speculate that surviving hair cells may play a role in the process of repair of the basilar papilla after noise trauma and that the changes in stereocilia structure described here are related to this role. RP RAPHAEL, Y (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 AVINASH GB, 1993, HEARING RES, V67, P139, DOI 10.1016/0378-5955(93)90241-R BORG E, 1989, J ACOUST SOC AM, V86, P1776, DOI 10.1121/1.398609 COTANCHE DA, 1987, HEARING RES, V28, P35, DOI 10.1016/0378-5955(87)90151-1 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, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 ENGSTROM B, 1983, HEARING RES, V12, P251, DOI 10.1016/0378-5955(83)90110-7 FISCHER FP, 1991, HEARING RES, V53, P281, DOI 10.1016/0378-5955(91)90061-D FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 HACKNEY CM, 1988, HEARING RES, V34, P207, DOI 10.1016/0378-5955(88)90109-8 HALL AL, 1988, J CELL BIOCHEM, V37, P285, DOI 10.1002/jcb.240370304 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 MARSH RR, 1990, HEARING RES, V46, P229, DOI 10.1016/0378-5955(90)90004-9 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 RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 SANTI PA, 1987, HEARING RES, V27, P47, DOI 10.1016/0378-5955(87)90025-6 SAUNDERS JC, 1991, J ACOUST SOC AM, V90, P136, DOI 10.1121/1.401307 SCHROEDER TE, 1978, DEV BIOL, V64, P42 SLEPECKY N, 1986, HEARING RES, V22, P307, DOI 10.1016/0378-5955(86)90107-3 SLEPECKY N, 1982, CELL TISSUE RES, V224, P15, DOI 10.1007/BF00217262 SMITH SM, 1991, BIOTECHNIQUES, V11, P340 THORNE PR, 1986, HEARING RES, V21, P41, DOI 10.1016/0378-5955(86)90044-4 THORNE PR, 1984, ACTA OTO-LARYNGOL, V97, P69, DOI 10.3109/00016488409130966 TILNEY LG, 1983, J CELL BIOL, V96, P822, DOI 10.1083/jcb.96.3.822 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 TILNEY LG, 1986, DEV BIOL, V16, P119 NR 34 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 1994 VL 73 IS 1 BP 85 EP 91 DI 10.1016/0378-5955(94)90285-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100009 PM 8157509 ER PT J AU SCHECTERSON, LC BOTHWELL, M AF SCHECTERSON, LC BOTHWELL, M TI NEUROTROPHIN AND NEUROTROPHIN RECEPTOR MESSENGER-RNA EXPRESSION IN DEVELOPING INNER-EAR SO HEARING RESEARCH LA English DT Article DE NEUROTROPHINS; TRK; P75; COCHLEA; COCHLEOVESTIBULAR GANGLION ID NERVE GROWTH-FACTOR; COCHLEO-VESTIBULAR GANGLION; TRK PROTOONCOGENE PRODUCT; AFFINITY NGF RECEPTOR; EMBRYONIC OTIC VESICLE; IMMUNOHISTOCHEMICAL LOCALIZATION; TYROSINE KINASE; MOLECULAR-CLONING; SENSORY GANGLIA; GENE-EXPRESSION AB Receptors which bind the neurotrophins NGF, BDNF, NT-3 and NT-4/5 were shown to be present in cochlear and vestibular ganglion cells during development, implying a neurotrophic role for these molecules in the inner ear. We have found by in situ hybridization that cochlear and vestibular sensory epithelial cells express BDNF and NT-3 mRNAs, but neither NGF or NT-4 mRNAs, in mouse embryos from embryonic day (E)11.5 through postnatal day (P)1. NT-3 mRNA was expressed throughout the sensory epithelium whereas BDNF mRNA appeared to be localized in hair cells (vestibular) and epithelial precursors of hair cells (cochlea). BDNF mRNA was also expressed in a subpopulation of cells in the cochleovestibular ganglion at E11.5 and E12.5. Additionally, cochlear and vestibular neurons contained mRNAs encoding the neurotrophin receptors p75 and trkB. TrkA mRNA. was transiently expressed in cochleovestibular ganglion cells at E12.5. These data suggest that BDNF and NT-3 play a role in cochleovestibular neuron survival and neurite outgrowth during development in the inner ear. RP SCHECTERSON, LC (reprint author), UNIV WASHINGTON,DEPT PHYSIOL & BIOPHYS,SJ-40,SEATTLE,WA 98195, USA. CR ACHESON A, 1991, NEURON, V7, P265, DOI 10.1016/0896-6273(91)90265-2 ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 ARD MD, 1984, INT J DEV NEUROSCI, V2, P535, DOI 10.1016/0736-5748(84)90031-5 BARDE YA, 1982, EMBO J, V1, P549 BERKEMEIER LR, 1991, NEURON, V7, P857, DOI 10.1016/0896-6273(91)90287-A BERND P, 1989, DEV BIOL, V134, P11, DOI 10.1016/0012-1606(89)90073-0 CORDONCARDO C, 1991, CELL, V66, P173, DOI 10.1016/0092-8674(91)90149-S DAVIES AM, 1987, NATURE, V326, P353, DOI 10.1038/326353a0 DAVIES AM, 1985, DEV BIOL, V111, P62, DOI 10.1016/0012-1606(85)90435-X DAVIES AM, 1986, J NEUROSCI, V6, P1897 DESPRES G, 1991, HEARING RES, V52, P157, DOI 10.1016/0378-5955(91)90195-F DESPRES G, 1988, NEUROSCI LETT, V85, P5, DOI 10.1016/0304-3940(88)90418-1 FINN PJ, 1987, J NEUROCYTOL, V16, P639, DOI 10.1007/BF01637656 GLASS DJ, 1991, CELL, V66, P405, DOI 10.1016/0092-8674(91)90629-D HALLBOOK F, 1991, NEURON, V6, P845, DOI 10.1016/0896-6273(91)90180-8 HAUGER SH, 1985, NEUROSCIENCE, V33, P241 HEMPSTEAD BL, 1991, NATURE, V350, P678, DOI 10.1038/350678a0 HOHN A, 1990, NATURE, V344, P339, DOI 10.1038/344339a0 IP NY, 1993, NEURON, V10, P137, DOI 10.1016/0896-6273(93)90306-C IP NY, 1992, P NATL ACAD SCI USA, V89, P3060, DOI 10.1073/pnas.89.7.3060 JONES KR, 1990, P NATL ACAD SCI USA, V87, P8060, DOI 10.1073/pnas.87.20.8060 KAPLAN DR, 1991, NATURE, V350, P158, DOI 10.1038/350158a0 KAPLAN DR, 1991, SCIENCE, V252, P554, DOI 10.1126/science.1850549 KLEIN R, 1990, CELL, V61, P647, DOI 10.1016/0092-8674(90)90476-U KLEIN R, 1991, CELL, V65, P189, DOI 10.1016/0092-8674(91)90419-Y LAMBALLE F, 1991, CELL, V66, P967, DOI 10.1016/0092-8674(91)90442-2 LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEFEBVRE PP, 1991, BRAIN RES, V567, P306, DOI 10.1016/0006-8993(91)90809-A LEIBROCK J, 1989, NATURE, V341, P149, DOI 10.1038/341149a0 LEVIMONT.R, 1968, PHYSIOL REV, V48, P534 LOEB DM, 1991, CELL, V66, P961, DOI 10.1016/0092-8674(91)90441-Z LU B, 1991, J NEUROSCI, V11, P318 MAISONPIERRE PC, 1990, SCIENCE, V247, P1446, DOI 10.1126/science.2321006 MBIENE JP, 1988, ANAT EMBRYOL, V177, P331, DOI 10.1007/BF00315841 MBIENE JP, 1986, J COMP NEUROL, V254, P271, DOI 10.1002/cne.902540210 MCPHEE JR, 1986, J EMBRYOL EXP MORPH, V97, P1 MIDDLEMAS DS, 1991, MOL CELL BIOL, V11, P143 MILLAN FA, 1991, DEVELOPMENT, V111, P131 NEBREDA AR, 1991, SCIENCE, V252, P558, DOI 10.1126/science.1850550 PELTON RW, 1991, J CELL BIOL, V115, P1091, DOI 10.1083/jcb.115.4.1091 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 RADEKE MJ, 1987, NATURE, V325, P593, DOI 10.1038/325593a0 REPRESA J, 1989, DEV BIOL, V134, P21, DOI 10.1016/0012-1606(89)90074-2 RODRIGUEZTEBAR A, 1990, NEURON, V4, P487, DOI 10.1016/0896-6273(90)90107-Q ROSENTHAL A, 1990, NEURON, V4, P767, DOI 10.1016/0896-6273(90)90203-R SCHECTERSON LC, 1992, NEURON, V9, P449, DOI 10.1016/0896-6273(92)90183-E SCHER, 1971, ACTA LARYNGOL S, V285, P1 SOPPET D, 1991, CELL, V65, P895, DOI 10.1016/0092-8674(91)90396-G SQUINTO SP, 1991, CELL, V65, P885, DOI 10.1016/0092-8674(91)90395-F SUTTER A, 1979, J BIOL CHEM, V254, P5972 VANDEWATER TR, 1992, ASS RES OTOLARYNGOL, V15, P47 VOGEL KS, 1991, NEURON, V7, P819, DOI 10.1016/0896-6273(91)90284-7 VONBARTHELD CS, 1991, DEVELOPMENT, V113, P455 WHEELER EF, 1994, IN PRESS HEAR RES WHEELER EF, 1992, J NEUROSCI, V12, P930 WILKINSON DG, 1989, DEVELOPMENT, V105, P131 YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C ZHOU XN, 1987, ACTA OTO-LARYNGOL, V104, P90, DOI 10.3109/00016488709109052 NR 58 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 1994 VL 73 IS 1 BP 92 EP 100 DI 10.1016/0378-5955(94)90286-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100010 PM 8157510 ER PT J AU MARCUS, DC LIU, JZ WANGEMANN, P AF MARCUS, DC LIU, JZ WANGEMANN, P TI TRANSEPITHELIAL VOLTAGE AND RESISTANCE OF VESTIBULAR DARK CELL EPITHELIUM FROM THE GERBIL AMPULLA SO HEARING RESEARCH LA English DT Article DE INNER EAR; TRANSEPITHELIAL CURRENT; OUABAIN; BUMETANIDE; MICRO USSING CHAMBER; DIDS ID NONSENSORY REGION; ELECTRICAL RESPONSES; APICAL MEMBRANE; UTRICLE; POTASSIUM; CL; PERMEABILITY; ENDOLYMPH; CHANNEL AB Transepithelial voltage (V-t) and resistance (R(t)) were measured across the dark cell epithelium of the gerbil ampulla using a micro Ussing chamber of improved design in order to test the view that the histologically similar epithelia in the utricle and in the ampullae exhibit similar electrophysiologic functions. V-t was found to be 8.0 +/- 0.3 mV and R(t) was 11.6 +/- 0.4 ohm-cm(2) (N = 179) when both sides of the tissue were perfused with symmetric perilymph-like solution. The equivalent short circuit current (I-sc = V-t/R(t)) was 712 +/- 18 mu A/cm(2) (N = 179). I-sc was reduced from 638 +/- 60 to 48 +/- 16 mu A/cm(2) (N = 14) by basolateral perfusion of 10(-3) M ouabain and from 538 +/- 27 to 27 +/- 4 mu A/cm(2) (N = 15) by basolateral perfusion of 5.10(-5) M bumetanide. Basolateral K+ steps (Na+ substitution) from 3.6 to 25 mM increased V-t from 6.5 +/- 0.5 to 12.2 +/- 0.6 mV and reduced R(t) from 9.7 +/- 0.7 to 7.4 +/- 0.5 ohm-cm(2) (N = 43). Apical K+ steps from 3.6 to 25, to 100 mM or to 145 mM led to a decrease in both V-t and R(t). The steady state V-t during apical perfusion of 145 mM K+ was near zero. Upon return to 3.6 mM K+, V-t transiently overshot its original level. Apical Cl- steps from 150 to 50 mM (gluconate substitution) monophasically decreased V-t from 5.9 +/- 0.7 to 4.1 +/- 0.8 mV (N 15) and increased R(t) from 9.6 +/- 1.3 to 12.0 +/- 1.5 ohm-cm(2) (N = 14). Apical perfusion of 5.10(-4) M DIDS increased V-t from 7.1 +/- 0.9 to a peak value of 11.9 +/- 1.7 mV (N = 6) and decreased R(t) from 10.2 +/- 2.1 to 9.0 +/- 1.7 ohm-cm(2) at the time of the peak V-t. The present results are qualitatively similar to data obtained in the utricle, suggesting a functional similarity between the dark cell epithelium in these two regions of the vestibular labyrinth. Further, the data support the hypothesis that the vestibular dark cells contribute a lumen-positive voltage only when the K+ concentration of endolymph falls below the level normally found in vivo. RP MARCUS, DC (reprint author), BOYS TOWN NATL RES HOSP,BIOPHYS LAB,555 N 30TH ST,OMAHA,NE 68131, USA. RI Wangemann, Philine/N-2826-2013 CR BERNARD C, 1986, J PHYSIOL-LONDON, V371, P17 BRAYDEN DJ, 1993, AM J PHYSIOL, V264, pG325 BRIDGES RJ, 1989, AM J PHYSIOL, V256, pC902 CABANTCH.ZI, 1974, J MEMBRANE BIOL, V15, P207, DOI 10.1007/BF01870088 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P359, DOI 10.1007/BF00588214 KUSAKARI J, 1976, LARYNGOSCOPE, V86, P132, DOI 10.1288/00005537-197601000-00025 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1987, HEARING RES, V30, P55, DOI 10.1016/0378-5955(87)90183-3 MARCUS DC, 1984, AM J PHYSIOL, V247, pC240 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 MARCUS NY, 1985, AM J OTOLARYNG, V6, P268, DOI 10.1016/S0196-0709(85)80054-5 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MARCUS NY, 1990, HEARING RES, V44, P13, DOI 10.1016/0378-5955(90)90018-K NINOYU O, 1986, ARCH OTO-RHINO-LARYN, V243, P141, DOI 10.1007/BF00453767 SALT AN, 1989, AM J OTOLARYNG, V10, P371, DOI 10.1016/0196-0709(89)90030-6 SELLICK PM, 1972, PFLUG ARCH EUR J PHY, V336, P21, DOI 10.1007/BF00589138 SHEN Z, 1994, ABSTR ASS RES OTOLAR TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 Wangemann Philine, 1992, Journal of General Physiology, V100, p64A WANGEMANN P, 1992, HEARING RES, V62, P149, DOI 10.1016/0378-5955(92)90180-U WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 ZUMGOTTESBERGE AMM, 1988, ACTA OTOLARYNGOL S S, V460, P18 NR 23 TC 45 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 FEB PY 1994 VL 73 IS 1 BP 101 EP 108 DI 10.1016/0378-5955(94)90287-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100011 PM 8157498 ER PT J AU GUTH, PS FERMIN, CD PANTOJA, M EDWARDS, R NORRIS, C AF GUTH, PS FERMIN, CD PANTOJA, M EDWARDS, R NORRIS, C TI HAIR-CELLS OF DIFFERENT SHAPES AND THEIR PLACEMENT ALONG THE FROG CRISTA-AMPULLARIS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; VESTIBULAR; FROG; SEMICIRCULAR CANAL; MORPHOLOGY; SHAPE ID VESTIBULAR NERVE; FISH EAR; INNERVATION; CHINCHILLA; TOADFISH; SACCULE AB The list of distinguishing morphological features of hair cells includes: Type I and Type II afferent innervation, and length, shapes and arrangements of stereo- and kinocilia. We now add to this list the shapes of the hair cells themselves and their placement within the mechanosensory organ, in this case the semicircular canal. Although hair cells of the crista ampullaris of the frog are only of Type II they may now be further classified into three sub-groups according to shape: club-, cigar- and pear-shaped. The cigar- and club-shaped hair cells are each about 40% while the pear-shaped cells are about 20% of the total numbers of hair cells in the crista. The differently-shaped hair cells also distribute differently along the crista. The cigar- and club-shaped are more-or-less uniformly distributed with somewhat higher concentrations at the ends of the crista than in the center. The pear-shaped hair cells, on the other hand, are mostly concentrated toward the center of the crista. This distribution of the pear-shaped hair cells, and their shape is reminiscent of the distribution of calyceal endings (Type I hair cell) in the cristae of amniotes [Goldberg et al., Hear. Res. 49, 89-102 (1990) in Chinchilla; Fernandez et al., Sec. Neurosci. Abstr. 17, 312 (1991) in Monkey]. There are some quantitative differences between hair cells of the same shape but from different portions of the crista. For instance, pear-shaped hair cells of the center are generally of greater cross-sectional area than those of the ends. Also, club-shaped hair cells are taller in the slopes of the crista than they are in the center. Lastly, hair cells of all three shapes have smaller cross-sectional areas after isolation from the crista as, for example, in preparation for patch-clamping. The greatest of these areal differences is seen in the pear-shaped hair cells. Thus, the emerging picture of the hair cell of the semicircular canal when considering both morphology and physiology is one of diversity and complexity suggesting a role in signal processing of greater importance than previously appreciated. C1 TULANE UNIV,SCH MED,DEPT PATHOL,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA 70112. UNIV VALLE,DEPT PHARMACOL,CALI 25360,COLOMBIA. RP GUTH, PS (reprint author), TULANE UNIV,SCH MED,DEPT PHARMACOL,1430 TULANE AVE,NEW ORLEANS,LA 70112, USA. CR BOHNE BA, 1985, J ACOUST SOC AM, V77, P153, DOI 10.1121/1.392279 BOYLE R, 1991, J NEUROPHYSIOL, V66, P1504 CHANG JSY, 1992, J COMP NEUROL, V324, P621, DOI 10.1002/cne.903240413 FERMIN CD, 1987, ACTA ANAT, V129, P188 FERMIN CD, 1982, ANN OTO RHINOL LARYN, V91, P44 FERNANDEZ C, 1991, Society for Neuroscience Abstracts, V17, P312 FERNANDEZ C, 1988, J NEUROPHYSIOL, V60, P167 FLOCK A, 1964, J CELL BIOL, V22, P413, DOI 10.1083/jcb.22.2.413 GOLDBERG JM, 1990, HEARING RES, V49, P89, DOI 10.1016/0378-5955(90)90097-9 GUTH P, 1993, HEARING RES, V66, P43 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HILLMAN DE, 1976, FROG NEUROBIOLOGY HOSHINO T, 1975, ACTA OTO-LARYNGOL, V80, P43, DOI 10.3109/00016487509121299 HOUSLEY GD, 1989, HEARING RES, V38, P259, DOI 10.1016/0378-5955(89)90070-1 JORGENSEN JM, ACTA ZOOLOGICA, V55, P289 LAPEYRE P, 1992, ACTA OTO-LARYNGOL, V112, P635, DOI 10.3109/00016489209137453 LOWENSTEIN O, 1964, PROC R SOC SER B-BIO, V160, P1, DOI 10.1098/rspb.1964.0026 LOWENSTEIN O, 1964, NATURE, V204, P97 MYERS SF, 1990, BRAIN RES, V534, P15, DOI 10.1016/0006-8993(90)90107-M NORRIS CH, 1992, J NEUROPHYSIOL, V68, P1642 NORRIS CH, 1992, ABSTE ASS RES OTOLAR, P119 POPPER AN, 1990, HEARING RES, V46, P211, DOI 10.1016/0378-5955(90)90003-8 POPPER AN, 1993, HEARING RES, V64, P211, DOI 10.1016/0378-5955(93)90008-O PRECHT W, 1976, PHYSL PERIPHERAL CEN, P481 RICCI AS, 1992, ABSTR ASS RES OTOLAR, P119 STEINACKER A, 1992, BRAIN RES, V574, P229, DOI 10.1016/0006-8993(92)90821-P STEINACKER A, 1991, ANN NY ACAD SCI, V656, P27 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 Weibel E R, 1969, Int Rev Cytol, V26, P235, DOI 10.1016/S0074-7696(08)61637-X WERSALL J, 1954, ACTA OTO-LARYNGOL, V44, P359, DOI 10.3109/00016485409128719 NR 30 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 1994 VL 73 IS 1 BP 109 EP 115 DI 10.1016/0378-5955(94)90288-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100012 PM 8157499 ER PT J AU SOHMER, H GOITEIN, K FREEMAN, S AF SOHMER, H GOITEIN, K FREEMAN, S TI IMPROVEMENT IN SENSORINEURAL AUDITORY THRESHOLD OF THE GUINEA-PIG FETUS FOLLOWING DELIVERY SO HEARING RESEARCH LA English DT Article DE THRESHOLD; FETUS; NEONATE; BONE CONDUCTION; AUDITORY NERVE-BRAIN-STEM EVOKED RESPONSE (ABR) ID BRAIN-STEM RESPONSE; HEARING-LOSS; POTENTIALS; HYPOXIA; OXYGEN; INFANTS; ORIGIN; SHEEP; ONSET; PO2 AB The human fetus in utero is hypoxic relative to the neonate due to differences between placental and pulmonary oxygenation. Comparable degrees of hypoxia induced in young and adult animals caused an elevation in hearing threshold of a sensorineural nature. It was hypothesised therefore that the human fetus may also have such an elevation of threshold. This was tested in this study by recording ABR thresholds to bone conducted stimuli in fetal guinea-pigs that were near full term and again in the same animals, after delivery and consequent pulmonary oxygenation. In every animal studied (n = 9), the neonatal threshold was better than that in the fetus. In those fetuses in which a response could be recorded (n = 5), the neonatal threshold was on average 20 dB better than in the fetus. These findings are probably due to a depression of the endocochlear potential induced by the relatively hypoxic state of the fetus. The hypoxic state would lead to a reduced transduction current in the hair cells in response to a stimulus and an elevated hearing threshold. At birth, with the shift to pulmonary oxygenation, the neonate becomes normoxic, the endocochlear potential rapidly reaches near maximal levels and threshold is improved. C1 HADASSAH UNIV HOSP,PEDIAT INTENS CARE UNIT,IL-91120 JERUSALEM,ISRAEL. RP SOHMER, H (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 91120,IL-91010 JERUSALEM,ISRAEL. CR Anggard L., 1965, ACTA OTOLARYNGOLOGIC, V203, P1 BIRNHOLZ JC, 1983, SCIENCE, V222, P516, DOI 10.1126/science.6623091 BOSHER SK, 1971, J PHYSL, V212, P736 CARTER AM, 1989, J DEV PHYSIOL, V12, P305 CYCOWICZ Y, 1988, HEARING RES, V33, P239, DOI 10.1016/0378-5955(88)90154-2 Draper RL, 1920, ANAT REC, V18, P369, DOI 10.1002/ar.1090180408 FAWER CL, 1982, NEUROPEDIATRICS, V13, P200, DOI 10.1055/s-2008-1059623 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 GAFNI M, 1976, ACTA OTO-LARYNGOL, V82, P354, DOI 10.3109/00016487609120919 GAGNON R, 1987, AM J OBSTET GYNECOL, V157, P375 GEALDOR M, 1993, HEARING RES, V69, P236, DOI 10.1016/0378-5955(93)90113-F HILDESHEIMER M, 1987, LARYNGOSCOPE, V97, P204 JACKSON BT, 1987, AM J PHYSIOL, V252, pR94 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X JOHNSTON.BM, 1972, Q REV BIOPHYS, V5, P1 LARY S, 1985, J PEDIATR-US, V107, P593, DOI 10.1016/S0022-3476(85)80030-5 LAWRENCE M, 1975, ANN OTO RHINOL LARYN, V84, P499 LONGO LD, 1977, J APPL PHYSIOL, V43, P885 METCALFE J, 1967, PHYSIOL REV, V47, P782 PUJOL R, 1973, ACTA OTO-LARYNGOL, V76, P1, DOI 10.3109/00016487309121476 RANKIN JHG, 1971, AM J PHYSIOL, V220, P1688 RAPHAEL Y, 1983, ARCH OTO-RHINO-LARYN, V237, P147, DOI 10.1007/BF00463614 RUSSELL IJ, 1983, NATURE, V301, P334, DOI 10.1038/301334a0 SALOMON G, 1993, SCREENING CHILDREN A, P191 SELLICK PM, 1974, PFLUG ARCH EUR J PHY, V352, P351, DOI 10.1007/BF00585687 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 SOHMER H, 1986, ELECTROEN CLIN NEURO, V64, P334, DOI 10.1016/0013-4694(86)90157-4 SOHMER H, 1989, HEARING RES, V40, P87, DOI 10.1016/0378-5955(89)90102-0 SOHMER H, 1991, HEARING RES, V55, P92, DOI 10.1016/0378-5955(91)90095-Q STARR A, 1977, PEDIATRICS, V60, P831 WALSH EJ, 1986, J ACOUST SOC AM, V79, P712, DOI 10.1121/1.393461 WOLFSON MR, 1990, ELECTROEN CLIN NEURO, V75, P242, DOI 10.1016/0013-4694(90)90177-L WOODS JR, 1985, OTOLARYNG HEAD NECK, V93, P759 NR 34 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 1994 VL 73 IS 1 BP 116 EP 120 DI 10.1016/0378-5955(94)90289-5 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100013 PM 8157500 ER PT J AU MARKOVITZ, NS POLLAK, GD AF MARKOVITZ, NS POLLAK, GD TI BINAURAL PROCESSING IN THE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS SO HEARING RESEARCH LA English DT Article DE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS; BINAURAL PROCESSING; INTERAURAL INTENSITY DISPARITIES; TIME-INTENSITY TRADE; EXCITATORY-INHIBITORY NEURONS ID SUPERIOR OLIVARY COMPLEX; BAT INFERIOR COLLICULUS; SOUND LOCATION SELECTIVITY; UNIT EXCITATORY RESPONSES; AUDITORY-SYSTEM; MUSTACHE BAT; PTERONOTUS-PARNELLII; INTERAURAL TIME; BRAIN-STEM; TONOTOPIC ORGANIZATION AB We studied the binaural properties of 72 neurons in the dorsal nucleus of the lateral lemniscus (DNLL) of the mustache bat. There are six main findings: 1) Conventional EI neurons that were excited by stimulation of the contralateral ear and inhibited by ipsilateral stimulation, comprise the majority (80%) of binaural DNLL cells. 2) For most EI neurons the quantitative features of their interaural intensity disparity (IID) functions, maximum inhibition, dynamic range and 50% point IIDs, were largely unaffected by the absolute intensity at the contralateral ear. 3) Although the net effect of the inhibition evoked by ipsilateral stimulation was to suppress discharges evoked by contralateral stimulation, our results indicate that the inhibitory inputs can act in three different ways. The first was a time-intensity trade, where increasing the intensity at the ipsilateral ear evoked inhibitory effects with progressively shorter latencies. The second way was that the latency of inhibition did not appear to decrease with ipsilateral intensity, but rather increasing ipsilateral intensity appeared only to increase the strength of the inhibition. The third way was that the lowest effective ipsilateral intensity suppressed the first spikes evoked by the contralateral stimulus and higher ipsilateral intensities then suppressed the later discharges of the train. Each of these inhibitory patterns was seen in about a third of the cells. 4) Neurons that had more complex binaural properties, such as the facilitated EI neurons (EI/F) and neurons that were driven by sound to either ear (EE neurons), represented about 20% of the binaural population. There were two types of EE neurons; those in which there was a simple summation of discharges evoked with certain IIDs, and those in which the spike-counts to binaural stimulation at certain IIDs were greater than a summation of the monaural counts and thus were facilitated. 5) Air binaural neurons were strongly inhibited with IIDs that favored the ipsilateral ear. Our findings indicate that the more complex binaural types, the facilitated EI neurons (EI/F) as well as the two types of EE neurons, may be constructed from conventional EI neurons by adding inputs from several sources that impart the more complex features to these neurons. We propose four circuits that could account for the different binaural response properties that we observed. The circuits' are based on the known connections of the DNLL and the neurochemistry of those connections. Finally, we compared the binaural properties of neurons in the mustache bat DNLL with those of neurons in the mustache bat inferior colliculus and lateral superior olive. The comparative features suggest that the processing of the interaural intensity disparities undergoes at least four types of response transformations along the ascending auditory system. C1 UNIV TEXAS,DEPT ZOOL,AUSTIN,TX 78712. CR ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 AITKIN LM, 1970, J NEUROPHYSIOL, V33, P421 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 BRUGGE JF, 1970, J NEUROPHYSIOL, V33, P441 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 BUCKTHOUGHT AD, 1993, ABSTR ASS RES OT, P126 CAIRD D, 1983, EXP BRAIN RES, V52, P385 CANT NB, 1984, HEARING SCI RECENT A, P371 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 COVEY E, 1991, J NEUROPHYSIOL, V66, P1080 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 ERULKAR SD, 1972, PHYSIOL REV, V52, P237 Faingold C. L., 1992, Society for Neuroscience Abstracts, V18, P1193 FINDLAYSON PG, 1991, J NEUROPHYSIOL, V65, P598 FINDLAYSON PG, 1989, HEARING RES, V38, P221 FUJITA I, 1991, J NEUROSCI, V11, P722 FUZESSERY ZM, 1984, SCIENCE, V225, P725, DOI 10.1126/science.6463649 FUZESSERY ZM, 1990, J NEUROPHYSIOL, V63, P1128 FUZESSERY ZM, 1985, J NEUROPHYSIOL, V54, P757 FUZESSERY ZM, 1992, J COMP PHYSIOL A, V170, P57 GALAMBOS R, 1959, AM J PHYSIOL, V197, P527 GLENDENNING KK, 1992, J COMP NEUROL, V319, P100, DOI 10.1002/cne.903190110 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GOLDBERG JAY M., 1968, J NEUROPHYSIOL, V31, P639 GROTHE B, 1992, P NATL ACAD SCI USA, V89, P5108, DOI 10.1073/pnas.89.11.5108 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 HALL JL, 1965, J ACOUST SOC AM, V37, P814, DOI 10.1121/1.1909447 HARNISCHFEGER G, 1985, J NEUROPHYSIOL, V53, P89 Henkel C. K., 1992, Society for Neuroscience Abstracts, V18, P1038 HUTSON KA, 1991, J COMP NEUROL, V312, P105, DOI 10.1002/cne.903120109 IWAHORI N, 1986, Neuroscience Research, V3, P196, DOI 10.1016/0168-0102(86)90002-7 KITZES LM, 1980, J COMP NEUROL, V192, P455, DOI 10.1002/cne.901920306 KUDO M, 1981, BRAIN RES, V221, P57, DOI 10.1016/0006-8993(81)91063-5 LARUE D T, 1991, Society for Neuroscience Abstracts, V17, P300 LI L, 1992, J NEUROSCI, V12, P4530 MARKOVITZ NS, 1993, ABSTR ASS RES OT, P110 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 Mills A. W., 1972, FOUNDATIONS MODERN A, V2, P303 PARK T, 1991, ABSTR ASS RES OT, P89 PARK T J, 1991, Society for Neuroscience Abstracts, V17, P300 PARK TJ, 1993, J NEUROSCI, V13, P2050 POLLAK GD, 1993, HEARING RES, V65, P99, DOI 10.1016/0378-5955(93)90205-F Pollak GD, 1989, NEURAL BASIS ECHOLOC POLLAK GD, 1992, ABSTR ASS RES OTOLAR, P79 POLLAK GD, 1988, HEARING RES, V36, P107, DOI 10.1016/0378-5955(88)90054-8 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 ROSS LS, 1988, J COMP NEUROL, V270, P488, DOI 10.1002/cne.902700403 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SANES DH, 1990, J NEUROSCI, V10, P3494 SANES DH, 1988, J NEUROSCI, V8, P682 SCHULLER G, 1986, J NEUROSCI METH, V18, P339, DOI 10.1016/0165-0270(86)90022-1 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 STOTLER WA, 1953, J COMP NEUROL, V98, P401, DOI 10.1002/cne.900980303 SUGA N, 1985, J NEUROPHYSIOL, V53, P1109 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 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 TSUCHITA.C, 1966, J NEUROPHYSIOL, V29, P684 VATER M, 1992, J COMP NEUROL, V325, P183, DOI 10.1002/cne.903250205 WENSTRUP JJ, 1988, J NEUROPHYSIOL, V60, P1369 WENSTRUP JJ, 1985, HEARING RES, V17, P191, DOI 10.1016/0378-5955(85)90021-8 WU SH, 1992, J NEUROPHYSIOL, V68, P1151 YANG L, 1993, IN PRESS SOC NEUR AB YANG LC, 1992, J NEUROPHYSIOL, V68, P1760 YIN TCT, 1985, J NEUROPHYSIOL, V53, P746 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 ZOOK JM, 1979, SOC NEUR ABSTR, V5, P34 ZOOK JM, 1985, J COMP NEUROL, V237, P307, DOI 10.1002/cne.902370303 ZOOK JM, 1987, J COMP NEUROL, V261, P347, DOI 10.1002/cne.902610303 ZOOK JM, 1982, J COMP NEUROL, V207, P14, DOI 10.1002/cne.902070103 NR 75 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 FEB PY 1994 VL 73 IS 1 BP 121 EP 140 DI 10.1016/0378-5955(94)90290-9 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MV541 UT WOS:A1994MV54100014 PM 8157501 ER PT J AU DECRAEMER, WF KHANNA, SM AF DECRAEMER, WF KHANNA, SM TI MODELING THE MALLEUS VIBRATION AS A RIGID-BODY MOTION WITH ONE ROTATIONAL AND ONE TRANSLATIONAL DEGREE-OF-FREEDOM SO HEARING RESEARCH LA English DT Article DE MALLEUS; VIBRATION MODE; INTERFEROMETER; CAT; RIGID BODY ID CAT; FREQUENCY; MANUBRIUM AB Vibration of a set of points distributed along the manubrium of cat was measured with a heterodyne interferometer-in response to sinusoidal acoustic signals. The observed motion did not fit pure rotation of the malleus around a fixed axis coinciding with the anterior mallar and posterior incudal ligament as is classically assumed. As a first approximation a model of motion consisting of a rotational and a translational component was used. At low frequencies the rotation is mostly predominant, but the situation may be entirely reversed at mid and high frequencies. The presence of a translation besides rotation was also found at some frequencies in the motion of the human malleus. C1 COLUMBIA UNIV,COLL PHYSICIANS & SURGEONS,DEPT OTOLARYNGOL,NEW YORK,NY 10032. RP DECRAEMER, WF (reprint author), UNIV ANTWERP,RIJKSUNIV CTR ANTWERP,BIOMED PHYS LAB,GROENENBORGERLAAN 171,B-2020 ANTWERP,BELGIUM. CR BARANY E, 1938, ACTA OTOLARYNGOL S S, V26 Dahmann H, 1929, Z HALS NASEN OHRENH, V24, P462 DECRAEMER WF, 1989, HEARING RES, V38, P1, DOI 10.1016/0378-5955(89)90123-8 DECRAEMER WF, 1990, HEARING RES, V47, P205, DOI 10.1016/0378-5955(90)90152-F DECRAEMER WF, 1991, HEARING RES, V54, P305, DOI 10.1016/0378-5955(91)90124-R DECRAEMER WF, 1992, 3 DIMENSIONAL DISPLA, P156 DECRAEMER WF, 1993, UNPUB 3 DIMENSIONAL DONAHUE KM, 1989, THESIS MIT CAMBRIDGE DONAHUE KM, 1991, CAN MOTION HUMAN MAL, P53 FUNNELL WRJ, 1992, J ACOUST SOC AM, V91, P2082, DOI 10.1121/1.403694 GRAHAM MD, 1978, ANN OTO RHINOL LARYN, V87, P426 GUNDERSEN T, 1976, ACTA OTO-LARYNGOL, V82, P16, DOI 10.3109/00016487609120858 GYO K, 1987, ACTA OTO-LARYNGOL, V103, P87, DOI 10.3109/00016488709134702 KHANNA SM, 1970, HOLOGRAPHIC STUDY TY Kirikae I., 1960, STRUCTURE FUNCTION M Press W. H., 1989, NUMERICAL RECIPES AR Wells D A, 1967, LAGRANGIAN DYNAMICS Wever EG, 1954, PHYSL ACOUSTICS Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 NR 19 TC 31 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 JAN PY 1994 VL 72 IS 1-2 BP 1 EP 18 DI 10.1016/0378-5955(94)90199-6 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300001 PM 8150727 ER PT J AU VELLUTI, RA PENA, JL PEDEMONTE, M NARINS, PM AF VELLUTI, RA PENA, JL PEDEMONTE, M NARINS, PM TI INTERNALLY-GENERATED SOUND STIMULATES COCHLEAR NUCLEUS UNITS SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS; SPONTANEOUS ACTIVITY; ELECTROCARDIOGRAM; INTERNAL SOUNDS; CAROTID OCCLUSION; WAKEFULNESS ID NERVE; SLEEP AB The body generates many physiological sounds. One of the most prominent is that produced by the blood flowing inside the vessels with each heart beat. On the other hand, the cochlea is a very sensitive receptor with a low threshold. Given the anatomical close proximity of the carotid artery and other vessels to the inner ear, the possibility of its being stimulated is very high. Cochlear nucleus spontaneous as well sound-responding auditory units were studied. A close relationship between the heart beat, that is the blood flow, and the cochlear nucleus firing was demonstrated, in anesthetized and awake guinea-pigs. Temporary mechanical interruption of the blood flow through the ipsilateral carotid artery abolished firing increments at the cochlear nucleus time-locked to the heart beat. We conclude that one component of the so called 'spontaneous' firing in the auditory system is actually evoked activity due to normal body-generated sounds or noises. C1 UNIV CALIF LOS ANGELES, DEPT BIOL, LOS ANGELES, CA USA. RP VELLUTI, RA (reprint author), UNIV REPUBLICA, FAC MED, DEPT FISIOL, GRAL FLORES 2125, MONTEVIDEO 11800, URUGUAY. CR Brownell W. E., 1986, NEUROBIOLOGY HEARING, P91 DEVRIES HL, 1952, J ACOUST SOC AM, V24, P527, DOI 10.1121/1.1906931 Kiang NY-s, 1965, DISCHARGE PATTERNS S KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 LEWIS ER, 1992, HEARING RES, V63, P7, DOI 10.1016/0378-5955(92)90067-W PENA JL, 1992, ARCH ITAL BIOL, V130, P179 SIEGEL W, 1978, HEART, P422 VELLUTI R, 1989, HEARING RES, V39, P203, DOI 10.1016/0378-5955(89)90091-9 NR 8 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 JAN PY 1994 VL 72 IS 1-2 BP 19 EP 22 DI 10.1016/0378-5955(94)90200-3 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300002 PM 8150736 ER PT J AU RYAN, AF BENNETT, TM WOOLF, NK AXELSSON, A AF RYAN, AF BENNETT, TM WOOLF, NK AXELSSON, A TI PROTECTION FROM NOISE-INDUCED HEARING-LOSS BY PRIOR EXPOSURE TO A NONTRAUMATIC STIMULUS - ROLE OF THE MIDDLE-EAR MUSCLES SO HEARING RESEARCH LA English DT Article DE NOISE TRAUMA; MIDDLE EAR MUSCLES; PREEXPOSURE; GERBIL ID PERIODIC REST; SUSCEPTIBILITY; SENSITIVITY; COCHLEA; DAMAGE AB Recent evidence suggests that prior exposure to a moderate-level acoustic stimulus can reduce damage to later exposure to the same stimulus at high intensity [Canlon et al, Hear. Res. 34, 197-200 (1988)]. To test the role of the middle ear muscles (MEMs) in this phenomenon, mongolian gerbils were conditioned by exposure to a two-octave band of noise (1414-5656 Hz) at 81 dB SPL without conditioning. The MEMs of one ear in each subject were cut, to determine their role in any noise trauma protection effects. In the unoperated ears, conditioning without a recovery period did not alter the effects of the 110 dB stimulus. Conditioning followed by a one week recovery period reduced both temporary (TTS) and permanent (PTS) threshold shift. MEM section had no effect on either TTS or PTS in unconditioned subjects, and did not alter the reduction in TTS or PTS seen with conditioning. It is concluded that the noise trauma resistance provided by acoustic conditioning is not mediated by the MEMs. C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. VET ADM MED CTR,LA JOLLA,CA 92093. SAHLGRENS UNIV HOSP,DEPT AUDIOL,GOTHENBURG,SWEDEN. RP RYAN, AF (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT SURG OTOLARYNGOL,LA JOLLA,CA 92093, USA. RI Legarth, Jonas/A-9156-2012 CR Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 BORG E, 1972, ACTA OTOLARYNGOL S, V304 BORG E, 1984, ACOUSTIC REFLEX, P413 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, 1992, NOISE INDUCED HEARIN, P489 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 DALLOS D, 1973, AUDITORY PERIPHERY DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 FLETCHER JOHN L., 1962, SOUND, V1, P17, DOI 10.1121/1.2369553 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C HENDERSON D, 1991, NOISE INDUCED HEARIN, P476 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 NEELY JG, 1991, HEARING RES, V52, P403, DOI 10.1016/0378-5955(91)90028-8 NEERGAARD EB, 1963, ACTA OTOLARYNGOL S, V188, P280 PAPAZIAN M, 1993, ASS RES OTOLARYNGOL, V16, P96 RAJAN R, 1988, BRAIN RES, V459, P241, DOI 10.1016/0006-8993(88)90640-3 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 RYAN A, 1978, J ACOUST SOC AM, V63, P1145, DOI 10.1121/1.381822 RYAN AF, 1992, HEARING RES, V61, P24, DOI 10.1016/0378-5955(92)90032-I Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 SOLOKOWSKI A, 1973, ARCH OHREN NASEN KEH, V203, P289 WOOLF N K, 1988, Society for Neuroscience Abstracts, V14, P475 ZAKRISSON JE, 1974, ACTA OTOLARYNGOL STO, V79, P1 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 27 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 1994 VL 72 IS 1-2 BP 23 EP 28 DI 10.1016/0378-5955(94)90201-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300003 PM 8150739 ER PT J AU HOUTGAST, T AOKI, S AF HOUTGAST, T AOKI, S TI STIMULUS-ONSET DOMINANCE IN THE PERCEPTION OF BINAURAL INFORMATION SO HEARING RESEARCH LA English DT Article DE PRECEDENCE EFFECT; SOUND LOCALIZATION; LATERALIZATION; SPACIOUSNESS; DICHOTIC SIGNALS; BINAURAL PROCESSING ID INTERAURAL DIFFERENCES; FREQUENCY; DISCRIMINATION; LEVEL AB With dichotic signals presented by headphone, stimulus-onset dominance (the 'precedence effect') was investigated for various types of binaural-processing-based percepts. The following three dichotic cues were considered: (1) inter-aural time delay (IATD, underlying the lateralization of the sound image), (2) inter-aural level difference (IALD, also underlying lateralization), and (3) inter-aural cross correlation (IACC, underlying the spaciousness of the sound image in terms of broadness/ compactness). For all three cases, the degree of stimulus-onset dominance is estimated by one and the same experimental paradigm, which is essentially the same as used by Aoki and Houtgast [Hear. Res. 59, 25-30 (1992)1: When subdividing a brief stimulus in two parts of equal duration, a leading and a trailing part, in which the dichotic cue has opposite values, the over-all sensation is found to be dominated by the cue in the leading part. This dominance can be compensated by shortening the leading part (while keeping total signal duration constant), providing a quantitative measure for the onset dominance. The signals were octave-band filtered noise (center frequencies 500 or 2000 Hz) or 7-kHz low-pass filtered noise, and total signal duration was 5, 10, 20 or 40 ms. The results obtained for the four signal durations have been converted to a weighting function, representing the perceptual weight of the dichotic information as a function of time-after-signal-onset. These estimated weighting functions (derived separately for IATD, IALD and IACC, and for each of the three types noise signals) show a peak during the first few milliseconds, followed by a brief period of reduced weight (5 to 10 ms after signal onset), recovering after, roughly, 20 ms. This typical peak-dip-shaped weighting function is most clear for IATD and IALD (lateralization), and is a little less pronounced for IACC (broadness/ compactness). C1 NIPPON TELEGRAPH & TEL PUBL CORP, HUMAN INTERFACE LABS, YOKOSUKA, KANAGAWA, JAPAN. RP HOUTGAST, T (reprint author), TNO, INST HUMAN FACTORS, POB 23, 3769 ZG SOESTERBERG, NETHERLANDS. CR AOKI S, 1992, HEARING RES, V59, P25, DOI 10.1016/0378-5955(92)90098-8 Blauert J., 1983, SPATIAL HEARING BUELL TN, 1988, J ACOUST SOC AM, V84, P2063, DOI 10.1121/1.397050 FITZGIBBONS PJ, 1983, J ACOUST SOC AM, V74, P67, DOI 10.1121/1.389619 GARDNER MB, 1968, J ACOUST SOC AM, V43, P1243, DOI 10.1121/1.1910974 HAAS H, 1972, J ACOUST ENG SOC, V20, P149 HAFTER ER, 1988, FUNCTIONS AUDITORY S HENNING GB, 1981, HEARING RES, V4, P185, DOI 10.1016/0378-5955(81)90005-8 RAATGEVER J, 1992, 13TH P ICA BEIJ WALLACH H, 1949, AM J PSYCHOL, V62, P315, DOI 10.2307/1418275 YOST WA, 1988, J ACOUST SOC AM, V83, P1846, DOI 10.1121/1.396520 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 13 TC 24 Z9 24 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 JAN PY 1994 VL 72 IS 1-2 BP 29 EP 36 DI 10.1016/0378-5955(94)90202-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300004 PM 8150742 ER PT J AU BROCK, M HENLEY, CM AF BROCK, M HENLEY, CM TI POSTNATAL CHANGES IN COCHLEAR POLYAMINE METABOLISM IN THE RAT SO HEARING RESEARCH LA English DT Article DE ORNITHINE DECARBOXYLASE; POLYAMINES; COCHLEA; DEVELOPMENT; RAT ID EAR ORNITHINE DECARBOXYLASE; ALPHA-DIFLUOROMETHYLORNITHINE; INNER-EAR; ACOUSTIC DISTORTION; HEARING-LOSS; GUINEA-PIGS; INHIBITOR; MECHANICS; NONLINEARITY; RESPONSES AB Ornithine decarboxylase (ODC), the initial enzyme in the polyamine biosynthetic pathway, is increased in the developing rat cochlea, suggesting that polyamine biosynthesis is important in cochlear development. Although cochlear polyamines have been detected in adult rats, they have not been identified in developing rats. We quantified polyamines in the developing and mature rat cochlea and further characterized ODC in the early postnatal period. Putrescine and spermidine in combined tissues of the organ of Corti and lateral wall of the cochlea were highest during the first 10 postnatal days, then declined to adult levels shortly thereafter. Spermine demonstrated a similar developmental trend. A high spermidine to spermine ratio was noted during this period as was rapidly increasing ODC activity. A high spermidine/spermine ratio was also noted in the cochlear nerve of developing and mature rats, suggesting that spermidine may be necessary for function and maintenance of the nerve. This is the first report of polyamines in the developing rat cochlea. The period of increased polyamine synthesis coincides with the critical period for ototoxicity induced by cr-difluoromethylornithine, a specific ODC inhibitor, and the period of rapid cochlear development. C1 BAYLOR COLL MED,DEPT OTORHINOLARYNGOL & COMMUNICAT SCI & PHARMACO,HOUSTON,TX 77030. CR ABELOFF MD, 1986, CANCER TREAT REP, V70, P843 ABELOFF MD, 1984, J CLIN ONCOL, V2, P124 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BROWN ND, 1982, J CHROMATOGR, V245, P101, DOI 10.1016/S0021-9673(00)82479-6 CRANN SA, 1991, CELL TISSUE RES, V265, P547, DOI 10.1007/BF00340878 GORMAN ALF, 1982, J PHYSIOL-LONDON, V333, P681 HENLEY C, 1990, J CELL BIOCH F S, V14, P22 HENLEY CM, 1987, BRAIN RES BULL, V19, P695, DOI 10.1016/0361-9230(87)90056-6 HENLEY CM, 1990, HEARING RES, V43, P141, DOI 10.1016/0378-5955(90)90223-C HENLEY CM, 1991, HEARING RES, V55, P45, DOI 10.1016/0378-5955(91)90090-V JANSEN C, 1989, ARCH OTOLARYNGOL, V115, P1234 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 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 LYOS AT, 1992, OTOLARYNG HEAD NECK, V107, P501 MARKS SC, 1991, HEARING RES, V53, P230, DOI 10.1016/0378-5955(91)90057-G MELVIN MAL, 1980, PHYSIOL CHEM PHYS M, V12, P431 METCALF BW, 1978, J AM CHEM SOC, V100, P2551, DOI 10.1021/ja00476a050 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PEGG AE, 1988, ISI ATLAS-BIOCHEM, P11 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 PUJOL R, 1986, ACTA OTOLARYNGOL, V249, P29 RUSSELL D, 1968, P NATL ACAD SCI USA, V60, P1420, DOI 10.1073/pnas.60.4.1420 RUSSELL DH, 1985, DRUG METAB REV, V16, P1, DOI 10.3109/03602538508991430 RYBAK LP, 1991, ORL J OTO-RHINO-LARY, V53, P72 SAFIEDDINE S, 1992, NEUROREPORT, V3, P1145, DOI 10.1097/00001756-199212000-00029 SALZER SJ, 1990, HEARING RES, V46, P101, DOI 10.1016/0378-5955(90)90143-D SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SCHWEITZER L, 1986, BRAIN RES BULL, V16, P215, DOI 10.1016/0361-9230(86)90035-3 SEILER N, 1980, PHYSIOL CHEM PHYS M, V12, P411 SEILER N, 1981, MED BIOL, V59, P334 Seiler N, 1991, Prog Drug Res, V37, P107 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SJOERDSMA A, 1984, T ASSOC AM PHYSICIAN, V97, P70 SLOTKIN TA, 1986, BRAIN RES BULL, V17, P307, DOI 10.1016/0361-9230(86)90236-4 Slotkin T A, 1983, Int J Dev Neurosci, V1, P7, DOI 10.1016/0736-5748(83)90004-7 SLOTKIN TA, 1979, LIFE SCI, V24, P1623, DOI 10.1016/0024-3205(79)90244-3 Uziel A, 1986, Acta Otolaryngol Suppl, V429, P23 WEDGWOOD MA, 1977, NEUROPHARMACOLOGY, V16, P445, DOI 10.1016/0028-3908(77)90087-9 WILLIAMS K, 1991, LIFE SCI, V48, P469, DOI 10.1016/0024-3205(91)90463-L NR 40 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 JAN PY 1994 VL 72 IS 1-2 BP 37 EP 43 DI 10.1016/0378-5955(94)90203-8 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300005 PM 8150743 ER PT J AU WEAVER, SP SCHWEITZER, L AF WEAVER, SP SCHWEITZER, L TI DEVELOPMENT OF GERBIL OUTER HAIR-CELLS AFTER THE ONSET OF COCHLEAR FUNCTION - AN ULTRASTRUCTURAL-STUDY SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEAR DEVELOPMENT; GERBIL; OUTER HAIR CELL; SUBSURFACE CISTERNAE ID EVOKED OTOACOUSTIC EMISSIONS; ELECTROKINETIC SHAPE CHANGES; GUINEA-PIG COCHLEA; BASILAR-MEMBRANE; MONGOLIAN GERBIL; FREQUENCY-SELECTIVITY; SUBSURFACE CISTERNAE; MAMMALIAN EAR; ORGAN; CORTI AB It has recently been proposed that elements which contribute to active cochlear processes develop at the same time (between postnatal day (PND) 12 and 21) as the shift of the place code in the developing gerbil cochlea. Since outer hair cells (OHCs) have been implicated in these processes, we have hypothesized that developing OHCs will exhibit changes in anatomical features that contribute to cochlear maturation. Our results demonstrate that the ultrastructural characteristics of OHCs change after the onset of hearing (PND 12), during the time that cochlear nonlinearities are being established (PND 12-21). Differences are primarily associated with the distribution of cytoplasmic organelles. The subsurface cisternae (SSC), which are thought to be related to the mechanical support of the outer hair cell, to cell motility, and therefore to cochlear mechanics, are present at PND 10 but remain immature, with cisternal layers added during the preweanling period. In immature OHCs, more mitochondria are centrally-located than in mature OHCs. During development mitochondria come to form a continuous row near the innermost leaflet of the SSC. These ultrastructural features undergo rapid change during the maturation of peripheral auditory function. C1 UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 ATWAL OS, 1988, AM J ANAT, V182, P42, DOI 10.1002/aja.1001820105 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DOUEK EE, 1983, J LARYNGOL OTOL, V93, P793 ECHTELER SM, 1993, ARO ABSTR, V16, P25 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 ENGSTROM H, 1954, ACTA OTO-LARYNGOL, V44, P490, DOI 10.3109/00016485409127660 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 FITZAKERLEY J, 1991, ABSTR ASS RES OT, V14, P132 FRIEDMANN I, 1962, BRIT MED BULL, V18, P209 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HE ZZ, 1993, ABSTR ASS RES OT, V16, P25 Henley C, 1989, HEARING RES, V43, P141 Kikuchi K, 1965, Acta Otolaryngol, V60, P207, DOI 10.3109/00016486509127003 HOLLEY M, 1991, BIOESSAYS, V13, P115, DOI 10.1002/bies.950130304 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 Karnovsky M. J, 1965, J CELL BIOL, V27, P137 KHANNA SM, 1986, HEARING RES, V23, P55, DOI 10.1016/0378-5955(86)90175-9 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X KRUAS HJ, 1981, HEARING RES, V4, P89 LIM DJ, 1985, ACTA OTO-LARYNGOL, V99, P478, DOI 10.3109/00016488509108941 Lim D, 1992, DEV AUDITORY VESTIBU, P33 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 NAGASAWA A, 1991, SCANNING MICROSCOPY, V5, P747 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PFEIFFER RR, 1973, BASIC MECHANISMS HEA, P555 PUJOL R, 1970, J COMP NEUROL, V139, P115, DOI 10.1002/cne.901390108 PUJOL R, 1991, HEARING RES, V57, P129, DOI 10.1016/0378-5955(91)90082-K Romand R., 1983, DEV AUDITORY VESTIBU, P47 ROMAND R, 1983, NEUROSCI LETT, V35, P271, DOI 10.1016/0304-3940(83)90329-4 ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 ROTH B, 1992, ANAT EMBRYOL, V185, P571, DOI 10.1007/BF00185616 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SAITO K, 1983, CELL TISSUE RES, V229, P467 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 Siegel S., 1956, NONPARAMETRIC STATIS SMITH CA, 1957, AM J ANAT, V100, P337, DOI 10.1002/aja.1001000304 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E THORN L, 1975, ADV ANAT EMBRYOL CEL, V51, P1 UEDA H, 1992, HEARING RES, V62, P199, DOI 10.1016/0378-5955(92)90187-R WALSH EJ, 1990, AM J OTOLARYNG, V11, P23, DOI 10.1016/0196-0709(90)90166-S Walsh Edward J., 1992, P161 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 55 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 JAN PY 1994 VL 72 IS 1-2 BP 44 EP 52 DI 10.1016/0378-5955(94)90204-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300006 PM 8150744 ER PT J AU ROMAND, R HIRNINGFOLZ, U EHRET, G AF ROMAND, R HIRNINGFOLZ, U EHRET, G TI N-MYC EXPRESSION IN THE EMBRYONIC COCHLEA OF THE MOUSE SO HEARING RESEARCH LA English DT Article DE N-MYC; PROTOONCOGENE; INNER EAR; ONTOGENY; SPIRAL GANGLION; KOLLIKERS ORGAN ID C-MYC; DIFFERENTIAL EXPRESSION; INSITU HYBRIDIZATION; GENE-EXPRESSION; MESSENGER-RNAS; INNER-EAR; ORGANOGENESIS; ONCOGENE; PROTEIN; CELLS AB N-myc expression in the mouse embryo was examined during the late cochlear organogenesis. Tissue distribution of N-myc expression was histologically analyzed by in situ hybridization of the transcript in the cochlea between 15 and 18 days of gestation. At 15 days of gestation, N-myc expression was found very conspicuous in nervous structure of the cochlea such as the auditory nerve and the spiral ganglion. Moreover, N-myc was also present in the Kollikers organ and in the epithelium surrounding the cochlear canal. A few days later, N-myc expression was still clearly present in the Kollikers organ but less so in nervous structures. This study shows that cochlear tissues derived from the otic placode present a significant level of N-myc transcript during late embryogenesis. N-myc expression seems to be related to cell differentiation in the inner ear. C1 UNIV ULM,KLIN GENET ABT,W-7900 ULM,GERMANY. UNIV ULM,VERGLEICHEND NEUROBIOL ABT,ULM,GERMANY. RP ROMAND, R (reprint author), UNIV BLAISE PASCAL CLERMONT II,NEUROBIOL & PHYSIOL DEV LAB,F-63177 CLERMONT FERRAND,FRANCE. CR ADAMSON ED, 1987, DEVELOPMENT, V99, P449 BERNARD O, 1992, NEURON, V9, P1217, DOI 10.1016/0896-6273(92)90079-S COX KH, 1984, DEV BIOL, V101, P485, DOI 10.1016/0012-1606(84)90162-3 DAMICOMARTEL A, 1983, AM J ANAT, V166, P445, DOI 10.1002/aja.1001660406 DEPINHO RA, 1991, ADV CANCER RES, V57, P1, DOI 10.1016/S0065-230X(08)60994-X DEPINHO RA, 1986, P NATL ACAD SCI USA, V83, P1827, DOI 10.1073/pnas.83.6.1827 DESPRES G, 1988, NEUROSCI LETT, V85, P5, DOI 10.1016/0304-3940(88)90418-1 DESPRES G, 1991, NEUROREPORT, V2, P639, DOI 10.1097/00001756-199111000-00001 DOWNS KM, 1989, GENE DEV, V3, P860, DOI 10.1101/gad.3.6.860 HIRNING U, 1991, MECH DEVELOP, V33, P119, DOI 10.1016/0925-4773(91)90078-K HIRVONEN H, 1990, ONCOGENE, V5, P1787 JACOBOVITS A, 1985, NATURE, V318, P188 KATO K, 1991, DEV GROWTH DIFFER, V33, P29 KERKHOFF E, 1991, ONCOGENE, V6, P93 KOHL NE, 1986, NATURE, V319, P73, DOI 10.1038/319073a0 KOHL NE, 1983, CELL, V35, P359, DOI 10.1016/0092-8674(83)90169-1 LARCHER JC, 1991, ONCOGENE, V6, P633 LIM DJ, 1985, ACTA OTOLARYNGOL S, V42, P1 Lim D, 1992, DEV AUDITORY VESTIBU, P33 MCCORMACK MA, 1992, MOL BRAIN RES, V12, P215, DOI 10.1016/0169-328X(92)90087-R MEICHLE A, 1992, BIOCHIM BIOPHYS ACTA, V1114, P126 MORGAN JI, 1991, ANNU REV NEUROSCI, V14, P421, DOI 10.1146/annurev.ne.14.030191.002225 MORGAN JI, 1989, ASSEMBLY NERVOUS SYS, P235 MUGRAUER G, 1988, J CELL BIOL, V107, P1325, DOI 10.1083/jcb.107.4.1325 MUGRAUER G, 1991, J CELL BIOL, V112, P13, DOI 10.1083/jcb.112.1.13 NECKERS LM, 1992, J IMMUNOTHER, V12, P162, DOI 10.1097/00002371-199210000-00003 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 RAMSAY G, 1986, MOL CELL BIOL, V6, P4450 REPRESA J, 1990, DEVELOPMENT, V110, P1081 SCHMID P, 1989, SCIENCE, V243, P226, DOI 10.1126/science.2911736 SLAMON DJ, 1986, SCIENCE, V232, P768, DOI 10.1126/science.3008339 STANTON BR, 1992, BRAIN PATHOL, V2, P71 WAKAMATSU Y, 1993, NEURON, V10, P1, DOI 10.1016/0896-6273(93)90236-K YAMADA S, 1992, DEV GROWTH DIFFER, V34, P239 ZIMMERMAN KA, 1986, NATURE, V319, P780, DOI 10.1038/319780a0 NR 35 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 1994 VL 72 IS 1-2 BP 53 EP 58 DI 10.1016/0378-5955(94)90205-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300007 PM 8150745 ER PT J AU KOSSL, M AF KOSSL, M TI OTOACOUSTIC EMISSIONS FROM THE COCHLEA OF THE CONSTANT FREQUENCY BATS, PTERONOTUS-PARNELLII AND RHINOLOPHUS-ROUXI SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSION; SPONTANEOUS AND EVOKED; DISTORTION PRODUCTS; 2F(1)-F(2); COCHLEAR RESONANCE; BASILAR MEMBRANE; ECHOLOCATION ID DOPPLER-SHIFTED ECHOES; CF-FM BAT; ACOUSTIC DISTORTION; MOUSTACHED BAT; MUSTACHE BAT; SPIRAL LIGAMENT; AUDITORY-SYSTEM; P-PARNELLII; INNER-EAR; RESONANCE AB During stimulation with continuous pure tones, the cochlea of each individual of the mustached bat, Pteronotus parnellii, produces a strong evoked stimulus-frequency otoacoustic emission (SFOAE) at about 62 kHz. The SFOAEs were on average 480 Hz above the dominant constant frequency component of the echolocation call (resting frequency, RF). In two out of nine individuals of Pteronotus the SFOAEs changed into spontaneous otoacoustic emissions of 25-40 dB SPL. In the rufuous horseshoe bat, Rhinolophus rouxi spontaneous emissions were not detected and only in two out of seven animals were there weak SFOAEs about 300 Hz above the RF of 78 kHz. This difference may be due to a stronger damping of underlying resonant processes in Rhinolophus (Henson et al., 1985a). Acoustic distortion products behaved quite similar in both species. The first lower sideband distortion 2f(1)-f(2) was measurable over a wide frequency range between 10 and 100 kHz. The optimum frequency separation Delta f of the two primary tones to evoke maximum 2f(1)-f(2) distortion was 0.8 to 5.8 kHz in Pteronotus and 1 to 7 kHz in Rhinolophus for frequencies outside the range of the constant frequency components of the call. This corresponds to ratios f(2)/f(1) of about 1.03 to 1.2. At the frequency of the SFOAE in Pteronotus (480 Hz above the RF) and about 300 Hz above the RF in Rhinolophus the optimum Delta f decreased sharply to values of 31-63 Hz in Pteronotus (ratio f(2)/f(1) of 1.0005-1.001), and to 39-590 Hz in Rhinolophus (ratio f(2)/f(1) of 1.0005-1.007). In Pteronotus a second minimum of Delta f was found at about 90 kHz (values of 180-620 Hz, ratios f(2)/f(1) of 1.002-1.007). In both bat species, the respective minima of Delta f are located at or close to frequencies where neuronal tuning sharpness is exceptionally high. This indicates a mechanical origin of enhanced tuning. After adjusting the frequency of f(2) to match the optimum Delta fs, 2f(1)-f(2) threshold curves were obtained. The distortion product threshold approximately parallels neuronal data and is in both species characterized by a pronounced insensitivity at the RF followed by a steep threshold minimum at frequencies 0.3-3 kHz above the RF. These features may be involved in reducing the cochlear response to the call such that the bats are able to focus on the Doppler-shifted echos which are slightly higher in frequency and thus within the range of the treshold minimum. RP KOSSL, M (reprint author), ZOOL INST,LUISENSTR 14,D-80021 MUNICH,GERMANY. CR 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 BRUNS V, 1976, J COMP PHYSIOL, V106, P77 FRANK G, 1993, 21TH P GOTT NEUR C T, P262 GAIONI SJ, 1990, J NEUROPHYSIOL, V64, P1801 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 HARRIS FP, 1992, HEARING RES, V64, P133, DOI 10.1016/0378-5955(92)90175-M HENSON MM, 1984, HEARING RES, V16, P231, DOI 10.1016/0378-5955(84)90112-6 HENSON MM, 1985, HEARING RES, V20, P207, DOI 10.1016/0378-5955(85)90025-5 HENSON MM, 1991, HEARING RES, V56, P122, DOI 10.1016/0378-5955(91)90161-2 HENSON MM, 1978, AM J ANAT, V153, P143, DOI 10.1002/aja.1001530109 HENSON OW, 1989, HEARING RES, V38, P213, DOI 10.1016/0378-5955(89)90066-X HENSON OW, 1985, J COMP PHYSIOL A, V157, P587, DOI 10.1007/BF01351353 HENSON OW, 1990, HEARING RES, V50, P259, DOI 10.1016/0378-5955(90)90050-Y HUFFMAN RF, 1993, J COMP PHYSIOL A, V171, P725, DOI 10.1007/BF00213069 Kemp D T, 1981, Ciba Found Symp, V85, P54 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KOSSL M, 1985, HEARING RES, V19, P157, DOI 10.1016/0378-5955(85)90120-0 KOSSL M, 1992, HEARING RES, V60, P156, DOI 10.1016/0378-5955(92)90018-I KOSSL M, 1992, NATURWISSENSCHAFTEN, V79, P425, DOI 10.1007/BF01138579 KOSSL M, 1993, 21TH P GOTT NEUR C, P264 KOSSL M, 1990, J COMP PHYSIOL A, V166, P711 KOSSL M, 1994, HEARING RES, V72, P73, DOI 10.1016/0378-5955(94)90207-0 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 MAIN IG, 1984, VIBRATIONS WAVES PHY MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MANLEY GA, 1990, MECH BIOPHYSICS HEAR, P210 METZNER W, 1987, J COMP PHYSL, V160, P385 NEUWEILER G, 1990, PHYSIOL REV, V70, P615 POLLAK G, 1979, J COMP PHYSIOL, V131, P255 POLLAK G, 1972, SCIENCE, V176, P66, DOI 10.1126/science.176.4030.66 SCHNITZL.HU, 1970, Z VERGL PHYSIOL, V68, P25, DOI 10.1007/BF00297809 SCHNITZL.HU, 1968, Z VERGL PHYSIOL, V57, P376, DOI 10.1007/BF00303062 SCHULLER G, 1979, EXP BRAIN RES, V34, P117 SCHULLER G, 1974, J COMP PHYSIOL, V89, P275, DOI 10.1007/BF00696191 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SMURZYNSKI J, 1992, HEARING RES, V58, P227, DOI 10.1016/0378-5955(92)90132-7 SUGA N, 1977, J EXP BIOL, V69, P207 SUGA N, 1975, J EXP BIOL, V63, P161 SUGA N, 1976, J COMP PHYSIOL, V106, P111 VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 Vater M., 1988, ANIMAL SONAR, P225 NR 45 TC 49 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 JAN PY 1994 VL 72 IS 1-2 BP 59 EP 72 DI 10.1016/0378-5955(94)90206-2 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300008 PM 8150746 ER PT J AU KOSSL, M AF KOSSL, M TI EVIDENCE FOR A MECHANICAL FILTER IN THE COCHLEA OF THE CONSTANT FREQUENCY BATS, RHINOLOPHUS-ROUXI AND PTERONOTUS-PARNELLII SO HEARING RESEARCH LA English DT Article DE DISTORTION PRODUCTS; 2F(1)-F(2); ECHOLOCATION; BASILAR MEMBRANE ID MUSTACHE BAT; DISTORTION PRODUCTS; ECHOLOCATION; RESONANCE; MEMBRANE; NUCLEUS; EAR; MAP AB To investigate the function of basilar membrane (BM) thickenings in the cochlea of bats which use constant frequency (CF) echolocation calls, acoustic distortion products were measured while placing the primary stimuli f(1) and f(2) at frequencies which are represented in the thickened BM regions. In Rhinolophus, for primary stimuli between about 80-100 kHz, pronounced maxima of the level of distortion products (2f(1)-f(2), 3f(1)-2f(2), 4f(1)-3f(2)) Can be measured if the frequency separation between the two primary tones is chosen so that the resulting distortion frequency matches the dominant CF frequency (resting frequency, RF). The distortion maxima extend from the individual RF down to frequencies which are 2-4 kHz lower. The data indicate that the thickened BM region in the basal halfturn of the cochlea strongly oscillates at the bats' RF and slightly below. The hearing threshold, however, is at a maximum at the RF (see Kossl 1993). Therefore, the RF oscillations are thought to be involved in absorbing the respective frequency such that the more apically located frequency place of the RF is insensitive and a mechanical notch filter is established. In Pteronotus, there are maxima of the level of 2f(1)-f(2) at distortion frequencies around the RF of about 61.5 kHz up to the frequency of a strong stimulus-frequency otoacoustic emission (SFOAE) which is a few hundred Hz higher. Pronounced distortions in the RF range can only be elicited when the stimulus frequencies are between about 62 to 72 kHz. Similar to the situation in Rhinolophus, this frequency band is represented on a stretch of thickened BM. RP KOSSL, M (reprint author), ZOOL INST,LUISENSTR 14,D-80021 MUNICH,GERMANY. CR ALLEN JB, 1993, ABSTR ASS RES OT, P103 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1992, P ROY SOC B-BIOL SCI, V250, P29, DOI 10.1098/rspb.1992.0126 BRUNS V, 1976, J COMP PHYSIOL, V106, P77 HENSON OW, 1989, HEARING RES, V38, P213, DOI 10.1016/0378-5955(89)90066-X HENSON OW, 1990, HEARING RES, V50, P259, DOI 10.1016/0378-5955(90)90050-Y KOLSTON PJ, 1989, J ACOUST SOC AM, V86, P133, DOI 10.1121/1.398332 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KOSSL M, 1992, HEARING RES, V60, P156, DOI 10.1016/0378-5955(92)90018-I KOSSL M, 1994, HEARING RES, V72, P59, DOI 10.1016/0378-5955(94)90206-2 KOSSL M, 1990, J COMP PHYSIOL A, V166, P711 KOSSL M, 1990, J COMP PHYSIOL A, V166, P695 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 METZNER W, 1987, J COMP PHYSL, V160, P385 NEUWEILER G, 1987, BEHAV ECOL SOCIOBIOL, V20, P53, DOI 10.1007/BF00292166 SUGA N, 1975, J EXP BIOL, V63, P161 VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 Vater M., 1988, ANIMAL SONAR, P225 WILSON JP, 1983, HEARING RES, V10, P15, DOI 10.1016/0378-5955(83)90016-3 ZWISLOCKI JJ, 1979, SCIENCE, V204, P639, DOI 10.1126/science.432671 ZWISLOCKI JJ, 1986, HEARING RES, V22, P155, DOI 10.1016/0378-5955(86)90091-2 NR 21 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 JAN PY 1994 VL 72 IS 1-2 BP 73 EP 80 DI 10.1016/0378-5955(94)90207-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300009 PM 8150747 ER PT J AU RYALS, BM WESTBROOK, EW AF RYALS, BM WESTBROOK, EW TI TEM ANALYSIS OF NEURAL TERMINALS ON AUTORADIOGRAPHICALLY IDENTIFIED REGENERATED HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE BIRD; HAIR CELLS; REGENERATION; NEURAL ID CHICKEN BASILAR PAPILLA; AVIAN INNER-EAR; ACOUSTIC TRAUMA; INNERVATION; COCHLEA; QUAIL AB Regenerated tall and short hair cells identified by autoradiography ([H-3]thymidine) were analyzed for their neural contacts using transmission electron microscopy. Ears from mature Coturnix quail(N = 5) exposed to pure tone overstimulation (1500 Hz, 115 dB, 12 h) and treated with [H-3] thymidine for 10 days were fixed, embedded, sectioned serially in 100 mu intervals and prepared for autoradiography. At fifty percent length along the papilla, alternating semi-thick (1 mu m) and thin (70 nm) sections were taken at 50 mu m intervals. Semi-thick sections were analyzed at the light microscope level for autoradiographic labeling of [H-3]thymidine over the hair cell nucleus. When an autoradiographically labelled hair cell was identified the corresponding serial thin sections were analyzed in the transmission electron microscope. Seven autoradiographically labeled hair cells in semi-thin sections were positively identified in immediately adjacent thin serial sections. Labeled hair cells were morphologically similar to adjacent cells with no label and generally appeared to receive similar innervation. Regenerated short hair cells showed large chalice shaped, efferent terminals, intermediate hair cells received both afferent and efferent innervation and tall hair cells were contacted by two to three afferent terminals with synaptic specializations. These results provide conclusive evidence of both efferent and afferent synaptic contacts on newly regenerated hair cells of all types 10 days following acoustic trauma. C1 DEPT VET AFFAIRS MED CTR,RICHMOND,VA. RP RYALS, BM (reprint author), JAMES MADISON UNIV,DEPT SPEECH PATHOL & AUDIOL,HARRISONBURG,VA 22807, USA. CR CHANDLER JP, 1984, J COMP NEUROL, V222, P506, DOI 10.1002/cne.902220405 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 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 FIRBAS W, 1983, HEARING RES, V10, P109, DOI 10.1016/0378-5955(83)90021-7 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 HIROKAWA N, 1978, J NEUROCYTOL, V7, P283, DOI 10.1007/BF01176994 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MANLEY GA, 1990, PERIPHERAL HEARING M, P206 MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 REBILLARD M, 1983, ACTA OTO-LARYNGOL, V96, P379, DOI 10.3109/00016488309132723 RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N RYALS BM, 1992, EXP NEUROL, V115, P18, DOI 10.1016/0014-4886(92)90214-B RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1989, HEARING RES, V43, P81, DOI 10.1016/0378-5955(89)90061-0 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 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 VONDURING M, 1985, FORTSCHRITTE ZOOL BD, V30 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P277, DOI 10.1016/0306-4522(85)90178-2 YALS BM, 1991, ABSTR ASS OT, V338, P123 NR 24 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 JAN PY 1994 VL 72 IS 1-2 BP 81 EP 88 DI 10.1016/0378-5955(94)90208-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300010 PM 8150748 ER PT J AU SHEPHERD, RK XU, SA CLARK, GM AF SHEPHERD, RK XU, SA CLARK, GM TI PARTIAL HEARING-LOSS IN THE MACAQUE FOLLOWING THE COADMINISTRATION OF KANAMYCIN AND ETHACRYNIC-ACID SO HEARING RESEARCH LA English DT Article DE OTOTOXICITY; NEPHROTOXICITY; HEARING LOSS; AMINOGLYCOSIDES; LOOP DIURETICS; DEAFNESS; COCHLEAR IMPLANTS ID GENTAMICIN-NEPHROTOXICITY; AUDITORY-NERVE; ELECTRICAL-STIMULATION; AMINOOXYACETIC ACID; COCHLEAR PATHOLOGY; GUINEA-PIGS; OTOTOXICITY; AMINOGLYCOSIDE; RAT; DEAFNESS AB Co-administration of kanamycin (KA) with the loop diuretic ethacrynic acid (EA) rapidly produces a profound hearing loss in the cat while maintaining normal renal function [Xu et al., Hear. Res. 70, 205-215 (1993)]. In the present paper we have applied this deafening procedure to the old world monkey Macaca fascicularis (macaque). Following the co-administration of KA and EA, the hearing loss in the macaque developed far slower than we observed in the cat. Moreover, unlike the cat, there was evidence of a partial recovery in the animal's hearing, resulting in a bilaterally symmetrical high frequency hearing loss. The extent of this hearing loss was dependent on the dose of the EA administered. Finally, the most unexpected result of the present study was the degree of acute nephrotoxicity experienced by these animals following the drug administration. The sensitivity of this species to renal failure restricted the dose of EA that could be safely administered. In conclusion, the co-administration of KA and EA cannot reliably produce a profound hearing loss in the macaque. While it can produce a dose dependent high frequency hearing loss the animal will also experience acute renal failure that requires careful management. RP SHEPHERD, RK (reprint author), UNIV MELBOURNE,DEPT OTOLARYNGOL,32 GISBORNE ST,MELBOURNE,VIC 3002,AUSTRALIA. RI Shepherd, Robert/I-6276-2012 CR ADELMAN RD, 1979, J INFECT DIS, V140, P342 Appel G.B., 1982, AMINOGLYCOSIDES MICR, P269 BAUCHAMAP D, 1990, J PHARMACOL EXP THER, V255, P858 BENNETT WM, 1982, J LAB CLIN MED, V99, P156 BENNETT WM, 1976, P SOC EXP BIOL MED, V151, P736 BOSHER SK, 1973, ACTA OTO-LARYNGOL, V75, P184, DOI 10.3109/00016487309139694 Brummett RE, 1982, AMINOGLYCOSIDES MICR, P419 BRUMMETT RE, 1979, ARCH OTOLARYNGOL, V105, P240 BRYANT GM, 1984, HEARING RES, V15, P173, DOI 10.1016/0378-5955(84)90048-0 CHIU PJS, 1978, ANTIMICROB AGENTS CH, V14, P214 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 HAWKINS J. E., 1959, ANN OTOL RHINOL AND LARYNGOL, V68, P698 HAWKINS JE, 1977, ACTA OTO-LARYNGOL, V83, P123, DOI 10.3109/00016487709128821 HAYASHIDA T, 1989, ACTA OTO-LARYNGOL, V108, P404, DOI 10.3109/00016488909125546 HIEL H, 1992, HEARING RES, V57, P157, DOI 10.1016/0378-5955(92)90148-G HUMES HD, 1984, J CLIN INVEST, V73, P134, DOI 10.1172/JCI111184 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JAVEL E, 1991, ASS RES OT MIDW M FL, V14, P130 KALOYANIDES GJ, 1980, KIDNEY INT, V18, P571, DOI 10.1038/ki.1980.175 KHANNA SM, 1986, HEARING RES, V23, P55, DOI 10.1016/0378-5955(86)90175-9 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 Kohonen A., 1965, ACTA OTO-LARYNGOL, V208, P1 LAWSON DH, 1972, J INFECT DIS, V126, P593 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1987, ANN OTO RHINOL LARYN, V96, P48 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 Mitruka B. M., 1977, CLIN BIOCH HEMATOLOG MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 NAKAI Y, 1981, ACTA OTO-LARYNGOL, V91, P199, DOI 10.3109/00016488109138500 Parker R. A., 1982, AMINOGLYCOSIDES MICR, P235 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PFINGST BE, 1979, ANN OTO RHINOL LARYN, V88, P613 POWELL TPS, 1962, J ANAT, V96, P249 PRAZMA J, 1972, ARCHIV OTOLARYNGOL, V95, P448 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E ROBERTSON D, 1979, J ACOUST SOC AM, V66, P466, DOI 10.1121/1.383097 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1363 SHEPHERD RK, 1984, P AUST PHYSL PHARM, V15 SHEPHERD RK, 1993, P AUST NEUROSCI SOC, V4, P112 SHEPHERD RK, 1989, STUDIES PEDIATRIC AU SHEPHERD RK, 1985, HEARING RES, V18, P105, DOI 10.1016/0378-5955(85)90001-2 STEBBINS WC, 1969, ANN OTO RHINOL LARYN, V78, P1007 SUTTON D, 1983, ANN OTO RHINOL LARYN, V92, P53 TACHIBANA M, 1985, HISTOCHEMISTRY, V83, P237, DOI 10.1007/BF00953990 HUY PTB, 1983, HEARING RES, V11, P191, DOI 10.1016/0378-5955(83)90078-3 VANDEWALLE A, 1981, KIDNEY INT, V19, P529, DOI 10.1038/ki.1981.50 WEDEEN RP, 1983, LAB INVEST, V48, P212 WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 WHELTON A, 1982, AMINOGLYCOSIDES MICR, P191 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 XU SA, 1993, HEARING RES, V70, P205, DOI 10.1016/0378-5955(93)90159-X XU SA, 1988, STUDIES PEDIATRIC AU NR 54 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 JAN PY 1994 VL 72 IS 1-2 BP 89 EP 98 DI 10.1016/0378-5955(94)90209-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300011 PM 8150749 ER PT J AU DURRANT, JD MARTIN, WH HIRSCH, B SCHWEGLER, J AF DURRANT, JD MARTIN, WH HIRSCH, B SCHWEGLER, J TI 3CLT ABR ANALYSES IN A HUMAN SUBJECT WITH UNILATERAL EXTIRPATION OF THE INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; AUDITORY PATHWAY; CENTRAL AUDITORY PATHOLOGY; INFERIOR COLLICULUS; 3-CHANNEL LISSAJOUS TRAJECTORY; STEREOTAXIC RADIOSURGERY ID AUDITORY BRAIN-STEM; EVOKED-POTENTIALS; LESIONS; CAT AB Reported are the results of analyses of three-channel Lissajous trajectories (3CLTs) of the auditory brain stem responses (ABRs) in a human subject in whom a focal lesion of the brain stem was caused by stereotactic radiosurgery, the 'gamma knife'. The surgery caused total destruction of the right inferior colliculus. The results, using multiple measures for defining ABR components, confirm findings from more conventional 2-channel recordings which, in turn, suggested the presence of an intact wave IV but a negligible, if not totally absent, wave V with stimulation of the left (contralateral) ear. The results thus support theories that wave V is generated by crossed pathways and that wave IV is an independent wave generated by the lateral lemniscus. Since magnetic resonance imaging suggested no destruction of tissue below the inferior colliculus, the findings also support theories of wave V generation at or rostral to the inferior colliculus. In practical terms, the results demonstrate the value of multichannel recordings of the ABR in component identification and in interpreting ABR abnormalities. C1 EYE & EAR INST PITTSBURGH,PITTSBURGH,PA 15213. TEMPLE UNIV,SCH MED,DEPT OTOLARYNGOL & BRONCHOESOPHOGOL,PHILADELPHIA,PA 19140. RP DURRANT, JD (reprint author), UNIV PITTSBURGH,MED CTR,DEPT OTOLARYNGOL,203 LOTHROP ST,PITTSBURGH,PA 15213, USA. CR DURRANT JD, 1990, EAR HEARING, V11, P215, DOI 10.1097/00003446-199006000-00009 GARDI JN, 1987, ELECTROEN CLIN NEURO, V68, P360, DOI 10.1016/0168-5597(87)90017-7 HASHIMOTO I, 1979, ARCH NEUROL-CHICAGO, V36, P161 HAUSLER R, 1980, BRAIN RES, V191, P589, DOI 10.1016/0006-8993(80)91312-8 KONDZIOLKA D, 1992, NEUROSURGERY, V31, P271 LEGATT AD, 1988, NEUROL CLIN, V6, P681 MARTIN WH, 1987, ELECTROEN CLIN NEURO, V68, P341, DOI 10.1016/0168-5597(87)90015-3 MARTIN WH, 1987, ELECTROEN CLIN NEURO, V68, P333, DOI 10.1016/0168-5597(87)90014-1 MARTIN WH, 1987, ELECTROEN CLIN NEURO, V68, P327, DOI 10.1016/0168-5597(87)90013-X MOLLER AR, 1982, ELECTROEN CLIN NEURO, V53, P612, DOI 10.1016/0013-4694(82)90137-7 MOORE JK, 1987, HEARING RES, V29, P33, DOI 10.1016/0378-5955(87)90203-6 OH SJ, 1981, NEUROLOGY, V31, P14 PRATT H, 1985, ELECTROEN CLIN NEURO, V61, P530, DOI 10.1016/0013-4694(85)90972-1 PRATT H, 1992, ELECTROEN CLIN NEURO, V84, P447, DOI 10.1016/0168-5597(92)90032-7 PRATT H, 1983, ELECTROEN CLIN NEURO, V56, P682, DOI 10.1016/0013-4694(83)90036-6 SHERG M, 1985, ELECTROEN CLIN NEURO, V62, P290 WILLISTON JS, 1981, BRAIN RES, V223, P181, DOI 10.1016/0006-8993(81)90820-9 NR 17 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 JAN PY 1994 VL 72 IS 1-2 BP 99 EP 107 DI 10.1016/0378-5955(94)90210-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300012 PM 8150750 ER PT J AU CONLEE, JW GERITY, LC WESTENBERG, IS CREEL, DJ AF CONLEE, JW GERITY, LC WESTENBERG, IS CREEL, DJ TI PIGMENT-DEPENDENT DIFFERENCES IN THE STRIA VASCULARIS OF ALBINO AND PIGMENTED GUINEA-PIGS AND RATS SO HEARING RESEARCH LA English DT Article DE ALBINISM; COCHLEA; INNER EAR; MELANOCYTES; MELANIN ID INNER-EAR; COCHLEAR POTENTIALS; ENDOLYMPH; MELANOCYTES; MELANIN; FLUIDS; MOUSE AB Functional models of the stria vascularis (SV) have ascribed roles for the marginal and basal cells, but not for the intermediate cells, which remain poorly understood. Intermediate cells have been identified as melanocytes, which produce melanin in most pigmented animals including humans. The relationship of melanin to intermediate cell function may be addressed through comparisons with the albino inner ear. Albinos have a normal distribution of melanocytes that are unable to synthesize melanin pigment. In the present study, the SV was compared between albino and pigmented littermates in both the guinea pig and the rat. Photomicrographic montages of the SV were analyzed from each of 7 cochlear regions in the guinea pig and 5 regions in the rat. Stereological procedures were used to determine the volume density (V-v) for each of the three main cell types in the stria, the surface density (S-v) of the marginal cells, and to derive estimates of absolute cell volume and surface area. In the guinea pig, comparisons between pigment groups showed that marginal cell V-v was larger across cochlear turns in the albinos, while intermediate cell V-v was smaller. Intermediate cell cytoplasmic and total cell volumes were smaller in the albino guinea pigs; however, marginal cell S-v and absolute area were larger. In the rat, intermediate cell V-v was also smaller across cochlear turns in the albinos. Similarly, intermediate cell cytoplasmic and total cell volumes were smaller in the albinos, while marginal cell total surface area per radial cross-section of the SV was larger. These results demonstrate that amelanotic melanocytes occupy significantly less volume than do pigmented melanocytes, and suggest that melanin may influence the structure and function of the SV. C1 VET AFFAIRS MED CTR,SALT LAKE CITY,UT. GLENDALE COMMUNITY COLL,DEPT PSYCHOL,GLENDALE,AZ. RP CONLEE, JW (reprint author), UNIV UTAH,SCH MED,DEPT ANAT,SALT LAKE CITY,UT 84132, USA. CR BADDELEY AJ, 1986, J MICROSC-OXFORD, V142, P259 BARRENAS ML, 1992, ACTA OTO-LARYNGOL, V112, P50, DOI 10.3109/00016489209100782 VONBEKESY G, 1952, J ACOUST SOC AM, V24, P72 Bonaccorsi P, 1965, Ann Laringol Otol Rinol Faringol, V64, P725 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 BRAENDGAARD H, 1986, J NEUROSCI METH, V18, P39 CABLE J, 1991, PIGM CELL RES, V4, P87, DOI 10.1111/j.1600-0749.1991.tb00320.x CARLISLE L, 1989, HEARING RES, V38, P111, DOI 10.1016/0378-5955(89)90132-9 CONLEE JW, 1991, HEARING RES, V55, P57, DOI 10.1016/0378-5955(91)90092-N CONLEE JW, 1993, HEARING RES, V65, P141, DOI 10.1016/0378-5955(93)90209-J CRUZORIVE LM, 1990, AM J PHYSIOL, V258, pL148 DEOL MS, 1970, PROC R SOC SER B-BIO, V175, P201, DOI 10.1098/rspb.1970.0019 DEOL MS, 1970, J EMBRYOL EXP MORPH, V23, P773 FORGE A, 1987, HEARING RES, V31, P253, DOI 10.1016/0378-5955(87)90195-X HILDING DA, 1977, ACTA OTO-LARYNGOL, V84, P24, DOI 10.3109/00016487709123939 HILL HZ, 1992, BIOESSAYS, V14, P49, DOI 10.1002/bies.950140111 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P348, DOI 10.1007/BF00588213 LAFERRIE.KA, 1974, ANN OTO RHINOL LARYN, V83, P685 LOHUIS PJFM, 1990, HEARING RES, V47, P95, DOI 10.1016/0378-5955(90)90169-P MCCARTY NA, 1992, PHYSIOL REV, V72, P1037 MISRAHY GA, 1958, AM J PHYSIOL, V194, P396 NUTTALL AL, 1986, NEUROBIOLOGY HEARING, P47 SALT AN, 1989, AM J OTOLARYNG, V10, P371, DOI 10.1016/0196-0709(89)90030-6 SANTI PA, 1983, HEARING RES, V11, P7, DOI 10.1016/0378-5955(83)90041-2 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1984, AM J PHYSIOL, V246, pF47 SUGA F, 1962, ANN OTO RHINOL LARYN, V73, P924 SYKA J, 1981, HEARING RES, V4, P287, DOI 10.1016/0378-5955(81)90013-7 Weibel E. R., 1979, STEREOLOGICAL METHOD, V1 WHITE FH, 1982, ARCH DERMATOL RES, V273, P307, DOI 10.1007/BF00409260 Witkop Jr CJ, 1983, METABOLIC BASIS INHE, P301 Wolff D, 1931, ARCHIV OTOLARYNGOL, V14, P195 ZUMGOTTESBERGE AMM, 1988, PIGM CELL RES, V1, P238 NR 33 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 JAN PY 1994 VL 72 IS 1-2 BP 108 EP 124 DI 10.1016/0378-5955(94)90211-9 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300013 PM 8150728 ER PT J AU POPELAR, J ERRE, JP ARAN, JM CAZALS, Y AF POPELAR, J ERRE, JP ARAN, JM CAZALS, Y TI PLASTIC CHANGES IN IPSI-CONTRALATERAL DIFFERENCES OF AUDITORY-CORTEX AND INFERIOR COLLICULUS EVOKED-POTENTIALS AFTER INJURY TO ONE EAR IN THE ADULT GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE ADULT GUINEA PIG; EVOKED POTENTIALS; AUDITORY CORTEX; INFERIOR COLLICULUS; NEURAL PLASTICITY ID UNILATERAL COCHLEAR ABLATION; SINGLE-UNIT RESPONSES; BINAURAL INTERACTION; BRAIN-STEM; SENSITIVE PERIOD; NMDA RECEPTORS; STRIATE CORTEX; BARN OWL; NUCLEUS; NEURONS AB In normal adult guinea pigs, evoked potentials recorded at the ipsilateral auditory cortex to monaural high-frequency acoustic stimuli present higher thresholds and lower amplitudes than at the contralateral cortex; in the inferior colliculus, such ipsi-contralateral differences (ICDs) are smaller than in the auditory cortex. Changes in the ICDs were studied after opposite ear injury. Following quasi-complete hair cell destruction induced by sisomicin injection into the contralateral inner ear, threshold ICDs almost disappeared after about two to six days and ipsilateral amplitudes progressively increased in two to three weeks. The occurrence of ICDs at higher auditory centers revealed in this study, indicates peculiar processing of high frequency stimuli in normal guinea pigs. The alteration of ICDs after opposite ear impairment provides a new possibility to study the auditory plasticity in adult animals. C1 ACAD SCI CZECH REPUBL,INST EXPTL MED,CS-12000 PRAGUE 2,CZECH REPUBLIC. RP POPELAR, J (reprint author), UNIV BORDEAUX 2,INSERM,U229,AUDIOL EXPTL LAB,BORDEAUX,FRANCE. RI Popelar, Jiri/H-2558-2014 CR AITKIN L, 1991, J NEUROPHYSIOL, V65, P383 ALEEENKO NY, 1968, ZH VYSS NERV DEAT, V18, P1001 ALTMAN JA, 1970, PHYSIOL BOHEMOSLOV, V19, P177 BENES FM, 1977, BRAIN RES, V122, P1, DOI 10.1016/0006-8993(77)90658-8 BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 CAZALS Y, 1983, ACTA OTO-LARYNGOL, V95, P211, DOI 10.3109/00016488309130937 CLOPTON BM, 1977, J NEUROPHYSIOL, V40, P1275 CONLEE JW, 1981, J COMP NEUROL, V202, P373, DOI 10.1002/cne.902020307 COTMAN CW, 1988, ANNU REV NEUROSCI, V11, P61, DOI 10.1146/annurev.neuro.11.1.61 DECKER TN, 1981, HEARING RES, V4, P251, DOI 10.1016/0378-5955(81)90010-1 DUPONT J, 1990, COLLOQUE PHYSIQUE S2, V51, P123 EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 FENG AS, 1971, BRAIN RES, V10, P97 GROSS NATHAN B., 1967, BRAIN RES, V5, P250, DOI 10.1016/0006-8993(67)90090-X HARRISON RV, 1992, ADV BIOSCI, V83, P625 HENDRY SHC, 1988, NEURON, V1, P701, DOI 10.1016/0896-6273(88)90169-9 HIND JE, 1960, NEURAL MECHANISMS AU HUBEL DH, 1977, PHILOS T ROY SOC B, V278, P377, DOI 10.1098/rstb.1977.0050 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 KAAS JH, 1983, ANNU REV NEUROSCI, V6, P325, DOI 10.1146/annurev.ne.06.030183.001545 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 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 KLEINSCHMIDT A, 1987, SCIENCE, V238, P355, DOI 10.1126/science.2443978 KNUDSEN EI, 1984, J NEUROSCI, V4, P1001 KNUDSEN EI, 1985, J NEUROSCI, V5, P3094 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 MOORE DR, 1990, J COMP NEUROL, V302, P810, DOI 10.1002/cne.903020412 MOORE DR, 1991, FETAL NEONATAL BRAIN, P161 MOORE DR, 1986, BRAIN RES, V373, P268, DOI 10.1016/0006-8993(86)90341-0 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 REALE RA, 1987, DEV BRAIN RES, V34, P281, DOI 10.1016/0165-3806(87)90215-X ROSENZWEIG MR, 1951, AM J PHYSIOL, V167, P147 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SASAKI CT, 1980, BRAIN RES, V194, P511, DOI 10.1016/0006-8993(80)91233-0 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 SYKA J, 1993, UNPUB HEAR RES TANIGUCHI I, 1978, P JPN ACAD B-PHYS, V54, P496, DOI 10.2183/pjab.54.496 TRUNE DR, 1993, J COMP NEUROL, V209, P425 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 TUNTURI AR, 1952, AM J PHYSIOL, V168, P712 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WIESEL TN, 1963, J NEUROPHYSIOL, V26, P1003 NR 51 TC 76 Z9 77 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 1994 VL 72 IS 1-2 BP 125 EP 134 DI 10.1016/0378-5955(94)90212-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300014 PM 8150729 ER PT J AU MAURER, J HEINRICH, UR MANN, W AF MAURER, J HEINRICH, UR MANN, W TI DIFFERENCES OF INNER AND OUTER HAIR-CELLS IN THE ORGAN OF CORTI OF THE GUINEA-PIG IN RESPECT TO THE CELLULAR CONTENT OF PRECIPITABLE CALCIUM SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; HAIR CELL; CALCIUM; ELECTRON; SPECTROSCOPIC IMAGING (ESI) ID ENERGY-LOSS SPECTROSCOPY; ELEMENTAL COMPOSITION; MECHANICAL RESPONSES; MOTILE RESPONSE; IONIC BASIS; PYROANTIMONATE; STIMULATION; POTASSIUM; TRANSDUCTION; COCHLEA AB Differences between inner and outer hair cells in the cellular content of precipitable calcium were detected using a potassium pyroantimonate precipitation method and the electron spectrospcopic imaging (ESI-) technique. The cytoplasm of the inner hair cells was scattered with a high number of calcium precipitates in all analysed animals, but only a few reaction products could be identified in the cytoplasm of the outer hair cells in all analyzed specimens. Even the well developed system of the subsurface fenestrated cisternae in the outer hair cells was nearly empty of calcium precipitates. A relatively high amount of reaction products could be identified in the nuclei of both types of nerve endings of the receptor cells. Significant differences regarding the content of precipitable calcium were found in the different types of nerve endings, which come into contact with the basal parts of both receptor cells. The observed differences in the content of precipitable calcium between the two types of hair cells are discussed with respect to their probable different roles in signal transduction processes. RP MAURER, J (reprint author), JOHANNES GUTENBERG UNIV,SCH MED,DEPT ENT,LANGENBECKSTR 1,D-55101 MAINZ,GERMANY. CR ANNIKO M, 1984, ACTA OTO-LARYNGOL, V98, P439, DOI 10.3109/00016488409107585 ARNOLD W, 1990, ACTA OTO-LARYNGOL, V109, P213, DOI 10.3109/00016489009107436 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 BAUER R, 1988, METHOD MICROBIOL, V20, P113, DOI 10.1016/S0580-9517(08)70050-3 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 Campbell A. K., 1983, INTRACELLULAR CALCIU CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 Carafoli E., 1985, SCI AM, V253, P50 CHANDLER JA, 1976, J HISTOCHEM CYTOCHEM, V24, P740 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 DALLOS P, 1972, SCIENCE, V177, P356, DOI 10.1126/science.177.4046.356 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, 1990, J NEUROSCI, V10, P1388 DULON D, 1991, HEARING RES, V52, P225, DOI 10.1016/0378-5955(91)90202-K EGLE W, 1984, ZEISS INFORMATION, V3, P4 EGLE W, 1984, EMSA P, V42, P566 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 HEINRICH UR, 1991, J MICROSC-OXFORD, V162, P123 HEINRICH UR, 1990, ULTRAMICROSCOPY, V32, P1, DOI 10.1016/0304-3991(90)90086-2 IKEDA K, 1991, ORL J OTO-RHINO-LARY, V53, P78 IKEDA K, 1993, HEARING RES, V66, P169, DOI 10.1016/0378-5955(93)90138-Q KOMNICK H, 1962, PROTOPLASMA, V55, P414, DOI 10.1007/BF01881781 LEGATO MJ, 1969, J CELL BIOL, V41, P401, DOI 10.1083/jcb.41.2.401 LIM DJ, 1989, ACTA OTO-LARYNGOL, V107, P398, DOI 10.3109/00016488909127529 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MANN W, 1988, ARCH OTO-RHINO-LARYN, V245, P185, DOI 10.1007/BF00464024 MAURER J, 1991, EUR ARCH OTO-RHINO-L, V248, P242 RASMUSSEN H, 1989, SCI AM, V261, P44 RAVAZZOLA M, 1976, J CELL SCI, V27, P107 REIMER L, 1989, TRANSMISSION ELECTRO ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 SAITO K, 1983, CELL TISSUE RES, V229, P467 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOSSACCHI J, 1988, PHYSL EAR, P271 SCHAFER H, 1979, ZELLKALZIUM ZELLFUNK SMALLS CM, 1977, J MORPHOL, V151, P213, DOI 10.1002/jmor.1051510204 SPOENDLIN H, 1978, EVOKED ELECTRICAL AC, P3 SPOENDLIN H, 1974, FACTS MODELS HEARING, P18 TANDLER CJ, 1970, J CELL BIOL, V45, P355, DOI 10.1083/jcb.45.2.355 WICK SM, 1982, J HISTOCHEM CYTOCHEM, V30, P939 YAROM R, 1974, J HISTOCHEM CYTOCHEM, V22, P147 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 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 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P457, DOI 10.3109/00016488809119501 ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V49, P304 NR 52 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 1994 VL 72 IS 1-2 BP 135 EP 142 DI 10.1016/0378-5955(94)90213-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300015 PM 8150730 ER PT J AU HURD, LB FELDMAN, ML AF HURD, LB FELDMAN, ML TI PURKINJE-LIKE CELLS IN RAT COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE CALBINDIN D-28 KDA; COCHLEAR NUCLEUS IMMUNOCYTOCHEMISTRY; PURKINJE CELLS; CARTWHEEL CELLS ID CALCIUM-BINDING PROTEIN; IMMUNOHISTOCHEMICAL LOCALIZATION; GOLGI IMPREGNATION; ACID DECARBOXYLASE; CARTWHEEL NEURONS; NERVOUS-SYSTEM; BRAIN-STEM; CEREBELLUM; IMMUNOREACTIVITY; CAT AB A unique class of cells, strongly immunopositive for anti-calbindin D-28 kDa was observed in and near the cochlear nucleus of young adult, male Sprague-Dawley rats. These cells are present in small numbers which are highly variable across animals and inconstant in position. They are preferentially located in the dorsal cochlear nucleus, with occasional examples being present in the ventral cochlear nucleus, as well as in adjacent brainstem locations. They have been referred to in other studies as displaced Purkinje cells or 'Purkinje cell-like cells', and are here designated 'Purkinje-like cells' (PLCs). PLCs have relatively large cell bodies, with thick, heavily spined dendrites, and are typically situated in an immediately subpial position. The dendritic arborization extends into the interior of the nucleus, away from the pial surface, a trajectory opposite in direction to that of the cerebellar Purkinje cells. The intense immunoreactivity exhibited by PLC somata and dendrites when treated with antiserum directed against calbindin is equivalent to that of cerebellar Purkinje cells, and markedly stronger than that of most other cell populations of the cochlear nucleus. However, in tissue treated with anti-parvalbumin, which also strongly labels cerebellar Purkinje cell somata and dendrites, PLC labeling, when present, is relatively weak, limited to the cell bodies and only the base of the dendrites of PLCs, indicating non-equivalence of the two cell types. In addition, the intensity of calbindin immunostaining in the PLCs appears to be more sensitive to glutaraldehyde in any of the fixative solutions than that seen in cerebellar Purkinje cells in the same sections. Of the cell types of the cochlear nucleus, the cartwheel cells would appear to be the most similar to the PLCs on morphological and immunocytochemical grounds. However, the subpial position and average somal dimensions of the PLCs, as well as the relatively modest immunoreactivity of the cartwheel cells for calbindin, rather clearly differentiate the PLCs from this class of neurons. The results of the present study suggest that the PLCs of the cochlear nucleus, although they may arise developmentally as ectopic cerebellar Purkinje cells and maintain certain Purkinje cell characteristics, represent a distinct neuronal cell type in the adult rat cochlear nucleus, exhibiting incomplete overlap of fixation, immunocytochemical and morphological characteristics with both cartwheel cells of the cochlear nucleus and cerebellar Purkinje cells. RP HURD, LB (reprint author), BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,80 E CONCORD ST,BOSTON,MA 02118, USA. CR ADAMS J C, 1988, Society for Neuroscience Abstracts, V14, P489 ALTMAN J, 1980, J COMP NEUROL, V194, P877, DOI 10.1002/cne.901940410 ALTMAN J, 1978, J COMP NEUROL, V179, P23, DOI 10.1002/cne.901790104 BAIMBRIDGE KG, 1982, BRAIN RES, V239, P519, DOI 10.1016/0006-8993(82)90526-1 BAIMBRIDGE KG, 1982, BRAIN RES, V245, P223, DOI 10.1016/0006-8993(82)90804-6 BERREBI AS, 1990, J NEUROCYTOL, V19, P643, DOI 10.1007/BF01188033 BLACKSTAD TW, 1984, NEUROSCIENCE, V13, P827, DOI 10.1016/0306-4522(84)90099-X BLACKSTAD TW, 1981, NEUROSCI LETT S, V7, pS73 Braun K, 1990, Prog Histochem Cytochem, V21, P1 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 BROWN BL, 1983, ANAT REC, V205, pA25 BROWNER RH, 1982, J COMP NEUROL, V211, P115, DOI 10.1002/cne.902110203 CAJAL SRY, 1952, HISTOLOGIE SYSTEME N, V2 CAJAL SRY, 1952, HISTOLOGIE SYSTEME N, V1 Cant NB, 1992, MAMMALIAN AUDITORY P, P66 CANT NB, 1984, HEARING SCI RECENT A, P371 CELIO MR, 1981, NATURE, V293, P300, DOI 10.1038/293300a0 CELIO MR, 1988, CELL CALCIUM, V9, P81, DOI 10.1016/0143-4160(88)90027-9 CELIO MR, 1990, CELL CALCIUM, V11, P599, DOI 10.1016/0143-4160(90)90014-L CELIO MR, 1986, SCIENCE, V231, P995, DOI 10.1126/science.3945815 CELIO MR, 1990, NEUROSCIENCE, V35, P375, DOI 10.1016/0306-4522(90)90091-H CHANPALAY V, 1981, P NATL ACAD SCI-BIOL, V78, P7787, DOI 10.1073/pnas.78.12.7787 CHANPALAY V, 1982, P NATL ACAD SCI-BIOL, V79, P2695, DOI 10.1073/pnas.79.8.2695 DECAMILLI P, 1984, NEUROSCIENCE, V11, P761, DOI 10.1016/0306-4522(84)90193-3 DISTERHOFT JF, 1980, J COMP NEUROL, V192, P687, DOI 10.1002/cne.901920405 ELDRED WD, 1983, J HISTOCHEM CYTOCHEM, V31, P285 FELDMAN SC, 1983, ENDOCRINOLOGY, V112, P290 GARCIASEGURA LM, 1984, BRAIN RES, V296, P75, DOI 10.1016/0006-8993(84)90512-2 Harrison J M, 1970, Contrib Sens Physiol, V4, P95 HEIZMANN CW, 1984, EXPERIENTIA, V40, P910, DOI 10.1007/BF01946439 JANDE SS, 1981, NATURE, V294, P765, DOI 10.1038/294765a0 KANE EC, 1974, J COMP NEUROL, V155, P301, DOI 10.1002/cne.901550303 KANE ES, 1981, J COMP NEUROL, V198, P483, DOI 10.1002/cne.901980308 KIYAMA H, 1985, NEUROSCIENCE, V14, P547, DOI 10.1016/0306-4522(85)90309-4 LEGRAND C, 1983, CELL TISSUE RES, V233, P389 LOHMANN SM, 1981, P NATL ACAD SCI-BIOL, V78, P653, DOI 10.1073/pnas.78.1.653 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MARANI E, 1977, J ANAT, V124, P335 MCBURNEY RN, 1987, TRENDS NEUROSCI, V10, P164, DOI 10.1016/0166-2236(87)90042-7 MOREST DK, 1990, J COMP NEUROL, V300, P230, DOI 10.1002/cne.903000207 MUGNAINI E, 1987, ARCH ITAL BIOL, V126, P41 MUGNAINI E, 1987, P NATL ACAD SCI USA, V84, P8692, DOI 10.1073/pnas.84.23.8692 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 Mugnaini E., 1972, COMP ANATOMY HISTOLO, P201 NILAVER G, 1982, NATURE, V295, P597, DOI 10.1038/295597a0 OSEN KK, 1985, NEUROSCI LETT S, V22, pS167 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 Palay SL, 1974, CEREBELLAR CORTEX CY Pochet R, 1989, Adv Exp Med Biol, V255, P435 ROGERS JH, 1989, NEUROSCIENCE, V31, P711, DOI 10.1016/0306-4522(89)90435-1 WASSEF M, 1984, NEUROSCIENCE, V13, P1217, DOI 10.1016/0306-4522(84)90295-1 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 WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X WILLARD FH, 1986, J COMP NEUROL, V248, P119, DOI 10.1002/cne.902480109 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 WOUTERLOOD FG, 1984, J NEUROCYTOL, V13, P639, DOI 10.1007/BF01148083 ZETTEL ML, 1991, J COMP NEUROL, V313, P1, DOI 10.1002/cne.903130102 ZIAI MR, 1988, J NEUROCHEM, V51, P1771, DOI 10.1111/j.1471-4159.1988.tb01158.x NR 60 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 1994 VL 72 IS 1-2 BP 143 EP 158 DI 10.1016/0378-5955(94)90214-3 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300016 PM 8150731 ER PT J AU KOPPL, C MANLEY, GA AF KOPPL, C MANLEY, GA TI SPONTANEOUS OTOACOUSTIC EMISSIONS IN THE BOBTAIL LIZARD .2. INTERACTIONS WITH EXTERNAL TONES SO HEARING RESEARCH LA English DT Article DE COCHLEA; SOAE; FREQUENCY TUNING; SUPPRESSION; BASILAR PAPILLA ID OTO-ACOUSTIC EMISSIONS; AUDITORY-NERVE FIBERS; TILIQUA-RUGOSA; 2-TONE SUPPRESSION; COCHLEA; EARS AB The response of spontaneous otoacoustic emissions to the presentation of external tones was studied in the Australian bobtail lizard. Three basic types of effects were observed: suppression (a reduction in the emission's amplitude), facilitation (an increase in the emission's amplitude) and frequency shifting. The suppressive effect was highly frequency selective. Iso-suppression tuning curves resembled the rate-threshold tuning curves of the high-frequency population of VIIIth nerve fibres in this species. The frequency with the lowest threshold for suppression corresponded, on average, to the emission's own frequency and did not show any systematic deviation from it. Facilitation of between 2 and 10 dB occurred, but only in response to frequencies within certain narrow ranges, and at sound pressure levels below those that suppressed. The most commonly-observed facilitation range lay between 0.2 and 0.6 octaves above the emission's own frequency and coincided in frequency with a characteristic notch in the iso-suppression tuning curve. In the same narrow frequency range, the input/output functions of amplitude suppression always showed a pronounced increase in slope. The emissions moved their own frequency away from that of an external tone. The observed shifts were comparatively large (up to -330 Hz) and were more pronounced in the downward direction. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 Baker R. J., 1989, COCHLEAR MECHANISMS, P349 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CAPRANCIA RR, 1973, J ACOUST SOC AM S, V55, pS85 Capranica R.R., 1976, P551 CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 DALLOS P, 1992, J NEUROSCI, V12, P4575 FENG AS, 1975, J COMP PHYSIOL, V100, P221 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 HARRIS FP, 1992, HEARING RES, V64, P133, DOI 10.1016/0378-5955(92)90175-M KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 Kemp DT, 1980, PSYCHOPHYSICAL PHYSL, P34 KOPPL C, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P489 KOPPL C, 1988, HEARING RES, V35, P209, DOI 10.1016/0378-5955(88)90119-0 KOPPL C, 1993, HEARING RES, V71, P157, DOI 10.1016/0378-5955(93)90031-U KOPPL C, 1990, J COMP PHYSIOL A, V167, P101 KOPPL C, 1990, J COMP PHYSIOL A, V167, P113 KOPPL C, 1993, J ACOUST SOC AM, V93, P2834 LONG GR, 1991, J ACOUST SOC AM, V89, P1201, DOI 10.1121/1.400651 LONG GR, 1988, HEARING RES, V36, P125, DOI 10.1016/0378-5955(88)90055-X MANLEY GA, 1993, IN PRESS BIOPHYSICS MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MANLEY GA, 1994, HEARING RES, V72, P171, DOI 10.1016/0378-5955(94)90216-X MANLEY GA, 1990, J COMP PHYSIOL A, V167, P89, DOI 10.1007/BF00192409 MANLEY GA, 1990, J COMP PHYSIOL A, V167, P129, DOI 10.1007/BF00192412 MANLEY GA, 1992, AUDITORY PHYSL PERCE, P151 MANLEY GA, 1992, EFFECT TEMPERATURE S, P156 MANLEY GA, 1993, J ACOUST SOC AM, V93, P2820, DOI 10.1121/1.405803 MANLEY GA, 1989, COCHLEAR MECH STRUCT, P143 MARTIN GK, 1988, HEARING RES, V33, P49, DOI 10.1016/0378-5955(88)90020-2 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MILLER MR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P463 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 OHYAMA K, 1991, HEARING RES, V56, P111, DOI 10.1016/0378-5955(91)90160-B Probst R, 1990, Adv Otorhinolaryngol, V44, P1 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 VANDIJK P, 1990, J ACOUST SOC AM, V88, P1779, DOI 10.1121/1.400199 VONDALLMAYR C, 1985, ACUSTICA, V59, P67 WHITEHEAD ML, 1993, SCAND AUDIOL, V22, P3, DOI 10.3109/01050399309046012 WILSON JP, 1990, COCHLEAR MECHANISMS, V7, P47 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 ZUREK PM, 1981, J ACOUST SOC AM, V70, P446, DOI 10.1121/1.386787 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 NR 46 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 JAN PY 1994 VL 72 IS 1-2 BP 159 EP 170 DI 10.1016/0378-5955(94)90215-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300017 PM 8150732 ER PT J AU MANLEY, GA KOPPL, C AF MANLEY, GA KOPPL, C TI SPONTANEOUS OTOACOUSTIC EMISSIONS IN THE BOBTAIL LIZARD .3. TEMPERATURE EFFECTS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSION; LIZARD; HEARING; TEMPERATURE; BASILAR PAPILLA ID RESPONSE PROPERTIES; GUINEA-PIG; DEPENDENCE; TILIQUA; FIBERS; FROG AB Spontaneous otoacoustic emissions (SOAE) in the ear canal of the Australian bobtail lizard are temperature sensitive. They shift their frequency up with an increase in temperature, an effect that is fully reversible. The degree of shift is dependent not only on the center frequency of the SOAE (lower-frequency SOAE show a smaller shift) but also on the temperature range in question. Rates of change of frequency are 0.014 to 0.04 oct/degrees C at 30 degrees C, and twice that at 22 degrees C. There was no strong and consistent effect of temperature on SOAE amplitudes. The above findings are very similar to those on the effect of temperature on SOAE of frogs and mammals. Suppression tuning curves of SOAE shifted with temperature, the largest effects being near the center frequency in the tuning-curve's tip region. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. CR BUTLER RA, 1960, AM J PHYSIOL, V199, P688 CAMPBELL HW, 1969, PHYSIOL ZOOL, V42, P183 COATS ALFRED C., 1965, SCIENCE, V15l), P1481 EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 EATOCK RA, 1976, J ACOUST SOC AM, V60, pS80, DOI 10.1121/1.2003544 FUCHS PA, 1988, J NEUROSCI, V8, P2460 GENOSSA TJ, 1989, J ACOUST SOC AM, V85, pS35 GUMMER AW, 1983, HEARING RES, V12, P367, DOI 10.1016/0378-5955(83)90006-0 HUFFMAN RF, 1993, J COMP PHYSIOL A, V171, P735, DOI 10.1007/BF00213070 HUFFMAN RF, 1993, J COMP PHYSIOL A, V171, P725, DOI 10.1007/BF00213069 KLINKE R, 1984, COMP PHYSL SENSORY S, P195 KOPPL C, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P489 KOPPL C, 1994, HEARING RES, V72, P159, DOI 10.1016/0378-5955(94)90215-1 KOPPL C, 1993, HEARING RES, V71, P157, DOI 10.1016/0378-5955(93)90031-U KOPPL C, 1990, J COMP PHYSIOL A, V167, P101 MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MANLEY GA, 1989, MECH HEARING, P143 MANLEY GA, 1992, EFFECT TEMPERATURE S, P156 MOFFAT AJM, 1976, J ACOUST SOC AM, V60, pS80, DOI 10.1121/1.2003543 OHYAMA K, 1992, ABSTR ASS RES OTOLAR, P150 OHYAMA K, 1991, HEARING RES, V56, P111, DOI 10.1016/0378-5955(91)90160-B SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SMOLDERS J, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P125 SMOLDERS JWT, 1984, J COMP PHYSIOL, V155, P19, DOI 10.1007/BF00610927 STIEBLER IB, 1990, HEARING RES, V46, P63, DOI 10.1016/0378-5955(90)90140-K VANDIJK P, 1990, HEARING RES, V44, P231, DOI 10.1016/0378-5955(90)90083-2 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 WERNER YI, 1976, J EXP ZOOL, V195, P319, DOI 10.1002/jez.1401950302 WERNER Y L, 1972, Journal of Herpetology, V6, P147, DOI 10.2307/1562767 WHITEHEAD ML, 1986, AUDITORY FREQUENCY S, P36 WILSON JP, 1985, PERIPHERAL AUDITORY, P137 NR 31 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 1994 VL 72 IS 1-2 BP 171 EP 180 DI 10.1016/0378-5955(94)90216-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300018 PM 8150733 ER PT J AU WEAVER, SP HOFFPAUIR, J SCHWEITZER, L AF WEAVER, SP HOFFPAUIR, J SCHWEITZER, L TI DISTRIBUTION OF ACTIN IN DEVELOPING OUTER HAIR-CELLS IN THE GERBIL SO HEARING RESEARCH LA English DT Article DE ACTIN; COCHLEA; DEVELOPMENT; HEARING; HAIR CELLS; IMMUNOCYTOCHEMISTRY ID GUINEA-PIG COCHLEA; MONGOLIAN GERBIL; BASILAR-MEMBRANE; STRUCTURAL BASIS; F-ACTIN; ORGAN; CORTI; FREQUENCY; ELECTROMOTILITY; CYTOSKELETON AB During the two weeks following the onset of cochlear function in the gerbil, active cochlear processes appear to mature. The active cochlear processes likely involve outer hair cells with their specialized lateral wall structures, including the subsurface cisternae and associated cytoskeletal elements. We have previously demonstrated that the subsurface cisternae mature gradually during the time that active cochlear processes mature in the gerbil. In the study reported here, we used postembedding immunocytochemical electron microscopy to investigate whether actin labelling associated with the cortical cytoskeleton of the gerbil outer hair cell increased concomitantly. In contrast to the gradual development of the subsurface cisternae, actin labelling in the region of the cortical cytoskeleton significantly increased during the onset of cochlear function and maintained this level during the time that active cochlear processes mature. Thus, it appears that increased actin adjacent to the lateral plasma membrane of the outer hair cell is related to the onset of cochlear function rather than to the maturation of active cochlear processes. C1 UNIV LOUISVILLE,SCH MED,HLTH SCI CTR,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 Bannister L H, 1988, Prog Brain Res, V74, P213 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1990, J NEUROSCI, V10, P1388 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HE ZZ, 1993, ONTOGENY OUTER HAIR, V97, P25 HENLEY CM, 1989, HEARING RES, P141 Kikuchi K, 1965, Acta Otolaryngol, V60, P207, DOI 10.3109/00016486509127003 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1992, J CELL SCI, V102, P569 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 HOLLEY M C, 1991, Journal of Cell Biology, V115, p345A JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 KHANNA SM, 1986, HEARING RES, V23, P55, DOI 10.1016/0378-5955(86)90175-9 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 LUNA EJ, 1992, SCIENCE, V258, P955, DOI 10.1126/science.1439807 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PIRVOLA U, 1991, HEARING RES, V52, P345, DOI 10.1016/0378-5955(91)90024-4 PUJOL R, 1991, HEARING RES, V57, P129, DOI 10.1016/0378-5955(91)90082-K ROTH B, 1992, ANAT EMBRYOL, V185, P571, DOI 10.1007/BF00185616 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P299, DOI 10.1121/1.392491 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 Siegel S., 1956, NONPARAMETRIC STATIS SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SLEPECKY N, 1986, CELL TISSUE RES, V245, P229 SLEPECKY NB, 1990, J ELECTRON MICR TECH, V15, P280, DOI 10.1002/jemt.1060150307 SLEPECKY NB, 1992, HEARING RES, V57, P201, DOI 10.1016/0378-5955(92)90152-D THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 WEAVER SP, 1994, HEARING RES, V72, P44, DOI 10.1016/0378-5955(94)90204-6 WEAVER SP, 1993, BRAIN RES BULL, V31, P225, DOI 10.1016/0361-9230(93)90029-B WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 YLIKOSKI J, 1992, HEARING RES, V60, P80, DOI 10.1016/0378-5955(92)90061-Q ZINE A, 1991, Society for Neuroscience Abstracts, V17, P29 NR 44 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 1994 VL 72 IS 1-2 BP 181 EP 188 DI 10.1016/0378-5955(94)90217-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300019 PM 8150734 ER PT J AU JOHNSON, AC CANLON, B AF JOHNSON, AC CANLON, B TI TOLUENE EXPOSURE AFFECTS THE FUNCTIONAL-ACTIVITY OF THE OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; COCHLEA; DISTORTION PRODUCT OTOACOUSTIC EMISSIONS; RATS; SOLVENT; HAIR CELLS ID ACOUSTIC-DISTORTION PRODUCTS; 2F1-F2 OTOACOUSTIC EMISSIONS; 2 DISCRETE SOURCES; HEARING-LOSS; COCHLEAR MECHANICS; AUDITORY-SENSITIVITY; GUINEA-PIGS; MUTANT MICE; RATS; NOISE AB Rats were exposed to toluene by inhalation (1400 ppm, 16 h/d, 8 days) and the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOEs) were used as measures of the auditory sensitivity. These measurements were made before the exposure to toluene, 3 and 5 days after the start of the exposure and 4 days after the end of the exposure. To quantify the repeated DPOE data the area under the curve of the DPOE amplitudes versus the stimuli levels was calculated and used for statistical analysis. Results demonstrate that 3 days of toluene exposure tended to lower DPOE amplitudes and elevate ABR thresholds. Similarly after 5 days of exposure significantly lower DPOE amplitudes were observed at most frequencies along with elevated ABR thresholds. At 4 days post-exposure DPOE amplitudes were greatly diminished at all frequencies and the ABR thresholds were raised by about 40 dB between 1.6 and 20 kHz. These results show a parallel shift between ABR thresholds and DPOE amplitudes during toluene exposure. Furthermore, the results from the DPOE measurements indicate that mainly the outer hair cells are adversely affected by toluene exposure. C1 KAROLINSKA INST,DEPT PHYSIOL & PHARMACOL,S-17177 STOCKHOLM,SWEDEN. RP JOHNSON, AC (reprint author), NATL INST OCCUPAT HLTH,DEPT NEUROMED,S-17184 SOLNA,SWEDEN. CR BARREGARD L, 1984, SCAND AUDIOL, V13, P151, DOI 10.3109/01050398409043054 BERGSTROM B, 1986, SCAND AUDIOL, V15, P227, DOI 10.3109/01050398609042148 BHATTACHARYYA TK, 1985, ANN OTO RHINOL LARYN, V94, P75 BORG E, 1987, HEARING RES, V30, P111, DOI 10.1016/0378-5955(87)90128-6 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 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 BRUMMETT RE, 1980, DRUGS, V19, P412, DOI 10.2165/00003495-198019060-00002 BUCHWALD JS, 1983, BASES AUDITORY BRAIN, P157 CODY RP, 1987, APPLIED STATISTICS S COLEMAN JW, 1976, ACTA OTO-LARYNGOL, V82, P33, DOI 10.3109/00016487609120860 CROFTON KM, 1993, IN PRESS NEUROTOXICO FORNAZZARI L, 1983, ACTA NEUROL SCAND, V67, P319 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C GORGA MP, 1993, J ACOUST SOC AM, V93, P2050, DOI 10.1121/1.406691 HENLEY CM, 1990, HEARING RES, V43, P141, DOI 10.1016/0378-5955(90)90223-C HORMES JT, 1986, NEUROLOGY, V36, P698 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 JOHNSON AC, 1990, ACTA OTO-LARYNGOL, V109, P34, DOI 10.3109/00016489009107412 JOHNSON AC, 1988, ACTA OTO-LARYNGOL, V105, P56, DOI 10.3109/00016488809119446 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KIM DO, 1980, HEARING RES, V2, P297, DOI 10.1016/0378-5955(80)90064-7 KIMBERLEY BP, 1989, J OTOLARYNGOL, V18, P365 LAURELL G, 1990, LARYNGOSCOPE, V100, P724 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LAZAR RB, 1983, NEUROLOGY, V33, P1337 LENOIR M, 1987, HEARING RES, V29, P265, DOI 10.1016/0378-5955(87)90173-0 LI HS, 1992, ARCH TOXICOL, V66, P382, DOI 10.1007/BF02035126 LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 Lonsbury-Martin B L, 1990, Ann Otol Rhinol Laryngol Suppl, V147, P3 Martin G K, 1990, Ann Otol Rhinol Laryngol Suppl, V147, P30 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E MORATA TC, 1990, 4 INT C COMB EFF ENV, P81 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NYLEN P, 1993, UNPUB TOLUENE PHARM PRYOR GT, 1984, NEUROBEH TOXICOL TER, V6, P223 PRYOR GT, 1983, NEUROBEH TOXICOL TER, V5, P53 PRYOR GT, 1984, NEUROBEH TOXICOL TER, V6, P111 REBERT CS, 1983, NEUROBEH TOXICOL TER, V5, P59 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 SMURZYNSKI J, 1990, ARCH OTOLARYNGOL, V116, P1309 SULLIVAN MJ, 1989, NEUROTOXICOL TERATOL, V10, P525 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 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 NR 48 TC 26 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 1994 VL 72 IS 1-2 BP 189 EP 196 DI 10.1016/0378-5955(94)90218-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300020 PM 8150735 ER PT J AU COLING, DE NAIK, RM SCHACHT, J AF COLING, DE NAIK, RM SCHACHT, J TI CALCIUM AND CALMODULIN INHIBIT PHOSPHORYLATION OF A NOVEL AUDITORY-NERVE PROTEIN SO HEARING RESEARCH LA English DT Article DE ACOUSTIC NERVE; CALCIUM; CALMODULIN; MYRISTOYLATED ALANINE RICH C KINASE SUBSTRATE (MARCKS); PROTEIN KINASE; PROTEIN PHOSPHORYLATION ID KINASE-C SUBSTRATE; BINDING PROTEIN; BRAIN; PURIFICATION; MEMBRANE; NEURONS; DOMAIN; MARCKS; ACID; SITE AB The growing use of cochlear prosthetic devices and demonstrations of direct ototoxic insult to spiral ganglion neurons make it imperative to gain an understanding of intracellular biochemical regulation in primary sensory neurons. Calcium and calmodulin regulate many aspects of neuronal cellular physiology through stimulation of protein kinase activity. We have previously demonstrated the presence of calmodulin-dependent protein kinase substrates in the guinea pig modiolus and, additionally, the presence of two proteins (12 kDa and 81 kDa, designated as p12 and p81) whose phosphorylation is blocked by calcium and calmodulin (Coling and Schacht, 1991). Here, we investigate three models for this unusual regulatory mechanism. The effects of calcium, calmodulin and trifluoperazine on dephosphorylation of both proteins suggests that calmodulin inhibits protein kinase activity. P81 was identified by immunoprecipitation as the myristoylated alanine-rich C kinase substrate (MARCKS), a ubiquitous actin-binding protein. Two observations indicate that MARCKS may be regulated differently in acoustic nerve than in cerebral cortex. P-32 incorporation was significantly higher in acoustic nerve than in brain. The calmodulin-dependent block of MARCKS phosphorylation was observed only in acoustic nerve. p12 shares several characteristics with myelin basic protein (MBP). We used a double label assay with P-32 autoradiography and immunoblotting to show that p12 is in fact distinct from MBP. We suggest that either p12 or p12 kinase may be either specific to the peripheral auditory system or novel marker proteins for that tissue. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR ALBERT KA, 1984, P NATL ACAD SCI-BIOL, V81, P3622, DOI 10.1073/pnas.81.12.3622 ALBERT KA, 1986, P NATL ACAD SCI USA, V83, P2822, DOI 10.1073/pnas.83.9.2822 BAUDIER J, 1991, J BIOL CHEM, V266, P229 Cohen P, 1988, CALMODULIN COHEN P, 1989, ANNU REV BIOCHEM, V58, P453, DOI 10.1146/annurev.bi.58.070189.002321 COLING DE, 1991, HEARING RES, V57, P113, DOI 10.1016/0378-5955(91)90080-S DUPONT J, 1993, HEARING RES, V68, P217, DOI 10.1016/0378-5955(93)90125-K GRAFF JM, 1989, J BIOL CHEM, V264, P21818 GRAND RJA, 1980, BIOCHEM J, V189, P227 HARTWIG JH, 1992, NATURE, V356, P618, DOI 10.1038/356618a0 HIDAKA H, 1990, BIOL MED SIGNAL TRAN, P485 HOUBRE D, 1991, J BIOL CHEM, V266, P7121 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LEFEBVRE PP, 1992, HEARING RES, V58, P185, DOI 10.1016/0378-5955(92)90127-9 LEFEBVRE PP, 1992, ACTA OTO-LARYNGOL, V112, P288 Martenson Russell E., 1992, P387 MELLONI E, 1989, TRENDS NEUROSCI, V12, P438, DOI 10.1016/0166-2236(89)90093-3 MUSTILLO P, 1984, AUDIOLOGY, V23, P145 NAIRN AC, 1985, ANNU REV BIOCHEM, V54, P931, DOI 10.1146/annurev.biochem.54.1.931 NESTLER EJ, 1980, P NATL ACAD SCI-BIOL, V77, P7479, DOI 10.1073/pnas.77.12.7479 NESTLER EJ, 1984, PROTEIN PHOSPHORYLAT Schwartz A. M, 1986, NEUROBIOLOGY HEARING, P271 SMITH PK, 1985, ANAL BIOCHEM, V150, P76, DOI 10.1016/0003-2697(85)90442-7 STEWART AA, 1982, FEBS LETT, V137, P80, DOI 10.1016/0014-5793(82)80319-0 STRATFORD CA, 1984, J NEUROCHEM, V42, P842, DOI 10.1111/j.1471-4159.1984.tb02758.x THELEN M, 1991, NATURE, V351, P320, DOI 10.1038/351320a0 TOKUMITSU H, 1989, BIOCHEM BIOPH RES CO, V163, P581, DOI 10.1016/0006-291X(89)92177-3 TYTELL M, 1980, P NATL ACAD SCI-BIOL, V77, P3042, DOI 10.1073/pnas.77.5.3042 UMEKAGE T, 1991, FEBS LETT, V286, P147, DOI 10.1016/0014-5793(91)80961-2 WENTHOLD RJ, 1982, J NEUROCHEM, V39, P27, DOI 10.1111/j.1471-4159.1982.tb04697.x WENTHOLD RJ, 1982, BRAIN RES, V253, P263, DOI 10.1016/0006-8993(82)90693-X WU WCS, 1982, P NATL ACAD SCI-BIOL, V79, P5249, DOI 10.1073/pnas.79.17.5249 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 JAN PY 1994 VL 72 IS 1-2 BP 197 EP 205 DI 10.1016/0378-5955(94)90219-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300021 PM 7512086 ER PT J AU NELKEN, I PRUT, Y VAADIA, E ABELES, M AF NELKEN, I PRUT, Y VAADIA, E ABELES, M TI POPULATION RESPONSES TO MULTIFREQUENCY SOUNDS IN THE CAT AUDITORY-CORTEX - ONE-PARAMETER AND 2-PARAMETER FAMILIES OF SOUNDS SO HEARING RESEARCH LA English DT Article DE PRIMARY AUDITORY CORTEX; COMPLEX SOUNDS; 2-TONE FACILITATION; CAT ID WIDE-SPECTRUM NOISE; AMPLITUDE-MODULATION; SQUIRREL-MONKEYS; COMBINED TONE; SINGLE UNITS; NEURONS; REPRESENTATION; STIMULI; ORGANIZATION; SENSITIVITY AB Population responses to multi-frequency sounds were recorded in primary auditory cortex of anesthetized cats. The sounds consisted of single-tone stimuli; two-tone stimuli; and nine-tone stimuli, with the tones evenly spaced on a linear frequency scale. The stimuli were presented through a sealed, calibrated sound delivery system. Single units, cluster activity (CA) and the short-time mean absolute value of the envelope of the neural signal (MABS) were recorded extracellularly from six microelectrodes simultaneously. The CA and MABS were interpreted as measures of the activity of large populations of neurons, in contrast with the single unit activity which is presumably recorded from single neurons. The responses of the MABS signal to simple stimuli were generally similar to those of the CA, but were more stable statistically. Thus, the MABS is better suited for studying the activity of populations of neurons. The responses to tones near the best frequency were strongly influenced by a second tone, even when the second tone was outside the single-tone response area. These influences could be both facilitatory and suppressory. They could not be predicted from the responses to single tones. The responses to the nine-tone stimuli could be explained qualitatively by the responses to the two-tone stimuli. It is concluded that the population responses in primary auditory cortex are shaped by the contributions of the individual frequencies appearing in the stimulus and by the interactions between pairs of frequencies. Interactions between stimulus components are therefore a necessary component of any attempt to explain the processing of complex sounds in the auditory cortex. They may play a role in a global representation of the stimulus spectrum in the primary auditory cortex. The presence of higher-order interactions cannot be excluded by the results presented here. C1 HADASSAH MED SCH,DEPT PHYSIOL,IL-91010 JERUSALEM,ISRAEL. RI Nelken, Israel/B-7753-2011; Vaadia, Eilon/E-9347-2011 OI Nelken, Israel/0000-0002-6645-107X; CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 ABELES M, 1972, BRAIN RES, V42, P337, DOI 10.1016/0006-8993(72)90535-5 ABELES M, 1970, J NEUROPHYSIOL, V33, P172 ABELES M, 1977, P IEEE, V65, P762, DOI 10.1109/PROC.1977.10559 AHISSAR M, 1992, J NEUROPHYSIOL, V67, P203 ECKHORN R, 1988, BIOL CYBERN, V60, P121, DOI 10.1007/BF00202899 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 EVANS EF, 1964, J PHYSIOL-LONDON, V171, P476 FROSTIG RD, 1983, BRAIN RES, V272, P211, DOI 10.1016/0006-8993(83)90567-X GERSTEIN GL, 1968, J NEUROPHYSIOL, V31, P526 GOLDSTEI.MH, 1968, J ACOUST SOC AM, V43, P444, DOI 10.1121/1.1910851 GRAY CM, 1989, NATURE, V338, P334, DOI 10.1038/338334a0 MATSUBARA JA, 1988, J COMP NEUROL, V268, P38, DOI 10.1002/cne.902680105 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 NELKEN I, 1994, HEARING RES, V72, P223, DOI 10.1016/0378-5955(94)90221-6 NELKEN I, 1991, THESIS NEWMAN JD, 1973, BRAIN RES, V54, P287, DOI 10.1016/0006-8993(73)90050-4 OONISHI S, 1965, JPN J PHYSIOL, V15, P342 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1986, J ACOUST SOC AM, V80, P177, DOI 10.1121/1.394178 PHILLIPS DP, 1985, HEARING RES, V18, P73, DOI 10.1016/0378-5955(85)90111-X PHILLIPS DP, 1985, HEARING RES, V18, P87, DOI 10.1016/0378-5955(85)90112-1 PHILLIPS DP, 1991, HEARING RES, V53, P17, DOI 10.1016/0378-5955(91)90210-Z PRUT Y, 1994, UNPUB RELATIONSHIPS RAJAN R, 1990, J NEUROPHYSIOL, V64, P888 SCHREINER C, 1983, HEARING PHYSL BASES, P169 SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 SCHWARZ DWF, 1990, J NEUROPHYSIOL, V64, P282 SHAMMA SA, 1993, J NEUROPHYSIOL, V69, P367 SHAMMA SA, 1985, HEARING RES, V19, P1, DOI 10.1016/0378-5955(85)90094-2 STEINSCHNEIDER M, 1990, BRAIN RES, V519, P158, DOI 10.1016/0006-8993(90)90074-L STEVENS JK, 1976, J NEUROPHYSIOL, V39, P213 SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 NR 37 TC 51 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 1994 VL 72 IS 1-2 BP 206 EP 222 DI 10.1016/0378-5955(94)90220-8 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300022 PM 8150737 ER PT J AU NELKEN, I PRUT, Y VADDIA, E ABELES, M AF NELKEN, I PRUT, Y VADDIA, E ABELES, M TI POPULATION RESPONSES TO MULTIFREQUENCY SOUNDS IN THE CAT AUDITORY-CORTEX - 4-TONE COMPLEXES SO HEARING RESEARCH LA English DT Article DE PRIMARY AUDITORY CORTEX; COMPLEX SOUNDS; NONLINEAR MODELING; CAT ID SPECIES-SPECIFIC VOCALIZATIONS; DORSAL COCHLEAR NUCLEUS; AMPLITUDE-MODULATION; NOISE STIMULI; SINGLE UNITS; NEURONS; REPRESENTATION; FIELDS; CELLS; MAPS AB Population responses to two-tone and four-tone sounds were recorded in primary auditory cortex of anesthetized cats. The stimuli were delivered through a sealed, calibrated sound delivery system. The envelope of the neural signal (short time mean absolute value, MAPS) was recorded extracellularly from six microelectrodes simultaneously. A new method was developed to describe the responses to the four-tone complexes. The responses were represented as sums of contributions of different orders. The first order contributions described the effect of the single frequencies appearing in the stimulus. The second order contributions described the modulatory effect of the pairs of frequencies. Higher order contributions could in principle be computed. This paper concentrates on the mean onset responses. The extent to which the first and second order contributions described the onset responses was assessed in two ways. First, the actual responses to two-tone stimuli were compared with those predicted using the contributions computed from the four-tone stimuli. Second, the residual variance in the responses, after the substraction of the first and second order contributions, was computed and compared with the variability in the responses to repetitions of the same stimulus. The first type of analysis showed good quantitative agreement between the predicted and the measured two-tone responses. The second type of analysis showed that the first and second order contributions were often sufficient to predict the responses to four-tone stimuli up to the level of the variability in the responses to repetitions of a single stimulus. In conjunction with the results of the companion paper (Nelken et al., 1994a) it is concluded that the onset responses to multifrequency sounds are shaped mainly by the single frequency content of the sound and by two-tone interactions, and that higher order interactions contribute much less to the responses. It follows that single-tone effects and two-tone interactions are necessary and sufficient to explain the mean population onset responses to the four-tone stimuli. More information can be coded in the temporal evolution of the responses. C1 HADASSAH MED SCH,DEPT PHYSIOL,IL-91010 JERUSALEM,ISRAEL. RI Nelken, Israel/B-7753-2011 OI Nelken, Israel/0000-0002-6645-107X CR ABELES M, 1972, BRAIN RES, V42, P337, DOI 10.1016/0006-8993(72)90535-5 AERTSEN AMHJ, 1981, BIOL CYBERN, V39, P195, DOI 10.1007/BF00342772 AERTSEN AMHJ, 1979, BIOL CYBERN, V32, P175, DOI 10.1007/BF00337394 CLOPTON BM, 1991, HEARING RES, V52, P329, DOI 10.1016/0378-5955(91)90023-3 EGGERMONT JJ, 1981, HEARING RES, V5, P109, DOI 10.1016/0378-5955(81)90030-7 EGGERMONT JJ, 1983, Q REV BIOPHYS, V16, P341 EGGERMONT JJ, 1983, HEARING RES, V10, P167, DOI 10.1016/0378-5955(83)90052-7 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 EPPING W, 1985, THESIS FROSTIG RD, 1983, BRAIN RES, V272, P211, DOI 10.1016/0006-8993(83)90567-X GOLDSTEIN MH, 1975, HDB SENSORY PHYSL 2, V5 HAMPEL FR, 1986, ROBUST STATISTICS AP JOHNSON DH, 1980, J ACOUST SOC AM, V68, P876, DOI 10.1121/1.384826 KIM PJ, 1993, IN PRESS J ACOUST SO MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 NELKEN I, 1991, THESIS NELKEN I, 1994, HEARING RES, V72, P237, DOI 10.1016/0378-5955(94)90222-4 NELKEN I, 1994, HEARING RES, V72, P206, DOI 10.1016/0378-5955(94)90220-8 NEWMAN JD, 1973, BRAIN RES, V54, P287, DOI 10.1016/0006-8993(73)90050-4 OONISHI S, 1965, JPN J PHYSIOL, V15, P342 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1986, J ACOUST SOC AM, V80, P177, DOI 10.1121/1.394178 PHILLIPS DP, 1985, HEARING RES, V18, P87, DOI 10.1016/0378-5955(85)90112-1 PRUT Y, 1994, UNPUB RELATIONSHIPS SACHS MB, 1984, HEARING SCI RECENT A, P263 SCHREINER C, 1983, HEARING PHYSL BASES, P169 SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 SCHWARZ DWF, 1990, J NEUROPHYSIOL, V64, P282 SHAMMA SA, 1993, J NEUROPHYSIOL, V69, P367 SMOLDERS JWT, 1979, BIOL CYBERN, V35, P11, DOI 10.1007/BF01845840 SOKAL RR, 1981, BIOMETRY, P180 SPIROU GA, 1991, J NEUROPHYSIOL, V66, P1750 STEINSCHNEIDER M, 1990, BRAIN RES, V519, P158, DOI 10.1016/0006-8993(90)90074-L SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 VICTOR JD, 1979, Q APPL MATH, V37, P113 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 WICKESBERG RE, 1984, HEARING RES, V14, P155, DOI 10.1016/0378-5955(84)90014-5 YESHURUN Y, 1985, BIOL CYBERN, V51, P383, DOI 10.1007/BF00350778 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 NR 41 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 JAN PY 1994 VL 72 IS 1-2 BP 223 EP 236 DI 10.1016/0378-5955(94)90221-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300023 PM 8150738 ER PT J AU NELKEN, I PRUT, Y VAADIA, E ABELES, M AF NELKEN, I PRUT, Y VAADIA, E ABELES, M TI IN SEARCH OF THE BEST STIMULUS - AN OPTIMIZATION PROCEDURE FOR FINDING EFFICIENT STIMULI IN THE CAT AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE PRIMARY AUDITORY CORTEX; COMPLEX SOUNDS; OPTIMAL STIMULI; CAT ID SPECIES-SPECIFIC VOCALIZATIONS; FREQUENCY-MODULATED STIMULI; FUNCTIONAL ARCHITECTURE; AMPLITUDE-MODULATION; VISUAL-CORTEX; SINGLE UNITS; NEURONS; RESPONSES; TONES; REPRESENTATION AB Units in the auditory cortex of cats respond to a large variety of stimuli: pure tones, AM- and FIM-modulated signals, clicks, wideband noise, natural sounds, and more. However, no single family of sounds was found to be optimal (in the sense that oriented lines are optimal in the visual cortex). The search for optimal complex sounds is hard because of the high dimensionality of the space of interesting sounds. In an effort to overcome this problem, an automatic search procedure for finding efficient stimuli in high-dimensional sound spaces was developed. This procedure chooses the stimuli to be presented according to the responses to past stimuli, trying to increase the strength of the response. The results of applying this method to. recordings of population activity in the primary auditory cortex of cats are described. The search was applied to single tones, two-tone stimuli, four-tone stimuli and to a two-dimensional subset of nine-tone stimuli, parametrized by the center frequency and the fixed difference between adjacent frequencies. The method was able to find efficient stimuli, and its performance improved with the dimension of the sound spaces. Efficient stimuli, found in different optimization runs using population activity recorded from the same electrode, often shared similar frequencies and pairs of frequencies, and tended to evoke similar levels of activity. This result indicates that a global analysis of the location of spectral peaks is performed at the level of the auditory cortex. C1 HADASSAH MED SCH,DEPT PHYSIOL,IL-91010 JERUSALEM,ISRAEL. RI Nelken, Israel/B-7753-2011; Vaadia, Eilon/E-9347-2011 OI Nelken, Israel/0000-0002-6645-107X; CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 ABELES M, 1972, BRAIN RES, V42, P337, DOI 10.1016/0006-8993(72)90535-5 Abeles M., 1982, LOCAL CORTICAL CIRCU AHISSAR M, 1992, J NEUROPHYSIOL, V67, P203 Aitkin L. M., 1990, AUDITORY CORTEX STRU BRUGGE JF, 1985, CEREBRAL CORTEX, V4 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GOLDSTEI.MH, 1970, J NEUROPHYSIOL, V33, P188 GOLDSTEIN MH, 1975, HDB SENSORY PHYSL 2, V5 GRAY CM, 1989, NATURE, V338, P334, DOI 10.1038/338334a0 HAMPEL FR, 1986, ROBUST STATISTICS AP HARTH E, 1974, VISION RES, V14, P1475, DOI 10.1016/0042-6989(74)90024-8 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 HUBEL DH, 1977, PROC R SOC SER B-BIO, V198, P1, DOI 10.1098/rspb.1977.0085 Huber P.J, 1981, ROBUST STATISTICS MATSUBARA JA, 1988, J COMP NEUROL, V268, P38, DOI 10.1002/cne.902680105 MENDELSON JR, 1992, HEARING RES, V58, P47, DOI 10.1016/0378-5955(92)90007-A MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MIDDLEBROOKS JC, 1981, J NEUROSCI, V1, P107 NELKEN I, 1994, HEARING RES, V72, P223, DOI 10.1016/0378-5955(94)90221-6 NELKEN I, 1994, HEARING RES, V72, P206, DOI 10.1016/0378-5955(94)90220-8 NEWMAN JD, 1973, BRAIN RES, V54, P287, DOI 10.1016/0006-8993(73)90050-4 ORAM MW, 1992, J NEUROPHYSIOL, V68, P70 PHILLIPS DP, 1985, HEARING RES, V18, P73, DOI 10.1016/0378-5955(85)90111-X Press WH, 1988, NUMERICAL RECIPES C PRUT Y, 1994, UNPUB RELATIONSHIPS Rabiner L.R., 1978, DIGITAL PROCESSING S RICE JJ, 1992, HEARING RES, V58, P132, DOI 10.1016/0378-5955(92)90123-5 SACHS MB, 1991, NEUROBIOLOGY HEARING, P79 SCHREINER C, 1983, HEARING PHYSL BASES, P169 SCHREINER C, 1988, ORG NEURAL NETWORKS SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 SCHWARZ DWF, 1990, J NEUROPHYSIOL, V64, P282 SHAMMA SA, 1993, J NEUROPHYSIOL, V69, P367 STEINSCHNEIDER M, 1990, BRAIN RES, V519, P158, DOI 10.1016/0006-8993(90)90074-L SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 TEICH MC, 1990, LECTURE NOTES BIOMAT, V87 TZANAKOU E, 1979, BIOL CYBERN, V35, P161, DOI 10.1007/BF00337061 WEINBERGER NM, 1987, PROG NEUROBIOL, V29, P1, DOI 10.1016/0301-0082(87)90014-1 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 YESHURUN Y, 1985, BIOL CYBERN, V51, P383, DOI 10.1007/BF00350778 NR 46 TC 31 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 JAN PY 1994 VL 72 IS 1-2 BP 237 EP 253 DI 10.1016/0378-5955(94)90222-4 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300024 PM 8150740 ER PT J AU WATAYA, H HANDA, K HOZAWA, K TAKASAKA, T CUNNINGHAM, D RUBEL, EW HAKOMORI, SI AF WATAYA, H HANDA, K HOZAWA, K TAKASAKA, T CUNNINGHAM, D RUBEL, EW HAKOMORI, SI TI A CHARACTERISTIC PROTEIN HIGHLY EXPRESSED IN GUINEA-PIG INNER-EAR, DEFINED BY MONOCLONAL-ANTIBODY WH-1 SO HEARING RESEARCH LA English DT Article DE GUINEA PIG COCHLEA; TECTORIAL MEMBRANE; OUTER HAIR STEREOCILIA; KIMURAS MEMBRANE; WESTERN BLOTTING; 40 KDA PROTEIN ID CARBOHYDRATE ANTIGENS; HAIR-CELLS; TUMOR; COCHLEA; ORGAN; CORTI AB A new monoclonal antibody (termed WH-1; isotype IgG(2b)) was established using a homogenate of dissected guinea pig cochleas (N = 60) as immunogen. Western blotting and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) identified the WH-1 antigen as a protein or glycoprotein with M(r) approximate to 40 kDa. Immunoperoxidase treatment of histologic cryosections of guinea pig cochlea, followed by light microscopic examination, revealed strong positive staining at three sites: (i) parts of Hensen's stripe, marginal band, covering net, and Kimura's membrane (within the tectorial membrane [TM]); (ii) Deiters' cells, pillar cells, Hensen's cells, and stereocilia of outer hair cells (within the organ of Corti); (iii) interdental cells, inner and outer sulcus cells, Reissner's membrane, and surface membrane of stria vascularis epithelium. Similar staining patterns were observed for cryosections of rat and mouse cochleas. Only a trace quantity of cross-reacting protein was detectable in brainstem. The protein was not detectable in tongue extract by Western blotting. However, sections of brainstem and tongue did show positive immunohistological staining with WH-1. Localization of WH-1 antigen was further examined by electron microscopy. WH-1 positivity on outer hair cell stereocilia, certain sites on the TM, interdental cell surface, Reissner's membrane epithelia, and inner and outer sulcus cells was confirmed. WH-1 antigen was not detected on inner hair cell stereocilia by light or electron microscopy. The localization of WH-1 antigen on outer hair cell stereocilia and TM suggests that it may play some role in adhesion between these structures. C1 BIOMEMBRANE INST,SEATTLE,WA 98119. UNIV WASHINGTON,DEPT PATHOBIOL,SEATTLE,WA 98195. TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,TOHOKU,JAPAN. UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. CR FEIZI T, 1985, NATURE, V314, P53, DOI 10.1038/314053a0 FENDERSON BA, 1990, BIOESSAYS, V12, P173, DOI 10.1002/bies.950120406 GILLOYZAGA P, 1985, HEARING RES, V20, P1 Hakomori S., 1983, SPHINGOLIPID BIOCH, P1 HAKOMORI S, 1984, ANNU REV IMMUNOL, V2, P103, DOI 10.1146/annurev.immunol.2.1.103 HAKOMORI SI, 1989, ADV CANCER RES, V52, P257, DOI 10.1016/S0065-230X(08)60215-8 HAKOMORI S, 1983, J NATL CANCER I, V71, P231 HOZAWA K, 1993, GLYCOBIOLOGY, V3, P47, DOI 10.1093/glycob/3.1.47 Kennett R. H., 1984, MONOCLONAL ANTIBODIE Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 KOHLER G, 1976, EUR J IMMUNOL, V6, P511, DOI 10.1002/eji.1830060713 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LOWRY OH, 1951, J BIOL CHEM, V193, P265 MCLEAN IW, 1974, J HISTOCHEM CYTOCHEM, V22, P1077 OBERHOLTZER JC, 1986, HEARING RES, V23, P161, DOI 10.1016/0378-5955(86)90013-4 PORSTMANN B, 1981, J CLIN CHEM CLIN BIO, V19, P435 PTOK M, 1991, HEARING RES, V57, P79, DOI 10.1016/0378-5955(91)90077-M RICHARDSON GP, 1987, DEV BIOL, V119, P217, DOI 10.1016/0012-1606(87)90223-5 RICHARDSON GP, 1990, J CELL BIOL, V110, P1055, DOI 10.1083/jcb.110.4.1055 RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 RUEDA J, 1988, GLYCOCONJUGATES MED, P338 SANTI PA, 1987, HEARING RES, V27, P47, DOI 10.1016/0378-5955(87)90025-6 TACHIBANA M, 1987, HEARING RES, V25, P115, DOI 10.1016/0378-5955(87)90084-0 TAKASAKA T, 1983, ANN OTOL RHINOL S101, V92, P112 THALMANN I, 1980, ARCH OTO-RHINO-LARYN, V226, P123, DOI 10.1007/BF00455126 THALMANN I, 1990, EUR ARCH OTO-RHINO-L, V248, P15, DOI 10.1007/BF00634774 THORN L, 1979, ANAT EMBRYOL, V115, P303 ZAJIC G, 1991, HEARING RES, V52, P59, DOI 10.1016/0378-5955(91)90187-E NR 29 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 JAN PY 1994 VL 72 IS 1-2 BP 254 EP 262 DI 10.1016/0378-5955(94)90223-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MT823 UT WOS:A1994MT82300025 PM 8150741 ER PT J AU BERLIN, CI HOOD, LJ WEN, H SZABO, P CECOLA, RP RIGBY, P JACKSON, DF AF BERLIN, CI HOOD, LJ WEN, H SZABO, P CECOLA, RP RIGBY, P JACKSON, DF TI CONTRALATERAL SUPPRESSION OF NONLINEAR CLICK-EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; CONTRALATERAL SUPPRESSION; EFFERENT SYSTEM; NONLINEAR CLICKS; HUMANS; RMS AMPLITUDE; TIME-SHIFT; ECHOES ID COCHLEAR MICROMECHANICAL PROPERTIES; EFFERENT OLIVOCOCHLEAR NEURONS; OTO-ACOUSTIC EMISSIONS; AUDITORY-NERVE FIBERS; ELECTRICAL-STIMULATION; MECHANICS AB Click-evoked otoacoustic emissions from nominal 80 dB pSP (peak sound pressure) 80-mu s pulses presented at 50 pulses per second were collected from the right ears of eleven normal hearing subjects using an IL08S Otodynamic Analyzer in the non-linear mode. Clicks, pure tones, and narrow bands of noise were then presented to their left ears through insert earphones. The 80-mu s contralateral clicks ranged in intensity from 80 dB pSP in 5 dB steps down to 60 dB pSP but data on only 10 of the subjects were collected successfully. The pure tones and narrow bands of noise centered at 250, 500, 1000, 2000, and 4000 Hz were also presented through insert phones at 20, 40, 60 and 80 dB HL (Hearing Level) to all 11 subjects. The mean overall 'echo amplitude' without contralateral stimuli was 11 dB SPL and underwent more than 3 dB of overall suppression in response to the noises which were the most effective of the contralateral suppressors. When we analyzed the echo suppression to noise in 2-ms segments, we found consistent contralateral suppression of 3-4 dB concentrated in the time zones after 8 ms. Time shifts of more than 200 mu s between the control and experimental traces were also observed in the same zones. The clicks were the next most effective suppressors, but showed their amplitude and time effects in somewhat earlier time zones. The tones were the least effective suppressors suggesting that efferent effects we measured in the human system are not strongly tonotopic. Because 'non-linear' mode high intensity clicks were deliberately selected as stimuli to evoke the TEOAE's, the emissions and their suppression can represent neither the 'true' TEOAE nor all of the efferent system's suppression abilities. RP BERLIN, CI (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES LAB,2020 GRAVIER ST,NEW ORLEANS,LA 70112, USA. CR BERLIN CI, 1991, ABSTR ASS RES OTOL BERLIN CI, 1993, HEARING RES, V65, P40, DOI 10.1016/0378-5955(93)90199-B BROWN SE, 1990, ABSTR ASS RES OT, P230 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1992, ABSTR ASS RES OT, P158 COLLET L, 1991, COMMUNICATION COLLET L, 1991, MAY INT S OT EM KANS DJUPESLAND G, ACTA OTOLARYNGOLOGIC, V71, P262 Glattke T.J., 1991, AM J AUDIOL, V1, P29 GROSE JH, 1983, J ACOUST SOC AM S1, V71, pS38 GUINAN JJ, 1988, ABSTR ASS RES OT, P174 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 JW, 1979, THESIS BAYLOR COLL M KILLION MC, 1946, HEAR INSTRU, V35, P28 KUJAWA S, 1989, ASHA, V31, P123 KUJAWA S, 1991, ABSTR ASS RES OT KUJAWA S, 1990, ASHA, V32, P156 MCCOY M, 1990, ASHA, V32, P156 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOUNTAIN DC, 1980, HEARING RES, V3, P231, DOI 10.1016/0378-5955(80)90049-0 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 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 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 STARR A, 1991, BRAIN, V114, P1157, DOI 10.1093/brain/114.3.1157 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr WB, 1986, NEUROBIOLOGY HEARING NR 32 TC 86 Z9 87 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 1993 VL 71 IS 1-2 BP 1 EP 11 DI 10.1016/0378-5955(93)90015-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800001 PM 8113128 ER PT J AU POPELKA, GR OSTERHAMMEL, PA NIELSEN, LH RASMUSSEN, AN AF POPELKA, GR OSTERHAMMEL, PA NIELSEN, LH RASMUSSEN, AN TI GROWTH OF DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS WITH PRIMARY-TONE LEVEL IN HUMANS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; DISTORTION PRODUCTS; METABOLICALLY ACTIVE; NONLINEAR COCHLEAR PROCESSES ID ACOUSTIC DISTORTION; AUDITORY-SENSITIVITY; HUMAN EARS; 2F1-F2; NONLINEARITY; PRESSURE; RABBIT AB This study addressed the hypotheses that the growth of the level of distortion product otoacoustic emissions (L(DP)) With primary-tone level reflects the behavior of a third-order nonlinear polynomial system, and that two sources exist for these distortion products. The results indicated that the 2f(1)-f(2) otoacoustic emission in humans can be measured over a much larger stimulus range than reported previously, even for stimuli (L(1) = L(2)) as low as 10 dB SPL (re 20 mu Pa). The input/output functions are best described as a straight line with a rate of growth of about 1 dB/dB of stimulus level. For stimulus levels at which metabolically active, nonlinear cochlear processes are in operation, the system does not behave as a simple third-order nonlinear polynomial. Small plateaus and sharp discontinuities or 'notches' can occur in the functions at stimulus levels of approximately 55 dB SPL. These characteristics are consistent with the notion of two separate sources of the L(DP), one at low stimulus levels, and one at high levels. An alternative explanation is that the measured otoacoustic emission does not represent only the activity ata single location along the basilar membrane but includes the effects of interactions among similar signals arising from multiple locations, or from the original source via multiple paths. C1 RIGSHOSP,DEPT OTOLARYNGOL,HEAD & NECK SURG AUDIOL LAB,COPENHAGEN,DENMARK. RP POPELKA, GR (reprint author), CENT INST DEAF,818 S EUCLID,ST LOUIS,MO 63110, USA. CR BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 FAHEY PF, 1988, BASIC ISSUES HEARING, P124 FAHEY PF, 1986, PERIPHERAL AUDITORY, P314 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 GOLDSTEIN JL, 1990, HEARING RES, V49, P39, DOI 10.1016/0378-5955(90)90094-6 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 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 LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 Lonsbury-Martin B L, 1990, Ann Otol Rhinol Laryngol Suppl, V147, P3 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MOULIN A, 1992, ACTA OTO-LARYNGOL, V112, P210 NAEVE SL, 1992, J ACOUST SOC AM, V91, P2091, DOI 10.1121/1.403695 NELSON DA, 1992, J SPEECH HEAR RES, V35, P1142 NIELSEN LH, 1993, IN PRESS SCAND AUDIO OSTERHAMMEL PA, 1993, SCAND AUDIOL, V22, P111, DOI 10.3109/01050399309046026 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 RAMIREZ RW, 1985, FFT FUNDAMENTALS CON, P101 RASMUSSEN AN, 1993, SCANDINAVIAN AUDIOLO, V22, P159 RASMUSSEN AN, 1992, SCAND AUDIOL, V21, P219, DOI 10.3109/01050399209046005 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L 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 ZUREK PM, 1992, EAR HEARING, V13, P307, DOI 10.1097/00003446-199210000-00008 ZWICKER E, 1990, J ACOUST SOC AM, V87, P2583, DOI 10.1121/1.399051 1991, ACOUSTICS STANDARD R NR 28 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 DEC PY 1993 VL 71 IS 1-2 BP 12 EP 22 DI 10.1016/0378-5955(93)90016-T PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800002 PM 8113130 ER PT J AU KITANO, I DOI, K MORI, N MATSUNAGA, T AF KITANO, I DOI, K MORI, N MATSUNAGA, T TI INVOLVEMENT OF CL- TRANSPORT IN FORSKOLIN-INDUCED ELEVATION OF ENDOCOCHLEAR POTENTIAL SO HEARING RESEARCH LA English DT Article DE CL- TRANSPORT; CAMP-ACTIVIATED CL- CHANNEL; FORSKOLIN; ADEQUATE CYCLASE; ENDOCOCHLEAR POTENTIAL ID ADENYLATE-CYCLASE MODULATION; COCHLEAR POTENTIALS; GUINEA-PIG; CHLORIDE; SECRETION; CELLS; CAMP AB To determine the possible involvement of C1(-) transport in the forskolin-induced endocochlear potential (EP) elevation, the effect of forskolin on the EP was examined in C1(-)-free artificial perilymph (aPL) as well as in the presence of Cl- channel blockers. The perfusion of scala vestibuli (SV) with forskolin (200 mu M) dissolved in Cl--free aPL failed to produce an EP elevation, while SV perfusion of forskolin dissolved in normal aPL elevated the EP. The application of DPC and IAA-94 (blockers of cAMP-activated Cl- channel) into SV completely suppressed the forskolin-induced EP elevation, while niflumic acid (a Ca2+-activated Cl- channel blocker) failed to do so. IAA-94 applied into scala tympani (ST) did not suppress this EP elevation. The results suggest that adenylate cyclase may modulate the EP by changing Cl- transport between SV and scala media (SM) across Reissner's membrane. C1 OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,OSAKA 553,JAPAN. KAGAWA MED SCH,DEPT OTOLARYNGOL,MIKI,KAGAWA 76107,JAPAN. RP KITANO, I (reprint author), NARA MED UNIV,DEPT OTOLARYNGOL,NARA,NARA 634,JAPAN. CR ANDERSON MP, 1991, P NATL ACAD SCI USA, V88, P6003, DOI 10.1073/pnas.88.14.6003 CLIFF WH, 1990, P NATL ACAD SCI USA, V87, P4956, DOI 10.1073/pnas.87.13.4956 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 KITANO I, 1992, ABSTR INN EAR BIOL, V29, P65 KITANO I, 1993, ABSTR ASS RES OT, V16, P135 KITANO L, 1992, ABSTR ASS RES OT, V15, P105 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P176, DOI 10.3109/00016487809124734 KORN SJ, 1991, J PHYSIOL-LONDON, V439, P423 KREUSEL KM, 1991, AM J PHYSIOL, V261, pC574 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P359, DOI 10.1007/BF00588214 LANDRY DW, 1987, J GEN PHYSIOL, V90, P779, DOI 10.1085/jgp.90.6.779 MACUS DC, 1984, AM J PHYSIOL, V247, pC240 SELLICK P M, 1975, Progress in Neurobiology (Oxford), V5, P337, DOI 10.1016/0301-0082(75)90015-5 SIMMONS NL, 1991, J PHYSIOL-LONDON, V432, P459 SINGH AK, 1991, AM J PHYSIOL, V260, pC51 SUNOSE H, 1993, ABSTR ASS RES OTOLAR, V16, P135 TASAKI I, 1954, J ACOUST SOC AM, V26, P765, DOI 10.1121/1.1907415 THALMANN I, 1982, Journal of the Acoustical Society of America, V71, pS99, DOI 10.1121/1.2019673 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 DEC PY 1993 VL 71 IS 1-2 BP 23 EP 27 DI 10.1016/0378-5955(93)90017-U PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800003 PM 8113141 ER PT J AU WARCHOL, ME CORWIN, JT AF WARCHOL, ME CORWIN, JT TI SUPPORTING CELLS IN AVIAN VESTIBULAR ORGANS PROLIFERATE IN SERUM-FREE CULTURE SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; SACCULE; UTRICLE; DEVELOPMENT; REGENERATION; CELL PROLIFERATION ID SENSORY HAIR-CELLS; INNER-EAR; ACOUSTIC TRAUMA; GROWTH-FACTORS; FISH EAR; REGENERATION; EPITHELIUM; MACULA; NUMBER; EVENTS AB Explants of saccules and utricles taken from hatchling chicks were cultured in medium that contained fetal bovine serum and in serum-free medium. The mitotic tracers [H-3]thymidine and bromo-deoxyuridine were added to the media to label proliferating cells. High numbers of labeled supporting cells were found in cultures that were maintained in both serum-containing and serum-free media. After seven days in culture, some of the labeled cells had begun to differentiate as hair cells. The results suggest that any mitogenic factors necessary for supporting cell proliferation and the factors required for the initial stages of hair cell differentiation are produced by cells contained within explants of the vestibular sensory epithelia. C1 UNIV VIRGINIA,SCH MED,DEPT NEUROSCI,CHARLOTTESVILLE,VA 22908. RP WARCHOL, ME (reprint author), UNIV VIRGINIA,SCH MED,DEPT OTOLARYNGOL HNS,POB 396,CHARLOTTESVILLE,VA 22908, USA. CR BALAK KJ, 1990, J NEUROSCI, V10, P2505 Banker G., 1991, CULTURING NERVE CELL BARRITAULT D, 1981, DIFFERENTIATION, V18, P29, DOI 10.1111/j.1432-0436.1981.tb01101.x BROOKS RF, 1976, NATURE, V260, P248, DOI 10.1038/260248a0 CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 CORWIN JT, 1986, BIOL CHANGE OTOLARYN, P291 CORWIN JT, 1991, CIBA FDN S, V160, P101 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1983, J COMP NEUROL, V217, P345, DOI 10.1002/cne.902170309 GAO WQ, 1991, NEURON, V6, P705, DOI 10.1016/0896-6273(91)90168-Y HASHINO E, 1993, J CELL SCI, V105, P23 HOLLEY RW, 1975, NATURE, V258, P487, DOI 10.1038/258487a0 JONES JE, 1993, J NEUROSCI, V13, P1022 JONES JE, 1991, THESIS U VIRGINIA CH JORGENSEN JM, 1989, J MORPHOL, V201, P187, DOI 10.1002/jmor.1052010208 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 KATAYAMA A, 1993, J COMP NEUROL, V333, P28, DOI 10.1002/cne.903330103 KELLEY MW, 1993, IN PRESS DEVELOPMENT KELLEY MW, 1992, ASS RES OTOLARYNGOL, V15, P145 LEWIS J, 1991, CIBA F SYMP, V160, P25 LILLIEN L, 1992, DEVELOPMENT, V115, P253 MCNEIL PL, 1989, J CELL BIOL, V109, P811, DOI 10.1083/jcb.109.2.811 PARDEE AB, 1989, SCIENCE, V246, P603, DOI 10.1126/science.2683075 PARDEE AB, 1974, P NATL ACAD SCI USA, V71, P1286, DOI 10.1073/pnas.71.4.1286 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 REPRESA J, 1989, DEV BIOL, V134, P21, DOI 10.1016/0012-1606(89)90074-2 REPRESA J, 1990, DEVELOPMENT, V110, P1081 REPRESA JJ, 1988, DEVELOPMENT, V103, P87 ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 STONE JS, 1993, ASS RES OTOLARYNGOL, V16, P104 WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 WARCHOL ME, 1992, ASS RES OTOLARYNGOL, V15, P106 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 ZETTERBERG A, 1985, P NATL ACAD SCI USA, V82, P5365, DOI 10.1073/pnas.82.16.5365 NR 39 TC 32 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 DEC PY 1993 VL 71 IS 1-2 BP 28 EP 36 DI 10.1016/0378-5955(93)90018-V PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800004 PM 8113143 ER PT J AU CLOCK, AE SALVI, RJ SAUNDERS, SS POWERS, NL AF CLOCK, AE SALVI, RJ SAUNDERS, SS POWERS, NL TI NEURAL CORRELATES OF TEMPORAL INTEGRATION IN THE COCHLEAR NUCLEUS OF THE CHINCHILLA SO HEARING RESEARCH LA English DT Article DE TEMPORAL INTEGRATION, COCHLEAR NUCLEUS, SINGLE UNIT, CHINCHILLA, 2-ALTERNATIVE FORCED-CHOICE ID HEARING-IMPAIRED CAT; RESPONSE PROPERTIES; BRAIN-SLICES; NOISE; CELLS; CLASSIFICATION; STIMULATION; REGULARITY; SUMMATION; MOUSE AB Single unit thresholds-were measured as a function of stimulus duration for Primary-like and Chopper units in the anteroventral cochlear nucleus (AVCN) of the chinchilla to examine the neural correlates of temporal integration. Thresholds were measured with a two-alternative, forced-choice (2AFC) adaptive tracking procedure. The time constants and the slopes of the threshold-duration functions were estimated by fitting the threshold data with an exponential function and a power law function. The results showed that Primary-like units exhibited greater threshold improvement and a longer time constant than Chopper units. Units with low characteristic frequencies (CF) showed a larger decrease in threshold with increasing duration and a longer time constant than mid-CF or high-CF units. Units with low spontaneous rates (SR) showed a smaller threshold decrease with increasing duration and a shorter time constant than mid-SR or high-SR units. The single unit time constants and the rate of threshold improvement are similar to those measured psychophysically in the chinchilla. C1 SUNY BUFFALO,HEARING RES LAB,BUFFALO,NY 14214. CR BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 CLARK WW, 1986, SENSORINEURAL HEARIN DOOLING RJ, 1985, J ACOUST SOC AM, V77, P1917, DOI 10.1121/1.391835 EGAN JP, 1975, SIGNAL DETECTION THE 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 GERKEN GM, 1990, J ACOUST SOC AM, V88, P767, DOI 10.1121/1.399726 GERKEN GM, 1979, J ACOUST SOC AM, V66, P728, DOI 10.1121/1.383223 GERKEN GM, 1991, HEARING RES, V53, P101, DOI 10.1016/0378-5955(91)90217-W GERSUNI GV, 1965, NEUROPSYCHOLOGIA, V3, P95, DOI 10.1016/0028-3932(65)90036-9 GREEN DM, 1957, J ACOUST SOC AM, V29, P523, DOI 10.1121/1.1908951 HENDERSO.D, 1969, J ACOUST SOC AM, V46, P474, DOI 10.1121/1.1911714 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 OERTEL D, 1985, J ACOUST SOC AM, V78, P328, DOI 10.1121/1.392494 OERTEL D, 1983, J NEUROSCI, V3, P2043 OLSEN WO, 1966, J ACOUST SOC AM, V40, P591, DOI 10.1121/1.1910123 PENNER MJ, 1978, J ACOUST SOC AM, V63, P195, DOI 10.1121/1.381712 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 POWERS NL, 1991, THESIS SUNY BUFFALO RELKIN EM, 1987, J ACOUST SOC AM, V82, P1679, DOI 10.1121/1.395159 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SHOFNER WP, 1989, J ACOUST SOC AM, V86, P2172, DOI 10.1121/1.398478 SOLECKI JM, 1990, J ACOUST SOC AM, V88, P779, DOI 10.1121/1.399727 VIEMEISTER NF, 1991, 9TH P INT S HEAR CAR VIEMEISTER NF, 1991, J ACOUST SOC AM, V90, P858, DOI 10.1121/1.401953 WALL L G, 1981, Journal of Auditory Research, V21, P29 WATSON CS, 1969, J ACOUST SOC AM, V46, P989, DOI 10.1121/1.1911819 WRIGHT HN, 1968, J SPEECH HEAR RES, V11, P842 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 ZWISLOCK.JJ, 1969, J ACOUST SOC AM, V46, P431, DOI 10.1121/1.1911708 ZWISLOCKI J, 1960, J ACOUST SOC AM, V32, P1046, DOI 10.1121/1.1908276 NR 35 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 1993 VL 71 IS 1-2 BP 37 EP 50 DI 10.1016/0378-5955(93)90019-W PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800005 PM 8113144 ER PT J AU MARKOVITZ, NS POLLAK, GD AF MARKOVITZ, NS POLLAK, GD TI THE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS IN THE MOUSTACHE BAT - MONAURAL PROPERTIES SO HEARING RESEARCH LA English DT Article DE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS; AUDITORY PHYSIOLOGY; MONAURAL RESPONSES; TEMPORAL RESPONSE PATTERNS; CHOPPERS; MOUSTACHE BAT ID SUPERIOR OLIVARY COMPLEX; VENTRAL COCHLEAR NUCLEUS; PHYSIOLOGICAL-RESPONSE PROPERTIES; INFERIOR COLLICULUS; HORSERADISH-PEROXIDASE; ASCENDING PROJECTIONS; PTERONOTUS-PARNELLII; AUDITORY-SYSTEM; BRAIN-STEM; FUNCTIONAL-ORGANIZATION AB Neurons in the mustache bat dorsal nucleus of the lateral lemniscus (DNLL) were examined in response to monaural stimulation. There are six main findings of this study. First, the mustache bat DNLL is tonotopically organized. Second, EI cells are the predominant aural type and comprise about 80% of DNLL neurons, whereas monaural and EE cells are far less numerous. Third, the majority of DNLL neurons have either monotonic or weakly nonmonotonic rate-intensity functions. Fourth, a chopping pattern is evoked by contralateral stimulation in 58% of DNLL neurons and is the predominant temporal response pattern. Fifth, neurons with different aural properties tend to exhibit different temporal response patterns: EI cells are largely choppers, while EO and EE cells are more often primarylike or primarylike-with-notch. Sixth, the sustained responses of EE units to contralateral stimulation differs dramatically from their onset responses to ipsilateral stimulation. Here we have demonstrated that although a large proportion of mustache bat DNLL neurons are EI choppers, the DNLL nonetheless contains a heterogeneous population of neurons based on physiological responses to pure tones. C1 UNIV TEXAS,DEPT ZOOL,AUSTIN,TX 78712. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V3, P265 ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 AITKIN LM, 1970, J NEUROPHYSIOL, V33, P421 BRUGGE JF, 1970, J NEUROPHYSIOL, V33, P441 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 BUCKTHOUGHT AD, 1993, ABSTR ASS RES OT, P126 CAIRD D, 1983, EXP BRAIN RES, V52, P385 Cant NB, 1992, MAMMALIAN AUDITORY P, P66 COVEY E, 1991, J NEUROPHYSIOL, V66, P1080 COVEY E, 1991, J NEUROSCI, V11, P3456 COVEY E, 1993, J NEUROPHYSIOL, V69, P842 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 GLENDENNING KK, 1992, J COMP NEUROL, V319, P100, DOI 10.1002/cne.903190110 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 GOLDBERG JAY M., 1968, J NEUROPHYSIOL, V31, P639 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GROTHE B, 1992, P NATL ACAD SCI USA, V89, P5108, DOI 10.1073/pnas.89.11.5108 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 HALL JL, 1965, J ACOUST SOC AM, V37, P814, DOI 10.1121/1.1909447 HARNISCHFEGER G, 1985, J NEUROPHYSIOL, V53, P89 Henkel C. K., 1992, Society for Neuroscience Abstracts, V18, P1038 Humason GL, 1979, ANIMAL TISSUE TECHNI HUTSON KA, 1991, J COMP NEUROL, V312, P105, DOI 10.1002/cne.903120109 IWAHORI N, 1986, Neuroscience Research, V3, P196, DOI 10.1016/0168-0102(86)90002-7 KANE ES, 1980, J COMP NEUROL, V192, P797, DOI 10.1002/cne.901920412 KUDO M, 1990, J COMP NEUROL, V298, P400, DOI 10.1002/cne.902980403 KUDO M, 1981, BRAIN RES, V221, P57, DOI 10.1016/0006-8993(81)91063-5 KUWABARA N, 1991, J COMP NEUROL, V314, P684, DOI 10.1002/cne.903140405 LARUE D T, 1991, Society for Neuroscience Abstracts, V17, P300 MARKOVITZ NS, 1993, ABSTR ASS RES OT, P110 MERCHAN MA, 1993, ABSTR ASS RES OT, P126 METZNER W, 1987, J COMP PHYSIOL A, V160, P395, DOI 10.1007/BF00613029 Oertel D., 1988, AUDITORY FUNCTION NE, P313 OLIVER DL, 1989, J NEUROSCI, V9, P967 ONEILL WE, 1985, J COMP PHYSIOL A, V157, P797, DOI 10.1007/BF01350077 PARK T, 1991, ABSTR ASS RES OT, P89 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 POLLAK G D, 1989, Society for Neuroscience Abstracts, V15, P1115 Pollak GD, 1989, NEURAL BASIS ECHOLOC RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1986, J NEUROPHYSIOL, V56, P262 Rhode WS, 1992, MAMMALIAN AUDITORY P, P94 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 ROSS LS, 1988, J COMP NEUROL, V270, P488, DOI 10.1002/cne.902700403 ROSS LS, 1989, J NEUROSCI, V9, P2819 ROUILLER EM, 1984, J COMP NEUROL, V225, P167, DOI 10.1002/cne.902250203 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SCHULLER G, 1986, J NEUROSCI METH, V18, P339, DOI 10.1016/0165-0270(86)90022-1 Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 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 SMITH PH, 1989, J COMP NEUROL, V282, P595, DOI 10.1002/cne.902820410 SUGA N, 1985, J NEUROPHYSIOL, V53, P1109 TANAKA K, 1985, BRAIN RES, V341, P252, DOI 10.1016/0006-8993(85)91064-9 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1985, J ACOUST SOC AM, V77, P1484, DOI 10.1121/1.392043 TSUCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 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 WONGRILEY M, 1979, BRAIN RES, V171, P11, DOI 10.1016/0006-8993(79)90728-5 WU SH, 1984, J NEUROSCI, V4, P1577 Yang L., 1993, Society for Neuroscience Abstracts, V19, P533 YANG LC, 1992, J NEUROPHYSIOL, V68, P1760 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 ZOOK JM, 1979, SOC NEUR ABSTR, V5, P34 ZOOK JM, 1985, J COMP NEUROL, V237, P307, DOI 10.1002/cne.902370303 ZOOK JM, 1987, J COMP NEUROL, V261, P347, DOI 10.1002/cne.902610303 ZOOK JM, 1982, J COMP NEUROL, V207, P14, DOI 10.1002/cne.902070103 ZOOK JM, 1982, J COMP NEUROL, V207, P1, DOI 10.1002/cne.902070102 ZOOK JM, 1985, J COMP NEUROL, V231, P530, DOI 10.1002/cne.902310410 NR 75 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 DEC PY 1993 VL 71 IS 1-2 BP 51 EP 63 DI 10.1016/0378-5955(93)90020-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800006 PM 8113145 ER PT J AU KIMITSUKI, T NAKAGAWA, T HISASHI, K KOMUNE, S KOMIYAMA, S AF KIMITSUKI, T NAKAGAWA, T HISASHI, K KOMUNE, S KOMIYAMA, S TI CISPLATIN BLOCKS MECHANOELECTRIC TRANSDUCER CURRENT IN CHICK COCHLEAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; CISPLATIN; MECHANOELECTRIC TRANSDUCTION CHANNEL; PATCH CLAMP TECHNIQUE; OTOTOXICITY ID OTOTOXICITY; CIS-DIAMMINEDICHLOROPLATINUM(II); DNA AB The effects of cisplatin (cis-dichlorodiammine platinum II, CDDP) on the mechano-electrical transduction (MET) current were investigated with a whole-cell patch-electrode voltage clamp technique in dissociated cochlear hair cells of chicks. CDDP blocked the MET channel in a dose-and voltage-dependent manner. At -50 mV, CDDP blocked the MET channel with a Hill coefficient of approximately 2 and a dissociation constant (K-D) of 1.5 x10(-3) M. The kinetics of CDDP blockade consist of a voltage-independent and a voltage-dependent component. RP KIMITSUKI, T (reprint author), KYUSHU UNIV,FAC MED,DEPT OTORHINOLARYNGOL,3-1-1 MAIDASHI,FUKUOKA 812,JAPAN. CR BARRON SE, 1987, HEARING RES, V26, P131, DOI 10.1016/0378-5955(87)90104-3 DECONTI RC, 1973, CANCER RES, V33, P1310 EASTMAN A, 1986, BIOCHEMISTRY-US, V25, P3912, DOI 10.1021/bi00361a026 ESTERM SA, 1981, OTOLARYNGOL HEAD NEC, V89, P638 Eyring H., 1949, REC CHEM PROGR, V10, P100 FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 HILLE B, 1984, IONIC CHANNELS EXCIT, P273 JORGENSEN F, 1988, J PHYSIOL-LONDON, V403, P577 KIMITSUKI T, 1992, J PHYSIOL-LONDON, V458, P27 KOMUNE S, 1981, OTOLARYNG HEAD NECK, V89, P275 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E MURRAY D, 1985, CANCER RES, V45, P6446 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 SAITO T, 1991, HEARING RES, V56, P143, DOI 10.1016/0378-5955(91)90163-4 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 WOODBURY JW, 1971, CHEM DYNAMICS PAPERS, P601 NR 20 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 1993 VL 71 IS 1-2 BP 64 EP 68 DI 10.1016/0378-5955(93)90021-R PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800007 PM 8113146 ER PT J AU GLEICH, O WILSON, S AF GLEICH, O WILSON, S TI THE DIAMETERS OF GUINEA-PIG AUDITORY-NERVE FIBERS - DISTRIBUTION AND CORRELATION WITH SPONTANEOUS RATE SO HEARING RESEARCH LA English DT Article DE HEARING; COCHLEA; HORSERADISH PEROXIDASE; SINGLE CELL LABELING; VIDEO IMAGE ANALYSIS ID RATE-INTENSITY FUNCTIONS; SPIRAL GANGLION; COCHLEAR NERVE; AFFERENT-FIBERS; LEVEL FUNCTIONS; CAT; NEURONS; ORGANIZATION; MORPHOMETRY; INNERVATION AB In the mammalian auditory nerve physiological recordings revealed that the spontaneous discharge rate of single auditory fibres correlates with the diversity of input-output functions which may be important for intensity discrimination (e.g., Sachs and Abbas, 1974, Liberman, 1978; Winter et al., 1990). In this study we determined if the spontaneous discharge rate of auditory nerve fibres in the guinea pig is correlated with an anatomical feature, namely the diameter of the respective fibres. The diameter of myelinated (Type I) guinea pig auditory nerve fibres was measured after staining with different techniques. Measurements were made on semithin sections using a video image analysis system. The diameters of fibres stained with toluidine blue from the portion of the auditory nerve containing fibres from the basal turn of the cochlea were found to have a normal distribution. Fibres were also labelled with horseradish peroxidase by bulk injection into the spiral ganglion. It was found that the presence of horseradish peroxidase within the fibres reduced the measured diameter in comparison to adjacent unlabelled fibres. A number of fibres were physiologically characterized with respect to spontaneous discharge rate and subsequently intracellularly labelled with horseradish peroxidase. Fibre diameter of a selected sample of intracellularly labelled fibres was measured over a distance of 800 mu m within the internal auditory meatus. At the positions nearest to the spiral ganglion fibres possessing low spontaneous rates were found to have smaller diameters than high spontaneous rate fibres. No difference in fibre diameter was found for the positions near the cochlear nucleus. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. QUEEN ELIZABETH II MED CTR,AUSTRALIAN NEUROMUSCULAR RES INST,NEDLANDS,WA 6009,AUSTRALIA. CR ALDER VA, 1978, J ACOUST SOC AM, V64, P684, DOI 10.1121/1.381993 ALVING BM, 1971, BRAIN RES, V25, P229, DOI 10.1016/0006-8993(71)90435-5 ANNIKO M, 1988, ARCH OTO-RHINO-LARYN, V245, P155, DOI 10.1007/BF00464018 ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BROWN MC, 1988, J COMP NEUROL, V278, P581, DOI 10.1002/cne.902780409 FRIEDE RL, 1984, J NEUROL SCI, V66, P193, DOI 10.1016/0022-510X(84)90007-8 GACEK RR, 1961, ANAT REC, V139, P455, DOI 10.1002/ar.1091390402 KARNES J, 1977, J NEUROL SCI, V34, P43, DOI 10.1016/0022-510X(77)90090-9 KAWASE T, 1992, J COMP NEUROL, V319, P312, DOI 10.1002/cne.903190210 KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 KIM DO, 1979, J NEUROPHYSIOL, V42, P16 LEAKE PA, 1989, J COMP NEUROL, V281, P612, DOI 10.1002/cne.902810410 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1988, HEARING RES, V34, P179, DOI 10.1016/0378-5955(88)90105-0 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 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MANLEY GA, 1976, J PHYSIOL-LONDON, V258, P323 Mesulam M. M., 1982, TRACING NEURAL CONNE, P1 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBERTSO.D, 1974, J COMP PHYSIOL, V91, P363, DOI 10.1007/BF00694467 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X SACHS MB, 1989, HEARING RES, V41, P61, DOI 10.1016/0378-5955(89)90179-2 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 SPOENDLIN H, 1979, ACTA OTO-LARYNGOL, V87, P381, DOI 10.3109/00016487909126437 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 NR 32 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 1993 VL 71 IS 1-2 BP 69 EP 79 DI 10.1016/0378-5955(93)90022-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800008 PM 7509334 ER PT J AU ELBARBARY, A ALTSCHULER, RA SCHACHT, J AF ELBARBARY, A ALTSCHULER, RA SCHACHT, J TI GLUTATHIONE S-TRANSFERASES IN THE ORGAN OF CORTI OF THE RAT - ENZYMATIC-ACTIVITY, SUBUNIT COMPOSITION AND IMMUNOHISTOCHEMICAL LOCALIZATION SO HEARING RESEARCH LA English DT Article DE GLUTATHIONE S-TRANSFERASES; HAIR CELLS; BASAL BODY; MICROTUBULE; DETOXIFICATION; WESTERN BLOT; DEITERS CELLS ID COCHLEAR HAIR-CELLS; MICROTUBULES; BRAIN; ORGANIZATION; GENTAMICIN; BINDING; CYTOSKELETAL; ASTROCYTES; HORMONES; PROTEINS AB Glutathione S-transferases (GSTs), a family of ubiquitous cytosolic isozymes, catalyze the detoxification of electrophilic substrates with reduced glutathione and participate in intracellular binding and transport of lipophilic substances. This study measured GST activity biochemically in the inner ear of the rat; determined the isozyme profile by Western blotting; and identified, immunohistochemically, the distribution of the mu and pi class GSTs in the organ of Corti. GST enzymatic activity in inner ear tissues ranged from 117 to 348 nmoles glutathione converted/min/mg protein, values somewhat higher than those found in brain (130) and much lower than in liver (1011). Of the GST isoforms, the pi class (identified by antibodies against the Y-p subunit) was most prominent, the mu class (Y-b1 subunit) clearly evident while the alpha class (Y-a subunit) was barely delectable on Western blots. Immunocytochemical analysis showed differential distribution of the Y-b1 and Y-p subunits. The Y-b1 subunit was present in the sensory cells, while supporting cells were not specifically stained. At the subcellular level, the isozyme was localized in the apical zones of inner (IHCs) and outer hair cells (OHCs) close to the cuticular plate. The extent of staining, however, varied between OHCs and IHCs. In the OHCs, staining appeared in discrete spots in the apical areas only, whereas in IHCs staining extended further towards the center of the cells. The Y-p subunit was mainly localized to Deiters cell processes and pillar cells. Both Y-b1 and Y-p colocalized with tubulin-specific antibody. The functional significance of GST in the cochlear receptor cells is speculative. However, a role anologous to that in other tissues (detoxification, prostaglandin synthesis) can be assumed. In addition, an association of GST with the microtubule system is possible based on immunohistochemical colocalization with tubulin. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. CR ABRAMOVITZ M, 1988, J NEUROCHEM, V50, P50, DOI 10.1111/j.1471-4159.1988.tb13228.x BASS NM, 1977, BIOCHIM BIOPHYS ACTA, V494, P131, DOI 10.1016/0005-2795(77)90141-6 BOYER TD, 1989, HEPATOLOGY, V9, P486, DOI 10.1002/hep.1840090324 BURGESS JR, 1987, BIOCHEM BIOPH RES CO, V142, P441, DOI 10.1016/0006-291X(87)90294-4 CAMMER W, 1989, J NEUROCHEM, V52, P876, DOI 10.1111/j.1471-4159.1989.tb02536.x CARILLO MC, 1991, BIOCHIM BIOPHYS ACTA, V1077, P325 CHANG M, 1990, J BIOL CHEM, V265, P5418 CHOU IN, 1984, CELL BIOL INT REP, V8, P441, DOI 10.1016/0309-1651(84)90165-6 DEGROOT JCMJ, 1990, HEARING RES, V50, P35, DOI 10.1016/0378-5955(90)90031-J DUSTIN P, 1984, MICROTUBULES, P98 ENGSTROM H, 1966, STRUCTURAL PATTERN O, P39 ERICKSONLAMY K, 1992, INVEST OPHTH VIS SCI, V33, P2631 ESCOUBET B, 1985, PROSTAGLANDINS, V29, P589 FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 GARETZ SL, 1992, ABSTR ASS RES OTOLAR GARETZ SL, 1993, ABSTR ASS RES OT HABIG WH, 1974, J BIOL CHEM, V249, P7130 HAYES JD, 1986, BIOCHEM J, V233, P779 HAYES PC, 1991, GUT, V32, P813, DOI 10.1136/gut.32.7.813 HIEL H, 1992, ACTA OTO-LARYNGOL, V112, P272 Kikuchi K, 1965, Acta Otolaryngol, V60, P207, DOI 10.3109/00016486509127003 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 Jakoby W B, 1978, Adv Enzymol Relat Areas Mol Biol, V46, P383 JOHNSON JA, 1993, J NEUROSCI, V13, P2013 KAWATA R, 1988, PROSTAGLANDINS, V35, P173, DOI 10.1016/0090-6980(88)90085-8 Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 KREIS TE, 1990, CELL MOTIL CYTOSKEL, V15, P67, DOI 10.1002/cm.970150202 LISTOWSKY I, 1988, DRUG METAB REV, V19, P305, DOI 10.3109/03602538808994138 MANNERVIK B, 1985, P NATL ACAD SCI USA, V82, P7202, DOI 10.1073/pnas.82.21.7202 Mannervik B, 1985, Adv Enzymol Relat Areas Mol Biol, V57, P357 MANNERVIK B, 1988, CRIT REV BIOCHEM MOL, V23, P283, DOI 10.3109/10409238809088226 MARUYAMA H, 1984, J BIOL CHEM, V259, P2449 MEISTER A, 1991, PHARMACOL THERAPEUT, V51, P155, DOI 10.1016/0163-7258(91)90076-X Ketterer B., 1988, P73 OBARA T, 1986, CARCINOGENESIS, V7, P801, DOI 10.1093/carcin/7.5.801 PEMBLE SE, 1986, BIOCHEM J, V240, P885 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 REED D J, 1984, Pharmacological Reviews, V36, p25S ROGIERS V, 1991, BIOCHEM PHARMACOL, V42, P491, DOI 10.1016/0006-2952(91)90310-2 SENJO M, 1986, NEUROSCI LETT, V66, P131, DOI 10.1016/0304-3940(86)90178-3 SHIRATORI Y, 1987, CANCER RES, V47, P6806 STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 TANSEY FA, 1991, J NEUROCHEM, V57, P95, DOI 10.1111/j.1471-4159.1991.tb02104.x THYBERG J, 1985, EXP CELL RES, V159, P1, DOI 10.1016/S0014-4827(85)80032-X TROMBETTA LD, 1992, TOXICOL LETT, V60, P329, DOI 10.1016/0378-4274(92)90292-R XU SH, 1992, ARCH BIOCHEM BIOPHYS, V296, P462, DOI 10.1016/0003-9861(92)90598-Q NR 47 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 DEC PY 1993 VL 71 IS 1-2 BP 80 EP 90 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800009 PM 8113147 ER PT J AU REN, TY NUTTALL, AL MILLER, JM AF REN, TY NUTTALL, AL MILLER, JM TI CONTRIBUTION OF THE ANTERIOR INFERIOR CEREBELLAR ARTERY TO COCHLEAR BLOOD-FLOW IN GUINEA-PIG - A MODEL-BASED ANALYSIS SO HEARING RESEARCH LA English DT Article DE MICROCIRCULATION; INNER EAR; HEMODYNAMICS; AUTOREGULATION; LASER DOPPLER FLOWMETRY ID AUTO-REGULATION; PRESSURE AB This study was performed to determine the contribution of the anterior inferior cerebellar artery (AICA) to cochlear blood flow (CBF) in guinea pig. The AICA and the basilar-vertebral arterial complex in twelve animals was exposed through the basal portion of the skull. The cochlea was ventrally approached and the CBF of the apical area monitored with laser Doppler flowmetry. A specially designed microclamp was held in a micromanipulator and used to obstruct the AICA. When the AICA was clamped, CBF decreased to approximately 60% of baseline (BL) (not to 'biological zero'), followed by a gradual increase. When the clamp was released, CBF quickly increased to more than 160% BL and then slowly declined to baseline. To quantify the contribution of AICA to CBF, we formulated an electrical analog model of the cochlear vessel system. With this model, AICA contribution to CBF and the relationship among blood pressure, blood flow, and vascular resistance or vascular conductance in the cochlea can be explored. Results in the present study indicate that the AICA contributes only about 45% of CBF to the cochlea; 55% of CBF must come from other supplying vessels. Contrary to previous reports, CBF response to AICA clamping did not exhibit a stable or constant decrease but showed time-dependent dynamic changes. In addition, the cochlear vascular system showed a marked autoregulatory response, instead of a passive response, to the perfusion pressure change. AICA clamping is, therefore, not a suitable model for investigation of ischemia effects in the guinea pig cochlea, but it is a useful approach to study autoregulation and the myogenic mechanism of the cochlear vascular system. C1 UNIV MICHIGAN,SCH MED,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. XIAN MED UNIV,AFFILIATED HOSP 1,DEPT OTOLARYNGOL,XIAN,PEOPLES R CHINA. CR AFZELIUS LE, 1979, ACTA OTO-LARYNGOL, V88, P183, DOI 10.3109/00016487909137158 Axellson A, 1968, ACTA OTO-LARYNGOL, V243, P1 BERNSTEI.JM, 1966, ARCHIV OTOLARYNGOL, V83, P422 BOHLEN HG, 1977, MICROVASC RES, V13, P125, DOI 10.1016/0026-2862(77)90121-2 COLE RR, 1988, AM J OTOL, V9, P211 COSTA OA, 1966, LARYNGOSCOPE, V76, P1874 GOW BS, 1980, HDB PHYSL 2, V2, P353 HOFFMAN JIE, 1990, PHYSIOL REV, V70, P331 HOUSE WF, 1975, OTOLARYNG CLIN N AM, V8, P515 KIMURA R., 1958, ANN OTOL RHINOL AND LARYNGOL, V67, P5 Lawrence M, 1980, Am J Otolaryngol, V1, P324, DOI 10.1016/S0196-0709(80)80035-4 Miller J M, 1986, Scand Audiol Suppl, V26, P11 MORFF RJ, 1982, CIRC RES, V51, P43 PERLMAN H B, 1959, Laryngoscope, V69, P591 PERLMAN H B, 1957, Ann Otol Rhinol Laryngol, V66, P537 PORTNOY HD, 1983, NEUROSURGERY, V13, P482 RANDOLF HB, 1990, EUR ARCH OTO-RHINO-L, V247, P226 REN TY, 1992, ABSTR SS RES OT, P305 SEIDMAN MD, 1992, EUR ARCH OTO-RHINO-L, V249, P332 SHORT SO, 1985, OTOLARYNG HEAD NECK, V93, P786 SPAAN JA, 1988, INSERM, V183, P54 NR 21 TC 20 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 1993 VL 71 IS 1-2 BP 91 EP 97 DI 10.1016/0378-5955(93)90024-U PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800010 PM 8113148 ER PT J AU MULROY, MJ DEMPEWOLF, SA CURTIS, S IIDA, HC AF MULROY, MJ DEMPEWOLF, SA CURTIS, S IIDA, HC TI GAP JUNCTIONAL CONNECTIONS BETWEEN HAIR-CELLS, SUPPORTING CELLS AND NERVES IN A VESTIBULAR ORGAN SO HEARING RESEARCH LA English DT Article DE INTERCELLULAR COMMUNICATION; CRISTA AMPULLARIS OF SEMICIRCULAR DUCT; ALLIGATOR LIZARD ID INTRACELLULAR-RECORDINGS; INNER-EAR; CORTI; RESPONSES AB The pattern of gap-junctional connections between cells in the vestibular neuroepithelium of the posterior semicircular duct of the alligator lizard are described based upon the study of freeze fracture replicas and ultrathin sections with a transmission electron microscope. Both type I and type II hair cells are coupled to adjacent supporting cells by a series of small macular gap junctions located in a ring around the hair cell at the level of the apical circumferential belt of actin filaments. Adjacent supporting cells are extensively interconnected by gap junctions. A few cases of gap junctions between afferent dendrites and supporting cells, and between afferent dendrites and calyceal nerve endings were seen. These morphological observations together with data from other studies in the literature suggest a possible role for supporting cells in altering the micromechanical properties of the hair cell receptor organs during stimulation. C1 MED COLL GEORGIA,OTOLARYNGOL SECT,AUGUSTA,GA 30912. RP MULROY, MJ (reprint author), MED COLL GEORGIA,DEPT CELLULAR BIOL ANAT,AUGUSTA,GA 30912, USA. CR ALBERTS B, 1989, MOL BIOL CELL, P798 BADENKRISTENSEN K, 1982, HEARING RES, V8, P295, DOI 10.1016/0378-5955(82)90021-1 BAIRD IL, 1978, ANAT REC, V191, P69, DOI 10.1002/ar.1091910107 BENNETT MVL, 1991, NEURON, V6, P305, DOI 10.1016/0896-6273(91)90241-Q BOITANO S, 1992, SCIENCE, V258, P292, DOI 10.1126/science.1411526 COREY DP, 1983, J NEUROSCI, V3, P942 DEW LA, 1993, HEARING RES, V66, P99, DOI 10.1016/0378-5955(93)90264-2 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 FURUKAWA T, 1985, J PHYSIOL-LONDON, V366, P107 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 GULLEY RL, 1976, J NEUROCYTOL, V5, P479, DOI 10.1007/BF01181652 GUTHRIE SC, 1989, TRENDS NEUROSCI, V12, P12, DOI 10.1016/0166-2236(89)90150-1 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 KOLB HA, 1991, REV PHYSIOL BIOCH P, V118, P1, DOI 10.1007/BFb0031480 MULROY MJ, 1974, NATURE, V249, P482, DOI 10.1038/249482a0 NADOL JB, 1978, ANN OTO RHINOL LARYN, V87, P70 NADOL JB, 1976, AM J ANAT, V147, P281, DOI 10.1002/aja.1001470304 OESTERLE E, 1986, HEARING RES, V22, P229, DOI 10.1016/0378-5955(86)90099-7 OESTERLE EC, 1990, J NEUROPHYSIOL, V64, P617 PETS A, 1976, FINE STRUCTURE NERVO, P174 SOMJEN GG, 1975, ANNU REV PHYSIOL, V37, P163, DOI 10.1146/annurev.ph.37.030175.001115 SPRAY DC, 1985, ANNU REV PHYSIOL, V47, P281 WEISS TF, 1974, J ACOUST SOC AM, V55, P606, DOI 10.1121/1.1914571 ZAHN DS, 1980, AM J ANAT, V158, P263 ZWISLOCKI JJ, 1992, HEARING RES, V57, P175, DOI 10.1016/0378-5955(92)90150-L NR 26 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 1993 VL 71 IS 1-2 BP 98 EP 105 DI 10.1016/0378-5955(93)90025-V PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800011 PM 8113149 ER PT J AU ATTIAS, J URBACH, D GOLD, S SHEMESH, Z AF ATTIAS, J URBACH, D GOLD, S SHEMESH, Z TI AUDITORY EVENT-RELATED POTENTIALS IN CHRONIC TINNITUS PATIENTS WITH NOISE-INDUCED HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE TINNITUS; NIHL; AUDITORY EVOKED POTENTIALS; P3; COGNITIVE PROCESSES ID EVOKED MAGNETIC-FIELDS; P300; SCHIZOPHRENIA; RESPONSES; NERVE AB In order to explore a possible deficit in auditory central neural activity in tinnitus with noise induced hearing loss (NIHL), auditory event related potentials (ERP) and reaction time (RT) were recorded (measures of central processing) from tinnitus patients (N = 12) and hearing and age matched controls (N = 12). Testing procedure included oddball paradigms and 1 KHz repetitive stimulus, as well as click-induced brainstem auditory evoked potentials (BAEP). ERP amplitudes (waves N1, P2 and P3) in tinnitus patients were significantly lower than in controls in all testing paradigms. No differences were found in ERP peak latencies, BAEP, RT, or response scoring. The lower ERP amplitudes may indicate attenuated or 'abnormal' auditory central processing in NIHL tinnitus patients. It is suggested that this dysfunction reflects an adaptive brain process response to the tinnitus and points to auditory central involvement in tinnitus sensation. C1 CHAIM SHEBA MED CTR,IDF,MED CORPS,EVOKED POTENTIALS LAB,IL-52621 RAMAT GAN,ISRAEL. RP ATTIAS, J (reprint author), CHAIM SHEBA MED CTR,IDF,MED CORPS,INST NOISE HAZARDS RES,BLDG 87,IL-52621 RAMAT GAN,ISRAEL. CR ATTIAS J, 1991, INT J NEUROSCI, V58, P95, DOI 10.3109/00207459108987186 ATTIAS J, 1990, ELECTROEN CLIN NEURO, V77, P127, DOI 10.1016/0168-5597(90)90026-A ATTIAS J, 1992, IN PRESS AUDIOLOGY ATTIAS J, 1990, SCAND AUDIOL, V19, P245, DOI 10.3109/01050399009070779 BARNEA G, 1990, AUDIOLOGY, V29, P36 BARRS DM, 1983, 2 P INT TINN SEM, P287 COLDINGJORGENSEN E, 1992, ELECTROEN CLIN NEURO, V83, P322, DOI 10.1016/0013-4694(92)90091-U COLES R, 1990, NOISE PUBLIC HLTH PR, V4, P87 Coles R. R. A., 1987, S BROWNS OTOLARYNGOL, V2, P368 ELMASSIOUI F, 1988, ELECTROEN CLIN NEURO, V70, P46 ERLANDSSON JJ, 1991, BRIT J AUDIOL, V25, P151 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 GERKEN GM, 1991, HEARING RES, V53, P101, DOI 10.1016/0378-5955(91)90217-W HALGREN E, 1980, SCIENCE, V210, P803, DOI 10.1126/science.7434000 HARALAMBOUS G, 1987, BEHAV RES THER, V25, P449 Hazell J, 1990, Acta Otolaryngol Suppl, V476, P202 HILLYARD SA, 1973, SCIENCE, V182, P177, DOI 10.1126/science.182.4108.177 HOKE M, 1989, HEARING RES, V37, P281, DOI 10.1016/0378-5955(89)90028-2 JACOBSON GP, 1991, HEARING RES, V56, P44, DOI 10.1016/0378-5955(91)90152-Y 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 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 LINDBERG P, 1990, BRIT J AUDIOL, V24, P51 MAGLIERO A, 1984, PSYCHOPHYSIOLOGY, V21, P171, DOI 10.1111/j.1469-8986.1984.tb00201.x MOLLER AR, 1984, ANN OTO RHINOL LARYN, V93, P39 MOLLER AR, 1992, LARYNGOSCOPE, V102, P187 PANTEV C, 1989, HEARING RES, V40, P261, DOI 10.1016/0378-5955(89)90167-6 PFEFFERBAUM A, 1984, ELECTROEN CLIN NEURO, V59, P104, DOI 10.1016/0168-5597(84)90027-3 PFEFFERBAUM A, 1989, ARCH GEN PSYCHIAT, V46, P1035 SEMLITSCH HV, 1986, PSYCHOPHYSIOLOGY, V23, P695, DOI 10.1111/j.1469-8986.1986.tb00696.x SHEMESH Z, 1993, AM J OTOLARYNG, V14, P94, DOI 10.1016/0196-0709(93)90046-A SUTTON S, 1965, SCIENCE, V150, P1127 TYLER RS, 1984, J LARYNGOL OTOL S, V9, P150 VAUGHAN HG, 1970, ELECTROEN CLIN NEURO, V28, P360, DOI 10.1016/0013-4694(70)90228-2 ZUNG WWK, 1965, ARCH GEN PSYCHIAT, V12, P63 1987, DIAGNOSTIC STATISTIC NR 36 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 DEC PY 1993 VL 71 IS 1-2 BP 106 EP 113 DI 10.1016/0378-5955(93)90026-W PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800012 PM 8113129 ER PT J AU BOHNE, BA HARDING, GW AF BOHNE, BA HARDING, GW TI COMBINED ORGAN OF CORTI-MODIOLUS TECHNIQUE FOR PREPARING MAMMALIAN COCHLEAS FOR QUANTITATIVE MICROSCOPY SO HEARING RESEARCH LA English DT Article DE COCHLEAR FIXATION AND DISSECTION; WHOLE MOUNTS; PLASTIC-EMBEDDING; DURCUPAN ID SPIRAL GANGLION; HAIR-CELLS; DEGENERATION; SEQUENCE AB An improved cochlear preparation technique is described with the following key features: 1) Preservation of the organ of Corti (OC) and the spiral ganglion cells (SGCs) in the same cochlea for quantitative, high-resolution microscopic evaluation; 2) Dissection of the plastic-embedded cochlea so that the entire OC can be prepared as whole mounts for quantitative study while the modiolus remains in a single block; 3) Decalcification and serial sectioning of the modiolus so that all SGC bodies are available for microscopic examination. This technique will be valuable for correlating the condition of the OC, nerve terminals, nerve fibers and the SGC bodies in normal and damaged cochleas. C1 WASHINGTON UNIV,SCH MED,DEPT NEUROL SURG,ST LOUIS,MO 63110. RP BOHNE, BA (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID AVE,ST LOUIS,MO 63110, USA. RI Bohne, Barbara/A-9113-2008 OI Bohne, Barbara/0000-0003-3874-7620 CR ANNIKO M, 1980, MICRON, V11, P73, DOI 10.1016/0047-7206(80)90141-7 ANNIKO M, 1977, ARCH OTO-RHINO-LARYN, V218, P67, DOI 10.1007/BF00469735 Axellson A, 1968, ACTA OTO-LARYNGOL, V243, P1 AXELSSON A, 1975, ACTA OTO-LARYNGOL, V79, P352, DOI 10.3109/00016487509124697 BOHNE BA, 1985, LARYNGOSCOPE, V95, P818 BOHNE BA, 1972, LARYNGOSCOPE, V82, P1 BOHNE BA, 1992, LARYNGOSCOPE, V102, P693, DOI 10.1288/00005537-199206000-00017 BROWNELL WE, 1984, SCANNING ELECTRON MI, V3, P1401 Engstrom H, 1966, STRUCTURAL PATTERN O EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P81, DOI 10.3109/00016488809107374 Hayasaka M., 1989, Proceedings of Japanese Society of Sugar Beet Technologists, P74 HAYAT MA, 1981, N ELECTRON MICROSCOP, P201 HUNTERDUVAR IM, 1978, ACTA OTOLARYNGOL S, V351, P1 JOHNSSON LG, 1974, ANN OTO RHINOL LARYN, V83, P294 KEITHLEY EM, 1987, J ACOUST SOC AM, V81, P1036, DOI 10.1121/1.394675 KEITHLEY EM, 1983, HEARING RES, V12, P381, DOI 10.1016/0378-5955(83)90007-2 NISHIMURA T, 1965, HIROSAKI MED J, V17, P1 RICHARDSON KC, 1960, STAIN TECHNOL, V35, P313 ROSS MD, 1973, ACTA OTO-LARYNGOL, V76, P381, DOI 10.3109/00016487309121526 Sando I, 1965, ACTA OTOLARYNG STOCK, V59, P417, DOI 10.3109/00016486509124577 SANTI PA, 1986, HEARING RES, V24, P179, DOI 10.1016/0378-5955(86)90017-1 SCHUKNECHT HF, 1963, ANN OTO RHINOL LARYN, V72, P687 SCHWARTZ IR, 1983, HEARING RES, V9, P185, DOI 10.1016/0378-5955(83)90027-8 SLEPECKY N, 1989, HEARING RES, V38, P135, DOI 10.1016/0378-5955(89)90135-4 SMITH CA, 1975, NERVOUS SYST, V3, P1 SMITH CA, 1951, LARYNGOSCOPE, V61, P1073 SMITH CA, 1957, AM J ANAT, V100, P337, DOI 10.1002/aja.1001000304 SOBKOWICZ HM, 1975, J NEUROCYTOL, V4, P543, DOI 10.1007/BF01351537 Spoendlin H, 1987, Acta Otolaryngol Suppl, V436, P25 SPOENDLI.H, 1974, ARCH OTO-RHINO-LARYN, V208, P137, DOI 10.1007/BF00453927 STROMINGER RN, 1993, ABSTR ASS RES OT, V16, P30 YOHMAN L, UNPUB 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 DEC PY 1993 VL 71 IS 1-2 BP 114 EP 124 DI 10.1016/0378-5955(93)90027-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800013 PM 7509332 ER PT J AU MAREAN, GC BURT, JM BEECHER, MD RUBEL, EW AF MAREAN, GC BURT, JM BEECHER, MD RUBEL, EW TI HAIR CELL REGENERATION IN THE EUROPEAN STARLING (STURNUS-VULGARIS) - RECOVERY OF PURE-TONE DETECTION THRESHOLDS SO HEARING RESEARCH LA English DT Article DE REGENERATION; FUNCTION; BEHAVIOR; THRESHOLDS; AVIAN; STARLING ID AVIAN INNER-EAR; ACOUSTIC TRAUMA; CHICK COCHLEA; STEREOCILIARY BUNDLES; INTENSE SOUND; EXPOSURE; HEARING; OTOTOXICITY; BUDGERIGAR; TOXICITY AB Behavioral detection thresholds were obtained from four starlings before, during, and after 11 days of subcutaneous injections of kanamycin. Birds were operantly conditioned to respond to pure-tones ranging in frequency from 0.25 kHz to 7 kHz using the method of constant stimuli and were tested daily for 141 days after the first injection of aminoglycoside. All four birds sustained hearing losses greater than 60 dB at frequencies from 4 kHz to 7 kHz by the end of the 11 day injection schedule. Two birds had a slight shift in threshold at 3 kHz. No change in threshold occurred for any of the birds at lower frequencies. Recovery of detection thresholds began soon after the injections ceased and continued for approximately 50 days. In all four birds there was some degree of permanent hearing loss: 5 dB to 15 dB at frequencies between 4 kHz and 6 kHz, and approximately 25 dB at 7 kHz. Scanning electron microscopy (SEM) was performed at 0 and 5 days post-injection in a separate group of starlings given the same injection schedule. Hair cell loss and damage was observed across the basal 34% to 36% of the basilar papilla. SEM in two behaviorally tested birds sacrificed 142 days after the first injection showed that there was regeneration of hair cells to populate the previously damaged region, but that disorientation of stereocilia bundles in the basal third of the basilar papilla was common. The other two behaviorally tested birds were treated with kanamycin again for 16 days beginning at 142 days after the first injection. Thresholds shifted again, but less than during the first dosing period. SEM of these birds' basilar papillae showed less hair cell loss than observed in the birds given only a single, 11 day dosing of kanamycin. This result suggests that birds may be less susceptible to the ototoxic effects of kanamycin in repeated treatments. In all four birds, the degree and position of damage observed with SEM corresponded with the extent and frequency of hearing loss. C1 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT SPEECH & HEARING SCI,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT PSYCHOL,SEATTLE,WA 98195. CR ADLER HJ, 1992, ABST ASS RES OT, V15, P160 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, 1991, CIBA F S, V160 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DOOLING RJ, 1986, B PSYCHONOMIC SOC, V24, P462 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 Fay R. R., 1988, HEARING VERTEBRATES GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 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, 1989, J ACOUST SOC AM, V85, P289, DOI 10.1121/1.397736 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 KONISHI M, 1985, ANNU REV NEUROSCI, V8, P125 KUHN A, 1982, NATURWISSENSCHAFTEN, V69, P245, DOI 10.1007/BF00398648 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MANLEY GA, 1990, PERIPHERAL HEANG MEC NORTON S, 1990, ARO ABSTR, V13, P62 OKANOYA K, 1987, J COMP PSYCHOL, V101, P7, DOI 10.1037//0735-7036.101.1.7 RAPHAEL Y, 1993, J COMP NEUROL, V330, P521, DOI 10.1002/cne.903300408 RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1989, HEARING RES, V43, P81, DOI 10.1016/0378-5955(89)90061-0 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 NR 29 TC 68 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 DEC PY 1993 VL 71 IS 1-2 BP 125 EP 136 DI 10.1016/0378-5955(93)90028-Y PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800014 PM 8113131 ER PT J AU BOETTCHER, FA MILLS, JH NORTON, BL AF BOETTCHER, FA MILLS, JH NORTON, BL TI AGE-RELATED-CHANGES IN AUDITORY-EVOKED POTENTIALS OF GERBILS .1. RESPONSE AMPLITUDES SO HEARING RESEARCH LA English DT Article DE AGING; AUDITORY BRAIN-STEM RESPONSE; EVOKED POTENTIALS; PRESBYCUSIS ID BRAIN-STEM RESPONSE; STIMULUS DEPENDENCIES; MONGOLIAN GERBILS; CLICK POLARITY; YOUNG; QUIET; NERVE; LEVEL; NOISE; BAER AB Auditory brainstem responses (ABRs) were recorded in young (6-10 month) and aged (36 month) Mongolian gerbils. For each subject, ABR thresholds and response amplitudes were measured at octave intervals from 1 through 16 kHz. Data from the young animals served as the baselines for comparison to aged animals which were categorized on the basis of auditory brainstem response (ABR) thresholds. The aged groups included subjects with thresholds (a) at the mean of a pool of 50 aged gerbils, (b) one standard deviation (SD) lower than the mean, (c) one sd higher than the mean, and (d) near normal for young gerbils. The amplitudes of ABR waveforms for the aged gerbils were reduced compared to the young subjects, particularly at high sound pressure levels. This was true even for aged subjects with thresholds similar to those for younger subjects. The slopes of the amplitude-intensity (I/O) functions were shallower in all aged subjects compared to young subjects. The results suggest that ABR amplitudes and I/O slopes decrease as a function of age and that the decreases are not a direct result of loss of auditory sensitivity. The reductions in ABR amplitudes from aged gerbils presumably reflect age-related pathology in the auditory periphery, as previous studies have shown reductions in amplitudes of the compound action potential of aged gerbils. RP BOETTCHER, FA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR Beagley H A, 1978, Br J Audiol, V12, P69, DOI 10.3109/03005367809078858 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 BURKARD R, 1993, J ACOUST SOC AM, V94, P2441, DOI 10.1121/1.407465 BURKARD R, 1989, J ACOUST SOC AM, V85, P2526, DOI 10.1121/1.397747 BURKARD R, 1989, J ACOUST SOC AM, V85, P2514, DOI 10.1121/1.397746 CHEAL M, 1986, EXP AGING RES, V12, P3 COSTA P, 1990, Electromyography and Clinical Neurophysiology, V30, P495 DUM N, 1980, ARCH OTO-RHINO-LARYN, V228, P249, DOI 10.1007/BF00660737 FELDMAN ML, 1991, ASS RES OT ABSTR, V14, P27 GRATTON MA, 1992, ASS RES OTOLARYNGOL, V15, P48 Hall J, 1992, HDB AUDITORY EVOKED HARKINS SW, 1981, INT J NEUROSCI, V15, P107, DOI 10.3109/00207458108985851 HARRISON J, 1982, NEUROBIOL AGING, V3, P163, DOI 10.1016/0197-4580(82)90036-7 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HENRY KR, 1980, ARCH OTO-RHINO-LARYN, V228, P233, DOI 10.1007/BF00660735 HENRY KR, 1978, ACTA OTO-LARYNGOL, V86, P366, DOI 10.3109/00016487809107515 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 JERGER J, 1980, ARCH OTOLARYNGOL, V106, P387 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KJAER M, 1980, ACTA NEUROL SCAND, V62, P20 MCGINN MD, 1987, HEARING RES, V31, P235, DOI 10.1016/0378-5955(87)90193-6 MELCHER JR, 1993, ASS RES OT ABSTR, V16, P63 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MITCHELL C, 1989, HEARING RES, V40, P75, DOI 10.1016/0378-5955(89)90101-9 MOLLER AR, 1988, ELECTROEN CLIN NEURO, V71, P198, DOI 10.1016/0168-5597(88)90005-6 MOLLER AR, 1985, HEARING RES, V17, P177, DOI 10.1016/0378-5955(85)90020-6 PSATTA DM, 1988, ELECTROEN CLIN NEURO, V71, P27, DOI 10.1016/0168-5597(88)90016-0 ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 SAND T, 1991, ELECTROEN CLIN NEURO, V78, P291, DOI 10.1016/0013-4694(91)90183-5 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SCHMIEDT RA, 1990, ASS RES OTOLARYNGOL, V13, P150 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SMITH DI, 1989, ELECTROEN CLIN NEURO, V72, P422, DOI 10.1016/0013-4694(89)90047-3 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V WHARTON JA, 1990, AUDIOLOGY, V29, P196 Willott J. F., 1991, AGING AUDITORY SYSTE 1987, VITAL HLTH STATISTIC, V3 NR 37 TC 40 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 DEC PY 1993 VL 71 IS 1-2 BP 137 EP 145 DI 10.1016/0378-5955(93)90029-Z PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800015 PM 8113132 ER PT J AU BOETTCHER, FA MILLS, JH NORTON, BL SCHMIEDT, RA AF BOETTCHER, FA MILLS, JH NORTON, BL SCHMIEDT, RA TI AGE-RELATED-CHANGES IN AUDITORY-EVOKED POTENTIALS OF GERBILS .2. RESPONSE LATENCIES SO HEARING RESEARCH LA English DT Article DE AGING; AUDITORY BRAIN-STEM RESPONSE; EVOKED POTENTIALS; PRESBYCUSIS ID BRAIN-STEM RESPONSES; MONGOLIAN GERBILS; YOUNG; QUIET; PRESBYCUSIS; DIAGNOSIS; SIZE; RATS; SEX AB Auditory brainstem responses (ABR) were recorded in young (6-10 month) and aged (36 month) Mongolian gerbils. Data from the young animals served as the baselines for comparison to aged animals which were categorized on the basis of ABR thresholds. Aged gerbils with normal thresholds (re young controls) had wave i and ii latencies of the ABR which were relatively normal at 1-4 kHz and slightly reduced at 8 and 16 kHz. Wave iv latencies in the aged gerbils with normal thresholds were reduced at all frequencies. Aged gerbils with 10-30 dB of hearing loss had wave i, ii, and iv latencies which were prolonged at low sound pressure levels and normal at high stimulus levels. Aged gerbils with 30 dB or greater losses had prolonged wave i, ii, and iv latencies at most levels. Slopes of latency-intensity (L/I) functions were steeper at 1-4 kHz than controls in aged subjects with hearing losses of 10 dB or greater. Slopes of L/I functions for wave iv were normal in aged subjects. The wave i-iv interval was shorter than normal in aged subjects with no hearing loss, normal in aged subjects with 10-30 dB of loss, and prolonged in subjects with greater than 30 dB of loss. RP BOETTCHER, FA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR ALLISON T, 1983, ELECTROEN CLIN NEURO, V55, P619, DOI 10.1016/0013-4694(83)90272-9 ALLISON T, 1984, ELECTROEN CLIN NEURO, V58, P14, DOI 10.1016/0013-4694(84)90196-2 Beagley H A, 1978, Br J Audiol, V12, P69, DOI 10.3109/03005367809078858 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z BURKARD R, 1993, J ACOUST SOC AM, V94, P2441, DOI 10.1121/1.407465 CHEAL M, 1986, EXP AGING RES, V12, P3 CHU NS, 1985, ELECTROEN CLIN NEURO, V62, P431, DOI 10.1016/0168-5597(85)90053-X CLEMIS JD, 1979, LARYNGOSCOPE, V89, P31 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F COSTA P, 1990, Electromyography and Clinical Neurophysiology, V30, P495 FELDMAN ML, 1991, ASS RES OT ABSTR, V14, P27 Hall J, 1992, HDB AUDITORY EVOKED HARKINS SW, 1981, INT J NEUROSCI, V15, P107, DOI 10.3109/00207458108985851 HARRISON J, 1982, NEUROBIOL AGING, V3, P163, DOI 10.1016/0197-4580(82)90036-7 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N 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 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KELLYBALLWEBER D, 1984, AUDIOLOGY, V23, P181 MARTINI A, 1991, ACTA OTOLARYNGOL S, V476, P97 MCGINN MD, 1987, HEARING RES, V31, P235, DOI 10.1016/0378-5955(87)90193-6 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MITCHELL C, 1989, HEARING RES, V40, P75, DOI 10.1016/0378-5955(89)90101-9 MOLLER AR, 1985, HEARING RES, V17, P177, DOI 10.1016/0378-5955(85)90020-6 OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 OTTAVIANI F, 1991, ACTA OTOLARYNGOL S S, V476, P110 OTTO WC, 1982, AUDIOLOGY, V21, P466 ROSENHALL U, 1986, SCAND AUDIOL, V15, P179, DOI 10.3109/01050398609042141 ROSENHALL U, 1985, ELECTROEN CLIN NEURO, V62, P426, DOI 10.1016/0168-5597(85)90052-8 ROSENHAMER HJ, 1980, SCAND AUDIOL, V9, P93, DOI 10.3109/01050398009076342 ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 SALVI RJ, 1979, HEARING RES, V1, P237, DOI 10.1016/0378-5955(79)90017-0 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SIMPSON GV, 1985, BRAIN RES, V348, P28, DOI 10.1016/0006-8993(85)90355-5 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V Willott J. F., 1991, AGING AUDITORY SYSTE NR 37 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 DEC PY 1993 VL 71 IS 1-2 BP 146 EP 156 DI 10.1016/0378-5955(93)90030-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800016 PM 8113133 ER PT J AU KOPPL, C MANLEY, GA AF KOPPL, C MANLEY, GA TI SPONTANEOUS OTOACOUSTIC EMISSIONS IN THE BOBTAIL LIZARD .1. GENERAL-CHARACTERISTICS SO HEARING RESEARCH LA English DT Article DE COCHLEA; SOAE; OTOACOUSTIC EMISSIONS; BASILAR PAPILLA; LIZARD ID AUDITORY-NERVE FIBERS; TILIQUA-RUGOSA; ACOUSTIC EMISSIONS; PATTERNS; PHASE AB Spontaneous otoacoustic emissions in the external ear canal of the bobtail lizard were identified on the basis of their consistent presence, their temperature- and hypoxia-dependence, and their supressibility by external tones. They were found in 86% of ears investigated, and each ear generated on average 10 emissions. Their sound-pressure levels lay between -10 and 9.3 dB SPL, and their centre frequencies between 0.93 and 4.61 kHz at 30 degrees C body temperature. Previous studies have shown that these frequencies are processed in the basal basilar-papillar segment by hair-cell areas that are strictly bidirectionally oriented and are covered by tectorial sallets. In contrast, no spontaneous otoacoustic emissions were found in the frequency range known to be processed by the apical, low-frequency segment of the basilar papilla. The mean frequency distance between emissions varied systematically across the frequency range in a way consistent with the hypothesis that they are generated by anatomically-defined groups of hair cells and their tectorial sallets. The 3dB-bandwidth of the emissions depended on their amplitude above the noise, but was at least 9 Hz. