FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Hall, RD Massengill, JL AF Hall, RD Massengill, JL TI The number of primary auditory afferents in the rat SO HEARING RESEARCH LA English DT Article DE spiral ganglion cell; cochlear nerve fiber; strain difference ID SPIRAL GANGLION-CELLS; COCHLEA; MORPHOLOGY; ORGAN; CORTI; MICE; AGE AB Published estimates of the number of primary auditory afferents in the rat differ by as much as 30%. We undertook to determine if the widely Varying estimates were related to methodological differences, especially the difference between counting cells in Rosenthal's canal and fibers in the cochlear nerve. Type I ganglion cells and myelinated cochlear nerve fibers in the same ears were counted in Long-Evans and Sprague-Dawley strains. Type II spiral ganglion cells were also counted. In each strain the numbers of myelinated fibers and type I ganglion cells were essentially the same. Means for the Long-Evans were 18,036 fibers and 17,749 cells. Means for Sprague-Dawleys were higher: 19,444 fibers and 19,229 cells. The mean number of type II ganglion cells was also greater in Sprague-Dawley than in Long-Evans rats: 1,388 and 1,170, respectively. Cell and fiber counts from the two ears of the same animal differed on average by only 1%. The number of auditory afferents did not change with age over the range (2-10 months) studied here. Several methodological differences have probably contributed to the varying estimates of type I primary auditory afferents, but the discrepancies are not inherent in counts of fibers and spiral ganglion cells. RP Hall, RD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,AUDITORY PROSTHESIS RES LAB,243 CHARLES ST,BOSTON,MA 02114, USA. 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PD JAN PY 1997 VL 103 IS 1-2 BP 75 EP 84 DI 10.1016/S0378-5955(96)00166-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800008 PM 9007576 ER PT J AU Baird, RA Steyger, PS Schuff, NR AF Baird, RA Steyger, PS Schuff, NR TI Intracellular distributions and putative functions of calcium-binding proteins in the bullfrog vestibular otolith organs SO HEARING RESEARCH LA English DT Article DE calbindin; calmodulin; calretinin; parvalbumin; S-100; sacculus; utriculus ID SACCULAR HAIR-CELLS; MAMMALIAN MYOSIN-I; COMPARATIVE TRANSDUCTION MECHANISMS; PERIPHERAL INNERVATION PATTERNS; ION-DEPENDENT CONDUCTANCES; PRESYNAPTIC ACTIVE ZONES; X-RAY-DIFFRACTION; INNER-EAR; SARCOPLASMIC-RETICULUM; ELECTRICAL RESONANCE AB Hair cells in the bullfrog vestibular otolith organs were immunolabeled by monoclonal and polyclonal antisera against calbindin (CaB), calmodulin (CaM), calretinin (CaR), and parvalbumin (PA). S-100, previously shown to immunolabel striolar hair cells in fish vestibular organs, only weakly immunolabeled hair cells in the bullfrog vestibular otolith organs. Immunolabeling was not detected in supporting cells. With the exception of CaR, myelinated axons and unmyelinated nerve terminals were immunolabeled by all of the above antisera. Immunolabeling was seen in all saccular hair cells, although hair cells at the macular margins were immunolabeled more intensely for CaB, CaM, and PA than more centrally located hair cells. As the macula margins are known to be a growth zone, this labeling pattern suggests that marginal hair cells up-regulate their calcium-binding proteins during hair cell development. In the utriculus, immunolabeling for CaM and PA was generally restricted to striolar hair cells. CaR immunolabeling was restricted to the stereociliary array. 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Res. PD JAN PY 1997 VL 103 IS 1-2 BP 85 EP 100 DI 10.1016/S0378-5955(96)00167-0 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800009 PM 9007577 ER PT J AU Scharf, B Magnan, J Chays, A AF Scharf, B Magnan, J Chays, A TI On the role of the olivocochlear bundle in hearing: 16 case studies SO HEARING RESEARCH LA English DT Article DE efferent system; olivocochlear bundle; selective attention; signal detection in noise; Meniere's disease ID COMPOUND ACTION-POTENTIALS; AUDITORY-NERVE RESPONSE; INTENSITY DISCRIMINATION; OTOACOUSTIC EMISSIONS; CONTRALATERAL SOUND; FILTER SHAPES; MASKED TONES; NOISE; STIMULATION; FREQUENCY AB Earlier we presented data (Scharf et al. (1994) Hear. Res. 75, 11-26) from a young patient (S.B.) who had undergone a vestibular neurotomy, during which the olivocochlear bundle (OCB) was severed. Those data are complemented by measurements on 15 other patients - some like S.B. with normal audiometric thresholds, none with a loss greater than 35 dB at experimental frequencies. Comparisons of performance for the same ear before and after surgery or between the operated and healthy ears do not provide evidence that the lack of OCB input impairs the following psychoacoustical functions: (I) detection of tonal signals, (2) intensity discrimination, (3) frequency selectivity, (4) loudness adaptation, (5) frequency discrimination within a tonal series, (6) in-head lateralization. Data on single-tone frequency discrimination are equivocal. These mostly negative results apply to listening both in the quiet and, where relevant, in noise. The only clear change in hearing after a vestibular neurotomy is that most patients detect signals at unexpected frequencies better than before. This change suggests an impaired ability to focus attention in the frequency domain. 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Res. PD JAN PY 1997 VL 103 IS 1-2 BP 101 EP 122 DI 10.1016/S0378-5955(96)00168-2 PG 22 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800010 PM 9007578 ER PT J AU Kajikawa, H Umemoto, M Mishiro, Y Sakagami, M Kubo, T Yoneda, Y AF Kajikawa, H Umemoto, M Mishiro, Y Sakagami, M Kubo, T Yoneda, Y TI Expression of highly polysialylated NCAM (NCAM-H) in developing and adult chicken auditory organ SO HEARING RESEARCH LA English DT Article DE highly polysialylated neural cell adhesion molecule (NCAM-H); developing chick inner ear; immunohistochemistry; neurogenesis; synaptogenesis ID CELL-ADHESION MOLECULES; VERTEBRATE NEURAL DEVELOPMENT; NERVOUS-SYSTEM; BASILAR PAPILLA; SPINAL-CORD; RAT; INNERVATION; EPITHELIUM; NEOCORTEX; BINDING AB Neural cell adhesion molecule (NCAM) is highly polysialylated (NCAM-H) in developing tissues, and recent findings suggest that NCAM-H is more essential for neural development than poorly sialylated NCAM (NCAM-L). In order to understand the precise role of NCAM-H in developing and adult inner ears, the immunohistochemical localization of NCAM-H in developing and adult chicken inner ears was examined using a monoclonal antibody which is only specific for NCAM-H. Immunoreactivity of NCAM-H was initially observed on acoustic ganglion at stage 24, when peripheral (afferent) fibers begin to emerge from the ganglion cells. At stage 38, when peripheral fibers form synapses with hair cells, NCAM-H was observed on peripheral fibers and the base of hair cells in the auditory epithelium. At stage 42, NCAM-H on nerve fibers disappeared, and only some acoustic ganglion cells were still positive for NCAM-H. This immunostain on ganglion cells was retained after birth. These data are consistent with the hypothesis that NCAM-H specifically regulates the afferent nerve fibers' growth and synaptogenesis with hair cells during inner ear development and may be associated with processing of auditory information and neuronal plasticity. C1 OSAKA UNIV,SCH MED,DEPT ANAT & CELL BIOL,SUITA,OSAKA 565,JAPAN. OSAKA UNIV,SCH MED,DEPT OTORHINOLARYNGOL,SUITA,OSAKA 565,JAPAN. HYOGO MED UNIV,DEPT OTOLARYNGOL,NISHINOMIYA,HYOGO 663,JAPAN. 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Res. PD JAN PY 1997 VL 103 IS 1-2 BP 123 EP 130 DI 10.1016/S0378-5955(96)00171-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800011 PM 9007579 ER PT J AU Killick, R Richardson, GP AF Killick, R Richardson, GP TI Antibodies to the sulphated, high molecular mass mouse tectorin stain hair bundles and the olfactory mucus layer SO HEARING RESEARCH LA English DT Article DE inner ear; tectorial membrane; extracellular matrix; hair cell; tectorin; olfactory mucus ID INNER-EAR; MONOCLONAL-ANTIBODY; KERATAN SULFATE; GUINEA-PIG; MEMBRANE; IDENTIFICATION; MATRIX; ULTRASTRUCTURE; PROTEOGLYCANS; ORGANIZATION AB Polyclonal antibodies were raised in chickens to the glycosylated forms of the high (H), medium (M) and low (L) molecular mass (MM) mouse tectorins. In the mouse cochlea, all three antibodies stained the tectorial membrane. Antibodies raised to HMM tectorin also stained the hair bundles of both inner and outer hair cells. A number of other mouse tissues were screened with the antitectorin antibodies to look for similar or antigenically related molecules. Staining was not observed in any other tissue type with the antibodies directed against the MMM and LMM tectorins. In the nose, the anti-HMM tectorin antibodies stained Bowman's glands and the mucus layer overlying the olfactory epithelium. The surface of the adjacent respiratory epithelium was not stained by these antibodies. HMM tectorin can be specifically radiolabelled by injecting neonatal mice with (SO4)-S-35 and undergoes a shift in electrophoretic mobility following treatment with keratanase, an endo-beta-galactosidase from Pseudomonas. However, when centrifuged on shallow CsCl gradients HMM tectorin has a buoyant density similar to that of glycoproteins and does not behave as a typical cartilage type proteoglycan. HMM tectorin does not react with mab 5D4, a monoclonal antibody that recognises keratan sulphate glycosaminoglycan from corneal and skeletal muscle proteoglycan. Unlike antibodies to HMM tectorin, mab 5D4 selectively stains the upper surface of the tectorial membrane, Hensen's stripe and the mucus layer overlying the respiratory epithelium. These studies indicate that the MMM and LMM tectorins may be unique to the cochlea, and that HMM may be a 'light' keratan sulphate proteoglycan that is antigenically related to either the mucins or a more specific component of the olfactory mucus layer. C1 UNIV SUSSEX,SCH BIOL SCI,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. 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PD JAN PY 1997 VL 103 IS 1-2 BP 131 EP 141 DI 10.1016/S0378-5955(96)00174-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800012 PM 9007580 ER PT J AU McFadden, SL Henderson, D Shen, YH AF McFadden, SL Henderson, D Shen, YH TI Low-frequency 'conditioning' provides long-term protection from noise-induced threshold shifts in chinchillas SO HEARING RESEARCH LA English DT Article DE auditory toughening; threshold shift; hearing loss; auditory plasticity; acoustic trauma ID REDUCES AUDITORY DESENSITIZATION; INDUCED HEARING-LOSS; ELECTRICAL-STIMULATION; ACOUSTIC STIMULATION; COCHLEAR EFFERENTS; GUINEA-PIGS; EXPOSURE; LEVEL; DEPENDENCE; STIMULUS AB Studies have shown that loss of auditory sensitivity caused by exposure to high-level acoustic stimuli can be significantly reduced by pre-exposing the subject to moderate-level acoustic stimuli. Although the protective effects of such 'conditioning' exposures have been well documented, very little is known about the persistence of conditioning-induced protection, or about the biological mechanisms underlying it. In the present study, the persistence of conditioning-induced protection was examined in chinchillas by imposing either a 30- or 60-day recovery period between conditioning (10 days of exposure to 0.5 kHz noise at 90 or 95 dB, 6 h/day) and high-level (0.5 kHz noise at 106 dB for 48 h) exposures. Comparisons of threshold shifts between conditioned animals and control animals exposed only to high-level noise indicated that conditioning provided significant protection from noise-induced threshold shifts for at least 2 months. Conditioned animals sustained outer hair cell losses similar to controls, ranging from 15 to 30% in the apical half of the cochlea. 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Res. PD JAN PY 1997 VL 103 IS 1-2 BP 142 EP 150 DI 10.1016/S0378-5955(96)00170-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800013 PM 9007581 ER PT J AU Morest, DK Kim, JN Bohne, BA AF Morest, DK Kim, JN Bohne, BA TI Neuronal and transneuronal degeneration of auditory axons in the brainstem after cochlear lesions in the chinchilla: Cochleotopic and non-cochleotopic patterns SO HEARING RESEARCH LA English DT Article DE transneuronal degeneration; cochlea; cochlear ablation; cochlear nucleus; superior olive; inferior colliculus ID DIFFERING SPONTANEOUS RATE; NERVE-FIBERS; CENTRAL PROJECTIONS; INFERIOR COLLICULUS; NUCLEUS; CAT; NOISE; GERBIL; ORGANIZATION; ARCHITECTURE AB Terminal axonal degeneration in the brain following cochlear lesions was studied with the Nauta-Rasmussen method. Losses of hair cells and myelinated cochlear fibers were assessed. The cochleotopic map projected, from apex to base, on the Ventral-to-dorsal axes of the cochlear nuclei. The cochleotopic correspondence was better for loss of cochlear nerve fibers and inner hair cells, than for outer hair cells. Cochlear fibers were traced to all parts of the cochlear nucleus, including the small-cell shell, also to cell-group Y and the flocculus. Terminal axonal degeneration in nuclei of the superior olivary complex, lateral lemniscus, and inferior colliculus was interpreted as transynaptic, since degenerated axons could not be traced to these locations from the cochlear nerve or trapezoid body. Moreover, biotinylated dextran amine injection in the basal turn of scala media of a normal cochlea labeled cochlear nerve fibers projecting to the high-frequency regions of the cochlear nuclei and to the flocculus, but not to more central auditory nuclei. 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Res. PD JAN PY 1997 VL 103 IS 1-2 BP 151 EP 168 DI 10.1016/S0378-5955(96)00172-4 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800014 PM 9007582 ER PT J AU Kim, JN Morest, DK Bohne, BA AF Kim, JN Morest, DK Bohne, BA TI Degeneration of axons in the brainstem of the chinchilla after auditory overstimulation SO HEARING RESEARCH LA English DT Article DE cochlea; noise trauma; cochlear nucleus; superior olive; inferior colliculus; transneuronal degeneration; tinnitus ID ANTEROVENTRAL COCHLEAR NUCLEUS; SPIRAL GANGLION-CELLS; GOLGI METHOD; NOMARSKI OPTICS; NERVE FIBERS; D-ASPARTATE; CAT; NOISE; INNERVATION; DAMAGE AB The patterns of axonal degeneration following acoustic overstimulation of the cochlea were traced in the brainstem of adult chinchillas. The Nauta-Rasmussen method for axonal degeneration was used following survivals of 1-32 days after a 105 min exposure to an octave-band noise with a center frequency of 4 kHz and a sound pressure level of 108 dB. Hair-cell and myelinated nerve-fiber loss were assessed in the cochlea. The cochleotopic pattern of terminal degeneration in the ventral cochlear nucleus correlated with the sites of myelinated fiber and inner-hair-cell loss: this correlation was less rigorous with outer-hair-cell loss, especially in the dorsal cochlear nucleus. These results are consistent with a dystrophic process with a slow time course depending on hair-cell loss and/or direct cochlear nerve-fiber damage. However, in a number of cases with no damage in the apical cochlea, fine fiber degeneration occurred with a faster course in low-frequency regions in the dorsal cochlear nucleus and, transynaptically, in a non-cochleotopic pattern in the superior olive and inferior colliculus. These findings suggest that neuronal hyperactivity plays a role in the central degeneration following acoustic overstimulation, possibly by an excitotoxic process. C1 UNIV CONNECTICUT,CTR HLTH,SCH MED,DEPT ANAT,FARMINGTON,CT 06030. WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,ST LOUIS,MO 63110. RI Bohne, Barbara/A-9113-2008 OI Bohne, Barbara/0000-0003-3874-7620 CR BERGLUND AM, 1994, HEARING RES, V75, P121, DOI 10.1016/0378-5955(94)90063-9 BOETTCHER FA, 1993, J ACOUST SOC AM, V94, P2123, DOI 10.1121/1.407484 Bohne B.A., 1982, NEW PERSPECTIVES NOI, P283 BOHNE BA, 1992, HEAR INSTRUMENTS, V41, P13 BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 BOHNE BA, 1976, ANN OTO RHINOL LARYN, V85, P711 BOHNE BA, 1985, ANN OTO RHINOL LARYN, V94, P122 BOHNE BA, 1992, HEAR INSTRUMENTS, V41, P58 BOURK TR, 1981, HEARING RES, V4, P215, DOI 10.1016/0378-5955(81)90008-3 BRAWER JR, 1975, J COMP NEUROL, V160, P491, DOI 10.1002/cne.901600406 COHEN ES, 1972, EXP NEUROL, V35, P470, DOI 10.1016/0014-4886(72)90117-3 Engstrom H, 1966, STRUCTURAL PATTERN O FELDMAN ML, 1969, J COMP NEUROL, V137, P267, DOI 10.1002/cne.901370303 GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 HUNTERDU.IM, 1973, J ACOUST SOC AM, V54, P1179, DOI 10.1121/1.1914364 JONES DR, 1984, HEARING RES, V15, P197, DOI 10.1016/0378-5955(84)90029-7 KALTENBACH JA, 1996, IN PRESS AUDIT NEURO KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 LEAKEJONES PA, 1989, J COMP NEUROL, V261, P613 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 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 LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 Lorente de No R., 1933, LARYNGOSCOPE, V43, P1 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MILLER JM, 1986, AM J OTOLARYNG, V7, P239, DOI 10.1016/S0196-0709(86)80045-X MOREST DK, 1983, HEARING RES, V9, P145, DOI 10.1016/0378-5955(83)90024-2 MOREST DK, 1996, ABSTR ASS RES OTOLAR, V19, P36 MOREST DK, 1987, ARO ABSTR, V10, P3 MOREST DK, 1978, ANAT REC, V193, P750 MOREST DK, 1982, NEW PERSPECTIVES NOI, P87 MOREST DK, 1989, ENG F C IMPL AUD PRO, P4 Morest DK, 1997, HEARING RES, V103, P151, DOI 10.1016/S0378-5955(96)00172-4 MOREST DK, 1990, J COMP NEUROL, V300, P230, DOI 10.1002/cne.903000207 OLIVER DL, 1983, J NEUROSCI, V3, P455 PERKINS RE, 1975, J COMP NEUROL, V163, P129, DOI 10.1002/cne.901630202 POWELL TPS, 1962, J ANAT, V96, P269 PUEL JL, 1994, J COMP NEUROL, V341, P241, DOI 10.1002/cne.903410209 RASMUSSEN GL, 1960, ANAT REC, V136, P344 RASMUSSEN GL, 1990, SPIRAL REMARKS COCHL, P1 Rose J.E., 1960, NEURAL MECHANISMS AU, P116 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 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 STOCKWEL.CW, 1969, ANN OTO RHINOL LARYN, V78, P1144 WEBSTER DB, 1971, J COMP NEUROL, V143, P323, DOI 10.1002/cne.901430305 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 NR 49 TC 69 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 JAN PY 1997 VL 103 IS 1-2 BP 169 EP 191 DI 10.1016/S0378-5955(96)00173-6 PG 23 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800015 PM 9007583 ER PT J AU Manabe, Y Yoshida, S Saito, H Oka, H AF Manabe, Y Yoshida, S Saito, H Oka, H TI Effects of lidocaine on salicylate-induced discharge of neurons in the inferior colliculus of the guinea pig SO HEARING RESEARCH LA English DT Article DE tinnitus; lidocaine; salicylate; inferior colliculus; guinea pig ID TINNITUS; MECHANISMS; POTENTIALS; PLASMA; MODEL AB Using the extracellular recording method, the effects of lidocaine (a local anesthetic known to relieve tinnitus) on discharge of inferior colliculus (IC) neurons of the guinea pig were studied before and after salicylate (200 mg/kg) administration. The salicylate-induced discharge was inhibited by intravenous injection of lidocaine at a concentration (1 mg/kg) clinically used for treating tinnitus. IC neurons could be classified into two groups according to the difference in sensitivity to lidocaine: (1) weakly-sensitive neurons and (2) highly-sensitive neurons. In weakly-sensitive neurons, the duration of the lidocaine effect lasted for less than 5 min, and the inhibitory action on the discharge of neurons was greater when the latency to sound stimulus became longer. In highly-sensitive neurons, on the other hand, the activity of neurons was almost completely inhibited for longer than 30 min, irrespective of the latency to sound stimulus. The clinical relevance of these types of neurons is discussed. C1 FUKUI MED SCH,DEPT OTOLARYNGOL,MATSUOKA,FUKUI 91011,JAPAN. FUKUI MED SCH,DEPT PHYSIOL,MATSUOKA,FUKUI 91011,JAPAN. CR Barany R., 1935, ACTA OTO-LARYNGOL, V23, P201 BERNHARD CG, 1954, ACTA PHYSL SCAND S, V31, P114 CHEN GD, 1995, HEARING RES, V82, P158, DOI 10.1016/0378-5955(94)00174-O EGGERMONT JJ, 1992, TINNITUS 91, P293 Evans E F, 1981, Ciba Found Symp, V85, P108 GARCIAMARTIN E, 1990, J NEUROCHEM, V55, P370, DOI 10.1111/j.1471-4159.1990.tb04147.x GEJORT T, 1976, ACTA OTOLARYNGOL, V82, P301 HILLE B, 1966, NATURE, V210, P1220, DOI 10.1038/2101220a0 HONRUBIA V, 1969, OTORHINOLARYNGOLOGY, V17, P470 JACKSON P, 1985, J LARYNGOL OTOL, V99, P663, DOI 10.1017/S0022215100097449 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 JASTREBOFF PJ, 1994, AM J OTOL, V15, P19 JASTREBOFF PJ, 1986, ARCH OTOLARYNGOL, V112, P1050 JOLLEY ME, 1981, J ANAL TOXICOL, V5, P236 JUHN SK, 1985, AUDITORY BIOCH, P488 LAURIKAINEN E, 1992, ACTA OTO-LARYNGOL, V112, P800, DOI 10.3109/00016489209137477 MARTIN WH, 1993, LARYNGOSCOPE, V103, P600 MCFADDEN D, 1984, HEARING RES, V16, P251, DOI 10.1016/0378-5955(84)90114-X MELDING PS, 1978, J LARYNGOL OTOL, V92, P115, DOI 10.1017/S002221510008511X MITCHELL C, 1973, ARCH OTOLARYNGOL, V98, P297 RITCHIE JM, 1979, ANNU REV NEUROSCI, V2, P341, DOI 10.1146/annurev.ne.02.030179.002013 RUTH RA, 1985, ARCH OTOLARYNGOL, V111, P799 SCHREINER CE, 1987, P 3 INT TINN SEM HAR, P100 SHEA JJ, 1978, LARYNGOSCOPE, V88, P1477 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E VELASCO M, 1982, INT J NEUROSCI, V17, P199 WARD PH, 1969, LARYNGOSCOPE, V79, P1605, DOI 10.1288/00005537-196909000-00006 NR 28 TC 43 Z9 49 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1997 VL 103 IS 1-2 BP 192 EP 198 DI 10.1016/S0378-5955(96)00181-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800016 PM 9007584 ER PT J AU Greenwood, DD AF Greenwood, DD TI The Mel Scale's disqualifying bias and a consistency of pitch-difference equisections in 1956 with equal cochlear distances and equal frequency ratios SO HEARING RESEARCH LA English DT Article DE pitch; mel scale; musical interval; cochlear map; critical bandwidth ID BASILAR-MEMBRANE; NERVE-FIBERS; RESPONSES; TONES AB In 1956, Stevens 'commissioned' an experiment to equisect a pitch difference between two tones. Results appear to reveal a methodological flaw that would invalidate the Mel Scale (Stevens and Volkmann, 1940). Stevens sought to distinguish sensory continua, e.g., loudness and pitch, on various criteria. He expected that the pitch continuum would not exhibit 'hysteresis'; i.e., that subjects dividing a pitch difference (Delta f) into equal-appearing parts would not set dividing frequencies higher when listening to notes in ascending order than in descending order. Seven subjects equisected a pitch difference, between tones of 400 and 7000 Hz, into equal-seeming parts by adjusting the frequencies of three intermediate tones. All seven exhibited hysteresis, contrary to expectation. This outcome bears on other issues. Years prior, Stevens suggested that equal pitch differences might correspond to equal cochlear distances, but not to equal frequency ratios nor to equal musical intervals (Stevens and Davis, 1938; Stevens and Volkmann, 1940). In 1960 (reported now), both the 1940 Mel Scale and the equal pitch differences of 1956 were compared to equal cochlear distances, using a frequency-position function that fitted Bekesy's cochlear map (Greenwood, 1961, 1990). When ascending and descending settings were combined to contra-pose biases, equal pitch differences did coincide with equal distances - which the Mel Scale did not. Further, the biased ascending-order data coincided with the Mel Scale, suggesting the Mel Scale was similarly biased. Thus, the combined-order equal pitch differences of 1956 - but not the Mel Scale - are consistent with equal cochlear distances. However, since the map between 400 and 7000 Hz is nearly logarithmic, equal frequency ratios also approximate equal distances. Ironically, above 400 Hz, Bekesy's map and Stevens' equal-distance hypothesis jointly imply that musical intervals will nearly agree with equal pitch differences, which Stevens thought he had disconfirmed. However, given Bekesy's map, only near the cochlear apex will equal distances not approximate equal frequency ratios; and Pratt's (Pratt, 1928) bisections of Delta fs greater than an octave indicated that equal pitch differences, on average, did agree with equal distances. However, they did so for only two of four subjects and coincided instead with equal frequency ratios for one musical subject. Historical distinctions suggest that between the parts of equisected Delta fs subjective equivalence may be of two kinds - one linked to musical intervals, leading to equal frequency ratios; a second linked to 'tone-height' and 'distance', leading to deviations from equal frequency ratios near the apex, though not appreciably if equisected Delta fs are less than an octave (or if perhaps subjects are musicians). Data of other kinds suggest that, if pure-tone pitch height were a function of place, the place could be the apical excitation-pattern edge, in any case not a maximum, which in neural data shifts and disappears with tone level. RP Greenwood, DD (reprint author), UNIV BRITISH COLUMBIA,SCH AUDIOL & SPEECH SCI,VANCOUVER,BC V5Z 1M9,CANADA. 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PD JAN PY 1997 VL 103 IS 1-2 BP 199 EP 224 DI 10.1016/S0378-5955(96)00175-X PG 26 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA WD588 UT WOS:A1997WD58800017 PM 9007585 ER PT J AU Schofield, BR Cant, NB AF Schofield, BR Cant, NB TI Projections from the ventral cochlear nucleus to the inferior colliculus and the contralateral cochlear nucleus in guinea pigs SO HEARING RESEARCH LA English DT Article DE auditory system; ascending pathway; fluorescent tracer; neuroanatomy ID SUPERIOR PARAOLIVARY NUCLEUS; BUSHY CELL AXONS; RETROGRADE TRANSPORT; HORSERADISH-PEROXIDASE; AFFERENT-PROJECTIONS; MULTIPOLAR CELLS; H-3 GLYCINE; CAT; NEURONS; OLIVE AB Multipolar cells in the ventral cochlear nucleus are the source of projections to numerous brainstem auditory nuclei, including the contralateral and ipsilateral inferior colliculi and the contralateral cochlear nucleus. Multiple fluorescent tracers were used to label the multipolar cells that project to each of these targets. Following injections of different tracers into each target, the ventral cochlear nucleus was examined for the presence of cells that contained more than one tracer. Such cells were never observed. In contrast, double-labeled cells were common in the dorsal cochlear nucleus, where cells frequently contained the two tracers that were injected into the ipsilateral and contralateral inferior colliculi. The distribution and somatic morphology of cells in the ventral cochlear nucleus that project to each of the three targets were examined. Each population contained cells with somas that ranged in shape from elongated to rounded, but there were differences in soma size. Projections to the ipsilateral and contralateral inferior colliculi arise predominantly from small to medium-sized cells, the average size being slightly less for cells with projections to the ipsilateral colliculus. Projections to the contralateral cochlear nucleus arise from cells with somas that range in size from small to large, including cells much larger than those that projected to either inferior colliculus. On the basis of these results, we conclude that projections from the ventral cochlear nucleus to the ipsilateral and contralateral inferior colliculi and to the contralateral cochlear nucleus arise in three different populations of multipolar cells. RP Schofield, BR (reprint author), DUKE UNIV, SCH MED, DEPT NEUROBIOL, POB 3209, DURHAM, NC 27710 USA. CR ADAMS JC, 1983, NEUROSCI LETT, V37, P205, DOI 10.1016/0304-3940(83)90431-7 ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1976, J COMP NEUROL, V170, P107, DOI 10.1002/cne.901700108 BENSON CG, 1990, J COMP NEUROL, V296, P415, DOI 10.1002/cne.902960307 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 BRAWER JR, 1975, J COMP NEUROL, V160, P491, DOI 10.1002/cne.901600406 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CANT NB, 1982, J COMP NEUROL, V212, P313, DOI 10.1002/cne.902120308 CANT NB, 1984, HEARING SCI RECENT A, P371 CANT NB, 1981, NEUROSCIENCE, V6, P2643, DOI 10.1016/0306-4522(81)90109-3 Cant N.B., 1992, Springer Handbook of Auditory Research, V1, P66 CANT NB, 1982, NEUROSCI LETT, V32, P241, DOI 10.1016/0304-3940(82)90300-7 CANT NB, 1986, J COMP NEUROL, V247, P457, DOI 10.1002/cne.902470406 DOUCET JR, 1996, ABSTR ASS RES OT, V19, P166 FRIAUF E, 1988, EXP BRAIN RES, V73, P263 GLENDENNING KK, 1985, J COMP NEUROL, V232, P261, DOI 10.1002/cne.902320210 HACKNEY CM, 1987, AUDITORY PATHWAY STR, P77 HACKNEY C M, 1986, British Journal of Audiology, V20, P215, DOI 10.3109/03005368609079018 KOLSTON J, 1992, ANAT EMBRYOL, V186, P443 KUWABARA N, 1991, J COMP NEUROL, V314, P684, DOI 10.1002/cne.903140405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MOORE JK, 1986, NEUROBIOLOGY HEARING, P283 MOREST DK, 1993, NATO ADV SCI INST SE, V239, P1 NODA Y, 1974, ARCH OTO-RHINO-LARYN, V208, P107, DOI 10.1007/BF00453924 NORDEEN KW, 1983, J COMP NEUROL, V214, P131, DOI 10.1002/cne.902140203 OERTEL D, 1990, J COMP NEUROL, V295, P136, DOI 10.1002/cne.902950112 OLIVER DL, 1987, J COMP NEUROL, V264, P24, DOI 10.1002/cne.902640104 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 Osen K.K., 1990, GLYCINE NEUROTRANSMI, P417 OSTAPOFF EM, 1996, ASS RES OT ABSTR, V19, P165 OSTAPOFF EM, 1994, J COMP NEUROL, V346, P19, DOI 10.1002/cne.903460103 PIRSIG W, 1968, Archiv fuer Klinische und Experimentelle Ohren- Nasen- und Kehlkopfheilkunde, V192, P333, DOI 10.1007/BF00411129 RHODE WS, 1992, SPRINGER HDB AUDITOR, V2, P94 ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 RYUGO DK, 1981, BRAIN RES, V210, P342, DOI 10.1016/0006-8993(81)90907-0 SAINTMARIE RL, 1990, BRAIN RES, V524, P244, DOI 10.1016/0006-8993(90)90698-B SCHOFIELD BR, 1991, J COMP NEUROL, V312, P68, DOI 10.1002/cne.903120106 SCHOFIELD BR, 1996, IN PRESS J COMP NEUR SCHOFIELD BR, 1995, J COMP NEUROL, V360, P135, DOI 10.1002/cne.903600110 SHORE SE, 1992, HEARING RES, V62, P16, DOI 10.1016/0378-5955(92)90199-W SMITH PH, 1993, J COMP NEUROL, V331, P245, DOI 10.1002/cne.903310208 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 SNYDER RL, 1988, J COMP NEUROL, V278, P209, DOI 10.1002/cne.902780205 THOMPSON AM, 1991, J COMP NEUROL, V303, P267, DOI 10.1002/cne.903030209 WARR WB, 1972, BRAIN RES, V40, P247 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WENTHOLD RJ, 1987, BRAIN RES, V415, P183, DOI 10.1016/0006-8993(87)90285-X WILLARD FH, 1983, NEUROSCIENCE, V10, P1203, DOI 10.1016/0306-4522(83)90109-4 NR 49 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 DEC 1 PY 1996 VL 102 IS 1-2 BP 1 EP 14 DI 10.1016/S0378-5955(96)00121-9 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000001 PM 8951445 ER PT J AU deSauvage, RC daCosta, DL Erre, JP Aran, JM AF deSauvage, RC daCosta, DL Erre, JP Aran, JM TI Changes in CM and CAP with sedation and temperature in the guinea pig: Facts and interpretation SO HEARING RESEARCH LA English DT Article DE xylazine; temperature; VIIth nerve compound action potential; convolution ID AUDITORY-NERVE FIBERS; UNIT RESPONSE; ROUND WINDOW; HYPOTHERMIA; DEPENDENCY; XYLAZINE; MASKING; COCHLEA; AGENTS; SYSTEM AB The influence of xylazine on the amplitude, latency and waveform of With nerve compound action potential (CAP) and cochlear microphonic (CM) in response to clicks at 95 dB SPL in normal awake preimplanted guinea pigs was investigated. The animals' temperature was monitored but no thermoregulation was exerted, except in one control experiment. Following a 0.2 mi injection of xylazine, CM showed minor variations while CAP audiograms for tone pips between 0.5 and 25 kHz remained normal. However, a progressive decrease in temperature and a strongly correlated increase in CAP amplitude and in N1 and N2 latencies were noticed. For peak N1 the changes were equivalent to linear amplitude and time expansions, and could be reproduced through CAP synthesis with convolution methods using time expanded unit response model and firing density functions. All changes were maximal after 2 h of sedation and recovered within approximately another 2 h. Whereas xylazine is known to induce hypothermia, all the changes disappeared if the animal was thermoregulated. Therefore the changes are interpreted as a result of hypothermia. The mechanism of N1 latency lengthening and increase in amplitude during hypothermia can be understood as a simultaneous increase in spike duration, hair cell/nerve synaptic delay and postsynaptic time constant. This hypothesis yielded a theoretical temperature coefficient for N1 latency (-52 mu s/degrees C) matching that measured experimentally (-55 mu s/degrees C). When compared with peak N1, peak N2 appeared relatively more expanded. Arguments about the origin of N2 are discussed. RP deSauvage, RC (reprint author), UNIV BORDEAUX 2,LAB AUDIOL EXPTL & CLIN,EQUIPE ACCUEIL UPR ES,HOP PELLEGRIN,F-33076 BORDEAUX,FRANCE. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 15 EP 27 DI 10.1016/S0378-5955(96)00137-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000002 ER PT J AU Gaihede, M AF Gaihede, M TI Tympanometric preconditioning of the tympanic membrane SO HEARING RESEARCH LA English DT Article DE compliance; admittance; preconditioning; repeatability; precision; retraction susceptibility AB Preconditioning is a general biomechanical phenomenon, where tissue characteristics change due to repetitive loading-unloading experiments, resulting in an increased compliance. Increasing compliance by repetitive tympanometric measurements has previously been described and may be related to rate of pressure change during recordings. Presently, 9 tympanometries were performed in a group of normal adults (n = 103 ears) at 4 different rates: 50, 100, 200, and 400 daPa/s. Compliance showed an initial larger increase from trial to trial, tending to reach a steady state during later trials, and the pattern was found identical in all 4 groups. However, stratifying data according to compliance at Ist trial of each ear, the preconditioning effect was found significantly correlated to compliance (P < 0.001), so that low compliance was associated with low preconditioning and vice versa. Stratification also illustrated that, while most ears reached a steady state, some ears with high compliance (greater than or equal to 1.04 cm(3)) did not. In this way identification is possible of tympanic membranes, which are less resistant to pressure loads and therefore may be susceptible to development of retraction pockets. Repeatable measures of compliance with insignificant effect of preconditioning could be obtained after 5 tympanometries, and measures of precision of compliance are reported. RP Gaihede, M (reprint author), AARHUS UNIV HOSP,DEPT OTOLARYNGOL,NORREBROGADE 44,DK-8000 AARHUS C,DENMARK. CR Ars B, 1995, Acta Oto-Rhino-Laryngologica Belgica, V49, P163 CRETEN WL, 1974, SCAND AUDIOL, V3, P39, DOI 10.3109/01050397409044963 DECRAEMER WF, 1980, J BIOMECH, V13, P463, DOI 10.1016/0021-9290(80)90338-3 Fung Y. 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PD DEC 1 PY 1996 VL 102 IS 1-2 BP 28 EP 34 DI 10.1016/S0378-5955(96)00146-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000003 PM 8951447 ER PT J AU Wiegrebe, L Schmidt, S AF Wiegrebe, L Schmidt, S TI Temporal integration in the echolocating bat, Megaderma lyra SO HEARING RESEARCH LA English DT Article DE psychophysics; temporal integration; bat ID ECHOES AB Temporal integration is a crucial feature of auditory temporal processing. We measured the psychophysical temporal integration of acoustic intensity in the echolocating bat Megaderma lyra using a two-alternative forced-choice procedure. A measuring paradigm was chosen in which the absolute threshold for pairs of short tone pips was determined as a function of the temporal separation between the pips. The time constants determined with this paradigm are a crucial characteristic of the sonar system of M. lyra, a species orientating in its environment by very short broadband sonar calls emitted at high rates. Two different carrier frequencies for the tone pips were used to obtain data from the lower and the higher half of the hearing area of M. lyra. Both in the lower and in the higher frequency range, M. lyra showed very short time constants of about 220 mu s. Our results are comparable to data from the echolocating dolphin, Tursiops truncatus, showing click integration times of about 260 mu s and to estimates of auditory temporal integration in the context of echo clutter interference in the big brown bat. RP Wiegrebe, L (reprint author), UNIV MUNICH,INST ZOOL,LUISENSTR 14,D-80333 MUNICH,GERMANY. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 35 EP 42 DI 10.1016/S0378-5955(96)00139-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000004 PM 8951448 ER PT J AU Ren, TY Nuttall, AL Miller, JM AF Ren, TY Nuttall, AL Miller, JM TI Electrically evoked cubic distortion product otoacoustic emissions from gerbil cochlea SO HEARING RESEARCH LA English DT Article DE electrical stimulation; cochlea; outer hair cell motility; acoustic emission; distortion product; gerbil ID OUTER HAIR-CELLS; GUINEA-PIG; SOUND PRESSURE; RESPONSES; MECHANICS AB It has been demonstrated that electrical stimulation of the cochlear partition results in basilar membrane vibration and otoacoustic emissions. Electromotility of stimulated outer hair cells (OHCs) elicits the electrically evoked otoacoustic emissions (EEOAEs). Although electrically evoked upper and lower sideband distortion products (DPs) have been reported, electrically evoked cubic DP has not been investigated. Since the acoustically evoked cubic DP is the most commonly used otoacoustic measure of cochlear nonlinearity, this study tested whether electrical stimuli evoke a cubic DP otoacoustic emission. An electrical current containing the frequency component fl and f2 (fl < f2) was delivered to the round window niche of the gerbil, and electrically induced sound pressure change in the external ear canal was measured with a microphone. It was found that, in addition to f1 and f2 EEOAEs, cubic DP (2f1-f2) and other emissions at 3f1-2f2, 2f2-f1 and f2-f1 frequencies are electrically evoked. The electrically evoked cubic DP growth is similar to that of an acoustically evoked cubic DP. An electrical stimulus at fl or f2 and an acoustic stimulus at f2 or fl produce an identical cubic DP to that evoked by two electrical stimuli and/or two acoustic stimuli at fl and f2 frequencies. An acoustic suppressor at a frequency near f2 can completely suppress an electrically evoked cubic DP emission. These data demonstrate that DPs can be provoked by a complex two frequency electrical current delivered to the round window niche. These stimuli elicit mechanical vibrations, from stimulated OHCs near the round window, which propagate apically toward their characteristic frequency places on the basilar membrane, and produce combination DPs. Electrically evoked cubic DPs appear to be produced by the same nonlinear mechanism that generates acoustically evoked DPs. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP Ren, TY (reprint author), OREGON HLTH SCI UNIV,OREGON HEARING RES CTR,3181 SW SAM JACKSON PK RD,NRC04,PORTLAND,OR 97201, USA. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 43 EP 50 DI 10.1016/S0378-5955(96)00145-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000005 PM 8951449 ER PT J AU Pedrozo, HA Schwartz, Z Luther, M Dean, DD Boyan, BD Wiederhold, ML AF Pedrozo, HA Schwartz, Z Luther, M Dean, DD Boyan, BD Wiederhold, ML TI A mechanism of adaptation to hypergravity in the statocyst of Aplysia californica SO HEARING RESEARCH LA English DT Article DE hypergravity; organ; calcification; Aplysia californica; gravity ID BONE; WEIGHTLESSNESS; MICROGRAVITY AB The gravity-sensing organ of Aplysia californica consists of bilaterally paired statocysts containing statoconia, which are granules composed of calcium carbonate crystals in an organic matrix. In early embryonic development, Aplysia contain a single granule called a statolith, and as the animal matures, statoconia production takes place. The objective of this study was to determine the effect of hypergravity on statoconia production and homeostasis and explore a possible physiologic mechanism for regulating this process. Embryonic Aplysia were exposed to normogravity or 3 x g or 5.7 x g and each day samples were analyzed for changes in statocyst, statolith, and body dimensions until they hatched. In addition, early metamorphosed Aplysia (developmental stages 7-10) were exposed to hypergravity (2 x g) for 3 weeks, and statoconia number and statocyst and statoconia volumes were determined. We also determined the effects of hypergravity on statoconia production and homeostasis in statocysts isolated from developmental stage 10 Aplysia. Since prior studies demonstrated that urease was important in the regulation of statocyst pH and statoconia formation, we also evaluated the effect of hypergravity on urease activity. The results show that hypergravity decreased statolith and body diameter in embryonic Aplysia in a magnitude-dependent fashion. In early metamorphosed Aplysia, hypergravity decreased statoconia number and volume. Similarly, there was an inhibition of statoconia production and a decrease in statoconia volume in isolated statocysts exposed to hypergravity in culture. Urease activity in statocysts decreased after exposure to hypergravity and was correlated with the decrease in statoconia production observed. In short, there was a decrease in statoconia production with exposure to hypergravity both in vivo and in vitro and a decrease in urease activity. It is concluded that exposure to hypergravity downregulates urease activity, resulting in a significant decrease in the formation of statoconia. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT ORTHOPAED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PERIODONT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PERIODONT,SAN ANTONIO,TX 78229. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 51 EP 62 DI 10.1016/S0378-5955(96)00147-5 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000006 PM 8951450 ER PT J AU Rarey, KE Ma, YL Gerhardt, KJ Fregly, MJ Garg, LC Rybak, LP AF Rarey, KE Ma, YL Gerhardt, KJ Fregly, MJ Garg, LC Rybak, LP TI Correlative evidence of hypertension and altered cochlear microhomeostasis: Electrophysiological changes in the spontaneously hypertensive rat SO HEARING RESEARCH LA English DT Article DE hypertension; compound action potential; endocochlear potential; potassium; inner ear ID EAR BLOOD-FLOW; AUTO-REGULATION; ALPHA-SUBUNIT; HEARING; AGE AB The spontaneously hypertensive rat model has been used to show that hypertension is an important pathophysiological risk factor in age-related hearing loss. In the present study, compound action potential (CAP), electrochemical potential (ECP), and potassium concentration (C-K(+)) measurements were taken from the cochlea of genetically predisposed, spontaneously hypertensive rats (SHR) and from normotensive Wistar-Kyoto (WKY) rats. In the SHR model, as the duration of hypertension increased with the animal's age (from 3 to 8 months), CAP thresholds increased, ECP increased in marginal cells only, and C-K(+) increased in both endolymph and marginal cells. Collectively, the data suggest that ionic alternations of cellular potentials are involved in hearing changes in the hypertensive state. Ultimately, such data may assist in understanding hearing loss in individuals who are diagnosed with hypertension. C1 UNIV FLORIDA,DEPT COMMUN PROC & DISORDERS,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. SO ILLINOIS UNIV,SCH MED,DEPT SURG,SPRINGFIELD,IL 62794. UNIV FLORIDA,DEPT PHARMACOL & THERAPEUT,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT PHYSIOL,GAINESVILLE,FL 32610. RP Rarey, KE (reprint author), UNIV FLORIDA,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32610, USA. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 63 EP 69 DI 10.1016/S0378-5955(96)00148-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000007 PM 8951451 ER PT J AU vanEmst, MG Klis, SFL Smoorenburg, GF AF vanEmst, MG Klis, SFL Smoorenburg, GF TI 4-Aminopyridine effects on summating potentials in the guinea pig SO HEARING RESEARCH LA English DT Article DE summating potential; 4-aminopyridine; perilymphatic perfusion; guinea pig ID OUTER HAIR-CELLS; COCHLEAR POTENTIALS; RECEPTOR POTENTIALS; MAMMALIAN COCHLEA; MOUSE COCHLEA; ROUND WINDOW; INNER; ORGAN; CORTI; RESPONSES AB DC receptor potentials measured in hair cells, and the associated extracellular DC potential known as the summating potential (SP), originate with nonlinear elements in the mechanoelectric transduction chain. Nonlinear electric conductance has been demonstrated in the basolateral membrane of the hair cell, and is commonly attributed to the presence of voltage- and time-dependent K+ conductances in this part of the hair cell membrane. To study a possible contribution of these K+ channels to the SP we perfused the perilymphatic spaces of the guinea pig cochlea with the K+ channel blocker 4-aminopyridine (4-AP). Since 4-AP might also affect the afferent fibers and, thus, interfere with SP measurement, we added tetrodotoxin (TTX) to the perfusion solutions to block the neuronal discharges. Sound-evoked (2-12 kHz) intracochlear potentials were recorded from the basal turn of both scala vestibuli and scala tympani. The results showed a frequency- and level-dependent effect of 4-AP on the magnitude of the SP. At low and moderate levels of 8 and 12 kHz stimuli 4-AP mostly reduced the SP amplitude, while at high levels of these stimuli and at all levels of 2 and 4 kHz stimuli 4-AP enlarged the SP amplitude. These effects were reversible and occurred in both scala vestibuli and scala tympani. We attribute these bi-directional effects on the SP amplitude to a differential effect of 4-AP on inner hair cell (IHC) and outer hair cell (OHC) physiology. The decrease in SP was found for stimulus conditions where the SP presumably depends mainly on contributions from basal turn IHCs. Blocking the 4-AP-sensitive Ki channel in the IHC membrane should lead to a reduced contribution from the IHCs to the SP, because of an increase in basolateral membrane resistance. The increase in SP was found for stimulus conditions where the SP is assumed to depend mainly on contributions from basal turn OHCs. In this case the OHCs seemed to respond to blocking of the 4-AP-sensitive K+ channel in the basolateral membrane with an increased contribution to the nonlinearity of the transduction chain. Administration of 4-AP did not affect the endocochlear potential. Light microscopic examination revealed no apparent changes in morphology after 4-AP perfusion. RP vanEmst, MG (reprint author), UNIV UTRECHT, DEPT OTORHINOLARYNGOL, LAB EXPTL AUDIOL, ROOM G02531, HEIDELBERGLAAN 100, NL-3584 CX UTRECHT, NETHERLANDS. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 70 EP 80 DI 10.1016/S0378-5955(96)00149-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000008 PM 8951452 ER PT J AU Komeda, M Raphael, Y AF Komeda, M Raphael, Y TI Gentamicin distribution in the basilar papilla: Possible association with regenerated hair cell orientation SO HEARING RESEARCH LA English DT Article DE gentamicin; regeneration; hair cell; basal body; chick ID AVIAN INNER-EAR; GLUTATHIONE S-TRANSFERASES; GUINEA-PIG COCHLEA; ACOUSTIC TRAUMA; CHICK COCHLEA; STEREOCILIARY BUNDLES; AMINOGLYCOSIDE OTOTOXICITY; KANAMYCIN OTOTOXICITY; FUNCTIONAL RECOVERY; ETHACRYNIC-ACID AB Gentamicin-specific immunolabeling was examined in the regenerating chick basilar papilla following gentamicin treatment. Surviving hair cells were labeled in the infracuticular area, predominantly in the basal body region. Label intensity in short hair cells (SHCs) was greater than tall hair cells (THCs). Quantitative examination of stereociliary bundle orientation in regenerated hair cells revealed a considerable degree of variability from normal. The orientation of SHC stereocilia was more varied than that of THC. The results suggest an association between the accumulation of gentamicin in the region of the basal body and the degree of disorientation of the cell surface. It is possible that gentamicin accumulation around the basal body compromises the ability of the centrosome to orient hair cells correctly. C1 UNIV MICHIGAN,SCH MED,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 81 EP 89 DI 10.1016/S0378-5955(96)00150-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000009 PM 8951453 ER PT J AU Campbell, KCM Rybak, LP Meech, RP Hughes, L AF Campbell, KCM Rybak, LP Meech, RP Hughes, L TI D-Methionine provides excellent protection from cisplatin ototoxicity in the rat SO HEARING RESEARCH LA English DT Article DE cisplatin; ototoxicity; methionine; protection ID HIGH-DOSE CISPLATIN; INDUCED LIPID-PEROXIDATION; INDUCED NEPHROTOXICITY; CANCER-PATIENTS; CIS-PLATINUM; GUINEA-PIG; PHASE-I; THIOETHER SUPPRESSION; ANTIOXIDANT SYSTEM; OVARIAN-CANCER AB Cisplatin (CDDP) is a widely used chemotherapeutic agent. Unfortunately, CDDP is highly ototoxic. We tested D-methionine (D-Met), a sulfur containing compound, as an otoprotectant in male Wistar rats. Complete data sets were obtained for five groups of five animals each, including a treated control group (16 mg/kg CDDP), an untreated control group (administered an equivalent volume of saline) and three groups that received either 75, 150, or 300 mg/kg D-Met 30 min prior to the 16 mg/kg CDDP dosing. Auditory brainstem response (ABR) thresholds were obtained in response to clicks, and 1 kHz, 4 kHz, 8 kHz, and 14 kHz toneburst stimuli, before and 3 days after drug administration. Scanning electron microscopy (SEM) was used to examine the outer hair cells of the apical, middle and basal turns of the cochlea. Animal weight was measured on the first and final day. D-Met provided excellent otoprotection even at the lowest level with complete otoprotection obtained for the 300 mg/kg dosing as measured by both ABR and SEM. D-Met also markedly reduced weight loss and mortality. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 90 EP 98 DI 10.1016/S0378-5955(96)00152-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000010 PM 8951454 ER PT J AU Henson, MM Xie, DH Wynne, RH Wilson, JL Henson, OW AF Henson, MM Xie, DH Wynne, RH Wilson, JL Henson, OW TI The course and distribution of medial efferent fibers in the cochlea of the mustached bat SO HEARING RESEARCH LA English DT Article DE cochlea; olivocochlear; bat; efferent; PHA-L; AChE ID CROSSED OLIVOCOCHLEAR BUNDLE; GUINEA-PIG COCHLEA; AUDITORY-NERVE FIBERS; BINAURAL ACOUSTIC STIMULATION; OUTER HAIR-CELLS; ELECTRICAL-STIMULATION; MOUSTACHED BAT; BRAIN-STEM; PTERONOTUS-PARNELLII; CONTRALATERAL SOUND AB The course and distribution of medial olivocochlear (MOC) nerve fibers were studied in the cochlea of the mustached bat. This animal is of interest because of the very sharp tuning of the ear and fine frequency resolution in small frequency bands near 60 and 90 kHz. The MOC fibers arise from about 400 cells in the dorsomedial periolivary (DMPO) nucleus and they are distributed to approximately 4500 outer hair cells (OHCs), resulting in an average OHC unit size of 11.25. Individual fibers appear to have a small number of branches and each branch entering the tunnel of Corti terminates on a patch of OHCs. The patch size is typically 1-3 OHCs with the smallest average patch sizes in the regions tuned to 60 and 90 kHz. The majority of the MOC terminals are derived from the contralateral DMPO. Contralateral vs. ipsilateral projecting fibers are not preferentially distributed within any of the three rows of OHCs or within specific regions throughout most of the cochlea. It can be concluded that the main differences between the mustached bat's MOC system and that of most other mammals are: (1) origin from a single nucleus; (2) relatively small sizes of the patches; (3) a single terminal on each OHC; (4) a gradient in the size of the terminals but not in the number of terminals from row to row or from base to apex. C1 UNIV N CAROLINA,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27599. UNIV WISCONSIN,CTR ENVIRONM REMOTE SENSING,MADISON,WI 53706. INDIANA UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,INDIANAPOLIS,IN 46202. RP Henson, MM (reprint author), UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CB 7090,TAYLOR HALL,CB 7090,CHAPEL HILL,NC 27599, USA. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 99 EP 115 DI 10.1016/0378-5955(96)00153-0 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000011 PM 8951455 ER PT J AU Yamasoba, T Suzuki, M Kaga, K AF Yamasoba, T Suzuki, M Kaga, K TI Influence of chronic kanamycin administration on basement membrane anionic sites in the labyrinth SO HEARING RESEARCH LA English DT Article DE kanamycin; ototoxicity; charge barrier; basement membrane anionic sites; stria vascularis; spiral limbus ID GUINEA-PIGS; STRIA VASCULARIS; BARRIER; POLYETHYLENEIMINE; OTOTOXICITY; SULFATE AB We studied the effect of chronic treatment with kanamycin on the basement membrane (BM) anionic sites in the cochlea and endolymphatic sac using polyethyleneimine (PEI) as a cationic tracer. Albino guinea pigs weighing 250-300 g received kanamycin (400 mg/kg/day, i.m.) for 10 or 17 consecutive days. The number of BM anionic sites as derived from the PEI area was not affected in Reissner's membrane, spiral prominence, basilar membrane or endolymphatic sac, whereas it was significantly decreased in the stria vascularis and spiral limbus, being more marked in the guinea pigs treated for 17 days than in those treated for 10 days. The number of BM anionic sites in these regions did not recover until 6 weeks after kanamycin treatment. These findings suggest that chronically administered kanamycin may selectively and progressively affect the BM anionic sites in the stria vascularis and spiral limbus, resulting in disruption of a barrier function in the cochlea, and that severely impaired BM anionic sites in the cochlea may not recover. C1 TOSEI NATL HOSP,DEPT OTOLARYNGOL,TOSEI,JAPAN. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 116 EP 124 DI 10.1016/S0378-5955(96)00159-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000012 PM 8951456 ER PT J AU Schmiedt, RA AF Schmiedt, RA TI Effects of aging on potassium homeostasis and the endocochlear potential in the gerbil cochlea SO HEARING RESEARCH LA English DT Article DE gerbil; endocochlear potential; endolymph; perilymph; potassium; presbyacusis; aging; cochlea ID AUDITORY-NERVE FIBERS; PRODUCT OTOACOUSTIC EMISSIONS; GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; INNER-EAR; ION-TRANSPORT; MERIONES-UNGUICULATUS; ENDOLYMPHATIC HYDROPS; WATER-DEPRIVATION; MONGOLIAN GERBIL AB Previous work has shown that the endocochlear potential (EP) decreases with age in the gerbil. Concomitant with the EP decrease is an age-related loss of activity of Na,K-ATPase in the lateral wall and stria vascularis. We hypothesized that the EP decrease is associated with a similar decrease in the endolymphatic potassium concentration [K-e(+)]. This hypothesis was tested using double-barrelled, K+-selective electrodes introduced into scala media through the round window in young and quiet-aged gerbils. Results show that the means (+/-S.D.) of the [K-e(+)] in young and aged gerbils were not significantly different (178.2+/-14.2 mM and 171.2+/-34.4 mM, respectively), although the intersubject variability was much greater in the aged animals than in the young. These values of [K-e(+)] are slightly higher than those found for other mammals and may reflect the higher plasma osmolarity found in the gerbil. The concentration of perilymphatic potassium [K-p(+)] in scala tympani at the round window was also similar for the young and aged groups (3.57+/-1.17 mM and 4.18+/-2.03 mM, respectively). On the other hand, mean EP values in the young and aged gerbils were 92.0+/-5.7 mV and 64.8+/-15.8 mV, respectively and were statistically different (P < 0.001). Overall, EP and [K-e(+)] showed little correlation (R(2)=0.23), except that when [K-e(+)] fell below 150 mM, the EP was always less than 60 mV. An analysis of the chemical potential for K-e(+) with respect to K-p(+) shows that,it was similar for young and aged gerbils (overall mean of 103.1+/-13.7 mV) and remained constant with respect to the EP, in spite of an overall electrochemical potential of K-e(+) that varied from 120 to 210 mV. Thus, the system maintains K-e(+) homeostasis at the expense of the EP, even when the EP is on the verge of collapse. RP Schmiedt, RA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 125 EP 132 DI 10.1016/S0378-5955(96)00154-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000013 PM 8951457 ER PT J AU Muller, M Smolders, JWT DingPfennigdorff, D Klinke, R AF Muller, M Smolders, JWT DingPfennigdorff, D Klinke, R TI Regeneration after tall hair cell damage following severe acoustic trauma in adult pigeons: Correlation between cochlear morphology, compound action potential responses and single fiber properties in single animals SO HEARING RESEARCH LA English DT Article DE bird; pigeon; acoustic trauma; regeneration; auditory nerve; basilar papilla ID CHICK BASILAR PAPILLA; INTENSE SOUND EXPOSURE; AVIAN INNER-EAR; TECTORIAL MEMBRANE; AUDITORY FUNCTION; GANGLION NEURONS; NEONATAL CHICK; DISCHARGE PATTERNS; THRESHOLD SHIFT; NOISE DAMAGE AB The time course of recovery of compound action potential (CAP) thresholds was observed in individual adult pigeons after severe acoustic trauma. Pigeons were overstimulated with a tone of 0.7 kHz and 136-142 dB SPL presented to one ear for 1 h under general anesthesia. Recovery of CAP audiograms was monitored at regular intervals after trauma. A new semi-stereotaxic approach to the peripheral part of the auditory nerve was developed. This permitted activity from single auditory nerve fibers to be recorded over a wide range of characteristic frequencies (CFs), including high CFs, without having to open the inner ear. Single unit recordings were made after three weeks and after 4 or more months of recovery. The time course of recovery, the single unit properties, and the morphological status of the basilar papilla were correlated. The CAP was abolished in all animals after overstimulation. Three groups of animals were identified according to the functional recovery of the CAP thresholds recorded at regular intervals with implanted electrodes: Group 1: Fast functional recovery starting immediately after trauma, followed by recovery to pre-exposure values within 3 weeks. Group 2: Slow functional recovery of threshold starting 1-2 weeks after trauma and ending 4-5 weeks after trauma. A mean residual hearing loss of 26.3 dB at 2 kHz remained. Group 3: No recovery of CAP thresholds up to 8 months after trauma. Three weeks after trauma, very few responsive neurons were found in groups 2 and 3. Tuning curves were very broad and sometimes irregular in shape. Thresholds were very high, around 120 dB SPL. Spontaneous firing rate was much reduced, especially in neurons with high CFs. After 4 or more months of recovery, the response properties of single units in group 1 had only partially recovered. Thresholds and sharpness of tuning of many single units were normal; however, in general they were still poorer than in control animals. Spontaneous firing rate was comparable to control animals. Neurons from animals in group 2 showed less recovery, especially at frequencies above the exposure frequency. Thresholds and sharpness of tuning were normal at frequencies below the exposure frequency, but were much poorer at frequencies above the exposure. Spontaneous firing rate was much reduced in fibers with high CFs. The basilar papilla in animals without recovery showed total loss of the sensory epithelium. The basal lamina of the basilar membrane, however, remained intact and was covered with cuboidal cells. In fast recovering animals, the papilla was repopulated with hair cells after 4 months. In slow recovering animals, short (abneural) hair cells were still missing over large parts of the papilla after 4 months of recovery. Residual short (abneural) hair cell loss was largest at two areas, one more basal and the other more apical to the characteristic place of the traumatizing frequency. The results show that functional recovery from severe damage to both short (abneural) and tall (neural) hair cells occurs in adult birds. However, the onset of recovery is delayed and the time course is slower than after destruction of short (abneural) hair cells alone. Furthermore recovery is incomplete, both functionally and morphologically. There are residual permanent hearing losses and regeneration of short (abneural) hair cells is incomplete. C1 UNIV FRANKFURT KLINIKUM,ZENTRUM PHYSIOL,D-60590 FRANKFURT,GERMANY. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 133 EP 154 DI 10.1016/S0378-5955(96)00155-4 PG 22 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000014 PM 8951458 ER PT J AU Agrup, C Berggren, PO Kohler, M Spangberg, ML BaggerSjoback, D AF Agrup, C Berggren, PO Kohler, M Spangberg, ML BaggerSjoback, D TI Morphological and functional characteristics of the different cell types in the stria vascularis: A comparison between cells obtained from fresh tissue preparations and cells cultured in vitro SO HEARING RESEARCH LA English DT Article DE inner ear; endolymph; guinea pig; Ca2+-transport ID INNER-EAR; FREE CA-2+; MELANOCYTES; MICROSCOPY; POTASSIUM AB Endolymph is the only extracellular fluid in the body which is characterized by an intracellular-like ion composition. The molecular mechanisms responsible for the production of endolymph and the regulation of endolymph composition are still unknown to a large extent, although the stria vascularis (SV) is believed to play an important role for these functions. A basic requirement for investigating the function of different cell types in the SV is the establishment of a method, which increases the accessibility of the tissue with maintained cell viability and function. In this study, fresh tissue preparations and cultured cells from SV, harvested from pigmented guinea pigs, were established. Marginal cells, intermediate/melanocyte-like cells and fibroblasts could be discerned in the cell cultures with bright-field microscopy, transmission and scanning electron microscopy as well as immunohistochemistry, using polyclonal antibodies against cytokeratin and vimentin. In order to study functional characteristics of the fresh tissue preparations and the cell cultures, changes in the cytoplasmic free Ca2+ concentration were determined with the fura-2 method. The cultured cells, of different types in the SV, are a suitable model for future studies of the molecular mechanisms behind the production of endolymph and the regulation of endolymph composition. C1 KAROLINSKA INST,KAROLINSKA HOSP,DEPT MOL MED,S-17176 STOCKHOLM,SWEDEN. RP Agrup, C (reprint author), KAROLINSKA INST,KAROLINSKA HOSP,DEPT OTORHINOLARYNGOL,S-17176 STOCKHOLM,SWEDEN. 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Res. PD DEC 1 PY 1996 VL 102 IS 1-2 BP 155 EP 166 DI 10.1016/S0378-5955(96)00156-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000015 PM 8951459 ER PT J AU Boettcher, FA Mills, JH Swerdloff, JL Holley, BL AF Boettcher, FA Mills, JH Swerdloff, JL Holley, BL TI Auditory evoked potentials in aged gerbils: Responses elicited by noises separated by a silent gap SO HEARING RESEARCH LA English DT Article DE aging; auditory brainstem response; evoked potential; hearing loss; presbyacusis ID SENSORINEURAL HEARING-LOSS; ANTEROVENTRAL COCHLEAR NUCLEUS; INFERIOR COLLICULUS NEURONS; SHORT-TERM ADAPTATION; BRAIN-STEM RESPONSES; C57BL/6J MICE; NEURAL SYNCHRONIZATION; AMPLITUDE-MODULATION; AZIMUTHAL LOCATION; MONGOLIAN GERBIL AB The compound action potential (CAP) and the auditory brainstem response (ABR; waves ii and iv) were recorded in young (4-8 month) and aged (33-37 month) gerbils using a paradigm similar to that used in some psychophysical studies of gap detection (a pair of identical low-pass noises separated by a silent gap). Response amplitudes were analyzed in terms of absolute amplitudes and the 'amplitude ratio' (the amplitude of the response to the second noise of a pair divided by that to the first). Response latencies were analyzed in terms of the absolute latencies as well as the 'latency shift' (the latency of the response to the second noise minus that to the first). Response amplitudes were much smaller in the aged subjects for both the first and second stimuli of a pair. There were minimal changes in amplitude ratios across age for both the CAP and ABR. Absolute latencies were similar between groups for the first stimulus of a pair, but latencies to wave iv were much longer for the aged subjects when the gap was short. Thus, the latency shift for the aged group was much longer for wave iv in the aged compared to the young group, but were similar between groups for the CAP or wave ii of the ABR. The results suggest that there may be changes in coding of temporal information in the auditory brainstem of aged gerbils which are not a direct result of abnormal temporal processing in the auditory periphery. RP Boettcher, FA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR AREHOLE S, 1989, AUDIOLOGY, V28, P92 BACKOFF PM, 1994, HEARING RES, V73, P163, DOI 10.1016/0378-5955(94)90231-3 BANAYSCHWARTZ M, 1993, NEUROCHEM RES, V18, P417, DOI 10.1007/BF00967245 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z BOETTCHER FA, 1995, HEARING RES, V89, P1, DOI 10.1016/0378-5955(95)00116-X BOETTCHER FA, 1995, OCCUP MED, V10, P577 BOETTCHER FA, 1990, HEARING RES, V48, P125, DOI 10.1016/0378-5955(90)90203-2 BOETTCHER FA, 1993, HEARING RES, V71, P146, DOI 10.1016/0378-5955(93)90030-5 BURKARD R, 1993, J ACOUST SOC AM, V94, P2441, DOI 10.1121/1.407465 BURKARD R, 1993, J ACOUST SOC AM, V93, P2069, DOI 10.1121/1.406693 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CASPARY DM, 1995, EXP GERONTOL, V30, P349, DOI 10.1016/0531-5565(94)00052-5 CLOCK AE, 1993, HEARING RES, V71, P37, DOI 10.1016/0378-5955(93)90019-W ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H 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 GIRAUDI D, 1980, J ACOUST SOC AM, V68, P802, DOI 10.1121/1.384818 GIRAUDIPERRY DM, 1982, J ACOUST SOC AM, V72, P1387, DOI 10.1121/1.388444 GRATTON MA, 1995, HEARING RES, V82, P44 GRATTON MA, 1995, HEARING RES, V83, P43, DOI 10.1016/0378-5955(94)00188-V HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N JORIS PX, 1994, J NEUROPHYSIOL, V71, P1022 JORIS PX, 1994, J NEUROPHYSIOL, V71, P1037 KALTENBACH JA, 1993, HEARING RES, V67, P35, DOI 10.1016/0378-5955(93)90229-T KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 MCFADDEN SL, 1994, HEARING RES, V78, P132, DOI 10.1016/0378-5955(94)90019-1 MCFADDEN SL, 1994, HEARING RES, V78, P115, DOI 10.1016/0378-5955(94)90018-3 Melcher JR, 1996, HEARING RES, V93, P52, DOI 10.1016/0378-5955(95)00200-6 Melcher JR, 1996, HEARING RES, V93, P28, DOI 10.1016/0378-5955(95)00179-4 MILBRANDT JC, 1994, NEUROBIOL AGING, V15, P699, DOI 10.1016/0197-4580(94)90051-5 Mills JH, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P181 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MOORE BCJ, 1992, J ACOUST SOC AM, V92, P1923, DOI 10.1121/1.405240 *NAT CTR HLTH STAT, 1987, VIT HLTH STAT 3, V25 RAZA A, 1994, HEARING RES, V77, P221, DOI 10.1016/0378-5955(94)90270-4 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 SCHMIEDT RA, 1996, IN PRESS J NEUROPHYS SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SHORE SE, 1995, HEARING RES, V82, P31 WALTON JP, 1995, HEARING RES, V88, P19, DOI 10.1016/0378-5955(95)00093-J WATANABE T, 1971, JPN J PHYSIOL, V21, P537 WESTERMAN LA, 1987, J ACOUST SOC AM, V81, P680, DOI 10.1121/1.394836 WILLOTT JF, 1994, HEARING RES, V74, P1, DOI 10.1016/0378-5955(94)90171-6 NR 44 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 DEC 1 PY 1996 VL 102 IS 1-2 BP 167 EP 178 DI 10.1016/S0378-5955(96)90016-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX780 UT WOS:A1996VX78000016 PM 8951460 ER PT J AU Evans, MG Kiln, J Pinch, D AF Evans, MG Kiln, J Pinch, D TI No evidence for functional GABA receptors in outer hair cells isolated from the apical half of the guinea-pig cochlea SO HEARING RESEARCH LA English DT Article DE outer hair cell; patch clamp; gamma-aminobutyric acid; acetylcholine; potassium current ID ACETYLCHOLINE; IMMUNOCYTOCHEMISTRY; CURRENTS AB Outer hair cells, isolated from the apical cochlear turns, did not respond to GABA during whole-cell recording. A few cells did respond to acetylcholine. Thus we have no evidence to suggest that GABA acts as an efferent neurotransmitter in the cochlea. C1 UNIV BRISTOL, SCH MED SCI, DEPT PHYSIOL, BRISTOL BS8 1TD, AVON, ENGLAND. RI evans, michael/C-4980-2009 OI evans, michael/0000-0002-8755-0034 CR ALTSCHULER RA, 1985, BRAIN RES, V338, P1, DOI 10.1016/0006-8993(85)90242-2 BOBBIN RP, 1970, NEUROPHARMACOLOGY, V9, P567, DOI 10.1016/0028-3908(70)90007-9 Evans MG, 1996, J PHYSIOL-LONDON, V491, P563 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 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 GITTER AH, 1992, EUR ARCH OTO-RHINO-L, V249, P62 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 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 Marty A, 1983, SINGLE CHANNEL RECOR, P107 NAKAGAWA T, 1994, BRAIN RES, V661, P293, DOI 10.1016/0006-8993(94)91207-6 PLINKERT PK, 1990, HEARING RES, V44, P25, DOI 10.1016/0378-5955(90)90019-L PLINKERT PK, 1993, EUR ARCH OTO-RHINO-L, V250, P351 PUJOL R, 1992, ADV BIOSCI, V83, P45 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X NR 16 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 1 EP 6 DI 10.1016/S0378-5955(96)00107-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900001 PM 8951427 ER PT J AU Pierson, M Li, DQ AF Pierson, M Li, DQ TI Cochlear integrity in rats with experimentally induced audiogenic seizure susceptibility SO HEARING RESEARCH LA English DT Article DE audiogenic seizure; epilepsy; cochlea; development; kanamycin ID EPILEPSY-PRONE RAT; KANAMYCIN; FREQUENCY; NOISE AB While chronic susceptibility of rodents to audiogenic seizures (AGSs) is often accompanied by cochlear lesions, it has not been demonstrated whether cochlear hair cell losses are essential to pathogenesis in this epileptic disorder. An alternative possibility is that the neonatal timing of hearing losses is what unites various models of chronic AGS susceptibility. In the latter case, either transient or permanent hearing losses might induce susceptibility as long as they concur with a critical period of development. To address this issue, it was examined whether lesions were universally present in cochleas of adult rats after having been made susceptible to sound-triggered seizures by different types and severities of neonatal auditory trauma. Neonatal treatments included: (1) an 8 min exposure of rat pups to intense noise (125 dB SPL) on postnatal day (PND) 14; (2) injections of low doses of kanamycin (KM: 100 mg/kg) on PNDs 9-12; or (3) injections of high doses of KM (500 mg/kg) on PNDs 9-12. As adults, rats in all experimental groups, but not in sham-treated groups, exhibited sound-triggerable seizure responses. Nonetheless, this outcome did not depend on integrity of cochleas. Hair cells were rarely missing in the cochleas of noise-exposed, low-dosage KM-treated, or sham-treated rats. By contrast, all inner and outer hair cells were missing from the basal 75% of cochleas of adult rats which had been treated with high-dose KM on PNDs 9-12. Results indicate that cochlear lesions are not requisite for the induction or expression of AGS susceptibility. At the same time, however, significant hair cell losses do not necessarily preclude susceptibility. It appears that the neonatal timing rather than the permanence of hearing losses may be what engenders chronic AGS susceptibility. RP Pierson, M (reprint author), TEXAS CHILDRENS HOSP,BAYLOR COLL MED,CAIN FDN LABS,6621 FANNIN,HOUSTON,TX 77030, USA. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 7 EP 13 DI 10.1016/S0378-5955(96)00125-6 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900002 PM 8951428 ER PT J AU Clerici, WJ Yang, LH AF Clerici, WJ Yang, LH TI Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function SO HEARING RESEARCH LA English DT Article DE cochlea; cochlear microphonic; compound action potential; hydroxyl radical; free radical; reactive oxygen species; superoxide anion ID OUTER HAIR CELL; GUINEA-PIG; FREE-RADICALS; CISPLATIN OTOTOXICITY; SUPEROXIDE-DISMUTASE; ANTIOXIDANT SYSTEM; DAMAGE; ALLOPURINOL; MECHANISM; INVITRO AB Reactive oxygen species (ROS) generation may play a role in ototoxicity, however, the specific effects of ROS generation upon cochlear function are unstudied. Therefore, guinea pig cochleas were instilled with artificial perilymph (AP), H2O2, or confirmed generating systems for the superoxide anion (O-2(-)) or the hydroxyl radical (OH.), or with an ROS system plus its respective scavenger - catalase (CAT), superoxide dismutase (SOD) or deferoxamine (DEF). O-2(-) generating system instillation led to significantly greater mean high frequency compound action potential (CAP) threshold shifts at 10 and 120 min post infusion than seen in AP control or SOD/O-2(-) groups. H2O2 group CAP threshold shifts were significantly greater than control and CAT/H2O2 group values at 10 (16-30 kHz), and 120 min (above 12 kHz). OH. generating system instillation led to significantly greater CAP threshold shifts at 10 (12-30 kHz) and 120 min (above 6 kHz) than seen in control or DEF/OH. groups. No significant CAP differences were found between controls and scavenger/ROS groups. Mean 1.0 mu V cochlear microphonic isopotential curve shift values did not systematically differ among groups. The rapid degradation of high frequency CAP threshold sensitivity seen here may provide insight into the portion of cochlear dysfunction which is ROS-mediated following noise, radiation or chemical exposures. RP Clerici, WJ (reprint author), UNIV KENTUCKY,ALBERT B CHANDLER MED CTR,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,COLL MED,LEXINGTON,KY 40536, USA. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 14 EP 22 DI 10.1016/S0378-5955(96)00126-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900003 PM 8951429 ER PT J AU Bibikov, NG Nizamov, SV AF Bibikov, NG Nizamov, SV TI Temporal coding of low-frequency amplitude modulation in the torus semicircularis of the grass frog SO HEARING RESEARCH LA English DT Article DE frog; auditory; amplitude modulation; torus semicircularis; adaptation ID DORSAL MEDULLARY NUCLEUS; GERBIL COCHLEAR NUCLEUS; AUDITORY-NERVE FIBERS; NORTHERN LEOPARD FROG; INFERIOR COLLICULUS; SINGLE NEURONS; COMPLEX SOUNDS; MIDBRAIN; SENSITIVITY; RESPONSES AB Single neuron responses to sinusoidal 20 Hz amplitude modulated lone bursts (612.5 ms stimulus-on time at the rate of once per 2.2 s) were studied in the auditory midbrain (torus semicircularis) of the immobilized grass frog (Rana temporaria temporaria). The characteristic frequency stimuli at 30 dB above the minimum threshold included 12 full modulation periods with fixed initial phase. Neurons generally showed good phase-locking to the envelope waveform. 160 of the 186 investigated neurons responded to 80% amplitude modulated stimuli with discharges synchronized to the modulation cycle. For this modulation depth the best phase-locking capability was observed for certain phasic and build-up units. The synchronous response to 10% modulated stimuli was observed in 104 units. Though a few (2 of 29) phasic units were capable of reproducing this modulation with very high fidelity, the general tendency was the increasing of phase-locking capacity for units with a substantial sustained activity. In this condition for 66 units (63% of the units displaying the synchronous response) we observed a significant improvement of phase-locking from the initial to the terminal periods of modulation. This effect could be interpreted as an initial stage of the enhancement of small amplitude changes in the course of the long-term adaptation. RP Bibikov, NG (reprint author), NN ANDREEV ACOUST INST,SCHWERN ST 4,MOSCOW 117036,RUSSIA. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 23 EP 44 DI 10.1016/S0378-5955(96)00128-1 PG 22 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900004 PM 8951430 ER PT J AU Pickles, JO BillieuxHawkins, DA Rouse, GW AF Pickles, JO BillieuxHawkins, DA Rouse, GW TI The incorporation and turnover of radiolabelled amino acids in developing stereocilia of the chick cochlea SO HEARING RESEARCH LA English DT Article DE stereocilia; protein; turnover; actin; chick; development; hair cell ID SERIAL-SECTION RECONSTRUCTION; ACTIN-FILAMENTS; HAIR-CELLS; ACOUSTIC TRAUMA; ULTRASTRUCTURAL-CHANGES; CUTICULAR PLATES; INNER-EAR; NOISE; ORGANIZATION; PROTEINS AB Hair cell stereocilia are composed of packed actin filaments, oriented such that the preferred end for the addition of actin monomers is at the tips of the stereocilia. It has therefore been suggested that when stereocilia grow, they do so from their tips (Tilney and DeRosier, 1986, Dev. Biol. 116, 119-129). In order to test the hypothesis, radiolabelled amino acids were applied to the air-sac of chicken eggs at day 17 of incubation, i.e., at the beginning of a phase in which the stereocilia have achieved their mature width, but are growing rapidly in length. Incorporation of radiolabel was studied autoradiographically, followed by image analysis and averaging grain counts over many hair cells. In contrast to the position expected from the above hypothesis, there was no sign of preferential incorporation of label in the upper part of the stereociliary bundle. The greatest density of labelling was found in the lower part of the bundle, while the upper part of the bundle was under-represented in the autoradiographic averages. The turnover time (to fall to l/e) was significantly greater in the bundle (16 days) than in the cuticular plate or in the rest of the cell (9 days). The results (i) give no support for the hypothesis that stereocilia grow from the tips, and (ii) suggest that during development at least some components of the stereocilia turn over with a relatively short time course. RP Pickles, JO (reprint author), UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,BRISBANE,QLD 4072,AUSTRALIA. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 45 EP 54 DI 10.1016/S0378-5955(96)00129-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900005 PM 8951431 ER PT J AU Crouch, JJ Schulte, BA AF Crouch, JJ Schulte, BA TI Identification and cloning of site C splice variants of plasma membrane Ca-ATPase in the gerbil cochlea SO HEARING RESEARCH LA English DT Article DE ion transport; inner ear; Ca homeostasis; reverse transcription polymerase chain reaction (RT-PCR) ID CALMODULIN-BINDING DOMAINS; SKELETAL-MUSCLE; MESSENGER-RNAS; CALCIUM; CA2+-ATPASE; PRODUCTS; PUMP; EXPRESSION; ISOFORM-3; PROTEINS AB Plasma membrane Ca-ATPase (PMCA) gene products were identified in the gerbil cochlea by reverse-transcription polymerase chain reaction (RT-PCR). Cochlear cDNA was amplified using PMCA isoform-specific primers from splice site C, the calmodulin binding domain. PCR products were cloned and sequenced. The putative housekeeping PMCA genes, 1b and 4b, as expected, were present in the gerbil cochlea and shared 98.6 and 100% amino acid homology with published rat sequences, at splice site C, respectively. PMCA2b, 3a and 3b splice variants also were detected in cochlear cDNAs and shared 95, 94.3 and 98% amino acid homology with their rat counterparts. PMCA isoforms 2 and 3 have been shown to occur in highly specialized tissues, such as muscle and brain, that require finely tuned regulation of intracellular free Ca2+ levels. The presence of several isoforms and splice variants of PMCA in the cochlea most probably reflects their differential expression among the several cell types that have been shown to contain immunoreactive PMCA. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 55 EP 61 DI 10.1016/S0378-5955(96)00132-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900006 PM 8951432 ER PT J AU Pantev, C Roberts, LE Elbert, T Ross, B Wienbruch, C AF Pantev, C Roberts, LE Elbert, T Ross, B Wienbruch, C TI Tonotopic organization of the sources of human auditory steady-state responses SO HEARING RESEARCH LA English DT Article DE human auditory cortex; magnetoencephalography; auditory evoked magnetic field; steady-state field ID EVOKED MAGNETIC-FIELDS; CORTICAL ORIGIN; CORTEX; POTENTIALS; FREQUENCY; AMPLITUDE; TRANSIENT; STIMULI; BRAIN; TONE AB Steady-state responses (SSRs) or steady-state fields (SSFs) show maximum amplitude when tone pulses are presented at repetition rates near 40 Hz. This result has led to the hypothesis that the SSR/SSF consists of superimposed transient 'middle latency' responses which display wave periods near 40 Hz and summate with one another when phase locked by 40 Hz steady-state stimulation. We evaluated this hypothesis by comparing the cortical sources of the 40 Hz auditory SSF with sources of the middle latency Pa wave which is prominent in electrical and magnetic recordings, and with the cortical sources of the familiar N1 wave, at different carrier frequencies between 250 and 4000 Hz. SSF sources determined for the different carrier frequencies were found to display a 'medial' tendency tonotopy resembling that of the N1m (sources for the higher frequencies represented more deeply within the supratemporal sulcus), opposite the 'lateral' tendency tonotopy of the middle latency Pam (sources for the higher frequencies situated more laterally). A medial SSF tonotopy was observed in each of the subjects investigated, including three subjects for whom Pam and Nlm maps were also available. These findings suggest that the 40 Hz SSF may not consist of summated or entrained middle latency responses, as has previously been proposed. Alternative mechanisms for the SSR are discussed. C1 MCMASTER UNIV, DEPT PSYCHOL, HAMILTON, ON L8S 4K1, CANADA. UNIV KONSTANZ, DEPT PSYCHOL, D-78434 CONSTANCE, GERMANY. RP Pantev, C (reprint author), UNIV MUNSTER, INST EXPT AUDIOL, CTR BIOMAGNETISM, KARDINAL VON GALEN RING 10, D-48129 MUNSTER, GERMANY. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 62 EP 74 DI 10.1016/S0378-5955(96)00133-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900007 PM 8951433 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 Gadolinium blocks mechano-electric transducer current in chick cochlear hair cells SO HEARING RESEARCH LA English DT Article DE hair cell; gadolinium; mechano-electric transduction channel; adaptation ID ACTIVATED ION CHANNELS; MECHANOELECTRIC TRANSDUCER; BULLFROGS SACCULUS; ADAPTATION; CALCIUM; DIHYDROSTREPTOMYCIN; AMILORIDE; BUNDLE AB We investigated the effects of gadolinium ion (Gd3+) On th, mechano-electrical transduction (MET) current using a whole-cell patch electrode voltage clamp technique in dissociated cochlear hair cells of chicks. Gd3+ blocked the MET channel in a concentration- and voltage-dependent manner. At -50 mV, Gd3+ blocked the MET channel, with a Hill coefficient of 1.14 and a dissociation constant (K-D) of 1.01 x 10(-5) M. Adaptation of the MET current disappeared after the introduction of Gd3+, a change that may be due to a decrease in inward going MET currents, specifically the Ca2+ component. RP Kimitsuki, T (reprint author), KYUSHU UNIV,FAC MED,DEPT OTORHINOLARYNGOL,3-1-1 MAIDASHI,FUKUOKA 812,JAPAN. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 75 EP 80 DI 10.1016/S0378-5955(96)00134-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900008 PM 8951434 ER PT J AU Cazals, Y Huang, ZW AF Cazals, Y Huang, ZW TI Average spectrum of cochlear activity: A possible synchronized firing, its olivo-cochlear feedback and alterations under anesthesia SO HEARING RESEARCH LA English DT Article DE cochlea; spontaneous activity; evoked activity; efferent feedback; anesthesia ID AUDITORY-NERVE ACTIVITY; RETINAL GANGLION-CELLS; GUINEA-PIG; OLIVOCOCHLEAR REFLEX; MASKED TONES; SPIKE RATE; CAT; FIBERS; OTOTOXICITY; ENHANCEMENT AB Average spectrum of electrophysiological cochlear activity (ASECA) recorded from the cochlea or the eighth nerve is related to firing of auditory neurons and has been used recently in search of an objective measure of tinnitus both in animal models and in humans. Little is known about neuro-sensory processes underlying the spectral features of ASECA. The present study used awake and/or anesthetized animals and investigated effects of various sounds presented contralaterally and ipsilaterally. Contralateral stimulation with noise bands at frequencies above about 8 kHz and below acoustic interaural cross-talk decreased the amplitude of the 1 kHz peak of ASECA. When presented ipsilaterally noises produced either an increase or a decrease of this spectral peak when the acoustic bandwidth was respectively above or below 1.5 kHz. Pure tones when presented contralaterally had no detectable effect. When presented ipsilaterally pure tones with frequencies higher than about 4 kHz decreased the 1 kHz peak of ASECA. The detailed time course of sound-induced variations of the 1 kHz peak was measured by time averaging. The resulting response patterns resemble PST histograms of the auditory nerve. Sedation and anesthesia deepened the 500 Hz trough of ASECA and shifted it towards 400 Hz. Sedation induced a diminution and anesthesia an almost complete suppression of the decrease of the 1 kHz peak induced by contralateral noise. Overall these data indicate that ASECA would reflect synchronized firings and they provide evidence for an influence of olivo-cochlear feedback sensitive to the state of awakeness. C1 HUBEI MED UNIV,AFFILIATED HOSP 1,ENT DEPT,WUHAN,PEOPLES R CHINA. RP Cazals, Y (reprint author), UNIV BORDEAUX 2,INSERM,LAB AUDIOL EXPT,HOP PELLEGRIN,PL A RABA LEON,F-33076 BORDEAUX,FRANCE. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 81 EP 92 DI 10.1016/S0378-5955(96)00135-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900009 PM 8951435 ER PT J AU Eybalin, M Norenberg, MD Renard, N AF Eybalin, M Norenberg, MD Renard, N TI Glutamine synthetase and glutamate metabolism in the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE glutamate-glutamine cycle; neurotransmission; excitotoxicity; ischemia; noise trauma; organ of Corti; immunocytochemistry ID SPIRAL GANGLION NEURONS; RAT-BRAIN; CEREBROSPINAL-FLUID; NERVOUS-SYSTEM; AMINO-ACIDS; INNER-EAR; LOCALIZATION; IMMUNOREACTIVITY; HIPPOCAMPUS; ASTROCYTES AB Glutamate is thought to act as a neurotransmitter of the sensory hair cells of the organ of Corti. Glutamine synthetase could be involved in a type of glutamate-glutamine cycle in the cochlea which could clear glutamate off the synaptic cleft and replenish the hair cell glutamate neurotransmitter store. Using both light and electron microscopic immunocytochemistry to localize this enzyme in the guinea pig cochlea, we have observed immunoreactive satellite glial cells surrounding parvalbumin-immunoreactive primary auditory neurons in the spiral ganglion. Glutamine synthetase was also detected in Schwann cells of the osseous spiral lamina which form the myelin sheath of nerve fibers. On the contrary, no immunoreactivity could be observed in the cochlear nerve and in the organ of Corti, although this organ contains structures able to take up glutamate. Although they confirm earlier works involving glutamine synthetase in the conversion of L-[H-3]glutamate taken up by glial cells, our results suggest that the cochlear glutamate-glutamine cycle is not primarily involved in the recycling and replenishment of hair cell neurotransmitter glutamate. Alternatively, it is proposed that glutamine synthetase functions to limit the perilymphatic glutamate concentrations. C1 UNIV MONTPELLIER 1,CHU HOP ST CHARLES,F-34295 MONTPELLIER 5,FRANCE. UNIV MIAMI,SCH MED,DEPT PATHOL D33,MIAMI,FL 33101. RP Eybalin, M (reprint author), INSERM U254 NERUOBIOL AUDIT PLAST SYNAPT,F-34295 MONTPELLIER 5,FRANCE. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 93 EP 101 DI 10.1016/S0378-5955(96)00136-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900010 PM 8951436 ER PT J AU vanDijk, P Narins, PM Wang, JX AF vanDijk, P Narins, PM Wang, JX TI Spontaneous otoacoustic emissions in seven frog species SO HEARING RESEARCH LA English DT Article DE spontaneous otoacoustic emission; frog; temperature ID TONOTOPIC ORGANIZATION; TEMPERATURE-DEPENDENCE; AMPHIBIAN PAPILLA; BASILAR PAPILLA; FREQUENCY; BULLFROG AB Spontaneous otoacoustic emissions were screened for in five advanced frog species (Hyla cinerea, n=10 ears; Hyla chrysoscelis, n = 10; Hyla versicolor, n = 7; Leptodactylus albilabris, n = 2; Rana pipiens pipiens, n = 8), and two primitive frog species (Xenopus laevis, n = 9; Bombina orientalis, n = 12). Emissions were found in 90% of the advanced species' ears, whereas none of the primitive species' ears had emissions. Emission frequencies ranged from 645 Hz to 1680 Hz. The absence of emissions in the primitive species correlates with (1) the absence of a tympanic membrane, and (2) a reduced length of the caudal extension of the amphibian papilla. In eight frogs, the effect of body temperature on emissions was investigated. As a function of temperature, the frequency changed at a rate between 0.009 and 0.091 oct/degrees C, and emission levels displayed a complex but consistent behavior. For 9 out of 15 spectral emission peaks encountered during the temperature experiments, the relation between the peak height and peak width was similar to that of an active oscillator. C1 UNIV CALIF LOS ANGELES,DEPT PHYSIOL SCI,LOS ANGELES,CA 90024. RP vanDijk, P (reprint author), UNIV GRONINGEN HOSP,ENT DEPT,NL-9700 RB GRONINGEN,NETHERLANDS. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 102 EP 112 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900011 PM 8951437 ER PT J AU Hood, LJ Berlin, CI Hurley, A Cecola, RP Bell, B AF Hood, LJ Berlin, CI Hurley, A Cecola, RP Bell, B TI Contralateral suppression of transient-evoked otoacoustic emissions in humans: Intensity effects SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; transient-evoked otoacoustic emission; contralateral suppression; human; intensity level ID COCHLEAR MICROMECHANICAL PROPERTIES; STIMULATED ACOUSTIC EMISSIONS; DEPENDENCE; RESPONSES; VARIABLES AB Transient evoked otoacoustic emissions (TEOAEs) were recorded to clicks presented at peak sound pressures of 50, 55, 60, 65 and 70 dB while continuous contralateral white noise was varied from 10 dB below to 10 dB above the click level. Suppression increased predictably with suppressor noise level for any given click level. However, when the suppressor noise level was held constant, suppression was greater for lower click levels. This observation is consistent with the association of suppression of otoacoustic emissions with active cochlear processes and efferent function at low intensity levels. RP Hood, LJ (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES LAB,2020 GRAVIER ST,NEW ORLEANS,LA 70112, USA. CR BERLIN CI, 1993, HEARING RES, V71, P1, DOI 10.1016/0378-5955(93)90015-S BERLIN CI, 1993, HEARING RES, V65, P40, DOI 10.1016/0378-5955(93)90199-B COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E GIFFORD ML, 1987, HEARING RES, V29, P179, DOI 10.1016/0378-5955(87)90166-3 KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 Killion MC, 1985, HEAR INSTRUM, V36, P34 NIEDER P, 1970, NATURE, V227, P184, DOI 10.1038/227184a0 RYAN S, 1991, British Journal of Audiology, V25, P391, DOI 10.3109/03005369109076614 VEUILLET E, 1991, J NEUROPHYSIOL, V65, P724 WARREN EH, 1989, HEARING RES, V37, P105, DOI 10.1016/0378-5955(89)90033-6 Wen H., 1993, ARO ABSTR, V16, P102 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 NR 14 TC 45 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 NOV 1 PY 1996 VL 101 IS 1-2 BP 113 EP 118 DI 10.1016/S0378-5955(96)00138-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900012 PM 8951438 ER PT J AU Matsunaga, T Kanzaki, J Hosoda, Y AF Matsunaga, T Kanzaki, J Hosoda, Y TI The vasculature of the peripheral portion of the human eighth cranial nerve SO HEARING RESEARCH LA English DT Article DE human; transmission electron microscopy; internal auditory artery; microvessel; peripheral nervous system; vestibular ganglion ID FINE-STRUCTURE; BLOOD-VESSELS; SCIATIC-NERVE; RAT; ROOTS; MICROENVIRONMENT; ULTRASTRUCTURE; PERMEABILITY; DIFFUSION; BARRIER AB The vasculature of the peripheral portion of the human eighth cranial nerve (VIIIN) was investigated by light and transmission electron microscopy. Arterioles and venules running longitudinally around the VIIIN formed the extrinsic vascular system. The anatomical relationship between these extrinsic vessels and the VIIIN sheath was similar to that between blood vessels on the surface of the brain and the pia mater. In the endoneurium, postcapillary venules and large capillaries were sparsely distributed and longitudinally arranged, and these microvessels formed the intrinsic microvascular system, which was supported by the extrinsic vascular system via anastomosing vessels. The ultrastructural features of the internal auditory artery and its main branches were the same as those of other intracranial arteries. Ultrastructural study also revealed myo-endothelial junctions in anastomosing arterioles, and endothelio-pericytic junctions in extrinsic and anastomosing venules. Microvascular endothelial cells were connected by tight junctions in both the vestibular ganglion and the rest of the VIIIN. These features of the vasculature were considered to be effective for maintenance of the endoneurial fluid and regulation of the circulation in the peripheral portion of the human VIIIN. C1 KEIO UNIV,SCH MED,DEPT OTOLARYNGOL,SHINJUKU KU,TOKYO 160,JAPAN. KEIO UNIV,SCH MED,DEPT PATHOL,SHINJUKU KU,TOKYO 160,JAPAN. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 119 EP 131 DI 10.1016/S0378-5955(96)00141-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900013 PM 8951439 ER PT J AU Nenov, AP Norris, C Bobbin, RP AF Nenov, AP Norris, C Bobbin, RP TI Acetylcholine response in guinea pig outer hair cells .1. Properties of the response SO HEARING RESEARCH LA English DT Article DE K+ channel; voltage dependence; desensitization ID CHOLINERGIC RECEPTOR; COCHLEA; CURRENTS; CHICK; HYPERPOLARIZES; RECTIFICATION; INHIBITION; CHANNELS AB The properties of the ACh (acetylcholine) response in guinea pig outer hair cells (OHCs)are not well understood. It has been shown that the response to ACh involves the activation of a Ca2+ dependent K+ selective conductance (referred to as K-sub where sub stands for suberyldicholine). In the present study, we examined the voltage dependence, the time dependence, and the desensitization of the ACh response. In addition, we examined the K+ selectivity of K-sub. These properties are important for aiding in the determination of the type of K+ channels activated by ACh. Patch-clamp technique in the whole-cell mode was used to record from single OHCs isolated from adult pigmented guinea pigs. ACh (100 mu M) was applied to the voltage-clamped OHCs and the ACh Induced currents (I-ACh) were measured. A voltage dependence of the ACh response was found with the ACh induced currents decaying monoexponentially at potentials positive to -30 mV. The decay of the ACh induced currents was faster soon after establishing the whole-cell mode of recording when compared to the decay of the currents some time later. This effect, referred to as the time dependence, was different from the desensitization of the response upon prolonged application of ACh. The desensitization of the ACh induced currents was about 50% after 2 min of continuous application of 100 mu M ACh. The examined characteristics of the ACh response in guinea pig OHCs indicate a voltage and time dependence of the response and strong K+ selectivity of the K-sub. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB SOUTH,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT OTORHINOLARYNGOL,NEW ORLEANS,LA 70112. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 132 EP 148 DI 10.1016/S0378-5955(96)00142-6 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900014 PM 8951440 ER PT J AU Nenov, AP Norris, C Bobbin, RP AF Nenov, AP Norris, C Bobbin, RP TI Acetylcholine response in guinea pig outer hair cells .2. Activation of a small conductance Ca2+-activated K+ channel SO HEARING RESEARCH LA English DT Article DE acetylcholine; outer hair cell; cesium; charybdotoxin; SK channel; apamin ID ION-DEPENDENT CONDUCTANCES; POTASSIUM CHANNELS; CHOLINERGIC RECEPTOR; VENTRICULAR MYOCYTES; CHROMAFFIN CELLS; CALCIUM; COCHLEA; CURRENTS; CHICK; PERMEABILITY AB The type of K+ channel involved in the acetylcholine (ACh) evoked response (K-sub; sub stands for suberyldicholine) in guinea pig outer hair cells (OHCs) is still uncertain. The present study tests the hypotheses that K-sub is one of the following: a big conductance Ca2+-dependent K+ channel (BK), a small conductance Ca2+-dependent K+ channel (SK), a K-A type of K+ channel, or a K-n type of K+ channel. Patch-clamp technique in the whole-cell mode was used to record from single guinea pig OHCs. ACh (100 mu M) was applied to voltage-clamped OHCs and the ACh-induced currents (I-ACh) were measured. Charybdotoxin (100 nM) had no effect on I-ACh, while apamin (1 mu M) blocked more than 90% of I-ACh. Lowering the external Ca2+ concentration caused a hyperpolarizing shift of the I-ACh monitored as a function of the prepulse voltage. Increasing internal Mg2+ (Mg-i(2+)) concentration caused a reduction in the outward I-ACh without affecting the inward I-ACh. The K-sub channel was found to be permeable to Cs+. In Cs+ solutions, I-ACh was 45% of the I-ACh in K+ solutions. The block of I-ACh by apamin, the dependence on extracellular Ca2+, the incomplete block of I-ACh by Cs+, and the ACh-induced Cs+ currents favor the hypothesis that K-sub belongs to the SK type of channels. An ionotropic/nicotinic nature of the ACh mechanism of action is favored. It is suggested that, in vivo, the amplitude of the ACh-induced hyperpolarization may depend on the Ca2+/Mg2+ ratio inside and outside the cell. C1 LOUISIANA STATE UNIV,MED CTR,KRESGE HEARING RES LAB SOUTH,DEPT OTORHINOLARYNGOL & BIOCOMMUN,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT OTORHINOLARYNGOL,NEW ORLEANS,LA 70112. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 149 EP 172 DI 10.1016/S0378-5955(96)00143-8 PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900015 PM 8951441 ER PT J AU Yamada, K Kaga, K Uno, A Shindo, M AF Yamada, K Kaga, K Uno, A Shindo, M TI Sound lateralization in patients with lesions including the auditory cortex: Comparison of interaural time difference (ITD) discrimination and interaural intensity difference (IID) discrimination SO HEARING RESEARCH LA English DT Article DE sound localization; dichotic study; temporal lobe; word deafness; auditory agnosia ID RATTUS-NORVEGICUS; LOCALIZATION; DISORDER AB We examined sound lateralization using dichotic presentation of noises in 15 patients with left unilateral (12 patients) or bilateral (3 patients) temporal lobe lesions, that included the auditory cortex, and evaluated their abilities to discriminate interaural time and intensity difference (ITD, IID) separately. On the ITD discrimination test, discrimination thresholds in patients with left unilateral lesions were significantly higher than those in normal subjects, but all patients with left unilateral lesions could detect ITD. However, none of 3 patients with bilateral lesions could detect ITD. On the IID discrimination test, all patients with either unilateral or bilateral lesions could detect IID. IID discrimination thresholds in these patients were significantly higher than those in normal subjects. The auditory cortex plays an important role in discriminating both cues, but appears to be necessary for discriminating ITD. C1 UNIV TOKYO,FAC MED,DEPT OTOLARYNGOL,TOKYO 113,JAPAN. NIMH,NATL CTR NEUROL & PSYCHIAT,TOKYO,JAPAN. RP Yamada, K (reprint author), TEIKYO UNIV,SCH MED,DEPT OTOLARYNGOL,ITABASHI KU,KAGA 2-11-1,TOKYO 173,JAPAN. 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Res. PD NOV 1 PY 1996 VL 101 IS 1-2 BP 173 EP 180 DI 10.1016/S0378-5955(96)00144-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900016 PM 8951442 ER PT J AU Takeuchi, S Kakigi, A Takeda, T Saito, H Irimajiri, A AF Takeuchi, S Kakigi, A Takeda, T Saito, H Irimajiri, A TI Intravascularly applied K+-channel blockers suppress differently the positive endocochlear potential maintained by vascular perfusion SO HEARING RESEARCH LA English DT Article DE endocochlear potential; K+ channel blocker; stria vascularis; guinea pig ID ION-TRANSPORT MECHANISMS; STRIA VASCULARIS; BASOLATERAL MEMBRANE; COCHLEAR POTENTIALS; MARGINAL CELLS; GAP-JUNCTIONS; POTASSIUM; BARIUM; DUCT AB We studied the effects of several K+ channel blockers on the positive endocochlear potential (EP) of guinea pigs undergoing perfusion via the anterior inferior cerebellar artery. The EP level was reversibly suppressed by 50-60% in the presence of Ba2+ (2 mM), quinine (2 mM) or verapamil (1 mM) in the perfusate, but not significantly affected by tetraethylammonium (20 mM) or 4-aminopyridine (5 mM). Although the effective site(s) of these blockers at the cell level has not been located yet, these findings indicate an important role for a K+ conductance in the generation of the EP. C1 KOCHI MED SCH,DEPT OTOLARYNGOL,NANKOKU,KOCHI 783,JAPAN. RP Takeuchi, S (reprint author), KOCHI MED SCH,DEPT PHYSIOL,NANKOKU,KOCHI 783,JAPAN. CR BLEICH M, 1990, PFLUG ARCH EUR J PHY, V415, P449, DOI 10.1007/BF00373623 FORGE A, 1984, HEARING RES, V13, P189, DOI 10.1016/0378-5955(84)90108-4 HILLE B, 1992, IONIC CHANNELS EXCIT, P83 HIRSCH J, 1993, PFLUG ARCH EUR J PHY, V424, P470, DOI 10.1007/BF00374910 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 ISHIKAWA T, 1993, J MEMBRANE BIOL, V133, P29 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KOBAYASHI T, 1984, ARCH OTO-RHINO-LARYN, V239, P243, DOI 10.1007/BF00464250 LEDAIN AC, 1994, J MEMBRANE BIOL, V141, P239 MARCUS DC, 1985, HEARING RES, V17, P79, DOI 10.1016/0378-5955(85)90133-9 MARCUS DC, 1984, AM J PHYSIOL, V247, pC240 MARCUS NY, 1990, HEARING RES, V44, P13, DOI 10.1016/0378-5955(90)90018-K NELSON MT, 1995, AM J PHYSIOL-CELL PH, V268, pC799 PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 RAMPE D, 1993, MOL PHARMACOL, V44, P642 REALE E, 1975, J ULTRA MOL STRUCT R, V53, P284, DOI 10.1016/S0022-5320(75)80030-X SALT AN, 1982, JPN J PHYSIOL, V32, P219 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 Takeuchi S, 1996, HEARING RES, V95, P18, DOI 10.1016/0378-5955(96)00016-0 TAKEUCHI S, 1995, HEARING RES, V83, P89, DOI 10.1016/0378-5955(94)00191-R Takeuchi S, 1996, J MEMBRANE BIOL, V150, P47, DOI 10.1007/s002329900029 WADA J, 1979, LARYNGOSCOPE, V89, P1457 WANG J, 1993, HEARING RES, V68, P152 WANGEMANN P, 1995, HEARING RES, V90, P149, DOI 10.1016/0378-5955(95)00157-2 WATSON S, 1994, TRENDS PHARMACOL SCI, P1 NR 26 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 1 PY 1996 VL 101 IS 1-2 BP 181 EP 185 DI 10.1016/S0378-5955(96)00151-7 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX209 UT WOS:A1996VX20900017 PM 8951443 ER PT J AU Lanford, PJ Presson, JC Popper, AN AF Lanford, PJ Presson, JC Popper, AN TI Cell proliferation and hair cell addition in the ear of the goldfish, Carassius auratus SO HEARING RESEARCH LA English DT Article DE bromodeoxyuridine; saccule; immunocytochemistry; fish ID POST-SYNAPTIC POTENTIALS; AVIAN INNER-EAR; CHICK COCHLEA; ACOUSTIC TRAUMA; NERVE-FIBERS; AMINOGLYCOSIDE TOXICITY; VESTIBULAR EPITHELIUM; POSTEMBRYONIC FISH; REGENERATION; GROWTH AB Cell proliferation and hair cell addition have not been studied in the ears of otophysan fish, a group of species who have specialized hearing capabilities. In this study we used the mitotic S-phase marker bromodeoxyuridine (BrdU) to identify proliferating cells in the ear of one otophysan species, Carassius auratus (the goldfish). Animals were sacrificed at 3 h or 5 days postinjection with BrdU and processed for immunocytochemistry. The results of the study show that cell proliferation occurs in all of the otic endorgans and results in the addition of new hair cells. BrdU-labeled cells were distributed throughout all epithelia, including the primary auditory endorgan (saccule), where hair cell phenotypes vary considerably along the rostrocaudal axis. This study lays the groundwork for our transmission electron microscopy study of proliferative cells in the goldfish ear (Presson et al., Hearing Research 100 (1996) 10-20) as well as future studies of hair cell development in this species. The ability to predict, based on epithelial location, the future phenotype of developing hair cells in the saccule of the goldfish make that endorgan a particularly powerful model system for the investigation of early hair cell differentiation. RP Lanford, PJ (reprint author), UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742, USA. CR BAIRD RA, 1993, HEARING RES, V65, P164, DOI 10.1016/0378-5955(93)90211-I 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 FAY RR, 1978, J ACOUST SOC AM, V63, P136, DOI 10.1121/1.381705 FAY RR, 1988, HEARING VERTEBRATES, P29 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P193 FURUKAWA T, 1967, J NEUROPHYSIOL, V30, P1377 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 Furukawa T, 1990, Neurosci Res Suppl, V12, pS27, DOI 10.1016/0921-8696(90)90006-O HAMA K, 1969, Z ZELLFORSCH MIK ANA, V94, P155, DOI 10.1007/BF00339353 HASHINO E, 1991, HEARING RES, V52, P356, DOI 10.1016/0378-5955(91)90025-5 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 KATAYAMA A, 1993, J COMP NEUROL, V333, P28, DOI 10.1002/cne.903330103 LANFORD PJ, 1994, 17 ANN MIDW M SOC RE LANFORD PJ, 1995, CELL PROLIFERATION G LAUDER G V, 1983, Bulletin of the Museum of Comparative Zoology, V150, P95 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 LOMBARTE A, 1994, J COMP NEUROL, V345, P419, DOI 10.1002/cne.903450308 LOMBARTE A, 1993, HEARING RES, V64, P166, DOI 10.1016/0378-5955(93)90002-I NAKAJIMA Y, 1974, J COMP NEUROL, V156, P403, DOI 10.1002/cne.901560403 PLATT C, 1977, J COMP NEUROL, V172, P283, DOI 10.1002/cne.901720207 PLATT C, 1984, SCANNING ELECT MICRO, V4, P1915 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 Popper Arthur N., 1993, P99 Presson JC, 1996, HEARING RES, V100, P10, DOI 10.1016/0378-5955(96)00109-8 PRESSON JC, 1995, J NEUROBIOL, V26, P579, DOI 10.1002/neu.480260410 PRESSON JC, 1994, HEARING RES, V80, P1, DOI 10.1016/0378-5955(94)90002-7 PRESSON JC, 1990, HEARING RES, V46, P9, DOI 10.1016/0378-5955(90)90135-C 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 Saidel WM, 1995, BRAIN BEHAV EVOLUT, V46, P362, DOI 10.1159/000113286 SENTO S, 1987, J COMP NEUROL, V258, P352, DOI 10.1002/cne.902580304 STONE JS, 1994, J COMP NEUROL, V341, P50, DOI 10.1002/cne.903410106 SUGIHARA H, 1986, HISTOCHEMISTRY, V85, P193, DOI 10.1007/BF00494803 SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P330 TSUE TT, 1994, J NEUROSCI, V14, P140 WEISLEDER P, 1992, EXP NEUROL, V115, P2, DOI 10.1016/0014-4886(92)90211-8 NR 43 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 1996 VL 100 IS 1-2 BP 1 EP 9 DI 10.1016/0378-5955(96)00110-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800002 PM 8922975 ER PT J AU Presson, JC Lanford, PJ Popper, AN AF Presson, JC Lanford, PJ Popper, AN TI Hair cell precursors are ultrastructurally indistinguishable from mature support cells in the ear of a postembryonic fish SO HEARING RESEARCH LA English DT Article DE support cell; hair cell; cell proliferation; S-phase; postembryonic development; saccule; ultrastructure ID AVIAN INNER-EAR; ACOUSTIC TRAUMA; CHICK COCHLEA; REGENERATION; GROWTH; DIFFERENTIATION; IDENTIFICATION; PROLIFERATION; EPITHELIUM; PROGENY AB The ultrastructure of S-phase cells in the postembryonic fish ear was compared with that of mature support cells. S-phase cells were identified by injecting animals with [H-3]thymidine and sacrificing 3 h later. Sensory epithelia (saccules, utricles, and canals) were processed for light-level autoradiography. Sections containing thymidine-labeled cells were re-embedded and re-examined using transmission electron microscopy. The results indicate that S-phase cells differ from mature support cells only in nuclear position and shape. Otherwise their cytoplasmic characteristics are indistinguishable. Both cell types, on the other hand, are readily distinguishable from hair cells. These data provide ultrastructural evidence for the ability of mature support cells to enter the cell cycle in postembryonic vertebrates. C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. 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, 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 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 FORGE A, 1994, ASS RES OT ABSTR, V17, P131 GORDON JI, 1994, CURR OPIN CELL BIOL, V6, P795, DOI 10.1016/0955-0674(94)90047-7 KATAYAMA A, 1993, J COMP NEUROL, V333, P28, DOI 10.1002/cne.903330103 KING DG, 1982, STAIN TECHNOL, V57, P307 Lanford PJ, 1996, HEARING RES, V100, P1, DOI 10.1016/0378-5955(96)00110-4 LANFORD PJ, 1996, ASS RES OT ABSTR, V19, P86 LASSAR AB, 1994, CURR OPIN CELL BIOL, V6, P788, DOI 10.1016/0955-0674(94)90046-9 LEFEBVRE PP, 1993, SCIENCE, V260, P692, DOI 10.1126/science.8480180 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 POPPER AN, 1979, J MORPHOL, V161, P241, DOI 10.1002/jmor.1051610302 POPPER AN, 1990, HEARING RES, V45, P33, DOI 10.1016/0378-5955(90)90180-W PRESSON JC, 1989, ASS RES OT ABSTR, V12, P351 PRESSON JC, 1995, J NEUROBIOL, V26, P579, DOI 10.1002/neu.480260410 PRESSON JC, 1994, HEARING RES, V80, P1, DOI 10.1016/0378-5955(94)90002-7 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 RAPHAEL Y, 1994, HEARING RES, V80, P53, DOI 10.1016/0378-5955(94)90008-6 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 Sauer FC, 1935, J COMP NEUROL, V62, P377, DOI 10.1002/cne.900620207 STONE JS, 1994, J COMP NEUROL, V341, P50, DOI 10.1002/cne.903410106 TSUE TT, 1994, J NEUROSCI, V14, P140 NR 28 TC 23 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1996 VL 100 IS 1-2 BP 10 EP 20 DI 10.1016/0378-5955(96)00109-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800003 PM 8922976 ER PT J AU Cosgrove, D Kornak, JM Samuelson, G AF Cosgrove, D Kornak, JM Samuelson, G TI Expression of basement membrane type IV collagen chains during postnatal development in the murine cochlea SO HEARING RESEARCH LA English DT Article DE cochlea; development; basement membrane; immunohistology ID RECESSIVE ALPORT SYNDROME; PIG INNER-EAR; MUTATIONS; PROTEINS; ANTIGEN; TISSUE AB An immunofluorescence study was performed to examine the temporal and spatial patterns of expression for the different type IV collagen chains during postnatal cochlear development. At birth, the classical chains (4A1 and 4A2) were widely expressed, while the novel chains (4A3, 4A4, and 4A5) were completely absent. Activation of the novel chains was observed at 4 days of age, with intense, widely distributed immunostaining suggesting that most of the cells in the cochlea express the novel chains at this developmental stage. From day 8 through day 14, developmental inactivation of the novel chains results in a reduction of generalized immunoreactivity with a concomitant elevation of specific staining in the membranous structures bounding the interdental cells of the spiral limbus, the inner sulcus, the basilar membrane, and in a fibrous bed of staining radiating from the spiral prominence into the region of the spiral ligament which corresponds to the location of the root cell processes. This pattern of intense immunostaining for the novel chains persists through adulthood. The classical chains are expressed in these same anatomical regions only transiently (from day 6 to day 10), after which a gradual developmental inactivation leads to the adult expression pattern where classical collagen chains are found primarily in the perineurium, in the membranes surrounding the spiral ganglion cell bodies, and in the vascular basement membranes of the spiral ligament and the stria vascularis. The complex developmental pattern of expression for the type IV collagen chains in the murine cochlea is similar to that observed in the murine kidney, which is the other major site for basement membrane pathology in Alport syndrome. RP Cosgrove, D (reprint author), BOYS TOWN NATL RES HOSP,DEPT GENET,555 N 30TH ST,OMAHA,NE 68131, USA. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 21 EP 32 DI 10.1016/0378-5955(96)00114-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800004 PM 8922977 ER PT J AU Zhou, SL Pickles, JO AF Zhou, SL Pickles, JO TI Postnatal changes in the reticular lamina of the guinea pig organ of Corti SO HEARING RESEARCH LA English DT Article DE guinea pig; hair cell; cuticular plate; stereocilia; development; age ID HAIR-CELLS; HAMSTER COCHLEA; DIFFERENTIATION; STEREOCILIA; MOUSE; MORPHOLOGY; GROWTH AB The dimensions of the apical surfaces of hair cells were measured in guinea pigs, aged from 3 weeks before term to 25 weeks after birth. In the basal two-thirds of the cochlea, the apical surfaces of the outer hair cells and their supporting cells changed with age, shrinking in a direction radial across the cochlear duct. There was an associated widening of the angle of the 'V' of the rows of stereocilia. Further apically, between 12 and 16 mm from the base of the cochlea, the outer hair cells and their supporting cells underwent the opposite change, becoming wider in a radial direction with age. The changes were seen before birth and continued for more than 3 weeks after birth. The results suggest that the guinea pig cochlea continues certain developmental processes for a considerable time after birth. RP Zhou, SL (reprint author), UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,ST LUCIA,QLD 4072,AUSTRALIA. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 33 EP 40 DI 10.1016/0378-5955(96)00117-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800005 PM 8922978 ER PT J AU Palombi, PS Caspary, DM AF Palombi, PS Caspary, DM TI Physiology of the young adult Fischer 344 rat inferior colliculus: Responses to contralateral monaural stimuli SO HEARING RESEARCH LA English DT Article DE Fischer 344 rat; inferior colliculus; dynamic range; rate/intensity function; first spike latency; receptive held ID SINGLE-UNIT RESPONSES; INTERAURAL TIME; CENTRAL NUCLEUS; BRAIN-STEM; INTENSITY DIFFERENCES; GABAERGIC INHIBITION; EXTERNAL NUCLEUS; HORSESHOE BATS; NEURONS; CAT AB This study was designed to establish the young adult (3 month) Fischer 344 (F344) rat as a model of inferior colliculus (IC) physiology, providing a baseline for analysis of changes in single unit responses as the animals age and for the study of noise induced hearing loss. The response properties of units localized to the central nucleus of the IC (CIC) and those localized to the external cortex of the IC (ECIC) were compared in order to better characterize differences between these two subnuclei in the processing of simple auditory stimuli. In vivo extracellular single unit recordings were made from IC neurons in ketamine/xylazine anesthetized young adult F344 rats. When a unit was electrically isolated, the spontaneous activity level, characteristic frequency (CF) and CF threshold were determined. Rate/intensity functions (RIFs) in response to contralateral CF;tones and to contralateral noise bursts were obtained as were tone isointensity functions. The recording site was marked by ejecting horseradish peroxidase (HRP) from an electrode. Locations of recorded units were determined from electrode track marks and HRP marks in serial brain sections. Recordings were made from 320 neurons in the IC; 176 were localized to the CIC and 87 to the ECIC. Thirteen percent of the units in each subdivision were found to be poorly responsive to auditory stimulation (clicks, tones or noise), and spontaneous activity was generally low. Characteristic frequencies representative of the full rat audiogram were found in each subdivision with the mean threshold significantly higher in the ECIC (28.7 dB SPL) than in the CIC (22.3 dB SPL). The mean maximum discharge rate to CF tone bursts was near 24 spikes/s in each subdivision. Dynamic range tended to be higher in the ECIC (28.3 dB) than in the CIC (23.2 dB), reflecting the lower percentage of nonmonotonic units found in the ECIC. Most units responded more robustly with a slower tone presentation rate, displayed lower levels of discharge to noise bursts than to tone bursts, and had differently shaped tone and noise RIFs. Most units were classified as onset responders to CF tone bursts in both subdivisions, with the percentage of onset responders higher in the ECIC (68.9%) than in the CIC (57.8%). First spike latency did not differ significantly between the subdivisions, but tended to be shorter in the CIC. The breadth of the excitatory receptive fields did not differ significantly between subdivisions, although the mean was slightly larger in the ECIC. These results are generally consistent with the results of CIC studies from other species, establishing the F344 rat as a model of CIC physiology. Differences between CIC and ECIC units included a higher percentage of nonmonotonic RIFs and lower percentage of onset temporal response patterns in the CIC than in the ECIC. Some properties which have been previously used as hallmarks for differentiation between CIC and ECIC units, namely broader tuning and longer first spike latencies in the ECIC, did not reach statistical significance in this study. These may reflect species differences and/or the highly variable and largely overlapping sets of responses evident in the large sample size used in this study. C1 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62702. CR Aitkin L., 1986, AUDITORY MIDBRAIN ST AITKIN L, 1994, EXP BRAIN RES, V98, P53 AITKIN L, 1991, J NEUROPHYSIOL, V65, P383 AITKIN L, 1990, HEARING RES, V50, P97, DOI 10.1016/0378-5955(90)90036-O AITKIN LM, 1978, J NEUROPHYSIOL, V41, P837 AITKIN LM, 1987, J NEUROPHYSIOL, V57, P1185 AITKIN LM, 1981, J COMP NEUROL, V196, P25, DOI 10.1002/cne.901960104 AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 BACKOFF PM, 1994, HEARING RES, V73, P163, DOI 10.1016/0378-5955(94)90231-3 Baker D. E. J., 1979, LAB RAT, V1, P153 BOCK GR, 1974, BRAIN RES, V76, P150, DOI 10.1016/0006-8993(74)90521-6 BOCK GR, 1972, J NEUROPHYSIOL, V35, P265 BRANDAO ML, 1993, BEHAV BRAIN RES, V58, P49, DOI 10.1016/0166-4328(93)90089-9 CAIRD D, 1987, EXP BRAIN RES, V68, P379 CARDOSO SH, 1994, BEHAV BRAIN RES, V63, P17, DOI 10.1016/0166-4328(94)90046-9 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 Caspary D. M., 1993, Society for Neuroscience Abstracts, V19, P1425 CASSEDAY JH, 1994, SCIENCE, V264, P847, DOI 10.1126/science.8171341 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 Covey E., 1993, Society for Neuroscience Abstracts, V19, P535 EHRET G, 1988, HEARING RES, V35, P1, DOI 10.1016/0378-5955(88)90035-4 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 FAINGOLD CL, 1991, HEARING RES, V52, P201, DOI 10.1016/0378-5955(91)90200-S Faingold C.L., 1991, NEUROBIOLOGY HEARING, P223 Fay R. R., 1988, HEARING VERTEBRATES FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 FENG AS, 1985, J COMP NEUROL, V235, P529, DOI 10.1002/cne.902350410 FINLAYSON PG, 1993, NEUROBIOL AGING, V14, P127, DOI 10.1016/0197-4580(93)90088-S FLAMMINO F, 1975, J ACOUST SOC AM, V57, P692, DOI 10.1121/1.380494 FUJITA I, 1991, J NEUROSCI, V11, P722 HAPLEA S, 1994, J COMP PHYSIOL A, V174, P671 HAZZARD DG, 1991, NEUROBIOL AGING, V12, P645, DOI 10.1016/0197-4580(91)90115-Z Helfert RH, 1991, NEUROBIOLOGY HEARING, P1 HUFFMAN RF, 1990, BRAIN RES REV, V15, P295, DOI 10.1016/0165-0173(90)90005-9 Irvine D.R.F., 1986, AUDITORY BRAINSTEM R IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 JOHNSTON MV, 1981, FETUS INDEPENDENT LI, P251 KELLY JB, 1994, J NEUROPHYSIOL, V71, P1078 KELLY JB, 1991, HEARING RES, V56, P273, DOI 10.1016/0378-5955(91)90177-B KONISHI M, 1985, AUDITORY FUNCTION NE, P721 LANGNER G, 1987, HEARING RES, V31, P197, DOI 10.1016/0378-5955(87)90127-4 LANGNER G, 1992, ADV BIOSCI, V83, P241 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MASORO EJ, 1991, NEUROBIOL AGING, V12, P639, DOI 10.1016/0197-4580(91)90114-Y MEININGER V, 1986, NEUROSCIENCE, V17, P1159, DOI 10.1016/0306-4522(86)90085-0 MOORE DR, 1984, HEARING RES, V13, P159, DOI 10.1016/0378-5955(84)90106-0 MOORE DR, 1983, BRAIN RES, V269, P69, DOI 10.1016/0006-8993(83)90963-0 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 NELSON PG, 1963, J NEUROPHYSIOL, V26, P908 Oliver D. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 41 EP 58 DI 10.1016/0378-5955(96)00115-3 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800006 PM 8922979 ER PT J AU Palombi, PS Caspary, DM AF Palombi, PS Caspary, DM TI Responses of young and aged Fischer 344 rat inferior colliculus neurons to binaural tonal stimuli SO HEARING RESEARCH LA English DT Article DE Rat; aging; inferior colliculus; binaural; interaural intensity difference; inhibition ID AUDITORY BRAIN-STEM; SUPERIOR OLIVARY COMPLEX; CNS STRUCTURAL ELEMENTS; SOUND PRESSURE LEVEL; LATERAL LEMNISCUS; GABAERGIC NEURONS; DORSAL NUCLEUS; GUINEA-PIG; AMINO-ACIDS; GABA-IMMUNOREACTIVITY AB The inferior colliculus (IC) is one nucleus of the central auditory system which displays age-related changes. Inputs to the IC use primarily the amino acid neurotransmitters glutamate and gamma-aminobutryic acid (GABA). Neurochemical and anatomical studies of the Fischer 344 (F344) rat IC have shown decreases in GABA and GABA receptor levels (see Caspary et al., 1995 for review). GABA neurotransmission affects binaural response properties in the IC (Faingold et al., 1991a,b; Vater et al., 1992a; Park and Pollak, 1993, 1994). We hypothesized that aged F344 rats would show alterations in binaural IC neuronal response properties due to an imbalance in the relative levels of inhibition and excitation. Extracellular recordings from 189 single units localized to the IC of anesthetized aged (24 month) F344 rats were compared to those obtained from 221 IC units in young adult (3 month) animals. Quantitative analyses were performed to determine the distribution of ipsilateral and binaural rate/intensity functions (RIFs) in the central nucleus of the IC and external cortex of the IC units. The majority of IC units in both young and aged F344 rats were not responsive to monaural ipsilateral characteristic frequency tone bursts. Although there was some shift in the distribution of binaural RIF shapes with age, it was not statistically significant. The shift included a reduction in the percentage of units classified as E/I (excited by contralateral stimulation/ipsilaterally inhibited during binaural stimulation), but an increase with age in the percentage of units classified as E/f(excited by contralateral stimulation/further facilitated by the addition of low intensity ipsilateral stimulation, but inhibited by higher intensity ipsilateral stimulation). Despite the role of inhibitory neurotransmission in binaural processing in the IC, age-related neurochemical deficits in the IC do not appear to result in a major deficit in the processing of simple binaural stimuli in F344 rats. C1 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62702. 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PD OCT PY 1996 VL 100 IS 1-2 BP 59 EP 67 DI 10.1016/0378-5955(96)00113-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800007 PM 8922980 ER PT J AU McFadden, SL Walsh, EJ McGee, J AF McFadden, SL Walsh, EJ McGee, J TI Onset and development of auditory brainstem responses in the Mongolian gerbil (Meriones unguiculatus) SO HEARING RESEARCH LA English DT Article DE auditory evoked potential; threshold sensitivity; auditory development ID MIDDLE-EAR DEVELOPMENT; OUTER HAIR-CELLS; POSTNATAL-DEVELOPMENT; COCHLEAR FUNCTION; NEONATAL GERBIL; SENSITIVITY; POTENTIALS; ONTOGENY AB The ontogeny of auditory function in the Mongolian gerbil (Meriones unguiculatus) was examined by measuring auditory brainstem response (ABR) thresholds for clicks and tone bursts at frequencies between 0.125 and 32 kHz. ABRs were elicited as early as 10 postnatal days (PND) in a small proportion of animals (28.6%). Three phases of development were identified based on the appearance of frequency-threshold curves: (a) an onset period (10-12 PND) during which ABRs could be elicited only by intense stimuli (95-110 dB SPL) within a restricted range of frequencies (0.25-8 kHz); (b) a transition period (13-14 PND) during which thresholds improved but frequency-threshold curves remained relatively flat; and (c) a refinement period (15-30 PND) during which frequency-threshold curves exhibited an adult-like ('V') shape and thresholds improved steadily to adult-like values. Opening of the external auditory meatus was associated with threshold improvements but not with changes in the frequency region of greatest sensitivity. Between the ages of 13 and 21 PND, low-frequency (0.125-1 kHz) and high-frequency (10-32 kHz) thresholds improved at statistically equivalent rates (4.9 and 5.6 dB/day, respectively), while thresholds for mid-frequency stimuli (2-8 kHz) improved at a significantly faster rate of 9.2 dB/day. C1 BOYS TOWN NATL RES HOSP,DEV AUDITORY PHYSIOL LAB,OMAHA,NE 68131. CR COHEN YE, 1993, AM J OTOLARYNG, V14, P191, DOI 10.1016/0196-0709(93)90029-7 COHEN YE, 1992, HEARING RES, V62, P187, DOI 10.1016/0378-5955(92)90185-P EHRET G, 1981, J COMP PHYSIOL PSYCH, V95, P304, DOI 10.1037/h0077770 Ehret G, 1983, DEV AUDITORY VESTIBU, P211 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 HE DZZ, 1994, HEARING RES, V78, P77, DOI 10.1016/0378-5955(94)90046-9 JAVEL E, 1986, ADV NEURAL BEHAVIORA, V2, P119 MCGUIRT JP, 1995, HEARING RES, V84, P52, DOI 10.1016/0378-5955(95)00015-V MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 RYAN AF, 1982, EXP BRAIN RES, V47, P428 SAUNDERS JC, 1993, COMP BIOCHEM PHYS A, V106, P7, DOI 10.1016/0300-9629(93)90030-8 SMITH DI, 1987, HEARING RES, V27, P157, DOI 10.1016/0378-5955(87)90016-5 SZYMANSKI MD, 1994, AUDIOLOGY, V33, P63 WALSH EJ, 1986, J ACOUST SOC AM, V79, P712, DOI 10.1121/1.393461 Walsh Edward J., 1992, P161 WEAVER SP, 1994, HEARING RES, V72, P44, DOI 10.1016/0378-5955(94)90204-6 Willott J. F., 1991, AGING AUDITORY SYSTE 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 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 OCT PY 1996 VL 100 IS 1-2 BP 68 EP 79 DI 10.1016/0378-5955(96)00108-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800008 PM 8922981 ER PT J AU Spicer, SS Schulte, BA AF Spicer, SS Schulte, BA TI The fine structure of spiral ligament cells relates to ion return to the stria and varies with place-frequency SO HEARING RESEARCH LA English DT Article DE fibrocyte; outer sulcus cell; K+ transport; ultrastructure; cochlea; gerbil ID BETA-SUBUNIT ISOFORMS; AGE-RELATED-CHANGES; GUINEA-PIG COCHLEA; SUPPORTING CELLS; INNER-EAR; GERBIL COCHLEA; ALPHA-SUBUNIT; INTERCELLULAR-JUNCTIONS; CONNECTIVE-TISSUE; MONGOLIAN GERBIL AB Ultrastructural analysis of cells in the cochlea's lateral wall was undertaken to investigate morophologic features relevant to the route of K+ cycling from organ of Corti (OC) to stria vascularis (StV) and to the question of a transcellular versus an extracellular path. The fine structure of outer sulcus cells (OSCs) evidenced their capacity for uptake of K+ from Claudius cells and from perilymph in inferior spiral ligament. Plasmalemmal amplification and mitochondrial density together with known content of Na,K-ATPase testified to activity of type II, IV and V fibrocytes in resorbing K+. Location and fine structure afforded a basis for distinguishing subtypes among the type I, II and IV cells. The type II, IV and V fibrocytes can be viewed as drawing K+ from surrounding perilymph and from OSCs and generating an intracellular downhill diffusion gradient for K+ flow through gap junctions to subtype Ib and Ia fibrocytes and strial basal cells. Pumping action enabled by extreme structural specialization of type II fibrocytes is considered to mediate K+ translocation across the interruption between the gap junction connected epithelial and gap junction connected fibrocyte systems and to explain ion flow directed toward StV through OSCs and fibrocytes despite their lack of polarity. The OSC bodies shrank, their root bundles expanded and the gap junction contact between OSCs and Claudius cells increased toward the base of the cochlea. Expanding root bundles and type I and IIb fibrocyte populations contrasted with shrinking OHCs and Deiters and tectal cells from he apex to the base of the cochlea. These differences indicated an increased magnitude and alternate route of K+ transport toward the StV in high as compared to low-frequency regions. The augmented K+ transport through spiral ligament in basal cochlea correlates with and provides a possible basis for the larger endocochlear potential in the base. The findings appear consistent with current flow extracellularly through scalae tympani and vestibuli and transcellularly through OC, OSCs and class I, II, IV and V fibrocytes. RP Spicer, SS (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR DUVALL AJ, 1969, LARYNGOSCOPE, V79, P1, DOI 10.1288/00005537-196901000-00001 ENGSTROM H, 1958, INT REV CYTOL, V7, P535, DOI 10.1016/S0074-7696(08)62695-9 GALIC M, 1989, ACTA OTOLARYNGOL S, V461, P3 HENSON MM, 1984, HEARING RES, V16, P231, DOI 10.1016/0378-5955(84)90112-6 HENSON MM, 1988, HEARING RES, V35, P237, DOI 10.1016/0378-5955(88)90121-9 IURATO S, 1976, ACTA OTO-LARYNGOL, V82, P57, DOI 10.3109/00016487609120863 IURATO S, 1967, SUBMICROSCOPIC STRUC, P61 IURATO S, 1962, Z ZELLFORSCH MIK ANA, V56, P40, DOI 10.1007/BF00326848 IWATA N, 1925, FOLIA ANAT JPN, V3, P37 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 Kimura R.S., 1984, ULTRASTRUCTURAL ATLA, P101 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUCUK B, 1990, ARCH HISTOL CYTOL, V53, P297, DOI 10.1679/aohc.53.297 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MARCUS DC, 1984, AM J PHYSIOL, V247, pC240 MCGUIRT JP, 1994, J HISTOCHEM CYTOCHEM, V42, P843 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 NADOL JB, 1978, ANN OTO RHINOL LARYN, V87, P70 NAKAZAWA K, 1995, J HISTOCHEM CYTOCHEM, V43, P981 OESTERLE EC, 1990, J NEUROPHYSIOL, V64, P617 REALE E, 1975, J ULTRA MOL STRUCT R, V53, P284, DOI 10.1016/S0022-5320(75)80030-X SALT AN, 1987, LARYNGOSCOPE, V97, P984 SALT AN, 1986, NEUROBIOLOGY HEARING, P123 SANTI PA, 1988, PHYSL EAR, P173 SANTOS-SACCHI J, 1983, HEARING RES, V9, P317, DOI 10.1016/0378-5955(83)90034-5 SANTOS-SACCHI J, 1987, HEARING RES, V25, P227, DOI 10.1016/0378-5955(87)90094-3 SANTOS-SACCHI J, 1991, HEARING RES, V52, P89, DOI 10.1016/0378-5955(91)90190-K 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 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 SPICER SS, 1987, LAB INVEST, V57, P535 SPICER SS, 1994, HEARING RES, V79, P161, DOI 10.1016/0378-5955(94)90137-6 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z SPOENDLIN H, 1967, SUBMICROSCOPIC STRUC, P149 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1985, AUDIOLOGY BIOCH, P473 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 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 ZIDANIC M, 1994, BIOPHYS J, V57, P1253 NR 42 TC 209 Z9 222 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 1996 VL 100 IS 1-2 BP 80 EP 100 DI 10.1016/0378-5955(96)00106-2 PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800009 PM 8922982 ER PT J AU Dazert, S Feldman, ML Keithley, EM AF Dazert, S Feldman, ML Keithley, EM TI Cochlear spiral ganglion cell degeneration in wild-caught mice as a function of age SO HEARING RESEARCH LA English DT Article DE auditory; inner ear; presbyacusis; aging ID DIFFERING SPONTANEOUS RATE; AUDITORY-NERVE FIBERS; SPATIAL-ORGANIZATION; INFERIOR COLLICULUS; CENTRAL PROJECTIONS; GRADED SERIES; CBA/J MICE; MOUSE; NUCLEUS; NEURONS AB Presbyacusis in humans is an age-related bilateral sensorineural hearing impairment generally associated with degeneration of cochlear hair cells and spiral ganglion cells (SGC) predominantly in the basal turn but present in the apical turn. Investigations of cochleas of aged rats and gerbils reveal a large loss of SGCs in the apical as well as the basal turns. Genetically inbred aged mice, on the other hand, seem to have variable amounts of SGC loss beginning in some strains very early in the life span of the animals and greatest in the basal turn. Three age groups of wild-caught, then laboratory-bred, mice were investigated to determine the pattern of SGC degeneration. In 18-19-month-old animals the main loss of SGCs occurred in the basal turn (49% loss compared to 2-3 months) followed by the apical turn (31%). The greatest SGC losses in the 28-31-month-old animals were in both the apical (76%) and basal turns (74%). Thus, this strain of mice is similar to other rodents in that both ends of the ganglion are affected by SGC degeneration associated with aging. C1 UNIV CALIF SAN DIEGO, SCH MED, DIV OTOLARYNGOL, LA JOLLA, CA 92093 USA. VET AFFAIRS MED CTR, LA JOLLA, CA 92093 USA. 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F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 Working Group on Speech Understanding Committee on Hearing Bioacoustics and Biomechanics, 1988, J ACOUST SOC AM, V83, P859 NR 32 TC 22 Z9 22 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 OCT PY 1996 VL 100 IS 1-2 BP 101 EP 106 DI 10.1016/0378-5955(96)00100-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800010 PM 8922983 ER PT J AU Syka, J Rybalko, N Brozek, G Jilek, M AF Syka, J Rybalko, N Brozek, G Jilek, M TI Auditory frequency and intensity discrimination in pigmented rats SO HEARING RESEARCH LA English DT Article DE hooded rat; frequency discrimination; intensity discrimination ID MONKEYS; THRESHOLDS; HUMANS AB Auditory function was investigated in seven pigmented hooded rats (strain Long-Evans) with the aid of an operant conditioning procedure. Frequency difference limen was measured at frequencies from 0.5 to 64 kHz at 50 dB sensation level (SL). Weber ratios (frequency difference limen/frequency) in this range varied between 3.7 and 7.3%. The decline in the intensity of the stimulus from 50 to 10 dB SL was accompanied by a slight increase in the frequency difference limen. The frequency difference limen values were similar for frequency shifts upwards or downwards. Intensity discrimination was measured at 50 dB SL at frequencies of 2, 8 and 32 kHz. Intensity difference limen was frequency independent and amounted to 2.9+/-0.5 dB in conditions of upward intensity shift. The values of intensity difference limen measured in conditions of downward intensity shift were significantly larger and amounted to 6.5+/-1.6 dB. The characteristics of hearing function found in these experiments correspond with those described by other authors in albino rats and indicate that albinism in the rat has no significant influence on auditory frequency and intensity discrimination. C1 CHARLES UNIV,FAC MED 2,INST PHYSIOL,PRAGUE,CZECH REPUBLIC. RP Syka, J (reprint author), ACAD SCI CZECH REPUBL,INST EXPT MED,VIDENSKA 1083,CR-14220 PRAGUE 4,CZECH REPUBLIC. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 107 EP 113 DI 10.1016/0378-5955(96)00101-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800011 PM 8922984 ER PT J AU Vass, Z Brechtelsbauer, PB Nuttall, AL Miller, JM AF Vass, Z Brechtelsbauer, PB Nuttall, AL Miller, JM TI Nitric oxide mediates capsaicin-induced increase in cochlear blood flow SO HEARING RESEARCH LA English DT Article DE inner ear; sensory neuron; capsaicin; substance P; nitric oxide; laser Doppler flowmetry; guinea pig ID SUBSTANCE-P; GUINEA-PIG; INVOLVEMENT; RELAXATION; ARTERIES; NERVES AB Capsaicin has been previously shown to increase cochlear blood flow (CBF) in a dose-dependent manner. The aim of this study was to define the role of nitric oxide (NO) in capsaicin-induced changes in CBF. This was investigated in the anesthetized guinea pig, utilizing laser Doppler flowmetry. Application of capsaicin (64.8 and 6.48 nmol in 2 mu l of saline) to the round window membrane (RWM) caused increases in CBF (34+/-2.8% of baseline (BL) and 28+/-2.3% BL, respectively (P <0.001)). Application of the NO synthase inhibitor, N-G-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg intravenously or topically to the RWM) reduced blood flow in the cochlea, as previously reported. After pretreatment with i.v. L-NAME, the effect of capsaicin on CBF was significantly decreased. With the dose of capsaicin at 64.8 nmol, the increase in CBF fell from 34+/-2.8% BL to 6.9+/-1.5% BL (P <0.001), and at 6.48 nmol it fell from 28+/-2.3% BL to 4.8+/-1.6% BL (P <0.001). RWM L-NAME application also decreased the capsaicin vasodilatation effect. A capsaicin dose of 64.8 nmol resulted in only a 10+/-2.5% BL increasein CBF, and with 6.48 nmol capsaicin the increase was 7.8+/-2.2% of BL (P <0.001). Capsaicin-sensitive sensory neurons in other systems are generally known to release substance P (SP), which;in turn elicits release of endothelium derived relaxing factor (NO). The results of this study indicate that NO is a mediator of capsaicin-sensitive sensory neuronal function in CBF regulation. C1 OREGON HLTH SCI UNIV,OREGON HEARING RES CTR,PORTLAND,OR 97201. UNIV MICHIGAN,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. ALBERT SZENT GYORGYI MED UNIV,DEPT OTOLARYNGOL,H-6701 SZEGED,HUNGARY. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 114 EP 119 DI 10.1016/0378-5955(96)00102-5 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800012 PM 8922985 ER PT J AU Kitzes, LM Hollrigel, GS AF Kitzes, LM Hollrigel, GS TI Response properties of units in the posterior auditory field deprived of input from the ipsilateral primary auditory cortex SO HEARING RESEARCH LA English DT Article DE primary auditory field; posterior auditory field; parallel processing; intracortical pathway; nonmonotonicity ID MEDIAL GENICULATE-BODY; SOMATOSENSORY CORTICAL AREA; REVERSIBLE INACTIVATION; MOUSTACHED BAT; CEREBRAL-CORTEX; SINGLE NEURONS; CAT; 2ND; PROJECTIONS; MONKEY AB The influence of the ipsilateral primary auditory field (AI) on the response properties of neurons in the posterior auditory field (Field P) was examined in three cats anesthetized with sodium pentobarbital. Rate/level functions were obtained, by extracellular recording, from single units in Field P before (n=38) and after (n=50) subpial aspiration of AI. The ablations were primarily confined to the medial ectosylvian gyrus, although in one case extended into the high-frequency portion of the anterior auditory field. Comparisons between the behavior of units isolated before and after AI ablation failed to demonstrate any changes in the response properties of neurons in Field P attributable to the ablation. Nonmonotonic response profiles, first spike latency, variability in latency, threshold and maximal discharge rates of the units to acoustic stimuli were not significantly altered by the AI ablation. These results indicate that the basic response properties of neurons in Field P do not depend on input from the ipsilateral AI. This suggests that these properties are most likely determined by thalamic input or by circuitry within Field P. RP Kitzes, LM (reprint author), UNIV CALIF IRVINE,DEPT NEUROBIOL & ANAT,IRVINE,CA 92717, USA. CR BURTON H, 1987, SOMATOSENS MOT RES, V4, P215 BURTON H, 1988, BRAIN RES, V448, P397, DOI 10.1016/0006-8993(88)91285-1 BURTON H, 1990, J COMP NEUROL, V291, P395, DOI 10.1002/cne.902910307 Clarey J.C., 1992, MAMMALIAN AUDITORY P, P232 CODE RA, 1985, J COMP NEUROL, V242, P485, DOI 10.1002/cne.902420404 DREHER B, 1975, J NEUROPHYSIOL, V38, P735 EDAMATSU H, 1993, J NEUROPHYSIOL, V69, P1700 FITZPATRICK DC, 1993, J NEUROSCI, V13, P931 GARRAGHTY PE, 1990, SOMATOSENS MOT RES, V7, P125 GIRARD P, 1989, J NEUROPHYSIOL, V62, P1287 IMIG TJ, 1981, J COMP NEUROL, V203, P1, DOI 10.1002/cne.902030102 Imig TJ, 1986, 2 HEMISPHERES ONE BR, P103 KELLY JP, 1981, BRAIN RES, V212, P1, DOI 10.1016/0006-8993(81)90027-5 KITZES LM, 1994, J NEUROPHYSIOL, V71, P1740 MANZONI T, 1979, EXP BRAIN RES, V34, P453 MATSUBARA JA, 1988, J COMP NEUROL, V268, P38, DOI 10.1002/cne.902680105 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MOREL A, 1987, J COMP NEUROL, V265, P119, DOI 10.1002/cne.902650109 OJIMA H, CEREB CORTEX, V1, P80 OJIMA H, 1992, Cerebral Cortex, V2, P197, DOI 10.1093/cercor/2.3.197 PANDYA DN, 1993, EXP NEUROL, V119, P220, DOI 10.1006/exnr.1993.1024 PHILLIPS DP, 1995, J NEUROPHYSIOL, V73, P674 PHILLIPS DP, 1984, J NEUROPHYSIOL, V51, P1984 PHILLIPS DP, 1991, HEARING RES, V53, P17, DOI 10.1016/0378-5955(91)90210-Z PHILLIPS DP, 1981, J NEUROPHYSIOL, V45, P48 PHILLIPS DP, 1994, EXP BRAIN RES, V102, P210 PONS TP, 1987, SCIENCE, V237, P417, DOI 10.1126/science.3603028 PONS TP, 1988, P NATL ACAD SCI USA, V85, P5279, DOI 10.1073/pnas.85.14.5279 REALE RA, 1983, P NATL ACAD SCI-BIOL, V80, P5449, DOI 10.1073/pnas.80.17.5449 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 RODRIGUESDAGAEFF C, 1989, HEARING RES, V39, P103, DOI 10.1016/0378-5955(89)90085-3 ROUILLER E, 1983, HEARING RES, V11, P235, DOI 10.1016/0378-5955(83)90081-3 ROUILLER EM, 1990, HEARING RES, V49, P249, DOI 10.1016/0378-5955(90)90107-Z ROUILLER EM, 1991, EXP BRAIN RES, V86, P483 SANDELL JH, 1982, J NEUROPHYSIOL, V48, P38 SCHILLER PH, 1977, BRAIN RES, V126, P366, DOI 10.1016/0006-8993(77)90734-X SCHREINER CE, 1992, EXP BRAIN RES, V92, P105 SHERK H, 1978, J NEUROPHYSIOL, V41, P204 SUGA N, 1990, SCI AM, V262, P60 SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUGA N, 1990, J NEUROPHYSIOL, V64, P225 SUGA N, 1989, J EXP BIOL, V146, P277 TURMAN AB, 1992, J NEUROPHYSIOL, V67, P411 WALLACE MN, 1991, EXP BRAIN RES, V86, P527 NR 44 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1996 VL 100 IS 1-2 BP 120 EP 130 DI 10.1016/0378-5955(96)00103-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800013 PM 8922986 ER PT J AU SamsDodd, F Capranica, RR AF SamsDodd, F Capranica, RR TI Representation of acoustic signals in the eighth nerve of the Tokay gecko .2. Masking of pure tones with noise SO HEARING RESEARCH LA English DT Article DE critical band; critical ratio; noise masking; reptile; spectral encoding; temporal encoding ID AUDITORY-NERVE; BACKGROUND-NOISE; FIBERS; RESPONSES; THRESHOLDS; VOWELS; SYSTEM; CATS AB Acoustic signals are generally encoded in the peripheral auditory system of vertebrates by a duality scheme. For frequency components that fall within the excitatory tuning curve, individual eighth nerve fibers can encode the effective spectral energy by a spike-rate code, while simultaneously preserving the signal waveform periodicity of lower frequency components by phase-locked spike-train discharges. To explore how robust this duality of representation may be in the presence of noise, we recorded the responses of auditory fibers in the eighth nerve of the Tokay gecko to tonal stimuli when masking noise was added simultaneously. We found that their spike-rate functions reached plateau levels fairly rapidly in the presence of noise, so the ability to signal the presence of a tone by a concomitant change in firing rate was quickly lost. On the other hand, their synchronization functions maintained a high degree of phase-locked firings to the tone even in the presence of high-intensity masking noise, thus enabling a robust detection of the tonal signal. Critical ratios (CR) and critical bandwidths showed that in the frequency range where units are able to phaselock to the tonal periodicity, the CR bands were relatively narrow and the bandwidths were independent of noise level. However, to higher frequency tones where phaselocking fails and only spike-rate codes apply, the CR bands were much wider and depended upon noise level, so that their ability to filter tones out of a noisy background degraded with increasing noise levels. The greater robustness of phase-locked temporal encoding contrasted with spike-rate coding verifies a important advantage in using lower frequency signals for communication in noisy environments. C1 CORNELL UNIV,NEUROBIOL & BEHAV SECT,ITHACA,NY 14853. 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PD OCT PY 1996 VL 100 IS 1-2 BP 131 EP 142 DI 10.1016/0378-5955(96)00104-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800014 PM 8922987 ER PT J AU Erichsen, S Zuo, J Curtis, L Rarey, K Hultcrantz, M AF Erichsen, S Zuo, J Curtis, L Rarey, K Hultcrantz, M TI Na,K-ATPase alpha- and beta-isoforms in the developing cochlea of the mouse SO HEARING RESEARCH LA English DT Article DE immunohistochemistry; inner ear; mouse; embryology; Na,K-ATPase; homeostasis, fluid and electrolyte ID RAT COCHLEA; GLUCOCORTICOID RECEPTOR; STRIA VASCULARIS; ATPASE ACTIVITY; GUINEA-PIG; INNER-EAR; EXPRESSION; LOCALIZATION; WALL AB Immunohistochemistry was used to investigate the presence of Na,K-ATPase alpha- and beta-subunits isoforms (alpha(1), alpha(2), alpha(3), beta(1) and beta(2)) in the cochlea of the mouse at different ages between embryological day (E) 19 and postnatal day (P)+30. alpha(1) was mainly found in the stria vascularis and in the spiral ligament; it increased steadily from p+4. These data correlates well with the morphological and electrophysiological maturation of the cochlea. alpha(3) predominated in the spiral ganglia and the cochlear nerve. This finding is well in accordance with reports that alpha(3) seems to be associated with the nervous system. The beta-subunit was found mainly in those tissues where staining of the alpha-subunit also was seen. Both subunits were localized in tissue regions where fluid regulation is expected to play an important role. For some isoforms, the expression pattern of Na,K-ATPase during development in the mouse is different from that in the rat. The expression of Na,K-ATPase and that of glucocorticoid receptors during development in the inner ear of the mouse show a similar pattern, which may indicate that glucocorticoid receptors could be involved in regulating the expression of Na,K-ATPase. C1 KAROLINSKA HOSP,DEPT OTORHINOLARYNGOL,S-17176 STOCKHOLM,SWEDEN. UNIV FLORIDA,DEPT ANAT & CELL BIOL,GAINESVILLE,FL. UNIV FLORIDA,DEPT OTOLARYNGOL,GAINESVILLE,FL. CR ANNIKO M, 1993, DEV AUDITORY VESTIBU, P375 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 CURTIS LM, 1993, EUR ARCH OTO-RHINO-L, V250, P265 DECOLLOGNE S, 1993, J CARDIOVASC PHARM, V22, P96 ERICHSEN S, 1996, IN PRESS ACTA OTOLAR, P116 Hultcrantz M, 1985, Scand Audiol Suppl, V24, P1 KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 LIM DJ, 1985, ACTA OTOLARYNGOL STO, V422, P5 LINGREL JB, 1992, J BIOENERG BIOMEMBR, V24, P263 MIKAELIAN D, 1964, ACTA OTOLARYNGOL STO, V59, P451 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 ORLOWSKI J, 1988, J BIOL CHEM, V263, P1043 RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1993, HEARING RES, V64, P205, DOI 10.1016/0378-5955(93)90007-N RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 ROSE AM, 1994, CLIN CHEM, V40, P1674 SALT AN, 1987, LARYNGOSCOPE, V97, P984 TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 YAO XF, 1994, HEARING RES, V80, P31, DOI 10.1016/0378-5955(94)90006-X YOSHIHARA T, 1987, ARCH OTO-RHINO-LARYN, V243, P395, DOI 10.1007/BF00464650 ZUO J, 1995, ACTA OTO-LARYNGOL, V115, P497, DOI 10.3109/00016489509139355 ZUO J, 1995, HEARING RES, V87, P220, DOI 10.1016/0378-5955(95)00092-I NR 22 TC 29 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1996 VL 100 IS 1-2 BP 143 EP 149 DI 10.1016/0378-5955(96)00105-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800015 PM 8922988 ER PT J AU Cransac, H Peyrin, L CottetEmard, JM Farhat, F Pequignot, JM Reber, A AF Cransac, H Peyrin, L CottetEmard, JM Farhat, F Pequignot, JM Reber, A TI Aging effects on monoamines in rat medial vestibular and cochlear nuclei SO HEARING RESEARCH LA English DT Article DE aging; monoamine; rat; cochlear nucleus; medial vestibular nucleus; neurochemistry ID CNS STRUCTURAL ELEMENTS; AGE-RELATED-CHANGES; BRAIN-STEM; VESTIBULOOCULAR REFLEX; DOPAMINERGIC-NEURONS; LOCUS-CERULEUS; OCULAR REFLEX; AMINO-ACIDS; SEROTONIN; NEUROTRANSMITTERS AB Noradrenaline (NA), dopamine (DA), serotonin (5-HT) and their metabolites-3-methoxy, 4-hydroxyphenylglycol (MHPG), 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA)-were determined using HPLC in medial vestibular nucleus (MVN), anteroventral cochlear nucleus (AVCN), dorsal+posteroventral cochlear nucleus (DCN+PVCN), locus coeruleus (LC) and raphe dorsalis of Dark Agouti-Hanovre (DA-HAN) rats aged 4, 21 and 24 months. In older rats, the main noradrenergic changes were a decrease of NA content with an increase of the MHPG/NA ratio in MVN and a selective NA increase in AVCN. 5-HT and 5-HIAA levels were increased in all the brainstem nuclei except raphe dorsalis. DA and DOPAC remained unchanged. These data show that noradrenergic neurons in sensory nuclei are differently affected by aging whereas serotonergic activation occurs in most of them possibly as a compensatory response to dysfunction of sensory input and processing. The increase of NA stores in the AVCN of aged rats is in line with the elevated auditory brainstem threshold reported in old rats and could improve the signal-to-noise ratio. Noradrenergic neurons in the MVN seem to be more sensitive to age effect than cochlear nuclei; however, even if neuronal loss occurs, NA synthesis and/or metabolism increase to ensure normal or increased noradrenergic activity. C1 FAC MED GRANGE BLANCHE, PHYSIOL LAB, F-69373 LYON 08, FRANCE. UNIV ROUEN, FAC SCI, LAB NEUROSCI & ENVIRONM, F-76821 MONT ST AIGNAN, FRANCE. RP Cransac, H (reprint author), FAC MED GRANGE BLANCHE, URA CNRS 1447, 8 AVE ROCKEFELLER, F-69373 LYON 08, FRANCE. CR AGID Y, 1973, NATURE-NEW BIOL, V245, P150 AMENTA F, 1991, MECH AGEING DEV, V61, P249, DOI 10.1016/0047-6374(91)90059-9 BACKOFF PM, 1994, HEARING RES, V73, P163, DOI 10.1016/0378-5955(94)90231-3 BALOH RW, 1993, EXP BRAIN RES, V95, P509 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P563, DOI 10.1007/BF00964919 CASPARY DM, 1990, J NEUROSCI, V10, P2363 CRANSAC H, 1996, INT S AC SIGN PROC C CRANSAC H, 1995, HEARING RES, V90, P65, DOI 10.1016/0378-5955(95)00147-X Cransac H, 1996, J NEURAL TRANSM, V103, P391, DOI 10.1007/BF01276416 DEMAREST KT, 1980, NEUROENDOCRINOLOGY, V31, P222, DOI 10.1159/000123078 Edeline JM, 1995, EXP BRAIN RES, V107, P221 FOOTE SL, 1983, PHYSIOL REV, V63, P844 GALLAGHER JP, 1992, ANN NY ACAD SCI, V656, P630, DOI 10.1111/j.1749-6632.1992.tb25241.x GOLDMAN G, 1981, NEUROBIOL AGING, V2, P33, DOI 10.1016/0197-4580(81)90056-7 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 KELLER EL, 1983, BRAIN RES, V258, P323, DOI 10.1016/0006-8993(83)91159-9 KLEPPER A, 1991, BRAIN RES, V557, P190, DOI 10.1016/0006-8993(91)90134-H KOSSL M, 1989, J NEUROSCI, V9, P4169 KUBANIS P, 1981, BEHAV NEURAL BIOL, V31, P115, DOI 10.1016/S0163-1047(81)91195-X LANNOU J, 1982, PFLUG ARCH EUR J PHY, V393, P42, DOI 10.1007/BF00582389 LESLIE FM, 1985, BRAIN RES, V359, P292, DOI 10.1016/0006-8993(85)91439-8 MCELLIGOTT JG, 1988, EXP BRAIN RES, V69, P509 MIYASHITA Y, 1984, NEUROSCI LETT, V51, P177, DOI 10.1016/0304-3940(84)90547-0 MONJI A, 1994, BRAIN RES, V641, P171, DOI 10.1016/0006-8993(94)91834-1 OOSTEVELD WF, 1983, HEARING BALANCE ELDE, P354 Paige G D, 1992, J Vestib Res, V2, P133 PICKLES JO, 1976, BRAIN RES, V105, P591, DOI 10.1016/0006-8993(76)90610-7 POMPEIANO O, 1994, PROG BRAIN RES, V100, P105 POMPEIANO O, 1991, PROG BRAIN RES, V88, P411 PRADHAN SN, 1980, LIFE SCI, V26, P1643, DOI 10.1016/0024-3205(80)90172-1 RAZA A, 1994, HEARING RES, V77, P221, DOI 10.1016/0378-5955(94)90270-4 REBER A, 1995, P 15 EUR WIN C BRAIN Schuknecht H., 1974, PATHOLOGY EAR, P388 SIMPKINS JW, 1977, ENDOCRINOLOGY, V100, P1672 STEINBUSCH HWM, 1991, ACTA OTO-LARYNGOL, P12 TERNAUX JP, 1987, PFLUG ARCH EUR J PHY, V409, P507, DOI 10.1007/BF00583808 VIBERT N, 1994, P 17 EUR NEUR ASS C, P123 WEISS B, 1984, HDB NEUROCHEMISTRY, V6, P595 Willott J. F., 1991, AGING AUDITORY SYSTE NR 41 TC 23 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 OCT PY 1996 VL 100 IS 1-2 BP 150 EP 156 DI 10.1016/0378-5955(96)00116-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800016 PM 8922989 ER PT J AU Harrison, RV Kakigi, A Hirakawa, H Harel, N Mount, RJ AF Harrison, RV Kakigi, A Hirakawa, H Harel, N Mount, RJ TI Tonotopic mapping in auditory cortex of the chinchilla SO HEARING RESEARCH LA English DT Article DE auditory perception; auditory pathway; brain mapping; cochleotopic organization; electrophysiology ID FERRET MUSTELA-PUTORIUS; FREQUENCY REPRESENTATION; ORGANIZATION; COCHLEA; MONKEY; FIELDS; CAT AB Using single-unit electrophysiological methods we have mapped sound frequency (or cochleotopic) representation in the auditory cortex of the chinchilla. We describe the surgical approach to expose this area. We report on maps from six subjects and note a considerable variation in shape between individuals. In general, the primary area has a cochleotopic/tonotopic organization in which low frequencies are represented rostrally and higher frequencies caudally. Neurons in the primary area have latency and tuning properties comparable to other mammalian species. A region anterior to the primary (AI) auditory area has a reverse tonotopic map and may be analogous to the anterior auditory field (AAF) reported in other species. RP Harrison, RV (reprint author), HOSP SICK CHILDREN,DEPT OTOLARYNGOL,AUDITORY SCI LAB,555 UNIV AVE,TORONTO,ON M5G 1X8,CANADA. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 157 EP 163 DI 10.1016/0378-5955(96)00120-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800017 PM 8922990 ER PT J AU Pantev, C Elbert, T Ross, B Eulitz, C Terhardt, E AF Pantev, C Elbert, T Ross, B Eulitz, C Terhardt, E TI Binaural fusion and the representation of virtual pitch in the human auditory cortex SO HEARING RESEARCH LA English DT Article DE hearing; pitch perception; binaural fusion; magnetoencephalography; auditory evoked magnetic field; human auditory cortex ID TONOTOPIC ORGANIZATION; COMPLEX TONES; MAGNETIC-FIELDS; ORIGIN; BRAIN AB The auditory system derives the pitch of complex tones from the tone's harmonics. Research in psychoacoustics predicted that binaural fusion was an important feature of pitch processing. Based on neuromagnetic human data, the first neurophysiological confirmation of binaural fusion in hearing is presented. The centre of activation within the cortical tonotopic map corresponds to the location of the perceived pitch and not to the locations that are activated when the single frequency constituents are presented. This is also true when the different harmonics of a complex tone are presented dichotically. We conclude that the pitch processor includes binaural fusion to determine the particular pitch location which is activated in the auditory cortex. C1 UNIV KONSTANZ,D-78434 CONSTANCE,GERMANY. TECH UNIV MUNICH,D-80290 MUNICH,GERMANY. RP Pantev, C (reprint author), UNIV MUNSTER,INST EXPT AUDIOL,CTR BIOMAGNETISM,KARDINAL GALEN RING 10,D-48129 MUNSTER,GERMANY. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 164 EP 170 DI 10.1016/0378-5955(96)00124-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800018 PM 8922991 ER PT J AU Wiegrebe, L Kossl, M Schmidt, S AF Wiegrebe, L Kossl, M Schmidt, S TI Auditory enhancement at the absolute threshold of hearing and its relationship to the Zwicker tone SO HEARING RESEARCH LA English DT Article DE threshold improvement; auditory enhancement; Zwicker tone; negative afterimages; temporary threshold shift ID POSTEXPOSURE RESPONSIVENESS; PREPROCESSING MODEL; ACTIVE FEEDBACK; SUPPRESSION; MASKING; SENSITIZATION; EMISSIONS; RESPONSES; STIMULI; SYSTEM AB Auditory enhancement describes an improvement in the detection of a tonal signal in a broad-band masker with a spectral gap at the signal frequency if the signal is delayed in its onset relative to the masker. This auditory enhancement may be based on an increase of the effective signal level instead of a decline in the effective masker level. In order to evaluate whether this signal enhancement also exists at the threshold of hearing, we measured the absolute threshold for pure-tone pulses of different frequencies with and without preceding band-rejected noise. Such noise also causes the sensation of the Zwicker tone-a faint pure tone lasting for a few seconds immediately after the noise presentation. The pitch of this sensation is a complex function of the noise parameters but always lies at a frequency within the rejected band. During the Zwicker tone sensation, auditory sensitivity for tone pulses at frequencies adjacent to the Zwicker tone was improved by up to 13 dB instead of being reduced which might be expected due to the presence of the simultaneously audible Zwicker tone. The failure to influence this threshold shift with low-frequency tones and measurements of the ear's acoustical response indicate that this threshold improvement may be produced through neuronal disinhibition rather than through a release from mechanical suppression in the cochlea. RP Wiegrebe, L (reprint author), UNIV MUNICH,INST ZOOL,LUISENSTR 14,D-80333 MUNICH,GERMANY. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 171 EP 180 DI 10.1016/0378-5955(96)00111-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800019 PM 8922992 ER PT J AU NicolasPuel, C Durrieu, JP Lenoir, M Huy, PTB Uziel, A Puel, JL AF NicolasPuel, C Durrieu, JP Lenoir, M Huy, PTB Uziel, A Puel, JL TI Electrical stimulation activates two different sites within the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE electrically evoked auditory brainstem response (EABR); cochlear implant; tetrodotoxin (TTX); strychnine; ototoxicity; hair cell; ganglion neuron ID BRAIN-STEM RESPONSE; OUTER HAIR-CELLS; NERVE ACTION-POTENTIALS; AUDITORY-NERVE; PHYSIOLOGICAL-PROPERTIES; ROUND WINDOW; RECORDINGS AB This study investigates whether auditory brainstem responses (ABRs) can be used to assess the functioning of electrically stimulated cochleas. Electrically evoked auditory brainstem responses (EABRs) were recorded in guinea pigs with normal hearing and guinea pigs deafened by amikacin, a powerful ototoxic antibiotic, combined with diuretic aminooxyacetic acid (AOAA). Two different types of EABRs were observed in normal animals, depending on the electrical pulse intensity applied to the round window: long-latency brainstem responses were evoked by low stimulation intensities, short-latency brainstem responses by high intensities. The absence of effect of strychnine applied intracochlearly ruled out the possibility of medial efferents being involved in these responses. Conversely, an intracochlear application of tetrodotoxin (TTX), an Na+-channel blocker, resulted in the disappearance of both types of responses, attesting that the sites activated by the electrical stimulation were located within the cochlea. In AOAA/amikacin poisoned cochleas, in which most of the hair cells were missing with apparently normal ganglion neurons, the long-latency brainstem responses evoked by low intensities were completely lacking. These findings suggest that low currents applied to the round window of the guinea pig cochlea primarily activate the hair cells, the neurons being directly excited at higher intensities. C1 UNIV MONTPELLIER,INSERM U254,LAB NEUROBIOL AUDIT PLAST SYNAPT,CHR ST CHARLES,F-34295 MONTPELLIER 5,FRANCE. CHU LARIBOISIERE,LAB OTOL EXPT,F-75010 PARIS,FRANCE. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 181 EP 191 DI 10.1016/0378-5955(96)00112-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800020 PM 8922993 ER PT J AU Li, L Frost, BJ AF Li, L Frost, BJ TI Azimuthal sensitivity of rat pinna reflex. EMG recordings from cervicoauricular muscles SO HEARING RESEARCH LA English DT Article DE sound localization; acoustic startle response; pinna reflex; cervicoauricular muscle; electromyogram; decerebrate rat ID PEDUNCULOPONTINE TEGMENTAL NUCLEUS; SOUND PRESSURE TRANSFORMATION; ACOUSTIC STARTLE RESPONSE; OWLS INFERIOR COLLICULUS; BRAIN-STEM PROJECTIONS; RETICULAR-FORMATION; FACIAL NUCLEUS; HORSERADISH-PEROXIDASE; INTERAURAL TIME; INTENSITY DIFFERENCES AB Electromyographic (EMG) responses of the cervicoauricular muscles (CAM) to free-field sounds were recorded in two groups of rats whose brainstems were dissected transversely either at a pretectal or transtectal level. After the rat recovered from anesthesia, wide-band noise pulses were presented and speaker positions were varied systematically in azimuth. Sound levels were set at 10-15 dB above empirically determined threshold for an EMG response to a sound from 0 degrees azimuth. In both animal groups, transient CAM EMGs with short latency were produced and three main types of azimuthal sensitivity of CAM EMG response were observed. (1) For the majority of the cases, an inverted 'U' type of azimuthal sensitivity was identified: the maximum activity occurred around 0 degrees azimuth, but as the speaker was moved toward either the ipsilateral or contralateral fields, the sound-evoked activity declined systematically. This directional tuning is quite different from the passive pinna directionality which is very lateral in the resting positions used in this study. (2) In a small number of cases, the spatial sensitivity curves were not symmetrical about the midline (0 degrees azimuth): the EMG response was vigorous in one hemifield and dropped off systematically as the speaker was moved toward extreme positions of the other hemifield. Regardless of shapes of EMG spatial tuning curves, obstruction of either the ipsilateral or contralateral meatus reduced the sound-elicited response dramatically and eliminated the spatial sensitivity. (3) Some cases exhibited an omnidirectional function: the EMG spike rate had no or minor systematical variation as the speaker position was changed in azimuth. The results of this study indicate that with either pretectal or transtectal decerebrate preparations, the acoustically evoked CAM EMG can exhibit an azimuthal sensitivity which is based on binaural processing. C1 QUEENS UNIV,DEPT PSYCHOL,VISUAL & AUDITORY NEUROSCI LAB,KINGSTON,ON K7L 3N6,CANADA. 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Res. PD OCT PY 1996 VL 100 IS 1-2 BP 192 EP 200 DI 10.1016/0378-5955(96)00119-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800021 PM 8922994 ER PT J AU Wangemann, P Shen, ZJ Liu, JZ AF Wangemann, P Shen, ZJ Liu, JZ TI K+-induced stimulation of K+ secretion involves activation of the I-sK channel in vestibular dark cells SO HEARING RESEARCH LA English DT Article DE inner ear; vestibular labyrinth; potassium secretion; I-sK channel ID ION-TRANSPORT MECHANISMS; TRANSEPITHELIAL VOLTAGE; POTASSIUM SECRETION; MARGINAL CELLS; GUINEA-PIG; INNER-EAR; CL; CONDUCTANCE; EPITHELIUM; PERILYMPH AB Vestibular dark cells in the inner ear secrete K+ from perilymph containing 4 mM K+ to endolymph containing 145 mM K+. Sensory transduction causes K+ to flow from endolymph to perilymph, thus threatening the homeostasis of the perilymphatic K+ concentration which is crucial for maintaining sensory transduction since the basolateral membranes of the sensory cells and adjacent neuronal elements need to be protected from K+-induced depolarization. The present study addresses the questions (1) whether increases in the perilymphatic K+ concentration by as little as 1 mM are sufficient to stimulate KCl uptake across the basolateral membrane of vestibular dark cells, (2) whether K+-induced stimulation of KCl uptake causes stimulation of the I-sK channel in the apical membrane, and (3) whether the rate of transepithelial K+ secretion depends on the perilymphatic (basolateral) K+ concentration when the apical side of the epithelium is bathed with a solution containing 145 mM K+, as in vivo. Uptake of KCl was monitored by measuring cell height as an indicator for cell volume. The current (I-IsK), conductance (g(IsK)) and inactivation time constant (tau(IsK)) of the I-sK channel as well as the apparent reversal potential of the apical membrane (V-r) were obtained with the cell-attached macro-patch technique. V-r was corrected for the membrane voltage previously measured with microelectrodes. The rate of transepithelial K+ secretion J(K) was obtained as equivalent short circuit current from measurements of the transepithelial voltage (V-t) and resistance (R(t)) measured in the micro-Ussing chamber. Cell height of vestibular dark cells was 7.2 mu M (average). Elevations of the extracellular K+ concentration from 3.5 to 4.5 mM caused cell swelling with an initial rate of cell height change of 11 mm/s. With 3.6 mM K+ in the pipette I-IsK was outwardly directed and elevation of the extracellular K+ concentration from 3.6 to 25 mM caused an increase of I-IsK from 12 to 65 pA, g(IsK) from 152 to 950 pS and tau(IsK) from 278 to 583 ms as well as a hyperpolarization of V-r from -50 to -60 mV. With 150 mM K+ in the pipette I-IsK was inwardly directed and the elevation of the extracellular K+ concentration caused an increase of I-IsK from -1 to -143 pA, g(IsK) from 141 to 1833 pS and tau(IsK) from 248 to 729 ms. V-r remained within+/-10 mV from zero. J(K) was 4.8 nmolxcm(-2)xs(-1) when the both the apical side and the basolateral side of the epithelium were perfused with a solution containing 3.5 mM K+. Elevation of the basolateral K+ concentration by 1 mM caused J(K) to increase by 1.1 nmolxcm(-2)xs(-1) or 23%. When the basolateral side of the epithelium was perfused with a solution containing 3.5 mM K+ and the apical side with a solution containing 145 mM K+, as in vivo, J(K) was 0.8 nmolxcm(-2)xs(-1) and elevation of the basolateral K+ concentration by 1 mM caused J(K) to increase by 0.8 nmolxcm(-2)xs(-1) or 100%. These data suggest that physiologically relevant increases in the perilymphatic K+ concentration increase J(K) by increasing KCl uptake across the basolateral membrane and activation of K+ release via the I-sK channel in the apical membrane. Thus, the data demonstrate that vestibular dark cells adjust the rate of K+ secretion into endolymph according to the perilymphatic K+ concentration. RP Wangemann, P (reprint author), BOYS TOWN NATL RES HOSP, CELL PHYSIOL LAB, 555 N 30TH ST, OMAHA, NE 68131 USA. 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PD OCT PY 1996 VL 100 IS 1-2 BP 201 EP 210 DI 10.1016/0378-5955(96)00127-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VX208 UT WOS:A1996VX20800022 PM 8922995 ER PT J AU Dais, CGD Prazma, J Ball, SS Zdanski, C Carrasco, V Pillsbury, HC AF Dais, CGD Prazma, J Ball, SS Zdanski, C Carrasco, V Pillsbury, HC TI Effect of sodium nitroprusside on compound action potential thresholds in the gerbil cochlea SO HEARING RESEARCH LA English DT Article DE nitric oxide; cochlea; hearing threshold; methylene blue; cyclic GMP; sodium nitroprusside ID NITRIC-OXIDE SYNTHASE; METHYLENE-BLUE; CYCLIC-GMP; VASODILATOR RESPONSES; GLUTAMATE RECEPTORS; SELECTIVE BLOCKADE; HIPPOCAMPAL SLICES; BLOOD-FLOW; INVIVO; SUPEROXIDE AB The presence of active nitric oxide synthase (NOS) in the spiral ganglion cells of the cochlea suggests that the neuromodulator nitric oxide (NO) may play a role in hearing. This study investigated the effects of sodium nitroprusside (SNP), an NO donor, upon cochlear function mediated through its activation of guanylate cyclase. In gerbils, cochlear compound action potential (CAP) thresholds were recorded after cochlear perfusions of control and test solutions in four experimental groups. Perfusions were performed using the following: artificial perilymph solution (APS); the NO donor SNP; the guanylate cyclase inhibitor methylene blue (MB); and sodium dodecyl sulfate (SDS), which facilitates MB entrance into cells. SNP caused significant elevations of CAP thresholds from baseline (25 dB SPL +/- 1.54 dB to 64.3 dB SPL +/- 2.54 dB). SNP with MB also resulted in significant CAP threshold elevations (29.4 dB SPL +/- 4.27 dB to 38.1 dB SPL +/- 4.0 dB); however, these elevations were significantly lower than those seen in SNP perfusions without MB. Drilling perfusion holes and perfusion of APS, APS/SDS, and MB/SDS/APS solutions did not significantly affect CAP thresholds. These results suggest that the NO donor nitroprusside does affect cochlear neuromodulation and effects this mediation in part through NO activation of guanylate cyclase. C1 UNIV N CAROLINA,SCH MED,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27599. OHIO STATE UNIV,COLL MED,COLUMBUS,OH 43210. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 1 EP 6 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800001 PM 8970807 ER PT J AU Magovcevic, I Berson, EL Morton, CC AF Magovcevic, I Berson, EL Morton, CC TI Detection of cone alpha transducin mRNA in human fetal cochlea: Negative mutation analysis in Usher syndrome SO HEARING RESEARCH LA English DT Article DE cone transducin alpha subunit; Usher syndrome, types I and II; cochlea; retina; retinitis pigmentosa; single-strand conformation polymorphism ID SYNDROME TYPE-I; RETINITIS-PIGMENTOSA; GENETIC-HETEROGENEITY; GEL-ELECTROPHORESIS; BINDING-PROTEIN; CYCLIC-GMP; LOCALIZATION; DNA; CHROMOSOME-1Q; CASCADE AB Cone alpha transducin (GNAT2), known to be expressed in photoreceptors, was found to be transcribed in human fetal cochlea. Due to the unexpected finding of expression of this gene in the inner ear and the success of the candidate gene approach in identifying mutations for a variety of heritable disorders, we investigated the possible role of this gene in Usher syndrome type I and type II. Single-strand conformation polymorphism (SSCP) was used to screen the GNAT2 coding region, as well as splice donor and acceptor sites, for mutations in a total of 140 unrelated patients. Two nucleotide changes leading to two silent amino acid changes and one rare polymorphism were found. In view of these results and those of a previously published Southern blot analysis, it is unlikely that mutations in GNAT2 are a common gene abnormality in Usher syndrome type I or type II. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. 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In the left/right localization tests, removal of both pinnae had no effect on localization acuity for broadband noise but did result in a small decrement in performance when localizing low-pass filtered noise. In the front/back localization tests, removal of a single pinna resulted in a small but consistent decrement in performance when the sound sources were located in the hemifield on the same side as the intact pinna, and a greater decrement when the sound sources were located in the hemifield on the side of the missing pinna; removal of both pinnae resulted in the largest decrement in performance. Finally, vertical localization acuity and performance when localizing low-pass filtered noise were greatly impaired following removal of both pinnae. These results demonstrate the importance of the pinnae in performing front/back and vertical localization tasks in which binaural cues are not available. RP Heffner, RS (reprint author), UNIV TOLEDO,DEPT PSYCHOL,TOLEDO,OH 43606, USA. 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PD SEP 15 PY 1996 VL 99 IS 1-2 BP 13 EP 21 DI 10.1016/S0378-5955(96)00074-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800003 PM 8970809 ER PT J AU Kong, WJ Ren, TY Nuttall, AL AF Kong, WJ Ren, TY Nuttall, AL TI Electrophysiological and morphological evaluation of the acute ototoxicity of sodium nitroprusside SO HEARING RESEARCH LA English DT Article; Proceedings Paper CT 18th Midwinter Research Meeting of the Association-for-Research-in-Otolaryngology CY FEB 05-09, 1995 CL ST PETERSBURG BEACH, FL SP Assoc Res Otolaryngol DE cochlea; nitric oxide; compound action potential; cochlear microphonics; endocochlear potential; cochlear microphonic quadratic difference tone; histopathology ID NITRIC-OXIDE SYNTHASE; GUINEA-PIG COCHLEA; SIGNAL TRANSDUCTION MECHANISM; HAIR CELL RESPONSES; GUANYLATE-CYCLASE; NERVOUS-SYSTEM; INHIBITION; GLUTAMATE; NEUROTOXICITY; ENHANCEMENT AB Nitric oxide (NO) is a messenger molecule that mediates several physiological functions and pathological processes. Sodium nitroprusside (SNP), a potent vasodilator, when given clinically as an anti-hypertension agent, exerts its function by releasing NO. It was reported recently that SNP causes a loss of auditory nerve compound action potential (CAP) after topical application of SNP on guinea pig round window membrane (RWM). The current study was designed to investigate the ototoxic target of SNP through both electrophysiological acid morphological approaches. The CAP threshold at frequencies ranging from 2 to 36 kHz, the cochlear microphonic quadratic distortion product (cmQDP, F2-F1, where F1 = 17.1 kHz; F2 = 18 kHz), and the cochlear microphonic (CM) at the frequency of F1 were recorded via a round window electrode before and up to 2 h after RWM application of 1 mu l of drug solution. Cochlear blood flow (CBF) and arterial blood pressure were monitored, The cochleae were then processed for morphological examination. The effect of SNP on endocochlear potential (EP) was also studied. Results showed that cmQDP, CM, and CAP, as well as EP, were suppressed in varying amounts, while CBF was substantially increased following drug application. Morphological evaluations showed swelling of the afferent inner radial dendrites within the basal cochlear turn in the higher concentration groups of SNP, while the hair cells presented no evidence of damage at the light microscopic level. The results indicate that SNP has an acute ototoxic effect in a concentration- and time-dependent manner. The targets of SNP ototoxicity are at least the afferent dendrites and stria vascularis. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. TONGJI MED UNIV,DEPT OTOLARYNGOL,WUHAN 430022,PEOPLES R CHINA. OREGON HLTH SCI UNIV,OREGON HEARING RES CTR,PORTLAND,OR 97201. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 22 EP 30 DI 10.1016/S0378-5955(96)00076-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800004 PM 8970810 ER PT J AU Vlajkovic, SM Thorne, PR Munoz, DJB Housley, GD AF Vlajkovic, SM Thorne, PR Munoz, DJB Housley, GD TI Ectonucleotidase activity in the perilymphatic compartment of the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE ectonucleotidase; ecto-ATPase; cochlea; adenosine 5'-triphosphate; purinoceptor ID OUTER HAIR-CELLS; ADENOSINE-TRIPHOSPHATASE-ACTIVITY; ECTO-ATPASE; EXTRACELLULAR ATP; 5'-TRIPHOSPHATE ATP; PHYSIOLOGICAL-ROLE; RAT; RECEPTOR; NUCLEOTIDES; RESPONSES AB It has been clearly demonstrated that extracellular adenosine 5'-triphosphate (ATP) exerts a potent modulatory activity in the cochlea through its interaction with P-2 purinoceptors. However, little is known regarding the metabolism of extracellular ATP in cochlear tissues via ectonucleotidases. This study provides evidence for the presence of ectonucleotidases in the perilymphatic compartment of the guinea pig cochlea. Using microperfusion, ATP (500 mu M) was introduced into the cochlear perilymph through the basal turn scala tympani, and effluent was collected from the basal turn scala vestibuli. Samples were subsequently analysed for the presence of adenine metabolites using high performance liquid chromatography (HPLC). Cell viability was evaluated by the activity of the intracellular enzyme lactate dehydrogenase (LDH) in the perfusate. ATP was degraded to 122.8 +/- 9.9 mu M (25.0 +/- 5.8%) during the passage through the cochlear perilymphatic compartment. Breakdown of ATP resulted in the formation of adenosine 5'-diphosphate (41.5 +/- 9.0 mu M), adenosine 5'-monophosphate (201.3 +/- 15.5 mu M), adenosine (108.6 +/- 8.3) and inosine (15.0 +/- 1.5 mu M). The degradation of ATP was significantly (P < 0.001, Student's t-test) inhibited in the absence of divalent cations, Ca2+ and Mg2+ in the perfusate. In control experiments, no spontaneous degradation of ATP was observed in vitro. LDH activity was similar during ATP perfusions (2.9 +/- 0.9%) to control perfusions with artificial perilymph (4.2 +/- 1.0%) indicating well preserved cell integrity in the cochlear perilymphatic compartment. The degradation of extracellular ATP in the presence of intact tissues and its inhibition in the absence of divalent cations, a cofactor for ectonucleotidases, provides evidence for ectonucleotidase activity in the perilymphatic fluid space of the cochlea. C1 UNIV AUCKLAND, DEPT PHYSIOL, AUCKLAND, NEW ZEALAND. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 31 EP 37 DI 10.1016/S0378-5955(96)00079-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800005 PM 8970811 ER PT J AU Mitchell, C Kempton, JB Creedon, T Trune, D AF Mitchell, C Kempton, JB Creedon, T Trune, D TI Rapid acquisition of auditory brainstem responses with multiple frequency and intensity tone-bursts SO HEARING RESEARCH LA English DT Article DE multiple stimulus; auditory brainstem response; tone-burst; threshold; latency; amplitude ID MAXIMUM LENGTH SEQUENCES; STEM-EVOKED-RESPONSES; STIMULI AB Auditory brainstem response (ABR) thresholds, latency and amplitude functions were obtained in mice using stimuli presented singly and as a multiple stimulus sequence. All stimuli were tone-bursts at frequencies from 4 to 32 kHz, The multiple stimulus consisted of a sequence of 20 tone-bursts of four different frequencies at five intensities separated by 12 ms. A comparison of responses to stimuli presented singly and those obtained with the 20-stimulus train showed no significant difference in thresholds. Also, no differences were found in response latencies or amplitudes, indicating that the responses from multiple stimuli were not adapted or otherwise affected. The use of this 20-stimulus train can result in a significant time savings for data acquisition compared with single stimuli. These findings demonstrate the feasibility of the rapid acquisition of unadapted cochlear and brainstem responses at different frequencies using a sequence of tone-bursts at different frequencies and intensities. RP Mitchell, C (reprint author), OREGON HLTH SCI UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,OREGON HEARING RES CTR,PORTLAND,OR 97201, USA. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 38 EP 46 DI 10.1016/S0378-5955(96)00081-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800006 PM 8970812 ER PT J AU Gratton, MA Schulte, BA HazenMartin, DJ AF Gratton, MA Schulte, BA HazenMartin, DJ TI Characterization and development of an inner ear type I fibrocyte cell culture SO HEARING RESEARCH LA English DT Article DE spiral ligament; cochlea; gerbil; lateral wall; morphology; ultrastructure; immunocytochemistry ID STRIAL MARGINAL CELLS; AUDITORY-NERVE FIBERS; GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; IMMUNOHISTOCHEMICAL LOCALIZATION; SPIRAL LIGAMENT; GERBIL; VASCULARIS; FUROSEMIDE; FIBROBLASTS AB A method has been developed that allows successful maintenance of secondary cell cultures derived from explants of the cochlear lateral wall of young adult gerbils. The secondary cultures were characterized morphologically with light and transmission electron microscopy and immunocytochemically with protein markers specific to various lateral wall cell types. Structural studies revealed fusiform-shaped cells with a paucity of cytoplasm surrounding the nucleus and slender processes. The cells showed little evidence of intercellular contact even when confluent. The cultures were immunopositive for vimentin, carbonic anhydrase isozyme II, creatine kinase isozyme BB and smooth endoplasmic reticulum Ca-ATPase, but lacked reactivity for cytokeratins and Na,K-ATPase. The results indicate that the cultures are comprised of type I fibrocytes from the spiral ligament. These findings are the first to demonstrate that inner ear spiral ligament cells can be isolated and maintained in secondary culture while retaining many of their in vivo characteristics. Based upon their location and content of ion transport enzymes, type I fibrocytes are thought to be involved in the recycling of potassium from perilymph into the stria vascularis. The establishment of this cell line provides a means to analyze the role of spiral ligament fibrocytes in maintenance of inner ear homeostasis. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP Gratton, MA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUNICAT SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 71 EP 78 DI 10.1016/S0378-5955(96)00080-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800008 PM 8970814 ER PT J AU Mandava, P Rupert, AL Moushegian, G AF Mandava, P Rupert, AL Moushegian, G TI Inferior colliculus neuronal responses to masking-level-difference stimuli SO HEARING RESEARCH LA English DT Article DE binaural masking-level difference; inferior colliculus neuron ID SUPERIOR OLIVARY NEURONS; BINAURAL MASKING; BACKWARD MASKING; INTERAURAL PHASE; CAT AB Seventy-one inferior colliculus neurons, with best frequencies below 1.5 kHz, were studied in a binaural, forward-masking paradigm in chinchilla. Masker and signal frequencies were presented at neuronal best frequency. Masker level was set 10-15 dB above neuronal threshold and varied to include a range of signal-to-masker ratios and overall intensities. Without the masker, 33 of the neurons preferred an in-phase signal (SO), 29 an out-of-phase (S pi) signal, and the remaining 9 had 'no-preference' (NP), responding equally well to SO and Sn. Complete protocols from 53 of the 71 neurons were obtained with and without maskers over a range of levels. With an in-phase masker (NO), some neurons responded better to dichotic (NOS rr) than to diotic (NOSO) sounds. Generally, they maintained a particular phase preference with and without masker. Some neurons, however, altered phase preference and responsivity when binaural maskers were added to signal. Signal-to-noise ratios between 0 and 30 dB were sufficient to differentiate neuronal responsiveness to NOSO and NOS pi. The results suggest that identical neural mechanisms are not involved in processing unmasked (SO or S pi) and masked binaural sounds (NOSO, NOS pi). Furthermore, changes in neuronal sensitivity favor the NOS pi condition upon addition of noise (NO) to the signal (SO or S pi). We conclude that greater neural activity is generated with stimuli which produce masking-level difference than stimuli that do not. C1 UNIV TEXAS,CALLIER CTR COMMUN DISORDERS,DALLAS,TX 75235. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 79 EP 84 DI 10.1016/S0378-5955(96)00085-8 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800009 PM 8970815 ER PT J AU Henley, CM Weatherly, RA Ou, CN Brown, RD AF Henley, CM Weatherly, RA Ou, CN Brown, RD TI Pharmacokinetics of kanamycin in the developing rat SO HEARING RESEARCH LA English DT Article DE kanamycin; pharmacokinetics; developing rat; ototoxicity ID ACOUSTIC DISTORTION PRODUCTS; 2F1-F2 OTOACOUSTIC EMISSIONS; POSTNATAL-DEVELOPMENT; AUDITORY FUNCTION; OTOTOXICITY; GENTAMICIN; NEPHROTOXICITY; AMIKACIN; MICE; TOBRAMYCIN AB The developing rat is hypersensitive to aminoglycoside ototoxicity during the period of anatomical and functional development of the cochlea. Toxicity is expressed only after a few days of treatment when kanamycin is given during the most sensitive period for production of ototoxicity (postnatal days 11-20). In contrast, when the drug is administered after the 20th postnatal day, the same dose and duration of treatment do not produce an ototoxic effect, Only after prolonged treatment (e.g., greater than or equal to 20 days) is there an observed effect. We characterized the pharmacokinetics of kanamycin in the serum of 12- and 25-day-old rats and observed a greater than 2.5-fold increase in elimination half-life in the 12- versus 25-day-old rat. The longer duration half-life of kanamycin in younger rats may explain the hypersensitivity of immature mammals to aminoglycoside ototoxicity. C1 BAYLOR COLL MED,DIV NEUROSCI,HOUSTON,TX 77030. UNIV MICHIGAN,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. LOUISIANA STATE UNIV,SCH MED,DEPT PEDIAT,CLIN PHARMACOL SECT,SHREVEPORT,LA 71130. RP Henley, CM (reprint author), BAYLOR COLL MED,DEPT PHARMACOL,BOBBY R ALFORD DEPT OTORHINOLARYNGOL & COMMUNICAT,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. 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PD SEP 15 PY 1996 VL 99 IS 1-2 BP 85 EP 90 DI 10.1016/S0378-5955(96)00094-9 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800010 PM 8970816 ER PT J AU Nitecka, LM Sobkowicz, HM AF Nitecka, LM Sobkowicz, HM TI The GABA/GAD innervation within the inner spiral bundle in the mouse cochlea SO HEARING RESEARCH LA English DT Article DE cochlear innervation; glutamic acid decarboxylase; gamma-aminobutyric acid; calcitonin gene-related peptide; growth-associated protein-43; inner hair cell ID GROWTH-ASSOCIATED PROTEIN; STEM AUDITORY NUCLEI; GUINEA-PIG ORGAN; ADULT-RAT BRAIN; OLIVOCOCHLEAR NEURONS; GLUTAMATE-DECARBOXYLASE; EFFERENT INNERVATION; GOLGI METHOD; CORTI; IMMUNOREACTIVITY AB Stains with antibodies to glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid (GABA) in the cochlea of postnatal and adult mice reveal within the inner spiral bundle a distinctive neuronal plexus intimately associated with the inner hair cells. This innervation provides endings that cradle the receptor poles of the sensory cells and lateral end collaterals that wind between the cells, distributing endings alongside and around them. Some GAD-positive fibers enter the inner pillar bundle, from where they distribute tunnel fibers to the outer hair cells and recurrent collaterals to the inner hair cells. The GABAergic innervation within the inner spiral bundle is present along the entire cochlear axis, with the highest density in its basal half. Stainings against calcitonin gene-related peptide (CGRP), which localizes in the cholinergic counterpart of the inner spiral bundle, reveal that some of these fibers parallel the GABAergic circuit. The present data, together with our previous demonstration of compound (serial, converging, triadic) efferent synapses within this pathway (Sobkowicz et al. (1995) Abst. ARO 18, 171) evidences the presence of a distinctive innervation to the inner hair cells, hitherto unrecognized. The expression of growth-associated protein-43 (GAP-43) within the inner hair cell innervation in the adult cochlea provides evidence for a continuous synaptic turnover and plasticity, thus emphasizing its functional importance. C1 UNIV WISCONSIN,DEPT NEUROL,MADISON,WI 53706. 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PD SEP 15 PY 1996 VL 99 IS 1-2 BP 91 EP 105 DI 10.1016/S0378-5955(96)00088-3 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800011 PM 8970817 ER PT J AU Laffon, E Angelini, E AF Laffon, E Angelini, E TI On the Deiters cell contribution to the micromechanics of the organ of Corti SO HEARING RESEARCH LA English DT Article DE supporting cell; cytoskeletal protein; cell stiffness; outer hair cell; cell mechanical coupling ID OUTER HAIR-CELLS; THERMAL FLUCTUATIONS; COCHLEA; RESPONSES; RIGIDITY; BUNDLES AB We give the first estimate of Young's modulus of the proteinaceous beam that makes the stiffness of the Deiters cell phalangeal processes. We show that the fundamental mode of vibration of an isolated phalanx is overdamped due to the damping imposed by the surrounding fluid. Then we consider the mechanical couplings that have so far been neglected in the micromechanics of the organ of Corti, Conclusions are drawn concerning the lack of significance of some expected resonant behaviour of isolated outer hair cells. C1 UNIV TALENCE,INST TECHNOL A,DEPT MESURES PHYS,F-33405 TALENCE,FRANCE. UNIV BORDEAUX 2,HOP PELLEGRIN,LAB AUDIOL EXPT,F-33076 BORDEAUX,FRANCE. RP Laffon, E (reprint author), CHU BORDEAUX,HOP HAUT LEVEQUE,NUCL MED SERV,AVE MAGELLAN,F-33600 PESSAC,FRANCE. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 106 EP 109 DI 10.1016/S0378-5955(96)00089-5 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800012 PM 8970818 ER PT J AU Beveridge, HA Carlyon, RP AF Beveridge, HA Carlyon, RP TI Effects of aspirin on human psychophysical tuning curves in forward and simultaneous masking SO HEARING RESEARCH LA English DT Article DE aspirin; salicylate; frequency selectivity; forward masking; simultaneous masking; psychophysical tuning curve; suppression ID SENSORINEURAL HEARING-LOSS; AUDITORY-NERVE FIBERS; OTOACOUSTIC EMISSIONS; PURE-TONE; LEVEL; SALICYLATE; INHIBITION; 2-TONE; MICROSTRUCTURE; MANIPULATIONS AB Psychophysical tuning curves (PTCs) at 4 kHz were measured in forward and simultaneous masking under two experimental conditions: 1 h after listeners had ingested three 320 mg capsules of aspirin every 6 h for 3 days (3.84 g/day), and after an identical schedule of placebo ingestion. Aspirin and placebo allocation was double-blind. In addition to raising thresholds at several audiometric frequencies, aspirin elevated the tips and reduced the slopes of the PTCs, indicating a reduction in frequency selectivity. The aspirin-induced reduction in PTC slopes did not differ significantly between forward and simultaneous masking, nor did the overall reduction differ significantly between the low- and high-frequency side. However, a separate analysis of the data obtained in simultaneous masking indicated that the broadening in tuning caused by aspirin was greatest on the high-frequency side of the PTC. C1 MRC,APPL PSYCHOL UNIT,CAMBRIDGE CB2 2EF,ENGLAND. UNIV SUSSEX,EXPT PSYCHOL LAB,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. RI Carlyon, Robert/A-5387-2010 CR ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 Bernstein J M, 1967, J Laryngol Otol, V81, P915, DOI 10.1017/S0022215100067852 BOETTCHER FA, 1989, HEARING RES, V42, P129, DOI 10.1016/0378-5955(89)90139-1 BONDING P, 1979, AUDIOLOGY, V18, P133 BROWN AM, 1993, J ACOUST SOC AM, V93, P3298, DOI 10.1121/1.405714 CARLYON RP, 1993, HEARING RES, V66, P233, DOI 10.1016/0378-5955(93)90143-O CHAMPLIN CA, 1993, J ACOUST SOC AM, V94, P1269, DOI 10.1121/1.408179 CODY AR, 1980, HEARING RES, V3, P3, DOI 10.1016/0378-5955(80)90004-0 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 Falbe-Hansen J., 1941, ACTA OTO-LARYNGOL, V44, P1 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GREEN DM, 1981, J ACOUST SOC AM, V69, P1758, DOI 10.1121/1.385911 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 GUINAN JJ, 1988, HEARING RES, V37, P29, DOI 10.1016/0378-5955(88)90075-5 HOUTGAST T, 1973, ACUSTICA, V29, P168 HOUTGAST T, 1972, J ACOUST SOC AM, V51, P1885, DOI 10.1121/1.1913048 JARDINI L, 1978, RHEUMATOL REHABIL, V17, P233, DOI 10.1093/rheumatology/17.4.233 KLIS JFL, 1988, HEARING RES, V36, P163, DOI 10.1016/0378-5955(88)90058-5 KOEGEL L, 1985, AM J OTOL, V6, P190 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 LONG GR, 1986, PERIPHERAL AUDITORY, P213 LONG GR, 1988, HEARING RES, V36, P125, DOI 10.1016/0378-5955(88)90055-X 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 MONGAN E, 1973, JAMA-J AM MED ASSOC, V226, P142, DOI 10.1001/jama.226.2.142 MOORE BCJ, 1978, J ACOUST SOC AM, V63, P524, DOI 10.1121/1.381752 MOORE BCJ, 1982, J ACOUST SOC AM, V72, P1374, DOI 10.1121/1.388441 MOORE BCJ, 1984, J ACOUST SOC AM, V76, P1057, DOI 10.1121/1.391425 MOORE BCJ, 1988, J ACOUST SOC AM, V83, P1102, DOI 10.1121/1.396055 Murugasu E., 1995, AUDIT NEUROSCI, V1, P139 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 NEFF DL, 1985, J ACOUST SOC AM, V78, P1966, DOI 10.1121/1.392653 NELSON DA, 1991, J SPEECH HEAR RES, V34, P360 NELSON DA, 1991, J SPEECH HEAR RES, V34, P374 NELSON DA, 1984, J ACOUST SOC AM, V75, P1570, DOI 10.1121/1.390866 OLOUGHLIN BJ, 1981, J ACOUST SOC AM, V69, P1119, DOI 10.1121/1.385691 Patterson RD, 1986, FREQUENCY SELECTIVIT, P123 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 RUSSELL IJ, 1995, AUDIT NEUROSCI, V1, P309 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 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 STELMACHOWICZ PG, 1985, J ACOUST SOC AM, V77, P620, DOI 10.1121/1.392378 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E TUNSTALL MJ, 1994, J PHYSL LOND P, V476, P75 TUNSTALL MJ, 1994, BRIT J AUDIOL, V27, P332 VOGTEN LLM, 1978, J ACOUST SOC AM, V63, P1520, DOI 10.1121/1.381846 WEBER DL, 1978, J ACOUST SOC AM, V64, P1392, DOI 10.1121/1.382105 WEBER DL, 1980, PSYCHOPHYSICAL PHYSL, P106 WIDIN GP, 1979, J ACOUST SOC AM, V66, P388, DOI 10.1121/1.383673 WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 Wightman F., 1977, PSYCHOPHYSICS PHYSL, P295 NR 57 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 15 PY 1996 VL 99 IS 1-2 BP 110 EP 118 DI 10.1016/S0378-5955(96)00091-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800013 PM 8970819 ER PT J AU Clark, JA Pickles, JO AF Clark, JA Pickles, JO TI The effects of moderate and low levels of acoustic overstimulation on stereocilia and their tip links in the guinea pig SO HEARING RESEARCH LA English DT Article DE acoustic trauma; hair cell; stereocilia; tip link; guinea pig ID HAIR-CELLS; NOISE TRAUMA; HEARING-LOSS; EXPOSURE; TRANSDUCTION; PROTECTION; STIMULATION; TEMPORARY; COCHLEA; OSMIUM AB Guinea pigs were exposed to pure tones of 10 kHz at intensities between 98 and 115 dB SPL for 5-30 min, to produce varying degrees of acoustic trauma. Changes in auditory thresholds were measured electrophysiologically, and the animals were immediately fixed for scanning electron microscopy. Correlation between morphological changes to the hair bundle and losses in threshold, showed that with the smallest degrees of trauma (98 dB SPL for 15 min, mean maximum threshold loss of 22 dB), damage was confined to a small stretch of inner hair cells (IHC), with only subtle changes to the stereocilia of the outer hair cells (OHC). At exposure intensities greater than 102 dB SPL (duration: 15 min) the IHC stereocilia in the centre of the lesion were always substantially disarrayed. Substantial damage to the OHC bundles was seen only with exposures above 110 dB SPL(duration: greater than or equal to 5 min), producing threshold losses of 50 dB or more. Tip links were lost only where the stereocilia were disarrayed. It is concluded that the tip links are not the most vulnerable components of the cochlear hair cell, but that relatively low levels of acoustic stimulation can cause significant damage to the stereociliary bundle of the IHCs. C1 UNIV BIRMINGHAM,DEPT PHYSIOL,BIRMINGHAM B15 2TJ,W MIDLANDS,ENGLAND. UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,BRISBANE,QLD 4072,AUSTRALIA. CR ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T CAMPO P, 1991, HEARING RES, V55, P195, DOI 10.1016/0378-5955(91)90104-H CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CANLON B, 1995, HEARING RES, V84, P112, DOI 10.1016/0378-5955(95)00020-5 COMIS SD, 1985, J NEUROCYTOL, V14, P113, DOI 10.1007/BF01150266 EVANS EF, 1979, AUDITORY INVESTIGATI, P324 GAO WY, 1992, HEARING RES, V62, P27, DOI 10.1016/0378-5955(92)90200-7 HILDESHEIMER M, 1990, HEARING RES, V43, P263, DOI 10.1016/0378-5955(90)90233-F KALTENBACH JA, 1992, HEARING RES, V60, P205, DOI 10.1016/0378-5955(92)90022-F LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 OSBORNE MP, 1984, CELL TISSUE RES, V237, P43 PATUZZI RB, 1991, HEARING RES, V54, P45, DOI 10.1016/0378-5955(91)90135-V PICKLES JO, 1984, HEARING RES, V14, P245, DOI 10.1016/0378-5955(84)90053-4 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PICKLES JO, 1992, TRENDS NEUROSCI, V15, P254, DOI 10.1016/0166-2236(92)90066-H PICKLES JO, 1987, HEARING RES, V25, P173, DOI 10.1016/0378-5955(87)90089-X RAJAN R, 1988, HEARING RES, V36, P53, DOI 10.1016/0378-5955(88)90137-2 RAJAN R, 1983, HEARING RES, V9, P279, DOI 10.1016/0378-5955(83)90032-1 REITER ER, 1995, J NEUROPHYSIOL, V73, P506 ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 SHAW EAG, 1974, J ACOUST SOC AM, V56, P1848, DOI 10.1121/1.1903522 SUBRAMANIAM M, 1991, HEARING RES, V56, P65, DOI 10.1016/0378-5955(91)90154-2 SUN JC, 1994, LARYNGOSCOPE, V104, P1251 TAKUMIDA M, 1989, J LARYNGOL OTOL, V103, P1125, DOI 10.1017/S002221510011117X THORNE PR, 1986, HEARING RES, V21, P41, DOI 10.1016/0378-5955(86)90044-4 NR 27 TC 32 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 119 EP 128 DI 10.1016/S0378-5955(96)00092-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800014 PM 8970820 ER PT J AU RinkwitzBrandt, S Arnold, HH Bober, E AF RinkwitzBrandt, S Arnold, HH Bober, E TI Regionalized expression of Nkx5-1, Nkx5-2, Pax2 and sek genes during mouse inner ear development SO HEARING RESEARCH LA English DT Article DE homeobox; Nkx5; Pax2; sek-gene; inner ear development ID PROGENITOR CELLS; REGULATORY GENE; PRECURSOR CELLS; HOMEOBOX GENES; PAIRED-BOX; DROSOPHILA; MUSCLE; HINDBRAIN; MUTATIONS; MESODERM AB Nkx5-1 and Nkx5-2 are two highly related homeobox genes which are expressed during mouse development in the inner ear. Here, we present the detailed expression of both genes within the developing ear and a comparison to the expression of other potential control genes in this organ. Both genes are active between E13.5 and birth in non-sensory epithelium of the semicircular canals, utricle and saccule. Nkx5-1 and Nkx5-2 are also expressed in the cochlea, where the expression is restricted to the stria vascularis. The endolymphatic duct is devoid of any Nkx5 transcripts. Pax2 is expressed in epithelial cells of the ventral part of the membranous labyrinth where it overlaps with the Nkx5 expression domain. sek shows a complementary pattern to Nkx5 in the vestibular epithelium. In the cochlea sek is expressed throughout the mesenchyme and epithelium but not in the stria vascularis. In the vestibulum Pax2 and sek is limited to the ventral part whereas Nkx5 genes are active thoroughout. These data suggest that Nkx5 genes, Pax2 and sek play different roles in the patterning of inner ear structures. C1 TECH UNIV CAROLO WILHELMINA BRAUNSCHWEIG,DEPT MOL & CELLULAR BIOL,D-38106 BRAUNSCHWEIG,GERMANY. 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Res. PD SEP 15 PY 1996 VL 99 IS 1-2 BP 129 EP 138 DI 10.1016/S0378-5955(96)00093-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800015 PM 8970821 ER PT J AU Blamey, PJ Dooley, GJ Parisi, ES Clark, GM AF Blamey, PJ Dooley, GJ Parisi, ES Clark, GM TI Pitch comparisons of acoustically and electrically evoked auditory sensations SO HEARING RESEARCH LA English DT Article DE cochlear prosthesis; pitch; electrical stimulation; hearing impairment ID CHANNEL COCHLEAR IMPLANT; INTRACOCHLEAR IMPLANT; STIMULATION; PERCEPTION; NERVE AB Cochlear implant users with some residual hearing in the non implanted ear compared the pitch sensations produced by acoustic pure tones and pulsatile electric stimuli. Pitch comparisons were obtained for pure tones and electrical stimuli presented at different positions (electrodes) in the scala tympani, keeping the electric pulse rate fixed at 100, 250, or 800 pps. Similarly, pitch comparisons were obtained for electrical stimuli with variable pulse rates presented to two fixed electrode positions (apical and basal) in the cochlea. Both electrode position and pulse rate influenced the perceived pitch of the electrical signal and 'matched' electric and acoustic signals were found over a wide range of frequencies. There was a large variation between listeners. For some stimuli, listeners had difficulty in deciding whether the acoustic or electric stimulus was higher in pitch. Despite the variability, consistent trends were obtained from the data: higher frequencies tended to be matched by more basal electrodes for all pulse rates. Higher frequencies tended to be marched by higher pulse rates for both electrode positions. 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PD SEP 15 PY 1996 VL 99 IS 1-2 BP 139 EP 150 DI 10.1016/S0378-5955(96)00095-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800016 PM 8970822 ER PT J AU Henry, KR AF Henry, KR TI Auditory nerve neurophonic produced by the frequency difference of two simultaneously presented tones SO HEARING RESEARCH LA English DT Article DE auditory nerve neurophonic; distortion product; gerbil; phase-locking; periodicity pitch; adaptation; compound action potential ID ODD-ORDER DISTORTION; HAIR CELL MOTOR; RESPONSES; 2-TONE; MODULATION; POTENTIALS; F2-F1 AB When two phase-locked sinusoidal stimuli having frequencies of F-1 and F-2 are simultaneously introduced to the ear of the gerbil, a difference tone (DT) can be observed (DT = F-2-F-1, where F-2>F-1) in the time-averaged electrical response recorded from the cochlear round window (RW). Tetrodotoxin (TTX), which blocks the axonal firing of the cochlear nerve fiber, greatly attenuates this DT response, suggesting it is primarily neural in origin. Alternating the polarity of a single phase-locked tone cancels out the RW cochlear microphonic (CM) from the time-averaged response, leaving a residual auditory nerve neurophonic (ANN) response if the stimulus frequency is low enough to result in phase-locked firing of cochlear nerve axons. Simultaneous presentation of 1 kHz (F-1) and 2 kHz (F-2) tones, each being phase-locked with alternating polarity, produces a small ANN in response to the original tones and a large time-averaged ANN in response to the DT. Even when the frequency of the individual tones is too high to support phase-locking, a large DT-ANN can also be measured in response to simultaneously presented tones. A robust time-averaged DT-ANN can be measured when the temporal and intensity relationships between F-1 and F-2 are varied widely, with the latency (but not amplitude) of the response following the stimulus envelope. The DT-ANN produced by pairs of tones having frequencies ranging from 500 Hz to 3.5 kHz is largest in response to a DT of approximately 700-1100 Hz. This is in contrast to the ANN generated in response to a single tone, which decreases in magnitude as the stimulus frequency increases from 500 to 1500 Hz. Robust DT-ANNs can be measured from the gerbil even when the F-2 frequency is greater than 30 kHz. RP Henry, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR BOBBIN RP, 1974, ACTA OTO-LARYNGOL, V77, P56, DOI 10.3109/00016487409124598 BROWN AM, 1994, J ACOUST SOC AM, V96, P2210, DOI 10.1121/1.410161 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P386 CHERTOFF ME, 1992, J SPEECH HEAR RES, V35, P157 Corso J. 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F., 1991, AGING AUDITORY SYSTE 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 SEP 15 PY 1996 VL 99 IS 1-2 BP 151 EP 159 DI 10.1016/S0378-5955(96)00096-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800017 PM 8970823 ER PT J AU Henry, KR AF Henry, KR TI Tuning curves of the difference tone auditory nerve neurophonic SO HEARING RESEARCH LA English DT Article DE audiogram; distortion product; gerbil; phase-locking; cochlea ID FREQUENCY-FOLLOWING RESPONSE; ODD-ORDER DISTORTION; HAIR CELL MOTOR; MONGOLIAN GERBIL; ENHANCEMENT; SUPPRESSION; MODULATION; MASKING; FIBERS; F2-F1 AB When a pair of tonal stimuli of different frequencies (F-1 and F-2, where F-2 > F-1) are simultaneously presented to the ear, an electrical response with a frequency of F-2-F-1 can be recorded from the round window (RW) of the gerbil's cochlea. By using phase-locked tones of alternating polarity, the cochlear microphonics are canceled, leaving a time-averaged difference tone-auditory nerve neurophonic (DT-ANN). When the F-1 frequency ranges from 1.25 to 30 kHz and F-2-F-1 approximate to 900 Hz, a DT-ANN audiogram can be constructed which parallels (but is at least 10 dB more sensitive than) the compound action potential (CAP) audiogram. In addition to this DT response, a smaller magnitude, higher threshold response having a frequency of 2 DT can often be measured. Both the DT-ANN and the 2 DT-ANN show non-monotonic amplitude input-output functions. The DT- and 2 DT-ANN responses can be forward masked. Masking of low level (e.g., 30 dB SPL) probe stimuli results in DT- and 2 DT-ANN V-shaped tuning curves (TC) with low tip thresholds (approximate to 20-30 dB SPL) and a tip frequency close to that of F-1 and F-2. The Q(10 dB) values of the forward masked DT-ANN TCs ranges from 1.54 to 20.0 for F-1 frequencies varying from 2 to 20 kHz, respectively. The V-shaped DT-ANN TCs generated with simultaneous maskers are often flanked, outside their high- and low-frequency slopes, by frequency-intensity domains where the masker enhances the amplitude of the DT-ANN response. These data (1) provide evidence that, in response to low-intensity tones, the DT-ANN is generated by a restricted population of neurons that have characteristic frequencies close to F-1 and F-2, and (2) provide evidence for sharply tuned, phase-locked activity occurring in response to low-intensity stimuli, by cochlear axons having characteristic frequencies as high as 20 kHz. RP Henry, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. 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PD SEP 15 PY 1996 VL 99 IS 1-2 BP 160 EP 167 DI 10.1016/S0378-5955(96)00097-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800018 PM 8970824 ER PT J AU Carlson, S Willott, JF AF Carlson, S Willott, JF TI The behavioral salience of tones as indicated by prepulse inhibition of the startle response: Relationship to hearing loss and central neural plasticity in C57BL/6J mice SO HEARING RESEARCH LA English DT Article DE neural plasticity; hearing loss; inbred mice; startle response; behavior ID INFERIOR COLLICULUS NEURONS; PEDUNCULOPONTINE TEGMENTAL NUCLEUS; ACOUSTIC STARTLE; AUDITORY-CORTEX; COCHLEAR NUCLEUS; RETICULAR-FORMATION; UNILATERAL DEAFNESS; GIANT-NEURONS; LESIONS; RAT AB Adult C57BL/6J mice exhibit high-frequency, sensorineural hearing loss accompanied by physiological changes in the upper auditory brainstem and cortex, referred to as hearing-loss induced (HLI) plasticity: as high-frequency sensitivity declines, many neurons come to respond better to still-audible, middle-frequency tones (especially 12-16 kHz). We used prepulse inhibition (PPI) to assess the relationship between the behavioral salience of tones and HLI plasticity. The ability of a tone 'prepulse' (S1), presented 100 ms before a startle-eliciting tone (S2), to 'inhibit' startle responses was measured in normal-hearing 1-month-olds and 5-month-olds with high-frequency hearing loss. Tone bursts of 4, 8, 12, 16, and 24 kHz were used as S1s and S2s in all possible combinations. PPI was significantly improved (more inhibition) in 5-month-olds with 12 or 16 kHz Sis. This effect was not influenced by S2 frequency or the size of the startle evoked by S2-only stimuli (smaller for high-frequency S2s in older mice). The increased salience of 12-16 kHz sis in 5-month-old C57 mice parallels changes in the central representation of tone frequency and implies a behavioral effect of HLI plasticity. C1 NO ILLINOIS UNIV,DEPT PSYCHOL,DE KALB,IL 60115. 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PD SEP 15 PY 1996 VL 99 IS 1-2 BP 168 EP 175 DI 10.1016/S0378-5955(96)00098-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VZ108 UT WOS:A1996VZ10800019 PM 8970825 ER PT J AU Hao, LF Khanna, SM AF Hao, LF Khanna, SM TI Reissner's membrane vibrations in the apical turn of a living guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE Reissner's membrane; cochlear mechanics; tuning; radial dependence ID BASILAR-MEMBRANE; MOSSBAUER TECHNIQUE; HOOK REGION; CAT COCHLEA; MECHANICS; EAR; MICROSCOPE; DAMAGE; INPUT; BASE AB Mechanical tuning curves were recorded at several radial locations on the Reissner's membrane, over a wide range of frequencies, and sound pressure levels. The position coordinates of each location were also recorded. The shape of the tuning curves changed dramatically with the radial location. 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(1) There are two kinds of ACh receptors on hair cells: muscarinic-like and nicotinic-like. (2) The nicotinic-like receptor mediates a hyperpolarizing response to ACh and a consequent reduction in afferent firing. (3) The muscarinic-like receptors mediate both a depolarization and a hyperpolarization of hair cells. (4) The hyperpolarization results in a reduction in afferent firing and (5) the depolarization results in an increase in afferent firing. C1 TULANE UNIV, SCH MED, DEPT OTOLARYNGOL, NEW ORLEANS, LA 70112 USA. RP Guth, PS (reprint author), TULANE UNIV, SCH MED, DEPT PHARMACOL, 1430 TULANE AVE, NEW ORLEANS, LA 70112 USA. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 1 EP 8 DI 10.1016/0378-5955(96)00031-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100001 PM 8880175 ER PT J AU Chen, C LeBlanc, C Bobbin, RP AF Chen, C LeBlanc, C Bobbin, RP TI Differences in cholinergic responses from outer hair cells of rat and guinea pig SO HEARING RESEARCH LA English DT Article DE cochlea; acetylcholine; receptor; voltage-clamp; patch-clamp ID ACETYLCHOLINE-RECEPTOR; CHANNEL; COCHLEA; SUBUNITS; INHIBITION; ALPHA-3; CALCIUM; ATP AB A cholinergic receptor on outer hair cells (OHC) in guinea pig cochlea induces a K+ current when it is activated by acetylcholine and suberyldicholine but not by nicotine or muscarine (Bobbin, 1995). This unusual receptor may contain an alpha 9-subunit. However, the pharmacology of the alpha 9-subunit cloned from rat and expressed in Xenopus oocytes does not completely match that obtained for the ACh receptor in guinea pig OHCs. The response to 1,1-dimethyl-4-phenylpiperazinium (DMPP) is large in guinea pig OHCs and small in oocytes containing receptors of the alpha 9-subunit. Therefore, we compared the effects of cholinergic receptor agonists in rat and guinea pig OHCs using the whole-cell variant of the patch-clamp technique. ACh caused the largest outward K+ current in OHCs from both rat and guinea pig. Carbachol- and suberyldicholine-induced responses were similar in magnitude in OHCs of rat and guinea pig. However, DMPP produced a small response in OHCs from rat and a large response in OHCs from guinea pig. At a concentration of 100 mu M, muscarine, oxotremorine M, nicotine and cytisine induced little response in guinea pig OHCs and none in rat OHCs. Results suggest that the ACh receptor on rat OHCs is similar to the alpha 9-subunit-containing receptor expressed in oocytes but different from the ACh receptor on guinea pig OHCs. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARGYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. CR BOBBIN RP, 1995, HAIR CELL HEARING AI, P29 BOULTER J, 1990, J BIOL CHEM, V265, P4472 CHEN C, 1995, HEARING RES, V86, P25, DOI 10.1016/0378-5955(95)00050-E CHEN C, 1995, HEARING RES, V88, P215, DOI 10.1016/0378-5955(95)00115-K COUTURIER S, 1990, J BIOL CHEM, V265, P17560 COUTURIER S, 1990, NEURON, V5, P847, DOI 10.1016/0896-6273(90)90344-F DOI T, 1993, HEARING RES, V67, P179, DOI 10.1016/0378-5955(93)90245-V ELGOYHEN AB, 1994, CELL, V79, P705, DOI 10.1016/0092-8674(94)90555-X EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EROSTEGUI C, 1994, HEARING RES, V81, P119, DOI 10.1016/0378-5955(94)90159-7 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FUCHS PA, 1992, P ROY SOC B-BIOL SCI, V248, P35, DOI 10.1098/rspb.1992.0039 FUCHS PA, 1992, J NEUROSCI, V12, P800 GERZANICH V, 1994, MOL PHARMACOL, V45, P212 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HOUSLEY GD, 1991, P ROY SOC B-BIOL SCI, V244, P161, DOI 10.1098/rspb.1991.0065 KAKEHATA S, 1993, J PHYSIOL-LONDON, V463, P227 KUJAWA SG, 1994, HEARING RES, V74, P122, DOI 10.1016/0378-5955(94)90181-3 LUEBKE AE, 1995, ABSTR 18 M ASS RES O, V772, P193 LUETJE CW, 1991, J NEUROSCI, V11, P837 SEGUELA P, 1993, J NEUROSCI, V13, P596 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X NR 22 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 9 EP 17 DI 10.1016/0378-5955(96)00049-4 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100002 PM 8880176 ER PT J AU Huang, JM Money, MK Berlin, CI Keats, BJB AF Huang, JM Money, MK Berlin, CI Keats, BJB TI Phenotypic patterns of distortion product otoacoustic emission in inbred and F-1 hybrid hearing mouse strains SO HEARING RESEARCH LA English DT Article DE CBA/J; curly-tail mouse; deafness mouse; genotype; heterosis; hybrid; inbred; MOLF/Rk; otoacoustic emission; phenotype ID DEAFNESS DN/DN MICE; ACOUSTIC DISTORTION; INNER-EAR; HETEROSIS; AGE; DN; DEGENERATION; THRESHOLDS; GENETICS; GANGLION AB Distortion product otoacoustic emissions (DPOE) were obtained from five different hearing mouse groups: CBA/J, MOLF/Rk, ct (homozygous normal mice of the curly-tail stock), and the F-1 hybrid offspring of the matings CBA/J x dn/dn and MOLF/Rk x dn/dn (dn/dn mice are the curly-tail stock with recessive deafness). The DPOE patterns of the CBA/J and ct strains were similar to each other and different from that of the MOLF/Rk. The two sets of F-1 hybrid mice, (CBA/J x dn/dn)F-1 and (MOLF/Rk x dn/dn)F-1, were found to have significantly larger DPOE amplitudes than their hearing parent strains, MOLF/Rk and CBA/J, respectively. In addition, the DPOE amplitudes were greater for the offspring of the MOLF/Rk x dn/dn cross than for those of the CBA/J x dn/dn cross, even though they were lower for MOLF/Rk than for CBA/J. The distinct features of DPOE patterns among these five groups suggest that DPOE testing can be used for auditory phenotyping. C1 LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. RP Huang, JM (reprint author), LOUISIANA STATE UNIV,DEPT OTORHINOLARGYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,2020 GRAVIER ST,NEW ORLEANS,LA 70112, USA. CR ALLEN JB, 1992, USER MANUAL CUBDIS D BERLIN CI, 1968, J SPEECH HEAR RES, V11, P159 BERLIN CI, 1963, J SPEECH HEAR RES, V6, P359 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 BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 DEOL M. S., 1958, HEREDITY, V12, P463, DOI 10.1038/hdy.1958.46 DOLAN TG, 1985, J ACOUST SOC AM, V77, P1475, DOI 10.1121/1.392042 Ehret G, 1976, J Am Audiol Soc, V1, P179 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Falconer D. S., 1981, INTRO QUANTITATIVE G, V3rd 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 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 HUANG JM, 1995, HEARING RES, V88, P61, DOI 10.1016/0378-5955(95)00099-P KEATS BJB, 1995, MAMM GENOME, V6, P8, DOI 10.1007/BF00350886 KIRSCH JP, 1993, HEARING RES, V67, P51, DOI 10.1016/0378-5955(93)90231-O KUMAR A, 1991, HEREDITY, V67, P275, DOI 10.1038/hdy.1991.90 LASKY R, 1992, EAR HEARING, V13, P430, DOI 10.1097/00003446-199212000-00009 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 LYNCH CB, 1986, GENET RES, V48, P95 MIKAMI H, 1985, GENET RES, V46, P85 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PARK JY, 1995, HEARING RES, V86, P147, DOI 10.1016/0378-5955(95)00065-C POONI HS, 1994, HEREDITY, V72, P628, DOI 10.1038/hdy.1994.86 PUJOL R, 1983, HEARING RES, V12, P57, DOI 10.1016/0378-5955(83)90118-1 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 SHULL GH, 1948, GENETICS, V33, P439 STEEL GP, 1983, ACTA OTOLARYNGOL, V96, P39 STEEL KP, 1980, NATURE, V288, P159, DOI 10.1038/288159a0 TSAFTARIS AS, 1987, ISOZYMES-CURR T BIOL, V16, P157 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 WILLOTT JF, 1984, HEARING RES, V16, P161, DOI 10.1016/0378-5955(84)90005-4 NR 35 TC 2 Z9 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 18 EP 21 DI 10.1016/0378-5955(96)00041-X PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100003 PM 8880177 ER PT J AU Long, GR VanDijk, P Wit, HP AF Long, GR VanDijk, P Wit, HP TI Temperature dependence of spontaneous otoacoustic emissions in the edible frog (Rana esculenta) SO HEARING RESEARCH LA English DT Article DE frog; Spontaneous otoacoustic emission; temperature ID PAPILLA; EAR AB The change in frequency of individual emissions in the European edible frog (Rana esculenta) when the temperature of the frog is modified, is part of a complex pattern of interaction between spontaneous otoacoustic emissions. At high temperatures (above 24 degrees C) two emissions are always detected (e.g., one near 800 Hz and one near 1200 Hz). The higher-frequency emission is lower in level and has a wider bandwidth than the lower-frequency emission. It is also often asymmetric and sometimes breaks into two emissions when an external suppressor tone is applied. When the temperature is decreased, these emissions are reduced in frequency at a rate of 0.04 octave/degrees C. The higher-frequency emission becomes narrower and taller, and the lower-frequency emissions becomes broader and less intense. At approximately 18 degrees C the lowest of these emissions (now between 600 and 700 Hz) disappears and is replaced by a new emission approximately 100 Hz lower in frequency. When the temperature is carefully controlled the two emissions can exist simultaneously. The lowest-frequency emission changes 0.015 degrees C/octave suggesting that the mechanisms controlling the frequency of this emission may be different than those determining the frequencies of the other emissions. All but the lowest-frequency emissions are maximal in level and have minimal bandwidth when the frequency is close to 700 Hz, which is interpreted as evidence that these emissions are filtered by a temperature-independent process. C1 UNIV GRONINGEN HOSP,ENT DEPT AUDIOL,NL-9700 RB GRONINGEN,NETHERLANDS. RP Long, GR (reprint author), PURDUE UNIV,DEPT AUDIOL & SPEECH SCI,W LAFAYETTE,IN 47907, USA. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 22 EP 28 DI 10.1016/0378-5955(96)00057-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100004 PM 8880178 ER PT J AU Hiel, H Happe, HK Warr, WB Morley, BJ AF Hiel, H Happe, HK Warr, WB Morley, BJ TI Regional distribution of a creatine transporter in rat auditory brainstem: An in-situ hybridization study SO HEARING RESEARCH LA English DT Article DE creatine transporter; in-situ hybridization; central auditory system; high-energy phosphate metabolism ID FUNCTIONAL EXPRESSION; INFERIOR COLLICULUS; KINASE ISOENZYMES; NERVOUS-SYSTEM; MUSCLE; CLONING; TISSUES; CDNA; FAMILY; ENERGY AB The expression of an mRNA encoding a creatine transporter (CRT1) was investigated in the rat auditory system under ambient sound conditions, using radiolabeled and non-radiolabeled oligonucleotide in-situ hybridization. The results indicated that CRT1 mRNA is widely distributed in auditory nuclei, including the fusiform and deep layers of the dorsal cochlear nucleus, the ventral cochlear nucleus, the superior olivary complex, the nuclei of the lateral lemniscus and the inferior colliculus. The molecular layer of the dorsal cochlear nucleus and the medial geniculate have low levels of label. Creatine provides cells with a reservoir of high-energy phosphate. Neurons do not synthesize creatine but accumulate it by a transport mechanism, which is probably the limiting step in the regulation of intracellular creatine. Therefore, the quantity of transporter expressed may reflect the utilization of creatine and could serve as an in-vitro indicator of endogenous high-energy metabolism in some cells. Although most auditory nuclei express CRT1 mRNA, the quantity of CRT1 mRNA varies among auditory nuclei, indicating that many auditory nuclei have high and fluctuating energy requirements. The level of CRT1 transcript or protein may be regulated by chronic metabolic changes in the auditory system that may occur, for example, with damage to the acoustic organ or the aging process. C1 BOYS TOWN NATL RES HOSP,NEUROCHEM LAB,OMAHA,NE 68131. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 29 EP 37 DI 10.1016/0378-5955(96)00046-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100005 PM 8880179 ER PT J AU Abdala, C Sininger, YS Ekelid, M Zeng, FG AF Abdala, C Sininger, YS Ekelid, M Zeng, FG TI Distortion product otoacoustic emission suppression tuning curves in human adults and neonates SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; distortion product; suppression; tuning curve ID BRAIN-STEM RESPONSES; STIMULATED ACOUSTIC EMISSIONS; 2 DISCRETE SOURCES; PHYSIOLOGICAL VULNERABILITY; FREQUENCY RESOLUTION; AUDITORY PATHWAY; BASILAR-MEMBRANE; EVOKED-RESPONSE; HAIR-CELLS; HUMAN EAR AB Distortion product otoacoustic emission (DPOAE) iso-suppression tuning curves (STC) were generated in 15 normal-hearing adults and 16 healthy term-born neonates for three f(2) frequencies. The 2f(1)-f(2) DPOAE was elicited using f(2)/f(1) = 1.2, L1 = 65 and L2 = 50 dB SPL. A suppressor tone was presented at frequencies ranging from 1 octave below to 1/4 octave above fz and varied in level until DPOAE amplitude was reduced by 6 dB. The suppressor level required for 6 dB suppression was plotted as function of suppressor frequency to generate a DPOAE STC. Forward-masked psychoacoustic tuning curves (PTC) were obtained for three of the adult subjects. Results indicate that DPOAE STCs are stable and show minimal inter- and intra-subject variability. The tip of the STC is consistently centered around the f(2) region and STCs are similar in shape, width (Q(10)) and slope to VIIIth-nerve TCs. PTCs and STCs measured in the same subject showed similar trends, although PTCs had narrower width and steeper slope. Neonatal STCs were recorded at 3000 and 6000 Hz only and were comparable in shape, width and slope to adult STCs. Results suggest: (1) suppression of the 2f(1)-f(2) DPOAE may provide an indirect measure of cochlear frequency resolution in humans and (2) cochlear tuning, and associated active processes in the cochlea, are mature by term birth for at least mid- and high-frequencies. These results provide significant impetus for continued study of DPOAE suppression as a means of evaluating cochlear frequency resolution in humans. RP Abdala, C (reprint author), CHILDRENS AUTITORY RES & EDUC CTR, HOUSE EAR INST, 2100 W 3RD ST, LOS ANGELES, CA 90057 USA. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 38 EP 53 DI 10.1016/0378-5955(96)00056-1 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100006 PM 8880180 ER PT J AU Michie, PT LePage, EL Solowij, N Haller, M Terry, L AF Michie, PT LePage, EL Solowij, N Haller, M Terry, L TI Evoked otoacoustic emissions and auditory selective attention SO HEARING RESEARCH LA English DT Article DE evoked otoacoustic emission; auditory efferent pathway; selective attention ID CROSSED OLIVOCOCHLEAR BUNDLE; CONTRALATERAL ACOUSTIC STIMULATION; ACTIVE MICROMECHANICAL PROPERTIES; TEMPORARY THRESHOLD SHIFTS; BRAIN-STEM; ELECTRICAL-STIMULATION; VISUAL-ATTENTION; COCHLEAR MECHANICS; STIMULUS VARIABLES; MAMMALIAN COCHLEA AB The auditory system has an extensive peripheral efferent innervation. The question addressed in this paper is whether the olivocochlear bundle (OCB) efferent system innervating the outer hair cells (OHC) of the cochlea plays a role in selective attention. As evoked otoacoustic emissions (EOAE) provide a measure of the active micromechanical properties of OHCs. they can be used to assess the role of the efferent system in attention. Six experiments using tone-pip EOAEs are reported, In each experiment, EOAEs generated by 1 or 2 kHz tone pips when they were attended were compared with EOAEs to the same stimuli when they were unattended. In three experiments (1-4), a non-linear stimulus difference method was used to record a pure cochlear component of EOAEs. In Exps. 1-5, 1 and 2 kHz tone pips were delivered to the same ear and the difficulty of the subjects' task was manipulated in order to produce a more focussed attentional state or contralateral noise was presented to determine whether attention effects are dependent upon having an already activated efferent system. In Exp. 6, the 1 and 2 kHz stimuli were delivered to opposite ears. A total of 70 subjects participated in the six experiments. There were no effects of attention on EOAEs in any of the experiments in the direction of previously reported effects. The results of these first six experiments employing simple attention switches between fixed auditory objects do not support active cochlear involvement in selective attention. C1 MACQUARIE UNIV, SCH BEHAV SCI, SYDNEY, NSW 2109, AUSTRALIA. NATL ACOUST LABS, HEARING LOSS PREVENT RES UNIT, CHATSWOOD, NSW 2067, AUSTRALIA. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 54 EP 67 DI 10.1016/0378-5955(96)00059-7 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100007 PM 8880181 ER PT J AU Skellett, RA Crist, JR Fallon, M Bobbin, RP AF Skellett, RA Crist, JR Fallon, M Bobbin, RP TI Chronic low-level noise exposure alters distortion product otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE noise exposure; distortion product otoacoustic emission; outer hair cell ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; TEMPORARY THRESHOLD SHIFT; ACOUSTIC DISTORTION; CONTRALATERAL SOUND; EFFERENT SYSTEM; RESPONSES; SALICYLATE; DAMAGE; CONSEQUENCES AB Chen et al. (1995) recently reported an altered response to the application of ATP in outer hair cells (OHC) isolated from guinea pigs continuously exposed for 10 or 11 days to a 65 dB SPL (A-scale) narrow-band noise (1.1-2.0 kHz). The primary goal of the present study was to test the hypothesis that the continuous low-level noise used by Chen et al. (1995) alters cochlear function. Cubic (2f(1)-f(2)) and quadratic (f(2)-f(1)) DPOAEs, as well as, the amount of contralateral suppression of DPOAE amplitudes were chosen for study. Responses were recorded in urethane-anesthetized guinea pigs with sectioned middle ear muscles. The animals had either been exposed to the low-level noise for 3 or 11 days or not exposed at all (n = 13 animals per group). Results demonstrate that this noise induces frequency-dependent and very localized reductions in 2f(1)-f(2) DPOAE input/output (I/O) functions, However, the f(2)-f(1) DPOAE I/O functions appear to be insensitive to the noise exposure. No noise-related changes were found in the amount of contralateral suppression between the different exposure groups, with the exception of one unexplainable data point (f(2)-f(1) DPOAE = 0.5 kHz; day 3) where it was reduced. The 2f(1)-f(2) DPOAE amplitude alterations lend support to the conclusions of Chen et al. (1995) that chronic low-level noise exposure induces molecular changes in the OHCs which may, in turn, alter cochlear function. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. 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D., 1976, EFFECTS NOISE HEARIN, P407 WARD WD, 1991, J ACOUST SOC AM, V90, P164, DOI 10.1121/1.401310 WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 NR 42 TC 20 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 SEP 1 PY 1996 VL 98 IS 1-2 BP 68 EP 76 DI 10.1016/0378-5955(96)00062-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100008 PM 8880182 ER PT J AU Pfingst, BE Holloway, LA Razzaque, SA AF Pfingst, BE Holloway, LA Razzaque, SA TI Effects of pulse separation on detection thresholds for electrical stimulation of the human cochlea SO HEARING RESEARCH LA English DT Article DE cochlear implant; detection threshold; electrical stimulation; human; pulse separation; psychophysics ID PSYCHOPHYSICAL DETECTION THRESHOLDS; AUDITORY-NERVE; PHASE DURATION; IMPLANTS; EXCITATION; MODEL; PREDICTORS; CONDUCTION; MONKEYS; FIBERS AB Effects of pulse separation on detection of electrical stimulation of the cochlea were studied in 12 profoundly deaf human subjects with Nucleus 22 cochlear implants. Biphasic symmetric pulses were used. Pulse separation is the time from offset of one biphasic pulse to the onset of the next biphasic pulse in the train. Effects of pulse separation were studied in the context of different covariables in four stages of the experiment. Effects of pulse separation seen in the different stages were similar, despite the different covariables. Both pulse separation and the total number of pulses per stimulus seem to be important variables affecting stimulus detection. For 0.5 ms/phase pulses, thresholds were lowest at the shortest pulse separations tested (0.2-1.1 ms) and increased as a function of pulse separation. For 2 ms/phase pulses, detection thresholds were lowest at pulse separations around 7.5 ms, in most cases, and higher at both longer and shorter pulse separations. These results suggest that interactions among adjacent pulses can either hinder or facilitate detection of the signal depending on the magnitudes of pulse separation and phase duration. Pulse separations at which thresholds measured for 2 ms/phase pulses were minimum were fairly consistent across subjects and did not correlate well with speech recognition scores. However, significant variation in this measure across species has been seen. RP Pfingst, BE (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,MED CTR,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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PD SEP 1 PY 1996 VL 98 IS 1-2 BP 77 EP 92 DI 10.1016/0378-5955(96)00071-8 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100009 PM 8880183 ER PT J AU Henley, CM Weatherly, RA Martin, GK LonsburyMartin, B AF Henley, CM Weatherly, RA Martin, GK LonsburyMartin, B TI Sensitive developmental periods for kanamycin ototoxic effects on distortion-product otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE kanamycin; neonatal rat; distortion-product emission; ototoxicity ID EAR ORNITHINE DECARBOXYLASE; INDUCED HEARING-LOSS; OUTER HAIR-CELLS; POSTNATAL-DEVELOPMENT; AUDITORY FUNCTION; AMINOGLYCOSIDE ANTIBIOTICS; COCHLEAR POTENTIALS; DEVELOPING RAT; GUINEA-PIGS; INNER AB The developing rat is hypersensitive to aminoglycoside toxicity, which is expressed early on as a destruction of outer hair cells (OHC). In the current study, distortion-product otoacoustic emissions (DPOAE), which specifically measure the micromechanical activity of OHCs, were used to assess functional effects of administering a regimen of kanamycin to three groups of neonatal rats representing discrete postnatal developmental periods. In this manner, pigmented rats were treated at postnatal days 1-10, 11-20, and 21-30. A series of input-output (I/O) functions obtained for the 2f(1)-f(2) DPOAE during the post-treatment period indicated that detection thresholds were significantly elevated for the animals treated on postnatal days 1-10 and 11-20, with the greatest elevations observed at the higher test frequencies. C1 BAYLOR COLL MED,DEPT PHARMACOL,HOUSTON,TX 77083. BAYLOR COLL MED,DIV NEUROSCI,HOUSTON,TX 77083. UNIV MICHIGAN,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. UNIV MIAMI,EAR INST,DEPT OTOLARYNGOL M805,MIAMI,FL 33101. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 93 EP 103 DI 10.1016/0378-5955(96)00077-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100010 PM 8880184 ER PT J AU Frank, G Kossl, M AF Frank, G Kossl, M TI The acoustic two-tone distortions 2f1-f2 and f2-f1 and their possible relation to changes in the operating point of the cochlear amplifier SO HEARING RESEARCH LA English DT Article DE acoustic two-tone distortion; low-frequency biasing; salicylate; DC current; cochlear amplifier; gain; operating point ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; LOW-FREQUENCY SOUND; BASILAR-MEMBRANE; OTOACOUSTIC EMISSIONS; MOUSE COCHLEA; PTERONOTUS-PARNELLII; TRANSDUCER CURRENTS; MAMMALIAN COCHLEA; RESPONSES AB Acoustic two-tone distortions are generated during non-linear mechanical amplification in the cochlea. Generation of the cubic distortion 2f1-f2 depends on asymmetric components of a non-linear transfer function whereas the difference tone f2-f1 relies on symmetric components. Therefore, a change of the operating point and hence the symmetry of the cochlear amplifier could be strongly reflected in the level of the f2-f1 distortion. To test this hypothesis, low-frequency tones (5 Hz) were used to bias the position of the cochlear partition in the gerbil. Phase-correlated changes of f2-f1 occurred at bias tone levels where there were almost no effects on 2f1-f2. Higher levels of the bias tone induced pronounced changes of both distortions. These results are qualitatively in good agreement with the results of a simulation in which the operating point of a Boltzman Function was shifted. This function is similar to those used to describe outer hair cell (OHC) transduction. To influence OHC motility, salicylate was injected. It caused a decrease of the 2f1-f2 level and an increase in the level of f2-f1. Such reciprocal changes of both distortions, again, can be interpreted in terms of a shift of the operating point of the cochlear amplifier along a non-linear transfer characteristic. To directly influence the cochlear amplifier, DC current was injected into the scala media. Large negative currents(> -2 mu A) caused a pronounced decrease of 2f1-f2 (> 15 dB) and positive currents had more complex effects with increasing and/or decreasing 2f1-f2 distortion level. The effects were time and primary level dependent. Changes of f2-f1 for DC currents > \mu 2A\ were in most cases larger compared to 2f1-f2 and reversed for certain primary levels. The current effects probably result from a combination of changing the endocochlear potential and shifting the operating point along a non-linear transfer function. RP Frank, G (reprint author), UNIV MUNICH, INST ZOOL, LUISENSTR 14, D-80021 MUNICH, GERMANY. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 104 EP 115 DI 10.1016/0378-5955(96)00083-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100011 PM 8880185 ER PT J AU Clerici, WJ Hensley, K DiMartino, DL Butterfield, DA AF Clerici, WJ Hensley, K DiMartino, DL Butterfield, DA TI Direct detection of ototoxicant-induced reactive oxygen species generation in cochlear explants SO HEARING RESEARCH LA English DT Article DE cochlea; electron paramagnetic resonance spectrometry; free radical; ototoxicity; reactive oxygen species ID ELECTRON-PARAMAGNETIC-RESONANCE; OUTER HAIR-CELLS; GUINEA-PIG; ETHACRYNIC-ACID; IN-VITRO; CISPLATIN OTOTOXICITY; SUPEROXIDE-DISMUTASE; RADICAL SCAVENGERS; ANTIOXIDANT SYSTEM; RAT HEPATOCYTES AB The proposal that free-radical generation contributes to the ototoxicities of several chemical agents was studied utilizing electron paramagnetic resonance (EPR) spectrometry to detect directly ototoxicant-induced reactive oxygen species formation in cochlear tissue. Guinea pig cochlear explants in chelexed artificial perilymph (AP; 200 mu l) were exposed to an ototoxicant or AP for 10 min. Ototoxic agents included gentamicin sulfate (4.0 mM), kanamycin monosulfate (4.0 mM), ethacrynic acid (0.5 mM), furosemide (0.3 mM), cisplatin (0.1 mM), trimethyltin chloride (0.1 mM), and quinine HCl (3.0 mM). Following incubation, 20 mu l of AP/ototoxicant mixture was replaced by the filtered spin trap, 5,5-dimethylpyrroline-N-oxide (DMPO). After 10 min, the EPR spectrum of the mixture was obtained. Four line EPR spectra of relative intensities 1:2:2:1, associated with hydroxyl radical (OH)/DMPO adduct formation, were evidenced by reaction mixtures containing cochlear explants exposed to each ototoxicant. Cisplatin, quinine and the loop diuretics produced weak OH-associated EPR signals in the absence of a cochlear explant, which were amplified in its presence. Deferoxamine quenched all OH spectral peaks. Peroxide levels, assayed in parallel experiments, were diminished by each ototoxicant relative to those seen following AP exposure, suggesting possible H2O2 conversion to OH. These data support the proposal that various ototoxic agents are capable of reactive oxygen species generation or promotion in cochlear tissues. C1 UNIV KENTUCKY,COLL MED,DEPT SURG,LEXINGTON,KY 40536. UNIV KENTUCKY,COLL MED,DEPT CHEM,LEXINGTON,KY 40536. UNIV KENTUCKY,COLL MED,COLL MEMBRANE SCI,LEXINGTON,KY 40536. CR ALI SF, 1992, NEUROTOXICOLOGY, V13, P637 BANNON AW, 1993, NEUROTOXICOLOGY, V14, P437 BARANAK CC, 1988, J NEURO-ONCOL, V6, P261, DOI 10.1007/BF00163711 BOSHER SK, 1980, ACTA OTO-LARYNGOL, V89, P407, DOI 10.3109/00016488009127156 BRANDON RJ, 1984, J MED CHEM, V27, P861, DOI 10.1021/jm00373a009 BRUMMETT RE, 1975, ACTA OTO-LARYNGOL, V80, P86, DOI 10.3109/00016487509121305 BUSZMAN E, 1984, BIOCHEM PHARMACOL, V33, P7, DOI 10.1016/0006-2952(84)90363-0 Butterfield D. 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Res. PD SEP 1 PY 1996 VL 98 IS 1-2 BP 116 EP 124 DI 10.1016/0378-5955(96)00075-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100012 PM 8880186 ER PT J AU Lichtenstein, V Stapells, DR AF Lichtenstein, V Stapells, DR TI Frequency-specific identification of hearing loss using transient-evoked otoacoustic emissions to clicks and tones SO HEARING RESEARCH LA English DT Article DE evoked otoacoustic emission; click; tone; sensorineural hearing loss; test performance ID BRAIN-STEM RESPONSES; CLINICAL-APPLICATIONS; ACOUSTIC EMISSIONS; NOTCHED NOISE; IMPAIRED SUBJECTS; EARS; INFANTS; THRESHOLDS; AUDIOMETRY; POTENTIALS AB Transient-evoked otoacoustic emissions (TEOAE) to clicks and to 500- and 2000-Hz brief tones were measured in 72 normal-hearing and hearing-impaired subjects (86 ears). The TEOAE's reproducibility parameter was used for the analyses. The purpose of the investigation was to determine which stimuli best predicted the presence of sensorineural hearing loss in a frequency-specific manner at 500, 1000, 2000, and 4000 Hz. Analyses of the TEOAEs filtered into frequency-specific bands showed that separation of normal and impaired ears at 1000, 2000 and 4000 Hz was best achieved by TEOAEs evoked by clicks. Identification of hearing loss al 500 Hz was best obtained using 500-Hz tone-evoked TEOAEs filtered using a band centered at 500 Hz. Octave- and half-octave-wide bands identified hearing loss equally well. An analysis sweep time of 20 ms provided slightly better results compared to 30 ms, except for 500 Hz, where the 30-ms sweep time slightly improved the identification of hearing loss. Increases in the audiometric criterion did not yield better test performance once hearing loss exceeded 20 dB HL. The findings from this study suggest that the combination of bandpass-filtered TEOAEs to clicks and TEOAEs to 500-Hz tones identifies with reasonable accuracy ears with sensorineural hearing loss at 500, 1000, 2000, and 4000 Hz. C1 UNIV BRITISH COLUMBIA,SCH AUDIOL & SPEECH SCI,VANCOUVER,BC V6T 1Z3,CANADA. ALBERT EINSTEIN COLL MED,AUDITORY EVOKED POTIENTIAL LABS,BRONX,NY 10461. CUNY GRAD SCH & UNIV CTR,PH D PROGRAM SPEECH & HEARING SCI,NEW YORK,NY 10036. 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PD SEP 1 PY 1996 VL 98 IS 1-2 BP 125 EP 136 DI 10.1016/0378-5955(96)00084-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100013 PM 8880187 ER PT J AU Felsheim, C Ostwald, J AF Felsheim, C Ostwald, J TI Responses to exponential frequency modulations in the rat inferior colliculus SO HEARING RESEARCH LA English DT Article DE auditory system; FM; modulation rate tuning; direction selective; single unit ID PRIMARY AUDITORY-CORTEX; STIMULI; NEURONS; TONES; SENSITIVITY; ORGANIZATION; TOPOGRAPHY; AMPLITUDE; SYSTEM; SWEEPS AB We examined responses to pure tones and exponentially frequency-modulated (FM) stimuli in the inferior colliculus of ketamine anesthetized rats. All units responded to both pure-tone and FM stimulation: units responding selectively to FM stimuli were not found. The comparison between responses to many different FM sweeps revealed that activity was elicited when the instantaneous frequency of a FM sweep entered the unit's pure-tone tuning curve. Units were tuned to the rate of frequency modulation. Most modulation rate transfer functions had bandpass characteristics. Best modulation rates covered a range from 4.8 to 1904 octaves/s with more than 90% between 10 and 400 octaves/s. In contrast to previous studies, modulation direction was not coded in unit responses and only few units demonstrated a weak change in response strength when sweep direction was altered. This is at least partly attributable to the FM stimulus design which, in the present study, was adapted to the logarithmic frequency representation in the rat auditory system and carefully matched to the units' pure-tone response area. In spite of the close relationship between pure tone and FM response behavior, modulation rate tuning cannot be completely explained on the basis of the units' pure-tone responses. RP Felsheim, C (reprint author), UNIV TUBINGEN,DEPT ANIM PHYSIOL,MORGENSTELLE 28,D-72076 TUBINGEN,GERMANY. 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PD SEP 1 PY 1996 VL 98 IS 1-2 BP 137 EP 151 DI 10.1016/0378-5955(96)00078-0 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100014 PM 8880188 ER PT J AU Chen, L Trautwein, PG Shero, M Salvi, RJ AF Chen, L Trautwein, PG Shero, M Salvi, RJ TI Tuning, spontaneous activity and tonotopic map in chicken cochlear ganglion neurons following sound-induced hair cell loss and regeneration SO HEARING RESEARCH LA English DT Article DE chicken; acoustic trauma; hair cell regeneration; tuning curve; spontaneous activity; frequency-place map ID SEVERE ACOUSTIC TRAUMA; BASILAR PAPILLA; ADULT CHICKENS; INTENSE SOUND; INNER-EAR; DISCHARGE PATTERNS; RECOVERY; ORGANIZATION; EXPOSURE; OVERSTIMULATION AB Adult chickens were exposed for 48 h to a 525 Hz, 120 dB SPL tone that destroyed the hair cells and tectorial membrane in a crescent-shaped patch along the abneural edge of the basilar papilla. Single-unit recordings were obtained from cochlear ganglion neurons 0-1, 5, 14 and 28 days post-exposure to determine what effect the cochlear lesion had on neural discharge patterns and if the discharge patterns fully recovered. Immediately after exposure, the tuning curves were extremely broad and CF thresholds were elevated by 30-40 dB. In addition, the average spontaneous rate and percentage of neurons with interspike interval histograms with preferred intervals were greatly reduced. Tuning curves and spontaneous activity started to recover by 5 days post-exposure; however, some W-shaped tuning curves with two distinct tips and a hypersensitive tail were observed at this time. W-shaped tuning curves disappeared and spontaneous activity recovered to normal levels 14-28 days post-exposure. However, the CF thresholds of the most sensitive neurons were still slightly elevated, tuning curve slopes below CF were shallower than normal, and thresholds in the low-frequency tail of the tuning curves were often hypersensitive. These functional deficits were most closely associated with residual damage to the upper fibrous layer of the tectorial membrane. To determine if the cochlear frequency-place map was altered by the cochlear lesion, four physiologically characterized neurons were labeled with biocytin at 5 days post-exposure. The CFs of the labeled neurons were consistent with the normal frequency-place map (Chen et al. (1994) Hearing Research 81, 130-136) indicating that the tonotopic map was not altered. RP Chen, L (reprint author), SUNY BUFFALO, DEPT COMMUNICAT DISORDERS & SCI, HEARING RES LABS, 215 PARKER HALL, BUFFALO, NY 14214 USA. 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PD SEP 1 PY 1996 VL 98 IS 1-2 BP 152 EP 164 DI 10.1016/0378-5955(96)00086-X PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100015 PM 8880189 ER PT J AU Wit, HP vanDijk, P Segenhout, HM AF Wit, HP vanDijk, P Segenhout, HM TI Frequency response for electromotility of isolated outer hair cells of the guinea pig SO HEARING RESEARCH LA English DT Article DE wiener kernel; cochlea; length change; motor function ID MOTILITY AB Frequency and impulse responses were determined for isolated guinea pig outer hair cells by electrically stimulating the cells between two wire electrodes with white noise. Cells were attached to the bottom of a small culture dish at one end while the other end was freely moving. Results have the character of a damped second-order system, with a cut-off frequency of approximately 7 kHz. Correspondingly. impulse responses show a single narrow peak roughly 50 mu s wide and have the shape of the impulse response for a critically damped harmonic oscillator. RP Wit, HP (reprint author), UNIV GRONINGEN HOSP,DEPT EXPT OTOLARYNGOL,POB 30 001,NL-9700 RB GRONINGEN,NETHERLANDS. RI Van Dijk, Pim/E-8019-2010 OI Van Dijk, Pim/0000-0002-8023-7571 CR Brownell W. 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PD SEP 1 PY 1996 VL 98 IS 1-2 BP 165 EP 168 DI 10.1016/0378-5955(96)00082-2 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100016 PM 8880190 ER PT J AU Waller, HJ Godfrey, DA Chen, KJ AF Waller, HJ Godfrey, DA Chen, KJ TI Effects of parallel fiber stimulation on neurons of rat dorsal cochlear nucleus SO HEARING RESEARCH LA English DT Article DE slice; spontaneous activity; glutamate; non-NMDA receptor; cartwheel cell; fusiform cell ID GUINEA-PIG; INTRACELLULAR-RECORDINGS; GRANULE CELLS; IN-VITRO; MICE; SLICES; INVITRO; CAT; CARTWHEEL; GOLGI AB We have compared the effects of parallel fiber stimuli on extracellularly recorded neurons showing regular or bursting spontaneous activity patterns in the dorsal cochlear nucleus of rat brainstem slices. Ninety percent of regular neurons failed to respond to stimulus currents (1.4 +/- 0.28 mA, mean +/- SEM) significantly greater than those (0.4 +/- 0.07 mA) that elicited responses from 96% of bursting neurons. Responses of bursting neurons were elicited from widely separated loci along the molecular layer. Kynurenic acid and CNQX or DNQX blocked both spontaneous firing and responses to parallel fiber stimuli of bursting neurons. The same agents also blocked responses of regular neurons but had little or no effect on their spontaneous firing rates. AP-5 caused small decreases in spontaneous rates of both bursting and regular neurons but did not appear to affect responses to stimuli. The data support the hypothesis that the responses of both regular and bursting neurons to parallel fiber stimulation are mediated by glutamate, acting mainly through non-NMDA receptors. Spontaneous activity of bursting, but not regular, neurons also requires non-NMDA glutamatergic transmission, suggesting that the spontaneous firing of bursting neurons, consisting largely of cartwheel cells, may depend upon granule cell activity. C1 MED COLL OHIO, DEPT OTOLARYNGOL, TOLEDO, OH 43699 USA. RP Waller, HJ (reprint author), MED COLL OHIO, DEPT NEUROL SURG, POB 10008, TOLEDO, OH 43699 USA. 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J., 1994, Society for Neuroscience Abstracts, V20, P137 WALLER HJ, 1994, ABSTR ASS RES OT, V17, P12 WICKESBERG RE, 1994, J COMP NEUROL, V339, P311, DOI 10.1002/cne.903390302 WICKESBERG RE, 1989, BRAIN RES, V486, P39, DOI 10.1016/0006-8993(89)91275-4 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1398 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1409 ZHANG S, 1994, J NEUROPHYSIOL, V71, P914 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1384 NR 36 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 SEP 1 PY 1996 VL 98 IS 1-2 BP 169 EP 179 DI 10.1016/0378-5955(96)00090-1 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VH191 UT WOS:A1996VH19100017 PM 8880191 ER PT J AU Wang, Y Raphael, Y AF Wang, Y Raphael, Y TI Re-innervation patterns of chick auditory sensory epithelium after acoustic overstimulation SO HEARING RESEARCH LA English DT Article DE chick; synapsin; regeneration; acoustic trauma; hair cell; efferent ID HAIR CELL REGENERATION; AVIAN INNER-EAR; INTENSE SOUND EXPOSURE; PROTEIN-KINASE-II; SYNAPSIN-I; BASILAR PAPILLA; BINDING-PROTEIN; NEONATAL CHICK; TRAUMA; RECOVERY AB There is evidence from several studies showing that sensory cells which are destroyed by trauma in the chick auditory epithelium are replaced by new cells. The fate of neurons that innervate the injured and degenerating sensory cells in the lesion, and the temporal sequence of re-innervation of regenerated hair cells are not well understood. This study examined efferent terminals in the chick auditory sensory epithelium following acoustic overstimulation using synapsin-specific immunocytochemistry. Chicks were exposed to an octave band noise (1.5 kHz center frequency, 116 dB SPL, 16 h) and killed on each day from 0 to 9 days postexposure. In the proximal half of control whole mounts of the basilar papillae, synapsin-specific immunoreactivity stained efferent terminals throughout the abneural portion of the sensory epithelium (the short hair cell region). In this area, the labeling appeared as 2-3 bouton-shaped clusters along the abneural edge of each hair cell. After acoustic overstimulation, a lesion was observed at the abneural edge of the papilla where many short hair cells were lost. The center of the lesion was located at 40% distance from the proximal end of each traumatized papilla. Synapsin-specific labeling was not found in sites where expanded supporting cells had replaced missing hair cells. Hair cells which survived the trauma exhibited a shrunken apical area, and synapsin-labeled boutons were observed near their basal domains. New hair cells, which first appeared in the papilla 4 days after trauma, were not initially associated with synapsin-labeled boutons. Regenerated hair cells first displayed contacts with synapsin-labeled boutons 7 days after trauma. Nine days after acoustic overstimulation? most new hair cells appeared to be associated with synapsin-labeled boutons which resembled the normal horseshoe configuration of efferent terminals. The data su est that direct contact with functional efferent synapses is not necessary for the generation and differentiation of new hair cells. C1 UNIV MICHIGAN,SCH MED,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 11 EP 18 DI 10.1016/S0378-5955(96)80003-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900002 PM 8844182 ER PT J AU Freeman, S Cherny, L Sohmer, H AF Freeman, S Cherny, L Sohmer, H TI Thyroxine affects physiological and morphological development of the ear SO HEARING RESEARCH LA English DT Article DE auditory nerve brainstem response; otoacoustic emission; distortion product; development; rat ID PRODUCT OTOACOUSTIC EMISSIONS; ACOUSTIC DISTORTION PRODUCTS; RAT CEREBELLAR CORTEX; 2 DISCRETE SOURCES; OUTER HAIR-CELLS; POSTNATAL-DEVELOPMENT; EARLY HYPOTHYROIDISM; BASILAR-MEMBRANE; ETHACRYNIC-ACID; NEONATAL RATS AB The onset and development of distortion product otoacoustic emissions (DPE) representing cochlear amplifier activity were studied in neonatal hyperthyroid (n = 10) and control (n = 10) rat pups. These were compared to the onset and development of auditory nerve-brainstem evoked responses (ABR) representing overall cochlear function, and to morphological development of the ear. DPEs were recorded at an earlier postnatal age to high (8 kHz) frequencies and progressed to lower (3 kHz) frequencies with age. ABRs to high-intensity clicks were recorded at least 2 days before DPEs, although DPE onset at 8 kHz preceded adult-like ABR thresholds. Both ABR and DPEs appeared earlier in the hyperthyroid rats. Histological evidence showed earlier morphological development of the ear in these animals. ABR thresholds and DPE amplitudes matured at a slower rate in the experimental group despite their earlier onset. There was no difference in ABR and DPE thresholds between adult hyperthyroid and control rats. However, in the experimental group, DPEs had smaller amplitudes to high (70 dB SPL) and to low (50 dB SPL) stimulus intensities at low frequencies. Hence, despite thyroxine-injected rat pups having earlier onset of auditory structure and function (lower ABR thresholds and earlier functioning active cochlear amplifier), it appeared that neonatal hyperthyroidism affected the later state of the cochlea, such that DPEs, especially to low-frequency stimuli, were depressed during and after maturation. C1 TEL AVIV UNIV,FAC LIFE SCI,DEPT ZOOL,RAMAT AVIV,ISRAEL. RP Freeman, S (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 12272,IL-91120 JERUSALEM,ISRAEL. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 19 EP 29 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900003 PM 8844183 ER PT J AU Merchant, SN Ravicz, ME Rosowski, JJ AF Merchant, SN Ravicz, ME Rosowski, JJ TI Acoustic input impedance of the stapes and cochlea in human temporal bones SO HEARING RESEARCH LA English DT Article DE cochlear impedance; stapes impedance; acoustic load on middle ear ID MIDDLE-EAR MECHANICS; V TYMPANOPLASTY; VIBRATION; MODEL; CAT; IV AB The acoustic input impedance of the stapes and cochlea Z(SC) represents the mechanical load driven by the tympanic membrane, malleus and incus. Z(SC) was calculated from broad-band measurements (20 Hz to 11 kHz) of stapes displacement made with an optical motion sensor and of sound pressure at the stapes head in a human temporal-bone preparation. Measurements were made in 12 fresh temporal bones with the round window insulated from the sound stimulus. Below 1 kHz, the magnitude of Z(SC) was approximately inversely proportional to frequency, and Z(SC) angle was between -0.10 and -0.20 periods, This behavior is consistent with a mixed stiffness and resistance. Between 1 and 4 kHz, Z(SC) was resistance-dominated with a magnitude between 40 and 100 mks acoustic GR that was roughly independent of frequency, and its angle was between -0.12 and 0 periods. Between 4 and 7 kHz, the magnitude of Z(SC) was either constant or increased with frequency while Z(SC) angle was near 0. Between 7 and 8 kHz, both Z(SC) magnitude and angle decreased sharply with frequency, and both increased somewhat at higher frequencies. The input impedance of the cochlea Z, was estimated in one ear from Z(SC) measurements made before and after draining the inner ear fluids. Z(C) was stiffness-dominated below 100 Hz, and resistance-dominated from 100 Hz to 5 kHz. The frequency-dependent magnitude of Z(SC) in our bones is similar to those reported by other investigators in cadaver temporal bones (Nakamura et al., 1992; Kurokawa and Goode, 1995). Our Z(SC) measurements are qualitatively similar to theoretical predictions (Zwislocki, 1962; Kringlebotn, 1988), but are a factor of 3 greater in magnitude, implying that Z(SC) may be more resistive and stiffer than previously thought. We found inter-ear variations of a factor of 4 (12 dB), which may explain some of the clinically observed variations in size of the air-bone gap in individuals with middle ear lesions or after middle-ear reconstructive surgery. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. RP Merchant, SN (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114, USA. 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J., 1975, NERVOUS SYSTEM, P45 NR 37 TC 80 Z9 81 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1996 VL 97 IS 1-2 BP 30 EP 45 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900004 PM 8844184 ER PT J AU Szczepaniak, WS Moller, AR AF Szczepaniak, WS Moller, AR TI Effects of (-)-baclofen, clonazepam, and diazepam on tone exposure-induced hyperexcitability of the inferior colliculus in the rat: Possible therapeutic implications for pharmacological management of tinnitus and hyperacusis SO HEARING RESEARCH LA English DT Article DE plasticity; auditory evoked potential; tinnitus; baclofen; clonazepam; diazepam ID UNILATERAL COCHLEAR ABLATION; AGE-RELATED DECREASE; EVOKED-POTENTIALS; AUDITORY-CORTEX; TEMPORAL INTEGRATION; ADULT MAMMALS; INTENSE SOUND; GUINEA-PIGS; NUCLEUS; NEURONS AB Recent investigations in the authors' laboratory have shown that acute tone exposure (4 kHz continuous tone, 104 dB sound pressure level (SPL), 30-min duration) induces increases in the amplitude of click-evoked potentials in the inferior colliculus (IC). These increases have been attributed to a decrease in GABA(A)-mediated inhibition on IC neurons. In the present study, we examined the effects of three compounds (diazepam, clonazepam, and (-)-baclofen) that are known to enhance GABAergic inhibition on these tone exposure-induced increases and on changes in temporal integration in the IC. (-)-Baclofen was the only one of the three compounds tested that reversed in a dose-dependent manner the effects of tone exposure on both the amplitude of the click-evoked potentials recorded from the IC and on measures of the changes in temporal integration based on these potentials. Diazepam and clonazepam exhibited remarkably different effects on the click-evoked potentials recorded from the surface of the IC. Diazepam caused a dose-dependent decrease in one of the components of the IC potentials that reflects postsynaptic activity in the IC, whereas clonazepam caused a dose-dependent decrease in a peak that reflects input to the IC from the superior olivary complex (SOC). At dosages up to 40 mg/kg, neither diazepam nor clonazepam reversed the changes in temporal integration in the IC that were induced by the tone exposure; diazepam caused a small, but statistically significant, enhancement of the effects of tone exposure on this function. The results of this study show that (-)-baclofen is a potent modulator of both the excitability of neurons in the ascending auditory pathway and the processing of auditory information by IC neurons. The finding of the present study that two benzodiazepines (clonazepam and diazepam) have remarkably different effects on evoked potentials, which reflects both input to the IC and postsynaptic events in the IC neurons, suggests heterogenicity of the GABA(A) receptor from one structure to another in the ascending auditory pathway. We suggest that (-)-baclofen may be clinically useful in treating disorders of the auditory system that are caused by plasticity in the ascending auditory pathway. C1 UNIV PITTSBURGH,SCH MED,DEPT NEUROL SURG,PITTSBURGH,PA 15213. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 46 EP 53 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900005 PM 8844185 ER PT J AU Cosgrove, D Samuelson, G Pinnt, J AF Cosgrove, D Samuelson, G Pinnt, J TI Immunohistochemical localization of basement membrane collagens and associated proteins in the murine cochlea SO HEARING RESEARCH LA English DT Article DE cochlea; basement membrane; immunohistology ID HEPARAN-SULFATE PROTEOGLYCAN; RECESSIVE ALPORT SYNDROME; IV COLLAGEN; EXTRACELLULAR-MATRIX; CORE PROTEIN; INNER-EAR; IDENTIFICATION; FIBRONECTIN; LAMININ; EXPRESSION AB Immunohistochemistry using antibodies specific for each of the basement membrane collagen chains was used to assess the location and composition of basement membranes in the mouse cochlea. The classical chains (COL4A1, 4A2) localized primarily in the osseous spiral lamina and in the capillaries of the spiral ligament. In contrast, the novel collagen chains (4A3, 4A4, and 4A5) localized to the interdental cells of the sulcus, the inner sulcus, the basilar membrane, and the region of type II fibrocytes in the spiral ligament. Antibodies against type 4A5 collagen also heavily stained the stria vascularis. Weak staining in the stria was observed with antibodies against 4A3. Basement membrane-associated proteins were also assessed. The basement membrane in the perineurium of the osseous spiral lamina immunostained using antibodies against laminin, heparan sulfate proteoglycan, and entactin. The basilar membrane contained only fibronectin in association with the novel collagen chains. The capillaries of the spiral ligament and the stria vascularis stained heavily for heparin sulfate proteoglycan and laminin. Generalized staining for laminin was observed in the spiral ligament. These results indicate that an abundance of basement membrane collagen containing extracellular matrix exists in the murine cochlea and that the composition of these matrices are surprisingly varied and tissue specific. RP Cosgrove, D (reprint author), BOYS TOWN NATL RES HOSP,DEPT GENET,555 N 30TH ST,OMAHA,NE 68131, USA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 54 EP 65 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900006 PM 8844186 ER PT J AU Jacobson, GP Calder, JA Newman, CW Peterson, EL Wharton, JA Ahmad, BK AF Jacobson, GP Calder, JA Newman, CW Peterson, EL Wharton, JA Ahmad, BK TI Electrophysiological indices of selective auditory attention in subjects with and without tinnitus SO HEARING RESEARCH LA English DT Article DE tinnitus; evoked potential; selective auditory attention ID EVOKED MAGNETIC-FIELDS; TONOTOPIC ORGANIZATION; NEURONAL-ACTIVITY; HUMAN-BRAIN; LOCALIZATION; POTENTIALS; CORTEX; NEGATIVITY; COMPONENT AB The present investigation was conducted in an attempt to determine whether selective auditory attention abilities differed between normal subjects and subjects with bothersome tinnitus. Subjects were 37 adults with tinnitus and high-frequency hearing loss (not affecting thresholds at 500 and 1000 Hz) and 15 subjects who were audiometrically and otologically normal. Results suggested that an electrophysiological index of early selective auditory attention (i.e., the negative difference wave, Nd) was of greater magnitude in tinnitus patients. Also, the cortical N1 component occurred significantly later in the presence of selective attention in tinnitus subjects only. Results of this investigation may support the view that early selective auditory attention in subjects with bothersome tinnitus differs from that of normal subjects. C1 CLEVELAND CLIN FDN,DIV AUDIOL,CLEVELAND,OH 44195. HENRY FORD HOSP,DIV BIOSTAT & RES EPIDEMIOL,DETROIT,MI 48202. HENRY FORD HOSP,DEPT NEUROL,DETROIT,MI 48202. RP Jacobson, GP (reprint author), HENRY FORD HOSP,DIV AUDIOL,2799 W GRAND BLVD,DETROIT,MI 48202, USA. 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L., 1990, EVENT RELATED BRAIN, P178 YAMAMOTO T, 1988, P NATL ACAD SCI USA, V85, P8732, DOI 10.1073/pnas.85.22.8732 NR 31 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 AUG PY 1996 VL 97 IS 1-2 BP 66 EP 74 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900007 PM 8844187 ER PT J AU Gerken, GM AF Gerken, GM TI Central tinnitus and lateral inhibition: An auditory brainstem model SO HEARING RESEARCH LA English DT Article DE tinnitus; hearing loss; aging; lateral inhibition; inferior colliculus; neural model ID RAT INFERIOR COLLICULUS; MIDDLE LATENCY RESPONSE; AGE-RELATED DECREASE; ELECTRICAL-STIMULATION; COCHLEAR NUCLEUS; NEURONS; SYSTEM; GABA; CAT; MECHANISMS AB Central tinnitus is used herein either to designate a tinnitus that originates in the central auditory system, or to refer to a component of a peripherally generated tinnitus that is exaggerated by auditory brain mechanisms. Findings from several research areas contribute to this analysis of central tinnitus. The inferior colliculus, in particular, is significant because of the distribution of lateral inhibition in this nucleus and because of the possible change in inhibition that follows hearing loss. There is also a convergence of auditory and non-auditory functions at inferior colliculus. One non-auditory function, the initiation of aversive behavioral responses, may be demonstrated with electrical or chemical stimulation of auditory nuclei in the vicinity of the midbrain. With reduction of central inhibition through hearing loss or aging, tinnitus activity may gain easier access to those subsystems that produce aversive responses. A neural model, conceptually based in inferior colliculus, assumes a pattern of lateral inhibition that is influenced by the distribution of cochlear pathology. Of special importance are the abrupt changes across the tonotopically organized outputs from the cochlea that are reflected in behavioral measures as an 'audiometric edge'. The neural response properties that derive from this assumption are related to properties of central tinnitus. C1 UNIV TEXAS,SW MED CTR,DEPT OTORHINOLARYNGOL,DALLAS,TX 75235. RP Gerken, GM (reprint author), UNIV TEXAS,CALLIER CTR COMMUN DISORDERS,1966 INWOOD RD,DALLAS,TX 75235, USA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 75 EP 83 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900008 PM 8844188 ER PT J AU Schweitzer, L Lutz, C Hobbs, M Weaver, SP AF Schweitzer, L Lutz, C Hobbs, M Weaver, SP TI Anatomical correlates of the passive properties underlying the developmental shift in the frequency map of the mammalian cochlea SO HEARING RESEARCH LA English DT Article DE hearing; frequency; place code; basilar membrane; cochlear mechanics ID OUTER HAIR-CELLS; MONGOLIAN GERBIL; BASILAR-MEMBRANE; POSTNATAL-DEVELOPMENT; INFERIOR COLLICULUS; PLACE PRINCIPLE; REPRESENTATION; STIFFNESS; ONTOGENY; ONSET AB As the cochlea develops, the cells in the basal cochlea become sensitive to progressively higher frequencies. To identify features of cochlear morphology that may underlie the place code shift, measurements of infant and adult gerbil cochleas were made at both the light and electron microscopic levels. The measurements included areas of the cochlear duct, basilar membrane, and organ of Corti, height and width of the basilar membrane, thickness of the tympanic cover layer, thickness of the upper and lower basilar membrane fiber bands, and optical density of the basilar membrane. The results indicated that basilar membrane dimensions do not change as the place code shifts and that regions that code for the roughly the same frequency (e.g., approximate to 11.2 kHz) at different ages can have basilar membranes of very different dimensions. In contrast, the size of the organ of Corti and the thickness of fiber bands inside the basilar membrane do change in ways consistent with the shift in the frequency map. RP Schweitzer, L (reprint author), UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292, USA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 84 EP 94 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900009 PM 8844189 ER PT J AU Marco, RAW Hoffman, LF Wackym, PA Micevych, PE Popper, P AF Marco, RAW Hoffman, LF Wackym, PA Micevych, PE Popper, P TI Distribution of calcitonin gene-related peptide immunoreactivity in vestibular efferent neurons of the chinchilla SO HEARING RESEARCH LA English DT Article DE calcitonin gene-related peptide; vestibular efferent; immunohistochemistry; in-situ hybridization ID MESSENGER-RNA; HORSERADISH-PEROXIDASE; END-ORGANS; INNER-EAR; RAT; SYSTEM; LOCALIZATION; TRANSMISSION; EXPRESSION AB The distribution of calcitonin gene-related peptide immunoreactivity (CGRPi) within efferent vestibular neurons in the chinchilla was investigated using fluorescent retrograde labeling combined with immunohistochemistry. Efferent vestibular neurons were found bilaterally in clusters: dorsolateral (group E1) and medial (group E2) to the genu of CN VII, as well as ventromedial to the descending CN VII fibers in the parvicellular reticular formation (PCR). The percentage of retrogradely labeled cells containing CGRPi was 77.1 +/- 5.7 for group E1 neurons, 90.3 +/- 3.8 in the E2 region. Among the PCR efferents more then half of the neurons (61.4 +/- 19.9%) expressed CGRP peptide or message. The wide distribution of CGRP among vestibular efferent neurons suggests that CGRP plays an important role in vestibular efferent function. In addition, the differential distribution among the groups of vestibular efferent neurons suggests that efferent modulation of vestibular function is different between the E cell group efferent neurons and the PCR efferent neurons. C1 UNIV CALIF LOS ANGELES,SCH MED,DIV HEAD & NECK SURG,GOODHILL EAR CTR,LAB VESTIBULAR NEUROSCI,LOS ANGELES,CA 90095. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 95 EP 101 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900010 PM 8844190 ER PT J AU McFadden, D Loehlin, JC Pasanen, EG AF McFadden, D Loehlin, JC Pasanen, EG TI Additional findings on heritability and prenatal masculinization of cochlear mechanisms: Click-evoked otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; heritability; prenatal auditory effect; hearing sensitivity; sex difference; ear difference; twins ID OPPOSITE-SEX TWINS; HEARING SENSITIVITY; DISTORTION PRODUCTS; ACOUSTIC EMISSIONS; MENSTRUAL-CYCLE; BREAST-CANCER; FREQUENCY; HORMONES; ASPIRIN; PREVALENCE AB A previous demonstration of a substantial genetic contribution to the expression of spontaneous otoacoustic emissions (SOAEs) is here extended to an aspect of click-evoked otoacoustic emissions (CEOAEs). CEOAEs were measured in the same twins and non-twins used for the SOAE heritability study. The stimuli were 100-mu s clicks presented at a nominal rate of 2/s; the emitted waveforms from 50 clicks were summed, and a 20-ms sample of that averaged waveform (beginning 6 ms after click presentation) was subjected to spectral analysis, The total power in the spectrum from 1 to 5 kHz in this temporal segment of the CEOAE waveform was used as the primary dependent variable. This overall power was significantly greater in female and right ears than in male and left ears, but the difference between dark- and light-eyed subjects was not significant. The overall power in the two left, and two right, ears of monozygotic co-twins was more highly correlated than in dizygotic co-twins, and structural modeling indicated that about 65-85% of the individual variation in the expression of CEOAE power could be attributed to genes-essentially the same heritability estimate as obtained previously from the SOAE data. Within-subject correlations between CEOAE power and number of SOAEs ranged from about 0.3 to 0.7, suggesting that these two forms of otoacoustic emission may depend upon somewhat different aspects of the same underlying mechanism and, thus, that heritability estimates based on one measure are not completely redundant to those from the other. While the average spectral power of the CEOAEs in opposite-sex dizygotic (OSDZ) females was smaller than that in same-sex dizygotic (SSDZ) females-and thus approached the value for males-the difference did not achieve statistical significance. Thus, the evidence for a prenatal masculinizing effect was less definitive in these CEOAE data than in the SOAE data obtained from the same subjects. An interpretation that accounts for both the CEOAE and SOAE results is that the strength of the so-called cochlear amplifiers is under genetic control that is to some extent mediated and/or modified through prenatal exposure to androgens. The indicated direction of effect is that weak cochlear amplifiers result when prenatal androgen levels are high. Under this view, then, androgen levels contribute both to the sex differences observed in otoacoustic emissions and the prenatal masculinizing effects observed in opposite-sex twins, and they may be a factor in individual differences in OAE expression as well. Additionally it is shown that, although the powers of the CEOAE waveforms were reasonably highly correlated for the two ears of subjects in all groups, and across MZ co-twins, cross-correlations on the fine structures of those same pairs of CEOAE waveforms were essentially zero-presumably owing largely to the synchronizing of (different) SOAE frequencies in the ears being compared. C1 UNIV TEXAS,INST NEUROSCI,AUSTIN,TX 78712. RP McFadden, D (reprint author), UNIV TEXAS,DEPT PSYCHOL,MEZES HALL 330,AUSTIN,TX 78712, USA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 102 EP 119 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900011 PM 8844191 ER PT J AU Khvoles, R Freeman, S Sohmer, H AF Khvoles, R Freeman, S Sohmer, H TI Transient evoked otoacoustic emissions can be recorded in the rat SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; animal; transient; evoked; rat ID ACOUSTIC DISTORTION PRODUCTS; 2 DISCRETE SOURCES; GUINEA-PIG; PHYSIOLOGICAL VULNERABILITY; NORMALLY-HEARING; RABBIT; ORGAN; CORTI AB Transient (click) evoked (TEOAE) and distortion product (DPOAE) otoacoustic emissions can be recorded in most normal human ears. Even though DPOAEs have been recorded in many laboratory animals, there has not been much success in recording TEOAEs in non-primate mammals except for guinea pigs. In this study, TEOAEs were unequivocally recorded in every rat (and guinea pig) ear studied by using short pulses (40 mu s) to generate the clicks and a short (1.1 ms) amplifier gain suppression period. The responses were reproducible in the same rat, above the noise floor and disappeared post-mortem They were shorter in duration in rats than in guinea pigs and were made up of a broadband frequency spectrum between 2 and 4 kHz. Post-mortem, the TEOAEs to 65 dB SPL clicks disappeared at about the same time as DPOAEs to low stimulus intensities and before the DPOAEs to high stimulus intensities. The ability to record TEOAEs in rats and other animals should permit further experimentation into the basic mechanisms of generation of otoacoustic emissions in general and TEOAEs in particular. C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,IL-91120 JERUSALEM,ISRAEL. CTR AUDIOL & HEARING REHABIL,TBILISI,REP OF GEORGIA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 120 EP 126 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900012 PM 8844192 ER PT J AU Code, RA Darr, MS Carr, CE AF Code, RA Darr, MS Carr, CE TI Chick cochlear efferent neurons are not immunoreactive for calcitonin gene-related peptide SO HEARING RESEARCH LA English DT Article DE olivocochlear; cholinergic motor neuron; choline acetyltransferase; superior olivary nucleus; dextran amine ID CENTRAL NERVOUS-SYSTEM; CHOLINE-ACETYLTRANSFERASE; GALLUS-DOMESTICUS; SPINAL-CORD; OLIVOCOCHLEAR NEURONS; NUCLEUS AMBIGUUS; FINE-STRUCTURE; LATERAL LINE; GUINEA-PIGS; BRAIN-STEM AB The fluorescent retrograde tracer, rhodamine dextran amine, was unilaterally injected into the cochlear duct of anesthetized chicks. Retrogradely labeled cells were found bilaterally in the brainstem ventromedial to the superior olivary nucleus and to the ventral facial nucleus, and in the caudal pontine reticular formation between the dorsal facial nucleus and the abducens nerve root. Tissue sections containing retrogradely labeled cells were incubated in an antiserum to calcitonin gene-related peptide (CGRP) and a fluorescently labeled secondary antiserum. No double-labeled neurons were found, suggesting that chick cochlear efferent neurons do not contain CGRP or that levels of CGRP in these cells may be too low to be detected immunohistochemically. C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. CR ADAMS JC, 1987, BRAIN RES, V419, P347, DOI 10.1016/0006-8993(87)90606-8 BATTEN TFC, 1988, J PHYSIOL-LONDON, V396, pP162 BATTEN TFC, 1988, BRAIN RES, V447, P314, DOI 10.1016/0006-8993(88)91134-1 BOBBIN RP, 1985, COMP BIOCHEM PHYS C, V80, P313, DOI 10.1016/0742-8413(85)90062-3 Code R. 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B., 1986, NEUROBIOLOGY HEARING, P333 Warr W. B., 1992, MAMMALIAN AUDITORY P, P410 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 WONG CJH, 1992, HEARING RES, V61, P31, DOI 10.1016/0378-5955(92)90033-J NR 56 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 1996 VL 97 IS 1-2 BP 127 EP 135 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900013 PM 8844193 ER PT J AU McAlpine, D Jiang, D Palmer, AR AF McAlpine, D Jiang, D Palmer, AR TI Interaural delay sensitivity and the classification of low best-frequency binaural responses in the inferior colliculus of the guinea pig SO HEARING RESEARCH LA English DT Article DE inferior colliculus; binaural responsiveness; interaural delay; characteristic delay; characteristic phase ID CHICK BRAIN-STEM; SUPERIOR OLIVARY COMPLEX; CENTRAL NUCLEUS; TIME DIFFERENCES; NOISE STIMULI; BARN OWL; CHANGING FREQUENCY; COCHLEAR NUCLEUS; SOUND FREQUENCY; NEURONS AB Monaural and binaural response properties of single units in the inferior colliculus (IC) of the guinea pig were investigated. Neurones were classified according to the effect of monaural stimulation of either ear alone and the effect of binaural stimulation. The majority (309/334) of IC units were excited (E) by stimulation of the contralateral ear, of which 41% (127/309) were also excited by monaural ipsilateral stimulation (EE), and the remainder (182/309) were unresponsive to monaural ipsilateral stimulation (EO). For units with best frequencies (BF) up to 3 kHz, similar proportions of EE and EO units were observed. Above 3 kHz, however, significantly more EO than EE units were observed. Units were also classified as either facilitated (F), suppressed (S), or unaffected (O) by binaural stimulation. More EO than EE units were suppressed or unaffected by binaural stimulation, and more EE than EO units were facilitated. There were more EO/S units above 1.5 kHz than below. Binaural beats were used to examine the interaural delay sensitivity of low-BF (BF < 1.5 kHz) units. The distributions of preferred interaural phases and, by extension, interaural delays, resembled those seen in other species, and those obtained using static interaural delays in the IC of the guinea pig. Units with best phase (BP) angles closer to zero generally showed binaural facilitation, whilst those with larger BPs generally showed binaural suppression. The classification of units based upon binaural stimulation with BF tones was consistent with their interaural-delay sensitivity. Characteristic delays (CD) were examined for 96 low-BF units. A clear relationship between BF and CD was observed. CDs of units with very low BFs (< 200 Hz) were long and positive, becoming progressively shorter as BF increased until, for units with BFs between 400 and 800 Hz, the majority of CDs were negative. Above 800 Hz, both positive and negative CDs were observed. A relationship between CD and characteristic phase (CP) was also observed, with CPs increasing in value as CDs became more negative. These results demonstrate that binaural processing in the guinea pig at low frequencies is similar to that reported in all other species studied. However, the dependence of CD on BF would suggest that the delay line system that sets up the interaural-delay sensitivity in the lower brainstem varies across frequency as well as within each frequency band. RP McAlpine, D (reprint author), UNIV NOTTINGHAM,MRC,INST HEARING RES,UNIV PK,NOTTINGHAM NG7 2RD,ENGLAND. 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Influence of local calcium-dependent mechanisms SO HEARING RESEARCH LA English DT Article DE adaptation; calcium; distortion product; non-linearity; outer hair cell; otoacoustic emission ID OUTER HAIR-CELLS; PRODUCT OTOACOUSTIC EMISSIONS; GUINEA-PIG COCHLEA; DISTORTION-PRODUCT; CONTRALATERAL SOUND; ACOUSTIC DISTORTION; BASILAR-MEMBRANE; EFFERENT SYSTEM; HEARING ORGAN; CHANNEL AB The distortion product otoacoustic emission (DPOAE) corresponding to the frequency f(2)-f(1) displays stereotyped, time-varying amplitude alterations during continuous primary tone stimulation. The origin of these alterations is unknown; however, evidence that efferent neurons contribute little to the changes has been presented (Kujawa et al., 1994a, 1995; Lowe and Robertson, 1995). The present investigation examines the hypothesis that these alterations in f(2)-f(1) amplitude are a reflection of local, Ca2+-dependent mechanisms involving the outer hair cell (OHC) response to sustained stimulation. Experiments were performed using urethane-anesthetized guinea pigs with sectioned middle ear muscles. Intracochlear perfusion was employed to reversibly lower perilymph Ca2+ levels and to introduce antagonists and agonists of L-type Ca2+ channels. Manipulations-that lowered available Ca2+ (zero Ca2+ artificial perilymph; zero Ca2+ with BAPTA) or that blocked its entry into the cell via L-type Ca2+ channels (nimodipine) reduced, prevented or reversed the perstimulatory changes in f(2)-f(1) DPOAE amplitude. These perilymph manipulations also reduced the overall amplitude of this distortion component while perfusion of an L-type Ca2+ channel agonist (Bay K 8644) increased its amplitude. Mg2+ did not substitute for Ca2+, suggesting that these are not merely divalent cation effects. Results are consistent with the hypothesis that continuous stimulation-related changes in f(2)-f(1) DPOAE amplitude are sensitive to perilymph Ca2+ levels and to the function of L-type Ca2+ channels. However, nimodipine also reduced the endocochlear potential (EP) and Bay K 8644 increased the EP. The sensitivity of both the perstimulatory changes in f(2)-f(1) DPOAE amplitude and the EP to the latter drugs leaves their site(s) of action unresolved. C1 LOUISIANA STATE UNIV, MED CTR, DEPT OTORHINOLARYNGOL & BIOCOMMUN, KRESGE HEARING RES LAB, NEW ORLEANS, LA 70112 USA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 153 EP 164 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900015 PM 8844195 ER PT J AU Phillips, DP Kitzes, LM Semple, MN Hall, SE AF Phillips, DP Kitzes, LM Semple, MN Hall, SE TI Stimulus-induced spike bursts in two fields of cat auditory cortex SO HEARING RESEARCH LA English DT Article DE auditory cortex; posterior field; single neuron; spike burst ID SINGLE NEURONS; POSTERIOR FIELD; RESPONSES; TIME; REPRESENTATION; STIMULATION; EXCITATION; NEOCORTEX; THALAMUS; UNITS AB The sound-evoked responses of extracellularly recorded cat primary auditory cortical neurons usually consist of a single spike or a short-term burst of 2-4 spikes, irrespective of the nature of the acoustic signal. In the cat's auditory cortex, the properties of such responses have to date been described only for cells in the primary field (AI). The purpose of the present study was to describe the properties of stimulus-evoked spike-burst responses seen in neurons of the posterior auditory field (P) and to compare those properties with those of a sample of AI neurons studied under similar conditions. The data come from 80 field P and 31 AI neurons studied with tonal and noise-burst stimuli in barbiturate-anesthetized cats, using calibrated, sealed stimulus delivery systems and conventional extracellular recording techniques. The mean inter-spike intervals (ISI) seen in the transient burst responses of posterior field cells were typically short (2-5 ms) and, where it was possible to test them, independent of the rise time of tonal signals, suggesting that they were also independent of the onset spectrum of the stimulus. The mean ISIs were often independent of the stimulus amplitude, even though the signal level had profound effects on the number of spikes evoked and the latency and regularity with which the responses were initiated. Each neuron was assigned a 'characteristic ISI', i.e., the mean ISI seen in the most vigorous responses. The distribution of characteristic ISIs for AI and P neurons overlapped, but were significantly different, with the characteristic ISIs of field P neurons being longer, In both AI and P populations, characteristic ISI was significantly correlated with minimal first-spike latency. The slopes of the regression lines of characteristic ISI on minimal latency for AI and for P cells were not significantly different from each other. Since the minimal latencies of AI neurons were usually shorter than those of field P neurons, the shorter characteristic ISIs of AI cells may thus be interpreted as secondary to their shorter latent periods. The general properties of stimulus-evoked spike bursts seen in field P neurons were thus very similar those previously described for AI cells. These data are consistent with the view that the majority of extracellular recordings in the cat's auditory cortex come from pyramidal neurons and an appropriate as a specialization for transfer of information to nonpyramidal, inhibitory interneurons. C1 DALHOUSIE UNIV,DEPT OTOLARYNGOL,HALIFAX,NS B3H 4J1,CANADA. UNIV CALIF IRVINE,DEPT ANAT & NEUROBIOL,IRVINE,CA 92717. NYU,CTR NEURAL SCI,NEW YORK,NY 10003. RP Phillips, DP (reprint author), DALHOUSIE UNIV,DEPT PSYCHOL,HALIFAX,NS B3H 4J1,CANADA. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 165 EP 173 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900016 PM 8844196 ER PT J AU Doan, DE Erulkar, JS Saunders, JC AF Doan, DE Erulkar, JS Saunders, JC TI Functional changes in the aging mouse middle ear SO HEARING RESEARCH LA English DT Article DE middle-ear function; umbo motion; laser interferometry; presbycusi AB Laser interferometry was used to measure sound-induced umbo velocity in the aging mouse middle ear. Velocity reductions of as much as 8 dB were seen as the mice aged. These functional differences suggest a variety of structural changes that may occur in the aging middle ear. C1 UNIV PENN,DEPT OTORHINOLARYNGOL HEAD & NECK SURG,PHILADELPHIA,PA 19104. UNIV PENN,DEPT BIOENGN,PHILADELPHIA,PA 19104. 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Res. PD AUG PY 1996 VL 97 IS 1-2 BP 174 EP 177 DI 10.1016/0378-5955(96)00060-3 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA VB549 UT WOS:A1996VB54900017 PM 8844197 ER PT J AU Chang, KW Norton, SJ AF Chang, KW Norton, SJ TI The effects of continuous versus interrupted noise exposures on distortion product otoacoustic emissions in guinea pigs SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; noise exposure; guinea pig ID PURE-TONE EXPOSURES; ACOUSTIC-DISTORTION; ALTERED SUSCEPTIBILITY; EAR; COCHLEA; DAMAGE; 2F1-F2; RABBIT; RESPONSES; BEHAVIOR AB Distortion product otoacoustic emissions (DPOAE) were measured serially in guinea pigs before and following 4-h exposures to a half-octave band of noise centered at 6 kHz, Stimulus parameters used to elicit the DPOAE were f(2)/f(1) = 1.26 and L(2) = L(1)-10. The 80 dB SPL exposures resulted in attenuation of emissions, which was maximal at the frequency one-half octave above the exposure when referenced to the f(2) stimulus, and which recovered back to baseline after 2 days. The 90 dB SPL exposures resulted in a permanent deficit in emissions elicited by high-frequency stimuli, as measured after 8 days of recovery. A statistically significant difference was also found between animals exposed continuously for 4 h versus animals given two 2-h exposures separated by a 1-h break. Measures of f(2)-f(1) and 3f(1)-2f(2) indicated that they were more sensitive than 2f(1)-f(2) to alterations in cochlear function after noise exposure. RP Chang, KW (reprint author), UNIV WASHINGTON,SCH MED,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,DEPT OTOLARYNGOL,SEATTLE,WA 98195, USA. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 1 EP 12 DI 10.1016/0378-5955(95)00225-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500001 PM 8817301 ER PT J AU Nakazawa, K Spicer, SS Gratton, MA Schulte, BA AF Nakazawa, K Spicer, SS Gratton, MA Schulte, BA TI Localization of actin in basal cells of stria vascularis SO HEARING RESEARCH LA English DT Article DE cochlea; immunohistochemistry; immunoelectron microscopy; vimentin; GLUTI ID INNER-EAR; IMMUNOHISTOCHEMICAL LOCALIZATION; MONOCLONAL-ANTIBODY; SUPPORTING CELLS; SPIRAL LIGAMENT; MUSCLE-ACTIN; ULTRASTRUCTURE; MELANOCYTES; EXPRESSION; FILAMENTS AB The distribution of actin in the lateral wall of the cochlear duct was investigated in the gerbil, rat, mouse and hamster, A monoclonal antibody specific for muscle alpha and gamma actins, and a polyclonal antiserum reactive with smooth muscle gamma and non-muscle beta actins yielded strong immunostaining of basal cells in the stria vascularis and of smooth muscle cells in lateral wall blood vessels. Both cell types stained in all four genera. Diffuse cytosolic staining was observed along the full-length of the basal cell layer including the blunt cell processes which they extend toward strial marginal cells. Immunoreactive basal cells appeared continuous with morphologically similar cells investing vessels penetrating the stria from the spiral ligament. The basal cells failed to bind antibodies to smooth muscle alpha actin and sarcomeric actin, By electron microscopic immunocytochemistry, gold labeling for actin was observed on dense, fine fibrils in the cytoplasm of the basal cells, In paraffin sections adjacent to those stained for actin, antibody to vimentin stained intermediate and basal cells in the stria vascularis whereas antibody to isoform 1 of the facilitated glucose transporter protein family (GLUT1) labeled only the non-overlapping apical and basal plasmalemma of basal cells. Content of vimentin, GLUT1 and muscle gamma actin supports the derivation of basal cells from mesoderm. The presence of stress fibers containing muscle gamma actin points to a possible contractile activity of basal cells which conceivably could be related to transport of K+ to and within the intrastrial compartment or regulation of blood flow in the stria vascularis. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,CHARLESTON,SC 29425. 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PD JUL PY 1996 VL 96 IS 1-2 BP 13 EP 19 DI 10.1016/0378-5955(96)00010-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500002 PM 8817302 ER PT J AU Gong, TWL Hegeman, AD Shin, JJ Adler, HJ Raphael, Y Lomax, MI AF Gong, TWL Hegeman, AD Shin, JJ Adler, HJ Raphael, Y Lomax, MI TI Identification of genes expressed after noise exposure in the chick basilar papilla SO HEARING RESEARCH LA English DT Article DE differential display; parathyroid hormone-related protein; calmodulin-regulated protein kinase II; CDC42; basilar papilla; acoustic trauma ID HORMONE-RELATED PEPTIDE; RNA DIFFERENTIAL DISPLAY; HAIR CELL REGENERATION; GTP-BINDING PROTEINS; MESSENGER-RNA; CDNA LIBRARY; ACOUSTIC TRAUMA; NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; HUMAN HOMOLOG AB We used differential display of mRNA, a method based on reverse transcriptase-PCR, to identify genes whose expression increases in response to acoustic trauma in the chick basilar papilla. Identifying these genes would provide insight into processes involved in repair of the damaged epithelium or in hair cell regeneration. We compared mRNA from the basilar papilla of normal chicks, from chicks exposed to an octave band noise (center frequency: 1.5 kHz) presented at 118 dB for 6 h, and from chicks exposed to noise and allowed to recover for 2 days. Thus far, we have identified 70 bands that appear to be differentially displayed on DNA sequencing gels; approximately 40 of these bands have been subcloned and sequenced. DNA sequences were compared with sequences in the GenBank database to identify genes with significant (70-85%) sequence identity to known genes. Chick cDNAs identified included: the parathyroid hormone-related protein, an immediate early gene; the delta-subunit of the neuronal-specific Ca2+/calmodulin-regulated protein kinase II; and the GTP-binding protein CDC42, a member of the ras superfamily of G proteins. A fourth cDNA had 84% sequence identity to an uncharacterized human cDNA (expressed sequence tag), indicating that this is a novel gene. Slot-blot hybridization analysis of these cDNAs probed with labeled DNA generated from mRNA from each experimental group indicated higher levels of mRNA for each of these four genes after noise exposure. These results indicate the potential involvement of both Ca2+/calmodulin-mediated signaling and GTPase cascades in the response to noise damage and during hair cell regeneration in the chick basilar papilla. C1 UNIV MICHIGAN,SCH MED,KRESGE HEARING RES INST,DEPT OTOLARYNGOL HEAD & NECK SURG,ANN ARBOR,MI 48109. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 20 EP 32 DI 10.1016/0378-5955(96)00013-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500003 PM 8817303 ER PT J AU Ratnanather, JT Zhi, M Brownell, WE Popel, AS AF Ratnanather, JT Zhi, M Brownell, WE Popel, AS TI Measurements and a model of the outer hair cell hydraulic conductivity SO HEARING RESEARCH LA English DT Article DE hydraulic skeleton; osmosis; mathematical model ID WATER PERMEABILITY; ELECTROMOTILITY AB The hydraulic conductivity of the cochlear outer hair cell (OHC) is central to the maintenance of the positive intracellular pressure necessary for its function as the cochlear amplifier, A mathematical model of osmotic water transport across the OHC membrane is formulated. The model relates the OHC hydraulic conductivity, L(p), to the rate of volume change in response to osmotic stimuli. L(p) is evaluated from osmotic experiments in which isolated OHCs are exposed to an hypotonic solution, The rate of volume increase in response to the hypotonic challenge was determined by a morphometric analysis of video images of cells. L, was found to be about 10(-14) m s(-1) Pa-1 or equivalently, P-f similar to 10(-4) cm s(-1). This is on the low side of values reported for different lipid bilayers and is 2 orders of magnitude lower than the hydraulic conductivity of red blood cells, The relation of the low OHC hydraulic conductivity to the composition and morphology of its membranes is discussed. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,BALTIMORE,MD 21205. RP Ratnanather, JT (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT BIOMED ENGN,ROOM 613,TRAYLOR RES BLDG,720 RUTLAND AVE,BALTIMORE,MD 21205, USA. RI Ratnanather, J. Tilak/A-3362-2010 OI Ratnanather, J. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 33 EP 40 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500004 PM 8817304 ER PT J AU Trune, DR Kempton, JB Mitchell, C AF Trune, DR Kempton, JB Mitchell, C TI Auditory function in the C3H/HeJ and C3H/HeSnJ mouse strains SO HEARING RESEARCH LA English DT Article DE mouse; C3H/HeJ substrain; C3H/HeSnJ substrain; auditory brainstem response; inner ear ID HEARING-LOSS; MICE AB The C3H inbred mouse strain arose in 1920 and includes several substrains, such as the C3H/HeJ and C3H/HeSnJ variants. However, use of these C3H mice in hearing research has been limited because their auditory function has not been described. Therefore, the purpose of this study was to characterize auditory function in two C3H representative substrains. C3H/HeJ and C3H/HeSnJ mice were obtained from Jackson Laboratories for auditory brainstem response (ABR) testing at ages from 2 to 30 months. Animals were tested with tone bursts at frequencies of 4, 8, 16, 24, and 32 kHz. These early responses were evaluated for age-related threshold shifts as an index of peripheral auditory function. Both strains show normal sensitivity up to 14 months of age, Thresholds for both strains were slightly elevated at most frequencies at 18 months. C3H/HeSnJ mice tested at 30 months demonstrated little hearing function due to extensive sensorineural degeneration. Thus, these C3H strains maintain excellent cochlear function past 1 year of age. RP Trune, DR (reprint author), OREGON HLTH SCI UNIV,OREGON HEARING RES CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,PORTLAND,OR 97201, USA. 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PD JUL PY 1996 VL 96 IS 1-2 BP 41 EP 45 DI 10.1016/0378-5955(96)00017-2 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500005 PM 8817305 ER PT J AU Zhang, MS Zwislocki, JJ AF Zhang, MS Zwislocki, JJ TI Intensity-dependent peak shift in cochlear transfer functions at the cellular level, its elimination by sound exposure, and its possible underlying mechanisms SO HEARING RESEARCH LA English DT Article DE outer hair cell; Hensen's cell; best frequency; sound exposure; active feedback ID BASILAR-MEMBRANE; NERVE-FIBERS; GUINEA-PIG; ORGAN; CORTI; CELLS; POTENTIALS; EMISSIONS; VIBRATION; NOISE AB Our systematic study of cochlear transfer functions has confirmed earlier results that, in a normal cochlea, the cochlear AC responses at any given cochlear location do not have a fixed best frequency at which the response is maximal. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 46 EP 58 DI 10.1016/0378-5955(96)00029-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500006 PM 8817306 ER PT J AU Capsius, B Leppelsack, HJ AF Capsius, B Leppelsack, HJ TI Influence of urethane anesthesia on neural processing in the auditory cortex analogue of a songbird SO HEARING RESEARCH LA English DT Article DE anesthesia; auditory cortex analogue; songbird; telencephalon; urethane ID WHITE-CROWNED SPARROW; FIELD-L; UNIT-ACTIVITY; FOREBRAIN; NEURONS; NUCLEUS; RAT; ORGANIZATION; INHIBITION; RESPONSES AB Functional maps of auditory response areas were derived from multi-unit recordings in the caudal telencephalon of the starling (Sturnus vulgaris L.). A regular grid of recording sites with distances of 200 mu m horizontally and 100 mu m vertically was placed over the auditory cortex analogue. Within one plane, mapping of auditory responses was first performed in the awake bird and then repeated under urethane anesthesia The data from both experimental approaches differ considerably. Urethane reduces the spontaneous discharge rate significantly. Under anesthesia, inhibition decreases in all auditory subunits. Excitation is less affected. Eight auditory subcenters were divided into three groups according to the changes in their excitatory responses. In the first group 'on' and sustained excitation changed only weakly. These areas are thought to receive direct inputs from the diencephalon. In the second group,'on' and sustained excitation are substantially reduced. These subcenters seem to receive projections from other forebrain areas. In subunits of the third group, an increase in sustained excitation is correlated to a decrease in inhibition. Within some specific centers, distinct natural calls for example the bird's own song, elicit stronger responses under anesthesia than other stimuli. C1 TECH UNIV MUNICH, INST ZOOL, D-85747 GARCHING, GERMANY. 