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY RES LAB,NEDLANDS,WA 6009,AUSTRALIA. RP KOPPL, C (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,D-85747 GARCHING,GERMANY. CR Ashmore J.F., 1989, COCHLEAR MECHANISMS, P107 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BURNS EM, 1984, HEARING RES, V16, P271, DOI 10.1016/0378-5955(84)90116-3 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407 GENOSSA TJ, 1989, J ACOUST SOC AM, V85, pS35 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 KOPPL C, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P489 KOPPL C, 1991, SPONTANEOUS OTOACOUS, P83 KOPPL C, 1988, HEARING RES, V35, P209, DOI 10.1016/0378-5955(88)90119-0 KOPPL C, 1994, IN PRESS HEAR RES KOPPL C, 1990, J COMP PHYSIOL A, V167, P139 KOPPL C, 1990, J COMP PHYSIOL A, V167, P101 KOPPL C, 1990, J COMP PHYSIOL A, V167, P113 KOPPL C, 1993, J ACOUST SOC AM, V93, P2834 KOSSL M, 1985, HEARING RES, V19, P157, DOI 10.1016/0378-5955(85)90120-0 LONSBURYMARTIN BL, 1988, HEARING RES, V34, P313, DOI 10.1016/0378-5955(88)90011-1 MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MANLEY GA, 1994, IN PRESS HEAR RES MANLEY GA, 1989, MECH HEARING, P143 MANLEY GA, 1990, J COMP PHYSIOL A, V167, P89, DOI 10.1007/BF00192409 MANLEY GA, 1990, J COMP PHYSIOL A, V167, P129, DOI 10.1007/BF00192412 MANLEY GA, 1992, EFFECT TEMPERATURE S, P156 MANLEY GA, 1993, J ACOUST SOC AM, V93, P2820, DOI 10.1121/1.405803 MARTIN GK, 1988, HEARING RES, V33, P49, DOI 10.1016/0378-5955(88)90020-2 Miller M.R., 1980, P169 MILLER MR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P463 MILLER MR, 1988, J COMP NEUROL, V271, P604, DOI 10.1002/cne.902710410 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 OHYAMA K, 1992, FREQUENCY INSTABILIT, P150 OHYAMA K, 1991, HEARING RES, V56, P111, DOI 10.1016/0378-5955(91)90160-B PALMER AR, 1981, J PHYSL, V324, pP66 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 TALMADGE CL, 1991, J ACOUST SOC AM, V89, P2391, DOI 10.1121/1.400958 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 VANDIJK P, 1990, J ACOUST SOC AM, V88, P1779, DOI 10.1121/1.400199 WHITEHEAD ML, 1993, SCAND AUDIOL, V22, P3, DOI 10.3109/01050399309046012 WILSON JP, 1990, ADV AUDIOL, V7, P47 WIT HP, 1989, COCHLEAR MECH STRUCT, P341 WIT HP, 1990, ADV AUDIOL, V7, P110 ZENNER HP, 1990, ADV AUDIOL, V7, P35 ZUREK PM, 1985, J ACOUST SOC AM, V78, P340, DOI 10.1121/1.392496 ZWICKER E, 1989, COCHLEAR MECHANISMS, P359 NR 44 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 DEC PY 1993 VL 71 IS 1-2 BP 157 EP 169 DI 10.1016/0378-5955(93)90031-U PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800017 PM 8113134 ER PT J AU TALMADGE, CL LONG, GR MURPHY, WJ TUBIS, A AF TALMADGE, CL LONG, GR MURPHY, WJ TUBIS, A TI NEW OFF-LINE METHOD FOR DETECTING SPONTANEOUS OTOACOUSTIC EMISSIONS IN HUMAN-SUBJECTS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; GENDER; BASILAR MEMBRANE ID DISTORTION-PRODUCT; FREQUENCY; PREVALENCE; AMPLITUDE AB Spontaneous otoacoustic emissions were evaluated in 36 female and 40 male subjects. In agreement with the results of previous surveys, emissions were found to be more prevalent in female subjects and there was a tendency for the male subjects to have fewer emissions in their left ears. The digitization of five minute samples of ear canal signals, combined with sophisticated data analysis, produced a substantial reduction in the emission detection threshold. 588 emissions were detected in 72% of the subjects and 56% of the ears. Of the observed emissions, 18 could be identified with cubic distortion products of other emissions, and 11 could be identified as harmonic products (i.e., integral frequency multiples of other emissions). The large number of emissions detected (one subject had 32 in her right ear and 25 in her left) permitted evaluation of the pattern of separation of emissions. The average effective separation along the basilar membrane (according to the Greenwood frequency map) for adjacent emissions of all ears was 0.427 mm with interquartile values of 0.387 mm and 0.473 mm. The relationship between emission power, frequency, and full width at half maximum appears to be in agreement with the implications of a noise perturbed Van der Pol oscillator model of spontaneous emissions. C1 PURDUE UNIV,DEPT AUDIOL & SPEECH SCI,W LAFAYETTE,IN 47907. RP TALMADGE, CL (reprint author), PURDUE UNIV,DEPT PHYS,W LAFAYETTE,IN 47907, USA. CR BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 BURNS EM, 1984, HEARING RES, V16, P271, DOI 10.1016/0378-5955(84)90116-3 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 DALLMAYR C, 1987, ACUSTICA, V63, P243 DALLMAYR C, 1985, ACUSTICA, V59, P67 GREENWOOD DD, 1991, HEARING RES, V54, P164, DOI 10.1016/0378-5955(91)90117-R GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 JONES K, 1986, PERIPHERAL AUDITORY, P266 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 KOHLER W, 1992, SCAND AUDIOL, V21, P55, DOI 10.3109/01050399209045982 LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 MARTIN GK, 1990, EAR HEARING, V11, P106 Press WH, 1988, NUMERICAL RECIPES C PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 RUSSELL AF, 1992, THESIS U ILLINOIS SHERA CA, 1993, UNPUB J ACOUST SOC A TALMADGE C, 1992, J ACOUST SOC AM, V91, P2380, DOI 10.1121/1.403333 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 VANDIJK P, 1990, J ACOUST SOC AM, V88, P1779, DOI 10.1121/1.400199 VANDIJK P, 1990, J ACOUST SOC AM, V88, P850, DOI 10.1121/1.399734 WHITEHEAD ML, 1991, HEARING RES, V53, P269, DOI 10.1016/0378-5955(91)90060-M WHITEHEAD ML, 1992, IN PRESS SCAND AUDIO WIT HP, 1990, MECH BIOPHYSICS HEAR, P259 ZWICKER E, 1990, HEARING RES, V44, P209, DOI 10.1016/0378-5955(90)90081-Y ZWICKER E, 1990, J ACOUST SOC AM, V88, P1639, DOI 10.1121/1.400324 NR 25 TC 93 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 DEC PY 1993 VL 71 IS 1-2 BP 170 EP 182 DI 10.1016/0378-5955(93)90032-V PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800018 PM 8113135 ER PT J AU MCLAREN, GM QUIRK, WS LAURIKAINEN, E COLEMAN, JKM SEIDMAN, MD DENGERINK, HA NUTTALL, AL MILLER, JM WRIGHT, JW AF MCLAREN, GM QUIRK, WS LAURIKAINEN, E COLEMAN, JKM SEIDMAN, MD DENGERINK, HA NUTTALL, AL MILLER, JM WRIGHT, JW TI SUBSTANCE-P INCREASES COCHLEAR BLOOD-FLOW WITHOUT CHANGING COCHLEAR ELECTROPHYSIOLOGY IN RATS SO HEARING RESEARCH LA English DT Article DE COCHLEAR BLOOD FLOW; BLOOD PRESSURE; COCHLEAR ACTION POTENTIAL; COCHLEAR MICROPHONICS; LASER DOPPLER FLOWMETER; SUBSTANCE P; RAT ID GENE-RELATED PEPTIDE; LASER DOPPLER; AUTO-REGULATION; ANGIOTENSIN-II; STIMULATION AB Carotid artery infusions of substance P yielded reductions in systemic blood pressure and elevations in cochlear blood flow (CoBF), measured via laser Doppler flowmeter, with no alterations in cochlear action potentials or cochlear microphonics in Wistar-Kyoto rats. Additionally, direct micro-infusions of substance P into the anterior inferior cerebellar artery, which contributes to the local vascular perfusion of the cochlea, yielded elevations in CoBF with no changes in systemic blood pressure. Pretreatment with a specific substance P receptor antagonist, ([D-Pro(2),D-Trp(7),(9)]SP) via the carotid artery or the anterior inferior cerebellar artery, diminished subsequent substance P-induced vascular responses. These results suggest that endogenous substance P, like other vasoactive peptides, may interact with a substance P-specific receptor population in the cochlea and may therefore participate in the ongoing regulation of CoBF. These findings also support the premise that vasodilatory hormones, along with vasoconstrictive agents, may be involved in the autoregulation of CoBF. C1 WAYNE STATE UNIV,DEPT OTOLARYNGOL,DETROIT,MI 48201. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. WASHINGTON STATE UNIV,DEPT PSYCHOL,PULLMAN,WA 99164. EAR RES FDN,SARASOTA,FL. RP MCLAREN, GM (reprint author), EDINBORO UNIV PENN,DEPT PSYCHOL,EDINBORO,PA 16444, USA. CR AXELSSON A, 1983, ACTA OTO-LARYNGOL, V96, P215, DOI 10.3109/00016488309132894 Bayliss WM, 1902, J PHYSIOL-LONDON, V28, P220 CARLISLE L, 1990, HEARING RES, V43, P107, DOI 10.1016/0378-5955(90)90219-F COLEMAN JKM, UNPUB AUTORADIOGRAPH DEFELICE AF, 1988, J PHARMACOL EXP THER, V246, P183 DENGERINK HA, 1988, PHYSL EAR, P327 DENGERINK HA, 1985, HEARING RES, V20, P31, DOI 10.1016/0378-5955(85)90056-5 DOLAN DF, 1988, J ACOUST SOC AM, V83, P1081, DOI 10.1121/1.396052 EULER U. S., 1931, JOUR PHYSIOL, V72, P74 FLYNN AJ, 1988, HEARING RES, V34, P201, DOI 10.1016/0378-5955(88)90108-6 GAZELIUS B, 1987, ACTA PHYSIOL SCAND, V130, P33, DOI 10.1111/j.1748-1716.1987.tb08108.x GILMAN A, 1990, GOODMAN GILMANS PHAR, P180 GOODWIN PC, 1984, ACTA OTO-LARYNGOL, V98, P403, DOI 10.3109/00016488409107581 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HULTCRANTZ E, 1982, ARCH OTO-RHINO-LARYN, V234, P151, DOI 10.1007/BF00453622 JOHNSON PC, 1986, CIRC RES, V59, P483 KRIEGER DT, 1981, NEW ENGL J MED, V304, P944, DOI 10.1056/NEJM198104163041605 LAROUERE MJ, 1989, OTOLARYNG HEAD NECK, V101, P375 LAWRENCE M, 1977, ACTA OTOLARYNGOL, V110, P305 LUNDBERG JM, 1982, ACTA PHYSIOL SCAND, V114, P329, DOI 10.1111/j.1748-1716.1982.tb06992.x LUNDBLAD L, 1983, ACTA PHYSIOL SCAND, V119, P7, DOI 10.1111/j.1748-1716.1983.tb07299.x MCEWAN JR, 1988, CIRCULATION, V77, P1072 MCLAREN GM, 1991, HEARING RES, V55, P1, DOI 10.1016/0378-5955(91)90086-O 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, 1984, ARCH OTOLARYNGOL, V110, P305 MULVANY MJ, 1990, PHYSIOL REV, V70, P921 PERNOW B, 1983, PHARMACOL REV, V35, P85 QUIRK WS, 1989, HEARING RES, V41, P53, DOI 10.1016/0378-5955(89)90178-0 QUIRK WS, 1988, HEARING RES, V32, P129 SEIDMAN MD, 1991, OTOLARYNG HEAD NECK, V105, P457 SNOW JB, 1972, VASCULAR DISORDERS H, P164 UDDMAN R, 1982, ARCH OTO-RHINO-LARYN, V236, P7, DOI 10.1007/BF00464052 UDDMANN R, 1988, NORADRENERGIC INNERV, P214 WRIGHT JW, 1981, J ACOUST SOC AM, V70, P1353, DOI 10.1121/1.387124 WRIGHT JW, 1985, HEARING RES, V17, P41, DOI 10.1016/0378-5955(85)90128-5 NR 36 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 1993 VL 71 IS 1-2 BP 183 EP 189 DI 10.1016/0378-5955(93)90033-W PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800019 PM 7509333 ER PT J AU PRIJS, VF KEIJZER, J VERSNEL, H SCHOONHOVEN, R AF PRIJS, VF KEIJZER, J VERSNEL, H SCHOONHOVEN, R TI RECOVERY CHARACTERISTICS OF AUDITORY-NERVE FIBERS IN THE NORMAL AND NOISE-DAMAGED GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE RECOVERY FUNCTION; GUINEA PIG; NOISE-INDUCED COCHLEAR DAMAGE; SPONTANEOUS ACTIVITY; AUDITORY NERVE FIBERS ID SINGLE-FIBER; ACTION-POTENTIALS; RESPONSES; CLICKS; FORM AB Spontaneous activity was analysed in auditory-nerve fibres innervating normal and noise-damaged cochleas. Spike occurrences were conceived as point processes. Joint interval distributions and serial correlation coefficients reveal a weak history effect for succeeding intervals. The point process is regarded as a renewal and the recovery function, being proportional to the hazard function, is determined from the interval probability density function. In 29 out of 60 fibres the latter shows peculiarities which result in a deviation from a monotonically increasing recovery function. For three fibres of low characteristic frequency the interval probability function shows an oscillatory pattern and for 26 fibres this function exhibits an early, sharp peak around 1.1 ms irrespective of characteristic frequency, spontaneous rate, or cochlear damage. The recovery function is not different between fibres with normal and those with abnormally high thresholds and exhibits an exponential recovery with one time constant of average value 1.6 ms. Bursting activity is found in only one fibre from the abnormally high threshold group. RP PRIJS, VF (reprint author), LEIDEN UNIV HOSP,ENT DEPT,POB 9600,2300 RC LEIDEN,NETHERLANDS. CR Bevington P. R., 1969, DATA REDUCTION ERROR BI Q, 1989, J ACOUST SOC AM, V85, P2504, DOI 10.1121/1.397745 BOSCH WR, 1990, P ASS RES OTOLARYNGO COOPER NP, 1989, THESIS U KEELE STAFF EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 EVANS EF, 1979, AUDITORY INVESTIGATI, P324 FRIJNS JHM, 1993, IN PRESS MED BIOL EN GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 GAUMOND RP, 1983, J ACOUST SOC AM, V74, P1392, DOI 10.1121/1.390164 GOLDBERG JM, 1964, J NEUROPHYSIOL, V27, P706 GRAY PR, 1967, BIOPHYS J, V7, P759, DOI 10.1016/S0006-3495(67)86621-9 GRAY PR, 1966, MIT451 RES LAB EL TE HARRISON RV, 1984, HEARING RES, V14, P79, DOI 10.1016/0378-5955(84)90070-4 JONES K, 1985, J ACOUST SOC AM, V78, P90, DOI 10.1121/1.392458 KARAMANOS N, 1988, BASIC ISSUES HEARING, P185 Kiang NY-s, 1965, DISCHARGE PATTERNS S KOHLLOFFEL LUE, 1975, ARCH OTO-RHINO-LARYN, V209, P179, DOI 10.1007/BF00453773 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LOWEN SB, 1992, J ACOUST SOC AM, V92, P803, DOI 10.1121/1.403950 LUTKENHONER B, 1980, SCAND AUDIOL S, V11, P25 LUTKENHONER B, 1982, THESIS MUNSTER MANLEY GA, 1976, J PHYSIOL-LONDON, V258, P323 MARK KE, 1992, J ACOUST SOC AM, V91, P989, DOI 10.1121/1.402504 MILLER MI, 1992, ADV BIOSCI, V83, P133 MILLER MI, 1985, J ACOUST SOC AM, V77, P1452, DOI 10.1121/1.392040 MOORE GP, 1966, ANNU REV PHYSIOL, V28, P493, DOI 10.1146/annurev.ph.28.030166.002425 PRIJS VF, 1980, ACUSTICA, V45, P1 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RUGGERO MA, 1973, J NEUROPHYSIOL, V36, P569 SCHOONHOVEN R, 1994, IN PRESS J ACOUST SO SIEGEL JH, 1992, HEARING RES, V59, P85, DOI 10.1016/0378-5955(92)90105-V Snyder D.L., 1991, RANDOM POINT PROCESS, Vsecond TEICH MC, 1980, BIOL CYBERN, V38, P187, DOI 10.1007/BF00337011 VERSNEL H, 1992, HEARING RES, V59, P138, DOI 10.1016/0378-5955(92)90111-Y VERSNEL H, 1992, HEARING RES, V59, P157, DOI 10.1016/0378-5955(92)90112-Z VERSNEL H, 1990, HEARING RES, V46, P147, DOI 10.1016/0378-5955(90)90145-F VERSNEL H, 1994, IN PRESS HEAR RES 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 DEC PY 1993 VL 71 IS 1-2 BP 190 EP 201 DI 10.1016/0378-5955(93)90034-X PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800020 PM 8113136 ER PT J AU WHITWORTH, C MORRIS, C SCOTT, V RYBAK, LP AF WHITWORTH, C MORRIS, C SCOTT, V RYBAK, LP TI DOSE-RESPONSE RELATIONSHIPS FOR FUROSEMIDE OTOTOXICITY IN RAT SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; COMPOUND ACTION POTENTIAL; ALBUMIN ID HAIR-CELLS; SERUM-ALBUMIN; BINDING; CHINCHILLA; SECRETION; KIDNEY AB Furosemide is an ototoxic loop diuretic which is highly bound to serum albumin. Previous studies have shown that rats deficient in albumin are more susceptible to furosemide ototoxicity than are rats with normal serum albumin concentrations: The present study was designed to compare the dose-response relationships for furosemide ototoxicity in rats with normal serum albumin concentration to rats without albumin in their serum. Young adult rats 50-80 days of age from each group were anesthetized with Rompun, and the endocochlear potential (EP) and compound action potential (CAP) thresholds were measured before and after furosemide injection. After a stable EP and CAP threshold were measured, each animal was injected with a single dose of furosemide through a cannula in the jugular vein. Rats with normal serum albumin had very little change in the EP or CAP threshold until the dose of furosemide was 40 mg/kg or greater. The dose-response curves for EP reduction and CAP threshold elevation then rose steeply to reach a maximum at 50 mg/kg. Albumin-deficient rats were much more sensitive to the effects of furosemide. The dose-response curves for both EP and CAP were shifted to the left. The doses resulting in half-maximal effects in the albumin-deficient rats were about half that found in the normal rats. These findings support the hypothesis that the access of furosemide to its site of ototoxic action in the cochlea depends on the quantity of unbound furosemide in the serum. C1 SO ILLINOIS UNIV,SCH MED,DEPT SURG,SPRINGFIELD,IL 62794. SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62794. CR ARNOLD W, 1981, ACTA OTOLARYNGOL, V91, P391 BESSEGHIR K, 1989, AM J PHYSIOL, V256, pF475 BOWMAN RH, 1975, AM J PHYSIOL, V229, P93 BROWN DR, 1991, DEV MED CHILD NEUROL, V33, P816 BROWN RD, 1979, TOXICOL APPL PHARM, V48, P157 CAISEY JD, 1980, CLIN CHEM, V26, P1877 COLOMBO R, 1982, PHARMACOLOGY, V25, P73, DOI 10.1159/000137726 Comis S D, 1981, Scand Audiol Suppl, V14 Suppl, P85 COMIS SD, 1990, ACTA OTO-LARYNGOL, V109, P49, DOI 10.3109/00016489009107414 DAVIS H, 1965, COLD SPRING HARB SYM, V30, P181 Forge A, 1982, Br J Audiol, V16, P109, DOI 10.3109/03005368209081455 GALLAGHER KL, 1979, ANN INTERN MED, V91, P744 GIDAL BE, 1993, ANN PHARMACOTHER, V27, P32 GREEN TP, 1981, J PHARMACOL EXP THER, V216, P537 HALL S, 1985, J PHARMACOL EXP THER, V232, P263 HAMMARLUND MM, 1982, BIOPHARM DRUG DISPOS, V3, P345, DOI 10.1002/bdd.2510030408 IKEDA K, 1989, ARCH OTOLARYNGOL, V115, P500 INOUE M, 1987, KIDNEY INT, V32, P198, DOI 10.1038/ki.1987.192 Jung W, 1975, Laryngol Rhinol Otol (Stuttg), V54, P411 Kshirsagar N A, 1978, J Postgrad Med, V24, P20 MATHOG RH, 1972, ANN OTO RHINOL LARYN, V81, P871 MORIZONO T, 1980, ARCH OTO-RHINO-LARYN, V229, P149, DOI 10.1007/BF00454238 NAGASE S, 1979, SCIENCE, V205, P590, DOI 10.1126/science.451621 PIKE DA, 1980, HEARING RES, V3, P79, DOI 10.1016/0378-5955(80)90009-X POSE I, 1983, BRAZ J MED BIOL RES, V16, P317 QUICK CA, 1975, ANN OTO RHINOL LARYN, V84, P94 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RUSSELL IJ, 1983, NATURE, V301, P334, DOI 10.1038/301334a0 RYBAK LP, 1993, ARCH OTOLARYNGOL, V119, P758 RYBAK LP, 1987, HEARING RES, V31, P169, DOI 10.1016/0378-5955(87)90123-7 RYBAK LP, 1993, OTOLARYNG CLIN N AM, V26, P829 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 RYBAK LP, 1985, LARYNGOSCOPE, V95, P1, DOI 10.1288/00005537-198509010-00001 RYBAK LP, 1992, HEARING RES, V59, P75, DOI 10.1016/0378-5955(92)90104-U RYBAK LP, 1991, LARYNGOSCOPE, V101, P1167 Sandroni S, 1988, J Fla Med Assoc, V75, P676 SEBILLE B, 1978, J CHROMATOGR, V167, P159, DOI 10.1016/S0021-9673(00)91155-5 SEWELL WF, 1984, J PHYSIOL-LONDON, V347, P685 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 SMITH DE, 1982, J PHARMACOKINET BIOP, V10, P663, DOI 10.1007/BF01062547 VIANI A, 1991, DEV PHARMACOL THERAP, V16, P33 ZINI R, 1976, EUR J CLIN PHARMACOL, V10, P139, DOI 10.1007/BF00609473 NR 42 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 1993 VL 71 IS 1-2 BP 202 EP 207 DI 10.1016/0378-5955(93)90035-Y PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800021 PM 8113137 ER PT J AU MCFADDEN, D MISHRA, R AF MCFADDEN, D MISHRA, R TI ON THE RELATION BETWEEN HEARING SENSITIVITY AND OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE AUDITORY SENSITIVITY; SPONTANEOUS OTOACOUSTIC EMISSIONS; SEX DIFFERENCES; EAR DIFFERENCES ID MICROSTRUCTURE; THRESHOLDS AB The auditory literature suggests that ears having spontaneous otoacoustic emissions (SOAEs) should also evidence overall better hearing in the quiet than ears with no SOAEs, but no direct tests of this presumed relationship have been made. Accordingly, hearing sensitivity was measured in both males and females having either no SOAEs or at least four SOAEs in the right ear. Averaged across frequencies, the hearing of the subjects with SOAEs was about 3 dB better, in both ears, than the hearing of the subjects with no SOAEs. In accord with past findings, sensitivity was also significantly better in right ears than left. However, the common finding of better hearing in females than males did not emerge, suggesting that this difference may exist only when the sex difference in SOAE prevalence is not taken into account. The existence of a direct relationship between hearing sensitivity in the quiet and the presence of SOAEs suggests that a common mechanism may be responsible for both. C1 UNIV TEXAS,INST NEUROSCI,AUSTIN,TX 78712. RP MCFADDEN, D (reprint author), UNIV TEXAS,DEPT PSYCHOL,MEZES HALL 330,AUSTIN,TX 78712, USA. CR Baker M A, 1977, Br J Audiol, V11, P65, DOI 10.3109/03005367709078835 BILGER RC, 1984, ASHA, V26, P175 BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 CHUNG DY, 1983, J ACOUST SOC AM, V73, P1277, DOI 10.1121/1.389276 COHEN MF, 1982, J ACOUST SOC AM, V71, P405, DOI 10.1121/1.387442 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 EMMERICH DS, 1988, NEUROPSYCHOLOGIA, V26, P133, DOI 10.1016/0028-3932(88)90036-X Kemp DT, 1979, SCAND AUDIOL S, V9, P35 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LONG GR, 1988, HEARING RES, V36, P125, DOI 10.1016/0378-5955(88)90055-X LONG GR, 1984, HEARING RES, V15, P73, DOI 10.1016/0378-5955(84)90227-2 MCFADDEN D, 1993, IN PRESS P NATL ACAD MCFADDEN D, 1993, HEARING RES, V68, P143, DOI 10.1016/0378-5955(93)90118-K PREVIC FH, 1991, PSYCHOL REV, V98, P299 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 STEVENS KN, 1987, J ACOUST SOC AM, V81, P470, DOI 10.1121/1.394913 SWANSON SJ, 1988, J SPEECH HEAR RES, V31, P569 WATSON CS, 1972, J ACOUST SOC AM, V52, P633, DOI 10.1121/1.1913153 WATSON CS, 1991, AM J OTOL, V12, P73 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 1989, ANSI S361989 AM NAT NR 21 TC 60 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 DEC PY 1993 VL 71 IS 1-2 BP 208 EP 213 DI 10.1016/0378-5955(93)90036-Z PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800022 PM 8113138 ER PT J AU ADLER, HJ POJE, CP SAUNDERS, JC AF ADLER, HJ POJE, CP SAUNDERS, JC TI RECOVERY OF AUDITORY FUNCTION AND STRUCTURE IN THE CHICK AFTER 2 INTENSE PURE-TONE EXPOSURES SO HEARING RESEARCH LA English DT Article DE THRESHOLD SHIFT; EVOKED POTENTIALS; TECTORIAL MEMBRANE; CHICKS; HEARING LOSS; AUDITORY FUNCTION ID HAIR CELL LOSS; MIDDLE-EAR DEVELOPMENT; SEVERE ACOUSTIC TRAUMA; TECTORIAL MEMBRANE; NEONATAL CHICK; BASILAR PAPILLA; SOUND EXPOSURE; COCHLEA; REGENERATION; OVERSTIMULATION AB Groups of neonatal chicks were examined in three experimental conditions that differed in the age and number of times they were exposed to a pure tone of 0.9 kHz at 120 dB SPL for 48 h. Several animals were exposed once at 2 or 16 days of age, while others were subjected twice to the above stimulus, first at 2 days and then at 16 days. Evoked potential measures of threshold shift, obtained at 0, 12 or 26 days post-exposure, were used to determine the degree of hearing loss and recovery. The average threshold loss in the mid-range frequencies was about 57 dB at 0 days for all three conditions. This level was reduced to about 15 dB in all three groups at 12 days of recovery, while in birds exposed once at 2 days, but allowed 26 days to recover, the post-exposure thresholds returned to pre-exposure levels. Scanning electron microscopic analysis of cochlear structure was conducted in groups of similarly exposed and recovered animals. Twelve days post-exposure, the structural analysis revealed regeneration of a single honeycomb-like tectorial membrane layer in both the once and twice-exposed cochleae. However, damage to, and repair of, the tectorial membrane after the second exposure revealed the production of a second honeycomb layer in about half the animals examined. The results indicated that chicks retain the capacity to repair receptor epithelium damage and recover considerably from hearing loss after multiple exposures to intense sound. C1 UNIV PENN,SCH MED,DEPT OTORHINOLARYNGOL HEAD & NECK SURG,PHILADELPHIA,PA 19104. RP ADLER, HJ (reprint author), UNIV PENN,SCH MED,DAVID MAHONEY INST NEUROL SCI,3400 SPRUCE ST,PHILADELPHIA,PA 19104, USA. CR ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X COHEN YE, 1992, J MORPHOL, V212, P257, DOI 10.1002/jmor.1052120305 COHEN YE, 1992, HEARING RES, V58, P1, DOI 10.1016/0378-5955(92)90002-5 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, 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, 1992, EXP NEUROL, V115, P23, DOI 10.1016/0014-4886(92)90215-C COTANCHE DA, 1990, HEARING RES, V46, P29, DOI 10.1016/0378-5955(90)90137-E HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 KILLICK R, 1992, HEARING RES, V64, P21, DOI 10.1016/0378-5955(92)90165-J 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 PUGLIANO FA, 1993, ACTA OTO-LARYNGOL, V113, P18, DOI 10.3109/00016489309135761 RAPHAEL Y, 1991, HEARING RES, V53, P173, DOI 10.1016/0378-5955(91)90052-B RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RYALS BM, 1985, HEARING RES, V19, P135, DOI 10.1016/0378-5955(85)90117-0 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 SAUNDERS JC, 1986, HEARING RES, V24, P227, DOI 10.1016/0378-5955(86)90021-3 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SAUNDERS JC, 1985, HEARING RES, V18, P253, DOI 10.1016/0378-5955(85)90042-5 SHIEL MJ, 1990, HEARING RES, V47, P147, DOI 10.1016/0378-5955(90)90172-L SMITH CA, 1985, FORM FUNCTIONS BIRDS, V3, P273 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 NR 30 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 DEC PY 1993 VL 71 IS 1-2 BP 214 EP 224 DI 10.1016/0378-5955(93)90037-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800023 PM 8113139 ER PT J AU PICKLES, JO AF PICKLES, JO TI AN ANALYSIS OF ACTIN ISOFORMS EXPRESSED IN HAIR-CELL ENRICHED FRACTIONS OF THE CHICK BASILAR PAPILLA BY THE POLYMERASE CHAIN-REACTION TECHNIQUE SO HEARING RESEARCH LA English DT Article DE ACTIN; STEREOCILIA; PCR; MESSENGER-RNA; CHICK ID ALPHA-CARDIAC ACTIN; BETA-ACTIN; BIRD COCHLEA; GENES; STEREOCILIA; FILAMENTS; CYTOSKELETAL; EVOLUTION; MUSCLE; ORGANIZATION AB Actin mRNA was characterised in hair-cell enriched fractions of the chick basilar papilla, by means of the reverse-transcription polymerase chain reaction technique. Primers were directed against the 3' untranslated portions of the actin mRNAs. Evidence for beta-cytoplasmic and gamma-cytoplasmic actin mRNA was found; no evidence was found for alpha-skeletal, alpha-cardiac or type 5 cytoplasmic actin mRNAs. Since beta-actin is known to form bundles of filaments whereas gamma-actin does not, this suggests that the hair-cell stereocilia are composed of beta-actin. RP PICKLES, JO (reprint author), UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,BRISBANE,QLD 4072,AUSTRALIA. CR BERGSMA DJ, 1985, MOL CELL BIOL, V5, P1151 CHANG KS, 1984, MOL CELL BIOL, V4, P2498 CHIRGWIN JM, 1979, BIOCHEMISTRY-US, V18, P5294, DOI 10.1021/bi00591a005 COUSILLAS H, 1988, HEARING RES, V32, P117, DOI 10.1016/0378-5955(88)90083-4 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 ERBA HP, 1988, MOL CELL BIOL, V8, P1775 ERBA HP, 1986, NUCLEIC ACIDS RES, V14, P5275, DOI 10.1093/nar/14.13.5275 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 GUNNING P, 1983, MOL CELL BIOL, V3, P1985 HAYWARD LJ, 1986, J CELL BIOL, V102, P1485, DOI 10.1083/jcb.102.4.1485 LLOYD C, 1992, J CELL BIOL, V117, P787, DOI 10.1083/jcb.117.4.787 OBERHOLTZER JC, 1986, HEARING RES, V23, P161, DOI 10.1016/0378-5955(86)90013-4 PICKLES JO, 1991, HEARING RES, V55, P244, DOI 10.1016/0378-5955(91)90109-M PONTE P, 1983, MOL CELL BIOL, V3, P1783 SCHEVZOV G, 1992, J CELL BIOL, V117, P775, DOI 10.1083/jcb.117.4.775 SHEPHERD GMG, 1990, P NATL ACAD SCI USA, V87, P8627, DOI 10.1073/pnas.87.21.8627 TILNEY LG, 1983, J CELL BIOL, V96, P822, DOI 10.1083/jcb.96.3.822 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 TILNEY LG, 1980, J CELL BIOL, V86, P244, DOI 10.1083/jcb.86.1.244 VANDEKERCKHOVE J, 1984, J MOL BIOL, V179, P391, DOI 10.1016/0022-2836(84)90072-X ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 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 DEC PY 1993 VL 71 IS 1-2 BP 225 EP 229 DI 10.1016/0378-5955(93)90038-3 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800024 PM 8113140 ER PT J AU ITO, M SPICER, SS SCHULTE, BA AF ITO, M SPICER, SS SCHULTE, BA TI IMMUNOHISTOCHEMICAL LOCALIZATION OF BRAIN-TYPE GLUCOSE-TRANSPORTER IN MAMMALIAN INNER EARS - COMPARISON OF DEVELOPMENTAL AND ADULT STAGES SO HEARING RESEARCH LA English DT Article DE INNER EAR; GLUCOSE TRANSPORTER; BLOOD-PERILYMPH BARRIER; IMMUNOHISTOCHEMISTRY ID INSULIN-RESPONSIVE TISSUES; HORSERADISH-PEROXIDASE; IMMUNOCYTOCHEMICAL LOCALIZATION; STRIA VASCULARIS; BLOOD; BARRIER; JUNCTIONS; PROTEIN; GLUT-1; PERMEABILITY AB Inner ears from five mammalian genera were examined immunohistochemically with a rabbit polyclonal antiserum against the brain type glucose transporter (GLUT1). Vascular endothelial cells distributed widely in soft tissues of the cochlea and vestibular system in all five genera showed uniform immunostaining. The basal cell layer of the stria vascularis also contained GLUT1 in all genera, and in the guinea pig, the strial marginal cells reacted as well. GLUT1 was expressed in satellite cells surrounding spiral ganglion neurons but only in the gerbil and cat. In the developing inner ear of the gerbil, endothelial cells expressed GLUT1 at 2 days after birth, the earliest stage examined. Immunoreactive transporter also was detected at this time in cells lying under strial marginal cells and interpreted as immature basal cells. Satellite cells acquired affinity for GLUT1 antibody between days 12 and 16 after birth. The expression of GLUT1 by the various cell types correlates well with their structural and functional maturation. GLUT1 apparently plays a role in glucose transport in the inner ear where it mediates efflux from blood vessels into perilymph. It also appears to facilitate uptake of glucose by the stria vascularis from interstitial fluid via the basal cell layer and, in some species, by spiral ganglion neurons through satellite cells. RP ITO, M (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR ANNIKO M, 1982, AM J OTOLARYNG, V3, P242, DOI 10.1016/S0196-0709(82)80062-8 BELL GI, 1990, DIABETES CARE, V13, P198, DOI 10.2337/diacare.13.3.198 BIBER JW, 1986, J BIOL CHEM, V261, P6180 BIRNBAUM MJ, 1986, P NATL ACAD SCI USA, V83, P5784, DOI 10.1073/pnas.83.16.5784 CARLISLE L, 1990, CELL TISSUE RES, V262, P329, DOI 10.1007/BF00309888 CHARRON MJ, 1989, P NATL ACAD SCI USA, V86, P2535, DOI 10.1073/pnas.86.8.2535 DERMIETZEL R, 1992, DEV DYNAM, V193, P152 DUVALL AJ, 1971, ARCHIV OTOLARYNGOL, V93, P304 FARRELL CL, 1992, J HISTOCHEM CYTOCHEM, V40, P193 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 FERRARY E, 1987, AM J PHYSIOL, V253, pF59 Fink A., 1972, J COMP PHYSIOL PSYCH, V78, P375 FROEHNER SC, 1988, J NEUROCYTOL, V17, P173, DOI 10.1007/BF01674204 FUKUMOTO H, 1989, J BIOL CHEM, V264, P7776 GERHART DZ, 1989, J NEUROSCI RES, V22, P464, DOI 10.1002/jnr.490220413 GOODWIN PC, 1984, HEARING RES, V15, P215, DOI 10.1016/0378-5955(84)90030-3 GOULD GW, 1990, TRENDS BIOCHEM SCI, V15, P18, DOI 10.1016/0968-0004(90)90125-U GRAHAM RC, 1966, J HISTOCHEM CYTOCHEM, V14, P291 HARIK SI, 1990, J NEUROSCI, V10, P3862 HARIK SI, 1990, P NATL ACAD SCI USA, V87, P4261, DOI 10.1073/pnas.87.11.4261 HUKEE MJ, 1985, ANN OTO RHINOL LARYN, V94, P297 ITO M, 1993, UNPUB HISTOCHEM J JAHNKE K, 1976, ACTA OTOLARYNGOL S S, V336, P5 KALARIA RN, 1988, ANN NEUROL, V24, P757, DOI 10.1002/ana.410240610 KASANICKI MA, 1990, DIABETES CARE, V13, P219, DOI 10.2337/diacare.13.3.219 KASANICKI MA, 1989, HISTOCHEM J, V21, P47, DOI 10.1007/BF01002471 KOESTNER KH, 1989, P NATL ACAD SCI USA, V86, P3150 MARCUS DC, 1978, LARYNGOSCOPE, V88, P1825 MCGUIRT JP, 1992, DEV ENDOCOCHLEAR POT, P106 MUECKLER M, 1985, SCIENCE, V229, P941, DOI 10.1126/science.3839598 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PARDRIDGE WM, 1990, J BIOL CHEM, V265, P18035 REALE E, 1975, J ULTRA MOL STRUCT R, V53, P284, DOI 10.1016/S0022-5320(75)80030-X SANTOS-SACCHI J, 1980, ACTA OTO-LARYNGOL, V89, P12, DOI 10.3109/00016488009127103 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TAKATA K, 1992, CELL TISSUE RES, V267, P407, DOI 10.1007/BF00319362 THALMANN R, 1972, LARYNGOSCOPE, V82, P2249, DOI 10.1288/00005537-197212000-00013 THORENS B, 1990, DIABETES CARE, V13, P209, DOI 10.2337/diacare.13.3.209 WINTHER FO, 1971, Z ZELLFORSCH MIK ANA, V114, P193, DOI 10.1007/BF00334000 WINTHER FO, 1971, Z ZELLFORSCH MIK ANA, V121, P499, DOI 10.1007/BF00560156 NR 42 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 DEC PY 1993 VL 71 IS 1-2 BP 230 EP 238 DI 10.1016/0378-5955(93)90039-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MN148 UT WOS:A1993MN14800025 PM 8113142 ER PT J AU SEWELL, WF MROZ, EA AF SEWELL, WF MROZ, EA TI FLAVIN ADENINE-DINUCLEOTIDE IS A MAJOR ENDOGENOUS FLUOROPHORE IN THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE HAIR CELL; AUDITORY SYSTEM; AUTOFLUORESCENCE; FLAVINS; GOLDFISH; FORMALDEHYDE ID CARASSIUS-AURATUS; GOLDFISH; AUTOFLUORESCENCE; CELLS AB When illuminated with visible light, hair cells can exhibit autofluorescence (Lewis et al. [1982] Science 215, 1641-1643) concentrated in the basal pole near the synapses (Sento and Furukawa [1987] J. Comp. Neurol. 258, 352-367). The autofluorescence is enhanced by formaldehyde. The level of fluorescence is high enough to interfere with fluorescence microscopy of hair cells and to suggest that the fluorescent substance might have a particular role in hair-cell function. To identify this substance, we extracted a substance with formaldehyde-enhanced fluorescence from the inner ears of goldfish and purified it chromatographically. The substance copurified with FAD and had the same fluorescence emission spectrum. Two further results supported the identity of the endogenous fluorescent substance with FAD. First, as is the case with flavins, the autofluorescence in inner ear tissue examined within a few hours after fixation was reduced by addition of dithionite. Second, as is the case with the formaldehyde-enhanced fluorophore, the fluorescence of FAD was enhanced by formaldehyde. FAD accounted for 90% of flavins in goldfish inner ears; its concentration in the sensory epithelium was estimated to be about 30 nmol/g tissue weight, one of the highest tissue concentrations known. The FAD is probably associated with an unidentified flavoprotein concentrated in the basal, synaptic region of the hair cell. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP SEWELL, WF (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR AUBIN JE, 1979, J HISTOCHEM CYTOCHEM, V27, P36 BENSON RC, 1979, J HISTOCHEM CYTOCHEM, V27, P44 BURCH HB, 1957, METHOD ENZYMOL, V3, P960, DOI 10.1016/S0076-6879(57)03485-0 CORRODI H, 1965, J HISTOCHEM CYTOCHEM, V13, P484 FRENCH D, 1945, ADV PROTEIN CHEM, V2, P277, DOI 10.1016/S0065-3233(08)60627-0 LEWIS ER, 1982, SCIENCE, V215, P1641, DOI 10.1126/science.6978525 Metcalf R. L., 1943, ARCH BIOCHEM, V2, P55 NAKAJIMA Y, 1974, J COMP NEUROL, V156, P403, DOI 10.1002/cne.901560403 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 SEWELL WF, 1990, HEARING RES, V50, P127, DOI 10.1016/0378-5955(90)90039-R SEWELL WF, 1987, J NEUROSCI, V7, P2465 SWEENEY TK, 1987, HEARING RES, V28, P153, DOI 10.1016/0378-5955(87)90046-3 THALMANN I, 1970, ANN OTO RHINOL LARYN, V79, P12 WEBER G, 1950, BIOCHEM J, V47, P114 NR 14 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 1993 VL 70 IS 2 BP 131 EP 138 DI 10.1016/0378-5955(93)90150-Y PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300001 PM 7904988 ER PT J AU MROZ, EA LECHENE, C AF MROZ, EA LECHENE, C TI CALCIUM AND MAGNESIUM TRANSPORT BY ISOLATED GOLDFISH HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; ELECTRON-PROBE ANALYSIS; ION TRANSPORT; CALCIUM; MAGNESIUM ID ION-DEPENDENT CONDUCTANCES; INTRACELLULAR CALCIUM; GUINEA-PIG; EXCHANGE; COCHLEA; DEPOLARIZATION; MECHANISMS; MICROSCOPY; MOTILITY; AXONS AB We used electron-probe analysis (EPA) to investigate the transport of the divalent cations calcium and magnesium across the plasma membranes of hair cells. Unlike ion-sensitive fluorescent dyes, EPA detects these ions regardless of the state of chemical combination inside the cell; changes in these cell ions determined by EPA indicate net transport across the cell membrane. Raising or lowering either extracellular divalent cation within 1 mM of its control level raised or lowered its cell contents, but further increases in extracellular concentration of either ion had little additional effect on the cell content of that ion. New steady-state contents could be obtained within minutes, but the net divalent cation currents required to account for the observed changes would have been smaller than most currents recorded electrophysiologically, less than 1 pA. The effects of replacing extracellular Na+ with other ions were consistent with the presence in hair cells of exchangers for divalent cations thought to occur in other tissues: electrically neutral sodium/magnesium exchange (2 Na+ per Mg2+) and electrogenic sodium/calcium exchange (at least 3 Na+ per Ca2+). The increase in cell Ca after 1 minute of pottasium-depolarization was similar to that expected from electrophysiological studies of voltage-sensitive calcium currents in goldfish hair cells. After that time in elevated potassium, however, either calcium-entry pathways were inhibited or calcium-export mechanisms were enhanced. C1 BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ABRAHAM EH, 1985, AM J PHYSIOL, V248, pC154 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 ASSAD JA, 1992, J NEUROSCI, V12, P3291 BAKER PF, 1983, CIBA F S, V122, P1 Baker P F, 1978, Ann N Y Acad Sci, V307, P250, DOI 10.1111/j.1749-6632.1978.tb41956.x CARAFOLI E, 1991, PHYSIOL REV, V71, P129 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 DIPOLO R, 1983, ANNU REV PHYSIOL, V45, P313, DOI 10.1146/annurev.ph.45.030183.001525 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, 1990, J NEUROSCI, V10, P1388 FLATMAN PW, 1991, ANNU REV PHYSIOL, V53, P259, DOI 10.1146/annurev.physiol.53.1.259 FUCHS PA, 1988, J NEUROSCI, V8, P2460 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 Hille B., 1992, IONIC CHANNELS EXCIT, V2nd HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 IKEDA K, 1992, PFLUG ARCH EUR J PHY, V420, P493, DOI 10.1007/BF00374624 IKEDA K, 1991, ORL J OTO-RHINO-LARY, V53, P78 IKEDA K, 1991, AM J PHYSIOL, V261, pC231 KIDD RC, 1990, HEARING RES, V49, P181, DOI 10.1016/0378-5955(90)90104-W LECHENE C, 1986, ANN NY ACAD SCI, V483, P270, DOI 10.1111/j.1749-6632.1986.tb34532.x LECHENE CP, 1977, ANNU REV BIOPHYS BIO, V6, P57, DOI 10.1146/annurev.bb.06.060177.000421 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 LIPP P, 1988, J PHYSIOL-LONDON, V403, P355 MROZ EA, 1993, HEARING RES, V70, P146, DOI 10.1016/0378-5955(93)90152-Q MROZ EA, 1993, HEARING RES, V70, P9, DOI 10.1016/0378-5955(93)90048-6 MROZ EA, 1993, HEARING RES, V70, P22, DOI 10.1016/0378-5955(93)90049-7 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 SEWELL WF, 1990, HEARING RES, V44, P71, DOI 10.1016/0378-5955(90)90023-I SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 TSIEN RY, 1989, ANNU REV NEUROSCI, V12, P227, DOI 10.1146/annurev.neuro.12.1.227 ULFENDAHL M, 1988, ARCH OTO-RHINO-LARYN, V245, P237, DOI 10.1007/BF00463935 YAMASHITA T, 1990, ACTA OTO-LARYNGOL, V109, P256, DOI 10.3109/00016489009107441 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 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 NOV PY 1993 VL 70 IS 2 BP 139 EP 145 DI 10.1016/0378-5955(93)90151-P PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300002 PM 8294257 ER PT J AU MROZ, EA LECHENE, C AF MROZ, EA LECHENE, C TI EXTRACELLULAR N-METHYL-D-GLUCAMINE LEADS TO LOSS OF HAIR-CELL SODIUM, POTASSIUM, AND CHLORIDE SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; ION TRANSPORT; PERMEABILITY; PH REGULATION ID EXCHANGE; PUMP AB The organic cation N-methyl-D-glucamine (NMDG) is often used to replace extracellular sodium in experimental studies. Replacing 100 mM of Na+ with NMDG(+) in the fluid bathing isolated goldfish hair cells led to a rapid loss not only of cell sodium, but also of cell potassium and chloride. The loss of inorganic cell solutes was accompanied by acidification of the cells. Cell volume did not change significantly. These results are consistent with passage of the cationic form of NMDG, a titratable amine with a pK(a) 9.6, across the hair-cell membrane. These results should have bearing in interpreting results of experiments in which this cation is used to replace extracellular sodium, particularly for periods of time longer than 3 min. C1 BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR AGAR G, 1989, FEBS LETT, V244, P231 AVDEEF A, 1993, ANAL CHEM, V65, P42, DOI 10.1021/ac00049a010 COOK DI, 1990, J MEMBRANE BIOL, V114, P37, DOI 10.1007/BF01869383 Dale HH, 1914, J PHARMACOL EXP THER, V6, P147 HARRIS RC, 1986, AM J PHYSIOL, V251, pC815 Hille B., 1992, IONIC CHANNELS EXCIT, V2nd HOUSLEY GD, 1992, J PHYSIOL-LONDON, V448, P73 IKEDA K, 1992, PFLUG ARCH EUR J PHY, V420, P493, DOI 10.1007/BF00374624 IKEDA K, 1992, J PHYSIOL-LONDON, V447, P627 LECHENE C, 1988, NA PLUS K PLUS PUM B, P171 LECHENE C, 1986, ANN NY ACAD SCI, V483, P270, DOI 10.1111/j.1749-6632.1986.tb34532.x MACKNIGHT ADC, 1989, RENAL PHYSIOL BIOCH, V12, P118 MROZ EA, 1993, HEARING RES, V70, P9, DOI 10.1016/0378-5955(93)90048-6 MROZ EA, 1993, HEARING RES, V70, P22, DOI 10.1016/0378-5955(93)90049-7 MUALLEM S, 1988, J MEMBRANE BIOL, V102, P153, DOI 10.1007/BF01870453 PALMER LG, 1988, BIOPHYS J, V55, P779 ROOS A, 1981, PHYSIOL REV, V61, P296 SKOU J C, 1992, News in Physiological Sciences, V7, P95 SMITH JB, 1987, J BIOL CHEM, V262, P11988 Stewart P. A., 1981, UNDERSTAND ACID BASE NR 20 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 1993 VL 70 IS 2 BP 146 EP 150 DI 10.1016/0378-5955(93)90152-Q PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300003 PM 8294258 ER PT J AU DURHAM, D MATSCHINSKY, FM RUBEL, EW AF DURHAM, D MATSCHINSKY, FM RUBEL, EW TI ALTERED MALATE-DEHYDROGENASE ACTIVITY IN NUCLEUS MAGNOCELLULARIS OF THE CHICKEN FOLLOWING COCHLEA REMOVAL SO HEARING RESEARCH LA English DT Article DE DEAFFERENTATION; OXIDATIVE METABOLISM; AUDITORY; COCHLEAR NUCLEUS ID STEM AUDITORY NUCLEI; CYTOCHROME-OXIDASE; AFFERENT INFLUENCES; PROTEIN-SYNTHESIS; ADULT-MOUSE; SYSTEM; NEURONS; DEPRIVATION AB The metabolism of second order auditory neurons in nucleus magnocellularis (NM) in the chick brainstem can be profoundly altered when excitatory input from the cochlea is removed. Within hours of cochlea removal, NM neurons show an increase in histochemical staining for the Kreb's cycle enzyme succinate dehydrogenase (SDH), followed in several days by decreases in SDH staining. We examined the activity of another Kreb's cycle enzyme, malate dehydrogenase (MDH) using a histochemical stain and a sensitive quantitative biochemical assay far comparison. We found changes in MDH staining similar in time course and magnitude to those of SDH; within 4 h of cochlea removal, MDH activity increases in ipsilateral NM neurons. By 9 days after cochlea removal MDH activity decreases, although not to the same degree as seen with SDH. Biochemical measurements of MDH activity also showed an early increase in activity in ipsilateral NM, followed at 9 days survival by a decrease in activity. Biochemical measurements of the activity of other enzymes in NM may be useful in further defining the metabolic consequences of deafferentation. C1 UNIV WASHINGTON,DEPT OTOLARYNGOL HEAD & NECK SURG,HEARING DEV LABS,SEATTLE,WA 98195. UNIV PENN,DEPT BIOCHEM & BIOPHYS,PHILADELPHIA,PA 19104. CR BOORD RL, 1969, ANN NY ACAD SCI, V167, P186, DOI 10.1111/j.1749-6632.1969.tb20444.x 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 DIETRICH WD, 1981, J NEUROSCI, V1, P929 DURHAM D, 1985, J COMP NEUROL, V231, P446, DOI 10.1002/cne.902310404 DURHAM D, 1985, Society for Neuroscience Abstracts, V11, P448 GODFREY DA, 1983, HEARING RES, V9, P3, DOI 10.1016/0378-5955(83)90129-6 HEIL P, 1986, J COMP NEUROL, V252, P279, DOI 10.1002/cne.902520302 HEVNER RF, 1990, J NEUROSCI, V10, P1331 HINTZ CS, 1980, AM J PHYSIOL, V239, pC58 HYDE GE, 1990, J COMP NEUROL, V297, P329, DOI 10.1002/cne.902970302 HYDE GE, 1993, IN PRESS J COMP NEUR HYDE GE, 1993, IN PRESS J NEUROSCI HYSON RL, 1989, J NEUROSCI, V9, P2835 KAGEYAMA GH, 1986, J COMP NEUROL, V246, P212, DOI 10.1002/cne.902460207 KATO T, 1973, J NEUROCHEM, V20, P151, DOI 10.1111/j.1471-4159.1973.tb12112.x LAND PW, 1987, J COMP NEUROL, V262, P78, DOI 10.1002/cne.902620107 LAND PW, 1987, BRAIN RES, V425, P178, DOI 10.1016/0006-8993(87)90497-5 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 Lowry OH, 1972, FLEXIBLE SYSTEM ENZY MATSCHIN.FM, 1968, J HISTOCHEM CYTOCHEM, V16, P29 MAWE GM, 1986, J COMP NEUROL, V249, P381, DOI 10.1002/cne.902490305 PARKS TN, 1978, J COMP NEUROL, V180, P439, DOI 10.1002/cne.901800303 Pearse A.G.E, 1980, HISTOCHEMISTRY THEOR RICHARDSON BE, 1990, HEARING RES, V46, P53 ROBB PJ, 1988, BLOCKADE 8TH NERVE A RUBEL EW, 1992, J COMP NEUROL, V318, P415, DOI 10.1002/cne.903180406 RUBEL E W, 1991, Brain Dysfunction, V4, P55 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 STEWARD O, 1985, J COMP NEUROL, V231, P385, DOI 10.1002/cne.902310308 YIP VS, 1987, BRAIN RES, V406, P157, DOI 10.1016/0006-8993(87)90780-3 NR 33 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 1993 VL 70 IS 2 BP 151 EP 159 DI 10.1016/0378-5955(93)90153-R PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300004 PM 8294259 ER PT J AU BROWN, AM AF BROWN, AM TI DISTORTION IN THE COCHLEA - ACOUSTIC F(2)-F(1) AT LOW STIMULUS LEVELS SO HEARING RESEARCH LA English DT Article DE COCHLEAR DISTORTION; ACOUSTIC EMISSION; NONLINEARITY; HAIR CELL MOTILITY ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; BASILAR-MEMBRANE; RESPONSES; TONES; ELECTROMOTILITY; SENSITIVITY; MOTILITY; PRODUCTS AB The stimulus level and frequency dependence of the quadratic difference tone (QDT) measured as an otoacoustic emission in the ear canal has been investigated in the guinea pig and compared with simultaneously measured cubic difference tone (CDT) and with the round window electrical response. Acoustic QDT level tended to be highly labile. Growth of the ear canal response with covaried stimuli was very gradual (slope < 0.5). Acoustic and CM responses shelved similar behaviour when f(2) alone was incremented. The QDT was strongly dependent on stimulus frequency separation for high frequency stimuli. It is suggested that, at low stimulus levels and high frequencies, the acoustic QDT may originate in the 'tonic' motile responses of outer hair cells as they follow the envelope of the two-tone stimulus. RP BROWN, AM (reprint author), UNIV SUSSEX,EXPTL PSYCHOL LAB,BRIGHTON BN1 9QG,ENGLAND. CR BROWN AM, 1985, HEARING RES, V19, P191, DOI 10.1016/0378-5955(85)90138-8 BROWN AM, 1989, 31ST INT C PHYS SCI BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BROWN AM, 1990, MECH BIOPHYSICS HEAR, P164 BROWN AM, 1988, HEARING RES, V34, P27, DOI 10.1016/0378-5955(88)90048-2 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 FAHEY PF, 1988, COCHLEAR MECHANISMS, P405 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HALL JL, 1974, J ACOUST SOC AM, V56, P1818, DOI 10.1121/1.1903519 HALL JL, 1972, J ACOUST SOC AM, V51, P1863, DOI 10.1121/1.1913045 HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 HUMES LE, 1983, J ACOUST SOC AM HUMES LE, 1979, J ACOUST SOC AM, V66, P1064, DOI 10.1121/1.383325 HUMES LE, 1980, J ACOUST SOC AM, V67, P2073, DOI 10.1121/1.384451 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 LEPAGE EL, 1990, MECH BIOPHYSICS HEAR, P278 NUTTALL, 1993, J ACOUST SOC AM, V93, P2061 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1992, P ROY SOC B-BIOL SCI, V247, P97, DOI 10.1098/rspb.1992.0014 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 SMOORENBURG GF, 1976, J ACOUST SOC AM, V59, P945, DOI 10.1121/1.380954 TONNDORF J, 1973, BASIC MECHANISMS HEA, P11 WENNER CH, 1967, J ACOUST SOC AM, V43, P77 ZUREK PM, 1976, J ACOUST SOC AM, V60, P155, DOI 10.1121/1.381057 ZWICKER E, 1979, HEARING RES, V1, P283, DOI 10.1016/0378-5955(79)90001-7 Zwicker E., 1955, Acustica, V5 NR 31 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 1993 VL 70 IS 2 BP 160 EP 166 DI 10.1016/0378-5955(93)90154-S PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300005 PM 8294260 ER PT J AU BROWN, JN MILLER, JM ALTSCHULER, RA NUTTALL, AL AF BROWN, JN MILLER, JM ALTSCHULER, RA NUTTALL, AL TI OSMOTIC PUMP IMPLANT FOR CHRONIC INFUSION OF DRUGS INTO THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; TETRODOTOXIN; COCHLEA; AUDITORY NERVE; SYNAPSE FLATTENING ID GUINEA-PIG; COCHLEAR NUCLEUS; POTENTIALS; NEOMYCIN; NEURONS; DENSITY AB Continuous long-term delivery of experimental drugs to the cochlea of a small animal, such as a young guinea pig, presents several technical problems. A method of placing and securing a cannula-osmotic pump system is described in this paper. Guinea pigs (225-410 g) were unilaterally implanted with an Alzet micro-pump and cannula for delivery of 20 mM tetrodotoxin (mt) (six animals) or saline (three animals) for three days (1 mu l/h). Auditory brainstem responses (ABRs) were recorded under light anesthesia on post-implant day 1 and day 3 and compared with pre-implant baseline values. In all six cochleas infused with TTX, most frequencies showed a 30-60dB decrease in sensitivity within 24 h. Saline control animals showed little or no change from baseline sensitivity for most frequencies. In three TTX-infused animals, the cannula-pump unit was removed on day 3, and ABRs were followed during recovery. Most frequencies returned to, or near, pre-implant levels after pump removal but recovery times varied. By day 6, all animals had recovered post-surgical weight loss and showed a gain of 10-40 g. Brains and cochleas were removed and processed for sectioning. Assessment of the cochlear nucleus of non-recovery TTX-treated animals showed a deafness-related flattening of auditory nerve active zones on the treated side. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR ALTSCHULER RA, 1990, 20TH SOC NEUR ANN M, P763 BORN DE, 1988, J NEUROSCI, V8, P901 GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 KINGMA GG, 1992, J NEUROSCI METH, V45, P127, DOI 10.1016/0165-0270(92)90050-N LEAKE PA, 1989, CONSEQUENCES CHRONIC, P268 LYNCH HJ, 1980, NEUROENDOCRINOLOGY, V31, P106, DOI 10.1159/000123059 MILLER JM, 1991, 4 INT C EFF NOIS AUD MORI N, 1986, ACTA OTO-LARYNGOL, V101, P217, DOI 10.3109/00016488609132830 NUTTALL AL, 1977, ACTA OTO-LARYNGOL, V83, P393, DOI 10.3109/00016487709128863 OHLSEN KA, 1991, CIRC RES, V69, P509 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 REES S, 1985, BRAIN RES, V325, P370, DOI 10.1016/0006-8993(85)90343-9 RYAN AF, 1987, J COMP NEUROL, V255, P606, DOI 10.1002/cne.902550411 SIE K, 1989, EARLY EFFECTS 8TH NE, P9 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 ZAPPIA JJ, 1989, HEARING RES, V40, P29, DOI 10.1016/0378-5955(89)90096-8 NR 17 TC 103 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 NOV PY 1993 VL 70 IS 2 BP 167 EP 172 DI 10.1016/0378-5955(93)90155-T PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300006 PM 8294261 ER PT J AU VETTER, DE SALDANA, E MUGNAINI, E AF VETTER, DE SALDANA, E MUGNAINI, E TI INPUT FROM THE INFERIOR COLLICULUS TO MEDIAL OLIVOCOCHLEAR NEURONS IN THE RAT - A DOUBLE-LABEL STUDY WITH PHA-L AND CHOLERA-TOXIN SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM; ACOUSTIC PATHWAYS; SUPERIOR OLIVE; RETROGRADE LABELING; ANTEROGRADE LABELING; IMMUNOCYTOCHEMISTRY ID COCHLEAR EFFERENT NEURONS; SUPERIOR OLIVARY COMPLEX; TMB REACTION-PRODUCT; BRAIN-STEM; GUINEA-PIG; HORSERADISH-PEROXIDASE; FLUORESCENT TRACERS; ACOUSTIC TRAUMA; TRAPEZOID BODY; ALBINO-RAT AB The inferior colliculus provides a strong descending influence capable of modulating the excitability levels of olivocochlear neurons (Rajan, 1990). In an attempt to anatomically demonstrate this pathway in rats, an experimental paradigm was designed by which anterogradely transported Phaseolus vulgaris-leucoagglutinin (PHA-L), which delineates axonal arbors, and retrogradely transported cholera toxin B subunit alone (CT-B) or conjugated to horseradish peroxidase (CT-HRP), which delineate dendritic arbors, are visualized in the same brainstem sections. PHA-L was injected unilaterally into the central nucleus of the inferior colliculus of adult rats 5-9 days prior to injection of CT-B or CT-HRP into either the contralateral or the ipsilateral cochlea. Descending collicular axons labeled with PHA-L densely innervate the Ventral nucleus of the trapezoid body (VNTB), which contains neurons of the medial olivocochlear system (MOCS), but do not enter the lateral superior olive, where the neurons of the lateral olivocochlear system (LOCS) are found. The collicular projection to VNTB is largely ipsilateral and supplies mostly the ventral half of the nucleus. Within VNTB, the collicular fibers intermingle with dendrites and, to a lesser extent, cell bodies of MOCS. Collicular boutons, predominantly of the en passant type, are often observed in close apposition to dendrites and, less frequently, cell bodies of both crossed and uncrossed MOCS. These light microscopic results suggest the existence of direct, synaptic contacts between descending collicular axons and ipsilateral crossed and uncrossed MOCS. Numerous collicular boutons were also seen at a distance from MOCS, suggesting that they establish synapses with other neuron types of the VNTB that do not send their axons to the cochlea. C1 UNIV CONNECTICUT,GRAD PROGRAM BIOBEHAV SCI,NEUROMORPHOL LAB,STORRS,CT 06269. UNIV SALAMANCA,FAC MED,DEPT BIOL CELULAR & PATOL,E-37007 SALAMANCA,SPAIN. RI Saldana, Enrique/C-4017-2011 CR ADAMS JC, 1983, J COMP NEUROL, V215, P275, DOI 10.1002/cne.902150304 ANDERSEN RA, 1980, J COMP NEUROL, V194, P649, DOI 10.1002/cne.901940311 ASCHOFF A, 1988, EXP BRAIN RES, V71, P252 ASCHOFF A, 1987, J COMP NEUROL, V264, P56, DOI 10.1002/cne.902640106 ASCHOFF A, 1988, EXP BRAIN RES, V71, P241 BISHOP AL, 1987, HEARING RES, V31, P175, DOI 10.1016/0378-5955(87)90124-9 BORG E, 1973, ACTA MORPHOL NEER SC, V11, P49 BRUCE K, 1992, J NEUROSCI METH, V45, P23, DOI 10.1016/0165-0270(92)90040-K CAICEDO A, 1993, J COMP NEUROL, V328, P377, DOI 10.1002/cne.903280305 CAMPBELL JP, 1988, HEARING RES, V35, P271, DOI 10.1016/0378-5955(88)90124-4 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 FAYELUND H, 1986, ANAT EMBRYOL, V175, P35, DOI 10.1007/BF00315454 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 FUJII M, 1984, Neuroscience Research, V1, P153, DOI 10.1016/S0168-0102(84)80012-7 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GROENEWEGEN HJ, 1990, HDB CHEM NEUROANATOM, V8, P47 HASHIKAWA T, 1983, J COMP NEUROL, V219, P241, DOI 10.1002/cne.902190209 HELFERT RH, 1988, J NEUROSCI, V8, P3111 KISS A, 1983, EXP BRAIN RES, V52, P315 KUWABARA N, 1991, J COMP NEUROL, V314, P684, DOI 10.1002/cne.903140405 LIANG F, 1991, J COMP NEUROL, V311, P356 LIANG FY, 1989, J NEUROSCI METH, V28, P155, DOI 10.1016/0165-0270(89)90031-9 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 MOORE RY, 1966, EXP NEUROL, V14, P429, DOI 10.1016/0014-4886(66)90127-0 Mugnaini E, 1985, HDB CHEM NEUROANAT 1, V4, P436 OLUCHA F, 1985, J NEUROSCI METH, V13, P131, DOI 10.1016/0165-0270(85)90025-1 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V RAJAN R, 1990, BRAIN RES, V506, P192, DOI 10.1016/0006-8993(90)91251-B RASMUSSEN GL, 1964, NEUROLOGICAL ASPECTS, P5 Rasmussen G.L, 1955, AM J PHYSIOL, V183, P653 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 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 RYE DB, 1984, J HISTOCHEM CYTOCHEM, V32, P1145 SALDANA E, 1909, SOC NEUR ABSTR, V16, P716 SALDANA E, 1993, MAMMALIAN COCHLEAR N, P153 SALDANA E, 1992, J COMP NEUROL, V319, P417, DOI 10.1002/cne.903190308 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 STRUTZ J, 1984, BRAIN RES, V299, P174, DOI 10.1016/0006-8993(84)90803-5 STRUTZ J, 1980, NEUROSCI LETT, V17, P227, DOI 10.1016/0304-3940(80)90027-0 STRUTZ J, 1981, ANN OTO RHINOL LARYN, V90, P158 SYKA J, 1988, AUDITORY PATHWAY STR, P299 TAKEYAMA M, 1992, ACTA OTO-LARYNGOL, V112, P205 THOMPSON AM, 1989, ASSON RES OTOLARYNGO, V12, P344 THOMPSON AM, 1988, J NEUROSCI METH, V25, P13, DOI 10.1016/0165-0270(88)90115-X THOMPSON AM, 1991, J COMP NEUROL, V303, P267, DOI 10.1002/cne.903030209 THOMPSON GC, 1986, J COMP NEUROL, V254, P246, DOI 10.1002/cne.902540208 VANNOORT J, 1969, STRUCTURE CONNECTION, P1 VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 VETTER DE, 1990, ARCH ITAL BIOL, V128, P331 VETTER DE, 1992, ANAT EMBRYOL, V185, P1, DOI 10.1007/BF00213596 VETTER D E, 1990, Society for Neuroscience Abstracts, V16, P716 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 Warr W.B., 1992, Springer Handbook of Auditory Research, V1, P410 WARR WB, 1993, ASS RES OT ABSTR, V16, P125 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WEINBERG RJ, 1991, J HISTOCHEM CYTOCHEM, V34, P1443 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WHITE JS, 1984, SOC NEUR ABSTR, V14, P393 WOUTERLOOD FG, 1985, BRAIN RES, V326, P188, DOI 10.1016/0006-8993(85)91402-7 WOUTERLOOD FG, 1987, J HISTOCHEM CYTOCHEM, V35, P131 NR 62 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 NOV PY 1993 VL 70 IS 2 BP 173 EP 186 DI 10.1016/0378-5955(93)90156-U PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300007 PM 8294262 ER PT J AU POLLICE, PA BROWNELL, WE AF POLLICE, PA BROWNELL, WE TI CHARACTERIZATION OF THE OUTER HAIR-CELLS LATERAL WALL MEMBRANES SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; SUBSURFACE CISTERNAE; C-6-NBD-CERAMIDE; DIOC(6); GOLGI APPARATUS; ENDOPLASMIC RETICULUM ID FLUORESCENT CERAMIDE ANALOG; GOLGI-APPARATUS; LIVING CELLS; ENDOPLASMIC-RETICULUM; SUBSURFACE CISTERNAE; PHYSICAL-PROPERTIES; ANIMAL-CELLS; FIXED CELLS; ELECTROMOTILITY; LOCALIZATION AB We examined the properties of outer hair cell (OHC) lateral wall membranes by application of 2 fluorescent membrane probes. The markers, C-6-NBD-Ceramide and DiOC(6), have been used in other cell types to label Golgi apparatus and endoplasmic reticulum, respectively. In living isolated OHCs NBD-Ceramide demonstrated uninterrupted fluorescence along the OHC lateral wall, while DiOC(6) labeling proved punctate and notably less uniform in this region. In aldehyde-fixed isolated OHCs both probes exhibited distinct, continuous lateral wall fluorescence. Fixed preparations of the organ of Corti labeled with each probe demonstrated diffuse fluorescence throughout the inner hair cell cytoplasm unlike the uniform, circumferential lateral wall fluorescence seen in OHCs. OHCs exposed to salicylate following NBD-Ceramide labeling displayed patchy, less distinct labeling along the OHC lateral wall. The thickness of lateral wall fluorescence in salicylate exposed cells was 49% greater than control OHCs. We interpreted the salicylate induced change in lateral wall labeling as a fluorescent representation of previously described ultrastructural dilatation and vesiculation of the subsurface cisternae. The distribution of these 2 fluorescent probes along OHC lateral wall membranes suggests that the OHCs subsurface cisternae are neither Golgi nor ER, but share characteristics of both. C1 JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,HNS,DEPT OTOLARYNGOL,BALTIMORE,MD 21205. CR BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DUNPHY WG, 1985, CELL, V42, P13, DOI 10.1016/S0092-8674(85)80097-0 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A FORGE A, 1993, HEARING RES, V64, P175, DOI 10.1016/0378-5955(93)90003-J GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 JOHNSON LV, 1981, J CELL BIOL, V88, P526, DOI 10.1083/jcb.88.3.526 JOHNSON LV, 1980, P NATL ACAD SCI-BIOL, V77, P990, DOI 10.1073/pnas.77.2.990 LEE C, 1988, CELL, V54, P37, DOI 10.1016/0092-8674(88)90177-8 LIPSKY NG, 1985, SCIENCE, V228, P745, DOI 10.1126/science.2581316 PAGANO R E, 1990, Current Opinion in Cell Biology, V2, P652, DOI 10.1016/0955-0674(90)90107-P PAGANO RE, 1990, BIOCHEM SOC T, V18, P361 PAGANO RE, 1989, J CELL BIOL, V109, P2067, DOI 10.1083/jcb.109.5.2067 PAGANO RE, 1988, BIOCHEMISTRY-US, V27, P4439, DOI 10.1021/bi00412a034 PAGANO RE, 1991, J CELL BIOL, V113, P1267, DOI 10.1083/jcb.113.6.1267 PAGANO RE, 1989, METHOD CELL BIOL, V29, P75 SAITO K, 1983, CELL TISSUE RES, V229, P467 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SIEGEL JH, 1986, J NEUROCYTOL, V15, P311, DOI 10.1007/BF01611434 SLEPECKY NB, 1992, J NEUROCYTOL, V21, P374, DOI 10.1007/BF01191705 TERASAKI M, 1984, CELL, V38, P101, DOI 10.1016/0092-8674(84)90530-0 NR 22 TC 32 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 NOV PY 1993 VL 70 IS 2 BP 187 EP 196 DI 10.1016/0378-5955(93)90157-V PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300008 PM 8294263 ER PT J AU KOMUNE, S NAKAGAWA, T HISASHI, K KIMITSUKI, T UEMURA, T AF KOMUNE, S NAKAGAWA, T HISASHI, K KIMITSUKI, T UEMURA, T TI MECHANISM OF LACK OF DEVELOPMENT OF NEGATIVE ENDOCOCHLEAR POTENTIAL IN GUINEA-PIGS WITH HAIR CELL LOSS SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; ENDOLYMPH; PERILYMPH; PERMEABILITY; CONDUCTANCE ID MUSTARD-N-OXIDE; BASOLATERAL MEMBRANE; COCHLEAR PARTITION; KANAMYCIN SULFATE; ETHACRYNIC-ACID; PERMEABILITY; EXCHANGER; POTASSIUM; TRANSPORT; CHLORIDE AB The endocochlear potential (EP), and the concentration of K+, Na+ and Cl- were measured simultaneously in endolymph of guinea pigs. The EP was 85.6+/-0.8 mV in normal guinea pigs, 90.7+/-0.8 mV in the kanamycin-treated animals, and 91.6+/-1.2 mV in those treated with nitrogen mustard-N-oxide (NMNO). Thirty minutes after the onset of anoxia, the EP (negative EP) was -29.3+/-1.0 mV in the normal group, -0.2+/-1.0 mV in the kanamycintreated group, and -1.9+/-1.3 mV in the NMNO-treated group. The permeability coefficients of K+ (P-k), Na+ (P-na) and Cl-(P-cl) across the endolymph-perilymph barrier during the period of 20-30 min after the onset of anoxia in the normal group were (341.6+38.2)x10(-9) cm(3) sec(-1), (53.0+/-8.1)x10(-9) cm(3) sec(-1) and (111.8+/-27.2)x10(-9) cm(3) sec(-1), respectively. P-k was decreased in the kanamycin- and NMNO-treated groups. P-na did not differ between the normal and treated groups. P-d was increased in the kanamycin- and NMNO-treated groups. The K+:Na+:Cl- permeability ratio was 1:0.16:0.32 in the normal group, 1:1.12:11.6 in the kanamycin-treated group, and 1:0.44:5.60 in the NMNO-treated group. The results indicate that the lack of development of a negative EP in the kanamycin- and NMNO-treated guinea pigs was attributable to the increased P-d and the decreased P-k across the endolymph-perilymph barrier, probably the organ of Corti, during anoxia. RP KOMUNE, S (reprint author), KYUSHU UNIV,FAC MED,DEPT OTORHINOLARYNGOL,HIGASHI KU,3-1-1 MAIDASHI,FUKUOKA 812,JAPAN. CR Ammann D., 1986, ION SELECTIVE MICROE ASAKUMA S, 1980, OTOLARYNG HEAD NECK, V88, P188 ASAKUMA S, 1984, ACTA OTO-LARYNGOL, V97, P273, DOI 10.3109/00016488409130989 ASAKUMA S, 1979, ARCH OTOLARYNGOL, V105, P145 BORON WF, 1989, KIDNEY INT, V36, P392, DOI 10.1038/ki.1989.208 BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 ERICSON A, 1982, AM J PHYSIOL, V243, pC140 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 FUJIMOTO M, 1976, JPN J PHYSIOL, V26, P631 GRINSTEIN S, 1986, J MEMBRANE BIOL, V90, P1, DOI 10.1007/BF01869680 HOTOKEBUCHI N, 1987, JPN J PHYSIOL, V37, P797, DOI 10.2170/jjphysiol.37.797 IKEDA K, 1989, ANN OTO RHINOL LARYN, V98, P379 KOMUNE S, 1982, ARCH OTOLARYNGOL, V108, P334 KOMUNE S, 1983, OTOLARYNG HEAD NECK, V91, P427 KONISHI T, 1980, EXP BRAIN RES, V40, P457 Konishi T, 1967, Acta Otolaryngol, V64, P107, DOI 10.3109/00016486709139097 KONISHI T, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 KONISHI T, 1979, ACTA OTO-LARYNGOL, V87, P506, DOI 10.3109/00016487909126459 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P359, DOI 10.1007/BF00588214 MARCUS DC, 1984, AM J PHYSIOL, V247, pC240 MORI H, 1985, HEARING RES, V17, P227, DOI 10.1016/0378-5955(85)90067-X OZAWA T, 1988, PFLUG ARCH EUR J PHY, V412, P509, DOI 10.1007/BF00582540 SASAKI S, 1988, J CLIN INVEST, V81, P1004, DOI 10.1172/JCI113410 SASAKI S, 1988, J CLIN INVEST, V81, P194, DOI 10.1172/JCI113294 SELLICK PM, 1975, PROG NEUROBIOL, V5, P335 WEINER ID, 1991, J CLIN INVEST, V87, P1551 WINGO CS, 1990, KIDNEY INT, V38, P985, DOI 10.1038/ki.1990.302 NR 27 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 NOV PY 1993 VL 70 IS 2 BP 197 EP 204 DI 10.1016/0378-5955(93)90158-W PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300009 PM 8294264 ER PT J AU XU, SA SHEPHERD, RK CHEN, Y CLARK, GM AF XU, SA SHEPHERD, RK CHEN, Y CLARK, GM TI PROFOUND HEARING-LOSS IN THE CAT FOLLOWING THE SINGLE COADMINISTRATION OF KANAMYCIN AND ETHACRYNIC-ACID SO HEARING RESEARCH LA English DT Article DE OTOTOXICITY; NEPHROTOXICITY; HEARING LOSS; ETHACRYNIC ACID; KANAMYCIN; COCHLEAR IMPLANT ID SPIRAL GANGLION-CELLS; GUINEA-PIG COCHLEA; AUDITORY-NERVE; IMPLANTATION; KITTENS; DAMAGE AB Co-administration of kanamycin (KA) with the loop diuretic ethacrynic acid (EA) has previously been shown to produce a rapid and profound hearing loss in guinea pigs. In the present study we describe a modified technique for developing a profound hearing loss in cats. By monitoring the animal's hearing status during the intravenous infusion of EA the technique minimizes the effects of individual variability to the drug regime. Seven cats received a subcutaneous injection of KA (300 mg/kg) followed by intravenous infusion of EA (1 mg/min). Click-evoked auditory brainstem responses (ABRs) were recorded to monitor the animal's hearing during the infusion. When the ABR thresholds rose rapidly to levels in excess of 90 dB SPL the infusion of EA was stopped. This occurred at EA doses of 10-25 mg/kg, indicating considerable individual variability to the deafening procedure. However, there was a strong negative correlation (r = -0.93) between the EA dose and body weight which accounted for much of this variability. Subsequent ABR monitoring showed that this profound hearing loss was both bilateral and permanent. Significantly, blood urea and creatinine levels, monitored for periods of up to three days after the procedure, remained within the normal range. Furthermore, there was no clinical evidence of renal dysfunction as indicated by weight loss or oliguria. Cochlear histopathology, examined after a two months to three year survival period, showed an absence of all inner and outer hair cells in the majority of cochleas. The extent of loss of spiral ganglion cells was dependent on their distance from the round window and the period of survival following the deafening procedure. Clearly, the degeneration of spiral ganglion cells continued for several years following the initial insult. Finally, we observed no evidence of renal histopathology. In conclusion, the co-administration of KA and EA produces a profound hearing loss in cats without evidence of renal impairment. Monitoring the animal's hearing status during the procedure ensures that the dose of EA can be optimised for individual animals. Moreover, it may be possible to adapt this procedure to produce animal models with controlled high frequency hearing losses. C1 UNIV MELBOURNE,DEPT OTOLARYNGOL,PARKVILLE,VIC 3052,AUSTRALIA. RI Shepherd, Robert/I-6276-2012 CR BREDBERG G, 1973, ADV OTORHINOLARYNGOL, V22, P102 BROWN M, 1992, HEARING RES, V59, P224, DOI 10.1016/0378-5955(92)90119-8 Brummett RE, 1982, AMINOGLYCOSIDES MICR, P419 BRUMMETT RE, 1979, ARCH OTOLARYNGOL, V105, P240 BURKARD R, 1984, ELECTROEN CLIN NEURO, V57, P83, DOI 10.1016/0013-4694(84)90010-5 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DUCKERT LG, 1983, LARYNGOSCOPE, V93, P841 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 Harrison R V, 1991, Acta Otolaryngol Suppl, V489, P5 HAWKINS J. E., 1959, ANN OTOL RHINOL AND LARYNGOL, V68, P698 JOHNSON AH, 1970, SOUTHERN MED J, V63, P511 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 LEAKEJONES PA, 1980, SEM, V3, P427 MATHOG RH, 1969, NEW ENGL J MED, V280, P1223, DOI 10.1056/NEJM196905292802208 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 MITRUKA BM, 1977, CLIN BIOCH HEMATOLOG, P145 NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 ORSULAKOVA A, 1981, ACTA OTOLARYNGOL STO, V93, P43 PUJOL R, 1970, J COMP NEUROL, V139, P115, DOI 10.1002/cne.901390108 ROMAND R, 1986, HEARING RES, V21, P161, DOI 10.1016/0378-5955(86)90036-5 RUSSELL NJ, 1979, ACTA OTO-LARYNGOL, V88, P369, DOI 10.3109/00016487909137181 SCHUKNECHT HF, 1984, PATHOLOGY EAR, P331 SHEPHERD RK, 1993, P AUST NEUROSCI SOC, V4, P112 SHEPHERD RK, 1988, STUDIES PEDIATRIC AU SHEPHERD RK, 1984, P AUST PHYSL PHARM S, V14 SHEPHERD RK, 1994, IN PRESS HEAR RES SHEPHERD RK, 1985, HEARING RES, V18, P105, DOI 10.1016/0378-5955(85)90001-2 SIMMONS FB, 1967, LARYNGOSCOPE, V77, P171, DOI 10.1288/00005537-196702000-00003 STEBBINS WC, 1969, ANN OTO RHINOL LARYN, V78, P1007 SUTTON D, 1983, ANN OTO RHINOL LARYN, V92, P53 SYKA J, 1984, SCAN AUDIOL S, V14, P63 HUY PTB, 1983, HEARING RES, V11, P191, DOI 10.1016/0378-5955(83)90078-3 WALSH EJ, 1987, HEARING RES, V28, P97, DOI 10.1016/0378-5955(87)90157-2 WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 XU SA, 1990, P AUST PHYSL PHARM S, V21, P44 Yamane H, 1988, Acta Otolaryngol Suppl, V447, P28 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P1 NR 38 TC 85 Z9 90 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 1993 VL 70 IS 2 BP 205 EP 215 DI 10.1016/0378-5955(93)90159-X PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300010 PM 8294265 ER PT J AU CAREY, MB ZELICK, R AF CAREY, MB ZELICK, R TI THE EFFECT OF SOUND LEVEL, TEMPERATURE AND DEHYDRATION ON THE BRAIN-STEM AUDITORY-EVOKED POTENTIAL IN ANURAN AMPHIBIANS SO HEARING RESEARCH LA English DT Article DE FROG; ANURAN; EVOKED POTENTIAL; AUDITORY BRAIN-STEM RESPONSE; TEMPERATURE; DEHYDRATION ID SUPERIOR OLIVARY COMPLEX; CENTRAL-NERVOUS-SYSTEM; DORSAL MEDULLARY; FIBER RESPONSE; TREE FROG; BULLFROG; MIDBRAIN; HYPOXIA; STATES AB Brainstem auditory evoked potentials (BAEPs) were used to examine the effects of sound level, temperature, and dehydration on the auditory pathway of three species of anuran amphibians: Rana pipiens, Bufo americanus and B. terrestris. BAEP latency, amplitude and a measure of threshold were determined for all stimulus and test conditions. Threshold values obtained with this technique were similar to other neural measures of threshold in anurans, and were stable for repeated measures within 12 h and over three days. Transient changes in temperature caused non-linear changes in BAEP threshold and latency. Above 20 degrees C small threshold shifts were elicited, while below 20 degrees C we observed rapid deterioration of threshold. Animals acclimated to a cold temperature (14 degrees C) were acoustically less sensitive than warm (21 degrees C) animals, even when both groups were tested at colder temperatures. Because peripheral components of the BAEP were most affected by both transient and acclimation (longer term) cooling and warming, the sensory epithelium appears to be the most temperature-sensitive component of the auditory pathway. Dehydrated frogs showed no auditory dysfunction until a critical level of dehydration was reached. More dehydration-resistant species (B. terrestris and B. americanus) were less susceptible to BAEP degradation near their critical dehydration level. C1 PORTLAND STATE UNIV,DEPT BIOL,PORTLAND,OR 97207. CR ALVARADO RH, 1972, PHYSIOL ZOOL, V45, P43 ANDREW RD, 1991, J NEUROL SCI, V101, P7, DOI 10.1016/0022-510X(91)90013-W ARIEFF AI, 1976, KIDNEY INT, V10, P104, DOI 10.1038/ki.1976.82 ATTIAS J, 1991, J THERM BIOL, V16, P249, DOI 10.1016/0306-4565(91)90012-Q BISHOP LG, 1967, MOL MECHANISMS TEMPE, P263 CAMPBELL HW, 1969, PHYSIOL ZOOL, V42, P183 Capranica R.R., 1976, P551 COREY DP, 1983, J NEUROSCI, V3, P962 CORWIN JT, 1982, ELECTROEN CLIN NEURO, V54, P629, DOI 10.1016/0013-4694(82)90117-1 COUNTER SA, 1985, COMP BIOCHEM PHYS A, V81, P837, DOI 10.1016/0300-9629(85)90916-8 COVEY E, 1991, J NEUROPHYSIOL, V66, P1080 DODGE P R, 1962, Trans Am Neurol Assoc, V87, P33 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 EWERT JP, 1974, J COMP PHYSIOL, V92, P117, DOI 10.1007/BF00694501 FAY RR, 1992, HEARING RES, V58, P9, DOI 10.1016/0378-5955(92)90003-6 FENG AS, 1991, J COMP NEUROL, V306, P613, DOI 10.1002/cne.903060407 FENG AS, 1991, J NEUROPHYSIOL, V65, P424 FUZESSERY ZM, 1983, J COMP PHYSIOL, V150, P107 GAGE PW, 1976, PHYSIOL REV, V56, P177 GERHARDT HC, 1978, SCIENCE, V199, P992, DOI 10.1126/science.199.4332.992 HALL JC, 1991, J NEUROPHYSIOL, V66, P955 HILLERY CM, 1984, SCIENCE, V225, P1037, DOI 10.1126/science.6474164 HILLMAN SS, 1980, COPEIA, P125, DOI 10.2307/1444142 HILLMAN SS, 1978, COMP BIOCHEM PHYS A, V61, P303, DOI 10.1016/0300-9629(78)90113-5 HILLMAN SS, 1987, PHYSIOL ZOOL, V60, P608 HILLMAN SS, 1988, PHYSIOL ZOOL, V61, P254 HUBL L, 1977, BEHAV PROCESS, V2, P305, DOI 10.1016/0376-6357(77)90001-8 HUBL L, 1979, J COMP PHYSIOL, V130, P17, DOI 10.1007/BF02582970 HUEY RB, 1982, BIOL REPTILIA, P26 KRAKAUER T, 1970, COMP BIOCHEM PHYSIOL, V33, P15, DOI 10.1016/0010-406X(70)90479-2 LEWIS ER, 1982, J COMP PHYSIOL, V145, P437 LEWIS ER, 1976, BRAIN BEHAV EVOLUT, V13, P196, DOI 10.1159/000123810 LOMBARD RE, 1982, J EXP BIOL, V91, P57 MACDONALD JA, 1981, J COMP PHYSIOL, V142, P411 MARSH RR, 1984, ELECTROEN CLIN NEURO, V57, P289, DOI 10.1016/0013-4694(84)90130-5 MEGELASIMMONS A, 1985, J ACOUST SOC AM, V78, P1236, DOI 10.1121/1.392892 MOHNEKE R, 1979, J COMP PHYSIOL, V130, P9, DOI 10.1007/BF02582969 NOLDY NE, 1990, NEUROPSYCHOBIOLOGY, V23, P48, DOI 10.1159/000118715 PUTNAM RW, 1981, ANIM BEHAV, V29, P502, DOI 10.1016/S0003-3472(81)80111-X ROSE GJ, 1985, J COMP PHYSIOL A, V157, P763, DOI 10.1007/BF01350073 ROSENBLUM SM, 1985, ANN OTOL RHINOL LARY, V94 SEAMAN RL, 1991, HEARING RES, V51, P301, DOI 10.1016/0378-5955(91)90046-C SHOEMAKER VH, 1964, COMP BIOCHEM PHYSIOL, V13, P261, DOI 10.1016/0010-406X(64)90121-5 Smith VDE, 1931, BIOL BULL-US, V60, P80, DOI 10.2307/1536792 SOTOS JF, 1960, PEDIATRICS, V26, P925 STAR RA, 1990, AM J MED SCI, V300, P402, DOI 10.1097/00000441-199012000-00012 STEIBLER IB, 1990, HEARING RES, V46, P63 STOCKARD JJ, 1978, ANN NEUROL, V3, P368, DOI 10.1002/ana.410030416 STRAIN GM, 1987, ELECTROEN CLIN NEURO, V67, P68, DOI 10.1016/0013-4694(87)90165-9 Thorson T, 1943, ECOLOGY, V24, P374, DOI 10.2307/1930538 THORSON TB, 1955, ECOLOGY, V36, P100, DOI 10.2307/1931435 VANDIJK P, 1990, HEARING RES, V44, P231, DOI 10.1016/0378-5955(90)90083-2 WERNER YI, 1976, J EXP ZOOL, V195, P319, DOI 10.1002/jez.1401950302 Wever EG, 1985, AMPHIBIAN EAR WILCZYNSKI W, 1984, PROG NEUROBIOL, V22, P1, DOI 10.1016/0301-0082(84)90016-9 ZAAROOR M, 1991, ELECTROEN CLIN NEURO, V80, P422, DOI 10.1016/0168-5597(91)90091-B NR 57 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 1993 VL 70 IS 2 BP 216 EP 228 DI 10.1016/0378-5955(93)90160-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300011 PM 8294266 ER PT J AU VONUNGE, M DECRAEMER, WF BAGGERSJOBACK, D DIRCKX, JJ AF VONUNGE, M DECRAEMER, WF BAGGERSJOBACK, D DIRCKX, JJ TI DISPLACEMENT OF THE GERBIL TYMPANIC MEMBRANE UNDER STATIC PRESSURE VARIATIONS MEASURED WITH A REAL-TIME DIFFERENTIAL MOIRE INTERFEROMETER SO HEARING RESEARCH LA English DT Article DE TYMPANIC MEMBRANE; ANIMAL MODEL; MOIRE INTERFEROMETRY; SHAPE; DISPLACEMENT; MECHANICAL PROPERTIES; ELASTICITY ID OTITIS-MEDIA; CHOLESTEATOMA AB It is thought that chronic middle ear disease ultimately causes changes in the stiffness and elasticity of the tympanic membrane, but it is unknown whether such changes occur early in the course of the disease. In order to analyze mechanical changes in different parts of the tympanic membrane, a full field moire interferometry technique was utilized to measure the shape and real-time displacement in response to positive and negative pressure gradients applied across the tympanic membrane. The measurements were performed on fresh isolated temporal bones from the Mongolian gerbil. In order to gain sufficient visual access to the pars tensa for the moire measurements, the tympanic bulla was opened, the tenser tympani muscle and the incudo-stapedial joint were cut, and part of the medial wall of the tympanic cavity was removed. The malleus and incus and their ligaments were kept intact. The specimens were kept continuously humidified with an evaporator or in a humid chamber, since otherwise the tympanic membrane dries out in a few minutes when its medial surface is exposed. This desiccation reduces the elasticity and cause shrinkage which results in a reduction of the height of the cone constituted by the pars tensa. Profiles of the tympanic membrane at rest and under different pressure conditions were extracted from the moire interferograms. The tympanic membrane and ossicular complex exhibit a hysteresis effect as differences in the displacement patterns under identical pressure gradients during the loading and the unloading phase; a residual displacement of the pars tensa was for instance seen after the pressure gradient across the tympanic membrane was eliminated. C1 KAROLINSKA SJUKHUSET,DEPT OTORHINOLARYNGOL,S-10401 STOCKHOLM,SWEDEN. KAROLINSKA INST,S-10401 STOCKHOLM,SWEDEN. UNIV ANTWERP,RIJKSUNIV CTR ANTWERP,BIOMED PHYS LAB,B-2020 ANTWERP,BELGIUM. CR CHOLE RA, 1989, ANN OTO RHINOL LARYN, V98, P761 DECRAEMER WF, 1980, J BIOMECH, V13, P463, DOI 10.1016/0021-9290(80)90338-3 DECRAEMER WF, 1980, J BIOMECH, V13, P559, DOI 10.1016/0021-9290(80)90056-1 DERHOVAN.J, 1971, APPL OPTICS, V10, P2734 ELNER A, 1971, ACTA OTO-LARYNGOL, V72, P255, DOI 10.3109/00016487109122480 FALK B, 1982, AM J OTOLARYNG, V3, P155, DOI 10.1016/S0196-0709(82)80048-3 FULGHUM RS, 1987, ARCH OTOLARYNGOL, V113, P521 FULGHUM RS, 1982, INFECT IMMUN, V36, P802 Fung Y., 1972, STRESS STRAIN HIST R KOBAYASHI T, 1986, ARCH OTOLARYNGOL, V112, P642 LIM D, 1970, ARCHIV OTOLARYNGOL, V91, P585 MAGNUSON B, 1978, ACTA OTO-LARYNGOL, V86, P408, DOI 10.3109/00016487809107520 MCGINN MD, 1982, ACTA OTO-LARYNGOL, V93, P61, DOI 10.3109/00016488209130853 SHANKS JE, 1988, J SPEECH HEAR DISORD, V53, P354 VONUNGE M, 1991, AM J OTOL, V12, P407 NR 15 TC 39 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 NOV PY 1993 VL 70 IS 2 BP 229 EP 242 DI 10.1016/0378-5955(93)90161-S PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300012 PM 8294267 ER PT J AU SCHWARTZ, DR SCHACHT, J MILLER, JM FREY, K ALTSCHULER, RA AF SCHWARTZ, DR SCHACHT, J MILLER, JM FREY, K ALTSCHULER, RA TI CHRONIC ELECTRICAL-STIMULATION REVERSES DEAFNESS-RELATED DEPRESSION OF ELECTRICALLY-EVOKED 2-DEOXYGLUCOSE ACTIVITY IN THE GUINEA-PIG INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE AUTORADIOGRAPHIC TECHNIQUE; [C-14] 2-DEOXYGLUCOSE; METABOLIC ACTIVITY; DEAFNESS; ELECTRICAL STIMULATION; AUDITORY BRAIN-STEM; IMPLANT ID MIDDLE LATENCY RESPONSE; COCHLEAR NUCLEUS; AUDITORY-SYSTEM; NERVE; CATS; PERFORMANCE; SURVIVAL; IMPLANT; NEURONS; RAT AB The [C-14]-2-deoxyglucose (2-DG) autoradiographic technique was used to study how auditory-related metabolic activity changes with deafness, and how chronic electrical stimulation of the deafened system may modify these changes. Guinea pigs were deafened by administration of kanamycin and ethacrynic acid. After nine weeks of deafness, the basal unstimulated uptake of 2-DG in the inferior colliculus (IC) was lower than in normal hearing control animals. 100 mu A Of acute cochlear electrical stimulation significantly increased 2-DG uptake in normal hearing animals but did not evoke a significant increase in four or nine week deafened animals. Electrically elicited 2-DG uptake in the IC is therefore depressed by prolonged deafness. In a second series of experiments, after four weeks of deafness, animals were chronically electrically stimulated via a cochlear implant 2.5-3.5 h a day, five days a week for five weeks at 100 mu A. Acute cochlear electrical stimulation following this chronic stimulation significantly increased 2-DG uptake in the contralateral IC over unstimulated levels. This suggests that some depressive effects of profound deafness on the auditory brain stem may be reduced or reversed with chronic electrical stimulation by a cochlear implant. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT NEUROL,ANN ARBOR,MI 48109. CR ALTSCHULER RA, 1990, ABSTR SOC NEUROSCI, V16, P723 BURTON MJ, 1989, ARCH OTOLARYNGOL, V115, P59 CHOUARD CH, 1983, ACTA OTO-LARYNGOL, V95, P639, DOI 10.3109/00016488309139456 Clark G., 1987, ADV OTORHINOLARYNGOL, V38, P1 DOWELL RC, 1986, ARCH OTOLARYNGOL, V112, P1054 GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 HULTCRANTZ M, 1991, HEARING RES, V54, P272, DOI 10.1016/0378-5955(91)90121-O JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 KILENY PR, 1991, ANN OTO RHINOL LARYN, V100, P563 KRAUS N, 1985, ELECTROEN CLIN NEURO, V62, P219, DOI 10.1016/0168-5597(85)90017-6 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LESPERANCE MM, 1992, ABSTR ASS RES OTOLAR, V15, P76 LOUSTEAU RJ, 1983, LARYNGOSCOPE, V97, P837 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 MILLER JM, 1991, NOISE INDUCED HEARIN, P130 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 REES S, 1985, BRAIN RES, V325, P370, DOI 10.1016/0006-8993(85)90343-9 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L RYAN AF, 1982, J COMP NEUROL, V207, P369, DOI 10.1002/cne.902070408 RYAN AF, 1988, BRAIN RES, V483, P293 SHANNONHARTMAN S, 1992, ABST ASS RES OT, V15, P54 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x TUCCI DL, 1993, IN PRESS HEAR RES WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 WEBSTER WR, 1978, NEUROSCI LETT, V10, P43, DOI 10.1016/0304-3940(78)90009-5 WEST BA, 1973, ARCH OTOLARYNGOL, V98, P32 NR 32 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 NOV PY 1993 VL 70 IS 2 BP 243 EP 249 DI 10.1016/0378-5955(93)90162-T PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MH433 UT WOS:A1993MH43300013 PM 8294268 ER PT J AU HORNER, KC HUANG, W ERRE, JP AF HORNER, KC HUANG, W ERRE, JP TI THE EFFECT OF A TAURINE MODIFIED DIET ON NORMAL AND HYDROPIC EARS OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE ENDOLYMPHATIC SAC; MENIERES DISEASE; COCHLEA; AUDITORY DISEASES; TAURINE; CALCIUM ID POSSIBLE CLINICAL-SIGNIFICANCE; INDUCED ENDOLYMPHATIC HYDROPS; POTASSIUM-INDUCED RELEASE; CELL-VOLUME REGULATION; HUMAN INFANT FORMULA; RETINAL DEGENERATION; AMINO-ACIDS; OSMOREGULATION; BRAIN; HYPONATREMIA AB Taurine is recognised as the major osmoregulating amino acid in the brain as well as other organs. Its possible influence on normal cochlear function and on hydropic cochleas of the guinea pig was investigated here. Normally hearing adult guinea pigs were placed on either a taurine-depleting diet (B-alanine) or a taurine-supplemented diet. At the end of 6 weeks the compound action potential audiograms (CAP) in the two groups were similar and appeared not to be different from a third control group receiving a non modified diet which suggested that a taurine-modified diet had not affected normal cochlear function. In hydropic ears the taurine-depleting diet was observed, in some cases, to moderately slow down the early phase of the characteristic progression of the CAP sensitivity loss. These data are in favor of a homeostatic role for taurine in the inner ear of the guinea pig under particular conditions such as osmoregulatory stress. C1 UNIV BORDEAUX 2,AUDIOL EXPTL LAB,INSERM,U229,F-33076 BORDEAUX,FRANCE. CR BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1990, HEARING RES, V46, P83, DOI 10.1016/0378-5955(90)90141-B BOWLUS RD, 1979, J EXP ZOOL, V208, P137, DOI 10.1002/jez.1402080202 DAVIES WE, 1990, TAURINE FUNCTIONAL N, P397 Davies W.E., 1985, P244 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x FORSTER RP, 1979, YALE J BIOL MED, V52, P497 FUGELLI K, 1986, J PHYSIOL-LONDON, V374, P245 GEGGEL HS, 1982, DOC OPHTHALMOL P SER, V31, P199 HARDING NJ, 1992, TINNITUS, V91, P123 HAYES KC, 1981, ANNU REV NUTR, V1, P401, DOI 10.1146/annurev.nu.01.070181.002153 HAYES KC, 1975, SCIENCE, V188, P947 HOOD JD, 1983, MENIERES DISEASE COM, P35 HORNER KC, 1993, HEARING RES, V58, P1 HORNER KC, 1991, HEARING RES, V52, P147, DOI 10.1016/0378-5955(91)90194-E HORNER KC, 1990, HEARING RES, V48, P281, DOI 10.1016/0378-5955(90)90068-Z HORNER KC, 1987, HEARING RES, V26, P319, DOI 10.1016/0378-5955(87)90067-0 HORNER KC, 1989, ACTA OTO-LARYNGOL, V108, P175, DOI 10.3109/00016488909125516 HUXTABLE RJ, 1979, J PHARMACOL EXP THER, V211, P465 IMAKI H, 1987, J NEUROSCI RES, V18, P602, DOI 10.1002/jnr.490180414 JACOBSEN JG, 1968, PHYSIOL REV, V48, P424 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x LAKE N, 1988, VISION RES, V28, P1071, DOI 10.1016/0042-6989(88)90133-2 LEHMANN A, 1984, NEUROSCI LETT, V52, P341, DOI 10.1016/0304-3940(84)90185-X NINOYU O, 1986, ARCH OTO-RHINO-LARYN, V243, P106, DOI 10.1007/BF00453759 PUKA M, 1991, BRAIN RES, V548, P267, DOI 10.1016/0006-8993(91)91131-J RABIN AR, 1973, INVEST OPHTH VISUAL, V12, P694 SCHWARTZ IR, 1983, HEARING RES, V9, P185, DOI 10.1016/0378-5955(83)90027-8 SPAETH DG, 1974, P SOC EXP BIOL MED, V147, P855 STURMAN JA, 1988, J NUTR, V118, P1169 STURMAN JA, 1984, INT J DEV NEUROSCI, V2, P121, DOI 10.1016/0736-5748(84)90003-0 SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 THURSTON JH, 1987, LIFE SCI, V40, P2539, DOI 10.1016/0024-3205(87)90076-2 THURSTON JH, 1980, LIFE SCI, V26, P1561, DOI 10.1016/0024-3205(80)90358-6 TRACHTMAN H, 1988, PEDIATR RES, V23, P35, DOI 10.1203/00006450-198801000-00008 TRACHTMAN H, 1990, PEDIATR RES, V27, P85, DOI 10.1203/00006450-199001000-00022 TRENKNER E, 1990, TAURINE FUNCTIONAL N, P129 TRENKNER E, 1991, INT J DEV NEUROSCI, V9, P77, DOI 10.1016/0736-5748(91)90075-W TYSON JE, 1989, PEDIATRICS, V83, P406 VALECALLESANDOV.MH, 1991, INT J DEV NEUROSCI, V9, P571 VANGELDER NM, 1983, NEUROCHEM RES, V8, P687 ZUMGOTTESBERGEORSULAKOVA AMM, 1986, ACTA OTO-LARYNGOL, V102, P93 NR 42 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 OCT PY 1993 VL 70 IS 1 BP 1 EP 8 DI 10.1016/0378-5955(93)90047-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000001 PM 8276726 ER PT J AU MROZ, EA NISSIM, KR LECHENE, C AF MROZ, EA NISSIM, KR LECHENE, C TI ELECTRON-PROBE ANALYSIS OF ISOLATED GOLDFISH HAIR-CELLS - IMPLICATIONS FOR PREPARING HEALTHY CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; ION COMPOSITION; ELECTRON-PROBE ANALYSIS; CULTURE MEDIA; CELL ISOLATION ID GUINEA-PIG COCHLEA; INNER-EAR; CONCANAVALIN-A; IONIC BASIS; TRANSPORT; CALCIUM; TRANSDUCTION; TRANSMISSION; CURRENTS; MODEL AB Electron-probe analysis provides an objective criterion for the physiological status of cells: whether they show the high potassium and low sodium that are expected of healthy animal cells. Preparing isolated goldfish hair cells that were healthy by this criterion required several precautions, including: limited exposure to enzymes and to simple salt solutions, a rest period between enzyme treatment and mechanical disruption of the tissue, and presence of bovine albumin in the medium both during the rest period and during mechanical dispersion and plating. Cells prepared with these precautions from the saccule and lagena and kept in an enriched medium had the following elemental composition (mole percentages with respect to phosphorus): K, 103; Na, 18; Cl, 23; S, 13; Mg, 8; Ca, 1.5. These mole percentages were close to these elements' total millimolar concentrations in the cells. If the precautions were not taken, cells with intact surface membranes (as assessed by exclusion and retention of dyes) could be obtained, but the cells had elevated cell sodium and low cell potassium. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ABRAHAM EH, 1985, AM J PHYSIOL, V248, pC154 AMSTERDAM A, 1978, METHOD CELL BIOL, V20, P362 ANNIKO M, 1984, ACTA OTO-LARYNGOL, V98, P439, DOI 10.3109/00016488409107585 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X BONE RC, 1980, LARYNGOSCOPE, V90, P1169, DOI 10.1288/00005537-198007000-00013 COHEN BJ, 1989, BIOL CELL, V66, P191, DOI 10.1016/0248-4900(89)90170-6 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1989, INT J RADIAT BIOL, V55, P1007, DOI 10.1080/09553008914551031 DULON D, 1990, J NEUROSCI, V10, P1388 FLATMAN PW, 1991, ANNU REV PHYSIOL, V53, P259, DOI 10.1146/annurev.physiol.53.1.259 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 GUTTENPLAN M, 1989, HEARING RES, V43, P47, DOI 10.1016/0378-5955(89)90058-0 HARRIS RC, 1986, AM J PHYSIOL, V251, pC815 IKEDA K, 1992, J PHYSIOL-LONDON, V447, P627 IKEDA K, 1990, EUR ARCH OTO-RHINO-L, V247, P43 IKEDA K, 1991, ARO ABSTR, V14, P125 KEHOE JS, 1978, NATURE, V274, P866, DOI 10.1038/274866a0 KONISHI T, 1983, HEARING RES, V11, P219, DOI 10.1016/0378-5955(83)90080-1 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 LARSSON L, 1986, ACTA PHYSIOL SCAND, V126, P321, DOI 10.1111/j.1748-1716.1986.tb07823.x LAWRENCE M, 1959, JAMA-J AM MED ASSOC, V171, P1927 LECHENE C, 1988, NA PLUS K PLUS PUM B, P171 LECHENE C, 1986, ANN NY ACAD SCI, V483, P270, DOI 10.1111/j.1749-6632.1986.tb34532.x LECHENE CP, 1977, ANNU REV BIOPHYS BIO, V6, P57, DOI 10.1146/annurev.bb.06.060177.000421 LIM DJ, 1985, ACTA OTO-LARYNGOL, V99, P478, DOI 10.3109/00016488509108941 MAYER ML, 1989, P NATL ACAD SCI USA, V86, P1411, DOI 10.1073/pnas.86.4.1411 MROZ EA, 1993, HEARING RES, V70, P22, DOI 10.1016/0378-5955(93)90049-7 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 ROOS A, 1981, PHYSIOL REV, V61, P296 RYAN AF, 1979, OTOLARYNG HEAD NECK, V87, P659 SALT AN, 1988, PHYSL EAR, P341 Schuknecht H. F., 1974, PATHOLOGY EAR Seglen P O, 1976, Methods Cell Biol, V13, P29, DOI 10.1016/S0091-679X(08)61797-5 SEWELL WF, 1987, J NEUROSCI, V7, P2465 SKOU J C, 1992, News in Physiological Sciences, V7, P95 SOLTOFF SP, 1988, ANNU REV PHYSIOL, V50, P207 Steinbach H. B., 1940, Cold Spring Harbor Symposia on Quantitative Biology, V8, P242 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STEWART PA, 1981, UNDERSTAND ACID BASE, P32 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 SUNOSE H, 1991, ARO ABSTR, V14, P14 SUNOSE H, 1992, ARO ABSTR, V15, P16 Tukey JW, 1977, EXPLORATORY DATA ANA, P688 WIDDOWSON EM, 1960, BIOCHEM J, V77, P30 ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 NR 53 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 OCT PY 1993 VL 70 IS 1 BP 9 EP 21 DI 10.1016/0378-5955(93)90048-6 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000002 PM 7506249 ER PT J AU MROZ, EA NISSIM, KR LECHENE, C AF MROZ, EA NISSIM, KR LECHENE, C TI RAPID RESTING ION FLUXES IN GOLDFISH HAIR-CELLS ARE BALANCED BY (NA+,K+)-ATPASE SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; CELL VOLUME; ION TRANSPORT; SODIUM-POTASSIUM ATPASE; ELECTRON-PROBE ANALYSIS; MENIERES DISEASE ID INNER-EAR; PUMP ACTIVITY; TRANSDUCTION; COCHLEA; K+; NA+,K+-ATPASE; POTENTIALS; SACCULUS; OUABAIN; MODEL AB Inhibition of sodium/potassium pumping by isolated goldfish hair cells led to a rapid gain of sodium and loss of potassium. Half-times for turnover were about 10 min, among the fastest of any cell type examined by electron-probe analysis. Pumping was inhibited by removal of extracellular potassium or by treatment with 1 mM ouabain, as expected of a classical (Na+,K+)-ATPase. The initial rate of entry of sodium after inhibition, about 4 mM/min, provided an estimate of resting sodium-entry and sodium-pumping rates. After return to control medium, cells loaded with sodium by removal of extracellular potassium could recover their normal high-potassium/low-sodium status. The initial rate of recovery (an estimate of the cells' maximum sodium-pumping rate) was sufficient to lower cell sodium by 10 mM/min. This functional estimate of hair-cell (Na+,K+)-ATPase activity was of the same order of magnitude as the biochemical activity of (Na+,K+)-ATPase previously reported for sensory epithelia of other species. The balance between sodium entry and sodium pumping determines hair-cell ionic composition, and thus the resting potential and the driving forces for sodium-coupled transport processes. Imbalance due to excess sodium entry or loss of pump capacity could have significant consequences for hair-cell function and integrity. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CELLULAR PHYSIOL LAB,BOSTON,MA 02115. RP MROZ, EA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ABRAHAM EH, 1985, AM J PHYSIOL, V248, pC154 ANNIKO M, 1984, ACTA OTO-LARYNGOL, V98, P439, DOI 10.3109/00016488409107585 ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X BROWNELL WE, 1983, J ACOUST SOC AM, V74, P792, DOI 10.1121/1.389866 COHEN BJ, 1990, AM J PHYSIOL, V258, pC24 COHEN BJ, 1989, BIOL CELL, V66, P191, DOI 10.1016/0248-4900(89)90170-6 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 HARRIS RC, 1986, AM J PHYSIOL, V251, pC815 HOFFMAN JF, 1969, J GEN PHYSIOL, V54, pS343 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P275 IKEDA K, 1990, EUR ARCH OTO-RHINO-L, V247, P43 KEITHLEY EM, 1992, ARO ABSTR, V15, P148 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, 1973, ACTA OTO-LARYNGOL, V76, P410, DOI 10.3109/00016487309121529 KONISHI T, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 Konishi T, 1966, Acta Otolaryngol, V62, P393, DOI 10.3109/00016486609119584 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 LAWRENCE M, 1959, JAMA-J AM MED ASSOC, V171, P1927 LECHENE C, 1988, NA PLUS K PLUS PUM B, P171 LECHENE C, 1986, ANN NY ACAD SCI, V483, P270, DOI 10.1111/j.1749-6632.1986.tb34532.x MATSCHINSKY FM, 1970, BIOCH MECHANISMS HEA, P265 MATSUURA S, 1971, JPN J PHYSIOL, V21, P563 MATSUURA S, 1968, SCIENCE, V160, P1117, DOI 10.1126/science.160.3832.1117 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 MROZ EA, 1993, HEARING RES, V70, P9, DOI 10.1016/0378-5955(93)90048-6 NAITO T, 1965, JAPANESE J OTOL, V68, P1628 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 RYAN AF, 1979, OTOLARYNG HEAD NECK, V87, P659 SALT AN, 1988, PHYSL EAR, P341 SCHNEIDER ME, 1987, HEARING RES, V31, P39, DOI 10.1016/0378-5955(87)90212-7 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SHAVER JLF, 1978, J CELL BIOL, V76, P278, DOI 10.1083/jcb.76.2.278 SKOU J C, 1992, News in Physiological Sciences, V7, P95 Steinbach H. B., 1940, Cold Spring Harbor Symposia on Quantitative Biology, V8, P242 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STEWART PA, 1981, UNDERSTAND ACID BASE, P32 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 SUNOSE H, 1992, ARO ABSTR, V15, P16 THALMANN R, 1972, LARYNGOSCOPE, V82, P2059, DOI 10.1288/00005537-197211000-00008 THOMAS RC, 1972, PHYSIOL REV, V52, P563 NR 44 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 1993 VL 70 IS 1 BP 22 EP 30 DI 10.1016/0378-5955(93)90049-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000003 PM 8276730 ER PT J AU HAGGERTY, HS LUSTED, HS MORTON, SC AF HAGGERTY, HS LUSTED, HS MORTON, SC TI STATISTICAL QUANTIFICATION OF 24-HOUR AND MONTHLY VARIABILITIES OF SPONTANEOUS OTOACOUSTIC EMISSION FREQUENCY IN HUMANS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; TIME SERIES ANALYSIS; COCHLEAR METABOLISM; MENSTRUAL CYCLE; BIOLOGICAL RHYTHMS ID OUTER HAIR-CELLS; ESTROUS-CYCLE; JET-LAG; MELATONIN; RECEPTOR; BENZODIAZEPINE; PROGESTERONE; RESPONSES; RHYTHMS; COCHLEA AB Previous evidence has suggested a relationship between spontaneous otoacoustic emissions (SOAEs) and established, biological cycles, although detailed statistical quantifications of the suggested relationships do not exist in the literature. In an attempt to statistically quantify the purported circadian and monthly influences on this phenomenon, two experiments were undertaken. The first experiment was conducted over eight weeks, investigating 31 SOAEs recorded from eight women and two men. Time series statistical analysis examined whether daily, weekly, and/or monthly cycles characterized SOAE frequency variability. Results yielded a significant monthly cycle for the majority of SOAEs recorded from the women but for none of the SOAEs recorded from the men. These results suggest the possibility that SOAE frequency fluctuation in women may be entrained to the monthly menstrual cycle. In the second experiment, hourly SOAE frequency stability was examined over a 24-h period to ascertain the nature of the daily frequency variation as precisely as possible. Four SOAEs from two subjects were examined, and time series analysis of these data included (1) modelling the autocorrelation structure of the measurements, (2) resolving each 24-h series of measurements into cyclical components of various periodicities, and (3) testing the statistical significance of given cycles within the spectrum of each series. Findings included a significant 24-h variability of frequency for each SOAE, suggesting the possibility of a circadian influence on frequency fluctuation. Results from the two experiments provide quantitative evidence supporting a hypothetical relationship between SOAEs and established, biological cycles. C1 UNIV S FLORIDA,DEPT SURG,TAMPA,FL 33612. STANFORD UNIV,MED CTR,SCH MED,DIV OTOLARYNGOL HEAD & NECK SURG,STANFORD,CA 94305. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 ARENDT J, 1985, CIBA F SYMP, V117, P266 ARENDT J, 1986, BRIT MED J, V292, P1170 ARENDT J, 1987, ERGONOMICS, V30, P1379, DOI 10.1080/00140138708966031 BELL A, 1992, HEARING RES, V58, P91, DOI 10.1016/0378-5955(92)90012-C BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 BITRAN D, 1991, BEHAV NEUROSCI, V105, P653, DOI 10.1037/0735-7044.105.5.653 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L Brownell W. E., 1986, PERIPHERAL AUDITORY, P369 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BROWNELL WE, 1983, HEARING PHYSL BASES, P103 BROWNELL WE, 1987, AUDITORY FREQUENCY S, P109 BRZEZINSKI A, 1992, FERTIL STERIL, V58, P526 BUSTO U, 1988, J CLIN PSYCHOPHARM, V8, P359 CALLACHAN H, 1987, PROC R SOC SER B-BIO, V231, P359, DOI 10.1098/rspb.1987.0049 Chatfield C., 1984, ANAL TIME SERIES INT CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 CZEISLER CA, 1986, SCIENCE, V233, P667, DOI 10.1126/science.3726555 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 GAVISH M, 1987, BRAIN RES, V409, P386, DOI 10.1016/0006-8993(87)90728-1 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 HAEFELY W, 1983, BENZODIAZEPINES MOL, P21 HARRISON NL, 1987, J PHARMACOL EXP THER, V241, P346 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 JOHNSSON LG, 1976, ANN OTO RHINOL LARYN, V85, P726 JUDD HL, 1979, ENDOCRINE RHYTHMS, P299 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 KLEIN DC, 1985, CIBA F SYMP, V117, P38 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 KOHLER W, 1986, ARCH OTO-RHINO-LARYN, V243, P43, DOI 10.1007/BF00457907 KUJAWA SG, 1992, HEARING RES, V61, P106, DOI 10.1016/0378-5955(92)90041-K LJUNG GM, 1978, BIOMETRIKA, V65, P297, DOI 10.1093/biomet/65.2.297 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 MAJEWSKA MD, 1986, SCIENCE, V232, P1004, DOI 10.1126/science.2422758 MEYER JH, 1982, SCIENCE, V217, P635, DOI 10.1126/science.217.4560.635 MITCHELL CK, 1991, VISUAL NEUROSCI, V7, P479 OLSEN RW, 1986, GABAERGIC TRANSMISSI, P21 PEREZ J, 1988, J PHARMACOL EXP THER, V244, P1005 PLINKERT PK, 1992, HNO, V40, P111 REITER RJ, 1984, PINEAL GLAND REPPERT SM, 1988, SCIENCE, V242, P78, DOI 10.1126/science.2845576 REPPERT SM, 1981, J NEUROSCI, V1, P1414 ROSS S, 1976, 1ST COURSE PROBABILI, P4 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SADUN AA, 1984, BRAIN RES, V302, P371, DOI 10.1016/0006-8993(84)90252-X SANDO I, 1971, ANN OTO RHINOL LARYN, V80, P826 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 Schuknecht H. F., 1974, PATHOLOGY EAR SMITH SS, 1987, BRAIN RES, V422, P52, DOI 10.1016/0006-8993(87)90539-7 SNEDECOR GW, 1980, STAT METHODS, P117 SPEROFF L, 1978, CLIN GYNECOLOGIC END, P116 SWANSON SJ, 1988, J SPEECH HEAR RES, V31, P569 Turi A, 1990, Acta Eur Fertil, V21, P207 WALDHAUSER F, 1985, ANN NY ACAD SCI, V453, P205, DOI 10.1111/j.1749-6632.1985.tb11811.x WESTERLING P, 1991, BRIT J PHARMACOL, V103, P1580 Wever R A, 1986, J Neural Transm Suppl, V21, P323 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WILKINSON M, 1983, BRAIN RES BULL, V11, P279, DOI 10.1016/0361-9230(83)90160-0 WILSON JP, 1981, TINNITUS, V85, P82 WILSON JP, 1986, PERIPHERAL AUDITORY, P229 WILSON MA, 1992, BRAIN RES BULL, V29, P165, DOI 10.1016/0361-9230(92)90022-P WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 WURTMAN RJ, 1986, J NEURAL TRANSM S, V21 WYNN VT, 1973, PROG NEUROBIO, V1, P113 ZUREK PM, 1981, J ACOUST SOC AM, V70, P446, DOI 10.1121/1.386787 1984, SAS ETS USERS GUIDE NR 70 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 OCT PY 1993 VL 70 IS 1 BP 31 EP 49 DI 10.1016/0378-5955(93)90050-B PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000004 PM 8276731 ER PT J AU MENSH, BD PATTERSON, MC WHITEHEAD, ML LONSBURYMARTIN, BL MARTIN, GK AF MENSH, BD PATTERSON, MC WHITEHEAD, ML LONSBURYMARTIN, BL MARTIN, GK TI DISTORTION-PRODUCT EMISSIONS IN RABBIT .1. ALTERED SUSCEPTIBILITY TO REPEATED PURE-TONE EXPOSURES SO HEARING RESEARCH LA English DT Article DE 2F(1)-F(2) DISTORTION-PRODUCT EMISSIONS; TEMPORARY-THRESHOLD SHIFT; SUSCEPTIBILITY; RESISTANCE; ACOUSTIC MIDDLE-EAR REFLEX; RABBIT ID REDUCES AUDITORY DESENSITIZATION; TEMPORARY THRESHOLD SHIFT; INDUCED HEARING-LOSS; ELECTRICAL-STIMULATION; OTOACOUSTIC EMISSIONS; COCHLEAR MECHANICS; PERIODIC REST; MUTANT MICE; GUINEA-PIGS; NOISE AB An important issue in understanding the development of noise-induced hearing loss is whether prior acoustic overstimulation alters the susceptibility of the cochlea to further damage. The present work was designed to establish a model of activity-dependent changes in the susceptibility of the cochlea to acoustic overstimulation by regularly exposing the ear to a low-frequency pure tone. As a quantitative index of cochlear function, 2f1-f2 distortion-product otoacoustic emissions (DPOAEs) were monitored systematically over time in three groups of rabbits, with each group experiencing a unique paradigm that incorporated repeated exposure to the low-frequency tone. Common to each rabbit's exposure protocol was that a given experimental session consisted of two exposure episodes, separated by a 40-min period. Experimental sessions were repeated three times, with 2- to 3-day recovery periods interposed between sessions. The rate of decrement in DPOAE amplitude over a prescribed time period was utilized as a measure of susceptibility to the acoustic trauma. The overall results indicated that ears were more susceptible to exposure 40 mins after the first exposure of a session than they were initially. A series of control experiments indicated that the robustness of the acoustic middle-ear reflex (AMR) did not change between the exposure episodes. Consequently, changes in the AMR could not account for the increased susceptibility seen following the first exposure. However, in awake rabbits with stronger AMRs, higher pure-tone exposure levels were needed to produce increased susceptibility to the second exposure. After 2-3 days of intersession recovery, susceptibility to the effects of excessive sound returned close to its original baseline level. The outcome of these studies demonstrated a reduced capacity for the ear to resist the harmful effects of exposure to a moderately intense tone, which was repeated twice over a brief 40-min period, but little change in susceptibility when identical exposures were repeated over longer intersession intervals of several days. C1 UNIV MIAMI,INST EAR M805,DEPT OTOLARYNGOL,POB 016960,MIAMI,FL 33101. BAYLOR COLL MED,DIV NEUROSCI,HOUSTON,TX 77030. BAYLOR COLL MED,MED SCIENTIST TRAINING PROGRAM,HOUSTON,TX 77030. GEORGETOWN UNIV,DEPT OTOLARYNGOL,WASHINGTON,DC 20057. CR Borg E, 1968, Acta Otolaryngol, V65, P575, DOI 10.3109/00016486809121001 Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 BORG E, 1972, ACTA OTO-LARYNGOL, V74, P163, DOI 10.3109/00016487209128437 Borg E, 1972, Acta Otolaryngol Suppl, V304, P1 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 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 CLARK WW, 1978, ANN OTOL RHINOL LA S, V51, P1 CLARK WW, 1992, NOISE INDUCED HEARIN, P445 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 CODY AR, 1988, HEARING RES, V35, P59, DOI 10.1016/0378-5955(88)90040-8 CODY AR, 1982, HEARING RES, V6, P199, DOI 10.1016/0378-5955(82)90054-5 CODY AR, 1992, NOISE INDUCED HEARIN, P11 DOLAN TG, 1985, J ACOUST SOC AM, V77, P1475, DOI 10.1121/1.392042 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C HANDROCK M, 1982, ARCH OTO-RHINO-LARYN, V234, P191, DOI 10.1007/BF00453630 HARRIS JD, 1955, J ACOUST SOC AM, V27, P177, DOI 10.1121/1.1907484 HENDERSON D, 1992, NOISE INDUCED HEARIN, P476 HIRSH IJ, 1955, J ACOUST SOC AM, V27, P1186, DOI 10.1121/1.1908157 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 LONSBURYMARTIN BL, 1978, J NEUROPHYSIOL, V41, P987 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 B D, 1989, Society for Neuroscience Abstracts, V15, P212 MENSH BD, 1993, HEARING RES, V70, P65, DOI 10.1016/0378-5955(93)90052-3 MOLLER AR, 1961, ANN OTO RHINOL LARYN, V70, P735 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PATTERSON M C, 1990, Society for Neuroscience Abstracts, V16, P872 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 RAJAN R, 1988, HEARING RES, V36, P75, DOI 10.1016/0378-5955(88)90138-4 RAJAN R, 1988, HEARING RES, V36, P53, DOI 10.1016/0378-5955(88)90137-2 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 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 STRINGER JL, 1983, BRAIN RES, V258, P159, DOI 10.1016/0006-8993(83)91244-1 SUBRAMANIAM M, 1991, HEARING RES, V56, P65, DOI 10.1016/0378-5955(91)90154-2 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H TERKILDSEN K, 1960, ARCHIV OTOLARYNGOL, V72, P339 WERSALL R, 1958, Acta Otolaryngol Suppl, V139, P1 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V YATES GK, 1983, HEARING RES, V12, P305, DOI 10.1016/0378-5955(83)90003-5 YOUNG E, 1973, J ACOUST SOC AM, V54, P1535, DOI 10.1121/1.1914451 NR 47 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 OCT PY 1993 VL 70 IS 1 BP 50 EP 64 DI 10.1016/0378-5955(93)90051-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000005 PM 8276732 ER PT J AU MENSH, BD LONSBURYMARTIN, BL MARTIN, GK AF MENSH, BD LONSBURYMARTIN, BL MARTIN, GK TI DISTORTION-PRODUCT EMISSIONS IN RABBIT .2. PREDICTION OF CHRONIC-NOISE EFFECTS BY BRIEF PURE-TONE EXPOSURES SO HEARING RESEARCH LA English DT Article DE PURE-TONE EXPOSURE; NOISE EXPOSURE; 2F(1)-F(2) DISTORTION-PRODUCT EMISSIONS; SUSCEPTIBILITY; RABBIT ID OTOACOUSTIC EMISSIONS; COCHLEAR MECHANICS; MUTANT MICE; SUSCEPTIBILITY; ORIGIN AB In an attempt to predict the susceptibility of the cochlea to the harmful influences of excessive sound, the effects of initially exposing the same rabbits to brief pure-tones were related to the subsequent effects of octave-band noise (OBN) exposure using measures of distortion-product otoacoustic emissions (DPOAEs). The pure-tone exposure paradigm consisted of determining the rate at which a 100-dB SPL, low-frequency tone reduced the amplitude of a 1.5-kHz DPOAE, elicited by 50-dB SPL primaries. To establish the stability of the rate-reduction index, the tonal-exposure protocol was repeated on three separate occasions for each subject. Subsequently, the same rabbits were exposed chronically to a 95-dB SPL OBN, centered at 1-kHz, until DPOAE amplitudes between 1-5 kHz were diminished to noise-floor levels, i.e., by 10-30 dB, in response to 45-dB SPL primaries. The results revealed a visually apparent relation between the slope of the tonal-induced DPOAE-loss functions and the number of days required to reach the criterion decrement in emission level during chronic exposure to noise. Analysis of the frequency extent of the noise-induced changes revealed significant correlations between the previously measured rate of pure-tone induced reductions of DPOAE amplitude and the subsequent amount of decrement produced by OBN exposure. Thus, rabbits exhibiting slow rates of tonal-induced decrements in low-frequency DPOAEs were resistant to the amplitude-reducing effects of a subsequent chronic OBN exposure in that it typically took more than four days to achieve the targeted amount of DPOAE loss. In contrast, animals showing rapid rates of tonal-induced DPOAE reduction tended to require only two to four days of noise exposure to attain the requisite decrease in the amplitudes of low-frequency DPOAEs. C1 UNIV MIAMI,INST EAR M805,DEPT OTOLARYNGOL,POB 016960,MIAMI,FL 33101. BAYLOR COLL MED,DEPT NEUROSCI,HOUSTON,TX 77030. BAYLOR COLL MED,MED SCIENTIST TRAINING PROGRAM,HOUSTON,TX 77030. CR ATTIAS J, 1985, AUDIOLOGY, V24, P149 BOHNE BA, 1976, ANN OTO RHINOL LARYN, V85, P711 CLARK WW, 1978, ANN OTOL RHINOL LA S, V51, P1 DOLAN TG, 1985, J ACOUST SOC AM, V77, P1475, DOI 10.1121/1.392042 Fosbroke J, 1830, LANCET, V1, P740 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C GREISEN L, 1951, ACTA OTO-LARYNGOL, V39, P132, DOI 10.3109/00016485109120289 HIRSH IJ, 1952, J ACOUST SOC AM, V24, P131, DOI 10.1121/1.1906867 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 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 MARTIN GK, 1983, HEARING RES, V12, P65, DOI 10.1016/0378-5955(83)90119-3 MENSH BD, 1990, ABSTR ASS RES OT, V13, P72 MENSH BD, 1993, HEARING RES, V70, P50, DOI 10.1016/0378-5955(93)90051-2 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Peyser A, 1930, DEUT MED WOCHENSCHR, V56, P150 RYAN A, 1978, J ACOUST SOC AM, V63, P1145, DOI 10.1121/1.381822 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 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 Ward W D, 1965, J Occup Med, V7, P595, DOI 10.1097/00043764-196512000-00001 WARD WD, 1958, J ACOUST SOC AM, V30, P944, DOI 10.1121/1.1909414 WHITEHAD ML, 1990, ABSTR ASS RES OT, V17, P67 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V Wilson R., 1984, ACOUSTIC REFLEX, P329 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 OCT PY 1993 VL 70 IS 1 BP 65 EP 72 DI 10.1016/0378-5955(93)90052-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000006 PM 8276733 ER PT J AU SLEPECKY, NB ULFENDAHL, M AF SLEPECKY, NB ULFENDAHL, M TI EVIDENCE FOR CALCIUM-BINDING PROTEINS AND CALCIUM-DEPENDENT REGULATORY PROTEINS IN SENSORY CELLS OF THE ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE HAIR CELL; CALCIUM; CALSEQUESTRIN; CALMODULIN; CALDESMON; CALBINDIN; PYROANTIMONATE ID OUTER HAIR-CELLS; ELECTRON-PROBE ANALYSIS; SARCOPLASMIC-RETICULUM; ENDOPLASMIC-RETICULUM; SMOOTH-MUSCLE; GUINEA-PIG; INNER-EAR; IMMUNOFLUORESCENT LOCALIZATION; IMMUNOCYTOCHEMICAL DETECTION; NONMUSCLE CELLS AB Calcium is thought to play a major signaling role in outer hair cells to control metabolism, cytoskeletal integrity, cell shape and cell excitability. For this to happen, in resting cells the concentration of free calcium ions must be maintained at low levels so that focal increases can trigger specific events. In this paper, the localization of calcium, calcium-binding and calcium-dependent regulatory proteins in sensory cells from the guinea pig inner ear was demonstrated using immunocytochemical and histochemical techniques. We found the calcium buffer and/or calcium sensor proteins calmodulin, calbindin and calsequestrin predominantly in sensory cells and that when present, these proteins can be enriched in the outer hair cells. Calmodulin is found in the stereocilia, in the cuticular plate and in the cytoplasm and calbindin is found only in the cuticular plate and cytoplasm of both the inner and outer hair cells. The staining for these proteins in the outer hair cells is homogeneous, with no apparent compartmentalization along the lateral wall. Calsequestrin, thought to store and release calcium from membrane bound intracellular storage sites is found only in the cytoplasm of outer hair cells. There, it has a more punctuate staining pattern than does calmodulin or calbindin suggesting that it may be present in calciosomes rather than soluble in the cytoplasm. We did not detect caldesmon and S-100. Using the potassium pyroantimonate technique, we found precipitates containing calcium ions distributed throughout the cytoplasm of outer hair cells, with no evidence that the subsurface cisterns along the lateral wall act as calcium storage sites. Thus, calcium in resting cells is found in the cytoplasm along with calbindin and calmodulin and appears to have a punctate distribution consistent with a co-localization with calsequestrin. The implications of this distribution with respect to the slow shortening and elongation seen in outer hair cells are discussed. C1 KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. RP SLEPECKY, NB (reprint author), SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244, USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BAIMBRIDGE KG, 1982, BRAIN RES, V239, P519, DOI 10.1016/0006-8993(82)90526-1 BAIMBRIDGE KG, 1984, BRAIN RES, V324, P85, DOI 10.1016/0006-8993(84)90624-3 BRETSCHER A, 1985, J CELL BIOL, V100, P1656, DOI 10.1083/jcb.100.5.1656 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1991, NEUROSCI LETT, V128, P77, DOI 10.1016/0304-3940(91)90763-J BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CAMPBELL KP, 1981, J BIOL CHEM, V256, P4626 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 CELIO MR, 1986, NATURE, V323, P715, DOI 10.1038/323715a0 CHANDLER JA, 1977, PRACTICAL METHODS EL CHRISTNER A, 1977, ACTA HISTOCHEM, V58, P39 DEARRUDA MV, 1990, J CELL BIOL, V111, P1069, DOI 10.1083/jcb.111.3.1069 DECHESNE CJ, 1988, DEV BRAIN RES, V40, P233, DOI 10.1016/0165-3806(88)90135-6 DECOUET HG, 1986, CELL TISSUE RES, V244, P315 DIFIGLIA M, 1989, J COMP NEUROL, V279, P653, DOI 10.1002/cne.902790411 DONATO R, 1986, CELL CALCIUM, V7, P123, DOI 10.1016/0143-4160(86)90017-5 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 GLENNEY JR, 1982, P NATL ACAD SCI-BIOL, V79, P4002, DOI 10.1073/pnas.79.13.4002 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 HARPER JF, 1980, P NATL ACAD SCI-BIOL, V77, P366, DOI 10.1073/pnas.77.1.366 HASHIMOTO S, 1988, J CELL BIOL, V107, P2423 HENKART MP, 1978, SCIENCE, V202, P1300, DOI 10.1126/science.725607 HENSON JH, 1989, J CELL BIOL, V109, P149, DOI 10.1083/jcb.109.1.149 HOWE CL, 1980, J CELL BIOL, V85, P916, DOI 10.1083/jcb.85.3.916 JANDE SS, 1981, NATURE, V294, P765, DOI 10.1038/294765a0 JORGENSEN AO, 1987, J HISTOCHEM CYTOCHEM, V35, P723 JORGENSEN AO, 1984, J CELL BIOL, V98, P1597, DOI 10.1083/jcb.98.4.1597 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KAKIUCHI S, 1982, CALMODULIN INTRACELL, P167 KARLSSON KK, 1990, NEUROSCI LETT, V116, P101, DOI 10.1016/0304-3940(90)90393-N KARLSSON KK, 1991, HEARING RES, V53, P95, DOI 10.1016/0378-5955(91)90216-V KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KOMNICK H, 1962, PROTOPLASMA, V55, P414, DOI 10.1007/BF01881781 KRAUS P, 1988, J ACOUST SOC AM S1, V83, pS96, DOI 10.1121/1.2025613 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 MACLENNA.DH, 1971, P NATL ACAD SCI USA, V68, P1231, DOI 10.1073/pnas.68.6.1231 MANN W, 1988, ARCH OTO-RHINO-LARYN, V245, P185, DOI 10.1007/BF00464024 MATUS A, 1975, NATURE, V258, P746, DOI 10.1038/258746a0 MEANS AR, 1982, PHYSIOL REV, V62, P1 MILNER RE, 1991, J BIOL CHEM, V266, P7155 OHMORI H, 1988, J PHYSIOL-LONDON, V399, P115 RABIE A, 1983, CELL TISSUE RES, V232, P691 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SANS A, 1986, BRAIN RES, V364, P190, DOI 10.1016/0006-8993(86)91003-6 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SLEPECKY N, 1986, CELL TISSUE RES, V245, P229 SLEPECKY NB, 1992, HEARING RES, V57, P201, DOI 10.1016/0378-5955(92)90152-D SLEPECKY NB, 1993, IN PRESS HEAR RES SOBUE K, 1982, BIOMED RES-TOKYO, V3, P188 SOMLYO AP, 1984, NATURE, V309, P516, DOI 10.1038/309516b0 SOMLYO AP, 1986, J CARDIOVASC PHARM, V8, pS42, DOI 10.1097/00005344-198600088-00009 SOMLYO AP, 1979, J CELL BIOL, V81, P316, DOI 10.1083/jcb.81.2.316 SOMLYO AV, 1985, EXPERIENTIA, V41, P841, DOI 10.1007/BF01970000 STOCLET JC, 1987, PROG NEUROBIOL, V29, P321, DOI 10.1016/0301-0082(87)90018-9 Ulfendahl M, 1989, Acta Otolaryngol Suppl, V467, P221 ULFENDAHL M, 1987, ACTA PHYSIOL SCAND, V130, P521, DOI 10.1111/j.1748-1716.1987.tb08171.x VINNIKOV YA, 1969, NATURE, V223, P641, DOI 10.1038/223641a0 VOLPE P, 1988, P NATL ACAD SCI USA, V85, P1091, DOI 10.1073/pnas.85.4.1091 WICK SM, 1982, J HISTOCHEM CYTOCHEM, V30, P1190 WOLOSEWICK J, 1982, BIOL CELL, V44, P85 WUYTACK F, 1987, BIOCHIM BIOPHYS ACTA, V899, P151, DOI 10.1016/0005-2736(87)90395-6 YAMASHITA T, 1990, ACTA OTO-LARYNGOL, V109, P256, DOI 10.3109/00016489009107441 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 71 TC 51 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 1993 VL 70 IS 1 BP 73 EP 84 DI 10.1016/0378-5955(93)90053-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000007 PM 8276734 ER PT J AU OESTERLE, EC TSUE, TT REH, TA RUBEL, EW AF OESTERLE, EC TSUE, TT REH, TA RUBEL, EW TI HAIR-CELL REGENERATION IN ORGAN-CULTURES OF THE POSTNATAL CHICKEN INNER-EAR SO HEARING RESEARCH LA English DT Article DE BIRD; AUDITORY; VESTIBULAR; HAIR CELLS; HAIR-CELL REGENERATION; ORGAN CULTURES ID ACOUSTIC TRAUMA; STEREOCILIARY BUNDLES; VESTIBULAR EPITHELIUM; POSSIBLE PRECURSORS; BASILAR PAPILLA; INTENSE SOUND; NOISE DAMAGE; COCHLEA; DIFFERENTIATION; OTOTOXICITY AB The sensory epithelium of the avian inner ear retains into adulthood progenitor cells for inner-ear hair cells and other cell types in the epithelium. Hair cells are produced normally on an ongoing basis in the vestibular sensory epithelium, and hair-cell production is increased after insult in both auditory and vestibular sensory epithelia. The details of postnatal hair-cell production are not understood. In particular, molecular factors involved in the initiation and regulation of hair-cell genesis and differentiation are not known. Studies of this phenomena have been hampered by the lack of cell culture models. An organ culture system was developed which encourages generation and differentiation of hair cells in mature inner-ear sensory epithelia. Continuous labeling with tritiated thymidine showed genesis of both supporting cells and hair cells in normal vestibular epithelia grown in culture, and an increase in hair-cell and supporting-cell proliferation in damaged sensory epithelia grown in culture as compared to undamaged controls. This demonstrates, in vitro, both the division and differentiation of hair-cell progenitor cells in normal vestibular epithelia, and the maintenance of the hair-cell regeneration process in damaged inner-ear epithelia. This culture system should be useful for studies of hair-cell genesis and differentiation as well as studies of hair-cell and supporting-cell functioning in general. C1 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT BIOL STRUCT,SEATTLE,WA 98195. RP OESTERLE, EC (reprint author), UNIV WASHINGTON,DEPT OTOLARYNGOL HEAD & NECK SURG,HEARING DEV LABS,RL-30,SEATTLE,WA 98195, USA. CR ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1991, REGENERATION VERTEBR, P103 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 DA, 1985, SCAN ELECTRON MICROS, P407 COTANCHE DA, 1987, HEARING RES, V25, P125, DOI 10.1016/0378-5955(87)90086-4 COTANCHE DA, 1991, CIBA F SYMP, V160, P131 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 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 Fell HB, 1928, ARCH EXP ZELLFORSCH, V7, P69 FRIEDMANN I, 1977, ANN OTO RHINOL LARYN, V86, P371 GAHWILER BH, 1981, J NEUROSCI METH, V4, P329, DOI 10.1016/0165-0270(81)90003-0 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 HIROKAWA N, 1986, HEARING RES, V22, P41, DOI 10.1016/0378-5955(86)90076-6 Iurato S, 1967, SUBMICROSCOPIC STRUC JANAS JJ, 1992, AVIAN COCHLEAR HAIR JORGENSEN JM, 1989, BRAIN BEHAV EVOLUT, V34, P273, DOI 10.1159/000116512 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 JORGENSEN JM, 1991, CIBA F SYMP, V160, P151 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 LOMBARTE A, 1993, HEARING RES, V64, P166, DOI 10.1016/0378-5955(93)90002-I MAREAN GC, 1993, IN PRESS HEAR RES MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 OESTERLE EC, 1993, HEARING RES, V66, P213, DOI 10.1016/0378-5955(93)90141-M OESTERLE EC, 1992, J COMP NEUROL, V318, P64, DOI 10.1002/cne.903180105 OESTERLE EC, 1993, ASS RES OT ABSTR, V16, P30 OESTERLE EC, 1992, ASS RES OT ABSTR, V15, P162 PRESSON JC, 1990, HEARING RES, V46, P9, DOI 10.1016/0378-5955(90)90135-C REBILLARD G, 1981, BRAIN RES, V229, P15, DOI 10.1016/0006-8993(81)90741-1 REH TA, 1989, J NEUROSCI, V9, P4179 REPRESA J, 1991, NATURE, V353, P561, DOI 10.1038/353561a0 REPRESA J, 1990, DEVELOPMENT, V110, P1081 ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 SANS A, 1993, ASS RES OT ABST, V16, P27 SOKOLOWSKI BHA, 1993, DEV BIOL, V155, P134, DOI 10.1006/dbio.1993.1013 STONE JS, 1991, J COMP NEUROL, V314, P614, DOI 10.1002/cne.903140315 STONE JS, 1992, J CELL SCI, V102, P671 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 TSUE TT, 1993, IN PRESS J NEUROSCI TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 WARCHOL ME, 1992, ASS RES OTOLARYNGOL, V15, P106 WEISLEDER P, 1991, THESIS U WASHINGTON 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 WEISLEDER P, 1992, ASS RES OT ABSTR, V15, P160 WERSALL J, 1956, ACTA OTOLARYNGOL S, V126 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 NR 55 TC 51 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 OCT PY 1993 VL 70 IS 1 BP 85 EP 108 DI 10.1016/0378-5955(93)90054-5 PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000008 PM 8276735 ER PT J AU AVAN, P BONFILS, P LOTH, D WIT, HP AF AVAN, P BONFILS, P LOTH, D WIT, HP TI TEMPORAL PATTERNS OF TRANSIENT-EVOKED OTOACOUSTIC EMISSIONS IN NORMAL AND IMPAIRED COCHLEAE SO HEARING RESEARCH LA English DT Article DE HUMAN COCHLEA; OTOACOUSTIC EMISSIONS; ACOUSTIC TRAUMA ID STIMULATED ACOUSTIC EMISSIONS; HUMAN EAR; MODEL; HEARING AB The spatial distribution of outer hair cells that participate in generating transient-EOE frequency-components has been investigated in man. According to several models (e.g. Wilson (1990) Hear. Res. 2, 527-532; Zwicker (1986) J. Acoust. Soc. Am. 80, 154-162; Wilson and Kemp (Eds.), Cochlear Mechanisms, Structures, Functions and Models, Plenum Press, NY), EOEs result from interferences between broadly distributed contributions, responsible for their long frequency-dependent delay. This work presents an analysis of the temporal patterns of click- and tone-burst-EOEs in human ears when contributions to EOEs are reduced by noise-induced lesions with audiometric notches centred around 4 kHz (N = 46). Although the auditory thresholds at the frequencies of the studied EOE-components were always normal, these components exhibited drastic and predictable changes compared to normal control ears (N = 40). (1) Their temporal pattern at the highest EOE frequency f(max) just below the audiometric notch appeared to be determined by the cochlear state at high frequencies (6 to 8 kHz). Either it was normal and the EOE exhibited a complicated beat-structure, or it was impaired and the time envelope of the EOE was simple. In contrast, any type of time pattern could be observed in normal ears. (2) The temporal patterns of EOEs one octave below f(max). always presented many beats and short delays. The proposed interpretation is that contributions to a transient-EOE component at frequency f can come from distant basal cochlear areas, i.e. more than 1 and sometimes 1.5 octaves from the place tuned to f. Therefore, the possible relationships between transient-EOEs and tuning mechanisms which presumably involve only a small number of OHC need further investigations. C1 HOP BOUCICAULT,DEPT EAR NOSE & THROAT,F-75730 PARIS 15,FRANCE. HOP LARIBOISIERE,DEPT BIOPHYS,F-75475 PARIS 10,FRANCE. UNIV HOSP GRONINGEN,INST AUDIOL,GRONINGEN,NETHERLANDS. RP AVAN, P (reprint author), FAC MED CLERMONT FERRAND,DEPT BIOPHYS,BP 38,F-63001 CLERMONT FERRAND,FRANCE. CR ARAN JM, 1988, PHYSL COCHLEE INSERM, P91 AVAN P, 1991, HEARING RES, V52, P99, DOI 10.1016/0378-5955(91)90191-B AVAN P, 1993, AUDIOLOGY, V32, P12 Avan P., 1991, Journal d'Acoustique, V4 BONFILS P, 1989, ANN OTO RHINOL LARYN, V98, P326 CODY AR, 1992, HEARING RES, V62, P166, DOI 10.1016/0378-5955(92)90182-M DANCER A, 1987, J ACOUSTIQUE, V81, P3 DEBOER E, 1983, J ACOUST SOC AM, V73, P577, DOI 10.1121/1.389004 EGGERMONT JJ, 1979, J ACOUST SOC AM, V65, P463, DOI 10.1121/1.382345 FUKAZAWA T, 1992, HEARING RES, V59, P17, DOI 10.1016/0378-5955(92)90097-7 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P462, DOI 10.1098/rspb.1948.0024 Gold T., 1988, COCHLEAR MECHANISMS, P299 GRANDORI F, 1985, AUDIOLOGY, V24, P71 Guinan JJ, 1990, MECH BIOPHYSICS HEAR, P170 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1980, PSYCHOPHYSICAL PHYSL, P75 KEMP DT, 1990, EAR HEARING, V11, P93 NARAYAN SS, 1992, ABSTR ASS RES OT, P158 NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 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 SIVARAMAKRISHNA.S, 1991, ABSTR ASS RES OT, P66 STOVER LJ, 1992, ABSTR ASS RES OT, P153 STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 Sutton GJ, 1983, MECHANICS HEARING, P83 WILSON JP, 1980, HEARING RES, V2, P527, DOI 10.1016/0378-5955(80)90090-8 WILSON JP, 1989, COCHLEAR MECHANISMS, P285 WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 Wit HP, 1983, MECHANICS HEARING, P101 WIT HP, 1979, J ACOUST SOC AM, V66, P911, DOI 10.1121/1.383202 Wit HP, 1980, PSYCHOPHYSICAL PHYSL, P53 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 ZWICKER E, 1986, J ACOUST SOC AM, V80, P154, DOI 10.1121/1.394176 ZWICKER E, 1989, COCHLEAR MECHANISMS, P359 NR 35 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 1993 VL 70 IS 1 BP 109 EP 120 DI 10.1016/0378-5955(93)90055-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000009 PM 8276727 ER PT J AU XUE, SW MOUNTAIN, DC HUBBARD, AE AF XUE, SW MOUNTAIN, DC HUBBARD, AE TI ACOUSTIC ENHANCEMENT OF ELECTRICALLY-EVOKED OTOACOUSTIC EMISSIONS REFLECTS BASILAR-MEMBRANE TUNING - EXPERIMENT RESULTS SO HEARING RESEARCH LA English DT Article DE GERBIL; OTOACOUSTIC EMISSIONS; ELECTRICALLY-EVOKED EMISSIONS; HEARING; COCHLEA ID GUINEA-PIG; MOSSBAUER TECHNIQUE; VIBRATION; COCHLEA AB Acoustic enhancement of the electrically-evoked otoacoustic emissions (EEOEs) was investigated by systematically varying acoustic frequency and intensity. The results demonstrated that simultaneous acoustic stimulation at frequencies around the characteristic frequency of the electrical current injection place was most effective in enhancing low-frequency EEOEs. Moreover, it was demonstrated that the enhancement was tuned and graded. The enhancement threshold tuning curves (defined as sound pressure level needed to achieve 1 dB of enhancement) resembled basilar membrane tuning at high sound pressure levels. The data suggest that the emissions were generated from a cochlear region near the electrode place, and the magnitude of the enhancement depends on the magnitude of the basilar membrane response to the acoustic stimulus. C1 BOSTON UNIV,DEPT OTOLARYNGOL,BOSTON,MA 02215. BOSTON UNIV,DEPT BIOMED ENGN,BOSTON,MA 02215. BOSTON UNIV,DEPT ELECT COMP & SYST ENGN,BOSTON,MA 02215. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWNELL WE, 1985, SCIENCE, V227, P195 CODY AR, 1992, HEARING RES, V62, P166, DOI 10.1016/0378-5955(92)90182-M HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 HUBBARD AE, 1990, HEARING RES, V43, P269, DOI 10.1016/0378-5955(90)90234-G JACK JJB, 1983, ELECTRIC CURRENT FLO MISRAHY GA, 1958, AM J PHYSIOL, V194, P396 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 Mountain DC, 1983, MECHANICS HEARING, P119 MOUNTAIN DC, 1986, PERIPHERAL AUDITORY, P179 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I NAKAJIMA HH, 1991, 1991 P IEEE 17TH ANN, P213, DOI 10.1109/IMTC.1991.161578 NAKAJIMA HH, 1990, ABSTR ASS RES OT FEB RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 RUGGERO MA, 1991, HEARING RES, V51, P215, DOI 10.1016/0378-5955(91)90038-B SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 TASAKI I, 1958, ANN REV PHYSL, V19, P417 XUE S, 1991, ABSTR ASS RES OT, P209 NR 20 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 OCT PY 1993 VL 70 IS 1 BP 121 EP 126 DI 10.1016/0378-5955(93)90056-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000010 PM 8276728 ER PT J AU CAMPBELL, DG DANIEL, HJ HUME, WG AF CAMPBELL, DG DANIEL, HJ HUME, WG TI AGING AND OTITIS-MEDIA AS SOURCES OF VARIANCE IN THE RAT AUDITORY BRAIN-STEM RESPONSE SO HEARING RESEARCH LA English DT Article DE AGING; AUDITORY BRAIN-STEM RESPONSE (ABR); MYCOPLASMA-PULMONIS; OTITIS MEDIA; RAT ID AGE-GRADED SERIES; LIGHT-MICROSCOPY; LABORATORY RATS; TRAPEZOID BODY; CELL COUNTS; COCHLEAS; NUCLEUS AB Auditory brainstem response (ABR) latencies were examined in normal female Sprague-Dawley rats at 6 months of age and in 10-12 month old animals which tested positive for Mycoplasma pulmonis, a frequently implicated pathogen in otitis media. Significant differences in the peak latencies of Waves I, II and IIIn were found between the two age groups. A significant age by intensity interaction effect was also identified for Waves II and IIIn. Since the age-related effects observed in Wave I were similarly reflected in Waves II and IIIn, it was concluded that the group differences were due to alterations of the auditory periphery and not to changes in the central auditory system. C1 E CAROLINA UNIV,DEPT SPEECH LANGUAGE & AUDITORY PATHOL,GREENVILLE,NC 27834. CR CASEY MA, 1988, NEUROSCIENCE, V24, P189, DOI 10.1016/0306-4522(88)90322-3 CASEY MA, 1982, NEUROBIOL AGING, V3, P187, DOI 10.1016/0197-4580(82)90039-2 CHEN TJ, 1991, EXP BRAIN RES, V85, P537 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F CROWLEY DE, 1974, PHYSIOL PSYCHOL, V2, P99 DANIEL HJ, 1971, J AUD RES, V11, P276 DANIEL HJ, 1973, PHYSIOL PSYCHOL, V1, P7 HOEFFDING V, 1988, J COMP NEUROL, V276, P537, DOI 10.1002/cne.902760408 JEWETT DL, 1972, BRAIN RES, V36, P105 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 LINDSEY JR, 1971, AM J PATHOL, V64, P675 MEANS LW, 1988, ANIM LEARN BEHAV, V16, P303, DOI 10.3758/BF03209081 MENDELSON T, 1979, ARCH OTOLARYNGOL, V105, P17 PENNY JE, 1986, LIFE SCI, V39, P887, DOI 10.1016/0024-3205(86)90370-X RETZLAFF E, 1960, Geriatrics, V15, P205 SHAW NA, 1988, PROG NEUROBIOL, V31, P19, DOI 10.1016/0301-0082(88)90021-4 SIMPSON GV, 1985, BRAIN RES, V348, P28, DOI 10.1016/0006-8993(85)90355-5 WEBSTER WR, 1985, RAT NERVOUS SYSTEM NR 19 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 OCT PY 1993 VL 70 IS 1 BP 127 EP 130 DI 10.1016/0378-5955(93)90057-8 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA MB750 UT WOS:A1993MB75000011 PM 8276729 ER PT J AU HOFFMAN, DW HOCHREITER, JS LANDRY, DR BRIMIJOIN, MR TREADWELL, MD GARDNER, PD ALTSCHULER, RA AF HOFFMAN, DW HOCHREITER, JS LANDRY, DR BRIMIJOIN, MR TREADWELL, MD GARDNER, PD ALTSCHULER, RA TI LOCALIZATION OF PREPROENKEPHALIN MESSENGER RNA-EXPRESSING CELLS IN RAT AUDITORY BRAIN-STEM WITH IN-SITU HYBRIDIZATION SO HEARING RESEARCH LA English DT Article DE OLIVOCOCHLEAR; AUDITORY EFFERENT; TRAPEZOID BODY; SUPERIOR OLIVE ID EFFERENT OLIVOCOCHLEAR NEURONS; SUPERIOR OLIVARY COMPLEX; ENKEPHALIN-LIKE IMMUNOREACTIVITY; ELECTRICAL-STIMULATION; GUINEA-PIG; NERVE-FIBERS; NEUROACTIVE SUBSTANCES; COCHLEAR NUCLEUS; MEDIAL ZONES; ORGAN AB Hair cells and auditory nerve dendrites in the inner ear are innervated by pontine neurons that have been demonstrated by immunochemical techniques to contain several neurotransmitters, including acetylcholine and the opioid peptide enkephalins and dynorphins. The functions of these nerve fibers are not known, but may involve modifying auditory sensitivity to low intensity stimuli. In the guinea pig the opioid pathways originate in the lateral superior olivary region. A recent study in the gerbil has reported cells expressing preproenkephalin mRNA present only in the ventral nucleus of the trapezoid body, and not in the superior olivary region. In the present study, a non-radioisotopically labeled in situ hybridization method was used to identify cells expressing mRNA coding for preproenkephalin in rat pontine neurons, specifically in the ventral nucleus of the trapezoid body. These cells may represent an enkephalin-containing medial olivocochlear system in the rat, the origin of the lateral system in the rat that differs markedly from the better-studied guinea pig and cat, or a non-olivocochlear enkephalin-containing system. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PSYCHIAT,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PHARMACOL,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT BIOCHEM,HANOVER,NH 03756. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR ABOUMADI L, 1987, HEARING RES, V30, P135, DOI 10.1016/0378-5955(87)90131-6 ADAMS JC, 1987, BRAIN RES, V419, P347, DOI 10.1016/0006-8993(87)90606-8 ALTSCHULER RA, 1985, HEARING RES, V17, P249, DOI 10.1016/0378-5955(85)90069-3 ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 ALTSCHULER RA, 1988, J HISTOCHEM CYTOCHEM, V36, P797 ALTSCHULER RA, 1984, J HISTOCHEM CYTOCHEM, V32, P839 ALTSCHULER RA, 1986, AM J OTOLARYNG, V7, P100, DOI 10.1016/S0196-0709(86)80038-2 ALTSCHULER RA, 1983, NEUROSCIENCE, V9, P621, DOI 10.1016/0306-4522(83)90178-1 ART JJ, 1984, J PHYSIOL-LONDON, V356, P507 DENERIS ES, 1988, NEURON, V1, P45, DOI 10.1016/0896-6273(88)90208-5 EYBALIN M, 1982, NEUROSCI LETT, V10, pS166 EYBALIN M, 1984, BRAIN RES, V305, P313, DOI 10.1016/0006-8993(84)90437-2 EYBALIN M, 1989, ARCH OTO-RHINO-LARYN, V246, P228, DOI 10.1007/BF00463561 FEX J, 1968, HEARING MECHANISMS V, P169 FEX J, 1981, P NATL ACAD SCI-BIOL, V78, P1255, DOI 10.1073/pnas.78.2.1255 GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 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 GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 GUINAN JJ, 1988, HEARING RES, V33, P115, DOI 10.1016/0378-5955(88)90024-X HOFFMAN DW, 1983, HEARING RES, V9, P71, DOI 10.1016/0378-5955(83)90135-1 HOFFMAN DW, 1984, BRAIN RES, V322, P59, DOI 10.1016/0006-8993(84)91180-6 HOFFMAN DW, 1986, NEUROBIOLOGY HEARING, P371 HOFFMAN DW, 1985, HEARING RES, V17, P47, DOI 10.1016/0378-5955(85)90129-7 HOKFELT T, 1977, NEUROSCI LETT, V5, P25, DOI 10.1016/0304-3940(77)90160-4 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 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 LU SM, 1987, HEARING RES, V31, P137, DOI 10.1016/0378-5955(87)90119-5 RAJAN R, 1988, BRAIN RES, V459, P241, DOI 10.1016/0006-8993(88)90640-3 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 Rasmussen G.L, 1942, ANAT REC, V82, P441 RYAN AF, 1991, EXP BRAIN RES, V87, P259 SABOL SL, 1983, BIOCHEM BIOPH RES CO, V113, P391, DOI 10.1016/0006-291X(83)91739-4 SAHLEY TL, 1991, HEARING RES, V55, P133, DOI 10.1016/0378-5955(91)90099-U VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WARR WB, 1980, ANN OTORHINOLARY S74, V74, P114 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 ZAMIR N, 1984, NATURE, V307, P643, DOI 10.1038/307643a0 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 SEP PY 1993 VL 69 IS 1-2 BP 1 EP 9 DI 10.1016/0378-5955(93)90087-H PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000001 PM 8226328 ER PT J AU PITOVSKI, DZ DRESCHER, MJ DRESCHER, DG AF PITOVSKI, DZ DRESCHER, MJ DRESCHER, DG TI HIGH-AFFINITY ALDOSTERONE BINDING-SITES (TYPE-I RECEPTORS) IN THE MAMMALIAN INNER-EAR SO HEARING RESEARCH LA English DT Article DE ALDOSTERONE; RECEPTOR; NA, K-ATPASE; COCHLEA; VESTIBULE ID ADRENOCORTICOSTEROID HORMONES; MINERALOCORTICOID RECEPTORS; STRIA VASCULARIS; RAT COCHLEAR; ABSENCE; CELLS; NA+,K+-ATPASE; MECHANISM AB The presence of aldosterone (Type I) binding sites in the mammalian inner ear has been previously suggested by an increase in inner ear Na, K-ATPase ouabain binding sites in response to the administration of aldosterone in vivo (Pitovski et al., 1993). Type I binding sites have now been identified and characterized in the lateral wall of the basal turn of the cochlea and in the ampullae of the semicircular canals of the guinea pig. In the presence of RU 28362, which blocks low-affinity binding of the labeled hormone to Type II sites, [H-3]-aldosterone binds to a single class of high-affinity (Type I) sites with K(d) values of 34.7 nM in lateral wall of the basal turn of the cochlea and 31.3 nM in the ampullae of the semicircular canals. B(max) is 17.1 fmol/mg dry tissue for the cochlear sample and 17.4 fmol/mg dry tissue for the ampullae, comparable to reported values in renal tissue (17-31 fmol/mg protein). Thus, the results of receptor-binding experimental protocols with [H-3]-aldosterone clearly suggest that these inner ear tissues are a target site of mineralocorticoid action. C1 WAYNE STATE UNIV,SCH MED,BIOOTOL LAB,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT BIOCHEM,DETROIT,MI 48201. RP PITOVSKI, DZ (reprint author), WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,540 E CANFIELD AVE,DETROIT,MI 48201, USA. CR BASTL CP, 1984, J BIOL CHEM, V259, P1186 BEAUMONT K, 1985, BRAIN RES, V342, P252, DOI 10.1016/0006-8993(85)91123-0 COIRINI H, 1985, BRAIN RES, V361, P212, DOI 10.1016/0006-8993(85)91291-0 ELMERNISSI G, 1983, PFLUG ARCH EUR J PHY, V399, P147 ERNST SA, 1979, CURR TOP MEMBRANES T, V13, P397 FUNDER JW, 1972, J STEROID BIOCHEMIST, V3, P209, DOI 10.1016/0022-4731(72)90052-0 FUNDER JW, 1988, SCIENCE, V242, P583, DOI 10.1126/science.2845584 FUNDER JW, 1973, ENDOCRINOLOGY, V92, P994 FUNDER JW, 1973, ENDOCRINOLOGY, V92, P1005 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 KERR TP, 1986, 9TH NASA GRAV SPAC B KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 LUTTGE W G, 1989, Steroids, V53, P59, DOI 10.1016/0039-128X(89)90146-3 MARVER D, 1983, MINER ELECTROL METAB, V9, P1 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PEARCE PT, 1986, ENDOCRINOLOGY, V118, P2072 PHILIBERT D, 1983, 65TH ANN M END SOC S, P335 PITOVSKI DZ, 1992, GLUCOCORTICOID TYPE, P11 PITOVSKI DZ, 1993, BRAIN RES, V601, P273, DOI 10.1016/0006-8993(93)91720-D QUIRK SJ, 1983, ENDOCRINOLOGY, V113, P1812 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 ROUSSEAU G, 1972, J STEROID BIOCHEMIST, V3, P219, DOI 10.1016/0022-4731(72)90053-2 SCHMIDT U, 1985, J CLIN INVEST, V55, P655 SCHULMAN G, 1986, J BIOL CHEM, V261, P2102 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 STEPHENSON G, 1984, AM J PHYSIOL, V247, pF665 TENCATE WJF, 1992, HEARING RES, V60, P199, DOI 10.1016/0378-5955(92)90021-E TENCATE WJF, 1990, ACTA OTO-LARYNGOL, V110, P234 VELDHUIS HD, 1982, ENDOCRINOLOGY, V110, P2044 NR 32 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 SEP PY 1993 VL 69 IS 1-2 BP 10 EP 14 DI 10.1016/0378-5955(93)90088-I PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000002 PM 8226329 ER PT J AU CHEN, L SALVI, RJ HASHINO, E AF CHEN, L SALVI, RJ HASHINO, E TI RECOVERY OF CAP THRESHOLD AND AMPLITUDE IN CHICKENS FOLLOWING KANAMYCIN OTOTOXICITY SO HEARING RESEARCH LA English DT Article DE COMPOUND ACTION POTENTIAL; HAIR CELL REGENERATION; CHICKENS; OTOTOXICITY ID HAIR CELL REGENERATION; ACOUSTIC TRAUMA; BASILAR PAPILLA; AMINOGLYCOSIDE ANTIBIOTICS; STEREOCILIARY BUNDLES; TECTORIAL MEMBRANE; COCHLEA; BUDGERIGAR; QUAIL AB Chickens were given a dose of kanamycin (400 mg/kg/d x 10 d) which destroyed hair cells over the basal 37-58% of the basilar papilla. Afterwards, the threshold and amplitude of the compound action potential were measured at recovery times ranging from 2 days to 10-20 weeks post-kanamycin treatment. At 2 days post-treatment, the thresholds at 1000, 2000 and 4000 Hz were elevated 40-60 dB while the thresholds at 250 and 500 Hz were elevated only 25 dB. By 10-20 weeks post-treatment, the threshold at 250 and 500 Hz had completely recovered whereas a residual threshold shift of 5 dB to 25 dB was present between 1000 to 4000 Hz. The maximum amplitude of the compound action potential was also reduced by more than 60% at all frequencies at 2 days post-treatment; however by 10-20 weeks post-treatment, the amplitude of the compound action potential had completely recovered at 500, 1000 and 2000 Hz. By contrast, the amplitude of the compound action potential at 4000 Hz was still reduced by more than 50% of its normal value 10-20 weeks post-treatment. The results of the present study indicate that the time course of recovery of the compound action potential is extremely slow and may lag behind the regeneration of hair cells by many weeks. The permanent deficits observed at the high frequencies could conceivably be due to functional deficits in regenerated hair cells, their afferent synapses or the loss of cochlear ganglion cells. C1 SUNY Buffalo, DEPT COMMUN DISORDERS & SCI, HEARING RES LAB, 215 PARKER HALL, BUFFALO, NY 14214 USA. RI Chen, Lin/N-8327-2013 OI Chen, Lin/0000-0002-5847-2989 CR ARAN JM, 1992, MAY MOL BIOL HEAR DE COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X 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, 1984, DEV BRAIN RES, V16, P181, DOI 10.1016/0165-3806(84)90024-5 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FUCHS PA, 1988, J NEUROSCI, V8, P2460 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 GRAY L, 1985, J ACOUST SOC AM, V77, P1162, DOI 10.1121/1.392180 HASHINO E, 1992, HEARING RES, V59, P46, DOI 10.1016/0378-5955(92)90101-R HASHINO E, 1992, EFFECTS NOISE AUDITO, P238 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 HASHINO E, 1988, J ACOUST SOC AM, V83, P2450, DOI 10.1121/1.396325 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 NORTON S, 1990, FEB ASS RES OT, P62 RUBEL EW, 1992, NOISE INDUCED HEARIN, P204 RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N RYALS BM, 1982, ACTA OTO-LARYNGOL, V93, P205, DOI 10.3109/00016488209130873 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1989, HEARING RES, V43, P81, DOI 10.1016/0378-5955(89)90061-0 SALVI R, 1980, HEARING RES, V2, P335, DOI 10.1016/0378-5955(80)90067-2 SALVI R, 1992, J COMP PHYSIOL A, V170, P2 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 NR 30 TC 28 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 SEP PY 1993 VL 69 IS 1-2 BP 15 EP 24 DI 10.1016/0378-5955(93)90089-J PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000003 PM 8226335 ER PT J AU SAUNDERS, JC TORSIGLIERI, AJ DEDIO, RM AF SAUNDERS, JC TORSIGLIERI, AJ DEDIO, RM TI THE GROWTH OF HEARING-LOSS IN NEONATAL CHICKS EXPOSED TO INTENSE PURE-TONES SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIALS; CHICKS; OVERSTIMULATION; HAIR CELL REGENERATION; HEARING LOSS; FREQUENCY SELECTIVITY ID HAIR CELL LOSS; TEMPORARY THRESHOLD SHIFTS; SEVERE ACOUSTIC TRAUMA; BASILAR PAPILLA; SOUND EXPOSURE; REGENERATION; COCHLEA; NOISE; EAR; MATURATION AB One-day-old chicks were exposed to an intense pure tone (0.9 kHz, 120 dB SPL) and assigned to one of eight groups based on continuous exposure durations from 1 to 200 h. As each animal was removed from the exposure, it was anesthetized and an electrode was placed in the nucleus magnocellularis. Sound-evoked potentials were used to measure absolute thresholds and frequency selectivity. Thresholds were measured at 10 frequencies between 0.1 and 4.5 kHz while frequency selectivity was assessed by a simultaneous masking tuning-curve procedure at five probe-tone frequencies between 0.3 and 2.5 kHz. Threshold shift was greatest at 1.3 kHz and reached a maximum loss of approximately 57 dB between 48 and 200 h of exposure. The shape of the threshold-shift curve as a function of exposure duration (for frequencies between 0.9 and 2.5 KHz) suggested the presence of an early and late effect. The loss in tuning sharpness was evaluated by comparing the values of Q10 dB for control and exposed tuning curves and expressing the difference between them as a percent change. Probe-tone tuning curves above 0.9 kHz became less selective as exposure duration increased. A maximum decrease in tuning of about 54 percent was reached by 48 h and this remained constant to 200 h. The low-frequency tuning curves (below 0.9 kHz) did not show any systematic loss in selectivity. The changes in sensitivity and selectivity are discussed in relation to the patterns of cochlear injury that occurred on the basilar papilla as exposure duration lengthened. C1 UNIV PENN,DEPT OTORHINOLARYNGOL & HUMAN COMMUN,PHILADELPHIA,PA 19104. CR ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 ANDERSON GJ, 1989, ABS ASS RES OT, V12, P145 CARDER HM, 1972, J SPEECH HEAR RES, V15, P603 COHEN YE, 1992, HEARING RES, V58, P1, DOI 10.1016/0378-5955(92)90002-5 COHEN YE, 1993, IN PRESS EXPER BRAIN CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 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, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1990, HEARING RES, V46, P29, DOI 10.1016/0378-5955(90)90137-E HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 HOU SM, 1973, POULTRY SCI, V52, P159 MANLEY GA, 1991, HEARING RES, V57, P1, DOI 10.1016/0378-5955(91)90068-K 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 MILLS JH, 1973, J SPEECH HEAR RES, V16, P426 MILLS JH, 1972, J SPEECH HEAR RES, V15, P624 PUGLIANO FA, 1993, IN PRESS NEUROSCI LE PUGLIANO FA, 1993, ACTA OTO-LARYNGOL, V113, P18, DOI 10.3109/00016489309135761 REBILLARD G, 1981, BRAIN RES, V229, P15, DOI 10.1016/0006-8993(81)90741-1 REBILLARD G, 1982, HEARING RES, V8, P77, DOI 10.1016/0378-5955(82)90036-3 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SAUNDERS J, 1974, P NATL ACAD SCI USA, V71, P1962, DOI 10.1073/pnas.71.5.1962 Saunders J.C., 1989, P35 SAUNDERS JC, 1986, SENSORINEURAL HEARIN, P29 SAUNDERS JC, 1980, BRAIN RES, V187, P69, DOI 10.1016/0006-8993(80)90495-3 SAUNDERS JC, 1986, HEARING RES, V24, P227, DOI 10.1016/0378-5955(86)90021-3 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 NR 30 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 1993 VL 69 IS 1-2 BP 25 EP 34 DI 10.1016/0378-5955(93)90090-N PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000004 PM 8226347 ER PT J AU MILLER, CA ABBAS, PJ ROBINSON, BK AF MILLER, CA ABBAS, PJ ROBINSON, BK TI CHARACTERIZATION OF WAVE-I OF THE ELECTRICALLY-EVOKED AUDITORY BRAIN-STEM RESPONSE IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; ELECTRICAL STIMULATION; COCHLEAR IMPLANT; EABR; MODELING ID COCHLEAR PATHOLOGY; PHYSIOLOGICAL-PROPERTIES; SENSORINEURAL DEAFNESS; AMINOOXYACETIC ACID; NERVE; STIMULATION; EXCITATION; PATTERNS; CATS; IMPLANTATION AB This paper examines the first component of the electrically evoked auditory brainstem response (EABR) of the guinea pig. Short (20 mus/phase) and long (4000 mus/phase) duration rectangular current pulses were applied through a bipolar intracochlear electrode in acute preparations. Short-duration pulses evoked a synchronized response relatively free of stimulus artifact; long pulses facilitated examination of the integrative capacities of nerve fibers at relatively low current levels. In deafened control subjects, wave I of the EABR consistently demonstrated two positive peaks having different latency-level and adaptation recovery functions. The early component (wave Ia) showed less decrement in latency with increasing stimulus level and recovered faster in a forward-masking paradigm. Non-monotonicities in the adaptation recovery curves were also observed, more consistently in the wave Ib data. It is proposed that wave la arises from stimulation of the axons proximal to the spiral ganglion while wave Ib is initiated at the peripheral dendritic processes. Implications for human cochlear implant research are discussed. C1 UNIV IOWA,DEPT SPEECH PATHOL & AUDIOL,IOWA CITY,IA 52242. UNIV IOWA,DEPT OTOLARYNGOL HEAD & NECK SURG,IOWA CITY,IA 52242. CR BLACK RC, 1983, ANN NY ACAD SCI, V405, P137, DOI 10.1111/j.1749-6632.1983.tb31626.x BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BROWN CJ, 1990, J ACOUST SOC AM, V88, P1385, DOI 10.1121/1.399716 BROWN M, 1992, HEARING RES, V59, P224, DOI 10.1016/0378-5955(92)90119-8 BRYANT GM, 1984, HEARING RES, V15, P173, DOI 10.1016/0378-5955(84)90048-0 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 FINLEY CC, 1978, COCHLEAR IMPLANTS MO, V53, P5 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HINOJOSA R, 1983, ANN NY ACAD SCI, V405, P459, DOI 10.1111/j.1749-6632.1983.tb31662.x JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1987, ANN OTO RHINOL LARYN, V96, P48 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 LIM HH, 1989, J ACOUST SOC AM, V86, P971, DOI 10.1121/1.398732 LINTHICUM FH, 1991, ACTA OTO-LARYNGOL, V111, P327, DOI 10.3109/00016489109137395 MCNEAL DR, 1976, IEEE T BIO-MED ENG, V23, P329, DOI 10.1109/TBME.1976.324593 MERZENICH MM, 1974, NERVOUS SYSTEM, V3, P537 Moxon E.C., 1971, THESIS MIT NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHEPHERD RK, 1990, INFORMATION PROCESSI, P281 SPOENDLI.H, 1974, ARCH OTO-RHINO-LARYN, V208, P137, DOI 10.1007/BF00453927 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 TONG YC, 1980, J LARYNGOL OTOL, V93, P679 VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 Weibel E. R., 1979, STEREOLOGICAL METHOD, V1 WHITE MW, 1984, ARCH OTOLARYNGOL, V110, P493 ZAPPIA JJ, 1991, ANN OTO RHINOL LARYN, V100, P914 NR 32 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 SEP PY 1993 VL 69 IS 1-2 BP 35 EP 44 DI 10.1016/0378-5955(93)90091-E PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000005 PM 8226348 ER PT J AU CHATTERJEE, M SMITH, RL AF CHATTERJEE, M SMITH, RL TI PHYSIOLOGICAL OVERSHOOT AND THE COMPOUND ACTION-POTENTIAL SO HEARING RESEARCH LA English DT Article DE CAP; ADAPTATION; 2-INTERVAL FORCED-CHOICE TECHNIQUE; SIGNAL-TO-NOISE RATIO; OVERSHOOT ID AUDITORY-NERVE FIBERS; RESPONSES; MASKING; ADAPTATION; THRESHOLDS AB The sensitivity of the compound action potential (CAP) of the auditory nerve of t he Mongolian gerbil (Meriones unguiculatus) to an added signal was studied as a function of the state of adaptation to a masker. The masker consisted of a train of tone bursts. A signal was added to one of the bursts and the threshold for detecting the signal was determined using a two-interval forced-choice technique. With a signal at the same frequency as the masker, there was little or no change in threshold with increasing adaptation to the masker, i.e., with the signal applied at masker onset or later on in the train. With a signal at a different frequency, considerably higher thresholds were obtained in the unadapted state than in the adapted state, a situation that appeared to resemble psychophysical overshoot phenomena. However, the interpretation of this result was complicated by the observation that the CAP response to a two-frequency stimulus is a sum of two slightly desynchronized waveforms arising from different cochlear regions. Synchronizing the two waveforms reduced the 'overshoot', but still resulted in higher thresholds in the unadapted state. The differences in threshold are accounted for by considering the changing signal-to-noise ratios at different states of adaptation. Possible relationships to psychophysically observed overshoot are discussed. C1 SYRACUSE UNIV,INST SENSORY RES,MERRILL LANE,SYRACUSE,NY 13244. SYRACUSE UNIV,DEPT BIOENGN & NEUROSCI,SYRACUSE,NY 13244. CR BACON SP, 1991, Q J EXP PSYCHOL-A, V43, P373 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 BACON SP, 1990, J ACOUST SOC AM, V88, P698, DOI 10.1121/1.399773 CARLYON RP, 1987, J ACOUST SOC AM, V82, P1078, DOI 10.1121/1.395329 CHATTERJEE M, 1990, J ACOUST SOC AM, V87, pS100 COOMBS S, 1989, J ACOUST SOC AM, V86, P925, DOI 10.1121/1.398727 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 EGGERMON.JJ, 1973, AUDIOLOGY, V12, P193 HARRISON RV, 1979, ARCH OTO-RHINO-LARYN, V224, P71, DOI 10.1007/BF00455226 KIANG NYS, 1976, ELECTROCOCHLEOGRAPHY KIMBERLEY BP, 1989, J ACOUST SOC AM, V85, P1660, DOI 10.1121/1.397954 MCFADDEN D, 1989, J ACOUST SOC AM, V85, P254, DOI 10.1121/1.397732 PEAKE WT, 1962, J ACOUST SOC AM, V34, P562, DOI 10.1121/1.1918169 RELKIN EM, 1991, HEARING RES, V53, P131, DOI 10.1016/0378-5955(91)90220-4 RELKIN EM, 1987, J ACOUST SOC AM, V82, P1679, DOI 10.1121/1.395159 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 SMITH RL, 1988, J ACOUST SOC AM, V84, pS55, DOI 10.1121/1.2026370 SMITH RL, 1971, J ACOUST SOC AM, V50, P1520, DOI 10.1121/1.1912805 SMITH RL, 1990, ARO ABSTR, V13, P191 SMITH RL, 1979, J ACOUST SOC AM, V50, P1520 SMITH RL, 1975, BIOL CYBERN, V17, P169, DOI 10.1007/BF00364166 SMITH RL, 1993, SENSORY RES MULTIMOD SOKOLICH WG, 1973, J ACOUST SOC AM, V54, pA283 TEAS DONALD C, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1438, DOI 10.1121/1.1918366 YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 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 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 1993 VL 69 IS 1-2 BP 45 EP 54 DI 10.1016/0378-5955(93)90092-F PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000006 PM 8226349 ER PT J AU RONKEN, DA BOSCH, WR MOLNAR, CE AF RONKEN, DA BOSCH, WR MOLNAR, CE TI EFFECTS OF SPIKE DISCHARGE HISTORY ON DISCHARGE PROBABILITY AND LATENCY IN FROG BASILAR PAPILLA UNITS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; SPIKE DISCHARGE; RECOVERY; REFRACTORY; CLICK; FROG ID PERIPHERAL AUDITORY-SYSTEM; NERVE-FIBER; RESPONSE PATTERNS; CAT; DEPENDENCE; STIMULUS; EFFERENT; AFFERENT; MASKING; EAR AB Gaumond et al. [(1982) J. Neurophysiol. 48, 856-873] showed in the cat that a multiplicative-intensity model can generally account quite well for reduction of the probability of an auditory-nerve spike by another spike preceding it by 4 to 25 ms, and that for smaller separations there is also an increased latency of the following spike. Bosch [(1990) D. Sc. Dissertation, Washington University, St. Louis, MO] made important improvements in experimental design and estimation techniques for studying these effects, and confirmed their presence in the gerbil. However, direct application of these methods to the frog does not yield reliable estimates. A clearer separation of discharge probability and latency effects in frog basilar papilla units is provided by the paired-click paradigm used in this study, which is applicable to low-spontaneous-rate units that generally respond to click stimuli with zero or one spike within a short interval following the click. The results confirm the existence in the frog of both spike-probability and spike-latency effects that are qualitatively similar to those found in mammals, although the absolute refractory time is much longer in frog, and the relative refractory time usually shorter. The paired-click paradigm also reveals a stimulus-history effect at stimulus levels which are near threshold: when there is no response to the first click, responses to the second click occur with increased probability and reduced latency. C1 WASHINGTON UNIV,SCH MED,INST BIOMED COMP,ST LOUIS,MO 63110. CR BARRETT EF, 1978, J PHYSIOL-LONDON, V279, P253 BOSCH WR, 1990, THESIS WASHINGTON U BOSCH WR, 1993, UNPUB HEAR RES CAPRANICA RR, 1975, J COMP PHYSIOL, V100, P231 FRISHKOP.LS, 1974, ACTA OTO-LARYNGOL, V77, P176, DOI 10.3109/00016487409124615 GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 GAUMOND RP, 1980, THESIS WASHINGTON U GOBLICK TJ, 1969, J ACOUST SOC AM, V46, P924, DOI 10.1121/1.1911812 GRAY PR, 1967, BIOPHYS J, V7, P759, DOI 10.1016/S0006-3495(67)86621-9 HALTER JA, 1991, J THEOR BIOL, V148, P345, DOI 10.1016/S0022-5193(05)80242-5 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 JOHNSON DH, 1983, J ACOUST SOC AM, V74, P493, DOI 10.1121/1.389815 KATZ B, 1965, J PHYSIOL-LONDON, V181, P656 Kiang N Y S, 1984, HDB PHYSL NERVOUS SY, VIII, P639 Kiang NY-s, 1965, DISCHARGE PATTERNS S LEWIS ER, 1982, SCIENCE, V215, P1641, DOI 10.1126/science.6978525 LEWIS ER, 1982, J COMP PHYSIOL, V145, P437 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1988, HEARING RES, V34, P179, DOI 10.1016/0378-5955(88)90105-0 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LUUTKENHONER B, 1986, HEARING RES, V24, P289 MEGELA AL, 1982, J ACOUST SOC AM, V71, P641, DOI 10.1121/1.387538 MEGELA AL, 1981, J NEUROPHYSIOL, V46, P465 Muller H., 1976, P1023 NARINS PM, 1989, J ACOUST SOC AM, V85, P1255, DOI 10.1121/1.397456 Paintal AS, 1978, PHYSL PATHOBIOLOGY A, P131 PFEIFFER RR, 1972, J ACOUST SOC AM, V52, P1669, DOI 10.1121/1.1913301 RONKEN DA, 1991, ABSTR ASS RES OT, P131 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 WARREN EH, 1989, HEARING RES, V37, P105, DOI 10.1016/0378-5955(89)90033-6 WEISS TF, 1988, HEARING RES, V33, P175, DOI 10.1016/0378-5955(88)90030-5 NR 32 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 1993 VL 69 IS 1-2 BP 55 EP 75 DI 10.1016/0378-5955(93)90093-G PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000007 PM 8226350 ER PT J AU YAO, WP GODFREY, DA AF YAO, WP GODFREY, DA TI CHOLINE-ACETYLTRANSFERASE IN COCHLEAR ROOT NEURONS SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINESTERASE; AUDITORY; CHOLINERGIC; COCHLEAR NUCLEUS; IMMUNOHISTOCHEMISTRY; QUANTITATIVE HISTOCHEMISTRY ID BRAIN-STEM; RAT; NUCLEUS; COMPLEX; SYSTEM AB Cochlear root neurons are a distinct group of cells located in the auditory nerve root in small rodents. Their transmitter is still unknown. Some of our preparations showed immunoreactivity of somata of cochlear root neurons with both polyclonal and monoclonal antibodies against choline acetyltransferase (ChAT) which, despite their very weak histochemical reaction for acetylcholinesterase (AChE), suggested that cochlear root neurons might be cholinergic. To test this, we used a radiometric assay to measure ChAT activities of rat auditory nerve root samples containing cochlear root neurons and of adjacent samples not containing them. There was no significant difference between the low mean ChAT activities of these two groups of samples. Thus, cochlear root neurons are not likely to be cholinergic. RP YAO, WP (reprint author), MED COLL OHIO,DEPT OTOLARYNGOL HEAD & NECK SURG,POB 10008,TOLEDO,OH 43699, USA. CR DUNNING D D, 1984, Society for Neuroscience Abstracts, V10, P682 ELBADAWI A, 1967, J HISTOCHEM CYTOCHEM, V15, P580 FONNUM F, 1973, J NEUROCHEM, V21, P1109, DOI 10.1111/j.1471-4159.1973.tb07565.x GODFREY DA, 1983, HEARING RES, V9, P3, DOI 10.1016/0378-5955(83)90129-6 GODFREY DA, 1993, MAMMALIAN COCHLEAR N, P267 GODFREY DA, 1976, J HISTOCHEM CYTOCHEM, V24, P697 Godfrey D.A., 1985, P163 GODFREY DA, 1987, HEARING RES, V31, P203, DOI 10.1016/0378-5955(87)90188-2 HARRISON JM, 1966, J COMP NEUROL, V126, P51, DOI 10.1002/cne.901260105 HARRISON JM, 1962, J COMP NEUROL, V119, P341, DOI 10.1002/cne.901190306 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 HEBB CO, 1957, PHYSIOL REV, V37, P196 HENDERSON Z, 1991, J COMP NEUROL, V314, P147, DOI 10.1002/cne.903140114 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 KARNOVSKY MJ, 1964, J HISTOCHEM CYTOCHEM, V12, P219 KATO T, 1985, J NEUROCHEM, V44, P675, DOI 10.1111/j.1471-4159.1985.tb12867.x LOPEZ DE, 1993, MAMMALIAN COCHLEAR N, P291 Lowry OH, 1972, FLEXIBLE SYSTEM ENZY MCCAMAN RE, 1970, J NEUROCHEM, V17, P1421, DOI 10.1111/j.1471-4159.1970.tb06877.x MERCHAN MA, 1988, J NEUROCYTOL, V17, P711, DOI 10.1007/BF01260998 OH JD, 1992, NEUROSCIENCE, V47, P807, DOI 10.1016/0306-4522(92)90031-V OSEN KK, 1991, J NEUROCYTOL, V20, P17, DOI 10.1007/BF01187131 POLAK JM, 1984, INTRO IMMUNOCYTOCHEM TAGO H, 1989, BRAIN RES, V495, P271, DOI 10.1016/0006-8993(89)90221-7 TATEHATA T, 1987, J HIRNFORSCH, V28, P707 VETTER DE, 1993, MAMMALIAN COCHLEAR N, P279 WAINER BH, 1984, NEUROCHEM INT, V6, P163, DOI 10.1016/0197-0186(84)90089-5 WEBSTER DB, 1982, AM J ANAT, V163, P103, DOI 10.1002/aja.1001630202 NR 29 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 SEP PY 1993 VL 69 IS 1-2 BP 76 EP 82 DI 10.1016/0378-5955(93)90094-H PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000008 PM 8226351 ER PT J AU GRAY, L AF GRAY, L TI SIMULTANEOUS MASKING IN NEWBORN CHICKENS SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; FREQUENCY ANALYSIS; MASKING; CHICK ID FREQUENCY DISCRIMINATION; RESPONSES; THRESHOLDS; INFANTS; NUCLEI; RAT AB Simultaneous masking was used to investigate the development of frequency analysis in newborn animals. The ability of young chickens to detect a tone in the presence of a second tone was measured. In the first experiment data were collected with a 500-Hz masker presented at 15 or 25 dB above absolute threshold. Signals to be detected varied up to an octave from the masker (+/- 1/9, +/- 2/9, +/- 1/3, +/- 2/3, and -1 octave). Receiver operating characteristics (ROCs) were constructed from delays in ongoing peeps that occur when chicks detect the presence of the signal over the masker. Psychometric functions were fit by probit analysis using areas under these ROCs. Amounts of masking were estimated by the degree to which psychometric functions were shifted toward the right by the presence of the masker. There is no developmental change in these masking patterns, corroborating recent data from human infants. Masking was shown in a second experiment to be similar at a higher frequency (given intensities corrected for improving absolute thresholds). In conclusion, masking patterns derived from chicks' peeps are like those from adult humans. Frequency analysis, as measured by simultaneous masking, appears to be mature in chickens at hatching. RP GRAY, L (reprint author), UNIV TEXAS,HLTH SCI CTR,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,6431 FANNIN,MSB 6132,HOUSTON,TX 77030, USA. CR CAMPBELL BA, 1983, J COMP PSYCHOL, V97, P3, DOI 10.1037/0735-7036.97.1.3 Ehmer RH, 1958, J ACOUST SOC AM, V31, P1115 EMMERICH DS, 1972, PERCEPT PSYCHOPHYS, V2, P65 Fay R. R., 1988, HEARING VERTEBRATES Finney D. J., 1971, PROBIT ANAL, V3rd Gelfand S. A., 1990, HEARING INTRO PSYCHO, V2nd Gibson E. J., 1969, PRINCIPLES PERCEPTUA Gottlieb G., 1981, DEV PERCEPTION, V1 GRAY L, 1985, MEASUREMENT AUDITION, P145 GRAY L, 1990, HEARING RES, V45, P169, DOI 10.1016/0378-5955(90)90118-9 GRAY L, 1990, DEV PSYCHOBIOL, V23, P297, DOI 10.1002/dev.420230402 GRAY L, 1992, DEV PSYCHOACOUSTICS, P89, DOI 10.1037/10119-003 GRAY L, 1992, J ACOUST SOC AM, V91, P1608, DOI 10.1121/1.402441 GRAY L, 1987, J ACOUST SOC AM, V82, P1608, DOI 10.1121/1.395151 GRAY L, 1985, J ACOUST SOC AM, V77, P1162, DOI 10.1121/1.392180 GREEN DM, 1966, SIGNAL DETECTION THE HYSON RL, 1987, DEV PSYCHOBIOL, V20, P189, DOI 10.1002/dev.420200208 JESTEADT W, 1985, J ACOUST SOC AM, V78, P365, DOI 10.1121/1.392500 JESTEADT W, 1975, J ACOUST SOC AM, V57, P1161, DOI 10.1121/1.380574 KERR LM, 1979, J EXP PSYCHOL ANIM B, V5, P97, DOI 10.1037//0097-7403.5.2.97 LICKLIDER JCR, 1951, HDB EXPT PSYCHOL LIPPE WR, 1987, HEARING RES, V25, P205, DOI 10.1016/0378-5955(87)90092-X LONG GR, 1981, HEARING RES, V4, P279, DOI 10.1016/0378-5955(81)90012-5 MANLEY GA, 1991, HEARING RES, V57, P1, DOI 10.1016/0378-5955(91)90068-K MCFADDEN D, 1983, ANNU REV PSYCHOL, V34, P95, DOI 10.1146/annurev.ps.34.020183.000523 MCKEE SP, 1985, PERCEPT PSYCHOPHYS, V37, P286, DOI 10.3758/BF03211350 NORUSIS MJ, 1990, SPSS PCPLUS ADV STAT OLSHO LW, 1985, INFANT BEHAV DEV, V8, P371, DOI 10.1016/0163-6383(85)90002-5 OLSHO LW, 1984, INFANT BEHAV DEV, V7, P27, DOI 10.1016/S0163-6383(84)80020-X PATTERSON RD, 1978, HDB PERCEPTION, V4 REBILLARD G, 1981, BRAIN RES, V229, P15, DOI 10.1016/0006-8993(81)90741-1 Rubel EW, 1988, AUDITORY FUNCTION NE, P3 RUBEL EW, 1975, J EXP PSYCHOL ANIM B, V1, P287 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RUDY JW, 1984, DEV PSYCHOBIOL, V17, P285, DOI 10.1002/dev.420170308 SAUNDERS JC, 1980, J EXP BIOL, V87, P331 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SCHNEIDER BA, 1989, J ACOUST SOC AM, V86, P1733, DOI 10.1121/1.398604 SCHNEIDER I, 1990, HEARING RES, V52, P281 SEVERNS M, 1985, PHYSIOL BEHAV, V34, P843, DOI 10.1016/0031-9384(85)90388-9 SPETNER NB, 1990, CHILD DEV, V61, P632, DOI 10.1111/j.1467-8624.1990.tb02808.x Swets J. A., 1982, EVALUATION DIAGNOSTI WATSON CS, 1964, J ACOUST SOC AM, V36, P283, DOI 10.1121/1.1918947 Wegel RL, 1924, PHYS REV, V23, P266, DOI 10.1103/PhysRev.23.266 WERNER LA, 1990, INFANT BEHAV DEV, V13, P355, DOI 10.1016/0163-6383(90)90040-F WERNER LA, 1991, PERCEPT PSYCHOPHYS, V50, P405, DOI 10.3758/BF03205057 Wilson W. R., 1984, PEDIAT AUDIOLOGY, P1 NR 48 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 SEP PY 1993 VL 69 IS 1-2 BP 83 EP 90 DI 10.1016/0378-5955(93)90095-I PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000009 PM 8226352 ER PT J AU DECHESNE, CJ WINSKY, L MONIOT, B RAYMOND, J AF DECHESNE, CJ WINSKY, L MONIOT, B RAYMOND, J TI LOCALIZATION OF CALRETININ MESSENGER-RNA IN RAT AND GUINEA-PIG INNER-EAR BY IN-SITU HYBRIDIZATION USING RADIOACTIVE AND NONRADIOACTIVE PROBES SO HEARING RESEARCH LA English DT Article DE CALRETININ; COCHLEA; VESTIBULE; IN-SITU HYBRIDIZATION; OLIGONUCLEOTIDE PROBE; DIGOXIGENIN; RAT; GUINEA PIG ID CALCIUM-BINDING PROTEIN; ALZHEIMER-TYPE DEMENTIA; CALBINDIN-D 28K; PARVALBUMIN IMMUNOCYTOCHEMISTRY; VESTIBULAR GANGLION; NERVOUS-SYSTEM; NEURONS; HIPPOCAMPUS; IMMUNOREACTIVITY; IDENTIFICATION AB The localization of calretinin mRNA was studied in the rat and guinea pig inner ear by in situ hybridization, and compared to the distribution of the protein previously examined by immunocytochemistry. Radioactive and non-radioactive in situ hybridizations (ISH) were performed using oligonucleotide probes labelled with S-35 or digoxigenin. Radioactive ISH was more sensitive than non-radioactive ISH. In cochlear and vestibular ganglia, calretinin mRNA was localized in subpopulations of neurons with patterns of distribution similar to those shown by immunocytochemistry. By contrast, the observations in the sensory epithelia differed with the two techniques, ISH revealing less positive structures than immunocytochemistry. Rat inner hair cells and guinea pig inner hair cells, Hensen's cells and Deiters cells, which had been described strongly immunoreactive, appeared positive with radioactive but not with non-radioactive ISH. On the other hand, rat vestibular type II hair cells and guinea pig interdental cells of the spiral limbus which were faintly immunoreactive were not positive with both ISH techniques. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP DECHESNE, CJ (reprint author), INSERM,U254,LAB NEUROPHYSIOL SENSORIELLE LAB,UM2,CP 089,PL BATAILLON,F-34095 MONTPELLIER 5,FRANCE. CR ARAI H, 1987, BRAIN RES, V418, P164, DOI 10.1016/0006-8993(87)90974-7 BAIMBRIDGE KG, 1992, TRENDS NEUROSCI, V15, P303, DOI 10.1016/0166-2236(92)90081-I DECHESNE CJ, 1991, BRAIN RES, V560, P139, DOI 10.1016/0006-8993(91)91224-O 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 DEMEMES D, 1991, MOL BRAIN RES, V9, P153, DOI 10.1016/0169-328X(91)90141-J DEMEMES D, 1992, BRAIN RES, V582, P168, DOI 10.1016/0006-8993(92)90334-6 DESMADRYL G, 1992, EXP BRAIN RES, V89, P105 HEIZMANN CW, 1991, TRENDS BIOCHEM SCI, V16, P98, DOI 10.1016/0968-0004(91)90041-S ICHIMIYA Y, 1989, BRAIN RES, V499, P402, DOI 10.1016/0006-8993(89)90793-2 LERANTH C, 1991, EXP BRAIN RES, V85, P129 MCGINN MD, 1992, NEUR ABS NORMAND E, 1991, J HISTOCHEM CYTOCHEM, V39, P1575 NORMAND E, 1992, HYBRIDATION IN SITU, P21 PARMENTIER M, 1990, ADV EXP MED BIOL, V269, P27 Raymond J, 1993, Acta Otolaryngol Suppl, V503, P114 ROGERS JH, 1987, J CELL BIOL, V105, P1343, DOI 10.1083/jcb.105.3.1343 SANS A, 1987, BRAIN RES, V435, P293, DOI 10.1016/0006-8993(87)91612-X SCHWARTZ IR, 1992, NEUR ABS SEQUIER JM, 1988, NEUROSCI LETT, V86, P155, DOI 10.1016/0304-3940(88)90563-0 SLOVITER RS, 1989, J COMP NEUROL, V280, P183, DOI 10.1002/cne.902800203 SLOVITER RS, 1991, J COMP NEUROL, V308, P381, DOI 10.1002/cne.903080306 SUTHERLAND MK, 1992, MOL BRAIN RES, V13, P239 WINSKY L, 1989, P NATL ACAD SCI USA, V86, P10139, DOI 10.1073/pnas.86.24.10139 Winsky L, 1991, NOVEL CALCIUM BINDIN, P277 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 SEP PY 1993 VL 69 IS 1-2 BP 91 EP 97 DI 10.1016/0378-5955(93)90096-J PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000010 PM 8226353 ER PT J AU FAINGOLD, CL ANDERSON, CAB RANDALL, ME AF FAINGOLD, CL ANDERSON, CAB RANDALL, ME TI STIMULATION OR BLOCKADE OF THE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS ALTERS BINAURAL AND TONIC INHIBITION IN CONTRALATERAL INFERIOR COLLICULUS NEURONS SO HEARING RESEARCH LA English DT Article DE DORSAL NUCLEUS OF THE LATERAL LEMNISCUS; INFERIOR COLLICULUS; GABA; BINAURAL INHIBITION; TONIC INHIBITION; ELECTRICAL STIMULATION ID GAMMA-AMINOBUTYRIC ACID; STEM AUDITORY NUCLEI; RESPONSE PROPERTIES; GUINEA-PIG; BRAIN-STEM; MEDIATED INHIBITION; GABAERGIC NEURONS; SINGLE NEURONS; GABA; RAT AB Recent studies have demonstrated that several specific types of acoustically-evoked GABA-mediated inhibition occur in neurons of the central nucleus of inferior colliculus (ICc). The dorsal nucleus of the lateral lemniscus (DNLL) provides a major GABAergic projection to ICc. The present study examined the effects of electrical or chemical stimulation or reversible blockade within the DNLL on the discharge characteristics of ICc neurons in anesthetized rats. Microinjection of a local anesthetic (lidocaine) or a GABA-A agonist (THIP) via a cannula placed into DNLL reversibly blocked acoustically-evoked binaural inhibition and increased spontaneous firing in most contralateral ICc neurons. Trains of electrical pulses or microinjection of the excitant amino acid, kainate, into DNLL resulted in reduced acoustically-evoked firing, which was similar to binaural inhibition, in most contralateral ICc neurons examined. The effects of DNLL electrical stimulation were reversibly blocked by microinjection of THIP into the stimulation site, suggesting that the effect of the electrical stimulation is mediated by direct effects on cell bodies of DNLL neurons. These data support the idea that contralateral GABAergic input from the DNLL is inhibitory to ICc neurons. Thus, binaural inhibition and tonic inhibition in ICc neurons may be mediated, in part, by the GABAergic projection from the contralateral DNLL. RP FAINGOLD, CL (reprint author), SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,POB 19230,SPRINGFIELD,IL 62794, USA. CR ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 ADAMS JC, 1979, NEUROSCIENCE, V4, P1947, DOI 10.1016/0306-4522(79)90067-8 AITKIN L, 1986, AUDITORY MIDBRAIN ST, P101 AITKIN LM, 1970, J NEUROPHYSIOL, V33, P421 BRISTOW DR, 1988, EUR J PHARMACOL, V148, P283, DOI 10.1016/0014-2999(88)90576-6 BRUGGE JF, 1970, J NEUROPHYSIOL, V33, P441 CAIRD D, 1991, NEUROBIOLOGY HEARING, V2, P253 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CHAN J C K, 1984, Society for Neuroscience Abstracts, V10, P844 Covey E., 1992, Society for Neuroscience Abstracts, V18, P150 FAINGOLD CL, 1991, NEUROBIOLOGY HEARING, V2, P223 FAINGOLD CL, 1986, EXP NEUROL, V93, P145, DOI 10.1016/0014-4886(86)90154-8 FAINGOLD CL, 1991, HEARING RES, V52, P201, DOI 10.1016/0378-5955(91)90200-S Faingold C. L., 1992, Society for Neuroscience Abstracts, V18, P1193 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 FISHER SK, 1976, J NEUROCHEM, V27, P1145, DOI 10.1111/j.1471-4159.1976.tb00321.x FLAMMINO F, 1975, J ACOUST SOC AM, V57, P692, DOI 10.1121/1.380494 FUJITA I, 1991, J NEUROSCI, V11, P722 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 HELFERT RH, 1991, NEUROBIOLOGY HEARING, V2, P1 HUTSON KA, 1991, J COMP NEUROL, V312, P105, DOI 10.1002/cne.903120109 KELLY JB, 1991, HEARING RES, V56, P273, DOI 10.1016/0378-5955(91)90177-B KIRZINGER A, 1990, J NEUROSCI METH, V33, P165, DOI 10.1016/0165-0270(90)90020-G KUDO M, 1981, BRAIN RES, V221, P57, DOI 10.1016/0006-8993(81)91063-5 KUWADA S, 1980, PSYCHOPHYSICAL PHYSL, P401 LI L, 1992, J NEUROSCI, V12, P4530 Li L., 1992, Society for Neuroscience Abstracts, V18, P1035 LOPEZCOLOME AM, 1978, NEUROSCIENCE, V3, P1069, DOI 10.1016/0306-4522(78)90124-0 MALPELI JG, 1979, J NEUROSCI METH, V1, P143, DOI 10.1016/0165-0270(79)90011-6 MILLAN MH, 1986, NEUROSCI LETT, V70, P69, DOI 10.1016/0304-3940(86)90439-8 MOISEFF A, 1985, Society for Neuroscience Abstracts, V11, P735 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 NAGAI T, 1985, J COMP NEUROL, V231, P260, DOI 10.1002/cne.902310213 NELSON PG, 1963, J NEUROPHYSIOL, V26, P908 OLIVER DL, 1989, J NEUROSCI, V9, P967 OLIVER DL, 1991, NEUROBIOLOGY HEARING, V2, P195 Ottersen O. P., 1984, HDB CHEM NEUROANATOM, V3, P141 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd POTASHNER S J, 1991, Society for Neuroscience Abstracts, V17, P300 RIAZ A, 1990, Society for Neuroscience Abstracts, V16, P781 RING JB, 1985, PHARMACOLOGIST, V27, P232 ROBERTS RC, 1987, J NEUROCYTOL, V16, P333, DOI 10.1007/BF01611345 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 SALLY SL, 1992, BRAIN RES, V572, P5, DOI 10.1016/0006-8993(92)90444-E 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 SIMSON PE, 1991, J PHARMACOL EXP THER, V259, P1288 SMITH D C, 1990, Society for Neuroscience Abstracts, V16, P187 Suneja S. K., 1992, Society for Neuroscience Abstracts, V18, P1036 TACHIBAN.M, 1974, BRAIN RES, V69, P370, DOI 10.1016/0006-8993(74)90017-1 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 VATER M, 1992, J COMP PHYSIOL A, V171, P541 WATANABE T, 1973, JPN J PHYSIOL, V23, P291 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, 1981, J NEUROPHYSIOL, V45, P35 YAMAUCHI R, 1989, NEUROSCI RES, V6, P446, DOI 10.1016/0168-0102(89)90006-0 YANG LC, 1992, J NEUROPHYSIOL, V68, P1760 NR 60 TC 96 Z9 97 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 1993 VL 69 IS 1-2 BP 98 EP 106 DI 10.1016/0378-5955(93)90097-K PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000011 PM 8226354 ER PT J AU WANGEMANN, P SHIGA, N MARCUS, DC AF WANGEMANN, P SHIGA, N MARCUS, DC TI THE NA+/H+ EXCHANGER IN TRANSITIONAL CELLS OF THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE NHE-1; ETHYLISOPROPYLAMILORIDE; BCECF; VESTIBULAR LABYRINTH; GERBIL ID INTRACELLULAR PH REGULATION; H+ EXCHANGER; MEMBRANE; CLONING; GERBIL; NHE-1 AB The cytosolic pH (pH(i)) of transitional cells from the ampulla of the gerbil was measured micro-fluorometrically with the pH-sensitive dye 2',7'-bicarboxyethyl-5(6)-carboxyfluorescein (BCECF) to assess the possible contribution of a Na+/H+ exchanger to the regulation of pH(i). All experiments were conducted in virtually HCO3--free solutions. Under control conditions, pH(i) was 7.19 and addition of 10(-5) M ethylisopropylamiloride (EIPA), a blocker of Na+/H+ exchange, caused a small but significant acidification of pH(i). A transient exposure to 21.4 mM NH4Cl caused a rapid cytosolic alkalinization followed by a brisk acidification and prompt recovery of pH(i) to its control value. The cytosolic buffer capacity (B(i)) was determined in the absence of Na+ from changes in pH(i) which were elicited by [NH4+] steps. B(i) was 4.7 mM/pH at pH(i) 7.19 and varied with pH(i). The initial net proton flux J(H), representative of Na+/H+ exchange activity, was calculated from the product of the initial rate of alkalinization after an NH4+-prepulse and B(i) at the corresponding pH(i). J(H) was dependent on the extracellular Na+ with an apparent K(m) of 64 mM, sensitive to the cytosolic [H+] with an apparent K(m) of 2.7 * 10(-7) M (i.e. pH 6.6), and inhibited by EIPA with an IC50 of 5 * 10(-7) M. These data suggest that transitional cells contain in the basolateral membrane a Na+/H+ exchanger of the amiloride-sensitive subtype. RP WANGEMANN, P (reprint author), BOYS TOWN NATL RES HOSP,CELL PHYSIOL LAB,555 N 30TH ST,OMAHA,NE 68131, USA. RI Wangemann, Philine/N-2826-2013 CR ARONSON PS, 1985, ANNU REV PHYSIOL, V47, P545 BORON WF, 1976, J GEN PHYSIOL, V67, P91, DOI 10.1085/jgp.67.1.91 BOYARSKY G, 1988, AM J PHYSIOL, V255, pC844 CLARK JD, 1991, AM J PHYSIOL, V261, pC945 GRINSTEIN S, 1986, J MEMBRANE BIOL, V90, P1, DOI 10.1007/BF01869680 GRINSTEIN S, 1989, BIOCHIM BIOPHYS ACTA, V988, P73, DOI 10.1016/0304-4157(89)90004-X KULANTHAIVEL P, 1992, BIOCHEM J, V284, P33 KURTZ I, 1988, J MEMBRANE BIOL, V106, P253, DOI 10.1007/BF01872163 MARCUS NY, 1985, AM J OTOLARYNG, V6, P268, DOI 10.1016/S0196-0709(85)80054-5 MOOLENAAR WH, 1986, ANNU REV PHYSIOL, V48, P363 MORI N, 1987, ARCH OTO-RHINO-LARYN, V244, P61, DOI 10.1007/BF00453493 NINOYU O, 1986, ARCH OTO-RHINO-LARYN, V243, P141, DOI 10.1007/BF00453767 ORLOWSKI J, 1992, J BIOL CHEM, V267, P9331 RENNER EL, 1989, AM J PHYSIOL, V256, pG44 RINK TJ, 1982, J CELL BIOL, V95, P189, DOI 10.1083/jcb.95.1.189 SALT AN, 1989, AM J OTOLARYNG, V10, P371, DOI 10.1016/0196-0709(89)90030-6 SHIGA N, 1993, KINETICS NAPLUS HPLU THOMAS JA, 1979, BIOCHEMISTRY-US, V18, P2210, DOI 10.1021/bi00578a012 TSE CM, 1992, J BIOL CHEM, V267, P9340 VILELLA S, 1992, PFLUG ARCH EUR J PHY, V420, P275, DOI 10.1007/BF00374459 VOELKL H, 1988, BIOCHIM BIOPHYS ACTA, V946, P5 WANGEMANN P, 1993, PH SENSITIVITY MEMBR WANGEMANN P, 1989, PFLUG ARCH EUR J PHY, V414, P656, DOI 10.1007/BF00582132 WANGEMANN P, 1993, IN PRESS PFLUGGERS A WANGEMANN P, 1989, FASEB Journal, V3, pA564 WEINTRAUB WH, 1989, AM J PHYSIOL, V257, pG317 ZWEIFACH A, 1992, J MEMBRANE BIOL, V128, P115 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 SEP PY 1993 VL 69 IS 1-2 BP 107 EP 114 DI 10.1016/0378-5955(93)90098-L PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000012 PM 8226330 ER PT J AU KOK, MR VANZANTEN, GA BROCAAR, MP AF KOK, MR VANZANTEN, GA BROCAAR, MP TI ASPECTS OF SPONTANEOUS OTOACOUSTIC EMISSIONS IN HEALTHY NEWBORNS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; CLICK-EVOKED OTOACOUSTIC EMISSIONS; NEWBORN ID OTO-ACOUSTIC EMISSIONS; HUMAN EARS; HEARING SUBJECTS; FREQUENCY; PREVALENCE; THRESHOLD; CHILDREN AB Spontaneous otoacoustic emissions (SOAEs) are pure-tone like signals, spontaneously present in the ear canal. In normal adult ears the prevalence of SOAEs is reported to be 30-70%, probably depending on the noise floor of the recordings. In infant studies, results on the SOAE prevalence are rare. SOAEs as well as evoked otoacoustic emissions (EOAEs) were recorded in healthy newborns. Their ages varied between 1 and 10 days. The recordings were done with commercially available equipment in a separate not sound treated -room of the obstetric department. The prevalence of SOAEs was 78%, which is higher than previously reported for adults as well as healthy newborns. The prevalence was not significantly different between left and right ears, or genders. The number of emissions per emitting ear amounted on average 5.5. The median number of SOAEs in boys (3.3) is significantly lower than in girls (4.6). The SOAE levels were between -2 and 42 dB SPL. The mean level per emitting ear was 8.0 dB SPL and not significantly different between right and left ears or genders. However, the level of the strongest emission per emitting ear was significantly higher for right than for left ears. In contrast with adults most of the emissions (70%) are at frequencies above 2 kHz. Comparing the levels of the EOAEs between ears with and without SOAEs we found a statistically significant higher EOAE level in ears with SOAEs. This supports our previous hypothesis that the higher EOAE level found in healthy newborns is partly due to the more frequent presence of stronger SOAEs in healthy newborns. Given these results in newborns and in view of the literature, we hypothesize that major developmental changes in the OAE phenomenon occur between 0 and 6 years of age. RP KOK, MR (reprint author), ERASMUS UNIV ROTTERDAM,DEPT OTORHINOLARYNGOL AUDIOL,EE 1655,POB 1738,3000 DR ROTTERDAM,NETHERLANDS. CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 BONFILS P, 1989, ARCH OTO-RHINO-LARYN, V246, P249, DOI 10.1007/BF00463565 BONFILS P, 1990, LARYNGOSCOPE, V100, P186 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 Cianfrone G, 1986, Scand Audiol Suppl, V25, P121 FRITZE W, 1983, ARCH OTO-RHINO-LARYN, V238, P189, DOI 10.1007/BF00454312 GLANVILLE J D, 1971, Journal of Laryngology and Otology, V85, P1 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Kemp D T, 1981, Ciba Found Symp, V85, P54 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KEMP DT, 1990, EAR HEARING, V11, P93 KOK MR, 1992, AUDIOLOGY, V31, P140 KOK MR, 1993, AUDIOLOGY, V32, P213 LONG GR, 1988, HEARING RES, V36, P125, DOI 10.1016/0378-5955(88)90055-X LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 MARTIN GK, 1990, EAR HEARING, V11, P106 MATHIS A, 1991, ARCH OTOLARYNGOL, V117, P674 NORTON SJ, 1991, MAY INT S OT EM KANS, P9 NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 PROBST R, 1987, AM J OTOLARYNG, V8, P73, DOI 10.1016/S0196-0709(87)80027-3 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 Rebillard G, 1987, Ann Otolaryngol Chir Cervicofac, V104, P363 SCHLOTH E, 1983, ACUSTICA, V53, P250 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 VANDIJK P, 1990, J ACOUST SOC AM, V88, P1779, DOI 10.1121/1.400199 VANDIJK P, 1988, BASIC ISSUES HEARING, P101 WIER CC, 1984, J ACOUST SOC AM, V76, P1248, DOI 10.1121/1.391376 WIT HP, 1981, J ACOUST SOC AM, V70, P437, DOI 10.1121/1.386786 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 ZWICKER E, 1990, COCHLEAR MECHANISMS, V7, P63 NR 35 TC 30 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 1993 VL 69 IS 1-2 BP 115 EP 123 DI 10.1016/0378-5955(93)90099-M PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000013 PM 8226331 ER PT J AU MARCUS, DC TAKEUCHI, S WANGEMANN, P AF MARCUS, DC TAKEUCHI, S WANGEMANN, P TI 2 TYPES OF CHLORIDE CHANNEL IN THE BASOLATERAL MEMBRANE OF VESTIBULAR DARK CELLS SO HEARING RESEARCH LA English DT Article DE GERBIL; 95 PS CL- CHANNEL; LARGE CONDUCTANCE (LC-TYPE) CL- CHANNEL; POTASSIUM SECRETION ID TRANSEPITHELIAL ELECTRICAL RESPONSES; GERBIL UTRICLE INVITRO; NONSENSORY REGION; APICAL MEMBRANE; EPITHELIAL-CELLS; CYSTIC-FIBROSIS; ANION CHANNELS; K+ CHANNEL; CONDUCTANCE; RAT AB Transepithelial and cell membrane potential measurements have suggested that the basolateral membrane of gerbil vestibular dark cells contains Cl- conductive pathways. We used the patch clamp technique to search this membrane for Cl- conductive channels which could account for the macroscopic observations. Two types of Cl- channel were found in both cell-attached and excised membrane patches. One type was found with an incidence of 19% and had a single-channel conductance of 95 +/- 1 pS (N = 20) in symmetrical Cl- solutions. The other type was found with an incidence of 3% and had a large single-channel conductance of 360 +/- 11 pS (N = 12) in symmetrical Cl- solutions (LC-type Cl- channel). Both types of Cl- channel had linear current-voltage relations and at least 2 substates. In asymmetrical Cl- solutions (gluconate substitution) the current-voltage relations fit the Goldman-Hodgkin-Katz current equation for Cl-. Neither channel was blocked by Zn2+, NPPB, DIDS, DNDS or quinine. The 95 pS channel exhibited a spontaneous 'rundown' of its activity within 1 to 10 min after being excised. This rundown was not reversed by the catalytic subunit of protein kinase A. Channel activity was not dependent on the presence of cytosolic Ca2+ nor markedly altered by variations in cytosolic pH between 6.5 and 8.0. The two Cl- channels were distinguished by the membrane voltage ranges in which they were active and by their anion selectivity. The open probability of the 95 pS channel was insensitive to voltage and the anions NO3-, I- and Br - were only half as permeable as Cl-. By contrast, the LC-type Cl- channel was mostly active between about +/- 30 mV and equally permeable to NO-, I-, Br- and Cl-. The 95 pS Cl- channel may account for the observed transepithelial and intracellular voltage responses to Cl- concentration steps and provide the path for the recirculation of Cl- across the basolateral membrane. The LC-type Cl- channel shows the same lack of anion discrimination as the anion pathway activated during hyposmotic challenge. RP MARCUS, DC (reprint author), BOYS TOWN NATL RES HOSP,BIOPHYS LAB,555 N 30TH ST,OMAHA,NE 68131, USA. RI Wangemann, Philine/N-2826-2013 CR ALTON EWFW, 1991, J PHYSIOL-LONDON, V443, P137 ANDERSON MP, 1992, AM J PHYSIOL, V263, pL1 BERNARD C, 1986, J PHYSIOL-LONDON, V371, P17 CHRISTENSEN O, 1989, PFLUG ARCH EUR J PHY, V415, P37, DOI 10.1007/BF00373139 COULOMBE A, 1992, PFLUG ARCH EUR J PHY, V422, P143, DOI 10.1007/BF00370413 DIENER M, 1989, J MEMBRANE BIOL, V108, P21, DOI 10.1007/BF01870422 FISHER H, 1991, J COMP PHYSIOL B, V161, P333 GOGELEIN H, 1988, BIOCHIM BIOPHYS ACTA, V947, P521, DOI 10.1016/0304-4157(88)90006-8 GREGER R, 1983, PFLUG ARCH EUR J PHY, V399, P29, DOI 10.1007/BF00652518 HANRAHAN JW, 1985, P NATL ACAD SCI USA, V82, P7791, DOI 10.1073/pnas.82.22.7791 HOLLUNDER-REESE F, 1991, Cellular Physiology and Biochemistry, V1, P238, DOI 10.1159/000154612 KUNZELMANN K, 1989, PFLUG ARCH EUR J PHY, V415, P172, DOI 10.1007/BF00370589 LIGHT DB, 1990, AM J PHYSIOL, V258, pF273 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1986, AM J PHYSIOL, V251, pC662 MARCUS DC, 1987, HEARING RES, V30, P55, DOI 10.1016/0378-5955(87)90183-3 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MARCUS NY, 1990, HEARING RES, V44, P13, DOI 10.1016/0378-5955(90)90018-K MCGILL JM, 1992, AM J PHYSIOL, V262, pG703 SCHMID A, 1989, J MEMBRANE BIOL, V111, P265, DOI 10.1007/BF01871011 SCHNEIDER GT, 1985, PFLUG ARCH EUR J PHY, V404, P354, DOI 10.1007/BF00585348 SOEJIMA M, 1988, PFLUGERS ARCH, V411, P301 TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 Wangemann Philine, 1992, Journal of General Physiology, V100, p64A WANGEMANN P, 1992, HEARING RES, V62, P149, DOI 10.1016/0378-5955(92)90180-U WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 WANGEMANN P, 1992, AM J PHYSIOL, V263, pC616 WOLL KH, 1987, PFLUG ARCH EUR J PHY, V410, P632, DOI 10.1007/BF00581324 ZIOMEK CA, 1980, J CELL BIOL, V86, P849, DOI 10.1083/jcb.86.3.849 NR 30 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 SEP PY 1993 VL 69 IS 1-2 BP 124 EP 132 DI 10.1016/0378-5955(93)90100-F PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000014 PM 8226332 ER PT J AU HAUSER, R PROBST, R HARRIS, FP AF HAUSER, R PROBST, R HARRIS, FP TI EFFECTS OF ATMOSPHERIC-PRESSURE VARIATION ON SPONTANEOUS, TRANSIENTLY EVOKED, AND DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN NORMAL HUMAN EARS SO HEARING RESEARCH LA English DT Article DE ATMOSPHERIC PRESSURE; MIDDLE EAR; OTOACOUSTIC EMISSIONS; HUMAN EARS ID SENSORINEURAL HEARING-LOSS; ACOUSTIC DISTORTION; ORIGIN AB The effects of atmospheric pressure changes on the frequency and amplitude of spontaneous (SOAEs), transiently evoked (TEOAEs) and distortion product (DPOAEs) otoacoustic emissions in normally hearing humans were compared. The purpose was to determine if the transmission of each form of OAE was influenced differently by the middle ear. Sixty-one subjects were tested in a pressure chamber. Twenty-seven SOAEs with a frequency range between 535 to 4729 Hz from 21 subjects were examined. Transiently evoked OAEs were studied in 20 subjects using clicks and tone-bursts at 0.5, 1, 2, 3, and 4 kHz. Distortion-product OAEs were generated at seven geometric mean frequencies between 1 and 8 kHz in another 20 subjects. Spontaneous OAEs were examined by applying atmospheric pressure up to 9 kPa and down to -2.5 kPa, for the measurement of TEOAEs and DPOAEs the pressure was varied from 0 kPa up to 8 kPa. In spite of large interindividual differences, results suggest that the influence of pressure on the three OAEs is frequency specific. The frequency and amplitude change of SOAEs, the modification of the amplitude and spectra of TEOAEs, and the amplitude change of DPOAEs are more influenced by changes in middle ear pressure below 4 kHz than are OAEs in the range at 4 kHz and above. C1 UNIV BASEL,KANTONSSPITAL,DEPT OTORHINOLARYNGOL,CH-4051 BASEL,SWITZERLAND. RP HAUSER, R (reprint author), UNIV BASEL,KANTONSSPITAL,DEPT OTORHINOLARYNGOL,CH-4031 BASEL,SWITZERLAND. CR BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 GROTH P, 1981, THESIS U LUND MALMO GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HAUSER R, 1991, EFFECTS VARIATION AT, P66 HAUSER R, 1992, ANN OTO RHINOL LARYN, V101, P994 Ingelstedt S, 1967, ACTA OTO-LARYNGOL, V228, P1 KEMP DT, 1980, HEARING RES, V2, P533, DOI 10.1016/0378-5955(80)90091-X Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1981, TINNITUS, P54 KHANNA SM, 1972, J ACOUST SOC AM, V51, P1904, DOI 10.1121/1.1913050 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KIMBERLEY BP, 1989, J OTOLARYNGOL, V18, P365 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1990, ANN OTO RHINOL LARYN, V99, P30 MATTHEWS JW, 1983, MECHANICS HEARING, P11 MATTHEWS JW, 1986, PERIPHERAL AUDITORY, P258 MATTHEWS JW, 1981, J ACOUST SOC AM, V69, P43 MOLLER AR, 1963, J ACOUST SOC AM, V35, P1526, DOI 10.1121/1.1918742 Munker G, 1972, FUNKTIONSANALYSE TUB NAEVE SL, 1992, J ACOUST SOC AM, V91, P2091, DOI 10.1121/1.403695 PROBST R, 1990, AM J OTOLARYNG, V11, P236, DOI 10.1016/0196-0709(90)90083-8 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L VONBEKESY G, 1942, AKUST Z, V7, P173 Wilson JP, 1981, TINNITUS, P82 ZOLLNER F, 1942, ANATOMIE PHYSL PATHO NR 30 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 SEP PY 1993 VL 69 IS 1-2 BP 133 EP 145 DI 10.1016/0378-5955(93)90101-6 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000015 PM 8226333 ER PT J AU LIM, HH JENKINS, OH MYERS, MW MILLER, JM ALTSCHULER, RA AF LIM, HH JENKINS, OH MYERS, MW MILLER, JM ALTSCHULER, RA TI DETECTION OF HSP-72 SYNTHESIS AFTER ACOUSTIC OVERSTIMULATION IN RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE HSP-72; NOISE; COCHLEA; HAIR CELL; IMMUNOBLOTTING; IMMUNOCYTOCHEMISTRY; RAT ID HEAT-SHOCK PROTEINS; GUINEA-PIG COCHLEA; STRESS PROTEIN; INSITU HYBRIDIZATION; TRANSIENT ISCHEMIA; RABBIT CEREBELLUM; OTOTOXIC DRUGS; MESSENGER-RNA; GERBIL BRAIN; NOISE AB The purpose of this study was to determine if high intensity acoustic stimulation would induce HSP 72 in rat cochlea. The animals were exposed to 110 dB SPL broad band noise for 1.5 h and sacrificed 4, 6 and 8 h after stimulation. Immunocytochemistry and western blotting were used to detect the expression of HSP 72 in the cochlear tissues. Western blots showed an intense 72 kD band in the noise exposed animals compared to a very light band in non-stimulated control animals. Immunocytochemical results in the cochlea revealed noise induced HSP 72 immunoreactive staining of outer hair cells. Only a few immunoreactive stained inner hair cells were seen and spiral ganglion cells were not stained. These results indicate that acoustic overstimulation can induce the expression of HSP 72 in outer hair cells of the rat cochlea. HSP 72 may serve as a marker for cellular stress and potential damage and may be involved in protection from insult. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,1301 E ANN ST,ANN ARBOR,MI 48109. CR BLAKE MJ, 1990, MOL BRAIN RES, V8, P89, DOI 10.1016/0169-328X(90)90014-5 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 BROWN IR, 1990, J NEUROSCI RES, V25, P14, DOI 10.1002/jnr.490250103 DANIEL GA, 1986, J CEREB BLOOD FLOW M, V6, P505 DECHESNE CJ, 1992, HEARING RES, V59, P195, DOI 10.1016/0378-5955(92)90116-5 ENGSTROM B, 1983, HEARING RES, V12, P251, DOI 10.1016/0378-5955(83)90110-7 ENGSTROM B, 1981, ARCH OTO-RHINO-LARYN, V230, P279, DOI 10.1007/BF00456330 Erlandsson B, 1980, Acta Otolaryngol Suppl, V367, P1 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 LIBERMAN MC, 1990, TOXICOL PATHOL, V18, P138 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 LINDQUIST S, 1986, ANNU REV BIOCHEM, V55, P1151, DOI 10.1146/annurev.bi.55.070186.005443 LINDQUIST S, 1988, ANNU REV GENET, V22, P631, DOI 10.1146/annurev.ge.22.120188.003215 MANZERRA P, 1990, NEUROCHEM RES, V15, P53, DOI 10.1007/BF00969184 MARINI AM, 1990, J NEUROCHEM, V54, P1509, DOI 10.1111/j.1471-4159.1990.tb01198.x MASING TE, 1989, NEUROCHEM RES, V14, P725, DOI 10.1007/BF00964949 MYERS MW, 1992, LARYNGOSCOPE, V102, P981 NEELY JG, 1991, HEARING RES, V52, P403, DOI 10.1016/0378-5955(91)90028-8 NOWAK TS, 1985, J NEUROCHEM, V45, P1635, DOI 10.1111/j.1471-4159.1985.tb07236.x NOWAK TS, 1991, J CEREBR BLOOD F MET, V11, P432 QUIRK WS, 1991, HEARING RES, V52, P217, DOI 10.1016/0378-5955(91)90201-J ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 SCHLESINGER MJ, 1990, J BIOL CHEM, V265, P12111 THOMPSON AM, 1992, OTOLARYNG HEAD NECK, V107, P769 TISSIERE.A, 1974, J MOL BIOL, V84, P389, DOI 10.1016/0022-2836(74)90447-1 TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350 VASS K, 1988, ACTA NEUROPATHOL, V77, P128 Welch W J., 1990, STRESS PROTEINS BIOL, P223 WELCH WJ, 1986, J CELL BIOL, V103, P2035, DOI 10.1083/jcb.103.5.2035 NR 32 TC 57 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 1993 VL 69 IS 1-2 BP 146 EP 150 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000016 PM 8226334 ER PT J AU LI, J YOUNG, ED AF LI, J YOUNG, ED TI DISCHARGE-RATE DEPENDENCE OF REFRACTORY BEHAVIOR OF CAT AUDITORY-NERVE FIBERS SO HEARING RESEARCH LA English DT Article DE REGULARITY; REFRACTORY PERIOD; HAZARD FUNCTION; AUDITORY NERVE; MODEL; CAT ID NEURAL SPIKE TRAIN; MODEL; ADAPTATION; RESPONSES; PATTERNS; PROBABILITY; STIMULUS; UNITS; TONES; NOISE AB A descriptive model for auditory-nerve (AN) refractory periods is described. The model assumes that interspike intervals consist of a constant-length absolute refractory period (ARP), followed by random-length relative refractory period (RRP) and a random-length waiting time to the next spike. Both the RRP and waiting time are exponentially distributed. This model fits AN hazard functions sufficiently well to provide estimates of the ARP and RRP durations for each fiber. The ARP is found to be constant, independent of discharge rate, with mean value between 0.56 and 0.86 ms in data from 7 experiments. The RRP decreases in duration as discharge rate increases; RRP mean length is less than 2 ms in most cases. There is an additional, slow component of recovery, lasting 20-40 ms, which is not modeled. The variation in RRP with discharge rate is shown to be capable of accounting for the deviation of AN. regularity from that predicted for a Poisson process. Finally, properties of peaks seen in hazard functions just at the end of the ARP are described; these peaks are not included in the model, but are shown to be especially prominent in low and medium spontaneous rate fibers. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOMED ENGN,505 TRAYLOR BLDG,720 RUTLAND AVE,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,BALTIMORE,MD 21205. CR BANKS MI, 1991, J NEUROPHYSIOL, V65, P606 BOSCH WR, 1990, THESIS WASHINGTON U COOPER NP, 1988, J PHYSIOL-LONDON, V407, pP64 Cox DR, 1962, RENEWAL THEORY Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 GRAY PR, 1967, BIOPHYS J, V7, P759, DOI 10.1016/S0006-3495(67)86621-9 JOHNSON DH, 1983, J ACOUST SOC AM, V74, P493, DOI 10.1121/1.389815 JOHNSON DH, 1986, HEARING RES, V21, P135, DOI 10.1016/0378-5955(86)90035-3 JONES K, 1985, J ACOUST SOC AM, V78, P90, DOI 10.1121/1.392458 KARAMANOS N, 1988, BASIC ISSUES HEARING, P185 Kiang NY-s, 1965, DISCHARGE PATTERNS S KUMAR A, 1984, 8409 RIC U DEP EL EN LI J, 1991, THESIS J HOPKINS U LUTKENHONER B, 1992, BIOL CYBERN, V67, P1, DOI 10.1007/BF00201797 LUTKENHONER B, 1986, HEARING RES, V24, P289, DOI 10.1016/0378-5955(86)90028-6 LUTKENHONER B, 1980, SCAND AUDIOL S, V11, P26 MARK KE, 1992, J ACOUST SOC AM, V91, P989, DOI 10.1121/1.402504 MILLER MI, 1992, J ACOUST SOC AM, V92, P202, DOI 10.1121/1.404284 MILLER MI, 1992, AUDITORY PHYSL PERCE, P133 MILLER MI, 1985, J ACOUST SOC AM, V77, P1452, DOI 10.1121/1.392040 MILLER MI, 1993, IN PRESS J ACOUST SO MOLNAR CE, 1968, PR INST ELECTR ELECT, V56, P993, DOI 10.1109/PROC.1968.6450 MULHERAN M, 1988, BRIT J AUDIOL, V22, P136 ROTHMAN JS, 1991, THESIS J HOPKINS U SCHROEDE.MR, 1974, J ACOUST SOC AM, V55, P1055, DOI 10.1121/1.1914647 SIEBERT WM, 1963, Q PROG REP RES LAB E, V71, P241 SMITH RL, 1982, BIOL CYBERN, V44, P107, DOI 10.1007/BF00317970 SOKOLICH WG, 1977, J ACOUST SOC AM, V62, pS12, DOI 10.1121/1.2016024 TEICH MC, 1990, HEARING RES, V46, P41, DOI 10.1016/0378-5955(90)90138-F TEICH MC, 1985, J ACOUST SOC AM, V77, P1110, DOI 10.1121/1.392176 WANG J, 1992, IN PRESS 1992 P COMP WESTERMAN LA, 1984, HEARING RES, V15, P249, DOI 10.1016/0378-5955(84)90032-7 YOUNG ED, 1992, IN PRESS MAMMALIAN C YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 NR 35 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 SEP PY 1993 VL 69 IS 1-2 BP 151 EP 162 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000017 PM 8226336 ER PT J AU HACKNEY, CM FETTIPLACE, R FURNESS, DN AF HACKNEY, CM FETTIPLACE, R FURNESS, DN TI THE FUNCTIONAL-MORPHOLOGY OF STEREOCILIARY BUNDLES ON TURTLE COCHLEAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEA; HAIR CELLS; STEREOCILIA; TURTLE ID GUINEA-PIG COCHLEA; MECHANOELECTRICAL TRANSDUCTION; ALLIGATOR LIZARD; EAR; ULTRASTRUCTURE; CHANNELS; BULLFROG; GROWTH; ORGANS; INNER AB The stereociliary bundles of hair cells from the basilar papilla of the red-eared turtle were examined with transmission and high resolution scanning electron microscopy to provide a description of their morphology, orientation and inter-ciliary connections for comparison with physiological observations. Bundles on hair cells in the basilar membrane region are of a uniform shape and orientation, but bundles on the apical and basal limbus are distinct in having elongated kinocilia more than twice the length of the tallest stereocilia. Bundles in the basilar membrane region show a roughly two-fold increase in height from 5 to 9 mum from base to apex. Electrical recordings from isolated hair cells indicate that the bundle height is inversely proportional to the cell's characteristic frequency. It is argued that the change in dimensions is insufficient to contribute significantly to the cochlea's frequency selectivity. The cytoplasm adjacent to the kinocilium is filled with microtubules and large vesicles, and there are coated pits in the apical membrane which, it is suggested, may be indicative of rapid turnover of the membrane in this region. C1 UNIV WISCONSIN,SCH MED,DEPT NEUROPHYSIOL,273 MED SCI BLDG,1300 UNIV AVE,MADISON,WI 53706. UNIV KEELE,DEPT COMMUN & NEUROSCI,KEELE ST5 5BG,STAFFS,ENGLAND. CR ART JJ, 1986, HEARING RES, V22, P31, DOI 10.1016/0378-5955(86)90073-0 ART JJ, 1987, J PHYSL, V356, P507 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 FETTIPLACE R, 1992, SENSORY TRANSDUCTION, P343 FETTIPLACE R, 1992, ANN NY ACAD SCI, V656, P1 FRISHKOPF LS, 1983, HEARING RES, V12, P393, DOI 10.1016/0378-5955(83)90008-4 FURNESS DN, 1986, HEARING RES, V21, P243, DOI 10.1016/0378-5955(86)90222-4 FURNESS DN, 1985, HEARING RES, V18, P177, DOI 10.1016/0378-5955(85)90010-3 FURNESS DN, 1990, EUR ARCH OTO-RHINO-L, V247, P12 GEISLER CD, 1993, HEARING RES, V65, P79, DOI 10.1016/0378-5955(93)90203-D HACKNEY CM, 1992, P ROY SOC B-BIOL SCI, V248, P215, DOI 10.1098/rspb.1992.0064 Hillman D.E., 1976, P452 HOLTON T, 1983, SCIENCE, V222, P508, DOI 10.1126/science.6623089 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 JORGENSEN J M, 1974, Acta Zoologica (Stockholm), V55, P289 KELLEY MW, 1992, HEARING RES, V59, P108 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 LEWIS ER, 1973, J MORPHOL, V139, P351, DOI 10.1002/jmor.1051390305 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MANLEY GA, 1986, AUDITORY FREQUENCY S, P63 MANLEY GA, 1989, COCHLEAR MECH STRUCT, P143 MILLER MR, 1978, AM J ANAT, V151, P409, DOI 10.1002/aja.1001510306 MULROY MJ, 1974, BRAIN BEHAV EVOLUT, V10, P69, DOI 10.1159/000124303 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H SNEARY MG, 1988, J COMP NEUROL, V276, P573, DOI 10.1002/cne.902760410 SNEARY MG, 1988, J COMP NEUROL, V276, P588, DOI 10.1002/cne.902760411 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 WEISS TF, 1985, HEARING RES, V20, P157, DOI 10.1016/0378-5955(85)90166-2 WEVER EG, 1978, REPTILE EAR NR 35 TC 38 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 1993 VL 69 IS 1-2 BP 163 EP 175 DI 10.1016/0378-5955(93)90104-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000018 PM 8226337 ER PT J AU GOBSCH, H TIETZE, G AF GOBSCH, H TIETZE, G TI INTERRELATION OF SPONTANEOUS AND EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSION; TRANSIENTLY EVOKED OTOACOUSTIC EMISSION; SPONTANEOUS OTOACOUSTIC EMISSION; SYNCHRONIZED SPONTANEOUS OTOACOUSTIC EMISSION; INTERRELATION OF OTOACOUSTIC EMISSION ID STIMULATED ACOUSTIC EMISSIONS; FINE-STRUCTURE; HUMAN EAR; HEARING; THRESHOLD; TINNITUS; INFANTS AB The interrelation of spontaneous otoacoustic emissions (SOAEs) that can be synchronised by acoustic stimuli and transiently evoked otoacoustic emissions (TEOAEs) was studied in different experiments in normal ears. Click evoked TEOAEs mixed with synchronised SOAEs were investigated in time windows of 102.4 ms. Frequency spectra were obtained from the whole time window, the first and second half and from each quarter separately. Synchronised SOAEs recorded by time domain averaging show exactly the same frequencies in the TEOAE spectra of all analysed time window quarters compared to SOAEs recorded by frequency domain averaging. Moreover, synchronised SOAEs can influence the response shape of the TEOAE additionally. This is shown in long lasting responses exceeding the inter stimulus interval (ISI). In this case superimposing of consecutive single responses takes place and the shape of the averaged response depends on the exact ISI value used. These effects were investigated by varying the ISI in steps of 0.1 ms. The ISI variation has more pronounced effects on the response shape at short ISI values (50 ms) and low stimulus levels (10 dB HL). Thus the wave form changes are not accompanied by a change of the frequency content poor phase cancellation takes place. This is confirmed by simulated phase interaction. It is suggested that the phase of an already synchronised SOAE has significant effects on the re-synchronisation of the SOAE by the next click. Both influences should be considered in TEOAE recordings if synchronised SOAEs are present. RP GOBSCH, H (reprint author), MED HSCH ERFURT,HNO KLIN,NORDHAUSER STR 74,POB 595,D-D-99012 ERFURT,GERMANY. CR BECK A, 1992, HNO, V40, P123 BONFILS P, 1988, AUDIOLOGY, V27, P27 BONFILS P, 1990, EAR HEARING, V11, P155, DOI 10.1097/00003446-199004000-00010 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BRAY PJ, 1989, THESIS U LONDON LOND BRIGHT K, 1986, SENSORINEURAL HEARIN, P201 Elberling C, 1985, Acta Otolaryngol Suppl, V421, P77 GOBSCH H, 1992, OTORHINOLARYNGOL NOV, V2, P253 HAUSER R, 1991, EUR ARCH OTO-RHINO-L, V248, P345 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, 1990, COCHLEAR MECHANISMS, V7, P77 KEMP DT, 1990, EAR HEARING, V11, P93 LAMPRECHT A, 1991, LARYNGO RHINO OTOL, V70, P1, DOI 10.1055/s-2007-997972 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 MATHIS A, 1991, HNO, V39, P55 NORTON SJ, 1990, EAR HEARING, V11, P159, DOI 10.1097/00003446-199004000-00011 PLINKERT PK, 1990, LARYNGO RHINO OTOL, V69, P108, DOI 10.1055/s-2007-998154 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 SCHLOTH E, 1983, ACUSTICA, V53, P250 SCHLOTH E, 1982, THESIS TU MUNCHEN MU STEVENS JC, 1990, EAR HEARING, V11, P128, DOI 10.1097/00003446-199004000-00007 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 WIT HP, 1981, J ACOUST SOC AM, V70, P437, DOI 10.1121/1.386786 WIT HP, 1979, J ACOUST SOC AM, V66, P911, DOI 10.1121/1.383202 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 ZWICKER E, 1990, AUDIOLOGY, V29, P241 NR 30 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 1993 VL 69 IS 1-2 BP 176 EP 181 DI 10.1016/0378-5955(93)90105-A PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000019 PM 8226338 ER PT J AU LUO, L KOUTNOUYAN, H BAIRD, A RYAN, AF AF LUO, L KOUTNOUYAN, H BAIRD, A RYAN, AF TI ACIDIC AND BASIC FGF MESSENGER-RNA EXPRESSION IN THE ADULT AND DEVELOPING RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE GROWTH FACTORS; COCHLEA; HAIR CELLS; SPIRAL GANGLION; DEVELOPMENT; FIBROBLAST GROWTH FACTOR; RAT ID FIBROBLAST GROWTH-FACTORS; AUDITORY NEURONS; INSITU HYBRIDIZATION; PERIPHERAL-NERVE; SPIRAL GANGLION; SCHWANN-CELLS; FACTOR FAMILY; HAIR-CELLS; RECEPTOR; TISSUES AB In situ hybridization was used to document the distribution of mRNA encoding acidic and basic fibroblast growth factor (aFGF and bFGF) in the rat cochlea from embryonic day (E) 16 to postnatal day (P) > 60. bFGF mRNA was not detected in the cochlea at any age. In the adult, aFGF mRNA was strongly expressed in spiral ganglion (SG) neurons, and this expression increased from base to apex. The stria vascularis (SV) and spiral prominence (SP) showed lesser expression which was equal in all turns. Developmentally, low level expression of aFGF mRNA was first seen in the SG at E-20, and remained low until P-4. Expression increased from P-6 to P-14, when adult levels were reached. aFGF mRNA was also observed in the developing hair cells of all turns at E-20. This expression increased after birth but disappeared after P-6. Expression in the SV and SP was first noted at E-20 and reached adult levels by P-16 and P-10, respectively. High levels of aFGF mRNA in the adult SG suggest that aFGF is important for the maintenance of SG neuron function and structure. aFGF in hair cells during the first postnatal week may be involved in the establishment of cochlear innervation. C1 UCSD,SCH MED,DEPT SURG,DIV OTOLARYNGOL,0666,9500 GILMAN DR,LA JOLLA,CA 92093. UCSD,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. VET ADM MED CTR,LA JOLLA,CA. WHITTER INST,LA JOLLA,CA. CR ANNIKO M, 1983, ACTA OTO-LARYNGOL, V95, P263, DOI 10.3109/00016488309130943 ANNIKO M, 1983, AM J OTOLARYNG, V4, P375, DOI 10.1016/S0196-0709(83)80043-X BAIRD A, 1986, RECENT PROG HORM RES, V42, P143 BAIRD A, 1987, BIOCHEM BIOPH RES CO, V142, P428, DOI 10.1016/0006-291X(87)90292-0 BAIRD A, 1991, CANCER CELL-MON REV, V3, P239 BAIRD A, 1989, BRIT MED BULL, V45, P438 CHEN JK, 1991, J NEUROSCI RES, V30, P321, DOI 10.1002/jnr.490300207 Coleman J.R., 1990, P205 CORDEIRO PG, 1989, PLAST RECONSTR SURG, V83, P1013, DOI 10.1097/00006534-198906000-00014 DAVIS JB, 1990, J CELL BIOL, V110, P1353, DOI 10.1083/jcb.110.4.1353 DEPRES G, 1991, NEUROREPORT, V2, P639 DIONNE CA, 1990, EMBO J, V9, P2685 ECHTELER SM, 1992, P NATL ACAD SCI USA, V89, P6324, DOI 10.1073/pnas.89.14.6324 ECKENSTEIN FP, 1991, J NEUROSCI, V11, P412 ECKENSTEIN FP, 1990, NEURON, V4, P623, DOI 10.1016/0896-6273(90)90120-5 Emoto N, 1989, Growth Factors, V2, P21, DOI 10.3109/08977198909069078 Fina M, 1991, Growth Factors, V5, P265, DOI 10.3109/08977199109000290 FOLKMAN J, 1988, AM J PATHOL, V130, P393 FRAUTSCHY SA, 1991, BRAIN RES, V553, P291, DOI 10.1016/0006-8993(91)90837-L GIACOBINI MMJ, 1991, EXP BRAIN RES, V86, P73 GONZALEZ AM, 1990, J CELL BIOL, V110, P753, DOI 10.1083/jcb.110.3.753 GOODRICH SP, 1989, NUCLEIC ACIDS RES, V17, P2867, DOI 10.1093/nar/17.7.2867 GOSPODAROWICZ D, 1990, CLIN ORTHOPAEDICS, V257, P231 HAFIDI A, 1990, J COMP NEUROL, V300, P153, DOI 10.1002/cne.903000202 HEARN MTW, 1991, BAILLIERE CLIN ENDOC, V5, P571 HUNTER C, 1992, OTOLARYNG CLIN N AM, V25, P1027 JOHNSON DE, 1990, MOL CELL BIOL, V10, P4728 LEFEBVRE PP, 1992, HEARING RES, V58, P185, DOI 10.1016/0378-5955(92)90127-9 LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEFEBVRE PP, 1991, NEUROREPORT, V2, P305, DOI 10.1097/00001756-199106000-00001 LEFEBVRE PP, 1992, ACTA OTO-LARYNGOL, V112, P288 LEFEBVRE PP, 1991, BRAIN RES, V567, P306, DOI 10.1016/0006-8993(91)90809-A LENOIR M, 1980, ANAT EMBRYOL, V160, P253, DOI 10.1007/BF00305106 Lim D, 1992, DEV AUDITORY VESTIBU, P33 LIN L, 1990, ENDOCRINOLOGY, V126, P1764 MATTSON MP, 1989, J NEUROSCI, V9, P3728 MORRISON RS, 1986, P NATL ACAD SCI USA, V83, P7537, DOI 10.1073/pnas.83.19.7537 OTTO D, 1987, NEUROSCI LETT, V83, P156, DOI 10.1016/0304-3940(87)90233-3 PIRVOLA U, 1991, HEARING RES, V52, P345, DOI 10.1016/0378-5955(91)90024-4 PUEL JL, 1992, ABSTR ARO, V15, P21 REPRESA J, 1991, NATURE, V353, P561, DOI 10.1038/353561a0 ROBINSON CJ, 1991, TRENDS PHARMACOL SCI, V12, P123, DOI 10.1016/0165-6147(91)90525-W ROMAND MR, 1990, J ELECTRON MICR TECH, V15, P144, DOI 10.1002/jemt.1060150206 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RYAN AF, 1991, NEUROREPORT, V2, P643, DOI 10.1097/00001756-199111000-00002 RYAN AF, 1991, HEARING RES, V56, P148, DOI 10.1016/0378-5955(91)90164-5 RYBAK PL, 1992, HAR RES, V59, P189 Schwartz A. M, 1986, NEUROBIOLOGY HEARING, P271 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 SHIMASAKI S, 1988, BIOCHEM BIOPH RES CO, V157, P256, DOI 10.1016/S0006-291X(88)80041-X SIMMONS DM, 1989, J HISTOTECHNOL, V12, P169 Sobkowicz HM, 1992, DEV AUDITORY VESTIBU, V2, P59 Spoendlin H, 1988, PHYSL EAR, P201 SWEETNAM PM, 1991, J NEUROCHEM, V57, P237, DOI 10.1111/j.1471-4159.1991.tb02121.x THOMAS KA, 1987, FASEB J, V1, P434 VANDEWATER TR, 1992, DEV AUDITORY VESTIBU, V2, P1 WALICKE P, 1986, P NATL ACAD SCI USA, V83, P3012, DOI 10.1073/pnas.83.9.3012 WALICKE PA, 1988, J NEUROSCI, V8, P2618 YOSHIDA K, 1991, BRAIN RES, V538, P118, DOI 10.1016/0006-8993(91)90385-9 NR 59 TC 65 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 1993 VL 69 IS 1-2 BP 182 EP 193 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000020 PM 7693641 ER PT J AU CRIST, JR FALLON, M BOBBIN, RP AF CRIST, JR FALLON, M BOBBIN, RP TI VOLUME REGULATION IN COCHLEAR OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS, OUTER; VOLUME REGULATION; OSMOLARITY ID ELECTROKINETIC SHAPE CHANGES; ACTIVATED ION CHANNELS; CALCIUM; MOTILITY; GADOLINIUM; LENGTH AB Many cells placed in a hypotonic medium initially swell and then rapidly undergo a regulatory volume decrease (RVD) to return towards original volume. Re-exposure to the isotonic solution results in the cells shrinking followed by a regulatory volume increase (RVI). Previous studies have shown that isolated outer hair cells (OHCs) placed in a hypotonic medium swell and maintain this shape until returned to the original medium. We re-examined this apparent lack of cell volume regulation in OHCs. OHCs were isolated from guinea pig cochleae, mechanically dissociated and dispersed, and placed in a Hank's balanced salt solution (HBS). In the cells studied, switching the perfusate to a hypotonic HBS (290-280 mmol/kg) for 15 min resulted in an immediate shortening of the OHCs (i.e., volume increase). In 26% of the cells, this increase was followed by a return to original length during the time the cell was perfused with the hypotonic medium, a RVD. Twelve percent of the cells demonstrating a RVD also displayed a RVI. Omitting collagenase and increasing Ca2+ concentration did not increase the percentage of cells displaying a RVD, while gadolinium (Gd3+, 10 muM) decreased the percentage to zero. This is the first report of isolated OHCs undergoing cell volume regulation. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB,NEW ORLEANS,LA 70112. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BIAGI BA, 1990, AM J PHYSIOL, V259, pC515 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CECOLA RP, 1992, HEARING RES, V61, P65, DOI 10.1016/0378-5955(92)90037-N CHRISTENSEN O, 1987, NATURE, V330, P66, DOI 10.1038/330066a0 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DING JP, 1991, HEARING RES, V56, P19, DOI 10.1016/0378-5955(91)90149-4 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 DULON D, 1990, J NEUROSCI, V10, P1388 FILIPOVIC D, 1991, AM J PHYSIOL, V260, pF119 GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 HOFFMANN EK, 1989, PHYSIOL REV, V69, P315 JANG HD, 1990, ARCH BIOCHEM BIOPHYS, V283, P318, DOI 10.1016/0003-9861(90)90649-J KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 MACKNIGHT ADC, 1988, RENAL PHYSIOL BIOCH, V11, P114 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A REUSS L, 1988, RENAL PHYSIOL BIOCH, V11, P187 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 ULFENDAHL M, 1988, ARCH OTO-RHINO-LARYN, V245, P237, DOI 10.1007/BF00463935 WELLING PA, 1988, AM J PHYSIOL, V255, pF853 YANG XC, 1989, SCIENCE, V243, P1068, DOI 10.1126/science.2466333 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 ZEUTHEN T, 1992, BIOCHIM BIOPHYS ACTA, V1113, P229, DOI 10.1016/0304-4157(92)90040-H NR 28 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 SEP PY 1993 VL 69 IS 1-2 BP 194 EP 198 DI 10.1016/0378-5955(93)90107-C PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000021 PM 8226339 ER PT J AU DIDIER, A MILLER, JM NUTTALL, AL AF DIDIER, A MILLER, JM NUTTALL, AL TI THE VASCULAR COMPONENT OF SODIUM-SALICYLATE OTOTOXICITY IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SODIUM SALICYLATE; LASER DOPPLER FLOWMETRY; COCHLEA; GUINEA PIG; HYDRALAZINE; TOPICAL DRUG APPLICATION ID PROSTAGLANDIN SYNTHESIS; HAIR-CELLS; ASPIRIN; COCHLEA; ELECTROMOTILITY; POTENTIALS; EMISSIONS AB Drugs of the salicylate family (aspirin-like drugs) are reversibly ototoxic. Electrophysiologic and ultrastructural evidence suggests an impairment of the sensory hair cells of the cochlea following salicylate treatment. In addition, since these drugs can cause vasoconstriction, the ototoxicity of salicylates may also involve an impairment of the blood circulation in inner ear. However, a vascular hypothesis of salicylate toxicity has not received much attention. In the current study, we simultaneously measured cochlear blood flow (by laser Doppler flowmetry) and the sound-evoked potentials from the round window. Sodium salicylate caused a decrease in cochlear blood flow that appeared within 30 min following an intramuscular injection of a low dose of sodium salicylate (100 mg/kg). This sodium salicylate dose did not cause a change in auditory sensitivity. For higher doses (200 mg/kg and 300 mg/kg), both cochlear blood flow and auditory sensitivity were affected. The 300 mg/kg dose decreased blood flow by about 25% and elevated compound action potential thresholds by 10 to 25 dB for high frequencies (greater-than-or-equal-to 8 kHz). Further experiments showed that salicylate-induced threshold shifts were significantly reduced for the mid-frequencies when cochlear blood flow is increased by the vasodilating drug hydralazine (negating the flow reduction caused by salicylate). These data indicate that in addition to the direct effect of systemically administered salicylate on neurosensory function a decreased blood flow contributes to the ototoxicity of salicylates. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,MED CTR,1301 E ANN ST,ANN ARBOR,MI 48109. UNIV LYON 1,NEUROPHYSIOL SENSORIELLE LAB,F-69621 VILLEURBANNE,FRANCE. CR AXELSSON A, 1987, HEARING RES, V31, P183, DOI 10.1016/0378-5955(87)90125-0 Bernstein J M, 1967, J Laryngol Otol, V81, P915, DOI 10.1017/S0022215100067852 BROWN MC, 1983, HEARING RES, V9, P131, DOI 10.1016/0378-5955(83)90023-0 BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 CAZALS Y, 1988, HEARING RES, V36, P89, DOI 10.1016/0378-5955(88)90139-6 CRIFO S, 1975, ORL J OTO-RHINO-LARY, V37, P27 DEER BC, 1982, J OTOLARYNGOL, V11, P260 DEMOURA LFP, 1968, ARCH OTOLARYNGOL, V87, P60 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DOUEK EE, 1983, J LARYNGOL OTOL, V93, P793 ESCOUBET B, 1985, PROSTAGLANDINS, V29, P589 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 HAWKINS JE, 1976, HDB SENSORY PHYSL, P708 ISHII T, 1967, ANN OTO RHINOL LARYN, V76, P368 JASTREBOFF PJ, 1988, LARYNGOSCOPE, V98, P280 JUNG TTK, 1991, ABSTR ASS RES OT, P377 Jung T T, 1992, Acta Otolaryngol Suppl, V493, P81 JUNG TTK, 1989, ABSTR ASS RES OT, P118 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 MCCABE PA, 1965, ANN OTO RHINOL LARYN, V74, P312 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MCPHERSO.DL, 1974, ARCH OTOLARYNGOL, V99, P304 MILLER JM, 1990, LASER DOPPLER BLOOD MITCHELL C, 1973, ARCH OTOLARYNGOL, V98, P297 MONCADA S, 1982, ARTERIOSCLEROSIS, V2, P193 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 NUTTALL AL, 1988, HEARING RES, V34, P215, DOI 10.1016/0378-5955(88)90001-9 OHLSEN A, 1993, ACTA OTO-LARYNGOL, V113, P55, DOI 10.3109/00016489309135767 OHLSEN AK, 1990, ABSTR ASS RES OT, P353 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 QUIRK WS, 1991, ABSTR ASS RES OT, P376 RAMSDEN RT, 1985, J LARYNGOL OTOL, V99, P1269, DOI 10.1017/S0022215100098510 RYAN AF, 1988, PHYSL EAR, P317 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SILVERST.H, 1967, ANN OTO RHINOL LARYN, V76, P118 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E THORNE PR, 1907, HEARING RES, V27, P1 VANE JR, 1971, NATURE-NEW BIOL, V231, P232 NR 39 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 SEP PY 1993 VL 69 IS 1-2 BP 199 EP 206 DI 10.1016/0378-5955(93)90108-D PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000022 PM 8226340 ER PT J AU OGAWA, K SCHACHT, J AF OGAWA, K SCHACHT, J TI RECEPTOR-MEDIATED RELEASE OF INOSITOL PHOSPHATES IN THE COCHLEAR AND VESTIBULAR SENSORY EPITHELIA OF THE RAT SO HEARING RESEARCH LA English DT Article DE INOSITOL PHOSPHATES; 2ND MESSENGER; COCHLEA; VESTIBULE; MUSCARINIC CHOLINERGIC RECEPTOR; PURINERGIC RECEPTOR; RAT ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; SIGNAL TRANSDUCTION; MOTILE RESPONSES; 2ND MESSENGER; INNER-EAR; EXTRACELLULAR ATP; SYSTEM; ACETYLCHOLINE; LOCALIZATION AB Various neurotransmitters, hormones and other modulators involved in intercellular communication exert their biological action at receptors coupled to phospholipase C (PLC). This enzyme catalyzes the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PtdInsP2) to inositol 1,4,5-trisphosphate (InsP3) and 1,2-diacylglycerol (DG) which act as second messengers. In the organ of Corti of the guinea pig, the InsP3 second messenger system is linked to muscarinic cholinergic and P2y purinergic receptors. However, nothing is known about the the InsP3 second messenger system in the vestibule. In this study, the receptor-mediated release of inositol phosphates (InsPs) in the vestibular sensory epithelia was compared to that in the cochlear sensory epithelia of Fischer-344 rats. After preincubation of the isolated intact tissues with myo-[H-3]inositol, stimulation with the cholinergic agonist carbamylcholine or the P2 purinergic agonist ATP-gamma-S resulted in a concentration-dependent increase in the formation of [H-3]InsPs in both epithelia. Similarly, the muscarinic cholinergic agonist muscarine enhanced InsPs release in both organs, while the nicotinic cholinergic agonist dimethylphenylpiperadinium (DMPP) was ineffective. The muscarinic cholinergic antagonist atropine completely suppressed the InsPs release induced by carbamylcholine, while the nicotinic cholinergic antagonist mecamylamine was ineffective. Potassium depolarization did not alter unstimulated or carbamylcholine-stimulated release of InsPs in either organ. In both tissues, the P2 purinergic agonist alpha,beta-methylene ATP also increased InsPs release, but the P1 purinergic agonist adenosine did not. These results extend our previous observations in the organ of Corti of the guinea pig to the rat and suggest a similar control of the InsP3 second messenger system in the vestibular sensory epithelia. In contrast to the cochlear sensory epithelia, atropine also significantly suppressed unstimulated InsPs release in the vestibular sensory epithelia. This suggests that the physiological mechanisms of the efferent nervous systems involving InsP3 second messenger system might be different in vestibular versus cochlear sensory epithelia. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,130 E ANN ST,ANN ARBOR,MI 48109. CR ANNIKO M, 1991, ACTA OTO-LARYNGOL, V111, P491, DOI 10.3109/00016489109138374 BARTOLAMI S, 1990, HEARING RES, V47, P229, DOI 10.1016/0378-5955(90)90154-H BERRIDGE MJ, 1984, NATURE, V312, P315, DOI 10.1038/312315a0 BERRIDGE MJ, 1983, BIOCHEM J, V212, P473 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 BROWN E, 1984, J NEUROCHEM, V42, P1379, DOI 10.1111/j.1471-4159.1984.tb02798.x BURNSTOCK G, 1981, J PHYSIOL-LONDON, V313, P1 BURNSTOCK G, 1990, ANN NY ACAD SCI, V603, P31 CANLON B, 1991, EUR J NEUROSCI, V3, P1338, DOI 10.1111/j.1460-9568.1991.tb00066.x CHALLISS RAJ, 1991, J NEUROCHEM, V57, P1042, DOI 10.1111/j.1471-4159.1991.tb08255.x DEAN NM, 1989, ANAL BIOCHEM, V183, P199, DOI 10.1016/0003-2697(89)90468-5 DECHESNE C, 1980, ACTA OTO-LARYNGOL, V90, P82, DOI 10.3109/00016488009131701 DRESCHER DG, 1992, J NEUROCHEM, V59, P765, DOI 10.1111/j.1471-4159.1992.tb09436.x DULON D, 1993, ABSTR ASS RES OT, V16, P117 DULON D, 1992, AM J OTOL, V13, P108 DULON D, 1990, J NEUROSCI, V10, P1388 EHRLICH YH, 1988, J NEUROCHEM, V50, P295, DOI 10.1111/j.1471-4159.1988.tb13263.x EVA C, 1986, J NEUROCHEM, V46, P1429, DOI 10.1111/j.1471-4159.1986.tb01758.x FISHER SK, 1991, J NEUROCHEM, V57, P1599, DOI 10.1111/j.1471-4159.1991.tb06357.x FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GOLDBERG JM, 1980, J NEUROPHYSIOL, V43, P986 GOLDBERG JM, 1975, ANNU REV PHYSIOL, V37, P129, DOI 10.1146/annurev.ph.37.030175.001021 GORDON JL, 1986, BIOCHEM J, V233, P309 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O 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 KAKEHATA S, 1992, P SENDAI S, V2, P25 KASTRITSIS CHC, 1992, J NEUROCHEM, V58, P1277 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 LEPEYRE PNM, 1991, J VESTIBUL RES-EQUIL, V1, P241 MAJERUS PW, 1988, J BIOL CHEM, V263, P3051 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 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 NISHIZUKA Y, 1984, SCIENCE, V225, P1365, DOI 10.1126/science.6147898 OGAWA K, 1993, ABST ASS RES OT, V16, P91 ONO T, 1989, NEUROCHEM INT, V14, P327, DOI 10.1016/0197-0186(89)90058-2 ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x SANS A, 1989, HEARING RES, V40, P117, DOI 10.1016/0378-5955(89)90105-6 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SCHACHT J, 1986, HEARING RES, V22, P94, DOI 10.1016/0378-5955(86)90086-9 SCHWARZ DWF, 1986, EXP BRAIN RES, V64, P19 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 SLEPECKY N, 1988, HEARING RES, V34, P119, DOI 10.1016/0378-5955(88)90099-8 SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M TACHIBANA M, 1984, HISTOCHEMISTRY, V81, P157, DOI 10.1007/BF00490110 TACHIBANA M, 1992, HEARING RES, V62, P82, DOI 10.1016/0378-5955(92)90204-Z THORNHILL RA, 1991, BRAIN RES, V561, P174, DOI 10.1016/0006-8993(91)90765-N VALAT J, 1991, NEUROSCI LETT, V127, P231, DOI 10.1016/0304-3940(91)90801-Y WACKYM PA, 1991, OTOLARYNG HEAD NECK, V105, P493 WANG SC, 1990, HEARING RES, V47, P53, DOI 10.1016/0378-5955(90)90166-M ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 ZENNER HP, 1990, HEARING RES, V50, P289, DOI 10.1016/0378-5955(90)90052-Q NR 55 TC 32 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 1993 VL 69 IS 1-2 BP 207 EP 214 DI 10.1016/0378-5955(93)90109-E PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000023 PM 8226341 ER PT J AU KURIYAMA, H ALBIN, RL ALTSCHULER, RA AF KURIYAMA, H ALBIN, RL ALTSCHULER, RA TI EXPRESSION OF NMDA-RECEPTOR MESSENGER-RNA IN THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE EXCITATORY AMINO ACID; NMDA RECEPTOR; COCHLEA; SPIRAL GANGLION CELLS; IN-SITU HYBRIDIZATION; RAT ID GUINEA-PIG COCHLEA; AMINO-ACID RECEPTORS; METHYL-D-ASPARTATE; INSITU HYBRIDIZATION; AUDITORY-NERVE; IMMUNOREACTIVITY; QUISQUALATE; ANTAGONISTS; AGONISTS; CLONING AB While there is considerable evidence that an excitatory amino acid and excitatory amino acid receptors are involved in the synapse between inner hair cells and the auditory nerve, evidence for the specific involvement of the N-methyl-D-aspartate (NMDA) receptor is more ambiguous. With the cloning of the NMDA receptor, probes are now available that can determine in which neurons the receptor is being expressed. In situ hybridization histochemical techniques were therefore utilized to examine the expression of NMDA receptor messenger ribonucleic acid (mRNA) in the rat cochlea. Expression of NMDA receptor mRNA was seen in spiral ganglion cells. These results suggest that NMDA receptor is a component of excitatory amino acid synapses in the cochlea. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT NEUROSCI,ANN ARBOR,MI 48109. CR ALTSCHULER RA, 1991, SOC NEUR ABSTR, P1214 ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 ARENTZEN R, 1985, J CELL BIOCHEM, V27, P415, DOI 10.1002/jcb.240270410 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BOBBIN RP, 1981, ABSTR ASS RES OT, P27 BOBBIN RP, 1987, HEARING RES, V25, P77, DOI 10.1016/0378-5955(87)90081-5 COLLINGRIDGE GL, 1988, J PHYSIOL-LONDON, V399, P301 COLLINGRIDGE GL, 1990, TRENDS PHARMACOL SCI, V11, P290, DOI 10.1016/0165-6147(90)90011-V COTMAN CW, 1987, TRENDS NEUROSCI, V10, P263, DOI 10.1016/0166-2236(87)90170-6 DOI K, 1992, ABSTR ASS RES OT, P19 DRESCHER GG, 1992, ABSTR ASS RES OT, P10 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x EHRENBERGER K, 1991, HEARING RES, V52, P73, DOI 10.1016/0378-5955(91)90188-F EYBALIN M, 1983, NEUROSCIENCE, V9, P863, DOI 10.1016/0306-4522(83)90274-9 Felix D., 1985, P68 FEX J, 1980, NEUROPHARMACOLOGY, V19, P809, DOI 10.1016/0028-3908(80)90076-3 FEX J, 1985, HEARING RES, V17, P101, DOI 10.1016/0378-5955(85)90014-0 GODFREY DA, 1976, J HISTOCHEM CYTOCHEM, V24, P468 GULLEY RL, 1979, ACTA OTO-LARYNGOL, V88, P177, DOI 10.3109/00016487909137157 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 KUMAR KN, 1991, NATURE, V354, P70 KURIYAMA H, 1992, SOC NEUR ABSTR, P1192 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 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 RYAN AF, 1991, NEUROREPORT, V2, P643, DOI 10.1097/00001756-199111000-00002 RYAN AF, 1991, HEARING RES, V56, P148, DOI 10.1016/0378-5955(91)90164-5 SCHWARTZ IR, 1986, NEUROBIOLOGY HEARING, P173 STARR PA, 1991, HEARING RES, V52, P23, DOI 10.1016/0378-5955(91)90185-C WATKINS JC, 1990, TRENDS PHARMACOL SCI, V11, P25, DOI 10.1016/0165-6147(90)90038-A YOUNG WS, 1986, P NATL ACAD SCI USA, V83, P9287 NR 33 TC 39 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 1993 VL 69 IS 1-2 BP 215 EP 220 DI 10.1016/0378-5955(93)90110-M PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000024 PM 8226342 ER PT J AU GOLDEY, ES KEHN, LS CROFTON, KM AF GOLDEY, ES KEHN, LS CROFTON, KM TI THE SENSITIVITY TO 3,3'-IMINODIPROPIONITRILE DIFFERS FOR HIGHFREQUENCY AND MIDFREQUENCY HEARING-LOSS IN THE DEVELOPING RAT SO HEARING RESEARCH LA English DT Article DE 3,3'-IMINODIPROPIONITRILE; OTOTOXICITY; COCHLEA; REFLEX MODIFICATION; ACOUSTIC STARTLE RESPONSE; DEVELOPMENT ID OTOACOUSTIC EMISSIONS; DEVELOPMENTAL-CHANGES; REFLEX MODIFICATION; AUDITORY FUNCTION; PLACE PRINCIPLE; COCHLEA; TRIMETHYLTIN; NEUROTOXICITY; OTOTOXICITY; KANAMYCIN AB 3,3'-Iminodipropionitrile (IDPN) has been demonstrated to produce a loss of hearing following both neonatal and adult exposures. Adult exposure induces a full spectrum hearing loss, whereas early postnatal exposure produces a high-frequency loss only. The purpose of this work was to delineate the period of development during which the rat becomes sensitive to the full ototoxic effects of IDPN. Primiparous Long Evans rats or their offspring were exposed to either saline or 300 mg/kg IDPN for three consecutive days. Ages of exposure were as follows: gestational days 15-17 or postnatal days (PND) 1-3, 5-7, 15-17, 20-22, 25-27, 30-32, 40-42, or 70-72. All animals were tested as adults for auditory thresholds to 5- and 40-kHz tones using reflex modification audiometry. Results demonstrate that adult-like susceptibility to IDPN was not reached until approximately PND 30-32. Early exposures (PND 5-22) to IDPN will induce a highfrequency selective hearing loss, sparing the lower frequency. Prenatal or early neonatal (PND 1-3) IDPN exposure resulted in a high degree of mortality ( > 70%). The long period of time between the susceptible period for the high frequency (PND 5-7) and the lower frequency (PND 30-32) does not correspond to the basal to apical ontogenic profile of any one physiological or anatomical process. These data suggest either a unique site of action for IDPN in the cochlea or the possibility of two different mechanisms, one operating at early postnatal ages and one at later ages. C1 MANTECH ENVIRONM TECHNOL INC,RES TRIANGLE PK,NC. RP GOLDEY, ES (reprint author), US EPA,DIV NEUROTOXICOL,MD 74B,RES TRIANGLE PK,NC 27711, USA. CR [Anonymous], 1989, SAS STAT USERS GUIDE, V2 AVERY DL, 1977, LAB ANIM SCI, V27, P110 AZIMA H, 1956, FED PROC, V15, P6 BENKE GM, 1975, TOXICOL APPL PHARM, V31, P254, DOI 10.1016/0041-008X(75)90161-1 BRODEUR J, 1963, P SOC EXP BIOL MED, V114, P509 BURDA H, 1985, HEARING RES, V17, P201, DOI 10.1016/0378-5955(85)90064-4 CADET JL, 1989, NEUROSCI BIOBEHAV R, V13, P39, DOI 10.1016/S0149-7634(89)80050-8 CARLIER E, 1980, ARCH OTO-RHINO-LARYN, V226, P129, DOI 10.1007/BF00455127 CHERNOFF N, 1989, TOXICOLOGY, V59, P111, DOI 10.1016/0300-483X(89)90050-4 CHOU SM, 1964, ACTA NEUROPATHOL, V3, P590 CLARK AW, 1980, J NEUROPATH EXP NEUR, V39, P42, DOI 10.1097/00005072-198001000-00004 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 Crofton K. M., 1992, NEUROTOXICOLOGY, P181 CROFTON KM, 1990, TOXICOL APPL PHARM, V105, P123, DOI 10.1016/0041-008X(90)90364-Z CROFTON KM, 1993, NEUROTOXICOL TERATOL, V15, P117, DOI 10.1016/0892-0362(93)90070-5 CROFTON KM, 1991, NEUROTOXICOL TERATOL, V13, P575, DOI 10.1016/0892-0362(91)90040-4 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 DAVIS M, 1982, J NEUROSCI, V2, P791 DEOL MS, 1976, ACTA OTO-LARYNGOL, V81, P429 Eggermont J J, 1986, Acta Otolaryngol Suppl, V429, P5 FECHTER LD, 1992, HEARING RES, V58, P166, DOI 10.1016/0378-5955(92)90125-7 FECHTER LD, 1986, HEARING RES, V23, P275, DOI 10.1016/0378-5955(86)90116-4 FORGACS J, 1960, Arch Ophtalmol Rev Gen Ophtalmol, V20, P275 FOWLER EP, 1947, JAMA-J AM MED ASSOC, V123, P87 GAINES TB, 1986, FUND APPL TOXICOL, V7, P299, DOI 10.1016/0272-0590(86)90160-0 GENTER MB, 1992, J PHARMACOL EXP THER, V263, P1432 HEATH H, 1968, EXP EYE RES, V7, P332, DOI 10.1016/S0014-4835(68)80046-6 HENLEY CM, 1991, HEARING RES, V55, P45, DOI 10.1016/0378-5955(91)90090-V ISON JR, 1984, NEUROBEH TOXICOL TER, V6, P437 JACOBSON A R, 1987, Molecular Toxicology, V1, P17 JANSSEN R, 1990, TOXICOLOGIST, V10, P306 JANSSEN R, 1991, BRAIN RES, V552, P255, DOI 10.1016/0006-8993(91)90090-I LENOIR M, 1980, ANAT EMBRYOL, V160, P253, DOI 10.1007/BF00305106 LENOIR M, 1986, BASIC APPLIED ASPECT, P227 LENOIR M, 1987, ANAT EMBRYOL, V175, P477, DOI 10.1007/BF00309683 LENOIR M, 1987, HEARING RES, V29, P265, DOI 10.1016/0378-5955(87)90173-0 LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 LLORENS J, 1991, NEUROTOXICOLOGY, V12, P583 Lu F C, 1965, Food Cosmet Toxicol, V3, P591, DOI 10.1016/S0015-6264(65)80206-1 MAROT M, 1980, HEARING RES, V2, P111, DOI 10.1016/0378-5955(80)90032-5 MIIKE T, 1981, SENTEN IJO CONG ANOM, V21, P407 MOSER VC, 1991, TOXICOLOGIST, V11, P167 MUIJSER H, 1988, TOXICOLOGY, V49, P331, DOI 10.1016/0300-483X(88)90016-9 MULLER M, 1991, HEARING RES, V56, P1, DOI 10.1016/0378-5955(91)90147-2 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W OLIVEIRA JA, 1989, AUDIOVESTIBULAR TOXI, V1 ONEJEME AU, 1984, TERATOLOGY, V29, P57, DOI 10.1002/tera.1420290108 OSAKO S, 1979, ACTA OTO-LARYNGOL, V88, P359, DOI 10.3109/00016487909137180 PRYOR GT, 1987, J APPL TOXICOL, V7, P55, DOI 10.1002/jat.2550070110 PRYOR GT, 1984, NEUROBEH TOXICOL TER, V6, P111 PUEL JL, 1987, DEV BRAIN RES, V37, P179, DOI 10.1016/0165-3806(87)90239-2 Pujol R, 1986, Acta Otolaryngol Suppl, V429, P29 REBERT CS, 1991, NEUROTOXICOL TERATOL, V13, P83, DOI 10.1016/0892-0362(91)90031-Q RUBEL EW, 1984, ANNU REV PHYSIOL, V46, P213 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RYBAK LP, 1992, OTOLARYNG HEAD NECK, V106, P677 SANDERS JC, 1982, ENV HLTH PERSPECT, V44, P63 SCHULZE GE, 1991, FUND APPL TOXICOL, V16, P602, DOI 10.1016/0272-0590(91)90099-P SELYE H, 1957, AM J OPHTHALMOL, V44, P763 STEFFEK AJ, 1972, TERATOLOGY, V5, P33, DOI 10.1002/tera.1420050107 Szulc-Kuberska J, 1976, MINERVA OTORINOLARIN, V26, P108 UZIEL A, 1985, DEV BRAIN RES, V19, P111, DOI 10.1016/0165-3806(85)90236-6 Uziel A, 1985, Acta Otolaryngol Suppl, V421, P57 UZIEL A, 1981, AUDIOLOGY, V20, P89 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V7, P733 WECKER JR, 1985, NEUROTOXICOL TERATOL, V7, P733 WILEY MJ, 1976, TERATOLOGY, V14, P43, DOI 10.1002/tera.1420140107 WILLHITE CC, 1981, TERATOLOGY, V23, P317, DOI 10.1002/tera.1420230306 WOLFF G, 1977, LIFE SCI, V20, P1163, DOI 10.1016/0024-3205(77)90487-8 YOUNG JS, 1986, TOXICOL APPL PHARM, V82, P87, DOI 10.1016/0041-008X(86)90441-2 YOUNG JS, 1983, J ACOUST SOC AM, V73, P1686, DOI 10.1121/1.389391 NR 73 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 1993 VL 69 IS 1-2 BP 221 EP 228 DI 10.1016/0378-5955(93)90111-D PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000025 PM 8226343 ER PT J AU FREEMAN, S GEALDOR, M SHIMONI, Y SOHMER, H AF FREEMAN, S GEALDOR, M SHIMONI, Y SOHMER, H TI THYROID-HORMONE INDUCES EARLIER ONSET OF AUDITORY FUNCTION IN NEONATAL RATS SO HEARING RESEARCH LA English DT Article DE ABR; DEVELOPMENT; THYROID HORMONES; NEONATE; FETUS; BONE CONDUCTION ID POTENTIALS; HYPOTHYROIDISM; PRETERM; COCHLEA; INFANTS; FLUIDS; EAR AB The effect of thyroid hormone injection on the development of auditory function in neonatal rats was evaluated using auditory nerve-brainstem evoked responses (ABR). The hormone induced earlier onset of auditory function. In order to differentiate between conductive and sensorineural factors, both air-conducted (AC) and bone-conducted (BC) ABR responses.were recorded. Neonatal rats were injected with thyroxine (T4), or with saline (control animals), from day of birth (post-natal day-PND-0), daily, until PND 9. AC- and BC-ABRs were recorded from PND 6 up to PND 20. It was found that both AC- and BC-ABR thresholds were lower in the T4-injected rats up to PND 15, after which no difference was found between the two groups. This indicated earlier maturity of both conductive (external and middle ears) and sensorineural (inner ear) factors and is probably due to the earlier appearance in the blood of higher T4 levels, following injection, than that occurring naturally during the neonatal period in these animals. RP FREEMAN, S (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 1172,IL-91010 JERUSALEM,ISRAEL. CR BERNARD PA, 1982, ARCH OTO-RHINO-LARYN, V234, P181, DOI 10.1007/BF00453627 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 DUSSAULT JH, 1975, ENDOCRINOLOGY, V97, P1321 FAWER CL, 1982, NEUROPEDIATRICS, V13, P200, DOI 10.1055/s-2008-1059623 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 FISHER DA, 1970, PEDIATRICS, V46, P208 GEALDOR M, 1992, HEARING RES, V69, P236 HEBERT R, 1987, CAN J PHYSIOL PHARM, V65, P424 Hoskins MM, 1927, J EXP ZOOL, V48, P373, DOI 10.1002/jez.1400480204 IWANO T, 1990, J HISTOCHEM CYTOCHEM, V38, P225 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 LARY S, 1985, J PEDIATR-US, V107, P593, DOI 10.1016/S0022-3476(85)80030-5 LENOIR M, 1980, ANAT EMBRYOL, V160, P301 LIN MH, 1978, J BIOL CHEM, V253, P723 MACKENZIE JM, 1989, ENDOCRINOLOGY, P646 MARSDEN CD, 1968, ACTA ENDOCRINOL-COP, V57, P353 RAPHAEL Y, 1983, ARCH OTO-RHINO-LARYN, V237, P147, DOI 10.1007/BF00463614 SALT AN, 1987, LARYNGOSCOPE, V97, P984 Sohmer H, 1976, ELECTROCOCHLEOGRAPHY, P431 STARR A, 1977, PEDIATRICS, V60, P831 UZIEL A, 1985, DEV BRAIN RES, V19, P111, DOI 10.1016/0165-3806(85)90236-6 UZIEL A, 1981, AUDIOLOGY, V20, P89 UZIEL A, 1983, HEARING RES, V11, P203, DOI 10.1016/0378-5955(83)90079-5 WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 WOOLF NK, 1988, HEARING RES, V35, P131, DOI 10.1016/0378-5955(88)90112-8 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 SEP PY 1993 VL 69 IS 1-2 BP 229 EP 235 DI 10.1016/0378-5955(93)90112-E PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000026 PM 8226344 ER PT J AU GEALDOR, M FREEMAN, S LI, G SOHMER, H AF GEALDOR, M FREEMAN, S LI, G SOHMER, H TI DEVELOPMENT OF HEARING IN NEONATAL RATS - AIR AND BONE CONDUCTED ABR THRESHOLDS SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; MATURATION; CONDUCTIVE; SENSORI-NEURAL; BONE CONDUCTION; ABR; FETUS; NEONATE ID BRAIN-STEM RESPONSE; MIDDLE-EAR; POTENTIALS; INFANTS; COCHLEA; ONSET; CAT; MATURATION; TERM AB While the human full-term neonate can hear at birth, in the rat the onset of auditory function as monitored by recording auditory nerve-brainstem evoked responses (ABR) has been reported to begin on post-natal day (PND) 12-14 and reaches adult thresholds at about 22 days. In order to determine the factors involved in this late onset and then rapid threshold improvement in rats, the ABR to both air conducted (AC) and bone-conducted (BC) auditory stimulation was determined in neonatal rats. ABR to maximal intensity BC stimuli (55 dB above adult rat ABR threshold - 55 dB HL*) could be recorded from PND 7-8 while AC responses to 80 dB HL* stimuli, only from PND 11. The air-bone gap (a measure of conductive immaturities only) disappeared on PND 15. This shows that there are both conductive (external and middle ear -Air-bone gap) and sensori-neural (inner ear - BC threshold) immaturities in the neonatal rat; the conductive factors are resolved by PND 15 while the sensori-neural continue after that. With respect to conductive factors, it seems that the state of the ear canal is not important while the chief conductive factors involved probably include mesenchyme resorption and/or ossicular ossification. The chief sensori-neural factor may be the development of the endocochlear potential, It is likely that the human fetus in-utero undergoes similar stages of development. C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 1172,IL-91010 JERUSALEM,ISRAEL. HADASSAH UNIV HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,IL-91240 JERUSALEM,ISRAEL. CR ADELMAN C, 1990, ELECTROEN CLIN NEURO, V77, P77, DOI 10.1016/0168-5597(90)90019-A ALPERT M, 1988, THESIS HEBREW U JERU Anggard L., 1965, ACTA OTOLARYNGOLOGIC, V203, P1 BLATCHLEY BJ, 1987, DEV BRAIN RES, V32, P75, DOI 10.1016/0165-3806(87)90140-4 BOEZEMAN EHJF, 1983, ELECTROEN CLIN NEURO, V56, P244, DOI 10.1016/0013-4694(83)90078-0 BOSHER SK, 1971, J PHYSL, V22, P739 CORNACCHIA L, 1983, AUDIOLOGY, V22, P430 FAWER CL, 1982, NEUROPEDIATRICS, V13, P200, DOI 10.1055/s-2008-1059623 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 GAGNON R, 1987, AM J OBSTET GYNECOL, V157, P1375 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X JONES TA, 1980, J NEUROSCI METH, V7, P261 KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 LARY S, 1985, J PEDIATR-US, V107, P593, DOI 10.1016/S0022-3476(85)80030-5 MAULDIN L, 1979, ARCH OTOLARYNGOL, V105, P656 RAPHAEL Y, 1983, ARCH OTO-RHINO-LARYN, V237, P147, DOI 10.1007/BF00463614 ROMAND R, 1976, J COMP NEUROL, V170, P1, DOI 10.1002/cne.901700102 ROMAND R, 1987, HEARING RES, V28, P1, DOI 10.1016/0378-5955(87)90148-1 RUBINSTEIN A, 1982, ANN OTO RHINOL LARYN, V91, P205 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 STARR A, 1977, PEDIATRICS, V60, P831 THOMAS JP, 1990, OTOLARYNG HEAD NECK, V103, P427 Tonndorf J., 1966, ACTA OTO-LARYNGOL, V213, P1 UZIEL A, 1981, AUDIOLOGY, V20, P89 WALSH EJ, 1986, J ACOUST SOC AM, V79, P712, DOI 10.1121/1.393461 WOLFSON MR, 1990, ELECTROEN CLIN NEURO, V75, P242, DOI 10.1016/0013-4694(90)90177-L WOODS JR, 1983, PEDIATR RES, V18, P83 WOOLF NK, 1986, AM J PHYSIOL, V250, pR493 WOOLF NK, 1988, HEARING RES, V35, P131, DOI 10.1016/0378-5955(88)90112-8 NR 31 TC 111 Z9 113 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 1993 VL 69 IS 1-2 BP 236 EP 242 DI 10.1016/0378-5955(93)90113-F PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000027 PM 8226345 ER PT J AU SHIVAPUJA, BG GU, ZP SAUNDERS, SS QUIRK, WS AF SHIVAPUJA, BG GU, ZP SAUNDERS, SS QUIRK, WS TI ACUTE EFFECTS OF COCAINE ON COCHLEAR FUNCTION SO HEARING RESEARCH LA English DT Article DE COCAINE; N(1) AMPLITUDE-INTENSITY FUNCTIONS; COCHLEAR BLOOD FLOW ID ACOUSTIC STARTLE; ABUSE; RAT AB The effect; of a single administration of cocaine on the cochlea was evaluated by measuring amplitude-intensity functions of the N1 response of the auditory nerve. Amplitude-intensity functions of the N1 response to tone-pips of. 500 Hz, 1, 2, 4 and 8 kHz were obtained before and after intraperitoneal injection of either saline, 3 mg/kg or 25 mg/kg of cocaine. N1 amplitudes were decreased after the administration of cocaine and this reduction was found to be dose dependent. The influence of cocaine on cochlear blood flow (CBF) was examined in order to test the possibility that cocaine induced reductions in CBF underlie these electro-physiological changes. Corresponding decreases in cochlear blood flow after cocaine exposure were observed. C1 BEIJING MED UNIV, FIRST HOSP, DEPT OTOLARYNGOL, BEIJING, PEOPLES R CHINA. SUNY Buffalo, HEARING SCI LABS, BUFFALO, NY 14260 USA. WAYNE STATE UNIV, DEPT OTOLARYNGOL, DETROIT, MI 48202 USA. RP SHIVAPUJA, BG (reprint author), HENRY FORD HOSP, DEPT OTOLARYNGOL, OTOL RES LABS, ER 7034, 2799 W GRAND BLVD, DETROIT, MI 48202 USA. CR Altschuler R. A., 1986, NEUROBIOLOGY HEARING AREHOLE S, 1987, HEARING RES, V30, P23, DOI 10.1016/0378-5955(87)90179-1 BEMENT C L, 1989, FASEB Journal, V3, pA297 BOZARTH MA, 1985, JAMA-J AM MED ASSOC, V254, P81, DOI 10.1001/jama.254.1.81 DAFNY N, 1979, PROG NEURO-PSYCHOPHA, V3, P353, DOI 10.1016/0364-7722(79)90046-8 DAVIS M, 1985, PSYCHOPHARMACOLOGY, V86, P31, DOI 10.1007/BF00431680 DENSERT O, 1974, ACTA OTO-LARYNGOL, V77, P185, DOI 10.3109/00016487409124616 GRITZKE R, 1988, ELECTROEN CLIN NEURO, V71, P389, DOI 10.1016/0168-5597(88)90042-1 HARTY TP, 1985, PSYCHOPHARMACOLOGY, V87, P396 HEISE GA, 1962, PSYCHOPHARMACOLOGIA, V3, P264, DOI 10.1007/BF00411367 Jaffe J, 1990, PHARMACOL BASIS THER, P522 Jones R T, 1984, NIDA Res Monogr, V50, P34 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 KONISHI T, 1968, J ACOUST SOC AM, V43, P471, DOI 10.1121/1.1910854 Lakoski J M, 1988, NIDA Res Monogr, V88, P78 LAURIKAINEN E, 1992, ACTA OTO-LARYNGOL, V112, P800, DOI 10.3109/00016489209137477 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 MISRAHY GA, 1958, J ACOUST SOC AM, V30, P70 MULE SJ, 1984, PSYCHIAT ANN, V14, P724 NANTWI KD, 1992, IN PRESS NEUROPHARMA NAYAK PK, 1976, J PHARMACOL EXP THER, V196, P556 RITCHIE JM, 1990, PHARMACOL BASIS THER, P311 SAHLEY TL, 1991, HEARING RES, V55, P133, DOI 10.1016/0378-5955(91)90099-U SHIH L, 1988, INT J PEDIATR OTORHI, V15, P245, DOI 10.1016/0165-5876(88)90079-1 Siegel R K, 1984, NIDA Res Monogr, V50, P92 SMART RG, 1987, J FORENSIC SCI, V32, P303 Spoendlin H, 1966, Acta Otolaryngol, V61, P423 TAYLOR D, 1978, RES COMMUN CHEM PATH, V21, P67 VANDYKE C, 1982, SCI AM, V246, P128 WEVER EG, 1949, AM J PHYSIOL, V159, P199 NR 30 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 1993 VL 69 IS 1-2 BP 243 EP 250 DI 10.1016/0378-5955(93)90114-G PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LW840 UT WOS:A1993LW84000028 PM 8226346 ER PT J AU WANG, J LI, QH DONG, WJ CHEN, JS AF WANG, J LI, QH DONG, WJ CHEN, JS TI EFFECTS OF K+-CHANNEL BLOCKERS ON COCHLEAR POTENTIALS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE COCHLEAR POTENTIALS; POTASSIUM-CHANNEL BLOCKERS; NOISE ID VERTEBRATE HAIR CELL; POTASSIUM CHANNEL; SMOOTH-MUSCLE; IONIC BASIS; INNER-EAR; ENDOLYMPH; NOISE AB The effects of different K+ channel blockers, 4-aminopyridine (4-AP), tetraethylammonium (TEA) and quinine, on the various cochlear potentials were observed by the means of perilymph infusion. Each of the three blockers depressed the compound action potential. However, they exerted quite different effects on other cochlear potentials, especially comparing 4-AP, a fast K+-channel blocker, with two other blockers. 4-AP induced a significant increase in the magnitude of summating potential, while TEA and quinine decreased it; 4-AP showed no effect on the general endocochlear potential (G-EP, the EP value recorded directly from the scala media, SM) and the negative EP component (N-EP), while TEA and Quinine increased G-EP and decreased the absolute value of N-EP. They also exerted different effects on the EP changes induced by exposure to intense noise. The results indicate the different roles of different K+-channels in the generation of cochlear potentials. The relationship of the two components of EP (positive and negative) and the G-EP was discussed. C1 NANJING RAILWAY MED COLL,AUDIOPHYSIOL LAB,NANJING,PEOPLES R CHINA. CR ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 BAKER M, 1987, J PHYSL, V383, P4567 CHOU JTY, 1975, EXPERIENTIA, V31, P554, DOI 10.1007/BF01932455 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 CREED KE, 1971, PFLUG ARCH EUR J PHY, V326, P115, DOI 10.1007/BF00586904 DALLOS P, 1985, J NEUROSCI, V5, P1591 FETTIPLACE R, 1987, TRENDS NEUROSCI, V10, P421, DOI 10.1016/0166-2236(87)90013-0 FUJII K, 1990, BRIT J PHARMACOL, V99, P779 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 HUDSPETH AJ, 1986, HEARING RES, V22, P21, DOI 10.1016/0378-5955(86)90070-5 INOUE R, 1985, PFLUG ARCH EUR J PHY, V405, P173, DOI 10.1007/BF00582557 KONISHI T, 1980, EXP BRAIN RES, V40, P457 Konishi T, 1967, Acta Otolaryngol, V64, P107, DOI 10.3109/00016486709139097 KONISHI T, 1973, ACTA OTO-LARYNGOL, V76, P410, DOI 10.3109/00016487309121529 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 MELICHAR I, 1987, HEARING RES, V25, P23, DOI 10.1016/0378-5955(87)90076-1 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 RICHER C, 1990, BRIT J PHARMACOL, V100, P557 ROPER J, 1989, J PHYSIOL-LONDON, V416, P93 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 SALT AN, 1982, JPN J PHYSIOL, V32, P219 SALT AN, 1979, HEARING RES, V1, P343, DOI 10.1016/0378-5955(79)90005-4 SELLICK PM, 1974, PFLUGER ARCH, V336, P406 Sitko S T, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P328 STEINACKER A, 1988, HEARING RES, V35, P265, DOI 10.1016/0378-5955(88)90123-2 WANG J, 1992, HEARING RES, V59, P31, DOI 10.1016/0378-5955(92)90099-9 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 AUG PY 1993 VL 68 IS 2 BP 152 EP 158 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800002 PM 8407601 ER PT J AU PICKLES, JO AF PICKLES, JO TI A MODEL FOR THE MECHANICS OF THE STEREOCILIAR BUNDLE ON ACOUSTICOLATERAL HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; TRANSDUCTION; MECHANICS; MODEL; STEREOCILIA; TIP LINK ID MECHANOELECTRICAL TRANSDUCTION CHANNELS; GUINEA-PIG COCHLEA; STIFFNESS; SENSITIVITY; LINKS; ORGAN; CORTI; FROG; EAR AB The stereociliar bundle on acousticolateral hair cells was modelled as a series of stiff rods (stereocilia), and springs (stereociliary links and rootlets). Predictions were made for the coupling of stimulus-induced deflections between the stereocilia on the hair bundle, and for the stretches of the different classes of link. Comparison of the results with the measured mechanical properties of hair bundles suggests that in the bullfrog sacculus the stiffness of a side link and a tip link are related to the rootlet's contribution to the stiffness of a stereocilium to deflection in approximately the ratios greater-than-or-equal-to 400:100:1. The results show that stretch of the tip links is closely related to the deflection of the hair bundle over a wide range of model parameters, while the stretch of the side links is more variable, and in some types of bundle the mean stretch of the side links may be zero or negative. The results are in accordance with the view that the tip links are in an appropriate position to detect the deflections, while the main role for the side links may be to couple the deflections between the stereocilia. The mechanical consequences of bundles of different configurations, as seen in different hair cell types, are investigated. CR ASSAD JA, 1992, IN PRESS J NEUROSCI ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X COREY D P, 1989, Society for Neuroscience Abstracts, V15, P208 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 HACKNEY CM, 1992, P ROY SOC B-BIOL SCI, V248, P215, DOI 10.1098/rspb.1992.0064 HOLTON T, 1986, J PHYSIOL-LONDON, V375, P195 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, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 JACOBS RA, 1990, COLD SH Q B, V55, P547 JORGENSEN F, 1988, J PHYSIOL-LONDON, V403, P577 KOSSL M, 1990, HEARING RES, V44, P217, DOI 10.1016/0378-5955(90)90082-Z NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 OSBORNE MP, 1988, HEARING RES, V35, P99, DOI 10.1016/0378-5955(88)90044-5 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PICKLES JO, 1989, COCHLEAR MECHANISMS, P37 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H RUSSELL IJ, 1986, NATURE, V321, P517, DOI 10.1038/321517a0 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 SHOTWELL SL, 1981, ANN NY ACAD SCI, V374, P1, DOI 10.1111/j.1749-6632.1981.tb30854.x STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 THURM U, 1981, BIOPHYS STRUCT MECH, V7, P245, DOI 10.1007/BF02425378 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 VATER M, 1992, J COMP NEUROL, V318, P380, DOI 10.1002/cne.903180404 ZWISLOCKI JJ, 1979, ACTA OTO-LARYNGOL, V87, P267, DOI 10.3109/00016487909126419 NR 27 TC 51 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 AUG PY 1993 VL 68 IS 2 BP 159 EP 172 DI 10.1016/0378-5955(93)90120-P PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800003 PM 8407602 ER PT J AU KUMOI, K SAITO, N TANAKA, C AF KUMOI, K SAITO, N TANAKA, C TI IMMUNOHISTOCHEMICAL LOCALIZATION OF GAMMA-AMINOBUTYRIC ACID- AND ASPARTATE-CONTAINING NEURONS IN THE GUINEA-PIG SUPERIOR OLIVARY COMPLEX SO HEARING RESEARCH LA English DT Article DE GAMMA-AMINOBUTYRIC ACID; ASPARTATE; IMMUNOHISTOCHEMISTRY; SUPERIOR OLIVARY COMPLEX; GUINEA PIG ID HORSERADISH-PEROXIDASE; OLIVOCOCHLEAR NEURONS; EFFERENT NEURONS; ENKEPHALIN-LIKE; BRAIN-STEM; COCHLEA; IMMUNOREACTIVITY; GABA; RAT; NUCLEI AB The immunohistochemical localization of gamma-aminobutyric acid (GABA)- and aspartate-containing neurons was demonstrated in the guinea pig superior olivary complex, using purified antisera to GABA and aspartate, respectively. Medium-sized oval GABA-containing neurons were found in the lateral superior olive, and bipolar medium-sized GABA-containing neurons were observed in the dorsal hilus of the lateral superior olive. Medium-sized to large round GABA-containing neurons were observed in the ventral nucleus of the trapezoid body. GABA-containing terminals were found throughout the superior olivary complex with the highest density in the ventral nucleus of the trapezoid body. Aspartate-like immunoreactivity was observed in medium-sized round or oval neurons in the lateral superior olive, small fusiform neurons in the ventral nucleus of the trapezoid body, fusiform medium-sized neurons in the medial superior olive and oval medium-sized neurons in the superior paraolivary nucleus and round medium-sized neurons in the medial nucleus of the trapezoid body. Double staining method demonstrated that aspartate-containing neurons in the medial nucleus of the trapezoid body were surrounded by GABA-containing terminals. The present results suggested the possible origin of GABAergic and aspartatergic olivocochlear bundles. C1 KOBE UNIV,SCH MED,DEPT PHARMACOL,7-5-2 KUSUNOKI CHO,CHUO KU,KOBE 650,JAPAN. KOBE UNIV,SCH MED,DEPT OTORHINOLARYNGOL,KOBE 650,JAPAN. CR ADAMS JC, 1983, J COMP NEUROL, V215, P272 ALTSCHULER RA, 1981, P NATL ACAD SCI-BIOL, V78, P6553, DOI 10.1073/pnas.78.10.6553 ALTSCHULER RA, 1984, J HISTOCHEM CYTOCHEM, V32, P839 ALTSCHULER RA, 1984, BRAIN RES, V291, P173, DOI 10.1016/0006-8993(84)90667-X ALTSCHULER RA, 1983, NEUROSCIENCE, V9, P621, DOI 10.1016/0306-4522(83)90178-1 FAGG GE, 1983, NEUROSCIENCE, V9, P701, DOI 10.1016/0306-4522(83)90263-4 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 HELFERT RH, 1988, J NEUROSCI, V8, P3111 KUMOI K, 1988, BRAIN RES, V439, P302, DOI 10.1016/0006-8993(88)91487-4 KUMOI K, 1987, BRAIN RES, V416, P22, DOI 10.1016/0006-8993(87)91492-2 MCLAUGHL.BJ, 1974, BRAIN RES, V76, P377, DOI 10.1016/0006-8993(74)90815-4 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 RASMUSSEN GL, 1953, J COMP NEUROL, V99, P61, DOI 10.1002/cne.900990105 SAITO N, 1986, NEUROSCI LETT, V65, P89, DOI 10.1016/0304-3940(86)90125-4 SAKAUE M, 1989, BIOMED RES-TOKYO, V10, P287 SCHWARTZ IR, 1990, J ELECTRON MICR TECH, V15, P225, DOI 10.1002/jemt.1060150304 SCHWARTZ IR, 1986, J COMP NEUROL, V246, P500, DOI 10.1002/cne.902460407 STORMMATHISEN J, 1983, NATURE, V301, P517, DOI 10.1038/301517a0 STRUTZ J, 1980, NEUROSCI LETT, V17, P227, DOI 10.1016/0304-3940(80)90027-0 THOMPSON GC, 1986, BRAIN RES, V372, P72, DOI 10.1016/0006-8993(86)91459-9 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WEBSTER WR, 1985, RAT NERVOUS SYSTEM, P153 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 NR 25 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 1993 VL 68 IS 2 BP 173 EP 179 DI 10.1016/0378-5955(93)90121-G PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800004 PM 8407603 ER PT J AU FOSTER, JD DRESCHER, MJ KHAN, KM DRESCHER, DG AF FOSTER, JD DRESCHER, MJ KHAN, KM DRESCHER, DG TI IMMUNOHISTOCHEMICAL LOCALIZATION OF S-100 PROTEIN IN THE SACCULE OF THE RAINBOW-TROUT (SALMO-GAIRDNERII R) SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; CALCIUM-BINDING PROTEINS; SACCULE; SALMO-GAIRDNERII ID CALCIUM-BINDING PROTEIN; OUTER HAIR-CELLS; HUMAN INNER-EAR; IMMUNOCYTOCHEMICAL DETECTION; NEURITE EXTENSION; XENOPUS-LAEVIS; S100 PROTEIN; RAT; BRAIN; COCHLEAR AB The distribution of S-100-like immunoreactivity in the trout saccule (a presumed organ of hearing in fish) has been determined by means of immunohistochemistry. Within the sensory epithelium of the saccular macula, hair cells and myelinated saccular nerve fibers were found to be immunoreactive. Hair-cell immunoreactivity was relatively uniform throughout the macula except at the extreme periphery (rostral, caudal, ventral and dorsal), where staining was either decreased or absent. The immunoreactivity associated with myelinated nerve fibers was greatest at the peripheral edges of the nerve processes, a position corresponding to the location of Schwann cells. However, the nerve processes themselves (within and subjacent to the sensory epithelium), as well as cell bodies within the saccular nerve, were also immunoreactive. Thus, the immunoreactivity of the saccular nerve observed above the basal lamina can be attributed to the saccular nerve processes as well as to nerve-associated Schwann cells. Overall, the immunoreactivity displayed by hair cells was less intense than that associated with myelinated saccular nerve, as evidenced by a disappearance of signal in hair cells first, upon serial dilution of antibody. No S-100-like immunoreactivity was observed in supporting cells within the sensory epithelium or in epithelial cells in non-sensory regions. A concentration of S-100-like immunoreactivity in hair cells and saccular nerve is suggestive of the presence of S-100 calcium-binding protein-mediated activities in these cell types. C1 WAYNE STATE UNIV,SCH MED,BIOOTOL LAB,DEPT OTOLARYNGOL,540 E CANFIELD AVE,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT BIOCHEM,DETROIT,MI 48201. AGA KHAN UNIV,DEPT ANAT,KARACHI,PAKISTAN. CR ALI SM, 1989, NATURE, V340, P313, DOI 10.1038/340313a0 COLING D, 1992, ABSTR ASS RES OT, V15, P10 COLING DE, 1991, HEARING RES, V57, P113, DOI 10.1016/0378-5955(91)90080-S DECHESNE CJ, 1988, HEARING RES, V33, P273, DOI 10.1016/0378-5955(88)90157-8 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DONATO R, 1983, FEBS LETT, V162, P310, DOI 10.1016/0014-5793(83)80778-9 DONATO R, 1985, FEBS LETT, V186, P65, DOI 10.1016/0014-5793(85)81340-5 DONATO R, 1991, CELL CALCIUM, V12, P713, DOI 10.1016/0143-4160(91)90040-L DRESCHER DG, 1989, BRAIN RES, V485, P225, DOI 10.1016/0006-8993(89)90565-9 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 DRESCHER MJ, 1987, SOC NEUR ABSTR, V17, P43 DRESCHER MJ, 1992, J NEUROCHEM, V59, P93, DOI 10.1111/j.1471-4159.1992.tb08879.x DRUST DS, 1988, NATURE, V331, P88, DOI 10.1038/331088a0 DULON D, 1990, J NEUROSCI, V10, P1388 ENDO T, 1983, FEBS LETT, V161, P235, DOI 10.1016/0014-5793(83)81015-1 Foster J. D., 1992, Society for Neuroscience Abstracts, V18, P1400 FUJI T, 1990, J BIOCHEM-TOKYO, V107, P133 GERKE V, 1984, EMBO J, V3, P227 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 Igarashi S, 1991, Acta Otolaryngol Suppl, V481, P163 ISHIKAWA H, 1983, NATURE, V303, P711, DOI 10.1038/303711a0 IWANAGA T, 1989, ARCH HISTOL CYTOL, V52, P13, DOI 10.1679/aohc.52.Suppl_13 KHAN KM, 1992, ABSTR ASS RES OT, V15, P85 KHAN KM, 1991, NEUROSCI LETT, V131, P109, DOI 10.1016/0304-3940(91)90348-W KLEE CB, 1988, BIOCHEMISTRY-US, V27, P6645, DOI 10.1021/bi00418a001 KLIGMAN D, 1988, TRENDS BIOCHEM SCI, V13, P437, DOI 10.1016/0968-0004(88)90218-6 KLIGMAN D, 1985, P NATL ACAD SCI USA, V82, P7136, DOI 10.1073/pnas.82.20.7136 MATA M, 1990, J NEUROCYTOL, V19, P432, DOI 10.1007/BF01188409 PERSECHINI A, 1989, TRENDS NEUROSCI, V12, P462, DOI 10.1016/0166-2236(89)90097-0 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A RABIE A, 1983, CELL TISSUE RES, V232, P691 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 RUSSELL IJ, 1971, J EXP BIOL, V54, P643 SAIDEL WM, 1990, HEARING RES, V47, P139, DOI 10.1016/0378-5955(90)90171-K SANS A, 1986, BRAIN RES, V364, P190, DOI 10.1016/0006-8993(86)91003-6 SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 SHI SR, 1992, LARYNGOSCOPE, V102, P734, DOI 10.1288/00005537-199207000-00002 SIEGEL JH, 1987, HEARING RES, V28, P131, DOI 10.1016/0378-5955(87)90044-X SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SUGIMURA K, 1989, MUSCLE NERVE, V12, P929, DOI 10.1002/mus.880121109 VANELDIK LJ, 1988, J BIOL CHEM, V263, P7830 VANELDIK LJ, 1991, BRAIN RES, V542, P280, DOI 10.1016/0006-8993(91)91579-P WACKYM PA, 1990, LARYNGOSCOPE, V100, P447 WINNINGHAMMAJOR F, 1989, J CELL BIOL, V107, pA729 WINNINGHAMMAJOR F, 1989, J CELL BIOL, V109, P3063, DOI 10.1083/jcb.109.6.3063 YAMAGISHI M, 1989, ANN OTO RHINOL LARYN, V98, P384 NR 46 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 AUG PY 1993 VL 68 IS 2 BP 180 EP 188 DI 10.1016/0378-5955(93)90122-H PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800005 PM 8407604 ER PT J AU WU, SH KELLY, JB AF WU, SH KELLY, JB TI RESPONSE OF NEURONS IN THE LATERAL SUPERIOR OLIVE AND MEDIAL NUCLEUS OF THE TRAPEZOID BODY TO REPETITIVE STIMULATION - INTRACELLULAR AND EXTRACELLULAR RECORDINGS FROM MOUSE-BRAIN SLICE SO HEARING RESEARCH LA English DT Article DE SUPERIOR OLIVARY COMPLEX; TRAPEZOID BODY; SOUND LOCALIZATION; BINAURAL INTEGRATION; ACOUSTIC CHIASM; TEMPORAL RESPONSE ID ANTEROVENTRAL COCHLEAR NUCLEUS; UNIT EXCITATORY RESPONSES; SINGLE AUDITORY UNITS; BINAURAL TONE BURSTS; BUSHY CELL AXONS; SOUND LOCALIZATION; PHYSIOLOGICAL-PROPERTIES; HORSERADISH-PEROXIDASE; DISCHARGE PATTERNS; EPTESICUS-FUSCUS AB The responses of neurons in the lateral superior olive (LSO) and medial nucleus of the trapezoid body (MNTB) to repeated electrical stimulation of the trapezoid body were investigated in a brain slice preparation of the mouse superior olivary complex. Brain slices, 400-500 mum thick, were cut in the frontal plane and were maintained for physiological recording in a bath of warm, oxygenated saline. Both intracellular and extracellular recordings were made with glass micropipettes filled with 4 M potassium acetate. Bipolar stimulating electrodes were placed on the trapezoid body ipsilateral and contralateral to the superior olive. Current levels were set so that an ipsilateral pulse elicited a single action potential in LSO and a contralateral pulse elicited a single action potential in MNTB. Trapezoid body fibers were then stimulated with trains consisting of 10 current pulses. Repeated stimulation at low rates resulted in a number of spikes equal to the number of current pulses. Pulse rate was then increased to determine the limits of response to repeated stimulation. In the MNTB, neurons were capable of following very high rates of stimulation without reduction in response probability. On the average, MNTB neurons responded with a probability of 0.9 at 667 Hz. In contrast, most LSO neurons were incapable of following high rates of stimulation. LSO neurons responded with a probability of 0.9 at 125 Hz. For some LSO neurons, application of strychnine (0.5 muM) to the bath increased the probability of firing at high rates. MNTB neurons were unaffected by strychnine. C1 CARLETON UNIV,DEPT PSYCHOL,SENSORY NEUROSCI LAB,329 LIFE SCI BLDG,OTTAWA K1S 5B6,ONTARIO,CANADA. CR ADAMS JC, 1990, HEARING RES, V49, P281, DOI 10.1016/0378-5955(90)90109-3 AOKI E, 1988, BRAIN RES, V442, P63, DOI 10.1016/0006-8993(88)91432-1 BAKER BN, 1986, ABSTR ASS RES OT, V9, P7 BANKS MI, 1992, J NEUROSCI, V12, P2819 BLEDSOE SC, 1990, BRAIN RES, V517, P189, DOI 10.1016/0006-8993(90)91025-C BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BROWNELL WE, 1979, BRAIN RES, V177, P189, DOI 10.1016/0006-8993(79)90930-2 BROWNER RH, 1975, BRAIN BEHAV EVOLUT, V11, P322, DOI 10.1159/000123643 CAIRD D, 1983, EXP BRAIN RES, V52, P385 Cant N. B., 1991, NEUROBIOLOGY HEARING, P99 CANT NB, 1984, J COMP NEUROL, V227, P63, DOI 10.1002/cne.902270108 CASPARY D M, 1991, P141 CASSEDAY JH, 1975, J NEUROPHYSIOL, V38, P842 COVEY E, 1986, J NEUROSCI, V6, P2926 COVEY E, 1991, J NEUROSCI, V11, P3456 FINLAYSON PG, 1989, HEARING RES, V38, P221, DOI 10.1016/0378-5955(89)90067-1 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 GLENDENNING KK, 1988, J COMP NEUROL, V275, P261 GLENDENNING KK, 1991, J COMP NEUROL, V310, P377, DOI 10.1002/cne.903100308 GOLDBERG JAY M., 1968, J NEUROPHYSIOL, V31, P639 GUINAN JJ, 1990, HEARING RES, V49, P321, DOI 10.1016/0378-5955(90)90111-2 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 Harrison J M, 1970, Contrib Sens Physiol, V4, P95 HARRISON JM, 1966, J COMP NEUROL, V126, P51, DOI 10.1002/cne.901260105 HARRISON JM, 1962, J COMP NEUROL, V119, P341, DOI 10.1002/cne.901190306 HELFERT RH, 1992, J COMP NEUROL, V323, P305, DOI 10.1002/cne.903230302 HELFERT RH, 1987, AM J ANAT, V179, P655 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 HELFERT RH, 1986, J COMP NEUROL, V244, P533, DOI 10.1002/cne.902440409 HUTSON K A, 1987, Society for Neuroscience Abstracts, V13, P548 JEANBAPTISTE M, 1975, J COMP NEUROL, V162, P111, DOI 10.1002/cne.901620107 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 KAVANAGH GL, 1992, J NEUROPHYSIOL, V67, P1643 KIANG NYS, 1965, MIT RES MONOGR, V35, P48 KUWABARA N, 1991, J COMP NEUROL, V314, P707, DOI 10.1002/cne.903140406 KUWABARA N, 1991, J COMP NEUROL, V314, P684, DOI 10.1002/cne.903140405 LENN NJ, 1966, AM J ANAT, V118, P375, DOI 10.1002/aja.1001180205 LI RYS, 1971, ANTIDROMIC ORTHODROM, V100, P227 LU SM, 1987, HEARING RES, V31, P137, DOI 10.1016/0378-5955(87)90119-5 MASTERTO.B, 1967, J NEUROPHYSIOL, V30, P341 MOLLER AR, 1969, ACTA PHYSIOL SCAND, V75, P542 MOORE CN, 1974, BRAIN RES, V82, P13, DOI 10.1016/0006-8993(74)90889-0 MOORE MJ, 1983, J NEUROSCI, V3, P237 MOREST D. KENT, 1968, BRAIN RES, V9, P288, DOI 10.1016/0006-8993(68)90235-7 NAKAJIMA Y, 1971, J CELL BIOL, V50, P121, DOI 10.1083/jcb.50.1.121 OERTEL D, 1985, J ACOUST SOC AM, V78, P328, DOI 10.1121/1.392494 Oertel D., 1988, AUDITORY FUNCTION NE, P313 OERTEL D, 1983, J NEUROSCI, V3 OLLO C, 1979, AM J ANAT, V155, P349, DOI 10.1002/aja.1001550306 ROUILLER EM, 1984, J COMP NEUROL, V225, P167, DOI 10.1002/cne.902250203 RYUGO DK, 1982, J COMP NEUROL, V210, P239, DOI 10.1002/cne.902100304 RYUGO DK, 1991, J COMP NEUROL, V305, P35, DOI 10.1002/cne.903050105 SAINTMARIE RL, 1990, BRAIN RES, V524, P244, DOI 10.1016/0006-8993(90)90698-B SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SANES DH, 1990, J NEUROSCI, V10, P3494 SCHWARTZ I, 1985, AUDITORY BIOCH, P258 Schwartz I. R., 1992, MAMMALIAN AUDITORY P, P117 SMITH P H, 1989, Society for Neuroscience Abstracts, V15, P746 SMITH PH, 1987, J COMP NEUROL, V266, P360, DOI 10.1002/cne.902660305 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 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 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3031, DOI 10.1016/0306-4522(82)90228-7 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 TSUCHITANI C, 1969, J ACOUST SOC AM, V46, P978 TSUCHITANI C, 1985, J ACOUST SOC AM, V77, P1484, DOI 10.1121/1.392043 TSUCHITA.C, 1966, J NEUROPHYSIOL, V29, P684 TSUCHITANI C, 1982, J NEUROPHYSIOL, V47, P479 TSUCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WARR WB, 1972, BRAIN RES, V40, P247 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WARR WB, 1966, EXP NEUROL, V14, P543 WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P987 WENTHOLD RJ, 1990, GLYCINE NEUROTRANSMI, P391 Wenthold RJ, 1991, NEUROBIOLOGY HEARING, P121 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 WU SH, 1992, J NEUROPHYSIOL, V68, P1151 WU SH, 1992, NEUROSCI LETT, V134, P257, DOI 10.1016/0304-3940(92)90529-G WU SH, 1986, J NEUROSCI, V6, P2691 WU SH, 1991, J NEUROPHYSIOL, V65, P230 WU SH, 1992, J NEUROSCI, V12, P3084 WU SH, 1993, ABSTR ASS RES OT, V16, P126 ZOOK JM, 1988, HEARING RES, V34, P141, DOI 10.1016/0378-5955(88)90101-3 NR 90 TC 79 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 AUG PY 1993 VL 68 IS 2 BP 189 EP 201 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800006 PM 8407605 ER PT J AU ZACKSENHOUSE, M JOHNSON, DH TSUCHITANI, C AF ZACKSENHOUSE, M JOHNSON, DH TSUCHITANI, C TI EXCITATION EFFECTS ON LSO UNIT SUSTAINED RESPONSES - POINT PROCESS CHARACTERIZATION SO HEARING RESEARCH LA English DT Article DE POINT PROCESS MODELS; LATERAL SUPERIOR OLIVE; EXCITATION ID LATERAL SUPERIOR OLIVE; BINAURAL TONE BURSTS; DISCHARGE PATTERNS; CAT; INHIBITION AB LSO units recover from a spike discharge in a characteristic way, modeled by an intrinsic recovery function that is stimulus invariant up to a scaling factor and a shifting constant. Data analysis shows that the effect of increasing excitatory stimulus level can be described by amplifying the intrinsic recovery function and by shifting it toward shorter intervals. The shifting process secondarily interacts with the absolute deadtime to produce the response characteristics of the three LSO unit types. Decreased excitation is clearly distinguished from inhibition, which affects the scaling, but not the time origin, of the recovery. We conclude that both excitatory and inhibitory stimulus levels are encoded in the timing of LSO unit discharges. C1 UNIV TEXAS,HLTH SCI CTR,GRAD SCH BIOMED SCI,CTR SENSORY SCI,HOUSTON,TX 77225. RP ZACKSENHOUSE, M (reprint author), RICE UNIV,DEPT ELECT & COMP ENGN,INST COMP & INFORMAT TECHNOL,HOUSTON,TX 77251, USA. CR Boudreau J C, 1970, Contrib Sens Physiol, V4, P143 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 Cox DR, 1962, RENEWAL THEORY GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 JOHNSON D, 1986, HEARING RES, V221, P135 JOHNSON DH, 1978, BIOPHYS J, V22, P413 OZAKI T, 1979, ANN I STAT MATH, V31, P145, DOI 10.1007/BF02480272 SMITH C, 1986, U S CAROLINA SC MINE, V1691 SMITH CE, 1986, BIOL CYBERN, V54, P41, DOI 10.1007/BF00337114 Snyder D.L., 1991, RANDOM POINT PROCESS, Vsecond TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 TSUCHITANI C, 1985, J ACOUST SOC AM, V77, P1484, DOI 10.1121/1.392043 TSUCHITANI C, 1982, J NEUROPHYSIOL, V47, P479 Tuckwell H. C., 1989, STOCHASTIC PROCESSES VERVEEN AA, 1968, PR INST ELECTR ELECT, V56, P906, DOI 10.1109/PROC.1968.6443 ZACKSENHOUSE M, 1992, HEARING RES, V62, P105, DOI 10.1016/0378-5955(92)90207-4 NR 17 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 1993 VL 68 IS 2 BP 202 EP 216 DI 10.1016/0378-5955(93)90124-J PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800007 PM 8407606 ER PT J AU DUPONT, J GUILHAUME, A ARAN, JM AF DUPONT, J GUILHAUME, A ARAN, JM TI NEURONAL DEGENERATION OF PRIMARY COCHLEAR AND VESTIBULAR INNERVATIONS AFTER LOCAL INJECTION OF SISOMICIN IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SPIRAL GANGLION; SCARPA GANGLION; NEURONAL DEGENERATION; GUINEA PIG; AMINOGLYCOSIDE OTOTOXICITY; MORPHOLOGY ID SPIRAL GANGLION; NEURAL DEGENERATION; INNER-EAR; RAT; LABYRINTHECTOMY; NERVE; CAT; DESTRUCTION; GENTAMICIN; CELLS AB This paper reports on a dynamic study of the morphological changes within the cochlear and vestibular ganglia of the guinea pig after local application of Sisomicin in the inner ear. The treatment leads to a rapid, complete and irreversible destruction of the sensory cells in the cochlear and vestibular neuroepithelia. A progressive degeneration of the type I and type II afferent neurons, presenting a decreasing gradient from the base toward the apex of the cochlea, is rapidly observed and becomes almost complete as early as 15 days after the peripheral injury. Five months after the treatment the spiral ganglion cells have almost completely disappeared. At this time the vestibular ganglion cell density appears normal but the neurons exhibit important signs of alteration. Such damage to the cochlear and vestibular afferent neurons may result from either retrograde neuronal degeneration and/or direct neurotoxic effect of the drug. Thus the combination of the two mechanisms could lead to neuronal losses in spiral and Scarpa's ganglia after the local aminoglycoside intoxication of the inner ear. The difference in the time course of degeneration for these two afferent ganglia could be due to their specific susceptibilities or to their different anatomical locations. C1 INSERM,AUDIOL EXPTL LAB,UNITE 229,F-33077 BORDEAUX,FRANCE. UNIV BORDEAUX 2,HOP PELLEGRIN,F-33076 BORDEAUX,FRANCE. CR ALEXANDER G, 1901, ARCH OHRENHEILK, V51, P109, DOI 10.1007/BF01809248 Anderson H, 1968, ACTA OTO-LARYNGOL, P1 ANNIKO M, 1983, DEV AUDITORY VESTIBU, V12, P375 ARAN JM, 1979, ACTA OTO-LARYNGOL, V87, P300, DOI 10.3109/00016487909126424 ARAN JM, 1982, ACTA OTOLARYNGOL S S, V390 Ballantyne J, 1969, J Laryngol Otol, V83, P19, DOI 10.1017/S002221510007002X BICHLER E, 1983, ARCH OTO-RHINO-LARYN, V237, P201, DOI 10.1007/BF00453725 CASS SP, 1989, OTOLARYNG HEAD NECK, V101, P459 CAUSSE R, 1949, ANN OTOLARYNGOL PARI, V66, P518 CAZALS Y, 1983, ARCH OTO-RHINO-LARYN, V238, P1, DOI 10.1007/BF00453735 CAZALS Y, 1979, ARCH OTO-RHINO-LARYN, V224, P61, DOI 10.1007/BF00455225 COHEN GM, 1990, J ELECTRON MICR TECH, V15, P165, DOI 10.1002/jemt.1060150208 COVELL W. P., 1957, LARYNGOSCOPE, V67, P118 CURTHOYS IS, 1981, ACTA OTO-LARYNGOL, V92, P107, DOI 10.3109/00016488109133244 DENO RL, 1931, ERGEBN PHYSL, V32, P73 DEOL MS, 1954, J GENET, V52, P562, DOI 10.1007/BF02985081 ERNSTSON S, 1971, ACTA OTOLARYNGOL STO, V711, P469 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 FERMIN CD, 1984, ACTA OTO-LARYNGOL, V97, P203, DOI 10.3109/00016488409130981 GULLEY RL, 1978, BRAIN RES, V158, P279, DOI 10.1016/0006-8993(78)90675-3 HAWKINS JE, 1973, ADV OTORHINOLARYNGOL, V250, P125 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HIEL H, 1992, HEARING RES, V57, P157, DOI 10.1016/0378-5955(92)90148-G HUY PTB, 1981, J INFECT DIS, V143, P476 IGARASHI M, 1970, ACTA OTO-LARYNGOL, V69, P247, DOI 10.3109/00016487009123360 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 JOHNSSON LG, 1974, ANN OTO RHINOL LARYN, V83, P294 KARNOVSK.MJ, 1965, J CELL BIOL, V27, pA137 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 KELLERHALS B, 1967, ACTA OTOLARYNGOL S S, V26, P1 KOHONEN A, 1965, ACTA OTOLARYNGOL S S, V208 KOITCHEV K, 1986, ACTA OTO-LARYNGOL, V102, P31, DOI 10.3109/00016488609108643 KOITCHEV K, 1982, ACTA OTO-LARYNGOL, V94, P431, DOI 10.3109/00016488209128931 LIBERMAN MC, 1978, ACTA OTOLARYNGOL S S, V358 LIM DJ, 1976, ANN OTO RHINOL LARYN, V85, P740 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 Lorente de No R., 1926, TRAV LAB INVEST BIOL, V24, P53 MAIR IWS, 1976, ARCH OTO-RHINO-LARYN, V212, P1, DOI 10.1007/BF00456358 MAIR IWS, 1973, ACTA OTOLARYNGOL S S, V314 MIKAELIA.DO, 1974, ACTA OTO-LARYNGOL, V77, P327, DOI 10.3109/00016487409124632 OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 REBILLARD G, 1976, ACTA OTO-LARYNGOL, V82, P48, DOI 10.3109/00016487609120862 RICHTER E, 1981, ACTA OTO-LARYNGOL, V92, P423, DOI 10.3109/00016488109133281 RICHTER E, 1981, ARCH OTO-RHINO-LARYN, V230, P251, DOI 10.1007/BF00456326 ROMAND R, 1985, HEARING RES, V18, P111, DOI 10.1016/0378-5955(85)90002-4 ROMAND R, 1984, ACTA OTO-LARYNGOL, V97, P239, DOI 10.3109/00016488409130985 ROSENBLUTH J, 1962, J CELL BIOL, V12, P329, DOI 10.1083/jcb.12.2.329 ROSSI G, 1976, ACTA OTO-LARYNGOL, V81, P270, DOI 10.3109/00016487609119962 RUEDA J, 1987, ACTA OTO-LARYNGOL, V104, P417, DOI 10.3109/00016488709128269 SCHACHT J, 1979, ARCH OTO-RHINO-LARYN, V224, P129, DOI 10.1007/BF00455236 SCHINDLER RA, 1977, ARCH OTOLARYNGOL, V103, P691 SCHUKNECHT HF, 1982, ANN OTO RHINOL LARYN, V91, P16 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 Spoendlin H., 1978, EVOKED ELECTRICAL AC, P21 SPOENDLIN H, 1979, ACTA OTO-LARYNGOL, V87, P381, DOI 10.3109/00016487909126437 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 SPOENDLIN H, 1977, ACTA OTO-LARYNGOL, V83, P130, DOI 10.3109/00016487709128822 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 SUGA F, 1976, ANN OTO RHINOL LARYN, V85, P169 SUZUKI Y, 1963, Arch Histol Jpn, V24, P9 TREVISI M, 1977, J SUBMICR CYTOL PATH, V9, P157 WARD PH, 1961, ANN OTO RHINOL LARYN, V70, P132 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 WEBSTER M, 1978, AM ZOOL, V18, P588 Wersall J., 1974, P123 WERSALL J, 1956, ACTA OTOLARYNGOL S S, V126 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P23 YLIKOSKI J, 1981, ACTA OTO-LARYNGOL, V91, P161, DOI 10.3109/00016488109138495 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P42 NR 70 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 1993 VL 68 IS 2 BP 217 EP 228 DI 10.1016/0378-5955(93)90125-K PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800008 PM 8407607 ER PT J AU PENNER, MJ GLOTZBACH, L HUANG, T AF PENNER, MJ GLOTZBACH, L HUANG, T TI SPONTANEOUS OTOACOUSTIC EMISSIONS - MEASUREMENT AND DATA SO HEARING RESEARCH LA English DT Article DE SOAES; EMISSIONS; TINNITUS ID HUMAN EARS; HEARING-LOSS; TINNITUS; SUPPRESSION; PREVALENCE; FREQUENCY; TONES AB Sounds from the ear canal were measured and then analyzed off-line. A peak-picking algorithm located spectral maxima which might be designated as spontaneous otoacoustic emissions (SOAEs). The output from a 0.5-cc syringe, used to simulate the volume of the ear canal, was also measured, analyzed and used to approximate the false-alarm rate of the measurement system. SOAE prevalence estimates depended on the false-alarm rate, just as the hit rate in a yes-no task does. With a false-alarm rate of zero, trends that have been found to be significant in the pooled results of other surveys were replicated: more SOAEs in the right ear, more SOAEs in females, and increased probability that the contralateral ear has an SOAE if the ipsilateral ear has an SOAE. In addition, many SOAEs failed to be detected in consecutive spectral analyses because they fluctuated in level. RP PENNER, MJ (reprint author), UNIV MARYLAND,DEPT PSYCHOL,COLL PK,MD 20742, USA. CR BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 BURNS EM, 1991, ABSTR ASS RES OT, P239 CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 DALLMAYR C, 1985, ACUSTICA, V59, P67 FRICK LR, 1988, EAR HEARING, V9, P190, DOI 10.1097/00003446-198808000-00004 GREEN DM, 1966, SIGNAL DETECTION THE HAMMEL DR, 1983, THESIS U ILLINOIS UR KEMP DT, 1980, HEARING RES, V2, P533, DOI 10.1016/0378-5955(80)90091-X KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KOHLER W, 1986, ARCH OTO-RHINO-LARYN, V243, P43, DOI 10.1007/BF00457907 MARTIN GK, 1990, EAR HEARING, V11, P106 McNemar Q, 1947, PSYCHOMETRIKA, V12, P153, DOI 10.1007/BF02295996 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1991, ACTA OTO-LARYNGOL, V111, P835, DOI 10.3109/00016489109138419 PENNER M J, 1992, British Journal of Audiology, V26, P115, DOI 10.3109/03005369209077879 PENNER MJ, 1989, J SPEECH HEAR RES, V32, P339 PENNER MJ, 1989, J SPEECH HEAR RES, V32, P458 PENNER MJ, 1988, ARCH OTOLARYNGOL, V114, P150 PENNER MJ, 1989, ARCH OTOLARYNGOL, V115, P871 PROBST R, 1987, AM J OTOLARYNG, V8, P73, DOI 10.1016/S0196-0709(87)80027-3 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 SCHLOTH E, 1983, ACUSTICA, V53, P250 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 TALMADGE CL, 1992, ABSTR ASS RES OT, P456 WHITEHEAD ML, 1991, HEARING RES, V53, P269, DOI 10.1016/0378-5955(91)90060-M WHITEHEAD M L, 1989, Society for Neuroscience Abstracts, V15, P209 WIER CC, 1984, J ACOUST SOC AM, V76, P1248, DOI 10.1121/1.391376 ZIZZ CA, 1988, J SPEECH HEAR RES, V31, P616 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 1975, ISO389 GEN SWITZ NR 32 TC 48 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 AUG PY 1993 VL 68 IS 2 BP 229 EP 237 DI 10.1016/0378-5955(93)90126-L PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800009 PM 8407608 ER PT J AU ZUCCA, G BOTTA, L MILESI, V VALLI, P AF ZUCCA, G BOTTA, L MILESI, V VALLI, P TI SENSORY ADAPTATION IN FROG VESTIBULAR ORGANS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; SENSORY ADAPTATION; SEMICIRCULAR CANAL; NA+-K+-ATPASE; OUABAIN ID SACCULAR HAIR-CELLS; SEMICIRCULAR CANALS; CALCIUM CURRENTS; INNER-EAR; TRANSDUCTION; DEPENDENCE; POTASSIUM; GLUTAMATE AB Adaptation, i.e., the decrease with time in sensory units' afferent discharge to a constant stimulus, appears to be a common feature of the receptors belonging to acoustico-lateralis system: However, the mechanisms underlaying this process are still a matter of debate. The present experiments demonstrate that sensory adaptation to both mechanical and electrical stimuli can be nearly suppressed after perilymphatic ouabain administration. This clearly indicates that the K+ homeostatic mechanisms [Valli et al., (1990) J. Physiol. (London) 430, 585-594] which control the K+ concentration gradient at both ends of vestibular hair cells play a predominant role in this process. The possible importance of different K+-dependent mechanisms in hair cell adaptation is discussed. C1 UNIV TURIN,DEPT ANIM BIOL,I-10124 TURIN,ITALY. RP ZUCCA, G (reprint author), UNIV PAVIA,INST GEN PHYSIOL,VIA FORLANINI 6,I-27100 PAVIA,ITALY. CR AKOEV GN, 1988, MECHANORECEPTORS THE ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 EATOCK RA, 1987, J NEUROSCI, V7, P2821 FERRARY E, 1992, ACTA OTO-LARYNGOL, V112, P294 FUCHS PA, 1990, J PHYSIOL-LONDON, V429, P553 GOLDBERG JM, 1975, ANNU REV PHYSIOL, V37, P129, DOI 10.1146/annurev.ph.37.030175.001021 HACOHEN N, 1989, J NEUROSCI, V9, P3988 HONRUBIA V, 1987, LARYNGOSCOPE, V97, P228 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 Konishi T, 1966, Acta Otolaryngol, V62, P393, DOI 10.3109/00016486609119584 MAYER ML, 1987, PROG NEUROBIOL, V28, P197, DOI 10.1016/0301-0082(87)90011-6 MCLAREN JW, 1977, THESIS U IOWA NAGEL G, 1991, CELL TISSUE RES, V265, P567, DOI 10.1007/BF00340881 NJEUGNA E, 1982, THESIS U LOUIS PASTE NJEUGNA E, 1990, INNOV TECH BIOL MED, V11, P65 OMAN CM, 1972, ACTA OTO-LARYNGOL, V74, P324, DOI 10.3109/00016487209128458 Precht W., 1976, P481 Prigioni I, 1992, J Vestib Res, V2, P31 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 STERKERS O, 1988, PHYSIOL REV, V68, P1083 Taglietti V, 1973, Arch Sci Biol (Bologna), V57, P73 VALLI P, 1990, J PHYSIOL-LONDON, V430, P585 VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 VALLI P, 1988, J COMP PHYSIOL A, V162, P173, DOI 10.1007/BF00606082 VALLI P, 1977, ACTA OTO-LARYNGOL, V84, P344, DOI 10.3109/00016487709123976 ZUCCA G, 1992, HEARING RES, V63, P52, DOI 10.1016/0378-5955(92)90073-V ZUCCA G, 1982, ACTA OTO-LARYNGOL, V93, P355, DOI 10.3109/00016488209130893 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 AUG PY 1993 VL 68 IS 2 BP 238 EP 242 DI 10.1016/0378-5955(93)90127-M PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800010 PM 8407609 ER PT J AU BENSER, ME ISSA, NP HUDSPETH, AJ AF BENSER, ME ISSA, NP HUDSPETH, AJ TI HAIR-BUNDLE STIFFNESS DOMINATES THE ELASTIC REACTANCE TO OTOLITHIC-MEMBRANE SHEAR SO HEARING RESEARCH LA English DT Article DE HAIR CELL; SACCULUS; STEREOCILIA; TRANSDUCTION; VESTIBULAR SYSTEM ID MECHANOELECTRICAL TRANSDUCTION; BULLFROGS SACCULUS; CELLS; EAR; CHANNELS; FROG; LOCALIZATION; SENSITIVITY AB Efficient transduction by acousticolateralis organs requires that a stimulus force principally deflect hair bundles, rather than flex other structural elements. Hair bundles might therefore be expected to provide a large fraction of the impedence to shear motions of otolithic membranes and other accessory structures. We measured the stiffness for shear motions of the bullfrog's saccular otolithic membrane, and determined the stiffness due to a single hair bundle and its associated extracellular filaments; this component is termed the elemental stiffness. Stiffness measurements were made by displacing the base of a flexible probe whose tip was coupled to the otolithic membrane, and simultaneously measuring the flexion of the probe and the displacement of the membrane. The average elemental stiffness, about 1350 muN . m-1, only modestly exceeded the stiffness of individual hair bundles. The hair bundles therefore provide the dominant component of stiffness in the bullfrog's sacculus, and thus account for a significant component of impedance to otolithic-membrane shear. As a corollary, stiffness changes or active movements in hair bundles should influence the mechanical responses of this and other receptor organs. C1 UNIV TEXAS,SW MED CTR,CTR BASIC NEUROSCI RES,5323 HARRY HINES BLVD,DALLAS,TX 75235. CR COREY DP, 1983, J NEUROSCI, V3, P942 COREY DP, 1980, J NEUROSCI METH, V3, P183, DOI 10.1016/0165-0270(80)90025-4 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 CRAWFORD AJJ, 1986, J PHYSL, V371, pP18 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 GUMMER AW, 1981, J ACOUST SOC AM, V70, P1298, DOI 10.1121/1.387144 HILLMAN DE, 1971, SCIENCE, V174, P416, DOI 10.1126/science.174.4007.416 Hillman D.E., 1976, P452 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 HOWARD J, 1987, SENSORY TRANSDUCTION, P138 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 HUDSPETH AJ, 1992, SENSORY TRANSDUCTION, P357 JACOBS RA, 1990, COLD SH Q B, V55, P547 JARAMILLO F, 1990, MECH BIOPHYSICS HEAR, P26 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 JARAMILLO F, 1993, P NATL ACAD SCI USA, V90, P1330, DOI 10.1073/pnas.90.4.1330 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A Kondrachuk A V, 1991, Physiologist, V34, pS212 KOYAMA H, 1982, BRAIN RES, V250, P168, DOI 10.1016/0006-8993(82)90964-7 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LANDAU LD, 1986, THEORY ELASTICITY, P22 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 MILLER CE, 1985, J ACOUST SOC AM, V77, P1465, DOI 10.1121/1.392041 NARINS PM, 1984, J ACOUST SOC AM, V76, P1384, DOI 10.1121/1.391455 OLSON ES, 1991, J ACOUST SOC AM, V89, P1262, DOI 10.1121/1.400535 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 RUSSELL IJ, 1989, HEARING RES, V43, P55, DOI 10.1016/0378-5955(89)90059-2 SHOTWELL SL, 1981, ANN NY ACAD SCI, V374, P1, DOI 10.1111/j.1749-6632.1981.tb30854.x NR 30 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 AUG PY 1993 VL 68 IS 2 BP 243 EP 252 DI 10.1016/0378-5955(93)90128-N PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800011 PM 8407610 ER PT J AU GEISLER, CD AF GEISLER, CD TI A REALIZABLE COCHLEAR MODEL USING FEEDBACK FROM MOTILE OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE COCHLEAR VIBRATION; OUTER HAIR CELL; FEEDBACK; MODEL ID RESPONSES; FREQUENCY; MECHANICS AB A physically realizable form of a recent cochlear model using feedback forces from motile outer hair cells [Geisler (1991) Hear. Res. 54, 105-117] has been developed. The model was computer-simulated in the frequency domain (necessarily linear). Its responses to pure tones are very realistic in terms of sharpness (Q10s of 3-5) and in terms of tip-to-tail ratios (50-60 dB). These large tips are due to the feedback forces, which act as negative resistances (energy-supplying elements) over restricted spatial ranges. Nyquist-criterion analysis indicates that the model is stable. The spatial patterns of the model's output also bear qualitative resemblances to several other phenomena observed in cochleas, both living and excised. C1 UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. RP GEISLER, CD (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,273 MED SCI BLDG,MADISON,WI 53706, USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BENDRE A, 1992, THESIS U SISCONSIN M BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DEBOER E, 1991, AUDITORY PHYSL PERCE GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P151 Kim DO, 1979, SCAND AUDIOL S, V63-81 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 REUTER G, 1990, HEARING RES, V43, P219, DOI 10.1016/0378-5955(90)90230-M REUTER G, 1992, HEARING RES, V60, P236, DOI 10.1016/0378-5955(92)90025-I 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 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 RUGGERO MA, 1987, J NEUROPHYSIOL, V58, P379 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SHAN X, 1988, THESIS U WISCONSIN M TUBIS A, 1989, COCHLEAR MECHANISMS, P323 WICKESBERG RE, 1985, PERIPHERAL AUDITORY, P113 WIT HP, 1985, PERIPHERAL AUDITORY, P221 ZWEIG G, 1990, MECHANICS BIOPHYSICS, P362 NR 20 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 AUG PY 1993 VL 68 IS 2 BP 253 EP 262 DI 10.1016/0378-5955(93)90129-O PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LR628 UT WOS:A1993LR62800012 PM 8407611 ER PT J AU LI, HS BORG, E AF LI, HS BORG, E TI AUDITORY DEGENERATION AFTER ACOUSTIC TRAUMA IN 2 GENOTYPES OF MICE SO HEARING RESEARCH LA English DT Article DE NOISE TRAUMA; AGING; GENOTYPE; INTERACTION; AUDITORY THRESHOLD ID INDUCED HEARING-LOSS; NOISE; MOUSE; AGE; PRESBYCUSIS; SENSITIVITY; EAR AB Two strains of mice, CBA/Ca and C57BL/6J, were exposed to a steady noise (27 kHz) of 120 dB SPL for 5 min at 1, 3, 6, or 12 months of age. Threshold shifts were determined by recording auditory brainstem response 1 month after exposure and thereafter up to the age of 16 months (C57BL) or 23-27 months (CBA). With increasing age of exposure, susceptibility to acoustic truama at middle frequencies (6.3-12.5 kHz) 1 month after exposure decreased in CBA mice but remained constant in C57BL mice. With increasing age after exposure, threshold shifts were retained at the middle frequencies in CBA mice exposed at 1 month of age and in C57BL mice of all exposed groups. The progress of the interaction between the previous noise damage and aging effects was generally the same for the two strains, first an additivity and then a blocking-like interaction. The rate of the progress in post-noise hearing did not exceed the spontaneous rate of aging. The differences between exposed and non-exposed groups decreased with advancing age. The results indicate that the interaction of noise trauma and aging effects depends on the susceptibility of the individual to acoustic trauma, affected frequencies. and the severity of noise-induced PTS. A previous noise damage did not potentiate the auditory degeneration either in CBA/Ca or in C57BL/6J mice. C1 KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. OREBRO MED CTR HOSP,DEPT AUDIOL,OREBRO,SWEDEN. CR BORG E, 1983, HEARING RES, V9, P247, DOI 10.1016/0378-5955(83)90029-1 BURNS W, 1973, NOISE MAN, P189 CODY AR, 1981, J ACOUST SOC AM, V70, P707, DOI 10.1121/1.386906 CODY AR, 1980, HEARING RES, V3, P93 CORSO JF, 1976, EFFECTS NOISE HEARIN, P497 CORSO JF, 1992, AUDIOLOGY, V31, P162 CORSO JF, 1980, AUDIOLOGY, V19, P221 DAVIS H, 1950, ACTA OTOLARYNGOL S, V195, P1 GLORIG A, 1960, Ann Otol Rhinol Laryngol, V69, P497 HARRISON DE, 1983, EXP AGING RES, V9, P245 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1983, AUDIOLOGY, V22, P372 HENRY KR, 1992, AUDIOLOGY, V31, P181 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 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 MACRAE JH, 1971, AUDIOLOGY, V10, P323 MCGINN MD, 1992, HEARING RES, V59, P1, DOI 10.1016/0378-5955(92)90094-4 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MILLS JH, 1992, NOISE INDUCED HEARIN, P237 MOLLICA V, 1969, INT AUDIO, V8, P305, DOI 10.3109/05384916909079071 PATUZZI R, 1992, HEARING RES, V60, P165, DOI 10.1016/0378-5955(92)90019-J 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 ROBINSON DW, 1970, HEARING NOISE IND, P100 ROP I, 1979, AUDIOLOGY, V18, P181 ROSENHALL U, 1990, EAR HEARING, V11, P257, DOI 10.1097/00003446-199008000-00002 SAUNDERS JC, 1991, J ACOUST SOC AM, V90, P136, DOI 10.1121/1.401307 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 Spoor A, 1967, INT AUDIOL, V6, P48, DOI 10.3109/05384916709074230 Willott J.F., 1983, AUDITORY PSYCHOBIOLO NR 32 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 JUN PY 1993 VL 68 IS 1 BP 19 EP 27 DI 10.1016/0378-5955(93)90060-E PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400002 PM 8376211 ER PT J AU MOORE, DR AF MOORE, DR TI AUDITORY BRAIN-STEM RESPONSES IN FERRETS FOLLOWING UNILATERAL COCHLEAR REMOVAL SO HEARING RESEARCH LA English DT Article DE DEAFNESS; DEVELOPMENT; PLASTICITY ID INFERIOR COLLICULUS; POSTNATAL-DEVELOPMENT; AFFERENT INFLUENCES; OTOCYST ABLATION; EVOKED-RESPONSE; STEM; NUCLEUS; NEURONS; PERIPHERY; SPECIFICITY AB To examine the effect of unilateral or asymmetric hearing loss on the developing brain, ferrets had the right cochlea removed at postnatal day (P)5, P25, P40 or P90. Auditory brainstem responses (ABR) to free-field click stimulation were obtained before and after cochlear removal in the P40 and P90 groups, and from P28 in the other groups. Acute cochlear removal did not lead to any change in the morphology of the ABR waveform or to any change in the ABR threshold in response to stimulation on the side of the intact ear. There was a small, progressive increase in the latency of the four main waves of the ABR. Long-term survival following cochlear removal did not lead to any change in ABR waveform or threshold, or to any further change in wave latency, regardless of age at the time of removal or survival time (up to 1-2 years). In contrast to initial expectations based on previous single-unit studies, these results suggest that cochlear removal in infancy does not produce any large compensatory change in the functional organization of the auditory brainstem. RP MOORE, DR (reprint author), UNIV OXFORD,PHYSIOL LAB,PK RD,OXFORD OX1 3PT,ENGLAND. CR 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 CARLILE S, 1991, HEARING RES, V51, P265, DOI 10.1016/0378-5955(91)90043-9 DEITCH JS, 1984, J COMP NEUROL, V229, P66, DOI 10.1002/cne.902290106 DOYLE WJ, 1991, HEARING RES, V54, P145, DOI 10.1016/0378-5955(91)90144-X FULLERTON BC, 1990, HEARING RES, V49, P363, DOI 10.1016/0378-5955(90)90114-5 HASHISAKI GT, 1989, J COMP NEUROL, V283, P465, DOI 10.1002/cne.902830402 KELLY JB, 1989, HEARING RES, V39, P231, DOI 10.1016/0378-5955(89)90043-9 KIL J, 1989, Society for Neuroscience Abstracts, V15, P745 KITZES L M, 1984, Brain Research, V306, P171, DOI 10.1016/0006-8993(84)90366-4 KITZES LM, 1986, BIOL CHANGE OTOLARYN KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 LEVIMONTALCINI R, 1949, J COMP NEUROL, V91, P209, DOI 10.1002/cne.900910204 LINDEN DC, 1981, J COMP NEUROL, V203, P189, DOI 10.1002/cne.902030204 MAIR IWS, 1985, ACTA OTO-LARYNGOL, V99, P377, DOI 10.3109/00016488509108926 MOORE DR, 1987, BR J AUDIOL, V21, P105 MOORE DR, 1992, DEV AUDITORY VESTIBU, V2 MOORE DR, 1990, J COMP NEUROL, V302, P810, DOI 10.1002/cne.903020412 MOORE DR, UNPUB AUDITORY BRAIN MOORE DR, 1992, DEV BRAIN RES, V66, P229, DOI 10.1016/0165-3806(92)90084-A MOORE DR, 1993, IN PRESS PROG BRAIN, V97 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, 1982, BRAIN RES, V253, P309, DOI 10.1016/0006-8993(82)90698-9 MOORE DR, 1992, NEUROREPORT, V3, P269, DOI 10.1097/00001756-199203000-00014 MOREY AL, 1990, DEV BRAIN RES, V52, P279, DOI 10.1016/0165-3806(90)90246-U NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 PARKS TN, 1979, J COMP NEUROL, V183, P665, DOI 10.1002/cne.901830313 PARKS TN, 1981, J COMP NEUROL, V202, P47, DOI 10.1002/cne.902020105 REALE RA, 1987, DEV BRAIN RES, V34, P281, DOI 10.1016/0165-3806(87)90215-X RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 RUSSEL FA, 1992, BRIT J AUDIOL, V26, P180 RYAN AF, 1992, DEV AUDITORY VESTIBU, V2, P243 RYAN A F, 1987, Society for Neuroscience Abstracts, V13, P79 SANES DH, 1992, J COMP NEUROL, V321, P1 SNODGRASS JG, 1977, NUMBERS GAME TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 Winer B. J., 1991, STATISTICAL PRINCIPL NR 38 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 1993 VL 68 IS 1 BP 28 EP 34 DI 10.1016/0378-5955(93)90061-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400003 PM 8376212 ER PT J AU JIANG, ZD ZHANG, L WU, YY LIU, XY AF JIANG, ZD ZHANG, L WU, YY LIU, XY TI BRAIN-STEM AUDITORY-EVOKED RESPONSES FROM BIRTH TO ADULTHOOD - DEVELOPMENT OF WAVE AMPLITUDE SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; HEARING; NEUROLOGY; NORMATIVE STUDY; CHILDREN; BRAIN-STEM AUDITORY EVOKED RESPONSE ID STEM RESPONSE; NEUROLOGICAL DISEASE; YOUNG-ADULTS; POTENTIALS; INFANTS; VARIABILITY; ELECTRODE; CHILDREN; LEVEL; AGE AB Brainstem auditory evoked response (BAER) was recorded in children from birth to 6 years and adults to study the development of wave amplitude. The amplitudes of all BAER waves increased with age, the greatest changes occurring during early infancy. Adult values were reached at 6 months of age for wave 1 and 2 years for wave V. The two waves continued to increase above the adult values until the highest amplitude value was reached at 3 years for wave 1 and 5 years for wave V. Subsequently, the amplitudes decreased towards the values in adults. The V/I amplitude ratio, which was slightly smaller than the adult value shortly after birth, decreased during the first year of life and reached the minimum value between 1 and 4 years. Thereafter, it increased towards the adult value. Throughout the maturational stages the ratio was smaller than in adults. The amplitude of wave V was relatively stable and its variation was much smaller than those of wave I and V/I amplitude ratio. Lower normative limits of these amplitude measures were given to provide a reference baseline for further study under the similar experimental conditions. We suggest that, in light of age-related differences of the V/I ratio, the normative criteria for the amplitude ratio should be established in relation to age. The amplitude of wave V is recommended to be useful in some clinical situations. C1 SHANGHAI MED UNIV,CHILDRENS HOSP,DEPT CHILD HLTH,SHANGHAI,PEOPLES R CHINA. CR BEATTIE RC, 1990, AM J OTOL, V11, P314 BEATTIE RC, 1988, SCAND AUDIOL, V17, P99, DOI 10.3109/01050398809070698 CHIAPPA KH, 1983, EVOKED POTENTIALS CL, P22 CHIAPPA KH, 1979, ARCH NEUROL-CHICAGO, V36, P81 CHIARENZA GA, 1991, EARLY HUM DEV, V27, P145, DOI 10.1016/0378-3782(91)90034-Z DUBOWITZ LM, 1970, J PEDIATR-US, V77, P1, DOI 10.1016/S0022-3476(70)80038-5 HAMID OA, 1986, AM J OTOL, V7, P333 HANNLEY M, 1983, AUDIOLOGY, V22, P20 HECOX KE, 1981, NEUROLOGY, V31, P1429 JEWETT DL, 1970, ELECTROEN CLIN NEURO, V28, P609, DOI 10.1016/0013-4694(70)90203-8 JIANG ZD, 1991, ACTA PAEDIATR SCAND, V80, P494, DOI 10.1111/j.1651-2227.1991.tb11892.x JIANG ZD, 1991, HEARING RES, V54, P67, DOI 10.1016/0378-5955(91)90137-X JIANG ZD, 1990, DEV MED CHILD NEUROL, V32, P473 JIANG ZD, 1991, AUDIOLOGY, V30, P173 JIANG ZD, 1988, THESIS SHANGHAI MED JIANG ZD, 1991, SCAND AUDIOL, V20, P41, DOI 10.3109/01050399109070789 JIANG ZD, 1990, EARLY HUM DEV, V23, P41, DOI 10.1016/0378-3782(90)90127-5 KEVANISHVILI Z, 1979, Scandinavian Audiology, V8, P51, DOI 10.3109/01050397909076301 KRUMHOLZ A, 1985, ELECTROEN CLIN NEURO, V62, P124, DOI 10.1016/0168-5597(85)90024-3 LAUTER JL, 1988, SCAND AUDIOL, V17, P87, DOI 10.3109/01050398809070696 MAURER K, 1985, EVOZIERTE POTENTIALE, P213 MOCHIZUKI Y, 1983, PROG NEUROBIOL, V20, P273, DOI 10.1016/0301-0082(83)90005-9 MOCHIZUKI Y, 1982, BRAIN DEV-JPN, V4, P127 MUSIEK FE, 1982, LARYNGOSCOPE, V92, P891 MUSIEK FE, 1984, EAR HEARING, V5, P52, DOI 10.1097/00003446-198401000-00011 PRATT H, 1981, ELECTROEN CLIN NEURO, V51, P80, DOI 10.1016/0013-4694(81)91511-X PSATTA DM, 1988, ELECTROEN CLIN NEURO, V71, P27, DOI 10.1016/0168-5597(88)90016-0 QIAN SG, 1980, CHIN J OBSTET GYNECO, V15, P198 ROWE MJ, 1981, EAR HEARING, V2, P41, DOI 10.1097/00003446-198101000-00008 ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 SALAMY A, 1986, MATURATION CNS EVOKE, P166 SALAMY A, 1976, ELECTROEN CLIN NEURO, V40, P418, DOI 10.1016/0013-4694(76)90193-0 SAND T, 1990, SCAND AUDIOL, V19, P131, DOI 10.3109/01050399009070764 STARR A, 1975, ARCH NEUROL-CHICAGO, V32, P761 STARR A, 1977, PEDIATRICS, V60, P831 STOCKARD JE, 1983, EAR HEARING, V4, P11, DOI 10.1097/00003446-198301000-00005 STOCKARD J J, 1978, American Journal of EEG Technology, V18, P177 STOCKARD JJ, 1977, NEUROLOGY, V27, P316 THORNTON ARD, 1978, EVOKED ELECTRICAL AC, P429 THORNTON ARD, 1975, SCAND AUDIOL, V4, P91, DOI 10.3109/01050397509043071 YANZ JL, 1985, EAR HEARING, V6, P98, DOI 10.1097/00003446-198503000-00007 ZHANG L, 1992, EARLY HUM DEV, V30, P61, DOI 10.1016/0378-3782(92)90087-W NR 42 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 1993 VL 68 IS 1 BP 35 EP 41 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400004 PM 8376213 ER PT J AU LEVI, EC FOLSOM, RC DOBIE, RA AF LEVI, EC FOLSOM, RC DOBIE, RA TI AMPLITUDE-MODULATION FOLLOWING RESPONSE (AMFR) - EFFECTS OF MODULATION RATE, CARRIER FREQUENCY, AGE, AND STATE SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIALS; AMPLITUDE MODULATION; COHERENCE; STEADY-STATE RESPONSES; AUDITORY DEVELOPMENT; SEDATION ID AUDITORY MIDDLE LATENCY; BRAIN-STEM RESPONSES; PURE-TONE AUDIOGRAM; INFERIOR COLLICULUS; EVOKED-POTENTIALS; COMPLEX TONES; ELECTROPHYSIOLOGICAL TECHNIQUES; THRESHOLD PREDICTION; SQUIRREL-MONKEYS; LOW PITCH AB Scalp responses to continuous amplitude-modulated (AM) tones were recorded from adults and 1-month-old infants. The amplitude-modulation following (or envelope) response (AMFR) was quantified using magnitude-squared coherence. This measurement indicates the strength of the frequency-following response relative to background neural noise. The optimal modulation rate for generating the AMFR was determined by studying the effects of stimulus modulation rate on the response. Stimulus AM rate was varied between 10 and 80 Hz for continuous tonal stimuli of 500 Hz, and between 20 and 80 Hz for continuous tonal stimuli of 2000 Hz. Optimal modulation rate was defined as the AM rate that provided the highest coherence estimate. Adult AMFR coherence increased between 10 and 40 Hz (20-40 Hz for 2000 Hz), and decreased between 40 and 80 Hz in both carrier frequency conditions. Infant AMFR coherence, in contrast, monotonically increased between 10 and 80 Hz (20-80 Hz for 2000 Hz). Thus, within the frequency range examined, 40 Hz is optimal for generating the AMFR in adults, whereas 80 Hz is optimal in infants. Adults were tested while awake and infants were tested during periods of sleep. Given the observed age difference in effective modulation rate, we examined modulation rate effects in a group of adults in both awake and sedated states. As in sleeping infants, 80 Hz was optimal for generating AMFRs in the sedated adults. C1 UNIV TEXAS,DEPT OTOLARYNGOL HEAD & NECK SURG,SAN ANTONIO,TX 78285. RP LEVI, EC (reprint author), UNIV WASHINGTON,CDMRC,DEPT SPEECH & HEARING SCI,WJ-10,BOX 47,SEATTLE,WA 98195, USA. CR BARAJAS JJ, 1988, SCAND AUDIOL, V17, P21, DOI 10.3109/01050398809042176 BATRA R, 1989, J NEUROPHYSIOL, V61, P257 CHAMBERS RD, 1986, J ACOUST SOC AM, V80, P1673, DOI 10.1121/1.394279 COHEN LT, 1991, J ACOUST SOC AM, V90, P2467, DOI 10.1121/1.402050 COLLET L, 1988, BRAIN DEV-JPN, V10, P169 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 DOBIE RA, 1990, ELECTROEN CLIN NEURO, V77, P205, DOI 10.1016/0168-5597(90)90039-G DOBIE RA, 1989, EAR HEARING, V10, P1 DOBIE RA, 1991, ELECTROEN CLIN NEURO, V80, P194, DOI 10.1016/0168-5597(91)90121-D DUNN OJ, 1961, J AM STAT ASSOC, V56, P52, DOI 10.2307/2282330 FASTL H, 1986, HEARING RES, V23, P199, DOI 10.1016/0378-5955(86)90016-X FEINBERG I, 1974, J PSYCHIAT RES, V10, P283, DOI 10.1016/0022-3956(74)90011-9 FERGUSON GA, 1981, STATISTICAL ANAL PSY GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GALBRAITH GC, 1990, ELECTROEN CLIN NEURO, V77, P295, DOI 10.1016/0168-5597(90)90068-O GORGA MP, 1988, J SPEECH HEAR RES, V31, P87 GORGA MP, 1985, EAR HEARING, V6, P105, DOI 10.1097/00003446-198503000-00008 GREENBERG S, 1987, HEARING RES, V25, P91, DOI 10.1016/0378-5955(87)90083-9 GRIFFITHS SK, 1991, EAR HEARING, V12, P235, DOI 10.1097/00003446-199108000-00002 HALL JW, 1979, SCIENCE, V205, P1297, DOI 10.1126/science.472748 HECOX K, 1974, ARCH OTOLARYNGOL, V99, P30 JAVEL E, 1980, J ACOUST SOC AM, V68, P133, DOI 10.1121/1.384639 JERGER J, 1986, EAR HEARING, V7, P240, DOI 10.1097/00003446-198608000-00004 KAVANAGH KT, 1984, ANN OTO RHINOL LARYN, V93, P1 KEEFE DH, IN PRESS J ACOUST SO KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KRAUS N, 1985, ELECTROEN CLIN NEURO, V62, P343, DOI 10.1016/0168-5597(85)90043-7 KRAUS N, 1989, EAR HEARING, V10, P339, DOI 10.1097/00003446-198912000-00004 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 KUWADA S, 1986, HEARING RES, V21, P179, DOI 10.1016/0378-5955(86)90038-9 LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 LEVI EC, 1992, THESIS U WASHINGTON LINDEN RD, 1985, EAR HEARING, V6, P167, DOI 10.1097/00003446-198505000-00008 LYNN JM, 1984, EAR HEARING, V5, P366, DOI 10.1097/00003446-198411000-00009 MAURIZI M, 1990, AUDIOLOGY, V29, P322 MILFORD C A, 1989, British Journal of Audiology, V23, P137, DOI 10.3109/03005368909077832 MORA JA, 1990, AUDIOLOGY, V29, P329 NIEDERMEYER E, 1982, ELECTROENCEPHALOGRAP, P107 PALASKAS CW, 1989, OTOLARYNG HEAD NECK, V101, P434 PICTON TW, 1987, J ACOUST SOC AM, V82, P165, DOI 10.1121/1.395560 PLOURDE G, 1990, ANESTH ANALG, V71, P460 PREUSS A, 1990, EXP BRAIN RES, V79, P207 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 RODRIGUEZ R, 1986, EAR HEARING, V7, P300, DOI 10.1097/00003446-198610000-00003 Rorke LB, 1969, MYELINATION BRAIN NE SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SMITH JC, 1978, SCIENCE, V201, P639, DOI 10.1126/science.675250 SOHMER H, 1978, ARCH NEUROL-CHICAGO, V35, P228 STAPELLS DR, 1987, ELECTROEN CLIN NEURO, V67, P260, DOI 10.1016/0013-4694(87)90024-1 STAPELLS DR, 1984, EAR HEARING, V5, P105 STAPELLS DR, 1988, ELECTROEN CLIN NEURO, V71, P289, DOI 10.1016/0168-5597(88)90029-9 SUZUKI T, 1984, AUDIOLOGY, V23, P599 Suzuki T, 1983, Br J Audiol, V17, P1, DOI 10.3109/03005368309081475 Suzuki T, 1983, Br J Audiol, V17, P5, DOI 10.3109/03005368309081476 TUCCI DL, 1990, ACTA OTO-LARYNGOL, V109, P195, DOI 10.3109/00016489009107434 VANDERDRIFT JFC, 1987, AUDIOLOGY, V26, P1 Yakovlev P. I., 1967, REGIONAL DEV BRAIN E, P3 NR 58 TC 67 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 JUN PY 1993 VL 68 IS 1 BP 42 EP 52 DI 10.1016/0378-5955(93)90063-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400005 PM 8376214 ER PT J AU CHERYCROZE, S MOULIN, A COLLET, L AF CHERYCROZE, S MOULIN, A COLLET, L TI EFFECT OF CONTRALATERAL SOUND STIMULATION ON THE DISTORTION-PRODUCT 2F(1)-F(2) IN HUMANS - EVIDENCE OF A FREQUENCY SPECIFICITY SO HEARING RESEARCH LA English DT Article DE 2F(1)-F(2) DISTORTION PRODUCT OTO-EMISSIONS; FREQUENCY SPECIFICITY; MEDIAL OLIVOCOCHLEAR EFFERENTS ID EFFERENT OLIVOCOCHLEAR NEURONS; AUDITORY-NERVE FIBERS; GUINEA-PIG COCHLEA; ELECTRICAL-STIMULATION; MICROMECHANICAL PROPERTIES; ACOUSTIC STIMULATION; EAR; CAT; SUPPRESSION; MORPHOLOGY AB The frequency characteristics of the suppression by contralateral stimulations, of the cubic 2f1-f2 distortion products (DPOAEs), were studied during 63 sessions performed in 39 humans with normal hearing. Each session consisted of exposure to five successive series of randomized contralateral NBN frequencies centered between 0.25 and 8 kHz, while measuring 2f1-f2 set at one of the four studied frequencies, i.e., 1, 2, 3 or 5 kHz. For each value of 2f1-f2, analysis of variance and Student's t-test were used in order to indicate and, if necessary, to localize, a possible significant frequency specificity. Results showed that the suppression exerted on 2f1-f2 DPOAEs by contralateral sound stimulation, is frequency specific, at least for middle frequencies of 1 and 2 kHz. The frequency specificity is specially marked when 2f1-f2 = 1 kHz with contralateral NBN central frequencies around 1 kHz. When 2f1-f2 = 2 kHz, central frequencies which induced a significant suppressive effect include frequencies around 2 kHz and also lower frequencies around 1 kHz. These observations support the interpretation that the suppression of the DPOAE is mediated by the medial olivo-cochlear efferent system. RP CHERYCROZE, S (reprint author), HOP EDOUARD HERRIOT,PAVILLON U,CNRS,URA 1447,F-69437 LYON 3,FRANCE. CR BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1990, ASS RES OTOLARYNGOL, P230 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, 1992, AUDIOLOGY, V31, P1 COLLET L, 1990, HEARING RES, V43, P252 COLLET L, 1990, ADV AUDIOL, P164 FROEHLICH P, 1990, BRAIN RES, V508, P286, DOI 10.1016/0006-8993(90)90408-4 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 GUINAN JJ, 1988, HEARING RES, V33, P115, DOI 10.1016/0378-5955(88)90024-X 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 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 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1993, HEARING RES, V65, P216, DOI 10.1016/0378-5955(93)90215-M MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K Probst R, 1990, Adv Otorhinolaryngol, V44, P1 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 ROBERTSON D, 1985, HEARING RES, V20, P63, DOI 10.1016/0378-5955(85)90059-0 SPOENDLIN H, 1985, AM J OTOLARYNG, V6, P453, DOI 10.1016/S0196-0709(85)80026-0 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 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 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, V19, P349 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 NR 29 TC 59 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 JUN PY 1993 VL 68 IS 1 BP 53 EP 58 DI 10.1016/0378-5955(93)90064-8 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400006 PM 8376215 ER PT J AU LEVINE, RA GARDNER, JC STUFFLEBEAM, SM FULLERTON, BC CARLISLE, EW FURST, M ROSEN, BR KIANG, NYS AF LEVINE, RA GARDNER, JC STUFFLEBEAM, SM FULLERTON, BC CARLISLE, EW FURST, M ROSEN, BR KIANG, NYS TI BINAURAL AUDITORY PROCESSING IN MULTIPLE-SCLEROSIS SUBJECTS SO HEARING RESEARCH LA English DT Article DE BRAIN-STEM AUDITORY EVOKED POTENTIALS; SOUND LATERALIZATION; MULTIPLE SCLEROSIS; MAGNETIC RESONANCE IMAGING; INTERAURAL DISCRIMINATION ID CENTRAL-NERVOUS-SYSTEM; EVOKED-POTENTIALS; CLICK LATERALIZATION; BRAIN; CAT; FIBERS AB In order to relate human auditory processing to physiological and anatomical experimental animal data, we have examined the interrelation-ships between behavioral, elecirophysiological and anatomical data obtained from human subjects with focal brainstem lesions. Thirty-eight subjects with multiple sclerosis were studied with tests of interaural time and level discrimination (just noticeable differences or jnds), brainstem auditory evoked potentials and magnetic resonance (MR) imaging. Interaural testing used two types of stimuli, high-pass ( > 4000 Hz) and low-pass ( < 1000 Hz) noise bursts. Abnormal time jnds (Tjnd) were far more common than abnormal level jnds (70% vs 11%); especially for the high-pass (Hp) noise (70% abnormal vs 40% abnormal for low-pass (Lp) noise). The HpTjnd could be abnormal with no other abnormalities; however, whenever the BAEPs, LpTjnd and/or level jnds were abnormal HpTjnd was always abnormal. Abnormal wave III amplitude was associated with abnormalities in both time jnds, but abnormal wave III latency with only abnormal HpTjnds. Abnormal wave V amplitude, when unilateral, was associated with a major HpTjnd abnormality, and, when bilateral, with both HpTjnd and LpTjnd major abnormalities. Sixteen of the subjects had their MR scans obtained with a uniform protocol and could be analyzed with objective criteria. In all four subjects with lesions involving the pontine auditory pathway, the BAEPs and both time jnds were abnormal. Of the twelve subjects with no lesions involving the pontine auditory pathway, all had normal BAEPs and level jnds, ten had normal LpTjnds, but only five had normal HpTjnds. We conclude that interaural time discrimination is closely related to the BAEPs and is dependent upon the stimulus spectrum. Redundant encoding of low-frequency sounds in the discharge patterns of auditory neurons, may explain why the HpTjnd is a better indicator of neural desynchrony than the LpTjnd. Encroachment of MS lesions upon the pontine auditory pathway always is associated with abnormal BAEPs and abnormal interaural time discrimination but may have normal interaural level discrimination. Our data provide one of the most direct demonstrations in humans of relationships among auditory performance, evoked potentials and anatomy. We present a model showing that many of these interrelationships can be readily interpreted using ideas developed from work on animals, even though these relationships could not have been predicted with confidence beforehand. This work provides a clear advance in our understanding of human auditory processing and should serve as a basis for future studies. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MIT,CAMBRIDGE,MA 02139. TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL. RP LEVINE, RA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ALLEN IV, 1979, J NEUROL SCI, V41, P81, DOI 10.1016/0022-510X(79)90142-4 CAIRD D, 1983, EXP BRAIN RES, V52, P385 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 FISCHER C, 1985, ELECTROEN CLIN NEURO, V61, P7, DOI 10.1016/0013-4694(85)91066-1 FULLERTON BC, 1987, ELECTROEN CLIN NEURO, V66, P547, DOI 10.1016/0013-4694(87)90102-7 FURST M, 1985, J ACOUST SOC AM, V78, P1644, DOI 10.1121/1.392802 FURST M, 1990, HEARING RES, V49, P347, DOI 10.1016/0378-5955(90)90113-4 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 HARRIS JO, 1991, ANN NEUROL, V29, P548, DOI 10.1002/ana.410290515 HAUSLER R, 1980, BRAIN RES, V191, P589, DOI 10.1016/0006-8993(80)91312-8 HOPF HC, 1978, ANN NEUROL, V4, P499, DOI 10.1002/ana.410040604 HOPF HC, 1983, ELECTROEN CLIN NEURO, V56, P31, DOI 10.1016/0013-4694(83)90004-4 JAVEL E, 1980, J ACOUST SOC AM, V68, P133, DOI 10.1121/1.384639 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 JEWETT DL, 1971, BRAIN, V94, P681, DOI 10.1093/brain/94.4.681 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 KENNEDY DN, 1986, THESIS MIT CAMBRIDGE Kiang NY-s, 1965, DISCHARGE PATTERNS S KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 LEVINE RA, 1993, EFFECTS MULTIPLE SCL, V68, P73 Lumsden CE, 1970, HDB CLINICAL NEUROLO, V9, P217 MATATHIAS O, 1985, ACTA OTO-LARYNGOL, V99, P369, DOI 10.3109/00016488509108925 MCDONALD W I, 1986, P112 NEWCOMBE J, 1991, BRAIN, V114, P1013, DOI 10.1093/brain/114.2.1013 PARVING A, 1981, AUDIOLOGY, V20, P123 PRINEAS JW, 1984, ANN NY ACAD SCI, V436, P11, DOI 10.1111/j.1749-6632.1984.tb14773.x Ramon, 1909, HISTOLOGIE SYSTEME N RUMBACH L, 1991, J NEUROL SCI, V104, P176, DOI 10.1016/0022-510X(91)90307-S STOTLER WA, 1953, J COMP NEUROL, V98, P401, DOI 10.1002/cne.900980303 THORNTON ARD, 1975, SCAND AUDIOL, V4, P91, DOI 10.3109/01050397509043071 van Noort J, 1969, STRUCTURE CONNECTION VANDERPOEL JC, 1988, BRAIN, V111, P1453, DOI 10.1093/brain/111.6.1453 WAXMAN SG, 1972, NATURE-NEW BIOL, V238, P217 Yin T. C. T., 1988, AUDITORY FUNCTION, P385 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 YOUNG IR, 1981, LANCET, V2, P1063 NR 38 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 JUN PY 1993 VL 68 IS 1 BP 59 EP 72 DI 10.1016/0378-5955(93)90065-9 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400007 PM 8376216 ER PT J AU LEVINE, RA GARDNER, JC FULLERTON, BC STUFFLEBEAM, SM CARLISLE, EW FURST, M ROSEN, BR KIANG, NYS AF LEVINE, RA GARDNER, JC FULLERTON, BC STUFFLEBEAM, SM CARLISLE, EW FURST, M ROSEN, BR KIANG, NYS TI EFFECTS OF MULTIPLE-SCLEROSIS BRAIN-STEM LESIONS ON SOUND LATERALIZATION AND BRAIN-STEM AUDITORY-EVOKED POTENTIALS SO HEARING RESEARCH LA English DT Article DE BRAIN-STEM AUDITORY EVOKED POTENTIALS; SOUND LATERALIZATION; MULTIPLE SCLEROSIS; MAGNETIC RESONANCE IMAGING; INTERAURAL DISCRIMINATION ID STEM RESPONSES ABRS; COCHLEAR NUCLEUS; CAT; GENERATION; SYSTEM AB Magnetic resonance (MR) imaging, brainstem auditory evoked potentials (BAEPs), and tests of interaural time and level discrimination were performed on sixteen subjects with multiple sclerosis (MS). Objective criteria were used to define MR lesions. Of the eleven subjects in whom no pontine lesions were detected and the one subject who had pontine lesions that did not encroach upon the auditory pathways, all had normal BAEPs and interaural level discrimination, although a few had abnormal interaural time discrimination. Of four subjects with lesions involving the pontine auditory pathway, all had both abnormal BAEPs and abnormal interaural time discrimination; one also had abnormal interaural level discrimination. Analysis of the data suggest the following: waves I and II are generated peripheral to the middle of the ventral acoustic stria (VAS); wave III is generated ipsilaterally in the region of the rostral VAS, caudal superior olivary complex (SOC) and trapezoid body (TB); and waves V and L are generated contralaterally, rostral to the SOC-TB. The region of the ipsilateral rostral SOC-TB is implicated as part of the pathway involved in the generation of waves V and L. Interaural time discrimination of both high and low frequency stimuli were affected by all brainstem lesions that encroached on auditory pathways. A unilateral lesion in the region of the LL affected interaural time discrimination for low-frequency stimuli less severely than bilateral lesions of the LL or a unilateral lesion of the VAS. The only interaural level discrimination abnormality occurred for a subject with a unilateral lesion involving the entire rostral VAS. It appears that detailed analysis of lesion locations coupled with electrophysiological and psychophysical data holds promise for testing hypotheses concerning the function of various human auditory brainstem structures. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MIT,CAMBRIDGE,MA 02139. TEL AVIV UNIV,IL-69978 TEL AVIV,ISRAEL. RP LEVINE, RA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ACHOR LJ, 1980, ELECTROEN CLIN NEURO, V48, P174, DOI 10.1016/0013-4694(80)90302-8 ADAMS JC, 1986, ARCH OTOLARYNGOL, V112, P1253 ALLEN IV, 1979, J NEUROL SCI, V41, P81, DOI 10.1016/0022-510X(79)90142-4 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 FISCHER C, 1985, ELECTROEN CLIN NEURO, V61, P7, DOI 10.1016/0013-4694(85)91066-1 FULLERTON BC, 1990, HEARING RES, V49, P363, DOI 10.1016/0378-5955(90)90114-5 FULLERTON BC, 1987, ELECTROEN CLIN NEURO, V66, P547, DOI 10.1016/0013-4694(87)90102-7 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 HENDLER T, 1990, EAR HEARING, V11, P403, DOI 10.1097/00003446-199012000-00002 HOPF HC, 1983, ELECTROEN CLIN NEURO, V56, P31, DOI 10.1016/0013-4694(83)90004-4 IRVINE DRF, 1986, AUDITORY BRAINSTEM, V7, P279 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 JORIS P X, 1990, Society for Neuroscience Abstracts, V16, P723 KIANG NYS, 1984, ADV AUDIOL, V1, P6 LEVINE RA, 1983, ELECTROEN CLIN NEURO, V55, P532, DOI 10.1016/0013-4694(83)90163-3 LEVINE RA, 1988, NEUROPSYCHOLOGIA, V26, P603, DOI 10.1016/0028-3932(88)90116-9 LEVINE RA, 1993, HEAR RES, V68 MELCHER JR, 1993, THESIS MIT MA MELCHER J R, 1990, Society for Neuroscience Abstracts, V16, P723 MOLLER AR, 1988, ELECTROEN CLIN NEURO, V71, P198, DOI 10.1016/0168-5597(88)90005-6 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 MOORE JK, 1971, FOLIA PRIMATOL, V16, P35, DOI 10.1159/000155390 NEWCOMBE J, 1991, BRAIN, V114, P1013, DOI 10.1093/brain/114.2.1013 OZDAMAR O, 1980, SOC NEUR ABSTR, V6, P595 PARVING A, 1981, AUDIOLOGY, V20, P123 PICTON TW, 1981, J OTOLARYNGOL S9, V10 RUMBACH L, 1991, J NEUROL SCI, V104, P176, DOI 10.1016/0022-510X(91)90307-S SCHAUF C L, 1981, Neurology, V31, P1337 STROMING.NL, 1971, J COMP NEUROL, V143, P217, DOI 10.1002/cne.901430205 VANDERPOEL JC, 1988, BRAIN, V111, P1453, DOI 10.1093/brain/111.6.1453 VOORDECKER R, 1988, ARCH NEUROL-CHICAGO, V45, P1272 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P352, DOI 10.1016/0013-4694(83)90261-4 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P340, DOI 10.1016/0013-4694(83)90260-2 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WILLOUGHBY EW, 1989, ANN NEUROL, V25, P43, DOI 10.1002/ana.410250107 WILMS G, 1991, J COMPUT ASSIST TOMO, V15, P359, DOI 10.1097/00004728-199105000-00003 NR 37 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 JUN PY 1993 VL 68 IS 1 BP 73 EP 88 DI 10.1016/0378-5955(93)90066-A PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400008 PM 8376217 ER PT J AU FORSS, N MAKELA, JP MCEVOY, L HARI, R AF FORSS, N MAKELA, JP MCEVOY, L HARI, R TI TEMPORAL INTEGRATION AND OSCILLATORY RESPONSES OF THE HUMAN AUDITORY-CORTEX REVEALED BY EVOKED MAGNETIC-FIELDS TO CLICK TRAINS SO HEARING RESEARCH LA English DT Article DE MAGNETOENCEPHALOGRAPHY; AUDITORY CORTEX; TEMPORAL INTEGRATION; EVOKED RESPONSE; 40-HZ RESPONSE; STEADY-STATE RESPONSE; HUMANS ID STEADY-STATE RESPONSES; HUMAN-BRAIN; VISUAL-CORTEX; ORGANIZATION; SOUNDS; CAT AB We recorded neuromagnetic evoked responses from the right auditory cortex of 7 healthy adults with a 24-channel planar SQUID gradiometer. The stimuli were 200-ms click trains presented at rates of 40, 80, 160 and 320 Hz, with interstimulus intervals (ISIs) of 1 and 4 s. The transient N100m response to the train onset depended on the click rate: the peak latency shortened to the same extent as the interval between successive clicks decreased in trains with rates from 40 Hz to 320 Hz. The N100m amplitude increased simultaneously, saturating at rates of 160-320 Hz. The mean N100m latency was slightly longer with the I-s than with the 4-s ISI for all click rates. The systematic changes of the N100m amplitude and latency according to click rate demonstrate the importance of temporal integration for N100m generation, and imply an integration time of 20-25 ms. The 20- and 40-Hz click trains also elicited oscillatory 40-Hz responses 80-250 ms after the train onset. The 40-Hz responses were more resistant than N100m to changes of the ISI, and their sources slightly differed from those of N100m. These two responses evidently reflect different aspects of auditory processing. RP FORSS, N (reprint author), HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. RI Hari, Riitta/J-1880-2012 OI Hari, Riitta/0000-0002-3142-2703 CR AHONEN AI, 1991, IEEE T MAGN, V27, P2786, DOI 10.1109/20.133789 BASAR E, 1980, RELATIONS BETWEEN EE DI S, 1992, J NEUROPHYSIOL, V68, P425 ECKHORN R, 1988, BIOL CYBERN, V60, P121, DOI 10.1007/BF00202899 ELBERLING C, 1980, SCAND AUDIOL, V9, P185, DOI 10.3109/01050398009076353 ELBERLING C, 1982, SCAND AUDIOL, V11, P61, DOI 10.3109/01050398209076201 Engel K, 1992, TRENDS NEUROSCI, V15, P218, DOI [10.1016/0166-2236(92)90039-B, DOI 10.1016/0166-2236(92)90039-B] GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GARNER WR, 1974, J EXP PSYCHOL, V37, P293 GHOSE GM, 1992, J NEUROPHYSIOL, V68, P1558 GRAY CM, 1989, NATURE, V338, P334, DOI 10.1038/338334a0 Hari R, 1986, Acta Otolaryngol Suppl, V432, P26 HARI R, 1982, ELECTROEN CLIN NEURO, V54, P561, DOI 10.1016/0013-4694(82)90041-4 Hari R, 1990, ADV AUDIOL, V6, P222 HARI R, 1987, AUDIOLOGY, V26, P31 HARI R, 1989, J ACOUST SOC AM, V86, P1033, DOI 10.1121/1.398093 HUGHES JW, 1946, PROC R SOC SER B-BIO, V133, P486, DOI 10.1098/rspb.1946.0026 JOUTSENIEMI SL, 1989, AUDIOLOGY, P325 KARMOS G, 1993, NEW DEVELOPMENTS IN EVENT-RELATED POTENTIALS, P87 KAUKORANTA E, 1986, EXP BRAIN RES, V63, P60 KAY RH, 1982, PHYSIOL REV, V62, P894 KNUUTILA J, 1987, REV SCI INSTRUM, V58, P2145, DOI 10.1063/1.1139478 KURIKI S, 1989, EXP BRAIN RES, V77, P127 LLINAS RR, 1991, NEUROSCIENCE, V44, P521, DOI 10.1016/0306-4522(91)90075-Y MAKELA JP, 1988, ELECTROEN CLIN NEURO, V69, P423, DOI 10.1016/0013-4694(88)90064-8 MAKELA JP, 1987, ELECTROEN CLIN NEURO, V66, P539, DOI 10.1016/0013-4694(87)90101-5 MURTHY VN, 1992, P NATL ACAD SCI USA, V89, P5670, DOI 10.1073/pnas.89.12.5670 ONISHI S, 1968, J ACOUST SOC AM, V44, P582, DOI 10.1121/1.1911124 OTTAVIANI F, 1990, AUDIOLOGY, V29, P212 PANTEV C, 1988, ELECTROEN CLIN NEURO, V69, P160, DOI 10.1016/0013-4694(88)90211-8 PANTEV C, 1986, AUDIOLOGY, V25, P263 PANTEV C, 1991, P NATL ACAD SCI USA, V88, P8996, DOI 10.1073/pnas.88.20.8996 PELIZZONE M, 1985, BIOMAGNETISM APPLICA, P326 PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 Plourde G, 1991, Acta Otolaryngol Suppl, V491, P153 RIBARY U, 1991, P NATL ACAD SCI USA, V88, P11037, DOI 10.1073/pnas.88.24.11037 TIIHONEN J, 1989, AUDIOLOGY, V28, P37 YAMAMOTO T, 1988, P NATL ACAD SCI USA, V85, P8732, DOI 10.1073/pnas.85.22.8732 NR 38 TC 46 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 JUN PY 1993 VL 68 IS 1 BP 89 EP 96 DI 10.1016/0378-5955(93)90067-B PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400009 PM 8376218 ER PT J AU KUJAWA, SG GLATTKE, TJ FALLON, M BOBBIN, RP AF KUJAWA, SG GLATTKE, TJ FALLON, M BOBBIN, RP TI CONTRALATERAL SOUND SUPPRESSES DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS THROUGH CHOLINERGIC MECHANISMS SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINE; COCHLEAR MECHANICS; CONTRALATERAL SOUND SUPPRESSION; OLIVOCOCHLEAR NEURONS; OUTER HAIR CELLS ID CROSSED OLIVOCOCHLEAR BUNDLE; COCHLEAR MICROMECHANICAL PROPERTIES; AUDITORY-NERVE RESPONSES; OTO-ACOUSTIC EMISSIONS; GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; STIMULUS VARIABLES; ACTION-POTENTIALS; EFFERENT NEURONS; STIMULATION AB Presentation of an acoustic signal to one ear can suppress sound-evoked activity recorded at the opposite ear. The suppression appears to be mediated by medial olivocochlear (MOC) efferent neurons synapsing with outer hair cells (OHCs) and acting through the MOC neurotransmitter, acetylcholine (ACh). The purpose of the present investigation was to study the suppression of distortion product otoacoustic emissions (DPOAEs) by contralateral sound and to examine whether the suppression could be blocked by known antagonists of olivocochlear (OC) efferent activity. Urethane-anesthetized guinea pigs were used. Perilymph spaces of ipsilateral cochleae were alternately perfused with artificial perilymph and drugs at 2.5 mul/min for 10 min. After each period of perfusion, DPOAEs were measured before, during and after contralateral wideband noise (WBN) stimulation. Pre-perfusion, contralateral WBN attenuated the ipsilateral DPOAEs between 1-3 dB. This suppression was blocked reversibly by strychnine (10 muM), curare (10 muM) and atropine (20 muM), known antagonists of OC efferent activity. These results confirm the findings of Puel and Rebillard (1990) that contralateral WBN can suppress DPOAEs in anesthetized guinea pigs. Furthermore, results suggest that this efferent control of the cochlear mechanical response can either be mediated by both nicotinic and muscarinic cholinergic receptors, or that a single receptor with as yet undescribed structure and pharmacology mediates effects seen. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. UNIV ARIZONA,DEPT SPEECH & HEARING SCI,TUCSON,AZ 85721. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 BERLIN CI, 1993, HEARING RES, V65, P40, DOI 10.1016/0378-5955(93)90199-B Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 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, 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 BROWN MC, 1989, HEARING RES, V40, P93, DOI 10.1016/0378-5955(89)90103-2 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 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 DEWSON JH, 1967, J NEUROPHYSIOL, V30, P817 FEX J, 1962, ACTA PHYSIOL SCAND, V55, P1 FOLSOM RC, 1987, ACTA OTO-LARYNGOL, V103, P262, DOI 10.3109/00016488709107792 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 KONISHI T, 1971, SCIENCE, V172, P483, DOI 10.1126/science.172.3982.483 KUJAWA SG, 1990, INFLUENCE CONTRALATE, P156 KUJAWA SG, 1989, INFLUENCE CONTRALATE, P123 KUJAWA SG, 1992, HEARING RES, V61, P106, DOI 10.1016/0378-5955(92)90041-K KUJAWA SG, 1992, HEARING RES, V65, P7 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 LITTMAN TA, 1992, J ACOUST SOC AM, V92, P1945, DOI 10.1121/1.405242 Moller AR, 1972, F MODERN AUDITORY TH, VII, P135 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1992, ACTA OTO-LARYNGOL, V112, P210 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 MURATA K, 1980, NEUROSCI LETT, V18, P289, DOI 10.1016/0304-3940(80)90299-2 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 ROBERTSON D, 1985, HEARING RES, V20, P63, DOI 10.1016/0378-5955(85)90059-0 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 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 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V WHITEHEAD ML, 1992, J ACOUST SOC AM, V91, P1587, DOI 10.1121/1.402440 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 NR 49 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 JUN PY 1993 VL 68 IS 1 BP 97 EP 106 DI 10.1016/0378-5955(93)90068-C PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400010 PM 8376219 ER PT J AU CHEATHAM, MA DALLOS, P AF CHEATHAM, MA DALLOS, P TI LONGITUDINAL COMPARISONS OF IHC AC AND DC RECEPTOR POTENTIALS RECORDED FROM THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; DISCHARGE RATE; HAIR CELL; RECEPTOR POTENTIAL; SYNCHRONY; SYNAPTIC PROCESSES ID OUTER HAIR-CELLS; AUDITORY-NERVE FIBERS; INTRACELLULAR-RECORDINGS; TIMING INFORMATION; TUNING CURVES; FREQUENCY; RESPONSES; INNER; STEREOCILIA; SUPPRESSION AB Recordings were made from inner hair cells (IHC) at three locations distributed in the apical half of the guinea pig cochlea. Longitudinal variations in ac and dc components of receptor potentials produced in response to single-tone inputs were studied to further understand the ways in which IHCs communicate with their innervating afferent dendrites. While neural synchrony probably depends on the ac receptor potential. discharge rate may be controlled by the dc receptor potential generated by the IHC transducer plus an ac component derived from the phasic receptor potential. The latter reflects low-pass filtering inherent in the hair cell's basolateral membrane and calcium-dependent synaptic processes. By comparing the frequency dependence of ac and dc components in cells with different characteristic frequencies, it may be possible to learn how neural response areas are formed and why their shapes change along the cochlear spiral. RP CHEATHAM, MA (reprint author), NORTHWESTERN UNIV,HUGH KNOWLES CTR,AUDITORY PHYSIOL LAB,2-240 FRANCES SEARLE BLDG,EVANSTON,IL 60208, USA. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P323 BADENKRISTENSEN K, 1983, J PHYSIOL-LONDON, V335, P699 BROWN MC, 1983, SCIENCE, V222, P69, DOI 10.1126/science.6623058 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P386 CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 CHEATHAM MA, 1983, THESIS NW U EVANSTON CHEATHAM MA, IN PRESS PROGR BR RE CHEATHAM MA, 1992, HEARING RES, V60, P1, DOI 10.1016/0378-5955(92)90052-O Cody AR, 1980, SCAND AUDIOL S, V12, P121 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1989, J ACOUST SOC AM, V86, P1790, DOI 10.1121/1.398611 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 DALLOS P, 1974, J ACOUST SOC AM, V55, P597, DOI 10.1121/1.1914570 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DANCER AL, 1992, NOISE INDUCED HEARIN DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 Evans EF, 1976, J PHYSIOL-LONDON, V256, P43 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 Harrison R V, 1979, SCAND AUDIOL S, P83 HENNING GB, 1966, J ACOUST SOC AM, V63, P486 Ishii D, 1968, Acta Otolaryngol, V66, P282, DOI 10.3109/00016486809126295 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KIDD RC, 1990, HEARING RES, V49, P181, DOI 10.1016/0378-5955(90)90104-W 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 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MOORE BCJ, 1909, INTRO PSYCHOL HEARIN OHLEMILLER KK, 1990, J COMP PHYSIOL A, V167, P329 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X PATUZZI R, 1983, J ACOUST SOC AM, V74, P1734, DOI 10.1121/1.390282 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PROSEN CA, 1991, HEARING RES, V57, P142, DOI 10.1016/0378-5955(91)90083-L PUJOL R, 1992, ADV BIOSCI, V83, P45 ROBERTSON D, 1987, HEARING RES, V25, P69, DOI 10.1016/0378-5955(87)90080-3 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 ROSE JE, 1971, J NEUROPHYSIOL, V34, P685 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 RUSSELL IJ, 1981, NEURONES IMPULSES TH, P117 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1978, J ACOUST SOC AM, V64, P502, DOI 10.1121/1.382000 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1984, J ACOUST SOC AM, V76, P1293, DOI 10.1121/1.391446 SCHUKNECHT HF, 1959, ARCHIV OTOLARYNGOL, V69, P549 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 WAKEFIELD GH, 1985, J ACOUST SOC AM, V77, P613, DOI 10.1121/1.391879 WEISS TF, 1988, HEARING RES, V33, P175, DOI 10.1016/0378-5955(88)90030-5 WEISS TF, 1988, HEARING RES, V33, P167, DOI 10.1016/0378-5955(88)90029-9 WRIGHT CG, 1973, BRAIN RES, V58, P37, DOI 10.1016/0006-8993(73)90822-6 Zwicker E., 1970, FREQUENCY ANAL PERIO, P376 ZWISLOCKI JJ, 1991, ACTA OTO-LARYNGOL, V111, P256, DOI 10.3109/00016489109137384 NR 58 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 JUN PY 1993 VL 68 IS 1 BP 107 EP 114 DI 10.1016/0378-5955(93)90069-D PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400011 PM 8376208 ER PT J AU HAN, Y COLBURN, HS AF HAN, Y COLBURN, HS TI POINT-NEURON MODEL FOR BINAURAL INTERACTION IN MSO SO HEARING RESEARCH LA English DT Article DE BINAURAL PROCESSING; NEURAL MODELING; MEDIAL SUPERIOR OLIVE ID ANTEROVENTRAL COCHLEAR NUCLEUS; AUDITORY-NERVE DATA; SUPERIOR OLIVE; PHYSIOLOGICAL-PROPERTIES; INFERIOR COLLICULUS; RESPONSES; TONES; DISCRIMINATION; TRANSDUCTION; SENSITIVITY AB A point-neuron model for the activity of individual cells in the medial superior olive (MSO) is described and shown to generate discharge patterns consistent with the activity of real neurons as reported in response to low-frequency sinusoidal stimulation. Inputs to the model cell are specified as primarylike firing patterns, and the cell membrane characteristics are specified in terms of constant-potential sources and time-varying conductances. Some conductances are determined in response to the input firings and some in response to output firing times, which are generated when the membrane potential of the model cell crosses threshold. Output firing patterns generated by the model cells are consistent with those reported from neurons in dog and cat MSO. These patterns are also compatible with those of the functionally specified coincidence model described in Colburn et al. (1990). Given these observations, the following questions are addressed: What parameter values in the point-neuron model are required to generate output patterns like those observed? How do these values compare to those expected or estimated from intracellular measurements in brainstem neurons? How might one reconcile the fact that inhibitory inputs are not necessary in the model for the generation of the observed firing patterns with the fact that MSO cells receive numerous inhibitory inputs? C1 BOSTON UNIV,DEPT BIOMED ENGN,44 CUMMINGTON ST,BOSTON,MA 02215. CR ADAMS JC, 1990, HEARING RES, V49, P281, DOI 10.1016/0378-5955(90)90109-3 ARLE JE, 1991, BIOL CYBERN, V64, P273, DOI 10.1007/BF00199590 BANKS MI, 1992, J NEUROSCI, V12, P2819 Bourk TR, 1976, THESIS MIT CAMBRIDGE CAJAL SRY, 1909, HISTOLOGIE SYSTEME N, pCH28 CANT NB, 1992, HEARING RES, V58, P28 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 CARNEY LH, 1993, J ACOUST SOC AM, V93, P401, DOI 10.1121/1.405620 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 CARR CE, 1988, P NATL ACAD SCI USA, V85, P8311, DOI 10.1073/pnas.85.21.8311 CLARK GM, 1969, BRAIN RES, V14, P293, DOI 10.1016/0006-8993(69)90111-5 COLBURN HS, 1973, J ACOUST SOC AM, V54, P1458, DOI 10.1121/1.1914445 COLBURN HS, 1990, HEARING RES, V49, P335 COLBURN HS, 1977, J ACOUST SOC AM, V61, P525, DOI 10.1121/1.381294 COLBURN HS, 1992, AUDITORY PERCEPTION CROW G, 1978, J ACOUST SOC AM, V64, P493, DOI 10.1121/1.381999 DIAZ JM, 1989, THESIS BOSTON U BOST Durlach NI, 1978, HDB PERCEPTION GAUMOND RP, 1982, J NEUROPHYSIOL, V48, P856 GOLDBERG JAY M., 1968, J NEUROPHYSIOL, V31, P639 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 HAN Y, 1992, THESIS BOSTON U BOST HARRISON JM, 1962, J COMP NEUROL, V119, P341, DOI 10.1002/cne.901190306 Held H, 1893, ARCH ANAT PHYSL ANAT, V3+4, P201 HYSON RL, 1989, ASS RES OTOLARYNGOL, V12, P34 JEFFRESS LA, 1958, J ACOUST SOC AM, V30, P802 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 Johnson D.H., 1974, THESIS MIT CAMBRIDGE JOHNSON DH, 1983, J ACOUST SOC AM, V74, P493, DOI 10.1121/1.389815 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 JORIS P X, 1990, Society for Neuroscience Abstracts, V16, P723 KUWADA S, 1991, Society for Neuroscience Abstracts, V17, P450 LINDSEY BG, 1975, J COMP NEUROL, V1609, P81 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MacGregor R, 1987, NEURAL BRAIN MODELIN MACGREGO.RJ, 1974, KYBERNETIK, V16, P53, DOI 10.1007/BF00270295 MANIS PB, 1991, J NEUROSCI, V11, P2865 MEDDIS R, 1988, J ACOUST SOC AM, V83, P1056, DOI 10.1121/1.396050 MEDDIS R, 1986, J ACOUST SOC AM, V79, P702, DOI 10.1121/1.393460 MILLER MI, 1992, AUDITORY PERCEPTION OERTEL D, 1983, J NEUROSCI, V3, P2043 OVERHOLT EM, 1992, J NEUROSCI, V12, P1698 PALMER AR, 1990, HEARING RES, V50, P71, DOI 10.1016/0378-5955(90)90034-M SCHWARTZ IR, 1980, AM J ANAT, V159, P25, DOI 10.1002/aja.1001590104 SIEBERT WM, 1970, PR INST ELECTR ELECT, V58, P723, DOI 10.1109/PROC.1970.7727 SMITH P H, 1989, Society for Neuroscience Abstracts, V15, P746 Smith P. H., 1992, Society for Neuroscience Abstracts, V18, P382 STOTLER WA, 1953, J COMP NEUROL, V98 STUTMAN ER, 1993, ABSTR ASS RES OT, V16, P121 VOIGT HF, 1991, COCHLEAR NUCLEUS STR WARR WB, 1986, CONTRIBUTIONS SENSOR, V7, P1 WARR WB, 1966, EXP NEUROL, V14, P453, DOI 10.1016/0014-4886(66)90130-0 WU SH, 1991, J NEUROPHYSIOL, V65, P230 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 NR 55 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 JUN PY 1993 VL 68 IS 1 BP 115 EP 130 DI 10.1016/0378-5955(93)90070-H PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400012 PM 8376209 ER PT J AU WERNER, LA FOLSOM, RC MANCL, LR AF WERNER, LA FOLSOM, RC MANCL, LR TI THE RELATIONSHIP BETWEEN AUDITORY BRAIN-STEM RESPONSE AND BEHAVIORAL THRESHOLDS IN NORMAL-HEARING INFANTS AND ADULTS SO HEARING RESEARCH LA English DT Article DE AUDITORY SENSITIVITY; AUDITORY DEVELOPMENT ID PURE-TONE SENSITIVITY; STEM RESPONSES; DEVELOPMENTAL-CHANGES; MULTIPLE-SCLEROSIS; WAVE-V; CHILDREN; FREQUENCY; MASKING; ABR; AUDIOMETRY AB The nature of age-related improvements in auditory sensitivity was explored by comparing behavioral and auditory brainstem response (ABR) thresholds in 3- and 6-month-old infants and in adults. Thresholds were estimated for tone pips at 1, 4, and 8 kHz, presented at a rate of 13.3/s. The time course of development of the two response measures was compared, and the correlation between thresholds for individual subjects was examined. Infant ABR threshold was adultlike at all frequencies, even among 3-month-olds. Infant behavioral thresholds were elevated relative to adult thresholds. Between 3 and 6 months, significant improvement occurred in the 8-kHz behavioral threshold, but no improvement occurred at other frequencies. This difference between ABR and behavioral measures in developmental time course suggests that peripheral sensitivity is not a major determinant of behavioral threshold elevation during infancy. The correlation between behavioral and ABR thresholds was significant at 4 kHz for 3-month-olds and at 8 kHz for adults. This suggests that variability in sensory function at these frequencies contributes to both behavioral and ABR thresholds, although other factors are likely to be involved as well. RP WERNER, LA (reprint author), UNIV WASHINGTON,CTR CHILD DEV & MENTAL RETARDAT,DEPT SPEECH & HEARING SCI,WJ-10,BOX 47,SEATTLE,WA 98195, USA. CR BERG KM, 1991, PERCEPT PSYCHOPHYS, V50, P314, DOI 10.3758/BF03212223 BERG KM, 1993, IN PRES PERCEPT PSYC BONFILS P, 1992, LARYNGOSCOPE, V102, P182 DALLOS P, 1988, AUDITORY FUNCTION NE, P153 DON M, 1984, SCAND AUDIOL, V13, P219, DOI 10.3109/01050398409042130 EGGERMONT JJ, 1991, ACTA OTO-LARYNGOL, V111, P220, DOI 10.3109/00016489109137378 EGGERMONT JJ, 1988, HEARING RES, V33, P35, DOI 10.1016/0378-5955(88)90019-6 Eggermont J J, 1985, Acta Otolaryngol Suppl, V421, P41 ELBERLING C, 1987, J ACOUST SOC AM, V81, P115, DOI 10.1121/1.395019 FOLSOM RC, 1987, AUDIOLOGY, V26, P117 FOLSOM RC, 1984, J ACOUST SOC AM, V75, P919, DOI 10.1121/1.390538 FOLSOM RC, 1987, J ACOUST SOC AM, V81, P412, DOI 10.1121/1.394906 FOLSOM RC, 1986, J ACOUST SOC AM, V80, P1057, DOI 10.1121/1.393847 GARNER WR, 1956, PSYCHOL REV, V63, P149, DOI 10.1037/h0042992 GORGA MP, 1988, J SPEECH HEAR RES, V31, P87 GORGA MP, 1989, J SPEECH HEAR RES, V32, P281 Gottlieb G., 1971, BIOPSYCHOLOGY DEV, P67 GRAY L, 1990, HEARING RES, V45, P169, DOI 10.1016/0378-5955(90)90118-9 HENDLER T, 1990, EAR HEARING, V11, P403, DOI 10.1097/00003446-199012000-00002 JACOBSON JT, 1987, EAR HEARING, V8, P115, DOI 10.1097/00003446-198704000-00009 KAGA K, 1980, ARCH OTOLARYNGOL, V106, P564 KLEIN AJ, 1984, HEARING RES, V16, P291, DOI 10.1016/0378-5955(84)90118-7 KLEIN AJ, 1986, J ACOUST SOC AM, V79, P755, DOI 10.1121/1.393464 NORTON SJ, 1990, EAR HEARING, V11, P121, DOI 10.1097/00003446-199004000-00006 OLSHO L W, 1988, Journal of the Acoustical Society of America, V84, P1316, DOI 10.1121/1.396630 OLSHO LW, 1987, DEV PSYCHOL, V23, P627, DOI 10.1037/0012-1649.23.5.627 PONTON CW, 1992, J ACOUST SOC AM, V91, P1576, DOI 10.1121/1.402439 PRIMUS MA, 1985, J SPEECH HEAR RES, V28, P539 RICKARD LK, 1988, THESIS U WASHINGTON Ruth R A, 1983, Scand Audiol Suppl, V17, P94 SASAMA R, 1990, AUDIOLOGY, V29, P76 SCHNEIDER B, 1980, SCIENCE, V7, P1003 SCHNEIDER BA, 1986, J ACOUST SOC AM, V79, P447, DOI 10.1121/1.393532 SCHNEIDER BA, 1989, J ACOUST SOC AM, V86, P1733, DOI 10.1121/1.398604 SINNOTT JM, 1983, INFANT BEHAV DEV, V6, P3, DOI 10.1016/S0163-6383(83)80003-4 SPETNER NB, 1990, CHILD DEV, V61, P632, DOI 10.1111/j.1467-8624.1990.tb02808.x TAYLOR MM, 1967, J ACOUST SOC AM, V41, P782, DOI 10.1121/1.1910407 TEAS DC, 1982, HEARING RES, V7, P19, DOI 10.1016/0378-5955(82)90080-6 THORPE LA, 1987, ABSTR SOC RES CHILD, V6, P273 TREHUB SE, 1980, J EXP CHILD PSYCHOL, V29, P282, DOI 10.1016/0022-0965(80)90020-X TREHUB SE, 1991, DEV PSYCHOL, V27, P40, DOI 10.1037//0012-1649.27.1.40 TREHUB SE, 1988, J EXP CHILD PSYCHOL, V46, P273, DOI 10.1016/0022-0965(88)90060-4 TREHUB SE, 1981, DEV PSYCHOL, V17, P872, DOI 10.1037//0012-1649.17.6.872 WERNER LA, 1990, INFANT BEHAV DEV, V13, P355, DOI 10.1016/0163-6383(90)90040-F WERNER LA, 1991, J ACOUST SOC AM, V90, P1867, DOI 10.1121/1.401666 YONESHIGE Y, 1981, J ACOUST SOC AM, V70, P1272, DOI 10.1121/1.387140 NR 46 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 JUN PY 1993 VL 68 IS 1 BP 131 EP 141 DI 10.1016/0378-5955(93)90071-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LL524 UT WOS:A1993LL52400013 PM 8376210 ER PT J AU CZIBULKA, A SCHWARTZ, IR AF CZIBULKA, A SCHWARTZ, IR TI GLIAL OR NEURONAL ORIGIN OF MICROCYSTS IN THE GERBIL PVCN SO HEARING RESEARCH LA English DT Article DE MICROCYSTS; ASTROCYTES; S-100; GFAP; RIP; GERBIL; COCHLEAR NUCLEUS; EXCITOTOXICITY AB This study used immunocytochemical markers for various classes of glial cells to investigate the relationship between glial elements and microcysts in the gerbil auditory system at the light and electron microscopic level. Monoclonal antibodies S-100, GFAP and Rip were used on tissue from 3- and 12-month old animals and acutely deafened 12 month old animals to localize astrocytes and oligodendrocytes and their processes around microcysts. No differences in the number and distribution of astrocytes were found in the PVCN as a result of aging or deafening. S-100 and GFAP labeling showed a high correlation between astrocytic processes and microcysts. The results indicate that up to 80% of microcysts are either contacted by astrocytic profiles over much of their perimeter or are labeled internally by the astrocytic markers S-100 or GFAP. Some microcysts appear to originate in neuronal dendrites or in axons. RP CZIBULKA, A (reprint author), YALE UNIV,SCH MED,OTOLARYNGOL SECT,333 CEDAR ST,NEW HAVEN,CT 06510, USA. CR BARRES BA, 1991, J NEUROSCI, V11, P3685 CZIBULKA A, 1991, HEARING RES, V52, P43, DOI 10.1016/0378-5955(91)90186-D CZIBULKA A, 1991, ABSTR ASS RES OT, V14, P42 CZIBULKA A, 1992, ABSTR ASS RES OT, V15, P76 Dahl D, 1986, ASTROCYTES, VIII, P1 DONATO R, 1986, CELL CALCIUM, V7, P123, DOI 10.1016/0143-4160(86)90017-5 FRIEDMAN B, 1989, GLIA, V2, P380, DOI 10.1002/glia.440020510 HAGLID K, 1974, NATURE, V251, P532, DOI 10.1038/251532b0 HANSSON HA, 1975, BRAIN RES, V93, P349, DOI 10.1016/0006-8993(75)90357-1 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KITZES L M, 1989, Society for Neuroscience Abstracts, V15, P743 MCGINN DMD, 1992, ABSTR ASS RES OT, V15, P77 MCGINN MD, 1987, HEARING RES, V31, P235, DOI 10.1016/0378-5955(87)90193-6 MCGINN MD, 1987, ABSTR ASS RES OT, V10, P208 MCGINN MD, 1988, ARO ABST, V11, P161 MCGINN MD, 1991, SOC NEUR ABSTR, V17, P281 MOREST DK, 1986, IUPS SAT S HEAR U CA, P80 OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 OSTAPOFF EM, 1987, ABSTR ASS RES OTOLAR, V10, P209 Roots BI, 1986, ASTROCYTES DEV MORPH, V1, P1 SCHWARTZ I R, 1988, Society for Neuroscience Abstracts, V14, P491 SCHWARTZ IR, 1982, STAIN TECHNOL, V57, P52 STATLER KD, 1988, ARO MIDW M, V11, P162 STATLER K D, 1989, Society for Neuroscience Abstracts, V15, P743 WOOLF N K, 1987, Society for Neuroscience Abstracts, V13, P1260 YU SM, 1989, STAIN TECHNOL, V64, P143 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 MAY PY 1993 VL 67 IS 1-2 BP 1 EP 12 DI 10.1016/0378-5955(93)90226-Q PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700001 PM 8340260 ER PT J AU TAKEUCHI, S WANGEMANN, P AF TAKEUCHI, S WANGEMANN, P TI AMINOGLYCOSIDE ANTIBIOTICS INHIBIT MAXI-K+ CHANNEL IN SINGLE ISOLATED COCHLEAR EFFERENT NERVE-TERMINALS SO HEARING RESEARCH LA English DT Article DE INNER EAR; COCHLEA; OTOTOXICITY; AXON TERMINAL; GERBIL ID RAT PROXIMAL TUBULE; OUTER HAIR-CELLS; TRANSMITTER RELEASE; GENTAMICIN-NEPHROTOXICITY; POTASSIUM CURRENT; CALCIUM; NEOMYCIN; MEMBRANE; BLOCKADE; NEURONS AB Patch clamp recordings were obtained from isolated cochlear efferent nerve terminals. The effect of aminoglycoside antibiotics on single maxi-K+ channels was determined. At positive voltages (cytosol with respect to extracellular side), neomycin, streptomycin, and kanamycin significantly reduced the single channel current amplitude of the maxi-K+ channel from the cytosolic side. The IC50 for neomycin was 9.10(-4) M from the cytosolic side and much greater than 10(-3) M from the extracellular side. Streptomycin and kanamycin were less potent. No significant difference in inhibition of the single channel current amplitude by 2.5.10(-4) M cytosolic neomycin was observed between 7.10(-4) M and 10(-6) M free cytosolic Ca2+. Neomycin had no significant effect on the open probability of the maxi-K+ channel either from the cytosolic or from the extracellular side. These findings demonstrate that the maxi-K+ channel in cochlear efferent nerve terminals can be a site of action for aminoglycoside antibiotics. C1 BOYS TOWN NATL RES HOSP,CELL PHYSIOL LAB,555 N 30TH ST,OMAHA,NE 68131. BOYS TOWN NATL RES HOSP,BIOPHYS LAB,OMAHA,NE 68131. RI Wangemann, Philine/N-2826-2013 CR ARAMAKI Y, 1986, BIOCHIM BIOPHYS ACTA, V862, P111, DOI 10.1016/0005-2736(86)90474-8 Aran JM, 1992, NOISE INDUCED HEARIN, P188 AUGUSTINE GJ, 1990, J PHYSIOL-LONDON, V431, P343 BROWN RD, 1972, ACTA OTO-LARYNGOL, V73, P335, DOI 10.3109/00016487209138949 BROWN RD, 1973, ACTA OTO-LARYNGOL, V76, P128, DOI 10.3109/00016487309121491 Cappas M.J., 1976, LARYNGOSCOPE, V87, P1100 Colquhoun D., 1983, SINGLE CHANNEL RECOR, P191 DELPOZO E, 1986, EUR J PHARMACOL, V128, P49, DOI 10.1016/0014-2999(86)90556-X DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 FIEKERS JF, 1983, J PHARMACOL EXP THER, V225, P487 HAGIWARA S, 1976, J GEN PHYSIOL, V67, P621, DOI 10.1085/jgp.67.6.621 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HAYASHIDA T, 1989, ACTA OTO-LARYNGOL, V108, P404, DOI 10.3109/00016488909125546 HIEL H, 1992, HEARING RES, V57, P157, DOI 10.1016/0378-5955(92)90148-G Hille B., 1992, IONIC CHANNELS EXCIT, P390 HINO N, 1982, PFLUG ARCH EUR J PHY, V394, P243, DOI 10.1007/BF00589099 HOCHNER B, 1986, P NATL ACAD SCI USA, V83, P8410, DOI 10.1073/pnas.83.21.8410 HUDSPETH AJ, 1983, J PHYSL, V345 INABA A, 1986, LIFE SCI, V39, P1345 Kohonen A., 1965, ACTA OTO-LARYNGOL, V208, P1 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LEFEBVRE PP, 1990, HEARING RES, V47, P83, DOI 10.1016/0378-5955(90)90168-O LIPSKY JJ, 1980, ANTIMICROB AGENTS CH, V18, P532 LODHI S, 1976, BIOCHIM BIOPHYS ACTA, V426, P781, DOI 10.1016/0005-2736(76)90147-4 LODHI S, 1992, AM J PHYSIOL, V262, pC1423 MORITA K, 1990, J NEUROSCI, V10, P2614 NATION PN, 1988, CAN J PHYSIOL PHARM, V66, P27 NOMURA K, 1990, J MEMBRNE BIOL, V1115, P241 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 OOSAWA Y, 1986, AM J PHYSIOL, V250, pC361 ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x PARSONS TD, 1992, J GEN PHYSIOL, V99, P491, DOI 10.1085/jgp.99.4.491 PRADO WA, 1978, ARCH INT PHARMACOD T, V231, P297 SCHACHT J, 1976, J ACOUST SOC AM, V59, P940, DOI 10.1121/1.380929 SILVERBLATT FJ, 1979, KIDNEY INT, V15, P335, DOI 10.1038/ki.1979.45 SUAREZKURTZ G, 1987, PFLUG ARCH EUR J PHY, V410, P517, DOI 10.1007/BF00586535 TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 WAGNER JA, 1987, NEW ENGL J MED, V317, P1669 WANGEMANN PH, 1992, ABSTR SOC NEUR WANGEMANN PH, 1992, ABSTR C MOL BIOL HEA WANGEMANN PH, 1993, HEARING RES, V66, P125 WEDEEN RP, 1983, LAB INVEST, V48, P212 WEINER ND, 1981, AMINOGLYCOSIDE OTOTO, P113 WILLIAMS PD, 1981, TOXICOL APPL PHARM, V61, P234, DOI 10.1016/0041-008X(81)90413-0 WILLIAMS PD, 1981, TOXICOL APPL PHARM, V61, P243, DOI 10.1016/0041-008X(81)90414-2 WRIGHT JM, 1977, J PHARMACOL EXP THER, V200, P576 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 MAY PY 1993 VL 67 IS 1-2 BP 13 EP 19 DI 10.1016/0378-5955(93)90227-R PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700002 PM 8340264 ER PT J AU KIRK, DL JOHNSTONE, BM AF KIRK, DL JOHNSTONE, BM TI MODULATION OF F2-F1 - EVIDENCE FOR A GABAERGIC EFFERENT SYSTEM IN APICAL COCHLEA OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE GABA; COCHLEA; DISTORTION TONES; EFFERENTS ID OLIVOCOCHLEAR BUNDLE STIMULATION; SUPERIOR OLIVARY COMPLEX; OUTER HAIR-CELLS; SOUND STIMULATION; MEDIAL ZONES; NEURONS; ORGAN; CORTI; IMMUNOREACTIVITY; MECHANICS AB f2-f1, but not 2f1-f2, was reduced in amplitude during continuous stimulation of the test ear with the primary tones, and with single tones near the primary frequencies. Stimulation of the contralateral ear, either with broad band noise or with single tones near the primary frequencies, also reduced f2-f1. Ipsilateral and contralateral effects were additive and were restricted to the frequency range between about 2 kHz and 7 kHz. Contralateral, but not ipsilateral suppression, was blocked after systemic administration of strychnine. Ipsilateral suppression was eliminated by perfusion of the cochlea with tetrodotoxin. Both contralateral and ipsilateral suppression were abolished after perfusion of the cochlea with The results are evidence for a role for a GABA-ergic efferent system in the modulation of outer hair cell mechanics in the apical cochlea. RP KIRK, DL (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 ALTSCHULER RA, 1984, HEARING RES, V16, P17, DOI 10.1016/0378-5955(84)90022-4 ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 Bekesy G., 1960, EXPT HEARING BOBBIN RP, 1971, NATURE-NEW BIOL, V231, P222 BROWN AM, 1988, HEARING RES, V34, P27, DOI 10.1016/0378-5955(88)90048-2 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CODY AR, 1982, J ACOUST SOC AM, V72, P280, DOI 10.1121/1.387993 CURTIS DR, 1971, BRAIN RES, V33, P57, DOI 10.1016/0006-8993(71)90305-2 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DESMEDT JE, 1961, NATURE, V192, P1263, DOI 10.1038/1921263a0 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x EYBALIN M, 1990, J ELECTRON MICR TECH, V15, P209, DOI 10.1002/jemt.1060150303 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 EYBALIN M, 1989, ARCH OTO-RHINO-LARYN, V246, P228, DOI 10.1007/BF00463561 FEX J, 1984, HEARING RES, V15, P123, DOI 10.1016/0378-5955(84)90043-1 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 GALLEY N, 1973, BRAIN RES, V64, P55, DOI 10.1016/0006-8993(73)90170-4 GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 GITTER AH, 1992, EUR ARCH OTO-RHINO-L, V249, P62 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 GULLEY RL, 1979, ACTA OTO-LARYNGOL, V88, P177, DOI 10.3109/00016487909137157 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 KAO CY, 1972, FED PROC, V31, P1117 KLINKE R, 1977, EXP BRAIN RES, V28, P311 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 MOULIN A, 1992, ACTA OTO-LARYNGOL, V112, P210 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PEYRET D, 1986, HEARING RES, V23, P115, DOI 10.1016/0378-5955(86)90008-0 PLINKERT PK, 1989, ARCH OTO-RHINO-LARYN, V246, P417, DOI 10.1007/BF00464301 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 Pujol R., 1986, NEUROBIOLOGY HEARING, P161 Rajan R, 1992, NOISE INDUCED HEARIN, P429 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 ROBERTSON D, 1985, HEARING RES, V20, P79, DOI 10.1016/0378-5955(85)90060-7 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X ROBERTSON D, 1987, HEARING RES, V25, P69, DOI 10.1016/0378-5955(87)90080-3 SCHWARTZ IR, 1983, HEARING RES, V9, P185, DOI 10.1016/0378-5955(83)90027-8 SCHWARZ DWF, 1988, HEARING RES, V32, P97, DOI 10.1016/0378-5955(88)90150-5 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 THOMPSON AM, 1991, J COMP NEUROL, V303, P267, DOI 10.1002/cne.903030209 THOMPSON GC, 1986, BRAIN RES, V372, P72, DOI 10.1016/0006-8993(86)91459-9 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WEIDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WHITEHEAD ML, 1991, HEARING RES, V51, P293, DOI 10.1016/0378-5955(91)90045-B ZWICKER E, 1979, HEARING RES, V1, P283, DOI 10.1016/0378-5955(79)90001-7 NR 53 TC 39 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 MAY PY 1993 VL 67 IS 1-2 BP 20 EP 34 DI 10.1016/0378-5955(93)90228-S PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700003 PM 8340272 ER PT J AU KALTENBACH, JA MELECA, RJ FALZARANO, PR MYERS, SF SIMPSON, TH AF KALTENBACH, JA MELECA, RJ FALZARANO, PR MYERS, SF SIMPSON, TH TI FORWARD MASKING PROPERTIES OF NEURONS IN THE DORSAL COCHLEAR NUCLEUS - POSSIBLE ROLE IN THE PROCESS OF ECHO SUPPRESSION SO HEARING RESEARCH LA English DT Article DE MASKING; FORWARD MASKING; DORSAL COCHLEAR NUCLEUS; PRECEDENCE EFFECT; ECHO SUPPRESSION ID SHORT-TERM ADAPTATION; AUDITORY-NERVE; INHIBITION; RESPONSES AB The majority of single unit studies in the auditory system have been carried out using stimuli whose temporal and spectral contexts are held constant. Relatively little attention has been given to the influence of context on unit response properties. Indeed, auditory nerve fiber responses are known to be context-dependent due to the property of forward masking, a phenomenon by which the response to one sound results in a reduction in the response to a subsequent sound. Forward masking might be expected to be even more influential at central levels of the auditory pathway where the responses are reshaped by additional synaptic interactions. The purpose of the present study was to characterize the forward masking properties of neurons in the dorsal cochlear nucleus (DCN). A tool was developed for measuring the response to a probe tone as a function of delay following a previous tone-burst. The frequency of the probe was held constant at the unit's characteristic frequency while the frequency of the leading tone (masker) was varied. These measures provided a description of neural masking effects in different temporal and spectral contexts. The data yielded two patterns of suppression. In the first pattern (Type A), the suppression of the probe response became evident immediately following offset of the masker; the suppression bandwidth showed a gradual narrowing as the delay between masker and probe was increased. In the second class (Type B), the suppression of the probe response did not become evident until well after offset of the masker; this pattern appeared more circumscribed in that the suppression bandwidth gradually increased as a function of delay up to a maximum then decreased with further increases in delay. The results imply that mechanisms intrinsic to the DCN contribute to further modification and reshaping of the spectral and temporal context of masking effects beyond those seen in the auditory nerve. It is hypothesized that such properties may be specialized for suppressing the response to echoes thus facilitating communication and localization of sound in enclosed spaces. C1 WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL,DETROIT,MI 48201. RP KALTENBACH, JA (reprint author), WAYNE STATE UNIV,SCH MED,DEPT AUDIOL,5E-UHC,4201 ST ANTOINE,DETROIT,MI 48201, USA. CR Boettcher F.A., 1988, P141 BOETTCHER FA, 1990, HEARING RES, V48, P125, DOI 10.1016/0378-5955(90)90203-2 DAVID EE, 1962, 4TH P INT C AC COP, pH24 DAVID EE, 1961, 3RD P INT C AC STUTT, V1, P144 ELLIOTT LL, 1962, J ACOUST SOC AM, V34, P1116, DOI 10.1121/1.1918254 ELLIOTT LL, 1967, J ACOUST SOC AM, V42, P143, DOI 10.1121/1.1910543 GARDNER MB, 1968, J ACOUST SOC AM, V43, P1243, DOI 10.1121/1.1910974 GASKELL H, 1983, HEARING RES, V11, P277 GUTTMAN N, 1960, J ACOUST SOC AM, V32, P1329, DOI 10.1121/1.1907902 HAFTER ER, 1989, AUDITORY FUNCTION NE, P647 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 HARRIS GERARD G., 1963, JOUR ACOUSTICAL SOC AMER, V35, P672, DOI 10.1121/1.1918583 HOUTGAST T, 1968, J ACOUST SOC AM, V44, P807, DOI 10.1121/1.1911178 KALTENBACH JA, 1991, HEARING RES, V51, P149, DOI 10.1016/0378-5955(91)90013-Y KIM DO, 1992, ASS RES OTOLARYNGOL, V15, P60 KOENIG W, 1950, J ACOUST SOC AM, V22, P61, DOI 10.1121/1.1906578 LINDEMANN W, 1983, J ACOUST SOC AM, V74, pS85, DOI 10.1121/1.2021185 LINDEMANN W, 1986, J ACOUST SOC AM, V80, P1623, DOI 10.1121/1.394326 MCFADDEN D, 1973, J ACOUST SOC AM, V54, P528, DOI 10.1121/1.1913611 RELKIN EM, 1988, J ACOUST SOC AM, V84, P584, DOI 10.1121/1.396836 SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 WALLACH H, 1949, AM J PSYCHOL, V52, P315 WATANABE T, 1971, JPN J PHYSIOL, V21, P537 WEBER DL, 1983, J ACOUST SOC AM, V73, P887, DOI 10.1121/1.389012 WESTERMAN LA, 1987, J ACOUST SOC AM, V81, P680, DOI 10.1121/1.394836 WICKESBERG RE, 1992, ASS RES OTOLARYNGOL, V15, P60 WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 WILSON RH, 1971, J ACOUST SOC AM, V49, P1254, DOI 10.1121/1.1912488 YOUNG ED, 1989, AUDITORY FUNCTION NE, P647 Zurek P. M., 1987, DIRECTIONAL HEARING, P85, DOI 10.1007/978-1-4612-4738-8_4 ZUREK PM, 1979, J ACOUST SOC AM, V66, P1750, DOI 10.1121/1.383648 ZUREK PM, 1980, J ACOUST SOC AM, V67, P952, DOI 10.1121/1.383974 ZUREK PM, 1975, J ACOUST SOC AM, V58, pS55, DOI 10.1121/1.2002193 NR 33 TC 40 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 MAY PY 1993 VL 67 IS 1-2 BP 35 EP 44 DI 10.1016/0378-5955(93)90229-T PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700004 PM 8340276 ER PT J AU FARMS, WB GODFREY, DA ASKARI, A AF FARMS, WB GODFREY, DA ASKARI, A TI EFFECT OF COPPER-DEFICIENT DIET ON METABOLISM IN RAT AUDITORY STRUCTURES SO HEARING RESEARCH LA English DT Article DE COPPER; COCHLEA; COCHLEAR NUCLEUS; INFERIOR COLLICULUS; GLUTAMINE; AMINO ACIDS ID AMINO-ACIDS; LIPID-PEROXIDATION; DISEASE; BRAIN; EPILEPSY AB Copper is a trace element known to be critical for abnormal brain function, and abnormal copper metabolism has been associated with some disorders involving the auditory system. We examined effects of copper deficiency on metabolism in major structures of the auditory system. Homogenates of cochlea, cochlear nucleus and inferior colliculus of rats, as well as whole brain, were assayed for activities of enzymes of oxidative and glycolytic energy metabolism - malate and lactate dehydrogenase, enzymes of acetylcholine metabolism - choline acetyltransferase and acetylcholinesterase, and concentrations of amino acids. Whole brain was also assayed for activity of superoxide dismutase, a copper-containing enzyme, and concentrations of minerals. For these chemicals and tissues, the only significant differences between copper-deficient and copper-adequate rats were: (1) decreased copper and magnesium and increased potassium concentrations in whole brain of copper-deficient rats and (2) an elevation of glutamine concentration in inferior colliculus and whole brain of copper-deficient rats. The elevated glutamine could not be related to any change in activity of glutamine synthetase or glutaminase, major enzymes of glutamine metabolism. It is speculated that the increase in glutamine might result from a net increase in ammonia accumulation in the brains of copper-deficient rats. C1 MED COLL OHIO,DEPT OTOLARYNGOL,POB 10008,TOLEDO,OH 43699. MED COLL OHIO,DEPT SURG,TOLEDO,OH 43699. CR ASKARI A, 1991, FASEB J, V5, pA1452 Bieri J. G., 1977, J NUTR, V107, P1340 BORNSTEIN RA, 1985, INT J NEUROSCI, V26, P239 CHUNG SH, 1984, PROC R SOC SER B-BIO, V221, P145, DOI 10.1098/rspb.1984.0028 Cooper J., 1991, BIOCH BASIS NEUROPHA, V6th CURTHOYS NP, 1973, J BIOL CHEM, V248, P162 EVANS GW, 1977, ADV NUTR RES, V1, P167 FAINGOLD CL, 1988, EXP NEUROL, V99, P678, DOI 10.1016/0014-4886(88)90184-7 FUJITA M, 1981, ANN NEUROL, V9, P42, DOI 10.1002/ana.410090108 GODFREY DA, 1990, HEARING RES, V48, P187, DOI 10.1016/0378-5955(90)90058-W HALL ED, 1989, FREE RADICAL BIO MED, V6, P303, DOI 10.1016/0891-5849(89)90057-9 HALL ED, 1988, STROKE, V19, P997 HILL DW, 1979, ANAL CHEM, V51, P1338, DOI 10.1021/ac50044a055 KARDOS J, 1989, NEUROSCI LETT, V103, P139, DOI 10.1016/0304-3940(89)90565-X KLEVAY LM, 1985, NUTR REP INT, V31, P963 KLINKE R, 1974, PHYSIOL REV, V54, P316 LEHNINGER AL, 1975, BIOCH LOWRY OH, 1951, J BIOL CHEM, V193, P265 LYNCH SM, 1989, BRIT J NUTR, V61, P345, DOI 10.1079/BJN19890122 Marklund SL, 1985, CRC HDB METHODS OXYG, P243 O'Dell BL, 1990, PRESENT KNOWLEDGE NU, P261 OLDENDORF WH, 1975, NERVOUS SYSTEM, V1, P279 ONO S, 1988, J NEUROL, V235, P397, DOI 10.1007/BF00314480 PATEL AJ, 1983, DEV BRAIN RES, V8, P31, DOI 10.1016/0165-3806(83)90154-2 PERRY T, 1983, GLUTAMINE GLUTAMATE, P581 QUARLES RH, 1989, BASIC NEUROCHEMISTRY, P697 ROSS CD, 1989, VISION RES, V29, P1079 SELLINGER OZ, 1962, J BIOL CHEM, V237, P2836 SHERWOOD G, 1989, J INHERIT METAB DIS, V12, P393 TYRER SP, 1979, AM J PSYCHIAT, V136, P937 WALTON JN, 1977, BRAINS DISEASES NERV WIET GJ, 1986, HEARING RES, V24, P137, DOI 10.1016/0378-5955(86)90058-4 WU XR, 1988, PEDIATR NEUROL, V4, P126, DOI 10.1016/0887-8994(88)90056-2 Zar JH, 1984, BIOSTATISTICAL ANAL NR 34 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 1993 VL 67 IS 1-2 BP 45 EP 50 DI 10.1016/0378-5955(93)90230-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700005 PM 8101836 ER PT J AU KIRSCH, JP MONEY, MK WEBSTER, DB AF KIRSCH, JP MONEY, MK WEBSTER, DB TI MICE HETEROZYGOUS FOR THE DEAFNESS GENE HAVE NORMAL AUDITORY-THRESHOLDS SO HEARING RESEARCH LA English DT Article DE AUDITORY THRESHOLDS; DEAFNESS MICE; ABRS; HETEROZYGOTES ID INNER-EAR; GANGLION; MOUSE AB Cochlear degeneration in the early postnatal period has been reported as a homozygous recessive mutation in deafness (dn/dn) mice of the curly-tail stock. Heterozygous (+/dn) mice of the same population exhibit hearing when tested by the Preyer reflex, and their cochlear morphology appears normal by light microscopy. However, whether the heterozygote's unmatched recessive deafness allele has deleterious effects not detected by this reflex has not been examined. This study compares the ABR thresholds of presumed homozygous dominant (+/+) and known heterozygous (+/dn) deafness mice, as well as CBA/J mice. Hearing thresholds in the heterozygotes were not significantly different from those of presumed homozygotes or CBA/J mice. A 'generational backtracking' method was used to increase the probability of identifying homozygous (+/+) animals of the curly-tail strain. C1 LOUISIANA STATE UNIV,MED CTR,KRESGE LAB 2020 ST,SUITE A,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,DEPT ANAT,NEW ORLEANS,LA 70112. TULANE UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,NEW ORLEANS,LA 70118. LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,DEPT BIOCOMMUN,KRESGE HEARING RES LAB,NEW ORLEANS,LA 70112. CR ANDERSON H, 1976, ACTA OTO-LARYNGOL, V82, P245, DOI 10.3109/00016487609120895 BERLIN CI, 1963, J SPEECH HEAR RES, V6, P359 BIRCH LM, 1968, J AUD RES, V8, P459 BOCK GR, 1983, ACTA OTO-LARYNGOL, V96, P39, DOI 10.3109/00016488309132873 BOCK GR, 1982, BRAIN RES, V239, P608, DOI 10.1016/0006-8993(82)90536-4 Conover WJ, 1980, PRACTICAL NONPARAMET, V2 DEOL M. S., 1958, HEREDITY, V12, P463, DOI 10.1038/hdy.1958.46 ELSTON RC, 1987, ESSENTIALS BIOSTATIS, P273 FRANK MP, 1983, ARCH OTOLARYNGOL, V109, P526 HOOD LJ, 1990, ABSTR ASS RES OT, V80, P68 KOCH GG, 1969, J AM STAT ASSOC, V64, P485, DOI 10.2307/2283634 MEREDITH R, 1992, J AUDIOL MED, V1, P11 MORRISON DF, 1990, MULTIVARIATE STATIST PUJOL R, 1983, HEARING RES, V12, P57, DOI 10.1016/0378-5955(83)90118-1 Shnerson A, 1983, AUDITORY PSYCHOBIOLO, P395 STEEL KP, 1980, NATURE, V288, P159, DOI 10.1038/288159a0 WEBSTER DB, 1985, HEARING RES, V18, P19, DOI 10.1016/0378-5955(85)90107-8 WEBSTER DB, 1992, EXP NEUROL, V115, P27, DOI 10.1016/0014-4886(92)90216-D 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 MAY PY 1993 VL 67 IS 1-2 BP 51 EP 54 DI 10.1016/0378-5955(93)90231-O PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700006 PM 8340277 ER PT J AU MCANALLY, KI CLARK, GM SYKA, J AF MCANALLY, KI CLARK, GM SYKA, J TI HAIR CELL-MEDIATED RESPONSES OF THE AUDITORY-NERVE TO SINUSOIDAL ELECTRICAL-STIMULATION OF THE COCHLEA IN THE CAT SO HEARING RESEARCH LA English DT Article DE ELECTROPHONIC; ELECTRICAL STIMULATION; HAIR CELL; COMPOUND ACTION POTENTIAL; TRANSDUCTION ID PHYSIOLOGICAL-PROPERTIES; GUINEA-PIG; FIBERS; ADAPTATION; RECORDINGS; EXPOSURE; PATTERNS; ALTERS AB Electrical stimulation of the cochlea elicits discharges of auditory nerve fibres which are mediated by the electrical or mechanical stimulation of inner hair cells (electrophonic responses). In order to isolate hair-cell mediated responses from those elicited by electrical stimulation of the nerve, the compound action potential (CAP) evoked by an acoustic probe was forward-masked by sinusoidal monopolar, or localized bipolar electrical stimulation of the base of the cochlea. The degree of masking of a given probe estimated the synaptically mediated response to the masker of the population of auditory nerve fibres innervating the cochlear location tuned to the probe. There was a peak of masking for probes close to the frequency of the electrical stimulus, suggesting a spatial tuning of the hair cell mediated response along the cochlea. This is consistent with excitation of the inner hair cells by a propagating mechanical response which is generated within the electrical field at the base of the cochlea. Furthermore, tuning curves for masking of a given probe were sharply tuned to electrical stimulation close to the probe frequency. This masking was not dependent upon the presence of functional outer hair cells close to the electrodes, suggesting an alternate transduction of electrical to mechanical energy. C1 CZECHOSLOVAK ACAD SCI,INST EXPTL MED,CS-11142 PRAGUE 1,CZECHOSLOVAKIA. RP MCANALLY, KI (reprint author), UNIV MELBOURNE,DEPT OTOLARYNGOL,PARKVILLE,VIC 3052,AUSTRALIA. RI Syka, Josef/H-3103-2014 CR ABBAS PJ, 1981, J ACOUST SOC AM, V69, P492, DOI 10.1121/1.385477 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BLACK RC, 1981, IEEE T BIO-MED ENG, V28, P721, DOI 10.1109/TBME.1981.324668 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CLARK GM, 1986, OTOLARYNG CLIN N AM, V19, P329 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DECORY L, 1991, HEARING RES, V52, P81, DOI 10.1016/0378-5955(91)90189-G DESMEDT JE, 1975, J PHYSIOL-LONDON, V247, P407 DESMEDT JE, 1975, HDB SENSORY PHYSIO 2, V5, P219 GORGA MP, 1981, J ACOUST SOC AM, V70, P1310, DOI 10.1121/1.387145 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 HUBBARD AE, 1990, HEARING RES, V43, P269, DOI 10.1016/0378-5955(90)90234-G ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JAVEL E, 1987, ANN OTOL RHINOL LA S, V128, P26 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 MICHELSON RP, 1975, ANN OTO RHINOL LARYN, V84, P494 MILLARD RE, 1992, J NEUROSCI METH, V44, P81, DOI 10.1016/0165-0270(92)90116-U MOUTAIN DC, 1989, HEARING RES, V42, P192 Moxon E.C., 1971, THESIS MIT CAMBRIDGE NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NORRIS CH, 1977, BRAIN RES, V123, P176, DOI 10.1016/0006-8993(77)90653-9 OLEARY SJ, 1985, HEARING RES, V18, P273, DOI 10.1016/0378-5955(85)90044-9 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 RAJAN R, 1983, HEARING RES, V12, P405, DOI 10.1016/0378-5955(83)90009-6 RAJAN R, 1991, HEARING RES, V53, P153, DOI 10.1016/0378-5955(91)90222-U SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WIENER FM, 1966, ACTA OTOLARYNG, V161, P255 NR 33 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 MAY PY 1993 VL 67 IS 1-2 BP 55 EP 68 DI 10.1016/0378-5955(93)90232-P PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700007 PM 8340278 ER PT J AU POPELAR, J SYKA, J AF POPELAR, J SYKA, J TI MIDDLE LATENCY RESPONSES TO ELECTRICAL-STIMULATION OF THE AUDITORY-NERVE IN UNANESTHETIZED GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE ELECTRICAL STIMULATION; COCHLEA; AUDITORY CORTEX; EVOKED RESPONSES ID COCHLEAR IMPLANTS; POTENTIALS; EXCITATION; MODEL; CATS; PSYCHOPHYSICS; NEURON AB Middle latency responses (MLR) to sinusoidal and pulsatile electrical stimulation (ES) of the cochlea and to acoustical stimulation (AS) were evaluated in awake guinea pigs with chronically implanted electrodes. The ear, which was later electrically stimulated, was deafened by local intracochlear application of gentamicin, the opposite ear was left intact. Waveforms and P1-P2 interpeak intervals of the electrically evoked MLR (ES-MLR) were similar to those evoked by acoustical stimulation of the intact ear (AS-MLR) and the latencies of the ES-MLR were shorter by about 1-3 ms. Thresholds of ES-MLR in the frequency range 0.5-32 kHz increased with increasing ES frequency (slope 3.2 dB/octave), thresholds were 3.5-9.5 dB lower for intracochlear than for extracochlear ES. Dynamic ranges for ES-MLR varied between 6-20 dB. MLR amplitude-intensity functions for ES were steeper (slope 2-12 muV/dB) than those for AS (slope 0.2-2 muV/dB). Maximal ES-MLR amplitudes exceeded usually 1.5-3 times the amplitudes of the acoustically evoked MLR. Both types of stimulations evoked larger MLR amplitudes to contralateral stimulation than to ipsilateral stimulation (average ratio = 4.1 +/- 2.2 for AS and 3.3 +/- 2.2 for ES). Because of the relatively long latency and therefore insensitivity to electrical artifact, the ES-MLR can be used for the evaluation of different strategies of the RP POPELAR, J (reprint author), CZECHOSLOVAK ACAD SCI,INST EXPTL MED,LEGEROVA 61,CS-12000 PRAGUE 2,CZECHOSLOVAKIA. RI Popelar, Jiri/H-2558-2014; Syka, Josef/H-3103-2014 CR ABBAS PJ, 1988, HEARING RES, V36, P153, DOI 10.1016/0378-5955(88)90057-3 ARAN JM, 1979, TECHNICAL BASIS AUDI, P233 AREZZO J, 1975, BRAIN RES, V90, P57, DOI 10.1016/0006-8993(75)90682-4 BARTH DS, 1990, J NEUROPHYSIOL, V64, P1527 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BUCHWALD JS, 1981, BRAIN RES, V205, P91, DOI 10.1016/0006-8993(81)90722-8 BURTON MJ, 1989, ARCH OTOLARYNGOL, V115, P59 BURTON MJ, 1989, ARCH OTOLARYNGOL, V115, P458 CLOPTON BM, 1984, HEARING RES, V14, P1, DOI 10.1016/0378-5955(84)90063-7 CLOPTON BM, 1982, ANN OTO RHINOL LARYN, V91, P285 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DOBIE RA, 1980, ARCH OTOLARYNGOL, V106, P573 FELLNER E, 1984, ARTIFICIAL AUDITORY, P65 FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 GLASS J, 1983, HEARING RES, V12, P233 Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 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 KRAUS N, 1985, ELECTROEN CLIN NEURO, V62, P219, DOI 10.1016/0168-5597(85)90017-6 LOEB GE, 1983, ANN NY ACAD SCI, V405, P123, DOI 10.1111/j.1749-6632.1983.tb31625.x MCNEAL DR, 1976, IEEE T BIO-MED ENG, V23, P329, DOI 10.1109/TBME.1976.324593 MEIKLE MB, 1981, ANN OTO RHINOL LARYN, V90, P9 MERZENIC.MM, 1973, ANN OTO RHINOL LARYN, V82, P486 Merzenich M.M., 1975, NERVOUS SYSTEM, V3, P537 PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 PFINGST BE, 1979, ANN OTO RHINOL LARYN, V88, P613 PFINGST BE, 1988, HEARING RES, V34, P243, DOI 10.1016/0378-5955(88)90005-6 PFINGST BE, 1984, ARCH OTOLARYNGOL, V110, P140 REILLY JP, 1985, IEEE T BIO-MED ENG, V32, P1001, DOI 10.1109/TBME.1985.325509 ROSENZWEIG MR, 1951, AM J PHYSIOL, V167, P147 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SIMMONS BF, 1972, ANN OTOL, V81, P731 SYKA J, 1993, UNPUB MODULATION THR VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VIVION MC, 1981, ANN OTO RHINOL LARYN, V90, P19 YAMANE H, 1981, OTOLARYNG HEAD NECK, V89, P117 NR 39 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 MAY PY 1993 VL 67 IS 1-2 BP 69 EP 74 DI 10.1016/0378-5955(93)90233-Q PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700008 PM 8340279 ER PT J AU KAWAMATA, S IGARASHI, Y AF KAWAMATA, S IGARASHI, Y TI GLYCOCONJUGATES IN THE COCHLEA AS REVEALED BY THE SILVER METHENAMINE METHOD SO HEARING RESEARCH LA English DT Article DE COCHLEA; GLYCOCONJUGATES; SILVER METHENAMINE; PERIODIC ACID-SCHIFF STAINING ID TECTORIAL MEMBRANE; INNER-EAR; GELATINOUS MEMBRANES; STRIA VASCULARIS; GUINEA-PIG; ORGANIZATION; CAPILLARIES; ORGAN; CORTI AB The glycoconjugates in the cochlea of the guinea pig were studied by staining samples by the silver methenamine method as well as after periodic acid-Schiff (PAS) staining. Results obtained by the two methods were similar but not identical. The silver methenamine method was much better in terms of resolution. However, this method of staining seemed less specific than the PAS reaction. When the silver methenamine method was used, the tectorial membrane and outer hair cells were specifically stained. Two types of fibrils were observed in the tectorial membrane. Thick fibrils were located in the fibrous layer. Thin fibrils were situated in the marginal band, the cover net, Hensen's stripe and the fibrous layer. The thick and thin fibrils appeared to correspond to type A and type B protofibrils, respectively. The outer hair cells were found to contain strongly stained particles which, presumably, consisted of glycogen. The basement membrane of the capillaries in the stria vascularis also gave a positive reaction, while that of other capillaries was essentially unstained. This finding suggests structural differences between these capillaries. C1 TOYAMA MED & PHARMACEUT UNIV,DEPT ANAT & OTORHINOLARYNGOL,TOYAMA,TOYAMA 93001,JAPAN. RP KAWAMATA, S (reprint author), TOYAMA MED & PHARMACEUT UNIV,DEPT ANAT,TOYAMA,TOYAMA 93001,JAPAN. CR ARIMA T, 1990, HEARING RES, V46, P289, DOI 10.1016/0378-5955(90)90010-M Arnold W, 1984, Ann Otol Rhinol Laryngol Suppl, V112, P119 ARNOLD W, 1976, ARCH OTO-RHINO-LARYN, V212, P99, DOI 10.1007/BF00454270 DEMARTIN.C, 1967, J ULTRA MOL STRUCT R, V19, P273, DOI 10.1016/S0022-5320(67)80221-1 FERMIN CD, 1990, ACTA ANAT, V138, P75 GILLOYZAGA P, 1985, HEARING RES, V20, P1 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 IGARASHI M, 1969, ACTA OTO-LARYNGOL, V68, P420, DOI 10.3109/00016486909121580 IGARASHI Y, 1993, HEARING RES, V67 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 MOWRY RW, 1959, J HISTOCHEM CYTOCHEM, V7, P288 MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 NOMURA Y, 1984, HUMAN HISTOLOGY, V7, P352 QICK CA, 1975, CLIN N AM, V8, P385 Rambourg A, 1971, Int Rev Cytol, V31, P57 RAMBOURG A, 1969, J CELL BIOL, V40, P395, DOI 10.1083/jcb.40.2.395 RAMBOURG A, 1967, J HISTOCHEM CYTOCHEM, V15, P409 SAKAGAMI M, 1982, CELL TISSUE RES, V226, P511 SAKAGAMI M, 1987, ACTA OTO-LARYNGOL, V103, P189, DOI 10.3109/00016488709107783 SAKAGAMI M, 1986, ACTA OTO-LARYNGOL, V101, P165, DOI 10.3109/00016488609132824 SANO Y, 1981, HISTOLOGICAL TECHNIC, P318 SLEPECKY NB, 1992, CELL TISSUE RES, V267, P413, DOI 10.1007/BF00319363 SUGIYAMA S, 1991, HEARING RES, V55, P263, DOI 10.1016/0378-5955(91)90111-L SUGIYAMA S, 1992, HEARING RES, V58, P35, DOI 10.1016/0378-5955(92)90006-9 TACHIBANA M, 1987, HEARING RES, V27, P239, DOI 10.1016/0378-5955(87)90005-0 THALMANN I, 1986, ORL J OTO-RHINO-LARY, V48, P107 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 VANHEYNI.HE, 1965, J HISTOCHEM CYTOCHEM, V13, P286 WISLOCKI GB, 1955, J ANAT, V89, P3 NR 30 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 MAY PY 1993 VL 67 IS 1-2 BP 75 EP 82 DI 10.1016/0378-5955(93)90234-R PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700009 PM 8340280 ER PT J AU IGARASHI, Y KAWAMATA, S MIZUKOSHI, K AF IGARASHI, Y KAWAMATA, S MIZUKOSHI, K TI GLYCOCONJUGATES IN THE VESTIBULAR ORGANS AS REVEALED BY THE SILVER METHENAMINE METHOD SO HEARING RESEARCH LA English DT Article DE GLYCOCONJUGATES; OTOLITHIC ORGANS; INNER EAR; OTOCONIA; SILVER METHENAMINE; PERIODIC ACID-SCHIFF STAINING ID GELATINOUS MEMBRANES; GUINEA-PIG; INNER-EAR; OTOLITH; CALCIUM; RAT; MANGANESE; MICE AB The glycoconjugates in the vestibular organs of the guinea pig were studied after staining by the silver methenamine method and by the periodic acid-Schiff (PAS) reaction. The organic matrix of otoconia, otolithic membranes and cupulae were stained to the same degree by the PAS reaction. In contrast, the mineralizing and non-mineralizing matrices were clearly distinguished by the silver methenamine method. The otoconia were surrounded by an intensely stained organic matrix, while the otolithic membranes and cupulae were moderately stained. This histochemical difference suggests that the positively stained organic matrix of otoconia is not identical to the otolithic membranes and cupulae in terms of its biochemical composition. The strongly stained material may play an important role in turnover of calcium in otoconia. The contact areas between type I hair cell and nerve calyx were contained silver methenamine-positive material which is probably involved in adhesion of these cell membranes. C1 TOYAMA MED & PHARMACEUT UNIV,DEPT ANAT,2630 SUGITANI,TOYAMA,TOYAMA 93001,JAPAN. TOYAMA MED & PHARMACEUT UNIV,DEPT OTORHINOLARYNGOL & ANAT,TOYAMA,TOYAMA 93001,JAPAN. CR BELANGER LF, 1960, CALCIFICATION BIOL S, P151 Endo S, 1991, Acta Otolaryngol Suppl, V481, P116 ERWAY L, 1970, J NUTR, V100, P643 FERMIN CD, 1990, ACTA ANAT, V138, P75 GILLOYZAGA P, 1985, HEARING RES, V18, P269, DOI 10.1016/0378-5955(85)90043-7 GULLEY RL, 1979, J NEUROCYTOL, V8, P591, DOI 10.1007/BF01208511 HAMILTON DW, 1968, J ULTRA MOL STRUCT R, V23, P98, DOI 10.1016/S0022-5320(68)80034-6 IGARASHI M, 1969, ACTA OTO-LARYNGOL, V68, P420, DOI 10.3109/00016486909121580 KAWAMATA S, 1991, ARCH HISTOL CYTOL, V54, P173, DOI 10.1679/aohc.54.173 KAWAMATA S, 1990, ARCH HISTOL CYTOL, V53, P397, DOI 10.1679/aohc.53.397 KAWAMATA S, 1993, HEAR RES, V67 Lim DJ, 1984, ULTRASTRUCTURAL ATLA, P245 MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 NAKAHARA H, 1979, ANAT REC, V193, P233, DOI 10.1002/ar.1091930205 PURICHIA N, 1972, DEV BIOL, V27, P395, DOI 10.1016/0012-1606(72)90178-9 Rambourg A, 1971, Int Rev Cytol, V31, P57 RAMBOURG A, 1967, J HISTOCHEM CYTOCHEM, V15, P409 ROSS MD, 1975, ANN OTO RHINOL LARYN, V84, P22 SALAMAT MS, 1980, ANN OTO RHINOL LARYN, V89, P229 SCARFONE E, 1991, CELL TISSUE RES, V266, P51, DOI 10.1007/BF00678710 SUGIYAMA S, 1991, HEARING RES, V55, P263, DOI 10.1016/0378-5955(91)90111-L SUZUKI H, 1992, HEARING RES, V60, P45, DOI 10.1016/0378-5955(92)90057-T TACHIBANA M, 1987, ARCH OTO-RHINO-LARYN, V244, P112, DOI 10.1007/BF00458560 VANHEYNI.HE, 1965, J HISTOCHEM CYTOCHEM, V13, P286 VEENHOF BV, 1969, DEV STATOCONIA MICE WISLOCKI GB, 1955, J ANAT, V89, P3 NR 26 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 MAY PY 1993 VL 67 IS 1-2 BP 83 EP 88 DI 10.1016/0378-5955(93)90235-S PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700010 PM 8340281 ER PT J AU SAMS, M HAMALAINEN, M HARI, R MCEVOY, L AF SAMS, M HAMALAINEN, M HARI, R MCEVOY, L TI HUMAN AUDITORY CORTICAL MECHANISMS OF SOUND LATERALIZATION .1. INTERAURAL TIME DIFFERENCES WITHIN SOUND SO HEARING RESEARCH LA English DT Article DE DIRECTIONAL HEARING; MAGNETOENCEPHALOGRAPHY; EVOKED RESPONSES; AUDITION; INTERAURAL TIME DIFFERENCE; AUDITORY SPACE ID HUMAN EVOKED-POTENTIALS; MAGNETIC-FIELDS; HUMAN-BRAIN; LOCALIZATION; CORTEX; RESPONSES; FREQUENCY; NOISE; STIMULI; NEURONS AB Neuromagnetic responses to 600-ms binaural click trains, presented once every 1.1 s, were recorded with a 24-channel gradiometer from 6 healthy humans. During the first 300 ms, the left-ear stimulus led the right by 0.7 ms and the sound was lateralized to the left ear. At 300 ms, the interaural time difference (ITD) changed and the lateralization moved to one of 5 different locations between the ears. An N100m response peaked about 110 ms after the sound onset and an N130m(c) response (c to stress a response to the change) about 135 ms after the ITD change. The source locations of N100m and N130m(c) agreed with activity in the supratemporal auditory cortex; this was confirmed in one subject by superimposing MEG results on MR images. The sources of N100m and N130m(c) did not differ statistically significantly from each other, nor were there differences in N130m(c) sources to various lateralization changes. N130m(c) grew larger when the ITD change increased, in parallel with the increase in the change of the perceived location. We suggest that N130m(c) is analogous to N100m, but is delayed due to postmasking induced by the early part of the sound. RP SAMS, M (reprint author), HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. RI Hamalainen, Matti/C-8507-2013; Hari, Riitta/J-1880-2012; Sams, Mikko/G-7060-2012 OI Hari, Riitta/0000-0002-3142-2703; CR AHONEN AI, 1991, IEEE T MAGN, V27, P2786, DOI 10.1109/20.133789 AITKIN L, 1969, AUDITORY CORTEX, V32, P1005 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 CARR CE, 1990, J NEUROSCI, V10, P3227 ELBERLING C, 1980, SCAND AUDIOL, V9, P185, DOI 10.3109/01050398009076353 HALLIDAY R, 1978, ELECTROEN CLIN NEURO, V45, P118, DOI 10.1016/0013-4694(78)90350-4 HARI R, 1980, EXP BRAIN RES, V40, P237 HARI R, 1989, SCIENCE, V244, P432, DOI 10.1126/science.2655083 HARI R, 1992, ELECTROEN CLIN NEURO, V82, P152, DOI 10.1016/0013-4694(92)90159-F Hari R., 1990, AUDITORY EVOKED MAGN, P222 Irvine DR, 1986, AUDITORY BRAINSTEM JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 JONES SJ, 1991, ELECTROEN CLIN NEURO, V80, P146, DOI 10.1016/0168-5597(91)90152-N JONES SJ, 1992, ELECTROEN CLIN NEURO, V84, P149, DOI 10.1016/0168-5597(92)90019-8 KAUKORANTA E, 1986, EXP BRAIN RES, V63, P60 KNUDSEN EI, 1978, J NEUROPHYSIOL, V41, P870 LOVELESS N, 1989, ELECTROEN CLIN NEURO, V74, P217, DOI 10.1016/0013-4694(89)90008-4 MAKELA JP, 1987, ELECTROEN CLIN NEURO, V69, P422 MAKELA JP, 1992, NEUROREPORT, V3, P94 MCEVOY L, 1993, HEARING RES, V67, P98, DOI 10.1016/0378-5955(93)90237-U MCEVOY LK, 1990, AUDIOLOGY, V29, P163 MCEVOY LK, 1991, EAR HEARING, V12, P389, DOI 10.1097/00003446-199112000-00003 MCEVOY LK, 1991, AUDIOLOGY, V30, P286 MIDDLEBROOKS JC, 1991, ANNU REV PSYCHOL, V42, P135, DOI 10.1146/annurev.ps.42.020191.001031 MIDDLEBROOKS JC, 1988, AUDITORY FUNCTION NE, P431 NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x NAATANEN R, 1988, ELECTROEN CLIN NEURO, V69, P523, DOI 10.1016/0013-4694(88)90164-2 ORMAN SS, 1984, J NEUROPHYSIOL, P1028 REALE RA, 1990, J NEUROPHYSIOL, V64, P1247 SAMS M, 1985, ELECTROEN CLIN NEURO, V62, P437, DOI 10.1016/0168-5597(85)90054-1 SAMS M, 1991, PSYCHOPHYSIOLOGY, V28, P21, DOI 10.1111/j.1469-8986.1991.tb03382.x SANCHEZLONGO LP, 1958, NEUROLOGY, V8, P119 SANCHEZLONGO LP, 1957, NEUROLOGY, V7, P665 Scherg M, 1989, J Cogn Neurosci, V1, P336, DOI 10.1162/jocn.1989.1.4.336 SUGA N, 1979, SCIENCE, V203, P270, DOI 10.1126/science.760193 UNGAN P, 1989, ELECTROEN CLIN NEURO, V73, P306, DOI 10.1016/0013-4694(89)90109-0 WALSH EG, 1957, BRAIN, V80, P222, DOI 10.1093/brain/80.2.222 Yin T. C. T., 1988, AUDITORY FUNCTION, P385 Zwicker E., 1990, PSYCHOACOUSTICS NR 41 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 MAY PY 1993 VL 67 IS 1-2 BP 89 EP 97 DI 10.1016/0378-5955(93)90236-T PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700011 PM 8340282 ER PT J AU MCEVOY, L HARI, R IMADA, T SAMS, M AF MCEVOY, L HARI, R IMADA, T SAMS, M TI HUMAN AUDITORY CORTICAL MECHANISMS OF SOUND LATERALIZATION .2. INTERAURAL TIME DIFFERENCES AT SOUND ONSET SO HEARING RESEARCH LA English DT Article DE MAGNETOENCEPHALOGRAPHY; EVOKED RESPONSES; AUDITORY CORTEX; INTERAURAL TIME DIFFERENCE; AUDITORY SPACE ID EVENT-RELATED POTENTIALS; MAGNETIC-FIELDS; HUMAN-BRAIN; NEUROMAGNETIC RESPONSES; SUPERIOR COLLICULUS; MUSTACHE BAT; CORTEX; FREQUENCY; LOCATION; STIMULI AB Neuromagnetic responses were recorded over the right temporal cortex using a 24-channel gradiometer. Stimuli were binaural click trains, presented with six separate interaural time differences (ITDs). N100m to sound onset was larger and earlier for stimuli presented with left- than with right-leading ITDs. With stimulus lateralization taken into account, monaural and binaural stimuli evoked responses of roughly equal amplitude. In selective adaptation and oddball experiments, stimuli presented with different ITDs excited overlapping neuronal populations, but the amount of overlap decreased as the ITD between the stimuli increased. There were no systematic differences in the cortical source locations of the N100m as a function of ITD, however. Thus it appears that ITD-sensitive neurons in the human auditory cortex are not organized into a large-scale, orderly representation, which could be resolved by MEG. C1 HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. RI Hari, Riitta/J-1880-2012; Sams, Mikko/G-7060-2012 OI Hari, Riitta/0000-0002-3142-2703; CR AHISSAR M, 1992, J NEUROPHYSIOL, V67, P203 BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BUTLER RA, 1972, NEUROPSYCHOLOGIA, V10, P219, DOI 10.1016/0028-3932(72)90063-2 ELBERLING C, 1980, SCAND AUDIOL, V9, P185, DOI 10.3109/01050398009076353 HARI R, 1980, EXP BRAIN RES, V40, P237 HARI R, 1992, ELECTROEN CLIN NEURO, V82, P152, DOI 10.1016/0013-4694(92)90159-F Hari R., 1990, AUDITORY EVOKED MAGN, P222 HARI R, 1988, EXP BRAIN RES, V71, P87 HARI R, 1984, NEUROSCI LETT, V50, P127, DOI 10.1016/0304-3940(84)90474-9 Ilmoniemi R J, 1991, Acta Otolaryngol Suppl, V491, P80 JAY MF, 1984, NATURE, V309, P345, DOI 10.1038/309345a0 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 KARMOS G, 1993, NEW DEVELOPMENTS IN EVENT-RELATED POTENTIALS, P95 KAUKORANTA E, 1989, HEARING RES, V41, P15, DOI 10.1016/0378-5955(89)90174-3 KNUDSEN EI, 1978, J NEUROPHYSIOL, V41, P870 LEVANEN S, UNPUB RESPONSES HUMA LOUNASMAA OV, 1989, EUROPHYS LETT, V9, P603, DOI 10.1209/0295-5075/9/6/019 MAKELA JP, 1988, PFLUG ARCH EUR J PHY, V412, P12 MIDDLEBROOKS JC, 1984, J NEUROSCI, V4, P2621 NAATANEN R, 1989, NEUROSCI LETT, V107, P237 NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x NAATANEN R, 1988, ELECTROEN CLIN NEURO, V69, P523, DOI 10.1016/0013-4694(88)90164-2 NAATANEN R, 1978, ACTA PSYCHOL, V42, P313, DOI 10.1016/0001-6918(78)90006-9 NAATANEN R, 1980, ACTA PSYCHOL, V44, P31, DOI 10.1016/0001-6918(80)90073-6 NAATANEN R, 1989, NEUROSCI LETT, V98, P217, DOI 10.1016/0304-3940(89)90513-2 NAATANEN R, 1990, BEHAV BRAIN SCI, V13, P201 PAAVILAINEN P, 1989, ELECTROEN CLIN NEURO, V73, P129, DOI 10.1016/0013-4694(89)90192-2 PANTEV C, 1986, AUDIOLOGY, V25, P54 RAJAN R, 1990, J NEUROPHYSIOL, V64, P888 REALE RA, 1990, J NEUROPHYSIOL, V64, P1247 REITE M, 1981, ELECTROEN CLIN NEURO, V51, P388, DOI 10.1016/0013-4694(81)90102-4 SAMS M, 1985, ELECTROEN CLIN NEURO, V61, P254, DOI 10.1016/0013-4694(85)91092-2 SAMS M, 1993, HEARING RES, V67, P89, DOI 10.1016/0378-5955(93)90236-T SAMS M, 1991, PSYCHOPHYSIOLOGY, V28, P21, DOI 10.1111/j.1469-8986.1991.tb03382.x SUGA N, 1979, SCIENCE, V203, P270, DOI 10.1126/science.760193 SUGA N, 1977, SCIENCE, V196, P64, DOI 10.1126/science.190681 TIIHONEN J, 1989, AUDIOLOGY, V28, P37 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 MAY PY 1993 VL 67 IS 1-2 BP 98 EP 109 DI 10.1016/0378-5955(93)90237-U PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700012 PM 8340283 ER PT J AU GRIGUER, C LEHOUELLEUR, J VALAT, J SAHUQUET, A SANS, A AF GRIGUER, C LEHOUELLEUR, J VALAT, J SAHUQUET, A SANS, A TI VOLTAGE-DEPENDENT REVERSIBLE MOVEMENTS OF THE APEX IN ISOLATED GUINEA-PIG VESTIBULAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE ISOLATED TYPE-I VESTIBULAR HAIR CELLS; REVERSIBLE MOTILE RESPONSES; MEMBRANE DEPOLARIZATION; GUINEA-PIG ID MECHANOELECTRICAL TRANSDUCTION; MOTILE RESPONSES; SENSORY CELLS; HUMAN FETUSES; ADAPTATION; LOCALIZATION; RECEPTORS; CHANNELS; BUNDLES AB Type I vestibular hair cells isolated from guinea pig were placed in the whole cell clamp configuration, and electrically stimulated by depolarizing voltage pulses. The voltage dependent reversible movements of the cell apex affected the length of the cell neck, the position of the cuticular plate, and the tilting and bending of the stereocilia. The cell neck shortened when the membrane was depolarized by 10 mV while cuticular plate and the stereocilia tilting did not begin until 20 mV. The shortening was 0.5 to 1 mum, and the cuticular plate tilting was up to 15-degrees for depolarization amplitudes of 20-40 mV. These movements were reversed within a few seconds. More complex, larger movements were induced by stronger depolarizations. The cuticular plate tilting and the hair bundle bending were always in the opposite direction to the kinocilium position. The small reversible movements of the mammalian type I vestibular hair cells are discussed in terms of mechanical adaptation processes and morphological features. It is suggested that such active movements of the vestibular hair cells occur in vivo. C1 UNIV MONTPELLIER 2,INSERM,U254,NEUROPHYSIOL CELLULAIRE & SENSORIELLE LABS,F-34060 MONTPELLIER,FRANCE. INSERM,CTR PHARMACOL ENDOCRINOL,CNRS,F-34100 MONTPELLIER,FRANCE. CR ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 CHENEY R E, 1992, Current Opinion in Cell Biology, V4, P27, DOI 10.1016/0955-0674(92)90055-H COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 EATOCK RA, 1987, J NEUROSCI, V7, P2821 FAVRE D, 1984, J NEUROSCI RES, V11, P293, DOI 10.1002/jnr.490110309 FAVRE D, 1979, ACTA OTO-LARYNGOL, V87, P97, DOI 10.3109/00016487909126393 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 GRIGUER C, 1993, PFLUG ARCH EUR J PHY, V422, P407, DOI 10.1007/BF00374300 HACOHEN N, 1989, J NEUROSCI, V9, P3988 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 LAPEYRE PNM, 1991, VESTIBULAR RES, V1, P241 MBIENE JP, 1986, J COMP NEUROL, V254, P271, DOI 10.1002/cne.902540210 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 RUSCH A, 1990, HEARING RES, V48, P247, DOI 10.1016/0378-5955(90)90065-W SANS A, 1989, HEARING RES, V40, P117, DOI 10.1016/0378-5955(89)90105-6 SANS A, 1989, ANAT EMBRYOL, V179, P457, DOI 10.1007/BF00319588 SCARFONE E, 1988, J NEUROSCI, V8, P4640 VALAT J, 1991, NEUROSCI LETT, V127, P231, DOI 10.1016/0304-3940(91)90801-Y ZENNER HP, 1991, ACTA OTO-LARYNGOL, V111, P291, DOI 10.3109/00016489109137390 ZENNER HP, 1990, HEARING RES, V50, P289, DOI 10.1016/0378-5955(90)90052-Q NR 23 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 MAY PY 1993 VL 67 IS 1-2 BP 110 EP 116 DI 10.1016/0378-5955(93)90238-V PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700013 PM 8340261 ER PT J AU BURNS, EM HARRISON, WA BULEN, JC KEEFE, DH AF BURNS, EM HARRISON, WA BULEN, JC KEEFE, DH TI VOLUNTARY CONTRACTION OF MIDDLE-EAR MUSCLES - EFFECTS ON INPUT IMPEDANCE, ENERGY REFLECTANCE AND SPONTANEOUS OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE MIDDLE EAR MUSCLES; OTOACOUSTIC EMISSIONS ID COCHLEAR MICROMECHANICAL PROPERTIES; OTO-ACOUSTIC EMISSIONS; STIMULATION; REFLEX AB Two types of measurements were performed on a subject able to voluntarily contract her middle ear muscles (MEM). First, wideband measurements (0-11 kHz) of middle ear input impedance and energy reflectance were obtained when the subject was relaxed and when she contracted her MEM. The changes in impedance observed with voluntary MEM contraction were similar to those reported in the literature for acoustically-elicited MEM contractions. The energy reflectance increased for frequencies below about 4 kHz. Second, the effects of voluntary MEM contraction on the frequencies and levels of spontaneous otoacoustic emissions (SOAEs) were measured and compared to effects evoked by contralateral acoustic stimulation. Effects on SOAEs appear to be a more sensitive indicator of MEM activity than changes in impedance, and the effects due to voluntary MEM contraction were qualitatively similar to those evoked by contralateral acoustic stimulation. These results suggest that in subjects with normally-functioning middle ears, only some effects on otoacoustic emissions caused by contralateral stimuli whose levels are below the contralateral acoustic reflex threshold can be unequivocally attributed to the action of cochlear efferents. The temporal aspects of SOAE frequency shifts caused by voluntary contraction of MEM show that voluntary contraction fatigues rapidly over a time period of tens of seconds. C1 UNIV WASHINGTON,SCH MUS,SEATTLE,WA 98195. RP BURNS, EM (reprint author), UNIV WASHINGTON,DEPT SPEECH & HEARING SCI,1417 NE 42ND ST,SEATTLE,WA 98195, USA. CR Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 BROWN SE, 1990, ABSTR ASS RES OT, V13, P230 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1992, AUDIOLOGY, V31, P1 DJUPESLAND G, 1984, ADV REFLEX CONSIDERA, P85 FLEER R, 1963, MIDDLE EAR FUNCTION GALAMBOS R, 1959, J ACOUST SOC AM, V31, P349, DOI 10.1121/1.1907723 GROSE JH, 1983, J ACOUST SOC AM S1, V74, P538 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 HARRISON WA, 1993, IN PRESS J ACOUST SO JEPSEN O, 1963, MODERN DEV AUDIOLOGY, P194 JEPSON O, 1955, THESIS U AARITUS DEN KEEFE DH, 1992, J ACOUST SOC AM, V91, P470, DOI 10.1121/1.402733 Kemp D T, 1981, Ciba Found Symp, V85, P54 LONG GR, 1989, ABSTR ASS RES OT, P228 METZ OTTO, 1951, ACTA OTO LARYNGOL, V39, P397, DOI 10.3109/00016485109119270 MOLLER A, 1961, 18 ROY I TECHN SPEEC MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1992, ACTA OTO-LARYNGOL, V112, P210 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Rabinowitz WM, 1977, THESIS MIT CAMBRIDGE RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 REGER S N, 1960, Ann Otol Rhinol Laryngol, V69, P1179 REGER SN, 1963, 576 US ARM MED RES L SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SEIGEL JH, 1982, HEARING RES, V6, P171 SIMMONS F. B., 1959, ANN OTOL RHINOL AND LARYNGOL, V68, P1126 Smith HD, 1943, ARCHIV OTOLARYNGOL, V38, P369 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V WHITHEAD ML, 1989, THESIS U KEELE Wilson J P, 1986, Scand Audiol Suppl, V25, P109 Wilson J P, 1981, Ciba Found Symp, V85, P82 ZITO F, 1980, AUDIOLOGY, V19, P395 1969, SPECIFICATIONS AUDIO NR 35 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 MAY PY 1993 VL 67 IS 1-2 BP 117 EP 127 DI 10.1016/0378-5955(93)90239-W PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700014 PM 8340262 ER PT J AU BARTSCH, E SCHMIDT, S AF BARTSCH, E SCHMIDT, S TI PSYCHOPHYSICAL FREQUENCY-MODULATION THRESHOLDS IN A FM-BAT, TADARIDA-BRASILIENSIS SO HEARING RESEARCH LA English DT Article DE FREQUENCY MODULATION THRESHOLDS; BAT; PSYCHOPHYSICS; FLUTTERING TARGET DISCRIMINATION ID GREATER HORSESHOE BATS; INFERIOR COLLICULUS; ECHOLOCATING BATS; CONSTANT-FREQUENCY; DISCRIMINATION; REPRESENTATION; RESPONSES; PATTERNS; INSECTS; SOUNDS AB Echolocating bats hunting flying insects discriminate complex temporal patterns of acoustic stimuli. For bats using frequency modulated sonar calls (FM bats), there are no behavioral data on the perception of sinusoidally frequency modulated (SFM) stimuli. Discrimination performance for SFM stimuli of varying modulation depth was measured in 4 Tadarida brasiliensis in a two-alternative, forced choice procedure. A center frequency of 40 kHz was modulated with rates between 10 and 2000 Hz. It was found that discrimination performance improved from a mean threshold modulation depth of 3.05 kHz at a modulation rate of 2000 Hz to 1.58 kHz at a modulation rate of 10 Hz. Psychoacoustical modulation depth thresholds of T. brasiliensis are thus distinctly larger than those observed in bat species emitting constant frequency (CF) components followed by an FM-sweep, in active echolocation experiments. The modulation thresholds of T brasiliensis are discussed in connection with the ability of bats to discriminate insect wingbeats. A comparison between non-echolocating mammals and the FM bat T brasiliensis shows that the ability to echolocate is not reflected in the modulation thresholds. C1 UNIV MUNICH,INST ZOOL,LUISENSTR 14,W-8000 MUNICH 2,GERMANY. CR AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 BODENHAMER RD, 1981, HEARING RES, V5, P317, DOI 10.1016/0378-5955(81)90055-1 EHRET G, 1985, J COMP PHYSIOL A, V156, P619, DOI 10.1007/BF00619111 EHRET G, 1985, SCIENCE, V227, P1245, DOI 10.1126/science.3975613 EHRET G, 1975, J COMP PHYSIOL, V102, P321 ELLIOTT DN, 1960, J ACOUST SOC AM, V32, P380, DOI 10.1121/1.1908071 FAY RR, 1988, HEARING VERTEBRATES, P451 Finney D. J., 1971, PROBIT ANAL, V3rd GOLDMAN LJ, 1977, BEHAV ECOL SOCIOBIOL, V2, P411, DOI 10.1007/BF00299509 HEFFNER HE, 1969, J AUD RES, V9, P12 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 HEILMANNRUDOLF U, 1984, THESIS EBERHARD KARL HENSON OW, 1970, BIOL BATS, P181 KELLY JB, 1970, THESIS VANDERBILT U, V70, P429 KOBER R, 1990, J ACOUST SOC AM, V87, P882, DOI 10.1121/1.398898 KOLLER S, 1967, TAFELN BEURTEILUNG H LANGEMANN U, 1991, THESIS I ZOOLOGIE TU LONG GR, 1983, J ACOUST SOC AM, V75, P184 NEUWEILER G, 1990, PHYSIOL REV, V70, P615 NEUWEILER G, 1984, NATURWISSENSCHAFTEN, V71, P446, DOI 10.1007/BF00455897 NITSCHE V, 1987, THESIS TU MUNCHEN POLLAK GD, 1978, J NEUROPHYSIOL, V41, P677 POLLAK GD, 1981, J NEUROPHYSIOL, V46, P605 RAVIZZA RJ, 1969, J AUD RES, V9, P1 RAVIZZA RJ, 1969, J AUD RES, V9, P8 ROVERUD RC, 1991, J COMP PHYSIOL A, V168, P259 SACHS L, 1978, STATISTISCHE AUSWERT SCHMIDT S, 1990, BRAIN PERCEPTION COG, P146 Schnitzler H.