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PD JUL PY 1996 VL 96 IS 1-2 BP 59 EP 70 DI 10.1016/0378-5955(96)00038-X PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500007 PM 8817307 ER PT J AU Trautwein, P Hofstetter, P Wang, J Salvi, R Nostrant, A AF Trautwein, P Hofstetter, P Wang, J Salvi, R Nostrant, A TI Selective inner hair cell loss does not alter distortion product otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE inner hair cell; outer hair cell; cochlear microphonic; distortion product otoacoustic emission; compound action potential; carboplatin; chinchilla ID WALTZER MUTANT MOUSE; BASILAR-MEMBRANE; COCHLEAR MECHANICS; CHINCHILLA COCHLEA; COMBINATION TONES; BIOMECHANICS; SUPPRESSION; CARBOPLATIN; RESPONSES; ORIGIN AB Outer hair cells (OHC) are believed to be the dominant source of distortion product otoacoustic emissions (DPOAE) in mammals; however, some studies in genetic mutants suggest that inner hair cell (IHC) loss may lead to a significant reduction of DPOAE amplitude. In the present study, we determined the extent to which MC loss altered DPOAE amplitude by using carboplatin to destroy selectively the IHCs in the chinchilla while sparing virtually all of the OHCs. IHC losses of 80-100% with normal retention of OHCs did not reduce the amplitude of the DPOAEs or the cochlear microphonic potential (CM); however, it completely abolished the compound action potential (CAP). The only time that the amplitude of the DPOAEs and CM were reduced was in cases where both the IHCs and OHCs were destroyed in the base of the cochlea. We conclude that the total loss of IHCs does not lead to a significant change in DPOAE amplitude. DPOAE amplitude was only reduced when there was a significant loss of OHCs. C1 SUNY BUFFALO,HEARING RES LAB,BUFFALO,NY 14214. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 71 EP 82 DI 10.1016/0378-5955(96)00040-8 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500008 PM 8817308 ER PT J AU Cai, YD Geisler, CD AF Cai, YD Geisler, CD TI Temporal patterns of the responses of auditory-nerve fibers to low-frequency tones SO HEARING RESEARCH LA English DT Article DE low-frequency tone; auditory nerve; peak-splitting; phase ID INNER HAIR-CELLS; GUINEA-PIG COCHLEA; RECEPTOR POTENTIALS; SPIKE INITIATION; SINGLE TONES; ROUND WINDOW; MODULATION; CHINCHILLA; MECHANICS; SOUND AB The temporal response patterns of auditory-nerve fibers to low-frequency tones were studied in anesthetized cats using period histograms. 'Peak-splitting' was observed mostly in fibers with lower characteristic frequencies (CF < 2 kHz) and with lower-frequency stimulation (less than or equal to 500 Hz). The occurrence of peak-splitting, the number of peaks, and the time between the peaks were all dependent upon the stimulus frequency. The phases of responses, although complex functions of stimulus frequency, intensity, and the fiber's CF, clearly showed traveling-wave characteristics for all frequencies at or above 100 Hz. The amount of phase change with intensity was generally small for lower-frequency stimuli (< similar to 50 degrees), although larger phase changes (e.g., similar to 180 degrees) were occasionally seen with higher-frequency stimuli. At 50 and 100 Hz, the phase of neural responses in the basal region roughly corresponds to the maximum velocity of the basilar membrane towards scala tympani (as inferred from cochlear microphonic recordings). C1 UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 83 EP 93 DI 10.1016/0378-5955(96)00033-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500009 PM 8817309 ER PT J AU Cai, YD Geisler, CD AF Cai, YD Geisler, CD TI Suppression in auditory-nerve fibers of cats using low-side suppressors .1. Temporal aspects SO HEARING RESEARCH LA English DT Article DE two-tone suppression; auditory nerve; suppression phase-lead ID INNER HAIR CELL; LOW-FREQUENCY TONES; GUINEA-PIG COCHLEA; BASILAR-MEMBRANE MOTION; 2-TONE RATE SUPPRESSION; MAMMALIAN COCHLEA; RATE RESPONSES; MODULATION; SENSITIVITY; STIMULATION AB Two-tone suppression was studied in the auditory nerve fibers of anesthetized cats, using low-frequency suppressors (50-2000 Hz). The response to the characteristic-frequency (CF) tone was suppressed in a phase-specific manner, attaining one or two minimums in 1 cycle of the suppressor (SUP) tone. The suppression phase-lead (i.e., the phase of maximum suppression leading the phase of response to the SUP tone) was about 1/4 cycle for lower-frequency suppressors (50, 100 and 200 Hz), and was close to 1/2 cycle for higher-frequency suppressors (500, 1000 and 2000 Hz). Both the phase of suppression and the suppression phase-lead are independent of fiber spontaneous rate (SR). Some fibers also show a secondary (minor) suppression at higher SUP intensities, which is always about 1/2 cycle away from the first (major) one. Fibers with higher CFs (> 2 kHz) are more likely to show a secondary suppression than those with lower CFs. The threshold difference between the major and minor suppressions is CF-dependent: lower CF fibers usually show differences of 10 dB or greater, while higher CF fibers show smaller differences. The secondary suppression is suppressor-frequency-dependent, usually restricted to lower-frequency suppressors (less than or equal to 200 Hz), No fibers showed a secondary suppression with a SUP frequency 1000 Hz or greater. The phases of suppressions (both the major and minor suppressions) are not affected by the intensity of the CF tone. Non-excitatory, low-frequency suppressors can also give rise to significant suppression. The threshold of synchronization to the SUP tone in the two-tone part was usually the lowest, while the SUP-alone rate threshold was highest. The threshold of synchronization in the SUP-alone segment and threshold of suppression were in between. In some low-SR fibers, complete suppression can be seen. C1 UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 CAI Y, 1995, THESIS U WISCONSIN M CAI Y, 1994, TEMPORAL ASPECTS 2 T, P98 Cai YD, 1996, HEARING RES, V96, P83, DOI 10.1016/0378-5955(96)00033-0 Cai YD, 1996, HEARING RES, V96, P141, DOI 10.1016/0378-5955(96)00037-8 Cai YD, 1996, HEARING RES, V96, P126, DOI 10.1016/0378-5955(96)00036-6 Cai YD, 1996, HEARING RES, V96, P113, DOI 10.1016/0378-5955(96)00035-4 CHEATHAM MA, 1992, HEARING RES, V60, P1, DOI 10.1016/0378-5955(92)90052-O CHEATHAM MA, 1995, ADV HEARING RES, P145 COOPER NP, 1995, HEARING RES, V82, P225, DOI 10.1016/0378-5955(94)00180-X DALLOS P, 1992, J NEUROSCI, V12, P4575 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DELGUTTE B, 1990, HEARING RES, V49, P225, DOI 10.1016/0378-5955(90)90106-Y DENG L, 1985, Journal of the Acoustical Society of America, V78, P1633, DOI 10.1121/1.392801 FAHEY PF, 1985, J ACOUST SOC AM, V77, P599, DOI 10.1121/1.391878 Galambos R, 1944, J NEUROPHYSIOL, V7, P287 GEISLER CD, 1992, HEARING RES, V63, P203, DOI 10.1016/0378-5955(92)90086-3 Geisler CD, 1996, J ACOUST SOC AM, V99, P1550, DOI 10.1121/1.414731 HILL KG, 1992, HEARING RES, V64, P52, DOI 10.1016/0378-5955(92)90167-L 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 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 NUTTALL AL, 1993, J ACOUST SOC AM, V93, P390, DOI 10.1121/1.405619 NUTTALL AL, 1981, BRAIN RES, V211, P171, DOI 10.1016/0006-8993(81)90078-0 OHLEMILLER KK, 1994, HEARING RES, V80, P174, DOI 10.1016/0378-5955(94)90109-0 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 PFEIFFER R R, 1970, Journal of the Acoustical Society of America, V48, P1373, DOI 10.1121/1.1912294 RELKIN EM, 1991, HEARING RES, V55, P215, DOI 10.1016/0378-5955(91)90106-J RHODE WS, 1993, HEARING RES, V66, P31, DOI 10.1016/0378-5955(93)90257-2 ROMAHN G, 1978, EXP BRAIN RES, V32, P423 RUGGERO MA, 1988, AUDITORY PATHWAY STR, P57 RUGGERO MA, 1995, ACTIVE HEARING, P321 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 SACHS MB, 1981, HEARING RES, V4, P309, DOI 10.1016/0378-5955(81)90015-0 SACHS MB, 1969, J ACOUST SOC AM, V45, P1205 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SELLICK PM, 1980, HEARING RES, V2, P439, DOI 10.1016/0378-5955(80)90080-5 SELLICK PM, 1982, HEARING RES, V7, P199, DOI 10.1016/0378-5955(82)90014-4 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 NR 42 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 JUL PY 1996 VL 96 IS 1-2 BP 94 EP 112 DI 10.1016/0378-5955(96)00034-2 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500010 PM 8817310 ER PT J AU Cai, YD Geisler, CD AF Cai, YD Geisler, CD TI Suppression in auditory-nerve fibers of cats using low-side suppressors .2. Effect of spontaneous rates SO HEARING RESEARCH LA English DT Article DE auditory nerve; spontaneous rate; two-tone suppression; afferent synapse ID INNER HAIR CELL; GUINEA-PIG COCHLEA; 2-TONE RATE SUPPRESSION; SPIRAL GANGLION-CELLS; BASILAR-MEMBRANE; RESPONSE PATTERNS; FREQUENCY; MODULATION; STIMULATION; VELOCITY AB The responses of auditory nerve fibers with different spontaneous rates were studied in anesthetized cats, using harmonically related characteristic frequency (CF) tone and suppressor (SUP) tone (50-2000 Hz) as stimuli. The relative-response index, defined as the ratio of the maximum response level in the two-tone segment to the response level in the CF-alone segment, at or near the intensity of maximum suppression (i.e., where the two-tone rate was lowest), was dependent on fiber's spontaneous rate (SR). For all the SUP frequencies used, lower-SR fibers almost always showed values less than unity, while high-SR fibers almost always gave values near or greater than unity, The phase of maximum suppression was not dependent upon fiber SR. In one experiment, a pair of low- and high-SR fibers with the same CF (12 kHz) were recorded consecutively in the same electrode penetration, and were studied with the same stimulus parameters. Their temporal responses showed dramatic temporal resemblances, with very similar phases of suppression and response. But the relative-response indexes were different. The similarities in the lower- and high-SR fibers support the idea that the basic response and suppression patterns in all fibers are formed at or before the inner hair cell (MC) stage, while the differences suggest that processes more central than the IHC receptor potential are important in determining the magnitudes of suppression, particularly in the lower-SR fibers. C1 UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 CAI Y, 1995, THESIS U WISCONSIN M CAI Y, 1995, 2 TONE SUPPRESSION A, P174 Cai YD, 1996, HEARING RES, V96, P83, DOI 10.1016/0378-5955(96)00033-0 Cai YD, 1996, HEARING RES, V96, P94, DOI 10.1016/0378-5955(96)00034-2 Cai YD, 1996, HEARING RES, V96, P141, DOI 10.1016/0378-5955(96)00037-8 CHEATHAM MA, 1992, HEARING RES, V59, P39, DOI 10.1016/0378-5955(92)90100-2 CHEATHAM MA, 1992, HEARING RES, V60, P1, DOI 10.1016/0378-5955(92)90052-O CHEATHAM MA, 1994, HEARING RES, V75, P103, DOI 10.1016/0378-5955(94)90061-2 CHEATHAM MA, 1990, HEARING RES, V50, P193, DOI 10.1016/0378-5955(90)90045-Q CHEATHAM MA, 1995, ADV HEARING RES, P145 COOPER NP, 1993, J NEUROPHYSIOL, V70, P370 DELGUTTE B, 1990, HEARING RES, V49, P225, DOI 10.1016/0378-5955(90)90106-Y 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 GEISLER CD, 1996, 2 TONE SUPPRESSION B, P56 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 HILL KG, 1992, HEARING RES, V6, P52 HILL KG, 1989, HEARING RES, V39, P75, DOI 10.1016/0378-5955(89)90083-X HILL KG, 1991, HEARING RES, V55, P167, DOI 10.1016/0378-5955(91)90101-E 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, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 NUTTALL AL, 1993, J ACOUST SOC AM, V93, P390, DOI 10.1121/1.405619 NUTTALL AL, 1981, BRAIN RES, V211, P171, DOI 10.1016/0006-8993(81)90078-0 PATUZZI R, 1984, HEARING RES, V13, P1, DOI 10.1016/0378-5955(84)90089-3 RELKIN EM, 1991, HEARING RES, V55, P215, DOI 10.1016/0378-5955(91)90106-J RHODE WS, 1993, HEARING RES, V66, P31, DOI 10.1016/0378-5955(93)90257-2 Rhode WS., 1977, PSYCHOPHYSICS PHYSL, P27 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 RUSSELL IJ, 1992, J NEUROSCI, V12, P1587 SACHS MB, 1969, J ACOUST SOC AM, V45, P1205 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SELLICK PM, 1980, HEARING RES, V2, P439, DOI 10.1016/0378-5955(80)90080-5 SELLICK PM, 1982, HEARING RES, V7, P199, DOI 10.1016/0378-5955(82)90014-4 SIEGEL JH, 1982, J NEUROPHYSL, V47, P33 YATES GK, 1980, PSYCHOPHYSICAL PHYSL, P200 ZAGAESKI M, 1994, J ACOUST SOC AM, V95, P3430, DOI 10.1121/1.409963 NR 41 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 JUL PY 1996 VL 96 IS 1-2 BP 113 EP 125 DI 10.1016/0378-5955(96)00035-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500011 PM 8817311 ER PT J AU Cai, YD Geisler, CD AF Cai, YD Geisler, CD TI Suppression in auditory-nerve fibers of cats using low-side suppressors .3. Model results SO HEARING RESEARCH LA English DT Article DE two-tone suppression; model; temporal; outer hair cell; inner hair cell; transfer function ID GUINEA-PIG COCHLEA; LOW-FREQUENCY TONES; OUTER HAIR-CELLS; BASILAR-MEMBRANE MOTION; 2-TONE SUPPRESSION; MAMMALIAN COCHLEA; RECEPTOR POTENTIALS; RESPONSES; INNER; MODULATION AB A phenomenological model which simulates auditory-nerve (AN) two-tone suppression was developed. The model uses the output of the outer hair cell (OHC) to control the gain of the cochlear amplifier, which presumably affects only frequencies near the characteristic frequency (CF). Among other things, the model can simulate basic AN suppression patterns including the 1/4 to 1/2 cycle relationships which exist between phase of suppression and phase of excitation to the suppressor (SUP) tone alone (Cai and Geisler, 1996a). Without any changes, it is also able to simulate the experimental low-frequency biasing data and the suppression of CF component by the low-frequency SUP tone in the OHC outputs (Cheatham and Dallos, 1994), These successful simulations of the suppression patterns support the basic assumption in the model, that the saturation of OHC transduction current produces two-tone suppression. However, the amplitude behavior of the model fits that obtained only from AN fibers with high spontaneous rates (and from inner hair cells (IHC)), but not fibers with lower spontaneous rates. It appears, therefore, that other unknown mechanism(s) operating at stages following the IHC potential are important in determining the magnitude of low-side suppression. C1 UNIV WISCONSIN, DEPT NEUROPHYSIOL, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT ELECT & COMP ENGN, MADISON, WI 53706 USA. CR ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 CAI Y, 1995, THESIS U WISCONSIN M Cai YD, 1996, HEARING RES, V96, P94, DOI 10.1016/0378-5955(96)00034-2 Cai YD, 1996, HEARING RES, V96, P113, DOI 10.1016/0378-5955(96)00035-4 CHEATHAM MA, 1992, HEARING RES, V59, P39, DOI 10.1016/0378-5955(92)90100-2 CHEATHAM MA, 1994, HEARING RES, V75, P103, DOI 10.1016/0378-5955(94)90061-2 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DALLOS P, 1992, J NEUROSCI, V12, P4575 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1992, SOC GEN PHY, V47, P371 DALLOS P, 1984, HEARING RES, V14, P281, DOI 10.1016/0378-5955(84)90055-8 GEISLER CD, 1993, BIOPHYSICS HAIR CELL, P330 GEISLER CD, 1992, HEARING RES, V63, P203, DOI 10.1016/0378-5955(92)90086-3 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 HOUSLEY GD, 1992, J PHYSIOL-LONDON, V448, P73 JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 NUTTALL AL, 1981, BRAIN RES, V211, P171, DOI 10.1016/0006-8993(81)90078-0 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, 1987, HEARING RES, V30, P83, DOI 10.1016/0378-5955(87)90186-9 RHODE WS, 1993, HEARING RES, V66, P31, DOI 10.1016/0378-5955(93)90257-2 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 RUSSELL IJ, 1986, HEARING RES, V22, P199, DOI 10.1016/0378-5955(86)90096-1 RUSSELL IJ, 1992, J NEUROSCI, V12, P1587 RUSSELL IJ, 1983, J PHYSIOL-LONDON, V338, P179 RUSSELL IJ, 1995, ADV HEARING RES, P136 SACHS MB, 1981, HEARING RES, V4, P309, DOI 10.1016/0378-5955(81)90015-0 SACHS MB, 1976, J ACOUST SOC AM, V60, P1157, DOI 10.1121/1.381218 SACHS MB, 1969, J ACOUST SOC AM, V45, P1205 SANTOS-SACCHI J, 1992, J NEUROSCI, V12, P1906 SELLICK PM, 1980, HEARING RES, V2, P439, DOI 10.1016/0378-5955(80)90080-5 SELLICK PM, 1982, HEARING RES, V7, P199, DOI 10.1016/0378-5955(82)90014-4 ZWICKER E, 1986, J ACOUST SOC AM, V80, P163, DOI 10.1121/1.394177 NR 37 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 JUL PY 1996 VL 96 IS 1-2 BP 126 EP 140 DI 10.1016/0378-5955(96)00036-6 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500012 PM 8817312 ER PT J AU Cai, YD Geisler, CD AF Cai, YD Geisler, CD TI Long-term suppression of the responses of auditory nerve fibers to a characteristic-frequency tone by a low-frequency suppressor SO HEARING RESEARCH LA English DT Article DE two-tone; suppression; long-term; efferent ID ACOUSTIC REFLEX; SOUND; CAT AB The classical two-tone suppression requires the characteristic-frequency (CF) tone and the suppressor (SUP) tone to act simultaneously. We report a novel phenomenon whereby the responses to the CF tone alone were 'suppressed' by a preceding low-side SUP tone. Increasing the repetition interval to about 3000 ms or longer eliminated such suppression. The magnitude of this 'long-term' Suppression was not dependent upon fiber CF, but fibers with low spontaneous rates (SR) generally showed more suppression than high-SR fibers did. The suppression threshold was not dependent upon fiber SR. This suppression of the CF responses did not affect the phases of responses to either the CF or SUP tone, or the phase of suppression. This phenomenon is not due to adaptation or fatigue, but due to the presence of the preceding SUP tone. The efferent system, particularly the 'slow' effect, might be responsible for it. C1 UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. CR ART JJ, 1985, J PHYSIOL-LONDON, V360, P397 ART JJ, 1982, PROC R SOC SER B-BIO, V216, P377, DOI 10.1098/rspb.1982.0081 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BORG E, 1990, BRAIN RES, V506, P79, DOI 10.1016/0006-8993(90)91201-Q BORG E, 1984, ACOUSTIC REFLEX, P413 BORG E, 1982, SCAND AUDIOL, V11, P237, DOI 10.3109/01050398209087473 CAI Y, 1995, THESIS U WISCONSIN M Cai YD, 1996, HEARING RES, V96, P83, DOI 10.1016/0378-5955(96)00033-0 Cai YD, 1996, HEARING RES, V96, P94, DOI 10.1016/0378-5955(96)00034-2 Cai YD, 1996, HEARING RES, V96, P126, DOI 10.1016/0378-5955(96)00036-6 Cai YD, 1996, HEARING RES, V96, P113, DOI 10.1016/0378-5955(96)00035-4 CASTILLO JD, 1954, J PHYSL, V124, P574 CODY AR, 1995, AUDIT NEUROSCI, V1, P351 FURUKAWA T, 1978, J PHYSIOL-LONDON, V276, P211 GEISLER CD, 1996, 2 TONE SUPPRESSION B, P56 GORGA MP, 1983, AUDIOLOGY, V22, P120 HAYASHI JH, 1985, J PHYSIOL-LONDON, V368, P179 HILL KG, 1992, HEARING RES, V64, P52, DOI 10.1016/0378-5955(92)90167-L KOBLER JB, 1992, J NEUROPHYSIOL, V68, P807 NELLIS A, 1979, J AM AUD SOC, V4, P184 Pang X-D, 1986, PERIPHERAL AUDITORY, P36 REITER ER, 1995, J NEUROPHYSIOL, V73, P506 SACHS MB, 1969, J ACOUST SOC AM, V45, P1205 SRIDHAR TS, 1995, J NEUROSCI, V15, P3667 TEIG E, 1973, ACTA PHYSIOL SCAND, V88, P382, DOI 10.1111/j.1748-1716.1973.tb05467.x WARREN EH, 1989, HEARING RES, V37, P89, DOI 10.1016/0378-5955(89)90032-4 NR 26 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1996 VL 96 IS 1-2 BP 141 EP 150 DI 10.1016/0378-5955(96)00037-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500013 PM 8817313 ER PT J AU Ma, YL Rarey, KE Gerhardt, KJ Curtis, LM Rybak, LP AF Ma, YL Rarey, KE Gerhardt, KJ Curtis, LM Rybak, LP TI Electrochemical potentials and potassium concentration profiles recorded from perilymph, endolymph and associated inner ear tissues in adrenalectomized rats SO HEARING RESEARCH LA English DT Article DE electrochemical potential; potassium determination; double-barrelled microelectrode; endolymph; perilymph; marginal cell; spiral ligament ID STRIA VASCULARIS; ION-TRANSPORT; COCHLEAR; MECHANISMS; MODEL AB This study evaluated the electrochemical potentials and potassium concentration (C-K+) profiles in the perilymph, endolymph, marginal cells, and spiral ligament of adrenalectomized rats in which endogenous corticosteroids had been removed. Electrochemical potentials recorded at the four cochlear sites were not affected by adrenalectomy (ADX). C-K+ was greater in the endolymph of the ADX animals as compared to control animals. Additionally, there was an increase of C-K+ in the marginal cells, perilymph, and spiral ligament tissues of the ADX animals as compared to control animals, although the observed increases were not statistically significant. In a previous study (Ma et al,, 1995a), it was found that potassium levels in the blood plasma of ADX animals were higher than those identified in normal rats; thus, ADX may have a systemic effect on C-K+ that is detectable in both tissues and fluids within the cochlea. Even though C-K+ was elevated within the cochlea in the ADX model, the functional response of the inner ear, as assessed electrophysiologically, was not altered. C1 UNIV FLORIDA,COLL MED,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT COMMUN PROC & DISORDERS,GAINESVILLE,FL 32610. SO ILLINOIS UNIV,SCH MED,DEPT SURG,SPRINGFIELD,IL 62794. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 151 EP 156 DI 10.1016/0378-5955(96)00051-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500014 PM 8817314 ER PT J AU Gates, TS Weedman, DL Pongstaporn, T Ryugo, DK AF Gates, TS Weedman, DL Pongstaporn, T Ryugo, DK TI Immunocytochemical localization of glycine in a subset of cartwheel cells of the dorsal cochlear nucleus in rats SO HEARING RESEARCH LA English DT Article DE auditory system; electron microscopy; glycine transporter; hearing ID GUINEA-PIG; SYNAPTIC CONNECTIONS; NMDA-RECEPTORS; AMINO-ACIDS; BRAIN; IMMUNOREACTIVITY; COMPLEX; NEURONS; CAT; MICE AB Glycine is an inhibitory neurotransmitter and a glutamate cofactor for N-methyl-D-aspartate (NMDA) receptors in the central nervous system. The distribution of glycine in the auditory system will therefore provide clues as to synaptic mechanisms underlying auditory signal processing. Previous studies have reported the immunocytochemical presence of glycine in the dorsal cochlear nucleus of a variety of mammals, but the specificity with respect to particular cell types has proven elusive at the light microscopic level. We sought to identify cell types in the superficial regions of the dorsal cochlear nucleus that were immunoreactive to glycine using light and electron microscopy in the rat. At the light microscopic level, glycine immunoreactivity was present in some but not all medium-sized cells in layers I and II, The somata of pyramidal and granule cells were not stained. At the electron microscopic level, using previously published ultrastructural criteria, we examined the glycine-labeled cells and determined that many but not all cartwheel cells were labeled. We also observed unlabeled unipolar brush cells, Golgi cells, and stellate cells. As some of the labeled cells could not be identified, we could not determine whether unipolar brush cells, Golgi cells or stellate cells had both labeled and unlabeled subpopulations. Our observations indicate that within the population of cartwheel cells, only a subset are glycine-immunoreactive. C1 JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,DEPT OTOLARYNGOL HEAD & NECK SURG,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,CTR HEARING SCI,DEPT NEUROSCI,BALTIMORE,MD 21205. CR AOKI E, 1988, BRAIN RES, V442, P63, DOI 10.1016/0006-8993(88)91432-1 BERREBI AS, 1991, ANAT EMBRYOL, V183, P427 BRAWER JR, 1974, J COMP NEUROL, V155, P251, DOI 10.1002/cne.901550302 CASPARY DM, 1990, GLYCINE NEUROTRANSMI, P453 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 CASPARY DM, 1987, BRAIN RES, V417, P273, DOI 10.1016/0006-8993(87)90452-5 DANGELO E, 1990, NATURE, V346, P467, DOI 10.1038/346467a0 FLETCHER EJ, 1988, EUR J PHARMACOL, V151, P161, DOI 10.1016/0014-2999(88)90711-X GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GOLDING NL, 1991, EXCITATORY INHIBITOR HACKNEY CM, 1990, ANAT EMBRYOL, V182, P123 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 JOHNSON JW, 1987, NATURE, V325, P529, DOI 10.1038/325529a0 KEMP JA, 1988, P NATL ACAD SCI USA, V85, P6547, DOI 10.1073/pnas.85.17.6547 KLECKNER NW, 1988, SCIENCE, V241, P835, DOI 10.1126/science.2841759 KOLSTON J, 1992, ANAT EMBRYOL, V186, P443 LANGOSCH D, 1990, EUR J BIOCHEM, V194, P1, DOI 10.1111/j.1432-1033.1990.tb19419.x LIU QR, 1993, J BIOL CHEM, V268, P22802 MANIS P, 1989, EVIDENCE FUNCTIONAL Martin M.R., 1985, P184 MONAGHAN DT, 1985, J NEUROSCI, V5, P2909 MUGNAINI E, 1980, J NEUROCYTOL, V9, P537, DOI 10.1007/BF01204841 NELKEN I, 1994, J NEUROPHYSIOL, V71, P2446 OERTEL D, 1989, J COMP NEUROL, V283, P228, DOI 10.1002/cne.902830206 Palay SL, 1974, CEREBELLAR CORTEX CY PEYRET D, 1987, ACTA OTO-LARYNGOL, V104, P71, DOI 10.3109/00016488709109049 POURCHO RG, 1992, NEUROSCIENCE, V46, P643, DOI 10.1016/0306-4522(92)90151-Q RYUGO DK, 1995, J COMP NEUROL, V358, P102, DOI 10.1002/cne.903580107 SAINTMARIE RL, 1991, HEARING RES, V51, P11, DOI 10.1016/0378-5955(91)90003-R SALT TE, 1989, BRAIN RES, V481, P403, DOI 10.1016/0006-8993(89)90823-8 SCHWARTZ IR, 1981, EXP NEUROL, V73, P601, DOI 10.1016/0014-4886(81)90199-0 SMITH KE, 1992, NEURON, V8, P927, DOI 10.1016/0896-6273(92)90207-T SPIROU GA, 1991, J NEUROPHYSIOL, V66, P1750 THOMSON AM, 1989, NATURE, V338, P422, DOI 10.1038/338422a0 VOIGT HF, 1980, J NEUROPHYSIOL, V44, P76 WENTHOLD RJ, 1987, BRAIN RES, V415, P183, DOI 10.1016/0006-8993(87)90285-X WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 WICKESBERG RE, 1994, J COMP NEUROL, V339, P311, DOI 10.1002/cne.903390302 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 WOUTERLOOD FG, 1984, J NEUROCYTOL, V13, P639, DOI 10.1007/BF01148083 WU SH, 1986, J NEUROSCI, V6, P2691 ZARA, 1995, J NEUROSCI, V15, P3952 NR 44 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 1996 VL 96 IS 1-2 BP 157 EP 166 DI 10.1016/0378-5955(96)00054-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500015 PM 8817315 ER PT J AU Goodyear, R Killick, R Legan, PK Richardson, GP AF Goodyear, R Killick, R Legan, PK Richardson, GP TI Distribution of beta-tectorin mRNA in the early posthatch and developing avian inner ear SO HEARING RESEARCH LA English DT Article DE inner ear; extracellular matrix; tectorial membrane; hair cell; supporting cell; development ID HAIR-CELL ANTIGEN; STEREOCILIARY BUNDLES; CHICK COCHLEA; MEMBRANE AB Expression of beta-tectorin mRNA in the inner ear of the embryonic and early posthatch (PH) chick was studied by in situ hybridisation. In the PH chick, beta-tectorin mRNA is expressed in the basilar papilla, in the clear and the cuboidal cells that lie either side of the papilla, in the striolar regions of the maculae, and in two small groups of cells lying adjacent to the midline in the cristae of the anterior and posterior ampullae. Expression of beta-tectorin is not observed in the lateral ampulla. In the sensory epithelia of the PH chick in which beta-tectorin mRNA is detected, expression is restricted to the supporting cell population. During development of the cochlear duct, beta-tectorin expression begins between embryonic (E) days 5 and 6. At E6, expression is observed throughout the length of the duct but is highest at the distal end. By E7, the pattern of expression is reversed and is highest at the proximal end of the cochlea, suggesting that a wave of high beta-tectorin expression passes disto-proximally along the papilla during E6 and E7. Expression of beta-tectorin mRNA is not detected in the homogene cells at any stage during the development of the cochlear duct, indicating that these cells do not synthesise one of the two major proteins of the avian tectorial membrane. The distribution of supporting cells expressing beta-tectorin mRNA in the different epithelia was compared with the distribution of sensory cells that have type B hair bundles, those with shaft links restricted to basal regions of their stereocilia, and sensory cells that have type A bundles, those with shaft links all over the entire surface of their stereocilia. Hair cells with type A hair bundles are never found in association with supporting cells expressing beta-tectorin. Although there is a correspondence in the basilar papilla and the maculae of the utriculus and lagena between the distribution of supporting cells expressing beta-tectorin mRNA and hair cells with type B bundles, this correlation does not generalise to the other sensory epithelia. C1 UNIV SUSSEX, SCH BIOL SCI, BRIGHTON BN1 9QG, E SUSSEX, ENGLAND. CR BARTOLAMI S, 1991, J COMP NEUROL, V314, P777, DOI 10.1002/cne.903140410 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X CORWIN JT, 1991, CIBA F SYMP, V160, P103 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 GOODYEAR R, 1992, J COMP NEUROL, V325, P243, DOI 10.1002/cne.903250208 GOODYEAR R, 1995, J COMP NEUROL, V351, P81, DOI 10.1002/cne.903510108 GOODYEAR R, 1994, HEARING RES, V80, P93, DOI 10.1016/0378-5955(94)90013-2 GOODYEAR R, 1994, J COMP NEUROL, V345, P267, DOI 10.1002/cne.903450208 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 KILLICK R, 1995, J CELL BIOL, V129, P535, DOI 10.1083/jcb.129.2.535 KILLICK R, 1992, HEARING RES, V64, P21, DOI 10.1016/0378-5955(92)90165-J LEWIS J, 1991, CIBA F SYMP, V160, P25 READY DF, 1976, DEV BIOL, V53, P217, DOI 10.1016/0012-1606(76)90225-6 SHIEL MJ, 1990, HEARING RES, V47, P147, DOI 10.1016/0378-5955(90)90172-L TAKEMURA T, 1994, HEARING RES, V79, P99, DOI 10.1016/0378-5955(94)90131-7 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 Wilkinson D, 1990, POSTIMPLANTATION MAM, P155 WILKINSON DG, 1992, IN SITU HYDRIDISATIO NR 19 TC 15 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1996 VL 96 IS 1-2 BP 167 EP 178 DI 10.1016/0378-5955(96)00045-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500016 PM 8817316 ER PT J AU Jock, BM Hamernik, RP Aldrich, LG Ahroon, WA Petriello, KL Johnson, AR AF Jock, BM Hamernik, RP Aldrich, LG Ahroon, WA Petriello, KL Johnson, AR TI Evoked-potential thresholds and cubic distortion product otoacoustic emissions in the chinchilla following carboplatin treatment and noise exposure SO HEARING RESEARCH LA English DT Article DE hearing loss; otoacoustic emission; carboplatin ID OUTER HAIR-CELLS; TUNING CURVES; OTOTOXICITY AB Twenty-two chinchillas were given either a single intraperitoneal (ip.) or intravenous (i.v.) injection (50 or 75 mg/kg) of Paraplatin(TM), an asymptotic threshold shift-producing noise or a combination of the drug acid noise in series. Auditory evoked potential (pure-tone) audiograms and cubic distortion product otoacoustic emissions were obtained on each animal before and after treatment, and the sensory epithelium of the cochlea was evaluated using the surface preparation method. Anatomical analysis indicated that the carboplatin alone caused relatively severe but scattered losses of inner hair cells throughout most of the cochlea which were dependent on dose and administration route. The outer sensory cell population remained essentially intact. In animals that had up to 40% scattered losses of only inner hair cells, evoked potential thresholds were near normal and the emission functions either were normal or showed an enhanced output. The severe losses of inner hair cells produced by the drug had no effect on the threshold shift dynamics produced by a five-day uninterrupted noise exposure. In general, there was not a consistent relation between the emission data and both the permanent threshold shift and outer hair cell losses. C1 SUNY COLL PLATTSBURGH,AUDITORY RES LAB,PLATTSBURGH,NY 12901. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 179 EP 190 DI 10.1016/0378-5955(96)00058-5 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500017 PM 8817317 ER PT J AU Schroger, E AF Schroger, E TI Interaural time and level differences: Integrated or separated processing? SO HEARING RESEARCH LA English DT Article DE spatial hearing; interaural cue; auditory evoked potential; mismatch negativity ID EVENT-RELATED POTENTIALS; AUDITORY SENSORY MEMORY; MISMATCH NEGATIVITY; HUMAN-BRAIN; STIMULUS DEVIANCE; COMPLEX SOUND; PITCH CHANGES; RESPONSES; CORTEX; ATTENTION AB The processing of interaural differences in time (IDT) and sound pressure level (IDL) was studied by using the mismatch negativity auditory evoked potential (MMN), which is a probe of pre-attentive auditory sensory memory. In a passive oddball experiment, subjects were reading in a book while they were presented with a standard stimulus (P = 0.88) having no IDTs or IDLs and three different deviant stimuli revealing an IDT, IDL, or both IDT and IDL. The different deviants elicited MMNs of comparable latencies indicating that memory representations of the IDTs and IDLs have been established. The MMN amplitudes to the IDT-IDL deviant were larger than those to changes in either IDT or IDL only. Moreover, the time-courses, amplitudes, and topographies of the MMNs to the IDT-IDL deviants were very similar to the sum of the MMNs elicited by the IDT and IDL deviants. These findings suggest that the representations of the binaural location cues were (at least partly) processed in parallel. It is argued that separate azimuth representations exist for IDT and IDL at a cortical level. RP Schroger, E (reprint author), UNIV MUNICH,INST PSYCHOL,LEOPOLDSTR 13,D-80802 MUNICH,GERMANY. 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Res. PD JUL PY 1996 VL 96 IS 1-2 BP 191 EP 198 DI 10.1016/0378-5955(96)00066-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500018 PM 8817318 ER PT J AU Yao, XF Rarey, KE AF Yao, XF Rarey, KE TI Detection and regulation of Cu/Zn-SOD and Mn-SOD in rat cochlear tissues SO HEARING RESEARCH LA English DT Article DE superoxide dismutase (SOD); ELISA; glucocorticoid; cochlea; methylprednisolone (MP) ID MANGANESE-SUPEROXIDE-DISMUTASE; LINKED-IMMUNOSORBENT-ASSAY; ANTIOXIDANT ENZYMES; FREE-RADICALS; DAMAGE; GLUCOCORTICOIDS; CELLS; STIMULATION; ALLOPURINOL AB Relative levels of copper/zinc-superoxide dismutase (Cu/Zn-SOD) and manganese-superoxide dismutase (Mn-SOD) in individual cochlear tissues were detected by the use of an enzyme-linked immunosorbent assay (ELISA). A heterogeneous distribution of Cu/Zn-SOD was observed in the individual tissues of control animals: high levels were measured in the stria vascularis (SV), intermediate levels of enzyme were measured in the spiral ligament (SL), and low levels were measured in the organ of Corti region (OC); collectively, these levels were not statistically significant (P = 0.0645). Levels of Mn-SOD in individual tissues of the control group were statistically significant (P < 0.05): high levels were measured in the SV, medium levels were detected in the SL, and low levels were identified in the OC. Following the administration of methylprednisolone (MP), a significant reduction of Cu/Zn-SOD in the SV (P < 0.05) and a non-significant, but noticeable, increase (> 30%) of Mn-SOD in the OC were observed. These results indicate that levels of SOD are tissue specific and that SOD is subject to glucocorticoid regulation. C1 UNIV FLORIDA,COLL MED,DEPT ANAT & CELL BIOL,JH MILLER HLTH CTR,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. 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H., 1960, LARYNGOSCOPE, V70, P351 YOSHIOKA T, 1994, KIDNEY INT, V45, P211, DOI 10.1038/ki.1994.25 ZELCK U, 1993, EUR ARCH OTO-RHINO-L, V250, P218 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 JUL PY 1996 VL 96 IS 1-2 BP 199 EP 203 DI 10.1016/0378-5955(96)00050-0 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UX135 UT WOS:A1996UX13500019 PM 8817319 ER PT J AU Fuzessery, ZM AF Fuzessery, ZM TI Monaural and binaural spectral cues created by the external ears of the pallid bat SO HEARING RESEARCH LA English DT Article DE sound localization; spectral cue; bat; pinna; external ear; spectral notche ID SOUND PRESSURE TRANSFORMATION; FALSE VAMPIRE BAT; ANTROZOUS-PALLIDUS; MEGADERMA-LYRA; MEDIAN PLANE; DIRECTIONAL HEARING; INFERIOR COLLICULUS; INSECTIVOROUS BAT; PLECOTUS-AURITUS; CARDIODERMA-COR AB The acoustic properties of external ears transform the spectra of incident sound in a location-dependent manner, and provide monaural and binaural spectral information used in 2-dimensional localization. Human studies suggest that binaural spectral differences, and spectral peaks and notches in monaural transfer functions, may all provide spatial information. This study examined the acoustic properties of;the pallid bat ear to determine directionality, interaural intensity differences, spectral peaks and notches in transfer functions, as well as acoustic gain. The pallid bat is a gleaning bat that uses passive sound localization to find prey, and echolocation for general orientation. It is capable of very accurate passive sound localization, and the primary focus of this study was to determine the spectral cues that might support this localization acuity. Results show that the external ears of this bat create spectral maxima and minima that vary systematically with azimuth and elevation. The monaural spectral cues resemble those reported in humans and cats, and suggest that similar spectral cues are used across taxa. The ears also create robust interaural spectral differences that vary systematically with both sound azimuth and elevation. These monaural and binaural spectral cues may provide the basis for the 1 degrees angular resolution apparent in it this bat's passive sound localization performance. C1 UNIV WYOMING,DEPT ZOOL,LARAMIE,WY 82071. UNIV WYOMING,DEPT PHYSIOL,LARAMIE,WY 82071. RP Fuzessery, ZM (reprint author), UNIV WYOMING,DEPT PSYCHOL,LARAMIE,WY 82071, USA. 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PD MAY PY 1996 VL 95 IS 1-2 BP 1 EP 17 DI 10.1016/0378-5955(95)00223-5 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200001 PM 8793503 ER PT J AU Takeuchi, S Irimajiri, A AF Takeuchi, S Irimajiri, A TI Maxi-K+ channel in plasma membrane of basal cells dissociated from the stria vascularis of gerbils SO HEARING RESEARCH LA English DT Article DE stria vascularis; basal cell; ion transport; maxi-K+ channel ID VESTIBULAR DARK CELLS; ACTIVATED POTASSIUM CHANNELS; APICAL MEMBRANE; NONSELECTIVE CATION; NONSENSORY REGION; MARGINAL CELLS; TETRAETHYLAMMONIUM; MECHANISMS; UTRICLE AB The plasma membrane of isolated strial basal cells has been probed for conductive pathways by the patch-clamp single-channel recording technique. Maxi-K+ channels were identified in 28 excised patches (i.e., 29%) out of 95, and these active patches each contained an average of 2.4 channel activities. In the cell-attached mode, activity of the maxi-K+ channel was also observed. Properties of the maxi-K+ channel thus revealed include: (1) linear I-V relations with 150 mM K+ on both sides of the membrane, (2) a unit conductance of 246.2 +/- 4.0 pS (n = 14), (3) Ca2+ sensitivity, (4) activation by membrane depolarization, (5) a complete block by Ba2+ (2 mM) from either side of the membrane, (6) a flickering block by quinine (0.1 mM) or verapamil (0.1 mM) from either side of the membrane, and (7) a complete block by tetraethylammonium (1 mM) from the outside only. The maxi-K+ channel may play a role in the generation of endocochlear potentials. RP Takeuchi, S (reprint author), KOCHI MED SCH,DEPT PHYSIOL,NANKOKU,KOCHI 783,JAPAN. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 18 EP 25 DI 10.1016/0378-5955(96)00016-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200002 PM 8793504 ER PT J AU Takemura, T Sakagami, M Takebayashi, K Umemoto, M Nakase, T Takaoka, K Kubo, T Kitamura, Y Nomura, S AF Takemura, T Sakagami, M Takebayashi, K Umemoto, M Nakase, T Takaoka, K Kubo, T Kitamura, Y Nomura, S TI Localization of bone morphogenetic protein-4 messenger RNA in developing mouse cochlea SO HEARING RESEARCH LA English DT Article DE bone morphogenetic protein-4; claudius; cell; basilar membrane; in situ hybridization ID INNER-EAR; IMMUNOHISTOCHEMICAL LOCALIZATION; DIFFERENTIAL EXPRESSION; RAT; IDENTIFICATION; FIBRONECTIN; INDUCTION; RECEPTOR; BETA-1; BRAIN AB Bone morphogenetic protein-4 (BMP-4) is a cytokine that belongs to the TGF-beta superfamily. It has been implicated that it plays an important role during embryogenesis including epithelial-mesenchymal interactions and mesenchymal cells condensation. To investigate whether BMP-4 is involved in the embryogenesis of the inner ear, we performed in situ hybridization at various stages of the developing inner ear of mice. BMP-4 mRNA was detected only in the developmental stage. Its initial expression was detected in part of the otic vesicle at 9 days post-coitum (PC). As development proceeded, the hair cells of the cochlear duct were morphologically distinguishable, and BMP-4 expressing cells were found in Claudius' cell region at 16 days PC, At this stage, the signal was most intense during development and the structure notably changed under the expressing cells. Mesenchymal cells were assembled and condensed underneath the BMP-4-expressing cells. The basilar membrane, with a rich extracellular matrix and elasticity, would be produced in the area between the Claudius' cells and condensed mesenchymal cells. Previous reports support the notion that BMP-4 expressed in the epithelium causes mesenchymal cell condensation and induces a structure with elasticity. In the developing cochlea, BMP-4 may be involved in the condensation and differentiation of the mesenchymal cells as well as basilar membrane formation. BMP-4 might be an essential factor for the normal development of the basilar membrane. C1 OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,SUITA,OSAKA 565,JAPAN. OSAKA UNIV,SCH MED,DEPT PATHOL,SUITA,OSAKA 565,JAPAN. HYOGO MED UNIV,DEPT OTOLARYNGOL,NISHINOMIYA,HYOGO 663,JAPAN. OSAKA UNIV,SCH MED,DEPT ORTHOPAED SURG,SUITA,OSAKA 565,JAPAN. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 26 EP 32 DI 10.1016/0378-5955(95)00233-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200003 PM 8793505 ER PT J AU Frijns, JHM deSnoo, SL tenKate, JH AF Frijns, JHM deSnoo, SL tenKate, JH TI Spatial selectivity in a rotationally symmetric model of the electrically stimulated cochlea SO HEARING RESEARCH LA English DT Article DE auditory prosthesis; electrical stimulation; spatial selectivity; electrical volume conduction; auditory nerve fibre; computational modelling ID AUDITORY-NERVE; CURRENT DISTRIBUTIONS; EXCITATION; IMPLANT; SYSTEM; FIBERS AB A rotationally symmetric model of electrical stimulation of the guinea pig cochlea with active neural elements is used to study the influence of temporal stimulus parameters and electrode configurations on the spatial selectivity of electrical stimulation by cochlear implants. The width of the excitation patterns is determined with respect to the position of the stimulating electrode pairs in the cochlea. Computed Q(10 dB) values are compared against single fibre data from the cat cochlear nerve as measured by Van den Honert and Stypulkowsky (1987). It turns out that the use of charge-balanced asymmetric rather than symmetric biphasic pulses approximately doubles the number of independent channels that can be applied in a cochlear implant with longitudinal bipolar electrodes, like a configuration with radial electrode pairs using symmetric biphasic pulse stimulation will also do. Finally, the influence on selectivity of the physiological variation in diameter of the cochlear nerve fibres and of a possible loss of their peripheral processes is studied. C1 DELFT UNIV TECHNOL,DEPT APPL PHYS,ACOUST PERCEPT GRP,DELFT,NETHERLANDS. RP Frijns, JHM (reprint author), UNIV LEIDEN HOSP,DEPT ENT,POB 9600,2300 RC LEIDEN,NETHERLANDS. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 33 EP 48 DI 10.1016/0378-5955(96)00004-4 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200004 PM 8793506 ER PT J AU Wangemann, P Liu, JZ AF Wangemann, P Liu, JZ TI Osmotic water permeability of capillaries from the isolated spiral ligament: New in-vitro techniques for the study of vascular permeability and diameter SO HEARING RESEARCH LA English DT Article DE cochlea; labyrinth; water permeability; blood vessel; capillary ID BLOOD-BRAIN-BARRIER; HYDRAULIC CONDUCTIVITY; LABYRINTH BARRIER; RAT; PERILYMPH; ENDOLYMPH; FLUIDS; ENTRY AB Perilymph is separated from blood by a barrier called the blood-labyrinth or blood-perilymph barrier in analogy to the blood-brain or blood-cerebrospinal fluid barrier. These barriers consist mainly of vascular endothelial cells. To characterize the blood-labyrinth barrier we developed in vitro techniques for the quantitative determination of the osmotic water permeability and for the determination of changes in the diameter of isolated inner ear capillaries. Both techniques rely on measurement of the velocity of marker red cells trapped in the lumen of capillaries. The velocity of marker red cells is a measure for the capillary permeability when a water flux across the capillary wall is induced by an osmotic gradient or a measure for a change in the capillary diameter. With these techniques the osmotic water permeability coefficient (P-f) and the pH sensitivity of isolated capillaries from the spiral ligament of the inner ear was determined. P-f at 23 degrees C was (1.49 +/- 0.17) 10(-3) cm/s at pH 7.4 and (1.61 +/- 0.23) 10(-3) cm/s at pH 6.8 (n = 12; mean +/- SEM; n = number of tissues). P-f at 37 degrees C was (2.26 +/- 0.23) 10(-3) cm/s at pH 7.4 and (2.35 +/- 0.17) 10(-3) cm/s at pH 6.8 (n = 13). No change in capillary diameter was observed when the pH of the interstitial fluid was lowered from pH 7.4 to 6.8. These data demonstrate that P-f and the capillary diameter of spiral ligament capillaries are pH independent and suggest that water crosses the blood-labyrinth barrier via an aqueous pathway. Further, these data suggest that the relatively low P-f is another characteristic shared by the blood-labyrinth and the blood-brain barrier. RP Wangemann, P (reprint author), BOYS TOWN NATL RES HOSP,CELL PHYSIOL LAB,555 N 30TH ST,OMAHA,NE 68131, USA. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 49 EP 56 DI 10.1016/0378-5955(96)00007-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200005 PM 8793507 ER PT J AU Trune, DR Kempton, JB Mitchell, C AF Trune, DR Kempton, JB Mitchell, C TI Decreased auditory function in the C3H/lpr autoimmune disease mouse SO HEARING RESEARCH LA English DT Article DE autoimmune disease; cochlea; C3H/lpr mouse; stria vascularis; auditory brainstem response ID SENSORINEURAL HEARING-LOSS; INNER-EAR DISEASES; LPR LPR MOUSE; STRAIN MOUSE; PATHOLOGY; COCHLEAR; AUTOANTIBODIES; ANTIBODIES; MECHANISM; SERUM AB To better understand autoimmune-related inner ear disease, cochlear structure and function were evaluated in the C3H/lpr autoimmune strain mouse, a model for systemic lupus erythematosus. C3H/lpr mice were examined at ages from 2 to 12 months along with age-matched C3H/HeJ controls. Autoimmune disease onset occurred at 3-4 months of age as serum immune complexes, antinuclear antibodies, and spleen weights were significantly elevated. Auditory brainstem response (ABR) audiometry showed normal auditory thresholds in C3H/lpr mice at 4 months of age, but elevated thresholds by 6 months, particularly in the high frequencies. Examination of the cochleas revealed no apparent loss of hair cells or spiral ganglion neurons, even in those mice with 50 dB SPL threshold shifts. However, changes were observed in the stria vascularis, including edematous spaces, enlarged capillaries, and thickened vessel linings. These findings imply that cochlear dysfunction in the autoimmune disease mice is the result of stria vascularis pathology. RP Trune, DR (reprint author), OREGON HLTH SCI UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,OREGON HEARING RES CTR,PORTLAND,OR 97201, USA. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 57 EP 62 DI 10.1016/0378-5955(96)00018-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200006 PM 8793508 ER PT J AU Ochi, K Eggermont, JJ AF Ochi, K Eggermont, JJ TI Effects of salicylate on neural activity in cat primary auditory cortex SO HEARING RESEARCH LA English DT Article DE salicylate; auditory cortex; single-unit, cross-correlation; spontaneous activity, bursting; tinnitus; cat ID GUINEA-PIG; SINGLE UNITS; OTOTOXICITY; TINNITUS; NIMODIPINE; ANESTHESIA; KETAMINE; CALCIUM; QUININE; SERUM AB The effect of systemically applied salicylate on single-unit firing activity in primary auditory cortex was investigated in six cats. A dose of 200 mg/kg sodium salicylate was administered intraperitoneally, and recordings from the same units were performed prior to application and continuously up to, on average, 6 h after administration. Local field potentials were used to track the threshold shifts and general input-output (I/O) behavior following salicylate administration. All animals showed 20-30 dB of threshold shift about 2 h after administration and showed no recovery during the following 4 h. I/O curves were invariably of the recruitment type. Significant changes were found in spontaneous firing rates for two groups of units separately. Low-spontaneous rate units (initial firing rate < 1 spike/s) showed an increase in spontaneous rate and high-spontaneous rate units (initial firing rate > 1 spike/s) showed a decrease in spontaneous firing rate. There were no significant changes in modal and mean values for interspike-interval (ISI) histograms. The duration-to-rebound peak in the autocorrelation function for spontaneous firings was prolonged significantly after salicylate administration. Peak cross-correlation coefficients for the firing patterns of simultaneously recorded cells showed no significant change but the correlogram's central peak was significantly narrower after salicylate application. The percentage of firings occurring in bursts showed no significant change after administration of salicylate. The best modulation frequency in response to stimulation with periodic click trains decreased after administration. Both the changes in the spontaneous autocorrelogram and in the temporal modulation transfer function suggest a prolongation in the duration of the Ca2+-activated K+ conductance of the cortical pyramidal cells following salicylate. This suggests that salicylates affect both the auditory periphery and the auditory cortex. C1 UNIV CALGARY,DEPT PSYCHOL,BEHAV NEUROSCI RES GRP,CALGARY,AB T2N 1N4,CANADA. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 63 EP 76 DI 10.1016/0378-5955(96)00019-6 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200007 PM 8793509 ER PT J AU Richter, CP Sauer, G Hoidis, S Klinke, R AF Richter, CP Sauer, G Hoidis, S Klinke, R TI Development of activity patterns in auditory nerve fibres of pigeons SO HEARING RESEARCH LA English DT Article DE pigeon; auditory; single fiber; activity pattern; development ID CHICKS BASILAR PAPILLA; AVIAN INNER-EAR; HAIR-CELLS; PLACE PRINCIPLE; COCHLEAR GANGLION; TONOTOPIC ORGANIZATION; INNERVATION PATTERNS; TECTORIAL MEMBRANE; DISCHARGE PATTERNS; FIBERS AB Little is known about inner ear development in pigeons. This paper addresses the question of maturation in activity patterns of pigeon auditory nerve fibres. Pigeons that were 1, 2 and 4 weeks and 1, 2, 3 and 4 years old were investigated. Adult-like activity patterns are found 4 weeks post-hatching. Spontaneous activities of fibres in immature animals (about 40 spikes/s) are half that found in adults. Spontaneous discharge rate does not increase with decreasing characteristic frequency (CF) of the fibre if the animals are immature. Rate thresholds are less sensitive in immature animals. Differences between the age groups are generally significant if the CFs of the fibres are below 1.3 kHz. Sharpness of tuning is already adult-like in 1-week-old animals. Inter-spike time interval histograms (ISTH) of auditory fibres recorded in animals of all age groups often show Poisson-like distributions. Preferred intervals are found in 10% of the ISTHs of fibres in immature animals but in 30% of adults. Cross-correlations between heart beats of the animal and spontaneous activities show good correlation for about 70% of the fibres in immature animals. With the growth of the animals, the number of fibres showing correlation of spontaneous activities and heart beats decreases to about 40%. The basilar papilla of a I-week-old animal is smaller than in an adult animal (by 10% in length and by 10% in width), judged by scanning electron microscopy (SEM). Changes of activity patterns in this study are likely to be a result of maturation of the middle ear. In addition to the latter, development of the inner ear is conceivable. C1 UNIV FRANKFURT KLINIKUM,ZENTRUM PHYSIOL,D-60590 FRANKFURT,GERMANY. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 77 EP 86 DI 10.1016/0378-5955(96)00020-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200008 PM 8793510 ER PT J AU Sziklai, I He, DZZ Dallos, P AF Sziklai, I He, DZZ Dallos, P TI Effect of acetylcholine and GABA on the transfer function of electromotility in isolated outer hair cells SO HEARING RESEARCH LA English DT Article DE outer hair cell; electromotility; GABA; acetylcholine, efferent influence; model of electromotility ID GUINEA-PIG COCHLEA; ELECTROKINETIC SHAPE CHANGES; AUDITORY SENSORY CELLS; OLIVOCOCHLEAR NEURONS; MECHANICAL RESPONSES; ORGAN; CORTI; MOTILITY; INNER; IMMUNOCYTOCHEMISTRY AB Outer hair cells (OHC) from high- and low-frequency regions were separately isolated from guinea pig cochleas. The cells were inserted with their ciliary pole first into a partitioning microchamber so that only 20-50% of the cell length was excluded. Somatic length changes due to transcellular electrical stimulation were measured at the cuticular plate in the inserted portion of the cells. Transfer curves of electromotility of the OHCs were obtained by both a series of brief (2.5 ms) and longer (30 ms) square pulses with opposite polarity and linearly increasing size from 40 to 280 mV in both negative and positive directions. Alterations in the transient and steady-state electromotility transfer curves were examined by application of acetylcholine (ACh) and gamma-aminobutyric acid (GABA) to the synaptic pole. ACh, in the concentration range of 10-30 mu M, evoked a significant magnitude and gain increase of electromotility in both transient and steady-state responses without a measurable shift in the operating point of the displacement-voltage transfer curve. A tonotopic response magnitude difference is found for ACh challenge. Basal turn OHCs responded with greater magnitude increase (+90% increase from control) than apical turn OHCs (+40%). GABA exerted an opposite effect, again in a location-dependent manner. :Magnitude response decreased about 30% for long cells and 14% for short ones. Atropin, a muscarinic receptor antagonist, completely blocked the increase in electromotility response due to ACh. However, D-tubocurarine, a nicotinic receptor antagonist, while hot blocking the ACh effect, altered the cell's apparent operating point. Bicuculline methiodide, a GABA(A)-receptor antagonist, completely arrested GABA influences on the electromotility response. These results suggest that both ACh and GABA can change the electromotile activity of OHCs, in a tonotopically biased manner. ACh challenge evokes greater magnitude responses in basal turn OHCs, whereas GABA induces greater motility response decrease in apical turn OHCs. The control of the gain and magnitude of electromotility by the transmitter substances appear to involve at least two mechanisms. One is probably related to conformational changes of the voltage-to-movement converter molecules and a change in their number in an effective operational pool, the other operates via changing the electrical resistance of the basolateral cell membrane. C1 NORTHWESTERN UNIV,DEPT COMMUN SCI & DISORDERS,AUDITORY PHYSIOL LAB,HUGH KNOWLES CTR,EVANSTON,IL 60208. NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL,EVANSTON,IL 60208. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 87 EP 99 DI 10.1016/0378-5955(96)00026-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200009 PM 8793511 ER PT J AU Sziklai, I AF Sziklai, I TI Human otosclerotic bone-derived peptide decreases the gain of the electromotility in isolated outer hair cells SO HEARING RESEARCH LA English DT Article DE otosclerosis; outer hair cell; electromotility; acetylcholine; caffeine; sensorineural hearing loss ID MECHANICAL RESPONSES; INHIBITION; PERILYMPH; MOVEMENT; CURRENTS; MOTILITY; COCHLEA; ORGAN; CORTI AB An otosclerotic peptide (OF) (Sziklai et al., 1985a,b) was purified from perilymph and stapes footplate of otosclerotic patients by Sephadex G-25 gel column chromatography and subsequent isotachophoretic (ITP) separation. The transfer function of the electromotility was measured by inserting the isolated outer hair cells (OHC) into a partitioning microchamber (Evens et al., 1991) and applying a series of pairs of brief square-pulse stimuli with opposite polarity and with increasing magnitude. Somatic length changes of the inserted part of the OHCs were measured by an optoelectronic system. The isotachophoretically homogenous peptide exerted a gain and magnitude decreasing effect on the transfer function of electromotility of isolated OHCs of the guinea pig, in vitro. The operating point of the electromotility did not change due to the effect of the peptide. The peptide decreased the electromotile performance within a minute and bath exchange to normal saline did not completely restore the transfer curve to baseline. Application of caffeine to the cells already under the effect of the otosclerotic peptide produced an opposite effect: gain and magnitude increase. Simultaneous application of acetylcholine (ACh) did not antagonize the effect of OF. The underlying mechanism of the action of OP on the transfer function of electromotility of OHCs is postulated to involve the modulation of intracellular Ca2+ concentration. C1 NORTHWESTERN UNIV,HUGH KNOWLES CTR,AUDITORY PHYSIOL LAB,EVANSTON,IL. RP Sziklai, I (reprint author), SEMMELWEIS UNIV MED,SCH MED,DEPT ENT,SZIGONY U 36,H-1083 BUDAPEST,HUNGARY. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 100 EP 107 DI 10.1016/0378-5955(96)00027-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200010 PM 8793512 ER PT J AU Seldon, HL Kawano, A Clark, GM AF Seldon, HL Kawano, A Clark, GM TI Does age at cochlear implantation affect the distribution of 2-deoxyglucose label in cat inferior colliculus? SO HEARING RESEARCH LA English DT Article DE plasticity; inferior colliculus; cochlear implant; 2-deoxyglucose; cat ID INTRACOCHLEAR ELECTRICAL-STIMULATION; AUDITORY BRAIN-STEM; NEONATALLY DEAFENED CAT; NORMAL-HEARING KITTENS; FREQUENCY REPRESENTATION; NUCLEUS; NEURONS; CHILDREN; DEAFNESS; CORTEX AB Cochlear implants are one treatment for children who are born deaf or become deaf before acquiring language. The question of optimum age for implantation arises. Using an animal model, we have studied the response of the auditory brainstem to implantation at various ages. Neonatally, pharmacologically deafened cats were implanted with a 4-electrode array in the left cochlea at ages from 100 to over 180 days. Eleven were chronically stimulated (1000 h if possible) with charge-balanced, biphasic current pulses; eight were unstimulated controls. In a terminal experiment, each animal received [(SC)-S-14]2-deoxyglucose i.v, preceding a 45-min stimulation program. The fraction of the right inferior colliculus (IC) with a significant accumulation of label was calculated. If age at implantation were a significant factor in determining the size of the responding region, the fraction would depend on the age; this was nor observed. However, there was considerable variation in the IC fraction sizes within both stimulated and unstimulated groups, leading to the conclusion that there are factors other than age which determine the size of the responding region. Thus, for deaf children of corresponding ages, age at implantation may not be of critical importance. C1 TOKYO MED COLL,DEPT OTOLARYNGOL,TOKYO 160,JAPAN. RP Seldon, HL (reprint author), UNIV MELBOURNE,DEPT OTOLARYNGOL,32 GISBORNE ST,MELBOURNE,VIC 3002,AUSTRALIA. CR Beggs W D, 1980, Br J Audiol, V14, P41, DOI 10.3109/03005368009078899 BROWN M, 1996, UNPUB INTENSITY FREQ BROWN M, 1996, UNPUB 3 DIMENSIONAL BROWN M, 1992, HEARING RES, V59, P224, DOI 10.1016/0378-5955(92)90119-8 BRUGGE JF, 1984, J ACOUST SOC AM, V75, P548 CLOPTON BM, 1980, MORPHOGENESIS MALFOR, P271 DAWSON PW, 1992, J SPEECH HEAR RES, V35, P401 DOWELL RC, 1991, AM J OTOL, V12, P137 Dowell R. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 108 EP 119 DI 10.1016/0378-5955(96)00028-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200011 PM 8793513 ER PT J AU Zhao, HB Liang, ZA AF Zhao, HB Liang, ZA TI Processing of modulation frequency in the dorsal cochlear nucleus of the guinea pig: Sinusoidal frequency-modulated tones SO HEARING RESEARCH LA English DT Article DE frequency modulation; phase-locking; dorsal cochlear nucleus; spontaneous rate; sound localization ID AUDITORY-NERVE FIBERS; DIFFERING SPONTANEOUS RATE; INFERIOR COLLICULUS; INHIBITORY INTERACTIONS; CENTRAL PROJECTIONS; UNIT RESPONSES; MUSTACHE BAT; NEURONS; CAT; AMPLITUDE AB Frequency- and amplitude-modulated (FM and AM, respectively) tones are important information-bearing elements in voice sounds and can also be produced by the spatial movement of sound sources. Zhao and Liang (1995) recently reported the response features of dorsal cochlear nucleus (DCN) neurons to AM tones. In the present study, the responses of the guinea pig DCN neurons to sinusoidal FM (SFM) tones were examined. Discharges of the DCN units to the SFM tones phase-locked to the stimulus modulation frequencies (f(m)). The phase-locked discharge patterns existed over broad ranges of modulation parameters and at stimulus levels as high as 95 dB SPL or modulation depths (d(m)) as low as 2%. Robust phase-locking to the f(m) was observed in samples of all DCN unit types studied. The means of best f(m) (B-fm) and upper limit f(m) (ULf(m)) of all recorded units were 510 Hz and 940 Hz, respectively. Pauser/Buildup (P/B) units had mean maximum synchronization index (SImax) of 0.57. ON units had the highest Bf(m) with the mean of 646 Hz and subtype ON-S showed the highest mean of SImax at 0.63. Phase-locking to the f(m) was independent of discharge rates and existed even when the discharge rates were reduced to the background spontaneous rate (SR). A few units showed stronger synchronous responses to the square and triangular FM stimuli instead of the SFM tones. The relationship between the modulated responses and the unit's response area were further examined. The f(m) phase-locking occurred to modulation bands (or frequency ranges) within the response area, with the modulation bands as narrow as +/-160 Hz in the central inhibitory areas of the type IV units, As the width of the modulation band changed within a unit's response area, the phases of the f(m) phase-locked responses of P/B units linearly changed while for Onset units, the change was lesser. The P/B and Onset units had a pi phase shift and a pi/2 phase change, respectively, as carrier frequencies (f(c)s) passed through characteristic frequencies (CF) and the excitatory/inhibitory response boundaries. The phase-locked responses to the f(m)s were dependent on the SR but were independent of the CF. Low-SR (less than or equal to 2 spikes/s) units had higher synchronization of responses to the f(m) than the high-SR(> 2 spikes/s) units (SImax = 0.64 and 0.42, respectively). These results suggest that the temporal characteristics:of the f(m) is effectively represented in the responses of DCN units to the SFM tones. Such temporal encoding behavior can play an important role in the processing of the complex sounds in the auditory system. These results also have implications for a possible role for the DCN is in identifying the spatial movement of a sound source. C1 CHINESE ACAD SCI,SHANGHAI INST PHYSIOL,SHANGHAI 200031,PEOPLES R CHINA. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 120 EP 134 DI 10.1016/0378-5955(96)00030-5 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200012 PM 8793514 ER PT J AU Fukazawa, T Tanaka, Y AF Fukazawa, T Tanaka, Y TI Spontaneous otoacoustic emissions in an active feed-forward model of the cochlea SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; cochlear model; computer simulation ID BASILAR-MEMBRANE; MOSSBAUER TECHNIQUE; ACOUSTIC EMISSIONS; FINE-STRUCTURE; SUPPRESSION; THRESHOLD; TONES AB Numerical simulation of spontaneous otoacoustic emissions (SOAE) was done using a 1-dimensional macromechanical cochlear model with an active 'feed-forward' force in every section of the basilar membrane (BM). When the activity of-the force was increased the model showed more stability than a 'feed-back' model and could have excitation curves with larger tips without divergence of the solution. The stability broke up when either (1) the damping of the BM was made slightly irregular throughout the BM or (2) the feed-forward force was switched off at a certain part of the BM, and limit cycle oscillations (LCO) emerged within the cochlea. Critical feed-forward value for the emergence of LCO in the first setting of BM (1), which was intended to simulate physiological variations in the distribution of outer hair cells, was searched utilizing the 'ringing' of delayed evoked otoacoustic emissions (DEOAE). In the course of the search, smooth transition from a DEOAE to a set of SOAEs was found to occur keeping the same spectral fine structure of the emissions when the feed-forward force surpassed a certain value. It was, as a result, suggested that the two kinds of emissions may have the same origin. In the second setting of BM (2), which was intended to simulate pathological cases, LCOs tended to be stronger than in the first one and they had similarity not only to real SOAEs but also to tinnitus in the way they showed up very close to or at the 'edge' of the switched-off part of the BM. RP Fukazawa, T (reprint author), DOKKYO UNIV, SCH MED, KOSHIGAYA HOSP, DEPT OTOLARYNGOL, KOSHIGAYA, SAITAMA 343, JAPAN. 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Res. PD MAY PY 1996 VL 95 IS 1-2 BP 135 EP 143 DI 10.1016/0378-5955(96)00039-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200013 PM 8793515 ER PT J AU Melcher, JR AF Melcher, JR TI Cellular generators of the binaural difference potential in cat SO HEARING RESEARCH LA English DT Article DE auditory system; cochlear nucleus; spherical cell; superior olivary complex; kainic acid; lesion ID AUDITORY BRAIN-STEM; ANTEROVENTRAL COCHLEAR NUCLEUS; SUPERIOR OLIVARY COMPLEX; INDUCED NEURONAL LOSS; EVOKED-POTENTIALS; TRAPEZOID BODY; INFERIOR COLLICULUS; INTERAURAL TIME; RESPONSES ABRS; KAINIC ACID AB In humans, lateralization and fusion of binaurally presented clicks are correlated with the latency and amplitude of the binaural difference potential (BDP) (e.g., Furst et al., 1985). The BDP is derived by subtracting the brainstem auditory evoked potential (BAEP) for binaural stimulation from the sum of the BAEPs for left and right monaural stimulation. Our aim in this work was to determine the cellular generators of the BDP and thus identify cells that may be crucial for specific types of binaural sound processing. To this end, we injected kainic acid into the superior olivary complex (SOC) or the cochlear nucleus (CN) in cats and examined the effects of the resulting lesions on the click-evoked BDP. Lesions confined to the anterior anteroventral CN (AVCNa) substantially reduced the BDP, while lesions primarily involving mon posterior parts of the CN had little or no effect. BDP reductions occurred for lesions involving either high (> 10 kHz) or lower (< 10 kHz) characteristic frequency (CF) regions of the AVCNa (as well as the posterior CN). Lesions involving the SOC reduced the BDP and, in one case, eliminated the high-pass filtered (270 Hz cutoff) BDP. Combining these results with published information about the physiology and anatomy of auditory brainstem cells, we conclude that: (1) spherical cells in the AVCNa are essential for BDP production, (2) the earliest part of the BDP is generated by medial superior olive (MSG) principal cells which receive spherical cell inputs, (3) a later part is probably generated by the cellular targets of MSO principal cells and, (4) the cells involved in BDP generation have CFs above, as well as below, 10 kHz. Since humans, like cats, have a well-developed MSG, we suggest that the MSO may also be essential for BDP production in humans. Thus, perceptual correlates of the BDP, binaural fusion and click lateralization, apparently involve the MSO. C1 MIT,CAMBRIDGE,MA 02139. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. 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PD MAY PY 1996 VL 95 IS 1-2 BP 144 EP 160 DI 10.1016/0378-5955(96)00032-9 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200014 PM 8793516 ER PT J AU Zheng, XY Wang, J Salvi, RJ Henderson, D AF Zheng, XY Wang, J Salvi, RJ Henderson, D TI Effects of kainic acid on the cochlear potentials and distortion product otoacoustic emissions in chinchilla SO HEARING RESEARCH LA English DT Article DE chinchilla; neural noise; auditory nerve; otoacoustic emission; kainic acid; electrical noise ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; MECHANICAL RESPONSES; REVERSE TRANSDUCTION; MOTILITY; INNER AB In absence of acoustic stimulation, the auditory nerve generates electrical noise with a spectral peak between 300 and 3000 Hz (Dolan et al., 1990). This electrical noise is eliminated when the dendrites of auditory nerve fibers are damaged by kainic acid (KA). We hypothesized that the KA-induced damage to the afferent dendrites might alter cochlear micromechanics or modify outer hair cell (OHC) electromotility. The KA-induced decrease in spontaneous electrical noise from the auditory nerve could conceivably reduce the spontaneous sounds recorded in the ear canal and the postulated change in cochlear micromechanics might alter distortion product otoacoustic emissions (DPOAE). To evaluate these hypotheses, we applied KA to the round window of the cochlea. KA reduced the spontaneous electrical noise recorded from the round window and significantly reduced the amplitude of the compound action potential (CAP) to tone bursts at 2, 4 and 8 kHz. KA caused only a slight reduction in the amplitude of the cochlear microphonic (CM) recorded from the round window; however, it had no effect on the spontaneous acoustic noise in the ear canal or on 2fl-f2 DPOAEs. These results suggest that the KA-induced reduction of electrical noise from the auditory nerve has no measurable effect on OHC electromotility as reflected in spontaneous otoacoustic emissions and that damage to the afferent dendrites has no effect on cochlear micromechanics as reflected in DPOAEs. C1 SUNY BUFFALO,HEARING RES LAB,BUFFALO,NY 14214. 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PD MAY PY 1996 VL 95 IS 1-2 BP 161 EP 167 DI 10.1016/0378-5955(96)00047-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UR782 UT WOS:A1996UR78200015 PM 8793517 ER PT J AU Lee, KH Cotanche, DA AF Lee, KH Cotanche, DA TI Potential role of bFGF and retinoic acid in the regeneration of chicken cochlear hair cells SO HEARING RESEARCH LA English DT Article DE epidermal growth factor receptor; basic fibroblast growth factor; fibroblast growth factor receptor; insulin-like growth factor receptor; insulin receptor; retinoic acid receptor beta; retinoic acid receptor gamma; retinoic acid; cochlea; reverse transcriptase PCR; regeneration; hair cell; chicken ID FIBROBLAST GROWTH-FACTOR; PIGMENT EPITHELIAL-CELLS; VEIN ENDOTHELIAL-CELLS; INTENSE SOUND EXPOSURE; AVIAN INNER-EAR; ACOUSTIC TRAUMA; BASILAR PAPILLA; VESTIBULAR EPITHELIUM; NEONATAL CHICK; NERVOUS-SYSTEM AB Messenger RNAs (mRNA) of several growth factor receptors and related genes were examined with reverse transcriptase polymerase chain reaction (RT-PCR) in normal and noise-damaged chicken basilar papillae (BP). Analysis of the amplification products indicated the presence of mRNAs for epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), insulin-like growth factor receptor (IGFR), insulin receptor (IR), retinoic acid receptor beta (RAR beta), retinoic acid receptor gamma (RXR gamma), and basic fibroblast growth factor (BFGF) in both normal and noise-damaged BP. The RT-PCR products generated were characterized by size and sequencing analysis to confirm the identities of the target molecules. The subcellular localization of the mature protein analogs for EGFR, FGFR, IGFR, RAR beta, and BFGF were identified using fluorescence immunocytochemistry and confocal laser scanning microscopy. These experiments indicated that EGFR is present in the stereociliary bundles in the hair cells, IGFR is not present in the cells of the BP, BFGF localizes in the nuclei of supporting cells in the BP, but not hair cells or hyaline cells, and that RAR beta localizes in the perinuclear regions of hair cells. The subcellular distributions of these proteins were consistent in both noise-damaged and control BP. FGFR, in contrast, changed its distribution in the tissue after noise damage. In normal BP, FGFR is concentrated in the stereocilia of hair cells. However, in damaged regions of noise-exposed chick cochleae, FGFR is heavily expressed in the expanded apical regions of the supporting cells. These findings suggest that BFGF and retinoic acid may potentially play a role in the mechanisms which regulate the regeneration of chicken cochlear hair cells. RP Lee, KH (reprint author), BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,80 E CONCORD ST,BOSTON,MA 02118, USA. 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PD MAY PY 1996 VL 94 IS 1-2 BP 1 EP 13 DI 10.1016/0378-5955(95)00220-0 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UQ838 UT WOS:A1996UQ83800001 PM 8789806 ER PT J AU Saffer, LD Gu, RD Corwin, JT AF Saffer, LD Gu, RD Corwin, JT TI An RT-PCR analysis of mRNA for growth factor receptors in damaged and control sensory epithelia of rat utricles SO HEARING RESEARCH LA English DT Article DE growth factor receptor; reverse transcriptase-polymerase chain reaction; hair cell; regeneration; balance; vestibular ID HAIR CELL REGENERATION; AVIAN INNER-EAR; ACOUSTIC TRAUMA; LATERAL LINE; EXPRESSION; ORGANS; PROLIFERATION; TOXICITY; BUNDLES; COCHLEA AB Sensory epithelia from normal rat utricles and those cultured with and without neomycin treatment were assayed for the presence of growth factor receptor mRNAs by RT-PCR (reverse transcriptase-polymerase chain reaction). Both undamaged and damaged utricles showed mRNA for Insulin receptor, IGF-I receptor, FGF receptor 1, EGF receptor, and PDGF alpha receptor. Neomycin-damaged sensory epithelia showed less PDGF alpha receptor mRNA than undamaged epithelia, suggesting that this message may be expressed at higher copy levels in hair cells than in supporting cells. Consistent with that hypothesis, immunohistochemistry revealed much stronger PDGF alpha receptor staining in the hair cells than in the supporting cells. Preliminary evidence suggests that IGF-I receptor message also my be lowered in neomycin-damaged epithelia. C1 UNIV VIRGINIA,SCH MED,DEPT OTOLARYNGOL HNS,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,SCH MED,DEPT NEUROSCI,CHARLOTTESVILLE,VA 22908. 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PD MAY PY 1996 VL 94 IS 1-2 BP 14 EP 23 DI 10.1016/0378-5955(95)00228-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UQ838 UT WOS:A1996UQ83800002 PM 8789807 ER PT J AU Ueda, N Ikeda, K Oshima, T Adachi, M Furukawa, M Takasaka, T AF Ueda, N Ikeda, K Oshima, T Adachi, M Furukawa, M Takasaka, T TI Subcellular distribution of protein kinase C in the living outer hair cell of the guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE protein kinase C; outer hair cell; immunohistochemistry; confocal laser microscopy; translocation ID RAT-BRAIN; IMMUNOCYTOCHEMICAL LOCALIZATION; PHORBOL ESTER; BETA-I; RELEASE; ACETYLCHOLINE; ACTIVATION; MECHANISM; SYSTEM; PKC AB Immunohistochemical staining using isoform-specific antibodies and intracellular localization using fluorescent probes for protein kinase C (PKC) were evaluated in the cochlear outer hair cell (OHC). Among three isoforms of classic PKC, PKC alpha was selectively stained in the fixed OHC as well as inner hair cells under a surface preparation method. Two types of fluorescent probes to detect subcellular localization of PKC were observed with a confocal laser scanning microscopy in the present study, fim-1 diacetate which binds to the ATP-competitive catalytic domain of PKC and Bodipy FL C-12-phorbol acetate which binds to specific site localized to the first cystein-rich loop of the C1 region in the regulatory domain. High fluorescence intensity of both dyes was observed in subcuticular and subsynaptic regions, infracuticular network, and along the lateral wall. The displacement experiments to evaluate binding specificity were performed by incubating Bodipy FL C-12-phorbol acetate in the presence of 10 mu M phorbol 12-myritate 13-acetate (PMA) and the fluorescence was totally disappeared. For the acute treatment of phorbol ester, cells were preincubated with 1 mu M PMA 30 min before loading with fim-1 diacetate. The brightest area in the plasma membrane became much larger as compared with untreated cells, which suggests a dramatic translocation of PKC to the plasma membrane. The biological functions involving PKC in the OHC are discussed. C1 TOHOKU UNIV,SCH MED,DEPT OTORHINOLARYNGOL,CELL PHYSIOL & BIOL LAB,AOBU KU,SENDAI,MIYAGI 98077,JAPAN. 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Res. PD MAY PY 1996 VL 94 IS 1-2 BP 24 EP 30 DI 10.1016/0378-5955(95)00219-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UQ838 UT WOS:A1996UQ83800003 PM 8789808 ER PT J AU Berglund, AM Benson, TE Brown, MC AF Berglund, AM Benson, TE Brown, MC TI Synapses from labeled type II axons in the mouse cochlear nucleus SO HEARING RESEARCH LA English DT Article DE auditory system; hearing; spiral ganglion neuron; outer hair cell; unmyelinated axon ID AUDITORY-NERVE FIBERS; DIFFERING SPONTANEOUS RATE; CENTRAL PROJECTIONS; SPIRAL GANGLION; HORSERADISH-PEROXIDASE; ADULT CATS; GUINEA-PIG; CELLS; BRANCHES; AFFERENT AB This study investigates the ultrastructure and central targets in the cochlear nucleus of axonal swellings of type II primary afferent neurons. Type II axons comprise only 5-10% of the ar;uns of the auditory nerve of mammals, but they alone provide the afferent innervation of the outer hail cells. In this study, type II axons were labeled with horseradish peroxidase, and serial-section electron microscopy was used to examine their swellings in: (1) the granule-cell lamina at its boundary with posteroventral cochlear nucleus, (2) the rostral anteroventral cochlear nucleus, and (3) the auditory nerve root. Only some (18%) of the type II terminal and en-passant swellings formed synapses. The synapses were asymmetric and contained clear round synaptic vesicles, suggesting that they are excitatory. Type II synapses were compared to those from type I fibers, the fibers providing the afferent innervation of the inner hair cells. Type II synapses tended to have slightly smaller and fewer synaptic vesicles had a greater proportion of the membrane apposition accompanied by a postsynaptic density, and often had densities that were discontinuous or 'perforated'. In all cochlear nucleus regions examined, the postsynaptic targets of type II synapses had characteristics of dendrites; in most cases these dendrites could not be traced to their cell bodies of origin. Some evidence suggests, however, that targets may include granule cells, spherical cells, and other cells in the nerve root. These results suggest afferent information from outer hair cells reaches diverse regions and targets within the cochlear nucleus. C1 HARVARD UNIV, SCH MED, DEPT OTOL & LARYNGOL, BOSTON, MA 02115 USA. BOSTON UNIV, DEPT BIOMED ENGN, BOSTON, MA 02215 USA. HARVARD UNIV, DIV HLTH SCI TECHNOL, CAMBRIDGE, MA 02138 USA. MIT, CAMBRIDGE, MA 02138 USA. 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Res. PD MAY PY 1996 VL 94 IS 1-2 BP 31 EP 46 DI 10.1016/0378-5955(95)00231-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UQ838 UT WOS:A1996UQ83800004 PM 8789809 ER PT J AU Faulstich, M Kossl, M Reimer, K AF Faulstich, M Kossl, M Reimer, K TI Analysis of non-linear cochlear mechanics in the marsupial Monodelphis domestica: Ancestral and modern mammalian features SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; distortion product; 2f1-f2; Monodelphis domestica; audiogram; cochlea ID ACOUSTIC DISTORTION PRODUCTS; OTOACOUSTIC EMISSION; FREQUENCY MAP; SUPPRESSION; 2F1-F2; EAR; RESPONSES; HUMANS; RABBIT AB The acoustic distortion product 2f1-f2 was measured in the ear canal of the gray short-tailed opossum, Monodelphis domestica, during stimulation with two pure tone stimuli of the frequencies f1 and f2 (f1 0). 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Res. PD MAY PY 1996 VL 94 IS 1-2 BP 157 EP 162 DI 10.1016/0378-5955(95)00229-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UQ838 UT WOS:A1996UQ83800016 PM 8789821 ER PT J AU Melcher, JR Knudson, IM Fullerton, BC Guinan, JJ Norris, BE Kiang, NYS AF Melcher, JR Knudson, IM Fullerton, BC Guinan, JJ Norris, BE Kiang, NYS TI Generators of the brainstem auditory evoked potential in cat .1. An experimental approach to their identification SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; superior olivary complex; kainic acid; lesion ID SUPERIOR OLIVARY COMPLEX; KAINIC ACID LESIONS; ANTEROVENTRAL COCHLEAR NUCLEUS; LATERAL GENICULATE-NUCLEUS; RAT INFERIOR COLLICULUS; INDUCED NEURONAL LOSS; STEM RESPONSES; TONOTOPIC ORGANIZATION; HORSERADISH-PEROXIDASE; BINAURAL RESPONSES AB This paper is the first in a series aimed at identifying the cellular generators of the brainstem auditory evoked potential (BAEP) in cats. The approach involves (1) developing experimental procedures for making small selective lesions and determining the corresponding changes in BAEP waveforms, (2) identifying brainstem regions involved in BAEP generation by examining the effects of lesions on the BAEP and, (3) identifying specific cell populations involved by combining the lesion results with electrophysiological and anatomical information from other kinds of studies. We created lesions in the lower brainstem by injecting kainic acid which is generally toxic for neuronal cell bodies but not for axons and terminals. This first paper describes the justifications for using kainic acid, explains the associated problems, and develops a methodology that addresses the main difficulties. The issues and aspects of the specific methods are generally applicable to physiological and anatomical studies using any neurotoxin, as well as to the present BAEP study. The methods chosen involved (1) measuring the BAEP at regular intervals until it reached a post-injection steady state and perfusing the animals with fixative shortly after the last BAEP recordings were made, (2) using objective criteria to distinguish injection-related BAEP changes from unrelated ones, (3) making control injections to identify effects not due to kainic acid toxicity, (4) verifying the anatomical and functional integrity of axons in lesioned regions, and (5) examining injected brainstems microscopically for cell loss and cellular abnormalities indicating dysfunction, This combination of methods enabled us to identify BAEP changes which are clearly correlated with lesion locations. C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. 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Res. PD APR PY 1996 VL 93 IS 1-2 BP 1 EP 27 DI 10.1016/0378-5955(95)00178-6 PG 27 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500001 PM 8735066 ER PT J AU Melcher, JR Guinan, JJ Knudson, IM Kiang, NYS AF Melcher, JR Guinan, JJ Knudson, IM Kiang, NYS TI Generators of the brainstem auditory evoked potential in cat .2. Correlating lesion sites with waveform changes SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; superior olivary complex; kainic acid; lesion ID SUPERIOR OLIVARY COMPLEX; BUSHY CELL AXONS; ANTEROVENTRAL COCHLEAR NUCLEUS; DORSAL LATERAL GENICULATE; INDUCED NEURONAL LOSS; KAINIC ACID; STEM RESPONSES; HORSERADISH-PEROXIDASE; EFFERENT PROJECTIONS; INFERIOR COLLICULUS AB Brainstem regions involved in generating the brainstem auditory evoked potential (BAEP) were identified by examining the effects of lesions on the click-evoked BAEP in cats. An excitotoxin, kainic acid, was injected into various parts of the cochlear nucleus (CN) or into the superior olivary complex (SOC), The locations of the resulting lesions were correlated with the changes produced in the various extrema of the BAEP waveforms, The results indicate that: (1) the earliest BAEP extrema (P1, N1 (recorded between vertex and the earbar ipsilateral to the stimulus) and P1a, P1b, (vertex to contralateral earbar)) are generated by cells with somata peripheral to the CN; (2) P2 is primarily generated by posterior anteroventral CN (AVCNp) and anterior posteroventral CN (PVCNa) cells; (3) SOC, anterior anteroventral CN (AVCNa), AVCNp, and PVCNa cells are involved in generating P3; (4) AVCNa cells are the main CN cells involved in P4, N4, and P5 generation; (5) both ipsilateral and contralateral SOC cells have a role in generating monaurally evoked P4 and P5; and (6) P5 is generated by cells with characteristic frequencies below 10 kHz. From (2) and (4), it is clear that P2 and P4-P5 are generated by cells in distinct, parallel pathways. C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. 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B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WUERTHELE SM, 1978, BRAIN RES, V149, P489, DOI 10.1016/0006-8993(78)90491-2 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 ZAAROOR M, 1991, ELECTROEN CLIN NEURO, V80, P422, DOI 10.1016/0168-5597(91)90091-B ZAAROOR M, 1991, ELECTROEN CLIN NEURO, V80, P436, DOI 10.1016/0168-5597(91)90092-C ZACZEK R, 1978, BRAIN RES, V152, P626, DOI 10.1016/0006-8993(78)91121-6 NR 46 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 APR PY 1996 VL 93 IS 1-2 BP 28 EP 51 DI 10.1016/0378-5955(95)00179-4 PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500002 PM 8735067 ER PT J AU Melcher, JR Kiang, NYS AF Melcher, JR Kiang, NYS TI Generators of the brainstem auditory evoked potential in cat .3. Identified cell populations SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; superior olivary complex; spherical cell; globular cell ID ANTEROVENTRAL COCHLEAR NUCLEUS; SUPERIOR OLIVARY COMPLEX; INDUCED NEURONAL LOSS; SINGLE UNIT-ACTIVITY; STEM RESPONSES ABRS; TRAPEZOID BODY; MEDIAL NUCLEUS; INFERIOR COLLICULUS; HORSERADISH-PEROXIDASE; LATERAL LEMNISCUS AB This paper examines the relationship between different brainstem cell populations and the brainstem auditory evoked potential (BAEP), First, we present a mathematical model relating the BAEP to underlying cellular activity, Then, we identify specific cellular generators of the click-evoked BAEP in cats by combining model-derived insights with key experimental data. These data include (a) a correspondence between particular brainstem regions and specific extrema in the BAEP waveform, determined from lesion experiments, and (b) values for model parameters derived from published physiological and anatomical information, Ultimately, we conclude (with varying degrees of confidence) that: (1) the earliest extrema in the BAEP are generated by spiral ganglion cells, (2) P2 is mainly generated by cochlear nucleus (CN) globular cells, (3) P3 is partly generated by CN spherical cells and partly by cells receiving inputs from globular cells, (4) P4 is predominantly generated by medial superior olive (MSG) principal cells, which are driven by spherical cells, (5) the generators of P5 are driven by MSO principal cells, and (6) the BAEP, as a whole, is generated mainly by cells with characteristic frequencies above 2 kHz, Thus, the BAEP in cats mainly reflects cellular activity in two parallel pathways, one originating with globular cells and the other with spherical cells, Since the globular cell pathway is poorly represented in humans, we suggest that the human BAEP is largely generated by brainstem cells in the spherical cell pathway. Given our conclusions, it should now be possible to relate activity in specific cell populations to psychophysical performance since the BAEP can be recorded in behaving humans and animals. C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. 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PD APR PY 1996 VL 93 IS 1-2 BP 52 EP 71 DI 10.1016/0378-5955(95)00200-6 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500003 PM 8735068 ER PT J AU Engdahl, B AF Engdahl, B TI Effects of noise and exercise on distortion product otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE distortion product otoacoustic emission; noise; exercise; temporary threshold shift ID COCHLEAR MICROMECHANICAL PROPERTIES; TEMPORARY THRESHOLD SHIFT; PURE-TONE EXPOSURES; ACOUSTIC DISTORTION; AUDITORY-SENSITIVITY; PHYSICAL EXERCISE; SOUND EXPOSURE; HEARING-LOSS; HUMAN EARS; STIMULATION AB The effect of physical exercise on both distortion product otoacoustic emissions (DPOAE), and on the temporary effects of noise on human cochlear function was examined. Changes in DPOAEs were compared to changes in behavioural thresholds and the possible relation between contralateral suppression of DPOAEs and susceptibility to noise exposure was investigated. Bekesy audiometry, tympanometry and DPOAEs were measured in 8 subjects on 3 separate occasions: before and after noise exposure; before and after exercise at 60% of maximal oxygen uptake (VO2max); and before and after a combination of noise exposure and exercise, all of 10 min duration. Noise exposure was third-octave band noise of 102 dB SPL centered at 2 kHz. The magnitude of the effect of noise exposure on DPOAE amplitude averaged in the 2-4 kHz range was comparable but weakly correlated to the magnitude of the temporary threshold shift (TTS) measured as the change in Bekesy threshold at 3 kHz. There was no effect of physical exercise without noise exposure on either the Bekesy threshold or the DPOAE amplitude. 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PD APR PY 1996 VL 93 IS 1-2 BP 72 EP 82 DI 10.1016/0378-5955(95)00197-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500004 PM 8735069 ER PT J AU Warr, WB Beck, JE AF Warr, WB Beck, JE TI Multiple projections from the ventral nucleus of the trapezoid body in the rat SO HEARING RESEARCH LA English DT Article DE auditory pathway; cochlear nucleus; olivocochlear bundle; superior olivary complex; inferior colliculus ID SUPERIOR OLIVARY COMPLEX; CHOLINE-ACETYLTRANSFERASE ACTIVITY; DORSAL COCHLEAR NUCLEUS; STEM AUDITORY NUCLEI; BUSHY CELL AXONS; INFERIOR COLLICULUS; GUINEA-PIG; BRAIN-STEM; DESCENDING PROJECTIONS; MEDIAL NUCLEUS AB An analysis of the central projections of the ventral nucleus of the trapezoid body (VNTB) in the rat, a region of the superior olivary complex known for its neuronal heterogeneity, was made using two anterograde axonal tracers, [H-3]leucine and biotinylated dextran amine (BDA). A mixture of these tracers was injected iontophoretically into the VNTB and the results analyzed by first assessing magnitudes of autoradiographic signal in nuclei receiving projections and then identifying the axons and terminals responsible for this signal in parallel sets of sections processed for BDA. Our analysis showed that in addition to its projections to each cochlea via the olivocochlear bundle, the VNTB has 3 major central sites of axonal terminations: (1) the cochlear nucleus, particularly the molecular layer of the contralateral dorsal cochlear nucleus, (2) the contralateral lateral superior olive, and (3) the ipsilateral inferior colliculus. Other sites receiving projections from the VNTB included the VNTB itself and the nuclei of the lateral lemniscus. Significantly, the relative magnitudes of labeling within the nuclei receiving inputs from the VNTB varied consistently as a function of the dorsoventral location of the injection site, confirming previous work showing that there is a partial segregation within this nucleus of neurons according to their projections. Our data also revealed an orderly topographic pattern of projections to the cochlear nuclei, lateral superior olive and the inferior colliculus which is consistent with the known tonotopic organization both of the VNTB and these projection targets. Methodologically, the co-injection of two tracers was advantageous in that patterns of silver grains in autoradiographs could be used to confirm whether axons and terminals labeled with BDA had originated from labeled somata at the injection site or were the result of uptake of BDA by fibers of passage. RP Warr, WB (reprint author), BOYS TOWN NATL RES HOSP, 555 N 30TH ST, OMAHA, NE 68131 USA. 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PD APR PY 1996 VL 93 IS 1-2 BP 83 EP 101 DI 10.1016/0378-5955(95)00198-0 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500005 PM 8735070 ER PT J AU Yan, J Suga, N AF Yan, J Suga, N TI The midbrain creates and the thalamus sharpens echo-delay tuning for the cortical representation of target-distance information in the mustached bat SO HEARING RESEARCH LA English DT Article DE auditory; bat; combination-sensitive neuron; echolocation; inferior colliculus; medial geniculate body ID COMBINATION-SENSITIVE NEURONS; AUDITORY-CORTEX; INFERIOR COLLICULUS; ECHOLOCATING BAT; NEURAL MECHANISMS; BIOSONAR SIGNALS; MYOTIS-LUCIFUGUS; CENTRAL NUCLEUS; MOUSTACHED BAT; RANGE AB Mustached bats emit complex biosonar 'pulses' for echolocation. A delay of an echo from the emitted pulse carries target-distance information. At the auditory periphery, distance information is expressed by a time interval between the responses of neurons to the emitted pulse and its echo. In the auditory cortex (AC), however, it is mapped by 'FM-FM' neurons which are tuned to particular echo delays. FM-FM neurons have been found not only in the AC but also in the inferior colliculus (IC) of the midbrain and the medial geniculate body (MGB) of the thalamus. In the present study, we found that the IC has a precursor of the cortical echo-delay axis for the systematic representation of target-distance information and that the MGB shows the improved neural representation of target-distance information. C1 WASHINGTON UNIV,DEPT BIOL,ST LOUIS,MO 63130. CR BERKOWITZ A, 1989, HEARING RES, V41, P255, DOI 10.1016/0378-5955(89)90017-8 BUTMAN JA, 1992, THESIS WASHINGTON U COVEY E, 1991, J NEUROSCI, V11, P3456 EDAMATSU H, 1989, J NEUROPHYSIOL, V61, P202 EDAMATSU H, 1993, J NEUROPHYSIOL, V69, P1700 FITZPATRICK KA, 1975, J COMP NEUROL, V164, P185, DOI 10.1002/cne.901640204 FRISINA RD, 1989, J COMP NEUROL, V284, P85, DOI 10.1002/cne.902840107 GRINNELL AD, 1963, J PHYSIOL-LONDON, V167, P38 HATTORI T, 1989, ASS RES OT ABST, P94 HORIKAWA J, 1988, P JPN ACAD B-PHYS, V64, P181, DOI 10.2183/pjab.64.181 KAWASAKI M, 1988, J NEUROPHYSIOL, V59, P623 MITTMANN DH, 1994, ASS RES OT ABST, P93 OLSEN JF, 1991, J NEUROPHYSIOL, V65, P1275 OLSEN JF, 1986, THESIS WASHINGTON U ONEILL WE, 1985, J COMP PHYSIOL A, V157, P797, DOI 10.1007/BF01350077 ONEILL WE, 1979, SCIENCE, V203, P69, DOI 10.1126/science.758681 ONEILL WE, 1982, J NEUROSCI, V2, P17 PARK TJ, 1993, J NEUROSCI, V13, P5172 SAITOH I, 1995, J NEUROPHYSIOL, V74, P1 SAITOH I, 1992, ASS RES OT ABST, P141 SEMPLE MN, 1979, J NEUROPHYSIOL, V42, P1626 SUGA N, 1986, J NEUROPHYSIOL, V55, P776 SUGA N, 1996, ASS RES OT ABST SUGA N, 1971, J PHYSIOL-LONDON, V217, P159 SUGA N, 1990, NEURAL NETWORKS, V3, P3, DOI 10.1016/0893-6080(90)90043-K SUGA N, 1995, ACTIVE HEARING, P13 SUGA N, 1979, SCIENCE, V206, P351, DOI 10.1126/science.482944 SUGA N, 1978, SCIENCE, V200, P778, DOI 10.1126/science.644320 SUGA N, 1994, DYNAMICS NEURAL PROC, P10 SUGA N, 1973, J ACOUST SOC AM, V54, P174, DOI 10.1121/1.1913561 SUGA N, 1983, J NEUROPHYSIOL, V49, P1573 SUGA N, 1970, SCIENCE, V170, P449, DOI 10.1126/science.170.3956.449 SULLIVAN WE, 1982, J NEUROPHYSIOL, V48, P1011 SULLIVAN WE, 1982, J NEUROPHYSIOL, V48, P1033 Teng H., 1995, Society for Neuroscience Abstracts, V21, P666 TENG H, 1994, ASS RES OT ABST, P344 Wenstrup Jeffrey J., 1993, Society for Neuroscience Abstracts, V19, P1426 WENSTRUP JJ, 1995, J NEUROSCI, V15, P4693 WONG D, 1991, NEUROBIOLOGY HEARING, P367 ZOOK JM, 1985, J COMP NEUROL, V231, P530, DOI 10.1002/cne.902310410 NR 40 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. 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PD APR PY 1996 VL 93 IS 1-2 BP 102 EP 110 DI 10.1016/0378-5955(95)00209-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500006 PM 8735071 ER PT J AU Mizuta, K Iwasa, KH Simonds, WF Tachibana, M AF Mizuta, K Iwasa, KH Simonds, WF Tachibana, M TI Ultrastructural localization of G-protein G(s) in the lateral wall of the guinea pig cochlear duct SO HEARING RESEARCH LA English DT Article DE G(s) protein; C-terminal peptide (RMHLRQYELL); immunocytochemistry; post-embedding immunogold; Lowicryl K4M; stria vascularis; Reissner's membrane ID ADENYLATE-CYCLASE; INNER-EAR; NONSELECTIVE CATION; STRIA VASCULARIS; ALPHA-SUBUNITS; BINDING-SITES; CL CHANNELS; RAT-KIDNEY; VASOPRESSIN; STIMULATION AB Immunocytochemical localization of a GTP-binding protein, G(s), in the various cells of the-lateral wall of guinea pig cochlear duct was investigated using a post-embedding immunogold method with antibody raised against a synthetic decapeptide (RMHLRQYELL) encoding the C-terminus of the alpha-subunit of G(s). In the stria vascularis, labeling was observed on the basolateral membrane infoldings of marginal cells, on the juxtaposed membrane of intermediate cells, and on the cell membrane of basal cell. In contrast, no significant labeling was observed on the luminal membrane of marginal cells. Immunoreactivity also was detected on the cell membranes of various other cells. These include spiral prominence epithelial cells, fibrocytes of spiral ligament, external sulcus cells, and epithelial and mesothelial cells of Reissner's membrane. Adenylylcyclase has been functionally implicated in some of the cell types with membranes labeled in this study. The significance of these findings is briefly discussed. C1 NIDOCD,LAB CELLULAR BIOL,BETHESDA,MD 20892. NIDDKD,METAB DIS BRANCH,BETHESDA,MD 20892. NIDOCD,MOLEC GENET LAB,BETHESDA,MD 20892. CR BERTORELLO A, 1989, AM J PHYSIOL, V256, pF57 BIRNBAUMER L, 1990, BIOCHIM BIOPHYS ACTA, V1031, P163, DOI 10.1016/0304-4157(90)90007-Y BRUNSKILL N, 1991, KIDNEY INT, V40, P997, DOI 10.1038/ki.1991.307 DOI K, 1990, EUR ARCH OTO-RHINO-L, V247, P16 FELDMAN AM, 1976, P NATL ACAD SCI USA, V73, P1761, DOI 10.1073/pnas.73.5.1761 GILMAN AG, 1987, ANNU REV BIOCHEM, V56, P615, DOI 10.1146/annurev.biochem.56.1.615 IWAKURA S, 1994, ABSTR SOC NEUROSCI, V20, P971 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 IWASA KH, 1994, NEUROSCI LETT, V172, P163, DOI 10.1016/0304-3940(94)90687-4 KANOH N, 1994, LARYNGOSCOPE, V104, P197 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KITANO I, 1993, HEARING RES, V71, P23, DOI 10.1016/0378-5955(93)90017-U KLEYMAN TR, 1994, AM J PHYSIOL, V266, pF506 KOCH T, 1991, EUR ARCH OTO-RHINO-L, V248, P459, DOI 10.1007/BF00627634 KOCH T, 1992, HEARING RES, V63, P197, DOI 10.1016/0378-5955(92)90085-2 KOCH T, 1988, ARCH OTO-RHINO-LARYN, V245, P82, DOI 10.1007/BF00481441 MARUNAKA Y, 1991, AM J PHYSIOL, V260, pC1071 MEES K, 1984, ARCH OTO-RHINO-LARYN, V240, P55, DOI 10.1007/BF00464345 ZUMGOTTESBERGE AMM, 1991, HEARING RES, V56, P86 MIZUTA K, 1995, IN PRESS HEAR RES MIZUTA K, 1994, ABSTR ASS RES OT, V17, P135 MORI N, 1986, ACTA OTO-LARYNGOL, V101, P217, DOI 10.3109/00016488609132830 NIELSEN S, 1993, P NATL ACAD SCI USA, V90, P11663, DOI 10.1073/pnas.90.24.11663 OGAWA K, 1994, HEARING RES, V74, P197, DOI 10.1016/0378-5955(94)90187-2 PITOVSKI DZ, 1993, HEARING RES, V69, P10, DOI 10.1016/0378-5955(93)90088-I SCHACHT J, 1985, HEARING RES, V20, P9, DOI 10.1016/0378-5955(85)90053-X SCHACHT J, 1982, AM J OTOLARYNG, V3, P328, DOI 10.1016/S0196-0709(82)80005-7 SIMONDS WF, 1989, P NATL ACAD SCI USA, V86, P7809, DOI 10.1073/pnas.86.20.7809 STOW JL, 1991, AM J PHYSIOL, V261, pF831 SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 TACHIBANA M, 1992, HEARING RES, V62, P82, DOI 10.1016/0378-5955(92)90204-Z TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P ZAJIC G, 1983, HEARING RES, V10, P249, DOI 10.1016/0378-5955(83)90090-4 ZENNER HP, 1979, ARCH OTO-RHINO-LARYN, V222, P275, DOI 10.1007/BF01261174 NR 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 APR PY 1996 VL 93 IS 1-2 BP 111 EP 119 DI 10.1016/0378-5955(95)00202-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500007 PM 8735072 ER PT J AU Rosbe, KW Burgess, BJ Glynn, RJ Nadol, JB AF Rosbe, KW Burgess, BJ Glynn, RJ Nadol, JB TI Morphologic evidence for three cell types in the human spiral ganglion SO HEARING RESEARCH LA English DT Article DE spiral ganglion; human; morphometry ID NEURONS; COCHLEA; FIBERS; NERVE AB Although two types of spiral ganglion cells (large type I and smaller type II) have classically been described by anatomic studies in both animal and human spiral ganglion, there is physiologic and morphologic evidence for subtypes of the large type I ganglion cell. In addition, in the animal and human, a variety of morphologic differences based on cytoplasmic content, myelinization, immunostaining and morphometric analysis have suggested more than one variety of type I ganglion cell. Light and electron microscopic serial sections of the spiral ganglion in two human specimens in the basal, middle and upper middle turns were pooled for morphometric analysis of the cell area, nuclear area and axon diameter. Analysis of variance, bivariate scatter plots and multivariate cluster analysis provided evidence for 3 types of ganglion cells in the human spiral ganglion: large, intermediate and small, varying from each other significantly on the basis of cell area. It was suggested, based on the morphologic findings and prevalence of the cell types, that the large and intermediate cells were subtypes of the classic type I spiral ganglion cell, whereas the small ganglion cell was consistent with the classically described type II ganglion cell. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. CR ADAMO NJ, 1973, J NEUROCYTOL, V2, P91, DOI 10.1007/BF01099211 BERGLUND AM, 1991, J COMP NEUROL, V306, P393, DOI 10.1002/cne.903060304 CHIONG CM, 1993, HEARING RES, V67, P211, DOI 10.1016/0378-5955(93)90249-Z ENGLEMAN L, 1990, BMDP STAT SOFTWARE M Hartigan J., 1975, CLUSTERING ALGORITHM KELLERHALS B, 1967, ACTA OTOLARYNGOL S S, P226 Kiang N.Y.S., 1984, P143 LIBERMAN MC, 1980, HEARING RES, V3, P45, DOI 10.1016/0378-5955(80)90007-6 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 NADOL JB, 1990, HEARING RES, V49, P141, DOI 10.1016/0378-5955(90)90101-T NADOL JB, 1990, ANN OTO RHINOL LARYN, V99, P340 OTA CY, 1980, ACTA OTO-LARYNGOL, V89, P53, DOI 10.3109/00016488009127108 ROMAND MR, 1987, ACTA OTO-LARYNGOL, V104, P29, DOI 10.3109/00016488709109044 ROSENBLUTH J, 1962, J CELL BIOL, V12, P329, DOI 10.1083/jcb.12.2.329 Spoendlin H., 1978, EVOKED ELECTRICAL AC, P21 SPOENDLI.H, 1972, ACTA OTO-LARYNGOL, V73, P235, DOI 10.3109/00016487209138937 NR 16 TC 15 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1996 VL 93 IS 1-2 BP 120 EP 127 DI 10.1016/0378-5955(95)00208-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500008 PM 8735073 ER PT J AU Veuillet, E DuverdyBertholon, F Collet, L AF Veuillet, E DuverdyBertholon, F Collet, L TI Effect of contralateral acoustic stimulation on the growth of click-evoked otoacoustic emissions in humans SO HEARING RESEARCH LA English DT Article DE click-evoked otoacoustic emission; contralateral acoustic stimulation; growth function; medial olivocochlear system; human ID CROSSED-OLIVOCOCHLEAR-BUNDLE; COCHLEAR MICROMECHANICAL PROPERTIES; AUDITORY-NERVE RESPONSES; ELECTRICAL-STIMULATION; SOUND STIMULATION; STIMULUS VARIABLES; ACTION-POTENTIALS; FIBER RESPONSES; EFFERENT SYSTEM; GUINEA-PIG AB Input-output (I/O) functions of click-evoked otoacoustic emissions (CEOAEs) were obtained over a 12 dB range for 64 normally hearing adult listeners with and without contralateral broadband noise (BBN). Contralateral acoustic stimulation (GAS) is a convenient way of suppressing responses to ipsilateral stimuli, probably acting via the medial olivocochlear system (MOCS). The present study shows that this contralateral sound suppression of CEOAEs is largest at low stimulus levels. In fact, the curves obtained under CAS approach the curves obtained without CAS as stimulus level rises. I/O slope analysis for the whole study population (n = 64) showed a slight but significant rise in slope with BBN, which may be interpreted as I/O function decompression. A loss of contralateral suppression effect at high ipsilateral stimulus levels was found in both very low and very high amplitude CEOAE subjects, despite the fact that I/O slopes differed between these two groups, whereas rise in slope under contralateral stimulation failed to be found for these same 2 groups of 16 subjects each. These findings clearly indicate that the MOCS is mostly functional at low sound levels, and suggest that the study of CEOAE I/O slope alteration under CAS may help specify one form of MOCS action on cochlear functioning. C1 CHU GRENOBLE,NEUROPHYSIOL LAB,F-38043 GRENOBLE,FRANCE. RP Veuillet, E (reprint author), HOP EDOUARD HERRIOT,LAB PHYSIOL SENSORIELLE AUDIT & VOIX,CNRS,URA 1447,PAVILLON U,3 PL ARSONVAL,F-69347 LYON,FRANCE. 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PD APR PY 1996 VL 93 IS 1-2 BP 128 EP 135 DI 10.1016/0378-5955(95)00212-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500009 PM 8735074 ER PT J AU Furness, DN Hackney, CM Benos, DJ AF Furness, DN Hackney, CM Benos, DJ TI The binding site on cochlear stereocilia for antisera raised against renal Na+ channels is blocked by amiloride and dihydrostreptomycin SO HEARING RESEARCH LA English DT Article DE cochlea; auditory; aminoglycoside; mechanotransduction; epithelial Na+ channel ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; TRANSDUCTION CHANNELS; MECHANOELECTRICAL TRANSDUCTION; SODIUM-CHANNELS; CROSS-LINKS; LOCALIZATION; BUNDLES; CALCIUM AB The mechanoelectrical transduction channels on hair cells have been suggested to be operated by tip links that are stretched when the hair bundle is deflected in the direction of the tallest row of stereocilia. Localising these channels is therefore an important test of this hypothesis. The transduction channels are known to be amiloride-sensitive and immunogold labelling with antibodies raised against the amiloride-sensitive epithelial Na+ channel from kidney (alpha NaCh), has suggested that sites with similar characteristics are located in the region where the tips of the shorter stereocilia appear to come into contact with the sides of the adjacent taller stereocilia rather than being associated directly with the tip links. Now, further immunocytochemical experiments have been performed to determine if amiloride and dihydrostreptomycin, both of which can block transduction, can affect this labelling. Immunofluorescent labelling of the stereocilia is obtained when surface preparations of the organ of Corti are fixed and incubated with alpha NaCh followed by an appropriate secondary antibody. This labelling is abolished by trypsinization prior to fixation but retained if the tissue is pretreated with amiloride and then trypsinized in its presence, Because amiloride is known to protect amiloride-binding sites from degradation by trypsin, these results suggest that alpha NaCh is revealing amiloride-binding sites on the stereocilia. Similarly, immunofluorescent labelling of the stereocilia is abolished if cochlear tissue is pretreated with dihydrostreptomycin (DHS) and fixed in its presence prior to incubation with alpha NaCh. Quantitative analysis of colloidal gold labelling using transmission electron microscopy shows that DHS treatment produces a significant reduction in the number of gold particles on stereocilia, especially in the region of contact between them. These results suggest that anti-Na+ recognises a site with characteristics similar to the mechanoelectrical transduction channels. C1 UNIV ALABAMA,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. 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PD APR PY 1996 VL 93 IS 1-2 BP 136 EP 146 DI 10.1016/0378-5955(95)00224-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500010 PM 8735075 ER PT J AU Zhou, X Hossain, WA Rutledge, A Baier, C Morest, DK AF Zhou, X Hossain, WA Rutledge, A Baier, C Morest, DK TI Basic fibroblast growth factor (FGF-2) affects development of acoustico-vestibular neurons in the chick embryo brain in vitro SO HEARING RESEARCH LA English DT Article DE rhombencephalon; nucleus magnocellularis; nucleus tangentialis vestibularis; cochlear nucleus; cell death; axon growth ID STEM AUDITORY NUCLEI; ADULT-RAT BRAIN; COCHLEOVESTIBULAR GANGLION; NEURITE EXTENSION; NERVOUS-SYSTEM; BASAL LAMINA; N-LAMINARIS; RECEPTOR; SURVIVAL; INVITRO AB The effects of basic fibroblast growth factor (FGF-2) on presumptive auditory and vestibular neurons from the medulla were studied in primary cell cultures. The part of the rhombic lip that forms nucleus magnocellularis (homologue of the mammalian anteroventral cochlear nucleus) was explanted from white leghorn chicken embryos at Hamburger-Hamilton stage 28 (E5.5), the time when precursors of the magnocellularis bushy cells migrate and begin to differentiate in situ. In vitro the neuroblasts migrated onto 2-D substrates of purified collagen, differentiated, and expressed neuronal markers. One-half of the cultures were supplemented with human recombinant FGF-2 (10 ng/ml daily) for 5-7 days; the others, with fetal bovine serum. FGF-2 more than doubled the length of neurite outgrowth during the first 3 day treatment compared to serum, but the number of migrating neuroblasts was unaffected. Although neurites attained greater lengths in FGF-2, they usually degenerated after 4-5 days; in serum their growth continued for several weeks. Differentiation of neuronal structure, including axons and dendrites, began within 1-2 days in bFGF but required at least 5-7 days in serum. Histochemical observations in vitro and in situ with antibodies to FGF receptor demonstrated immunopositive patches on acoustico-vestibular neuroblasts at stage 28, when they are migrating and first forming their axons. The findings suggest that FGF-2 stimulates neurite outgrowth in the cochlear and vestibular nuclei. FGF-2 may accelerate cell death by overstimulating neuroblasts, but other factors are needed to sustain their further development. C1 UNIV CONNECTICUT,CTR HLTH,DEPT ANAT,FARMINGTON,CT 06030. 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Res. PD APR PY 1996 VL 93 IS 1-2 BP 147 EP 166 DI 10.1016/0378-5955(95)00222-7 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500011 PM 8735076 ER PT J AU Malmierca, MS LeBeau, FEN Rees, A AF Malmierca, MS LeBeau, FEN Rees, A TI The topographical organization of descending projections from the central nucleus of the inferior colliculus in guinea pig SO HEARING RESEARCH LA English DT Article DE inferior colliculus; lateral lemniscus; superior olivary complex; cochlear nuclear complex; auditory neuroanatomy-neurophysiology ID DORSAL COCHLEAR NUCLEUS; BRAIN-STEM NUCLEI; LATERAL LEMNISCUS; ALBINO-RAT; COMPUTER RECONSTRUCTION; OLIVOCOCHLEAR NEURONS; EFFERENT PROJECTIONS; CAT; CONNECTIONS; MORPHOLOGY AB We describe the descending projections from the central nucleus of the inferior colliculus (CMC) in guinea pig. Focal injections of the tracer biocytin, made in physiologically defined frequency regions of the CNIC, labelled laminated axonal terminal fields in the ipsilateral dorsal nucleus of the lateral lemniscus, and bilaterally in the ventral nucleus of the trapezoid body and the dorsal cochlear nucleus. Labelling was also present in the rostral periolivary nucleus, but we could not distinguish a clear border between the terminal fields in this nucleus and those in the ventral nucleus of the trapezoid body. Labelling observed in the ventral nucleus of the lateral lemniscus, and to a lesser extent in the dorsal nucleus of the lateral lemniscus, was accompanied by retrogradely labelled somata and therefore we cannot conclude unequivocally that the CNIC projects to these lemniscal nuclei. Where the labelling was ordered topographically, its position varied as a function of the best frequency at the injection site. High-frequency regions in the CNIC project to the medial parts of the ventral nucleus of the trapezoid body and dorsal cochlear nucleus, while low-frequency regions in the CNIC project to the lateral parts of the ventral nucleus of the trapezoid body and dorsal cochlear nucleus. Additional axonal labelling with terminal boutons, but with no apparent topographical arrangement, was present in the ipsilateral horizontal cell group, sagulum, and also bilaterally in the superficial granule cell layer of the ventral cochlear nucleus and layer 2 of the dorsal cochlear nucleus. Our findings are consistent with the existence of tonotopically organised feedback projections from the CNIC to the brainstem nuclei that project to it. C1 UNIV NEWCASTLE UPON TYNE, SCH MED, DEPT PHYSIOL SCI, NEWCASTLE UPON TYNE NE2 4HH, TYNE & WEAR, ENGLAND. 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Res. PD APR PY 1996 VL 93 IS 1-2 BP 167 EP 180 DI 10.1016/0378-5955(95)00227-8 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500012 PM 8735077 ER PT J AU Erway, LC Shiau, YW Davis, RR Krieg, EF AF Erway, LC Shiau, YW Davis, RR Krieg, EF TI Genetics of age-related hearing loss in mice .3. Susceptibility of inbred and F1 hybrid strains to noise-induced hearing loss SO HEARING RESEARCH LA English DT Article DE noise-induced; age-related; brainstem; inbred; hybrid; mice ID ACOUSTIC TRAUMA; C57BL/6J MICE; GENOTYPE; DAMAGE; CBA/CA; MOUSE AB Some humans and mice are genetically predisposed to age-related hearing loss (AHL), and others are variously susceptible to noise-induced hearing loss (NIHL). The inbred C57BL/6J (B6) mice exhibit AHL at an early age, whereas the inbred CBA/CaJ (CB) mice do not. The B6 mice are much more susceptible to NIHL than are the CB mice (Shone et al., 1991; Li, 1992a). The B6 mice possess an Ahl gene which maps to chromosome 10 (Erway et al., 1995). This study was designed, using these two inbred strains plus two F1 hybrid strains of mice, to begin to test the hypothesis that the Ahl genotypes may influence the susceptibility to NIHL. These strains of mice (with putative genotypes) are: inbred CB (+/+) and B6 (Ahl/Ahl); hybrid CBBBF1 (+/Ahl) and B6D2F1 (Ahl/Ahl; D2 represents inbred DBA/2J). Twenty-four mice of each of these four strains were exposed to noise (110 dB for 0, 1 or 2 h) and tested for auditory-evoked brainstem response (ABR) thresholds. The CB and CBB6F1 strains of mice did not differ significantly from each other, exhibiting mostly temporary threshold shifts. The B6 and B6D2F1 strains of mice did not differ significantly from each other, but did exhibit permanent threshold shifts. These results support the hypothesis that genetic predisposition to AHL may be revealed at a younger age by NIHL. This suggests that it may be possible to use the NIHL to distinguish segregating genotypes (+/Ahl vs. Ahl/Ahl) among backcross progeny and thereby to identify and map single genes for AHL. C1 UNIV CINCINNATI,DEPT COMMUN SCI & DISORDERS,CINCINNATI,OH 45221. CTR DIS CONTROL & PREVENT,BIOACOUST & OCCUPAT VIBRAT SECT,PHYS AGENT EFFECTS BRANCH,NIOSH,CINCINNATI,OH 45221. CTR DIS CONTROL & PREVENT,STAT ACTIV,DIV BIOMED & BEHAV SCI,NIOSH,CINCINNATI,OH 45221. RP Erway, LC (reprint author), UNIV CINCINNATI,DEPT BIOL SCI,CINCINNATI,OH 45221, USA. RI Davis, Rickie/A-3186-2008 CR CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X DAVIS RR, 1989, J ACOUST SOC AM, V58, P963 DAVIS RR, 1994, EFFECTS NOISE HEARIN ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H Erway LC, 1996, SCIENTIFIC BASIS OF NOISE-INDUCED HEARING LOSS, P56 ERWAY LC, 1995, ARO MIDW M, P548 HENDERSON D, 1991, J ACOUST SOC AM, V89, P1350, DOI 10.1121/1.400658 HENRY KR, 1992, ACTA OTO-LARYNGOL, V112, P599, DOI 10.3109/00016489209137447 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1983, AUDIOLOGY, V22, P372 HENRY KR, 1982, BEHAV GENET, V12, P563, DOI 10.1007/BF01070410 Li H S, 1992, Scand Audiol Suppl, V36, P1 LI HS, 1993, AUDIOLOGY, V32, P195 LI HS, 1993, HEARING RES, V68, P19, DOI 10.1016/0378-5955(93)90060-E LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 LING XB, 1995, ARP MIDW RES M NEWLANDER JK, 1995, ARO MIDW RES M SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 TAYLOR W, 1965, J ACOUST SOC AM, V38, P113, DOI 10.1121/1.1909580 Willott J. F., 1991, AGING AUDITORY SYSTE NR 21 TC 103 Z9 104 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 1996 VL 93 IS 1-2 BP 181 EP 187 DI 10.1016/0378-5955(95)00226-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500013 PM 8735078 ER PT J AU Lewis, ER Henry, KR AF Lewis, ER Henry, KR TI Nonlinear effects of noise on phase-locked cochlear-nerve responses to sinusoidal stimuli SO HEARING RESEARCH LA English DT Article DE adaptation; AC responsiveness; slow nonlinearity; instantaneous nonlinearity ID AUDITORY-NERVE; FIBER RESPONSES; HAIR-CELLS; TONES; ADAPTATION; MODEL; INTENSITY; DISCRIMINATION; BACKGROUNDS; SUPPRESSION AB It is well known that, in a cochlear afferent axon with background spike activity, a sinusoidal stimulus (tone) of sufficiently low frequency will produce periodic modulation of the instantaneous spike rate, the alternating half cycles of which comprise excursions above and below the mean background spike rate, It also is known that if the amplitude of the stimulus is sufficiently small, the instantaneous spike rate follows very nearly a sinusoidal trajectory through these positive and negative excursions. For such cases, we define the AC responsiveness of a primary auditory afferent axon to be the amplitude of sinusoidal modulation of the instantaneous spike rate divided by the amplitude of the tone producing that modulation. In the experiments described in this paper, changes in AC responsiveness were followed during and after sudden changes in the background noise level. When the amplitude of the tone was sufficiently small relative to that of the noise, we found that the AC responsiveness can be strongly dependent on the time elapsed since the last change in noise level, while being nearly independent of the amplitude of the tone itself. Under those circumstances, after transitions between noise levels 20 dB apart, we observed changes in AC responsiveness that consistently followed time courses similar to those of the short-term mean (background) spike rate (approximating the adapting response to the noise alone), unfolding over several milliseconds or tens of milliseconds. At the time of the transition between noise levels, there was another change in AC responsiveness, which appeared to be instantaneous; as the noise level increased, the AC responsiveness immediately increased with it. This seemingly paradoxical effect and the similarity of the time courses of AC responsiveness and short-term mean spike rate both are consistent with a simple, descriptive model of spike generation involving the shifting of threshold along a bell curve. C1 UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616. RP Lewis, ER (reprint author), UNIV CALIF BERKELEY,DEPT EECS,BERKELEY,CA 94720, USA. 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M., 1968, RECOGNIZING PATTERNS, P104 SMITH RL, 1982, BIOL CYBERN, V44, P107, DOI 10.1007/BF00317970 SMITH RL, 1985, J ACOUST SOC AM, V78, P1310, DOI 10.1121/1.392900 Stein RB, 1970, NEUROSCIENCES, P597 TEICH MC, 1991, MECHANICS BIOPHYSICS, P354 WESTERMAN LA, 1988, J ACOUST SOC AM, V83, P2266, DOI 10.1121/1.396357 WIESENFELD K, 1995, NATURE, V373, P33, DOI 10.1038/373033a0 WINSLOW RL, 1988, HEARING RES, V35, P165, DOI 10.1016/0378-5955(88)90116-5 YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 YU XL, 1989, IEEE T BIO-MED ENG, V36, P36, DOI 10.1109/10.16447 NR 46 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 1995 VL 92 IS 1-2 BP 1 EP 16 DI 10.1016/0378-5955(95)00189-1 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800001 PM 8647731 ER PT J AU Janas, JD Cotanche, DA Rubel, EW AF Janas, JD Cotanche, DA Rubel, EW TI Avian cochlear hair cell regeneration: Stereological analyses of damage and recovery from a single high dose of gentamicin SO HEARING RESEARCH LA English DT Article DE regeneration; aminoglycoside otoxicity; chicks; Basilar papilla ID SEVERE ACOUSTIC TRAUMA; CHICK COCHLEA; INNER-EAR; AMINOGLYCOSIDE OTOTOXICITY; STEREOCILIARY BUNDLES; FUNCTIONAL RECOVERY; BASILAR PAPILLA; KANAMYCIN; TOXICITY; DUCT AB Hair cell regeneration after acoustic trauma has been conclusively documented in birds. Previous studies of aminoglycoside ototoxicity have typically used 5-10 day courses of drug to damage the cochlea and trigger regeneration, This long-term lesion prevented analysis of the early events of regeneration. We set out to determine how much damage would occur and how recovery would proceed after a single high-dose injection of the aminoglycoside gentamicin. White Leghorn chicks were given a single high dose of gentamicin (100 mg/kg). Three post-injection survival groups with age-matched controls were studied: short-term (3-5 days), intermediate-term (2 weeks) and long-term (5 weeks). After sacrifice, cochleae were dissected and processed for scanning electron microscopy. Using stereological techniques, a quantitative analysis of cochlear hair cell counts along the proximal 50% of the cochlea was performed from scanning electron micrographs on 4-7 chicks from each group. Variable degrees of damage were seen 3-5 days after the drug injection. All hair cells were lost from the proximal 20% of the cochlea in all chicks. This complete hair cell loss could extend to 50% of the cochlea. Immature appearing hair cells could be first identified by their immature stereocilia at 3 days, Immature appearing hair cells were present in greatest number in regions which had been denuded of native hair cells and in regions where partial loss occurred. Interestingly, immature appearing hair cells also occasionally appeared in adjacent areas in which there was no apparent loss of native hair cells. Two-week survivors showed an elevation in hair cell number compared to controls in regions which had sustained damage and immediately adjacent regions. This elevation implies that an overproduction of hair cells might occur as part of the regeneration response. By 5 weeks after damage hair cell numbers approximated controls. C1 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT OTOLARYNGOL HEAD & NECK SURG,SEATTLE,WA 98195. CR BHAVE SA, 1995, J NEUROSCI, V15, P4618 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, 1984, DEV BRAIN RES, V16, P181, DOI 10.1016/0165-3806(84)90024-5 COTANCHE DA, 1990, HEARING RES, V46, P29, DOI 10.1016/0378-5955(90)90137-E COTANCHE DA, 1991, STRUCTURAL REORGANIZ CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DUCKERT LG, 1993, J COMP NEUROL, V331, P75, DOI 10.1002/cne.903310105 DUCKERT LG, 1990, HEAR RES, V48 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 GUNDERSEN HJG, 1988, APMIS, V96, P379 HASHINO E, 1992, HEARING RES, V59, P46, DOI 10.1016/0378-5955(92)90101-R HASHINO E, 1993, J CELL SCI, V105, P23 HASHINO E, 1991, HEARING RES, V52, P356, DOI 10.1016/0378-5955(91)90025-5 HASHINO E, 1988, J ACOUST SOC AM, V83, P2450, DOI 10.1121/1.396325 JANAS JD, 1994, ASS RES OT M ST PET KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y 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, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 RYALS BM, 1985, HEARING RES, V19, P73, DOI 10.1016/0378-5955(85)90099-1 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 RYALS BM, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 Saunders J. C., 1982, NEW PERSPECTIVES NOI, P229 STONE JS, 1994, J COMP NEUROL, V341, P50, DOI 10.1002/cne.903410106 STONE JS, 1992, J CELL SCI, V102, P671 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 Tomei L. D., 1991, APOPTOSIS MOL BASIS TSUE TT, 1994, P NATL ACAD SCI USA, V91, P1584, DOI 10.1073/pnas.91.4.1584 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 NR 35 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 1995 VL 92 IS 1-2 BP 17 EP 29 DI 10.1016/0378-5955(95)00190-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800002 PM 8647739 ER PT J AU Ren, TY Brown, NJ Zhang, MS Nuttall, AL Miller, JM AF Ren, TY Brown, NJ Zhang, MS Nuttall, AL Miller, JM TI A reversible ischemia model in gerbil cochlea SO HEARING RESEARCH LA English DT Article DE cochlear blood flow; laser Doppler flowmetry; ischemia/reperfusion injury; cochlea; otoacoustic emission ID STIMULATED ACOUSTIC EMISSIONS; BLOOD-FLOW; PHYSIOLOGICAL VULNERABILITY; DISTORTION PRODUCTS; HEARING-LOSS; EAR; OCCLUSION; RABBIT AB A completely reversible cochlear-ischemia animal model was developed, and an initial study of ischemia/reperfusion-induced cochlear function change is presented. The bulla of the anesthetized gerbil was opened through a ventral approach and the anterior inferior cerebellar artery and its branches were exposed. Cochlear blood flow (CBF) from the basal turn of the cochlea was monitored with a laser Doppler flowmeter. An electrically isolated microclamp was used to occlude the labyrinthine artery (LA). During LA clamping, the cubic distortion product (DP) was continuously recorded. The LA was repeatedly clamped for different durations in all animals, and CBF consistently showed full recovery after clamp release. No obvious change in vessel diameter or flow pattern was observed under a stereomicroscope. Mean blood pressure did not show significant change during clamping. Immediately upon LA clamping, CBF decreased rapidly nearly to zero. After damp release, CBF demonstrated an immediate rapid increase, followed by a secondary gradual recovery to baseline. CBF recovery patterns were clamp duration-related. Within a few seconds of occlusion, DP decreased and reached a minimum of approximately 24% of the initial level in less than 30 s. Following reperfusion of the cochlea, DP gradually increased, decreased again, then slowly recovered. Time delay between CBF reperfusion and the first increase of DP was proportional to clamping duration, and the increased amplitudes demonstrated a negative relationship to clamp duration. We assume that the first decrease in DP during clamping was caused by ischemia in the cochlea; the second decrease, during the cochlear reperfusion, could be a form of reperfusion-induced change in cochlear function. This ischemia/reperfusion model in gerbil cochlea demonstrates excellent repeatability and reversibility. Since DP and other measurements can be used to dynamically monitor cochlear or hair cell functions, this model is useful in studies of auditory physiology and pathophysiology. C1 XIAN MED UNIV,DEPT OTOLARYNGOL,XIAN,PEOPLES R CHINA. RP Ren, TY (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,SCH MED,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 30 EP 37 DI 10.1016/0378-5955(95)00192-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800003 PM 8647743 ER PT J AU Supin, AY Popov, VV AF Supin, AY Popov, VV TI Envelope-following response and modulation transfer function in the dolphin's auditory system SO HEARING RESEARCH LA English DT Article DE modulation transfer function; envelope-following response; auditory brainstem response; dolphin ID AMPLITUDE-MODULATION; TEMPORAL GAPS; SCALP POTENTIALS; FREQUENCY REGION; COCHLEAR NUCLEUS; EVOKED-RESPONSES; NOISE; BANDWIDTH; HEARING; SOUNDS AB Potentials following the envelopes of sinusoidally amplitude-modulated tones (envelope following response, EFR) were recorded from the head surface in bottle-nosed dolphins. EFR appeared at modulation rates from 300 to 3400 Hz. EFR amplitude was higher at rates from 500 to 1400 Hz with peaks at 600 and 1000 Hz and troughs at 700-850, 1200, and 2000 Hz; at rates above 1700 Hz it fell steeply. EFR dependence on modulation depth was linear except at the highest response amplitudes, which made it possible to obtain the modulation transfer function (MTF). EFR appears to be generated by several sources. One source had a latency of about 4 ms and followed modulation rates up to 1700 Hz, while another had a latency of 2 ms and followed modulation rates up to 3.4 kHz. The latencies of both sources coincided with those of waves of the auditory brainstem response (ABR). Comparison of MTF with the ABR spectrum had shown that several MTF peaks and troughs reflected the ABR spectrum. The latencies of the two sources were consistent with origins in the midbrain and auditory nerve, respectively. RP Supin, AY (reprint author), RUSSIAN ACAD SCI, INST ECOL & EVOLUT, 33 LENINSKY PROSP, MOSCOW 117071, RUSSIA. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 38 EP 46 DI 10.1016/0378-5955(95)00194-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800004 PM 8647744 ER PT J AU Kuriki, S Nogai, T Hirata, Y AF Kuriki, S Nogai, T Hirata, Y TI Cortical sources of middle latency responses of auditory evoked magnetic field SO HEARING RESEARCH LA English DT Article DE middle latency auditory evoked field; auditory evoked field; auditory cortex; magnetoencephalography; SQUID AB In the recordings of middle latency responses of auditory evoked magnetic fields in 4 male subjects, we observed distinct components at 11, 19 and 33 ms after click stimulus. Equivalent current dipole sources of these components were located in the supratemporal auditory cortex, where the earliest component source was found at the most medial site. C1 OKAZAKI NATL RES INST,NATL INST PHYSIOL SCI,OKAZAKI,AICHI 444,JAPAN. RP Kuriki, S (reprint author), HOKKAIDO UNIV,RES INST ELECT SCI,KITA KU,N-12,W-6,SAPPORO,HOKKAIDO 060,JAPAN. CR CELESIA GG, 1976, BRAIN, V99, P403, DOI 10.1093/brain/99.3.403 LEE YS, 1984, BRAIN, V107, P115, DOI 10.1093/brain/107.1.115 LIEGEOISCHAUVEL C, 1994, ELECTROEN CLIN NEURO, V92, P204, DOI 10.1016/0168-5597(94)90064-7 MAKELA JP, 1994, ELECTROEN CLIN NEURO, V92, P414, DOI 10.1016/0168-5597(94)90018-3 MCEVOY L, 1994, HEARING RES, V78, P249, DOI 10.1016/0378-5955(94)90031-0 PANTEV C, 1995, ELECTROEN CLIN NEURO, V94, P26, DOI 10.1016/0013-4694(94)00209-4 PELIZZONE M, 1987, NEUROSCI LETT, V82, P303, DOI 10.1016/0304-3940(87)90273-4 Scherg M., 1989, ADV BIOMAGNETISM, P97 YOSHIURA T, 1994, NEUROSCI LETT, V172, P159, DOI 10.1016/0304-3940(94)90686-6 NR 9 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 1995 VL 92 IS 1-2 BP 47 EP 51 DI 10.1016/0378-5955(95)00195-6 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800005 PM 8647745 ER PT J AU Strominger, RN Bohne, BA Harding, GW AF Strominger, RN Bohne, BA Harding, GW TI Regenerated nerve fibers in the noise-damaged chinchilla cochlea are not efferent SO HEARING RESEARCH LA English DT Article DE regenerated nerve fiber; inner ear; AChE-staining; noise; chinchilla ID HAIR CELL REGENERATION; INNER-EAR; ACOUSTIC TRAUMA; NEURONS; GROWTH; DEAFNESS; ORGAN; CORTI AB Nerve-fiber regeneration in the chinchilla cochlea following a traumatic noise exposure was systematically described by Bohne and Harding (1992). However, their study did not determine the origin of the regenerated nerve fibers (RNFs). In the present study, 23 chinchillas were exposed for 12 h to a 0.5 kHz octave band of noise at 120 dB SPL. After a 3-month or 1-year recovery period, their right cochleas were incubated to demonstrate acetylcholinesterase (AChE) activity and then briefly counterstained with Neutral Red or OsO4. Their left cochleas were fixed with OsO4 and dissected using a combined organ of Corti (OC)/modiolus technique that preserved both structures for high-resolution microscopy. All cochleas were prepared as plastic-embedded flat preparations. Damage was located in the basal two-thirds of the cochlea and generally consisted of multiple lesions in the OC, often involving total degeneration of one or more OC segments (i.e., OC wipeouts). The OC wipeouts were separated from one another by areas which contained some identifiable cells of the OC (i.e., OC remnants). Most RNFs were found in OC wipeouts adjacent to OC remnants. In those animals (83%) with significant OC damage, 13 (100%) 3-month-recovery chinchillas had 1-96 RNFs while 6 (86%) 1-year-recovery chinchillas had 7-62 RNFs. In the AChE-stained cochleas, none of the RNFs were AChE-positive, but normal AChE-positive fibers were found in the undamaged apical turn. A variable number of surviving spiral ganglion cells was present in those regions of Rosenthal's canal that had originally innervated the missing hair cells in the OC wipeouts and remnants. It is concluded that RNFs are not part of the efferent cochlear system and therefore, most likely belong to the afferent system. C1 WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,ST LOUIS,MO 63110. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 52 EP 62 DI 10.1016/0378-5955(95)00196-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800006 PM 8647746 ER PT J AU Popelar, J Hartmann, R Syka, J Klinke, R AF Popelar, J Hartmann, R Syka, J Klinke, R TI Middle latency responses to acoustical and electrical stimulation of the cochlea in cats SO HEARING RESEARCH LA English DT Article DE cat; middle latency response; acoustical stimulation; electrical stimulation ID AUDITORY EVOKED-POTENTIALS; TONOTOPIC ORGANIZATION; HEARING-LOSS; GUINEA-PIGS; CORTEX; NERVE; EXCITATION; IMPLANT; COMPONENTS; MODEL AB The middle latency responses (MLR) to acoustical stimulation (A-MLR) as well as to electrical stimulation (E-MLR) of the inner ear were recorded in pentobarbital-anaesthetised cats. Monopolar and bipolar MLR recordings were performed with electrodes located at different places on the primary auditory cortex (AI). The cochlea was electrically stimulated (ES) through a single round-window electrode or through a multichannel intracochlear implant. The slope of amplitude-intensity functions of the A-MLR was steeper when the stimulus frequency of the acoustical stimuli corresponded to the tonotopical recording place on the auditory cortex. Other response properties (waveshape, thresholds and latencies) were related to the recording site and stimulus frequency in only two-thirds of animals. Parameters of E-MLRs evoked by high-frequency (> 4 kHz) and low-intensity ES in hearing cats, which produced an electrophonic effect, were similar to parameters of acoustically evoked MLRs. In deafened cats, the properties of responses to extracochlear ES were different from those recorded to acoustical stimulation and they were almost uniform in all cortical places, Variations in thresholds, in latencies and in the slope of the amplitude-intensity functions of the E-MLRs recorded in individual tonotopical cortical places were observed when the auditory nerve was stimulated with different configurations of electrodes through a multichannel intracochlear implant. C1 UNIV FRANKFURT,ZENTRUM PHYSIOL,D-60590 FRANKFURT,GERMANY. RP Popelar, J (reprint author), ACAD SCI CZECH REPUBL,INST EXPTL MED,VIDENSKA 1083,CR-14220 PRAGUE 4,CZECH REPUBLIC. 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N., 1960, NEURAL MECH AUDITORY, P165 Woolsey CN, 1942, B JOHNS HOPKINS HOSP, V71, P315 XU SA, 1993, HEARING RES, V70, P205, DOI 10.1016/0378-5955(93)90159-X NR 72 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 DEC PY 1995 VL 92 IS 1-2 BP 63 EP 77 DI 10.1016/0378-5955(95)00199-9 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800007 PM 8647747 ER PT J AU Furuta, H Mori, N Luo, L Ryan, AF AF Furuta, H Mori, N Luo, L Ryan, AF TI Detection of mRNA encoding guanylate cyclase A atrial natriuretic peptide receptor in the rat cochlea by competitive polymerase chain reaction and in situ hybridization SO HEARING RESEARCH LA English DT Article DE ANP receptor; cochlea; guanylate cyclase A; in situ hybridization; polymerase chain reaction; rat ID BINDING-SITES; GUINEA-PIG; INNER-EAR; BRAIN; TRANSPORT; GENE; RNA; BIOCHEMISTRY; VASOPRESSIN; EXPRESSION AB Expression of mRNA encoding guanylate cyclase A (GC-A)/atrial natriuretic peptide (ANP) receptor in the rat cochlea was examined by polymerase chain reaction (PCR) and in situ hybridization (ISH). After reverse-transcription, PCR amplification, subcloning, and sequencing, we found that GC-A mRNA with sequence identical to that previously cloned from the rat brain (Chinkers et al., 1989) was expressed in the rat spiral ligament as well as in the spiral ganglion, However, GC-A mRNA was not detected in the stria vascularis. Competitive PCR using internal standard DNAs indicated that the expression of GC-A in the cochlea occurred at a level approximately 16 times less than that measured in kidney cortex. ISH histochemistry using a S-35-labeled antisense riboprobe showed the highest level of expression of GC-A mRNA to be in oligodendrocytes of the cochlear nerve root. The results suggest that ANP may play a role in the cochlear nerve function. C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT SURG OTOLARYNGOL,LA JOLLA,CA 92093. HOUSE EAR RES INST,DEPT NEUROANAT,LOS ANGELES,CA 90059. RP Furuta, H (reprint author), KAGAWA MED SCH,DEPT OTOLARYNGOL,1750-1,MIKI,KAGAWA 76107,JAPAN. CR BEAUMONT K, 1990, J NEUROSCI RES, V25, P256, DOI 10.1002/jnr.490250215 BIDZSERANOVA A, 1991, PHARMACOL BIOCHEM BE, V40, P61, DOI 10.1016/0091-3057(91)90320-2 BRENNER BM, 1990, PHYSIOL REV, V70, P665 CHINKERS M, 1989, NATURE, V338, P78, DOI 10.1038/338078a0 ERMISCH A, 1992, PROG BRAIN RES, V91, P155 FORSSMANN WG, 1986, EUR J CLIN INVEST, V16, P439, DOI 10.1111/j.1365-2362.1986.tb02159.x FULLER F, 1988, J BIOL CHEM, V263, P9395 FURUTA H, 1994, HEARING RES, V78, P175, DOI 10.1016/0378-5955(94)90023-X GENEST J, 1988, REV PHYSIOL BIOCH P, V110, P1, DOI 10.1007/BFb0027530 HORISBERGER JD, 1992, HYPERTENSION, V19, P221 JARD S, 1983, CURR TOP MEMBR TRANS, V18, P255 KOCH T, 1992, HEARING RES, V63, P197, DOI 10.1016/0378-5955(92)90085-2 LUO L, 1993, HEARING RES, V69, P182 MANTYH CR, 1986, HYPERTENSION, V8, P712 MORI N, 1989, ACTA OTO-LARYNGOL, V107, P80, DOI 10.3109/00016488909127482 NUDEL U, 1983, NUCLEIC ACIDS RES, V11, P1759, DOI 10.1093/nar/11.6.1759 PERRIN S, 1990, NUCLEIC ACIDS RES, V18, P7433, DOI 10.1093/nar/18.24.7433 PITOVSKI DZ, 1993, HEARING RES, V69, P10, DOI 10.1016/0378-5955(93)90088-I RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 SAAVEDRA JM, 1991, CAN J PHYSIOL PHARM, V69, P1567 SAIKI RK, 1985, SCIENCE, V230, P1350, DOI 10.1126/science.2999980 SCHULZ S, 1989, CELL, V58, P1155, DOI 10.1016/0092-8674(89)90513-8 SIMMONS DM, 1989, J HISTOTECHNOL, V12, P169 STIEGER M, 1991, J VIROL METHODS, V34, P149, DOI 10.1016/0166-0934(91)90095-H YAMAGUCHI M, 1990, J BIOL CHEM, V265, P20414 YAMAMOTO T, 1994, AM J PHYSIOL, V267, pF318 ZUMGOTTESBERGE AMM, 1989, ACTA OTO-LARYNGOL, V468, P53 NR 27 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 DEC PY 1995 VL 92 IS 1-2 BP 78 EP 84 DI 10.1016/0378-5955(95)00203-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800008 PM 8647748 ER PT J AU Miller, CA Woodruff, KE Pfingst, BE AF Miller, CA Woodruff, KE Pfingst, BE TI Functional responses from guinea pigs with cochlear implants .1. Electrophysiological and psychophysical measures SO HEARING RESEARCH LA English DT Article DE animal model; cochlear implant; electrical stimulation; evoked potential; guinea pig; psychophysics ID BRAIN-STEM RESPONSE; STIMULATED AUDITORY-NERVE; ELECTRICAL-STIMULATION; DETECTION THRESHOLDS; PHASE DURATION; FIBERS; EXCITATION; ELECTRODES; FREQUENCY; PATTERNS AB We examined electrophysiological and psychophysical measures of the electrically stimulated auditory system of guinea pigs implanted with chronic intracochlear electrodes, Guinea pigs were trained to detect low-level acoustic stimuli and then unilaterally deafened and implanted with one extracochlear and two intracochlear electrodes, Electrically evoked auditory brainstem responses (EABRs) and psychophysical detection thresholds were obtained from the same animals using pulsatile stimuli. Supplementary EABR data were obtained from additional, untrained, animals. Thresholds were obtained as a function of stimulus phase duration and monopolar and longitudinal-bipolar electrode configurations. The slopes of the EABR and psychophysical functions for bipolar stimulation, averaged across subjects within 1 month after implantation, were -5.25 and -6.18 dB per doubling of pulse duration, respectively. These slopes were obtained with pulse durations ranging from 20 to 400 mu s/phase; slope was reduced at longer pulse durations. Strength-duration slope also varied as a function of electrode configuration: monopolar stimulation produced steeper functions than did bipolar stimulation. Differences between EABR and psychophysical strength-duration measures suggest the existence of central mechanisms of stimulus integration in addition to that occurring at the level of the auditory nerve, Differences observed with variation of stimulus parameters (e.g., monopolar vs. bipolar stimulation modes) suggest that the specific mode of intracochlear electrical stimulation can influence stimulus integration. Such observations may be useful in the design of prosthetic devices and furthering our understanding of electrical excitation of the auditory system. C1 UNIV MICHIGAN,MED CTR,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. CR ABBAS PJ, 1991, HEARING RES, V51, P139, DOI 10.1016/0378-5955(91)90012-X ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W BEITEL RE, 1995, ABSTR ASS RES OT, P181 Bevington P. R., 1969, DATA REDUCTION ERROR BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P59 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P41 BRISMAR T, 1981, ACTA PHYSIOL SCAND, V113, P161, DOI 10.1111/j.1748-1716.1981.tb06877.x BROWN CJ, 1994, EAR HEARING, V15, P168, DOI 10.1097/00003446-199404000-00006 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BRUMMER SB, 1977, IEEE T BIO-MED ENG, V24, P59, DOI 10.1109/TBME.1977.326218 CHIU SY, 1981, J PHYSIOL-LONDON, V313, P415 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 Fletcher H., 1953, SPEECH HEARING COMMU GOLDSTEIN MH, 1958, J ACOUST SOC AM, V30, P107, DOI 10.1121/1.1909497 HAYES D, 1982, SCAND AUDIOL, V11, P133, DOI 10.3109/01050398209076210 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 Hill AV, 1936, PROC R SOC SER B-BIO, V119, P305, DOI 10.1098/rspb.1936.0012 HODGES AV, 1994, ARCH OTOLARYNGOL, V120, P1093 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 LAFONTAINE S, 1982, J PHYSIOL-LONDON, V323, P287 Lapicque L, 1907, J PHYSIOL-PARIS, V9, P622 Leake PA, 1985, COCHLEAR IMPLANTS, P55 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 MARSH RR, 1981, OTOLARYNG HEAD NECK, V89, P125 MASON SM, 1993, ADV COCHLEAR IMPLANT, P44 MILLER CA, 1993, HEARING RES, V69, P35, DOI 10.1016/0378-5955(93)90091-E MILLER CA, 1993, HEARING RES, V66, P130, DOI 10.1016/0378-5955(93)90134-M MOON AK, 1993, HEARING RES, V67, P166, DOI 10.1016/0378-5955(93)90244-U 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 PETERSEN MR, 1977, J EXP ANAL BEHAV, V27, P529, DOI 10.1901/jeab.1977.27-529 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PFINGST BE, 1993, J ACOUST SOC AM, V94, P1287, DOI 10.1121/1.408155 PFINGST BE, 1995, HEARING RES, V85, P76, DOI 10.1016/0378-5955(95)00037-5 PROSEN CA, 1978, J ACOUST SOC AM, V63, P559, DOI 10.1121/1.381754 RANCK JB, 1975, BRAIN RES, V98, P417, DOI 10.1016/0006-8993(75)90364-9 SHALLOP JK, 1991, ANN OTO RHINOL LARYN, V100, P896 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 Shepherd R K, 1983, Acta Otolaryngol Suppl, V399, P19 Smith D.G., 1995, ABSTR ASS RES OTOL, P177 SMITH DW, 1995, J ACOUST SOC AM, V98, P211, DOI 10.1121/1.413755 SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMITH DW, 1993, ADV COCHLEAR IMPLANT, P8 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 THOMSEN E, 1966, ACTA OTOLARYNGOL S, V224, P442 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 Weisberg S., 1985, APPLIED LINEAR REGRE Weiss G, 1901, ARCH ITAL BIOL, V35, P413 White M.W., 1984, AUDIOL ITAL, V1, P77 YAMANE H, 1981, OTOLARYNG HEAD NECK, V89, P117 ZHOU R, 1994, THESIS U IOWA NR 58 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 DEC PY 1995 VL 92 IS 1-2 BP 85 EP 99 DI 10.1016/0378-5955(95)00204-9 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800009 PM 8647749 ER PT J AU Miller, CA Faulkner, MJ Pfingst, BE AF Miller, CA Faulkner, MJ Pfingst, BE TI Functional responses from guinea pigs with cochlear implants .2. Changes in electrophysiological and psychophysical measures over time SO HEARING RESEARCH LA English DT Article DE animal model; cochlear implant; electrical stimulation; evoked potential; guinea pig; psychophysics ID INTRACOCHLEAR ELECTRICAL-STIMULATION; NEONATALLY DEAFENED CATS; SPIRAL GANGLION-CELLS; BRAIN-STEM RESPONSE; AUDITORY-NERVE; TEMPORAL BONES; PHASE DURATION; FIBERS; EXCITATION; SURVIVAL AB This study, the second of a two-part investigation, assessed changes over time in functional measures of the electrically stimulated auditory system following ototoxic deafening. Guinea pigs were trained to respond behaviorally to threshold level acoustic stimuli and then unilaterally deafened and implanted with a bipolar pair of electrodes within the cochlea and a single extracochlear electrode. Using pulsatile stimuli, thresholds for the electrically evoked auditory brainstem response (EABR) and psychophysical detection were repeatedly collected from the same animals over 3-month post-implantation periods. Thresholds were obtained as a function of stimulus phase duration primarily using bipolar intracochlear stimulation. As in earlier studies, the threshold measures exhibited both intra- and intersubject variability. Analysis of group data failed to show any statistically significant changes over time in either EABR or psychophysical threshold at any fixed pulse duration. However, significant changes over time were found in the slopes of the strength-duration functions for both measures. Slopes became shallower with time, suggesting a reduction in the efficiency of stimulus current integration, a trend presumed to occur with neural degeneration. This result suggests that strength-duration functions could be useful as a clinical diagnostic measure. C1 UNIV MICHIGAN,MED CTR,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. CR ABBAS PJ, 1995, ABSTR ASS RES OT, P180 Bevington P. R., 1969, DATA REDUCTION ERROR BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P59 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P41 BRISMAR T, 1981, ACTA PHYSIOL SCAND, V113, P161, DOI 10.1111/j.1748-1716.1981.tb06877.x BROWN CJ, 1994, EAR HEARING, V15, P168, DOI 10.1097/00003446-199404000-00006 Brown C.J., 1995, EAR HEARING, V16, P1 CHIU SY, 1981, J PHYSIOL-LONDON, V313, P415 Clopton B. M., 1995, Annals of Otology Rhinology and Laryngology, V104, P115 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DORMAN MF, 1992, J SPEECH HEAR RES, V35, P1126 FAYAD J, 1991, ANN OTO RHINOL LARYN, V100, P807 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 GANTZ BJ, 1993, ANN OTO RHINOL LARYN, V102, P909 HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U HARTSHORN DO, 1991, OTOLARYNG HEAD NECK, V104, P311 Hill AV, 1936, PROC R SOC SER B-BIO, V119, P305, DOI 10.1098/rspb.1936.0012 HINOJOSA R, 1983, ANN NY ACAD SCI, V405, P459, DOI 10.1111/j.1749-6632.1983.tb31662.x JYUNG RW, 1989, OTOLARYNG HEAD NECK, V101, P670 KOITCHEV K, 1986, ACTA OTO-LARYNGOL, V102, P31, DOI 10.3109/00016488609108643 LAFONTAINE S, 1982, J PHYSIOL-LONDON, V323, P287 Lapicque L, 1907, J PHYSIOL-PARIS, V9, P622 LEAKE PA, 1992, HEARING RES, V64, P99, DOI 10.1016/0378-5955(92)90172-J LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEAKE PA, 1995, HEARING RES, V82, P65 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MARSH RR, 1981, OTOLARYNG HEAD NECK, V89, P125 MILLER CA, 1993, HEARING RES, V69, P35, DOI 10.1016/0378-5955(93)90091-E MILLER CA, 1994, HEARING RES, V78, P11, DOI 10.1016/0378-5955(94)90039-6 MILLER JM, 1983, ANN OTO RHINOL LARYN, V92, P599 MILLER JM, 1995, IN PRESS AUDITORY PL MILLER JM, 1995, ABSTR ASS RES OT, P181 MOON AK, 1993, HEARING RES, V67, P166, DOI 10.1016/0378-5955(93)90244-U NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 NAGASE S, 1995, ABSTR ASS RES OT, P181 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1990, HEARING RES, V50, P225, DOI 10.1016/0378-5955(90)90047-S RUBINSTEIN JT, 1995, BIOPHYS J, V68, P779 SHANNON RV, 1993, 1993 C IMPL AUD PROS SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 SMITH DW, 1994, HEARING RES, V81, P1, DOI 10.1016/0378-5955(94)90147-3 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 STEEL KP, 1984, HEARING RES, V15, P59, DOI 10.1016/0378-5955(84)90225-9 STYPULKOWSKI PH, 1986, OTOLARYNG CLIN N AM, V19, P249 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 WALTZMAN SB, 1991, OTOLARYNG HEAD NECK, V105, P797 WEBSTER M, 1981, BRAIN RES, V212, P17, DOI 10.1016/0006-8993(81)90028-7 Weiss G, 1901, ARCH ITAL BIOL, V35, P413 ZAPPIA JJ, 1991, ANN OTO RHINOL LARYN, V100, P914 ZHOU R, 1994, THESIS U IOWA NR 55 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 DEC PY 1995 VL 92 IS 1-2 BP 100 EP 111 DI 10.1016/0378-5955(95)00205-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800010 PM 8647732 ER PT J AU Crouch, JJ Schulte, BA AF Crouch, JJ Schulte, BA TI Expression of plasma membrane Ca-ATPase in the adult and developing gerbil cochlea SO HEARING RESEARCH LA English DT Article DE Calcium; ion transport; hair cell; endolymph; homeostasis; immunohistochemistry ID OUTER HAIR-CELLS; INNER-EAR; IMMUNOHISTOCHEMICAL LOCALIZATION; BINDING PROTEINS; GUINEA-PIG; FIBROCYTES; ORGAN AB The distribution of the plasma membrane Ca-ATPase (PMCA) was mapped in the adult and developing gerbil cochlea by immunostaining with a monoclonal antibody against the human erythrocyte PMCA. In the mature cochlea, intense immunoreactivity was present at the surface of stereocilia of both inner (IHC) and outer (OHC) hair cells. The basolateral plasma membrane of IHCs but not OHCs stained strongly whereas that of strial marginal cells and the epithelial cell layer of Reissner's membrane showed only weak reactivity. Nerve terminals underlying IHCs were also selectively stained. At birth, strong to moderate reactivity for PMCA was present in the basolateral plasma membrane of IHCs and OHCs, strial marginal cells, and epithelial cells lining the scala media surface of Reissner's membrane and in the neurolemma of spiral ganglion cells. Immunostaining in the basolateral plasmalemma of OHCs, strial marginal cells, and epithelial cells lining Reissner's membrane remained strong to moderate up to 14 days after birth when it diminished or disappeared entirely, suggesting a developmental role for PMCA activity in these sites. Expression of PMCA at the surface of IHC and OHC stereocilia was first observed at 10 days after birth and staining reached adult levels by 14 days after birth. The abundance of PMCA in the stereociliary plasma membrane of mature hair cells supports the suggested involvement of Ca2+ in regulating transduction and adaptation mechanisms. RP Crouch, JJ (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR ASSAD JA, 1992, J NEUROSCI, V12, P3291 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 PUJOL R, 1991, HEARING RES, V57, P129, DOI 10.1016/0378-5955(91)90082-K ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 SALT AN, 1994, HEARING RES, V74, P115, DOI 10.1016/0378-5955(94)90180-5 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 SCHULTE BA, 1993, HEARING RES, V65, P262, DOI 10.1016/0378-5955(93)90219-Q SEWELL WF, 1990, HEARING RES, V44, P71, DOI 10.1016/0378-5955(90)90023-I SHEPHERD GMG, 1989, P NATL ACAD SCI USA, V86, P4973, DOI 10.1073/pnas.86.13.4973 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z STAHL WL, 1990, J HISTOCHEM CYTOCHEM, V38, P1099 STREHLER EE, 1991, J MEMBRANE BIOL, V120, P1, DOI 10.1007/BF01868586 WALKER RG, 1993, P NATL ACAD SCI USA, V90, P2807, DOI 10.1073/pnas.90.7.2807 WEAVER SP, 1994, HEARING RES, V72, P44, DOI 10.1016/0378-5955(94)90204-6 YAMAMOTO T, 1994, BRAIN RES, V648, P296, DOI 10.1016/0006-8993(94)91130-4 YOSHIHARA T, 1987, ARCH OTO-RHINO-LARYN, V243, P395, DOI 10.1007/BF00464650 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 ZUMGOTTESBERGE AMM, 1988, ACTA OTOLARYNGOL S S, V460, P18 ZUMGOTTESBERGE AMM, 1987, AVIAT SPACE ENV ME A, pA240 NR 20 TC 46 Z9 49 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1995 VL 92 IS 1-2 BP 112 EP 119 DI 10.1016/0378-5955(95)00201-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800011 PM 8647733 ER PT J AU Curtis, LM Rarey, KE AF Curtis, LM Rarey, KE TI Effect of stress on cochlear glucocorticoid protein .2. Restraint SO HEARING RESEARCH LA English DT Article DE immobilization; stress; inner ear; corticosteroid ID INNER-EAR; RECEPTOR; RAT; BINDING AB The effect of restraint stress via immobilization on rat cochlear glucocorticoid receptor (GR) levels was determined using an enzyme-linked immunosorbent assay (ELISA). Results demonstrated that GR levels in cochlear tissues exhibited tissue-specific and time-dependent responses to immobilization (6 hours daily). Similar responses of the GR were observed in rats restrained during two different times of the day. A significant quadratic trend (P = 0.019, R(2) = 0.58) was observed in levels of GR in spiral ligament tissues of rats restrained from 10:00 to 16:00 h; levels of GR were elevated by day 2, and by day 21 GR levels had returned to near normal levels. GR levels in the spiral ligament tissues also were found to increase significantly after 2 days in response to repeated restraint stress administered from 06:00 to 12:00 h (P = 0.017, R(2) = 0.34). Interestingly, a subtle, but statistically significant, decreasing trend in the organ of Cord's GR levels was detected when the daily restraint stress was applied from 06:00 to 12:00 h for up to 7 days. No significant trends (P > 0.05) were observed in GR levels of stria vascularis tissues regardless of the time of day of the restraint protocol. Stress has been implicated as an etiological factor in Meniere's disease and other ear pathologies. The data presented here indicate that the effect of stress is specific to tissue region and that, as in tissues of other systems, the GR of cochlear tissues are responsive to stress. C1 UNIV FLORIDA,J HILLIS MILLER HLTH CTR,DEPT ANAT & CELL BIOL,COLL MED,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. CR Akioka K, 1991, Acta Otolaryngol Suppl, V481, P139 ALEXANDROVA M, 1992, J STEROID BIOCHEM, V42, P493, DOI 10.1016/0960-0760(92)90261-G BAULIEU EE, 1989, ENDOCRINOLOGY, P16 CARLSTEDTDUKE J, 1982, P NATL ACAD SCI-BIOL, V79, P4260, DOI 10.1073/pnas.79.14.4260 GOLDMAN HB, 1962, NEW YORK STATE J MED, V62, P377 GUSTAFSSON JA, 1987, ENDOCR REV, V8, P185 MILLER AH, 1990, AM J PHYSIOL, V259, pE405 MUCHNIK C, 1992, HEARING RES, V58, P101, DOI 10.1016/0378-5955(92)90013-D MUNCK A, 1984, ENDOCR REV, V5, P25 MUNCK A, 1990, AM REV RESPIR DIS, V141, pS2 OTTENWELLER JE, 1979, ACTA ENDOCRINOL-COP, V91, P150 RAREY KE, 1993, HEARING RES, V64, P205, DOI 10.1016/0378-5955(93)90007-N RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 RAREY KE, 1995, HEARING RES, V82, P135, DOI 10.1016/0378-5955(94)00171-L SAPOLSKY RM, 1983, EXP GERONTOL, V18, P55, DOI 10.1016/0531-5565(83)90051-7 Ten Cate Wouter-Jan F., 1994, American Journal of Physiology, V266, pE269 TENCATE WJF, 1992, HEARING RES, V60, P199, DOI 10.1016/0378-5955(92)90021-E TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 WATANABE Y, 1992, BRAIN RES, V588, P341, DOI 10.1016/0006-8993(92)91597-8 NR 19 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 DEC PY 1995 VL 92 IS 1-2 BP 120 EP 125 DI 10.1016/0378-5955(95)00207-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800012 PM 8647734 ER PT J AU Akizuki, H Yoshie, H Morita, Y Takahashi, K Hara, A Watanabe, T Uchiyama, Y Kusakari, J AF Akizuki, H Yoshie, H Morita, Y Takahashi, K Hara, A Watanabe, T Uchiyama, Y Kusakari, J TI Nuclear transition of heat shock protein in guinea pig cochlea after hyperthermia SO HEARING RESEARCH LA English DT Article DE heat shock protein 70 family; immunohistochemical study; hyperthermal stress; nuclear transition ID INSITU HYBRIDIZATION; TRANSIENT ISCHEMIA; RAT COCHLEA; RNA LEVELS; INDUCTION; BRAIN; CELLS; LOCALIZATION; GENE AB The main reaction of heat shock protein (hsp) 70 family to hear shock is 2-fold, one is an increased synthesis in the cytoplasm and the other is a transition from the cytoplasm to the nucleus. Although the former has been already reported in the cochlea by several authors, there has been no description as to the latter. The present study was designed to determine whether this nuclear transition of hsp70 family is also present in the cochlea as in the other organs. Albino guinea pigs subjected to hyperthermia treatment (42 degrees C, 10 min) were killed at 0, 6, 18 or 24 h after the cessation of hyperthermia treatment. Immunohistochemical studies in the cochlea of the untreated animals revealed anti-hsp70 family immunoreactivity mainly in the cytoplasm of the various cells in the cochlea, including the interdental cells, the spiral ganglion cells or the outer hair cells. However, immunoreactivity remarkably increased in the nucleus immediately after the cessation of hyperthermia treatment and this increased immunoreactivity disappeared at 6 h or later. It is concluded that the nuclear transition of hsp70 family also takes place under hyperthermal stress in the cells of the cochlea as in other organs. C1 UNIV TSUKUBA,INST CLIN MED,DEPT OTOLARYNGOL,TSUKUBA,IBARAKI 305,JAPAN. UNIV TSUKUBA,INST BASIC MED SCI,DEPT ANAT,TSUKUBA,IBARAKI 305,JAPAN. OSAKA UNIV,SCH MED,DEPT CELL BIOL & ANAT,OSAKA 565,JAPAN. CR BECKMANN RP, 1990, SCIENCE, V241, P1817 BROWN IR, 1989, NEURON, V2, P1559, DOI 10.1016/0896-6273(89)90044-5 CHAPPELL TG, 1986, CELL, V45, P3, DOI 10.1016/0092-8674(86)90532-5 CHIRICO WJ, 1988, NATURE, V332, P805, DOI 10.1038/332805a0 DECHESNE CJ, 1992, HEARING RES, V59, P195, DOI 10.1016/0378-5955(92)90116-5 LEWIS MJ, 1985, EMBO J, V4, P3137 LIM HH, 1993, HEARING RES, V69, P146 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, 1990, J NEUROCHEM, V54, P451, DOI 10.1111/j.1471-4159.1990.tb01893.x PELHAM HRB, 1986, CELL, V46, P959, DOI 10.1016/0092-8674(86)90693-8 POLLA BS, 1988, IMMUNOL TODAY, V9, P134, DOI 10.1016/0167-5699(88)91199-1 SCHLESINGER MJ, 1986, J CELL BIOL, V103, P321, DOI 10.1083/jcb.103.2.321 SPRANG GK, 1987, MOL BRAIN RES, V3, P89, DOI 10.1016/0169-328X(87)90049-0 THOMPSON AM, 1992, OTOLARYNG HEAD NECK, V107, P769 TOMASOVIC SP, 1989, LIFE CHEM REPORTS, V1, P33 UNEY JB, 1993, J NEUROCHEM, V60, P659, DOI 10.1111/j.1471-4159.1993.tb03198.x UNGEWICKELL E, 1985, EMBO J, V4, P3385 WELCH WJ, 1984, J BIOL CHEM, V259, P4501 NR 19 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 DEC PY 1995 VL 92 IS 1-2 BP 126 EP 130 DI 10.1016/0378-5955(95)00210-3 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800013 PM 8647735 ER PT J AU Shepherd, RK Martin, RL AF Shepherd, RK Martin, RL TI Onset of ototoxicity in the cat is related to onset of auditory function SO HEARING RESEARCH LA English DT Article DE ototoxicity; cochlear development; hearing loss; deafness; aminoglycoside; loop diuretic ID ETHACRYNIC-ACID; POSTNATAL-DEVELOPMENT; COCHLEAR NUCLEUS; HEARING-LOSS; FREQUENCY REPRESENTATION; BASILAR PAPILLA; DEVELOPING RAT; GUINEA-PIG; HAIR-CELLS; INNER-EAR AB Cats are altricial mammals; they are born deaf and undergo rapid maturation of the auditory periphery late in the first and throughout the 2nd week of life. Previous studies, using multiple aminoglycoside administration over several days or weeks, have indicated that there is a reduction in the degree of ototoxicity in young animals provided the drug is administered prior to the onset of auditory function. In order to provide a more precise relationship between the degree of ototoxicity and auditory development, we used a single administration of Kanamycin (KA) and the loop diuretic ethacrynic acid (EA), as the co-administration of these drugs is known to produce a rapid and profound hearing loss in adult animals. Thirty kittens were administered with KA and EA at ages that varied from 2 to 16 days after birth (DAB) using a fixed dose per kilogram body weight sufficient to profoundly deafen adult animals. All animals made an uneventful recovery from the procedure. At 26 DAB, tone-pip-evoked auditory brainstem responses (ABR) were recorded from each animal in order to establish the extent of the hearing loss, The degree of hearing loss was compared with normal ABR audiograms recorded from 6 age-matched control animals. All animals treated with KA/EA at 9 DAB or older had a profound hearing loss similar to adult animals. Animals treated between 2 and 8 DAB exhibited severe high-frequency hearing losses. The extent of the loss was correlated with age (r = 0.63) and body weight (r = 0.72) such that hearing loss tended to spread towards lower frequencies as age and/or weight increased. All animals exhibited bilaterally symmetrical hearing losses which remained relatively stable over monitoring periods of up to 6 months following the drug treatment. These findings imply that the onset of ototoxicity is related, at least in part, to the onset of auditory function in the kitten, The rapid onset of deafness following this procedure makes it a useful technique in the study of both ototoxicity and cochlear development. C1 UNIV MELBOURNE,COOPERAT RES CTR COCHLEAR IMPLANT SPEECH & HEARIN,MELBOURNE,VIC 3002,AUSTRALIA. RP Shepherd, RK (reprint author), UNIV MELBOURNE,DEPT OTOLARYNGOL,32 GISBORNE ST,MELBOURNE,VIC 3002,AUSTRALIA. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 131 EP 142 DI 10.1016/0378-5955(95)00211-1 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800014 PM 8647736 ER PT J AU Reimer, K AF Reimer, K TI Ontogeny of hearing in the marsupial, Monodelphis domestica, as revealed by brainstem auditory evoked potentials SO HEARING RESEARCH LA English DT Article DE marsupial; ontogeny; brainstem auditory evoked potential; audiogram ID SHORT-TAILED OPOSSUM; NORTHERN NATIVE CAT; POSTNATAL-DEVELOPMENT; INFERIOR COLLICULUS; STEM RESPONSE; DASYURUS-HALLUCATUS; THRESHOLDS; SYSTEM; NEUROGENESIS; MATURATION AB Auditory development was studied in the Brazilian short-tailed opossum, Monodelphis domestica, using the brainstem auditory evoked potential (BAEP). Consistent responses can first be recorded 29 days after birth. The hearing range at the onset of hearing is limited to 5-20 kHz with lowest thresholds of 60 dB SPL at 8-12 kHz. During ontogeny, the hearing range expands towards lower and higher frequencies and thresholds decrease until the adult audiogram is obtained by about day 40. Peak latencies and central conduction times are very long at the onset of hearing and decrease until about day 37. In Monodelphis, ontogenetic changes of auditory function are in good agreement with those described for eutherian mammals, suggesting that this small marsupial species can be used as a general model system for auditory development in mammals. RP Reimer, K (reprint author), UNIV ULM, ABT VERGLEICHENDE NEUROBIOL, D-89069 ULM, GERMANY. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 143 EP 150 DI 10.1016/0378-5955(95)00213-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800015 PM 8647737 ER PT J AU Nuttall, AL Ren, TY AF Nuttall, AL Ren, TY TI Electromotile hearing: Evidence from basilar membrane motion and otoacoustic emissions SO HEARING RESEARCH LA English DT Article DE cochlear electric stimulation; basilar membrane vibration; laser Doppler velocimeter; electrophonic hearing; outer hair cell electromotility; guinea ID OUTER HAIR-CELLS; MECHANICAL RESPONSES; COCHLEA; MOTILITY; ORGAN; CORTI AB Electrical stimulation of the cochlea is known to cause auditory sensations in humans and other animals. It also has been shown to produce emissions of sound from the inner ear. In the current study we investigate the relationship between electrically induced motion of the basilar membrane (BM) and the production of otoacoustic emissions. We test the hypothesis that electrical current-induced movements of the outer hair cell (OHC electromotility) result in intracochlear acoustic pressure which causes traveling waves on the BM. Our results demonstrate that the dominant response of the guinea pig inner ear to electric stimulation, at the round window membrane (RW) or across the cochlear duct, is a mechanical response of the organ of Corti. We observed that electrical stimulation of the cochlea produced traveling wave activity on the BM, measured with a laser Doppler velocimeter. The BM motion was accompanied by sound emitted by the cochlea for frequencies up to at least 25 kHz. Furthermore, bipolar rectangular current stimulation produced steady, bipolar displacements of the BM (to 2 nm), indicating functional elongation or contraction of OHCs occurs depending on the polarity of the current pulse. All of the evoked responses were absent after drug treatments eliminated the OHCs. Our data indicate that OHCs undergo electrically evoked displacements capable of producing high-fidelity, high-frequency acoustic energy. The electrically evoked intracochlear energy results in conventional traveling waves within the cochlea, as well as emissions of sound from the cochlea. These data provide direct support for a mechanism of cochlear sensitivity and tuning involving high-frequency OHC electromotility. Moreover, the data also indicate that any intra- or extracochlear electric current which affects the electric polarization of OHCs could induce BM traveling waves and cause 'electromotile hearing'. This form of hearing would be one component under the more general definition of the electrophonic effect. C1 XIAN MED UNIV,DEPT OTOLARYNGOL,XIAN 710061,PEOPLES R CHINA. RP Nuttall, AL (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,5032 KHRI,POB 0506,ANN ARBOR,MI 48109, USA. 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PD DEC PY 1995 VL 92 IS 1-2 BP 170 EP 177 DI 10.1016/0378-5955(95)00216-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800017 PM 8647740 ER PT J AU Ren, TY Nuttall, AL AF Ren, TY Nuttall, AL TI Extracochlear electrically evoked otoacoustic emissions: A model for in vivo assessment of outer hair cell electromotility SO HEARING RESEARCH LA English DT Article DE electrical stimulation; cochlea; outer hair cell motility; acoustic emission ID REVERSE TRANSDUCTION; GUINEA-PIG; COCHLEA AB Cochlear outer hair cell (OHC) motion in response to changes in membrane potential (electromotility) has been extensively studied in vitro. Electromotility is thought to actively control the micromechanical properties of the sensory epithelium. In order to understand how OHC electromotility contributes to normal cochlear responses, its role must be assessed in vivo. We have developed a novel animal model for the study of electromotility in vivo. Alternating current is delivered by an electrode to the round window (RW) of gerbil cochlea and the electrically evoked otoacoustic emission (EEOE) is measured from the external ear canal. As much as 45 dB SPL sound could be generated by about 200 mu A RMS extracochlear current delivered to the RW. Except for the fine structure of EEOE transfer function curves, the magnitude of the EEOE has a bandpass appearance ranging from about 4 to 32 kHz and shows a positive linear relationship to the current intensity. The phase has a linear relationship with frequency and shows no significant change with current intensity. Local intracochlear perfusion of 4% paraformaldehyde caused EEOE to decrease by approximately 20 dB. These results indicate that the EEOE is probably generated by OHCs near the electrode location and propagates to the external ear canal. In addition, the force generated by OHCs in vivo is a linear function of the electrical stimulus. The major advantages of our model include: (1) non-invasive procedure and normal cochlea; (2) wide dynamic range of the measurement; (3) simple and easy preparation. With these features this model has potential applications in basic hearing research and in the diagnosis and treatment of otological patients. C1 XIAN MED UNIV,DEPT OTOLARYNGOL,XIAN 710061,PEOPLES R CHINA. RP Ren, TY (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 178 EP 183 DI 10.1016/0378-5955(95)00217-0 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800018 PM 8647741 ER PT J AU Steyger, PS Wiederhold, ML AF Steyger, PS Wiederhold, ML TI Visualization of newt aragonitic otoconial matrices using transmission electron microscopy SO HEARING RESEARCH LA English DT Article DE otoconia; extracellular matrix; vestibular; tannic acid; transmission electron microscopy ID CRYSTAL-GROWTH; PROTEIN AB Otoconia are calcified protein matrices within the gravity-sensing organs of the vertebrate vestibular system. These protein matrices are thought to originate from the supporting or hair cells in the macula during development. Previous studies of mammalian calcitic, barrel-shaped otoconia revealed an organized protein matrix consisting of a thin peripheral layer, a well-defined organic core and a flocculent matrix inbetween. No studies have reported the microscopic organization of the aragonitic otoconial matrix, despite its protein characterization. Pote et al. (1993b) used densitometric methods and inferred that prismatic (aragonitic) otoconia have a peripheral protein distribution, compared to that described for the barrel-shaped, calcitic otoconia of birds, mammals, and the amphibian utricle. By using tannic acid as a negative stain, we observed three kinds of organic matrices in preparations of fixed, decalcified saccular otoconia from the adult newt: (1) fusiform shapes with a homogenous electron-dense matrix; (2) singular and multiple strands of matrix; and (3) more significantly, prismatic shapes outlined by a peripheral organic matrix. These prismatic shapes remain following removal of the gelatinous matrix, revealing an internal array of organic matter. We conclude that prismatic otoconia have a largely peripheral otoconial matrix, as inferred by densitometry. C1 UNIV TEXAS,HLTH SCI CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,SAN ANTONIO,TX 78284. 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Res. PD DEC PY 1995 VL 92 IS 1-2 BP 184 EP 191 DI 10.1016/0378-5955(95)00221-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TY898 UT WOS:A1995TY89800019 PM 8647742 ER PT J AU Kawase, T Takasaka, T AF Kawase, T Takasaka, T TI The effects of contralateral noise on masked compound action potential in humans SO HEARING RESEARCH LA English DT Article DE contra sound; masking; efferent; cochlear; human ID CROSSED OLIVOCOCHLEAR BUNDLE; COCHLEAR MICROMECHANICAL PROPERTIES; AUDITORY-NERVE FIBERS; ELECTRICAL-STIMULATION; RESPONSE PROPERTIES; EFFERENT NEURONS; GUINEA-PIG; CAT; SOUND; DISCRIMINATION AB The effects of contralateral noise on the masked compound action potential (CAP) were examined in human subjects. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 1 EP 6 DI 10.1016/0378-5955(95)00145-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900001 PM 8647711 ER PT J AU Sato, K Kuriyama, H Altschuler, RA AF Sato, K Kuriyama, H Altschuler, RA TI Expression of glycine receptor subunits in the cochlear nucleus and superior olivary complex using non-radioactive in-situ hybridization SO HEARING RESEARCH LA English DT Article DE glycine receptor; cochlear nucleus; superior olivary complex; hybridization, in situ; rat ID MICROSCOPIC AUTORADIOGRAPHIC LOCALIZATION; CENTRAL NERVOUS-SYSTEM; DEVELOPING RAT-BRAIN; GUINEA-PIG; MESSENGER-RNA; SPINAL-CORD; WIDESPREAD EXPRESSION; FUNCTIONAL EXPRESSION; REGIONAL DISTRIBUTION; AUDITORY PATHWAY AB The distribution of glycine receptor (GlyR) subunit mRNAs was examined in the cochlear nucleus (CN) and superior olivary complex of 5-6-week-old and 8-10-week-old rats using a non-radioactive in-situ hybridization method. In the younger rats, GlyR alpha 1-, alpha 2-, alpha 3- and beta-subunits were observed in all major ventral cochlear nucleus (VCN) and superior olivary complex (SOC) neurons, while only alpha 1-, alpha 3- and beta-subunits were observed in dorsal cochlear nucleus (DCN) neurons. In 8-10-week-old rats, GlyR alpha 1-, alpha 3- and beta-subunits were observed in all major CN and SOC neurons, while mRNA for GlyR alpha 2-subunit was not observed. These results indicate that GlyR is being expressed all major CN and SOC neurons, with alpha 1-, alpha 3- and beta-subunit components of the mature receptor and the alpha 2-subunit, a component of the immature GlyR, which is not down-regulated until after 6 weeks of age in most CN and SOC neurons. C1 UNIV MICHIGAN, KRESGE HEARING RES INST, ANN ARBOR, MI 48109 USA. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 7 EP 18 DI 10.1016/0378-5955(95)00156-5 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900002 PM 8647726 ER PT J AU Felder, E SchrottFischer, A AF Felder, E SchrottFischer, A TI Quantitative evaluation of myelinated nerve fibres and hair cells in cochleae of humans with age-related high-tone hearing loss SO HEARING RESEARCH LA English DT Article DE presbycusis; ageing; cochlea; neuronal degeneration; block surface; micro-dissection ID PATHOLOGY AB In this study 9 human temporal bones from 8 individuals were fixed with Karnovsky solution by perilymphatic perfusion within 1-3 h after death and examined using the 'block-surface method' (Spoendlin and Brun, 1974; Spoendlin and Schrott, 1987) and the 'micro-dissection method' (Johnsson and Hawkins, 1967). The audiogram of 7 individuals showed high-tone hearing loss, typical for sensory-neural presbycusis. The inner (IHC) and outer hair cells (OHC) and the myelinated nerve fibers in the osseous spiral lamina were counted to correlate audiometric curves with hair-cell and nerve-fiber densities. The 'block-surface' method allows accurate hair-cell and myelinated nerve-fiber enumeration with maximal preservation of cochlear structures. The most significant change in the cochlea was not the expected loss of hair cells but an evident loss of nerve fibres in the spiral lamina along the entire length of the cochlea. This loss of nerve fibres was found to be age-related. Reductions up to 30-40% in comparison to normal-hearing middle-aged persons were found in cochleae from persons older than 60 years. In 2 cases only 13% of the fibres remained in some regions of the cochlea. The hair-cell counts showed a reduction of approximately 80% of the OHCs, mainly in the apical parts of the cochlea, and only little differences in the number of IHCs as compared with a group of normal-hearing middle-aged persons. We conclude that neither loss of hair cells nor primary degeneration of nerve fibres alone can fully explain the high-tone loss. Probably injuries of hair cells or neuronal elements at the cellular level can cause threshold elevation. RP Felder, E (reprint author), UNIV INNSBRUCK, DEPT OTOLARYNGOL, HALS NASEN OHREN KLIN, ANICHSTR 35, A-6020 INNSBRUCK, AUSTRIA. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 19 EP 32 DI 10.1016/0378-5955(95)00158-1 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900003 PM 8647720 ER PT J AU Diaz, ME VarelaRamirez, A Serrano, EE AF Diaz, ME VarelaRamirez, A Serrano, EE TI Quantity, bundle types, and distribution of hair cells in the sacculus of Xenopus laevis during development SO HEARING RESEARCH LA English DT Article DE amphibian; hair cell; inner ear; stereocilia bundle; ultrastructure; Xenopus laevis ID ACOUSTIC TRAUMA; TELEOST FISH; CHICK COCHLEA; INNER-EAR; REGENERATION; BULLFROG; GROWTH; SENSITIVITY; INNERVATION; GENTAMICIN AB Proliferation of saccular hair cells of the amphibian, Xenopus laevis, was examined at various stages of development. Numbers of total hair cells and of hair cell bundle types were determined in larval (stages 47, 52 and 56), recently metamorphosed juvenile (1 g), and adult (60 g) animals with scanning electron microscopy (SEM). Hair cells were identified by ultrastructural analysis of the stereociliary bundle. Two general bundle types were present on the sensory epithelium: long stereociliary (LS) and short stereociliary (SS) bundles. Based on the kinocilium length, the SS bundle type was further divided into SS1 (kinocilium greater than or equal to 8 mu m) and SS2 (kinocilium < 8 mu m). The sensory epithelium was composed of a central zone containing all LS and some SS bundles, and a peripheral zone containing only SS bundles. Our results show that in X. laevis, the number of LS and SS bundles, as well as the ratio of LS/SS bundles increased continuously during larval and post-metamorphic development, with an associated enlargement in the sensory epithelium area. These increases were more pronounced during larval life. The percentage of hair cells with SS1 bundles was greater in larval stages, while that of hair cells with SS2 bundles was comparatively higher in juvenile and adult specimens. C1 NEW MEXICO STATE UNIV,DEPT BIOL,LAS CRUCES,NM 88003. 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PD NOV PY 1995 VL 91 IS 1-2 BP 33 EP 42 DI 10.1016/0378-5955(95)00159-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900004 PM 8647723 ER PT J AU Souter, M Nevill, G Forge, A AF Souter, M Nevill, G Forge, A TI Postnatal development of membrane specialisations of gerbil outer hair cells SO HEARING RESEARCH LA English DT Article DE outer hair cell; development; membrane specialisation; gerbil ID GUINEA-PIG COCHLEA; INTERCELLULAR-JUNCTIONS; TECTORIAL MEMBRANE; MONGOLIAN GERBIL; RETICULAR LAMINA; TIGHT JUNCTIONS; FREEZE-FRACTURE; RAT COCHLEA; ORGAN; CORTI AB Using a combination of freeze-fracture and thin sections, this study examines the maturation of the membrane specialisations of the gerbil outer hair cells (OHC) between 2 and 16 days after birth (DAB). The apical membrane, the junctional region around the neck of the cell, and the lateral and basal membranes are described. The results suggest a sequential development of the different components of the lateral wall. Intramembrane protein particles (IMP), the putative OHC motor elements, were found to be present at low density at 2 DAB and increased in density from 2200 IMP/mu m(2) at 2 DAB to 4131/mu m(2) at 8 DAB. OHCs have been reported as showing electromotility from 8 DAB onward. IMPs continue to increase in density until mature values are attained at 16 DAB. Sub-surface cistemae did not appear until 8 DAB, with a single layer being complete by 10 DAB. Pillar structures, proposed to be related to the cytoskeletal lattice, first appear at 10 DAB. The apical membrane of the immature hair cell is characterised by the presence of pits related to the endocytosis of vesicles, and tip-links between stereocilia, thought to be associated with sites of ion channel opening, are present at 2 DAB. The junctional region comprises two areas which mature at differing rates: an apical-most region which attains an adult-like appearance by 8 DAB and a basal-ward region which continues to increase in complexity until mature at 16 DAB. The functional significance of the results are discussed in relation to the possible roles of the junctional regions and the proposed sites of the OHC motor elements. RP Souter, M (reprint author), UCL, SCH MED, INST LARYNGOL & OTOL, 330-332 GRAYS INN RD, LONDON WC1X 8EE, ENGLAND. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 43 EP 62 DI 10.1016/0378-5955(95)00163-8 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900005 PM 8647724 ER PT J AU Song, JK Yan, HY Popper, AN AF Song, JK Yan, HY Popper, AN TI Damage and recovery of hair cells in fish canal (but not superficial) neuromasts after gentamicin exposure SO HEARING RESEARCH LA English DT Article DE hair cell; lateral line; canal neuromast; superficial neuromast; fish; gentamicin ID INNER-EAR; LEPISOSTEUS-PLATYRHINCUS; FINE-STRUCTURE; FLORIDA GAR; REGENERATION; OTOTOXICITY; INNERVATION; MORPHOLOGY; EPITHELIUM; UTRICLE AB Recent evidence demonstrating the presence of two types of sensory hair cell in the ear of a teleost fish (Astronotus ocellatus, the oscar) indicates that hair cell heterogeneity may exist not only in amniotic vertebrates but also in anamniotes. Here we report that a similar heterogeneity between hair cell types may also occur in the other mechanosensory organ of the oscar, the lateral line. We exposed oscars to the aminoglycoside (ototoxic) antibiotic gentamicin sulfate and found damaged sensory hair cells in one class of the lateral line receptors, the canal neuromasts, but not in the other class, the superficial neuromasts. This effect was not due to the canal environment. Moreover, new ciliary bundles on hair cells of the canal neuromasts were found after, and during, gentamicin exposure. The pattern of hair cell destruction and recovery in canal neuromasts is similar to that of type I-like hair cells found in the striolar region of the utricle and lagena of the oscar after gentamicin treatment. These results suggest that the hair cells in the canal and superficial neuromasts may be similar to type I-like and type II hair cells, respectively, in the fish ear. RP Song, JK (reprint author), UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742, USA. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 63 EP 71 DI 10.1016/0378-5955(95)00170-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900006 PM 8647725 ER PT J AU Nozza, RJ AF Nozza, RJ TI Estimating the contribution of non-sensory factors to infant adult differences in behavioral thresholds SO HEARING RESEARCH LA English DT Article DE hearing; human; infant; development; masking ID SPEECH-SOUND DISCRIMINATION; MASKING; FREQUENCY; INTENSITY; NOISE AB Estimates of behavioral thresholds of infants are elevated relative to those of adults. Explanations for the differences include auditory sensory factors and non-sensory factors, but no direct estimates of the relative contributions of these two factors have been made. In this investigation, thresholds in quiet and in increasing levels of a masking noise for a 1 kHz tone, in infants 8 to 11 months old and in adults, were determined. The infant-adult difference in unmasked threshold was compared to the infant-adult difference in an estimate of the minimum masking level (MML) that was derived from the masking data. The intensity level of a masking noise at which masking begins is assumed to be independent of the non-sensory factors that impact on the threshold value itself. Therefore, it is reasoned that the infant-adult difference in MML reflects more closely differences in auditory sensory factors than does the infant-adult difference in unmasked threshold. In the region of 1 kHz, the infant-adult difference in behavioral threshold was 12 dB and the infant-adult difference in MML was 8 dB. Therefore, according to our assumptions, 8 dB of the infant-adult difference in unmasked threshold is accounted for by sensory factors and the remaining 4 dB must be attributable to non-sensory factors. RP Nozza, RJ (reprint author), UNIV GEORGIA,DEPT COMMUN SCI & DISORDERS,565 ADERHOLD HALL,ATHENS,GA 30602, USA. CR FEIGIN JA, 1989, EAR HEARING, V10, P254 HOGAN DD, 1975, AUDITORY ASSESSMENT, P262 KEEFE DH, 1993, J ACOUST SOC AM, V94, P2617, DOI 10.1121/1.407347 NOZZA RJ, 1987, J ACOUST SOC AM, V81, P1928, DOI 10.1121/1.394757 NOZZA RJ, 1990, J ACOUST SOC AM, V87, P339, DOI 10.1121/1.399301 NOZZA RJ, 1988, J SPEECH HEAR RES, V31, P212 NOZZA RJ, 1984, J SPEECH HEAR RES, V27, P613 OLSHO L W, 1988, Journal of the Acoustical Society of America, V84, P1316, DOI 10.1121/1.396630 Schneider B. A., 1992, DEV PSYCHOACOUSTICS, P3, DOI 10.1037/10119-001 Viemeister N. 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PD NOV PY 1995 VL 91 IS 1-2 BP 72 EP 78 DI 10.1016/0378-5955(95)00171-9 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900007 PM 8647727 ER PT J AU Ma, YL Gerhardt, KJ Curtis, LM Rybak, LP Whitworth, C Rarey, KE AF Ma, YL Gerhardt, KJ Curtis, LM Rybak, LP Whitworth, C Rarey, KE TI Combined effects of adrenalectomy and noise exposure on compound action potentials, endocochlear potentials and endolymphatic potassium concentrations SO HEARING RESEARCH LA English DT Article DE endocochlear potential; potassium; compound action potential; noise exposure; adrenalectomy ID NA-K-ATPASE; QUANTITATIVE LOCALIZATION; ADENOSINE-TRIPHOSPHATASE; COCHLEAR POTENTIALS; NEPHRON SEGMENTS; STRIA VASCULARIS; CELLS; RAT; HYDROPS AB The effects of removal of endogenous corticosteroids via bilateral adrenalectomy in combination with noise exposure (30 min at 100 dB) were determined by recording compound action potentials (CAP) and endocochlear potentials (EP), and by measuring potassium concentrations (K-e(+)) within the endolymph. Thirty-eight Long-Evans rats were divided into groups according to experimental treatments: adrenalectomy (ADX) or non-ADX and noise exposure or non-noise exposure. CAP thresholds, EP and K-e(+) values were subjected to repeated-measures analysis of variance with group and time as factors classifying the measurements. Noise exposure resulted in significant elevations of CAP thresholds in both the ADX and non-ADX animals, but had no effect on either EP or endolymphatic K-e(+) Recovery was noted during all post-exposure measurement periods and was significantly faster for ADX animals. EP and K-e(+) did not change during or after noise exposure. ADX animals showed a non-significant reduction of EP and a statistically significant increase of K-e(+) during all measurement periods as compared to non-ADX animals. C1 UNIV FLORIDA,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT COMMUN PROC & DISORDERS,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. SO ILLINOIS UNIV,SCH MED,DEPT SURG,SPRINGFIELD,IL 62794. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 79 EP 86 DI 10.1016/0378-5955(95)00172-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900008 PM 8647728 ER PT J AU Taschenberger, G Gallo, L Manley, GA AF Taschenberger, G Gallo, L Manley, GA TI Filtering of distortion-product otoacoustic emissions in the inner ear of birds and lizards SO HEARING RESEARCH LA English DT Article DE otoacoustic emission; tectorial membrane; auditory filter; bird; lizard ID ACOUSTIC DISTORTION; TECTORIAL MEMBRANE; FREQUENCY; COCHLEA AB When the output magnitude of more than one order of distortion-product otoacoustic emission (DPOAE) is measured, they reach their maximum at the same DPOAE frequency. This fact led several authors to the assumption that, subsequent to their generation in the cochlea, the DPOAE are band-pass filtered. It was suggested that the tectorial membrane is the structure responsible for this filtering. In this report, we show that the same kind of 'DPOAE tuning' is shown by animals which have hearing organs with tectorial structures of very different morphology, or even with no tectorial membrane at all. We therefore conclude that it is unlikely that the filter is the tectorial membrane. C1 TECH UNIV MUNICH, INST ZOOL, D-85747 GARCHING, GERMANY. 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PD NOV PY 1995 VL 91 IS 1-2 BP 87 EP 92 DI 10.1016/0378-5955(95)00174-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900009 PM 8647729 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: A model SO HEARING RESEARCH LA English DT Article DE cochlea; otoacoustic emission; model; hearing; cable equation ID GUINEA-PIG; MONGOLIAN GERBIL; COCHLEA; MECHANICS AB A simple model for the acoustic enhancement of electrically evoked otoacoustic emissions (EEOEs) is presented in this paper. The model is based on the assumption that the enhancement is a result of the local interaction between the electrical current spreading in the scala media and the basilar membrane (BM) response to acoustic input. The analytical, steady-state response of the 1-dimensional linear cable to sinusoidal current injection is derived and is used to predict the current spreading in the cochlea. Acoustic enhancement at an emission generator is modeled as a magnitude change that is a sigmoid function of the local BM motion. The model results are in good agreement with the experimental findings and support our interpretation that the acoustic enhancement of EEOEs reflects BM tuning. C1 BOSTON UNIV,DEPT BIOMED ENGN,BOSTON,MA 02215. BOSTON UNIV,DEPT OTOLARYNGOL,BOSTON,MA 02215. BOSTON UNIV,DEPT ELECT COMP & SYST ENGN,BOSTON,MA 02215. RP Xue, SW (reprint author), DUKE UNIV,MED CTR,DIV OTOLARYNGOL HEAD & NECK SURG,BOX 3550,DURHAM,NC 27710, USA. CR DIEPENDAAL RJ, 1987, J ACOUST SOC AM, V82, P917, DOI 10.1121/1.395290 HUBBARD AE, 1990, HEARING RES, V43, P269, DOI 10.1016/0378-5955(90)90234-G JACK JJB, 1983, ELECTRIC CURRENT FLO JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 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, 1993, BIOPHYSICS HAIR CELL, P409 Mountain DC, 1983, MECHANICS HEARING, P119 MURATA K, 1991, HEARING RES, V55, P201, DOI 10.1016/0378-5955(91)90105-I NAKAJIMA HH, 1994, J ACOUST SOC AM, V96, P786, DOI 10.1121/1.410316 PLASSMANN W, 1987, BRAIN BEHAV EVOLUT, V30, P82, DOI 10.1159/000118639 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 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 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 TASAKI I, 1957, HEAR ANN REV PHYSL, V19, P417 XUE S, 1992, THESIS BOSTON U XUE SW, 1993, HEARING RES, V70, P121, DOI 10.1016/0378-5955(93)90056-7 ZWISLOCK.JJ, 1974, J ACOUST SOC AM, V55, P578, DOI 10.1121/1.1914567 NR 22 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 1995 VL 91 IS 1-2 BP 93 EP 100 DI 10.1016/0378-5955(95)00175-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900010 PM 8647730 ER PT J AU Fechter, LD Liu, Y AF Fechter, LD Liu, Y TI Elevation of intracellular calcium levels in spiral ganglion cells by trimethyltin SO HEARING RESEARCH LA English DT Article DE ototoxicity; trimethyltin; intracellular calcium; excitotoxicity; spiral ganglion cell; calcium channel ID GUINEA-PIG COCHLEA; DEVELOPING RAT COCHLEA; GLUTAMATE NEUROTOXICITY; KAINIC ACID; HAIR-CELLS; NEURONS; CA-2+; NMDA; HIPPOCAMPAL; ACTIVATION AB The neurotoxicant, trimethyltin (TMT) produces cochlear impairment at far lower dose levels and far more rapidly than it does central nervous system effects. The initial effects of TMT in the cochlea, in vivo, are consistent with disruption of the inner hair cell type-1 spiral ganglion cell synapse although it is uncertain whether the effect is on presynaptic and/or postsynaptic units. This synapse is believed to be an excitatory glutamatergic one, providing the possibility that TMT could induce an excitotoxic process resulting in elevations in intracellular calcium ([Ca2+](i)). The objective of this study was to determine whether TMT had direct toxic effects on the postsynaptic spiral ganglion cells studied in primary culture and to identify the role of extracellular calcium in such an effect. The marker of interest was the effect of this agent on [Ca2+](i) levels as determined using quantitation of the fluorescent calcium dye, Fura-2. TMT did induce a marked and sustained elevation in [Ca2+](i) level in the spiral ganglion cells that appeared to have a rapid initial phase and a slower saturating phase. Studies performed using calcium-free medium showed that elevation of [Ca2+](i) in spiral ganglion cells by TMT was attenuated but not entirely blocked. Further, the L-type calcium channel blocker, nifedipine, was able to inhibit the initial increase in [Ca2+](i), suggesting that at least this phase of the TMT effect was mediated by calcium channels, although nifedipine had no significant effect on the time to reach the maximal [Ca2+](i) level. Parallel control experiments performed using application of exogenous glutamate and depolarizing K+ concentrations also produced elevation in [Ca2+](i) levels. The data indicate that TMT elevates [Ca2+](i) in isolated spiral ganglion cells both by increasing extracellular uptake via Ca2+ channels and also by releasing Ca2+ from intracellular stores. Thus TMT ototoxicity appears to include a direct postsynaptic toxic event. RP Fechter, LD (reprint author), UNIV OKLAHOMA,HLTH SCI CTR,COLL PHARM,TOXICOL PROGRAM,POB 26901,OKLAHOMA CITY,OK 73190, USA. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 101 EP 109 DI 10.1016/0378-5955(95)00176-X PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900011 PM 8647712 ER PT J AU McAnally, KI Calford, MB AF McAnally, KI Calford, MB TI Phase effects in forward masking of the compound action potential: A comparison of responses to stimulus and distortion frequencies SO HEARING RESEARCH LA English DT Article DE auditory nerve; auditory non-linearity; distortion product; phase; masking; compound action potential ID TUNING CURVES; 2-TONE; SENSITIVITY; PERCEPTION; 2F1-F2; TONES AB When a complex stimulus is presented, new frequencies (distortion products, DPs) are generated within the cochlea. The most intense DPs are lower in frequency than the stimulus tones (primaries). It is not clear whether the relative phase of stimuli is encoded by neural channels tuned to the primaries or by channels tuned to the DPs. We estimated the response of auditory nerve fibres tuned to each of these channels as a function of the relative phase of harmonic stimuli. The compound action potential (CAP) evoked by probes at the primary or distortion frequencies was masked by harmonic 2-tone maskers and cochlear generated DPs. The degree of masking reflected the response to the masker of fibres tuned to the probe. Changes in relative phase of the primaries resulted in a large modulation of the response of fibres tuned to the DPs. Except for a primary frequency ratio of 1:2, the response of fibres tuned to the primaries was only shallowly modulated by changes in relative phase. However, the level of response to the DPs was much lower than the response to the stimulus tones. C1 UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,ST LUCIA,QLD 4072,AUSTRALIA. RI Calford, Mike/B-4637-2009 OI Calford, Mike/0000-0002-5727-0234 CR BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P386 BUUNEN TJF, 1977, J ACOUST SOC AM, V61, P508, DOI 10.1121/1.381292 CHEATHAM MA, 1990, HEARING RES, V43, P135, DOI 10.1016/0378-5955(90)90222-B DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 GOLDSTEI.JL, 1967, J ACOUST SOC AM, V41, P676, DOI 10.1121/1.1910396 HALL JL, 1972, J ACOUST SOC AM, V51, P1872, DOI 10.1121/1.1913046 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HENRY KR, 1988, J ACOUST SOC AM, V84, P1354, DOI 10.1121/1.396634 KIM DO, 1980, J ACOUST SOC AM, V67, P1704, DOI 10.1121/1.384297 MCANALLY KI, 1992, HEARING RES, V58, P213, DOI 10.1016/0378-5955(92)90130-F MCANALLY KI, 1990, HEARING RES, V44, P51, DOI 10.1016/0378-5955(90)90021-G NORRIS CH, 1984, HEARING RES, V15, P281, DOI 10.1016/0378-5955(84)90034-0 OHM GS, 1943, VORRICHTUNGEN ANN PH, V59, P513 PATTERSON RD, 1987, J ACOUST SOC AM, V82, P1560, DOI 10.1121/1.395146 Plomp R, 1976, ASPECTS TONE SENSATI RADIONOVA EA, 1986, J EVOL BIOCHEM PHYS, V21, P310 RADIONOVA EA, 1990, HEARING RES, V48, P221, DOI 10.1016/0378-5955(90)90062-T SCHMIEDT RA, 1990, J ACOUST SOC AM, V87, P1357, DOI 10.1121/1.399512 von Helmholtz Hermann, 1912, SENSATIONS TONE NR 19 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. 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PD NOV PY 1995 VL 91 IS 1-2 BP 110 EP 118 DI 10.1016/0378-5955(95)00177-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900012 PM 8647713 ER PT J AU Pack, AK Slepecky, NB AF Pack, AK Slepecky, NB TI Cytoskeletal and calcium-binding proteins in the mammalian organ of Corti: Cell type-specific proteins displaying longitudinal and radial gradients SO HEARING RESEARCH LA English DT Article DE inner ear; cochlea; longitudinal gradient; actin; tubulin; calcium-binding protein ID OUTER HAIR-CELLS; INTERMEDIATE FILAMENT PROTEINS; GUINEA-PIG COCHLEA; INNER-EAR; ACTIN; LOCALIZATION; MICROTUBULES; RAT; EXPRESSION; GERBIL AB Whole mounts and tissue sections of the organ of Corti from two representative mammalian species, the Mongolian gerbil (Meriones unguiculatus) and the guinea pig (Caven porcellus) were probed with antibodies to cytoskeletal and calcium-binding proteins (actin, tubulin, including post-translational modifications, spectrin, fimbrin, calmodulin, parvalbumin, calbindin, S-100 and calretinin). kll of the proteins tested were expressed in both species. New findings include the following. Actin is present in large accumulations in cell bodies of the Deiters cells under the outer hair cells (OHC), as well as in the filament networks previously described. These accumulations are more prominent in the apical turns. Tubulin is present in sensory cells in the tyrosinated (more dynamic) form, while tubulin in the supporting cells is post-translationally modified, indicating greater stability. Fimbrin, present in the stereocilia of both IHCs and OHCs, is similar to the isoform of fimbrin found in the epithelial cells of the intestine (fimbrin-I), which implies that actin bundling by fimbrin is reduced in the presence of increased calcium. Parvalbumin appears to be an IHC-specific calcium-binding protein in the gerbil as well as in the guinea pig; labeling displays a longitudinal gradient, with hair cells at the apex staining intensely and hair cells at the base staining weakly. Calbindin displays a similar longitudinal gradient, with staining intense in the IHCs and OHCs at the apex and weak to absent in the base. In the middle turns of the guinea pig cochlea, OHCs in the first row near the pillar cells lose immunoreactivity to calbindin before those in the second and third rows. Calmodulin is found throughout the whole cochlea in the IHCs and OHCs in the stereocilia, cuticular plate, and cell body. Calretinin is present in IHCs and Deiters cells in both species, as well as the tectal cell (modified Hensen cell) in the gerbil. S-100 is a supporting cell-specific calcium-binding protein which has not been localized in the sensory cells of these two species. The supporting cells containing S-100 include the inner border, inner phalangeal, pillar, Deiters, tectal (in gerbil) and Hensen cells, where labeling displays a longitudinal gradient decreasing in intensity towards the apex (opposite to what has been seen with labeling for other proteins in the cochlea). C1 SYRACUSE UNIV,INST SENSORY RES,DEPT BIOENGN & NEUROSCI,SYRACUSE,NY 13244. SUNY HLTH SCI CTR,DEPT ANAT & CELL BIOL,SYRACUSE,NY 13210. 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PD NOV PY 1995 VL 91 IS 1-2 BP 119 EP 135 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900013 PM 8647714 ER PT J AU Slepecky, NB Henderson, CG Saha, S AF Slepecky, NB Henderson, CG Saha, S TI Post-translational modifications of tubulin suggest that dynamic microtubules are present in sensory cells and stable microtubules are present in supporting cells of the mammalian cochlea SO HEARING RESEARCH LA English DT Article DE inner ear; cochlea; tubulin; tubulin, tyrosinated; tubulin, acetylated; tubulin, detyrosinated; tubulin, polyglutamated ID ACETYLATED ALPHA-TUBULIN; HAIR-CELLS; INNER-EAR; GUINEA-PIG; POSTTRANSLATIONAL MODIFICATIONS; TYROSINATION DETYROSINATION; CEREBELLAR MACRONEURONS; MONOCLONAL-ANTIBODY; ELEVATED LEVELS; BETA-TUBULIN AB Post-translational modifications to tubulin in the sensory and supporting cells of the cochlea were studied using antibodies specific to the tyrosinated, detyrosinated, acetylated and polyglutamylated isoforms. In the sensory cells, microtubules which label intensely with antibodies to tyrosinated tubulin are found in networks within the cytoplasm. Microtubules which label with antibodies to detyrosinated tubulin and polyglutamylated tubulin, but not acetylated tubulin, form a small component of the microtubules found in the cytoplasm only in the region below the cuticular plate. Microtubules in the supporting cells (inner and outer pillar cells and Deiters cells) are arranged in bundles and contain little tyrosinated tubulin. They are composed instead of predominantly post-translationally modified isoforms which include detyrosinated, acetylated and polyglutamylated tubulin. The findings suggest that microtubules in the sensory cells form dynamic structures, since microtubules that undergo cyclic polymerization and depolymerization predominantly contain tubulin that has not yet had its carboxy-terminal tyrosine residue removed. The presence of microtubules in the supporting cells in which the tubulin has been polymerized into microtubules long enough to be post-translationally modified, provides evidence that these microtubules are stable, long-lived and could contribute to the structural support of the sensory organ of Corti. C1 UNIV ST ANDREWS,SCH BIOL & MED SCI,ST ANDREWS,FIFE,SCOTLAND. RP Slepecky, NB (reprint author), SYRACUSE UNIV,INST SENSORY RES,DEPT BIOENGN & NEUROSCI,SYRACUSE,NY 13244, USA. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 136 EP 147 DI 10.1016/0378-5955(95)00184-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900014 PM 8647715 ER PT J AU Cotanche, DA Messana, EP Ofsie, MS AF Cotanche, DA Messana, EP Ofsie, MS TI Migration of hyaline cells into the chick basilar papilla during severe noise damage SO HEARING RESEARCH LA English DT Article DE noise damage; hyaline cell; regeneration; actin; hair cell; cochlea; confocal microscopy ID OUTER HAIR-CELLS; AVIAN INNER-EAR; ACOUSTIC TRAUMA; EXTRACELLULAR-MATRIX; SPIRAL LIGAMENT; COCHLEA; REGENERATION; ACTIN; PROTEINS; OVERSTIMULATION AB Severe acoustic damage in the chick cochlea causes a destruction of both hair cells and supporting cells in a localized area on the basilar papilla. In this region, the sensory cells are replaced by a layer of flattened epithelial cells. We have employed scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM) to examine the structure and cytoskeletal changes involved in this process. Immunocytochemical staining for actin indicates that the flattened cells are derived from the hyaline cells normally located along the inferior edge of the basilar papilla. In control cochleae the hyaline cells contain dense bundles of actin filaments that anchor into the basal surface of the cells. The hyaline cells appear to redistribute into the severely damaged region by extending the actin bundles at their basal surfaces. Moreover, the efferent nerves that normally form a network among the hyaline cells move into the severely damaged area along with the hyaline cells. In moderately damaged cochleae, where only hair cells are lost, the hyaline cells do not spread into the damaged region. 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PD NOV PY 1995 VL 91 IS 1-2 BP 148 EP 159 DI 10.1016/0378-5955(95)00185-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900015 PM 8647716 ER PT J AU Ebert, U Ostwald, J AF Ebert, U Ostwald, J TI GABA alters the discharge pattern of chopper neurons in the rat ventral cochlear nucleus SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; gamma-aminobutyric acid; inhibition; iontophoresis; temporal discharge pattern; rat ID SUPERIOR OLIVARY COMPLEX; STEM AUDITORY NUCLEI; GUINEA-PIG; DESCENDING PROJECTIONS; RESPONSE PROPERTIES; HORSERADISH-PEROXIDASE; REGULARITY ANALYSIS; GLYCINE; CAT; IMMUNOREACTIVITY AB The effect of microiontophoretically applied gamma-aminobutyric acid (GABA) on chopper neurons in the ventral cochlear nucleus of the rat is described. The predominantly inhibitory effect of GABA resulted in a change of the regular discharge pattern. The interspike interval increased and the pattern became less regular as indicated by an increase of its coefficient of variation. These results suggest that the release of GABA may be responsible for the transient chopper behavior of some neurons which loose their regular discharge pattern within 20 ms after onset of the response to pure-tone stimulation. C1 UNIV TUBINGEN,TUBINGEN,GERMANY. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 160 EP 166 DI 10.1016/0378-5955(96)83100-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900016 PM 8647717 ER PT J AU Souter, M AF Souter, M TI Suppression of stimulus frequency otoacoustic emissions by contralateral noise SO HEARING RESEARCH LA English DT Article DE stimulus frequency otoacoustic emission; contralateral noise; efferent; human ID CROSSED OLIVOCOCHLEAR BUNDLE; BINAURAL ACOUSTIC STIMULATION; SOUND STIMULATION; GUINEA-PIG; DISTORTION PRODUCTS; COCHLEAR MECHANICS; ACTION-POTENTIALS; EFFERENT NEURONS; THRESHOLD SHIFT; TONIC ACTIVITY AB The effect of different bands of contralaterally presented noise at low and moderate intensities on stimulus frequency otoacoustic emissions (SFOAE) from human ears is examined. A SFOAE evoked by a continuous stimulus tone and suppressed by a second tone to produce an SFOAE residual was chosen as the probe to determine the effect of the efferent input. At low levels of contralateral noise, a band centred on the ipsilateral stimulus frequency was the most effective suppressor of the SFOAE residual. For higher levels of the contralateral stimulus, noise bands containing higher frequency components produced most reductions in the SFOAE residual. Small changes in the phase of the SFOAE residual during the contralateral noise were also recorded. Increases in the SFOAE residual onset latency were also found to be small, being around 1 ms. In some cases increases in the level of the SFOAE residual produced by low-frequency suppressors were recorded during the contralateral noise presentation. The results are discussed in the context of current knowledge of the functioning of the auditory efferent innervation, and it is suggested that the method of evoking SFOAEs presents a viable method for determining the effect of efferent stimulation on cochlear mechanics which also allows possible artifact contamination to be readily identified. RP Souter, M (reprint author), UCL, SCH MED, INST LARYNGOL & OTOL, 330-332 GRAYS INN RD, LONDON WC1X 8EE, ENGLAND. 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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 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 NR 38 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 NOV PY 1995 VL 91 IS 1-2 BP 167 EP 177 DI 10.1016/0378-5955(95)00187-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900017 PM 8647718 ER PT J AU Vater, M Siefer, W AF Vater, M Siefer, W TI The cochlea of Tadarida brasiliensis: Specialized functional organization in a generalized bat SO HEARING RESEARCH LA English DT Article DE cochlear frequency map; hair cell; echolocation ID OUTER HAIR-CELLS; SCANNING ELECTRON-MICROSCOPY; GUINEA-PIG COCHLEA; CF-FM BAT; FREQUENCY REPRESENTATION; PTERONOTUS-PARNELLII; TECTORIAL MEMBRANE; SPIRAL LIGAMENT; HORSESHOE BAT; MUSTACHE BAT AB Tadarida brasiliensis mexicana employs a broad-band sonar system at frequencies between 80 and 20 kHz and is characterized by non-specialized hearing capabilities. The cochlear frequency map was determined with extracellular horseradish peroxidase tracing in relation to quantitative morphological data obtained with light, scanning and transmission electron microscopy. These data reveal distinct species characteristic specializations clearly separate from the patterns observed in other bats with either broad-band or narrow-band sonar systems. The basilar membrane (BM) is coiled to 2.5 turns and about 12 mm long. Its thickness and width only change within the extreme basal and apical ends. The frequency range from about 30 to 80 kHz is represented in the lower basal turn with a typically mammalian mapping coefficient of about 3 mm/octave. This region exhibits morphological features correlated with non-specialized processing of high frequencies. (1) The BM is radially segmented by thickenings of pars tecta and pars pectinata. (2) The 3 rows of outer hair cells (OHCs) have similar morphology. Between 35 and 86% distance from base, frequencies between 30 and 12 kHz are represented with a slightly expanded mapping coefficient of about 6 mm/octave. In analogy to previous work, this cochlea region is termed 'acoustic fovea'. It includes the frequency range of maximum sensitivity and sharpest tuning (21-27 kHz) but also frequencies below the sonar signals. The fovea is characterized by several morphological specializations. (1) The BM features a continuous radial thickening mainly composed of hyaline substance. (2) There is an increased number of layers of tension fibroblasts in the spiral ligament. (3) There are morphological differences in the arrangements of stereocilia bundles among the 3 rows of OHCs. 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Res. PD NOV PY 1995 VL 91 IS 1-2 BP 178 EP 195 DI 10.1016/0378-5955(95)00188-3 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900018 PM 8647719 ER PT J AU Hisashi, K Nakagawa, T Yasuda, T Kimitsuki, T Komune, S Komiyama, S AF Hisashi, K Nakagawa, T Yasuda, T Kimitsuki, T Komune, S Komiyama, S TI Voltage-dependent Ca2+ channels in the spiral ganglion cells of guinea pig cochlea SO HEARING RESEARCH LA English DT Article DE spiral ganglion cell; guinea pig; patch-clamp technique; calcium channel; calcium antagonist ID CHICK SENSORY NEURONS; CALCIUM CHANNELS AB Voltage-dependent Ca2+ channels in spiral ganglion cells (SGCs) isolated from guinea pig cochlea were investigated using the patch-clamp technique in a whole-cell recording mode. The voltage-dependent Na+ and K+ currents were blocked by adding tetrodotoxin, 4-aminopyridine, and tetraethylammonium to the external solution and by using choline or Cs+ in the external and internal solutions instead of Na+ or K+, respectively. The depolarizing voltage steps evoked inward currents with slow current decay. The maximum amplitude of the inward current increased in a hyperbolic manner with increasing extracellular Ca2+ concentration, indicating that the inward current was a voltage-dependent Ca2+ current (I-Ca) In 5 mM Ca2+ external solution, the I-Ca activated from a membrane potential around -60 mV and reached full activation at about -10 mV. The I-Ca inactivated from about -60 mV and became fully inactivated at about 0 mV, consistent with the high-voltage-activated Ca2+ channel subtype. Ionic selectivities for Ca2+ channels in SGCs were as follows: Ca2+ > Ba2+ > Sr2+. Effects of both inorganic and organic Ca2+ antagonists also were examined. 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PD NOV PY 1995 VL 91 IS 1-2 BP 196 EP 201 DI 10.1016/0378-5955(95)00191-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900019 PM 8647721 ER PT J AU FerberViart, C Savourey, G Garcia, C Duclaux, R Bittel, J Collet, L AF FerberViart, C Savourey, G Garcia, C Duclaux, R Bittel, J Collet, L TI Influence of hyperthermia on cochlear micromechanical properties in humans SO HEARING RESEARCH LA English DT Article DE body temperature; otoacoustic emission, click evoked; cochlear micromechanical activity ID SPONTANEOUS OTOACOUSTIC EMISSIONS; TEMPERATURE-DEPENDENCE; ATTENTION; TASK AB We investigated the effect of body temperature on transient evoked otoacoustic emissions (TEOAEs) in humans. Hyperthermic conditions were obtained in adults in a climatic chamber. During hyperthermia up to an average temperature of 38.4 degrees C, significant falls were found in total amplitude and peak values of TEOAEs: by 1.3 dB SPL/degrees C and 2.3 dB/degrees C, respectively. This inhibition affected all spectrum components equally. These findings indicate that the outer hair cell micromechanical activity that is presumed to be measured by TEOAEs is not independent of variations in body temperature. The reduction found in hyperthermia suggests that temperature-dependent mechanisms are involved in the generation of TEOAEs. C1 UNIV LYON 1,HOP EDOUARD HERRIOT,LAB PERCEPT & MECAN AUDITIFS,CNRS,URA 1447,F-69437 LYON,FRANCE. CRSSA,LAB THERMOPHYSIOL,F-38700 LA TRONCHE,FRANCE. RP FerberViart, C (reprint author), CTR HOSP LYON SUD,SERV EXPLORAT FONCTIONNELLE NEUROSENSORIELLE,HOSPICES CIVILS LYON,PAV 3A,F-69495 PIERRE BENITE,FRANCE. CR ATTIAS J, 1991, J THERM BIOL, V16, P249, DOI 10.1016/0306-4565(91)90012-Q AVAN P, 1992, HEARING RES, V57, P269, DOI 10.1016/0378-5955(92)90156-H BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 FLOCK A, 1985, ACTA OTO-LARYNGOL, V99, P495, DOI 10.3109/00016488509108943 FROEHLICH P, 1994, HEARING RES, V75, P184, DOI 10.1016/0378-5955(94)90069-8 FROEHLICH P, 1990, BRAIN RES, V508, P286, DOI 10.1016/0006-8993(90)90408-4 FROEHLICH P, 1993, PHYSIOL BEHAV, V53, P679, DOI 10.1016/0031-9384(93)90173-D HARDY JD, 1961, PHYSIOL REV, V41, P521 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 KOHSHI K, 1990, J APPL PHYSIOL, V69, P1419 LEWIS ER, 1982, J COMP PHYSIOL, V145, P437 MERIC C, 1993, ACTA OTO-LARYNGOL, V113, P471, DOI 10.3109/00016489309135848 PUEL JL, 1989, NATO ASI SER, P315 VANDIJK P, 1987, J ACOUST SOC AM, V82, P2147, DOI 10.1121/1.395660 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L WILSON JP, 1986, AUDITORY FREQUENCY S, P39 WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 ZUREK PM, 1981, J ACOUST SOC AM, V69, P513 NR 22 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 NOV PY 1995 VL 91 IS 1-2 BP 202 EP 207 DI 10.1016/0378-5955(95)00193-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TU889 UT WOS:A1995TU88900020 PM 8647722 ER PT J AU SOUTER, M AF SOUTER, M TI STIMULUS FREQUENCY OTOACOUSTIC EMISSIONS FROM GUINEA-PIG AND HUMAN-SUBJECTS SO HEARING RESEARCH LA English DT Article DE STIMULUS FREQUENCY OTOACOUSTIC EMISSION; GUINEA PIG; HUMAN ID ACOUSTIC DISTORTION; STIMULATION; EAR; MECHANICS; PATTERNS; COCHLEA AB Stimulus frequency otoacoustic emissions (SFOAEs) have previously been recorded from human subjects by the suppression of a continuous stimulus tone generated OAE by a second tone (Kemp et al., 1990). This study presents comparative data from guinea pig and human subjects using a similar method. Differences between human and guinea pig responses to suppressor tones of higher frequency than the stimulus tone are reported. The most effective suppressors of the SFOAE in human subjects was found to be a tone of the same or slightly higher frequency than the continuous stimulus tone. In guinea pigs, this stimulus condition was found to be less effective than higher-frequency suppressors. Large phase changes were found in the SFOAE from guinea pigs when higher-frequency suppressors were employed. These were not seen in the human data. Changes in the SFOAE latency from guinea pig ears were also found as the suppressing tone frequency moved above that of the stimulus tone. These level and phase effects, when taken together with latency changes, may be indicative of the differing contributions of stimulus-place generated OAEs and those from more basal elements to the total emission recorded in the meatus in guinea pig. The results are discussed in view of the known species differences in the tuning characteristics at the frequency region studied. RP SOUTER, M (reprint author), UNIV COLL & MIDDLESEX SCH MED, INST LARYNGOL & OTOL, 330-332 GRAYS INN RD, LONDON WC1X 8EE, ENGLAND. CR AVAN P, 1993, HEARING RES, V70, P109, DOI 10.1016/0378-5955(93)90055-6 BRASS D, 1993, J ACOUST SOC AM, V93, P920, DOI 10.1121/1.405453 BRASS D, 1991, J ACOUST SOC AM, V90, P2415, DOI 10.1121/1.402046 BROWN AM, 1990, J ACOUST SOC AM, V88, P840, DOI 10.1121/1.399733 BROWN AM, 1993, J ACOUST SOC AM, V93, P3291, DOI 10.1121/1.405713 Evans E. F., 1989, BRIT J AUDIOL, V23, P151 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 Guinan JJ, 1990, MECH BIOPHYSICS HEAR, P170 KEMP DT, 1990, LECT NOTES BIOMATH, V87, P202 KEMP DT, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 Kemp DT, 1980, PSYCHOPHYSICAL PHYSL, P34 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 MASTERTO.B, 1969, J ACOUST SOC AM, V45, P966, DOI 10.1121/1.1911574 MOORE BCJ, 1983, J ACOUST SOC AM, V74, P750, DOI 10.1121/1.389861 NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 ROBERTSON D, 1985, HEARING RES, V20, P63, DOI 10.1016/0378-5955(85)90059-0 ROSOWSKI JJ, 1991, J ACOUST SOC AM, V90, P124, DOI 10.1121/1.401306 RUGGERO MA, 1990, J ACOUST SOC AM, V87, P1612, DOI 10.1121/1.399409 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 NR 20 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 1995 VL 90 IS 1-2 BP 1 EP 11 DI 10.1016/0378-5955(95)00124-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300001 PM 8974986 ER PT J AU SALT, AN DEMOTT, JE AF SALT, AN DEMOTT, JE TI ENDOLYMPH VOLUME CHANGES DURING OSMOTIC DEHYDRATION MEASURED BY 2 MARKER TECHNIQUES SO HEARING RESEARCH LA English DT Article DE COCHLEA; ENDOLYMPH; ENDOLYMPHATIC HYDROPS; MENIERES DISEASE; OSMOLARITY ID GUINEA-PIG COCHLEA; INNER-EAR; ION-TRANSPORT; SCALA MEDIA; FLOW-RATE; HYDROPS; PERMEABILITY; PERILYMPH AB The processes underlying endolymph volume regulation during osmotic disturbances were investigated in vivo using ionic volume markers. The markers utilized were tetramethylammonium (TMA(+)) or hexafluoroarsenate (AsF6-). Both ions were used in concentrations low enough not to be toxic, but readily detectable by ion-selective microelectrodes (typically < 1 mM). Two marker techniques were developed. In one, termed the 'perfused volume marker' (PVM) method, the marker was loaded into endolymph throughout the cochlea by perfusion of the perilymphatic space. Concentration changes of the marker were measured with a double-barreled ion-selective microelectrode. These recordings were insensitive to longitudinal movements of endolymph. The second technique, termed the 'iontophoresed volume marker' (IVM) method, utilized a localized, iontophoretic injection of marker into endolymph. In this method, marker changes were recorded from two ion-selective electrodes, one placed basal and one placed apical to the injection site. These data were used to compute changes in cross-sectional area and longitudinal movements of endolymph. Changes in endolymph volume were induced by perfusion of the perilymphatic space with hypertonic media. The endolymph potassium increase produced by osmotic dehydration was of similar magnitude and time course to that of a volume marker loaded by the PVM method. Using the IVM method, it was shown that these concentration increases arose by two distinct processes. One component was the area decrease of scala media. A second component was a small apically directed movement of endolymph during dehydration, thereby concentrating the available electrolytes within a smaller volume. This latter component was estimated to contribute approximately one third of the electrolyte increase during dehydration. Both the present and previous studies show that in the undisturbed state, longitudinal endolymph movements are extremely small and cannot make a significant contribution to ionic homeostasis. However, when endolymph volume is disturbed, longitudinal movements contribute to the electrolyte changes and are part of the compensation process. This study provides the first direct evidence supporting the long-standing hypotheses that local, radial homeostasis and longitudinal volume corrections both occur in the mammalian cochlea. RP SALT, AN (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID,ST LOUIS,MO 63110, USA. CR BARTOLI E, 1989, AM J PHYSIOL, V257, pF341 COHEN J, 1985, ARCH OTO-RHINO-LARYN, V241, P285, DOI 10.1007/BF00453702 DOI K, 1992, ACTA OTO-LARYNGOL, V112, P667, DOI 10.3109/00016489209137457 FELDMAN AM, 1976, P NATL ACAD SCI USA, V76, P1761 Guild SR, 1927, AM J ANAT, V39, P57, DOI 10.1002/aja.1000390103 HOBBIE RK, 1978, INTERMEDIATE PHYSICS JOHNSTONE BM, 1981, MENIERES DISEASE PAT, P44 JULIEN N, 1994, PFLUG ARCH EUR J PHY, V426, P446, DOI 10.1007/BF00388309 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KIMURA RS, 1982, AM J OTOLARYNG, V3, P447, DOI 10.1016/S0196-0709(82)80023-9 KITANO I, 1993, HEARING RES, V71, P23, DOI 10.1016/0378-5955(93)90017-U KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P176, DOI 10.3109/00016487809124734 KONISHI T, 1984, HEARING RES, V15, P51, DOI 10.1016/0378-5955(84)90224-7 LAWRENCE M, 1980, OTOLARYNG CLIN N AM, V13, P577 LAWRENCE M, 1961, ANN OTO RHINOL LARYN, V70, P753 LUNDQUIST PG, 1964, ACTA OTOLARYNGOL S, V188, P194 NAFTALIN L, 1958, J Laryngol Otol, V72, P118, DOI 10.1017/S0022215100053731 OHYAMA K, 1988, HEARING RES, V35, P119, DOI 10.1016/0378-5955(88)90111-6 PITOVSKI DZ, 1993, BRAIN RES, V601, P273, DOI 10.1016/0006-8993(93)91720-D RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1993, HEARING RES, V64, P205, DOI 10.1016/0378-5955(93)90007-N SALT AN, 1986, HEARING RES, V23, P141, DOI 10.1016/0378-5955(86)90011-0 Salt AN, 1989, MENIERES DIS, P69 SALT AN, 1995, IN PRESS ANN OTO RHI SALT AN, 1994, HEARING RES, V74, P165, DOI 10.1016/0378-5955(94)90184-8 SALT AN, 1991, HEARING RES, V56, P37, DOI 10.1016/0378-5955(91)90151-X SALT AN, 1988, HEARING RES, V33, P279, DOI 10.1016/0378-5955(88)90158-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, 1988, PHYSL EAR, P341 SHINKAWA H, 1986, ACTA OTO-LARYNGOL, V101, P43, DOI 10.3109/00016488609108606 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1984, AM J PHYSIOL, V246, pF47 STERKES O, 1982, AM J PHYSIOL, pF173 SYKOVA E, 1987, HEARING RES, V28, P161, DOI 10.1016/0378-5955(87)90047-5 SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 THALMANN R, 1989, 2 INT S MEN DIS, P55 ZIDANIC M, 1990, BIOPHYS J, V57, P1253 ZUMGOTTESBERGE AMM, 1988, ACTA OTOLARYNGOL S S, V460, P18 NR 40 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1995 VL 90 IS 1-2 BP 12 EP 23 DI 10.1016/0378-5955(95)00142-0 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300002 PM 8974989 ER PT J AU KITANO, I MORI, N MATSUNAGA, T AF KITANO, I MORI, N MATSUNAGA, T TI ROLE OF ATP-SENSITIVE K+ CHANNELS IN ANOXIA-SENSITIVE NEGATIVE POTENTIAL OF ENDOLYMPH SO HEARING RESEARCH LA English DT Article DE ATP-SENSITIVE K+ CHANNELS; GLYBENCLAMIDE; DIAZOXIDE; FUROSEMIDE; COCHLEAR ENDOLYMPH; ANOXIA-SENSITIVE NEGATIVE POTENTIAL ID ISOLATED HEART-CELLS; STRIA VASCULARIS; GUINEA-PIG; INHIBITION; FUROSEMIDE; MEMBRANE; OUABAIN; MUSCLE AB To investigate the possible role of the ATP-sensitive K+ channels (K-ATP channels) in the generation of the anoxia-sensitive negative potential (ASNP), the effects of the treatment with glybenclamide and diazoxide on the endocochlear potential (EP) and K+ activity (A(K)) in the scala media were examined with double-barrelled K+-selective microelectrodes. The experiments were carried out in guinea pig cochleae, using glybenclamide as a K-ATP channel blocker and diazoxide as a K-ATP channel opener. Perilymphatic perfusion of glybenclamide decreased the amplitude of the ASNP and shortened its duration, whereas perfusion of diazoxide increased ASNP amplitude and prolonged its duration. Glybenclamide enhanced the decrease of endolymphatic A(K) by anoxia, whereas diazoxide suppressed this A(K) decrease. The results suggest that K-ATP channels may be involved in the generation of the ASNP. C1 OSAKA MED COLL,DEPT PHYSIOL,OSAKA 569,JAPAN. KAGAWA MED SCH,DEPT OTOLARYNGOL,KAGAWA 76107,JAPAN. RP KITANO, I (reprint author), NARA MED UNIV,DEPT OTOLARYNGOL,840 SHIJO CHO,KASHIHARA,NARA 634,JAPAN. CR AMMANN D, 1975, HELV CHIM ACTA, V58, P1535, DOI 10.1002/hlca.19750580605 ASHFORD MLJ, 1989, J PHYSL, V409, P53 BENNDORF K, 1992, J PHYSIOL-LONDON, V454, P339 BENNDORF K, 1991, PFLUG ARCH EUR J PHY, V419, P108, DOI 10.1007/BF00373754 BOTT A, 1992, EUR J PHARMACOL, V213, P141, DOI 10.1016/0014-2999(92)90244-X CIAMPOLILLO F, 1992, J PHARMACOL EXP THER, V260, P254 COVINGTON AK, 1975, ANAL CHIM ACTA, V78, P219, DOI 10.1016/S0003-2670(01)84768-1 FINDLAY I, 1992, J PHARMACOL EXP THER, V261, P540 JIANG C, 1992, J PHYSIOL-LONDON, V448, P599 KOBAYASHI T, 1985, Practica Otologica Kyoto, V78, P569 KUIJPERS W, 1970, PFLUG ARCH EUR J PHY, V320, P359, DOI 10.1007/BF00588214 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 NICHOLS CG, 1991, AM J PHYSIOL, V261, pH1675 OFFNER FF, 1991, J MEMBRANE BIOL, V123, P171, DOI 10.1007/BF01998087 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PATEL MN, 1992, BRAIN RES, V539, P114 Robinson R. A., 1970, ELECTROLYTE SOLUTION SAKAGAMI M, 1991, HEARING RES, V56, P168, DOI 10.1016/0378-5955(91)90166-7 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHWIETERT R, 1992, EUR J PHARMACOL, V211, P87, DOI 10.1016/0014-2999(92)90267-8 SELLICK PM, 1974, PFLUG ARCH EUR J PHY, V352, P339, DOI 10.1007/BF00585686 SHUGYO A, 1990, EUR ARCH OTO-RHINO-L, V248, P79 SILBERBERG SD, 1992, PFLUG ARCH EUR J PHY, V420, P118, DOI 10.1007/BF00378653 SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 TSUCHIYA K, 1992, P NATL ACAD SCI USA, V89, P6418, DOI 10.1073/pnas.89.14.6418 WEISS JN, 1992, J PHYSIOL-LONDON, V447, P649 NR 27 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 OCT PY 1995 VL 90 IS 1-2 BP 24 EP 30 DI 10.1016/0378-5955(95)00143-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300003 PM 8975002 ER PT J AU EPSTEIN, JE COTANCHE, DA AF EPSTEIN, JE COTANCHE, DA TI SECRETION OF A NEW BASAL LAYER OF TECTORIAL MEMBRANE FOLLOWING GENTAMICIN-INDUCED HAIR CELL LOSS SO HEARING RESEARCH LA English DT Article DE GENTAMICIN; OTOTOXICITY; TECTORIAL MEMBRANE; COCHLEA; REGENERATION ID SEVERE ACOUSTIC TRAUMA; CHICK COCHLEA; AMINOGLYCOSIDE OTOTOXICITY; INNER-EAR; STEREOCILIARY BUNDLES; FUNCTIONAL RECOVERY; NOISE DAMAGE; REGENERATION; KANAMYCIN; ADULT AB Scanning electron microscopy (SEM) and video-enhanced DIC light microscopy were used to assess morphological changes in the chick tectorial membrane (TM) following gentamicin-induced hair cell loss. Gentamicin was administered (100 mg/kg/day for 3 days) and isolated and in-situ TMs were examined in both fixed and unfixed preparations at days 5 and 10 after the initial injection. Although this protocol induced hair cell damage extending up to 75% of the length of the basilar papilla, there was no apparent damage to the TM itself. However, the ejection of damaged hair cells appeared to sever the filamentous attachments between the TM and the apical surface of the basilar papilla. In SEM preparations this detachment caused the TM to shrink back toward the superior edge. Interestingly, despite the lack of TM damage, gentamicin treatment did reveal the secretion of a new basal layer of TM. Secretion of this new basal layer had begun by day 5 and it was well organized by day 10. This new layer formed attachments to both the recovering basilar papilla and the overlying original TM, a step thought to be necessary for the restoration of auditory function in the regenerating cochlea. RP EPSTEIN, JE (reprint author), BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,80 E CONCORD ST,BOSTON,MA 02118, USA. CR ADLER HJ, 1993, HEARING RES, V71, P214, DOI 10.1016/0378-5955(93)90037-2 ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 Alexander CM, 1991, CELL BIOL EXTRACELLU, P255 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X COTANCHE DA, 1987, HEARING RES, V30, P197, DOI 10.1016/0378-5955(87)90136-5 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1992, EXP NEUROL, V115, P23, DOI 10.1016/0014-4886(92)90215-C COTANCHE DA, 1991, CIBA F SYMP, V160, P131 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 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 FEE WE, 1980, LARYNGOSCOPE, V90, P1, DOI 10.1288/00005537-198010001-00001 FREEMAN DM, 1994, HEARING RES, V79, P197, DOI 10.1016/0378-5955(94)90141-4 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 GOODYEAR R, 1994, HEARING RES, V80, P93, DOI 10.1016/0378-5955(94)90013-2 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 JANAS JD, 1995, UNPUB AVIAN COCHLEAR KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 KILLICK R, 1992, HEARING RES, V64, P21, DOI 10.1016/0378-5955(92)90165-J MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y MOFFAT DA, 1977, J LARYNGOL OTOL, V91, P511, DOI 10.1017/S0022215100083985 RAPHAEL Y, 1991, HEARING RES, V53, P173, DOI 10.1016/0378-5955(91)90052-B REMEZAL M, 1993, HEARING RES, V66, P23, DOI 10.1016/0378-5955(93)90256-Z RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 SHIEL MJ, 1990, HEARING RES, V47, P147, DOI 10.1016/0378-5955(90)90172-L STONE JS, 1992, J CELL SCI, V102, P671 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 TUCCI DL, 1990, OTOLARYNG HEAD NECK, V103, P443 WESTBROOK EW, 1993, ABSTR ASS RES OT, V16, P141 NR 33 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 1995 VL 90 IS 1-2 BP 31 EP 43 DI 10.1016/0378-5955(95)00141-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300004 PM 8975003 ER PT J AU MORLET, T LAPILLONNE, A FERBER, C DUCLAUX, R SANN, L PUTET, G SALLE, B COLLET, L AF MORLET, T LAPILLONNE, A FERBER, C DUCLAUX, R SANN, L PUTET, G SALLE, B COLLET, L TI SPONTANEOUS OTOACOUSTIC EMISSIONS IN PRETERM NEONATES - PREVALENCE AND GENDER EFFECTS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSION; PRETERM NEONATE; MATURATION; COCHLEA; HUMAN ID EVOKED ACOUSTIC EMISSIONS; HEARING-LOSS; DISTORTION-PRODUCT; HEALTHY NEWBORNS; CHILDREN; INFANTS; EAR; COCHLEA; SYSTEM; TERM AB A number of lines of evidence indicate that the human cochlea is fully functional as a mature sound transducer by 6 months of age. However, information about the development of the active cochlear mechanisms and notably the development of outer hair cell (OHC) activity is yet incomplete. Recording and analysis of otoacoustic emissions (OAEs), probably generated by the OHCs of the organ of Corti, have led to a better understanding, in humans, of how sounds are analysed in the cochlea by means of active mechanisms. Evoked OAEs (EOAEs) and spontaneous OAEs (SOAEs), when they can be recorded in full-term and preterm neonates, show different characteristics from those in adults, suggesting that maturation of the peripheral auditory system is incomplete at birth, To learn more about this maturation, using the best-established facts concerning SOAEs in adults, such as their greater prevalence in females and also in right ears, SOAEs were studied in more detail in 81 preterm neonates, from 30 to 40 weeks of conceptional age, all presenting bilateral EOAEs according to objective criteria. The first finding of this study was that SOAEs existed and could be recorded as of 30 weeks of conceptional age in humans. Some SOAE characteristics in preterm neonates, such as prevalence, peak number and acoustic frequencies, showed similarity with full-term neonates. Comparison of other criteria between the two populations, such as greater SOAE prevalence in right ears and higher SOAE peak number in females, suggested that these developmental factors emerge around term in humans. Comparison of SOAE characteristics between male and female preterms suggested that male preterms were less advanced in peripheral auditory development than were female preterms. C1 HOP EDOUARD HERRIOT,SERV NEONATOL,F-69003 LYON,FRANCE. CTR HOSP LYON SUD,PHYSIOL SENSORIELLE LAB,LYON,FRANCE. HOP DEBROUSSE,EXPLORAT FONCTIONNELLE NEUROSENSORIELLE LAB,LYON,FRANCE. HOP DEBROUSSE,SERV NEONATOL,LYON,FRANCE. RP MORLET, T (reprint author), HOP EDOUARD HERRIOT,PHYSIOL SENSORIELLE AUDIT & VOIX LAB,CNRS,URA 1447,PAVILLON U,3 PL ARSONVAL,F-69003 LYON,FRANCE. CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 BALKANY TJ, 1978, LARYNGOSCOPE, V88, P398, DOI 10.1288/00005537-197803000-00003 BENCH RJ, 1974, SOUND RECEPTION MAMM, P11 BILGER RC, 1990, J SPEECH HEAR RES, V33, P418 BONFILS P, 1988, ARCH OTOLARYNGOL, V114, P887 BONFILS P, 1988, ARCH OTO-RHINO-LARYN, V245, P53, DOI 10.1007/BF00463550 BONFILS P, 1989, ARCH OTO-RHINO-LARYN, V246, P249, DOI 10.1007/BF00463565 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 BRAY P, 1989, THESIS U COLLEGE LON BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BURNS EM, 1992, J ACOUST SOC AM, V91, P1571, DOI 10.1121/1.402438 COLLET L, 1992, INT J NEUROSCI, V62, P113 COLLET L, 1993, BRAIN DEV-JPN, V15, P249, DOI 10.1016/0387-7604(93)90018-4 Eggermont J. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 44 EP 54 DI 10.1016/0378-5955(95)00144-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300005 PM 8975004 ER PT J AU MAGOVCEVIC, I KHETARPAL, U BIEBER, FR MORTON, CC AF MAGOVCEVIC, I KHETARPAL, U BIEBER, FR MORTON, CC TI GNAZ IN HUMAN FETAL COCHLEA - EXPRESSION, LOCALIZATION, AND POTENTIAL ROLE IN INNER-EAR FUNCTION SO HEARING RESEARCH LA English DT Article DE G PROTEIN; HYBRIDIZATION IN SITU; IMMUNOHISTOCHEMISTRY; COCHLEAR IONIC BALANCE ID PURIFIED MUSCARINIC RECEPTORS; PROTEIN ALPHA-SUBUNIT; GTP-BINDING PROTEIN; ADENYLATE-CYCLASE; STRIA VASCULARIS; MOLECULAR MECHANISM; CYCLIC-AMP; MOUSE; NA+,K+-ATPASE; FAMILY AB Dissociation of an activated alpha-subunit from the beta-gamma complex directly regulates secondary messenger proteins. To address the potential role of G proteins expressed in human fetal cochlea, degenerate oligonucleotide primers corresponding to the 3'-end of the conserved region of a-subunits were used for polymerase chain reaction amplification of reverse-transcribed total human fetal cochlear mRNAs; GNAZ and GNAQ were isolated. These two G proteins are unique among the G-protein family because they lack a typical pertussis modification site. GNAZ is expressed in high levels in neural tissue while GNAQ is ubiquitously expressed. We characterized GNAZ expression using Northern blots, tissue in-situ hybridization and immunohistochemistry techniques to elucidate the potential role of this protein in inner ear function. Our data suggest that GNAZ may play a role in maintaining the ionic balance of perilymphatic and endolymphatic cochlear fluids. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. 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PD OCT PY 1995 VL 90 IS 1-2 BP 55 EP 64 DI 10.1016/0378-5955(95)00146-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300006 PM 8975005 ER PT J AU CRANSAC, H COTTETEMARD, JM PEQUIGNOT, JM PEYRIN, L AF CRANSAC, H COTTETEMARD, JM PEQUIGNOT, JM PEYRIN, L TI MONOAMINES (NORADRENALINE, DOPAMINE, SEROTONIN) IN THE RAT COCHLEAR NUCLEI - ENDOGENOUS LEVELS AND TURNOVER SO HEARING RESEARCH LA English DT Article DE MONOAMINE; RAT; COCHLEAR NUCLEUS; LOCUS COERULEUS; RAPHE DORSALIS; NEUROCHEMISTRY; HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY; TURNOVER ID LOCUS COERULEUS; AUDITORY-NERVE; UNIT-ACTIVITY; DORSAL; NEURONS; BRAIN; CAT; ORGANIZATION; INNERVATION; FIBERS AB Noradrenaline (NA), dopamine (DA), serotonin (5-HT) and their metabolites, 3-methoxy,4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA), were determined using high-performance liquid chromatography with electrochemical detection in the rat anteroventral cochlear nucleus (AVCN), in the dorsal part of the nucleus including the dorsal cochlear nucleus (DCN) and the posteroventral cochlear nucleus (PVCN) and as a comparison, in the locus coeruleus (LC) and dorsal raphe nucleus (RD) which contain the corresponding noradrenergic and serotonergic cell bodies. In both cochlear nuclei (CN), the endogenous levels of NA, 5-HT and related metabolites were smaller than in LC or RD. NA turnover assessed from the ratio MHPG/NA or after treatment with alpha-methylparatyrosine was faster in the CN than in LC; in contrast, 5-HT turnover was lower in the CN than in RD as shown by the ratio 5-HIAA/5-HT. In agreement with previous histological findings, NA and 5-HT were more concentrated in AVCN than in DCN + PCVN; however, the turnover of both monoamines was faster in the dorsal nuclei. In addition, the CN contained small amounts of dopamine and DOPAC; both DA levels and the ratio DA/NA (0.10 vs. 0.04) were greater in the dorsal than in the ventral part suggesting the presence of non-precursor-specific DA pools. Our data suggest that the functional involvement of monoamines may be different in cochlear subnuclei. RP CRANSAC, H (reprint author), FAC MED LYON,PHYSIOL LAB,8 AVE ROCKEFELLER,F-69373 LYON,FRANCE. CR BELL C, 1981, J NEUROCHEM, V36, P563 BORG E, 1973, BRAIN RES, V49, P101, DOI 10.1016/0006-8993(73)90404-6 BOUTHENET ML, 1991, BRAIN RES, V564, P203, DOI 10.1016/0006-8993(91)91456-B BRODIE BB, 1966, J PHARMACOL EXP THER, V154, P493 BUDA M, 1983, BRAIN RES, V273, P197, DOI 10.1016/0006-8993(83)90844-2 CHIKAMORI Y, 1980, BRAIN RES, V194, P53, DOI 10.1016/0006-8993(80)91318-9 DAVIS M, 1982, J NEUROSCI, V2, P791 EBERT U, 1992, NEUROSCI LETT, V145, P51, DOI 10.1016/0304-3940(92)90201-H EVANS EF, 1973, EXP BRAIN RES, V17, P402 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FEX J, 1976, BRAIN RES, V109, P575, DOI 10.1016/0006-8993(76)90036-6 FOOTE SL, 1983, PHYSIOL REV, V63, P844 FRITSCHY JM, 1989, NEUROSCIENCE, V30, P181, DOI 10.1016/0306-4522(89)90364-3 FUXE K, 1965, ACTA PHYSL SCAN S247, V62, P39 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 HEYM J, 1982, BRAIN RES, V232, P29, DOI 10.1016/0006-8993(82)90608-4 KLEPPER A, 1991, BRAIN RES, V557, P190, DOI 10.1016/0006-8993(91)90134-H KOHNO Y, 1981, J NEUROCHEM, V36, P286, DOI 10.1111/j.1471-4159.1981.tb02405.x KOSSL M, 1989, J NEUROSCI, V9, P4169 KOSSL M, 1988, J COMP NEUROL, V269, P523, DOI 10.1002/cne.902690405 KROMER LF, 1980, ANAT EMBRYOL, V158, P227, DOI 10.1007/BF00315908 KROMER LF, 1976, BRAIN RES, V118, P531, DOI 10.1016/0006-8993(76)90327-9 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MENA F, 1976, ENDOCRINOLOGY, V99, P445 PALKOVITS M, 1988, MAPS GUIDE MICRODISE PARENT A, 1981, NEUROSCIENCE, V6, P115, DOI 10.1016/0306-4522(81)90050-6 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd PICKLES JO, 1976, BRAIN RES, V105, P591, DOI 10.1016/0006-8993(76)90610-7 RHODE WS, 1987, J NEUROPHYSIOL, V57, P414 RYUGO DK, 1993, J COMP NEUROL, V329, P20, DOI 10.1002/cne.903290103 RYUGO DK, 1991, J COMP NEUROL, V305, P35, DOI 10.1002/cne.903050105 SAINTMARIE RL, 1991, HEARING RES, V51, P11, DOI 10.1016/0378-5955(91)90003-R SPIROU GA, 1991, J NEUROPHYSIOL, V66, P1750 Steinbusch H. W. M., 1984, HDB CHEM NEUROANAT 2, V3, P68 STEINBUSCH HWM, 1981, NEUROSCIENCE, V6, P557, DOI 10.1016/0306-4522(81)90146-9 VERSTEEG DHG, 1976, BRAIN RES, V113, P563, DOI 10.1016/0006-8993(76)90057-3 VERTES RP, 1994, J COMP NEUROL, V340, P11, DOI 10.1002/cne.903400103 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WENTHOLD RJ, 1987, BRAIN RES, V415, P183, DOI 10.1016/0006-8993(87)90285-X Young E. D., 1988, AUDITORY FUNCTION NE, P277 NR 41 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1995 VL 90 IS 1-2 BP 65 EP 71 DI 10.1016/0378-5955(95)00147-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300007 PM 8975006 ER PT J AU NAITO, Y NAITO, E HONJO, I NEWMAN, A HONRUBIA, V AF NAITO, Y NAITO, E HONJO, I NEWMAN, A HONRUBIA, V TI EFFECT OF VESTIBULAR NERVE-SECTION ON CYTOCHROME-OXIDASE ACTIVITY IN THE VESTIBULAR GANGLION-CELLS OF THE SQUIRREL-MONKEY SO HEARING RESEARCH LA English DT Article DE CYTOCHROME OXIDASE; VESTIBULAR GANGLION; CELL SIZE; SQUIRREL MONKEY ID INNERVATING SEMICIRCULAR CANALS; NEURONS; REGENERATION; HISTOCHEMISTRY; LOCALIZATION; PHYSIOLOGY; DYNAMICS; BULLFROG; NUCLEUS; SYSTEM AB Cytochrome oxidase (GO) activity of the vestibular ganglion cells of the squirrel monkey was demonstrated histochemically under normal and experimental conditions. Under general anesthesia, right vestibular nerve section was performed on adult squirrel monkeys between the vestibular ganglion and brain stem. The left side was left intact and was used as a within-animal normal control. One squirrel monkey that did not undergo vestibular nerve section was also included in the normal group. Following a survival period of seven months, neurons in the vestibular ganglion of both sides were examined. In the normal control sides, a significant negative correlation between the size of the neuron and its optical density for CO stain was observed. Many neurons in the vestibular ganglion survived after vestibular nerve section, but their cell sizes and optical densities of CO stain decreased compared with those of the control side. C1 UNIV CALIF LOS ANGELES,SCH MED,DIV HEAD & NECK SURG,LOS ANGELES,CA 90024. RP NAITO, Y (reprint author), KYOTO UNIV,FAC MED,DEPT OTOLARYNGOL,SAKYO KU,KYOTO 60601,JAPAN. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 72 EP 78 DI 10.1016/0378-5955(95)00148-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300008 PM 8975007 ER PT J AU YEH, T VANDENABBEELE, T MARIANOVSKI, R HERMAN, P HUY, PTB AF YEH, T VANDENABBEELE, T MARIANOVSKI, R HERMAN, P HUY, PTB TI LUMINAL NONSELECTIVE CATION AND OUTWARDLY RECTIFYING CHLORIDE CHANNELS IN CULTURED STRIAL MARGINAL CELLS FROM GERBIL SO HEARING RESEARCH LA English DT Article DE COCHLEA; STRIA VASCULARIS; IONIC CHANNEL; PATCH CLAMP; ENDOLYMPH ID NASAL EPITHELIAL-CELLS; NONSELECTIVE CATION; GUINEA-PIG; APICAL MEMBRANE; CL CHANNELS; INNER-EAR; VASCULARIS; MECHANISMS; POTENTIALS; INVITRO AB Ionic channels located on the luminal side of strial marginal cells (MCs) of gerbil in culture were investigated using the patch-clamp technique. Two types of channels were identified. The most frequently recorded single-channel activity corresponded to a non-selective cation (NSC) channel with a conductance of 23.7 +/- 0.2 pS (n = 18) in symmetrical NaCl conditions. The channel was activated by internal Ca2+ and inhibited by internal adenine nucleotides and flufenamic acid. Spontaneous activity of NSC channels was found in 16% of the cell-attached patches and with a very high density (9 +/- 2 levels/patch, n = 28) in 100% of the excised patches. An outwardly rectifying chloride (ORC) channel was also identified in 14% of the patches but only after excision. The channel exhibited at 0 mV a unit conductance of 26.8 +/- 1.3 pS (n = 8) and a strong outward rectification in symmetrical NaCl conditions, and the open probability increased with depolarization. The luminal NSC channel and the ORC channel evidenced in this study might participate in the production of endolymph. Although extrapolation of the presents results to the in vivo situation should be made with caution, this study suggests that culture of strial MCs may be a suitable model for investigation of endolymph physiology. C1 UNIV PARIS 07,UFR LARIBOISIERE ST LOUIS,ORL EXPTL LAB,PARIS,FRANCE. NATL TAIWAN UNIV HOSP,ENT DEPT,TAIPEI,TAIWAN. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 79 EP 88 DI 10.1016/0378-5955(95)00149-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300009 PM 8975008 ER PT J AU RIGGS, GH COOPER, NGF SCHWEITZER, L AF RIGGS, GH COOPER, NGF SCHWEITZER, L TI PATTERNS OF GFAP-IMMUNOREACTIVITY PARALLEL THE TONOTOPIC AXIS IN THE DEVELOPING DORSAL COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE GLIA; AUDITORY SYSTEM; DORSAL COCHLEAR NUCLEUS; AXON GUIDANCE; HAMSTER; TONOTOPIC ID FIBRILLARY ACIDIC PROTEIN; LATERAL GENICULATE-NUCLEUS; FETAL MONKEY NEOCORTEX; CENTRAL-NERVOUS-SYSTEM; EARLY POSTNATAL MOUSE; INFERIOR COLLICULUS; SOMATOSENSORY CORTEX; MONOCLONAL-ANTIBODY; CELL MIGRATION; RADIAL GLIA AB The role of glia in the development of tonotopic and laminar organization in the auditory central nervous system has not been well characterized. In other systems, glia immunoreactive for glial fibrillary acidic protein (GFAP) appear to function in development of radial, laminar and topographic organization. Using a polyclonal antibody to GFAP, we have characterized the development of GFAP-immunoreactivity in the dorsal cochlear nucleus (DCN), a laminated and tonotopically organized central auditory system structure. Results suggest that in this nucleus, the GFAP-immunoreactive processes are not found within or between developing laminae, rather glial processes are observed parallel to presumptive isofrequency sheets before primary afferents have invaded the nucleus. Thus, GFAP-immunoreactive processes are positioned to play an early role in establishing the tonotopic axis of the DCN. C1 UNIV LOUISVILLE, SCH MED, DEPT ANAT SCI & NEUROBIOL, LOUISVILLE, KY 40292 USA. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 89 EP 96 DI 10.1016/0378-5955(95)00150-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300010 PM 8975009 ER PT J AU WHITE, PN THORNE, PR HOUSLEY, GD MOCKETT, B BILLETT, TE BURNSTOCK, G AF WHITE, PN THORNE, PR HOUSLEY, GD MOCKETT, B BILLETT, TE BURNSTOCK, G TI QUINACRINE STAINING OF MARGINAL CELLS IN THE STRIA VASCULARIS OF THE GUINEA-PIG COCHLEA - A POSSIBLE SOURCE OF EXTRACELLULAR ATP SO HEARING RESEARCH LA English DT Article DE ADENOSINE 5'-TRIPHOSPHATE; GUINEA-PIG COCHLEA; STRIA VASCULARIS; MARGINAL CELL; QUINACRINE STAINING ID OUTER HAIR-CELLS; INNERVATION; NUCLEOTIDES; NEURONS; NERVES AB There is accumulating evidence for a purinergic humoral system involved in the control of cochlear function. Evidence of specific P-2 purinoceptors on cochlear tissues implies a role for extracellular adenosine triphosphate (ATP) in the cochlea. To further this hypothesis a study was undertaken to determine if there was any specific source of purine compounds in cochlear tissues. Cochlear tissues (the sensory epithelium and lateral wall) from the guinea pig were incubated with the acridine derivative quinacrine dihydrochloride (5 X 10(-6) M in phosphate-buffered saline for 30 min at room temperature) which fluoresces on binding to high concentrations of ATP. Most cochlear tissues showed a diffuse green fluorescence slightly above the background level. However, a region of the marginal cells of the stria vascularis showed a specific punctate fluorescence. Optical sectioning of these cells by confocal microscopy revealed that the fluorescent structures in these marginal cells was confined to a region up to 10 mu m from their endolymphatic surface. Similar cells studied by transmission electron microscopy showed membrane-bound vesicles located in the same region of the cell. These data imply that purine compounds are localized in discrete structures, perhaps vesicles, within the marginal cells which could serve as a source of extracellular ATP in the cochlea. C1 UNIV AUCKLAND, DEPT PHYSIOL, AUCKLAND, NEW ZEALAND. UCL, DEPT ANAT & DEV BIOL, LONDON, ENGLAND. CR Alberts B., 1995, MOL BIOL CELL ALUND M, 1980, J AUTONOM NERV SYST, V2, P281, DOI 10.1016/0165-1838(80)90017-X ALUND M, 1978, HISTOCHEMISTRY, V58, P153, DOI 10.1007/BF00495714 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 ASHMORE JF, 1993, BIOPHYSICS HAIR CELL, P151 BEAN BP, 1990, ION CHANNELS, P169 BENHAM CD, 1992, NATURE, V359, P103, DOI 10.1038/359103a0 BURNSTOCK G, 1978, BRIT J PHARMACOL, V63, P125 BURNSTOCK G, 1993, DRUG DEVELOP RES, V28, P301, DOI 10.1002/ddr.430280320 BURNSTOC.G, 1972, PHARMACOL REV, V24, P509 BURNSTOCK G, 1979, BRIT J PHARMACOL, V65, P377 BURNSTOCK G, 1986, CIRC RES, V58, P319 COCKS T, 1979, EUR J PHARMACOL, V54, P261, DOI 10.1016/0014-2999(79)90085-2 CROWE R, 1984, BRAIN RES BULL, V12, P387, DOI 10.1016/0361-9230(84)90110-2 DAPRADA M, 1978, PLATELETS MULTIDISCI, P331 DUBYAK GR, 1991, AM J RESP CELL MOL, V4, P295 DULON D, 1993, CELL CALCIUM, V14, P245, DOI 10.1016/0143-4160(93)90071-D EDWARDS FA, 1992, NATURE, V359, P144, DOI 10.1038/359144a0 EKELUND M, 1980, HISTOCHEMISTRY, V66, P1, DOI 10.1007/BF00493240 FRIEDMAN I, 1984, ULTRASTRUCTURAL ATLA GORDON JL, 1986, BIOCHEM J, V233, P309 HOUSLEY GD, 1993, BIOPHYSICS HAIR CELL, P116 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HOUSLEY GD, 1995, UNPUB IDENTIFICATION IRVIN JL, 1954, J BIOL CHEM, V210, P45 KNIGHT GE, 1992, COMP BIOCHEM PHYS C, V102, P305, DOI 10.1016/0742-8413(92)90116-O KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KURNICK NB, 1962, J LAB CLIN MED, V60, P669 LEITNER JW, 1975, ENDOCRINOLOGY, V96, P662 LERMAN LS, 1963, P NATL ACAD SCI USA, V49, P94, DOI 10.1073/pnas.49.1.94 MOCKETT BG, 1994, J NEUROSCI, V14, P1692 MOCKETT BG, 1995, HEARING RES, V84, P177, DOI 10.1016/0378-5955(95)00024-X MUNOZ DJB, 1995, HEARING RES, V90, P119, DOI 10.1016/0378-5955(95)00153-5 MUNOZ DJB, 1995, HEARING RES, V90, P106, DOI 10.1016/0378-5955(95)00152-3 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 OLSON L, 1976, CELL TISSUE RES, V171, P407 Sato T, 1967, J ELECTRONMICROSC, V16, P133 SURPRENANT A, 1995, TRENDS NEUROSCI, V18, P224, DOI 10.1016/0166-2236(95)93907-F THORNE PR, 1994, DRUG DEVELOP RES, V31, P328 NR 39 TC 71 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 OCT PY 1995 VL 90 IS 1-2 BP 97 EP 105 DI 10.1016/0378-5955(95)00151-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300011 PM 8975010 ER PT J AU MUNOZ, DJB THORNE, PR HOUSLEY, GD BILLETT, TE BATTERSBY, JM AF MUNOZ, DJB THORNE, PR HOUSLEY, GD BILLETT, TE BATTERSBY, JM TI EXTRACELLULAR ADENOSINE 5'-TRIPHOSPHATE (ATP) IN THE ENDOLYMPHATIC COMPARTMENT INFLUENCES COCHLEAR FUNCTION SO HEARING RESEARCH LA English DT Article DE ADENOSINE 5'-TRIPHOSPHATE; P-2 PURINOCEPTOR; GUINEA-PIG COCHLEA; COCHLEAR FUNCTION; ENDOCOCHLEAR POTENTIAL; COCHLEAR MICROPHONIC; ENDOLYMPH; PERILYMPH ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; RELEASE; INNER; ORGAN; CORTI; FUROSEMIDE; PERFUSION; POTASSIUM; NEURONS AB There is strong evidence for the presence of P-2 purinoceptors on cochlear tissues, but the role of extracellular ATP in cochlear function is still unclear. Our previous studies have determined the presence of ATP in the cochlear fluids and indicated that the purinoceptors are substantially localized to the tissues lining the endolymphatic compartment. This implies that extracellular ATP may have an humoral role confined to the endolymphatic space. In order to study the influence of extracellular ATP in the endolymphatic space, a series of studies were undertaken in which ATP (10 mu M to 10 mM) in artificial endolymph (EL) (test solution: 2-12.5 nl) was injected into the scala media and the effect on the cochlear microphonic (CM) and endocochlear potential (EP) evaluated. A double-barrelled pipette, with one barrel containing the test solution and the other artificial EL (control solution) was inserted into scala media of the third turn of the guinea-pig cochlea. A known volume (2-12.5 nl) of test or control solution was then pressure-injected into the space. ATP had a significant dose-dependent suppressive effect on both EP and CM with a threshold of approximately 2 X 10(-14) mel; the response was readily reversible, also in a dose-dependent fashion. Artificial EL of the same volume had no effect on EP and CM. The ATP effect on EP was blocked by the P-2 purinoceptor antagonists suramin and reactive blue 2 (RB2). Neither adenosine (2 x 10(-13) to 2 X 10(-11) mol) nor suramin or RB2 on their own had any effect on EP and CM. This study provides the first evidence for an effect of extracellular ATP in the endolymphatic compartment on cochlear function which is mediated via P-2 purinoceptors. This provides supporting evidence for an humoral role for extracellular ATP in the modulation of cochlear function. C1 UNIV AUCKLAND,SCH MED,DEPT PHYSIOL,AUCKLAND,NEW ZEALAND. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V360, P397 ASHMORE JF, 1993, BIOPHYSICS HAIR CELL, P151 AUBERT A, 1994, NEUROSCIENCE, V62, P963, DOI 10.1016/0306-4522(94)90487-1 BEAN BP, 1990, ION CHANNELS, P169 BURNSTOCK G, 1993, DRUG DEVELOP RES, V28, P195, DOI 10.1002/ddr.430280303 CROWE R, 1984, BRAIN RES BULL, V12, P387, DOI 10.1016/0361-9230(84)90110-2 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DAVIS H, 1965, COLD SPRING HARB SYM, V30, P181 DULON D, 1991, NEUROREPORT, V2, P69, DOI 10.1097/00001756-199102000-00001 EDWARDS FA, 1992, NATURE, V359, P144, DOI 10.1038/359144a0 EVANS RJ, 1992, NATURE, V357, P503, DOI 10.1038/357503a0 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 FITZGERALD JJ, 1993, HEARING RES, V67, P147, DOI 10.1016/0378-5955(93)90242-S GORDON JL, 1986, BIOCHEM J, V233, P309 HOUSLEY GD, 1993, BIOPHYSICS HAIR CELL, P116 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x KOLSTON PJ, 1992, J PHYSIOL-LONDON, V446, pP389 KONISHI T, 1979, ACTA OTO-LARYNGOL, V88, P41, DOI 10.3109/00016487909137138 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 MOCKETT BG, 1994, J NEUROSCI, V14, P1692 MOCKETT BG, 1993, BIOPHYSICS HAIR CELL, P226 MOCKETT BG, 1995, HEARING RES, V84, P177, DOI 10.1016/0378-5955(95)00024-X MUNOZ DJB, 1995, HEARING RES, V90 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 NILLES R, 1994, HEARING RES, V73, P27, DOI 10.1016/0378-5955(94)90279-8 NUTTALL AL, 1977, ACTA OTO-LARYNGOL, V83, P393, DOI 10.3109/00016487709128863 OGAWA K, 1994, HEARING RES, V74, P197, DOI 10.1016/0378-5955(94)90187-2 OGAWA K, 1993, HEARING RES, V69, P207, DOI 10.1016/0378-5955(93)90109-E PATTON HD, 1989, TXB PHYSL, P17 Pickles JO, 1988, INTRO PHYSL HEARING RUGGERO MA, 1991, J NEUROSCI, V11, P1057 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 STERKERS O, 1988, PHYSIOL REV, V68, P1083 SYKOVA E, 1987, HEARING RES, V28, P161, DOI 10.1016/0378-5955(87)90047-5 TAKEUCHI S, 1991, ANN OTO RHINOL LARYN, V100, P244 WHITE PN, 1995, HEARING RES, V50, P97 NR 42 TC 62 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 OCT PY 1995 VL 90 IS 1-2 BP 106 EP 118 DI 10.1016/0378-5955(95)00152-3 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300012 PM 8974987 ER PT J AU MUNOZ, DJB THORNE, PR HOUSLEY, GD BILLETT, TE AF MUNOZ, DJB THORNE, PR HOUSLEY, GD BILLETT, TE TI ADENOSINE 5'-TRIPHOSPHATE (ATP) CONCENTRATIONS IN THE ENDOLYMPH AND PERILYMPH OF THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE ADENOSINE 5'-TRIPHOSPHATE; GUINEA-PIG COCHLEA; ENDOLYMPH; PERILYMPH; CEREBROSPINAL FLUID ID OUTER HAIR-CELLS; CEREBROSPINAL-FLUID; EXTRACELLULAR ATP; ORGAN; CORTI; BLOOD AB The concentration of adenosine S-triphosphate (ATP) in endolymph (EL), perilymph (PL) and cerebrospinal fluid (CSF), collected from anesthetized guinea pigs was determined using the luciferase-luciferin reaction. The cochlea was exposed by a ventrolateral approach and the bone overlying scala media of the third turn (EL) or scala vestibuli of the first turn (PL) was shaved to a thin layer and a small fenestrum made. For EL sampling, a double-barrelled pipette was inserted through the spiral ligament-stria vascularis complex. One barrel was filled with 150 mM KCl to record the endocochlear potential (EP) and upon the appearance of the positive EP, 0.12-1.22 mu l of fluid was aspirated into the other barrel by gentle negative pressure. For PL sampling, a single-barrelled pipette was advanced into scala vestibuli and 0.3-1.6 mu l of fluid was collected by capillarity. CSF (0.36-1.75 mu l) was obtained from the cisterna magna. The cochleae were removed and processed for light microscopy to determine the extent of tissue damage from the sampling procedure. ATP concentrations (mean +/- SEM, nM) for EL, PL and CSF were 12.95 +/- 2.4 (n = 10), 10.5 +/- 3.9 (n = 11) and 16.1 +/- 5.4 (n = 11) respectively. Differences in ATP concentrations among fluids were not statistically significant. To test the effect of hypoxia on ATP levels, a group of guinea pigs was subjected to a 90 s period of respiratory anoxia prior to sampling of EL, PL or CSF. ATP concentrations were 14.4 +/- 3.5 (n = 11), 20.7 +/- 4.1 (n = 10) and 13.5 +/- 4.6 (n = 4) for EL, PL and CSF, respectively; only PL ATP concentrations were statistically different (P = 0.018, Wilcoxon rank sum test) to basal conditions. This is the first study which demonstrates the presence of free ATP in cochlear fluids. The results indicate that ATP is present in cochlear fluids at concentrations close to those known to cause hair cell depolarization in vivo. C1 UNIV AUCKLAND,SCH MED,DEPT PHYSIOL,AUCKLAND,NEW ZEALAND. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 119 EP 125 DI 10.1016/0378-5955(95)00153-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300013 PM 8974988 ER PT J AU LIN, T GOLDSTEIN, JL AF LIN, T GOLDSTEIN, JL TI QUANTIFYING 2-FACTOR PHASE-RELATIONS IN NONLINEAR RESPONSES FROM LOW CHARACTERISTIC-FREQUENCY AUDITORY-NERVE FIBERS SO HEARING RESEARCH LA English DT Article DE NONLINEAR COCHLEAR SOUND ANALYSIS; MODEL OF 2-FACTOR RESPONSE; COCHLEAR PHASE-ADAPTATION HYPOTHESIS ID 2-TONE RATE SUPPRESSION; LEVEL; DEPENDENCE; STIMULUS; COCHLEA; MODEL AB Auditory-nerve excitation by two response factors that can be in antiphase has been hypothesized by Kiang (1990) on the basis of non-linear interference in responses to tones (Kiang et al., 1969). The general conditions for antiphasic responses and the relevance of the hypothesis for other auditory stimuli are unknown. Clarification was sought in a systematic modeling study of published data on level-dependent non-linear responses from low characteristic-frequency (CF) auditory-nerve fibers for a broad variety of acoustic stimuli. The MBPNL non-linear I/O model of cochlear frequency analysis (Goldstein, 1990), which incorporates the 2-factor hypothesis, was used to simulate the reported non-linear phenomena. It was found that experiments with paired click stimuli (Goblick and Pfeiffer, 1969) and with octave-band complex tones (Horst et al., 1990), in addition to experiments with single clicks or tones, are sensitive to the phase difference between factors. Surprisingly, the paired-click transient responses require a quadrature phase, while the complex-tone steady-state responses require an antiphase relation. The MBPNL model simulations of all low-CF data surveyed, for simple and complex stimuli, are consistent with a quadrature phase for transient responses and antiphase relation for steady-state responses. It is hypothesized that some adaptive, low-CF, cochlear mechanism, not described by the basic MBPNL model, produces a temporal transition of the '2-factor' response from an initial quadrature relation (tip leading) to a final antiphase relation. New experimental and modeling research guided by this working hypothesis is proposed. C1 WASHINGTON UNIV,CENT INST DEAF,ST LOUIS,MO 63110. CR ABBAS PJ, 1976, J ACOUST SOC AM, V59, P112, DOI 10.1121/1.380841 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 Cooper N. 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V., 1975, DIGITAL SIGNAL PROCE RUGGERO MA, 1994, AUDIOLOGY, V33, P131 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 WESTERMAN LA, 1988, J ACOUST SOC AM, V83, P2266, DOI 10.1121/1.396357 NR 37 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 1995 VL 90 IS 1-2 BP 126 EP 138 DI 10.1016/0378-5955(95)00154-7 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300014 PM 8974990 ER PT J AU DUNNEBIER, EA SEGENHOUT, JM KALICHARAN, D JONGEBLOED, WL WIT, HP ALBERS, FWJ AF DUNNEBIER, EA SEGENHOUT, JM KALICHARAN, D JONGEBLOED, WL WIT, HP ALBERS, FWJ TI LOW-VOLTAGE FIELD-EMISSION SCANNING ELECTRON-MICROSCOPY OF NON-COATED GUINEA-PIG HAIR CELL STEREOCILIA SO HEARING RESEARCH LA English DT Article DE FIELD-EMISSION SCANNING ELECTRON MICROSCOPY; NONCOATING; STEREOCILIA; GLYCOCALYX; CROSS-LINK; MECHANOELECTRICAL TRANSDUCTION ID COCHLEA; BUNDLES; LINKS AB The stereociliar structures of the guinea-pig cochlear organ of Corti were studied at low-voltage (1-5 kV) with field-emission scanning electron microscope (SEM) using various pre- and post-fixation methods, such as OTOTO (OsO4/thiocarbohydrazide/OsO4/thiocarbohydrazide/OsO4) and TAO (tannic acid/arginine/OsO4), and different dissection procedures of the cochlea. A perfusion and immersion pre-fixation with glutaraldehyde, in combination with removal of the bony wall and stria vascularis from the cochlea, followed by the TAO non-coating treatment, gave the best result at 2 kV acceleration voltage. Due to these new techniques, several interesting delicate structures of the stereocilia, in particular fine surface structures, were detected for the first time using SEM. These findings include the different types of cross-links and tip links, i.e., the fine surface morphology of the stereocilia and their attachments and imprints in the tectorial membrane (TM). One of the most interesting findings in this study is a network of long filamentous structures, which has been identified mainly at the top of the longest stereocilia and the undersurface of the TM and which may represent the glycocalyx. These findings and their possible implications in the process of mechanoelectrical transduction will be discussed. C1 UNIV GRONINGEN,CELL BIOL & ELECTRON MICROSCOPY LAB,9700 RB GRONINGEN,NETHERLANDS. RP DUNNEBIER, EA (reprint author), UNIV GRONINGEN HOSP,DEPT OTORHINOLARYNGOL,9700 RB GRONINGEN,NETHERLANDS. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 139 EP 148 DI 10.1016/0378-5955(95)00155-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300015 PM 8974991 ER PT J AU WANGEMANN, P AF WANGEMANN, P TI COMPARISON OF ION-TRANSPORT MECHANISMS BETWEEN VESTIBULAR DARK CELLS AND STRIAL MARGINAL CELLS SO HEARING RESEARCH LA English DT Article DE ENDOLYMPH; ENDOCOCHLEAR POTENTIAL; POTASSIUM ION; STRIAL MARGINAL CELL; VESTIBULAR DARK CELL; VESTIBULAR LABYRINTH; COCHLEA ID ADENYLATE-CYCLASE; INNER-EAR; NONSELECTIVE CATION; APICAL MEMBRANE; CELLULAR-LOCALIZATION; NONSENSORY REGION; POTASSIUM CHANGES; GERBIL UTRICLE; CL CHANNELS; GUINEA-PIG AB Morphologic similarities between strial marginal cells and vestibular dark cells have long been recognized and it has long been accepted that both of these cell types are involved in the secretion of K+ into endolymph. Functional similarities of these two epithelia, however, were considered unlikely as long as strial marginal cells were assumed to generate the endocochlear potential which has no equivalent in the vestibular labyrinth. The recently introduced concept that strial marginal cells transport K+ but that the mechanism for the generation of the endocochlear potential is located in another cell type provided the basis to hypothesize that ion transport mechanisms and their regulation are similar in vestibular dark and strial marginal cells. The present review compiles evidence in support of this hypothesis. 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 AHLSTROM P, 1975, LARYNGOSCOPE, V85, P1241, DOI 10.1288/00005537-197507000-00016 FERRARY E, 1991, ACTA OTO-LARYNGOL, V111, P281, DOI 10.3109/00016489109137388 FERRARY E, 1991, EUR ARCH OTO-RHINO-L, V248, P275 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 Jahnke K, 1975, Acta Otolaryngol Suppl, V336, P1 JOHNSTONE BM, 1989, J PHYSIOL-LONDON, V408, P77 JOHNSTON.BM, 1972, Q REV BIOPHYS, V5, P1 KIKUCHI T, 1995, ANAT EMBRYOL, V191, P101, DOI 10.1007/BF00186783 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 KONISHI T, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 KUSAKARI J, 1978, ACTA OTO-LARYNGOL, V86, P336, DOI 10.3109/00016487809107512 LIU J, 1995, IN PRESS AUDIT NEURO MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1993, HEARING RES, V69, P124, DOI 10.1016/0378-5955(93)90100-F MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 1994, J GEN PHYSIOL, V104, pA16 MARCUS DC, 1994, HEARING RES, V73, P101, DOI 10.1016/0378-5955(94)90287-9 MARCUS DC, 1987, HEARING RES, V30, P55, DOI 10.1016/0378-5955(87)90183-3 MARCUS DC, 1994, AM J PHYSIOL, V267, pC857 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 RYAN AF, 1994, P SEND S, V4, P47 SAKAGAMI M, 1991, HEARING RES, V56, P168, DOI 10.1016/0378-5955(91)90166-7 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SALT AN, 1993, ANN OTO RHINOL LARYN, V102, P64 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 SHINDO M, 1992, JPN J PHYSIOL, V42, P617, DOI 10.2170/jjphysiol.42.617 STEEL KP, 1989, DEVELOPMENT, V107, P453 SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 SUNOSE H, 1995, ASS RES OTOLARYNGOL, V18, P26 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 TAKEUCHI S, 1992, AM J PHYSIOL, V262, pC1430 TAKEUCHI S, 1995, HEARING RES, V83, P89, DOI 10.1016/0378-5955(94)00191-R TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 VALLI P, 1990, J PHYSIOL-LONDON, V430, P585 WANGEMANN P, 1995, HEARING RES, V84, P19, DOI 10.1016/0378-5955(95)00009-S WANGEMANN P, 1990, DIURETICS, V3, P220 WANGEMANN P, 1992, HEARING RES, V62, P149, DOI 10.1016/0378-5955(92)90180-U WANGEMANN P, 1995, ASS RES OTOLARYNGOL, V18, P25 WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 WANGEMANN P, 1995, J MEMBRANE BIOL, V147, P263 WANGEMANN P, 1995, J MEMBRANE BIOL, V147, P255 ZAJIC G, 1983, HEARING RES, V10, P249, DOI 10.1016/0378-5955(83)90090-4 ZIDANIC M, 1990, BIOPHYS J, V57, P1253 NR 50 TC 144 Z9 152 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 1995 VL 90 IS 1-2 BP 149 EP 157 DI 10.1016/0378-5955(95)00157-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300016 PM 8974992 ER PT J AU LIBERMAN, MC GAO, WY AF LIBERMAN, MC GAO, WY TI CHRONIC COCHLEAR DE-EFFERENTATION AND SUSCEPTIBILITY TO PERMANENT ACOUSTIC INJURY SO HEARING RESEARCH LA English DT Article DE OLIVOCOCHLEAR; EFFERENT; OUTER HAIR CELL; COCHLEA; ACOUSTIC TRAUMA; SLOW EFFECT ID CROSSED OLIVOCOCHLEAR BUNDLE; TEMPORARY THRESHOLD SHIFTS; SUPERIOR OLIVARY COMPLEX; GUINEA-PIG COCHLEA; IMMUNOELECTRON MICROSCOPY; ELECTRICAL-STIMULATION; HORSERADISH-PEROXIDASE; AUDITORY-SENSITIVITY; MEDIAL ZONES; NEURONS AB The question of whether olivocochlear (OC) efferent feedback can decrease permanent damage from acoustic overexposure was investigated by comparing the chronic threshold shifts and cochlear histopathology in guinea pigs either surgically de-efferented or sham-operated and then exposed (awake and unrestrained) to a 109- or 112-dB narrow-band noise centered at 10 kHz for 2 h. Threshold shifts were estimated using compound action potentials; hair cell loss and stereocilia condition were evaluated via light-microscopic examination of plastic-embedded surface preparations, and the degree of de-efferentation was assessed by measuring OC fascicles in the tunnel of Corti. Among animals exposed to 109-dB noise, the mean permanent threshold shift (PTS) was less than 25 dB, and there were no significant differences between normal and de-efferented animals with respect to either physiological or histological measures of acoustic injury. Among animals exposed to 112 dB, the mean peak PTS was roughly 50 dB. There was a small (but statistically significant) increase in PTS for de-efferented animals, especially at frequencies above the region of peak threshold shift; however, the patterns of hair cell loss and stereocilia damage were statistically indistinguishable. 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PD OCT PY 1995 VL 90 IS 1-2 BP 158 EP 168 DI 10.1016/0378-5955(95)00160-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300017 PM 8974993 ER PT J AU SENARITA, M THALMANN, I SHIBASAKI, O THALMANN, R AF SENARITA, M THALMANN, I SHIBASAKI, O THALMANN, R TI CALCIUM-BINDING PROTEINS IN ORGAN OF CORTI AND BASILAR PAPILLA - CBP-15, AN UNIDENTIFIED CALCIUM-BINDING PROTEIN OF THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; BASILAR PAPILLA; CALCIUM-BINDING PROTEIN; CALMODULIN; CALBINDIN; PARVALBUMIN ID OUTER HAIR-CELLS; POLYACRYLAMIDE GELS; ACID AB In a previous paper (Thalmann et al., 1993) we reported that the amino acid sequence of OCP2, a low molecular weight acidic protein present in extremely high concentrations in the organ of Corti and absent in the basilar papilla, exhibits a rudimentary EF-hand - a potential calcium-binding domain. The present study was undertaken to determine whether OCP2 binds 45-calcium under non-denaturing conditions following separation by isoelectric focusing and transblotting. The same criterion was used to determine whether the EF-hands of several other calcium-binding proteins (CBP) are functional in organ of Corti and basilar papilla. OCP2 exhibited no 45-calcium binding. Calmodulin, present in the organ of Corti in extremely high concentrations and lower in basilar papilla, showed strong 45-calcium binding in both structures. While calbindin represents a major protein in basilar papilla and binds 45-calcium, this protein is a minor component in the organ of Corti; whether it binds 45-calcium remains to be decided. By extending the pi range in the acidic region of isoelectric focusing, a 15 kDa, highly acidic (pi approximate to 3.1) protein was revealed that constitutes a major protein in the organ of Corti; the protein was not detectable in the basilar papilla, spiral ligament/stria vascularis complex and numerous other organs tested. It remains to be resolved whether this protein represents an isoform of parvalbumin or a novel CBP. The differential make-up of CBPs between the mammalian organ of Corti and the avian basilar papilla is discussed. C1 WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,ST LOUIS,MO 63110. UNIV TSUKUBA,INST CLIN MED,DEPT OTOLARYNGOL,TSUKUBA,IBARAKI 305,JAPAN. CR ANDERSON L, 1988, 2 DIMENSIONAL ELECTR ANGHILERI LJ, 1990, ROLE CALCIUM BIOL SY, V5 CHEN H, 1995, IN PRESS CDNA CLONIN DULON D, 1994, BIOCHEM BIOPH RES CO, V201, P1263, DOI 10.1006/bbrc.1994.1841 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1990, J NEUROSCI, V10, P1388 EYBALIN M, 1990, CR ACAD SCI III-VIE, V310, P639 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FOHR UG, 1993, EUR J BIOCHEM, V215, P719, DOI 10.1111/j.1432-1033.1993.tb18084.x HEIZMANN CW, 1992, TRENDS NEUROSCI, V15, P259, DOI 10.1016/0166-2236(92)90067-I HEIZMANN CW, 1991, NOVEL CALCIUM BINDIN MOORE BW, 1988, NEUROCHEM RES, V13, P693, DOI 10.1007/BF00971590 NAKAYAMA S, 1994, ANNU REV BIOPH BIOM, V23, P473, DOI 10.1146/annurev.bb.23.060194.002353 OAKLEY BR, 1980, ANAL BIOCHEM, V105, P361, DOI 10.1016/0003-2697(80)90470-4 OBERHOLTZER JC, 1988, P NATL ACAD SCI USA, V85, P3387, DOI 10.1073/pnas.85.10.3387 PACK AK, 1995, 18TH MIDW M ARO ST P, P161 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 SENARITA M, 1994, 17TH MIDW 7 ARO ST P, P138 SLEPECKY NB, 1993, HEARING RES, V70, P73, DOI 10.1016/0378-5955(93)90053-4 SMITH PK, 1985, ANAL BIOCHEM, V150, P76, DOI 10.1016/0003-2697(85)90442-7 TAKAHASHI K, 1989, J ACOUST SOC AM, V85, pS31, DOI 10.1121/1.2026909 THALMANN I, 1990, LARYNGOSCOPE, V100, P99 THALMANN I, 1993, HEARING RES, V64, P191, DOI 10.1016/0378-5955(93)90005-L THALMANN L, 1995, BIOCHEM BIOPH RES CO, V215, P142 THALMANN R, 1976, HDB AUDITORY VESTIBU, P359 THALMANN R, 1970, LARYNGOSCOPE, V80, P1619, DOI 10.1288/00005537-197011000-00001 TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 28 TC 7 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1995 VL 90 IS 1-2 BP 169 EP 175 DI 10.1016/0378-5955(95)00161-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300018 PM 8974994 ER PT J AU HENRY, KR AF HENRY, KR TI AUDITORY-NERVE NEUROPHONIC RECORDED FROM THE ROUND WINDOW OF THE MONGOLIAN GERBIL SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE NEUROPHONIC; COCHLEAR MICROPHONIC; COMPOUND ACTION POTENTIAL; GERBIL; TETRODOTOXIN; FREQUENCY-FOLLOWING RESPONSE; PHASE-LOCKING ID FREQUENCY-FOLLOWING RESPONSE; COCHLEAR NERVE; ADAPTATION; RECOVERY; SUPPRESSION; MASKING; FIBERS; TONES; ANN AB In the Mongolian gerbil, round window (RW) recordings of averaged responses to phase-locked acoustic stimuli which are not alternated in polarity can include both the cochlear microphonic (CM) and auditory nerve neurophonic (ANN). The ANN can dominate the recordings when the RW electrode is referenced to some portion of the body that allows the two electrodes to straddle the auditory nerve. Concentric bipolar RW electrodes are biased in favor of the CM. When there is a substantial ANN component in the RW response, as the sinusoidal stimulus intensity increases there is a non-monotonic increase of amplitude and a pronounced change of phase of the response. When the phase-locked stimuli are alternated in polarity in order to cancel the CM, a residual response is often observed. This residual response has twice the frequency of the stimulus and is decreased in amplitude by forward masking. It also shows a pattern of amplitude decrement following the stimulus onset, resembling adaptation of the firing rate of cochlear nerve axons. Tetrodotoxin (TTX) eliminates the non-monotonic RW amplitude input-output (I/O) function, reduces the phase changes of the response as the stimulus intensity is increased, eliminates the residual non-canceled response to alternated stimuli, and the time-limited amplitude decrements which resemble adaptation. Following application of TTX, the RW response of the gerbil to stimuli with non-alternated polarity much more closely resembles the CM responses of other animals. It is concluded that the gerbil's residual response following cancellation of the CM is the ANN, and that the RW of the gerbil is a convenient site for recording measures of phase-locked cochlear axonal activity. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 176 EP 184 DI 10.1016/0378-5955(95)00162-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300019 PM 8974995 ER PT J AU MITTMANN, DH WENSTRUP, JJ AF MITTMANN, DH WENSTRUP, JJ TI COMBINATION-SENSITIVE NEURONS IN THE INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE AUDITORY PATHWAYS; BAT; BIOSONAR; COMBINATION SENSITIVE; COMPLEX SOUND; INFERIOR COLLICULUS ID PRIMARY AUDITORY-CORTEX; MEDIAL GENICULATE-BODY; MUSTACHED BAT; FUNCTIONAL-ORGANIZATION; MOUSTACHED BAT; PTERONOTUS-PARNELLII; BIOSONAR SIGNALS; TUNING CURVES; TARGET RANGE; REPRESENTATION AB We examined whether neurons in the inferior colliculus of the mustached bat (Pteronotus parnellii) are combination sensitive, responding to both low- and high-frequency components of the bat's sonar signal. These neurons, previously reported in the thalamus and cortex, analyze sonar target features including distance. Of 82 single units and 36 multiple units from the 58-112 kKz representations of the inferior colliculus, most (86%) displayed sensitivity to low-frequency sounds that was tuned in the range of the fundamental biosonar component (24-31 kHz). All histologically localized units were in the central nucleus of the inferior colliculus (ICC). There were two major types of combination-sensitive influences. Many neurons were facilitated by low-frequency sounds and selective for particular delays between the low- and high-frequency components. In other neurons, the low-frequency signal was inhibitory if presented simultaneously or a few milliseconds prior to the high-frequency signal. The results indicate that mechanisms creating specialized frequency comparisons and delay sensitivity in combination-sensitive neurons operate at the ICC or below. Since combination sensitivity or multipeaked tuning curves occur in the auditory systems of many species, ICC neurons in these animals may also respond to species-specific frequency combinations. C1 NE OHIO UNIV,COLL MED,DEPT NEUROBIOL,ROOTSTOWN,OH 44272. UNIV AKRON,DEPT BIOMED ENGN,AKRON,OH 44326. CR DEAR SP, 1993, J NEUROPHYSIOL, V70, P1988 Ehret G, 1988, Brain Res, V472, P139 FITZPATRICK DC, 1993, J NEUROSCI, V13, P931 FRISINA RD, 1989, J COMP NEUROL, V284, P85, DOI 10.1002/cne.902840107 FUZESSERY ZM, 1983, J COMP PHYSIOL, V150, P333 Irvine D. R. F., 1986, PROGR SENSORY PHYSL, V7 KANWAL JS, 1994, J ACOUST SOC AM, V96, P1229, DOI 10.1121/1.410273 KATSUKI Y, 1958, J NEUROPHYSIOL, V21, P569 KAWASAKI M, 1988, J NEUROPHYSIOL, V59, P623 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 MARGOLIASH D, 1992, J NEUROSCI, V12, P4309 Mittmann D. 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Res. PD OCT PY 1995 VL 90 IS 1-2 BP 185 EP 191 DI 10.1016/0378-5955(95)00164-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300020 PM 8974996 ER PT J AU ZIMMERMANN, CE BURGESS, BJ NADOL, JB AF ZIMMERMANN, CE BURGESS, BJ NADOL, JB TI PATTERNS OF DEGENERATION IN THE HUMAN COCHLEAR NERVE SO HEARING RESEARCH LA English DT Article DE NEURAL DEGENERATION; SPIRAL GANGLION; SENSORINEURAL HEARING LOSS ID SENSORINEURAL HEARING-LOSS; SPIRAL GANGLION-CELLS; RETROGRADE DEGENERATION; NEURAL DEGENERATION; AUDITORY-NERVE; PATHOLOGY; DEAFNESS; IMPLANTATION; NEURONS; CATS AB The patterns of neural degeneration of the spiral ganglion were studied in 12 human pathologic specimens and 2 normal neonatal specimens. Morphometric analysis of spiral ganglion cells included the maximum cross-sectional areas of both large (type 1) and small (type II) spiral ganglion cells. The organ of Corti in segments corresponding to the spiral ganglion, was evaluated for the presence or absence of inner (IHC) and outer (OHC) hair cells and supporting cells. The relationship between degeneration of spiral ganglion cells and degeneration in the organ of Corti, the age, sex, duration of deafness, cochlear location and delay between death and fixation was evaluated statistically. Both primary and secondary degeneration of the spiral ganglion were more severe in the basal than apical half of the cochlea. Degeneration of the spiral ganglion was most severe when both IHCs and OHCs were absent in the organ of Corti. No survival advantage was identified for type II ganglion cells as has been previously reported. That is, there was no correlation between the degree of degeneration of the spiral ganglion and the prevalence of type II ganglion cells. In fact, there was more severe degeneration of type II cells when the corresponding organ of Corti was severely degenerated. These findings in the human were compared with animal models of degeneration of the spiral ganglion, and the implications for cochlear implantation were discussed. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. CR ARNESEN AR, 1982, J LARYNGOL OTOL, V96, P503, DOI 10.1017/S002221510009277X BAIRD IL, 1967, ANAT REC, V159, P281, DOI 10.1002/ar.1091590306 BICHLER E, 1983, ARCH OTO-RHINO-LARYN, V237, P201, DOI 10.1007/BF00453725 Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 CAVANAGH JB, 1964, INT REV EXP PATHOL, V3, P219 Felix H, 1990, Acta Otolaryngol Suppl, V470, P71 GUILD STACY R., 1931, ACTA OTO LARYNGOL, V15, P269, DOI 10.3109/00016483109119096 HINOJOSA R, 1980, ARCH OTOLARYNGOL, V106, P193 ISHII T, 1977, ANN OTO RHINOL LARYN, V86, P541 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 JOHNSSON LG, 1976, ANN OTO RHINOL LARYN, V85, P725 KEITHLEY EM, 1979, J COMP NEUROL, V188, P429, DOI 10.1002/cne.901880306 Kellerhals B., 1967, ACTA OTO-LARYNGOL, V226, P1 Kiang N.Y.S., 1984, P143 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 LAWRENCE M, 1973, ANN OTO RHINOL LARYN, V82, P464 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 NADOL JB, 1990, HEARING RES, V49, P141, DOI 10.1016/0378-5955(90)90101-T NADOL JB, 1989, ANN OTO RHINOL LARYN, V98, P411 NADOL JB, 1977, ANN OTO RHINOL LARYN, V86, P507 NADOL JB, 1987, ANN OTO RHINOL LARYN, V96, P449 Nadol J B Jr, 1995, Acta Otolaryngol Suppl, V519, P47 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 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 PAULER M, 1986, ARCH OTO-RHINO-LARYN, V243, P200, DOI 10.1007/BF00470622 PUJOL R, 1977, ACTA OTO-LARYNGOL, V83, P59, DOI 10.3109/00016487709128813 SCHUKNECHT HF, 1986, ARCH OTO-RHINO-LARYN, V243, P1, DOI 10.1007/BF00457899 SCHUKNECHT HF, 1993, ANN OTOL RHINOL LA S, V158, P1 SCHUKNECHT H F, 1953, Trans Am Acad Ophthalmol Otolaryngol, V57, P366 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 SPOENDLIN H, 1988, ACTA OTO-LARYNGOL, V105, P403, DOI 10.3109/00016488809119493 SPOENDLIN H, 1990, ACTA OTOLARYNGOL S S, V450, P61 SPOENDLIN H, 1975, ACTA OTO-LARYNGOL, V79, P266, DOI 10.3109/00016487509124683 SPOENDLIN H, 1984, ANN OTO RHINOL LARYN, V93, P76 SPOENDLI.H, 1974, BRAIN, V97, P41, DOI 10.1093/brain/97.1.41 SPOENDLIN H, 1976, ACTA OTO-LARYNGOL, V81, P228, DOI 10.3109/00016487609119954 Suzuka Y, 1988, Acta Otolaryngol Suppl, V450, P1 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P23 YLIKOSKI J, 1981, ACTA OTO-LARYNGOL, V91, P161, DOI 10.3109/00016488109138495 NR 41 TC 57 Z9 62 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1995 VL 90 IS 1-2 BP 192 EP 201 DI 10.1016/0378-5955(95)00165-1 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300021 PM 8974997 ER PT J AU DALDIN, C PUEL, JL LEDUCQ, R CRAMBES, O EYBALIN, M PUJOL, R AF DALDIN, C PUEL, JL LEDUCQ, R CRAMBES, O EYBALIN, M PUJOL, R TI EFFECTS OF A DOPAMINERGIC AGONIST IN THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE GUINEA PIG COCHLEA; LATERAL OLIVOCOCHLEAR INNERVATION; EXCITOTOXICITY; DOPAMAINE; PIRIBEDIL; D2/D3 RECEPTOR ID METABOLISM; INNER; RATS AB This study investigates the role of dopamine, a putative lateral efferent neurotransmitter/modulator, in cochlear physiology and physiopathology. Cochlear potentials were recorded in guinea pigs after intracochlear perfusion of increasing doses (0.1-1 mM) of piribedil, an agonist of the D2/D3 receptors. A dose-dependent reduction in the amplitude of auditory nerve compound action potential (CAP) was observed, predominantly at high-intensity tone-burst stimulations, and without significant effect on CAP threshold. There was no variation of cochlear microphonic and summating potential. When 1 mM piribedil was perfused into the cochlea during continuous 130 dB SPL pure tone exposure (6 kHz, 15 min), CAP threshold shifts were significantly less than in control animals with artificial perilymph-perfused cochleas. No dendritic damage was observed, although there was evident hair cell damage. Similarly, radial dendrites were clearly protected against ischemia-induced damage when 1 mM piribedil was applied prior to a 10-min ischemia. These results suggest that dopamine modulates the activity of radial afferent fibers via D2/D3 receptors. The protective effect of piribedil during acoustic trauma or ischemia suggests that this modulation corresponds to a prevention of excitotoxicity due to dysfunction of inner hair cell neurotransmission. C1 INST RECH INT SERVIER,F-92415 COURBEVOIE,FRANCE. RP DALDIN, C (reprint author), CHU MONTPELLIER,HOP ST CHARLES,INSERM,U254,NEUROBIOL AUDIT & PLASTIC SYNAPTIQUE LAB,F-34295 MONTPELLIER,FRANCE. CR Bobbin R.P., 1974, ACTA OTO-LARYNGOL, V77, P55 BOBBIN RP, 1981, PHARM HEARING, P19 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X Drescher D. G., 1994, Society for Neuroscience Abstracts, V20, P972 EYBALIN M, 1993, NEUROSCIENCE, V54, P133, DOI 10.1016/0306-4522(93)90389-W EYBALIN M, 1995, ACTIVE HEARING, P76 EYBALIN M, 1993, PHYSIOL REV, V73, P309 GILLOYZAGA P, 1989, DEV BRAIN RES, V48, P157, DOI 10.1016/0165-3806(89)90100-4 GILLOYZAGA P, 1993, BRAIN RES, V623, P177, DOI 10.1016/0006-8993(93)90027-K JONES N, 1987, HEARING RES, V30, P33, DOI 10.1016/0378-5955(87)90180-8 LIPTON SA, 1989, TRENDS NEUROSCI, V7, P265 MILLAN MJ, 1994, EUR J PHARMACOL, V260, pR3, DOI 10.1016/0014-2999(94)90353-0 PUEL JL, 1991, NEUROSCIENCE, V45, P63, DOI 10.1016/0306-4522(91)90103-U PUEL JL, 1994, J COMP NEUROL, V341, P241, DOI 10.1002/cne.903410209 PUEL JL, 1995, CR ACAD SCI III-VIE, V318, P67 Pujol R, 1991, NOISE INDUCED HEARIN, P196 PUJOL R, 1992, NEUROREPORT, V3, P299, DOI 10.1097/00001756-199204000-00002 ROBERTSON D, 1983, HEARING RES, V9, P263, DOI 10.1016/0378-5955(83)90031-X SAFIEDDINE S, 1994, 59TH ASS RES OTOL ST SANCHEZGARZON M, 1990, ADV OTO-RHINO-LARYNG, V45, P99 SARATI S, 1991, PSYCHOPHARMACOLOGY, V105, P541, DOI 10.1007/BF02244377 Usami S, 1988, Acta Otolaryngol Suppl, V447, P36 VINCENT SR, 1988, J COMP NEUROL, V268, P584, DOI 10.1002/cne.902680408 YLIKOSKI J, 1989, ACTA OTO-LARYNGOL, V107, P417, DOI 10.3109/00016488909127533 ZILLES K, 1992, ANN ANAT, V174, P383 NR 25 TC 62 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 OCT PY 1995 VL 90 IS 1-2 BP 202 EP 211 DI 10.1016/0378-5955(95)00167-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300022 PM 8974998 ER PT J AU SUZUKI, H IKEDA, K TAKASAKA, T AF SUZUKI, H IKEDA, K TAKASAKA, T TI BIOLOGICAL CHARACTERISTICS OF THE GLOBULAR SUBSTANCE IN THE OTOCONIAL MEMBRANE OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE OTOCONIA; PRECURSOR; GLOBULAR SUBSTANCE; CALCIUM; UTRICLE; CONFOCAL LASER SCANNING MICROSCOPY ID UTRICULAR MACULA; INNER-EAR; CALCIUM; CELLS; CHLOROTETRACYCLINE; FLUORESCENCE; LOCALIZATION; PROBE; RAT AB Biological characteristics of the globular substance, which is considered to be a precursor of otoconia, were investigated by means of confocal laser scanning microscopy. The shape of the globular substance was a complete sphere, 3-10 mu m in diameter. Its surface stained positively with both rhodamine 123 and DiOC(6)(3), implying similarity to intracellular organelles, whereas no fluorescence was seen when stained with chlortetracycline, a membrane-associated Ca2+ dye. Meanwhile, this substance showed very little affinity for six kinds of lectins, indicating the lack of a surface structure of carbohydrates. The fluorescence of fluo-3 in the globular substance increased markedly after the application of ionomycin. But this was completely inhibited by the depletion of external Ca2+. This reaction suggests that the surface of the globular substance exhibits characteristics of a biological membrane and that the influx of external Ca2+ occurs through membrane-combined ionomycin. Internal free Ca2+ concentration varied from 1.1 X 10(-9) to 1.6 X 10(-4) M, the geometric mean being 3.3 X 10(-7) M, which is higher than normal resting level of intracellular Ca2+ concentration but lower than the calcium content of the globular substance estimated by X-ray microanalysis in previous studies. RP SUZUKI, H (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,AOBA KU,1-1 SEIRYO MACHI,SENDAI,MIYAGI 98077,JAPAN. CR ANNIKO M, 1987, ACTA OTO-LARYNGOL, V104, P285, DOI 10.3109/00016488709107330 BELANGER LF, 1960, CALCIFICATION BIOL S, P151 CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 CASWELL AH, 1971, BIOCHEM BIOPH RES CO, V42, P43, DOI 10.1016/0006-291X(71)90359-7 CHANDLER DE, 1978, J CELL BIOL, V76, P371, DOI 10.1083/jcb.76.2.371 DULON D, 1990, J NEUROSCI, V10, P1355 Endo S, 1991, Acta Otolaryngol Suppl, V481, P116 FERMIN CD, 1985, ACTA ANAT, V123, P148 HALE JE, 1987, J BIOL CHEM, V262, P1916 HALLETT M, 1972, J MEMBRANE BIOL, V10, P31, DOI 10.1007/BF01867846 Harada Y, 1983, Adv Otorhinolaryngol, V30, P258 HARADA Y, 1982, Japanese Journal of Clinical Electron Microscopy, V15, P1 HARADA Y, 1978, J CLIN ELECT MICROSC, V11, P5 HIROTA S, 1994, CELL TECHNOL JAPAN, V13, P1072 IKEDA K, 1993, HEARING RES, V66, P169, DOI 10.1016/0378-5955(93)90138-Q JOHNSON LV, 1980, P NATL ACAD SCI-BIOL, V77, P990, DOI 10.1073/pnas.77.2.990 KAO JPY, 1989, J BIOL CHEM, V264, P8179 Kawamata S, 1993, Acta Otolaryngol Suppl, V504, P30 KIDO T, 1993, ACTA OTO-LARYNGOL, V113, P128, DOI 10.3109/00016489309135780 KIDO T, 1991, AM J OTOLARYNG, V12, P191, DOI 10.1016/0196-0709(91)90119-Z Lim D J, 1973, Ann Otol Rhinol Laryngol, V82, P23 MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 NACCACHE PH, 1979, J CELL BIOL, V83, P179, DOI 10.1083/jcb.83.1.179 NAKAHARA H, 1979, ANAT REC, V193, P233, DOI 10.1002/ar.1091930205 POTE KG, 1993, BIOCHEMISTRY-US, V32, P5017, DOI 10.1021/bi00070a007 ROE MW, 1990, CELL CALCIUM, V11, P63, DOI 10.1016/0143-4160(90)90060-8 Ross M D, 1979, Adv Otorhinolaryngol, V25, P26 ROSS MD, 1985, AUDITORY BIOCH, P500 SALAMAT MS, 1980, ANN OTO RHINOL LARYN, V89, P229 SHRADER RE, 1973, TERATOLOGY, V8, P257, DOI 10.1002/tera.1420080305 SUZUKI H, 1992, HEARING RES, V60, P45, DOI 10.1016/0378-5955(92)90057-T TACHIBANA M, 1992, HEARING RES, V62, P11, DOI 10.1016/0378-5955(92)90198-V TAKEMURA T, 1994, HEARING RES, V79, P99, DOI 10.1016/0378-5955(94)90131-7 TAKUMIDA M, 1992, ACTA OTO-LARYNGOL, V112, P643, DOI 10.3109/00016489209137454 TERASAKI M, 1984, CELL, V38, P101, DOI 10.1016/0092-8674(84)90530-0 YOON K, 1987, BIOCHEM BIOPH RES CO, V148, P1129, DOI 10.1016/S0006-291X(87)80250-4 NR 36 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1995 VL 90 IS 1-2 BP 212 EP 218 DI 10.1016/0378-5955(95)00168-7 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300023 PM 8974999 ER PT J AU LORENZI, C MICHEYL, C BERTHOMMIER, F AF LORENZI, C MICHEYL, C BERTHOMMIER, F TI NEURONAL CORRELATES OF PERCEPTUAL AMPLITUDE-MODULATION DETECTION SO HEARING RESEARCH LA English DT Article DE NEURAL MODELING; PSYCHOMETRIC FUNCTION; AMPLITUDE MODULATION; COCHLEAR NUCLEUS; INFERIOR COLLICULUS; MODULATION THRESHOLD ID ANTEROVENTRAL COCHLEAR NUCLEUS; PURE-TONE STIMULI; INFERIOR COLLICULUS; AUDITORY-SYSTEM; BAND NOISE; FREQUENCY; RESPONSES; CAT; PROJECTIONS; REGION AB The goal of the present paper is to relate the coding of amplitude modulation (AM) in the auditory pathway to the behavioral detection performance. To address this issue, the detectability of AM was estimated by modelling a single neuron located in the central nucleus of the inferior colliculus (IC). The computational model is based on cochlear nucleus responses and a coincidence detection mechanism. The model replicated the main feature of the neuronal AM transfer function, namely a bandpass function. The IC-unit model was initially tuned to a 200-Hz modulation frequency. A single neurometric function for AM detection at this modulation frequency was generated using a 2-interval, 2-alternative forced-choice paradigm. On each trial of the experiments, AM was taken to be correctly detected by the model if the number of spikes in response to the modulated signal exceeded the number of spikes in an otherwise identical interval that contained an unmodulated signal. Psychometric functions for 4 human subjects were also measured under the same stimulus conditions. Comparison of the simulated neurometric and psychometric functions suggested that there was sufficient information in the rate response of an IC neuron well-tuned in the modulation-frequency domain to support behavioral detection performance. C1 INST NATL POLYTECH GRENOBLE,INST COMMUN PARLEE,CNRS,URA 368,F-38031 GRENOBLE,FRANCE. UNIV LYON 2,INST PSYCHOL,DEPT PSYCHOL COGNIT,PERCEPT COGNIT HANDICAP LAB,F-69676 BRON,FRANCE. HOP EDOUARD HERRIOT,PHYSIOL SENSORIELLE LAB,CNRS,URA 1447,F-69437 LYON,FRANCE. RI Lorenzi, Christian/F-5310-2012 CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 AINSWORTH WA, 1994, J ACOUST SOC AM, V96, P687, DOI 10.1121/1.410306 ARLE JE, 1991, BIOL CYBERN, V64, P273, DOI 10.1007/BF00199590 AVRON E, 1991, BIOL CYBERN, V65, P487, DOI 10.1007/BF00204662 BACON SP, 1989, J ACOUST SOC AM, V85, P2575, DOI 10.1121/1.397751 BANKS MI, 1991, BIOL CYBERN, V64, P273 BERTHOMMIER F, 1990, P INNC90 PARIS KLUWE, V1, P467 BERTHOMMIER F, 1991, COGNITIVA 90 : AT THE CROSSROADS OF ARTIFICIAL INTELLIGENCE, COGNITIVE SCIENCE, AND NEUROSCIENCE, P25 BERTHOMMIER F, 1992, THESIS U J FOURIER G BLACKBURN CC, 1989, J NEUROPHYSIOL, V62, P1303 EDDINS DA, 1993, J ACOUST SOC AM, V93, P470, DOI 10.1121/1.405627 EHRET G, 1988, BRAIN RES REV, V13, P139, DOI 10.1016/0165-0173(88)90018-5 FORREST TG, 1987, J ACOUST SOC AM, V82, P1933, DOI 10.1121/1.395689 FRISINA RD, 1990, HEARING RES, V44, P99, DOI 10.1016/0378-5955(90)90074-Y FRISINA RD, 1989, J COMP NEUROL, V284, P85, DOI 10.1002/cne.902840107 GHOSHAL S, 1992, HEARING RES, V58, P153, DOI 10.1016/0378-5955(92)90124-6 Goldberg JM, 1969, J NEUROPHYSIOL, V32, P940 GREEN DM, 1974, SIGNAL DETECTION THE HEWITT MJ, 1992, J ACOUST SOC AM, V91, P2096, DOI 10.1121/1.403696 HEWITT MJ, 1994, J ACOUST SOC AM, V95, P2145, DOI 10.1121/1.408676 HODGKIN AL, 1982, J PHYSL, V117, P500 HOUTGAST T, 1989, J ACOUST SOC AM, V85, P1676, DOI 10.1121/1.397956 JORIS PX, 1992, J ACOUST SOC AM, V91, P215, DOI 10.1121/1.402757 LANGNER G, 1992, HEARING RES, V60, P115, DOI 10.1016/0378-5955(92)90015-F LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 LORENZI C, 1993, J ACOUST SOC AM, V93, P2313, DOI 10.1121/1.406381 MOLLER AR, 1976, ACTA PHYSIOL SCAND, V98, P157, DOI 10.1111/j.1748-1716.1976.tb00235.x NEWSOME WT, 1989, NATURE, V341, P52, DOI 10.1038/341052a0 OERTEL D, 1985, J ACOUST SOC AM, V78, P328, DOI 10.1121/1.392494 OLIVER DL, 1987, J COMP NEUROL, V264, P24, DOI 10.1002/cne.902640104 REES A, 1987, HEARING RES, V27, P129, DOI 10.1016/0378-5955(87)90014-1 REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 RODENBURG M, 1977, PSYCHOPHYSICS PHYSIO ROSE JE, 1971, J NEUROPHYSIOL, V34, P685 STRICKLAND EA, 1994, J ACOUST SOC AM A, V95, P2964, DOI 10.1121/1.409026 VIEMEISTER NF, 1979, J ACOUST SOC AM, V74, P765 ZOHARY E, 1994, NATURE, V370, P140, DOI 10.1038/370140a0 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 OCT PY 1995 VL 90 IS 1-2 BP 219 EP 227 DI 10.1016/0378-5955(95)00169-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TK343 UT WOS:A1995TK34300024 PM 8975000 ER PT J AU BOETTCHER, FA MILLS, JH DUBNO, JR SCHMIEDT, RA AF BOETTCHER, FA MILLS, JH DUBNO, JR SCHMIEDT, RA TI MASKING OF AUDITORY BRAIN-STEM RESPONSES IN YOUNG AND AGED GERBILS SO HEARING RESEARCH LA English DT Article DE AGING; AUDITORY BRAIN-STEM RESPONSE; EVOKED POTENTIAL; GERBIL; HEARING LOSS; MASKING; PRESBYCUSIS ID SENSORINEURAL HEARING-LOSS; CHRONIC COCHLEAR PATHOLOGY; FREQUENCY-SELECTIVITY; BASILAR-MEMBRANE; THRESHOLD SHIFT; NERVE FIBERS; LISTENERS; SPREAD; QUIET; RECOGNITION AB Auditory brainstem responses (ABR) were recorded in the presence of low-pass (1 kHz cutoff) or high-pass (8 kHz cutoff) filtered noise in young (4-8 month) and aged (36 month) gerbils. For low-pass maskers, aged gerbils had higher masked thresholds at 2 and 4 kHz than young subjects. This was true for all aged subjects, including those with quiet thresholds similar to those of young controls. For high-pass masking, the majority of aged subjects had higher masked thresholds at 2 and 4 kHz than young controls; however, aged subjects with relatively normal quiet thresholds had masked thresholds similar to those of young subjects. A modified power-law (MPL) model was used to predict masked thresholds for aged subjects. Thresholds measured in the presence of low-pass noise were higher than predicted in many of the aged subjects, particularly those with near-normal quiet thresholds. In contrast, thresholds measured in the presence of the high-pass masker were similar to the predicted thresholds. These results suggest that: (a) excess masking occurred in aged subjects for low-pass, but not high-pass, maskers; (b) the excess masking occurred independently of quiet thresholds; and (c) excess upward spread of masking was related to the spectrum of the masker and not the 2 and 4 kHz regions of the auditory periphery. RP BOETTCHER, FA (reprint author), MED UNIV S CAROLINA,DEPT OTORHINOLARYNGOL & COMMUNICAT SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR BILGER RC, 1956, J ACOUST SOC AM, V28, P623, DOI 10.1121/1.1908426 BOETTCHER FA, 1994, ASS RES OTOLARYNGOL, V17, P153 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z BOETTCHER FA, 1993, HEARING RES, V71, P146, DOI 10.1016/0378-5955(93)90030-5 BURKARD R, 1993, J ACOUST SOC AM, V94, P2441, DOI 10.1121/1.407465 DEATHERAGE BH, 1957, J ACOUST SOC AM, V29, P512, DOI 10.1121/1.1908944 DEATHERAGE BH, 1957, J ACOUST SOC AM, V29, P132, DOI 10.1121/1.1908641 DUBNO JR, 1992, J ACOUST SOC AM, V91, P2110, DOI 10.1121/1.403697 FLORENTINE M, 1980, J SPEECH HEAR RES, V23, P646 GAGNE JP, 1988, J ACOUST SOC AM, V83, P2311 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HUMES LE, 1988, J ACOUST SOC AM, V83, P188, DOI 10.1121/1.396420 HUMES LE, 1989, J ACOUST SOC AM, V85, P1285, DOI 10.1121/1.397459 KLEIN AJ, 1990, J ACOUST SOC AM, V87, P1266, DOI 10.1121/1.398802 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 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 MARTIN ES, 1970, J SPEECH HEAR RES, V13, P426 MILLS JH, 1983, HEARING RES THEORY, V2, P233 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 Mills J.H., 1982, NEW PERSPECTIVES NOI, P249 OMALLEY H, 1979, J ACOUST SOC AM, V66, P1075, DOI 10.1121/1.383326 PATTERSON RD, 1982, J ACOUST SOC AM, V72, P1788, DOI 10.1121/1.388652 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O SALVI RJ, 1983, HEARING RES, V10, P37, DOI 10.1016/0378-5955(83)90017-5 SCHMIEDT RA, 1984, J ACOUST SOC AM, V76, P1293, DOI 10.1121/1.391446 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 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SMITH DI, 1989, ELECTROEN CLIN NEURO, V72, P422, DOI 10.1016/0013-4694(89)90047-3 TREES DE, 1986, AUDIOLOGY, V25, P70 Wegel RL, 1924, PHYS REV, V23, P266, DOI 10.1103/PhysRev.23.266 Wightman F., 1977, PSYCHOPHYSICS PHYSL, P295 NR 33 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1995 VL 89 IS 1-2 BP 1 EP 13 DI 10.1016/0378-5955(95)00116-X PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700001 PM 8600113 ER PT J AU VINCENT, DA GRATTON, MA SMYTH, BJ SCHULTE, BA AF VINCENT, DA GRATTON, MA SMYTH, BJ SCHULTE, BA TI EFFECT OF POSTMORTEM AUTOLYSIS ON NA,K-ATPASE ACTIVITY AND ANTIGENICITY IN THE GERBIL COCHLEA SO HEARING RESEARCH LA English DT Article DE NA,K-ATPASE; COCHLEA; AUTOLYSIS; IMMUNOHISTOCHEMISTRY; ANTIGENICITY; GERBIL ID POTENTIALS; CELLS; AGE AB Alterations in the enzymatic activity and antigenicity of Na,K-ATPase as well as changes in cochlear morphology were assessed in gerbil inner ears harvested at selected time intervals up to 18 h postmortem. Na,K-ATPase activity was assayed biochemically in one cochlea from each animal and the other cochlea was fixed and embedded in paraffin for evaluation by light microscopy. Na,K-ATPase antigenicity was assessed by immunostaining with a broad-spectrum antiserum reactive with all known isoforms of the enzyme, and structural preservation was evaluated on adjacent sections stained with hematoxylin and eosin. The results showed a downward trend in enzymatic activity of Na,K-ATPase in lateral wall tissues within 1 h of death. In contrast, Na,K-ATPase immunoreactivity was fairly well preserved with postmortem fixation delays up to 12 h, despite the considerable structural degradation of cochlear tissues which began 2-3 h postmortem. It is concluded that under controlled environmental conditions, cochleas collected up to 4 h postmortem are suitable for morphological and immunohistochemical study of Na,K-ATPase by light microscopy. Cochleas collected more than 5 h postmortem were useful only for relatively gross immunohistochemical studies. It is suggested that cochleas intended for biochemical assays of Na,K-ATPase and probably most other enzymes should be collected within 1 h of death. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP VINCENT, DA (reprint author), MED UNIV S CAROLINA,DEPT OTORHINOLARYNGOL & COMMUNICAT SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR BREDBERG G, 1972, ACTA OTOLARYNGOLOG S, V301 COMIS SD, 1990, ACTA OTO-LARYNGOL, V109, P361, DOI 10.3109/00016489009125156 FERNANDEZ C, 1958, Laryngoscope, V68, P1586, DOI 10.1288/00005537-195809000-00002 FORBUSH B, 1983, ANAL BIOCHEM, V128, P159, DOI 10.1016/0003-2697(83)90356-1 GRATTON MA, 1995, HEARING RES, V83, P43, DOI 10.1016/0378-5955(94)00188-V HAWKINS JE, 1976, HDB AUDITORY VESTIBU, P5 HAZENMARTIN DJ, 1993, ENVIRON HEALTH PERSP, V101, P510, DOI 10.2307/3431588 HIEBER V, 1989, J NEUROSCI RES, V23, P9, DOI 10.1002/jnr.490230103 JOHNSON JP, 1986, AM J PHYSIOL, V251, pC186 JORGENSEN PL, 1988, METHOD ENZYMOL, V156, P291 MATSCHIN.FM, 1967, ANN OTO RHINOL LARYN, V76, P638 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 RUTLEDGE LJ, 1969, LARYNGOSCOPE, V79, P2104, DOI 10.1288/00005537-196912000-00006 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K THALMANN R, 1972, LARYNGOSCOPE, V82, P2249, DOI 10.1288/00005537-197212000-00013 VINCENT DA, 1993, ABSTR ASS RES OT, V16, P137 ZOLOTARJOVA N, 1994, BBA-BIOMEMBRANES, V1192, P125, DOI 10.1016/0005-2736(94)90152-X NR 18 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 1995 VL 89 IS 1-2 BP 14 EP 20 DI 10.1016/0378-5955(95)00117-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700002 PM 8600119 ER PT J AU LEVI, EC FOLSOM, RC DOBIE, RA AF LEVI, EC FOLSOM, RC DOBIE, RA TI COHERENCE ANALYSIS OF ENVELOPE-FOLLOWING RESPONSES (EFRS) AND FREQUENCY-FOLLOWING RESPONSES (FFRS) IN INFANTS AND ADULTS SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED POTENTIAL; AUDITORY DEVELOPMENT; COHERENCE; STEADY-STATE RESPONSE; THRESHOLD ID MODULATION-FOLLOWING RESPONSE; AUDITORY-NERVE FIBERS; SCALP POTENTIALS; AMPLITUDE; TONES; HUMANS; SPEECH; STATE AB The frequency-following response (FFR) and the envelope-following response (EFR) were recorded in 1-month-old infants and in adults to examine the development of temporal coding. The stimuli were amplitude-modulated (AM) tones. A modulation frequency of 80 Hz was used in infants; modulation frequencies of 40 and 80 Hz were used in adults. The effects of intensity, carrier frequency, and modulation frequency on these responses were studied. Responses were analyzed using magnitude-squared coherence. The effect of intensity on the growth of FFR- and EFR-coherence were similar in infants and adults. In addition, the growth functions were not affected by the carrier frequency or the modulation frequency of the stimulus. FFR thresholds did not differ across age groups. 'Best frequency' (i.e., infant 80 Hz and adult 40 Hz) EFR thresholds were the same for infants and adults at 500 and 1000 Hz, but infant EFR thresholds were poorer than adult thresholds at 2000 Hz. Thus, although FFRs and EFRs are primarily adult-like at 1 month of age, there are some age differences in the EFR that deserve further study. C1 UNIV TEXAS,DEPT OTOLARYNGOL HEAD & NECK SURG,SAN ANTONIO,TX 78285. RP LEVI, EC (reprint author), UNIV WASHINGTON,CTR CHILD DEV & MENTAL RETARDAT,DEPT SPEECH & HEARING SCI,INFANT HEARING LAB,SEATTLE,WA 98105, USA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 21 EP 27 DI 10.1016/0378-5955(95)00118-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700003 PM 8600128 ER PT J AU CHEN, L TRAUTWEIN, PG MILLER, K SALVI, RJ AF CHEN, L TRAUTWEIN, PG MILLER, K SALVI, RJ TI EFFECTS OF KANAMYCIN OTOTOXICITY AND HAIR CELL REGENERATION ON THE DC ENDOCOCHLEAR POTENTIAL IN ADULT CHICKENS SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; KANAMYCIN; OTOTOXICITY; HAIR CELL REGENERATION; COCHLEAR MICROPHONIC; COMPOUND ACTION POTENTIAL; CHICKEN ID AVIAN INNER-EAR; GENTAMICIN TREATMENT; ETHACRYNIC-ACID; COCHLEAR FLUIDS; GUINEA-PIGS; POTASSIUM; RESPONSES; RECOVERY; PERMEABILITY; FUROSEMIDE AB High doses of aminoglycoside antibiotics cause massive damage to the avian basilar papilla. The resulting functional loss could conceivably arise from the reduction in the DC endocochlear potential (EP) due to impairment of the tegmentum vasculosum (TV) or to shunting of current through the damaged sensory epithelium. To test this hypothesis, the EP was measured in adult chickens after destroying hair cells in the basal half of the cochlea with a high dose (400 mg/kg per day for 10 days) of kanamycin (KM). KM treatment caused an increase in the steady-state EP from + 18.1 to + 23.3 mV and a decrease in the magnitude of the negative EP from -42.0 to -19.2 mV. The EP showed almost no change between 1 and 2 days and 1 week post-KM treatment. After 4 weeks of recovery, most hair cells had regenerated; however, the steady-state EP was still elevated by 13% and the negative EP was depressed by 37%. These results suggest that functional loss as shown by the large reduction in cochlear microphonic (CM) and the elevated thresholds of compound action potential (CAP) following KM treatment is not due to a reduction in the EP but may arise from functional deficits in the hair cells and/or the auditory nerve. RP CHEN, L (reprint author), SUNY BUFFALO,DEPT COMMUNICAT DISORDERS & SCI,HEARING RES LABS,215 PARKER HALL,BUFFALO,NY 14214, USA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 28 EP 34 DI 10.1016/0378-5955(95)00119-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700004 PM 8600130 ER PT J AU LASKY, RE SNODGRASS, EB LAUGHLIN, NK HECOX, KE AF LASKY, RE SNODGRASS, EB LAUGHLIN, NK HECOX, KE TI DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN MACACA-MULATTA AND HUMANS SO HEARING RESEARCH LA English DT Article DE DISTORTION PRODUCT OTOACOUSTIC EMISSION; MACACA MULATTA; NORMAL HEARING HUMAN ADULT ID ACOUSTIC DISTORTION; NONHUMAN PRIMATE; BASIC FEATURES; 2F1-F2; RESPONSES; COCHLEA; RABBIT; EARS AB Distortion product otoacoustic emissions (DPOAEs) were compared in eight rhesus monkeys (Macaca mulatta) and eight normal hearing humans. DPOAEs were recorded in three conditions. In the first condition, DPOAEgrams were generated for monkeys and humans from approximately f(2) = 0.5-20 kHz. Monkeys had larger amplitude DPOAEs at all frequencies except around f(2) = 1 kHz. In the second condition, DPOAE amplitudes increased and then decreased as the separation between the primaries increased. These functions were similar in the two species except at the lowest frequencies assessed. In the third condition, the levels of the primaries were varied independently. Monkeys had steeper input/output (I/O) functions than humans. The slopes of DPOAE I/O functions increased with frequency in both species. When the levels of both primaries were increased simultaneously, DPOAE I/O functions were well described by power functions throughout the intensity range assessed (from threshold to 65 dB SPL). Monkey I/O functions tended to be expansive power functions at all but the lowest frequencies, while human I/O functions tended to be compressive power functions except at the highest frequencies assessed. Other differences in I/O functions at f(2) = 8 kHz may indicate species specific differences at high (for human) frequencies. C1 UNIV WISCONSIN,HARLOW PRIMATE LAB,MADISON,WI 53792. RP LASKY, RE (reprint author), UNIV WISCONSIN,SCH MED,DEPT NEUROL,H6-573 CLIN SCI BLDG,600 HIGHLAND AVE,MADISON,WI 53792, USA. 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PD SEP PY 1995 VL 89 IS 1-2 BP 35 EP 51 DI 10.1016/0378-5955(95)00120-1 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700005 PM 8600131 ER PT J AU GOLDSTEIN, JL AF GOLDSTEIN, JL TI RELATIONS AMONG COMPRESSION, SUPPRESSION, AND COMBINATION TONES IN MECHANICAL RESPONSES OF THE BASILAR-MEMBRANE - DATA AND MBPNL MODEL SO HEARING RESEARCH LA English DT Article DE NONLINEAR COCHLEAR MECHANICS; TEST OF I/O MODEL; COMPRESSION; SUPPRESSION; COMBINATION TONES ID AUDITORY-NERVE FIBERS; 2-TONE RATE SUPPRESSION; OUTER HAIR-CELLS; COCHLEAR MECHANICS; TUNING CURVES; ACOUSTIC DISTORTION; MOSSBAUER TECHNIQUE; EAR; FREQUENCY; NONLINEARITY AB Recent observations of combination tones and low-frequency suppression in the mechanical response of the basilar membrane have eliminated uncertainty of the existence of these non-linear phenomena at this stage of the cochlea (Robles et al., 1991; Ruggero et al., 1992b; Rhode and Cooper, 1993), and provide the first opportunity to test and extend theoretical understanding of these non-linear responses. This paper reports a systematic study of the new data for the chinchilla with the MBPNL (multiple band-pass non-linearity) non-linear model for rapid compression in cochlear filtering (Goldstein, 1990). The two key findings are that: (1) the large differences in suppression growth rates for low- and high-frequency suppressors are closely predicted by the model, although a statistically significant small bias in the prediction was found; and (2) combination tones of frequency 2f2-f1 were well predicted by the model, while reported levels of 2f1-f2 were underestimated by the model. The most likely explanation of the result for 2f1-f2 is that the model correctly predicts the distributed generation of combination tones, but does not include a propagating medium that allows combination tones to accumulate at their tuned site. Alternative explanations requiring experimental clarification are suggested. The general finding of this study is that the complex level-dependent properties of suppression and combination tones are closely related to the three regions characterizing the tuned response of the basilar membrane, in which linear-like responses at low and high sound levels are joined by a compressive range. The MBPNL model describes this general relationship quantitatively and is a reliable basis for further modeling research. RP GOLDSTEIN, JL (reprint author), CENT INST DEAF,ST LOUIS,MO 63110, USA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 52 EP 68 DI 10.1016/0378-5955(95)00121-3 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700006 PM 8600132 ER PT J AU HU, BH JIANG, SC AF HU, BH JIANG, SC TI EFFECT OF FOCAL COCHLEAR VASCULAR LESION ON ENDOCOCHLEAR POTENTIAL IN GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE COCHLEAR MICROCIRCULATION; ENDOCOCHLEAR POTENTIAL; INTRAVITAL MICROSCOPY; PHOTOCHEMISTRY; FOCAL MICROVESSEL LESION ID PLATELET-AGGREGATION; BLOOD-FLOW; STRIA VASCULARIS; HEARING-LOSS; MICROCIRCULATION; MODEL; INFARCTION; THROMBOSIS; INVIVO; LIGHT AB The alteration endocochlear potential (EP) in response to total cochlear ischemia induced by various experimental manipulations has been studied. However, the effect of restricted areal damage to the microvessels (restricted to small area in the lateral wall of a cochlear turn) on the EP value is still unknown. In the current investigation we adopted a photochemical method to produce a focal (i.e., restricted area) microvessel injury in the lateral wall of the guinea pig cochlea and examined the effect of these insults on EP recorded in the same region. The small area of the microvessel lesion (small fenestra: approximately 0.2 x 0.4 mm(2)) induced by photoactivation did not yield significant EP changes, suggesting that damage to such a small area of microcirculation in the lateral wall of the cochlea has no statistically significant effects on EP values. In subjects with a large area of the microvessel lesion (large fenestra: approximate to 0.2 X 0.8 mm(2)), a decrease in the EP value (mean +/- SEM 7.9 +/- 0.8 mV) was noted. However, the control group animals with a large fenestra but without microvessel lesion also displayed a decrease (8.6 +/- 0.8 mV) in EP. In the current study we were unable to differentiate whether the EP changes in animals with the large fenestra microvessel lesions were caused by the cochlear blood flow decrease or by the surgical preparation. However, the results of this study indicated if the EP value was affected by the large area of the microvessel lesion, the level of decrease would not be large. That is, the EP decrease was less than the EP change in the control group (mean: 8.6 mV). Considering the dependence of EP on blood flow, the data of this study suggest that compensatory mechanisms in the cochlea may maintain the EP following a focal lesion in the lateral wall of the cochlea. This study also indicates that the photochemical method provides a reliable approach to produce the animal model with the focal microvessel lesion in the lateral wall of the cochlea. C1 CHINESE GREAT WALL HOSP,INST OTORHINOLARYNGOL,BEIJING 100853,PEOPLES R CHINA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 69 EP 75 DI 10.1016/0378-5955(95)00122-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700007 PM 8600133 ER PT J AU YAO, WP GODFREY, DA AF YAO, WP GODFREY, DA TI IMMUNOHISTOCHEMISTRY OF MUSCARINIC ACETYLCHOLINE-RECEPTORS IN RAT COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINESTERASE; AUDITORY; CENTRIFUGAL PATHWAY; CHOLINERGIC; CHOLINE ACETYLTRANSFERASE; IMAGING ID CHOLINE-ACETYLTRANSFERASE; BRAIN-STEM; AUTORADIOGRAPHIC LOCALIZATION; MONOCLONAL-ANTIBODIES; DORSAL HIPPOCAMPUS; NEURONS; LESIONS; SYSTEM AB Neurons of the cochlear nucleus (CN) receive extrinsic and intrinsic cholinergic inputs, the effects of which appear to be mediated primarily by muscarinic acetylcholine receptors (mAChRs). To investigate the distribution of mAChRs and the correlation of pre- and post-synaptic cholinergic markers in CN, we used a monoclonal anti-mAChR antibody (M35) and a monoclonal antibody against choline acetyltransferase (ChAT) to perform immunohistochemistry on rat brain sections, and we also carried out histochemistry for acetylcholinesterase (AChE) activity. The density distributions of ChAT immunohistochemistry and AChE activity histochemistry agreed well with previous quantitative measurements of the activity distributions of these enzymes. A generally close correlation between densities of M35 and ChAT immunoreactivities was found across subregions of rat CN. The localizations of M35 and ChAT immunoreactivities suggest that cholinergic synapses are mostly axosomatic in ventral CN and possibly mostly axodendritic in dorsal CN. Prominent differences in density and appearance between M35 immunoreactivity and AChE activity were found in the regions of the rat CN where granule cells predominate. RP YAO, WP (reprint author), MED COLL OHIO,DEPT OTOLARYNGOL HEAD & NECK SURG,POB 10008,TOLEDO,OH 43699, USA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 76 EP 85 DI 10.1016/0378-5955(95)00123-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700008 PM 8600134 ER PT J AU VASS, Z NUTTALL, AL COLEMAN, JKM MILLER, JM AF VASS, Z NUTTALL, AL COLEMAN, JKM MILLER, JM TI CAPSAICIN-INDUCED RELEASE OF SUBSTANCE-P INCREASES COCHLEAR BLOOD-FLOW IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SUBSTANCE P; CAPSAICIN; COCHLEAR BLOOD FLOW; SENSORY NEURON; GUINEA PIG ID NERVE; NEUROPEPTIDES; INNERVATION; RESPONSES; RECEPTORS; ARTERIES; ENDINGS; SYSTEM; RAT AB Physiological evidence from several studies suggests that endogenous vasoactive peptides, such as substance P (SP), and their respective receptor populations may participate in the mechanisms that govern the autoregulatory capacity of the cochlear vascular system. However, these studies do not provide evidence regarding the origin or mechanism of action of SP. Capsaicin sensitivity has been used as a marker for sensory neurons, and the release of SP following capsaicin treatment suggests a sensory transmitter role for SP. The present investigation examines the relationship between the capsaicin-sensitive sensory neurons and SP in the regulation of cochlear blood flow (CBF). In 75 pigmented guinea pigs, the cochlea was surgically exposed and a laser Doppler flowmeter probe placed on the bony surface of the first turn to monitor CBF. Capsaicin solutions (2 mu l, 0.01%, 0.001% and 0.0001%) applied to the round-window membrane (RWM) resulted in a dose-related CBF increase, without change in the systemic blood pressure. This effect could be inhibited by application of a specific SP receptor antagonist, [D-Pro(2),D-Trp(7,9)]-SP, after which none of the capsaicin concentrations used induced a change in CBF. Moreover, after RWM application of 50 nmol/2 mu l of SP there was a significant increase in CBF. No CBF change was observed with the lower concentrations of 10 nmol SP or 100 pmol SP. These results indicate a role of SP in CBF regulation and give indirect evidence that SP is released from capsaicin-sensitive primary sensory neurons. C1 UNIV MICHIGAN,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. ALBERT SZENT GYORGYI MED UNIV,DEPT OTOLARYNGOL,H-6701 SZEGED,HUNGARY. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 86 EP 92 DI 10.1016/0378-5955(95)00127-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700009 PM 8600135 ER PT J AU MOORE, DR LIPPE, WR RUBEL, EW AF MOORE, DR LIPPE, WR RUBEL, EW TI EFFECTS OF MIDDLE-EAR PRESSURE ON FREQUENCY REPRESENTATION IN THE CENTRAL AUDITORY-SYSTEM SO HEARING RESEARCH LA English DT Article DE HEARING; OTITIS MEDIA; GERBIL; INFERIOR COLLICULUS ID OTOACOUSTIC EMISSIONS; INFERIOR COLLICULUS; CHILDREN AB Changes in middle ear pressure (MEP) are known to produce an attenuation of sound transmission through the outer and middle ear, but the effects on frequency representation in the auditory system have not previously been studied. This issue is of particular interest because of changes in MEP occurring during episodes of otitis media. We have investigated the effect of changes in MEP on the tuning of neurons in the inferior colliculus (IC) of the gerbil to calibrated tone stimulation of the contralateral, pressurized ear. Both negative and positive non-atmospheric MEP produced an elevation of neural thresholds that was inversely related to IC neuron best frequency (BF). A robust, linear relationship was found between BF at atmospheric MEP (control) and BF at -20 daPa MEP. Higher resolution analysis was performed on a sub-sample of neurons that had particularly stable BFs with repeated, control MEP. For the majority of these neurons, alternation of MEP between control and -20 daPa had no effect on BF. However, a few neurons showed small (up to 5%), significant shifts in BF with -20 daPa MEP. These results are consistent with previous reports of the effects of MEP on spontaneous otoacoustic emissions. We conclude that non-atmospheric MEP acts as a high-pass filter on the input to the cochlea, but does not change the frequency organization of the auditory system to any marked extent. C1 UNIV WASHINGTON,SCH MED RL30,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED RL30,DEPT OTOLARYNGOL HNS,SEATTLE,WA 98195. CR Aitkin L., 1986, AUDITORY MIDBRAIN ST BRANDES PJ, 1981, J SPEECH HEAR DISORD, V46, P301 CALFORD MB, 1983, HEARING RES, V11, P395, DOI 10.1016/0378-5955(83)90070-9 FINKELSTEIN Y, 1992, ACTA OTO-LARYNGOL, V112, P88, DOI 10.3109/00016489209100788 FREEMAN BA, 1979, CLIN PEDIATR, V18, P205, DOI 10.1177/000992287901800403 KALTENBACH JA, 1987, EXP NEUROL, V96, P406, DOI 10.1016/0014-4886(87)90058-6 LAMBERT PR, 1986, ARCH OTOLARYNGOL, V112, P1043 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MILLS DM, 1993, J ACOUST SOC AM, V94, P2108, DOI 10.1121/1.407483 Moller A. R., 1983, AUDITORY PHYSL PALMER AR, 1982, HEARING RES, V7, P305, DOI 10.1016/0378-5955(82)90042-9 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 TAKAHASHI H, 1991, ANN OTO RHINOL LARYN, V100, P469 Wever EG, 1942, J EXP PSYCHOL, V30, P40, DOI 10.1037/h0061283 Wever EG, 1954, PHYSL ACOUSTICS WHITEHEAD ML, 1988, THESIS U KEELE WILSON JP, 1981, CIBA F S, P82 NR 19 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 1995 VL 89 IS 1-2 BP 93 EP 100 DI 10.1016/0378-5955(95)00125-0 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700010 PM 8600136 ER PT J AU CHABBERT, C CANITROT, Y SANS, A LEHOUELLEUR, J AF CHABBERT, C CANITROT, Y SANS, A LEHOUELLEUR, J TI CALCIUM HOMEOSTASIS IN GUINEA-PIG TYPE-I VESTIBULAR HAIR CELL - POSSIBLE INVOLVEMENT OF AN NA+-CA2+ EXCHANGER SO HEARING RESEARCH LA English DT Article DE CA2+ HOMEOSTASIS; VESTIBULE; NA+-CA2+ EXCHANGE; GUINEA PIG; FURA-2; SODIUM BENZOFURAN ISOPHTHALATE ID ROD OUTER SEGMENTS; NA-CA EXCHANGE; CRISTA-AMPULLARIS; SQUID AXONS; POTASSIUM; FLUORESCENCE; REQUIRES; SODIUM; HYPERPOLARIZES; TRANSMISSION AB In type-I vestibular hair cells (VHCs), the mechanisms involved in intracellular calcium homeostasis have not yet been established. In order to investigate the involvement of an Na+-dependent ionic exchanger in the regulation of cytosolic free calcium concentration, we analyzed the effect of the removal of external sodium on the cytosolic concentration of calcium ions ([Ca2+](i)), sodium ions ([Na+](i)), and protons (pH(i)). These concentrations were measured in type-I VHCs isolated from guinea pig labyrinth, using Fura-2, sodium benzofuran isophtalate (SBFI), and 1,4 diacetoxy-2,3 dicyanobenzol (ADB) respectively. Complete replacement of Na+ in the superfusion solution with N-methyl-D-glucamine (NMDG(+)), reversibly increased [Ca2+](i) by 276 +/- 89% (n = 46) and decreased [Na+](i), by 23 +/- 6% (n = 14). Both responses were prevented by removing external Ca2+ or chelating internal Ca2+. This suggests the presence of coupled Ca2+ and Na+ transport. The [Ca2+](i) increase evoked by Na+-free solution was reduced by about 55% with the application of amiloride derivatives and was totally abolished in the presence of high [Mg2+](o). No pH(i) variation was detected during [Na+](o) reduction. In the absence of external K+, the Na+-free solution failed to induce [Ca2+](i) increase; the readmission of external K+ restored the [Ca2+](i) response. These results are consistent with a Na+-Ca2+ exchanger operating in reverse mode. An K+ dependence of this exchange is also suggested. C1 INSERM,U432,NEUROPHYSIOL SENSORIELLE & CELLULAIRE LAB,F-34095 MONTPELLIER,FRANCE. UNIV PERPIGNAN,CHIM PHYS LAB,F-66860 PERPIGNAN,FRANCE. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 101 EP 108 DI 10.1016/0378-5955(95)00126-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700011 PM 8600114 ER PT J AU KAZEE, AM HAN, LY SPONGR, VP WALTON, JP SALVI, RJ FLOOD, DG AF KAZEE, AM HAN, LY SPONGR, VP WALTON, JP SALVI, RJ FLOOD, DG TI SYNAPTIC LOSS IN THE CENTRAL NUCLEUS OF THE INFERIOR COLLICULUS CORRELATES WITH SENSORINEURAL HEARING-LOSS IN THE C57BL/6 MOUSE MODEL OF PRESBYCUSIS SO HEARING RESEARCH LA English DT Article DE PRESBYCUSIS; C57 MOUSE; INFERIOR COLLICULUS; SYNAPTIC MORPHOMETRY; CYTOCOCHLEOGRAM; AUDITORY BRAIN-STEM RESPONSE ID DORSAL COCHLEAR NUCLEUS; AGE-RELATED LOSS; CBA/J MICE; AUDITORY-SENSITIVITY; AGING C57BL/6J; NEURONS; YOUNG; RAT; CAT; MORPHOLOGY AB Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the central nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the central nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%, A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the central nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the central nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the central deficits of presbycusis. C1 UNIV ROCHESTER,DEPT NEUROL,ROCHESTER,NY 14642. UNIV ROCHESTER,DEPT SURG,DIV OTOLARYNGOL,ROCHESTER,NY 14642. SUNY BUFFALO,HEARING RES LAB,BUFFALO,NY. RP KAZEE, AM (reprint author), UNIV ROCHESTER,DEPT PATHOL & LAB MED,601 ELMWOOD AVE,BOX 626,ROCHESTER,NY 14642, USA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 109 EP 120 DI 10.1016/0378-5955(95)00128-6 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700012 PM 8600115 ER PT J AU NAKAZAWA, K SCHULTE, BA SPICER, SS AF NAKAZAWA, K SCHULTE, BA SPICER, SS TI THE ROSETTE COMPLEX IN GERBIL DEITERS CELLS CONTAINS GAMMA-ACTIN SO HEARING RESEARCH LA English DT Article DE ACTIN; VIMENTIN; DEITERS CELL; COCHLEA; CYTOSKELETON; GERBIL; COCHLEAR MECHANICS; FREQUENCY ENCODING; TUNING ID INNER-EAR; MONOCLONAL-ANTIBODY; SUPPORTING CELLS; MUSCLE-ACTIN; FILAMENTS; LOCALIZATION; POTENTIALS; COCHLEA; AGE AB The relationship of selected cytoskeletal elements with the rosette complex of Deiters cells was examined immunocytochemically in the gerbil cochlea. By light microscopy, the staining pattern for actin in the apical portion of Deiters cells corresponded with the location of the rosette complex. At the ultrastructural level, the actin antibodies bound selectively at the periphery of the dense trabeculae in the center of the complex. Comparative staining with a battery of polyclonal and isoform-specific monoclonal antibodies revealed selective presence of the gamma muscle actin isoform in this location. The loose meshwork at the periphery of the rosette complex stained selectively with a monoclonal antibody to vimentin. beta-tubulin was not associated with the rosette complex but occurred in abundance in the microtubule-rich stalk. Actin and vimentin were not detected in the apical compartment of Deiters cells at the extreme base of the cochlea, thus confirming their association with the rosette complex which is not present in regions of the gerbil cochlea tuned to frequencies of 20 kHz or higher (Spicer and Schulte, 1993, 1994). The cytoarchitecture of the rosette complex and its preferential distribution along the place-frequency map promote speculation that Deiters cells may play a role in regulating ion homeostasis and/or micromechanical response properties of the organ of Corti. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 121 EP 129 DI 10.1016/0378-5955(95)00129-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700013 PM 8600116 ER PT J AU BRECHTELSBAUER, PB REN, TY MILLER, JM NUTTALL, AL AF BRECHTELSBAUER, PB REN, TY MILLER, JM NUTTALL, AL TI AUTOREGULATION OF COCHLEAR BLOOD-FLOW IN THE HYDROPIC GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE NITRIC OXIDE; SYMPATHETIC BLOCKADE; ENDOLYMPHATIC HYDROPS; LASER DOPPLER FLOWMETRY ID EXPERIMENTAL ENDOLYMPHATIC HYDROPS; STIMULATION; PRESSURE; GANGLION AB Previous data suggest that regulation of cochlear blood flow (CBF) may be abnormal in the hydropic guinea pig. The purpose of this study was to employ the technique of anterior inferior cerebellar artery (AICA) occlusion to measure CBF autoregulation in experimental endolymphatic hydrops. This study also addresses the role of the cochlear sympathetic neural innervation and nitric oxide in CBF regulation with hydrops. In anesthetized guinea pigs, CBF was measured with a laser Doppler flowmeter probe while the AICA was intermittently occluded with a microvascular occluder. The CBF response was measured in normal, 6-week, and 12-week chronically hydropic animals. The gain factors (0 = no autoregulation, 1 = complete autoregulation) for 1-min occlusion were 0.95 +/- 0.16 (control), 0.77 +/- 0.28 (6 week, P = 0.164), and 0.67 +/- 0.25 (12 week, P = 0.037). N-G-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of nitric oxide synthase, was infused intravenously to assess basal nitric oxide (an endogenous vasodilator) production in the hydropic ear. With infusion of L-NAME, CBF was reduced by 9.16 +/- 11%, 10.7 +/- 10% (P = 0.87), and 16.6 +/- 18% (P = 0.95), in the control, 6-week, and 12-week animals, respectively. In a separate group of 12-week hydropic animals, the left superior cervical ganglion (SCG) was anesthetized with lidocaine, and AICA occlusions were performed pre-and post-blockade. Prior to blocking the SCG, the gain was 0.712 +/- 0.02 and afterwards 0.708 +/- 0.051 (P = 0.93). The above results show that there was a statistically significant reduction in CBF autoregulation in the 12-week hydropic animals. There was no difference in basal nitric oxide production in normal versus hydropic animals nor was there a change in autoregulation following blockade of the SCG. These data provide clear evidence for reduced CBF autoregulation in experimental endolymphatic hydrops. C1 XIAN MED UNIV,DEPT OTOLARYNGOL,XIAN 710061,PEOPLES R CHINA. RP BRECHTELSBAUER, PB (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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Res. PD SEP PY 1995 VL 89 IS 1-2 BP 130 EP 136 DI 10.1016/0378-5955(95)00130-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700014 PM 8600117 ER PT J AU CHEN, KJ WALLER, HJ GODFREY, DA AF CHEN, KJ WALLER, HJ GODFREY, DA TI MUSCARINIC RECEPTOR SUBTYPES IN RAT DORSAL COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE CHOLINERGIC; ACETYLCHOLINE; PIRENZEPINE; TROPICAMIDE; AUDITORY; BRAIN SLICE ID POLYMERASE CHAIN-REACTION; HEXAHYDRO-SILA-DIFENIDOL; MOUSE ISOLATED STOMACH; ACETYLCHOLINE-RECEPTOR; PHARMACOLOGICAL CHARACTERIZATION; BINDING-PROPERTIES; ACID-SECRETION; GUINEA-PIG; CELLS; ANTAGONIST AB We previously reported that responses of spontaneously active rat dorsal cochlear nucleus (DCN) neurons to cholinergic agonists are mediated predominantly by muscarinic receptors. We have now tested the effects of 7 antagonists with differing affinities for the muscarinic receptor subtypes M(1)-M(4) on the responses to constant, submaximal doses of carbachol in rat brainstem slices. Each slice was exposed to one or more concentrations of one antagonist applied during extracellular recording of a DCN neuron. The concentrations yielding 50% reduction of test responses (IC50) of regular and bursting neurons were estimated for each antagonist. Correlation coefficients were calculated between log(IC50) values and log(K-i) values of the drugs for the receptor subtypes. Correlation coefficients for both regular and bursting neurons were not significant (P > 0.05) for M(1) and M(3), but were significant (P < 0.02) for M(4). Bursting but not regular neurons also showed a significant correlation for M(2) (P < 0.05). Our results suggest that (1) M(4) contributes to the cholinergic responses in DCN and M(2) may also contribute to the responses of bursting neurons, but the contribution of other subtypes cannot be completely excluded; (2) muscarinic subtypes in DCN probably differ from those reported for cochlea and some brain regions. C1 MED COLL OHIO,DEPT OTOLARYNGOL,TOLEDO,OH 43699. MED COLL OHIO,DEPT NEUROL SURG,TOLEDO,OH 43699. CR BARLOW RB, 1976, BRIT J PHARMACOL, V58, P613 BERREBI AS, 1991, ANAT EMBRYOL, V183, P427 BONNER TI, 1988, NEURON, V1, P403, DOI 10.1016/0896-6273(88)90190-0 BONNER TI, 1987, SCIENCE, V237, P527, DOI 10.1126/science.3037705 BUCKLEY NJ, 1989, MOL PHARMACOL, V35, P469 BURGARD EC, 1993, NEUROSCIENCE, V54, P377, DOI 10.1016/0306-4522(93)90259-I CAULFIELD MP, 1991, BRIT J PHARMACOL, V104, P39 CHEN K, 1993, ABSTR ASS RES OT, V16, P122 Chen K., 1992, Society for Neuroscience Abstracts, V18, P1036 CHEN K, 1994, ABSTR ASS RES OT, V17, P13 CHEN KJ, 1994, HEARING RES, V77, P168 DOLEZAL V, 1990, J PHARMACOL EXP THER, V252, P739 DORJE F, 1991, J PHARMACOL EXP THER, V256, P727 DRESCHER DG, 1992, J NEUROCHEM, V59, P765, DOI 10.1111/j.1471-4159.1992.tb09436.x DUTAR P, 1988, J NEUROSCI, V8, P4214 EGLEN RM, 1990, BRIT J PHARMACOL, V99, P637 ELTZE M, 1985, EUR J PHARMACOL, V112, P211, DOI 10.1016/0014-2999(85)90498-4 FERNANDO JCR, 1991, EUR J PHARM-MOLEC PH, V207, P297, DOI 10.1016/0922-4106(91)90003-Z GIACHETTI A, 1986, LIFE SCI, V38, P1663, DOI 10.1016/0024-3205(86)90410-8 GODFREY DA, 1993, MAMMALIAN COCHLEAR N, P267 GODFREY DA, 1992, J NEUROSCI METH, V41, P167, DOI 10.1016/0165-0270(92)90058-L GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HAAS HL, 1979, J NEUROSCI METH, V1, P323, DOI 10.1016/0165-0270(79)90021-9 HAMMER R, 1980, NATURE, V283, P90, DOI 10.1038/283090a0 HAMMER R, 1986, LIFE SCI, V38, P1653, DOI 10.1016/0024-3205(86)90409-1 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 HULME EC, 1990, ANNU REV PHARMACOL, V30, P633, DOI 10.1146/annurev.pa.30.040190.003221 KASHIHARA K, 1992, LIFE SCI, V51, P955, DOI 10.1016/0024-3205(92)90403-C KRAUTH J, 1988, DISTRIBUTION FREE ST, V2 KROMER W, 1991, TRENDS PHARMACOL SCI, V12, P11, DOI 10.1016/0165-6147(91)90482-8 KROMER W, 1990, N-S ARCH PHARMACOL, V341, P165 KROMER W, 1991, N-S ARCH PHARMACOL, V343, P7 LAMBRECHT G, 1988, EUR J PHARMACOL, V152, P193, DOI 10.1016/0014-2999(88)90856-4 LAZARENO S, 1990, MOL PHARMACOL, V38, P805 LAZARENO S, 1993, BRIT J PHARMACOL, V109, P1120 LIAO CF, 1989, J BIOL CHEM, V264, P7328 MANIS PB, 1993, MAMMALIAN COCHLEAR N, P361 MCKINNEY M, 1993, J PHARMACOL EXP THER, V264, P74 MEI L, 1991, J PHARMACOL EXP THER, V256, P689 MENG YQ, 1990, MEMBRANE BIOCHEM, V9, P293, DOI 10.3109/09687689009025848 MICHELETTI R, 1990, J PHARMACOL EXP THER, V253, P310 OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 PITLER TA, 1990, BRAIN RES, V534, P257, DOI 10.1016/0006-8993(90)90137-Z RICHARDS MH, 1990, BRIT J PHARMACOL, V99, P753 STOCKTON JM, 1983, MOL PHARMACOL, V23, P551 VETTER DE, 1993, MAMMALIAN COCHLEAR N, P279 VILARO MT, 1991, NEUROSCIENCE, V40, P159, DOI 10.1016/0306-4522(91)90181-M WAELBROECK M, 1990, MOL PHARMACOL, V38, P267 WALLER HJ, 1991, ABSTR ASS RES OT, V14, P142 WALLER HJ, 1994, J NEUROPHYSIOL, V71, P467 WALLER HJ, 1994, ABSTR ASS RES OT, V17, P12 WHITHAM EM, 1991, EUR J PHARM-MOLEC PH, V206, P181, DOI 10.1016/S0922-4106(05)80017-3 WOUTERLOOD FG, 1984, J COMP NEUROL, V227, P136, DOI 10.1002/cne.902270114 ZHANG S, 1994, J NEUROPHYSIOL, V71, P914 ZHANG S, 1993, J NEUROPHYSIOL, V69, P1384 NR 55 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 SEP PY 1995 VL 89 IS 1-2 BP 137 EP 145 DI 10.1016/0378-5955(95)00131-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700015 PM 8600118 ER PT J AU FAY, RR AF FAY, RR TI PERCEPTION OF SPECTRALLY AND TEMPORALLY COMPLEX SOUNDS BY THE GOLDFISH (CARASSIUS-AURATUS) SO HEARING RESEARCH LA English DT Article DE HEARING; FISH; COMPLEX SOUND; PITCH; TIMBRE ID STURNUS-VULGARIS; SONGBIRD; PITCH AB Behavioral studies on complex sound perception in goldfish were carried out in order to help determine what, if any, differences exist between the sense of hearing of fishes and other vertebrates. A stimulus generalization paradigm was used with classical conditioning in three experiments to determine: (1) the perceptual relations between a pure tone and harmonic complexes having a fundamental frequency equal to that of the tone; (2) the combined effects on perception of pulse repetition rate and spectral envelope; and (3) whether goldfish can be shown to identify a complex source when presented simultaneously with another complex source. Experiment 1 showed that the perceptions of tones and harmonic complexes differ profoundly even for the cases in which they have common periodicities and frequency components. Experiment 2 demonstrated that pulse repetition rate and spectral location simultaneously control behavior, and that repetition rate exerts behavioral control independent of spectral location. Experiment 3 indicates that goldfish did not 'hear out' or analyze a complex target source within a mixture of complex sources. In general, goldfish appear to be aware of multiple acoustic dimensions of complex sounds, suggesting both pitch-like and timbre-like perceptual dimensions. These results do not permit a qualitative distinction between the sense of hearing of goldfish and that of other vertebrates. 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 Blackwell HR, 1943, J EXP PSYCHOL, V33, P407, DOI 10.1037/h0057863 BRANTLEY RK, 1994, ETHOLOGY, V96, P213 BULLOCK TH, 1992, EVOLUTIONARY BIOL HE CYNX J, 1993, J COMP PSYCHOL, V107, P140, DOI 10.1037/0735-7036.107.2.140 CYNX J, 1986, J COMP PSYCHOL, V100, P356 DEBOER E, 1976, HDB SENSORY PHYSL, V5, P479 ECHTELER SM, 1985, J COMP PHYSIOL A, V156, P267, DOI 10.1007/BF00610868 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, 1994, HEARING RES, V76, P158, DOI 10.1016/0378-5955(94)90097-3 FAY RR, 1986, J ACOUST SOC AM, V79, P1883, DOI 10.1121/1.393196 GUTTMAN N, 1963, PSYCHOL STUDY SCI, V5 Hartmann W. M., 1988, AUDITORY FUNCTION, P623 HEFFNER H, 1976, J ACOUST SOC AM, V59, P915, DOI 10.1121/1.380951 HONIG WK, 1981, J EXP ANAL BEHAV, V36, P405, DOI 10.1901/jeab.1981.36-405 JENKINS HM, 1960, J EXP PSYCHOL, V59, P246, DOI 10.1037/h0041661 LU Z, 1994, J COMP PHYSL, V123, P33 Malott R. W., 1970, ANIMAL PSYCHOPHYSICS, P363 MCCORMICK CA, 1992, EVOLUTIONARY BIOL HE MOSTOFSKY DI, 1965, STIMULUS GENERALIZAT MYRBERG AA, 1981, HEARING SOUND COMMUN PATTERSO.RD, 1973, J ACOUST SOC AM, V53, P1565, DOI 10.1121/1.1913504 PLOMP R, 1970, FREQUENCY ANAL PERIO Shepard R. N, 1965, STIMULUS GENERALIZAT STOVER LJ, 1983, J ACOUST SOC AM, V73, P1701, DOI 10.1121/1.389393 TERHARDT E, 1974, ACUSTICA, V30, P201 THOMPSON RF, 1962, J COMP PHYSIOL PSYCH, V55, P279, DOI 10.1037/h0047856 YOST WA, 1989, J ACOUST SOC AM, V86, P2138, DOI 10.1121/1.398474 NR 31 TC 23 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1995 VL 89 IS 1-2 BP 146 EP 154 DI 10.1016/0378-5955(95)00132-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700016 PM 8600120 ER PT J AU SADANAGA, M MORIMITSU, T AF SADANAGA, M MORIMITSU, T TI DEVELOPMENT OF ENDOCOCHLEAR POTENTIAL AND ITS NEGATIVE COMPONENT IN MOUSE COCHLEA SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; NEGATIVE ENDOCOCHLEAR POTENTIAL; COCHLEAR DEVELOPMENT; MOUSE; STRIA VASCULARIS ID INNER-EAR; RAT; ANOXIA AB The chronological developmental processes of endocochlear potential (EP) and negative endocochlear potential (-EP) were investigated as a function of age from birth in the basal and second cochlear turns in normal ICR-strain mice. The EP of the basal turn developed between 5 and 17 days after birth (DAB). The -EP of the basal turn attained to its mature level on 11 DAB and it increased its absolute value further between 12 and 16 DAB and then, recovered to its mature level again on 20 DAB. The developmental processes of EP and -EP of the second turn followed similar courses to these of the basal turn although they were several millivolts different on each day in detail. The results suggest that the developmental processes of the + EP and the -EP are different. The time of reaching minimum -EP during anoxia were measured and the rate of EP decline were calculated on each animal. The rate of EP decline increased rapidly on 10 DAB, almost coinciding the day which EP began to increase abruptly. Although the rate of EP decline is influenced by several processes, this result showed one of the possibility that the sensitivity of the stria vascularis to hypoxia may develop parallel to the development of the EP. RP SADANAGA, M (reprint author), MIYAZAKI MED COLL,DEPT OTORHINOLARYNGOL,5200 KIHARA KIYOTAKE,MIYAZAKI 88916,JAPAN. CR Anggard L., 1965, ACTA OTOLARYNGOLOGIC, V203, P1 ANNIKO M, 1988, PROG NEUROBIOL, V30, P209, DOI 10.1016/0301-0082(88)90007-X VONBEKESY G, 1952, J ACOUST SOC AM, V24, P72 BOCK GR, 1983, ACTA OTO-LARYNGOL, V96, P39, DOI 10.3109/00016488309132873 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 DAVIS H, 1957, PHYSIOL REV, V37, P1 FERNANDEZ C, 1974, ACTA OTOLARYNGOL, V60, P207 KONISHI T, 1961, J ACOUST SOC AM, V33, P349, DOI 10.1121/1.1908659 KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 OHMURA M, 1990, EUR ARCH OTO-RHINO-L, V248, P8, DOI 10.1007/BF00634771 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 SCHMIDT RS, 1963, J EXP ZOOL, V153, P227, DOI 10.1002/jez.1401530305 STEEL KP, 1989, DEVELOPMENT, V107, P453 STEEL KP, 1983, BEHAV NEUROSCI, V97, P381, DOI 10.1037//0735-7044.97.3.381 WOOLF NK, 1986, AM J PHYSIOL, V250, pR493 NR 15 TC 40 Z9 40 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1995 VL 89 IS 1-2 BP 155 EP 161 DI 10.1016/0378-5955(95)00133-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700017 PM 8600121 ER PT J AU MCPHERSON, DL STARR, A AF MCPHERSON, DL STARR, A TI AUDITORY TIME-INTENSITY CUES IN THE BINAURAL INTERACTION COMPONENT OF THE AUDITORY-EVOKED POTENTIALS SO HEARING RESEARCH LA English DT Article DE BINAURAL INTERACTION; EVOKED POTENTIAL; BRAIN-STEM AUDITORY EVOKED POTENTIAL; MIDDLE LATENCY AUDITORY EVOKED POTENTIAL; BINAURAL FUSION; LATERALIZATION ID BRAIN-STEM RESPONSES; MIDDLE-LATENCY; CLICK LATERALIZATION; SOUND LATERALIZATION; MULTIPLE-SCLEROSIS; GUINEA-PIG; STIMULI; NEURONS; LESIONS; CAT AB Binaural interaction in the brainstem and middle latency auditory evoked potentials to intensity (dI) and timing differences (dT) between the two ears was studied in 10 normal hearing young adults. A component reflecting binaural interaction in the brainstem potentials occurred at approximately 7 ms and was of largest amplitude when dI and dT were 0. The latency of the binaural interaction component gradually shifted and its amplitude decreased as dI or dT increased and binaural interaction became undetectable when dI = 16 dB or when dT greater than or equal to 1.6 ms. In the middle latency potentials binaural interaction components peaking at 20, 32, and 45 ms were defined that were also largest when dl and dT= 0. The latency of the interaction did not shift with changes in dT and dI whereas the amplitude gradually decreased but binaural interaction components were still evident even at the largest values of dI (30 dB) and dT (3 ms). Psychophysical judgments of binaural perceptions showed binaural fusion of the stimuli to persist with dT values up to 1.6 ms and that lateralization of the intracranial image was complete when either dT = 1.6 ms or when dI = 16 dB. The results suggest that the presence of a binaural interaction component of auditory brainstem potentials correlates with the fusion of binaural click stimuli and the amplitude of the binaural interaction component correlates inversely with the degree of lateralization of the intracranial image. Binaural interaction components of middle latency potentials persist and continue to change even after the binaural stimuli cannot be fused. C1 UNIV CALIF IRVINE,DEPT NEUROL,IRVINE,CA 92717. RP MCPHERSON, DL (reprint author), BRIGHAM YOUNG UNIV,PROGRAM AUDIOL,129 TLRB,PROVO,UT 84602, USA. CR BERLIN CI, 1984, HEARING SCI RECENT A, P461 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 CAIRD D, 1983, EXP BRAIN RES, V52, P385 DIAMOND IT, 1957, J NEUROPHYSIOL, V20, P300 DIAMOND IT, 1962, J NEUROPHYSIOL, V25, P223 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 FULLERTON BC, 1979, SOC NEUR ABSTR, V5, P20 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 GALAMBOS R, 1959, AM J PHYSIOL, V197, P527 GARDI JN, 1981, ARCH OTOLARYNGOL, V197, P164 GAUMOND RP, 1991, J ACOUST SOC AM, V89, P454, DOI 10.1121/1.400482 Hosford HL, 1979, J ACOUST SOC AM, V65, P86 IRVING R, 1967, J COMP NEUROL, V130, P77, DOI 10.1002/cne.901300105 JEFFRESS LA, 1971, J ACOUST SOC AM, V49, P1169, DOI 10.1121/1.1912479 JONES SJ, 1990, ELECTROEN CLIN NEURO, V77, P214, DOI 10.1016/0168-5597(90)90040-K LEVINE RA, 1993, HEARING RES, V68, P73, DOI 10.1016/0378-5955(93)90066-A MCPHERSON DL, 1993, HEARING RES, V66, P91, DOI 10.1016/0378-5955(93)90263-Z MCPHERSON DL, 1989, ELECTROEN CLIN NEURO, V74, P124, DOI 10.1016/0168-5597(89)90017-8 MILLS AW, 1960, J ACOUST SOC AM, V32, P132, DOI 10.1121/1.1907864 MOLLER AR, 1981, ELECTROEN CLIN NEURO, V52, P18, DOI 10.1016/0013-4694(81)90184-X MOUSHEGIAN G, 1975, J NEUROPHYSIOL, V38, P1037 MOUSHEGIAN G, 1972, F MODERN AUDITORY TH OZDAMAR O, 1986, ELECTROEN CLIN NEURO, V63, P476, DOI 10.1016/0013-4694(86)90129-X STARR A, 1976, ELECTROEN CLIN NEURO, V41, P595, DOI 10.1016/0013-4694(76)90005-5 STARR A, 1991, BRAIN, V114, P1157, DOI 10.1093/brain/114.3.1157 VANDERPOEL JC, 1988, BRAIN, V111, P1453, DOI 10.1093/brain/111.6.1453 WADA SI, 1989, ELECTROEN CLIN NEURO, V72, P535, DOI 10.1016/0013-4694(89)90231-9 WERNICK JS, 1968, J NEUROPHYSIOL, V31, P428 WREGE KS, 1981, ARCH NEUROL-CHICAGO, V38, P572 YOST WA, 1981, J ACOUST SOC AM, V70, P397, DOI 10.1121/1.386775 YOST WA, 1985, FUNDAMENTALS HEARING, P156 NR 34 TC 25 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1995 VL 89 IS 1-2 BP 162 EP 171 DI 10.1016/0378-5955(95)00134-1 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700018 PM 8600122 ER PT J AU RIGGS, GH WALSH, EJ SCHWEITZER, L AF RIGGS, GH WALSH, EJ SCHWEITZER, L TI THE DEVELOPMENT OF GLYCINE-LIKE IMMUNOREACTIVITY IN THE DORSAL COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE INHIBITION; GLYCINE; HEARING; COCHLEAR NUCLEUS; DEVELOPMENT; GLUTAMIC ACID DECARBOXYLASE ID AUDITORY BRAIN-STEM; GUINEA-PIG; AUTORADIOGRAPHIC LOCALIZATION; RETROGRADE TRANSPORT; AMINO-ACIDS; HAMSTER; GABA; CAT; RECEPTOR; RESPONSES AB Both anatomical and physiological lines of evidence suggest that inhibitory influences are active early in the development of the dorsal cochlear nucleus (DCN). Data from physiological/pharmacological studies suggest that in the adult these inhibitory influences may be mediated at least in part by the neurotransmitter glycine. Using a polyclonal antibody to examine the development of glycine in the DCN, we have observed that glycine-like immunoreactive cell bodies and punctate label are present in the DCN by the day of birth in the hamster and in the kitten at least 10 days prior to birth. In contrast to the development of immunoreactivity for glutamic acid decarboxylase (GAD) (Schweitzer et al., 1993), glycine-like immunoreactivity shows a homogeneous distribution throughout the DCN from the day of birth through adulthood. In addition, glycine immunoreactivity is present earlier than GAD-immunoreactivity and is present well before these brain structures become responsive to air-borne sounds. Thus, glycine is present in the very young animal and may mediate inhibitory effects that occur early in development. C1 UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. BOYS TOWN NATL RES HOSP,OMAHA,NE 68131. CR ALTSCHULER RA, 1986, BRAIN RES, V369, P316, DOI 10.1016/0006-8993(86)90542-1 ALTSCHULER RA, 1986, AM J OTOLARYNG, V7, P100, DOI 10.1016/S0196-0709(86)80038-2 AOKI C, 1987, J NEUROSCI, V7, P2214 BENSON CG, 1990, J COMP NEUROL, V296, P415, DOI 10.1002/cne.902960307 CASPARY DM, 1979, BRAIN RES, V172, P179, DOI 10.1016/0006-8993(79)90909-0 CHERUBINI E, 1991, TRENDS NEUROSCI, V14, P515, DOI 10.1016/0166-2236(91)90003-D CODE RA, 1989, HEARING RES, V40, P167, DOI 10.1016/0378-5955(89)90109-3 FRIAUF E, 1994, ASS RES OT ABSTR, V10 FROSTHOLM A, 1985, BRAIN RES BULL, V15, P473, DOI 10.1016/0361-9230(85)90038-3 FROSTHOLM A, 1986, BRAIN RES BULL, V16, P189, DOI 10.1016/0361-9230(86)90033-X GLEICH O, 1994, ASS RES OT ABSTR, V10 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 GODFREY DA, 1977, J HISTOCHEM CYTOCHEM, V25, P417 GODFREY DA, 1978, J HISTOCHEM CYTOCHEM, V26, P118 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P549 HYSON RL, 1991, ASS RES OT ABSTR, V14, P141 Kandler K., 1993, Society for Neuroscience Abstracts, V19, P889 KOLSTON J, 1992, ANAT EMBRYOL, V186, P443 MARTIN MR, 1982, NEUROPHARMACOLOGY, V21, P201, DOI 10.1016/0028-3908(82)90188-5 OBATA K, 1978, BRAIN RES, V144, P179, DOI 10.1016/0006-8993(78)90447-X PEYRET D, 1987, ACTA OTO-LARYNGOL, V104, P71, DOI 10.3109/00016488709109049 SAINTMARIE RL, 1991, HEARING RES, V51, P11, DOI 10.1016/0378-5955(91)90003-R Sanes D. H., 1993, Society for Neuroscience Abstracts, V19, P616 SANES DH, 1987, J NEUROSCI, V7, P3793 SCHWARTZ IR, 1981, EXP NEUROL, V73, P601, DOI 10.1016/0014-4886(81)90199-0 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, 1993, HEARING RES, V65, P240, DOI 10.1016/0378-5955(93)90217-O SCHWEITZER L, 1987, NEUROSCIENCE, V23, P1123, DOI 10.1016/0306-4522(87)90186-2 SCHWEITZER L, 1991, DEV BRAIN RES, V59, P39, DOI 10.1016/0165-3806(91)90027-G 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 WALSH EJ, 1987, HEARING RES, V28, P97, DOI 10.1016/0378-5955(87)90157-2 WALSH EJ, 1990, J NEUROPHYSIOL, V64, P961 WENTHOLD RJ, 1987, BRAIN RES, V415, P183, DOI 10.1016/0006-8993(87)90285-X WENTHOLD RJ, 1990, GLYCINE NEUROTRANSMI, P391 WENTHOLD RJ, 1987, NEUROSCIENCE, V22, P897, DOI 10.1016/0306-4522(87)92968-X WENTHOLD RJ, 1988, J COMP NEUROL, V276, P423, DOI 10.1002/cne.902760307 WICKESBERG RE, 1994, J COMP NEUROL, V339, P311, DOI 10.1002/cne.903390302 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 WU SH, 1986, J NEUROSCI, V6, P2691 WU SH, 1987, HEARING RES, V30, P99 NR 42 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 1995 VL 89 IS 1-2 BP 172 EP 180 DI 10.1016/0378-5955(95)00139-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700019 PM 8600123 ER PT J AU RACHEL, JD DZIADZIOLA, JK QUIRK, WS AF RACHEL, JD DZIADZIOLA, JK QUIRK, WS TI ATRIAL-NATRIURETIC-PEPTIDE PARTICIPATES IN THE REGULATION OF VESTIBULAR BLOOD-FLOW SO HEARING RESEARCH LA English DT Article DE VESTIBULAR BLOOD FLOW; ATRIAL NATRIURETIC PEPTIDE ID INNER-EAR; RATS; RESISTANCE AB Atrial natriuretic peptide (ANP) is a cardiac hormone which exerts natriuretic, diuretic and vasorelaxant effects. Among the many organs and vascular beds populated with ANP receptors (Genest and Cantin, 1988) are the vestibular and auditory organs of the inner ear (Lamprecht and Meyer zum Gottesberge, 1988). The purpose of the current study was to assess the potential influence of ANP on vestibular blood flow in the guinea pig. The inner ear was exposed with a posterior-lateral approach medially through the mastoid cortex. The laser Doppler probe was placed adjacent to the ampulla of the posterior semicircular canal. Baseline measurements of mean blood pressure (BP), heart rate (HR) and vestibular blood flow were established. ANP dissolved in physiologic saline was infused intravenously at concentrations of 15, 150 or 300 ng/kg/min at 10 mu l/min for 30 min. Measurements were recorded during the infusion and for a recovery period of 65 min. The control group was treated equivalently and infused with 0.15 M NaCl. Baseline BP and HR for all animals were 40.1 +/- 6.67 and 190 +/- 15.7, respectively. BP, HR and vestibular blood flow remained stable during the baseline, control and recovery conditions of saline infused subjects. Infusion of ANP (15 ng/kg/min) induced a mild elevation of BP followed by a small decrease in pressure during the post-infusion period. Vestibular blood flow showed a decrease to approximately 20% below baseline during infusion and stabilized at this level during the recovery period. Infusion of higher concentrations of ANP (150 and 300 ng/kg/min) induced a similar pattern of BP change in a dose-dependent manner. Vestibular blood flow, however, evidenced significant elevations during the post-infusion periods for both concentrations. These increases (22% and 26%, for 150 and 300 ng/kg/min, respectively) were significantly different from vestibular blood flow changes in the saline and low dose groups. The HR remained stable for baseline, infusion and recovery periods for each of the ANP infused subjects. This investigation demonstrates the systemic and local effects of ANP suggest a possible role for ANP in local regulation of vestibular blood flow. C1 WAYNE STATE UNIV,DEPT OTOLARYNGOL 5E UHC,MICROCIRCULAT LAB,DETROIT,MI 48201. CR ANANDSRIVASTAVA MB, 1986, BIOCHEM BIOPH RES CO, V138, P427, DOI 10.1016/0006-291X(86)90299-8 ANGELBORG C, 1985, J OTOLARYNGOL, V14, P41 BROWN JN, 1994, AM J PHYSIOL, V266, pH458 CHIEN YW, 1987, AM J PHYSIOL, V252, pH894 DEMEY JG, 1987, J PHARMACOL EXP THER, V240, P937 GENEST J, 1988, REV PHYSIOL BIOCH P, V110, P1, DOI 10.1007/BFb0027530 HAMET P, 1984, BIOCHEM BIOPH RES CO, V123, P515, DOI 10.1016/0006-291X(84)90260-2 HARRISONBERNARD LM, 1991, AM J PHYSIOL, V260, pR247 KIMURA RS, 1986, AM J OTOLARYNG, V7, P130, DOI 10.1016/S0196-0709(86)80042-4 KOH GY, 1993, HYPERTENSION, V22, P634 LAMPRECHT J, 1988, ARCH OTO-RHINO-LARYN, V245, P300, DOI 10.1007/BF00464636 LYON MJ, 1993, HEARING RES, V67, P157, DOI 10.1016/0378-5955(93)90243-T MCLAREN GM, 1991, HEARING RES, V55, P1, DOI 10.1016/0378-5955(91)90086-O MCLAREN GM, 1993, HEARING RES, V71, P183, DOI 10.1016/0378-5955(93)90033-W ZUMGOTTESBERGE AMM, 1991, HEARING RES, V56, P86 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 NAKASHIMA T, 1991, ACTA OTO-LARYNGOL, V111, P738, DOI 10.3109/00016489109138406 NEEDLEMAN P, 1986, NEW ENGL J MED, V314, P828 QUIRK WS, 1989, HEARING RES, V41, P53, DOI 10.1016/0378-5955(89)90178-0 QUIRK WS, 1994, AM J OTOL, V15, P56 SHEN YT, 1991, AM J PHYSIOL, V260, pH1893 WANAMAKER HH, 1990, OTOLARYNG HEAD NECK, V103, P586 NR 23 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 SEP PY 1995 VL 89 IS 1-2 BP 181 EP 186 DI 10.1016/0378-5955(95)00135-3 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700020 PM 8600124 ER PT J AU PREYER, S HEMMERT, W ZENNER, HP GUMMER, AW AF PREYER, S HEMMERT, W ZENNER, HP GUMMER, AW TI ABOLITION OF THE RECEPTOR POTENTIAL RESPONSE OF ISOLATED MAMMALIAN OUTER HAIR-CELLS BY HAIR-BUNDLE TREATMENT WITH ELASTASE - A TEST OF THE TIP-LINK HYPOTHESIS SO HEARING RESEARCH LA English DT Article DE MECHANOELECTRICAL TRANSDUCTION; OUTER HAIR CELL; GUINEA PIG; ELASTASE; TIP-LINK ID GUINEA-PIG COCHLEA; TRANSDUCTION CHANNELS; STEREOCILIA; ORGAN; CORTI; ANTIBIOTICS AB To test the hypothesis that the tip-links of hair-cell stereocilia are essential for mechanoelectrical transduction, tip-links of isolated outer hair cells (OHCs) of the guinea-pig cochlea were eliminated with a proteolytic enzyme, elastase, and the influence on the receptor potential measured with the whole-cell patch-clamp technique. Within 45 s of immersion of the hair bundle in 20 IU/ml elastase, the receptor potential in response to direct deflection of the hair bundle was irreversibly abolished. The electrical input impedance of the cell remained unchanged, implying that the channels of the basolateral membrane were not affected by elastase. The effect of elastase on the receptor potential was comparable to changes seen after mechanically induced hair-bundle damage. As a further control, a putative transduction-channel blocker, dihydrostreptomycin (68 mu M), which does not affect tip-links, was applied to the hair bundle. Although the receptor potential was also blocked by dihydrostreptomycin, the effect was reversible. The results suggest that tip-links are required for mechanoelectrical transduction of mammalian OHCs. C1 UNIV TUBINGEN,DEPT OTORHINOLARYNGOL,PHYSIOL ACOUST & COMMUN SECT,D-72076 TUBINGEN,GERMANY. CR ASSAD JA, 1991, NEURON, V7, P985, DOI 10.1016/0896-6273(91)90343-X COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 COREY DP, 1983, J NEUROSCI, V3, P962 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1983, HEARING RES, V12, P89, DOI 10.1016/0378-5955(83)90120-X EVANS BN, 1993, P NATL ACAD SCI USA, V90, P8347, DOI 10.1073/pnas.90.18.8347 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 HUDSPETH AJ, 1994, NEURON, V12, P1, DOI 10.1016/0896-6273(94)90147-3 HUDSPETH AJ, 1979, P NATL ACAD SCI USA, V76, P1506, DOI 10.1073/pnas.76.3.1506 HUDSPETH AJ, 1982, J NEUROSCI, V2, P1 JARAMILLO F, 1991, NEURON, V7, P409, DOI 10.1016/0896-6273(91)90293-9 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 OSBORNE MP, 1988, HEARING RES, V35, P99, DOI 10.1016/0378-5955(88)90044-5 OSBORNE MP, 1990, ACTA OTO-LARYNGOL, V110, P37, DOI 10.3109/00016489009122513 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PREYER S, 1994, HEARING RES, V77, P116, DOI 10.1016/0378-5955(94)90259-3 PREYER WT, 1900, BEOBACHTUNGEN GEISTI, P57 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 TAKUMIDA M, 1993, ORL J OTO-RHINO-LARY, V55, P77 ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 NR 22 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 1995 VL 89 IS 1-2 BP 187 EP 193 DI 10.1016/0378-5955(95)00136-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700021 PM 8600125 ER PT J AU TANYERI, H LOPEZ, I HONRUBIA, V AF TANYERI, H LOPEZ, I HONRUBIA, V TI HISTOLOGICAL EVIDENCE FOR HAIR CELL REGENERATION AFTER OTOTOXIC CELL DESTRUCTION WITH LOCAL APPLICATION OF GENTAMICIN IN THE CHINCHILLA CRISTA-AMPULLARIS SO HEARING RESEARCH LA English DT Article DE HAIR CELL REGENERATION; CRISTA AMPULLARIS; CHINCHILLA; GENTAMICIN OTOTOXICITY; BROMODEOXYURIDINE ID INNER-EAR; VESTIBULAR EPITHELIUM; PROLIFERATION; TOXICITY; GROWTH AB Two experiments were conducted to study the ototoxic effects of local gentamicin (GM) administration and the subsequent hair cell (HC) regeneration process in the chinchilla cristae ampullares (CA). In the first experiment, 3 different doses of GM (0.1, 0.2 and 1.2 mg) were administered by surgical implantation of GM-soaked Gelfoam(R) pledgets in the perilymphatic space in the otic capsule of the left superior semicircular canal. The CA was histologically processed for light-microscopic examination. In the second experiment, 6 groups of 2 chinchillas each were treated with 0.1 mg of GM. To document cell proliferation and HC regeneration, Alzet(R) micro-osmotic pumps were implanted in each chinchilla to deliver bromodeoxyuridine (BrdU) at 125 mu g/h for 1 week. Chinchillas were subsequently killed at 1 and 3 days and 1, 2, 4 and 8 weeks post-treatment (PT). The CA was processed for light microscopy and BrdU immunocytochemistry. In the first experiment the smallest dose produced damage restricted to HCs alone, while the medium and large doses produced severe damage in the sensory epithelium, including supporting cells and HCs. Results in the second experiment demonstrated that at 1 and 4 days PT the HCs showed extensive damage, including clumping of nuclear material. By 4 days PT the supporting cell nuclei lost their monolayer configuration. Calyceal terminals appeared empty, and vacuolized remnants of nerve calyces were evident in the basal portion. At 1 week PT complete disappearance of HCs from the sensory epithelium was evident, and there was cytoplasmic extrusion into the endolymphatic space. At 2 weeks PT there was complete HC loss, the supporting cell nuclei were scattered randomly in the crista, and the nerve fibers were retracted from the sensory epithelium. At 4 weeks PT there was evidence of sensory epithelium repair and HC regeneration. Short cells resembling type-II HCs were evident in the surface of the sensory epithelium. At 8 weeks PT the number of HCs increased in a uniform fashion on the surface of the sensory epithelium, and the supporting cell nuclei were realigned on the basal membrane. Nerve fibers with growth cones penetrated the basal membrane. Supporting cell proliferation was evident by the presence of mitotic figures and BrdU immunoreactivity in the chromatin material of dividing cells at 2 weeks PT. The labeling was more evident in newly formed cells at 4 and 8 weeks PT. These results demonstrate that in chinchillas the vestibular organs have the capacity of self-repair and the process includes HC regeneration after local administration of GM. The overall process involves changes in different cells in the sensory epithelium and neural elements, all of which show modifications with an orderly pattern. C1 UNIV CALIF LOS ANGELES,SCH MED,VICTOR GOODHILL EAR CTR,DIV HEAD & NECK SURG,LOS ANGELES,CA 90024. CR BAIRD RA, 1995, ASS RES OT ABST, V45, P178 BAIRD RA, 1993, HEARING RES, V65, P164, DOI 10.1016/0378-5955(93)90211-I BAIRD RA, 1993, ASS RES OT ABST, V103, P412 BALAK KJ, 1990, J NEUROSCI, V10, P2502 BAREGGI R, 1990, PHARMACOL RES, V22, P635, DOI 10.1016/S1043-6618(05)80056-8 BASERGA R, 1985, BIOL CELL REPRODUCTI CARRANZA A, 1994, 17TH ASS RES OT, V37, P137 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, 1991, CIBA F SYMP, V160, P103 DUCKERT LG, 1993, J COMP NEUROL, V331, P75, DOI 10.1002/cne.903310105 FERNANDEZ C, 1995, J NEUROPHYSIOL, V73, P1253 FORGE A, 1993, SCIENCE, V259, P1616, DOI 10.1126/science.8456284 GOLDBERG JM, 1992, ANN NY ACAD SCI, V656, P92, DOI 10.1111/j.1749-6632.1992.tb25202.x GOLDSTEIN BJ, 1994, ASS RES OT ABST, V131, P524 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V73, P319 KIMURA RS, 1991, ACTA OTO-LARYNGOL, V111, P1021, DOI 10.3109/00016489109138445 KIMURA RS, 1988, ANN OTO RHINOL LARYN, V97, P577 LOPEZ I, 1990, BRAIN RES, V5530, P170 LUNDQUIST PG, 1967, GENTAMICIN, P26 POPPER AN, 1984, HEARING RES, V15, P133, DOI 10.1016/0378-5955(84)90044-3 ROBERSON DF, 1992, HEARING RES, V57, P166, DOI 10.1016/0378-5955(92)90149-H RUBEL EW, 1995, SCIENCE, V267, P701, DOI 10.1126/science.7839150 TANYERI HM, 1994, 17TH ASS RES OT MIDW, P248 TSUE TT, 1994, OTOLARYNG HEAD NECK, V111, P281, DOI 10.1016/S0194-5998(94)70603-4 WARCHOL ME, 1993, SCIENCE, V259, P1619, DOI 10.1126/science.8456285 WEISLEDER P, 1995, HEARING RES, V82, P125 WEISLEDER P, 1993, J COMP NEUROL, V331, P97, DOI 10.1002/cne.903310106 Wersall J., 1981, AMINOGLYCOSIDE OTOTO, P197 NR 30 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 SEP PY 1995 VL 89 IS 1-2 BP 194 EP 202 DI 10.1016/0378-5955(95)00137-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700022 PM 8600126 ER PT J AU PIJL, S SCHWARZ, DWF AF PIJL, S SCHWARZ, DWF TI INTONATION OF MUSICAL INTERVALS BY MUSICAL INTERVALS BY DEAF SUBJECTS STIMULATED WITH SINGLE BIPOLAR COCHLEAR IMPLANT ELECTRODES SO HEARING RESEARCH LA English DT Article DE MUSICAL PITCH; COCHLEAR IMPLANT; TEMPORAL CODE; ADJUSTMENT METHOD ID AUDITORY-NERVE FIBERS; ELECTRICAL-STIMULATION; ABSOLUTE IDENTIFICATION; PITCH; PERCEPTION; PATTERNS; MONKEYS AB Some subjects with cochlear implants have been shown to associate electrical stimulus pulse rates with the pitches of musical tones. In order to clarify the role of these pitch sensations in a musical context, the present investigation examined the intonation accuracy achieved by implant subjects when adjusting pulse rates in the reconstruction of musical intervals. Using a method of adjustment, the subjects altered a variable pulse rate, relative to a fixed reference rate, on one electrode, in the tuning of musical intervals abstracted from familiar melodies. At low pulse rates, subjects generally tuned the intervals to the same frequency ratios which define tonal musical intervals in normal-hearing listeners, with error margins comparable to musically untrained subjects. Two subjects were, in addition, able to transpose these melodic intervals from a standard reference pulse rate to higher and lower reference rates (reference and target pulse rates with geometric means of the intervals ranging from 81 to 466 pulses/s). Generally, the intervals were adjusted on a ratio scale, according to the same frequency ratios which define analogous acoustical musical intervals. These results support the hypothesis that, at low pulse rates, a temporal code in the auditory nerve alone is capable of defining musical pitch. C1 UNIV BRITISH COLUMBIA,CTR ROTARY HEARING,VANCOUVER,BC V6T 2B5,CANADA. RP PIJL, S (reprint author), ST PAULS HOSP,DIV OTOLARYNGOL,2614-1081 BURRARD ST,VANCOUVER,BC V6Z 1Y6,CANADA. CR ATTNEAVE F, 1971, AM J PSYCHOL, V84, P147, DOI 10.2307/1421351 BILGER RC, 1977, ANN OTO RHINOL LARYN, V86, P92 Burns E. M., 1982, PSYCHOL MUSIC, P241 BURNS EM, 1981, J ACOUST SOC AM, V70, P1655, DOI 10.1121/1.387220 BURNS EM, 1978, J ACOUST SOC AM, V63, P456, DOI 10.1121/1.381737 Burns EM, 1983, HEARING PHYSL BASES, P327 BURNS EM, 1976, J ACOUST SOC AM, V60, P863, DOI 10.1121/1.381166 CHOUARD CH, 1978, OTOLARYNG CLIN N AM, V11, P217 DOWLING WJ, 1978, PSYCHOL REV, V85, P341, DOI 10.1037/0033-295X.85.4.341 EDDINGTON D K, 1978, Annals of Otology Rhinology and Laryngology, V87, P5 EDDINGTON DK, 1978, T AM SOC ART INT ORG, V24, P1 ELLIOT J, 1987, PERCEPT PSYCHOPHYS, V42, P594, DOI 10.3758/BF03207991 GFELLER K, 1991, J SPEECH HEAR RES, V34, P916 GREENWOOD D, 1961, J ACOUST SOC AM, V33, P1344, DOI 10.1121/1.1908437 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HARTMANN WM, 1993, J ACOUST SOC AM, V93, P3400, DOI 10.1121/1.405695 HOCHMAIRDESOYER IJ, 1983, ANN NY ACAD SCI, V405, P295, DOI 10.1111/j.1749-6632.1983.tb31642.x HOUTSMA AJM, 1984, MUSIC PERCEPT, V1, P296 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 MOORE BCJ, 1979, J EXP PSYCHOL, V31, P229 NADOL JB, 1991, ANN OTO RHINOL LARYN, V100, P712 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PIJL S, 1995, J ACOUST SOC AM, V98, P886, DOI 10.1121/1.413514 PIJL S, 1992, OTOLARYNG HEAD NECK, V107, P472 PIJL S, 1994, THESIS U BRIT COLUMB ROSE JE, 1967, J NEUROPHYSIOL, V30, P769 SACHS MB, 1983, COCHLEAR PROSTHESES, V405, P510 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 SHANNON RV, 1990, J ACOUST SOC AM, V87, P905, DOI 10.1121/1.398902 SIEGEL JA, 1977, PERCEPT PSYCHOPHYS, V21, P143, DOI 10.3758/BF03198717 Simmons F. B., 1966, ARCH OTOLARYNGOL, V84, P24 SIMMONS FB, 1979, ACTA OTO-LARYNGOL, V87, P170, DOI 10.3109/00016487909126403 SIMMONS FB, 1983, ANN NY ACAD SCI, V405, P259, DOI 10.1111/j.1749-6632.1983.tb31638.x SPILLMANN T, 1982, APPL NEUROPHYSIOL, V45, P32 TEICH MC, 1993, J STAT PHYS, V70, P257, DOI 10.1007/BF01053967 TONG YC, 1985, J ACOUST SOC AM, V77, P1881, DOI 10.1121/1.391939 TOWNSHEND B, 1987, J ACOUST SOC AM, V82, P106, DOI 10.1121/1.395554 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VERNON M, 1967, LARYNGOSCOPE, V77, P1856, DOI 10.1288/00005537-196710000-00008 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 SEP PY 1995 VL 89 IS 1-2 BP 203 EP 211 DI 10.1016/0378-5955(95)00138-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700023 PM 8600127 ER PT J AU LASKY, RE MAIER, MM SNODGRASS, EB LAUGHLIN, NK HECOX, KE AF LASKY, RE MAIER, MM SNODGRASS, EB LAUGHLIN, NK HECOX, KE TI AUDITORY-EVOKED BRAIN-STEM AND MIDDLE LATENCY RESPONSES IN MACACA-MULATTA AND HUMANS SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED BRAIN-STEM RESPONSE; MIDDLE LATENCY RESPONSE; MAXIMUM LENGTH SEQUENCE; MACACA MULATTA; NORMAL-HEARING HUMAN ADULT ID MAXIMUM LENGTH SEQUENCES; STEM RESPONSES; RHESUS-MONKEY; POTENTIALS; NOISE; STIMULATION; GENERATORS; STIMULUS; MASKING; RATES AB Early (ABRs) and middle (MLRs) surface-recorded auditory evoked potentials were compared in eight adult monkeys (Macaca mulatta) and eight adult humans. Responses whose probable generators were the cochlear nucleus and lateral lemniscus were of shorter latency and larger amplitude in monkeys. Relative to humans, ABR response latencies in monkeys were less affected by stimulus intensity, stimulus rate, and masker level. In contrast, monkey amplitudes were relatively more affected by those same stimulus parameters. The most prominent MLR wave was longer in latency and greater in amplitude in humans than the homologous wave in monkeys. The reduction in amplitude of that wave with increasing rate was greater for humans than monkeys. Temporal interactions (the effect of prior stimuli on the response to current stimulation) were investigated from a non-linear systems identification framework using maximum length sequences (MLSs). Both monkey and human auditory systems were second and probably third-order systems at the levels assessed. As the separations between the stimulus pulses decreased, evidence for temporal interactions became more prominent, reached a maximum, and then decreased with further decreases in stimulus pulse separation. At the highest stimulus rates presented, variations in temporal spacing among stimuli had less of an effect on monkey than human evoked responses. C1 UNIV WISCONSIN,HARLOW PRIMATE LAB,MADISON,WI 53715. RP LASKY, RE (reprint author), UNIV WISCONSIN,SCH MED,DEPT NEUROL,H6-573 CLIN SCI BLDG,600 HIGHLAND AVE,MADISON,WI 53792, USA. CR ALLEN AR, 1978, ELECTROEN CLIN NEURO, V45, P53, DOI 10.1016/0013-4694(78)90341-3 AREZZO J, 1975, BRAIN RES, V90, P57, DOI 10.1016/0006-8993(75)90682-4 BURKARD R, 1994, J ACOUST SOC AM, V95, P2126, DOI 10.1121/1.408674 BURKARD R, 1990, J ACOUST SOC AM, V87, P1656, DOI 10.1121/1.399413 BURKARD R, 1994, J ACOUST SOC AM, V95, P2136, DOI 10.1121/1.408675 BURKARD R, 1991, J ACOUST SOC AM, V90, P1398, DOI 10.1121/1.401931 BURKARD R, 1990, J ACOUST SOC AM, V87, P1665, DOI 10.1121/1.399414 BURKARD R, 1993, ASS RES OTOL, P16 CHAN FHY, 1992, MED BIOL ENG COMPUT, V30, P32, DOI 10.1007/BF02446190 DEIBER MP, 1988, ELECTROEN CLIN NEURO, V71, P187, DOI 10.1016/0168-5597(88)90004-4 DON M, 1977, ANN OTO RHINOL LARYN, V86, P186 DOYLE WJ, 1983, ELECTROEN CLIN NEURO, V56, P210, DOI 10.1016/0013-4694(83)90075-5 EGGERMONT JJ, 1993, HEARING RES, V66, P177, DOI 10.1016/0378-5955(93)90139-R EYSHOLDT U, 1982, AUDIOLOGY, V21, P242 FRIA TJ, 1982, OTOLARYNG HEAD NECK, V90, P824 Hall J, 1992, HDB AUDITORY EVOKED HECOX KE, 1989, EAR HEARING, V10, P346, DOI 10.1097/00003446-198912000-00005 JACOBSON G P, 1990, Brain Topography, V2, P229, DOI 10.1007/BF01140591 KRAUS N, 1985, HEARING RES, V17, P219, DOI 10.1016/0378-5955(85)90066-8 LASKKY RE, 1995, IN PRESS NEROTOX TER LASKY RE, 1991, DEV PSYCHOBIOL, V24, P51, DOI 10.1002/dev.420240105 LASKY RE, 1995, UNPUB DISTORTION PRO LASKY RE, 1987, ELECTROEN CLIN NEURO, V68, P45, DOI 10.1016/0168-5597(87)90069-4 LASKY RE, 1982, HEARING RES, V6, P315, DOI 10.1016/0378-5955(82)90063-6 LASKY RE, 1993, J ACOUST SOC AM, V93, P2077, DOI 10.1121/1.406694 LASKY RE, 1995, ABSTR ASS RES OT, V18, P551 Lasky R E, 1992, J Am Acad Audiol, V3, P383 LASKY RE, 1984, ELECTROEN CLIN NEURO, V59, P411, DOI 10.1016/0168-5597(84)90042-X LEE YS, 1984, BRAIN, V107, P115, DOI 10.1093/brain/107.1.115 LINAGRANADE G, 1994, AUDIOLOGY, V33, P218 Marmarelis PZ, 1978, ANAL PHYSL SYSTEMS MARSH RR, 1992, EAR HEARING, V13, P396, DOI 10.1097/00003446-199212000-00004 MOLLER AR, 1986, ELECTROEN CLIN NEURO, V65, P361, DOI 10.1016/0168-5597(86)90015-8 Oppenheim A.V., 1983, SIGNALS SYSTEMS PICTON TW, 1992, ELECTROEN CLIN NEURO, V84, P90, DOI 10.1016/0168-5597(92)90071-I SHERG M, 1986, ELECTROEN CLIN NEURO, V65, P344 SHI Y, 1990, THESIS U WISCONSIN M Shi Y, 1991, IEEE Trans Biomed Eng, V38, P834 Sutter E. E., 1987, ADV METHODS PHYSL SY, P303 THORNTON ARD, 1993, BRIT J AUDIOL, V27, P205, DOI 10.3109/03005369309076694 Volterra V., 1959, THEORY FUNCTIONALS I Weber B A, 1993, J Am Acad Audiol, V4, P157 1985, GUIDE CARE USE LABOR NR 43 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 SEP PY 1995 VL 89 IS 1-2 BP 212 EP 225 DI 10.1016/0378-5955(95)00140-7 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TH367 UT WOS:A1995TH36700024 PM 8600129 ER PT J AU FOWLER, T CANLON, B DOLAN, D MILLER, JM AF FOWLER, T CANLON, B DOLAN, D MILLER, JM TI THE EFFECT OF NOISE TRAUMA FOLLOWING TRAINING EXPOSURES IN THE MOUSE SO HEARING RESEARCH LA English DT Article DE NOISE TRAUMA; AUDITORY BRAIN-STEM RESPONSE; TRAINING; MOUSE ID INDUCED HEARING-LOSS; ACOUSTIC STIMULATION; COCHLEAR DAMAGE; SUSCEPTIBILITY; AGE AB The effect of moderate level acoustic stimulation, or 'training', on a subsequent high intensity noise exposure was studied in CBA/Ca mice. Eight groups of mice were exposed to a variety of training paradigms as well as different intensity traumatic exposures. We sought a combination which would result in the maximum protective effect from acoustic trauma as measured by the auditory brainstem responses. Using a narrow band noise centered at 4.5 kHz, we investigated the effects of a 10-day 'interval' training regimen, allowing a rest period between successive training exposures, as well as several continuous training exposures. These training paradigms were followed by a 24 h traumatic noise exposure (also centered at 4.5 kHz) at one of three intensities, 107, 110, or 117 dB SPL which induce a temporary, a moderate, or a severe permanent threshold shift, respectively. In none of these trained groups was a protective effect demonstrated at any time up to one month following a subsequent traumatic noise exposure. Several groups demonstrated higher compound threshold shifts after the traumatic noise exposure compared to controls. After a recovery period of 4 weeks nearly all trained groups demonstrated a tendency toward higher permanent threshold shifts than the control, untrained, animals. While no protective effect was demonstrated, examination of the threshold shifts following the training periods and after the traumatic noise exposures raised interesting questions for future investigation regarding the inherent resistance to noise induced threshold shifts in the mouse. C1 KAROLINSKA INST,DEPT PHYSIOL & PHARMACOL,S-17177 STOCKHOLM,SWEDEN. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR BORG E, 1982, HEARING RES, V8, P117, DOI 10.1016/0378-5955(82)90070-3 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, 1991, EFFECTS NOISE AUDITO CANLON B, 1983, HEARING RES, V10, P217, DOI 10.1016/0378-5955(83)90055-2 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 Engström B, 1983, Acta Otolaryngol Suppl, V402, P5 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HENRY KR, 1983, AUDIOLOGY, V22, P372 LI HS, 1993, AUDIOLOGY, V32, P195 LI HS, 1991, ACTA OTO-LARYNGOL, V111, P827, DOI 10.3109/00016489109138418 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MIYAKITA T, 1992, HEARING RES, V60, P149, DOI 10.1016/0378-5955(92)90017-H RYAN AF, 1994, HEARING RES, V72, P23, DOI 10.1016/0378-5955(94)90201-1 SAUNDERS JC, 1977, J ACOUST SOC AM, V61 STOPP PE, 1983, HEARING RES, V11, P55, DOI 10.1016/0378-5955(83)90045-X SUBRAMANIAM M, 1991, HEARING RES, V58, P57 SUBRAMANIAM M, 1992, J ACOUST SOC AM, V93 SUBRAMANIAM M, 1992, HEARING RES, V65, P234 YANZ JL, 1982, J ACOUST SOC AM, V72, P1450, DOI 10.1121/1.388678 NR 22 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 AUG PY 1995 VL 88 IS 1-2 BP 1 EP 13 DI 10.1016/0378-5955(95)00062-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300001 PM 8575986 ER PT J AU HUANG, JM BERLIN, CI CULLEN, JK WICKREMASINGHE, AR AF HUANG, JM BERLIN, CI CULLEN, JK WICKREMASINGHE, AR TI DEVELOPMENT OF THE VIIITH-NERVE COMPOUND ACTION-POTENTIAL EVOKED BY LOW-INTENSITY TONE PIPS IN THE MONGOLIAN GERBIL SO HEARING RESEARCH LA English DT Article DE AUDITORY DEVELOPMENT; AUDITORY NERVE COMPOUND ACTION POTENTIAL; GERBIL ID INPUT-OUTPUT FUNCTIONS; POSTNATAL-DEVELOPMENT; FREQUENCY; CAT; SENSITIVITY; LATENCIES; COCHLEA AB Maturation of the cochlea and afferent auditory units is reflected by changes in VIIIth nerve compound action potential (CAP) parameters. We studied auditory nerve CAPs evoked by low-intensity stimuli in Mongolian gerbils (Meriones unguiculatus) ranging in age from 22 to 92 days after birth. The gerbil CAP development is characterized by marked changes in latency, threshold, and amplitude during the first few weeks of life. CAP latency and CAP threshold reach adult-like values at about 1 month of age. In contrast, the CAP amplitude continues to grow in size even after 2 months. This dichotomy suggests that the development of afferent auditory nerve function in the gerbil is preceded by maturation of the mechanical processes of the middle ear and cochlea. C1 LOUISIANA STATE UNIV,DEPT COMMUN SCI & DISORDERS,BATON ROUGE,LA 70803. LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. RP HUANG, JM (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112, USA. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 BERLIN CI, 1990, 13TH MIDW RES M ASS, P220 CHURCH MW, 1984, DEV BRAIN RES, V14, P23, DOI 10.1016/0165-3806(84)90005-1 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FELDMAN DS, 1987, ABCUS CONCEPTS STATV, V2 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N IWASA H, 1982, OTOLARYNG HEAD NECK, V90, P95 NETER J, 1985, APPLIED LINEAR STATI, P346 OZDAMAR O, 1976, J ACOUST SOC AM, V59, P143 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 SCHWEITZER L, 1987, HEARING RES, V25, P249, DOI 10.1016/0378-5955(87)90096-7 SMITH DI, 1987, HEARING RES, V27, P157, DOI 10.1016/0378-5955(87)90016-5 SORANT AJM, 1989, SUBROUTINE PACKAGE F TEAS DC, 1966, J ACOUST SOC AM, V39, P1077, DOI 10.1121/1.1909994 WALSH EJ, 1986, J ACOUST SOC AM, V79, P712, DOI 10.1121/1.393461 WALSH EJ, 1992, HEARING RES, V60, P53, DOI 10.1016/0378-5955(92)90058-U 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 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 22 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1995 VL 88 IS 1-2 BP 14 EP 18 DI 10.1016/0378-5955(95)00094-K PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300002 PM 8575989 ER PT J AU WALTON, JP FRISINA, RD MEIERHANS, LR AF WALTON, JP FRISINA, RD MEIERHANS, LR TI SENSORINEURAL HEARING-LOSS ALTERS RECOVERY FROM SHORT-TERM ADAPTATION IN THE C57BL/6 MOUSE SO HEARING RESEARCH LA English DT Article DE ADAPTATION; HEARING LOSS; TEMPORAL RESOLUTION; MOUSE; ABR ID INFERIOR COLLICULUS NEURONS; AUDITORY-NERVE RESPONSES; COCHLEAR NUCLEUS; IMPAIRED LISTENERS; EVOKED-RESPONSE; CBA/J MICE; MASKING; AGE; CHINCHILLAS; FIBERS AB Several strains of laboratory mouse (Mus musculus) have a pattern of hearing loss which resembles that found in humans. The C57BL/6 strain of mouse has a genetic defect that results in degeneration of the organ of Corti, originating in the basal, high-frequency region and then proceeding apically over time. The end result is a severe-to-profound sensorineural hearing loss (SNHL) by 14 months of age. In contrast, auditory function of the CBA strain remains normal through its early life span then slowly declines later in life, much like that typified by human presbycusis. The purpose of the present study was to compare ABR (peak 5) forward masking recovery functions in young, normal-hearing CBA and C57BL/6 mice to hearing-impaired C57BL/6 mice. ABR audiograms were obtained prior to collecting the tone-on-tone forward masking data. Masking was defined as a 50% reduction in the P5 component of the ABR, elicited and masked by 12 kHz tone bursts, using masker/probe time delays from 0 to 100 ms. Time constants were computed from an exponential model fit to the recovery functions (masker level vs. time delay). In hearing-impaired animals there was a significant increase in recovery from short-term adaptation as measured by the time constants, as well as a significant latency shift in the P5 component. The effects of SNHL on the recovery of the P5 component from short-term adaptation was comparable to that reported behaviorally for human hearing-impaired listeners and physiologically from the inferior colliculus (IC) of chinchillas suffering permanent threshold shifts. C1 UNIV ROCHESTER,SCH MED & DENT,DEPT PHYSIOL,ROCHESTER,NY 14642. RP WALTON, JP (reprint author), UNIV ROCHESTER,SCH MED & DENT,DEPT SURG,DIV OTOLARYNGOL,POB 629,601 ELMWOOD AVE,ROCHESTER,NY 14642, USA. CR ABBAS PJ, 1981, J ACOUST SOC AM, V69, P492, DOI 10.1121/1.385477 AREHOLE S, 1987, HEARING RES, V27, P193, DOI 10.1016/0378-5955(87)90001-3 AREHOLE S, 1989, AUDIOLOGY, V28, P92 BOETTCHER FA, 1990, HEARING RES, V48, P125, DOI 10.1016/0378-5955(90)90203-2 CHIMENTO TC, 1990, J ACOUST SOC AM, V88, P857, DOI 10.1121/1.399735 CUDAHY E, 1982, NEW PERSPECTIVES NOI DANAHER EM, 1978, AUDIOLOGY, V17, P324 ERWAY LC, 1993, HEARING RES, V65, P125, DOI 10.1016/0378-5955(93)90207-H FITZGIBBONS PJ, 1982, J ACOUST SOC AM, V72, P1387 GORGA MP, 1981, J ACOUST SOC AM, V70, P1310, DOI 10.1121/1.387145 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 HENRY KR, 1980, AUDIOLOGY, V19, P369 KALTENBACH JA, 1993, HEARING RES, V67, P35, DOI 10.1016/0378-5955(93)90229-T KAZEE AM, 1995, IN PRESS HEARING RES KIDD G, 1984, J ACOUST SOC AM, V75, P937, DOI 10.1121/1.390558 KRAMER SJ, 1982, J ACOUST SOC AM, V73, P795 LI HS, 1992, ACTA OTO-LARYNGOL, V112, P956, DOI 10.3109/00016489209137496 LUSHER E, 1947, ACTA OTOLARYNGOL, V35, P428 NELSON DA, 1980, S PSYCHOL BEHAVIORAL, P175 NELSON DA, 1987, J ACOUST SOC AM, V81, P709, DOI 10.1121/1.395131 SHANNON RV, 1990, HEARING RES, V47, P159, DOI 10.1016/0378-5955(90)90173-M SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 SNYDER RL, 1985, HEARING RES, V20, P45, DOI 10.1016/0378-5955(85)90058-9 TYLER RS, 1982, J ACOUST SOC AM, V72, P740, DOI 10.1121/1.388254 WALTON JP, 1994, ASS RES OT, V16, P324 WESTERMAN LA, 1984, HEARING RES, V15, P249, DOI 10.1016/0378-5955(84)90032-7 WESTERMAN LA, 1987, J ACOUST SOC AM, V81, P680, DOI 10.1121/1.394836 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., 1983, AUDITORY PSYCHOBIOLO WILLOTT JF, 1994, NEUROBIOL AGING, V15, P175, DOI 10.1016/0197-4580(94)90109-0 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 NR 33 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 AUG PY 1995 VL 88 IS 1-2 BP 19 EP 26 DI 10.1016/0378-5955(95)00093-J PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300003 PM 8575994 ER PT J AU VANEMST, MG KLIS, SFL SMOORENBURG, GF AF VANEMST, MG KLIS, SFL SMOORENBURG, GF TI TETRAETHYLAMMONIUM EFFECTS ON COCHLEAR POTENTIALS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SUMMATING POTENTIAL; TETRAETHYLAMMONIUM; COMPOUND ACTION POTENTIAL; PERILYMPHATIC PERFUSION ID OUTER HAIR-CELLS; RECEPTOR POTENTIALS; MAMMALIAN COCHLEA; INNER; RESPONSES; MEMBRANE; ORGAN; CORTI; SENSITIVITY; CURRENTS AB Voltage-dependent K+ channels in the basolateral membrane of hair cells in guinea-pig cochlea might contribute to the non-linear current-voltage relationships in these hair cells and, thereby, to generation of the extracellular summating potential (SP). To evaluate the role of K+ channels in the generation of the SP the perilymphatic perfusion technique was used to introduce the K+-channel blocker tetraethylammonium (TEA) into the cochlea. Sound-evoked cochlear potentials were measured subsequently. Without blocking nerve activity TEA induced reversible shifts of the SP in the negative direction, irrespective of whether we recorded from scala vestibuli or scala tympani. Shifts in the negative direction were probably due to TEA acting directly on the afferent fibres, since removal of nerve activity by the potent Na+-channel blocker tetrodotoxin (TTX) prevented TEA from shifting the SP in the negative direction. Once nerve activity had been removed by TTX, administration of TEA caused a small decrease in the magnitude of the SP, both in scala vestibuli and in scala tympani, irrespective of its polarity. The decrease was significant for the highest test frequencies only (8-12 kHz), and completely reversible. The rapidly activated K+ channel in the inner hair cell (IHC) is probably blocked by TEA and this blocking might be responsible for the small decrease in magnitude of the SP. The asymmetric contribution from this K+ channel to the IHC's current-voltage relationship seems to be only partly responsible for the generation of the SP, since blocking of this K+ channel with TEA caused relatively small decreases in the amplitude of the SP. TEA did not affect the endocochlear potential. RP VANEMST, MG (reprint author), UNIV UTRECHT, DEPT OTORHINOLARYNGOL, EXPTL AUDIOL LAB, ROOM G02531, HEIDELBERGLAAN 100, 3584 CX UTRECHT, NETHERLANDS. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 27 EP 35 DI 10.1016/0378-5955(95)00095-L PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300004 PM 8576000 ER PT J AU LIN, X HUME, RI NUTTALL, AL AF LIN, X HUME, RI NUTTALL, AL TI DIHYDROPYRIDINES AND VERAPAMIL INHIBIT VOLTAGE-DEPENDENT K+ CURRENT IN ISOLATED OUTER HAIR-CELLS OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; DIHYDROPYRIDINE; VERAPAMIL; VOLTAGE-DEPENDENT K+ CURRENT; GUINEA PIG ID CALCIUM-CHANNEL; MECHANICAL RESPONSES; IONIC CURRENTS; COCHLEA; RECEPTORS; CONDUCTANCE; QUININE; NEURONS AB Dihydropyridines and verapamil are widely used as blockers of voltage-dependent Ca++ channels. In this work we show that these compounds can have a direct blocking action on a class of voltage-activated potassium channels. Voltage-dependent whole-cell currents were recorded from isolated guinea-pig outer hair cells (OHCs) under conditions such that the free Ca++ concentration in both the internal and external solutions was minimized. A substantial Ca++-independent K+ current was revealed by this procedure. Both conventional K+ and Ca++ channel ligands inhibited this current. The order of potency (in terms of the half inhibitory concentrations (IC50) of channel inhibitors) was: nimodipine (6 mu M) > Bay K 8644 (8 mu M) > verapamil (11 mu M)> 4-aminopyridine (22 mu M) > nifedipine (32 mu M) > quinine (49 mu M) > TEA (10236 mu M). Except for verapamil, these channel ligands reduced the size of the K+ currents without much alteration of the time course of the currents. In contrast, verapamil caused a more than 10-fold increase in the apparent inactivation rate of the K+ currents without significantly altering the activation of the currents. The observation that relatively low concentrations of calcium channel ligands can directly inhibit potassium currents in isolated OHCs indicates that caution should be taken when these pharmacological agents are used as tools for studying cochlear hair cell physiology. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT BIOL,ANN ARBOR,MI 48109. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 36 EP 46 DI 10.1016/0378-5955(95)00096-M PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300005 PM 8576001 ER PT J AU LAUTERMANN, J SONG, B MCLAREN, J SCHACHT, J AF LAUTERMANN, J SONG, B MCLAREN, J SCHACHT, J TI DIET IS A RISK FACTOR IN CISPLATIN OTOTOXICITY SO HEARING RESEARCH LA English DT Article DE CISPLATIN; OTOTOXICITY; METABOLISM; GLUTATHIONE ID CANCER-PATIENTS; RENAL-FUNCTION; PLATINUM; NEPHROTOXICITY; METABOLISM AB This study demonstrates that cisplatin ototoxicity depends on dietary factors and correlates with decreased levels of cochlear glutathione and serum albumin. After 12 days of injections, cisplatin (1 mg/kg body weight, s.c.) caused a small hearing loss in guinea pigs fed a regular, full-protein diet (9 +/- 6 dB at 8 kHz and 10 +/- 9 dB at 18 kHz) but a significantly higher hearing loss in animals on a low-protein diet (23 +/- 17 dB at 8 kHz and 32 +/- 23 dB at 18 kHz). Animals on the low-protein diet gained significantly less weight than those on the regular diet, and cisplatin treatment lowered the weight gain in both groups. The low-protein diet also significantly reduced cochlear glutathione levels from 180 +/- 50 to 90 +/- 21 nmol/mg protein and serum albumin from 2.32 +/- 0.04 to 1.75 +/- 0.06 g/dl. Cisplatin treatment tended to decrease glutathione and serum albumin in animals on a full-protein diet but not on the low-protein diet. Renal function was assessed by measuring blood urea nitrogen (BUN) and serum creatinine. While BUN and creatinine values indicated some cisplatin-induced nephrotoxicity, there was no correlation with the severity of ototoxicity. Furthermore, serum platinum levels did not differ between animals on either diet, ruling out a potential influence of altered pharmacokinetics on ototoxicity. These results suggest that the metabolic state of the animal is a risk factor for cisplatin ototoxicity. C1 UNIV MICHIGAN,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 47 EP 53 DI 10.1016/0378-5955(95)00097-N PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300006 PM 8576002 ER PT J AU HELLSTROM, PA AF HELLSTROM, PA TI THE RELATIONSHIP BETWEEN SOUND TRANSFER-FUNCTIONS AND HEARING LEVELS SO HEARING RESEARCH LA English DT Article DE SOUND TRANSFER FUNCTION; NOISE-INDUCED HEARING LOSS; EAR CANAL ACOUSTICS; MINIATURE MICROPHONE ID TEMPORARY THRESHOLD SHIFT; HUMAN EAR; PRESSURE LEVEL; EARDRUM; TRANSFORMATION; FREQUENCY; PATTERNS; FIELD; PLANE; WAVES AB The effects of individual differences in sound transfer function (STF) from free sound field to the tympanic membrane on hearing levels was studied in the right and left ears of 55 young male and 45 young female subjects. Furthermore, canal volumes and lengths have been recorded. STFs were measured in 1/3-octave bands using a miniature microphone and an attached probe. STF measurements were performed in the 0.5-16 kHz frequency range. Audiograms were registered with linear frequency sweep from 0.25 to 8 kHz. Transfer function spectra and magnitudes as well as ear canal dimensions were compared to hearing levels. There was a significant relationship between the dimensions of the ear canal and hearing levels. Large, compared to small, ear canal volumes resulted in a shift of STFs towards lower frequencies. STF spectra and magnitudes had a significant effect on hearing levels. Subject with low-frequency-dominated STFs have higher hearing thresholds than subjects with lower magnitude STFs. RP HELLSTROM, PA (reprint author), LINDHOLMEN DEV HEARING RES LAB,POB 8714,S-40275 GOTHENBURG,SWEDEN. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 54 EP 60 DI 10.1016/0378-5955(95)00102-A PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300007 PM 8576003 ER PT J AU HUANG, JM MONEY, MK BERLIN, CI KEATS, BJB AF HUANG, JM MONEY, MK BERLIN, CI KEATS, BJB TI AUDITORY PHENOTYPING OF HETEROZYGOUS SOUND-RESPONSIVE (+/DN) AND DEAFNESS (DN/DN) MICE SO HEARING RESEARCH LA English DT Article DE AUDITORY PHENOTYPING; AUDITORY BRAIN-STEM RESPONSE; OTOACOUSTIC EMISSION; DEAFNESS MOUSE ID OTOACOUSTIC EMISSIONS; INNER-EAR; DEGENERATION AB Accurate phenotyping of offspring from backcross matings between F-1 heterozygous sound-responsive and deafness mice is an important step for the identification of the deafness (dn) gene (Keats et al., 1995). Here, we report the results of auditory phenotyping of backcross offspring who are either sound-responsive or deaf by recording the Preyer reflex elicited by hand clap, auditory brainstem responses (ABRs), and 2f(1)-f(2) distortion product otoacoustic emissions (DPOEs). Our results show that the Preyer reflex observation alone is inadequate for auditory phenotyping; a more precise test such as a click-evoked ABR recording is needed for auditory phenotyping. DPOE recording results in identification of sound-responsive or deaf mice as accurately as the click-evoked ABR testing. In addition, because the DPOE amplitude function is in good agreement with the ABR threshold in frequency sensitivity and specificity for stimulus frequencies between 1 and 16 kHz, the DPOE recording can be considered as an alternate test for auditory phenotyping. C1 LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. 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PD AUG PY 1995 VL 88 IS 1-2 BP 61 EP 64 DI 10.1016/0378-5955(95)00099-P PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300008 PM 8576004 ER PT J AU OKOYAMA, S MORIIZUMI, T KITAO, Y KAWANO, J KUDO, M AF OKOYAMA, S MORIIZUMI, T KITAO, Y KAWANO, J KUDO, M TI POSTNATAL-DEVELOPMENT OF THE PROJECTION FROM THE MEDIAL SUPERIOR OLIVE TO THE INFERIOR COLLICULUS IN THE RAT SO HEARING RESEARCH LA English DT Article DE AUDITORY PATHWAY; INFERIOR COLLICULUS; MEDIAL SUPERIOR OLIVE; POSTNATAL DEVELOPMENT; AXONAL GROWTH; RAT ID AUDITORY BRAIN-STEM; NORTH-AMERICAN OPOSSUM; CENTRAL NUCLEUS; ASCENDING PROJECTIONS; ORGANIZATION; CONNECTIONS; NEURONS; CAT; MOLE; BAT AB Normal projection development from the medial superior olive (MSG) to the inferior colliculus (IC) was examined by injecting Fluoro-Gold (FG), a retrograde tracer, into the IC unilaterally at postnatal days 0 (P0), P3, P7 and maturity. The rats were killed 1 day after FG injection. At all ages, labeled neurons in the MSO appeared on the ipsilateral side only, as in adult controls. The total number of MSO neurons counted in Nissl-stained sections was constant throughout the postnatal periods. The labeled frequency index of MSO neurons was increased stepwise (from 35% to 90%) with increasing postnatal stages (from PO to adulthood), suggesting differential growth of early- and late-developing axons. C1 KANAZAWA UNIV,SCH MED,DEPT ANAT,KANAZAWA,ISHIKAWA 920,JAPAN. 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R., 1992, MAMMALIAN AUDITORY P, P117 SCHWEIZER H, 1981, J COMP NEUROL, V201, P25, DOI 10.1002/cne.902010104 WILLARD FH, 1984, BRAIN RES, V303, P171, DOI 10.1016/0006-8993(84)90225-7 WILLARD FH, 1983, NEUROSCIENCE, V10, P1203, DOI 10.1016/0306-4522(83)90109-4 WILLARD FH, 1982, AUDITORY PSYCHOBIOLO, P201 ZOOK JM, 1982, J COMP NEUROL, V207, P14, DOI 10.1002/cne.902070103 NR 36 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1995 VL 88 IS 1-2 BP 65 EP 70 DI 10.1016/0378-5955(95)00100-I PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300009 PM 8576005 ER PT J AU OKOYAMA, S MORIIZUMI, T KITAO, Y KAWANO, J KUDO, M AF OKOYAMA, S MORIIZUMI, T KITAO, Y KAWANO, J KUDO, M TI ANATOMICAL PLASTICITY IN THE MEDIAL SUPERIOR OLIVE FOLLOWING ABLATION OF THE INFERIOR COLLICULUS IN NEONATAL AND ADULT-RATS SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; MEDIAL SUPERIOR OLIVE; ABERRANT PROJECTION; RETROGRADE CELL DEGENERATION; PLASTICITY; RAT ID AUDITORY BRAIN-STEM; COCHLEAR NUCLEUS; EARLY LESIONS; PROJECTIONS; NEURONS; MONKEYS; REMOVAL; DEATH AB We evaluated the consequences of unilateral ablation of the inferior colliculus (IC) upon the ascending projection from the medial superior olive (MSG) to the IC. Ablation of the IC was performed in rats aged between postnatal day 1 (P1) and maturity. All the rats were given injections of Fluoro-Gold (FG) into the ipsilateral IC at birth (PO) (before the ipsilateral IC was ablated in any case) so that growth of early-developing axons to the ipsilateral IC could be examined for any labeled neurons in the ipsilateral MSG. Upon reaching adulthood, the rats received injections of Fluoro-Ruby (FR) into the contralateral (intact) IC so that aberrant crossed projections to the intact IC could be examined for any labeled neurons in the ipsilateral MSG. These rats were killed 2 days after FR injections. The number of surviving cells in the ipsilateral MSO were counted in Nissl-stained sections for quantitative analysis of retrograde degeneration. The results show that: (1) the total number of neurons was reduced to 64-34% in the ipsilateral MSO as a result of IC ablation; (2) cell reduction by retrograde degeneration followed a U-shaped curve with a maximal effect in rats operated at P7 (reduced to 34%); (3) adult ablation of the IC led to retrograde degeneration that was less severe than that in late neonatal (P7) ablation; (4) an aberrant projection from the MSO to the contralateral IC occurred in rats operated at P1 and P3 but not in rats operated at P7 or maturity. Thus, our findings suggest that growth of late-developing axons is a major factor in the plasticity of this system of projection. C1 KANAZAWA UNIV,SCH MED,DEPT ANAT,KANAZAWA,ISHIKAWA 920,JAPAN. CR BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 BREGMAN BS, 1983, DEV BRAIN RES, V9, P137, DOI 10.1016/0165-3806(83)90047-0 CAICEDO A, 1993, J COMP NEUROL, V328, P377, DOI 10.1002/cne.903280305 Coleman J.R., 1990, P205 COLEMAN JR, 1979, EXP NEUROL, V64, P553, DOI 10.1016/0014-4886(79)90231-0 Cowan WM, 1970, CONT RES METHODS NEU, P217 CUNNINGHAM TJ, 1982, INT REV CYTOL, V74, P163, DOI 10.1016/S0074-7696(08)61172-9 FOERSTER AP, 1982, J COMP NEUROL, V210, P335, DOI 10.1002/cne.902100403 FRIAUF E, 1990, NEUROSCI LETT, V120, P58, DOI 10.1016/0304-3940(90)90167-8 GLENDENNING KK, 1981, J COMP NEUROL, V197, P673, DOI 10.1002/cne.901970409 GOLDBERGER ME, 1978, ANAT REC, V190, P403 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 ITO M, 1994, ACTA ANAT, V151, P124 KANDLER K, 1993, J COMP NEUROL, V328, P161, DOI 10.1002/cne.903280202 KUDO M, 1988, AUDITORY PATHWAY STR, P171 KUPFER C, 1964, EXP NEUROL, V9, P400, DOI 10.1016/0014-4886(64)90074-3 Kuypers HGJM, 1984, ADV CELL NEUROBIOL, V5, P307 MAXWELL B, 1988, ANAT REC, V220, pA62 Dardennes R, 1984, Brain Res, V318, P159 MERLINE M, 1990, J COMP NEUROL, V296, P506, DOI 10.1002/cne.902960313 MERZENICH MM, 1984, J COMP NEUROL, V224, P591, DOI 10.1002/cne.902240408 MERZENICH MM, 1983, NEUROSCIENCE, V10, P639, DOI 10.1016/0306-4522(83)90208-7 MOORE DR, 1990, J COMP NEUROL, V302, P810, DOI 10.1002/cne.903020412 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 OKOYAMA S, 1995, HEARING RES, V88, P65, DOI 10.1016/0378-5955(95)00100-I Okoyama S., 1994, Society for Neuroscience Abstracts, V20, P1108 PYSH JJ, 1969, AM J ANAT, V124, P411, DOI 10.1002/aja.1001240402 SCHEFFE H, 1953, BIOMETRIKA, V40, P87, DOI 10.1093/biomet/40.1-2.87 SCHMUED LC, 1989, J NEUROCYTOL, V18, P333, DOI 10.1007/BF01190836 SCHNEIDE.GE, 1973, BRAIN BEHAV EVOLUT, V8, P73, DOI 10.1159/000124348 SO KF, 1978, BRAIN RES, V147, P277, DOI 10.1016/0006-8993(78)90840-5 TORVIK A, 1956, J NEUROPATH EXP NEUR, V15, P119, DOI 10.1097/00005072-195604000-00001 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 XU XM, 1989, J COMP NEUROL, V279, P368, DOI 10.1002/cne.902790304 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 AUG PY 1995 VL 88 IS 1-2 BP 71 EP 78 DI 10.1016/0378-5955(95)00101-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300010 PM 8576006 ER PT J AU SALT, AN HENSON, MM GEWALT, SL KEATING, AW DEMOTT, JE HENSON, OW AF SALT, AN HENSON, MM GEWALT, SL KEATING, AW DEMOTT, JE HENSON, OW TI DETECTION AND QUANTIFICATION OF ENDOLYMPHATIC HYDROPS IN THE GUINEA-PIG COCHLEA BY MAGNETIC-RESONANCE MICROSCOPY SO HEARING RESEARCH LA English DT Article DE MAGNETIC RESONANCE; MRI; MR MICROSCOPY; ENDOLYMPH; PERILYMPH; ENDOLYMPHATIC HYDROPS; COCHLEA ID MENIERES-DISEASE; INNER-EAR; 3-DIMENSIONAL RECONSTRUCTION; DUCT AB Three-dimensional magnetic resonance microscopy (MRM) was used to study normal and hydropic cochleae of the guinea pig. With this technique consecutive serial slices representing the entire volume of isolated, fixed cochleae were obtained. The voxels (volume elements) making up the contiguous slices were isotropic (25 mu m(3)) and in each slice the boundaries of scala media, including the position of Reissner's membrane, were clearly delineated. Three-dimensional reconstructions of the endolymphatic and perilymphatic scalae were generated. Custom software was developed to quantify cross-sectional area (CSA) of all scalae. In the normal cochlea all 3 scalae, including scala media, showed a gradual decrease in CSA from base to apex. Marked differences existed between our findings and previously reported cochlear dimensions, especially for the perilymphatic scalae in the basal turn. In hydropic cochleae the scala media was enlarged to a varying extent in different turns and marked changes in the degree of distension of Reissner's membrane occurred along the cochlea. MRM and subsequent computer analysis of the isotropic data provide excellent methods for imaging and quantifying the fluid spaces of normal and hydropic cochleae. C1 UNIV N CAROLINA,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27599. DUKE UNIV,MED CTR,DEPT RADIOL,CTR VIVO MICROSCOPY,DURHAM,NC 27710. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. RP SALT, AN (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,ST LOUIS,MO 63110, USA. CR ANTUNEZ JCM, 1980, ANN OTO RHINOL LARYN, V89, P23 BAGGERSJOBACK D, 1990, ARCH OTOLARYNGOL, V116, P345 BANSON ML, 1992, INVEST RADIOL, V27, P157, DOI 10.1097/00004424-199202000-00013 BROGAN M, 1991, AM J NEURORADIOL, V12, P1 DENK W, 1993, P NATL ACAD SCI USA, V90, P1595, DOI 10.1073/pnas.90.4.1595 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 HEBBAR GK, 1991, ANN OTO RHINOL LARYN, V100, P219 HENSON MM, 1994, HEARING RES, V75, P75, DOI 10.1016/0378-5955(94)90058-2 JOHNSON GA, 1993, MAGN RESON QUART, V9, P1 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 KOIZUKA I, 1991, ORL J OTO-RHINO-LARY, V53, P357 LAU SK, 1993, AM J OTOL, V14, P79 LEUWER R, 1993, LARYNGO RHINO OTOL, V72, P288, DOI 10.1055/s-2007-997902 OKUNO T, 1987, ANN OTO RHINOL LARYN, V96, P438 SALT AN, 1994, HEARING RES, V74, P165, DOI 10.1016/0378-5955(94)90184-8 SALT AN, 1993, ANN OTO RHINOL LARYN, V102, P64 SALT AN, 1988, PHYSL EAR, P341 SHINKAWA H, 1986, ACTA OTO-LARYNGOL, V101, P43, DOI 10.3109/00016488609108606 TANIOKA H, 1992, EUR J RADIOL, V15, P83, DOI 10.1016/0720-048X(92)90211-Q TIEN RD, 1993, MAGN RESON IMAGING, V11, P429, DOI 10.1016/0730-725X(93)90077-Q VOIE AH, 1993, J MICROSC-OXFORD, V170, P229 VOIE AH, 1994, ASS RES OT, V17, P92 ZHOU XH, 1993, JMRI-J MAGN RESON IM, V3, P803, DOI 10.1002/jmri.1880030518 NR 23 TC 34 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1995 VL 88 IS 1-2 BP 79 EP 86 DI 10.1016/0378-5955(95)00103-B PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300011 PM 8576007 ER PT J AU ZHOU, RZ ASSOULINE, JG ABBAS, PJ MESSING, A GANTZ, BJ AF ZHOU, RZ ASSOULINE, JG ABBAS, PJ MESSING, A GANTZ, BJ TI ANATOMICAL AND PHYSIOLOGICAL MEASURES OF AUDITORY-SYSTEM IN MICE WITH PERIPHERAL MYELIN DEFICIENCY SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; TRANSGENIC MOUSE; MYELIN DEFICIENCY; COCHLEA; MYELIN; SCHWANN CELL ID BRAIN-STEM RESPONSE; TREMBLER-J MOUSE; ELECTRICAL-STIMULATION; SPIRAL GANGLION; NERVE SURVIVAL; SCHWANN-CELLS; NEUROPATHY; DEAFNESS; MUTATION AB Animal models with genetic abnormalities have been increasingly used in auditory research. Both Tr(J) mice and P-o-DT-A mice are animals with peripheral myelin deficiency. In Tr(J) mice, the defect is due to a mutated PMP-22 gene. In P-o-DT-A mice, the defect is produced by a transgene using the rat P-o promotor to direct the expression of gene encoding for the bacterial diphtherial toxin A chain (DT-A). This study evaluates the auditory system both physiologically and histologically in these two strains of mice. Histological examination revealed that there was myelin deficiency of the auditory nerve fibers, accompanied by a loss of dendrites and a loss of spiral ganglion cell bodies in both strains of mice. In general, histological deficits in Tr(J) mice were greater than those in P-o-DT-A mice. There was a strong correlation between the degree of myelin deficiency and the survival of spiral ganglion neurons. ABR measurements exhibited differences in threshold, latency and slope of the ABR growth function between myelin-deficient mice and their respective controls. These results suggest that the integrity of the myelin in the auditory nerve is important both for neural survival and for normal electrophysiological function of spiral ganglion neurons. C1 UNIV IOWA,DEPT SPEECH PATHOL & AUDIOL,IOWA CITY,IA 52242. UNIV IOWA,DEPT OTOLARYNGOL HEAD & NECK SURG,IOWA CITY,IA 52242. UNIV WISCONSIN,SCH VET MED,DEPT PATHOBIOL SCI,MADISON,WI. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 87 EP 97 DI 10.1016/0378-5955(95)00104-C PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300012 PM 8576008 ER PT J AU ZHOU, RZ ABBAS, PJ ASSOULINE, JG AF ZHOU, RZ ABBAS, PJ ASSOULINE, JG TI ELECTRICALLY-EVOKED AUDITORY BRAIN-STEM RESPONSE IN PERIPHERALLY MYELIN-DEFICIENT MICE SO HEARING RESEARCH LA English DT Article DE MYELIN DEFICIENCY; ELECTRICALLY EVOKED AUDITORY BRAIN-STEM RESPONSE; ELECTROPHYSIOLOGY; TRANSGENIC MOUSE ID RAT NERVE-FIBERS; STEM RESPONSE; CATS; STIMULATION; CONDUCTION; SURVIVAL; CELLS AB The integrity of the myelin sheath is important for normal electrophysiological function and survival of neurons that make up the auditory nerve. It is hypothesized that myelin deficiency of the auditory nerve may change the electrophysiologic characteristics of the auditory system, especially the temporal properties. In this study, the electrically evoked auditory brainstem response (EABR) was systematically evaluated in Tr(J) and P-o-DT-A mice. Both of these mice have a deficit of their peripheral myelin. Correlation between the EABR and degree of myelin deficiency was also evaluated. The EABR in both strains of poorly myelinated mice exhibited prolonged latency, decreased amplitude, elevated threshold of wave I evoked by short-duration stimuli (20 mu s/phase). A 2-pulse stimulation paradigm was used to evaluate refractory properties. Myelin-deficient mice exhibited slower recovery from the refractory state than controls. Long-duration stimuli (4 ms/phase) were used to assess integration properties. Myelin-deficient mice demonstrated prolonged wave I latency and more gradual latency changes with current level. Myelin thickness showed a strong correlation with EABR threshold for short-duration stimulation (r=-0.784), maximum wave I latency (r=-0.778) and the time constant of the wave I latency-current level function (r=-0.736) for long-duration stimulation and normalized wave I recovery functions (r=-0.718). These findings suggest that EABR measurement may be a promising tool to assess the electrically stimulated properties of auditory neurons, particularly related to the status of myelin sheath. C1 UNIV IOWA,DEPT SPEECH PATHOL & AUDIOL,IOWA CITY,IA 52242. UNIV IOWA,DEPT OTOLARYNGOL HEAD & NECK SURG,IOWA CITY,IA 52242. 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PD AUG PY 1995 VL 88 IS 1-2 BP 98 EP 106 DI 10.1016/0378-5955(95)00105-D PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300013 PM 8576009 ER PT J AU ITO, M SPICER, SS SCHULTE, BA AF ITO, M SPICER, SS SCHULTE, BA TI CYTOLOGICAL CHANGES RELATED TO MATURATION OF THE ORGAN OF CORTI AND OPENING OF CORTIS TUNNEL SO HEARING RESEARCH LA English DT Article DE GERBIL; COCHLEA; SUPPORTING CELL; DEVELOPMENT; MICROTUBULE; TUBULIN; ULTRASTRUCTURE; ORGAN OF CORTI; DEITERS CELL; PILLAR CELL; IMMUNOHISTOCHEMISTRY ID HAIR CELL-DIFFERENTIATION; INNER-EAR; IMMUNOHISTOCHEMICAL LOCALIZATION; MONGOLIAN GERBIL; ENDOPLASMIC-RETICULUM; COCHLEAR INNERVATION; AUDITORY FUNCTION; BASILAR PAPILLA; RAT; CYTOSKELETAL AB Maturation of the organ of Corti in the gerbil was analyzed between 2 and 16 days after birth (DAB) by electron microscopy and immunostaining for beta-tubulin. At 2 DAB, the organ of Corti consisted of stratified epithelium bearing immature sensory hair cells (HCs) and supporting cells. Maturation of OHCs and Deiters cells progressed in a medial-to-lateral direction and cytoskeletal development in inner pillar cells preceded that in outer pillar cells at the single location studied along the frequency-place map. Pillar cell differentiation progressed through a unique stage characterized by the appearance and stratification of structural features apparently concerned with opening of Corti's tunnel and subsequently showed other structural changes related to maturity toward the adult form. Development of the microtubule cytoskeleton occurred first in the cell's apex and proceeded basally. Ruffling of a middle region of the cell surface by microvilli appeared to promote separation between inner and outer pillar cells and initiate tunnel opening at 4 DAB. Proliferation of distended cisternae of granular reticulum evidenced proteinaceous secretion by these cells between 4 and 8 DAB. Subsequent tunnel expansion at about 14 DAB coincided with appearance in outer pillar cells of tubulocistemal endoplasmic reticulum and associated Golgi complexes that are thought to mediate fluid and ion secretion. Sixteen days postnatally after disappearance of granular and tubulocistemal reticula and Gorgi complexes and at the time of clearing of tunnel fluid, lysosomes interpreted as mediating catabolism of endocytosed protein congregated beneath the apical and apicolateral plasmalemmae of inner pillar cells. As with pillar cells, development of the microtubule system in Deiters cells proceeded from the cell's apex to base. Following differentiation of their microtubule system by 8 DAB, Deiters cells showed expansion of Golgi cisternae between 10 and 15 DAB and development of tubulocistemal endoplasmic reticulum at 15 DAB. Hair cells possessed abundant, distinctively large mitochondria from 4 to 10 DAB. The subsurface cisternae matured earlier in medial as opposed to lateral outer hair cells. Vesicles budding from underlying cisternae appeared associated with development of subsurface cisternae and at 16 DAB were still observed in third row but not in more mature first row HCs. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 107 EP 123 DI 10.1016/0378-5955(95)00106-E PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300014 PM 8575987 ER PT J AU TYKOCINSKI, M SHEPHERD, RK CLARK, GM AF TYKOCINSKI, M SHEPHERD, RK CLARK, GM TI REDUCTION IN EXCITABILITY OF THE AUDITORY-NERVE FOLLOWING ELECTRICAL-STIMULATION AT HIGH STIMULUS RATES SO HEARING RESEARCH LA English DT Article DE MULTICHANNEL COCHLEAR IMPLANT; HIGH-RATE ELECTRICAL STIMULATION; AUDITORY NERVE; STIMULATING ELECTRODE; AUDITORY BRAIN-STEM RESPONSE; ELECTRICALLY EVOKED AUDITORY BRAIN-STEM RESPONSE ID BRAIN-STEM RESPONSE; NEURONAL INJURY; EXTRACELLULAR POTASSIUM; COCHLEAR IMPLANT; NEURAL DAMAGE; GUINEA-PIG; CAT; CALCIUM; PATTERNS; FIBERS AB While recent studies have suggested that electrical stimulation of the auditory nerve at high stimulus rates (e.g., 1000 pulses/s) may lead to an improved detection of the fine temporal components in speech among cochlear implant patients, neurophysiological studies have indicated that such stimulation could place metabolic stress on the auditory nerve, which may lead to neural degeneration. To examine this issue we recorded the electrically evoked auditory brainstem response (EABR) of guinea pigs following acute bipolar intracochlear electrical stimulation using charge-balanced biphasic current pulses at stimulus rates varying from 100 to 1000 pulses/s and stimulus intensities ranging from 0.16 to 1.0 mu C/phase. Charge density was held constant (similar to 75 mu C cm(-2) geom/phase) in those experiments. To monitor the recovery in excitability of the auditory nerve following this acute stimulation, EABR thresholds, wave I and III amplitudes and their latencies were determined for periods of up to 12 h following the acute stimulation. Higher stimulus rates and, to a lesser extent, higher intensities led to greater decrements in the post-stimulus EABR amplitude and prolonged the recovery period. While continuous stimulation at 100 pulses/s induced no decrement in the EABR, stimulation at 200 and 400 pulses/s produced an increasingly significant post-stimulus reduction of the EABR amplitude, which showed only partial recovery during the monitoring period. No EABR response could be evoked immediately following stimulation at 1000 pulses/s, using a probe intensity 16-19 dB below the stimulus intensity. However, partial EABR recovery was observed for wave III following stimulation at the lowest stimulus intensity (0.16 mu C/phase). These stimulus-induced reductions in the EABR amplitude were also reflected in increased thresholds and latencies. Providing stimulus rate and intensity were held constant, stimulation at different charge densities (37.7, 75.5 and 150.7 mu C cm(-2) geom/phase) had no influence on the post-stimulus EABR recovery. Significantly, the introduction of a 50% duty cycle into the stimulus pulse train resulted in a more rapid and complete post-stimulus recovery of the EABR compared to continuous stimulation. These data suggest that stimulus rate is a major contributor to the observed reduction in excitability of the electrically stimulated auditory nerve. This reduction may be a result of an activity-induced depletion of neural energy resources required to maintain homeostasis. The present findings have implications for the design of safe speech-processing strategies for use in multichannel cochlear implants. C1 UNIV MELBOURNE,DEPT OTOLARYNGOL,MELBOURNE,VIC 3052,AUSTRALIA. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 124 EP 142 DI 10.1016/0378-5955(95)00108-G PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300015 PM 8575988 ER PT J AU WILLOTT, JF ERWAY, LC ARCHER, JR HARRISON, DE AF WILLOTT, JF ERWAY, LC ARCHER, JR HARRISON, DE TI GENETICS OF AGE-RELATED HEARING-LOSS IN MICE .2. STRAIN DIFFERENCES AND EFFECTS OF CALORIC RESTRICTION ON COCHLEAR PATHOLOGY AND EVOKED-RESPONSE THRESHOLDS SO HEARING RESEARCH LA English DT Article DE GENETICS; INBRED MICE; COCHLEA; PRESBYCUSIS; CALORIC RESTRICTION ID DIETARY RESTRICTION; CBA/J MICE; MOUSE; NUCLEUS; PRESBYACUSIS; MORPHOLOGY; C57BL/6J; NEURONS AB The effects of genotype and diet on age-related hearing loss were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 5 inbred mouse strains, CBA/H-T6J (CH), DBA/2J (D2), C57BL/6J (B6), BALB/cByJ (BY) and WB/ReJ (WE), and their 10 F1 hybrid strains. The mice had been maintained since weaning on either a high-energy (HE) control diet or low-energy (LE) calorically restricted diet. ABR thresholds were obtained when the mice were 23 months old; the mice were allowed to age until they died from natural causes prior to obtaining the histological material. The severity of post-mortem cochlear pathology in mice maintained with the HE diet supports our earlier genetic model which postulated that B6, BY, and WE strains each possessed a different recessive allele causing age-related hearing loss, D2 mice possessed all 3 genes, and CH mice possessed none. The histopathology indicates that the genes act at the cochlear level. Dietary restriction resulted in increased longevity in a number of strains, but age-related changes in cochlear pathology were not ameliorated in any of these; indeed, in some strains long-lived LE mice exhibited severe cochlear degeneration. In strains for which longevity was not extended by caloric restriction, only B6 mice exhibited an ameliorative effect of the LE diet on cochlear pathology. ABRs in 23-month-olds indicated a slowing of age-related hearing loss in LE mice of 3 F1 hybrid strains. C1 UNIV CINCINNATI,DEPT BIOL SCI,CINCINNATI,OH 45221. JACKSON LAB,BAR HARBOR,ME 04609. 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PD AUG PY 1995 VL 88 IS 1-2 BP 143 EP 155 DI 10.1016/0378-5955(95)00107-F PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300016 PM 8575990 ER PT J AU HASHINO, E TINHAN, EK SALVI, RJ AF HASHINO, E TINHAN, EK SALVI, RJ TI BASE-TO-APEX GRADIENT OF CELL-PROLIFERATION IN THE CHICK COCHLEA FOLLOWING KANAMYCIN-INDUCED HAIR CELL LOSS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; REGENERATION; AMINOGLYCOSIDE; BROMODEOXYURIDINE; CHICKEN ID ACOUSTIC TRAUMA; BASILAR PAPILLA; INNER-EAR; REGENERATION; RECOVERY; OTOTOXICITY; GENTAMICIN; DEATH; BUDGERIGAR; BUNDLES AB In order to elucidate the mechanisms that drive cell proliferation in the avian cochlea, we investigated the spatio-temporal relationship between hair cell degeneration and cell proliferation after aminoglycoside ototoxicity. Neonatal chicks were given a daily intramuscular injection of kanamycin (KM) at 400 mg/kg per day for 10 consecutive days. At various times during or after KM administration, proliferating cells were labeled over a period of 2 days with bromodeoxyuridine (BrdU) and visualized with peroxidase immunohistochemistry. Changes in the location of the hair cell lesion during the KM treatment were monitored by phalloidin immunofluorescence or scanning electron microscopy. Hair cell loss began at the base of the cochlea 6 days after the start of KM injections, whereas cell proliferation was first observed in the basal region between days 6 and 8 of the KM treatment. This indicates that the latency between cell loss and cell proliferation is less than 48 h. The region of cell proliferation shifted from the base toward the apex of the cochlea over a period of 6-8 days, but cell proliferation in a specific region of the cochlea only occurred for 2-4 days. The latency as well as the total duration of cell proliferation after KM ototoxicity was virtually equivalent to that observed after acoustic trauma (Hashino and Salvi, 1993), suggesting that similar cellular events are involved in triggering cell proliferation after mechanical destruction and metabolic destruction of avian hair cells. The spatio-temporal gradient of cell proliferation followed the pattern of hair cell loss, suggesting that some aspect of hair cell degeneration provides trigger signals for cell proliferation. C1 SUNY BUFFALO,DEPT ANAT & CELL BIOL,BUFFALO,NY 14214. RP HASHINO, E (reprint author), SUNY BUFFALO,CTR HEARING & DEAFNESS,BUFFALO,NY 14214, USA. 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PD AUG PY 1995 VL 88 IS 1-2 BP 156 EP 168 DI 10.1016/0378-5955(95)00109-H PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300017 PM 8575991 ER PT J AU LENOIR, M RIPOLL, C VAGO, P AF LENOIR, M RIPOLL, C VAGO, P TI STRUCTURAL AND ULTRASTRUCTURAL ASPECTS OF ISOLATED IMMATURE COCHLEAR OUTER HAIR-CELLS MAINTAINED IN SHORT-TERM CULTURE SO HEARING RESEARCH LA English DT Article DE ISOLATED OUTER HAIR CELL; COCHLEA; DEVELOPMENT; TRANSMISSION ELECTRON MICROSCOPY; LASER SCANNING IMAGE CYTOMETRY; RAT ID SCANNING ELECTRON-MICROSCOPY; HORSESHOE BATS ORGAN; GUINEA-PIG COCHLEA; RAT COCHLEA; POSTNATAL-DEVELOPMENT; SUBSURFACE CISTERNAE; MOTILE RESPONSE; SHAPE CHANGES; CORTI; STIMULATION AB Immature outer hair cells (OHCs), isolated from developing rat cochlea without using proteolytic enzymes, were maintained in short-term culture in a clot of coagulated plasma. Cell viability was assessed by a laser scanning image cytometer, using double-fluorescent labeling. Light and transmission electron microscopy was used to study the morphology of isolated cells. Ten to 60 healthy OHCs were obtained from one cochlea, either as single isolated cells or clusters containing 2-10 cells from the same row. Although dead cells were observed only 1 h after dissociation, there were still viable cells after 6 h. Isolated OHCs were not perfectly cylindrical, due to the immaturity of their cortical structures. One hour after dissociation the ultrastructural organization of the isolated cells was generally well preserved, but this was followed by dilatation of the Golgi apparatus and endoplasmic reticulum. Specific changes in isolated OHCs were also observed at the subsurface cistemae and cuticular plate. Although degenerating OHCs generally showed a classic pattern of necrosis, certain morphological features reminiscent of apoptosis were also observed. This study emphasises the difficulty involved in investigating isolated immature OHCs in vitro and provides a basis for future research into the physiological requirements of isolated immature OHCs. C1 UNIV MONTPELLIER 1,CHU HOP,F-34295 MONTPELLIER,FRANCE. RP LENOIR, M (reprint author), INSERM,U254,F-34295 MONTPELLIER,FRANCE. 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Although a distinct correlation between inherited hypothyroidism and hearing loss in humans exists, there has been no previous evaluation of the auditory system in these mutant mice. We determined hearing thresholds by auditory-evoked brainstem response testing and noted a 40-45 dB elevation in the hyt/hyt mouse compared to littermate heterozygote (hyt/+) animals and normal progenitor controls BALB/cByJ (+/+). Conventional light microscopy was used to examine the general anatomy of the cochlea in these animals, and the surface structure of the organ of Corti was further evaluated with scanning electron microscopy. Heterozygote and normal control mice had no significant abnormalities of the cochlea, however the hyt/hyt mice displayed consistent morphologic abnormalities of the stereocilia on both inner and outer hair cell systems. 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Res. PD AUG PY 1995 VL 88 IS 1-2 BP 181 EP 189 DI 10.1016/0378-5955(95)00111-G PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300019 PM 8575993 ER PT J AU HEFFNER, RS HEFFNER, HE KOAY, G AF HEFFNER, RS HEFFNER, HE KOAY, G TI SOUND LOCALIZATION IN CHINCHILLAS .2. FRONT/BACK AND VERTICAL LOCALIZATION SO HEARING RESEARCH LA English DT Article DE PINNA; ELEVATION; MONAURAL CUE; NOISE BAND; ULTRASOUND; EVOLUTION ID SPECTRAL CUES; BINAURAL LOCALIZATION; HEARING CONDITIONS; AUDITORY SPACE; ACUITY; CAT; TOPOGRAPHY; FREQUENCY; PINNA AB The ability of chinchillas to make front/back and vertical locus discriminations was examined behaviorally using a conditioned avoidance procedure. Their minimum audible angle for localizing single broadband noise bursts was 36 degrees for front/back localization and 23 degrees for vertical localization. Sound localization tests using filtered noise demonstrated that the signal must contain high frequencies in order for chinchillas to make front/back and vertical locus judgements and that frequencies in their highest audible octave (i.e., above 16 kHz) contribute to localization. These results support the view that a major selective advantage of high-frequency hearing in mammalian evolution was its utility for monaural as well as binaural sound localization. RP HEFFNER, RS (reprint author), UNIV TOLEDO,DEPT PSYCHOL,TOLEDO,OH 43606, USA. 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E., 1995, METHODS COMP PSYCHOA, P79 HEFFNER RS, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P691 HEFFNER RS, 1988, ARO ABSTR, V11, P233 HEFFNER RS, 1986, BEHAV NEUROSCI, V100, P93, DOI 10.1037/0735-7044.100.1.93 HEFFNER RS, 1995, UNPUB SOUND LOCALIZA, V3 HEFFNER RS, 1988, J COMP PSYCHOL, V102, P66, DOI 10.1037/0735-7036.102.1.66 HEFFNER RS, 1988, HEARING RES, V36, P221, DOI 10.1016/0378-5955(88)90064-0 HEFFNER RS, 1993, ARO ABSTR, V16, P49 HEFFNER RS, 1991, HEARING RES, V52, P13, DOI 10.1016/0378-5955(91)90183-A HEFFNER RS, 1989, ARO ABSTR, V12, P166 HEFFNER RS, 1994, HEARING RES, V80, P247, DOI 10.1016/0378-5955(94)90116-3 IVARSSON C, 1980, HEARING RES, V3, P241, DOI 10.1016/0378-5955(80)90050-7 Knudsen E.I., 1980, P289 KONISHI M, 1993, AM SCI, V61, P414 MARTIN RL, 1987, HEARING RES, V30, P239, DOI 10.1016/0378-5955(87)90140-7 MASTERTO.B, 1969, J ACOUST SOC AM, V45, P966, DOI 10.1121/1.1911574 MOONEY S, 1992, THESIS U TOLEDO TOLE 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 OLDFIELD SR, 1986, PERCEPTION, V15, P67, DOI 10.1068/p150067 OLDFIELD SR, 1984, PERCEPTION, V13, P581, DOI 10.1068/p130581 RICE JJ, 1992, HEARING RES, V58, P132, DOI 10.1016/0378-5955(92)90123-5 SUTHERLAND DP, 1993, ASS RES OTOLARYNGOL, V16, P109 THOMPSON M, 1990, BEHAV RES METH INSTR, V22, P449, DOI 10.3758/BF03203193 NR 38 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1995 VL 88 IS 1-2 BP 190 EP 198 DI 10.1016/0378-5955(95)00112-H PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300020 PM 8575995 ER PT J AU MIZUTA, K IWASA, KH TACHIBANA, M BENOS, DJ LIM, DJ AF MIZUTA, K IWASA, KH TACHIBANA, M BENOS, DJ LIM, DJ TI AMILORIDE-SENSITIVE NA+ CHANNEL-LIKE IMMUNOREACTIVITY IN THE LUMINAL MEMBRANE OF SOME NONSENSORY EPITHELIA OF THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE AMILORIDE-SENSITIVE NA+ CHANNEL; IMMUNOGOLD LABELING; STRIA VASCULARIS; SPIRAL PROMINENCE; AMPULLAR DARK CELL; REISSNERS MEMBRANE ID STRIA VASCULARIS; NONSELECTIVE CATION; APICAL MEMBRANE; SODIUM-CHANNEL; CL CHANNELS; DARK CELLS; K PUMP; LOCALIZATION; MECHANISMS; POTENTIALS AB Some non-sensory epithelia of the inner ear were examined for the localization of immunoreactivity to polyclonal antibodies raised against amiloride-sensitive Na+ channels from the bovine kidney. The pre-embedding immunogold technique was used for this purpose. Labelings were found on the membrane of the endolymphatic surface of strial marginal cells, epithelial cells of spiral prominence and Reissner's membrane, and ampullar dark cells. In contrast, no labeling was found on the luminal membrane of mesothelial cells of Reissner's membrane, the cells lining the supra-strial perilymphatic space, transitional cells and ampullar ceiling cells. Since the antibodies used may also label non-selective cation channels and non-functional sodium channel precursors as suggested by others, it was not possible to determine the labelings are solely due to amiloride-sensitive Na+ channels. However, the observed result was consistent with the previous studies that amiloride blocks ion transport in strial marginal cells and the semicircular canal. It is therefore likely that the observed labeling includes amiloride-sensitive Naf channels. These labeled ion channels in a variety of epithelial cells lining the endolymphatic space could be important in the inner ear fluid regulation. C1 NATL INST DEAFNESS & OTHER COMMUN DISORDERS,CELLULAR BIOL LAB,BETHESDA,MD 20892. NATL INST DEAFNESS & OTHER COMMUN DISORDERS,GENET MOLEC LAB,BETHESDA,MD 20892. UNIV ALABAMA,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. CR BURNHAM JA, 1984, HEARING RES, V13, P261, DOI 10.1016/0378-5955(84)90079-0 DEWEER P, 1988, ANNU REV PHYSIOL, V50, P225, DOI 10.1146/annurev.physiol.50.1.225 FERRARY E, 1989, AM J PHYSIOL, V257, pF182 GARTY H, 1988, PHYSIOL REV, V68, P309 HACKNEY CM, 1991, SCANNING MICROSCOPY, V5, P741 IWASA KH, 1994, NEUROSCI LETT, V172, P163, DOI 10.1016/0304-3940(94)90687-4 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 KOEFOEDJOHNSEN V, 1958, ACTA PHYSIOL SCAND, V42, P298, DOI 10.1111/j.1748-1716.1958.tb01563.x MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 1994, HEARING RES, V73, P101, DOI 10.1016/0378-5955(94)90287-9 MARCUS DC, 1987, HEARING RES, V30, P55, DOI 10.1016/0378-5955(87)90183-3 MARCUS DC, 1994, AM J PHYSIOL, V267, pC857 MARCUS NY, 1987, AM J PHYSIOL, V253, pF613 MCGUIRT JP, 1994, J HISTOCHEM CYTOCHEM, V42, P843 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 MIZUTA K, 1994, ABSTR ASS RES OT, V17, P135 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SARIBANSOHRABY S, 1986, AM J PHYSIOL, V250, pC175 SELLICK P M, 1975, Progress in Neurobiology (Oxford), V5, P337, DOI 10.1016/0301-0082(75)90015-5 SORSCHER EJ, 1988, AM J PHYSIOL, V255, pC835 SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 SZIKLAI I, 1992, LARYNGOSCOPE, V102, P431, DOI 10.1288/00005537-199204000-00011 TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P TOUSSON A, 1989, J CELL SCI, V93, P349 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 NR 29 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 AUG PY 1995 VL 88 IS 1-2 BP 199 EP 205 DI 10.1016/0378-5955(95)00113-I PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300021 PM 8575996 ER PT J AU KOIKE, H NAKAMURA, K NISHIMURA, K KASHIMA, I WIEDERHOLD, ML ASASHIMA, M AF KOIKE, H NAKAMURA, K NISHIMURA, K KASHIMA, I WIEDERHOLD, ML ASASHIMA, M TI NONINVASIVE ASSESSMENT OF OTOLITH FORMATION DURING DEVELOPMENT OF THE JAPANESE RED-BELLIED NEWT, CYNOPS-PYRRHOGASTER SO HEARING RESEARCH LA English DT Article DE OTOLITH; DEVELOPMENT; X-RAY; COMPUTED RADIOGRAPH; PHOTO-STIMULATED LUMINESCENCE LEVEL; CALCIFICATION AB Pre-mated adult female newts and embryos have been flown on the International Microgravity Laboratory-2 (IML-2) Space Shuttle flight in 1994 (Wiederhold et al., 1992b). With the specimens available from this flight, the calcification of otoliths, ulna, radius and backbone of the flown larvae and adult newts were analyzed. The experiments presented here studied the development of the otoliths on the ground. Otoliths of living newts, from embryo to adult, were observed in situ with the application of a new X-ray and bio-imaging analyzer system. For the establishment of this method, newts at different developmental stages were used. An imaging plate temporarily stores the X-ray energy pattern at the bio-imaging analyzer. A latent image on the imaging plate was transformed into a digital time series signal with an image reader. Acquired digital information was computed with the image processor. The processed information was recorded on film with an image recorder, in order to visualize it on an enlargement computed radiograph. To analyze development of the otoliths, photo-stimulated luminescence level was detected by an image analyzer, using transmitted X-ray photons. A single clump of otoconia could first be seen at stage 33. Stage-36 embryos first have distinguishable otoliths, with the utricle in front and saccule behind. Our results show that this X-ray method detects the otoliths equally as well as sectioning. In the newt, the mandibular/maxillary bone formed before the spine. It is suspected that for the newt embryo, living in water, feeding becomes necessary prior to support of the body. C1 UNIV TOKYO,DEPT BIOL,MEGURO KU,TOKYO 153,JAPAN. YOKOHAMA CITY UNIV,DEPT BIOL,KANAZAWA KU,YOKOHAMA,KANAGAWA 236,JAPAN. KANAGAWA DENT COLL,DEPT ORAL & MAXILLOFACIAL RADIOL,YOKOSUKA,KANAGAWA 238,JAPAN. UNIV TEXAS,HLTH SCI CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,SAN ANTONIO,TX 78284. CR AMEMIYA Y, 1987, SCIENCE, V273, P164 AMEMIYA Y, 1988, NATURE, V336, P89, DOI 10.1038/336089a0 BAIRD IL, 1974, BRAIN BEHAV EVOLUT, V10, P11, DOI 10.1159/000124300 CHRISTENSENDALG.D, 1993, J COMP PHYSIOL A, V173, P653 Lim D J, 1973, Ann Otol Rhinol Laryngol, V82, P23 LOWENSTAM HA, 1981, SCIENCE, V211, P1126, DOI 10.1126/science.7008198 MAXWELL SS, 1924, LARYNGOSCOPE, V34, P849 NISHIMURA K, 1993, JPN J AEROSPACE ENV, V30, P1 Okada YK, 1947, JPN J EXP MORPHOL, V3, P1 SHICHIRI T, 1986, J CRYST GROWTH, V78, P491 SHICHIRI T, 1987, KOUBUTUGAKU ZASSHI, V18, P173 Spangenberg D, 1985, Physiologist, V28, pS151 STEYGER PS, 1995, HEARING RES, V84, P61, DOI 10.1016/0378-5955(95)00013-T WIEDERHOLD ML, 1994, ADV SPACE RES, V14, P327, DOI 10.1016/0273-1177(94)90419-7 WIEDERHOLD ML, 1994, ARO MIDW ABST, V17, P38 WIEDERHOLD ML, 1992, 18TH P INT S SPAC TE, V18, P2103 WIEDERHOLD ML, 1995, HEARING RES, V84, P41, DOI 10.1016/0378-5955(95)00012-S WIEDERHOLD ML, 1993, ASGSB B, V7, P64 WIEDERHOLD ML, 1992, 9TH P ISAS SPAC UT S, P127 NR 19 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 AUG PY 1995 VL 88 IS 1-2 BP 206 EP 214 DI 10.1016/0378-5955(95)00114-J PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300022 PM 8575997 ER PT J AU CHEN, C NENOV, A BOBBIN, RP AF CHEN, C NENOV, A BOBBIN, RP TI NOISE EXPOSURE ALTERS THE RESPONSE OF OUTER HAIR-CELLS TO ATP SO HEARING RESEARCH LA English DT Article DE VOLTAGE-CLAMP; PATCH-CLAMP; ATP-GATED CHANNEL; COCHLEA; NOISE EXPOSURE ID GUINEA-PIG COCHLEA; HEARING-LOSS; MAMMALIAN COCHLEA; PERIODIC REST; SUSCEPTIBILITY; RABBIT AB The outer hair cells (OHCs) are one target of noise-induced effects. To date there are few studies which examine changes in the function of OHCs induced by noise exposure. There is increasing evidence that ATP may be a neuromodulator acting on OHCs. Therefore, we examined the possibility that the response to ATP may be altered by low-level noise exposure. ATP was tested on cation currents recorded from outer hair cells (OHCs) isolated from chronic noise-exposed guinea pigs and compared to currents recorded from normal control animals. The whole-cell variant of the patch-clamp technique was used. The incidence of response to 100 mu M ATP was decreased in OHCs from noise-exposed animals as compared to controls when normal internal and external solutions were employed. When K+ was substituted by N-methyl-glucamine (NMG(+)) in the pipette solution, there were significant differences in the magnitudes of ATP-evoked currents between cells from noise-exposed and control animals. This was observed in both normal and 20 mM Ba2+ external solutions. In addition, the response to ATP exhibited a dependency on OHC length. In short OHCs (< 65 mu m) from noise-exposed animals the magnitude of the response to ATP was significantly reduced. By contrast, the response in long OHCs (> 65 mu m) from noise-exposed animals was increased. Results suggest that low-level noise exposure induces changes in OHCs which affect the response of the cell to ATP. C1 LOUISIANA STATE UNIV, MED CTR, DEPT PHYSIOL, NEW ORLEANS, LA 70112 USA. LOUISIANA STATE UNIV, MED CTR, DEPT OTORHINOLARYNGOL & BIOCOMMUN, KRESGE HEARING RES LAB S, NEW ORLEANS, LA 70112 USA. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 AUBERT A, 1994, NEUROSCIENCE, V62, P963, DOI 10.1016/0306-4522(94)90487-1 AUBERT A, 1995, NEUROSCIENCE, V64, P1153, DOI 10.1016/0306-4522(94)00434-7 BERRIDGE MJ, 1994, MOL CELL ENDOCRINOL, V98, P119, DOI 10.1016/0303-7207(94)90129-5 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T BOHNE BA, 1976, ANN OTO RHINOL LARYN, V85, P711 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, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 DECORY L, 1992, NOISE INDUCED HEARIN, P73 EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 EYBALIN M, 1993, PHYSIOL REV, V73, P309 FRANKLIN DJ, 1991, HEARING RES, V53, P185, DOI 10.1016/0378-5955(91)90053-C HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 KUJAWA SG, 1995, HEARING RES, V85, P142, DOI 10.1016/0378-5955(95)00041-2 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 MAYNARD KI, 1992, BRIT J PHARMACOL, V107, P833 MENSH BD, 1993, HEARING RES, V70, P50, DOI 10.1016/0378-5955(93)90051-2 MOCKETT BG, 1994, J NEUROSCI, V14, P6992 MORLEY P, 1994, BRAIN PATHOL, V4, P37 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 NILLES R, 1994, HEARING RES, V73, P27, DOI 10.1016/0378-5955(94)90279-8 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUJOL R, 1992, ADV BIOSCI, V83, P45 RICCI AJ, 1994, COMP BIOCHEM PHYS A, V107, P13, DOI 10.1016/0300-9629(94)90266-6 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 SUBRAMANIAM M, 1994, HEARING RES, V74, P204, DOI 10.1016/0378-5955(94)90188-0 NR 34 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 AUG PY 1995 VL 88 IS 1-2 BP 215 EP 221 DI 10.1016/0378-5955(95)00115-K PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TF523 UT WOS:A1995TF52300023 PM 8575998 ER PT J AU CHEN, C NENOV, A SKELLETT, R FALLON, M BRIGHT, L NORRIS, CH BOBBIN, RP AF CHEN, C NENOV, A SKELLETT, R FALLON, M BRIGHT, L NORRIS, CH BOBBIN, RP TI NITROPRUSSIDE SUPPRESSES COCHLEAR POTENTIALS AND OUTER HAIR CELL RESPONSES SO HEARING RESEARCH LA English DT Article DE NITRIC OXIDE; FERRICYANIDE; FERROCYANIDE; S-NITROSO-N-ACETYLPENICILLAMINE; ELECTROMOTILITY; VOLTAGE-CLAMP ID GUINEA-PIG COCHLEA; NITRIC-OXIDE; ELECTROMOTILITY; MECHANISM; CURRENTS; BLOCKADE; NEURONS AB Biochemical and pharmacological evidence supports a role for nitric oxide (NO) in the cochlea. In the present experiments, we tested sodium nitroprusside (SNP), an NO donor, applied by intracochlear perfusions on sound-evoked responses of the cochlea (CM, cochlear microphonic; SP, summating potential; EP, endocochlear potential; CAP, compound action potential) and in vitro on outer hair cell (OHC) voltage-induced length changes and current responses. In vivo application of SNP in increasing concentrations (10, 33, 100, 330 and 1000 mu M) reduced all sound-evoked responses starting at about 300 mu M. The responses continued to decline after a postdrug wash. At 1 mM SNP decreased EP slowly (approximate to 80 min) whereas at 10 mM it reduced EP more rapidly (approximate to 20 min). Ferricyanide (1 mM) and S-nitroso-N-acetylpenicillamine (SNAP; 1 mM) had no effect on sound-evoked cochlear potentials. Ferricyanide(1 mM and 10 mM) and ferrocyanide (10 mM) had no effect on EP. In vitro, SNP (10 mM) significantly reduced both OHC voltage-induced length changes and whole-cell outward currents. Results suggest that SNP, possibly acting by released NO, influences cochlear function through effects at the stria vascularis and at the OHCs. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA 70112. CR BLATTER LA, 1994, CELL CALCIUM, V15, P122, DOI 10.1016/0143-4160(94)90051-5 BLEDSOE SC, 1981, HEARING RES, V4, P109, DOI 10.1016/0378-5955(81)90040-X BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BOBBIN RP, 1981, PHARM HEARING, P19 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 BRECHTELSBAUER PB, 1993, ASS RES OTOLARYNGOL, V368, pP92 CHEN C, 1994, IN PRESS J PHYSL CHEN C, 1993, EUR J PHARMACOL, V243, P83, DOI 10.1016/0014-2999(93)90171-D EAST SJ, 1991, EUR J PHARMACOL, V209, P119, DOI 10.1016/0014-2999(91)90021-H EROSTEGUI C, 1994, HEARING RES, V74, P135, DOI 10.1016/0378-5955(94)90182-1 FESSENDEN JD, 1994, BRAIN RES, V668, P9, DOI 10.1016/0006-8993(94)90505-3 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 IGNARRO LJ, 1990, HYPERTENSION, V16, P477 KALINEC F, 1993, NEUROSCI LETT, V157, P231, DOI 10.1016/0304-3940(93)90744-6 KIEDROWSKI L, 1992, MOL PHARMACOL, V41, P779 KUJAWA SG, 1994, HEARING RES, V74, P122, DOI 10.1016/0378-5955(94)90181-3 MANZONI O, 1992, NEURON, V8, P653, DOI 10.1016/0896-6273(92)90087-T MONCADA S, 1991, PHARMACOL REV, V43, P109 MURASE K, 1989, NEUROSCI LETT, V103, P56, DOI 10.1016/0304-3940(89)90485-0 OHLSEN A, 1993, ACTA OTO-LARYNGOL, V113, P55, DOI 10.3109/00016489309135767 RICCI AJ, 1994, COMP BIOCHEM PHYS A, V107, P13, DOI 10.1016/0300-9629(94)90266-6 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SCHUMAN EM, 1994, ANNU REV NEUROSCI, V17, P153, DOI 10.1146/annurev.neuro.17.1.153 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 SOUTHAM E, 1991, NEUROSCI LETT, V130, P107, DOI 10.1016/0304-3940(91)90239-P ZDANSKI CJ, 1994, HEARING RES, V79, P39, DOI 10.1016/0378-5955(94)90125-2 NR 28 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 JUL PY 1995 VL 87 IS 1-2 BP 1 EP 8 DI 10.1016/0378-5955(95)00071-B PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600001 PM 8567427 ER PT J AU LEE, KH COTANCHE, DA AF LEE, KH COTANCHE, DA TI DETECTION OF BETA-ACTIN MESSENGER-RNA BY RT-PCR IN NORMAL AND REGENERATING CHICKEN COCHLEAE SO HEARING RESEARCH LA English DT Article DE ACTIN; COCHLEA; REVERSE TRANSCRIPTASE PCR; REGENERATION; HAIR CELL; CHICKEN ID POLYMERASE CHAIN-REACTION; HAIR CELL REGENERATION; BIRD COCHLEA; CUTICULAR PLATE; MESSENGER-RNA; STEREOCILIARY BUNDLES; NOISE DAMAGE; FILAMENTS; CYTOSKELETAL; PROTEIN AB Reverse transcriptase polymerase chain reaction (RT-PCR) was used to show that beta-actin RNA levels can be detected in total RNA isolations from as few as two cochleae. In functionally mature chicken cochleae, a low homeostatic level of beta-actin message should be expressed in order to synthesize enough actin to maintain the stereocilia, cuticular plate, junctional complexes of hair cells and the cytoskeletal components of the supporting cells. The RT-PCR product obtained has been characterized by size, restriction digest analysis, and DNA sequencing analysis. These procedures have confirmed that the product is amplified from a chicken beta-actin mRNA target. Subsequently, semi-quantitative RT-PCR techniques were used to demonstrate an upregulation of beta-actin mRNA transcription levels in the cells of the basilar papilla during regeneration following damage from acoustic overstimulation. These studies suggest that RT-PCR can be utilized for analysis of limited quantities of tissue such as that found in the chicken cochlea and indicate promise for further qualitative and quantitative studies on the molecular mechanisms of hair cell transduction and regeneration. RP LEE, KH (reprint author), BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,80 E CONCORD ST,BOSTON,MA 02118, USA. CR 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 COTANCHE DA, 1991, CIBA F SYMP, V160, P131 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DEROSIER DJ, 1989, J CELL BIOL, V109, P2853, DOI 10.1083/jcb.109.6.2853 DRENCKHAHN D, 1991, J CELL BIOL, V112, P641, DOI 10.1083/jcb.112.4.641 DRESCHER DG, 1993, J NEUROCHEM, V61, P143 DRESCHER DG, 1992, J NEUROCHEM, V59, P765, DOI 10.1111/j.1471-4159.1992.tb09436.x FATH KR, 1990, DEVELOPMENT, V109, P449 FLOCK A, 1977, J CELL BIOL, V75, P39 HIROKAWA N, 1982, J CELL BIOL, V95, P249, DOI 10.1083/jcb.95.1.249 HOUSLEY GD, 1994, HEARING RES, V75, P47, DOI 10.1016/0378-5955(94)90054-X Innis M. A., 1990, PCR PROTOCOLS GUIDE KAWASAKI ES, 1987, P NATL ACAD SCI USA, V85, P5698 KOST TA, 1983, NUCLEIC ACIDS RES, V11, P8287, DOI 10.1093/nar/11.23.8287 LAWRENCE JB, 1986, CELL, V45, P407, DOI 10.1016/0092-8674(86)90326-0 LEE JJ, 1995, ASS RES OTOLARYNGOL, V18, P162 MULLIS K, 1986, COLD SPRING HARB SYM, V51, P263 RAPHAEL Y, 1994, HEARING RES, V76, P173, DOI 10.1016/0378-5955(94)90098-1 RICKLES JO, 1993, HEARING RES, V71, P225 Siebert P.D., 1993, QUANTITATIVE RT PCR SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 STONE JS, 1992, J CELL SCI, V102, P671 SUNDELL CL, 1991, SCIENCE, V253, P1275, DOI 10.1126/science.1891715 SUNDELL CL, 1990, J CELL BIOL, V111, P2397, DOI 10.1083/jcb.111.6.2397 TILNEY LG, 1986, DEV BIOL, V116, P119, DOI 10.1016/0012-1606(86)90048-5 TILNEY LG, 1988, J CELL BIOL, V106, P355, DOI 10.1083/jcb.106.2.355 TILNEY LG, 1983, J CELL BIOL, V96, P822, DOI 10.1083/jcb.96.3.822 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 WEAVER SP, 1993, BRAIN RES BULL, V31, P225, DOI 10.1016/0361-9230(93)90029-B NR 32 TC 14 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 9 EP 15 DI 10.1016/0378-5955(95)00072-C PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600002 PM 8567447 ER PT J AU LAURELL, G TEIXEIRA, M STERKERS, O FERRARY, E AF LAURELL, G TEIXEIRA, M STERKERS, O FERRARY, E TI EFFECT OF CISPLATIN ADMINISTRATION ON THE ELECTROCHEMICAL COMPOSITION OF ENDOLYMPH IN THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE INNER EAR FLUIDS; LD50; ENDOCOCHLEAR POTENTIAL ID HIGH-DOSE CISPLATIN; GUINEA-PIG; STRIA VASCULARIS; MARGINAL CELLS; OTOTOXICITY; PLATINUM; HEARING; CHANNELS; FLUIDS; ENTRY AB The effect of cisplatin on the electrochemical composition of the cochlear endolymph was studied in Long-Evens rats three days after a single intraperitoneal injection (8 mg/kg b.w.). A dose 2/3 of LD50 induced a decrease of the endolymphatic concentration of potassium whereas the endocochlear potential was unaffected. The discrepancy between these two findings indicated that cisplatin did not alter the mechanisms involved in the genesis of the endocochlear potential but modified the passive K transport into endolymph. C1 UNIV PARIS 07,FAC XAVIER BICHAT,DEPT PHYSIOL,INSERM,U251,F-75018 PARIS,FRANCE. CR BARRON SE, 1987, HEARING RES, V26, P131, DOI 10.1016/0378-5955(87)90104-3 BOSHER SK, 1979, J PHYSIOL-LONDON, V293, P329 ESTREM SA, 1981, OTOLARYNG HEAD NECK, V89, P638 FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 JULIEN N, IN PRESS PFLUGERS AR KOCIBA RJ, 1971, CANCER CHEMOTH REP 1, V55, P1 KOMMUNE S, 1981, OTOLARYNGOL HEAD NEC, V89, P275 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 KOPELMAN J, 1988, LARYNGOSCOPE, V98, P858 LAURELL G, 1990, LARYNGOSCOPE, V100, P724 LAURELL G, 1989, HEARING RES, V38, P19, DOI 10.1016/0378-5955(89)90124-X LAURELL G, 1989, HEARING RES, V38, P27, DOI 10.1016/0378-5955(89)90125-1 LAURELL G, 1991, ACTA OTO-LARYNGOL, V111, P891, DOI 10.3109/00016489109138427 LIU DS, 1991, ACTA OTO-LARYNGOL, V111, P298, DOI 10.3109/00016489109137391 MARATSUKA Y, 1989, HEARING RES, V39, P241 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E REDDEL RR, 1982, CANCER TREAT REP, V66, P19 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHWEITZER VG, 1986, OTOLARYNG HEAD NECK, V94, P458 STERKERS O, 1987, AM J PHYSIOL, V253, pF50 STERKERS O, 1984, AM J PHYSIOL, V247, pF602 STERKERS O, 1982, AM J PHYSIOL, V243, pF173 SZIKLAI I, 1992, EUR ARCH OTO-RHINO-L, V249, P149 TAKAHASHI M, 1980, OTOL FUKUOKA, V26, P416 TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P TANGE RA, 1984, ARCH OTO-RHINO-LARYN, V239, P41, DOI 10.1007/BF00454261 NR 26 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 JUL PY 1995 VL 87 IS 1-2 BP 16 EP 20 DI 10.1016/0378-5955(95)00074-E PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600003 PM 8567433 ER PT J AU MOORE, JK PERAZZO, LM BRAUN, A AF MOORE, JK PERAZZO, LM BRAUN, A TI TIME-COURSE OF AXONAL MYELINATION IN THE HUMAN BRAIN-STEM AUDITORY PATHWAY SO HEARING RESEARCH LA English DT Article DE AXONS; COCHLEAR NERVE; AUDITORY PATHWAYS; MYELIN SHEATH; OLIGODENDROGLIA ID STEM POTENTIALS; MATURATION; LATENCY; SOUND; LIFE AB Structures in the human brainstem auditory pathway, from the proximal end of the cochlear nerve to the inferior colliculus, undergo myelination between the 26th and 29th fetal weeks. By the 26th week of gestation, axons in the cochlear nerve and brainstem pathways have acquired linear arrays of oligodendroctyes, and faint myelin sheaths can be distinguished. By the 29th week, definitive myelination is present in all auditory pathways, including the proximal end of the cochlear nerve, trapezoid body, lateral lemniscus, dorsal commissure of the lemniscus, commissure of the inferior colliculus and brachium of the inferior colliculus. Subsequent to the 29th gestational week, density of myelination increases in all pathways until at least 1 year postnatal age. The time of onset of myelination coincides with the onset of acousticomotor reflexes and brainstem auditory evoked responses, processes which depend on rapid, synchronized conduction of auditory impulses in the cochlear nerve and brainstem. The cotemporality in appearance of myelin, reflex responses, and evoked responses supports the idea that the 26th to 28th gestational weeks are a critical period in the onset of human central auditory function. The subsequent increase in myelin density is likely to be a factor in the steady decrease in ABR wave III-V latencies observed during the perinatal period. C1 UNIV CHICAGO,SCH MED,CHICAGO,IL 60637. SUNY STONY BROOK,DEPT PATHOL,STONY BROOK,NY 11794. RP MOORE, JK (reprint author), HOUSE EAR RES INST,DEPT NEUROANAT,2100 W 3RD ST,5TH FLOOR,LOS ANGELES,CA, USA. 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I., 1967, REGIONAL DEV BRAIN E, P3 NR 33 TC 81 Z9 83 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 21 EP 31 DI 10.1016/0378-5955(95)00073-D PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600004 PM 8567438 ER PT J AU SUZUKI, H KATORI, Y IKEDA, K TAKASAKA, T AF SUZUKI, H KATORI, Y IKEDA, K TAKASAKA, T TI CARBOHYDRATE DISTRIBUTION IN THE LIVING UTRICULAR MACULA OF THE GUINEA-PIG DETECTED BY LECTINS SO HEARING RESEARCH LA English DT Article DE UTRICLE; GUINEA PIG; CARBOHYDRATE; LECTIN; CONFOCAL LASER SCANNING MICROSCOPY; SIALIDASE ID VESTIBULAR END ORGANS; INNER-EAR; GELATINOUS MEMBRANES; CELL COAT; COCHLEA; CORTI; LOCALIZATION; STEREOCILIA; TECTORIAL AB Carbohydrate distribution in the fresh utricular macula of the guinea pig was analysed using lectins such as Concanavalin A (ConA), Dolichos biflorus agglutinin (DBA), peanut agglutinin (PNA), soybean agglutinin (SEA), Ulex europeus agglutinin (UEA-I) and wheat germ agglutinin (WGA) by means of confocal laser scanning microscopy. The ciliary bundle was strongly reactive to ConA, PNA, SEA and WGA but not to DBA and UEA-I, showing that the ciliary bundle has abundant D-galactose (Gal), N-acetyl-D-glucosamine (GlcNAc), D-mannose (Man) and sialic acid(s) (Sia) but not detectable amounts of L-fucose (Fuc) and terminal N-acetyl-D-galactosamine (GalNAc). Similar patterns of lectin bindings with moderate-to-weak intensities were observed on the non-cilial apical surface, on the surface of the otoconia and in the gelatinous layer of the otoconial membrane. On the contrary, the globular substance, a precursor of the otoconia, was scarcely reactive to any lectin examined, implying that it lacks glycoconjugates on its surface. Previous histochemical studies reported that the otoconial membrane possesses a much higher affinity for lectins than does the sensory epithelium (including the cilia) in the vestibular organ. This discrepancy suggests that factors in the preparation process may affect the otoconial membrane or the surface coat of the cilia to change their lectin affinity. Meanwhile, sialidase treament augmented the affinity of the ciliary bundle for DBA and PNA, indicating that sialylated GalNAc and Gal are present on the vestibular ciliary bundle. C1 YAMAGATA UNIV,SCH MED,DEPT ANAT,YAMAGATA 99023,JAPAN. RP SUZUKI, H (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,AOBA KU,1-1 SEIRYO MACHI,SENDAI,MIYAGI 980,JAPAN. CR BAIRD RA, 1993, HEARING RES, V65, P151, DOI 10.1016/0378-5955(93)90210-R BAKER DA, 1983, BIOCHEMISTRY-US, V22, P2741, DOI 10.1021/bi00280a023 BELANGER L F, 1956, Ann Otol Rhinol Laryngol, V65, P1060 CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 Endo S, 1991, Acta Otolaryngol Suppl, V481, P116 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 FURNESS DN, 1985, HEARING RES, V18, P177, DOI 10.1016/0378-5955(85)90010-3 GILLOYZAGA P, 1985, HEARING RES, V18, P269, DOI 10.1016/0378-5955(85)90043-7 Harada Y, 1983, Adv Otorhinolaryngol, V30, P258 HARADA Y, 1982, Japanese Journal of Clinical Electron Microscopy, V15, P1 HOZAWA K, 1993, GLYCOBIOLOGY, V3, P47, DOI 10.1093/glycob/3.1.47 HULTCRANTZ M, 1992, EUR ARCH OTO-RHINO-L, V249, P134 IKEDA K, 1993, HEARING RES, V66, P169, DOI 10.1016/0378-5955(93)90138-Q KAHN KM, 1990, J HISTOCHEM CYTOCHEM, V38, P1615 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LOTAN R, 1975, J BIOL CHEM, V250, P8518 Luftig R B, 1981, Int Rev Cytol Suppl, V12, P309 MANCINI P, 1993, HEARING RES, V64, P151, DOI 10.1016/0378-5955(93)90001-H MUNYER PD, 1991, HEARING RES, V52, P369, DOI 10.1016/0378-5955(91)90026-6 OSBORNE MP, 1984, CELL TISSUE RES, V237, P43 POTE KG, 1986, J ULTRA MOL STRUCT R, V95, P61, DOI 10.1016/0889-1605(86)90029-7 POTE KG, 1993, BIOCHEMISTRY-US, V32, P5017, DOI 10.1021/bi00070a007 PRIETO JJ, 1986, HEARING RES, V24, P237, DOI 10.1016/0378-5955(86)90022-5 ROSS MD, 1985, AUDITORY BIOCH, P500 ROSS MD, 1981, ANN NY ACAD SCI, V374, P808, DOI 10.1111/j.1749-6632.1981.tb30921.x ROSS MD, 1987, ACTA OTO-LARYNGOL, V103, P56, DOI 10.3109/00016488709134698 SLEPECKY N, 1985, HEARING RES, V17, P281, DOI 10.1016/0378-5955(85)90072-3 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 TAKEMURA T, 1994, HEARING RES, V79, P99, DOI 10.1016/0378-5955(94)90131-7 TAKUMIDA M, 1989, ORL J OTO-RHINO-LARY, V51, P144 TAKUMIDA M, 1988, ACTA OTO-LARYNGOL, V106, P130, DOI 10.3109/00016488809107380 TAKUMIDA M, 1993, OTOL JPN, V3, P822 TAKUMIDA M, 1989, J LARYNGOL OTOL, V103, P357, DOI 10.1017/S0022215100108953 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 JUL PY 1995 VL 87 IS 1-2 BP 32 EP 40 DI 10.1016/0378-5955(95)00075-F PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600005 PM 8567440 ER PT J AU SKELLETT, RA CRIST, JR FALLON, M BOBBIN, RP AF SKELLETT, RA CRIST, JR FALLON, M BOBBIN, RP TI CAFFEINE-INDUCED SHORTENING OF ISOLATED OUTER HAIR-CELLS - AN OSMOTIC MECHANISM OF ACTION SO HEARING RESEARCH LA English DT Article DE HAIR CELL, OUTER; CAFFEINE; OSMOLARITY; RYANODINE RECEPTOR ID ISOLATED SARCOPLASMIC-RETICULUM; CA-2+-INDUCED CA-2+ RELEASE; SMOOTH-MUSCLE CELLS; INTRACELLULAR CALCIUM; VOLUME REGULATION; GUINEA-PIG; CHANNEL; INVOLVEMENT; MOTILITY; CURRENTS AB The application of caffeine to the bathing medium of isolated cochlear outer hair cells (OHCs) induces shortening of the cells (Slepecky et al., 1988). This study was designed to test the hypothesis that a 'smooth muscle-like' mechanism was responsible for the caffeine-induced shortening of OHCs as suggested by Slepecky et al. OHCs were isolated from guinea pig cochleae and length measurements were taken during various drug perfusions. Antagonists of the ryanodine receptor/Ca2+-induced Ca2+ release (CICR; tetracaine, ruthenium red, and ryanodine) failed to block the caffeine-induced shortening of the OHCs. Application of the Ca2+ ionophore A23187 caused cell length to increase. These results did not support this hypothesis and therefore, an osmotic mechanism was proposed. 