-U., 1983, P235 Schnitzler H. U., 1980, ANIMAL SONAR SYSTEMS, P109, DOI 10.1007/978-1-4684-7254-7_6 SCHNITZL.HU, 1968, Z VERGL PHYSIOL, V57, P376, DOI 10.1007/BF00303062 SCHNITZLER HU, 1983, J COMP PHYSIOL A, P385 SCHORER E, 1989, ACUSTICA, V68, P183 SCHULLER G, 1979, J COMP PHYSIOL, V132, P47 SIEFER W, 1990, THESIS LUDWIG MAXIMI SIMMONS JA, 1978, J COMP PHYSL, V3125, P291 Suga N., 1973, BASIC MECH HEARING, P675 SUM YW, 1988, J COMP PHYSIOL A, V163, P349, DOI 10.1007/BF00604010 VATER M, 1979, J COMP PHYSIOL, V131, P137 VONDEREMDE G, 1986, J COMP PHYSIOL A, V159, P765 VONDEREMDE G, 1990, J COMP PHYSIOL A, V167, P423 VONDEREMDE G, 1989, J COMP PHYSIOL A, V164, P663 ZOFEL P, 1988, STATISTIK PRAXIS Zwicker E., 1990, PSYCHOACOUSTICS FACT NR 44 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 MAY PY 1993 VL 67 IS 1-2 BP 128 EP 138 DI 10.1016/0378-5955(93)90240-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700015 PM 8340263 ER PT J AU AVINASH, GB NUTTALL, AL RAPHAEL, Y AF AVINASH, GB NUTTALL, AL RAPHAEL, Y TI 3-D ANALYSIS OF F-ACTIN IN STEREOCILIA OF COCHLEAR HAIR-CELLS AFTER LOUD NOISE EXPOSURE SO HEARING RESEARCH LA English DT Article DE 3-D OPTICAL MICROSCOPY; IMAGE PROCESSING, F-ACTIN; STEREOCILIA; COCHLEAR HAIR CELL; LOUD NOISE ID SERIAL-SECTION RECONSTRUCTION; ULTRASTRUCTURAL-CHANGES; CUTICULAR PLATES; ACOUSTIC TRAUMA; CONSEQUENCES; FILAMENTS; INJURY AB Fluorescence microscopy can be a useful tool in the early detection of pathological changes in the stereocilia of outer hair cells which have undergone acoustic overstimulation. Fluorescent phalloidin, a highly specific F-actin stain, can be used to label F-actin in stereocilia. In this study, phalloidin label is used to determine quantitative changes of F-actin in the stereocilia of guinea pigs exposed to loud noise (117 dB; octave band noise, centered at 1 kHz; 4 h). Reliably determining three-dimensional (3-D) structural changes in stereocilia is a challenging problem in optical microscopy since stereocilia diameter is close to the optical resolution limit. In order to alleviate the problem, a computational 3-D microscopy technique is used (Avinash et al., 1992). Whole-mounts of the cochlear second and third turns were examined in a Leitz Orthoplan microscope through a Leitz Plan Apo objective lens (100 X; 1.32 N.A.; 170/0.17). Images were acquired with a charge-coupled device camera where the focus was shifted in 0.2 mum steps using a piezoelectric translator. Images were processed with the appropriate point spread function of the optical system. Analysis of control cochleas indicate that our technique can resolve single stereocilia and distinguish between various intensities of label along each stereocilia. In noise-exposed cochleas, our data show length and intensity changes in the phalloidin label. These results suggest that both depolymerization and polymerization of F-actin can occur in stereocilia of outer hair cells after acoustic overstimulation. Our findings demonstrate the applicability of computational 3-D microscopy to quantitative and qualitative analysis of stereocilia. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. CR AVINASH G, 1993, IN PRESS IEEE T MED CANLON B, 1989, ABSTR ASS RES OT ENGSTROM B, 1983, HEARING RES, V12, P251, DOI 10.1016/0378-5955(83)90110-7 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 HIRAOKA Y, 1987, SCIENCE, V238, P36, DOI 10.1126/science.3116667 KORN ED, 1987, SCIENCE, V238, P638, DOI 10.1126/science.3672117 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 RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 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 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 NR 13 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 MAY PY 1993 VL 67 IS 1-2 BP 139 EP 146 DI 10.1016/0378-5955(93)90241-R PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700016 PM 8340265 ER PT J AU FITZGERALD, JJ ROBERTSON, D JOHNSTONE, BM AF FITZGERALD, JJ ROBERTSON, D JOHNSTONE, BM TI EFFECTS OF INTRA-COCHLEAR PERFUSION OF SALICYLATES ON COCHLEAR MICROPHONIC AND OTHER AUDITORY RESPONSES IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SALICYLATE; OTOTOXICITY; COCHLEAR MICROPHONIC; CAP, OLIVOCOCHLEAR ACTION, HEARING LOSS ID SPONTANEOUS OTOACOUSTIC EMISSIONS; CROSSED OLIVOCOCHLEAR BUNDLE; ELECTRICAL-STIMULATION; ASPIRIN; THRESHOLD; ORGAN; CORTI AB The ototoxic action of salicylate was investigated in the guinea pig by perfusion of both salicylate and bromosalicylate through scala tympani. The results qualitatively confirmed experiments using intravenous administration in cats (Stypulkowski, 1990), showing dose-dependent elevations in compound action potential (CAP) thresholds, increases in cochlear microphonics (CM) and level-dependent reductions in 2f1-f2 acoustic distortion products. The endocochlear potential was not significantly affected and iontophoretic injection of salicylate into scala media had no measurable effect on CAP thresholds, consistent with an action on the basolateral walls of the hair cells. Perfusion with indomethacin produced effects similar to those of the salicylates, but at non-physiological doses. Together with the great effectiveness of 5-bromosalicylate, this suggests that salicylate does not act by inhibiting prostaglandin synthesis. The results are qualitatively consistent with the proposition that salicylates act on the basolateral walls of the outer hair cells. However, the magnitude of the CM increases, particularly at high drug concentrations, and the fact that salicylate reduced, but did not eliminate the effects of olivocochlear efferent stimulation on CM amplitude indicate that a simple explanation for salicylate effects based solely on a conductance increase in the outer hair cell membranes may be inadequate. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR ALTMAN RD, 1988, POSTGRAD MED, V84, P206 CRIFO S, 1975, J HISTOCHEM CYTOCHEM, V37, P27 DALLOS P, 1983, HEARING RES, V12, P89, DOI 10.1016/0378-5955(83)90120-X DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 ESCOUBET B, 1985, PROSTAGLANDINS, V29, P589 FERREIRA SH, 1971, NATURE-NEW BIOL, V231, P237 GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 HUMES JL, 1981, P NATL ACAD SCI-BIOL, V78, P2053, DOI 10.1073/pnas.78.4.2053 HUY PTB, 1987, ACTA OTO-LARYNGOL, V103, P558 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 KAWATA R, 1988, PROSTAGLANDINS, V35, P173, DOI 10.1016/0090-6980(88)90085-8 KLINKE R, 1974, PHYSIOL REV, V54, P316 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E MCCABE PA, 1965, ANN OTO RHINOL LARYN, V74, P312 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 PATUZZI R, 1990, HEARING RES, V45, P15, DOI 10.1016/0378-5955(90)90179-S PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 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 PENNER MJ, 1989, ARCH OTOLARYNGOL, V115, P871 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 NETO FR, 1980, EUR J PHARMACOL, V68, P155, DOI 10.1016/0014-2999(80)90316-7 SHEHATA WE, 1990, 13TH MIDW M ASS RES, P252 SILVERST.H, 1967, ANN OTO RHINOL LARYN, V76, P118 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E VARGAFTIG BB, 1977, EUR J PHARMACOL, V43, P125, DOI 10.1016/0014-2999(77)90125-X WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 NR 32 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 MAY PY 1993 VL 67 IS 1-2 BP 147 EP 156 DI 10.1016/0378-5955(93)90242-S PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700017 PM 8340266 ER PT J AU LYON, MJ WANAMAKER, HH AF LYON, MJ WANAMAKER, HH TI BLOOD-FLOW AND ASSESSMENT OF CAPILLARIES IN THE AGING RAT POSTERIOR CANAL CRISTA SO HEARING RESEARCH LA English DT Article DE VESTIBULAR; AGING; BLOOD FLOW; MICROCIRCULATION; STEREOLOGY; RAT ID SURFACE-AREA; INNER-EAR; PATHOLOGICAL RESEARCH; VESTIBULAR APPARATUS; VASCULAR MECHANISMS; MICROSPHERE METHOD; VERTICAL SECTIONS; MENIERES-DISEASE; NERVOUS-SYSTEM; GUINEA-PIG AB Vascular change has been proposed as an etiological factor in inner ear aging and in several inner ear disorders. Moreover, some successful medical management of the episodic vertigo and tinnitus associated with Meniere's disease has been directed toward pharmacologically increasing blood flow, changing vascular permeability or ion homeostasis. While there are many studies of cochlear capillary morphology and blood flow, there are very few examining these variables in the vestibular system and none with respect to aging. The purpose of this study was to examine the rat posterior canal ampullary crista for age-related changes in blood flow and capillary morphology. By combining stereological techniques with microsphere injection, we have determined that in the rat posterior canal crista there is a statistically significant age-related decrease in blood flow (75%), mean capillary diameter (31%), and volume fraction of capillary lumen (31%). There is also an overall 18% decrease in the volume of the ampullary crista, a 72% decrease in blood flow/unit volume and a 36% increase in capillary length/unit volume. There were no significant changes in the capillary surface area/unit volume, the absolute capillary length, or the absolute capillary surface area. These data suggest impaired blood flow and degenerative loss of the ampullary crista may be relate to impaired end organ function. C1 SUNY,HLTH SCI CTR SYRACUSE,DEPT ANAT & CELL BIOL,SYRACUSE,NY 13210. RP LYON, MJ (reprint author), SUNY,HLTH SCI CTR SYRACUSE,DEPT OTOLARYNGOL & COMMUN SCI,ROOM 156 WEISKOTTEN HALL,750 E ADAMS ST,SYRACUSE,NY 13210, USA. CR ANGELBORG C, 1988, VERTIGO NAUSEA TINNI, P193 ANGELBORG C, 1985, ANN OTO RHINOL LARYN, V94, P181 Angelborg C, 1988, Adv Otorhinolaryngol, V42, P39 ANGELBORG C, 1984, ARCH OTOLARYNGOL, V110, P297 ANGELBORG C, 1985, J OTOLARYNGOL, V14, P41 ANGELBORG C, 1987, VESTIBULAR SYSTEM NE, P157 AXELSSON A, 1971, ACTA OTO-LARYNGOL, V72, P172, DOI 10.3109/00016487109122470 BADDELEY AJ, 1986, J MICROSC-OXFORD, V142, P259 COHEN GM, 1988, CRIT REV NEUROBIOL, V4, P179 DENSERT O, 1975, ACTA OTO-LARYNGOL, V79, P96, DOI 10.3109/00016487509124660 DIXON WJ, 1983, BMDP STATISTICAL SOF Fischer A J, 1991, Acta Otolaryngol Suppl, V479, P24 GRAD A, 1989, ARCH NEUROL-CHICAGO, V46, P282 GROSS PM, 1987, J CEREBR BLOOD F MET, V7, P154 GULYA AJ, 1990, CURRENT THERAPY OTOL, P4 GUNDERSEN HJG, 1988, APMIS, V96, P379 GUNDERSEN HJG, 1987, J MICROSC-OXFORD, V147, P229 GUNDERSEN HJG, 1986, J MICROSC-OXFORD, V143, P3 GUNDERSEN HJG, 1988, APMIS, V96, P857 GUSSEN R, 1983, OTOLARYNG HEAD NECK, V91, P68 GUSSEN R, 1982, ARCH OTOLARYNGOL, V108, P544 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 HORAK FB, 1989, NEUROBIOL AGING, V10, P727, DOI 10.1016/0197-4580(89)90010-9 HOZAWA K, 1989, ACTA OTO-LARYNGOL, V107, P171, DOI 10.3109/00016488909127496 HULTCRANTZ E, 1978, ORL J OTO-RHINO-LARY, V40, P65 HULTCRANTZ E, 1988, AM J OTOLARYNG, V9, P317, DOI 10.1016/S0196-0709(88)80039-5 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P364 KIMURA RS, 1986, AM J OTOLARYNG, V7, P130, DOI 10.1016/S0196-0709(86)80042-4 KOBAYASHI H, 1982, BRAIN RES, V244, P374, DOI 10.1016/0006-8993(82)90101-9 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 LARSEN HC, 1984, HEARING RES, V16, P127, DOI 10.1016/0378-5955(84)90002-9 LYON MJ, 1992, SOC NEUR ABSTR, V22, P1401 MICHEL RP, 1988, J MICROSC-OXFORD, V150, P117 MOORADIAN AD, 1991, NEUROCHEM RES, V16, P447, DOI 10.1007/BF00965565 NAKAI Y, 1990, MENIERES DIS, P35 NAKAI Y, 1986, SCAN ELECTRON MICROS, V2, P543 NAKASHIMA T, 1991, ACTA OTO-LARYNGOL, V111, P738, DOI 10.3109/00016489109138406 PARK JC, 1987, HEARING RES, V28, P87, DOI 10.1016/0378-5955(87)90156-0 PERLMAN H B, 1959, Laryngoscope, V69, P591 PRAZMA J, 1990, ARCH OTOLARYNGOL, V116, P932 RODGERS GK, 1986, ARCH OTOLARYNGOL, V112, P180 Schuknecht H. F., 1974, PATHOLOGY EAR SMITH CA, 1953, LARYNGOSCOPE, V63, P87 SMITH CA, 1972, VASCULAR DISORDERS H SOHMER H, 1986, ELECTROEN CLIN NEURO, V64, P334, DOI 10.1016/0013-4694(86)90157-4 SOHMER H, 1989, HEARING RES, V40, P87, DOI 10.1016/0378-5955(89)90102-0 SOKOLOFF L, 1977, J NEUROCHEM, V28, P897, DOI 10.1111/j.1471-4159.1977.tb10649.x SOKOLOFF L, 1981, FED PROC, V40, P2311 SPOENDLIN H, 1966, ACTA OTOLARYNGOL, V61, P432 TERAYAMA Y, 1973, ACTA OTO-LARYNGOL, V76, P244, DOI 10.3109/00016487309121505 TODA N, 1991, AM J PHYSIOL, V260, pH1443 VERICEL E, 1991, AGE, V14, P1, DOI 10.1007/BF02434840 WANAMAKER HH, 1990, OTOLARYNG HEAD NECK, V103, P586 NR 54 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 1993 VL 67 IS 1-2 BP 157 EP 165 DI 10.1016/0378-5955(93)90243-T PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700018 PM 8340267 ER PT J AU MOON, AK ZWOLAN, TA PFINGST, BE AF MOON, AK ZWOLAN, TA PFINGST, BE TI EFFECTS OF PHASE DURATION ON DETECTION OF ELECTRICAL-STIMULATION OF THE HUMAN COCHLEA SO HEARING RESEARCH LA English DT Article DE AUDITORY PROSTHESIS; ELECTRICAL STIMULATION; HUMAN; PSYCHOPHYSICS; DETECTION THRESHOLDS; PHASE DURATION ID TEMPORAL RESPONSE PATTERNS; AUDITORY-NERVE FIBERS; IMPLANT; PERFORMANCE; PREDICTORS; RECOGNITION; THRESHOLDS AB Detection thresholds for biphasic symmetric pulses were measured in fourteen human subjects implanted with the Cochlear Corporation Nucleus 22 Implant. The effects of phase duration on thresholds were studied using single pulses, and 500 ms pulse trains at 100 pps. Psychophysical detection thresholds decreased as a function of phase duration with a change in slope at approximately 0.5 ms/phase. Mean single-pulse and pulse-train slopes were -3.60 and -4.25 dB/doubling of phase duration for pulse durations of less than about 0.5 ms/phase. For pulse durations greater than 0.5 ms/phase, mean slopes were -5.71 and -7.54 dB/doubling for single pulses and pulse trains, respectively. Thresholds for pulse trains decreased as a function of stimulus duration for durations up to at least 300 ms, with the rate of decrease being dependent on the phase duration of the pulse. Effects of stimulus duration were greater for longer phase duration signals. We hypothesize that the longer phase duration pulses activate multiple spikes in a single fiber and/or more effective patterns of spikes across fibers, which may explain why slopes of psychophysical threshold functions are steeper than those of functions for single auditory nerve fibers for longer duration pulses. Thresholds were compared to respective speech perception scores (CID sentences) since thresholds for long phase duration signals have been shown previously to be correlated with nerve survival patterns, and nerve survival patterns may affect speech perception. Correlation coefficients ranged from -0.59 to -0.81, depending on stimulus parameters and subject selection. C1 UNIV MICHIGAN,MED CTR,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,1301 E ANN ST,BOX 0506,ANN ARBOR,MI 48109. CR BLANEY PJ, 1992, ANN OTO RHINOL LARYN, V101, P342 CARHART R, 1959, J SPEECH HEAR DISORD, V24, P220 Clark G., 1987, ADV OTORHINOLARYNGOL, V38, P1 FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 Hill AV, 1936, PROC R SOC SER B-BIO, V119, P440, DOI 10.1098/rspb.1936.0015 JAVEL E, 1987, ANN OTOL RHINOL LA S, V128, P26 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KILENY PR, 1991, ANN OTO RHINOL LARYN, V100, P563 KNUTSON JF, 1991, ANN OTO RHINOL LARYN, V100, P817 KUK FK, 1990, SCAND AUDIOL, V19, P139, DOI 10.3109/01050399009070765 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 PFINGST BE, 1985, HEARING RES, P305 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PFINGST BE, 1992, ABSTR ASS RES OT, P7 PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1988, HEARING RES, V34, P243, DOI 10.1016/0378-5955(88)90005-6 PFINGST BE, 1984, ABSTR ASS RES OTOLAR, P10 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 SHANNON RV, 1990, J ACOUST SOC AM, V87, P905, DOI 10.1121/1.398902 Shannon R.V, 1989, COCHLEAR IMPLANT MOD, P187 SKINNER MW, 1991, EAR HEARING, V12, P3, DOI 10.1097/00003446-199102000-00002 VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 NR 26 TC 48 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 MAY PY 1993 VL 67 IS 1-2 BP 166 EP 178 DI 10.1016/0378-5955(93)90244-U PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700019 PM 8340268 ER PT J AU DOI, T OHMORI, H AF DOI, T OHMORI, H TI ACETYLCHOLINE INCREASES INTRACELLULAR CA2+ CONCENTRATION AND HYPERPOLARIZES THE GUINEA-PIG OUTER HAIR CELL SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINE; HAIR CELL; POTASSIUM CONDUCTANCE; INTRACELLULAR CA2+ ID RECEPTOR; COCHLEA; CALCIUM; BUNDLE; CHICK; STIMULATION; CHANNELS; MEMBRANE; VOLTAGE; TURTLE AB Extracellularly applied acetylcholine (ACh) induced outward currents in isolated outer hair cells of a guinea-pig cochlea. The ACh induced current was carried by K+ ions. The current amplitude was ACh dose dependent with a K(D) of 12 muM. The ACh induced outward current was reversibly blocked by extracellularly applied atropine (1 muM), d-tubocurarine (d-TC, 1 muM), apamin (1 muM) and strychnine (0.1-10 muM). D-TC (10 muM) not only blocked the ACh induced outward current, but also reduced the amplitude of depolarization induced outward current. ACh induced a rise of intracellular Ca2+ concentration ([Ca2+]i). D-TC (10 muM) reduced but did not totally block the increase of [Ca2+]i. In a low Ca2+ (0.1 mM) extracellular medium, the amplitude of ACh induced current was reduced rapidly and was recovered gradually to the normal level after the extracellular Ca2+ concentration was resumed. It is probable that ACh hyperpolarizes the guinea-pig outer hair cell membrane by activation of a Ca2+-activated K+ conductance. C1 NATL INST PHYSIOL SCI,OKAZAKI,JAPAN. RP DOI, T (reprint author), KANSAI MED UNIV,DEPT OTOLARYNGOL,FUMIZONO CHO,MORIGUCHI,OSAKA 570,JAPAN. CR ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 ART JJ, 1984, J PHYSIOL-LONDON, V356, P525 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BAYLOR DA, 1970, J PHYSIOL-LONDON, V207, P77 BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BOBBIN RP, 1971, NATURE-NEW BIOL, V231, P222 BROWN D, 1987, J PHYSL, V397, P149 CHABALA LD, 1985, BIOPHYS J, V48, P241 CHURCHILL J. A., 1956, LARYNGOSCOPE, V66, P1 COOK NS, 1985, J PHYSIOL-LONDON, V358, P373 DOI T, 1991, JPN J PHYSL S, V41, P240 FEX J, 1968, HEARING MECHANISMS V, P169 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 FU T, 1988, BIOCHEM BIOPH RES CO, V157, P1429 FUCHS PA, 1992, J NEUROSCI, V12, P800 GUTH PS, 1976, PHARMACOL REV, V28, P95 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HELD H, 1926, HDB NORMALEN PATHOLO, V2, P467 HOUSLEY GD, 1991, 21ST ANN M SOC NEUR, P633 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 KAKEHATA S, 1993, IN PRESS J PHYSL KIMITSUKI T, 1992, J PHYSIOL-LONDON, V458, P27 KRISHTAL OA, 1980, NEUROSCIENCE, V5, P2325, DOI 10.1016/0306-4522(80)90149-9 MAGLEBY KL, 1972, J PHYSIOL-LONDON, V223, P151 OHMORI H, 1988, J PHYSIOL-LONDON, V399, P115 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 SHIGEMOTO T, 1991, J PHYSIOL-LONDON, V442, P669 SPOENDIN H, 1978, AUDIOLOGIA TONIATRIA, V1, P1 SUGAI T, 1992, HEARING RES, V61, P56, DOI 10.1016/0378-5955(92)90036-M NR 30 TC 69 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 MAY PY 1993 VL 67 IS 1-2 BP 179 EP 188 DI 10.1016/0378-5955(93)90245-V PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700020 PM 8340269 ER PT J AU POTE, KG ROSS, MD AF POTE, KG ROSS, MD TI UTRICULAR OTOCONIA OF SOME AMPHIBIANS HAVE CALCITIC MORPHOLOGY SO HEARING RESEARCH LA English DT Article DE INNER EAR; VESTIBULAR SYSTEM; SCANNING ELECTRON MICROSCOPY; OTOCONIA; CALCITE; AMPHIBIANS ID INNER-EAR; RAT; MICROSCOPY; STATOCONIA; CHICK AB This report concerns the morphological features of otoconia removed from the inner ear of four amphibian species. Results from scanning electron microscopic examination are compared based on the site of origin. These results show that utricular otoconia have a mineral structure that mimics calcite, rather than the widely accepted idea that they are mineralized by calcium carbonate of the aragonite polymorph. C1 NASA,AMES RES CTR,MOFFETT FIELD,CA 94035. RP POTE, KG (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT OTOLARYNGOL & COMMUN DISORDERS,300 LONGWOOD AVE,BOSTON,MA 02115, USA. CR Anniko M, 1980, Am J Otolaryngol, V1, P400, DOI 10.1016/S0196-0709(80)80021-4 ASHCROFT DW, 1934, J PHYSL, V81, P23 BALLARINO J, 1985, AM J ANAT, V174, P131, DOI 10.1002/aja.1001740204 BERRY LG, 1959, MINERALOGY BRANDENBERGER E, 1945, HELV MED ACTA S, V16, P1 BRESCHET G, 1938, RESCHERCHES ANATOMIQ CAMPOS A, 1984, ACTA OTO-LARYNGOL, V97, P475, DOI 10.3109/00016488409132924 CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 CIGES M, 1983, ACTA OTO-LARYNGOL, V95, P522, DOI 10.3109/00016488309139436 DEVINCENTIIS M, 1969, J EMBRYOL EXP MORPH, V15, P349 FERMIN CD, 1985, ACTA ANAT, V123, P148 Harada Y, 1973, Adv Otorhinolaryngol, V19, P50 HARADA Y, 1972, ACTA OTO-LARYNGOL, V73, P316, DOI 10.3109/00016487209138947 HENLE, 1966, HUMAN COMP HISTOLOGY, P86 IMOTO T, 1983, ACTA OTO-LARYNGOL, V96, P227, DOI 10.3109/00016488309132895 LEWIS ER, 1982, SCIENCE, V215, P1641, DOI 10.1126/science.6978525 LIM DJ, 1974, BRAIN BEHAV EVOLUT, V10, P37, DOI 10.1159/000124301 Lim D J, 1969, Acta Otolaryngol Suppl, V255, P1 Lindeman H H, 1973, Adv Otorhinolaryngol, V20, P405 Lippmann F., 1973, SEDIMENTARY CARBONAT LYON MF, 1955, J EMBRYOL EXP MORPH, V3, P213 MANN S, 1983, PROC R SOC SER B-BIO, V218, P415, DOI 10.1098/rspb.1983.0048 MARMO F, 1981, CELL TISSUE RES, V218, P265 MARMO F, 1983, CELL TISSUE RES, V233, P35 McNally WJ, 1925, AM J PHYSIOL, V75, P155 MOFFAT AJM, 1976, J COMP PHYSIOL, V105, P1 POTE KG, 1993, IN PRESS HEAR RES POTE KG, 1991, COMP BIOCHEM PHYS B, V98, P287, DOI 10.1016/0305-0491(91)90181-C Retzius G, 1881, GEHORORGAN WIRBELTIE Romer AS, 1970, VERTEBRATE BODY ROSS M, 1984, MINERAL PHASES BIOL, P35 ROSS MD, 1980, ADV PHYSL SCI, V19, P243 SALAMAT MS, 1980, ANN OTO RHINOL LARYN, V89, P229 VASQUEZ C. S., 1955, ANN OTOL RHINOL AND LARYNGOL, V64, P1019 VEENHOF VB, 1969, THESIS U AMSTERDAM VILSTRUP T, 1951, ANN OTO RHINOL LARYN, V60, P974 Whiteside B, 1922, AM J ANAT, V30, P231, DOI 10.1002/aja.1000300204 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 MAY PY 1993 VL 67 IS 1-2 BP 189 EP 197 DI 10.1016/0378-5955(93)90246-W PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700021 PM 8340270 ER PT J AU MULLER, M WESS, FP BRUNS, V AF MULLER, M WESS, FP BRUNS, V TI COCHLEAR PLACE-FREQUENCY MAP IN THE MARSUPIAL MONODELPHIS-DOMESTICA SO HEARING RESEARCH LA English DT Article DE COCHLEA; PLACE-FREQUENCY MAP; MARSUPIAL; HRP ID POSSUM TRICHOSURUS-VULPECULA; BRUSH-TAILED POSSUM; PACHYUROMYS-DUPRASI; AUDITORY MIDBRAIN; SPIRAL GANGLION; REPRESENTATION; BAT; CORTEX; GERBIL; CAT AB In order to determine the place-frequency map of the cochlea in the marsupial Monodelphis domestica, iontophoretic HRP-injections were made at several locations in the ventral cochlear nucleus. Prior to iontophoresis the auditory neurons at these locations were characterized electrophysiologically. The resulting distribution of retrogradely labeled cochlear spiral ganglion cells was analysed by means of a three dimensional reconstruction of the cochlea. The map was established for frequencies between 2.4 and 44.5 kHz, corresponding to positions between 95 to 14% of basilar membrane length (base = 0%). The maximum slope amounted to 1.8 mm/octave. Over the basal-most 60% of the cochlea the slope of the place-frequency map was larger than 1.5 mm/octave, further apically the slope rapidly decreased to values below 0.8 min/octave. The shape of the cochlear place-frequency map is similar to that described in placental mammals. C1 UNIV FRANKFURT,INST ZOOL,W-6000 FRANKFURT 1,GERMANY. RP MULLER, M (reprint author), JW GOETHE UNIV KLINIKUM,ZENTRUM PHYSIOL,THEODOR STERN KAI 7,W-6000 FRANKFURT 70,GERMANY. CR AITKIN LM, 1978, BRAIN RES, V150, P29, DOI 10.1016/0006-8993(78)90651-0 AITKIN LM, 1983, BRAIN BEHAV EVOLUT, V22, P75, DOI 10.1159/000121509 AITKIN LM, 1986, BRAIN BEHAV EVOLUT, V29, P17, DOI 10.1159/000118669 AITKIN LM, 1979, J EXP ZOOL, V209, P317, DOI 10.1002/jez.1402090212 Bekesy G., 1960, EXPT HEARING BRUNS V, 1976, J COMP PHYSIOL, V106, P87 CLEMENS WA, 1977, BIOL MARSUPIALS, P51 EHRET G, 1975, J COMP PHYS, V106, P329 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 FROST SB, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P655 FROST SB, 1989, 12TH MINW M, P232 GATES GR, 1982, HEARING RES, V7, P1, DOI 10.1016/0378-5955(82)90078-8 Gates G.R., 1984, P191 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 JOHNSON JI, 1977, BIOL MARSUPIALS KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KRAUS HJ, 1982, VERH DTSCH ZOOL GES, P279 LEWIS ER, 1985, VERETEBRATE INNER EA LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 Manley G.A., 1988, P3 MULLER M, 1991, HEARING RES, V56, P191, DOI 10.1016/0378-5955(91)90169-A MULLER M, 1990, EXP BRAIN RES, V81, P140 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 MULLER M, 1992, J COMP PHYSIOL A, V171, P469 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 VONBEKESY NG, 1944, TIERE AKUSTISCHE Z, V9, P3 NR 28 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 MAY PY 1993 VL 67 IS 1-2 BP 198 EP 202 DI 10.1016/0378-5955(93)90247-X PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700022 PM 8340271 ER PT J AU BARTOLAMI, S PLANCHE, M PUJOL, R AF BARTOLAMI, S PLANCHE, M PUJOL, R TI INHIBITION OF THE CARBACHOL-EVOKED SYNTHESIS OF INOSITOL PHOSPHATES BY OTOTOXIC DRUGS IN THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE AMINOGLYCOSIDES; CISPLATIN; ETHACRYNATE; MERCURIC CHLORIDE; INOSITOL PHOSPHATES; COCHLEAR MUSCARINIC RECEPTORS ID OUTER HAIR-CELLS; MUSCARINIC ACETYLCHOLINE-RECEPTOR; GTP-BINDING PROTEINS; INNER-EAR TISSUES; GUINEA-PIG; AMINOGLYCOSIDE ANTIBIOTICS; SIGNAL TRANSDUCTION; ETHACRYNIC-ACID; CALCIUM ENTRY; CISPLATIN AB The ability of amikacin, neomycin, ethacrynate, mercuric chloride and cisplatin to alter the inositol phosphate (IP) signalling pathway was assessed in the 12-day-old rat cochlea, where the turnover of IPs is coupled to muscarinic receptors. This study was motivated by: (1) the demonstration of neomycin binding to phosphatidylinositol 4,5-biphosphate, the precursor of IPs, and (2) the fact that ototoxic drugs induce some common symptoms in outer hair cells. At concentrations below 1 mM, none of the compounds changed the control H-3-IP formation. Mercuric chloride, cisplatin and ethacrynate inhibited the carbachol-induced formation of IPs in a dose-dependent manner with IC50 values of 74, 340 and 430 muM, respectively. The aminoglycosides were less efficient in reducing the carbachol-stimulated accumulation of IPs, since neither amikacin nor neomycin, both at 1 mM, had any significant effect. However, neomycin applied at 15 and 30 muM induced 29% and 43% of inhibition of the stimulated IP response. Finally, additive effects are obtained between some of the toxic drugs. The results suggest that a block of the IP transduction system, associated with the cholinergic efferent innervation of the organ of Corti, is a feature that may be involved in some types of ototoxicity. The inefficiency of aminoglycosides and the putative targets of the ototoxic agents are discussed. C1 UNIV MONTPELLIER 2,NEUROBIOL AUDIT LAB,F-34060 MONTPELLIER,FRANCE. RP BARTOLAMI, S (reprint author), CHU ST CHARLES,INSERM,U254,NEUROBIOL AUDIT,F-34059 MONTPELLIER 1,FRANCE. CR ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 ANNIKO M, 1978, ACTA OTO-LARYNGOL, V85, P213, DOI 10.3109/00016487809111928 ARONSTAM RS, 1978, MOL PHARMACOL, V14, P575 BARRON SE, 1987, HEARING RES, V26, P131, DOI 10.1016/0378-5955(87)90104-3 BARTOLAMI S, 1990, HEARING RES, V47, P229, DOI 10.1016/0378-5955(90)90154-H BARTOLAMI S, 1992, ABSTR SOC NEUROSCI, V1, pA10 BARTOLAMI S, 1992, ABSTR INN EAR BIOL W, V297, P79 BERRIDGE MJ, 1984, NATURE, V312, P315, DOI 10.1038/312315a0 BERRIDGE MJ, 1982, BIOCHEM J, V206, P587 CANLON B, 1991, EUR J NEUROSCI, V3, P1338, DOI 10.1111/j.1460-9568.1991.tb00066.x COLE KS, 1992, BRAIN RES, V575, P223 DANNHOF BJ, 1991, CELL TISSUE RES, V266, P89, DOI 10.1007/BF00678715 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 FALK SA, 1974, ARCH PATHOL, V97, P297 FLORIO VA, 1985, J BIOL CHEM, V260, P3477 FORGE A, 1985, HEARING RES, V19, P171, DOI 10.1016/0378-5955(85)90121-2 GARETZ SL, 1992, ABSTR ASS RES OT, V15, P328 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O GUIRAMAND J, 1990, TOXICOL LETT, V51, P331, DOI 10.1016/0378-4274(90)90076-X HAGA K, 1986, J BIOL CHEM, V261, P133 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HAYASHIDA T, 1989, ACTA OTO-LARYNGOL, V108, P404, DOI 10.3109/00016488909125546 HEDLUND B, 1979, MOL PHARMACOL, V15, P531 HERRMANN E, 1988, FEBS LETT, V229, P49, DOI 10.1016/0014-5793(88)80795-6 HOSTETLER KY, 1982, BIOCHIM BIOPHYS ACTA, V710, P506, DOI 10.1016/0005-2760(82)90136-9 HUANG MY, 1989, MED TOXICOL ADV DRUG, V4, P452 HUANG MY, 1990, BIOCHEM PHARMACOL, V40, pR11, DOI 10.1016/0006-2952(90)90077-X HUXTABLE RJ, 1992, PHYSIOL REV, V72, P101 KAY IS, 1990, EUR ARCH OTO-RHINO-L, V247, P37 KOCH T, 1991, EUR ARCH OTO-RHINO-L, V248, P459, DOI 10.1007/BF00627634 KOECHEL DA, 1984, J PHARMACOL EXP THER, V228, P799 KONISHI T, 1979, ACTA OTO-LARYNGOL, V88, P41, DOI 10.3109/00016487909137138 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 KONISHI T, 1979, ACTA OTO-LARYNGOL, V88, P203, DOI 10.3109/00016487909137161 KOSSL M, 1990, HEARING RES, V44, P217, DOI 10.1016/0378-5955(90)90082-Z KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LAURELL G, 1989, HEARING RES, V38, P19, DOI 10.1016/0378-5955(89)90124-X LAURELL G, 1991, ACTA OTO-LARYNGOL, V111, P891, DOI 10.3109/00016489109138427 LENOIR M, 1980, ANAT EMBRYOL, V160, P253, DOI 10.1007/BF00305106 LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LODHI S, 1976, BIOCHIM BIOPHYS ACTA, V426, P781, DOI 10.1016/0005-2736(76)90147-4 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 NIEDZIELSKI AS, 1992, HEARING RES, V59, P250, DOI 10.1016/0378-5955(92)90121-3 NISHIZUKA Y, 1984, SCIENCE, V225, P1365, DOI 10.1126/science.6147898 NUTTALL AL, 1977, ACTA OTO-LARYNGOL, V83, P393, DOI 10.3109/00016487709128863 ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x Pujol R, 1986, Acta Otolaryngol Suppl, V429, P29 RAMSAMMY LS, 1988, J PHARMACOL EXP THER, V247, P989 Riché G., 1989, Cahiers de la Recherche-Développement, P57 RICHARDSON GP, 1991, HEARING RES, V53, P293, DOI 10.1016/0378-5955(91)90062-E RUSSELL NJ, 1979, ACTA OTO-LARYNGOL, V88, P369, DOI 10.3109/00016487909137181 RYBAK LP, 1986, NEUROBIOLOGY HEARING, P441 SAITO T, 1991, HEARING RES, V56, P143, DOI 10.1016/0378-5955(91)90163-4 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SCHACHT J, 1979, ARCH OTO-RHINO-LARYN, V224, P129, DOI 10.1007/BF00455236 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SIMMONS DD, 1990, HEARING RES, V49, P127, DOI 10.1016/0378-5955(90)90100-4 STOCKHORST E, 1977, ACTA OTO-LARYNGOL, V83, P401, DOI 10.3109/00016487709128864 TAKADA A, 1982, HEARING RES, V8, P179, DOI 10.1016/0378-5955(82)90073-9 THALMANN R, 1977, ACTA OTO-LARYNGOL, V83, P221, DOI 10.3109/00016487709128836 VALLEE BL, 1972, ANNU REV BIOCHEM, V41, P91, DOI 10.1146/annurev.bi.41.070172.000515 WANG BM, 1984, BIOCHEM PHARMACOL, V33, P3257, DOI 10.1016/0006-2952(84)90087-X WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 WINSLOW JW, 1987, J BIOL CHEM, V262, P4501 ZUNINO F, 1989, CHEM-BIOL INTERACT, V70, P89, DOI 10.1016/0009-2797(89)90065-3 NR 67 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 MAY PY 1993 VL 67 IS 1-2 BP 203 EP 210 DI 10.1016/0378-5955(93)90248-Y PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700023 PM 8340273 ER PT J AU CHIONG, CM BURGESS, BJ NADOL, JB AF CHIONG, CM BURGESS, BJ NADOL, JB TI POSTNATAL MATURATION OF HUMAN SPIRAL GANGLION-CELLS - LIGHT AND ELECTRON-MICROSCOPIC OBSERVATIONS SO HEARING RESEARCH LA English DT Article DE SPIRAL GANGLION; MORPHOMETRY; NEONATE; HUMAN ID ADULT CATS; INNERVATION; AFFERENT; COCHLEAE; NEURONS; FIBERS; COUNTS; RAT AB The presence of two types of ganglion cells, based on cell size and other morphologic parameters, is well established in the adult mammalian and human spiral ganglion. On the other hand, there is little data concerning cell morphology in the neonatal spiral ganglion. The present study was undertaken to evaluate the differences in the morphometry and distribution of cell types in the spiral ganglion of the human neonate as compared to the adult. A total of five human temporal bones from two neonates and three infants were included in this study. Light microscopic analysis of all specimens was performed, and electron microscopic evaluation of a 14 day old neonatal spiral ganglion was accomplished. The segmental density of spiral ganglion cells was higher in the neonate than in the adult. The prevalence of type II spiral ganglion cells was higher in the neonate than has been reported in the adult, particularly in the middle and apical turns where type II cells constituted 24% and 26% of all ganglion cells, respectively. The prevalence of type II ganglion cells decreased with age, particularly in the middle and apical turns. In the neonate, the maximal cross sectional area of type I neurons increased from the base to the apex and seemed to increase with age especially in the basal turn. The present study strongly supports a clear differentiation of type I and type Il ganglion cells in the human neonate and that the prevalence of type II cells is greater in the neonate than the adult. This finding is discussed with reference to postnatal development of the spiral ganglion. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114. SUNNYBROOK HLTH SCI CTR,DEPT OTOLARYNGOL,TORONTO,ON,CANADA. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. CR ANNIKO M, 1988, ORL J OTO-RHINO-LARY, V50, P103 ARNOLD WJ, 1982, AM J OTOL, V3, P266 BAIRD IL, 1967, ANAT REC, V159, P281, DOI 10.1002/ar.1091590306 Bast T. H., 1949, TEMPORAL BONE EAR BERG DK, 1982, NEURONAL DEV Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 HAMBURGER V, 1949, J EXP ZOOL, V111, P457, DOI 10.1002/jez.1401110308 HINOJOSA R, 1985, ACTA OTO-LARYNGOL, V99, P8, DOI 10.3109/00016488509119139 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 KELLERHALS B, 1967, ACTA OTOLARYNGOL S S, P226 KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 Kiang N.Y.S., 1984, P143 KIMURA R S, 1979, Annals of Otology Rhinology and Laryngology, V88, P1 KONIGSMARK BW, 1970, CONT RES METHODS NEU, P314 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MERCK W, 1977, ARCH OTO-RHINO-LARYN, V217, P441, DOI 10.1007/BF00464466 NADOL JB, 1985, J COMP NEUROL, V237, P333, DOI 10.1002/cne.902370305 NADOL JB, 1988, AM J OTOLARYNG, V9, P47, DOI 10.1016/S0196-0709(88)80007-3 NADOL JB, 1990, ANN OTO RHINOL LARYN, V99, P340 NISHIMURA T, 1965, HIROSAKI MED J, V17, P1 OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PAULER M, 1986, ARCH OTO-RHINO-LARYN, V243, P200, DOI 10.1007/BF00470622 PUJOL R, 1992, ACTA OTO-LARYNGOL, V112, P259 PUJOL R, 1980, HEARING RES, V2, P423, DOI 10.1016/0378-5955(80)90078-7 Rasmussen AT, 1940, LARYNGOSCOPE, V50, P67 ROMAND R, 1986, HEARING RES, V21, P161, DOI 10.1016/0378-5955(86)90036-5 ROMAND R, 1984, ACTA OTO-LARYNGOL, V97, P239, DOI 10.3109/00016488409130985 ROSENBLUTH J, 1962, J CELL BIOL, V12, P329, DOI 10.1083/jcb.12.2.329 RUBEN RJ, 1992, ACTA OTO-LARYNGOL, V112, P192 Schwartz A. M, 1986, NEUROBIOLOGY HEARING, P271 SIMMONS DD, 1988, J COMP NEUROL, V270, P132, DOI 10.1002/cne.902700111 SPOENDLIN H, 1979, ACTA OTO-LARYNGOL, V87, P381, DOI 10.3109/00016487909126437 SPOENDLIN H, 1988, ACTA OTO-LARYNGOL, V105, P403, DOI 10.3109/00016488809119493 SPOENDLIN H, 1972, ACTA OTOLARYNGOL STO, V73, P381 THORN W, 1976, VERH ANAT GES, V70, P517 Wright A, 1987, Acta Otolaryngol Suppl, V444, P1 NR 40 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 MAY PY 1993 VL 67 IS 1-2 BP 211 EP 219 DI 10.1016/0378-5955(93)90249-Z PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700024 PM 8340274 ER PT J AU BUTLER, RA MUSICANT, AD AF BUTLER, RA MUSICANT, AD TI BINAURAL LOCALIZATION - INFLUENCE OF STIMULUS FREQUENCY AND THE LINKAGE TO COVERT PEAK AREAS SO HEARING RESEARCH LA English DT Article DE SPECTRAL CUES; SPATIAL REFERENTS; MONAURAL LOCALIZATION; BINAURAL LOCALIZATION; HEAD-RELATED-TRANSFER-FUNCTIONS ID SOUND LOCALIZATION; MEDIAN PLANE; EXTERNAL EAR; SENSITIVITY AB The influence of selectively filtering a broadband stimulus on binaural localization was investigated. First, head-related-transfer-functions were obtained by placing a miniature microphone at the entrance of the ear canal and presenting broadband noise bursts from each of 104 loudspeakers arrayed in the listener's left hemifield. The microphone's output was transformed into frequency spectra using a Fast Fourier Transform. The microphone and loudspeaker characteristics were accounted for by repeating the procedure with the microphone suspended in space. The in-ear data were divided by the in-space data thereby providing an account of the pinna's interaction with the incident sound wave. Extracted from these data were the covert peak areas (CPAs) associated with different frequency segments. A CPA was defined as the spatial location of those loudspeakers, which when generating the stimulus, produced a sound pressure level at the ear canal entrance within 1 dB of the maximum level recorded for a particular frequency segment. A series of localization tests was conducted using a bandstop stimulus - one in which differently-centered 2.0-kHz wide frequency segments were filtered from a broadband noise. We predicted that when a given frequency segment was filtered, binaural listeners would less often report a sound as originating from the CPA associated with that segment compared to their performances when the sound was unfiltered. This prediction was substantiated by the data (P < 0.0001). While localization accuracy was decreased for the filtered stimuli, the decrement was significantly greater (P < 0.01) for sounds originating in the CPA. We interpreted the results to mean that monaural spectral cues contribute significantly to the accuracy of binaural localization and that the basis of the contribution is the spatial referents of stimulus frequencies, C1 UNIV CHICAGO,DEPT SURG,CHICAGO,IL 60637. MIDDLE TENNESSEE STATE UNIV,DEPT PSYCHOL,MURFREESBORO,TN 37130. RP BUTLER, RA (reprint author), UNIV CHICAGO,DEPT PSYCHOL,5848 UNIV AVE,CHICAGO,IL 60637, USA. CR BATTEAU DW, 1967, PROC R SOC SER B-BIO, V168, P158, DOI 10.1098/rspb.1967.0058 BLAUERT J, 1969, ACUSTICA, V22, P205 BUTLER RA, 1974, FED PROC, V33, P1920 BUTLER RA, 1987, PERCEPT PSYCHOPHYS, V41, P1, DOI 10.3758/BF03208206 BUTLER RA, 1971, PERCEPT PSYCHOPHYS, V9, P99, DOI 10.3758/BF03213038 BUTLER RA, 1980, PERCEPT PSYCHOPHYS, V28, P449, DOI 10.3758/BF03204889 CARLILE S, 1987, HEARING RES, V31, P123, DOI 10.1016/0378-5955(87)90118-3 CARLILE S, 1990, J ACOUST SOC AM, V88, P2196, DOI 10.1121/1.400116 Durlach N. I., 1978, HDB PERCEPTION, V4, P365 GARDNER MB, 1973, J ACOUST SOC AM, V53, P400, DOI 10.1121/1.1913336 Healy M.J.R., 1988, GLIM INTRO Hosmer DW, 1989, APPLIED LOGISTIC REG Knudsen E.I., 1980, P289 McCullagh P., 1989, GENERALIZED LINEAR M, V2nd MIDDLEBROOKS JC, 1989, J ACOUST SOC AM, V86, P89, DOI 10.1121/1.398224 MUSICANT AD, 1990, J ACOUST SOC AM, V87, P757, DOI 10.1121/1.399545 MUSICANT AD, 1984, J ACOUST SOC AM, V75, P1195, DOI 10.1121/1.390770 MUSICANT AD, 1984, HEARING RES, V14, P185, DOI 10.1016/0378-5955(84)90017-0 PETTIGREW A, 1978, NATURE, V272, P138, DOI 10.1038/272138a0 Pierce A. H., 1901, STUDIES AUDITORY VIS Pratt CC, 1930, J EXP PSYCHOL, V13, P278, DOI 10.1037/h0072651 ROFFLER SK, 1968, J ACOUST SOC AM, V43, P1255, DOI 10.1121/1.1910976 ROFFLER SK, 1968, J ACOUST SOC AM, V43, P1260, DOI 10.1121/1.1910977 ROGERS ME, 1992, PERCEPT PSYCHOPHYS, V52, P536, DOI 10.3758/BF03206715 SEARLE C L, 1976, Journal of the Acoustical Society of America, V60, P1164, DOI 10.1121/1.381219 SHAW EAG, 1966, J ACOUST SOC AM, V39, P465, DOI 10.1121/1.1909913 SHAW EAG, 1968, J ACOUST SOC AM, V44, P240, DOI 10.1121/1.1911059 Yost W.A., 1987, DIRECTIONAL HEARING, P49 NR 28 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 1993 VL 67 IS 1-2 BP 220 EP 229 DI 10.1016/0378-5955(93)90250-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LH027 UT WOS:A1993LH02700025 PM 8340275 ER PT J AU WANGEMANN, P TAKEUCHI, S AF WANGEMANN, P TAKEUCHI, S TI MAXI-K+ CHANNEL IN SINGLE ISOLATED COCHLEAR EFFERENT NERVE-TERMINALS SO HEARING RESEARCH LA English DT Article DE AXON TERMINAL; CHARYBDOTOXIN; INNER EAR; COCHLEA; GERBIL ID ACTIVATED POTASSIUM CHANNELS; GALLBLADDER EPITHELIUM; CALCIUM CHANNELS; CELLS; TETRAETHYLAMMONIUM; CHARYBDOTOXIN; CONDUCTANCE; BUNDLE; MUSCLE AB Patch clamp recordings were obtained from isolated cochlear efferent nerve terminals. Channel activity was found in 85% of membrane patches, was present in on-terminal and excised patches and was characterized to originate from a maxi-K+ channel. An average of 2.0+/-0.1 (N = 33) maxi-K+ channels were found per active patch. In symmetrical solutions, the current-voltage relationship was linear and the single-channel conductance was 221+/-5 pS (N = 22). The open probability of the maxi-K+ channel increased with depolarization of the membrane potential and with an increasing free Ca2+-concentration on the cytosolic side. The open probability was insensitive to changes in the free Ca2+ concentration on the extracellular side. TEA (20 mM) and charybdotoxin (10(-7) M) decreased the open probability to nearly zero from the extracellular side but had no effect from the cytosolic side. The high incidence with which this channel was found suggests that the maxi-K+ channel is physiologically relevant which might include protection against overstimulation of the efferent synapse. C1 BOYSTOWN NATL RES HOSP,BIOPHYS LAB,OMAHA,NE. RP WANGEMANN, P (reprint author), BOYSTOWN NATL RES HOSP,CELL PHYSIOL LAB,555 N 30TH ST,OMAHA,NE 68131, USA. RI Wangemann, Philine/N-2826-2013 CR BIELEFELDT K, 1992, J PHYSIOL-LONDON, V458, P41 Colquhoun D., 1983, SINGLE CHANNEL RECOR, P191 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 GUGGINO SE, 1987, AM J PHYSIOL, V252, pC128 HERMANN A, 1987, J GEN PHYSIOL, V90, P27, DOI 10.1085/jgp.90.1.27 IWATSUKI N, 1985, J MEMBRANE BIOL, V86, P139, DOI 10.1007/BF01870780 KARNOVSKY MJ, 1964, J CELL BIOL, V23, P217, DOI 10.1083/jcb.23.2.217 LEMOS JR, 1986, NATURE, V319, P410, DOI 10.1038/319410a0 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 LINDGREN CA, 1989, J PHYSIOL-LONDON, V414, P201 MALLART A, 1985, J PHYSIOL-LONDON, V368, P577 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MILLER C, 1985, NATURE, V313, P316, DOI 10.1038/313316a0 MORITA K, 1990, J NEUROSCI, V10, P2614 OBAID AL, 1989, J GEN PHYSIOL, V93, P715, DOI 10.1085/jgp.93.4.715 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 RAYAN R, 1988, J NEUROPHYSIOL, V60, P549 ROBITAILLE R, 1992, J NEUROSCI, V12, P297 SEGAL Y, 1990, AM J PHYSIOL, V259, pC56 SEGAL Y, 1990, J GEN PHYSIOL, V95, P791, DOI 10.1085/jgp.95.5.791 SINGER JJ, 1987, PFLUG ARCH EUR J PHY, V408, P98, DOI 10.1007/BF00581337 STANLEY EF, 1991, NEURON, V7, P585, DOI 10.1016/0896-6273(91)90371-6 TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 WANGEMANN P, 1992, ABSTR ASS RES OTOLAR, P12 WANGEMANN P, 1992, C MOL BIOL HEARING D WANGEMANN P, 1992, SOC NEUROSCI Warr W.B., 1992, Springer Handbook of Auditory Research, V1, P410 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WONG BS, 1986, PFLUG ARCH EUR J PHY, V407, P279, DOI 10.1007/BF00585303 NR 29 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 APR PY 1993 VL 66 IS 2 BP 123 EP 129 DI 10.1016/0378-5955(93)90133-L PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000001 PM 7685332 ER PT J AU MILLER, CA ABBAS, PJ BROWN, CJ AF MILLER, CA ABBAS, PJ BROWN, CJ TI ELECTRICALLY EVOKED AUDITORY BRAIN-STEM RESPONSE TO STIMULATION OF DIFFERENT SITES IN THE COCHLEA SO HEARING RESEARCH LA English DT Article DE ELECTRICAL STIMULATION; COCHLEAR IMPLANT; EABR ID SPIRAL GANGLION-CELLS; STEM RESPONSE; AMINOOXYACETIC ACID; IMPLANT; NERVE; ELECTRODE; CATS; KANAMYCIN; PATHOLOGY; DEAFNESS AB It is often assumed that stimulation of the eighth nerve with brief current pulses results in a highly synchronous discharge of action potentials from the ensemble of excited nerve fibers. Latency data derived from the electrically evoked auditory brainstem response (EABR) of the guinea pig and human indicate that there is a baso-apical gradient of response latencies in both species. Place-specific stimulation of different regions of the guinea pig cochlea was achieved by positioning a narrowly spaced bipolar electrode into each of the four spiral turns. Peak latencies of EABR waves I and III both revealed longer latencies with increasing distance from the base. Different amplitude growth functions were obtained from each turn. Place-specific stimulation in humans implanted with the Nucleus 22-electrode device was achieved by presenting current pulses across electrodes spaced 1.5 mm apart. A gradient of wave V latencies was observed in all subjects studied. The presence of a latency gradient would influence results obtained in efforts to correlate evoked potential amplitude measures with nerve survival. It may also provide information useful in characterizing the surviving fiber population in human implant subjects. C1 UNIV IOWA,DEPT SPEECH PATHOL & AUDIOL,IOWA CITY,IA 52242. UNIV IOWA,DEPT OTOLARYNGOL HEAD & NECK SURG,IOWA CITY,IA 52242. CR ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W ABBAS PJ, 1990, USE FORWARD MASKING ABEL SM, 1986, SCAND AUDIOL, V15, P197, DOI 10.3109/01050398609042144 ARNESEN AR, 1978, J COMP NEUROL, V178, P661, DOI 10.1002/cne.901780405 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BRIGHTWELL A, 1985, COCHLEAR IMPLANTS, P343 BROWN CJ, 1990, J ACOUST SOC AM, V88, P1385, DOI 10.1121/1.399716 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P440, DOI 10.1109/TBME.1977.326179 BRYANT GM, 1984, HEARING RES, V15, P173, DOI 10.1016/0378-5955(84)90048-0 CLARK GM, 1983, J ACOUST SOC AM, V74, P1911, DOI 10.1121/1.390239 CROSBY PA, 1985, Patent No. 14532930 DONALDSON JA, 1992, SURGICAL ANATOMY TEM EGGERMONT JJ, 1983, BASES AUDITORY BRAIN, P287 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P365 HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U HERMANN B, 1990, 2 INT COCHL IMPL S I, P57 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1987, ANN OTO RHINOL LARYN, V96, P48 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 LIM HH, 1989, J ACOUST SOC AM, V86, P971, DOI 10.1121/1.398732 LUSTED HS, 1984, LARYNGOSCOPE, V94, P878 MERZENICH MM, 1979, BIOMED ENG INSTRUMEN, V3, P321 MILLER CM, 1992, THESIS U IOWA MILLER JM, 1983, ANN OTO RHINOL LARYN, V92, P599 MORRISON D, 1975, ACTA OTO-LARYNGOL, V79, P11, DOI 10.3109/00016487509124649 Moxon E.C., 1971, THESIS MIT NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 NAGEL D, 1974, ARCH OTO-RHINO-LARYN, V206, P293, DOI 10.1007/BF00460282 RATTAY F, 1987, J THEOR BIOL, V125, P339, DOI 10.1016/S0022-5193(87)80066-8 Schuknecht H. F., 1974, PATHOLOGY EAR SHALLOP JK, 1990, EAR HEARING, V11, P5, DOI 10.1097/00003446-199002000-00004 SHANNON RV, 1990, J ACOUST SOC AM, V87, P905, DOI 10.1121/1.398902 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 SPOENDLIN H, 1989, HEARING RES, V43, P23 TEAS DONALD C, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1438, DOI 10.1121/1.1918366 VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 YAMANE H, 1981, OTOLARYNG HEAD NECK, V89, P117 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P23 ZAPPIA JJ, 1991, ANN OTO RHINOL LARYN, V100, P914 NR 42 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 1993 VL 66 IS 2 BP 130 EP 142 DI 10.1016/0378-5955(93)90134-M PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000002 PM 8509305 ER PT J AU GUTH, P NORRIS, C FERMIN, CD PANTOJA, M AF GUTH, P NORRIS, C FERMIN, CD PANTOJA, M TI THE CORRELATED BLANCHING OF SYNAPTIC BODIES AND REDUCTION IN AFFERENT FIRING RATES CAUSED BY TRANSMITTER-DEPLETING AGENTS IN THE FROG SEMICIRCULAR CANAL SO HEARING RESEARCH LA English DT Article DE SYNAPTIC BODIES; HAIR CELLS; POSTERIOR CRISTA; FROG; SEMICIRCULAR CANAL; VESTIBULAR ID HAIR-CELLS; ORGAN; CORTI; SYNAPSES; MEMBRANE; MICE AB Synaptic bodies (SBs) associated with rings of synaptic vesicles and well-defined, pre-and post-synaptic membrane structures are indicators of maturity in most hair cell-afferent nerve junctions. The role of the SBs remains elusive despite several experiments showing that they may be involved in storage of neurotransmitter. Our results demonstrate that SBs of the adult posterior semicircular canal (SCC) cristae hair cells become less electron dense following incubation of the SCC with the transmitter-depleting drug tetrabenazine (TBZ). Objective quantification and comparison of the densities of the SBs in untreated and TBZ-treated frog SCC demonstrated that TBZ significantly decreased the electron density of SBs. This reduction in electron density was accompanied by a reduction in firing rates of afferent fibers innervating the posterior SCC. A second transmitter-depleting drug, guanethidine, previously shown to reduce the electron density of hair cell SBs, also reduced the firing rates of afferent fibers innervating the posterior SCC. In contrast, the electron density of dense granules (DG), similar in size and shape to synaptic bodies (SB) in hair cells, did not change after incubation in TBZ, thus indicating that granules and SBs are not similar in regard to their electron density. The role of SBs in synaptic transmission and the transmitter, if any, stored in the SBs remain unknown. Nonetheless, the association of the lessening of electron density with a reduction in afferent firing rate provides impetus for the further investigation of the SB's role in neurotransmission. C1 TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT PATHOL,NEW ORLEANS,LA 70112. UNIV VALLE,DEPT PHARMACOL,CALI,COLOMBIA. RP GUTH, P (reprint author), TULANE UNIV,SCH MED,DEPT PHARMACOL,1430 TULANE AVE,RM 3730,NEW ORLEANS,LA 70112, USA. CR DOUGLAS W, 1965, PHARMACOL BASIS THER, P615 DUNN RF, 1980, J COMP NEUROL, V193, P255, DOI 10.1002/cne.901930117 FERMIN CD, 1990, J ELECT MICROSC TECH, V15, P85 FERMIN CD, 1992, J MICROSC-OXFORD, V167, P85 FERMIN CD, 1991, 3RD IBRO WORLD C NEU, P271 Glauert A. M., 1972, PRACTICAL METHODS EL GLAUERT AM, 1984, FIXATION DEHYDRATION GUTH PS, 1986, ACTA OTO-LARYNGOL, V102, P194, DOI 10.3109/00016488609108666 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HAYAT MA, 1970, BIOL APPLICATIONS, V1 HIROKAWA N, 1978, J NEUROCYTOL, V7, P283, DOI 10.1007/BF01176994 HOUSLEY GD, 1988, HEARING RES, V35, P87, DOI 10.1016/0378-5955(88)90043-3 KING TS, 1982, J NEUROCYTOL, V11, P19, DOI 10.1007/BF01258002 Lewis ER, 1985, VERTEBRATE INNER EAR MONAGHAN P, 1975, CELL TISSUE RES, V163, P239 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 OSBORNE AMP, 1972, Z ZELLFORSCH, V127, P347 PARK JC, 1987, HEARING RES, V28, P87, DOI 10.1016/0378-5955(87)90156-0 Schaeffer S F, 1976, Cold Spring Harb Symp Quant Biol, V40, P521 SHORE PA, 1966, PHARMACOL REV, V18, P561 SIEGEL JH, 1981, BRAIN RES, V220, P188, DOI 10.1016/0006-8993(81)90224-9 SIEGEL JH, 1986, J NEUROCYTOL, V15, P311, DOI 10.1007/BF01611434 SJOSTRAND FS, 1958, J ULTRA MOL STRUCT R, V2, P122, DOI 10.1016/S0022-5320(58)90050-9 SOBKOWICZ HM, 1986, J NEUROCYTOL, V15, P693, DOI 10.1007/BF01625188 SOBKOWICZ HM, 1975, J NEUROCYTOL, V4, P543, DOI 10.1007/BF01351537 SOBKOWICZ HM, 1982, J NEUROSCI, V2, P942 SZAMIER RB, 1974, AM J ANAT, V139, P567, DOI 10.1002/aja.1001390407 WOODS AD, 1987, ACTA OTO-LARYNGOL, V104, P193, DOI 10.3109/00016488709107318 ZIMMERMANN H, 1989, CELL BIOL INT REP, V13, P993, DOI 10.1016/0309-1651(89)90015-5 NR 29 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 1993 VL 66 IS 2 BP 143 EP 149 DI 10.1016/0378-5955(93)90135-N PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000003 PM 8389740 ER PT J AU FAVRE, E PELIZZONE, M AF FAVRE, E PELIZZONE, M TI CHANNEL INTERACTIONS IN PATIENTS USING THE INERAID MULTICHANNEL COCHLEAR IMPLANT SO HEARING RESEARCH LA English DT Article DE COCHLEAR IMPLANTS; ELECTRICAL STIMULATION; CHANNEL INTERACTIONS; PSYCHOPHYSICAL THRESHOLDS ID ELECTRICAL-STIMULATION; RECOGNITION AB Electrode interactions were investigated on two totally deaf patients fitted with the Ineraid multichannel cochlear implant. Currents were applied to the most apical electrode (the 'perturbation' electrode) and their effects on psychophysical thresholds on the other electrodes (the 'test' electrodes) of the intracochlear array were studied. Two experimental protocols were used. In experiment I, we used a detection protocol to study how the perception of signals presented on each test electrode was affected by subthreshold, simultaneous or non-simultaneous stimulation of the perturbation electrode. Strong electrode interactions were observed with simultaneous stimulation and monotonically decreased as a function of electrode separation. Electrode interactions were weak with non-simultaneous stimulation. In experiment II, we used a discrimination protocol to study how the perception of signals presented on the test electrode was affected by suprathreshold, non-simultaneous stimulation of the perturbation electrode. Subjects could discriminate stimulation of 'perturbation+test' versus 'perturbation alone' when the level of stimulation on the test electrode was near threshold. These results demonstrate that strong electrode interactions in the Ineraid multichannel cochlear implant system are generated by electrical field summation due to simultaneous stimulation of different electrodes, and that one can reduce electrode interactions by sequential activation of the electrodes. These observations might help to understand basic phenomena underlying recent significant improvements in speech recognition scores when switching from simultaneous to interleaved pulsatile stimulation in patients wearing the same cochlear implant system C1 HOP CANTONAL GENEVA,DEPT OTOLARYNGOL,ORL CLIN,CH-1211 GENEVA 4,SWITZERLAND. CR DORMAN MF, 1989, EAR HEARING, V10, P44 EDDINGTON DK, 1992, IN PRESS ELECTROANAT, V2 EDDINGTON DK, 1978, ANN OTOL RHINOL LA S, V53, P1 EDDINGTON DK, 1980, J ACOUST SOC AM, V68, P885, DOI 10.1121/1.384827 GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LIM HH, 1989, J ACOUST SOC AM, V86, P971, DOI 10.1121/1.398732 MONTANDON P, 1992, ORL J OTO-RHINO-LARY, V54, P314 SCHLAUCH RS, 1990, J ACOUST SOC AM, V88, P732, DOI 10.1121/1.399776 SHANNON RV, 1983, HEARING RES, V12, P1, DOI 10.1016/0378-5955(83)90115-6 TONG YC, 1983, SCIENCE, V219, P993, DOI 10.1126/science.6823564 WHITE MW, 1984, ARCH OTOLARYNGOL, V110, P493 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 NR 13 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 APR PY 1993 VL 66 IS 2 BP 150 EP 156 DI 10.1016/0378-5955(93)90136-O PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000004 PM 8509306 ER PT J AU HAFNER, H PRATT, H BLAZER, S SUJOV, P AF HAFNER, H PRATT, H BLAZER, S SUJOV, P TI CRITICAL AGES IN BRAIN-STEM DEVELOPMENT REVEALED BY NEONATAL 3-CHANNEL LISSAJOUS TRAJECTORY OF AUDITORY BRAIN-STEM EVOKED-POTENTIALS SO HEARING RESEARCH LA English DT Article DE NEWBORNS; AUDITORY BRAIN-STEM; EVOKED POTENTIALS; DEVELOPMENT; 3-CHANNEL LISSAJOUS TRAJECTORIES ID STEM RESPONSE; NEWBORN-INFANTS; MATURATION; LESIONS; INTENSITY; STIMULUS; SUBJECT; TERM AB Auditory brainstem evoked potentials (ABEPs) were recorded from 91 newborns from 7 age groups between 26 to 43 weeks of gestation. In addition to the widely used vertex-mastoid derivation, potentials were recorded from three orthogonal electrode configurations, and represented in 3 dimensional voltage-space as three-channel Lissajous' trajectories (3CLTs). ABEPs were evoked by alternating polarity, monaural 75 dBnHL clicks presented at rates of 10/s, 55/s and 80/s. Potentials were also recorded to 45 dBnHL and 15 dBnHL clicks presented at 10/s. 3CLT point by point (apex latencies, amplitudes and orientation) as well as planar segment (planar segment position and duration) descriptors, along with peak latencies of the vertex-mastoid peaks, were followed for effects of age, stimulus intensity and rate. ABEPs began to appear consistently at 29 weeks of gestation to high stimulus intensities, with a rapid decrease of ABEP thresholds up to 34 weeks. At 35 weeks, thresholds stabilized approximately at adult values. The results indicate a significant effect of stimulus rate and intensity as well as of gestational age group on apex latencies. The findings also showed changes in apex orientations associated with stimulus rate and intensity interacting with gestational age. 3CLT descriptors enhanced the understanding of these results in relation to developmental and maturational aspects of the auditory system. The results may be explained by maturational change in relative contributions of constituents of the complex ABEP generators. C1 RAMBAM MED CTR,NEONATAL INTENS CARE UNIT,HAIFA,ISRAEL. RP HAFNER, H (reprint author), TECHNION ISRAEL INST TECHNOL,EVOKED POTENTIALS LAB,GUTWIRTH BLDG,IL-32000 HAIFA,ISRAEL. CR Cohen B A, 1987, Electromyogr Clin Neurophysiol, V27, P469 DESPLAND PA, 1980, PEDIATR RES, V14, P154, DOI 10.1203/00006450-198002000-00018 DUBOWITZ LM, 1970, J PEDIATR-US, V77, P1, DOI 10.1016/S0022-3476(70)80038-5 EGGERMONT JJ, 1988, ELECTROEN CLIN NEURO, V70, P293, DOI 10.1016/0013-4694(88)90048-X Eggermont J J, 1985, Acta Otolaryngol Suppl, V421, P41 EYRE JA, 1988, BRIT MED BULL, V44, P1076 FAWER CL, 1982, NEUROPEDIATRICS, V13, P200, DOI 10.1055/s-2008-1059623 FUJIKAWA SM, 1977, J AM AUDITORY SOC, V3, P147 GARDI JN, 1987, ELECTROEN CLIN NEURO, V68, P360, DOI 10.1016/0168-5597(87)90017-7 GOLDSTEIN PJ, 1979, AM J OBSTET GYNECOL, V135, P622 HAFNER H, 1991, HEARING RES, V51, P33, DOI 10.1016/0378-5955(91)90005-T HAKAMADA S, 1981, BRAIN DEV-JPN, V3, P339 HAREL Z, 1984, MATH BIOSCI, V69, P1, DOI 10.1016/0025-5564(84)90011-7 HITNER HM, 1977, J PEDIATR, V91, P455 ISAACSON G, 1986, ATLAS FETAL STIONAL JEWETT DL, 1987, ELECTROEN CLIN NEURO, V68, P386, DOI 10.1016/0168-5597(87)90020-7 KENDROR A, 1987, ELECTROEN CLIN NEURO, V68, P209, DOI 10.1016/0168-5597(87)90028-1 KILENY P, 1985, J OTOLARYNGOL, V14, P34 KRUMHOLZ A, 1985, ELECTROEN CLIN NEURO, V62, P124, DOI 10.1016/0168-5597(85)90024-3 LASKY RL, 1984, ELECTROEN CLIN NEURO, V59, P345 MARSHALL RE, 1980, J PEDIATR-US, V96, P731, DOI 10.1016/S0022-3476(80)80755-4 MARTIN WH, 1986, ELECTROEN CLIN NEURO, V63, P54, DOI 10.1016/0013-4694(86)90062-3 MCPHERSON DL, 1985, ANN OTO RHINOL LARYN, V94, P236 MOLLER AR, 1981, ELECTROEN CLIN NEURO, V52, P18, DOI 10.1016/0013-4694(81)90184-X PAQUEREAU J, 1986, AUDIOLOGY, V25, P107 PRATT H, 1976, ARCH OTO-RHINO-LARYN, V212, P85, DOI 10.1007/BF00454268 PRATT H, 1990, ADV AUDIOL, V6, P331 PRATT H, 1981, ELECTROEN CLIN NEURO, V51, P80, DOI 10.1016/0013-4694(81)91511-X PRATT H, 1984, ELECTROEN CLIN NEURO, V58, P83, DOI 10.1016/0013-4694(84)90204-9 PRATT H, 1991, HEARING RES, V53, P237, DOI 10.1016/0378-5955(91)90058-H PRATT H, 1985, ELECTROEN CLIN NEURO, V61, P530, DOI 10.1016/0013-4694(85)90972-1 PRATT H, 1983, ELECTROEN CLIN NEURO, V56, P682, DOI 10.1016/0013-4694(83)90036-6 PRATT H, 1987, AUDIOLOGY, V26, P247 ROTTEVEEL JJ, 1987, HEARING RES, V26, P21, DOI 10.1016/0378-5955(87)90033-5 SALAMY A, 1984, J CLIN NEUROPHYSIOL, V1, P293, DOI 10.1097/00004691-198407000-00003 SCHERG M, 1985, ELECTROEN CLIN NEURO, V62, P290, DOI 10.1016/0168-5597(85)90006-1 SCHULMANGALAMBOS C, 1975, J SPEECH HEAR RES, V18, P456 STARR A, 1977, PEDIATRICS, V60, P831 STEVEN AJ, 1984, INT MED CARE J HOSPI, P9 STEVEN AJ, 1984, INT MED CARE J HOSPI, P83 STOCKARD JE, 1979, ARCH NEUROL-CHICAGO, V36, P823 WALSH E, 1983, THESIS OMAHA WILLISTON JS, 1981, BRAIN RES, V223, P181, DOI 10.1016/0006-8993(81)90820-9 ZIMMERMAN MC, 1987, ANN OTO RHINOL LARYN, V96, P291 NR 44 TC 5 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 1993 VL 66 IS 2 BP 157 EP 168 DI 10.1016/0378-5955(93)90137-P PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000005 PM 8509307 ER PT J AU IKEDA, K TAKASAKA, T AF IKEDA, K TAKASAKA, T TI CONFOCAL LASER MICROSCOPIC IMAGES OF CALCIUM DISTRIBUTION AND INTRACELLULAR ORGANELLES IN THE OUTER HAIR CELL ISOLATED FROM THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE FREE CALCIUM; MEMBRANE-BOUND CALCIUM; SUBSURFACE CISTERN; MITOCHONDRIA; F-ACTIN ID SENSORY CELLS; MOTILITY; ACTIN; LOCALIZATION; RESPONSES; MOVEMENT; LENGTH AB We report the use of a confocal laser fluorescence microscope to observe the distribution of cytosolic Ca2+ and the localization of intracellular organelles and cytoskeleton in the isolated outer hair cell (OHC). Membrane-bound Ca2+ stained by chlortetracycline was mainly seen in the subcuticular region, the infranuclear region, and the region adjacent to the lateral wall. In contrast, the central portion of the cytoplasm and nucleus were devoid of detectable fluorescence of membrane-associated Ca2+, but were relatively rich in free Ca2+. The cuticular plate showed a lack of both membrane-bound and free Ca2+. Fluorescent clusters of mitochondria and endoplasmic reticulum were predominantly seen in the infracuticular and infranuclear regions, and some were associated with the lateral wall. These two types of cytosolic organelles which fluoresced upon chlortetracycline treatment are therefore presumed to sequester calcium. The characteristic distribution of the endoplasmic reticulum was observed in coincidence with the infracuticular network of F-actin. The subsurface cistern, which was shown to be analogous to the endoplasmic reticulum in terms of its biological function, is likely to be the source of Ca2+ for the actin-mediated process. RP IKEDA, K (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. CR ALTSCHULER RA, 1991, ABSTR ASS RES OT, P13 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BERRIDGE MJ, 1989, NATURE, V341, P197, DOI 10.1038/341197a0 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 CANLON B, 1991, HEARING RES, V53, P7, DOI 10.1016/0378-5955(91)90209-R CARAFOLI E, 1987, ANNU REV BIOCHEM, V56, P395, DOI 10.1146/annurev.biochem.56.1.395 CHANDLER DE, 1978, J CELL BIOL, V76, P371, DOI 10.1083/jcb.76.2.371 Chen L B, 1982, Cold Spring Harb Symp Quant Biol, V46 Pt 1, P141 DEMARTINIS FD, 1987, AM J PHYSIOL, V253, pC783 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 HASHIMOTO S, 1987, ACTA OTO-LARYNGOL, V103, P64 HOLLEY MC, 1990, J CELL SCI, V96, P283 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 IKEDA K, 1991, AM J PHYSIOL, V261, pC231 IKEDA K, 1990, EUR ARCH OTO-RHINO-L, V247, P43 JOHNSON LV, 1980, P NATL ACAD SCI-BIOL, V77, P990, DOI 10.1073/pnas.77.2.990 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KUBA K, 1991, NEUROSCI RES, V10, P245, DOI 10.1016/0168-0102(91)90082-A LIM DJ, 1985, ACTA OTO-LARYNGOL, V99, P478, DOI 10.3109/00016488509108941 MELDOLESI J, 1990, BIOCHIM BIOPHYS ACTA, V1055, P130, DOI 10.1016/0167-4889(90)90113-R NAKAGAWA T, 1991, NEUROSCI LETT, V125, P81, DOI 10.1016/0304-3940(91)90136-H ORMAN S, 1983, HEARING RES, V11, P261, DOI 10.1016/0378-5955(83)90061-8 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SLEPECKY N, 1989, HEARING RES, V38, P135, DOI 10.1016/0378-5955(89)90135-4 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 TERASAKI M, 1984, CELL, V38, P101, DOI 10.1016/0092-8674(84)90530-0 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 VANBREEMEN C, 1989, ANNU REV PHYSIOL, V51, P315, DOI 10.1146/annurev.physiol.51.1.315 WILLIAMS DA, 1990, CELL CALCIUM, V11, P589, DOI 10.1016/0143-4160(90)90013-K YLIKOSKI J, 1991, 28TH INN EAR BIOL, P6 ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V149, P304, DOI 10.1016/0006-291X(87)91639-1 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 39 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 APR PY 1993 VL 66 IS 2 BP 169 EP 176 DI 10.1016/0378-5955(93)90138-Q PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000006 PM 8509308 ER PT J AU LECHNER, TP AF LECHNER, TP TI A HYDROMECHANICAL MODEL OF THE COCHLEA WITH NONLINEAR FEEDBACK USING PVF(2) BENDING TRANSDUCERS SO HEARING RESEARCH LA English DT Article DE COCHLEA; NONLINEAR FEEDBACK; HYDROMECHANICAL MODEL; PVF(2) BENDING TRANSDUCERS ID OTOACOUSTIC EMISSIONS; PREPROCESSING MODEL; ACTIVE FEEDBACK; MECHANICS; COILING; TONE AB A single-channel hydromechanical model of the human cochlea with nonlinear feedback on the membrane is introduced. The piezoelectric transducers for displacement measurement and force exertion on the membrane are constructed of PVF2 in the bimorph bending type. The passive response shows high-frequency slopes of about 60 dB/oct and a shortest wavelength of about 17 mm corresponding to 0.9 Bark in the human cochlea. High-frequency slopes and Q10 dB with one feedback loop are within the range of animal data, where as dynamic compression does not exceed 20 dB. Input impedance and phase response are in good agreement with nature, which is ascribed to longitudinal stiffness of the membrane. C1 TECH UNIV MUNICH,LEHRSTUHL ELEKTROAKUST,W-8000 MUNICH 2,GERMANY. CR ALLEN JB, 1977, J ACOUST SOC AM, V61, P110, DOI 10.1121/1.381272 DEBOER E, 1981, J ACOUST SOC AM, V69, P1369, DOI 10.1121/1.385818 DEBOER E, 1983, J ACOUST SOC AM, V73, P577, DOI 10.1121/1.389004 DEBOER E, 1982, J ACOUST SOC AM, V72, P1427, DOI 10.1121/1.388675 DIEPENDAAL RJ, 1989, J ACOUST SOC AM, V85, P803, DOI 10.1121/1.397553 DIESTEL HG, 1954, ACUSTICA, V4, P421 FURST M, 1982, J ACOUST SOC AM, V72, P717, DOI 10.1121/1.388252 HELLE R, 1974, THESIS TU MUNCHEN HOLMES MH, 1980, J ACOUST SOC AM, V68, P482, DOI 10.1121/1.384747 HOLMES MH, 1984, J ACOUST SOC AM, V76, P767, DOI 10.1121/1.391300 IURATO SALVATORE, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1386, DOI 10.1121/1.1918355 KELLER JB, 1985, J ACOUST SOC AM, V77, P2107, DOI 10.1121/1.391735 KOHLLOFFEL LUE, 1990, HEARING RES, V49, P19, DOI 10.1016/0378-5955(90)90092-4 KOLSTON PJ, 1989, J ACOUST SOC AM, V86, P133, DOI 10.1121/1.398332 KOLSTON PJ, 1988, J ACOUST SOC AM, V83, P1481, DOI 10.1121/1.395903 LOH CH, 1984, J ACOUST SOC AM, V74, P95 LYNCH TJ, 1982, J ACOUST SOC AM, V72, P108, DOI 10.1121/1.387995 Nedzelnitsky V, 1974, FACTS MODELS HEARING, P45 NEELY ST, 1981, J ACOUST SOC AM, V69, P1386, DOI 10.1121/1.385820 NOVOSELOVA SM, 1989, HEARING RES, V51, P215 OETINGER R, 1961, ACUSTICA, V11, P161 PEISL W, 1990, THESIS TU MUNCHEN RHODE WS, 1971, J ACOUST SOC AM, V49, P1212 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SHERA CA, 1991, J ACOUST SOC AM, V89, P1276, DOI 10.1121/1.400650 STEELE CR, 1981, J ACOUST SOC AM, V69, P1107, DOI 10.1121/1.385679 STEELE CR, 1979, J ACOUST SOC AM, V65, P1001, DOI 10.1121/1.382569 STEELE CR, 1985, J ACOUST SOC AM, V77, P1849, DOI 10.1121/1.391935 STEELE CR, 1974, J ACOUST SOC AM, V56, P1252, DOI 10.1121/1.1903416 STEELE CR, 1980, J ACOUST SOC AM, V68, P147, DOI 10.1121/1.384640 TABER LA, 1981, J ACOUST SOC AM, V70, P426, DOI 10.1121/1.386785 VIERGEVER MA, 1980, MECHANICS INNER EAR VOLDRICH L, 1978, ACTA OTO-LARYNGOL, V86, P331, DOI 10.3109/00016487809107511 VONBEKESY G, 1942, AKUST Z, V7, P173 VONBEKESY G, 1941, AKUST Z, V6, P265 VONBEKESY G, 1966, EXPT HEARING von Bekesy G, 1928, PHYS Z, V29, P793 VONBEKESY G, 1947, J ACOUST SOC AM, V19, P452 ZWICKER E, 1974, ACTA OTO-LARYNGOL, V78, P65, DOI 10.3109/00016487409126327 ZWICKER E, 1986, J ACOUST SOC AM, V80, P154, DOI 10.1121/1.394176 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 Zwicker E., 1967, OHR ALS NACHRICHTENE ZWICKER E, 1990, HEARING RES, V44, P209, DOI 10.1016/0378-5955(90)90081-Y ZWICKER E, 1990, J ACOUST SOC AM, V88, P1639, DOI 10.1121/1.400324 ZWICKER E, 1986, J ACOUST SOC AM, V80, P146, DOI 10.1121/1.394175 ZWICKER E, 1979, BIOL CYBERN, V35, P24 ZWISLOCKI JJ, 1948, ACTA OTO LARYNGOL S, V72 NR 48 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 1993 VL 66 IS 2 BP 202 EP 212 DI 10.1016/0378-5955(93)90140-V PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000008 PM 8509310 ER PT J AU OESTERLE, EC RUBEL, EW AF OESTERLE, EC RUBEL, EW TI POSTNATAL PRODUCTION OF SUPPORTING CELLS IN THE CHICK COCHLEA SO HEARING RESEARCH LA English DT Article DE BIRD; AUDITORY; COCHLEA; BASILAR PAPILLA; SUPPORTING CELLS; HAIR-CELL REGENERATION ID REGENERATED HAIR-CELLS; ACOUSTIC TRAUMA; INNER-EAR; POSSIBLE PRECURSORS; MACULA NEGLECTA; NERVOUS-SYSTEM; COTURNIX QUAIL; GANGLION-CELL; FISH EAR; GROWTH AB The auditory receptor organ in birds, the basilar papilla, is mitotically active after acoustic overstimulation or pharmological insult and is capable of self-repair. The damaged epithelium is repopulated with new hair cells and supporting cells. The cell production that underlies this regenerative self-repair is believed to be a response evoked by damage in populations of cells that normally become mitotically quiescent even before hatching. In contrast, regeneration in the vertebrate nervous system is often correlated with continued or recent neurogenesis in the tissue concerned. The hypothesis that there may be ongoing postnatal production of cells in the normal avian basilar papilla was investigated. Autoradiographic analysis of tritiated-thymidine-injected animals was used to look for the existence of newly formed cells in the basilar papilla of normal posthatch chickens. Several types of supporting cells, namely, organ supporting cells, border cells and hyaline cells, are produced postnatally in the normal chicken. Typically, they are added interstitially to the apical (distal) half of the basilar papilla. C1 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. CR BALAK KJ, 1990, J NEUROSCI, V10, P2502 BARBER VC, 1985, CELL TISSUE RES, V241, P597 BIRSE SC, 1980, J COMP NEUROL, V194, P291, DOI 10.1002/cne.901940202 Cavalieri B., 1966, GEOMETRIA INDIVISIBI CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 CORWIN JT, 1986, BIOL CHANGE OTOLARYN, P291 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1983, J COMP NEUROL, V217, P345, DOI 10.1002/cne.902170309 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1985, SCAN ELECTRON MICROS, P407 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 EASTER SS, 1981, J NEUROSCI, V1, P793 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 GROSSET L, 1975, CELL TISSUE KINET, V8, P91, DOI 10.1111/j.1365-2184.1975.tb01210.x HOLDER N, 1988, TRENDS NEUROSCI, V11, P94, DOI 10.1016/0166-2236(88)90151-8 JORGENSEN JM, 1981, ACTA ZOOL-STOCKHOLM, V62, P171 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 LEWIS ER, 1973, J MORPHOL, V139, P351, DOI 10.1002/jmor.1051390305 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 LYON MJ, 1987, J COMP NEUROL, V255, P511, DOI 10.1002/cne.902550404 MCFARLAN.PW, 1973, J CELL SCI, V13, P821 OESTERLE EC, 1992, J COMP NEUROL, V318, P64, DOI 10.1002/cne.903180105 PAKKENBERG B, 1988, J MICROSC-OXFORD, V150, P1 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W PRESSON JC, 1990, HEARING RES, V46, P9, DOI 10.1016/0378-5955(90)90135-C RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RUBEN RJ, 1967, ACTA OTOLARYNGOL S, V220, P4 RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N RYALS BM, 1988, HEARING RES, V36, P1, DOI 10.1016/0378-5955(88)90133-5 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 STERIO DC, 1984, J MICROSC-OXFORD, V134, P127 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 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TESTER AL, 1969, PAC SCI, V23, P1 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 TSUE TT, 1993, IN PRESS J NEUROSCI WEISLEDER P, 1992, EXP NEUROL, V115, P2, DOI 10.1016/0014-4886(92)90211-8 YAN HY, 1992, ASS RES OTOLARYNGOL, V15, P161 NR 46 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 APR PY 1993 VL 66 IS 2 BP 213 EP 224 DI 10.1016/0378-5955(93)90141-M PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000009 PM 8509311 ER PT J AU POTE, KG WEBER, CH KRETSINGER, RH AF POTE, KG WEBER, CH KRETSINGER, RH TI INFERRED PROTEIN-CONTENT AND DISTRIBUTION FROM DENSITY-MEASUREMENTS OF CALCITIC AND ARAGONITIC OTOCONIA SO HEARING RESEARCH LA English DT Article DE OTOCONIA; XENOPUS-LAEVIS; RATTUS-NORVEGICUS; DENSITY; BIOMINERALIZATION ID BIOMINERALIZATION; STATOCONIA; CRYSTALS AB Otoconia from the peripheral portion of the vestibular system contain specific proteins and are mineralized by several polymorphs of calcium carbonate. To infer the internal distribution of their mineral and protein components, we have measured the densities, by equilibrium centrifugation, and the lengths of aragonitic otoconia from the African clawed frog (Xenopus laevis) and calcitic otoconia from the Norway rat (Rattus norvegicus). The densities are statistically dependent on the length of the otoconia Further, this dependence is not the same for aragonitic and calcitic otoconia. Aragonitic otoconia are statistically more dense when smaller and less dense when larger. For calcitic otoconia the opposite is true; the smaller otoconia are statistically less dense than larger otoconia. Because the organic and inorganic phases have different densities, this indicates that the otoconial proteins and the mineral phases have different distributions within these two types of otoconia. C1 UNIV VIRGINIA,DEPT BIOL,CHARLOTTESVILLE,VA 22903. CR ADDADI L, 1987, P NATL ACAD SCI USA, V84, P2732, DOI 10.1073/pnas.84.9.2732 ADDADI L, 1985, P NATL ACAD SCI USA, V82, P4110, DOI 10.1073/pnas.82.12.4110 BALLARINO J, 1985, THESIS CORNELL U ITH BERMAN A, 1990, SCIENCE, V250, P664, DOI 10.1126/science.250.4981.664 BORMAN AH, 1982, EUR J BIOCHEM, V129, P179, DOI 10.1111/j.1432-1033.1982.tb07037.x CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 FERMIN CD, 1985, ACTA ANAT, V123, P148 FERMIN CD, 1987, HEARING RES, V28, P23, DOI 10.1016/0378-5955(87)90150-X KAWAMATA S, 1991, ARCH HISTOL CYTOL, V54, P173, DOI 10.1679/aohc.54.173 MANN S, 1983, P ROY SOC LOND B BIO, V18, P415 MARMO F, 1983, CELL TISSUE RES, V233, P35 MATTHEWS BW, 1968, J MOL BIOL, V33, P491, DOI 10.1016/0022-2836(68)90205-2 MATTHEWS BW, 1974, J MOL BIOL, V82, P513, DOI 10.1016/0022-2836(74)90245-9 POTE KG, 1986, J ULTRA MOL STRUCT R, V95, P61, DOI 10.1016/0889-1605(86)90029-7 POTE KG, 1992, UNPUB HEARING RES POTE KG, 1992, IN PRESS BIOCHEMISTR POTE KG, 1991, COMP BIOCHEM PHYS B, V98, P287, DOI 10.1016/0305-0491(91)90181-C ROSS MD, 1973, ANAT REC, V175, P429 WATABE N, 1974, J CRYST GROWTH, V24, P116, DOI 10.1016/0022-0248(74)90288-7 WHEELER AP, 1984, AM ZOOL, V24, P933 WRAY JL, 1957, J AM CHEM SOC, V79, P2031, DOI 10.1021/ja01566a001 1970, CRC HDB CHEM PHYSICS, pE40 NR 22 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 APR PY 1993 VL 66 IS 2 BP 225 EP 232 DI 10.1016/0378-5955(93)90142-N PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000010 PM 8509312 ER PT J AU CARLYON, RP BUTT, M AF CARLYON, RP BUTT, M TI EFFECTS OF ASPIRIN ON HUMAN AUDITORY FILTERS SO HEARING RESEARCH LA English DT Article DE ASPIRIN; SALICYLATE; FREQUENCY SELECTIVITY; FILTER SHAPES; FORWARD MASKING; TEMPORAL INTEGRATION; GROWTH OF MASKING ID HEARING-LOSS; SALICYLATE OTOTOXICITY; INTENSE SOUNDS; SHAPES AB Auditory filter shapes were measured in eight male volunteers with normal hearing, using a notched-noise forward-masking paradigm and a signal frequency of 4 kHz. The measurements were made under three conditions: after listeners had taken eight doses of three 320 mg aspirin tablets every six hours; after an identical schedule of placebo ingestion; and one week after testing in the first two conditions had been completed. Half of the listeners did the placebo condition first, and half did the aspirin condition first. Aspirin and placebo were administered double-blind, and testing took place approximately one hour after the last dose. Filter shapes were significantly broader in the aspirin condition than in the placebo and post-test conditions, indicating that even a modest dose affects auditory frequency selectivity. Two-point measures of growth of masking did not differ significantly between conditions. RP CARLYON, RP (reprint author), UNIV SUSSEX,EXPTL PSYCHOL LAB,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. RI Carlyon, Robert/A-5387-2010 CR BOETTCHER FA, 1991, AM J OTOLARYNG, V12, P33, DOI 10.1016/0196-0709(91)90071-M BOETTCHER FA, 1989, HEARING RES, V42, P129, DOI 10.1016/0378-5955(89)90139-1 BONDING P, 1979, AUDIOLOGY, V18, P133 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 FALBEHANSEN J, 1941, ACTA OTOLARYNGOL S, V414 FESTEN JM, 1983, J ACOUST SOC AM, V73, P652, DOI 10.1121/1.388957 Glasberg B R, 1989, Scand Audiol Suppl, V32, P1 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T HOUTGAST T, 1972, J ACOUST SOC AM, V51, P1885, DOI 10.1121/1.1913048 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 MCCABE PA, 1965, ANN OTO RHINOL LARYN, V74, P312 MCFADDEN D, 1990, J ACOUST SOC AM, V87, P2634, DOI 10.1121/1.399056 MCFADDEN D, 1984, HEARING RES, V16, P251, DOI 10.1016/0378-5955(84)90114-X MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MCFADDEN D, 1984, AM J OTOLARYNG, V5, P235, DOI 10.1016/S0196-0709(84)80033-2 MCFADDEN D, 1983, HEARING RES, V9, P295, DOI 10.1016/0378-5955(83)90033-3 MOORE BCJ, 1983, J ACOUST SOC AM, V74, P750, DOI 10.1121/1.389861 MOORE BCJ, 1987, J ACOUST SOC AM, V81, P1873, DOI 10.1121/1.394751 MOORE BCJ, 1984, J ACOUST SOC AM, V76, P1057, DOI 10.1121/1.391425 MOORE BCJ, 1981, J ACOUST SOC AM, V69, P1003 PATTERSON RD, 1980, J ACOUST SOC AM, V67, P229, DOI 10.1121/1.383732 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 PEDERSEN CB, 1974, AUDIOLOGY, V13, P311 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E YOUNG LL, 1982, AUDIOLOGY, V21, P342 1969, SPECIFICATIONS AUDIO NR 29 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 APR PY 1993 VL 66 IS 2 BP 233 EP 244 DI 10.1016/0378-5955(93)90143-O PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000011 PM 8509313 ER PT J AU PTOK, M NAIR, T CAREY, TE ALTSCHULER, RA AF PTOK, M NAIR, T CAREY, TE ALTSCHULER, RA TI DISTRIBUTION OF KHRI-3 EPITOPES IN THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE MONOCLONAL ANTIBODY; INNER EAR; SUPPORTING CELLS; IMMUNOCYTOCHEMISTRY; WESTERN BLOTTING ID GUINEA-PIG ORGAN; MONOCLONAL-ANTIBODIES; CORTI; IMMUNOREACTIVITY; ANTIGENS; COCHLEA; CELLS AB Murine monoclonal antibodies against cochlear structures were previously generated to obtain probes for elucidating the function of cochlear cell subsets. Preliminary immunocytochemical characterization showed that the monoclonal antibody KHRI 3 binds to supporting cells but not sensory cells in the guinea pig cochlea. We have now investigated KHRI 3 epitopes in other species and other parts of the inner ear. The KHRI 3 epitope appears to be species-specific since no immunolabeling was seen in rat inner ear nor in chick inner ear. In immunocytochemical assays in. the guinea pig vestibular tissues KHRI 3 stained saccular wall cells and transitional epithelial cells in the utricle and ampules as well as clusters of cells in the endolymphatic sac. In Western blots KHRI 3 stained a broad 70-75 kDa band in lanes loaded with guinea pig cochlea homogenates - as seen previously - as well as in lanes loaded with vestibular tissue homogenates. The immunolabeling patterns suggest that KHRI 3 epitopes are cell membrane components or related to membrane structures. Thus the monoclonal antibody KHRI 3 appears to define a nonsensory cell subset in the guinea pig inner ear that can be identified by expression of KHRI 3 epitopes. C1 KRESGE HEARING RES INST,ANN ARBOR,MI. RP PTOK, M (reprint author), UNIV TUBINGEN,DEPT OTOLARYNGOL,HNO HEARING RES LABS,SILCHERSTR 5,W-7400 TUBINGEN 1,GERMANY. CR ALTSCHULER RA, 1985, HEARING RES, V17, P249, DOI 10.1016/0378-5955(85)90069-3 ALTSCHULER RA, 1985, BRAIN RES, V327, P379, DOI 10.1016/0006-8993(85)91541-0 FEX J, 1985, HEARING RES, V17, P101, DOI 10.1016/0378-5955(85)90014-0 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 FEX J, 1981, P NATL ACAD SCI-BIOL, V78, P1255, DOI 10.1073/pnas.78.2.1255 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 OROZCO CR, 1990, LARYNGOSCOPE, V100, P941 PTOK M, 1991, HEARING RES, V57, P79, DOI 10.1016/0378-5955(91)90077-M PTOK M, 1989, 26 WORKSH INN EAR BI, P50 PTOK M, 1989, ARCH OTORHINOLARYN S, V2, P73 TOWBIN H, 1979, P NATL ACAD SCI USA, V73, P2599 ZAJIC G, 1991, HEARING RES, V52, P59, DOI 10.1016/0378-5955(91)90187-E NR 13 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 APR PY 1993 VL 66 IS 2 BP 245 EP 252 DI 10.1016/0378-5955(93)90144-P PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000012 PM 7685333 ER PT J AU PEDERSEN, AD MORTON, JI TRUNE, DR AF PEDERSEN, AD MORTON, JI TRUNE, DR TI INNER-EAR BASIC FIBROBLAST GROWTH-FACTOR IN CBA/J, C3H/HEJ, AND AUTOIMMUNE PALMERSTON-NORTH MICE SO HEARING RESEARCH LA English DT Article DE BASIC FIBROBLAST GROWTH FACTOR; AUTOIMMUNE DISEASE; PALMERSTON-NORTH MOUSE; INNER EAR; OSTEOGENESIS; BONE LINING CELLS ID COCHLEO-VESTIBULAR GANGLION; EMBRYONIC OTIC VESICLE; HUMAN TEMPORAL BONE; LINING CELL; FACTOR BFGF; OTOSCLEROSIS; MOUSE; DIFFERENTIATION; LOCALIZATION; OSTEOGENESIS AB Basic fibroblast growth factor (bFGF) has a mitogenic effect on fibroblasts and osteoblasts for matrix proliferation and on endothelial cells for neovascularization. Because otic capsule osteogenesis in autoimmune disease subjects often involves abnormal matrix and vascular changes, bFGF may serve as a potential mediator for such bone disorders. To investigate this relationship, bFGF was evaluated in the Palmerston North autoimmune strain mouse, which develops otic capsule sclerotic lesions during the progression of its systemic disease. Inner ears from PN mice, along with control CBA/J and C3H/HeJ mice, were immunohistochemically stained with antibodies against bFGF to identify its presence and possible role in otic capsule disease. Although cells reactive for bFGF were observed along the lining of the otic capsule in all three strains, a significantly higher frequency was observed in the PN mice. Other sites of staining included connective tissue around the tensor tympani muscle and the geniculate ganglion. This identification of bFGF in the otic capsule raises the possibility that it may play some role in normal bone maintenance, as well as abnormal bone or connective tissue remodeling in autoimmune disease. C1 OREGON HLTH SCI UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,OREGON HEARING RES CTR,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED,DIV ARTHRIT & RHEUMAT DIS,PORTLAND,OR 97201. CR BAIRD A, 1989, BRIT MED BULL, V45, P438 BAROTTE C, 1989, NEUROSCI LETT, V101, P197, DOI 10.1016/0304-3940(89)90530-2 BERND P, 1989, DEV BIOL, V134, P11, DOI 10.1016/0012-1606(89)90073-0 BLATT IM, 1961, ARCHIV OTOLARYNGOL, V73, P639 DAVIDSON WF, 1982, J IMMUNOL, V129, P751 FINKLESTEIN SP, 1988, BRAIN RES, V460, P253, DOI 10.1016/0006-8993(88)90370-8 FISHER ER, 1961, ARCH PATHOL, V72, P572 FRENZ DA, 1991, ABSTR ASS RES OT, P136 FRENZ DA, 1990, ANN NY ACAD SCI, V593, P340, DOI 10.1111/j.1749-6632.1990.tb16138.x GUSSEN R, 1977, ARCH OTO-RHINO-LARYN, V217, P263, DOI 10.1007/BF00465544 HANNEKEN A, 1989, J CELL PHYSIOL, V138, P115, DOI 10.1002/jcp.1041380116 HARRIS JP, 1986, ANN OTO RHINOL LARYN, V95, P176 HAUSCHKA PV, 1988, CIBA F SYMP, V136, P207 HERTLER CK, 1990, OTOLARYNG HEAD NECK, V103, P713 JANET T, 1988, J NEUROSCI RES, V19, P195, DOI 10.1002/jnr.490190204 Jenkins H A, 1981, Am J Otolaryngol, V2, P99, DOI 10.1016/S0196-0709(81)80026-9 JOSEPHSILVERSTEIN J, 1989, J CELL BIOL, V108, P2459, DOI 10.1083/jcb.108.6.2459 JOYCE ME, 1990, J CELL BIOL, V110, P2195, DOI 10.1083/jcb.110.6.2195 LEFEBVRE PP, 1992, ABSTR ASS RES OT, P162 LIM DJ, 1987, AM J OTOLARYNG, V8, P282, DOI 10.1016/S0196-0709(87)80047-9 LIM DJ, 1985, HEARING LOSS DIZZINE, P43 MARKS SC, 1988, AM J ANAT, V183, P1, DOI 10.1002/aja.1001830102 MAURIZI M, 1988, AM J OTOLARYNG, V9, P68, DOI 10.1016/S0196-0709(88)80010-3 MENTON DN, 1984, ANAT REC, V209, P29, DOI 10.1002/ar.1092090105 MILLER SC, 1987, CALCIFIED TISSUE INT, V41, P1, DOI 10.1007/BF02555122 MILLER SC, 1980, ANAT REC, V198, P163, DOI 10.1002/ar.1091980204 MILLER SC, 1981, DEV BIOL, V87, P52, DOI 10.1016/0012-1606(81)90060-9 NIJWEIDE PJ, 1986, PHYSIOL REV, V66, P855 NIJWEIDE PJ, 1988, CIBA FDN S, P61 PEDERSEN AD, 1991, OTOLARYNGOL HEAD NEC, V105, P190 RAREY KE, 1986, AM J OTOLARYNG, V4, P387 REPRESA J, 1991, ANAT EMBRYOL, V184, P421, DOI 10.1007/BF01236048 REPRESA J, 1989, DEV BIOL, V134, P21, DOI 10.1016/0012-1606(89)90074-2 SCHRADER M, 1990, ANN OTO RHINOL LARYN, V99, P349 SHIPLEY GD, 1989, J CELL PHYSIOL, V138, P511, DOI 10.1002/jcp.1041380310 SLACK JMW, 1990, PHILOS T ROY SOC B, V327, P75, DOI 10.1098/rstb.1990.0044 SORENSEN MS, 1988, ACTA OTO-LARYNGOL, V105, P242, DOI 10.3109/00016488809097004 TANG XM, 1986, CHINESE MED J-PEKING, V99, P950 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, 1991, AM J OTOLARYNG, V12, P259, DOI 10.1016/0196-0709(91)90003-X TRUNE DR, 1990, OTOLARYNGOL HEAD NEC, V103, P230 VANDERWIEL CJ, 1978, CLIN ORTHOP RELAT R, V134, P350 VANDEWATER TR, 1990, ANN NY ACAD SCI, V593, P371 WALKER SE, 1978, J LAB CLIN MED, V92, P932 WOLFF D, 1965, ANN OTO RHINOL LARYN, V74, P507 YANAGITA N, 1987, LARYNGOSCOPE, V97, P345 YOO TJ, 1987, AM J OTOLARYNG, V8, P317, DOI 10.1016/S0196-0709(87)80050-9 YOO TJ, 1984, ANN OTO RHINOL LARYN, V93, P28 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 52 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 APR PY 1993 VL 66 IS 2 BP 253 EP 259 DI 10.1016/0378-5955(93)90145-Q PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA LA880 UT WOS:A1993LA88000013 PM 8509314 ER PT J AU FROEHLICH, P COLLET, L VALATX, JL MORGON, A AF FROEHLICH, P COLLET, L VALATX, JL MORGON, A TI SLEEP AND ACTIVE COCHLEAR MICROMECHANICAL PROPERTIES IN HUMAN-SUBJECTS SO HEARING RESEARCH LA English DT Article DE TRANSIENTLY EVOKED OTOACOUSTIC EMISSIONS; SLEEP; OLIVOCOCHLEAR; EFFERENT ID SPONTANEOUS OTOACOUSTIC EMISSIONS; ACOUSTIC STIMULATION; EVOKED-POTENTIALS; FREQUENCY; BAEP; EAR AB In this paper the effect of sleep on the cochlea is studied by transiently evoked otoacoustic emissions (TEOAEs). Amplitude increases considerably (e.g., 4 dB) and the effect of a contralateral noise on the TEOAEs decreases during the night. These modifications can be related to sleep, although there is no link to electroencephalographic sleep stage. During sleep onset, the effect of contralateral noise disappears: this could correspond to a functional rest of the auditory pathway during that period. C1 HOP EDOUARD HERRIOT,CNRS,URA 1447,PAVILLON U,3 PL ARSONVAL,F-69003 LYON,FRANCE. UNIV LYON 1,DEPT MED EXPTL,INSERM,U52,F-69365 LYON 2,FRANCE. CR AMADEO M, 1973, PSYCHOPHYSIOLOGY, V10, P244, DOI 10.1111/j.1469-8986.1973.tb00523.x BASTUJI H, 1988, ELECTROEN CLIN NEURO, V70, P9, DOI 10.1016/0013-4694(88)90189-7 BENZINGER TH, 1963, TEMP ITS MEAS, V3, P637 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 CAMPBELL KB, 1986, ELECTROEN CLIN NEURO, V65, P142, DOI 10.1016/0168-5597(86)90047-X COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1990, ADV AUDIOL, V7, P164 EVANS EF, 1981, TINNITUS, P108 FROEHLICH P, 1990, BRAIN RES, V508, P286, DOI 10.1016/0006-8993(90)90408-4 HELLEKSON C, 1979, ELECTROEN CLIN NEURO, V47, P742, DOI 10.1016/0013-4694(79)90302-X HUGHES JR, 1984, INT J NEUROSCI, V24, P267, DOI 10.3109/00207458409089815 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 PESSAH MA, 1972, SCIENCE, V178, P773, DOI 10.1126/science.178.4062.773 Puel J.L., 1989, COCHLEAR MECHANISMS, P315 PUEL JL, 1988, BRAIN RES, V447, P380, DOI 10.1016/0006-8993(88)91144-4 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 Rechtschaffen A, 1968, MANUAL STANDARDIZED VELLUTI R, 1989, HEARING RES, V39, P203, DOI 10.1016/0378-5955(89)90091-9 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WEBB WB, 1970, SCIENCE, V18, P145 WHITEHEAD ML, 1991, HEARING RES, V53, P269, DOI 10.1016/0378-5955(91)90060-M WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 NR 28 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 MAR PY 1993 VL 66 IS 1 BP 1 EP 7 DI 10.1016/0378-5955(93)90254-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000001 PM 8473241 ER PT J AU DANNHOF, BJ BRUNS, V AF DANNHOF, BJ BRUNS, V TI THE INNERVATION OF THE ORGAN OF CORTI IN THE RAT SO HEARING RESEARCH LA English DT Article DE INNERVATION; AFFERENT; EFFERENT; HAIR CELL; RAT ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; SPIRAL GANGLION-CELLS; AGE-GRADED SERIES; HORSERADISH-PEROXIDASE; EFFERENT SYNAPSES; CAT COCHLEA; ADULT CATS; QUANTITATIVE-ANALYSIS; AFFERENT INNERVATION AB To date our knowledge of the baso-apical distribution of the afferent and efferent nerve fibers innervating the organ of Corti is only fragmentary. This study makes an effort to lay the basis for a comprehensive analysis of cochlear innervation. Using a quantitative electronmicroscopic method, the fiber density of all cochlear fibers along the entire length of the cochlear duct was investigated in adult rats, Rattus norvegicus. Myelinated and unmyelinated nerve fibers in the primary osseous spiral lamina and afferent and efferent nerve fibers to the outer hair cells (OHCs) in the tunnel of Corti were counted. The rat cochlea is innervated by 19000 nerve fibers which consist of 79% afferent and 21% efferent fibers, The inner hair cells (IHCs) are innervated by 14000 afferent and 2000 efferent fibers. The OHCs are innervated by 1000 afferent and 2000 efferent fibers. The maximum fiber density of IHC afferents, OHC afferents and IHC efferents was found in the middle of the cochlea. This corresponds to the region at the basilar membrane where the frequency range of maximum sensitivity is located [8 kHz-31 kHz; Kelly and Masterton, J. Comp. Physiol. Psychol. 91, 930-936 (1977)]. The efferent nerve fibers to the OHCs consists of two different morphological sub-types: large fibers containing mitochondria and neurotubules (type I) and small fibers containing neurofilaments (type II). The fiber density of type I OHC efferents decreases from base to apex corresponding to the frequency dispersion along the basilar membrane. The fiber density of type II OHC efferents has maxima at the base and at the apex and a minimum in the middle of the cochlea. This minimum corresponds to the region at the basilar membrane where the frequency range of maximum sensitivity is located. RP DANNHOF, BJ (reprint author), UNIV FRANKFURT,INST ZOOL,SIESMAYERSTR 70,W-6000 FRANKFURT 11,GERMANY. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 ASCHOFF A, 1987, J COMP NEUROL, V264, P56, DOI 10.1002/cne.902640106 ASCHOFF A, 1988, EXP BRAIN RES, V71, P241 BALLAST L, 1984, THESIS JW GOETHE U F BENSON TE, 1987, SOC NEUR ABSTR, V17, P1258 BERGLUND AM, 1986, BRAIN RES, V383, P327, DOI 10.1016/0006-8993(86)90034-X BERGLUND AM, 1987, J COMP NEUROL, V255, P560, DOI 10.1002/cne.902550408 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BROWN M C, 1985, Society for Neuroscience Abstracts, V11, P1052 BRUNS V, 1985, FORTS ZOOL, V30, P653 BRUNS V, 1984, Acta Zoologica Fennica, V171, P129 BURDA H, 1988, J MORPHOL, V198, P2669 BURDA H, 1985, HEARING RES, V14, P315 DANNHOF BJ, 1988, SENSE ORGANS INTERFA, P183 DANNHOF BJ, 1991, CELL TISSUE RES, V266, P89, DOI 10.1007/BF00678715 DELASEN JCR, 1987, ACTA OTOL, V104, P417 EHRET G, 1979, J COMP NEUROL, V183, P73, DOI 10.1002/cne.901830107 EYBALIN M, 1990, J ELECTRON MICR TECH, V15, P209, DOI 10.1002/jemt.1060150303 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 GINZBERG RD, 1984, HEARING RES, V14, P109, DOI 10.1016/0378-5955(84)90011-X HASHIMOTO S, 1987, ACTA OTO-LARYNGOL, V103, P64 HASHIMOTO S, 1990, ACTA OTO-LARYNGOL, V109, P228, DOI 10.3109/00016489009107438 KEITHLEY EM, 1987, J ACOUST SOC AM, V81, P1036, DOI 10.1121/1.394675 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 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 LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 MERCHANPEREZ A, 1991, 28TH WORKSH INN EAR, P90 MORRISON D, 1975, ACTA OTO-LARYNGOL, V79, P11, DOI 10.3109/00016487509124649 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 PERKINS RE, 1975, J COMP NEUROL, V163, P129, DOI 10.1002/cne.901630202 PLINKERT PK, 1989, ARCH OTO-RHINO-LARYN, V246, P417, DOI 10.1007/BF00464301 ROBERTSON D, 1985, HEARING RES, V20, P79, DOI 10.1016/0378-5955(85)90060-7 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 ROMAND MR, 1987, ACTA OTO-LARYNGOL, V104, P29, DOI 10.3109/00016488709109044 ROSSEL SH, 1986, SCANDINAVICA, V25, P49 ROTH B, 1992, ANAT EMBRYOL, V185, P559, DOI 10.1007/BF00185615 ROTH B, 1991, ANAT EMBRYOL, V183, P483 ROTH B, 1992, ANAT EMBRYOL, V185, P571, DOI 10.1007/BF00185616 SIMMONS DD, 1988, J COMP NEUROL, V270, P132, DOI 10.1002/cne.902700111 SIMMONS DD, 1988, J COMP NEUROL, V270, P145, DOI 10.1002/cne.902700112 SIMMONS DD, 1990, HEARING RES, V49, P127, DOI 10.1016/0378-5955(90)90100-4 SPOENDLI.H, 1969, ACTA OTO-LARYNGOL, V67, P239, DOI 10.3109/00016486909125448 Spoendlin H, 1973, BASIC MECHANISMS HEA, P185 SPOENDLIN H, 1979, ACTA OTO-LARYNGOL, V87, P381, DOI 10.3109/00016487909126437 SPOENDLIN H, 1988, ACTA OTO-LARYNGOL, V105, P403, DOI 10.3109/00016488809119493 SPOENDLI.H, 1974, ARCH OTO-RHINO-LARYN, V208, P137, DOI 10.1007/BF00453927 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 SPOENDLIN H, 1979, ARCH OTO-RHINO-LARYN, V223, P1, DOI 10.1007/BF00455076 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 Takasaka T, 1987, Acta Otolaryngol Suppl, V435, P7 WALTHER Y, 1991, THESIS JW GOETHE U F Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 NR 65 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 MAR PY 1993 VL 66 IS 1 BP 8 EP 22 DI 10.1016/0378-5955(93)90255-Y PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000002 PM 8473248 ER PT J AU REMEZAL, M GILLOYZAGA, P AF REMEZAL, M GILLOYZAGA, P TI INCORPORATION OF D3H GLUCOSAMINE TO THE ADULT AND DEVELOPING COCHLEAR TECTORIAL MEMBRANE OF NORMAL AND HYPOTHYROID RATS SO HEARING RESEARCH LA English DT Article DE COCHLEA; TECTORIAL MEMBRANE; DEVELOPMENT; D-GLUCOSAMINE; HYPOTHYROIDISM; RAT ID ORGAN; CORTI; ORGANIZATION AB The uptake of D-H-3-glucosamine by the developing cochlea of normal and hypothyroid rats was examined using light microscopic radioautography. During postnatal development, normal and hypothyroid rat cochleas exhibited a layer of radiolabelling in the tectorial membrane (TM). This layer first appeared in the TM region which covers the spiral limbus and the Kolliker's organ (KO), then progressively reached the apical part of the TM covering the organ of Corti. Radiolabelling was significantly greater in hypothyroid than in normal cochleas. These findings suggests that the enormous size reached by the TM in the congenital hypothyroidism could be related to an increase of epithelial secretion, at least for carbohydrates. It also suggests that TM, in normal and hypothyroid cochleas, could be formed during development by the addition of successive layers. Older layers could be displaced upwards by the new ones. Cochleas of normal young adult rats, treated with D-H-3-glucosamine, showed a very scarce and diffuse radiolabelling. Cochleas of hypothyroid young adult rats exhibited a thickened and distorted TM, which incorporated a significant amount of carbohydrates. These results suggest that TM secretion is highly reduced in young adult normal animals, while in young adult hypothyroid ones it is still active. During cochlear maturation, thyroxine seems to be neccesary, not only for the synthesis of normal glycoproteins (as suggested by previous reports), but also for the control of glycoprotein secretion. C1 UNIV COMPLUTENSE MADRID,FAC MED,DEPT CIENCIAS MORFOL,APDO CORREOS 60075,E-28080 MADRID,SPAIN. CR ARNOLD W, 1973, ACTA OTO-LARYNGOL, V75, P192, DOI 10.3109/00016487309139695 BELANGER LF, 1953, SCIENCE, V118, P520, DOI 10.1126/science.118.3070.520 DAMJANOV I, 1987, LAB INVEST, V57, P5 DEBRUYNE F, 1983, AUDIOLOGY, V22, P404 DEOL MS, 1976, ACTA OTO-LARYNGOL, V81, P429 DEOL MS, 1973, J MED GENET, V10, P235, DOI 10.1136/jmg.10.3.235 DIEDEREN JHB, 1987, CELL TISSUE RES, V248, P215, DOI 10.1007/BF01239983 GABRION J, 1984, HEARING RES, V13, P203, DOI 10.1016/0378-5955(84)90074-1 GILLOYZAGA P, 1985, HEARING RES, V20, P1 GILLOYZAGA P, 1991, HEARING RES, V57, P38, DOI 10.1016/0378-5955(91)90072-H GILLOYZAGA P, 1990, HEARING RES, V45, P151, DOI 10.1016/0378-5955(90)90191-Q HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 Haubrich J, 1975, Acta Otolaryngol Suppl, V332, P1 KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 Kuijpers W, 1986, Acta Otolaryngol Suppl, V429, P35 LARRA F, 1970, Journal de Microscopie (Paris), V9, P845 LEBLOND CP, 1979, J HISTOCHEM CYTOCHEM, V27, P1185 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 LIM DJ, 1987, HEARING RES, V28, P9 MEYERHOFF WL, 1976, LARYNGOSCOPE, V86, P483, DOI 10.1288/00005537-197604000-00002 PARVING HH, 1982, CLIN ENDOCRINOL, V16, P207, DOI 10.1111/j.1365-2265.1982.tb03166.x PRIETO JJ, 1990, HEARING RES, V45, P51, DOI 10.1016/0378-5955(90)90182-O PRIETO JJ, 1990, HEARING RES, V45, P1283 PRIETO JJ, 1990, DEV BRAIN RES, V52, P141, DOI 10.1016/0165-3806(90)90229-R PRIETO JJ, 1991, HEARING RES, V54, P59, DOI 10.1016/0378-5955(91)90136-W RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 RUEDA J, 1988, GLYCOCONJUGATES MED, P338 STEEL K, 1980, ACTA OTO-LARYNGOL, V89, P27, DOI 10.3109/00016488009127104 STEEL KP, 1986, NEUROBIOLOGY HEARING, P139 STEEL KP, 1983, HEARING RES, V9, P327, DOI 10.1016/0378-5955(83)90035-7 TACHIBANA M, 1987, HEARING RES, V25, P115, DOI 10.1016/0378-5955(87)90084-0 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 THORN L, 1979, ANAT EMBRYOL, V155, P303, DOI 10.1007/BF00317643 THORN L, 1978, ARCH OHREN NASEN KEH, V221, P123, DOI 10.1007/BF00455883 THORN L, 1977, C INSERM, V68, P37 TROTTER WR, 1960, BRIT MED BULL, V16, P92 UZIEL A, 1981, ACTA OTO-LARYNGOL, V92, P469, DOI 10.3109/00016488109133286 UZIEL A, 1980, BRAIN RES, V182, P172, DOI 10.1016/0006-8993(80)90840-9 UZIEL A, 1983, DEV BRAIN RES, V7, P295, DOI 10.1016/0165-3806(83)90186-4 UZIEL A, 1983, HEARING RES, V11, P203, DOI 10.1016/0378-5955(83)90079-5 VANMIDDLESWORTH L, 1980, ENDOCRINOLOGY, V106, P1686 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 MAR PY 1993 VL 66 IS 1 BP 23 EP 30 DI 10.1016/0378-5955(93)90256-Z PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000003 PM 8473243 ER PT J AU RHODE, WS COOPER, NP AF RHODE, WS COOPER, NP TI 2-TONE SUPPRESSION AND DISTORTION PRODUCTION ON THE BASILAR-MEMBRANE IN THE HOOK REGION OF CAT AND GUINEA-PIG COCHLEAE SO HEARING RESEARCH LA English DT Article DE COCHLEAR MECHANICS; BASILAR MEMBRANE; 2-TONE SUPPRESSION; 2-TONE DISTORTION ID AUDITORY-NERVE FIBERS; LOW-FREQUENCY TONES; OUTER HAIR-CELLS; MAMMALIAN COCHLEA; RATE-INTENSITY; TUNING CURVES; RESPONSES; SENSITIVITY; MODEL; MODULATION AB Two-tone suppression and two-tone distortion were investigated at the level of the basilar membrane in the hook region of cat and guinea pig cochleae using a displacement-sensitive laser interferometric measurement system. The system allowed measurements to be performed at physiological stimulus levels in the cochlear region tuned to 30-35 kHz in cat and 29 kHz in guinea pig. The amplitude of vibration of the basilar membrane due to a probe tone at the characteristic frequency (CF) was attenuated during the presentation of a simultaneous suppressor tone either above or below CF. The amount of suppression depended on the intensities of both probe and suppressor, and the relationship of the suppressor frequency to the CF. Suppressors at frequencies more than an octave below the CF attenuated the responses to the CF probe at a rate of up to 1 dB/dB, with little variation based on suppressor frequency. As the suppressor frequency was increased above CF the Tate of suppression decreased rapidly. The lowest suppressor intensity at which attenuation of the probe response was observed did not vary in direct proportion to the probe intensity. This suppression threshold often varied only a few dB SPL when the probe was varied over a 20 dB SPL range. In a few instances the rate of attenuation was as much as a factor of two greater at the lowest probe intensities than at higher intensities. It is noteworthy that suppression was found when the frequency of the suppressor was either above or below CF in the same preparation. Low frequency suppressor tones suppress basilar membrane motion at the CF when the basilar membrane undergoes displacement toward either scala. The maximum suppression occurs around 100 mus after the peak excursions caused by the low frequency biasing tone. Two-tone distortion products were often observed even at stimulus levels below those causing two-tone suppression at the site studied. The cubic difference tone (CDT) was the most prominent of the distortion products. The level of the CDT component varied nonmonotonically with the level of either of the primary tones. Responses at the difference frequency between the two primaries were usually below the noise floor of the recording system. The existence of both two-tone distortion and two-tone suppression was dependent on the presence of a cochlear nonlinearity. RP RHODE, WS (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,1300 UNIV AVE,MADISON,WI 53706, USA. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 CODY AR, 1989, HEARING RES, V41, P89, DOI 10.1016/0378-5955(89)90002-6 COOPER NP, 1992, HEARING RES, V63, P191, DOI 10.1016/0378-5955(92)90084-Z COOPER NP, 1992, HEARING RES, V63, P163, DOI 10.1016/0378-5955(92)90083-Y COSTALUPES JA, 1987, HEARING RES, V26, P155, DOI 10.1016/0378-5955(87)90107-9 Covell WP, 1936, AM J PHYSIOL, V116, P524 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DEBOER E, 1976, HDB SENSORY PHYSL, V3 DELGUTTE B, 1990, HEARING RES, V49, P225, DOI 10.1016/0378-5955(90)90106-Y DUIFHUIS H, 1975, J ACOUST SOC AM, V59, P408 ENGEBRET.AM, 1968, J ACOUST SOC AM, V44, P548, DOI 10.1121/1.1911119 EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 Fay R. R., 1988, HEARING VERTEBRATES GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GOLDSTEI.JL, 1968, PR INST ELECTR ELECT, V56, P981, DOI 10.1109/PROC.1968.6449 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 GOLDSTEIN JL, 1990, HEARING RES, V49, P39, DOI 10.1016/0378-5955(90)90094-6 GREENWOOD DD, 1986, J ACOUST SOC AM, V79, P1857, DOI 10.1121/1.393194 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 Hall E. R., 1981, MAMMALS N AM, V1, P1 HIND JE, 1967, J NEUROPHYSIOL, V30, P794 JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 KIM DO, 1973, J ACOUST SOC AM, V54, P1517, DOI 10.1121/1.1914449 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 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIBERMAN MC, 1978, ACTA OTOLARYNGOL S, V358 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 NEELY ST, 1982, HEARING RES, P123 NORTON SJ, 1984, J ACOUST SOC AM, V76, P44, DOI 10.1121/1.391034 NUTTALL AL, 1990, MECHANICS BIOPHYSICS, V87, P288 PATUZZI R, 1984, HEARING RES, V13, P9, DOI 10.1016/0378-5955(84)90090-X PATUZZI R, 1984, HEARING RES, V13, P19, DOI 10.1016/0378-5955(84)90091-1 PATUZZI R, 1984, HEARING RES, V13, P1, DOI 10.1016/0378-5955(84)90089-3 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PFEIFFER R R, 1970, Journal of the Acoustical Society of America, V48, P1373, DOI 10.1121/1.1912294 PRIJS VF, 1989, HEARING RES, V42, P73, DOI 10.1016/0378-5955(89)90118-4 Rhode WS., 1977, PSYCHOPHYSICS PHYSL, P27 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 ROBLES L, 1989, COCHLEAR MECH STRUCT, P369 ROBLES L, 1990, MECHANICS BIOPHYSICS, V87, P304 Ruggero M.A., 1989, COCHLEAR MECH STRUCT, P259 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1989, HEARING RES, V41, P61, DOI 10.1016/0378-5955(89)90179-2 SACHS MB, 1976, J ACOUST SOC AM, V60, P1157, DOI 10.1121/1.381218 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P615, DOI 10.1121/1.1913152 SMOORENBURG GF, 1980, HEARING RES, V2, P347, DOI 10.1016/0378-5955(80)90069-6 Wever EG, 1940, J ACOUST SOC AM, V12, P268, DOI 10.1121/1.1916102 WILSON JP, 1973, NATURE, V241, P206, DOI 10.1038/241206a0 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M YATES GK, 1989, COCHLEAR MECHANISMS, P177 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 ZWICKER E, 1981, J ACOUST SOC AM, V70, P1277, DOI 10.1121/1.387141 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 ZWICKER E, 1976, J ACOUST SOC AM, V61, P1031 ZWISLOCKI JJ, 1986, HEARING RES, V22, P155, DOI 10.1016/0378-5955(86)90091-2 NR 69 TC 82 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 MAR PY 1993 VL 66 IS 1 BP 31 EP 45 DI 10.1016/0378-5955(93)90257-2 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000004 PM 8473244 ER PT J AU WOODS, DL ALAIN, C COVARRUBIAS, D ZAIDEL, O AF WOODS, DL ALAIN, C COVARRUBIAS, D ZAIDEL, O TI FREQUENCY-RELATED DIFFERENCES IN THE SPEED OF HUMAN AUDITORY PROCESSING SO HEARING RESEARCH LA English DT Article DE EVOKED POTENTIAL; AUDITORY; CORTEX; LATENCY; FREQUENCY; REACTION TIME ID HEARING-IMPAIRED SUBJECTS; RISE-FALL TIME; MIDDLE COMPONENTS; EVOKED-POTENTIALS; CORTEX; PERCEPTION; PHYSIOLOGY; INTENSITY; RESPONSES; DURATION AB Three experiments were performed, two comparing the peak latencies of auditory evoked potentials (AEPs) elicited by 250 Hz and 4000 Hz tone pips and a third comparing simple reaction times (RTs) to the same stimuli. In the AEP experiments, the latencies of brainstem, middle and long-latency components were delayed following 250 Hz tone pips in comparison with the latencies of the same components evoked by loudness-matched 4000 Hz tones. Frequency-related latency differences increased with component latency, ranging from less than 1.0 ms for wave V of the brainstem AEP, to more than 20.0 ms for the cortical NI component. Interpeak latency differences were also significantly lengthened following the 250 Hz tone pips. In the behavioral study, RTs were 14.6 ms slower following 250 than 4000 Hz tone pips. The results suggest that the time required for the sensory analysis of auditory signals varies inversely with their frequency. C1 UNIV CALIF DAVIS,DEPT NEUROL,DAVIS,CA 95616. UNIV CALIF DAVIS,CTR NEUROBIOL,DAVIS,CA 95616. RP WOODS, DL (reprint author), VET ADM MED CTR,NEUROL SERV,CLIN NEUROPHYSIOL LAB,150 MUIR RD,MARTINEZ,CA 94553, USA. CR BEATTIE RC, 1984, J SPEECH HEAR DISORD, V49, P114 BOER E, 1987, ANNU REV PSYCHOL, V38, P181 DOUGHTY JM, 1947, J EXP PSYCHOL, V37, P351, DOI 10.1037/h0061516 FLORENTINE M, 1983, 11TH P INT C AC, P103 GEISLER CD, 1982, J ACOUST SOC AM, V72, P781, DOI 10.1121/1.388259 GULICK WL, 1989, HEARING PHYSL NEURAL HECOX K, 1976, J ACOUST SOC AM, V60, P1187, DOI 10.1121/1.381194 HENNING GB, 1974, J ACOUST SOC AM, V55, P84, DOI 10.1121/1.1928135 JACOBSON GP, 1992, EAR HEARING, V13, P300, DOI 10.1097/00003446-199210000-00007 KODERA K, 1979, AUDIOLOGY, P395 LIBERMAN AM, 1989, SCIENCE, V243, P489, DOI 10.1126/science.2643163 LIVINGSTONE M, 1988, SCIENCE, V240, P740, DOI 10.1126/science.3283936 MASTERTON RB, 1984, ANNU REV PHYSIOL, V46, P275 MAURIZI M, 1984, AUDIOLOGY, V23, P5669 MCFARLAND WH, 1977, J SPEECH HEAR RES, V20, P781 MOORE BCJ, 1973, J ACOUST SOC AM, V54, P610, DOI 10.1121/1.1913640 NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x ONISHI S, 1968, J ACOUST SOC AM, V44, P582, DOI 10.1121/1.1911124 PANTEV C, 1988, ELECTROEN CLIN NEURO, V69, P160, DOI 10.1016/0013-4694(88)90211-8 PICTON TW, 1977, J OTOLARYNGOL, V6, P90 RAPIN I, 1966, ELECTROEN CLIN NEURO, V21, P335, DOI 10.1016/0013-4694(66)90039-3 REDIES H, 1989, J COMP NEUROL, V282, P473, DOI 10.1002/cne.902820402 SCHARF B, 1986, HDB PERCEPTION PSYCH, V6, P1 SMALL AM, 1987, J ACOUST SOC AM, V82, P1957, DOI 10.1121/1.395640 STAPELLS DR, 1990, AUDIOLOGY, V29, P262 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 THORNTON AR, 1977, J SPEECH HEAR RES, V20, P81 WOODS DL, 1985, ELECTROEN CLIN NEURO, V60, P122, DOI 10.1016/0013-4694(85)90018-5 WOODS DL, 1993, IN PRESS J EXP PSYCH WOODS DL, 1993, IN PRESS PSYCHOPHYSI WOODS DL, 1993, IN PRESS PERCEPTION WOODS D L, 1989, Society for Neuroscience Abstracts, V15, P112 Yost W.A., 1987, DIRECTIONAL HEARING, P49 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 MAR PY 1993 VL 66 IS 1 BP 46 EP 52 DI 10.1016/0378-5955(93)90258-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000005 PM 8473245 ER PT J AU ZAJIC, G FORGE, A SCHACHT, J AF ZAJIC, G FORGE, A SCHACHT, J TI MEMBRANE STAINS AS AN OBJECTIVE MEANS TO DISTINGUISH ISOLATED INNER AND OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS, INNER, OUTER; MEMBRANE STAINS ID GUINEA-PIG; POTASSIUM AB The use of isolated cochlear outer and inner hair cells has become widespread. While the morphological features of these two cell types in general are sufficiently different to allow discrimination, there are situations where confusion can arise. Small outer hair cells, particularly when they are swollen or distorted, can take on an appearance suggestive of inner hair cells. We describe here two fluorescent membrane stains, 3,3'-dihexyloxacarbocyanine iodide and rhodamine B hexyl ester, as an objective means to distinguish between cochlear hair cell types. Both stains mark the subsurface cisternae of outer hair cells thereby delineating the cell outline, and the interior of the cell shows discrete structure. On the other hand, in inner hair cells, the outline of the cell is not resolved while the interior is diffusely fluorescent. Since the two probes have different excitation and emission wavelengths (fluorescein- and rhodamine-like, respectively), this staining procedure can even be used in the presence of another fluorescent marker (for example, a calcium-indicating dye) by appropriate choice of the membrane stain. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. UNIV LONDON UNIV COLL,INST LARYNGOL & OTOL,LONDON WC1E 6BT,ENGLAND. CR BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DULON D, 1990, J NEUROSCI, V10, P1388 DULON D, 1991, HEARING RES, V52, P225, DOI 10.1016/0378-5955(91)90202-K FORGE A, IN PRESS HEAR RES GITTER AH, 1990, HEARING RES, V45, P87, DOI 10.1016/0378-5955(90)90185-R KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 TERASAKI M, 1992, J CELL SCI, V101, P315 THALMANN R, 1972, LARYNGOSCOPE, V82, P2059, DOI 10.1288/00005537-197211000-00008 YAMASHITA T, 1990, ACTA OTO-LARYNGOL, V109, P256, DOI 10.3109/00016489009107441 YAMASHITA T, 1991, ACTA OTO-LARYNGOL, V111, P879, DOI 10.3109/00016489109138425 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 12 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 1993 VL 66 IS 1 BP 53 EP 57 DI 10.1016/0378-5955(93)90259-4 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000006 PM 7682544 ER PT J AU TANAKA, H WONG, D AF TANAKA, H WONG, D TI THE INFLUENCE OF TEMPORAL PATTERN OF STIMULATION ON DELAY TUNING OF NEURONS IN THE AUDITORY-CORTEX OF THE FM BAT, MYOTIS-LUCIFUGUS SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; DELAY SENSITIVITY; TEMPORAL SEQUENCE; VELOCITY SENSITIVITY; ECHOLOCATION; FM BAT ID COMBINATION-SENSITIVE NEURONS; PTERONOTUS-P-PARNELLII; ECHOLOCATING BAT; BIOSONAR SIGNALS; MUSTACHED BAT; TARGET RANGE; REPRESENTATION; INFORMATION; CAT; COLLICULUS AB In echolocating bats, delay-sensitive neurons show facilitative responses to simulated pulse-echo pairs at particular echo delays. Three experiments examined how the temporal pattern of stimulation affected the delay tuning of neurons in the auditory cortex of the awake FM bat, Myotis lucifugus. First, delay tuning was compared using a series of pulse-echo pairs fixed in echo delay ('standard' stimuli), and a series of pulse-echo pairs in which successive sound pairs decreased by a fixed echo-delay step ('approach' stimuli). Similar best delays were measured with both stimulation patterns presented at repetition rates in which the neuron was delay-sensitive. At the higher delay-sensitive pulse repetition rates, approach stimuli evoked larger delay-dependent responses. Second, approach stimuli were fixed at different intertrial intervals. The best delay was unaffected by intertrial interval, although some neurons showed larger responses for longer intertrial intervals (0.5, 1.0 s), especially at the higher delay-sensitive pulse repetition rates. Third, approach stimuli were fixed at different echo-delay steps to simulate target velocity. The majority of neurons showed some sensitivity to echo-delay step, with clear preference for target velocity mainly between 1.8-7.0 m/s. This suggests that delay-sensitive neurons compute target velocity by rate of change of echo delay over successive echoes. Thus, response properties of cortical neurons are influenced by dynamic acoustic conditions found in target-directed flight. C1 INDIANA UNIV,SCH MED,DEPT ANAT,MED SCI BLDG,ROOM 205,INDIANAPOLIS,IN 46202. CR ABELES M, 1972, BRAIN RES, V42, P337, DOI 10.1016/0006-8993(72)90535-5 BERKOWITZ A, 1989, HEARING RES, V41, P255, DOI 10.1016/0378-5955(89)90017-8 FENG AS, 1978, SCIENCE, V202, P645, DOI 10.1126/science.705350 Griffin D. R., 1960, Animal Behaviour, V8, P141, DOI 10.1016/0003-3472(60)90022-1 Griffin DR, 1958, LISTENING DARK HABERSETZER J, 1983, J COMP PHYSIOL, V152, P275 HENSON OW, 1982, HEARING RES, V7, P127, DOI 10.1016/0378-5955(82)90010-7 HOCHERMAN S, 1981, J NEUROPHYSIOL, V45, P987 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1275 ONEILL WE, 1982, J NEUROSCI, V2, P17 PHILLIPS DP, 1985, HEARING RES, V19, P253, DOI 10.1016/0378-5955(85)90145-5 Sales GD, 1974, ULTRASONIC COMMUNICA Schnitzler H. U., 1980, ANIMAL SONAR SYSTEMS, P109, DOI 10.1007/978-1-4684-7254-7_6 SCHNITZL.HU, 1970, Z VERGL PHYSIOL, V68, P25, DOI 10.1007/BF00297809 SCHNITZLER HU, 1987, J COMP PHYSIOL A, V161, P267, DOI 10.1007/BF00615246 SCHNITZL.HU, 1968, Z VERGL PHYSIOL, V57, P376, DOI 10.1007/BF00303062 Schnitzler H.-U., 1984, P211 SCHULLER G, 1991, EUR J NEUROSCI, V3, P1165, DOI 10.1111/j.1460-9568.1991.tb00051.x SCHULLER G, 1979, J COMP PHYSIOL, V132, P47 SCHULLER G, 1974, J COMP PHYSIOL, V89, P275, DOI 10.1007/BF00696191 SHAMMA SA, 1985, HEARING RES, V19, P1, DOI 10.1016/0378-5955(85)90094-2 Simmons J. A., 1988, ANIMAL SONAR PROCESS, P353 SIMMONS JA, 1974, J ACOUST SOC AM, V56, P672, DOI 10.1121/1.1903307 SIMMONS JA, 1975, AM SCI, V63, P204 SUGA N, 1986, J NEUROPHYSIOL, V55, P776 SUGA N, 1990, GOLD SPRING HARBOR S, V55, P585 SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUGA N, 1978, SCIENCE, V200, P778, DOI 10.1126/science.644320 SUGA N, 1983, J NEUROPHYSIOL, V49, P1573 SULLIVAN WE, 1982, J NEUROPHYSIOL, V48, P1011 SUTHERS RA, 1965, J EXP ZOOL, V158, P319, DOI 10.1002/jez.1401580307 TANAKA H, 1992, J COMP PHYSIOL A, V171, P29 WENSTRUP JJ, 1984, J COMP PHYSIOL, V155, P75, DOI 10.1007/BF00610933 WONG D, 1992, J COMP PHYSIOL A, V170, P393 WONG D, 1984, HEARING RES, V16, P261, DOI 10.1016/0378-5955(84)90115-1 WONG D, 1988, BRAIN RES, V453, P349, DOI 10.1016/0006-8993(88)90176-X NR 36 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 1993 VL 66 IS 1 BP 58 EP 66 DI 10.1016/0378-5955(93)90260-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000007 PM 8473246 ER PT J AU SHOFNER, WP YOST, WA SHEFT, S AF SHOFNER, WP YOST, WA SHEFT, S TI INCREMENT DETECTION OF BAND-LIMITED NOISES IN THE CHINCHILLA SO HEARING RESEARCH LA English DT Article DE INTENSITY DISCRIMINATION; CHINCHILLA; NOISE; BANDWIDTH ID INTENSITY DISCRIMINATION; MODULATION THRESHOLDS; HEARING-LOSS; BANDWIDTH; RESPONSES; MASKING; LEVEL AB A positive reinforcement, adaptive tracking procedure was used to study the intensity discrimination abilities of six chinchillas to noise signals. Increment detection thresholds were obtained using a two-down, one-up tracking rule. The effect of overall noise masker level and the effect of noise bandwidth on increment detection thresholds were studied. The continuous noise masker and the signal increment had equal bandwidths. Increment detection thresholds are independent of overall level for wideband noise; the asymtotic DL for wideband noise is 1.334 dB. In addition, increment detection thresholds decrease as the bandwidth of the noise increases. The observed slope of the bandwidth function for the chinchilla is independent of overall level and is around - 2.8 dB/decade. The slope of the bandwidth function obtained for the chinchilla is similar to values reported for human subjects under similar conditions, but is less than the slope predicted by the ideal energy detector model. RP SHOFNER, WP (reprint author), LOYOLA UNIV,PARMLY HEARING INST,6525 N SHERIDAN AVE,CHICAGO,IL 60626, USA. CR Bendat J., 1971, RANDOM DATA ANAL MEA BOS CE, 1966, J ACOUST SOC AM, V39, P708, DOI 10.1121/1.1909945 BUUS S, 1990, J ACOUST SOC AM, V87, P2643, DOI 10.1121/1.399057 CAMPBELL RA, 1964, J ACOUST SOC AM, V36, P570, DOI 10.1121/1.1919004 CARDER HM, 1972, J SPEECH HEAR RES, V15, P603 CLARK WW, 1974, J ACOUST SOC AM, V56, P1202, DOI 10.1121/1.1903409 CLOPTON BM, 1972, J EXP ANAL BEHAV, V17, P473, DOI 10.1901/jeab.1972.17-473 Creelman C. D., 1991, DETECTION THEORY USE DAVIES OL, 1984, STATISTICAL METHODS DEBOER E, 1966, J ACOUST SOC AM, V40, P552, DOI 10.1121/1.1910118 Fay R. R., 1988, HEARING VERTEBRATES FAY RR, 1985, J ACOUST SOC AM, V78, P1296, DOI 10.1121/1.392899 GOLDBERG JM, 1906, J NEUROPHYSIOL, V29, P72 GRANTHAM DW, 1982, J ACOUST SOC AM, V72, P406, DOI 10.1121/1.388092 Green D. M., 1988, PROFILE ANAL AUDITOR GREEN DM, 1960, J ACOUST SOC AM, V32, P121, DOI 10.1121/1.1907862 GREEN DM, 1975, PSYCHOL REV, V82, P483, DOI 10.1037//0033-295X.82.6.483 GREENWOO.DD, 1970, J ACOUST SOC AM, V47, P1022, DOI 10.1121/1.1912002 GREENWOO.DD, 1965, J NEUROPHYSIOL, V28, P863 HENDERSON D, 1984, J ACOUST SOC AM, V75, P1177, DOI 10.1121/1.390767 LESHOWIT.B, 1971, J ACOUST SOC AM, V49, P1180, DOI 10.1121/1.1912480 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 MILLER GA, 1947, J ACOUST SOC AM, V19, P609, DOI 10.1121/1.1916528 MOORE BCJ, 1975, J ACOUST SOC AM, V57, P391, DOI 10.1121/1.380454 MOORE BCJ, 1975, J ACOUST SOC AM, V57, P400, DOI 10.1121/1.380455 NIEMIEC AJ, 1992, J ACOUST SOC AM, V92, P2636, DOI 10.1121/1.404380 RAAB DH, 1975, J ACOUST SOC AM, V57, P437, DOI 10.1121/1.380467 RUGGERO MA, 1973, J NEUROPHYSIOL, V36, P569 SALVI RJ, 1982, J ACOUST SOC AM, V71, P424, DOI 10.1121/1.387445 SAUNDERS SS, 1987, J ACOUST SOC AM, V82, P1604, DOI 10.1121/1.395150 SCHACKNOW PN, 1976, J ACOUST SOC AM, V60, P893, DOI 10.1121/1.381170 SCHALK TB, 1980, J ACOUST SOC AM, V67, P903, DOI 10.1121/1.383970 SMALL AM, 1959, J ACOUST SOC AM, V31, P508, DOI 10.1121/1.1907743 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 NR 35 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 MAR PY 1993 VL 66 IS 1 BP 67 EP 80 DI 10.1016/0378-5955(93)90261-X PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000008 PM 8473247 ER PT J AU XIE, DH HENSON, MM BISHOP, AL HENSON, OW AF XIE, DH HENSON, MM BISHOP, AL HENSON, OW TI EFFERENT TERMINALS IN THE COCHLEA OF THE MOUSTACHED BAT - QUANTITATIVE DATA SO HEARING RESEARCH LA English DT Article DE COCHLEA; EFFERENT; OLIVOCOCHLEAR; HAIR CELL; BAT ID GUINEA-PIG COCHLEA; SUPERIOR OLIVARY COMPLEX; DOPPLER-SHIFTED ECHOES; PTERONOTUS-PARNELLII; FREQUENCY REPRESENTATION; OLIVOCOCHLEAR NEURONS; AUDITORY-SYSTEM; IMMUNOREACTIVITY; FIBERS; INNERVATION AB Efferent terminals in the cochlea of the mustached bat were stained for acetylcholinesterase (AChE) and quantitative data were obtained for the number and size of the endings on the outer hair cells (OHCs) in each row, from base to apex. From TEM micrographs and AChE-stained, surface preparations it was determined that every OHC had a single, large terminal. The mean size of the terminals was significantly different in each row, with the largest occurring in the first row (7.1 mum2); the mean size in the second and third rows was 5.7 and 5.0 mum2 respectively. In specific frequency processing regions, the largest mean size (8.4 mum2) for first row OHCs was consistently found in the distal densely innervated (DDI) area. This region has afferent neurons that are sharply tuned to the second harmonic, constant frequency component of the bat's biosonar signals. Sudden changes in the size of the terminals were observed exactly at the boundaries of the DDI with adjacent sparsely innervated regions. Similar, but less striking, size changes also occurred in and adjacent to the proximal densely innervated (PDI) region, a harmonically related, sharply tuned region, which processes the bat's 91.5 kHz, third harmonic, constant frequency signals. The region of the cochlea with the smallest first row terminals (mean 5.3 mum2) was the large, sparsely innervated region of the basal turn, a region that does not appear to process biosonar signals. Although the significance of differences in efferent terminal size is not known, the data suggest a possible correlation between OHC stimulation and sharp tuning. The potentially greater influence of the efferent fibers on the first row of OHCs, compared to other rows, is consistent with observations made on other mammals; in the latter, however, the greater influence has been suggested more by number than size. Unlike other mammals, the OHC efferents in the mustached bat have no clear base-to-apex gradient in the number or size of the efferent terminals. It is suggested that this might reflect the high frequency nature of the ear (6-120 kHz) and absence of low frequency hearing. C1 UNIV N CAROLINA,DEPT CELL BIOL & ANAT,108 TAYLOR HALL,CB 7090,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27599. GLAXO INC,RESP CLIN RES,RES TRIANGLE PK,NC. CR ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 Bishop AL, 1988, ANIMAL SONAR, P307 BISHOP AL, 1987, HEARING RES, V31, P175, DOI 10.1016/0378-5955(87)90124-9 BODIAN D, 1980, J COMP NEUROL, V192, P785, DOI 10.1002/cne.901920411 BODIAN D, 1983, HEARING RES, V9, P201, DOI 10.1016/0378-5955(83)90028-X BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BRUNS V, 1989, J MORPHOL, V199, P103, DOI 10.1002/jmor.1051990109 BRUNS V, 1980, HEARING RES, V3, P27, DOI 10.1016/0378-5955(80)90006-4 CHURCHILL JOHN A., 1959, HENRY FORD HOSP MED BULL, V7, P202 DANNHOF BJ, 1991, CELL TISSUE RES, V266, P89, DOI 10.1007/BF00678715 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 FEX J, 1984, HEARING RES, V15, P123, DOI 10.1016/0378-5955(84)90043-1 FEX J, 1982, HEARING RES, V7, P149, DOI 10.1016/0378-5955(82)90011-9 FEX J, 1981, P NATL ACAD SCI-BIOL, V78, P1255, DOI 10.1073/pnas.78.2.1255 FIRBAS W, 1970, ACTA OTO-LARYNGOL, V70, P329 GINZBERG RD, 1984, HEARING RES, V14, P109, DOI 10.1016/0378-5955(84)90011-X GODFREY DA, 1985, ANN OTO RHINOL LARYN, V94, P409 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 HASHIMOTO S, 1987, ACTA OTO-LARYNGOL, V103, P64 HENSON MM, 1984, HEARING RES, V16, P231, DOI 10.1016/0378-5955(84)90112-6 HENSON MM, 1973, J ACOUST SOC AM, V53, P1739, DOI 10.1121/1.1913529 HENSON MM, 1982, HEARING RES, V7, P91, DOI 10.1016/0378-5955(82)90083-1 HENSON MM, 1983, HEARING RES, V10, P153, DOI 10.1016/0378-5955(83)90051-5 HENSON MM, 1991, HEARING RES, V56, P122, DOI 10.1016/0378-5955(91)90161-2 HENSON OW, 1985, J COMP PHYSIOL A, V157, P587, DOI 10.1007/BF01351353 HUFFMAN RF, 1992, IN PRESS J COMP PH A Ishii D, 1968, Acta Otolaryngol, V66, P282, DOI 10.3109/00016486809126295 Ishii T, 1967, Acta Otolaryngol, V64, P267, DOI 10.3109/00016486709139116 ISHII T, 1967, ANN OTO RHINOL LARYN, V76, P69 IURATO S, 1978, J COMP NEUROL, V182, P57, DOI 10.1002/cne.901820105 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KOSSL M, 1990, J COMP PHYSIOL A, V166, P711 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 NAKAI Y, 1974, ACTA OTO-LARYNGOL, V77, P393, DOI 10.3109/00016487409124641 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 POLLAK GD, 1981, J NEUROPHYSIOL, V46, P605 POLLAK G, 1972, SCIENCE, V176, P66, DOI 10.1126/science.176.4030.66 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 ROTH B, 1991, ANAT EMBRYOL, V183, P483 SCHNITZL.HU, 1970, Z VERGL PHYSIOL, V68, P25, DOI 10.1007/BF00297809 SCHNITZLER H-U, 1970, Bijdragen tot de Dierkunde, V40, P77 SIMMONS DD, 1990, HEARING RES, V49, P127, DOI 10.1016/0378-5955(90)90100-4 Smith C A, 1973, Adv Otorhinolaryngol, V20, P296 SMITH CA, 1961, J ULTRA MOL STRUCT R, V5, P523, DOI 10.1016/S0022-5320(61)80025-7 SMITH CA, 1975, ANN OTO RHINOL LARYN, V84, P443 SPOENDLIN H, 1963, ANN OTO RHINOL LARYN, V72, P60 SUGA N, 1977, J EXP BIOL, V69, P207 SUGA N, 1975, J EXP BIOL, V63, P161 TAGO H, 1986, J HISTOCHEM CYTOCHEM, V34, P1431 Takasaka T, 1987, Acta Otolaryngol Suppl, V435, P7 TEAS DC, 1972, J ACOUST SOC AM, V51, P1256, DOI 10.1121/1.1912969 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WIEDERHOLD ML, 1967, THESIS MIT WILSON JL, 1991, HEARING RES, V55, P98, DOI 10.1016/0378-5955(91)90096-R ZOOK JM, 1989, J COMP NEUROL, V290, P243, DOI 10.1002/cne.902900206 NR 60 TC 9 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 1993 VL 66 IS 1 BP 81 EP 90 DI 10.1016/0378-5955(93)90262-Y PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000009 PM 7682545 ER PT J AU MCPHERSON, DL STARR, A AF MCPHERSON, DL STARR, A TI BINAURAL INTERACTION IN AUDITORY EVOKED-POTENTIALS - BRAIN-STEM, MIDDLE-LATENCY AND LONG-LATENCY COMPONENTS SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIAL; BRAIN-STEM; MIDDLE-LATENCY; LONG-LATENCY; BINAURAL INTERACTION; EVOKED POTENTIAL; ADULTS ID RESPONSES; STEM; LESIONS; CORTEX; ORIGIN AB Binaural interaction occurs in the auditory evoked potentials when the sum of the monaural auditory evoked potentials are not equivalent to the binaural evoked auditory potentials. Binaural interaction of the early- (0-10 ms), middle- (10-50 ms) and long-latency (50-200 ms) auditory evoked potentials was studied in 17 normal young adults. For the early components, binaural interaction was maximal at 7.35 ms accounting for a reduction of 21% of the amplitude of the binaural evoked potentials. For the middle latency auditory evoked potentials, binaural interaction was maximal at 39.6 ms accounting for a reduction of 48% of the binaural evoked potential. For the long-latency auditory evoked potentials, binaural interaction was maximal at 145 ms accounting for a reduction of 38% of the binaural evoked potential. In all of the auditory evoked potentials binaural interaction was long lasting around the maxima. The binaural interaction component extends for several milliseconds in the brainstem to tens of milliseconds in the middle- and long-latency components. Binaural interaction takes the form of a reduction of amplitude of the binaural evoked potential relative to the sum of the monaural responses, suggests that inhibitory processes are represented in binaural interaction using evoked potentials. Binaural processing in the auditory pathway is maximal in the time domain of the middle-latency components reflecting activity in the thalamo-cortical portions of the auditory pathways. C1 UNIV CALIF IRVINE,DEPT NEUROL,IRVINE,CA 92717. RP MCPHERSON, DL (reprint author), BRIGHAM YOUNG UNIV,HEARING & SPEECH SCI LAB,PROGRAM AUDIOL,129 TLRB,PROVO,UT 84602, USA. CR BAILEY BJR, 1977, J AM STAT ASSOC, V72, P468 BAILEY BJR, 1977, J AM STAT ASSOC, V72, P358 BERLIN CI, 1984, HEARING SCI RECENT A, P461 BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 BUTLER RA, 1969, ACTA OTO-LARYNGOL, V68, P317, DOI 10.3109/00016486909121570 DECKER TN, 1981, J ACOUST SOC AM, V69, P1084, DOI 10.1121/1.385687 DOBIE RA, 1979, ARCH OTOLARYNGOL, V105, P391 DOBIE RA, 1980, ELECTROEN CLIN NEURO, V49, P303, DOI 10.1016/0013-4694(80)90224-2 DOBIE RA, 1982, J ACOUST SOC AM, V71, P1031, DOI 10.1121/1.387584 GEISSER S, 1958, ANN MATH STAT, V29, P885, DOI 10.1214/aoms/1177706545 JEWETT DL, 1971, BRAIN, V94, P681, DOI 10.1093/brain/94.4.681 KELLYBALLWEBER D, 1984, AUDIOLOGY, V3, P181 Kemp EH, 1937, AM J PHYSIOL, V120, P316 KRAUS N, 1982, ELECTROEN CLIN NEURO, V54, P275, DOI 10.1016/0013-4694(82)90177-8 LEVINE RA, 1983, ELECTROEN CLIN NEURO, V55, P532, DOI 10.1016/0013-4694(83)90163-3 LOTT IT, 1986, ELECTROEN CLIN NEURO, V64, P218, DOI 10.1016/0013-4694(86)90169-0 MCPHERSON DL, 1989, ELECTROEN CLIN NEURO, V74, P124, DOI 10.1016/0168-5597(89)90017-8 MENDEL MI, 1983, AUDIOLOGY, V10, P141 MOLLER AR, 1981, ELECTROEN CLIN NEURO, V52, P18, DOI 10.1016/0013-4694(81)90184-X MOORE DR, 1991, AUDIOLOGY, V1, P125 PELIZZONE M, 1987, NEUROSCI LETT, V82, P303, DOI 10.1016/0304-3940(87)90273-4 PERONNET F, 1977, PROGR CLIN NEUROPHYS, V2, P130 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 ROSENZWEIG MR, 1955, EXPERIENTIA, V11, P498, DOI 10.1007/BF02166840 STARR A, 1976, ELECTROEN CLIN NEURO, V41, P595, DOI 10.1016/0013-4694(76)90005-5 TIIHONEN J, 1989, AUDIOLOGY, V28, P37 WERNICK JS, 1968, J NEUROPHYSIOL, V3, P428 WREGE KS, 1981, ARCH NEUROL-CHICAGO, V38, P572 NR 28 TC 61 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 MAR PY 1993 VL 66 IS 1 BP 91 EP 98 DI 10.1016/0378-5955(93)90263-Z PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000010 PM 8473249 ER PT J AU DEW, LA OWEN, RG MULROY, MJ AF DEW, LA OWEN, RG MULROY, MJ TI CHANGES IN SIZE AND SHAPE OF AUDITORY HAIR-CELLS INVIVO DURING NOISE-INDUCED TEMPORARY THRESHOLD SHIFT SO HEARING RESEARCH LA English DT Article DE TEMPORARY DEAFNESS; ACOUSTIC TRAUMA; RELAXATION; OSMOSIS; SYNAPTIC VESICLE MEMBRANE; COCHLEA; EAR; LIZARD ID GUINEA-PIG COCHLEA; ALLIGATOR LIZARD; ACTIN-FILAMENTS; ACOUSTIC TRAUMA; STEREOCILIA; EXPOSURE; ORGANIZATION; ENDOCYTOSIS; RESPONSES; INVITRO AB In this study we describe changes in the size and shape of auditory hair cells of the alligator lizard in vivo during noise-induced temporary threshold shift. These changes consist of a decrease in cell volume, a decrease in cell length and an increase in cell width. We speculate that these changes are due to relaxation of cytoskeletal contractile elements and osmotic loss of intracellular water. We also describe a decrease in the surface area of the hair cell plasmalemma, and speculate that it is related to the endocytosis and intracellular accummulation of cell membrane during synaptic vesicle recycling. Finally we describe an increase in the endolymphatic surface area of the hair cell, and speculate that this could alter the micromechanics of the stereociliary tuft to attenuate the effective stimulus. C1 MED COLL GEORGIA,DEPT CELLULAR BIOL & ANAT,AUGUSTA,GA 30912. MED COLL GEORGIA,OTOLARYNGOL SECT,AUGUSTA,GA 30912. CR Beagley H A, 1965, Acta Otolaryngol, V60, P479, DOI 10.3109/00016486509127031 BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 DECORY L, 1991, HEARING RES, V52, P81, DOI 10.1016/0378-5955(91)90189-G DUNN DE, 1979, ABST ASS RES OTOLARY, P37 FLOCK A, 1984, HEARING RES, V15, P11 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FREEMAN DM, 1990, HEARING RES, V48, P1, DOI 10.1016/0378-5955(90)90195-U HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 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 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 MILLER TM, 1984, J CELL BIOL, V98, P685, DOI 10.1083/jcb.98.2.685 MODEL PG, 1975, BRAIN RES, V98, P209, DOI 10.1016/0006-8993(75)90002-5 MULROY MJ, 1984, SCANNING ELECT MICRO, V2, P831 MULROY MJ, 1987, HEARING RES, V25, P11, DOI 10.1016/0378-5955(87)90075-X MULROY MJ, 1990, HEARING RES, V49, P79, DOI 10.1016/0378-5955(90)90096-8 MULROY MJ, 1985, J COMP NEUROL, V233, P463, DOI 10.1002/cne.902330405 MULROY MJ, 1986, SCANNING ELECTRON MI, V4, P1451 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A ROBERTSON D, 1983, HEARING RES, V9, P263, DOI 10.1016/0378-5955(83)90031-X SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 Schaeffer S F, 1976, Cold Spring Harb Symp Quant Biol, V40, P521 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 STOPP P, 1982, NEW PERSPECTIVES NOI, P331 STOPP PE, 1983, HEARING RES, V11, P55, DOI 10.1016/0378-5955(83)90045-X SYZMKO YM, 1992, HEARING RES, V59, P241 THORNE PR, 1986, HEARING RES, V21, P41, DOI 10.1016/0378-5955(86)90044-4 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 TILNEY LG, 1980, J CELL BIOL, V86, P244, DOI 10.1083/jcb.86.1.244 WEISS TF, 1974, J ACOUST SOC AM, V55, P606, DOI 10.1121/1.1914571 ZAMORA AJ, 1984, NEUROSCIENCE, V13, P105, DOI 10.1016/0306-4522(84)90263-X ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 36 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 MAR PY 1993 VL 66 IS 1 BP 99 EP 107 DI 10.1016/0378-5955(93)90264-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000011 PM 7682546 ER PT J AU SHEPHERD, RK HATSUSHIKA, S CLARK, GM AF SHEPHERD, RK HATSUSHIKA, S CLARK, GM TI ELECTRICAL-STIMULATION OF THE AUDITORY-NERVE - THE EFFECT OF ELECTRODE POSITION ON NEURAL EXCITATION SO HEARING RESEARCH LA English DT Article DE COCHLEAR IMPLANTS; ELECTRODE ARRAY; EVOKED POTENTIALS; COCHLEAR PATHOLOGY ID BRAIN-STEM RESPONSE; COCHLEAR IMPLANT PATIENTS; AMINOOXYACETIC ACID; INSERTION TRAUMA; SPIRAL GANGLION; TEMPORAL BONES; SCALA TYMPANI; ARRAY; OTOTOXICITY; KANAMYCIN AB Histological studies have shown that the Melbourne/Cochlear electrode array lies along the outer wall of the scala tympani and is therefore some distance from the residual VIII(th) nerve elements. In order to investigate the influence of electrode position on neural excitation we systematically varied the position of the electrode array within the cat scala tympani while recording electrically evoked auditory brainstem responses (EABRs). Using both normal hearing and long-term deafened animals, we observed significant reductions in EABR thresholds as the electrode array was moved from the outer wall towards the modiolus. Further threshold reductions were observed when the array was placed underneath the osseous spiral lamina (OSL) close to the peripheral dendrites. These changes were independent of the bipolar inter-electrode separation, and were observed over a wide range of cochlear pathologies varying from normal to a moderate spiral ganglion cell loss. Interestingly, the one animal exhibiting extensive neural loss showed no correlation between EABR threshold and electrode position. There was also a general decrease in the gradient of the EABR input-output function as the electrode array was moved closer to the neural elements. This was, however, only statistically significant when the electrode was positioned adjacent to the peripheral dendrites. Significant reductions in EABR threshold were also observed as the inter-electrode spacing of the bipolar electrodes was increased. The gradient of the EABR input-output function also increased with increasing inter-electrode spacing, although again, this was only significant when the electrode array was positioned close to the neural elements. The present results indicate that the optimum placement of a Melbourne/Cochlear electrode array is adjacent to the peripheral dendrites. However, such a site would be difficult to achieve in practice while minimizing insertion trauma. An array lying adjacent to the modiolus would be a safe alternative while ensuring a significant reduction in threshold compared with the existing site (outer wall). This placement should result in more localized neural excitation patterns, an increase in the number of bipolar electrodes available, together with an increase in their dynamic range. These changes may lead to further improvements in speech perception among cochlear implant patients. C1 UNIV MELBOURNE,DEPT OTOLARYNGOL,PARKVILLE,VIC 3052,AUSTRALIA. RI Shepherd, Robert/I-6276-2012 CR ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W ABBAS PJ, 1988, HEARING RES, V36, P156 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BLAMEY PJ, 1992, ANN OTO RHINOL LARYN, V101, P342 BROWN M, 1992, HEARING RES, V59, P224, DOI 10.1016/0378-5955(92)90119-8 BRUMMETT RE, 1982, AMINOGLYCOSIDES MICR BRYANT GM, 1984, HEARING RES, V15, P173, DOI 10.1016/0378-5955(84)90048-0 CLARK GM, 1983, ANN NY ACAD SCI, V405, P191, DOI 10.1111/j.1749-6632.1983.tb31632.x Clark G M, 1988, Acta Otolaryngol Suppl, V448, P1 CLARK GM, 1977, J LARYNGOL OTOL, V91, P185, DOI 10.1017/S0022215100083560 Eddington D. K., 1978, ANN OTOL S, V53, P5 FINLEY C, 1990, P IEEE ENG MED BIOL, V12, P2290 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HATSUSHIKA S, 1990, ANN OTO RHINOL LARYN, V99, P871 HATSUSHIKA SI, 1989, 14 WORLD C OT HEAD N, P75 HINOJOSA R, 1980, ARCH OTOLARYNGOL, V106, P193 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 KENNEDY DW, 1987, LARYNGOSCOPE, V97, P42 LEAKE PA, 1987, ANN OTO RHINOL LARYN, V96, P48 LEAKEJONES PA, 1983, ANN NY ACAD SCI, V405, P203, DOI 10.1111/j.1749-6632.1983.tb31634.x LIM HH, 1989, J ACOUST SOC AM, V86, P971, DOI 10.1121/1.398732 LUKIES PM, 1987, ANN OTO RHINOL LARYN, V96, P24 LUSTED HS, 1984, LARYNGOSCOPE, V94, P878 MARSH RR, 1981, OTOLARYNG HEAD NECK, V89, P125 MERZENICH MM, 1977, FUNCTIONAL ELECT STI, P321 NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 PFINGST BE, 1979, ANN OTO RHINOL LARYN, V88, P613 PFINGST BE, 1990, COCHLEAR IMPLANTS MO, P161 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L SAPOZHNIKOV A, 1990, THESIS U MELBOURNE A SCHINDLER RA, 1977, ARCH OTOLARYNGOL, V103, P691 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHEPHERD RK, 1990, INFORMATION PROCESSI, P281 SHEPHERD RK, 1985, ANN OTO RHINOL LARYN, V94, P55 SHEPHERD RK, 1988, 4TH U MELB DEP OT Q Shepherd R K, 1983, Acta Otolaryngol Suppl, V399, P19 SHEPHERD RK, 1987, 2ND U MELB DEP OT Q SHEPHERD RK, 1990, P AUST PHYSL PHARM S, V21 SHEPHERD RK, 1985, HEARING RES, V18, P105, DOI 10.1016/0378-5955(85)90001-2 SIMMONS FB, 1984, ANN OTO RHINOL LARYN, V93, P97 SIMMONS FB, 1967, LARYNGOSCOPE, V77, P171, DOI 10.1288/00005537-196702000-00003 SIMMONS FB, 1972, ANN OTO RHINOL LARYN, V81, P731 SUTTON D, 1983, ANN OTO RHINOL LARYN, V92, P53 TONG YC, 1985, J ACOUST SOC AM, V77, P1881, DOI 10.1121/1.391939 TONG YC, 1982, J ACOUST SOC AM, V71, P153, DOI 10.1121/1.387342 VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 WALLOCH RA, 1974, ARCH OTOLARYNGOL, V100, P19 XU SA, 1990, P AUST PHYSL PHARM S, V21 XU SA, 1992, P AUST SOC OTOLARYNG, P59 XU SA, 1992, P AUST NEUROSCI SOC, V3, P130 ZAPPIA JJ, 1991, ANN OTO RHINOL LARYN, V100, P914 NR 54 TC 179 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 MAR PY 1993 VL 66 IS 1 BP 108 EP 120 DI 10.1016/0378-5955(93)90265-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KW200 UT WOS:A1993KW20000012 PM 8473242 ER PT J AU GREENWOOD, DD AF GREENWOOD, DD TI THE INTENSITIVE DL OF TONES - DEPENDENCE OF SIGNAL MASKER RATIO ON TONE LEVEL AND ON SPECTRUM OF ADDED NOISE SO HEARING RESEARCH LA English DT Article DE INTENSITY DISCRIMINATION; MASKING; TTS; COCHLEA; NEURAL PATTERNS ID COCHLEAR NERVE-FIBERS; AUDITORY-NERVE; FREQUENCY-SELECTIVITY; BASILAR-MEMBRANE; MOSSBAUER TECHNIQUE; COMBINATION BANDS; ACOUSTIC TRAUMA; DISCRIMINATION; CAT; MASKING AB In Greenwood [J. Acoust. Soc. Am. 33, 484-502 (1961a)] the ratio of masked signal threshold to masker level (S/M) decreased about 4 dB at a masker level of about 50 dB SL, the 'transition' level, when noise bands were subcritical but not when supercritical. Schlauch et al. [J. Acoust. Soc. Am. 71, S73 (1982)] report a related result. A pilot study [Greenwood, Harvard Psychoacoustic Lab. Status Report 37, 8-9 (1961)] in which pure tones masked identical tones in-phase showed a larger change in S/M. Detailed tone-tone growth-of-masking curves from over a dozen subjects in 1967-69, and in 1960, are reported here. A transition in slope, of variable abruptness, often begins to occur at about 50 dB SL, dropping S/M ratio by 6 to 8 dB or more [Rabinowitz et al., J. Acoust. Soc. Am. 35, 1053 (1976)]; the curves sometimes possess two segments, sometimes are simply convex. All have overall slopes less than 1.0, known also as the 'near miss'. Consistent with other results [Zwicker, Acustica 6, 365-396 (1956); Viemeister, J. Acoust. Soc. Am. 51, 1265-1296 (1972); Moore and Raab, J. Acoust. Soc. Am. 55, 1049-1060 (1974)], addition of low-level wide-band and high-pass noise was found to counteract the change in S/M, i.e., to raise the high-level section of the growth-of-masking curve. However, the ability of narrow 'band-pass' noise to exert this effect was greatest when added at a frequency ratio (band/masking-tone) of 1.3 to 1.5, which seems more closely to link the effects of added noise to the effects of increasing a masking band from sub- to supercritical width (above). Interpretation of the decrease in DL with level begins by noting that the 'transition' level correlates approximately with the level at which a primary unit population excited by a given pure tone begins rapidly to expand basally. Underlying this, the basalward shift of a tone's displacement envelope peak accelerates at about the same level [Rhode, J. Acoust. Soc. Am. 49, 1218-1231 (1971); Sellick et al., J. Acoust. Soc. Am. 72, 131-141 (1982)]. Given the hypothesis that the DL may (normally) be determined by detection of the shift in the basal-edge of the tone's neural excitation zone, explanations of changes in the size of the DL - with level and with addition of high-side noise-must be cast first in terms of cochlear physics, in order to account for the level change needed for a tone to dominate more territory, i.e., to recruit more basal area and receptors at the expense of other components. Then, second, neuro-anatomical and physiological explanation is needed to specify (a) how the mechanically determined edge, between zones of dominance, is preserved at central synapses by the differences in neural discharge on either side of, and at, the edge (in rate, phase-locked timing, and/or variance) and (b) what determines the size of the minimal edge-shift needed for detection. In short, primary units recruited by a tone change their firing patterns - including positive or negative rate change, but the edge-shift itself may be what 'registers' in the CNS to determine an intensitive DL, as when a spot of light, with diameter increasing and edges shifting on the retina, is perceived to expand. C1 HARVARD UNIV,PSYCHOACOUST LAB,CAMBRIDGE,MA 02138. RP GREENWOOD, DD (reprint author), UNIV BRITISH COLUMBIA,SCH AUDIOL & SPEECH SCI,5804 FAIRVIEW CRESENT,VANCOUVER V6T 1Z3,BC,CANADA. CR BILGER RC, 1976, HEARING DAVIS ESSAYS, P191 BOS CE, 1966, J ACOUST SOC AM, V39, P708, DOI 10.1121/1.1909945 BRUGGE JF, 1969, J NEUROPHYSIOL, V27, P287 CARLYON RP, 1984, J ACOUST SOC AM, V76, P1369, DOI 10.1121/1.391453 CODY AR, 1980, HEARING RES, V3, P3, DOI 10.1016/0378-5955(80)90004-0 CODY AR, 1981, J ACOUST SOC AM, V70, P707, DOI 10.1121/1.386906 COOPER NP, 1992, ABSTR ASS RES OT, V49, P19 DAVIS H, 1950, ACTA OTOLARYNGOL S, V88, P4 DEATHERAGE BH, 1957, J ACOUST SOC AM, V29, P512, DOI 10.1121/1.1908944 DEBOER E, 1962, J ACOUST SOC AM, V34, P985, DOI 10.1121/1.1918235 DELGUTTE B, 1986, PSYCHOPHYSICS SPEECH, P333 EGAN JP, 1950, J ACOUST SOC AM, V22, P622, DOI 10.1121/1.1906661 EVANS EF, 1977, PSYCHOPHYSICS PHYSL, P320 EVANS EF, 1971, 7TH P INT C AC BUD, V3, P453 Fletcher H, 1940, REV MOD PHYS, V12, P0047, DOI 10.1103/RevModPhys.12.47 Fletcher H., 1953, SPEECH HEARING COMMU FLORENTINE M, 1983, J ACOUST SOC AM, V74, P1375, DOI 10.1121/1.390162 FLORENTINE M, 1981, J ACOUST SOC AM, V70, P1646, DOI 10.1121/1.387219 Galambos R, 1943, J NEUROPHYSIOL, V6, P39 Galambos R, 1944, J NEUROPHYSIOL, V7, P287 GARNER WR, 1947, J ACOUST SOC AM, V19, P600, DOI 10.1121/1.1916527 Garner WR, 1944, J EXP PSYCHOL, V34, P450, DOI 10.1037/h0059786 GOLDBERG JM, 1966, J NEUROPHYSIOL, V29, P72 GREEN DM, 1962, J ACOUST SOC AM, V34, P745, DOI 10.1121/1.1937328 GREEN DM, 1967, J ACOUST SOC AM, V41, P1517, DOI 10.1121/1.1910514 GREENBERG S, 1986, J ACOUST SOC AM, V79, P1010, DOI 10.1121/1.393373 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P484, DOI 10.1121/1.1908699 GREENWOO.DD, 1972, J ACOUST SOC AM, V52, P1144, DOI 10.1121/1.1913227 GREENWOOD DD, 1983, UNPUB TONE NOISE BAN GREENWOOD DD, 1983, J ACOUST SOC AM S1, V73, pS91, DOI 10.1121/1.2020633 GREENWOOD DD, 1961, HARVARD PSYCHOACOUST, V37, P8 GREENWOOD DD, 1991, J NEUROPHYSIOL, V54, P209 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 GREENWOO.DD, 1970, J ACOUST SOC AM, V47, P1022, DOI 10.1121/1.1912002 GREENWOO.DD, 1965, J NEUROPHYSIOL, V28, P863 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 GREENWOO.DD, 1972, J ACOUST SOC AM, V52, P1155, DOI 10.1121/1.1913228 GREENWOO.DD, 1971, J ACOUST SOC AM, V50, P502, DOI 10.1121/1.1912668 HAMILTON PM, 1957, J ACOUST SOC AM, V29, P506, DOI 10.1121/1.1908942 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 JESTEADT W, 1977, J ACOUST SOC AM, V61, P169, DOI 10.1121/1.381278 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 KIANG N, 1968, J ACOUST SOC AM, V42, P1341 KIM DO, 1980, SCAND AUDIOL S, V9, P83 KIM DO, 1979, J NEUROPHYSIOL, V42, P16 Kohllöffel L U, 1971, Acta Otolaryngol Suppl, V288, P1 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIM JS, 1974, THESIS MIT CAMBRIDGE LONSBURYMARTIN BL, 1978, J NEUROPHYSIOL, V41, P987 McFadden D., 1986, BASIC APPL ASPECTS N, P295 MCGILL WJ, 1968, J ACOUST SOC AM, V44, P576, DOI 10.1121/1.1911123 MCMAHON L, 1962, HARVARD PSYCHOACOUST, V40, P8 MILLER GA, 1947, J ACOUST SOC AM, V19, P609, DOI 10.1121/1.1916528 MOLLER AR, 1977, PSYCHOPHYSICS PHYSL, P195 MOLLER AR, 1977, J ACOUST SOC AM, V62, P135 MOLLER AR, 1983, BIOL CYBERN, V47, P95, DOI 10.1007/BF00337083 MOLLER AR, 1978, ACTA PHYSIOL SCAND, V104, P24, DOI 10.1111/j.1748-1716.1978.tb06247.x MOORE BCJ, 1974, J ACOUST SOC AM, V55, P1049, DOI 10.1121/1.1914646 NIENHUYS TGW, 1979, ACTA OTO-LARYNGOL, V88, P350, DOI 10.3109/00016487909137179 PENNER MJ, 1974, PERCEPT PSYCHOPHYS, V15, P568, DOI 10.3758/BF03199303 PFEIFFER R, 1975, J ACOUST SOC AM, V57, P867 PICKLES JO, 1979, J ACOUST SOC AM, V66, P1725, DOI 10.1121/1.383645 PICKLES JO, 1975, ACTA OTO-LARYNGOL, V80, P245, DOI 10.3109/00016487509121325 PICKLES JO, 1976, J ACOUST SOC AM, V60, P1151, DOI 10.1121/1.381217 RAAB DH, 1963, J ACOUST SOC AM, V35, P1053, DOI 10.1121/1.1918653 RABINOWITZ WM, 1976, J ACOUST SOC AM, V59, P1506, DOI 10.1121/1.381000 Reisz R. R., 1928, PHYS REV, V31, P867 RHODE WS, 1978, J NEUROPHYSIOL, V41, P692 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 ROSE JE, 1974, J NEUROPHYSIOL, V37, P218 ROSE JE, 1971, J NEUROPHYSIOL, V34, P685 SCHACKNO.PN, 1973, PERCEPT PSYCHOPHYS, V14, P449, DOI 10.3758/BF03211182 SCHAEFER TH, 1953, J ACOUST SOC AM, V22, P490 SCHLAUCH, 1982, J ACOUST SOC AM S1, V71, pS73 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SMALL AM, 1959, J ACOUST SOC AM, V31, P1619, DOI 10.1121/1.1907670 Stevens S S, 1940, Science, V92, P583, DOI 10.1126/science.92.2399.583 STEVENS SS, 1941, J PSYCHOL, V54, P315 VIEMEIST.NF, 1972, J ACOUST SOC AM, V51, P1265, DOI 10.1121/1.1912970 VIEMEISTER NF, 1983, SCIENCE, V221, P1206, DOI 10.1126/science.6612337 VIEMEISTER NF, 1988, AUDITORY FUNCTION WARD WD, 1959, J ACOUST SOC AM, V31, P522, DOI 10.1121/1.1907746 WARD WD, 1960, J ACOUST SOC AM, V32, P135, DOI 10.1121/1.1907865 WARD WD, 1960, J ACOUST SOC AM, V32, P235, DOI 10.1121/1.1908023 WILSON JP, 1975, J ACOUST SOC AM, V68, P1523 ZHANG M, 1992, ABSTR ASS RES OT, V47, P18 Zwicker E., 1970, FREQUENCY ANAL PERIO, P376 Zwicker E., 1956, Acustica, V6 ZWISLOCKI J, 1958, J ACOUST SOC AM, V30, P254, DOI 10.1121/1.1909559 NR 92 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 1993 VL 65 IS 1-2 BP 1 EP 39 DI 10.1016/0378-5955(93)90198-A PG 39 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300001 PM 8458743 ER PT J AU BERLIN, CI HOOD, LJ CECOLA, RP JACKSON, DF SZABO, P AF BERLIN, CI HOOD, LJ CECOLA, RP JACKSON, DF SZABO, P TI DOES TYPE-I AFFERENT NEURON DYSFUNCTION REVEAL ITSELF THROUGH LACK OF EFFERENT SUPPRESSION SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; CONTRALATERAL SUPPRESSION; AFFERENT AUDITORY SYSTEM; EFFERENT AUDITORY SYSTEM; ABSENT AUDITORY BRAIN-STEM RESPONSE; NORMAL PURE TONE SENSITIVITY; ABSENT MASKING LEVEL DIFFERENCE; ABSENT MIDDLE EAR MUSCLE REFLEXES ID COCHLEAR MICROMECHANICAL PROPERTIES; STIMULATED ACOUSTIC EMISSIONS; MASKING LEVEL DIFFERENCES; AUDITORY-NERVE FIBERS; OTOACOUSTIC EMISSIONS; CONTRALATERAL EAR; ELECTRICAL-STIMULATION; OLIVOCOCHLEAR NEURONS; SOUND STIMULATION; HEARING-LOSS AB We present here two patients and three control subjects to demonstrate the clinical utility of studying evoked otoacoustic emissions and their contralateral suppression, as an aid to the delineation of afferent neuron dysfunction and possible lack of efferent suppression. The key patients here who fail to show contralateral suppression of their very robust otoacoustic emissions, concomitantly show paradoxically absent auditory brainstem responses (ABRs) and absence of middle ear muscle reflexes despite normal audiograms in the 2 kHz region and normal tympanograms. One of these patients has nearly normal pure tone sensitivity up to 3 kHz. The other has normal sensitivity in the 2 kHz region, but poor sensitivity on either side of that frequency. In addition, the two patients of interest show absent masking level differences and inordinately poor speech discrimination. Three 'foils' are presented: one patient with poor hearing on either side of 2 kHz, one with Bell's Palsy, and the third with bilateral temporal lobe disease. These patients show respectively that (1) isolated normal hearing at 2 kHz, (2) absence of middle ear muscle reflexes and (3) conscious cortical awareness of sound do not contribute directly to this intriguing clinical state. We propose that these patients with absent ABRs suffer from an auditory nervous system dysfunction which disrupts access to the efferent system. This condition also disables whatever systems contribute to the neural synchrony inherent in recording compound far-field action potentials such as the ABR. There are a number of hypotheses to be considered here. One suggests that the key patients are deficient in synchronous activation of Type I afferent fibers to the degree that they cannot activate efferent feedback, or they may be able to use only so-called Type II afferent neurons to support their normal zones of pure tone sensitivity. A less likely consideration focuses on the notion that discharge of primary neurons might be in some way synchronized by an efferent system which in these patients is the primary source of deficit. RP BERLIN, CI (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES LAB,2020 GRAVIER ST,NEW ORLEANS,LA 70112, USA. CR BERLIN CI, 1978, OTOLARYNG HEAD NECK, V86, P111 BERLIN CI, VOLTA REV, V84, P352 BERLIN CI, 1991, ABSTR ASS RES OT BERLIN CI, 1982, STUDIES USE AMPLIFIC, P44 BUNO W, 1978, EXP NEUROL, V59, P62, DOI 10.1016/0014-4886(78)90201-7 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1991, MAY INT S OT EM KANS DJUPESLAND G, 1975, HDB CLIN IMPEDANCE A Glattke T.J., 1991, AM J AUDIOL, V1, P29 GROSE JH, 1983, J ACOUST SOC AM S1, V74, pS38, DOI 10.1121/1.2020934 GUINAN JJ, 1988, ABSTR ASS RES OT, P174 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 JW, 1979, THESIS BAYLOR COLLEG HANNLEY M, 1983, AUDIOLOGY, V22, P20 HIRSH IJ, 1948, J ACOUST SOC AM, V20, P536, DOI 10.1121/1.1906407 HOOD LJ, 1989, ASHA, V31, P109 HOOD LJ, 1986, NEUROBIOLOGY HEARING JERGER J, 1969, ACTA OTO-LARYNGOL, V258, P7 Jerger S., 1981, AUDITORY DISORDERS Katz J., 1985, HDB CLIN AUDIOLOGY 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, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 KILLION MC, 1984, HEARING INSTRUMENTS, V35, P30 Kim D. O., 1984, HEARING SCI RECENT A, P241 KRAUS N, 1984, LARYNGOSCOPE, V94, P400 LANDAU WM, 1957, NEUROLOGY, V7, P915 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1988, HEARING RES, V34, P179, DOI 10.1016/0378-5955(88)90105-0 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 LICKLIDER JCR, 1948, J ACOUST SOC AM, V20, P150, DOI 10.1121/1.1906358 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOUNTAIN DC, 1980, HEARING RES, V3, P231, DOI 10.1016/0378-5955(80)90049-0 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORTON SJ, 1990, EAR HEARING, V11, P121, DOI 10.1097/00003446-199004000-00006 OLSEN WO, 1976, AUDIOLOGY, V15, P287 PATUZZI R, 1991, MAY INT S OT EM KANS PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 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 SALONNA I, 1990, Bollettino Societa Italiana Biologia Sperimentale, V66, P167 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 STARR A, 1991, BRAIN, V114, P1157, DOI 10.1093/brain/114.3.1157 UZIEL AS, 1991, MAY INT S OT EM KANS VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr WB, 1986, NEUROBIOLOGY HEARING WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WORTHINGTON DW, 1980, EAR HEARING, V1, P281, DOI 10.1097/00003446-198009000-00009 1989, S361989 AM NAT STAND NR 54 TC 81 Z9 96 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 1993 VL 65 IS 1-2 BP 40 EP 50 DI 10.1016/0378-5955(93)90199-B PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300002 PM 8458758 ER PT J AU FRITZSCH, B NICHOLS, DH AF FRITZSCH, B NICHOLS, DH TI DII REVEALS A PRENATAL ARRIVAL OF EFFERENTS AT THE DIFFERENTIATING OTOCYST OF MICE SO HEARING RESEARCH LA English DT Article DE OLIVOCOCHLEAR EFFERENTS; VESTIBULAR EFFERENTS; MOTOR NEURON DEVELOPMENT; CENTRIFUGAL VESTIBULAR FIBERS; DEVELOPMENT ID HAIR CELL-DIFFERENTIATION; COCHLEAR INNERVATION; VESTIBULAR SYSTEM; BRAIN-STEM; MOUSE; RAT; FIBERS; NEURONS; EXPRESSION; GANGLIA AB We have reinvestigated the time of arrival of efferent fibers at the developing otocyst of mice employing diffusion of the lipophilic dye DiI in fixed tissue. In contrast to almost all previous reports, our data indicate a prenatal arrival of efferent fibers. A few efferent fibers were found to enter the eighth nerve root at embryonic day (ED) 10 1/2. Retrogradely labelled efferent cell bodies were at this stage coextensive with those of the facial motor nucleus, but started to segregate by ED 12. In contrast to retrogradely labelled facial motor neurons, labelled efferent neurons were bilaterally distributed in the hindbrain with a few projecting to both otocysts as early as ED 12. Anterograde labelling from the brain showed efferent fibers in the vestibular ganglion by ED 11. Invasion of the future vestibular sensory epithelia started by ED 12. Growth cones of efferent fibers had also reached the future cochlear sensory epithelium but invasion was only achieved by a few filopodia at this stage. The early arrival of efferents at the future sensory epithelia demonstrated here may allow an as yet unexplored interaction of efferent fibers with the proliferating and/or differentiating hair cells. RP FRITZSCH, B (reprint author), CREIGHTON UNIV,DEPT BIOMED SCI,OMAHA,NE 68178, USA. CR ALTMAN J, 1980, J COMP NEUROL, V194, P877, DOI 10.1002/cne.901940410 ALTMAN J, 1982, ADV ANAT EMBRYOL CEL, V74, P1 Anniko M., 1983, DEV AUDITORY VESTIBU, P375 CAMPBELL JP, 1988, HEARING RES, V35, P271, DOI 10.1016/0378-5955(88)90124-4 EMMERLING MR, 1990, J ELECTRON MICR TECH, V15, P123, DOI 10.1002/jemt.1060150205 FAVRE D, 1978, BRAIN RES, V142, P333, DOI 10.1016/0006-8993(78)90639-X FRITZSCH B, 1990, TRENDS NEUROSCI, V13, P14, DOI 10.1016/0166-2236(90)90056-G FRITZSCH B, 1987, NEUROSCI LETT, V81, P48, DOI 10.1016/0304-3940(87)90338-7 FRITZSCH B, 1990, J COMP NEUROL, V300, P405 FRITZSCH B, 1991, J NEUR ABSTR, V17, P632 Gacek R R, 1982, Adv Otorhinolaryngol, V28, P1 GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 GODEMENT P, 1987, DEVELOPMENT, V101, P687 GOFFINET AM, 1984, J ANAT, V138, P207 GOLDBERG JM, 1980, J NEUROPHYSIOL, V43, P986 HAFIDI A, 1990, J COMP NEUROL, V300, P153, DOI 10.1002/cne.903000202 Hogan B, 1986, MANIPULATING MOUSE E HONIG MG, 1989, TRENDS NEUROSCI, V12, P333, DOI 10.1016/0166-2236(89)90040-4 IURATO S, 1974, HDB SENSORY PHYSL, V5, P261 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC LUMSDEN A, 1990, TRENDS NEUROSCI, V13, P329, DOI 10.1016/0166-2236(90)90144-Y NODEN DM, 1991, BRAIN BEHAV EVOLUT, V38, P190, DOI 10.1159/000114388 OPPENHEIM RW, 1991, ANNU REV NEUROSCI, V14, P453, DOI 10.1146/annurev.neuro.14.1.453 PIRVOLA U, 1991, HEARING RES, V52, P345, DOI 10.1016/0378-5955(91)90024-4 Pujol R., 1986, BIOL CHANGE OTOLARYN, P47 Ramon, 1909, HISTOLOGIE SYSTEME N REPRESA J, 1991, ANAT EMBRYOL, V184, P421, DOI 10.1007/BF01236048 ROBERTS BL, 1992, EVOLUTIONARY BIOL HE, P182 ROTH B, 1991, ANAT EMBRYOL, V183, P483 Ruben R. J., 1967, ACTA OTO-LARYNGOL, V220, P1 SANS A, 1982, J COMP NEUROL, V206, P1, DOI 10.1002/cne.902060102 SCARFONE E, 1991, J NEUROSCI, V11, P1173 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 Shnerson A., 1982, DEV BRAIN RES, V2, P77 SIMMONS DD, 1990, HEARING RES, V49, P127, DOI 10.1016/0378-5955(90)90100-4 SOBKOWICZ HM, 1989, J NEUROCYTOL, V18, P209, DOI 10.1007/BF01206663 TELLO JF, 1931, TRAV LAB RECH BIOL, V27, P151 Theiler K, 1989, HOUSE MOUSE THOENEN H, 1991, TRENDS NEUROSCI, V14, P165, DOI 10.1016/0166-2236(91)90097-E VACA K, 1988, BRAIN RES REV, V13, P261, DOI 10.1016/0165-0173(88)90009-4 VANDEWATER TR, 1983, DEV AUDITORY VESTIBU, P337 VANDEWATER TR, 1988, DEVELOPMENT, V103, P185 WARR WB, 1992, ANATOMY MAMMALIAN AU, P410 WILM C, 1992, J NEUROBIOL, V23, P692, DOI 10.1002/neu.480230608 WILSON JL, 1991, HEARING RES, V55, P98, DOI 10.1016/0378-5955(91)90096-R NR 45 TC 91 Z9 91 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 1993 VL 65 IS 1-2 BP 51 EP 60 DI 10.1016/0378-5955(93)90200-K PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300003 PM 8458759 ER PT J AU MACKERSIE, C DOWN, KE STAPELLS, DR AF MACKERSIE, C DOWN, KE STAPELLS, DR TI PURE-TONE MASKING PROFILES FOR HUMAN AUDITORY BRAIN-STEM AND MIDDLE LATENCY RESPONSES SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; MIDDLE LATENCY RESPONSE; FREQUENCY SELECTIVITY; HUMAN ID EVOKED-POTENTIALS; FREQUENCY-SELECTIVITY; ELECTROPHYSIOLOGICAL EVIDENCE; STEM RESPONSES; TUNING CURVES; CRITICAL BAND; HEARING-LOSS; GUINEA-PIG; WAVE; SPECIFICITY AB Several studies have compared the frequency selectivity of waves I and V of the auditory brainstem response (ABR) in humans, however little is known about the frequency selectivity of the middle latency response (MLR). Simultaneous recordings of ABRs and MLRs to 60 dB peSPL 2000-Hz probe tones were obtained in the presence of 0.5, 1.0, 1.41, 2.0, 2.83 and 4.0 kHz maskers presented at 40, 60, and 80 dB SPL. ABR/MLR iso-intensity masking profiles showing the percentage of the unmasked amplitudes as a function of frequency were constructed for ABR peak V-Vn and MLR peaks Na-Pa and Nb-Pb at each masker intensity. No significant differences were found between the frequency selectivity of the ABR and MLR, and the effects of masking on the amplitudes of these responses were similar. These results are consistent with the suggestion that frequency tuning is similar up to the level of the primary auditory cortex. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,ROSE F KENNEDY CTR,DEPT OTOLARYNGOL,ROOM 817,BRONX,NY 10461. CUNY,GRAD CTR,PHD PROGRAM SPEECH SCI,NEW YORK,NY 10021. CR BEITER RC, 1973, ELECTROEN CLIN NEURO, V34, P203, DOI 10.1016/0013-4694(73)90050-3 BROWN CJ, 1987, HEARING RES, V25, P193, DOI 10.1016/0378-5955(87)90091-8 BURKARD R, 1989, J ACOUST SOC AM, V85, P2514, DOI 10.1121/1.397746 BURROWS DL, 1990, J ACOUST SOC AM, V88, P180, DOI 10.1121/1.399938 BUTLER RA, 1972, ELECTROEN CLIN NEURO, V33, P277, DOI 10.1016/0013-4694(72)90154-X BUTLER RA, 1968, J ACOUST SOC AM, V44, P945, DOI 10.1121/1.1911233 CALFORD MB, 1983, HEARING RES, V11, P395, DOI 10.1016/0378-5955(83)90070-9 DAUMAN R, 1988, ACTA OTO-LARYNGOL, V105, P50, DOI 10.3109/00016488809119445 DOLAN TG, 1985, HEARING RES, V18, P203, DOI 10.1016/0378-5955(85)90038-3 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 FOLSOM RC, 1984, J ACOUST SOC AM, V75, P919, DOI 10.1121/1.390538 FOLSOM RC, 1987, J ACOUST SOC AM, V81, P412, DOI 10.1121/1.394906 GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GREENHOUSE SW, 1959, PSYCHOMETRIKA, V24, P95, DOI 10.1007/BF02289823 HYDE ML, 1985, J OTOLARYNGOL, V14, P19 KILENY P, 1987, ELECTROEN CLIN NEURO, V66, P108, DOI 10.1016/0013-4694(87)90180-5 KILENY PR, 1987, ARCH OTOLARYNGOL, V113, P1072 KLEIN AJ, 1983, ARCH OTOLARYNGOL, V109, P74 KLEIN AJ, 1981, J ACOUST SOC AM, V70, P1045, DOI 10.1121/1.386955 KLEIN AJ, 1981, J ACOUST SOC AM, V69, P760, DOI 10.1121/1.385576 KRAMER SJ, 1982, HEARING RES, V8, P317, DOI 10.1016/0378-5955(82)90022-3 KRAMER SJ, 1982, J ACOUST SOC AM, V72, P795, DOI 10.1121/1.388186 KRAUS N, 1985, ELECTROEN CLIN NEURO, V62, P343, DOI 10.1016/0168-5597(85)90043-7 KRAUS N, 1987, HEARING RES, V27, P165, DOI 10.1016/0378-5955(87)90017-7 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 KRAUS N, 1984, LARYNGOSCOPE, V94, P400 Kraus N, 1990, J Am Acad Audiol, V1, P130 LEGATT AD, 1988, NEUROL CLIN, V6, P681 MILLER JM, 1989, CROSS SPECIES COMP A, P31 MILLS JH, 1983, HEARING RES THEORY, V2, P233 MITCHELL C, 1980, J ACOUST SOC AM, V68, P896, DOI 10.1121/1.384829 Moore B. C. J., 1989, INTRO PSYCHOL HEARIN NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x OZDAMAR O, 1983, AUDIOLOGY, V22, P34 OZDAMAR O, 1982, ELECTROEN CLIN NEURO, V53, P224, DOI 10.1016/0013-4694(82)90027-X PARKER D J, 1978, Scandinavian Audiology, V7, P73, DOI 10.3109/01050397809043135 PATTERSON RD, 1976, J ACOUST SOC AM, V59, P640, DOI 10.1121/1.380914 Pickles JO, 1988, INTRO PHYSL HEARING PICTON TW, 1978, ELECTROEN CLIN NEURO, V45, P186, DOI 10.1016/0013-4694(78)90003-2 PORTMANN M, 1983, ACTA OTO-LARYNGOL, V95, P657, DOI 10.3109/00016488309139459 ROBINSON K, 1977, BRAIN, V100, P19, DOI 10.1093/brain/100.1.19 SCHERG M, 1983, ELECTROEN CLIN NEURO, V56, P443, DOI 10.1016/0013-4694(83)90227-4 SCHERG M, 1986, ELECTROEN CLIN NEURO, V65, P344, DOI 10.1016/0168-5597(86)90014-6 SMITH DI, 1990, HEARING RES, V43, P95, DOI 10.1016/0378-5955(90)90218-E STAPELLS DR, 1981, EAR HEARING, V2, P20 STAPELLS DR, 1988, ELECTROEN CLIN NEURO, V71, P289, DOI 10.1016/0168-5597(88)90029-9 STAPELLS DR, 1990, AUDIOLOGY, V29, P262 Stapells DR, 1985, AUDITORY BRAINSTEM R, P147 STAPELLS D R, 1989, Seminars in Hearing, V10, P229 WEBER B A, 1987, Ear and Hearing, V8, p49S, DOI 10.1097/00003446-198708001-00010 ZERLIN S, 1986, J ACOUST SOC AM, V79, P1612, DOI 10.1121/1.393297 NR 51 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 FEB PY 1993 VL 65 IS 1-2 BP 61 EP 68 DI 10.1016/0378-5955(93)90201-B PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300004 PM 8458760 ER PT J AU YLIKOSKI, J PIRVOLA, U MOSHNYAKOV, M PALGI, J ARUMAE, U SAARMA, M AF YLIKOSKI, J PIRVOLA, U MOSHNYAKOV, M PALGI, J ARUMAE, U SAARMA, M TI EXPRESSION PATTERNS OF NEUROTROPHIN AND THEIR RECEPTOR MESSENGER-RNAS IN THE RAT INNER-EAR SO HEARING RESEARCH LA English DT Article DE NEUROTROPHIN-3; BRAIN-DERIVED NEUROTROPHIC FACTOR; ORGAN OF CORTI; VESTIBULAR ORGANS; COCHLEOVESTIBULAR NEURONS; HYBRIDIZATION, INSITU ID NERVE GROWTH-FACTOR; TYROSINE KINASE RECEPTOR; ADULT SENSORY NEURONS; SUBSTANCE-P; VESTIBULAR GANGLION; SYMPATHETIC-GANGLIA; TRK PROTOONCOGENE; MOLECULAR-CLONING; FACTOR FAMILY; FACTOR NGF AB In situ hybridization was used to study the expression of mRNAs of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-5 (NT-5) and the components of their high-affinity receptors in the early postnatal and adult rat inner ears. NGF or NT-5 transcripts were not detected in the inner ear neuroepithelium or in the innervating neurons. NT-3 mRNA was intensely expressed over the one-week-old and adult inner hair cells (IHCs) but in the outer hair cells (OHCs) and vestibular maculae only during the early postnatal period. BDNF mRNA was expressed in the IHCs and OHCs of the early postnatal cochlea but not in the adult organ of Corti. High levels of BDNF transcripts were observed in the sensory epithelia of all vestibular end organs. mRNAs of low affinity NGF receptor. trk B and trk C, but not of trk, were expressed in the spiral and vestibular ganglia. In addition, the non-catalytic form of trk B mRNA localized to the sensory epithelia of maculae utriculi and sacculi. The present results show that of the neurotrophins examined, NT-3 is the predominant neurotrophin in the adult organ of Corti and BDNF is that in vestibular organs. The expression patterns of NT-3 and BDNF mRNAs suggest that these neurotrophins may participate in the maintenance of mature cochleovestibular neurons and they may be involved in the survival response of injured neurons. C1 UNIV HELSINKI,DEPT PATHOL,SF-00100 HELSINKI 10,FINLAND. UNIV HELSINKI,INST BIOTECHNOL,SF-00100 HELSINKI 10,FINLAND. ESTONIAN ACAD SCI,INST CHEM PHYS & BIOPHYS,TALLINN,ESTONIA. RP YLIKOSKI, J (reprint author), UNIV KUOPIO,DEPT OTOLARYNGOL,POB 1777,SF-70211 KUOPIO,FINLAND. CR ADLER JE, 1984, SCIENCE, V225, P1499, DOI 10.1126/science.6206570 LINDSAY RM, 1989, NATURE, V337, P362, DOI 10.1038/337362a0 ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 BANERJEE SP, 1973, P NATL ACAD SCI USA, V70, P2519, DOI 10.1073/pnas.70.9.2519 BARDE YA, 1982, EMBO J, V1, P549 BAYER SA, 1982, SCIENCE, V216, P890, DOI 10.1126/science.7079742 BERKEMEIER LR, 1991, NEURON, V7, P857, DOI 10.1016/0896-6273(91)90287-A BRADY ST, 1991, NEURON, V7, P521, DOI 10.1016/0896-6273(91)90365-7 DAVIES AM, 1987, NATURE, V326, P353, DOI 10.1038/326353a0 DIAMOND J, 1987, P NATL ACAD SCI USA, V84, P6596, DOI 10.1073/pnas.84.18.6596 FERMIN CD, 1982, ANN OTO RHINOL LARYN, V91, P44 Fritsch E., 1989, MOL CLONING GACEK RR, 1960, NEURAL MECHANISMS AU, P276 HALLBOOK F, 1991, NEURON, V6, P845, DOI 10.1016/0896-6273(91)90180-8 HEMPSTEAD BL, 1991, NATURE, V350, P678, DOI 10.1038/350678a0 HEUMANN R, 1984, EMBO J, V3, P3183 HOHN A, 1990, NATURE, V344, P339, DOI 10.1038/344339a0 IGARASHI M, 1970, ACTA OTO-LARYNGOL, V69, P247, DOI 10.3109/00016487009123360 KAPLAN DR, 1991, NATURE, V350, P158, DOI 10.1038/350158a0 KESSLER JA, 1980, P NATL ACAD SCI-BIOL, V77, P649, DOI 10.1073/pnas.77.1.649 KING AJ, 1991, TRENDS NEUROSCI, V14, P31, DOI 10.1016/0166-2236(91)90181-S KLEIN R, 1990, DEVELOPMENT, V109, P845 KLEIN R, 1991, CELL, V66, P395, DOI 10.1016/0092-8674(91)90628-C LAMBALLE F, 1991, CELL, V66, P967, DOI 10.1016/0092-8674(91)90442-2 LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEFEBVRE PP, 1992, ACTA OTO-LARYNGOL, V112, P288 LEFEBVRE PP, 1991, ACTA OTO-LARYNGOL, V111, P304, DOI 10.3109/00016489109137392 LEIBROCK J, 1989, NATURE, V341, P149, DOI 10.1038/341149a0 LEVIMONT.R, 1968, PHYSIOL REV, V48, P534 LEVIMONTALCINI R, 1987, SCIENCE, V237, P1154, DOI 10.1126/science.3306916 LINDSAY RM, 1988, J NEUROSCI, V8, P2394 Lurie M. H., 1944, LARYNGOSCOPE, V54, P375 MACLEAN DB, 1989, BRAIN RES, V478, P349, DOI 10.1016/0006-8993(89)91515-1 MAISONPIERRE PC, 1990, SCIENCE, V247, P1446, DOI 10.1126/science.2321006 MARTINZANCA D, 1989, MOL CELL BIOL, V9, P24 MERLIOI JP, 1992, IN PRESS NEUROSCIENC METSIS M, 1992, IN PRESS GENE MIDDLEMAS DS, 1991, MOL CELL BIOL, V11, P143 MORRISON D, 1975, ACTA OTO-LARYNGOL, V79, P11, DOI 10.3109/00016487509124649 OPPENHEIM RW, 1988, SCIENCE, V240, P919, DOI 10.1126/science.3363373 PIRVOLA U, 1992, P NATL ACAD SCI USA, V89, P9915, DOI 10.1073/pnas.89.20.9915 RADEKE MJ, 1987, NATURE, V325, P593, DOI 10.1038/325593a0 RICHTER E, 1981, ACTA OTO-LARYNGOL, V92, P423, DOI 10.3109/00016488109133281 Ruben R. J., 1967, ACTA OTO-LARYNGOL, V220, P1 SAXEN A, 1937, ACTA OTOLARYNGOL S, V23, P1 SIMMONS DD, 1991, HEARING RES, V55, P81, DOI 10.1016/0378-5955(91)90094-P SOPPET D, 1991, CELL, V65, P895, DOI 10.1016/0092-8674(91)90396-G SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 SQUINTO SP, 1991, CELL, V65, P885, DOI 10.1016/0092-8674(91)90395-F SWANSON GJ, 1990, DEV BIOL, V137, P243, DOI 10.1016/0012-1606(90)90251-D Usami S, 1991, Acta Otolaryngol Suppl, V481, P166 USAMI SI, 1992, IN PRESS ACTA OTOLAR VANDEWATER TR, 1984, ANN OTO RHINOL LARYN, V93, P558 VONBARTHELD CS, 1991, DEVELOPMENT, V113, P455 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 WHITTEMORE SR, 1988, J NEUROSCI RES, V20, P403, DOI 10.1002/jnr.490200402 Wilkinson D, 1990, POSTIMPLANTATION MAM, P155 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P5 YLIKOSKI J, 1992, MOL BIOL HEARING DEA Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P23 YLIKOSKI J, 1990, EUR ARCH OTO-RHINO-L, V247, P211 Ylikoski J, 1981, Am J Otolaryngol, V2, P81, DOI 10.1016/S0196-0709(81)80024-5 YLIKOSKI J, 1989, ACTA OTO-LARYNGOL, V107, P417, DOI 10.3109/00016488909127533 YLIKOSKI J, 1984, J LARYNGOL OTOL, V98, P759, DOI 10.1017/S0022215100147413 NR 65 TC 230 Z9 243 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 1993 VL 65 IS 1-2 BP 69 EP 78 DI 10.1016/0378-5955(93)90202-C PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300005 PM 8080462 ER PT J AU GEISLER, CD AF GEISLER, CD TI A MODEL OF STEREOCILIARY TIP-LINK STRETCHES SO HEARING RESEARCH LA English DT Article DE MODEL; TIP-LINK STRETCHES; STEREOCILIA; CILIARY MOTION; VERTEBRATES ID GUINEA-PIG COCHLEA; CROSS-LINKS; CELLS; ORGAN; CORTI AB A model of the tip-link stretches produced by angular deflections of the stereocilia of vertebrate acoustico-lateralis hair cells is presented. It is shown that tip-link stretch in the model is proportional to the angle of stereociliary deflection. By contrast, the stretch of a horizontal (e.g.. row-to-row) link is proportional to the square of the angle of stereociliary deflection. Possible roles of these stretches in sensory transduction are discussed. C1 UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. RP GEISLER, CD (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,273 MED SCI BLDG,MADISON,WI 53706, USA. CR COREY DP, 1983, J NEUROSCI, V3, P942 ENGSTROM H, 1978, HEARING RES, V1, P49, DOI 10.1016/0378-5955(78)90009-6 Flock A., 1977, PSYCHOPHYSICS PHYSL, P15 FURNESS DN, 1985, HEARING RES, V18, P177, DOI 10.1016/0378-5955(85)90010-3 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 OSBORNE MP, 1984, CELL TISSUE RES, V237, P43 OSBORNE MP, 1988, HEARING RES, V35, P99, DOI 10.1016/0378-5955(88)90044-5 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 NR 10 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 1993 VL 65 IS 1-2 BP 79 EP 82 DI 10.1016/0378-5955(93)90203-D PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300006 PM 8458761 ER PT J AU FREEMAN, DM HENDRIX, DK SHAH, D FAN, LF WEISS, TF AF FREEMAN, DM HENDRIX, DK SHAH, D FAN, LF WEISS, TF TI EFFECT OF LYMPH COMPOSITION ON AN INVITRO PREPARATION OF THE ALLIGATOR LIZARD COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; INVITRO PREPARATION; LYMPH COMPOSITION; HAIR CELLS ID OUTER HAIR-CELLS; INNER-EAR; INDUCED MOTILITY; GUINEA-PIG; TECTORIAL MEMBRANE; MENIERES-DISEASE; DEPOLARIZATION; TRANSDUCTION; TRANSMISSION; MECHANISM AB The effects of different artificial lymphs on the cochlear duct of the alligator lizard were studied in an in vitro preparation. The duct was dissected and cemented to the glass floor of a chamber that had been filled with an artificial lymph. The vestibular membrane was removed and latex beads (1-5 mum in diameter) were allowed to settle on the endolymphatic surface of the duct. During perfusion with an artificial lymph solution, the positions of beads were measured and video images of the duct were obtained. Artificial lymphs were isosmotic and included artificial endolymph (AE), artificial perilymph (AP), Leibovitz's L-15 culture medium, an AE solution whose calcium concentration was the same as that of AP, and AE and AP solutions in which gluconate was substituted for chloride ions. Results obtained in AE were consistently different from those in other lymphs. The displacements of beads, the projected area of the papilla, the occurrence of blebs, and direct observation of cells in the duct all indicated that the tissue swelled in AE (with or without 2 mmol/l Ca) but showed no consistent shrinking or swelling in any of the other artificial lymphs. Thus for the solutions we used, the presence of both potassium and chloride was required to elicit the swelling response to isosmotic artificial lymphs. There were some regional differences in the swelling response: the swelling of the endolymphatic surface of the tissue in a direction orthogonal to the basilar membrane surface was smaller on the free-standing region of the basilar papilla than either on the tectorial membrane or on the hyaline epithelial cells. The preparation was osmotically stable in AP and in both AE and AP solutions in which gluconate was substituted for chloride ions. After exposure to these solutions for as much as 300 min, the preparation showed no gross signs of deterioration visible with the light microscope, and continued to exhibit a highly specific osmotic response to the composition of the bathing medium. C1 MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114. RP FREEMAN, DM (reprint author), MIT,DEPT ELECT ENGN & COMP SCI,ROOM 36-865,77 MASSACHUSETTS AVE,CAMBRIDGE,MA 02139, USA. CR ASHMORE JF, 1991, ANNU REV PHYSIOL, V53, P465, DOI 10.1146/annurev.physiol.53.1.465 BRACHO H, 1978, J PHYSIOL-LONDON, V281, P445 BROWNELL WE, 1990, MECHANICS BIOPHYSICS, P41 COOK RO, 1979, APPL OPTICS, V18, P3230, DOI 10.1364/AO.18.003230 DIDIER A, 1990, HEARING RES, V46, P171, DOI 10.1016/0378-5955(90)90147-H DOHLMANN GF, 1976, ARCH OTO-RHINO-LARYN, V212, P301, DOI 10.1007/BF00453678 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 FREEMAN AR, 1967, J GEN PHYSIOL, V50, P423 FREEMAN DM, 1990, HEARING RES, V48, P1, DOI 10.1016/0378-5955(90)90195-U FREEMAN DM, 1990, HEARING RES, V48, P37, DOI 10.1016/0378-5955(90)90198-X FRISHKOPF LS, 1983, HEARING RES, V12, P393, DOI 10.1016/0378-5955(83)90008-4 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 GUTTENPLAN M, 1989, HEARING RES, V43, P47, DOI 10.1016/0378-5955(89)90058-0 Hoffmann EK, 1987, CELL VOLUME CONTROL, P125 HOLTON T, 1983, SCIENCE, V222, P508, DOI 10.1126/science.6623089 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 KRONESTERFREI A, 1979, ARCH OTO-RHINO-LARYN, V224, P3, DOI 10.1007/BF00455217 Kronester-Frei A, 1978, SCANNING ELECT MICRO, V2, P943 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 MACKNIGHT ADC, 1977, PHYSIOL REV, V57, P510 MULROY MJ, 1985, J COMP NEUROL, V233, P463, DOI 10.1002/cne.902330405 MULROY MJ, 1986, J COMP NEUROL, V248, P263, DOI 10.1002/cne.902480209 MULROY MJ, 1974, BRAIN BEHAV EVOLUT, V10, P69, DOI 10.1159/000124303 NADOL JB, 1976, AM J ANAT, V147, P281, DOI 10.1002/aja.1001470304 NADOL JB, 1989, MENIERES DISEASE ORMAN SS, 1986, AM J OTOLARYNG, V7, P140, DOI 10.1016/S0196-0709(86)80043-6 PARKER JC, 1983, AM J PHYSIOL, V244, pC313 PETERSON SK, 1978, J COMP PHYSIOL, V126, P1 REUBEN JP, 1964, J GEN PHYSIOL, V47, P1141, DOI 10.1085/jgp.47.6.1141 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 SIEBENS AW, 1985, KIDNEY PHYSL PATHOPH, P91 STERKERS O, 1988, PHYSIOL REV, V68, P1083 ULFENDAHL M, 1988, ARCH OTO-RHINO-LARYN, V245, P237, DOI 10.1007/BF00463935 WEISS TF, 1985, HEARING RES, V20, P157, DOI 10.1016/0378-5955(85)90166-2 ZENNER HP, 1986, ARCH OTO-RHINO-LARYN, V243, P108, DOI 10.1007/BF00453760 NR 38 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 FEB PY 1993 VL 65 IS 1-2 BP 83 EP 98 DI 10.1016/0378-5955(93)90204-E PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300007 PM 8458762 ER PT J AU POLLAK, GD PARK, TJ AF POLLAK, GD PARK, TJ TI THE EFFECTS OF GABAERGIC INHIBITION ON MONAURAL RESPONSE PROPERTIES OF NEURONS IN THE MOUSTACHE BATS INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE GABAERGIC INHIBITION; MONAURAL RESPONSE PROPERTIES; INFERIOR COLLICULUS; MOUSTACHE BAT ID COMBINATION-SENSITIVE NEURONS; SOUND LOCATION SELECTIVITY; MEDIAL GENICULATE-BODY; 60-KHZ EI UNITS; ASCENDING PROJECTIONS; CENTRAL NUCLEUS; ISOFREQUENCY REGION; LATERAL LEMNISCUS; BINAURAL NEURONS; DORSAL NUCLEUS AB The effects of GABAergic inhibition on response properties of neurons in the inferior colliculus were investigated. The experimental animals were mustache bats and responses were monitored from neurons in the hypertrophied 60 kHz isofrequency contour of the inferior colliculus. The features we report on here are: 1) the maximum discharge rates evoked by tone bursts at each unit's best frequency; 2) the forms of the Tate-level functions; 3) the discharge patterns evoked by best frequency tone bursts; and 4) the changes in these response features that were observed when GABAergic inhibition was blocked with bicuculline, an antagonist specific for GABA(A) receptors. There were three main findings. The first is that bicuculline caused the discharge rate to increase in the majority of neurons. The maximum firing rates in more than half of the units increased by at least 100%, and in 15% of the cells the maximum spike-count increased 400% or more. Of particular interest were the 13 cells that were nearly unresponsive to any tone burst, but responded vigorously to the same stimuli after application of bicuculline. The second main finding is that the increased discharge rates were due either to a change from a phasic to a tonic discharge pattern, or to a change in overall excitability with no change in discharge pattern. The third main finding was that bicuculline changed the shape of the rate-level functions in almost half of the cells studied. The general trend was that units whose pre-drug rate-level functions were upper-threshold were most likely to be changed, followed by regular nonmonotonic and non-saturated monotonic. Units with saturated monotonic functions were the least likely to be affected by bicuculline. These results lead us to suggest that GABAergic inhibition acts on collicular cells in two principal ways. The first way is to modify the effects of the excitatory innervation and thereby shape the response features of collicular neurons. The formation of rate-level functions is but one illustration of the shaping action of GABAergic inhibition. Other features that are shaped by GABAergic inhibition include discharge patterns, thresholds, latencies and tuning curves. The second way is to provide a regulated suppression of evoked activity. We propose that the suppression is situation dependent and may act to enhance the operating range of collicular neurons in situations of particular importance to the animal, such as during periods of selective attention and perhaps in other situations as well. RP POLLAK, GD (reprint author), UNIV TEXAS,DEPT ZOOL,AUSTIN,TX 78712, USA. CR ADAMS JC, 1984, BRAIN RES BULL, V13, P585, DOI 10.1016/0361-9230(84)90041-8 ADAMS JC, 1979, NEUROSCIENCE, V4, P1947, DOI 10.1016/0306-4522(79)90067-8 Aitkin L., 1986, AUDITORY MIDBRAIN ST AOKI E, 1988, BRAIN RES, V442, P63, DOI 10.1016/0006-8993(88)91432-1 BORMANN J, 1988, TRENDS NEUROSCI, V11, P112, DOI 10.1016/0166-2236(88)90156-7 Cooper J. R., 1982, BIOCH BASIS NEUROPHA DYKES RW, 1984, J NEUROPHYSIOL, V52, P1066 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 FUJITA I, 1991, J NEUROSCI, V11, P722 FUZESSERY ZM, 1990, J NEUROPHYSIOL, V63, P1128 FUZESSERY ZM, 1985, J NEUROPHYSIOL, V54, P757 HAVEY DC, 1980, ELECTROEN CLIN NEURO, V48, P249, DOI 10.1016/0013-4694(80)90313-2 Irvine D. R. F., 1986, PROGR SENSORY PHYSL, V7 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 LARUE D T, 1991, Society for Neuroscience Abstracts, V17, P300 MULLER CM, 1988, J NEUROPHYSIOL, V59, P1673 OLIVER DL, 1991, J COMP NEUROL, V303, P75, DOI 10.1002/cne.903030108 OLIVER D L, 1988, Society for Neuroscience Abstracts, V14, P490 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1275 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1254 ONEILL WE, 1985, J COMP PHYSIOL A, V157, P797, DOI 10.1007/BF01350077 PALOMBI PS, 1992, J NEUROPHYSIOL, V67, P738 PARK T, 1991, ABSTR ASS RES OT, P89 PARK T J, 1991, Society for Neuroscience Abstracts, V17, P300 POLLAK GD, 1981, J NEUROPHYSIOL, V46, P605 POLLAK G D, 1989, Society for Neuroscience Abstracts, V15, P1115 Pollak GD, 1989, NEURAL BASIS ECHOLOC POLLAK GD, 1992, IN PRESS PRINCIPLES Purves RD, 1981, MICROELECTRODE METHO ROBERTS RC, 1987, J NEUROCYTOL, V16, P333, DOI 10.1007/BF01611345 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 ROSS LS, 1988, J COMP NEUROL, V270, P488, DOI 10.1002/cne.902700403 ROSS LS, 1989, J NEUROSCI, V9, P2819 ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 RYAN A, 1977, J NEUROPHYSIOL, V40, P943 SACHS MB, 1989, HEARING RES, V41, P61, DOI 10.1016/0378-5955(89)90179-2 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SCHULLER G, 1986, J NEUROSCI METH, V18, P339, DOI 10.1016/0165-0270(86)90022-1 SCHUMWAY CA, 1988, J COMP PHYSL, V164, P391 SEMPLE MN, 1980, EXP BRAIN RES, V41, P19 SHNEIDERMAN A, 1989, J COMP NEUROL, V286, P28, DOI 10.1002/cne.902860103 SILLITO AM, 1975, J PHYSIOL-LONDON, V250, P305 Suga N., 1984, DYNAMIC ASPECTS NEOC, P315 TSUCHITA.C, 1966, J NEUROPHYSIOL, V29, P684 WARR WB, 1982, CONTRIBUTIONS SENSOR, P1 WATANABE T, 1973, JPN J PHYSIOL, V23, P291 WENSTRUP JJ, 1988, J NEUROPHYSIOL, V60, P1369 WENSTRUP JJ, 1988, J NEUROPHYSIOL, V60, P1384 WENSTRUP JJ, 1986, J NEUROSCI, V6, P962 WENTHOLD RJ, 1990, GLYCINE NEUROTRANSMI, P391 YANG L, 1992, IN PRESS J NEUROPHYS ZOOK JM, 1982, J COMP NEUROL, V207, P14, DOI 10.1002/cne.902070103 ZOOK JM, 1985, J COMP NEUROL, V231, P530, DOI 10.1002/cne.902310410 NR 55 TC 103 Z9 106 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 1993 VL 65 IS 1-2 BP 99 EP 117 DI 10.1016/0378-5955(93)90205-F PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300008 PM 8384613 ER PT J AU KRAUS, N MICCO, AG KOCH, DB MCGEE, T CARRELL, T SHARMA, A WIET, RJ WEINGARTEN, CZ AF KRAUS, N MICCO, AG KOCH, DB MCGEE, T CARRELL, T SHARMA, A WIET, RJ WEINGARTEN, CZ TI THE MISMATCH NEGATIVITY CORTICAL EVOKED-POTENTIAL ELICITED BY SPEECH IN COCHLEAR-IMPLANT USERS SO HEARING RESEARCH LA English DT Article DE COCHLEAR IMPLANTS; AUDITORY EVOKED POTENTIALS; MISMATCH NEGATIVITY; EVENT-RELATED POTENTIALS ID EVENT-RELATED POTENTIALS; AUDITORY STIMULUS; DISCRIMINATION; RESPONSES; ATTENTION; DEVIANCE; CORTEX; TONES AB The mismatch negativity (MMN) event-related potential is a non-task related neurophysiologic index of auditory discrimination. The MMN was elicited in eight cochlear implant recipients by the synthesized speech stimulus pair /da/ and /ta/. The response was remarkably similar to the MMN measured in normal-hearing individuals to the same stimuli. The results suggest that the central auditory system can process certain aspects of speech consistently, independent of whether the stimuli are processed through a normal cochlea or mediated by a cochlear prosthesis. The MMN shows promise as a measure for the objective evaluation of cochlear-implant function, and for the study of central neurophysiological processes underlying speech perception. C1 NORTHWESTERN UNIV,DEPT COMMUN SCI & DISORDERS,EVANSTON,IL 60201. NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL,EVANSTON,IL 60201. NORTHWESTERN UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,EVANSTON,IL 60201. CR AALTONEN O, 1987, BIOL PSYCHOL, V24, P197, DOI 10.1016/0301-0511(87)90002-0 ALHO K, 1986, PSYCHOPHYSIOLOGY, V23, P613, DOI 10.1111/j.1469-8986.1986.tb00680.x ALHO K, 1992, ELECTROEN CLIN NEURO, V82, P356, DOI 10.1016/0013-4694(92)90005-3 BLAMEY PJ, 1987, J ACOUST SOC AM, V82, P38, DOI 10.1121/1.395542 BUCHWALD J, 1989, BRAIN DYNAMICS, V2 Cazals Y, 1990, Acta Otolaryngol Suppl, V469, P150 CSEPE V, 1987, ELECTROEN CLIN NEURO, V66, P571, DOI 10.1016/0013-4694(87)90103-9 CSEPE V, 1988, SLEEP 86 Davis PA, 1939, J NEUROPHYSIOL, V2, P494 Galey F R, 1984, Acta Otolaryngol Suppl, V411, P38 GANTZ BJ, 1988, OTOLARYNGOL HEAD NEC, V1, P171 GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 GIARD MH, 1990, PSYCHOPHYSIOLOGY, V27, P627, DOI 10.1111/j.1469-8986.1990.tb03184.x HALGREN E, 1986, EVOKED POTENTIALS, V3 HARI R, 1984, NEUROSCI LETT, V50, P127, DOI 10.1016/0304-3940(84)90474-9 HARRISON JB, 1988, ELECTROEN CLIN NEURO, V69, P55, DOI 10.1016/0013-4694(88)90035-1 KAGA K, 1991, LARYNGOSCOPE, V101, P905 KAUKORANTA E, 1989, HEARING RES, V41, P15, DOI 10.1016/0378-5955(89)90174-3 KLATT DH, 1980, J ACOUST SOC AM, V67, P971, DOI 10.1121/1.383940 KOCH DB, 1990, HEAR INSTR, V41, P28 KRAUS N, 1992, EAR HEARING, V13, P158, DOI 10.1097/00003446-199206000-00004 NAATANEN R, 1987, CURRENT TRENDS EVE S, V40, P129 NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x NAATANEN R, 1978, ACTA PSYCHOL, V42, P313, DOI 10.1016/0001-6918(78)90006-9 NAATANEN R, 1990, BEHAV BRAIN SCI, V13, P201 NOVAK GP, 1990, ELECTROEN CLIN NEURO, V75, P255, DOI 10.1016/0013-4694(90)90105-S Oviatt D. L., 1991, AM J AUDIOLOGY, V1, P48 PAAVILAINEN P, 1989, ELECTROEN CLIN NEURO, V73, P129, DOI 10.1016/0013-4694(89)90192-2 SAMS M, 1985, ELECTROEN CLIN NEURO, V62, P437, DOI 10.1016/0168-5597(85)90054-1 Sams M, 1990, J Cogn Neurosci, V2, P344, DOI 10.1162/jocn.1990.2.4.344 SAMS M, 1991, PSYCHOPHYSIOLOGY, V28, P21, DOI 10.1111/j.1469-8986.1991.tb03382.x WOLDORFF MG, 1991, ELECTROEN CLIN NEURO, V79, P170, DOI 10.1016/0013-4694(91)90136-R WOODS DL, 1992, ELECTROEN CLIN NEURO, V82, P341, DOI 10.1016/0013-4694(92)90004-2 NR 33 TC 75 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 FEB PY 1993 VL 65 IS 1-2 BP 118 EP 124 DI 10.1016/0378-5955(93)90206-G PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300009 PM 8458744 ER PT J AU ERWAY, LC WILLOTT, JF ARCHER, JR HARRISON, DE AF ERWAY, LC WILLOTT, JF ARCHER, JR HARRISON, DE TI GENETICS OF AGE-RELATED HEARING-LOSS IN MICE .1. INBRED AND F1-HYBRID STRAINS SO HEARING RESEARCH LA English DT Article DE GENETICS; INBRED MICE; F1 HYBRIDS; PRESBYCUSIS; AUDITORY EVOKED BRAIN RESPONSE ID INFERIOR COLLICULUS NEURONS; BRAIN-STEM RESPONSE; LABORATORY MOUSE; THRESHOLDS; C57BL/6 AB The auditory-evoked brainstem response (ABR) was used to assess hearing loss in five inbred strains of mice and all ten combinations of F1 hybrids. The inbred strains are CBA/H-T6J (CH), DBA/2J (D2), C57BL/6J (B6), BALB/cByJ (BY) and WB/ReJ (WB). The Fl hybrids are CHD2, CHB6, CHBY, CHWB, D2B6, D2BY, D2WB, B6BY, B6WB, and BYWB. At middle age (12, 16 months), mice were tested with click stimuli. At a relatively old age (23 months, near inbreds' median life span), they were tested with both click and tone-pip stimuli. The CH mice and their four F1 hybrid strains exhibit lower thresholds than the other strains, with the F1 strains being most sensitive (i.e., hybrid vigor). The D2 inbred and the three D2 Fl hybrids (excluding CHD2) exhibit the earliest and most severe hearing losses. The B6, BY and WB inbred strains exhibit severe hearing losses between 16 and 23 months of age; however, the B6BY, B6WB and BYWB F1 hybrids have significantly lower thresholds than their parental strains (genetic complementation). These data support a genetic model for recessive alleles at three different loci which contribute to age-related hearing loss. The CH mice have none of the recessive alleles, and the D2 mice are homozygous recessive for all three; the B6, BY and WB inbred strains are homozygous recessive respectively for one of the three loci. C1 NO ILLINOIS UNIV,DEPT PSYCHOL,DE KALB,IL 60115. UNIV CINCINNATI,DEPT BIOL SCI,CINCINNATI,OH 45221. JACKSON LAB,BAR HARBOR,ME 04609. CR ALLEN ND, 1990, CELL, V61, P853, DOI 10.1016/0092-8674(90)90195-K FARRER LA, 1992, AM J HUM GENET, V50, P528 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1992, AUDIOLOGY, V31, P190 HENRY KR, 1986, J COMP PSYCHOL, V100, P46, DOI 10.1037/0735-7036.100.1.46 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1979, ELECTROEN CLIN NEURO, V46, P452 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 JOHNSON KR, 1992, IN PRESS MAMMALIAN G LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 PARHAM K, 1988, Behavioral Neuroscience, V102, P881, DOI 10.1037/0735-7044.102.6.881 RALLS K, 1967, ANIM BEHAV, V15, P123, DOI 10.1016/S0003-3472(67)80022-8 Schuknecht H. F., 1974, PATHOLOGY EAR SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 WENNGREN BI, 1988, ACTA OTO-LARYNGOL, V106, P238, DOI 10.3109/00016488809106431 Willott J. F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1984, HEARING RES, V16, P161, DOI 10.1016/0378-5955(84)90005-4 WILLOTT JF, 1981, J NEUROPHYSIOL, V45, P35 NR 19 TC 169 Z9 170 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 1993 VL 65 IS 1-2 BP 125 EP 132 DI 10.1016/0378-5955(93)90207-H PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300010 PM 8458745 ER PT J AU PLATT, C AF PLATT, C TI ZEBRAFISH INNER-EAR SENSORY SURFACES ARE SIMILAR TO THOSE IN GOLDFISH SO HEARING RESEARCH LA English DT Article DE HAIR CELL; INNER EAR; OTOLITH; TELEOST; ZEBRAFISH ID RETICULOSPINAL NEURONS; OSTARIOPHYSAN FISHES; GROWTH; CELL AB The inner ear of the zebrafish (Brachydanio rerio) is very similar to that of the goldfish in its structural details, including the distribution and orientation of mechanosensory hair cell populations. Both species have been used in studying different aspects of the acoustic startle response. These structural similarities suggest that the zebrafish is a valid representative model for understanding peripheral hearing specializations in otophysan fishes. RP PLATT, C (reprint author), UNIV MARYLAND,DEPT ZOOL,COLL PK,MD 20742, USA. CR COOMBS S, 1979, J COMP PHYSIOL, V132, P203 CORWIN JT, 1978, J COMP NEUROL, V218, P345 Diamond J., 1971, FISH PHYSIOL, P265 EATON RC, 1980, J COMP PHYSIOL, V140, P337 EISEN JS, 1986, NATURE, V320, P269, DOI 10.1038/320269a0 Faber D.S., 1978, NEUROBIOLOGY MAUTHNE FABER DS, 1989, ANN NY ACAD SCI, V563, P11, DOI 10.1111/j.1749-6632.1989.tb42187.x FAY RR, 1988, SENSORY BIOL AQUATIC, P710 FAY RR, 1984, SCIENCE, V225, P951, DOI 10.1126/science.6474161 FAY RR, 1983, HEARING OTHER SENSES, P123 FINK SV, 1981, ZOOL J LINN SOC-LOND, V72, P297, DOI 10.1111/j.1096-3642.1981.tb01575.x HAMA K, 1969, Z ZELLFORSCH MIK ANA, V94, P155, DOI 10.1007/BF00339353 HUDSPETH AJ, 1985, SCIENCE, V230, P745, DOI 10.1126/science.2414845 JENKINS DB, 1979, AM J ANAT, V154, P81, DOI 10.1002/aja.1001540106 LEE RKK, 1991, J COMP NEUROL, V304, P34 Lewis ER, 1985, VERTEBRATE INNER EAR LIN JW, 1983, BRAIN RES, V274, P319, DOI 10.1016/0006-8993(83)90710-2 Lowenstein O., 1971, P207 Lowenstein O, 1974, HDB SENSORY PHYSL, P75 METCALFE WK, 1986, J COMP NEUROL, V251, P147, DOI 10.1002/cne.902510202 NELSON JS, 1984, FISHES WORLD, P2 Platt C., 1981, HEARING SOUND COMMUN, P3 PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 PLATT C, 1984, SCANNING ELECT MICRO, V4, P1915 Platt C., 1988, P783 Platt C, 1983, FISH NEUROBIOLOGY, V1, P89 PLATT C, 1981, ABSTR SOC NEUROSCI, V7, P536 POPPER AN, 1977, J MORPHOL, V153, P397, DOI 10.1002/jmor.1051530306 POPPER AN, 1983, J MORPHOL, V176, P121, DOI 10.1002/jmor.1051760202 POPPER AN, 1973, J ACOUST SOC AM, V53, P1515, DOI 10.1121/1.1913496 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1982, TRENDS NEUROSCI, V5, P276, DOI 10.1016/0166-2236(82)90171-0 POPPER AN, 1982, AM ZOOL, V22, P311 NR 33 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 FEB PY 1993 VL 65 IS 1-2 BP 133 EP 140 DI 10.1016/0378-5955(93)90208-I PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300011 PM 8458746 ER PT J AU CONLEE, JW BENNETT, ML AF CONLEE, JW BENNETT, ML TI TURN-SPECIFIC DIFFERENCES IN THE ENDOCOCHLEAR POTENTIAL BETWEEN ALBINO AND PIGMENTED GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE ALBINISM; ENDOCOCHLEAR POTENTIAL; INNER EAR; MELANIN PIGMENTATION; STRIA VASCULARIS ID STRIA VASCULARIS; INNER-EAR; COCHLEAR POTENTIALS; K+ CONCENTRATION; CELLS; MELANOCYTES; MELANIN; ABNORMALITIES; CHINCHILLA; RESPONSES AB Recent findings indicate that structural differences exist in the stria vascularis (SV) between albino and pigmented guinea pigs. In the higher cochlear turns, volume density for marginal cells in the albino SV is abnormally large, while that for intermediate cells (melanocytes) is abnormally small. These anatomical variations suggest that functional differences between albino and pigmented inner ears also may be found. To examine this possibility, four strains of guinea pigs were studied, consisting of Hartley albino (N = 9) and NIH outbred pigmented (N = 15) guinea pigs, as well as albino (N = 11) and pigmented (N = 15) guinea pig siblings born to mixed litters. Tracheotomy and carotid artery cannulation were performed. Animals were mechanically ventilated, with periodic samples drawn for arterial blood gas analysis. Blood pressure, heart rate and rectal temperature were monitored. Compound action potentials were measured first to assess cochlear viability. Positive endocochlear potentials (+EP) then were recorded, beginning with the fourth turn, followed by the first, second and third turns. Results showed that the +EP in albinos remained relatively constant across cochlear turns, but decreased significantly from base to apex in the pigmented inner ears. Across all animals, mean +EPs (mV +/- S.E.M.) for turns 1-4 in albinos were: 72.5 (2.5), 68.7 (2.3), 59.2 (2.7). 68.1 (3.3); pigmented values were: 72.9 (2.9), 66.9 (2.6), 53.8 (3.0), 57.0 (2.7). One-way ANOVAs did not show a significant difference in albino +EPs between any of the cochlear turns, but did indicate a highly significant difference between turns in the pigmented inner ears (P < 0.000004). Post hoc comparisons demonstrated +EPs in turns 3 and 4 were smaller than in turn 1. Since turn 3 was recorded last in these experiments, and was reduced in value relative to turn 4 in both groups, it is likely that cochlear deterioration contributed to this result more than any other factor. These results, combined with previous anatomical data, indicate that a diminution of melanocyte cell volume in the albino SV is accompanied by an increase in marginal cell volume density and larger +EPs in the higher cochlear turns, at least at resting levels. C1 UNIV UTAH,SCH MED,DEPT PEDIAT,SALT LAKE CITY,UT 84112. VET AFFAIRS MED CTR,SALT LAKE CITY,UT. RP CONLEE, JW (reprint author), UNIV UTAH,SCH MED,DEPT ANAT,SALT LAKE CITY,UT 84132, USA. CR ANGGARD L, 1965, ACTA OTOLARYNGOL S S, V203 ANNIKO M, 1976, ACTA OTO-LARYNGOL, V82, P70, DOI 10.3109/00016487609120864 BARILAN A, 1980, PFLUG ARCH EUR J PHY, V384, P93, DOI 10.1007/BF00589520 BARZA M, 1976, ANTIMICROB AGENTS CH, V10, P569 VONBEKESY G, 1952, J ACOUST SOC AM, V24, P72 BENITEZ LD, 1972, J ACOUST SOC AM, V52, P1115, DOI 10.1121/1.1913222 BILLINGHAM RE, 1960, Q REV BIOL, V35, P1, DOI 10.1086/402951 BOCK GR, 1984, HEARING RES, V13, P201, DOI 10.1016/0378-5955(84)90109-6 Bonaccorsi P, 1965, Ann Laringol Otol Rinol Faringol, V64, P725 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 BROWN JN, 1989, LAB ANIM SCI, V39, P142 BROWN MC, 1983, HEARING RES, V10, P345, DOI 10.1016/0378-5955(83)90097-7 BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 BRUMMETT R, 1977, ACTA OTO-LARYNGOL, V83, P98, DOI 10.3109/00016487709128819 BUTLER RA, 1965, J ACOUST SOC AM, V37, P429, DOI 10.1121/1.1909346 CABLE J, 1991, PIGM CELL RES, V4, P87, DOI 10.1111/j.1600-0749.1991.tb00320.x CONLEE JW, 1989, ACTA OTO-LARYNGOL, V107, P48, DOI 10.3109/00016488909127478 CONLEE JW, 1991, HEARING RES, V55, P57, DOI 10.1016/0378-5955(91)90092-N CONLEE JW, 1984, J COMP NEUROL, V225, P141, DOI 10.1002/cne.902250115 Corti A., 1851, Z WISS ZOOL, V3, P109 Crovetto M A, 1988, Rev Laryngol Otol Rhinol (Bord), V109, P453 DALLOS P, 1985, J NEUROSCI, V5, P1591 DEOL MS, 1970, PROC R SOC SER B-BIO, V175, P201, DOI 10.1098/rspb.1970.0019 DEOL MS, 1970, J EMBRYOL EXP MORPH, V23, P773 Dräger U C, 1987, Neurosci Res Suppl, V6, pS75, DOI 10.1016/0921-8696(87)90009-0 ECHANDIA EL, 1965, Z ZELLFORSCH MIK ANA, V67, P600, DOI 10.1007/BF00340327 FARMER JB, 1968, BRIT J PHARMACOL, V32, P193 GREEN EL, 1966, BIOL LABORATORY MOUS HILDING DA, 1977, ACTA OTO-LARYNGOL, V84, P24, DOI 10.3109/00016487709123939 HINOJOSA R, 1966, AM J ANAT, V118, P631, DOI 10.1002/aja.1001180218 HOEFFDING V, 1991, HEARING RES, V54, P39, DOI 10.1016/0378-5955(91)90134-U Ito Z, 1991, Acta Otolaryngol Suppl, V481, P83 KIMURA RS, 1970, ACTA OTO-LARYNGOL, V69, P415, DOI 10.3109/00016487009123387 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 KONIGSMARK BW, 1976, GENETIC METABOLIC DE KUIJPERS W, 1970, PFLEUGERS ARCH, V320, P248 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P359, DOI 10.1007/BF00588214 LARSSON B, 1979, BIOCHEM PHARMACOL, V28, P1181, DOI 10.1016/0006-2952(79)90326-5 LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LEFERRIERE K, 1974, ANN OTOL RHINO LARYN, V83, P685 LINDQUIST NG, 1973, ACTA RADIOL STOCKH S, V325 LYTTKENS L, 1979, ACTA OTO-LARYNGOL, V88, P61, DOI 10.3109/00016487909137141 MARSHALL LH, 1956, P SOC EXP BIOL MED, V92, P31 MASON HS, 1960, ARCH BIOCHEM BIOPHYS, V86, P225, DOI 10.1016/0003-9861(60)90409-4 MCGINNES.J, 1974, SCIENCE, V183, P853, DOI 10.1126/science.183.4127.853 MEIKLE MB, 1977, OTO RHINOL LARYNGOL, V84, P183 MELICHAR I, 1977, PFLUG ARCH EUR J PHY, V372, P207, DOI 10.1007/BF01063854 MISRAHY GA, 1958, AM J PHYSIOL, V194, P396 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 RAREY KE, 1982, HEARING RES, V6, P15, DOI 10.1016/0378-5955(82)90004-1 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHROTT A, 1987, ACTA OTO-LARYNGOL, V103, P451 SMITH CA, 1958, AM J PHYSIOL, V193, P203 SPITZER A, 1971, AM J PHYSIOL, V221, P1431 STEEL KP, 1987, HEARING RES, V27, P11, DOI 10.1016/0378-5955(87)90022-0 STEEL KP, 1989, DEVELOPMENT, V107, P453 STEEL KP, 1983, ARCH OTOLARYNGOL, V109, P22 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1984, AM J PHYSIOL, V246, pF47 SUGA F, 1962, ANN OTO RHINOL LARYN, V73, P924 SYKA J, 1981, HEARING RES, V4, P287, DOI 10.1016/0378-5955(81)90013-7 TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 VERNON J, 1976, METHODS PHYSL PSYCHO, P3 WASTERSTROM SA, 1984, SCAND AUDIOL S, V23 Witkop Jr CJ, 1983, METABOLIC BASIS INHE, P301 Wolff D, 1931, ARCHIV OTOLARYNGOL, V14, P195 WRIGHT CG, 1989, ACTA OTO-LARYNGOL, V108, P190, DOI 10.3109/00016488909125518 ZUMGOTTESBERGE AMM, 1988, PIGM CELL RES, V1, P238 NR 69 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 1993 VL 65 IS 1-2 BP 141 EP 150 DI 10.1016/0378-5955(93)90209-J PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300012 PM 8458747 ER PT J AU BAIRD, RA SCHUFF, NR BANCROFT, J AF BAIRD, RA SCHUFF, NR BANCROFT, J TI REGIONAL DIFFERENCES IN LECTIN BINDING PATTERNS OF VESTIBULAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE LECTINS; GLYCOCONJUGATES; OTOLITH ORGANS; SEMICIRCULAR CANALS; BULLFROG; GUINEA PIG ID WHEAT-GERM-AGGLUTININ; TROUT SACCULAR MACULA; VICIA-VILLOSA SEEDS; INNER-EAR; CARBOHYDRATE-BINDING; SURFACE GLYCOPROTEINS; LOTUS-TETRAGONOLOBUS; SUPPORTING CELLS; COMBINING SITES; ULEX-EUROPAEUS AB Surface glycoconjugates of hair cells and supporting cells in the vestibular endorgans of the bullfrog were identified using biotinylated lectins with different carbohydrate specificities. Lectin binding in hair cells was consistent with the presence of glucose and mannose (CON A). galactose (RCA-1), N-acetylglucosamine (WGA), N-acetylgalactosamine (VVA), but not fucose (UEA-I) residues. Hair cells in the bullfrog sacculus, unlike those in the utriculus and semicircular canals. did not stain for N-acetylglucosamine (WGA) or N-acetylgalactosamine (VVA). By contrast, WGA and, to a lesser extent, VVA, differentially stained utricular and semicircular canal hair cells, labeling hair cells located in peripheral, but not central, regions. In mammals. WGA uniformly labeled Type I hair cells while labeling, as in the bullfrog, Type 11 hair cells only in peripheral regions. These regional variations were retained after enzymatic digestion. We conclude that vestibular hair cells differ in their surface glycoconjugates and that differences in lectin binding patterns can be used to identify hair cell types and to infer the epithelial origin of isolated vestibular hair cells. RP BAIRD, RA (reprint author), GOOD SAMARITAN HOSP,RS DOW NEUROL SCI INST,1120 NW 20TH AVE,PORTLAND,OR 97209, USA. CR ALLEN HJ, 1977, IMMUNOL COMMUN, V6, P585, DOI 10.3109/08820137709093469 ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X BAENZIGER JU, 1979, J BIOL CHEM, V254, P9795 BAIRD RA, 1986, BRAIN RES, V369, P48, DOI 10.1016/0006-8993(86)90512-3 BAIRD R A, 1991, Society for Neuroscience Abstracts, V17, P313 BAIRD RA, 1992, ANN NY ACAD SCI, V656, P12, DOI 10.1111/j.1749-6632.1992.tb25197.x BAIRD RA, 1993, HEAR RES, V65 BAIRD RA, 1993, UNPUB J NEUROPHYSIOL BAKER DA, 1983, BIOCHEMISTRY-US, V22, P2741, DOI 10.1021/bi00280a023 CORREIA MJ, 1989, J NEUROPHYSIOL, V62, P924 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 DEBRAY H, 1981, EUR J BIOCHEM, V117, P41 DEGROOT JCMJ, 1988, HEARING RES, V35, P39, DOI 10.1016/0378-5955(88)90038-X DODD J, 1986, J EXP BIOL, V124, P225 EATOCK RA, 1987, J NEUROSCI, V7, P2821 EBISU S, 1978, CARBOHYD RES, V61, P129, DOI 10.1016/S0008-6215(00)84473-0 EDELMAN GM, 1984, ANNU REV NEUROSCI, V7, P339 Endo S, 1991, Acta Otolaryngol Suppl, V481, P116 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 GILLOYZAGA P, 1985, HEARING RES, V20, P1 GILLOYZAGA P, 1985, HEARING RES, V18, P269, DOI 10.1016/0378-5955(85)90043-7 GILLOYZAGA P, 1988, HEARING RES, V34, P149, DOI 10.1016/0378-5955(88)90102-5 GLICK MC, 1978, GLYCOCONJUGATES, V2, P337 Goldstein I J, 1978, Adv Carbohydr Chem Biochem, V35, P127 Goldstein I.J., 1986, LECTINS PROPERTIES F, P33 GOLDSTEIN IJ, 1981, J BIOL CHEM, V256, P3890 HENNIGAR LM, 1987, STAIN TECHNOL, V62, P317 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HOOK M, 1984, ANNU REV BIOCHEM, V53, P847 KALADAS PM, 1981, MOL IMMUNOL, V18, P969, DOI 10.1016/0161-5890(81)90114-0 KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 KHAN KM, 1990, J HISTOCHEM CYTOCHEM, V38, P1615 KHAN KM, 1991, HEARING RES, V53, P223, DOI 10.1016/0378-5955(91)90056-F KORNFELD R, 1985, ANNU REV BIOCHEM, V54, P631, DOI 10.1146/annurev.biochem.54.1.631 KOYAMA H, 1982, BRAIN RES, V250, P168, DOI 10.1016/0006-8993(82)90964-7 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 LEWIS ER, 1982, SCIENCE, V215, P1641, DOI 10.1126/science.6978525 LI CW, 1979, ANN OTO RHINOL LARYN, V88, P427 Lim DJ, 1979, SCANNING ELECTRON MI, V3, P929 LIM DJ, 1990, ACTA OTO-LARYNGOL, V110, P224, DOI 10.3109/00016489009122541 LIM DJ, 1976, SCANNING ELECT MIC 5, V2, P269 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 LINDEMAN HH, 1969, ACTA OTO-LARYNGOL, V67, P177, DOI 10.3109/00016486909125441 LIS H, 1986, ANNU REV BIOCHEM, V55, P35, DOI 10.1146/annurev.bi.55.070186.000343 LOOMIS RE, 1987, ARCH BIOCHEM BIOPHYS, V258, P452, DOI 10.1016/0003-9861(87)90366-3 LUFT JH, 1976, INT REV CYTOL, V45, P291 MONSIGNY M, 1980, EUR J BIOCHEM, V104, P147, DOI 10.1111/j.1432-1033.1980.tb04410.x NEUGEBAUER DC, 1986, NATURWISSENSCHAFTEN, V73, P508, DOI 10.1007/BF00367202 PEINADO A, 1987, BRAIN RES, V410, P335, DOI 10.1016/0006-8993(87)90333-7 PEREIRA MEA, 1978, ARCH BIOCHEM BIOPHYS, V185, P108, DOI 10.1016/0003-9861(78)90149-2 PETERS BP, 1979, BIOCHEMISTRY-US, V18, P5505, DOI 10.1021/bi00591a038 PRIETO JJ, 1986, HEARING RES, V24, P237, DOI 10.1016/0378-5955(86)90022-5 PRIETO JJ, 1990, DEV BRAIN RES, V52, P141, DOI 10.1016/0165-3806(90)90229-R RENNIE KJ, 1991, HEARING RES, V51, P279, DOI 10.1016/0378-5955(91)90044-A RUEDA J, 1988, GLYCOCONJUGATES MED, P338 SANTI PA, 1987, HEARING RES, V27, P47, DOI 10.1016/0378-5955(87)90025-6 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SHARON N, 1982, SCIENCE, V231, P227 SLEPECKY N, 1985, HEARING RES, V17, P281, DOI 10.1016/0378-5955(85)90072-3 SPICER SS, 1992, J HISTOCHEM CYTOCHEM, V40, P1 SUGII S, 1982, CARBOHYD RES, V99, P99, DOI 10.1016/S0008-6215(00)80982-9 SUGIYAMA S, 1991, HEARING RES, V55, P263, DOI 10.1016/0378-5955(91)90111-L TACHIBANA M, 1987, HEARING RES, V25, P115, DOI 10.1016/0378-5955(87)90084-0 TACHIBANA M, 1987, HEARING RES, V27, P239, DOI 10.1016/0378-5955(87)90005-0 TACHIBANA M, 1987, ARCH OTO-RHINO-LARYN, V244, P112, DOI 10.1007/BF00458560 TAKADA A, 1985, HEARING RES, V19, P245, DOI 10.1016/0378-5955(85)90144-3 TAKUMIDA M, 1989, ACTA OTO-LARYNGOL, V107, P39, DOI 10.3109/00016488909127477 TAKUMIDA M, 1989, HEARING RES, V37, P163, DOI 10.1016/0378-5955(89)90037-3 TAKUMIDA M, 1989, ARCH OTO-RHINO-LARYN, V246, P26, DOI 10.1007/BF00454130 TAKUMIDA M, 1989, J LARYNGOL OTOL, V103, P357, DOI 10.1017/S0022215100108953 TOLLEFSEN SE, 1983, J BIOL CHEM, V258, P5172 VALAT J, 1989, HEARING RES, V40, P255, DOI 10.1016/0378-5955(89)90166-4 WERSALL J, 1974, HDB SENSORY PHYSL 1, P124 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 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 FEB PY 1993 VL 65 IS 1-2 BP 151 EP 163 DI 10.1016/0378-5955(93)90210-R PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300013 PM 8458748 ER PT J AU BAIRD, RA TORRES, MA SCHUFF, NR AF BAIRD, RA TORRES, MA SCHUFF, NR TI HAIR CELL REGENERATION IN THE BULLFROG VESTIBULAR OTOLITH ORGANS FOLLOWING AMINOGLYCOSIDE TOXICITY SO HEARING RESEARCH LA English DT Article DE OTOTOXICITY; HAIR CELL; REGENERATION; OTOLITH ORGANS; BULLFROG ID AVIAN INNER-EAR; ACOUSTIC TRAUMA; CHICK COCHLEA; FISH EAR; GENTAMICIN; OTOTOXICITY; GROWTH; TRANSDUCTION; STEREOCILIA; GLYCOCALYX AB Adult bullfrogs were given single intraotic injections of the aminoglycoside antibiotic gentamicin sulfate and sacrificed at postinjection times ranging from 0.5 to 9 days. The saccular and utricular maculae of normal and injected animals were examined in wholemount and cross-section. Intraotic 200 muM gentamicin concentrations resulted in the uniform destruction of the hair bundles and, at later times, the cell bodies of saccular hair cells. In the utriculus, striolar hair cells were selectively damaged while extrastriolar hair cells were relatively unaffected. Regenerating hair cells, identified in sectioned material by their small cell bodies and short, well-formed hair bundles, were seen in the saccular and utricular maculae as early as 24-48 h postinjection. Immature versions of mature hair cell types in both otolith organs were recognized by the presence or absence of a bulbed kinocilia and the relative lengths of their kinocilia and longest stereocilia. Utricular hair cell types with kinocilia longer than their longest stereocilia were observed at earlier times than hair cell types with shorter kinocilia. In the sacculus, the hair bundles of gentamicin-treated animals, even at 9 days postinjection, were significantly smaller than those of normal animals. The hair bundles of utricular hair cells, on the other hand, reached full maturity within the same time period. RP BAIRD, RA (reprint author), GOOD SAMARITAN HOSP,RS DOW NEUROL SCI INST,1120 NW 20TH AVE,PORTLAND,OR 97209, USA. CR BAIRD RA, 1986, BRAIN RES, V369, P48, DOI 10.1016/0006-8993(86)90512-3 BAIRD RA, 1992, ANN NY ACAD SCI, V656, P12, DOI 10.1111/j.1749-6632.1992.tb25197.x BAIRD RA, 1993, IN PRESS ASS RES OTO, V16 BAIRD RA, 1993, UNPUB J NEUROPHYSIOL BERRIDGE MJ, 1989, NATURE, V341, P197, DOI 10.1038/341197a0 CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 CORWIN JT, 1989, J COMP NEUROL, V288, P529, DOI 10.1002/cne.902880402 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 DEGROOT JCMJ, 1990, HEARING RES, V50, P35, DOI 10.1016/0378-5955(90)90031-J DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 HASHINO E, 1991, HEARING RES, V52, P356, DOI 10.1016/0378-5955(91)90025-5 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 JAMARILLO F, 1991, NEURON, V7, P409 JONES TA, 1992, ASS RES OTOLARYNGOL, V15, P161 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 KROESE ABA, 1980, NATURE, V283, P395, DOI 10.1038/283395a0 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 LI CW, 1979, ANN OTO RHINOL LARYN, V88, P427 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 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 NISHIZUKA Y, 1984, SCIENCE, V225, P1365, DOI 10.1126/science.6147898 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RUBEL EW, 1991, NOISE INDUCED HEARIN, P204 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X TAKADA A, 1985, HEARING RES, V19, P245, DOI 10.1016/0378-5955(85)90144-3 TAKUMIDA M, 1989, ACTA OTO-LARYNGOL, V107, P39, DOI 10.3109/00016488909127477 TAKUMIDA M, 1989, HEARING RES, V37, P163, DOI 10.1016/0378-5955(89)90037-3 TAKUMIDA M, 1989, ARCH OTO-RHINO-LARYN, V246, P26, DOI 10.1007/BF00454130 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WEISLEDER P, 1992, EXP NEUROL, V115, P2, DOI 10.1016/0014-4886(92)90211-8 WERSALL J, 1974, HDB SENSORY PHYSL 1, P124 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 NR 44 TC 75 Z9 80 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 1993 VL 65 IS 1-2 BP 164 EP 174 DI 10.1016/0378-5955(93)90211-I PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300014 PM 8458749 ER PT J AU EGGERMONT, JJ AF EGGERMONT, JJ TI DIFFERENTIAL-EFFECTS OF AGE ON CLICK-RATE AND AMPLITUDE MODULATION-FREQUENCY CODING IN PRIMARY AUDITORY-CORTEX OF THE CAT SO HEARING RESEARCH LA English DT Article DE CAT; PRIMARY AUDITORY CORTEX; AMPLITUDE MODULATION; REPETITION RATE; TEMPORAL MODULATION TRANSFER FUNCTIONS; MATURATION ID TEMPORAL CHARACTERISTICS; NEURONS; MIDBRAIN; TIME; REPRESENTATION; SENSITIVITY; STIMULATION; RESPONSES; GRASSFROG; ONSET AB Recordings were made from 185 neurons in the primary auditory cortex of cats in the age range of 15 to 297 days. A comparison was made between the tuning for click repetition-rate and for amplitude modulation-frequency of a noise burst on the basis of temporal Modulation Transfer Functions (tMTF). 90 of the 185 units had a clear band-pass type tMTF for both repetition rate and modulation frequency, there was, however, no correlation between the respective Best Modulation Frequencies (BMF). Amplitude modulated noise (AMnoise) was the more effective stimulus in young kittens while click-train stimulation was more effective in adult cats. For all neurons with significant synchronization, BMFs for both click-train and AMnoise increased with age from about 4 Hz in kittens younger than 30 days to about 10 Hz in adult cats. In the approximately 50% of the neurons that were tuned both to click rate and modulation frequency. however, the BMF to AMnoise was consistently and significantly higher than that for clicks. In this group the mean BMF for kittens younger than 30 days were 7.94 Hz for AMnoise and 3.29 Hz for clicks and in the adults 10.91 Hz for AMnoise and 7.71 Hz for clicks. RP EGGERMONT, JJ (reprint author), UNIV CALGARY,DEPT PSYCHOL,BEHAV NEUROSCI RES GRP,2500 UNIV DR NW,CALGARY T2N 1N4,ALBERTA,CANADA. CR AITKIN L., 1990, AUDITORY CORTEX CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 EGGERMONT JJ, 1991, HEARING RES, V56, P153, DOI 10.1016/0378-5955(91)90165-6 EGGERMONT JJ, 1989, HEARING RES, V40, P147, DOI 10.1016/0378-5955(89)90108-1 EGGERMONT JJ, 1991, HEARING RES, V57, P45, DOI 10.1016/0378-5955(91)90073-I EGGERMONT JJ, 1992, HEARING RES, V61, P1, DOI 10.1016/0378-5955(92)90029-M ELLIOTT LL, 1986, J ACOUST SOC AM, V80, P1250, DOI 10.1121/1.393819 EPPING WJM, 1986, HEARING RES, V24, P55, DOI 10.1016/0378-5955(86)90005-5 EPPING WJM, 1986, HEARING RES, V24, P37, DOI 10.1016/0378-5955(86)90004-3 MARDIA KV, 1972, STATISTICS DIRECTION MCCORMICK DA, 1985, J NEUROPHYSIOL, V54, P782 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 SALGANICOFF M, 1988, J NEUROSCI METH, V25, P181, DOI 10.1016/0165-0270(88)90132-X SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SCHREINER CE, 1988, AUDITORY FUNCTION NE, P337 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 Suga N., 1973, BASIC MECH HEARING, P675 ZEKI S, 1990, SIGNAL SENSE LOCAL G, P85 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 FEB PY 1993 VL 65 IS 1-2 BP 175 EP 192 DI 10.1016/0378-5955(93)90212-J PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300015 PM 8458750 ER PT J AU MOULIN, A COLLET, L DUCLAUX, R AF MOULIN, A COLLET, L DUCLAUX, R TI CONTRALATERAL AUDITORY-STIMULATION ALTERS ACOUSTIC DISTORTION PRODUCTS IN HUMANS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; ACOUSTIC DISTORTION PRODUCTS; MEDIAL EFFERENT COCHLEAR SYSTEM ID COCHLEAR MICROMECHANICAL PROPERTIES; SPONTANEOUS OTOACOUSTIC EMISSIONS; CROSSED OLIVOCOCHLEAR BUNDLE; NORMALLY HEARING SUBJECTS; GUINEA-PIG COCHLEA; EFFERENT NEURONS; ELECTRICAL-STIMULATION; SOUND STIMULATION; ACTION-POTENTIALS; NERVE FIBERS AB It is now generally accepted that otoacoustic emissions (OAE) represent the only objective and non-intrusive means of functional exploration of the active micromechanical characteristics of the outer hair cells of the organ of Corti. Previous studies showed a decrease of the transiently evoked otoacoustic emissions and spontaneous otoacoustic emissions in humans, during acoustic stimulation of the contralateral ear, and attributed this effect to the medial efferent system. Such an effect has been shown on acoustic distortion product otoacoustic emissions (DPOAE) in guinea pigs, but has not been investigated for DPOAEs recorded in humans, although DPOAEs represent the easiest means of exploring active micromechanical cochlear properties both in humans and in laboratory animals. The present study sought to investigate the existence and characteristics of a contralateral auditory stimulation effect on DPOAEs recorded in humans. This study shows that contralateral broad-band noise (BBN) has a suppressive effect on DPOAEs recorded from 0.5 kHz to 5 kHz. This effect is not due to air conduction, as no change in the noise floor occurred under increasing contralateral stimulation, and as no reduction in DPOAE amplitude was obtained in subjects whose contralateral ear was sealed with a plastic ear plug. Moreover, cross-over attenuation by bone transmission has been ruled out, as no change in DPOAE amplitude was recorded in the healthy ear of total unilaterally deaf patients during acoustic stimulation of the deaf ear. The effect seen was not entirely due to the acoustic reflex, as it was found and could indeed be even greater in subjects with no acoustic reflex. Results presented here show that the contralateral BBN effect is greater at low levels of ipsilateral stimulation, which leads us to discuss the involvement of both passive and active mechanisms in DPOAE generation at high stimulation levels. The contralateral BBN effect seems to be greater in mid frequency cochlear regions. There is strong evidence that the medial efferent system is involved and that afferent and efferent inputs are, at least partly, integrated at a brainstem level in order to ensure cochlear interaction. DPOAEs provide an interesting model for functional exploration of the efferent system, since they seem to be the only type of otoacoustic emission that can be recorded in both humans and in the majority of animals, and since results are obtained in the same way from both animals and humans, which allows experimental animal models very close to the human model. C1 FAC MED LYON SUD,PHYSIOL SENSORIELLE LAB,PIERRE BENITE,FRANCE. RP MOULIN, A (reprint author), HOP EDOUARD HERRIOT,CNRS,URA 1447,PAVILLON U,3 PL ARSONVAL,F-69003 LYON,FRANCE. CR BORG E, 1971, EXP NEUROL, V31, P301, DOI 10.1016/0014-4886(71)90234-2 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 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 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 COLLET L, 1992, AUDIOLOGY, V31, P1 FEX J, 1962, ACTA PHYSIOL SCAND, V55, P1 FOLSOM RC, 1987, ACTA OTO-LARYNGOL, V103, P262, DOI 10.3109/00016488709107792 FURST M, 1988, J ACOUST SOC AM, V84, P215, DOI 10.1121/1.396968 GALAMBOS R, 1956, J NEUROPHYSIOL, V19, P424 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 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 J J Jr, 1986, Scand Audiol Suppl, V25, P53 HARRIS FP, 1990, MECH BIOPHYSICS HEAR, P178 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 INNITZER J, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P137 JOSEPH MP, 1985, J COMP NEUROL, V23, P43 KEMP DT, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 KEMP DT, 1990, EAR HEARING, V11, P93 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LIBERMAN MC, 1988, J NEUROPHYSIOL, V60, P1779 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P3 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 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 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 PROBST R, 1990, ADV AUDIOL, V7, P117 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RAJAN R, 1988, BRAIN RES, V459, P241, DOI 10.1016/0006-8993(88)90640-3 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 ROBERTSON D, 1985, HEARING RES, V20, P63, DOI 10.1016/0378-5955(85)90059-0 SIEGEL JH, 1982, HEARING RES, V6, P172 SMURZYNSKI J, 1992, HEARING RES, V58, P227, DOI 10.1016/0378-5955(92)90132-7 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 Warr W. B., 1986, NEUROBIOLOGY HEARING, P333 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WIER CC, 1988, J ACOUST SOC AM, V84, P130 ZENNER HP, 1989, NATO ASI SER, P93 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 NR 45 TC 103 Z9 109 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 1993 VL 65 IS 1-2 BP 193 EP 210 DI 10.1016/0378-5955(93)90213-K PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300016 PM 8458751 ER PT J AU HARDING, NJ DAVIES, WE AF HARDING, NJ DAVIES, WE TI CELLULAR-LOCALIZATION OF TAURINE IN THE ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE TAURINE; GUINEA PIG; OUTER HAIR CELL; CONFOCAL MICROSCOPY ID GUINEA-PIG COCHLEA; POTASSIUM-INDUCED RELEASE; RETINAL DEGENERATION; HAIR-CELLS; OTOTOXICITY; SUBSTANCES; GABA AB The cellular localisation of taurine in the organ of Corti has been established using a monoclonal antibody and confocal fluorescence microscopy. The bulk of the taurine was found in the outer hair cells with very little present in the inner hair cells and supporting structures. The outer hair cells which probably function as an amplification/attenuation gain system, control inner hair cell output to the brain. Taurine is tentatively postulated as being related to calcium fluxes involved in outer hair cell response to sound or olivocochlear bundle stimulation. Other possibilities are also discussed. C1 UNIV BIRMINGHAM,SCH MED,DEPT PHARMACOL,BIRMINGHAM B15 2TT,W MIDLANDS,ENGLAND. CR ASHMORE J, 1992, NATURE, V356, P111, DOI 10.1038/356111a0 BIRNSO OV, 1989, P PHYSL SOC J PHYSL, V416, pP22 BOBBIN RP, 1991, HEARING RES, V54, P135, DOI 10.1016/0378-5955(91)90143-W BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1990, HEARING RES, V46, P83, DOI 10.1016/0378-5955(90)90141-B CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 Davies W.E., 1985, P244 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x HAYES KC, 1975, SCIENCE, V188, P949, DOI 10.1126/science.1138364 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 HUXTABLE RJ, 1990, TAURINE FUNCTIONAL N, P185 HUXTABLE RJ, 1986, TRENDS PHARMACOL SCI, V7, P481, DOI 10.1016/0165-6147(86)90433-5 IMAKI H, 1987, J NEUROSCI RES, V18, P602, DOI 10.1002/jnr.490180414 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x KAY IS, 1990, EUR ARCH OTO-RHINO-L, V247, P37 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 MAGNUSSON KR, 1988, J NEUROSCI, V8, P4551 MANDEL P, 1976, TRANSMITTERS VISUAL, P89 RUSSELL IJ, 1987, BRIT MED BULL, V43, P802 SAWAMURA A, 1990, CELL CALCIUM, V11, P251, DOI 10.1016/0143-4160(90)90001-B SCHWARTZ IR, 1983, HEARING RES, V9, P185, DOI 10.1016/0378-5955(83)90027-8 STORMMATHISEN J, 1986, NEUROHISTOCHEMISTRY, P21 TAKIHARA K, 1988, BIOCHEM PHARMACOL, V37, P2651 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 WRIGHT CE, 1986, ANNU REV BIOCHEM, V55, P427, DOI 10.1146/annurev.bi.55.070186.002235 NR 25 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 FEB PY 1993 VL 65 IS 1-2 BP 211 EP 215 DI 10.1016/0378-5955(93)90214-L PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300017 PM 8458752 ER PT J AU MOULIN, A COLLET, L VEUILLET, E MORGON, A AF MOULIN, A COLLET, L VEUILLET, E MORGON, A TI INTERRELATIONS BETWEEN TRANSIENTLY EVOKED OTOACOUSTIC EMISSIONS, SPONTANEOUS OTOACOUSTIC EMISSIONS AND ACOUSTIC DISTORTION PRODUCTS IN NORMALLY HEARING SUBJECTS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; CLICK-EVOKED OTOACOUSTIC EMISSIONS; ACOUSTIC DISTORTION PRODUCTS; ACTIVE COCHLEAR MECHANISMS ID COCHLEAR MICROMECHANICAL PROPERTIES; HUMAN EARS; 2F1-F2; STIMULATION; INFANTS; BEHAVIOR; FREQUENCY; CHILDREN; SYSTEM; TONES AB Active cochlear mechanisms and especially outer hair cells seem to be involved in oto-acoustic emissions (OAEs) genesis. This study sought to investigate basic characteristics of spontaneous otoacoustic emissions (SOAEs), click-evoked otoacoustic emissions (TOAEs) and interrelations between SOAEs, TOAEs and 2f1-f2 and 2f2-f1 distortion product OAEs (DPOAEs) in 135 normally hearing subjects. A gender effect was shown on TOAEs and DPOAEs amplitude, and is attributed to the higher incidence of SOAEs in women (58%) than in men (22%). Moreover, SOAEs presence seems to mask the age effect found, especially at high frequency components, on TOAEs amplitude. A general influence of SOAEs on TOAEs and DPOAEs is shown, especially at frequencies ranging from 1 kHz to 3 kHz. collecting more than 66% of the SOAEs peaks recorded. Lastly, correlations between TOAEs frequency band amplitude and 2f1-f2 DPOAEs amplitude, shows frequency specificity, at least at low frequencies (i.e., from 0.5 to 2 kHz) in agreement with previous works suggesting that the 2f1-f2 DPOAEs generation site is at the geometric mean of the primaries. The same correlations calculated with 2f2-f1 DPOAEs amplitude show frequency specificity at low frequencies i.e., at 800 Hz and 1600 Hz. 2f2-f1 DPOAEs in humans are shown to be generated near the 2f2-f1 frequency region on the cochlear partition. C1 UNIV CLAUDE BERNARD,HOP EDOUARD HERRIOT,PHYSIOL SENSORIELLE AUDIT & VOIX LAB,CNRS,UNITE 1447,F-69003 LYON,FRANCE. CTR HOSP LYON SUD,PHYSIOL SENSORIELLE LAB,F-69310 PIERRE BENITE,FRANCE. CR BARGONES JY, 1988, J ACOUST SOC AM, V83, P1809, DOI 10.1121/1.396515 BONFILS P, 1988, ARCH OTOLARYNGOL, V114, P887 BONFILS P, 1989, LARYNGOSCOPE, V99, P752 BONFILS P, 1988, ARCH OTO-RHINO-LARYN, V245, P53, DOI 10.1007/BF00463550 BONFILS P, 1988, AUDIOLOGY, V27, P27 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BROWN SE, 1990, ABSTR ASS RES OT, V13, P230 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 CIANFRONE M, 1990, ADV AUDIOL, V7, P126 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COLLET L, 1990, ANN OTO RHINOL LARYN, V99, P993 COLLET L, 1992, INT J NEUROSCI, V62, P113 COLLET L, 1992, AUDIOLOGY, V31, P1 COLLET L, 1989, ARCH OTOLARYNGOL, V115, P1060 COLLET L, 1991, AUDIOLOGY, V30, P164 DOLAN TG, 1985, J ACOUST SOC AM, V77, P1475, DOI 10.1121/1.392042 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 Gleeson M, 1987, Acta Otolaryngol Suppl, V436, P103 GRANDORI F, 1985, AUDIOLOGY, V24, P71 HARRIS FP, 1991, AUDIOLOGY, V30, P135 HARRIS FP, 1990, MECH BIOPHYSICS HEAR, P178 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HOUSTON HG, 1985, BIOL PSYCHIAT, V20, P419, DOI 10.1016/0006-3223(85)90044-7 JOHNSEN NJ, 1983, SCAND AUDIOL, V12, P17, DOI 10.3109/01050398309076220 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 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, 1982, COCHLEAR ECHOES IMPL, P189 KEMP DT, 1990, EAR HEARING, V11, P93 LONG GR, 1988, HEARING RES, V36, P125, DOI 10.1016/0378-5955(88)90055-X LONSBURYMARTIN BL, 1991, J ACOUST SOC AM, V89, P1749, DOI 10.1121/1.401009 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P3 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 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 MARTIN G K, 1990, Seminars in Hearing, V11, P186, DOI 10.1055/s-0028-1091347 MARTIN GK, 1990, ANN OTO RHINOL LARYN, V99, P30 MARTIN GK, 1990, EAR HEARING, V11, P121 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOULIN A, 1992, ACTA OTO-LARYNGOL, V112, P210 MOULIN A, 1991, ACTA OTO-LARYNGOL, V111, P835, DOI 10.3109/00016489109138419 NORTON SJ, 1990, EAR HEARING, V11, P121, DOI 10.1097/00003446-199004000-00006 NORTON SJ, 1989, HEARING RES, V38, P243, DOI 10.1016/0378-5955(89)90069-5 PROBST R, 1987, AM J OTOLARYNG, V8, P73, DOI 10.1016/S0196-0709(87)80027-3 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 PROBST R, 1990, ADV AUDIOL, V7, P117 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SCHMIEDT RA, 1981, HEARING RES, V5, P195 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WHITEHEAD ML, 1989, BRIT J AUDIOL, V23, P149 WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 NR 61 TC 65 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 1993 VL 65 IS 1-2 BP 216 EP 233 DI 10.1016/0378-5955(93)90215-M PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300018 PM 8458753 ER PT J AU SUBRAMANIAM, M HENDERSON, D SPONGR, VP AF SUBRAMANIAM, M HENDERSON, D SPONGR, VP TI PROTECTION FROM NOISE INDUCED HEARING-LOSS - IS PROLONGED CONDITIONING NECESSARY SO HEARING RESEARCH LA English DT Article DE CONDITIONING; NUMBER OF EXPOSURES; THRESHOLD SHIFT ID AUDIBILITY CURVE; EXPOSURE; CHINCHILLA; RESISTANCE; LEVEL AB The effect of prior 'conditioning' noise exposures on the protection from subsequent higher level exposures was studied using four groups of chinchillas. The three experimental groups were 'conditioned' using a 0.5 kHz octave band noise at 95 dB SPL for 6 h a day. The first group was exposed to the noise once and allowed to recover for nine days prior to the second exposure. The second and third groups were exposed for ten and twenty days respectively. The first group showed only small reductions in threshold shift (TS) following the second exposure. The other two groups showed significant reductions in TS with repeated exposures. Following the last 'conditioning' exposure, all three experimental groups were allowed to recover for five days before exposing them to the same noise at 106 dB SPL for 48 h. Threshold shifts recorded following the 106 dB exposure were compared against those recorded in a control group exposed only to the higher level. Each of the three experimental groups developed significantly less permanent threshold shifts than the control group. However, there were no significant differences among the three experimental groups and the differences in hair cell losses were insignificant. RP SUBRAMANIAM, M (reprint author), SUNY BUFFALO,DEPT COMMUNICAT DISORDERS & SCI,HEARING RES LAB 215,BUFFALO,NY 14214, USA. CR Bohne B.A., 1982, NEW PERSPECTIVES NOI, P283 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 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 GRATTON MA, 1990, HEARING RES, V50, P211, DOI 10.1016/0378-5955(90)90046-R HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 Mills J. H., 1976, EFFECTS NOISE HEARIN, P265 MILLS JH, 1981, J ACOUST SOC AM, V70, P390, DOI 10.1121/1.386774 SPONGR VP, 1992, ARCH OTOLARYNGOL, V118, P157 SUBRAMANIAM M, 1991, HEARING RES, V56, P65, DOI 10.1016/0378-5955(91)90154-2 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H NR 12 TC 17 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 FEB PY 1993 VL 65 IS 1-2 BP 234 EP 239 DI 10.1016/0378-5955(93)90216-N PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300019 PM 8458754 ER PT J AU SCHWEITZER, L CECIL, T WALSH, EJ AF SCHWEITZER, L CECIL, T WALSH, EJ TI DEVELOPMENT OF GAD-IMMUNOREACTIVITY IN THE DORSAL COCHLEAR NUCLEUS OF THE HAMSTER AND CAT - LIGHT AND ELECTRON-MICROSCOPIC OBSERVATIONS SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEAR NUCLEUS; DEVELOPMENT; GLUTAMIC ACID DECARBOXYLASE; GABA ID GLUTAMIC-ACID DECARBOXYLASE; GAMMA-AMINOBUTYRIC-ACID; STEM AUDITORY NUCLEI; BRAIN-STEM; GUINEA-PIG; IMMUNOCYTOCHEMICAL LOCALIZATION; GABAERGIC NEURONS; GABA IMMUNOREACTIVITY; SYNAPTIC ORGANIZATION; FUSIFORM CELLS AB Physiologic and pharmacologic evidence suggests that inhibitory influences are active in the mammalian dorsal cochlear nucleus (DCN) by the onset of hearing, while anatomical evidence suggests that inhibitory synapses are not present until days or weeks later. One inhibitory neurotransmitter in the DCN is gamma aminobutyric acid (GABA) and its presence can be indexed by immunohistochemical localization of its synthetic enzyme glutamic acid decarboxylase (GAD). The present study investigated the ingrowth and synapse formation of GAD-immunoreactive inputs in the DCN of cat and hamster. GAD-immunoreactive puncta are present in the DCN of the cat at birth and of the hamster on postnatal day (PND) 3. Thus, the present data correlate well with the physiologic and pharmacologic evidence. In both species the first labelled puncta are near the dorsal acoustic stria and may originate from efferent axons in the stria. Several days later a band of labelled puncta is found in the fusiform cell layer. This location is equivalent to the termination zone of cartwheel cells, GAD- immunoreactive interneurons in the DCN. Based on this spatiotemporal sequence in the appearance of GAD-immunoreactive puncta, we suggest that sources of GABA extrinsic to the DCN mature first, followed by intrinsic sources. C1 BOYS TOWN NATL RES HOSP,OMAHA,NE. RP SCHWEITZER, L (reprint author), UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292, USA. CR ADAMS JC, 1987, J COMP NEUROL, V262, P375, DOI 10.1002/cne.902620305 ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 BARARDI N, 1984, J PHYSIOL-LONDON, V357, P525 BERREBI AS, 1991, ANAT EMBRYOL, V183, P427 BRUGGE JF, 1984, J ACOUST SOC AM, V75, P1548, DOI 10.1121/1.390826 BRUGGE JF, 1978, ANNU REV NEUROSCI, V1, P363, DOI 10.1146/annurev.ne.01.030178.002051 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 CODE RA, 1989, J COMP NEUROL, V284, P504, DOI 10.1002/cne.902840403 COHEN ES, 1972, EXP NEUROL, V35, P470, DOI 10.1016/0014-4886(72)90117-3 DAVIES W E, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P155 EVANS EF, 1973, EXP BRAIN RES, V17, P428 FITZPATRICK D, 1990, P NATL ACAD SCI USA, V87, P449, DOI 10.1073/pnas.87.1.449 FROSTHOLM A, 1986, BRAIN RES BULL, V16, P189, DOI 10.1016/0361-9230(86)90033-X GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GODFREY DA, 1975, J COMP NEUROL, V162, P269, DOI 10.1002/cne.901620207 GOLDBERG JM, 1973, BRAIN RES, V64, P35, DOI 10.1016/0006-8993(73)90169-8 HENRY S, 1989, NEUROSCI LETT, V100, P301, DOI 10.1016/0304-3940(89)90703-9 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 JONG YJ, 1986, DEV BRAIN RES, V25, P83, DOI 10.1016/0165-3806(86)90154-9 JUIZ JM, 1989, BRAIN RES, V504, P173, DOI 10.1016/0006-8993(89)91620-X KANE EC, 1974, ANAT REC, V179, P67, DOI 10.1002/ar.1091790106 KANE EC, 1974, J COMP NEUROL, V155, P301, DOI 10.1002/cne.901550303 KANE ES, 1981, J COMP NEUROL, V198, P483, DOI 10.1002/cne.901980308 KANE ES, 1978, AM J ANAT, V153, P321, DOI 10.1002/aja.1001530302 KIANG NYS, 1975, NERVOUS SYSTEM, P81 KUNKEL DD, 1986, J NEUROSCI, V6, P541 MANIS PB, 1983, J NEUROPHYSIOL, V50, P1156 MCLEAN IW, 1974, J HISTOCHEM CYTOCHEM, V22, P1077 MERCHANPEREZ A, 1990, EUR ARCH OTO-RHINO-L, V248, P4, DOI 10.1007/BF00634770 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 Mugnaini E, 1985, HDB CHEM NEUROANAT 1, V4, P436 OERTEL WH, 1981, NEUROSCIENCE, V6, P2715, DOI 10.1016/0306-4522(81)90115-9 OERTEL WH, 1981, NEUROSCIENCE, V6, P2689, DOI 10.1016/0306-4522(81)90113-5 Osen K.K., 1990, GLYCINE NEUROTRANSMI, P417 Ottersen O. P., 1984, HDB CHEM NEUROANATOM, V3, P141 POTASHNER SJ, 1985, AUDITORY BIOCH, P141 POTASHNER SJ, 1985, J NEUROCHEM, V45, P1558, DOI 10.1111/j.1471-4159.1985.tb07227.x PURVES D, 1985, PRINCIPLES NEURAL DE RIBAK CE, 1978, BRAIN RES, V140, P315, DOI 10.1016/0006-8993(78)90463-8 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 SAINTMARIE RL, 1991, HEARING RES, V51, P11, DOI 10.1016/0378-5955(91)90003-R SANES DH, 1988, J NEUROSCI, V8, P682 SAVELLS K, 1991, ANAT REC, V229, P79 SCHWEITZER L, 1992, HEARING RES, V60, P34, DOI 10.1016/0378-5955(92)90056-S SCHWEITZER L, 1987, HEARING RES, V25, P249, DOI 10.1016/0378-5955(87)90096-7 SCHWEITZER L, 1991, NEUROTOXICOL TERATOL, V13, P189, DOI 10.1016/0892-0362(91)90010-T SCHWEITZER L, 1984, J COMP NEUROL, V225, P228, DOI 10.1002/cne.902250208 SCHWEITZER L, 1985, DEV BRAIN RES, V20, P69, DOI 10.1016/0165-3806(85)90088-4 SCHWEITZER L, 1990, DEV BRAIN RES, V56, P19, DOI 10.1016/0165-3806(90)90159-V SERESS L, 1988, DEV BRAIN RES, V44, P197, DOI 10.1016/0165-3806(88)90218-0 SHIPLEY C, 1980, BRAIN RES, V182, P313, DOI 10.1016/0006-8993(80)91191-9 SHIRAISHI T, 1985, BRAIN RES, V347, P183, DOI 10.1016/0006-8993(85)90910-2 SHOTWELL SL, 1986, J NEUROSCI, V6, P1410 TACHIBAN.M, 1974, BRAIN RES, V69, P370, DOI 10.1016/0006-8993(74)90017-1 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 WALSH EJ, 1986, J ACOUST SOC AM, V79, P745, DOI 10.1121/1.393463 Walsh Edward J., 1992, P161 WALSH EJ, 1990, J NEUROPHYSIOL, V64, P961 WARTON SS, 1990, DEV BRAIN RES, V52, P95, DOI 10.1016/0165-3806(90)90225-N WENTHOLD RJ, 1986, BRAIN RES, V380, P7, DOI 10.1016/0006-8993(86)91423-X WENTHOLD RJ, 1979, BRAIN RES, V162, P338, DOI 10.1016/0006-8993(79)90294-4 WOLFF JR, 1981, ADV EXP MED BIOL, V181, P215 WU SH, 1987, HEARING RES, V30, P99 YAJIMA Y, 1990, EXP BRAIN RES, V81, P581, DOI 10.1007/BF02423507 YOUNG ED, 1988, AUDITORY FUNCTION NE, P817 NR 66 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 1993 VL 65 IS 1-2 BP 240 EP 252 DI 10.1016/0378-5955(93)90217-O PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300020 PM 8458755 ER PT J AU AOYAGI, M KIREN, T KIM, Y SUZUKI, Y FUSE, T KOIKE, Y AF AOYAGI, M KIREN, T KIM, Y SUZUKI, Y FUSE, T KOIKE, Y TI OPTIMAL MODULATION FREQUENCY FOR AMPLITUDE-MODULATION FOLLOWING RESPONSE IN YOUNG-CHILDREN DURING SLEEP SO HEARING RESEARCH LA English DT Article DE AMPLITUDE-MODULATION FOLLOWING RESPONSE; MODULATION FREQUENCY; AGE EFFECT; EFFECT OF SLEEP; PHASE SPECTRAL ANALYSIS ID STEADY-STATE RESPONSES; EVENT-RELATED POTENTIALS; EVOKED-POTENTIALS; TONES; SCALP; CAT AB In young children, there appears to be no advantage to recording steady-state response (SSR) at a stimulus rate of 40 Hz. To determine the optimal modulation frequency in auditory SSR evoked by sinusoidally amplitude-modulated (SAM) tones (amplitude-modulation following response: AMFR) in children during sleep and compare response patterns of AMFR at different modulation frequencies while awake with those during sleep, AMFR was examined in 10 adults with normal hearing while awake and during sleep and in 10 young children with normal hearing during sleep. The stimulus was a 1000 Hz, 50 dBnHL SAM tone with a modulation depth of 95%. Modulation frequency was varied from 20 to 200 Hz in 20 Hz steps. Response was determined by phase spectral analysis and the S/N ratio calculated by spectral amplitude at the modulation frequency and noise level around the modulation frequency using fast Fourier transform. Although AMFR was clearly evoked only by a modulation frequency of 40 Hz in adults while awake, AMFRs at modulation frequencies of 80 and 100 Hz were detected during sleep, in addition to 40 Hz AMFR. In children, 40 Hz AMFR was difficult to detect, but response could be clearly detected at higher modulation rates, especially at modulation frequencies of 80 and 100 Hz, compared with response in adults during sleep. Modulation frequencies from 80 to 100 Hz would thus appear optimal for detecting AMFR during sleep in children. RP AOYAGI, M (reprint author), YAMAGATA UNIV,SCH MED,DEPT OTOLARYNGOL,YAMAGATA 99023,JAPAN. CR AOYAGI M, 1991, PLACTICA OTOLOGICA S, V51, P1 AOYAGI M, 1991, Audiology Japan, V34, P149 BATRA R, 1986, HEARING RES, V21, P167, DOI 10.1016/0378-5955(86)90037-7 DOBIE RA, 1991, ELECTROEN CLIN NEURO, V80, P194, DOI 10.1016/0168-5597(91)90121-D DOLPHIN WF, 1992, HEARING RES, V58, P70, DOI 10.1016/0378-5955(92)90010-K FRIDMAN J, 1984, AUDIOLOGY, V23, P99 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 GREENBLATT E, 1985, AUDIOLOGY, V24, P228 Hotelling H, 1931, ANN MATH STAT, V2, P360, DOI 10.1214/aoms/1177732979 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 KUWADA S, 1986, HEARING RES, V21, P179, DOI 10.1016/0378-5955(86)90038-9 LINDEN RD, 1985, EAR HEARING, V6, P167, DOI 10.1097/00003446-198505000-00008 MAKELA JP, 1990, HEARING RES, V45, P41, DOI 10.1016/0378-5955(90)90181-N MAURIZI M, 1990, AUDIOLOGY, V29, P322 OKITSU T, 1984, SCAND AUDIOL, V13, P83, DOI 10.3109/01050398409043044 PICTON TW, 1987, J ACOUST SOC AM, V82, P165, DOI 10.1121/1.395560 PICTON TW, 1987, ELECTROEN CLIN NEURO, V68, P119, DOI 10.1016/0168-5597(87)90039-6 REES A, 1986, HEARING RES, V23, P123, DOI 10.1016/0378-5955(86)90009-2 Rickards F.W., 1984, EVOKED POTENTIAL, VII, P163 RODRIGUEZ R, 1986, EAR HEARING, V7, P300, DOI 10.1097/00003446-198610000-00003 SPYDELL JD, 1985, ELECTROEN CLIN NEURO, V62, P193, DOI 10.1016/0168-5597(85)90014-0 STAPELLS DR, 1988, ELECTROEN CLIN NEURO, V71, P289, DOI 10.1016/0168-5597(88)90029-9 SUZUKI T, 1984, AUDIOLOGY, V23, P599 VICTOR JD, 1991, ELECTROEN CLIN NEURO, V78, P378, DOI 10.1016/0013-4694(91)90099-P NR 25 TC 82 Z9 87 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 1993 VL 65 IS 1-2 BP 253 EP 261 DI 10.1016/0378-5955(93)90218-P PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300021 PM 8458756 ER PT J AU NISHIDA, Y FUJIMOTO, T TAKAGI, A HONJO, I OGAWA, K AF NISHIDA, Y FUJIMOTO, T TAKAGI, A HONJO, I OGAWA, K TI FODRIN IS A CONSTITUENT OF THE CORTICAL LATTICE IN OUTER HAIR-CELLS OF THE GUINEA-PIG COCHLEA - IMMUNOCYTOCHEMICAL EVIDENCE SO HEARING RESEARCH LA English DT Article DE FODRIN; CORTICAL LATTICE; OUTER HAIR CELL; COCHLEA; CYTOSKELETON ID ERYTHROCYTE-MEMBRANE; ACTIN; SPECTRIN; SKELETON; VISUALIZATION; RESPONSES; COMPONENT; MOTILITY; PROTEIN; SHAPE AB Localization of fodrin, a membrane skeletal protein, in the outer hair cell of the guinea pig cochlea was examined by immunocytochemical techniques. By immunofluorescence microscopy, fodrin was observed in the cuticular plate, in the infracuticular network and along the lateral wall. By immunoelectron microscopy of ultrathin cryosections, labeling for fodrin along the lateral wall was localized between the cell membrane and the outermost layer of the subsurface cisternae. Furthermore, pre-embedding immunoelectron microscopy of permeabilized specimens showed that most immunogolds for fodrin were on the thin cross-linking component of the cortical lattice. The results indicate that fodrin is a constituent of the cortical lattice which is thought to play an important role in outer hair cell motility. C1 KYOTO UNIV,FAC MED,DEPT ANAT,KYOTO 606,JAPAN. RP NISHIDA, Y (reprint author), KYOTO UNIV,FAC MED,DEPT OTOLARYNGOL,SAKYO KU,KYOTO 606,JAPAN. CR ALTSCHULER RA, 1991, ABSTR ASS RES OT, V14, P12 ARIMA T, 1991, CELL TISSUE RES, V263, P91, DOI 10.1007/BF00318403 ARNOLD W, 1990, ACTA OTO-LARYNGOL, V109, P213, DOI 10.3109/00016489009107436 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Bannister L H, 1988, Prog Brain Res, V74, P213 BENNETT V, 1988, PROTOPLASMA, V145, P89, DOI 10.1007/BF01349343 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BYERS TJ, 1985, P NATL ACAD SCI USA, V82, P6153, DOI 10.1073/pnas.82.18.6153 COLEMAN TR, 1989, CELL MOTIL CYTOSKEL, V12, P225, DOI 10.1002/cm.970120405 DING JP, 1991, HEARING RES, V56, P19, DOI 10.1016/0378-5955(91)90149-4 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1990, J NEUROSCI, V10, P1388 EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 FISHKIND DJ, 1987, CELL MOTIL CYTOSKEL, V7, P304, DOI 10.1002/cm.970070403 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FUJIMOTO T, 1991, J HISTOCHEM CYTOCHEM, V39, P1485 FUJIMOTO T, 1989, J HISTOCHEM CYTOCHEM, V37, P1345 HIROKAWA N, 1983, CELL, V32, P953, DOI 10.1016/0092-8674(83)90080-6 HOLLEY M, 1991, BIOESSAYS, V13, P115, DOI 10.1002/bies.950130304 HOLLEY MC, 1990, J CELL SCI, V96, P283 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 HOLLEY MC, 1990, EUR ARCH OTO-RHINO-L, V247, P4 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 LIM DJ, 1989, ACTA OTO-LARYNGOL, V107, P398, DOI 10.3109/00016488909127529 RAPHAEL Y, 1986, J SUBMICR CYTOL PATH, V18, P731 SACHS F, 1988, CRIT REV BIOMED ENG, V16, P141 SHEN BW, 1986, J CELL BIOL, V102, P997, DOI 10.1083/jcb.102.3.997 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, 1992, HEARING RES, V57, P201, DOI 10.1016/0378-5955(92)90152-D SOBUE K, 1987, Biomedical Research (Tokyo), V8, P13 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 VERTESSY BG, 1989, BIOPHYS J, V55, P255 YLIKOSKI J, 1990, HEARING RES, V43, P199, DOI 10.1016/0378-5955(90)90228-H 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 NR 38 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 FEB PY 1993 VL 65 IS 1-2 BP 274 EP 280 DI 10.1016/0378-5955(93)90220-U PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KN113 UT WOS:A1993KN11300023 PM 8458757 ER PT J AU MANCINI, P SANTI, PA AF MANCINI, P SANTI, PA TI LOCALIZATION OF THE GM1 GANGLIOSIDE IN THE VESTIBULAR SYSTEM USING CHOLERA-TOXIN SO HEARING RESEARCH LA English DT Article DE INNER EAR; CHOLERA TOXIN; GM1; HISTOCHEMISTRY ID MYELINATED NERVE-FIBERS; BINDING-SITES; THYROTROPIN RECEPTORS; BEHAVIORAL RECOVERY; CELLS; STIMULATION; ENDOLYMPH; MEMBRANES; GROWTH; LESION AB Cholera toxin is an ubiquitous activator of intracellular adenylate cyclase and is divided in two major components: A and B. The B-component consists of several subunits that specifically bind to the external cell membrane. The receptor for the toxin, the GM1 ganglioside, is concentrated in nervous tissues. The B subunit of the cholera toxin, conjugated to different molecules (i.e., choleragenoid) is therefore a sensitive anatomical tracer and has been used to detect the presence of GM1 in mammalian tissues. Using choleragenoid, unlabeled and labeled with FITC, we have determined the distribution of the GM1 ganglioside in the vestibular system of the chinchilla. Vestibular tissues were fixed in 4% paraformaldehyde in phosphate buffer, decalcified in 10% EDTA and prepared as either whole-mount, surface-preparations, or for radial cryosections. Positive control tissue consisted of binding to normal brain tissues. Negative controls consisted of several treatments: masking of the GM1 receptors with unlabeled choleragenoid, tissue extraction of GM1 using ethanol, and preabsorbing the choleragenoid with bovine GM1. In addition, to exclude staining of glycoproteins that may have a carbohydrate structure similar to GM1, tissues were digested with trypsin prior to choleragenoid exposure. In the vestibular system, a strongly positive reaction was observed in: the sensory stereocilia and supporting cells of the maculae and cristae, epithelial cells of the planum semilunatum, and polygonal cells of the semicircular canal. Positive but less strong reactivity was observed in the sensory cell body of maculae and cristae, nerve fibers, epithelial cells of utricle and ampulla walls and flattened epithelial cells of the semicircular canals. No reactivity was present in the supporting connective tissue cells and fibrils, blood vessels, gelatinous cupula of the cristae ampullaris and statoconial membranes. Brain tissue showed strong choleragenoid reactivity. The negative controls showed no or greatly reduced reactivity to choleragenoid. Trypsin digestion did not decrease reactivity to choleragenoid. C1 UNIV MINNESOTA,SCH MED,DEPT OTOLARYNGOL,ROOM 282,LIONS RES BLDG,2001 6TH ST SE,MINNEAPOLIS,MN 55455. CR ACKERMAN GA, 1980, J HISTOCHEM CYTOCHEM, V28, P1100 APORTI F, 1984, COMP PHYSL SENSORY S, P189 APORTI F, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P371 APORTI F, 1977, ARCH ITAL OTOL RINOL, V5, P25 APORTI F, 1981, ACTA OTO-LARYNGOL, V92, P433, DOI 10.3109/00016488109133282 BAIRATI A, 1960, EXP CELL RES, V20, P77, DOI 10.1016/0014-4827(60)90224-X BARTHEL LK, 1990, J HISTOCHEM CYTOCHEM, V38, P1383 BESANCON F, 1974, NATURE, V252, P478, DOI 10.1038/252478a0 BREZICKA FT, 1989, CANCER RES, V49, P1300 CECCARELLI B, 1976, EFFECTS BRAIN DISEAS, P275 DONTA ST, 1973, NATURE-NEW BIOL, V243, P246 FELDMAN AM, 1976, P NATL ACAD SCI USA, V73, P1761, DOI 10.1073/pnas.73.5.1761 FISHMAN PH, 1976, SCIENCE, V194, P906, DOI 10.1126/science.185697 FISHMAN PH, 1982, J MEMBRANE BIOL, V69, P85, DOI 10.1007/BF01872268 FUXE K, 1989, ACTA PHYSIOL SCAND, V137, P551, DOI 10.1111/j.1748-1716.1989.tb08796.x GANSER AL, 1984, J NEUROSCI RES, V12, P245, DOI 10.1002/jnr.490120212 GANSER AL, 1983, J NEUROCYTOL, V12, P921, DOI 10.1007/BF01153342 GARVIN JL, 1988, AM J PHYSIOL, V255, pF711 GILL DM, 1977, ADV CYCLIC NUCLEOTID GILL DM, 1976, BIOCHEMISTRY-US, V15, P1242, DOI 10.1021/bi00651a011 GORIO A, 1983, NEUROSCIENCE, V8, P417, DOI 10.1016/0306-4522(83)90189-6 GREGORY D, 1981, INVEST OPHTH VIS SCI, V20, P371 HANSSON HA, 1977, P NATL ACAD SCI USA, V74, P3782, DOI 10.1073/pnas.74.9.3782 Harada Y, 1989, Acta Otolaryngol Suppl, V468, P17 HARRIS PL, 1978, J AM CHEM SOC, V100, P6738, DOI 10.1021/ja00489a032 HOLLENBE.MD, 1973, P NATL ACAD SCI USA, V70, P2964, DOI 10.1073/pnas.70.10.2964 Humason G.L., 1967, ANIMAL TISSUE TECHNI IWAMASA T, 1987, ACTA NEUROPATHOL, V73, P357 KARPIAK SE, 1987, STROKE, V18, P184 KARPIAK SE, 1984, J NEUROSCI RES, V12, P485, DOI 10.1002/jnr.490120231 KASUI GJ, 1966, J INFECT DIS, V116, P606 KIELCZYNSKI W, 1991, BIOCHEMISTRY-US, V88, P1991 KIMURA R, 1964, Acta Otolaryngol, V57, P517, DOI 10.3109/00016486409137114 KOCH T, 1988, ARCH OTO-RHINO-LARYN, V245, P82, DOI 10.1007/BF00481441 LEDEEN RW, 1984, J NEUROSCI RES, V12, P147, DOI 10.1002/jnr.490120204 LEDEEN RW, 1981, IMPLICATION DISTRIBU, P211 LEDEEN RW, 1978, J SUPRAMOL STR CELL, V8, P1, DOI 10.1002/jss.400080102 LEDLEY FD, 1976, BIOCHEM BIOPH RES CO, V69, P852, DOI 10.1016/0006-291X(76)90452-6 MISHIMA H, 1982, CELL TISSUE RES, V223, P241, DOI 10.1007/BF01258486 MULLIN BR, 1976, P NATL ACAD SCI USA, V73, P842, DOI 10.1073/pnas.73.3.842 MULLIN BR, 1976, P NATL ACAD SCI USA, V73, P1679, DOI 10.1073/pnas.73.5.1679 OLSNES S, 1974, J IMMUNOL, V113, P842 PACUSZKA T, 1990, J BIOL CHEM, V265, P7673 PARKINSON ME, 1989, FEBS LETT, V242, P309, DOI 10.1016/0014-5793(89)80491-0 PETROSINI L, 1987, BEHAV BRAIN RES, V23, P117, DOI 10.1016/0166-4328(87)90049-0 ROBERTSON B, 1989, J NEUROCYTOL, V18, P77, DOI 10.1007/BF01188426 ROISEN FJ, 1988, NEW TRENDS GANGLIOSI, P361 ROISEN FJ, 1981, SCIENCE, V214, P577, DOI 10.1126/science.7291999 Schauer R, 1980, Adv Exp Med Biol, V125, P283 SIMPSON LL, 1971, J NEUROCHEM, V18, P1751, DOI 10.1111/j.1471-4159.1971.tb03750.x SPARROW JR, 1982, EXP NEUROL, V77, P230, DOI 10.1016/0014-4886(82)90157-1 SPIEGEL S, 1988, BIOCHIM BIOPHYS ACTA, V938, P270, DOI 10.1016/0005-2736(88)90165-4 SPIEGEL S, 1987, P NATL ACAD SCI USA, V84, P141, DOI 10.1073/pnas.84.1.141 SUZUKI K, 1965, J NEUROCHEM, V12, P969, DOI 10.1111/j.1471-4159.1965.tb10256.x SUZUKI K, 1976, CATABOLISM SIALIL CO, P159 VANHEYNINGEN W, 1961, J GEN MICROBIOL, V24, P107 VAUGHAN M, 1970, NATURE, V226, P658, DOI 10.1038/226658a0 WOLFF J, 1973, P NATL ACAD SCI USA, V70, P2741, DOI 10.1073/pnas.70.10.2741 NR 58 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 JAN PY 1993 VL 64 IS 2 BP 151 EP 165 DI 10.1016/0378-5955(93)90001-H PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700001 PM 8432686 ER PT J AU LOMBARTE, A YAN, HY POPPER, AN CHANG, JS PLATT, C AF LOMBARTE, A YAN, HY POPPER, AN CHANG, JS PLATT, C TI DAMAGE AND REGENERATION OF HAIR CELL CILIARY BUNDLES IN A FISH EAR FOLLOWING TREATMENT WITH GENTAMICIN SO HEARING RESEARCH LA English DT Article DE FISH; OTOTOXICITY; HAIR CELL; INNER EAR; GENTAMICIN ID ACOUSTIC TRAUMA; CHICK COCHLEA; JUNCTIONAL PROTEINS; POSSIBLE PRECURSORS; INNER-EAR; GROWTH; REORGANIZATION; CYTOSKELETAL; DEGENERATION; SENSITIVITY AB Sensory hair cells in the striolar regions of the utricle and lagena of a teleost fish, the oscar (Astronotus ocellatus), were damaged following intramuscular injections of gentamicin sulfate. In order to determine whether fish can regenerate hair cells, the time course of damage and recovery was followed over a period of four weeks by scanning electron microscopy. Maximum loss of ciliary bundles occurred at about day 10 after the first of four daily injections of gentamicin (20 mg/kg) in 4-6 cm long fish. The striolar regions were almost totally denuded of ciliary bundles, and there was evidence of considerable hair cell loss. The time course for damage was longer in larger fish, but the recovery of the ciliary bundles appeared to be complete about 10 days after maximal damage was seen in both the smaller and larger fish. These data indicate that Astronotus is able to repair damage to hair cells for an extended period of time post-embryonically. C1 UNIV MARYLAND,DEPT ZOOL,COLL PK,MD 20742. RI Lombarte, Antoni/D-3142-2013 CR BALAK KJ, 1990, J NEUROSCI, V10, P2502 CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 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, 1992, EXP NEUROL, V115, P7, DOI 10.1016/0014-4886(92)90212-9 CORWIN JT, 1983, J COMP NEUROL, V217, P345, DOI 10.1002/cne.902170309 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 FORGE A, 1985, HEARING RES, V19, P171, DOI 10.1016/0378-5955(85)90121-2 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 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 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 KELLEY MW, 1992, HEARING RES, V59, P108 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MCDOWELL B, 1989, HEARING RES, V40, P221, DOI 10.1016/0378-5955(89)90163-9 Nadol JJ, 1981, AMINOGLYCOSIDE OTOTO, P409 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W PRESSON JC, 1991, ABST ASS RES OTOLARY, V14, P96 PRESSON JC, 1990, HEARING RES, V46, P9, DOI 10.1016/0378-5955(90)90135-C RAPHAEL Y, 1992, EXP NEUROL, V115, P32, DOI 10.1016/0014-4886(92)90217-E RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H 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 SEIDMAN DA, 1989, ABSTR ASS RES OTOLAR, V12, P135 WEISLEDER P, 1992, EXP NEUROL, V115, P2, DOI 10.1016/0014-4886(92)90211-8 WERNER CL. F., 1933, ZEITSCHR GES ANAT ABT I ZEITSCHR ANAT U ENTWICK LUNGSGESCH, V99, P696, DOI 10.1007/BF02118586 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 NR 34 TC 78 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 JAN PY 1993 VL 64 IS 2 BP 166 EP 174 DI 10.1016/0378-5955(93)90002-I PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700002 PM 8432687 ER PT J AU FORGE, A ZAJIC, G LI, L NEVILL, G SCHACHT, J AF FORGE, A ZAJIC, G LI, L NEVILL, G SCHACHT, J TI STRUCTURAL VARIABILITY OF THE SUBSURFACE CISTERNAE IN INTACT, ISOLATED OUTER HAIR-CELLS SHOWN BY FLUORESCENT LABELING OF INTRACELLULAR MEMBRANES AND FREEZE-FRACTURE SO HEARING RESEARCH LA English DT Article DE 3,3'-DIHEXYLOXACARBOCYANINE IODIDE; ENDOPLASMIC RETICULUM; FLUORESCENT MEMBRANE LABELING; HAIR CELLS; LATERAL CISTERNAE; FREEZE-FRACTURE ID ENDOPLASMIC-RETICULUM; SUBSURFACE CISTERNAE; ORGAN; CORTI; ULTRASTRUCTURE; CONTRACTIONS; SALICYLATE; COCHLEA; SYSTEM; ACTIN AB The intracellular membrane systems in intact, isolated outer hair cells were visualised using the fluorescent membrane probe 3,3'-dihexyloxacarbocyanine iodide (DiOC6) and by freeze-fracture, and f-actin distribution was examined with rhodamine-phalloidin. DiOC6 stained the sub-surface cisternal membranes in the lateral wall and revealed a membrane system running in the centre of the cell from the nucleus to the sub-cuticular region. In optical sections of the lateral wall of fluorescently labelled cells, obtained by scanning laser confocal microscopy, the sub-surface membrane appeared as a fenestrated sheet or a fine network of tubules. Freeze-fracture replicas of rapidly-frozen, unfixed outer hair cells also showed the sub-surface membrane as a fenestrated sheet in some cells or as a network of tubules in others. These combined studies indicate that the interruptions within the cisternal membranes as seen in normal thin sections of outer hair cells are not fixation artefacts but may reflect the dynamic and plastic properties of this membrane system. Double staining of cells with rhodamine-phalloidin and DiOC6 showed substantial co-localisation of intracellular membranes and f-actin. The results suggest there may be a continuous, dynamic endoplasmic reticulum system, forming a core in the centre of the cell, broadening in the subcuticular region and extending down the lateral wall, that may have a role in the turnover and distribution of cytoskeletal assemblies within the outer hair cell. C1 UNIV MICHIGAN, KRESGE HEARING RES INST, ANN ARBOR, MI 48109 USA. RP FORGE, A (reprint author), UCL, INST LARYNGOL & OTOL, 330-332 GRAYS INN RD, LONDON WC1X 8EE, ENGLAND. CR BAUMANN O, 1990, J STRUCT BIOL, V105, P154, DOI 10.1016/1047-8477(90)90109-P BRIDGMAN PC, 1986, J CELL BIOL, V102, P1510, DOI 10.1083/jcb.102.4.1510 BROWNELL WE, 1986, AUDITORY FREQUENCY S, P109 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DODSON HC, 1982, ACTA OTO-LARYNGOL, V94, P193, DOI 10.3109/00016488209128905 DOUEK EE, 1983, J LARYNGOL OTOL, V97, P793, DOI 10.1017/S0022215100095025 DULON D, 1990, J NEUROSCI, V10, P1388 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FORGE A, 1991, J NEUROCYTOL, V20, P471, DOI 10.1007/BF01252275 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 FORGE A, 1982, CELL TISSUE RES, V226, P375 FORGE A, 1989, COCHLEAR MECHANISMS, P29 GULLEY RL, 1977, ANAT REC, V189, P109, DOI 10.1002/ar.1091890108 HOLLEY MC, 1992, ADV BIOSCI, V83, P27 HOLLEY MC, 1990, J CELL SCI, V96, P283 KARLSSON KK, 1991, ACTA OTO-LARYNGOL, V111, P500, DOI 10.3109/00016489109138375 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MCDOWELL B, 1989, HEARING RES, V40, P221, DOI 10.1016/0378-5955(89)90163-9 SAITO K, 1983, CELL TISSUE RES, V229, P467 SLEPECKY N, 1982, ACTA OTO-LARYNGOL, V93, P329, DOI 10.3109/00016488209130890 SPOENDLIN H, 1957, Pract Otorhinolaryngol (Basel), V19, P192 STEYGER PS, 1989, HEARING RES, V42, P1, DOI 10.1016/0378-5955(89)90113-5 TERASAKI M, 1984, CELL, V38, P101, DOI 10.1016/0092-8674(84)90530-0 TERASAKI M, 1992, J CELL SCI, V101, P315 THIERY G, 1976, J MICROSC BIOL CELL, V26, P103 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X NR 29 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 JAN PY 1993 VL 64 IS 2 BP 175 EP 183 DI 10.1016/0378-5955(93)90003-J PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700003 PM 8432688 ER PT J AU FRANCIS, HW NADOL, JB AF FRANCIS, HW NADOL, JB TI PATTERNS OF INNERVATION OF OUTER HAIR-CELLS IN A CHIMPANZEE .1. AFFERENT AND RECIPROCAL SYNAPSES SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; ORGAN OF CORTI; AFFERENT INNERVATION ID HUMAN ORGAN; CORTI; COCHLEA; CAT AB Three varieties of synaptic specialization, afferent, efferent, and reciprocal, have been demonstrated at the base of outer hair cells of one chimpanzee. The purpose of the present study was to investigate the innervation density of afferent and reciprocal synapses in the three rows and three turns of the organ of Corti. The data presented is based on light and electron microscopy from one aged chimpanzee using serial section electron microscopy. Afferent fibers make contact with outer hair cells as either terminal swellings or en passant contacts. In addition to membrane specialization, presynaptic bodies were present at the majority of afferent synapses. The mean innervation density of afferent endings was highest in the middle turn. Reciprocal endings were found on 74% of all outer hair cells. The average number of reciprocal endings increased from the base to apex and, except in the apical turn, from the first to third row of outer hair cells. On the basis of morphological criteria, endings with a reciprocal synapses were more similar to afferent than to efferent endings. C1 MASSACHUSETTS EYE & EAR INFIRM,OTOPATHOL LAB,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. CR BAIRD IL, 1967, ANAT REC, V159, P281, DOI 10.1002/ar.1091590306 DOWLING JE, 1966, PROC R SOC SER B-BIO, V166, P80, DOI 10.1098/rspb.1966.0086 DUNN RA, 1975, P NATL ACAD SCI USA, V72, P3599, DOI 10.1073/pnas.72.9.3599 DUNN RF, 1976, ORL, V82, P188 ENGSTROM H, 1958, Acta Otolaryngol, V49, P109, DOI 10.3109/00016485809134734 FAMIGLIE.EV, 1970, BRAIN RES, V20, P181, DOI 10.1016/0006-8993(70)90287-8 HASHIMOTO S, 1987, ACTA OTO-LARYNGOL, V103, P64 KIMURA R, 1962, Acta Otolaryngol, V55, P11, DOI 10.3109/00016486209127336 KIMURA RS, 1975, INT REV CYTOL, V42, P173, DOI 10.1016/S0074-7696(08)60981-X LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 MCDONALD DM, 1975, J NEUROCYTOL, V4, P177, DOI 10.1007/BF01098781 NADOL JB, 1988, ORL J OTO-RHINO-LARY, V50, P363 NADOL JB, 1981, ANN OTO RHINOL LARYN, V93, P247 NADOL JB, 1984, ANN OTO RHINOL LARYN, V93, P247 NADOL JB, 1985, J COMP NEUROL, V237, P333, DOI 10.1002/cne.902370305 NADOL JB, 1990, ANN OTO RHINOL LARYN, V99, P215 NADOL JB, 1983, LARYNGOSCOPE, V93, P780 NADOL JB, 1988, AM J OTOLARYNG, V9, P47, DOI 10.1016/S0196-0709(88)80007-3 NADOL JB, 1988, HEARING RES, V34, P253, DOI 10.1016/0378-5955(88)90006-8 PUOL R, 1981, DEV BRAIN RES, V3, P151 SCHUKNECHT HF, 1960, NEURAL MECHANISMS AU, P76 SIMMONS DD, 1988, J COMP NEUROL, V270, P145, DOI 10.1002/cne.902700112 SMITH CA, 1961, J ULTRA MOL STRUCT R, V5, P523, DOI 10.1016/S0022-5320(61)80025-7 SMITH CA, 1963, J CELL BIOL, V26, P63 SPOENDLIN H, 1989, 2ND P INT AC C IMM O YAMAUCHI A, 1975, J ULTRA MOL STRUCT R, V50, P47, DOI 10.1016/S0022-5320(75)90007-6 NR 26 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 JAN PY 1993 VL 64 IS 2 BP 184 EP 190 DI 10.1016/0378-5955(93)90004-K PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700004 PM 8432689 ER PT J AU THALMANN, I SUZUKI, H MCCOURT, DW COMEGYS, TH THALMANN, R AF THALMANN, I SUZUKI, H MCCOURT, DW COMEGYS, TH THALMANN, R TI PARTIAL AMINO-ACID-SEQUENCES OF ORGAN OF CORTI PROTEINS OCP1 AND OCP2 - A PROGRESS REPORT SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; PROTEIN; AMINO ACID SEQUENCE; GUINEA PIG ID ANTIGENIC DETERMINANTS; NUCLEOTIDE-SEQUENCE; SECONDARY-STRUCTURE; PREDICTION; PEPTIDE AB Progress in amino acid sequencing of two low-molecular weight acidic proteins of unknown function which are present at high concentrations in the organ of Corti is reported. These two proteins, provisionally termed OCP1 and OCP2, were originally demonstrated by two-dimensional polyacrylamide gel electrophoresis; their presence at high concentrations in the inner ear sensory epithelia strongly suggests that OCP1 and OCP2 serve some important function in the ear. In the present paper, extension of the amino-terminal sequence of OCP2 to 71 residues is described. In addition, the first results on sequencing of OCP1 are presented. Computer algorithms are used to predict important structural features, and the sequences are analyzed for probable phosphorylation, glycosylation, and Ca-binding sites. Projected further studies in immunochemistry and molecular biology of OCP1 and OCP2 based on the amino acid sequencing data are discussed. C1 WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,ST LOUIS,MO 63110. TOHOKU UNIV,DEPT OTOLARYNGOL,SENDAI,MIYAGI 980,JAPAN. RP THALMANN, I (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID AVE,ST LOUIS,MO 63110, USA. CR BARKER WC, 1989, PROTEIN SEQUENCE DAT Chou P Y, 1978, Adv Enzymol Relat Areas Mol Biol, V47, P45 CLEVELAND DW, 1977, J BIOL CHEM, V252, P1102 DEVEREUX J, 1984, NUCLEIC ACIDS RES, V12, P387, DOI 10.1093/nar/12.1Part1.387 EMINI EA, 1985, J VIROL, V55, P836 GARNIER J, 1978, J MOL BIOL, V120, P97, DOI 10.1016/0022-2836(78)90297-8 GRIBSKOV M, 1990, METHOD ENZYMOL, V183, P146, DOI 10.1016/0076-6879(90)83011-W HOPP TP, 1981, P NATL ACAD SCI-BIOL, V78, P3824, DOI 10.1073/pnas.78.6.3824 HOWARD PK, 1985, GENE, V35, P321, DOI 10.1016/0378-1119(85)90011-3 HUDSON GS, 1984, J MOL BIOL, V180, P1023, DOI 10.1016/0022-2836(84)90269-9 JAMESON BA, 1988, COMPUT APPL BIOSCI, V4, P181 KARPLUS PA, 1985, NATURWISSENSCHAFTEN, V72, P212, DOI 10.1007/BF01195768 KENNEDY TE, 1988, P NATL ACAD SCI USA, V85, P7008, DOI 10.1073/pnas.85.18.7008 KRAUS P, 1988, BIOL CHEM H-S, V369, P1204 KYTE J, 1982, J MOL BIOL, V157, P105, DOI 10.1016/0022-2836(82)90515-0 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LIPMAN DJ, 1985, SCIENCE, V227, P1435, DOI 10.1126/science.2983426 TAKAHASHI K, 1989, J ACOUST SOC AM, V85, pS31, DOI 10.1121/1.2026909 THALMANN I, 1980, ARCH OTO-RHINO-LARYN, V226, P123, DOI 10.1007/BF00455126 THALMANN I, 1988, J ACOUST SOC AM, V83, pS6 THALMANN I, 1990, LARYNGOSCOPE, V100, P99 THALMANN I, 1990, EUR ARCH OTO-RHINO-L, V248, P15, DOI 10.1007/BF00634774 THALMANN R, 1976, HDB AUDITORY VESTIBU, P359 WELLNER D, 1990, P NATL ACAD SCI USA, V87, P1947, DOI 10.1073/pnas.87.5.1947 NR 24 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 JAN PY 1993 VL 64 IS 2 BP 191 EP 198 DI 10.1016/0378-5955(93)90005-L PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700005 PM 8432690 ER PT J AU LAURIKAINEN, EA KIM, D DIDIER, A REN, TY MILLER, JM QUIRK, WS NUTTALL, AL AF LAURIKAINEN, EA KIM, D DIDIER, A REN, TY MILLER, JM QUIRK, WS NUTTALL, AL TI STELLATE GANGLION DRIVES SYMPATHETIC REGULATION OF COCHLEAR BLOOD-FLOW SO HEARING RESEARCH LA English DT Article DE COCHLEAR BLOOD FLOW; ELECTRICAL STIMULATION; SYMPATHETIC; STELLATE GANGLION; ALPHA-RECEPTOR; GUINEA PIG ID INNER-EAR; INNERVATION AB The functional properties of the sympathetic fibers innervating the cochlea are not well understood. Adrenergic fibers supplying lateral wall structures of the cochlea have been observed terminating on radiating arterioles and collecting venules. Adrenergic fibers also terminate as 'free' endings in the spiral osseous lamina. Stimulation or transection of sympathetic fibers originating from superior cervical chain and supplying the cochlea have yielded mixed results concerning many aspects of cochlea physiology. In order to clarify the origin of sympathetic fibers and their role in control of cochlear blood flow (CBF), we examined the effect of electrical stimulation of the stellate ganglion (ESS) and transection of postganglionic fibers from the stellate on CBF measured by laser Doppler flowmetry and on systemic blood pressure (BP) in the guinea pig. ESS produced a 20-35% increase in BP and 10-15% decrease in CBF. The decrease in CBF presumably reflects the net result of increased perfusion pressure, local autoregulatory mechanisms, and a direct sympathetic-induced vasoconstriction. Section of the immediate postganglionic sympathetic trunk had little or no effect on the ESS-related change in BP; however, it eliminated the CBF reduction. Intravenously infused beta1-blocker diminished the BP increase due to ESS, while the electrically-evoked reduction in CBF remained. Local application of an alpha-blocker on the round window blocked ESS evoked CBF reductions without altering the BP increase. These data confirm the functional role of sympathetic projections from the stellate ganglion in CBF regulation in guinea pig. Taken together with previous studies showing that the superior cervical ganglion mediates a sympathetic input into inner ear vasculature in guinea pig, our results indicate the action of two or more autonomic sympathetic fiber systems in the control of CBF. C1 UNIV MICHIGAN,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. UNIV LYON 1,NEUROPHYSIOL SENSORIELLE LAB,F-69621 VILLEURBANNE,FRANCE. XIAN MED UNIV,FIRST AFFILIATED HOSP,DEPT OTOLARYNGOL,XIAN,PEOPLES R CHINA. WAYNE STATE UNIV,DEPT OTOLARYNGOL,DETROIT,MI 48202. UNIV HOSP TURKU,DEPT OTOLARYNGOL,TURKU,FINLAND. CR ANGELBORG C, 1977, ACTA OTO-LARYNGOL, V83, P92, DOI 10.3109/00016487709128818 BEAUSANGLINDER M, 1980, ACTA PHYSIOL SCAND, V109, P433, DOI 10.1111/j.1748-1716.1980.tb06617.x BRECHTELSBAUER PB, 1990, OTOLARYNG HEAD NECK, V103, P566 CARRASCO VN, 1990, ARCH OTOLARYNGOL, V116, P411 DENSERT O, 1974, ACTA OTO-LARYNGOL, V77, P185, DOI 10.3109/00016487409124616 DENSERT O, 1974, ACTA OTO-LARYNGOL, V78, P345, DOI 10.3109/00016487409126365 FRAZER P, 1936, J LARYNGOL OTOL, V51, P579, DOI 10.1017/S0022215100042985 GERO J, 1978, BLOOD VESSELS, V15, P277 HULTCRANTZ E, 1980, ORL J OTO-RHINO-LARY, V42, P304 LARSEN HC, 1982, ARCH OTO-RHINO-LARYN, V234, P145, DOI 10.1007/BF00453621 LAURIKAINEN E, 1991, 1991 INN EAR BIOL C MILLER JM, 1990, LASER DOPPLER FLOWME, P319 MILLER JM, 1988, AM J OTOLARYNG, V9, P302, DOI 10.1016/S0196-0709(88)80038-3 MILLER JM, 1984, ARCH OTOLARYNGOL, V110, P305 OHLSEN KA, 1991, CIRC RES, V69, P509 PERLMAN H B, 1955, Ann Otol Rhinol Laryngol, V64, P1176 QUIRK WS, 1989, HEARING RES, V41, P53, DOI 10.1016/0378-5955(89)90178-0 REN TY, 1992, UNPUB EFFECTS INTRAN REN TY, 1992, UNPUB EFFECTS ELECTR Spoendlin H, 1966, Acta Otolaryngol, V61, P423 Spoendlin H, 1981, Adv Otorhinolaryngol, V27, P1 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 NR 22 TC 33 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 JAN PY 1993 VL 64 IS 2 BP 199 EP 204 DI 10.1016/0378-5955(93)90006-M PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700006 PM 8381781 ER PT J AU RAREY, KE CURTIS, LM TENCATE, WJF AF RAREY, KE CURTIS, LM TENCATE, WJF TI TISSUE SPECIFIC LEVELS OF GLUCOCORTICOID RECEPTOR WITHIN THE RAT INNER-EAR SO HEARING RESEARCH LA English DT Article DE ADRENAL STEROIDS; COCHLEA; VESTIBULAR ENDORGANS; ELISA; BUGR2 ID AMPULLAR DARK CELLS; ADRENOCORTICOSTEROID HORMONES; STRIA VASCULARIS; ABSENCE; CORTICOSTEROIDS; FIBROBLASTS; HYALURONAN; MODULATION; BINDING AB Individual, rat inner ear tissues were isolated and processed for determination of levels of glucocorticoid (GR) receptor by an Enzyme Linked Immuno-Sorbant Assay (ELISA). Differing levels of GR receptor between seven sampled inner ear regions were measured. Levels of GR receptors in the spiral ligament tissues were found to be significantly higher compared to all other tissue samples. GR levels in the tissues of stria vascularis and organ of Corti were different from one another but both were statistically higher than those detected in the vestibular tissue samples (dark cell regions, cristae ampullares and maculae utriculi), which had the lowest GR receptor levels measured. Intermediate levels of GR receptor were found in the endolymphatic sac region. It is suggested that the varying levels of inner ear GR receptors may be indicative of differing biological responses among the given tissues, as well as differences in the magnitudes of such responses to circulating glucocorticoids. C1 UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. RP RAREY, KE (reprint author), UNIV FLORIDA,COLL MED,DEPT ANAT & CELL BIOL,J HILLIS MILLER HLTH CTR,POB 100235,GAINESVILLE,FL 32610, USA. CR ANNIKO M, 1986, HEARING RES, V22, P279, DOI 10.1016/0378-5955(86)90104-8 BALLARD PL, 1974, ENDOCRINOLOGY, V94, P998 BAULIEU EE, 1989, ENDOCRINOLOGY, P16 BAXTER JD, 1979, GLUCOCORTICOID HORMO, P10 BLOOM E, 1980, J STEROID BIOCHEM, V12, P175, DOI 10.1016/0022-4731(80)90267-8 BUTLER DM, 1988, ARTHRITIS RHEUM, V31, P1281, DOI 10.1002/art.1780311010 FRIBERG U, 1989, ACTA OTO-LARYNGOL, V108, P62, DOI 10.3109/00016488909107393 GARG LC, 1985, AM J PHYSIOL, V248, pF487 GOLDMAN HB, 1962, NEW YORK STATE J MED, V62, P377 GUSTAFSSON JA, 1987, ENDOCR REV, V8, P185 HACKETT PH, 1988, AVIAT SPACE ENVIR MD, V59, P950 JANSSON B, 1991, ORL J OTO-RHINO-LARY, V53, P68 JOHNSON TS, 1984, NEW ENGL J MED, V310, P683, DOI 10.1056/NEJM198403153101103 JUNG TTK, 1992, ABSTR ASS RES O 0202, P71 LISTON S, 1987, DISEASES EAR HEARING, P1 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 MORRISON AW, 1975, MANAGEMENT SENSORINE PITOVSKI DZ, 1991, SOV NEUR, V17 PITOVSKI DZ, 1992, ABSTR ASS RES O 0202 PULEC JL, 1984, HEARING DISORDERS, P135 RAREY KE, 1991, LARYNGOSCOPE, V101, P1081 RAREY KE, 1992, IN PRESS AM J OTOL RAREY KE, 1989, 2ND INT S MEN DIS, P173 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 RYAN A F, 1991, Molecular and Cellular Neuroscience, V2, P179, DOI 10.1016/1044-7431(91)90011-C SCHIFF M, 1974, LARYNGOSCOPE, V84, P1959 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SHEA JJ, 1992, 9TH SHAMB SHEA OT C SMITH TJ, 1988, METABOLISM, V37, P179, DOI 10.1016/S0026-0495(98)90015-4 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z STEIN WH, 1948, J BIOL CHEM, V176, P337 TENCATE WJF, 1992, HEARING RES, V60, P199, DOI 10.1016/0378-5955(92)90021-E TENCATE WJF, 1991, ARCH OTOLARYNGOL, V117, P96 TENCATE WJF, 1990, ACTA OTO-LARYNGOL, V110, P234 TREVISI M, 1980, ACTA OTOLARYNGOL S, V373, P1 TURNER BB, 1986, ENDOCRINOLOGY, V118, P1211 WILSON WR, 1980, ARCH OTOLARYNGOL, V106, P772 NR 38 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 JAN PY 1993 VL 64 IS 2 BP 205 EP 210 DI 10.1016/0378-5955(93)90007-N PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700007 PM 8432691 ER PT J AU POPPER, AN SAIDEL, WM CHANG, JSY AF POPPER, AN SAIDEL, WM CHANG, JSY TI 2 TYPES OF SENSORY HAIR CELL IN THE SACCULE OF A TELEOST FISH SO HEARING RESEARCH LA English DT Article DE HAIR CELL; TYPE-I; TYPE-II; FISH; SACCULE; EAR ID GOLDFISH; EAR; AFFERENT; INNERVATION; UTRICLE; FIBERS AB Previous investigations have demonstrated significant ultrastructural differences in hair cells located in various regions of the utricle of the oscar, Astronotus ocellatus. In this study, we used TEM and SEM to examine cells from the central and marginal regions of the saccule to determine if similar hair cell ultrastructural differences exist in this endorgan. Based upon ultrastructural characteristics, central saccular cells closely resemble utricular striolar cells while marginal cells are intermediate in ultrastructure between striolar and extrastriolar cells of the utricle. C1 UNIV MARYLAND,DEPT POULTRY SCI,COLL PK,MD 20742. RP POPPER, AN (reprint author), UNIV MARYLAND,DEPT ZOOL,COLL PK,MD 20742, USA. CR CHANG JSY, 1992, J COMP NEUROL, V324, P621, DOI 10.1002/cne.903240413 CHANG J, 1991, Society for Neuroscience Abstracts, V17, P630 DALE T, 1976, Norwegian Journal of Zoology, V24, P85 DESMADRYL G, 1990, DEV BRAIN RES, V52, P183, DOI 10.1016/0165-3806(90)90234-P Dijkgraaf S., 1949, PHYSL COMP OECOL, V2, P81 FAY RR, 1978, J ACOUST SOC AM, V63, P136, DOI 10.1121/1.381705 von Frisch K, 1938, NATURE, V141, P8, DOI 10.1038/141008a0 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 HAMA K, 1969, Z ZELLFORSCH MIK ANA, V94, P155, DOI 10.1007/BF00339353 JORGENSEN JM, 1988, ACTA ZOOL-STOCKHOLM, V69, P169 JORGENSEN JM, 1989, J MORPHOL, V201, P187, DOI 10.1002/jmor.1052010208 Lewis ER, 1985, VERTEBRATE INNER EAR LOWENSTEIN O, 1964, PROC R SOC SER B-BIO, V160, P1, DOI 10.1098/rspb.1964.0026 NAKAJIMA Y, 1974, J COMP NEUROL, V156, P403, DOI 10.1002/cne.901560403 Platt C., 1981, HEARING SOUND COMMUN, P3 POPPER AN, 1977, J MORPHOL, V153, P397, DOI 10.1002/jmor.1051530306 POPPER AN, 1990, HEARING RES, V46, P211, DOI 10.1016/0378-5955(90)90003-8 POPPER AN, 1981, HEARING RES, V5, P245, DOI 10.1016/0378-5955(81)90049-6 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, 1982, TRENDS NEUROSCI, V5, P276, DOI 10.1016/0166-2236(82)90171-0 POPPER AN, 1981, J COMP PHYSIOL, V144, P27 PRESSON JC, 1992, BRAIN BEHAV EVOLUT, V39, P196 SAIDEL WM, 1990, HEARING RES, V47, P139, DOI 10.1016/0378-5955(90)90171-K SAIDEL WM, 1990, J COMP NEUROL, V302, P629, DOI 10.1002/cne.903020317 Schellart NAM, 1992, COMP EVOLUTIONARY BI, P295 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 STEINACKER A, 1992, BRAIN RES, V574, P229, DOI 10.1016/0006-8993(92)90821-P SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 WEGNER N, 1982, ACTA ZOOL-STOCKHOLM, V63, P133 WERSALL J, 1960, ACTA OTO-LARYNGOL, V163, P25 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 NR 32 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 JAN PY 1993 VL 64 IS 2 BP 211 EP 216 DI 10.1016/0378-5955(93)90008-O PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700008 PM 8432692 ER PT J AU FRANCIS, HW NADOL, JB AF FRANCIS, HW NADOL, JB TI PATTERNS OF INNERVATION OF OUTER HAIR-CELLS IN A CHIMPANZEE .2. EFFERENT ENDINGS SO HEARING RESEARCH LA English DT Article DE EFFERENT INNERVATION; OUTER HAIR CELL; ORGAN OF CORTI ID GUINEA-PIG ORGAN; ENKEPHALIN-LIKE IMMUNOREACTIVITY; CORTI; LOCALIZATION; COCHLEA; MICROSCOPY AB A morphometric analysis of the efferent innervation of the outer hair cells in the organ of Corti of one chimpanzee was performed. There was a wide variability in the size of efferent endings which ranged from approximately 0.1 to 4.5 mum3 in volume. Based on the size distribution of endings, a volume of 1.0 mum3 was chosen to divide efferent endings into two groups, 'large' and 'small'. The incidence of large efferent fibers decreased from base to apex and from the first to third row of each turn, whereas the incidence of small efferents increased from base to apex and from the first to third row in each turn. This data was interpreted to suggest that at least two types of efferent endings may exist at the base of outer hair cells of the organ of Corti in the chimpanzee. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,OTOPATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. CR ALTSCHULER RA, 1985, HEARING RES, V17, P249, DOI 10.1016/0378-5955(85)90069-3 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 CHURCHILL JOHN A., 1959, HENRY FORD HOSP MED BULL, V7, P202 CHURCHILL J. A., 1956, LARYNGOSCOPE, V66, P1 ENGSTROM H, 1954, ACTA OTO-LARYNGOL, V44, P490, DOI 10.3109/00016485409127660 ENGSTROM H, 1958, Acta Otolaryngol, V49, P109, DOI 10.3109/00016485809134734 EYBALIN M, 1990, J ELECTRON MICR TECH, V15, P209, DOI 10.1002/jemt.1060150303 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 HASHIMOTO S, 1987, ACTA OTOLARYNGOL, V105, P64 Ishii D, 1968, Acta Otolaryngol, V66, P282, DOI 10.3109/00016486809126295 IURATO S, 1962, EXP CELL RES, V27, P162, DOI 10.1016/0014-4827(62)90057-5 KIMURA R, 1962, Acta Otolaryngol, V55, P11, DOI 10.3109/00016486209127336 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 NADOL JB, 1988, ORL J OTO-RHINO-LARY, V50, P363 Rasmussen G.L., 1942, ANAT REC, V82, P44 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 SMITH CA, 1963, ANN OTO RHINOL LARYN, V72, P489 SMITH CA, 1961, J ULTRA MOL STRUCT R, V5, P523, DOI 10.1016/S0022-5320(61)80025-7 SPOENDLIN HH, 1963, ANN OTO RHINOL LARYN, V72, P660 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 NR 21 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 JAN PY 1993 VL 64 IS 2 BP 217 EP 221 DI 10.1016/0378-5955(93)90009-P PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KK687 UT WOS:A1993KK68700009 PM 8432693 ER PT J AU FELIX, D EHRENBERGER, K AF FELIX, D EHRENBERGER, K TI THE EFFERENT MODULATION OF MAMMALIAN INNER HAIR CELL AFFERENTS SO HEARING RESEARCH LA English DT Article DE INNER HAIR CELL; EFFERENTS; NEUROTRANSMITTERS; MICROIONTOPHORESIS; GABA; GLUTAMATE; ACETYLCHOLINE ID GUINEA-PIG COCHLEA; METHYL-D-ASPARTATE; CHOLINE-ACETYLTRANSFERASE; OLIVOCOCHLEAR NEURONS; AMINO-ACIDS; ORGAN; CORTI; NEUROTRANSMISSION; TRANSMITTER; GLUTAMATE AB The results of immunocytochemical, enzymatic and electrophysiological studies have indicated that acetylcholine and GABA may act as neurotransmitters in lateral olivocochlear efferent endings on inner hair cell afferent dendrites. Since spike activity can be recorded in the dendritic region of inner hair cells, microiontophoretic techniques were used for testing the possible neurotransmitter candidates, acetylcholine and GABA, on spontaneous and induced firing of the afferent dendrites. The experiments were carried out in anaesthetised guinea-pigs, the third and fourth turns of the cochlea being exposed for electrode penetration. Ejection of acetylcholine resulted in a pronounced dose-dependent increase in subsynaptic spiking activity. Furthermore, acetylcholine enhanced glutamate-induced activity. In contrast, even at high doses, GABA had very little effect on the spontaneous cochlear firing rate. When the firing rate had first been enhanced by glutamate or N-methyl-D-aspartate, however, this activation could be reduced by the ejection of GABA. A similar reduction was observed when the firing rate had been enhanced with acetylcholine. The results of our studies support the hypothesis that these substances are involved in efferent neurotransmission on inner hair cell afferent fibres. It should be pointed out, however, that besides acetylcholine and GABA, several opioids such as enkephalins and dynorphins seem to be involved in efferent cochlear innervation. C1 UNIV VIENNA,DEPT ENT 1,A-1010 VIENNA,AUSTRIA. RP FELIX, D (reprint author), UNIV BERN,DIV NEUROBIOL,ERLACHSTR 9A,CH-3012 BERN,SWITZERLAND. CR ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BOBBIN RP, 1979, EXP BRAIN RES, V34, P389 BOBBIN RP, 1970, NEUROPHARMACOLOGY, V9, P567, DOI 10.1016/0028-3908(70)90007-9 CHURCHILL J. A., 1956, LARYNGOSCOPE, V66, P1 COMIS SD, 1979, EXP BRAIN RES, V36, P119 DALLOS P, 1985, J NEUROSCI, V5, P1591 EHRENBERGER K, 1991, HEARING RES, V52, P73, DOI 10.1016/0378-5955(91)90188-F EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 EYBALIN M, 1989, ARCH OTO-RHINO-LARYN, V246, P228, DOI 10.1007/BF00463561 FELIX D, 1991, 28TH WORKSH INN EAR 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 FEX J, 1984, HEARING RES, V15, P123, DOI 10.1016/0378-5955(84)90043-1 FEX J, 1976, BRAIN RES, V109, P575, DOI 10.1016/0006-8993(76)90036-6 Fex J, 1973, BASIC MECHANISMS HEA, P377 FEX J, 1968, HEARING MECHANISMS V, P169 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 JASSER A, 1973, J NEUROCHEM, V20, P45, DOI 10.1111/j.1471-4159.1973.tb12103.x JENISON GL, 1986, COMP BIOCHEM PHYS C, V84, P385, DOI 10.1016/0742-8413(86)90110-6 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 KLINKE R, 1981, ACTA OTO-LARYNGOL, V91, P541, DOI 10.3109/00016488109138540 KLINKE R, 1977, EXP BRAIN RES, V30, P145 LEFEBVRE PP, 1991, BRAIN RES, V555, P75, DOI 10.1016/0006-8993(91)90862-P 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 MULLER M, 1991, HEARING RES, V57, P63, DOI 10.1016/0378-5955(91)90075-K PTOK M, 1992, OTORHINOLARYNGOL NOV, V2, P21 PTOK M, 1992, NOVA, V2, P12 PUEL JL, 1991, HEARING RES, V51, P255, DOI 10.1016/0378-5955(91)90042-8 ROBERTSON D, 1978, HEARING RES, V1, P31, DOI 10.1016/0378-5955(78)90006-0 SIEGEL JH, 1986, HEARING RES, V22, P245, DOI 10.1016/0378-5955(86)90101-2 TANAKA Y, 1966, J NEUROPHYSIOL, V29, P94 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WIET GJ, 1986, HEARING RES, V24, P137, DOI 10.1016/0378-5955(86)90058-4 YATES GK, 1992, TRENDS NEUROSCI, V15, P57, DOI 10.1016/0166-2236(92)90027-6 NR 37 TC 53 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 DEC PY 1992 VL 64 IS 1 BP 1 EP 5 DI 10.1016/0378-5955(92)90163-H PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900001 PM 1362722 ER PT J AU CABLE, J BARKWAY, C STEEL, KP AF CABLE, J BARKWAY, C STEEL, KP TI CHARACTERISTICS OF STRIA VASCULARIS MELANOCYTES OF VIABLE-DOMINANT SPOTTING (WV/WV) MOUSE MUTANTS SO HEARING RESEARCH LA English DT Article DE MELANOCYTES; STRIA VASCULARIS; INNER EAR; VIABLE DOMINANT-SPOTTING MUTANT; W-LOCUS; C-KIT ID C-KIT RECEPTOR; TYROSINE KINASE RECEPTOR; W-LOCUS; INNER-EAR; PROTO-ONCOGENE; SI-LOCUS; MICE; EXPRESSION; MUTATIONS; LIGAND AB The W(v) mutation lies in the kinase domain of the proto-oncogene c-kit which is expressed in a variety of cells including neural crest derived melanoblasts. The mutation results in the abnormal migration, proliferation, survival and/or differentiation of melanoblasts. Viable Dominant Spotting (W(v)/W(v)) mouse mutants have a white coat due to the absence of melanocytes. The majority of these animals have no melanocytes within the stria vascularis and no endocochlear potential (EP). A proportion of homozygous mutants partially escape the effects of the mutation: 47.2% of pinnae and 21% of vestibular regions were pigmented and 10.8% of ears had an EP. All ears with an EP that were available for histology had some pigmentation of the stria. There was no obvious correlation between external and internal spotting in W(v)/W(v) mice, and asymmetrical pigmentation of the ears was common. Both light and dark intermediate cells (which are derived from melanocytes) were present in the middle and/or basal turns of these cochlear ducts and they appeared to function normally in enabling the stria to produce an EP (although the EP was usually lower than normal). This suggests that the c-kit gene product is needed only during development of the stria, and not for mature melanocyte function because the melanocytes present in the mutant strias were carrying the mutant version of the c-kit gene. Melanocytes were similar in appearance in controls and mutants, except that fewer melanin granules were observed in the strias of W(v)/W(v) mice. The observations that strial melanocytes with very few melanin granules in W(v)/W(v) mutants are able to support EP production, together with previous observations that albino animals with strial melanocytes but no melanin have a normal EP, suggest that melanocytes but not melanin are essential for normal strial function. RP CABLE, J (reprint author), MRC,INST HEARING RES,UNIV PK,NOTTINGHAM NG7 2RD,ENGLAND. RI Cable, Joanne/A-4360-2010 CR BOSHER SK, 1973, ACTA OTO-LARYNGOL, V75, P184, DOI 10.3109/00016487309139694 BROWN PG, 1969, ACTA OTO-LARYNGOL, V68, P14, DOI 10.3109/00016486909121538 CABLE J, 1991, PIGM CELL RES, V4, P87, DOI 10.1111/j.1600-0749.1991.tb00320.x CARLISLE L, 1990, CELL TISSUE RES, V262, P329, DOI 10.1007/BF00309888 CHABOT B, 1988, NATURE, V335, P88, DOI 10.1038/335088a0 COPELAND NG, 1990, CELL, V63, P175, DOI 10.1016/0092-8674(90)90298-S DAMICOMARTEL A, 1983, AM J ANAT, V166, P445, DOI 10.1002/aja.1001660406 DEOL MS, 1970, PROC R SOC SER B-BIO, V175, P201, DOI 10.1098/rspb.1970.0019 DEOL MS, 1970, J EMBRYOL EXP MORPH, V23, P773 GEISSLER EN, 1988, CELL, V55, P185, DOI 10.1016/0092-8674(88)90020-7 HARRISON RV, 1984, ARCH OTO-RHINO-LARYN, V240, P271 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUANG E, 1990, CELL, V63, P225, DOI 10.1016/0092-8674(90)90303-V KESHET E, 1991, EMBO J, V10, P2425 Kikuchi K, 1966, Acta Otolaryngol, V62, P277, DOI 10.3109/00016486609119573 KOCK CA, 1991, SCIENCE, V252, P668 LEWIS PR, 1988, PRACTICAL METHODS EL MANOVA K, 1991, DEV BIOL, V146, P312, DOI 10.1016/0012-1606(91)90233-S MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MAYER TC, 1968, DEV BIOL, V18, P62, DOI 10.1016/0012-1606(68)90023-7 MAYER TC, 1970, DEV BIOL, V23, P297, DOI 10.1016/0012-1606(70)90100-4 NOCKA K, 1990, EMBO J, V9, P1805 NOCKA K, 1989, GENE DEV, V3, P816, DOI 10.1101/gad.3.6.816 ORRURTREGER A, 1990, DEVELOPMENT, V109, P911 RASKANDERSEN H, 1987, HEARING RES, V26, P177, DOI 10.1016/0378-5955(87)90110-9 REITH AD, 1990, GENE DEV, V4, P390, DOI 10.1101/gad.4.3.390 RUGH R, 1990, MOUSE ITS REPRODUCTI Russell E S, 1979, Adv Genet, V20, P357, DOI 10.1016/S0065-2660(08)60549-0 RUSSELL ES, 1968, ARCH BIOCHEM BIOPHYS, V125, P594, DOI 10.1016/0003-9861(68)90617-6 SCHROTT A, 1990, HEARING RES, V46, P1, DOI 10.1016/0378-5955(90)90134-B SCHROTT A, 1987, ACTA OTO-LARYNGOL, V103, P451 Silvers W.K., 1979, COAT COLORS MICE STEEL KP, 1980, NATURE, V288, P159, DOI 10.1038/288159a0 STEEL KP, 1987, HEARING RES, V27, P11, DOI 10.1016/0378-5955(87)90022-0 STEEL KP, 1989, DEVELOPMENT, V107, P453 STEEL KP, 1983, ARCH OTOLARYNGOL, V109, P922 STEEL KP, 1992, IN PRESS DEVELOPMENT SUGA F, 1964, ANN OTO RHINOL LARYN, V73, P924 ULLRICH A, 1990, CELL, V61, P203, DOI 10.1016/0092-8674(90)90801-K VANDUINEN SG, 1983, HISTOPATHOLOGY, V7, P35 Wada T., 1923, American Anatomical Memoir, Vno. 10, P1 Wästerström S A, 1984, Scand Audiol Suppl, V23, P1 ZSEBO KM, 1990, CELL, V63, P213, DOI 10.1016/0092-8674(90)90302-U NR 43 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 DEC PY 1992 VL 64 IS 1 BP 6 EP 20 DI 10.1016/0378-5955(92)90164-I PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900002 PM 1490901 ER PT J AU KILLICK, R MALENCZAK, C RICHARDSON, GP AF KILLICK, R MALENCZAK, C RICHARDSON, GP TI THE PROTEIN-COMPOSITION OF THE AVIAN TECTORIAL MEMBRANE SO HEARING RESEARCH LA English DT Article DE EAR, INTERNAL; COCHLEA; TECTORIAL MEMBRANE; EXTRACELLULAR MATRIX ID OTOLITHIC MEMBRANE; ORGANIZATION AB Gel electrophoretic analysis of the avian tectorial membrane under non-reducing conditions reveals the presence of 2 major proteins with apparent molecular masses of 195 and 41 kDa on 8.25% gels. Under reducing conditions, 6 polypeptides with apparent molecular masses of 146, 60, 56, 43, 35 and 31 kDa are consistently observed. None of these six polypeptides observed under reducing conditions are sensitive to digestion with collagenase, and all, except for the 43 kDa component, are degraded by treatment with cold acidic pepsin. The 60, 56 and 43 kDa polypeptides bind the peroxidase conjugated lectins from Canavalia ensiformis and Triticum vulgaris, indicating the presence of mannose, N-acetyl glucosamine and/or sialic acid. The 146, 60 and 56 kDa bands undergo a shift in electrophoretic mobility after treatment of native tectorial membranes with the enzyme neuroaminidase. Fibronectin and Type II collagen cannot be detected in the avian tectorial membrane by either immunoblotting or immunofluorescence techniques. Polyclonal antisera raised against the different polypeptides after partial purification by one dimensional gel electrophoresis confirm that these proteins are all components of the tectorial membrane, and show that they are restricted to the otolithic and tectorial membranes within the inner ear. Analysis of a wide variety of other tissue types indicates that the 60, 43 and 35 kDa components can only be detected within the inner ear, and that the antisera recognising the 146 and 31 kDa components only show cross-reactivity within the head, with the anti-146 kDa antibodies staining the mucus ducts supplying the olfactory epithelium and the anti-31 kDa antibodies staining granular elements in the cells of the respiratory epithelium. The results suggest that certain of the tectorial membrane components may be novel matrix molecules unique to the inner ear, and that some of the other proteins may be antigenically related to mucins. C1 UNIV SUSSEX,SCH BIOL SCI,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. CR ALLEN A, 1983, TRENDS BIOCHEM SCI, V8, P169, DOI 10.1016/0968-0004(83)90166-4 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X DOHLMAN GF, 1971, ACTA OTO-LARYNGOL, V71, P89, DOI 10.3109/00016487109125337 FERMIN CD, 1990, ACTA ANAT, V138, P75 GILLOYZAGA P, 1985, HEARING RES, V20, P1 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 JAHNKE V, 1969, ACTA OTO-LARYNGOL, V67, P583, DOI 10.3109/00016486909125485 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 KHAN KM, 1990, HEARING RES, V43, P149, DOI 10.1016/0378-5955(90)90224-D OFARRELL PH, 1975, J BIOL CHEM, V250, P4007 RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 SHEEHAN JK, 1991, AM REV RESPIR DIS, V144, pS4 SHIEL MJ, 1990, HEARING RES, V47, P147, DOI 10.1016/0378-5955(90)90172-L SLEPECKY NB, 1992, MATRIX, V11, P80 SLEPECKY NB, 1992, CELL TISSUE RES, V267, P413, DOI 10.1007/BF00319363 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 NR 18 TC 23 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 1992 VL 64 IS 1 BP 21 EP 38 DI 10.1016/0378-5955(92)90165-J PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900003 PM 1490898 ER PT J AU LAVIGNEREBILLARD, M BAGGERSJOBACK, D AF LAVIGNEREBILLARD, M BAGGERSJOBACK, D TI DEVELOPMENT OF THE HUMAN STRIA VASCULARIS SO HEARING RESEARCH LA English DT Article DE HUMAN COCHLEA; STRIA VASCULARIS; DEVELOPMENT; TRANSMISSION ELECTRON MICROSCOPY ID HUMAN FETUSES; CELLS AB Fifteen human fetal cochleas were investigated by light microscopy and transmission electron microscopy in order to observe the development of the stria vascularis. The earliest signs of strial cell differentiation take place during the 11th week of gestation. Subsequently, the first stages of the stria vascularis development occur quikly. At week 14 the three types of cells, namely, marginal, intermediate and basal cells are discernable. Moreover at this stage, signs of specific activity are already present. The adult-like appearance of the stria vascularis is reached by week 21 but its maturation is completed only during the last trimester of pregnancy. This is in good agreement both with the development of the organ of Corti structures and with the maturation of the human auditory function. C1 UNIV MONTPELLIER 2,F-34060 MONTPELLIER,FRANCE. KAROLINSKA HOSP,DEPT OTORHINOLARYNGOL,S-10401 STOCKHOLM 60,SWEDEN. RP LAVIGNEREBILLARD, M (reprint author), CHR ST CHARLES,INSERM,U254,NEUROBIOL AUDIT LAB,F-34059 MONTPELLIER 01,FRANCE. CR Anggard L., 1965, ACTA OTOLARYNGOLOGIC, V203, P1 ANNIKO M, 1984, ULTRASTRUCTURAL ATLA, P184 BAGGERSJOBACK D, 1987, ACTA OTO-LARYNGOL, V103, P64, DOI 10.3109/00016488709134699 VONBEKESY G, 1952, J ACOUST SOC AM, V24, P72 BIRNHOLZ JC, 1983, SCIENCE, V222, P516, DOI 10.1126/science.6623091 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 Corti A., 1851, Z WISS ZOOL, V3, P109 DUVALL AJ, 1980, ANN OTO RHINOL LARYN, V89, P335 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 FUJIMOTO S, 1981, ARCH HISTOL JAPON, V44, P223 GUILD S, 1927, AM J ANAT, V309, P57 HINOJOSA R, 1966, AM J ANAT, V118, P631, DOI 10.1002/aja.1001180218 JOHANSSON B, 1964, Acta Otolaryngol, V57, P188, DOI 10.3109/00016486409136960 Kikuchi K, 1966, Acta Otolaryngol, V62, P277, DOI 10.3109/00016486609119573 KIMURA RS, 1970, ACTA OTO-LARYNGOL, V69, P415, DOI 10.3109/00016487009123387 KIMURA RS, ACTA OTOLARYNGOL STO, V70, P301 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 LAVIGNEREBILLARD M, 1990, J ELECTRON MICR TECH, V15, P115, DOI 10.1002/jemt.1060150204 LAVIGNEREBILLARD M, 1988, ACTA OTO-LARYNGOL, V105, P398, DOI 10.3109/00016488809119492 LAVIGNEREBILLARD M, 1986, ANAT EMBRYOL, V174, P369, DOI 10.1007/BF00698787 NAKAI Y, 1970, PRACT-OTO-RHINO-LARY, V32, P257 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 Pujol R., 1986, BIOL CHANGE OTOLARYN, P47 PUJOL R, 1988, HDB HUMAN GROWTH D B, V1, P109 Pujol R, 1985, Acta Otolaryngol Suppl, V423, P43 RODRIGUEZECHAND.EL, 1965, Z ZELLFORSCH, V67, P600 RYBAK LP, 1991, ORL J OTO-RHINO-LARY, V53, P72 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SANTOS-SACCHI J, 1982, HEARING RES, V6, P7, DOI 10.1016/0378-5955(82)90003-X Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 SMITH CA, 1957, ANN OTO RHINOL LARYN, V66, P531 SPOENDLIN H, 1967, SUBMICROSCOPIC STRUC, P131 STARR A, 1977, PEDIATRICS, V60, P831 TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 THORN L, 1985, ACTA ANAT, V124, P159 WEIBEL E. R., 1957, ACTA ANAT, V29, P53 NR 36 TC 16 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 1992 VL 64 IS 1 BP 39 EP 51 DI 10.1016/0378-5955(92)90166-K PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900004 PM 1490899 ER PT J AU HILL, KG GEISLER, CD AF HILL, KG GEISLER, CD TI 2-TONE SUPPRESSION, EXCITATION AND THE AFTER EFFECT IN RATE RESPONSES IN AUDITORY-NERVE FIBERS IN THE CAT SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE FIBER; 2-TONE SUPPRESSION ID SHORT-TERM ADAPTATION; HAIR-CELLS; GUINEA-PIG; FIBERS; STIMULI; INTENSITY; PATTERNS; GOLDFISH; CONTOURS; NOISE AB Responses were recorded from single, auditory nerve fibres in the anaesthetized cat. Acoustic stimuli consisted of two tones, one of which was at characteristic frequency (CF), the other (the suppressor) was at considerably lower frequency. Tones were presented in simultaneous and sequential configurations. For simultaneous presentations, well-known response properties were observed. The rising limb of the two-tone rate-intensity function closely matched that of the appropriately adapted response to the suppressor tone presented alone. Also, whether strongly suppressed relative to CF-driven rate, or equal to CF-driven rate, rate responses to the two-tone stimuli persisted unchanged when the CF tone was terminated and the suppressor tone continued alone. These results support the hypothesis that the suppressor tone has dual influences, suppressive and excitatory, that are distinct and additive. Peristimulus response histograms confirm in the cat that depression and slow recovery of sensitivity to CF may follow termination of the suppressor tone, as reported for the guinea pig [Hill, K.G. and Palmer, A.R. (1991) Hear. Res. 55, 167-176]. This delay in recovery of normal sensitivity to CF appeared to be directly related to the amount of excitation of the fibre that is attributable to the suppressor tone. A similar, delayed re-establishment of sensitivity also occurred in the response to a tone at CF, presented immediately following excitation by a suppressor tone. However, no delay occurred in the onset of response to the suppressor when preceded by the CF tone. This observation indicates that the influence of the suppressor tone on subsequent sensitivity to CF can occur with or without the simultaneous presentation of the CF tone. C1 UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. RP HILL, KG (reprint author), AUSTRALIAN NATL UNIV,RES SCH BIOL SCI,DEV NEUROBIOL GRP,POB 475,CANBERRA,ACT 2601,AUSTRALIA. CR ARTHUR RM, 1976, BIOL CYBERN, V22, P21, DOI 10.1007/BF00340229 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 CHEATHAM MA, 1992, HEARING RES, V59, P39, DOI 10.1016/0378-5955(92)90100-2 DENG L, 1985, Journal of the Acoustical Society of America, V78, P1633, DOI 10.1121/1.392801 EVANS EF, 1974, HDB SENSORY PHYSL FAY RR, 1990, HEARING RES, V48, P93, DOI 10.1016/0378-5955(90)90201-Y FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 GEISLER CD, 1980, HEARING RES, V3, P317 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 HILL KG, 1989, HEARING RES, V39, P75, DOI 10.1016/0378-5955(89)90083-X HILL KG, 1989, HEARING RES, V39, P49, DOI 10.1016/0378-5955(89)90081-6 HILL KG, 1991, HEARING RES, V55, P167, DOI 10.1016/0378-5955(91)90101-E JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 KIANG NYS, 1965, MIT MONOGR, V35 RELKIN EM, 1991, HEARING RES, V55, P215, DOI 10.1016/0378-5955(91)90106-J Rhode WS, 1976, CURRENT COMPUTER TEC RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1969, J ACOUST SOC AM, V45, P1025, DOI 10.1121/1.1911493 SACHS MB, 1976, J ACOUST SOC AM, V60, P1157, DOI 10.1121/1.381218 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 SMITH RL, 1975, BIOL CYBERN, V17, P169, DOI 10.1007/BF00364166 YATES GK, 1985, HEARING RES, V17, P1, DOI 10.1016/0378-5955(85)90124-8 YATES GK, 1989, COCHLEAR MECHANISMS, P177 NR 29 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 1992 VL 64 IS 1 BP 52 EP 60 DI 10.1016/0378-5955(92)90167-L PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900005 PM 1490900 ER PT J AU LAROCHE, C HETU, R QUOC, HT JOSSERAND, B GLASBERG, B AF LAROCHE, C HETU, R QUOC, HT JOSSERAND, B GLASBERG, B TI FREQUENCY-SELECTIVITY IN WORKERS WITH NOISE-INDUCED HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE FREQUENCY SELECTIVITY; NOISE-INDUCED HEARING LOSS; AUDITORY FILTER BANDWIDTH ID AUDITORY FILTER SHAPES; EXCITATION PATTERNS; MASKING; BANDWIDTHS; LISTENERS; THRESHOLD; ASYMMETRY; FORMULAS; SPREAD; LEVEL AB This study was undertaken in order to document, in a group of subjects affected by a noise-induced hearing loss, the relation between the loss of auditory sensitivity and the loss of frequency selectivity at mid-frequencies, namely 1000 and 3000 Hz. Auditory filter shapes were estimated using the notched noise method. Twelve notch widths were tested, six symmetrical and six asymmetrical with respect to the signal frequency; the spectral level of the noise was set at 50 dB SPL. Data were collected with 22 noise-exposed workers having different degrees of hearing loss. The findings indicate that above a certain degree of hearing loss, which seems to be around 30 dB HL, frequency selectivity tends to decrease linearly with increase in loss of sensitivity. Even when the degree of hearing loss is similar in origin and in magnitude, there is a wide variation among subjects in auditory filter bandwidth. Based on the data collected in this study, it is not possible to adequately predict the auditory filter bandwidth of an individual from hearing threshold levels. C1 UNIV MONTREAL,ACOUST GRP,CP 6128,MONTREAL H3C 3J7,QUEBEC,CANADA. UNIV CAMBRIDGE,DEPT EXPTL PSYCHOL,CAMBRIDGE,ENGLAND. CR BERGMAN M, 1992, British Journal of Audiology, V26, P15, DOI 10.3109/03005369209077867 CHUNG DY, 1981, J SPEECH HEAR RES, V24, P506 COLEMAN GJ, 1980, TM8001 REP COLEMAN GJ, 1984, TM841 I OCC MED REP EVANS EF, 1975, AUDIOLOGY, V14, P419 FAULKNER A, 1990, British Journal of Audiology, V24, P381, DOI 10.3109/03005369009076579 FERGUSON GA, 1972, STATISTICAL ANAL PSY, P371 FESTEN JM, 1983, J ACOUST SOC AM, V73, P652, DOI 10.1121/1.388957 FLORENTINE M, 1980, J SPEECH HEAR RES, V23, P646 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 GLASBERG BR, 1984, J ACOUST SOC AM, V75, P536, DOI 10.1121/1.390487 HETU R, 1979, J OCCUP ENVIRON MED, V21, P251 HETU R, 1992, CAHIERS AUDIT, V5, P10 LAROCHE C, 1991, APPL ACOUST, V32, P193, DOI 10.1016/0003-682X(91)90003-W LUDVIGSEN C, 1985, J ACOUST SOC AM, V78, P1271, DOI 10.1121/1.392896 LUTMAN ME, 1991, J ACOUST SOC AM, V89, P320, DOI 10.1121/1.400513 MOORE BCJ, 1987, J ACOUST SOC AM, V81, P1633, DOI 10.1121/1.394518 MOORE BCJ, 1983, J ACOUST SOC AM, V74, P750, DOI 10.1121/1.389861 MOORE BCJ, 1990, J ACOUST SOC AM, V88, P132, DOI 10.1121/1.399960 MOORE BCJ, 1987, HEARING RES, V28, P209, DOI 10.1016/0378-5955(87)90050-5 PATTERSON RD, 1980, J ACOUST SOC AM, V67, P229, DOI 10.1121/1.383732 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, 1986, FREQUENCY SELECTIVIT, P123 PETERS RW, 1992, IN PRESS 9TH INT S H PETERS RW, 1992, J ACOUST SOC AM, V91, P256, DOI 10.1121/1.402769 PICARD M, 1985, AUDIOLOGY, V24, P81 Pick G., 1977, PSYCHOPHYSICS PHYSL, P273 PICK GF, 1980, PSYCHOPHYSICAL PHYSL, P476 QUOC HT, 1991, J SPEECH LANG PATHOL, V15, P21 TREES DE, 1986, AUDIOLOGY, V25, P70 Tyler R. S., 1986, FREQUENCY SELECTIVIT, P309 TYLER RS, 1984, J ACOUST SOC AM, V76, P1363, DOI 10.1121/1.391452 WEBSTER JC, 1950, J ACOUST SOC AM, V22, P483, DOI 10.1121/1.1906631 WEBSTER JC, 1950, J ACOUST SOC AM, V22, P473, DOI 10.1121/1.1906630 ZWICKER E, 1965, PSYCHOL REV, V72, P3, DOI 10.1037/h0021703 1986, AM NATIONAL STANDARD NR 38 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 DEC PY 1992 VL 64 IS 1 BP 61 EP 72 DI 10.1016/0378-5955(92)90168-M PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900006 PM 1490902 ER PT J AU KUJAWA, SG FALLON, M BOBBIN, RP AF KUJAWA, SG FALLON, M BOBBIN, RP TI INTRACOCHLEAR SALICYLATE REDUCES LOW-INTENSITY ACOUSTIC AND COCHLEAR MICROPHONIC DISTORTION PRODUCTS SO HEARING RESEARCH LA English DT Article DE SALICYLATE; DISTORTION PRODUCT EMISSIONS; ACTIVE PROCESS ID GUINEA-PIG COCHLEA; SPONTANEOUS OTOACOUSTIC EMISSIONS; ACTIVE PROCESS; HEARING-LOSS; ASPIRIN; ELECTROMOTILITY; OTOTOXICITY; POTENTIALS; GENTAMICIN; PERILYMPH AB Salicylate is well-known to produce reversible hearing loss and tinnitus. The site and mechanism of salicylate's ototoxic actions, however, remain unresolved. Recent experiments demonstrating primarily low-intensity effects on cochlear afferent outflow and effects on otoacoustic emissions (OAEs) suggest that salicylate acts to compromise active, energy-enhancing processes within the cochlea (i.e., the active process). We tested this hypothesis by examining the effect of salicylate on distortion product emissions. Distortion product responses to two-tone stimulation were monitored in the guinea pig before, during, and after intracochlear administration of increasing concentrations of salicylate (0.6-5 mM). These responses were recorded as acoustic signals in the ear canal spectrum (ADP), and as present in the cochlear microphonic (CM) recorded from a wire in basal turn scala vestibuli (CMDP). We also recorded the CM response to a single tone. Cochlear perfusion of salicylate resulted in a dose-responsive reduction in ADPs that was greater for low intensities of stimulation. CMDPs also demonstrated a concentration-dependent reduction at low intensities, but were increased slightly, though not significantly, by salicylate when elicited by high intensity primaries. CM was essentially unchanged by intracochlear salicylate. These results are consistent with an action of salicylate that involves the outer hair cells (OHCs) and are in harmony with the hypothesis that salicylate may selectively compromise the active process. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB,NEW ORLEANS,LA 70112. UNIV ARIZONA,DEPT SPEECH & HEARING SCI,TUCSON,AZ 85721. CR BARRON SE, 1987, HEARING RES, V31, P147, DOI 10.1016/0378-5955(87)90120-1 BOBBIN RP, 1992, NOISE INDUCED HEARIN, P38 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1991, HEARING RES, V56, P101, DOI 10.1016/0378-5955(91)90159-7 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, 1990, MECH BIOPHYSICS HEAR, P52 BROWNELL WE, 1990, BIOMECHANICS ACTIVE, P493 CAZALS Y, 1988, HEARING RES, V36, P89, DOI 10.1016/0378-5955(88)90139-6 Dallos P, 1988, ASHA, V30, P50 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 ESCOUBET B, 1985, PROSTAGLANDINS, V29, P589 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 JASTREBOFF PJ, 1986, ARCH OTOLARYNGOL, V112, P1050 JOHNSEN NJ, 1982, SCAND AUDIOL, V11, P3, DOI 10.3109/01050398209076194 JUNG TTK, 1988, HEAD NECK SURG, V99, P154 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 KUJAWA SG, 1992, HEARING RES, V61, P106, DOI 10.1016/0378-5955(92)90041-K LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 LONG GR, 1986, PERIPHERAL AUDITORY, P213 MARTIN GK, 1988, HEARING RES, V33, P49, DOI 10.1016/0378-5955(88)90020-2 MCCABE PA, 1965, ANN OTO RHINOL LARYN, V74, P312 MCFADDEN D, 1984, HEARING RES, V16, P251, DOI 10.1016/0378-5955(84)90114-X MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MCFADDEN D, 1983, HEARING RES, V9, P295, DOI 10.1016/0378-5955(83)90033-3 MITCHELL C, 1973, ARCH OTOLARYNGOL, V98, P297 MONGAN E, 1973, JAMA-J AM MED ASSOC, V226, P142, DOI 10.1001/jama.226.2.142 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W NUTTALL AL, 1986, NEUROBIOLOGY HEARING, P47 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 SANTOSSACCHI J, 1988, PHYSL EAR, P271 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SILVERST.H, 1967, ANN OTO RHINOL LARYN, V76, P118 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E THALMANN R, 1975, NERVOUS SYSTEM, V3, P31 WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 NR 41 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 DEC PY 1992 VL 64 IS 1 BP 73 EP 80 DI 10.1016/0378-5955(92)90169-N PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900007 PM 1490903 ER PT J AU GLASBERG, BR MOORE, BCJ AF GLASBERG, BR MOORE, BCJ TI EFFECTS OF ENVELOPE FLUCTUATIONS ON GAP DETECTION SO HEARING RESEARCH LA English DT Article DE GAP DETECTION; TEMPORAL RESOLUTION; TEMPORAL FLUCTUATIONS; LOUDNESS RECRUITMENT; HEARING IMPAIRMENT ID HEARING-IMPAIRED LISTENERS; MODULATION TRANSFER-FUNCTIONS; TEMPORAL WINDOW; NOISE; FREQUENCY; EARS; BANDWIDTH; LOUDNESS; LEVEL; SINUSOIDS AB The inherent fluctuations present in narrowbands of noise may limit the ability to detect gaps in the noise; 'dips' in the noise may be confused with the gap to be detected. For subjects with cochlear bearing loss, loudness recruitment may effectively magnify the fluctuations and this could partly account for the reduced ability to detect gaps in noise bands that is usually found in subjects with cochlear hearing loss. In the present experiments we tested these ideas by processing noise bands to alter the amount of envelope fluctuation. The envelopes of the noise bands were raised to a power, N. Powers greater than 1 result in expansion of the envelope (magnified fluctuations, simulating loudness recruitment), while powers less than 1 result in compression of the envelope (decreased fluctuations). Thresholds for detecting gaps in processed noise bands centered at 1 kHz were measured as a function of noise bandwidth and of N. To prevent the detection of spectral changes introduced by the gap or by the processing, stimuli were either presented in background noise, or at a low sensation level (20 dB). Three normally hearing subjects, two subjects with unilateral cochlear hearing loss and two subjects with bilateral cochlear hearing loss were tested. Gap thresholds generally increased with increasing N. This effect was large for small noise bandwidths (50 Hz or less) and smaller for larger noise bandwidths (200 Hz or more). For both the normal and impaired ears, gap thresholds at narrow bandwidths were improved relative to those for unprocessed noise bands (N = 1) by compressing the envelope fluctuations (N < 1). The results support the idea that fluctuations in narrowband noises affect gap detection, and that loudness recruitment may adversely affect the ability to detect gaps in noise bands. They also show that compression of the fluctuations in the noise can improve gap detection. C1 UNIV CAMBRIDGE,DEPT EXPTL PSYCHOL,DOWNING ST,CAMBRIDGE CB2 3EB,ENGLAND. RI Moore, Brian/I-5541-2012 CR ALVEY N, 1982, INTRO GENSTAT BACON SP, 1992, J SPEECH HEAR RES, V35, P642 BACON SP, 1985, AUDIOLOGY, V24, P117 Buus S, 1985, TIME RESOLUTION AUDI, P159 EVANS EF, 1975, AUDIOLOGY, V14, P419 FITZGIBBONS PJ, 1983, J ACOUST SOC AM, V74, P67, DOI 10.1121/1.389619 FITZGIBBONS PJ, 1982, J ACOUST SOC AM, V72, P761, DOI 10.1121/1.388256 FLORENTINE M, 1984, J SPEECH HEAR RES, V27, P449 FLORENTINE M, 1983, 11TH P INT C AC, V3, P103 Fowler EP, 1936, ARCHIV OTOLARYNGOL, V24, P731 Glasberg B R, 1989, Scand Audiol Suppl, V32, P1 GLASBERG BR, 1987, J ACOUST SOC AM, V81, P1546, DOI 10.1121/1.394507 GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T HELLMAN RP, 1978, J ACOUST SOC AM, V63, P1114, DOI 10.1121/1.381819 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 Moore B. C. J., 1989, INTRO PSYCHOL HEARIN MOORE BCJ, 1992, UNPUB JA COUST SOC A MOORE B C J, 1988, British Journal of Audiology, V22, P93, DOI 10.3109/03005368809077803 MOORE BCJ, 1992, IN PRESS BR J AUDIOL MOORE BCJ, 1992, IN PRESS EAR HEAR MOORE BCJ, 1989, J ACOUST SOC AM, V85, P1266, DOI 10.1121/1.397457 Moore B C, 1987, J Rehabil Res Dev, V24, P181 MOORE BCJ, 1988, J ACOUST SOC AM, V83, P1102, DOI 10.1121/1.396055 MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1505, DOI 10.1121/1.392045 MOORE BCJ, 1988, J ACOUST SOC AM, V83, P1093, DOI 10.1121/1.396054 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PHILLIPS DP, 1987, J ACOUST SOC AM, V82, P1, DOI 10.1121/1.395547 Pickles JO, 1988, INTRO PHYSL HEARING PLACK CJ, 1990, J ACOUST SOC AM, V87, P2178, DOI 10.1121/1.399185 PLACK CJ, 1991, J ACOUST SOC AM, V90, P3069, DOI 10.1121/1.401781 PLOMP R, 1964, J ACOUST SOC AM, V36, P277, DOI 10.1121/1.1918946 PLOMP R, 1988, J ACOUST SOC AM, V83, P2322, DOI 10.1121/1.396363 SCHWARTZ M, 1970, INFORMATION TRANSMIS SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 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 TYLER RS, 1982, J ACOUST SOC AM, V72, P740, DOI 10.1121/1.388254 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M ZENG FG, 1991, Q J EXP PSYCHOL-A, V43, P565 NR 40 TC 72 Z9 73 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 1992 VL 64 IS 1 BP 81 EP 92 DI 10.1016/0378-5955(92)90170-R PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900008 PM 1490904 ER PT J AU ELKINDHIRSCH, KE WALLACE, E STACH, BA JERGER, JF AF ELKINDHIRSCH, KE WALLACE, E STACH, BA JERGER, JF TI CYCLIC STEROID REPLACEMENT ALTERS AUDITORY BRAIN-STEM RESPONSES IN YOUNG-WOMEN WITH PREMATURE OVARIAN FAILURE SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; HORMONE REPLACEMENT; ESTROGEN EFFECT; PROGESTERONE EFFECT ID COCHLEAR NUCLEUS; SUPERIOR OLIVE; ACID; RECEPTORS; ESTROGEN; GABA; RAT AB To determine the independent contributions of estradiol and progesterone to the auditory brainstem response (ABR) latency changes associated with the menstrual cycle, we obtained ABRs on young women with premature ovarian failure who were undergoing cyclic hormone replacement therapy (HRT). We evaluated the influence of cyclic HRT on the ABRs of young women in three controlled phases of the same replacement cycles: 1) no steroid replacement, 2) estrogen-only replacement (E2-only), and 3) estrogen-plus-progesterone replacement (E2-PluS-P). A significant lengthening of wave V peak latency and I-V interpeak interval was found during E2-only replacement. Despite equivalent circulating estradiol levels, both wave V peak latencies and wave I-V interpeak intervals significantly decreased during the E2-Plus-P replacement phase as compared to the E2-only replacement phase. These findings are compatible with the hypothesis that estradiol potentiates secretion of the inhibitory neurotransmitter gamma-amino-butyric acid (GABA) at auditory nerve synapses, leading to delayed synaptic conduction time. Progesterone is known to blunt E2-potentiated GABA release and may antagonize its prolongation of wave V latency. C1 BAYLOR COLL MED,DEPT OTORHINOLARYNGOL & COMMUNICAT SCI,HOUSTON,TX 77030. RP ELKINDHIRSCH, KE (reprint author), METHODIST HOSP,DEPT CHEM,6565 FANNIN ST,B200,HOUSTON,TX 77030, USA. CR ADAMS JC, 1990, HEARING RES, V49, P281, DOI 10.1016/0378-5955(90)90109-3 ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 CASPARY DM, 1984, HEARING RES, V13, P113, DOI 10.1016/0378-5955(84)90102-3 Caspary D.M., 1986, NEUROBIOLOGY HEARING, P303 DEHAN CP, 1990, LARYNGOSCOPE, V100, P18 ELKINDHIRSCH KE, 1992, HEARING RES, V60, P143, DOI 10.1016/0378-5955(92)90016-G EYBALIN M, 1989, ARCH OTO-RHINO-LARYN, V246, P228, DOI 10.1007/BF00463561 FRANKFURT M, 1984, NEUROSCI LETT, V50, P245, DOI 10.1016/0304-3940(84)90493-2 MARTIN J V, 1991, Society for Neuroscience Abstracts, V17, P264 MARTIN MR, 1982, EXP NEUROL, V76, P675, DOI 10.1016/0014-4886(82)90135-2 McEwen B, 1984, FRONT NEUROENDOCRIN, V8, P153 MCGINNIS MY, 1980, J NEUROCHEM, V34, P785, DOI 10.1111/j.1471-4159.1980.tb09648.x MEIER E, 1984, J NEUROCHEM, V43, P1737, DOI 10.1111/j.1471-4159.1984.tb06102.x MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 OSTAPOFF EM, 1990, J CHEM NEUROANAT, V3, P285 PEREZ J, 1986, J NEUROCHEM, V47, P1798, DOI 10.1111/j.1471-4159.1986.tb13091.x ROOSENRUNGE G, 1984, EXP BRAIN RES, V54, P575 SCHUMACHER M, 1989, NEUROENDOCRINOLOGY, V50, P315, DOI 10.1159/000125239 SCHWARTZ IR, 1986, NEUROBIOLOGY HEARING, P173 YEN SCC, 1986, REPRODUCTIVE ENDOCRI NR 20 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 DEC PY 1992 VL 64 IS 1 BP 93 EP 98 DI 10.1016/0378-5955(92)90171-I PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900009 PM 1490905 ER PT J AU LEAKE, PA SNYDER, RL HRADEK, GT REBSCHER, SJ AF LEAKE, PA SNYDER, RL HRADEK, GT REBSCHER, SJ TI CHRONIC INTRACOCHLEAR ELECTRICAL-STIMULATION IN NEONATALLY DEAFENED CATS - EFFECTS OF INTENSITY AND STIMULATING ELECTRODE LOCATION SO HEARING RESEARCH LA English DT Article DE SPIRAL GANGLION; ELECTRICAL STIMULATION; HISTOPATHOLOGY; COCHLEAR IMPLANT; AUDITORY SYSTEM DEVELOPMENT; NEOMYCIN; OTOTOXICITY ID CONDUCTIVE HEARING-LOSS; STEM AUDITORY NUCLEI; BRAIN-STEM; INFERIOR COLLICULUS; COCHLEAR NUCLEUS; ACOUSTIC DEPRIVATION; NEURONS; PROJECTIONS; DEGENERATION; PLASTICITY AB An earlier study conducted in this laboratory suggested that chronic intracochlear electrical stimulation at moderate current levels can at least partially delay or prevent the retrograde degeneration of primary auditory (spiral ganglion) neurons that otherwise is progressive after neonatal deafness induced by ototoxic drug administration. Increased survival of spiral ganglion neurons was observed within the basal cochlear region near the stimulating bipolar electrode pairs, while in more apical regions there was no significant difference between the stimulated and control cochleas. The mechanisms underlying this maintenance of spiral ganglion neurons induced by chronic electrical stimulation are uncertain, especially since increased neuronal survival was observed over broader sectors of the ganglion than would be expected to be directly activated by the bipolar electrodes and moderate stimulation intensity (6 dB above electrically evoked auditory brainstem response threshold) used. In this report, data are presented from a second series of neonatally deafened and chronically stimulated cats. The parameters for chronic electrical stimulation were manipulated in two simple ways. First, the intensity of the electrical stimulus was reduced from the earlier study, while the duration of chronic stimulation periods was increased; and secondly, two different intracochlear positions of stimulating electrodes were employed in different experimental groups. Results indicate that electrical stimulation of the cochlea at an extremely low intensity (2 dB above electrically evoked auditory brainstem response threshold) is sufficient to at least partially prevent or delay ganglion cell degeneration in the deafened cochlea. In addition, data suggest a differential distribution of the maintained or conserved ganglion cells, such that when the stimulating electrode pair was positioned near the base of the cochlea increased ganglion survival was observed in a more basal cochlear sector, while stimulation at a more apical site resulted in increased neuronal survival extending to more apical regions. C1 UNIV CALIF SAN FRANCISCO,COLEMAN LAB,SAN FRANCISCO,CA 94143. RP LEAKE, PA (reprint author), UNIV CALIF SAN FRANCISCO,EPSTEIN LAB,DEPT OTOLARYNGOL,BOX 0732,SAN FRANCISCO,CA 94143, USA. CR BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 COLEMAN J R, 1979, Experimental Neurology, V64, P533 Eggermont J.J., 1986, ACTA OTOLARYNGOL S, V429, P1 EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 HAWKINS JE, 1977, ACTA OTO-LARYNGOL, V83, P123, DOI 10.3109/00016487709128821 JOHNSSON LG, 1974, ANN OTO RHINOL LARYN, V83, P294 JOHNSSON LG, 1981, AMINOGLYCOSIDE OTOTO, P389 KNUDSEN EI, 1984, J NEUROSCI, V4, P1012 KOHENEN A, 1965, ACTA OTOLARYNGOL S, V208 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 LEAKE PA, 1990, NEURAL PROSTHESES FU, P253 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 Leake-Jones P A, 1980, Scan Electron Microsc, P427 LEAKE-JONES P A, 1979, Scanning Electron Microscopy, P983 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 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 Nadol JJ, 1981, AMINOGLYCOSIDE OTOTO, P409 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 RUBEL EW, 1984, HEARING SCI, P109 RUBEN RJ, 1980, ANN OTO RHINOL LARYN, V89, P303 Ruben R J, 1986, Acta Otolaryngol Suppl, V429, P61 SCHMIDT JT, 1985, CELL MOL NEUROBIOL, V5, P5, DOI 10.1007/BF00711083 SCHMIDT JT, 1989, COMMENTS DEV NEUROBI, V1, P11 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 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 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 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 Weibel E. R., 1979, STEREOLOGICAL METHOD, V1 YLIKOSKI J, 1974, ACTA OTOLARYNGOL, V79, P266 NR 40 TC 71 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 DEC PY 1992 VL 64 IS 1 BP 99 EP 117 DI 10.1016/0378-5955(92)90172-J PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900010 PM 1490906 ER PT J AU YAMASHITA, H SEKITANI, T BAGGERSJOBACK, D AF YAMASHITA, H SEKITANI, T BAGGERSJOBACK, D TI EXPRESSION OF CARBONIC-ANHYDRASE ISOENZYME-LIKE IMMUNOREACTIVITY IN THE LIMBUS SPIRALIS OF THE HUMAN FETAL COCHLEA SO HEARING RESEARCH LA English DT Article DE LIMBUS SPIRALIS; COCHLEA; CARBONIC ANHYDRASE; EMBRYONIC DEVELOPMENT; HUMAN FETUS ID SKELETAL-MUSCLE FIBERS; INNER-EAR; GUINEA-PIG; DIFFERENTIATION; PURIFICATION; LOCALIZATION; MEMBRANE; RAT AB The distribution of carbonic anhydrase isoenzymes (CA I, II, III, V) was analyzed in the 14-, 15- and 16-week-old human fetal cochleae using immunohistochemical methods. The interdental cells in the limbus spiralis were strongly labelled with antibodies against CA I and III and the spiral ligament was also Positive for CA I and III. The stria vascularis and organ of Corti were however negative for CA I, II, III and V. These results suggest that the interdental cells in the human fetus may be related to fluid and ion transport of endolymph especially in the early stages of development. C1 KAROLINSKA INST,KAROLINSKA HOSP,DEPT OTOLARYNGOL,S-10401 STOCKHOLM 60,SWEDEN. RP YAMASHITA, H (reprint author), YAMAGUCHI UNIV,SCH MED,DEPT OTOLARYNGOL,UBE,YAMAGUCHI 755,JAPAN. CR ALTMANN F, 1950, ANN OTO RHINOL LARYN, V59, P657 BORGHESAN E, 1957, Laryngoscope, V67, P1266 DODGSON SJ, 1980, P NATL ACAD SCI-BIOL, V77, P5562, DOI 10.1073/pnas.77.9.5562 DRESCHER DG, 1977, P NATL ACAD SCI USA, V74, P892, DOI 10.1073/pnas.74.3.892 ERULKAR SD, 1961, NATURE, V189, P459, DOI 10.1038/189459a0 FERNLEY RT, 1979, FEBS LETT, V105, P299, DOI 10.1016/0014-5793(79)80634-1 Hsu C J, 1985, Acta Otolaryngol Suppl, V418, P1 IURATO S, 1962, Z ZELLFORSCH MIK ANA, V56, P40, DOI 10.1007/BF00326848 LAURILA AL, 1989, J HISTOCHEM CYTOCHEM, V37, P1375 LIM D J, 1970, Journal of Laryngology and Otology, V84, P1241, DOI 10.1017/S0022215100072984 LIM DJ, 1983, AM J OTOLARYNG, V4, P33, DOI 10.1016/S0196-0709(83)80005-2 SAXEN A, 1951, ACTA OTO-LARYNGOL, V40, P23, DOI 10.3109/00016485109138904 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TASHIAN RE, 1983, ISOZYMES-CURR T BIOL, V7, P79 THORN L, 1979, ANAT EMBRYOL, V155, P303, DOI 10.1007/BF00317643 VAANANEN HK, 1985, HISTOCHEMISTRY, V83, P231, DOI 10.1007/BF00953989 VAANANEN HK, 1982, J HISTOCHEM CYTOCHEM, V30, P1109 Voldrich L, 1967, Acta Otolaryngol, V63, P503 WATANABE K, 1984, ANN OTO RHINOL LARYN, V93, P262 WHITNEY PL, 1982, J BIOL CHEM, V257, P2056 YAMASHITA H, 1992, ACTA OTO-LARYNGOL, V112, P628, DOI 10.3109/00016489209137452 YAMASHITA H, 1992, J LARYNGOL OTOL, V106, P98, DOI 10.1017/S0022215100118808 YAMASHITA H, 1991, EUR ARCH OTO-RHINO-L, V248, P479, DOI 10.1007/BF00627638 NR 23 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 DEC PY 1992 VL 64 IS 1 BP 118 EP 122 DI 10.1016/0378-5955(92)90173-K PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900011 PM 1490894 ER PT J AU HICKS, ML BACON, SP AF HICKS, ML BACON, SP TI FACTORS INFLUENCING TEMPORAL EFFECTS WITH NOTCHED-NOISE MASKERS SO HEARING RESEARCH LA English DT Article DE MASKING; TEMPORAL EFFECTS; ADAPTATION ID ON-TONE MASKING; OVERSHOOT; LEVEL AB Temporal effects in simultaneous masking were studied by measuring the reduction in the amount of masking produced by a gated masker when that masker was preceded by a 400-ms noise (the precursor) that was usually spectrally identical to the masker. The signal frequency (f(s)) was 1.0 or 4.0 kHz. Experiment 1 revealed a temporal effect only when there was a spectral notch (centered at f(s)) in the masker and precursor. For a relative notchwidth of 0.4 f(s), the temporal effect was larger at 4.0 than at 1.0 kHz. In experiment 2, where the masker and precursor both consisted of two bands of noise separated by a spectral notch of 0.4 f(s), the size of the temporal effect remained essentially constant as the bandwidth of these noise bands increased from 0.2-0.8 kHz. The results from experiment 3 indicated that the temporal effect was largest when the level of the precursor was equal to the level of the masker. Finally, the results from experiment 4 suggested that the temporal effect may depend upon the frequency region below as well as above f(s), but that the frequency region above f(s) is probably more important. C1 ARIZONA STATE UNIV,DEPT SPEECH & HEARING,PSYCHOACOUST LAB,TEMPE,AZ 85287. CR BACON SP, 1986, HEARING RES, V23, P257, DOI 10.1016/0378-5955(86)90114-0 BACON SP, 1991, Q J EXP PSYCHOL-A, V43, P373 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 BACON SP, 1990, J ACOUST SOC AM S1, V88, pS50, DOI 10.1121/1.2029033 BACON SP, 1990, J ACOUST SOC AM, V88, P698, DOI 10.1121/1.399773 BACON SP, 1987, J ACOUST SOC AM, V81, P1073, DOI 10.1121/1.395125 BREGMAN AS, 1978, CAN J PSYCHOL, V32, P19, DOI 10.1037/h0081664 CARLYON RP, 1989, HEARING RES, V41, P223, DOI 10.1016/0378-5955(89)90014-2 CARLYON RP, 1987, J ACOUST SOC AM, V81, P418, DOI 10.1121/1.395117 ELLIOTT LL, 1967, J ACOUST SOC AM, V38, P738 ELLIOTT LL, 1965, J ACOUST SOC AM, V42, P143 FASTL H, 1976, ACUSTICA, V35, P287 GREEN DM, 1969, J ACOUST SOC AM, V46, P939, DOI 10.1121/1.1911813 LESHOWIT.B, 1972, J ACOUST SOC AM, V51, P1921, DOI 10.1121/1.1913051 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 MCFADDEN D, 1992, J ACOUST SOC AM, V92, P144, DOI 10.1121/1.404279 MCFADDEN D, 1990, J ACOUST SOC AM, V88, P711, DOI 10.1121/1.399774 NELSON DA, 1991, J SPEECH HEAR RES, V34, P374 PATTERSON RD, 1976, J ACOUST SOC AM, V59, P640, DOI 10.1121/1.380914 SCHMIDT S, 1991, J ACOUST SOC AM, V89, P1324, DOI 10.1121/1.400656 Viemeister NF, 1980, PSYCHOPHYSICAL PHYSL, P190 WRIGHT BA, 1991, THESIS U TEXAS AUSTI 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 1969, SPECIFICATIONS AUDIO 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 DEC PY 1992 VL 64 IS 1 BP 123 EP 132 DI 10.1016/0378-5955(92)90174-L PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900012 PM 1490895 ER PT J AU HARRIS, FP PROBST, R XU, L AF HARRIS, FP PROBST, R XU, L TI SUPPRESSION OF THE 2F1-F2 OTOACOUSTIC EMISSION IN HUMANS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSION; DISTORTION PRODUCT; SUPPRESSION; COCHLEAR MECHANICS; TUNING CURVES ID DISTORTION PRODUCTS F2-F1; OTO-ACOUSTIC EMISSIONS; COMBINATION TONES; AUDITORY-NERVE; RESPONSES; PRESSURE; ORIGIN AB Suppression of the 2f1-f2 distortion-product otoacoustic emission (DPOAE), stimulated with primaries, f1 and f2, in the frequency regions of 1, 2, and 4 kHz was measured in one ear of 14 human subjects with normal hearing. Suppression Tate functions were generated with a suppressor at either 1, 2, or 4 kHz increasing in level from 30 to 76 dB SPL for the corresponding f1 and f2 combinations. Stimulus levels for DPOAEs were L1 = 70 dB SPL and L2 adjusted to produce the highest amplitude DPOAE for each ear (range, 0 to 6 dB below L1). Results indicated that DPOAEs were reduced 3 dB in amplitude for a mean suppressor level of 61 dB SPL Maximum amplitude reduction occurred at a mean suppressor level of 69 dB SPL. These levels varied little for the three stimulus frequency regions. Mean slopes of the rate functions decreased as stimulus frequency region increased. Suppression tuning curves (STCs) were generated in the same three frequency regions and with L1 at either 70 or 55 dB SPL and L2 adjusted individually for each ear. The tips of the STCs were at frequencies associated with f1 and f2. The tip regions of the STCs for the 4-kHz stimulus condition were more complex in that they contained more multiple minima than did those for the 1- and 2-kHz regions. Results confirm that optimal suppression of the 2f1-f2 DPOAE occurs for frequencies in the vicinity of f1 and f2 rather than at 2f1-f2. RP HARRIS, FP (reprint author), KANTONSSPITAL,HNO KLIN,DEPT OTORHINOLARYNGOL,CH-4031 BASEL,SWITZERLAND. CR BARGONES JY, 1988, J ACOUST SOC AM, V83, P1809, DOI 10.1121/1.396515 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BUUNEN TJF, 1978, J ACOUST SOC AM, V64, P772, DOI 10.1121/1.382042 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 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 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HARRIS FP, 1990, MECH BIOPHYSICS HEAR, P178 HARRIS FP, 1991, EAR HEARING, V12, P399, DOI 10.1097/00003446-199112000-00004 KEMP DT, 1983, HEARING PHYSL BASES, P82 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 LONSBURYMARTIN B, 1989, ANN OTOL RHINOL LA S, V236, P14 MANLEY GA, 1990, MECH BIOPHYSICS HEAR, P210 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SIEGEL JH, 1982, J NEUROPHYSIOL, V47, P303 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P615, DOI 10.1121/1.1913152 SMOORENBURG GF, 1976, J ACOUST SOC AM, V59, P945, DOI 10.1121/1.380954 ZWICKER E, 1990, J ACOUST SOC AM, V87, P2583, DOI 10.1121/1.399051 Zwicker E., 1955, Acustica, V5 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 NR 23 TC 45 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 DEC PY 1992 VL 64 IS 1 BP 133 EP 141 DI 10.1016/0378-5955(92)90175-M PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900013 PM 1490896 ER PT J AU CANLON, B LI, H OLSON, L HULTCRANTZ, M BORG, E AF CANLON, B LI, H OLSON, L HULTCRANTZ, M BORG, E TI STAGE DEPENDENT DEVELOPMENT OF INTRAOCULAR COCHLEAR GRAFTS SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEA; DEVELOPMENT; INTRAOCULAR GRAFTING; TRANSPLANTATION AB The intraocular grafting technique was employed to test whether the peripheral hearing organ, the cochlea, is capable of survival and an organized development in total isolation from the temporal bone. Rat cochleae obtained from gestation day 16, postnatal day 1 and 7 were chosen for transplantation into the anterior chamber of the eye of adult Sprague-Dawley rats. The grafts were maintained in the anterior chamber for 6, 10, or 15 weeks survival time. The salient features of this study is that 1) cochlear structures survive and, 2) the cochlear structures develop beyond their pre-grafted stage as determined from light and electron micrographs. In the present study, the grafts obtained at gestation day 16 (GD 16) and postnatal day 1 gave a much higher rate of survival and development than the postnatal day 7 grafts. In addition, grafts maintained for either 6 or 10 weeks had a better survival rate than those grafts left for 15 weeks. It is estimated from light and electron micrographs that the gestation day 16 otocysts that were maintained for 10 weeks, developed to the equivalent of a postnatal day 10 cochlea. The grafts obtained from postnatal day one rats developed to the equivalent of approximately 14 days after birth. Interestingly, in the absence of synaptic contact, the inner and outer hair cells were capable of survival, differentiation and maturation. It remains to be determined if the spiral ganglion cells require additional neurotrophic factors for survival in the anterior chamber of the eye. C1 KAROLINSKA INST,DEPT HISTOL,S-10401 STOCKHOLM 60,SWEDEN. OREBRO MED CTR HOSP,OREBRO,SWEDEN. KAROLINSKA HOSP,DEPT OTOLARYNGOL,S-10401 STOCKHOLM 60,SWEDEN. RP CANLON, B (reprint author), KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. CR ANNIKO M, 1983, AM J OTOLARYNG, V4, P375, DOI 10.1016/S0196-0709(83)80043-X HUGHES SE, 1992, EXP NEUROL, V115, P37, DOI 10.1016/0014-4886(92)90218-F Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 Romand R., 1983, DEV AUDITORY VESTIBU, P47 Ruben R. J., 1967, ACTA OTO-LARYNGOL, V220, P1 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 Stromberg I, 1983, ADV CELL NEUROBIOL, V4, P407 VANDEWATER T, 1985, HEARING SCI, P49 NR 8 TC 1 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 1992 VL 64 IS 1 BP 142 EP 148 DI 10.1016/0378-5955(92)90176-N PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA KG739 UT WOS:A1992KG73900014 PM 1490897 ER PT J AU HENRY, KR LEWIS, ER AF HENRY, KR LEWIS, ER TI ONE-TONE SUPPRESSION IN THE COCHLEAR NERVE OF THE GERBIL SO HEARING RESEARCH LA English DT Article DE ONE-TONE SUPPRESSION; GERBIL; 2-TONE SUPPRESSION ID AUDITORY-NERVE; TUNING CURVES; 2-TONE SUPPRESSION; FIBERS; RESPONSES; PIGEON; INHIBITION; EXCITATION; PATTERNS AB One-tone rate suppression has been reported several times for auditory nerve fibers of mammalian and non-mammalian vertebrates. Because its properties are very similar to those of two-tone rate suppression, the possibility exists that one-tone rate suppression is the result of an interaction within the inner ear of the suppressing tonal stimulus and some ongoing extraneous acoustic stimulus. For this reason, reports of one-tone rate suppression often elicit suspicions that the investigators were not sufficiently careful in controlling leaks in their acoustic barriers or in the electrical pathways to their acoustic drivers. Recent reports of one-tone rate suppression in pigeon basilar-papillar fibers and goldfish saccular fibers were accompanied by descriptions of measures taken to avoid such leaks. In this paper, we describe one-tone rate suppression in a mammal, the Mongolian gerbil; and we demonstrate that the background spike activity being suppressed is not driven by either external sounds coming from outside the acoustic isolation test chamber or by non-stimulus electrical inputs to the acoustic driver. The suppressed background spike activity evidently arises from sources within the animal. These sources may be non-acoustic, associated with spontaneous pre- or post-synaptic ion-channel activity; or they may be acoustic sources - internal sound or vibration generators. C1 UNIV CALIF BERKELEY,DEPT ELECT ENGN & COMP SCI,BERKELEY,CA 94720. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 CHAMBERLAIN SC, 1977, J COMP NEUROL, V171, P193, DOI 10.1002/cne.901710205 DOLAN DF, 1990, J ACOUST SOC AM, V87, P2621, DOI 10.1121/1.399054 FAY RR, 1990, HEARING RES, V48, P93, DOI 10.1016/0378-5955(90)90201-Y FAY RR, 1986, AUDITORY FREQUENCY S, P137 FRISHKOPF LS, 1963, J ACOUST SOC AM, V35, P1219, DOI 10.1121/1.1918676 FRISHKOPF LS, 1964, J ACOUST SOC AM, V36, P1016, DOI 10.1121/1.2143197 GOLDSTEIN MH, 1962, J ACOUST SOC AM, V34, P734, DOI 10.1121/1.1937265 GROSS NB, 1976, BRAIN RES, V101, P209, DOI 10.1016/0006-8993(76)90264-X HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HENRY KR, 1989, COCHLEAR MECHANISMS, P251 HILL KG, 1989, HEARING RES, V39, P37, DOI 10.1016/0378-5955(89)90080-4 HILL KG, 1989, HEARING RES, V39, P75, DOI 10.1016/0378-5955(89)90083-X HILL KG, 1989, HEARING RES, V39, P49, DOI 10.1016/0378-5955(89)90081-6 HOUTGAST T, 1973, ACUSTICA, V29, P168 KATSUKI Y., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1396, DOI 10.1121/1.1918357 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 LEWIS ER, 1990, ABSTR ASS RES OT, P199 LEWIS ER, 1989, HEARING RES, V39, P209, DOI 10.1016/0378-5955(89)90092-0 LEWIS ER, 1988, BASIC ISSUES HEARING, P177 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1978, ACTA OTO-LARYNGOL, V85, P167, DOI 10.3109/00016487809111923 NOMOTO M, 1964, J NEUROPHYSIOL, V27, P768 PALMER AR, 1987, BRIT MED BULL, V43, P838 PATUZZI RB, 1988, COCHLEAR MECHANISMS, P257 RHODE WS, 1976, PSYCHOPHYSICS PHYSL, P27 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RUPERT A, 1963, J NEUROPHYSIOL, V26, P449 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1969, J ACOUST SOC AM, V45, P1025, DOI 10.1121/1.1911493 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SHANNON RV, 1976, J ACOUST SOC AM, V59, P1460, DOI 10.1121/1.381007 TASAKI I, 1954, J NEUROPHYSIOL, V17, P97 TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 NR 38 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 1992 VL 63 IS 1-2 BP 1 EP 6 DI 10.1016/0378-5955(92)90066-V PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100001 PM 1464563 ER PT J AU LEWIS, ER HENRY, KR AF LEWIS, ER HENRY, KR TI MODULATION OF COCHLEAR NERVE SPIKE RATE BY CARDIAC ACTIVITY IN THE GERBIL SO HEARING RESEARCH LA English DT Article DE COCHLEAR NERVE; ONE-TONE SUPPRESSION; CARDIAC; GERBIL ID AUDITORY-NERVE; SUPPRESSION; FIBERS; BRAIN AB Among primary auditory axons with characteristic frequencies (CFs) below 2500 Hz, a substantial subpopulation was found in which spike activity was driven by cardiac events. The presence of cardiac-driven activity was inferred from cycle histograms triggered on the peak of the electrocardiogram (ECG). This driven activity was either like a simple onset response (often followed by a reduction of spike activity to below background level), or as a longer lasting series of peaks and troughs. In two axons with high CFs (7 kHz and 12.5 kHz), cardiac-driven suppression was observed. Recordings made by a probe microphone revealed the presence of heart-related sound in the external ear canal. The onset of that sound coincided with the onset of cardiac-driven spike activity (and suppression). C1 UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616. UNIV CALIF BERKELEY,DEPT ELECT ENGN & COMP SCI,BERKELEY,CA 94720. CR BIRREN JE, 1963, SCIENCE, V140, P195, DOI 10.1126/science.140.3563.195-a CALLAWAY E, 1965, ELECTROEN CLIN NEURO, V19, P476, DOI 10.1016/0013-4694(65)90186-0 DELFINI LF, 1972, PSYCHOPHYSIOLOGY, V9, P484, DOI 10.1111/j.1469-8986.1972.tb01801.x DOLAN DF, 1990, J ACOUST SOC AM, V87, P2621, DOI 10.1121/1.399054 FAY RR, 1990, HEARING RES, V48, P93, DOI 10.1016/0378-5955(90)90201-Y HENRY KR, 1992, HEARING RES, V63, P1, DOI 10.1016/0378-5955(92)90066-V HILL KG, 1989, HEARING RES, V39, P49, DOI 10.1016/0378-5955(89)90081-6 LACEY BC, 1978, AM PSYCHOL, V33, P99, DOI 10.1037//0003-066X.33.2.99 MANLEY GA, 1978, ACTA OTO-LARYNGOL, V85, P167, DOI 10.3109/00016487809111923 MCGINN MD, 1987, HEARING RES, V31, P235, DOI 10.1016/0378-5955(87)90193-6 MCGINN MD, 1985, ABSTR ASS RES OT, V8, P120 PATUZZI RB, 1989, COCHLEAR MECHANISMS, P257 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RUBEL EW, 1984, HEARING SCI RUPERT A, 1963, J NEUROPHYSIOL, V26, P449 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 WALKER BB, 1979, PSYCHOPHYSIOLOGY, V19, P520 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WYNN VT, 1980, BRIT J PSYCHOL, V71, P155 NR 20 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 NOV PY 1992 VL 63 IS 1-2 BP 7 EP 11 DI 10.1016/0378-5955(92)90067-W PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100002 PM 1464576 ER PT J AU HENRY, KR AF HENRY, KR TI DERIVED AND ENHANCED COMPOUND ACTION-POTENTIALS AT NEAR-THRESHOLD LEVELS - FORWARD MASKING INCREASES SENSITIVITY OF AUDIOGRAMS AND TUNING CURVES SO HEARING RESEARCH LA English DT Article DE COCHLEA; ENHANCEMENT; DERIVED CAP; TUNING CURVES; AUDIOGRAM; FACILITATION ID HEARING; RESPONSES AB The amplitude of a cochlear nerve compound action potential (CAP) can be increased by forward maskers having levels close to the visual detection threshold of the CAP. This effect, termed enhancement, varies as a function of the frequency of the masker and probe stimulus, and is nonmonotonic with respect to the level of the masker. Other studies using the derived CAP have used a subtraction technique to evaluate the ability of simultaneous maskers having levels near the CAP visual detection threshold to influence the CAP produced by an above threshold tone. The present paper compares audiograms produced by the conventional nonmasked CAP visual detection threshold technique with audiograms produced by both forward masked derived CAPs and forward masked enhanced CAPs. In response to low and middle frequency stimuli, both masked CAP measures produce more sensitive audiograms than does the conventional nonmasking method. Forward masked amplitude tuning curves (TCs) were also produced, comparing the conventional 50% amplitude reduction and 20 muV amplitude reduction methods with TCs obtained with derived and enhanced CAPs. When the same criteria are used, both masked CAP measures result in sharply tuned amplitude TCs that are approximately 60 dB more sensitive than the conventional CAP technique. At near-threshold levels, the properties of forward masked enhanced and derived CAPs appear to be similar. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR BERLIN CI, 1987, ABSTR ASS RES OT, V10, P172 BERLIN CI, 1991, HEARING RES, V52, P271, DOI 10.1016/0378-5955(91)90017-4 BERLIN CI, 1981, CIBA F S, V85, P130 CACACE AT, 1986, HEARING RES, V23, P223, DOI 10.1016/0378-5955(86)90111-5 EGGERMONT JJ, 1985, AUDITORY SYSTEM CLIN ELMASIAN R, 1975, J ACOUST SOC AM, V58, P229, DOI 10.1121/1.380650 HENRY KR, 1985, AUDIOLOGY, V24, P92 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1991, HEARING RES, V56, P197, DOI 10.1016/0378-5955(91)90170-E HENRY KR, 1991, AUDIOLOGY, V30, P33 HENRY KR, 1992, J ACOUST SOC AM, V91, P2824, DOI 10.1121/1.402963 HENRY KR, 1991, HEARING RES, V56, P239, DOI 10.1016/0378-5955(91)90174-8 HOOD LJ, 1987, ABSTR ASS RES OT, V10, P172 HOOD LJ, 1991, HEARING RES, V55, P109, DOI 10.1016/0378-5955(91)90097-S HUDSPETH AJ, 1985, SCIENCE, V230, P745, DOI 10.1126/science.2414845 LEWIS ER, 1989, HEARING RES, V39, P209, DOI 10.1016/0378-5955(89)90092-0 LEWIS ER, 1992, MODULATION COCHLEAR, V63, P7 LEWIS ER, 1987, HEARING RES, V25, P83, DOI 10.1016/0378-5955(87)90082-7 PEAKE WT, 1962, J ACOUST SOC AM, V34, P571, DOI 10.1121/1.1918170 PEDERSEN CB, 1972, ACTA OTO-LARYNGOL, V74, P398, DOI 10.3109/00016487209128469 RONKEN DA, 1991, ABSTR ASS RES OT, P131 SALT AN, 1990, AUDIOLOGY, V29, P135 SALT AN, 1990, J ACOUST SOC AM, V88, P1392, DOI 10.1121/1.399717 SIEGEL JH, 1987, HEARING RES, V29, P169, DOI 10.1016/0378-5955(87)90165-1 ZWISLOCKI J, 1959, J ACOUST SOC AM, V31, P9, DOI 10.1121/1.1907619 ZWISLOCKI J, 1960, J ACOUST SOC AM, V32, P1046, DOI 10.1121/1.1908276 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 NOV PY 1992 VL 63 IS 1-2 BP 12 EP 18 DI 10.1016/0378-5955(92)90068-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100003 PM 1464566 ER PT J AU SCHEIBE, F HAUPT, H LUDWIG, C AF SCHEIBE, F HAUPT, H LUDWIG, C TI INTENSITY-DEPENDENT CHANGES IN OXYGENATION OF COCHLEAR PERILYMPH DURING ACOUSTIC EXPOSURE SO HEARING RESEARCH LA English DT Article DE OXYGEN PARTIAL PRESSURE; PERILYMPH; ACOUSTIC EXPOSURE; COCHLEAR FUNCTION; CARDIORESPIRATORY VARIABLES; GUINEA PIG ID LOUD SOUND EXPOSURE; LASER DOPPLER MEASUREMENTS; BLOOD-FLOW; DEOXYGLUCOSE UPTAKE; STIMULATION ALTERS; NEEDLE ELECTRODES; GUINEA-PIG; NOISE; TENSION AB This study examined the effects of acoustic exposure at different intensities on local oxygenation of the cochlea. The oxygen partial pressure (pO2) of perilymph in the basal scala tympani was measured polarographically in anesthetized guinea pigs exposed to either wide-band noise at 85 dB SPL or a 10 kHz pure tone at 90, 105, or 125 dB SPL for 1 h. Cochlear temperature, heart rate, arterial blood pressure and acid-base status were monitored. The cochlear microphonics (CM) and compound action potentials (CAP) were recorded before and after exposure. There were clear intensity-dependent differences in the effect of acoustic exposure on perilymphatic oxygenation. Moderate exposure intensities (85-90 dB SPL) were found to increase the pO2 by an average of about 20% of the initial level. In contrast, high intensity acoustic exposure (125 dB SPL) resulted in a mean decrease of about 20%. These changes persisted within a subsequent 30-min post-exposure period. There was no significant change in cochlear temperature and cardiorespiratory variables during and after any of the exposures as compared to the controls. CM and CAP amplitudes showed an extensive loss after acoustic overstimulation (125 dB SPL), but no permanent change with lower exposure intensities. These findings suggest that intracochlear oxygenation plays an important role in inner ear physiology during acoustic stimulation. RP SCHEIBE, F (reprint author), HUMBOLDT UNIV,HNO KLIN CHARITE,SCHUMANNSTR 20-21,O-1040 BERLIN,GERMANY. CR BOHNE BD, 1973, MEDIZINTECHNIK, V13, P13 CANLON B, 1983, HEARING RES, V10, P217, DOI 10.1016/0378-5955(83)90055-2 CANLON B, 1984, COMP BIOCHEM PHYS A, V78, P43, DOI 10.1016/0300-9629(84)90089-6 GOODWIN PC, 1984, HEARING RES, V15, P215, DOI 10.1016/0378-5955(84)90030-3 HAUPT H, 1988, 8 INT COCHL S 1987, P93 HAUPT H, 1991, EUR ARCH OTO-RHINO-L, V248, P413, DOI 10.1007/BF01463566 HULTCRANTZ E, 1979, ACTA PHYSIOL SCAND, V106, P29, DOI 10.1111/j.1748-1716.1979.tb06366.x HULTCRANTZ E, 1979, ARCH OTO-RHINO-LARYN, V224, P103, DOI 10.1007/BF00455231 KOLDE Y, 1960, ANN OTO RHINOL LARYN, V69, P661 LAMM K, 1988, HNO, V36, P367 MAASS B, 1976, ARCH OTO-RHINO-LARYN, V214, P109, DOI 10.1007/BF00453607 MAASS B, 1978, ARCH OHREN NASEN KEH, V221, P269, DOI 10.1007/BF00491463 MISRAHY GA, 1958, J ACOUST SOC AM, V30, P247, DOI 10.1121/1.1909555 MISRAHY GA, 1958, J ACOUST SOC AM, V30, P701, DOI 10.1121/1.1909734 NUTTALL AL, 1981, HEARING RES, V5, P285, DOI 10.1016/0378-5955(81)90052-6 NUTTALL AL, 1979, J ACOUST SOC AM S1, V65, P12 OKAMOTO A, 1990, ACTA OTO-LARYNGOL, V109, P378, DOI 10.3109/00016489009125158 PERLMAN H B, 1962, Acta Otolaryngol, V54, P99, DOI 10.3109/00016486209126927 PRAZMA J, 1983, ARCH OTOLARYNGOL, V109, P611 PRAZMA J, 1987, ARCH OTOLARYNGOL, V113, P36 QUIRK WS, 1991, HEARING RES, V52, P217, DOI 10.1016/0378-5955(91)90201-J RYAN AF, 1982, BRAIN RES, V234, P213, DOI 10.1016/0006-8993(82)90863-0 RYAN AF, 1988, ACTA OTO-LARYNGOL, V105, P232, DOI 10.3109/00016488809097003 SCHEIBE F, 1990, 27TH P WORKSH INN EA, P20 SCHEIBE F, 1986, 23RD WORKSH INN EAR, P46 SCHEIBE F, 1990, EUR ARCH OTO-RHINO-L, V247, P84 SCHEIBE F, 1989, Z VERSUCHSTIERKD, V32, P25 SCHEIBE F, 1988, 8 INT COCHL S 1987 M, P87 STURZEBECHER E, 1983, EXPT METHODEN WISSEN, P1 THORNE PR, 1989, ACTA OTO-LARYNGOL, V107, P71, DOI 10.3109/00016488909127481 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 WAGNER H, 1974, ARCH OTO-RHINO-LARYN, V206, P283, DOI 10.1007/BF00465541 NR 32 TC 25 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 1992 VL 63 IS 1-2 BP 19 EP 25 DI 10.1016/0378-5955(92)90069-Y PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100004 PM 1464569 ER PT J AU HARDING, GW BAGGOT, PJ BOHNE, BA AF HARDING, GW BAGGOT, PJ BOHNE, BA TI HEIGHT CHANGES IN THE ORGAN OF CORTI AFTER NOISE EXPOSURE SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI HEIGHT CHANGES; NOISE EXPOSURE; PATHOLOGY ID PHASE-CONTRAST MICROSCOPY; THRESHOLD SHIFTS; TEMPORARY; DAMAGE; OVERSTIMULATION AB To determine whether or not exposure to noise causes an alteration in the height of the organ of Corti (OC), 16 cochleas which had been exposed for one or two hours to an octave band of noise with a center frequency of 4 kHz and a sound pressure level of 108 dB were examined microscopically as whole mounts. These specimens were divided into four groups: early ears (N = 3) recovered less than 0.6 hours following the exposure; intermediate ears (N = 5) recovered 0.6-4.0 hours; 1 -day ears (N = 3) recovered 24 hours; and late ears (N = 5) recovered 2-21 days. Height was measured at three positions across the OC and at multiple percentage locations from apex to base. The OC-height data from the noise-exposed cochleas were compared statistically to those from ten control cochleas. A significant reduction (P less-than-or-equal-to 0.01) in OC height at the third outer hair cell (OHC) was first evident in the early ears in the region 65-95% distance from the apex. The height was reduced even further in the intermediate ears and included a region from 15-25% distance from the apex as well as the 65-95% region. In the late ears, heights had returned to control values, except within focal OC lesions. Height at the first row of OHCs was less affected than at the third row, and height at the inner hair cell (IHC) was least affected. These height changes were accompanied by distortion of the shape and position of OHCs, the shape of Deiters' cells and buckling of inner and outer pillar bodies. Sometimes IHCs had distorted shapes and were displaced from their usual positions. Although no functional measures were obtained from these ears, data from the literature indicate that the exposure described above would have produced a sizable threshold shift. Transient reduction in OC height likely accounts for some portion of noise-induced threshold shifts. C1 WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID AVE,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT NEUROL SURG,ST LOUIS,MO 63110. 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, 1987, HEARING RES, V29, P251, DOI 10.1016/0378-5955(87)90172-9 BOHNE BA, 1972, LARYNGOSCOPE, V82, P1 BOHNE BA, 1976, HEARING DAVIS ESSAYS, P85 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 CARDER HM, 1972, J SPEECH HEAR RES, V15, P603 DAVIS H, 1950, Acta Otolaryngol Suppl, V88, P1 ENGSTROM H, 1960, Acta Otolaryngol Suppl, V158, P219 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P81, DOI 10.3109/00016488809107374 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P373, DOI 10.3109/00016488809122260 HIRSH IJ, 1952, J ACOUST SOC AM, V24, P131, DOI 10.1121/1.1906867 HUNTERDUVAR IM, 1977, SCANNING ELECT MICRO, V2, P421 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 LUZ GA, 1971, J ACOUST SOC AM, V49, P1770, DOI 10.1121/1.1912580 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLS JH, 1973, J SPEECH HEAR RES, V16, P426 PICKLES JO, 1982, INTRO PHYSL HEARING, P125 RICHARDSON KC, 1960, STAIN TECHNOL, V35, P313 SAUNDERS JC, 1986, HEARING RES, V23, P245, DOI 10.1016/0378-5955(86)90113-9 STACK CR, 1971, ACTA OTO-LARYNGOL, V71, P483, DOI 10.3109/00016487109125392 WARD WD, 1970, J ACOUST SOC AM, V48, P561, DOI 10.1121/1.1912172 WARD WD, 1960, J ACOUST SOC AM, V32, P497, DOI 10.1121/1.1908111 WARD WD, 1958, J ACOUST SOC AM, V30, P944, DOI 10.1121/1.1909414 WARD WD, 1971, ANN OTO RHINOL LARYN, V80, P881 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 NOV PY 1992 VL 63 IS 1-2 BP 26 EP 36 DI 10.1016/0378-5955(92)90070-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100005 PM 1464572 ER PT J AU THALMANN, I COMEGYS, TH LIU, SZ ITO, Z THALMANN, R AF THALMANN, I COMEGYS, TH LIU, SZ ITO, Z THALMANN, R TI PROTEIN PROFILES OF PERILYMPH AND ENDOLYMPH OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE PERILYMPH; ENDOLYMPH; PROTEIN PROFILE; COCHLEAR FLUIDS ID INNER-EAR FLUIDS; HORSERADISH-PEROXIDASE; CEREBROSPINAL-FLUID; FLOW-RATE; COCHLEA; POTASSIUM; BLOOD; PERMEABILITY; TRANSPORT; BARRIER AB Results of protein separation of guinea pig plasma, perilymph, and endolymph by means of high-resolution two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis are presented. Several proteins are present in perilymph at levels in basic accord with the total protein gradient with respect to plasma; however, others are present in perilymph at levels comparable to plasma levels, and one protein low molecular weight protein, PLS:33, is eight times higher. In addition, a high molecular weight protein is shown to be present at similar levels in the two compartments. These findings indicate that ultrafiltration cannot be the sole mechanism of perilymph production. Endolymph proteins are uniformly five to eight times lower than perilymph levels, essentially following the total protein concentration gradient between the two compartments. This supports the view that endolymph is derived from perilymph rather than directly from blood. C1 UNIV TSUKUBA,TSUKUBA,JAPAN. RP THALMANN, I (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID AVE,ST LOUIS,MO 63110, USA. CR ANDERSON L, 1988, 2 DIMENSIONAL ELECTR ANDERSON NL, 1984, PLASMA PROTEINS, V4, P221 ARRER E, 1988, ACTA OTO-LARYNGOL, V106, P117, DOI 10.3109/00016488809107378 ARRER E, 1990, EUR ARCH OTO-RHINO-L, V247, P271 BECK C, 1965, HALS NASEN OHREN HEI, P115 BORGHESAN E, 1957, Laryngoscope, V67, P1266 BROOKS BR, 1989, CEREBROSPINAL FLUID, P167 CHEVANCE LG, 1976, ARCH OTOLARYNGOL, V102, P363 DUVALL AJ, 1971, ARCHIV OTOLARYNGOL, V93, P304 FERRARY E, 1987, AM J PHYSIOL, V22, pF59 GHOSH S, 1988, ANAL BIOCHEM, V169, P227, DOI 10.1016/0003-2697(88)90278-3 GORGAS K, 1974, ANAT EMBRYOL, V146, P33, DOI 10.1007/BF00341381 HARA A, 1989, HEARING RES, V42, P265 HUKEE MJ, 1985, ANN OTO RHINOL LARYN, V94, P297 INAMURA N, 1992, HEARING RES, V61, P12, DOI 10.1016/0378-5955(92)90030-Q ISHIYAMA E, 1970, ACTA OTO-LARYNGOL, V70, P319 JAHNKE K, 1981, 1ST INT S MEN DIS ST, P67 JAHNKE K, 1980, ARCH OTO-RHINO-LARYN, V228, P29, DOI 10.1007/BF00455891 JUHN SK, 1981, MENIERES DISEASE PAT, P59 JUHN SK, 1981, ANN OTO RHINOL LARYN, V90, P135 JUHN SK, 1982, AM J OTOLARYNG, V3, P392, DOI 10.1016/S0196-0709(82)80016-1 KIMURA RS, 1974, ACTA OTO-LARYNGOL, V77, P231 KONISHI T, 1980, EXP BRAIN RES, V40, P457 KONISHI T, 1973, ACTA OTO-LARYNGOL, V76, P410, DOI 10.3109/00016487309121529 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 MAKIMOTO K, 1974, ANN OTO RHINOL LARYN, V83, P174 MAKIMOTO K, 1978, ARCH OHREN NASEN KEH, V220, P259, DOI 10.1007/BF00455361 MARCUS DC, 1976, ARCH OTORHINOLARYNGO, V224, P155 MEES K, 1984, ARCH OTO-RHINO-LARYN, V240, P55, DOI 10.1007/BF00464345 MERRIL CR, 1990, NATURE, V343, P779, DOI 10.1038/343779a0 MIYAMOTO H, 1981, ROLE ELECTROLYTES DI, P39 OAKLEY BR, 1980, ANAL BIOCHEM, V105, P361, DOI 10.1016/0003-2697(80)90470-4 OHYAMA K, 1988, HEARING RES, V35, P119, DOI 10.1016/0378-5955(88)90111-6 RAUCH S, 1964, BIOCH HORORGANS SALT AN, 1986, HEARING RES, V23, P141, DOI 10.1016/0378-5955(86)90011-0 SALT AN, 1991, ACTA OTO-LARYNGOL, V111, P899, DOI 10.3109/00016489109138428 SALT AN, 1988, HEARING RES, V33, P279, DOI 10.1016/0378-5955(88)90158-X SALT AN, 1988, PHYSL EAR, P341 SANTOS-SACCHI J, 1980, ACTA OTO-LARYNGOL, V89, P12, DOI 10.3109/00016488009127103 SCHEIBE F, 1985, HEARING RES, V17, P61, DOI 10.1016/0378-5955(85)90131-5 SCHEIBE F, 1984, ARCH OTO-RHINO-LARYN, V240, P43, DOI 10.1007/BF00464343 SCHNIEDE.EA, 1974, ANN OTO RHINOL LARYN, V83, P76 SILVERST.H, 1966, ARCHIV OTOLARYNGOL, V84, P395 SMITH CA, 1954, LARYNGOSCOPE, V64, P141 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1987, AM J PHYSIOL, V253, pF50 STERKERS O, 1982, AM J PHYSIOL, V243, pF173 THALMANN I, 1991, UNPUB THALMANN I, 1987, LARYNGOSCOPE, V97, P357 THALMANN R, 1981, LARYNGOSCOPE, V91, P1785 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 WINTHER FO, 1971, Z ZELLFORSCH MIK ANA, V114, P193, DOI 10.1007/BF00334000 NR 52 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 NOV PY 1992 VL 63 IS 1-2 BP 37 EP 42 DI 10.1016/0378-5955(92)90071-T PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100006 PM 1464573 ER PT J AU LANGEMANN, U KLUMP, GM AF LANGEMANN, U KLUMP, GM TI FREQUENCY DISCRIMINATION IN THE EUROPEAN STARLING (STURNUS-VULGARIS) - A COMPARISON OF DIFFERENT MEASURES SO HEARING RESEARCH LA English DT Article DE FREQUENCY-DIFFERENCE LIMEN; FREQUENCY RESOLUTION; STARLING; BIRD ID BUDGERIGARS MELOPSITTACUS-UNDULATUS; DETECTION THRESHOLDS; CRITICAL RATIOS; HEART-RATE; MODULATION; TONES; RECOGNITION; PERCEPTION; AMPLITUDE AB Frequency-difference limens (DL) were determined in a songbird, the European starling (Sturnus vulgaris), for stimuli differing in the type of frequency change. Four different types of frequency change were studied: an increase in frequency between pulsed tones (type FSU), a single sinusoidal sweep upward (type SSU) starting in the center of an 800 ms signal, an asymmetrical periodic sinusoidal frequency modulation that extended only above the reference frequency (type ASFM), and a symmetrical periodical sinusoidal frequency modulation extending to both sides of the reference frequency (type SSFM). Frequency DLs at two reference frequencies, 1 and 4 kHz, were studied. At 1 kHz, the starling showed the lowest DL for pulsed tones (11.4 Hz), slightly higher DLs for single sweeps and asymmetrical frequency modulation at modulation frequencies of less-than-or-equal-to 40 Hz (15.9 Hz for stimulus SSU, and 15.3 Hz for low modulation frequencies of stimulus type ASFM). At a reference frequency of 1 kHz, the DL for symmetrical modulation (type SSFM) at modulation frequencies less-than-or-equal-to 40 Hz was about twice as large (21.6 Hz) than for pulsed tones. Furthermore, the DLs for periodically modulated signals at a modulation frequency of 320 Hz were about twice as large as those at low modulation frequencies. At a reference frequency of 4 kHz, the differences in the DLs for various stimulus types were insignificant (27.7 Hz for type FSU, 23.3 Hz for type SSU, 28.0 Hz for type ASFM and low modulation frequencies, and 24.6 Hz for type SSFM and low modulation frequencies). Only at high modulation frequencies (greater-than-or-equal-to 320 Hz) were the DLs increased. The results are discussed with respect to similar effects of stimulus type and reference frequency on the frequency-difference limen in humans and with respect to the frequency DLs in other bird species. C1 TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,W-8046 GARCHING,GERMANY. CR ADRET-HAUSBERGER M, 1989, Bioacoustics, V2, P137 BAUR A, 1989, THESIS TU MUNICH BRAUCKER R, 1986, NATURWISSENSCHAFTEN, V73, P563, DOI 10.1007/BF00368171 CYNX J, 1986, J COMP PSYCHOL, V100, P356 DEMANY L, 1989, J ACOUST SOC AM, V85, P1295, DOI 10.1121/1.397460 DOOLING RJ, 1986, B PSYCHONOMIC SOC, V24, P462 DOOLING RJ, 1987, J COMP PSYCHOL, V101, P139, DOI 10.1037/0735-7036.101.2.139 FASTL H, 1989, 13TH P INT C AC BELG, V3, P11 FASTL H, 1978, J ACOUST SOC AM, V63, P275, DOI 10.1121/1.381725 Fay R. R., 1988, HEARING VERTEBRATES Greenewalt CH, 1968, BIRD SONG ACOUSTICS Hulse S.H., 1989, P331 HURLY TA, 1990, ANIM BEHAV, V40, P176, DOI 10.1016/S0003-3472(05)80677-3 KLUMP GM, 1989, J COMP PHYSIOL A, V164, P531, DOI 10.1007/BF00610446 KLUMP GM, 1991, HEARING RES, V52, P1, DOI 10.1016/0378-5955(91)90182-9 KLUMP GM, 1992, IN PRESS J ACOUST SO KNIPSCHILD M, 1992, HEARING RES, V57, P216, DOI 10.1016/0378-5955(92)90153-E KUHN A, 1980, NATURWISSENSCHAFTEN, V67, P102, DOI 10.1007/BF01054703 KUHN A, 1982, NATURWISSENSCHAFTEN, V69, P245, DOI 10.1007/BF00398648 LANGEMANN U, 1992, ABSTR ASS RES OT, P26 Moore B. C. J., 1989, INTRO PSYCHOL HEARIN MOORE BCJ, 1989, J ACOUST SOC AM, V86, P1722, DOI 10.1121/1.398603 Nelson D.A., 1990, COMP PERCEPTION, V2, P443 NELSON DA, 1988, BEHAVIOUR, V106, P158, DOI 10.1163/156853988X00142 OKANOYA K, 1990, HEARING RES, V50, P185, DOI 10.1016/0378-5955(90)90044-P PAGE SC, 1989, J EXP PSYCHOL ANIM B, V15, P137, DOI 10.1037/0097-7403.15.2.137 SAUNDERS JC, 1979, HEARING RES, V1, P303, DOI 10.1016/0378-5955(79)90003-0 SCHORER E, 1989, ACUSTICA, V68, P183 SCHORER E, 1989, ACUSTICA, V68, P268 SINNOTT JM, 1980, J COMP PHYSIOL PSYCH, V94, P401, DOI 10.1037/h0077681 Swets J.A., 1964, SIGNAL DETECTION REC WEARY DM, 1990, ANIM BEHAV, V39, P459 WIER CC, 1977, J ACOUST SOC AM, V61, P178, DOI 10.1121/1.381251 Zwicker E., 1982, PSYCHOAKUSTIK ZWICKER E, 1990, PSYCHACUSTICS ZWICKER E, 1957, J ACOUST SOC AM, V29, P548, DOI 10.1121/1.1908963 NR 36 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 1992 VL 63 IS 1-2 BP 43 EP 51 DI 10.1016/0378-5955(92)90072-U PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100007 PM 1464574 ER PT J AU ZUCCA, G BOTTA, L MILESI, V DAGANI, F VALLI, P AF ZUCCA, G BOTTA, L MILESI, V DAGANI, F VALLI, P TI EVIDENCE FOR L-GLUTAMATE RELEASE IN FROG VESTIBULAR ORGANS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; NEUROTRANSMITTER; SEMICIRCULAR CANAL; GLUTAMATE ID POTASSIUM-INDUCED RELEASE; SEMICIRCULAR CANALS; XENOPUS-LAEVIS; LATERAL-LINE; AMINO-ACIDS; INVITRO; TISSUE; SKATE; BRAIN AB The present study was devised in order to ascertain whether L-glutamate (Glu) is the neurotransmitter at the primary afferent synapse in frog vestibular organs. To this end different groups of frog isolated semicircular canals were stimulated by means of solutions slightly enriched in K+ (5 mM K+-rich solutions are sufficient to produce a strong, long-lasting, transmitter release from the basal pole of sensory cells) both in normal conditions and after low-Ca2+-high-Mg2+ impairment of the synaptic transmission. The concentration of Glu in the surrounding medium, determined by means of a bioluminescence-enzymatic method, was evaluated in two different experimental conditions: a) when the canals (5 canals placed inside little net bags) were immersed in a 5 mM K+-stimulating solution; b) during the superfusion of the canals (25 canals placed into a little perfusion chamber) with a 5 mM K+-stimulating solution. The net bag experiments demonstrated that K+-rich solutions can provoke an outflow of Glu from canal organs only if the crista ampullaris is present and functioning. Glu fluctuations were in fact suppressed by employing canals deprived of the ampulla or after low-Ca2+-high-Mg2+ synaptic blockade. The superfusion experiments demonstrated that the time course of 5 mM K+-induced release of Glu from the sensory organ strictly parallels the time course of 5 mM K+-induced EPSPs and spike discharge in afferent axons. These results strongly support the hypothesis that Glu is, or is released with, the afferent transmitter in frog inner ear sensory organs, C1 UNIV PAVIA,INST PHARMACOL,I-27100 PAVIA,ITALY. UNIV TURIN,DEPT ANIM BIOL,I-10124 TURIN,ITALY. RP ZUCCA, G (reprint author), UNIV PAVIA,INST GEN PHYSIOL,VIA FORLANINI 6,I-27100 PAVIA,ITALY. CR AKOEV G, 1991, J COMP PHYSIOL A, V168, P639 AKOEV GN, 1980, NEUROSCI LETT, V20, P307, DOI 10.1016/0304-3940(80)90165-2 BLEDSOE SC, 1980, EXP BRAIN RES, V40, P97 BLEDSOE SC, 1989, BRAIN RES, V493, P113, DOI 10.1016/0006-8993(89)91005-6 BOBBIN RP, 1984, HEARING SCI RECENT A, P159 DECHESNE C, 1984, ANN OTO RHINOL LARYN, V93, P163 DELUCA M, 1978, METHOD ENZYMOL, V57 DREJER J, 1985, J NEUROCHEM, V45, P145, DOI 10.1111/j.1471-4159.1985.tb05486.x DRESCHER MJ, 1987, BRAIN RES, V417, P39, DOI 10.1016/0006-8993(87)90177-6 FOSSE VM, 1986, J NEUROCHEM, V47, P340 GUTH PS, 1988, HEARING RES, V33, P223, DOI 10.1016/0378-5955(88)90152-9 HANSEN AJ, 1985, PHYSIOL REV, V65, P101 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x MEZA G, 1982, BRAIN RES, V241, P157, DOI 10.1016/0006-8993(82)91238-0 NICHOLLS DG, 1987, J NEUROCHEM, V49, P50, DOI 10.1111/j.1471-4159.1987.tb03393.x ROSSI ML, 1977, BRAIN RES, V135, P67, DOI 10.1016/0006-8993(77)91052-6 THORNHIL.RA, 1972, COMPARATIVE, V3, P89, DOI 10.1016/0010-4035(72)90045-6 VALLI P, 1990, J PHYSIOL-LONDON, V430, P585 VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 VALLI P, 1988, J COMP PHYSIOL A, V162, P173, DOI 10.1007/BF00606082 VALLI P, 1977, ACTA OTO-LARYNGOL, V84, P344, DOI 10.3109/00016487709123976 VALLI P, 1976, ACTA OTO-LARYNGOL, V81, P395, DOI 10.3109/00016487609107493 ZUCCA G, 1992, HEARING RES, V59, P70, DOI 10.1016/0378-5955(92)90103-T NR 23 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 1992 VL 63 IS 1-2 BP 52 EP 56 DI 10.1016/0378-5955(92)90073-V PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100008 PM 1361183 ER PT J AU MASTERTON, RB GRANGER, EM GLENDENNING, KK AF MASTERTON, RB GRANGER, EM GLENDENNING, KK TI PSYCHOACOUSTICAL CONTRIBUTION OF EACH LATERAL LEMNISCUS SO HEARING RESEARCH LA English DT Article DE SUPERIOR OLIVE; NOISE-DETECTION THRESHOLD; TONE-DETECTION THRESHOLD; FM-DETECTION THRESHOLD; AM-DETECTION THRESHOLD ID CENTRAL AUDITORY-SYSTEM; SOUND-LOCALIZATION; SUPERIOR OLIVE; ACOUSTIC CHIASM; BRAIN-STEM; CAT; SENSITIVITY; MECHANISMS; HEARING; LESIONS AB Although each lateral lemniscus is required for sound localization in its contralateral hemifield, no auditory function is yet known for the neural activity evoked in the lemniscus ipsilateral to a sound source. In an attempt to assess the role played by the ipsilateral lemniscus, monaural cats were tested on an array of psychoacoustical tasks before and after surgical section of one or the other lateral lemniscus. The results show that the lemniscus contralateral to the remaining intact ear is either necessary or sufficient for 24 of the 26 tests administered. However, the lemniscus ipsilateral to the intact ear is both necessary and sufficient (or alternatively, the contralateral lemniscus makes no obvious contribution) to normal thresholds in two of the tasks: detection of low-frequency tones ( < 4 kHz) and detection of low-frequency AM modulation. Because of their projections to the ipsilateral inferior colliculus via the ipsilateral lateral lemniscus, the anatomical substrate of these two unusual tasks is probably the fibers from the MSO and possibly, the LSO, ipsilateral to the intact ear. RP MASTERTON, RB (reprint author), FLORIDA STATE UNIV,DEPT PSYCHOL,PROGRAM NEUROSCI,R-54,TALLAHASSEE,FL 32306, USA. CR BRUGGE JF, 1978, ANNU REV NEUROSCI, V1, P363, DOI 10.1146/annurev.ne.01.030178.002051 GLENDENNING KK, 1992, COMP NEUROL, V319, P100 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 GLENDENNING KK, 1986, ASS RES OTOLARYNGOL, V9, P38 GLENDENNING KK, 1983, J NEUROSCI, V3, P1521 GRANGER DEM, 1987, THESIS FLORIDA STATE HARRISON JM, 1978, HDB BEHAVIORAL NEURO, P409 HEFFNER HE, 1992, ASS RES OTOLARYNGOL, V15, P52 HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 HUTSON KA, 1991, J COMP NEUROL, V312, P105, DOI 10.1002/cne.903120109 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 KAVANAGH GL, 1987, J NEUROPHYSIOL, V57, P1746 Kelly J.B., 1970, THESIS VANDERBILT U KELLY JB, 1985, J NEUROPHYSIOL, V53, P361 MASTERTO.B, 1969, J ACOUST SOC AM, V45, P966, DOI 10.1121/1.1911574 MASTERTON RB, 1984, ANNU REV PHYSIOL, V46, P275 MASTERTON RB, 1988, J NEUROPHYSIOL, V60, P1841 MASTERTON RB, 1991, ASS RES OTOLARYNGOL, V14, P32 MASTERTON RB, 1981, NEURONAL MECHANISMS, P263 MASTERTON RB, 1975, J COMP PHYSIOL PSYCH, V80, P379 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 THOMPSON GC, 1978, J NEUROPHYSIOL, V41, P1183 YIN TCT, 1983, J NEUROPHYSIOL, V50, P1020 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 NR 27 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 1992 VL 63 IS 1-2 BP 57 EP 70 DI 10.1016/0378-5955(92)90074-W PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100009 PM 1464575 ER PT J AU HUTCHINGS, ME MEYER, SE MOORE, DR AF HUTCHINGS, ME MEYER, SE MOORE, DR TI BINAURAL MASKING LEVEL DIFFERENCES IN INFANTS WITH AND WITHOUT OTITIS-MEDIA WITH EFFUSION SO HEARING RESEARCH LA English DT Article DE HEARING; PSYCHOACOUSTICS; DEVELOPMENT ID BRAIN-STEM POTENTIALS; DEVELOPMENTAL-CHANGES; HEARING; FREQUENCY; ADULTS; SENSITIVITY; THRESHOLDS; SOUND; DISCRIMINATION; LOCALIZATION AB The binaural masking level difference (MLD) was measured in two groups of infants (aged 7-10 months) who either had or did not have a documented history of otitis media with effusion (OME). Subjects were trained to detect a 500 Hz signal (either in or out-of-phase between the ears) against an in-phase, narrow band noise masker centred at 500 Hz. Non-OME infants had elevated masked thresholds and reduced MLDs compared with normal-hearing older (7-12 years) children and adults (20-27 years). OME infants also had elevated masked thresholds and reduced MLDs but, in contrast to studies using older subjects, their results were similar to those of the non-OME infants. These results suggest that, during at least the first year of life, infants are disadvantaged compared with adults or children when listening in noisy environments. They also suggest that OME does not further compromise infants' ability to detect sounds in those environments. C1 UNIV OXFORD,PHYSIOL LAB,PK RD,OXFORD OX1 3PT,ENGLAND. CR ASHMEAD DH, 1987, DEV PSYCHOL, V23, P641, DOI 10.1037//0012-1649.23.5.641 ASLIN RN, 1989, J ACOUST SOC AM, V86, P582, DOI 10.1121/1.398237 BIRNHOLZ JC, 1983, SCIENCE, V222, P516, DOI 10.1126/science.6623091 BROWNING GG, 1989, ANN OTO RHINOL LARYN, V98, P245 BRUGGE JF, 1988, AUDITORY FUNCTION NE, P113 CLIFTON RK, 1981, CHILD DEV, V52, P833, DOI 10.1111/j.1467-8624.1981.tb03121.x CLIFTON RK, 1985, AUDITORY DEV INFANCY, P85 Durlach N. I., 1978, HDB PERCEPTION, V4, P365 DURLACH NI, 1981, AUDIOLOGY, V20, P181 EGAN JP, 1969, PERCEPT PSYCHOPHYS, V6, P209, DOI 10.3758/BF03207019 EGGERMONT JJ, 1988, HEARING RES, V33, P35, DOI 10.1016/0378-5955(88)90019-6 Finney D. J., 1971, PROBIT ANAL, V3rd Green D. M., 1975, HDB SENSORY PHYSL, V2, P461 HAGGARD MP, 1991, SCREENINGS CHILDRENS Hall J W 3rd, 1990, J Am Acad Audiol, V1, P81 HALL JW, 1986, ANN OTO RHINOL LARYN, V95, P525 HAUSLER R, 1983, ACTA OTOLARYNGOL S, V400 HECOX K, 1975, INFANT PERCEPTION SE, V2, P151 HEFFNER HE, 1990, J NEUROPHYSIOL, V64, P915 KAGA K, 1980, ARCH OTOLARYNGOL, V106, P564 KLEIN AJ, 1984, HEARING RES, V16, P291, DOI 10.1016/0378-5955(84)90118-7 KNUDSEN EI, 1988, AUDITORY FUNCTION NE, P137 MOCHIZUKI Y, 1982, BRAIN DEV-JPN, V4, P127 MOORE DR, 1988, HDB HUMAN GROWTH DEV, V1, P131 MOORE DR, 1990, SEMIN PERINATOL, V14, P294 MOORE DR, 1991, AUDIOLOGY, V30, P90 MOORE DR, 1991, FETAL NEONATAL BRAIN, P161 MORRONGIELLO BA, 1988, INFANT BEHAV DEV, V11, P127, DOI 10.1016/S0163-6383(88)80001-8 Movshon J.A., 1990, P155 NOZZA RJ, 1988, J SPEECH HEAR RES, V31, P212 NOZZA RJ, 1984, J SPEECH HEAR RES, V27, P613 NOZZA RJ, 1987, INFANT BEHAV DEV, V10, P105, DOI 10.1016/0163-6383(87)90010-5 OLSHO LW, 1987, J ACOUST SOC AM, V82, P454, DOI 10.1121/1.395446 PILLSBURY HC, 1991, ARCH OTOLARYNGOL, V117, P718 ROLAND PS, 1989, ARCH OTOLARYNGOL, V115, P1049 Rubel EW, 1988, AUDITORY FUNCTION NE, P3 SALAMY A, 1976, ELECTROEN CLIN NEURO, V40, P418, DOI 10.1016/0013-4694(76)90193-0 SCHNEIDER BA, 1988, J ACOUST SOC AM, V83, P1124, DOI 10.1121/1.396057 SCHNEIDER BA, 1986, J ACOUST SOC AM, V79, P447, DOI 10.1121/1.393532 SCHNEIDER BA, 1989, J ACOUST SOC AM, V86, P1733, DOI 10.1121/1.398604 STARR A, 1977, PEDIATRICS, V60, P831 TEAS DC, 1982, HEARING RES, V7, P19, DOI 10.1016/0378-5955(82)90080-6 TOWNSEND TH, 1970, J ACOUST SOC AM, V51, P621 TREHUB SE, 1981, J SPEECH HEAR RES, V24, P202 TREHUB SE, 1989, AUDIOLOGY, V28, P241 WERNER LA, 1992, J ACOUST SOC AM, V90, P1867 WITHINGTONWRAY DJ, 1990, DEV BRAIN RES, V51, P225, DOI 10.1016/0165-3806(90)90279-8 YOST WA, 1988, J ACOUST SOC AM, V83, P1517, DOI 10.1121/1.395907 ZWICKER E, 1991, HEARING RES, V53, P141, DOI 10.1016/0378-5955(91)90221-T NR 49 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 1992 VL 63 IS 1-2 BP 71 EP 78 DI 10.1016/0378-5955(92)90075-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100010 PM 1464577 ER PT J AU OHLEMILLER, KK SIEGEL, JH AF OHLEMILLER, KK SIEGEL, JH TI THE EFFECTS OF MODERATE COOLING ON GROSS COCHLEAR POTENTIALS IN THE GERBIL - BASAL AND APICAL DIFFERENCES SO HEARING RESEARCH LA English DT Article DE COCHLEAR TEMPERATURE; ENDOCOCHLEAR POTENTIAL; COCHLEAR MICROPHONIC POTENTIAL; SUMMATING POTENTIAL ID OUTER HAIR-CELLS; COMPOUND ACTION-POTENTIALS; GUINEA-PIG COCHLEA; MONGOLIAN GERBIL; TUNING CURVES; CARBON-MONOXIDE; NERVE-FIBERS; BLOOD-FLOW; FREQUENCY; RESPONSES AB Changes in the threshold of the compound action potential (CAP) response in the gerbil to low- and high-frequency tonebursts were monitored during uniform cooling of the cochlea by 7-8-degrees-C below normal body temperature. Recordings of the endocochlear potential (EP), cochlear microphonic (CM), and summating potentials (SP) were also obtained from the base and apex of the cochlea under the same conditions. Cooling-related changes in the CAP, as well as the CM and SP response obtained near the best frequency of the recording location, were greater in the base than in the apex. In contrast, reductions in the EP appeared uniform throughout the cochlea. Thus the greater vulnerability of CAP thresholds in the base does not result from a greater vulnerability of the stria vascularis in this region. Our results suggest that the enhanced susceptibility to cooling of the CAP in the cochlear base reflects changes in hair cell mechanisms. C1 NORTHWESTERN UNIV, DEPT NEUROBIOL & PHYSIOL, EVANSTON, IL 60201 USA. CR AXELSSON A, 1974, HDB SENSORY PHYSL, V5, P212 BILLETT TE, 1989, HEARING RES, V41, P189, DOI 10.1016/0378-5955(89)90010-5 BOHNE BA, 1976, ANN OTO RHINOL LARYN, V85, P711 BOHNE BA, 1985, ANN OTO RHINOL LARYN, V94, P122 BROWN AM, 1973, J COMP PHYSIOL, V83, P393, DOI 10.1007/BF00696354 BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 BUTLER RA, 1960, AM J PHYSIOL, V199, P688 BUTLER RA, 1965, J ACOUST SOC AM, V37, P429, DOI 10.1121/1.1909346 CHAMBERLAIN SC, 1977, J COMP NEUROL, V171, P193, DOI 10.1002/cne.901710205 CHEATHAM MA, 1984, HEARING RES, V16, P189, DOI 10.1016/0378-5955(84)90009-1 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1972, ACTA OTO-LARYNGOL, P1 DALLOS P, 1983, HEARING RES, V12, P89, DOI 10.1016/0378-5955(83)90120-X DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 DALLOS P, 1974, J ACOUST SOC AM, V55, P597, DOI 10.1121/1.1914570 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 Dallos P., 1973, AUDITORY PERIPHERY B de Brey H B, 1978, Acta Otolaryngol, V85, P363, DOI 10.3109/00016487809121465 DRESCHER DG, 1976, J ACOUST SOC AM, V59, P401, DOI 10.1121/1.380877 DRESCHER DG, 1974, SCIENCE, V185, P273, DOI 10.1126/science.185.4147.273 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FECHTER LD, 1987, HEARING RES, V27, P37, DOI 10.1016/0378-5955(87)90024-4 FERNANDEZ C, 1958, Acta Otolaryngol, V49, P189, DOI 10.3109/00016485809134747 GEISLER CD, 1986, HEARING RES, V24, P125, DOI 10.1016/0378-5955(86)90056-0 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 GUMMER AW, 1983, HEARING RES, V12, P367, DOI 10.1016/0378-5955(83)90006-0 HARRISON JB, 1965, PHYSIOL ZOOL, V38, P34 HENRY KR, 1984, HEARING RES, V16, P225, DOI 10.1016/0378-5955(84)90111-4 KAHANA L, 1950, AM J PHYSIOL, V163, P213 KONISHI T, 1981, HEARING RES, V4, P265, DOI 10.1016/0378-5955(81)90011-3 MANLEY JA, 1974, J COMP PHYSIOL, V88, P43, DOI 10.1007/BF00695922 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 NEDZIELSKI A, 1991, ABSTR ASS RES OT, V14, P135 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 OHLEMILLER KK, 1990, J COMP PHYSIOL A, V167, P329 OHLEMILLER KK, 1990, ABSTR SOC NEUROSCI, V16, P1079 OHLEMILLER KK, 1989, ABSTR ASS RES OT, V12, P119 OHLEMILLER KK, 1990, ABSTR ASS RES OT, V13, P257 OHLEMILLER KK, 1990, THESIS NW U OZDAMAR O, 1978, BRAIN RES, V155, P169, DOI 10.1016/0006-8993(78)90320-7 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 PRIJS VF, 1981, HEARING RES, V4, P23, DOI 10.1016/0378-5955(81)90034-4 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 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 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 Schuknecht H. F., 1974, PATHOLOGY EAR SHORE SE, 1985, J ACOUST SOC AM, V77, P590, DOI 10.1121/1.391877 SLEPECKY N, 1987, ACTA OTO-LARYNGOL, V103, P176, DOI 10.3109/00016488709107781 WHITFIEL.IC, 1965, J ACOUST SOC AM, V38, P126, DOI 10.1121/1.1909586 YOUNG JS, 1987, HEARING RES, V26, P37, DOI 10.1016/0378-5955(87)90034-7 NR 58 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 NOV PY 1992 VL 63 IS 1-2 BP 79 EP 89 DI 10.1016/0378-5955(92)90076-Y PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100011 PM 1464578 ER PT J AU HENRY, KR PRICE, JM AF HENRY, KR PRICE, JM TI SUPRATHRESHOLD COMPARISONS OF DERIVED AND ENHANCED COMPOUND ACTION-POTENTIALS SO HEARING RESEARCH LA English DT Article DE ENHANCEMENT; DERIVED CAP; COCHLEA; LATENCY ID LOUDNESS ENHANCEMENT; BURSTS; PAIRS AB The Derived cochlear nerve compound action potential (CAP) and the Enhanced CAP are both measures which demonstrate the ability of a forward masker to increase the amplitude of the CAP produced by a probe stimulus. Enhancement occurs whenever the amplitude of a masked CAP is larger than that of a nonmasked CAP, whereas the derived CAP is produced by the subtraction of the entire masked CAP waveform from that of the nonmasked waveform. Therefore, a derived CAP is created whenever the masker produces a difference of amplitude, latency, and/or waveform shape. The present experiments compare these two measures by observing the effects of 13 kHz maskers varying from levels of - 10 to + 70 dB SPL on CAPs produced by 50 or 60 dB SPL, 13 kHz probe stimuli. Enhancement is characterized by a nonmonotonic increase of CAP amplitude (and sometimes a decrease of latency) as a function of increasing levels of the forward masker, whereas this pattern seldom occurs with the derived CAP. Enhancement is typically seen with forward making, but seldom seen with simultaneous masking, whereas the derived CAP is very similar under these two types of masking. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR BERLIN CI, 1991, HEARING RES, V52, P271, DOI 10.1016/0378-5955(91)90017-4 BERLIN CI, 1987, ABSTR ASS RES OT, P172 CACACE AT, 1986, HEARING RES, V23, P223, DOI 10.1016/0378-5955(86)90111-5 ELMASIAN R, 1975, J ACOUST SOC AM, V58, P229, DOI 10.1121/1.380650 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1992, ABSTR ASS RES OT HENRY KR, 1991, HEARING RES, V56, P197, DOI 10.1016/0378-5955(91)90170-E HENRY KR, 1992, J ACOUST SOC AM, V91, P2824, DOI 10.1121/1.402963 HENRY KR, 1992, HEARING RES, V63, P8 HENRY KR, 1991, HEARING RES, V56, P239, DOI 10.1016/0378-5955(91)90174-8 HENRY KR, UNPUB ENHANCEMENT AM HOOD LJ, 1987, ABSTR ASS RES OT, V10, P172 HOOD LJ, 1991, HEARING RES, V55, P109, DOI 10.1016/0378-5955(91)90097-S IRWIN RJ, 1971, PERCEPT PSYCHOPHYS, V10, P189, DOI 10.3758/BF03205785 RONKEN DA, 1991, ABSTR ASS RES OT RUBIN H, 1960, J ACOUST SOC AM, V32, P670, DOI 10.1121/1.1908177 SALT AN, 1990, AUDIOLOGY, V29, P135 SALT AN, 1990, J ACOUST SOC AM, V88, P1392, DOI 10.1121/1.399717 SIEGEL JH, 1987, HEARING RES, V29, P169, DOI 10.1016/0378-5955(87)90165-1 ZWICKER E, 1957, J ACOUST SOC AM, V29, P548, DOI 10.1121/1.1908963 ZWISLOCKI J, 1959, J ACOUST SOC AM, V31, P9, DOI 10.1121/1.1907619 ZWISLOCK.JJ, 1974, PERCEPT PSYCHOPHYS, V16, P91, DOI 10.3758/BF03203257 ZWISLOCK.JJ, 1974, PERCEPT PSYCHOPHYS, V16, P87 NR 23 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 1992 VL 63 IS 1-2 BP 90 EP 96 DI 10.1016/0378-5955(92)90077-Z PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100012 PM 1464579 ER PT J AU PRICE, JM HENRY, KR AF PRICE, JM HENRY, KR TI LATENCY ENHANCEMENT OF THE COCHLEAR NERVE COMPOUND ACTION-POTENTIAL (CAP) SO HEARING RESEARCH LA English DT Article DE ENHANCEMENT; COCHLEA; GERBIL; TUNING CURVES; LATENCY; HAIR CELL; ADAPTATION ID OUTER HAIR-CELLS; TUNING CURVES; GUINEA-PIG; RESPONSES; INTENSITY; INNER AB Forward maskers within two frequency-intensity domains are capable of decreasing (enhancing) CAP latency: one region flanks the low frequency tail, the other flanks the tip/high frequency slope regions of the latency tuning curve (TC). By contrast, amplitude enhancement typically does not flank the high frequency slope region. RP PRICE, JM (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR Bekesy G., 1960, EXPT HEARING BERLIN CI, 1991, HEARING RES, V52, P271, DOI 10.1016/0378-5955(91)90017-4 BROWN CJ, 1987, HEARING RES, V25, P193, DOI 10.1016/0378-5955(87)90091-8 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CACACE AT, 1986, HEARING RES, V23, P223, DOI 10.1016/0378-5955(86)90111-5 COATS AC, 1976, ELECTROCOCHLEOGRAPHY, P387 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 HENRY KR, 1990, AUDIOLOGY, V29, P122 HENRY KR, 1991, HEARING RES, V56, P197, DOI 10.1016/0378-5955(91)90170-E HENRY KR, 1979, AUDIOLOGY, V18, P93 HENRY KR, 1991, AUDIOLOGY, V30, P33 HENRY KR, 1992, J ACOUST SOC AM, V91, P2824, DOI 10.1121/1.402963 HENRY KR, 1991, HEARING RES, V56, P239, DOI 10.1016/0378-5955(91)90174-8 HENRY KR, 1992, UNPUB ENHANCEMENT AB Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 MOLLER AR, 1985, HEARING RES, V17, P177, DOI 10.1016/0378-5955(85)90020-6 OZDAMAR O, 1978, BRAIN RES, V155, P169, DOI 10.1016/0006-8993(78)90320-7 RONKEN DA, 1991, ABSTR ASS RES OT RUGGERO MA, 1987, J NEUROPHYSIOL, V58, P379 RUSSELL IJ, 1989, HEARING RES, V43, P55, DOI 10.1016/0378-5955(89)90059-2 SALVI RJ, 1979, HEARING RES, V1, P237, DOI 10.1016/0378-5955(79)90017-0 SIEGEL JH, 1987, HEARING RES, V29, P169, DOI 10.1016/0378-5955(87)90165-1 STRELIOFF D, 1985, HEARING RES, V18, P169, DOI 10.1016/0378-5955(85)90009-7 NR 28 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 1992 VL 63 IS 1-2 BP 97 EP 101 DI 10.1016/0378-5955(92)90078-2 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100013 PM 1464580 ER PT J AU QUIRK, WS AVINASH, G NUTTALL, AL MILLER, JM AF QUIRK, WS AVINASH, G NUTTALL, AL MILLER, JM TI THE INFLUENCE OF LOUD SOUND ON RED-BLOOD-CELL VELOCITY AND BLOOD-VESSEL DIAMETER IN THE COCHLEA SO HEARING RESEARCH LA English DT Article DE LOUD SOUND; INTRAVITAL MICROSCOPY; RED BLOOD CELL VELOCITY; VESSEL DIAMETER; GUINEA PIG ID GUINEA-PIG; NOISE EXPOSURE; FLOW; RAT AB Using intravital microscopy, we observed both decreases in red blood cell velocity and possible vasoconstriction in stria vascularis capillaries of the rat cochlea in response to loud sound (Quirk et al., 1991). However, our observation of vasoconstriction was subject to error in measurements from the two dimensional images obtained with our silicon intensified (SIT) camera due to the influence of focus causing image blur. The purpose of the current study was to apply an extended focus microscopy technique to obtain quantitative assessment of vessel diameter changes (Avinash et al., 1992), as well as to extend these studies to the guinea pig model. Broad-band sound stimulation at intensities of 84 dB SPL and 110 dB SPL were used. The results show that loud sound induces a sequence of changes in cochlear blood flow. Stimulation with 110 dB SPL resulted in a mean increase (maximum = 27%) in red blood cell velocity for the first 20 min of exposure followed by a gradual decrease below baseline (minimum = - 12%) prior to termination of the signal. This velocity decrease and subsequent recovery were associated with significant changes in vessel diameters of selected and measured capillaries. In contrast, the 84 dB SPL stimulus caused an increase in red blood cell velocity (maximum = 20%) and vessel diameter (mean = 7.5) during the stimulation period. No recovery was observed during the 10 min observation period following sound. Several possible mechanisms responsible for these changes are discussed. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP QUIRK, WS (reprint author), WAYNE STATE UNIV,DEPT OTOLARYNGOL,5E UHC,540 E CANFIELD,DETROIT,MI 48201, USA. CR Angelborg C, 1979, Adv Otorhinolaryngol, V25, P41 AXELSSON A, 1990, ACTA OTOLARYNGOL STO, V109, P262 AXELSSON A, 1981, ACTA OTO-LARYNGOL, V91, P237, DOI 10.3109/00016488109138504 AXELSSON A, 1982, NEW PERSPECTIVES NOI, P49 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 CANLON B, 1983, HEARING RES, V10, P217, DOI 10.1016/0378-5955(83)90055-2 DENGERINK H, 1985, ACTA OTO-LARYNGOL, V100, P19, DOI 10.3109/00016488509108582 DUVALL AJ, 1974, ANN OTO RHINOL LARYN, V83, P498 FRUHSTORFER B, 1988, INT J NEUROSCI, V39, P197, DOI 10.3109/00207458808985704 GRANGER HJ, 1988, AM J OTOLARYNG, V9, P264, DOI 10.1016/S0196-0709(88)80035-8 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HILLERDAL M, 1987, ACTA OTO-LARYNGOL, V104, P270, DOI 10.3109/00016488709107328 MCLAREN GM, 1991, HEARING RES, V55, P1, DOI 10.1016/0378-5955(91)90086-O MILES FP, 1989, HEARING RES, V33, P191 MORIMITS.T, 1965, ANN OTO RHINOL LARYN, V74, P22 NUTTALL AL, 1981, HEARING RES, V5, P285, DOI 10.1016/0378-5955(81)90052-6 NUTTALL AL, 1987, HEARING RES, V27, P111, DOI 10.1016/0378-5955(87)90012-8 PERLMAN H B, 1962, Acta Otolaryngol, V54, P99, DOI 10.3109/00016486209126927 PRAZMA J, 1983, ARCH OTOLARYNGOL, V109, P611 PRAZMA J, 1987, ARCH OTOLARYNGOL, V113, P36 QUIRK WS, 1991, HEARING RES, V52, P217, DOI 10.1016/0378-5955(91)90201-J QUIRK WS, UNPUB MICROVASCULAR RYAN AF, 1988, ACTA OTO-LARYNGOL, V105, P232, DOI 10.3109/00016488809097003 SCHIEBE F, 1990, ERU ARCH OTORHINOILA, V247, P84 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 WRIGHT JW, 1981, J ACOUST SOC AM, V70, P1353, DOI 10.1121/1.387124 NR 26 TC 34 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 NOV PY 1992 VL 63 IS 1-2 BP 102 EP 107 DI 10.1016/0378-5955(92)90079-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100014 PM 1464564 ER PT J AU HEIL, P RAJAN, R IRVINE, DRF AF HEIL, P RAJAN, R IRVINE, DRF TI SENSITIVITY OF NEURONS IN CAT PRIMARY AUDITORY-CORTEX TO TONES AND FREQUENCY-MODULATED STIMULI .1. EFFECTS OF VARIATION OF STIMULUS PARAMETERS SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; FM RATE SENSITIVITY; FM DIRECTIONAL SENSITIVITY; SPIKE TIMING; INTENSITY ID TIME-VARYING STIMULI; INFERIOR COLLICULUS; SINGLE NEURONS; FUNCTIONAL-ORGANIZATION; COCHLEAR NUCLEUS; UNIT RESPONSES; AMPLITUDE; REPRESENTATION; NOISE; TOPOGRAPHY AB In the primary auditory cortex (AI) of barbiturate-anesthetized cats multi-unit responses to tones and to frequency-modulated (FM) tonal stimuli were analyzed, Characteristic frequency (CF), sharpness of tuning, minimum threshold, and dynamic range of spike count - intensity functions were determined. Minimum threshold and dynamic range were positively correlated. The response functions to unidirectional FM sweeps of varying linear rate of change of frequency (RCF) that traversed the excitatory frequency response areas (FRAs) displayed a variety of shapes. Preferences for fast RCFs ( > 1000 kHz/s) were most common. Best RCF was not correlated with measures of sharpness of tuning. Directional preference and sensitivity were quantified by a DS index which varied with RCF. About two-thirds of the multi-unit responses showed a preference for downward sweeps. Directional sensitivity was independent of CF and independent of best RCF. Measurements of latencies of phasic responses to unidirectional FM sweeps of different RCF demonstrated that the discharges of a given multi-unit over its effective RCF range were initiated at the same instantaneous frequency (effective F(i)), independent of RCF. Effective F(i)s fell within the excitatory FRA of a given multi-unit. The relationships of effective F(i)s to CF show that responses were evoked only when the frequency of the signal was modulated towards CF and not when modulated away from it, and that responses were initiated before the modulation reached CF. Changes in the range and depth of modulation had only minor, if any, effects on RCF response characteristics, FM directional sensitivity, and effective F(i)s, as long as the beginning and ending frequencies of FM sweeps fell outside a multi-unit's FRA. Stimulus intensity also had only moderate effects on RCF response characteristics and DS. However, effective F(i)s were influenced in systematic fashions: with increases in intensity, effective F(i)s to upward and downward sweeps decreased and increased, respectively. Thus, for higher intensities FM responses were initiated at instantaneous frequencies occuring earlier in the signal. The results are compared with previous data on tone and FM sensitivity of auditory neurons in cortical and subcortical structures, and mechanisms of FM rate and directional sensitivity are discussed. The topographic representations of these neuronal properties in AI are reported in the companion report. C1 MONASH UNIV,DEPT PSYCHOL,CLAYTON,VIC 3168,AUSTRALIA. RI Rajan, Ramesh/A-5945-2008; Irvine, Dexter/F-7474-2011 CR ABELES M, 1970, J NEUROPHYSIOL, V33, P172 BRITT R, 1976, J NEUROPHYSIOL, V39, P179 BROWN KA, 1978, DEV PSYCHOBIOL, V11, P559, DOI 10.1002/dev.420110605 BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 CALFORD MB, 1992, UNPUB CHANGES FREQUE ERULKAR SD, 1968, J NEUROPHYSIOL, V31, P537 GOLDSTEIN MH, 1970, J ACOUST SOC AM, V43, P444 HEIL P, 1992, UNPUB HEAR RES HEIL P, 1992, IN PRESS J COMP PH A HEIL P, 1989, THESIS TU DARMSTADT HEIL P, 1992, RHYTHMOGENESIS NEURO, P203 HEIL P, 1991, BRAIN RES, V539, P110, DOI 10.1016/0006-8993(91)90692-O HEIL P, 1991, BRAIN RES, V539, P121, DOI 10.1016/0006-8993(91)90693-P ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 KELLY JB, 1971, J NEUROPHYSIOL, V34, P802 MARLER P, 1959, DARWINS BIOL WORK SO MARLER P, 1960, PUBL AM I BIOL SCI, V7 MENDELSON JR, 1985, BRAIN RES, V327, P331, DOI 10.1016/0006-8993(85)91530-6 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MOLLER AR, 1969, ACTA PHYSIOL SCAND, V76, P503, DOI 10.1111/j.1748-1716.1969.tb04497.x MOLLER AR, 1977, AUDIOLOGY, V17, P446 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x MOLLER AR, 1971, ACTA PHYSIOL SCAND, V81, P540, DOI 10.1111/j.1748-1716.1971.tb04931.x NELSON PG, 1966, J NEUROPHYSIOL, V29, P834 NOMOTO M, 1980, JPN J PHYSIOL, V30, P427 OONISHI S, 1965, JPN J PHYSIOL, V15, P342 PHILLIPS DP, 1985, HEARING RES, V19, P253, DOI 10.1016/0378-5955(85)90145-5 PHILLIPS DP, 1987, EXP BRAIN RES, V67, P479 PHILLIPS DP, 1988, BRAIN RES, V443, P281, DOI 10.1016/0006-8993(88)91622-8 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1985, HEARING RES, V18, P73, DOI 10.1016/0378-5955(85)90111-X PHILLIPS DP, 1985, EXP BRAIN RES, V58, P443 PHILLIPS DP, 1989, HEARING RES, V37, P269, DOI 10.1016/0378-5955(89)90027-0 PHILLIPS DP, 1981, J NEUROPHYSIOL, V45, P48 POON PWF, 1991, EXP BRAIN RES, V83, P598 RAJAN R, 1991, HEARING RES, V53, P153, DOI 10.1016/0378-5955(91)90222-U REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 RHODE WS, 1976, CURRENT COMPUTER TEC, P543 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1442 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SHAMMA SA, 1985, HEARING RES, V19, P1, DOI 10.1016/0378-5955(85)90094-2 SHORE SE, 1987, J ACOUST SOC AM, V82, P471, DOI 10.1121/1.395448 SINEX DG, 1981, HEARING RES, V4, P127, DOI 10.1016/0378-5955(81)90001-0 Smith J.C., 1975, Symposia Zool Soc Lond, VNo. 37, P317 SOKOLICH WG, 1981, Patent No. 4251686 SUGA N, 1965, J PHYSIOL-LONDON, V179, P26 SUGA N, 1968, J PHYSIOL-LONDON, V198, P51 Suga N., 1973, BASIC MECH HEARING, P675 Suga N., 1984, DYNAMIC ASPECTS NEOC, P315 SUGA N, 1965, J PHYSIOL-LONDON, V181, P671 SUGA N, 1969, J PHYSIOL-LONDON, V200, P555 SUTTER ML, 1991, ABSTR ASS RES OT, V14, P21 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 WATANABE T, 1972, JPN J PHYSIOL, V22, P569 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 NR 58 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 NOV PY 1992 VL 63 IS 1-2 BP 108 EP 134 DI 10.1016/0378-5955(92)90080-7 PG 27 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100015 PM 1464565 ER PT J AU HEIL, P RAJAN, R IRVINE, DRF AF HEIL, P RAJAN, R IRVINE, DRF TI SENSITIVITY OF NEURONS IN CAT PRIMARY AUDITORY-CORTEX TO TONES AND FREQUENCY-MODULATED STIMULI .2. ORGANIZATION OF RESPONSE PROPERTIES ALONG THE ISOFREQUENCY DIMENSION SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; TOPOGRAPHY; INTENSITY CODING; FM RATE SENSITIVITY; FM DIRECTIONAL SENSITIVITY ID SINGLE NEURONS; REPRESENTATION; AMPLITUDE; TOPOGRAPHY; INTENSITY; COCHLEA; NOISE; TIME; BAT; AI AB The spatial distribution of neuronal responses to tones and frequency-modulated (FM) stimuli was mapped along the 'isofrequency' dimension of the primary auditory cortex (AI) of barbiturate-anesthetized cats. In each cat, electrode penetrations roughly orthogonal to the cortical surface were closely spaced (average separation almost-equal-to 130 mum) along the dorsoventral extent of a single 'isofrequency' strip in high frequency parts of AI ( > 15 kHz). Characteristic frequency (CF), minimum threshold, sharpness of frequency tuning (Q10 and Q20), the dynamic range of the spike count-intensity function at CF, sensitivity to the rate of change of frequency (RCF) and to the direction of frequency-modulation (DS) were determined for contralaterally-presented tone and FM stimuli. Sharpness of tuning attained maximum values at central loci along the dorsoventral 'isofrequency' axis and values declined towards more dorsal and more ventral locations. Minimum threshold and dynamic range varied between high and low values in a similar and correlated periodic fashion. Their combined organization yielded an orderly spatial representation of response strength, relative to maximum, as a function of stimulus amplitude. The distributions of the most common forms of FM rate sensitivity (RCF response categories) and best RCF along 'isofrequency' strips were significantly non-random although there was a considerable degree of variability between cats. FM directional preference and sensitivity appeared to be randomly distributed. Sharpness of tuning may be related to the analysis of the spectral content of an acoustic stimulus, both minimum threshold and dynamic range are related to the encoding of stimulus intensity, and measures of FM rate and directional sensitivity assess the coding of temporal changes of stimulus spectra. The independent, or for minimum threshold and dynamic range dependent, topographic organizations of these neuronal parameters therefore suggest parallel and independent processing of these aspects of acoustic signals, in AI. C1 MONASH UNIV, DEPT PSYCHOL, CLAYTON, VIC 3168, AUSTRALIA. RI Rajan, Ramesh/A-5945-2008; Irvine, Dexter/F-7474-2011 CR AITKIN LM, 1986, J COMP NEUROL, V252, P175, DOI 10.1002/cne.902520204 ASANUMA A, 1983, J NEUROPHYSIOL, V50, P1182 CROSS EM, 1982, EDUC PSYCHOL MEAS, V42, P25, DOI 10.1177/0013164482421003 EHIL P, 1989, NEURAL MECHANISMS BE, P126 HEIL P, 1991, P AUST NEUROSCI SOC, V2, pS28 HEIL P, 1992, HEARING RES, V63, P108, DOI 10.1016/0378-5955(92)90080-7 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 KELLY JB, 1971, J NEUROPHYSIOL, V34, P802 KNIGHT PL, 1977, BRAIN RES, V130, P447, DOI 10.1016/0006-8993(77)90108-1 MENDELSON JR, 1985, BRAIN RES, V327, P331, DOI 10.1016/0006-8993(85)91530-6 MENDELSON JR, 1988, ABSTR ASS RES OT, V11, P199 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MIDDLEBROOKS JC, 1980, BRAIN RES, V181, P31, DOI 10.1016/0006-8993(80)91257-3 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1985, HEARING RES, V18, P73, DOI 10.1016/0378-5955(85)90111-X PHILLIPS DP, 1985, EXP BRAIN RES, V58, P443 PHILLIPS DP, 1981, J NEUROPHYSIOL, V45, P48 RAJAN R, 1990, J NEUROPHYSIOL, V64, P888 RAJAN R, 1991, HEARING RES, V53, P153, DOI 10.1016/0378-5955(91)90222-U REALE RA, 1986, J NEUROPHYSIOL, V56, P663 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 SCHREINER CE, 1984, J NEUROPHYSIOL, V51, P1284 SCHREINER CE, 1988, ABSTR ASS RES OT, V11, P198 SCHREINER CE, 1990, J NEUROPHYSIOL, V64, P1142 SHAMA SA, 1990, TR9045 U MARYL SYST SHAMMA SA, 1991, AUDITORY PHYSL PERCE STIEBLER I, 1986, NEUROSCI LETT, V65, P336, DOI 10.1016/0304-3940(86)90285-5 Suga N., 1984, DYNAMIC ASPECTS NEOC, P315 SUGA N, 1977, SCIENCE, V196, P64, DOI 10.1126/science.190681 SUTTER ML, 1991, ABSTR ASS RES OT, V14, P21 SUTTER ML, 1991, J NEUROPHYSIOL, V65, P1207 SWINDALE NV, 1991, NATO ADV SCI I A-LIF, V200, P111 TUNTURI AR, 1952, AM J PHYSIOL, V168, P712 Woolsey CN, 1942, B JOHNS HOPKINS HOSP, V71, P315 NR 36 TC 108 Z9 109 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 1992 VL 63 IS 1-2 BP 135 EP 156 DI 10.1016/0378-5955(92)90081-W PG 22 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100016 PM 1464567 ER PT J AU BOBBIN, RP FALLON, M AF BOBBIN, RP FALLON, M TI INTENSE SOUND INCREASES THE LEVEL OF AN UNIDENTIFIED AMINE FOUND IN PERILYMPH SO HEARING RESEARCH LA English DT Article DE HAIR CELL; GLUTAMATE; SODIUM; AMINO ACIDS; NEUROTRANSMITTER; COCHLEA ID GUINEA-PIG COCHLEA; POTASSIUM-INDUCED RELEASE; XENOPUS-LAEVIS; LATERAL-LINE; ACID CONTENT; HAIR-CELLS; SUBSTANCES; GLUTAMATE; NEURONS; RAT AB The hypothesis tested was that intense sound increases the levels of a substance such as glutamate, a putative neurotransmitter and neurotoxic substance, in the perilymph compartment of the cochlea. Artificial perilymph was perfused through the perilymphatic compartment of the guinea pig cochlea and the effluent collected during successive 10-min periods. The effects of perfusing an artificial perilymph containing normal levels of Na+ (NARP) were compared to the effects of perfusing an artificial perilymph containing very low concentrations of Na+ (VLNa). The effluent was collected during ambient noise and during increasing intensities of broad-band noise (10 min at 106, 112, 118 and 124 dB SPL). Levels of amines in the effluent were measured by HPLC utilizing precolumn o-phthalaldehyde (OPA) derivatization and fluorescence detection. VLNa increased the levels of glutamate and several other amines in effluent from the cochlea compared to levels obtained in NARP. Compared with its level during ambient room noise, the concentration of an unidentified amine labeled Unk 2.5 increased during intense noise (124 dB SPL). Intense noise induced no detectable changes in the concentrations of glutamate and fifteen other amines. The chemical identity and role of Unk 2.5 remain to be determined. RP BOBBIN, RP (reprint author), LOUISIANA STATE UNIV,MED CTR,KRESGE HEARING RES LAB 5,DEPT OTORHINOLARYNGOL & BIOCOMMUN,NEW ORLEANS,LA 70112, USA. CR Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BLEDSOE SC, 1980, EXP BRAIN RES, V40, P97 BLEDSOE SC, 1989, BRAIN RES, V493, P113, DOI 10.1016/0006-8993(89)91005-6 BOBBIN RP, 1991, HEARING RES, V54, P135, DOI 10.1016/0378-5955(91)90143-W BOBBIN RP, 1990, HEARING RES, V46, P83, DOI 10.1016/0378-5955(90)90141-B BOBBIN RP, 1992, CHARACTERISTICS UNID, P100 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 BOX GEP, 1978, STATISTICS EXPT DANCER AL, 1992, NOISE INDUCED HEARIN, P554 DRESCHER MJ, 1987, BRAIN RES, V417, P39, DOI 10.1016/0006-8993(87)90177-6 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x ERECINSKA M, 1987, BIOCHEM PHARMACOL, V36, P3547, DOI 10.1016/0006-2952(87)90001-3 EYBALIN M, 1983, NEUROSCIENCE, V9, P863, DOI 10.1016/0306-4522(83)90274-9 FERKANY J, 1986, J NEUROSCI RES, V16, P491, DOI 10.1002/jnr.490160305 HERTZ L, 1979, PROG NEUROBIOL, V13, P277, DOI 10.1016/0301-0082(79)90018-2 JANSSEN R, 1991, BRAIN RES, V552, P255, DOI 10.1016/0006-8993(91)90090-I JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x Joseph M.H., 1986, HPLC SMALL MOL PRACT, P13 JUIZ JM, 1989, HEARING RES, V40, P65, DOI 10.1016/0378-5955(89)90100-7 KONISHI T, 1968, J ACOUST SOC AM, V43, P471, DOI 10.1121/1.1910854 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 LEFEBVRE PP, 1991, BRAIN RES, V555, P75, DOI 10.1016/0006-8993(91)90862-P LEFEBVRE PP, 1990, HEARING RES, V47, P83, DOI 10.1016/0378-5955(90)90168-O MEDINA JE, 1981, NEUROSCIENCE, V6, P505, DOI 10.1016/0306-4522(81)90142-1 MELAMED B, 1982, HEARING RES, V7, P13, DOI 10.1016/0378-5955(82)90079-X PUEL JL, 1991, NEUROSCIENCE, V45, P63, DOI 10.1016/0306-4522(91)90103-U PUJOL R, 1991, ACTA OTOLARYNGOL S S, V476, P32 SEWELL WF, 1978, SCIENCE, V202, P910, DOI 10.1126/science.30998 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 NR 29 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 1992 VL 63 IS 1-2 BP 157 EP 162 DI 10.1016/0378-5955(92)90082-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100017 PM 1361182 ER PT J AU COOPER, NP RHODE, WS AF COOPER, NP RHODE, WS TI BASILAR-MEMBRANE MECHANICS IN THE HOOK REGION OF CAT AND GUINEA-PIG COCHLEAE - SHARP TUNING AND NONLINEARITY IN THE ABSENCE OF BASE-LINE POSITION SHIFTS SO HEARING RESEARCH LA English DT Article DE COCHLEAR MECHANICS; BASILAR MEMBRANE ID OUTER HAIR-CELLS; AUDITORY-NERVE FIBERS; MOSSBAUER TECHNIQUE; MAMMALIAN COCHLEA; HIGH-FREQUENCIES; VIBRATION; AMPLITUDE; PHASE; RESPONSES; CURVES AB A heterodyne laser interferometer was used to observe the movements of small (approximately 20 mum) stainless-steel beads placed on the basilar membrane in the hook region of cat and guinea-pig cochleae. In several preparations, the displacement patterns observed exhibited sharp nonlinear tuning; in one cat this tuning was comparable to that commonly observed in single auditory-nerve fibers. The most sensitive frequencies of the preparations ranged from 31-40 kHz in the cat, and 28-32 kHz in the guinea-pig. The sharp tuning and nonlinearity of the basilar membrane responses was not apparent in surgically or acoustically traumatized preparations. The response nonlinearities were susceptible to temporary threshold shifts and disappeared within a few minutes post-mortem. Stimulus-related shifts in the baseline position of the basilar membrane were not apparent at low stimulus levels. Such shifts were occasionally observed at higher stimulus levels (e.g., > 90 dB SPL), but never approached the fundamental (oscillatory) component of basilar membrane vibration in magnitude. These findings are discussed in relation to previous observations by other workers. C1 UNIV WISCONSIN, DEPT NEUROPHYSIOL, MADISON, WI 53706 USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BOBROFF N, 1987, APPL OPTICS, V26, P2676, DOI 10.1364/AO.26.002676 BONBEKESY G, 1960, EXPT HEARING, P1 BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BUUNEN TJF, 1981, J ACOUST SOC AM, V69, P744, DOI 10.1121/1.385574 COOPER NP, 1992, HEARING RES, V63, P191, DOI 10.1016/0378-5955(92)90084-Z COOPER NP, 1992, COCHLEAR MECHANICS C COOPER NP, 1992, UNPUB NONLINEAR MECH DECRAEMER WF, 1989, HEARING RES, V38, P1, DOI 10.1016/0378-5955(89)90123-8 DECRAEMER WF, 1990, HEARING RES, V47, P205, DOI 10.1016/0378-5955(90)90152-F DECRAEMER WF, 1991, HEARING RES, V54, P305, DOI 10.1016/0378-5955(91)90124-R EVANS BN, 1990, LECT NOTES BIOMATH, V87, P61 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P409 FAY RR, 1988, HEARING RES, V34, P295, DOI 10.1016/0378-5955(88)90009-3 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 Johnstone BM, 1967, SCIENCE, V158, P390 JOHNSTONE JR, 1977, PSYCHOPHYSICS PHYSL, P89 JOHNSTON.BM, 1970, J ACOUST SOC AM, V47, P504, DOI 10.1121/1.1911921 KHANNA SM, 1983, HEARING OTHER SENSES, P65 KHANNA SM, 1986, HEARING RES, V23, P55, DOI 10.1016/0378-5955(86)90175-9 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KHANNA SM, 1986, HEARING RES, V23, P37, DOI 10.1016/0378-5955(86)90174-7 KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 KOHLLOFFEL LUE, 1975, OTORHINOLARYNGOL, V209, P179 KOHLLOFF.LU, 1972, ACUSTICA, V27, P66 LEONARD DGB, 1984, J ACOUST SOC AM, V75, P515, DOI 10.1121/1.390485 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 LEPAGE EL, 1980, HEARING RES, V2, P183, DOI 10.1016/0378-5955(80)90056-8 LEPAGE EL, 1990, LECT NOTES BIOMATH, V87, P278 LEPAGE EL, 1981, THESIS U W AUSTR NED LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 MOLLER AR, 1963, J ACOUST SOC AM, V35, P1526, DOI 10.1121/1.1918742 NUTTALL AL, 1990, LECT NOTES BIOMATH, V87, P288 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PATUZZI R, 1984, HEARING RES, V13, P99, DOI 10.1016/0378-5955(84)90100-X Rhode W. S., 1973, BASIC MECHANISMS HEA, P49 RHODE WS, 1980, J ACOUST SOC AM, V67, P1696, DOI 10.1121/1.384296 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, 1992, UNPUB 2 TONE SUPPRES RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBERTSON, 1974, SCIENCE, V186, P623 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 ROBLES L, 1989, COCHLEAR MECH STRUCT, P369 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 ROBLES L, 1976, J ACOUST SOC AM, V59, P926, DOI 10.1121/1.380953 ROBLES L, 1990, LECT NOTES BIOMATH, V87, P304 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 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 SHORE SE, 1985, J ACOUST SOC AM, V77, P590, DOI 10.1121/1.391877 TONNDORF J, 1957, J ACOUST SOC AM, V29, P558, DOI 10.1121/1.1908965 TONNDORF J, 1968, J ACOUST SOC AM, V44, P1546, DOI 10.1121/1.1911295 von Bekesy G, 1928, PHYS Z, V29, P793 Wilson JP, 1983, MECH HEARING, P30 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 NR 59 TC 142 Z9 145 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 1992 VL 63 IS 1-2 BP 163 EP 190 DI 10.1016/0378-5955(92)90083-Y PG 28 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100018 PM 1464568 ER PT J AU COOPER, NP RHODE, WS AF COOPER, NP RHODE, WS TI BASILAR-MEMBRANE TONOTOPICITY IN THE HOOK REGION OF THE CAT COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEAR MECHANICS; BASILAR MEMBRANE; TONOTOPICITY ID MOSSBAUER TECHNIQUE; MECHANICS; INPUT AB Middle-ear to basilar membrane (BM) velocity transfer functions are reported for seven locations in the hook region of a single cat cochlea. These transfer functions were recorded at high sound pressure levels in a linearized, or passive cochlea, and resemble those reported previously by Wilson and Evans (1983). They demonstrate longitudinal tonotopicity with a gradient of approximately 3.6 mm/octave. When allowances are made for the nonlinear mechanisms previously demonstrated in active hook region preparations (Cooper and Rhode, 1992), the data are also consistent with the tonotopic map derived from the intracellular dye-filling studies of Liberman (1982). C1 UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. CR COOPER NP, 1992, BASILAR MEMBRANE MEC, V63, P163 HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 KHANNA SM, 1986, HEARING RES, V23, P55, DOI 10.1016/0378-5955(86)90175-9 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KHANNA SM, 1986, HEARING RES, V23, P37, DOI 10.1016/0378-5955(86)90174-7 KOHLLOFFEL LUE, 1975, ARCH OTO-RHINO-LARYN, V209, P179, DOI 10.1007/BF00453773 LEONARD DGB, 1984, J ACOUST SOC AM, V75, P515, DOI 10.1121/1.390485 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 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 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 Wilson JP, 1983, MECH HEARING, P30 NR 14 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 NOV PY 1992 VL 63 IS 1-2 BP 191 EP 196 DI 10.1016/0378-5955(92)90084-Z PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100019 PM 1464570 ER PT J AU KOCH, T GLODDEK, B GUTZKE, S AF KOCH, T GLODDEK, B GUTZKE, S TI BINDING-SITES OF ATRIAL-NATRIURETIC-PEPTIDE (ANP) IN THE MAMMALIAN COCHLEA AND STIMULATION OF CYCLIC-GMP SYNTHESIS SO HEARING RESEARCH LA English DT Article DE ATRIAL NATRIURETIC PEPTIDE; CGMP; CAMP; STRIA VASCULARIS; G-PROTEINS ID PIG INNER-EAR; ADENYLATE-CYCLASE STIMULATION; GUINEA-PIG; VASOPRESSIN AB The distribution of binding sites for atrial natriuretic peptide (ANP) has been examined in frozen sections of the guinea pig inner ear by means of autoradiography. The highest density was found in the stria vascularis of all cochlear turns. In membrane preparations of stria vascularis in vitro, the production of the second messenger cGMP was strongly stimulated by synthetic ANP in a dose dependent manner. Adenylate cyclase was neither stimulated nor inhibited by ANP, thus suggesting. that the binding sites coincide with an ANP receptor, which is coupled to guanylate cyclase but not negatively coupled to an adenylate cyclase molecule. The production of cyclic GMP could not be reduced by GDP-betaS, a strong inhibitor of the G(s) protein. We conclude the existence of an ANP receptor-guanylate cyclase signal transfer system, similar to the beta2 receptor-adenylate cyclase system in the inner ear, without coupling to a G protein. ANP might play a role in sodium and water regulation of the endolymph and might antagonize the action of vasopressin. C1 UNIV HANNOVER,MED HSCH,DEPT OTORHINOLARNGOL,W-3000 HANNOVER,GERMANY. CR AHSLSTROM P, 1974, LARYNGOSCOPE, V85, P1241 ANANDSRIVASTAVA MB, 1986, BIOCHEM BIOPH RES CO, V138, P427, DOI 10.1016/0006-291X(86)90299-8 DOI K, 1992, HEARING RES, V58, P221, DOI 10.1016/0378-5955(92)90131-6 DOI K, 1990, EUR ARCH OTO-RHINO-L, V247, P16 ECKSTEIN F, 1979, J BIOL CHEM, V254, P9829 FRIEDL A, 1986, J NEUROCHEM, V46, P1522, DOI 10.1111/j.1471-4159.1986.tb01771.x FUJII K, 1986, J PHYSIOL-LONDON, V377, P315 GOETZ KL, 1988, AM J PHYSIOL, V254, P1 HAMET P, 1984, BIOCHEM BIOPH RES CO, V123, P515, DOI 10.1016/0006-291X(84)90260-2 HAMET P, 1986, J HYPERTENS, V4, P49 HEISLER S, 1986, MOL CELL ENDOCRINOL, V44, P125, DOI 10.1016/0303-7207(86)90054-7 KOCH T, 1988, ARCH OTO-RHINO-LARYN, V245, P82, DOI 10.1007/BF00481441 LAMPRECHT J, 1988, ARCH OTO-RHINO-LARYN, V245, P300, DOI 10.1007/BF00464636 MANTYH CR, 1986, HYPERTENSION, V8, P712 MEES K, 1989, LARYNGO RHINO OTOL, V68, P225, DOI 10.1055/s-2007-998323 ZUMGOTTESBERGE AMM, 1991, HEARING RES, V56, P86 MORI N, 1989, ACTA OTO-LARYNGOL, V107, P80, DOI 10.3109/00016488909127482 UMEMURA S, 1985, BIOCHEM BIOPH RES CO, V127, P943, DOI 10.1016/S0006-291X(85)80035-8 WINQUIST RJ, 1984, P NATL ACAD SCI-BIOL, V81, P7661, DOI 10.1073/pnas.81.23.7661 WINQUIST RJ, 1986, FASEB J, V45, P2371 ZENNER HP, 1979, ARCH OTO-RHINO-LARYN, V222, P275, DOI 10.1007/BF01261174 NR 21 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 1992 VL 63 IS 1-2 BP 197 EP 202 DI 10.1016/0378-5955(92)90085-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100020 PM 1334479 ER PT J AU GEISLER, CD AF GEISLER, CD TI 2-TONE SUPPRESSION BY A SATURATING FEEDBACK MODEL OF THE COCHLEAR PARTITION SO HEARING RESEARCH LA English DT Article DE MODEL; COCHLEA; SUPPRESSION; NONLINEAR; FEEDBACK ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; BASILAR-MEMBRANE; MAMMALIAN COCHLEA; AUDITORY-NERVE; RESPONSES; INNER AB A model of a small strip of cochlear partition was computer simulated. The model is composed of two elements, approximations to the transfer functions of an inner hair cell (IHC) and an outer hair cell (OHC), respectively. The IHC element was insensitive to DC stimulation. Input was one or two sinusoids. One sinusoid, at the characteristic frequency (CF), was multiplied by the gain of the 'cochlear amplifier'. A second sinusoid, representing a tone with much lower frequency, was not affected by the amplifier gain. This gain was determined by the OHC transfer function. In one form of the model ('fixed-gain'), this gain was set at a fixed number determined from the furthest point reached on the OHC transfer function. This form of the model produced very realistic single-tone responses as well as showing 'two-tone suppression': that is, the IHC DC response produced by CF stimulation was reduced when the lower-frequency sinusoid, at suitable intensities, was added to the stimulus. When a DC component was added to the two-tone stimulus, the magnitude of this two-tone suppression was enhanced. In the second form of the model ('variable-gain'), the cochlear-amplifier gain varied throughout the stimulus cycle. Its value was re-calculated at each instant, determined by the point on the OHC transfer function current at that particular instant. This form of the model showed two-tone suppression only when a DC component was added to the two-tone stimulus. C1 UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. RP GEISLER, CD (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706, USA. CR ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BRUNDIN L, 1991, NEUROSCI LETT, V128, P77, DOI 10.1016/0304-3940(91)90763-J CHEATHAM MA, 1992, HEARING RES, V60, P1, DOI 10.1016/0378-5955(92)90052-O DENG L, 1985, Journal of the Acoustical Society of America, V78, P1633, DOI 10.1121/1.392801 DOLAN DF, 1989, J ACOUST SOC AM, V86, P1007, DOI 10.1121/1.398091 GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 HALL JL, 1977, J ACOUST SOC AM, V61, P802, DOI 10.1121/1.381369 HILL KG, 1989, JHEAR RES, V639, P37 HILL KG, 1992, IN PRESS HEARING RES HIND JE, 1967, J NEUROPHYSIOL, V30, P794 JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 KIM DO, 1986, LECTURE NOTES BIOMAT, V64, P239 KIM DO, 1973, J ACOUST SOC AM, V54, P1517, DOI 10.1121/1.1914449 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 PATUZZI R, 1983, J ACOUST SOC AM, V74, P1734, DOI 10.1121/1.390282 PFEIFFER R R, 1970, Journal of the Acoustical Society of America, V48, P1373, DOI 10.1121/1.1912294 RHODE WS, 1992, UNPUB HEAR RES RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 SACHS MB, 1968, J ACOUST SOC AM, V45, P1025 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SELLICK PM, 1982, HEARING RES, V7, P199, DOI 10.1016/0378-5955(82)90014-4 YATES GK, 1989, COCHLEAR MECHANISMS, P177 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 ZWICKER E, 1986, J ACOUST SOC AM, V80, P146, DOI 10.1121/1.394175 NR 28 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 NOV PY 1992 VL 63 IS 1-2 BP 203 EP 211 DI 10.1016/0378-5955(92)90086-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JZ831 UT WOS:A1992JZ83100021 PM 1464571 ER PT J AU CHIMENTO, TC SCHREINER, CE AF CHIMENTO, TC SCHREINER, CE TI ADAPTATION AND RECOVERY FROM ADAPTATION OF THE AUDITORY-NERVE NEUROPHONIC (ANN) USING LONG DURATION TONES SO HEARING RESEARCH LA English DT Article DE FORWARD MASKING; COMPOUND ACTION POTENTIAL; PHASE LOCKING; CAT; TIME CONSTANT ID SHORT-TERM ADAPTATION; FREQUENCY-FOLLOWING RESPONSE; FIBER RESPONSES; MASKING; MODEL AB The time course of the interaction between adaptation and the recovery from adaptation of the auditory nerve neurophonic (ANN) responses was examined. The interaction between the process of recovery and the adaptation process of long probe tones which follow a masker. the so called whole tone recovery, was determined for the ANN response for different silent intervals between masker offset and probe onset. The auditory nerve neurophonic (ANN) reflects the ensemble response of phase-locked firing in single auditory nerve fibers to sustained signals. Consequently, neural response properties such as adaptation and recovery from adaptation of these coherent, time-locked responses can be studied. Recovery from adaptation was determined by recording the response of a 290 ms duration probe tone following a 100 ms masker tone, equal in frequency to the probe, ranging from -5 to 20 dB relative to the probe amplitude. Two different time patterns of the whole tone recovery were observed. If short silent intervals and/or loud maskers were used, the time course of the probe tone can be described as an exponential increase in amplitude toward a steady state expressed by the equation: A(tp) = A(ss) - Y(r) e(-tp/tauRr) ('ascending exponential'). For longer silent intervals and/or fainter maskers, the time course ot the probe tone can be described by an exponential decrease expressed by the equation: A(tp) = Y(r) e(-tp/tauRr) + Y(s) e(-tp/tauRs) + A(ss) ('declining exponential'). C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. CR ABBAS PJ, 1981, J ACOUST SOC AM, V69, P492, DOI 10.1121/1.385477 BRACHMAN ML, 1980, THESIS SYRACUSE U SY CHIMENTO TC, 1990, ELECTROEN CLIN NEURO, V75, P88, DOI 10.1016/0013-4694(90)90156-E CHIMENTO TC, 1990, J ACOUST SOC AM, V88, P857, DOI 10.1121/1.399735 CHIMENTO TC, 1991, J ACOUST SOC AM, V90, P263, DOI 10.1121/1.401296 EGGERMON.JJ, 1973, AUDIOLOGY, V12, P193 EGGERMON.JJ, 1973, AUDIOLOGY, V12, P221 EGGERMONT JJ, 1985, HEARING RES, V18, P57, DOI 10.1016/0378-5955(85)90110-8 GARDI J, 1979, AUDIOLOGY, V18, P353 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 HUANG CM, 1981, ELECTROEN CLIN NEURO, V52, P394, DOI 10.1016/0013-4694(81)90021-3 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 MOLLER A, 1988, HEARING RES, V38, P163 SMITH RL, 1979, J ACOUST SOC AM, V65, P166, DOI 10.1121/1.382260 SMITH RL, 1982, BIOL CYBERN, V44, P107, DOI 10.1007/BF00317970 SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 SMITH RL, 1975, BIOL CYBERN, V17, P169, DOI 10.1007/BF00364166 SNYDER RL, 1985, HEARING RES, V20, P45, DOI 10.1016/0378-5955(85)90058-9 SNYDER RL, 1984, HEARING RES, V15, P261, DOI 10.1016/0378-5955(84)90033-9 Spoor A., 1976, ELECTROCOCHLEOGRAPHY, P183 WESTERMAN LA, 1984, HEARING RES, V15, P249, DOI 10.1016/0378-5955(84)90032-7 WESTERMAN LA, 1985, THESIS SYRACUSE U SY YOUNG E, 1973, J ACOUST SOC AM, V54, P1535, DOI 10.1121/1.1914451 NR 23 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 1992 VL 62 IS 2 BP 131 EP 141 DI 10.1016/0378-5955(92)90178-P PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500001 PM 1429255 ER PT J AU REBILLARD, G LAVIGNEREBILLARD, M AF REBILLARD, G LAVIGNEREBILLARD, M TI EFFECT OF REVERSIBLE HYPOXIA ON THE COMPARED TIME COURSES OF ENDOCOCHLEAR POTENTIAL AND 2F1-F2 DISTORTION PRODUCTS SO HEARING RESEARCH LA English DT Article DE ACOUSTIC DISTORTION PRODUCT; HYPOXIA; COCHLEAR MICROMECHANICS; ENDOCOCHLEAR POTENTIAL ID OUTER HAIR-CELLS; STIMULATED ACOUSTIC EMISSIONS; ELECTROKINETIC SHAPE CHANGES; BASILAR-MEMBRANE; GUINEA-PIGS; EAR; RESPONSES; COCHLEA; MECHANICS; GERBIL AB In order to study the effects of a controlled hypoxia on the cochlear active mechanisms, the 2f1-f2 distortion product (DP) and the endocochlear potential (EP) were recorded simultaneously in the same ear, in guinea pigs artificially respired with gas mixtures containing different percentages of oxygen. The data show an important difference in the behavior of the two parameters. While the EP undergoes a reduction of amplitude starting shortly after the establishment of the hypoxia, reaches a steady state, and recovers monotonically after a return to normoxic conditions, the time course of the DP is more complex. Its level also declines shortly after the beginning of the hypoxia though it slightly lags behind the EP decline. After switching back to normoxic conditions, the DP rises with an eventual delay with respect to the EP, overshoots, and then dramatically falls again. A slow recovery subsequently takes place and normal values are reached within 5 to 10 min. These results indicate a certain independence of the DP versus the EP. During the exposure to hypoxic conditions, differences in the time course and in the variation of amplitude of the two recorded parameters seem to indicate that the DPs could be more related to the OHC physiology than to the EP. The DP post-hypoxia effect observed after a return to normoxic conditions, indicates that a normal EP is not sufficient for the generation of normal DPs. Different hypotheses which could explain the DP post-hypoxia effect are discussed. C1 UNIV MONTREAL,MONTREAL H3C 3J7,QUEBEC,CANADA. RP REBILLARD, G (reprint author), CHR ST CHARLES,NEUROBIOL AUDIT LAB,INSERM,U254,F-34059 MONTPELLIER 01,FRANCE. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ATTIAS J, 1990, HEARING RES, V45, P257 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 BROWN AM, 1985, HEARING RES, V19, P191, DOI 10.1016/0378-5955(85)90138-8 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CHOI DW, 1990, ANNU REV NEUROSCI, V13, P171, DOI 10.1146/annurev.ne.13.030190.001131 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 EYBALIN M, 1987, EXP BRAIN RES, V65, P261 EYBALIN M, 1989, ARCH OTO-RHINO-LARYN, V246, P228, DOI 10.1007/BF00463561 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUBBARD AE, 1983, SCIENCE, V222, P510, DOI 10.1126/science.6623090 ISHII D, 1969, ACTA OTO-LARYNGOL, V67, P573, DOI 10.3109/00016486909125484 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 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 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 KUJAWA SG, 1991, FEB ASS RES OT ST PE LAWRENCE M, 1977, ACTA OTO-LARYNGOL, V83, P146, DOI 10.3109/00016487709128825 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 LOTZ P, 1977, C I NATIONAL SANTE R, V68, P238 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 PUEL JL, 1991, IN PRESS ADV BIOSCIE PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 ROSOWSKI JJ, 1984, HEARING RES, V13, P141, DOI 10.1016/0378-5955(84)90105-9 RUBEL EW, 1992, IN PRESS HEAR RES RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SIEGEL JH, 1982, HEARING RES, V6, P173 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 ZUREK PM, 1985, J ACOUST SOC AM, V78, P340, DOI 10.1121/1.392496 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 ZWICKER E, 1981, HEARING RES, V4, P43, DOI 10.1016/0378-5955(81)90035-6 NR 39 TC 33 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 1992 VL 62 IS 2 BP 142 EP 148 DI 10.1016/0378-5955(92)90179-Q PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500002 PM 1429256 ER PT J AU WANGEMANN, P MARCUS, DC AF WANGEMANN, P MARCUS, DC TI THE MEMBRANE-POTENTIAL OF VESTIBULAR DARK CELLS IS CONTROLLED BY A LARGE CL- CONDUCTANCE SO HEARING RESEARCH LA English DT Article DE GERBIL; INNER EAR; POTASSIUM; CHLORIDE CHANNEL; PIRETANIDE ID NONSENSORY REGION; STRIA VASCULARIS; GERBIL UTRICLE; ENDOLYMPH; TRANSPORT; CHANNELS; INVITRO AB The K+ secretory epithelium of the vestibular labyrinth (dark cells) was impaled with glass microelectrodes in order to test the hypothesis that it contains a large Cl- conductance. In the first series of experiments, the short-circuited epithelium was perfused on both sides by a solution containing 150 mmol/1 Cl-. The membrane voltage (PD) was -18 +/- 1 mV (N = 101), showed a Gaussian distribution, and the estimated input resistance of the cell (R('cell')) was 17 +/- 3 MOMEGA. The PD responded to 10(-4) mol/l ouabain with a depolarization, suggesting the presence of a (Na+ + K+)-ATPase. The PD responses to Cl- steps yielded an apparent transference number t(Cl) = 0.34 +/- 0.03 (N = 65) and those to K+ steps yielded a t(K) = 0.16 +/- 0.01 (N = 48). In the second series of experiments, cells presumed to be Cl--depleted were impaled in Cl--free solutions. The distribution of the PD was not Gaussian; PDs as negative as -90 mV were observed. Cells with a highly negative PD also had a high R('cell'). With the addition of Cl- the PD collapsed to -19 +/- 1 mV and R collapsed to 16 +/- 3 MOMEGA (N = 145) which are not significantly different from values obtained in the first series of experiments when cells were impaled in a solution containing 150 mmol/l Cl-. Alternating the bath perfusate between Cl--free and Cl--containing solutions led to large PD transients. Cl--induced PD transients could be mimicked by other anions suggesting an ion selectivity of Cl- > Br- > NO3- > I - much greater than glutamate- = isethionate- = gluconate-. Cl--induced PD transients could not be abolished by a blocker of the Na+/Cl-/K+ cotransporter, 10(-4) mol/l piretanide (N = 5); by a blocker of various anion transport systems, 10(-3) Mol/l 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS; N = 2); or by several blockers of epithelial Cl-channels, 10(-4) mol/l 5-nitro-2(3-phenylpropylamino)-benzoic acid (NPPB; N = 2), and 10(-4) Mol/l dichloro-di-phenyl-amine-2-carboxylic acid (DCDPC; N = 2). In a solution containing 15 mmol/l Cl- the apparent transference numbers were t(CL) = 0.56 +/- 0.03 (N = 19) and t(K) = 0.44 +/- 0.02 (N = 66). The PD responses to K+ steps were not abolished by the K+ channel blockers barium, quinidine or TEA suggesting that the observed PD deflections were only partly due to a K+ conductance and that the apparent t(K) is overestimating the contribution of the K+ conductance. The response to piretanide was variable. However, in a solution containing 15 mmol/l Cl- hyperpolarizations up to -80 mV were observed. These results demonstrate that vestibular dark cells contain a dominating Cl- conductance and suggest that this Cl- conductance is a manifestation of a Cl- channel. RP WANGEMANN, P (reprint author), BOYS TOWN NATL RES HOSP,CELL PHYSIOL & BIOPHYS LAB,555 N 30TH ST,OMAHA,NE 68131, USA. RI Wangemann, Philine/N-2826-2013 CR BERNARD C, 1986, J PHYSIOL-LONDON, V371, P17 CHOU JTY, 1979, ACTA OTO-LARYNGOL, V88, P187, DOI 10.3109/00016487909137159 CHRISTENSEN O, 1989, PFLUG ARCH EUR J PHY, V415, P37, DOI 10.1007/BF00373139 FERRARY E, 1989, AM J PHYSIOL, V257, pF182 GREGER R, 1991, KIDNEY INT, V40, pS119 HOFFMANN EK, 1986, BIOCHIM BIOPHYS ACTA, V864, P1, DOI 10.1016/0304-4157(86)90014-6 Jahnke K, 1975, Acta Otolaryngol Suppl, V336, P1 KUNZELMANN K, 1989, PFLUG ARCH EUR J PHY, V415, P172, DOI 10.1007/BF00370589 LASSEN UV, 1971, J MEMBRANE BIOL, V6, P269, DOI 10.1007/BF02116574 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1987, HEARING RES, V30, P45 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 MARCUS D, 1988, FASEB J, V2, pA753 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 MORGENSTERN C, 1982, AM J OTOLARYNG, V3, P323, DOI 10.1016/S0196-0709(82)80004-5 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 SALT AN, 1987, LARYNGOSCOPE, V87, P984 SHIGA N, 1992, VESTIBULAR DARK CELL TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 TAKEUCHI S, 1992, CHLORIDE CHANNELS BA WANGEMANN P, 1990, DIURETICS, V3, P220 WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 WANGEMANN P, 1992, AM J PHYSIOL, V263, pC616 WANGEMANN P, 1989, MEMBRANE POTENTIAL M WANGEMANN P, 1986, PFLUG ARCH EUR J PHY, V407, pS128, DOI 10.1007/BF00584942 WANGEMANN P, 1989, PFLUG ARCH EUR J PHY, V414, P656, DOI 10.1007/BF00582132 WELCH MJ, 1983, J MEMBRANE BIOL, V71, P219 NR 28 TC 32 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 OCT PY 1992 VL 62 IS 2 BP 149 EP 156 DI 10.1016/0378-5955(92)90180-U PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500003 PM 1331015 ER PT J AU BERNSTEIN, LR TRAHIOTIS, C AF BERNSTEIN, LR TRAHIOTIS, C TI DETECTION OF ANTIPHASIC SINUSOIDS ADDED TO THE ENVELOPES OF HIGH-FREQUENCY BANDS OF NOISE SO HEARING RESEARCH LA English DT Article DE BINAURAL HEARING; MASKING-LEVEL DIFFERENCES; BINAURAL SLUGGISHNESS ID CORRELATION DISCRIMINATION; NARROW BANDS; DETECTABILITY; MASKING; DEPENDENCE; BANDWIDTH; DELAYS AB Listeners' sensitivities to antiphasic sinusoids added to the envelopes of high-frequency bands of noise were measured as a function of the frequency of the sinusoid and the bandwidth of the masking noise. The stimuli were constructed such that the added sinusoid produced interaural intensitive differences (IIDs) that fluctuated at a rate that was equal to the frequency of the sinusoid and was independent of the bandwidth of the masking noise. The data indicated that performance was relatively unaffected by the rate of modulation for rates between 5 and 160 Hz. Greater rates of modulation resulted in substantial degradations of performance. The results are pertinent to Zurek and Durlach's (1987) suggestions concerning the relatively small binaural masking-level differences typically measured with high-frequency signals and broadband maskers in the N0S(pi) configuration. Specifically, it appears that listeners' performance is greatly affected by an insensitivity to rapidly fluctuating IIDs but is relatively unaffected by any 'spectral interference' produced by masking energy beyond the monaural critical band. Interestingly, the data corroborate Grantham's (1984) insightful proposal that the binaural system may possess two independent averaging mechanisms, one for the processing of interaural temporal disparities (ITDs) and the other for the processing of IIDs. C1 UNIV CONNECTICUT,CTR HLTH,DEPT SURG OTOLARYNGOL,FARMINGTON,CT 06032. RP BERNSTEIN, LR (reprint author), UNIV CONNECTICUT,CTR HLTH,CTR NEUROL SCI,SURG RES CTR,FARMINGTON,CT 06030, USA. CR AMENTA CA, 1987, HEARING RES, V29, P147, DOI 10.1016/0378-5955(87)90163-8 BERNSTEIN LR, 1991, HEARING RES, V52, P189, DOI 10.1016/0378-5955(91)90198-I BERNSTEIN LR, 1992, J ACOUST SOC AM, V91, P306, DOI 10.1121/1.402773 Blauert J., 1983, SPATIAL HEARING BLAUERT J, 1986, J ACOUST SOC AM, V79, P806, DOI 10.1121/1.393471 BOURBON WT, 1966, THESIS U TEXAS AUSTI COLBURN HS, 1978, HEARING, V4 Davenport WB, 1958, INTRO THEORY RANDOM DURLACH NI, 1986, J ACOUST SOC AM, V79, P1548, DOI 10.1121/1.393681 DURLACH NI, 1972, F MODERN AUDITORY TH, V2 DURLACH NI, 1964, J ACOUST SOC AM, V36, P576, DOI 10.1121/1.1919006 GABRIEL KJ, 1981, J ACOUST SOC AM, V69, P1394, DOI 10.1121/1.385821 GABRIEL KJ, 1983, THESIS MIT CAMBRIDGE GLASBERG BR, 1990, HEARING RES, V47, P103, DOI 10.1016/0378-5955(90)90170-T GRANTHAM DW, 1978, J ACOUST SOC AM, V63, P511, DOI 10.1121/1.381751 GRANTHAM DW, 1984, J ACOUST SOC AM, V76, P71, DOI 10.1121/1.391009 HAFTER ER, 1971, J ACOUST SOC AM, V50, P1116, DOI 10.1121/1.1912743 HALL JW, 1983, J ACOUST SOC AM, V73, P894, DOI 10.1121/1.389013 HIRSH IJ, 1948, J ACOUST SOC AM, V20, P536, DOI 10.1121/1.1906407 HIRSH IJ, 1958, J ACOUST SOC AM, V30, P827, DOI 10.1121/1.1909781 JAIN M, 1991, J ACOUST SOC AM, V90, P1918, DOI 10.1121/1.401671 JEFFRESS LA, 1956, J ACOUST SOC AM, V28, P416, DOI 10.1121/1.1908346 LICKLIDER JCR, 1948, J ACOUST SOC AM, V20, P150, DOI 10.1121/1.1906358 MCFADDEN D, 1976, J ACOUST SOC AM, V59, P634, DOI 10.1121/1.380913 MCFADDEN D, 1966, J ACOUST SOC AM, V40, P1414, DOI 10.1121/1.1910241 MILLS AW, 1958, J ACOUST SOC AM, V30, P237, DOI 10.1121/1.1909553 OSMAN E, 1971, J ACOUST SOC AM, V50, P1494, DOI 10.1121/1.1912803 ROBINSON DE, 1972, PERCEPT PSYCHOPHYS, V12, P333, DOI 10.3758/BF03207216 SCHARF B, 1970, F MODERN AUDITORY TH, V1 SEVER JC, 1979, J ACOUST SOC AM, V66, P1343, DOI 10.1121/1.383528 SRINIVAS.R, 1971, J ACOUST SOC AM, V50, P616, DOI 10.1121/1.1912677 TRAHIOTIS C, 1990, J ACOUST SOC AM, V87, P810, DOI 10.1121/1.398892 TRAHIOTIS C, 1981, J ACOUST SOC AM S1, V69, pS63, DOI 10.1121/1.386148 TRAHIOTIS C, 1990, J ACOUST SOC AM, V87, P1359, DOI 10.1121/1.399513 WEBSTER FA, 1951, J ACOUST SOC AM, V23, P452, DOI 10.1121/1.1906787 WIGHTMAN FL, 1971, J ACOUST SOC AM, V50, P623, DOI 10.1121/1.1912678 ZUREK P M, 1985, Journal of the Acoustical Society of America, V78, pS18, DOI 10.1121/1.2022675 ZUREK PM, 1987, J ACOUST SOC AM, V81, P459, DOI 10.1121/1.394911 ZWICKER E, 1985, HEARING RES, V19, P29, DOI 10.1016/0378-5955(85)90096-6 NR 39 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 1992 VL 62 IS 2 BP 157 EP 165 DI 10.1016/0378-5955(92)90181-L PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500004 PM 1429257 ER PT J AU CODY, AR AF CODY, AR TI ACOUSTIC LESIONS IN THE MAMMALIAN COCHLEA - IMPLICATIONS FOR THE SPATIAL-DISTRIBUTION OF THE ACTIVE PROCESS SO HEARING RESEARCH LA English DT Article DE ACTIVE PROCESS; SPATIAL DISTRIBUTION; ACOUSTIC LESION ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; BASILAR-MEMBRANE; TUNING CURVES; MECHANICAL TRAUMA; RESPONSES; GANGLION; SUPPRESSION; THRESHOLDS; ELEMENTS AB The spatial contribution of mechanically active hair cells to tuning and sensitivity at a single point in the mammalian cochlea has been investigated in the basal turn of the guinea pig cochlea. Following the destruction of outer hair cells with acoustic overstimulation it was possible to record apparently normal tuning and sensitivity from spiral ganglion neurones innervating inner hair cells located on the apical edges of substantial lesions. The distance between the recording site, where neurones showed normal sensitivity, and areas of the cochlea showing 60-100% of the outer hair cells either damaged or missing varied between 0.2 and 1.3 mm which incorporates approximately 70 to 450 outer hair cells. In one animal neurones that demonstrated normal sensitivity were recorded within 0.2 nun of a lesion where 67% of the outer hair cells were either missing or showed severe damage to their stereocilia and within 0.5 mm of areas of the organ of Corti showing damage to 97% of the outer hair cells. This distance includes approximately 50 inner hair cells or 180 outer hair cells. The location of these neurones, whose sharp tuning presumably mirrors basilar membrane mechanics, suggests that a substantial proportion of point tuning in the cochlea may be derived over a distance of less than 0.5 mm and involve fewer than 200 active outer hair cells C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. RP CODY, AR (reprint author), UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,ST LUCIA,QLD 4072,AUSTRALIA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CODY AR, 1980, HEARING RES, V3, P3, DOI 10.1016/0378-5955(80)90004-0 CODY AR, 1980, ACTA OTO-LARYNGOL, V89, P440, DOI 10.3109/00016488009127160 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 Dallos P, 1973, BASIC MECHANISMS HEA, P335 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DEBOER E, 1983, J ACOUST SOC AM, V73, P567, DOI 10.1121/1.389002 DIEPENDAAL RJ, 1987, J ACOUST SOC AM, V82, P917, DOI 10.1121/1.395290 DIEPENDAAL RJ, 1986, J ACOUST SOC AM, V80, P124, DOI 10.1121/1.394460 Evans EF, 1976, J PHYSIOL-LONDON, V256, P43 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 KIM DO, 1980, PSYCHOPHYSICAL PHYSL, P242 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 MOUNTAIN DC, 1986, NEUROBIOLOGY HEARING, P77 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 PATUZZI R, 1984, HEARING RES, V13, P19, DOI 10.1016/0378-5955(84)90091-1 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 ROBERTSON D, 1979, J ACOUST SOC AM, V66, P466, DOI 10.1121/1.383097 ROBERTSO.D, 1974, J COMP PHYSIOL, V91, P363, DOI 10.1007/BF00694467 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 ROBERTSON D, 1981, J ACOUST SOC AM, V69, P1096, DOI 10.1121/1.385689 ROBERTSON D, 1980, J OTOLARYNGOL SOC AU, V4, P285 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 ROBLES L, 1989, COCHLEAR MECH STRUCT, P369 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SIEGAL JH, 1981, HEARING RES, V6, P171 WEIDERHOLD ML, 1970, J ACOUST SOC AM, V48, P966 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 35 TC 31 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 OCT PY 1992 VL 62 IS 2 BP 166 EP 172 DI 10.1016/0378-5955(92)90182-M PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500005 PM 1429258 ER PT J AU DODD, F CAPRANICA, RR AF DODD, F CAPRANICA, RR TI A COMPARISON OF ANESTHETIC AGENTS AND THEIR EFFECTS ON THE RESPONSE PROPERTIES OF THE PERIPHERAL AUDITORY-SYSTEM SO HEARING RESEARCH LA English DT Article DE ANESTHESIA; AUDITORY PHYSIOLOGY; REPTILES ID BRAIN-STEM; KETAMINE; NEURONS; RABBIT; TONES AB Anesthetic agents were compared in order to identify the most appropriate agent for use during surgery and electrophysiological recordings in the auditory system of the tokay gecko (Gekko gecko). Each agent was first screened for anesthetic and analgesic properties and, if found satisfactory, it was subsequently tested in electrophysiological recordings in the auditory nerve. The following anesthetic agents fulfilled our criteria and were selected for further screening: sodium pentobarbital (60 mg/kg); sodium pentobarbital (30 mg/kg) and oxymorphone (1 mg/kg); 3.2% isoflurane; ketamine (440 mg/kg) and oxymorphone (I mg/kg). These agents were subsequently compared on the basis of their effect on standard response properties of auditory nerve fibers. Our results verified that different anesthetic agents can have significant effects on most of the parameters commonly used in describing the basic response properties of the auditory system in vertebrates. We therefore conclude from this study that the selection of an appropriate experimental protocol is critical and must take into consideration the effects of anesthesia on auditory responsiveness. In the tokay gecko, we recommend 3.2% isoflurane for general surgical procedures; and for electrophysiological recordings in the eighth nerve we recommend barbituate anesthesia of appropriate dosage in combination if possible with an opioid agent to provide additional analgesic action. C1 CORNELL UNIV,NEUROBIOL & BEHAV SECT,W-255 SEELEY G MUDD HALL,ITHACA,NY 14853. CR BARKER JL, 1973, SCIENCE, V182, P720, DOI 10.1126/science.182.4113.720 BERGJOHNSEN J, 1986, ACTA PHYSIOL SCAND, V128, P613, DOI 10.1111/j.1748-1716.1986.tb08019.x BOBBIN RP, 1979, ARCH OTOLARYNGOL, V105, P467 BORG E, 1975, ACTA PHYSIOL SCAND, V94, P327, DOI 10.1111/j.1748-1716.1975.tb05893.x CARLSSON KH, 1986, NEUROSCI LETT, V71, P356, DOI 10.1016/0304-3940(86)90647-6 CHURCH MW, 1987, BRAIN RES, V403, P72, DOI 10.1016/0006-8993(87)90124-7 COHEN MS, 1982, ANESTH ANALG, V61, P338 COLLINS JG, 1986, ANESTH ANALG, V65, P1123 EATOCK RA, 1981, J COMP PHYSIOL, V142, P203 EVANS EF, 1973, EXP BRAIN RES, V17, P402 HILL KG, 1989, HEARING RES, V39, P37, DOI 10.1016/0378-5955(89)90080-4 KULLI J, 1991, TINS, V41, P6 KUWADA S, 1989, J NEUROPHYSIOL, V61, P269 MARGOLIASH D, 1983, J NEUROSCI, V3, P1039 OLSEN RW, 1982, ANNU REV PHARMACOL, V22, P245, DOI 10.1146/annurev.pa.22.040182.001333 OSHIMA E, 1988, EUR J PHARMACOL, V148, P25, DOI 10.1016/0014-2999(88)90450-5 PASTERNAK GW, 1988, JAMA-J AM MED ASSOC, V259, P1362, DOI 10.1001/jama.259.9.1362 SANDERS RA, 1979, J OTOLARYNGOL, V8, P24 Short C. E., 1987, PRINCIPLES PRACTICE SINEX DG, 1981, HEARING RES, V4, P127, DOI 10.1016/0378-5955(81)90001-0 SMOLDERS JWT, 1986, HEARING RES, V24, P89, DOI 10.1016/0378-5955(86)90052-3 SULLIVAN WE, 1986, P NATL ACAD SCI USA, V83, P8400, DOI 10.1073/pnas.83.21.8400 TURNER RG, 1987, HEARING RES, V26, P287, DOI 10.1016/0378-5955(87)90064-5 VRIESLANDER JD, 1990, J ACOUST SOC AM, V87, pS25, DOI 10.1121/1.2028142 WILKINSON L, 1987, SYSYAT SYSTEM STATIS WILLOW M, 1983, INT REV NEUROBIOL, V24, P15, DOI 10.1016/S0074-7742(08)60219-6 NR 26 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 OCT PY 1992 VL 62 IS 2 BP 173 EP 180 DI 10.1016/0378-5955(92)90183-N PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500006 PM 1429259 ER PT J AU JONES, TA NELSON, RC AF JONES, TA NELSON, RC TI RECOVERY OF VESTIBULAR FUNCTION FOLLOWING HAIR CELL DESTRUCTION BY STREPTOMYCIN SO HEARING RESEARCH LA English DT Article DE VESTIBULAR RECOVERY; CHICK; AMINOGLYCOSIDES; HAIR CELL REGENERATION; OTOTOXICITY ID PULSED LINEAR ACCELERATION; AVIAN INNER-EAR; ACOUSTIC TRAUMA; REGENERATION; CHICK AB Can the vestibular periphery of warm-blooded vertebrates recover functionally from severe sensory hair cell loss? Recent findings in birds suggest a mechanism for recovery but in fact no direct functional evidence has been reported. We produced vestibular hair cell lesions using the ototoxic agent streptomycin sulfate (600 mg/kg/day, 8 days, chicks, Gallus domesticus). Compound action potentials of the vestibular nerve were used as a direct measure of peripheral vestibular function. Vestibular thresholds, neural activation latencies and amplitudes were documented. Eight days of drug treatment elevated thresholds significantly (P < 0.001) and eliminated all but remnants of vestibular activity. Virtually complete physiological recovery occurred in all animals studied over a period of 70 days following treatment. Thresholds recovered within two weeks of drug treatment whereas the return of response morphologies including activation latencies and amplitudes required an additional 6-8 weeks. RP JONES, TA (reprint author), UNIV NEBRASKA,MED CTR,COLL DENT,DEPT ORAL BIOL,40TH & HOLDREGE ST,LINCOLN,NE 68583, USA. CR CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 HASHINO E, 1989, J ACOUST SOC AM, V85, P289, DOI 10.1121/1.397736 HASHINO E, 1988, J ACOUST SOC AM, V83, P2450, DOI 10.1121/1.396325 JONES TA, 1992, ELECTROEN CLIN NEURO, V82, P377, DOI 10.1016/0013-4694(92)90007-5 JONES TA, 1989, J NEUROSCI METH, V27, P115, DOI 10.1016/0165-0270(89)90094-0 JONES TA, 1989, AM J OTOLARYNG, V10, P327, DOI 10.1016/0196-0709(89)90108-7 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 NAZARETH AM, 1991, NEUR ABS, V17, P29 NAZARETH AM, 1991, THESIS U NEBRASKA ME ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WEISLEDER P, 1992, EXP NEUROL, V115, P2, DOI 10.1016/0014-4886(92)90211-8 WEISLEDER P, 1990, ELECTROEN CLIN NEURO, V76, P362, DOI 10.1016/0013-4694(90)90037-K NR 15 TC 47 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 OCT PY 1992 VL 62 IS 2 BP 181 EP 186 DI 10.1016/0378-5955(92)90184-O PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500007 PM 1429260 ER PT J AU COHEN, YE BACON, CK SAUNDERS, JC AF COHEN, YE BACON, CK SAUNDERS, JC TI MIDDLE-EAR DEVELOPMENT-III - MORPHOMETRIC CHANGES IN THE CONDUCTING APPARATUS OF THE MONGOLIAN GERBIL SO HEARING RESEARCH LA English DT Article DE MIDDLE-EAR; ANATOMY; DEVELOPMENT; MONGOLIAN GERBIL ID ONTOGENY; COCHLEA; FREQUENCY; 2-DEOXYGLUCOSE; MAP AB Middle-ear structural ontogeny was examined in 12 age groups of Mongolian gerbils between 2 and 42 days after birth. Measurements of tympanic membrane surface area; depth of the tympanic membrane cone; the lengths of the malleus and incus long processes; and stapes footplate, annular space, and oval window areas were obtained using video micrographs and computer digitization techniques. The incus long process matured first at 3.5 days after birth, while the pars flaccida surface area was the last middle-ear variable studied to reach adult size (26 days after birth). The incus long process increased its length by 30% from 0.5 mm to 0.65 mm. The malleus long process, however, demonstrated much more relative growth (47%). Pars tensa area expanded from 6.35 mm2 at two days after birth to its adult size of 16.9 mm2 and the stapes footplate expanded by 50%. The developmental changes observed in middle-ear anatomy are then discussed with regard to their contribution to the functional maturation of both the middle ear and more central auditory function. C1 UNIV PENN,DEPT BIOENGN,5 SILVERSTEIN ORL,3400 SPRUCE ST,PHILADELPHIA,PA 19104. UNIV PENN,DEPT OTORHINOLARYNGOL,PHILADELPHIA,PA 19104. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 COHEN YE, 1992, J MORPHOL, V212, P257, DOI 10.1002/jmor.1052120305 COHEN YE, 1991, ABSTR ASS RES OT, V14, P121 DOAN DE, 1992, ABSTR ASS RES OT, V15, P144 ECHTELER SM, 1987, NEUR ABSTR, V13, P540 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 HARRIS DM, 1990, HEARING RES, V50, P1, DOI 10.1016/0378-5955(90)90029-O HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HOROWITZ P, 1980, ART ELECTRONICS HUNGFU M, 1983, J MORPHOL, V176, P249 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 LAY DOUGLAS, 1972, J MORPHOL, V138, P41, DOI 10.1002/jmor.1051380103 LYNCH TJ, 1981, THESIS MIT CAMBRIDGE MCGUIRT JP, 1992, ABST ASS RES OT, V15, P312 MCGUIRT JP, 1991, ABST ASS RES OT, V14, P79 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W RELKIN EM, 1979, J ACOUST SOC AM, V66, P133, DOI 10.1121/1.383066 RELKIN EM, 1980, ACTA OTO-LARYNGOL, V90, P6, DOI 10.3109/00016488009131692 RUBEL EW, 1984, ANNU REV PHYSIOL, V46, P213 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RYAN AF, 1982, EXP BRAIN RES, V47, P428 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SANES DH, 1988, J NEUROSCI, V8, P682 THOMAS JP, 1990, OTOLARYNG HEAD NECK, V103, P427 VRETTAKOS PA, 1988, AM J OTOLARYNG, V9, P58, DOI 10.1016/S0196-0709(88)80009-7 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 WOOLF NK, 1986, AM J PHYSIOL, V250, pR493 WOOLF NK, 1988, HEARING RES, V35, P131, DOI 10.1016/0378-5955(88)90112-8 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 32 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 1992 VL 62 IS 2 BP 187 EP 193 DI 10.1016/0378-5955(92)90185-P PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500008 PM 1429261 ER PT J AU FREDELIUS, L WERSALL, J AF FREDELIUS, L WERSALL, J TI HAIR CELL-DAMAGE AFTER CONTINUOUS AND INTERRUPTED PURE-TONE OVERSTIMULATION - A SCANNING ELECTRON-MICROSCOPIC STUDY IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE ACOUSTIC TRAUMA; COCHLEAR DAMAGE; SCANNING ELECTRON MICROSCOPY ID THRESHOLD SHIFT; IMPULSE NOISE; EXPOSURE; COCHLEA AB In our earlier investigations [Fredelius et al., Hear. Res. 30, 157-167 (1987)] acoustic trauma was studied after continuous 3.85-kHz pure tone exposures of different intensities and durations. In the present investigation, the importance of the introduction of a break during longer 3.85-kHz pure tone exposures was studied. Female pigmented guinea pigs were exposed to 108, 114, or 120 dB SPL for 6 h with or without a 1-h break after the first 3 h. Four weeks after exposure the cochleas were prepared for scanning electron microscopy and the resulting hair cell damage was evaluated according to a 4-grade damage scale. Significant differences could be demonstrated in the hair cell damage in the animals exposed to continuous acoustic overstimulation and those exposed to intermittent overstimulation. The importance of rest periods to decrease hair cell damage during long periods of acoustic overstimulation was clearly demonstrated. RP FREDELIUS, L (reprint author), KAROLINSKA INST,KAROLINSKA HOSP,DEPT OTOLARYNGOL,S-10401 STOCKHOLM 60,SWEDEN. CR BLAKESLEE EA, 1978, J ACOUST SOC AM, V63, P876, DOI 10.1121/1.381767 BOHNE BA, 1987, HEARING RES, V29, P251, DOI 10.1016/0378-5955(87)90172-9 BREDBERG G, 1970, SCIENCE, V170, P861, DOI 10.1126/science.170.3960.861 FREDELIUS L, 1987, HEARING RES, V30, P157, DOI 10.1016/0378-5955(87)90133-X FREDELIUS L, 1988, THESIS STOCKHOLM HENDERSON D, 1979, J ACOUST SOC AM, V65, P1231, DOI 10.1121/1.382790 LIBERMAN MC, 1984, HEARING RES, V16, P33, DOI 10.1016/0378-5955(84)90023-6 MALICK LE, 1975, SCAN ELECTRON MICR, V1, P269 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MORRISON D, 1975, ACTA OTO-LARYNGOL, V79, P11, DOI 10.3109/00016487509124649 MURAKAMI T, 1974, Archivum Histologicum Japonicum, V36, P189 NILSSON P, 1982, NEW PERSPECTIVES NOI, P69 ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 SOUDIJN ER, 1976, ANN OTOL RHINOL LA S, V29, P1 STOPP PE, 1983, HEARING RES, V11, P55, DOI 10.1016/0378-5955(83)90045-X Ward W. D., 1976, EFFECTS NOISE HEARIN, P407 WARD W D, 1971, Journal of the Acoustical Society of America, V49, P91, DOI 10.1121/1.1976136 NR 17 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 1992 VL 62 IS 2 BP 194 EP 198 DI 10.1016/0378-5955(92)90186-Q PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500009 PM 1429262 ER PT J AU UEDA, H HATTORI, T SAWAKI, M NIWA, H YANAGITA, N AF UEDA, H HATTORI, T SAWAKI, M NIWA, H YANAGITA, N TI THE EFFECT OF FUROSEMIDE ON EVOKED OTOACOUSTIC EMISSIONS IN GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSION; GUINEA PIG; FUROSEMIDE ID STIMULATED ACOUSTIC EMISSIONS; HAIR-CELLS; COCHLEAR; RESPONSES; EARS AB After recording transiently evoked otoacoustic emissions (TEOAEs) to a click stimulus in guinea pigs by using the IL088 which was developed by Bray and Kemp (1987) for easy recording and analysis of TEOAE, the changes after intravenous administration of furosemide (30 mg/kg or 50 mg/kg) were examined. The wave of the TEOAE could be detected from 20 of 24 ears (83%). After the i.v. injection of furosemide (30 mg/kg), TEOAE powers (total echo power and highest peak power in FFT pictures) decreased quickly and showed minimum values after 5-10 min. Then they increased rapidly and recovered normally within 60 min after injection. However, no ears showed TEOAEs during the 5- to 10-min period following the injection of the 50-mg/kg dose of furosemide. They then recovered slowly as compared with the group treated with the lower dose of furosemide (30 mg/kg). These changes are similar to those of the endocochlear potential (EP) after furosemide injection. These data support the notion that the EP can contribute to the mechanism of TEOAE generation. RP UEDA, H (reprint author), NAGOYA UNIV,SCH MED,DEPT OTORHINOLARYNGOL,65 TSURUMAI CHO,SHOWA KU,NAGOYA,AICHI 466,JAPAN. CR ANDERSON SD, 1979, ARCH OTO-RHINO-LARYN, V224, P47, DOI 10.1007/BF00455223 AVAN P, 1990, HEARING RES, V44, P151, DOI 10.1016/0378-5955(90)90077-3 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 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 COMIS SD, 1990, ACTA OTO-LARYNGOL, V109, P49, DOI 10.3109/00016489009107414 INAMURA N, 1991, OTOL JPN, V1, P40 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 KIANG NYS, 1986, HEARING RES, V22, P171 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 WILSON JP, 1983, P INT UNION PHYSL SC, V15, P100 WIT HP, 1982, HEARING RES, V8, P1, DOI 10.1016/0378-5955(82)90030-2 WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P457, DOI 10.3109/00016488809119501 ZWICKER E, 1981, HEARING RES, V4, P43, DOI 10.1016/0378-5955(81)90035-6 NR 20 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 OCT PY 1992 VL 62 IS 2 BP 199 EP 205 DI 10.1016/0378-5955(92)90187-R PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500010 PM 1429263 ER PT J AU HEFFNER, RS HEFFNER, HE AF HEFFNER, RS HEFFNER, HE TI HEARING AND SOUND LOCALIZATION IN BLIND MOLE RATS (SPALAX-EHRENBERGI) SO HEARING RESEARCH LA English DT Article DE EVOLUTION; SUBTERRANEAN; AUDIOGRAM; VISION; COMPARATIVE; RODENT ID SEISMIC COMMUNICATION; VOCAL COMMUNICATION; GUINEA-PIG; SENSITIVITY; PERCEPTION; SPECIATION; EVOLUTION; MOUSE AB Two blind mole rats were tested for their ability to detect and localize sound. The results indicate that blind mole rats have severely limited, and probably degenerate, auditory abilities. Although their 60-dB low-frequency hearing limit of 54 Hz is within the range for other rodents, the highest frequency they can hear at a level of 60 dB SPL is only 5.9 kHz, giving them the poorest high-frequency sensitivity yet observed in any mammal. In addition they have poor sensitivity as indicated by the fact that their lowest threshold is only 32 dB SPL (at 1 kHz). Finally, they are unable to localize brief sounds but retain a rudimentary ability to localize sounds of 0.5 s or longer. These results, combined with those of previous studies of subterranean species (i.e., blind mole rats, naked mole rats, and pocket gophers), suggest that poor auditory sensitivity, the loss of high-frequency hearing, and an inability to localize brief sounds is a degenerate state which may be characteristic of subterranean mammals. Thus it appears that an exclusive adaptation to a subterranean lifestyle (where airborne sound propagates poorly and where directional responses are limited by the tunnels) can result in vestigial auditory abilities just as the absence of light results in vestigial vision. RP HEFFNER, RS (reprint author), UNIV TOLEDO,DEPT PSYCHOL,TOLEDO,OH 43606, USA. CR BRONCHTI G, 1989, J COMP NEUROL, V284, P253, DOI 10.1002/cne.902840209 BRONCHTI G, 1991, DEV BRAIN RES, V58, P159, DOI 10.1016/0165-3806(91)90002-Z BRUNS V, 1988, HEARING RES, V33, P1, DOI 10.1016/0378-5955(88)90017-2 BURDA H, 1990, EVOLUTION SUBTERRANE, P269 CAPRANICA RR, 1973, J ACOUST SOC AM, V54, pS121 CONESA J, 1991, ASS RES OT ABSTR, V14, P24 DEJONG WW, 1990, EVOLUTION SUBTERRANE, P383 Fay R. R., 1988, HEARING VERTEBRATES HEFFNER H, 1980, J ACOUST SOC AM, V68, P1584, DOI 10.1121/1.385213 HEFFNER HE, 1985, J COMP PSYCHOL, V99, P275, DOI 10.1037//0735-7036.99.3.275 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 HEFFNER RS, 1990, HEARING RES, V48, P231, DOI 10.1016/0378-5955(90)90063-U Heffner R. S., 1990, COMP PERCEPTION, VI, P285 HEFFNER RS, 1992, J COMP NEUROL, V317, P219, DOI 10.1002/cne.903170302 HEFFNER RS, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P691 HEFFNER RS, 1991, ABSTR ASS RES OTOLAR, V14, P24 HEFFNER RS, 1991, HEARING RES, V55, P109 HEFFNER RS, 1990, HEARING RES, V46, P239, DOI 10.1016/0378-5955(90)90005-A HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 HEFFNER RS, 1992, ARO ABSTR, V15, P50 HEFFNER RS, UNPUB HETEROCEPHALUS HEFFNER RS, 1989, ASS RES OT ABSTR, V12, P233 HETH G, 1986, EXPERIENTIA, V42, P1287, DOI 10.1007/BF01946426 HETH G, 1987, BEHAV ECOL SOCIOBIOL, V21, P31, DOI 10.1007/BF00324432 HETH G, 1988, J MAMMAL, V69, P121, DOI 10.2307/1381755 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KNUDSEN EI, 1989, J NEUROSCI, V9, P3306 MASTERTO.B, 1969, J ACOUST SOC AM, V45, P966, DOI 10.1121/1.1911574 MOONEY SE, 1990, ASS RES OT ABSTR, V13, P176 MUSICANT AD, 1984, J ACOUST SOC AM, V75, P1195, DOI 10.1121/1.390770 NEVO E, 1979, ANNU REV ECOL SYST, V10, P269, DOI 10.1146/annurev.es.10.110179.001413 NEVO E, 1991, P NATL ACAD SCI USA, V88, P1256, DOI 10.1073/pnas.88.4.1256 NEVO E, 1987, P NATL ACAD SCI USA, V84, P3312, DOI 10.1073/pnas.84.10.3312 Nevo E., 1961, Mammalia Paris, V25, P127, DOI 10.1515/mamm.1961.25.2.127 NEVO E, 1990, BEHAVIOUR, V114, P249, DOI 10.1163/156853990X00158 PEVET P, 1984, J EXP ZOOL, V232, P41, DOI 10.1002/jez.1402320106 RADO R, 1989, HEARING RES, V41, P23, DOI 10.1016/0378-5955(89)90175-5 RADO R, 1987, ANIM BEHAV, V35, P1249, DOI 10.1016/S0003-3472(87)80183-5 RADO R, 1991, ANIM BEHAV, V42, P15, DOI 10.1016/S0003-3472(05)80601-3 RAPHAEL Y, 1991, J COMP NEUROL, V314, P367, DOI 10.1002/cne.903140211 ROFFLER SK, 1968, J ACOUST SOC AM, V43, P1255, DOI 10.1121/1.1910976 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SANYAL S, 1990, INVEST OPHTH VIS SCI, V31, P1398 SAUNDERS JC, 1979, ASSESSMENT HEARING A, P487 SAVIC IR, 1990, EVOLUTION SUBTERRANE, P120 THOMPSON GC, 1978, J NEUROPHYSIOL, V41, P1183 THOMPSON M, 1990, BEHAV RES METH INSTR, V22, P449, DOI 10.3758/BF03203193 WITHINGTONWRAY DJ, 1990, EUR J NEUROSCI, V2, P682, DOI 10.1111/j.1460-9568.1990.tb00458.x NR 48 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 OCT PY 1992 VL 62 IS 2 BP 206 EP 216 DI 10.1016/0378-5955(92)90188-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500011 PM 1429264 ER PT J AU BOETTCHER, FA SPONGR, VP SALVI, RJ AF BOETTCHER, FA SPONGR, VP SALVI, RJ TI PHYSIOLOGICAL AND HISTOLOGICAL-CHANGES ASSOCIATED WITH THE REDUCTION IN THRESHOLD SHIFT DURING INTERRUPTED NOISE EXPOSURE SO HEARING RESEARCH LA English DT Article DE NOISE INDUCED HEARING LOSS; HAIR CELLS; COCHLEA; COMPOUND ACTION POTENTIAL; COCHLEAR MICROPHONIC; SCANNING ELECTRON MICROSCOPY ID CHRONIC COCHLEAR PATHOLOGY; GUINEA-PIG COCHLEA; HEARING-LOSS; HAIR-CELLS; ACOUSTIC TRAUMA; TUNING CURVES; STEREOCILIA DAMAGE; PERIODIC REST; NERVE-FIBERS; OVERSTIMULATION AB The compound action potential (AP) was recorded from one group of chinchillas exposed to interrupted noise (95 dB SPL, octave band centered at 500 Hz, 3 h on, 9 h off) for 15 days. A second group of chinchillas was exposed to the same interrupted noise for 1, 2 or 15 days and their cochleas were analyzed by scanning electron microscopy (SEM). During the first few days of the exposure, the AP threshold was elevated approximately 40 dB at the low-to-mid frequencies; however, the threshold shifts decreased with increasing exposure duration so that the threshold shift was only about 10 dB after the 15th day of exposure. The amplitude of the AP also recovered with exposure time. In contrast to the improvement in A.P threshold, the number of missing hair cells increased and the condition of the stereocilia on inner and outer hair cells deteriorated between the first and 15th day of the exposure. C1 SUNY BUFFALO,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214. SO ILLINOIS UNIV,SCH MED,DEPT SURG,DIV OTOLARYNGOL,SPRINGFIELD,IL 62708. CR AREHOLE S, 1989, AUDIOLOGY, V28, P92 BOETTCHER FA, 1987, EAR HEARING, V8, P192, DOI 10.1097/00003446-198708000-00003 BOHNE BA, 1986, J ACOUST SOC AM, V80, P1729, DOI 10.1121/1.394285 BYRNE C, 1988, RECENT ADV RES COMBI, P239 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CANLON B, 1992, NOISE INDUCED HEARIN, P489 CARDER H M, 1971, Transactions of the American Academy of Ophthalmology and Oto-Laryngology, V75, P1346 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 CLARK WW, 1989, ABSTR ASS RES OT, P218 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X COLLETTI V, 1986, BASIC APPL ASPECTS N, P247 COTANCHE DA, 1987, HEARING RES, V30, P197, DOI 10.1016/0378-5955(87)90136-5 CRANE HD, 1983, HEARING RES THEORY, V2, P126 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 FIORINO FG, 1989, VALSALVA S1, V54, P36 GRATTON MA, 1990, HEARING RES, V50, P211, DOI 10.1016/0378-5955(90)90046-R Hamernik RP, 1980, SCAND AUDIOL SS, VS12, P128 HENDERSON D, 1992, NOISE INDUCED HEARIN, P476 HENDERSON D, 1973, J ACOUST SOC AM, V48, P513 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 HUMES LE, 1984, J ACOUST SOC AM, V76, P1318, DOI 10.1121/1.391447 LIBERMAN MC, 1986, BASIC APPL ASPECTS N, P163 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, 1982, NEW PERSPECTIVES NOI, P109 MILLER JD, 1963, ACTA OTOLARYNGOL S, V176 MULROY MJ, 1990, HEARING RES, V49, P79, DOI 10.1016/0378-5955(90)90096-8 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 Rajan R, 1992, NOISE INDUCED HEARIN, P429 RAJAN R, 1983, HEARING RES, V9, P279, DOI 10.1016/0378-5955(83)90032-1 RAPHAEL Y, 1991, HEARING RES, V53, P173, DOI 10.1016/0378-5955(91)90052-B ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 SALVI R, 1980, HEARING RES, V2, P335, DOI 10.1016/0378-5955(80)90067-2 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SALVI RJ, 1982, AM J OTOLARYNG, V3, P408, DOI 10.1016/S0196-0709(82)80018-5 SALVI RJ, 1983, HEARING RES, V10, P37, DOI 10.1016/0378-5955(83)90017-5 SALVI RJ, 1979, HEARING RES, V1, P237, DOI 10.1016/0378-5955(79)90017-0 SAUNDERS JC, 1977, J ACOUST SOC AM, V61, P558, DOI 10.1121/1.381298 SAUNDERS JC, 1986, HEARING RES, V23, P245, DOI 10.1016/0378-5955(86)90113-9 SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 SUBRAMANIAM M, 1991, HEARING RES, V56, P65, DOI 10.1016/0378-5955(91)90154-2 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 WARD WD, 1970, J ACOUST SOC AM, V48, P561, DOI 10.1121/1.1912172 ZAKRISSO.JE, 1974, AUDIOLOGY, V13, P231 NR 48 TC 53 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 OCT PY 1992 VL 62 IS 2 BP 217 EP 236 DI 10.1016/0378-5955(92)90189-T PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500012 PM 1429265 ER PT J AU SUNOSE, H IKEDA, K SAITO, Y NISHIYAMA, A TAKASAKA, T AF SUNOSE, H IKEDA, K SAITO, Y NISHIYAMA, A TAKASAKA, T TI MEMBRANE-POTENTIAL MEASUREMENT IN ISOLATED OUTER HAIR-CELLS OF THE GUINEA-PIG COCHLEA USING CONVENTIONAL MICROELECTRODES SO HEARING RESEARCH LA English DT Article DE COCHLEA; OUTER HAIR CELL; MICROELECTRODE; MEMBRANE POTENTIAL; NA+, K+ ATPASE; K+ PERMEABILITY; NA+ PERMEABILITY ID INTRACELLULAR-RECORDINGS; MECHANICAL RESPONSES; SUPPORTING CELLS; POTASSIUM-IONS; CELLULAR BASIS; NA+,K+-ATPASE; OUABAIN; NA+; K+; CURRENTS AB Membrane potential of the isolated outer hair cells (OHCs) from the guinea pig cochlea was measured using conventional microelectrodes filled with 200 mM KCl. The resting membrane potential during superfusion with the standard physiological saline solution containing 3.5 mM K+ was -47.3 +/- 1.4 mV (N = 72), which was higher than those previously reported for isolated OHCs studied by using microelectrodes. Addition of ouabain (10(-5) - 10(-3) M), the specific Na+, K+ ATPase inhibitor, depolarized the cell slowly and progressively, indicating the presence of low but definite Na+, K+ ATPase activity in the plasma membrane of OHCs. The magnitude of membrane potential was mainly dependent on the extracellular K+ concentration ([K+]O). A ten-fold increase of [K+]O depolarized the membrane potential by 49.6 +/- 1.0 mV (N = 58). A decrease of [Na+]O to one tenth of the control hyperpolarized the membrane potential by about 2 mV. Decreasing extracellular Cl-from 131.3 mM to 27.5 mM did not cause a significant change in the membrane potential. Using the Goldman-Hodgkin-Katz equation, assuming a negligible contribution of Cl- to the membrane potential and total monovalent cat ion concentration of the cytosol similar to the extracellular fluid, we calculated the permeability ratio of K+ versus Na+ to 131 +/- 19 and intracellular K+ concentration to 33.3 +/- 1.9 mM. C1 TOHOKU UNIV,SCH MED,DEPT PHYSIOL,SENDAI,MIYAGI 980,JAPAN. RP SUNOSE, H (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,1-1 SEIRYO MACHI,AOBAKU,SENDAI,MIYAGI 980,JAPAN. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Ashmore J F, 1988, Prog Brain Res, V74, P3 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BLATT MR, 1983, J MEMBRANE BIOL, V72, P223, DOI 10.1007/BF01870589 BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1990, J NEUROSCI, V10, P1388 FROMM M, 1981, J MEMBRANE BIOL, V62, P239, DOI 10.1007/BF01998169 GADSBY DC, 1985, NATURE, V315, P63, DOI 10.1038/315063a0 GITTER AH, 1987, PFLUG ARCH S1, V408, pR58 GITTER AH, 1990, HEARING RES, V45, P87, DOI 10.1016/0378-5955(90)90185-R GITTER A H, 1987, Pfluegers Archiv European Journal of Physiology, V408, pR71 GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 GLYNN IM, 1975, ANNU REV PHYSIOL, V37, P13, DOI 10.1146/annurev.ph.37.030175.000305 HAMA K, 1977, J NEUROCYTOL, V6, P1, DOI 10.1007/BF01175410 HARADA Y, 1988, ADV OTO-RHINO-LARYNG, V44, P7 HODGKIN AL, 1949, J PHYSL, V108, P33 HODGKIN AL, 1959, J PHYSIOL-LONDON, V148, P127 HUDSPETH AJ, 1985, SCIENCE, V230, P745, DOI 10.1126/science.2414845 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 IKEDA K, 1992, J PHYSIOL-LONDON, V447, P627 IKEDA K, 1990, EUR ARCH OTO-RHINO-L, V247, P43 IKEDA K, 1992, IN PRESS PFLUGERS AR IWANO T, 1990, J HISTOCHEM CYTOCHEM, V38, P225 Jahnke K, 1975, Acta Otolaryngol Suppl, V336, P1 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, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P348, DOI 10.1007/BF00588213 MATSUI H, 1982, J BIOCHEM-TOKYO, V92, P193 MESS K, 1983, ACTA OTOLARYNGOL, V95, P277 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 OESTERLE EC, 1989, J ACOUST SOC AM, V86, P1013, DOI 10.1121/1.398092 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 PALMER LG, 1977, J MEMBRANE BIOL, V33, P41, DOI 10.1007/BF01869511 ROBINSON JD, 1979, BIOCHIM BIOPHYS ACTA, V549, P145, DOI 10.1016/0304-4173(79)90013-2 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SMITH CA, 1954, LARYNGOSCOPE, V64, P141 SUNOSE H, 1991, ABSTR ASS RES OT, P14 THOMPSON SM, 1982, J MEMBRANE BIOL, V66, P41, DOI 10.1007/BF01868480 ULFENDAHL M, 1988, ARCH OTO-RHINO-LARYN, V245, P237, DOI 10.1007/BF00463935 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 51 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 1992 VL 62 IS 2 BP 237 EP 244 DI 10.1016/0378-5955(92)90190-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JU265 UT WOS:A1992JU26500013 PM 1429266 ER PT J AU KUIJPERS, W TONNAER, ELGM PETERS, TA RAMAEKERS, FCS AF KUIJPERS, W TONNAER, ELGM PETERS, TA RAMAEKERS, FCS TI DEVELOPMENTALLY-REGULATED COEXPRESSION OF VIMENTIN AND CYTOKERATINS IN THE RAT INNER-EAR SO HEARING RESEARCH LA English DT Article DE INTERMEDIATE FILAMENTS; VIMENTIN; CYTOKERATIN; RAT; INNER EAR; DEVELOPMENT ID INTERMEDIATE-FILAMENT PROTEINS; MONOCLONAL-ANTIBODIES; CO-EXPRESSION; SURGICAL PATHOLOGY; EPITHELIAL-CELLS; CULTURED-CELLS; GUINEA-PIG; KERATINS; MOUSE; DIFFERENTIATION AB In the present study the expression of vimentin-type intermediate filament proteins and cytokeratins was studied immunohistochemically in the rat inner ear from 12 days postconception up to 40 days after birth. With the use of a broad spectrum monoclonal antibody, cytokeratin expression was found to be present in the whole epithelial lining except for the sensory cells, throughout all the developmental stages examined. Vimentin was detected in the mesenchymal cells, the mesenchyme-derived tissues and the intermediate cells of the stria vascularis, confirming their origin from melanocyte precursor cells. In addition, the coexpression of vimentin and cytokeratins in the epithelial lining of the membranous inner ear was found to be developmentally regulated. During the final stages of differentiation, vimentin expression disappeared from the majority of the cell types. In the mature cochlea the coexpression of vimentin and cytokeratins was still found in the supporting cells of the organ of Corti, in the cells of Claudius and in external sulcus cells. As far as we could conclude from this study, the sensory cells showed only vimentin expression but not cytokeratin expression. A possible relationship between vimentin expression in adult epithelial cells of the inner ear and a specialised function of these cells is discussed. C1 UNIV LIMBURG,DEPT MOLEC CELL BIOL,6200 MD MAASTRICHT,NETHERLANDS. RP KUIJPERS, W (reprint author), CATHOLIC UNIV NIJMEGEN,DEPT OTORHINOLARYNGOL,PH VAN LEYDENLAAN 15,6500 HB NIJMEGEN,NETHERLANDS. CR ANNIKO M, 1987, ACTA OTOLARYNGOL S, V437, P49 ANNIKO M, 1986, ORL J OTO-RHINO-LARY, V48, P98 ARNOLD W, 1990, LARYNGO RHINO OTOL, V69, P24, DOI 10.1055/s-2007-998135 BENZEEV A, 1984, J CELL BIOL, V99, P1424, DOI 10.1083/jcb.99.4.1424 CZERNOBILSKY B, 1985, EUR J CELL BIOL, V37, P175 Franke W W, 1982, Cold Spring Harb Symp Quant Biol, V46 Pt 1, P431 HENZENLOGMANS SC, 1987, VIRCHOWS ARCH A, V410, P347, DOI 10.1007/BF00711291 HOLTHOFER H, 1984, LAB INVEST, V50, P552 KASPER M, 1989, ACTA HISTOCHEM, V86, P85 KASPER M, 1987, ARCH OTO-RHINO-LARYN, V244, P66, DOI 10.1007/BF00453494 KASPER M, 1989, DIFFERENTIATION, V40, P207, DOI 10.1111/j.1432-0436.1989.tb00600.x KHONG TY, 1986, CELL TISSUE RES, V246, P189 KUIJPERS W, 1991, HISTOCHEMISTRY, V96, P511, DOI 10.1007/BF00267077 KUIPERS W, 1991, HEARING RES, V52, P133 LANE EB, 1983, NATURE, V303, P701, DOI 10.1038/303701a0 LAROCCA PJ, 1984, CANCER RES, V44, P2991 MCLEAN IW, 1974, J HISTOCHEM CYTOCHEM, V22, P1077 MUIJEN GNP, 1987, LAB INVEST, V57, P359 OESTERLE EC, 1990, HEARING RES, V47, P1, DOI 10.1016/0378-5955(90)90162-I OSBORN M, 1984, ANN NY ACAD SCI, V455, P669 OSBORN M, 1984, EUR J CELL BIOL, V34, P137 OSBORN M, 1983, LAB INVEST, V48, P372 PARANKO J, 1986, DEV BIOL, V117, P135, DOI 10.1016/0012-1606(86)90356-8 RAMAEKERS F, 1987, EXP CELL RES, V170, P235, DOI 10.1016/0014-4827(87)90133-9 RAMAEKERS F, 1990, AM J PATHOL, V136, P641 RAMAEKERS FCS, 1983, J CLIN INVEST, V71, P635, DOI 10.1172/JCI110810 RAMAEKERS FCS, 1983, P NATL ACAD SCI-BIOL, V80, P2618, DOI 10.1073/pnas.80.9.2618 RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x SATO M, 1985, CANCER RES, V45, P3878 SCHROTT A, 1988, ARCH OTO-RHINO-LARYN, V245, P250, DOI 10.1007/BF00463937 SCHROTT A, 1987, ACTA OTO-LARYNGOL, V103, P451 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 TONNAER EL, 1990, J HISTOCHEM CYTOCHEM, V38, P1223 Traub P., 1985, INTERMEDIATE FILAMEN VERHAGEN APM, 1988, PROSTATE, V13, P25, DOI 10.1002/pros.2990130104 VIEBAHN C, 1987, DIFFERENTIATION, V34, P175, DOI 10.1111/j.1432-0436.1987.tb00065.x VIEBAHN C, 1988, CELL TISSUE RES, V253, P553 VIRTANEN I, 1981, J CELL SCI, V50, P45 WANG E, 1985, INTERMEDIATE FILAMEN, P455 WIKSTROM SO, 1988, ACTA OTO-LARYNGOL, V106, P71, DOI 10.3109/00016488809107373 NR 40 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 SEP PY 1992 VL 62 IS 1 BP 1 EP 10 DI 10.1016/0378-5955(92)90197-U PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700001 PM 1385376 ER PT J AU TACHIBANA, M MORIOKA, H AF TACHIBANA, M MORIOKA, H TI GLUCURONIC ACID-CONTAINING GLYCOSAMINOGLYCANS OCCUR IN OTOCONIA - CYTOCHEMICAL EVIDENCE BY HYALURONIDASE-GOLD LABELING SO HEARING RESEARCH LA English DT Article DE GLYCOSAMINOGLYCANS; HYALURONIDASE-GOLD; OTOCONIA; UTRICLE; MONGOLIAN GERBIL ID INNER-EAR AB Localization of glucuronic acid-containing glycosaminoglycans in the gerbil utricle was examined, using a hyaluronidase-gold labeling technique with special emphasis on the otoconia. Otoconia and the gelatinous layer of the otoconial membrane were strongly labeled by hyaluronidase-gold. The secretory granules in supporting cells were also strongly labeled, suggesting that the organic matrix of otoconia is secreted from the supporting cells. Otoconia seem to lose labeling while they degenerated. The degenerating otoconia were observed to be absorbed into dark cells. Glucuronic acid-containing glycosaminoglycans occur in otoconia. These glycosaminoglycans may play a crucial role in the formation and degeneration of otoconia. C1 MEIJI COLL ORIENTAL MED,DEPT OTOLARYNGOL,KYOTO,JAPAN. KYOTO PREFECTURAL UNIV MED,ELECTRON MICROSCOPY LAB,KYOTO 602,JAPAN. CR BELANGER LF, 1960, CALCIFICATION BIOL S, P151 BELANGER LF, 1956, SCIENCE, V123, P1074, DOI 10.1126/science.123.3207.1074 BELANGER LF, 1953, SCIENCE, V118, P520, DOI 10.1126/science.118.3070.520 DODGSON KS, 1968, CARBOHYD METABOL, V1, P169 FRENS G, 1973, NATURE-PHYS SCI, V241, P20 GILLOYZAGA P, 1985, HEARING RES, V18, P269, DOI 10.1016/0378-5955(85)90043-7 HULTCRANTZ M, 1985, AM J OTOLARYNG, V6, P79, DOI 10.1016/S0196-0709(85)80044-2 IGARASHI M, 1969, ACTA OTO-LARYNGOL, V68, P420, DOI 10.3109/00016486909121580 KHAN KM, 1990, HEARING RES, V43, P149, DOI 10.1016/0378-5955(90)90224-D Lim DJ, 1984, ULTRASTRUCTURAL ATLA, P245 Lim D J, 1984, Ann Otol Rhinol Laryngol Suppl, V112, P17 Lim D J, 1973, Ann Otol Rhinol Laryngol, V82, P23 LONDONO I, 1988, J HISTOCHEM CYTOCHEM, V36, P1005 MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 ROSS MD, 1973, ANAT REC, V175, P429 ROSS MD, 1985, AUDITORY BIOCH, P500 SHRADER RE, 1973, TERATOLOGY, V8, P257, DOI 10.1002/tera.1420080305 VISTRUP T, 1954, ANN OTO RHINOL LARYN, V63, P151 WISLOCKI GB, 1955, J ANAT, V78, P3 Yamane H, 1984, Acta Otolaryngol Suppl, V406, P263 NR 20 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 SEP PY 1992 VL 62 IS 1 BP 11 EP 15 DI 10.1016/0378-5955(92)90198-V PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700002 PM 1429247 ER PT J AU SHORE, SE GODFREY, DA HELFERT, RH ALTSCHULER, RA BLEDSOE, SC AF SHORE, SE GODFREY, DA HELFERT, RH ALTSCHULER, RA BLEDSOE, SC TI CONNECTIONS BETWEEN THE COCHLEAR NUCLEI IN GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE HORSERADISH PEROXIDASE-WHEAT-GERM AGGLUTININ; CONTRALATERAL COCHLEAR NUCLEUS; VENTRAL COCHLEAR NUCLEUS; DORSAL COCHLEAR NUCLEUS; COMMISSURAL CONNECTIONS; BINAURAL HEARING ID SUPERIOR OLIVARY COMPLEX; DESCENDING PROJECTIONS; NEURONAL ARCHITECTURE; CAT; DORSAL; CELLS; ORGANIZATION; CHINCHILLA; RESPONSES AB This study provides a detailed analysis of the appearances and distributions of neurons projecting from one cochlear nucleus to the other. Injections of wheatgerm agglutinin conjugated to horseradish peroxidase were made into ventral or dorsal cochlear nucleus of the guinea pig. Retrogradely labeled cells in the opposite cochlear nucleus were examined and quantified. Three major categories of labeled cells were discerned on the basis of their soma shape: elongate, round-to-oval, and polygonal. All injections resulted in widespread labeling of cells in all of these categories, but especially round-to-oval cells, in the opposite ventral cochlear nucleus and sparse labeling in the dorsal cochlear nucleus. The results suggest that there is a significant cochlear nucleus commissural projection involving heterogeneous cell types which could have diverse functions in binaural auditory signal processing. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP SHORE, SE (reprint author), MED COLL OHIO,DEPT OTOLARYNGOL,TOLEDO,OH 43699, USA. CR ADAMS JC, 1976, J COMP NEUROL, V11, P49 ADAMS JC, 1983, J COMP NEUROL, V215, P275, DOI 10.1002/cne.902150304 ALTSCHULER RA, 1986, BRAIN RES, V369, P316, DOI 10.1016/0006-8993(86)90542-1 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 CANT NB, 1982, J COMP NEUROL, V212, P313, DOI 10.1002/cne.902120308 CANT NB, 1979, NEUROSCIENCE, V4, P1925, DOI 10.1016/0306-4522(79)90066-6 CANT NB, 1984, HEARING SCI RECENT A, P371 CANT NB, 1981, NEUROSCIENCE, V6, P2643, DOI 10.1016/0306-4522(81)90109-3 Godfrey DA, 1988, AUDITORY PATHWAY, P107 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 HACKNEY CM, 1990, ANAT EMBRYOL, V182, P123 HARRISON JM, 1966, J COMP NEUROL, V126, P15 HARRISON JM, 1962, J COMP NEUROL, V119, P341, DOI 10.1002/cne.901190306 HOCHFELD PR, 1973, THESIS MIT CAMBR KLINKE R, 1969, PFLUG ARCH EUR J PHY, V306, P165, DOI 10.1007/BF00586883 MAST TE, 1970, J NEUROPHYSIOL, V33, P108 MAST TE, 1973, BRAIN RES, V62, P61, DOI 10.1016/0006-8993(73)90619-7 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 MOORE JK, 1986, NEUROBIOLOGY HEARING, P283 MOREST D. KENT, 1968, BRAIN RES, V9, P288, DOI 10.1016/0006-8993(68)90235-7 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 PFALZ REINHARD K. J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1472, DOI 10.1121/1.1918372 PIRSIG W, 1968, Archiv fuer Klinische und Experimentelle Ohren- Nasen- und Kehlkopfheilkunde, V192, P333, DOI 10.1007/BF00411129 PIRSIG W, 1968, Kumamoto Medical Journal, V21, P75 SHORE SE, 1991, HEARING RES, V52, P255, DOI 10.1016/0378-5955(91)90205-N SHORE SE, 1985, J ACOUST SOC AM, V78, P1286, DOI 10.1121/1.392898 STOTLER WA, 1953, J COMP NEUROL, V98, P401, DOI 10.1002/cne.900980303 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3013, DOI 10.1016/0306-4522(82)90227-5 TSUCHITANI C, 1977, J NEUROPHYSIOL, V40, P296 VANNOORT J, 1969, PSYCHIAT NEUROL NEUR, V72, P109 WENTHOLD RJ, 1987, BRAIN RES, V415, P183, DOI 10.1016/0006-8993(87)90285-X WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 NR 34 TC 79 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 SEP PY 1992 VL 62 IS 1 BP 16 EP 26 DI 10.1016/0378-5955(92)90199-W PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700003 PM 1385377 ER PT J AU GAO, WY DING, DL ZHENG, XY RUAN, FM LIU, YJ AF GAO, WY DING, DL ZHENG, XY RUAN, FM LIU, YJ TI A COMPARISON OF CHANGES IN THE STEREOCILIA BETWEEN TEMPORARY AND PERMANENT HEARING LOSSES IN ACOUSTIC TRAUMA SO HEARING RESEARCH LA English DT Article DE ACOUSTIC TRAUMA; STEREOCILIA; TEMPORARY THRESHOLD SHIFT; PERMANENT THRESHOLD SHIFT; CUTICULAR PLATE ID GUINEA-PIG COCHLEA; SERIAL-SECTION RECONSTRUCTION; ULTRASTRUCTURAL-CHANGES; CUTICULAR PLATES; IMPULSE NOISE; ORGAN; CORTI; THRESHOLD; EXPOSURE; DAMAGE AB A comparison of stereociliary changes at different post-exposure intervals in ears with temporary and permanent hearing losses has been made. Twenty guinea pigs were exposed to either 110 dB SPL broadband white noise for 30 min (N = 10) or 120 dB SPL white noise for 150 min (N = 10). The recovery patterns for threshold shifts for both groups were systematically assessed at regular post-exposure intervals for 80 days, using the auditory cortex evoked response to tone bursts between 0.5 and 8kHz. Thirty-two animals that had been exposed to the same noise at either 110 dB for 30 min (N = 16) or 120 dB for 150 min (N = 16) were decapitated for scanning electron microscopic examination at the same post-exposure intervals. The threshold shifts induced by 110 dB noise were reversible while those induced by 120 dB were generally irreversible, although extreme variabilities existed among the animals. In the acute TTS ears, damage was confined to the third row of OHCs, where only the tips of the stereocilia were affected. Neither discontinuity of cuticular plate nor expelled cytoplasm was found in these cells. In the lesions of PTS, either all the three rows of OHCs or the IHCs and the first row of OHCs were involved. The entire length of the stereocilia, more severe in the lower part was always damaged. Expelled cytoplasm and fusion between stereocilia were frequently seen. In the chronic TTS ears, no abnormalities of stereocilia were found while in the PTS ears, a complete absence of the organ of Corti was noticed. The results of the present study clearly suggest that the status of the lower part of the stereocilia and the continuity of the cuticular plate play an important role in determining the reversibility of threshold shifts. C1 RENJI HOSP,DEPT OTOLARYNGOL,SHANGHAI,PEOPLES R CHINA. RP GAO, WY (reprint author), CHANG ZHENG HOSP,DEPT OTOLARYNGOL,HEARING RES LAB,972 XIANG YIN RD,SHANGHAI 200433,PEOPLES R CHINA. CR BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DUVALL AJ, 1967, ANN OTO RHINOL LARYN, V76, P688 ENGSTROM B, 1983, HEARING RES, V12, P251, DOI 10.1016/0378-5955(83)90110-7 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P81, DOI 10.3109/00016488809107374 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P373, DOI 10.3109/00016488809122260 GAO WY, 1991, HEARING RES, V54, P296 HUNTERDUVAR IM, 1977, SCANNING ELECTRON MI, V2 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 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, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PICKLES JO, 1987, HEARING RES, V25, P173, DOI 10.1016/0378-5955(87)90089-X ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 SLEPECKY N, 1982, ACTA OTO-LARYNGOL, V93, P329, DOI 10.3109/00016488209130890 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 THORNE PR, 1986, HEARING RES, V21, P41, DOI 10.1016/0378-5955(86)90044-4 THORNE PR, 1984, ACTA OTO-LARYNGOL, V97, P69, DOI 10.3109/00016488409130966 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 NR 25 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 SEP PY 1992 VL 62 IS 1 BP 27 EP 41 DI 10.1016/0378-5955(92)90200-7 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700004 PM 1429249 ER PT J AU MCCREERY, DB YUEN, TGH AGNEW, WF BULLARA, LA AF MCCREERY, DB YUEN, TGH AGNEW, WF BULLARA, LA TI STIMULATION WITH CHRONICALLY IMPLANTED MICROELECTRODES IN THE COCHLEAR NUCLEUS OF THE CAT - HISTOLOGIC AND PHYSIOLOGICAL-EFFECTS SO HEARING RESEARCH LA English DT Article DE CAT; COCHLEAR NUCLEUS; ELECTRIC STIMULATION; MICROELECTRODES; MICROSTIMULATION; NEURAL DAMAGE ID DEFINED CHARGE-DENSITIES; ELECTRICAL-STIMULATION; NERVOUS-SYSTEM; ELECTRODES; INJECTION; SALINE AB The effects of several hours of continuous electrical stimulation in the cats' cochlear nucleus with chronically implanted activated iridium microelectrodes was investigated from the changes in the evoked response near the inferior colliculus and also by histologic evaluation of the stimulated tissue. The stimulating microelectrodes had geometric surface areas of 75-500 mu m2. They were pulsed continuously for 4 h, at a pulse repetition rate of 200 Hz, using charge-balanced pulse pairs. The charge per phase was 1.8 or 3.6 nC/ph. The animals were sacrificed for histologic evaluation 2 h, or several days later. The only remarkable histologic change resulting from the 4 h of stimulation was some aggregation of lymphocytes at the site of stimulation. However, depression of the electrical excitability of neurons near the sites often persisted for several days after 4 h of stimulation at 3.6 nC/phase. The charge per phase of the stimulus pulse pair was correlated strongly with the depression of excitability, and there was a weaker correlation between the depression and the amplitude of the first phase of voltage transient induced across the electrode-tissue interface. The charge density, calculated from the geometric surface area of the stimulating electrodes, was poorly correlated with the severity of the depression. The findings suggest a means of detecting impending stimulation-induced neural damage while it is still reversible. RP MCCREERY, DB (reprint author), HUNTINGTON MED RES INST,NEUROL RES LAB,734 FAIRMOUNT AVE,PASADENA,CA 91105, USA. CR ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W 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 BEEBE X, 1988, IEEE T BIO-MED ENG, V35, P494, DOI 10.1109/10.2122 Bockris J., 1970, MODERN ELECTROCHEMIS BRUMMER SB, 1975, BIOELECTROCH BIOENER, V2, P13, DOI 10.1016/0302-4598(75)80002-X BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P59, DOI 10.1109/TBME.1977.326218 BULLARA LA, 1983, J NEUROSCI METH, V9, P15, DOI 10.1016/0165-0270(83)90104-8 Gorsuch R. L., 1983, FACTOR ANAL MCCREERY DB, 1986, EXP NEUROL, V92, P147, DOI 10.1016/0014-4886(86)90131-7 MCCREERY DB, 1990, IEEE T BIO-MED ENG, V37, P996, DOI 10.1109/10.102812 ROBBLEE LS, 1983, J ELECTROCHEM SOC, V130, P731, DOI 10.1149/1.2119793 Robblee L.S., 1990, NEURAL PROSTHESES ROBBLEE LS, 1990, NINDS N01NS82313 CON YUEN TGH, 1981, NEUROSURGERY, V9, P292 NR 15 TC 44 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 SEP PY 1992 VL 62 IS 1 BP 42 EP 56 DI 10.1016/0378-5955(92)90201-W PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700005 PM 1429250 ER PT J AU LIDAN, D YEDGAR, S BENARONSON, H SOHMER, H AF LIDAN, D YEDGAR, S BENARONSON, H SOHMER, H TI INFLUENCE OF EXPERIMENTALLY ELEVATED BLOOD-VISCOSITY ON THE AUDITORY NERVE-BRAIN-STEM EVOKED-RESPONSE AND THRESHOLD SO HEARING RESEARCH LA English DT Article DE BLOOD VISCOSITY; AUDITORY NERVE-BRAIN-STEM RESPONSE; POLYCYTHEMIA; HEMATOCRIT ID COCHLEAR ACTION-POTENTIALS; LASER-DOPPLER FLOWMETRY; HEMODILUTION AB Blood viscosity, due to its effect on blood flow, is one of the determinants of oxygen delivery. Therefore the influence of elevated blood viscosity on hearing was studied in rats using the auditory brainstem response (ABR) threshold, wave 1 latency, brainstem transmission time (BTT) and wave 1/4 amplitude ratio. Whole blood viscosity (WBV) was elevated by 15-21% in two different ways: elevating the hematocrit (Polycythemia) by acclimation in a hypobaric chamber, or elevating the plasma viscosity by infusing a solution of Polyvinylpyrrolidone-360 (PVP). ABR was recorded before and 24 h after the blood viscosity was elevated, so that each rat served as its own control. Paired t-tests showed that there was no statistically significant difference in the ABR parameters in each of the groups as a consequence of blood viscosity elevation. In conclusion, the elevation of WBV to this degree for this duration, using two different techniques had no effect either on the function of the auditory nerve and the more peripheral sites, or on the central auditory pathway as studied by ABR. C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 1172,IL-91010 JERUSALEM,ISRAEL. HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT BIOCHEM,IL-91010 JERUSALEM,ISRAEL. HADASSAH UNIV HOSP,DEPT ANESTHESIOL,JERUSALEM,ISRAEL. CR AFIFI A M, 1971, Journal of Laryngology and Otology, V85, P275, DOI 10.1017/S0022215100073424 Burton A., 1972, PHYSL BIOPHYSICS CIR CHARLESWORTH D, 1981, CLIN ASPECTS BLOOD V, P67 Chien S., 1984, HDB PHYSL 2, P217 DAVIS EC, 1965, LARYNGOSCOPE, V75, P1847 Dormandy J, 1981, CLIN ASPECTS BLOOD V, P67 Dormandy J A, 1970, Ann R Coll Surg Engl, V47, P211 GAFNI M, 1976, ACTA OTO-LARYNGOL, V82, P354, DOI 10.3109/00016487609120919 HAYNES RH, 1961, T SOC RHEOL, V5, P85 HILDESHEIMER M, 1982, HEARING RES, V8, P187, DOI 10.1016/0378-5955(82)90074-0 HILDESHEIMER M, 1990, CLIN HEMORHEOL, V10, P59 HULTCRANTZ E, 1987, AM J OTOLARYNG, V8, P16, DOI 10.1016/S0196-0709(87)80014-5 JANDLE JH, 1987, BLOOD TXB HEMATOLOGY NUTTALL AL, 1988, HEARING RES, V34, P215, DOI 10.1016/0378-5955(88)90001-9 SALMON SE, 1988, CECIL TXB INT MED, P1026 SCHMIDSCHONBEIN H, 1981, CLIN ASPECTS BLOOD V, P49 SCOTT H, 1983, PHYSICAL PHARM PHYSI, P592 SOHMER H, 1989, HEARING RES, V40, P87, DOI 10.1016/0378-5955(89)90102-0 SOHMER H, 1982, ELECTROEN CLIN NEURO, V53, P506, DOI 10.1016/0013-4694(82)90063-3 SOHMER H, 1986, ELECTROEN CLIN NEURO, V64, P328, DOI 10.1016/0013-4694(86)90156-2 STONE HO, 1968, AM J PHYSIOL, V214, P913 WELLS M, 1977, CLIN OTOLARYNGOL, V2, P327, DOI 10.1111/j.1365-2273.1977.tb01376.x YEDGAR S, 1985, AM J PHYSIOL, V248, pE10 YOFFEY JM, 1968, ANN NY ACAD SCI, V149, P179, DOI 10.1111/j.1749-6632.1968.tb15151.x Zar JH, 1984, BIOSTATISTICAL ANAL 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 SEP PY 1992 VL 62 IS 1 BP 57 EP 62 DI 10.1016/0378-5955(92)90202-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700006 PM 1429251 ER PT J AU NI, DF SHEPHERD, RK SELDON, HL XU, SA CLARK, GM MILLARD, RE AF NI, DF SHEPHERD, RK SELDON, HL XU, SA CLARK, GM MILLARD, RE TI COCHLEAR PATHOLOGY FOLLOWING CHRONIC ELECTRICAL-STIMULATION OF THE AUDITORY-NERVE .1. NORMAL HEARING KITTENS SO HEARING RESEARCH LA English DT Article DE COCHLEAR IMPLANTS; ELECTRICAL STIMULATION; COCHLEAR PATHOLOGY, ELECTRODE IMPEDANCE; ABR; EABR ID BRAIN-STEM RESPONSE; SPIRAL GANGLION; IMPLANT PATIENT; SCALA TYMPANI; AUDIOMETRY; MASKING; CELLS; TERM; DEAF AB The present study examines the histopathological effects of long-term intracochlear electrical stimulation in young normal hearing animals. Eight-week old kittens were implanted with scala tympani electrode arrays and stimulated for periods of up to 1500 h using charge balanced biphasic current pulses at charge densities in the range 21-52 muC cm-2 geom. per phase. Both click and electrically evoked auditory brainstem responses were periodically recorded to monitor the status of the hair cell and spiral ganglion cell populations. In addition, the impedance of the stimulating electrodes was measured daily to monitor their electrical characteristics during chronic implantation. Histopathological examination of the cochleas showed no evidence of stimulus induced damage to cochlear structures when compared with implanted, unstimulated control cochleas. Indeed, there was no statistically significant difference in the ganglion cell density adjacent to the stimulating electrodes when compared with a similar population in implanted control cochleas. In addition, hair cell loss, which was restricted to regions adjacent to the electrode array, was not influenced by the degree of electrical stimulation. These histopathological findings were consistent with the evoked potential recordings. Finally, electrode impedance data correlated well with the degree of tissue growth observed within the scala tympani. The present findings indicate that the young mammalian cochlea is no more susceptible to cochlear pathology following chronic implantation and electrical stimulation than is the adult. C1 UNIV MELBOURNE,DEPT OTOLARYNGOL,32 GISBORNE ST,MELBOURNE,VIC 3002,AUSTRALIA. RI Shepherd, Robert/I-6276-2012 CR AGNEW WF, 1983, NIH NS02319 PROGR RE BABB TL, 1977, J NEUROSURG, V47, P353, DOI 10.3171/jns.1977.47.3.0353 Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 CLARK GM, 1988, ACTA OTOLARYNGOL S, V448, P5 CLARK GM, 1984, ACTA OTO-LARYNGOL, P5 CLARK GM, 1991, EAR HEAR S, P15 CLARK GM, 1973, J LARYNGOL OTOL, V87, P92 CLARK GM, 1977, J LARYNGOL OTOL, V91, P185, DOI 10.1017/S0022215100083560 DAVIS H, 1984, AUDIOLOGY, V23, P59 DAWSON PW, 1992, J SPEECH HEAR RES, V35, P401 DODSON HC, 1987, HEARING RES, V31, P65, DOI 10.1016/0378-5955(87)90214-0 DODSON HC, 1986, NATURE, V320, P65, DOI 10.1038/320065a0 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 DOWELL RC, 1991, AM J OTOL, V12, P137 EVANS EF, 1982, AUDIOLOGY, V21, P204 FRANZ B, 1984, ACTA OTO-LARYNGOL, V410, P17 GYO K, 1988, ACTA OTO-LARYNGOL, V105, P248, DOI 10.3109/00016488809097005 HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U HARRISON JM, 1977, BRAIN BEHAV EVOLUT, V14, P87, DOI 10.1159/000125577 HOUSE WF, 1985, EAR HEARING, V6, P245 JOHNSSON LG, 1982, ANN OTO RHINOL LARYN, V91, P74 Leake PA, 1985, COCHLEAR IMPLANTS, P55 LEAKE PA, 1990, NEURAL PROSTHESES FU, P253 LEAKEJONES PA, 1983, ANN NY ACAD SCI, V405, P203, DOI 10.1111/j.1749-6632.1983.tb31634.x LINTHICUM FH, 1991, AM J OTOL, V12, P8 MARSH MA, 1992, AM J OTOL, V13, P241 Osberger M. J., 1991, EAR HEAR S, V12, P66 Patrick J., 1990, COCHLEAR PROSTHESES, p99 SCHINDLE.RA, 1974, ANN OTO RHINOL LARYN, V83, P202 SCHINDLER RA, 1977, ARCH OTOLARYNGOL, V103, P691 SCHUKNECHT HF, 1953, AMA ARCH OTOLARYNGOL, V58, P377 SELDON HL, 1991, BRAIN RES, V551, P185, DOI 10.1016/0006-8993(91)90932-L SHEPHERD RK, 1989, 7TH NIH PROGR REP NI Shepherd RK, 1990, COCHLEAR PROSTHESES, P69 SHEPHERD RK, 1990, NIH NONS72342 PROGR Shepherd R K, 1983, Acta Otolaryngol Suppl, V399, P19 SHEPHERD RK, 1991, ACTA OTO-LARYNGOL, V111, P848, DOI 10.3109/00016489109138421 SHEPHERD RK, 1985, HEARING RES, V18, P105, DOI 10.1016/0378-5955(85)90001-2 SHUTE SA, 1990, THESIS U MELBOURNE A SIMMONS FB, 1967, LARYNGOSCOPE, V77, P171, DOI 10.1288/00005537-196702000-00003 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 STYPULKOWSKI PH, 1986, OTOLARYNG CLIN N AM, V19, P249 SUTTON D, 1980, ANN OTO RHINOL LARYN, V89, P11 SUTTON D, 1983, ANN OTO RHINOL LARYN, V92, P53 WALSH SM, 1982, HEARING RES, V7, P266 XU SA, 1992, IN PRESS AM J OTOL ZAPPIA JJ, 1991, ANN OTO RHINOL LARYN, V100, P914 NR 47 TC 41 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 SEP PY 1992 VL 62 IS 1 BP 63 EP 81 DI 10.1016/0378-5955(92)90203-Y PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700007 PM 1429252 ER PT J AU TACHIBANA, M WILCOX, E YOKOTANI, N SCHNEIDER, M FEX, J AF TACHIBANA, M WILCOX, E YOKOTANI, N SCHNEIDER, M FEX, J TI SELECTIVE AMPLIFICATION AND PARTIAL SEQUENCING OF CDNAS ENCODING G-PROTEIN ALPHA-SUBUNITS FROM COCHLEAR TISSUES SO HEARING RESEARCH LA English DT Article DE G-PROTEIN; RNA; CDNA; POLYMERASE CHAIN REACTION; ORGAN OF CORTI; LATERAL WALL; COCHLEA ID PURIFIED MUSCARINIC RECEPTORS; INOSITOL PHOSPHATE FORMATION; POLYMERASE CHAIN-REACTION; ENZYMATIC AMPLIFICATION; RAT COCHLEA; GUINEA-PIG; SIGNAL TRANSDUCTION; MOLECULAR-CLONING; ADENYLATE-CYCLASE; DNA-POLYMERASE AB An approach utilizing the polymerase chain reaction (PCR) was devised to clone members of a family of cDNAs encoding the a subunit of G proteins in the cochlea. RNA was extracted from the whole cochlea of the mouse and from the organ of Corti or the lateral wall of the cochlea microdissected from the guinea pig cochlea. The RNA was reverse-transcribed to cDNA which was selectively amplified by PCR using degenerate primers corresponding to two conserved regions of the G protein coding sequence. PCR products were cloned into a plasmid for sequencing. The following seven cDNA clones of particular interest were obtained: three clones putatively coding for part of the alpha-subunit of a stimulatory G protein (G(S)), one clone putatively coding for part of the alpha-subunit of an inhibitory G protein (G(i)) and three clones putatively coding for part of the alpha-subunit of a transducin (G(t))-like protein. Possible functions in the cochlea of putative G proteins with alpha-subunits partly encoded by these cDNA clones are briefly discussed and future studies are suggested. RP TACHIBANA, M (reprint author), NIDOLD,MOLEC BIOL LAB,BLDG 36,ROOM 5D-08,BETHESDA,MD 20892, USA. CR AIYAR N, 1989, ARCH BIOCHEM BIOPHYS, V268, P698, DOI 10.1016/0003-9861(89)90338-X ASHKENAZI A, 1989, TRENDS PHARMACOL SCI, P16 BARTOLAMI S, 1990, HEARING RES, V47, P229, DOI 10.1016/0378-5955(90)90154-H BRAY P, 1986, P NATL ACAD SCI USA, V83, P8893, DOI 10.1073/pnas.83.23.8893 BURNSTOCK G, 1990, ANN NY ACAD SCI, V603, P1 GILMAN AG, 1987, ANNU REV BIOCHEM, V56, P615, DOI 10.1146/annurev.biochem.56.1.615 GOMPERTS BD, 1990, G PROTEINS, P601 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HAGA K, 1985, NATURE, V316, P731, DOI 10.1038/316731a0 HAGA K, 1986, J BIOL CHEM, V261, P133 HEILING JS, 1989, CURRENT PROTOCOLS MO HELMREICH EJM, 1985, TRENDS PHARMACOL SCI, V4, P438 HOMBURGER V, 1989, 26TH WORKSH INN EAR, P13 INNIS MA, 1988, P NATL ACAD SCI USA, V85, P9436, DOI 10.1073/pnas.85.24.9436 ITOH H, 1986, P NATL ACAD SCI USA, V83, P3776, DOI 10.1073/pnas.83.11.3776 ITOH H, 1988, J BIOL CHEM, V263, P6656 JONES DT, 1987, J BIOL CHEM, V262, P14241 JONES DT, 1989, SCIENCE, V244, P790, DOI 10.1126/science.2499043 KAZIRO Y, 1990, G PROTEINS MEDIATORS, P47 KINGSTON RE, 1989, CURRENT PROTOCOLS MO KOZASA T, 1988, P NATL ACAD SCI USA, V85, P2081, DOI 10.1073/pnas.85.7.2081 LIBERT F, 1989, SCIENCE, V244, P569, DOI 10.1126/science.2541503 LITOSCH I, 1990, INOSITOL PHOSPHATE M, P151 LOCHRIE MA, 1985, SCIENCE, V228, P96, DOI 10.1126/science.3856323 MATTERA R, 1986, FEBS LETT, V206, P36, DOI 10.1016/0014-5793(86)81336-9 MORI N, 1987, ACTA OTO-LARYNGOL, V104, P66, DOI 10.3109/00016488709109048 MORI N, 1989, ACTA OTO-LARYNGOL, V107, P80, DOI 10.3109/00016488909127482 MORI N, 1986, ACTA OTO-LARYNGOL, V101, P217, DOI 10.3109/00016488609132830 MULLIS K, 1986, COLD SPRING HARB SYM, V51, P263 NIEDZIELSKI A, 1991, ABSTR ASS RES OT, V14, P135 NIEDZIELSKI AS, 1991, THESIS OKAYAMA H, 1987, METHOD ENZYMOL, V154, P3 RALL T, 1987, FEBS LETT, V224, P365, DOI 10.1016/0014-5793(87)80486-6 RAPORT CJ, 1989, J BIOL CHEM, V264, P7122 SAIKI RK, 1985, SCIENCE, V230, P1350, DOI 10.1126/science.2999980 SAIKI RK, 1988, SCIENCE, V239, P487, DOI 10.1126/science.2448875 SANGER F, 1977, P NATL ACAD SCI USA, V74, P5463, DOI 10.1073/pnas.74.12.5463 SCHACHT J, 1985, HEARING RES, V20, P93 SHUGYO A, 1989, ORL J OTO-RHINO-LARY, V51, P156 SOKOLOVSKY M, 1980, BIOCHEM BIOPH RES CO, V94, P487, DOI 10.1016/0006-291X(80)91257-7 SULLIVAN KA, 1986, P NATL ACAD SCI USA, V83, P6687, DOI 10.1073/pnas.83.18.6687 TANABE T, 1985, NATURE, V315, P242, DOI 10.1038/315242a0 VANMEGEN YJB, 1988, BRAIN RES, V474, P185, DOI 10.1016/0006-8993(88)90682-8 WILBUR WJ, 1983, P NATL ACAD SCI-BIOL, V80, P726, DOI 10.1073/pnas.80.3.726 ZENNER HP, 1979, ARCH OTO-RHINO-LARYN, V222, P275, DOI 10.1007/BF01261174 NR 45 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 SEP PY 1992 VL 62 IS 1 BP 82 EP 88 DI 10.1016/0378-5955(92)90204-Z PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700008 PM 1429253 ER PT J AU MELICHAR, I GITTER, AH DARTSCH, PC ZENNER, HP AF MELICHAR, I GITTER, AH DARTSCH, PC ZENNER, HP TI CHARACTERIZATION OF MARGINAL AND CLAUDIUS CELLS GROWING FROM COCHLEAR EXPLANTS INVITRO SO HEARING RESEARCH LA English DT Article DE STRIA VASCULARIS; PRIMARY CELL CULTURE; MARGINAL CELLS; CLAUDIUS CELLS; CYTOKERATIN; VIMENTIN ID INTERMEDIATE-SIZED FILAMENTS; INNER-EAR; EPITHELIAL-CELLS; GUINEA-PIG; EXPRESSION; VIMENTIN; CYTOKERATINS; PROTEINS; ANTIBODY; CULTURE AB Tissue specimens of stria vascularis together with spiral ligament were transferred from the guinea pig cochlea to tissue culture dishes. To characterize and identify cells growing out from the explants, indirect immunofluorescence microscopy was used. The expression of the intermediate-sized filaments vimentin and cytokeratin 18 in cells on the surface of tissue specimens and in cells growing out from the explants after different cultivation periods were compared. Basically, three types of cells grew from the explants during several days: marginal cells, Claudius' cells and fibroblast-like cells. In primary cultures of explants, growth of marginal cells was observed in 25% of the dishes. Their proliferative activity, estimated by the use of the BrdUrd-DNA antibody, started in the stria vascularis and continued across the attachment of Reissner's membrane down to the bottom of the cell culture dish. The newly-formed marginal cells expressed cytokeratin 18 in the same way that original marginal cells on the tissue specimen do. If the newly-formed marginal cells were in contact with fibroblast-like cells or were forming groups (domes) on the bottom, they expressed vimentin. In 3% of the dishes growth of Claudius' cells was observed. Proliferative activity of these cells was found at the point where the basilar membrane was attached to the spiral ligament. New Claudius' cells spread at the opposite side of an explant when compared with the location of new marginal cells. Original as well as newly-formed Claudius' cells contained cytokeratin 18. Fibroblast-like cells were commonly present in cultures and contained only vimentin. C1 UNIV TUBINGEN,DEPT OTOLARYNGOL,SILCHERSTR 5,W-7400 TUBINGEN 1,GERMANY. HNO HEARING RES LABS & SFB NEUROBIOL,TUBINGEN,GERMANY. CR ADCHOUCHE J, 1989, PRIMARY CULTURE STRI ANNIKO M, 1990, EUR ARCH OTO-RHINO-L, V247, P182 BENZEEV A, 1985, ANN NY ACAD SCI, V455, P597, DOI 10.1111/j.1749-6632.1985.tb50439.x BENZEEV A, 1984, J CELL BIOL, V99, P1424, DOI 10.1083/jcb.99.4.1424 DARTSCH PC, 1990, LABOR MED, V13, P450 FRANKE WW, 1979, EXP CELL RES, V123, P25, DOI 10.1016/0014-4827(79)90418-X FRANKE WW, 1978, P NATL ACAD SCI USA, V75, P5034, DOI 10.1073/pnas.75.10.5034 GRATZNER HG, 1975, EXP CELL RES, V95, P88, DOI 10.1016/0014-4827(75)90612-6 IURATO S, 1962, Z ZELLFORSCH MIK ANA, V56, P40, DOI 10.1007/BF00326848 KASPER M, 1987, ARCH OTO-RHINO-LARYN, V244, P66, DOI 10.1007/BF00453494 KUIJPERS W, 1991, HEARING RES, V52, P133, DOI 10.1016/0378-5955(91)90193-D MELICHAR I, 1991, EUR ARCH OTO-RHINO-L, V248, P358 RAMAEKERS F, 1983, LAB INVEST, V49, P353 RAREY KE, 1989, HEARING RES, V38, P277, DOI 10.1016/0378-5955(89)90071-3 SCHROTT A, 1988, ARCH OTO-RHINO-LARYN, V245, P250, DOI 10.1007/BF00463937 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 STEINERT PM, 1985, ANNU REV CELL BIOL, V1, P41 NR 17 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 1992 VL 62 IS 1 BP 89 EP 98 DI 10.1016/0378-5955(92)90205-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700009 PM 1385378 ER PT J AU DIRCKX, JJJ DECRAEMER, WFS AF DIRCKX, JJJ DECRAEMER, WFS TI AREA CHANGE AND VOLUME DISPLACEMENT OF THE HUMAN TYMPANIC MEMBRANE UNDER STATIC PRESSURE SO HEARING RESEARCH LA English DT Article DE EARDRUM; STATIC PRESSURE; AREA; VOLUME ID MOIRE TOPOGRAMS; MIDDLE-EAR AB Direct measurements are presented of the area change and volume displacement of a human tympanic membrane under static pressures in the range of - 1.6 KPa to + 1.6 kPa. The area change is given separately for the pars tensa and the pars flaccida. For the pars tensa a strong asymmetry in area change under positive and negative pressure is observed. The volume displacement is also given separately for the pars tensa and the pars flaccida. The volume displacement of the entire TM agrees very well with volume displacement data in literature on tympanometry. It is shown further that a linear relationship between umbo displacement and volume displacement exists. The compliance of the tympanic membrane under static pressure load is compared to acoustic compliance measurements at low frequencies, and found to be a factor 2.5 higher than the compliance at 500 Hz. C1 UNIV ANTWERP,RIJKSUNIV CTR ANTWERPEN,BIOMED PHYS LAB,GROENENBORGELAAN 171,B-2020 ANTWERP,BELGIUM. CR Bekesy G., 1960, EXPT HEARING DECRAEMER WF, 1991, HEARING RES, V51, P107, DOI 10.1016/0378-5955(91)90010-7 DECRAEMER WF, 1980, J BIOMECH, V13, P559, DOI 10.1016/0021-9290(80)90056-1 Dirckx J, 1990, HEARING RES, V51, P93 DIRCKX JJJ, 1989, REV SCI INSTRUM, V60, P3698, DOI 10.1063/1.1140477 DIRCKX JJJ, 1990, APPL OPTICS, V29, P1474, DOI 10.1364/AO.29.001474 DIRCKX JJJ, 1988, APPL OPTICS, V27, P1164, DOI 10.1364/AO.27.001164 DIRCKX JJJ, 1991, APPL OPTICS, V30, P2757, DOI 10.1364/AO.30.002757 ELNER A, 1971, Acta Oto-Laryngologica, V72, P397, DOI 10.3109/00016487109122499 FLISBERG K, 1963, Acta Otolaryngol Suppl, V182, P43 GRONTVED A, 1989, ACTA OTO-LARYNGOL, V108, P101, DOI 10.3109/00016488909107399 HERGILS L, 1985, ARCH OTOLARYNGOL, V111, P86 KEITH A, 1918, ENQUIRY ANAL MECHAN Kirikae I., 1960, STRUCTURE FUNCTION M RABINOWITZ WM, 1981, J ACOUST SOC AM, V70, P1025, DOI 10.1121/1.386953 ROSS S, 1968, J ACOUST SOC AM, V43, P491, DOI 10.1121/1.1910857 SCHWALBE G, 1887, LEHRBUCH ANATOMY SIN Shinkawa H, 1987, Acta Otolaryngol Suppl, V435, P107 Stuhlman O. Jr., 1937, Journal of the Acoustical Society of America, V9, DOI 10.1121/1.1915915 von Bekesy G., 1941, AKUST Z, V6, P1 von Bekesy G, 1936, ANN PHYS-BERLIN, V25, P0413 Wever EG, 1954, PHYSL ACOUSTICS ZWISLOCKI J, 1957, J ACOUST SOC AM, V29, P349, DOI 10.1121/1.1908887 NR 23 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 SEP PY 1992 VL 62 IS 1 BP 99 EP 104 DI 10.1016/0378-5955(92)90206-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700010 PM 1429254 ER PT J AU ZACKSENHOUSE, M JOHNSON, DH TSUCHITANI, C AF ZACKSENHOUSE, M JOHNSON, DH TSUCHITANI, C TI EXCITATORY INHIBITORY INTERACTION IN THE LSO REVEALED BY POINT PROCESS MODELING SO HEARING RESEARCH LA English DT Article DE POINT PROCESS MODELS; BINAURAL PROCESSING; LATERAL SUPERIOR; OLIVE INHIBITION OLIVE ID LATERAL SUPERIOR OLIVE; BINAURAL TONE BURSTS; DISCHARGE PATTERNS; GLYCINE IMMUNOREACTIVITY; COCHLEAR NUCLEUS; CAT; UNITS; RESPONSES; NEURONS; COMPLEX AB We studied lateral superior olivary (LSO) unit responses to binaural tone-bursts using a general point process approach. We show that inhibition of the ipsilaterally elicited response by contralateral stimulation cannot be modeled simply as a reduction of the ipsilateral input. Statistical analyses reveal that inhibition operates by scaling the intensity of the point process describing the ipsilateral response. In some cases the scaling process has secondary effects: Binaurally elicited discharges produce bimodal interspike interval histograms from units that produce unimodal interval histograms under monaural stimulation. We present a specific point process model that describes the scaling process and successfully replicates the observed responses to monaural and binaural stimulation of the three types of LSO units: slow choppers, fast choppers, and bimodal units. We interpret scaling as a shunting inhibitory process in these LSO neurons. By relating scaling magnitude to interaural level difference, we demonstrate the spatial sensitivity of LSO units. C1 UNIV TEXAS,HLTH SCI CTR,GRAD SCH BIOMED SCI,CTR SENSORY SCI,HOUSTON,TX 77225. RP ZACKSENHOUSE, M (reprint author), RICE UNIV,DEPT ELECT & COMP ENGN,INST COMP & INFORMAT TECHNOL,HOUSTON,TX 77251, USA. CR BLOMFIELD S, 1974, BRAIN RES, P69 BORMANN J, 1987, J PHYSIOL-LONDON, V385, P243 Boudreau J C, 1970, Contrib Sens Physiol, V4, P143 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P422 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 COLBURN HS, 1981, NEURONAL MECH HEARIN, P283 Cox DR, 1962, RENEWAL THEORY DINGLEDINE R, 1980, BRAIN RES, V185, P277, DOI 10.1016/0006-8993(80)91068-9 FINLAYSON PG, 1989, HEARING RES, V38, P221, DOI 10.1016/0378-5955(89)90067-1 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GOLDBERG JM, 1964, J NEUROPHYSIOL, V27, P706 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 Hille B., 1992, IONIC CHANNELS EXCIT, V2nd IRVINE DRF, 1987, HEARING RES, V26, P267, DOI 10.1016/0378-5955(87)90063-3 JOHNSON DH, 1983, J ACOUST SOC AM, V74, P493, DOI 10.1121/1.389815 JOHNSON DH, 1990, HEARING RES, V49, P301, DOI 10.1016/0378-5955(90)90110-B JOHNSON DH, 1978, BIOPHYS J, V22, P413 JOHNSON DH, 1986, HEARING RES, V21, P135, DOI 10.1016/0378-5955(86)90035-3 Kandel E. R., 1985, PRINCIPLES NEURAL SC LINEBARGER DA, 1986, HEARING RES, V23, P185, DOI 10.1016/0378-5955(86)90015-8 MOORE MJ, 1983, J NEUROSCI, V3, P237 OZAKI T, 1979, ANN I STAT MATH, V31, P145, DOI 10.1007/BF02480272 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 RODIECK RW, 1962, BIOPHYS J, V2, P351 SANES DH, 1990, J NEUROSCI, V10, P3494 SMITH CE, 1986, BIOL CYBERN, V54, P41, DOI 10.1007/BF00337114 Snyder D.L., 1991, RANDOM POINT PROCESS, Vsecond TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P164 TSUCHITANI C, 1988, J NEUROPHYSIOL, V59, P184 TSUCHITANI C, 1985, J ACOUST SOC AM, V77, P1484, DOI 10.1121/1.392043 TSUCHITANI C, 1982, J NEUROPHYSIOL, V47, P479 TSUCHITA.C, 1969, J ACOUST SOC AM, V46, P979, DOI 10.1121/1.1911818 Tuckwell H. C., 1989, STOCHASTIC PROCESSES WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X WU SH, 1991, J NEUROPHYSIOL, V65, P230 Yamada W. M., 1989, METHODS NEURONAL MOD, P97 ZACKSENHOUSE M, 1992, UNPUB POINT PROCESS 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 SEP PY 1992 VL 62 IS 1 BP 105 EP 123 DI 10.1016/0378-5955(92)90207-4 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JQ287 UT WOS:A1992JQ28700011 PM 1429246 ER PT J AU EGGERMONT, JJ AF EGGERMONT, JJ TI STIMULUS INDUCED AND SPONTANEOUS RHYTHMIC FIRING OF SINGLE UNITS IN CAT PRIMARY AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE CAT; DEVELOPMENT; AUDITORY CORTEX; SINGLE UNIT; SPONTANEOUS ACTIVITY; PERIODICITY CODING; AUTOCORRELATION; RHYTHMIC FIRING ID VISUAL-CORTEX; NEURONS; OSCILLATIONS; NEOCORTEX; SYNCHRONIZATION; RESPONSES AB Recordings were made under ketamine anesthesia from 385 neurons in primary auditory cortex in adult cat and from 265 neurons in 10-55 day old kittens. The temporal Modulation Transfer Function for the response to repetitive click stimuli peaked at 8 Hz. After a click a suppression period of 130-155 ms in duration, depending on click-rate, was observed. This suppression period limited the response to high click rates and thereby determined the `resonance' in the click response. The suppression duration in kittens decreased in exponential fashion toward the adult value with a time constant of about 1 month. After the one second duration click-trains an oscillatory rebound with a mean period of 113 ms was observed in about 60% of the recordings in the adult cat. Spontaneous activity showed in about 30% of the neurons an oscillatory auto-correlogram with an average period of 126 ms in the adult cats and 170 ms in kittens. RP EGGERMONT, JJ (reprint author), UNIV CALGARY,DEPT PSYCHOL,BEHAV NEUROSCI RES GRP,CALGARY T2N 1N4,ALBERTA,CANADA. CR Abeles M., 1982, LOCAL CORTICAL CIRCU CHAGNACAMITAI Y, 1989, J NEUROPHYSIOL, V62, P1149 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 De Ribaupierre F, 1972, Brain Res, V48, P205, DOI 10.1016/0006-8993(72)90179-5 De Ribaupierre F, 1972, Brain Res, V48, P185, DOI 10.1016/0006-8993(72)90178-3 ECKHORN R, 1988, BIOL CYBERN, V60, P121, DOI 10.1007/BF00202899 EGGERMONT JJ, 1990, HEARING RES, V43, P181, DOI 10.1016/0378-5955(90)90227-G Eggermont JJ, 1990, CORRELATIVE BRAIN TH EGGERMONT JJ, 1991, HEARING RES, V56, P153, DOI 10.1016/0378-5955(91)90165-6 EGGERMONT JJ, 1991, HEARING RES, V57, P45, DOI 10.1016/0378-5955(91)90073-I EGGERMONT JJ, 1991, IN PRESS J NEUROPHYS ENGEL AK, 1991, SCIENCE, V252, P1177, DOI 10.1126/science.252.5009.1177 Freeman W.J., 1975, MASS ACTION NERVOUS Getting P. A., 1989, METHODS NEURONAL MOD, P171 GRAY CM, 1989, P NATL ACAD SCI USA, V86, P1698, DOI 10.1073/pnas.86.5.1698 GRAY CM, 1989, OSCILLATORY RESPONSE LLINAS RR, 1988, SCIENCE, V242, P1654, DOI 10.1126/science.3059497 LLINAS RR, 1991, P NATL ACAD SCI USA, V88, P897, DOI 10.1073/pnas.88.3.897 Magleby KL, 1987, SYNAPTIC FUNCTION, P21 MCCORMICK DA, 1985, J NEUROPHYSIOL, V54, P782 PURPURA DP, 1965, J NEUROPHYSIOL, V28, P925 SILVA LR, 1991, SCIENCE, V251, P432, DOI 10.1126/science.1824881 STERIADE M, 1988, PHYSIOL REV, V68, P649 NR 23 TC 76 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 AUG PY 1992 VL 61 IS 1-2 BP 1 EP 11 DI 10.1016/0378-5955(92)90029-M PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800001 PM 1526882 ER PT J AU INAMURA, N SALT, AN AF INAMURA, N SALT, AN TI PERMEABILITY CHANGES OF THE BLOOD-LABYRINTH BARRIER MEASURED INVIVO DURING EXPERIMENTAL TREATMENTS SO HEARING RESEARCH LA English DT Article DE COCHLEA; PERILYMPH; BLOOD-LABYRINTH BARRIER; ION-SELECTIVE ELECTRODES ID GUINEA-PIG COCHLEA; CEREBROSPINAL-FLUID; BRAIN-BARRIER; PERILYMPH; FLOW AB The communication between blood and cochlear perilymph was investigated using the tracer ion trimethylphenylammonium (TMPA). TMPA can be detected in micromolar concentrations by ion-selective microelectrodes, allowing it to be used as an almost ideal marker to study intercommunication between fluid compartments. TMPA-sensitive electrodes were sealed into the cochlear scalae, using procedures which avoided the artifactual displacement of perilymph by cerebrospinal fluid (CSF). TMPA was infused intravenously at a low rate to produce a plasma concentration of approximately 0.5.mM. The time course of entry into perilymph of scala tympani (ST), scala vestibuli (SV) and into CSF were compared. After 90 min infusion, the mean CSF concentration reached 14.3% of that measured in plasma. The TMPA concentrations measured in ST and SV perilymph were significantly lower than those recorded in CSF, only reaching an average of 6.5% and 3.7% of the plasma concentration respectively after 90 min. The slow entry of TMPA confirms the existence of a tight blood-labyrinth barrier, equivalent to the blood-brain or blood-CSF barriers. The rate of TMPA entry into perilymph was increased by epinephrine-induced hypertension or by simultaneous administration of histamine and prostaglandin E2. These treatments are presumed to increase the permeability of the blood-labyrinth barrier. Characterization and manipulation of blood-labyrinth barrier permeability could be important to our understanding cochlear pathology. C1 WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,BOX 8115,517 S EUCLID AVE,ST LOUIS,MO 63110. CR ALTMANN F, 1947, ANN OTO RHINOL LARYN, V56, P684 ALTMANN F, 1950, ANN OTO RHINOL LARYN, V59, P657 CHOO YB, 1964, ANN OTO RHINOL LARYN, V73, P92 HAGGENDA.E, 1972, ACTA NEUROL SCAND, V48, P271 HARA A, 1989, HEARING RES, V42, P265 HARDEBO JE, 1977, ACTA PHYSIOL SCAND, V101, P342, DOI 10.1111/j.1748-1716.1977.tb06016.x HAWKINS JE, 1968, 3RD S ROL VEST ORG S, P241 JAHNKE K, 1981, MENIERES DIS, P67 Johansson BB, 1989, IMPLICATIONS BLOOD B, P389 JUHN SK, 1981, MENIERES DISEASE PAT, P59 JUHN SK, 1981, ANN OTO RHINOL LARYN, V90, P135 JUHN SK, 1982, AM J OTOLARYNG, V3, P392, DOI 10.1016/S0196-0709(82)80016-1 Juhn S K, 1988, Acta Otolaryngol Suppl, V458, P79 KAUPP H, 1980, ARCH OTO-RHINO-LARYN, V229, P245, DOI 10.1007/BF02565527 OHYAMA K, 1988, HEARING RES, V35, P119, DOI 10.1016/0378-5955(88)90111-6 RAPPORT SI, 1976, EXP NEUROL, V52, P467 SALT AN, 1991, ACTA OTO-LARYNGOL, V111, P899, DOI 10.3109/00016489109138428 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 SCHEIBE F, 1985, HEARING RES, V17, P61, DOI 10.1016/0378-5955(85)90131-5 SCHNIEDE.EA, 1974, ANN OTO RHINOL LARYN, V83, P76 SCHUKNECHT HF, 1963, ANN OTO RHINOL LARYN, V72, P687 SOKRAB TEO, 1988, ACTA NEUROPATHOL, V75, P557 TAKAHASHI T, 1970, Acta Oto-Laryngologica, V69, P46, DOI 10.3109/00016487009123335 NR 24 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 1992 VL 61 IS 1-2 BP 12 EP 18 DI 10.1016/0378-5955(92)90030-Q PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800002 PM 1526884 ER PT J AU GREENBERG, AB MYERS, MW HARTSHORN, DO MILLER, JM ALTSCHULER, RA AF GREENBERG, AB MYERS, MW HARTSHORN, DO MILLER, JM ALTSCHULER, RA TI COCHLEAR ELECTRODE REIMPLANTATION IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE COCHLEAR PROSTHESIS; SPIRAL GANGLION CELL; ELECTRODE REIMPLANTATION; SAFETY; PATHOLOGY ID IMPLANTATION AB Cochlear implants are being applied to an ever widening patient population, including children in whom lifetime use of these devices is anticipated. Replacement of implants can be expected for reasons of device failure as well as future upgrading. This investigation was undertaken to examine the effect of cochlear electrode explantation and reimplantation on spiral ganglion cell survival. Guinea pigs with normal ears were initially implanted and either explanted or explanted and reimplanted (at 2 months) with a single wire ball-tip intracochlear electrode or a silastic carrier (each remaining for an additional 2 months). Little loss of hair cells or auditory nerve was observed across experimental groups and normal controls. Restricted basal turn cochlear and spiral ganglion cell loss was observed in a few animals in each group and was likely associated with mechanical damage from initial implantation. Likewise the scattered organ of Corti damage and hair cell loss observed was noted in only a few cochleae in each experimental group. Therefore, no significant differences in the average pathology across experimental groups and controls were observed. Thus, explantation or explantation with subsequent reimplantation does not appear to constitute an additional significant pathological risk compared to implantation alone. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. CR HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 Leake PA, 1985, COCHLEAR IMPLANTS, P55 LEAKE PA, 1989, ARO MIDWINTER RES M, V12, P268 LEAKEJONES PA, 1983, ANN NY ACAD SCI, V405, P203, DOI 10.1111/j.1749-6632.1983.tb31634.x Lousteau R. J., 1987, LARYNGOSCOPE, V97, P837 MILLER JM, 1991, IN PRESS 4 INT C EFF MILLER N, 1987, SPAZ SOC-SPACE SOC, V10, P54 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 SCHINDLER RA, 1979, LARYNGOSCOPE, V89, P752 SCHINDLE.RA, 1974, ANN OTO RHINOL LARYN, V83, P202 SCHINDLER RA, 1976, J LARYNGOL OTOL, V90, P445, DOI 10.1017/S002221510008230X WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 ZAPPIA JJ, 1989, HEARING RES, V40, P29, DOI 10.1016/0378-5955(89)90096-8 NR 15 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 1992 VL 61 IS 1-2 BP 19 EP 23 DI 10.1016/0378-5955(92)90031-H PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800003 PM 1526892 ER PT J AU RYAN, AF AXELSSON, GA WOOLF, NK AF RYAN, AF AXELSSON, GA WOOLF, NK TI CENTRAL AUDITORY METABOLIC-ACTIVITY INDUCED BY INTENSE NOISE EXPOSURE SO HEARING RESEARCH LA English DT Article DE NOISE DAMAGE; COCHLEA; 2-DEOXYGLUCOSE; GERBIL; AUDITORY NEURONS ID 2-DEOXYGLUCOSE; SYSTEM; GERBIL; STIMULATION AB Neural activity in the central auditory system was mapped by measuring 2-deoxyglucose (2-DG) uptake during a one hour exposure to a two-octave (1414-5656 Hz) band of noise. Gerbils were exposed to 100, 110 or 120 dB SPL, intensities which can produce only temporary (100 dB) or both temporary and permanent (120 dB) hearing loss. Exposure to 100 dB SPL evoked high levels of neural-activity throughout responsive regions of auditory nuclei. At 110 dB SPL, a central region of low neural activity was surrounded by areas exhibiting increased activity. At 120 dB SPL, neural activity was low in almost all areas of auditory nuclei. To study the effects of permanent hearing loss on auditory neuronal activity, other animals were given 2-DG during exposure to 65 dB SPL broad band noise as a test stimulus, two months after exposure to the noise band at 110 dB SPL. Central auditory nuclei showed a tonotopic region of low neural activity corresponding to an approximately 3 kHz pure tone, surrounded by regions of evoked activity. The deficits in evoked metabolic activity observed both during and long after noise exposure appear to exceed those predicted from the degree of temporary and permanent threshold shift produced by the same noise exposures. C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. SAHLGRENS UNIV HOSP,DEPT AUDIOL,S-41345 GOTHENBURG,SWEDEN. RP RYAN, AF (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT SURG OTOLARYNGOL,900 GILMAN DK,LA JOLLA,CA 92093, USA. CR ACKERMANN RF, 1984, J NEUROSCI, V4, P251 LONSBURYMARTIN BL, 1978, J NEUROPHYSIOL, V41, P987 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 POPELAR J, 1982, HEARING RES, V8, P273, DOI 10.1016/0378-5955(82)90019-3 ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 RYAN A, 1978, J ACOUST SOC AM, V63, P1145, DOI 10.1121/1.381822 RYAN AF, 1982, BRAIN RES, V252, P177, DOI 10.1016/0006-8993(82)90994-5 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 RYAN AF, 1989, BRAIN RES, V483, P293 SALVI RJ, 1979, ARCH OTO-RHINO-LARYN, V224, P111, DOI 10.1007/BF00455233 SHARP FR, 1981, BRAIN RES, V230, P87, DOI 10.1016/0006-8993(81)90393-0 SHARP FR, 1983, BRAIN RES, V263, P97, DOI 10.1016/0006-8993(83)91204-0 SOKOLOFF L, 1977, J NEUROCHEM, V29, P13, DOI 10.1111/j.1471-4159.1977.tb03919.x THEURICH M, 1984, BRAIN RES, V322, P157, DOI 10.1016/0006-8993(84)91197-1 TOOTELL RBH, 1988, J NEUROSCI, V8, P1531 WEBSTER WR, 1978, NEUROSCI LETT, V10, P43, DOI 10.1016/0304-3940(78)90009-5 NR 18 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 1992 VL 61 IS 1-2 BP 24 EP 30 DI 10.1016/0378-5955(92)90032-I PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800004 PM 1326506 ER PT J AU WONG, CJH TO, EC SCHWARZ, DWF AF WONG, CJH TO, EC SCHWARZ, DWF TI LOCATION OF MOTONEURONS INNERVATING THE MIDDLE-EAR MUSCLE OF THE CHICKEN, (GALLUS-DOMESTICUS) SO HEARING RESEARCH LA English DT Article DE MIDDLE EAR; MUSCULUS-COLUMELLAE; STAPEDIUS; FACIAL NUCLEUS; BIRDS ID COTURNIX-COTURNIX-JAPONICA; COUPLED OXIDATION REACTION; PIGEON COLUMBA-LIVIA; STAPEDIUS MUSCLE; HORSERADISH-PEROXIDASE; DIRECTIONAL HEARING; CAT; IDENTIFICATION; ORGANIZATION; PATHWAYS AB The motoneuron pool for the musculus columellae, the avian equivalent to the m. stapedius, was identified by retrograde labeling with WGA-HRP. It consists of a discrete group of approximately 65 neurons located along the dorsolateral border in the ventral subnucleus of the facial nuclear complex. Other facial motoneurons were only labeled when diffusion of the tracer into neighbor structures was not excluded. The dorsal subnucleus of the facial nerve innervates the m. depressor mandibulae. C1 UNIV BRITISH COLUMBIA,ROTARY HEARING CTR,DIV OTOLARYNGOL,VANCOUVER V6T 1W5,BC,CANADA. UNIV BRITISH COLUMBIA,DEPT PHYSIOL,VANCOUVER V6T 1W5,BC,CANADA. CR BOORD RL, 1969, ANN NY ACAD SCI, V167, P186, DOI 10.1111/j.1749-6632.1969.tb20444.x Borg E., 1984, ACOUSTIC REFLEX BASI, P63 COLES RB, 1980, J EXP BIOL, V86, P153 COUNTER SA, 1979, ACTA OTO-LARYNGOL, V88, P13, DOI 10.3109/00016487909137134 COUNTER SA, 1982, ACTA OTO-LARYNGOL, V94, P267, DOI 10.3109/00016488209128913 Evans H.E., 1979, P505 GOLUBEVA TB, 1972, J EVOLUT BIOC PHYL, V8, P149 GRASSI S, 1983, ARCH ITAL BIOL, V121, P37 GRASSI S, 1990, BRAIN RES, V529, P158, DOI 10.1016/0006-8993(90)90823-T GRASSI S, 1988, J COMP PHYSIOL A, V162, P525, DOI 10.1007/BF00612517 GUINAN JJ, 1989, J COMP NEUROL, V287, P134, DOI 10.1002/cne.902870110 HILL KG, 1980, J EXP BIOL, V86, P135 ITOH K, 1979, BRAIN RES, V175, P341, DOI 10.1016/0006-8993(79)91013-8 JOSEPH MP, 1985, J COMP NEUROL, V232, P43, DOI 10.1002/cne.902320105 LUNDQUIS.I, 1971, ANAL BIOCHEM, V41, P567, DOI 10.1016/0003-2697(71)90179-5 LYON MJ, 1978, BRAIN RES, V143, P437, DOI 10.1016/0006-8993(78)90355-4 Moller A, 1984, ACOUSTIC REFLEX, P1 OECKINGHAUS H, 1983, J COMP PHYSIOL, V150, P61 PARK TJ, 1991, J COMP PSYCHOL, V105, P125, DOI 10.1037/0735-7036.105.2.125 Pohlman AG, 1921, J MORPHOL, V35, P229 ROSOWSKI JJ, 1980, J COMP PHYSIOL, V136, P183 ROUILLER EM, 1989, BRAIN RES, V476, P21, DOI 10.1016/0006-8993(89)91532-1 SCHWARZ DWF, 1992, IN PRESS HEAR RES SCHWARZ IE, 1981, J COMP NEUROL, V196, P1, DOI 10.1002/cne.901960102 SHAW MD, 1983, J COMP NEUROL, V216, P10, DOI 10.1002/cne.902160103 Smith G, 1904, Q J MICROSC SCI, V48, P11 THOMPSON GC, 1985, J COMP NEUROL, V231, P270, DOI 10.1002/cne.902310214 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 WILD JM, 1980, J COMP NEUROL, V192, P175, DOI 10.1002/cne.901920112 NR 29 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 1992 VL 61 IS 1-2 BP 31 EP 34 DI 10.1016/0378-5955(92)90033-J PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800005 PM 1382048 ER PT J AU SCHULTE, BA SCHMIEDT, RA AF SCHULTE, BA SCHMIEDT, RA TI LATERAL WALL NA,K-ATPASE AND ENDOCOCHLEAR POTENTIALS DECLINE WITH AGE IN QUIET-REARED GERBILS SO HEARING RESEARCH LA English DT Article DE COCHLEA; STRIA VASCULARIS; PRESBYACUSIS; AGING; ENDOCOCHLEAR POTENTIAL; GERBIL; NA,K-ATPASE ID AUDITORY-NERVE FIBERS; HAIR CELL LOSS; INNER-EAR; MONGOLIAN GERBIL; STRIA VASCULARIS; GUINEA-PIG; COCHLEA; LOCALIZATION; DEGENERATION; SUPPRESSION AB Changes in the integrity of cochlear ion transport systems with age were examined in gerbils raised for 5-38 months in a quiet environment. Ion transport function was assessed by light microscopic immunohistochemical staining for the enzyme, Na,K-ATPase and by measurement of the endocochlear potential (EP). Small foci of strial atrophy accompanied by loss of immunostaining for Na,K-ATPase were observed in the stria vascularis of the apical and basal turns as early as 5 months of age. Cochleas from 29-38 month-old gerbils showed a loss of immunostaining for Na,K-ATPase in the stria in most of the apical turn with the degeneration extending well into the middle turn in many of the oldest ears. The extent of strial atrophy and loss of immunoreactive Na,K-ATPase in the basal turn varied considerably among the oldest cochleas. Populations of lateral wall fibrocytes (type II fibrocytes) normally rich in Na,K-ATPase exhibited a corresponding decrease in enzyme content in regions of advanced strial atrophy. The volume of immunostained stria vascularis correlated well with the magnitude of the resting EP. The results demonstrate that lateral wall ion transport systems in the gerbil cochlea degenerate as a function of age. The findings also provide good evidence for a functional relationship between the stria vascularis and the Na,K-ATPase-rich type Il fibrocytes in generating and maintaining the EP. C1 MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,CHARLESTON,SC 29425. RP SCHULTE, BA (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR BHATTACHARYYA TK, 1985, ANN OTO RHINOL LARYN, V94, P75 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 BURG MB, 1986, KIDNEY, P145 CHEAL M, 1986, EXP AGING RES, V12, P3 CHOLE RA, 1988, ANN OTO RHINOL LARYN, V97, P78 CHOLE R A, 1981, American Journal of Otology, V2, P204 COHEN GM, 1988, CRIT REV NEUROBIOL, V4, P179 COVELL W. P., 1957, LARYNGOSCOPE, V67, P118 GRATTON MA, 1992, ABSTR ASS RES OT, V48 GULYA AJ, 1990, ASHA REPORTS, V19, P126 Hawkins J E Jr, 1973, Adv Otorhinolaryngol, V20, P125 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HIEBER V, 1989, J NEUROSCI RES, V23, P9, DOI 10.1002/jnr.490230103 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 JOHNSSON LG, 1972, LARYNGOSCOPE, V82, P1105, DOI 10.1288/00005537-197207000-00002 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 Koeppen B M, 1985, Soc Gen Physiol Ser, V39, P89 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 MIKAELIA.DO, 1974, ACTA OTO-LARYNGOL, V77, P327, DOI 10.3109/00016487409124632 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 NADOL JB, 1980, AGING COMMUNICATION, P63 PAULER M, 1988, LARYNGOSCOPE, V98, P754 RYAN A, 1978, J ACOUST SOC AM, V63, P1145, DOI 10.1121/1.381822 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 Schuknecht H., 1974, PATHOLOGY EAR, P388 Schuknecht H. F., 1965, ACTA OTO-LARYNGOL, V59, P154, DOI 10.3109/00016486509124549 SCHUKNEC.HF, 1974, LARYNGOSCOPE, V84, P1777 SCHUKNECHT HF, 1964, ARCHIV OTOLARYNGOL, V80, P369 SCHUKNECHT HF, 1956, LARYNGOSCOPE, V65, P402 Schuknecht HF, 1989, GERIATRIC OTORHINOLA, P40 SCHULTE BA, 1989, ABSTR ASS RES OT, V47 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 SMITH DI, 1990, HEARING RES, V43, P95, DOI 10.1016/0378-5955(90)90218-E SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TACHIBANA M, 1984, ACTA OTO-LARYNGOL, V97, P257, DOI 10.3109/00016488409130987 TAKAHASH.T, 1971, ANN OTO RHINOL LARYN, V80, P721 TAKAHASHI T, 1970, Acta Oto-Laryngologica, V69, P46, DOI 10.3109/00016487009123335 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V THALMANN R, 1981, ACTA OTO-LARYNGOL, V91, P535, DOI 10.3109/00016488109138539 NR 50 TC 134 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 AUG PY 1992 VL 61 IS 1-2 BP 35 EP 46 DI 10.1016/0378-5955(92)90034-K PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800006 PM 1326507 ER PT J AU VEUILLET, E COLLET, L MORGON, A AF VEUILLET, E COLLET, L MORGON, A TI DIFFERENTIAL-EFFECTS OF EAR-CANAL PRESSURE AND CONTRALATERAL ACOUSTIC STIMULATION ON EVOKED OTOACOUSTIC EMISSIONS IN HUMANS SO HEARING RESEARCH LA English DT Article DE EVOKED OTOACOUSTIC EMISSION; PRESSURE VARIATION; CONTRALATERAL ACOUSTIC STIMULATION; MEDIAL OLIVOCOCHLEAR SYSTEM; COCHLEAR VULNERABILITY ID CROSSED OLIVOCOCHLEAR BUNDLE; SUPERIOR OLIVARY COMPLEX; PERILYMPHATIC FLUID; MEDIAL ZONES; TRANSMISSION; PROJECTIONS; DEPENDENCE; CATS AB The effect of ear canal pressure variation (ECPV) on click evoked otoacoustic emissions (EOAEs) was compared to the suppressive effect observed with contralateral acoustic stimulation (CAS) in 11 healthy subjects. Both total EOAE amplitude and amplitude of 200 Hz frequency bands (22) were analyzed. Our results revealed that the ECPV as the CAS induced a decrease of the total EOAE amplitude; these two factors showed an additive effect when they are conjoint. The study of the EOAE frequency bands showed that the majority of them decreased under CAS and ECPV; however, a few bands are not affected. Moreover, it appeared that amplitude of the EOAE frequency bands were not modified in a similar way between the two factors: indeed some bands around 4.1 kHz did not decrease either by CAS or ECPV. These results suggest that these applied factors exert different actions on EOAEs. Moreover, the lack of a decrease effect for the same bands, both with CAS and ECPV, may explain the vulnerability of some cochlear locations. RP VEUILLET, E (reprint author), UNIV CLAUDE BERNARD,HOP EDOUARD HERRIOT,PHYSIOL SENSORIELLE AUDIT & VOIX LAB,CNRS,UA 1447,F-69374 LYON,FRANCE. CR BERLIN CI, 1991, ABSTR ASS RES OT, V14, P83 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BRAY P, 1989, THESIS U COLLEGE MID, P201 COLLET L, 1990, ADV AUDIOL, V7, P164 COLLET L, 1992, AUDIOLOGY, V62, P113 COLLET L, 1990, HEARING RES, V43, P252 COLLET L, 1991, AUDIOLOGY, V30, P164 DENSERT B, 1986, ACTA OTO-LARYNGOL, V102, P186, DOI 10.3109/00016488609108665 DENSERT O, 1981, ACTA OTO-LARYNGOL, V91, P55, DOI 10.3109/00016488109138482 Enander A, 1967, Acta Otolaryngol, V64, P543, DOI 10.3109/00016486709139139 GUINAN JJ, 1984, J COMP NEUROL, V226, P21, DOI 10.1002/cne.902260103 GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 ITO J, 1990, ACTA OTO-LARYNGOL, V110, P203, DOI 10.3109/00016489009122538 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1991, J NEUROPHYSIOL, V65, P123 NAEVE SL, 1991, ABSTR ASS RES OT, V14, P68 OHMURA M, 1987, ACTA OTO-LARYNGOL, V104, P255, DOI 10.3109/00016488709107326 RAJAN R, 1989, HEARING RES, V39, P263, DOI 10.1016/0378-5955(89)90046-4 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZWICKER E, 1990, HEARING RES, V47, P185, DOI 10.1016/0378-5955(90)90150-N NR 25 TC 59 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 AUG PY 1992 VL 61 IS 1-2 BP 47 EP 55 DI 10.1016/0378-5955(92)90035-L PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800007 PM 1526893 ER PT J AU SUGAI, T YANO, J SUGITANI, M OOYAMA, H AF SUGAI, T YANO, J SUGITANI, M OOYAMA, H TI ACTIONS OF CHOLINERGIC AGONISTS AND ANTAGONISTS ON THE EFFERENT SYNAPSE IN THE FROG SACCULUS SO HEARING RESEARCH LA English DT Article DE VESTIBULAR EFFERENT SYNAPSE; HAIR CELL; ACETYLCHOLINE RECEPTOR; FROG; SACCULUS ID COCHLEAR HAIR-CELLS; LATERAL LINE ORGAN; BURBOT LOTA-LOTA; ACETYLCHOLINE-RECEPTORS; NERVE-FIBERS; STIMULATION; INHIBITION; TRANSMISSION; ORGANIZATION; TURTLE AB Intracellular recordings were made from hair cells in the frog saccular epithelium isolated with its innervating nerves. Inhibitory post-synaptic potentials (IPSPs) were recorded from hair cells when the efferent fibers were activated by electrical stimulation. The effects of acetylcholine (ACh), cholinomimetics, and cholinergic antagonists on the efferent synapse were studied in a preparation where the IPSPs can be observed directly. ACh or carbachol (CCh) produced a transient membrane hyperpolarization with a decrease in input resistance followed by an abolition or reduction of the IPSP. In a low Ca2+ medium where efferent synaptic activity was abolished, ACh or CCh still induced hyperpolarization, though the response appeared to be smaller than that in normal medium. Neither nicotinic (dimethyl-4-phenyl-piperazinium (DMPP), phenyltrimethylammonium (PTMA) and nicotine) nor muscarinic (muscarine, methacholine, bethanechol and oxotremorine) agonists induced the membrane hyperpolarization, but the former drugs inhibited the IPSPs while the latter drugs did not. Both d-tubocurarine and atropine inhibited the IPSP, but the d-tubocurarine was more potent, causing inhibition even at a dose of 0.5-mu-M while 2-mu-M or more atropine was needed. The ACh- or CCh-induced hyperpolarization was inhibited completely by d-tubocurarine (5-mu-M), but only slightly by atropine (5-mu-M). These results may indicate that the IPSP and the effects of ACh or CCh are based on a direct interaction between ACh or CCh and ACh receptors on the hair cells. RP SUGAI, T (reprint author), KANAZAWA MED UNIV,DEPT PHYSIOL,UCHINADA,ISHIKAWA 92002,JAPAN. CR ART JJ, 1985, J PHYSIOL-LONDON, V360, P397 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 ASHMORE JF, 1982, J PHYSIOL-LONDON, V329, pP25 BERNARD C, 1985, BRAIN RES, V338, P225, DOI 10.1016/0006-8993(85)90151-9 DESMEDT JE, 1963, NATURE, V200, P472, DOI 10.1038/200472b0 FLOCK A, 1973, J PHYSIOL-LONDON, V235, P591 FLOCK A, 1976, J PHYSIOL-LONDON, V257, P45 FURUKAWA T, 1981, J PHYSIOL-LONDON, V315, P203 GUTH PS, 1986, ACTA OTOLARYNGOL, V102, P186 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 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 KEHOE J, 1972, J PHYSIOL-LONDON, V225, P115 KLINKE R, 1974, PHYSIOL REV, V54, P316 KOKETSU K, 1958, AM J PHYSIOL, V193, P213 LINDMAR R, 1967, EXPERIENTIA, V23, P933, DOI 10.1007/BF02136230 NORRIS CH, 1985, TRENDS PHARMACOL SCI, V6, P15 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 PRIGIONI I, 1983, BRAIN RES, V269, P83, DOI 10.1016/0006-8993(83)90964-2 ROSSI ML, 1980, BRAIN RES, V185, P984 SEWELL WF, 1991, J NEUROPHYSIOL, V65, P1158 SHIGEMOTO T, 1990, J PHYSIOL-LONDON, V420, P127 STEINACKER A, 1988, HEARING RES, V35, P265, DOI 10.1016/0378-5955(88)90123-2 SUGAI T, 1989, JPN J PHYSL S, V39, P168 SUGAI T, 1990, JPN J PHYSL S, V40, P186 SUGAI T, 1991, JPN J PHYSIOL, V41, P217, DOI 10.2170/jjphysiol.41.217 VALLI P, 1986, BRAIN RES, V362, P92, DOI 10.1016/0006-8993(86)91402-2 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WONG LA, 1989, NATURE, V341, P439, DOI 10.1038/341439a0 NR 30 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 AUG PY 1992 VL 61 IS 1-2 BP 56 EP 64 DI 10.1016/0378-5955(92)90036-M PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800008 PM 1526894 ER PT J AU CECOLA, RP BOBBIN, RP AF CECOLA, RP BOBBIN, RP TI LOWERING EXTRACELLULAR CHLORIDE CONCENTRATION ALTERS OUTER HAIR CELL-SHAPE SO HEARING RESEARCH LA English DT Article DE HAIR CELLS, OUTER; CHLORIDE; TURGOR; VOLUME REGULATION ID MOTILITY; VOLUME; ACTIN; ACETYLCHOLINE; MECHANISMS; TRANSPORT; LENGTH; MODEL; NA+ AB In general, increasing external K+ concentration, as well as exposure to hypotonic medium, induces a shortening of outer hair cells (OHCs) accompanied by an increase in width and volume. One possible mechanism suggested for these changes is a movement of Cl- and/or water across the cell membrane. We therefore examined the role of Cl- in OHC volume maintenance by testing the effect of decreasing extracellular Cl- concentration on OHC length and shape. In addition, the effect of hypotonic medium was examined. OHCs were isolated from guinea pig cochleae, mechanically dissociated and dispersed, and placed in a modified Hanks balanced salt solution (HBS). Exposing the cells to a Cl--free HBS produced an initial shortening, which was rapidly followed by an increase in length. After about 9 min of exposure to Cl--free HBS, the cells appeared to lose all water and collapsed. Upon return to normal HBS, the OHCs returned to their normal shape. We speculate that the collapse of the OHCs may be due to the loss of intracellular Cl-, which, in turn, resulted in the loss of intracellular K+ and water. The results indicate that Cl- contributes greatly to the maintenance of OHC volume. In addition, we confirmed that isolated OHCs swell in hypotonic medium and maintain their swollen state until returned to normal medium. The mechanism for maintenance of the swollen state is unknown. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. CR BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 GRAF J, 1988, RENAL PHYSIOL BIOCH, V11, P202 HODGKIN AL, 1959, J PHYSIOL-LONDON, V148, P127 HOFFMANN EK, 1989, PHYSIOL REV, V69, P315 HOLLEY MC, 1990, J CELL SCI, V96, P283 LARSEN EH, 1987, J MEMBRANE BIOL, V99, P25, DOI 10.1007/BF01870619 LEWIS SA, 1985, J MEMBRANE BIOL, V83, P119, DOI 10.1007/BF01868744 MACKNIGHT ADC, 1985, PFLUG ARCH EUR J PHY, V405, pS12, DOI 10.1007/BF00581773 MACKNIGHT ADC, 1988, RENAL PHYSL BIOCH, V3, P114 MOUNTAIN DC, 1986, NEUROBIOLOGY HEARING, P77 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A REUSS L, 1988, RENAL PHYSIOL BIOCH, V11, P187 SLEPECKY N, 1988, HEARING RES, V34, P119, DOI 10.1016/0378-5955(88)90099-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 ULFENDAHL M, 1988, ARCH OTO-RHINO-LARYN, V245, P237, DOI 10.1007/BF00463935 WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 WELLING PA, 1988, AM J PHYSIOL, V255, pF853 WELLING PA, 1990, AM J PHYSIOL, V258, pF951 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1986, NEUROBIOLOGY HEARING, P1 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 NR 32 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 1992 VL 61 IS 1-2 BP 65 EP 72 DI 10.1016/0378-5955(92)90037-N PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800009 PM 1526895 ER PT J AU LI, L KELLY, JB AF LI, L KELLY, JB TI BINAURAL RESPONSES IN RAT INFERIOR COLLICULUS FOLLOWING KAINIC ACID LESIONS OF THE SUPERIOR OLIVE - INTERAURAL INTENSITY DIFFERENCE FUNCTIONS SO HEARING RESEARCH LA English DT Article DE SUPERIOR OLIVARY COMPLEX; MEDIAL SUPERIOR OLIVE; LATERAL SUPERIOR OLIVE; BINAURAL INTERACTION; INTERAURAL INTENSITY ID SINGLE AUDITORY UNITS; SOUND PRESSURE LEVEL; CENTRAL NUCLEUS; BRAIN-STEM; LATERAL LEMNISCUS; ACOUSTIC CHIASM; ALBINO-RAT; COCHLEAR NUCLEUS; DORSAL NUCLEUS; CAT AB The binaural responses of cells in the rat's inferior colliculus were determined following either unilateral or bilateral lesions of the superior olivary complex (SOC). The lesions were made by local injection of kainic acid through a glass micropipette lowered stereotaxically into the auditory brain stem After a recovery period of at least two weeks, neural responses to pure tone pulses were recorded from the inferior colliculus with tungsten microelectrodes inserted into the central nucleus. Attention was focused on neurons that exhibited binaural suppression, ie., were excited by contralateral and inhibited by bilateral stimulation. Binaural suppression responses were still present following complete unilateral destruction of the superior olive either ipsilateral or contralateral to the recording site. Binaural responses were also present following bilateral lesions of the SOC. Furthermore, the shape and slope of interaural intensity difference functions were not statistically different for normal animals and animals with either unilateral or bilateral SOC lesions. No differences were found among lesion groups or between recording sites ipsilateral or contralateral to the lesions. These data suggest that the superior olive is not essential for binaural interaction and that supraolivary structures play a significant role in shaping binaural responses in the inferior colliculus. C1 CARLETON UNIV,DEPT PSYCHOL,SENSORY NEUROSCI LAB,OTTAWA K1S 5B6,ONTARIO,CANADA. CR ADAMS JC, 1983, J COMP NEUROL, V215, P275, DOI 10.1002/cne.902150304 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 AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 AOKI E, 1988, BRAIN RES, V442, P63, DOI 10.1016/0006-8993(88)91432-1 BANIKS MI, 1990, SOC NEUR ABSTR, V16, P722 BENEVENT.LA, 1970, BRAIN RES, V17, P387, DOI 10.1016/0006-8993(70)90248-9 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P442 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CAIRD D, 1983, EXP BRAIN RES, V52, P385 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 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 FLAMMINO F, 1975, J ACOUST SOC AM, V57, P692, DOI 10.1121/1.380494 GEISLER CD, 1969, J NEUROPHYSIOL, V32, P960 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GLENDENNING KK, 1983, J NEUROSCI, V3, P1521 GLENN SL, 1991, ASS RES OTOLARYNGOL, V14, P22 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GOLDBERG JM, 1967, J COMP NEUROL, V129, P143, DOI 10.1002/cne.901290203 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 GUINAN JJ, 1972, INT J NEUROSCI, V4, P101, DOI 10.3109/00207457209147165 Harrison J M, 1970, Contrib Sens Physiol, V4, P95 HUTSON KA, 1991, J COMP NEUROL, V312, P105, DOI 10.1002/cne.903120109 HUTSON K A, 1987, Society for Neuroscience Abstracts, V13, P548 INBODY SB, 1981, BRAIN RES, V210, P361, DOI 10.1016/0006-8993(81)90910-0 IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KELLY JB, 1991, HEARING RES, V56, P273, DOI 10.1016/0378-5955(91)90177-B MASTERTON RB, 1979, BRAIN RES, V173, P156, DOI 10.1016/0006-8993(79)91105-3 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 NELSON PG, 1966, J NEUROPHYSIOL, V26, P908 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 D L, 1986, Society for Neuroscience Abstracts, V12, P1271 ROONEY BJ, 1991, J NEUROSCI METH, V39, P65, DOI 10.1016/0165-0270(91)90094-G ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SALLY SL, 1992, BRAIN RES, V572, P5, DOI 10.1016/0006-8993(92)90444-E SEMPLE MN, 1987, J NEUROPHYSIOL, V57, P1130 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SEMPLE MN, 1979, J NEUROPHYSIOL, V42, P1626 SHNEIDERMAN A, 1988, J COMP NEUROL, V276, P188, DOI 10.1002/cne.902760204 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 STILLMAN RD, 1972, EXP NEUROL, V36, P118, DOI 10.1016/0014-4886(72)90140-9 STOPP PE, 1983, HEARING PHYSL BASES, P176 STRUTZ J, 1984, BRAIN RES, V299, P174, DOI 10.1016/0006-8993(84)90803-5 SYKA J, 1981, EXP BRAIN RES, V44, P11, DOI 10.1007/BF00238744 SYKA J, 1981, NEURONAL MECH HEARIN, P137 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 TSUCHITA.C, 1969, J ACOUST SOC AM, V46, P979, DOI 10.1121/1.1911818 WENSTRUP JJ, 1988, J NEUROPHYSIOL, V60, P1369 WENSTRUP JJ, 1985, HEARING RES, V17, P91 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 NR 59 TC 38 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 AUG PY 1992 VL 61 IS 1-2 BP 73 EP 85 DI 10.1016/0378-5955(92)90038-O PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800010 PM 1526896 ER PT J AU TAKEUCHI, S MARCUS, DC WANGEMANN, P AF TAKEUCHI, S MARCUS, DC WANGEMANN, P TI CA-2+-ACTIVATED NONSELECTIVE CATION, MAXI K+ AND CL- CHANNELS IN APICAL MEMBRANE OF MARGINAL CELLS OF STRIA VASCULARIS SO HEARING RESEARCH LA English DT Article DE GERBIL; INNER EAR; PATCH CLAMP TECHNIQUE; POTASSIUM SECRETION ID TRANSEPITHELIAL ELECTRICAL RESPONSES; NONSENSORY REGION; GERBIL UTRICLE; INTRACELLULAR CALCIUM; SODIUM-TRANSPORT; COLLECTING DUCT; GUINEA-PIG; POTASSIUM; RAT; POTENTIALS AB Patch clamp recordings on the apical membrane of marginal cells of the stria vascularis of the gerbil were made in the cell-attached and excised configuration. Marginal cells are thought to secrete K+ into and absorb Na+ from endolymph. Four types of channel were identified; the most frequently observed channel was a small, nonselective cation channel which was highly similar to that found in the apical membrane of vestibular dark cells (Marcus et al., (1992) Am. J. Physiol. 262, C1423-C1429). The small nonselective cation channel was equally conductive (26.7 +/- 0.3 pS; N = 49) for K+, Na+, Rb+, Li+ and Cs+, 1.6 times more permeable to NH4+, but not permeable to Cl-, Ca2+, Ba2+ or N-methyl-D-glucamine. This channel yielded linear current-voltage relations which passed nearly through the origin (intercept: - 2.2 +/- 0.4 mV, N = 49) when conductive monovalent cations were present on both sides of the membrane in equal concentrations. Channel activity required the presence of Ca2+ at the cytosolic face but not the extracellular (endolymphatic) face; there was essentially no activity for cytosolic Ca2+ less-than-or-equal-to 10(-7) M Ca2+ and full activity for greater-than-or-equal-to 10(-5) M. Cell-attached recordings had a conductance of 28.6 +/- 2.2 pS (N = 6) and a reversal voltage of - 2.2 +/- 5.2 mV (N = 3) which was interpreted to reflect the intracellular potential of marginal cells under the present conditions. The three other types of channel were a Cl- channel (approximately 50 pS; N = 2), a maxi-K+ channel (approximately 230 pS; N = 1), and another large channel, probably cation nonselective (approximately 170 pS; N = 1). The 27 pS nonselective cation channel may be involved in K+ secretion and Na+ absorption under stimulated conditions which produce an elevated intracellular Ca2+; however, consideration of the apparent channel density in relation to the total transepithelial K+ flux suggests that these channels are not sufficient to account for K+ secretion. C1 BOYS TOWN NATL RES HOSP,BIOPHYS LAB,OMAHA,NE 68131. RI Wangemann, Philine/N-2826-2013 CR BEAR CE, 1990, AM J PHYSIOL, V258, pC421 COLQUHOUN D, 1983, SINGLE CHANNEL RECOR, P170 COOK DI, 1990, J MEMBRANE BIOL, V114, P37, DOI 10.1007/BF01869383 GOGELEIN H, 1989, PFLUG ARCH EUR J PHY, V413, P287, DOI 10.1007/BF00583543 GOGELEIN H, 1990, BIOCHIM BIOPHYS ACTA, V1027, P191, DOI 10.1016/0005-2736(90)90084-2 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HEBERT RL, 1991, J CLIN INVEST, V87, P1992, DOI 10.1172/JCI115227 HILLE B, 1992, IONIC CHANNELS EXCIT, P371 JOHNSTON.BM, 1972, Q REV BIOPHYS, V5, P1 KATSUKI Y, 1966, SCIENCE, V151, P1544, DOI 10.1126/science.151.3717.1544 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 LIGHT DB, 1988, AM J PHYSIOL, V255, pF278 LIU DS, 1991, ACTA OTO-LARYNGOL, V111, P298, DOI 10.3109/00016489109137391 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1978, LARYNGOSCOPE, V88, P1825 MARCUS DC, 1983, HEARING RES, V12, P17, DOI 10.1016/0378-5955(83)90116-8 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MARCUS NY, 1990, HEARING RES, V44, P13, DOI 10.1016/0378-5955(90)90018-K MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 NITSCHKE R, 1991, PFLUG ARCH EUR J PHY, V417, P622, DOI 10.1007/BF00372961 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PARTRIDGE LD, 1988, TRENDS NEUROSCI, V11, P69, DOI 10.1016/0166-2236(88)90167-1 RAE JL, 1990, EXP EYE RES, V50, P373, DOI 10.1016/0014-4835(90)90138-K SALT AN, 1982, JPN J PHYSIOL, V32, P219 SCHON F, 1983, ARCH OTO-RHINO-LARYN, V237, P125, DOI 10.1007/BF00463611 SELLICK P M, 1975, Progress in Neurobiology (Oxford), V5, P337, DOI 10.1016/0301-0082(75)90015-5 STERKERS O, 1982, AM J PHYSIOL, V243, pF173 TAKEUCHI S, 1991, J GEN PHYSIOL, V98, pA28 TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 THALMANN R, 1989, 2 INT S MEN DIS, P55 WANGEMANN P, 1989, PFLUG ARCH EUR J PHY, V414, P656, DOI 10.1007/BF00582132 WEBER A, 1989, PFLUG ARCH EUR J PHY, V414, P564, DOI 10.1007/BF00580992 YELLEN G, 1982, NATURE, V296, P357, DOI 10.1038/296357a0 NR 37 TC 55 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 AUG PY 1992 VL 61 IS 1-2 BP 86 EP 96 DI 10.1016/0378-5955(92)90039-P PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800011 PM 1382049 ER PT J AU GRATTON, MA WRIGHT, CG AF GRATTON, MA WRIGHT, CG TI ALTERATIONS OF INNER-EAR MORPHOLOGY IN EXPERIMENTAL HYPERCHOLESTEROLEMIA SO HEARING RESEARCH LA English DT Article DE CHINCHILLA; COCHLEA; GLYCOGEN; OUTER HAIR CELLS; STRIA VASCULARIS ID HEARING-LOSS; HYPERLIPIDEMIA; CHOLESTEROL; GLYCOGEN; NOISE; CHINCHILLA; MEMBRANE AB Previous clinical and experimental studies have indicated that auditory function may be compromised by hypercholesterolemia. In this investigation, inner ear tissue from chinchillas maintained on a cholesterol-supplemented diet for 3 months was examined for morphological alterations which might underlie the physiological changes observed with this condition in earlier studies. Ultrastructural analysis of cochleas from 16 hypercholesterolemic chinchillas revealed alterations in both the stria vascularis and outer hair cells. Strial marginal cells throughout the cochlea and outer hair cells of the apical turn, contained electron-lucent patches of an amorphous material. These patches had the morphological characteristics and histochemical properties of glycogen. Mild extracellular edema and increased numbers of lysosomes were also noted in the stria vascularis of experimental animals. These alterations suggest that chronic hypercholesterolemia metabolically stresses inner ear tissue. It is hypothesized that such changes could increase susceptibility of the cochlea to ototraumatic agents. C1 UNIV TEXAS,SW MED CTR,DEPT OTORHINOLARYNGOL,DALLAS,TX 75230. CR AXELSSON A, 1985, ACTA OTO-LARYNGOL, V100, P379, DOI 10.3109/00016488509126561 COOPER RA, 1975, J CLIN INVEST, V55, P115, DOI 10.1172/JCI107901 CUNNINGH.DR, 1974, AUDIOLOGY, V13, P470 DEBRUIJN WC, 1973, J ULTRA MOL STRUCT R, V42, P29, DOI 10.1016/S0022-5320(73)80004-8 DROCHMANS P, 1962, J ULTRA MOL STRUCT R, V6, P141, DOI 10.1016/S0022-5320(62)90050-3 DUVALL AJ, 1974, ANN OTO RHINOL LARYN, V83, P498 DUVALL AJ, 1976, ANN OTO RHINOL LARYN, V85, P234 FALBE-HANSEN J, 1963, Acta Otolaryngol, V56, P429, DOI 10.3109/00016486309127434 HILDESHEIMER M, 1982, HEARING RES, V8, P187, DOI 10.1016/0378-5955(82)90074-0 HUI SW, 1980, J CELL BIOL, V85, P283, DOI 10.1083/jcb.85.2.283 ISHII D, 1969, ACTA OTO-LARYNGOL, V67, P573, DOI 10.3109/00016486909125484 KARRER HE, 1960, J ULTRA MOL STRUCT R, V4, P191, DOI 10.1016/S0022-5320(60)90053-8 KYTE J, 1981, NATURE, V292, P201, DOI 10.1038/292201a0 LOPUKHIN YM, 1984, SOVIET SCI REV SUPPL, V4 MCCORMICK JG, 1972, J ACOUST SOC AM, V52, pA143 MINIO F, 1966, J ULTRA MOL STRUCT R, V16, P339, DOI 10.1016/S0022-5320(66)80067-9 MORIZONO T, 1978, ANN OTO RHINOL LARYN, V87, P804 MORIZONO T, 1982, OTOLARYNG HEAD NECK, V90, P814 MORIZONO T, 1985, ACTA OTO-LARYNGOL, V99, P516 PERLMAN H B, 1955, Ann Otol Rhinol Laryngol, V64, P1176 PILLSBURY HC, 1986, LARYNGOSCOPE, V96, P1112 PRIETO JJ, 1990, DEV BRAIN RES, V51, P138, DOI 10.1016/0165-3806(90)90268-4 REVEL JP, 1960, J BIOPHYS BIOCHEM CY, V8, P575, DOI 10.1083/jcb.8.3.575 ROSA F, 1967, J HISTOCHEM CYTOCHEM, V15, P14 ROSEN S, 1965, ARCHIV OTOLARYNGOL, V82, P236 ROSEN S, 1964, Trans Am Acad Ophthalmol Otolaryngol, V68, P433 RUBINSTEIN M, 1977, GERONTOLOGY, V23, P4 SHIGA T, 1980, EXPERIENTIA, V36, P127, DOI 10.1007/BF02004015 SIKORA MA, 1986, ACTA OTO-LARYNGOL, V102, P372, DOI 10.3109/00016488609119420 SPICER SS, 1982, HUM PATHOL, V13, P343, DOI 10.1016/S0046-8177(82)80224-4 THIERY JP, 1967, J MICROSC-OXFORD, V6, P987 THOMOPOULOS GN, 1987, J ELECTRON MICR TECH, V5, P17, DOI 10.1002/jemt.1060050103 TSAI MT, 1989, OTOLARYNGOL HEAD NEC, V101, pS200 WRIGHT CG, 1988, ANN OTO RHINOL LARYN, V97, P67 YANG XR, 1990, FASEB J, V4, P3140 NR 35 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 AUG PY 1992 VL 61 IS 1-2 BP 97 EP 105 DI 10.1016/0378-5955(92)90040-T PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800012 PM 1526897 ER PT J AU KUJAWA, SG GLATTKE, TJ FALLON, M BOBBIN, RP AF KUJAWA, SG GLATTKE, TJ FALLON, M BOBBIN, RP TI INTRACOCHLEAR APPLICATION OF ACETYLCHOLINE ALTERS SOUND-INDUCED MECHANICAL EVENTS WITHIN THE COCHLEAR PARTITION SO HEARING RESEARCH LA English DT Article DE EFFERENTS; ACETYLCHOLINE; ACOUSTIC DISTORTION PRODUCTS; COCHLEAR MECHANICS; OLIVOCOCHLEAR NEURONS; OUTER HAIR CELLS ID OUTER HAIR-CELLS; CROSSED OLIVOCOCHLEAR BUNDLE; AUDITORY-NERVE FIBERS; ACOUSTIC DISTORTION; STIMULATION; RESPONSES; SYSTEM; CAT AB Activation of olivocochlear (OC) efferent fibers has been suggested to alter micromechanical events occurring within the cochlear partition, possibly through an effect of the efferent neurotransmitter (acetylcholine; ACh) on outer hair cells (OHCs). Based on the widely-accepted assumption that otoacoustic emissions reflect OHC activity, we investigated the in vivo influence of ACh on OHCs by studying alterations in emission amplitude with local ACh application. Distortion product otoacoustic emissions (DPOAEs) were measured in anesthetized guinea pigs before, during, and after intracochlear application of ACh (250-mu-M) with the cholinesterase inhibitor, eserine (20-mu-M). Perfusion of ACh/eserine was associated with a desensitizing reduction in DPOAE amplitude of approximately 4.4 dB. This reduction was intensity-dependent, with greater and more consistent reductions observed for DPOAEs elicited by low- than by moderate-intensity primaries. The response reduction was not seen during consecutive ACh perfusions performed without an intervening artificial perilymph wash, and was effectively blocked in the presence of pharmacologic antagonists of OC efferent activity (curare, 50-mu-M; strychnine, 50-mu-M). Finally, a similar alteration in DPOAE amplitude was never seen during perfusion of the control (artificial perilymph) solution alone. It is argued that these results support the hypothesis that OC efferent activation can alter sound-induced cochlear mechanical events. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. UNIV ARIZONA,DEPT PHARMACEUT RES,TUCSON,AZ 85721. CR [Anonymous], 1985, NIH PUBLICATION ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BOBBIN RP, 1971, NATURE-NEW BIOL, V231, P222 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 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 BROWN SE, 1990, ABSTR ASS RES OT, V13, P230 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E DALLOS P, 1985, P207 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DESMEDT J. E., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1478, DOI 10.1121/1.1918374 DOLAN DF, 1988, J ACOUST SOC AM, V77, P1475 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 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, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 KUJAWA SG, 1991, ABSTR ASS RES OT, V14, P127 LEVINE RR, 1989, TRENDS PHARM SCI S LITTMAN TA, 1990, THESIS LOUISIANA STA MOULIN A, 1992, ABSTR ASS RES OT, V15, P157 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NORRIS CH, 1988, HEARING RES, V32, P197, DOI 10.1016/0378-5955(88)90092-5 PATUZZI R, 1991, INT S OTOACOUSTIC EM PLINKERT PK, 1990, HEARING RES, V44, P25, DOI 10.1016/0378-5955(90)90019-L PUEL JL, 1990, J ACOUST SOC AM, V76, P1713 RUBEL EW, 1991, ABSTR ASS RES OT, V14, P84 RUGGERO MA, 1990, J ACOUST SOC AM, V87, P1612, DOI 10.1121/1.399409 SALT AN, 1986, NEUROBIOLOGY HEARING, P109 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SLEPECKY N, 1988, HEARING RES, V34, P119, DOI 10.1016/0378-5955(88)90099-8 TONNDORF J, 1962, ANN OTO RHINOL LARYN, V71, P801 WATSON S, 1990, TRENDS PHARM SCI S WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WIEDERHOLD ML, 1985, J ACOUST SOC AM S1, V77, pS95, DOI 10.1121/1.2022609 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 NR 48 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 AUG PY 1992 VL 61 IS 1-2 BP 106 EP 116 DI 10.1016/0378-5955(92)90041-K PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800013 PM 1326504 ER PT J AU NICOL, KMM HACKNEY, CM EVANS, EF PRATT, SR AF NICOL, KMM HACKNEY, CM EVANS, EF PRATT, SR TI BEHAVIORAL EVIDENCE FOR RECOVERY OF AUDITORY FUNCTION IN GUINEA-PIGS FOLLOWING KANAMYCIN ADMINISTRATION SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEA; GUINEA PIG; HAIR CELL; KANAMYCIN ID HAIR CELL REGENERATION; CHRONIC GENTAMICIN TREATMENT; SEVERE ACOUSTIC TRAUMA; CHICK COCHLEA; AMINOGLYCOSIDE OTOTOXICITY; THRESHOLDS; NERVE; ANTIBIOTICS; TOXICITY; DAMAGE AB Deterioration followed by recovery of behavioural absolute threshold and frequency selectivity has been observed in guinea pigs following kanamycin administration of 200 mg/kg body weight daily for 16 days. Deterioration in function consistently follows a high-to-low frequency pattern and recovery generally occurs at the lowest of the high (8-32 kHz) frequencies affected. The degree of recovery is related to the magnitude of the threshold elevation; where large (40-45 dB) elevations occur initially, the process appears to be partial since threshold recovers only to within 5-12 dB of pre-administration levels. In instances where smaller threshold elevations (5-20 dB) take place initially, recovery can sometimes be complete. However, when threshold elevations of over 50 dB occur, no recovery is apparent. Recovery is relatively slow, taking place over periods of up to 100 days post-kanamycin administration. Hair cell counts have established that the threshold elevation which remains in instances of partial recovery is not related to a reduction in hair cell numbers at the light microscope level. C1 UNIV KEELE, DEPT COMMUN & NEUROSCI, KEELE ST5 5BG, STAFFS, ENGLAND. CR ADELMAN C, 1989, ANN OTO RHINOL LARYN, V98, P283 ARAN JM, 1975, ACTA OTO-LARYNGOL, V79, P24, DOI 10.3109/00016487509124650 BALLANTY.J, 1973, AUDIOLOGY, V12, P325 COLDING H, 1989, ACTA PAEDIATR SCAND, V6, P840 CORWIN JT, 1986, BIOL CHANGE OTOLARYN, P291 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 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, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DALLOS P, 1974, AUDIOLOGY, V13, P227 Evans E. F., 1989, BRIT J AUDIOL, V23, P151 EVANS EF, 1992, ADV BIOSCI, V83, P159 EVANS E F, 1978, Scandinavian Audiology Supplementum, P9 EVANS EF, 1975, AUDIOLOGY, V14, P419 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 FEE WE, 1980, LARYNGOSCOPE, V90, P1, DOI 10.1288/00005537-198010001-00001 FORGE A, 1985, HEARING RES, V19, P171, DOI 10.1016/0378-5955(85)90121-2 FORGE A, 1987, HEARING RES, V31, P253, DOI 10.1016/0378-5955(87)90195-X FROST JO, 1960, OTOTOXICITY AM REV R, V82, P23 FURNESS DN, 1985, HEARING RES, V18, P177, DOI 10.1016/0378-5955(85)90010-3 GLASBERG BR, 1984, J ACOUST SOC AM, V75, P536, DOI 10.1121/1.390487 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HACKNEY CM, 1987, BR J AUDIOL, V21, P319 HACKNEY CM, 1989, BR J AUDIOL, V23, P160 HACKNEY CM, 1990, LECT NOTES BIOMATH, V87, P10 HARRISON RV, 1977, INNER EAR BIOL, P105 HAWKINS JE, 1977, C INNER EAR BIOL, P327 HAWKINS J. E., 1959, ANN OTOL RHINOL AND LARYNGOL, V68, P698 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 KAING NYS, 1970, CIBA F S SENSORINEUR, P241 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 KOHOLET D, 1990, PAEDIATRIC RES, V28, P232 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MCCRORIE TI, 1989, AM J DIS CHILD, V143, P1328 MOFFAT DA, 1977, J LARYNGOL OTOL, V91, P511, DOI 10.1017/S0022215100083985 OUCHI J, 1969, PRACT-OTO-RHINO-LARY, V31, P218 Pick G., 1977, PSYCHOPHYSICS PHYSL, P273 Pick G, 1983, HEARING PHYSL BASES, P393 PICK GF, 1980, J ACOUST SOC AM, V68, P1085, DOI 10.1121/1.384979 PRATT SR, 1988, 25TH WORKSH INN EAR, P96 PRATT SR, 1983, BR J AUDIOL, V17, P120 Pratt S R, 1982, Br J Audiol, V16, P117, DOI 10.3109/03005368209081456 PRATT SR, 1984, BR J AUDIOL, V18, P248 Prosen C. A., 1980, EXPT CLIN NEUROTOXIC, P62 PROSEN CA, 1978, J ACOUST SOC AM, V63, P599 ROBERTSON D, 1979, J ACOUST SOC AM, V66, P466, DOI 10.1121/1.383097 ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 RUBEN RJ, 1967, ACTA OTOLARYNGOL S, V220 RUSSELL NJ, 1979, ACTA OTO-LARYNGOL, V88, P369, DOI 10.3109/00016487909137181 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 RYAN A, 1979, J ACOUST SOC AM, V66, P370, DOI 10.1121/1.383194 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X STEBBINS WC, 1975, BEHAVIOURAL TOXICOLO, P401 STUPP H, 1967, ARCHIV OTOLARYNGOL, V86, P515 SYKA J, 1980, HEARING RES, V3, P205, DOI 10.1016/0378-5955(80)90047-7 TAYLOR MM, 1967, J ACOUST SOC AM, V41, P282 THEOPOLD HM, 1977, ACTA OTO-LARYNGOL, V84, P57, DOI 10.3109/00016487709123942 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WEST P D B, 1990, British Journal of Audiology, V24, P89, DOI 10.3109/03005369009077849 WILSON JP, 1972, CAPACITIVE PROBE MEA, P172 WINKEL O, 1978, ACTA OTO-LARYNGOL, V86, P212, DOI 10.3109/00016487809124738 YLIKOSKI J, 1974, ACTA OTO-LARYNGOL, P5 NR 67 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 AUG PY 1992 VL 61 IS 1-2 BP 117 EP 131 DI 10.1016/0378-5955(92)90042-L PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800014 PM 1526883 ER PT J AU HANGFU, M ZHAO, JY DIN, DL AF HANGFU, M ZHAO, JY DIN, DL TI THE PROPHYLACTIC EFFECT OF THYROXINE ON KANAMYCIN OTOTOXICITY IN GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE THYROXINE; OTOTOXICITY; KANAMYCIN CONCENTRATION AB Guinea pigs receiving intramuscular kanamycin sulfate 400 mg/kg daily and thyroxin 10 mg/kg orally every other day for 9 days were studied to determine whether thyroxin prevents toxic damage to the cochlea from kanamycin. The auditory brainstem response thresholds of wave IV evoked by tone pip stimuli at 4 and 8 kHz were found to be 19.1 dB and 27.2 dB poorer, respectively, for the kanamycin-only animals. Less than 10% of outer hair cells were damaged in 80% of basal turns but without any involvement in the rest turns in animals given thyroxin. Over 50% of outer hair cells were damaged in 65.4% of basal turns and over 50% of the second and third turns were also involved in the kanamycin-only group. Our study suggests that thyroxin reduces the accumulation of kanamycin in the perilymph and prevents the ototoxicity of kanamycin. RP HANGFU, M (reprint author), SHANGHAI MED UNIV 2,REN JI HOSP,DEPT OTOLARYNGOL,145 SHAN DONG C RD,SHANGHAI,PEOPLES R CHINA. CR HILGER J A, 1956, Ann Otol Rhinol Laryngol, V65, P395 KONONEN A, 1971, LARYNGOSCOPE, V81, P947 MEYERHOFF WL, 1976, LARYNGOSCOPE, V86, P483, DOI 10.1288/00005537-197604000-00002 Mizukoshi O, 1967, Acta Otolaryngol, V64, P45, DOI 10.3109/00016486709139091 POST JAMES T., 1964, LARYNGOSCOPE, V74, P221 RITTER FN, 1960, LARYNGOSCOPE, V60, P393 STUPP H, 1967, ARCHIV OTOLARYNGOL, V86, P515 WHITHERS BT, 1972, LARYNGOSCOPE, V82, P779 NR 8 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 1992 VL 61 IS 1-2 BP 132 EP 136 DI 10.1016/0378-5955(92)90043-M PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800015 PM 1526885 ER PT J AU HARVEY, D STEEL, KP AF HARVEY, D STEEL, KP TI THE DEVELOPMENT AND INTERPRETATION OF THE SUMMATING POTENTIAL RESPONSE SO HEARING RESEARCH LA English DT Article DE SUMMATING POTENTIALS; COCHLEAR RESPONSES; DEVELOPMENT; MOUSE ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; MAMMALIAN COCHLEA; MOUSE COCHLEA; INNER-EAR; FREQUENCY; GERBIL AB The development of cochlear responses in the mouse was investigated, recording from the round window. Positive summating potentials (SP) could be detected as early as 7 days after birth in some individuals, the first signs of negative SP occurred in mice aged 10 days, and compound action potentials were first detected at 11 days of age. These early responses were obtained with relatively low frequency stimuli (usually 6 kHz). All waveforms recorded from 20 day old mice could be interpreted as simple additions of positive and negative SP and compound action potentials, each with different amplitudes and latencies. Positive SP showed both fast and slow components. Our observations are consistent with the positive SP with only a fast component arising from the basal turn inner hair cells, the positive SP with fast and slow components being generated by both inner and outer hair cells in the basal turn, and the negative SP seen at low frequencies of stimulation originating from depolarisation of hair cells in the apical turn. Summating potentials may thus be useful for investigating inner and outer hair cell function seperately in abnormal cochleas in which it is not known which cell type primarily is affected. C1 MRC, INST HEARING RES, UNIV PK, NOTTINGHAM NG7 2RD, ENGLAND. CR Anggard L., 1965, ACTA OTOLARYNGOLOGIC, V203, P1 ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 BOCK GR, 1983, ACTA OTO-LARYNGOL, V96, P39, DOI 10.3109/00016488309132873 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V315, P317 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1972, ACTA OTO-LARYNGOL, P1 Dallos P., 1973, AUDITORY PERIPHERY B DAVIS H, 1958, AM J PHYSIOL, V195, P251 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 GOLDSTEIN R, 1954, AM J PHYSIOL, V178, P331 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HARVEY D, 1989, THESIS U NOTTINGHAM HARVEY D, 1992, UNPUB FOCAL POINT DE HENRY KR, 1985, HEARING RES, V18, P245, DOI 10.1016/0378-5955(85)90041-3 HONRUBIA VH, 1969, J ACOUST SOC AM, V45, P1443, DOI 10.1121/1.1911622 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 JOHNSTON.JR, 1966, J ACOUST SOC AM, V40, P1405, DOI 10.1121/1.1910240 KONISHI T, 1963, J ACOUST SOC AM, V35, P1448, DOI 10.1121/1.1918712 Mikaelian D, 1965, ACTA OTO-LARYNGOL, V59, P451, DOI DOI 10.3109/00016486509124579 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X PESTALOZZA G, 1956, AM J PHYSIOL, V185, P595 PUJOL R, 1985, ACTA OTOLARYNGOL S, V421, P56 Romand R., 1983, DEV AUDITORY VESTIBU, P47 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1977, NATURE, V267, P858, DOI 10.1038/267858a0 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SCHMIDT RS, 1963, J EXP ZOOL, V153, P227, DOI 10.1002/jez.1401530305 STEEL KP, 1992, DEV AUDITORY VESTIBU, V2 STEEL KP, 1989, DEVELOPMENT, V107, P453 STEEL KP, 1983, BEHAV NEUROSCI, V97, P381, DOI 10.1037//0735-7044.97.3.381 VANDEELEN GW, 1986, ACTA OTO-LARYNGOL, V101, P207, DOI 10.3109/00016488609132829 WOOLF NK, 1988, HEARING RES, V35, P131, DOI 10.1016/0378-5955(88)90112-8 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 41 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 AUG PY 1992 VL 61 IS 1-2 BP 137 EP 146 DI 10.1016/0378-5955(92)90044-N PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800016 PM 1526886 ER PT J AU MCGEE, T KRAUS, N LITTMAN, T NICOL, T AF MCGEE, T KRAUS, N LITTMAN, T NICOL, T TI CONTRIBUTIONS OF MEDIAL GENICULATE-BODY SUBDIVISIONS TO THE MIDDLE LATENCY RESPONSE SO HEARING RESEARCH LA English DT Article DE AUDITORY MIDDLE LATENCY RESPONSE; MEDIAL GENICULATE BODY; AUDITORY PATHWAY, PRIMARY AND NONPRIMARY ID GUINEA-PIG; CAT; ORGANIZATION; DIVISION; SYSTEMS; SLEEP; MLRS AB Ongoing studies in our laboratory, concerned with identifying the neural pathways responsible for the auditory middle latency response (MLR), have involved analysis of surface and intracranial potentials following pharmacologic inactivation (with lidocaine) of small regions in the guinea pig brain. Previous studies indicate that MLR surface waves recorded over the temporal lobe originate from pathways anatomically distinct from those that generate MLR waves recorded over the midline. The medial geniculate body (MG) contributes to both MLR responses. At issue here are the relative contributions of ventral and caudomedial subdivisions, which have been linked to primary and non-primary auditory pathways, respectively. Ventral and caudomedial subdivisions contributed to the surface-recorded MLR in a distinctive manner. Lidocaine injections to both areas reduced the amplitude of the surface temporal response. Caudomedial injections had a much greater effect on the surface midline responses than did injections in the ventral portion. Thus, the ventral division, a part of the primary auditory pathway, contributes chiefly to the temporal response. The caudomedial portion, which may be linked to non-primary auditory pathways, contributes to both responses. RP MCGEE, T (reprint author), NORTHWESTERN UNIV,EVOKED POTENTIALS LAB,2299 SHERIDAN RD,EVANSTON,IL 60208, USA. CR ANDERSEN RA, 1980, J COMP NEUROL, V194, P663, DOI 10.1002/cne.901940312 CALFORD MB, 1983, J NEUROSCI, V3, P2350 CHEN BM, 1986, ELECTROEN CLIN NEURO, V65, P373, DOI 10.1016/0168-5597(86)90016-X HILLE B, 1966, NATURE, V210, P1220, DOI 10.1038/2101220a0 KRAUS N, 1990, ADV AUDIOL, V6, P141 KRAUS N, 1989, EAR HEARING, V10, P339, DOI 10.1097/00003446-198912000-00004 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 KRAUS N, 1992, IN PRESS AUDITORY SY, V2 KRAUS N, 1992, IN PRESS BRAIN RES LITTMAN T, 1992, IN PRESS ELECTROENCE Luparello T. J., 1967, STEREOTAXIC ATLAS FO MCGEE T, 1991, BRAIN RES, V544, P211, DOI 10.1016/0006-8993(91)90056-2 MCGEE TJ, 1983, AM J OTOLARYNG, V4, P116, DOI 10.1016/S0196-0709(83)80013-1 NIIMI K, 1979, ADV ANATOMY EMBRYOLO, V57 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 RODRIGUESDAGAEFF C, 1989, HEARING RES, V39, P103, DOI 10.1016/0378-5955(89)90085-3 SMITH DI, 1987, AM J OTOLARYNG, V8, P241, DOI 10.1016/S0196-0709(87)80010-8 WINER JA, 1984, HEARING RES, V15, P225, DOI 10.1016/0378-5955(84)90031-5 WINER JA, 1983, J NEUROSCI, V3, P2629 NR 20 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 AUG PY 1992 VL 61 IS 1-2 BP 147 EP 154 DI 10.1016/0378-5955(92)90045-O PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800017 PM 1526887 ER PT J AU DEMEMES, D SCARFONE, E AF DEMEMES, D SCARFONE, E TI FODRIN IMMUNOCYTOCHEMICAL LOCALIZATION IN THE STRIATED ORGANELLES OF THE RAT VESTIBULAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE FODRIN; VESTIBULAR HAIR CELL; IMMUNOCYTOCHEMICAL; DISTRIBUTION; STRIATED ORGANELLES ID SENSORY CELLS; BRUSH-BORDER; GUINEA-PIG; IMMUNOELECTRON MICROSCOPY; PARIETAL-CELLS; HUMAN FETUSES; ACTIN; SPECTRIN; IDENTIFICATION; MICROTUBULES AB The immunocytochemical distribution of a spectrin-related protein, fodrin was studied at the electron microscopic level in the rat vestibular hair cells. As previously demonstrated [Scarfone et al., Neurosci. Lett. 93, 13-18, 1988], an intense immunoreactivity was found in the cuticular plates. We demonstrate furthermore, here, for the first time the association of fodrin immunoreactivity with the striated infracuticular structures called striated organelles (SO). Fodrin was found in striated structures clearly identified as SO in both Type I and Type II hair cells. SO were labelled regardless of their location, subcuticular or associated with the plasma membrane of the cells. We suggest that fodrin, as in the cuticular plate, could participate to the Ca2+ dependent cross-linking of the actin filaments of the striated organelles and could play a role in their interaction with the submembraneous cytoskeleton. RP DEMEMES, D (reprint author), UNIV MONTPELLIER 2,NEUROPHYSIOL SENSORIELLE LAB,INSERM,U254,CP 089,PL E BATAILLON,F-34095 MONTPELLIER 5,FRANCE. CR BENNETT V, 1985, ANNU REV BIOCHEM, V54, P273, DOI 10.1146/annurev.biochem.54.1.273 CARLIN RK, 1983, J CELL BIOL, V96, P443, DOI 10.1083/jcb.96.2.443 CHABBERT C, 1991, NEUROREPORT, V2, P243, DOI 10.1097/00001756-199105000-00007 DIDIER A, 1990, HEARING RES, V46, P171, DOI 10.1016/0378-5955(90)90147-H DRENCKHAHN D, 1985, AUDITORY BIOCH, P312 Engström H, 1972, Acta Otolaryngol Suppl, V301, P75 FACH BL, 1985, CAN J BIOCHEM CELL B, V63, P372 FAVRE D, 1983, ACTA OTO-LARYNGOL, V96, P15, DOI 10.3109/00016488309132870 FAVRE D, 1986, DEV BRAIN RES, V25, P137, DOI 10.1016/0165-3806(86)90161-6 FLOCK A, 1981, J NEUROCYTOL, V10, P133, DOI 10.1007/BF01181749 FRIEDMANN I, 1963, J ULTRA MOL STRUCT R, V9, P123, DOI 10.1016/S0022-5320(63)80040-4 FUJIMOTO T, 1989, J HISTOCHEM CYTOCHEM, V37, P1589 FUJIMOTO T, 1989, J HISTOCHEM CYTOCHEM, V37, P1345 GLENNEY JR, 1983, J CELL BIOL, V96, P1491, DOI 10.1083/jcb.96.5.1491 HIROKAWA N, 1983, CELL, V32, P953, DOI 10.1016/0092-8674(83)90080-6 HOSHINO T, 1975, ACTA OTO-LARYNGOL, V80, P43, DOI 10.3109/00016487509121299 ISHIKAWA M, 1983, J BIOCHEM-TOKYO, V94, P1209 Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 KOBAYASHI N, 1988, CELL MOTIL CYTOSKEL, V11, P167, DOI 10.1002/cm.970110304 MANGEAT PH, 1988, BIOL CELL, V64, P261, DOI 10.1016/0248-4900(88)90001-9 MERCIER F, 1989, J CELL BIOL, V108, P441, DOI 10.1083/jcb.108.2.441 MIZUNO M, 1989, ACTA HISTOCHEM CYTOC, V22, P593 MOOSEKER MS, 1983, CELL, V35, P11, DOI 10.1016/0092-8674(83)90202-7 JORGENSEN JM, 1982, ACTA OTO-LARYNGOL, V94, P241, DOI 10.3109/00016488209128909 OHMORI H, 1988, J PHYSIOL-LONDON, V399, P115 PERRIN D, 1985, NATURE, V315, P589, DOI 10.1038/315589a0 RODMAN JS, 1986, EUR J CELL BIOL, V42, P319 ROSS M, 1982, PHYSIOLOGIST S, V25, pS113 ROSS MD, 1983, SCIENCE, V220, P622, DOI 10.1126/science.6682246 SANS A, 1989, HEARING RES, V40, P117, DOI 10.1016/0378-5955(89)90105-6 SANS A, 1989, ANAT EMBRYOL, V179, P457, DOI 10.1007/BF00319588 SCARFONE E, 1988, NEUROSCI LETT, V93, P13, DOI 10.1016/0304-3940(88)90004-3 SCARFONE E, 1989, TYPE 1 VESTIBULAR HA SHIMOOKA T, 1986, J NEUROCYTOL, V15, P715, DOI 10.1007/BF01625189 SLEPECKY N, 1981, ACTA OTO-LARYNGOL, V91, P189, DOI 10.3109/00016488109138499 SLEPECKY N, 1982, CELL TISSUE RES, V224, P15, DOI 10.1007/BF00217262 SOBIN A, 1983, ACTA OTO-LARYNGOL, V96, P407, DOI 10.3109/00016488309132726 SPOENDLIN H, 1966, ADV OTO-RHINO-LARYNG, V13, P19 VALAT J, 1991, NEUROSCI LETT, V127, P231, DOI 10.1016/0304-3940(91)90801-Y YONEDA K, 1990, J INVEST DERMATOL, V94, P724, DOI 10.1111/1523-1747.ep12876298 ZAGON IS, 1986, J NEUROSCI, V6, P2977 ZENNER HP, 1990, HEARING RES, V50, P289, DOI 10.1016/0378-5955(90)90052-Q NR 42 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 1992 VL 61 IS 1-2 BP 155 EP 160 DI 10.1016/0378-5955(92)90046-P PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800018 PM 1526888 ER PT J AU DEMANY, L SEMAL, C AF DEMANY, L SEMAL, C TI DETECTION OF INHARMONICITY IN DICHOTIC PURE-TONE DYADS SO HEARING RESEARCH LA English DT Article DE HARMONICITY PERCEPTION; FREQUENCY RATIOS; DICHOTIC LISTENING; SCENE ANALYSIS; PACS NUMBERS 4366JH, 4366RQ, 4375CD ID COMPLEX TONES; FREQUENCY-MODULATION; OCTAVE TEMPLATES; ORIGIN; PITCH; RECOGNITION; THRESHOLDS; PARTIALS; HEARING; CHROMA AB Thresholds for the detection of quasi-sinusoidal frequency ratio fluctuations were measured with stimuli consisting of dichotic dyads of simultaneous pure tones. The two component tones of each dyad were slowly modulated in frequency, in such a way that the ratio of their instantaneous frequencies oscillated (or not) around some standard frequency ratio (SFR). As in a previous study [Demany and Semal (1988) J. Acoust. Soc. Am. 83, 687-695), it was found that smaller oscillations could be detected when the SFR was precisely an octave (2/1) than when it was slightly smaller or larger (2/1 +/-50 or 100 cents). Similar `harmonicity effects' were obtained here for SFRs in the vicinity of a fifth (3/2), a twelfth (3/1), or a double octave (4/1). However, these harmonicity effects were generally less pronounced than those observed in the vicinity of an octave. Each of our four subjects provided evidence for a central sensitivity to the octave harmonicity, but the same consistency could not be found with respect to other kinds of harmonicity. C1 LAB AUDIOL EXPTL,INSERM,UNITE 229,BORDEAUX,FRANCE. RP DEMANY, L (reprint author), UNIV BORDEAUX 2,PSYCHOACOUST LAB,146 RUE LEO SAIGNAT,F-33076 BORDEAUX,FRANCE. RI Semal, Catherine/D-8592-2014 OI Semal, Catherine/0000-0002-2075-6265 CR Bachem A, 1937, J ACOUST SOC AM, V9, P146, DOI 10.1121/1.1915919 BEERENDS JG, 1989, J ACOUST SOC AM, V85, P813, DOI 10.1121/1.397974 BROADBENT DE, 1957, J ACOUST SOC AM, V29, P708, DOI 10.1121/1.1909019 BUELL TN, 1991, J ACOUST SOC AM, V90, P1894, DOI 10.1121/1.401668 BURNS EM, 1978, J ACOUST SOC AM, V63, P456, DOI 10.1121/1.381737 CARLYON RP, 1991, J ACOUST SOC AM, V89, P329, DOI 10.1121/1.400468 CARLYON RP, 1989, J ACOUST SOC AM, V85, P2563, DOI 10.1121/1.397750 CARLYON RP, 1992, J ACOUST SOC AM, V91, P279, DOI 10.1121/1.402770 DARWIN CJ, 1992, AUDITORY PHYSL PERCE DEMANY L, 1991, J ACOUST SOC AM, V90, P3019, DOI 10.1121/1.401776 DEMANY L, 1988, J ACOUST SOC AM, V83, P687, DOI 10.1121/1.396164 DEMANY L, 1989, PSYCHOACOUSTIQUE PER, P43 DEMANY L, 1989, 13TH P INT C AC BELG, V3, P15 DEMANY L, 1990, J ACOUST SOC AM, V88, P2126, DOI 10.1121/1.400109 DEMANY L, 1984, J ACOUST SOC AM, V76, P57, DOI 10.1121/1.391006 DEMANY L, 1991, PUBLICATIONS LABORAT, V128, P177 HARTMANN WM, 1990, J ACOUST SOC AM, V88, P1712, DOI 10.1121/1.400246 HOUTSMA AJM, 1968, J ACOUST SOC AM, V44, P383, DOI 10.1121/1.1970636 HOUTSMA AJM, 1972, J ACOUST SOC AM, V51, P520, DOI 10.1121/1.1912873 KALLMAN HJ, 1979, PERCEPT PSYCHOPHYS, V26, P32, DOI 10.3758/BF03199859 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 McAdams S., 1984, THESIS STANFORD U MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1853, DOI 10.1121/1.391936 MOORE BCJ, 1986, J ACOUST SOC AM, V80, P479, DOI 10.1121/1.394043 MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1861, DOI 10.1121/1.391937 OHGUSHI K, 1983, J ACOUST SOC AM, V73, P1694, DOI 10.1121/1.389392 Plomp R, 1976, ASPECTS TONE SENSATI ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 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 AUG PY 1992 VL 61 IS 1-2 BP 161 EP 166 DI 10.1016/0378-5955(92)90047-Q PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800019 PM 1526889 ER PT J AU FISCHER, FP AF FISCHER, FP TI QUANTITATIVE-ANALYSIS OF THE INNERVATION OF THE CHICKEN BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE BIRD; COCHLEA; HAIR CELL; INNERVATION ID SERIAL SECTION RECONSTRUCTION; OUTER HAIR-CELLS; EFFERENT INNERVATION; HUMAN ORGAN; INNER-EAR; AVIAN COCHLEA; NERVE-ENDINGS; NEURAL POLES; CORTI; ORGANIZATION AB Unlike the organ of Corti in mammals, the avian basilar papilla has no distinct populations of hair cells. Instead, there is a continuous change between the extreme forms (tall hair cells = THC, and short hair cells = SHC). The hair-cell innervation pattern is complicated, there being no simple gradient between THC (mainly innervated by afferent fibers) and SHC (mainly innervated by efferent fibers). In the basal half of the papilla, SHC have only efferent innervation. The lack of afferent innervation indicates that the function of basal SHC is restricted to the basilar papilla itself, perhaps modifying its mechanical properties. RP FISCHER, FP (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,W-8046 GARCHING,GERMANY. CR BILLETT TE, 1989, HEARING RES, V41, P189, DOI 10.1016/0378-5955(89)90010-5 CHANDLER JP, 1984, J COMP NEUROL, V222, P506, DOI 10.1002/cne.902220405 CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407 COLE KS, 1990, EXP BRAIN RES, V82, P585 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 FIRBAS W, 1983, HEARING RES, V10, P109, DOI 10.1016/0378-5955(83)90021-7 FISCHER FP, 1991, HEARING RES, V53, P281, DOI 10.1016/0378-5955(91)90061-D FISCHER FP, 1988, HEARING RES, V34, P87, DOI 10.1016/0378-5955(88)90053-6 GLEICH O, 1988, THESIS TU MUNCHEN HASHIMOTO S, 1989, ACTA OTO-LARYNGOL, V107, P387, DOI 10.3109/00016488909127527 HASHIMOTO S, 1990, ACTA OTO-LARYNGOL, V109, P228, DOI 10.3109/00016489009107438 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 NADOL JB, 1990, J ELECTRON MICR TECH, V15, P187, DOI 10.1002/jemt.1060150210 NADOL JB, 1983, LARYNGOSCOPE, V93, P599 NADOL JB, 1990, ANN OTO RHINOL LARYN, V99, P215 NADOL JB, 1983, LARYNGOSCOPE, V93, P780 PARK JC, 1984, ACTA OTO-LARYNGOL, V98, P72, DOI 10.3109/00016488409107536 Pujol R., 1986, NEUROBIOLOGY HEARING, P161 REBILLARD M, 1983, ACTA OTO-LARYNGOL, V96, P379, DOI 10.3109/00016488309132723 REYNOLDS ES, 1963, J CELL BIOL, V17, P208, DOI 10.1083/jcb.17.1.208 SMITH CA, 1985, FORM FUNCTIONS BIRDS, V3, P273 Takasaka T, 1987, Acta Otolaryngol Suppl, V435, P7 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 THORN L, 1972, SEP EXPERIENTIA, V28, P835 TILNEY LG, 1986, HEARING RES, V22, P55, DOI 10.1016/0378-5955(86)90077-8 TILNEY MS, 1987, HEARING RES, V25, P141, DOI 10.1016/0378-5955(87)90087-6 VANDERDURING M, 1985, FORTSCHRITTE ZOOLOGI, V30 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P277, DOI 10.1016/0306-4522(85)90178-2 NR 33 TC 111 Z9 112 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 1992 VL 61 IS 1-2 BP 167 EP 178 DI 10.1016/0378-5955(92)90048-R PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800020 PM 1526890 ER PT J AU SHANNONHARTMAN, S WONG, D MAEKAWA, M AF SHANNONHARTMAN, S WONG, D MAEKAWA, M TI PROCESSING OF PURE-TONE AND FM STIMULI IN THE AUDITORY-CORTEX OF THE FM BAT, MYOTIS-LUCIFUGUS SO HEARING RESEARCH LA English DT Article DE SPECTRAL PROCESSING; AUDITORY CORTEX; FREQUENCY ORGANIZATION; FM SWEEP; ECHOLOCATING BATS ID ECHOLOCATING BAT; SENSITIVE NEURONS; EPTESICUS-FUSCUS; MUSTACHE BAT; BIOSONAR SIGNALS; TARGET RANGE; REPRESENTATION; INFORMATION; FREQUENCY AB FM bats perceive their surroundings during echolocation by analyzing frequency-modulated (FM) acoustic signals. Results from this study indicate a cortical organization in Myotis lucifugus which is largely made up of neurons sensitive to FM sounds (FM-sensitive neurons). Three types of neurons were distinguished by their responses to pure-tone and FM stimuli: (1) Type I FM-sensitive units (83%), Type II FM-sensitive units (13%) and pure-tone sensitive units (4%). Type I FM-sensitive units responded to pure tones, but exhibited greater response magnitudes to FM stimuli when the best FM swept through the BF. An orderly frequency representation was found when the frequencies of pure tones essential for response (EPTs) in Type I units were mapped along the cortical surface. The EPTs for Type I neurons were usually found within the last millisecond of a downward FM sweep. As outlined by two neuronal network models, both the responses of Type I and II units could likely result from the convergence of excitatory and inhibitory lower level neurons with slightly differing BFs. Type II units were selective for an FM sweep and showed negligible to no response to pure-tone stimuli. Pure-tone sensitive units exhibited weak or no responses to FM stimuli. These neurons were clustered in a small area located rostrodorsal to the tonotopic zone and had significantly lower best frequencies than adjacent EPT frequencies of Type I FM-sensitive neurons. C1 INDIANA UNIV,SCH MED,DEPT ANAT,INDIANAPOLIS,IN 46202. CR BERKOWITZ A, 1989, HEARING RES, V41, P255, DOI 10.1016/0378-5955(89)90017-8 FENG AS, 1978, SCIENCE, V202, P645, DOI 10.1126/science.705350 FRIEND JH, 1966, J CELL PHYSIOL, V67, P319, DOI 10.1002/jcp.1040670212 Griffin DR, 1958, LISTENING DARK GRINNELL AD, 1963, J PHYSIOL-LONDON, V167, P38 HABERSETZER J, 1983, J COMP PHYSIOL, V152, P275 JEN PHS, 1989, J COMP PHYSIOL A, V165, P1, DOI 10.1007/BF00613794 MENDELSON JR, 1985, BRAIN RES, V327, P331, DOI 10.1016/0006-8993(85)91530-6 MOSS CF, 1989, J COMP PHYSIOL A, V165, P383, DOI 10.1007/BF00619357 NOVICK A, 1961, J EXP ZOOL, V148, P125, DOI 10.1002/jez.1401480203 ONEILL WE, 1979, SCIENCE, V203, P69, DOI 10.1126/science.758681 ONEILL WE, 1982, J NEUROSCI, V2, P17 PHILLIPS DP, 1985, EXP BRAIN RES, V58, P443 Sales GD, 1974, ULTRASONIC COMMUNICA SHANNON SL, 1988, THESIS PURDUE U W LA SHANNON S L, 1989, Society for Neuroscience Abstracts, V15, P111 SIMMONS JA, 1979, SCIENCE, V207, P1336 SIMMONS JA, 1990, J COMP PHYSIOL A, V166, P449 SIMMONS JA, 1974, SCIENCE, V186, P1330 SUGA N, 1965, J PHYSIOL-LONDON, V179, P26 SUGA N, 1968, J PHYSIOL-LONDON, V198, P51 Suga N., 1973, BASIC MECH HEARING, P675 SUGA N, 1965, J PHYSIOL-LONDON, V181, P671 SUGA N, 1988, FUNCTIONS AUDITORY S, P679 SUGA N, 1979, SCIENCE, V203, P270, DOI 10.1126/science.760193 SUGA N, 1969, J PHYSIOL-LONDON, V200, P555 SUGA N, 1978, SCIENCE, V200, P778, DOI 10.1126/science.644320 SUGA N, 1983, J NEUROPHYSIOL, V49, P1573 SULLIVAN WE, 1982, J NEUROPHYSIOL, V48, P1011 WHITFIEL.IC, 1965, J NEUROPHYSIOL, V28, P655 WOLLBERG Z, 1972, SCIENCE, V175, P212, DOI 10.1126/science.175.4018.212 WONG D, 1992, J COMP PHYSIOL A, V170, P393 WONG D, 1988, BRAIN RES, V453, P349, DOI 10.1016/0006-8993(88)90176-X NR 33 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 AUG PY 1992 VL 61 IS 1-2 BP 179 EP 188 DI 10.1016/0378-5955(92)90049-S PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800021 PM 1326505 ER PT J AU SOHMER, H FRIEDMAN, I AF SOHMER, H FRIEDMAN, I TI PROLONGED CONDUCTIVE HEARING-LOSS IN RAT PUPS CAUSES SHORTER BRAIN-STEM TRANSMISSION TIME SO HEARING RESEARCH LA English DT Article DE CONDUCTIVE HEARING LOSS; AUDITORY NERVE BRAIN-STEM EVOKED RESPONSES; DEPRIVATION; TRANSMISSION TIME; INFANCY ID AUDITORY EVOKED-POTENTIALS; MIDDLE-EAR EFFUSION; OTITIS-MEDIA; MULTIPLE-SCLEROSIS; ACOUSTIC DEPRIVATION; LANGUAGE-DEVELOPMENT; COCHLEAR NUCLEI; STEM RESPONSES; CHILDREN; DISEASE AB A carefully controlled study was conducted in rats to determine whether a reversible conductive hearing loss during the neonatal period could induce changes in central conduction and thereby perhaps contribute to an understanding of learning problems seen in children following conductive hearing loss in infancy. Ear plugs were inserted from post-natal day 9 in rat pups and auditory nerve brainstem evoked responses were recorded in the presence of ear plugs and following their removal on post-natal day 23. The I-IV interpeak latency (brainstem transmission time) was significantly shorter in the experimental rats several days after plug removal (day 28) compared to untreated control rats. This difference was not related to residual conductive loss, nor to different body weights and was present even in response to equal sensation level stimuli, and was not present in adult rats with similarly induced conductive hearing losses. It seems therefore that conductive hearing loss in the young animal (critical period?) can induce changes in central auditory conduction and may be related to the findings of smaller brainstem auditory neurons in sound deprived animals. These results have implications for neonatal hearing loss in humans. C1 HADASSAH UNIV HOSP,CTR SPEECH & HEARING,JERUSALEM,ISRAEL. RP SOHMER, H (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 1172,IL-91010 JERUSALEM,ISRAEL. CR ANTEBY I, 1986, INT J PEDIATR OTORHI, V12, P1, DOI 10.1016/S0165-5876(86)80051-9 BLAKEMOR.C, 1970, NATURE, V228, P477, DOI 10.1038/228477a0 BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 COATS AC, 1977, ARCH OTOLARYNGOL, V103, P605 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 DOYLE WJ, 1991, HEARING RES, V54, P145, DOI 10.1016/0378-5955(91)90144-X EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 FOLSOM RC, 1983, ANN OTO RHINOL LARYN, V92, P249 GUNNARSON AD, 1991, J SPEECH HEAR RES, V34, P1207 HAFNER H, 1986, INT J PEDIATR OTORHI, V12, P13 HAUSLER R, 1980, BRAIN RES, V191, P589, DOI 10.1016/0006-8993(80)91312-8 HENNEMAN E, 1965, J NEUROPHYSIOL, V28, P560 HOOD LJ, 1990, AUDIOLOGY TODAY, V2, P30 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X KAWAI S, 1989, BIOL NEONATE, V55, P268 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LENHARDT ML, 1985, ARCH OTOLARYNGOL, V111, P315 MATATHIAS O, 1985, ACTA OTO-LARYNGOL, V99, P369, DOI 10.3109/00016488509108925 MEYER SE, 1991, BR J AUDIOL, V25, P56 MOORE DR, 1990, SEMIN PERINATOL, V14, P294 Moore D R, 1985, Acta Otolaryngol Suppl, V421, P19 MOORE DR, 1991, AUDIOLOGY, V30, P91 MUSTILLO P, 1984, AUDIOLOGY, V23, P145 RACH GH, 1988, INT J PEDIATR OTORHI, V15, P253, DOI 10.1016/0165-5876(88)90080-8 RAPIN I, 1979, ANN OTO RHINOL LARYN, V88, P3 SAK RJ, 1981, ANN OTO RHINOL LARYN, V90, P546 SOHMER H, 1991, ACTA OTO-LARYNGOL, V111, P206, DOI 10.3109/00016489109137376 STURZEBECHER E, 1985, SCAND AUDIOL, V14, P83, DOI 10.3109/01050398509045927 TOMASULO RA, 1988, ANN NEUROL, V23, P204, DOI 10.1002/ana.410230218 WALGER M, 1989, LARYNGO RHINO OTOL, V58, P626 WALLACE IF, 1988, J SPEECH HEAR DISORD, V53, P245 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1983, EXP NEUROL, V79, P130, DOI 10.1016/0014-4886(83)90384-9 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 WIESEL TN, 1963, J NEUROPHYSIOL, V26, P978 NR 37 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 1992 VL 61 IS 1-2 BP 189 EP 196 DI 10.1016/0378-5955(92)90050-W PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JJ938 UT WOS:A1992JJ93800022 PM 1526891 ER PT J AU ELKINDHIRSCH, KE STONER, WR STACH, BA JERGER, JF AF ELKINDHIRSCH, KE STONER, WR STACH, BA JERGER, JF TI ESTROGEN INFLUENCES AUDITORY BRAIN-STEM RESPONSES DURING THE NORMAL MENSTRUAL-CYCLE SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; MENSTRUAL CYCLE; ESTROGEN EFFECT; ORAL CONTRACEPTIVES ID STEM RESPONSE; GENDER; AGE AB We evaluated the impact of the menstrual cycle on auditory brainstem response (ABR) latency in nine normally cycling women. Subjects (age 23-40 years) using no hormonal therapy were recruited and underwent ABR testing during four different phases of the same menstrual cycle: early follicular (cycle days 1 to 3); mid-cycle (cycle days 12 to 15); mid-luteal (cycle days 17 to 22), and premenstrual (cycle days 25-27). Cycles were verified by basal body temperature, an&serum estrogen (E2), progesterone (P), and gonadotropin levels. A control group of nine women (age 23-40 years) on oral contraceptives (Nordette-28) was also studied four times during a pill cycle. Results show a significant increase in the latency of wave III and wave V peak latencies and in the I-V interpeak interval associated with a high estrogen state at the mid-cycle phase. No statistically significant variations in latency were found in the birth control pill group. These data suggest the existence of brainstem auditory neural pathways that are sensitive to fluctuations in E2 levels during the menstrual cycle. C1 METHODIST HOSP,BAYLOR COLL MED,DEPT OTORHINOLARYNGOL,HOUSTON,TX 77030. METHODIST HOSP,BAYLOR COLL MED,DEPT COMMUN SCI,HOUSTON,TX 77030. RP ELKINDHIRSCH, KE (reprint author), METHODIST HOSP,BAYLOR COLL MED,DEPT MED,6565 FANNIN ST,B200,HOUSTON,TX 77030, USA. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 Beagley H A, 1978, Br J Audiol, V12, P69, DOI 10.3109/03005367809078858 Caspary D.M., 1986, NEUROBIOLOGY HEARING, P303 DEHAN CP, 1990, LARYNGOSCOPE, V100, P18 EYBALIN M, 1986, ARCH OTORHINOLAYNGOL, V246, P228 FAGAN PL, 1986, AUDIOLOGY, V25, P321 JERGER J, 1988, EAR HEARING, V9, P168, DOI 10.1097/00003446-198808000-00002 JERGER J, 1980, ARCH OTOLARYNGOL, V106, P387 MARTIN J V, 1991, Society for Neuroscience Abstracts, V17, P264 MARTIN MR, 1982, EXP NEUROL, V76, P675, DOI 10.1016/0014-4886(82)90135-2 MCCLELLAND RJ, 1979, AUDIOLOGY, V18, P462 ROOSENRUNGE G, 1984, EXP BRAIN RES, V54, P575 SCHWARTZ IR, 1986, NEUROBIOLOGY HEARING, P173 STOCKARD J J, 1978, American Journal of EEG Technology, V18, P177 TRUNE DR, 1978, HEARING RES, V32, P165 NR 15 TC 53 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 JUL PY 1992 VL 60 IS 2 BP 143 EP 148 DI 10.1016/0378-5955(92)90016-G PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800002 PM 1639724 ER PT J AU MIYAKITA, T HELLSTROM, PA FRIMANSON, E AXELSSON, A AF MIYAKITA, T HELLSTROM, PA FRIMANSON, E AXELSSON, A TI EFFECT OF LOW-LEVEL ACOUSTIC STIMULATION ON TEMPORARY THRESHOLD SHIFT IN YOUNG HUMANS SO HEARING RESEARCH LA English DT Article DE NOISE INDUCED HEARING LOSS; TEMPORARY THRESHOLD SHIFT; SUSCEPTIBILITY; TRAINING; MOTILITY ID COCHLEAR MECHANICS; NOISE; DAMAGE; EXPOSURE; HEARING AB To assess the effect of a low level acoustic stimulation on the susceptibility to noise, young human subjects were exposed to music at 70 dBA for 6 h per day during 9 days (training period). Noise sensitivity was assessed by measuring temporary threshold shift (TTS) induced by 105 dBSPL, 1/3 octave band noise at 2 kHz for 10 min. On the fifth day of the training period, a significant decrease of TTS was observed in the frequency range 3-3.5 kHz, in comparison with the baseline TTS obtained before being trained. As the training continued, the frequency range which showed a significant reduction of TTS expanded to 2-5 kHz. C1 LINDHOLMEN DEV AB,HEARING RES LAB,GOTHENBURG,SWEDEN. SAHLGRENS UNIV HOSP,DEPT AUDIOL & OTOLARYNGOL,S-41345 GOTHENBURG,SWEDEN. RP MIYAKITA, T (reprint author), KUMAMOTO UNIV,SCH MED,DEPT HYG,KUMAMOTO 860,JAPAN. CR BORG E, 1984, ACOUSTIC REFLEX, P413 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CANLON B, 1991, NOISE INDUCED HEARIN, P489 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 Flock A, 1988, Prog Brain Res, V74, P297 Gelfand S. A., 1990, HEARING INTRO PSYCHO, V2nd HAMERNIK RP, 1989, J ACOUST SOC AM, V86, P2129, DOI 10.1121/1.398473 HELLSTROM PA, 1991, J SOUND VIB, V151 HELLSTROM PA, 1992, UNPUB RELATIONSHIP S HENDERSON D, 1991, NOISE INDUCED HEARIN, P476 HENRY KR, 1984, HEARING RES, V16, P225, DOI 10.1016/0378-5955(84)90111-4 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBSCOMB DM, 1977, ACTA OTOLARYNGOL, V84, P44 Lindgren F., 1986, BASIC APPL ASPECTS N, P313 Miyakita T., 1980, Journal of the Acoustical Society of Japan, V36 MIYAKITA T, 1987, BRIT J IND MED, V44, P41 MOLLER AR, 1980, PUBLIC HLTH PREVENTI, P790 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Pickles JO, 1988, INTRO PHYSL HEARING RAJAN R, 1983, HEARING RES, V12, P185, DOI 10.1016/0378-5955(83)90105-3 RYAN AF, 1992, COMMUNICATION Sandén A, 1981, Acta Otolaryngol Suppl, V377, P75 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 27 TC 42 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 JUL PY 1992 VL 60 IS 2 BP 149 EP 155 DI 10.1016/0378-5955(92)90017-H PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800003 PM 1639725 ER PT J AU KOSSL, M AF KOSSL, M TI HIGH-FREQUENCY DISTORTION PRODUCTS FROM THE EARS OF 2 BAT SPECIES, MEGADERMA-LYRA AND CAROLLIA-PERSPICILLATA SO HEARING RESEARCH LA English DT Article DE COCHLEA; DISTORTION PRODUCTS; 2F1-F2, BAT; SALICYLATE ID OUTER HAIR-CELLS; ACOUSTIC DISTORTION; RESPONSE CHARACTERISTICS; OTOACOUSTIC EMISSIONS; MECHANICAL RESPONSES; MUSTACHE BAT; SENSITIVITY; COCHLEA; 2F1-F2 AB In two echolocating bat species, Megaderma lyra and Carollia perspicillata 2f1-f2 distortion products were measured acoustically in the outer ear canal for f1 frequencies between 5 and 95 kHz in an attempt to study nonlinear cochlear processes at high frequencies. Similar to other mammals, the input/output (I/O) functions of 2f1 - f2 show non-monotonicities and notches at f1 levels between 40-70 dB SPL. The slope of the initial rise of the 2f1 - f2 I/O functions increased with f1 frequency from 0.73 (5 kHz) to 1.41 (95 kHz) in Megaderma and from 0.66 (7.5 kHz) to 1.47 (95 kHz) in Carollia. With increasing f1 frequency the optimum frequency ratio f2/f1 in order to evoke maximum distortion level decreases from 1. 1 8 (5 kHz) to 1.09 (95 kHz) in Megaderma and from 1.21 (7.5 kHz) to 1.11 (95 kHz) in Carollia. This is taken as indication of a general increase of the quality of tuning of the distortion generating mechanism with frequency. The f1 levels that were sufficient to elicit distortion levels of - 10 dB SPL were used to construct iso-distortion threshold curves which lay on average 37.2 dB (Megaderma) and 33.9 dB (Carollia) above the neuronal threshold curves [Rubsamen et al., J. Comp. Physiol. A 163 (1988); Sterbing et al., Proc. 18th Gottingen Neurobiol. Conf. Thieme Verlag, Stuttgart (1990)] and roughly paralleled these. Highest distortion levels (40-50 dB SPL with f1 levels of 80 dB SPL) and lowest distortion thresholds were measured in the f1 frequency range of 10-30 kHz (Megaderma) and 15-30 kHz (Carollia). For both bat species these respective frequency ranges correlate with broad minima in the neuronal audiogram. Thus in these animals distortion measurement can be used as noninvasive means to assess relative bearing threshold. Systemic application of salicylate (100-400 mg/kg) which is known to block outer hair cell (OHC) motility (Shehata et al., 1991) reduced the level of distortion by up to 25 dB (f1 frequency: 20 kHz) and up to 36 dB (f1 frequency: 70 kHz). RP KOSSL, M (reprint author), ZOOL INST,LUISENSTR 14,W-8000 MUNICH 2,GERMANY. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 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, 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 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DALLOS P, 1985, J NEUROSCI, V5, P1591 Dallos P, 1991, Curr Opin Neurobiol, V1, P215, DOI 10.1016/0959-4388(91)90081-H EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 Evans E. F., 1975, HDB SENSORY PHYSL, V5, P1 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 GOLD T, 1948, P ROY SOC B, V210, P71 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 KOSSL M, 1985, HEARING RES, V19, P157, DOI 10.1016/0378-5955(85)90120-0 KOSSL M, 1990, J COMP PHYSIOL A, V166, P711 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MARKL H, 1973, Zeitschrift fuer Tierpsychologie, V33, P274 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 Mountain DC, 1983, MECHANICS HEARING, P119 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 RUBSAMEN R, 1988, J COMP PHYSIOL A, V163, P271, DOI 10.1007/BF00612436 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SANTOSSACCHI J, 1990, MECH BIOPHYSICS HEAR, P69 SCHROTT A, 1991, HEARING RES, V52, P245, DOI 10.1016/0378-5955(91)90204-M SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 STERBING S, 1990, 18TH P GOTT NEUR C, P140 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 Wilson J., 1980, Proceedings of the Eighth Annual Canadian Conference on Information Science ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 35 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 JUL PY 1992 VL 60 IS 2 BP 156 EP 164 DI 10.1016/0378-5955(92)90018-I PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800004 PM 1639726 ER PT J AU PATUZZI, R RAJAN, R AF PATUZZI, R RAJAN, R TI ADDITIVITY OF THRESHOLD ELEVATIONS PRODUCED BY DISRUPTION OF OUTER HAIR CELL-FUNCTION SO HEARING RESEARCH LA English DT Article DE SENSORINEURAL HEARING LOSS; ADDITIVITY; ACTIVE PROCESS; RECEPTOR CURRENT ID CROSSED OLIVOCOCHLEAR BUNDLE; LOW-FREQUENCY TONES; BASILAR-MEMBRANE MOTION; ELECTRICAL-STIMULATION; MAMMALIAN COCHLEA; GUINEA-PIG; MECHANICAL RESPONSES; AUDITORY-SENSITIVITY; ACOUSTIC TRAUMA; MODULATION AB We present a simple model describing the additivity of hearing loss in the mammalian cochlea produced by disruption of the outer hair cell transduction processes. The validity of this model has been tested experimentally in the guinea-pig by inducing threshold elevations using two simultaneous cochlear manipulations, including acoustic overstimulation, two-tone suppression, low-frequency acoustic biasing of the cochlear partition and electrical stimulation of the medial olivo-cochlear system of efferent fibres. The results of these experiments suggest that the model presented is an adequate description, within the measurement error of our experiments, of the hearing losses produced. RP PATUZZI, R (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. RI Rajan, Ramesh/A-5945-2008 CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Black LJ, 1936, P SOC EXP BIOL MED, V33, P509 BROWN MC, 1983, SCIENCE, V222, P69, DOI 10.1126/science.6623058 Brownell W. E., 1983, MECH HEARING, P5 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CODY AR, 1980, HEARING RES, V3, P3, DOI 10.1016/0378-5955(80)90004-0 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 MCCRAE JH, 1991, J ACOUST SOC AM, V90, P2513 PATTUZZI R, 1988, PHYS REV, V68, P1005 PATUZZI R, 1984, HEARING RES, V13, P9, DOI 10.1016/0378-5955(84)90090-X PATUZZI R, 1984, HEARING RES, V13, P19, DOI 10.1016/0378-5955(84)90091-1 PATUZZI R, 1984, HEARING RES, V13, P1, DOI 10.1016/0378-5955(84)90089-3 PATUZZI R, 1990, HEARING RES, V45, P15, DOI 10.1016/0378-5955(90)90179-S PATUZZI R, 1986, NATO ASI SERIES A, V111, P123 PATUZZI R, 1984, HEARING RES, V13, P99, DOI 10.1016/0378-5955(84)90100-X 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, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 Pickles JO, 1988, INTRO PHYSL HEARING RAJAN R, 1989, HEARING RES, V39, P299, DOI 10.1016/0378-5955(89)90049-X RAJAN R, 1988, BRAIN RES, V459, P241, DOI 10.1016/0006-8993(88)90640-3 RAJAN R, 1983, HEARING RES, V9, P279, DOI 10.1016/0378-5955(83)90032-1 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SCHMIEDT RA, 1984, J ACOUST SOC AM, V76, P1293, DOI 10.1121/1.391446 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SIEGEL JH, 1987, HEARING RES, V28, P131, DOI 10.1016/0378-5955(87)90044-X Spoor A, 1967, INT AUDIOL, V6, P48, DOI 10.3109/05384916709074230 SPOOR A, 1973, 1973 P INT C NOIS PU, P281 ZWICKER E, 1979, J ACOUST SOC AM, V59, P166 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 JUL PY 1992 VL 60 IS 2 BP 165 EP 177 DI 10.1016/0378-5955(92)90019-J PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800005 PM 1639727 ER PT J AU MELSSEN, WJ EPPING, WJM AF MELSSEN, WJ EPPING, WJM TI SELECTIVITY FOR TEMPORAL CHARACTERISTICS OF SOUND AND INTERAURAL TIME DIFFERENCE OF AUDITORY MIDBRAIN NEURONS IN THE GRASSFROG - A SYSTEM THEORETICAL APPROACH SO HEARING RESEARCH LA English DT Article DE ACOUSTIC CLICK; GRASSFROG; INTERAURAL TIME DIFFERENCE; SOUND LOCALIZATION; SYSTEM IDENTIFICATION; TORUS-SEMICIRCULARIS ID DORSAL MEDULLARY NUCLEUS; AMPLITUDE-MODULATED SOUNDS; FROG RANA-TEMPORARIA; LOW-FREQUENCY CELLS; CROSS-CORRELATION; BINAURAL INTERACTION; DIRECTIONAL HEARING; INFERIOR COLLICULUS; NERVE-FIBERS; HAIR-CELLS AB The selectivity for temporal characteristics of sound and interaural time difference (ITD) was investigated in the torus semicircularis (TS) of the grassfrog. Stimuli were delivered by means of a closed sound system and consisted of binaurally presented Poisson distributed condensation clicks, and pseudo-random (RAN) or equidistant (EQU) click trains of which ITD was varied. With RAN and EQU trains, 86% of the TS units demonstrated a clear selectivity for ITD. Most commonly, these units had monotonically increasing ITD-rate functions. In general, units responding to Poisson clicks, responded also to RAN and EQU trains. One category of units which showed strong time-locking had comparable selectivities for ITD with both stimulus ensembles. A second category of units showed a combined selectivity for temporal structure and ITD. These units responded exclusively to EQU trains in a nonsynchronized way. From the responses obtained with the Poisson click ensemble so-called Poisson system kernels were determined, in analogy to the Wiener-Volterra functional expansion for nonlinear systems. The kernel analysis was performed up to second order. Contralateral (CL) first order kernels usually had positive or combinations of positive and negative regions, indicating that the contralateral ear exerted an excitatory or combined excitatory-inhibitory influence upon the neural response. Ipsilateral (IL), units were characterized by first order kernels which were not significantly different from zero, or kernels in which a single negative region was present. A large variety of CL second order kernels has been observed whereas rarely IL second order kernels were encountered. About 35% of the units possessed nonzero second order cross kernels, which indicates that CL and IL neural processes are interacting in a nonlinear way. Units demonstrating a pronounced selectivity for ITD, were generally characterized by positive CL combined with negative IL first order kernels. Findings.suggested that, in the grassfrog, neural selectivity for ITD mainly is established by linear interaction of excitatory and inhibitory processes originating from the CL and IL ear, respectively. Units exhibiting strong time-locking to Poisson clicks and RAN and EQU trains had significantly shorter response latencies than moderately time-locking units. In the first category of units, a substantial higher number of nonzero first and second order kernels was observed. It was concluded that nonlinear response properties, as observed in TS units, most likely have to be ascribed to nonlinear characteristics of neural components located in the auditory nervous system peripheral to the torus semicircularis. C1 CATHOLIC UNIV NIJMEGEN,DEPT MED PHYS & BIOPHYS,NIJMEGEN,NETHERLANDS. CR AERTSEN AMHJ, 1979, BIOL CYBERN, V32, P175, DOI 10.1007/BF00337394 AERTSEN AMHJ, 1985, BRAIN RES, V340, P341, DOI 10.1016/0006-8993(85)90931-X AERTSEN AMHJ, 1986, HEARING RES, V21, P17, DOI 10.1016/0378-5955(86)90043-2 BATRA R, 1989, J NEUROPHYSIOL, V61, P257 BIBIKOV N G, 1981, Biophysics (English Translation of Biofizika), V26, P346 BIBIKOV NG, 1981, NEUROPHYSIOLOGY, V12, P185, DOI 10.1007/BF01068051 BRILLINGER DR, 1975, ANN PROBAB, V3, P909, DOI 10.1214/aop/1176996218 BRZOSKA J, 1984, ZOOL JAHRB ALLG ZOOL, V88, P179 BRZOSKA J, 1977, J COMP PHYSIOL, V118, P173 CAPRANIC.RR, 1966, J ACOUST SOC AM, V40, P1131, DOI 10.1121/1.1910198 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 Cox D., 1980, POINT PROCESSES CRAWFORD AC, 1981, J PHYSIOL-LONDON, V315, P317 DEBOER E, 1968, IEEE T BIO-MED ENG, VBM15, P169, DOI 10.1109/TBME.1968.4502561 DERIBAUPIERRE F, 1980, HEARING RES, V3, P65, DOI 10.1016/0378-5955(80)90008-8 EGGERMONT JJ, 1990, HEARING RES, V43, P181, DOI 10.1016/0378-5955(90)90227-G Eggermont J.J., 1988, P307 EGGERMONT JJ, 1985, HEARING RES, V18, P57, DOI 10.1016/0378-5955(85)90110-8 EPPING WJM, 1990, HEARING RES, V45, P1, DOI 10.1016/0378-5955(90)90178-R EPPING WJM, 1986, HEARING RES, V24, P55, DOI 10.1016/0378-5955(86)90005-5 EPPING WJM, 1985, HEARING RES, V18, P223, DOI 10.1016/0378-5955(85)90040-1 EPPING WJM, 1987, J NEUROPHYSIOL, V57, P1464 EPPING WJM, 1986, HEARING RES, V24, P37, DOI 10.1016/0378-5955(86)90004-3 EPPING WJM, 1985, HEARING RES, V19, P15, DOI 10.1016/0378-5955(85)90095-4 Fay R.R., 1987, P179 FENG AS, 1981, J COMP PHYSIOL, V144, P419 FENG AS, 1978, J NEUROPHYSIOL, V41, P43 FENG AS, 1981, HEARING RES, V5, P201, DOI 10.1016/0378-5955(81)90046-0 FENG AS, 1982, HEARING RES, V6, P241, DOI 10.1016/0378-5955(82)90057-0 FENG AS, 1976, J NEUROPHYSIOL, V39, P871 FENG AS, 1975, J COMP PHYSIOL, V100, P221 FRISHKOP.LS, 1968, PR INST ELECTR ELECT, V56, P969, DOI 10.1109/PROC.1968.6448 Fuzessery Z.M., 1988, P253 FUZESSERY ZM, 1983, J COMP PHYSIOL, V150, P107 GERHARDT HC, 1988, J COMP PHYSIOL A, V162, P261, DOI 10.1007/BF00606090 GERSTEIN GL, 1985, J NEUROPHYSIOL, V54, P1513 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GRINVALD A, 1984, TRENDS NEUROSCI, V7, P143, DOI 10.1016/S0166-2236(84)80125-3 HALL JC, 1988, HEARING RES, V36, P261, DOI 10.1016/0378-5955(88)90067-6 HUDSPETH AJ, 1983, TRENDS NEUROSCI, V6, P366, DOI 10.1016/0166-2236(83)90166-2 IRVINE DRF, 1987, HEARING RES, V30, P169, DOI 10.1016/0378-5955(87)90134-1 Itoh K., 1984, Transactions of the Institute of Electronics and Communication Engineers of Japan, Section E (English), VE67 JOHANNESMA PIM, 1985, ACTA APPL MATH, V4, P201, DOI 10.1007/BF00052461 KLUMP GM, 1989, NATURWISSENSCHAFTEN, V76, P35, DOI 10.1007/BF00368312 KNOX CK, 1974, BIOPHYS J, V14, P567 KRAUSZ HI, 1975, BIOL CYBERN, V19, P217, DOI 10.1007/BF00334442 KRUGER J, 1988, J NEUROPHYSIOL, V60, P798 Kuwada S., 1987, P146 LEE YW, 1965, INT J CONTROL, V2, P237, DOI 10.1080/00207176508905543 MARDIA KV, 1972, STATISTICS DIRECTION Marmarelis PZ, 1978, ANAL PHYSL SYSTEMS MEGELA AL, 1981, J NEUROPHYSIOL, V46, P465 MEGELA AL, 1984, J ACOUST SOC AM, V75, P1155, DOI 10.1121/1.390764 MELSSEN WJ, 1990, HEARING RES, V44, P35, DOI 10.1016/0378-5955(90)90020-P MELSSEN WJ, 1987, BIOL CYBERN, V57 MELSSEN WJ, 1990, HEARING RES, V47, P235, DOI 10.1016/0378-5955(90)90155-I MELSSEN WJ, 1988, BASIC ISSUES HEARING, P279 MICHELSEN A, 1986, NATURWISSENSCHAFTEN, V73, P682, DOI 10.1007/BF00366697 MOORE GP, 1970, BIOPHYS J, V10, P876 PINDER AC, 1983, PROC R SOC SER B-BIO, V219, P371, DOI 10.1098/rspb.1983.0079 PITCHFORD S, 1987, HEARING RES, V27, P75, DOI 10.1016/0378-5955(87)90027-X RHEINLAENDER J, 1979, J COMP PHYSIOL, V133, P247 ROSE GJ, 1984, J COMP PHYSIOL, V154, P211, DOI 10.1007/BF00604986 ROSE GJ, 1985, J NEUROPHYSIOL, V53, P446 Schetzen M., 1980, VOLTERRA WIENER THEO, Vfirst SURMEIER DJ, 1985, BRAIN RES, V331, P180, DOI 10.1016/0006-8993(85)90732-2 VANSTOKKUM IHM, 1990, HEARING RES, V43, P231, DOI 10.1016/0378-5955(90)90231-D VANSTOKKUM IHM, 1987, HEARING RES, V29, P223, DOI 10.1016/0378-5955(87)90169-9 VANGELDER JJ, 1978, J ANIM ECOL, V47, P667 VANSTOKKUM IHM, 1991, HEARING RES, V52, P113, DOI 10.1016/0378-5955(91)90192-C VANSTOKKUM IHM, 1988, ACTA BIOL HUNG, V29, P291 VANSTOKKUM IHM, 1986, BIOL CYBERN, V55, P17 VANSTOKKUM IHM, 1989, HEARING RES, V41, P71, DOI 10.1016/0378-5955(89)90180-9 VLAMING MSMG, 1984, HEARING RES, V14, P191, DOI 10.1016/0378-5955(84)90018-2 Walkowiak W., 1988, P275 WALKOWIAK W, 1982, BEHAV ECOL SOCIOBIOL, V11, P247, DOI 10.1007/BF00299301 WALKOWIAK W, 1984, J COMP PHYSIOL, V155, P57, DOI 10.1007/BF00610931 Wiener N., 1958, NONLINEAR PROBLEMS R Wilczynski W., 1988, P209 YIN TCT, 1987, J NEUROPHYSIOL, V58, P562 ZELICK R, 1985, HEARING RES, V17, P161, DOI 10.1016/0378-5955(85)90019-X NR 81 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 JUL PY 1992 VL 60 IS 2 BP 178 EP 198 DI 10.1016/0378-5955(92)90020-N PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800006 PM 1639728 ER PT J AU TENCATE, WJF CURTIS, LM RAREY, KE AF TENCATE, WJF CURTIS, LM RAREY, KE TI IMMUNOCHEMICAL DETECTION OF GLUCOCORTICOID RECEPTORS WITHIN RAT COCHLEAR AND VESTIBULAR TISSUES SO HEARING RESEARCH LA English DT Article DE INNER EAR; STEROID RECEPTOR; ELISA; WESTERN BLOT ID MONOCLONAL-ANTIBODY; LOCALIZATION; BINDING; NEURONS AB A monoclonal antibody, BuGR2, to liver glucocorticoid receptor sites was tested for its reactivity and specificity in inner ear tissue supernatants by an Enzyme Linked Immuno Sorbant Assay (ELISA) and a Western blotting technique. Results demonstrated that this antibody specifically recognized a protein of 93 kDa in inner ear supernatant fractions, which conformed to the reported molecular weights of the glucocorticoid receptor in other tissues. Antigenic sites were determined to be higher within cochlear supernatant fractions compared to vestibular supernatant fractions by ELISA. This anti-glucocorticoid receptor antibody combined with the quantitative ELISA provides a sensitive means to further investigate the inner ear glucocorticoid receptor system. C1 UNIV FLORIDA,COLL MED,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32611. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32611. CR BALLARD PL, 1974, ENDOCRINOLOGY, V94, P998 Baxter J.D., 1979, GLUCOCORTICOID HORMO, P1 BLOOM E, 1980, J STEROID BIOCHEM, V12, P175, DOI 10.1016/0022-4731(80)90267-8 EISEN HJ, 1981, J BIOL CHEM, V256, P2920 EISEN LP, 1985, J BIOL CHEM, V260, P1805 EISEN LP, 1986, J BIOL CHEM, V261, P3725 GAMETCHU B, 1984, ENDOCRINOLOGY, V114, P274 GUSTAFSSON JA, 1987, ENDOCR REV, V8, P185 HARRISON RW, 1987, RECENT ADV STEROID H, P467 LAFOND RE, 1988, EXP CELL RES, V175, P52, DOI 10.1016/0014-4827(88)90254-6 LIPOSITS Z, 1987, HISTOCHEMISTRY, V87, P407, DOI 10.1007/BF00496811 MIESFELD R, 1986, CELL, V46, P389, DOI 10.1016/0092-8674(86)90659-8 RAFESTINOBLIN ME, 1986, J STEROID BIOCHEM, V24, P259, DOI 10.1016/0022-4731(86)90061-0 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 STEIN WH, 1948, J BIOL CHEM, V176, P337 UHT RM, 1988, J NEUROSCI RES, V19, P405 NR 16 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 1992 VL 60 IS 2 BP 199 EP 204 DI 10.1016/0378-5955(92)90021-E PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800007 PM 1639729 ER PT J AU KALTENBACH, JA SCHMIDT, RN KAPLAN, CR AF KALTENBACH, JA SCHMIDT, RN KAPLAN, CR TI TONE-INDUCED STEREOCILIA LESIONS AS A FUNCTION OF EXPOSURE LEVEL AND DURATION IN THE HAMSTER COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; STEREOCILIA; NOISE-INDUCED HEARING LOSS; ACOUSTIC TRAUMA; HAMSTER ID CROSSED OLIVOCOCHLEAR BUNDLE; TEMPORARY THRESHOLD SHIFTS; ELECTRICAL-STIMULATION PARAMETERS; REDUCES AUDITORY DESENSITIZATION; GUINEA-PIG COCHLEA; EFFERENT INNERVATION; DEPENDENCE; NOISE; SENSITIVITY; PATHOLOGY AB The present study presents an atlas of the effects of 10 kHz tone exposures of different levels and durations on cochlear hair cells and their stereocilia in the Syrian golden hamster. Animals were sound exposed while under anesthesia. The exposure conditions were varied over an intensity range of 90-129 dB SPL; at the highest levels (126-129 dB SPL) the exposure periods were varied over a range of 30 min to 4 h. In animals with mild damage the lesions were commonly restricted to either the inner hair cells and/or the first row of outer hair cells; the order of damage susceptibility was IHC, OHC1, OHC2, OHC3. Damage to the second and third rows of outer hair cells were found only in animals with the severest lesions. Possible mechanisms underlying the row-specific distributions of these lesions and relative susceptibilities of the 4 rows of hair cells are discussed. C1 WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL,DETROIT,MI 48201. RP KALTENBACH, JA (reprint author), WAYNE STATE UNIV,SCH MED,DEPT AUDIOL,5E-UHC,4201 ST ANTOINE,DETROIT,MI 48201, USA. CR CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DECORY L, 1989, COCHLEAR MECHANISMS, P225 ENGSTROM B, 1981, ARCH OTO-RHINO-LARYN, V230, P279, DOI 10.1007/BF00456330 ENGSTROM B, 1983, ACTA OTOLARYNGOL S, V402, P4 FREDELIUS L, 1987, HEARING RES, V30, P157, DOI 10.1016/0378-5955(87)90133-X GUINAN JJ, 1983, J COMP NEUROL, V221, P358, DOI 10.1002/cne.902210310 HAMERNIK RP, 1982, NEW PERSPECTIVES NOI LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 LIBERMAN MC, 1986, BASIC APPL ASPECTS N, P163 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 LIBERMAN MC, 1984, HEARING RES, V16, P33, DOI 10.1016/0378-5955(84)90023-6 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1986, HEARING RES, V24, P17, DOI 10.1016/0378-5955(86)90003-1 LIBERMAN MC, 1990, J NEUROPHYSIOL, V65, P123 MALICK LE, 1975, EVALUATION MODIFIED, P259 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 NILSSON P, 1982, NEW PERSPECTIVES NOI, P69 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V RAJAN R, 1988, HEARING RES, V36, P75, DOI 10.1016/0378-5955(88)90138-4 RAJAN R, 1988, HEARING RES, V36, P53, DOI 10.1016/0378-5955(88)90137-2 RAJAN R, 1990, BRAIN RES, V506, P192, DOI 10.1016/0006-8993(90)91251-B RAJAN R, 1988, J NEUROPHYSIOL, V60, P569 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 SAUNDERS C, J ACOUST SOC AM, V90, P136 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SIMMONS DD, 1990, HEARING RES, V49, P127, DOI 10.1016/0378-5955(90)90100-4 STINSON MR, 1986, LECTURE NOTES BIOMAT, V64 SYKA J, 1989, SENSORY PHYSL, V9, P97 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 NR 32 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 JUL PY 1992 VL 60 IS 2 BP 205 EP 215 DI 10.1016/0378-5955(92)90022-F PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800008 PM 1639730 ER PT J AU RAJAN, R PATUZZI, RB AF RAJAN, R PATUZZI, RB TI ADDITIVITY OF THRESHOLD LOSSES PRODUCED BY ACUTE ACOUSTIC TRAUMA SO HEARING RESEARCH LA English DT Article DE THRESHOLD LOSSES; ACUTE NOISE EXPOSURES; ADDITIVITY; ACTIVE PROCESS ID CROSSED OLIVOCOCHLEAR BUNDLE; AUDITORY-SENSITIVITY; ELECTRICAL-STIMULATION; EXPOSURE; SHIFTS; NOISE; COCHLEA; SYSTEM AB We have previously [Patuzzi and Rajan, Hear. Res. 60, 165-177, 1992] formulated a model to describe how the threshold elevations produced by a variety of independent, short-term cochlear manipulations add when the manipulations are combined. The manipulations were presumed to affect only the 'active process' in the cochlea. The present report applied this model to the effects observed after acute acoustic trauma in normal-hearing guinea pigs and in guinea pigs with idiopathic threshold losses. Successive loud pure-tone exposures were presented to the normal-hearing guinea pigs, while only a single exposure was presented to the guinea pigs with idiopathic hearing losses. Various parameters of exposure and inter-exposure delays were used to create a variety of threshold elevations, and the total hearing losses observed in the various groups were compared to the total hearing losses predicted by the model. In most cases a statistically-valid 1 : 1 relationship was obtained between the predicted values and the observed values. In cases where the model's predictions were found not to fit the data, this appeared to be due to inclusion of data previously defined to be outside the scope of the model. When such data were excluded, there was good agreement between the model's predictions and the observed data. The model was further tested by comparing its predictions with data obtained in studies of acute noise trauma in chinchillas and humans by other researchers. The model's predictions were found to agree with these data as well. Thus, across a number of different types and conditions of exposures, the model appears to provide a very good description of the additivity of threshold losses produced by acute acoustic trauma. The generality of and constraints on the model are discussed. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. RP RAJAN, R (reprint author), MONASH UNIV,DEPT PSYCHOL,CLAYTON,VIC 3168,AUSTRALIA. RI Rajan, Ramesh/A-5945-2008 CR BROWNELL WE, 1986, AUDITORY FREQUENCY S, P109 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CODY AR, 1980, ACTA OTO-LARYNGOL, V89, P440, DOI 10.3109/00016488009127160 DALLOS P, 1985, P207 GRENNER J, 1990, THESIS U LUND MALMO Hamemik R. P., 1976, EFFECTS NOISE HEARIN, P291 JOHNSTONE JR, 1979, J ACOUST SOC AM, V49, P1762 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 LOEB M, 1963, J AUD RES, V3, P213 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLS JH, 1970, J ACOUST SOC AM, V48, P524, DOI 10.1121/1.1912167 MILLS JH, 1973, J SPEECH HEAR RES, V16, P700 PATUZZI R, 1992, HEARING RES, V60, P165, DOI 10.1016/0378-5955(92)90019-J PATUZZI R, 1990, INFORMATION PROCESSI, P45 PATUZZI R, 1988, PHYSIOL REV, V68, P1005 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V RAJAN R, 1989, HEARING RES, V39, P299, DOI 10.1016/0378-5955(89)90049-X RAJAN R, 1988, BRAIN RES, V459, P241, DOI 10.1016/0006-8993(88)90640-3 RAJAN R, 1983, HEARING RES, V9, P279, DOI 10.1016/0378-5955(83)90032-1 RAJAN R, 1983, HEARING RES, V12, P185, DOI 10.1016/0378-5955(83)90105-3 RAJAN R, 1988, J NEUROPHYSIOL, V60, P549 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 Ward W. D., 1976, EFFECTS NOISE HEARIN, P407 WARD WD, 1959, J ACOUST SOC AM, V31, P791, DOI 10.1121/1.1907787 WARD WD, 1958, J ACOUST SOC AM, V30, P944, DOI 10.1121/1.1909414 WARD WD, 1963, MODERN DEV AUDIOLOGY, P241 NR 27 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 JUL PY 1992 VL 60 IS 2 BP 216 EP 230 DI 10.1016/0378-5955(92)90023-G PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800009 PM 1639731 ER PT J AU ZENG, FG SHANNON, RV AF ZENG, FG SHANNON, RV TI LOUDNESS BALANCE BETWEEN ELECTRIC AND ACOUSTIC STIMULATION SO HEARING RESEARCH LA English DT Article DE LOUDNESS BALANCE; ELECTRIC STIMULATION; LOUDNESS FUNCTION ID COCHLEAR IMPLANTS; PSYCHOPHYSICS AB Binaural loudness balance between electric and acoustic stimulation is obtained in auditory brainstem implant listeners who had substantial acoustic hearing in one ear. The data are well described by a linear relationship between acoustic decibels and electric microamps. Based upon this linear relationship, we propose an exponential model of loudness growth in electric stimulation. The exponential model predicts that the loudness growth function can be determined solely by the threshold and the uncomfortable loudness level in electric stimulation. This prediction is consistent with previous psychophysical data on loudness functions. Implications of this finding for speech processor designs are discussed. RP ZENG, FG (reprint author), HOUSE EAR RES INST,2100 W 3RD ST,LOS ANGELES,CA 90057, USA. RI Zeng, Fan-Gang/G-4875-2012 CR BARRETT JP, 1974, AM STAT, V28, P19, DOI 10.2307/2683523 Clark G.M., 1978, J OTOLARYNGOL SOC AU, V4, P208 EDDINGTON D K, 1978, Annals of Otology Rhinology and Laryngology, V87, P5 Eisenberg L S, 1987, J Rehabil Res Dev, V24, P9, DOI 10.1682/JRRD.1987.07.0009 HERNDON MK, 1981, 9065 STANF U INT CIR HOCHMAIRDESOYER IJ, 1985, ANN OTO RHINOL LARYN, V94, P65 HOUSE WF, 1982, ANN OTO RHINOL LARYN, V91, P104 MATHEWS RG, 1978, 53063 STANF U INT CI MULLER C, 1981, J ACOUST SOC AM, V70, pS52 OLSEN WO, 1974, ARCH OTOLARYNGOL, V99, P94 PFINGST BE, 1984, ARCH OTOLARYNGOL, V110, P140 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 SHANNON RV, 1985, HEARING RES, V18, P135, DOI 10.1016/0378-5955(85)90005-X SHANNON RV, 1992, IN PRESS AUDITION SP STEVENS SS, 1955, J ACOUST SOC AM, V27, P815, DOI 10.1121/1.1908048 TONG YC, 1979, J LARYNGOL OTOL, V93, P679, DOI 10.1017/S0022215100087545 VUREK LS, 1981, ANN OTO RHINOL LARYN, V90, P21 WALKER MG, 1978, 53064 STANF U INT CI WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 ZENG FG, 1991, HEARING RES, V55, P223, DOI 10.1016/0378-5955(91)90107-K 1969, ANSI S361969 AM NAT NR 22 TC 58 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 JUL PY 1992 VL 60 IS 2 BP 231 EP 235 DI 10.1016/0378-5955(92)90024-H PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800010 PM 1639732 ER PT J AU REUTER, G GITTER, AH THURM, U ZENNER, HP AF REUTER, G GITTER, AH THURM, U ZENNER, HP TI HIGH-FREQUENCY RADIAL MOVEMENTS OF THE RETICULAR LAMINA INDUCED BY OUTER HAIR CELL MOTILITY SO HEARING RESEARCH LA English DT Article DE COCHLEAR AMPLIFIER; FREQUENCY SELECTIVITY; SPEECH DISCRIMINATION; HEARING LOSS ID BASILAR-MEMBRANE; MECHANICAL-PROPERTIES; AMPULLARY KINOCILIA; MAMMALIAN COCHLEA; TRAVELING-WAVE; RESPONSES; ORGAN; CORTI AB Recently, it was shown in cochlear explants from the guinea pig cochlea that electrokinetic motile responses of outer hair cells can induce radial and transverse motion of the reticular lamina. Here we demonstrate, that the radial component of these motions can be measured up to high frequencies (15 kHz). Cochlear explants were taken from guinea pig inner ears and exposed to a sinusoidal electric field. A double photodiode was used as a linear position detector with high spatial and temporal resolution to detect radial movements in the plane of the reticular lamina. The organ of Corti of the second, third and fourth cochlear turns was stimulated with frequencies of the electrical field between 0.5 Hz and 20 kHz. Sinusoidal movements of up to 15 kHz were recorded. At higher frequencies the signal-to-noise ratio became too small. The largest responses were measured at the three rows of outer hair cells. If the strength of the eiectrical field was 2 kV/m, into which the cochlear explants were placed, the amplitudes of outer hair cell movements were around 1-mu-m at 1 Hz and 10 nm at 10 kHz. Uncoupling of the outer hair cells from the tunnel of Corti and from the inner hair cells decreased the oscillations of inner hair cells but did not affect outer hair cells. The movements showed frequency dependent amplitudes like a complex low-pass filter but no best frequency was observed. C1 UNIV TUBINGEN,DEPT OTOLARYNGOL,HALS NASEN OHREN HEARING RES LAB,SILCHERSTR 5,W-7400 TUBINGEN 1,GERMANY. UNIV MUNSTER,DEPT NEUROBIOL,W-4400 MUNSTER,GERMANY. CR 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 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DEBOER E, 1990, HEARING RES, V44, P83, DOI 10.1016/0378-5955(90)90024-J GITTER AH, 1988, BASIC ISSUES HEARING, P32 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 JOHNSTON.BM, 1967, SCIENCE, V158, P389, DOI 10.1126/science.158.3799.389 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P183 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P163 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 Kim D. O., 1984, HEARING SCI RECENT A, P241 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 REUTER G, 1990, HEARING RES, V43, P219, DOI 10.1016/0378-5955(90)90230-M RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 RUSCH A, 1990, HEARING RES, V48, P247, DOI 10.1016/0378-5955(90)90065-W RUSCH A, 1986, ORL J OTO-RHINO-LARY, V48, P76 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 VONBEKESY G, 1953, J ACOUST SOC AM, V25, P770 ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V149, P304, DOI 10.1016/0006-291X(87)91639-1 ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 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 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P457, DOI 10.3109/00016488809119501 ZWISLOCKI JJ, 1988, ACTA OTO-LARYNGOL, V105, P450, DOI 10.3109/00016488809119500 NR 29 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 JUL PY 1992 VL 60 IS 2 BP 236 EP 246 DI 10.1016/0378-5955(92)90025-I PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JD658 UT WOS:A1992JD65800011 PM 1639733 ER PT J AU CHEATHAM, MA DALLOS, P AF CHEATHAM, MA DALLOS, P TI 2-TONE SUPPRESSION IN INNER HAIR CELL RESPONSES - CORRELATES OF RATE SUPPRESSION IN THE AUDITORY-NERVE SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELL; NONLINEARITY; 2-TONE SUPPRESSION ID BASILAR-MEMBRANE MECHANICS; INPUT-OUTPUT FUNCTIONS; COCHLEAR-NERVE; TUNING CURVES; RECEPTOR POTENTIALS; GUINEA-PIG; TIMING INFORMATION; CHINCHILLA COCHLEA; ALLIGATOR LIZARD; FIBER RESPONSES AB Inner hair cell (IHC) recordings were made from second turn of the guinea pig cochlea where characteristic frequencies are approximately 4000 Hz. In order to compare IHC responses with rate suppression measured in the auditory nerve, suppressors were introduced that produced little or no response in the hair cell. The effects of a variable-frequency suppressor on a constant-frequency probe, placed near characteristic frequency, were also investigated since this paradigm is commonly used in single unit experiments. Resulting magnitude changes were measured in the fundamental component of the ac receptor potential and/or in the total dc produced in the region of temporal overlap between the two stimulus inputs. This latter component is especially important when considering how changes in IHC responses relate to decreases in discharge rate in single auditory nerve fibers. Since the ac receptor potential is filtered by the hair cell's basolateral membrane, the dc component probably controls transmitter release at the characteristic frequency of these second-turn IHCs. Based on results from these and previous experiments, a proposal is advanced to explain the evolution of two-tone suppression in the peripheral auditory system. The paper also discusses the use of excitatory versus non-excitatory suppressors and includes a description of two-tone suppression areas at the mechanical, IHC and single unit levels. The explanation of low-side suppression areas is of special interest since hitherto they have been difficult to model (Kim, 1985). RP CHEATHAM, MA (reprint author), NORTHWESTERN UNIV, AUDITORY PHYSIOL LAB, HUGH KNOWLES CTR, FRANCES SEARLE BLDG, EVANSTON, IL 60208 USA. CR ABBAS PJ, 1978, J ACOUST SOC AM, V63, P1878, DOI 10.1121/1.381929 ALLEN JB, 1980, PSYCHOPHYSICAL PHYSL, P85 ALLEN JB, 1983, MECH HEARING, P193 RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 ARTHUR RM, 1971, J PHYSL, V212, P21 CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 CHEATHAM MA, 1992, HEARING RES, V59, P39, DOI 10.1016/0378-5955(92)90100-2 CHEATHAM MA, 1990, HEARING RES, V50, P193, DOI 10.1016/0378-5955(90)90045-Q CHEATHAM MA, 1990, HEARING RES, V43, P135, DOI 10.1016/0378-5955(90)90222-B COSTALUPES JA, 1987, HEARING RES, V26, P155, DOI 10.1016/0378-5955(87)90107-9 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1990, J ACOUST SOC AM, V87, P1636, DOI 10.1121/1.399411 DALLOS P, 1974, FACTS MODELS HEARING, P312 DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DEBOER E, 1983, J ACOUST SOC AM, V73, P567, DOI 10.1121/1.389002 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 DELGUTTE B, 1989, J ACOUST SOC AM, V85, pS14, DOI 10.1121/1.2026806 DIEPENDAAL RJ, 1987, J ACOUST SOC AM, V82, P917, DOI 10.1121/1.395290 DOLAN DF, 1989, J ACOUST SOC AM, V86, P1007, DOI 10.1121/1.398091 ENGEBRET.AM, 1968, J ACOUST SOC AM, V44, P548, DOI 10.1121/1.1911119 Evans E. F., 1975, HDB SENSORY PHYSL, V5, P1 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 FRIEDMAN DH, 1990, LECT NOTES BIOMATH, V87, P372 GEISLER CD, 1990, LECT NOTES BIOMATH, V87, P86 GEISLER CD, 1991, HEARING RES, V54, P105, DOI 10.1016/0378-5955(91)90140-5 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GEISLER CD, 1980, HEARING RES, V3, P317 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HIND JE, 1967, J NEUROPHYSIOL, V30, P794 JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 Kiang N Y S, 1984, HDB PHYSL NERVOUS SY, VIII, P639 KIDD RC, 1990, HEARING RES, V49, P181, DOI 10.1016/0378-5955(90)90104-W KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KIM DO, 1985, PERIPHERAL AUDITORY, P239 KOLSTON PJ, 1990, J ACOUST SOC AM, V88, P1794, DOI 10.1121/1.400200 Mountain DC, 1983, MECHANICS HEARING, P119 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 NUTTALL AL, 1991, 2 TONE SUPPRESSION I, P132 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X PFEIFFER R R, 1970, Journal of the Acoustical Society of America, V48, P1373, DOI 10.1121/1.1912294 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 Rhode WS., 1977, PSYCHOPHYSICS PHYSL, P27 ROBERTSON D, 1981, J ACOUST SOC AM, V69, P1096, DOI 10.1121/1.385689 ROBLES L, 1989, COCHLEAR MECH STRUCT, P369 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 ROSE JE, 1971, J NEUROPHYSIOL, V34, P685 RUGGERO MA, 1992, UNPUB J NEUROPHYSIOL RUGGERO MA, 1992, IN PRESS PHYSL MAMMA RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1976, J ACOUST SOC AM, V60, P1157, DOI 10.1121/1.381218 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1978, J ACOUST SOC AM, V64, P502, DOI 10.1121/1.382000 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SOKOLOWSKI BHA, 1989, HEARING RES, V41, P115, DOI 10.1016/0378-5955(89)90005-1 WEISS TF, 1974, J ACOUST SOC AM, V55, P606, DOI 10.1121/1.1914571 WEISS TF, 1988, HEARING RES, V33, P167, DOI 10.1016/0378-5955(88)90029-9 YATES GK, 1989, COCHLEAR MECHANISMS, P177 ZWEIG G, 1991, J ACOUST SOC AM, V89, P1229, DOI 10.1121/1.400653 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 ZWISLOCKI JJ, 1980, J ACOUST SOC AM, V67, P1679 ZWISLOCKI JJ, 1980, PSYCHOPHYSICAL PHYSL, P16 NR 74 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 JUN PY 1992 VL 60 IS 1 BP 1 EP 12 DI 10.1016/0378-5955(92)90052-O PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800001 PM 1500370 ER PT J AU GITTER, AH FROMTER, E ZENNER, HP AF GITTER, AH FROMTER, E ZENNER, HP TI C-TYPE POTASSIUM CHANNELS IN THE LATERAL CELL-MEMBRANE OF GUINEA-PIG OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE CELL MEMBRANE POTENTIAL DIFFERENCE; COCHLEA; ION CHANNELS; OUTER HAIR CELL; POTASSIUM PERMEABILITY ID CULTURED RAT MUSCLE; ION CHANNELS; COCHLEA; CHICK; INNER; KINETICS; CURRENTS; INVITRO AB The basolateral cell membrane of outer hair cells (OHC) from the mammalian cochlea is known to contain K+-channels. The prevailing type, a high-conductance K+-channel was further characterized in the present study in order to support its classification as C channel. OHC were isolated from the 3rd and 4th turn of the guinea-pig cochlea. Cell-attached and excised inside-out patches of the lateral cell membrane were investigated. The C-type channel had a selectivity for K+ over Na+ of 12:1 to 20:1 and displayed Goldman-type rectification and voltage-dependence of the open probability. The kinetics of both opening and closing could be described by time constants in the range of ms. The channel provides a calcium- and voltage-activated pathway through OHC lateral membranes for passive K+ transport. C1 UNIV TUBINGEN,HALS NASEN OHREN KLIN,SILCHERSTR 5,W-7400 TUBINGEN 1,GERMANY. UNIV FRANKFURT,ZENTRUM PHYSIOL,W-6000 FRANKFURT 1,GERMANY. CR ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 CATTERALL WA, 1988, SCIENCE, V242, P50, DOI 10.1126/science.2459775 COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1984, HEARING RES, V12, P89 DAVIS H, 1958, Ann Otol Rhinol Laryngol, V67, P789 FUCHS PA, 1988, J NEUROSCI, V8, P2460 GITTER AH, 1987, PFLUG ARCH EUR J PHY, V408, P282, DOI 10.1007/BF02181471 GITTER AH, 1988, BASIC ISSUES HEARING GITTER AH, 1987, PFLUG ARCH EUR J PHY, V408, P194, DOI 10.1007/BF00581351 GITTER AH, 1990, HEARING RES, V45, P87, DOI 10.1016/0378-5955(90)90185-R GITTER AH, 1986, ORL J OTO-RHINO-LARY, V48, P68 Goldman David E., 1943, JOUR GEN PHYSIOL, V27, P37, DOI 10.1085/jgp.27.1.37 Hille B., 1984, IONIC CHANNELS EXCIT HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 LATORRE R, 1983, J MEMBRANE BIOL, V71, P11, DOI 10.1007/BF01870671 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 MAGLEBY KL, 1983, J PHYSIOL-LONDON, V344, P605 MAGLEBY KL, 1983, J PHYSIOL-LONDON, V344, P585 MARQUARDT DW, 1963, J SOC IND APPL MATH, V11, P431 MARTY A, 1984, J PHYSIOL-LONDON, V357, P293 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 OHMORI H, 1987, J PHYSIOL-LONDON, V387, P589 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 Sakmann B., 1983, SINGLE CHANNEL RECOR Schultz S, 1980, IUPAB BIOPHYSICS SER ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 NR 30 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 JUN PY 1992 VL 60 IS 1 BP 13 EP 19 DI 10.1016/0378-5955(92)90053-P PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800002 PM 1500373 ER PT J AU ZHOU, N PARKS, TN AF ZHOU, N PARKS, TN TI GAMMA-D-GLUTAMYLAMINOMETHYL SULFONIC-ACID (GAMS) DISTINGUISHES SUBTYPES OF GLUTAMATE RECEPTOR IN THE CHICK COCHLEAR NUCLEUS (NUC MAGNOCELLULARIS) SO HEARING RESEARCH LA English DT Article DE KAINIC ACID; DOMOIC ACID; QUISQUALIC ACID; QUINOXALINEDIONES; AUDITORY SYSTEM ID EXCITATORY AMINO-ACID; D-ASPARTATE RECEPTORS; AUDITORY-NERVE; SYNAPTIC TRANSMISSION; ALPHA-AMINOADIPATE; EVOKED EXCITATION; ANTAGONISTS; NEURONS; RAT; CAT AB Because kainic acid (KA) is more potent than other excitatory amino acids (EAAs) in affecting synaptic transmission in the cochlear nucleus, previous reports have concluded that primary afferent neurotransmission to the cochlear nucleus in birds and mammals is mediated by KA-preferring non-N-methyl-D-aspartate (non-NMDA) EAA receptors. Since this conclusion is at odds with a number of studies suggesting that rapid excitatory neurotransmission in the CNS is mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring non-NMDA receptors, we re-examined the pharmacology of synaptic transmission between the cochlear nerve and nucleus magnocellularis (NM) in chickens, using bath application of drugs and recording of field potentials evoked in NM by electrical stimulation of the cochlear nerve in vitro. A series of EAA agonists produced complete, concentration-dependent and reversible suppression of postsynaptic responses: the order of potency was domoic acid (DO) > KA > AMPA >> quisqualic acid >> L-glutamic acid (Glu). Three quinoxalinedione antagonists of non-6-nitro-7-sulphamobenzo[f]quinoxaline-2,3-dione NMDA receptors also produced complete, concentration-dependent and reversible suppression of postsynaptic responses in NM without affecting the presynaptic action potential; the half-maximal inhibitory concentrations (IC50's) were 2.7 +/- 0.4-mu-M for 6-nitro-7-sulphamobenzo[f]quinoxaline-2,3-dione (NBQX), 5.3 +/- 0.1-mu-M for 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and 10.6 +/- 1.2-mu-M for 6,7-dinitroquinoxaline-2,3-dione (DNQX). At concentrations that were without effect on postsynaptic responses elicited by stimulation of the cochlear nerve, gamma-D-glutamylaminomethyl sulfonic acid (GAMS), a competitive glutamate antagonist that has shown some selectivity for KA receptors in mammalian spinal cord, significantly reversed the suppression of postsynaptic responses produced by KA or AMPA but not by Glu. Taken together with other relevant experimental findings, these data suggest that 1) GAMS-sensitive and GAMS-insensitive non-NMDA receptors exist in NM and 2) the receptors mediating synaptic transmission in NM are AMPA-preferring and GAMS-insensitive. C1 UNIV UTAH, SCH MED, DEPT ANAT, SALT LAKE CITY, UT 84132 USA. CR BARNARD EA, 1990, TRENDS PHARMACOL SCI, V11, P500, DOI 10.1016/0165-6147(90)90051-9 BLAKE JF, 1989, BRIT J PHARMACOL, V97, P71 COLLINGRIDGE GL, 1989, PHARMACOL REV, V41, P143 DAVIES J, 1985, BRAIN RES, V327, P113, DOI 10.1016/0006-8993(85)91505-7 DINGLEDINE R, 1991, TRENDS PHARMACOL SCI, V12, P360, DOI 10.1016/0165-6147(91)90602-O Gasic G P, 1991, Curr Opin Neurobiol, V1, P20, DOI 10.1016/0959-4388(91)90006-S HACKETT JT, 1982, NEUROSCIENCE, V7, P1455, DOI 10.1016/0306-4522(82)90257-3 HONORE T, 1989, MED RES REV, V9, P1, DOI 10.1002/med.2610090102 JACKSON H, 1985, NEUROSCIENCE, V16, P171, DOI 10.1016/0306-4522(85)90054-5 JACKSON H, 1982, J NEUROSCI, V2, P1736 Konishi M, 1988, AUDITORY FUNCTION NE, P721 KROGSGAARDLARSE.P, 1991, EXCITATORY AMINO ACI, P433 KULKARNI SK, 1990, LIFE SCI, V46, P481, DOI 10.1016/0024-3205(90)90003-A MARTIN MR, 1979, NEUROSCIENCE, V4, P1097, DOI 10.1016/0306-4522(79)90191-X MARTIN MR, 1985, HEARING RES, V17, P153, DOI 10.1016/0378-5955(85)90018-8 MARTIN MR, 1980, NEUROPHARMACOLOGY, V19, P519, DOI 10.1016/0028-3908(80)90021-0 MARTIN MR, 1985, HEARING RES, V20, P215, DOI 10.1016/0378-5955(85)90026-7 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 OERTEL D, 1984, BRAIN RES, V302, P213, DOI 10.1016/0006-8993(84)90233-6 ORTEGA A, 1991, NEUROSCIENCE, V41, P335, DOI 10.1016/0306-4522(91)90331-H Rubel EW, 1988, AUDITORY FUNCTION NE, P3 SUGIYAMA H, 1989, NEUROSCI RES, V7, P164, DOI 10.1016/0168-0102(89)90057-6 TRUSSELL L O, 1991, Society for Neuroscience Abstracts, V17, P1166 WARCHOL ME, 1990, J COMP PHYSIOL A, V166, P721 WATKINS JC, 1990, TRENDS PHARMACOL SCI, V11, P25, DOI 10.1016/0165-6147(90)90038-A Wenthold R.J., 1985, P125 WICKESBERG RE, 1989, BRAIN RES, V486, P39, DOI 10.1016/0006-8993(89)91275-4 ZHOU N, 1990, SOC NEUR ABSTR, V16 ZHOU N, 1992, IN PRESS DEV BRAIN R, V67 NR 30 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 JUN PY 1992 VL 60 IS 1 BP 20 EP 26 DI 10.1016/0378-5955(92)90054-Q PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800003 PM 1379999 ER PT J AU TONO, T MORIZONO, T AF TONO, T MORIZONO, T TI LOW-FREQUENCY MODULATION OF COMPOUND ACTION-POTENTIAL IN EXPERIMENTAL PERILYMPHATIC FISTULA AND ENDOLYMPHATIC HYDROPS SO HEARING RESEARCH LA English DT Article DE PERILYMPHATIC FISTULA; ENDOLYMPHATIC HYDROPS; COMPOUND ACTION POTENTIAL; LOW-FREQUENCY BIAS, GUINEA PIG ID MORPHOLOGICAL-CHANGES; MENIERES-DISEASE; INDUCED MOTILITY; ROUND WINDOW; HAIR-CELLS; THRESHOLDS AB We have tested the hypothesis that the cause of cochlear dysfunction associated with perilymphatic fistula (PLF) is closely related to endolymphatic hydrops (ELH). Using guinea pigs, we studied the tone-burst elicited compound action potential (CAP) and its modulation as caused by a 50 Hz biasing tone in experimental PLF. We compared these results with those of experimental ELH. Following perilymph aspiration through the perforated round window membrane, mild but significant elevations of CAP thresholds at tested frequencies were found. A reduction in the amplitude of cochlear microphonics (CM) for a 50 Hz sine wave appeared to correlate with these CAP threshold changes. However, there were no significant changes in the modulation effect of the 50 Hz biasing tone on the CAP elicited by an 8 kHz tone burst. This finding differed from that in ears with experimental ELH, in which significant reductions of both 50 Hz CM and the degree of CAP modulation were consistently observed. We concluded that it is unlikely that the underlying mechanisms of a modification to the low frequency response of the base of the cochlea following perilymph aspiration is linked to that of experimental ELH. C1 UNIV MINNESOTA,SCH MED,DEPT OTOLARYNGOL,RES E BLDG,2630 UNIV AVE SE,MINNEAPOLIS,MN 55414. CR ALBERS FWJ, 1987, ANN OTO RHINOL LARYN, V96, P282 ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 ARENBERG IK, 1988, OTOLARYNG HEAD NECK, V99, P435 AXELSSON A, 1977, ACTA OTO-LARYNGOL, V84, P1, DOI 10.3109/00016487709123937 BOHMER A, 1990, LARYNGOSCOPE, V100, P389 COHEN J, 1984, ACTA OTO-LARYNGOL, V98, P398, DOI 10.3109/00016488409107580 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 DALLOS P, 1971, J ACOUST SOC AM, V49, P1144, DOI 10.1121/1.1912476 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 FLINT P, 1988, OTOLARYNG HEAD NECK, V99, P380 FUNAI H, 1988, AM J OTOLARYNG, V9, P244, DOI 10.1016/S0196-0709(88)80034-6 HARA M, 1990, ANN OTO RHINOL LARYN, V99, P316 HORNER KC, 1990, HEARING RES, V45, P145, DOI 10.1016/0378-5955(90)90190-Z HOUSE HP, 1967, LARYNGOSCOPE, V77, P410 KLIS JFL, 1988, HEARING RES, V32, P175, DOI 10.1016/0378-5955(88)90089-5 KLIS SFL, 1990, ANN OTO RHINOL LARYN, V99, P566 KOHUT RI, 1986, ANN OTO RHINOL LARYN, V95, P466 LAMM H, 1984, ACTA OTO-LARYNGOL, V98, P454, DOI 10.3109/00016488409107586 MEYERHOFF WL, 1990, OTOLARYNG HEAD NECK, V102, P678 MILLER JD, 1970, J ACOUST SOC AM, V48, P512 MORIZONO T, 1985, ANN OTO RHINOL LARYN, V94, P191 MORIZONO T, 1986, EAR RES JAPAN S1, V17, P84 MORIZONO T, 1984, ANN OTO RHINOL LARYN, V93, P225 MORIZONO T, 1989, 2ND INT S MEN DIS, P363 MUCHNIK C, 1990, AUDIOLOGY, V29, P55 NOMURA Y, 1987, ACTA OTO-LARYNGOL, V103, P469 OSHIRO EM, 1989, ANN OTO RHINOL LARYN, V98, P491 STEELE CR, 1985, J ACOUST SOC AM, V78, P84, DOI 10.1121/1.393090 VANDEELEN GW, 1987, ARCH OTO-RHINO-LARYN, V244, P167 ZENNER HP, 1986, ARCH OTO-RHINO-LARYN, V243, P108, DOI 10.1007/BF00453760 NR 30 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 JUN PY 1992 VL 60 IS 1 BP 27 EP 33 DI 10.1016/0378-5955(92)90055-R PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800004 PM 1500374 ER PT J AU SCHWEITZER, L CECIL, T AF SCHWEITZER, L CECIL, T TI MORPHOLOGY OF HRP-LABELED COCHLEAR NERVE AXONS IN THE DORSAL COCHLEAR NUCLEUS OF THE DEVELOPING HAMSTER SO HEARING RESEARCH LA English DT Article DE AUDITORY; AXONS; DEVELOPMENT; COCHLEAR NERVE; COCHLEAR NUCLEUS; TONOTOPIC; TUNING ID FREQUENCY-SELECTIVITY; NEONATAL CAT; GANGLION; FIBERS; ORGANIZATION; ELIMINATION; INNERVATION; REDUCTION; RESPONSES; ONTOGENY AB To study the development of the central terminal arbors of the cochlear nerve fibers in the dorsal cochlear nucleus, horseradish peroxidase-labelled axons in young and adult hamsters were analyzed morphometrically. Brainstem slices with whole cochlear nuclei were maintained in a slice chamber and the cochlear nerve root was injected with a mixture of wheat germ agglutinin-horseradish peroxidase, horseradish peroxidase and poly-L-ornithine. The poly-L-ornithine was added to keep the injection site small; small injections resulted in only a few axons being labelled and permitted reconstruction of individual fibers. Axons underwent an initial period of ingrowth that was completed prior to the onset of hearing (postnatal day 16). After this time the morphology and area of influence of the axons remained unchanged but the nucleus continued to increase in size. Since no additional cochlear nerve axons grow into the nucleus during this period of nuclear growth, the existing axons necessarily become more widely spaced as development proceeds. These anatomical changes may contribute to the progressive narrowing of auditory cell tuning curves. RP SCHWEITZER, L (reprint author), UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292, USA. CR ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1208 BLACKSTAD TW, 1984, NEUROSCIENCE, V13, P827, DOI 10.1016/0306-4522(84)90099-X BROWN MC, 1991, J COMP NEUROL, V303, P300, DOI 10.1002/cne.903030211 BROWN MC, 1989, HEARING RES, V49, P105 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BROWN MC, 1988, J COMP NEUROL, V278, P581, DOI 10.1002/cne.902780409 COLLINGE C, 1991, HEARING RES, V53, P159, DOI 10.1016/0378-5955(91)90051-A COWAN WM, 1984, SCIENCE, V225, P1258, DOI 10.1126/science.6474175 DENNIS MJ, 1981, ANNU REV NEUROSCI, V4, P43, DOI 10.1146/annurev.ne.04.030181.000355 EASTER SS, 1985, SCIENCE, V230, P507, DOI 10.1126/science.4048944 FELDMAN ML, 1969, J COMP NEUROL, V137, P267, DOI 10.1002/cne.901370303 JACKSON H, 1982, J NEUROSCI, V2, P1736 JENSEN JK, 1987, FREQUENCY INTENSITY JOHNSON DA, 1981, J PHYSIOL-LONDON, V318, P143 KALTENBACH JA, 1991, HEARING RES, V51, P149, DOI 10.1016/0378-5955(91)90013-Y KERR LM, 1979, J EXP PSYCHOL ANIM B, V5, P97, DOI 10.1037//0097-7403.5.2.97 LEVAY S, 1978, J COMP NEUROL, V179, P1 LICHTMAN JW, 1980, J PHYSIOL-LONDON, V301, P213 Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MASON CA, 1984, J NEUROSCI, V4, P1715 MOORE DR, 1979, BRAIN RES, V163, P49, DOI 10.1016/0006-8993(79)90150-1 PURVES D, 1985, PRINCIPLES NEURAL DE ROMAND R, 1983, NEUROSCI LETT, V35, P271, DOI 10.1016/0304-3940(83)90329-4 ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 ROUILLER EM, 1986, J COMP NEUROL, V249, P261, DOI 10.1002/cne.902490210 SACHS GM, 1986, J COMP NEUROL, V246, P395, DOI 10.1002/cne.902460308 SAUNDERS JC, 1980, BRAIN RES, V187, P69, DOI 10.1016/0006-8993(80)90495-3 SCHURR A, 1987, BRAIN SLICES FUNDAME SCHWEITZER L, 1987, HEARING RES, V25, P249, DOI 10.1016/0378-5955(87)90096-7 SCHWEITZER L, 1987, NEUROSCIENCE, V23, P1123, DOI 10.1016/0306-4522(87)90186-2 SCHWEITZER L, 1984, J COMP NEUROL, V225, P228, DOI 10.1002/cne.902250208 SHNERSON A, 1979, EXP BRAIN RES, V37, P373 Shnerson A., 1982, DEV BRAIN RES, V2, P65 Siegel S., 1956, NONPARAMETRIC STATIS WALSH EJ, 1990, AM J OTOLARYNG, V11, P23, DOI 10.1016/0196-0709(90)90166-S WILLOTT JF, 1978, BRAIN RES, V148, P230, DOI 10.1016/0006-8993(78)90395-5 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 YAJIMA Y, 1989, EXP BRAIN RES, V75, P381 NR 39 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 1992 VL 60 IS 1 BP 34 EP 44 DI 10.1016/0378-5955(92)90056-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800005 PM 1500375 ER PT J AU SUZUKI, H LEE, YC TACHIBANA, M HOZAWA, K WATAYA, H TAKASAKA, T AF SUZUKI, H LEE, YC TACHIBANA, M HOZAWA, K WATAYA, H TAKASAKA, T TI QUANTITATIVE CARBOHYDRATE ANALYSES OF THE TECTORIAL AND OTOCONIAL MEMBRANES OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; OTOCONIAL MEMBRANE; CARBOHYDRATE COMPOSITION; HIGH-PERFORMANCE ANION-EXCHANGE CHROMATOGRAPHY; GLYCOPEPTIDASE-F; ENDO-BETA-GALACTOSIDASE ID ANION-EXCHANGE CHROMATOGRAPHY; LOCALIZATION; COLLAGEN; LECTINS; PROTEIN AB Carbohydrate composition of the tectorial membrane (TM) and the otoconial membrane (OM) of the guinea pig was analyzed after hydrolysis, using high-performance anion-exchange chromatography and pulsed amperometric detection. Both of the tissues were highly glycosylated; the carbohydrate content being 24-42% of protein. GlcN, Gal, Glc and Man were found to be the major component sugars of TM, whereas little GalN was found. Fuc and NANA were also present, but NGNA was not detectable. After digestion with thermolysin for solubilization, OM was separated into two fractions: insoluble mineral particles of the otoconia (OM-ppt) and a soluble fraction from the gelatinous layer (OM-sup). These two fractions showed distinct carbohydrate composition from each other. Further analyses using glycosidases revealed that TM contained asialyl and monosialyl but little di-, tri- and tetrasialyl N-glycosides, and OM-sup did not seem to be susceptible to endo-beta-galactosidase, which is known to cleave some N-acetyl-polylactosamine and keratan sulfate. Based on these analyses, it can be suggested that most of the carbohydrates in TM are likely to be asialyl and monosialyl N-glycosides. N-Glycosides may be predominant in the otoconia as well, and a polymer structure consisting of GlcN(Ac) and Gal other than N-acetyl-poly-lactosamine may exist in the gelatinous layer of OM. O-Glycosylation of the usual type appeared to be minor in all the fractions. C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. NIDOCD,MOLEC BIOL LAB,BETHESDA,MD. RP SUZUKI, H (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,1-1 SEIRYO CHO,SENDAI,MIYAGI 980,JAPAN. CR ALLEN G, 1981, LAB TECHNIQUES BIOCH, P43 BITTER T, 1962, ANAL BIOCHEM, V4, P330, DOI 10.1016/0003-2697(62)90095-7 BUTLER WT, 1966, J BIOL CHEM, V241, P3882 CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 CARREY EA, 1989, PROTEIN STRUCTURE PR, P117 GILLOYZAGA P, 1985, HEARING RES, V20, P1 GILLOYZAGA P, 1985, HEARING RES, V18, P269, DOI 10.1016/0378-5955(85)90043-7 GILLOYZAGA P, 1990, HEARING RES, V45, P151, DOI 10.1016/0378-5955(90)90191-Q IGARASHI M, 1969, ACTA OTO-LARYNGOL, V68, P420, DOI 10.3109/00016486909121580 INOUE S, 1975, ANAL BIOCHEM, V65, P164, DOI 10.1016/0003-2697(75)90502-3 IURATO S, 1960, Z ZELLFORSCH MIK ANA, V52, P105, DOI 10.1007/BF00344642 JOHNSON DC, 1986, CHROMATOGRAPHY FORUM, V1, P37 KENNEDY JF, 1979, PROTEOGLYCANS BIOL C, P97 KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 KOBAYASHI M, 1990, ANAL BIOCHEM, V189, P122, DOI 10.1016/0003-2697(90)90056-F LEE YC, 1990, ANAL BIOCHEM, V189, P151, DOI 10.1016/0003-2697(90)90099-U LI YT, 1982, METHOD ENZYMOL, V83, P610 Lim D J, 1973, Ann Otol Rhinol Laryngol, V82, P23 MILLER EJ, 1971, BIOCHEMISTRY-US, V10, P1652, DOI 10.1021/bi00785a024 MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 OLECHNO JD, 1989, TECHNIQUES PROTEIN C, P364 PRIETO JJ, 1990, HEARING RES, V45, P283, DOI 10.1016/0378-5955(90)90127-B RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 ROSS MD, 1974, AM J ANAT, V139, P449, DOI 10.1002/aja.1001390402 ROSS MD, 1973, ANAT REC, V175, P429 ROSS MD, 1985, AUDITORY BIOCH, P500 RUEDA J, 1988, GLYCOCONJUGATES MED, P338 SAITO H, 1970, ACTA OTO-LARYNGOL, V69, P333, DOI 10.3109/00016487009123373 SANTI PA, 1990, J ELECTRON MICR TECH, V15, P293, DOI 10.1002/jemt.1060150308 SPIRO RG, 1967, J BIOL CHEM, V242, P4813 STOWELL CP, 1978, ANAL BIOCHEM, V85, P572, DOI 10.1016/0003-2697(78)90256-7 SUGIYAMA S, 1991, HEARING RES, V55, P263, DOI 10.1016/0378-5955(91)90111-L TACHIBANA M, 1987, HEARING RES, V25, P115, DOI 10.1016/0378-5955(87)90084-0 TACHIBAN.M, 1973, ACTA OTO-LARYNGOL, V76, P37, DOI 10.3109/00016487309121481 TAKUMIDA M, 1989, ORL J OTO-RHINO-LARY, V51, P144 TARENTINO AL, 1985, BIOCHEMISTRY-US, V24, P4665, DOI 10.1021/bi00338a028 THALMANN I, 1986, ORL J OTO-RHINO-LARY, V48, P107 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 TOWNSEND RR, 1989, ANAL BIOCHEM, V182, P1 WISLOCKI GB, 1955, J ANAT, V89, P3 NR 40 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 JUN PY 1992 VL 60 IS 1 BP 45 EP 52 DI 10.1016/0378-5955(92)90057-T PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800006 PM 1500376 ER PT J AU WALSH, EJ GORGA, M MCGEE, J AF WALSH, EJ GORGA, M MCGEE, J TI COMPARISONS OF THE DEVELOPMENT OF AUDITORY BRAIN-STEM RESPONSE LATENCIES BETWEEN CATS AND HUMANS SO HEARING RESEARCH LA English DT Article DE EVOKED POTENTIAL; AUDITORY EVOKED BRAIN-STEM RESPONSE; HUMAN; CAT; DEVELOPMENT ID INTENSIVE-CARE NURSERY; EVOKED-POTENTIALS; STEM RESPONSES; TECTORIAL MEMBRANE; NORMAL PATTERNS; TUNING CURVES; HUMAN INFANTS; HUMAN ADULTS; FREQUENCY; HEARING AB Developmental changes in the peak latencies of auditory brainstem responses (ABR) recorded from humans and kittens were compared to test the hypothesis that developmental time courses among mammals are the same when appropriately normalized. Response latencies were computed as the difference from adult latency and conceptional ages were represented as percentages relative to the age that ABR wave latencies achieved a criterion value within 0.2 ms of asymptotic latency (i.e., adulthood). An underlying assumption of this exercise is that far-field response latency is an appropriate index of overall 'auditory development'. Results of this analysis suggest that developmental changes in latency of responses arising within the auditory periphery are similar between humans and cats, when appropriately normalized, and that more central changes show less correspondence. Consequently, absolute time course differences for specific developmental parameters must be considered and caution should be exercised when extrapolating results acquired from one species to the other. RP WALSH, EJ (reprint author), BOYS TOWN NATL RES HOSP,555 N 30TH ST,OMAHA,NE 68132, USA. CR AINSLIE PJ, 1980, ELECTROEN CLIN NEURO, V49, P291, DOI 10.1016/0013-4694(80)90223-0 Anniko M, 1987, Acta Otolaryngol Suppl, V436, P51 BARGONES JY, 1988, J ACOUST SOC AM, V83, P1809, DOI 10.1121/1.396515 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 Conel J., 1941, POSTNATAL DEV HUMAN, V2 Conel J. L, 1939, POSTNATAL DEV HUMAN, V1-8 Conel J. L. R., 1967, POSTNATAL DEV HUMAN, V8 Conel J. L. R., 1963, POSTNATAL DEV HUMAN, V7 CONEL JL, 1959, POSTNATAL DEV HUMAN, V6 CONEL JL, 1947, POSTNATAL DEV HUMAN, V3 CONEL JLR, 1955, POSTNATAL DEV HUMAN, V5 CONEL JLR, 1951, POSTNATAL DEV HUMAN, V4 DENNIS J, 1984, AM J OTOLARYNG, V3, P201 DUM N, 1981, HEARING RES, V5, P271, DOI 10.1016/0378-5955(81)90051-4 DURIEUXSMITH A, 1985, J OTOLARYNGOL, V14, P12 Eggermont J J, 1985, Acta Otolaryngol Suppl, V421, P102 EGGERMONT JJ, 1986, ARCH NEUROL-CHICAGO, V43, P116 FOLSOM RC, 1987, J ACOUST SOC AM, V81, P412, DOI 10.1121/1.394906 FOLSOM RC, 1986, J ACOUST SOC AM, V80, P1057, DOI 10.1121/1.393847 FULLERTON BC, 1987, ELECTROEN CLIN NEURO, V66, P547, DOI 10.1016/0013-4694(87)90102-7 GALAMBOS R, 1980, PEDIATR RES, V14, P159, DOI 10.1203/00006450-198002000-00019 GORGA MP, 1988, EAR HEARING, V9, P144, DOI 10.1097/00003446-198806000-00007 GORGA MP, 1987, J SPEECH HEAR RES, V30, P311 GORGA MP, 1989, J SPEECH HEAR RES, V32, P281 HECOX K, 1982, ANN NY ACAD SCI, V388, P538, DOI 10.1111/j.1749-6632.1982.tb50815.x HECOX K, 1974, ARCH OTOLARYNGOL, V99, P30 HINOJOSA R, 1977, ACTA OTO-LARYNGOL, V84, P238, DOI 10.3109/00016487709123963 HYDE ML, 1984, J OTOLARYNGOL, V13, P49 JAVEL E, 1986, ADV NEURAL BEHAVIORA, V2, P119 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X KLEIN AJ, 1984, HEARING RES, V16, P291, DOI 10.1016/0378-5955(84)90118-7 KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 LAVIGNEREBILLARD M, 1986, ANAT EMBRYOL, V174, P369, DOI 10.1007/BF00698787 Lavigne-Rebillard M, 1985, Ann Otolaryngol Chir Cervicofac, V102, P493 Lavigne-Rebillard M, 1987, Acta Otolaryngol Suppl, V436, P43 LEVENTHAL AS, 1964, CHILD DEV, V35, P759, DOI 10.1111/j.1467-8624.1964.tb05215.x LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 LIM DJ, 1977, INNER EAR BIOL, P47 LIM DJ, 1987, HEARING RES, V28, P9 LINDEMAN HH, 1971, ACTA OTO-LARYNGOL, V72, P229, DOI 10.3109/00016487109122478 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 PUJOL R, 1973, ACTA OTO-LARYNGOL, V76, P1, DOI 10.3109/00016487309121476 Pujol R, 1985, Acta Otolaryngol Suppl, V423, P43 SALAMY A, 1975, BRAIN RES, V96, P361, DOI 10.1016/0006-8993(75)90748-9 FERNANDEZ JMS, 1983, ACTA OTO-LARYNGOL, V95, P460, DOI 10.3109/00016488309139430 SHIPLEY C, 1980, BRAIN RES, V182, P313, DOI 10.1016/0006-8993(80)91191-9 Siebert W. M., 1968, RECOGNIZING PATTERNS, P104 SINNOTT JM, 1985, J ACOUST SOC AM, V78, P1986, DOI 10.1121/1.392655 TANAKA K, 1979, ANN OTO RHINOL LARYN, V88, P749 TREHUB SE, 1980, J EXPT CHILD PSYCHOL, V29, P283 WALSH EJ, 1986, J ACOUST SOC AM, V79, P712, DOI 10.1121/1.393461 WALSH EJ, 1987, HEARING RES, V28, P97, DOI 10.1016/0378-5955(87)90157-2 WALSH EJ, 1986, J ACOUST SOC AM, V79, P745, DOI 10.1121/1.393463 WALSH EJ, 1986, J ACOUST SOC AM, V79, P725, DOI 10.1121/1.393462 WALSH EJ, 1983, THESIS CREIGHTON U O Yakovlev P. I., 1967, REGIONAL DEV BRAIN E, P3 NR 57 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 JUN PY 1992 VL 60 IS 1 BP 53 EP 63 DI 10.1016/0378-5955(92)90058-U PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800007 PM 1500377 ER PT J AU KAWASAKI, K YAMAMOTO, A OMORI, K IWANO, T KUMAZAWA, T TASHIRO, Y AF KAWASAKI, K YAMAMOTO, A OMORI, K IWANO, T KUMAZAWA, T TASHIRO, Y TI QUANTITATIVE IMMUNOELECTRON MICROSCOPIC LOCALIZATION OF NA, K-ATPASE ALPHA-SUBUNIT IN THE EPITHELIAL-CELLS OF RAT VESTIBULAR APPARATUS SO HEARING RESEARCH LA English DT Article DE QUANTITATIVE IMMUNOGOLD ELECTRON-MICROSCOPY; NA; K-ATPASE; RAT; VESTIBULAR APPARATUS ID SQUIRREL-MONKEY; COCHLEAR DUCT; NA+,K+-ATPASE; NITROCELLULOSE; PURIFICATION; ANTIBODIES; PROTEINS; (NA+; WALL AB Na, K-ATPase was quantitatively localized in the epithelial cells of rat vestibular apparatus such as macula utriculi, macula sacculi and crista ampullaris. Immunogold localization method was carried out at the saturation level of antibody using an affinity purified antibody against the alpha-subunit of rat kidney Na, K-ATPase. Numerous gold particles were found on the basolateral membrane of the dark cells, a small number of gold particles were found on the basolateral membrane of the transitional epithelium cells and hair cells, but the luminal surface membranes of the hair cells, transitional epithelium cells, planum semilunatum cells and dark cells were rarely labeled by gold particles. Significance of the abundant localization of Na, K-ATPase on the basolateral surface of the dark cells in the production of endolymph was discussed. C1 KANSAI MED UNIV,DEPT PHYSIOL,MORIGUCHI,OSAKA 570,JAPAN. KANSAI MED UNIV,DEPT OTOLARYNGOL,MORIGUCHI,OSAKA 570,JAPAN. CR AKAYAMA M, 1986, CELL STRUCT FUNCT, V11, P259 BURNETTE WN, 1981, ANAL BIOCHEM, V112, P195, DOI 10.1016/0003-2697(81)90281-5 FUKUI Y, 1992, IN PRESS J HISTOCHEM IWANO T, 1990, J HISTOCHEM CYTOCHEM, V38, P225 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 KAWASAKI K, 1990, Cell Structure and Function, V15, P487 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 MCDONOUGH AA, 1982, J MEMBRANE BIOL, V69, P13, DOI 10.1007/BF01871237 Nakai Y, 1968, Acta Otolaryngol, V66, P120, DOI 10.3109/00016486809126280 SELLICK PM, 1972, PFLUG ARCH EUR J PHY, V336, P21, DOI 10.1007/BF00589138 SELLICK PM, 1972, PFLUG ARCH EUR J PHY, V336, P28, DOI 10.1007/BF00589139 SLOT JW, 1985, EUR J CELL BIOL, V38, P87 SMITH DE, 1984, J CELL BIOL, V99, P20, DOI 10.1083/jcb.99.1.20 SPICER SS, 1990, HEARING RES, V43, P205, DOI 10.1016/0378-5955(90)90229-I TAKADA T, 1989, Cell Structure and Function, V14, P921 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V104, P22, DOI 10.3109/00016488709109043 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 NR 18 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 JUN PY 1992 VL 60 IS 1 BP 64 EP 72 DI 10.1016/0378-5955(92)90059-V PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800008 PM 1323557 ER PT J AU NEWTON, EH COOPER, WA COLEMAN, JR AF NEWTON, EH COOPER, WA COLEMAN, JR TI RATE AND FREQUENCY INTERACTIONS IN THE AUDITORY BRAIN-STEM RESPONSE OF THE ADULT-RAT SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM; TONAL STIMULI; RATE; LATENCY; AMPLITUDE; RAT ID COMPOUND ACTION-POTENTIALS; STIMULUS REPETITION RATE; STEM RESPONSES; MULTIPLE-SCLEROSIS; EVOKED-POTENTIALS; LATENCY; CAT; HUMANS; SCALP; AGE AB Tone pip stimuli were used at different repetition rates to examine influences upon auditory brainstem response components. Rate increases to 80.1/s result in significant latency increases in waves IV and V at all test frequencies. Rate effects occur in rostral brainstem response components which show frequency related latencies different from wave I. Amplitude measures decline at higher repetition rates for waves I and IV at most test frequencies. Rate effects are most pronounced at 8 kHz stimulation which is around the optimal behavioral frequency in rat. At higher rates the second peak of wave I is enhanced at 8 kHz. whereas the third peak of wave I at 40 kHz disappears. These results demonstrate that tone-specific stimuli provide sensitive measures of latency, amplitude and wave morphology of components of the auditory brainstem response as a function of stimulus repetition. C1 UNIV S CAROLINA,DEPT SPEECH PATHOL & AUDIOL,COLUMBIA,SC 29208. UNIV S CAROLINA,DEPT PSYCHOL & PHYSIOL,COLUMBIA,SC 29208. CR ANGELLO R, 1990, AUDIOLOGY, V29, P326 BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 BLATCHLEY BJ, 1987, DEV BRAIN RES, V32, P74 BUCHWALD JS, 1983, BASES AUDITORY BRAIN, P157 BURKARD R, 1983, J ACOUST SOC AM, V74, P1204, DOI 10.1121/1.390024 CHIAPPA KH, 1979, ARCH NEUROL-CHICAGO, V36, P81 COLEMAN JR, 1986, P INT UNION PHYSL SC, V16, P203 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F DEBRUYNE F, 1986, AUDIOLOGY, V25, P101 DESPLAND PA, 1980, PEDIATR RES, V14, P154, DOI 10.1203/00006450-198002000-00018 DON M, 1977, ANN OTO RHINOL LARYN, V86, P186 FUNAI H, 1980, AUDIOLOGY, V22, P9 HENRY KR, 1979, AUDIOLOGY, V18, P93 HUANG C, 1980, ELECTROEN CLIN NEURO, V49, P15, DOI 10.1016/0013-4694(80)90347-8 HUMPHREY DR, 1968, ELECTROEN CLIN NEURO, V25, P421, DOI 10.1016/0013-4694(68)90152-1 JACOBSON JT, 1987, EAR HEARING, V8, P115, DOI 10.1097/00003446-198704000-00009 JEWETT DL, 1972, BRAIN RES, V36, P101, DOI 10.1016/0006-8993(72)90769-X JEWETT DL, 1971, BRAIN, V94, P681, DOI 10.1093/brain/94.4.681 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 MAIR IWS, 1979, AUDIOLOGY, V18, P265 MOLLER AR, 1988, ELECTROEN CLIN NEURO, V71, P198, DOI 10.1016/0168-5597(88)90005-6 MOLLER AR, 1983, EXP NEUROL, V80, P633, DOI 10.1016/0014-4886(83)90313-8 Moller AR, 1985, AUDITORY BRAINSTEM R, P13 PRATT H, 1976, ARCH OTORHINOLARYNGO, V63, P839 PRIJS VF, 1981, HEARING RES, V4, P23, DOI 10.1016/0378-5955(81)90034-4 ROBINSON K, 1977, BRAIN, V100, P19, DOI 10.1093/brain/100.1.19 ROWE MJ, 1981, EAR HEARING, V2, P41, DOI 10.1097/00003446-198101000-00008 SMITH DI, 1990, HEARING RES, V43, P95, DOI 10.1016/0378-5955(90)90218-E SUZUKI T, 1986, ELECTROEN CLIN NEURO, V65, P150, DOI 10.1016/0168-5597(86)90048-1 TSUCHITANI C, 1983, BASES AUDITORY BRAIN, P67 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P326, DOI 10.1016/0013-4694(83)90259-6 1977, ANSI S311977 AM NAT 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 JUN PY 1992 VL 60 IS 1 BP 73 EP 79 DI 10.1016/0378-5955(92)90060-Z PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800009 PM 1500378 ER PT J AU YLIKOSKI, J PIRVOLA, U LEHTONEN, E AF YLIKOSKI, J PIRVOLA, U LEHTONEN, E TI DISTRIBUTION OF F-ACTIN AND FODRIN IN THE HAIR-CELLS OF THE GUINEA-PIG COCHLEA AS REVEALED BY CONFOCAL FLUORESCENCE MICROSCOPY SO HEARING RESEARCH LA English DT Article DE IMMUNOHISTOCHEMISTRY; HAIR CELLS; CYTOSKELETON; SURFACE SPECIMENS ID MOTILE RESPONSES; ORGAN; SPECTRIN; CORTI; ORGANIZATION; CYTOSKELETAL; EPITHELIUM; MECHANICS; MEMBRANE; LATTICE AB We double-stained paraformaldehyde fixed guinea pig cochleas with rhodaminated phalloidin to detect F-actin and with a monoclonal antibody against non-erythroid spectrin (fodrin). The hair cells were studied in surface specimens of the organ of Corti with confocal fluorescence microscopy. In serial optical sections, phalloidin stained the stereocilia, cuticular plate, and a circumferential ring beneath it in the inner and outer hair cells (IHCs and OHCs). The cytoplasm of the IHCs and the OHCs was unlabelled, but the infracuticular network of the OHCs in the upper turns showed a strong reaction. The lateral plasma membrane was unreactive with phalloidin in the IHCs and OHCs, except in the basal turn, where a moderate reaction, probably representing actin of Deiter's cups, was seen along the lateral walls of the basal pole of the OHCs. Fodrin was similarly seen in the cuticular plate, in a circumferential ring beneath it, and in the infracuticular network of the apical OHCs. The most interesting finding was the fodrin-specific distinct labelling of the lateral cell surface in the OHCs of the basal cochlear turn. This staining, diminished towards the apex and was practically absent in the OHCs located above the level of 15 mm from the round window. The lateral cell surface of IHCs showed moderate fodrin labelling in all cochlear turns. This staining was much weaker than that seen in the basal OHCs. Fodrin labelling revealed deformation from the regular cylindrical shape in midportion of the OHC bodies in the basal turn of the cochlea. This change seems not to be a fixation artefact, even though effects of other physical and chemical factors are not excluded. If not an artefact, the shape change indicates reduced rigidity of the cortical cytoskeleton of the OHCs at this location. The differences in the distribution and organization ot actin and fodrin among the hair cells of different rows and turns of the cochlea probably reflect differences in their mechanisms of function. C1 UNIV HELSINKI,DEPT PATHOL,SF-00100 HELSINKI 10,FINLAND. EUROPEAN MOLEC BIOL LAB,W-6900 HEIDELBERG,GERMANY. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BACALLAO R, 1989, J CELL BIOL, V109, P2817, DOI 10.1083/jcb.109.6.2817 BEAVEN GH, 1985, EUR J CELL BIOL, V36, P299 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 CARLISLE L, 1988, HEARING RES, V33, P201, DOI 10.1016/0378-5955(88)90033-0 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DEBOER E, 1983, J ACOUST SOC AM, V73, P567, DOI 10.1121/1.389002 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1991, HEARING RES, V52, P225, DOI 10.1016/0378-5955(91)90202-K ESKELINEN S, 1991, IN PRESS J CELL PHYS FLOCK A, 1982, HEARING RES, V6, P75 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FUNG LWM, 1989, LIFE SCI, V44, P735, DOI 10.1016/0024-3205(89)90385-8 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HIROKAWA N, 1986, HEARING RES, V22, P41, DOI 10.1016/0378-5955(86)90076-6 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1990, BIOPHYS SCI, V2, P49 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 LIM DJ, 1989, ACTA OTO-LARYNGOL, V107, P398, DOI 10.3109/00016488909127529 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LIU SC, 1987, J CELL BIOL, V104, P527, DOI 10.1083/jcb.104.3.527 REUTER G, 1990, HEARING RES, V43, P219, DOI 10.1016/0378-5955(90)90230-M SAITO K, 1983, CELL TISSUE RES, V229, P467 SAXTON MJ, 1989, BIOPHYS J, V55, P21 SCARFONE E, 1991, HEARING RES, V54, P247, DOI 10.1016/0378-5955(91)90119-T SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 STELZER EHK, 1989, SCANNING IMAGINGS, P146 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 YLIKOSKI J, 1990, HEARING RES, V43, P199, DOI 10.1016/0378-5955(90)90228-H ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 37 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 JUN PY 1992 VL 60 IS 1 BP 80 EP 88 DI 10.1016/0378-5955(92)90061-Q PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800010 PM 1500379 ER PT J AU DENK, W WEBB, WW AF DENK, W WEBB, WW TI FORWARD AND REVERSE TRANSDUCTION AT THE LIMIT OF SENSITIVITY STUDIED BY CORRELATING ELECTRICAL AND MECHANICAL FLUCTUATIONS IN FROG SACCULAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR BUNDLE; THERMAL NOISE; HEARING ID ION-DEPENDENT CONDUCTANCES; BASILAR-MEMBRANE MOTION; MECHANOELECTRICAL TRANSDUCTION; BULLFROGS SACCULUS; BULL-FROG; RANA-CATESBEIANA; NERVE-FIBERS; INNER-EAR; TURTLE; CHANNELS AB The spontaneous fluctuations of the intracellular voltage and the position of the sensory hairbundle were measured concurrently using intracellular microelectrodes and an optical differential micro interferometer. Magnitude and frequency distribution of the hair bundles' spontaneous motion suggest that it consists mostly of Brownian motion. The electrical noise, however, exceeds the value expected for thermal Johnson noise by several orders of magnitude, and its frequency distribution reflects the transduction tuning properties of the hair cells. Frequently, a strong correlation was observed between the fluctuations of the hair bundle position and the intracelluar electrical noise. From the properties of the correlation and from experiments involving mechanical stimulation we conclude that in most cases mechano-electrical transduction of the bundles' Brownian motion causes this correlation. Small signal transduction sensitivities ranged from 18 to 500-mu-V/nm. Bundle motion that was observed in response to current injection in more than half of the cells suggests the existence of a fast reverse (electro-mechanical) transduction mechanism to be common in these cells. The sensitivities could be as high as 600 pm of bundle deflection per millivolt of membrane potential change. In a significant minority (4 in 44) of cells, all showing excess electrical noise, we found 'non-causal' components of the electro-mechanical correlation, and in two of those cells narrow-band bundle motion in excess of their thermal motion at frequencies coincident with peaks in the intracellular noise was observed. C1 CORNELL UNIV,SCH APPL & ENGN PHYS,ITHACA,NY 14853. AT&T BELL LABS,DEPT PHYS,MURRAY HILL,NJ 07974. RI Webb, Watt/B-5905-2011; denk, winfried/I-6627-2012 CR ADAMS PR, 1982, NATURE, V296, P746, DOI 10.1038/296746a0 ALLEN RD, 1968, Z WISS MIKR MIKROTEC, V69, P193 ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1985, PROC R SOC SER B-BIO, V226, P325, DOI 10.1098/rspb.1985.0098 ASHMORE JF, 1983, NATURE, V304, P535 ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 Bendat J., 1971, RANDOM DATA ANAL MEA BIALEK W, 1984, PHYS LETT A, V104, P173, DOI 10.1016/0375-9601(84)90371-2 COREY DP, 1979, BIOPHYS J, V26, P499 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 COREY DP, 1983, J NEUROSCI, V3, P942 COREY DP, 1980, J NEUROSCI METH, V3, P183, DOI 10.1016/0165-0270(80)90025-4 COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V315, P317 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 DENK W, 1989, P NATL ACAD SCI USA, V86, P5371, DOI 10.1073/pnas.86.14.5371 DENK W, 1989, THESIS CORNELL U ITH DENK W, 1989, COCHLEAR MECH STRUCT, P125 DENK W, 1989, PHYS REV LETT, V63, P207, DOI 10.1103/PhysRevLett.63.207 DENK W, 1990, APPL OPTICS, V29, P2382, DOI 10.1364/AO.29.002382 DEVRIES HL, 1948, PHYSICA, V14, P48, DOI 10.1016/0031-8914(48)90060-3 EATOCK RA, 1987, J NEUROSCI, V7, P2821 FELLER W, 1968, INTRO PROBABILITY TH, V1, P230 FLEROV MI, 1976, BIOFIZIKA+, V21, P1092 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P462, DOI 10.1098/rspb.1948.0024 GUHARAY F, 1984, J PHYSIOL-LONDON, V352, P685 HACOHEN N, 1989, J NEUROSCI, V9, P3988 HARRIS GG, 1968, J ACOUST SOC AM, V44, P176, DOI 10.1121/1.1911052 HILL BC, 1977, SCIENCE, V196, P426, DOI 10.1126/science.850785 HOLTON T, 1986, J PHYSIOL-LONDON, V375, P195 HOROWITZ P, 1980, ART ELECTRONICS HOWARD J, 1987, P NATL ACAD SCI USA, V84, P3064, DOI 10.1073/pnas.84.9.3064 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P275 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 HUDSPETH AJ, 1983, J PHYSIOL-LONDON, V345, pP66 HUDSPETH AJ, 1983, ANNU REV NEUROSCI, V6, P187, DOI 10.1146/annurev.ne.06.030183.001155 HUDSPETH AJ, 1979, P NATL ACAD SCI USA, V76, P1506, DOI 10.1073/pnas.76.3.1506 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 HUDSPETH AJ, 1978, AM J PHYSIOL, V234, pC56 IWASA K, 1980, SCIENCE, V210, P338, DOI 10.1126/science.7423196 Johnson JB, 1927, NATURE, V119, P50, DOI 10.1038/119050c0 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LEWIS ER, 1988, BIOPHYS J, V53, P441 LEWIS RS, 1983, HEARING PHYSL BASES, P17 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 MAURO A, 1970, J GEN PHYSIOL, V55, P497, DOI 10.1085/jgp.55.4.497 MURALT P, 1986, IBM J RES DEV, V30, P443 NARINS PM, 1984, J ACOUST SOC AM, V5, P1384 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 NEHER E, 1977, ANNU REV BIOPHYS BIO, V6, P345, DOI 10.1146/annurev.bb.06.060177.002021 OHMORI H, 1988, J PHYSIOL-LONDON, V399, P115 PALMER AR, 1981, J PHYSL, V324, pP66 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PITCHFORD S, 1987, HEARING RES, V27, P75, DOI 10.1016/0378-5955(87)90027-X ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 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 SIGWORTH FJ, 1980, J PHYSIOL-LONDON, V307, P97 TERAKAWA S, 1984, J PHYSL, V369, P229 WEISS TF, 1982, HEARING RES, V7, P353, DOI 10.1016/0378-5955(82)90045-4 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 NR 71 TC 86 Z9 88 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 1992 VL 60 IS 1 BP 89 EP 102 DI 10.1016/0378-5955(92)90062-R PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800011 PM 1500380 ER PT J AU OBERHOLTZER, JC BUETTGER, C SUMMERS, MC MATSCHINSKY, FM AF OBERHOLTZER, JC BUETTGER, C SUMMERS, MC MATSCHINSKY, FM TI METABOLIC LABELING AND QUANTITATION OF PROTEINS SYNTHESIZED BY SINGLE CHICK COCHLEAS SO HEARING RESEARCH LA English DT Article DE AVIAN; COCHLEA; PROTEIN SYNTHESIS; QUANTITATION ID SENSORY HAIR-CELLS; BASILAR PAPILLA; INNER-EAR; ACOUSTIC TRAUMA; STEREOCILIA; REGENERATION; TRANSDUCTION AB Molecular studies of the peripheral auditory system are made difficult by the small quantities of tissue available and by their relative inaccessibility. In addition, the cochlea and other hair cell-containing receptor organs are composed of both hair cells and supporting cells, as well as several other cell types. The identification of known proteins and the characterization of specific and novel protein molecules from these tissues require the use of sensitive techniques and a consideration of the complex histology. The chick cochlea was selected as an experimental system since the cochlea is relatively accessible in the bird, the receptor neuroepithelium contains a large number of hair cells compacted in a small area, and the physiology of the auditory periphery has been studied extensively. A general procedure is described for the metabolic radiolabelling of proteins from single cochleas followed by their solubilization, separation by high-resolution two-dimensional gel electrophoresis, and accurate quantitation. The method is highly reproducible and sensitive, and should prove useful in studies of proteins from the specialized cell types of the chick cochlea, including the identification of those whose rates of synthesis are modified in response to acoustic stimulation and sound damage or recovery. C1 UNIV PENN,SCH MED,DIABET RES CTR,DEPT BIOCHEM & BIOPHYS,501 STEMMLER BLDG,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. CR CELIS JE, 1990, ELECTROPHORESIS, V11, P1072, DOI 10.1002/elps.1150111203 CELIS JE, 1990, ELECTROPHORESIS, V11, P989, DOI 10.1002/elps.1150111202 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 DRESCHER DG, 1989, BRAIN RES, V485, P225, DOI 10.1016/0006-8993(89)90565-9 GARRELS JI, 1984, 2 DIMENSIONAL GEL EL, P38 GARRELS JI, 1983, METHOD ENZYMOL, V100, P411 GARRELS JI, 1989, J BIOL CHEM, V264, P5283 GARRELS JI, 1989, J BIOL CHEM, V264, P5299 GARRELS JI, 1989, J BIOL CHEM, V264, P5269 GARRELS JI, 1990, ELECTROPHORESIS, V11, P1114, DOI 10.1002/elps.1150111204 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 GILLESPIE PG, 1991, P NATL ACAD SCI USA, V88, P2563, DOI 10.1073/pnas.88.6.2563 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 OBERHOLTZER JC, 1986, HEARING RES, V23, P161, DOI 10.1016/0378-5955(86)90013-4 OBERHOLTZER JC, 1988, P NATL ACAD SCI USA, V85, P3387, DOI 10.1073/pnas.85.10.3387 RICHARDSON GP, 1990, J CELL BIOL, V110, P1055, DOI 10.1083/jcb.110.4.1055 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SCHNEIDER ME, 1987, HEARING RES, V31, P39, DOI 10.1016/0378-5955(87)90212-7 SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 SMITH C, 1971, CONTRIBUTIONS SENSOR TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 THALMANN I, 1980, ARCH OTO-RHINO-LARYN, V226, P123, DOI 10.1007/BF00455126 THALMANN I, 1990, LARYNGOSCOPE, V100, P99 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 TILNEY MS, 1989, J CELL BIOL, V109, P1711, DOI 10.1083/jcb.109.4.1711 VANBOGELEN RA, 1990, ELECTROPHORESIS, V11, P1131, DOI 10.1002/elps.1150111205 NR 31 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 JUN PY 1992 VL 60 IS 1 BP 103 EP 109 DI 10.1016/0378-5955(92)90063-S PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800012 PM 1500371 ER PT J AU SCHWARZ, DWF SCHWARZ, IE DEZSO, A AF SCHWARZ, DWF SCHWARZ, IE DEZSO, A TI COCHLEAR EFFERENT NEURONS PROJECTING TO BOTH EARS IN THE CHICKEN, GALLUS-DOMESTICUS SO HEARING RESEARCH LA English DT Article DE COCHLEAR EFFERENTS; BILATERAL PROJECTION; AUDITORY PATHWAY; BIRDS ID PIGEON COLUMBA-LIVIA; VESTIBULAR NEURONS; RETROGRADE AB Different retrograde neuroanatomical tracers were injected into each cochlea of adult chicken. The number of cells labeled in the cochlear efferent cell group found bilaterally within the caudal pontine reticular formation depended upon the tracer, with True Blue and Fluoro Gold yielding maximal average counts of 332 efferent neurons per injection. Double labeling of less than 1% of these cells was possible with the combination of True Blue and Diamidino Yellow. Thus the contribution of efferent neurons with axon collaterals projecting to both ears is not fundamentally different in birds and other vertebrates. C1 UNIV BRITISH COLUMBIA,ROTARY HEARING CTR,DIV OTOLARYNGOL,VANCOUVER V6T 1W5,BC,CANADA. UNIV BRITISH COLUMBIA,DEPT PHYSIOL,VANCOUVER V6T 1W5,BC,CANADA. UNIV PECS,OTOLARYNGOL CLIN,H-7622 PECS,HUNGARY. CR COLE KS, 1990, EXP BRAIN RES, V82, P585 FRITZSCH B, 1989, NEUROSCI LETT, V96, P241, DOI 10.1016/0304-3940(89)90385-6 KHALSA SBS, 1981, ACTA OTO-LARYNGOL, V92, P83, DOI 10.3109/00016488109133241 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 ROBERTSON D, 1987, HEARING RES, V25, P69, DOI 10.1016/0378-5955(87)90080-3 SCHWARZ DWF, 1978, BRAIN RES, V155, P103, DOI 10.1016/0006-8993(78)90308-6 SCHWARZ IE, 1981, J COMP NEUROL, V196, P1, DOI 10.1002/cne.901960102 STRUTZ J, 1982, ACTA OTO-LARYNGOL, V94, P45, DOI 10.3109/00016488209128888 THOMPSON GC, 1986, J COMP NEUROL, V254, P246, DOI 10.1002/cne.902540208 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 NR 10 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 JUN PY 1992 VL 60 IS 1 BP 110 EP 114 DI 10.1016/0378-5955(92)90064-T PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA JB648 UT WOS:A1992JB64800013 PM 1500372 ER PT J AU HARA, A SENARITA, M KOMENO, M KUSAKARI, J AF HARA, A SENARITA, M KOMENO, M KUSAKARI, J TI METALLIC ELEMENTS IN THE PERILYMPH MEASURED WITH AN INDUCTIVELY-COUPLED PLASMA ATOMIC EMISSION SPECTROMETER SO HEARING RESEARCH LA English DT Article DE INDUCTIVELY-COUPLED PLASMA ATOMIC EMISSION SPECTROMETRY; CATION; PERILYMPH ID COCHLEAR ENDOLYMPH; MAGNESIUM CONCENTRATION; GUINEA-PIG; CSF; COPPER; ZINC; FLUID AB Metallic elements in the perilymph of the scala tympani in normal and acoustically overstimulated guinea pigs were measured using a new method, an inductively-coupled plasma atomic emission spectrometry. The concentrations of phosphorus and eight metallic elements, i.e. calcium, copper, iron, potassium, magnesium, sodium, lead and zinc were measured simultaneously in a 2-mu-l sample of perilymph. The mean concentration values of calcium, copper, iron, magnesium, phosphorus, lead and zinc were 2.03 mM, 38.5-mu-M, 69.3-mu-M, 0.822 mM, 0.851 mM, 43.5-mu-M and 25.0-mu-M, respectively. There was no significant effect of acoustic overstimulation on the concentrations of these elements except for magnesium, which decreased significantly after the exposure to a intense sound (2 kHz, 115 dB SPL) for 15 min. This is the first report describing the synchronous determination of metallic poly-elements, including copper, iron, lead and zinc, in the perilymph. RP HARA, A (reprint author), UNIV TSUKUBA,INST CLIN MED,DEPT OTORHINOLARYNGOL,1-1-1 TENNODAI,TSUKUBA 305,JAPAN. CR BOSHER SK, 1978, NATURE, V273, P377, DOI 10.1038/273377a0 CITRON L, 1957, P ROY SOC MED, V50, P697 DOMINICI C, 1986, CLIN CHIM ACTA, V158, P207, DOI 10.1016/0009-8981(86)90284-6 DORMANDY TL, 1978, LANCET, V1, P647 HALLIWELL B, 1985, TRENDS NEUROSCI, V8, P22, DOI 10.1016/0166-2236(85)90010-4 HARA A, 1988, GLYCOCONJUGATES MED, P333 HARA A, 1989, HEARING RES, V42, P265 IKEDA K, 1987, HEARING RES, V26, P117, DOI 10.1016/0378-5955(87)90040-2 IKEDA K, 1988, HEARING RES, V32, P103, DOI 10.1016/0378-5955(88)90081-0 IKEDA K, 1988, ARCH OTO-RHINO-LARYN, V245, P142, DOI 10.1007/BF00464015 JOACHIMS Z, 1983, J ACOUST SOC AM, V74, P104, DOI 10.1121/1.389726 JUHN SK, 1976, LARYNGOSCOPE, V2, P273 JUHN SK, 1981, ANN OTO RHINOL LARYN, V90, P135 KANEKO A, 1975, J PHYSIOL-LONDON, V252, P509 KAPAKI E, 1989, ACTA NEUROL SCAND, V79, P373 KATZ B, 1967, J PHYSIOL-LONDON, V192, P407 MARKLUND SL, 1982, P NATL ACAD SCI-BIOL, V79, P7634, DOI 10.1073/pnas.79.24.7634 NISHIKAWA N, 1990, EAR RES JPN, V21, P311 PALL HS, 1987, LANCET, V2, P238 PALM R, 1986, ACTA NEUROL SCAND, V74, P308 PETERSON SK, 1978, J COMP PHYSIOL, V126, P1 RAUCH S, 1974, HDB SENSORY PHYSL, V1, P647 SAHU RN, 1988, BIOL PSYCHIAT, V24, P480, DOI 10.1016/0006-3223(88)90190-4 WEISNER B, 1987, J NEUROL SCI, V79, P229, DOI 10.1016/0022-510X(87)90275-9 NR 24 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 MAY PY 1992 VL 59 IS 2 BP 117 EP 120 DI 10.1016/0378-5955(92)90108-Y PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600001 PM 1618704 ER PT J AU GREENWOOD, DD AF GREENWOOD, DD TI CRITICAL BANDWIDTH AND CONSONANCE - THEIR OPERATIONAL DEFINITIONS IN RELATION TO COCHLEAR NONLINEARITY AND COMBINATION TONES SO HEARING RESEARCH LA English DT Article DE CRITICAL BANDWIDTH; MASKING; COCHLEA; COMBINATION TONES; NOTCHED-NOISE ID DISTORTION PRODUCTS F2-F1; AUDITORY FILTER SHAPES; DIFFERENCE; MASKING; NEURONS; NUCLEUS; 2F1-F2; BANDS; LEVEL; PHASE AB In a part of the paper cited above, it was suggested that detection of combination components might well determine the initial fall in signal threshold when an experimeter separates two bands of noise masking a signal centered between them-the notched-noise paradigm developed by Patterson (1976). Unfortunately, I mis-stated the bandwidths of the noise bands used by Patterson despite his clear description of their widths and despite the fact that I have also generated noises in the same way. I erred by stating the bandwidths to be half of what they were. Given this error, I calculated examples of the cochlear distribution of the combination components that would be produced by Patterson's noise bands, by themselves and in combination with the signal. The calculated combination-band frequency limits and their cochlear positions, using the wrong primary-noise bandwidth, therefore do not apply to Patterson's experiment. Here the errors are corrected. The modified distribution is not affected in principle. However, for some readers it might seem less probable that detection of combination components in frequency regions lower than the lower band of masking noise could determine the initial fall in threshold (rather than detection of events created by the signal in a cochlear region given by the notch in the two-band masker). But in any case this is an empirical question requiring the direct study that was being urged by the reasoning and calculations presented. There is still reason to suspect that combination tones may have played a role in the two-band experiments, as is illustrated here by figures from Greenwood (1972b) and Krammer (1973) in which the masking stimuli were much narrower. In one figure, given a tone and noise-band masker, a wide array of separated combination bands is generated at lower frequencies, which can mask signals of external origin. They will also either mask, or fail to mask, signal-masker generated combination bands created when an external signal is added in the gap or notch within the two-part primary masker. If signal-masker combination bands are not absolutely everywhere masked by the two-part masker and its combination bands, the signal-masker bands may permit detection of the added signal's presence (thus lowering 'signal' threshold). If the masker bands are widened (as by the above corrections, with notch constant), the combination bands generated by them will join and overlap, to mask more uniformly in the lower frequencies, but their distribution will not be the same as if the notch were filled. Whether they will be able everywhere to mask also-wider signal-masker combination bands is the critical question posed by these figures, which indicate that an experimental study, varying notch and bandwidth parameters, would be of considerable interest whatever answer emerged. RP GREENWOOD, DD (reprint author), UNIV BRITISH COLUMBIA,SCH AUDIOL & SPEECH SCI,5804 FAIRVIEW CRESENT,VANCOUVER V6T 1W5,BC,CANADA. CR DEATHERAGE BH, 1957, J ACOUST SOC AM, V29, P512, DOI 10.1121/1.1908944 GREENWOO.DD, 1972, J ACOUST SOC AM, V52, P1144, DOI 10.1121/1.1913227 GREENWOOD DD, 1977, PSYCHOPHYSICS PHYSL, P40 GREENWOOD DD, 1991, HEARING RES, V54, P209, DOI 10.1016/0378-5955(91)90118-S GREENWOOD DD, 1988, HEARING RES, V32, P207, DOI 10.1016/0378-5955(88)90093-7 GREENWOO.DD, 1972, J ACOUST SOC AM, V52, P1137, DOI 10.1121/1.1913226 GREENWOOD DD, 1976, J ACOUST SOC AM, V59, P607, DOI 10.1121/1.380906 GREENWOOD DD, 1969, S FREQUENCY ANAL PER, P436 GREENWOO.DD, 1972, J ACOUST SOC AM, V52, P1155, DOI 10.1121/1.1913228 GREENWOO.DD, 1971, J ACOUST SOC AM, V50, P502, DOI 10.1121/1.1912668 HALL JL, 1972, J ACOUST SOC AM, V51, P1863, DOI 10.1121/1.1913045 HALL JL, 1972, J ACOUST SOC AM, V51, P1872, DOI 10.1121/1.1913046 HORST JW, 1985, J ACOUST SOC AM, V78, P1898, DOI 10.1121/1.392779 HORST JW, 1986, J ACOUST SOC AM, V79, P398, DOI 10.1121/1.393528 KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 KRAMMER FG, 1973, J ACOUST SOC AM, V55, P402 KRAMMER FG, 1973, THESIS U BRIT COLUMB, P1 MOORE BCJ, 1990, J ACOUST SOC AM, V88, P132, DOI 10.1121/1.399960 PATTERSON RD, 1976, J ACOUST SOC AM, V70, P1003 SHAILER MJ, 1990, J ACOUST SOC AM, V88, P141, DOI 10.1121/1.399961 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P615, DOI 10.1121/1.1913152 SMOORENB.GF, 1972, J ACOUST SOC AM, V52, P603, DOI 10.1121/1.1913151 SMOORENBURG GF, 1976, J ACOUST SOC AM, V59, P945, DOI 10.1121/1.380954 Wegel RL, 1924, PHYS REV, V23, P266, DOI 10.1103/PhysRev.23.266 ZWICKER E, 1973, ACUSTICA, V29, P336 ZWICKER E, 1981, J ACOUST SOC AM, V70, P1277, DOI 10.1121/1.387141 NR 26 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 1992 VL 59 IS 2 BP 121 EP 128 DI 10.1016/0378-5955(92)90109-Z PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600002 PM 1352282 ER PT J AU OVERBECK, GW CHURCH, MW AF OVERBECK, GW CHURCH, MW TI EFFECTS OF TONE BURST FREQUENCY AND INTENSITY ON THE AUDITORY BRAIN-STEM RESPONSE (ABR) FROM ALBINO AND PIGMENTED RATS SO HEARING RESEARCH LA English DT Article DE ALBINO RATS; AUDITORY BRAIN-STEM RESPONSE; BRAIN-STEM AUDITORY EVOKED POTENTIAL; PIGMENTED RATS; STIMULUS FREQUENCY; STIMULUS INTENSITY; STRAIN DIFFERENCES ID EVOKED-POTENTIALS; STEM ANOMALIES; DIFFERENTIAL SUSCEPTIBILITY; LABORATORY MOUSE; HEARING-LOSS; GUINEA-PIGS; STIMULUS; STRAINS; MICE; CATS AB Young adult male Sprague-Dawley (SD) and Long-Evans (LE) rats were evaluated using the auditory brainstem response (ABR). ABRs were evoked by stimuli with intensities ranging from 15 to 100 dB peSPL. Stimuli were tone bursts of 2000, 4000 and 8000 Hz. As stimulus intensity decreased from 100 to 15 dB, the ABR peak latencies prolonged, interpeak latencies (IPLs) shortened and amplitudes decreased. As stimulus frequency decreased from 8000 to 2000 Hz, ABR latencies prolonged, amplitudes decreased and ABR thresholds increased. The longest IPLs were in response to the 4000 Hz tone bursts. SD rats had ABRs with shorter peak latencies, larger amplitudes and lower thresholds than LE rats. The IPLs usually did not show significant strain-dependent differences. Our observations on stimulus intensity and frequency are consistent with previous reports. Our observations also suggest that the SD (albino) rat has better auditory acuity than the LE (pigmented) rat over the frequency range of 2000 to 8000 Hz. This implies that previous concerns about the use of albino animals in audiological research are somewhat overstated. C1 WAYNE STATE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT AUDIOL,DETROIT,MI 48201. CR ANTICAGLIA J, 1970, PHYSL EFFECTS NOISE, P143 ATTIAS J, 1985, AUDIOLOGY, V24, P149 BERMAN RF, 1992, IN PRESS ALCOHOL CLI BOCK GR, 1984, HEARING RES, V13, P201, DOI 10.1016/0378-5955(84)90109-6 CHEN TJ, 1990, ACTA PHYSIOL SCAND, V138, P529, DOI 10.1111/j.1748-1716.1990.tb08881.x CHURCH MW, 1987, BRAIN RES, V403, P72, DOI 10.1016/0006-8993(87)90124-7 CHURCH MW, 1984, ELECTROEN CLIN NEURO, V59, P328, DOI 10.1016/0168-5597(84)90050-9 CHURCH MW, 1986, AUDIOLOGY, V25, P363 CHURCH M W, 1991, Society for Neuroscience Abstracts, V17, P1597 CHURCH MW, 1991, TERATOLOGY, V43, P561, DOI 10.1002/tera.1420430610 CHURCH MW, 1990, NEUROTOXICOL TERATOL, V14, P345 CHURCH MW, 1988, BRAIN RES, V456, P224, DOI 10.1016/0006-8993(88)90221-1 CHURCH M W, 1988, Society for Neuroscience Abstracts, V14, P800 COATS AC, 1978, ARCH OTOLARYNGOL, V104, P709 CONLEE JW, 1986, HEARING RES, V23, P81, DOI 10.1016/0378-5955(86)90177-2 CONLEE JW, 1989, HEARING RES, V41, P43, DOI 10.1016/0378-5955(89)90177-9 CONLEE JW, 1984, J COMP NEUROL, V225, P141, DOI 10.1002/cne.902250115 CONLEE JW, 1988, ACTA OTO-LARYNGOL, V106, P64, DOI 10.3109/00016488809107372 CONLEE JW, 1986, BRAIN RES, V363, P28, DOI 10.1016/0006-8993(86)90655-4 CREEL D, 1983, BRAIN RES, V260, P1, DOI 10.1016/0006-8993(83)90758-8 CREEL D, 1980, SCIENCE, V209, P1253, DOI 10.1126/science.7403883 CREEL DJ, 1984, NEUROBEH TOXICOL TER, V6, P447 DEBRUYNE F, 1982, ORL J OTO-RHINO-LARY, V44, P36 GARBER SR, 1982, EAR HEARING, V3, P207, DOI 10.1097/00003446-198207000-00004 GORGA MP, 1988, J SPEECH HEAR RES, V31, P87 GOUREVITCH G, 1970, ANIMAL PSYCHOPHYSICS, P67 GRINNELL AD, 1963, J PHYSIOL-LONDON, V167, P38 HARPUR ES, 1976, EXPERIENTIA, V32, P1562, DOI 10.1007/BF01924454 HENRY KR, 1982, ACTA OTO-LARYNGOL, V93, P1, DOI 10.3109/00016488209130846 HENRY KR, 1975, BEHAV GENET, V5, P137, DOI 10.1007/BF01066807 HENRY KR, 1982, J GERONTOL, V37, P275 HENRY KR, 1979, J AM AUDITORY SOC, V4, P173 HENRY KR, 1978, ACTA OTO-LARYNGOL, V86, P366, DOI 10.3109/00016487809107515 KARSAI LK, 1972, ARCHIV OTOLARYNGOL, V96, P499 LINDQUIST N G, 1973, Acta Radiologica Supplementum, V325, P1 POST RH, 1964, EUGEN QUART, V11, P65 PUJOL R, 1977, ACTA OTO-LARYNGOL, V83, P59, DOI 10.3109/00016487709128813 RALLS K, 1967, ANIM BEHAV, V15, P123, DOI 10.1016/S0003-3472(67)80022-8 ROSSI GT, 1984, ELECTROEN CLIN NEURO, V57, P143, DOI 10.1016/0013-4694(84)90173-1 STOCKARD JE, 1979, ARCH NEUROL-CHICAGO, V36, P823 YIN TCT, 1990, J COMP NEUROL, V295, P438, DOI 10.1002/cne.902950308 NR 41 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 1992 VL 59 IS 2 BP 129 EP 137 DI 10.1016/0378-5955(92)90110-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600003 PM 1618705 ER PT J AU VERSNEL, H SCHOONHOVEN, R PRIJS, VF AF VERSNEL, H SCHOONHOVEN, R PRIJS, VF TI SINGLE-FIBER AND WHOLE-NERVE RESPONSES TO CLICKS AS A FUNCTION OF SOUND INTENSITY IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE POSTSTIMULUS TIME HISTOGRAM; INTENSITY; CLICK; COMPOUND ACTION POTENTIAL; CONVOLUTION; GUINEA PIG ID AUDITORY-NERVE; COCHLEAR NERVE; REVERSE-CORRELATION; FREQUENCY-SELECTIVITY; PHASE-LOCKING; ROUND WINDOW; FIBERS; CAT; POTENTIALS; PATTERNS AB This paper describes a study of the intensity dependence of click-evoked responses of auditory-nerve fibres in relation to the simultaneously recorded compound action potential (CAP). Condensation and rarefaction clicks were presented to normal hearing guinea pigs over an intensity range of 60 dB. The recorded poststimulus time histograms (PSTHs) were characterized by the latency (t(p)), amplitude (A(p)) and synchronization (S(p)) of their dominant peak, parameters that are particularly important for the understanding of the CAP. For all fibres t(p) decreased monotonically with increasing intensity, in a continuous way for fibres with high characteristic frequency (CF > 3 kHz), and in discrete steps of one CF-cycle for low-CF (CF less-than-or-equal-to 3 kHz) fibres. An additional analysis of PSTH envelopes revealed that average latency shifts with intensity are similar for all CFs above 2 kHz. For all fibres A(p) increased monotonically with intensity; the increase was stronger and maximum values were larger for low-CF than for high-CF fibres. A schematic model PSTH was then formulated on the basis of the experimental data. A sum of these model PSTHs from a hypothesized fibre population was convolved with an elemental unit response (Versnel et al., 1992) in order to simulate the compound action potential. Synthesized CAPs agreed with experimental CAPs in their main aspects. C1 LEIDEN UNIV HOSP,DEPT EAR NOSE & THROAT,2333 AA LEIDEN,NETHERLANDS. CR ANTOLICANDELA F, 1978, EVOKED ELECTRICAL AC, P165 BAPPERT E, 1980, SCAND AUDIOL S, V11, P45 Bevington P. R., 1969, DATA REDUCTION ERROR BURDA H, 1984, HEARING RES, V14, P315, DOI 10.1016/0378-5955(84)90058-3 COOPER NP, 1989, THESIS U KEELE de Boer E, 1975, J Acoust Soc Am, V58, P1030, DOI 10.1121/1.380762 DEBOER E, 1978, J ACOUST SOC AM, V63, P115, DOI 10.1121/1.381704 DEBOER E, 1979, SCAND AUDIOL S, V11, P17 DESAUVAGE RC, 1983, J ACOUST SOC AM, V73, P616 DOLAN DF, 1983, J ACOUST SOC AM, V73, P580, DOI 10.1121/1.389005 EGGERMONT JJ, 1976, HDB SENSORY PHYSL, V5, P626 EGGERMONT JJ, 1983, Q REV BIOPHYS, V16, P341 Elberling C, 1976, ELECTROCOCHLEOGRAPHY, P151 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 EVANS EF, 1979, AUDITORY INVESTIGATI, P324 Goldstein JL, 1971, PHYSL AUDITORY SYSTE, P133 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 GRASHUIS JL, 1974, THESIS U NIJMEGEN HARRISON RV, 1982, HEARING RES, V6, P303, DOI 10.1016/0378-5955(82)90062-4 HARRISON RV, 1981, J ACOUST SOC AM, V70, P1036, DOI 10.1121/1.386954 Kiang NYS, 1976, ELECTROCOCHLEOGRAPHY, P95 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KIM DO, 1979, J NEUROPHYSIOL, V42, P16 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LUTKENHONER B, 1980, SCAND AUDIOL S, V11, P25 MOLLER AR, 1983, HEARING RES, V11, P267, DOI 10.1016/0378-5955(83)90062-X MOLLER AR, 1985, HEARING RES, V17, P177, DOI 10.1016/0378-5955(85)90020-6 MOLLER AR, 1977, J ACOUST SOC AM, V62, P135 MOLLER AR, 1986, AUDIOLOGY, V25, P29 Moller AR, 1985, AUDITORY BRAINSTEM R, P13 OZDAMAR O, 1978, BRAIN RES, V155, P169, DOI 10.1016/0006-8993(78)90320-7 PEAKE WT, 1962, BIOPHYS J, V2, P23 PFEIFFER RR, 1972, J ACOUST SOC AM, V52, P1669, DOI 10.1121/1.1913301 PRIJS VF, 1980, ACUSTICA, V44, P283 PRIJS VF, 1990, MECHANICS BIOPHYSICS, P154 PRIJS VF, 1986, HEARING RES, V21, P127, DOI 10.1016/0378-5955(86)90034-1 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBLES L, 1976, J ACOUST SOC AM, V59, P926, DOI 10.1121/1.380953 ROSE JE, 1971, J NEUROPHYSIOL, V34, P685 RUGGERO MA, 1991, IN PRESS AUDITORY PH SACHS MB, 1989, HEARING RES, V41, P61, DOI 10.1016/0378-5955(89)90179-2 SALVI RJ, 1979, HEARING RES, V1, P237, DOI 10.1016/0378-5955(79)90017-0 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 VERSNEL H, 1992, HEARING RES, V59, P157, DOI 10.1016/0378-5955(92)90112-Z VERSNEL H, 1990, HEARING RES, V46, P147, DOI 10.1016/0378-5955(90)90145-F Wang B, 1979, THESIS MIT CAMBRIDGE WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E NR 49 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 MAY PY 1992 VL 59 IS 2 BP 138 EP 156 DI 10.1016/0378-5955(92)90111-Y PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600004 PM 1618706 ER PT J AU VERSNEL, H PRIJS, VF SCHOONHOVEN, R AF VERSNEL, H PRIJS, VF SCHOONHOVEN, R TI ROUND-WINDOW RECORDED POTENTIAL OF SINGLE-FIBER DISCHARGE (UNIT RESPONSE) IN NORMAL AND NOISE-DAMAGED COCHLEAS SO HEARING RESEARCH LA English DT Article DE UNIT RESPONSE; NOISE TRAUMA; SINGLE FIBER; GUINEA PIG ID GUINEA-PIG COCHLEA; AUDITORY-NERVE; STEREOCILIA; FIBERS; MODEL AB Unit responses (URs) of eighth-nerve fibres have been determined at the round window by spike-triggered averaging in both normal and pathological guinea pig cochleas. The pathology was mainly noise-induced damage. The URs have been analysed with respect to their dependence on the fibre's threshold, characteristic frequency (CF) and spontaneous rate (SR). The results from normal cochleas confirmed earlier data (Prijs, 1986): the UR has a diphasic waveform and the amplitude of its negative first peak is about 0.1-mu-V. From the six parameters (amplitude, latency, and width of the two peaks) by which the UR was described only the amplitude of the positive peak showed a significant variation with CF: a small decrease with increasing CF (CF-range 0.1 to 20 kHz). This finding may possibly be caused by oscillations in the spike-triggered average for low CFs. URs for most low- and medium-SR fibres were found to be large (greater than 0.3-mu-V). However. this result is interpreted as an artefact caused by synchrony of fibre spontaneous activity. In damaged cochleas only slight changes of the UR were found: the waveform duration became significantly shorter and on some occasions the positive peak increased in amplitude, but latency and amplitude of the negative component of the UR remained unchanged. C1 LEIDEN UNIV HOSP,DEPT EAR NOSE & THROAT,2333 AA LEIDEN,NETHERLANDS. CR Bevington P. R., 1969, DATA REDUCTION ERROR BIONDI E, 1975, INT J BIOMED COMPUT, V6, P157, DOI 10.1016/0020-7101(75)90001-X BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 CANLON B, 1987, HEARING RES, V30, P65, DOI 10.1016/0378-5955(87)90184-5 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X de Boer E, 1975, J Acoust Soc Am, V58, P1030, DOI 10.1121/1.380762 DESAUVAGE RC, 1983, J ACOUST SOC AM, V73, P616 DESAUVAGE RC, 1987, HEARING RES, V29, P105, DOI 10.1016/0378-5955(87)90159-6 DOLAN DF, 1983, J ACOUST SOC AM, V73, P580, DOI 10.1121/1.389005 EVANS EF, 1987, BRIT J AUDIOL, V21, P103 EVANS EF, 1979, AUDITORY INVESTIGATI, P324 GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P1075 GYDIKOV AA, 1986, BIOL CYBERN, V53, P363, DOI 10.1007/BF00318202 HERINGA A, 1989, J APPL PHYS, V66, P2724, DOI 10.1063/1.344213 HOKE M, 1979, SCAND AUDIOL S, V9, P141 Kiang NYS, 1976, ELECTROCOCHLEOGRAPHY, P95 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, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 Lorente de No R., 1947, STUD ROCKEFELLER I M, V132, P384 PRIJS VF, 1980, ACUSTICA, V44, P283 PRIJS VF, 1981, HEARING RES, V4, P23, DOI 10.1016/0378-5955(81)90034-4 PRIJS VF, 1986, HEARING RES, V21, P127, DOI 10.1016/0378-5955(86)90034-1 ROBERTSON D, 1983, HEARING RES, V9, P263, DOI 10.1016/0378-5955(83)90031-X SCHOONHOVEN R, 1989, IL VALSALVA S1, V54, P48 SCHOONHOVEN R, 1986, IEEE T BIO-MED ENG, V33, P327, DOI 10.1109/TBME.1986.325718 SCHOONHOVEN R, 1991, CRIT REV BIOMED ENG, V19, P47 SIEGEL JH, 1986, HEARING RES, V22, P245, DOI 10.1016/0378-5955(86)90101-2 Suzuka Y, 1988, Acta Otolaryngol Suppl, V450, P1 VERSNEL H, 1992, HEARING RES, V59, P138, DOI 10.1016/0378-5955(92)90111-Y VERSNEL H, 1990, HEARING RES, V46, P147, DOI 10.1016/0378-5955(90)90145-F Wang B, 1979, THESIS MIT CAMBRIDGE NR 32 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 1992 VL 59 IS 2 BP 157 EP 170 DI 10.1016/0378-5955(92)90112-Z PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600005 PM 1618707 ER PT J AU KEITHLEY, EM RYAN, AF FELDMAN, ML AF KEITHLEY, EM RYAN, AF FELDMAN, ML TI COCHLEAR DEGENERATION IN AGED RATS OF 4 STRAINS SO HEARING RESEARCH LA English DT Article DE AGING; PRESBYACUSIS; COCHLEA; MELANIN; ALBINO ID PIGMENTED GUINEA-PIGS; GRADED SERIES; CELL COUNTS; ALBINO; MELANIN; SUSCEPTIBILITY; NUCLEUS AB Animals with various degrees of inbreeding, some of which are albino, are frequently used in biological research. Albinos do not produce melanin and it is therefore absent from the cochlea. While the function of melanin is unknown, it has been hypothesized that it is involved in cochlear homeostasis. It is possible then, that age-related degeneration may be affected by the presence or absence of melanin. We therefore evaluated young (2-6 months old) and aged (24-36 months old) cochleas in 4 different rat strains: albino Fischer 344 and Lewis rats and pigmented Lewis-Brown Norway F1 rats and Brown Norway rats. Cochlear morphology was the same across all strains of young adult animals with the exception that the pigmented animals had small, darkly stained granules in the stria vascularis. The aged pigmented animals all had large granules as well as small ones. Degeneration of spiral ganglion cells in the apical region of the ganglion had occurred in the old animals of all strains. Strial degeneration at the apex was also present in aged animals. There was no correlation between the presence or absence of melanin and the magnitude of cochlear degenerative changes in the aged animals. The presence or absence of melanin therefore, appears to have no effect on cochlear degeneration in the aged rat cochlea. C1 UNIV CALIF SAN DIEGO,VET ADM MED CTR,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,LA JOLLA,CA 92093. BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,BOSTON,MA 02118. CR BARRENAS ML, 1990, SCAND AUDIOL, V19, P97, DOI 10.3109/01050399009070759 COHEN J, 1977, STATISTICAL POWER AN CONLEE JW, 1986, HEARING RES, V23, P81, DOI 10.1016/0378-5955(86)90177-2 CONLEE JW, 1989, ACTA OTO-LARYNGOL, V107, P48, DOI 10.3109/00016488909127478 CONLEE JW, 1988, ACTA OTO-LARYNGOL, V106, P64, DOI 10.3109/00016488809107372 CONLEE JW, 1986, BRAIN RES, V363, P28, DOI 10.1016/0006-8993(86)90655-4 CREEL D, 1983, BRAIN RES, V260, P1, DOI 10.1016/0006-8993(83)90758-8 Dräger U C, 1987, Neurosci Res Suppl, V6, pS75, DOI 10.1016/0921-8696(87)90009-0 DUM N, 1983, Z SAUGETIERKD, V48, P95 EAGLES EL, 1961, T AM ACAD OPTHALMOL, V65, P260 GARBER SR, 1982, EAR HEARING, V3, P207, DOI 10.1097/00003446-198207000-00004 GENSLER HL, 1987, REV BIOL RES AGING, V3, P451 GODFREY DA, 1987, HEARING RES, V31, P203, DOI 10.1016/0378-5955(87)90188-2 HOEFFDING V, 1988, J ACOUST SOC AM, V84, P2067, DOI 10.1121/1.397051 HOOD JD, 1976, J ACOUST SOC AM, V59, P706, DOI 10.1121/1.380923 JACOBSON SG, 1984, DOC OPHTHALMOL, V56, P337, DOI 10.1007/BF00155678 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 Kiang N.Y.S., 1984, P143 KINNEAR PE, 1985, SURV OPHTHALMOL, V30, P75, DOI 10.1016/0039-6257(85)90077-3 KORNER A, 1982, SCIENCE, V217, P1163, DOI 10.1126/science.6810464 MOORE DR, 1988, HEARING RES, V35, P275, DOI 10.1016/0378-5955(88)90125-6 PYE A, 1987, ARCH OTO-RHINO-LARYN, V243, P411, DOI 10.1007/BF00464654 ROYSTER LH, 1980, J ACOUST SOC AM, V68, P551, DOI 10.1121/1.384769 Schuknecht H., 1974, PATHOLOGY EAR, P388 Sealy R. C., 1980, FREE RADICAL BIO MED, V4, P209 SEIJI M, 1965, J BIOCHEM-TOKYO, V57, P457 WASTERSTROM SA, 1986, AM J OTOL, V7, P11 WILLOTT JF, 1991, AGE RELATED COCHLEA, P16 YANZ JL, 1985, AUDIOLOGY, V24, P260 NR 31 TC 77 Z9 77 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 1992 VL 59 IS 2 BP 171 EP 178 DI 10.1016/0378-5955(92)90113-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600006 PM 1618708 ER PT J AU HOORMANN, J FALKENSTEIN, M HOHNSBEIN, J BLANKE, L AF HOORMANN, J FALKENSTEIN, M HOHNSBEIN, J BLANKE, L TI THE HUMAN FREQUENCY-FOLLOWING RESPONSE (FFR) - NORMAL VARIABILITY AND RELATION TO THE CLICK-EVOKED BRAIN-STEM RESPONSE SO HEARING RESEARCH LA English DT Article DE FREQUENCY-FOLLOWING RESPONSE; NORMATIVE VALUES; FREQUENCY FUNCTION; FREQUENCY CONTENTS; BRAIN-STEM EVOKED RESPONSE ID STEM RESPONSES; AUDITORY-NERVE; POTENTIALS; COMPLEX; TONES; CAT AB The frequency-following response (FFR) was recorded from twenty human subjects (11 female and 9 male) over a frequency range of 128-832 Hz in order to study the normal variability of this evoked potential and its dependence on age and sex. Moreover the relation of the FFR to the click-evoked brain stem response (BER) was analyzed in order to contribute to the FFR source discussion. The FFR had a maximum amplitude of about 400 nV and a latency of about 6.4 ms for stimulus frequencies around 350 Hz; the inter-individual variance of the best frequency and of the shape of the frequency function was considerable. Large second harmonics were seen in the FFR to stimuli below about 200 Hz. The FFR amplitude tended to be larger in younger subjects, whereas no such effect was found for the BER. No significant sex effect was found for the FFR amplitude, whereas the BER waves IV and VI were larger for females than for males. There were no correlations between FFR and BER latencies. Significant correlations were found between the amplitudes of the FFR and of BER components II, III and IV, but not of waves V and VI. The results support the notion that the FFR and the BER reflect different mechanisms. Moreover the results do not favor the common hypothesis that the inferior colliculus is the major source of the scalp-recorded human FFR, but rather point to lower brainstem levels. C1 INST ARBEITSPHYSIOL,SINNES & NEUROPHYSIOL ABT,ARDEYSTR 67,W-4600 DORTMUND,GERMANY. CR BATRA R, 1986, HEARING RES, V21, P167, DOI 10.1016/0378-5955(86)90037-7 CHIMENTO TC, 1990, ELECTROEN CLIN NEURO, V75, P88, DOI 10.1016/0013-4694(90)90156-E DAVIS H, 1976, AUDIOLOGY, V15, P181 DAVIS RL, 1984, HEARING RES, V15, P29, DOI 10.1016/0378-5955(84)90222-3 DEMBON H, 1989, ELECTROEN CLIN NEURO, V74, P46, DOI 10.1016/0168-5597(89)90050-6 DEMBON H, 1984, BIOMED TECHNIK, V29, P223, DOI 10.1515/bmte.1984.29.s1.223 DIXON WJ, 1990, BMDP STATISTICAL SOF EGGERMONT JJ, 1976, J ACOUST SOC AM, V50, P1132 ELDREDGE DH, 1974, HDB SENSORY PHYSL, V5, P549 ERNE NS, 1990, ADV NEUROL, V54, P167 EULER M, 1981, ELECTROEN CLIN NEURO, V52, P400, DOI 10.1016/0013-4694(81)90022-5 GALBRAITH GC, 1990, ELECTROEN CLIN NEURO, V77, P295, DOI 10.1016/0168-5597(90)90068-O GARDI J, 1979, AUDIOLOGY, V18, P353 GARDI J, 1979, J ACOUST SOC AM, V65, P1491, DOI 10.1121/1.382913 GLASER EM, 1976, ELECTROEN CLIN NEURO, V40, P25, DOI 10.1016/0013-4694(76)90176-0 GREENBERG S, 1987, HEARING RES, V25, P91, DOI 10.1016/0378-5955(87)90083-9 Huis in't Veld F., 1977, SCAND AUDIOL, V6, P27 KIANG NYS, 1990, HEARING RES, V49, P1 LAVINE RA, 1971, J NEUROPHYSIOL, V34, P467 MARSH JT, 1975, ELECTROEN CLIN NEURO, V38, P113, DOI 10.1016/0013-4694(75)90220-5 MAURER K, 1982, AKUSTISCH EVOZIERTE MICHALEWSKI HJ, 1980, ELECTROEN CLIN NEURO, V48, P351, DOI 10.1016/0013-4694(80)90271-0 MOLLER AR, 1981, ELECTROEN CLIN NEURO, V52, P18, DOI 10.1016/0013-4694(81)90184-X MOLLER AR, 1982, ELECTROEN CLIN NEURO, V53, P612, DOI 10.1016/0013-4694(82)90137-7 MOUSHEGI.G, 1973, ELECTROEN CLIN NEURO, V35, P665, DOI 10.1016/0013-4694(73)90223-X PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 ROSE JE, 1967, J NEUROPHYSIOL, V30, P768 ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 SCHERG M, 1985, ELECTROEN CLIN NEURO, V62, P290, DOI 10.1016/0168-5597(85)90006-1 SCHERG M, 1979, SCAND AUDIOL S, V9, P197 SMITH JC, 1975, ELECTROEN CLIN NEURO, V39, P465, DOI 10.1016/0013-4694(75)90047-4 SNYDER RL, 1984, HEARING RES, V15, P261, DOI 10.1016/0378-5955(84)90033-9 SOHMER H, 1977, ELECTROEN CLIN NEURO, V42, P656, DOI 10.1016/0013-4694(77)90282-6 STILLMAN RD, 1976, AUDIOLOGY, V15, P10 YAMADA O, 1977, ELECTROEN CLIN NEURO, V43, P362, DOI 10.1016/0013-4694(77)90259-0 ZWISLOCK.JJ, 1969, J ACOUST SOC AM, V46, P431, DOI 10.1121/1.1911708 1970, ANSI S361969 AM NAT NR 37 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 MAY PY 1992 VL 59 IS 2 BP 179 EP 188 DI 10.1016/0378-5955(92)90114-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600007 PM 1618709 ER PT J AU RYBAK, LP WHITWORTH, C SCOTT, V AF RYBAK, LP WHITWORTH, C SCOTT, V TI DEVELOPMENT OF ENDOCOCHLEAR POTENTIAL AND COMPOUND ACTION-POTENTIAL IN THE RAT SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; COMPOUND ACTION POTENTIAL; COCHLEAR DEVELOPMENT; RAT; STRIA VASCULARIS ID STRIA VASCULARIS; INNER-EAR; FREQUENCY-SELECTIVITY; POSTNATAL-DEVELOPMENT; HAIR-CELLS; MIDDLE-EAR; COCHLEA; MOUSE; HEARING; ONSET AB The present study was designed to investigate the developmental changes of the endocochlear potential and compound action potential simultaneously from rat pups of various ages. Animals were anesthetized with ketamine/xylazine, and the endocochlear potential was measured with a glass microelectrode. At the same time, a wire electrode was placed on the round window to record the click-evoked compound action potential. The endocochlear potential was found to be very low during the first few days of postnatal life. A rapid increase in the value of the endocochlear potential was noted between eleven and thirteen days of age, and adult-like values were recorded by seventeen days of age. Compound action potential responses were recorded at thirteen days of age to high intensity clicks, followed by a progressive improvement of thresholds and reduction of latencies. The development of the endocochlear potential and compound action potential was found to be reciprocally related - as the magnitude of the endocochlear potential increased, the compound action potential threshold declined with increasing age. The development of the endocochlear potential was found to closely approximate the development of enzymatic activity of sodium, potassium-ATPase in the stria vascularis reported by Kuijpers (1974). RP RYBAK, LP (reprint author), SO ILLINOIS UNIV,SCH MED,DEPT SURG,POB 19230,SPRINGFIELD,IL 62794, USA. CR ANGAARD L, 1965, ACTA OTO-LARYNGOL, V203, P1 ANNIKO M, 1981, HEARING RES, V4, P11, DOI 10.1016/0378-5955(81)90033-2 ANNIKO M, 1988, PROG NEUROBIOL, V30, P209, DOI 10.1016/0301-0082(88)90007-X ANNIKO M, 1981, ANN OTO RHINOL LARYN, V90, P25 AXELSSON A, 1986, ACTA OTO-LARYNGOL, V101, P75, DOI 10.3109/00016488609108610 BOSHER SK, 1972, ACTA OTO-LARYNGOL, V73, P203, DOI 10.3109/00016487209138931 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 CARLIER E, 1978, BRAIN RES, V147, P174, DOI 10.1016/0006-8993(78)90784-9 CARLIER E, 1979, HEARING RES, V1, P197, DOI 10.1016/0378-5955(79)90013-3 CARLISLE L, 1990, CELL TISSUE RES, V262, P329, DOI 10.1007/BF00309888 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 DAVIS H, 1965, COLD SPRING HARB SYM, V30, P181 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 Kikuchi K, 1965, Acta Otolaryngol, V60, P207, DOI 10.3109/00016486509127003 KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 LENG G, 1980, HEARING RES, V3, P17, DOI 10.1016/0378-5955(80)90005-2 LENOIR M, 1987, ANAT EMBRYOL, V175, P477, DOI 10.1007/BF00309683 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 MELICHAR I, 1987, HEARING RES, V25, P25 MOORE DR, 1981, BRAIN RES, V219, P29, DOI 10.1016/0006-8993(81)90265-1 MORIZONO T, 1980, ARCH OTO-RHINO-LARYN, V229, P149, DOI 10.1007/BF00454238 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PUJOL R, 1973, ACTA OTO-LARYNGOL, V76, P1, DOI 10.3109/00016487309121476 PUJOL R, 1978, J COMP NEUROL, V177, P529, DOI 10.1002/cne.901770311 Romand R., 1983, DEV AUDITORY VESTIBU, P47 ROMAND R, 1976, J COMP NEUROL, V170, P1, DOI 10.1002/cne.901700102 ROMAND R, 1985, HEARING RES, V18, P111, DOI 10.1016/0378-5955(85)90002-4 RUSSELL IJ, 1983, NATURE, V301, P334, DOI 10.1038/301334a0 RYBAK LP, 1988, AUDITORY PATHWAY, P41 RYBAK LP, 1991, ASS RES OT ABSTR, V14, P107 RYBAK L P, 1990, Society for Neuroscience Abstracts, V16, P871 SCHMIDT RS, 1963, J EXP ZOOL, V153, P227, DOI 10.1002/jez.1401530305 SCHROTT A, 1990, HEARING RES, V46, P1, DOI 10.1016/0378-5955(90)90134-B Shnerson A., 1982, DEV BRAIN RES, V2, P77 STEEL KP, 1987, HEARING RES, V27, P11, DOI 10.1016/0378-5955(87)90022-0 STEEL KP, 1989, DEVELOPMENT, V107, P453 THOMAS JP, 1990, OTOLARYNG HEAD NECK, V103, P427 UZIEL A, 1981, AUDIOLOGY, V20, P89 Wada T., 1923, American Anatomical Memoir, Vno. 10, P1 WALSH EJ, 1990, AM J OTOLARYNG, V11, P23, DOI 10.1016/0196-0709(90)90166-S WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 WOOLF NK, 1986, AM J PHYSIOL, V250, pR493 WOOLF NK, 1988, HEARING RES, V35, P131, DOI 10.1016/0378-5955(88)90112-8 YOSHIE N, 1968, LARYNGOSCOPE, V78, P198, DOI 10.1288/00005537-196802000-00002 NR 45 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 MAY PY 1992 VL 59 IS 2 BP 189 EP 194 DI 10.1016/0378-5955(92)90115-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600008 PM 1319988 ER PT J AU DECHESNE, CJ KIM, HN NOWAK, TS WENTHOLD, RJ AF DECHESNE, CJ KIM, HN NOWAK, TS WENTHOLD, RJ TI EXPRESSION OF HEAT-SHOCK PROTEIN, HSP72, IN THE GUINEA-PIG AND RAT COCHLEA AFTER HYPERTHERMIA - IMMUNOCHEMICAL AND INSITU HYBRIDIZATION ANALYSIS SO HEARING RESEARCH LA English DT Article DE HSP72; HYPERTHERMIA; COCHLEA; IMMUNOBLOTTING; IMMUNOCYTOCHEMISTRY; INSITU HYBRIDIZATION; GUINEA PIG; RAT ID MESSENGER-RNA; INNER-EAR; BRAIN; ISCHEMIA; INDUCTION; LOCALIZATION; TRAUMA; GENE; TISSUES; DAMAGE AB The induction of the heat shock protein, HSP72, was studied in the cochlea of guinea pigs and rats subjected to a hyperthermic stress. Analyses were done by immunoblotting and immunocytochemistry at 6 and 12 h after heat shock, using a commercially available monoclonal antibody (Amersham), and by in situ hybridization 1 h after heat shock using an oligonucleotide probe. In guinea pig immunoblots of the cochlea, HSP72 was present in both unstressed and heat stressed animals and immunocytochemistry did not reveal any difference of staining between them. As opposed to guinea pig, HSP72 was not found in unstressed rat cochlea. Heat shock induced HSP72 expression in most inner ear tissues of the rat examined by immunoblotting. Immunocytochemistry and in situ hybridization localized HSP72 synthesis in ganglion neurons, Schwann cells, spiral limbus, spiral ligament and stria vascularis. The strongest immunoreactivity and highest density of silver grains were seen in the stria vascularis. All blood vessels were strongly immunoreactive and were outlined with silver grains. These results show that HSP72 synthesis can be induced by hyperthermia in rat cochlea and suggest that this protein could be a useful marker for assessment of the effects of specific stresses in this organ. C1 NIDCD,NEUROCHEM LAB,BETHESDA,MD. NINCDS,STROKE BRANCH,BETHESDA,MD 20892. RP DECHESNE, CJ (reprint author), UNIV MONTPELLIER 2,INSERM,U254,NEUROPHYSIOL SENSORIELLE LAB,CP 089,PL BATAILLON,F-34095 MONTPELLIER 05,FRANCE. CR ANNIKO M, 1984, ULTRASTRUCTURAL ATLA, P184 BARBE MF, 1988, SCIENCE, V241, P1817, DOI 10.1126/science.3175623 BROWN IR, 1989, NEURON, V2, P1559, DOI 10.1016/0896-6273(89)90044-5 BROWN IR, 1990, J NEUROSCI RES, V25, P14, DOI 10.1002/jnr.490250103 CAIRO G, 1985, HEPATOLOGY, V5, P357, DOI 10.1002/hep.1840050303 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CURRIE RW, 1981, SCIENCE, V214, P72, DOI 10.1126/science.7280681 CURRIE RW, 1987, J MOL CELL CARDIOL, V19, P795 DECHESNE CJ, 1991, BRAIN RES, V545, P223, DOI 10.1016/0006-8993(91)91290-H DWYER BE, 1989, EXP NEUROL, V104, P28, DOI 10.1016/0014-4886(89)90005-8 GRAUR D, 1991, NATURE, V351, P649, DOI 10.1038/351649a0 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LIBERMAN MC, 1990, TOXICOL PATHOL, V18, P138 LINDQUIST S, 1988, ANNU REV GENET, V22, P631, DOI 10.1146/annurev.ge.22.120188.003215 LOWRY OH, 1951, J BIOL CHEM, V193, P265 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MARINI AM, 1990, J NEUROCHEM, V54, P1509, DOI 10.1111/j.1471-4159.1990.tb01198.x MASING TE, 1989, NEUROCHEM RES, V14, P725, DOI 10.1007/BF00964949 MYERS MW, 1991, 14TH MIDW RES M ARO, P61 NEELY JG, 1991, HEARING RES, V52, P403, DOI 10.1016/0378-5955(91)90028-8 NISHIMURA RN, 1991, MOL BRAIN RES, V9, P39, DOI 10.1016/0169-328X(91)90128-K NOWAK TS, 1990, J NEUROCHEM, V54, P451, DOI 10.1111/j.1471-4159.1990.tb01893.x NOWAK TS, 1991, J CEREBR BLOOD F MET, V11, P432 PELHAM H, 1988, NATURE, V332, P776, DOI 10.1038/332776a0 PUJOL R, 1991, ACTA OTOLARYNGOL S S, V476, P32 RIABOWOL KT, 1988, SCIENCE, V242, P433, DOI 10.1126/science.3175665 RYBAK LP, 1986, NEUROBIOLOGY HEARING, P441 SCHLESINGER MJ, 1990, J BIOL CHEM, V265, P12111 SLEPECKY N, 1986, HEARING RES, V22, P307, DOI 10.1016/0378-5955(86)90107-3 SPRANG GK, 1987, MOL BRAIN RES, V3, P89, DOI 10.1016/0169-328X(87)90049-0 TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350 UNEY JB, 1988, FEBS LETT, V235, P215, DOI 10.1016/0014-5793(88)81265-1 VASS K, 1988, ACTA NEUROPATHOL, V77, P128 WADA K, 1989, NATURE, V342, P684, DOI 10.1038/342684a0 WATOWICH SS, 1988, MOL CELL BIOL, V8, P393 WELCH WJ, 1989, STRESS INDUCED PROTE, P187 WENTHOLD RJ, 1991, NOISE INDUCED HEARIN, P28 NR 37 TC 33 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 1992 VL 59 IS 2 BP 195 EP 204 DI 10.1016/0378-5955(92)90116-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600009 PM 1618710 ER PT J AU SINNOTT, JM BROWN, CH BROWN, FE AF SINNOTT, JM BROWN, CH BROWN, FE TI FREQUENCY AND INTENSITY DISCRIMINATION IN MONGOLIAN GERBILS, AFRICAN MONKEYS AND HUMANS SO HEARING RESEARCH LA English DT Article DE COMPARATIVE; FREQUENCY DLS; INTENSITY DLS; GERBIL; MONKEY; HUMAN ID OLD-WORLD MONKEYS; AUDITORY-NERVE FIBERS; CERCOPITHECUS-MITIS; HEARING; COMMUNICATION; DEGENERATION; SENSITIVITY; RESPONSES; PRIMATES; VOWELS AB Frequency (DELTA-F) and intensity (DELTA-I) difference limens were directly compared in Mongolian gerbils (Meriones unguiculatus), Old World African Monkeys (Cercopithecus mitis, Cercocebus albigena), and humans. Methods employed a repeating, background AX discrimination procedure, and positive (food) reinforcement for animals. For DELTA-I, there were small quantitative differences between the species. At 1 kHz, 70 dB SPL, DLs averaged 2.82 dB for gerbils, 2.29 dB for monkeys, and 0.75 dB for humans. For DELTA-F, there were larger differences between the species. At 1 kHz, 60 dB SPL, frequency DLs were highest for gerbils, averaging 108 Hz. DLs were lower for monkeys, averaging 32.6 Hz, similar to recently reported DLs for other Old World monkeys (Prosen et al., 1990). Human DLs, averaging 2.27 Hz, were markedly lower than those of either monkeys or gerbils. These results suggest that animals provide better models of human DELTA-I than DELTA-F. RP SINNOTT, JM (reprint author), UNIV SO ALABAMA,DEPT PSYCHOL,COMPARAT HEARING LAB,MOBILE,AL 36688, USA. CR BROWN C H, 1990, International Journal of Comparative Psychology, V4, P79 BROWN CH, 1984, EXP AGING RES, V10, P35 BROWN CH, 1986, J ACOUST SOC AM, V79, P1058, DOI 10.1121/1.393378 BROWN CH, 1984, ANIM BEHAV, V32, P66, DOI 10.1016/S0003-3472(84)80325-5 BURKARD R, 1989, J ACOUST SOC AM, V85, P2514, DOI 10.1121/1.397746 BUUS S, 1991, J ACOUST SOC AM, V90, P1371, DOI 10.1121/1.401928 CZIBULKA A, 1991, HEARING RES, V52, P43, DOI 10.1016/0378-5955(91)90186-D ELLIOTT DN, 1960, J ACOUST SOC AM, V32, P380, DOI 10.1121/1.1908071 ERELL A, 1988, J ACOUST SOC AM, V84, P204, DOI 10.1121/1.396966 Fay R. R., 1988, HEARING VERTEBRATES FAY RR, 1991, EVOLUTIONARY BIOL HE, P229 GOUREVITCH G, 1970, ANIMAL PSYCHOPHYSICS, P67 GREENWOOD D, 1990, J ACOUST SOC AM, V87, P1364 HARRIS DM, 1990, HEARING RES, V50, P1, DOI 10.1016/0378-5955(90)90029-O HEFFNER RS, 1988, BEHAV NEUROSCI, V102, P422, DOI 10.1037/0735-7044.102.3.422 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HIENZ R, 1987, COMP DIFFERENT METHO, P84 HIENZ RD, 1988, J ACOUST SOC AM, V84, P186, DOI 10.1121/1.396963 HIENZ RD, 1981, J ACOUST SOC AM, V70, P699, DOI 10.1121/1.386933 KOJIMA S, 1990, FOLIA PRIMATOL, V55, P62, DOI 10.1159/000156501 MCGINN MD, 1987, HEARING RES, V31, P235, DOI 10.1016/0378-5955(87)90193-6 MCGINN MD, 1990, HEARING RES, V48, P265, DOI 10.1016/0378-5955(90)90066-X PROSEN CA, 1990, J ACOUST SOC AM, V88, P2152, DOI 10.1121/1.400112 RONKEN DA, 1986, J ACOUST SOC AM, V79, P417, DOI 10.1121/1.393529 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L SAUNDERS SS, 1987, J ACOUST SOC AM, V82, P1604, DOI 10.1121/1.395150 SCHMIEDT RA, 1982, J ACOUST SOC AM, V72, P142, DOI 10.1121/1.387998 SINNOTT JM, 1989, J ACOUST SOC AM, V86, P557, DOI 10.1121/1.398235 SINNOTT JM, 1987, J COMP PSYCHOL, V101, P126, DOI 10.1037/0735-7036.101.2.126 SINNOTT JM, 1976, J ACOUST SOC AM, V60, P687, DOI 10.1121/1.381140 SINNOTT JM, 1991, J ACOUST SOC AM, V89, P2421, DOI 10.1121/1.400974 SINNOTT JM, 1985, J ACOUST SOC AM, V78, P1977, DOI 10.1121/1.392654 SMITH RL, 1985, J ACOUST SOC AM, V78, P1310, DOI 10.1121/1.392900 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 STATLER KD, 1990, HEARING RES, V50, P275, DOI 10.1016/0378-5955(90)90051-P STEBBINS WC, 1973, AM J PHYS ANTHROPOL, V38, P357, DOI 10.1002/ajpa.1330380233 WESTERMAN LA, 1987, J ACOUST SOC AM, V81, P680, DOI 10.1121/1.394836 WOOLF NK, 1984, HEARING RES, V13, P277, DOI 10.1016/0378-5955(84)90081-9 NR 39 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 MAY PY 1992 VL 59 IS 2 BP 205 EP 212 DI 10.1016/0378-5955(92)90117-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600010 PM 1618711 ER PT J AU KALTENBACH, JA CZAJA, JM KAPLAN, CR AF KALTENBACH, JA CZAJA, JM KAPLAN, CR TI CHANGES IN THE TONOTOPIC MAP OF THE DORSAL COCHLEAR NUCLEUS FOLLOWING INDUCTION OF COCHLEAR LESIONS BY EXPOSURE TO INTENSE SOUND SO HEARING RESEARCH LA English DT Article DE TONOTOPIC MAPS; PLASTICITY; REORGANIZATION; COCHLEAR NUCLEUS ID ACOUSTIC INJURY; DEGENERATION; PATHOLOGY; NERVE AB Hamsters were exposed to intense tones (10 kHz) al levels and durations sufficient to cause stereocilia lesions. The purpose was to determine how the tonotopic map of the dorsal cochlear nucleus (DCN) readjusts to loss of receptor sensitivity. Neural Population thresholds and tonotopic organization was mapped over the surface of the DCN in normal unexposed animals and those showing tone-induced lesions. The results indicate that cochlear lesions characterized mainly by loss of stereocilia in a restricted portion of the organ of Corti cause changes in a corresponding region of the tonotopic map which reflect primarily changes in the shape and thresholds of neural tuning curves. In many cases the center of the lesion was represented in the DCN as a distinct characteristic frequency (CF) gap in the tonotopic map in which responses were either extremely weak or absent. In almost all cases the map area representing the center of the lesion was bordered by an expanded region of near-constant CF, a feature superficially suggestive of map reorganization. These expanded map areas had abnormal tip thresholds and showed other features suggesting that their CFs had been shifted downward by distortion and deterioration of their original tips. Such changes in neural tuning are similar to those observed by others in the auditory nerve following acoustic trauma, and thus would seem to have a peripheral origin. Thus, it is not necessary to invoke plastic changes in the cochlear nucleus to explain the changes observed in the tonotopic map. C1 LOYOLA UNIV,SCH MED,DEPT OTOLARYNGOL,CHICAGO,IL 60611. RP KALTENBACH, JA (reprint author), WAYNE STATE UNIV,SCH MED,DEPT AUDIOL,5E-UHC,4201 ST ANTOINE,DETROIT,MI 48201, USA. CR HALL JG, 1976, ACTA OTO-LARYNGOL, V81, P344, DOI 10.3109/00016487609119972 HALL JG, 1974, SCAND AUDIOL, V4, P31 HARRISON RV, 1991, HEARING RES, V54, P11, DOI 10.1016/0378-5955(91)90131-R ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 KALTENBACH JA, 1991, HEARING RES, V51, P149, DOI 10.1016/0378-5955(91)90013-Y KANE EC, 1974, ANAT REC, V179, P67, DOI 10.1002/ar.1091790106 LAMOTTE CC, 1989, J COMP NEUROL, V288, P311, DOI 10.1002/cne.902880209 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 LIBERMAN MC, 1984, HEARING RES, V16, P33, DOI 10.1016/0378-5955(84)90023-6 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X Malick L. E., 1975, Scanning Electron Microscopy 1975 MCMAHON SB, 1991, J COMP NEUROL, V304, P307, DOI 10.1002/cne.903040211 MOREST DK, 1983, HEARING RES, V9, P145, DOI 10.1016/0378-5955(83)90024-2 PASIC TR, 1989, J COMP NEUROL, V283, P474, DOI 10.1002/cne.902830403 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 RAJAN R, 1992, NOISE INDUCED HEARIN, P119 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 SCHMIEDT RA, 1984, J ACOUST SOC AM, V76, P1293, DOI 10.1121/1.391446 Sowiński H, 1975, Neuropatol Pol, V13, P367 STRAKHOV A B, 1970, Byulleten' Eksperimental'noi Biologii i Meditsiny, V69, P95 Syka J, 1989, PROGR SENSORY PHYSL, V9, P97 TARMAS J, 1974, Folia Morphologica (Wroclaw), V33, P5 NR 23 TC 56 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 MAY PY 1992 VL 59 IS 2 BP 213 EP 223 DI 10.1016/0378-5955(92)90118-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600011 PM 1618712 ER PT J AU BROWN, M SHEPHERD, RK WEBSTER, WR MARTIN, RL CLARK, GM AF BROWN, M SHEPHERD, RK WEBSTER, WR MARTIN, RL CLARK, GM TI COCHLEOTOPIC SELECTIVITY OF A MULTICHANNEL SCALA TYMPANI ELECTRODE ARRAY USING THE 2-DEOXYGLUCOSE TECHNIQUE SO HEARING RESEARCH LA English DT Article DE COCHLEAR PROSTHESES; 2-DEOXYGLUCOSE; ELECTRICAL STIMULATION; COCHLEAR NUCLEUS; INFERIOR COLLICULUS ID STIMULATED AUDITORY-NERVE; INFERIOR COLLICULUS; ELECTRICAL-STIMULATION; C-14 2-DEOXYGLUCOSE; NEURONAL ARCHITECTURE; CURRENT DISTRIBUTIONS; COCHLEAR NUCLEUS; CAT; ORGANIZATION; PATTERNS AB The 2-deoxyglucose (2-DG) technique was used to study the cochleotopic selectivity of a multichannel scala tympani electrode array in four cats with another acting as an unstimulated control. Each animal was unilaterally deafened and a multichannel electrode array inserted 6 mm into the scala tympani. Thresholds to electrical stimulation were determined by recording electrically evoked auditory brainstem responses (EABRs). Each animal was injected with 2-DG, and electrically stimulated using bipolar electrodes located either distal or proximal to the round window. The contralateral ear was stimulated with acoustic tone pips at frequencies that matched the electrode place. Stimulation of both distal and proximal bipolar electrodes at 3 X EABR threshold, evoked localized 2-DG labelling in both ipsilateral cochlear nucleus (CN) and the contralateral inferior colliculus (IC), which was very similar in orientation and breadth to labelling evoked by the contralateral tone pips. The cochleotopic position of labelling to proximal stimulation was located in the 24-26 kHz region of each structure, whereas the distal labelling was located around 12 kHz. Distal stimulation at 10 X EABR threshold produced very broad 2-DG labelling in IC centered around the 12 kHz place. The present 2-DG results clearly illustrate cochleotopic selectivity using multichannel bipolar scala tympani electrodes. The extent of this selectivity is dependent on electrical stimulus levels. The 2-DG technique has great potential in evaluating the efficacy of new electrode array designs. C1 MONASH UNIV,DEPT PSYCHOL,CLAYTON,VIC 3168,AUSTRALIA. UNIV MELBOURNE,DEPT OTOLARYNGOL,PARKVILLE,VIC 3052,AUSTRALIA. RI Shepherd, Robert/I-6276-2012 CR ACKERMANN RF, 1984, J NEUROSCI, V4, P251 Aitkin L, 1984, HDB PHYSL 1, P675 AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 AUKER CR, 1983, J NEUROPHYSIOL, V49, P1504 BLACK RC, 1983, ANN NY ACAD SCI, V405, P137, DOI 10.1111/j.1749-6632.1983.tb31626.x Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 Bourk TR, 1976, THESIS MIT CAMBRIDGE BOURK TR, 1981, HEARING RES, V4, P215, DOI 10.1016/0378-5955(81)90008-3 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 DURHAM D, 1977, BRAIN RES, V137, P169, DOI 10.1016/0006-8993(77)91022-8 DURHAM D, 1978, J COMP NEUROL, V178, P629, DOI 10.1002/cne.901780403 Eddington D. K., 1978, ANN OTOL S, V53, P5 EVANS DA, 1990, LARYNGOSCOPE, V100, P129 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 Foley J.D., 1982, FUNDAMENTALS INTERAC GALLISTEL CR, 1982, NEUROSCI BIOBEHAV R, V6, P409, DOI 10.1016/0149-7634(82)90024-0 Hartmann R., 1990, COCHLEAR IMPLANTS MO, P135 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HATSUSHIKA S, 1990, ANN OTO RHINOL LARYN, V99, P871 HUANG C, 1986, EXP BRAIN RES, V26, P327 HUBEL DH, 1978, J COMP NEUROL, V177, P361, DOI 10.1002/cne.901770302 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 LIBERMAN CC, 1982, J ACOUST SOC AM, V75, P1441 LIM HH, 1989, J ACOUST SOC AM, V86, P971, DOI 10.1121/1.398732 LIPPE WR, 1980, BRAIN RES, V196, P43, DOI 10.1016/0006-8993(80)90715-5 LUKIES PM, 1987, ANN OTO RHINOL LARYN, V96, P24 MARTIN RL, 1988, HEARING RES, V33, P245, DOI 10.1016/0378-5955(88)90155-4 MERZENICH MM, 1977, FUNCTIONAL ELECT STI, P321 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 Moxon E.C., 1971, THESIS MIT CAMBRIDGE NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 OLEARY SJ, 1985, HEARING RES, V18, P15 ROSE JE, 1959, B J HOPKINS HOSP, V103, P211 ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 RYAN AF, 1990, HEARING RES, V50, P57, DOI 10.1016/0378-5955(90)90033-L SAPOZHINKOV A, 1990, THESIS U MELBOURNE A SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SCHWARTZ WJ, 1979, SCIENCE, V205, P723, DOI 10.1126/science.462184 SERVIERE J, 1981, NEUROSCI LETT, V27, P113, DOI 10.1016/0304-3940(81)90253-6 SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHARP FR, 1983, BRAIN RES, V263, P97, DOI 10.1016/0006-8993(83)91204-0 SHEPHERD RK, 1990, INFORMATION PROCESSI, P281 Shepherd R K, 1983, Acta Otolaryngol Suppl, V399, P19 SHEPHERD RK, 1984, P AUST PHYSL PHARM S, V14 SHEPHERD RK, 1990, STUDIES PEDIATRIC AU SKEEN LC, 1978, BRAIN RES, V142, P538, DOI 10.1016/0006-8993(78)90915-0 SOKOLOFF L, 1977, J NEUROCHEM, V29, P13, DOI 10.1111/j.1471-4159.1977.tb03919.x THERUICH M, 1984, BRAIN RES, V322, P157 TONG YC, 1982, J ACOUST SOC AM, V71, P153, DOI 10.1121/1.387342 VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 WEBSTER WR, 1978, NEUROSCI LETT, V19, P43 WEBSTER WR, 1985, J NEUROSCI, V5, P1820 WEBSTER WR, 1984, EXP BRAIN RES, V56, P427 YAMANE H, 1980, OTOLARYNGOL HEAD NEC, V89, P117 NR 60 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 MAY PY 1992 VL 59 IS 2 BP 224 EP 240 DI 10.1016/0378-5955(92)90119-8 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600012 PM 1618713 ER PT J AU SZYMKO, YM DIMITRI, PS SAUNDERS, JC AF SZYMKO, YM DIMITRI, PS SAUNDERS, JC TI STIFFNESS OF HAIR BUNDLES IN THE CHICK COCHLEA SO HEARING RESEARCH LA English DT Article DE STIFFNESS; HAIR BUNDLES; AVIAN; WATER JET ID GUINEA-PIG COCHLEA; MECHANICAL-PROPERTIES; THRESHOLD SHIFT; CELLS; STEREOCILIA; RESPONSES; FROG AB The stiffness of hair bundles from isolated chick cochlear hair cells was measured in tissue culture medium. A water jet was used to deflect fiberglass fibers, quartz fibers, and hair bundles of isolated hair cells. A voltage-displacement curve was generated for a water jet ramp stimulus applied to miniature fiberglass and quartz fibers. Fiber displacements were measured using video image subtraction techniques. A force-voltage calibration curve was then derived for the fibers by modelling them as cantilever beams subjected to point forces at the tips. A voltage-displacement curve was then generated for isolated hair cell stereociliary bundles using the same procedure as for the fibers. A corresponding force-displacement curve was derived for isolated hair cells under water jet stimulation by correlating maximum ramp voltage from the hair cell's voltage-displacement curve to a corresponding force applied to a fiber from the fiberglass fiber calibration curve. The stiffness of the hair bundle. which is the slope of the hair cell's force-displacement curve, was then calculated using Hooke's law. assuming the force was distributed along the entire length of the hair bundle. The mean stiffness value was 5.04 +/- 2.68 x 10(-4) N/m for 14 hair cells, and was in close agreement with previously reported stiffness values of several investigators utilizing different animal models and procedures. C1 UNIV PENN,DEPT BIOENGN,PHILADELPHIA,PA 19104. UNIV PENN,DEPT OTORHINOLARYNGOL HEAD & NECK SURG,PHILADELPHIA,PA 19104. CR ASHMORE JF, 1984, J PHYSIOL-LONDON, V350, pP20 Brundin L, 1989, Acta Otolaryngol Suppl, V467, P229 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 FLOCK A, 1984, NATURE, V310, P597, DOI 10.1038/310597a0 FOX RW, 1985, INTRO FLUID MECHANIC FREEMAN DM, 1990, HEARING RES, V48, P1, DOI 10.1016/0378-5955(90)90195-U GUTTENPLAN M, 1989, HEARING RES, V43, P47, DOI 10.1016/0378-5955(89)90058-0 HALLIDAY D, 1988, FUNDAMENTALS PHYSICS HOWARD J, 1987, P NATL ACAD SCI USA, V84, P3064, DOI 10.1073/pnas.84.9.3064 HOWARD J, 1986, HEARING RES, V23, P93, DOI 10.1016/0378-5955(86)90178-4 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 PARK JB, 1984, BIOMATERIALS SCI ENG, P104 RUSSELL IJ, 1989, HEARING RES, V43, P55, DOI 10.1016/0378-5955(89)90059-2 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 SAUNDERS JC, 1989, J ACOUST SOC AM, V86, P1797, DOI 10.1121/1.398612 SAUNDERS JC, 1989, COCHLEAR MECHANISMS, P135 SAUNDERS JC, 1986, BASIC APPL ASPECTS N, P11 SAUNDERS JC, 1986, HEARING RES, V23, P245, DOI 10.1016/0378-5955(86)90113-9 SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 Stevens K., 1987, STATICS STRENGTH MAT STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 TILNEY LG, 1983, J CELL BIOL, V96, P807, DOI 10.1083/jcb.96.3.807 VANVLACK LH, 1980, ELEMENTS MATERIALS S, P523 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 MAY PY 1992 VL 59 IS 2 BP 241 EP 249 DI 10.1016/0378-5955(92)90120-C PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600013 PM 1618714 ER PT J AU NIEDZIELSKI, AS ONO, T SCHACHT, J AF NIEDZIELSKI, AS ONO, T SCHACHT, J TI CHOLINERGIC REGULATION OF THE PHOSPHOINOSITIDE 2ND MESSENGER SYSTEM IN THE GUINEA-PIG ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE COCHLEA; EFFERENTS; INOSITOL; MUSCARINIC RECEPTOR; OUTER HAIR CELL; 2ND MESSENGERS ID OUTER HAIR-CELLS; INOSITOL PHOSPHATE FORMATION; RAT COCHLEA; ACETYLCHOLINE; BINDING; MOTILITY; STIMULATION; CARBACHOL; RESPONSES; SPECTRIN AB The effect of cholinergic agents on the phosphoinositide second messenger system was investigated in the cochlea of the adult guinea pig in vivo and in vitro. In vivo, phospholipids were labeled with [P-32]-orthophosphate by perilymphatic perfusion and their hydrolysis assayed in 'chase' experiments with non-radioactive orthophosphate. Carbachol (1 mM) reduced the content of P-32-labeled phosphatidylinositol 4,5-bisphosphate in the organ of Corti from 31 % to 21 % of total P-32-lipids, indicating stimulated hydrolysis. The pharmacology of this effect was studied in detail in vitro via the release of inositol phosphates from phosphoinositides pre-labeled with H-3-inositol. Release was increased 2-fold by 1 mM carbachol, 1.6-fold by 1 mM muscarine, but was unaffected by dimethylphenylpiperazinium; the stimulation was blocked by 1-mu-M atropine but not mecamylamine. These responses indicate the coupling of phosphoinositides to a muscarinic receptor. Furthermore, stimulated inositol phosphate release was higher in the base of the organ of Corti than in the apex which correlates with the increased cholinergic efferent innervation of outer hair cells in the basal region. These results suggest that muscarinic-stimulated inositol phosphate release occurs at the level of the outer hair cell and thus may have an important modulatory role in auditory transduction. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. CR BARTOLAMI S, 1990, HEARING RES, V47, P229, DOI 10.1016/0378-5955(90)90154-H BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CANLON B, 1989, ACTA PHYSIOL SCAND, V137, P549, DOI 10.1111/j.1748-1716.1989.tb08795.x COLING DE, 1991, HEARING RES, V57, P113, DOI 10.1016/0378-5955(91)90080-S DEAN NM, 1989, ANAL BIOCHEM, V183, P199, DOI 10.1016/0003-2697(89)90468-5 DESMEDT JE, 1961, NATURE, V193, P1263 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1990, J NEUROSCI, V10, P1388 FEX J, 1978, BRAIN RES, V159, P440, DOI 10.1016/0006-8993(78)90555-3 FISHER SK, 1983, J BIOL CHEM, V258, P7358 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GODFREY PP, 1990, NEUROCHEM INT, V17, P515, DOI 10.1016/0197-0186(90)90038-U GONZALES RA, 1984, J NEUROSCI, V4, P3120 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 JAMES WM, 1983, HEARING RES, V9, P113, DOI 10.1016/0378-5955(83)90139-9 MEGEN YJB, 1988, BRAIN RES, V474, P185 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NIEDZIELSKI A S, 1991, Society for Neuroscience Abstracts, V17, P1213 NIEDZIELSKI A, 1991, ABSTR ASS RES OT, V14, P135 NIEDZIELSKI AS, 1991, HEARING RES, V57, P107, DOI 10.1016/0378-5955(91)90079-O NISHIZUKA Y, 1989, JAMA-J AM MED ASSOC, V262, P1826, DOI 10.1001/jama.262.13.1826 NUTTALL AL, 1977, ACTA OTO-LARYNGOL, V83, P393, DOI 10.3109/00016487709128863 ONO T, 1989, NEUROCHEM INT, V14, P327, DOI 10.1016/0197-0186(89)90058-2 ONO T, 1987, AUDIOL JPN, V30, P607 ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x PLINKERT PK, 1990, HEARING RES, V44, P25, DOI 10.1016/0378-5955(90)90019-L SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 Schacht J, 1981, Methods Enzymol, V72, P626 SLEPECKY N, 1988, HEARING RES, V34, P119, DOI 10.1016/0378-5955(88)90099-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SPOENDLIN H, 1985, AM J OTOLARYNG, V6, P453, DOI 10.1016/S0196-0709(85)80026-0 TAKADA A, 1982, HEARING RES, V8, P179, DOI 10.1016/0378-5955(82)90073-9 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 YLIKOSKI J, 1990, HEARING RES, V43, P199, DOI 10.1016/0378-5955(90)90228-H NR 38 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 MAY PY 1992 VL 59 IS 2 BP 250 EP 254 DI 10.1016/0378-5955(92)90121-3 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HU756 UT WOS:A1992HU75600014 PM 1319989 ER PT J AU MCGINN, MD BEANKNUDSEN, D ERMEL, RW AF MCGINN, MD BEANKNUDSEN, D ERMEL, RW TI INCIDENCE OF OTITIS-MEDIA IN CBA/J AND CBA/CAJ MICE SO HEARING RESEARCH LA English DT Article DE AGING; AUDITORY THRESHOLD; LABYRINTHITIS; PASTEURELLA-PNEUMOTROPICA; TETRACYCLINE ID HEARING-LOSS; BACTERIAL; RATS AB The inbred CBA/J mouse has become a standard experimental animal for auditory study because of its lifelong good hearing. In a newly established mouse breeding colony that housed CBA/J and CBA/CaJ mice to reared as auditory subjects, otitis media frequently afflicted CBA/J mice, reaching an incidence of 90% in animals > 400 days of age. Otitis media was not found in CBA/CaJ mice. Three attempts to establish a colony that was free of otitis were unsuccessful. Although the primary pathogen was not clearly established, Pasteurella pneumotropica was isolated from infected bullae. Partial control of otitis media followed the introduction of tetracycline prophylaxis. The CBA/CaJ mice may be suitable replacements for CBA/J mice in studies that require inbred mice with good hearing, since their auditory thresholds did not differ significantly from those of otitis-free CBA/J mice. C1 UNIV CALIF DAVIS,SCH VET MED,COMPARAT BIOL LAB,DAVIS,CA 95616. UNIV CALIF DAVIS,SCH VET MED,ANIM RESOURCES SERV,DAVIS,CA 95616. RP MCGINN, MD (reprint author), UNIV CALIF DAVIS,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,OTOL RES LAB,SURGE 3,DAVIS,CA 95616, USA. CR AHMED A, 1977, J EXP MED, V145, P101, DOI 10.1084/jem.145.1.101 ALTMAN PL, 1979, INBRED GENETICALLY D, P45 BRODIE HA, 1987, AM J OTOLARYNG, V8, P342, DOI 10.1016/S0196-0709(87)80053-4 CARLTON WW, 1978, PATHOLOGY LABORATORY, V2, P1368 Dickie MM, 1966, MOUSE NEWS LETT, V34, P30 EAMENS GJ, 1984, LAB ANIM SCI, V34, P480 FIDLER IJ, 1977, NATURE, V270, P735, DOI 10.1038/270735a0 GOLDSTEIN E, 1967, J BACTERIOL, V63, P1651 GOODMAN MG, 1979, J IMMUNOL, V123, P2482 HARKNESS JE, 1975, LAB ANIM SCI, V25, P315 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1992, IN PRESS AUDIOLOGY HENRY KR, 1978, ACTA OTO-LARYNGOL, V86, P366, DOI 10.3109/00016487809107515 HENRY KR, 1981, ARCH OTOLARYNGOL, V107, P92 HOAG WG, 1962, J INFECT DIS, V111, P135 HOOPER DG, 1977, AM J VET RES, V38, P565 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 KELEMEN G, 1978, PATHOLOGY LAB ANIMAL, V1, P620 KOHN DF, 1974, LAB ANIM SCI, V24, P823 KOHN DF, 1980, J AM VET MED ASSOC, V177, P815 MACPHERSON CW, 1963, LAB ANIM CARE, V13, P737 MCGINN MD, 1984, ACTA OTO-LARYNGOL, V97, P297, DOI 10.3109/00016488409130992 MOORE GJ, 1978, LAB ANIM, V12, P227, DOI 10.1258/002367778781088413 MORIZONO T, 1984, RECENT ADV OTITIS ME, P341 OBRIEN AD, 1979, J IMMUNOL, V123, P720 OLSON LD, 1968, LAB ANIM CARE, V18, P478 Ratcliffe H.L., 1949, RAT LAB INVESTIGATIO, P515 Schuknecht H. F., 1974, PATHOLOGY EAR SIDMAN RL, 1965, J HERED, V56, P23 SMITH GS, 1973, J NATL CANCER I, V50, P1195 THONG YH, 1980, CLIN EXP IMMUNOL, V39, P728 WAGNER JE, 1976, LAB ANIM SCI, V26, P902 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 Willott J.F., 1983, AUDITORY PSYCHOBIOLO NR 34 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 APR PY 1992 VL 59 IS 1 BP 1 EP 6 DI 10.1016/0378-5955(92)90094-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600001 PM 1629038 ER PT J AU NOMOTO, M AF NOMOTO, M TI ENHANCEMENT AND SUPPRESSION IN THE AUDITORY MIDBRAIN NUCLEUS (MLD) OF THE PIGEON SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIAL; AUDITORY SPIKE RESPONSE; ENHANCEMENT; SUPPRESSION; NUCLEUS MESENCEPHALICUS LATERALIS PARS DORSALIS; AUDITORY NERVOUS SYSTEM; PIGEON ID 2-TONE SUPPRESSION; NERVE; RESPONSES; MASKING; FIBERS AB Auditory evoked potentials (AEPs) and spike responses were recorded from the same recording site in the nucleus mesencephalicus lateralis pars dorsalis (MLD) in pigeons with a tungsten microelectrode. Depending on the recording sites within the MLD, enhancement and suppression of the AEPs in response to clicks were observed at particular frequencies of a background continuous pure tone. Post stimulus time histograms (PSTs) of the spike responses, if available in such cases, were recorded from the same position by the same electrode. Suppression of the AEPs always occurred but enhancement occurred in only 21% of the trials. The frequencies of tone bursts that caused maximum AEP were vaguely related to the frequencies of continuous pure tones that elicited maximum suppression of the AEPs in response to clicks. However, enhancement was produced by a continuous pure tone of approximately 1.5 kHz, independent of the frequencies of tone bursts that produced maximum AEPs. Most of the PSTs in such instances showed parallel relations between the spike responses and the amplitudes of the AEPs. The nature of the enhancement and suppression of the click evoked AEPs during continuous pure tones was clearly different from those in recordings from the nucleus magnocellularis, nucleus angularis and Field L in respect to the probability of occurrence of enhancement and suppression. RP NOMOTO, M (reprint author), HINO HOSP,DEPT PSYCHIAT,3-9-3 HINO,KONAN KU,YOKOHAMA 233,JAPAN. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 ANANTHANARAYAN AK, 1983, ELECTROEN CLIN NEURO, V55, P223, DOI 10.1016/0013-4694(83)90191-8 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BOORD RL, 1969, ANN NY ACAD SCI, V167, P186, DOI 10.1111/j.1749-6632.1969.tb20444.x CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 DALLOS P, 1977, J ACOUST SOC AM, V62, P1048, DOI 10.1121/1.381598 Evans E. F., 1975, HDB SENSORY PHYSL, V5, P1 GERKEN GM, 1973, ELECTROEN CLIN NEURO, V34, P509, DOI 10.1016/0013-4694(73)90068-0 GOLDSTEI.JL, 1968, PR INST ELECTR ELECT, V56, P981, DOI 10.1109/PROC.1968.6449 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 Karten H.J., 1967, STEREOTAXIC ATLAS BR KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KRAMER SJ, 1982, J ACOUST SOC AM, V72, P795, DOI 10.1121/1.388186 NOMOTO M, 1985, HEARING RES, V17, P13, DOI 10.1016/0378-5955(85)90125-X NOMOTO M, 1964, J NEUROPHYSIOL, V27, P768 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 RUPERT A, 1963, J NEUROPHYSIOL, V26, P449 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 Suga N, 1988, AUDITORY FUNCTION NE, P679 NR 20 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 1992 VL 59 IS 1 BP 7 EP 13 DI 10.1016/0378-5955(92)90095-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600002 PM 1629048 ER PT J AU TACHIBANA, M SENUMA, H KUMAMOTO, K AF TACHIBANA, M SENUMA, H KUMAMOTO, K TI ENKEPHALIN-LIKE IMMUNOREACTIVITY IN COCHLEAR EFFERENTS IN THE BAT, RHINOLOPHUS-FERRUMEQUINUM SO HEARING RESEARCH LA English DT Article DE BAT; RHINOLOPHUS-FERRUMEQUINN; METHIONINE-ENKEPHALIN; IMMUNOHISTOCHEMISTRY ID GENE-RELATED PEPTIDE; GUINEA-PIG; MET-ENKEPHALIN; NERVE-FIBERS; ORGAN; CORTI; LOCALIZATION; INNERVATION; ORIGINS; RAT AB The cochlear efferent of the bat is anatomically different from other mammals. The olivocochlear bundle of the greater horse shoe bat, Rhinolophus ferrumequinum, projects only to outer hair cells. To examine the neurochemical nature of the olivocochlear bundle, we examined methionine-enkephalin-like immunoreactivity in this species. We observed immunoreactivity in the inner spiral bundles and in nerve fibers in the osseous spiral lamina. Sometimes immunostained inner spiral bundles were found to project towards inner hair cells. These data, as well as data from previous studies, suggest that cochlear efferents of different species of mammals share some common neurochemical features. C1 MEIJI COLL ORIENTAL MED,DEPT OTOLARYNGOL,KYOTO,JAPAN. MEIJI COLL ORIENTAL MED,DEPT ANAT,KYOTO,JAPAN. CR ADAMS JC, 1987, BRAIN RES, V419, P347, DOI 10.1016/0006-8993(87)90606-8 ALTSCHULER RA, 1984, HEARING RES, V16, P17, DOI 10.1016/0378-5955(84)90022-4 ASCHOFF A, 1987, J COMP NEUROL, V264, P56, DOI 10.1002/cne.902640106 BISHOP AL, 1987, HEARING RES, V31, P175, DOI 10.1016/0378-5955(87)90124-9 BISHOP AL, 1988, NATO ASI SERIES A, V156, P307 BRUNS V, 1980, HEARING RES, V3, P27, DOI 10.1016/0378-5955(80)90006-4 EYBALIN M, 1984, BRAIN RES, V305, P313, DOI 10.1016/0006-8993(84)90437-2 EYBALIN M, 1983, CR ACAD SCI III-VIE, V296, P1125 EYBALIN M, 1984, HEARING RES, V13, P135, DOI 10.1016/0378-5955(84)90104-7 FEX J, 1981, P NATL ACAD SCI-BIOL, V78, P1255, DOI 10.1073/pnas.78.2.1255 FIRBAS W, 1970, ACTA OTO-LARYNGOL, V70, P329 HOFFMAN DW, 1983, HEARING RES, V9, P71, DOI 10.1016/0378-5955(83)90135-1 HOFFMAN DW, 1984, BRAIN RES, V322, P59, DOI 10.1016/0006-8993(84)91180-6 Ishii D, 1968, Acta Otolaryngol, V66, P282, DOI 10.3109/00016486809126295 Ishii T, 1967, Acta Otolaryngol, V64, P267, DOI 10.3109/00016486709139116 KANEKO Y, 1968, LARYNGOSCOPE, V78, P1566, DOI 10.1288/00005537-196809000-00008 KITAJIRI M, 1985, BRAIN RES, V358, P394, DOI 10.1016/0006-8993(85)90992-8 SLINSKAKOWALSKA M, 1989, HEARING RES, V42, P83 TAKEDA N, 1987, ACTA OTO-LARYNGOL, V103, P567 VETTER DE, 1991, SYNAPSE, V7, P21, DOI 10.1002/syn.890070104 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WARR WB, 1975, J COMP NEUROL, V161, P152 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 NR 23 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 1992 VL 59 IS 1 BP 14 EP 16 DI 10.1016/0378-5955(92)90096-6 PG 3 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600003 PM 1629041 ER PT J AU FUKAZAWA, T AF FUKAZAWA, T TI EVOKED OTOACOUSTIC EMISSIONS IN A NONLINEAR MODEL OF THE COCHLEA SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; COCHLEAR MODEL; COMPUTER SIMULATION ID STIMULATED ACOUSTIC EMISSIONS; ACTIVE ELEMENTS; BIOMECHANICS; RESPONSES; TINNITUS; ECHOES; WAVE AB A nonlinear, transmission-line-analog model of the ear is presented for the purpose of simulating the experimental data of delayed evoked otoacoustic emissions (DEOAEs). The model produces echoes very similar to DEOAEs in the latency, saturation and spectral features when hypothetical, highly damped points arranged on the BM with an equal spacing are assumed. Special attention is paid to the reason for the long latency of DEOAEs. In the model, the delay occurs spuriously by cancellation of components scattered from the irregular points and is longer than the simple round trip time of the travelling wave from the stapes to the place of characteristic frequency. The echoes in the model are basically linear for the low intensity stimuli and only when the stimuli surpass a certain level they saturate owing to the nonlinearity of the BM damping. C1 KYOTO UNIV,SCH MED,DEPT OTOLARYNGOL,KYOTO 606,JAPAN. CR Antonelli A, 1986, Scand Audiol Suppl, V25, P97 DALLMAYR C, 1987, ACUSTICA, V63, P243 DEBOER E, 1983, HEARING RES, V13, P101 FURST M, 1988, J ACOUST SOC AM, V84, P222, DOI 10.1121/1.396969 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 Kemp D. T., 1983, MECH HEARING, P75 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, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 LONG GR, 1985, PERIPHERAL AUDITORY LONSBURYMARTIN BL, 1988, HEARING RES, V33, P69, DOI 10.1016/0378-5955(88)90021-4 LYNCH TJ, 1982, J ACOUST SOC AM, V72, P108, DOI 10.1121/1.387995 NEELY ST, 1981, J ACOUST SOC AM, V69, P1386, DOI 10.1121/1.385820 NEELY ST, 1988, J ACOUST SOC AM, V83, P652, DOI 10.1121/1.396542 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NEELY ST, 1988, BASIC ISSUES HEARING, P106 PETERSON LC, 1950, J ACOUST SOC AM, V22, P369, DOI 10.1121/1.1906615 SCHROEDER MR, 1972, J ACOUST SOC AM, V53, P429 STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 Sutton GJ, 1983, MECHANICS HEARING, P83 VIERGEVER MA, 1977, J ENG MATH, V11, P11, DOI 10.1007/BF01535585 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X WILSON JP, 1980, HEARING RES, V2, P527, DOI 10.1016/0378-5955(80)90090-8 WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 WIT HP, 1981, J ACOUST SOC AM, V70, P437, DOI 10.1121/1.386786 ZERLIN S, 1969, J ACOUST SOC AM, V46, P1011, DOI 10.1121/1.1911792 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 ZWICKER E, 1988, BASIC ISSUES HEARING, P14 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 ZWICKER E, 1988, NATO ASI SERIES NR 30 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 APR PY 1992 VL 59 IS 1 BP 17 EP 24 DI 10.1016/0378-5955(92)90097-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600004 PM 1629042 ER PT J AU AOKI, S HOUTGAST, T AF AOKI, S HOUTGAST, T TI A PRECEDENCE EFFECT IN THE PERCEPTION OF INTER-AURAL CROSS-CORRELATION SO HEARING RESEARCH LA English DT Article DE PRECEDENCE EFFECT; LOCALIZATION; LATERALIZATION; DIFFUSENESS COMPACTNESS; BINAURAL PROCESSING ID SOUND AB Does the precedence effect, well known in the field of sound localization or lateralization, also apply to other percepts based on binaural processing? We have compared, with one and the same experimental paradigm, a manifestation of the traditional precedence effect in lateralization with a possible similar effect in the perception of diffuseness or compactness of a sound image. With dichotic headphone stimulation, lateralization was controlled by the inter-aural time delay (IATD), and diffuseness/compactness by the inter-aural cross correlation (IACC). The experimental paradigm rests on the principle of estimating the over-all sensation of a 20-ms noise burst, which was subdivided in two parts, with the relevant dichotic information (IATD or IACC) in the leading part being opposite to that in the trailing part. When each part is 10 ms, it is found that the overall sensation is slightly dominated by the information in the leading part, both for lateralization and for compactness/diffuseness. This dominance of the leading part can be compensated by a certain decrease of its duration and/or amplitude relative to that of the trailing part. It is found that this quantitative measure for the 'strength' of the precedence effect for the present stimulus is essentially the same for IATD and IACC, suggesting that the precedence effect does not apply exclusively to sound localization or lateralization, but to at least one other percept based on binaural processing as well, namely the processing of inter-aural cross correlation. C1 TNO, INST PERCEPT, SOESTERBERG, NETHERLANDS. RP AOKI, S (reprint author), NIPPON TELEGRAPH & TEL PUBL CORP, MUSASHINO ELECT COMMUN LAB, HUMAN INTERFACE LABS, MUSASHINO, TOKYO 180, JAPAN. CR ANDO Y, 1986, J ACOUST SOC AM, V80, P833, DOI 10.1121/1.393906 GARDNER MB, 1968, J ACOUST SOC AM, V43, P1243, DOI 10.1121/1.1910974 GARDNER MB, 1969, J ACOUST SOC AM, V46, P339, DOI 10.1121/1.1911695 HAAS H, 1972, J ACOUST ENG SOC, V20, P149 RAATGEVER J, 1986, J ACOUST SOC AM, V80, P429, DOI 10.1121/1.394039 RAKERD B, 1986, J ACOUST SOC AM, V80, P1695, DOI 10.1121/1.394282 STEVENS SS, 1957, J ACOUST SOC AM, V29, P603, DOI 10.1121/1.1908979 TOBIAS JV, 1959, J ACOUST SOC AM, V31, P1595, DOI 10.1121/1.1907665 WALLACH H, 1949, AM J PSYCHOL, V62, P315, DOI 10.2307/1418275 YANAGAWA H, 1989, J ACOUST SOC AM S1, V86 YANAGAWA H, 1988, J ACOUST SOC AM, V84, P1728, DOI 10.1121/1.397187 ZUREK PM, 1980, J ACOUST SOC AM, V67, P952, DOI 10.1121/1.383974 NR 12 TC 13 Z9 13 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 APR PY 1992 VL 59 IS 1 BP 25 EP 30 DI 10.1016/0378-5955(92)90098-8 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600005 PM 1629043 ER PT J AU WANG, J LI, QH DONG, WJ CHEN, JS AF WANG, J LI, QH DONG, WJ CHEN, JS TI EFFECTS OF VARIOUS NOISE EXPOSURES ON ENDOCOCHLEAR POTENTIALS CORRELATED WITH COCHLEAR GROSS RESPONSES SO HEARING RESEARCH LA English DT Article DE NOISE; ENDOCOCHLEAR POTENTIAL; GROSS COCHLEAR POTENTIALS; GUINEA PIG ID GUINEA-PIG; BASILAR-MEMBRANE; BLOOD-FLOW; ACTIVE PROCESS; HAIR CELL; ENDOLYMPH; SENSITIVITY; MECHANICS AB Changes in endocochlear potentials (EP), cochlear microphonics (CM), and compound action potentials (CAP) with noise exposure were investigated in guinea pigs. The animals were anesthetized and immobilized and exposed to white noise at intensities ranging from 105 to 125 dB. The negative EP (N-EP) was induced by anoxia and was investigated during and after noise exposure. It was found that the general EP (G-EP, the sum of both positive EP (P-EP) and N-EP) increased remarkably during exposure to 115 dB noise but decreased during exposure to 125 dB noise. A smaller absolute value of N-EP was encountered only during exposure to 125 dB noise. The results shed light on the relationship between EP and CM, CAP changes, and the potential mechanism of EP change and its significance in noise-induced hearing loss. RP WANG, J (reprint author), NANJING RAILWAY MED COLL,DEPT FUNDAMENTAL MED,AUDIOPHYSIOL LAB,DINJIA QIAO RD 87,NANJING 210009,PEOPLES R CHINA. CR AXELSSON A, 1981, ACTA OTO-LARYNGOL, V91, P237, DOI 10.3109/00016488109138504 BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 CHOU JTY, 1975, EXPERIENTIA, V31, P554, DOI 10.1007/BF01932455 DALLOS P, 1985, P207 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DUVALL AJ, 1974, ANN OTO RHINOL LARYN, V83, P498 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HUDSPETH AJ, 1986, HEARING RES, V22, P21, DOI 10.1016/0378-5955(86)90070-5 IKEDA K, 1988, HEARING RES, V32, P103, DOI 10.1016/0378-5955(88)90081-0 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 KIM DO, 1986, HEARING RES, V26, P199 KONISHI T, 1980, EXP BRAIN RES, V40, P457 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 MAASS B, 1978, ARCH OHREN NASEN KEH, V221, P269, DOI 10.1007/BF00491463 MELICHAR I, 1987, HEARING RES, V25, P23, DOI 10.1016/0378-5955(87)90076-1 MELICHAR I, 1980, Hearing Research, V2, P55, DOI 10.1016/0378-5955(80)90016-7 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 MOUNTAIN DC, 1986, NEUROBIOLOGY HEARING, P77 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 OZDAMAR O, 1976, J ACOUST SOC AM, V59, P143 PATUZZI R, 1985, BASIC APPLIED ASPECT, P123 PATUZZI R, 1984, HEARING RES, V13, P999 PRAZMA J, 1983, ARCH OTOLARYNGOL, V109, P611 PRAZMA J, 1987, ARCH OTOLARYNGOL, V113, P36 PRAZMA J, 1975, ARCH OTO-RHINO-LARYN, V209, P1, DOI 10.1007/BF00454023 PRAZMA J, 1969, ACTA OTOLARYNGOL, V68, P58 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 ROBLES L, 1976, J ACOUST SOC AM, V59, P926, DOI 10.1121/1.380953 SALT AN, 1981, J ACOUST SOC AM, V69, P1746, DOI 10.1121/1.385954 SALT AN, 1979, HEARING RES, V1, P343, DOI 10.1016/0378-5955(79)90005-4 SELLICK PM, 1974, PFLUGER ARCH, V336, P406 Sitko S T, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P328 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 SYKA J, 1981, HEARING RES, V4, P287, DOI 10.1016/0378-5955(81)90013-7 THORNE PR, 1985, ANN OTO RHINOL LARYN, V230, P285 VERTES D, 1981, ACTA OTO-LARYNGOL, V92, P15, DOI 10.3109/00016488109133233 Wang J A, 1990, Hear Res, V44, P143, DOI 10.1016/0378-5955(90)90076-2 WEISS TF, 1982, HEARING RES, V7, P353, DOI 10.1016/0378-5955(82)90045-4 WRIGHT JW, 1985, HEARING RES, V17, P41, DOI 10.1016/0378-5955(85)90128-5 NR 41 TC 5 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 1992 VL 59 IS 1 BP 31 EP 38 DI 10.1016/0378-5955(92)90099-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600006 PM 1629044 ER PT J AU CHEATHAM, MA DALLOS, P AF CHEATHAM, MA DALLOS, P TI PHYSIOLOGICAL CORRELATES OF OFF-FREQUENCY LISTENING SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELL; NONLINEARITY; OFF-FREQUENCY LISTENING; 2-TONE SUPPRESSION ID AUDITORY-NERVE FIBERS; HAIR CELL RESPONSES; BASILAR-MEMBRANE; GUINEA-PIG; RECEPTOR POTENTIALS; MOSSBAUER TECHNIQUE; 2-TONE SUPPRESSION; TIMING INFORMATION; ALLIGATOR LIZARD; TUNING CURVES AB Recordings are made from inner hair cells (IHC) in the second turn of the guinea pig cochlea where characteristic frequencies (CF) are approximately 4000 Hz. Results from experiments using two stimulus inputs suggest that the characterization of two-tone suppression at this more-basal recording location is similar to that reported for IHCs in the third cochlear turn (Cheatham and Dallos, 1989, 1990a, 1990b). For example, introduction of a suppressor causes IHC frequency response functions to become narrower with the smallest magnitude reductions occurring between 1/2 to 1 octave below CF. In this frequency region, where suppression is minimal, it was also observed that suppressor magnitude was reduced by the probe. In other words, the mutual suppression of probe and suppressor may contribute to the sharpening of these functions. Since the peak of the frequency response function shifts to a lower frequency in the presence of the suppressor, these results may provide a physiological correlate of the psychophysical phenomenon known as 'off-frequency listening.' RP CHEATHAM, MA (reprint author), NORTHWESTERN UNIV,HUGH KNOWLES CTR,AUDITORY PHYSIOL LAB,FRANCES SEARLE BLDG,EVANSTON,IL 60208, USA. CR ALLEN JB, 1983, J ACOUST SOC AM, V73, P2071, DOI 10.1121/1.389575 ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 CHEATHAM MA, 1990, HEARING RES, V50, P193, DOI 10.1016/0378-5955(90)90045-Q CHEATHAM MA, 1990, HEARING RES, V43, P135, DOI 10.1016/0378-5955(90)90222-B CHEATHAM MA, 1992, IN PRESS HEAR RES, V59 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1974, FACTS MODELS HEARING, P312 DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 DELGUTTE B, 1989, J ACOUST SOC AM, V85, pS14, DOI 10.1121/1.2026806 DENG L, 1985, Journal of the Acoustical Society of America, V78, P1633, DOI 10.1121/1.392801 GEISLER CD, 1982, J ACOUST SOC AM, V71, P1201, DOI 10.1121/1.387768 HIND JE, 1967, J NEUROPHYSIOL, V30, P794 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 JOHNSONDAVIES D, 1979, J ACOUST SOC AM, V65, P765, DOI 10.1121/1.382490 KIDD RC, 1990, HEARING RES, V49, P181, DOI 10.1016/0378-5955(90)90104-W NUTTALL AL, 1991, 2 TONE SUPPRESSION I, P132 OLOUGHLIN BJ, 1981, J ACOUST SOC AM, V69, P1119, DOI 10.1121/1.385691 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X PATTERSON RD, 1976, J ACOUST SOC AM, V59, P640, DOI 10.1121/1.380914 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 ROBLES L, 1989, COCHLEAR MECH STRUCT, P369 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SINEX DG, 1986, J NEUROPHYSIOL, V56, P1763 WEISS TF, 1974, J ACOUST SOC AM, V55, P606, DOI 10.1121/1.1914571 WEISS TF, 1988, HEARING RES, V33, P167, DOI 10.1016/0378-5955(88)90029-9 NR 33 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 1992 VL 59 IS 1 BP 39 EP 45 DI 10.1016/0378-5955(92)90100-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600007 PM 1629045 ER PT J AU HASHINO, E TANAKA, Y SALVI, RJ SOKABE, M AF HASHINO, E TANAKA, Y SALVI, RJ SOKABE, M TI HAIR CELL REGENERATION IN THE ADULT BUDGERIGAR AFTER KANAMYCIN OTOTOXICITY SO HEARING RESEARCH LA English DT Article DE HAIR CELL REGENERATION; KANAMYCIN; OTOTOXICITY; BUDGERIGAR; HEARING LOSS ID SEVERE ACOUSTIC TRAUMA; AVIAN INNER-EAR; BASILAR PAPILLA; CHICK COCHLEA; AUDITORY-THRESHOLDS; INTENSE SOUND; HEARING-LOSS; STEREOCILIA; EXPOSURE; PIGEON AB Adult budgerigars were given kanamycin at a dose of 200 mg/kg/day for 10 successive days. At 1, 7, 14 and 28 days after the drug treatment, the cochleae of the birds were processed for scanning electron microscopy (SEM). Complete degeneration of sensory hair cells was observed in the basal 55-75% of the basilar papilla immediately after the treatment. Regenerating hair cells, characterized by clusters of microvilli and small apical surfaces, were present in the basal end of the papilla as early as one day post-treatment. During the 28 day recovery period, the number of hair cells progressively increased beginning at the base and spreading toward the apex. Although the appearance of the basilar papilla had improved considerably by 28 days post-treatment, the sensory epithelium still contained a number of pathologies, most noticeably, incomplete restoration of hair cell number in the most apical part of the damaged region and the disorganization of hair cell packing. These remaining pathologies may be responsible for the permanent threshold shifts observed in budgerigars exposed to the same dose of kanamycin treatment (Hashino and Sokabe, 1989). C1 DOKKYO UNIV,SCH MED,DEPT OTOLARYNGOL,SAITAMA,JAPAN. NAGOYA UNIV,SCH MED,DEPT PHYSIOL,NAGOYA,AICHI 466,JAPAN. RP HASHINO, E (reprint author), SUNY BUFFALO,HEARING RES LABS,215 PARKER HALL,BUFFALO,NY 14214, USA. CR Bekesy G., 1960, EXPT HEARING CORWIN JT, 1989, J COMP NEUROL, V288, P529, DOI 10.1002/cne.902880402 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1986, ASS RES OTOLARYNGOL, V9, P32 COTANCHE DA, 1987, HEARING RES, V28, P35, DOI 10.1016/0378-5955(87)90151-1 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, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 FISCHER FP, 1988, HEARING RES, V34, P87, DOI 10.1016/0378-5955(88)90053-6 GIROD AG, IN PRESS LARYNGOSCOP GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 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 HASHINO E, 1991, NOISE INDUCED HEARIN, P228 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 INOUE T, 1989, J ELECTRON MICROSC, V38, P246 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 LODHI S, 1980, BIOCHEM PHARMACOL, V29, P597, DOI 10.1016/0006-2952(80)90382-2 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MARSH RR, 1990, HEARING RES, V46, P229, DOI 10.1016/0378-5955(90)90004-9 PROSEN CA, 1978, J ACOUST SOC AM, V63, P559, DOI 10.1121/1.381754 RUBEL EW, 1991, NOISE INDUCED HEARIN, P204 RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N RYALS BM, 1982, ACTA OTOLARYNGOL, V98, P93 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1989, HEARING RES, V43, P81, DOI 10.1016/0378-5955(89)90061-0 RYAN A, 1979, J ACOUST SOC AM, V66, P370, DOI 10.1121/1.383194 SCHERMULY L, 1990, HEARING RES, V48, P69, DOI 10.1016/0378-5955(90)90199-Y SEIDMAN DA, 1989, ABSTR ASS RES OTOLAR, V12, P135 STEBBINS WC, 1981, AMINOGLYCOSIDE OTOTO, P5 TILNEY MS, 1987, HEARING RES, V25, P141, DOI 10.1016/0378-5955(87)90087-6 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 NR 36 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 APR PY 1992 VL 59 IS 1 BP 46 EP 58 DI 10.1016/0378-5955(92)90101-R PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600008 PM 1629046 ER PT J AU AVAN, P LOTH, D MENGUY, C TEYSSOU, M AF AVAN, P LOTH, D MENGUY, C TEYSSOU, M TI HYPOTHETICAL ROLES OF MIDDLE-EAR MUSCLES IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE MIDDLE EAR; ACOUSTIC REFLEX; STAPEDIUS MUSCLE; GUINEA PIG; RABBIT; COCHLEAR MICROPHONICS; IMPEDANCE AUDIOMETRY; ELECTROMYOGRAPHY ID STAPEDIUS MUSCLE; REFLEX AB The attenuation of incoming sounds induced by acoustic reflex triggering was evaluated from the cochlear microphonic response to test tones in 45 awake guinea-pigs. Although control electromyographic measurements proved that the stapedius muscle was contracting, neither impedance changes nor attenuation induced by contralateral reflex-eliciting sounds were detectable in 30 cases out of 45. For ipsi- and bilateral stimulations, an attenuation was detectable for 7 guinea-pigs out of 10. In the guinea-pigs for which a reflex-induced change was found on CM, the mean attenuation was weak i.e. of the order of 2 dB at 20 dB above reflex threshold. These results were quite different from those obtained during control experiments in the rabbit for which CM attenuation was much larger. However, large attenuations associated with middle ear muscle contractions were found in the guinea-pig in other circumstances, i.e. during self-vocalization or when spontaneous muscle contractions occurred during anaesthesia. It is concluded that middle ear muscles can have several different functions, and that even when it exists. attenuation of loud sounds might not be their primary role. RP AVAN, P (reprint author), UNIV PARIS 07,FAC MED LARIBOISIERE,CENT SERV BIOPHYS & NUCL MED,10 AVE VERDUN,F-75010 PARIS,FRANCE. CR ANDERSON H, 1969, NOBEL S, V10, P49 ANNIKO M, 1981, ARCH OTO-RHINO-LARYN, V230, P109, DOI 10.1007/BF00456139 AVAN P, 1988, NOISE 88 P, P15 BERGE H, 1990, HEARING RES, V48, P209 Borg E, 1968, Acta Otolaryngol, V65, P575, DOI 10.3109/00016486809121001 Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 BORG E, 1973, BRAIN RES, V49, P101, DOI 10.1016/0006-8993(73)90404-6 Borg E., 1984, ACOUSTIC REFLEX BASI, P63 BORG E, 1975, ACTA OTO-LARYNGOL, V79, P325, DOI 10.3109/00016487509124694 BORG E, 1972, ACTA OTOLARYNGOL S, V304 BORG E, 1971, ACTA PHYSL SCAND, V86, P175 BOSATRA A, 1984, ACOUSTIC REFLEX, P301 COUNTER SA, 1982, ACTA OTO-LARYNGOL, V94, P267, DOI 10.3109/00016488209128913 COUNTER SA, 1989, AUDIOLOGY, V28, P135 DALLOS P, 1972, J ACOUST SOC AM, V52, P1263, DOI 10.1121/1.1913241 DJUPESLA.G, 1971, ACTA OTO-LARYNGOL, V71, P262, DOI 10.3109/00016487109125361 GALAMBOS R, 1959, J ACOUST SOC AM, V31, P349, DOI 10.1121/1.1907723 GERHARDT KJ, 1986, AUDIOLOGY, V25, P309 HENSON OW, 1965, J PHYSIOL-LONDON, V180, P871 HORNER KC, 1986, HEARING RES, V24, P117, DOI 10.1016/0378-5955(86)90055-9 JOSEPH MP, 1985, J COMP NEUROL, V232, P43, DOI 10.1002/cne.902320105 Kato T, 1913, PFLUG ARCH GES PHYS, V150, P569, DOI 10.1007/BF01681012 KOBLER JB, 1987, BRAIN RES, V425, P372, DOI 10.1016/0006-8993(87)90523-3 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 LEPAGE EL, 1990, 4TH C EFF NOIS AUD S, P106 LIBERMAN MC, 1988, HEARING RES, V34, P179, DOI 10.1016/0378-5955(88)90105-0 LOTZ P, 1969, ARCH KLIN EXP OHR, V195, P47, DOI 10.1007/BF00343034 Moller A, 1984, ACOUSTIC REFLEX, P1 MOLLER A R, 1964, Acta Otolaryngol, V58, P525, DOI 10.3109/00016486409121413 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MORGAN DE, 1978, J ACOUST SOC AM, V63, P6 MURATA K, 1986, HEARING RES, V23, P169, DOI 10.1016/0378-5955(86)90014-6 NUTTALL AL, 1974, J ACOUST SOC AM, V56, P1239, DOI 10.1121/1.1903414 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V RAJAN R, 1990, 4TH C EFF NOIS AUD S, P429 VACHER SR, 1989, J COMP NEUROL, V289, P401, DOI 10.1002/cne.902890306 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V Wiggers HC, 1937, AM J PHYSIOL, V120, P771 WROBLEWSKI R, 1981, J ULTRA MOL STRUCT R, V76, P46, DOI 10.1016/S0022-5320(81)80049-4 NR 39 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 APR PY 1992 VL 59 IS 1 BP 59 EP 69 DI 10.1016/0378-5955(92)90102-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600009 PM 1629047 ER PT J AU ZUCCA, G VEGA, R BOTTA, L PEREZ, ME VALLI, P SOTO, E AF ZUCCA, G VEGA, R BOTTA, L PEREZ, ME VALLI, P SOTO, E TI STREPTOMYCIN BLOCKS THE AFFERENT SYNAPSE OF THE ISOLATED SEMICIRCULAR CANALS OF THE FROG SO HEARING RESEARCH LA English DT Article DE VESTIBULAR SYSTEM; STREPTOMYCIN; AMINOGLYCOSIDE; HAIR CELL; INNER EAR; GLUTAMATE RECEPTOR; EXCITATORY AMINO ACID ID HAIR-CELLS; PLANAR BILAYERS; TRANSDUCTION; ANTIBIOTICS; GLUTAMATE; CHANNELS; CURRENTS; NEOMYCIN AB This study aimed to define the acute electrophysiological effects of the perilymphatic perfusion of streptomycin in the sensory apparatus of the semicircular canals of the frog. The ampullary DC potential, the vestibular nerve multiunit discharge, the nerve DC potential and the unitary EPSP activity were recorded in isolated semicircular canals of the frog (Rana esculenta L). The results demonstrated that perilymphatic microperfusion of streptomycin (0.1, 0.3, 1 and 3 mM) reduced both resting and mechanically evoked afferent discharge, while the response of the hair cells remains unchanged. Intracellular recordings from single afferent axons showed that the reduction of the afferent discharge was mainly due to a reduction of the amplitude, but not the frequency, of the EPSPs. These results indicate that streptomycin, when applied in the fluid bathing the synaptic pole of the sensory cells, can act as an antagonist of the vestibular afferent transmitter at the postsynaptic level. C1 UNIV AUTONOMA PUEBLA,ICUAP,DEPT CIENCIAS FISIOL,14 SUR 6301 CU,APARTADO POSTAL 406,PUEBLA 72000,MEXICO. UNIV PAVIA,IST FISIOL GEN,I-27100 PAVIA,ITALY. UNIV TURIN,DIPARTIMENTO BIOL ANIM,I-10124 TURIN,ITALY. RI Soto, Enrique/C-4073-2013 CR PITTINGE.C, 1972, ANNU REV PHARMACOLOG, V12, P169, DOI 10.1146/annurev.pa.12.040172.001125 ANDERSON DJ, 1981, AMINOGLYCOSIDE OTOTO, P161 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 KROESE ABA, 1980, NATURE, V283, P395, DOI 10.1038/283395a0 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 MATSUURA S, 1968, SCIENCE, V160, P1117, DOI 10.1126/science.160.3832.1117 NOMURA K, 1990, J MEMBRANE BIOL, V115, P241, DOI 10.1007/BF01868639 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 ONODERA K, 1977, NEUROPHARMACOLOGY, V16, P171, DOI 10.1016/0028-3908(77)90092-2 PEREZ ME, 1991, BRAIN RES, V563, P221, DOI 10.1016/0006-8993(91)91537-B SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SOKABE M, 1983, P JPN ACAD B-PHYS, V59, P33, DOI 10.2183/pjab.59.33 SOTO E, 1988, BRAIN RES, V462, P104, DOI 10.1016/0006-8993(88)90591-4 SOTO E, 1991, EXCITATORY AMINO ACI, P293 SUAREZKURTZ G, 1987, PFLUG ARCH EUR J PHY, V410, P517, DOI 10.1007/BF00586535 VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 VALLI P, 1977, ACTA OTO-LARYNGOL, V84, P344, DOI 10.3109/00016487709123976 VALLI P, 1976, ACTA OTO-LARYNGOL, V81, P395, DOI 10.3109/00016487609107493 WAUD DR, 1968, J PHARMACOL EXP THER, V159, P123 WERSALL J, 1964, LIFE SCI, V3, P1151, DOI 10.1016/0024-3205(64)90132-8 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 ZUCCA G, 1982, ACTA OTO-LARYNGOL, V93, P355, DOI 10.3109/00016488209130893 NR 23 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 1992 VL 59 IS 1 BP 70 EP 74 DI 10.1016/0378-5955(92)90103-T PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600010 PM 1629049 ER PT J AU RYBAK, LP WHITWORTH, C WEBERG, A SCOTT, V AF RYBAK, LP WHITWORTH, C WEBERG, A SCOTT, V TI EFFECTS OF ORGANIC-ACIDS ON THE EDEMA OF THE STRIA VASCULARIS INDUCED BY FUROSEMIDE SO HEARING RESEARCH LA English DT Article DE STRIA VASCULARIS; ELECTRON MICROSCOPY; FUROSEMIDE; OTOTOXICITY; ORGANIC ACIDS; ENDOCOCHLEAR POTENTIAL ID MAMMALIAN ENDOLYMPH SYSTEM; THICK ASCENDING LIMB; CELL-VOLUME DENSITY; PIG INNER-EAR; ETHACRYNIC-ACID; GUINEA-PIG; LOOP DIURETICS; CHOROID-PLEXUS; POTASSIUM CONCENTRATION; TUBULAR SECRETION AB Furosemide is a loop diuretic which is ototoxic. Investigations have shown the stria vascularis to be the target tissue of this ototoxic drug. The purpose of the present study was to investigate the effects of furosemide on the stria vascularis in chinchillas, in controls and in animals pretreated with the above organic acids. Control animals were injected with 0.5 ml alkalinized saline followed by furosemide IV 30 min later. Experimental animals received probenecid, penicillin or sodium salicylate IV. Thirty minutes later, furosemide was injected in the same dose as in the controls. The basal turn of the stria vascularis was rapidly removed at various times from 10 to 30 min after furosemide administration and processed for transmission electron microscopy. Control animals were found to have reversible edema of the stria vascularis. Experimental animals had variable findings. Those animals pretreated with penicillin had virtually no edema of the stria vascularis at any time. Salicylate and probenecid pretreated animals had significantly less edema from one to 10 min after furosemide injection, but more edema than controls at later times. These findings suggest a discrepancy between ultrastructural pathology and functional status of the cochlea in experimental animals pretreated with probenecid or sodium salicylate followed by furosemide. On the other hand, good structure function correlations were seen in controls and in experimental animals pretreated with penicillin. C1 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62708. RP RYBAK, LP (reprint author), SO ILLINOIS UNIV,SCH MED,DEPT SURG,POB 19230,SPRINGFIELD,IL 62708, USA. CR ARNOLD W, 1981, ACTA OTOLARYNGOL, V91, P391 BARANY EH, 1971, ACTA PHYSIOL SCAND, V83, P220, DOI 10.1111/j.1748-1716.1971.tb05072.x BARANY EH, 1973, ACTA PHYSIOL SCAND, V88, P412, DOI 10.1111/j.1748-1716.1973.tb05470.x BECKER B, 1960, AM J OPHTHALMOL, V50, P862 BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V89, P407, DOI 10.3109/00016488009127156 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P40, DOI 10.3109/00016488009131696 BRUMMETT R, 1977, ACTA OTO-LARYNGOL, V83, P98, DOI 10.3109/00016487709128819 BRUSILOW SW, 1976, CAN J PHYSIOL PHARM, V54, P42 DEER BC, 1982, J OTOLARYNGOL, V11, P260 DUVALL AJ, 1989, ACTA OTO-LARYNGOL, V108, P397, DOI 10.3109/00016488909125545 ERNST A, 1989, J LIPID MEDIATOR, V1, P297 ERNST A, 1989, PROSTAGLANDINS, V38, P523, DOI 10.1016/0090-6980(89)90146-9 ERNST A, 1989, HEARING RES, V40, P39, DOI 10.1016/0378-5955(89)90097-X ERNST A, 1990, J LIPID MEDIATOR, V2, P33 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P409 FERRARY E, 1989, AM J PHYSIOL, V257, pF182 FISHMAN RA, 1966, ARCH NEUROL-CHICAGO, V15, P113 FORBUSH B, 1983, J BIOL CHEM, V258, P1787 Forge A, 1982, Br J Audiol, V16, P109, DOI 10.3109/03005368209081455 FORGE A, 1976, CLIN OTOLARYNGOL, V1, P211, DOI 10.1111/j.1365-2273.1976.tb00879.x GARDINER TH, 1976, J PHARMACOL EXP THER, V196, P455 GARDINER TH, 1977, GEN PHARMACOL, V8, P235, DOI 10.1016/0306-3623(77)90019-2 GOTTL KH, 1985, N-S ARCH PHARMACOL, V331, P275, DOI 10.1007/BF00634249 GREGER R, 1987, RENAL PHYSIOL BIOCH, V10, P174 GREGER R, 1985, PHYSIOL REV, V65, P760 GRINSTEIN S, 1986, J MEMBRANE BIOL, V90, P1, DOI 10.1007/BF01869680 HARA A, 1986, J ACOUST SOC AM S, V80, P76 HARA A, 1987, PRONOUNCED DIFFERENC, P25 HIRASHIMA N, 1978, ANN OTO RHINOL LARYN, V87, P32 Hommerich C P, 1990, Adv Otorhinolaryngol, V44, P92 HORI R, 1991, J PHARMACOKINET BIOP, V19, P51, DOI 10.1007/BF01062192 HUY PTB, 1986, FEB ASS RES OT CLEAR, P48 JAKUBOVICZ DE, 1987, BRAIN RES, V435, P138, DOI 10.1016/0006-8993(87)91594-0 KIM CS, 1981, BRAIN RES, V224, P209, DOI 10.1016/0006-8993(81)91135-5 KIM CS, 1983, BRAIN RES, V259, P340, DOI 10.1016/0006-8993(83)91271-4 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 LANT A, 1986, DRUGS, V31, P40 MATTHIAS R, 1984, 21 WORKSH INN EAR BI, P76 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 MICHEL O, 1987, 24TH WORKSH INN EAR, P53 MOLLER JV, 1983, PHARMACOL REV, V34, P315 MORIZONO T, 1980, ARCH OTO-RHINO-LARYN, V229, P149, DOI 10.1007/BF00454238 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 NIERENBERG DW, 1987, J PHARMACOL EXP THER, V240, P712 ODLIND B, 1979, J PHARMACOL EXP THER, V211, P238 PIKE DA, 1980, HEARING RES, V3, P79, DOI 10.1016/0378-5955(80)90009-X POLLARD TJ, 1981, ACTA OTO-LARYNGOL, V92, P249, DOI 10.3109/00016488109133261 PRITCHARD JB, 1987, BIOCHIM BIOPHYS ACTA, V906, P295, DOI 10.1016/0304-4157(87)90015-3 QUICK CA, 1975, ANN OTO RHINOL LARYN, V84, P94 QUICK CA, 1973, LARYNGOSCOPE, V83, P1469, DOI 10.1288/00005537-197309000-00007 REDDY VN, 1979, INVEST OPHTH VIS SCI, V18, P1000 RENNICK BR, 1972, ANNU REV PHARMACOLOG, V12, P141, DOI 10.1146/annurev.pa.12.040172.001041 RENNICK BR, 1981, AM J PHYSIOL, V240, pF83 ROSS CR, 1983, ANNU REV PHARMACOL, V23, P65, DOI 10.1146/annurev.pa.23.040183.000433 RUGGERO MA, 1991, J NEUROSCI, V11, P1057 RYBAK LP, 1986, ARCH OTO-RHINO-LARYN, V243, P180, DOI 10.1007/BF00470616 RYBAK LP, 1990, HEARING RES, V46, P95, DOI 10.1016/0378-5955(90)90142-C RYBAK LP, 1982, HEARING RES, V7, P223, DOI 10.1016/0378-5955(82)90015-6 RYBAK LP, 1991, ARCH OTORHINOLARYNGO, V248, P353 RYBAK LP, 1986, ANNU REV PHARMACOL, V26, P79 RYBAK LP, 1985, LARYNGOSCOPE, V95, P1, DOI 10.1288/00005537-198509010-00001 RYBAK LP, 1987, HEARING RES, V26, P89, DOI 10.1016/0378-5955(87)90037-2 RYBAK LP, 1984, J PHARMACOL EXP THER, V230, P706 RYBAK LP, 1991, LARYNGOSCOPE, V101, P1167 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 SANTI PA, 1985, HEARING RES, V18, P283, DOI 10.1016/0378-5955(85)90045-0 SCHLATTER E, 1983, PFLUG ARCH EUR J PHY, V396, P210, DOI 10.1007/BF00587857 SCHROTT A, 1989, HEARING RES, V42, P17, DOI 10.1016/0378-5955(89)90114-7 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 SOLIS JM, 1990, J NEUROSCI RES, V26, P159, DOI 10.1002/jnr.490260205 SPECTOR R, 1990, PHARMACOLOGY, V40, P1, DOI 10.1159/000138632 STONE RA, 1979, INVEST OPHTH VIS SCI, V18, P807 SUZUKI H, 1987, J PHARMACOL EXP THER, V243, P1147 SYKA J, 1985, HEARING RES, V20, P267, DOI 10.1016/0378-5955(85)90031-0 WALLIN JD, 1978, J PHARMACOL EXP THER, V205, P471 WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 NR 78 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 APR PY 1992 VL 59 IS 1 BP 75 EP 84 DI 10.1016/0378-5955(92)90104-U PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600011 PM 1629050 ER PT J AU SIEGEL, JH AF SIEGEL, JH TI SPONTANEOUS SYNAPTIC POTENTIALS FROM AFFERENT TERMINALS IN THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE SYNAPTIC TRANSMISSION; INNER HAIR CELL; SPONTANEOUS ACTIVITY ID AUDITORY-NERVE FIBERS; SERIAL SECTION RECONSTRUCTION; OUTER HAIR-CELLS; SENSORY EPITHELIUM; EFFERENT SYNAPSES; VESTIBULAR NERVE; RIBBON SYNAPSES; FINE-STRUCTURE; NEURAL POLES; CAT COCHLEA AB Records of spontaneous activity from units likely to be radial afferents were analyzed to find the origin of spontaneous action potentials in single auditory nerve fibers. Single synaptic events (excitatory postsynaptic potentials or EPSPs) nearly all triggered action potentials (spikes). An abrupt increase in slope during the rising phase of the EPSP often signalled the initiation of an action potential. Synaptic potentials that did not trigger spikes occurred frequently during the refractory period. These events sometimes appeared to be composed of subunits. Refractoriness appears to be the primary reason these EPSPs were ineffective. Distributions of the onset slopes of postsynaptic potentials were highly skewed. Skewing was not a consequence of refractoriness, but most likely because the amplitude distribution of spontaneous potentials is not gaussian. C1 NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL,EVANSTON,IL 60208. RP SIEGEL, JH (reprint author), NORTHWESTERN UNIV,DEPT COMMUN SCI & DISORDERS,EVANSTON,IL 60208, USA. CR ADLER EM, 1991, J NEUROSCI, V11, P1496 ANNONI JM, 1984, J NEUROSCI, V4, P2106 BAIRD RA, 1988, J NEUROPHYSIOL, V60, P182 BLAKELEY AGH, 1979, J PHYSIOL-LONDON, V296, P85 COOMBS JS, 1955, J PHYSIOL-LONDON, V130, P374 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 CURTIS DR, 1959, J PHYSIOL-LONDON, V145, P529 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 FAVRE D, 1986, BRAIN RES, V384, P379, DOI 10.1016/0006-8993(86)91176-5 FLOCK A, 1973, BASIC MECHANISMS HEA, P273 FURUKAWA T, 1978, J COMP NEUROL, V180, P807, DOI 10.1002/cne.901800411 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 FURUKAWA T, 1985, AUDITORY BIOCH, P31 GEISLER CD, 1981, BRAIN RES, V212, P198, DOI 10.1016/0006-8993(81)90051-2 GINZBERG RD, 1984, HEARING RES, V14, P109, DOI 10.1016/0378-5955(84)90011-X HASHIMOTO S, 1990, ACTA OTO-LARYNGOL, V109, P228, DOI 10.3109/00016489009107438 HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 KRIEBEL ME, 1974, J GEN PHYSIOL, V64, P85, DOI 10.1085/jgp.64.1.85 KUNO M, 1971, J PHYSIOL-LONDON, V213, P545 KUNO M, 1974, SYNAPTIC TRANSMISSIO, P79 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1990, J COMP NEUROL, V301, P443, DOI 10.1002/cne.903010309 MANDELL JW, 1990, NEURON, V5, P19, DOI 10.1016/0896-6273(90)90030-J McLachlan E M, 1978, Int Rev Physiol, V17, P49 MCLACHLAN EM, 1975, J PHYSIOL-LONDON, V245, P447 NADOL JB, 1983, LARYNGOSCOPE, V93, P599 NADOL JB, 1983, LARYNGOSCOPE, V93, P780 ROSSI ML, 1989, J GEN PHYSIOL, V94, P303, DOI 10.1085/jgp.94.2.303 ROSSI ML, 1977, BRAIN RES, V135, P67, DOI 10.1016/0006-8993(77)91052-6 RUSSELL I, 1986, AUDITORY FREQUENCY S, P199 SAIDEL WM, 1983, J MORPHOL, V177, P301, DOI 10.1002/jmor.1051770307 SAITO K, 1980, J ULTRA MOL STRUCT R, V71, P222, DOI 10.1016/S0022-5320(80)90108-2 SAITO K, 1984, CELL TISSUE RES, V238, P437 SCARFONE E, 1988, J NEUROSCI, V8, P4640 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 SEWELL WF, 1990, HEARING RES, V44, P71, DOI 10.1016/0378-5955(90)90023-I SIEGEL JH, 1990, J ELECTRON MICR TECH, V15, P197, DOI 10.1002/jemt.1060150302 SIEGEL JH, 1987, NEUR ABST, V13, P540 SIEGEL JH, 1986, HEARING RES, V22, P245, DOI 10.1016/0378-5955(86)90101-2 SIEGEL JH, 1986, ASS RES OT ABSTR, V9, P60 SIEGEL JH, 1987, HEARING RES, V28, P131, DOI 10.1016/0378-5955(87)90044-X SMITH CA, 1961, ANN OTO RHINOL LARYN, V70, P504 SOBKOWICZ HM, 1982, J NEUROSCI, V2, P942 Spoendlin H, 1966, ADV OTORHINOLARYNGOL, V13, P1 TREMBLAY JP, 1983, BRAIN RES REV, V6, P299, DOI 10.1016/0165-0173(83)90009-7 YAMAGUCHI K, 1990, J PHYSIOL-LONDON, V420, P185 NR 46 TC 48 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 APR PY 1992 VL 59 IS 1 BP 85 EP 92 DI 10.1016/0378-5955(92)90105-V PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600012 PM 1629051 ER PT J AU WONG, ML YOUNG, JS NILAVER, G MORTON, JI TRUNE, DR AF WONG, ML YOUNG, JS NILAVER, G MORTON, JI TRUNE, DR TI COCHLEAR IGG IN THE C3H LPR AUTOIMMUNE STRAIN MOUSE SO HEARING RESEARCH LA English DT Article DE AUTOIMMUNE DISEASE; MOUSE; INNER EAR; IMMUNOGLOBULIN G; LPR GENE ID SENSORINEURAL HEARING-LOSS; SYSTEMIC LUPUS-ERYTHEMATOSUS; INNER-EAR; MENIERES-DISEASE; COGAN SYNDROME; WEGENERS GRANULOMATOSIS; TEMPORAL BONE; MANIFESTATIONS; DEAFNESS; LESIONS AB The inner ear of the C3H/lpr autoimmune strain mouse was evaluated to identify potential mechanisms by which systemic autoimmune disease interferes with auditory function. The inner ears were immunohistochemically stained for IgG at ages before (2 months) and after (6-10 months) autoimmune disease onset and compared to age-matched nonautoimmune C3H/HeJ controls. Immunoreactivity for IgG was not seen in the 2 month C3H/lpr autoimmune mice or in either age group of the C3H/HeJ controls. On the other hand, all older C3H/lpr mice showed reaction product in the vessels of the cochlea, particularly the stria vascularis and bony capsule. Less frequent sites of staining were the geniculate ganglion, marrow cavities of the bony capsule, tensor tympani muscle, and on one occasion, a hair cell of the organ of Corti. These findings indicate that IgG is widespread within the cochlea and its vessels during systemic autoimmune disease and not directed against any specific sensorineural structure. This suggests a generalized or indirect mechanism whereby such systemic disease affects the inner ear. C1 OREGON HLTH SCI UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,OREGON HEARING RES CTR,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED,DIV ARTHRIT & RHEUMAT DIS,PORTLAND,OR 97201. CR ARNOLD W, 1980, ACTA OTO-LARYNGOL, V89, P330, DOI 10.3109/00016488009127145 ARNOLD W, 1984, ANN OTO RHINOL LARYN, V93, P119 BICKNELL JM, 1978, NEUROLOGY, V28, P278 BOWMAN CA, 1986, OTOLARYNG HEAD NECK, V94, P197 BROOKES GB, 1986, ARCH OTOLARYNGOL, V112, P536 BROOKES GB, 1985, J ROY SOC MED, V78, P47 CALONIUS IH, 1980, J LARYNGOL OTOL, V94, P649, DOI 10.1017/S0022215100089362 CODY DTR, 1971, LARYNGOSCOPE, V81, P1208, DOI 10.1288/00005537-197108000-00004 COMERFOR.FR, 1968, LAB INVEST, V19, P643 DJUPESLA.G, 1974, ARCH OTOLARYNGOL, V99, P218 GUSSEN R, 1977, ARCH OTO-RHINO-LARYN, V217, P263, DOI 10.1007/BF00465544 HARRIS JP, 1984, ANN OTO RHINOL LARYN, V93, P157 HARRIS JP, 1990, LARYNGOSCOPE, V100, P516 HARRIS JP, 1987, LARYNGOSCOPE, V97, P63 HAYNES BF, 1980, MEDICINE, V59, P426 HERTLER CK, 1990, OTOLARYNG HEAD NECK, V103, P713 Hughes G B, 1988, Laryngoscope, V98, P251 HUGHES GB, 1983, OTOLARYNG HEAD NECK, V91, P24 HUGHES GB, 1984, LARYNGOSCOPE, V94, P758 HUGHES GB, 1983, LARYNGOSCOPE, V93, P410 Jenkins H A, 1981, Am J Otolaryngol, V2, P99, DOI 10.1016/S0196-0709(81)80026-9 Kanzaki J, 1983, Acta Otolaryngol Suppl, V393, P77 LEONE CA, 1984, ANN OTO RHINOL LARYN, V93, P208 MCCABE BF, 1979, ANN OTO RHINOL LARYN, V88, P585 MCDONALD TJ, 1978, LARYNGOSCOPE, V88, P38 MCMENOMEY SO, 1992, IN PRESS OTOLARYNGOL MCNEIL NF, 1952, ANN INTERN MED, V37, P1253 MORGAN GJ, 1984, AM J OTOLARYNG, V5, P258 Murphy E. D., 1978, Genetic control of autoimmune disease. Proceedings of the workshop on the genetic control of autoimmune disease held in Bloomfield Hills, Michigan, USA, on July 10-12, 1978., P207 MURPHY ED, 1981, IMMUNOLOGIC DEFECTS, V2, P143 Peitersen E, 1966, Acta Otolaryngol, V61, P189, DOI 10.3109/00016486609127055 QUICK CA, 1973, LARYNGOSCOPE, V83, P1469, DOI 10.1288/00005537-197309000-00007 RAREY KE, 1986, AM J OTOLARYNG, V4, P387 STEPHENS SDG, 1982, AUDIOLOGY, V21, P128 TAKAHASHI M, 1988, LARYNGOSCOPE, V98, P1133 THEOFILOPOULOS AN, 1980, CLIN IMMUNOL IMMUNOP, V15, P258, DOI 10.1016/0090-1229(80)90039-2 THEOFILOPOULOS AN, 1985, ADV IMMUNOL, V37, P269, DOI 10.1016/S0065-2776(08)60342-9 TRUNE DR, 1990, HEARING RES, V48, P241, DOI 10.1016/0378-5955(90)90064-V TRUNE DR, 1992, IN PRESS AM J OTOLAR TRUNE DR, 1989, HEARING RES, V38, P57, DOI 10.1016/0378-5955(89)90128-7 VELDMAN JE, 1984, LARYNGOSCOPE, V94, P501, DOI 10.1288/00005537-198404000-00014 WILLIAMS LL, 1987, ARCH OTOLARYNGOL, V113, P397 WOLFF D, 1965, ANN OTO RHINOL LARYN, V74, P507 WOLFF SM, 1974, ANN INTERN MED, V81, P513 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, P28 YOON TH, 1989, LARYNGOSCOPE, V99, P600 YOUNG JS, 1988, DISTRIBUTION IGG INN, P225 NR 49 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 APR PY 1992 VL 59 IS 1 BP 93 EP 100 DI 10.1016/0378-5955(92)90106-W PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600013 PM 1629052 ER PT J AU FAY, RR AF FAY, RR TI ANALYTIC LISTENING BY THE GOLDFISH SO HEARING RESEARCH LA English DT Article DE HEARING; GOLDFISH; ANALYTIC LISTENING; FREQUENCY ANALYSIS; PSYCHOPHYSICS ID CARASSIUS-AURATUS; FREQUENCY AB A stimulus generalization paradigm was used with classical respiratory conditioning to study analytic listening in the goldfish. Animals were first conditioned to suppress respiration upon the presentation of a long-duration complex sound comprised of two sinusoidal components, 166 and 724 Hz. Conditioned animals were then presented with a set of eight novel test tones with frequencies between 95 and 1514 Hz, and including 166 and 724 Hz. Response magnitudes were greatest at the frequencies of the components making up the complex to which the animals were initially conditioned. This is a demonstration that the goldfish had acquired independent information about the frequencies of the individual sinusoidal components making up a complex sound. and thus had listened to the complex analytically. To my knowledge, this is the first demonstration of simultaneous frequency analysis and analytic listening by a nonhuman animal, and suggests that this fundamental aspect of human hearing may be a primitive character shared with the fishes and perhaps with all living vertebrates. C1 LOYOLA UNIV,DEPT PSYCHOL,CHICAGO,IL 60626. RP FAY, RR (reprint author), LOYOLA UNIV,PARMLY HEARING INST,6525 N SHERIDAN RD,CHICAGO,IL 60626, USA. CR Bregman AS., 1990, AUDITORY SCENE ANAL BURNS EM, 1982, J ACOUST SOC AM, V72, P1394, DOI 10.1121/1.388445 COOMBS S, 1989, J ACOUST SOC AM, V86, P925, DOI 10.1121/1.398727 FAY RR, 1972, J ACOUST SOC AM, V52, P660, DOI 10.1121/1.1913155 Fay R. R., 1988, HEARING VERTEBRATES Fay R. R., 1969, 605 US NAV SUBM MED, P1 FAY RR, 1970, J EXP ANAL BEHAV, V14, P353, DOI 10.1901/jeab.1970.14-353 FAY R, 1969, J AUD RES, V9, P112 FAY RR, 1970, J COMP PHYSIOL PSYCH, V73, P175, DOI 10.1037/h0030245 FAY RR, 1992, IN PRESS EFFECTS TEM FREED DJ, 1990, J ACOUST SOC AM, V87, P311, DOI 10.1121/1.399298 Hartmann W. M., 1988, AUDITORY FUNCTION, P623 Malott R. W., 1970, ANIMAL PSYCHOPHYSICS, P363 NELSON DA, 1989, SCIENCE, V244, P976, DOI 10.1126/science.2727689 NR 14 TC 29 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 APR PY 1992 VL 59 IS 1 BP 101 EP 107 DI 10.1016/0378-5955(92)90107-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600014 PM 1629039 ER PT J AU KELLEY, MW OCHIAI, CK CORWIN, JT AF KELLEY, MW OCHIAI, CK CORWIN, JT TI MATURATION OF KINOCILIA IN AMPHIBIAN HAIR-CELLS - GROWTH AND SHORTENING RELATED TO KINOCILIARY BULB FORMATION SO HEARING RESEARCH LA English DT Article DE CILIA; MICROTUBULES; DEVELOPMENT; POLARITY; TRASDUCTION ID INNER-EAR; ACTIN-FILAMENTS; BIRD COCHLEA; BULLFROG; ULTRASTRUCTURE; STEREOCILIA; INJECTION; DYNAMICS AB New hair cells are added to the amphibian sacculus throughout life, primarily at its outer edge. The stereociliary bundles near that edge are heterogeneous, but eventually develop the more homogeneous morphology of the overwhelming majority of mature cells near the center of the epithelium. During their development the kinocilium grows and a kinociliary bulb forms. It has been proposed that initial elongation of the kinocilium is followed by shortening, and that the bulb may form during shortening. To test those hypotheses, amphibian sacculi were examined by scanning electron microscopy and the length of the kinocilium, the width of the kinociliary bulb, and the length of the tallest stereocilia were measured for 159 hair cells. The length of the tallest stereocilia on each hair cell was used as an indicator of the relative maturity of that cell, so that changes in the structure of each cell's kinocilium could be related to that cell's stage of development. Results indicate that initial elongation of the kinocilium is followed by shortening. Kinociliary bulbs first appear and increase in volume as shortening proceeds. These findings support the hypotheses. Models are proposed to explain how the formation of the bulb could result from depolymerization of apical cytoskeletal elements, and how kinocilium growth and shortening may contribute to hair bundle reorientation in the developing ear. C1 UNIV VIRGINIA, DEPT NEUROSCI, CHARLOTTESVILLE, VA 22908 USA. RP KELLEY, MW (reprint author), UNIV VIRGINIA, SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,BOX 396, COBB HALL, ROOM 1057, CHARLOTTESVILLE, VA 22908 USA. CR BAIRD RA, 1986, BRAIN RES, V369, P48, DOI 10.1016/0006-8993(86)90512-3 CAVALIER.T, 1974, J CELL SCI, V16, P529 CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 CORWIN JT, 1985, P NATL ACAD SCI USA, V82, P3911, DOI 10.1073/pnas.82.11.3911 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 DENTLER WL, 1977, J CELL BIOL, V74, P747, DOI 10.1083/jcb.74.3.747 DENTLER WL, 1989, CILIARY FLAGELLAR ME, P31 DENTLER WL, 1987, INT REV CYTOL, P391 FURUKAWA T, 1978, J COMP NEUROL, V180, P807, DOI 10.1002/cne.901800411 Kikuchi K, 1965, Acta Otolaryngol, V60, P207, DOI 10.3109/00016486509127003 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 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 KELLOGG K, 1989, SPAZ SOC-SPACE SOC, V12, P80 Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 LEWIS ER, 1975, BRAIN RES, V83, P35, DOI 10.1016/0006-8993(75)90856-2 LEWIS ER, 1982, SCIENCE, V215, P1641, DOI 10.1126/science.6978525 LEWIS ER, 1973, J MORPHOL, V139, P351, DOI 10.1002/jmor.1051390305 LEWIS ER, 1976, BRAIN BEHAV EVOLUT, V13, P196, DOI 10.1159/000123810 LEWIS ER, 1981, BRAIN RES, V219, P149, DOI 10.1016/0006-8993(81)90274-2 PORTMAN RW, 1987, J CELL SCI, V87, P85 SAMMAK PJ, 1988, NATURE, V332, P724, DOI 10.1038/332724a0 SCHULZE E, 1987, J CELL BIOL, V104, P277, DOI 10.1083/jcb.104.2.277 SCHULZE E, 1988, NATURE, V334, P356, DOI 10.1038/334356a0 SHORT G, 1991, BIOL BULL, V180, P466, DOI 10.2307/1542347 SOKOLOWSKI BHA, 1987, J MORPHOL, V194, P323, DOI 10.1002/jmor.1051940311 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 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 NR 30 TC 14 Z9 14 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 APR PY 1992 VL 59 IS 1 BP 108 EP 115 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HN566 UT WOS:A1992HN56600015 PM 1629040 ER PT J AU CHAMBERS, RD AF CHAMBERS, RD TI DIFFERENTIAL AGE EFFECTS FOR COMPONENTS OF THE ADULT AUDITORY MIDDLE LATENCY RESPONSE SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED RESPONSE; MIDDLE LATENCY RESPONSE; AGE-RELATED; RETICULAR ACTIVATING SYSTEM ID AVERAGED ELECTROENCEPHALIC RESPONSE; CONSTANT LEVEL CLICKS; BRAIN-STEM RESPONSE; EVOKED-RESPONSES; BINAURAL INTERACTION; POTENTIALS; SLEEP; VERTEX AB The middle latency components of the auditory evoked response were obtained from a young (20-24 years of age) and an older (51 to 71 years of age) group of normal-hearing, healthy female subjects. Recording procedures and stimulus repetition rates were chosen to promote the resolution of both Pa and Pb. The absolute and peak-to-peak amplitudes of Pa and Pb were significantly larger for the older subjects at all stimulus rates. An amplitude reduction of Pb with increasing stimulus rate was much more pronounced for the young than for the older subjects. This, combined with a shorter latency for Pb in the older subjects, may have contributed to partial and/or complete fusion of Pa and Pb observed in 10 of the 17 older subjects. An apparent positive shift in the response baseline for older subjects also may have contributed to the age-related amplitude effects. RP CHAMBERS, RD (reprint author), UNIV ILLINOIS,DEPT SPEECH & HEARING SCI,901 S 6TH ST,CHAMPAIGN,IL 61820, USA. CR BRENT G, 1977, PSYCHOPHYSIOLOGY, V14, P96 BUCHWALD JS, 1991, ELECTROEN CLIN NEURO, V80, P303, DOI 10.1016/0168-5597(91)90114-D BUCHWALD JS, 1989, ELECTROEN CLIN NEURO, V74, P378, DOI 10.1016/0168-5597(89)90005-1 BUCHWALD JS, 1988, NEUROSCI ABST, V14, P771 BUCHWALD JS, 1981, BRAIN RES, V205, P91, DOI 10.1016/0006-8993(81)90722-8 CHAMBERS RD, 1991, HEARING RES, V51, P1, DOI 10.1016/0378-5955(91)90002-Q CHEN BM, 1986, ELECTROEN CLIN NEURO, V65, P373, DOI 10.1016/0168-5597(86)90016-X DICKINSON L, 1986, NEUR ABSTR, V12, P1130 DOBIE RA, 1980, ELECTROEN CLIN NEURO, V49, P303, DOI 10.1016/0013-4694(80)90224-2 DRECHSLER F, 1978, J NEUROL, V218, P197, DOI 10.1007/BF00313013 DUSTMAN RE, 1966, SCIENCE, V151, P1013, DOI 10.1126/science.151.3713.1013 DUSTMAN RE, 1969, ELECTROEN CLIN NEURO, V26, P2, DOI 10.1016/0013-4694(69)90028-5 ERWIN R, 1986, ELECTROEN CLIN NEURO, V65, P383, DOI 10.1016/0168-5597(86)90017-1 ERWIN RJ, 1986, ELECTROEN CLIN NEURO, V64, P417, DOI 10.1016/0013-4694(86)90075-1 Ford J. M., 1985, ADV PSYCHOPHYSIOLOGY, V1, P301 FORD JM, 1980, AGING 1980S PSYCHOL, P115, DOI 10.1037/10050-008 HEFFLEY E, 1985, NEUROBEH TOXICOL TER, V7, P399 HINMAN CL, 1983, BRAIN RES, V264, P57, DOI 10.1016/0006-8993(83)91120-4 HOOD LJ, 1990, HEARING RES, V45, P115, DOI 10.1016/0378-5955(90)90187-T HYDE ML, 1985, AUDITORY BRAINSTEM R, P133 JERGER J, 1988, Seminars in Hearing, V9, P75, DOI 10.1055/s-0028-1085653 JERGER J, 1980, ARCH OTOLARYNGOL, V106, P387 KELLYBALLWEBER D, 1984, AUDIOLOGY, V23, P181 KILENY P, 1983, ELECTROEN CLIN NEURO, V55, P268, DOI 10.1016/0013-4694(83)90204-3 KLEIN AJ, 1983, ARCH OTOLARYNGOL, V109, P6 KRAUS N, 1982, ELECTROEN CLIN NEURO, V54, P275, DOI 10.1016/0013-4694(82)90177-8 LUDERS H, 1970, ELECTROEN CLIN NEURO, V29, P450, DOI 10.1016/0013-4694(70)90062-3 MCFARLAND WH, 1977, J SPEECH HEAR RES, V20, P781 MENDEL MI, 1974, AUDIOLOGY, V13, P23 MENDEL MI, 1971, J SPEECH HEAR RES, V14, P829 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 OZDAMAR O, 1983, AUDIOLOGY, V22, P34 PFEFFERBAUM A, 1979, ELECTROEN CLIN NEURO, V46, P81, DOI 10.1016/0013-4694(79)90052-X PFEFFERBAUM A, 1980, ELECTROEN CLIN NEURO, V49, P266, DOI 10.1016/0013-4694(80)90221-7 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 ROWE JW, 1987, SCIENCE, V237, P143, DOI 10.1126/science.3299702 Scheibel ME, 1975, AGING, V1, P11 Shallop J K, 1983, Adv Otorhinolaryngol, V29, P124 Smith D.B.D., 1980, AGING 80S, P135, DOI 10.1037/10050-010 SMITH DBD, 1978, 11TH INT C GER TOK WOODS DL, 1986, ELECTROEN CLIN NEURO, V65, P297, DOI 10.1016/0168-5597(86)90008-0 NR 41 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 MAR PY 1992 VL 58 IS 2 BP 123 EP 131 DI 10.1016/0378-5955(92)90122-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600001 PM 1568935 ER PT J AU RICE, JJ MAY, BJ SPIROU, GA YOUNG, ED AF RICE, JJ MAY, BJ SPIROU, GA YOUNG, ED TI PINNA-BASED SPECTRAL CUES FOR SOUND LOCALIZATION IN CAT SO HEARING RESEARCH LA English DT Article DE SOUND LOCALIZATION; PINNA; MONAURAL SPECTRAL CUES; CAT ID PRIMARY AUDITORY-CORTEX; HORIZONTAL PLANE; MEDIAN PLANE; EXTERNAL EAR; MONAURAL LOCALIZATION; PRESSURE TRANSFORMATION; INFERIOR COLLICULUS; SUPERIOR COLLICULUS; GUINEA-PIG; FREE-FIELD AB The directional dependence of the transfer function from free field plane waves to a point near the tympanic membrane (TM) was measured in anesthetized domestic cats. A probe tube microphone was placed almost-equal-to 3 mm from the TM from beneath the head in order to keep the pinna intact. Transfer functions were computed as the ratio of the spectrum of a click recorded near the TM to the spectrum of the click in freefield. We analyze the transfer functions in three frequency ranges: low frequencies (< 5 kHz) where interaural level differences vary smoothly with azimuth; midfrequencies (5-18 kHz) where a prominent spectral notch is observed; and high frequencies (> 18 kHz) where the transfer functions vary greatly with source location. Because no two source directions produce the same transfer function, the spectrum of a broadband sound at the TM could serve as a sound localization cue for both elevation and azimuth. In particular, we show that source direction is uniquely determined, for source directions in front of the cat, from the frequencies of the midfrequency spectral notches in the two ears. The validity of the transfer functions as measures of the acoustic input to the auditory system is considered in terms of models of sound propagation in the ear canal. C1 JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,DEPT OTOLARYNGOL HEAD & NECK SURG,BALTIMORE,MD 21205. RP RICE, JJ (reprint author), JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,DEPT BIOMED ENGN,ROOM 505 TRAYLOR BLDG,BALTIMORE,MD 21205, USA. CR AITKIN L, 1990, HEARING RES, V50, P97, DOI 10.1016/0378-5955(90)90036-O AITKIN LM, 1987, J NEUROPHYSIOL, V57, P1185 BATTEAU DW, 1967, PROC R SOC SER B-BIO, V168, P158, DOI 10.1098/rspb.1967.0058 BELENDIUK K, 1975, J ACOUST SOC AM, V58, P701, DOI 10.1121/1.380717 BLAUERT J, 1969, ACUSTICA, V22, P205 Blauert J., 1983, SPATIAL HEARING BUTLER RA, 1980, PERCEPT PSYCHOPHYS, V28, P449, DOI 10.3758/BF03204889 CALFORD MB, 1984, HEARING RES, V14, P13, DOI 10.1016/0378-5955(84)90064-9 CARLILE S, 1990, J ACOUST SOC AM, V88, P2180, DOI 10.1121/1.400115 CARLILE S, 1987, HEARING RES, V31, P111, DOI 10.1016/0378-5955(87)90117-1 CARLILE S, 1990, J ACOUST SOC AM, V88, P2196, DOI 10.1121/1.400116 CASSEDAY JH, 1973, J ACOUST SOC AM, V54, P365, DOI 10.1121/1.1913586 Crouch JE, 1969, TEXT ATLAS CAT ANATO GARDNER MB, 1973, J ACOUST SOC AM, V53, P400, DOI 10.1121/1.1913336 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 HEBRANK J, 1974, J ACOUST SOC AM, V56, P935, DOI 10.1121/1.1903351 HEBRANK J, 1974, J ACOUST SOC AM, V56, P1829, DOI 10.1121/1.1903520 IRVINE DRF, 1987, HEARING RES, V26, P267, DOI 10.1016/0378-5955(87)90063-3 JEN PHS, 1988, HEARING RES, V34, P101, DOI 10.1016/0378-5955(88)90098-6 JENKINS WM, 1984, J NEUROPHYSIOL, V52, P819 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 KHANNA SM, 1986, 12TH P INT C AC Kuhn GF, 1987, DIRECTIONAL HEARING, P3 MARTIN RL, 1987, HEARING RES, V30, P239, DOI 10.1016/0378-5955(87)90140-7 MIDDLEBROOKS JC, 1989, J ACOUST SOC AM, V86, P89, DOI 10.1121/1.398224 MIDDLEBROOKS JC, 1981, J NEUROSCI, V1, P107 MIDDLEBROOKS JC, 1987, J NEUROPHYSIOL, V57, P672 Mills A. W., 1972, FOUNDATIONS MODERN A, V2, P303 MUSICANT AD, 1985, J ACOUST SOC AM S, V77, pS94, DOI 10.1121/1.2022605 MUSICANT AD, 1990, J ACOUST SOC AM, V87, P757, DOI 10.1121/1.399545 MUSICANT AD, 1985, J ACOUST SOC AM, V77, P202, DOI 10.1121/1.392259 MUSICANT AD, 1984, J ACOUST SOC AM, V75, P1195, DOI 10.1121/1.390770 MUSICANT AD, 1984, HEARING RES, V14, P185, DOI 10.1016/0378-5955(84)90017-0 NETI C, 1990, THESIS J HOPKINS U B PALMER AR, 1985, HEARING RES, V17, P267, DOI 10.1016/0378-5955(85)90071-1 PHILLIPS DP, 1982, HEARING RES, V8, P13, DOI 10.1016/0378-5955(82)90031-4 RABBITT RD, 1988, J ACOUST SOC AM, V83, P1064, DOI 10.1121/1.396051 ROFFLER SK, 1968, J ACOUST SOC AM, V43, P1255, DOI 10.1121/1.1910976 ROSOWSKI JJ, 1988, J ACOUST SOC AM, V84, P1695, DOI 10.1121/1.397185 SEARLE C L, 1973, Journal of the Acoustical Society of America, V54, P308, DOI 10.1121/1.1978213 SEARLE CL, 1975, J ACOUST SOC AM, V57, P448, DOI 10.1121/1.380442 SHAW EAG, 1974, J ACOUST SOC AM, V56, P1848, DOI 10.1121/1.1903522 SHAW EAG, 1968, J ACOUST SOC AM, V44, P240, DOI 10.1121/1.1911059 SHAW EAG, 1972, J ACOUST SOC AM, V51, P150, DOI 10.1121/1.1981568 SOKOLICH WG, 1977, J ACOUST SOC AM, V62, pS12, DOI 10.1121/1.2016024 SUN XD, 1987, HEARING RES, V27, P207 THOMPSON GC, 1978, J NEUROPHYSIOL, V41, P1183 THURLOW WR, 1967, J ACOUST SOC AM, V42, P480, DOI 10.1121/1.1910604 WIENER FM, 1966, ACTA OTOLARYNGOL, V61, P225 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P858, DOI 10.1121/1.397557 WIGHTMAN FL, 1987, DIRECTIONAL HEARING, P26 YOUNG E D, 1990, Society for Neuroscience Abstracts, V16, P875 NR 52 TC 182 Z9 183 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 1992 VL 58 IS 2 BP 132 EP 152 DI 10.1016/0378-5955(92)90123-5 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600002 PM 1568936 ER PT J AU GHOSHAL, S KIM, DO NORTHROP, RB AF GHOSHAL, S KIM, DO NORTHROP, RB TI AMPLITUDE-MODULATED TONE ENCODING BEHAVIOR OF COCHLEAR NUCLEUS NEURONS - MODELING STUDY SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS; NEURAL MODEL; AMPLITUDE MODULATION; SIGNAL ENCODING ID PHYSIOLOGICAL-RESPONSE PROPERTIES; HORSERADISH-PEROXIDASE; CELLS; CAT; FREQUENCY; SLICES AB A recent study of amplitude-modulated (AM) tone encoding behavior of dorsal and posteroventral cochlear nucleus (DCN and PVCN) neurons by Kim et al. [Hear. Res. 45, 95-113, 1990] observed that certain neurons (e.g., pause/build type-III neurons and chop-S neurons) tended to exhibit band-pass modulation transfer functions (MTFs) and intrinsic oscillations (IOs) whereas certain other neurons (e.g., chop-T neurons) tended to exhibit low-pass MTFs and no IOs. The goal of the present study was to develop models of these response characteristics in an attempt to understand the underlying neuronal mechanisms. We hypothesized that chopper neurons corresponded to stellate cells and pause/build neurons corresponded to fusiform cells. We also hypothesized that, with right input combination, appropriate models of a single stellate and fusiform cell could account for band-pass and low-pass MTFs as well as the associated IOs. The neuron models developed by Arle and Kim [Biol. Cybern. 64, 273-283, 1991] for the stellate and fusiform cells were used in this study. The models are modified versions of MacGregor type neuron model incorporating cell-specific nonlinear voltage-dependent conductances. The AM tone excitation via the auditory nerve fibers was represented by a current at the soma of the neuron model, which consisted of dc, ac and a zero-mean Gaussian noise. The dc, ac and noise represent a high-frequency carrier beyond the neuron's phase-locking limit, an envelope, and randomness of the system, respectively. With systematic variation of dc, ac and noise amplitudes, we observed the following: the band-pass MTF behaviors of pause/build and chop-S neurons were reproduced by the fusiform cell model and the stellate cell model with a strong dc/noise ratio, respectively. The low-pass MTF behavior of a chop-T neuron was reproduced by the stellate cell model with a weak dc/noise ratio. It was observed that the stellate cell model was more susceptible to the noise, in the sense that an increase in noise tended to abolish the IO and change the MTF of the model from band-pass to low-pass more readily in the stellate cell model than in the fusiform cell model. Kim et al. (1990) observed a close correlation between the IO frequency and the best envelope frequency (BEF). In the models, a similar correlation was observed between the two measures for both the stellate and fusiform cell models. The present results support the hypothesis that intrinsic cellular mechanisms of fusiform and stellate cells similar to those postulated in these cell models underlie the observed MTF behavior of CN neurons in response to AM tone stimuli. C1 UNIV CONNECTICUT,CTR HLTH,CTR NEUROL SCI,SURG RES CTR,DIV OTOLARYNGOL,BIOENGN PROGRAM,FARMINGTON,CT 06030. CR ARLE JE, 1991, BIOL CYBERN, V64, P273, DOI 10.1007/BF00199590 BRACHMAN ML, 1980, ISRS19 I SENS RES SP Cooper G. R., 1967, METHODS SIGNAL SYSTE DEVROYE L, 1986, NONUNIFORM RANDOM VA, P379 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 GHOSHAL S, 1991, 17TH P ANN IEEE NE B, P5 GHOSHAL S, 1990, Society for Neuroscience Abstracts, V16, P871 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P535 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KIM DO, 1992, UNPUB HEAR RES MacGregor R, 1987, NEURAL BRAIN MODELIN 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 OERTEL D, 1983, J NEUROSCI, V3, P2043 RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 TEICH MC, 1979, J ACOUST SOC AM, V66, P1738, DOI 10.1121/1.383647 VATER M, 1982, J COMP PHYSIOL, V149, P369 WU SH, 1984, J NEUROSCI, V4, P1577 Young E. D., 1988, AUDITORY FUNCTION NE, P277 NR 24 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 1992 VL 58 IS 2 BP 153 EP 165 DI 10.1016/0378-5955(92)90124-6 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600003 PM 1568937 ER PT J AU FECHTER, LD CLERICI, WJ YAO, L HOEFFDING, V AF FECHTER, LD CLERICI, WJ YAO, L HOEFFDING, V TI RAPID DISRUPTION OF COCHLEAR FUNCTION AND STRUCTURE BY TRIMETHYLTIN IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE OTOTOXICITY; TRIMETHYLTIN; COCHLEA; ENDOCOCHLEAR POTENTIAL; COMPOUND ACTION POTENTIAL; COCHLEAR MICROPHONIC ID INTOXICATION; INJURY; RAT; EXPOSURE; PROTEIN AB Trimethyltin (TMT) is a potent ototoxicant which acutely disrupts generation of the action potential evoked by a broad range of tone frequencies and subsequently produces selective high frequency impairment and outer hair cell (OHC) damage in the extreme basal turn of the cochlea. We investigated the development of TMT ototoxicity in the guinea pig 6-48 h following treatment using the compound action potential (CAP), cochlear microphonic (CM), endocochlear potential (EP) and light and electron microscopic examinations. At all time intervals studied, TMT reduced CAP sensitivity and CM amplitude. The effect was relatively broad across test frequencies at 6 h and subsequently became restricted to higher frequencies. No disruption of the EP was observed between 6 and 24 h following TMT. OHC pathology in the basal turn of the cochlea 12 h following TMT consisted of vacuolization in the supranuclear region and disruption of the cuticular plate; some mitochondria exhibited dark inclusions. Type 1 spiral ganglion cells appeared swollen at 24 h with separation of myelin from the cell bodies. No pathological changes were observed in the inner hair cells (IHC). The present data identify the OHC as targets responsible for the loss of CM sensitivity after TMT as the EP was unaffected. These data suggest that CAP and CM recovery at low and middle frequencies following acute TMT administration is accompanied by recovery of neurotransmission at the IHC or Type 1 SGC level and OHC recovery at apical regions of the cochlea. C1 JOHNS HOPKINS MED INST,DEPT PHARM & ALLIED HLTH PROFESS,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT OTOLARYNGOL HEAD & NECK SURG,BALTIMORE,MD 21205. CR ALDRIDGE WN, 1981, ANALYST, V106, P60, DOI 10.1039/an9810600060 BOULDIN TW, 1984, J NEUROPATH EXP NEUR, V43, P162, DOI 10.1097/00005072-198403000-00006 BOULDIN TW, 1981, AM J PATHOL, V104, P237 BROCK TO, 1987, J NEUROSCI, V7, P931 BROWN AW, 1979, AM J PATHOL, V97, P59 CHANG LW, 1982, ENVIRON RES, V29, P445, DOI 10.1016/0013-9351(82)90045-7 CLERICI WJ, 1991, TOXICOL APPL PHARM, V109, P547, DOI 10.1016/0041-008X(91)90017-9 COSTA LG, 1986, TOXICOL APPL PHARM, V86, P189, DOI 10.1016/0041-008X(86)90049-9 CROFTON KM, 1990, TOXICOL APPL PHARM, V105, P123, DOI 10.1016/0041-008X(90)90364-Z FECHTER LD, 1990, TOXICOL APPL PHARM, V105, P133, DOI 10.1016/0041-008X(90)90365-2 FECHTER LD, 1986, HEARING RES, V23, P275, DOI 10.1016/0378-5955(86)90116-4 HOEFFDING V, 1991, NEUROTOXICOL TERATOL, V13, P135, DOI 10.1016/0892-0362(91)90003-F HOEFFDING V, 1990, TOXICOLOGIST, V10, P109 PETERS A, 1972, J COMP NEUROL, V144, P253, DOI 10.1002/cne.901440302 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 TOEWS AD, 1986, BRAIN RES, V393, P298 TOEWS AD, 1988, NEUROCHEM PATHOL, V8, P63 YOUNG JS, 1986, TOXICOL APPL PHARM, V82, P87, DOI 10.1016/0041-008X(86)90441-2 NR 18 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 MAR PY 1992 VL 58 IS 2 BP 166 EP 174 DI 10.1016/0378-5955(92)90125-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600004 PM 1568938 ER PT J AU BRUNDIN, L FLOCK, B FLOCK, A AF BRUNDIN, L FLOCK, B FLOCK, A TI SOUND INDUCED DISPLACEMENT RESPONSE OF THE GUINEA-PIG HEARING ORGAN AND ITS RELATION TO THE COCHLEAR POTENTIALS SO HEARING RESEARCH LA English DT Article DE COCHLEA; OUTER HAIR CELL; MOTILITY; TUNING; HEARING ID OUTER HAIR-CELLS; MAMMALIAN COCHLEA AB The sound induced motion of the cells within the fourth turn of the guinea pig organ of Corti was studied in an in vitro preparation (Ulfendahl et al. 1989). The cells were visualised by relief microscopy, achieved by an oblique illumination technique. The motion of the sensory cells was observed during the recording of the extracellular receptor potentials; the cochlear microphonics (CM) and the summating potential (SP). Our results show that the temporal bone preparation sustains an endocochlear potential and maintains the receptor potentials for 3-4 h. During the tone stimulus the outer hair cells were seen to elongate and the surface of the organ of Corti was displaced in the direction of scala vestibuli. The displacement response showed two frequency maxima, one at 150 and one at 300 Hz. The mechanical tuning of the sensory organ coincided with the tuning of the receptor potentials. Both the mechanical and the electrical responses at the 300 Hz peak were vulnerable to the administration of methylene blue suggesting cyclic GMP dependence, whereas the 150 Hz peak was unaffected. We conclude that the outer hair cells provide active tuning in the organ of Corti. RP BRUNDIN, L (reprint author), KAROLINSKA INST,DEPT PHYSIOL 2,BOX 60400,S-10401 STOCKHOLM 60,SWEDEN. CR Adrian E. D., 1931, J PHYSL, V71 Bekesy G., 1960, EXPT HEARING VONBEKESY G, 1952, J ACOUST SOC AM, V24, P72 BRUNDIN L, 1991, NEUROSCI LETT, V128, P77, DOI 10.1016/0304-3940(91)90763-J BRUNDIN L, 1991, UNPUB TUNED DISPLACE BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DAVIS H, 1950, P NATL ACAD SCI USA, V36, P580, DOI 10.1073/pnas.36.10.580 HARRIS GG, 1969, J ACOUST SOC AM, V45, P300, DOI 10.1121/1.1971325 HONRUBIA VH, 1969, J ACOUST SOC AM, V45, P1443, DOI 10.1121/1.1911622 JOHNSTON.BM, 1972, Q REV BIOPHYS, V5, P1 KHANNA SM, 1990, COCHLEAR MECHANISMS, V7, P13 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 LEPAGE EL, 1987, J ACOUST SOC AM, V82, P139, DOI 10.1121/1.395557 MITTAL CK, 1982, HDB EXPT PHARM, V58, P225 Murad F, 1978, Adv Cyclic Nucleotide Res, V9, P145 PANTIN CFA, 1946, NOTES MICROSCOPICA 2, P54 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 STEIVE H, 1986, MOL MECHANISMS PHOTO ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 Wever EG, 1930, P NATL ACAD SCI USA, V16, P344, DOI 10.1073/pnas.16.5.344 NR 23 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 MAR PY 1992 VL 58 IS 2 BP 175 EP 184 DI 10.1016/0378-5955(92)90126-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600005 PM 1568939 ER PT J AU LEFEBVRE, PP WEBER, T RIGO, JM STAECKER, H MOONEN, G VANDEWATER, TR AF LEFEBVRE, PP WEBER, T RIGO, JM STAECKER, H MOONEN, G VANDEWATER, TR TI PERIPHERAL AND CENTRAL TARGET-DERIVED TROPHIC FACTOR(S) EFFECTS ON AUDITORY NEURONS SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; ASTROCYTES; NEURONOTROPHIC EFFECTS; CONDITIONED MEDIUM ID NERVE GROWTH-FACTOR; INNER-EAR; COCHLEAR IMPLANTATION; RAT; GANGLION; DEGENERATION; POPULATIONS; ASTROCYTES; CULTURE; CHICK AB In the developing inner ear, a naturally occurring programmed cell death of cochleovestibular ganglion (CVG) neurons as well as peripheral and central target-derived trophic effects on survival of embryonic CVG neurons are known. To further analyze these target derived trophic interactions, spiral ganglion explants obtained from 5 day postpartum (P5) rat pups were cultured with an intact organ of Corti and in the absence of Corti's organ. Both neuronal survival and neurite extension were influenced by the presence of this peripheral target tissue. Local destruction of Corti's organ caused both neuritic retraction and neuronal cell death to occur in a corresponding portion of the spiral ganglion. This peripheral target-derived neurotrophic effect may be mediated by a diffusible factor(s) since organ of Corti conditioned medium also had a neurotrophic effect on the survival of auditory neurons in cell cultures of dissociated spiral ganglia from P5 rat pups. A component of central target tissue, i.e. astrocytes, was also shown to release a diffusible factor(s) that supported the survival of dissociated P5 rat spiral ganglion neurons. The neurotrophic effects on the in vitro survival of spiral ganglion neurons by both of these conditioned medium factors were concentration dependent. C1 STATE UNIV LIEGE,DEPT HUMAN PHYSIOL,B-4000 LIEGE,BELGIUM. STATE UNIV LIEGE,DEPT PATHOPHYSIOL,B-4000 LIEGE,BELGIUM. STATE UNIV LIEGE,DEPT OTORHINOLARYNGOL,B-4000 LIEGE,BELGIUM. STATE UNIV LIEGE,DEPT AUDIOPHONOL,B-4000 LIEGE,BELGIUM. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,INST COMMUN DISORDERS,BRONX,NY 10461. RI Rigo, Jean-Michel/E-3456-2010 CR ABE H, 1991, ACTA OTO-LARYNGOL, V111, P691, DOI 10.3109/00016489109138401 APPEL SH, 1981, ANN NEUROL, V10, P499, DOI 10.1002/ana.410100602 ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 ARD MD, 1984, INT J DEV NEUROSCI, V2, P535, DOI 10.1016/0736-5748(84)90031-5 BICHLER E, 1983, ARCH OTO-RHINO-LARYN, V237, P201, DOI 10.1007/BF00453725 BOTTENSTEIN JE, 1979, P NATL ACAD SCI USA, V76, P514, DOI 10.1073/pnas.76.1.514 DAMICOMARTEL A, 1983, AM J ANAT, V166, P445, DOI 10.1002/aja.1001660406 DESPRES G, 1988, NEUROSCI LETT, V85, P5, DOI 10.1016/0304-3940(88)90418-1 FERRARA N, 1988, BRAIN RES, V462, P223, DOI 10.1016/0006-8993(88)90550-1 GUILD STACY R., 1931, ACTA OTO LARYNGOL, V15, P269, DOI 10.3109/00016483109119096 KOITCHEV K, 1984, ACTA OTOLARYNGOL STO, V94, P431 LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEFEBVRE PP, 1991, ACTA OTO-LARYNGOL, V111, P304, DOI 10.3109/00016489109137392 LEVIMONTALCINI R, 1987, SCIENCE, V237, P1154, DOI 10.1126/science.3306916 Lindsay R M, 1985, J Cell Sci Suppl, V3, P115 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PATEL AJ, 1989, NEUROSCI LETT, V99, P223, DOI 10.1016/0304-3940(89)90294-2 SCHMIDT JM, 1985, ACTA OTO-LARYNGOL, V99, P14, DOI 10.3109/00016488509119140 SPOENDLI.H, 1971, ARCH KLIN EXP OHR, V200, P275, DOI 10.1007/BF00373310 SUTTON D, 1980, ANN OTOL RHINOL LA S, V89, P1 THOENEN H, 1980, PHYSIOL REV, V60, P1284 VANDEWATER TR, 1984, ANN OTO RHINOL LARYN, V93, P558 VANDEWATER TR, 1983, ACTA OTO-LARYNGOL, V95, P470, DOI 10.3109/00016488309139431 Varon S, 1980, Curr Top Dev Biol, V16, P207 WALSH SM, 1982, HEARING RES, V7, P281, DOI 10.1016/0378-5955(82)90041-7 WILKIN GP, 1990, TRENDS NEUROSCI, V13, P43, DOI 10.1016/0166-2236(90)90065-I ZHOU XN, 1987, ACTA OTO-LARYNGOL, V104, P90, DOI 10.3109/00016488709109052 NR 27 TC 48 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 1992 VL 58 IS 2 BP 185 EP 192 DI 10.1016/0378-5955(92)90127-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600006 PM 1568940 ER PT J AU MCLAMB, WT PARK, JC AF MCLAMB, WT PARK, JC TI CHOLINESTERASE ACTIVITY IN VESTIBULAR ORGANS OF YOUNG AND OLD MICE SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINESTERASE; BUTYRYLCHOLINESTERASE; VESTIBULAR; AGE-RELATED; MICE; INNER EAR ID ACETYLCHOLINESTERASE; DEGENERATION; BUTYRYLCHOLINESTERASE; COCHLEA; SYSTEM; MOUSE; AGE AB The activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were studied by histochemical methods in the semicircular canal end organs, the utricle and the saccule of young and old mice. AChE was located on the plasma membrane of efferent nerve terminals beneath vestibular hair cells, and along the basement membrane. In the ampulla, stained efferent terminals were more prevalent on the slopes of the crista than in the central region. In all organs examined, there were no discernible differences in AChE activity between young and old mice. BChE activity was observed in the epithelial light cells and supporting cells of the saccule, utricle, and ampulla. Its distribution was similar in both young and old mice in the ampulla, but decreased significantly with age in the utricle. Preliminary data suggest that BChE activity is also weak in old saccular supporting cells. Unlike the utricle, old saccular light cells retained intense BChE activity. C1 FLORIDA INST TECHNOL,DEPT BIOL SCI,150 W UNIV BLVD,MELBOURNE,FL 32901. CR ADLER M, 1990, FEBS LETT, V267, P107, DOI 10.1016/0014-5793(90)80300-8 ATACK JR, 1987, J NEUROCHEM, V48, P1687, DOI 10.1111/j.1471-4159.1987.tb05724.x CHUBB IW, 1983, NEUROSCIENCE, V10, P1369, DOI 10.1016/0306-4522(83)90118-5 COHEN GM, 1990, J ELECTRON MICR TECH, V15, P165, DOI 10.1002/jemt.1060150208 COHEN GM, 1992, UNPUB AGE RELATED CH COHEN GM, 1987, HEARING RES, V28, P57, DOI 10.1016/0378-5955(87)90153-5 DOHLMAN GF, 1964, ANN OTO RHINOL LARYN, V73, P708 EMMERLING MR, 1990, J ELECTRON MICR TECH, V15, P123, DOI 10.1002/jemt.1060150205 GACEK R R, 1965, Acta Otolaryngol, V59, P541, DOI 10.3109/00016486509124585 GREENFIELD SA, 1984, EXP BRAIN RES, V54, P513 HARADA Y, 1985, ACTA OTO-LARYNGOL, V99, P411, DOI 10.3109/00016488509108932 HEDREEN JC, 1985, J HISTOCHEM CYTOCHEM, V33, P134 HILDING D, 1962, Acta Otolaryngol, V55, P205, DOI 10.3109/00016486209127354 Iurato S, 1971, Acta Otolaryngol Suppl, V279, P1 IURATO S, 1972, BRAIN RES, V37, P429 IURATO S, 1971, ACTA OTO-LARYNGOL, V71, P147, DOI 10.3109/00016487109125343 KARNOVSKY MJ, 1964, J HISTOCHEM CYTOCHEM, V12, P219 KIMURA R, 1964, Acta Otolaryngol, V57, P517, DOI 10.3109/00016486409137114 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 MCMARTIN DN, 1979, MECH AGEING DEV, V10, P241, DOI 10.1016/0047-6374(79)90038-1 MESROBIAN RJO, 1987, ARCH OTOLARYNGOL, V113, P543 NOMURA Y, 1965, ARCHIV OTOLARYNGOL, V81, P335 PARK JC, 1987, HEARING RES, V28, P87, DOI 10.1016/0378-5955(87)90156-0 PARK J C, 1987, Society for Neuroscience Abstracts, V13, P1261 ROSSI G, 1961, Acta Otolaryngol Suppl, V170, P1 SIRVIO J, 1988, EXP GERONTOL, V23, P473, DOI 10.1016/0531-5565(88)90059-9 SMITH DO, 1982, J NEUROPHYSIOL, V48, P100 SOBKOWICZ HM, 1989, J NEUROCYTOL, V18, P209, DOI 10.1007/BF01206663 VAUGHAN DW, 1990, EXP NEUROL, V109, P224, DOI 10.1016/0014-4886(90)90077-6 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 MAR PY 1992 VL 58 IS 2 BP 193 EP 199 DI 10.1016/0378-5955(92)90128-A PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600007 PM 1568941 ER PT J AU DABAK, AG JOHNSON, DH AF DABAK, AG JOHNSON, DH TI FUNCTION-BASED MODELING OF BINAURAL PROCESSING - INTERAURAL PHASE SO HEARING RESEARCH LA English DT Article DE BINAURAL PROCESSING; MEDIAL SUPERIOR OLIVE; FUNCTION-BASED MODELING ID BRAIN-STEM; DISCRIMINATION; ORGANIZATION; FIBERS; CAT AB The intent of function-based modeling is to predict from theoretical considerations the input/output characteristics of a neuron if it were to perform a specific signal processing task within a sensory system. In this study, the sensory task is localization within the horizontal plane of a sustained low-frequency tone using interaural phase cue's alone. The stimulus is assumed to be represented by primary-like discharge patterns from each ear. These patterns serve as the input to a system whose task is to extract the information needed to determine azimuthal angle. The optimal system resembles the classic Jeffress model, but differs from it in important details. In particular, the Jeffress model is shown to be a sub-optimal approximation in that it ignores the characteristic frequency of the inputs. The physical realization of either model by a structure resembling currently known MSO anatomy and innervation is discussed. C1 RICE UNIV,INST COMP & INFORMAT TECHNOL,DEPT ELECT & COMP ENGN,HOUSTON,TX 77251. CR BOUDREAU JC, 1968, J NEUROPHYSIOL, V31, P422 Bourk TR, 1976, THESIS MIT CAMBRIDGE BROWNELL WE, 1975, BRAIN RES, V94, P413, DOI 10.1016/0006-8993(75)90226-7 CARR CE, 1988, P NATL ACAD SCI USA, V85, P8311, DOI 10.1073/pnas.85.21.8311 COLBURN HS, 1973, J ACOUST SOC AM, V54, P1458, DOI 10.1121/1.1914445 Colburn HS, 1978, HDB PERCEPTION, VIV, P467 DABAK AG, 1990, FUNCTION BASED MODEL GOLDBERG JAY M., 1968, J NEUROPHYSIOL, V31, P639 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GREEN DM, 1970, INTRO HEARING, P200 GUINAN JJ, 1972, INT J NEUROSCI, V4, P147 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 JOHNSON DH, 1976, BIOPHYS J, V16, P719 Johnson D.H., 1974, THESIS MIT CAMBRIDGE JOHNSON DH, 1990, HEARING RES, V49, P301, DOI 10.1016/0378-5955(90)90110-B JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 KIANG NYS, 1975, NERVOUS SYSTEM, V3, P81 Kiang NY-s, 1965, DISCHARGE PATTERNS S KUHN GF, 1977, J ACOUST SOC AM, V62 Kuhn GF, 1987, DIRECTIONAL HEARING, P3 Licklider J. C. R., 1959, PSYCHOL STUDY SCI, P41 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 ROTH GL, 1980, J ACOUST SOC AM, V68, P1643, DOI 10.1121/1.385196 RZHEVKIN SN, 1963, THEORY SOUND SHAMMA SA, 1989, J ACOUST SOC AM, V86, P989, DOI 10.1121/1.398734 SIEBERT WM, 1968, RECOGNIZING PATTERNS SIEBERT WM, 1970, PR INST ELECTR ELECT, V58, P723, DOI 10.1109/PROC.1970.7727 Snyder D. L., 1975, RANDOM POINT PROCESS STOTLER WA, 1953, J COMP NEUROL, V98, P401, DOI 10.1002/cne.900980303 van Noort J, 1969, STRUCTURE CONNECTION VanTrees H, 1968, DETECTION ESTIMATI 1 WARR WB, 1966, EXP NEUROL, V14, P453, DOI 10.1016/0014-4886(66)90130-0 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 YOUNG SR, 1983, J NEUROSCI, V3, P1373 NR 35 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 MAR PY 1992 VL 58 IS 2 BP 200 EP 212 DI 10.1016/0378-5955(92)90129-B PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600008 PM 1568942 ER PT J AU MCANALLY, KI CALFORD, MB AF MCANALLY, KI CALFORD, MB TI COHERENCE OF FREQUENCY-MODULATION IS ENCODED BY COCHLEAR-GENERATED DISTORTION SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; FREQUENCY MODULATION; COHERENCE; DISTORTION PRODUCTS; COCHLEAR MICROPHONIC ID TONES; PHASE; ENHANCEMENT; PERCEPTION; RESPONSES; CAT AB Nonlinearities of the peripheral auditory system generate distortion products which present to the central auditory system as apparent acoustic stimuli. The frequency and amplitude of distortion products reflect the frequency, phase and amplitude relationship of the components of a complex stimulus. When the stimulus consists of harmonically-related primaries, the amplitudes of the major distortion products are a function of the relative phase of the presented (primary) tones. We have previously shown (McAnally and Calford, 1990) that the variation of amplitude of the distortion as a function of the relative phase of a pair of harmonically-related primaries is well modelled as a function of the interaction of the multiple modes of distortion which fall at the same frequency (e.g. difference frequency and cubic difference frequency). A possibility raised by this result is that coherence of frequency modulation (that which maintains harmonicity) could be encoded in the amplitude of distortion. This was examined in measurements of both the cochlear microphonic potential (CM) and the responses of auditory nerve fibres in anaesthetized cats. Very small deviations from coherence of frequency modulation produced changes in the amplitude of the CM potential at the frequency of distortion. Also the discharges of auditory nerve fibres tuned to the frequency of distortion were found to be modulated at the same frequency as the amplitude changes observed in the CM. There was no variation in distortion amplitude in the CM and no modulation of auditory nerve discharges when primaries were frequency modulated coherently. It is suggested that amplitude modulation of distortion gives the auditory system its demonstrated sensitivity to minor departures from coherence of frequency-modulated, harmonically-related tones. RI Calford, Mike/B-4637-2009 OI Calford, Mike/0000-0002-5727-0234 CR Batschelet E, 1981, CIRCULAR STATISTICS BUUNEN TJF, 1977, J ACOUST SOC AM, V61, P508, DOI 10.1121/1.381292 CALFORD MB, 1984, HEARING RES, V14, P13, DOI 10.1016/0378-5955(84)90064-9 CARLYON RP, 1991, J ACOUST SOC AM, V89, P329, DOI 10.1121/1.400468 Dallos P, 1973, AUDITORY PERIPHERY Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 GARDNER RB, 1986, PERCEPT PSYCHOPHYS, V40, P183, DOI 10.3758/BF03203015 HALL JL, 1972, J ACOUST SOC AM, V51, P1872, DOI 10.1121/1.1913046 HORNER K, 1983, HEARING RES, V11, P343, DOI 10.1016/0378-5955(83)90066-7 HORST JW, 1985, J ACOUST SOC AM, V78, P1898, DOI 10.1121/1.392779 HORST JW, 1986, PERIPHERAL AUDITORY, P298 HORST JW, 1986, AUDITORY FREQUENCY S, P229 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 KUBOVY M, 1979, J ACOUST SOC AM, V66, P100, DOI 10.1121/1.383061 MCADAMS S, 1984, THESIS STANFORD MCADAMS S, 1989, J ACOUST SOC AM, V86, P2148, DOI 10.1121/1.398475 MCANALLY KI, 1989, HEARING RES, V41, P237, DOI 10.1016/0378-5955(89)90015-4 MCANALLY KI, 1990, HEARING RES, V44, P51, DOI 10.1016/0378-5955(90)90021-G RASCH RA, 1978, ACUSTICA, V40, P21 RHODE WS, 1976, TEST SIGNIFICANCE ME SCHROEDER MR, 1975, P IEEE, V63, P1332, DOI 10.1109/PROC.1975.9941 SCHWARTZ M, 1959, INFORMATION TRANSMIS Shower EG, 1931, J ACOUST SOC AM, V3, P275, DOI 10.1121/1.1915561 WIT HP, 1986, HEARING RES, V21, P59, DOI 10.1016/0378-5955(86)90046-8 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 MAR PY 1992 VL 58 IS 2 BP 213 EP 220 DI 10.1016/0378-5955(92)90130-F PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600009 PM 1568943 ER PT J AU DOI, K KITANO, I MORI, N AF DOI, K KITANO, I MORI, N TI ADENYLATE-CYCLASE MODULATION OF ENDOCOCHLEAR POTENTIAL DURING SUPPRESSION OF STRIAL NA+-K+ ATPASE SO HEARING RESEARCH LA English DT Article DE ADENYLATE CYCLASE; FORSKOLIN; NA+-K+ ATPASE; OUABAIN; ENDOCOCHLEAR POTENTIAL; K+-SELECTIVE MICROELECTRODE ID INNER-EAR; COCHLEAR POTENTIALS; GUINEA-PIG; MOUSE; LOCALIZATION; VASCULARIS; OUABAIN AB Forskolin, an adenylate cyclase activator, produces a reversible elevation of the endocochlear potential (EP) (Doi et al., 1990a). To determine whether strial Na+-K+ ATPase activity is essential for the forskolin-dependent EP elevation, we examined, by means of K+-selective microelectrodes, the effects of forskolin on the EP and the endolymphatic K+ activity ([K+]) while strial Na+-K+ ATPase was suppressed by ouabain. Perilymphatic perfusion with ouabain (10(-3) M) decreased the EP from 78.5 +/- 2.4 mV to -27.6 +/- 2.4 mV (N = 8) at 37.9 +/- 3.7 min after the start of perfusion and decreased the [K+] from 138.7 +/- 5.4 mM to 103.7 +/- 3.7 mM (N = 3). Successive perfusion with forskolin (2 X 10(-4) M) with ouabain (10(-3) M) increased the EP by 15.1 +/- 1.5 mV (N = 8) but did not influence the [K+] decrease from 101 +/- 3.6 mM to 95 +/- 1.3 mM (N = 3). Forskolin (2 X 10(-4) M) with ouabain (10-(-3) M) without a preceding ouabain perfusion decreased the EP from 76.2 +/- 2.3 mV to -12.9 +/- 1.8 mV (N = 6) at 65.3 +/- 2.1 min after the start of perfusion. These results indicate that adenylate cyclase can modulate the EP in the absence of strial Na+-K+ ATPase activity and that adenylate cyclase activation can attenuate the EP drop induced by strial Na+-K+ ATPase suppression. C1 OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,SUITA,OSAKA 565,JAPAN. NARA MED SCH,DEPT OTOLARYNGOL,NARA,JAPAN. KAGAWA UNIV,SCH MED,DEPT OTOLARYNGOL,TAKAMATSU,KAGAWA 760,JAPAN. CR AHLSTROM P, 1975, LARYNGOSCOPE, V85, P1241, DOI 10.1288/00005537-197507000-00016 ARAKAWA E, 1987, HEARING RES, V31, P1, DOI 10.1016/0378-5955(87)90209-7 BAGGERSJOBACK D, 1980, ARCH OTO-RHINO-LARYN, V228, P217, DOI 10.1007/BF00454231 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 BUTLER RA, 1963, J ACOUST SOC AM, V35, P1188, DOI 10.1121/1.1918672 DAVIS H, 1958, AM J PHYSIOL, V195, P251 DOI K, 1990, Society for Neuroscience Abstracts, V16, P872 DOI K, 1990, HEARING RES, V45, P157, DOI 10.1016/0378-5955(90)90192-R DOI K, 1991, ABSTR ASS RES OT, P107 JOHNSTONE BM, 1981, MENIERES DISEASE PAT, P44 KOCH T, 1988, ARCH OTO-RHINO-LARYN, V245, P82, DOI 10.1007/BF00481441 KONISHI T, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P176, DOI 10.3109/00016487809124734 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P359, DOI 10.1007/BF00588214 KUROKAWA S, 1965, JAP J OTOL TOKYO, V68, P1177 MARCUS DC, 1981, HEARING RES, V4, P149, DOI 10.1016/0378-5955(81)90002-2 MEES K, 1984, ARCH OTO-RHINO-LARYN, V240, P55, DOI 10.1007/BF00464345 MORI H, 1985, HEARING RES, V17, P227, DOI 10.1016/0378-5955(85)90067-X PRAZMA J, 1978, AM J PHYSIOL, V235, pF317 SCHACHT J, 1985, HEARING RES, V20, P9, DOI 10.1016/0378-5955(85)90053-X SCHOMIG A, 1990, J CARDIOVASC PHARM, V16, P5105 STEINER AL, 1972, J BIOL CHEM, V247, P1121 STERKERS O, 1984, AM J PHYSIOL, V246, pF47 TASAKI I, 1954, J ACOUST SOC AM, V26, P765, DOI 10.1121/1.1907415 THALMANN I, 1982, J ACOUST SOC AM, V71, P599 ZAJIC G, 1983, HEARING RES, V10, P249, DOI 10.1016/0378-5955(83)90090-4 NR 26 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 1992 VL 58 IS 2 BP 221 EP 226 DI 10.1016/0378-5955(92)90131-6 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600010 PM 1314796 ER PT J AU SMURZYNSKI, J KIM, DO AF SMURZYNSKI, J KIM, DO TI DISTORTION-PRODUCT AND CLICK-EVOKED OTOACOUSTIC EMISSIONS OF NORMALLY-HEARING ADULTS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; COCHLEAR MECHANICS; HUMAN EAR; DISTORTION PRODUCT; CLICK ID OTO-ACOUSTIC EMISSIONS; HUMAN EAR; COCHLEAR MECHANICS; SUPPRESSION; BEHAVIOR; PRESSURE; ORIGIN; ECHOES AB The purpose of this study was to compare distortion-product otoacoustic emissions (DPOEs) and click-evoked otoacoustic emissions (CEOEs) for normally-hearing human adults. The statistical analysis consisted of computing the DPOE and CEOE levels versus frequency corresponding to the 10th, 25th, 50th, 75th, and 90th percentiles among normal adult ears. The mean and standard deviations of the DPOEs and CEOEs were computed. A direct comparison of the DPOE and CEOE data obtained from the same ears showed that, in a 1-4 kHz frequency region, there was a statistically significant correlation between the levels of the two types of otoacoustic emissions. This finding supports the hypothesis that DPOEs and CEOEs arise from some common mechanisms of the cochlea such as active nonlinear biomechanical mechanisms of the outer hair cells. C1 UNIV CONNECTICUT,CTR HLTH,DEPT SURG,DIV OTOLARYNGOL,263 FARMINGTON AVE,FARMINGTON,CT 06030. UNIV CONNECTICUT,CTR HLTH,CTR NEUROL SCI,FARMINGTON,CT 06030. UNIV CONNECTICUT,CTR HLTH,SURG RES CTR,FARMINGTON,CT 06030. CR BONFILS P, 1988, AUDIOLOGY, V27, P27 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 JOHNSEN NJ, 1982, SCAND AUDIOL, V11, P3, DOI 10.3109/01050398209076194 JOHNSEN NJ, 1988, SCAND AUDIOL, V17, P27, DOI 10.3109/01050398809042177 KEMP DT, 1980, HEARING RES, V2, P533, DOI 10.1016/0378-5955(80)90091-X Kemp D T, 1986, Scand Audiol Suppl, V25, P71 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, 1990, EAR HEARING, V11, P93 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 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 KIM DO, 1992, NOISE INDUCED HEARIN, P98 KIMBERLEY BP, 1989, J OTOLARYNGOL, V18, P365 LAFRENIERE D, 1991, ARCH OTOLARYNGOL, V117, P1382 LEONARD G, 1990, ADV AUDIOL, V7, P139 LIND O, 1990, J OTOLARYNGOL, V19, P252 LONG GR, 1986, PERIPHERAL AUDITORY, P213 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P3 LONSBURYMARTIN BL, 1991, ASS RES OT ABSTR, V14, P67 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1990, ANN OTO RHINOL LARYN, V99, P30 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 ROHLF FJ, 1981, STATISTICAL TABLES SMURZYNSKI J, 1990, ARCH OTOLARYNGOL, V116, P1309 SPEKTOR Z, 1991, LARYNGOSCOPE, V101, P965 WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 WIT HP, 1981, J ACOUST SOC AM, V70, P437, DOI 10.1121/1.386786 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 NR 33 TC 70 Z9 73 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 1992 VL 58 IS 2 BP 227 EP 240 DI 10.1016/0378-5955(92)90132-7 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HH086 UT WOS:A1992HH08600011 PM 1568944 ER PT J AU COHEN, YE RUBIN, DM SAUNDERS, JC AF COHEN, YE RUBIN, DM SAUNDERS, JC TI MIDDLE-EAR DEVELOPMENT .1. EXTRA-STAPEDIUS RESPONSE IN THE NEONATAL CHICK SO HEARING RESEARCH LA English DT Article DE EXTRA-STAPEDIUS, MIDDLE-EAR, DEVELOPMENT; CHICK ID TYMPANIC MEMBRANE; DIRECTIONAL HEARING; FREQUENCY-RESPONSE; BASILAR PAPILLA; HAIR-CELLS; INNER-EAR; ADMITTANCE; HAMSTER; VIBRATIONS; MODEL AB A laser interferometry system was used to study the ontogeny of tympanic membrane mechanical responses to sound as measured at the tip of the extra-stapedius (ES) in chicks. The ES velocity and phase responses in the frequency range between 0.2 and 10.0 kHz were measured in animals ranging from 3 days of age to adult. The slope of the low frequency response remained constant with age while the ES low frequency sensitivity increased by 11 dB. The sensitivity improvement indicated an increase in low frequency middle-ear admittance. However, there was no consistent developmental improvement in high frequency ES sensitivity. Comparisons between the growth of low frequency ES velocity, the development of admittance magnitude, and evoked potential threshold sensitivity developmental data indicated no clear relation between these measures. C1 UNIV PENN,DEPT OTOLARYNGOL HEAD & NECK SURG,PHILADELPHIA,PA 19104. RP COHEN, YE (reprint author), UNIV PENN,DEPT BIOENGN,5 SILVERSTEIN ORL,3400 SPRUCE ST,PHILADELPHIA,PA 19104, USA. CR ADLER HJ, 1991, IN PRESS ACTA OTOLAR BOCK GR, 1978, AUDIOLOGY, V17, P193 BOCK GR, 1977, SCIENCE, V197, P396, DOI 10.1126/science.877565 BUNNEN TJF, 1981, J ACOUST SOC AM, V69, P744 CHANDLER JP, 1984, J COMP NEUROL, V222, P523, DOI 10.1002/cne.902220406 COHEN YC, 1991, IN PRESS J MORPHOL COLES RB, 1980, J EXP BIOL, V86, P153 DECRAEMER WF, 1989, HEARING RES, V38, P1, DOI 10.1016/0378-5955(89)90123-8 DECRAEMER WF, 1990, HEARING RES, V47, P200 FERMIN CD, 1984, ACTA OTO-LARYNGOL, V97, P39, DOI 10.3109/00016488409130963 FUNNELL WRJ, 1987, J ACOUST SOC AM, V81, P1851, DOI 10.1121/1.394749 Gaudin E P, 1968, Acta Otolaryngol, V65, P316, DOI 10.3109/00016486809120971 Gottlieb G., 1971, BIOPSYCHOLOGY DEV, P67 GRAY L, 1981, J COMP PHYSIOL PSYCH, V95, P188, DOI 10.1037/h0077750 GUINAN JJ, 1967, J ACOUST SOC AM, V51, P1904 GUMMER AW, 1989, HEARING RES, V39, P1, DOI 10.1016/0378-5955(89)90077-4 KONISHI M, 1973, P NATL ACAD SCI USA, V70, P1795, DOI 10.1073/pnas.70.6.1795 MANLEY GA, 1972, NATURE, V237, P112, DOI 10.1038/237112a0 MCFADDEN EA, 1987, HEARING RES, V30, P197 MOFFAT AJM, 1978, J COMP PHYSIOL, V127, P97 MOLLER AR, 1963, J ACOUST SOC AM, V35, P1526, DOI 10.1121/1.1918742 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 RACICZ ME, 1990, J ACOUST SOC AM S, V87, P101 REBILLARD G, 1981, BRAIN RES, V229, P15, DOI 10.1016/0006-8993(81)90741-1 RELKIN EM, 1979, J ACOUST SOC AM, V66, P133, DOI 10.1121/1.383066 RELKIN EM, 1980, ACTA OTO-LARYNGOL, V90, P6, DOI 10.3109/00016488009131692 ROSOWSKI JJ, 1984, HEARING RES, V1, P205 ROSOWSKI JJ, 1980, J COMP PHYSIOL, V136, P183 ROSOWSKI JJ, 1985, HEARING RES, V20, P139, DOI 10.1016/0378-5955(85)90165-0 ROSOWSKI JJ, 1988, J ACOUST SOC AM, V84, P1695, DOI 10.1121/1.397185 RUBEL EW, 1984, ANNU REV PHYSIOL, V46, P213 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 SAUNDERS JC, 1972, ACTA OTO-LARYNGOL, V73, P353, DOI 10.3109/00016487209138952 SAUNDERS JC, 1986, HEARING RES, V24, P227, DOI 10.1016/0378-5955(86)90021-3 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SAUNDERS JC, 1985, HEARING RES, V18, P253, DOI 10.1016/0378-5955(85)90042-5 SAUNDERS JC, 1974, MIN OTO, V24, P221 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 Vanzulli A., 1963, ACTA NEUROL LATINOAM, V9, P19 VLAMING MSMG, 1984, HEARING RES, V14, P191, DOI 10.1016/0378-5955(84)90018-2 ZWILLENBERG D, 1981, OTOLARYNG HEAD NECK, V89, P856 NR 41 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 FEB PY 1992 VL 58 IS 1 BP 1 EP 8 DI 10.1016/0378-5955(92)90002-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300001 PM 1559899 ER PT J AU FAY, RR REAM, TJ AF FAY, RR REAM, TJ TI THE EFFECTS OF TEMPERATURE-CHANGE AND TRANSIENT HYPOXIA ON AUDITORY-NERVE FIBER RESPONSE IN THE GOLDFISH (CARASSIUS-AURATUS) SO HEARING RESEARCH LA English DT Article DE HEARING; GOLDFISH; AUDITORY NERVE FIBERS; TEMPERATURE; HYPOXIA ID HAIR-CELLS; FREQUENCY; SACCULUS; MODEL AB Temperature change and hypoxia produce consistent, reversible effects on the response of single auditory nerve fibers in the goldfish. Cooling and hypoxia produce reductions of a cell's spontaneous activity, sensitivity, most excitatory or best frequency (BF) at a given signal level, and overall responsiveness to acoustic stimulation. Warming above ambient temperatures increases a cell's spontaneous activity, sensitivity, BF, and responsiveness. Adaptation, or the tendency for responsiveness to decline with time during a stimulus, increases during hypoxia and cooling, and decreases during warming. The effects of temperature change and hypoxia on a fiber's BF are similar to the effects of overall sound level. Since BF normally increases with sound level, the BF-shift with temperature change and hypoxia can be understood as a change in sensitivity or the overall effectiveness of a stimulus at a given sound level. The effects on neural response of temperature change and hypoxia are probably due in part to changes in the release and replenishment of neurotransmitter at the synapses between hair cells and auditory nerve fibers. C1 LOYOLA UNIV,PARMLY HEARING INST,CHICAGO,IL 60626. RP FAY, RR (reprint author), LOYOLA UNIV,DEPT PSYCHOL,6525 N SHERIDAN RD,CHICAGO,IL 60626, USA. CR CORWIN JT, 1991, ANNU REV NEUROSCI, V14, P301, DOI 10.1146/annurev.neuro.14.1.301 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 EVANS EF, 1974, J PHYSL, V238, P65 Fay R. R., 1988, HEARING VERTEBRATES 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 RR, 1990, HEARING RES, V48, P93, DOI 10.1016/0378-5955(90)90201-Y FAY RR, 1991, HEARING RES, V55, P177, DOI 10.1016/0378-5955(91)90102-F FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 GUMMER AW, 1983, HEARING RES, V12, P367, DOI 10.1016/0378-5955(83)90006-0 HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P275 ISHII Y, 1971, JPN J PHYSIOL, V21, P91 KLINKE R, 1977, PSYCHOPHYSICS PHYSL, P100 MOFFAT AJM, 1976, J ACOUST SOC AM, V60, pS80, DOI 10.1121/1.2003543 SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SMOLDERS JWT, 1984, J COMP PHYSIOL, V155, P19, DOI 10.1007/BF00610927 STEIBLER IB, 1990, HEARING RES, V46, P63 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 SUZUE T, 1987, J NEUROPHYSIOL, V58, P1066 WESTERMAN LA, 1988, J ACOUST SOC AM, V83, P2266, DOI 10.1121/1.396357 NR 22 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 FEB PY 1992 VL 58 IS 1 BP 9 EP 18 DI 10.1016/0378-5955(92)90003-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300002 PM 1348502 ER PT J AU OHLSEN, KA DIDIER, A BALDWIN, D MILLER, JM NUTTALL, AL HULTCRANTZ, E AF OHLSEN, KA DIDIER, A BALDWIN, D MILLER, JM NUTTALL, AL HULTCRANTZ, E TI COCHLEAR BLOOD-FLOW IN RESPONSE TO DILATING AGENTS SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; HYDRALAZINE; SODIUM NITROPRUSSIDE; NICOTINIC ACID; PAPAVERINE; VERAPAMIL; HISTAMINE ID LASER DOPPLER MEASUREMENTS; GUINEA-PIG; PERMEABILITY; NITROPRUSSIDE; HYDRALAZINE; EXPOSURE AB Reduced cochlear blood flow (CBF) has been implicated in various pathologies of the inner ear, including sudden deafness, noise-induced hearing loss and Meniere's disease. Thus the aim of some current therapeutic regimens to treat these conditions is to increase CBF and thereby improve oxygenation of the inner ear tissues. Most of the vasodilating agents in clinical use, however, do not have specific experimental evidence to support their effects on CBF. The hypotension which can follow systemic administration may limit their local effectiveness and general utility, just as it complicates the interpretation of the data in animal experiments. In the current study we investigated the effect of six agents, known for their systemic cardiovascular actions, on CBF: hydralazine, sodium nitroprusside, papaverine, nicotinic acid, verapamil and histamine. The effect of these drugs was studied after topical applications on the round window membrane (RWM) and systemic intravenous administrations. CBF was monitored with a laser Doppler flowmeter (LDF). Topical administration of sodium nitroprusside was the most effective in increasing CBF, followed, in order, by hydralazine and histamine. No change in CBF was observed for papaverine, verapamil or nicotinic acid. Systemic administrations of all the agents caused a marked decrease in blood pressure and variable effects on CBF. We discuss the CBF changes in relation to the different pharmacological mechanisms of action of each drug. The study demonstrates the effectiveness of topical application of vasodilating agents in increasing CBF. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. CR AXELSSON A, 1971, ACTA OTO-LARYNGOL, V72, P172, DOI 10.3109/00016487109122470 BROWN MC, 1983, HEARING RES, V9, P131, DOI 10.1016/0378-5955(83)90023-0 CUMMINGHAM DR, 1974, AUDIOLOGY, V13, P470 ESCOUBET B, 1985, PROSTAGLANDINS, V29, P589 Goodman L.S., 1985, PHARM BASIS THERAPEU GREENBERG S, 1983, PHYSL PHARM MICROCIR, V1 HULTCRANTZ E, 1982, ARCH OTO-RHINO-LARYN, V234, P151, DOI 10.1007/BF00453622 HULTCRANTZ E, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P271 HULTCRANTZ E, 1988, AM J OTOLARYNG, V9, P317, DOI 10.1016/S0196-0709(88)80039-5 IGNARRO LJ, 1989, FASEB J, V3, P31 ITO Z, 1991, 14TH MIDW M ASS RES, P108 JOHNSON A, 1984, J OTOLARYNGOL, V13, P201 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P364 LAWRENCE M, 1975, ANN OTO RHINOL LARYN, V84, P499 LUNDMAN LA, 1987, ACTA OTO-LARYNGOL, V104, P472, DOI 10.3109/00016488709128277 MATTOX DE, 1980, ACTA OTOLARYNGOL, V80, P111 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, 1984, ARCH OTOLARYNGOL, V110, P305 MORIZONO T, 1989, RECENT ADV OTITIS ME NAKATSU K, 1989, CAN J PHYSIOL PHARM, V67, P251 NELSON SH, 1988, ANESTHESIOLOGY, V68, P541, DOI 10.1097/00000542-198804000-00011 NUTTALL AL, 1988, AM J OTOLARYNG, V9, P291, DOI 10.1016/S0196-0709(88)80037-1 OLHLSEN KA, 1991, CIRC RES, V69, P509 PRAZMA J, 1981, ARCH OTOLARYNGOL, V107, P227 PRAZMA J, 1981, ACTA OTO-LARYNGOL, V92, P459, DOI 10.3109/00016488109133284 RYBAK LP, 1984, ARCH OTO-RHINO-LARYN, V240, P207 SHEPHERD AMM, 1986, J CARDIOVASC PHARM, V8, P527, DOI 10.1097/00005344-198605000-00014 SILLMAN JS, 1988, ANN OTO RHINOL LARYN, V97, P1 SNOW JB, 1973, ARCH OTOLARYNGOL, V97, P365 TAMI TA, 1985, OTOLARYNG HEAD NECK, V93, P235 TANAKA K, 1981, ARCH OTO-RHINO-LARYN, V233, P67, DOI 10.1007/BF00464276 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 WALDMAN SA, 1987, PHARMACOL REV, V39, P163 WOODWARD DF, 1986, AGENTS ACTIONS, V18, P504, DOI 10.1007/BF01964954 ZAJTCHUK JT, 1979, HEAD NECK SURG, V87, P268 NR 36 TC 38 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 FEB PY 1992 VL 58 IS 1 BP 19 EP 25 DI 10.1016/0378-5955(92)90004-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300003 PM 1559902 ER PT J AU CANT, NB HYSON, RL AF CANT, NB HYSON, RL TI PROJECTIONS FROM THE LATERAL NUCLEUS OF THE TRAPEZOID BODY TO THE MEDIAL SUPERIOR OLIVARY NUCLEUS IN THE GERBIL SO HEARING RESEARCH LA English DT Article DE AUDITORY SYSTEM; SUPERIOR OLIVARY COMPLEX; NEUROANATOMY ID ANTEROVENTRAL COCHLEAR NUCLEUS; STEM AUDITORY NUCLEI; GLYCINE IMMUNOREACTIVITY; NEURONAL ARCHITECTURE; GUINEA-PIG; CAT; COMPLEX; ORGANIZATION; SENSITIVITY; PEROXIDASE AB We made small injections of horseradish peroxidase into the medial superior olivary nucleus (MSO) of gerbils in order to examine the sources of input into that nucleus. As previously described, the MSO receives inputs from neurons in the rostral part of both anteroventral cochlear nuclei. In addition, we found evidence for a projection from the ipsilateral lateral nucleus of the trapezoid body (LNTB). Our results are also compatible with previous reports that the medial nucleus of the trapezoid body (MNTB) projects to the MSO. It is likely that these projections into the MSO from the LNTB and MNTB are sources of inhibitory synaptic inputs. C1 UNIV WASHINGTON,HEARING DEV LABS,SEATTLE,WA 98195. RP CANT, NB (reprint author), DUKE UNIV,MED CTR,DEPT NEUROBIOL,POB 3209,DURHAM,NC 27710, USA. CR ADAMS J C, 1987, Society for Neuroscience Abstracts, V13, P1259 ADAMS JC, 1981, J HISTOCHEM CYTOCHEM, V29, P775 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 CANT NB, 1991, NEUROBIOLOGY HEARING, V2, P99 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 CLARK GM, 1969, BRAIN RES, V15, P548, DOI 10.1016/0006-8993(69)90181-4 CLARK GM, 1969, BRAIN RES, V14, P293, DOI 10.1016/0006-8993(69)90111-5 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 GOLDBERG JAY M., 1968, J NEUROPHYSIOL, V31, P639 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 Irvine D. R. F., 1986, PROGR SENSORY PHYSL, V7 KUWABARA N, 1990, NEUR ABSTR, V6, P723 LINDSEY BG, 1975, J COMP NEUROL, V160, P81, DOI 10.1002/cne.901600106 MOORE MJ, 1983, J NEUROSCI, V3, P237 MOREST D. KENT, 1968, BRAIN RES, V9, P288, DOI 10.1016/0006-8993(68)90235-7 NORDEEN KW, 1983, J COMP NEUROL, V214, P131, DOI 10.1002/cne.902140203 Osen K. K., 1970, EXCITATORY SYNAPTIC, P295 OSTAPOFF EM, 1990, J CHEM NEUROANAT, V3, P285 PERKINS RE, 1973, J COMP NEUROL, V148, P387, DOI 10.1002/cne.901480306 Rasmussen G.L., 1967, SENSORINEURAL HEARIN, P61 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 RYAN AF, 1982, J COMP NEUROL, V207, P369, DOI 10.1002/cne.902070408 SCHWARTZ IR, 1984, CONTRIB SENS PHYSL, V8, P99 SMITH PH, 1990, SOC NEUR ABSTR, V15, P746 SMITH PH, 1991, J COMP NEUROL, V304, P387, DOI 10.1002/cne.903040305 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 SPIROU GA, 1990, J NEUROPHYSIOL, V63, P1169 STRAUS W, 1982, J HISTOCHEM CYTOCHEM, V30, P491 TOLBERT LP, 1982, NEUROSCIENCE, V7, P3031, DOI 10.1016/0306-4522(82)90228-7 van Noort J, 1969, STRUCTURE CONNECTION WARR WB, 1972, BRAIN RES, V40, P247 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WARR WB, 1966, EXP NEUROL, V14, P453, DOI 10.1016/0014-4886(66)90130-0 WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X Yin T. C. T., 1988, AUDITORY FUNCTION, P385 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 NR 39 TC 91 Z9 92 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 1992 VL 58 IS 1 BP 26 EP 34 DI 10.1016/0378-5955(92)90005-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300004 PM 1559903 ER PT J AU SUGIYAMA, S SPICER, SS MUNYER, PD SCHULTE, BA AF SUGIYAMA, S SPICER, SS MUNYER, PD SCHULTE, BA TI ULTRASTRUCTURAL-LOCALIZATION AND SEMIQUANTITATIVE ANALYSIS OF GLYCOCONJUGATES IN THE TECTORIAL MEMBRANE SO HEARING RESEARCH LA English DT Article DE LECTIN-GOLD CYTOCHEMISTRY; HISTOCHEMISTRY; GLYCOCONJUGATES; GERBIL; COCHLEA; INNER EAR; TECTORIAL MEMBRANE ID WHEAT-GERM AGGLUTININ; STRUCTURAL DETERMINANTS; GOLD COMPLEXES; LIMAX-FLAVUS; LECTIN; OLIGOSACCHARIDES; BINDING; ORGAN; CORTI; SPECIFICITY AB The tectorial membrane of the gerbil cochlea was analyzed with lectin-gold cytochemical methods for demonstrating and characterizing glycoconjugates (GCs) in situ. Binding of lectins from Limax flavus (LFA), Lens culinaris (LCA), Datura stramonium (DSA), Ricinus communis (RCA I), Ulex europeus (UEA I) and Phaseolus vulgaris (PHA L) was assayed semiquantitatively on ultrathin sections. Binding occurred throughout the tectorial membrane with all lectins except UEA I but the labelling density with a given lectin differed among substructures. The cover net disclosed the highest level of GC with four lectins whereas the fibrous layer revealed the lowest level. DSA, LCA and PHA L demonstrated considerable similarity between the cover net and the marginal band in content of GC with N-linked oligosaccharide. The cover net differed from the marginal band, however, in containing more RCA I reactive GC with terminal lactosamine. Hensen's stripe, with which inner hair cell stereocilia are thought to interact, differed from other substructures in containing the highest level of PHA L-reactive triantennate N-linked chains and except for the basal layer the lowest concentration of GC with terminal lactosamine. Fucosylated GC detectable with UEA I-gold was present at low levels in all substructures except the cover net and marginal band. Distribution of GCs in the fibrous layer and less consistently in the cover net differed between limbal and middle zones. The differences observed here in the carbohydrate composition among substructures in the tectorial membrane support and extend previous cytochemical observations and imply a role for different classes of GCs in determining the biophysical and physiological properties of the tectorial membrane. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425. CR ALLEN AK, 1976, BIOCHEM J, V155, P127 ARNOLD W, 1973, ACTA OTO-LARYNGOL, V75, P192, DOI 10.3109/00016487309139695 BAENZIGER JU, 1979, J BIOL CHEM, V254, P9795 CROWLEY JF, 1984, ARCH BIOCHEM BIOPHYS, V231, P524, DOI 10.1016/0003-9861(84)90417-X CUMMINGS RD, 1982, J BIOL CHEM, V257, P1230 DEBRAY H, 1981, EUR J BIOCHEM, V117, P41 FERMIN CD, 1990, ACTA ANAT, V138, P75 GILLOYZAGA P, 1985, HEARING RES, V20, P1 GILLOYZAGA P, 1988, HEARING RES, V34, P149, DOI 10.1016/0378-5955(88)90102-5 GILLOYZAGA P, 1990, HEARING RES, V45, P151, DOI 10.1016/0378-5955(90)90191-Q Goldstein I J, 1978, Adv Carbohydr Chem Biochem, V35, P127 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 LIM DJ, 1972, ARCHIV OTOLARYNGOL, V96, P199 LIM DJ, 1990, ACTA OTO-LARYNGOL, V110, P224, DOI 10.3109/00016489009122541 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MILLER RL, 1982, J BIOL CHEM, V257, P7574 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 PEREIRA MEA, 1978, ARCH BIOCHEM BIOPHYS, V60, P244 PRIETO JJ, 1990, DEV BRAIN RES, V52, P141, DOI 10.1016/0165-3806(90)90229-R PRIETO JJ, 1990, HEARING RES, V45, P283, DOI 10.1016/0378-5955(90)90127-B RADEMACHER TW, 1988, ANNU REV BIOCHEM, V57, P785 RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 ROSS MD, 1974, AM J ANAT, V139, P449, DOI 10.1002/aja.1001390402 ROTH J, 1978, J HISTOCHEM CYTOCHEM, V26, P163 ROTH J, 1983, J HISTOCHEM CYTOCHEM, V31, P987 ROTH J, 1984, J HISTOCHEM CYTOCHEM, V32, P1167 RUEDA J, 1988, GLYCOCONJUGATES MED, P338 SAITO J, 1970, ACTA OTOLARYNGOL STO, V69, P333 SANTI PA, 1990, J ELECTRON MICR TECH, V15, P293, DOI 10.1002/jemt.1060150308 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHULTE BA, 1990, LUNG BIOL HLTH DISEA, P147 SPICER SS, 1987, J HISTOCHEM CYTOCHEM, V35, P1231 SUGIYAMA S, 1991, J HISTOCHEM CYTOCHEM, V39, P425 SUGIYAMA S, 1991, HEARING RES, V55, P263, DOI 10.1016/0378-5955(91)90111-L TACHIBAN.M, 1973, ACTA OTO-LARYNGOL, V76, P37, DOI 10.3109/00016487309121481 TACHIBANA M, 1987, HEARING RES, V27, P239, DOI 10.1016/0378-5955(87)90005-0 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 THOMOPOULOS GN, 1987, J ELECTRON MICR TECH, V5, P17, DOI 10.1002/jemt.1060050103 TOMODA K, 1984, EAR RES JPN, V15, P199 NR 43 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 FEB PY 1992 VL 58 IS 1 BP 35 EP 46 DI 10.1016/0378-5955(92)90006-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300005 PM 1559904 ER PT J AU MENDELSON, JR AF MENDELSON, JR TI NEURAL SELECTIVITY FOR INTERAURAL FREQUENCY DISPARITY IN CAT PRIMARY AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE PRIMARY AUDITORY CORTEX; INTERAURAL FREQUENCY DISPARITY; CAT ID INTENSITY DIFFERENCE SENSITIVITY; BINAURAL INTERACTION; SUPERIOR COLLICULUS; SINGLE NEURONS; RESPONSES; REPRESENTATION; ORGANIZATION AB Single-unit responses to interaural frequency disparities (IFDs) were examined in 74 neurons in cat primary auditory cortex (AI). Thirty-three of these cells were classified as EE (binaural facilitators), 39 were classified as EI (binaural inhibitors), and 2 were classified as EO (binaural occluders). The best frequency (BF) was presented to the dominant (usually the contralateral) ear while tones of the same or different frequency (either higher or lower than BF) were presented simultaneously to the nondominant (usually the ipsilateral) ear. Most cells displayed sensitivity to IFDs and thus were classified according to the IFD condition that elicited the strongest facilitatory or inhibitory response. The stimulus condition which evoked the strongest binaural response is referred to as the best IFD. For 50 cells (68%), the best IFD response was obtained when tones of different frequency were presented to each ear. Across the entire sample, binaural IFD responses of cortical neurons were categorized into one of three groups: Those preferring a lower frequency than BF in the ipsilateral ear (referred to as the 'lower IFD group'), those preferring a frequency equal to BF (the 'zero IFD group'), or those preferring a frequency higher than BF (the 'higher IFD group'). Among EE cells, approximately one third were maximally facilitated when the ipsilateral ear frequency was lower than BF, one third when it was equal to BF, and one third when it was higher than BF. Among EI cells, 50% exhibited deepest inhibition for higher IFDs with relatively fewer cells showing inhibition for zero or lower IFDs. Overall, EI cells responded over a broader range of IFD conditions than EE cells. Finally, approximately 50% of all units exhibited bimodal responses such that cells classified as EE displayed some inhibitory response characteristics when stimulated with certain IFD conditions and vice versa. C1 UNIV TORONTO,DEPT PSYCHOL,SCARBOROUGH,ONTARIO,CANADA. CR BROADBENT DE, 1957, J ACOUST SOC AM, V29, P708, DOI 10.1121/1.1909019 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 Cherry C., 1953, J ACOUST SOC AM, V25, P975, DOI 10.1121/1.1907229 DEATHERAGE B, 1961, J ACOUST SOC AM, V33, P139, DOI 10.1121/1.1908602 EHRET G, 1988, AUDITORY FUNCTION NE, P363 FIDELL S, 1983, J ACOUST SOC AM, V73, P628, DOI 10.1121/1.389008 Fletcher H, 1940, REV MOD PHYS, V12, P0047, DOI 10.1103/RevModPhys.12.47 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 KITZES LM, 1980, J COMP NEUROL, V192, P455, DOI 10.1002/cne.901920306 KLINKE R, 1970, FREQUENCY ANAL PERIO, P161 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 MARGOLIS RH, 1975, J SPEECH HEAR RES, V18, P571 MENDELSON JR, 1991, UNPUB J NEUROSCI MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MIDDLEBROOKS JC, 1981, J NEUROSCI, V1, P107 Moore B. C. J., 1988, AUDITORY FUNCTION NE, P585 PERROTT DR, 1970, J ACOUST SOC AM, V48, P1022, DOI 10.1121/1.1912225 PHILLIPS DP, 1981, HEARING RES, V4, P299, DOI 10.1016/0378-5955(81)90014-9 PHILLIPS DP, 1985, EXP BRAIN RES, V58, P443 REALE RA, 1986, J NEUROPHYSIOL, V56, P663 REPP BH, 1984, PERCEPT PSYCHOPHYS, V36, P523, DOI 10.3758/BF03207512 SCHARF B, 1976, SENS PROCESS, V1, P109 Scharf B, 1970, FOUNDATIONS MODERN A, V1, P157 THURLOW WR, 1959, J ACOUST SOC AM, V31, P1606, DOI 10.1121/1.1907666 THURLOW WR, 1957, J ACOUST SOC AM, V29, P515, DOI 10.1121/1.1908946 van den Brink G, 1970, FREQUENCY ANAL PERIO, P362 WHEATSTONE C, 1838, PHILOS T ROY SOC LON, V11, P371 WISE LZ, 1984, HEARING RES, V16, P181, DOI 10.1016/0378-5955(84)90008-X WISE LZ, 1985, J NEUROPHYSIOL, V54, P185 NR 29 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 1992 VL 58 IS 1 BP 47 EP 56 DI 10.1016/0378-5955(92)90007-A PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300006 PM 1559905 ER PT J AU SUBRAMANIAM, M HENDERSON, D CAMPO, P SPONGR, V AF SUBRAMANIAM, M HENDERSON, D CAMPO, P SPONGR, V TI THE EFFECT OF CONDITIONING ON HEARING-LOSS FROM A HIGH-FREQUENCY TRAUMATIC EXPOSURE SO HEARING RESEARCH LA English DT Article DE HEARING LOSS; CONDITIONING; HIGH FREQUENCY TRAUMATIC EXPOSURE; BASE VS APEX ID AUDIBILITY CURVE; CHINCHILLA; NOISE AB The role of high frequency, low level 'conditioning' exposures as moderators of hearing loss from subsequent exposure to the same noise at a higher level was studied using monaural chinchillas. All the animals in the experimental groups were exposed to an octave band noise centered at 4 kHz at 85 dB SPL for 6 h a day for 10 days. One of the experimental groups was allowed to recover for 5 days and the other was allowed to recover for 18 h, prior to the higher level exposure at 100 dB for 48 h. A third group exposed only to the higher level constituted the control group. A comparison of threshold shifts and hair cell loss after 4 weeks of recovery across the three groups revealed: (a) the 5-day recovery group incurred greater threshold shifts than the other two groups; the hair cell loss in this group was greater than in the 18-h recovery group, but the same as in the control group and (b) the 18-h recovery group incurred considerably less threshold shift as well as hair cell loss than the other two groups. The results were also compared with the results from similar exposures using low frequency noise which indicated that the base vs. apex differences in the cochlea appear to extend to the effects of 'conditioning' exposures. C1 INST NATL RECH & SECUR,VANDOEUVRE NANCY,FRANCE. RP SUBRAMANIAM, M (reprint author), SUNY BUFFALO,DEPT COMMUN DISORDERS SCI,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214, USA. CR BOHNE BA, 1987, HEARING RES, V29, P251, DOI 10.1016/0378-5955(87)90172-9 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 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 MILLER JD, 1963, ACTA OTOLARYNG S, V176 Pujol R., 1986, NEUROBIOLOGY HEARING, P161 Smith C A, 1968, Adv Sci, V24, P419 SOENDLIN H, 1969, ACTA OTOLARYNG, V87, P381 SUBRAMANIAM M, 1991, IN PRESS HEAR RES THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 VONBEKESY G, 1947, J ACOUST SOC AM, P452 NR 14 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 FEB PY 1992 VL 58 IS 1 BP 57 EP 62 DI 10.1016/0378-5955(92)90008-B PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300007 PM 1559906 ER PT J AU CHAMPLIN, CA AF CHAMPLIN, CA TI METHODS FOR DETECTING AUDITORY STEADY-STATE POTENTIALS RECORDED FROM HUMANS SO HEARING RESEARCH LA English DT Article DE STEADY-STATE POTENTIAL; FREQUENCY-DOMAIN METHOD; MAGNITUDE; PHASE; COHERENCE ID EVOKED-POTENTIALS; MIDDLE-LATENCY; RESPONSES; COHERENCE; AUDIOLOGY; OTOLOGY; TONES; SCALP; SLEEP AB Auditory steady-state potentials were recorded from the scalp of adult humans. The stimuli were 100-mu-s clicks presented at a rate of 39.1/s. Four stimulus levels were used (- 20, 0, 10, and 20 dB SL). The presence or absence of a response was determined by three frequency-domain methods and examiners. The frequency-domain methods were: magnitude-squared coherence (MSC), phase coherence (PC), and magnitude only (MO). The MSC method generally had the highest d' values, indicating that it was the most sensitive method for detecting responses. The hearing threshold predicted by the MSC method was the lowest, and it was within 4 dB of the behaviorally measured threshold for the click stimuli. Further, the amplitude of the response was significantly more variable than its phase, and no relation was found between the variability of the amplitude of the response and the amplitude of the noise. In summary, response detection methods that incorporate phase information (such as MSC and PC) should be chosen over methods which incorporate only amplitude information. C1 UNIV TEXAS,INST NEUROSCI,AUSTIN,TX 78712. RP CHAMPLIN, CA (reprint author), UNIV TEXAS,DEPT SPEECH COMMUN,CMA 2-102,AUSTIN,TX 78712, USA. CR BATRA R, 1986, HEARING RES, V21, P167, DOI 10.1016/0378-5955(86)90037-7 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 DOBIE RA, 1989, EAR HEARING, V10, P2 DOBIE RA, 1991, ELECTROEN CLIN NEURO, V80, P194, DOI 10.1016/0168-5597(91)90121-D EDWARDS AL, 1954, STATISTICAL METHODS FRIDMAN J, 1984, AUDIOLOGY, V23, P99 GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GREEN DM, 1966, SIGNAL DETECTION THE Jasper H. H., 1958, ELECTROENCEPHALOGRAP, V10, P371, DOI DOI 10.1016/0013-4694(58)90053-1 JERGER J, 1986, EAR HEARING, V7, P240, DOI 10.1097/00003446-198608000-00004 JERVIS BW, 1983, IEEE T BIO-MED ENG, V30, P43, DOI 10.1109/TBME.1983.325165 KEPPERL G, 1973, DSIGN ANAL RES HDB KILENY P, 1986, J SPEECH HEAR RES, V29, P20 KUWADA S, 1986, HEARING RES, V21, P179, DOI 10.1016/0378-5955(86)90038-9 LINDEN RD, 1985, EAR HEARING, V6, P167, DOI 10.1097/00003446-198505000-00008 MAKEIG S, 1985, THESIS U CALIFORNIA MARDIA KV, 1972, STATISTICS DIRECTION PICTON TW, 1987, ELECTROEN CLIN NEURO, V68, P119, DOI 10.1016/0168-5597(87)90039-6 REGAN D, 1966, ELECTROEN CLIN NEURO, V20, P238, DOI 10.1016/0013-4694(66)90088-5 SHALLOP JK, 1983, SCAND AUDIOL, V12, P91, DOI 10.3109/01050398309076230 STAPELLS DR, 1987, ELECTROEN CLIN NEURO, V67, P260, DOI 10.1016/0013-4694(87)90024-1 STAPELLS DR, 1984, EAR HEARING, V5, P105 TUCCI DL, 1990, ACTA OTOLARYNGOL, V9, P195 1978, ANSI S3211978 AM NAT NR 25 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 FEB PY 1992 VL 58 IS 1 BP 63 EP 69 DI 10.1016/0378-5955(92)90009-C PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300008 PM 1559907 ER PT J AU DOLPHIN, WF MOUNTAIN, DC AF DOLPHIN, WF MOUNTAIN, DC TI THE ENVELOPE FOLLOWING RESPONSE - SCALP POTENTIALS ELICITED IN THE MONGOLIAN GERBIL USING SINUSOIDALLY AM ACOUSTIC-SIGNALS SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIALS; AMPLITUDE MODULATION; GERBIL; GROUP DELAY ID FREQUENCY-FOLLOWING RESPONSES; AMPLITUDE-MODULATED SOUNDS; AUDITORY-EVOKED-RESPONSES; INFERIOR COLLICULUS; COCHLEAR NUCLEUS; PHASE-LOCKING; GUINEA-PIG; HAIR-CELLS; NEURONS; TONES AB Scalp potentials which follow the low frequency envelope of a sinusoidally amplitude modulated stimulus waveform were evoked and recorded in anesthetized gerbils. This envelope following response (EFR) is presumably due to the synchronized discharge of populations of neurons in the auditory pathway. The magnitude of the EFR increased and the latency decreased in a near monotonic fashion with increased stimulus intensity and modulation depth. The modulation rate transfer function (MRTF) was determined for modulation frequencies between 10 and 920 Hz imposed on carrier frequencies ranging from 1 to 7 kHz. The MRTF was low pass in character having a corner frequency of 100-120 Hz. Measurements of the group delay, determined from the phase of the response relative to the stimulus phase, indicate that the response is generated in at least three distinct regions within the auditory pathway. C1 BOSTON UNIV,DEPT OTOLARYNGOL,BOSTON,MA 02215. BIOL SYST RES CORP,HINGHAM,MA. RP DOLPHIN, WF (reprint author), BOSTON UNIV,DEPT BIOMED ENGN,BOSTON,MA 02215, USA. CR ANDERSON DJ, 1971, J ACOUST SOC AM, V62, P930 BATRA R, 1989, J NEUROPHYSIOL, V61, P257 BATRA R, 1986, HEARING RES, V21, P167, DOI 10.1016/0378-5955(86)90037-7 Bode H. W., 1945, NETWORK ANAL FEEDBAC BURKARD R, 1983, J ACOUST SOC AM, V74, P1204, DOI 10.1121/1.390024 BURKARD R, 1989, J ACOUST SOC AM, V85, P2514, DOI 10.1121/1.397746 CAMPBELL FW, 1977, PROG CLIN NEUROPHYS, V2, P68 COX LC, 1985, AUDITORY BRAINSTEM R, P297 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 DOLPHIN WF, 1991, 17TH P ANN NE BIOENG, P215 FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y FRISINA RD, 1982, HEARING RES, V6, P402 GARDI J, 1979, AUDIOLOGY, V18, P494 GUMMER AW, 1984, J ACOUST SOC AM, V76, P1388, DOI 10.1121/1.391456 HALL JW, 1979, SCIENCE, V205, P1297, DOI 10.1126/science.472748 HARRISON RV, 1979, ARCH OTO-RHINO-LARYN, V224, P71, DOI 10.1007/BF00455226 HECOX K, 1974, ARCH OTOLARYNGOL, V99, P30 JEWETT DL, 1970, ELECTROEN CLIN NEURO, V28, P609, DOI 10.1016/0013-4694(70)90203-8 KUWADA S, 1986, HEARING RES, V21, P179, DOI 10.1016/0378-5955(86)90038-9 MARSH JT, 1974, ELECTROEN CLIN NEURO, V36, P415, DOI 10.1016/0013-4694(74)90192-8 MOLLER AR, 1974, EXP NEUROL, V45, P104, DOI 10.1016/0014-4886(74)90104-6 MOLLER AR, 1986, HEARING RES, V24, P203, DOI 10.1016/0378-5955(86)90019-5 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x MOUSHEGI.G, 1973, ELECTROEN CLIN NEURO, V35, P665, DOI 10.1016/0013-4694(73)90223-X Oppenheim A. V., 1989, DISCRETE TIME SIGNAL OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X 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, 1986, HEARING RES, V23, P123, DOI 10.1016/0378-5955(86)90009-2 Rickards F.W., 1984, EVOKED POTENTIAL, VII, P163 RODENBUR.M, 1972, AUDIOLOGY, V11, P283 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SCHREINER C, 1983, HEARING PHYSL BASES, P169 SOKOLICH W, 1976, J ACOUST SOC AM, V54, P283 STARR A, 1975, ARCH NEUROL-CHICAGO, V32, P761 STATLER KD, 1990, HEARING RES, V50, P275, DOI 10.1016/0378-5955(90)90051-P STOCKARD JE, 1979, ARCH NEUROL-CHICAGO, V36, P823 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 WOOLF NK, 1981, HEARING RES, V4, P335, DOI 10.1016/0378-5955(81)90017-4 YIN TCT, 1984, J ACOUST SOC AM, V76, P1401, DOI 10.1121/1.391457 NR 42 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 FEB PY 1992 VL 58 IS 1 BP 70 EP 78 DI 10.1016/0378-5955(92)90010-K PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300009 PM 1559908 ER PT J AU DYNES, SBC DELGUTTE, B AF DYNES, SBC DELGUTTE, B TI PHASE-LOCKING OF AUDITORY-NERVE DISCHARGES TO SINUSOIDAL ELECTRIC-STIMULATION OF THE COCHLEA SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; COCHLEAR IMPLANTS; PHASE LOCKING; ELECTRICAL STIMULATION ID TEMPORAL RESPONSE PATTERNS; PITCH PERCEPTION; FIBER RESPONSES; MODEL; IMPLANT; INFORMATION; EXCITATION; FREQUENCY; SYNCHRONY; NEURON AB The activity of auditory-nerve fibers were recorded in anesthetized cats in response to sinusoidal electric stimuli applied through a bipolar electrode pair inserted about 5 mm into the cochlea through the round window. The synchronization index was calculated from period histograms for frequencies ranging from 0.2 to over 10 kHz. The stimulus artifact was largely eliminated through the use of differential micropipettes and an adaptive digital filter. Measured synchronization indices were many times larger than the indices that could be attributed to the residual stimulus artifact. Synchronization indices at each stimulus frequency varied considerably from fiber to fiber, even in the same animal. The dependence of synchrony on stimulus frequency was also variable, decreasing monotonically in some fibers and nonmonotonically in others. The average electric synchronization index for all fibers did not fall as steeply with frequency as does the average synchrony for acoustic stimuli. The finding of significant phase locking to electric stimuli well above 1 kHz suggests that the poor frequency discrimination of cochlear-implant recipients for single-channel stimulation above this frequency may be due to the inability of the central processor to make effective use of the available phase-locking information for monaural stimulation. C1 MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. RP DYNES, SBC (reprint author), MASSACHUSETTS EYE & EAR HOSP,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. CR ANDERSON DJ, 1973, J ACOUST SOC AM, V54, P361, DOI 10.1121/1.1913585 Carlson R., 1975, AUDITORY ANAL PERCEP, P55 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DELGUTTE B, 1984, J ACOUST SOC AM, V75, P866, DOI 10.1121/1.390596 Delgutte B, 1987, PSYCHOPHYSICS SPEECH, P333 DENG L, 1987, J ACOUST SOC AM, V82, P2001, DOI 10.1121/1.395644 DENT LJ, 1987, J ACOUST SOC AM S1, V82, pS72, DOI 10.1121/1.2024955 DYNES SBC, 1989, 12TH MIDW RES M ASS, P269 EDDINGTON DK, 1978, ANN OTOL RHINOL S53, V87 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 GHITZA O, 1988, J PHONETICS, V16, P109 GLASS I, 1984, EXP BRAIN RES, V55, P386 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HARTMANN R, 1990, COCHLEAR IMPLANTS MO HARTMANN R, 1987, COCHLEAR IMPLANTS CU, P73 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HOCHMAIRDESOYER IJ, 1983, ANN NY ACAD SCI, V405, P295, DOI 10.1111/j.1749-6632.1983.tb31642.x Javel E., 1990, COCHLEAR IMPLANTS MO JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 JOHNSON DH, 1978, BIOPHYS J, V22, P413 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 Kiang NY, 1970, SENSORINEURAL HEARIN, P241 KIANG NYS, 1979, ACTA OTO-LARYNGOL, V87, P204, DOI 10.3109/00016487909126408 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 LOEB GE, 1983, BIOL CYBERN, V47, P149, DOI 10.1007/BF00337005 MEDDIS R, 1991, J ACOUST SOC AM, V89, P2866, DOI 10.1121/1.400725 MOXON EC, 1967, THESIS MIT CAMBRIDGE Moxon E.C., 1971, THESIS MIT CAMBRIDGE 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 PFEIFFER RR, 1975, J ACOUST SOC AM, V58, P867, DOI 10.1121/1.380735 ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 RUBINSTEIN JT, 1991, IN PRESS BIOPHYS J SENEFF S, 1988, J PHONETICS, V16, P55 SHAMMA SA, 1985, J ACOUST SOC AM, V78, P1622, DOI 10.1121/1.392800 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHANNON RV, 1990, J ACOUST SOC AM, V88, P741, DOI 10.1121/1.399777 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 STEINBAC.AB, 1971, J GEN PHYSIOL, V58, P580, DOI 10.1085/jgp.58.5.580 TONG YC, 1982, J ACOUST SOC AM, V71, P153, DOI 10.1121/1.387342 TOWNSHEND B, 1987, J ACOUST SOC AM, V82, P106, DOI 10.1121/1.395554 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 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 WEISS TF, 1988, HEARING RES, V33, P167, DOI 10.1016/0378-5955(88)90029-9 WIDROW B, 1975, P IEEE, V63, P1692, DOI 10.1109/PROC.1975.10036 WILSON BS, 1991, NATURE, V352, P236, DOI 10.1038/352236a0 WILSON BS, 1990, SPEECH PROCESSORS AU YOUNG ED, 1979, J ACOUST SOC AM, V66, P1381, DOI 10.1121/1.383532 NR 53 TC 63 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 FEB PY 1992 VL 58 IS 1 BP 79 EP 90 DI 10.1016/0378-5955(92)90011-B PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300010 PM 1559909 ER PT J AU BELL, A AF BELL, A TI CIRCADIAN AND MENSTRUAL RHYTHMS IN FREQUENCY VARIATIONS OF SPONTANEOUS OTOACOUSTIC EMISSIONS FROM HUMAN EARS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSION; CIRCADIAN RHYTHM; MENSTRUAL CYCLE; BLOOD PRESSURE; CEREBROSPINAL FLUID PRESSURE ID COCHLEAR AQUEDUCT; PERILYMPHATIC PRESSURE; CEREBROSPINAL-FLUID; CAT AB This paper reports hourly and daily monitoring of the frequencies of spontaneous otoacoustic emissions. Regular circadian variations in frequency were found in two of three subjects. Consistent monthly variations, in step with the menstrual cycle, were seen in three of four women. The circadian cycle typically showed a rise in frequency of 0.6-1% while asleep and a similar fall while awake. The monthly cycle typically saw frequencies rise and fall by 0.4-0.6%, reaching a minimum near the onset of menstruation, and rising to a peak close to ovulation. A review of the literature revealed that certain cardiovascular parameters such as arterial blood pressure follow, over both daily and menstrual cycles, a broadly similar time course to SOAE frequency. Further experiments produced data supporting a relationship between blood pressure and SOAE frequency, and it is therefore suggested that much of the circadian-linked, menstrual-linked, and background variation in SOAE frequency may arise from cardiovascular changes. A likely causal mechanism, involving cerebrospinal fluid, is discussed. C1 AUSTRALIAN NATL UNIV,RES SCH BIOL SCI,CANBERRA,ACT 2601,AUSTRALIA. CR BEENTJES BI, 1972, ACTA OTO-LARYNGOL, V73, P112, DOI 10.3109/00016487209138919 BERING EA, 1974, FED PROC, V33, P2061 BRASK T, 1978, SCAND AUDIOL S, V7 CARLBORG B, 1980, ACTA OTO-LARYNGOL, V90, P209, DOI 10.3109/00016488009131717 CARLBORG B, 1981, ACTA OTO-LARYNGOL, V91, P19, DOI 10.3109/00016488109138478 CARLBORG B, 1990, ACTA OTO-LARYNGOL, V110, P386, DOI 10.3109/00016489009107459 Casselbrant M, 1979, Acta Otolaryngol Suppl, V362, P3 COX JR, 1980, EAR HEARING, V1, P219, DOI 10.1097/00003446-198007000-00008 Davson H., 1967, PHYSL CEREBROSPINAL DENSERT O, 1981, ACTA OTO-LARYNGOL, V91, P55, DOI 10.3109/00016488109138482 Dyrenfurth I, 1974, BIORHYTHMS HUMAN REP, P171 Engel P., 1974, BIORHYTHMS HUMAN PRO, P325 FERIN M, 1974, BIORHYTHMS HUMAN REP Floras JS, 1978, CLIN SCI MOL MED, V55, P395 FREEDMAN SH, 1974, BIORHYTHMS HUMAN REP, P259 FRITZE W, 1983, ARCH OTO-RHINO-LARYN, V238, P189, DOI 10.1007/BF00454312 HAGGERTY HS, 1990, SPONTANEOUS OTOACOUS HAGGERTY HS, 1989, J ACOUST SOC AM, V86 HAGGERTY HS, 1991, VARIANCE FREQUENCY T Kapuściński A, 1978, Adv Neurol, V20, P321 KATZENELBOGEN S, 1935, CEREBROSOPINAL FLUID KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KEMP DT, 1981, TINNITUS, P54 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 KLOCKHOFF I, 1966, ACTA OTOLARYNGOL, V84, P220 LAUGEL GR, 1987, HEARING RES, V31, P245, DOI 10.1016/0378-5955(87)90194-8 LOPESFO O, 1978, J OTOLARYNGOL, V7, P439 MACRAE JH, 1972, J SPEECH HEAR RES, V15, P330 MARCHBANKS R J, 1990, British Journal of Audiology, V24, P179, DOI 10.3109/03005369009076554 MEYER JH, 1982, SCIENCE, V217, P635, DOI 10.1126/science.217.4560.635 MILLARCRAIG MW, 1978, LANCET, V1, P795 NEDZELNITSKY V, 1980, J ACOUST SOC AM, V68, P1676, DOI 10.1121/1.385200 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 REID A, 1990, British Journal of Audiology, V24, P123, DOI 10.3109/03005369009077853 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SORENSEN PS, 1985, REGUL PEPTIDES, V10, P115 STRICKLAND E, 1984, J ACOUST SOC AM, V75 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 TALMADGE CL, 1991, J ACOUST SOC AM, V89, P2391, DOI 10.1121/1.400958 VERNON J, 1990, TINNITUS TODAY, V15, P14 WHITEHEAD ML, 1989, THESIS U KEELE KEELE Wilson J P, 1986, Scand Audiol Suppl, V25, P109 Wilson JP, 1981, TINNITUS, P82 WILSON JP, 1985, PERIPHERAL AUDITORY, P229 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 WLODYKA J, 1978, ANN OTO RHINOL LARYN, V87, P22 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 NR 49 TC 57 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 FEB PY 1992 VL 58 IS 1 BP 91 EP 100 DI 10.1016/0378-5955(92)90012-C PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300011 PM 1559910 ER PT J AU MUCHNIK, C SAHARTOV, E PELEG, E HILDESHEIMER, M AF MUCHNIK, C SAHARTOV, E PELEG, E HILDESHEIMER, M TI TEMPORARY THRESHOLD SHIFT DUE TO NOISE EXPOSURE IN GUINEA-PIGS UNDER EMOTIONAL-STRESS SO HEARING RESEARCH LA English DT Article DE HYPERSYMPATHETIC ACTIVITY; TEMPORARY THRESHOLD SHIFT; EMOTIONAL STRESS ID COCHLEAR BLOOD-FLOW; LOUD SOUND EXPOSURE; CATECHOLAMINES; RATS AB One of the factors which can affect the amount of temporary threshold shift (TTS) due to acoustic overstimulation is known to be the general metabolic state of the exposed subject. The present study was conducted to elucidate how preexisting intense emotional stress in awake guinea pigs could influence the TTS induced by exposure of 4 kHz at 120 dB SPL for 20 min. Considering the hypersympathetic activity in both 'stress' and 'noise' it was assumed that the two factors would act synergetically on the cochlear function. However, an unexpected result was obtained. The mean threshold for the stressed animals following noise exposure was significantly lower (better) than that of the controlled, sedated, guinea pigs. C1 CHAIM SHEBA MED CTR,HYPERTENS UNIT,IL-52621 TEL HASHOMER,ISRAEL. TEL AVIV UNIV,SACKLER SCH MED,TEL AVIV,ISRAEL. RP MUCHNIK, C (reprint author), CHAIM SHEBA MED CTR,DEPT COMMUN DISORDERS SPEECH LANGUAGE & HEARING,IL-52621 TEL HASHOMER,ISRAEL. CR ALARIO P, 1987, J STEROID BIOCHEM, V28, P433, DOI 10.1016/0022-4731(87)91062-4 ARMARIO A, 1984, BEHAV NEURAL BIOL, V41, P71, DOI 10.1016/S0163-1047(84)90745-3 BORRELL J, 1980, NEUROENDOCRINOLOGY, V31, P53, DOI 10.1159/000123050 BOSATRA A B, 1961, Acta Otolaryngol Suppl, V169, P1 CARLISLE L, 1990, HEARING RES, V43, P107, DOI 10.1016/0378-5955(90)90219-F DENSERT O, 1974, ACTA OTO-LARYNGOL, V77, P185, DOI 10.3109/00016487409124616 DeWeese D D, 1973, Adv Otorhinolaryngol, V20, P191 HANKIN RI, 1963, AM J PHYSIOL, V204, P710 HILDESHEIMER M, 1979, ACTA OTO-LARYNGOL, V88, P37, DOI 10.3109/00016487909137137 HULCRANTZ E, 1979, ACTA PHYSL SCAND, V106, P29 JOHNSON GA, 1977, CURR THER RES CLIN E, V21, P898 KAWAMOTO H, 1976, Medical Journal of Osaka University, V27, P77 MUCHNIK C, 1980, ARCH OTO-RHINO-LARYN, V228, P295, DOI 10.1007/BF00660742 MUCHNIK C, 1983, ARCH OTOLARYNGOL, V109, P530 OKAMOTO A, 1990, ACTA OTO-LARYNGOL, V109, P378, DOI 10.3109/00016489009125158 Ross M D, 1971, Acta Otolaryngol Suppl, V286, P1 RUBIN W, 1968, LARYNGOSCOPE, V78, P829, DOI 10.1288/00005537-196805000-00013 RYAN AF, 1988, ACTA OTO-LARYNGOL, V105, P232, DOI 10.3109/00016488809097003 SELYE H, 1985, ANN OTO RHINOL LARYN, V94, P87 SIEGEL RA, 1983, EUR J PHARMACOL, V91, P49, DOI 10.1016/0014-2999(83)90360-6 SNOW JB, 1973, VASCULAR DISORDERS H, P167 Spoendlin H, 1967, Arch Klin Exp Ohren Nasen Kehlkopfheilkd, V189, P346, DOI 10.1007/BF00440938 Spoendlin H, 1966, Acta Otolaryngol, V61, P423 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 TAGGART P, 1973, LANCET, V2, P341 TERAYAMA Y, 1968, ANN OTO RHINOL LARYN, V77, P1152 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 NR 27 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 FEB PY 1992 VL 58 IS 1 BP 101 EP 106 DI 10.1016/0378-5955(92)90013-D PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300012 PM 1559900 ER PT J AU DAVIS, RL SEWELL, WF AF DAVIS, RL SEWELL, WF TI NEURITE REGENERATION FROM SINGLE PRIMARY-AUDITORY NEURONS INVITRO SO HEARING RESEARCH LA English DT Article DE GOLDFISH; CONDITIONING LESIONS; INTRINSIC REGULATION; ENDOGENOUS DETERMINANTS; REGENERATION; PERIPHERAL NERVE ID 8TH CRANIAL NERVE; ADULT GOLDFISH RETINA; OPTIC-NERVE; GROWTH CONES; CONDITIONING LESION; CENTRAL PROJECTIONS; EXPLANT CULTURE; FIBERS; CELLS; BULLFROG AB Neurons of the VIII(th) cranial nerve in lower vertebrates precisely reconnect with their targets after sustaining injury. It is not known, however, whether the regenerating neurites are guided entirely by external cues or may also be directed by intrinsic mechanisms. To address this issue, single adult primary-auditory neurons were dissected from goldfish and placed in an in vitro environment, devoid of the normal complement of satellite cells, neighboring neurons, and synaptic targets, to observe their patterns of growth. Because acutely isolated neurons showed little neurite outgrowth, neurite regeneration was enhanced by focally crushing the VIII(th) cranial nerve 2 to 24 h prior to removal for tissue culture. Neurons that regenerated under identical culture conditions showed growth patterns that could be categorized into three separate groups based on both their morphology and growth patterns. They either 1) remained unbranched (54%), 2) bifurcated or trifurcated into major branches directly from the myelinated stump (V-shaped) (19%), or 3) bifurcated from a regenerated process (Y-shaped), sometimes with a third, smaller branch (27%). Unbranched and V-shaped neurites grew at a constant elongation rate, while Y-shaped neurites grew variably, with alternating retractions and elongations. Neurite elongation was completed in a uniform time period of approximately 15 days despite the differences in elongation rate, maximum length, and latency to growth onset. The neurite branching morphology and manner of growth revealed in this study indicated that adult regenerating neurons can reproduce some elements of the final branching patterns in the absence of extrinsic cues, a capability which may ultimately contribute to the fidelity of reconnection seen in vivo. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,EATON PEABODY LAB,BOSTON,MA 02114. CR ACKLIN SE, 1990, J NEUROSCI, V10, P1082 BANKER GA, 1988, INTRINSIC DETERMINAN, P61 BENTLEY D, 1983, NATURE, V304, P62, DOI 10.1038/304062a0 Bloom W., 1968, TXB HISTOLOGY BROCKES JP, 1979, BRAIN RES, V165, P105, DOI 10.1016/0006-8993(79)90048-9 CADAY CG, 1989, MOL BRAIN RES, V5, P45, DOI 10.1016/0169-328X(89)90016-8 CAJAL SRY, 1956, DEGENERATION REGENER, V1 DAVIES AM, 1989, NATURE, V337, P553, DOI 10.1038/337553a0 DENO LR, 1933, LARYNGOSCOPE, V43, P1 DODD J, 1988, SCIENCE, V242, P692, DOI 10.1126/science.3055291 EISEN JS, 1986, NATURE, V320, P269, DOI 10.1038/320269a0 FURUKAWA T, 1978, J COMP NEUROL, V180, P807, DOI 10.1002/cne.901800411 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1337 GAGE FH, 1988, BRAIN INJURY RECOVER, P201 Gleisner L, 1975, Acta Otolaryngol Suppl, V333, P1 GRUMBACHERREINERT S, 1989, P NATL ACAD SCI USA, V86, P7270, DOI 10.1073/pnas.86.18.7270 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HARRIS WA, 1986, NATURE, V320, P266, DOI 10.1038/320266a0 HOPKINS JM, 1985, J NEUROSCI, V5, P3030 KUWADA JY, 1986, SCIENCE, V233, P740, DOI 10.1126/science.3738507 LANDRETH GE, 1976, BRAIN RES, V118, P299, DOI 10.1016/0006-8993(76)90714-9 LANDRETH GE, 1979, BRAIN RES, V161, P39, DOI 10.1016/0006-8993(79)90194-X LETOURNEAU PC, 1975, DEV BIOL, V44, P92, DOI 10.1016/0012-1606(75)90379-6 MARBEY D, 1984, HEARING RES, V15, P89, DOI 10.1016/0378-5955(84)90228-4 MCQUARRIE IG, 1982, BRAIN RES, V251, P25, DOI 10.1016/0006-8993(82)91270-7 MCQUARRIE IG, 1981, BRAIN RES, V216, P253, DOI 10.1016/0006-8993(81)90128-1 MONTAGUE PR, 1989, P NATL ACAD SCI USA, V86, P7223, DOI 10.1073/pnas.86.18.7223 NAKAJIMA Y, 1974, J COMP NEUROL, V156, P375, DOI 10.1002/cne.901560402 NEWMAN A, 1987, LARYNGOSCOPE, V97, P1219 NEWMAN A, 1986, LARYNGOSCOPE, V96, P484, DOI 10.1288/00005537-198605000-00003 NEWMAN A, 1989, LARYNGOSCOPE, V99, P162 Peters A., 1976, FINE STRUCTURE NERVO RAPER JA, 1983, J NEUROSCI, V3, P31 ROSENBLUM J, 1961, J BIOPHYS BIOCHEM CY, V9, P853, DOI 10.1083/jcb.9.4.853 ROUSSELET A, 1990, DEV BIOL, V137, P33, DOI 10.1016/0012-1606(90)90005-4 RUNYON RP, 1977, NONPARAMETRIC STAT, P45 RUNYON RP, 1977, DESCRIPTIVE INFERENT, P179 SCHWARTZ M, 1987, CRIT REV BIOCHEM MOL, V22, P89, DOI 10.3109/10409238709083737 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 SPERRY RW, 1963, P NATL ACAD SCI USA, V50, P703, DOI 10.1073/pnas.50.4.703 SPERRY RW, 1945, AM J PHYSIOL, V144, P735 STEWART WW, 1978, CELL, V14, P741, DOI 10.1016/0092-8674(78)90256-8 SZPIR MR, 1990, J COMP NEUROL, V295, P530, DOI 10.1002/cne.902950403 YASUDA T, 1990, BRAIN RES, V524, P54, DOI 10.1016/0006-8993(90)90491-S ZAKON H, 1981, SCIENCE, V213, P242, DOI 10.1126/science.6972599 ZAKON H, 1981, BRAIN RES, V209, P325, DOI 10.1016/0006-8993(81)90157-8 ZAKON HH, 1983, J NEUROPHYSIOL, V49, P1410 NR 47 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 1992 VL 58 IS 1 BP 107 EP 121 DI 10.1016/0378-5955(92)90014-E PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA HD563 UT WOS:A1992HD56300013 PM 1559901 ER PT J AU HIEL, H SCHAMEL, A ERRE, JP HAYASHIDA, T DULON, D ARAN, JM AF HIEL, H SCHAMEL, A ERRE, JP HAYASHIDA, T DULON, D ARAN, JM TI CELLULAR AND SUBCELLULAR-LOCALIZATION OF TRITIATED GENTAMICIN IN THE GUINEA-PIG COCHLEA FOLLOWING COMBINED TREATMENT WITH ETHACRYNIC-ACID SO HEARING RESEARCH LA English DT Article DE AMINOGLYCOSIDE ANTIBIOTICS; AUTORADIOGRAPHY; HAIR CELLS; LOOP DIURETICS; LYSOSOMES; OTOTOXICITY; 8TH-NERVE ACTION POTENTIAL ID HAIR-CELLS; MECHANOELECTRICAL TRANSDUCTION; AMINOGLYCOSIDE ANTIBIOTICS; CALCIUM; ANTAGONISM; BLOCKADE AB Guinea pigs (GPs) receiving one intra-muscular injection of gentamicin (GM) (150 mg/kg) in which 2 mg of tritiated GM (2 mCi) were incorporated, followed 1.5 h later by an intra-cardiac injection of ethacrynic acid (EA) (30 mg/kg) were sacrificed 25 min, 1, 4 and 24 h after the EA injection. Other GPs were treated with one injection of GM or EA alone and sacrificed 24 h later. Cochlear function was monitored by recording VIIIth nerve compound action potential (CAP) responses to clicks at 70 dB peak-equivalent Sound Pressure Level (pe SPL) and CAP audiograms. At 24 h thresholds were significantly elevated for high frequencies only in GPs treated with the GM/EA combination. GM was revealed in the cochlea and kidney by autoradiography using light and electron microscopy. In the kidney GM was already detected in the proximal tubule cells at 25 min and at 24 h. In the cochlea GM was systematically not observed at 25 min. At 1 h a weak labelling was detected in vessels of the stria vascularis and in sensory cells at the base of the cochlea. At 4 h the labelling disappeared in stria vascularis but increased in the hair cells. At 24 h GM labelling was found exclusively in hair cells, particularly outer hair cells, with a gradient from base to apex and from first to 3rd row, this distribution pattern correlating well with the pattern of threshold changes prominent at high frequencies. Inside the hair cells, labelling was diffuse in the cytoplasm at an early stage but at 24 h it was clearly localized in the hair bundle area, the cuticular plate, particularly dense on the lysosomes concentrated below the cuticular plate, and over the nucleus. This specific cellular and intracellular localization of GM, and its progressive accumulation inside the hair cell body, along with the development of functional changes, tend to indicate that the toxicity results from specific intracellular effects of the aminoglycoside molecule. C1 UNIV BORDEAUX,CYTOL LAB,CNRS,UA 339,TALENCE,FRANCE. UNIV BORDEAUX 2,HOP PELLEGRIN,F-33076 BORDEAUX,FRANCE. RP ARAN, JM (reprint author), LAB AUDIOL EXPTL,INSERM,U229,BORDEAUX,FRANCE. CR PITTINGE.C, 1972, ANNU REV PHARMACOLOG, V12, P169, DOI 10.1146/annurev.pa.12.040172.001125 Aran J M, 1982, Acta Otolaryngol Suppl, V390, P1 ARAN JM, 1979, OXFORD MED ENG SERIE, P233 ARAN JM, 1991, EFFECTS NOISE HEARIN, P188 ARAN JM, 1990, B ACAD NATL MED, V107, P939 ARAN JM, 1990, ADV AUDIOL, V7, P42 BEAUCHAMP D, 1990, J PHARMACOL EXP THER, V255, P858 DARROUZET J, 1974, ETUDE EXPT MICROSCOP, V95, P601 DEGROOT JCM, 1990, HEARING RES, V50, P34 DELPOZO E, 1986, EUR J PHARMACOL, V128, P49, DOI 10.1016/0014-2999(86)90556-X DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 GONZALEZ G, 1972, ANN OTO RHINOL LARYN, V81, P127 HANCOCK REW, 1981, J ANTIMICROB CHEMOTH, V8, P429, DOI 10.1093/jac/8.6.429 Hawkins Jr JE, 1976, HDB SENSORY PHYSIOLO, P707 HAYASHIDA T, 1989, ACTA OTO-LARYNGOL, V108, P404, DOI 10.3109/00016488909125546 HOUGHTON DC, 1986, AM J PATHOL, V123, P183 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 HUANG MY, 1990, BIOCHEM PHARMACOL, V40, pR11, DOI 10.1016/0006-2952(90)90077-X HUANG MY, 1991, CYTOSOLIC ENZYMES CO, P73 HUDSPETH AJ, 1985, SCIENCE, V230, P745, DOI 10.1126/science.2414845 JARLSTEDT J, 1977, ACTA OTO-LARYNGOL, V84, P361, DOI 10.3109/00016487709123978 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 PRADO WA, 1978, ARCH INT PHARMACOD T, V231, P297 RYBAK LP, 1986, ANNU REV PHARMACOL, V26, P79 SPOENDLI.H, 1966, PRACT-OTO-RHINO-LARY, V28, P305 TAKADA A, 1982, HEARING RES, V8, P179, DOI 10.1016/0378-5955(82)90073-9 Tran Ba Huy P, 1981, J INFECT DIS, V143, P476 TRAN BHP, 1986, J CLIN INVEST, V77, P1492 VANDEWALLE A, 1981, KIDNEY INT, V19, P529, DOI 10.1038/ki.1981.50 WEDEEN RP, 1983, LAB INVEST, V48, P212 NR 31 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 JAN PY 1992 VL 57 IS 2 BP 157 EP 165 DI 10.1016/0378-5955(92)90148-G PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700001 PM 1733909 ER PT J AU ROBERSON, DF WEISLEDER, P BOHRER, PS RUBEL, EW AF ROBERSON, DF WEISLEDER, P BOHRER, PS RUBEL, EW TI ONGOING PRODUCTION OF SENSORY CELLS IN THE VESTIBULAR EPITHELIUM OF THE CHICK SO HEARING RESEARCH LA English DT Article DE VESTIBULAR SYSTEM; HAIR CELL; AVIAN; CELL PROLIFERATION; 3H-THYMIDINE; BROMODEOXYURIDINE ID HAIR CELL; INNER-EAR; ACOUSTIC TRAUMA; FISH EAR; REGENERATION; GROWTH; BROMODEOXYURIDINE; PROLIFERATION; COCHLEA AB Recent studies have shown that the vestibular and auditory systems of some species of birds have the capacity to generate sensory hair cells postnatally. We used a traditional technique, H-3-thymidine autoradiography, and a newer method, bromodeoxyuridine immunocytochemistry, to determine whether ongoing proliferation of hair cells occurs in the intact chick vestibular epithelium. A ten-day course of H-3-thymidine, bromodeoxyuridine, or both was administered to twelve-day-old chicks. Both autoradiographic and immunocytochemical labeling demonstrated ongoing production of supporting cells and Type II hair cells in all chick vestibular organs. No evidence for production of Type I hair cells was seen in this investigation. New sensory cells were distributed throughout the epithelium; there was no peripheral growth zone analogous to that found in other vertebrates. Labeled Type II hair cells were frequently seen immediately above labeled supporting cells. This observation suggests that supporting cells are precursors for new hair cells. The ongoing, postnatal regeneration of vestibular epithelial cells also suggests that this epithelium may retain the potential for repair after trauma or ototoxic damage. C1 UNIV WASHINGTON,DEPT OTOLARYNGOL HEAD & NECK SURG,HEARING DEV LABS,RL-30,SEATTLE,WA 98195. RI Weisleder, Pedro/C-8990-2009 CR CORWIN JT, 1981, J COMP NEUROL, V201, P541, DOI 10.1002/cne.902010406 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, 1983, J COMP NEUROL, V217, P345, DOI 10.1002/cne.902170309 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 EDWARDS AL, 1967, STATISTICAL METHODS FLOCK A, 1964, J CELL BIOL, V22, P413, DOI 10.1083/jcb.22.2.413 FRIEDMANN I, 1959, J BIOPHYS BIOCHEM CY, V5, P263, DOI 10.1083/jcb.5.2.263 Iurato S, 1967, SUBMICROSCOPIC STRUC JORGENSEN JM, 1981, ACTA ZOOL-STOCKHOLM, V62, P171 JORGENSEN JM, 1989, BRAIN BEHAV EVOLUT, V34, P273, DOI 10.1159/000116512 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 MILLER MW, 1988, BRAIN RES, V457, P44, DOI 10.1016/0006-8993(88)90055-8 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W PRESSON JC, 1990, HEARING RES, V46, P9, DOI 10.1016/0378-5955(90)90135-C RAMPRASHAD F, 1986, ACTA OTOLARYNGOL S, V427 RETZIUS G, 1894, GEHORORGAN WIRBELTIE, V2 RUBEN RJ, 1967, ACTA OTOLARYNGOL S, V220 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SUGIHARA H, 1986, HISTOCHEMISTRY, V85, P193, DOI 10.1007/BF00494803 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 TAPSCOTT SJ, 1989, SCIENCE, V245, P532, DOI 10.1126/science.2547249 WEISLEDER P, 1991, ASS RES OT ABSTR, V14, P154 WERSALL J, 1956, ACTA OTOLARYNGOL S, V126 WERSALL J, 1960, NEURAL MECHANISMS AU, P247 NR 28 TC 110 Z9 114 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 1992 VL 57 IS 2 BP 166 EP 174 DI 10.1016/0378-5955(92)90149-H PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700002 PM 1733910 ER PT J AU ZWISLOCKI, JJ SLEPECKY, NB CEFARATTI, LK SMITH, RL AF ZWISLOCKI, JJ SLEPECKY, NB CEFARATTI, LK SMITH, RL TI IONIC COUPLING AMONG CELLS IN THE ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELLS; SUPPORTING CELLS; ELECTRICAL POTENTIALS; GAP JUNCTIONS ID GAP-JUNCTIONS; INTRACELLULAR-RECORDINGS; INTERCELLULAR-JUNCTIONS; SUPPORTING CELLS; HAIR-CELLS; GUINEA-PIG; TRANSMISSION AB Gap junctions have been demonstrated morphologically among the supporting cells of the mammalian organ of Corti but, in contradistinction to reptiles, evidence for their existence between the supporting cells and hair cells is equivocal. The literature is ambiguous with respect to electrical coupling and dye coupling among the supporting cells, and no coupling of either kind has been demonstrated for the hair cells. We found strong coupling of both kinds among the supporting cells in the cochleas of live Mongolian gerbils and a less stable coupling between the supporting cells and the outer hair cells. The electrical coupling was established by recording alternating receptor potentials in the hair cells and following their decrement in the population of Hensen's cells; the dye coupling, by injecting Lucifer yellow electrophoretically into the hair cells or the supporting cells and investigating its spread to the neighboring cells. The electrical recordings were made by means of microelectrodes filled with either 1.5 or 3 M KCl or 1 M LiCl with 6% Lucifer yellow, the latter used for dye injection. The electrode resistances ranged from about 20 to 60 M-OMEGA in the first instance, and from about 50 to 110 M-OMEGA, in the second. The electrodes were inserted into the organ of Corti through scala media according to the method of Dallos, Santos-Sacchi and Flock (1982) modified by us. The alternating potential in Hensen's cells was usually larger than in the outer tunnel of Corti and remained practically constant up to the outer margin of the Hensen's-cell population. Its phase was the same as in the outer hair cells. When the dye was injected into a Hensen's cell, it always spread to neighboring Hensen's cells and often to Deiter's cells. Dye injected into outer hair cells (identified according to anatomical and physiological criteria) also spread to Deiter's and Hensen's cells and, usually, to other outer hair cells. Stained cells were identified in surface preparations and, on two occasions, in serial sections from plastic embedded cochleas. RP ZWISLOCKI, JJ (reprint author), SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244, USA. CR DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1983, HEARING RES, V12, P89, DOI 10.1016/0378-5955(83)90120-X DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 GULLEY RL, 1976, J NEUROCYTOL, V5, P479, DOI 10.1007/BF01181652 HAMA K, 1980, J NEUROCYTOL, V9, P845, DOI 10.1007/BF01205023 IURATO S, 1976, ACTA OTO-LARYNGOL, V82, P57, DOI 10.3109/00016487609120863 JASLOVE SW, 1987, CELL CELL COMMUNICAT MILLER MR, 1990, J COMP NEUROL, V293, P223, DOI 10.1002/cne.902930206 NADOL JB, 1978, ANN OTO RHINOL LARYN, V87, P70 NADOL JB, 1976, AM J ANAT, V147, P281, DOI 10.1002/aja.1001470304 OESTERLE EC, 1989, J ACOUST SOC AM, V86, P1013, DOI 10.1121/1.398092 PERACCHIA C, 1980, J CELL BIOL, V87, P273 PERACCHIA C, 1980, J CELL BIOL, V87, P708, DOI 10.1083/jcb.87.3.708 RAVIOLA E, 1973, P NATL ACAD SCI USA, V70, P1677, DOI 10.1073/pnas.70.6.1677 SANTOS-SACCHI J, 1983, HEARING RES, V9, P317, DOI 10.1016/0378-5955(83)90034-5 SANTOS-SACCHI J, 1984, HEARING RES, V14, P203, DOI 10.1016/0378-5955(84)90019-4 SANTOS-SACCHI J, 1986, CELL TISSUE RES, V245, P525 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 WEISS TF, 1971, J ACOUST SOC AM, V50, P587, DOI 10.1121/1.1912675 ZIDANIC M, 1989, IL VALSALVA, V54, P20 ZWISLOCKI JJ, 1988, HEARING RES, V33, P207, DOI 10.1016/0378-5955(88)90151-7 ZWISLOCKI JJ, 1986, AUDITORY FREQUENCY S NR 22 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 JAN PY 1992 VL 57 IS 2 BP 175 EP 194 DI 10.1016/0378-5955(92)90150-L PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700003 PM 1733911 ER PT J AU BERGGREN, D VANDEWATER, TR ANNIKO, M AF BERGGREN, D VANDEWATER, TR ANNIKO, M TI AGE-DEPENDENT DISRUPTION OF BASAL LAMINA AND EXTRACELLULAR-MATRIX FORMATION IN L-PROLINE ANALOG TREATED OTIC EXPLANTS SO HEARING RESEARCH LA English DT Article DE INVITRO; OTIC ANLAGE; L-AZETIDINE-2-CARBOXYLIC ACID; EXTRACELLULAR MATRIX; COLLAGEN; BASAL LAMINA ID CARTILAGE AB L-azetidine-2-carboxylic acid, LACA, a naturally occurring vegetable imino acid, can be incorporated into mammal proteins instead of proline. This incorporation has an especially inhibitive effect on collagen secretion. Exposure of embryonic mouse inner ear explants to LACA causes dysmorphogenesis and retarded differentiation, reduces the number of collagen fibrils in the perilymphatic spaces and capsules, and gives rise to a dose-dependent derangement of the basal lamina. In control specimens, both in vivo and in vitro, the inner ear epithelia had a dense contiguous basal lamina overlying a well-developed network of collagen fibrils. When the inner ears were exposed to LACA at a concentration of 150-mu-g per ml of medium, there was a loss of the collagen network and gaps appeared in the basal lamina. At exposure to 300-mu-g LACA/ml, scarcely any collagen fibrils were present and the basal lamina was disrupted in many areas, especially beneath the sensory epithelia. C1 UMEA UNIV HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,S-90185 UMEA,SWEDEN. UNIV UPPSALA HOSP,DEPT OTORHINOLARYNGOL & HEAD & NECK SURG,UPPSALA,SWEDEN. YESHIVA UNIV ALBERT EINSTEIN COLL MED,KENNEDY CTR,DEPT OTORHINOLARYNGOL,DEV OTOBIOL LAB,BRONX,NY 10461. CR ANNIKO M, 1984, ULTRASTRUCTURAL ATLA, P184 ANNIKO M, 1984, ARCH OTO-RHINO-LARYN, V240, P27, DOI 10.1007/BF00464341 BROWN KS, 1981, J EMBRYOL EXP MORPH, V62, P165 EHLING UH, 1966, GENETICS, V54, P1381 FOWDEN L, 1963, BIOCHIM BIOPHYS ACTA, V71, P459, DOI 10.1016/0006-3002(63)91104-1 Gospodarowicz D., 1981, BIOL NORMAL HUMAN GR, P1 Hay ED, 1981, CELL BIOL EXTRACELLU, P379 HAY ED, 1978, GROWTH, V42, P399 HEINEGAR.D, 1972, BIOCHIM BIOPHYS ACTA, V285, P193, DOI 10.1016/0005-2795(72)90191-2 Jost A, 1985, C R Acad Sci III, V301, P225 JOST A, 1988, P NATL ACAD SCI USA, V85, P8094, DOI 10.1073/pnas.85.21.8094 KARNOVSK.MJ, 1965, J CELL BIOL, V27, pA137 KEFALIDES NA, 1975, J INVEST DERMATOL, V65, P85, DOI 10.1111/1523-1747.ep12598062 KLEINMAN HK, 1982, IMMUNOCHEMISTRY EXTR, V2, P151 TAKEUCHI T, 1969, BIOCHIM BIOPHYS ACTA, V175, P142, DOI 10.1016/0005-2795(69)90153-6 Theiler K, 1972, HOUSE MOUSE TRELSTAD RL, 1974, J CELL BIOL, V62, P815, DOI 10.1083/jcb.62.3.815 VANDEWATER TR, 1978, DEV SIGNIFICANCE EPI, P24 VANDEWATER TR, 1973, ANN OTOL RHINOL L S4, V82, P19 WESSELLS NK, 1968, DEV BIOL, V18, P294, DOI 10.1016/0012-1606(68)90037-7 ZAGARI A, 1990, BIOPOLYMERS, V30, P951, DOI 10.1002/bip.360300909 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 JAN PY 1992 VL 57 IS 2 BP 195 EP 200 DI 10.1016/0378-5955(92)90151-C PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700004 PM 1733912 ER PT J AU SLEPECKY, NB ULFENDAHL, M AF SLEPECKY, NB ULFENDAHL, M TI ACTIN-BINDING AND MICROTUBULE-ASSOCIATED PROTEINS IN THE ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE INNER EAR; HAIR CELL; ACTIN; TUBULIN; ACTIN-BINDING PROTEINS; MAPS; TAU; FREEZE-DRY ID OUTER HAIR-CELLS; AMINO-ACID-SEQUENCE; INNER-EAR; SUPPORTING CELLS; GUINEA-PIG; F-ACTIN; IMMUNOFLUORESCENT LOCALIZATION; CONTRACTILE PROTEINS; MEMBRANE-SKELETON; EPITHELIAL-CELLS AB Actin-binding and microtubule-associated proteins regulate microfilament and microtubule number, length, organization and location in cells. In freeze-dried preparations of the guinea pig cochlea, both actin and tubulin are found in the sensory and supporting cells of the organ of Corti. Fodrin (brain spectrin) co-localized with actin in the cuticular plates of both inner and outer hair cells and along the lateral wall of the outer hair cells. Alpha-actinin co-localized with actin in the cuticular plates of the hair cells and in the head and foot plates of the supporting cells. It was also found in the junctional regions between hair cells and supporting cells. Profilin co-localized with actin in the cuticular plates of the sensory hair cells. Myosin was detected only in the cuticular plates of the outer hair cells and in the supporting cells in the region facing endolymph. Gelsolin was found in the region of the nerve fibers. Tubulin is found in microtubules in all cells of the organ of Corti. In supporting cells, microtubules are bundled together with actin microfilaments and tropomyosin, as well as being present as individual microtubules arranged in networks. An intensely stained network of microtubules is found in both outer and inner sensory hair cells. The microtubules in the outer hair cells appear to course throughout the entire length of the cells, and based on their staining with antibodies to the tyrosinated form of tubulin they appear to be more dynamic structures than the microtubules in the supporting cells. The microtubule-associated protein MAP-2 is present only in outer hair cells within the organ of Corti and co-localizes with tubulin in these cells. No other MAPs (1,3,4,5) are present. Tau is found in the nerve fibers below both inner and outer hair cells and in the osseous spiral lamina. It is clear that the actin-binding and microtubule-associated proteins present in the cochlea co-localize with actin and tubulin and that they modulate microfilament and microtubule structure and function in a manner similar to that seen in other cell types. The location of some of these proteins in outer hair cells suggests a role for microfilaments and microtubules in outer hair cell motility. C1 KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. RP SLEPECKY, NB (reprint author), SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244, USA. CR Angelborg C, 1972, Acta Otolaryngol Suppl, V301, P49 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 BENNETT V, 1985, ANNU REV BIOCHEM, V54, P273, DOI 10.1146/annurev.biochem.54.1.273 BRANTON B, 1981, CELL, V11, P14 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BURRIDGE K, 1981, NATURE, V294, P565, DOI 10.1038/294565a0 CARLISLE L, 1988, HEARING RES, V33, P201, DOI 10.1016/0378-5955(88)90033-0 CARLSSON L, 1977, J MOL BIOL, V115, P465, DOI 10.1016/0022-2836(77)90166-8 CLARKE M, 1977, ANNU REV BIOCHEM, V46, P797, DOI 10.1146/annurev.bi.46.070177.004053 CRAIG SW, 1979, J CELL BIOL, V80, P203, DOI 10.1083/jcb.80.1.203 DAVISON MD, 1988, CELL, V52, P159, DOI 10.1016/0092-8674(88)90503-X DECHESNE C, 1990, ABSTR ASS RES OT, V362 DECHESNE CJ, 1988, HEARING RES, V33, P273, DOI 10.1016/0378-5955(88)90157-8 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 DULON D, 1990, J NEUROSCI, V10, P1388 EYBALIN M, 1990, CR ACAD SCI III-VIE, V310, P639 FLOCK A, 1982, HEARING RES, V6, P75 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FURNESS DN, 1990, J ELECTRON MICR TECH, V15, P261, DOI 10.1002/jemt.1060150306 GARRELS JI, 1976, CELL, V9, P793, DOI 10.1016/0092-8674(76)90142-2 GEIGER B, 1981, J CELL BIOL, V91, P614, DOI 10.1083/jcb.91.3.614 GLENNEY JR, 1982, CELL, V28, P843, DOI 10.1016/0092-8674(82)90063-0 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 GRIFFITH LM, 1978, J CELL BIOL, V78, P958, DOI 10.1083/jcb.78.3.958 GUNDERSEN GG, 1984, CELL, V38, P779, DOI 10.1016/0092-8674(84)90273-3 HERZOG W, 1978, EUR J BIOCHEM, V92, P1, DOI 10.1111/j.1432-1033.1978.tb12716.x HIROKAWA N, 1983, CELL, V32, P953, DOI 10.1016/0092-8674(83)90080-6 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HOFFMAN EP, 1987, NATURE, V330, P754, DOI 10.1038/330754a0 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 HUBER G, 1984, J NEUROSCI, V4, P151 KOTANI S, 1985, J BIOL CHEM, V260, P779 KREIS TE, 1987, EMBO J, V6, P2597 LAZARIDES E, 1982, CELL, V31, P505, DOI 10.1016/0092-8674(82)90306-3 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LUBITZ DKJ, 1981, CELL TISSUE RES, V220, P787 MATUS A, 1986, NEUROSCIENCE, V17, P371, DOI 10.1016/0306-4522(86)90253-8 MATUS A, 1988, ANNU REV NEUROSCI, V11, P29, DOI 10.1146/annurev.neuro.11.1.29 MURPHY DB, 1975, P NATL ACAD SCI USA, V72, P2696, DOI 10.1073/pnas.72.7.2696 NADOL JB, 1983, LARYNGOSCOPE, V93, P780 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NELSON WJ, 1986, J CELL BIOL, V103, P1751, DOI 10.1083/jcb.103.5.1751 OLMSTED JB, 1986, ANN NY ACAD SCI, V466, P292, DOI 10.1111/j.1749-6632.1986.tb38401.x PAPASOZOMENOS SC, 1987, CELL MOTIL CYTOSKEL, V8, P210, DOI 10.1002/cm.970080303 POLLARD TD, 1986, ANNU REV BIOCHEM, V55, P987, DOI 10.1146/annurev.biochem.55.1.987 RABIE A, 1983, CELL TISSUE RES, V232, P691 RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x SAITO K, 1983, CELL TISSUE RES, V229, P467 SATTILARO RF, 1981, J CELL BIOL, V90, P467, DOI 10.1083/jcb.90.2.467 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 SLEPECKY N, 1988, BASIC ISSUES HEARING, P49 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SLEPECKY N, 1987, CELL TISSUE RES, V248, P63, DOI 10.1007/BF01239963 SLEPECKY N, 1986, CELL TISSUE RES, V245, P229 SLEPECKY N, 1983, HEARING RES, V10, P359, DOI 10.1016/0378-5955(83)90098-9 SLEPECKY N, 1982, CELL TISSUE RES, V224, P15, DOI 10.1007/BF00217262 SLEPECKY NB, 1988, CYTOL PATHOL, V20, P37 Small J V, 1982, Cold Spring Harb Symp Quant Biol, V46 Pt 2, P599 SOBEL JS, 1988, DEV BIOL, V126, P47, DOI 10.1016/0012-1606(88)90237-0 SOBIN A, 1983, ACTA OTO-LARYNGOL, V96, P407, DOI 10.3109/00016488309132726 Spoendlin H, 1966, ADV OTORHINOLARYNGOL, V13, P1 STEYGER PS, 1989, BR J AUDIOL, V23, P143 THALMANN I, 1990, LARYNGOSCOPE, V100, P99 THALMANN R, 1970, LARYNGOSCOPE, V80, P1619, DOI 10.1288/00005537-197011000-00001 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 TILNEY LG, 1980, J CELL BIOL, V86, P244, DOI 10.1083/jcb.86.1.244 ULFENDAHL M, 1992, UNPUB CALCIUM BINDIN VANDEKERCKHOVE J, 1978, J MOL BIOL, V126, P783, DOI 10.1016/0022-2836(78)90020-7 WEBSTER DR, 1987, P NATL ACAD SCI USA, V84, P9040, DOI 10.1073/pnas.84.24.9040 YLIKOSKI J, 1990, HEARING RES, V43, P199, DOI 10.1016/0378-5955(90)90228-H ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 83 TC 66 Z9 68 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 1992 VL 57 IS 2 BP 201 EP 215 DI 10.1016/0378-5955(92)90152-D PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700005 PM 1733913 ER PT J AU KNIPSCHILD, M DORRSCHEIDT, GJ RUBSAMEN, R AF KNIPSCHILD, M DORRSCHEIDT, GJ RUBSAMEN, R TI SETTING COMPLEX TASKS TO SINGLE UNITS IN THE AVIAN AUDITORY FOREBRAIN .1. PROCESSING OF COMPLEX ARTIFICIAL STIMULI SO HEARING RESEARCH LA English DT Article DE AVES; EUROPEAN STARLING; AUDITORY FOREBRAIN; COMPLEX STIMULI; REVERSE CORRELATION; PHASE LOCKING ID SPECIES-SPECIFIC CALLS; FOWL NUMIDA-MELEAGRIS; INFERIOR COLLICULUS; GUINEA FOWL; AMPLITUDE-MODULATION; COCHLEAR NUCLEUS; FIELD-L; FUNCTIONAL-ORGANIZATION; TONOTOPIC ORGANIZATION; DYNAMIC PROPERTIES AB In the auditory forebrain (field L) of the European starling (Sturnus vulgaris), single unit responses were recorded for a wide range of complex stimuli, comprising different forms of amplitude and frequency modulation. About two-third of the units locked to sinusoidal modulation regardless of whether frequency (SFM) or amplitude (SAM) was modulated. On average, however, frequency led to stronger synchronization. Both the proportion of phase locking and its mean strength showed a low-pass dependence on modulation frequency. The lower efficiency of amplitude modulation is also visible in unit responses when SAM is combined with (random) frequency modulation. For the assessment of response strength and its comparison across the tested repertoire of complex stimuli, a new index (REX) is introduced which primarily weighs similarity of the spike trains in identically repeated stimulus runs. Applied to a set of 311 field L neurons, also this approach discloses the two stimulus classes lacking frequency modulation (pure tone and SAM) as the least effective. A new measure for response latency, the Effective Response Delay (ERD), based on the spike-triggered analysis of responses to randomly frequency-modulated sounds (RFM), reflects physiological delays better than conventional latency. So, ERD correction of SAM and SFM Period Histograms allowed to disclose response effective stimulus ranges independent of modulation frequency. C1 RUHR UNIV BOCHUM,LEHRSTUHL ALLGEMEINE ZOOL & NEUROBIOL,W-4630 BOCHUM 1,GERMANY. CR AERTSEN AMHJ, 1980, BIOL CYBERN, V38, P235, DOI 10.1007/BF00337016 AITKIN LM, 1972, J NEUROPHYSIOL, V35, P365 BIGALKEKUNZ B, 1987, J COMP PHYSIOL A, V161, P255, DOI 10.1007/BF00615245 BONKE D, 1979, J COMP PHYSIOL, V132, P243 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 DEBOER E, 1968, IEEE T BIO-MED ENG, VBM15, P169, DOI 10.1109/TBME.1968.4502561 DOOLING RJ, 1981, J COMP PHYSIOL, V143, P383 DORRSCHEIDT GJ, 1988, SENSE ORGANS ENV BEH, P169 EVANS EF, 1973, EXP BRAIN RES, V17, P402 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 GREENWOOD JA, 1955, ANN MATH STAT, V26, P233, DOI 10.1214/aoms/1177728540 HOSE B, 1987, BRAIN RES, V422, P367, DOI 10.1016/0006-8993(87)90946-2 Johannesma PIM, 1972, P IPO S HEARING THEO, P58 KONISHI M, 1970, Z VERGL PHYSIOL, V66, P257, DOI 10.1007/BF00297829 KUHN A, 1982, NATURWISSENSCHAFTEN, V69, P245, DOI 10.1007/BF00398648 LANGNER G, 1983, EXP BRAIN RES, V52, P333 LEPPELSA.HJ, 1974, J COMP PHYSIOL, V88, P271, DOI 10.1007/BF00697959 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1977, INNER EAR BIOL, P127 MCCORNACK RL, 1965, J AM STAT ASSOC, V60, P864, DOI 10.2307/2283253 MOLLER AR, 1986, HEARING RES, V24, P203, DOI 10.1016/0378-5955(86)90019-5 MOLLER AR, 1975, J NEUROPHYSIOL, V38, P812 MOLLER AR, 1973, BRAIN RES, V57, P443, DOI 10.1016/0006-8993(73)90148-0 MULLER CM, 1985, EXP BRAIN RES, V59, P589 MULLER SC, 1985, J COMP PHYSIOL A, V156, P1, DOI 10.1007/BF00610661 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 ROSE M, 1914, J PSYCHOL NEUROL, V21, P278 RUBSAMEN R, 1986, J COMP PHYSIOL A, V158, P639, DOI 10.1007/BF00603820 Sachs M.B., 1980, P323 SCHAFER M, 1992, HEARING RES, V57, P231, DOI 10.1016/0378-5955(92)90154-F SCHEICH H, 1979, CELL TISSUE RES, V204, P17 SCHEICH H, 1979, J COMP PHYSIOL, V132, P257 SCHEICH H, 1983, ADV VERTEBRATE NEURO, P731 SCHREINER CE, 1988, HEARING RES, V32, P49, DOI 10.1016/0378-5955(88)90146-3 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 Ziemer R. E., 1976, PRINCIPLES COMMUNICA NR 38 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 1992 VL 57 IS 2 BP 216 EP 230 DI 10.1016/0378-5955(92)90153-E PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700006 PM 1733914 ER PT J AU SCHAFER, M RUBSAMEN, R DORRSCHEIDT, GJ KNIPSCHILD, M AF SCHAFER, M RUBSAMEN, R DORRSCHEIDT, GJ KNIPSCHILD, M TI SETTING COMPLEX TASKS TO SINGLE UNITS IN THE AVIAN AUDITORY FOREBRAIN .2. DO WE REALLY NEED NATURAL STIMULI TO DESCRIBE NEURONAL RESPONSE CHARACTERISTICS SO HEARING RESEARCH LA English DT Article DE AVES; EUROPEAN STARLING; AUDITORY FOREBRAIN; FEATURE DETECTION; SPECIES-SPECIFIC SOUND STIMULI; REVERSE CORRELATION ID TEMPORAL RECEPTIVE-FIELD; TONOTOPIC ORGANIZATION; VOCALIZATIONS; SONGBIRD; MIDBRAIN; CALLS AB The response characteristic of auditory forebrain neurons in the European starling was established both with artificial stimuli (AS) and a conspecific territorial song as a natural stimulus (NS1). Applying experimenter-centred statistical methods for response detection and for scaling response strength, and spike-triggered analyses for the delimitation of the key sound parameters (spectrotemporal receptive field STRF, Aertsen et al. 1980) the study aimed at disclosing differences in the processing of the two stimulus classes, AS and NS. With the STRF as reference, we find congruence (1) in the best frequency with those determined under sweep and bandpass noise stimulation, (2) in response latency, and (3) in response-intensity dependence, further similarity in the overall frequency characteristic. Partitioning the song into 42 acoustically defined segments allowed to further delimit the response criteria under natural stimulation. They are easily understood from the AS response characteristics: (1) In the neuronal sample as a whole, long segments are more effective than short and, among the short, loud segments are more effective than faint; (2) Units showing their best excitatory response to AS in a certain frequency band are most probably excited by segments with a high proportion of their power concentrated upon or near this band; (3) Units with a slow (build-up) AS response react to a lower number of song segments than those dynamically following AS transients. Our data give no hint towards adaptive, feature detection properties of single neurons in field L. Instead, these neurons appear to base their response solely on the short-time spectrotemporal structure of the stimulus, irrespective of its natural or artificial origin. C1 RUHR UNIV BOCHUM,LEHRSTUHL ALLGEMEINE ZOOL & NEUROBIOL,W-4630 BOCHUM 1,GERMANY. CR AERTSEN AMHJ, 1981, BIOL CYBERN, V39, P195, DOI 10.1007/BF00342772 AERTSEN AMHJ, 1979, BIOL CYBERN, V32, P175, DOI 10.1007/BF00337394 AERTSEN AMHJ, 1980, BIOL CYBERN, V38, P235, DOI 10.1007/BF00337016 BIGALKEKUNZ B, 1987, J COMP PHYSIOL A, V161, P255, DOI 10.1007/BF00615245 BONKE D, 1979, COMP PHYSL, V132, P257 Bullock TH, 1961, SENS COMMUN, P717 BULLOCK TH, 1977, LIFE SCI RES REP, V5 CREUTZFELDT O, 1980, EXP BRAIN RES, V39, P87 DEBOER E, 1968, IEEE T BIO-MED ENG, VBM15, P169, DOI 10.1109/TBME.1968.4502561 EGGERMONT JJ, 1983, HEARING RES, V10, P191, DOI 10.1016/0378-5955(83)90053-9 EGGERMONT JJ, 1986, HEARING RES, V24, P255, DOI 10.1016/0378-5955(86)90024-9 EGGERMONT JJ, 1983, HEARING RES, V10, P167, DOI 10.1016/0378-5955(83)90052-7 EWERT JP, 1987, BEHAV BRAIN SCI, V10, P337 FRISHKOP.LS, 1968, PR INST ELECTR ELECT, V56, P969, DOI 10.1109/PROC.1968.6448 GLASS I, 1979, EXP BRAIN RES, V34, P489 Johannesma PIM, 1972, P IPO S HEARING THEO, P58 JOHNSTON.BM, 1970, NATURE, V227, P625, DOI 10.1038/227625a0 KNIPSCHILD M, 1992, HEARING RES, V57, P216, DOI 10.1016/0378-5955(92)90153-E LEPPELSACK HJ, 1976, J COMP PHYSIOL, V107, P263 LEPPELSACK HJ, 1980, 17 ACT C INT ORN 197, P728 Leppelsack H.-J., 1983, NATO ASI (Advanced Science Institutes) Series Series A Life Sciences, V56, P783 LETTVIN JY, 1959, P IRE, V47, P1940, DOI 10.1109/JRPROC.1959.287207 MARGOLIASH D, 1983, J NEUROSCI, V3, P1039 MULLER CM, 1985, EXP BRAIN RES, V59, P587 NEWMAN JD, 1973, J EXP NEUROL, V40, P821 RUBSAMEN R, 1986, J COMP PHYSIOL A, V158, P639, DOI 10.1007/BF00603820 SCHEICH H, 1979, J COMP PHYSIOL, V132, P257 SCHEICH H, 1977, J COMP PHYSIOL, V117, P245 SCHEICH H, 1977, LIFE SCI RES REP, V5, P161 SCHEICH H, 1983, NATO ASI SER, V56, P731 SCHULZ W, 1986, J ORNITHOL, V127, P380 Siegel S., 1956, NONPARAMETRIC STATIS SUGA N, 1978, FED PROC, V37, P2342 SYMMES D, 1980, HEARING RES, V3, P133, DOI 10.1016/0378-5955(80)90041-6 SYMMES D, 1981, HEARING RES, V4, P203, DOI 10.1016/0378-5955(81)90007-1 WINTER P, 1973, EXP BRAIN RES, V18, P498 WORDEN FG, 1972, NEUROSCI PROG RES B, V10 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 JAN PY 1992 VL 57 IS 2 BP 231 EP 244 DI 10.1016/0378-5955(92)90154-F PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700007 PM 1733915 ER PT J AU PEAKE, WT ROSOWSKI, JJ LYNCH, TJ AF PEAKE, WT ROSOWSKI, JJ LYNCH, TJ TI MIDDLE-EAR TRANSMISSION - ACOUSTIC VERSUS OSSICULAR COUPLING IN CAT AND HUMAN SO HEARING RESEARCH LA English DT Article DE MIDDLE EAR; COCHLEAR WINDOWS; MODELS; ABNORMAL MIDDLE EARS ID RANA-TEMPORARIA L; DIRECTIONAL HEARING; AUDITORY BULLA; NETWORK MODEL; SOUND; FROG; INPUT; VIBRATION; EVOLUTION; MECHANICS AB Otologic surgeons consider the action of sound pressure on the cochlear windows to be of major importance in certain cases of middle-ear pathology, yet previously published network models of mammalian middle ears do not include such a mechanism. A unified middle-ear model is developed in which it is assumed that the difference of acoustic pressures acting on the windows adds to the ossicular-chain pressure to produce cochlear input. From a network model of the cat middle-ear cavities we estimate the contributions of pressures on the cochlear windows for both normal and abnormal cat ears. For the human ear we use the model of Kringlebotn (1988) and measurements of Bekesy (1947). We determine that the pressure difference across the cochlear windows is negligibly small in normal cat and human ears. Thus, it is a reasonable approximation to ignore this mechanism in normal ears. For ears with a drastically altered tympanic membrane and/or ossicular chain, acoustic coupling to the cochlear windows can-to a considerable extent-explain residual hearing in human. The model predicts hearing levels for type IV tympanoplastic reconstructions that agree with the best results obtained surgically. C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OTOLARYNGOL,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114. RP PEAKE, WT (reprint author), MIT,ELECTR RES LAB,ROOM 36-825,77 MASSACHUSETTS AVE,CAMBRIDGE,MA 02139, USA. CR AERTSEN AMHJ, 1986, HEARING RES, V21, P17, DOI 10.1016/0378-5955(86)90043-2 Allen J. B., 1986, PERIPHERAL AUDITORY, P44 BALLANTYNE JC, 1978, SYNOPSIS OTOLARYNGOL Baranek LL, 1954, ACOUSTICS Bekesy G., 1960, EXPT HEARING CARHART R, 1950, ARCH OTOLARYNGOL, V51, P798 DALLOS P, 1970, J ACOUST SOC AM, V48, P489, DOI 10.1121/1.1912163 Desoer C. A., 1969, BASIC CIRCUIT THEORY DICK JC, 1951, J PHYSIOL-LONDON, V112, P102 DIRKS DD, 1985, HDB CLIN AUDIOLOGY, P202 EHRET G, 1990, NATURWISSENSCHAFTEN, V77, P192, DOI 10.1007/BF01131168 FENG AS, 1981, HEARING RES, V5, P201, DOI 10.1016/0378-5955(81)90046-0 FROOTKO NJ, 1987, SCOTTBROWNS OTOLARYN, V3, pCH11 GISSELSSON L, 1958, J Laryngol Otol, V72, P329, DOI 10.1017/S0022215100053986 GOODE RL, 1988, ADV AUDIOL, V4, P22 GOTAYRODRIGUEZ VM, 1977, LARYNGOSCOPE, V87, P522 GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 GYO K, 1988, ADV AUDIOL, V4, P107 HARKNESS RD, 1961, BIOL REV, V36, P399, DOI 10.1111/j.1469-185X.1961.tb01596.x HARTLINE PH, 1971, J EXP BIOL, V54, P349 HAUT RC, 1969, J BIOMECH, V2, P289, DOI 10.1016/0021-9290(69)90085-2 HILL KG, 1980, J EXP BIOL, V86, P135 HOODHILL V, 1979, EAR DISEASES DEAFNES HOUGH J, 1988, ANN OTO RHINOL LARYN, V97, P650 HOUGH J V, 1959, Laryngoscope, V69, P644 HUNT RM, 1974, J MORPHOL, V143, P21, DOI 10.1002/jmor.1051430103 Jahnke K, 1988, Adv Otorhinolaryngol, V39, P65 JERGER J, 1975, HDB CLIN IMPEDANCE A, P189 Keen J. A., 1941, Transactions of the Royal Society of South Africa, V28, P307 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 Kirikae I., 1960, STRUCTURE FUNCTION M KODERA K, 1988, ADV AUDIOL, V4, P97 KOHLLOFFEL LUE, 1984, HEARING RES, V13, P83, DOI 10.1016/0378-5955(84)90098-4 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 LEE K, 1971, LARYNGOSCOPE, V81, P529, DOI 10.1288/00005537-197104000-00004 LYNCH TJ, 1982, J ACOUST SOC AM, V72, P108, DOI 10.1121/1.387995 LYNCH TJ, 1981, THESIS MIT CAMBRIDGE MANIGLIA AJ, 1988, ANN OTO RHINOL LARYN, V97, P3 MARGOLIS RH, 1978, ACTA OTO-LARYNGOL, V86, P428, DOI 10.3109/00016487809107522 MATTHEWS JW, 1983, MECHANICS HEARING MCDONALD TJ, 1986, OTOLARYNGOLOGY HEAD, P3081 MCELVEEN JT, 1982, ANN OTO RHINOL LARYN, V91, P526 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 MUNDIE JR, 1963, 576 US ARM MED RES R, P63 NADOL JB, 1990, COMMUNICATION NADOL JB, 1989, COMMUNICATION NARINS PM, 1988, P NATL ACAD SCI USA, V85, P1508, DOI 10.1073/pnas.85.5.1508 NOVACEK MJ, 1977, MAMMAL REV, V7, P131, DOI 10.1111/j.1365-2907.1977.tb00366.x NUTTALL AL, 1974, J ACOUST SOC AM, V56, P1231, DOI 10.1121/1.1903413 NUTTALL AL, 1974, J ACOUST SOC AM, V56, P1239, DOI 10.1121/1.1903414 ONCHI Y, 1961, J ACOUST SOC AM, V33, P794, DOI 10.1121/1.1908801 PALVA T, 1982, CHOLESTEATOMA MASTOI, P491 PAPARELLA M, 1973, OTOLARYNGOLOGY, V2 PEAKE WT, 1967, MIT RES LAB ELECTRON, V84, P320 PINDER AC, 1983, PROC R SOC SER B-BIO, V219, P371, DOI 10.1098/rspb.1983.0079 PROCTOR B, 1964, ARCHIV OTOLARYNGOL, V79, P176 Roark R. J., 1975, FORMULAS STRESS STRA ROSOWSKI JJ, 1990, ANN OTO RHINOL LARYN, V99, P403 ROSOWSKI JJ, 1987, ACCESSORY ACOUSTIC P ROSOWSKI JJ, 1980, J COMP PHYSIOL, V136, P183 ROSOWSKI JJ, 1991, J ACOUST SOC AM, V90, P124, DOI 10.1121/1.401306 ROSOWSKI JJ, 1988, J ACOUST SOC AM, V84, P1695, DOI 10.1121/1.397185 SATALOFF, 1966, HEARING LOSS Schuknecht H. F., 1974, PATHOLOGY EAR SHERA CA, 1991, COMMUNICATION SHERA CA, 1989, UNPUB TRANSFER MATRI STROMBER.DD, 1969, J APPL PHYSIOL, V26, P857 SUZUKI J, 1985, ACTA OTO-LARYNGOL, V99, P313, DOI 10.3109/00016488509108915 SUZUKI JI, 1988, ADV AUDIOL, V4 TONNDORF J, 1972, F MODERN AUDITORY TH, V2, P197 VLAMING MSMG, 1986, CLIN OTOLARYNGOL, V11, P411, DOI 10.1111/j.1365-2273.1986.tb00145.x VLAMING MSMG, 1984, HEARING RES, V14, P191, DOI 10.1016/0378-5955(84)90018-2 von Bekesy G., 1941, AKUST Z, V6, P1 von Bekesy G., 1947, ACTA OTO-LARYNGOL, V35, p[301, 115] VONBEKESY G, 1948, J ACOUST SOC AM, V20, P727 VONBEKESY G, 1932, ANN PHYSIK, V79, P111 WEVER EG, 1950, J ACOUST SOC AM, V22, P460, DOI 10.1121/1.1906628 WEVER EG, 1948, ARCH OTOLARYNGOL, V48, P19 Wever EG, 1954, PHYSL ACOUSTICS WILLIAMS M, 1990, SCAND AUDIOL, V19, P161, DOI 10.3109/01050399009070767 WILSON EP, 1990, AM J OTOLARYNG, V11, P149, DOI 10.1016/0196-0709(90)90029-U Wullstein H, 1967, ANN OTO RHINOL LARYN, V65, P1020 ZWISLOCKI J, 1963, J ACOUST SOC AM, V35, P1034, DOI 10.1121/1.1918650 ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 ZWISLOCKI JJ, 1970, ASHA MONOGRAPH, V15 NR 88 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 JAN PY 1992 VL 57 IS 2 BP 245 EP 268 DI 10.1016/0378-5955(92)90155-G PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700008 PM 1733916 ER PT J AU AVAN, P BONFILS, P AF AVAN, P BONFILS, P TI ANALYSIS OF POSSIBLE INTERACTIONS OF AN ATTENTIONAL TASK WITH COCHLEAR MICROMECHANICS SO HEARING RESEARCH LA English DT Article DE COCHLEAR MECHANICS; OTOACOUSTIC EMISSIONS; EFFERENT PATHWAYS; SELECTIVE ATTENTION ID PRODUCT OTOACOUSTIC EMISSIONS; CROSSED OLIVOCOCHLEAR BUNDLE; AUDITORY EVOKED-POTENTIALS; STIMULATION; RESPONSES; SYSTEM; EARS AB Several contradictory studies have been published regarding the effect of selective attention on cochlear mechanics, possibly modulated through efferent pathways. Click-evoked otoacoustic emissions have been proposed as a highly sensitive tool for testing the hypothesis of such a modulation. In this study, two other types of evoked otoacoustic emissions (i.e. distortion products and stimulus frequency emissions between 1 and 4 kHz) were measured on 20 normal subjects in absence and presence of a visual selective attention task. The duration of measurements at a given frequency was short enough to eliminate possible artefacts due to long-time averaging. No significant change was observed in these signals, considered as probes of cochlear micromechanics. It is concluded that in this set of experimental conditions, selective attention has a negligible effect on peripheral sensitivity. C1 FAC MED LARIBOISIERE,BIOPHYS LAB PAM NEUROSENSORIEL,PARIS,FRANCE. HOP BOUCICAULT,DEPT EAR NOSE & THROAT,F-75730 PARIS 15,FRANCE. CR AVAN P, 1991, HEARING RES, V52, P99, DOI 10.1016/0378-5955(91)90191-B Bonfils P, 1990, Ann Otolaryngol Chir Cervicofac, V107, P224 BONFILS P, 1991, IN PRESS ARCH OTOLAR BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BRIX R, 1984, ACTA OTO-LARYNGOL, V98, P89, DOI 10.3109/00016488409107538 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 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E FAYELUND H, 1986, ANAT EMBRYOL, V175, P35, DOI 10.1007/BF00315454 FLOCK A, 1983, HEARING PHYSL BASES, P2 FROEHLICH P, 1990, BRAIN RES, V508, P286, DOI 10.1016/0006-8993(90)90408-4 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 Guinan JJ, 1990, MECH BIOPHYSICS HEAR, P170 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HERNANDEZPEON R, 1957, ACTA NEUROL LATINOAM, V3, P144 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 LEONARD G, 1990, ADV AUDIOL, V7, P139 LUKAS JH, 1981, INT J NEUROSCI, V12, P137 LUKAS JH, 1980, PSYCHOPHYSIOLOGY, V17, P444, DOI 10.1111/j.1469-8986.1980.tb00181.x 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 OATMAN LC, 1976, EXP NEUROL, V51, P41, DOI 10.1016/0014-4886(76)90052-2 PAPANICOLAOU AC, 1986, BRAIN LANG, V27, P50, DOI 10.1016/0093-934X(86)90004-0 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P191, DOI 10.1016/0013-4694(74)90156-4 PROBST R, 1990, AM J OTOLARYNG, V11, P236, DOI 10.1016/0196-0709(90)90083-8 Puel J.L., 1989, COCHLEAR MECHANISMS, P315 PUEL JL, 1988, BRAIN RES, V447, P380, DOI 10.1016/0006-8993(88)91144-4 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 ROUILLER EM, 1991, IN PRESS INTRO ANATO RUBEL EW, 1991, VVULNERABILITY OTOAC SIEGEL JH, 1982, HEARING RES, V6, P1271 SMURZYNSKI J, 1990, ARCH OTOLARYNGOL, V116, P1309 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P966, DOI 10.1121/1.1912235 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 ZWICKER E, 1990, HEARING RES, V47, P185, DOI 10.1016/0378-5955(90)90150-N NR 37 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 JAN PY 1992 VL 57 IS 2 BP 269 EP 275 DI 10.1016/0378-5955(92)90156-H PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GX097 UT WOS:A1992GX09700009 PM 1733917 ER PT J AU MANLEY, GA KAISER, A BRIX, J GLEICH, O AF MANLEY, GA KAISER, A BRIX, J GLEICH, O TI ACTIVITY PATTERNS OF PRIMARY AUDITORY-NERVE FIBERS IN CHICKENS - DEVELOPMENT OF FUNDAMENTAL PROPERTIES SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; CHICKEN; PRIMARY AUDITORY NEURONS; COCHLEAR GANGLION; AUDITORY PHYSIOLOGY; BIRD ID HAIR CELL LOSS; BASILAR PAPILLA; TONOTOPIC ORGANIZATION; ACOUSTIC TRAUMA; PREFERRED INTERVALS; DISCHARGE PATTERNS; MAMMALIAN COCHLEA; PRIMARY AFFERENTS; PLACE PRINCIPLE; SINGLE FIBERS AB We have examined the activity patterns of single auditory-nerve fibres in the chicken and tested for possible changes during post-hatching development. For this purpose, we recorded from fibres in the cochlear ganglion of chickens of two age groups (about P2 and P21) and investigated their spontaneous and sound-evoked activity patterns under nembutal-chloralhydrate anaesthesia. The spontaneous activity of primary auditory neurones was irregular, the average rates were between 20.5 (P2) and 23 (P21) spikes/s. Many low-frequency fibres from both age groups showed preferred intervals in their spontaneous activity. Tuning characteristics, including the range of characteristic frequencies, the presence of primary and two-tone suppression, the slopes of tuning-curve flanks and Q10 dB values were similar to those previously reported for the starling and were statistically indistinguishable between the two age groups. However, there was a difference in fibre thresholds at the highest frequencies. Systematic differences were also present between the two age groups with regard to some characteristics of the rate-intensity functions. These data indicate that whereas the tuning properties of primary auditory fibres of the chicken cochlea are mature as early as post-hatching day 2, the intensity functions are not. RP MANLEY, GA (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,W-8046 GARCHING,GERMANY. CR ANASTASIO TJ, 1985, J NEUROPHYSIOL, V54, P335 ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 BOORD RL, 1963, J COMP NEUROL, V120, P463, DOI 10.1002/cne.901200305 CHANDLER JP, 1984, J COMP NEUROL, V222, P506, DOI 10.1002/cne.902220405 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 COTANCHE DA, 1984, DEV BRAIN RES, V16, P181, DOI 10.1016/0165-3806(84)90024-5 COTANCHE D A, 1984, Society for Neuroscience Abstracts, V10, P529 COUSILLAS H, 1985, HEARING RES, V19, P217, DOI 10.1016/0378-5955(85)90141-8 CRAWFORD AC, 1985, J PHYSL, V364, P659 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 EATOCK RA, 1981, J COMP PHYSIOL, V142, P203 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FERMIN CD, 1984, ACTA OTO-LARYNGOL, V97, P39, DOI 10.3109/00016488409130963 FERMIN CD, 1984, ACTA OTO-LARYNGOL, V98, P42, DOI 10.3109/00016488409107533 GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 GLEICH O, 1988, HEARING RES, V32, P81, DOI 10.1016/0378-5955(88)90148-7 GLEICH O, 1987, NEW FRONTIERS BRAIN, P101 GLEICH O, 1987, ABSTR ASS RES OT, P22 GRAY L, 1985, J ACOUST SOC AM, V77, P1162, DOI 10.1121/1.392180 GROSS NB, 1976, BRAIN RES, V101, P209, DOI 10.1016/0006-8993(76)90264-X GUMMER AW, 1989, 26TH WORKSH INN EAR GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 HAESELER C, 1989, DYNAMICS PLASTICITY, P282 HILL KG, 1989, HEARING RES, V39, P37, DOI 10.1016/0378-5955(89)90080-4 HILL KG, 1989, HEARING RES, V39, P49, DOI 10.1016/0378-5955(89)90081-6 HILL KG, 1989, HEARING RES, V39, P63, DOI 10.1016/0378-5955(89)90082-8 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 LIPPE W, 1985, J COMP NEUROL, V237, P273, DOI 10.1002/cne.902370211 LIPPE WR, 1987, HEARING RES, V25, P205, DOI 10.1016/0378-5955(87)90092-X 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, 1984, NATURWISSENSCHAFTEN, V71, P592, DOI 10.1007/BF01189191 MANLEY GA, 1991, HEARING RES, V56, P211, DOI 10.1016/0378-5955(91)90172-6 MANLEY GA, 1991, IN PRESS EVOLUTIONAR Manley G.A., 1988, P3 Manley G., 1983, P207 MANLEY GA, 1990, PERIPHERAL HEARLING MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1977, 14TH INN EAR BIOL WO, P127 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 PATUZZI R, 1983, J ACOUST SOC AM, V74, P1734, DOI 10.1121/1.390282 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 REBILLARD G, 1981, BRAIN RES, V229, P15, DOI 10.1016/0006-8993(81)90741-1 REBILLARD G, 1982, HEARING RES, V8, P77, DOI 10.1016/0378-5955(82)90036-3 REBILLARD M, 1983, ACTA OTO-LARYNGOL, V96, P379, DOI 10.3109/00016488309132723 ROMAND R, 1984, EXP BRAIN RES, V56, P395 ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RUBEL EW, 1984, ANN OTO RHINOL LARYN, V93, P609 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, 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, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 Sachs M.B., 1980, P323 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SAUNDERS JC, 1986, HEARING RES, V24, P227, DOI 10.1016/0378-5955(86)90021-3 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SCHERMULY L, 1990, J COMP PHYSIOL A, V166, P355 SCHWARTZKOPFF J, 1963, J PHYSIOL-PARIS, V55, P495 SINGER I, 1989, 26TH INN EAR BIOL M TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 TEMCHIN AN, 1980, DOKL AKAD NAUK SSSR+, V253, P773 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P277, DOI 10.1016/0306-4522(85)90178-2 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P255, DOI 10.1016/0306-4522(85)90177-0 NR 69 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 DEC PY 1991 VL 57 IS 1 BP 1 EP 15 DI 10.1016/0378-5955(91)90068-K PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500001 PM 1774201 ER PT J AU SHAPIRO, SM CONLEE, JW AF SHAPIRO, SM CONLEE, JW TI BRAIN-STEM AUDITORY EVOKED-POTENTIALS CORRELATE WITH MORPHOLOGICAL-CHANGES IN GUNN RAT PUPS SO HEARING RESEARCH LA English DT Article DE BILIRUBIN ENCEPHALOPATHY; BRAIN-STEM AUDITORY EVOKED POTENTIALS; HEARING LOSS; HYPERBILIRUBINEMIA; JAUNDICE; KERNICTERUS; TRAPEZOID BODY; COCHLEAR NUCLEUS; SUPERIOR OLIVE ID ACUTE BILIRUBIN ENCEPHALOPATHY; STEM; SULFADIMETHOXINE AB The relationship of brainstem structure and function in bilirubin encephalopathy is incompletely understood. The present experiments compare quantitative measures of brainstem structures with brainstem auditory evoked potentials (BAEPs) in infant jaundiced (jj) and nonjaundiced (Nj) Gunn rats. Ten jj's from 4 litters were injected with sulfadimethoxine at 11-12 days of age to raise their brain bilirubin concentration. Littermate controls were jj's given saline, and Nj's given sulfadimethoxine or saline. At 15-17 days of age BAEPs were recorded, and rats were prepared for histological examination, as was reported in the previous paper (Conlee and Shapiro, 1991). Significant differences between groups were seen for BAEP wave I latency (P = 0.002), I-II interwave interval (P = 0.001), and amplitudes of waves I, II, III, and IV (each P < 0.0005) due to increased latencies and decreased amplitudes in the jj-sulfa group. Animals with the most severe BAEP abnormalities had the most severe histological abnormalities. Cochlear nucleus volume had a positive linear correlation with the amplitude of BAEP waves I, II, and IV, and an inverse correlation with wave I latency and I-II interwave interval (P less-than-or-equal-to 0.001). The highest correlations were BAEP I-II interwave interval and amplitude of waves I and II with cochlear nucleus volume (r = -0.78, 0.71 and 0.70, respectively, P < 0.0005). In the cochlear nucleus, spherical cell area correlated with wave I latency and amplitude, and wave III amplitude (P < 0.001), the I-II interwave interval, and the amplitudes of waves II and IV (P < 0.01). In contrast, globular cells, which were not affected anatomically, did not correlate significantly with later BAEP waves. Cell area in the nucleus of the trapezoid body correlated with amplitude of I and II (P < 0.01). There were no significant correlations of cell area in the superior olive with any of the BAEP values. These results show that BAEPs are sensitive indicators of morphometric abnormalities in the brainstem of jaundiced Gunn rats, and help to establish the predictive validity of BAEPs in determining the specific sites of bilirubin-induced brain damage. C1 VET AFFAIRS MED CTR,SALT LAKE CITY,UT. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PEDIAT,RICHMOND,VA 23298. UNIV UTAH,SCH MED,DEPT ANAT,SALT LAKE CITY,UT 84112. RP SHAPIRO, SM (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT NEUROL,DIV CHILD NEUROL,BOX 211,MCV STN,RICHMOND,VA 23298, USA. CR AHDABBARMADA M, 1984, J NEUROPATH EXP NEUR, V43, P45, DOI 10.1097/00005072-198401000-00004 BLANC WA, 1959, J NEUROPATH EXP NEUR, V18, P165, DOI 10.1097/00005072-195901000-00011 CONLEE JW, 1991, HEARING RES, V52, P23 DIAMOND I, 1966, J CLIN INVEST, V45, P678, DOI 10.1172/JCI105383 DUBLIN W, 1976, FUNDAMENTALS SENSORI DUBLIN W, 1974, ARCH OTOLARYNGOL, V100, P55 DUBLIN WB, 1951, AM J CLIN PATHOL, V21, P935 ELBARBARY A, 1991, UNPUB HEARING RES Harrison J.M., 1974, P283 HAYMAKER W, 1961, KERNICTERUS ITS IMPO, P21 HUANG CM, 1977, BRAIN RES, V137, P291 JEW JY, 1979, ARCH NEUROL-CHICAGO, V36, P149 JEW JY, 1977, J ANAT, V124, P599 JOHNSON L, 1959, AMA J DIS CHILD, V97, P591 KELEMEN G, 1956, ARCHIV OTOLARYNGOL, V63, P392 Keppel G., 1982, DESIGN ANAL RES HDB LARROCHE JC, 1968, HDB CLIN NEUROLOGY, P491 MATKIN ND, 1966, ARCHIV OTOLARYNGOL, V84, P502 MOLLER AR, 1983, EXP NEUROL, V80, P633, DOI 10.1016/0014-4886(83)90313-8 PLANTZ RG, 1974, BRAIN RES, V68, P55, DOI 10.1016/0006-8993(74)90533-2 ROSE AL, 1979, J NEUROPATH EXP NEUR, V38, P152, DOI 10.1097/00005072-197903000-00006 SCHUTTA HS, 1971, LAB INVEST, V24, P82 SCHUTTA HS, 1967, J NEUROPATH EXP NEUR, V26, P377, DOI 10.1097/00005072-196707000-00003 SCHUTTA HS, 1969, J PEDIATR, V75, P1070, DOI 10.1016/S0022-3476(69)80351-3 SHAPIRO SM, 1988, PEDIATR RES, V23, P306, DOI 10.1203/00006450-198803000-00015 SHAPIRO SM, 1989, ANN OTO RHINOL LARYN, V98, P308 SHAPIRO SM, 1988, DEV BRAIN RES, V41, P147, DOI 10.1016/0165-3806(88)90178-2 SHAPIRO SM, 1991, IN PRESS HEAR RES STREBEL L, 1971, PEDIATR RES, V5, P548, DOI 10.1203/00006450-197110000-00007 UZIEL A, 1983, ACTA OTO-LARYNGOL, V95, P651, DOI 10.3109/00016488309139458 ZHANG S, 1989, BRAIN RES, V501, P194, DOI 10.1016/0006-8993(89)91043-3 Zimmerman HM, 1933, AM J DIS CHILD, V45, P740 NR 32 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 DEC PY 1991 VL 57 IS 1 BP 16 EP 22 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500002 PM 1774207 ER PT J AU CONLEE, JW SHAPIRO, SM AF CONLEE, JW SHAPIRO, SM TI MORPHOLOGICAL-CHANGES IN THE COCHLEAR NUCLEUS AND NUCLEUS OF THE TRAPEZOID BODY IN GUNN RAT PUPS SO HEARING RESEARCH LA English DT Article DE BILIRUBIN ENCEPHALOPATHY; BRAIN-STEM AUDITORY EVOKED POTENTIALS; HEARING LOSS; HYPERBILIRUBINEMIA; JAUNDICE; KERNICTERUS; TRAPEZOID BODY; COCHLEAR NUCLEUS; SUPERIOR OLIVE ID ACUTE BILIRUBIN ENCEPHALOPATHY; BRAIN-STEM ANOMALIES; EVOKED-POTENTIALS; SUPERIOR OLIVE; ALBINO CATS; ABNORMALITIES; SULFADIMETHOXINE; RESPONSES; LESIONS AB Mechanisms underlying bilirubin encephalopathy and hearing loss remain poorly understood, including the way bilirubin enters the nervous system and how bilirubin accumulates in circumscribed regions of the brain. The present experiments examined the auditory brainstem in heterozygous (Nj) and homozygous (jj) Gunn rats at an age when serum bilirubin levels were highest, and after brain bilirubin concentration was artificially raised by sulfadimethoxine administration. In four litters of 11-12 day old Gunn rats, Nj and jj littermates received a single intraperitoneal injection of sulfadimethoxine (100 mg/kg) or a comparable volume of saline. At 16-17 days of age, brainstem auditory evoked potentials were recorded to assess the severity of bilirubin toxicity in the Nj and jj animals. Following the recordings, each animal was perfusion-fixed and frozen sections of the brainstem were cut in the transverse plane from medullary through mesencephalic levels. Sections were mounted on slides, stained with thionin and coded to avoid observer bias. Quantitative analysis revealed no differences between saline and sulfa-treated Nj rats for cochlear nucleus volume, or for cell size in the cochlear nucleus or superior olive. In the sulfa-treated jj rats, cochlear nucleus volume, and cross-sectional areas of spherical cells in the anteroventral cochlear nucleus and principal cells in the nucleus of the trapezoid body, were all significantly smaller than in the combined groups of Nj animals. The affected areas in the cochlear nucleus and superior olive are innervated by large axosomatic end-bulbs of Held or calyceal endings, and were associated with bilirubin staining of glia in the most severely jaundiced jj sulfa-treated rats. The findings suggest that cells receiving synaptic input from end-bulbs or calyces are early targets of bilirubin toxicity in the auditory system. C1 VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA,DEPT NEUROL,DIV CHILD NEUROL, BOX 211,MCV STN, RICHMOND, VA 23298 USA. UNIV UTAH, SCH MED, DEPT ANAT, SALT LAKE CITY, UT 84112 USA. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT PEDIAT, RICHMOND, VA 23298 USA. VET AFFAIRS MED CTR, SALT LAKE CITY, UT USA. RP SHAPIRO, SM (reprint author), VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA,DEPT NEUROL,DIV CHILD NEUROL, BOX 211, MCV STN, RICHMOND, VA 23298 USA. CR AHDABBARMADA M, 1984, J NEUROPATH EXP NEUR, V43, P45, DOI 10.1097/00005072-198401000-00004 BERGMAN I, 1985, J PEDIATR, V106, P5 BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 BRUGGE JF, 1987, 10TH MIDW M ARO, P97 CHEN HC, 1965, AM J PATHOL, V46, P331 CHIAPPA KH, 1982, NEW ENGL J MED, V306, P1140, DOI 10.1056/NEJM198205133061904 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 COLLINGRIDGE GL, 1989, PHARMACOL REV, V41, P143 CONLEE JW, 1984, J COMP NEUROL, V225, P141, DOI 10.1002/cne.902250115 CREEL D, 1983, BRAIN RES, V260, P1, DOI 10.1016/0006-8993(83)90758-8 DIAMOND I, 1966, J CLIN INVEST, V45, P678, DOI 10.1172/JCI105383 DUBLIN W, 1976, FUNDAMENTALS SENSORI DUBLIN WB, 1951, AM J CLIN PATHOL, V21, P935 Friede R. L., 1975, DEV NEUROPATHOLOGY Godfrey DA, 1988, AUDITORY PATHWAY, P107 HARRISON JM, 1962, J COMP NEUROL, V119, P341, DOI 10.1002/cne.901190306 JEW JY, 1979, ARCH NEUROL-CHICAGO, V36, P149 JEW JY, 1977, J ANAT, V124, P599 JOHNSON L, 1961, AM J DIS CHILD, V101, P322 JOHNSON L, 1959, AMA J DIS CHILD, V97, P591 LING EA, 1973, J COMP NEUROL, V149, P73, DOI 10.1002/cne.901490105 LUCEY JF, 1964, EXP NEUROL, V9, P43, DOI 10.1016/0014-4886(64)90042-1 MACDONALD JW, 1990, SOC NEUROSCI, V16, P1123 MACDONALD JW, 1990, ANN NEUROL, V28, P413 MOREST D. KENT, 1968, BRAIN RES, V9, P288, DOI 10.1016/0006-8993(68)90235-7 ODELL GB, 1970, PEDIATRICS, V46, P16 ROSE AL, 1979, J NEUROPATH EXP NEUR, V38, P152, DOI 10.1097/00005072-197903000-00006 RYUGO DK, 1982, J COMP NEUROL, V210, P239, DOI 10.1002/cne.902100304 SALAMY A, 1989, J PEDIATR-US, V114, P847, DOI 10.1016/S0022-3476(89)80151-9 SAWASAKI Y, 1976, J NEUROCHEM, V27, P577, DOI 10.1111/j.1471-4159.1976.tb12285.x SCHUTTA HS, 1971, LAB INVEST, V24, P82 SCHUTTA HS, 1967, J NEUROPATH EXP NEUR, V26, P377, DOI 10.1097/00005072-196707000-00003 SCHUTTA HS, 1970, J NEUROPATH EXP NEUR, V29, P296, DOI 10.1097/00005072-197004000-00010 SCHUTTA HS, 1969, J PEDIATR, V75, P1070, DOI 10.1016/S0022-3476(69)80351-3 SHAPIRO SM, 1988, PEDIATR RES, V23, P306, DOI 10.1203/00006450-198803000-00015 SHAPIRO SM, 1989, ANN OTO RHINOL LARYN, V98, P308 SHAPIRO SM, 1991, HEARING RES, V57, P16 SHAPIRO SM, 1988, DEV BRAIN RES, V41, P147, DOI 10.1016/0165-3806(88)90178-2 STARR A, 1976, ELECTROEN CLIN NEURO, V41, P595, DOI 10.1016/0013-4694(76)90005-5 STREBEL L, 1971, PEDIATR RES, V5, P548, DOI 10.1203/00006450-197110000-00007 STURROCK RR, 1978, NEUROPATH APPL NEURO, V4, P209, DOI 10.1111/j.1365-2990.1978.tb00538.x TREMAIN KE, 1982, EXP BRAIN RES, V45, P243 TRUNE DR, 1987, ABSTR ASS RES OT, P66 UZIEL A, 1983, ACTA OTO-LARYNGOL, V95, P651, DOI 10.3109/00016488309139458 VAZQUEZ J, 1988, J BIOL CHEM, V263, P1255 VOLPE JJ, 1987, NEUROLOGY NEWBORN, P386 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P352, DOI 10.1016/0013-4694(83)90261-4 WEBSTER DB, 1982, AM J ANAT, V163, P103, DOI 10.1002/aja.1001630202 WENTHOLD RJ, 1985, AUDITORY BIOCH ZHANG S, 1989, BRAIN RES, V501, P194, DOI 10.1016/0006-8993(89)91043-3 Zimmerman HM, 1933, AM J DIS CHILD, V45, P740 NR 52 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 1991 VL 57 IS 1 BP 23 EP 30 DI 10.1016/0378-5955(91)90070-P PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500003 PM 1774208 ER PT J AU ULFENDAHL, M KHANNA, SM FLOCK, A AF ULFENDAHL, M KHANNA, SM FLOCK, A TI EFFECTS OF OPENING AND RESEALING THE COCHLEA ON THE MECHANICAL RESPONSE IN THE ISOLATED TEMPORAL BONE PREPARATION SO HEARING RESEARCH LA English DT Article DE COCHLEAR MECHANICS; ORGAN OF CORTI; HAIR CELL; MICROMECHANICS ID BASILAR-MEMBRANE; MOSSBAUER TECHNIQUE; VIBRATION; EAR AB The isolated temporal bone preparation has been used previously for studying the micromechanical behaviour of the cochlea. Mechanical tuning curves have been obtained from several cells and structures within the hearing organ. In order to obtain access to the apical turns the bony shell of the cochlea has to be opened. To study how the opening affects the mechanical response of the cochlea, experiments were performed in which the cochlea was opened and then sealed with a glass window. Responses were measured from the same identified cells in the opened and in the sealed cochlea. The opening of the cochlea reduced the vibration amplitude mainly at frequencies below 300 Hz. Below the mechanical resonance frequency the slope of the tuning curve became steeper. The shape was not affected appreciably above the resonance frequency. The relative vibration amplitude of different cells remained unchanged by opening and closing the cochlea. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT OTOLARYNGOL,NEW YORK,NY 10032. RP ULFENDAHL, M (reprint author), KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. CR Bekesy G., 1960, EXPT HEARING HUXLEY AF, 1969, NATURE, V221, P935, DOI 10.1038/221935a0 JOHNSTON.BM, 1967, SCIENCE, V158, P389, DOI 10.1126/science.158.3799.389 KARLSSON KK, 1991, HEARING RES, V53, P95, DOI 10.1016/0378-5955(91)90216-V KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P189 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P163 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P157 KHANNA SM, 1981, MATH MODELING HEARIN, P70 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P151 Koester C J, 1989, Acta Otolaryngol Suppl, V467, P27 KOHLLOFF.LU, 1972, ACUSTICA, V27, P49 LEPAGE EL, 1980, HEARING RES, V2, P183, DOI 10.1016/0378-5955(80)90056-8 Lund D T, 1989, Acta Otolaryngol Suppl, V467, P77 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SOKOLICH WG, 1977, J ACOUST SOC AM, V56, pS12 ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 Ulfendahl M, 1989, Acta Otolaryngol Suppl, V467, P145 Ulfendahl M, 1989, Acta Otolaryngol Suppl, V467, P91 ULFENDAHL M, 1991, ABSTR ASS RES OT ST, P396 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 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 DEC PY 1991 VL 57 IS 1 BP 31 EP 37 DI 10.1016/0378-5955(91)90071-G PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500004 PM 1774209 ER PT J AU GILLOYZAGA, P GABRION, J REMEZAL, M NGUYENTHANDAO, B UZIEL, A AF GILLOYZAGA, P GABRION, J REMEZAL, M NGUYENTHANDAO, B UZIEL, A TI INCORPORATION OF D-[H-3]-GLUCOSAMINE AND L-[H-3]-FUCOSE INTO THE DEVELOPING RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; DEVELOPMENT; D-GLUCOSAMINE; L-FUCOSE; AUTORADIOGRAPHY ID TECTORIAL MEMBRANE; GLYCOPROTEINS; ORGANIZATION; ORGAN AB The uptake of two tritiated carbohydrates, D-[H-3]-glucosamine and L-[H-3]-fucose, to the developing rat cochlea was examined using light and electron microscopic radioautography. Both carbohydrates, administered to in vitro developing rat cochleas, shared a similar ultrastructural labeling pattern on the microvilli and apical cell region and on the tectorial membrane (TM) fibrils. On embryonic day 18, the radiolabeling appeared on the apical surface of the undifferentiated epithelium that will develop into both spiral limbus and Kolliker's organ (KO), while on postnatal day (PD) 1, it was only located on the apical surface of the KO. When D-[H-3]-glucosamine was administered in vivo to newborn rats, the radiolabeling was observed in the TM covering the KO at PD 3. Lastly, D-[H-3]-glucosamine administered in vivo to PD 7 rats, appeared at PD 9 in the TM region lying just above the organ of Corti. The present findings support the previously suggested leading role of the spiral limbus and KO in the secretion of the TM during cochlear development. The secretion of carbohydrates, and probably of other matrix components, starts on the spiral limbus and KO region and progressively extends to the organ of Corti. C1 CHR ST CHARLES,INSERM,U254,NEUROBIOL AUDIT LAB,MONTPELLIER,FRANCE. UNIV MONTPELLIER 2,CNRS,UA 1197,F-34060 MONTPELLIER,FRANCE. RP GILLOYZAGA, P (reprint author), UNIV COMPLUTENSE MADRID,DEPT CIENCIAS MORFOL,APARTADO CORREOS,E-28080 MADRID,SPAIN. CR ARNOLD W, 1973, ACTA OTO-LARYNGOL, V75, P192, DOI 10.3109/00016487309139695 BELANGER LF, 1953, SCIENCE, V118, P520, DOI 10.1126/science.118.3070.520 BENNETT G, 1986, AM J ANAT, V177, P441, DOI 10.1002/aja.1001770403 DENIS P, 1902, ARCH BIOL, V18, P377 DIEDEREN JHB, 1987, CELL TISSUE RES, V248, P215, DOI 10.1007/BF01239983 GILLOYZAGA P, 1985, HEARING RES, V20, P1 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 HINOJOSA R, 1977, ACTA OTO-LARYNGOL, V84, P238, DOI 10.3109/00016487709123963 KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 Kuijpers W, 1986, Acta Otolaryngol Suppl, V429, P35 LARRA F, 1970, Journal de Microscopie (Paris), V9, P845 LEBLOND CP, 1979, J HISTOCHEM CYTOCHEM, V27, P1185 LENOIR M, 1987, ANAT EMBRYOL, V175, P477, DOI 10.1007/BF00309683 Lim D J, 1985, Acta Otolaryngol Suppl, V422, P1 LIM DJ, 1987, HEARING RES, V28, P9 PRIETO JJ, 1990, DEV BRAIN RES, V52, P141, DOI 10.1016/0165-3806(90)90229-R RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 RUEDA J, 1988, GLYCOCONJUGATES MED, P338 STEEL K, 1980, ACTA OTO-LARYNGOL, V89, P27, DOI 10.3109/00016488009127104 STEEL KP, 1986, NEUROBIOLOGY HEARING, P139 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 THORN L, 1979, ANAT EMBRYOL, V155, P303, DOI 10.1007/BF00317643 THORN L, 1978, ARCH OHREN NASEN KEH, V221, P123, DOI 10.1007/BF00455883 THORN L, 1977, C INSERM, V68, P37 VANDEWATER TR, 1976, ANN OTOL RHINOL LA S, V33, P1 NR 25 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 1991 VL 57 IS 1 BP 38 EP 44 DI 10.1016/0378-5955(91)90072-H PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500005 PM 1774210 ER EF