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 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L CECOLA RP, 1992, HEARING RES, V61, P65, DOI 10.1016/0378-5955(92)90037-N CRIST JR, 1993, HEARING RES, V69, P194, DOI 10.1016/0378-5955(93)90107-C 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 EHRLICH BE, 1994, TRENDS PHARMACOL SCI, V15, P145, DOI 10.1016/0165-6147(94)90074-4 ENDO M, 1977, EXCITATION CONTRACT FEINSTEI.MB, 1969, FED PROC, V28, P1643 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 Harada N, 1993, Acta Otolaryngol Suppl, V500, P39 HAZAMA A, 1990, BIOCHEM BIOPH RES CO, V167, P287, DOI 10.1016/0006-291X(90)91763-I HERRMANNFRANK A, 1991, PFLUG ARCH EUR J PHY, V418, P353, DOI 10.1007/BF00550873 LUFT JH, 1971, ANAT REC, V171, P369, DOI 10.1002/ar.1091710303 MEISSNER G, 1986, J BIOL CHEM, V261, P6300 OHNISHI ST, 1979, J BIOCHEM-TOKYO, V86, P1147 OHTA T, 1993, J PHYSIOL-LONDON, V465, P149 PALADE P, 1987, J BIOL CHEM, V262, P6142 PALADE P, 1987, J BIOL CHEM, V262, P6135 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SOMLYO AP, 1989, FASEB J, V3, P2266 TUNSTALL J, 1994, EXP PHYSIOL, V79, P435 WONG SME, 1986, AM J PHYSIOL, V250, pC841 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZHOLOS AV, 1991, J PHYSIOL-LONDON, V443, P555 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 JUL PY 1995 VL 87 IS 1-2 BP 41 EP 48 DI 10.1016/0378-5955(95)00076-G PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600006 PM 8567441 ER PT J AU BOBBIN, RP FALLON, M LEBLANC, C BABER, A AF BOBBIN, RP FALLON, M LEBLANC, C BABER, A TI EVIDENCE THAT GLUTATHIONE IS THE UNIDENTIFIED AMINE (UNK-2.5) RELEASED BY HIGH POTASSIUM INTO COCHLEAR FLUIDS SO HEARING RESEARCH LA English DT Article DE RELEASE; HPLC; AMINE; DEPOLARIZATION; HAIR CELL ID GUINEA-PIG COCHLEA; XENOPUS-LAEVIS; LATERAL-LINE; SUBSTANCES; GLUTAMATE; PERILYMPH; ACIDS; GABA AB An unidentified substance, Unk 2.5, may be important in the function of the cochlea. The efflux of Unk 2.5 into cochlear fluids is increased by intense sound (Bobbin and Fallen, 1992) and by exposure of the cochlear tissue to high concentrations of K+ (Bobbin et al., 1990,1991; Bobbin and Fallen, 1992). The unidentified chemical eluted at 2.5 min in chromatograms obtained by HPLC utilizing fluorescence detection and precolumn o-phthalaldehyde (OPA) derivatization of samples of effluent from the cochlea (e.g., Bobbin et al., 1990). The purpose of this investigation was to provide evidence as to the identity of this unidentified chemical we call Unk 2.5. Therefore, we carried out additional HPLC assays on samples obtained during perfusion of the cochlear perilymph compartment. Glutathione (GSH) was found to elute at the same time (@ 2.5 min) as Unk 2.5 in HPLC chromatograms utilizing precolumn derivatization with OPA and mercaptoethanol. In addition, both Unk 2.5 and GSH reacted with OPA without mercaptoethanol present in the reaction mixture to give a peak at 2.5 min in the chromatogram, but failed to show this peak if stored in solutions with a pH > 7 for several days before the reaction. Results indicate that Unk 2.5 is GSH or a closely related compound. Given this probable identification GSH, aka Unk 2.5, has been demonstrated to be released from tissue in the cochlea by high concentrations of K+ (Bobbin et al., 1990,1991) and by intense sound (124 dB SPL; Bobbin and Fallen, 1992). RP BOBBIN, RP (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112, USA. CR ANDERSON ME, 1985, METHOD ENZYMOL, V113, P548 ARIAS IM, 1976, GLUTATHIONE METABOLI, P382 BARBARY AE, 1993, HEARING RES, V71, P80, DOI 10.1016/0378-5955(93)90023-T Benet LZ, 1990, GOODMAN GILMANS PHAR, P1 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BLEDSOE SC, 1988, EXP BRAIN RES, 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, HEARING RES, V63, P157, DOI 10.1016/0378-5955(92)90082-X DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x EYBALIN M, 1993, PHYSIOL REV, V73, P309 GARETZ SL, 1994, HEARING RES, V77, P75, DOI 10.1016/0378-5955(94)90254-2 GARETZ SL, 1994, HEARING RES, V77, P81, DOI 10.1016/0378-5955(94)90255-0 HOFFMAN DW, 1987, HEARING RES, V31, P217, DOI 10.1016/0378-5955(87)90190-0 HOFFMAN DW, 1988, ANN OTO RHINOL LARYN, V97, P36 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x MEHLER AH, 1992, TXB BIOCH CLIN CORRE, P491 NEUSCHWANDERTETRI, 1989, ANAL BIOCHEM, V179, P236 SEWELL WF, 1978, SCIENCE, V202, P910, DOI 10.1126/science.30998 Sies H., 1988, GLUTATHIONE CONJUGAT ZANGERLE L, 1992, J NEUROCHEM, V59, P181, DOI 10.1111/j.1471-4159.1992.tb08889.x NR 23 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 49 EP 54 DI 10.1016/0378-5955(95)00077-H PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600007 PM 8567442 ER PT J AU LINAGRANADE, G COLLET, L AF LINAGRANADE, G COLLET, L TI EFFECT OF INTERSTIMULUS-INTERVAL ON EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; OUTER HAIR CELL; COCHLEA; STIMULUS RATE; ADAPTATION ID STIMULATED ACOUSTIC EMISSIONS; HAIR-CELLS; ADAPTATION; COCHLEAR; POTENTIALS; RESPONSES; SYSTEM; HUMANS AB In order to explore extensively the effect of interstimulus interval, including very short interstimulus intervals, on evoked otoacoustic emissions (EOAEs), several EOAE recordings were carried out using pairs of clicks: a suppressor click preceded the stimulus click generating an EOAE, with various intervals between the two clicks. EOAEs elicited by two clicks separated by intervals under 8-9 ms had significantly smaller amplitudes than EOAEs evoked by the stimulus alone. The amplitude decay correlated with the interclick interval, and was about 40% when the interclick interval decreased from 12 to 1 ms. This phenomenon has been noted before but not precisely quantified. It might reflect an adaptive mechanism within the outer hair cells, which has been previously described, or else mechanical interactions on the basilar membrane. The delay in EOAE decrease is of the same order as the first phase of neural adaptation, known as 'rapid adaptation', and these thus may prove to be correlated. RP LINAGRANADE, G (reprint author), UNIV LYON 1,HOP EDOUARD HERRIOT,DEPT OTORHINOLARYNGOL,PHYSIOL SENSORIELLE LAB,CNRS,URA 1447,F-69437 LYON 03,FRANCE. CR ANDERSON SD, 1980, HEARING RES, V2, P273, DOI 10.1016/0378-5955(80)90063-5 CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 EATOCK RA, 1987, J NEUROSCI, V7, P2821 EGGERMON.JJ, 1974, AUDIOLOGY, V13, P1 EGGERMONT JJ, 1985, HEARING RES, V18, P57, DOI 10.1016/0378-5955(85)90110-8 EYSHOLDT U, 1982, AUDIOLOGY, V21, P242 GRANDORI F, 1985, AUDIOLOGY, V24, P71 HOWARD J, 1987, P NATL ACAD SCI USA, V94, P3064 HUDSPETH AJ, 1994, NEURON, V12, P1, DOI 10.1016/0896-6273(94)90147-3 KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, EAR HEARING, V11, P93 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 LINAGRANADE G, 1994, AUDIOLOGY, V33, P218 PICTON TW, 1993, EAR HEARING, V14, P299, DOI 10.1097/00003446-199310000-00001 PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SMITH RL, 1985, ACTA OTO-LARYNGOL, V100, P1, DOI 10.3109/00016488509108580 THORNTON ARD, 1975, ELECTROEN CLIN NEURO, V39, P399, DOI 10.1016/0013-4694(75)90103-0 THORNTON ARD, 1993, J ACOUST SOC AM, V94, P132, DOI 10.1121/1.407090 VEUILLET E, 1992, HEARING RES, V61, P47, DOI 10.1016/0378-5955(92)90035-L WEISS TF, 1984, ANNU REV PHYSIOL, V46, P247 NR 22 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 55 EP 61 DI 10.1016/0378-5955(95)00078-I PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600008 PM 8567443 ER PT J AU SU, ZL JIANG, SC GU, R YANG, WP AF SU, ZL JIANG, SC GU, R YANG, WP TI 2 TYPES OF CALCIUM CHANNELS IN BULLFROG SACCULAR HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE CALCIUM CHANNEL; HAIR CELLS; PATCH-CLAMP TECHNIQUE ID ION-DEPENDENT CONDUCTANCES; CHICK SENSORY NEURONS; GUINEA-PIG; SYMPATHETIC NEURONS; CURRENTS; COCHLEA; TRANSDUCTION; ADAPTATION; KINETICS; MODES AB Ca2+ channels were studied in cell-attached recordings from the basolateral membrane of the bullforg saccular hair cells with the EPC-9 patch-clamp system. Pipettes contained 110 mM Ba2+ and the membrane potential was zeroed with isotonic potassium aspartate. Data acquisition and analysis were performed using E9SCREEN and M2LAB software. L-type channel was distinguished by a single-channel conductance of 26 pS, activation range between -10 and +40 mV and intense activity even at a holding potential of -40 mV. The L-type channel showed characteristic bursts of brief openings (mode 1) interrupted occasionally by longer openings (mode 2). Bay K 8644 promoted the mode 2 activity and nifedipine inhibited L-type channel activity. Another type of calcium channels, 20 pS channel, was detected by -50 to +10 mV depolarizing steps from a holding potential of -40 or -80 mV. This channel was insensitive to dihydropyridines and resembled the N-type channel. RP SU, ZL (reprint author), PEOPLES LIBERAT ARMY GEN HOSP,INST OTOLARYNGOL,28 FUXING RD,BEIJING 100853,PEOPLES R CHINA. CR ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 ASSAD JA, 1992, J NEUROSCI, V12, P3291 AUGUSTINE GJ, 1991, CALCIUM CHANNELS THE, P87 BEAN BP, 1985, J GEN PHYSIOL, V86, P1, DOI 10.1085/jgp.86.1.1 Colquhoun D., 1983, SINGLE CHANNEL RECOR, P191 CRAWFORD AC, 1990, J PHYSIOL-LONDON, V420, pP90 CRAWFORD AC, 1991, J PHYSIOL-LONDON, V434, P369 DELCOUR AH, 1993, J NEUROSCI, V13, P181 Flock A, 1988, Prog Brain Res, V74, P297 FORTI L, 1993, NEURON, V10, P437, DOI 10.1016/0896-6273(93)90332-L FOX AP, 1987, J PHYSIOL-LONDON, V394, P149 FOX AP, 1987, J PHYSIOL-LONDON, V394, P173 FUCHS PA, 1990, J PHYSIOL-LONDON, V429, P553 FUCHS PA, 1992, PROG NEUROBIOL, V39, P493, DOI 10.1016/0301-0082(92)90003-W HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HESS P, 1984, NATURE, V311, P538, DOI 10.1038/311538a0 HIRNING LD, 1988, SCIENCE, V239, P57, DOI 10.1126/science.2447647 HOWARD J, 1987, P NATL ACAD SCI USA, V84, P3064, DOI 10.1073/pnas.84.9.3064 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 JORGENSEN F, 1983, ACTA PHYSIOL SCAND, V118, P423, DOI 10.1111/j.1748-1716.1983.tb07292.x KIMITSUKI T, 1994, ACTA OTO-LARYNGOL, V114, P144, DOI 10.3109/00016489409126033 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 LIPSCOMBE D, 1988, P NATL ACAD SCI USA, V85, P2398, DOI 10.1073/pnas.85.7.2398 NAKAGAWA T, 1991, NEUROSCI LETT, V125, P81, DOI 10.1016/0304-3940(91)90136-H NOWYCKY MC, 1985, NATURE, V316, P440, DOI 10.1038/316440a0 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A RENNIE KJ, 1991, HEARING RES, V51, P279, DOI 10.1016/0378-5955(91)90044-A RUSCH A, 1991, J PHYSIOL-LONDON, V434, pP52 SCOTT RH, 1991, PROG NEUROBIOL, V36, P485, DOI 10.1016/0301-0082(91)90014-R SIGWORTH FJ, 1987, BIOPHYS J, V52, P1047 TSIEN RW, 1988, TRENDS NEUROSCI, V11, P431, DOI 10.1016/0166-2236(88)90194-4 NR 33 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 JUL PY 1995 VL 87 IS 1-2 BP 62 EP 68 DI 10.1016/0378-5955(95)00079-J PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600009 PM 8567444 ER PT J AU CODE, RA CARR, CE AF CODE, RA CARR, CE TI ENKEPHALIN-LIKE IMMUNOREACTIVITY IN THE CHICK BRAIN-STEM - POSSIBLE RELATION TO THE COCHLEAR EFFERENT SYSTEM SO HEARING RESEARCH LA English DT Article DE SUPERIOR OLIVARY NUCLEUS; LATERAL LEMNISCAL NUCLEI; COCHLEAR EFFERENT NEURON; CHAT-IMMUNOREACTIVITY ID PREPROENKEPHALIN MESSENGER-RNA; SUPERIOR OLIVARY COMPLEX; GUINEA-PIG; OLIVOCOCHLEAR NEURONS; CHOLINE-ACETYLTRANSFERASE; GALLUS-DOMESTICUS; MET-ENKEPHALIN; RAT; LOCALIZATION; PROJECTIONS AB Mammalian lateral olivocochlear (LOG) neurons that are immunoreactive for choline acetyltransferase (ChAT) are also immunoreactive for enkephalin (Enk). To determine whether cochlear efferent neurons in birds might also contain Enk-like immunoreactivity (Enk-LI), we studied the auditory brainstem of the domestic chicken using antisera to ChAT, leucine-enkephalin (L-Enk) and methionine-enkephalin (M-Enk). Enk-LI terminals are found around, but not within, the superior olivary nucleus (SO) and the nucleus of the lateral lemniscus, pars intermedia (LLi). A moderate concentration of Enk-LI terminals is found ventromedial to the ventral facial nucleus (VIIv) where the ventrolateral group of ChAT-I cochlear efferent neurons is located. After colchicine injections into the lateral ventricle, a population of intensely stained Enk-LI perikarya was found in the nucleus of the lateral lemniscus, pars ventralis (LLv) with scattered cells in the LLi and the nucleus subceruleus ventralis (SCv). The distribution of Enk-LI and ChAT-I somata, however, never overlapped, even in adjacent sections. Thus, in the chick, Enk-LI perikarya are not distributed in areas where cochlear efferent neurons are found. Instead, a dense concentration of Enk-I terminals can be found in areas containing ChAT-I cochlear efferent neurons. The source of these enkephalinergic terminals may be a population of Enk-LI cells in the LLv. C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. 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Res. PD JUL PY 1995 VL 87 IS 1-2 BP 69 EP 83 DI 10.1016/0378-5955(95)00080-N PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600010 PM 8567445 ER PT J AU FINLAYSON, PG AF FINLAYSON, PG TI DECREASED INHIBITION TO LATERAL SUPERIOR OLIVE NEURONS IN YOUNG AND AGED SPRAGUE-DAWLEY RATS SO HEARING RESEARCH LA English DT Article DE LATERAL SUPERIOR OLIVE; AGING; SPRAGUE-DAWLEY RAT; INHIBITORY DEFICITS ID UNIT EXCITATORY RESPONSES; BINAURAL TONE BURSTS; INFERIOR COLLICULUS; TRAPEZOID BODY; MEDIAL NUCLEUS; COCHLEAR NUCLEUS; PRINCIPAL CELLS; CBA/J MICE; COMPLEX; CAT AB Lateral superior olive (LSO) neurons in young and aged Sprague-Dawley rats have functional properties consistent with a limited contralateral inhibition, which is markedly different from other animals. An unusually low proportion of LSO cells (36/113) exhibited contralateral inhibition (and ipsilateral excitation, IE), while over 25% of LSO units exhibited excitatory responses to contralateral stimuli. Inhibition of most IE LSO neurons was evident only when the contralateral intensity was greater than the ipsilateral intensity, resulting in a marked shift in sensitivity to interaural intensity differences (IID). The firing rate of IE neurons was also affected more by a change in intensity of ipsilateral compared to contralateral stimuli. The shift in the IID sensitivity and the relative decrease in effectiveness of contralaterally driven inhibition in Sprague-Dawley rat LSO neurons could be due to decreased inhibitory inputs from the MNTB principal cells, increased contralateral excitatory effects and/or increased ipsilateral excitatory effects, Age-related decreases in the numbers of MNTB neurons observed anatomically is not reflected in a change in LSO function. The Sprague-Dawley rat may be a useful model for the effect of reduced inhibition in the superior olivary complex on auditory behavior. RP FINLAYSON, PG (reprint author), UNIV BRITISH COLUMBIA,CTR ROTARY HEARING,DEPT SURG OTOLARYNGOL,2211 WESBROOK MALL,ROOM F-150,VANCOUVER,BC V6T 2B5,CANADA. CR BANAYSCHWARTZ M, 1989, NEUROCHEM RES, V14, P555, DOI 10.1007/BF00964918 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 BROWN CH, 1984, EXP AGING RES, V10, P35 CAIRD D, 1983, EXP BRAIN RES, V52, P385 Cant N. 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PD JUL PY 1995 VL 87 IS 1-2 BP 84 EP 95 DI 10.1016/0378-5955(95)00081-E PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600011 PM 8567446 ER PT J AU BERLIN, CI HOOD, LJ HURLEY, AE WEN, H KEMP, DT AF BERLIN, CI HOOD, LJ HURLEY, AE WEN, H KEMP, DT TI BINAURAL NOISE SUPPRESSES LINEAR CLICK-EVOKED OTOACOUSTIC EMISSIONS MORE THAN IPSILATERAL OR CONTRALATERAL NOISE SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; EFFERENT SUPPRESSION; BINAURAL; IPSILATERAL; CONTRALATERAL; FORWARD MASKING ID MASKING PARADIGM; EFFERENT SYSTEM; SOUND; STIMULATION; BEHAVIOR AB We studied the efferent suppression of click-evoked otoacoustic emissions with 65 dB SPL of white noise presented to left, right, or sometimes both, ears for 408 ms. Each burst of noise preceded a series of four unipolar 80 mu s 65 dB peak Sound Pressure clicks, presented to the left ear only. The first click of the four-click group followed the end of the noise by either 1, 2, 5, 10, 20, 50, 100 or 200 ms; each subsequent click was offset by 20 additional ms via an ILO88 system with special programming modifications. Conditions were alternated so that a 'without noise' condition preceded a 'with noise' condition for three repetitions of 600 clicks per trial. Seven subjects with normal hearing participated in the study, and three of the seven participated in a Lest-retest reliability study. Results showed the greatest suppression followed binaural stimulation ending within one to five ms of the first click in the pulse train. Somewhat less suppression was seen following ipsilateral stimulation. The least amount of suppression was seen following contralateral stimulation, suggesting that previous research using contralateral stimulation may underestimate efferent effects. We saw no effects when the end of the noise was 100 ms or more away from the beginning of the click train. RP BERLIN, CI (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112, USA. 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PD JUL PY 1995 VL 87 IS 1-2 BP 96 EP 103 DI 10.1016/0378-5955(95)00082-F PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600012 PM 8567448 ER PT J AU MONEY, MK PIPPIN, GW WEAVER, KE KIRSCH, JP WEBSTER, DB AF MONEY, MK PIPPIN, GW WEAVER, KE KIRSCH, JP WEBSTER, DB TI AUDITORY BRAIN-STEM RESPONSES OF CBA/J MICE WITH NEONATAL CONDUCTIVE HEARING LOSSES AND TREATMENT WITH GM1 GANGLIOSIDE SO HEARING RESEARCH LA English DT Article DE GM1 GANGLIOSIDE; CONDUCTIVE HEARING LOSS; AUDITORY BRAIN-STEM RESPONSE; CBA/J MICE ID ANTEROVENTRAL COCHLEAR NUCLEUS; SPINAL-CORD INJURY; GM-1 GANGLIOSIDE; ACOUSTIC DEPRIVATION; SOUND DEPRIVATION; LABORATORY MOUSE; STEM RESPONSES; RAT; NERVE; NEUROTOXICITY AB Exogenous administration of GM1 ganglioside to CBA/J mice with a neonatal conductive hearing loss ameliorates the atrophy of spiral ganglion neurons, ventral cochlear nucleus neurons, and ventral cochlear nucleus volume. The present investigation demonstrates the extent of a conductive loss caused by atresia and tests the hypothesis that GM1 ganglioside treatment will ameliorate the conductive hearing loss. Auditory brainstem responses were recorded from four groups of seven mice each: two groups received daily subcutaneous injections of saline (one group had normal hearing; the other had a conductive hearing loss); the other two groups received daily subcutaneous injections of GM1 ganglioside (one group had normal hearing; the other had a conductive hearing loss). In mice with a conductive loss, decreases in hearing sensitivity were greatest at high frequencies. The decreases were determined by comparing mean ABR thresholds of the conductive loss mice with those of normal hearing mice. The conductive hearing loss induced in the mice in this study was similar to that seen in humans with congenital aural atresias. GM1 ganglioside treatment had no significant effect on ABR wave I thresholds or latencies in either group. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. PK CENT INST,ST LOUIS,MO. LOUISIANA STATE UNIV,MED CTR,DEPT ANAT,NEW ORLEANS,LA 70112. 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Res. PD JUL PY 1995 VL 87 IS 1-2 BP 104 EP 113 DI 10.1016/0378-5955(95)00083-G PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600013 PM 8567428 ER PT J AU MANDAVA, P RUPERT, AL MOUSHEGIAN, G AF MANDAVA, P RUPERT, AL MOUSHEGIAN, G TI VOWEL AND VOWEL SEQUENCE PROCESSING BY COCHLEAR NUCLEUS NEURONS SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS NEURONS; VOWEL SEQUENCES; CODING PROPERTIES ID AUDITORY-NERVE FIBERS; SHORT-TERM ADAPTATION; DISCHARGE PATTERNS; CAT; ARCHITECTURE; MASKING; DORSAL; ROOT; RESPONSES; PARALLEL AB This study examined neuronal discharge rates and temporal patterns to vowels and vowel sequences in chinchilla. The properties of primary-like, chopper, and onset neurons were studied using vowels /i/, /a/, and /u/ individually and paired with separations (0-100 ms), at sound levels above and below thresholds. The interspike interval, period, and post-stimulus-time histograms of all neuronal types to a vowel were modified when in a sequence. Primary-like and chopper discharges were reduced and enhanced depending on vowel sequence parameters; onset neurons exhibited discharge rate reductions only and not enhancements. In addition to rate changes, novel discharge intervals appeared with vowel pairs. An unexpected finding on choppers was that subthreshold levels of the preceding vowel in a paired sequence enhanced discharges to the succeeding one. Reducing levels of preceding or increasing levels of following vowels evoked changes not predictable from single vowel data. Thus the responses to paired vowels in a sequence are interactive. Patterns of discharges and rate functions to vowel sounds from neurons of the same type varied greatly. The cochlear nuclei harbor anatomically and functionally diverse neurons. Because of this heterogeneity, the neural transformations of vowel segments by all cochlear nucleus neuronal types can not be predicted from sinusoidal data. 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Res. PD JUL PY 1995 VL 87 IS 1-2 BP 114 EP 131 DI 10.1016/0378-5955(95)00084-H PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600014 PM 8567429 ER PT J AU VASAMA, JP MAKELA, JP AF VASAMA, JP MAKELA, JP TI AUDITORY PATHWAY PLASTICITY IN ADULT HUMANS AFTER UNILATERAL IDIOPATHIC SUDDEN SENSORINEURAL HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED FIELD; AUDITORY CORTEX; HEARING DISORDER; SENSORINEURAL; UNILATERAL HEARING LOSS; INTERSTIMULUS INTERVAL; PLASTICITY; HUMAN ID CORTEX AB We recorded auditory evoked magnetic fields from 8 patients with unilateral, idiopathic, sudden, sensorineural hearing loss and from 8 healthy controls, using a 122-channel whole-scalp neuromagnetometer. The stimuli were 50-ms 1-kHz tons bursts, delivered to the healthy ear at interstimulus intervals (ISIs) of 1, 2, 4, 8, and 16 s. On average, as in normal-hearing controls, the dipole moments and the latencies of N100m, the 100-ms response, increased as a function of ISI over both hemispheres to left- and right-ear stimulation. Four patients had shorter response latencies and 4 had stronger dipole moments over the hemisphere ipsilateral to the stimulation. In 3 patients, one additional source was observed over the anterolateral right hemisphere and another near head midline. These findings suggest that unilateral sensorineural hearing loss may modify information processing in the central auditory pathways. RP VASAMA, JP (reprint author), HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. CR AHONEN AI, 1993, PHYS SCRIPTA, VT49A, P198, DOI 10.1088/0031-8949/1993/T49A/033 BIGNALL KE, 1968, ELECTROENCEPHALOGR C, V26, P206 Coles R. R. A., 1987, S BROWNS OTOLARYNGOL, V2, P368 GIARD MH, 1994, ELECTROEN CLIN NEURO, V92, P238, DOI 10.1016/0168-5597(94)90067-1 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, 1988, EXP BRAIN RES, V71, P87 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JACOBSON GP, 1991, HEARING RES, V56, P44, DOI 10.1016/0378-5955(91)90152-Y KAUKORANTA E, 1986, EXP BRAIN RES, V63, P60 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 Makela J. P., 1993, Human Brain Mapping, V1, P48, DOI 10.1002/hbm.460010106 MAKELA JP, 1994, ELECTROEN CLIN NEURO, V92, P414, DOI 10.1016/0168-5597(94)90018-3 PANDYA DN, 1969, BRAIN RES, V14, P49, DOI 10.1016/0006-8993(69)90030-4 PELLIZZONE M, 1986, NEUROSCI LETT, V68, P192 POPELAR J, 1994, HEARING RES, V72, P125, DOI 10.1016/0378-5955(94)90212-7 SAMS M, 1993, J COGNITIVE NEUROSCI, V5, P363, DOI 10.1162/jocn.1993.5.3.363 VASAMA JP, 1994, HEARING RES, V78, P91, DOI 10.1016/0378-5955(94)90047-7 VASAMA JP, 1995, NEUROREPORT, V6, P961, DOI 10.1097/00001756-199505090-00003 WILLOTT JF, 1993, J COMP NEUROL, V329, P402, DOI 10.1002/cne.903290310 NR 20 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 JUL PY 1995 VL 87 IS 1-2 BP 132 EP 140 DI 10.1016/0378-5955(95)00086-J PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600015 PM 8567430 ER PT J AU NAITO, Y NEWMAN, A LEE, WS BEYKIRCH, K HONRUBIA, V AF NAITO, Y NEWMAN, A LEE, WS BEYKIRCH, K HONRUBIA, V TI PROJECTIONS OF THE INDIVIDUAL VESTIBULAR END-ORGANS IN THE BRAIN-STEM OF THE SQUIRREL-MONKEY SO HEARING RESEARCH LA English DT Article DE AFFERENT INNERVATION; VESTIBULAR RECEPTOR; VESTIBULAR NUCLEUS; SQUIRREL MONKEY ID HORSERADISH-PEROXIDASE; LABYRINTHINE INFLUENCES; EFFERENT CONNECTIONS; DIDELPHIS-VIRGINIANA; AMERICAN OPOSSUM; GUINEA-PIG; CAT; NUCLEI; NERVE; FIBERS AB The central nervous system (CNS) projections of primary afferent neurons from individual vestibular receptors were studied using horseradish peroxidase (HRP) or biocytin labeling in 14 ears from 7 adult squirrel monkeys using the technique developed in the chinchilla (Lee et al., 1989,1992). The specificity of labeling was verified by examining the location of the labeled fibers and cell bodies in the vestibular nerve and Scarpa's ganglion, Labeled fibers and cells were restricted to nerves and areas belonging to groups of cells in either the superior or the inferior ganglion of the vestibular nerve. In the vestibular nerve root, labeled primary afferent fibers also exhibited a receptor-dependent segregation at the entrance to the medulla. Fibers from the HSC and the SSC were found rostrally and those from the PSC and the SAC were found in the caudal area, The UTR fibers were situated intermediate between these two groups of fibers. (A bundle of fibers, probably vestibular efferents, was identified immediately rostrally and ventromedially to the UTR fibers.) The primary afferent fibers bifurcated into secondary ascending and descending fibers at the lateral border of the vestibular nuclei, forming a longitudinal rostrocaudal vestibular tract, The secondary fibers from individual end-organs occupied specific locations in the tract: the UTR fibers were dorsal to the SSC and the HSC fibers, PSC fibers were found most medially, and the SAC fibers occupied the lateralmost area. The secondary UTR fibers overlapped considerably with those of the SSC and the HSC. The orderly receptor-dependent segregation of fibers was more prominent in the descending tracts than in the ascending tracts. In the vestibular nuclei complex the location of the tertiary branches of various end-organs exhibited considerable overlap within the major vestibular nuclei (SN, superior nucleus; LN, lateral nucleus; MN, medial nucleus; DN, descending nucleus). There were still differences, however, in the projection pattern. Fibers from the SAC ran primarily in the lateral area, fibers from the SSC and the UTR were found ventromedially to the SAC fibers, and the HSC projected slightly medially to the fibers from the SSC. The PSC fibers projected most medially, The UTR and SAC sent numerous fibers to the cerebellum. Fibers from the semicircular canals projected through the rostrodorsal region of the SN and presumably also projected to the cerebellum. The precise termination of fibers was evaluated by studying the location of labeled boutons, which were identified in all major vestibular nuclei. Labeled boutons from all the receptors were in the rostral and central areas of the SN, and in the MN mainly in the rostral two-thirds. In the LN, boutons from all the receptors were in the rostroventral part, most of which were from the UTR and SAG. No labeled boutons were in the caudodorsal part of this nucleus. Labeled boutons in the DN primarily surrounded the descending tract fibers and were particularly prominent medially, In specimens in which superior vestibular nerve receptor organs were scratched vestibular efferent fibers were also labeled, These fibers traveled in the most ventral part of the vestibular nerve root and projected in the ventral aspect of the LN to labeled soma in the ipsilateral and contralateral brain stem. Specificity the in projection patterns of efferent fibers from different end-organs could not be ascertained. C1 UNIV CALIF LOS ANGELES,SCH MED,VICTOR GOODHILL EAR CTR,LOS ANGELES,CA 90024. KYOTO UNIV,DEPT OTOLARYNGOL,KYOTO 606,JAPAN. YONSEI UNIV,DEPT OTOLARYNGOL,SEOUL 120749,SOUTH KOREA. 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Res. PD JUL PY 1995 VL 87 IS 1-2 BP 141 EP 155 DI 10.1016/0378-5955(95)00085-I PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600016 PM 8567431 ER PT J AU KLUMP, GM LANGEMANN, U AF KLUMP, GM LANGEMANN, U TI COMODULATION MASKING RELEASE IN A SONGBIRD SO HEARING RESEARCH LA English DT Article DE MASKING; MASKING RELEASE; COMODULATION; COMODULATION MASKING RELEASE; BIRD ID STARLING STURNUS-VULGARIS; MODULATION TRANSFER-FUNCTIONS; SPEECH-RECEPTION THRESHOLD; GAP DETECTION; MASKER BANDWIDTH; FLANKING-BAND; ON-FREQUENCY; TIME-DELAY; SIGNAL; COMMUNICATION AB Comodulation masking release (CMR) describes the reduced masking of a pure tone when the masking is a noise that is coherently amplitude modulated (comodulated) over the total range of the spectrum compared to masking by an unmodulated noise of the same bandwidth and overall energy. The masking release results from cues available within a critical band and from cues generated by comparisons across critical bands ('true' CMR). Here we report data on masking release and 'true' CMR in a songbird, the European starling (Sturnus vulgaris), that was demonstrated in a psychoacoustic experiment using a GO/NOGO paradigm. Masked thresholds for 2-kHz tones centered in digitally generated continuous masking noise of different bandwidths were determined, and the amount of masking release was calculated as the threshold difference between the unmodulated and the comodulated condition. In the first experiment the modulator was a 50-Hz lowpass noise. A masking release of 11.8 dB was found for the noise masker with the largest bandwidth (1600 Hz). With the masker bandwidth decreasing to 50 Hz, the birds' release from masking was reduced to 1.6 dB. The starling's 'true' CMR was 4 dB or 8 dB, depending on the definition that was applied. In a second experiment the masker bandwidth was constant (1600 Hz) and the cut-off frequency of the modulator was varied. A release from masking of 17.8 dB was found for a modulator cut-off frequency of 12.5 Hz. It decreased to 6.1 dB with an increase in the modulator cut-off frequency to 400 Hz. The duration of the test signal (100-750 ms) had little effect on the release from masking. Given the similarities in the release from masking and in CMR of starlings and humans, the starling may provide an excellent model for studying the mechanisms that underlie the generation of CMR. RP KLUMP, GM (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,D-85748 GARCHING,GERMANY. 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Res. PD JUL PY 1995 VL 87 IS 1-2 BP 157 EP 164 DI 10.1016/0378-5955(95)00087-K PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600017 PM 8567432 ER PT J AU ZINE, A HAFIDI, A ROMAND, R AF ZINE, A HAFIDI, A ROMAND, R TI FIMBRIN EXPRESSION IN THE DEVELOPING RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE STEREOCILIA; HAIR CELL; CYTOSKELETAL PROTEIN; ACTIN; ONTOGENY ID ACTIN-BINDING-PROTEINS; VERTEBRATE HAIR-CELLS; INNER-EAR; BRUSH-BORDER; GUINEA-PIG; F-ACTIN; LOCALIZATION; STEREOCILIA; FILAMENTS; ORGANIZATION AB The expression of fimbrin in the developing rat cochlea was analyzed using an immunohistochemical technique with fimbrin antibody. The cochlea displayed temporal and lateral-longitudinal gradients for fimbrin expression during development. Fimbrin immunoreactivity first appeared in the inner hair cell stereocilia of the basal turn on the first gestational day studied (day 18). At birth, both inner (IHC) and outer hair cell (OHC) stereocilia of the basal turn showed positive labeling with fimbrin antibody. The progression of appearance was always from IHCs to OHCs and fimbrin immunostaining appeared in the apical hair cells by postnatal day 6. Immunostaining was restricted to stereocilia and the cuticular plate, and no immunoreactivity was observed in neighboring structures of the epithelium. Double labeling using both fimbrin antibody and phalloidin binding revealed similar chronological expression from the earliest stage studied. Increasing fimbrin immunoreactivity was observed in hair cells until late postnatal and adult stages. This study suggests that fimbrin is expressed with F-actin during development and fimbrin together with actin may constitute the two basic molecules that participate in stereocilia formation. We speculate that fimbrin may help maintain the parallel growth of actin filaments within the stereocilia. These data additionally support previous findings that hair cell maturation occurs from the base to the apex and from IHCs to OHCs. C1 UNIV CLERMONT FERRAND,NEUROBIOL LAB,F-63177 CLERMONT FERRAND,FRANCE. CR BRETSCHER A, 1980, J CELL BIOL, V86, P335, DOI 10.1083/jcb.86.1.335 BRETSCHER A, 1981, P NATL ACAD SCI-BIOL, V78, P6849, DOI 10.1073/pnas.78.11.6849 BRETSCHER A, 1978, J CELL BIOL, V79, P839, DOI 10.1083/jcb.79.3.839 DEARRUDA MV, 1990, J CELL BIOL, V111, P1069, DOI 10.1083/jcb.111.3.1069 DEROSIER DJ, 1980, NATURE, V287, P291, DOI 10.1038/287291a0 DRENCKHAHN D, 1991, J CELL BIOL, V122, P641 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 EZZELL RM, 1989, DEVELOPMENT, V106, P407 FLOCK A, 1984, HEARING RES, V15, P11 FLOCK A, 1981, J NEUROCYTOL, V10, P133, DOI 10.1007/BF01181749 FLOCK A, 1982, HEARING RES, V6, P75 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FLOCK A, 1965, COLD SPRING HARB SYM, V30, P133 HUDSPETH AJ, 1979, P NATL ACAD SCI USA, V76, P1506, DOI 10.1073/pnas.76.3.1506 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 JONSSON R, 1986, J IMMUNOL METHODS, V88, P109, DOI 10.1016/0022-1759(86)90058-X KUIJPERS W, 1991, HISTOCHEMISTRY, V96, P511, DOI 10.1007/BF00267077 LAZARIDES E, 1975, J CELL BIOL, V65, P549, DOI 10.1083/jcb.65.3.549 LENOIR M, 1987, ANAT EMBRYOL, V175, P477, DOI 10.1007/BF00309683 MATSUDAIRA P, 1983, NATURE, V301, P209, DOI 10.1038/301209a0 MOOSEKER MS, 1983, CELL, V35, P11, DOI 10.1016/0092-8674(83)90202-7 ROMAND R, 1993, CELL MOTIL CYTOSKEL, V25, P213, DOI 10.1002/cm.970250302 ROMAND R, 1987, HEARING RES, V28, P1, DOI 10.1016/0378-5955(87)90148-1 SLEPECKY N, 1985, HEARING RES, V20, P245, DOI 10.1016/0378-5955(85)90029-2 SLEPECKY NB, 1990, J ELECTRON MICR TECH, V15, P280, DOI 10.1002/jemt.1060150307 SOBIN A, 1983, ACTA OTO-LARYNGOL, V96, P407, DOI 10.3109/00016488309132726 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 TILNEY LG, 1986, HEARING RES, V22, P55, DOI 10.1016/0378-5955(86)90077-8 TILNEY LG, 1980, J CELL BIOL, V86, P244, DOI 10.1083/jcb.86.1.244 TILNEY MS, 1989, J CELL BIOL, V109, P1711, DOI 10.1083/jcb.109.4.1711 WEEDS A, 1982, NATURE, V296, P811, DOI 10.1038/296811a0 ZENNER HP, 1980, ARCH OTORHINOLARYNGO, V230, P81 NR 32 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 JUL PY 1995 VL 87 IS 1-2 BP 165 EP 169 DI 10.1016/0378-5955(95)00088-L PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600018 PM 8567434 ER PT J AU FRIJNS, JHM DESNOO, SL SCHOONHOVEN, R AF FRIJNS, JHM DESNOO, SL SCHOONHOVEN, R TI POTENTIAL DISTRIBUTIONS AND NEURAL EXCITATION PATTERNS IN A ROTATIONALLY SYMMETRICAL MODEL OF THE ELECTRICALLY STIMULATED COCHLEA SO HEARING RESEARCH LA English DT Article DE AUDITORY PROSTHESIS; ELECTRICAL STIMULATION; ELECTRICAL VOLUME CONDUCTION; BOUNDARY ELEMENT METHOD; AUDITORY NERVE FIBER; COMPUTATIONAL MODELING ID AUDITORY-NERVE; FIBERS AB In spite of many satisfactory results, the clinical outcome of cochlear implantation is poorly predictable and Further insight into the fundamentals of electrical nerve stimulation in this complex geometry is necessary. For this purpose we developed a rotationally symmetric volume conductor model of the implanted cochlea, using the Boundary Element Method (BEM). This configuration mimics the cochlear anatomy more closely than previous, unrolled models. The calculated potential distribution in the cochlea due to stimulating electrodes is combined with a multiple non-linear node model of auditory nerve fibres, which we recently developed. The combined model is used to compute excitation profiles of the auditory nerve for a variety of stimulus levels and electrode positions. The model predicts that the excitation threshold, the spatial selectivity and the dynamic range depend on the exact position of the electrode in the scala tympani. These results are in good agreement with recently published electrical ABR data. It is shown that the use of actively modelled nerve fibres is essential to obtain correct predictions for the biphasic stimuli typically used in cochlear implants and that unrolling the cochlear duct as done in previous models leads to erroneous predictions regarding modiolar stimulation. RP FRIJNS, JHM (reprint author), LEIDEN UNIV HOSP,DEPT ENT,ROOM J2-56,POB 9600,2300 RC LEIDEN,NETHERLANDS. RI Frijns, Johan/H-6249-2011 CR BALKANY TJ, 1986, OTOLARYNG CLIN N AM, V19, P215 Binns K.J., 1992, ANAL NUMERICAL SOLUT BLACK RC, 1983, ANN NY ACAD SCI, V405, P137, DOI 10.1111/j.1749-6632.1983.tb31626.x BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 DEMUNCK JC, 1992, IEEE T BIO-MED ENG, V39, P986, DOI 10.1109/10.256433 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FINLEY CC, 1987, 9TH P IEEE EMBS C, P1901 FRANKENHAEUSER B, 1964, J PHYSIOL-LONDON, V171, P302 FRIJNS JHM, 1994, MED BIOL ENG COMPUT, V32, P391, DOI 10.1007/BF02524690 FRIJNS JHM, 1994, IEEE T BIO-MED ENG, V41, P556, DOI 10.1109/10.293243 GANTZ BJ, 1990, LARYNGOSCOPE, V98, P1100 GANTZ BJ, 1993, ANN OTO RHINOL LARYN, V102, P909 Girzon G., 1987, THESIS MIT GLEICH O, 1993, HEARING RES, V71, P69, DOI 10.1016/0378-5955(93)90022-S HODGKIN AL, 1952, J PHYSIOL-LONDON, V117, P500 IFUKUBE T, 1987, IEEE T BIO-MED ENG, V34, P883, DOI 10.1109/TBME.1987.326009 LIBERMAN MC, 1984, J COMP NEUROL, V223, P163, DOI 10.1002/cne.902230203 MEIJS JWH, 1989, IEEE T BIO-MED ENG, V36, P1038, DOI 10.1109/10.40805 MOTZ H, 1986, NEUROSCIENCE, V18, P699, DOI 10.1016/0306-4522(86)90064-3 NIJDAM HF, 1982, THESIS GRONINGEN U OLEARY SJ, 1985, HEARING RES, V18, P273, DOI 10.1016/0378-5955(85)90044-9 RATTAY F, 1989, IEEE T BIO-MED ENG, V36, P676, DOI 10.1109/10.32099 RATTAY F, 1993, IEEE T BIO-MED ENG, V40, P1201, DOI 10.1109/10.250575 RATTAY F, 1990, ELECTRICAL NERVE STI REILLY JP, 1985, IEEE T BIO-MED ENG, V32, P1001, DOI 10.1109/TBME.1985.325509 SAPOZHNIKOV A, 1990, THESIS U MELBOURNE A SCHWARZ JR, 1987, PFLUG ARCH EUR J PHY, V409, P569, DOI 10.1007/BF00584655 SHEPHERD RK, 1993, HEARING RES, V66, P108, DOI 10.1016/0378-5955(93)90265-3 SPELMAN FA, 1982, ANN OTO RHINOL LARYN, V91, P3 Strang G., 1973, ANAL FINITE ELEMENT STRELIOF.D, 1973, J ACOUST SOC AM, V54, P620, DOI 10.1121/1.1913642 SUESSERMAN MF, 1993, IEEE T BIO-MED ENG, V40, P237, DOI 10.1109/10.216407 Suesserman M.F., 1992, THESIS U WASHINGTON VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VANDERWEIDEN RM, 1989, COMPUT MECH, V4, P283 van Oosterom A, 1991, Acta Otolaryngol Suppl, V491, P70 WARMAN EN, 1992, IEEE T BIO-MED ENG, V39, P1244, DOI 10.1109/10.184700 NR 39 TC 86 Z9 86 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 170 EP 186 DI 10.1016/0378-5955(95)00090-Q PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600019 PM 8567435 ER PT J AU SHAH, DM FREEMAN, DM WEISS, TF AF SHAH, DM FREEMAN, DM WEISS, TF TI THE OSMOTIC RESPONSE OF THE ISOLATED, UNFIXED MOUSE TECTORIAL MEMBRANE TO ISOSMOTIC SOLUTIONS - EFFECT OF NA+, K+, AND CA2+ CONCENTRATION SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; LYMPH COMPOSITION; MOUSE ID GUINEA-PIG COCHLEA; HAIR-CELLS; TRANSDUCER CURRENTS; INNER-EAR; ADAPTATION; ENDOLYMPH; MICROMECHANICS; ORGANIZATION; MOVEMENT; FLUIDS AB Changes in the size, shape, and structure of the isolated tectorial membrane (TM) of the mouse were measured in response to isosmotic changes in the ionic composition of the bathing solution. Substitution of artificial perilymph (AP) for artificial endolymph (AE) caused a small(approximate to 1%) shrinkage of the TM's thickness. This substitution alters not only the predominate cation (from K+ to Na+) but also the Ca2+ concentration(from 20 mu mol/l to 2 mmol/l). When the predominate cation was changed from K+ to Na+, while holding Ca2+ concentration constant, results depended on Ca2+ concentration: there was a small(approximate to 1%) swelling for 20 mu mol/l Ca2+, larger (approximate to 14%) swelling for lower (< 7 mu mol/l) concentrations of Ca2+, and little response for 2 mmol/l Ca2+ or for solutions containing the Ca2+ chelator EGTA. Addition of Ca2+ while holding the predominate cation constant caused shrinkage of the TM; both removal of Ca2+ and addition of the Ca2+ chelator EGTA caused swelling. Swelling responses were largely reversible if the magnitude of the swelling was small. Responses greater than a few percent were only partially reversible and caused long-lasting changes. Changes in ionic composition of the bath affected not only the thickness of the TM but also its other dimensions. Solution changes that increase TM thickness tend to cause radial shearing motions of the surfaces of the TM, which are accompanied by small decreases in width. Little change in length was observed. Although the responses were non-isotropic, increases in thickness were highly correlated with increases in volume. Swelling of the TM was also accompanied by a reduction in prominence of its radially oriented fibrillar structure. These results for the isolated TM of the mouse are qualitatively similar to those obtained previously for the isolated chick TM (Freeman et al., 1994) but different from those obtained for the in vitro mouse TM (Kronester-Frei, 1979a). C1 MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,BALTIMORE,MD 21203. CR ALLEN JB, 1980, J ACOUST SOC AM, V68, P1660, DOI 10.1121/1.385198 ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 BOSHER SK, 1978, NATURE, V273, P377, DOI 10.1038/273377a0 CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 EATOCK RA, 1987, J NEUROSCI, V7, P2821 FREEMAN DM, 1993, HEARING RES, V65, P83, DOI 10.1016/0378-5955(93)90204-E FREEMAN DM, 1994, HEARING RES, V79, P197, DOI 10.1016/0378-5955(94)90141-4 GRODZINSKY AJ, 1983, CRIT REV BIOMED ENG, V9, P133 HASKO JA, 1988, HEARING RES, V35, P21, DOI 10.1016/0378-5955(88)90037-8 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 Iurato S, 1967, SUBMICROSCOPIC STRUC KAWAMATA S, 1993, HEARING RES, V67, P75, DOI 10.1016/0378-5955(93)90234-R KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 KILLICK R, 1992, HEARING RES, V64, P21, DOI 10.1016/0378-5955(92)90165-J KONISHI T, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 KRONESTERFREI A, 1977, THESIS TU MUNICH 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 KRONESTERFREI A, 1978, CELL TISSUE RES, V193, P11 KROS CJ, 1992, P ROY SOC B-BIOL SCI, V249, P185, DOI 10.1098/rspb.1992.0102 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 MELICHAR I, 1977, PFLUG ARCH EUR J PHY, V372, P207, DOI 10.1007/BF01063854 MELICHAR I, 1980, Hearing Research, V2, P55, DOI 10.1016/0378-5955(80)90016-7 MELICHAR I, 1978, HEARING RES, V1, P35, DOI 10.1016/0378-5955(78)90007-2 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 ORMAN SS, 1986, AM J OTOLARYNG, V7, P140, DOI 10.1016/S0196-0709(86)80043-6 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 RUSSELL IJ, 1987, HEARING RES, V31, P9, DOI 10.1016/0378-5955(87)90210-3 SALT AN, 1979, HEARING RES, V1, P343, DOI 10.1016/0378-5955(79)90005-4 SELLICK PM, 1972, PFLUGERS ARCH, V336, P1 STEEL K, 1980, ACTA OTO-LARYNGOL, V89, P27, DOI 10.3109/00016488009127104 STEEL KP, 1983, HEARING RES, V12, P265, DOI 10.1016/0378-5955(83)90111-9 STEEL KP, 1983, HEARING RES, V9, P327, DOI 10.1016/0378-5955(83)90035-7 STERKERS O, 1988, PHYSIOL REV, V68, P1083 STERKERS O, 1984, AM J PHYSIOL, V247, pF602 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 TABER LA, 1981, J ACOUST SOC AM, V70, P426, DOI 10.1121/1.386785 TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 TANAKA T, 1981, SCI AM, V244, P124 THALMANN I, 1986, J OTORHINOLARYNGOL, V48, P106 THALMANN I, 1993, ARCH BIOCHEM BIOPHYS, V307, P391, DOI 10.1006/abbi.1993.1605 THALMANN I, 1987, LARYNGOSCOPE, V97, P357 THALMANN I, 1993, CONNECT TISSUE RES, V29, P191, DOI 10.3109/03008209309016826 VASSOUT P, 1984, ACTA OTO-LARYNGOL, V98, P199, DOI 10.3109/00016488409107555 WEAVER SP, 1994, HEARING RES, V76, P1, DOI 10.1016/0378-5955(94)90081-7 ZWISLOCKI JJ, 1989, HEARING RES, V42, P211, DOI 10.1016/0378-5955(89)90146-9 ZWISLOCKI JJ, 1980, J ACOUST SOC AM, V657, P1679 NR 53 TC 35 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 187 EP 207 DI 10.1016/0378-5955(95)00089-M PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600020 PM 8567436 ER PT J AU BOETTCHER, FA WHITE, DR MILLS, JH SCHMIEDT, BN AF BOETTCHER, FA WHITE, DR MILLS, JH SCHMIEDT, BN TI AGE-RELATED-CHANGES IN AUDITORY-EVOKED POTENTIALS OF GERBILS .3. LOW-FREQUENCY RESPONSES AND REPETITION RATE EFFECTS SO HEARING RESEARCH LA English DT Article DE AGING; AUDITORY BRAIN-STEM RESPONSE; EVOKED POTENTIAL; GERBIL; HEARING LOSS; PRESBYACUSIS ID BRAIN-STEM RESPONSE; VENTRAL COCHLEAR NUCLEUS; MONGOLIAN GERBIL; INTERSTIMULUS-INTERVAL; STIMULUS DEPENDENCIES; NERVE FIBERS; CLICK LEVEL; LATENCY; YOUNG; QUIET AB The auditory brainstem response (ABR) was recorded non-invasively from Mongolian gerbils ranging in age from 6 to 36 months. The ABR was elicited using gaussian tone bursts at octave intervals from 1 to 16 kHz. Responses were bandpass filtered from 30 to 300 Hz (LF-ABR; low-frequency component) and from 300 to 3000 Hz (HF-ABR; high-frequency component). In Experiment A, the thresholds of the two components (HF- and LF-ABR) were compared in 6- and 36-month subjects. The LF-ABR varied more with age than did the HF-ABR, particularly at stimulus frequencies of 2 kHz and above. As shown previously for the HF-ABR, the latencies of the LF-ABR increased as a function of hearing loss in aged gerbils whereas amplitudes of the LF-ABR were reduced in all aged gerbils, regardless of age-related threshold elevation. In Experiment B, tone bursts were presented at rates of 11-91/s to gerbils aged 6, 18, 30, and 36 months. Increased repetition rate resulted in an increase in the latency of both the HF- and LF-ABR, but to the same degree in each age group. Similarly, the interpeak intervals of the HF-ABR increased as a function of repetition rate in all subjects to the same degree. Increased age and increased repetition rate both resulted in significant reductions in ABR amplitudes, but rate did not interact with age. The data suggest that(1) the LF-ABR may be more sensitive to aging than is the HF-ABR and (2) there are no age-related changes in the HF- or LF-ABR which are dependent upon the repetition rate. RP BOETTCHER, FA (reprint author), MED UNIV S CAROLINA,DEPT OTORHINOLARYNGOL & COMMUNICAT SCI,CHARLESTON,SC 29425, USA. CR BACKOFF PM, 1994, HEARING RES, V73, P163, DOI 10.1016/0378-5955(94)90231-3 Beagley H A, 1978, Br J Audiol, V12, P69, DOI 10.3109/03005367809078858 BEATTIE RC, 1984, J SPEECH HEAR DISORD, V49, P114 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z BOETTCHER FA, 1993, HEARING RES, V71, P146, DOI 10.1016/0378-5955(93)90030-5 BURKARD R, 1983, J ACOUST SOC AM, V74, P1204, DOI 10.1121/1.390024 BURKARD R, 1987, J ACOUST SOC AM, V81, P1050, DOI 10.1121/1.394677 BURKARD R, 1993, J ACOUST SOC AM, V94, P2441, DOI 10.1121/1.407465 BURKARD R, 1989, J ACOUST SOC AM, V85, P2514, DOI 10.1121/1.397746 CHEAL M, 1986, EXP AGING RES, V12, P3 CHIAPPA KH, 1979, ARCH NEUROL-CHICAGO, V36, P81 DALY DM, 1977, ELECTROEN CLIN NEURO, V43, P151, DOI 10.1016/0013-4694(77)90123-7 DAVIS H, 1979, AUDIOLOGY, V18, P445 DAVIS H, 1976, ANN OTOL S28, V85 DAVIS KA, 1994, ABSTR ASS RES OT, V17, P17 DEBRUYNE F, 1986, AUDIOLOGY, V25, P101 DING J, 1994, ABSTR ASS RES OT, V17, P17 DON M, 1977, ANN OTO RHINOL LARYN, V86, P186 FADDIS BT, 1993, EXP NEUROL, V120, P160, DOI 10.1006/exnr.1993.1051 FOWLER CG, 1983, J SPEECH HEAR RES, V26, P560 FUJIKAWA SM, 1977, J AM AUDITORY SOC, V3, P147 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 GRATTON MA, 1995, HEARING RES, V83, P43, DOI 10.1016/0378-5955(94)00188-V Hall J, 1992, HDB AUDITORY EVOKED HARKINS SW, 1981, INT J NEUROSCI, V15, P107, DOI 10.3109/00207458108985851 HARKINS SW, 1979, INT J NEUROSCI, V10, P7 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HELLSTROM LI, 1991, HEARING RES, V53, P217, DOI 10.1016/0378-5955(91)90055-E HENRY KR, 1980, ARCH OTO-RHINO-LARYN, V228, P233, DOI 10.1007/BF00660735 JACOBSON JT, 1987, EAR HEARING, V8, P115, DOI 10.1097/00003446-198704000-00009 JEWETT DL, 1971, BRAIN, V94, P681, DOI 10.1093/brain/94.4.681 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KJAER M, 1980, ACTA NEUROL SCAND, V62, P20 KLEIN AJ, 1983, ARCH OTOLARYNGOL, V109, P6 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 OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 OTTO WC, 1982, AUDIOLOGY, V21, P466 PICTON T, 1974, ELECTROEN CLIN NEURO, V36, P197 PICTON TW, 1981, J OTOLARYNGOL, V10, P1 PRATT H, 1976, ARCH OTO-RHINO-LARYN, V212, P85, DOI 10.1007/BF00454268 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 ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 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 SCOTT ML, 1978, INT J NEUROSCI, V8, P147, DOI 10.3109/00207457809150392 SMITH DI, 1991, HEARING RES, V54, P1, DOI 10.1016/0378-5955(91)90130-2 SMITH DI, 1989, ELECTROEN CLIN NEURO, V72, P422, DOI 10.1016/0013-4694(89)90047-3 STAPELLS DR, 1981, EAR HEARING, V2, P20 STARR A, 1975, ARCH NEUROL-CHICAGO, V32, P761 SUZUKI T, 1986, ELECTROEN CLIN NEURO, V65, P150, DOI 10.1016/0168-5597(86)90048-1 SUZUKI T, 1985, ELECTROEN CLIN NEURO, V65, P150 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V TERKILDSEN K, 1975, SCAND AUDIOL, V4, P167, DOI 10.3109/01050397509043078 WHARTON JA, 1990, AUDIOLOGY, V29, P196 YAGI T, 1979, ARCH OHREN NASEN KEH, V222, P91, DOI 10.1007/BF00469746 NR 59 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1995 VL 87 IS 1-2 BP 208 EP 219 DI 10.1016/0378-5955(95)00091-H PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600021 PM 8567437 ER PT J AU ZUO, J CURTIS, LM YAO, XF TENCATE, WJF BAGGERSJOBACK, D HULTCRANTZ, M RAREY, KE AF ZUO, J CURTIS, LM YAO, XF TENCATE, WJF BAGGERSJOBACK, D HULTCRANTZ, M RAREY, KE TI GLUCOCORTICOID RECEPTOR EXPRESSION IN THE POSTNATAL RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE GLUCOCORTICOID RECEPTOR; IMMUNOCYTOCHEMISTRY; DEVELOPMENT ID MESSENGER-RNA; INNER-EAR; ONTOGENY AB The glucocorticoid receptor (GR) expression in the neonatal rat cochlea was investigated by utilization of a polyclonal antibody against GR, the immunoreactivity of which exhibited a distinct, age-dependent developmental pattern in tissues of the spiral ligament (SL). Immunostaining of GR appeared initially at the 7th postnatal day (PND), increased rapidly between the 14th and 21st PND, and reached adult-like expression levels by the 21st PND. Less pronounced, developmentally regulated expression patterns of GR were observed in cells of the spiral limbus (SLi), spiral ganglion (SG), organ of Corti (OC), and cochlear nerve (CN). For example, high expression levels of GR were observed in the SLi, SG and OC at 3 PND; subsequently, GR immunoreactivity levels decreased from 7 to 14 PND, and then GR immunoreactivity intensified in these regions by 21 PND. No remarkable changes in GR expression were observed in stria vascularis (SV). These data indicate that GR expression in the inner ear is tissue and age-specific, and that GR expression parallels both Na,K-ATPase expression and endocochlear potential development. C1 UNIV FLORIDA,COLL MED,DEPT ANAT,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT CELL BIOL,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. 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Res. PD JUL PY 1995 VL 87 IS 1-2 BP 220 EP 227 DI 10.1016/0378-5955(95)00092-I PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA TB396 UT WOS:A1995TB39600022 PM 8567439 ER PT J AU BRUCKNER, S RUBSAMEN, R AF BRUCKNER, S RUBSAMEN, R TI BINAURAL RESPONSE CHARACTERISTICS IN ISOFREQUENCY SHEETS OF THE GERBIL INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; BINAURAL RESPONSES; CONVERGENCE; ISOFREQUENCY SHEETS; MERIONES UNGUICULATUS ID SUPERIOR OLIVARY COMPLEX; SOUND PRESSURE LEVEL; CENTRAL NUCLEUS; TONOTOPIC ORGANIZATION; COCHLEAR NUCLEUS; FUNCTIONAL-ORGANIZATION; NEURONAL ARCHITECTURE; AFFERENT-PROJECTIONS; FREQUENCY NEURONS; LATERAL LEMNISCUS AB The spatial distribution of neurons with different binaural response properties was studied in two isofrequency areas of the inferior colliculus (IC) of the gerbil (Meriones unguiculatus). Single units were recorded in dorsomedial-to-ventrolaterally oriented electrode penetrations at different rostrocaudal positions, within a low (1-2 kHz; N=108) and a high (23-27 kHz; N=90) 'iso-frequency' sheet. Response types were not equally represented within the two layers. Within low-frequency regions, 41% of the units were excited following sound stimulation of either ear (EE), 21% received an excitatory input from one and an inhibitory input from the other ear (EI), and 12% were monaural (EO), while within high-frequency regions the distribution was 20% EE, 47% EI and 18% EO. However, the spatial arrangement of EE, EI and EO, within the dorsomedial-to-ventrolateral extent of the isofrequency sheets, was on the whole comparable within the two regions: EE-units were accumulated dorsomedially and EI-units ventrolaterally in the respective isofrequency sheets. EO-units were distributed equally within the low-frequency sheet but occurred more frequently in the middle part of the high-frequency lamina. About equal proportions of the units (low frequencies 9%; high frequencies 7%) had complex binaural response characteristics and were characterized as E/IE. In the rostrocaudal dimension of the nucleus, orderly arrangement of different unit types was less obvious. The results show that there is a tendency for grouping of different binaural unit types within the inferior colliculus. However, these unit types are not strictly segregated. Furthermore, it was shown that, despite the differences found in low- and high-frequency sites, there is a common scheme of 'binaural representation' across frequencies within the IC. Provided that EE-, EI-, and monaural response characteristics originate from separate sources, the data point to a convergence of binaural brainstem afferents within the IC. C1 RUHR UNIV BOCHUM,LEHRSTUHL ALLGEMEINE ZOOL & NEUROBIOL,D-44780 BOCHUM,GERMANY. 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C. T., 1988, AUDITORY FUNCTION, P385 YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 ZOOK JM, 1985, J COMP NEUROL, V231, P530, DOI 10.1002/cne.902310410 NR 54 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 JUN PY 1995 VL 86 IS 1-2 BP 1 EP 14 DI 10.1016/0378-5955(95)00048-9 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200001 PM 8567406 ER PT J AU LAUTERMANN, J MCLAREN, J SCHACHT, J AF LAUTERMANN, J MCLAREN, J SCHACHT, J TI GLUTATHIONE PROTECTION AGAINST GENTAMICIN OTOTOXICITY DEPENDS ON NUTRITIONAL-STATUS SO HEARING RESEARCH LA English DT Article DE GENTAMICIN; OTOTOXICITY; DIET; GLUTATHIONE; PROTECTION ID MONOETHYL ESTER; DEFICIENCY; METABOLITE; THERAPY; LIVER; RAT AB This study demonstrates that gentamicin ototoxicity depends on dietary factors and correlates with tissue glutathione levels. After 15 days of gentamicin injections (100 mg/kg/day s.c.) guinea pigs on a regular protein diet (18.5% protein) had an average hearing loss of 9 dB at 3 kHz, 31 dB at 8 khz and 42 dB at 18 kHz. Guinea pigs on a 7% protein diet showed an increased hearing loss of 52 dB at 3 kHz, 63 dB at 8 kHz and 74 dB at 18 kHz. Supplementing the low protein diet with either essential or sulfur-containing amino acids did not protect against gentamicin ototoxicity. Glutathione levels in the cochlear sensory epithelium were decreased in animals on a low protein diet and could be restored to normal by oral administration of glutathione monoethyl ester (1.2 g/kg/day) in combination with vitamin C (100 mg/kg/day). Glutathione supplementation significantly reduced the magnitude of hearing loss in the low protein diet group at all frequencies (43 dB reduction at 3 kHz, 27 dB reduction at 8 kHz and 21 dB reduction at 18 kHz). In animals on a full protein diet, dietary glutathione neither increased cochlear glutathione levels nor attenuated hearing loss. Serum gentamicin levels did not differ between animals on the various diets with or without glutathione supplement. These results suggest that gentamicin toxicity and detoxifying mechanisms are affected by the metabolic state of the animal and the glutathione content of the tissue. Thus, compounds that could potentially protect against gentamicin ototoxicity may be more correctly assessed in animal models of deficient nutritional states in which endogenous detoxifying mechanisms are compromised. This animal model might also be more realistically related to the clinical situation of a critically ill patient receiving gentamicin treatment. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. 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J., 1984, Laboratory animal medicine, P149 MCLEAN AEM, 1975, BIOCHEM PHARMACOL, V24, P37, DOI 10.1016/0006-2952(75)90310-X MEISTER A, 1992, BIOCHEM PHARMACOL, V44, P1905, DOI 10.1016/0006-2952(92)90091-V MEISTER A, 1991, PHARMACOL THERAPEUT, V51, P155, DOI 10.1016/0163-7258(91)90076-X NEUSCHWANDERTETRI, 1989, ANAL BIOCHEM, V179, P236 PIERSON MG, 1980, HEARING RES, V4, P79 PRASAD JS, 1978, CHEMOTHERAPY, V24, P333 PRAZMA J, 1983, ANN OTO RHINOL LARYN, V92, P178 PRIUSKA E, 1995, ABSTR ASS RES OT, V18, P79 RAPHAEL Y, 1990, HEARING RES, V51, P173 RICEEVANS CA, 1993, FREE RADICAL BIO MED, V15, P77, DOI 10.1016/0891-5849(93)90127-G SAMOTRA K, 1985, EUR J CLIN PHARMACOL, V29, P255, DOI 10.1007/BF00547433 SCHACHT J, 1993, OTOLARYNG CLIN N AM, V26, P845 SPENCER PS, 1993, SCIENCE, V262, P825, DOI 10.1126/science.8235599 STAAL FJT, 1992, LANCET, V339, P909, DOI 10.1016/0140-6736(92)90939-Z TEICHER BA, 1988, CANCER, V62, P1275, DOI 10.1002/1097-0142(19881001)62:7<1275::AID-CNCR2820620705>3.0.CO;2-I WHITING PH, 1988, BRIT J EXP PATHOL, V69, P35 ZENNER HP, 1994, EUR ARCH OTO-RHINO-L, V251, P84 NR 37 TC 85 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 JUN PY 1995 VL 86 IS 1-2 BP 15 EP 24 DI 10.1016/0378-5955(95)00049-A PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200002 PM 8567412 ER PT J AU CHEN, C NENOV, A NORRIS, CH BOBBIN, RP AF CHEN, C NENOV, A NORRIS, CH BOBBIN, RP TI ATP MODULATION OF L-TYPE CALCIUM-CHANNEL CURRENTS IN GUINEA-PIG OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE ION CHANNEL; VOLTAGE-CLAMP; DIHYDROPYRIDINE; COCHLEA ID INTRACELLULAR CALCIUM; SYMPATHETIC NEURONS; VERTEBRATE CELLS; CHROMAFFIN CELLS; COCHLEA; NEUROTRANSMITTERS; TRANSMISSION; RESPONSES; CHICK AB Ca2+ channel currents and their modulation by adenosine 5'-triphosphate (ATP) in acutely isolated guinea pig outer hair cells (OHCs) were investigated using the whole-cell patch-clamp technique. The current-voltage (I-V) relation of OHCs indicated that the Ca2+ channel opened near -30 mV, and the current reached a maximum at +10 and 0 mV in 20 mM Ca2+ and Ba2+ external solutions, respectively. BayK 8644 (BayK, 2 mu M) caused a 3.5-fold increase in peak Ca2+ currents and shifted the I-V curves toward more negative potentials. These results suggest that the majority of Ca2+ channels in OHCs have L-type characteristics. The effects of ATP on Ca2+ channels of OHCs were heterogenous. ATP (100 mu M) decreased Ca2+ channel currents by 31.7 +/- 5.6% at 0 mV and shifted Ca2+ tail activation curves toward more depolarized potentials in some cells (N = 6). By contrast, in others, ATP enhanced the currents by 43.5 +/- 12.5% at +10 mV (N = 6). In the presence of BayK, however, ATP-induced inhibition or enhancement of Ca2+ channel currents was attenuated. In addition, 100 mu M ATP produced little effect on Ca2+ channel currents in another subpopulation of cells (N = 12). This heterogenous neuromodulation of Ca2+ channel currents by ATP may reflect a functional diversity among OHCs. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 25 EP 33 DI 10.1016/0378-5955(95)00050-E PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200003 PM 8567418 ER PT J AU TRUY, E DEIBER, MP CINOTTI, L MAUGUIERE, F FROMENT, JC MORGON, A AF TRUY, E DEIBER, MP CINOTTI, L MAUGUIERE, F FROMENT, JC MORGON, A TI AUDITORY-CORTEX ACTIVITY CHANGES IN LONG-TERM SENSORINEURAL DEPRIVATION DURING CRUDE COCHLEAR ELECTRICAL-STIMULATION - EVALUATION BY POSITRON EMISSION TOMOGRAPHY SO HEARING RESEARCH LA English DT Article DE LONG-TERM DEAFNESS; CRUDE ELECTRICAL COCHLEAR STIMULATION; POSITRON EMISSION TOMOGRAPHY; AUDITORY CORTEX; ACTIVATION ID CEREBRAL BLOOD-FLOW; INTRAVENOUS (H2O)-O-15; IMPLANT; METABOLISM; SYSTEM; TIME AB We studied three right-handed human volunteers who have been prelingually deaf for 16 to 26 years. We measured cerebral regional activity (rA) using O-15 labelled water and positron emission tomography (PET) during rest and during electrical cochlear stimulation of the right ear. The stimulus consisted of crude constant current squared pulses, it is currently employed in cochlear implant screening. Two subjects described a subjective auditory sensation under cochlear stimulation, the third did not. An increment of the rA (which is linked to the regional cerebral blood flow) in the auditory cortex was observed in all subjects, activation was ipsilateral to stimulation in one subject and contralateral in two subjects. These findings suggest 1) that auditory pathways to the cortex can remain functional a long time after prelinguistic auditory deprivation, 2) that the auditory cortex can be activated by a crude electrical stimulation of the cochlea in the absence of perception of the auditory stimulus, 3) that PET does not seem to offer any advantage for screening patients who have been prelingually deaf for a long time. C1 HOP EDOUARD HERRIOT,DEPT PHYSIOL SENSORIELLE AUDIT & VOIX,CNRS,URA 1447,LYON,FRANCE. CTR ETUD & RECH MED EMISS POSITONS,LYON,FRANCE. HOP NEUROL & NEUROCHIRURG P WERTHEIMER,DEPT IMAGERIE RESONANCE MAGNET,LYON,FRANCE. RP TRUY, E (reprint author), HOP EDOUARD HERRIOT,DEPT OTORHINOLARYNGOL CHIRURG CERVICOFACIALE & PH,PL ARSONVAL,F-69437 LYON 03,FRANCE. RI Deiber, Marie-Pierre/M-5949-2014 CR BAILEY DL, 1991, J CEREB BLOOD FLO S2, V11, pS150 BANFAI P, 1988, AM J OTOL, V9, P203 CELESIA GG, 1982, ELECTROEN CLIN NEURO, V54, P243, DOI 10.1016/0013-4694(82)90174-2 Chouard C H, 1983, Ann Otolaryngol Chir Cervicofac, V100, P417 FINKENZELLER P, 1987, COCHLEAR IMPLANT, P31 FOX PT, 1989, J NUCL MED, V10, P141 FOX PT, 1984, J CEREBR BLOOD F MET, V4, P329 FOX PT, 1988, J CEREBR BLOOD F MET, V8, P642 FRISTON KJ, 1990, J CEREBR BLOOD F MET, V10, P458 GANTZ BJ, 1989, OTOLARYNG CLIN N AM, V22, P239 HERSCOVITCH P, 1983, J NUCL MED, V24, P782 HERZOG H, 1991, OTORHINOLARYGOL NOVA, V1, P37 ITO J, 1990, ARCH OTOLARYNGOL, V116, P1437 KANNO I, 1987, J CEREBR BLOOD F MET, V7, P143 KANNO I, 1991, J NUCL MED, V32, P1931 LAUTER JL, 1988, AUDITORY PATHWAY, P313 LAUTER JL, 1992, CENTRAL AUDITORY PRO, P61 LAUTER JL, 1985, HEARING RES, V20, P199, DOI 10.1016/0378-5955(85)90024-3 LEE L, 1983, ANN OTO RHINOL LARYN, V92, P19 LESCAO Y, 1991, CIRCULATION METABOLI, V9, P103 LUXFORD WM, 1989, AM J OTOL, V10, P95 MAZOYER B, 1990, IEEE T NUCL SCI, V37, P778, DOI 10.1109/23.106714 MAZZIOTTA JC, 1982, NEUROLOGY, V32, P921 MILLER J, 1897, AM J OTOL, V8, P220 MINTUN MA, 1989, J CEREB BLOOD FLOW M, V9, P574 MOORE D, 1983, ACTA OTOLARYNGOL S S, V421, P19 MOORE JK, 1992, ARO, V15, P153 PONTON CW, 1993, ELECTROEN CLIN NEURO, V88, P473 RACZKOWSKI D, 1980, NEUROPSYCHOLOGIA, V18, P213 Raichle ME, 1987, HDB PHYSL NERVOUS SY, P643 RAICHLE ME, 1983, J NUCL MED, V24, P790 SOKOLOFF L, 1981, FED PROC, V40, P2311 Talairach J., 1988, COPLANAR STEREOTAXIC WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WONGRILEY MTT, 1981, ANN OTO RHINOL LARYN, V90, P30 1985, ISO389 INT ORG STAND NR 36 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 JUN PY 1995 VL 86 IS 1-2 BP 34 EP 42 DI 10.1016/0378-5955(95)00052-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200004 PM 8567419 ER PT J AU ADLER, HJ NIEMIEC, AJ MOODY, DB RAPHAEL, Y AF ADLER, HJ NIEMIEC, AJ MOODY, DB RAPHAEL, Y TI TECTORIAL MEMBRANE REGENERATION IN ACOUSTICALLY DAMAGED BIRDS - AN IMMUNOCYTOCHEMICAL TECHNIQUE SO HEARING RESEARCH LA English DT Article DE CHICK; QUAIL; BASILAR PAPILLA; ACOUSTIC OVERSTIMULATION; REGENERATION; TECTORIAL MEMBRANE ID CHICK; TRAUMA AB A novel immunocytochemical method was used to determine whether the sound-damaged adult quail ear can repair its tectorial membrane (TM) and to compare the repair in quail to that in chicks. Birds were exposed to an octave band noise with a center frequency of 1.5 kHz at 116 dB SPL for 4 h. The chicks were grouped based on recovery duration (0 and 7 days), while the quail were divided into 0-, 7- and 14-day recovered groups. At the end of the recovery period, the animals were sacrificed, and their basilar papillae labeled with a TM-specific monoclonal primary antibody solution followed by a diaminobenzidine process. Examinations under a stereoscope revealed that a patch lesion devoid of TM was located on all 0-day recovered papillae. Seven days later, a honeycomb-patterned layer was observed covering the lesion. In 14-day recovered quail ears, the honeycomb layer appeared similar to that seen at 7 days post-exposure. These observations indicated that both chicks and quail were able to repair their TM within 7 days following exposure to intense sound. RP ADLER, HJ (reprint author), UNIV MICHIGAN,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 COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X COTANCHE DA, 1987, HEARING RES, V30, P197, DOI 10.1016/0378-5955(87)90136-5 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 GOODYEAR R, 1994, HEARING RES, V80, P93, DOI 10.1016/0378-5955(94)90013-2 MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 NIEMIEC AJ, 1994, HEARING RES, V79, P1, DOI 10.1016/0378-5955(94)90122-8 RAPHAEL Y, 1993, J COMP NEUROL, V330, P521, DOI 10.1002/cne.903300408 SHEETS WCP, 1994, 1994 SENS MECH REG C TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 NR 10 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 1995 VL 86 IS 1-2 BP 43 EP 46 DI 10.1016/0378-5955(95)00051-5 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200005 PM 8567420 ER PT J AU KETTEMBEIL, S MANLEY, GA SIEGL, E AF KETTEMBEIL, S MANLEY, GA SIEGL, E TI DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS AND THEIR ANESTHESIA SENSITIVITY IN THE EUROPEAN STARLING AND THE CHICKEN SO HEARING RESEARCH LA English DT Article DE DISTORTION-PRODUCT EMISSION; DPOAE; OTOACOUSTIC EMISSION; BIRD HEARING ID NORMALLY HEARING SUBJECTS; 2 DISCRETE SOURCES; ACOUSTIC DISTORTION; BASILAR PAPILLA; BOBTAIL LIZARD; PHYSIOLOGICAL VULNERABILITY; EAR; 2F1-F2; HUMANS; RABBIT AB The aim of the present experimental series was to provide further information on the distortion-product otoacoustic emissions (DP) of birds and contribute to a general understanding of DP generation. Basic characteristics of the DP 2f(1)-f(2) and 2f(2)-f(1) were measured in the ear canal of both awake and anaesthetized European Starlings and chickens. The effect of a third suppressive tone and the behaviour of the DP under anaesthesia were also studied. In general, the DP characteristics of both bird species resembled those of lizards and mammals, but first appeared at somewhat higher primary-tone levels. The best frequencies of third tones suppressing 2f(1)-f(2) lay near the first primary tone (f(1)), but for 2f(2)-f(1), the situation was more complex. Facilitation via a third tone was also seen for both DP, often at levels below those eliciting suppression. The DP 2f(1)-f(2) disappeared completely at the onset of deep anaesthesia and recovered to its original magnitude when the anaesthesia was lightened, sometimes with a considerable delay. The compound action potential (CAP) was somewhat more sensitive to anaesthesia than the DP. Control experiments showed that the anaesthesia effect was not a result of hypoxia. Avian DP at low and intermediate sound levels are thus physiologically-sensitive manifestations of normal hair-cell function that are, in contrast to mammals, also anaesthesia-sensitive. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. CR 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 FISCHER FP, 1994, HEARING RES, V73, P1, DOI 10.1016/0378-5955(94)90277-1 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 GASKILL SA, 1990, J ACOUST SOC AM, V88, P821, DOI 10.1121/1.399732 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 HARRIS FP, 1989, J ACOUST SOC AM, V85, P220, DOI 10.1121/1.397728 HORNER KC, 1985, J ACOUST SOC AM, V78, P1603, DOI 10.1121/1.392798 JARAMILLO F, 1993, NATURE, V364, P527, DOI 10.1038/364527a0 Kemp D. T., 1983, MECH HEARING, P75 KEMP DT, 1983, HEARING PHYSL BASES, P82 KLINKE R, 1993, PROG BRAIN RES, V97, P31 KONISHI M, 1970, Z VERGL PHYSIOL, V66, P257, DOI 10.1007/BF00297829 KOPPL C, 1990, J COMP PHYSIOL A, V167, P139 KOPPL C, 1993, J ACOUST SOC AM, V93, P2834 KUHN A, 1982, NATURWISSENSCHAFTEN, V69, P245, DOI 10.1007/BF00398648 LANGEMANN U, 1992, HEARING RES, V63, P43, DOI 10.1016/0378-5955(92)90072-U 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 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1987, HEARING RES, V26, P257, DOI 10.1016/0378-5955(87)90062-1 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1992, AUDITORY PHYSL PERCE, P151 MANLEY GA, 1993, J ACOUST SOC AM, V93, P2820, DOI 10.1121/1.405803 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MATTHEWS JW, 1986, PERIPHERAL AUDITORY, P258 MOULIN A, 1993, HEARING RES, V65, P193, DOI 10.1016/0378-5955(93)90213-K NORTON SJ, 1990, MECH BIOPHYSICS HEAR, P219 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 WHITEHEAD ML, 1991, HEARING RES, V51, P293, DOI 10.1016/0378-5955(91)90045-B WHITEHEAD ML, 1992, J ACOUST SOC AM, V92, P2662, DOI 10.1121/1.404382 WHITEHEAD ML, 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 ZHENG Y, 1995, 18TH ASS RES OT MIDW ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 ZWICKER E, 1980, HEARING RES, V2, P513, DOI 10.1016/0378-5955(80)90088-X NR 40 TC 34 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1995 VL 86 IS 1-2 BP 47 EP 62 DI 10.1016/0378-5955(95)00053-7 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200006 PM 8567421 ER PT J AU BARBARA, M MODESTI, A AF BARBARA, M MODESTI, A TI NERVE-FIBERS OF THE ENDOLYMPHATIC SAC - ELECTRON-MICROSCOPIC FINDINGS IN THE MONGOLIAN GERBIL SO HEARING RESEARCH LA English DT Article DE NERVE FIBERS; ENDOLYMPHATIC SAC; TRANSMISSION ELECTRON MICROSCOPY; MONGOLIAN GERBIL ID GUINEA-PIG; INNERVATION AB The presence of separate bundles of nerve fibres in the gerbilline endolymphatic sac (ES) is described, paying particular attention to their ultrastructure and localization. One bundle, localized in the area of the subepithelium which separates the sigmoid sinus from the ES, is composed only of myelinated fascicles which, moreover, seem to have an isolated contact with the ES area. Other two single nerve fibres, much smaller in caliber, are localized in the ES subepithelium and laterally to the ES area, still close to the sigmoid sinus. These fibres, composed of myelinated and unmyelinated fascicles, seem to have a rather longitudinal orientation and, moreover, contract close relationships with the rich vascular network of the ES subepithelial tissue. As far as the course is concerned, the serial sectioning technique would suggest that the nerve fibres get very close to the ES epithelial cell layer, going proximal to distal. Speculations on the origin of this nerve contingent in the ES are proposed and discussed in view of possible new theories for pathogenesis and therapy of some inner ear diseases. C1 UNIV G DANNUNZIO,DEPT PATHOL,CHIETI,ITALY. RP BARBARA, M (reprint author), UNIV ROMA LA SAPIENZA,DEPT OTORHINOLARYNGOL,I-00185 ROME,ITALY. CR Adlington P, 1968, J Laryngol Otol, V82, P101, DOI 10.1017/S0022215100068559 BAGGERSJOBACK D, 1986, ARCH OTOLARYNGOL, V112, P398 BARBARA M, 1992, ATTUALITA NELLA RICE, P115 BARBARA M, 1989, J LARYNGOL OTOL, V103, P137, DOI 10.1017/S0022215100108308 BIRGERSSON L, 1992, ORL J OTO-RHINO-LARY, V54, P188 BRECHTELSBAUER PB, 1992, ARCH OTOLARYNGOL, V118, P260 Guild SR, 1927, AM J ANAT, V39, P1, DOI 10.1002/aja.1000390102 HASSF C, 1873, ANAT STUDIEN, V1, P765 Hozawa K, 1993, Acta Otolaryngol Suppl, V506, P14 HOZAWA K, 1989, ACTA OTO-LARYNGOL, V107, P171, DOI 10.3109/00016488909127496 KIMURA RS, 1965, PRACT-OTO-RHINO-LARY, V27, P343 LINDVALL M, 1978, SCIENCE, V201, P176, DOI 10.1126/science.663649 LUNDQUIST PG, 1965, ACTA OTOLARYNGOL S S, V201, P1 RASKANDERSEN H, 1991, ANN OTO RHINOL LARYN, V100, P148 VANEGMOND AAJ, 1956, ACTA OTOLARYNGOL STO, V46, P285 WACKYM PA, 1987, J LARYNGOL OTOL, V101, P768, DOI 10.1017/S0022215100102713 NR 16 TC 0 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1995 VL 86 IS 1-2 BP 63 EP 67 DI 10.1016/0378-5955(95)00054-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200007 PM 8567422 ER PT J AU SUZUKI, M IKEDA, K SUNOSE, H HOZAWA, K KUSAKARI, C KATORI, Y TAKASAKA, T AF SUZUKI, M IKEDA, K SUNOSE, H HOZAWA, K KUSAKARI, C KATORI, Y TAKASAKA, T TI ATP-INDUCED INCREASE IN INTRACELLULAR CA2+ CONCENTRATION IN THE CULTURED MARGINAL CELL OF THE STRIA VASCULARIS OF GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE MARGINAL CELL; CELL CULTURE; NA+/K+ ATPASE; INTRACELLULAR CA2+ CONCENTRATION; ATP ID OUTER HAIR-CELLS; EXTRACELLULAR ATP; COCHLEAR EXPLANTS; CALCIUM; GENERATION; MICROSCOPY; RELEASE; GROWTH; ORGAN; CORTI AB The primary culture of marginal cells from the explant of the stria vascularis of guinea-pigs was established and confirmed by morphological, immunohistochemical and physiological characters of the cultivated cells. The positive stain of cytokeratin 18 without vimentin and desmin expressions indicated the epithelial origin of the cultured polygonal cells. Electron microscopical findings of cultured cells resembled the morphological characteristics of marginal cells. The addition of 100 mu M ouabain to the cultured cells significantly increased the intracellular Na+ concentration, providing the evidence for the presence of Na+ pump. Using the cultured marginal cells identified by the above-mentioned findings, the effects of neurotransmitters and hormones in regulating intracellular Ca2+ concentration ([Ca2+](i)) were investigated. The addition of 10(-4) M ATP caused an increase in [Ca2+](i), which was independent of the presence of extracellular Ca2+. The rank order of agonist potency was ATP > alpha,beta-methylene ATP > ADP. Adenosine, however, evoked no response. Cultured marginal cells may possess P-2-purinergic receptors which mobilize Ca2+ from the intracellular Ca2+ pool. [Marginal cell, Cell culture, Na+/K(+)ATPase, Intracellular Ca2+ concentration, ATP]. C1 TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,SENDAI,MIYAGI,JAPAN. CR ACHOUCHE J, 1991, ANN OTO RHINOL LARYN, V100, P999 ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BENHAM CD, 1987, NATURE, V328, P375 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 ERNST SA, 1979, CURR TOP MEMBR TRANS, V13, P355 GORDON JL, 1986, BIOCHEM J, V233, P309 GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440 HALLAM TJ, 1986, FEBS LETT, V207, P95, DOI 10.1016/0014-5793(86)80019-9 HAROOTUNIAN AT, 1989, J BIOL CHEM, V264, P19458 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 IKEDA K, 1992, PFLUG ARCH EUR J PHY, V420, P493, DOI 10.1007/BF00374624 IKEDA K, 1995, IN PRESS CELL CALCIU IKEDA K, 1990, EUR ARCH OTO-RHINO-L, V248, P19, DOI 10.1007/BF00634775 KASPER M, 1987, ARCH OTO-RHINO-LARYN, V244, P66, DOI 10.1007/BF00453494 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 KUJAWA SG, 1994, HEARING RES, V78, P181, DOI 10.1016/0378-5955(94)90024-8 KUPFERMANN I, 1991, PHYSIOL REV, V71, P683 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MELICHAR I, 1992, HEARING RES, V62, P89, DOI 10.1016/0378-5955(92)90205-2 MELICHAR I, 1992, ACTA OTO-LARYNGOL, V112, P762, DOI 10.3109/00016489209137471 MELICHAR I, 1991, EUR ARCH OTO-RHINO-L, V248, P358 NIEDZIELSKI AS, 1992, NEUROREPORT, V3, P273, DOI 10.1097/00001756-199203000-00015 NILLES R, 1994, HEARING RES, V73, P27, DOI 10.1016/0378-5955(94)90279-8 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 OGAWA K, 1993, HEARING RES, V69, P207, DOI 10.1016/0378-5955(93)90109-E RAREY KE, 1989, HEARING RES, V38, P277, DOI 10.1016/0378-5955(89)90071-3 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 SUZUKI M, 1993, ABSTR ASS RES OT, V16, P135 SUZUKI M, 1994, ABSTR ASS RES OT, V17, P135 NR 32 TC 20 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 1995 VL 86 IS 1-2 BP 68 EP 76 DI 10.1016/0378-5955(95)00055-9 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200008 PM 8567423 ER PT J AU LESPERANCE, MM HELFERT, RH ALTSCHULER, RA AF LESPERANCE, MM HELFERT, RH ALTSCHULER, RA TI DEAFNESS INDUCED CELL-SIZE CHANGES IN ROSTRAL AVCN OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE PLASTICITY; COCHLEAR NUCLEUS; AUDITORY; DEAFNESS; CELL SIZE ID ANTEROVENTRAL COCHLEAR NUCLEUS; STEM AUDITORY NUCLEI; BRAIN-STEM; ELECTRICAL-STIMULATION; ACOUSTIC DEPRIVATION; SOUND DEPRIVATION; REMOVAL; NEURONS; DENSITY; NUMBER AB The right cochleae of 250-350 g guinea pigs were lesioned by topical administration of neomycin in the middle ear cavity. Eight weeks after the lesion, the cochleae and cochlear nuclei were analyzed. Cochlear hair cell loss was assessed, and cell areas of spherical bushy cells in the rostral anteroventral cochlear nucleus (AVCN) were compared between the lesioned and normal hearing sides for each animal. In five animals with both inner and outer hair cell loss in the lesioned cochlea, the average area of neuronal somata in the rostral AVCN in the lesioned side was 22% smaller than the average area of these cells in the normal hearing side. In two animals with outer hair cell loss but inner hair cells remaining, there was no difference in cell size between the lesioned and non-lesioned AVCN. These results provide evidence that there is significant shrinkage in AVCN cell size in the mature mammal after hearing loss associated with inner hair cell loss. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109. SO ILLINOIS UNIV,SCH MED,DEPT SURG,SPRINGFIELD,IL 62794. 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 CANT NB, 1984, HEARING SCI RECENT A, P371 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 FINGER PA, 1993, INFLUENCE STIMULATIO, P55 Hashisaki G T, 1989, J Comp Neurol, V283, P5 HULTCRANTZ M, 1991, HEARING RES, V54, P272, DOI 10.1016/0378-5955(91)90121-O KALIL R, 1980, J COMP NEUROL, V189, P483, DOI 10.1002/cne.901890305 KILENY PR, 1991, ANN OTO RHINOL LARYN, V100, P563 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 MCGEE TM, 1962, ARCHIV OTOLARYNGOL, V75, P295 MILLER JM, 1991, NOISE INDUCED HEARIN, P130 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 OSEN KK, 1969, ACTA OTO-LARYNGOL, V67, P352, DOI 10.3109/00016486909125462 PASIC TR, 1990, J COMP NEUROL, V283, P474 POWELL TPS, 1962, J ANAT, V96, P249 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 SCHWARTZ DR, 1995, IN PRESS HEAR RES SENTO S, 1989, J COMP NEUROL, V305, P553 SIE KCY, 1992, J COMP NEUROL, V320, P501, DOI 10.1002/cne.903200407 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 TUCCI DL, 1995, UNPUB HEAR RES WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1978, ANAT REC, V190, P578 WEBSTER DB, 1983, INT J PEDIATR OTORHI, V6, P107 ZAPPIA JJ, 1989, HEARING RES, V40, P29, DOI 10.1016/0378-5955(89)90096-8 NR 28 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 PY 1995 VL 86 IS 1-2 BP 77 EP 81 DI 10.1016/0378-5955(95)00056-A PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200009 PM 8567424 ER PT J AU FUKAZAWA, K SAKAGAMI, M UMEMOTO, M KUBO, T AF FUKAZAWA, K SAKAGAMI, M UMEMOTO, M KUBO, T TI ENDOCYTOSIS AND TRANSEPITHELIAL TRANSPORT OF ENDOLYMPH IN THE ENDOLYMPHATIC SAC SO HEARING RESEARCH LA English DT Article DE ENDOLYMPHATIC SAC; CATIONIZED FERRITIN; ENDOCYTOSIS; TRANSEPITHELIAL TRANSPORT; ACID PHOSPHATASE ID NEWBORN RAT; MEMBRANE; CELLS AB The fate of cationized ferritin (CF) injected into the endolymphatic space of the endolymphatic sac was observed by transmission electron microscopy. At 10 min after the injection, CF particles bound to the apical plasma membrane of epithelial cells of the sac and were then endocytosed with coated pits. However, they never passed through the junctional complexes between the epithelial cells. At 30 min after the injection, the CF particles were transferred to endosomes and lysosomes by small vesicles of 100-150 mm in diameter. CF particles were also found in small vesicles close to Golgi cisternae and in multivesicular bodies. Acid phosphatase positive lysosomes were found close to endosomes containing CF particles. In addition, a small fraction of the small vesicles containing CF particles became inserted into the basolateral plasma membrane. At 60 min after the injection, many CF particles were found in acid phosphatase positive secondary lysosomes. These observations suggest that endocytosis of endolymph is actively performed by the epithelial cells of the sac, and transepithelial vesicular transport across the epithelial cells occurs. C1 KINKI CENT HOSP,DEPT OTOLARYNGOL,ITAMI,HYOGO 664,JAPAN. OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,SUITA,OSAKA 565,JAPAN. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 82 EP 88 DI 10.1016/0378-5955(95)00058-C PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200010 PM 8567425 ER PT J AU SPATZ, WB LOHLE, E AF SPATZ, WB LOHLE, E TI CALCIUM-BINDING PROTEINS IN THE SPIRAL GANGLION OF THE MONKEY, CALLITHRIX-JACCHUS SO HEARING RESEARCH LA English DT Article DE MARMOSET; POSTNATAL DEVELOPMENT; CALBINDIN; CALRETININ; PARVALBUMIN; IMMUNOHISTOCHEMISTRY ID RAT NERVOUS-SYSTEM; LATERAL GENICULATE-NUCLEUS; GUINEA-PIG COCHLEA; INNER-EAR; PARVALBUMIN IMMUNOREACTIVITY; CYTOCHROME-OXIDASE; HAIR-CELLS; CALRETININ; NEURONS; LOCALIZATION AB Calcium-binding proteins can act as intermediaries between changing levels of free intracellular calcium ions and the physiological response of neurons. Some of these proteins, among them calbindin (CB), calretinin (CR) and parvalbumin (PV), can act as calcium buffers. A survey of previous studies in rodents and human fetuses leads to the impression that many spiral ganglion cells co-express CB, CR, and PV. The findings of the present study suggest that, in the adult marmoset, the expression of CB is restricted to a small number of cells, most likely type II ganglion cells, and that at least some of the numerous type I ganglion cells co-express CR and PV. In the neonate marmoset, large numbers of putative type I ganglion cells from the apical cochlear turn transiently expressed a light and granular labeling for CB-like immunoreactivity, in addition to the cells we believe to be type II ganglion cells exhibiting a strong and solid CB-like staining. The spiral ganglion cells in all developmental stages co-expressed the mitochondrial enzyme cytochrome oxidase. 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PD JUN PY 1995 VL 86 IS 1-2 BP 89 EP 99 DI 10.1016/0378-5955(95)00059-D PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200011 PM 8567426 ER PT J AU KNIPPER, M ZIMMERMANN, U KOPSCHALL, I ROHBOCK, K JUNGLING, S ZENNER, HP AF KNIPPER, M ZIMMERMANN, U KOPSCHALL, I ROHBOCK, K JUNGLING, S ZENNER, HP TI IMMUNOLOGICAL IDENTIFICATION OF CANDIDATE PROTEINS INVOLVED IN REGULATING ACTIVE SHAPE CHANGES OF OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; MOTILITY; ANION EXCHANGER; PROTEIN 4.1; SPECTRIN; ANKYRIN ID HUMAN-ERYTHROCYTE-MEMBRANE; AUDITORY SENSORY CELLS; GUINEA-PIG COCHLEA; CYTOPLASMIC DOMAIN; CORTICAL LATTICE; MOTILE RESPONSES; STRUCTURAL BASIS; ANION-EXCHANGER; BAND-3 PROTEIN; LENGTH CHANGES AB By employing immunological methods, it has been demonstrated that myosin, myosin light chain (MLC) and myosin light chain kinase (MLCK) proteins in outer hair cells (OHC) are immunologically different from isoforms in platelets, smooth muscle and heart muscle, and are probably more related to isoforms found in red blood cells (RBC). Moreover, proteins related to band 3 protein (b3p) and protein 4.1 (p 4.1), ankyrin as well as fodrin and spectrin, but not glycophorin, have been identified in isolated OHCs. Both OHCs and RBC differ from other motile non-muscle cells in their lack of smooth muscle isoforms of actin, their common high levels of spectrin-, ankyrin- and band 3-like proteins, as well as the expression of the 80 kDa protein 4.1 isoform. The data support the notion that motility of OHC may be based upon regulation of the b3p/p 4.1/ankyrin complex, and thus may be reminiscent to the active shape changes in RBC. RP KNIPPER, M (reprint author), UNIV TUBINGEN,CTR HEARING RES,DEPT OTOLARYNGOL,RONTGENWEG 11,D-72076 TUBINGEN,GERMANY. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 100 EP 110 DI 10.1016/0378-5955(95)00060-H PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200012 PM 8567407 ER PT J AU OGATA, Y SLEPECKY, NB AF OGATA, Y SLEPECKY, NB TI IMMUNOCYTOCHEMICAL COMPARISON OF POSTTRANSLATIONALLY MODIFIED FORMS OF TUBULIN IN THE VESTIBULAR END-ORGANS OF THE GERBIL - TYROSINATED, ACETYLATED AND POLYGLUTAMYLATED TUBULIN SO HEARING RESEARCH LA English DT Article DE POSTTRANSLATIONAL MODIFICATION; ACETYLATED TUBULIN; TYROSINATED TUBULIN; POLYGLUTAMYLATED TUBULIN; MICROTUBULE; VESTIBULAR END-ORGAN ID CHLAMYDOMONAS ALPHA-TUBULIN; COCHLEAR HAIR-CELLS; GUINEA-PIG ORGAN; DETYROSINATED TUBULIN; SUPPORTING CELLS; SENSORY CELLS; INNER-EAR; HUMAN-NEUTROPHILS; MOTILE RESPONSES; MICROTUBULES AB Specific antibodies against alpha-tubulin, acetylated alpha-tubulin, tyrosinated alpha-tubulin and polyglutamylated alpha- and beta-tubulin were used to compare the distribution of posttranslationally modified tubulin in the vestibular end-organs of the gerbil. Antibodies to acetylated tubulin labeled a dense network of microtubules in the hair cells and bundles of microtubule in the supporting cells. Nerve fibers within and below the epithelium were weakly labeled. This localization paralleled that seen with antibodies to cu-tubulin which labeled all microtubules present in the cells. Antibodies to tyrosinated tubulin labeled networks and bundles of microtubules in both hair cells and supporting cells and in addition gave intense, diffuse labeling in the cytoplasm of both cell types. It also labeled the nerve fibers. Antibodies to polyglutamylated tubulin were localized mainly in nerve fibers, and in the calyces the labeled microtubules were found running circumferentially around the type I sensory hair cells. Thus, tyrosinated tubulin was found in the fine networks of microtubules in both the sensory and supporting cells. Acetylated tubulin was found in the dense networks and bundles of microtubules in the sensory and supporting cells, but did not colocalize with polyglutamylated tubulin, which was found predominantly in the nerve fibers. The labeling patterns for the tyrosinated tubulin and posttranslationally modified tubulins in the sensory and supporting cells of the vestibular end organs differ from that seen in the organ of Corti and may reflect differences in the stability of the microtubules and the mechanical properties of the sensory epithelium. C1 YAMAGUCHI UNIV,SCH MED,DEPT OTOLARYNGOL,UBE,YAMAGUCHI 755,JAPAN. RP OGATA, Y (reprint author), SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13210, USA. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 125 EP 131 DI 10.1016/0378-5955(95)00063-A PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200014 PM 8567409 ER PT J AU GEISLER, CD SANG, CN AF GEISLER, CD SANG, CN TI A COCHLEAR MODEL USING FEEDFORWARD OUTER-HAIR-CELL FORCES SO HEARING RESEARCH LA English DT Article DE COCHLEAR VIBRATIONS; OUTER HAIR CELL; ACTIVE MODEL; COCHLEAR AMPLIFIER ID BASILAR-MEMBRANE MECHANICS; GUINEA-PIG COCHLEA; CHINCHILLA-COCHLEA; FREQUENCY MAP; TUNING CURVES; SUPPRESSION; AMPLIFIER; NONLINEARITY; ENHANCEMENT; RESPONSES AB A linear (frequency-domain) model of the cat cochlea (implemented in both 1- and 2-dimensional versions) has been developed which uses outer hair cell (OHC) forces in a geometry which includes the longitudinal (base-to-apex) tilt of the outer hair cells (OHCs). When positive (contractile) real OHC force-constants are used, very large (50 + dB) response peaks along with very rapidly accumulating phase lags (which can reach -50 pi radians) are obtained, The wider the longitudinal segmentation, the broader the peaks and the less the phase accumulation; 71-mu m segmentation produced the most realistic responses. These large response peaks are achieved by a small zone of negative resistance (ca. 1 mm) just basal to the response peak and the virtual 'zeroing' of the basilar membrane's effective impedance over the entire peak region (ca. 2.5 mm). To produce these peaks, the OHCs generate about 25-times the incoming acoustic power. Inclusion of low-pass filtering in the model's OHC representation produces, by contrast, very unrealistic notch-and-peak displacement complexes accompanied by very large phase lags, for all segmentation widths used. However, when phase reversals of OHC forces are also added, achieved by imbedding a resonant system within the tectorial membrane, very realistic peaks and phase functions are produced. More power must, however, be generated by the OHCs (about 70-times the incoming). The end result is output which mimics quite closely the living basilar membrane's responses to low-intensity high-frequency tones. C1 UNIV WISCONSIN,DEPT ELECT & COMP ENGN,MADISON,WI 53706. RP GEISLER, CD (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,1300 UNIV AVE,MADISON,WI 53706, USA. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 132 EP 146 DI 10.1016/0378-5955(95)00064-B PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200015 PM 8567410 ER PT J AU PARK, JY CLARK, WW COTICCHIA, JM ESSELMAN, GH FREDRICKSON, JM AF PARK, JY CLARK, WW COTICCHIA, JM ESSELMAN, GH FREDRICKSON, JM TI DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN RHESUS (MACACA-MULATTA) MONKEY EARS - NORMATIVE FINDINGS SO HEARING RESEARCH LA English DT Article DE DISTORTION PRODUCT OTOACOUSTIC EMISSIONS; RHESUS MONKEY; NORMATIVE DATA; ANIMAL MODEL ID STIMULATED ACOUSTIC EMISSIONS; 2 DISCRETE SOURCES; AUDITORY-SENSITIVITY; COCHLEAR MECHANICS; PHYSIOLOGICAL VULNERABILITY; NONHUMAN PRIMATE; BASIC FEATURES; NORMAL-HEARING; MUTANT MICE; GUINEA-PIG AB Distortion product otoacoustic emissions (DPOAEs) in rhesus monkeys were characterized and the optimal parameters for their generation were determined. Robust DPOAEs were readily measurable from the ear canals of six rhesus monkeys (n = 12 ears). The nonmonotonic behavior of the f(2)/f(1) ratio functions in rhesus monkeys was found to be similar to other animals and humans. The optimal mean f(2)/f(1) ratio of 1.21 and the effect of the primary frequency and level on the optimal f(2)/f(1) ratios were also similar to human measurements. The contour of the rhesus monkey DPOAE 'audiograms' and their behavior were also comparable to human measurements with slight differences in peak frequencies. The rhesus monkey DPOAE input/output (I/O) functions were generally monotonic with a slope approaching unity with increasing frequency. Therefore, our study shows that many basic DPOAE characteristics are remarkably similar in the two species and emphasizes the appropriateness of the rhesus monkey as a model for DPOAE research. Detailed studies of the behavior of DPOAEs can be carried out in a model that is phylogenetically close to human both in hearing and in the gross structure and histology of the inner ear. C1 WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,ST LOUIS,MO 63110. CENT INST DEAF,ST LOUIS,MO 63110. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 147 EP 162 DI 10.1016/0378-5955(95)00065-C PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200016 PM 8567411 ER PT J AU TRUNE, DR BERG, DM DEGAGNE, JM AF TRUNE, DR BERG, DM DEGAGNE, JM TI COMPUTERIZED DIGITAL PHOTOGRAPHY IN AUDITORY RESEARCH - A COMPARISON OF PUBLICATION-QUALITY DIGITAL PRINTERS WITH TRADITIONAL DARKROOM METHODS SO HEARING RESEARCH LA English DT Article DE EAR; DIGITAL PHOTOGRAPHY; DYE SUBLIMATION PRINTERS; COMPUTERIZED IMAGE PROCESSING AB Digital photography is the rapidly developing field of computer processing of images generated either directly from a digital camera or from scanned conventional film. Subsequent photographs output from digital color printers are publication-quality and superior to conventional darkroom prints because of greater image control (exposure, contrast, color correction). Because final print quality is the most critical factor in the research application of digital photography, we evaluated the photographic output of several continuous-tone digital printers. Digital images from selected microscopic sections of the middle and inner ear were generated by scanning black and white film and Ektachrome color transparencies and sent to commercial representatives for printing. Photographs from some printers were as good or better than traditional darkroom prints of the same film when evaluated for resolution, image quality, and costs. It is our hope that the hearing research field will benefit enormously by adoption of chemical-free digital photography because of its quality, convenience, speed, and low cost. C1 TYCO TOYS INC,VIEW MASTER,PORTLAND,OR. RP TRUNE, DR (reprint author), OREGON HLTH SCI UNIV,OREGON HEARING RES CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,PORTLAND,OR 97201, USA. CR AALAND M, 1992, DIGITAL PHOTOGRAPHY ANDERSON C, 1994, SCIENCE, V263, P317, DOI 10.1126/science.8278802 BERG DM, 1994, ASS RES OT ABSTR, P57 BRESLOW N, 1991, BASIC DIGITAL PHOTOG FRASER B, 1993, MACUSER MAY, V9, P151 FRASER B, 1994, MACUSER APR, V10, P77 FRASER B, 1994, MACUSER NOV, V10, P82 HEID J, 1992, MACWORLD APR, V9, P227 HEID J, 1994, MACWORLD JUL, V11, P106 NEGRINO T, 1992, MACWORLD APR, V9, P136 PERNICIARO C, 1993, MAYO CLIN PROC, V68, P1220 STONE MD, 1992, PC MAGAZINE 1124, V11, P255 TAUBES G, 1994, SCIENCE, V263, P318, DOI 10.1126/science.8278803 NR 13 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 PY 1995 VL 86 IS 1-2 BP 163 EP 170 DI 10.1016/0378-5955(95)00067-E PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200017 PM 8567413 ER PT J AU HARPER, A BLYTHE, WR GROSSMAN, G PETRUSZ, P PRAZMA, J PILLSBURY, HC AF HARPER, A BLYTHE, WR GROSSMAN, G PETRUSZ, P PRAZMA, J PILLSBURY, HC TI IMMUNOCYTOCHEMICAL LOCALIZATION OF ASPARTATE AND GLUTAMATE IN THE PERIPHERAL VESTIBULAR SYSTEM SO HEARING RESEARCH LA English DT Article DE ASPARTATE; GLUTAMATE; VESTIBULAR HAIR CELLS; NEUROTRANSMISSION ID AMINO-ACID RECEPTORS; RAT SPINAL-CORD; GUINEA-PIG; HAIR-CELLS; NEUROTRANSMITTER; CAT; GABA; AMINOTRANSFERASE; NEURONS; RELEASE AB Controversy exists concerning the identity of the neurotransmitter in the mammalian peripheral vestibular system. Several candidates have been proposed, including the excitatory amino acids glutamate and aspartate and the inhibitory amino acid gamma-aminobutyric acid (GABA). Previous studies have demonstrated vestibulonerual electrophysiological activity associated with glutamate and aspartate. Paraffin sections of rat vestibular ganglia and end-organs were examined for the presence of glutamate-like and aspartate-like immunoreactivity. Our results demonstrate the presence of both aspartate-like and glutamate-like immunoreactivity in vestibular hair cells, peripheral vestibular nerve fibers, and vestibular ganglion cells. Minimal immunoreactivity was noted in the tissues surrounding these cells. These data add support to the hypothesis that the excitatory amino acids glutamate and aspartate are involved in vestibular neurotransmission. C1 UNIV N CAROLINA,SCH MED,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC. RP HARPER, A (reprint author), UNIV N CAROLINA,SCH MED,DIV OTOLARYNGOL HEAD & NECK SURG,610 BURNETT WOMACK BLDG,CB 7070,CHAPEL HILL,NC 27599, USA. CR ABDULLAH LH, 1992, NEUROSCIENCE, V51, P729, DOI 10.1016/0306-4522(92)90311-O BOLZ J, 1985, NEUROSCI LETT, V53, P315, DOI 10.1016/0304-3940(85)90557-9 COCHRAN SL, 1989, SYNAPSE, V1, P102 DEMEMES D, 1990, HEARING RES, V46, P261, DOI 10.1016/0378-5955(90)90007-C DEMEMES D, 1984, BRAIN RES, V304, P188, DOI 10.1016/0006-8993(84)90880-1 DEVAU G, 1993, EUR J NEUROSCI, V5, P1210, DOI 10.1111/j.1460-9568.1993.tb00975.x DEWAELE C, 1990, EXP BRAIN RES, V81, P125 DIDIER A, 1990, CELL TISSUE RES, V260, P415, DOI 10.1007/BF00318645 DRESCHER MJ, 1987, BRAIN RES, V417, P39, DOI 10.1016/0006-8993(87)90177-6 DRESCHER MJ, 1992, J NEUROCHEM, V59, P93, DOI 10.1111/j.1471-4159.1992.tb08879.x EYBALIN M, 1993, PHYSIOL REV, V73, P309 FONNUM F, 1984, J NEUROCHEM, V42, P1, DOI 10.1111/j.1471-4159.1984.tb09689.x GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HEPLER JR, 1988, J HISTOCHEM CYTOCHEM, V36, P13 JESSELL TM, 1986, J EXP BIOL, V124, P239 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 KUMOI K, 1987, BRAIN RES, V416, P22, DOI 10.1016/0006-8993(87)91492-2 LOPEZ I, 1992, BRAIN RES, V589, P341, DOI 10.1016/0006-8993(92)91297-R LOPEZ I, 1990, BRAIN RES, V530, P170, DOI 10.1016/0006-8993(90)90677-4 MEZA G, 1992, ANN NY ACAD SCI, V656, P943, DOI 10.1111/j.1749-6632.1992.tb25302.x MONAGHAN DT, 1989, ANNU REV PHARMACOL, V29, P365 NAKANISHI S, 1992, SCIENCE, V258, P597, DOI 10.1126/science.1329206 ORDRONNEAU P, 1981, J HISTOCHEM CYTOCHEM, V29, P1397 PETRUSZ P, 1990, BRAIN RES, V529, P339, DOI 10.1016/0006-8993(90)90848-6 PETRUSZ P, 1975, HISTOCHEMISTRY, V46, P9, DOI 10.1007/BF02463558 PRIGIONI I, 1990, HEARING RES, V46, P253, DOI 10.1016/0378-5955(90)90006-B RAYMOND J, 1984, EXP BRAIN RES, V56, P523 RAYMOND J, 1988, PROG BRAIN RES, V76, P29 ROSS CD, 1985, J HISTOCHEM CYTOCHEM, V33, P624 RUSTIONI A, 1992, HYPERALGESIA ALLODYN, P267 SHUPLIAKOV O, 1993, EXP BRAIN RES, V96, P404 TANAKA M, 1990, EUR ARCH OTO-RHINO-L, P119 VACCA LL, 1980, J HISTOCHEM CYTOCHEM, V28, P297 VALLI P, 1985, BRAIN RES, V330, P1, DOI 10.1016/0006-8993(85)90002-2 WALBERG F, 1990, EXP BRAIN RES, V79, P547 WIET GJ, 1990, ANN OTO RHINOL LARYN, V99, P353 ZUCCA G, 1992, HEARING RES, V63, P52, DOI 10.1016/0378-5955(92)90073-V NR 37 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 JUN PY 1995 VL 86 IS 1-2 BP 171 EP 182 DI 10.1016/0378-5955(95)00068-F PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200018 PM 8567414 ER PT J AU YAO, XF BUHI, WC ALVAREZ, IM CURTIS, LM RAREY, KE AF YAO, XF BUHI, WC ALVAREZ, IM CURTIS, LM RAREY, KE TI DE-NOVO SYNTHESIS OF GLUCOCORTICOID HORMONE-REGULATED INNER-EAR PROTEINS IN RATS SO HEARING RESEARCH LA English DT Article DE COCHLEA; 2D-SDS-PAGE; GLUCOCORTICOIDS; PROTEINS; RAT ID RECEPTOR AB Changes of rat inner ear de novo protein synthesis in response to dexamethasone (DEX), a synthetic glucocorticoid, have been analyzed by high resolution two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis (2D-SDS-PAGE) and fluorography. Two proteins (M(r) 41 000 and 35 000) were amplified and one protein (M(r) 47 000) was suppressed by DEX in a cochlear culture medium, In the culture medium conditioned by vestibular tissue, three proteins (M(r) 67 000, 57 000 and 50 000) were amplified after DEX administration. In cochlear and vestibular tissues, glucocorticoid-responsive protein synthesis was down-regulated by DEX, including two proteins (M(r) 39 000 and 35 000) in the cochlea and five proteins (M(,) 80 000, 64 000, 59 000, 56 000 and 40 000) in the vestibule. The regulation of these inner ear proteins by DEX suggests that glucocorticoid may play an important role in normal inner ear microhomeostasis, as well as in the treatment of some inner ear disorders. C1 UNIV FLORIDA,J HILLIS MILLER HLTH CTR,COLL MED,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT OBSTET & GYNECOL,GAINESVILLE,FL 32610. CR Baxter J.D., 1979, GLUCOCORTICOID HORMO, P1 BUHI WC, 1992, J EXP ZOOL, V262, P426, DOI 10.1002/jez.1402620409 CURTIS LM, 1993, EUR ARCH OTO-RHINO-L, V250, P265 ELLIS D, 1988, IN VITRO CELL DEV B, V24, P811 HAMILTON JA, 1981, ARTHRITIS RHEUM, V24, P1296, DOI 10.1002/art.1780241010 IVARIE RD, 1978, CELL, V13, P41, DOI 10.1016/0092-8674(78)90136-8 MIESFELD R, 1986, CELL, V46, P389, DOI 10.1016/0092-8674(86)90659-8 MULDOON TG, 1986, ENDOCR REV, V1, P339 PITOVSKI DZ, 1994, HEARING RES, V77, P216, DOI 10.1016/0378-5955(94)90269-0 RAREY KE, 1993, HEARING RES, V64, P205, DOI 10.1016/0378-5955(93)90007-N RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 ROBERTS RM, 1984, MOL CHEM CHARACTERIZ, P61 SHEA JJ, 1988, INSTRUCTIONAL COURSE, P219 SHEA JJ, 1993, AM J OTOL, V14, P224 TENCATE WJF, 1993, LARYNGOSCOPE, V103, P865 VASSALLI JD, 1978, CELL, V8, P271 NR 16 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 JUN PY 1995 VL 86 IS 1-2 BP 183 EP 188 DI 10.1016/0378-5955(95)00069-G PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200019 PM 8567415 ER PT J AU BROWN, JN MILLER, JM NUTTALL, AL AF BROWN, JN MILLER, JM NUTTALL, AL TI AGE-RELATED-CHANGES IN COCHLEAR VASCULAR CONDUCTANCE IN MICE SO HEARING RESEARCH LA English DT Article DE LASER DOPPLER FLOWMETRY; PRESBYCUSIS; SODIUM NITROPRUSSIDE ID GUINEA-PIGS; RAT; PRESBYCUSIS; RABBIT AB Vascular changes contribute to age-related hearing loss but the mechanisms involved in microvascular reactivity, particularly in the aged ear, are still incompletely understood. In this study, possible age-related changes in cochlear blood flow (CBF) and vascular reactivity were studied in presbycusic mice (C57BL/6) and young, age-matched, and old controls (CBA/J) without presbycusis. Reactivity was monitored by laser Doppler flowmetry and assessed by change in cochlear vascular conductance (VC) (defined as the ratio of CBF to blood pressure) in response to round window-applied sodium nitroprusside, a vasodilating agent. Mean VC response of C57BL/6 mice differed from controls both in maximum response and in post-drug recovery time. In C57BL/6 mice, mean VC increased about 28%, in contrast to an increase of over 40% in young and age-matched CBA/J controls. A less elevated VC response, similar to that of the presbycusic mice, was shown by aged (20-21 month) controls. Also, VC response in C57BL/6 mice was sustained throughout the 60 min observation period, while response of most CBA/J controls recovered in 50 min or less. These changes suggest age-dependent, pathologically-related altered responsiveness in cochlear vascular reactivity. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR BARILAN A, 1980, PFLUG ARCH EUR J PHY, V384, P93, DOI 10.1007/BF00589520 BROWN JN, 1989, LAB ANIM SCI, V39, P142 CAVAZZUTI M, 1987, J CEREBR BLOOD F MET, V7, P806 CHOLE RA, 1983, AUDIOLOGY, V22, P384 COX RH, 1977, AM J PHYSIOL, V233, pH256 FLEISCH JH, 1971, BRIT J PHARMACOL, V42, P311 FLEISCH JH, 1976, CIRC RES, V38, P243 GREEN C J, 1975, Laboratory Animals (London), V9, P161, DOI 10.1258/002367775780994574 GREEN CJ, 1979, ANIMAL ANESTHESIA HAYASHI S, 1978, BRIT J PHARMACOL, V64, P229 HENRY KR, 1980, AUDIOLOGY, V19, P369 OHLSEN KA, 1992, HEARING RES, V58, P19, DOI 10.1016/0378-5955(92)90004-7 SCHLAGER G, 1966, NATURE, V212, P519, DOI 10.1038/212519a0 SCHNERSON A, 1981, DEV BRAIN RES, V2, P65 SCHUKNECHT HF, 1993, ANN OTO RHINOL LARYN, V102, P1 SHONE G, 1991, HEARING RES, V56, P173, DOI 10.1016/0378-5955(91)90167-8 STEVENSON NR, 1988, MICROVASC RES, V35, P278, DOI 10.1016/0026-2862(88)90082-9 WILLOTT JF, 1988, HEARING RES, V37, P15, DOI 10.1016/0378-5955(88)90074-3 WRIGHT JL, 1972, ARCHIV OTOLARYNGOL, V96, P16 NR 19 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1995 VL 86 IS 1-2 BP 189 EP 194 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200020 PM 8567416 ER PT J AU CHURCH, MW KALTENBACH, JA BLAKLEY, BW BURGIO, DL AF CHURCH, MW KALTENBACH, JA BLAKLEY, BW BURGIO, DL TI THE COMPARATIVE EFFECTS OF SODIUM THIOSULFATE, DIETHYLDITHIOCARBAMATE, FOSFOMYCIN AND WR-2721 ON AMELIORATING CISPLATIN-INDUCED OTOTOXICITY SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE (ABR); CANCER THERAPY; CHEMO-PROTECTION; CISPLATIN; DIETHYLDITHIOCARBAMATE; FOSFOMYCIN; HAMSTER; NEUROPATHY; OTOTOXICITY; SODIUM THIOSULFATE; WR-2721 ID HIGH-DOSE CISPLATIN; BRAIN-STEM; HEARING-LOSS; RESPONSES; PROTECTION; RESCUE; MOUSE; TRIAL; RAT AB The efficacies of four agents in ameliorating cisplatin-induced ototoxicity were investigated. Hamsters were given a series of 5 cisplatin injections (3 mg/kg/injection once every other day, i.p.) either alone or in combination with 1600 mg/kg/injection sodium thiosulfate (STS), 300 mg/kg/injection diethyldithiocarbamate (DDTC), 18 mg/kg/injection WR-2721, or 300 mg/kg/injection fosfomycin (n = 10/group). Ototoxicity was assessed electrophysiologically by auditory brainstem responses (ABRs) and anatomically by cochlear histology. The greatest auditory protection was given by STS, followed by DDTC. WR-2721 and fosfomycin did not provide any protection. All of the animals in the STS and DDTC groups survived, while some fatalities occurred in the fosfomycin, WR-2721, and cisplatin-only groups. Thus, the agents that were protective against ototoxicity were also protective against mortality. The ABRs also provided evidence of cisplatin-induced neuropathy. In summary, STS and DDTC hold promise for ameliorating the ototoxic effects of cisplatin chemotherapy and the hamster proved to be an excellent model of cisplatin ototoxicity. C1 WAYNE STATE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DETROIT,MI. WAYNE STATE UNIV,SCH MED,DEPT AUDIOL,DETROIT,MI. WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL,DETROIT,MI. 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Res. PD JUN PY 1995 VL 86 IS 1-2 BP 195 EP 203 DI 10.1016/0378-5955(95)00066-D PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RM842 UT WOS:A1995RM84200021 PM 8567417 ER PT J AU ZHANG, MS ZWISLOCKI, JJ AF ZHANG, MS ZWISLOCKI, JJ TI OHC RESPONSE RECRUITMENT AND ITS CORRELATION WITH LOUDNESS RECRUITMENT SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELLS; RESPONSE RECRUITMENT; ACTIVE FEEDBACK; NOISE EXPOSURE ID OUTER HAIR-CELLS; COCHLEAR NERVE-FIBERS; GUINEA-PIG COCHLEA; INTRACELLULAR-RECORDINGS; TUNING CURVES; SALICYLATE; ELECTROMOTILITY; POTENTIALS; EARS AB After proper noise exposure, Hensen's cells, which have been shown to follow closely the response characteristics of the outer hair cells, suffered a loss of sensitivity at low and moderate SPLs. The lower the stimulus level, the greater was the loss. When the low-SPL loss did not exceed about 40 dB, input-output functions showed an increased rate of amplitude growth, so that the post-exposure response caught up with its pre-exposure counterpart between 60 and 90 dB SPL, depending on the severity of the loss. These results, together with preceding clinical observations, led us to the conclusion that loudness recruitment occurs at least in part at the hair cell level and is basically a local event as opposed to a pathological spread of excitation. The response recruitment we have discovered appears to result from a decreased effect of the active feedback when the passive cochlear mechanisms are intact. Evidence for these relationships is presented and an explanation is offered for previous experimental successes and failures in observing a steepening of rate-intensity functions in auditory nerve fibers after noise exposures or administration of ototoxic drugs. C1 SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244. SYRACUSE UNIV,DEPT BIOENGN,SYRACUSE,NY 13244. CR DALLOS P, 1992, J NEUROSCI, V12, P4575 DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 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 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P409 EVANS EF, 1975, AUDIOLOGY, V14, P419 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P385 HALLPIKE CS, 1967, SENSORINEURAL HEARIN, P489 HELLMAN RP, 1970, J ACOUST SOC AM, V48, P500, DOI 10.1121/1.1912164 HENDERSON D, 1982, PERSONAL HEARING PRO JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1505, DOI 10.1121/1.392045 Moxon EC, 1970, SENSORINEURAL HEARIN OESTERLE EC, 1989, J ACOUST SOC AM, V86, P1013, DOI 10.1121/1.398092 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 RUGGERO MA, 1990, MECHANICS BIOPHYSICS, P314 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SHEHATA WE, 1991, ACTA OTO-LARYNGOL, V111, P707, DOI 10.3109/00016489109138403 STILLMAN JA, 1993, J ACOUST SOC AM, V93, P425, DOI 10.1121/1.405622 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E THORNTON AR, 1980, J ACOUST SOC AM, V67, P638, DOI 10.1121/1.383888 VEIMEISTER VF, 1974, J ACOUST SOC AM, V56, P1594 ZENG FG, 1990, THESIS SYRACUSE U ZHANG M, 1992, ARO ABSTR, V15, P18 ZHANG M, 1993, THESS SYRACUSE U SYR ZWISLOCKI JJ, 1991, ACTA OTO-LARYNGOL, V111, P256, DOI 10.3109/00016489109137384 ZWISLOCKI JJ, 1988, NATO ADV RES WORKS A, V164, P163 ZWISLOCKI JJ, 1986, P NOBEL S, V63, P155 ZWISLOCKI JJ, 1990, MECH BIOPHYSICS HEAR, P114 ZWISLOCKI JJ, 1992, HEARING RES, V57, P175, DOI 10.1016/0378-5955(92)90150-L ZWISLOCKI LJ, 1986, NATO ASI SERIES A, V119, P3 NR 34 TC 19 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 1995 VL 85 IS 1-2 BP 1 EP 10 DI 10.1016/0378-5955(95)00026-Z PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700001 PM 7559163 ER PT J AU KITANO, I NARIO, K MORI, N MATSUNAGA, T AF KITANO, I NARIO, K MORI, N MATSUNAGA, T TI THE EFFECT OF PROTEIN-KINASE-C STIMULATOR AND INHIBITOR ON COCHLEAR POTENTIALS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE PROTEIN KINASE C; SOUND-EVOKED COCHLEAR POTENTIALS; INNER HAIR CELLS; NEUROTRANSMITTER; NEUROMODULATION ID PHORBOL ESTERS; AGONISTS; CELLS AB To determine a possible role of protein kinase C (PKC) in the cochlea, the effects of a PKC stimulator (phorbol-12-myristate-13-acetate; PMA), an inactive analogue of PKC stimulator (4 alpha-phorbol-12,13-didecanoate; 4 alpha-PDD) and a PKC inhibitor (D-sphingosine) on cochlear potentials were examined in the guinea pig. The perilymphatic perfusion with PMA (3 x 10(-6) M) produced an increase in compound action potential (CAP) amplitude and no change in N-1 latency, the amplitudes of negative summating potential (-SP), cochlear microphonics (CM) and endocochlear potential (EP). The perfusion with 4 alpha-PDD (3 x 1O(-6) M) did not change the sound-evoked cochlear potentials and the EP. The perfusion with D-sphingosine (10(-5) M) produced a decrease in CAP amplitude and no change in N-1 latency and the amplitudes of -SP, CM and EP. The results suggest that PKC may be involved in the mechanism underlying the CAP generation. C1 KAGAWA MED SCH,DEPT OTOLARYNGOL,KAGAWA 76107,JAPAN. RP KITANO, I (reprint author), NARA MED UNIV,DEPT OTOLARYNGOL,840 SHIJO CHO,KASHIHARA,NARA 634,JAPAN. CR CASTAGNA M, 1982, J BIOL CHEM, V257, P7847 COLING DE, 1991, HEARING RES, V57, P113, DOI 10.1016/0378-5955(91)90080-S GERARD C, 1986, J CLIN INVEST, V77, P61, DOI 10.1172/JCI112302 HVALBY O, 1988, EXP BRAIN RES, V71, P588, DOI 10.1007/BF00248751 NISHIZUKA Y, 1986, SCIENCE, V233, P305, DOI 10.1126/science.3014651 NISHIZUKA Y, 1988, NATURE, V334, P661, DOI 10.1038/334661a0 RYU SH, 1990, J BIOL CHEM, V265, P17941 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SCORNIK F, 1990, BRAIN RES, V525, P280, DOI 10.1016/0006-8993(90)90875-C STERKERS O, 1988, PHYSIOL REV, V68, P1083 TACHIBANA M, 1987, HEARING RES, V26, P171, DOI 10.1016/0378-5955(87)90109-2 TERBUSH DR, 1986, J BIOL CHEM, V261, P7099 TOUNY SE, 1990, J BIOL CHEM, V265, P16437 Yanagisawa K, 1988, Prog Brain Res, V74, P313 NR 14 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1995 VL 85 IS 1-2 BP 11 EP 17 DI 10.1016/0378-5955(95)00027-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700002 PM 7559166 ER PT J AU NUMMELA, S AF NUMMELA, S TI SCALING OF THE MAMMALIAN MIDDLE-EAR SO HEARING RESEARCH LA English DT Article DE ALLOMETRY; ISOMETRY; MIDDLE EAR OSSICLES; TYMPANIC MEMBRANE; FUNCTIONAL ANATOMY; MAMMALS ID ELEPHANT ELEPHAS-MAXIMUS; HEARING; SOUND; CALLS AB This study considers the general question how animal size limits the size and information receiving capacity of sense organs. To clarify this in the case of the mammalian middle ear, I studied 63 mammalian species, ranging from a small bat to the Indian elephant. I determined the skull mass and the masses of the ossicles malleus, incus and stapes (M, I and S), and measured the tympanic membrane area, A(1). The ossicular mass (in mg) is generally negatively allometric to skull mass (in g), the regression equation for the whole material (excluding true seals) being y = 1.373 X(0.513). However, for very small mammals the allometry approaches isometry. Within a group of large mammals no distinct allometry can be discerned. The true seals (Phocidae) are exceptional by having massive ossicles. The size relations within the middle ear are generally rather constant. However, the I/M relation is slightly positively allometric, y = 0.554 X(1.162). TWO particularly isometric relations were found; the S/(M + I) relation for the ossicles characterized by the regression equation y = 0.054 X(0.993), and the relation between a two-dimensional measure of the ossicles and the tympanic membrane area, (M + I)(2/3)/A(1). As in isometric ears the sound energy collected by the tympanic membrane is linearly related to its area, the latter isometry suggests that, regardless of animal size, a given ossicular cross-sectional area is exposed to a similar sound-induced stress. Possible morphological middle ear adaptations to particular acoustic environments are discussed. RP NUMMELA, S (reprint author), HELSINKI UNIV,DEPT ZOOL,POB 17 P RAUTATIEKATU 13,SF-00014 HELSINKI,FINLAND. CR AITKIN LM, 1982, BRAIN BEHAV EVOLUT, V21, P49, DOI 10.1159/000121616 BIEWENER AA, 1982, J EXP BIOL, V98, P289 COHEN YE, 1992, HEARING RES, V62, P187, DOI 10.1016/0378-5955(92)90185-P Cooper CF, 1928, PHILOS T R SOC LON B, V216, P265, DOI 10.1098/rstb.1928.0005 Daniel H.J. 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M., 1982, THESIS U CHICAGO ROSOWSKI JJ, 1991, ZOOL J LINN SOC-LOND, V101, P131, DOI 10.1111/j.1096-3642.1991.tb00890.x SAUNDERS JC, 1982, J COMP PHYSIOL, V146, P517 SCHOBER W, 1989, GUIDE BATS BRIT EURO SEGALL W, 1973, ACTA ANAT, V86, P96 SHOSHANI J, 1982, ELEPHAS MAXIMUS MAMM SOLNTSEVA G N, 1975, Zoologicheskii Zhurnal, V54, P1529 Spector WS, 1956, HDB BIOL DATA STROGANOV SU, 1945, J MAMMAL, V26, P412, DOI 10.2307/1375161 VRETTAKOS PA, 1988, AM J OTOLARYNG, V9, P58, DOI 10.1016/S0196-0709(88)80009-7 Wever EG, 1954, PHYSL ACOUSTICS WILKIE HC, 1929, P ZOOL SOC LOND, P61 WILKIE HC, 1925, P ZOOL SOC, P1283 NR 39 TC 65 Z9 67 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1995 VL 85 IS 1-2 BP 18 EP 30 DI 10.1016/0378-5955(95)00030-8 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700003 PM 7559173 ER PT J AU HEMILA, S NUMMELA, S REUTER, T AF HEMILA, S NUMMELA, S REUTER, T TI WHAT MIDDLE-EAR PARAMETERS TELL ABOUT IMPEDANCE MATCHING AND HIGH-FREQUENCY HEARING SO HEARING RESEARCH LA English DT Article DE ISOMETRY; OSSICLE INERTIA; TRANSFORMER RATIO; COCHLEAR ACOUSTIC IMPEDANCE; MAMMALS ID INPUT IMPEDANCE AB Acoustic energy enters the mammalian cochlea aided by an anatomical impedance matching performed by the middle ear. The purpose of this paper is to analyse the functional consequences of changes in scale of the middle ear when going from the smallest mammals to the largest. Our anatomical measurements in mammals of different sizes ranging from bats to elephants indicate that middle ear proportions are largely isometric. Thus the calculated transformer ratio is basically independent of animal size, a typical value lying between 30 and 80. Similarly, the calculated specific acoustic input impedance of the inner ear is independent of animal size, the average value being about 140 kPa s/m. We show that if the high frequency hearing limit of isometric ears is limited by ossicle inertia, it should be inversely proportional to the cubic root of the ossicular mass. This prediction is in reasonable agreement with published audiogram data. We then present a three-parameter model of the middle ear where some obvious deviations from perfect isometry are taken into account. The high frequency hearing limits of different species generally agree well with the predictions of this simple model. However, the hearing limits of small rodents clearly deviate from the model calculation. We interpret this observation as indicating that the hearing limit towards very high frequencies may be set by cochlear transduction mechanisms. Further we discuss the exceptional high frequency hearing of the cat and the amphibious hearing of seals. C1 HELSINKI UNIV TECHNOL,PHYS LAB,SF-02150 ESPOO,FINLAND. UNIV HELSINKI,DEPT ZOOL,SF-00100 HELSINKI,FINLAND. CR BARANY E, 1938, ACTA OTOLARYNGOLOG S, V26 DECORY L, 1989, THESIS U BORDEAUX 2 Evans E, 1982, SENSES, P239 Fay R. 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J., 1986, PERIPHERAL AUDITORY, P3 ROSOWSKI JJ, 1991, ZOOL J LINN SOC-LOND, V101, P131, DOI 10.1111/j.1096-3642.1991.tb00890.x SAUNDERS JC, 1982, J COMP PHYSIOL, V146, P517 von Bekesy G., 1941, AKUST Z, V6, P1 VOSS SE, 1994, J ACOUST SOC AM, V95, P372, DOI 10.1121/1.408329 ZWISLOCKI J., 1962, JOUR ACOUSTICAL SOC AMER, V34, P1514, DOI 10.1121/1.1918382 Zwislocki J. J., 1975, NERVOUS SYSTEM, P45 NR 36 TC 60 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 MAY PY 1995 VL 85 IS 1-2 BP 31 EP 44 DI 10.1016/0378-5955(95)00031-X PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700004 PM 7559177 ER PT J AU KING, C MCGEE, T RUBEL, EW NICOL, T KRAUS, N AF KING, C MCGEE, T RUBEL, EW NICOL, T KRAUS, N TI ACOUSTIC FEATURES AND ACOUSTIC CHANGE ARE REPRESENTED BY DIFFERENT CENTRAL PATHWAYS SO HEARING RESEARCH LA English DT Article DE INTERAURAL PHASE DIFFERENCE; BINAURAL PROCESSING; AUDITORY EVOKED POTENTIALS; MISMATCH NEGATIVITY; PRIMARY VS NONPRIMARY PATHWAYS ID MASKING-LEVEL DIFFERENCE; MEDIAL GENICULATE-BODY; MIDDLE LATENCY RESPONSE; MISMATCH NEGATIVITY; INFERIOR COLLICULUS; BINAURAL MASKING; GUINEA-PIG; GENERATING-SYSTEM; SPEECH STIMULI; SINGLE UNITS AB The central processing of acoustic stimulus changes can be observed neurophysiologically in the mismatch negativity auditory evoked potential (MMN). Stimuli differing in interaural phase were used to investigate the contributions of the primary and non-primary auditory pathways to the encoding of binaural stimuli and to investigate passively elicited measures of binaural processing in experimental animals. In guinea pigs, the MMN was obtained in response to 1000 Hz tones embedded in white noise (S:N = 2 dB). Using a modified oddball paradigm (that is, two stimuli presented in a series, each with a different probability of occurrence), stimuli were presented binaurally with both the tone and noise in-phase to the two ears (S0N0) as the standard stimulus and the tone 180 degrees out-of-phase (SPiN0) as the deviant stimulus. The MMN, by definition, should occur only in response to a change, or 'mismatch,' between the standard and deviant stimuli. The response to the deviant stimulus in the oddball paradigm was compared to the response to the same stimulus when presented in a series alone. The responses to S0N0 and SPiN0 collected in a series alone, termed the intrinsic responses, were also compared. Responses were recorded from two surface epidural electrodes - one at the posterior midline and one over the left temporal lobe. AEPs from these locations have been shown to reflect the activity of primary and non-primary thalamo-cortical pathways respectively. A significant MMN was observed at the midline electrode, but no MMN was observed over the temporal lobe. However, there was a significant difference in the intrinsic responses to the two stimuli over the temporal lobe while no difference in the intrinsic responses was seen over the midline. The results suggest that the primary and non-primary auditory pathways appear to provide distinctly different contributions to the encoding of changes in binaural phase. Additionally, the MMN to stimuli differing in interaural phase can be obtained in anesthetized animals and may provide a useful measure of binaural processing. C1 UNIV WASHINGTON,DEPT OTOLARYNGOL,SEATTLE,WA 98195. NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL,EVANSTON,IL 60208. NORTHWESTERN UNIV,DEPT OTOLARYNGOL,CHICAGO,IL 60611. RP KING, C (reprint author), NORTHWESTERN UNIV,DEPT COMMUN SCI & DISORDERS,AUDITORY NEUROSCI LAB,FRANCES SEARLE BLDG,EVANSTON,IL 60208, USA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 45 EP 52 DI 10.1016/0378-5955(95)00028-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700005 PM 7559178 ER PT J AU FRISINA, RD ZETTEL, ML KELLEY, PE WALTON, JP AF FRISINA, RD ZETTEL, ML KELLEY, PE WALTON, JP TI DISTRIBUTION OF CALBINDIN D-28K IMMUNOREACTIVITY IN THE COCHLEAR NUCLEUS OF THE YOUNG-ADULT CHINCHILLA SO HEARING RESEARCH LA English DT Article DE HEARING; IMMUNOCYTOCHEMISTRY; COCHLEAR NUCLEUS; CALBINDIN; AUDITORY SYSTEM; CHINCHILLA ID CALCIUM-BINDING PROTEIN; VESTIBULAR HAIR-CELLS; INFERIOR COLLICULUS; AUDITORY-SYSTEM; NERVOUS-SYSTEM; IMMUNOCYTOCHEMICAL DETECTION; NEURONAL ARCHITECTURE; AMPLITUDE-MODULATION; SPEECH-PERCEPTION; CARTWHEEL NEURONS AB Calbindin is a 28 kD calcium-binding protein found in neural tissue. Although its functional role in nerve cell physiological processing is still uncertain, previous investigations have suggested that because of its intracellular calcium buffering and regulation properties, it could influence temporal precision of neuronal firing to subserve temporal processing in the auditory brainstem, or could mediate monaural versus binaural coding, or be involved in synaptic plasticity (learning). The present study demonstrates differential calbindin immunoreactivity in the cochlear nuclear complex of the chinchilla, a rodent with exceptionally good low-frequency hearing. The most intense labeling in the cochlear nucleus was in somata of cartwheel and fusiform cells of the fusiform cell layer, and somata and processes of the molecular layer of the dorsal cochlear nucleus (DCN). Only a relatively few scattered neurons were stained in the deep layers of DCN. In contrast, moderate labeling of neurons and neuropil throughout the ventral cochlear nucleus was seen. For instance, moderately stained spherical and elongate cells of the anteroventral cochlear nucleus were observed in contact with labeled puncta and amidst stained fibers. In the cochlear nerve root region, stained auditory nerve fibers and globular cells were noted. In the posteroventral cochlear nucleus, principal cells of elongate and octopus shape were observed, in contact with labeled swellings and surrounded by labeled neuropil. C1 UNIV NEW MEXICO,DIV OTOLARYNGOL HEAD & NECK SURG,ALBUQUERQUE,NM 87131. RP FRISINA, RD (reprint author), UNIV ROCHESTER,SCH MED & DENT,DEPT PHYSIOL,DEPT SURG,DIV OTOLARYNGOL,601 ELMWOOD AVE,ROCHESTER,NY 14642, USA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 53 EP 68 DI 10.1016/0378-5955(95)00029-4 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700006 PM 7559179 ER PT J AU WOODS, DL ALAIN, C COVARRUBIAS, D ZAIDEL, O AF WOODS, DL ALAIN, C COVARRUBIAS, D ZAIDEL, O TI MIDDLE LATENCY AUDITORY-EVOKED POTENTIALS TO TONES OF DIFFERENT FREQUENCY SO HEARING RESEARCH LA English DT Article DE AUDITORY; CORTEX; EVOKED POTENTIALS; DISTRIBUTION; TONOTOPY; THALAMUS; ATTENTION; FREQUENCY; DICHOTIC; LATENCY ID MEDIAL GENICULATE-BODY; BINAURAL INTERACTION; TEMPORAL COMPONENTS; SELECTIVE ATTENTION; GENERATOR SYSTEMS; BRAIN-STEM; RESPONSES; CORTEX; CAT; TOPOGRAPHY AB The scalp distributions of middle latency auditory evoked potentials (MAEPs) elicited by tone bursts of 250 and 4000 Hz were compared in two experiments. Na (19.9 ms), Pa (29.8 ms), and Pb (51.4 ms) components elicited by tones of either frequency had fronto-central distributions, whereas the Nb component (38.4 ms) was maximal at parietal sites. Although the distributions of MAEP components varied as a function of the ear of stimulation, no significant differences were found as a function of tone frequency. The results are consistent with suggestions that MAEPs reflect activation of non-tonotopically organized generators. C1 UNIV CALIF DAVIS,NO CALIF SYST CLIN,CTR NEUROSCI,MARTINEZ,CA 94553. RP WOODS, DL (reprint author), UNIV CALIF DAVIS,NO CALIF SYST CLIN,DEPT NEUROL,CLIN NEUROPHYSIOL LAB,150 MUIR RD,MARTINEZ,CA 94553, USA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 69 EP 75 DI 10.1016/0378-5955(95)00035-3 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700007 PM 7559180 ER PT J AU PFINGST, BE MORRIS, DJ MILLER, AL AF PFINGST, BE MORRIS, DJ MILLER, AL TI EFFECTS OF ELECTRODE CONFIGURATION ON THRESHOLD FUNCTIONS FOR ELECTRICAL-STIMULATION OF THE COCHLEA SO HEARING RESEARCH LA English DT Article DE AUDITORY PROSTHESIS; COCHLEAR IMPLANT; ELECTRICAL STIMULATION; ELECTRODE CONFIGURATION; NONHUMAN PRIMATES; PSYCHOPHYSICS ID PSYCHOPHYSICAL DETECTION THRESHOLDS; AUDITORY-NERVE; PHASE DURATION; IMPLANTS; EXCITATION; PATTERNS; MODEL AB Psychophysical detection threshold vs frequency functions for sinusoidal electrical stimulation of the deafened cochlea were measured in 18 nonhuman primate subjects. Functions for monopolar or widely-spaced (> 2.5 mm) bipolar stimulation were lower and usually had steeper slopes than those for more narrowly-spaced (< 2.0 mm) bipolar stimulation. In 56% of the cases the difference between thresholds for narrowly-spaced bipolar stimulation and more widely-spaced bipolar or monopolar stimulation was greater for low frequency stimuli (63 or 100 Hz) than for high frequency stimuli (800 or 1,000 Hz) by 5 dB or more. Two cases were compared in more detail using pulsatile stimuli. For sinusoidal stimuli, one of these cases showed a moderate frequency dependent effect of electrode configuration and the other did not. The case with the frequency dependent effect of electrode configuration for sinusoids also showed a phase-duration dependent effect of electrode configuration for detection of single biphasic pulses: strength-duration curves (detection threshold in decibels vs pulse duration in ms/phase) were steeper for monopolar stimulation than for narrowly-spaced (0.7 mm) bipolar stimulation. This effect was not seen in the case that showed little or no frequency dependence in the effect of electrode configuration for sinusoidal stimuli. Slopes of threshold vs pulse rate functions where pulse duration was held constant at 2 ms/phase were not affected by electrode configuration in either subject. RP PFINGST, BE (reprint author), UNIV MICHIGAN,MED CTR,DEPT OTOLARYNGOL,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 76 EP 84 DI 10.1016/0378-5955(95)00037-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700008 PM 7559181 ER PT J AU MUNYER, PD SCHULTE, BA AF MUNYER, PD SCHULTE, BA TI DEVELOPMENTAL EXPRESSION OF PROTEOGLYCANS IN THE TECTORIAL AND BASILAR-MEMBRANE OF THE GERBIL COCHLEA SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; BASILAR MEMBRANE; COCHLEAR DEVELOPMENT; PROTEOGLYCANS; GERBIL ID MONOCLONAL-ANTIBODIES; GELATINOUS MEMBRANES; MONGOLIAN GERBIL; INNER-EAR; LOCALIZATION; GLYCOSAMINOGLYCANS; IDENTIFICATION; ULTRASTRUCTURE; ORGANIZATION; FREQUENCY AB The appearance and distribution of specific proteoglycans (PGs) was assessed during development and maturation of the tectorial (TM) and basilar membranes (BM) in the gerbil cochlea. At birth, monoclonal antibodies against keratan sulfate (KSPG) and chondroitin 4- or 6-sulfate (4S CSPG, 68 CSPG) reacted with the upper fibrous layer of the TM with staining for anti-KSPG predominating. Reactivity for 48 CSPG remained constant whereas that for 6S CSPG increased through day 20 when it exceeded that of 48 CSPG. The region of Kollikers organ near the developing tunnel of Corti stained positively with all three PG antibodies from birth through day 8. In contrast, cells in the developing inner spiral sulcus lacked immunoreactive KSPG but expressed CSPG. PGs were first detectable in the BM of the basal turn at day 8 and increased to near adult levels by 16 days after birth. Anti-KSPG again showed the strongest staining with labeling density for 4S and 68 CSPG being about equal at maturity. Staining with all three antibodies was localized along the margins of the BM. Reactivity of the TM and BM in the upper turns lagged behind that of the basal turns by 24-48 h. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 85 EP 94 DI 10.1016/0378-5955(95)00032-Y PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700009 PM 7559182 ER PT J AU MROWINSKI, D GERULL, G NUBEL, K SCHOLZ, G AF MROWINSKI, D GERULL, G NUBEL, K SCHOLZ, G TI MASKING AND PITCH SHIFT OF TONE BURSTS AND CLICKS BY LOW-FREQUENCY TONES SO HEARING RESEARCH LA English DT Article DE LOW TONE MASKING; PITCH SHIFT; ENDOLYMPHATIC HYDROPS ID ENDOLYMPHATIC HYDROPS; MAMMALIAN COCHLEA; MODULATION; SENSITIVITY; POTENTIALS AB From experiments in animals and investigations in humans it is known that the normally phase-dependent masking of a short stimulus by a low-frequency continuous tone does not occur in the case of endolymphatic hydrops. The recording of the masked threshold of short tone stimuli in a loud tone of 30 Hz is to be evaluated for the clinical diagnostics of Meniere's disease. To this purpose, the main parameters of the measurement (type, frequency, duration of the stimulus, and intensity of the masker) and their effect on phase-dependent masking and pitch-shift are investigated. Stimuli above 2 kHz are masked less than those of lower frequencies. Wide-band stimuli are less useful, since only the low-frequency component of their spectrum is masked. The tone stimuli should be short (1 - 2 ms) in order to make the measurement of the phase dependence more accurate. With increasing masker level the masking at phase 0 degrees corresponds to the increase in level, at phase 270 degrees the amount is twice as much. The pitch shift which is perceived in low-tone masking depends on the phase of the stimulus, and on the levels of the stimulus and the masking tone. The use of brain stem recordings in the investigation of phase-dependent low tone masking is problematic since well-synchronizing stimuli with high frequency spectral components are masked poorly. RP MROWINSKI, D (reprint author), FREE UNIV BERLIN,RUDOLF VIRCHOW HOSP,DEPT ENT,AUGUSTENBURGER PL 1,D-13353 BERLIN,GERMANY. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 95 EP 102 DI 10.1016/0378-5955(95)00033-Z PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700010 PM 7559183 ER PT J AU KUROKAWA, T SAITO, H AF KUROKAWA, T SAITO, H TI RETROGRADE AXONAL-TRANSPORT OF DIFFERENT FLUORESCENT TRACERS FROM THE NEOCORTEX TO THE SUPRAGENICULATE NUCLEUS IN THE RAT SO HEARING RESEARCH LA English DT Article DE MOTOR CORTEX; AUDITORY CORTEX; SUPRAGENICULATE NUCLEUS; DOUBLE LABELING METHOD; FLUORESCENT TRACERS; RAT ID MEDIAL GENICULATE-BODY; POSTERIOR THALAMIC NUCLEI; AUDITORY-CORTEX; MOTOR CORTEX; CAT; ORGANIZATION; PROJECTIONS; CONNECTIONS; NEURONS; CYTOARCHITECTURE AB The retrograde fluorescent tracers in a combination of two different dyes (Fluoro gold/Nuclear yellow or Fast blue/Fluoro gold) were used for the study of the projections from the medial geniculate body to the frontal and temporal cortices in rats. There were only single-labeled cells, no double-labeled ones in the medial geniculate body (MGB). The suprageniculate nucleus (SG) was considered to be the origin of the rat direct pathway to the frontal cortex. The present results suggest that projections from the suprageniculate nucleus to the frontal cortex and the temporal cortex consist of separate neuronal groups in the rat MGB and SG. The inputs to the SG from the auditory and oculomotor system may be processed in different ways. RP KUROKAWA, T (reprint author), FUKUI MED SCH,DEPT OTOLARYNGOL,FUKUI 91011,JAPAN. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 103 EP 108 DI 10.1016/0378-5955(95)00034-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700011 PM 7559164 ER PT J AU DAI, HP NGUYEN, QT GREEN, DM AF DAI, HP NGUYEN, QT GREEN, DM TI A 2-FILTER MODEL FOR FREQUENCY DISCRIMINATION SO HEARING RESEARCH LA English DT Article DE FREQUENCY DISCRIMINATION; SPECTRAL-SHAPE DISCRIMINATION; AUDITORY FILTER ID TONES; MODULATION; MECHANISMS; INTENSITY AB In this paper, we explore a two-filter model, the simplest version of multi-channel models for frequency discrimination of simple tones. According to this model, frequency discrimination is based on a change in the relative output levels of two auditory filters, one centered below and the other above the frequency of the tone. This idea can explain the experimental results that frequency discrimination is relatively unaffected by randomization of stimulus level. Moreover, it suggests a close relationship between the ability of listeners to perform frequency discrimination of simple tones and spectral-shape discrimination of two-tone complexes. The ability of three listeners to perform these two tasks was measured at six frequencies (from 0.25 to 8 kHz). The results from the spectral-shape-discrimination task were used to predict frequency-difference limens. There was a high correlation between obtained and predicted values. RP DAI, HP (reprint author), UNIV FLORIDA,DEPT PSYCHOL,PSYCHOACOUST LAB,GAINESVILLE,FL 32611, USA. 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PD MAY PY 1995 VL 85 IS 1-2 BP 109 EP 114 DI 10.1016/0378-5955(95)00036-4 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700012 PM 7559165 ER PT J AU HALLWORTH, R WIEDERHOLD, ML CAMPBELL, JB STEYGER, PS AF HALLWORTH, R WIEDERHOLD, ML CAMPBELL, JB STEYGER, PS TI ATOMIC-FORCE MICROSCOPE OBSERVATIONS OF OTOCONIA IN THE NEWT SO HEARING RESEARCH LA English DT Article DE OTOCONIA; ATOMIC FORCE MICROSCOPE; BIOMINERALIZATION ID INNER-EAR; PROTEIN; BIOMINERALS; AMPHIBIANS; CALCITE AB Calcitic and aragonitic otoconia from the Japanese red-bellied newt, Cynops pyrrhogaster, were examined using an atomic force microscope. The surface structure of both otoconial polymorphs consisted of arrays of elements approximately 50 nm in diameter. Elements were generally round and were separated by shallow depressions of no more than 20 nm. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 115 EP 121 DI 10.1016/0378-5955(95)00038-6 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700013 PM 7559167 ER PT J AU RYBAK, LP WHITWORTH, C MORRIS, C SCOTT, V KANNO, H AF RYBAK, LP WHITWORTH, C MORRIS, C SCOTT, V KANNO, H TI COCHLEAR EFFECTS OF INDACRINONE ARE NOT ALTERED BY PENICILLIN SO HEARING RESEARCH LA English DT Article DE LOOP DIURETICS; ENDOCOCHLEAR POTENTIAL; COMPOUND ACTION POTENTIAL; PENICILLIN OTOTOXICITY ID ETHACRYNIC-ACID; ORGANIC-ACIDS; STRIA VASCULARIS; LOOP DIURETICS; FUROSEMIDE; OTOTOXICITY; CHINCHILLA; ENDOLYMPH; TRANSPORT; PERILYMPH AB Indacrinone is a loop diuretic structurally related to ethacrynic acid. Indacrinone is a racemic mixture. Previous studies have shown that the (-) enantiomer caused reduction of endocochlear potential (EP) and elevation of compound action potential (CAP) threshold (Rybak and Whitworth, 1987a). It has been demonstrated that organic acids such as penicillin, probenecid and sodium salicylate prevent the reduction of EP normally observed after furosemide administration (Rybak et al., 1992a). The present study was designed to determine whether penicillin pretreatment could prevent changes in EP and CAP threshold in (-)-indacrinone treated chinchillas. Adult chinchillas were anesthetized with ketamine and pentobarbital. A microelectrode was advanced into the scala media using the round window approach, and CAP responses to clicks were measured. One group was treated with (-)-indacrinone 100 mg/kg via the jugular vein. A second group of animals received penicillin 50 mg/kg IV thirty minutes before(-)-indacrinone. The mean EP change in the indacrinone-treated animals was 38.38 +/- 19.32 millivolts (my). The reduction of EP in the group receiving penicillin was 24.43 +/- 20.74 mv (P > 0.09). The mean CAP threshold changes in animals receiving indacrinone was 20 +/- 14.14 dB whereas those pretreated with penicillin showed a threshold shift of 21.43 +/- 20.35 dB (P > 0.05). These findings are consistent with previous studies which showed that the effect of ethacrynic acid on the EP and CAP was not changed by the pretreatment with penicillin (Rybak et al., 1990). C1 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,SPRINGFIELD,IL 62794. RP RYBAK, LP (reprint author), SO ILLINOIS UNIV,SCH MED,DEPT SURG,POB 19230,SPRINGFIELD,IL 62794, USA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 122 EP 126 DI 10.1016/0378-5955(95)00039-7 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700014 PM 7559168 ER PT J AU IRVINE, DRF PARK, VN MATTINGLEY, JB AF IRVINE, DRF PARK, VN MATTINGLEY, JB TI RESPONSES OF NEURONS IN THE INFERIOR COLLICULUS OF THE RAT TO INTERAURAL TIME AND INTENSITY DIFFERENCES IN TRANSIENT STIMULI - IMPLICATIONS FOR THE LATENCY HYPOTHESIS SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; LATENCY; INTERAURAL INTENSITY DIFFERENCE; INTERAURAL TIME DIFFERENCE; BINAURAL PROCESSING; EXCITATORY - INHIBITORY NEURONS ID PRIMARY AUDITORY-CORTEX; SOUND PRESSURE LEVEL; CATS SUPERIOR COLLICULUS; OLIVARY COMPLEX LESIONS; KAINIC ACID LESIONS; LATERAL LEMNISCUS; DORSAL NUCLEUS; BINAURAL INTERACTION; FREQUENCY NEURONS; ACOUSTIC STIMULI AB Although the sensitivity to interaural intensity differences (IIDs) of neurons receiving excitatory - inhibitory binaural input (EI neurons) has been examined in numerous studies, the mechanisms underlying this sensitivity remain unclear. According to the 'latency hypothesis', neuronal sensitivity to IIDs reflects sensitivity to differences in the timing of ipsilateraI and contralateral inputs that are produced as a consequence of the effects of intensity upon latency. If the latency hypothesis is correct, a neuron's responses over any given IID range should be predicted by its responses to the interauraI time differences (ITDs) that are 'equivalent' to the IIDs tested, in the sense that they produce the same changes in the relative timing of inputs. This prediction from the latency hypothesis was examined by determining the sensitivity of ET neurons in the inferior colliculus of anesthetized rats to IIDs and ITDs in click stimuli, under conditions that allowed 'equivalent' ITDs to be estimated. In approximately 10% of the 41 neurons tested, the IID-sensitivity function was a perfect or near-perfect match to the equivalent-ITD function, indicating that IID sensitivity could be entirely accounted for in terms of sensitivity to intensity-produced neural time differences, as asserted by the latency hypothesis. For the majority of neurons, however, sensitivity to equivalent ITDs accounted only partially for the characteristics of the IID-sensitivity function; other features of the function in these cases appeared to reflect the operation of an additional factor, most probably the relative magnitude of the inputs from the two ears. Although the conclusions are qualified by the fact that one of the assumptions on which the estimation of equivalent ITDs was based was probably not satisfied for some neurons, the results suggest that intensity-produced changes in both the magnitude and the timing of excitatory and inhibitory inputs shape the IID sensitivity of most EI neurons. RP IRVINE, DRF (reprint author), MONASH UNIV,DEPT PSYCHOL,CLAYTON,VIC 3168,AUSTRALIA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 127 EP 141 DI 10.1016/0378-5955(95)00040-B PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700015 PM 7559169 ER PT J AU KUJAWA, SG FALLON, M BOBBIN, RP AF KUJAWA, SG FALLON, M BOBBIN, RP TI TIME-VARYING ALTERATIONS IN THE F(2)-F(1) DPOAE RESPONSE TO CONTINUOUS PRIMARY STIMULATION .1. RESPONSE CHARACTERIZATION AND CONTRIBUTION OF THE OLIVOCOCHLEAR EFFERENTS SO HEARING RESEARCH LA English DT Article DE OLIVOCOCHLEAR EFFERENTS; OTOACOUSTIC EMISSIONS; OUTER HAIR CELLS; QUADRATIC NONLINEARITY; CUBIC NONLINEARITY ID CONTRALATERAL SOUND; COCHLEAR MECHANICS; HAIR-CELLS; RECEPTOR SHOWS; GUINEA-PIG; DISTORTION; BUNDLE; ADAPTATION; NEURONS; SYSTEM AB The f(2)-f(1) distortion product otoacoustic emission (DPOAE) can be observed to undergo gradual alterations in amplitude during continuous ipsilateral stimulation with primary tones. In the present experiments, we characterized the dependence of these amplitude alterations on several stimulus variables (intensity, duration, frequency) and on DPOAE type (quadratic vs cubic) and tested the hypothesis that such alterations are mediated by the olivocochlear (OC) efferents. Responses were recorded in urethane-anesthetized guinea pigs with sectioned middle ear muscles before and after intracochlear application of antagonists (curare, 1 mu M; bicuculline, 10 mu M; tetrodotoxin, 1 mu M) or before and after OC efferent section at the midline of the floor of the IVth ventricle. We confirm previous reports of continuous stimulation-related alterations in the amplitude of the quadratic distortion product, f(2)-f(1) and report a novel, suppressive 'off-effect' apparent in f(2)-f(1) amplitude following a short rest from such stimulation. Response alterations were sensitive to primary intensity and to duration of rest from continuous stimulation, but were not clearly frequency-dependent over the ranges tested. Corresponding alterations in the amplitude of the cubic nonlinearity, 2f(1)-f(2) were very small or absent. Amplitude alterations in f(2)-f(1) were reduced but not blocked by OC efferent antagonists (curare, bicuculline) and were largely unaffected by TTX or by midline brainstem section. All of these manipulations, however, prevented completely the known efferent-mediated contralateral sound suppression of both f(2)-f(1) and 2f(1)-f(2) DPOAEs. Taken together, these results do not provide support for efferent control of the f(2)-f(1) amplitude alterations observed during continuous ipsilateral stimulation. RP KUJAWA, SG (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES INST,NEW ORLEANS,LA 70112, USA. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 142 EP 154 DI 10.1016/0378-5955(95)00041-2 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700016 PM 7559170 ER PT J AU WU, MI JEN, PHS AF WU, MI JEN, PHS TI RESPONSES OF PONTINE NEURONS OF THE BIG BROWN BAT, EPTESICUS-FUSCUS, TO TEMPORALLY PATTERNED SOUND PULSES SO HEARING RESEARCH LA English DT Article DE BATS; PONTINE NEURONS; PULSE REPETITION RATE; PULSE DURATION ID AUDITORY SPACE REPRESENTATION; FM BAT; INFERIOR COLLICULUS; MYOTIS-LUCIFUGUS; REPETITION RATE; ECHOLOCATING BATS; TARGET DISTANCE; SINGLE NEURONS; CORTEX; SYSTEM AB Under free field stimulation conditions, this study examined the responses of pontine neurons of Eptesicus fuscus to temporally patterned sound pulses by means of repetitive single pulses and pulse trains. Among 93 pontine neurons isolated, 90 always discharged less than 5 impulses to sound pulses presented during this study and 3 discharged impulses throughout the whole duration of each presented pulse. Responses to sound pulses at different repetition rates were examined in 65 neurons. The number of impulses of individual neurons discharged to each pulse varied within a given repetition rate and among different repetition rates. Although these pontine neurons showed different degrees of habituation to high repetition rates, more than 25% could follow the highest repetition rate tested (100 pps). However, they did not always discharge maximal number of impulses to this repetition rate. The total number of impulses discharged by a neuron was also affected by pulse duration. Thus, each pontine neuron discharged maximally to a specific combination of pulse repetition rate and duration. Using a 50% difference between the maximal and minimal responses as a criterion, the response function with respect to repetition rate and duration can be described as band-pass, low-pass, high-pass, all-pass and irregular. These response properties reflect more those of inferior collicular neurons than auditory cortical neurons. This study also showed that response latencies of pontine neurons examined were lengthened by increasing pulse repetition rate and duration. In addition, whereas minimum thresholds of pontine neurons were elevated by increasing repetition rate, they were lowered by increasing pulse duration. C1 UNIV MISSOURI,DIV BIOL SCI,COLUMBIA,MO 65211. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 155 EP 168 DI 10.1016/0378-5955(95)00042-3 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700017 PM 7559171 ER PT J AU PETERS, TA KUIJPERS, W TONNAER, ELGM VANMUIJEN, GNP JAP, PHK AF PETERS, TA KUIJPERS, W TONNAER, ELGM VANMUIJEN, GNP JAP, PHK TI DISTRIBUTION AND FEATURES OF MELANOCYTES DURING INNER-EAR DEVELOPMENT IN PIGMENTED AND ALBINO-RATS SO HEARING RESEARCH LA English DT Article DE MELANOCYTES; DEVELOPMENT; RAT; INNER EAR; ALBINO PIGMENTED ID STRIA VASCULARIS; MONOCLONAL-ANTIBODIES; GUINEA-PIGS; CELLS; MOUSE; LINEAGE; MICE AB In this developmental study, the distribution and features of melanocytes in the inner ear of pigmented and albino rats was investigated with the use of an antibody, which specifically reacts with a melanocyte differentiation antigen present in the membranes of (pre)melanosomes. Melanocyte precursors could be traced from 13 days post conception onwards and the course was followed to their targets in the inner ear. Melanocytes which settle in the modiolus appeared to reach their target along another pathway than strial and vestibular melanocytes. No difference was observed in the melanocyte distribution between pigmented and albino rats. The integration of melanocytes into the stria vascularis was associated with an increased rate of melanosome production in both strains, but in the albinos far fewer melanosomes were produced. After the stria had reached maturity, melanosome production was arrested and melanosomes were subject to lysosomal digestion. In the stria of the pigmented rats, cells with aggregations of disintegrating melanosomes appeared and persisted into adulthood. In the adult, the majority of the intermediate cells contained only a few scattered melanosomes, while melanosomes could only rarely be detected in the albinos. These observations indicate that there is a close relationship between melanosome production and the process of interdigitation of melanocytes with the marginal cells. It seems unlikely that melanosomes or melanin make any important contribution to the function of the adult stria vascularis. Outside the stria, the features of melanocytes in both strains were similar to skin melanocytes. C1 UNIV NIJMEGEN,DEPT OTORHINOLARYNGOL,6500 HB NIJMEGEN,NETHERLANDS. UNIV NIJMEGEN,DEPT PATHOL,NIJMEGEN,NETHERLANDS. UNIV NIJMEGEN,DEPT HISTOL & CELL BIOL,NIJMEGEN,NETHERLANDS. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 169 EP 180 DI 10.1016/0378-5955(95)00043-4 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700018 PM 7559172 ER PT J AU MCFADDEN, D LOEHLIN, JC AF MCFADDEN, D LOEHLIN, JC TI ON THE HERITABILITY OF SPONTANEOUS OTOACOUSTIC EMISSIONS - A TWINS STUDY SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; HERITABILITY; PRENATAL AUDITORY EFFECTS; HEARING SENSITIVITY; SEX DIFFERENCES; EAR DIFFERENCES; TWINS ID OTO-ACOUSTIC EMISSIONS; SEX-DIFFERENCES; COCHLEAR MECHANICS; HAIR-CELLS; HUMAN EARS; FREQUENCY; STIMULATION; HEARING; PREVALENCE; CHILDREN AB Spontaneous otoacoustic emissions (SOAEs) were measured in human monozygrotic (MZ) and dizygotic (DZ) twins and in a sample of non-twins. The number of SOAEs exhibited was more highly correlated in MZ co-twins than in same-sex DZ co-twins. Model-fitting to the correlations suggested that about three-quarters of the individual variation in the expression of SOAEs is attributable to genes. There was no convincing evidence far the heritability of specific SOAE frequencies. In accord with past surveys, SOAEs were more numerous in right than left ears, and in female than male subjects. Also investigated were the numbers of SOAEs exhibited by dark- versus light-eyed people and by MZ versus DZ twins. Those differences in our data were small and not statistically significant, but they were in a direction consistent with other studies: more SOAEs in dark-eyed individuals and in MZ twins. The view presented here is that SOAEs themselves are unlikely objects for natural selection, and probably are epiphenomena resulting from selection for those cochlear mechanisms that contribute to good hearing sensitivity-which is related to SOAE expression. It is argued that, in addition to genetics, other factors have the potential to affect the specific numbers of SOAEs that are expressed. For example, same aspects of the complex prenatal process of producing a male fetus are presumed to be responsible for the smaller number of SOAEs seen in males than females. C1 UNIV TEXAS,INST NEUROSCI,AUSTIN,TX 78712. RP MCFADDEN, D (reprint author), UNIV TEXAS,DEPT PSYCHOL,MEZES HALL 330,AUSTIN,TX 78712, USA. 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PD MAY PY 1995 VL 85 IS 1-2 BP 181 EP 198 DI 10.1016/0378-5955(95)00045-6 PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700019 PM 7559174 ER PT J AU LUCIANO, L REISS, G IURATO, S REALE, E AF LUCIANO, L REISS, G IURATO, S REALE, E TI THE JUNCTIONS OF THE SPINDLE-SHAPED CELLS OF THE STRIA VASCULARIS - A LINK THAT COMPLETES THE BARRIER BETWEEN PERILYMPH AND ENDOLYMPH SO HEARING RESEARCH LA English DT Article DE INDUSTRIAL COMPARTMENT; CELL JUNCTIONS; FILIPIN; CHOLESTEROL; FREEZE-FRACTURE; SCANNING ELECTRON MICROSCOPY ID EPITHELIAL TIGHT JUNCTIONS; HORSERADISH-PEROXIDASE; MAMMALIAN COCHLEA; LEAKY EPITHELIA; CYTO-CHEMISTRY; CHOLESTEROL; PERMEABILITY; TRANSPORT; MEMBRANE; HYDROPS AB It is current opinion that the intercellular spaces of the stria vascularis represent a closed compartment isolated from the endolymph by the tight junctions of the marginal cells and from the perilymph by the junctional complexes of the basal cells. However, it has not yet been investigated whether these two barriers meet at the stria margins toward Reissner's membrane and the spiral prominence. Possible candidates for this sealing could be junctions between the spindle-shaped cells. In the present study freeze-fracture replicas of guinea pig specimens fixed in the presence of filipin were used in order to investigate the junctions of the spindle-shaped cells and to localize the cholesterol in their plasma membrane. Replicas reveal that, below the belt-like apical zonula occludens, the basolateral plasma membranes of the spindle-shaped cells adjacent to each other and to the basal cells are joined over their entire extension by a large number of junctional strands intermingled with numerous filipin-cholesterol-complexes. Gap junctions are present in the meshes formed by these junctional strands. Thus, the plasma membrane of the spindle-shaped cells shows morphological and cytochemical characteristics which indicate that they are the anatomical components completing the barrier isolating the intrastrial compartment from the surrounding fluids. C1 UNIV BARI,DEPT BIOACOUST,I-70124 BARI,ITALY. RP LUCIANO, L (reprint author), HANNOVER MED SCH,CELL BIOL & ELECTRON MICROSCOPY,KONSTANTY GUTSCHOW STR 8,D-30625 HANNOVER,GERMANY. 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Res. PD MAY PY 1995 VL 85 IS 1-2 BP 199 EP 209 DI 10.1016/0378-5955(95)00047-8 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700020 PM 7559175 ER PT J AU LOPEZ, CA OLSON, ES ADAMS, JC MOU, K DENHARDT, DT DAVIS, RL AF LOPEZ, CA OLSON, ES ADAMS, JC MOU, K DENHARDT, DT DAVIS, RL TI OSTEOPONTIN EXPRESSION DETECTED IN ADULT COCHLEAE AND INNER-EAR FLUIDS SO HEARING RESEARCH LA English DT Article DE INNER EAR; CHOROID PLEXUS; IN SITU HYBRIDIZATION; IMMUNOHISTOCHEMISTRY; WESTERN BLOT ID SECRETED PHOSPHOPROTEIN-1 SPP-1; INSITU HYBRIDIZATION; NEOPLASTIC TRANSFORMATION; BONE PHOSPHOPROTEIN; MOLECULAR-CLONING; TUMOR PROMOTER; MESSENGER-RNA; RAT BONE; PROTEIN; KIDNEY AB Localization of protein epitopes and mRNA expression showed that there was a wide-spread distribution of osteopontin (OPN) within the membranous labyrinth of the adult mammalian cochlea. Immunoreaction product and mRNA were found within the stria vascularis, VIIIth cranial nerve, spiral ligament and limbus. Only specific cell types within these regions contained abundant OPN mRNA or protein, the main cell type being fibrocytes that populate the spiral limbus and spiral ligament. Epithelial cells that line the luminal surface of the stria vascularis (marginal cells) and neurons that compose the vestibular and auditory ganglia also showed high opn expression. The pattern of anti-OPN staining within the membranous labyrinth was comparable to that observed in tissues such as gall bladder, breast and kidney. In those tissues, luminal epithelial cells, corresponding to the marginal cells of the stria vascularis, may be responsible for manufacturing and secreting OPN into the luminal fluids. Consistent with those observations, we detected OPN epitopes in cochlear fluids withdrawn from the scala media and tympani of the cochlea. We found that the protein species in cochlear fluid differed from those present in cerebrospinal fluid (CSF) suggesting that OPN exists in tissue-specific isoforms that may correspond to particular cellular functions. C1 RUTGERS STATE UNIV,DEPT BIOL SCI,PISCATAWAY,NJ 08855. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. CR ADAMS JC, 1992, J HISTOCHEM CYTOCHEM, V40, P1457 ARCANGELI A, 1993, J CELL BIOL, V122, P1131, DOI 10.1083/jcb.122.5.1131 BRAHIC M, 1978, P NATL ACAD SCI USA, V75, P6125, DOI 10.1073/pnas.75.12.6125 BROWN LF, 1992, MOL BIOL CELL, V3, P1169 CHAMBERS AF, 1992, ANTICANCER RES, V12, P43 CHEN Y, 1992, J BIOL CHEM, V267, P24871 COX KH, 1984, DEV BIOL, V101, P485, DOI 10.1016/0012-1606(84)90162-3 CRAIG AM, 1989, J BIOL CHEM, V264, P9682 DENHARDT DT, 1993, FASEB J, V7, P1475 FET V, 1989, GENOMICS, V5, P375, DOI 10.1016/0888-7543(89)90074-8 GIACHELLI C, 1991, BIOCHEM BIOPH RES CO, V177, P867, DOI 10.1016/0006-291X(91)91870-I GIACHELLI CM, 1994, KIDNEY INT, V45, P515, DOI 10.1038/ki.1994.67 HAFEN E, 1983, EMBO J, V2, P617 HAYASHI S, 1978, J HISTOCHEM CYTOCHEM, V26, P677 HWANG S, 1994, J BIOL CHEM, V269, P711 ICHIMIYA I, 1994, ACTA OTO-LARYNGOL, V114, P167, DOI 10.3109/00016489409126037 KASUGAI S, 1991, BONE MINER, V13, P235, DOI 10.1016/0169-6009(91)90071-7 KIMURA RS, 1970, ACTA OTO-LARYNGOL, V69, P415, DOI 10.3109/00016487009123387 LOPEZ CA, UNPUB ACTIVATION SIG LOPEZ CA, 1993, LAB INVEST, V69, P355 MARK MP, 1987, J HISTOCHEM CYTOCHEM, V35, P707 MARK MP, 1988, CELL TISSUE RES, V251, P23, DOI 10.1007/BF00215443 MCKEE M, IN PRESS NY ACAD SCI MELTON DA, 1984, NUCLEIC ACIDS RES, V12, P7035, DOI 10.1093/nar/12.18.7035 NEMIR M, 1989, J BIOL CHEM, V264, P18202 PRINCE CW, 1987, J BIOL CHEM, V262, P2900 RODRIGUEZECHAND.EL, 1965, Z ZELLFORSCH, V67, P600 SAKAGAMI M, 1994, ASS RES OTOLARYNGOL, V17, P557 SALT AN, 1979, ACTA OTO-LARYNGOL, V88, P198, DOI 10.3109/00016487909137160 SALT AN, 1986, NEUROBIOLOGY HEARING, P109 SCHWARTZ M A, 1992, Trends in Cell Biology, V2, P304, DOI 10.1016/0962-8924(92)90120-C SCHWARTZ MA, 1994, J BIOL CHEM, V269, P11133 SENGER DR, 1989, ANTICANCER RES, V9, P1291 SENGER DR, 1994, MOL BIOL CELL, V5, P565 SENGER DR, 1989, BIOCHIM BIOPHYS ACTA, V996, P43, DOI 10.1016/0167-4838(89)90092-7 SENGER DR, 1988, CANCER RES, V48, P5770 SHANKAR G, 1993, J CELL SCI, V105, P61 SHIRAGA H, 1992, P NATL ACAD SCI USA, V89, P426, DOI 10.1073/pnas.89.1.426 SILVERSTEIN H, 1976, HDB AUDITORY VESTIBU, P420 SINGH K, 1992, J BIOL CHEM, V267, P23847 SINGH RP, 1990, J EXP MED, V171, P1931, DOI 10.1084/jem.171.6.1931 SMITH JH, 1987, J CELL BIOCHEM, V34, P13, DOI 10.1002/jcb.240340103 SPICER SS, 1992, J HISTOCHEM CYTOCHEM, V40, P185 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z SPICER SS, 1990, HEARING RES, V43, P205, DOI 10.1016/0378-5955(90)90229-I SWANSON GJ, 1989, HEARING RES, V41, P169, DOI 10.1016/0378-5955(89)90008-7 TAKAHASHI T, 1970, Acta Oto-Laryngologica, V69, P46, DOI 10.3109/00016487009123335 THALMANN I, 1992, HEARING RES, V63, P37, DOI 10.1016/0378-5955(92)90071-T ULLRICH O, 1991, J BIOL CHEM, V266, P3518 WORCESTER EM, 1992, J BONE MINER RES, V7, P1029 NR 50 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 1995 VL 85 IS 1-2 BP 210 EP 222 DI 10.1016/0378-5955(95)00046-7 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA RE527 UT WOS:A1995RE52700021 PM 7559176 ER PT J AU HILGER, AW FURNESS, DN WILSON, JP AF HILGER, AW FURNESS, DN WILSON, JP TI THE POSSIBLE RELATIONSHIP BETWEEN TRANSIENT EVOKED OTOACOUSTIC EMISSIONS AND ORGAN OF CORTI IRREGULARITIES IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE EVOKED OTOACOUSTIC EMISSIONS; COCHLEA; HAIR CELL; GUINEA PIG ID STIMULATED ACOUSTIC EMISSIONS; COCHLEA; EAR; SUPPRESSION; RESPONSES; TINNITUS AB Otoacoustic emissions are believed to arise from an active process associated with the outer hair cells in the mammalian organ of Corti. They have been attributed to the presence of impedance discontinuities on the basilar membrane which might be caused by hair cell irregularities. To test this hypothesis we have investigated the possible relationship between transient evoked otoacoustic emissions (TEOAEs) and anatomical integrity in the organ of Corti. Click-evoked TEOAEs have been measured from the ear canals of normal, pigmented guinea pigs using an Otodynamics ILO88 analyser. Emissions were present in 18 out of 19 animals tested and the major frequencies observed were consistently present in different measurements over periods of up to ten weeks provided recording conditions were satisfactory. The frequency spectra of the TEOAEs resembled those measured in humans but the latencies of the responses were considerably shorter. In one acute experiment, the TEOAEs were shown to be dependent on metabolic energy as they were lost rapidly following termination with an overdose of anaesthetic. In another case, evoked emissions of long duration (sustained) at about 1 KHz were obtained from both ears. All cochleae examined showed irregularities, especially patches of mainly apical outer hair cell loss of differing extents. However, there was no evidence that substantial lesions coincided consistently with the frequency regions corresponding to the major emissions. Nevertheless, it was noted that the total energy level of emissions was proportional to the total outer hair cell loss, except in one case, where the outer hair cell loss was substantial and the energy level of TEOAEs was considerably lower. Although there is no clear relationship between TEOAEs of specific frequencies and abnormalities at the corresponding cochloetopic location in the organ of Corti which could represent impedance discontinuities, the degree of irregularity may determine the overall emission level. This finding is consistent with the idea that emissions arise as a result of irregularity producing variations in the reflection coefficient. C1 UNIV KEELE,DEPT COMMUN & NEUROSCI,KEELE ST5 5BG,STAFFS,ENGLAND. N STAFFORDSHIRE HOSP,DEPT EAR NOSE & THROAT,STOKE ON TRENT ST4 7LN,STAFFS,ENGLAND. CR 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, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 CLARK WW, 1978, ANN OTOL RHINOL LA S, V51, P1 CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 EVANS EF, 1992, ADV BIOSCI, V83, P159 Evans E F, 1981, Ciba Found Symp, V85, P108 FURNESS DN, 1985, HEARING RES, V18, P177, DOI 10.1016/0378-5955(85)90010-3 FURNESS DN, 1988, BRIT J AUDIOL, V22, P142 FURNESS DN, 1990, ACTA OTO-LARYNGOL, V109, P66, DOI 10.3109/00016489009107416 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 JIANG D, 1993, BRIT J AUDIOL, V27, P195, DOI 10.3109/03005369309076693 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, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 LONSBURYMARTIN BL, 1988, HEARING RES, V33, P66 Manley GA, 1983, MECH HEARING, P36 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 MOUNTAIN DC, 1986, PERIPHERAL AUDITORY, P179 OHYAMA K, 1991, HEARING RES, V56, P111, DOI 10.1016/0378-5955(91)90160-B PROBST R, 1991, J ACOUST SOC AM, V89, P2027, DOI 10.1121/1.400897 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 Shera CA, 1993, BIOPHYSICS HAIR CELL, P54 SIMONCELLI C, 1992, LARYNGO RHINO OTOL, V71, P319, DOI 10.1055/s-2007-997304 STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 Sutton GJ, 1983, MECHANICS HEARING, P83 UEDA H, 1992, HEARING RES, V62, P199, DOI 10.1016/0378-5955(92)90187-R 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 ZENNER HP, 1993, BRIT J AUDIOL, V27, P73, DOI 10.3109/03005369309077894 ZWICKER E, 1990, HEARING RES, V47, P185, DOI 10.1016/0378-5955(90)90150-N ZWICKER E, 1981, HEARING RES, V4, P43, DOI 10.1016/0378-5955(81)90035-6 NR 33 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 1995 VL 84 IS 1-2 BP 1 EP 11 DI 10.1016/0378-5955(95)00007-Q PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200001 PM 7642443 ER PT J AU LUTZ, C SCHWEITZER, L AF LUTZ, C SCHWEITZER, L TI LONGITUDINAL AND RADIAL DIFFERENCES IN THE SUBSURFACE CISTERNAL SYSTEM IN THE GERBIL COCHLEA SO HEARING RESEARCH LA English DT Article DE GRADIENTS; OUTER HAIR CELLS; SUBSURFACE CISTERNAE; OTOTOXICITY; ELECTROMOTILITY ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; FREEZE-FRACTURE; INNER-EAR; ORGAN; CORTI; INNERVATION; ELECTROMOTILITY; ULTRASTRUCTURE; MORPHOLOGY AB Many features of cochlear anatomy vary systematically radially and longitudinally within the organ of Corti. There is limited evidence that along the longitudinal axis of the cochlea the thickness of the subsurface cisternal system in the outer hair cells (OHCs) changes. Similarly a radial gradient may exist. The thickness of the subsurface cisternal system in OHCs was measured in gerbils to determine if there are differences between the three rows of OHCs and in OHCs in different locations along the length of the organ of Corti. The results suggest that there is a longitudinal as well as a radial gradient of subsurface cisternal system thickness. These gradients are the inverse to those for efferent innervation of OHCs. It is possible that these differences may contribute to the increased susceptibility to trauma and ototoxic compounds characteristic of the innermost and basalmost OHCs. C1 UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. CR Alberts B., 1989, MOL BIOL CELL ARNOLD W, 1990, LARYNGO RHINO OTOL, V69, P177, DOI 10.1055/s-2007-998171 BOHNE BA, 1973, ACOUST SOC AM, V53, P292 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 DANNHOF BJ, 1993, HEARING RES, V66, P8, DOI 10.1016/0378-5955(93)90255-Y DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DULON D, 1990, J NEUROSCI, V10, P1388 FORGE A, 1991, CELL TISSUE RES, V265, P473, DOI 10.1007/BF00340870 FORGE A, 1993, J NEUROCYTOL, V22, P854, DOI 10.1007/BF01186357 FORGE A, 1993, HEARING RES, V64, P175, DOI 10.1016/0378-5955(93)90003-J FORGE A, 1989, COCHLEAR MECHANISMS, P29 FRANCIS HW, 1993, HEARING RES, V64, P217, DOI 10.1016/0378-5955(93)90009-P FURNESS DN, 1990, EUR ARCH OTO-RHINO-L, V247, P12 GITTER AH, 1993, PFLUG ARCH EUR J PHY, V424, P9, DOI 10.1007/BF00375096 HALLWORTH R, 1993, J NEUROPHYSIOL, V70, P549 HARADA N, 1993, BRAIN RES, V614, P205, DOI 10.1016/0006-8993(93)91036-R HARADA Y, 1986, SCAN ELECT MICROSC, V2, P531 HOLLEY MC, 1992, AUDITORY PHYSL PERCE, P27 KALTENBACH JA, 1992, HEARING RES, V60, P205, DOI 10.1016/0378-5955(92)90022-F KARNOVSK.MJ, 1965, J CELL BIOL, V27, pA137 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 Kimura R S, 1966, Acta Otolaryngol, V61, P55, DOI 10.3109/00016486609127043 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, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 NADOL JB, 1990, J ELECTRON MICR TECH, V15, P187, DOI 10.1002/jemt.1060150210 NAGASAWA A, 1991, SCANNING MICROSCOPY, V5, P747 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 ROTHMAN SM, 1987, TRENDS NEUROSCI, V10, P299, DOI 10.1016/0166-2236(87)90177-9 SAITO K, 1983, CELL TISSUE RES, V229, P467 SCHULTE BA, 1993, HEARING RES, V65, P262, DOI 10.1016/0378-5955(93)90219-Q Siegel S., 1956, NONPARAMETRIC STATIS SMITH CA, 1957, AM J ANAT, V100, P337, DOI 10.1002/aja.1001000304 VONLUBITZ DKJE, 1981, CELL TISSUE RES, V220, P787 WEAVER SP, 1994, HEARING RES, V72, P44, DOI 10.1016/0378-5955(94)90204-6 XIE DH, 1993, HEARING RES, V66, P81, DOI 10.1016/0378-5955(93)90262-Y YLIKOSKI J, 1993, HEARING RES, V65, P69, DOI 10.1016/0378-5955(93)90202-C NR 37 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 APR PY 1995 VL 84 IS 1-2 BP 12 EP 18 DI 10.1016/0378-5955(95)00008-R PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200002 PM 7642445 ER PT J AU WANGEMANN, P LIU, JZ MARCUS, DC AF WANGEMANN, P LIU, JZ MARCUS, DC TI ION-TRANSPORT MECHANISMS RESPONSIBLE FOR K+ SECRETION AND THE TRANSEPITHELIAL VOLTAGE ACROSS MARGINAL CELLS OF STRIA VASCULARIS IN-VITRO SO HEARING RESEARCH LA English DT Article DE STRIA VASCULARIS; COCHLEA; MARGINAL CELLS; VIBRATING PROBE; MICRO-USSING CHAMBER ID VESTIBULAR DARK CELLS; ELECTRICAL RESPONSES; NONSELECTIVE CATION; NONSENSORY REGION; ETHACRYNIC-ACID; CELLULAR-MODEL; GERBIL UTRICLE; POTASSIUM-FREE; COCHLEAR DUCT; CL CHANNELS AB It has long been accepted that marginal cells of stria vascularis are involved in the generation of the endocochlear potential and the secretion of Kf. The present study was designed to provide evidence for this hypothesis and for a cell model proposed to explain KC secretion and the generation of the endocochlear potential. Stria vascularis from the cochlea of the gerbil was isolated and mounted into a micro-Ussing chamber such that the apical and basolateral membrane of marginal cells could be perfused independently. In this preparation, the transepithelial voltage (V-t) and resistance (R(t)) were measured across marginal cells and the resulting equivalent short circuit current (I-sc) was calculated (I-sc = V-t/R(t)). Further, K+ secretion (J(K+),(probe)) was measured with a K+-selective vibrating probe in the vicinity of the apical membrane. In the absence of extrinsic chemical driving forces, when both sides of the marginal cell epithelium were bathed with a perilymph-like solution, V-t was 8 mV (apical side positive), R(t) was 10 ohm-cm(2) and I-sc was 850 mu A/cm(2) (N = 27). J(K+,probe) was outwardly directed from the apical membrane and reversibly inhibited by basoiateral bumetanide, a blocker of the Na+/Cl-/K+ cotransporter. On the basolateral but not apical side, ouabain and bumetanide each caused a decline of V, and an increase of R(t) suggesting the presence of the Na,K-ATPase and the Na+/Cl-/K+ cotransporter in the basolateral membrane. The responses to [Cl-] steps demonstrated a significant Cl- conductance in the basolateral membrane and a small Cl- conductance in the paracellular pathway or the apical membrane. The responses to [Na+] steps demonstrated no significant Na+ conductance in the basolateral membrane and a small Na+ or nonselective cation conductance in the apical membrane or paracellular pathway. The responses to [K+] steps demonstrated a large K+ conductance in the apical membrane. Apical application of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) and basolateral elevation of K+ caused an increase in V-t and a decrease in R(t) consistent with stimulation of the apical K+ conductance. Similar observations have been made in vestibular dark cells, which suggest that strial marginal cells and Vestibular dark cells are homologous and transport ions by the same pathways. Taken together, these observations are incompatible with a model for the generation of the endocochlear potential which ascribes the entire potential to the strial marginal cells [Offner et al. (1987) Hear. Res. 29, 117-124]. However, the data are compatible with the notion that marginal cells contribute not more than a few mV to the endocochlear potential as suggested by Salt et al. [Laryngoscope 97, 984-991, 1987]. C1 BOYS TOWN NATL RES HOSP,BIOPHYS LAB,OMAHA,NE 68131. 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 FERRARY E, 1989, AM J PHYSIOL, V257, P182 FORGE A, 1984, HEARING RES, V13, P189, DOI 10.1016/0378-5955(84)90108-4 HODGKIN AL, 1959, J PHYSIOL-LONDON, V148, P127 Hsu C J, 1985, Acta Otolaryngol Suppl, V418, P1 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 IKEDA K, 1989, HEARING RES, V40, P111, DOI 10.1016/0378-5955(89)90104-4 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 Jahnke K, 1975, Acta Otolaryngol Suppl, V336, P1 JOHNSTON.BM, 1972, Q REV BIOPHYS, V5, P1 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 KONISHI T, 1970, Acta Oto-Laryngologica, V69, P192, DOI 10.3109/00016487009123353 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUHTREIBER WM, 1990, J CELL BIOL, V110, P1565, DOI 10.1083/jcb.110.5.1565 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 KUSAKARI J, 1978, ACTA OTO-LARYNGOL, V86, P336, DOI 10.3109/00016487809107512 LIU J, 1995, ASS RES OTOLARYNGOL, V18, P100 MARCUS DC, 1985, HEARING RES, V17, P79, DOI 10.1016/0378-5955(85)90133-9 MARCUS DC, 1978, LARYNGOSCOPE, V88, P1825 MARCUS DC, 1994, ABSTR ASS RES OT, V17, P529 MARCUS DC, 1993, HEARING RES, V69, P124, DOI 10.1016/0378-5955(93)90100-F MARCUS DC, 1981, HEARING RES, V4, P149, DOI 10.1016/0378-5955(81)90002-2 MARCUS DC, 1994, BIOPHYS J, V66, P1939 MARCUS DC, 1994, HEARING RES, V73, P101, DOI 10.1016/0378-5955(94)90287-9 MARCUS DC, 1987, HEARING RES, V30, P55, DOI 10.1016/0378-5955(87)90183-3 MARCUS DC, 1994, AM J PHYSIOL, V267, pC857 MARCUS DC, 1984, AM J PHYSIOL, V247, pC240 MARCUS DC, 1994, ABSTR J GEN PHYSL, V104, pA16 MARCUS DC, 1989, BIOCHIM BIOPHYS ACTA, V987, P56, DOI 10.1016/0005-2736(89)90454-9 MARCUS DC, 1992, AM J PHYSIOL, V262, pC143 MARCUS NY, 1990, HEARING RES, V44, P13, DOI 10.1016/0378-5955(90)90018-K OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 RYBAK LP, 1986, ACTA OTO-LARYNGOL, V101, P59, DOI 10.3109/00016488609108608 SAKAGAMI M, 1991, HEARING RES, V56, P168, DOI 10.1016/0378-5955(91)90166-7 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1994, HEARING RES, V78, P65, DOI 10.1016/0378-5955(94)90045-0 SHEN Z, 1994, ASS RES OTOLARYNGOL, V17, P134 SHINDO M, 1992, JPN J PHYSIOL, V42, P617, DOI 10.2170/jjphysiol.42.617 SMITH PR, 1991, ANNU REV PHYSIOL, V53, P509, DOI 10.1146/annurev.ph.53.030191.002453 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z SUNOSE H, 1994, HEARING RES, V80, P86, DOI 10.1016/0378-5955(94)90012-4 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 TAKEUCHI S, 1994, ASS RES OTOLARYNGOL, V17, P133 TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 WADA J, 1979, ARCH OTO-RHINO-LARYN, V225, P79, DOI 10.1007/BF00455206 WANGEMANN P, 1990, DIURETICS, V3, P220 WANGEMANN P, 1990, PFLUG ARCH EUR J PHY, V416, P262, DOI 10.1007/BF00392062 NR 49 TC 176 Z9 188 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 1995 VL 84 IS 1-2 BP 19 EP 29 DI 10.1016/0378-5955(95)00009-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200003 PM 7642451 ER PT J AU CLERICI, WJ DIMARTINO, DL PRASAD, MR AF CLERICI, WJ DIMARTINO, DL PRASAD, MR TI DIRECT EFFECTS OF REACTIVE OXYGEN SPECIES ON COCHLEAR OUTER HAIR CELL-SHAPE IN-VITRO SO HEARING RESEARCH LA English DT Article DE AUDITORY; CYTOPLASMIC BLEB; FREE RADICAL; HYDROGEN PEROXIDE; HYDROXYL RADICAL; SUPEROXIDE ANION ID CENTRAL-NERVOUS-SYSTEM; RAT CEREBRAL-CORTEX; GUINEA-PIG COCHLEA; FREE-RADICALS; SUPEROXIDE-DISMUTASE; INDUCED OTOTOXICITY; OXIDATIVE STRESS; STRIA VASCULARIS; ATP DEPLETION; MOTILITY AB Reactive oxygen species (ROS) have been implicated in the ototoxicity of various agents. This study examines the effects of superoxide anion (O-2(.)), hydroxyl radical (OH.) and hydrogen peroxide (H2O2), on isolated cochlear outer hair cell (OHC) morphology. OHCs were superfused with artificial perilymph (AP) or AP containing a specific ROS scavenger, and then with AP, ROS system or scavenger plus ROS system for 90 min. The generation of ROS as well as the scavenging properties of other agents were confirmed by specific biochemical assays. Control cells decreased 4.8% in mean length, and showed no obvious membrane damage. Generation of O-2(.) Or OH. resulted in high rates (85.7 and 42.9%, respectively) of bleb formation at the synaptic pole, and decreased (O-2(.), 15.2%; OH.; 17.3%) mean cell length. Length change and bleb formation rate were H2O2 concentration-dependent. 20 mM H2O2 led to 33.3% decreased mean cell length, and only 20% bleb formation; 0.1 mM H2O2 led to 83.3% bleb formation, with no length decrease. Superoxide dismutase, deferoxamine and catalase protected against O-2(.), OH. and H2O2 effects, respectively. Bleb formation and diminished cell length likely represent differential lipid peroxidative outcomes at supra- and infranuclear membranes, and are consistent with effects of certain ototoxicants. C1 UNIV KENTUCKY,COLL MED,DEPT SURG,DIV NEUROSURG,LEXINGTON,KY 40536. RP CLERICI, WJ (reprint author), UNIV KENTUCKY,COLL MED,UK CHANDLER MED CTR,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,LEXINGTON,KY 40536, USA. 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0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1995 VL 84 IS 1-2 BP 30 EP 40 DI 10.1016/0378-5955(95)00010-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200004 PM 7642453 ER PT J AU WIEDERHOLD, ML YAMASHITA, M LARSEN, KA BATTEN, JS KOIKE, H ASASHIMA, M AF WIEDERHOLD, ML YAMASHITA, M LARSEN, KA BATTEN, JS KOIKE, H ASASHIMA, M TI DEVELOPMENT OF THE OTOLITH ORGANS AND SEMICIRCULAR CANALS IN THE JAPANESE RED-BELLIED NEWT, CYNOPS-PYRRHOGASTER SO HEARING RESEARCH LA English DT Article DE OTOCONIA; OTOLITH; UTRICLE; SACCULE; SEMICIRCULAR CANALS; DEVELOPMENT ID X-RAY-DIFFRACTION; OTOCONIA AB The sequence in which the otoliths and semicircular canals and their associated sensory epithelia appear and develop in the newt are described. Three-dimensional reconstruction of serial sections through the otic vesicle of newt embryos from stages 31 through 58 demonstrate the first appearance, relative position and growth of the otoliths. A single otolith is first seen in stage 33 embryos (approximately 9 days old); this splits into separate utricular and saccular otoliths at stage 40 (13 days). The lateral semicircular canal is the first to appear, at stage 41 (14 days). The anterior and posterior canals appear approximately one week later and the vestibular apparatus is essentially fully formed at stage 58 (approximately 5 weeks). The data reported here will serve as ground-based controls for fertilized newt eggs flown on the International Microgravity Laboratory-2 Space Shuttle night, to investigate the influence of microgravity on the development of the gravity-sensing organs. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. INST SPACE & ASTRONAUT SCI,SAGAMIHARA,KANAGAWA 229,JAPAN. UNIV TOKYO,TOKYO,JAPAN. RP WIEDERHOLD, ML (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. CR Anson BJ, 1973, OTOLARYNGOLOGY, V1, P3 BALLARINO J, 1984, AM J PHYSIOL, V246, pR305 CARLSTROM DD, 1963, BIOL BULL, V125, P441, DOI 10.2307/1539358 GAULDIE RW, 1993, J MORPHOL, V218, P1, DOI 10.1002/jmor.1052180102 HOWLAND HC, 1981, VESTIBULAR SYSTEM FU, P77 KOIKE H, 1995, NONINVASIVE ASSESSME LIM DJ, 1974, AEROSPACE MED, V45, P705 LYCHAKOV DV, 1985, KOSM BIOL AVIAK MED+, V19, P48 MARMO F, 1981, CELL TISSUE RES, V218, P265 MARMO F, 1983, ACTA ZOOL-STOCKHOLM, V64, P219 MARMO F, 1992, ACTA ZOOL-STOCKHOLM, V73, P203 MARMO F, 1983, CELL TISSUE RES, V233, P35 OKADA T, 1989, DEV VERTEBRATES Okada YK, 1947, JPN J EXP MORPHOL, V3, P1 OKADA YK, 1989, JAP J EXPT MORPH PATERSON NF, 1949, P ZOOL SOC LOND, V119, P269 PEDROZO HA, 1994, HEARING RES, V79, P137, DOI 10.1016/0378-5955(94)90135-X POTE KG, 1991, COMP BIOCHEM PHYS B, V98, P287, DOI 10.1016/0305-0491(91)90181-C SHICHIRI T, 1986, J CRYST GROWTH, V78, P493, DOI 10.1016/0022-0248(86)90151-X SOKOLOWSKI BHA, 1987, J MORPHOL, V194, P323, DOI 10.1002/jmor.1051940311 STEYGER PS, 1995, HEAR RES WIEDERHOLD ML, 1992, 9TH P ISAS SPAC UT S, V9, P127 WIEDERHOLD ML, 1994, ARO MIDW ABST, V17, P38 WIEDERHOLD ML, 1992, 18TH P INT S SPAC TE, V18, P2103 WIEDERHOLD ML, 1995, UNPUB DEV CRYST FORM 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 APR PY 1995 VL 84 IS 1-2 BP 41 EP 51 DI 10.1016/0378-5955(95)00012-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200005 PM 7642454 ER PT J AU MCGUIRT, JP SCHMIEDT, RA SCHULTE, BA AF MCGUIRT, JP SCHMIEDT, RA SCHULTE, BA TI DEVELOPMENT OF COCHLEAR POTENTIALS IN THE NEONATAL GERBIL SO HEARING RESEARCH LA English DT Article DE COCHLEA; DEVELOPMENT; GERBIL; COMPOUND ACTION POTENTIAL; COCHLEAR MICROPHONIC; ENDOCOCHLEAR POTENTIAL ID AGE-RELATED-CHANGES; MONGOLIAN GERBIL; GUINEA-PIG; INNER-EAR; ENDOCOCHLEAR; EMISSIONS; TIME; RAT AB The onset and maturation of hearing was examined in separate groups of sibling and nonsibling neonatal Mongolian gerbils (Meriones unguiculatus). Auditory nerve compound action potentials (CAP) and cochlear microphonics (CM) were measured at the round window, and the endocochlear potential(EP) was recorded at three different locations in pups aged 13 to 30 days after birth (DAB) and in 90 day-old animals. Maturational trends for the three potentials were similar to those previously reported for gerbil neonates. However, CAP thresholds continued to decrease, and CM and CAP input/output functions and EP continued to increase beyond 30 days of age, a time at which many investigators have considered hearing in the gerbil to be mature. The EP developed simultaneously throughout the cochlea and approached 80 mV by 20 DAB. CAP thresholds showed a highly correlated log-linear relationship with EP in groups of nonlittermates and in siblings studied at different ages. In contrast, maximum CAP and CM amplitudes increased with increasing EP, but did not show significant growth until the EP exceeded 70 mV. C1 MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,CHARLESTON,SC 29425. RP MCGUIRT, JP (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 52 EP 60 DI 10.1016/0378-5955(95)00015-V PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200006 PM 7642455 ER PT J AU STEYGER, PS WIEDERHOLD, ML BATTEN, J AF STEYGER, PS WIEDERHOLD, ML BATTEN, J TI THE MORPHOGENIC FEATURES OF OTOCONIA DURING LARVAL DEVELOPMENT OF CYNOPS-PYRRHOGASTER, THE JAPANESE RED-BELLIED NEWT SO HEARING RESEARCH LA English DT Article DE OTOCONIA; VESTIBULAR; MORPHOGENESIS; BIOMINERALIZATION; EXTRACELLULAR MATRIX ID ENDOLYMPHATIC SAC; CRYSTAL-GROWTH; PROTEIN; STATOCONIA; MEMBRANE AB Otoconia are calcified protein matrices within the gravity-sensing organs of the vertebrate vestibular system. Mammalian otoconia are barrel-shaped with triplanar facets at each end. Reptilian otoconia are commonly prismatic or fusiform in shape. Amphibians have all three otoconial morphologies, barrel-shaped otoconia within the utricle, with prismatic and fusiform otoconia in the saccule. Scanning electron microscopy revealed a sequential appearance of all three otoconial morphologies during larval development of the newt, Cynops pyrrhogaster. The first otoconia appear within a single, developing otolith, and some resemble adult barrel-shaped otoconia. As the larvae hatch, around stages 39-42, the single otolith divides into two anatomically separate regions, the utricle and saccule, and both contain otoconia similar to those seen in the single otolith. Throughout development, these otoconia may have variable morphologies, with serrated surfaces, or circumferential striations with either separated facets or adjacent facets in the triplanar end-regions. small fusiform otoconia occur later, at stage 51, and only in the saccule. Prismatic otoconia appear later still, at stage 55, and again only in the saccule. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 61 EP 71 DI 10.1016/0378-5955(95)00013-T PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200007 PM 7642456 ER PT J AU EGERT, D LEWIS, ER AF EGERT, D LEWIS, ER TI TEMPERATURE-DEPENDENCE OF SACCULAR NERVE-FIBER RESPONSE IN THE NORTH-AMERICAN BULLFROG SO HEARING RESEARCH LA English DT Article DE FROG; SACCULUS; TEMPERATURE; TUNING; AUDITORY NERVE ID HAIR-CELLS; RANA-CATESBEIANA; ALLIGATOR LIZARD; AUDITORY-SYSTEM; FROG; FREQUENCY; COCHLEA; EAR AB A clinical microwave device was used to heat the head and ear of the North American bullfrog in order to observe the temperature dependence of tuning in the sacculus, an organ known to possess the capability of electrical resonance in its hair cells. In tuning curves derived from reverse correlation analysis with noise stimuli, the temperature dependencies of the frequencies of tuning peaks and notches typically exhibited Q(10)s less than 1.1; whereas the frequencies of electrical resonances are expected to have Q(10)s Of the order of 1.7. Therefore we conclude that electrical resonances are not significantly involved in tuning in the bullfrog sacculus. C1 UNIV CALIF BERKELEY,CTR BECHTEL ENGN 230,BIOENGN PROGRAM,BERKELEY,CA 94720. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 72 EP 80 DI 10.1016/0378-5955(95)00019-Z PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200008 PM 7642457 ER PT J AU HENRY, WR MULROY, MJ AF HENRY, WR MULROY, MJ TI AFFERENT SYNAPTIC CHANGES IN AUDITORY HAIR-CELLS DURING NOISE-INDUCED TEMPORARY THRESHOLD SHIFT SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELL; NOISE-INDUCED HEARING LOSS; TTS; ALLIGATOR LIZARD; SYNAPSE; SYNAPTIC BODY ID ALLIGATOR LIZARD COCHLEA; GUINEA-PIG COCHLEA; NERVE-ENDINGS; INNER-EAR; FREQUENCY-SELECTIVITY; STRUCTURAL-CHANGES; ACTIN-FILAMENTS; STEREOCILIA; SYNAPSES; ORGANIZATION AB This study presents evidence in support of the hypothesis that one of the sites of failure during noise-induced temporary threshold shift (TTS) is the afferent synapse between auditory hair cells and auditory nerve fibers. Our results show clear evidence indicating changes in the quantity of afferent synapses and the morphology of presynaptic structures in the alligator lizard auditory hair cells during TTS. In TTS hair cells there are statistically significant decreases in: 1) the number of afferent synapses, 2) the number of synaptic vesicles at the afferent synapses, 3) the size of synaptic bodies, and 4) the packing density of synaptic vesicles around the synaptic body. These results suggest that the presynaptic components of the afferent synapse reflect the functional state of the synapse, and that the reduction of these synapses, both in number and component size, contributes to TTS. C1 MED COLL GEORGIA,DEPT CELLULAR BIOL & ANAT,AUGUSTA,GA 30912. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 81 EP 90 DI 10.1016/0378-5955(95)00014-U PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200009 PM 7642458 ER PT J AU HALL, JW GROSE, JH MENDOZA, LL AF HALL, JW GROSE, JH MENDOZA, LL TI MASKER INTERAURAL PHASE AND THE MLD - EFFECTS OF CONDUCTIVE HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE MASKING-LEVEL DIFFERENCE; BINAURAL HEARING; CONDUCTIVE HEARING LOSS; MIDDLE EAR MECHANICS ID BINAURAL HEARING; LEVEL AB Sensitivity to binaural signals that were interaurally antiphasic with respect to the masking noise was examined as a function of the interaural phase of the masking noise, for listeners with normal hearing, and listeners with conductive hearing losses. Some of the hearing-impaired listeners were tested bath before and after middle ear surgery. In agreement with previous findings, the normal-hearing listeners showed the lowest thresholds when the masking noise had no interaural phase shift, with thresholds increasing monotonically as the interaural phase of the center frequency of the masker approached +/- 180 degrees. Although many of the masked threshold functions of the hearing-impaired listeners showed significant changes in thresholds as a function of masker interaural phase, most of the functions were abnormal in shape, and few showed peaks far the interaural masker phase of 0 degrees. Although functions often continued to be abnormal after middle ear surgery, a few subjects obtained postsurgery functions that were correlated with the average normal function. The results indicate that although normal-hearing listeners generally have the lowest antiphasic signal threshold for a masker with 0 degrees interaural phase, conductively-impaired listeners often do not show a clear minimum for antiphasic signal threshold at any particular masker interaural phase. RP HALL, JW (reprint author), UNIV N CAROLINA,SCH MED,DIV OTOLARYNGOL HEAD & NECK SURG,CB 7070,CHAPEL HILL,NC 27599, USA. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 91 EP 98 DI 10.1016/0378-5955(95)00016-W PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200010 PM 7642459 ER PT J AU HENLEY, CM SALZER, TA COKER, NJ SMITH, G HADDOX, MK AF HENLEY, CM SALZER, TA COKER, NJ SMITH, G HADDOX, MK TI LOCALIZATION OF ORNITHINE DECARBOXYLASE (ODC) IN THE COCHLEA OF THE IMMATURE RAT SO HEARING RESEARCH LA English DT Article DE ORNITHINE DECARBOXYLASE; COCHLEA; COCHLEAR DEVELOPMENT; POLYAMINES ID INNER-EAR; ALPHA-DIFLUOROMETHYLORNITHINE; PARATHYROID-HORMONE; POLYAMINES; INHIBITION; RECEPTOR; INVITRO; CELLS AB Ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine synthesis, is important in cochlear development. Whereas tissue specific differences in cochlear ODC activity have been demonstrated, cellular localization of ODC protein in the inner ear of the immature rat has not. ODC was localized in inner ear structures using an ODC polyclonal antibody and the effects of cycloheximide on ODC immunoreactivity and enzymatic activity were determined. Tissues demonstrating elevated enzymatic activity contained cells with the strong immunoreactivity. ODC activity was highest in the organ of Corti and lateral wall followed by the cochlear nerve. Immunoreactivity was demonstrated throughout the cochlea with intense staining of the hair cells, pillar cells, Deiter's cells, inner sulcus cells, basilar membrane, stria vascularis, spiral ganglion cell bodies and cochlear nerve fibers. Cycloheximide rapidly diminished cochlear ODC activity and expression of ODC protein. The half-life of cochlear ODC was 30 min. Localization of cellular sites of ODC is important in understanding the role of the ODC-polyamine pathway in cochlear development and will be a valuable marker for tissue damage from ototoxic agents. C1 BAYLOR COLL MED,DEPT PHARMACOL,HOUSTON,TX 77030. BAYLOR COLL MED,DIV NEUROSCI,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT NEUROSURG,HOUSTON,TX 77030. UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,HOUSTON,TX 77030. RP HENLEY, CM (reprint author), BAYLOR COLL MED,DEPT OTOLARYNGOL & COMMUN SCI,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 99 EP 111 DI 10.1016/0378-5955(95)00017-X PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200011 PM 7543894 ER PT J AU CANLON, B FRANSSON, A AF CANLON, B FRANSSON, A TI MORPHOLOGICAL AND FUNCTIONAL PRESERVATION OF THE OUTER HAIR-CELLS FROM NOISE TRAUMA BY SOUND CONDITIONING SO HEARING RESEARCH LA English DT Article DE AUDITORY; COCHLEA; DISTORTION PRODUCT EMISSION; NOISE; PROTECTION; SOUND CONDITIONING ID ACOUSTIC-DISTORTION PRODUCTS; CROSSED OLIVOCOCHLEAR BUNDLE; TEMPORARY THRESHOLD SHIFT; GUINEA-PIG; MECHANICAL RESPONSES; HEARING-LOSS; STIMULATION; EXPOSURE; 2F1-F2; LEVEL AB Guinea pigs were sound conditioned to a low-level, long-term pure tone stimulus (1 kHz, 81 dB SPL, 24 days) before exposure to a traumatic noise (1 kHz, 105 dB SPL, 72 h). Auditory brainstem response thresholds and distortion product otoacoustic emissions were obtained at selected frequencies before sound conditioning and at day 1, 5, 10, and 15 during sound conditioning as well as on the final 24th day. Auditory brainstem responses at 1 and 2 kHz were not affected at any time during sound conditioning. The amplitude of the distortion product otoacoustic emission showed minor alterations (below 10 dB) at selected frequencies only during the initial stages (day 1, 5, and 10) of sound conditioning in some, but not all the animals. Distortion product amplitudes were similar to control values on the 15th and 24th day of conditioning. Surface preparations of the organ of Corti did not reveal any significant hair cell loss induced by sound conditioning. The effect of a traumatic exposure (1 kHz, 105 dB SPL, 72 h) on a control group and a sound conditioned group was determined. The distortion product otoacoustic emission amplitude measured 4 weeks after the cessation of the traumatic exposure revealed significant differences. The amplitude of the distortion product otoacoustic emission for the control group was depressed at all tested frequencies and at lower frequencies (2.8, 2.1, and 1.75 kHz) the emissions did not show an increase in response to increases in intensity. of the primaries. The sound conditioned group showed increases in distortion product amplitude with increases in the intensity of the primaries for all tested frequencies and statistically significant reductions from the pre-exposure values were not found. Surface preparations from the control group indicated that the traumatic noise exposure affected nearly 100% of the outer hair cells around the 14 mm distance from the round window. The sound conditioned group showed a significantly less (50%) outer hair cell loss than the control group. The sound conditioned group illustrated an altered pattern of damage after subsequent noise trauma. There were two distinct regions of outer hair cell loss, one being around the 16 mm distance and the other around the 12 mm distances from the round window. These results imply that the intrinsic properties of the outer hair cells and/or the organ of Corti have been altered by sound conditioning. RP CANLON, B (reprint author), KAROLINSKA INST,DEPT PHYSIOL & PHARMACOL,S-17177 STOCKHOLM,SWEDEN. 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PD APR PY 1995 VL 84 IS 1-2 BP 112 EP 124 DI 10.1016/0378-5955(95)00020-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200012 PM 7642444 ER PT J AU ONEILL, MP BEARDEN, A AF ONEILL, MP BEARDEN, A TI LASER-FEEDBACK MEASUREMENTS OF TURTLE BASILAR-MEMBRANE MOTION USING DIRECT REFLECTION SO HEARING RESEARCH LA English DT Article DE REPTILE EAR; COCHLEA; BASILAR PAPILLA; FREQUENCY TUNING; LASER-FEEDBACK INTERFEROMETRY ID COCHLEAR HAIR-CELLS; FREQUENCY-SELECTIVITY; INNER-EAR; INTERFEROMETRY; MECHANICS; VIBRATION; BUNDLES; LIZARD; CAT AB In mammalian hearing, the frequency-dependent spatial pattern of movement in the basilar membrane/organ of Corti complex forms the basis of frequency discrimination. This is not necessarily the case in lower vertebrates; the turtle, for example, has an electrical resonance mechanism in its auditory receptor cells that varies in best frequency from cell to cell. But how much, if any, of the frequency separation by the turtle is done mechanically by the basilar membrane complex? Attempts to find an investigative approach that avoided placing objects on the basilar membrane led to the rediscovery of laser-feedback interferometry. Laser-feedback interferometric investigations of the vibrational amplitude and phase of the turtle basilar membrane in response to imposed nanometer displacements of the eardrum reveal that the membrane reflects the broadly-tuned middle-ear filter characteristics. Phase-angle measurements of the basilar membrane as a function of frequency, and the best frequency of the obtained amplitude tuning curves, did not vary as a function of position within each specimen. 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PD APR PY 1995 VL 84 IS 1-2 BP 125 EP 138 DI 10.1016/0378-5955(95)00018-Y PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200013 PM 7642446 ER PT J AU KUHN, B VATER, M AF KUHN, B VATER, M TI THE ARRANGEMENTS OF F-ACTIN, TUBULIN AND FODRIN IN THE ORGAN OF CORTI OF THE HORSESHOE BAT (RHINOLOPHUS-ROUXI) AND THE GERBIL (MERIONES-UNGUICULATUS) SO HEARING RESEARCH LA English DT Article DE COCHLEA; CYTOSKELETON; IMMUNOCYTOCHEMISTRY; HAIR CELLS; SUPPORTING CELLS ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; SUPPORTING CELLS; INNER-EAR; ELECTRON-MICROSCOPY; MEMBRANE SKELETON; ECHOLOCATING BATS; ULTRASTRUCTURE; ORGANIZATION; MICROTUBULES AB The composition of cytoskeletal elements in hair cells and non-sensory cells was studied in paraformaldehyde fixed cochleae of the horseshoe bat and the gerbil using phallotoxins and antibodies directed against actin, alpha-tubulin and fodrin. In both species, cryostat sections of the organ of Corti were studied using confocal fluorescence microscopy; in the bat, ultrathin sections were investigated using actin-immunoelectron and classical electron microscopy. F-actin was found in stereocilia and cuticular plates of inner and outer hair cells (IHCs and OHCs) of both species. In fixed material from both species, no F-actin staining was detected in the cytoplasm or along the lateral cell membrane of OHCs, whereas in freshly isolated OHCs of the gerbil, a faint F-actin staining was detected along the lateral wall. In the bat, the patterns of F-actin staining were confirmed with actin-immunoelectron microscopy. The alpha-tubulin antibody strongly labeled IHCs of both species. They contained a complex network of microtubules especially in the neck portion. In the bat, OHCs showed no distinct alpha-tubulin reactivity, as would be expected given the scarcity of microtubules observed at the ultrastructural level. In the gerbil, alpha-tubulin reactivity was found throughout the OHC body with highest intensity in the cell apex. In Deiters cells, pillar cells and Boettcher cells of both species, F-actin and microtubules were colocalized at contact zones with the basilar membrane. In Deiters cups, F-actin staining was most pronounced in the the basal turn of the bat cochlea. In the gerbil, a distinct baso-apical gradient was found in immunostaining properties and morphology of the Deiters cells. Intense fodrin reactivity was found in the cuticular plates and along the lateral cell membrane of both types of hair cells of the bat. Cytoplasmic fodrin staining was localized within the IHCs of the bat. In the gerbil, intense fodrin staining was only found in cuticular prates of hair cells and staining of the lateral cell membrane of hair cells was faint. A faint fodrin staining was also seen in Deiters cells of both species. The basic arrangement of the cytoskeletal elements in the bats organ of Corti is similar to that of other mammals, however, certain features suggest the presence of subtle differences in micromechanical properties: there is an increased concentration of microtubules in the neck portion of IHCs, an increase in the amount of F-actin within the Deiters cups and a reduced amount of microtubules in the OHCs. RP KUHN, B (reprint author), UNIV REGENSBURG,INST ZOOL,UNIV STR 31,D-93040 REGENSBURG,GERMANY. CR ALTSCHULER RA, 1991, ABSTR ASS RES OT, V14, P12 Amos L. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 139 EP 156 DI 10.1016/0378-5955(95)00021-U PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200014 PM 7642447 ER PT J AU CHITTAJALLU, SK PALAKAL, MJ WONG, D AF CHITTAJALLU, SK PALAKAL, MJ WONG, D TI ANALYSIS AND CLASSIFICATION OF DELAY-SENSITIVE CORTICAL-NEURONS BASED ON RESPONSE TO TEMPORAL PARAMETERS IN ECHOLOCATION SIGNALS SO HEARING RESEARCH LA English DT Article ID AUDITORY-CORTEX; FM BAT; MYOTIS-LUCIFUGUS; MUSTACHED BAT; REPRESENTATION; SONAR AB Echolocating bats generate an acoustic image of their target by processing target-reflected echoes of their emitted biosonar pulses. Efforts in building computational models of auditory processing in the bat auditory system, using extensive neurophysiological data from cortical studies are challenged by the intrinsic complexity and the significant variability in neural response to stimuli. In this paper, we use a computerized method for the analysis and classification of delay-sensitive neurons to classify neurons from the auditory cortex of Myotis lucifugus, a species that echolocates with FM signals. The coefficients of the hi-linear fit to the best delay response surfaces (mean R(2) = 0.01) were used in classifying the neurons. Six classes were derived that corresponded to the four previously characterized neurophysiologically. The first class corresponded to delay-tuned neurons which exhibited a constant best delay at different pulse repetition rates and pulse durations. Three other classes corresponded to the different subtypes of tracking neurons which changed their best delay to one or both of these stimulus temporal parameters. Two additional classes were differentiated although their best-delay response were similar to either the delay-tuned or the duration and pulse-repetition rate sensitive class. Artificial delay-sensitive neurons built from the parameters of the centroid of each class, will serve a key role in the FM bat auditory system model that we are building. C1 INDIANA UNIV PURDUE UNIV,DEPT COMP SCI,INDIANAPOLIS,IN 46202. INDIANA UNIV PURDUE UNIV,DEPT ANAT,INDIANAPOLIS,IN 46202. RP CHITTAJALLU, SK (reprint author), INDIANA UNIV PURDUE UNIV,DEPT MECH ENGN,SL 2250,723 W MICHIGAN,INDIANAPOLIS,IN 46202, USA. CR ALTES RA, 1976, J ACOUST SOC AM, V59, P97, DOI 10.1121/1.380831 Busnel R. 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PD APR PY 1995 VL 84 IS 1-2 BP 157 EP 166 DI 10.1016/0378-5955(95)00022-V PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200015 PM 7642448 ER PT J AU LANGEMANN, U KLUMP, GM DOOLING, RJ AF LANGEMANN, U KLUMP, GM DOOLING, RJ TI CRITICAL BANDS AND CRITICAL-RATIO BANDWIDTH IN THE EUROPEAN STARLING SO HEARING RESEARCH LA English DT Article DE BIRD; FREQUENCY SELECTIVITY; CRITICAL RATIO BANDWIDTH; CRITICAL BAND ID STURNUS-VULGARIS; GAP DETECTION; FREQUENCY-SELECTIVITY; THRESHOLDS; HEARING; CHINCHILLA; NEURONS AB Critical bands (CB) and critical-ratio (CR) bandwidth were determined in five European starlings (Stumus vulgaris) using a GO/NOGO procedure and the method of constant stimuli. Test-tone frequencies were 1, 2, 4, and 6.3 kHz. Critical ratios were independent of the level of the white noise masker. The lowest CR of 21.8 dB was found at 1 kHz, and the CR monotonically increased on average by 2.3 dB per octave. CR-bandwidths at a masker spectrum level of 41 dB were 151, 191, 437, and 501 Hz at 1, 2, 4, and 6.3 Mit, respectively. With the exception of the test-tone frequency of 6.3 kHz, the size of the critical bands measured with a band-narrowing procedure was similar to that of the CR-bandwidth. CBs were 135, 233, 345, and 1156 Hz at 1, 2, 4, and 6.3 kHz, respectively. A repeat measurement at 6.3 kHz with another speaker position yielded a CB of 860 Hz. The results of this psychoacoustic study in the starling are discussed with respect to comparative data from other vertebrates and to neurophysiological bandwidth measurements of tuning curves of auditory-nerve fibres. C1 UNIV MARYLAND,DEPT PSYCHOL,COLLEGE PK,MD 20742. RP LANGEMANN, U (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,D-85748 GARCHING,GERMANY. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 167 EP 176 DI 10.1016/0378-5955(95)00023-W PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200016 PM 7642449 ER PT J AU MOCKETT, BG BO, XN HOUSLEY, GD THORNE, PR BURNSTOCK, G AF MOCKETT, BG BO, XN HOUSLEY, GD THORNE, PR BURNSTOCK, G TI AUTORADIOGRAPHIC LABELING OF P-2 PURINOCEPTORS IN THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE EXTRACELLULAR ATP; [H-3] ALPHA,BETA-METHYLENE-ATP; BETA,GAMMA-METHYLENE-ATP; [S-35] DATP-ALPHA-S; 2-METHYLTHIO-ATP; ORGAN OF CORTI; STRIA VASCULARIS; SPIRAL GANGLION; HAIR CELLS ID OUTER HAIR-CELLS; H-3 ALPHA,BETA-METHYLENE ATP; RAT VAS-DEFERENS; EXTRACELLULAR ATP; BINDING-SITES; URINARY-BLADDER; RECEPTOR; P2-PURINOCEPTORS; EXPRESSION; MECHANISM AB Two different radioligands were used to identify extracellular ATP binding sites specific to P-2 purinoceptors in guinea-pig cochlear tissue. Deoxyadenosine 5'-(alpha-[S-35]thio)triphosphate ([S-35]dATP alpha S; 10 nM) provided a high activity probe for the P-2y purinoceptor subtype on the basis of selective block by 2-methylthio-ATP (2MeSATP; 100 mu M). [H-3]alpha, beta-methylene-ATP (10 nM), a high affinity probe for a P-2x purinoceptor subtype was selectively blocked by inclusion of the related compound beta,gamma-methylene-ATP (100 mu M). Both probes labelled the organ of Corti, stria vascularis and spiral prominence regions. The P-2x purinoceptor probe also bound to lateral wall tissue below the spiral prominence and insertion point of the basilar membrane within the scala tympani compartment, a region which failed to show significant binding using [S-35]dATP alpha S. Frozen sections of whole cochlea permitted analysis of radioligand binding to the cell body region (spiral ganglion in Rosenthal's canal) of the primary auditory afferents and the auditory nerve itself, which lies within the central region of the modiolus of the cochlea. Both these regions exhibited 2MeSATP blockable [S-35]dATP alpha S binding whereas specific [H-3]alpha,beta-methylene-ATP binding was absent from spiral ganglion and minimal in the auditory nerve region. These results demonstrate a mixed P-2 purinoceptor distribution in cochlear tissues and suggest that complex purine-mediated neurohumoral mechanisms may influence cochlear function at a number of sites. C1 UNIV AUCKLAND,SCH MED,DEPT PHYSIOL,AUCKLAND,NEW ZEALAND. UNIV LONDON UNIV COLL,DEPT ANAT & DEV BIOL,LONDON WC1E 6BT,ENGLAND. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 177 EP 193 DI 10.1016/0378-5955(95)00024-X PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200017 PM 7642450 ER PT J AU WALSH, EJ MCGEE, JA FITZAKERLEY, JL AF WALSH, EJ MCGEE, JA FITZAKERLEY, JL TI ACTIVITY-DEPENDENT RESPONSES OF DEVELOPING COCHLEAR NUCLEAR NEURONS TO MICROIONOPHORETICALLY-APPLIED AMINO-ACIDS SO HEARING RESEARCH LA English DT Article DE NEUROTRANSMITTER; VOLTAGE-DEPENDENT; AUDITORY; EAA; MICROIONTOPHORESIS ID METHYL-D-ASPARTATE; INFERIOR COLLICULUS; HIPPOCAMPAL-NEURONS; PROTEIN-SYNTHESIS; SPINAL NEURONS; RECEPTOR; GLUTAMATE; CULTURE; HAMSTER; GABA AB The experimental purpose of this investigation was to determine whether the efficacy of glutamate, N-methyl-D-aspartate (NMDA) and/or GABA is related to the activity state of neurons in the cochlear nuclear complex (CN). The hypothesis tested was that changes in discharge activity produced by glutamatergic and GABAergic ligands are, or may be, greater when neurons are stimulated at moderate to high acoustic levels compared to near threshold stimulation levels, when activity levels are high or low, respectively. All neurons from which discharge rate vs. sound pressure level curves were tested during simultaneous administration of amino acids exhibited characteristics commensurate with an activity-dependent system; at high sound levels, when discharge rates were elevated relative to rates produced by low level stimuli, both glutamate-induced increments and GABA-induced decrements in discharge rate were enhanced. The relationship between discharge rate and amino acid efficacy was a uniform property of neurons sampled throughout the first two postnatal weeks of development. In adults, preliminary indications are that activity-dependent neurotransmitter efficacy is characteristic of some cells, but not others. The activity-dependent nature of endogenous amino acid neurotransmission was demonstrated through the microionsphoretic administration of NMDA and GABA(A) selective antagonists, D-alpha-aminoadipate (D alpha AA) and 2-amino-5-phosphonovalerate (APV), and bicuculline (BIC), respectively. These results suggest that postsynaptic actions elicited by membrane receptors subserving amino acid neurotransmission within the CN are activity-dependent. C1 CREIGHTON UNIV,SCH MED,DEPT OTOLARYNGOL,OMAHA,NE 68131. CREIGHTON UNIV,SCH MED,DEPT PHYSIOL,OMAHA,NE 68131. RP WALSH, EJ (reprint author), BOYS TOWN NATL RES HOSP,DEV AUDITORY PHYSIOL LAB,555 NORTH ST,OMAHA,NE 68131, USA. 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Res. PD APR PY 1995 VL 84 IS 1-2 BP 194 EP 204 DI 10.1016/0378-5955(95)00011-R PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QV812 UT WOS:A1995QV81200018 PM 7642452 ER PT J AU AZZENA, GB CONTI, G SANTARELLI, R OTTAVIANI, F PALUDETTI, G MAURIZI, M AF AZZENA, GB CONTI, G SANTARELLI, R OTTAVIANI, F PALUDETTI, G MAURIZI, M TI GENERATION OF HUMAN AUDITORY STEADY-STATE RESPONSES (SSRS) .1. STIMULUS RATE EFFECTS SO HEARING RESEARCH LA English DT Article DE MIDDLE LATENCY RESPONSE; STEADY-STATE RESPONSE; REPETITION RATE; ADAPTATION; AUDITORY SYSTEM ID MIDDLE LATENCY RESPONSE; EVOKED-POTENTIALS; EEG; CAT; COMPONENTS; TRANSIENT; RABBIT; FIELDS; BRAIN; SLOW AB Auditory evoked responses were recorded in 16 normally hearing subjects in order to investigate the mechanisms underlying the generation of the 40 Hz steady-state response (SSR). In the first part of our study, auditory potentials were evoked by 0.1 ms clicks presented at 105 dB p.e. SPL with repetition rates of 7.9 (to obtain middle latency response, MLR), 20, 30, 40, 50, 60 Hz. In each subject predictions of the responses recorded at stimulus repetition rates of 30, 40, 50, 60 Hz were synthesized by superimposing MLRs at suitable time intervals. The calculated mean amplitude/rate and phase/rate functions behaved similarly for the recorded and predicted curves, showing the highest amplitude at 40 Hz and a linear increase of phase values when increasing the stimulus rate. Nevertheless the synthetic curves closely predicted amplitude and phase values of the recorded responses only at 40 Hz. At frequencies below 40 Hz, the mean amplitude of the predicted curve was lower than that of the recorded one while at frequencies above 40 Hz the mean amplitude was higher. Predicted phase values were found lagging at 30 Hz, and leading at 50 Hz and 60 Hz in comparison to phase values calculated on the recorded responses. Our findings suggest that a model based on the linear addition of transient MLRs is not able to adequately predict steady-state responses at stimulus rates other than at 40 Hz. Other mechanisms related to the recovery cycle of the activated system come into play in the steady-state response generation causing a decrease in amplitude and an increase in phase fag when increasing the stimulus repetition rate. C1 UNIV CATTOLICA SACRO CUORE,ORL CLIN,I-00168 ROME,ITALY. INST HUMAN PHYSIOL,ROME,ITALY. CR BARINAGA M, 1990, SCIENCE, V249, P856, DOI 10.1126/science.2392677 BASAR E, 1979, BIOL CYBERN, V34, P1, DOI 10.1007/BF00336852 BASAR E, 1987, INT J NEUROSCI, V33, P103 Basar E., 1980, EEG BRAIN DYNAMICS BASAR E, 1979, BIOL CYBERN, V34, P21, DOI 10.1007/BF00336853 BOUYER JJ, 1981, ELECTROEN CLIN NEURO, V51, P244, DOI 10.1016/0013-4694(81)90138-3 BRESSLER SL, 1990, TRENDS NEUROSCI, V13, P161, DOI 10.1016/0166-2236(90)90039-D BRESSLER SL, 1980, ELECTROEN CLIN NEURO, V50, P19, DOI 10.1016/0013-4694(80)90319-3 CHAMBERS RD, 1992, HEARING RES, V58, P123, DOI 10.1016/0378-5955(92)90122-4 Crick F., 1990, Seminars in the Neurosciences, V2, P263 DAVIS H, 1966, ELECTROEN CLIN NEURO, V21, P105, DOI 10.1016/0013-4694(66)90118-0 ERWIN RJ, 1986, ELECTROEN CLIN NEURO, V64, P417, DOI 10.1016/0013-4694(86)90075-1 GALAMBOS R, 1982, ANN NY ACAD SCI, V88, P722 GALAMBOS R, 1988, DYNAMICS SENSORY COG, P103 GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 HARI R, 1989, J ACOUST SOC AM, V86, P1033, DOI 10.1121/1.398093 HYDE ML, 1976, BRIT J AUDIOL, V10, P41, DOI 10.3109/03005367609078806 KRAUS N, 1988, ELECTROEN CLIN NEURO, V70, P541, DOI 10.1016/0013-4694(88)90152-6 LENARZ T, 1986, ORL J OTO-RHINO-LARY, V48, P24 MAKELA JP, 1987, ELECTROEN CLIN NEURO, V66, P539, DOI 10.1016/0013-4694(87)90101-5 OTTAVIANI F, 1990, AUDIOLOGY, V29, P212 PANTEV C, 1993, ELECTROEN CLIN NEURO, V88, P389, DOI 10.1016/0168-5597(93)90015-H PANTEV C, 1991, P NATL ACAD SCI USA, V88, P8996, DOI 10.1073/pnas.88.20.8996 PICTON TW, 1992, ELECTROEN CLIN NEURO, V84, P90, DOI 10.1016/0168-5597(92)90071-I Plourde G, 1991, Acta Otolaryngol Suppl, V491, P153 Regan D., 1989, HUMAN BRAIN ELECTROP ROTHMAN HH, 1970, ELECTROEN CLIN NEURO, V29, P225, DOI 10.1016/0013-4694(70)90135-5 STAPELLS DR, 1984, EAR HEARING, V5, P105 STAPELLS DR, 1988, ELECTROEN CLIN NEURO, V71, P289, DOI 10.1016/0168-5597(88)90029-9 STURZEBECHER E, 1985, SCAND AUDIOL, V14, P214 SUZUKI T, 1986, ELECTROEN CLIN NEURO, V65, P150, DOI 10.1016/0168-5597(86)90048-1 TERKILDSEN K, 1975, SCAND AUDIOL, V4, P215, DOI 10.3109/01050397509043084 TIITINEN H, 1993, NATURE, V364, P59, DOI 10.1038/364059a0 1985, ISO389 NR 34 TC 38 Z9 40 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1995 VL 83 IS 1-2 BP 1 EP 8 DI 10.1016/0378-5955(94)00184-R PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000001 PM 7607975 ER PT J AU SANTARELLI, R MAURIZI, M CONTI, G OTTAVIANI, F PALUDETTI, G PETTOROSSI, VE AF SANTARELLI, R MAURIZI, M CONTI, G OTTAVIANI, F PALUDETTI, G PETTOROSSI, VE TI GENERATION OF HUMAN AUDITORY STEADY-STATE RESPONSES (SSRS) .2. ADDITION OF RESPONSES TO INDIVIDUAL STIMULI SO HEARING RESEARCH LA English DT Article DE MIDDLE LATENCY RESPONSES; 40 HZ STEADY-STATE RESPONSES; RESONANT FREQUENCY; AUDITORY SYSTEM ID EVOKED-POTENTIALS; ELECTROENCEPHALIC RESPONSE; MIDDLE LATENCY; COMPONENTS; SLEEP; EEG; CAT; FREQUENCY; RABBIT; FIELDS AB In order to investigate the generation of the 40 Hz steady-state response (SSR), auditory potentials evoked by clicks were recorded in 16 healthy subjects in two stimulating conditions. Firstly, repetition rates of 7.9 and 40 Hz were used to obtain individual middle latency responses (MLRs) and 40 Hz-SSRs, respectively. In the second condition, eight click trains were presented at a 40 Hz repetition rate and an inter-train interval of 126 ms. We extracted from the whole train response: (1) the response-segment taking place after the last click of the train (last click response, LCR), (2) a modified LCR (mLCR) obtained by clearing the LCR from the amplitude enhancement due to the overlapping of the responses to the clicks preceding the last within the stimulus train. In comparison to MLRs, the most relevant feature of the evoked activity following the last click of the train (LCRs, mLCRs) was the appearance in the 50-110 ms latency range of one (in 11 subjects) or two (in 2 subjects) additional positive-negative deflections having the same periodicity as that of MLR waves. The grand average (GA) of the 40 Hz-SSRs was compared with three predictions synthesized by superimposing: (1) the GA of MLRs, (2) the GA of LCRs, (3) the GA of mLCRs. Both the MLR and mLCR predictions reproduced the recorded signal in amplitude while the LCR prediction amplitude resulted almost twice that of the 40 Hz-SSR. With regard to the phase, the MLR, LCR and mLCR closely predicted the recorded signal. Our findings confirm the effectiveness of the linear addition mechanism in the generation of the 40 Hz-SSR. However the responses to individual stimuli within the 40 Hz-SSR differ from MLRs because of additional periodic activity. These results suggest that phenomena related to the resonant frequency of the activated system may play a role in the mechanisms which interact to generate the 40 Hz-SSR. C1 UNIV CATTOLICA SACRO CUORE,ORL CLIN,I-00168 ROME,ITALY. INST HUMAN PHYSIOL,ROME,ITALY. UNIV PERUGIA,INST HUMAN PHYSIOL,I-06100 PERUGIA,ITALY. CR AZZENA GB, 1995, HEARING RES, V83, P1, DOI 10.1016/0378-5955(94)00184-R BASAR E, 1979, BIOL CYBERN, V34, P1, DOI 10.1007/BF00336852 BASAR E, 1987, INT J NEUROSCI, V33, P103 BASAR E, 1979, BIOL CYBERN, V34, P21, DOI 10.1007/BF00336853 BRESSLER SL, 1980, ELECTROEN CLIN NEURO, V50, P19, DOI 10.1016/0013-4694(80)90319-3 ERWIN R, 1986, ELECTROEN CLIN NEURO, V65, P383, DOI 10.1016/0168-5597(86)90017-1 GALAMBOS R, 1982, ANN NY ACAD SCI, V88, P722 GALAMBOS R, 1981, P NATL ACAD SCI-BIOL, V78, P2643, DOI 10.1073/pnas.78.4.2643 HARI R, 1989, J ACOUST SOC AM, V86, P1033, DOI 10.1121/1.398093 KAVANAGH KT, 1984, ANN OTO RHINOL LARYN, V93, P1 MAKEIG S, 1989, Society for Neuroscience Abstracts, V15, P113 MAKELA JP, 1990, HEARING RES, V45, P41, DOI 10.1016/0378-5955(90)90181-N MAKELA JP, 1987, ELECTROEN CLIN NEURO, V66, P539, DOI 10.1016/0013-4694(87)90101-5 MENDEL MI, 1971, J SPEECH HEAR RES, V14, P829 OTTAVIANI F, 1990, AUDIOLOGY, V29, P212 PANTEV C, 1993, ELECTROEN CLIN NEURO, V88, P389, DOI 10.1016/0168-5597(93)90015-H PANTEV C, 1991, P NATL ACAD SCI USA, V88, P8996, DOI 10.1073/pnas.88.20.8996 PICTON TW, 1978, OTOLARYNG CLIN N AM, V11, P263 PICTON TW, 1992, ELECTROEN CLIN NEURO, V84, P90, DOI 10.1016/0168-5597(92)90071-I PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 Plourde G, 1991, Acta Otolaryngol Suppl, V491, P153 STAPELLS DR, 1984, EAR HEARING, V5, P105 STAPELLS DR, 1988, ELECTROEN CLIN NEURO, V71, P289, DOI 10.1016/0168-5597(88)90029-9 THORNTON AR, 1977, J SPEECH HEAR RES, V20, P81 1985, ISO389 NR 25 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 MAR PY 1995 VL 83 IS 1-2 BP 9 EP 18 DI 10.1016/0378-5955(94)00185-S PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000002 PM 7607994 ER PT J AU RICHTER, CP HEYNERT, S KLINKE, R AF RICHTER, CP HEYNERT, S KLINKE, R TI RATE-INTENSITY-FUNCTIONS OF PIGEON AUDITORY PRIMARY AFFERENTS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE FIBER; RATE-INTENSITY FUNCTION; NONLINEARITY; PIGEON ID BASILAR-MEMBRANE NONLINEARITY; NERVE FIBERS; GUINEA-PIG; COCHLEAR GANGLION; MOSSBAUER TECHNIQUE; DISCHARGE PATTERNS; LEVEL FUNCTIONS; SINGLE FIBERS; DISCRIMINATION; NEURONS AB Rate-intensity-functions (RI-functions) were determined in 150 primary auditory afferents in anaesthetized pigeon. Acoustic stimulation was either at characteristic frequency (CF) or half an octave below or above CF. Stimulated at CF, 37% of the fibres showed saturating RI-functions, whereas 50% showed sloping and 13% straight RI-functions. In the sloping RI-functions, a bend was found about 20 dB above the fibres' thresholds. For non-CF stimuli, the general shape of the RI-functions remained constant. However, the maximum evoked discharge rates were lower for frequencies below CF and higher for frequencies above CF. The data show that a population of neurones, the sloping and straight ones, code stimulus intensities over a wide intensity range. In combination with the scatter of the thresholds, intensity ranges greater than 100 dB are conceivable. It was concluded that the nonlinearities found in pigeon are not caused by basilar membrane (BM) mechanics, rather an origin at the hair cell-afferent nerve fibre system has to be considered. RP RICHTER, CP (reprint author), UNIV FRANKFURT,ZENTRUM PHYSIOL,THEODOR STERN KAI 7,D-60590 FRANKFURT,GERMANY. 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Res. PD MAR PY 1995 VL 83 IS 1-2 BP 19 EP 25 DI 10.1016/0378-5955(94)00186-T PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000003 PM 7607985 ER PT J AU SONE, M NARIUCHI, H SAITO, K YANAGITA, N AF SONE, M NARIUCHI, H SAITO, K YANAGITA, N TI A SUBSTRAIN OF NZB MOUSE AS AN ANIMAL-MODEL OF AUTOIMMUNE INNER-EAR DISEASE SO HEARING RESEARCH LA English DT Article DE AUTOIMMUNE MOUSE; STRIA VASCULARIS; CAPILLARY BASEMENT MEMBRANE; HEARING DYSFUNCTION ID SENSORINEURAL HEARING-LOSS; SYSTEMIC LUPUS-ERYTHEMATOSUS; NEW-ZEALAND MICE; STRAIN MOUSE; ENDOLYMPHATIC HYDROPS; SERUM ANTIBODIES; IMMUNOFLUORESCENCE; AUTOANTIBODIES; PATHOLOGY AB A substrain of an autoimmune-prone mouse, NZB/kl, was found to show spontaneous elevation of the auditory brainstem response (ABR) threshold with age. Morphological examination of-the inner ear in NZB/kl mice with high ABR thresholds revealed pathological changes confined to the stria vascularis, including marked thickening of the capillary basement membrane which contained many foamy structures, and vacuolar degeneration of the intermediate cells. Circular or granular IgM deposits and some IgG deposits were found in the stria vascularis in the mice with high ABR thresholds, suggesting that deposits of immune complexes (mainly IgM antibodies) could cause strial damage that resulted in the ABR threshold elevation. Another substrain of NZB mice, NZB/san, showed lower levels of IgM immune complexes and anti-ss DNA antibodies, and did not develop either inner ear morphological changes or a high ABR threshold. NZB/kl mice may provide a useful animal model for studying the mechanism of autoimmune inner ear disease. C1 UNIV TOKYO,INST MED SCI,DEPT ALLERGOL,TOKYO,JAPAN. GUNMA UNIV,SCH MED,COLL MED CARE & TECHNOL,MAEBASHI,GUMMA 371,JAPAN. RP SONE, M (reprint author), NAGOYA UNIV,SCH MED,DEPT OTORHINOLARYNGOL,SHOWA KU,65 TSURUMAI CHO,NAGOYA,AICHI 466,JAPAN. 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Res. PD MAR PY 1995 VL 83 IS 1-2 BP 26 EP 36 DI 10.1016/0378-5955(94)00189-W PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000004 PM 7607988 ER PT J AU KITANO, I MORI, N MATSUNAGA, T AF KITANO, I MORI, N MATSUNAGA, T TI ROLE OF ENDOLYMPHATIC ANION TRANSPORT IN FORSKOLIN-INDUCED CL- ACTIVITY INCREASE OF SCALA MEDIA SO HEARING RESEARCH LA English DT Article DE CL- CHANNEL; NA+/K+/2CL(-) COTRANSPORT; CL-/HCO3-; EXCHANGE; ENDOLYMPH HOMEOSTASIS; FORSKOLIN; ENDOCOCHLEAR POTENTIAL ID GUINEA-PIG; CHLORIDE; DEPENDENCE; BUMETANIDE; BICARBONATE; COTRANSPORT; MEMBRANE; EXCHANGE; CELLS AB To determine the role of anion transport in the forskolin-induced Cl- increase of scala media (SM), effects of forskolin on the EP (endocochlear potential) and Cl- activity (A(Cl)) in SM were examined with double-barrelled Cl--selective microelectrodes. The experiments were carried out on guinea pig cochleae, using a few anion transport inhibitors: IAA-94 for a Cl- channel blocker, bumetanide (BU) for an Na+/K+/2Cl(-) cotransport blocker, and SITS and DIDS for Cl-/HCO3- exchange blockers. The application of forskolin (200 mu M) into scala vestibuli (SV) caused a 20 mEq increase of endolymphatic A(Cl) and a 15 mV elevation of EP, and IAA-94 with forskolin completely abolished these responses. Although each application of BU, SITS or DIDS did not completely suppress EP elevation, the concurrent application of these inhibitors completely suppressed EP with endolymphatic A(Cl) increase. The results indicate the involvement of Cl- channels, Na+/K-/2Cl(-) cotransport and Cl-/HCO3- exchange in forskolin-induced increase of A(Cl) and EP. The role of adenylate cyclase activation and Cl- transport in endolymph homeostasis was discussed. C1 OSAKA MED COLL,DEPT PHYSIOL,OSAKA 569,JAPAN. KAGAWA MED SCH,DEPT OTOLARYNGOL,KAGAWA 76107,JAPAN. RP KITANO, I (reprint author), NARA MED UNIV,DEPT OTOLARYNGOL,840 SHIJO CHO,KASHIHARA,NARA 634,JAPAN. CR AALKJAER C, 1991, J PHYSIOL-LONDON, V436, P57 AMMANN D, 1975, HELV CHIM ACTA, V58, P1535, DOI 10.1002/hlca.19750580605 CHAO AC, 1987, AM J PHYSIOL, V253, pC343 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 FONG P, 1991, AM J PHYSIOL, V261, pL290 GUGGINO WB, 1983, J MEMBRANE BIOL, V71, P227, DOI 10.1007/BF01875464 HAAS M, 1990, AM J PHYSIOL, V259, pC557 HADDAD P, 1991, AM J PHYSIOL, V261, pG340 HEGARTY JL, 1991, AM J PHYSIOL, V261, pC521 HUME JR, 1991, AM J PHYSIOL, V261, pC339 IMAI Y, 1993, J OTOLARYNGOL JPN, V96, P1833 KITANO I, 1994, HEARING RES, V78, P58, DOI 10.1016/0378-5955(94)90044-2 KITANO I, 1993, HEARING RES, V71, P23, DOI 10.1016/0378-5955(93)90017-U KUSAKARI J, 1978, ACTA OTO-LARYNGOL, V86, P336, DOI 10.3109/00016487809107512 KUWAHARA M, 1991, AM J PHYSIOL, V260, pF635 LAMBERT RW, 1991, AM J PHYSIOL, V260, pG517 LANDRY DW, 1987, J GEN PHYSIOL, V90, P779, DOI 10.1085/jgp.90.6.779 MARCUS DC, 1994, HEARING RES, V73, P101, DOI 10.1016/0378-5955(94)90287-9 MORI N, 1993, EUR ARCH OTO-RHINO-L, V250, P186 RESTREPO D, 1991, AM J PHYSIOL, V260, pC535 Robinson R. A., 1970, ELECTROLYTE SOLUTION SHINDO M, 1992, JPN J PHYSIOL, V42, P617, DOI 10.2170/jjphysiol.42.617 SINGH AK, 1991, AM J PHYSIOL, V260, pC51 STERKERS O, 1988, PHYSIOL REV, V68, P1083 SUNOSE H, 1993, AM J PHYSIOL, V266, pC72 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 1995 VL 83 IS 1-2 BP 37 EP 42 DI 10.1016/0378-5955(94)00187-U PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000005 PM 7607989 ER PT J AU GRATTON, MA SMYTH, BJ SCHULTE, BA VINCENT, DA AF GRATTON, MA SMYTH, BJ SCHULTE, BA VINCENT, DA TI NA,K-ATPASE ACTIVITY DECREASES IN THE COCHLEAR LATERAL WALL OF QUIET-AGED GERBILS SO HEARING RESEARCH LA English DT Article DE NA,K-ATPASE; STRIA VASCULARIS; ORGAN OF CORTI; AGING; GERBIL; ION TRANSPORT ID BICINCHONINIC ACID; K+-ATPASE; NA+,K+-ATPASE; LOCALIZATION; CELLS; ASSAY; NA+; RAT AB Alterations in the distribution and activity of Na,K-ATPase have been implicated in declining cell function with age. However, the location, size and anatomical complexity of the cochlea have limited study of this essential enzyme. Here we describe a micro-colorimetric assay which measures Na,K-ATPase activity in subregions of individual cochleae. Na,K-ATPase activity was determined in lateral wall and organ of Corti tissues by measuring liberation of inorganic phosphate (P-i) from ATP against a standard phosphate curve. Na,K-ATPase specific activity, expressed as mu mol P-i liberated/mg protein/h, was calculated as the difference between total P-i liberated versus P-i liberated in the presence of ouabain. Na,K-ATPase specific activity and total protein content in the lateral wall significantly exceeded those of the organ of Corti. Although lateral wall protein content remained constant with age, Na,K-ATPase specific activity declined in some older gerbils, suggesting a basis for age-related reductions in magnitude of the endocochlear potential and confirming previous histochemical results. This microassay offers a sensitive, reliable means to assay enzyme activity in subregions or single turns of the cochlea that unlike other methods does not rely on use of radioisotopes, enzymatic cycling or sample pooling. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP GRATTON, MA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD MAR PY 1995 VL 83 IS 1-2 BP 43 EP 50 DI 10.1016/0378-5955(94)00188-V PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000006 PM 7607990 ER PT J AU RYALS, BM STALFORD, MD LAMBERT, PR WESTBROOK, EW AF RYALS, BM STALFORD, MD LAMBERT, PR WESTBROOK, EW TI RECOVERY OF NOISE-INDUCED CHANGES IN THE DARK CELLS OF THE QUAIL TEGMENTUM VASCULOSUM SO HEARING RESEARCH LA English DT Article DE BIRD; HAIR CELLS; REGENERATION; TEGMENTUM VASCULOSUM ID INTENSE SOUND EXPOSURE; SEVERE ACOUSTIC TRAUMA; CHICK COCHLEA; TECTORIAL MEMBRANE; COTURNIX QUAIL; REGENERATION AB Morphologic changes in the tegmentum vasculosum (TV) of adult quail after high intensity sound exposure were studied. Quail were continuously exposed to 115 dB SPL, 1500 Hz pure tone in a sound field for 12 h and either sacrificed immediately (0 day), 1, 2, 3, 4, 6 or 10 days later. Serial sections through the basilar papilla at 100 mu m intervals from base to apex were obtained for study with light microscopy and TEM. Significant morphologic changes were found within the TV of quail sacrificed on days 0-4. On a quantitative scale, the majority of recovery occurred within the first 24 h. After four days survival the tegmentum appeared nearly normal. This recovery correlates well with the temporal pattern of threshold shift recovery. These results demonstrate a temporal correlation between ultrastructural changes in the TV and functional recovery of hearing after intense sound exposure. A potential etiologic role of the TV in avian temporary threshold shift is suggested. C1 UNIV VIRGINIA,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,CHARLOTTESVILLE,VA 22908. MCGUIRE DEPT VET AFFAIRS MED CTR,RICHMOND,VA. RP RYALS, BM (reprint author), JAMES MADISON UNIV,DEPT COMMUN SCI & DISORDERS,HARRISONBURG,VA 22807, USA. CR AXELSSON A, 1982, NEW PERSPECTIVES NOI, P49 CHEN L, 1991, CHIN J OTORHINOLARYN, V26, P70 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, 1992, EXP NEUROL, V115, P23, DOI 10.1016/0014-4886(92)90215-C COTANCHE DA, 1987, HEARING RES, V25, P125, DOI 10.1016/0378-5955(87)90086-4 COTANCHE DA, 1982, SCANNED ELECT MICROS, V3, P1283 DUVALL AJ, 1974, ANN OTO RHINOL LARYN, V83, P498 HASHINO E, 1988, J ACOUST SOC AM, V83, P2450, DOI 10.1121/1.396325 ISHIYAMA M, 1970, ANN OTOL RHINO LARYN, V79, P997 Manley G. A., 1990, PERIPHERAL HEARING M 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 RETZIUS G, 1884, GEHORORGAN WIRBELTIE, V1 RYALS BM, 1993, ABSTR ASS RES OT, V16, P171 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 SAUNDERS J, 1974, P NATL ACAD SCI USA, V71, P1962, DOI 10.1073/pnas.71.5.1962 SAUNDERS JC, 1991, J ACOUST SOC AM, V90, P136, DOI 10.1121/1.401307 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SCHNEIDER ME, 1987, HEARING RES, V31, P39, DOI 10.1016/0378-5955(87)90212-7 SEWELL DA, 1994, ABSTR ASS RES OT, V17, P483 STONE JS, 1992, J CELL SCI, V102, P671 VOSSIECK T, 1991, HEARING RES, V56, P93, DOI 10.1016/0378-5955(91)90158-6 YAMANE H, 1991, ACTA OTO-LARYNGOL, V111, P85, DOI 10.3109/00016489109137358 NR 26 TC 27 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1995 VL 83 IS 1-2 BP 51 EP 61 DI 10.1016/0378-5955(94)00190-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000007 PM 7607991 ER PT J AU BEAUBIEN, AR KARPINSKI, K ORMSBY, E AF BEAUBIEN, AR KARPINSKI, K ORMSBY, E TI TOXICODYNAMICS AND TOXICOKINETICS OF AMIKACIN IN THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE PHARMACODYNAMICS; PHARMACOKINETICS; OUTER HAIR CELLS; AMINOGLYCOSIDE ANTIBIOTIC; OTOTOXICITY; NONLINEAR MODELING; CHARACTERIZATION OF EFFECTS; 4-PARAMETER LOGISTIC ID OUTER HAIR CELLS; OTOTOXICITY; GENTAMICIN; KANAMYCIN; RADIOLIGAND; RESPONSES; THRESHOLD; POSITION; ABSENCE; ORGAN AB An extensive overview of the relationship between cochlear toxicity and amikacin blood concentrations in the guinea pig is provided which should assist in the clinical application of this class of antibiotic. A data set previously used to relate the incidence of amikacin ototoxicity to dosing rates and blood concentrations was re-examined to assess the toxicodynamics of amikacin in terms of decibels of hearing loss across dosing rate, hearing frequency and time following drug exposure. Animals in this data set had received continuously i.v. infused amikacin over an 8-fold range of dosing rates. Preliminary analysis indicated that the data were consistent with a sigmoid relationship between hearing loss (decibels) and area under the amikacin plasma concentration vs time curve cumulated over the entire course of drug administration (cAUC). The sigmoid model was therefore used as the backbone of a far more comprehensive toxicodynamic model which described all the data with a single equation. Testing with this model showed that the cAUC required to produce half-maximum hearing loss (cAUC-1/2) was related to dosing rate (P < 0.01), to hearing frequency (P < 0.00001), and to post-drug interval (P < 0.00001). Maximum hearing loss (difference between upper and lower sigmoid asymptotes) was less than total and was significantly related to frequency (P < 0.00001). No effects could be detected on the sigmoid slope. Further modelling of the significant effects detected by the comprehensive toxicodynamic model was done to determine if they could be described by simple relationships or by biologically relevant sub-models. Modelling of maximum hearing loss (postulated to represent loss of mainly outer hair cell function) indicated that this parameter was constant at about 61 decibels for 2-12 kHz and linearly decreased with log frequency for frequencies > 12 kHz. Modelling of cAUC-1/2 on frequency indicated that there was a strong inverse linear relationship to log frequency. Modelling of cAUC-1/2 on post-drug interval indicated that delayed ototoxicity continued at progressively slower rates for at least 56 days after drug administration-had ceased. Modelling of cAUC-1/2 on dosing rate showed an increased requirement for drug as the dosing rate decreased. However, cAUC-1/2 changed no more than 20% across the range of dosing rates compared to the 8-fold difference in mean steady-state plasma concentrations, suggesting that plasma concentration is not a primary determinant of ototoxicity. A toxicokinetic model was developed which explained the dosing rate effect on cAUC-1/2 very successfully. This model postulated (1) zero order accumulation of drug in the ototoxic pool at a rate directly proportional to steady-state amikacin plasma concentration, (2) first order disappearance kinetics from the ototoxic pool, and (3) that the level of drug accumulation in the ototoxic pool required to produce a given severity of hearing loss is the same for all dosing rates or plasma concentrations. The disappearance half-life from the ototoxic pool calculated from the fit of this toxicokinetic model to the data was about 80 days. Since the sloping portion of the sigmoid relationship for any one frequency covered several octaves of differential sensitivity to drug, it would appear that the slope results principally from row-to-row and to within row differences in drug sensitivity rather than to longitudinal differences. Cluster analysis of standardized hearing loss values (obtained by removing the influence of all significant effects from the residuals to the final toxicodynamic model) about a common sigmoid curve indicated that the hearing loss data falls into 4 main clusters whose means are about 20 dB apart, presumably corresponding to the loss of 0, 1, 2 or 3 rows of outer hair cells. These results show that, for a limited range of dosing exposures, amikacin-induced hearing loss in the guinea pig cochlea is well described as a sigmoid function of cAUC (R(2) = 0.71 With statistically significant parameters modelled in), and that sensitivity to drug can be expressed as a complex mathematical function of hearing frequency, dosing rate and post exposure time within an expanded sigmoid model. The estimate of a very long disappearance half-life of drug at the ototoxic pool has important clinical implications. C1 FOODS DIRECTORATE,BUR BIOSTAT & COMP APPLICAT,OTTAWA,ON K1A 0L2,CANADA. HLTH & WELF CANADA,HLTH PROTECT BRANCH,DRUGS DIRECTORATE,DIV BIOMETR & COMP SCI,OTTAWA,ON K1A 0L2,CANADA. RP BEAUBIEN, AR (reprint author), DRUGS DIRECTORATE,DIV BIOPHARMACEUT & PHARMACODYNAM,FREDERICK G BANTING BLDG,TUNNEYS PASTURE,OTTAWA,ON K1A 0L2,CANADA. CR ARAN JM, 1975, ACTA OTO-LARYNGOL, V79, P24, DOI 10.3109/00016487509124650 BEAUBIEN AR, 1990, ACTA OTO-LARYNGOL, V109, P345, DOI 10.3109/00016489009125154 BEAUBIEN AR, 1989, AM J OTOLARYNG, V10, P234, DOI 10.1016/0196-0709(89)90002-1 BEAUBIEN AR, 1991, ANTIMICROB AGENTS CH, V35, P1070 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 DEGROOT JCMJ, 1991, ACTA OTO-LARYNGOL, V111, P273, DOI 10.3109/00016489109137387 DULON D, 1993, CR ACAD SCI III-VIE, V316, P682 FINNEY DJ, 1976, BIOMETRICS, V32, P721, DOI 10.2307/2529258 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X PROSEN CA, 1980, NEUROTOXICOLOGY, V1, P497 RATKOWSKY DA, 1986, BIOMETRICS, V42, P575, DOI 10.2307/2531207 RYAN A, 1975, NATURE, V253, P44, DOI 10.1038/253044a0 RYAN AF, 1980, HEARING RES, V3, P335, DOI 10.1016/0378-5955(80)90027-1 SIEGENTHALER WE, 1986, AM J MED, V80, P2, DOI 10.1016/0002-9343(86)90473-0 TANGE RA, 1982, ARCH OTO-RHINO-LARYN, V236, P173, DOI 10.1007/BF00454037 THORNE PR, 1984, J ACOUST SOC AM, V76, P440, DOI 10.1121/1.391136 TRAN BHP, 1986, J CLIN INVEST, V77, P1492 WASTERSTROM SA, 1986, AM J OTOL, V7, P19 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P42 NR 22 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 1995 VL 83 IS 1-2 BP 62 EP 79 DI 10.1016/0378-5955(94)00192-S PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000008 PM 7607992 ER PT J AU GOLDSMITH, JD KUJAWA, SG MCLAREN, JD BLEDSOE, SC AF GOLDSMITH, JD KUJAWA, SG MCLAREN, JD BLEDSOE, SC TI IN-VIVO RELEASE OF NEUROACTIVE AMINO-ACIDS FROM THE INFERIOR COLLICULUS OF THE GUINEA-PIG USING BRAIN MICRODIALYSIS SO HEARING RESEARCH LA English DT Article DE NEUROTRANSMITTER; AMINO ACIDS; GABA; GLYCINE; GLUTAMATE ID MICROSCOPIC AUTORADIOGRAPHIC LOCALIZATION; STEM AUDITORY NUCLEI; LATERAL LEMNISCUS; DORSAL NUCLEUS; GABAERGIC PROJECTION; COCHLEAR NUCLEUS; GLYCINE RECEPTOR; INTERAURAL TIME; RAT; CAT AB Microdialysis techniques were used to measure in vivo release of neuroactive amino acids from the central nucleus of the inferior colliculus (ICC) in anesthetized guinea pigs. Concentric dialysis probes were implanted in the ICC and perfused with Ringer solution of various compositions at a flow rate of 2.0 mu l/min. Consecutive 10-min fractions of the dialysate were collected for up to 3 h under different experimental conditions, frozen and assayed for amino acid content by high performance liquid chromatography (HPLC). There was an initial high outflow of amino acids which declined to stable baseline levels,after 2 h. Following this stabilization period, perfusion with a medium containing 100 mM KCl produced an increase in the extracellular levels of aspartate (Asp), glutamate (Glu), gamma-aminobutyric acid (GABA) and glycine (Gly). Only the increases in GABA and Gly were statistically significant. None of the increases occurred in the presence of 2.0 mM cobalt suggesting the release of amino acids is calcium dependent. Histological examination revealed that tissue damage was minimal and largely confined to the immediate vicinity of the probes. We were also able to show that the blood brain barrier (BBB) appeared to heal 2 h after probe implantation. Thus, following intravenous injection of [H-3]alpha-aminoisobutyric acid (AIB), which does not cross the intact BBB, no isotope was recovered in the dailysate. These results demonstrate that microdialysis is a unique and suitable method to monitor changes in the extracellular levels of amino acid neurotransmitters in a central auditory structure. They also provide in vivo data that supports the notion that inhibitory amino acids play a functional role in processing acoustic information in the inferior colliculus. C1 UNIV MICHIGAN,SCH MED,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. UNIV ARIZONA,DEPT SPEECH & HEARING SCI,TUCSON,AZ 85721. CR ADAMS JC, 1987, ABSTR ASS RES OTOLAR, V10, P62 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 ADAMS JC, 1979, NEUROSCIENCE, V4, P1947, DOI 10.1016/0306-4522(79)90067-8 AOKI E, 1988, BRAIN RES, V442, P63, DOI 10.1016/0006-8993(88)91432-1 BENVENISTE H, 1989, J NEUROCHEM, V52, P1667, DOI 10.1111/j.1471-4159.1989.tb07243.x BENVENISTE H, 1990, PROG NEUROBIOL, V35, P195, DOI 10.1016/0301-0082(90)90027-E BLASBERG RG, 1983, J CEREBR BLOOD F MET, V3, P8 BLEDSOE SC, 1989, BRAIN RES, V493, P113, DOI 10.1016/0006-8993(89)91005-6 BRISTOW DR, 1988, EUR J PHARMACOL, V148, P283, DOI 10.1016/0014-2999(88)90576-6 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CAIRD D, 1987, EXP BRAIN RES, V68, P379 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 CASPARY DM, 1990, J NEUROSCI, V10, P2363 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 CONTRERAS NEIR, 1979, EXP BRAIN RES, V36, P573 DICHIARA G, 1990, TRENDS PHARMACOL SCI, V11, P116, DOI 10.1016/0165-6147(90)90197-G FAINGOLD CL, 1991, NEUROBIOLOGY HEARING, V2, P223 FAINGOLD CL, 1986, EXP NEUROL, V93, P145, DOI 10.1016/0014-4886(86)90154-8 FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 FISHER SK, 1976, J NEUROCHEM, V27, P1145, DOI 10.1111/j.1471-4159.1976.tb00321.x Gaddum J., 1961, J PHYSIOL-LONDON, V155, P1 GLOBUS MY, 1988, J NEUROCHEM, V1, P1455 GOLDEN GT, 1989, NEUROCHEM RES, V14, P465, DOI 10.1007/BF00964862 HAMBERGER A, 1985, IN VIVO PERFUSION RE, P119 KUWADA S, 1980, PSYCHOPHYSICAL PHYSL, P401 LOPEZCOLOME AM, 1978, NEUROSCIENCE, V3, P1069, DOI 10.1016/0306-4522(78)90124-0 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 NAGAI T, 1985, J COMP NEUROL, V231, P260, DOI 10.1002/cne.902310213 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, 1988, Society for Neuroscience Abstracts, V14, P490 PAULSEN RE, 1989, J NEUROCHEM, V52, P1823, DOI 10.1111/j.1471-4159.1989.tb07263.x PEYRET D, 1987, ACTA OTO-LARYNGOL, V104, P71, DOI 10.3109/00016488709109049 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 ROCKEL AJ, 1973, J COMP NEUROL, V147, P61, DOI 10.1002/cne.901470104 SAINTMARIE RL, 1990, BRAIN RES, V524, P244, DOI 10.1016/0006-8993(90)90698-B SAINTMARIE RL, 1989, J COMP NEUROL, V279, P382 SANDBERG M, 1986, J NEUROCHEM, V47, P178 SANES DH, 1987, J NEUROSCI, V7, P3793 SEIGHART W, 1986, J NEUROCHEM, V47, P920 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SHNEIDERMAN A, 1993, J NEUROCHEM, V60, P72, DOI 10.1111/j.1471-4159.1993.tb05824.x SHNEIDERMAN A, 1988, J COMP NEUROL, V276, P188, DOI 10.1002/cne.902760204 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 UNGERSTEDT U, 1987, LIFE SCI, V41, P861, DOI 10.1016/0024-3205(87)90181-0 WALZ W, 1985, NEUROMETHODS AMINO A, P239 WATANABE T, 1973, JPN J PHYSIOL, V23, P291 WESTERINK BHC, 1989, J NEUROCHEM, V52, P705, DOI 10.1111/j.1471-4159.1989.tb02512.x YOUNG AMJ, 1986, J NEUROCHEM, V47, P1399, DOI 10.1111/j.1471-4159.1986.tb00771.x ZARBIN MA, 1981, J NEUROSCI, V1, P532 NR 55 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 MAR PY 1995 VL 83 IS 1-2 BP 80 EP 88 DI 10.1016/0378-5955(94)00193-T PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000009 PM 7607993 ER PT J AU TAKEUCHI, S ANDO, M KOZAKURA, K SAITO, H IRIMAJIRI, A AF TAKEUCHI, S ANDO, M KOZAKURA, K SAITO, H IRIMAJIRI, A TI ION CHANNELS IN BASOLATERAL MEMBRANE OF MARGINAL CELLS DISSOCIATED FROM GERBIL STRIA VASCULARIS SO HEARING RESEARCH LA English DT Article DE MARGINAL CELL; ION TRANSPORT; NONSELECTIVE CATION CHANNEL; CL- CHANNEL ID NONSELECTIVE CATION CHANNEL; VESTIBULAR DARK CELLS; CHLORIDE CHANNELS; EPITHELIAL-CELLS; ETHACRYNIC-ACID; APICAL MEMBRANE; CELLULAR-MODEL; CL CHANNELS; CALCIUM; FUROSEMIDE AB The basolateral membrane of isolated strial marginal cells has been probed for conductive pathways by the patch-damp technique. Two types of voltage-insensitive channels were identified in both cell-attached and excised patches. Of these, frequently (69% of excised patches) observed was a Ca2+-activated nonselective cation channel having a unit conductance of 24.9 +/- 0.5 pS (N = 16). Other characteristics of this type in excised patches include: 1) linear I-V relations with 150 mM K+ (pipette)/150 mM Na+ (bath), 2) a permeability sequence of NH4+ > Na+ = K+ = Rb+ > Li+, 3) a flickering block by quinine or quinidine (both 1 mM), and 3) a dose dependent block of its activity by ADP or ATP (IC50,ATP/IC50,ADP = 20-35), both from the cytosolic side. Channels with similar characteristics were found in the apical membrane of the same cell; however, the basolateral channels were 2-4 times more densely distributed than the apical counterparts. Also frequently (57%) detected was a Cl- channel of 80.0 +/- 0.5 pS (N = 6), whose activity was Ca2+ independent. Additionally, this Cl- channel had: 1) linear I-V relations with symmetric Cl-, 2) a permeability sequence of Cl- > Br- > I- greater than or equal to NO3- greater than or equal to gluconate(-), and 3) a complete and reversible block by 1 mM diphenylamine-2-carboxylate. In contrast to the apical Cl- channels, the basolateral ones had a much higher density (57% vs. < 1%) as well as a higher unit conductance (80 pS vs. 50 pS) than the apical counterpart. The relative abundance of these two types as the major conductive pathways for Na+, K+, and Cl- in the basolateral region must be taken into account when addressing the role of strial marginal cells in generating the positive endocochlear potential. The Cl- channel may facilitate Cl- distribution across the basolateral membrane. C1 KOCHI MED SCH,DEPT OTOLARYNGOL,NANKOKU,KOCHI 783,JAPAN. RP TAKEUCHI, S (reprint author), KOCHI MED SCH,DEPT PHYSIOL,NANKOKU,KOCHI 783,JAPAN. CR ALTON EWFW, 1991, J PHYSIOL-LONDON, V443, P137 BOSHER SK, 1980, ARCH OTORHINOLARYNGO, V244, P346 FISCHER H, 1991, J COMP PHYSIOL B, V161, P333 GOGELEIN H, 1988, BIOCHIM BIOPHYS ACTA, V947, P521, DOI 10.1016/0304-4157(88)90006-8 GRAY MA, 1990, BIOCHIM BIOPHYS ACTA, V1029, P33, DOI 10.1016/0005-2736(90)90433-O HAGIWARA S, 1982, J PHYSIOL-LONDON, V331, P231 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 IKEDA K, 1989, HEARING RES, V40, P111, DOI 10.1016/0378-5955(89)90104-4 KATAGIRI S, 1968, ACTA OTOLARYNGOL, V68, P386 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KUNZELMANN K, 1989, PFLUG ARCH EUR J PHY, V415, P172, DOI 10.1007/BF00370589 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 LIM DJ, 1985, AM J OTOLARYNG, V6, P153, DOI 10.1016/S0196-0709(85)80078-8 MARCUS DC, 1992, AM J PHYSIOL, V262, pC1423 MARCUS DC, 1993, HEARING RES, V69, P124, DOI 10.1016/0378-5955(93)90100-F Marty A, 1983, SINGLE CHANNEL RECOR, P107 MARUYAMA Y, 1984, J MEMBRANE BIOL, P83 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 QUICK CA, 1970, LARYNGOSCOPE, V80, P954, DOI 10.1288/00005537-197006000-00009 RAE JL, 1990, EXP EYE RES, V50, P373, DOI 10.1016/0014-4835(90)90138-K RYBAK LP, 1982, HEARING RES, V7, P223, DOI 10.1016/0378-5955(82)90015-6 RYBAK LP, 1986, HEARING RES, V24, P133, DOI 10.1016/0378-5955(86)90057-2 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHMID A, 1989, J MEMBRANE BIOL, V111, P265, DOI 10.1007/BF01871011 SELLICK P M, 1975, Progress in Neurobiology (Oxford), V5, P337, DOI 10.1016/0301-0082(75)90015-5 SIMONS K, 1985, ANNU REV CELL BIOL, V1, P243 STURGESS NC, 1986, FEBS LETT, V208, P397, DOI 10.1016/0014-5793(86)81056-0 STURGESS NC, 1987, PFLUG ARCH EUR J PHY, V409, P607, DOI 10.1007/BF00584661 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 TAKEUCHI S, 1994, ASS RES OTOLARYNGOL, V17, P133 TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P WANGEMANN P, 1992, HEARING RES, V62, P149, DOI 10.1016/0378-5955(92)90180-U ZIOMEK CA, 1980, J CELL BIOL, V86, P849, DOI 10.1083/jcb.86.3.849 NR 34 TC 39 Z9 43 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1995 VL 83 IS 1-2 BP 89 EP 100 DI 10.1016/0378-5955(94)00191-R PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000010 PM 7541786 ER PT J AU NAIR, TS RAPHAEL, Y DOLAN, DF PARRETT, TJ PERLMAN, LS BRAHMBHATT, VR WANG, Y HOU, XM GANJEI, G NUTTALL, AL ALTSCHULER, RA CAREY, TE AF NAIR, TS RAPHAEL, Y DOLAN, DF PARRETT, TJ PERLMAN, LS BRAHMBHATT, VR WANG, Y HOU, XM GANJEI, G NUTTALL, AL ALTSCHULER, RA CAREY, TE TI MONOCLONAL-ANTIBODY INDUCED HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE MONOCLONAL ANTIBODIES; SUPPORTING CELLS; STEREOCILIA; AUDITORY BRAIN-STEM RESPONSES; MICE ID AUTOIMMUNE STRAIN MOUSE; INNER-EAR ANTIGENS; GUINEA-PIG; INTEGRIN ALPHA-6-BETA-4; SQUAMOUS CARCINOMA; COCHLEAR; CELLS; AUTOANTIBODIES; PEMPHIGUS; DISORDERS AB Monoclonal antibodies KHRI-3 and KHRI-5 identify antigens expressed on inner ear supporting cells and auditory hair cells respectively. To determine if these antibodies affect inner ear function groups of syngeneic Balb/c mice were inoculated with hybridomas KHRI-3, KHRI-5 and other Ig-secreting hybridomas. Hybridomas UM-A9, UM-7F11, the non-secreting SP2/0 myeloma and mice with no hybridoma were used as controls. Animals were tested for auditory brainstem responses (ABR) for frequencies of 4, 8, 16 and 24 kHz, before the inoculation of the hybridomas and at intervals of 6 to 10 days thereafter or daily once tumors became palpable. In normal mice there were no changes in ABR thresholds over the course of the experiment. Other control animals showed little change in ABR even when the growth of the hybridoma or myeloma tumors were far advanced, Of the KHRI-5 hybridoma bearing animals only one of seven animals exhibited threshold shifts greater than 15 dB. In contrast, most mice bearing the KHRI-3 hybridoma exhibited high frequency threshold shifts of 40-50 dB that coincided temporally with the growth of the hybridoma, the presence of circulating KHRI-3 antibody, and greatly increased immunoglobulin titers. Ears from KHRI-3-bearing mice that developed high frequency hearing loss also had a novel type of lesion in the basal turn of the cochlea that was characterized by loss of outer hair cells and absence of typical supporting cell scars. Such changes were not found in control hybridoma-bearing mice. These findings suggest that KHRI-3 antibody has an effect on hearing that is secondary to damage to the organ of Corti and loss of outer hair cells. Our results have important implications for antibody-mediated mechanisms of hearing loss and provide an animal model in which to study this phenomenon. C1 UNIV MICHIGAN,KRESGE HEARING RES INST 6020,CELL BIOL LAB,ANN ARBOR,MI 48109. CR AMAGAI M, 1992, J CLIN INVEST, V90, P919, DOI 10.1172/JCI115968 ANHALT GJ, 1982, NEW ENGL J MED, V306, P1189, DOI 10.1056/NEJM198205203062001 ANHALT GJ, 1981, J CLIN INVEST, V68, P1097, DOI 10.1172/JCI110333 ARNOLD W, 1985, ACTA OTO-LARYNGOL, V99, P437, DOI 10.3109/00016488509108935 BATES RC, 1994, J CELL BIOL, V125, P403, DOI 10.1083/jcb.125.2.403 BOETTCHER FA, 1992, HEARING RES, V62, P217, DOI 10.1016/0378-5955(92)90189-T CHEVANCE L G, 1960, Acta Otolaryngol, V52, P41, DOI 10.3109/00016486009123124 CRUZ O L M, 1990, American Journal of Otology, V11, P342 DELUCA M, 1990, P NATL ACAD SCI USA, V87, P6888 HARRIS JP, 1990, AM J OTOLARYNG, V11, P304, DOI 10.1016/0196-0709(90)90059-5 HARRIS JP, 1990, LARYNGOSCOPE, V100, P516 HARRIS JP, 1987, LARYNGOSCOPE, V97, P63 HARRIS JP, 1983, OTOLARYNGOL HEAD NEC, V91, P17 Hughes G B, 1988, Laryngoscope, V98, P251 JOLIAT T, 1992, ANN OTO RHINOL LARYN, V101, P1000 Kanzaki J, 1983, Acta Otolaryngol Suppl, V393, P77 KIMMEL KA, 1986, CANCER RES, V46, P3614 KOHLER G, 1975, NATURE, V256, P495, DOI 10.1038/256495a0 KUMAGAMI H, 1976, ORL J OTO-RHINO-LARY, V38, P334 KUSAKARI C, 1992, ANN OTO RHINOL LARYN, V101, P82 LEE EC, 1992, J CELL BIOL, V117, P671, DOI 10.1083/jcb.117.3.671 LOTZ MM, 1990, CELL REGUL, V1, P249 MCCABE BF, 1991, ADV OTO-RHINO-LARYNG, V46, P78 MCCABE BF, 1979, ANN OTO RHINOL LARYN, V88, P585 MOGI G, 1982, ARCH OTOLARYNGOL, V108, P270 NAIR TS, 1992, ASS RES OTOLARYNGOL OROZCO CR, 1990, LARYNGOSCOPE, V100, P941 PALVA T, 1981, ANN OTO RHINOL LARYN, V76, P23 PTOK M, 1991, HEARING RES, V57, P79, DOI 10.1016/0378-5955(91)90077-M PTOK M, 1993, HEARING RES, V66, P245, DOI 10.1016/0378-5955(93)90144-P PTOK M, 1993, EUR ARCH OTO-RHINO-L, V250, P345 RAPHAEL Y, 1992, J NEUROCYTOL, V21, P663, DOI 10.1007/BF01191727 RAPHAEL Y, 1991, HEARING RES, V51, P173, DOI 10.1016/0378-5955(91)90034-7 RAPHAEL Y, 1991, CELL MOTIL CYTOSKEL, V18, P215, DOI 10.1002/cm.970180307 SALOMON P, 1993, ACTA OTO-LARYNGOL, V113, P318, DOI 10.3109/00016489309135816 TAGO C, 1992, ANN OTO RHINOL LARYN, V101, P87 UNO K, 1993, ANN OTO RHINOL LARYN, V102, P537 VANWAES C, 1991, CANCER RES, V51, P2395 VELDMAN JE, 1984, LARYNGOSCOPE, V94, P501, DOI 10.1288/00005537-198404000-00014 WONG ML, 1992, HEARING RES, V59, P93, DOI 10.1016/0378-5955(92)90106-W YOO TJ, 1983, SCIENCE, V222, P65, DOI 10.1126/science.6623056 ZAJIC G, 1991, HEARING RES, V52, P59, DOI 10.1016/0378-5955(91)90187-E NR 42 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 1995 VL 83 IS 1-2 BP 101 EP 113 DI 10.1016/0378-5955(94)00194-U PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000011 PM 7607976 ER PT J AU MONSELL, EM CODY, DD BONE, HG DIVINE, GW WINDHAM, JP JACOBSON, GP NEWMAN, CW PATEL, SC AF MONSELL, EM CODY, DD BONE, HG DIVINE, GW WINDHAM, JP JACOBSON, GP NEWMAN, CW PATEL, SC TI HEARING-LOSS IN PAGETS-DISEASE OF BONE - THE RELATIONSHIP BETWEEN PURE-TONE THRESHOLDS AND MINERAL DENSITY OF THE COCHLEAR CAPSULE SO HEARING RESEARCH LA English DT Article DE COCHLEAR CAPSULE; BONE MINERAL DENSITY; PAGETS DISEASE; BEHAVIORAL AUDIOMETRY; CONDUCTIVE HEARING LOSS ID TEMPORAL BONE; OTOSCLEROSIS AB We have developed a unique method of quantitative computed tomography (QCT) that enables measurement of the density of the cochlear capsule in vivo. We performed pure-tone audiometry and QCT on 67 ears from 35 subjects with radiographically confirmed Paget's disease of the skull and on 40 ears from twenty volunteer subjects. The Pearson product-moment correlation coefficients (age- and sex-adjusted) in the group affected by Paget's disease were -0.63 for left ears and -0.73 for right ears for high-frequency air conduction pure-tone thresholds (mean of 1, 2, and 4 kHz) versus cochlear capsule density. Correlation coefficients (age- and sex-adjusted) between cochlear capsule density and air-bone gap (mean at 0.5 and 1 kHz) for the affected group were -0.67 for left ears and -0.63 for right ears. Ah correlations between hearing thresholds and cochlear capsule density in pagetic subjects were significant at p < 0.001. The regressions were consistent throughout the ranges of hearing level. There were no significant correlations between cochlear capsule mean density and hearing level in the volunteer subjects. These findings demonstrate the feasibility of precise and accurate density measurements in the temporal bone in vivo and support the use of the mean cochlear capsule density as a marker of disease effect. Alteration of cochlear capsule bone density may be related to the mechanisms of hearing loss in Paget's disease of bone. C1 HENRY FORD HOSP,DEPT DIAGNOST RADIOL,DIV RADIOL PHYS & ENGN,DETROIT,MI 48202. HENRY FORD HOSP,CTR BONE & JOINT SPECIALTY,DIV BONE & MINERAL,DETROIT,MI 48202. HENRY FORD HOSP,HENRY FORD HLTH SCI CTR,DIV BIOSTAT & RES EPIDEMIOL,DETROIT,MI 48202. HENRY FORD HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,DIV AUDIOL,DETROIT,MI 48202. HENRY FORD HOSP,DEPT NEUROL,DETROIT,MI 48202. HENRY FORD HOSP,DEPT DIAGNOST RADIOL,DIV NEURORADIOL,DETROIT,MI 48202. RP MONSELL, EM (reprint author), HENRY FORD HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,DIV OTOL & NEUROTOL,DETROIT,MI 48202, USA. CR APPLEBAUM EL, 1977, LARYNGOSCOPE, V87, P1753 CLEMIS JD, 1967, ANN OTO RHINOL LARYN, V76, P611 CODY DD, 1989, MED PHYS, V161, P766 DAMSMA H, 1984, RADIOL CLIN N AM, V22, P37 DAVIES DG, 1968, ACTA OTOLARYNGOL S S, V242, P1 DAVIES DG, 1968, J LARYNGOL OTOL, V8, P331 DAVIES D G, 1970, Journal of Laryngology and Otology, V84, P553, DOI 10.1017/S002221510007225X DEGROOT JAM, 1985, ANN OTO RHINOL LARYN, V94, P223 HUIZING EH, 1987, ACTA OTO-LARYNGOL, V103, P464 KANIS JA, 1991, PATHOPHYSIOLOGY TREA, P123 KHETARPAL U, 1990, ANN OTOL RHINOL S145, V99 MONSELL EM, 1993, AM J OTOL, V14, P1 NAGER GT, 1975, ANN OTO RHINOL LARYN, V84, P1 NAGER GT, 1993, PATHOLOGY EAR TEMPOR, P1011 PROOPS D, 1985, J OTOLARYNGOL, V14, P20 Rüedi L, 1968, Acta Otolaryngol, V65, P13, DOI 10.3109/00016486809120937 RUEGSEGGER P, 1991, BONE, V12, P99, DOI 10.1016/8756-3282(91)90007-6 SORENSEN MS, 1992, ACTA OTOLARYNGOL S S, V496, P4 Valvassori G E, 1973, Otolaryngol Clin North Am, V6, P379 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 MAR PY 1995 VL 83 IS 1-2 BP 114 EP 120 DI 10.1016/0378-5955(94)00196-W PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000012 PM 7607977 ER PT J AU SAGARA, T FURUKAWA, H MAKISHIMA, K FUJIMOTO, S AF SAGARA, T FURUKAWA, H MAKISHIMA, K FUJIMOTO, S TI DIFFERENTIATION OF THE RAT STRIA VASCULARIS SO HEARING RESEARCH LA English DT Article DE STRIA VASCULARIS; DIFFERENTIATION; EPITHELIAL-MESENCHYMAL INTERACTION; MARGINAL CELL; APICAL TUBULE; NA+ K+ ATPASE ID CELLS; LOCALIZATION; FIBRONECTIN; LAMININ; MUCOSA; LIVER AB The differentiation of the rat stria vascularis (SV) was investigated by light- and electron microscopy and by immunocytochemistry. Loss of the basal lamina at the epithelial-mesenchymal interface of SVs as indicated by immunoreactions of laminin and fibronectin induces the formation of vascular feet by basal infoldings of the marginal cells (MCs), and the development of the strial capillaries (SCs) by mesenchymal cells in a manner of vasculogenesis is progressing at the same time. The production of fibronectin in the rough endoplasmic reticulum of mesenchymal cells and the involvement of this glycoprotein in a mechanical linkage between the vasoformative mesenchymal cells and endothelial ones of the SCs are indicated by immunocytochemistry. The plasma membrane of the marginal cells (MCs) begins to show immunoreactions of Na+. K+ ATPase at postnatal day 5 and is conjugated to each other by tight junctions at postnatal day 14. The apical tubules of the differentiating MCs do not seem to be involved in the endocytotic activity but are involved in the plasma membrane supply for the rapid differentiation. C1 UNIV OCCUPAT & ENVIRONM HLTH,SCH MED,DEPT ANAT,KITAKYUSHU,FUKUOKA 807,JAPAN. UNIV OCCUPAT & ENVIRONM HLTH,SCH MED,DEPT OTORHINOLARYNGOL,KITAKYUSHU,FUKUOKA 807,JAPAN. 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Res. PD MAR PY 1995 VL 83 IS 1-2 BP 121 EP 132 DI 10.1016/0378-5955(94)00195-V PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000013 PM 7607978 ER PT J AU LOWE, M ROBERTSON, D AF LOWE, M ROBERTSON, D TI THE BEHAVIOR OF THE F(2)-F(1) ACOUSTIC DISTORTION-PRODUCT - LACK OF EFFECT OF BRAIN-STEM LESIONS IN ANESTHETIZED GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE ACOUSTIC DISTORTION PRODUCTS; MICROMECHANICS; OLIVOCOCHLEAR EFFERENTS; BRAIN-STEM LESIONS ID CONTRALATERAL SOUND STIMULATION; HAIR CELL MOTILITY; OLIVOCOCHLEAR NEURONS; COCHLEAR MECHANICS; EFFERENT SYSTEM; BUNDLE; ORGAN; CORTI; 2F1-F2; TRANSDUCTION AB Two tones of frequency f(1) and f(2) (the primary tones), when presented simultaneously to the ear, generate acoustic distortion products in the external ear canal. One of these distortion products, of frequency f(2)-f(1), has been shown to undergo a reversible change in amplitude when the primary tones generating distortion are presented continuously to the test (ipsilateral) ear (Brown, 1988; Kirk and Johnstone, 1993). The effect is apparent for low and moderate primary tone intensities and has been postulated to be caused by the action of a neural feedback loop via the superior olivary complex. We have carried out a series of studies of this phenomenon in anaesthetized guinea pigs, making brainstem lesions positioned so as to interrupt the known medial and/or lateral efferent projections to the cochlea from the superior olivary complex. We could not demonstrate any consistent change after lesioning, either in the baseline level of f(2)-f(1) or in the alteration of f(2)-f(1) caused by continuous monaural primary tones. These results are not consistent with the suggestion by others that a neural feedback loop involving either the medial (Brown, 1988) or lateral (Kirk and Johnstone, 1993) olivocochlear efferents may be responsible for the effect. We therefore conclude that either 1) the changes in f(2)-f(1) produced by continuous low-level primary tones reflect the operation of intrinsic hair cell mechanisms and do not involve efferent feedback via brainstem nuclei or 2) a neural feedback loop does play a role, but this loop involves an unknown pathway that was not interrupted by our lesions. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. 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Res. PD MAR PY 1995 VL 83 IS 1-2 BP 133 EP 141 DI 10.1016/0378-5955(94)00198-Y PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000014 PM 7607979 ER PT J AU MORIOKA, I REUTER, G REISS, P GUMMER, AW HEMMERT, W ZENNER, HP AF MORIOKA, I REUTER, G REISS, P GUMMER, AW HEMMERT, W ZENNER, HP TI SOUND-INDUCED DISPLACEMENT RESPONSES IN THE PLANE OF THE ORGAN OF CORTI IN THE ISOLATED GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; OUTER HAIR CELL; VIBRATION; FREQUENCY SELECTIVITY; TEMPORAL-BONE PREPARATION ID OUTER HAIR-CELLS; TEMPORAL BONE PREPARATION; HEARING ORGAN; MOTILE RESPONSES; FREQUENCY; DEPOLARIZATION; MOVEMENTS; FIBERS; NERVE; CAT AB Sound-induced displacement responses in the plane of the organ of Corti were studied in the apical turn in the isolated temporal-bone preparation of the guinea-pig cochlea. Swept sinusoidal sound stimuli (100-500 Hz) were delivered closed-field to the external auditory meatus. The surface of the organ of Corti was continuously monitored using a CCD video camera. Displacement responses in the plane of the organ of Corti were determined by analyzing the change of the location of the cells (pixel-by-pixel) within the visual field of the microscope. Displacement responses followed the stimulus amplitude and were observable at Hensen's cells, three rows of outer hair cells and inner hair cells. The most prominent displacement responses were over the outer hair cells; the maximum amplitude was 0.6-1.7 mu m at 100 dB SPL. Tuned displacement responses were found; the Q(10 dB) was 1.3 +/- 0.6. The best frequency was tonotopically organized, decreasing toward the apex with a space constant of 0.4-0.9 mm/oct. The motion was directed either strial-apically or strial-basally in a frequency dependent manner. With the aid of laser interferometric measurements of the transverse displacement, it was concluded that sound stimulation does not induce slow DC motion in the organ of Corti for the isolated temporal-bone preparation. C1 UNIV TUBINGEN,DEPT OTOLARYNGOL,HNO,HEARING RES LAB,D-72076 TUBINGEN,GERMANY. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 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, 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 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 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GITTER AH, 1988, BASIC ISSUES HEARING, P32 GUMMER AW, 1993, BIOPHYSICS HAIR CELL, P229 KHANNA SM, 1989, ACTA OTOLARYNGOL S, V467 Kim D. O., 1980, PSYCHOPHYSICAL PHYSL, P7 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 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 SANTOS-SACCHI J, 1991, J NEUROSCI, V11, P3096 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 STROMER H, 1991, THESIS U TUBINGEN TU, P19 ULFENDAHL M, 1991, HEARING RES, V57, P31, DOI 10.1016/0378-5955(91)90071-G ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 YAMASHITA T, 1990, ACTA OTO-LARYNGOL, V109, P256, DOI 10.3109/00016489009107441 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 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 28 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 MAR PY 1995 VL 83 IS 1-2 BP 142 EP 150 DI 10.1016/0378-5955(95)00002-L PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000015 PM 7607980 ER PT J AU FRANK, G KOSSL, M AF FRANK, G KOSSL, M TI THE SHAPE OF 2F(1)-F(2) SUPPRESSION TUNING CURVES REFLECTS BASILAR-MEMBRANE SPECIALIZATIONS IN THE MOUSTACHED BAT, PTERONOTUS-PARNELLII SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSION; DISTORTION PRODUCTS; 2F(1)-F(2); SUPPRESSION; TUNING CURVES; BASILAR MEMBRANE ID MOUSTACHED BAT; GUINEA-PIG; ACOUSTIC EMISSIONS; COCHLEA; SOUND; EAR; ECHOLOCATION; SYSTEM AB Iso-suppression tuning curves (STCs) of the 2f(1)-f(2) distortion product (dp) were measured over a primary frequency range of 20 to 93 kHz in mustached bats, Pteronotus pamellii pamellii. Primary levels were chosen to produce dp levels between 0 and 7 dB SPL. At frequencies outside the ranges of 60 - 72 kHz and 90 - 93 kHz the shapes of the STCs were symmetrical or asymmetrical with a steep high frequency slope. In the vicinity of 61 kHz where a strong stimulus frequency otoacoustic emission (SFOAE) is present, the asymmetry of the STCs was inverted with a very steep low frequency slope(max. -89 dB/kHz) and a shallow high frequency slope. The inverted STCs resemble neuronal tuning curves of the same species with best frequencies at about 61 kHz. Close to 61 kHz the STCs were sharply tuned with Q(10dB) values up to 177. The STC-thresholds were about 20 dB above the neuronal thresholds. Thickenings of the basilar membrane located just basal to the cochlear place of the SFOAE frequency are probably involved in creating the asymmetric STCs. Cochlear resonance at the SFOAE frequency and an increased longitudinal coupling within the thickened basilar membrane region are thought to contribute to the specialized STC shape. In the range of 40 - 93 kHz, the STCs are also sharply tuned with inverted asymmetry which is probably not due to an harmonic effect of the specialized cochlear mechanics in the 60 kHz region but may be caused by an independent mechanism. RP FRANK, G (reprint author), UNIV MUNICH,INST ZOOL,LUISENSTR 14,D-80021 MUNICH,GERMANY. 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PD MAR PY 1995 VL 83 IS 1-2 BP 151 EP 160 DI 10.1016/0378-5955(94)00197-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000016 PM 7607981 ER PT J AU BAJO, VM ROUILLER, EM WELKER, E CLARKE, S VILLA, AEP DERIBAUPIERRE, Y DERIBAUPIERRE, F AF BAJO, VM ROUILLER, EM WELKER, E CLARKE, S VILLA, AEP DERIBAUPIERRE, Y DERIBAUPIERRE, F TI MORPHOLOGY AND SPATIAL-DISTRIBUTION OF CORTICOTHALAMIC TERMINALS ORIGINATING FROM THE CAT AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE CAT; AUDITORY CORTEX; MEDIAL GENICULATE BODY; BIOCYTIN; ANTEROGRADE TRACER ID MEDIAL GENICULATE-BODY; ANTEROVENTRAL COCHLEAR NUCLEUS; SQUIRREL SCIURUS-CAROLINENSIS; LEUKOAGGLUTININ PHA-L; TONOTOPIC ORGANIZATION; FUNCTIONAL-ORGANIZATION; RESPONSE PROPERTIES; CORTICAL FIELDS; SINGLE NEURONS; BARREL CORTEX AB In this paper we studied the morphology and spatial distribution of corticothalamic axons and terminals originating from the auditory cortical fields of the cat. The anterograde tracer biocytin was injected at electrophysiologically characterized loci in the primary (AI) (N = 2), anterior (AAF) (N = 1), posterior (PAF) (N = 1) and secondary (AII) (N = 2) auditory fields. In all cases, two different types of labeled terminals were found in the auditory thalamus: small spherical endings (1-2 mu m) and giant, finger-like endings (5-10 mu m). After biocytin injections in AI and AAF, the majority of anterogradely labeled axons terminated in the rostral half of the pars lateralis (LV) of the ventral division of the medial geniculate body (vMGB). In LV, the corticothalamic axons ramified profusely, giving rise to dense terminal fields forming well delineated curved stripes, with small spherical endings. Additional terminal fields formed by small endings were observed in the medial division of the medial geniculate body (mMGB). Giant endings were observed in a small area in the dorsal nucleus (D) of the dorsal division of the medial geniculate body (dMGB), near its border with the vMGB. PAF projections were located in the caudal half of vMGB and in mMGB, where only small terminals were found. Giant endings were seen in the superficial part of dMGB emerging from labeled corticothalamic axons oriented in parallel to the dorsal surface of the MGB. Projections from AII gave rise to a main terminal field of small endings in D; a second terminal field consisting of giant endings intermingled with small endings was found in the deep dorsal nucleus (DD) of dMGB. We conclude that small terminals serve the feedback projection to the thalamic nucleus from which the injected cortical field receives its main input, whereas giant terminals cross the borders between the parallel ascending auditory pathways. C1 INST ANAT,LAUSANNE,SWITZERLAND. INST PHYSIOL,FRIBOURG,SWITZERLAND. DEPT BIOL CELULAR & PATOL,SALAMANCA,SPAIN. RP BAJO, VM (reprint author), UNIV LAUSANNE,INST PHYSIOL,RUE BUGON 7,LAUSANNE,SWITZERLAND. 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Res. PD MAR PY 1995 VL 83 IS 1-2 BP 161 EP 174 DI 10.1016/0378-5955(94)00199-Z PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000017 PM 7607982 ER PT J AU BORG, E VIBERG, A AF BORG, E VIBERG, A TI EXTRA INNER HAIR-CELLS - PREVALENCE AND NOISE SUSCEPTIBILITY SO HEARING RESEARCH LA English DT Article DE RABBIT; COCHLEA; MORPHOLOGY; SCANNING ELECTRON-MICROSCOPY ID GUINEA-PIG; STEREOCILIA; COCHLEA; RAT AB A total of 39 cochleae, 10 non-exposed and 29 noise exposed cochleae, were analyzed in a scanning electronmicroscope. Inner hair cells (IHCs) localized on the modiolar side of the ordinary row of IHCs were described. The mean number of such extra IHCs was 11 per cochlea both for non-exposed and exposed ears, ranging from 0-37. They showed a bimodal distribution with a maximum number at apex and 6-9 mm from apex. The dimension of the cuticular plate was slightly but significantly larger than for the ordinary IHCs. The extra IHCs suffered significantly less damage to their stereocilia than the ordinary IHCs after short-term high-level noise exposure. There was a significant negative correlation between the number of extra IHCs and the size of the post exposure permanent threshold shift. There was no evidence of postexposure generation of extra IHCs in or near the region of hair cell damage. It was concluded that extra IHCs normally occur in rabbits and that they are less susceptible to noise trauma than ordinary IHCs. The negative correlation between extra IHC occurrence and noise susceptibility needs further analysis. C1 OREBRO MED CTR HOSP,DEPT AUDIOL,S-70185 OREBRO,SWEDEN. RP BORG, E (reprint author), KAROLINSKA INST,DEPT PHYSIOL & PHARMACOL,S-17177 STOCKHOLM,SWEDEN. CR BORG E, 1993, NOISE MAN 93 NOISE P, V3, P161 BORG E, 1990, BRAIN RES, V506, P79, DOI 10.1016/0006-8993(90)91201-Q BORG E, 1989, J ACOUST SOC AM, V86, P1776, DOI 10.1121/1.398609 BREDBERG G, 1968, ACTA OTOLARYNGOLOG S, V236 ENGSTROM B, 1984, SCAND AUDIOL, V13, P87, DOI 10.3109/01050398409043045 ENGSTROM B, 1983, SCAND AUDIOL S, V19 Engstrom H, 1966, STRUCTURAL PATTERN O Ernstson S, 1972, Acta Otolaryngol Suppl, V297, P1 FURNESS DN, 1986, HEARING RES, V21, P243, DOI 10.1016/0378-5955(86)90222-4 LAVIGNEREBILLAR.M, 1987, ACTA OTOLARYNGOL S S, V436, P43 LIM DJ, 1985, ACTA OTOLARYNGOL S S, V422 RAPHAEL Y, 1991, J COMP NEUROL, V314, P367, DOI 10.1002/cne.903140211 Retzius G, 1884, GEHORORGAN WIRBELTIE, pII STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 WRIGHT A, 1984, HEARING RES, V13, P89, DOI 10.1016/0378-5955(84)90099-6 NR 15 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 MAR PY 1995 VL 83 IS 1-2 BP 175 EP 182 DI 10.1016/0378-5955(94)00200-A PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000018 PM 7607983 ER PT J AU RELKIN, EM DOUCET, JR STERNS, A AF RELKIN, EM DOUCET, JR STERNS, A TI RECOVERY OF THE COMPOUND ACTION-POTENTIAL FOLLOWING PRIOR STIMULATION - EVIDENCE FOR A SLOW COMPONENT THAT REFLECTS RECOVERY OF LOW SPONTANEOUS-RATE AUDITORY NEURONS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; ADAPTATION; CHINCHILLA; COMPOUND ACTION POTENTIAL; FORWARD MASKING; RECOVERY ID NERVE-FIBERS; GUINEA-PIG; INTENSITY; RESPONSES; THRESHOLDS; MASKING; NOISE; CATS AB Relkin and Doucet (1991) have shown that recovery of single auditory-nerve neurons from the effects of prior stimulation by a 100 ms pure tone varies with the spontaneous activity of the neuron. Recovery of thresholds for low spontaneous-rate (SR) neurons takes up to 2.0 s, a factor of 10 times greater than the 200 ms required for recovery of high SR neurons. The purpose of this study was to see if the different recovery rates for the two classes of neurons is reflected in recovery of the amplitude of the compound action potential (CAP) recorded in response to a brief probe tone with similar prior stimulation. We present evidence for two components in the recovery of the CAP amplitude, a slow and fast component, that have time courses similar to those for the recovery of responses for single low and high SR neurons, respectively. Thus, we conclude that the recovery of the CAP amplitude does indeed reflect the underlying recovery processes of single auditory-nerve neurons. C1 SYRACUSE UNIV,DEPT BIOENGN & NEUROSCI,SYRACUSE,NY 13244. RP RELKIN, EM (reprint author), SYRACUSE UNIV,INST SENSORY RES,MERRILL LANE,SYRACUSE,NY 13244, USA. 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PD MAR PY 1995 VL 83 IS 1-2 BP 183 EP 189 DI 10.1016/0378-5955(95)00004-N PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000019 PM 7607984 ER PT J AU CONDON, CJ CHANG, SH FENG, AS AF CONDON, CJ CHANG, SH FENG, AS TI CLASSIFICATION OF THE TEMPORAL DISCHARGE PATTERNS OF SINGLE AUDITORY NEURONS IN THE FROG SUPERIOR OLIVARY NUCLEUS SO HEARING RESEARCH LA English DT Article DE FROG; AUDITORY; FIRING PATTERN; BRAIN-STEM ID DORSAL MEDULLARY NUCLEUS; EFFERENT INNERVATION PATTERNS; AMPLITUDE-MODULATED SOUNDS; UNIT EXCITATORY RESPONSES; VENTRAL COCHLEAR NUCLEUS; NORTHERN LEOPARD FROG; BINAURAL TONE BURSTS; INFERIOR COLLICULUS; FREQUENCY-SELECTIVITY; RANA-CATESBEIANA AB Temporal discharge patterns of neurons in the superior olivary nucleus (SON) of the northern leopard frog (Rana pipiens pipiens) were studied by evaluating peri-stimulus time histograms and interspike interval histograms generated from responses to tone bursts at the neuron's characteristic frequency and at 10 dB above neuron's characteristic threshold. Four basic discharge patterns were observed, i.e., primary-like, phasic-burst, phasic, and pauser. Additionally, within each class, different neurons exhibited further subtle differences in temporal discharge patterns and thus subclasses were distinguishable. For most SON neurons, changes in signal lever did not affect the discharge pattern. However, there were a few notable exceptions. The firing pattern of 12% of SON neurons changed from one class to another with a change in signal level. Two-thirds of phasic-burst neurons showed increased regularity (i.e., chopping pattern) in their discharges as the signal level was increased. The majority of SON neurons showed monotonic rate-level functions, but one-fourth gave non-monotonic rate-level functions. The presence of a fairly large number of non-monotonic units in the frog SON suggests an additional role of this nucleus in information processing beyond the simple coding of stimulus level. The discharge patterns displayed by SON neurons resembled those seen in the frog cochlear nucleus and in the mammalian superior olivary complex. C1 UNIV ILLINOIS,DEPT PHYSIOL & BIOPHYS,NEUROSCI PROGRAM,URBANA,IL 61801. UNIV ILLINOIS,BECKMAN INST,URBANA,IL 61801. 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M., 1993, Society for Neuroscience Abstracts, V19, P533 NR 64 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1995 VL 83 IS 1-2 BP 190 EP 202 DI 10.1016/0378-5955(95)00005-O PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QQ710 UT WOS:A1995QQ71000020 PM 7607986 ER PT J AU RAREY, KE GERHARDT, KJ CURTIS, LM TENCATE, WJF AF RAREY, KE GERHARDT, KJ CURTIS, LM TENCATE, WJF TI EFFECT OF STRESS ON COCHLEAR GLUCOCORTICOID PROTEIN - ACOUSTIC STRESS SO HEARING RESEARCH LA English DT Article DE ACOUSTIC STRESS; GLUCOCORTICOIDS; COCHLEA ID RAT COCHLEA; GUINEA-PIG; NOISE; TISSUES; HEAT AB Levels of glucocorticoid (GR) receptor protein were determined by a quantitative enzyme-linked immunosorbent assay (ELISA) technique in inner ear tissues of rats exposed daily to 85 dB SPL white noise for 4 hours on 3 consecutive days. GR levels in spiral ligament and organ of Corti tissues were detected using a monoclonal antibody to the GR receptor, BuGR(2). A non-significant 13% decrease in GR levels of spiral ligament tissues was observed in the noise exposed animals relative to untreated animals. A statistically significant decrease of 27% in GR protein levels was seen in the organ of Corti region (P < 0.03), however. There was a concomitant increase of serum corticosterone levels (P < 0.03) in noise exposed animals as opposed to those of controls. These results indicate a tissue specific response of GR receptor to acoustic stress. Inner ear GR protein therefore may be a useful marker in determining the effect of stress on the inner ear. Finally, such data may be applicable to support the hypothesis that stress is an etiological agent in Meniere's disease. C1 UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT COMMUN PROC & DISORDERS,GAINESVILLE,FL 32611. RP RAREY, KE (reprint author), UNIV FLORIDA,COLL MED,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32610, USA. 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PD FEB PY 1995 VL 82 IS 2 BP 135 EP 138 DI 10.1016/0378-5955(94)00171-L PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900001 PM 7775279 ER PT J AU JONES, SM JONES, TA AF JONES, SM JONES, TA TI NEURAL TUNING CHARACTERISTICS OF AUDITORY PRIMARY AFFERENTS IN THE CHICKEN-EMBRYO SO HEARING RESEARCH LA English DT Article DE AVES; FREQUENCY TUNING; BASILAR PAPILLA; COCHLEA; ONTOGENY; DEVELOPMENT ID INFRASOUND SENSITIVE NEURONS; COCHLEAR GANGLION NEURONS; BASILAR PAPILLA; TONOTOPIC ORGANIZATION; DISCHARGE PATTERNS; HAIR-CELLS; CHARACTERISTIC FREQUENCY; INNERVATION PATTERNS; PREFERRED INTERVALS; PLACE PRINCIPLE AB Primary afferent activity was recorded from the cochlear ganglion in chicken embryos (Gallus domesticus) at 19 days of incubation (E19). The ganglion was accessed via the recessus scala tympani and impaled with glass micropipettes. Frequency tuning curves were obtained using a computerized threshold tracking procedure. Tuning curves were evaluated to determine characteristic frequencies (CFs), CF thresholds, slopes of low and high frequency flanks, and tip sharpness (Q(10dB)). The majority of tuning curves exhibited the typical 'V' shape described for older birds and, on average, appeared relatively mature based on mean values for CF thresholds (59.6 +/- 20.3 dBSPL) and tip sharpness (Q(10dB) = 5.2 +/- 3). The mean slopes of low (61.9 +/- 37 dB/octave) and high (64.6 +/- 33 dB/octave) frequency flanks although comparable were somewhat less than those reported for 21-day-old chickens. Approximately 14% of the tuning curves displayed an unusual 'saw-tooth' pattern. CFs ranged from 188 to 1623 Hz. The highest CF was well below those reported for post-hatch birds. In addition, a broader range of Q(10dB) values (1.2 to 16.9) may relate to a greater variability in embryonic tuning curves. Overall, these data suggest that an impressive functional maturity exists in the embryo at E19. The most significant sign of immaturity was the limited expression of high frequencies. it is argued that the limited high CF in part may be due to the developing middle ear transfer function and/or to a functionally immature cochlear base. C1 UNIV MISSOURI,SCH MED,DEPT SURG,DIV OTOLARYNGOL,COLUMBIA,MO 65212. CR COHEN GM, 1978, ACTA OTO-LARYNGOL, V86, P342, DOI 10.3109/00016487809107513 Cohen G M, 1993, Physiologist, V36, pS75 COHEN YE, 1992, HEARING RES, V58, P1, DOI 10.1016/0378-5955(92)90002-5 COTANCHE DA, 1984, DEV BRAIN RES, V16, P181, DOI 10.1016/0165-3806(84)90024-5 COTANCHE DA, 1983, ARCH OTO-RHINO-LARYN, V237, P191, DOI 10.1007/BF00453723 COTANCHE DA, 1985, SCANNING ELECT MICRO, V1, P407 COUSILLAS H, 1985, HEARING RES, V19, P217, DOI 10.1016/0378-5955(85)90141-8 FERMIN CD, 1984, ACTA OTO-LARYNGOL, V97, P39, DOI 10.3109/00016488409130963 GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 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 HEMOND SG, 1991, DEV BRAIN RES, V61, P87, DOI 10.1016/0165-3806(91)90117-2 JONNES SM, 1995, IN PRESS HEAR RES, V82 KLINKE R, 1986, HEARING RES, V22, P183, DOI 10.1016/0378-5955(86)90094-8 KNOWLTON VY, 1967, J MORPHOL, V121, P179, DOI 10.1002/jmor.1051210302 LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 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, 1988, BASIC ISSUES HEARING, P64 MANLEY GA, 1984, NATURWISSENSCHAFTEN, V71, P592, DOI 10.1007/BF01189191 MANLEY GA, 1991, HEARING RES, V57, P1, DOI 10.1016/0378-5955(91)90068-K MANLEY GA, 1991, HEARING RES, V56, P211, DOI 10.1016/0378-5955(91)90172-6 Manley G.A., 1988, P3 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 Sachs M.B., 1980, P323 SALVI RJ, 1992, J COMP PHYSIOL A, V170, P227 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SAUNDERS JC, 1985, HEARING RES, V18, P253, DOI 10.1016/0378-5955(85)90042-5 SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SCHERMULY L, 1990, HEARING RES, V48, P69, DOI 10.1016/0378-5955(90)90199-Y SCHERMULY L, 1990, J COMP PHYSIOL A, V166, P355 TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 Vanzulli A., 1963, ACTA NEUROL LATINOAM, V9, P19 WARCHOL ME, 1990, J COMP PHYSIOL A, V166, P721 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 40 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 FEB PY 1995 VL 82 IS 2 BP 139 EP 148 DI 10.1016/0378-5955(94)00172-M PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900002 PM 7775280 ER PT J AU JONES, SM JONES, TA AF JONES, SM JONES, TA TI THE TONOTOPIC MAP IN THE EMBRYONIC CHICKEN COCHLEA SO HEARING RESEARCH LA English DT Article DE AVES; BASILAR PAPILLA; AUDITION; DEVELOPMENT; BIOCYTIN; PRIMARY AFFERENTS ID STEM AUDITORY NUCLEI; HAIR CELL REGENERATION; BASILAR PAPILLA; ACOUSTIC TRAUMA; PLACE PRINCIPLE; MIDDLE-EAR; ONTOGENETIC CHANGES; GERBIL COCHLEA; ORGANIZATION; FREQUENCY AB The purpose of the present study was to determine the tonotopic map in the chicken cochlea at 19 days of incubation (E19) by obtaining characteristic frequencies (CFs) for primary afferents, labeling the characterized neurons, and documenting their projections to the papilla. The lowest and highest CFs recorded were 188 and 1623 Hz respectively. The embryonic tonotopic map coincided with maps reported for post-hatch chicks. There was no evidence that neurons selective to low frequencies project inappropriately to more basal locations of the embryonic papilla. Linear regression was used to estimate the frequency gradient (b = 0.037 +/- 0.012 In Hz/% [b +/- SE(b)]) and intercept (In C, where C = 111 Hz) of the semilog plot of frequency versus cochlear position (in % distance from apex). From these estimates the octave distribution was calculated to be 18.7%/octave or 0.58 man/octave. These quantities were not significantly different from those found in post hatch chickens. We conclude that the tonotopic map of the avian cochlea for CFs between 100 and 1700 Hz is stable and relatively mature from age E19 to post-hatch day 21 (P21). The most striking sign of immaturity in the E19 embryo is the limited range of high CFs. We offer the hypothesis that, between the ages of E19 and P21, improvements in middle ear admittance alone or in combination with functional maturation of the cochlear base may be the principal factors responsible for the appearance of adult-like high CF limits and not an apically shifting tonotopic map. C1 UNIV MISSOURI,SCH MED,DEPT SURG,DIV OTOLARYNGOL,COLUMBIA,MO 65212. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 COHEN GM, 1978, ACTA OTO-LARYNGOL, V86, P342, DOI 10.3109/00016487809107513 Cohen G M, 1993, Physiologist, V36, pS75 COHEN YE, 1992, HEARING RES, V58, P1, DOI 10.1016/0378-5955(92)90002-5 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 COTANCHE DA, 1984, DEV BRAIN RES, V16, P181, DOI 10.1016/0165-3806(84)90024-5 COTANCHE DA, 1983, ARCH OTO-RHINO-LARYN, V237, P191, DOI 10.1007/BF00453723 COUSILLAS H, 1985, HEARING RES, V19, P217, DOI 10.1016/0378-5955(85)90141-8 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FERMIN CD, 1984, ACTA OTO-LARYNGOL, V97, P39, DOI 10.3109/00016488409130963 GINZBERG RD, 1983, HEARING RES, V10, P227, DOI 10.1016/0378-5955(83)90056-4 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HEMOND SG, 1991, DEV BRAIN RES, V61, P87, DOI 10.1016/0165-3806(91)90117-2 JONES SM, 1995, IN PRESS HEAR RES, V82 KONISHI M, 1973, P NATL ACAD SCI USA, V70, P1795, DOI 10.1073/pnas.70.6.1795 LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 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, 1991, HEARING RES, V57, P1, DOI 10.1016/0378-5955(91)90068-K MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 PUJOL R, 1978, J COMP NEUROL, V177, P529, DOI 10.1002/cne.901770311 ROMAND R, 1987, HEARING RES, V288, P117 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 RUBEL EW, 1984, ANN OTO RHINOL LARYN, V93, P609 RUBEL EW, 1976, J COMP NEUROL, V166, P469, DOI 10.1002/cne.901660408 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 SALVI RJ, 1992, J COMP PHYSIOL A, V170, P227 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 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, 1983, DEV AUDITORY VESTIBU, P3 Vanzulli A., 1963, ACTA NEUROL LATINOAM, V9, P19 WARCHOL ME, 1990, J COMP PHYSIOL A, V166, P721 WARCHOL ME, 1989, J COMP PHYSIOL A, V166, P83 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 ZAR JH, 1984, BIOSTAT ANAL, P205 NR 42 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 FEB PY 1995 VL 82 IS 2 BP 149 EP 157 DI 10.1016/0378-5955(94)00173-N PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900003 PM 7775281 ER PT J AU CHEN, GD JASTREBOFF, PJ AF CHEN, GD JASTREBOFF, PJ TI SALICYLATE-INDUCED ABNORMAL ACTIVITY IN THE INFERIOR COLLICULUS OF RATS SO HEARING RESEARCH LA English DT Article DE SALICYLATE; SPONTANEOUS ACTIVITY; INFERIOR COLLICULUS; TINNITUS ID SPONTANEOUS OTOACOUSTIC EMISSIONS; PHANTOM AUDITORY-PERCEPTION; TERM THERAPEUTIC USE; OUTER HAIR-CELLS; GUINEA-PIG; DISTORTION PRODUCTS; NEURAL ACTIVITY; FETAL TOXICITY; TINNITUS; CALCIUM AB The evaluation of the spontaneous activity of 471 units from the external nucleus of the IC revealed that salicylate induces an increase of the spontaneous activity and the emergence of a bursting type of activity longer than 4 spikes. For sharply tuned units, the affected cells were from the frequency range of 10-16 Id-It, which corresponds to the behaviorally measured pitch of salicylate-induced tinnitus in rats. An exogenous calcium supplement, provided under the conditions shown to attenuate the behavioral manifestation of salicylate-induced tinnitus, abolished the modification of the spontaneous activity induced by salicylate. Finally, profound changes of activity were observed for cells not responding to contralateral sound. We propose that the observed long bursts of discharges represent tinnitus-related neuronal activity. The results are consistent with the hypothesis that GABA-mediated disinhibition is involved in the processing of tinnitus-related neuronal activity. C1 UNIV MARYLAND,SCH MED,DEPT SURG,BALTIMORE,MD 21201. CR ASHMORE JF, 1989, J PHYSIOL-LONDON, V412, pP46 ASSAD JA, 1992, J NEUROSCI, V12, P3291 ASSAD JA, 1992, P NATL ACAD SCI USA, V86, P2918 AXELSSON A, 1991, NOISE INDUCED HEARIN, P269 BOBBIN RP, 1992, NOISE INDUCED HEARIN, P38 BOBBIN RP, 1991, HEARING RES, V56, P101, DOI 10.1016/0378-5955(91)90159-7 BOETTCHER FA, 1991, AM J OTOLARYNG, V12, P33, DOI 10.1016/0196-0709(91)90071-M BRENNAN JF, 1991, ACTA NEUROBIOL EXP, V51, P15 BUSTO U, 1988, J CLIN PSYCHOPHARM, V8, P359 BUSTO U, 1986, NEW ENGL J MED, V315, P854, DOI 10.1056/NEJM198610023151403 CARLYON RP, 1993, HEARING RES, V66, P233, DOI 10.1016/0378-5955(93)90143-O CLARK WG, 1972, TOXICOL APPL PHARM, V23, P191, DOI 10.1016/0041-008X(72)90182-2 DIDIER A, 1993, HEARING RES, V69, P199, DOI 10.1016/0378-5955(93)90108-D DIELER R, 1991, J NEUROCYTOL, V20, P637, DOI 10.1007/BF01187066 DIELER R, 1991, ASS RES OTOLARYNGOL, V14, P13 DOUEK EE, 1983, J LARYNGOL OTOL, V93, P793 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 EGGERMONT JJ, 1990, HEARING RES, V48, P111, DOI 10.1016/0378-5955(90)90202-Z Evans E F, 1982, Br J Audiol, V16, P101, DOI 10.3109/03005368209081454 Evans E F, 1981, Ciba Found Symp, V85, P108 FAINGOLD CL, 1991, HEARING RES, V52, P201, DOI 10.1016/0378-5955(91)90200-S 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 FITZGERALD JJ, 1993, HEARING RES, V67, P147, DOI 10.1016/0378-5955(93)90242-S FLOWER RJ, 1980, PHARMACOL BASIS THER, P682 GUTH PS, 1991, HEARING RES, V56, P69, DOI 10.1016/0378-5955(91)90155-3 HACOHEN N, 1989, J NEUROSCI, V9, P3988 HAWKINS JE, 1991, TINNITUS 91, P135 HERRGESE.JD, 1967, J AM VET MED ASSOC, V151, P452 HU S, 1994, ASS RES OTOLARYNGOL, V17, P49 JASTREBOFF P, 1991, ASS RES OTOLARYNGOL, V14, P75 JASTREBOFF PJ, 1988, BEHAV NEUROSCI, V102, P811, DOI 10.1037/0735-7044.102.6.811 JASTREBOFF PJ, 1990, NEUROSCI RES, V8, P221, DOI 10.1016/0168-0102(90)90031-9 JASTREBOFF P J, 1985, Society for Neuroscience Abstracts, V11, P244 JASTREBOFF PJ, 1994, AUDIOLOGY, V33, P202 JASTREBOFF PJ, 1994, AM J OTOL, V15, P19 JASTREBOFF P J, 1989, Society for Neuroscience Abstracts, V15, P210 JASTREBOFF PJ, 1988, ARCH OTOLARYNGOL, V114, P186 JASTREBOFF PJ, 1991, ASS RES OTOLARYNGOL, V14, P145 JASTREBOFF PJ, 1992, TINNITUS 91, P309 JASTREBOFF PJ, 1991, ARCH OTOLARYNGOL, V117, P1162 JASTREBOFF PJ, 1986, ARCH OTOLARYNGOL, V112, P1050 JASTREBOFF PJ, 1985, J ACOUST SOC AM, V80, P1384 JUNG TTK, 1993, OTOLARYNG CLIN N AM, V26, P791 JURNA I, 1992, PAIN, V49, P2496 KAUBE H, 1993, HEADACHE, V33, P541, DOI 10.1111/j.1526-4610.1993.hed3310541.x KAUER JS, 1982, LARYNGOSCOPE, V92, P1401 KELLOGG CK, 1991, BEHAV NEUROSCI, V105, P640, DOI 10.1037/0735-7044.105.5.640 Kiang N Y, 1970, Ciba Found Symp, P241 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 KUJAWA SG, 1992, HEARING RES, V64, P73, DOI 10.1016/0378-5955(92)90169-N KUMAGAI M, 1992, Hokkaido Journal of Medical Science, V67, P216 LEES P, 1985, VET RECORD 0427, P479 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LONG GR, 1991, J ACOUST SOC AM, V89, P1201, DOI 10.1121/1.400651 MACDONALD RL, 1993, EPILEPSIA, V34, pS1, DOI 10.1111/j.1528-1157.1993.tb05918.x MARKUS HS, 1994, STROKE, V25, P1760 McFadden D, 1982, TINNITUS FACTS THEOR MCFADDEN D, 1984, HEARING RES, V16, P251, DOI 10.1016/0378-5955(84)90114-X MOLLER AR, 1984, ANN OTO RHINOL LARYN, V93, P39 MOLLER AR, 1992, LARYNGOSCOPE, V102, P1165 MOLLER AR, 1991, TINNITUS 91, P165 MOLLER AR, 1992, LARYNGOSCOPE, V102, P187 MOLLER AR, 1993, SURG CRANIAL NERVES, P105 MOLLER MB, 1993, LARYNGOSCOPE, V103, P421 MULHERAN M, 1990, THESIS U KEELE STAFF, P1 NINOYU O, 1988, ARCH OTORHINOLARYNGO, V243, P106 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A PUEL JL, 1990, OTOLARYNG HEAD NECK, V102, P66 SAITO H, 1982, RES COMMUN CHEM PATH, V38, P209 SALVI RJ, 1991, HEARING RES, V1, P97 SALVI RJ, 1983, J SPEECH HEAR RES, V26, P629 SASAKI CT, 1981, LARYNGOSCOPE, V91, P2018 SASAKI CT, 1980, BRAIN RES, V194, P511, DOI 10.1016/0006-8993(80)91233-0 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 SHEPHERD GMG, 1994, IN PRESS J NEUROSCI STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E Trinder P., 1953, BRANCHED CHAIN FATTY, V57, P301 UENO K, 1983, RES COMMUN CHEM PATH, V39, P179 WIER CC, 1988, J ACOUST SOC AM, V84, P230, DOI 10.1121/1.396970 ZUMGOTTESBERGE AM, 1988, MENIERES DISEASE, P343 ZUMGOTTESBERGEO.AM, 1986, ACTA OTO-LARYNGOL, V102, P93 NR 84 TC 130 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 FEB PY 1995 VL 82 IS 2 BP 158 EP 178 DI 10.1016/0378-5955(94)00174-O PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900004 PM 7775282 ER PT J AU ARAN, JM CHAPPERT, C DULON, D ERRE, JP AUROUSSEAU, C AF ARAN, JM CHAPPERT, C DULON, D ERRE, JP AUROUSSEAU, C TI UPTAKE OF AMIKACIN BY HAIR-CELLS OF THE GUINEA-PIG COCHLEA AND VESTIBULE AND OTOTOXICITY - COMPARISON WITH GENTAMICIN SO HEARING RESEARCH LA English DT Article DE AMINOGLYCOSIDE ANTIBIOTICS; COCHLEOTOXICITY; VESTIBULOTOXICITY; IMMUNOCYTOCHEMICAL LABELING; CONFOCAL MICROSCOPY ID ACOUSTIC STIMULATION; ETHACRYNIC-ACID; DESTRUCTION; RESPONSES AB The distribution of amikacin (AK), an exclusive cochleo-toxic aminoglycosidic antibiotic (AA), and of gentamicin (GM), which is bath cochleo- and vestibule-toxic, has been studied in cochlear and vestibular hair cells. Guinea pigs were treated during six days with one daily injection of AK (450 mg/kg/day) or GM (60 mg/kg/day). AAs were detected, using immunocytochemical technique with scanning laser confocal microscopy, in isolated cells from guinea pigs sacrificed from 2 to 30 days after the end of the treatments. Results demonstrate a rapid uptake (as soon as after 2-day treatment) of both AAs by cochlear and vestibular hair cells and a very slow clearance. Particularly GM and AK are detected in type I and type II hair cells of the utricles and cristae ampullaris. The presence of these two molecules with different toxic potentialities towards cochlear and vestibular hair cells indicates that the selective ototoxicity of aminoglycosides cannot be explained simply on the basis of particular uptake and accumulation in the different sensory hair cells. C1 UNIV BORDEAUX 2,HOP PELLEGRIN,F-33076 BORDEAUX,FRANCE. RP ARAN, JM (reprint author), INSERM,U229,AUDIOL EXPTL LAB,PL AMELIE RABAN LEON,F-33076 BORDEAUX,FRANCE. CR ARAN J, 1981, AMINOGLYCOSIDE OTOTO, P31 ARAN JM, 1979, ACTA OTO-LARYNGOL, V87, P300, DOI 10.3109/00016487909126424 Aran J M, 1982, Acta Otolaryngol Suppl, V390, P1 ARAN JM, 1982, NEPHROTOXICITE OTOTO, P377 ARAN JM, 1979, AUDITORY INVESTIGATI, P233 CAZALS Y, 1980, SCIENCE, V210, P83, DOI 10.1126/science.6968092 CAZALS Y, 1979, ARCH OTO-RHINO-LARYN, V224, P61, DOI 10.1007/BF00455225 DEGROOT JCM, 1990, HEARING RES, V50, P34 DULON D, 1986, ANTIMICROB AGENTS CH, V30, P96 DULON D, 1993, CR ACAD SCI III-VIE, V316, P682 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 HIEL H, 1992, ACTA OTO-LARYNGOL, V112, P272 HIEL H, 1993, AUDIOLOGY, V32, P78 HUY PTB, 1986, J CLIN INVEST, V17, P1492 SCARFONE E, 1991, CELL TISSUE RES, V266, P51, DOI 10.1007/BF00678710 SCHACHT J, 1993, OTOLARYNG CLIN N AM, V26, P845 VALAT J, 1989, HEARING RES, V40, P255, DOI 10.1016/0378-5955(89)90166-4 NR 18 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 FEB PY 1995 VL 82 IS 2 BP 179 EP 183 DI 10.1016/0378-5955(94)00175-P PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900005 PM 7775283 ER PT J AU VONUNGE, M DECRAEMER, WF DIRCKX, JJ BAGGERSJOBACK, D AF VONUNGE, M DECRAEMER, WF DIRCKX, JJ BAGGERSJOBACK, D TI SHAPE AND DISPLACEMENT PATTERNS OF THE GERBIL TYMPANIC MEMBRANE IN EXPERIMENTAL OTITIS-MEDIA WITH EFFUSION SO HEARING RESEARCH LA English DT Article DE OTITIS MEDIA; EFFUSION; SEROUS; MUCOID; ANIMAL MODEL; MOIRE INTERFEROMETRY; DISPLACEMENT; EARDRUM STIFFNESS ID CHOLESTEATOMA; PRESSURE AB This study assesses the visco-elastic properties of the tympanic membrane (TM) in isolated gerbilline temporal bones as a function of time after inducing experimental otitis media with effusion (OME). To do this we measured the TM displacements produced by application of sequences of static pressures across the TM, with a high resolution, real-time, differential moire interferometer, and the results were compared with measurements on healthy ears. Two methods of producing OME were used: in one group tubal plugging was performed to produce mild OME (the 'TP group'); in the other group electro-cauterization of the nasopharyngeal orifice of the Eustachian tube was used to cause a severe form of OME (the 'EC group'). The measurements were performed from one day up to ten weeks after surgery. In the TP group the displacement fringe patterns were normal, i.e. qualitatively they resembled the patterns of the control group. Quantitatively there was a significant decrease of displacement for a given pressure on the first day after surgery, followed by a trend of increase with time; after seven to ten days the displacement was larger than in the control group. In the EC group the displacement was significantly reduced after half a week, followed by a trend of increase with time, similar to what was found in the TP group; at one week the displacement was larger than in the control group, and at ten weeks the largest displacement was recorded. In the EC group the displacement patterns were often irregular; in some cases with changes suggesting the presence of weak spots in the TM where retraction pockets most likely could develop. OME seems to affect the stiffness of the TM promptly so that it is a potential parameter for early diagnosis. The stiffness changes may, if measurable in the clinical situation, become prognostic parameters in the treatment of OME. C1 KAROLINSKA INST,S-10401 STOCKHOLM,SWEDEN. UNIV ANTWERP,RIJKSUNIV CTR ANTWERP,BIOMED PHYS LAB,B-2020 ANTWERP,BELGIUM. RP VONUNGE, M (reprint author), KAROLINSKA SJUKHUSET,DEPT OTORHINOLARYNGOL,S-10401 STOCKHOLM,SWEDEN. CR BLUESTONE CD, 1972, ANN OTOL RHINOL LA S, V25, P182 DECRAEMER WF, 1980, J BIOMECH, V13, P559, DOI 10.1016/0021-9290(80)90056-1 FALK B, 1982, AM J OTOLARYNG, V3, P155, DOI 10.1016/S0196-0709(82)80048-3 MAES M, 1989, J BIOMECH, V22, P1203, DOI 10.1016/0021-9290(89)90222-4 MAGNUSON B, 1978, ACTA OTO-LARYNGOL, V86, P408, DOI 10.3109/00016487809107520 MOLLER P, 1981, ACTA OTO-LARYNGOL, V91, P215 SADE J, 1993, ANN OTO RHINOL LARYN, V102, P712 SHIMADA T, 1971, ANN OTO RHINOL LARYN, V80, P210 VONUNGE M, 1991, AM J OTOL, V12, P407 VONUNGE M, 1994, AM J OTOL, V15, P663 VONUNGE M, 1993, HEARING RES, V70, P229, DOI 10.1016/0378-5955(93)90161-S VONUNGE M, 1994, THESIS KAROLINSKA I WOLFMAN DE, 1986, ANN OTO RHINOL LARYN, V95, P639 NR 13 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 FEB PY 1995 VL 82 IS 2 BP 184 EP 196 DI 10.1016/0378-5955(94)00017-K PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900006 PM 7775284 ER PT J AU POJE, CP SEWELL, DA SAUNDERS, JC AF POJE, CP SEWELL, DA SAUNDERS, JC TI THE EFFECTS OF EXPOSURE TO INTENSE SOUND ON THE DC ENDOCOCHLEAR POTENTIAL IN THE CHICK SO HEARING RESEARCH LA English DT Article DE AUDITORY SYSTEM; ACOUSTIC TRAUMA; CHICK; COCHLEA; ENDOCOCHLEAR POTENTIAL; HEARING RECOVERY ID HAIR CELL REGENERATION; SEVERE ACOUSTIC TRAUMA; BASILAR PAPILLA; NEONATAL CHICKS; COCHLEAR FLUIDS; PURE-TONES; INNER-EAR; RECOVERY; GROWTH; NERVE AB Chicks were exposed to an intense pure tone (0.9 kHz, 120 dB SPL) for 48 h. The DC endocochlear potential was measured with a microelectrode inserted into scala media in six separate groups of animals between 0 and 12 days post exposure. Similar data were obtained from seven groups of unexposed control chicks between 2 and 15 days of age. One to nine animals were tested in each control or exposed group. The results in the control chicks revealed that the EP at 2 days of age (6.7 mV) was 36% of the mature value (15.2 mV) noted at 6 days of age. In the exposed animals, at 0-days recovery, the EP showed a 63% reduction relative to that measured in age matched control chicks. The level of EP in the exposed animals quickly recovered, and by 3 and 6 days post exposure exhibited a loss of only 7 and 3 percent relative to the age-matched controls. The recovery of EP was plotted against the recovery of evoked potential thresholds reported by others, and the time-course of the recovery functions were very similar. This relationship suggested that recovery of auditory function in the chick was highly correlated with the restoration of the EP. Damage to the tegmentum vasculosum and its capacity to secrete potassium, as well as the shunting of current through the damaged basilar papilla, are considered as mechanisms for the reduction of EP loss in the exposed ear. C1 UNIV PENN,DEPT OTORHINOLARYNGOL HEAD & NECK SURG,PHILADELPHIA,PA 19104. CHILDRENS HOSP PHILADELPHIA,DIV OTOLARYNGOL,PHILADELPHIA,PA 19104. CR ADLER HJ, 1993, HEARING RES, V71, P214, DOI 10.1016/0378-5955(93)90037-2 ADLER HJ, 1992, ACTA OTO-LARYNGOL, V112, P444, DOI 10.3109/00016489209137425 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 COHEN YE, 1993, EXP BRAIN RES, V95, P205 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, 1987, HEARING RES, V25, P125, DOI 10.1016/0378-5955(87)90086-4 COTANCHE DA, 1982, SCANNED ELECT MICROS, V3, P1283 COUSILLAS H, 1985, HEARING RES, V19, P217, DOI 10.1016/0378-5955(85)90141-8 FISCHER FP, 1992, HEARING RES, V61, P167, DOI 10.1016/0378-5955(92)90048-R HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 JORGENSEN FO, 1976, ACTA PHYSL SCAND, V100, P393 KLINKE R, 1993, PROG BRAIN RES, V97, P31 KNOWLTON VY, 1967, J MORPHOL, V191, P179 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 NECKER R, 1970, Z VERGL PHYSIOL, V69, P367, DOI 10.1007/BF00333768 PUGLIANO FA, 1993, ACTA OTO-LARYNGOL, V113, P18, DOI 10.3109/00016489309135761 RUBEL EW, 1983, SCIENCE, V219, P522 RUNHAAR G, 1991, HEARING RES, V56, P227, DOI 10.1016/0378-5955(91)90173-7 RYALS BM, 1993, ABSTR ASS RES OT, V16, P43 RYALS BM, 1985, HEARING RES, V19, P135, DOI 10.1016/0378-5955(85)90117-0 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 RYBAK LP, 1992, HEARING RES, V59, P189, DOI 10.1016/0378-5955(92)90115-4 Saunders J. C., 1982, NEW PERSPECTIVES NOI, P229 SAUNDERS JC, 1973, BRAIN RES, V37, P59 SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A SAUNDERS JC, 1993, HEARING RES, V69, P25, DOI 10.1016/0378-5955(93)90090-N SCHMIDT RS, 1963, COMP BIOCHEM PHYSIOL, V10, P83, DOI 10.1016/0010-406X(63)90105-1 SCHMIDT RS, 1962, J CELL COMPAR PHYSL, V59, P311, DOI 10.1002/jcp.1030590311 SCHNEIDER ME, 1987, HEARING RES, V31, P39, DOI 10.1016/0378-5955(87)90212-7 SCHWARTZKOPFF J, 1973, BASIC MECHANISMS HEA, P423 STERKERS O, 1988, PHYSIOL REV, V68, P1083 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 NR 38 TC 28 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 FEB PY 1995 VL 82 IS 2 BP 197 EP 204 DI 10.1016/0378-5955(94)00177-R PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900007 PM 7775285 ER PT J AU POLYAKOV, A PRATT, H AF POLYAKOV, A PRATT, H TI 3-CHANNEL LISSAJOUS TRAJECTORY OF THE BINAURAL INTERACTION COMPONENTS OF HUMAN AUDITORY MIDDLE-LATENCY EVOKED-POTENTIALS SO HEARING RESEARCH LA English DT Article DE AUDITORY; MIDDLE LATENCY EVOKED POTENTIALS; BINAURAL INTERACTION; 3-CHANNEL LISSAJOUS TRAJECTORY ID BRAIN-STEM RESPONSE; CORTICAL-LESIONS; GUINEA-PIG; CAT; GENERATORS; ORGANIZATION; LOCALIZATION; STIMULI; PATIENT; AGNOSIA AB Three-channel Lissajous' trajectories (3-CLTs) of the binaural interaction component (BI) of auditory middle latency evoked potentials (AMLEPs) were derived from 14 normally hearing adults by subtracting the response to binaural clicks from the algebraic sum of monaural responses. AMLEPs were recorded in response to 65 dB nHL, rarefaction clicks, presented at a rate of 3.3/s. A normative set of BI 3-CLT measures was calculated and compared with the corresponding measures of simultaneously recorded, single-channel vertex-left mastoid and vertex-neck derivations of BI and of AMLEP to binaural stimulation (B). 3-CLT measures included: apex latency, amplitude and orientation, as well as planar segment duration, orientation, size and shape. The results showed seven main apices and associated planar segments ('Be','Bf,'Bg', 'Bh','Bi,','Bi-2' and 'Bj') in the 3-CLT of BI. Apex latencies of the BI 3-CLT were comparable to peak latencies of the vertex-left mastoid and vertex-neck AMLEP and BI records, both in their absolute values and in intersubject variability. Durations of BI planar segments were approximately 5.0 ms, Apex amplitudes of BI 3-CLT were larger than the respective peak amplitudes of the vertex-mastoid and vertex-neck BI records, while their intersubject variabilities were comparable. The lateralization of BI components may indicate asymmetric processing of binaural auditory input, or may be connected with anatomical asymmetry such as skull thickness. Preliminary analyses did not reveal a clear correlation between the lateralization of the BI component 'Bi,' and the handedness of the subject. We suggest that BI components of AMLEP may be associated with the primary auditory cortex and subcortical ascending structures. C1 TECHNION ISRAEL INST TECHNOL,EVOKED POTENTIALS LAB,IL-32000 HAIFA,ISRAEL. 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Res. PD FEB PY 1995 VL 82 IS 2 BP 205 EP 215 DI 10.1016/0378-5955(94)00178-S PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900008 PM 7775286 ER PT J AU ZENG, FG SHANNON, RV AF ZENG, FG SHANNON, RV TI POSSIBLE ORIGINS OF THE NONMONOTONIC INTENSITY DISCRIMINATION FUNCTION IN FORWARD MASKING SO HEARING RESEARCH LA English DT Article DE INTENSITY DISCRIMINATION; FORWARD MASKING; ADAPTATION; ELECTRIC STIMULATION; COCHLEAR IMPLANT; AUDITORY BRAIN-STEM IMPLANT; CONTRALATERAL STIMULATION ID AUDITORY-NERVE FIBERS; ANTEROVENTRAL COCHLEAR NUCLEUS; HAIR CELL; ELECTRIC-STIMULATION; LOUDNESS ENHANCEMENT; NEURAL TRANSDUCTION; CENTRAL PROJECTIONS; RESPONSE PATTERNS; ADAPTATION; NEURONS AB A non-monotonic intensity discrimination function in forward masking has been recently reported [Zeng et al. (1991) Hear. Res. 55, 223-230; Zeng and Turner (1992) J. Acoust Sec. Am. 92, 782-787] in which just-noticeable-differences (jnds) in intensity are largest for midlevel tones and smaller for soft and loud tones following an intense narrow-band noise, One hypothesis was that this midlevel hump reflects the contribution of low-spontaneous rate (SR) neurons to intensity coding, based on the differential recovery from forward masking of low-SR and high-SR neurons [Relkin and Doucet (1991) Hear. Res. 55, 215-222]. The present study conducted three experiments stimulating different stages of the auditory system in an attempt to determine the peripheral and central origins of the midlevel hump. First, in two cochlear implant (CI) listeners, the forward masker produced a midlevel hump on the intensity discrimination function, suggesting that the synapses between the hair cell and the eighth nerve are probably not responsible for the hump, as they are bypassed and the eighth nerve is stimulated directly. Second, in auditory brainstem implant (ABI) listeners, the forward masker produced no midlevel hump, but the masked jnds were larger than those without a masker. The absence of the midlevel hump in the ABI listeners suggests that the occurrence of the hump requires physiological mechanisms in the auditory nerve transmission, or the intrinsic processing circuits of the cochlear nuclei, or both. Third, in normal-hearing listeners, an ipsilateral, 90 dB SPL, pure-tone forward masker produced a midlevel hump, which is similar to that using a narrow-band noise masker; whereas a contralateral forward masker produced essentially no midlevel hump, suggesting that binaural interactions at superior olivary complex and more central sites are probably not responsible. RP ZENG, FG (reprint author), HOUSE EAR RES INST,2100 W 3RD ST,LOS ANGELES,CA 90057, USA. 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PD FEB PY 1995 VL 82 IS 2 BP 216 EP 224 DI 10.1016/0378-5955(94)00179-T PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900009 PM 7775287 ER PT J AU COOPER, NP RHODE, WS AF COOPER, NP RHODE, WS TI NONLINEAR MECHANICS AT THE APEX OF THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEAR MECHANICS; REISSNERS MEMBRANE; BASILAR MEMBRANE; PEAK-SPLITTING ID BASILAR-MEMBRANE MECHANICS; AUDITORY-NERVE FIBERS; OUTER HAIR-CELLS; DISPLACEMENT RESPONSE; MOSSBAUER TECHNIQUE; HEARING ORGAN; TUNING CURVES; FREQUENCY; VIBRATION; POSITION AB A heterodyne laser interferometer was used to observe the sound-evoked displacement patterns of Reissner's membrane and various other structures in the apical turn of the guinea-pig cochlea. Most structures (including the basilar membrane) were similarly tuned, and had best frequencies in the 200-350Hz range. A distinct notch was usually observed similar to 0.7 octaves above the best frequency, and amplitude- and phase-plateaus were observed at higher frequencies. In most other respects, however, the mechanical tuning resembled the frequency-threshold curves of low frequency cochlear nerve fibers. In five reasonably intact, in vivo preparations, the frequency of the mechanical sensitivity notch was intensity-dependent: Compressive nonlinearities were observed above similar to 80 dB SPL on the low-frequency side of the notch, with antagonistically expansive nonlinearities on the high-frequency side. Two-tone suppression was observed in one of these preparations. Stimulus-related baseline position shifts were observed in another in vivo preparation. No such nonlinearities were observed in structurally damaged and/or > 1 hour post-mortem preparations. However, more robust nonlinearities were observed in all preparations at higher levels of stimulation (e.g. > 100-110 dB SPL). These high-level nonlinearities diminished only slowly after death, and gave rise to various effects, including time-dependent (i.e. adapting) and severely distorted (e.g. peak-split and/or de-shifted) responses. RP COOPER, NP (reprint author), UNIV WISCONSIN,DEPT NEUROPHYSIOL,275 MED SCI BLDG,1300 UNIV AVE,MADISON,WI 53706, USA. CR ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 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 CARNEY LH, 1988, J NEUROPHYSIOL, V60, P1653 Cooper N. 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C., 1976, THESIS HARVARD U CAM MANLEY GA, 1974, J ACOUST SOC AM, V56, P571, DOI 10.1121/1.1903292 MOUNTAIN DC, 1989, COCHLEAR MECH STRUCT, P153 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PFEIFFER RR, 1972, J ACOUST SOC AM, V52, P1670 PRIJS VF, 1989, HEARING RES, V42, P73, DOI 10.1016/0378-5955(89)90118-4 Rhode W. 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Res. PD FEB PY 1995 VL 82 IS 2 BP 225 EP 243 DI 10.1016/0378-5955(94)00180-X PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900010 PM 7775288 ER PT J AU ZHAO, HB LIANG, ZA AF ZHAO, HB LIANG, ZA TI PROCESSING OF MODULATION FREQUENCY IN THE DORSAL COCHLEAR NUCLEUS OF THE GUINEA-PIG - AMPLITUDE-MODULATED TONES SO HEARING RESEARCH LA English DT Article DE MODULATION INFORMATION; TEMPORAL ENCODING; AMPLITUDE MODULATION; DORSAL COCHLEAR NUCLEUS; GUINEA PIG ID INFERIOR COLLICULUS; AUDITORY-CORTEX; NERVE FIBERS; RESPONSES; NEURONS; SOUNDS; CAT; STIMULI; REPRESENTATION; FLUCTUATIONS AB The modulation frequency (Fm), particularly high Fm (> 200 Hz), in amplitude modulated (AM) tones can elicit the perception of the periodicity pitch (Langner, 1992). In this study, single unit responses to the Fms of the sinusoidal AM tones were investigated at 50 to 90 dB SPL. The recordings were made from the dorsal cochlear nucleus (DCN) of neuroleptic anesthetized guinea pigs with an intact cerebellum The DCN units show a good capability of phase-locking to Fm at 400-1200 Hz. On-S-type II and Pauser/Buildup (P/B) units have a high modulation gain (7.2-8.3 dB). P/B units can preserve the high modulation gain (5-9 dB) up to 90 dB SPL. The modulation gain exponentially increases with decreasing modulation depth (Dm) and the phase-locking is detectable even at the Dm as low as 2-5%. The 'central skipping' of the phase-locking peak has been found at deep Dms in a few cases. The synchronization is independent of the discharge rate and can remain high even when the responses to AM tones are inhibited below the spontaneous activity. Such encoding behaviors over the unit's response area show that the Fm phase-locking is strong near or at its characteristic frequency (CF). The synchronization index (SI) versus carrier frequency (Fc) curve is similar to the inverse shape of tuning curve but more narrowly tuned than the iso-intensity function of pure tones at moderate to high intensity levels. The phase-locking is related to the unit's spontaneous rate (SR). The average modulation gain of the lower SR (less than or equal to 2 spikes/s) units is 5 dB higher than that of the higher SR (> 2 spikes/s) units (8.16 and 2.92 dB, respectively) at 70 dB SPL. These results suggest that AM information is temporally encoded over broad ranges of modulation parameters in the DCN and is conveyed by the Fc channel. Such a timing mechanism can play an important role in processing of complex sounds under normal acoustic conditions. C1 CHINESE ACAD SCI,SHANGHAI INST PHYSIOL,SHANGHAI 200031,PEOPLES R CHINA. 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PD FEB PY 1995 VL 82 IS 2 BP 244 EP 256 DI 10.1016/0378-5955(94)00181-O PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900011 PM 7775289 ER PT J AU AITKIN, L AF AITKIN, L TI THE AUDITORY NEUROBIOLOGY OF MARSUPIALS - A REVIEW SO HEARING RESEARCH LA English DT Article DE MARSUPIAL; AUDITORY PATHWAY; NEUROGENESIS; ONSET OF HEARING; AUDIOGRAM ID NORTH-AMERICAN OPOSSUM; POSSUM TRICHOSURUS-VULPECULA; CAT DASYURUS-HALLUCATUS; BRUSH-TAILED POSSUM; INFERIOR COLLICULUS; BRAIN-STEM; MONODELPHIS-DOMESTICA; EXTERNAL NUCLEUS; COCHLEAR NUCLEUS; NEURONS AB The marsupials, the large group of mammals which develop during fetal life in an externalized pouch, have been given little attention by auditory neurobiologists. In this review the structure of the auditory systems of the handful of marsupials which have been studied is described, the course of auditory development mapped, and the behavioral and electrophysiological manifestations bf hearing examined. It is argued that research on the highly accessible developing marsupial will provide information about the development of hearing difficult to obtain from, but applicable to all, mammalian species. C1 MONASH UNIV,DEPT PHYSIOL,MELBOURNE,VIC 3168,AUSTRALIA. 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PD FEB PY 1995 VL 82 IS 2 BP 257 EP 266 DI 10.1016/0378-5955(94)00182-P PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900012 PM 7775290 ER PT J AU MAREAN, GC CUNNINGHAM, D BURT, JM BEECHER, MD RUBEL, EW AF MAREAN, GC CUNNINGHAM, D BURT, JM BEECHER, MD RUBEL, EW TI REGENERATED HAIR-CELLS IN THE EUROPEAN STARLING - ARE THEY MORE RESISTANT TO KANAMYCIN OTOTOXICITY THAN ORIGINAL HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE REGENERATION; OTOTOXICITY; RESISTANCE; AVIAN; STARLING ID TOXICITY; COCHLEA AB Previous work from our laboratory [Marean et al. (1993) Hear. Res. 71, 125-136] has shown that a 10 day dose of 200 mg/kg/day kanamycin produced damage to the basal 34% of the starling basilar papilla. We also observed that repeating the dosing schedule following a 4 month survival period resulted in significantly less damage to the regenerated auditory epithelium. The present study investigated whether or not this apparent resistance was the result of a tendency for regenerated hair cells to be less susceptible to kanamycin ototoxicity, or if other, systemic factors may be involved. Eight European starlings were given subcutaneous injections of 200 mg/kg/day kanamycin for 10 days. Serum levels of kanamycin were measured at the time of sacrifice for all birds, and the basilar papillae of all birds were examined by scanning electron microscopy (SEM). Two of these birds (Group 1) were sacrificed immediately following the dosing period. Two of the birds were allowed to survive for 60 days (Group 2). Two of the birds were redosed with 200 mg/kg/day for 10 days after 60 days survival (Group 3). Finally, two birds were redosed with 250 mg/kg/day until serum levels of kanamycin were the same as Group 1 when sacrificed(> 9 mu g/ml). The SEM results showed that the regenerated auditory epthelium of the birds dosed a second time sustained less damage compared to previously untreated ears, even though the dosing regimen was the same (Group 3 versus Group 1). The regenerated auditory epethelium of birds dosed a second time sustained the same damage as previously untreated animals when the dosage was increased to attain similar serum levels (Group 4 versus Group 1). These results suggest metabolic changes occur in the starling in response to the initial dose of kanamycin which do not necessarily involve changes in hair cell resistance to ototoxicity. C1 UNIV WASHINGTON, VIRGINIA MERRIL BLOEDEL HEARING RES CTR, DEPT OTOLARYNGOL HEAD & NECK SURG, SEATTLE, WA 98195 USA. UNIV WASHINGTON, DEPT SPEECH & HEARING SCI, SEATTLE, WA 98195 USA. UNIV WASHINGTON, DEPT PSYCHOL, SEATTLE, WA 98195 USA. CR CONNEY AH, 1967, PHARMACOL REV, V19, P317 COTANCHE DA, 1994, ANAT EMBRYOL, V189, P1 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 GIBALDY M, 1991, BIOPHARMACEUTICS CLI HASHINO E, 1992, HEARING RES, V59, P46, DOI 10.1016/0378-5955(92)90101-R Kucers A, 1987, USE ANTIBIOTICS LIPPE WR, 1991, HEARING RES, V56, P203, DOI 10.1016/0378-5955(91)90171-5 Manley G. A., 1990, PERIPHERAL HEARING M MAREAN GC, 1993, HEARING RES, V71, P125, DOI 10.1016/0378-5955(93)90028-Y NR 9 TC 19 Z9 23 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 FEB PY 1995 VL 82 IS 2 BP 267 EP 276 DI 10.1016/0378-5955(94)00183-Q PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QM319 UT WOS:A1995QM31900013 PM 7775291 ER PT J AU AUTHIER, S MANLEY, GA AF AUTHIER, S MANLEY, GA TI A MODEL OF FREQUENCY TUNING IN THE BASILAR PAPILLA OF THE TOKAY GECKO, GEKKO-GECKO SO HEARING RESEARCH LA English DT Article DE GECKO; LIZARD; TUNING MODEL; BASILAR PAPILLA; FREQUENCY TUNING; HEARING ID ALLIGATOR LIZARD COCHLEA; GUINEA-PIG COCHLEA; HAIR-CELLS; TONOTOPIC ORGANIZATION; BUNDLES; STEREOCILIA; RESONANCE; SELECTIVITY; STIFFNESS; TILIQUA AB This paper uses the quantitative details of the anatomy of the auditory papilla in the Tokay gecko Gekko gecko (as described in the companion paper) to make a quantitative model predicting the tonotopic organization of two of the three papillar areas. Assuming that hair-cell bundle stiffness is similar to that of other species, a model of resonance frequencies for the apical areas of the papilla was constructed, taking into account factors such as the number of hair cells per resonant unit, their bundle dimensions, the volume of the tectorial mass, etc. The model predicts that the apical pre- and postaxial areas, although anatomically adjacent, respond to different frequency ranges, a phenomenon not yet reported from any vertebrate. The model predicts that together, these areas respond best to frequencies between 1.1 and 5.3 kHz, close to the range found physiologically [Eatock et al. (1981) J. Comp. Physiol. 142, 203-218] (0.8 to 5 kHz) for the high-frequency range for this species. Only physiological experiments tracing responses to specific papillar nerve fibres can confirm or refute these interesting predictions of the model. The model also indicates that, compared to free-standing hair-cell bundles, the semi-isolated tectorial structures called sallets not only lower the range of characteristic frequencies but also increase the frequency selectivity of the attached hair eels. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. CR CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DING D, 1991, SYNAPSE TRANSMISSION, P102 DOOLING RJ, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P545 EATOCK RA, 1981, J COMP PHYSIOL, V142, P203 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 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 HOLTON T, 1983, SCIENCE, V222, P508, DOI 10.1126/science.6623089 HOLTON T, 1983, J PHYSIOL-LONDON, V345, P241 KOPPL C, 1989, THESIS TU MUNCHEN 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, 1991, ABSTR SOC RES OT, P83 KOPPL C, 1990, J COMP PHYSIOL A, V167, P101 KOPPL C, 1995, HEARING RES, V82, P14 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MANLEY GA, 1989, MECH HEARING, P143 MANLEY GA, 1993, BIOPHYSICS HAIR CELL, P33 MANLEY GA, 1991, ABSTR ASS RES OT, P83 MANLEY GA, 1986, AUDITORY FREQUENCY S, P63 MANLEY GA, 1994, 17TH ASS RES OT, P53 MILLER MR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P463 MILLER MR, 1973, Z ZELLFORSCH MIK ANA, V136, P307, DOI 10.1007/BF00307037 MULROY MJ, 1987, HEARING RES, V25, P11, DOI 10.1016/0378-5955(87)90075-X NETTEN SM, 1987, HEARING RES, V29, P55 PATUZZI RB, 1987, HEARING RES, V30, P83, DOI 10.1016/0378-5955(87)90186-9 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 STRELIOFF D, 1985, HEARING RES, V18, P169, DOI 10.1016/0378-5955(85)90009-7 STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 TURNER RG, 1981, SCIENCE, V213, P1519, DOI 10.1126/science.7280673 TURNER RG, 1987, HEARING RES, V26, P287, DOI 10.1016/0378-5955(87)90064-5 WEISS TF, 1985, HEARING RES, V20, P157, DOI 10.1016/0378-5955(85)90166-2 WEVER EG, 1974, J MORPHOL, V143, P121, DOI 10.1002/jmor.1051430202 ZUREK PM, 1985, J ACOUST SOC AM, V78, P340, DOI 10.1121/1.392496 ZWISLOCKI JJ, 1989, HEARING RES, V42, P211, DOI 10.1016/0378-5955(89)90146-9 NR 37 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 JAN PY 1995 VL 82 IS 1 BP 1 EP 13 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500001 PM 7744705 ER PT J AU KOPPL, C AUTHIER, S AF KOPPL, C AUTHIER, S TI QUANTITATIVE ANATOMICAL BASIS FOR A MODEL OF MICROMECHANICAL FREQUENCY TUNING IN THE TOKAY GECKO, GEKKO-GECKO SO HEARING RESEARCH LA English DT Article DE HEARING; LIZARD; BASILAR PAPILLA; COCHLEA; HAIR CELL ID ALLIGATOR LIZARD COCHLEA; NERVE FIBER ACTIVITY; HAIR-CELLS; TONOTOPIC ORGANIZATION; TECTORIAL MEMBRANE; BUNDLES; SELECTIVITY; RESONANCE; TILIQUA; EAR AB The basilar papilla of the Tokay gecko was studied with standard light- and scanning electron microscopy methods. Several parameters thought to be of particular importance for the mechanical response properties of the system were quantitatively measured, separately for the three different hair-cell areas that are typical for this lizard family. In the basal third, papillar structure was very uniform. The apical two-thirds are subdivided into two hair-cell areas running parallel to each other along the papilla and covered by very different types of tectorial material. Both of those areas showed prominent gradients in hair-cell bundle morphology, i.e., in the height of the stereovillar bundles and the number of stereovilli per bundle, as well as in hair cell density and the size of their respective tectorial covering. Based on the direction of the observed anatomical gradients, a 'reverse' tonotopic organization is suggested, with the highest frequencies represented at the apical end. RP KOPPL, C (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,D-85747 GARCHING,GERMANY. CR AUTHIER S, 1995, HEARING RES, V82, P1 CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407 CRAWFORD AC, 1985, J PHYSIOL-LONDON, V364, P359 DALLOS P, 1992, J NEUROSCI, V12, P4575 EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 EATOCK RA, 1981, J COMP PHYSIOL, V142, P203 FETTIPLACE R, 1987, TRENDS NEUROSCI, V10, P421, DOI 10.1016/0166-2236(87)90013-0 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 HOLTON T, 1983, SCIENCE, V222, P508, DOI 10.1126/science.6623089 HOLTON T, 1983, J PHYSIOL-LONDON, V345, P241 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, 1990, J COMP PHYSIOL A, V167, P101 KRONESTERFREI A, 1979, HEARING RES, V1, P81, DOI 10.1016/0378-5955(79)90019-4 Lewis ER, 1985, VERTEBRATE INNER EAR LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 Manley G. A., 1990, PERIPHERAL HEARING M MANLEY GA, 1988, HEARING RES, V33, P181, DOI 10.1016/0378-5955(88)90031-7 MANLEY GA, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P561 MANLEY GA, 1989, MECH HEARING, P143 MANLEY GA, 1986, AUDITORY FREQUENCY S, P63 MILLER MR, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P463 MILLER MR, 1988, J COMP NEUROL, V271, P604, DOI 10.1002/cne.902710410 MILLER MR, 1973, Z ZELLFORSCH MIK ANA, V136, P307, DOI 10.1007/BF00307037 MILLER MR, 1974, BRAIN BEHAV EVOLUT, V10, P95, DOI 10.1159/000124305 PEAKE WT, 1980, J ACOUST SOC AM, V67, P1736, DOI 10.1121/1.384300 PICKLES JO, 1993, HEARING RES, V68, P159, DOI 10.1016/0378-5955(93)90120-P RUNHAAR G, 1989, HEARING RES, V37, P179, DOI 10.1016/0378-5955(89)90039-7 SAMSDODD F, 1994, HEARING RES, V76, P16, DOI 10.1016/0378-5955(94)90083-3 SNEARY MG, 1988, J COMP NEUROL, V276, P573, DOI 10.1002/cne.902760410 TURNER RG, 1981, SCIENCE, V213, P1519, DOI 10.1126/science.7280673 TURNER RG, 1987, HEARING RES, V26, P287, DOI 10.1016/0378-5955(87)90064-5 WEISS TF, 1985, HEARING RES, V20, P157, DOI 10.1016/0378-5955(85)90166-2 WEVER EG, 1978, REPTILE EAR WEVER EG, 1974, J MORPHOL, V143, P121, DOI 10.1002/jmor.1051430202 WEVER EG, 1967, J MORPHOL, V123, P355, DOI 10.1002/jmor.1051230404 WEVER EG, 1967, J MORPHOL, V122, P307, DOI 10.1002/jmor.1051220403 NR 38 TC 21 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1995 VL 82 IS 1 BP 14 EP 25 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500002 PM 7744709 ER PT J AU CODE, RA AF CODE, RA TI EFFERENT NEURONS TO THE MACULA LAGENA IN THE EMBRYONIC CHICK SO HEARING RESEARCH LA English DT Article DE DII; RETICULAR FORMATION; SUPERIOR OLIVE; COCHLEAR EFFERENTS ID GALLUS-DOMESTICUS; COCHLEA; FIBERS; PIGEON AB The lipophilic dye, DiI, was placed into the macula lagena of paraformaldehyde-fixed embryonic chicks. Retrogradely labeled cells were found bilaterally in the pontine reticular formation (RF) between the dorsal facial nucleus and the abducens nerve root. This location is similar to that of the dorsomedial group of efferent cells that project to the basilar papilla. No lagenar efferent neurons, however, were found near the superior olivary nucleus where the ventrolateral group of cochlear efferents is located. Whether efferent neurons in the pontine RF send collaterals to both the basilar papilla and to the macula lagena has yet to be determined. C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. CR BOORD RL, 1963, J COMP NEUROL, V120, P463, DOI 10.1002/cne.901200305 BOORD RL, 1974, BRAIN BEHAV EVOLUT, V10, P228, DOI 10.1159/000124314 CODE RA, 1994, J COMP NEUROL, V340, P161, DOI 10.1002/cne.903400203 COLE KS, 1990, EXP BRAIN RES, V82, P585 FISCHER FP, 1994, J MORPHOL, V220, P71, DOI 10.1002/jmor.1052200107 HONIG MG, 1989, TRENDS NEUROSCI, V12, P333, DOI 10.1016/0166-2236(89)90040-4 KAISER A, 1994, ASS RES OT ABSTR, V17, P26 KOPPL C, 1994, J COMP NEUROL, V339, P438, DOI 10.1002/cne.903390310 Kuenzel WJ, 1988, STEREOTAXIC ATLAS BR SCHWARZ DWF, 1992, HEARING RES, V60, P110, DOI 10.1016/0378-5955(92)90064-T 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 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P277, DOI 10.1016/0306-4522(85)90178-2 WHITEHEAD MC, 1981, NEUROSCIENCE, V6, P2351, DOI 10.1016/0306-4522(81)90022-1 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P255, DOI 10.1016/0306-4522(85)90177-0 NR 16 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 1995 VL 82 IS 1 BP 26 EP 30 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500003 PM 7744710 ER PT J AU SHORE, SE AF SHORE, SE TI RECOVERY OF FORWARD-MASKED RESPONSES IN VENTRAL COCHLEAR NUCLEUS NEURONS SO HEARING RESEARCH LA English DT Article DE VENTRAL COCHLEAR NUCLEUS; NEURON RESPONSE; MEMBRANE; TONEBURSTS; RECOVERY ID AUDITORY-NERVE FIBERS; SHORT-TERM ADAPTATION; GUINEA-PIG; HORSERADISH-PEROXIDASE; DESCENDING PROJECTIONS; DISCHARGE PATTERNS; PRIOR STIMULATION; ECHO SUPPRESSION; CAT; MASKING AB Single unit responses were obtained from and classes of cells in the ventral cochlear nucleus: Primarylike, Primarylike with characteristic frequencies below 1 kHz, Primarylike-Notch, Sustained Chopper, Transient-Chopper, Low-intensity Chopper; Onset with later activity and On-Chopper. Stimuli were paired tonebursts, a masker preceding a probe, separated by time delta t ms. The decrement in discharge rate to the probe was measured as a function of delta t and constituted the forward-masking recovery function. The recovery functions of primarylike units were similar to those reported for auditory nerve fibers, but recovered more slowly than all other classes of units in the ventral cochlear nucleus. Some units, such as onset units, were completely masked at short masker-probe intervals, while others, such as the low-intensity choppers, were less affected by the masker. More masking occurred in the first 2 ms of the response (onset rate) than in the overall response (average rate). Using shorter maskers and measuring the onset rate produced greater differences in masking functions between unit classes. Units with high spontaneous activity were more resistant to the effects of the masker than units with low and medium spontaneous activity. This was especially evident at high masker levels and short masker-probe intervals. Units other than primarylike often showed non-monotonic relationships between the firing rate evoked by the masker and the firing rate decrement in response to the probe, suggesting that both adaptation and inhibition are operating to produce the observed effects. C1 MED COLL OHIO,DEPT OTOLARYNGOL,TOLEDO,OH 43699. 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Res. PD JAN PY 1995 VL 82 IS 1 BP 31 EP 43 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500004 PM 7744711 ER PT J AU GRATTON, MA SCHULTE, BA AF GRATTON, MA SCHULTE, BA TI ALTERATIONS IN MICROVASCULATURE ARE ASSOCIATED WITH ATROPHY OF THE STRIA VASCULARIS IN QUIET-AGED GERBILS SO HEARING RESEARCH LA English DT Article DE STRIA VASCULARIS; AGING; MORPHOMETRY; PRESBYACUSIS; COCHLEA; PATHOLOGY ID INNER-EAR; COCHLEAR; CHINCHILLA; POTENTIALS; YOUNG; WALL AB Age-related changes in the integrity of the stria vascularis and its microvasculature were assessed in whole mount preparations of the gerbil cochlear lateral wall. Small focal regions containing few or no capillaries were present at the extreme ends of the stria vascularis in most 5-9 month-old gerbils. A few ears in this age range also contained small regions devoid of capillaries at the extreme basal end of the stria. These degenerate foci expanded in a systematic fashion toward the middle turn of the cochlea with increasing age. Gerbils aged 33 months or older exhibited a normal strial vasculature pattern only in portions of the middle and upper basal turns. The remainder of the stria in these older gerbils contained degenerate regions which showed both loss of capillaries and atrophy of strial marginal cells. Quantification via computer-aided image analysis confirmed that the areas of strial atrophy correlated well with the loss of strial capillaries at all ages. However, regions containing capillaries with decreased diameter were not necessarily accompanied by atrophic changes in marginal cells. The results suggest that degeneration of the stria vascularis begins prior to onset of auditory threshold shift and is preceded and possibly initiated by changes in the strial microvasculature. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP GRATTON, MA (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR AXELSSON A, 1971, ACTA OTO-LARYNGOL, V72, P172, DOI 10.3109/00016487109122470 AXELSSON A, 1986, ACTA OTO-LARYNGOL, V101, P75, DOI 10.3109/00016488609108610 BHATTACHARYYA TK, 1985, ANN OTO RHINOL LARYN, V94, P75 BOETTCHER FA, 1993, HEARING RES, V71, P137, DOI 10.1016/0378-5955(93)90029-Z BOETTCHER FA, 1993, HEARING RES, V71, P146, DOI 10.1016/0378-5955(93)90030-5 BOHNE BA, 1990, HEARING RES, V48, P79, DOI 10.1016/0378-5955(90)90200-9 CARLISLE L, 1989, HEARING RES, V38, P111, DOI 10.1016/0378-5955(89)90132-9 COVELL W. P., 1957, LARYNGOSCOPE, V67, P118 GRAHAM RC, 1966, J HISTOCHEM CYTOCHEM, V14, P291 HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N JOHNSON PC, 1973, VASCULAR DISORDERS H, P119 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P364 KEITHLEY EM, 1992, HEARING RES, V59, P171, DOI 10.1016/0378-5955(92)90113-2 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MUMBYJONES CJ, 1984, AM J OTOLARYNG, V5, P127 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 PAULER M, 1988, LARYNGOSCOPE, V98, P754 PRAZMA J, 1990, ARCH OTOLARYNGOL, V116, P932 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SCHUKNEC.HF, 1974, LARYNGOSCOPE, V84, P1777 SCHUKNECHT HF, 1964, ARCHIV OTOLARYNGOL, V80, P369 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K Sugar J O, 1972, Acta Otolaryngol Suppl, V301, P61 TANGE RA, 1986, HEARING RES, V23, P135, DOI 10.1016/0378-5955(86)90010-9 TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V NR 25 TC 66 Z9 69 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1995 VL 82 IS 1 BP 44 EP 52 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500005 PM 7744712 ER PT J AU CHEOURLUHTANEN, M ALHO, K KUJALA, T SAINIO, K REINIKAINEN, K RENLUND, M AALTONEN, O EEROLA, O NAATANEN, R AF CHEOURLUHTANEN, M ALHO, K KUJALA, T SAINIO, K REINIKAINEN, K RENLUND, M AALTONEN, O EEROLA, O NAATANEN, R TI MISMATCH NEGATIVITY INDICATES VOWEL DISCRIMINATION IN NEWBORNS SO HEARING RESEARCH LA English DT Article DE NEWBORNS; VOWEL PERCEPTION; AUDITORY DISCRIMINATION; EVENT-RELATED POTENTIAL; MISMATCH NEGATIVITY ID EVENT-RELATED POTENTIALS; INTERMODAL SELECTIVE ATTENTION; COMPLEX SOUND PATTERNS; HUMAN AUDITORY-CORTEX; BRAIN POTENTIALS; MEMORY TRACE; VISUAL-STIMULI; SENSORY MEMORY; SPEECH STIMULI; RESPONSES AB The present study shows that an infrequent vowel ('deviant') presented among frequent vowels ('standard') elicits in sleeping human newborns a negativity in the auditory event-related potential (ERP) resembling the mismatch negativity (MMN) recorded in adults. Thus, the MMN appears to provide means to investigate brain mechanisms of vowel perception in infants. C1 UNIV HELSINKI,DEPT NEUROPEDIAT,HELSINKI,FINLAND. UNIV HELSINKI,DEPT OBSTET & GYNECOL,HELSINKI,FINLAND. UNIV TURKU,DEPT COGNIT NEUROSCI,TURKU,FINLAND. RP CHEOURLUHTANEN, M (reprint author), UNIV HELSINKI,DEPT PSYCHOL,COGNIT PSYCHOPHYSIOL RES UNIT,POB 11,SF-00014 HELSINKI,FINLAND. RI Alho, Kimmo/G-2997-2013 CR AALTONEN O, 1987, BIOL PSYCHOL, V24, P197, DOI 10.1016/0301-0511(87)90002-0 AALTONEN O, 1983, AUDIOLOGY, V22, P410 ALHO K, 1990, ELECTROEN CLIN NEURO, V77, P151, DOI 10.1016/0168-5597(90)90031-8 ALHO K, 1989, PSYCHOPHYSIOLOGY, V26, P514, DOI 10.1111/j.1469-8986.1989.tb00704.x ALHO K, 1993, NEUROREPORT, V4, P391, DOI 10.1097/00001756-199304000-00012 ALHO K, 1992, ELECTROEN CLIN NEURO, V82, P356, DOI 10.1016/0013-4694(92)90005-3 AULANKO R, 1993, NEUROREPORT, V4, P1356, DOI 10.1097/00001756-199309150-00018 Campbell K., 1991, SLEEP AROUSAL PERFOR, P88 COURCHESNE E, 1981, CHILD DEV, V52, P804, DOI 10.1111/j.1467-8624.1981.tb03117.x Courchesne E, 1990, EVENT RELATED BRAIN, P210 CSEPE V, 1992, 10TH INT C EV REL PO GALAMBOS R, 1982, CLIN APPLICATION CER, P323 GIARD MH, 1990, PSYCHOPHYSIOLOGY, V27, P627, DOI 10.1111/j.1469-8986.1990.tb03184.x GRAVEL J S, 1989, Seminars in Hearing, V10, P216 Hall J, 1992, HDB AUDITORY EVOKED HARI R, 1984, NEUROSCI LETT, V50, P127, DOI 10.1016/0304-3940(84)90474-9 HILPERT PL, 1983, DISS ABSTR HUOTILAINEN M, 1993, NEUROREPORT, V4, P1279, DOI 10.1097/00001756-199309000-00018 KANE NM, 1993, LANCET, V341, P688, DOI 10.1016/0140-6736(93)90453-N KLATT DH, 1980, J ACOUST SOC AM, V67, P971, DOI 10.1121/1.383940 KORPILAHTI P, 1992, 10TH INT C EV REL PO KRAUS N, 1993, ELECTROEN CLIN NEURO, V88, P123, DOI 10.1016/0168-5597(93)90063-U KRAUS N, 1992, EAR HEARING, V13, P158, DOI 10.1097/00003446-199206000-00004 KURTZBERG D, 1986, EVOKED POTENTIAL, P513 KURTZBERG D, 1985, CLIN PERINATOL, V12, P277 LANG AH, 1990, PSYCHOPHYSIOLOGICAL, V1, P294 LAWSON EA, 1981, BIOL PSYCHOL, V13, P281, DOI 10.1016/0301-0511(81)90043-0 LEPPANEN P, 1992, 10TH INT C EV REL PO LYYTINEN H, 1992, PSYCHOPHYSIOLOGY, V29, P523, DOI 10.1111/j.1469-8986.1992.tb02025.x Mayeux R, 1991, PRINCIPLES NEURAL SC, P839 Naatanen R., 1992, ATTENTION BRAIN FUNC NAATANEN R, 1989, NEUROSCI LETT, V107, P347, DOI 10.1016/0304-3940(89)90844-6 NAATANEN R, 1987, PSYCHOPHYSIOLOGY, V24, P375, DOI 10.1111/j.1469-8986.1987.tb00311.x NAATANEN R, 1993, NEUROREPORT, V4, P503 NAATANEN R, 1995, UNPUB MISMATCH NEGAT NAATANEN R, 1978, ACTA PSYCHOL, V42, P313, DOI 10.1016/0001-6918(78)90006-9 NIELSENBOHLMAN L, 1991, ELECTROEN CLIN NEURO, V79, P281, DOI 10.1016/0013-4694(91)90124-M PAAVILAINEN P, 1993, BIOL PSYCHOL, V35, P139, DOI 10.1016/0301-0511(93)90010-6 Paavilainen P, 1987, Electroencephalogr Clin Neurophysiol Suppl, V40, P246 PAAVILAINEN P, 1989, ELECTROEN CLIN NEURO, V73, P129, DOI 10.1016/0013-4694(89)90192-2 PICTON TW, 1981, J OTOLARYNGOL, V10, P1 SAMS M, 1985, ELECTROEN CLIN NEURO, V62, P437, DOI 10.1016/0168-5597(85)90054-1 SAMS M, 1985, ELECTROEN CLIN NEURO, V61, P254, DOI 10.1016/0013-4694(85)91092-2 Sams M, 1990, J Cogn Neurosci, V2, P344, DOI 10.1162/jocn.1990.2.4.344 Scherg M, 1989, J Cogn Neurosci, V1, P336, DOI 10.1162/jocn.1989.1.4.336 SCHROGER E, 1992, NEUROSCI LETT, V146, P183, DOI 10.1016/0304-3940(92)90073-G SHARMA A, 1993, ELECTROEN CLIN NEURO, V88, P64, DOI 10.1016/0168-5597(93)90029-O TIITINEN H, 1993, PSYCHOPHYSIOLOGY, V30, P537, DOI 10.1111/j.1469-8986.1993.tb02078.x VAUGHAN HG, 1992, MINN SYM CHILD PSYCH, V24, P1 WERNER SS, 1977, ATLAS NEONATAL ELECT, P37 WOODS DL, 1992, ELECTROEN CLIN NEURO, V82, P341, DOI 10.1016/0013-4694(92)90004-2 NR 51 TC 112 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 1995 VL 82 IS 1 BP 53 EP 58 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500006 PM 7744713 ER PT J AU YOSHIDA, M AOYAGI, M MAKISHIMA, K AF YOSHIDA, M AOYAGI, M MAKISHIMA, K TI EFFECTS OF ACOUSTIC OVERSTIMULATION ON 2F(1)-F(2) DISTORTION-PRODUCT IN THE COCHLEAR MICROPHONICS SO HEARING RESEARCH LA English DT Article DE ACOUSTIC OVERSTIMULATION; COCHLEAR MICROPHONICS; 2F(1)-F(2); DISTORTION PRODUCT; ACTIVE PROCESS ID BASILAR-MEMBRANE; AUDITORY-SYSTEM; ACTIVE PROCESS; INJURY; CONSEQUENCES; SUPPRESSION; TRAUMA AB The cochlear microphonics (CM) in response to two-tone stimuli as well as the threshold of compound action potential (CAP) were measured before and after exposure to 4 kHz pure tone at 100 dB SPL for 10 min. Although the loss of CM output at the primary frequencies was limited to around 2 dB, the 2f(1)-f(2) distortion products in the CM (CM-DPs) were markedly reduced immediately after the exposure, especially at low primary levels (i.e. less than 65 dB). The low level CM-DPs recovered gradually near the initial level within 7 days from the exposure. The elevation of CAP threshold closely paralleled with the reduction of CM-DPs in not only the acute phase but also in the recovery phase from the exposure. These results show that the active transduction process in the cochlea was affected by acoustic overstimulation. This impairment of the active transduction was postulated to play an important role in developing the noise induced temporary threshold shift. RP YOSHIDA, M (reprint author), UNIV OCCUPAT & ENVIRONM HLTH,SCH MED,DEPT OTORHINOLARYNGOL,KITAKYUSHU,FUKUOKA 807,JAPAN. CR BROWN AM, 1985, HEARING RES, V19, P191, DOI 10.1016/0378-5955(85)90138-8 BROWN AM, 1989, HEARING RES, V42, P143, DOI 10.1016/0378-5955(89)90140-8 CHEATHAM MA, 1985, HEARING RES, V18, P291, DOI 10.1016/0378-5955(85)90046-2 CODY AR, 1980, HEARING RES, V3, P3, DOI 10.1016/0378-5955(80)90004-0 CODY AL, 1991, NOISE INDUCED HEARIN, P11 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DALLOS P, 1969, J ACOUST SOC AM, V46, P1437, DOI 10.1121/1.1911882 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 KEMP DT, 1984, HEARING RES, V13, P39, DOI 10.1016/0378-5955(84)90093-5 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 KUJAWA SG, 1992, HEARING RES, V64, P73, DOI 10.1016/0378-5955(92)90169-N MOUNTAIN DC, 1986, NEUROBIOLOGY HEARING, P77 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 ROBLES L, 1991, NATURE, V349, P413, DOI 10.1038/349413a0 RUGGERO MA, 1992, J NEUROPHYSIOL, V68, P1087 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 STYPULKOWSKI PH, 1990, HEARING RES, V46, P113, DOI 10.1016/0378-5955(90)90144-E WARD WD, 1963, MODERN DEV AUDIOLOGY, P241 Wever EG, 1940, J ACOUST SOC AM, V12, P268, DOI 10.1121/1.1916102 WIEDERHOLD ML, 1986, PERIPHERAL AUDITORY, P322 NR 25 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 1995 VL 82 IS 1 BP 59 EP 64 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500007 PM 7744714 ER PT J AU LEAKE, PA SNYDER, RL HRADEK, GT REBSCHER, SJ AF LEAKE, PA SNYDER, RL HRADEK, GT REBSCHER, SJ TI CONSEQUENCES OF CHRONIC EXTRACOCHLEAR ELECTRICAL-STIMULATION IN NEONATALLY DEAFENED CATS 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; COCHLEAR NUCLEUS; INFERIOR COLLICULUS; BRAIN-STEM; ACOUSTIC DEPRIVATION; NEURONS; NERVE; PROJECTIONS; REPRESENTATION AB This investigation examined the consequences of neonatal deafness and chronic electrical stimulation of the cochlea in the developing auditory system. Cats were bilaterally deafened by daily ototoxic drug administration for two weeks after birth. Electrical stimulation was initiated at 6-9 weeks of age and continued for up to 6 months, using monopolar round window electrodes that synchronously excited auditory neurons throughout the cochlea. Morphometric evaluation of the density of spiral ganglion cell somata within Rosenthal's canal demonstrated that chronic stimulation induced an increase of about 6% in neuronal survival. Although this difference was statistically significant, extracochlear stimulation in these cats was less effective in preventing neural degeneration than lower intensity, more restricted intracochlear stimulation that was shown in a previous study to induce an average increase of about 13% in neuronal survival. Electrophysiological recording experiments conducted in the inferior colliculus in these animals indicated that monopolar extracochlear stimulation can induce profound alterations in the spatial (frequency) selectivity of the auditory midbrain. On average, results were similar to those previously reported for bipolar intracochlear stimulation, showing about a two-fold expansion of the central representation of chronically stimulated electrodes. However, results with extracochlear stimulation showed much greater variability among individual animals. The results presented suggest that it is problematic to effect consistent 'whole' nerve stimulation using monopolar round window electrodes. Moreover, this mode of stimulation can induce profound functional alterations in the central nervous system and is substantially less effective in forestalling the degeneration of auditory neurons than intracochlear stimulation. Both these results contraindicate the implantation of such electrodes in young children for the purpose of maintaining the integrity of the auditory system for later application of a multichannel cochlear implant. RP LEAKE, PA (reprint author), UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,EPSTEIN LAB,U490,SAN FRANCISCO,CA 94143, USA. 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 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 HARRISON RV, 1993, ACTA OTO-LARYNGOL, V113, P296, DOI 10.3109/00016489309135812 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, 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, 1994, ADV COCHLEAR IMPLANT, P50 LEAKE PA, 1990, NEURAL PROSTHESES FU, P253 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 LUSTIG LR, 1994, HEARING RES, V74, P29, DOI 10.1016/0378-5955(94)90173-2 MATSUSHIMA JI, 1991, HEARING RES, V56, P133, DOI 10.1016/0378-5955(91)90162-3 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MILLER JM, 1991, NOISE INDUCED HEARIN, P130 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 Moxon E.C., 1971, THESIS MIT CAMBRIDGE 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, 1985, NEUROSCIENCE, V14, P535, DOI 10.1016/0306-4522(85)90308-2 SCHMIDT JT, 1989, COMMENTS DEV NEUROBI, V1, P11 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 SNYDER RL, IN PRESS J NEUROPHYS 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 VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 VUREK LS, 1981, ANN OTO RHINOL LARYN, V90, P21 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 YLIKOSKI J, 1974, ACTA OTOLARYNGOL, V79, P266 NR 50 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 JAN PY 1995 VL 82 IS 1 BP 65 EP 80 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500008 PM 7744715 ER PT J AU GLEICH, O KLUMP, GM AF GLEICH, O KLUMP, GM TI TEMPORAL-MODULATION TRANSFER-FUNCTIONS IN THE EUROPEAN STARLING (STURNUS-VULGARIS) .2. RESPONSES OF AUDITORY-NERVE FIBERS SO HEARING RESEARCH LA English DT Article DE TEMPORAL RESOLUTION; AMPLITUDE MODULATION; AUDITORY NERVE; BIRD; HEARING ID GAP DETECTION; AMPLITUDE-MODULATION; COCHLEAR-NERVE; GUINEA-PIG; FIBERS; THRESHOLDS; GOLDFISH; RECEPTOR; NEURONS; SYSTEM AB The temporal resolution of cochlear-nerve fibres in the European starling was determined with sinusoidally amplitude-modulated noise stimuli similar to those previously used in a psychoacoustic study in this species (Klump and Okanoya, 1991). Temporal modulation transfer curves (TMTFs) were constructed for cochlear afferents allowing a direct comparison with the starling's behavioural performance. On average, the neuron's detection of modulation was less sensitive than that obtained in the behavioural experiments, although the most sensitive cells approached the values determined psychophysically. The shapes of the neural TMTFs generally resembled low-pass or band-pass filter functions, and the shapes of the averaged neural functions were very similar to those obtained in the behavioural study for two different types of stimuli (gated and continuous carrier). Minimum integration times calculated from the upper cut-off frequency of the neural TMTFs had a median of 0.97 ms with a range of 0.25 to 15.9 ms. The relations between the minimum integration times and the tuning characteristics of the cells (tuning curve bandwidth, Q(10) dB-value, high- and low-frequency slopes of the tuning curves) are discussed. Finally, we compare the TMTF data recorded in the starling auditory nerve with data from neurophysiological and behavioural observations on temporal resolution using other experimental paradigms in this and other vertebrate species. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. 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Res. PD JAN PY 1995 VL 82 IS 1 BP 81 EP 92 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500009 PM 7744716 ER PT J AU NAKAZAWA, K SPICER, SS SCHULTE, BA AF NAKAZAWA, K SPICER, SS SCHULTE, BA TI POSTNATAL EXPRESSION OF THE FACILITATED GLUCOSE-TRANSPORTER, GLUT-5, IN GERBIL OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE GLUCOSE TRANSPORT; GLUT 5; COCHLEA; OUTER HAIR CELL; IMMUNOHISTOCHEMISTRY; DEVELOPMENT ID INNER-EAR; MONGOLIAN GERBIL; SMALL-INTESTINE; IMMUNOHISTOCHEMICAL LOCALIZATION; FUNCTIONAL-CHARACTERIZATION; FRUCTOSE TRANSPORTER; MESSENGER-RNA; COCHLEA; TISSUE; BRAIN AB The fifth isoform from the family of facilitative glucose transporters (GLUT 5) was identified in the gerbil cochlea by light and electron microscopic immunohistochemistry. The immunostaining procedure employed a polyclonal antibody raised against a synthetic peptide representing the carboxy terminus of human GLUT 5. Immunoreactive GLUT 5 was abundant in the basolateral plasma membrane of outer hair cells (OHCs) in the mature gerbil cochlea. No immunostaining was observed in any other site in the cochlea or vestibular system. During postnatal development of the gerbil inner ear, OHCs were first observed to express GLUT 5 in a punctate pattern at 10 days after birth. Immunostaining intensity increased gradually and developed a linear pattern along the entire OHC basolateral plasmalemma between 10 and 16 days after birth when it approached adult levels. The developmental expression of GLUT 5 corresponded with the appearance of glycogen in OHCs and structural maturation of the organ of Corti. This time period also coincided with the onset and rapid maturation of auditory function in the gerbil. GLUT 5 apparently supports OHC function by facilitating uptake of glucose which enables these cells to sustain a high level of metabolic activity in a relatively anaerobic environment. RP NAKAZAWA, K (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD JAN PY 1995 VL 82 IS 1 BP 93 EP 99 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500010 PM 7744717 ER PT J AU GLEICH, O KLUMP, GM DOOLING, RJ AF GLEICH, O KLUMP, GM DOOLING, RJ TI PERIPHERAL BASIS FOR THE AUDITORY DEFICIT IN BELGIAN WATERSLAGER CANARIES (SERINUS-CANARIUS) SO HEARING RESEARCH LA English DT Article DE BIRD; HEARING DEFICIT; COCHLEA; MIDDLE EAR; EVOKED POTENTIAL ID COCHLEAR GANGLION NEURONS; HAIR CELL REGENERATION; NERVE FIBERS; ACTIVITY PATTERNS; ACOUSTIC TRAUMA; CHICK COCHLEA; GUINEA-PIG; THRESHOLDS; RESPONSES; PAPILLA AB Recently, behavioural thresholds obtained in canaries of the Belgian Waterslager strain showed that these birds have an inherited auditory deficit. Canaries of this strain have absolute auditory thresholds at frequencies above 2.0 kHz that are as much as 40 dB above the threshold of canaries of other strains. We obtained audiograms from cochlear microphonics and from compound action potentials from the 8th nerve of Waterslager and non-Waterslager canaries and compare these results to previous behavioural data on hearing in this species. We also examined the growth of evoked potential amplitude-intensity functions in Waterslager and non-Waterslager canaries. Together with reflectance measurements of middle-ear function from both Waterslager and non-Waterslager canaries, we conclude that the origin of the auditory deficit in Waterslager canaries lies in the cochlea. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. UNIV MARYLAND,DEPT PSYCHOL,COLLEGE PK,MD 20742. CR 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 DINGPFENNIGDORF.D, 1992, THESIS GOETHE U FRAN DOOLING RJ, 1993, ABSTR ASS RES OT, P88 DOOLING RJ, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P545 DOOLING RJ, 1971, J ACOUST SOC AM, V50, P700, DOI 10.1121/1.1912686 GLEICH O, 1989, HEARING RES, V37, P255, DOI 10.1016/0378-5955(89)90026-9 GLEICH O, 1994, HEARING RES, V79, P123, DOI 10.1016/0378-5955(94)90134-1 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 GUTTINGER HR, 1985, BEHAVIOUR, V92, P255 HUDDE H, 1983, J ACOUST SOC AM, V73, P242, DOI 10.1121/1.388855 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 JORGENSEN FO, 1977, ACTA PHYSIOL SCAND, V100, P393 KLUHS W, 1992, KANARIENFREUND, V43, P324 KOPPL C, 1993, J COMP PHYSKL, V117, P695 KUHNE R, 1985, FORM FUNCTION BIRDS, V3, P227 LEFEBVRE PP, 1993, SCIENCE, V260, P692, DOI 10.1126/science.8480180 Manley G. 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Res. PD JAN PY 1995 VL 82 IS 1 BP 100 EP 108 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500011 PM 7744706 ER PT J AU FURST, M LEVINE, RA KORCZYN, AD FULLERTON, BC TADMOR, R ALGOM, D AF FURST, M LEVINE, RA KORCZYN, AD FULLERTON, BC TADMOR, R ALGOM, D TI BRAIN-STEM LESIONS AND CLICK LATERALIZATION IN PATIENTS WITH MULTIPLE-SCLEROSIS SO HEARING RESEARCH LA English DT Article DE CLICK LATERALIZATION; MULTIPLE SCLEROSIS; MAGNETIC RESONANCE IMAGING; AUDITORY PATHWAY ID AUDITORY-EVOKED-POTENTIALS; CAT AB The ability to lateralize dichotic clicks with either interaural time delays (ITD) or interaural level differences (ILD) was tested in seven multiple sclerosis (MS) subjects who had normal audiograms. Along with the psychoacoustical tests, magnetic resonance images (MRI) of the subjects' brainstem were obtained. After matching each MRI section with the corresponding section of a computerized atlas of the brainstem, the parts of the auditory pathway affected by each MS lesion were determined. Of the seven subjects two performed normally with both types of interaural asymmetry and had no brainstem lesions involving the auditory pathway. Two subjects performed normally only with level differences, but perceived all the dichotic clicks with different ITDs in the center of the head; both had lesions involving the trapezoid body. Three subjects could not perform normally with either task, perceiving the clicks to the sides and never in the center for both ITDs and ILDs; all three had unilateral lesions of the lateral lemniscus. A multi-level decision making model is proposed to account for these results. C1 MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TEL AVIV UNIV,SACKLER FAC MED,DEPT NEUROL,IL-69978 TEL AVIV,ISRAEL. TEL AVIV UNIV,SACKLER FAC MED,DEPT PHYSIOL & PHARMACOL,IL-69978 TEL AVIV,ISRAEL. TEL AVIV UNIV,SACKLER FAC MED,DEPT RADIOL,IL-69978 TEL AVIV,ISRAEL. BAR ILAN UNIV,DEPT PSYCHOL,IL-52900 RAMAT GAN,ISRAEL. RP FURST, M (reprint author), TEL AVIV UNIV,FAC ENGN,DEPT ELECT ENGN SYST,IL-69978 TEL AVIV,ISRAEL. CR ALGOM D, 1988, J ACOUST SOC AM, V846, P1302 CAIRD D, 1983, EXP BRAIN RES, V52, P385 COLBURN HS, 1990, HEARING RES, V49, P335 COLBURN HS, 1987, DIRECTIONAL HEARING, P261 Durlach N. 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Res. PD JAN PY 1995 VL 82 IS 1 BP 109 EP 124 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500012 PM 7744707 ER PT J AU WEISLEDER, P TSUE, TT RUBEL, EW AF WEISLEDER, P TSUE, TT RUBEL, EW TI HAIR CELL REPLACEMENT IN AVIAN VESTIBULAR EPITHELIUM - SUPPORTING CELL TO TYPE-I HAIR CELL SO HEARING RESEARCH LA English DT Article DE VESTIBULAR SYSTEM; CHICKEN; INNER EAR; REGENERATION ID WEAKLY ELECTRIC FISH; INNER-EAR; ACOUSTIC TRAUMA; POSTNATAL-DEVELOPMENT; POSSIBLE PRECURSORS; PROGENITOR CELLS; SENSORY ORGANS; CHICK COCHLEA; TELEOST FISH; REGENERATION AB Previous investigations have demonstrated that the sensory epithelium of the avian vestibular system possesses the capacity to replace hair cells both on an ongoing basis and following severe damage. Supporting cells, within the sensory epithelium, are believed to be the progenitors of the regenerated hair cells. In the present study we describe the series of events leading to the formation of a regenerated vestibular hair cell in post-hatched birds. Young chickens received injections of streptomycin sulfate in order to damage the sensory epithelium of the vestibular system. These injections were followed by injections of the cell proliferation marker tritiated-thymidine. At predetermined intervals, the animals were killed, and the vestibular organs were processed for tissue autoradiography. Our results confirm that hair cells originate from supporting cells. The data also indicate that postmitotic cells migrate towards the lumen of the epithelium where they differentiate into Type II hair cells. At a later time, some of the new Type II hair cells further differentiate into Type I hair cells. These results suggest that both types of avian vestibular hair cells have a common ancestor. The data also provide evidence in support of the hypothesis that calyx enclosed Type I hair cells, only present in birds and mammals, are a more differentiated stage of Type II hair cells. C1 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT OTOLARYNGOL HEAD & NECK SURG,SEATTLE,WA 98195. 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PD JAN PY 1995 VL 82 IS 1 BP 125 EP 133 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QH195 UT WOS:A1995QH19500013 PM 7744708 ER PT J AU SMITH, DW FINLEY, CC VANDENHONERT, C OLSZYK, VB KONRAD, KEM AF SMITH, DW FINLEY, CC VANDENHONERT, C OLSZYK, VB KONRAD, KEM TI BEHAVIORAL AND ELECTROPHYSIOLOGICAL RESPONSES TO ELECTRICAL-STIMULATION IN THE CAT .1. ABSOLUTE THRESHOLDS SO HEARING RESEARCH LA English DT Article DE COCHLEAR PROSTHESIS; ELECTRICAL STIMULATION; EABR; SINGLE-AUDITORY NEURON; THRESHOLD; CAT ID BRAIN-STEM RESPONSE; AUDITORY-NERVE AB Estimates of electrical auditory brainstem response (EABR) thresholds are compared with behavioral thresholds for electrical stimulation in the same subject using identical stimuli and electrode configurations. Four cats were behaviorally trained to measure acoustic auditory thresholds using food as a reward in an operant reinforcement paradigm. One of the animals was then implanted, in an otherwise normal ear, with a scaled-UCSF multi-contact;electrode array containing four intracochlear electrodes. Three animals were implanted with an electrode array containing eight intracochlear contacts and one extracochlear contact under the temporalis muscle following unilateral cochlear perfusion with 10% neomycin solution. Stimuli for the behavioral studies were single presentations of 200 us/phase biphasic current pulses. For the EABR studies, the same stimulus was presented at a rate of 32/s. In general, for the animal with the four-contact array and two of the three subjects with the eight-contact implant, changes in electrode configuration produced well-differentiated changes in threshold. For these three subjects, comparisons of behavioral and EABR thresholds for the majority of monopolar and bipolar electrode configurations tested showed excellent agreement (r(2) = 0.88). Correlations between behavioral and EABR measures in these animals were comparable for bipolar and monopolar arrangements (r(2) = 0.88 for bipolar and 0.87 for monopolar). For one subject with the eight-contact electrode, who showed similar monopolar and bipolar electrode behavioral thresholds for all tested electrode spacings or configurations, most EABR thresholds were substantially higher than, and poorly correlated with, behavioral thresholds (r(2) = 0.15; r(2) = 0.28 for monopolar arrangements, and r(2) = 0.12 for bipolar arrangements). C1 RES TRIANGLE INST,NEUROSCI PROGRAM OFF,RES TRIANGLE PK,NC 27709. RP SMITH, DW (reprint author), DUKE UNIV,MED CTR,DIV OTOLARYNGOL HEAD & NECK SURG,BOX 3550,DURHAM,NC 27710, USA. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 1 EP 10 DI 10.1016/0378-5955(94)90147-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800001 PM 7737916 ER PT J AU COHEN, YE SAUNDERS, JC AF COHEN, YE SAUNDERS, JC TI THE EFFECT OF ACOUSTIC OVEREXPOSURE ON THE TONOTOPIC ORGANIZATION OF THE NUCLEUS MAGNOCELLULARIS SO HEARING RESEARCH LA English DT Article DE ACOUSTIC OVEREXPOSURE; NUCLEUS MAGNOCELLULARIS; TONOTOPIC ORGANIZATION ID HAIR CELL REGENERATION; DORSAL COCHLEAR NUCLEUS; STEM AUDITORY NUCLEI; INTENSE SOUND EXPOSURE; BRAIN-STEM; TECTORIAL MEMBRANE; NEONATAL CHICK; RESPONSE PATTERNS; THRESHOLD SHIFT; BASILAR PAPILLA AB We assessed the effect a sound-induced cochlear lesion had on the tonotopic organization of the nucleus magnocellularis (NM) immediately after acoustic overexposure and following a twelve day recovery period. The acoustic overexposure was a 0.9 kHz tone at 120 dB sound pressure level (SPL) for 48 h. Initially after the acoustic overexposure, the tonotopic organization of the NM was statistically different from that of age-matched controls. Specifically, it appeared that the center frequencies of units in the frequency region of the NM associated with the acoustic overexposure had higher center frequencies than their control counterparts. Following a twelve day recovery period, when threshold sensitivity and frequency selectivity were operating normally, the tonotopic organization of the NM was not statistically different from age-matched controls. We suggest that the sound-induced changes in the tonotopic organization of the NM reflect peripheral damage in the basilar papilla. It has been well documented that similar exposure paradigms produce a loss of short hair cells and a degeneration of the tectorial membrane in the region of the basilar membrane associated with the overexposure. We postulate that the loss of these structures alters the micromechanics and tuning of the basilar membrane which is reflected in the observed changes in NM tonotopy. Following the recovery period, when those structures destroyed by the overexposure had regenerated and basilar membrane micromechanics were operating normally, the tonotopic organization of the NM returned to normal. C1 UNIV PENN,DEPT OTORHINOLARYNGOL HEAD & NECK SURG,PHILADELPHIA,PA 19104. UNIV PENN,DEPT BIOENGN,PHILADELPHIA,PA 19104. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 11 EP 21 DI 10.1016/0378-5955(94)90148-1 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800002 PM 7737919 ER PT J AU MARTIN, F MARIANOWSKI, R TU, TY HERMAN, P HUY, PTB AF MARTIN, F MARIANOWSKI, R TU, TY HERMAN, P HUY, PTB TI MODULATION OF CYCLIC-AMP PRODUCTION BY STRIAL MARGINAL CELLS FROM GERBIL IN CULTURE SO HEARING RESEARCH LA English DT Article DE MARGINAL CELLS; ENDOLYMPH; CYCLIC AMP; CELL CULTURE ID COCHLEAR FLUID BALANCE; PIG INNER-EAR; ADENYLATE-CYCLASE; BIOCHEMICAL CHARACTERISTICS; VASCULARIS; STIMULATION; VASOPRESSIN; MECHANISM; PROTEINS; BINDING AB To further investigate the role of marginal cells (MCs) in the secretion of endolymph and because of the limitations encountered in investigating these cells in vivo, we used primary cultures of MCs derived from explants of gerbil stria vascularis and investigated modulation of the adenylate cyclase-cyclic AMP system. After 10 days on type I collagen coated plastic dishes, a confluent monolayer of epithelial-like cells was obtained which exhibited the morphologic and immunohistochemical features of the native marginal cells. The cyclic AMP (cAMP) content was determined at 37 degrees C, after 5 min of incubation with various agents, in the presence of a specific inhibitor of type III cAMP-dependent phosphodiesterase, RO 20-1724. The adenylate cyclase-cAMP system was associated with beta(2)-adrenergic receptors. The cAMP content was increased by isoproterenol (23-fold), a beta-agonist, but not by octopamine, an alpha-agonist, and the affinity for ICI 118.551, a specific beta(2)-antagonist, was greater than for CGP 20712A, a specific beta(1)-antagonist (Kd: 0.03 X 10(-6) M and 15 X 10(-6) M respectively). The cAMP content was maximally increased by prostaglandin E(2) > beta(2)-adrenergic agonist >> vasopressine type 2 receptor agonist (26-, 23-, and 3-fold the basal cAMP content, respectively). The present study demonstrates that cultured marginal cells retain some of their in vivo properties including a modulated enzymatic cAMP system. This culture model should allow further in-depth investigation of the function of marginal cells. C1 FAC MED LARIBOISIERE,OTOL EXPTL LAB,F-75010 PARIS,FRANCE. FAC MED LARIBOISIERE,FRA CLAUDE BERNARD,F-75010 PARIS,FRANCE. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 33 EP 41 DI 10.1016/0378-5955(94)90150-3 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800004 PM 7737927 ER PT J AU FUKAZAWA, T TANAKA, Y AF FUKAZAWA, T TANAKA, Y TI DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN AN ACTIVE NONLINEAR MODEL OF THE COCHLEA SO HEARING RESEARCH LA English DT Article DE DISTORTION PRODUCT OTOACOUSTIC EMISSIONS; COCHLEAR MODEL; COMPUTER SIMULATION ID OUTER HAIR-CELLS; PHYSIOLOGICAL VULNERABILITY; EAR; FEEDBACK; RESPONSES; MECHANICS; RABBIT; WAVE AB An active nonlinear model of the cochlea in the form of a transmission line was presented, in which the active feedback system by outer hair cells (OHCs) was expressed as a series of low-pass filters on the basilar membrane (BM) which were transducing basilar membrane displacement to feedback force. The model could produce distortion product oto-acoustic emissions (DPOAEs) explicitly as well as sharp tuning curves of BM, and it was possible to discuss the cause of DPOAEs in terms of the active feedback. It was inferred that the nonlinearity of the cochlea which causes DPOAEs may be related to a saturating property of the feedback system by OHCs. RP FUKAZAWA, T (reprint author), DOKKYO UNIV,KOSHIGAYA HOSP,SCH MED,DEPT OTOLARYNGOL,KOSHIGAYA,SAITAMA 343,JAPAN. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 42 EP 48 DI 10.1016/0378-5955(94)90151-1 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800005 PM 7737928 ER PT J AU NADOL, JB BURGESS, BJ AF NADOL, JB BURGESS, BJ TI SUPRANUCLEAR EFFERENT SYNAPSES ON OUTER HAIR-CELLS AND DEITERS CELLS IN THE HUMAN ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE EFFERENT; SYNAPSE; OUTER HAIR CELL; DEITERS CELL; SYNAPTOPHYSIN ID GUINEA-PIG ORGAN; IMMUNOELECTRON MICROSCOPY; COCHLEAR MECHANICS; LOCALIZATION; INNERVATION AB Synaptophysin immunoreactivity and transmission electron microscopy have demonstrated vesiculated nerve endings synapsing on the supranuclear zone of outer hair cells and also of Deiters' cells in the human organ of Corti. These fibers seem similar to supranuclear fibers, apparently derived from the olivocochlear efferent system, which have been described in the animal. However, these endings were found throughout the cochlea in the human whereas in the animal such fibers were limited to the apical cochlea. Although such fibers have been demonstrated among supporting cells by immunohistochemical techniques, this is the first demonstration by transmission electron microscopy of morphology consistent with a chemical synapse between such fibers and Deiters' cells. Although the role of such fibers is unknown, neurophysiologic evidence suggests that they may modify the micromechanics of the outer hair cell. The function of neural innervation of Deiters' cells is speculative. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. RP NADOL, JB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. 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PD DEC PY 1994 VL 81 IS 1-2 BP 49 EP 56 DI 10.1016/0378-5955(94)90152-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800006 PM 7737929 ER PT J AU MCGINN, MD FADDIS, BT AF MCGINN, MD FADDIS, BT TI EXPOSURE TO LOW-FREQUENCY NOISE DURING REARING INDUCES SPONGIFORM LESIONS IN GERBIL COCHLEAR NUCLEUS - HIGH-FREQUENCY EXPOSURE DOES NOT SO HEARING RESEARCH LA English DT Article DE SPONGIFORM LESION; GERBIL; ACOUSTIC ISOLATION; FREQUENCY; TONOTOPIC ID SUSTAINED ELECTRICAL-STIMULATION; CENTRAL AUDITORY-SYSTEM; EPILEPTIC BRAIN-DAMAGE; MONGOLIAN GERBIL; PERFORANT PATH; IMMUNOCYTOCHEMICAL LOCALIZATION; SPONGY DEGENERATION; NERVOUS-SYSTEM; NMDA RECEPTOR; KANGAROO RAT AB Spongiform lesions of the gerbil cochlear nucleus are reduced in number and extent by rearing in acoustic isolation compared with rearing while exposed to normal colony low-frequency background noise. This study tested whether rearing under exposure to noise bands of moderate intensity would increase the number and extent of cochlear nucleus spongiform lesions. Gerbils were reared from weaning to young adulthood in acoustic isolation chambers while continually exposed to moderately intense bands of either high frequency or low frequency noise. Exposure to low frequency noise resulted in lesion number and area densities that were more than twice those seen in gerbils exposed to high frequency noise. Lesion extent in the low frequency group was similar to that in colony-reared gerbils; lesion extent in the high frequency group was similar to gerbils reared in acoustic isolation. Comparisons within the posterior ventral cochlear nucleus revealed that the differences in lesion extent were most pronounced in the middle and dorsal-medial portions, the regions that are most responsive to middle and high frequencies. These finding suggest that the regional restriction of spongiform lesions within the cochlear nucleus does not have a tonotopic basis. RP MCGINN, MD (reprint author), UNIV CALIF DAVIS,SCH MED,DEPT OTOLARYNGOL,1515 NEWTON COURT,ROOM 209,DAVIS,CA 95616, USA. 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PD DEC PY 1994 VL 81 IS 1-2 BP 57 EP 65 DI 10.1016/0378-5955(94)90153-8 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800007 PM 7737930 ER PT J AU KILLIAN, MJP KLIS, SFL SMOORENBURG, GF AF KILLIAN, MJP KLIS, SFL SMOORENBURG, GF TI ADAPTATION IN THE COMPOUND ACTION-POTENTIAL RESPONSE OF THE GUINEA-PIG 8TH NERVE TO ELECTRIC-STIMULATION SO HEARING RESEARCH LA English DT Article DE COCHLEAR IMPLANT; ELECTRICALLY EVOKED COMPOUND ACTION POTENTIAL; FATIGUE; FORWARD MASKING; BACKWARD MASKING; RECOVERY FROM ADAPTATION ID TEMPORARY THRESHOLD SHIFTS; REDUCES AUDITORY DESENSITIZATION; CROSSED OLIVOCOCHLEAR BUNDLE; COCHLEAR BLOOD-FLOW; ROUND WINDOW; INNER-EAR; PHYSIOLOGICAL-PROPERTIES; FIBER RESPONSES; MASKING; CAT AB An experimental study, carried out in guinea pigs, was designed to investigate whether forward masking measured psychophysically in 3M-House cochlear implant users might have a correlate in VIIIth nerve activity. The study was based on electrically evoked VIIIth nerve compound action potentials (ECAPs), using a masking paradigm comparable to the one used in the psychophysical study. Trains of 50 maskers with inter-masker-intervals of 509 ms appeared to induce a long-term fatigue effect that could influence the recovery from adaptation measurements. Fatigue stabilized within about 1 to 3 min when masker trains were repeated with intervening silent intervals of 10.5 s. The change in amplitude of probe-evoked ECAPs with increasing masker-probe delays was determined within the steady fatigue state. The recovery-from-adaptation functions obtained from these measurements resembled the forward masking functions found in 3M-House cochlear implant users. No correlate of psychophysical backward masking was found at the VIIIth nerve level. To examine whether hair cells were involved in fatigue and recovery from adaptation, the measurements described above were carried out in intact cochleas and in cochleas without hair cells. Results were essentially the same in the different preparations. The results suggest that processes at the level of the VIIIth nerve could, at least partly, account for forward masking found in 3M-House cochlear implant users. Backward masking must be attributed to mechanisms located centrally to the VIIIth nerve. C1 UNIV UTRECHT,DEPT OTORHINOLARYNGOL,EXPTL AUDIOL LAB,3508 GA UTRECHT,NETHERLANDS. 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PD DEC PY 1994 VL 81 IS 1-2 BP 66 EP 82 DI 10.1016/0378-5955(94)90154-6 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800008 PM 7737931 ER PT J AU LAMM, K ZAJIC, G SCHACHT, J AF LAMM, K ZAJIC, G SCHACHT, J TI LIVING ISOLATED CELLS FROM INNER-EAR VESSELS - A NEW APPROACH FOR STUDYING THE REGULATION OF COCHLEAR MICROCIRCULATION AND VASCULAR-PERMEABILITY SO HEARING RESEARCH LA English DT Article DE MICROCIRCULATION; COCHLEA; COCHLEAR BLOOD FLOW; ENDOTHELIUM, VASCULAR; PERICYTES; MUSCLE, SMOOTH, VASCULAR; CELL CULTURE; GUINEA PIG ID CAPILLARY ENDOTHELIAL-CELLS; LOW-DENSITY LIPOPROTEIN; SMOOTH-MUSCLE CELLS; MICROVASCULAR PERICYTES; STRIA VASCULARIS; GUINEA-PIG; SPIRAL LIGAMENT; ULTRASTRUCTURE; CURRENTS; NYCODENZ AB The spiral modiolar artery with its proximal branches and the microvessels in the spiral ligament and the stria vascularis were microdissected from the guinea pig cochlea. After incubation with proteolytic and collagenolytic enzymes the mixed cell suspension was fractionated by gradient centrifugation. The cells migrated according to their buoyant densities into the fractions of 1.04 g/ml (endothelial cells), 1.06 g/ml (vascular smooth muscle cells obtained from the spiral modiolar artery; strial pericytes) and 1.08 g/ml (pericytes obtained from the spiral ligament). To test for viability cells were loaded with a fluorescent vital stain (BCECF-AM); for identification, cell-specific staines were used. Identity of endothelial cells (ECs) was confirmed using acetylated low density lipoprotein fluorescently labeled with dioctadecyl-tetramethyl-indocarbocyanine perchlorate (DiI-Ac-LDL). Pericytes were identified immunofluorescently using th method according to Nayak et al. (1988). Vascular smooth muscle cells were stained for F-actin with rhodamin-phalloidin. This in vitro technique may open new approaches to study local factors involved in microcirculation and vessel permeability of various cochlear vascular beds. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP LAMM, K (reprint author), TECH UNIV MUNICH,UNIV CLIN KLINIKUM RECHTS ISAR,HNO,DEPT OTORHINOLARYNGOL,ISMANINGERSTR 22,D-81675 MUNICH,GERMANY. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 83 EP 90 DI 10.1016/0378-5955(94)90155-4 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800009 PM 7737932 ER PT J AU LOVELESS, N VASAMA, JP MAKELA, J HARI, R AF LOVELESS, N VASAMA, JP MAKELA, J HARI, R TI HUMAN AUDITORY CORTICAL MECHANISMS OF SOUND LATERALIZATION .3. MONAURAL AND BINAURAL SHIFT RESPONSES SO HEARING RESEARCH LA English DT Article DE AUDITION; AUDITORY SPACE; DIRECTIONAL HEARING; INTERAURAL INTENSITY DIFFERENCE; MAGNETOENCEPHALOGRAPHY; EVOKED RESPONSE ID INTERAURAL TIME DIFFERENCES; HUMAN EVOKED-POTENTIALS; MIDDLE-LATENCY; NEUROMAGNETIC RESPONSES; MAGNETIC-FIELDS; HUMAN-BRAIN; LATERALIZATION; CORTEX; NOISE; STIMULI AB Neuromagnetic responses were recorded over the whole head with a 122-channel gradiometer. A pair of 150-ms 1-kHz tones separated by an interval of 150 ms was presented to one ear every 2 s. The other ear received either no input, an identical pair simultaneous to the first, an identical pair alternating with the first or a continuous 600-ms tone. The 'monaural shift' condition in which stimuli alternated between ears produced a clear perception of changing lateralisation, but the evoked response could be explained as merely the sum of simple monaural onset and offset responses; thus we found no evidence for a separate response to interaural intensity difference in this condition. The 'binaural shift' condition, in which intensity changed in one ear while the other received a continuous tone, evoked a transient response (N130m) at a latency of about 130 ms. N130m was larger over the hemisphere contralateral to the direction of shift, and larger than the corresponding monaural response, whether to an onset or an offset. We concluded that N130m also was not a separate directional response, but was analogous to a simple monaural response, the prolonged latency being due to masking and the enhanced amplitude to facilitation by the sustained response to the continuous tone. C1 HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 91 EP 99 DI 10.1016/0378-5955(94)90156-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800010 PM 7737933 ER PT J AU TROUTT, LL VANHEUMEN, WRA PICKLES, JO AF TROUTT, LL VANHEUMEN, WRA PICKLES, JO TI THE CHANGING MICROTUBULE ARRANGEMENTS IN DEVELOPING HAIR-CELLS OF THE CHICK COCHLEA SO HEARING RESEARCH LA English DT Article DE MICROTUBULES; HAIR CELLS; DEVELOPMENT; STEREOCILIA; KINOCILIUM ID ACTIN-FILAMENTS; BASILAR PAPILLA; SENSORY CELLS; INNER-EAR; STEREOCILIA; REGENERATION; ORGANIZATION; MEMBRANE; PROTEINS; BUNDLES AB It has been suggested that microtubules in auditory hair cells might be involved in directing the morphological and hence functional polarisation of the sensory hair bundles. The distribution of microtubules was studied in hair cells of the chick cochlea, during the developmental stages when the stereocilia and cuticular plate were being formed. Cochleae were immunofluorescently labelled with antibodies to tubulin at specific stages in development, and hair cell ultrastructure was observed by electron microscopy. We found that the microtubule array changed from a simple symmetrical apical plate with a central kinocilium before the cuticular plate forms, to a ring with the kinocilium to one side when the cuticular plate begins to form, through to a cup-like arrangement below the cuticular plate once the plate has formed. In the earliest stages, no asymmetries were observed in the distribution of the microtubules, suggesting that structures other than the microtubules set up the functional polarisation of the stereociliary bundle. C1 UNIV QUEENSLAND,VIS TOUCH & HEARING RES CTR,DEPT PHYSIOL & PHARMACOL,BRISBANE,QLD 4072,AUSTRALIA. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 100 EP 108 DI 10.1016/0378-5955(94)90157-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800011 PM 7737917 ER PT J AU HYSON, RL OVERHOLT, EM LIPPE, WR AF HYSON, RL OVERHOLT, EM LIPPE, WR TI COCHLEAR MICROPHONIC MEASUREMENTS OF INTERAURAL TIME DIFFERENCES IN THE CHICK SO HEARING RESEARCH LA English DT Article DE SOUND LOCALIZATION; INTERAURAL PHASE DIFFERENCE; INTERAURAL CANAL; INTERAURAL INTENSITY DIFFERENCES; NUCLEUS LAMINARIS ID PIGEON COLUMBA-LIVIA; COTURNIX-COTURNIX-JAPONICA; SOUND LOCALIZATION; BRAIN-STEM; DIRECTIONAL HEARING; ACOUSTIC PROPERTIES; BARN OWL; CIRCUIT; NEURONS; EAR AB The major cues for the sound localization are the interaural differences in the timing and intensity of acoustic information. This poses a difficult coding problem for animals with relatively small heads, such as birds, because interaural time differences (ITDs) would have a small range and magnitude and interaural intensity differences (IIDs) would be significant for only high frequency sounds. It has been suggested that this coding problem is mitigated in birds by an enhancement of ITDs and IIDs resulting from the acoustic coupling of the two middle ear cavities through an interaural canal. In this report, the functional ITDs for sounds at different azimuthal locations were recorded in young chicks, and the contribution of middle ear acoustic coupling was evaluated. ITDs were calculated from simultaneous cochlear microphonic (CM) recordings evoked by pure tone stimuli. These effective ITDs were larger than predicted by the physical separation of the two ears, and this enhancement was more pronounced at low (0.8 and 1 kHz) than at high (2 and 4 kHz) frequencies, reaching maximum values of approximately 180 and 100 mu s, respectively. The amplitude of the CM also varied as a function of sound source location. This variation was as much as +/-30%, even for the low frequency tones. This suggests that IID cues are also available to the chick. To determine the contribution of middle ear acoustic coupling to the timing and amplitude of the CM response, the CM in one ear was measured prior to, and following occlusion of the contralateral external auditory canal. The cochlear microphonic from the ear distal to the sound source advanced in time and increased in amplitude when the ear proximal to the sound source was sealed. These effects were more pronounced for low frequency sounds. These findings confirm that acoustic coupling of the middle ear cavities plays a role in enhancing sound localization cues in the chick. C1 UNIV WASHINGTON,SCH MED,VIRGINIA MERRIL BLOEDEL HEARING RES CTR,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,SEATTLE,WA 98195. CR CALFORD MB, 1988, J COMP PHYSIOL A, V162, P503, DOI 10.1007/BF00612515 CALFORD MB, 1988, J COMP PHYSIOL A, V162, P491, DOI 10.1007/BF00612514 CARR CE, 1990, J NEUROSCI, V10, P3227 COLES RB, 1980, J EXP BIOL, V86, P153 COLES RB, 1988, J COMP PHYSIOL A, V163, P117, DOI 10.1007/BF00612002 FENG AS, 1980, J ACOUST SOC AM, V68, P1107, DOI 10.1121/1.384981 FENG AS, 1981, HEARING RES, V5, P201, DOI 10.1016/0378-5955(81)90046-0 Henson O.W. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 109 EP 118 DI 10.1016/0378-5955(94)90158-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800012 PM 7737918 ER PT J AU EROSTEGUI, C NENOV, AP NORRIS, CH BOBBIN, RP AF EROSTEGUI, C NENOV, AP NORRIS, CH BOBBIN, RP TI ACETYLCHOLINE ACTIVATES A K+ CONDUCTANCE PERMEABLE TO CS+ IN GUINEA-PIG OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE ION CHANNELS; BARIUM; CALCIUM; N-METHYLGLUCAMINE ID IONIC CURRENTS; COCHLEA; STIMULATION; INHIBITION; RESPONSES; FROG AB Acetylcholine (ACh), the major neurotransmitter released by efferent nerve fibers in the cochlea, has been shown to activate a Ca2+-dependent K+ conductance in outer hair cells (OHCs). Previously we reported that this ACh operated conductance is permeable to Cs+. The purpose of the present study was to characterize further this Cs+-permeable channel and its dependency on Ca2+ using isolated OHCs and the patch clamp technique in the whole cell configuration. The changes in the ACh response were examined when Cs+, Ba2+, Cd2+, N-methyl-D-glucamine (NMG(+)) and tetraethylammonium (TEA(+)) were placed in the external or internal solutions. Cs+ substituted for K+ in carrying the ACh-evoked Ca2+-dependent K+ current. When NMG(+)\TEA(+) was substituted for internal K+ ACh-evoked an inward and an outward current, and Cs+ substituted for external K+ blocked the outward but not the inward current evoked by ACh suggesting it was carried by K+. In the NMG(+)\TEA(+) condition, when the cell was held at different V-h values for an extended period of time, the ACh-induced K+ current rectified. In Ba2+ (3 mM) with zero Ca2+ ACh failed to induce any detectable current and the ACh response slowly recovered from the Ba2+ block, suggesting a block at an intracellular site. Cd2+ (1 mM) readily and reversibly blocked ACh-induced currents even when carried by Cs+. This data suggests that ACh opens a channel selective for K+, conductive to Cs+ and dependent on Ca2+. C1 DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,DEPT PHYSIOL,NEW ORLEANS,LA 70112. 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PD DEC PY 1994 VL 81 IS 1-2 BP 119 EP 129 DI 10.1016/0378-5955(94)90159-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800013 PM 7537728 ER PT J AU CHEN, L SALVI, R SHERO, M AF CHEN, L SALVI, R SHERO, M TI COCHLEAR FREQUENCY-PLACE MAP IN ADULT CHICKENS - INTRACELLULAR BIOCYTIN LABELING SO HEARING RESEARCH LA English DT Article DE CHICKEN; BASILAR PAPILLA; TONOTOPIC MAP; COCHLEAR GANGLION NEURONS; BIOCYTIN; INTRACELLULAR STAINING ID AUDITORY-NERVE FIBERS; HAIR CELL LOSS; ACOUSTIC TRAUMA; BASILAR PAPILLA; TONOTOPIC ORGANIZATION; INNER-EAR; REGENERATION; PATTERNS; OTOTOXICITY; INNERVATION AB A cochlear frequency-place map was developed for adult chickens by labeling cochlear ganglion neurons with biocytin and correlating the location of each labeled fiber along the basilar papilla with the characteristic frequency of the unit's tuning curve. Labeled fibers showed little or no branching within the sensory epithelium and most fibers appeared to terminate on a single hair cell along the neural side of the basilar papilla. The CFs of the labeled neurons ranged from 353 Hz to 3145 Hz and the location of the labeled neurons ranged from 30.1% to 74.4% of the total distance from the apex of the papilla. CFs increased in an orderly manner from the apex towards the base of the papilla. The cochlear frequency map for adult chickens was similar to that estimated from previous cochlear lesion studies carried out on 30 day old chicks, although the predicted frequencies in the adults were slightly higher in some regions of the basilar papilla than in 30 day old animals. However, previous maps developed in younger animals (less than or equal to 21 days) using lesion or labeling data predict significantly lower frequencies for a given location than in adult animals particularly in the basal half of the cochlea. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 130 EP 136 DI 10.1016/0378-5955(94)90160-0 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800014 PM 7737920 ER PT J AU KING, AJ CARLILE, S AF KING, AJ CARLILE, S TI RESPONSES OF NEURONS IN THE FERRET SUPERIOR COLLICULUS TO THE SPATIAL LOCATION OF TONAL STIMULI SO HEARING RESEARCH LA English DT Article DE SUPERIOR COLLICULUS; AUDITORY SPACE MAP; PINNA; FREQUENCY INTEGRATION; SPECTRAL LOCALIZATION CUES ID PRIMARY AUDITORY-CORTEX; CAT INFERIOR COLLICULUS; INTERAURAL INTENSITY DIFFERENCES; SOUND PRESSURE LEVEL; GUINEA-PIG; RECEPTIVE-FIELDS; AZIMUTHAL SENSITIVITY; FREQUENCY NEURONS; CENTRAL NUCLEUS; EXTERNAL EAR AB Using multi-unit recordings, we compared the azimuthal spatial selectivity of auditory neurons in the deep layers of the ferret superior colliculus (SC) to broadband and tonal stimuli. Responses to noise were tuned at different sound levels to a single location, which varied topographically along the rostrocaudal axis of the nucleus to form a map of sound azimuth. Frequency response profiles tended to be multi-peaked, so the spatial tuning was examined at two or more frequencies in each case; Some of the azimuthal response profiles obtained with tonal stimuli were bilobed, as expected from the spatially ambiguous cues available at individual frequencies, although the rest were tuned to a single region of space. The preferred sound directions usually varied with the frequency used, and the range of auditory best positions at each recording site was significantly greater with tones than with noise. Comparison with the acoustical properties of the auditory periphery suggested that the near-threshold positional selectivity of many of the tonal responses may be determined by the monaural directionality of the outer ear. When the sound level was raised by 20 dB so that both ears were stimulated at all speaker locations, the range of tonal best positions obtained at each frequency increased and some of the units responded best to pure tones located in the ipsilateral hemifield. The lack of topographic order in the distribution of tonal spatial selectivity along the rostrocaudal axis of the SC indicates the need for a broadband input, incorporating the spectral localization cues provided by the outer ear, in the construction of a neural map of auditory space. RP KING, AJ (reprint author), UNIV OXFORD,PHYSIOL LAB,PARKS RD,OXFORD OX1 3PT,ENGLAND. 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S., 1938, EXPT PSYCHOL YIN TCT, 1990, J NEUROPHYSIOL, V64, P465 YOUNG ED, 1992, PHILOS T ROY SOC B, V336, P407, DOI 10.1098/rstb.1992.0076 NR 65 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 1994 VL 81 IS 1-2 BP 137 EP 149 DI 10.1016/0378-5955(94)90161-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800015 PM 7737921 ER PT J AU SHEPHERD, RK MATSUSHIMA, J MARTIN, RL CLARK, GM AF SHEPHERD, RK MATSUSHIMA, J MARTIN, RL CLARK, GM TI COCHLEAR PATHOLOGY FOLLOWING CHRONIC ELECTRICAL-STIMULATION OF THE AUDITORY-NERVE .2. DEAFENED KITTENS SO HEARING RESEARCH LA English DT Article DE COCHLEAR IMPLANTS; OTOTOXIC DRUGS; COCHLEAR HISTOPATHOLOGY; EABR; SPIRAL GANGLION CELL SURVIVAL; ELECTRICAL STIMULATION; ELECTRODE IMPEDANCE ID BRAIN-STEM RESPONSE; AFFERENT INFLUENCES; CATS; KANAMYCIN; NEURONS; HEARING; DEGENERATION; OTOTOXICITY; IMPLANTS; SURVIVAL AB The present study examines the effects of long-term electrical stimulation of the auditory nerve on cochlear histopathology and spiral ganglion cell survival in young sensorineural deafened cats. Eight kittens were deafened using kanamycin and ethacrynic acid, and implanted with bipolar or monopolar scala tympani electrodes. Following recovery from surgery the animals were unilaterally stimulated using charge balanced biphasic current pulses for 450-1730 hours over implant periods of up to four months. Charge densities varied from 0.6-0.9 mu C.cm(-2) geom. per phase for monopolar electrodes to 12-26 mu C.cm(-2) geom. per phase for the bipolar electrodes. Electrically-evoked auditory brainstem responses (EABRs) were periodically monitored during stimulation to confirm that the stimulus levels were above threshold, and to monitor any change in the response of the auditory nerve. Following completion of the stimulation program cochleae were prepared for histological examination. EABRs exhibited relatively stable thresholds for both stimulated and implanted, unstimulated control cochleae for the stimulus duration. While the growth in response amplitude as a function of stimulus current remained stable for the bipolar control and monopolar stimulated cochleae, the five cochleae chronically stimulated using bipolar electrodes exhibited a moderate to large increase in response amplitude. These increases were associated with a more widespread fibrous tissue response which may have altered the current distribution within these cochleae. Implanted control cochleae exhibited significantly less tissue response within the scala tympani. Importantly, we observed no statistically significant difference in the spiral ganglion cell density associated with chronic electrical stimulation when compared with unstimulated control cochleae. While the present study supports the safe application of cochlear implants in young profoundly deafened children, it does not corroborate previous studies that have reported electrical stimulation providing a trophic effect on degenerating auditory nerve fibres. RP SHEPHERD, RK (reprint author), UNIV MELBOURNE,DEPT OTOLARYNGOL,32 GISBANE ST,MELBOURNE,VIC 3002,AUSTRALIA. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 150 EP 166 DI 10.1016/0378-5955(94)90162-7 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800016 PM 7737922 ER PT J AU JAVEL, E AF JAVEL, E TI SHAPES OF CAT AUDITORY-NERVE FIBER TUNING CURVES SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; TUNING CURVE; COCHLEAR MECHANICS; ACTIVE PROCESS ID OUTER HAIR-CELLS; COCHLEAR-FREQUENCY MAP; BASILAR-MEMBRANE; MAMMALIAN COCHLEA; SINGLE TONES; RESPONSES; MODEL; INTENSITY; MECHANICS; STIMULUS AB Tuning curves of auditory nerve fibers in normal-hearing cats were fitted by a computational model comprising four processes. One process accounts for sensitivity in tuning curve tails and consists of an approximation to bandpass filtering by extracochlear structures. The second and third processes describe passive and active components of basilar membrane (BM) mechanics, respectively. The former consists of a lowpass filter function, which provides baseline threshold sensitivity and filtering above characteristic frequency (CF), and the latter consists of a Gaussian that accounts for sharp tuning and high sensitivity around CF. A fourth process, modeled as a high-pass filter, was needed in many fits to account for breaks and plateaus in threshold sensitivity at frequencies above CF. The latter three processes operated on cochlear spatial coordinates rather than stimulus frequency. The four-process description closely accounted for shapes of most tuning curves. Tuning curve tails possessed minima at 40-80 dB SPL, and minima increased with fiber CF. High-frequency cutoffs of tail filters tended to increase with CF, but low-frequency cutoffs were generally constant across CF. Functions describing tails varied from ear to ear but behaved in a similar manner for fibers from a single ear. Passive components of BM resonances possessed baselines with sensitivities that decreased with CF and cutoff slopes that increased with CF. The magnitude of the active component increased smoothly with CF over an 80 + dB range, and its spatial extent was essentially constant at 1.5 mm or 6% of cochlear length regardless of gain magnitude, fiber CF, or threshold sensitivity. Tuning curves from fibers with high and medium spontaneous rates (SRs) and similar CFs had nearly identical shapes, with the sole difference being essentially constant differences in sensitivity across the entire excitatory frequency range. Tuning curve shapes from fibers with low SRs were more variable. These could either resemble those obtained from similarly-tuned fibers with higher SRs, or they could exhibit lower tip-to-tail ratios and reduced active component magnitudes. 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PD DEC PY 1994 VL 81 IS 1-2 BP 167 EP 188 DI 10.1016/0378-5955(94)90163-5 PG 22 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800017 PM 7737923 ER PT J AU SHVAREV, YN AF SHVAREV, YN TI BRAIN-STEM AUDITORY-EVOKED POTENTIALS CHARACTERISTICS IN MICE - THE EFFECT OF GENOTYPE SO HEARING RESEARCH LA English DT Article DE BRAIN-STEM AUDITORY EVOKED POTENTIALS; STIMULUS INTENSITY; MOUSE; STRAIN DIFFERENCES ID SUPERIOR OLIVARY COMPLEX; NERVE ACTION POTENTIALS; INDUCED NEURONAL LOSS; STEM RESPONSE; LABORATORY MOUSE; HEARING-LOSS; COCHLEAR NUCLEUS; GUINEA-PIG; CAT; SENSITIVITY AB Brainstem auditory evoked potentials (BAEPs) elicited by sound clicks were recorded as a function of stimulus intensity in pentobarbital anesthetized C57BL/6J and BALB/c male mice, 2.5 months old. At high stimulus intensities the BAEPs of both strains consisted of 4 positive and 4 negative waves (labelled P1-P4 and N1-N4, correspondingly). However, great interstrain differences were observed. BALB/c mice were characterized by higher thresholds, less amplitudes, beginning with P1 peak, longer latencies and steeper in slope latency-intensity profiles. The data suppose that by this age C57BL/6J mice have better auditory acuity, than BALB/c, and in BALB/c mice the pronounced abnormalities appear to arise in cochlear-auditory nerve system. Analysis of BAEPs using interpeak latencies (IPLs) and amplitude ratios intensities (ARs) profiles technique demonstrated no general trend that could fit for all IPLs as well as for all Ars changes by varying stimulus intensity. The obtained interstrain and interpeak differences in BAEPs parameters suggest that auditory information processing may vary greatly as a function of brainstem level. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 189 EP 198 DI 10.1016/0378-5955(94)90164-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800018 PM 7737924 ER PT J AU ATTANASIO, G SPONGR, VP HENDERSON, D AF ATTANASIO, G SPONGR, VP HENDERSON, D TI LOCALIZATION OF F-ACTIN AND FODRIN ALONG THE ORGAN OF CORTI IN THE CHINCHILLA SO HEARING RESEARCH LA English DT Article DE ORGAN OF CORTI; CHINCHILLA; F-ACTIN; FODRIN; CONFOCAL FLUORESCENCE MICROSCOPY ID OUTER HAIR-CELLS; GUINEA-PIG COCHLEA; MOTILE RESPONSES; EAR; MECHANISM; PROTEINS; CYTOSKELETAL; STEREOCILIA; FILAMENTS; SPECTRIN AB The distribution of the two cytoskeletal proteins, filamentous actin (F-actin) and fodrin, was investigated along the organ of Corti of the chinchilla using laser scanning confocal fluorescence microscopy. High intensity labeling of F-actin was seen in outer and inner hair cells, including the stereocilia. High intensity staining was also seen for fodrin in outer and inner hair cells, but not in their stereocilia. Staining intensity of both proteins along the lateral cell wall of the outer hair cells appeared to be greater in the middle and basal cochlear turns than in the apical turn. Pillars and Deiters cells also exhibited high intensity labeling of F-actin. The lack of significant differences in the distribution of fodrin between outer and inner hair cells makes the role of this protein in the active processes still unclear. Comparison of the distribution of F-actin and fodrin in the chinchilla with those reported in the guinea pigs suggest possible species differences. C1 SUNY BUFFALO,HEARING RES LAB,BUFFALO,NY 14214. UNIV ROMA LA SAPIENZA,DEPT OTOLARYNGOL,ENT CLIN 3,I-00161 ROME,ITALY. CR ARIMA T, 1987, HEARING RES, V25, P61, DOI 10.1016/0378-5955(87)90079-7 ARNOLD W, 1990, CELL TISSUE RES, V263, P91 Brownell W. 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Res. PD DEC PY 1994 VL 81 IS 1-2 BP 199 EP 207 DI 10.1016/0378-5955(94)90165-1 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800019 PM 7537729 ER PT J AU WIT, HP VANDIJK, P AVAN, P AF WIT, HP VANDIJK, P AVAN, P TI ON THE SHAPE OF (EVOKED) OTOACOUSTIC EMISSION-SPECTRA SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; PERIODICITY; IRREGULARITY; CONVOLUTION AB In a preceding paper [Wit et al., (1994) Hear. Res. 73, 141-147] it was shown that realistic time-frequency plots for click evoked otoacoustic emissions can be synthesized by adding a large number of gammatones. It is necessary in such a synthesis to make the inner ear frequency to place map, from which the central frequencies of the gammatones are taken, slightly irregular along the entire cochlear partition. The present paper shows that this approach leads, in a rather straightforward way, to (quasi-) periodicity in synthesized spectra of evoked otoacoustic emissions. These spectra show good resemblance with spectra from real ear emission measurements. C1 FAC MED CLERMONT FERRAND,BIOPHYS LAB,CLERMONT FERRAND,FRANCE. RP WIT, HP (reprint author), UNIV GRONINGEN HOSP,INST AUDIOL,POB 30001,9700 RB GRONINGEN,NETHERLANDS. RI Van Dijk, Pim/E-8019-2010 OI Van Dijk, Pim/0000-0002-8023-7571 CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 BONFILS P, 1988, ARCH OTO-RHINO-LARYN, V245, P53, DOI 10.1007/BF00463550 Gold T., 1988, COCHLEAR MECHANISMS, P299 GREENWOOD DD, 1990, J ACOUST SOC AM, V87, P2592, DOI 10.1121/1.399052 HORST JW, 1993, PHYSL BASES PSYCHOPH, P89 Kemp DT, 1979, SCAND AUDIOL S, V9, P35 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 PAPOULIS A, 1962, FOURIER INTEGRAL ITS, P85 PATTERSON RD, 1992, AUDITORY PHYSL PERCE, P429 SCHLOTH E, 1983, ACUSTICA, V53, P250 Shera CA, 1993, BIOPHYSICS HAIR CELL, P54 WILLIAMS JEF, 1992, MODERN METHODS ANAL, P59 WIT HP, 1994, HEARING RES, V73, P141, DOI 10.1016/0378-5955(94)90228-3 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 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 DEC PY 1994 VL 81 IS 1-2 BP 208 EP 214 DI 10.1016/0378-5955(94)90166-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA QD778 UT WOS:A1994QD77800020 PM 7737925 ER PT J AU CROFTON, KM JANSSEN, R PRAZMA, J PULVER, S BARONE, S AF CROFTON, KM JANSSEN, R PRAZMA, J PULVER, S BARONE, S TI THE OTOTOXICITY OF 3,3'-IMINODIPROPIONITRILE - FUNCTIONAL AND MORPHOLOGICAL EVIDENCE OF COCHLEAR DAMAGE SO HEARING RESEARCH LA English DT Article DE IMINODIPROPIONITRILE; OTOTOXICITY; REFLEX MODIFICATION AUDIOMETRY; BRAIN-STEM AUDITORY EVOKED RESPONSE; COCHLEAR DAMAGE ID DEVELOPING RAT COCHLEA; REFLEX MODIFICATION; AUDITORY FUNCTION; HEARING-LOSS; SENSITIVITY; BETA,BETA'-IMINODIPROPIONITRILE; DEGENERATION; DYSFUNCTION; AUDIOMETRY; CAT AB Previous reports have suggested that IDPN may be ototoxic (Wolff et al., 1977; Crofton and Knight, 1991). The purpose of this research was to investigate the ototoxicity of IDPN using behavioral, physiological and morphological approaches. Three groups of adult rats were exposed to IDPN (0-400 mg/kg/day) for three consecutive days. In the first group, at 9-10 weeks post-exposure, thresholds for hearing of 5.3- and 38-kHz filtered clicks were measured electrophysiologically and brainstem auditory evoked responses (BAERs) were also recorded to a suprathreshold broadband click stimulus. A second set of animals was tested at 9 weeks for behavioral hearing thresholds (0.5- to 40-kHz tones) and at 11-12 weeks post-exposure for BAER thresholds (5- to 80-kHz filtered clicks). A third group of animals was exposed (as above), and killed at 12-14 weeks post-exposure for histological assessment. Kanamycin sulfate was used as a positive control for high-frequency selective hearing loss. Surface preparations of the organ of Corti were prepared in order to assess hair cells, and mid-modiolar sections of the cochlea were used to examine Rosenthal's canal and the stria vascularis. Functional data demonstrate a broad-spectrum hearing loss ranging from 0.5 kHz (30 dB deficit) to 80 kHz (40 dB deficit), as compared to a hearing deficit in kanamycin-exposed animals that was only apparent at frequencies greater than 5 kHz. Surface preparations revealed IDPN-induced hair cell loss in all turns of the organ of Corti, with a basal-to-apical gradient (more damage in the basal turns) at the lower dosages. At higher dosages there was complete destruction of the organ of Corti. There was also a dosage-related loss of spiral ganglion cells in all turns of the cochlea, again with a basal-to-apical gradient at the lower dosages. These data demonstrate that IDPN exposure in the rat results in extensive hearing loss and loss of neural structures in the cochlea. C1 MANTECH ENVIRONM TECHNOL INC,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,SCH MED,DIV OTOLARYNGOL,CHAPEL HILL,NC. RP CROFTON, KM (reprint author), US EPA,HLTH EFFECTS RES LAB,DIV NEUROTOXICOL,MD-74B,RES TRIANGLE PK,NC 27114, USA. 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Res. PD NOV PY 1994 VL 80 IS 2 BP 129 EP 140 DI 10.1016/0378-5955(94)90104-X PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PW206 UT WOS:A1994PW20600001 PM 7896571 ER PT J AU WABLE, J COLLET, L AF WABLE, J COLLET, L TI CAN SYNCHRONIZED OTOACOUSTIC EMISSIONS REALLY BE ATTRIBUTED TO SOAES SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; TRANSIENTLY EVOKED OTOACOUSTIC EMISSIONS; HUMAN ID NORMALLY HEARING SUBJECTS; ACOUSTIC EMISSIONS; FREQUENCY AB In this study, spontaneous and transiently evoked otoacoustic emissions (SOAEs and TOAEs, respectively) were recorded in 15 normal-hearing subjects. An analysis of the TOAE spectrum was performed with three time intervals : 20 ms-40 ms, 40 ms-60 ms, 60 ms-80 ms (the spectra found are labelled TOAE(2-4), TOAE(4-6), TOAE(6-8)). The frequencies of the peaks observed were compared to the SOAE frequencies. We found that 78.8% of the TOAE(2-4) peaks also were observed as SOAEs and 91.2% of the SOAE peaks were recorded in the TOAE(2-4) spectrum. Peaks that were not observed by either method had lower amplitude than the others, and SOAE peaks that were not in TOAE(2-4) spectrum had higher frequencies than those that were observed in the TOAE(2-4) spectrum. We conclude that the TOAE spectrum recorded after 20 ms does not include all of the SOAE frequencies and is not composed solely of SOAEs. Therefore, frequencies exist which are synchronized specifically to the stimulus and SOAEs exist which can't be synchronized more than 20 ms. C1 UNIV LYON 1,HOP EDOUARD HERRIOT,PHYSIOL SENSORIELLE LAB,CNRS,URA 1447,F-69003 LYON,FRANCE. CR KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KILLION MC, 1986, J ACOUST SOC AM S, V1, P79 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 MCFADDEN D, 1984, J ACOUST SOC AM, V76, P443, DOI 10.1121/1.391585 MOULIN A, 1993, HEARING RES, V65, P216, DOI 10.1016/0378-5955(93)90215-M PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 WHITEHEAD ML, 1989, BRIT J AUDIOL, V23, P149 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 NR 10 TC 24 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1994 VL 80 IS 2 BP 141 EP 145 DI 10.1016/0378-5955(94)90105-8 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PW206 UT WOS:A1994PW20600002 PM 7896572 ER PT J AU SIEGEL, JH HIROHATA, ET AF SIEGEL, JH HIROHATA, ET TI SOUND CALIBRATION AND DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS AT HIGH-FREQUENCIES SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSIONS; DISTORTION PRODUCT; ACOUSTIC CALIBRATION; HIGH-FREQUENCY ID SENSORINEURAL HEARING-LOSS; ACOUSTIC DISTORTION; COCHLEAR MECHANICS; EAR; RESPONSES; BEHAVIOR; 2F1-F2; HUMANS; PRESSURE; RABBIT AB Distortion product otoacoustic emissions offer the potential for assessing inner ear function at high frequencies. However, commonly employed methods for calibrating the acoustic system used in these studies can lead to errors of +/-20 dB or more in the estimate of eardrum sound pressure levels above 2-3 kHz [Siegel, J. Acoust. Soc. Am. 95, 2589-2597 (1994)]. We assessed the magnitude of these errors by measuring the distortion product emission 2f(1)-f(2) (f(1)3.0.CO;2-D FAUSTI SA, 1984, AM J OTOLARYNG, V5, P177, DOI 10.1016/S0196-0709(84)80009-5 FAUSTI SA, 1992, J INFECT DIS, V165, P1026 FORNAZZARI L, 1983, ACTA NEUROL SCAND, V67, P319 GODFREY DA, 1985, ANN OTO RHINOL LARYN, V94, P409 GODFREY DA, 1986, NEUROBIOLOGY HEARING, P149 GOUREVIT.G, 1966, J COMP PHYSIOL PSYCH, V62, P289, DOI 10.1037/h0023669 ISON JR, 1984, NEUROBEH TOXICOL TER, V6, P437 JACOBSON EJ, 1969, J AUD RES, V9, P379 JANSSEN R, 1991, BRAIN RES, V552, P255, DOI 10.1016/0006-8993(91)90090-I 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, V75, P201, DOI 10.1016/0378-5955(94)90071-X JOHNSON AC, 1994, HEARING RES, V72, P189, DOI 10.1016/0378-5955(94)90218-6 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 LI HS, 1992, ARCH TOXICOL, V66, P382, DOI 10.1007/BF02035126 MATTSSON JL, 1990, PHARMACOL BIOCHEM BE, V36, P683, DOI 10.1016/0091-3057(90)90274-L METRICK SA, 1982, ANN NEUROL, V12, P553, DOI 10.1002/ana.410120609 MORATA TC, 1989, SCAND AUDIOL, V18, P53, DOI 10.3109/01050398909070723 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, 1987, J APPL TOXICOL, V7, P44 PRYOR GT, 1983, NEUROBEH TOXICOL TER, V5, P53 PRYOR GT, 1992, NEUROTOXICOLOGY, V13, P225 PRYOR GT, 1986, NEUROTOXICOL TERATOL, V8, P103 REBERT CS, 1991, NEUROTOXICOL TERATOL, V13, P83, DOI 10.1016/0892-0362(91)90031-Q REBERT CS, 1983, NEUROBEH TOXICOL TER, V5, P59 RUPPERT PH, 1984, TOXICOL LETT, V22, P33, DOI 10.1016/0378-4274(84)90042-0 RYBAK LP, 1992, OTOLARYNG HEAD NECK, V106, P677 SCHULTE BA, 1993, HEARING RES, V65, P262, DOI 10.1016/0378-5955(93)90219-Q SEITZ B, 1972, SOC MED HYG TRA 0410 SULLIVAN MJ, 1989, NEUROTOXICOL TERATOL, V10, P525 TANGE RA, 1985, ARCH OTO-RHINO-LARYN, V242, P77, DOI 10.1007/BF00464411 VELASQUEZ J, 1969, 16 INT C OCC HLTH TO YANO BL, 1992, TOXICOL PATHOL, V20, P1 YOUNG JS, 1983, J ACOUST SOC AM, V73, P1686, DOI 10.1121/1.389391 1992, TOXICOLOGICAL PROFIL, P98 NR 50 TC 89 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 OCT PY 1994 VL 80 IS 1 BP 25 EP 30 DI 10.1016/0378-5955(94)90005-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400004 PM 7852200 ER PT J AU YAO, XF TENCATE, WJF CURTIS, LM RAREY, KE AF YAO, XF TENCATE, WJF CURTIS, LM RAREY, KE TI EXPRESSION OF NA+,K+-ATPASE ALPHA-1 SUBUNIT MESSENGER-RNA IN THE DEVELOPING RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE HYBRIDIZATION, IN SITU; NA+,K+-ATPASE; MESSENGER-RNA; COCHLEAR DEVELOPMENT; RAT ID MESSENGER-RNAS; INSITU HYBRIDIZATION; ION-TRANSPORT; TISSUES; ATPASE; BRAIN AB The distribution of Na+,K+-ATPase alpha 1 subunit mRNA was identified using in situ hybridization in the developing rat cochlea. The expression of alpha 1 subunit mRNA in stria vascularis (SV) was observed in all time points studied, 1 to 30 postnatal day (pnd) rats. The adult expression level was attained between 11 to 14 pnd. Surprisingly, alpha 1 subunit mRNA in spiral ligament (SL) and spiral limbus (SLi) was expressed in a more distinct time-dependent manner. At 7 pnd, the alpha 1 subunit mRNA expression was observed initially in the tissues of the SL. At 11 pnd, alpha 1 subunit expression appeared in SLi. Between 11 and 14 pnd, an adult-like pattern of Na+,K+-ATPase alpha 1 subunit mRNA expression was attained in the SL and SLi. These data suggest that the expression of Na+,K+-ATPase alpha 1 subunit mRNA in these areas are closely related to the development of the rat EP, as its expression in the stria vascularis. C1 UNIV FLORIDA,J HILLIS MILLER HLTH CTR,COLL MED,DEPT ANAT & CELL BIOL,GAINESVILLE,FL 32610. UNIV FLORIDA,COLL MED,DEPT OTOLARYNGOL,GAINESVILLE,FL 32610. CR ABDELLAT.AA, 1967, J NEUROCHEM, V14, P1133, DOI 10.1111/j.1471-4159.1967.tb06160.x BOSHER SK, 1972, ACTA OTO-LARYNGOL, V73, P203, DOI 10.3109/00016487209138931 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 EMANUEL JR, 1987, P NATL ACAD SCI USA, V84, P9030, DOI 10.1073/pnas.84.24.9030 FERNANDE.C, 1974, ACTA OTO-LARYNGOL, V78, P173, DOI 10.3109/00016487409126343 GEERING K, 1982, J BIOL CHEM, V257, P338 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 KUIJPERS W, 1974, ACTA OTO-LARYNGOL, V78, P341, DOI 10.3109/00016487409126364 KUIJPERS W, 1968, BIOCHIM BIOPHYS ACTA, P477 ORLOWSKI J, 1988, J BIOL CHEM, V263, P10436 REMEZAL M, 1993, HEARING RES, V66, P23, DOI 10.1016/0378-5955(93)90256-Z RYAN A F, 1991, Molecular and Cellular Neuroscience, V2, P179, DOI 10.1016/1044-7431(91)90011-C RYAN AF, 1991, HEARING RES, V56, P148, DOI 10.1016/0378-5955(91)90164-5 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 SCHMITT CA, 1986, J BIOL CHEM, V261, P439 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SIMMONS DM, 1989, J HISTOTECHNOL, V12, P169 SPICER SS, 1991, HEARING RES, V56, P53, DOI 10.1016/0378-5955(91)90153-Z TONNDORF J, 1962, ANN OTO RHINOL LARYN, V71, P801 NR 22 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 OCT PY 1994 VL 80 IS 1 BP 31 EP 37 DI 10.1016/0378-5955(94)90006-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400005 PM 7852201 ER PT J AU VANDERHEIJDEN, M KOHLRAUSCH, A AF VANDERHEIJDEN, M KOHLRAUSCH, A TI USING AN EXCITATION-PATTERN MODEL TO PREDICT AUDITORY MASKING SO HEARING RESEARCH LA English DT Article DE EXCITATION PATTERN; MODEL; MASKING; AUDITORY FILTERS; ROEX FILTERS ID PSYCHOPHYSICAL TUNING CURVES; FILTER SHAPES; NOISE; LEVEL; FREQUENCY; INTENSITY; SIGNALS; BAND AB This paper evaluates the extent to which auditory masking can be reliably predicted from excitation patterns. For this purpose a quantitative model proposed by Glasberg and Moore [Hear. Res. 47, 103-138 (1990)] was used to calculate excitation patterns evoked by stationary sounds. Model simulations were performed for a number of masking experiments, reported in the literature, by calculating excitation patterns for the masker-alone as well as for the masker-plus-target conditions. As a threshold criterion, a difference between the two patterns of 1 dB at any frequency was imposed. For narrow-band-noise masking patterns, the method yields a fairly precise prediction of experimental data. For other conditions, however, systematic deviations between model predictions and data are observed. For instance, the model does not reproduce the typical tip-tail shape of psychophysical tuning curves. Furthermore, the nonlinearities in level dependence are not correctly described, and the model fails to reproduce a realistic two-tone masking curve. C1 INST PERCEPT RES, 5600 MB EINDHOVEN, NETHERLANDS. 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Res. PD OCT PY 1994 VL 80 IS 1 BP 38 EP 52 DI 10.1016/0378-5955(94)90007-8 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400006 PM 7852202 ER PT J AU RAPHAEL, Y ADLER, HJ WANG, Y FINGER, PA AF RAPHAEL, Y ADLER, HJ WANG, Y FINGER, PA TI CELL-CYCLE OF TRANSDIFFERENTIATING SUPPORTING CELLS IN THE BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE BASILAR PAPILLA; NOISE; CHICK; MITOSIS; TEM; REGENERATION ID SEVERE ACOUSTIC TRAUMA; CHICK COCHLEA; HAIR CELL; INNER-EAR; REGENERATION; REORGANIZATION; DIFFERENTIATION; REPRODUCTION; EPITHELIUM; EMBRYOS AB Mitosis of supporting cells has been shown to contribute to the cellular repopulation of the basilar papilla after acoustic trauma. In the present work we report data obtained with light and transmission electron microscopy after acoustic trauma in chicks. We report changes that occur in cell shape, surface morphology, intercellular junctions, nuclear shape and location, and cytoplasmic organization of supporting cells after trauma. The findings strongly suggest that supporting cells transdifferentiate and that the proliferative pattern is similar to interkinetic nuclear migration, as previously shown in the developing neural tube and basilar papilla. S-phase nuclei were positioned adjacent to the basement membrane, suggesting that interaction with the extracellular matrix may occur during the cell cycle. Supporting cells divided with the long axis of the spindle parallel to the reticular lamina and displayed no signs of intercellular communication during mitosis. This suggested to us that the fate of the progeny cells is determined prior to mitosis and that the progeny may be of identical phenotypic fate. Dividing cells had a smooth apical surface. The smooth surface may provide a marker to help identify dividing cells with scanning electron microscope analysis. RP RAPHAEL, Y (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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Res. PD OCT PY 1994 VL 80 IS 1 BP 53 EP 63 DI 10.1016/0378-5955(94)90008-6 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400007 PM 7852203 ER PT J AU WEISLEDER, P PARK, TJ AF WEISLEDER, P PARK, TJ TI BELGIAN WATERSLAGER CANARIES ARE AFFLICTED BY SCHEIBE-LIKE DYSPLASIA SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; CONGENITAL HEARING LOSS; INNER EAR; AVIAN ID HAIR CELL REGENERATION; SERINUS-CANARIUS; AUDITORY-THRESHOLDS; ACOUSTIC TRAUMA AB Behavioral investigations of Belgian Waterslager canaries (BWCs) have demonstrated a congenital hearing impairment that primarily affects high frequencies. Research into the surface anatomy of the basilar papilla of these birds has pointed to the hair cells as the site of the lesion. Given that the basilar papilla and the vestibular organs bath develop from the otocyst, we were interested in ascertaining whether the vestibular sensory epithelia also displayed abnormal hair cells. The inner ear of adult BWCs was examined by scanning electron microscopy. As expected, hair cells in the basilar papilla of BWCs were abnormal. As for the vestibular parenchyma, abnormal hair cells were detected in only one structure: the sacculus. Morphological abnormalities of the cochlea and sacculus are pathognomonic signs of Scheibe's dysplasia, the most common inner ear defect associated with congenital hearing loss. Our results suggest that BWCs are afflicted by this genetic disorder. RP WEISLEDER, P (reprint author), UNIV TEXAS,DEPT ZOOL,GOOD HAIRDAY LAB,AUSTIN,TX 78712, USA. 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F., 1965, ACTA OTO-LARYNGOL, V59, P154, DOI 10.3109/00016486509124549 WEISLEDER P, 1993, J COMP NEUROL, V331, P97, DOI 10.1002/cne.903310106 NR 16 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 1994 VL 80 IS 1 BP 64 EP 70 DI 10.1016/0378-5955(94)90009-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400008 PM 7852204 ER PT J AU SIMMONS, DD BERTOLOTTO, C NARINS, PM AF SIMMONS, DD BERTOLOTTO, C NARINS, PM TI MORPHOLOGICAL GRADIENTS IN SENSORY HAIR-CELLS OF THE AMPHIBIAN PAPILLA OF THE FROG, RANA-PIPIENS PIPIENS SO HEARING RESEARCH LA English DT Article DE TONOTOPY; TUNING; CELL BODY LENGTH; CROSS-SECTIONAL AREA; INNER EAR ID AUDITORY-NERVE FIBERS; PERIPHERAL ORIGINS; COCHLEA; FREQUENCY; BULLFROG; SENSITIVITIES; CONDUCTANCES; MEMBRANE; GOLDFISH; TURTLE AB The sensory hair cells of the amphibian papilla (AP) of the northern leopard frog were examined in a light-microscopic analysis. Hair cell length and cross-sectional area were found to vary systematically along the rostro-caudal axis of the endorgan. The AP was readily divided into three morphological regions. Rostrally-located hair cells are tall, cylindrically-shaped cells with large crosssectional areas and long stereocilia; caudally-located hair cells are short, goblet-shaped cells with small cross-sectional areas and short stereocilia. In the middle region, hair cells exhibit features intermediate to those of hair cells located at the AP extremes. The detailed pattern of changes in hair cell morphology along the endorgan correlates well with its observed tonotopy and may have implications for the intrinsic tuning of the AP. C1 UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. RP SIMMONS, DD (reprint author), UNIV CALIF LOS ANGELES, DEPT BIOL, 405 HILDEGARD AVE, LOS ANGELES, CA 90024 USA. 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Res. PD OCT PY 1994 VL 80 IS 1 BP 71 EP 78 DI 10.1016/0378-5955(94)90010-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400009 PM 7852205 ER PT J AU KEITHLEY, EM LO, J RYAN, AF AF KEITHLEY, EM LO, J RYAN, AF TI 2-DEOXYGLUCOSE UPTAKE PATTERNS IN RESPONSE TO PURE-TONE STIMULI IN THE AGED RAT INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE PRESBYCUSIS; AGING; 2-DEOXYGLUCOSE; AUDITORY PERCEPTION; PLASTICITY; NEURAL METABOLISM ID CEREBRAL GLUCOSE-UTILIZATION; TONOTOPIC ORGANIZATION; AUDITORY-SYSTEM; C-14 2-DEOXYGLUCOSE; COCHLEAR NUCLEUS; FISCHER-344 RAT; GRADED SERIES; CELL COUNTS; YOUNG; IMMUNOREACTIVITY AB The tonotopic map of the inferior colliculus (IC) of aged rats (25 months old) was examined to determine whether age-related changes known to occur in the cochlea are reflected in the 2-deoxyglucose (2-DG) uptake pattern of the IC. Because aged animals have hearing losses, auditory brainstem response thresholds were measured. Animals with threshold shifts of no greater than 30 dB relative to young animals were used. Animals were injected with radiolabeled 2-DG and stimulated with continuous pure tones presented at 70 dB above the behavioral thresholds for young animals at either 1, 4 or 32 kHz for one hour in a sound attenuated booth. The stimulus sound pressure levels were chosen to achieve comparable sensation levels between the young and aged animals. The tonotopic map of the IC in aged rats was different from that reported previously for young animals (Ryan et al., 1988), in that, the regions stimulated by 1 and 4 kHz were shifted towards the higher frequencies and the uptake areas were twice as broad for the aged animals as for the young animals. The observed 2-DG uptake patterns are consistent with an activation pattern of a high intensity stimulus and a loss of responsive elements in the cochlear apex. Similar broad and shifted bands of activated tissue may contribute to difficulties in auditory perception in aged humans with increased thresholds and sound amplification; C1 UNIV CALIF SAN DIEGO,SCH MED,DIV OTOLARYNGOL,LA JOLLA,CA. VET ADM MED CTR,LA JOLLA,CA. UNIV CALIF SAN DIEGO,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. CR Bredberg G, 1968, ACTA OTO-LARYNGOL, V236, P1 CASEY MA, 1990, NEUROBIOL AGING, V11, P391, DOI 10.1016/0197-4580(90)90004-J CASPARY DM, 1990, J NEUROSCI, V10, P2363 CLERICI WJ, 1987, NEUROBIOL AGING, V8, P171, DOI 10.1016/0197-4580(87)90028-5 COLEMAN JR, 1982, OTOLARYNG HEAD NECK, V90, P795 COOPER WA, 1990, HEARING RES, V43, P171, DOI 10.1016/0378-5955(90)90226-F CROWLEY DE, 1972, ANN OTO RHINOL LARYN, V81, P739 DALLOS P, 1977, PSYCHOPHYSICS PHYSL, P1 EHRET G, 1991, BRAIN RES, V567, P350, DOI 10.1016/0006-8993(91)90819-H FINLAYSON PG, 1993, NEUROBIOL AGING, V14, P127, DOI 10.1016/0197-4580(93)90088-S HUANG C, 1986, EXP BRAIN RES, V61, P506 HUNGERBUHLER JP, 1981, EXP NEUROL, V71, P104, DOI 10.1016/0014-4886(81)90074-1 KEITHLEY EM, 1990, NEUR ABSTR, V16, P796 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1993, J COMP NEUROL, V327, P612, DOI 10.1002/cne.903270411 KEITHLEY EM, 1990, HEARING RES, V49, P169, DOI 10.1016/0378-5955(90)90103-V KEITHLEY EM, 1989, J ACOUST SOC AM, V81, P1036 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 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LONDON ED, 1981, J NEUROCHEM, V37, P217, DOI 10.1111/j.1471-4159.1981.tb05311.x NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 REIMER K, 1993, BRAIN RES, V616, P339, DOI 10.1016/0006-8993(93)90229-G RYAN AF, 1989, BRAIN RES, V483, P283, DOI 10.1016/0006-8993(89)90172-8 RYAN AF, 1988, HEARING RES, V36, P181, DOI 10.1016/0378-5955(88)90060-3 RYAN AF, 1987, NEUR ABSTR, V13, P79 RYAN AF, 1992, HEARING RES, V61, P24, DOI 10.1016/0378-5955(92)90032-I RYAN AF, 1982, J COMP NEUROL, V207, P369, DOI 10.1002/cne.902070408 SCHEICH H, 1979, CELL TISSUE RES, V204, P17 SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SMITH CB, 1980, BRAIN, V103, P351, DOI 10.1093/brain/103.2.351 SOKOLOFF L, 1977, J NEUROCHEM, V29, P13, DOI 10.1111/j.1471-4159.1977.tb03919.x WEBSTER WR, 1985, J NEUROSCI, V5, P1820 WILLOTT JF, 1988, EXP NEUROL, V99, P615, DOI 10.1016/0014-4886(88)90178-1 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1984, BRAIN RES, V309, P159, DOI 10.1016/0006-8993(84)91022-9 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 OCT PY 1994 VL 80 IS 1 BP 79 EP 85 DI 10.1016/0378-5955(94)90011-6 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400010 PM 7852206 ER PT J AU SUNOSE, H IKEDA, K SUZUKI, M TAKASAKA, T AF SUNOSE, H IKEDA, K SUZUKI, M TAKASAKA, T TI VOLTAGE-ACTIVATED K-CHANNEL IN LUMINAL MEMBRANE OF MARGINAL CELLS OF STRIA-VASCULARIS DISSECTED FROM GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE POTASSIUM; SLOWLY ACTIVATING; ISK; COCHLEA; STRIA VASCULARIS; GUINEA PIG ID CL CHANNELS; NONSELECTIVE CATION; APICAL MEMBRANE; PROTEIN; CLONING; ISK; LOCALIZATION; EXPRESSION; MECHANISMS; HEART AB Inward rectifying K channel activity was observed in the luminal membrane of the marginal cell by use of the patch clamp technique. When pipette solution contained 150 mM KCl, the current reversed at 10.2 +/- 8.8 mV (N = 27). The channel current showed multiple subconductance levels and depolarization activated the channel very slowly (order of seconds). Current-voltage relationships in cell-attached mode showed inward rectification. The calculated slope conductance of inward and outward currents were 18 +/- 7 pS and 5.4 +/- 2.0 pS (N = 27), respectively. When pipette solution contained 75 mM NaCl and 75 mM KCI, the current reversed - 7.0 +/- 7.6 mV (N = 6). When pipette solution contained NaCl or Na gluconate, the channel currents were outwardly directed within a range of -60 to 60 mV. These results suggested that the channel is selective to K+. The channel showed immediate run down after excision, and this rundown was not prevented by elimination of cytoplasmic Ca2+. The channel activity was not affected by an increase of intracellular cAMP and cGMP, an application of cytoplasmic catalytic subunit of PKA with ATP. Taking its density into consideration, the channel seems to contribute considerably to the K+ conductance of the luminal membrane of the marginal cell. C1 TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,AOBA KU,SENDAI,MIYAGI 980,JAPAN. CR ATTALI B, 1993, NATURE, V365, P850, DOI 10.1038/365850a0 BENZANILLA F, 1985, BIOPHYS J, V47, P437 FOLANDER K, 1990, P NATL ACAD SCI USA, V87, P2975, DOI 10.1073/pnas.87.8.2975 HODGKIN AL, 1949, J PHYSL, V108, P33 HONORE E, 1991, EMBO J, V10, P2805 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KOMUNE S, 1993, ORL J OTO-RHINO-LARY, V55, P61 MARCUS DC, 1994, AM J PHYSIOL, V267, pC857 MELICHAR I, 1987, HEARING RES, V25, P35, DOI 10.1016/0378-5955(87)90077-3 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 SAKAGAMI M, 1991, HEARING RES, V56, P168, DOI 10.1016/0378-5955(91)90166-7 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SELLICK P M, 1975, Progress in Neurobiology (Oxford), V5, P337, DOI 10.1016/0301-0082(75)90015-5 SUGIMOTO T, 1990, J MEMBRANE BIOL, V113, P39, DOI 10.1007/BF01869604 SUNOSE H, 1993, AM J PHYSIOL, V265, pC72 TAKEUCHI S, 1992, HEARING RES, V61, P86, DOI 10.1016/0378-5955(92)90039-P TAKUMI T, 1988, SCIENCE, V242, P1042, DOI 10.1126/science.3194754 WANGEMANN P, 1994, FASEB J, V8, pA562 NR 19 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 OCT PY 1994 VL 80 IS 1 BP 86 EP 92 DI 10.1016/0378-5955(94)90012-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400011 PM 7531683 ER PT J AU GOODYEAR, R HOLLEY, M RICHARDSON, G AF GOODYEAR, R HOLLEY, M RICHARDSON, G TI VISUALIZATION OF DOMAINS IN THE AVIAN TECTORIAL AND, OTOLITHIC MEMBRANES WITH MONOCLONAL-ANTIBODIES SO HEARING RESEARCH LA English DT Article DE EAR, INTERNAL; COCHLEA; INNER EAR; EXTRACELLULAR MATRIX; OTOCONIA; ACCESSORY MEMBRANE ID HAIR BUNDLES; PROTEINS; EAR AB The staining patterns observed with six monoclonal antibodies (mAbs) raised in vitro against a fraction derived from the utricular macula were examined with cryosections of the auditory and vestibular organs of the avian inner ear. These antibodies revealed several distinct domains within the gelatinous membranes. Three different labelling patterns were observed in the tectorial membrane. Staining was seen either throughout the entire tectorial membrane, restricted to its core, or in a narrow zone lying close to the surface of the basilar papilla. In the maculae, the mAbs stained either the striolar region of the otolithic membrane or the entire structure: One monoclonal which labelled otoconia, stained small otoconia in their entirety, whilst larger otoconia were only labelled around their periphery. Only one of the mAbs stained the cupulae of the semi-circular canal ampullae and this antibody stained neither the tectorial nor the otolithic membranes. These results suggest that there are biochemically distinct regions in the gelatinous membranes of the inner ear and indicate that these matrices are not simply homogeneous extracellular structures. C1 UNIV SUSSEX,SCH BIOL SCI,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. SCH MED SCI BRISTOL,DEPT PHYSIOL,BRISTOL BS8 1TD,AVON,ENGLAND. CR BENSER ME, 1993, HEARING RES, V68, P243, DOI 10.1016/0378-5955(93)90128-N COHEN GM, 1985, HEARING RES, V18, P29, DOI 10.1016/0378-5955(85)90108-X DALE T, 1976, Norwegian Journal of Zoology, V24, P85 DOHLMAN GF, 1971, ACTA OTO-LARYNGOL, V71, P89, DOI 10.3109/00016487109125337 Flock A., 1965, ACTA OTO LARYNG ST S, V199, P1 GILLESPIE PG, 1991, J CELL BIOL, V112, P625, DOI 10.1083/jcb.112.4.625 GOODYEAR R, 1992, J COMP NEUROL, V325, P243, DOI 10.1002/cne.903250208 Hillman D.E., 1976, P452 IGARASHI M, 1969, ACTA OTO-LARYNGOL, V68, P43, DOI 10.3109/00016486909121541 JAHNKE V, 1969, ACT AOTOLARYNGOL, V67, P581 JOHNSSON LG, 1967, SCIENCE, V157, P1454, DOI 10.1126/science.157.3795.1454 KACHAR B, 1990, HEARING RES, V45, P179, DOI 10.1016/0378-5955(90)90119-A KELLY JP, 1991, J MORPHOL, V207, P23, DOI 10.1002/jmor.1052070105 KHAN KM, 1990, HEARING RES, V43, P149, DOI 10.1016/0378-5955(90)90224-D KILLICK R, 1992, HEARING RES, V64, P21, DOI 10.1016/0378-5955(92)90165-J Lim DJ, 1984, ULTRASTRUCTURAL ATLA, P245 LIM DJ, 1974, AEROSPACE MED, V95, P705 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 MARCO J, 1971, ACTA OTO-LARYNGOL, V71, P1, DOI 10.3109/00016487109125326 MONEY KE, 1972, COMP BIOCHEM PHYSIOL, V42, P353, DOI 10.1016/0300-9629(72)90116-8 POTE KG, 1986, J ULTRA MOL STRUCT R, V95, P61, DOI 10.1016/0889-1605(86)90029-7 POTE KG, 1991, COMP BIOCHEM PHYS B, V98, P287, DOI 10.1016/0305-0491(91)90181-C Retzius G., 1884, GEHORORGAN REPTILIEN, V2 REYNOLDS ES, 1963, J CELL BIOL, V17, P208, DOI 10.1083/jcb.17.1.208 ROSS MD, 1985, AUDITORY BIOCH, P500 ROSS MD, 1987, ACTA OTO-LARYNGOL, V103, P56, DOI 10.3109/00016488709134698 SHIEL MJ, 1990, HEARING RES, V47, P147, DOI 10.1016/0378-5955(90)90172-L TANAKA K, 1975, ANN OTO RHINOL LARYN, V84, P287 WERNER CL. F., 1933, ZEITSCHR GES ANAT ABT I ZEITSCHR ANAT U ENTWICK LUNGSGESCH, V99, P696, DOI 10.1007/BF02118586 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 YAN HY, 1991, P ROY SOC B-BIOL SCI, V245, P133, DOI 10.1098/rspb.1991.0099 NR 31 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 1994 VL 80 IS 1 BP 93 EP 104 DI 10.1016/0378-5955(94)90013-2 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400012 PM 7531684 ER PT J AU OXENHAM, AJ MOORE, BCJ AF OXENHAM, AJ MOORE, BCJ TI MODELING THE ADDITIVITY OF NONSIMULTANEOUS MASKING SO HEARING RESEARCH LA English DT Article DE MASKING; TEMPORAL RESOLUTION; TEMPORAL INTEGRATION ID BACKWARD-MASKING; MASKER DURATION; TEMPORAL GAPS; AUDITORY FUNCTIONS; FREQUENCY REGION; BASILAR-MEMBRANE; NORMAL-HEARING; NOISE; BANDWIDTH; INTENSITY AB Thresholds were measured for detecting a brief 6-kHz sinusoidal signal preceded by a broadband noise masker (forward masking), followed by the masker (backward masking), or both preceded by and followed by the masker (combined masking). The masker-signal interval was systematically varied. Consistent with the literature, thresholds in the combined-masking condition were higher than would be predicted by an energy-sum of the effects of the individual forward and backward maskers. This is often referred to as 'excess' masking. The data were modeled by subjecting the amplitude of the stimuli to a power-law nonlinearity followed by a sliding temporal integrator ('window'). It was assumed that threshold corresponds to a fixed signal-to-noise ratio at the output of the window. The best fits to the data were obtained using a power less than unity (0.5 to 0.7), i.e. by a compressive nonlinearity. Generally good fits to the data were achieved, indicating that the model is able to account for the decay of forward and backward masking as well as the effects of combining pairs of maskers (excess masking). The temporal windows derived from the data are also able to predict thresholds in decrement and increment detection tasks, and to account for the longer-term effects of masker duration in forward masking. RP OXENHAM, AJ (reprint author), UNIV CAMBRIDGE,DEPT EXPTL PSYCHOL,DOWNING ST,CAMBRIDGE CB2 3EB,ENGLAND. 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Res. PD OCT PY 1994 VL 80 IS 1 BP 105 EP 118 DI 10.1016/0378-5955(94)90014-0 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400013 PM 7852196 ER PT J AU QUIRK, WS COLEMAN, JKM HANESWORTH, JM HARDING, JW WRIGHT, JW AF QUIRK, WS COLEMAN, JKM HANESWORTH, JM HARDING, JW WRIGHT, JW TI NOISE-INDUCED ELEVATIONS OF PLASMA ENDOTHELIN (ET-3) SO HEARING RESEARCH LA English DT Article ID ANGIOTENSIN-II; IMMUNOREACTIVE ENDOTHELIN; CORTICOSTERONE RESPONSES; CEREBROSPINAL-FLUID; STRESS; RATS; CATECHOLAMINE; RECEPTOR; EXPOSURE; CLONING AB The endothelins (ETs) are a novel family of peptides which participate in hemodynamic homeostasis. Elevated levels of circulating ETs are evident in several stress related conditions and are associated with a variety of vascular pathophysiologies. The purpose of the current study was to test the possibility that plasma concentrations of endothelin increase following noise exposure- using radioimmunoassay (RIA). No difference in plasma endothelin was detected in rats subjected to brief noise exposure (30 min of 100 dB SPL broad-band noise) compared to control animals. Statistically significant elevations in plasma endothelin (ET-3) were measured in animals exposed to prolonged noise exposure (90 min and 72 h of 100 dB SPL broad-band noise). These results suggest that hemodynamic alterations, and potential vascular pathophysiologies accompanying prolonged exposure to noise are mediated by endothelin. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. WASHINGTON STATE UNIV,DEPT VET & COMPARAT ANAT PHARMACOL & PHYSIOL,PULLMAN,WA 99164. WASHINGTON STATE UNIV,DEPT PSYCHOL,PULLMAN,WA 99164. RP QUIRK, WS (reprint author), WAYNE STATE UNIV,DEPT OTOLARYNGOL,MICROCIRCULAT LAB,5E UHC,E CANFIELD,DETROIT,MI 48201, USA. 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Res. PD OCT PY 1994 VL 80 IS 1 BP 119 EP 122 DI 10.1016/0378-5955(94)90015-9 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400014 PM 7852197 ER PT J AU OHNO, K TAKEDA, N KUBO, T KIYAMA, H AF OHNO, K TAKEDA, N KUBO, T KIYAMA, H TI UP-REGULATION OF GAP-43 (B50/F1) GENE-EXPRESSION IN VESTIBULAR EFFERENT NEURONS FOLLOWING LABYRINTHECTOMY IN THE RAT - IN-SITU HYBRIDIZATION USING AN ALKALINE PHOSPHATASE-LABELED PROBE SO HEARING RESEARCH LA English DT Article DE REGENERATION; NERVE INJURY; GAP-43 GENE; INNER EAR ID PERIPHERAL-NERVE INJURY; ROOT GANGLION NEURONS; SPINAL-CORD; PROTEIN GAP-43; MESSENGER-RNA; GROWTH; CELLS; GALANIN AB Growth-associated protein (GAP)-43 plays a significant role in nerve regeneration and synaptic remodeling. We examined the profiles of GAP-43 mRNA expression in vestibular efferent neurons after labyrinthectomy in adult rats, and clearly demonstrated that labyrinthectomy increased GAP-43 expression in these neurons. This finding suggests the ability of vestibular efferent nerves to regenerate after nerve injury. C1 OSAKA UNIV,SCH MED,BIOMED RES CTR,DEPT NEUROANAT,SUITA,OSAKA 565,JAPAN. RP OHNO, K (reprint author), OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,2-2 YAMADAOKA,SUITA,OSAKA 565,JAPAN. 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Res. PD OCT PY 1994 VL 80 IS 1 BP 123 EP 127 DI 10.1016/0378-5955(94)90016-7 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PP044 UT WOS:A1994PP04400015 PM 7852198 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; BASILAR PAPILLA; REORGANIZATION; 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. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 1 EP 16 DI 10.1016/0378-5955(94)90122-8 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900001 PM 7806472 ER PT J AU NEUMANN, J UPPENKAMP, S KOLLMEIER, B AF NEUMANN, J UPPENKAMP, S KOLLMEIER, B TI CHIRP EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE TRANSIENTLY EVOKED OTOACOUSTIC EMISSIONS; AUDIOMETRY; HEARING THRESHOLD ID OTO-ACOUSTIC EMISSIONS; FINE-STRUCTURE; FREQUENCY; SUPPRESSION; THRESHOLD; EARS AB The principles of short frequency sweeps (chirps) and their application to evoke transiently evoked otoacoustic emissions (TEOAE) are developed in comparison to using standard click stimuli. In contrast to click stimuli, chirp signals have the advantage of stimulating a freely selectable frequency range. In addition, chirp signals contain more energy than a click stimulus with the same maximum amplitude. The effects of different stimuli on TEOAE were investigated in normal hearing and hearing-impaired subjects. Using wide-band chirp signals yields a better signal-to-noise ratio compared to click stimulation. In addition, the stimulation of selected regions of the basilar membrane with frequency-limited chirps evokes TEOAE with frequency components that lie within the stimulated frequency range. The characteristic fine structure of this spectrum was found to be independent of the stimulus applied. The utilization of chirp stimuli appears to be useful for evoking TEOAE in, e.g., clinical applications. C1 UNIV GOTTINGEN,DRITTES PHYS INST,W-3400 GOTTINGEN,GERMANY. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 17 EP 25 DI 10.1016/0378-5955(94)90123-6 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900002 PM 7806479 ER PT J AU MEITELES, LZ RAPHAEL, Y AF MEITELES, LZ RAPHAEL, Y TI SCAR FORMATION IN THE VESTIBULAR SENSORY EPITHELIUM AFTER AMINOGLYCOSIDE TOXICITY SO HEARING RESEARCH LA English DT Article DE VESTIBULAR EPITHELIUM; AMINOGLYCOSIDES; MAMMAL; DEGENERATION; REGENERATION; HAIR CELLS ID EXPERIMENTAL PERILYMPHATIC FISTULA; INNER-EAR AB Hair cell degeneration and the repair process due to differing types of trauma have been studied extensively in the organ of Corti. It has been determined that, during scar formation, after differing types of trauma to the auditory sensory system, the reticular lamina is maintained with adherens junctions and tight junctions. We investigated the repair process within the vestibular epithelium. Hair cell degeneration was induced by the unilateral application of streptomycin to the inner ears of guinea pigs. Whole mount preparations of all five vestibular organs were processed and examined by fluorescence, light and electron microscopy. Scar formation was seen as early as 4 days post-treatment with streptomycin and was noted to coincide with hair cell degeneration. Neighboring supporting cells swelled and filled the space beneath the degenerating hair cell. Between three and five supporting cells participate in the reparative process. The distribution of cytokeratin is also altered during scar formation. The area once occupied by the hair cell becomes filled with cytokeratin-rich processes of supporting cells. It appears that differing numbers of supporting cells are involved in the reparative process within the vestibular sensory epithelium as compared to the auditory system. The reticular lamina remains intact at all times. This may possibly prevent mixing of fluids between different compartments in the inner ear and dysfunction of the vestibular sensory organs. C1 UNIV MICHIGAN,MED CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 26 EP 38 DI 10.1016/0378-5955(94)90124-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900003 PM 7528737 ER PT J AU ZDANSKI, CJ PRAZMA, J PETRUSZ, P GROSSMAN, G RAYNOR, E SMITH, TL PILLSBURY, HC AF ZDANSKI, CJ PRAZMA, J PETRUSZ, P GROSSMAN, G RAYNOR, E SMITH, TL PILLSBURY, HC TI NITRIC-OXIDE SYNTHASE IS AN ACTIVE ENZYME IN THE SPIRAL GANGLION-CELLS OF THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE NITRIC OXIDE SYNTHASE; CITRULLINE; NEURONAL NADPH DIAPHORASE; SPIRAL GANGLION CELLS; NEUROTRANSMISSION; NEUROTOXICITY ID GUINEA-PIG COCHLEA; METHYL-D-ASPARTATE; NADPH-DIAPHORASE; KAINIC ACID; IMMUNOCYTOCHEMICAL LOCALIZATION; GLUTAMATE NEUROTOXICITY; NERVOUS-SYSTEM; NEUROTRANSMISSION; QUISQUALATE; ARGININE AB Nitric oxide (NO) mediates the effects of the excitatory amino acids in the central nervous system. Excitatory amino acids, in particular L-glutamate, are thought to be the neurotransmitter(s) present at the cochlear hair cell-afferent nerve synapse. To our knowledge, no studies to date have documented the presence of NO in the cochlea nor attempted to elucidate the role of NO in hearing. Rat cochlea frozen sections were examined for the presence of nitric oxide synthase (NOS) by NADPH diaphorase histochemistry. Vibratome sections of rat cochlea were examined by immunocytochemistry with an antibody to citrulline, an indication of NOS activity. Spiral ganglion cells in the rat cochlea were positive by NADPH diaphorase histochemistry and by anti-citrulline immunocytochemistry. These results indicate that NOS is present and that the enzyme actively produces nitric oxide in the spiral ganglion cells of the rat cochlea. Given our current understanding of neurotransmission in the cochlea, it is reasonable to postulate that the actions of NO in cochlear neuronal tissue are similar to the actions of NO in the CNS and that NO acts as a neurotransmitter/neuromodulator in the cochlea. In addition, because NO has been implicated as a mediator of excitotoxicity in the CNS, NO may play a role in neurotoxicity in the cochlea. C1 UNIV N CAROLINA,SCH MED,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC. RI Raynor, Eileen/F-7572-2013 CR ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 ALTSCHULER RA, 1984, BRAIN RES, V291, P173, DOI 10.1016/0006-8993(84)90667-X BECKMAN JS, 1990, P NATL ACAD SCI USA, V87, P1620, DOI 10.1073/pnas.87.4.1620 BLEDSOE SC, 1981, HEARING RES, V4, P109, DOI 10.1016/0378-5955(81)90040-X BOBBIN RP, 1979, EXP BRAIN RES, V34, P389 BREDT DS, 1990, P NATL ACAD SCI USA, V87, P682, DOI 10.1073/pnas.87.2.682 BREDT DS, 1989, P NATL ACAD SCI USA, V86, P9030, DOI 10.1073/pnas.86.22.9030 BRUNE B, 1989, J BIOL CHEM, V264, P8455 COYLE JT, 1983, J NEUROCHEM, V41, P1 DAWSON VL, 1991, P NATL ACAD SCI USA, V88, P6368, DOI 10.1073/pnas.88.14.6368 EHRENBERGER K, 1991, HEARING RES, V52, P73, DOI 10.1016/0378-5955(91)90188-F EYBALIN M, 1993, PHYSIOL REV, V73, P309 GARTHWAITE J, 1991, TRENDS NEUROSCI, V14, P60, DOI 10.1016/0166-2236(91)90022-M GARTHWAITE J, 1989, J NEUROCHEM, V53, P1952, DOI 10.1111/j.1471-4159.1989.tb09266.x GARTHWAITE J, 1989, EUR J PHARM-MOLEC PH, V172, P413, DOI 10.1016/0922-4106(89)90023-0 HIBBS JB, 1988, BIOCHEM BIOPH RES CO, V157, P87, DOI 10.1016/S0006-291X(88)80015-9 HOPE BT, 1991, P NATL ACAD SCI USA, V88, P2811, DOI 10.1073/pnas.88.7.2811 IZUMI Y, 1992, NEUROSCI LETT, V135, P227, DOI 10.1016/0304-3940(92)90442-A JANSSEN R, 1991, BRAIN RES, V552, P255, DOI 10.1016/0006-8993(91)90090-I 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 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 KNOWLES RG, 1989, P NATL ACAD SCI USA, V86, P5159, DOI 10.1073/pnas.86.13.5159 LEFEBVRE PP, 1991, BRAIN RES, V555, P75, DOI 10.1016/0006-8993(91)90862-P MONCADA S, 1991, PHARMACOL REV, V43, P109 NAKAGAWA T, 1991, J NEUROPHYSIOL, V65, P715 PASQUALOTTO BA, 1991, NEUROSCI LETT, V128, P155, DOI 10.1016/0304-3940(91)90250-W PETRUSZ P, 1993, J HISTOCHEM CYTOCHEM, V41, P1126 PUEL JL, 1991, NEUROSCIENCE, V45, P63, DOI 10.1016/0306-4522(91)90103-U PUJOL R, 1985, HEARING RES, V18, P145, DOI 10.1016/0378-5955(85)90006-1 SCHERERSINGLER U, 1983, J NEUROSCI METH, V9, P229, DOI 10.1016/0165-0270(83)90085-7 WOOD PL, 1990, J NEUROCHEM, V55, P346, DOI 10.1111/j.1471-4159.1990.tb08859.x NR 32 TC 61 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 SEP PY 1994 VL 79 IS 1-2 BP 39 EP 47 DI 10.1016/0378-5955(94)90125-2 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900004 PM 7528738 ER PT J AU YOST, WA SHEFT, S AF YOST, WA SHEFT, S TI MODULATION DETECTION INTERFERENCE - ACROSS-FREQUENCY PROCESSING AND AUDITORY GROUPING SO HEARING RESEARCH LA English DT Article DE AMPLITUDE MODULATION; MODULATION DETECTION INTERFERENCE; SOUND SOURCE DETERMINATION; ACROSS-SPECTRAL PROCESSING ID COMODULATION MASKING RELEASE; AMPLITUDE-MODULATION; CHANNEL MASKING; HEARING; SIGNALS; TONES AB Modulation Detection Interference (MDI) is the loss of sensitivity in processing amplitude modulation of a probe tone when a masker is similarly modulated. MDI was measured in four experiments to investigate two past claims concerning MDI: 1) That MDI represents across-spectral processing, and 2) that MDI is the consequence of the auditory system using common patterns of amplitude modulation to group spectral components into a single auditory source. Experiment I studied MDI when the envelope phase of the masker and probe modulators were different and was used to address the issue of the extent to which MDI is a consequence of spectral grouping based on common amplitude modulation. Measures of MDI for conditions in which the frequency separation between the probe and masker carriers was varied (Experiment II), estimates of modulation depth discrimination (Experiment III), and signal detection thresholds for brief sinusoidal signals masked by amplitude modulated tones (Experiment IV) were all used to address issues related to across-spectral processing of amplitude modulation. The conclusions of these studies is that MDI is largely an across-frequency phenomenon and that the role of auditory grouping based on a common pattern of modulation can not be ruled out as having a relationship to MDI. RP YOST, WA (reprint author), LOYOLA UNIV,PARMLY HEARING INST,6525 N SHERIDAN RD,CHICAGO,IL 60626, USA. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 48 EP 58 DI 10.1016/0378-5955(94)90126-0 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900005 PM 7806484 ER PT J AU KHETARPAL, U ROBERTSON, NG YOO, TJ MORTON, CC AF KHETARPAL, U ROBERTSON, NG YOO, TJ MORTON, CC TI EXPRESSION AND LOCALIZATION OF COL2A1 MESSENGER-RNA AND TYPE-II COLLAGEN IN HUMAN FETAL COCHLEA SO HEARING RESEARCH LA English DT Article DE HUMAN FETAL COCHLEA; COLLAGEN TYPE II, ALPHA 1; HYBRIDIZATION, IN SITU; IMMUNOHISTOCHEMISTRY ID INSITU HYBRIDIZATION; MESSENGER-RNAS; GENE COL2A1; TRANSIENT EXPRESSION; TECTORIAL MEMBRANE; 3' END; PROCOLLAGEN; CARTILAGE; CLONES; CDNA AB The expression and localization of COL2A1 mRNA and protein was examined in human fetal cochlea to study the role of this gene in hearing and to begin to understand the pathogenesis of mutations in COL2A1 in hearing disorders. Northern blot analysis revealed COL2A1 expression in fetal membranous cochlea to be markedly greater than that in fetal skin, kidney, cartilage, eye and brain. In situ hybridization revealed COL2A1 expression in marrow cells, osteoblasts, fibroblasts and some osteocytes, in addition to chondrocytes in otic capsule. In the membranous cochlea, connective tissue elements (spiral ligament, spiral limbus and modiolar connective tissue), neuronal cells, secretory cells (stria vascularis) and organ of Corti cells (sensory hair cells) were found to express COL2A1. Immunohistochemistry was performed to assess distribution of type TI collagen and correlation with COL2A1 mRNA in these morphologically and functionally diverse cell populations. In otic capsule, only cartilage was found to stain positively, and in membranous cochlea, only connective tissue structures including spiral ligament, spiral limbus, tectorial and basilar membranes, modiolar and spiral lamina cartilage contained type II collagen. Nonconnective tissue cells, marrow cells and osteoblasts did not contain immunohistochemically identifiable protein. Absence of type II collagen in a subset of cochlear cells may reflect potentially either inability to detect low levels of protein in these cells or posttranscriptional regulation. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV TENNESSEE,DEPT MED,DIV ALLERGY & IMMUNOL,MEMPHIS,TN 38163. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 59 EP 73 DI 10.1016/0378-5955(94)90127-9 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900006 PM 7806485 ER PT J AU MORGAN, YV RYUGO, DK BROWN, MC AF MORGAN, YV RYUGO, DK BROWN, MC TI CENTRAL TRAJECTORIES OF TYPE-II (THIN) FIBERS OF THE AUDITORY-NERVE IN CATS SO HEARING RESEARCH LA English DT Article DE TYPE II NEURONS; PRIMARY AFFERENTS; HORSERADISH PEROXIDASE; CAT ID CENTRAL PROJECTIONS; COCHLEAR NUCLEUS; SPIRAL GANGLION; HORSERADISH-PEROXIDASE; AFFERENT-FIBERS; ADULT CATS; INNERVATION; CELLS; NEURONS; MOUSE AB This paper describes the central projections of thin fibers of the auditory nerve in cats. Both thin (type II) and thick (type I) fibers are labeled by extracellular injections of horseradish peroxidase (HRP) into the auditory nerve. Type I and almost all type II fibers bifurcate upon reaching the auditory nerve root of the cochlear nucleus. For a given bundle of auditory nerve fibers labeled by a discrete injection of HRP, bifurcations of type II and type I fibers are restricted to a narrow region of the nerve root. After the bifurcation, the pathways of type II branches within the anteroventral cochlear nucleus (AVCN) and posteroventral cochlear nucleus (PVCN) are similar to those of type I branches. This similarity in bifurcation and course of type I and type II fibers was observed in the ventral as well as dorsal parts of the ventral cochlear nucleus. The complete axonal course of most type II fibers could not be reconstructed, however, due to fading of the reaction product. Type II fibers produce very few collaterals in the cochlear nucleus (CN), but possess many 'en passant' swellings along their main processes and collaterals. Compared with type II fibers previously studied in mice (Berglund and Brown, 1989; 1994; Brown and Ledwith, 1990), cat type II fibers are similar in their general projections within the main body of the nucleus and in the frequency of 'en passant' swellings per length of fiber, but cat fibers have a higher percentage of 'complex' or pedunculated 'en passant' swellings. C1 MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,BOSTON,MA 02114. JOHNS HOPKINS UNIV HOSP,CTR HEARING SCI,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. 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PD SEP PY 1994 VL 79 IS 1-2 BP 74 EP 82 DI 10.1016/0378-5955(94)90128-7 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900007 PM 7806486 ER PT J AU MUNYER, PD SCHULTE, BA AF MUNYER, PD SCHULTE, BA TI IMMUNOHISTOCHEMICAL LOCALIZATION OF KERATAN SULFATE AND CHONDROITIN 4-SULFATE AND 6-SULFATE PROTEOGLYCANS IN SUBREGIONS OF THE TECTORIAL AND BASILAR MEMBRANES SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; BASILAR MEMBRANE; COCHLEA; PROTEOGLYCANS; IMMUNOHISTOCHEMISTRY; GERBIL ID ELECTRON-MICROSCOPIC LOCALIZATION; SILVER METHENAMINE METHOD; INNER-EAR; GELATINOUS MEMBRANES; MONOCLONAL-ANTIBODIES; GUINEA-PIG; GERBIL; COCHLEA; GLYCOSAMINOGLYCANS; FIBRONECTIN AB Proteoglycans containing keratan sulfate (KSPG) and 4- and 6-sulfated epitopes of chondroitin sulfate (CSPG) were identified in distinct domains of the tectorial and basilar membranes by ultrastructural immunogold labeling with monoclonal antibodies. In the tectorial membrane (TM), the highest concentration of gold particles was present in the upper fibrous layers of the limbal, middle and marginal zones with all three antibodies. Reactivity with anti-KSPG exceeded that with anti-4S and anti-6S CSPG, especially in the marginal zone. The cover net showed no reactivity for any antibody. Labeling density of gold particles with all three antibodies increased markedly from base to apex. In the basilar membrane (BM), all three PGs were most highly concentrated in regions of amorphous ground substance bordering the upper and lower filamentous bands. As in the TM, reactivity for anti-KSPG in the BM exceeded that for either CSPG antibody and staining with all three antibodies was stronger and more widespread in the apical as compared to the basal turns. These results provide the first ultrastructural demonstration of KSPG and CSPG in distinct subregions of the TM and BM. The preferential distribution and marked increase in PGs from base to apex in both TM and BM supports a role for these macromolecules in regulating structural and mechanical properties of these highly specialized extracellular membranes. RP MUNYER, PD (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 83 EP 93 DI 10.1016/0378-5955(94)90129-5 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900008 PM 7528739 ER PT J AU DOBIE, RA WILSON, MJ AF DOBIE, RA WILSON, MJ TI PHASE WEIGHTING - A METHOD TO IMPROVE OBJECTIVE DETECTION OF STEADY-STATE EVOKED-POTENTIALS SO HEARING RESEARCH LA English DT Article DE MAGNITUDE-SQUARED COHERENCE; PHASE WEIGHTING; STEADY-STATE EVOKED POTENTIALS ID COHERENCE AB Objective response detection statistics such as magnitude-squared coherence (MSC) reflect the degree to which subaverage phases are clustered or dispersed, but not their agreement with an expected, or target, phase. Using signal-plus-noise simulations and human 40-Hz auditory evoked potentials, we tested MSC performance with and without phase weighting, in which MSC values were multiplied by weights related to the phase error between measured phase and target phase. Phase weighting improved MSC performance for both simulated and 40-Hz auditory evoked potential data. However, the improvement was greater for the simulations, probably because target phase was precisely known. RP DOBIE, RA (reprint author), UNIV TEXAS,HLTH SCI CTR,DIV OTOLARYNGOL HEAD & NECK SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. 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PD SEP PY 1994 VL 79 IS 1-2 BP 94 EP 98 DI 10.1016/0378-5955(94)90130-9 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900009 PM 7806487 ER PT J AU TAKEMURA, T SAKAGAMI, M NAKASE, T KUBO, T KITAMURA, Y NOMURA, S AF TAKEMURA, T SAKAGAMI, M NAKASE, T KUBO, T KITAMURA, Y NOMURA, S TI LOCALIZATION OF OSTEOPONTIN IN THE OTOCONIAL ORGANS OF ADULT-RATS SO HEARING RESEARCH LA English DT Article DE OSTEOPONTIN; OTOCONIA; SENSORY HAIR CELL; HYBRIDIZATION, IN SITU ID BONE PHOSPHOPROTEIN OSTEOPONTIN; URINARY STONE PROTEIN; INSITU HYBRIDIZATION; MESSENGER-RNA; DEVELOPMENTAL EXPRESSION; 2AR OSTEOPONTIN; HISTOCHEMISTRY; GLYCOPROTEIN; MEMBRANES; CLONING AB Although it is known that mammalian otoconia consist of calcium bicarbonate and organic materials, none of the protein components have been identified in mammals at the molecular level, and the mechanisms of morphogenesis and calcification of the otoconia is still unclear. In the present study, we demonstrated the presence of osteopontin (OPN) in rat otoconia by using immunohistochemistry, and detected OPN mRNA in the sensory hair cells by a non-radioisotopic in situ hybridization technique. These results indicate that OPN is one of the protein components in rat otoconia and suggest that sensory hair cells are involved in the production of otoconia. C1 OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,SUITA,OSAKA 565,JAPAN. OSAKA UNIV,SCH MED,DEPT ORTHOPAED SURG,SUITA,OSAKA 565,JAPAN. OSAKA UNIV,SCH MED,DEPT PATHOL,SUITA,OSAKA 565,JAPAN. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 99 EP 104 DI 10.1016/0378-5955(94)90131-7 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900010 PM 7806488 ER PT J AU MORIYAMA, T HOU, TT WU, M JEN, PHS AF MORIYAMA, T HOU, TT WU, M JEN, PHS TI RESPONSES OF INFERIOR COLLICULAR NEURONS OF THE FM BAT, EPTESICUS-FUSCUS, TO PULSE TRAINS WITH VARIED PULSE AMPLITUDES SO HEARING RESEARCH LA English DT Article DE BAT; INFERIOR COLLICULUS; TEMPORALLY PATTERNED SOUNDS ID BIG BROWN BAT; AUDITORY SPACE REPRESENTATION; RHINOLOPHUS-FERRUMEQUINUM; MYOTIS-LUCIFUGUS; REPETITION RATE; ECHOLOCATING BATS; TARGET DISTANCE; HORSESHOE BAT; CORTEX; SYSTEM AB Under free field stimulation conditions, we studied the responses of inferior collicular neurons of the FM bat, Eptesicus fuscus, to pulse trains with varied pulse amplitudes. Each pulse train consisted of 7 pulses of 4 ms delivered at 24 ms interpulse-intervals (i.e. 42 pulses/s). For a control pulse train, ah pulse amplitudes were equal to a neuron's best amplitude which, when delivered in single pulses, elicited maximal number of impulses from the neuron. The amplitudes of individual pulses of the remaining pulse trains were linearly increased or decreased at a slope of 0, 14, 28, 42, 56 and 69 dB/s. All 56 inferior collicular neurons discharged to pulse trains were of two main types. Type I (N43, 77%) neurons discharged to each pulse within a train while type II(N11, 20%) neurons discharged to the first pulse of a train stimulus only. Discharge patterns of the remaining (N2, 3%) neurons changed between type I and type II when stimulated with different pulse trains. The number of impulses discharged by a neuron varied with different pulse trains. In addition, the number of impulses discharged to each pulse by type I neurons also varied among individual pulses within the train. Only 14 neurons (25%) discharged maximally to the control pulse train. Responses of the remaining neurons to other pulse trains were either 30%-120% larger than (N17, 30%) or within 30% (N25, 45%) of the control pulse train response. Furthermore, half of 56 neurons selectively discharged to a most preferred pulse train with a response magnitude which was at least 50% larger than the response to the least preferred pulse train. Possible mechanisms underlying the different discharge patterns are discussed in terms of a neuron's recovery cycle, minimum threshold and inhibitory period relative to the temporal characteristics (pulse repetition rate and amplitude) of the pulse trains. C1 UNIV MISSOURI,DIV BIOL SCI,COLUMBIA,MO 65211. TOKYO MED & DENT UNIV,DEPT NEUROPHYSIOL,TOKYO 113,JAPAN. CHANG GUNG MED COLL,DEPT PHYSIOL,TAIPEI,TAIWAN. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 105 EP 114 DI 10.1016/0378-5955(94)90132-5 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900011 PM 7806473 ER PT J AU CONLEE, JW GERITY, LC BENNETT, ML AF CONLEE, JW GERITY, LC BENNETT, ML TI ONGOING PROLIFERATION OF MELANOCYTES IN THE STRIA VASCULARIS OF ADULT GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE ALBINISM; COCHLEA; INNER EAR; MELANIN; PIGMENTATION ID INNER-EAR; DIFFERENTIAL SUSCEPTIBILITY; MITOTIC-ACTIVITY; ACOUSTIC TRAUMA; CELLS; GENTAMICIN; PIGMENT; ALBINO; CHINCHILLA; EXPOSURE AB The intermediate cells of the stria vascularis are melanocytes derived from the neural crest. These internalized pigment cells have been thought to be a static population, distinct from those found in the skin. However, this investigation demonstrates that the melanocytes of the adult stria vascularis undergo continuous replication. Cell proliferation was studied using [H-3]-thymidine autoradiography and bromodeoxyuridine (BrdU) immunohistochemistry. Single or multiple injections of [H-3]-thymidine within a six hour period labeled a mean of 9 intermediate cells. In pigmented guinea pigs, single daily injections of [H-3]-thymidine for 2 or 4 days labeled a mean of 24 and 69 intermediate cells, respectively; Pigmented guinea pigs given BrdU once daily for 2 or 4 days labeled a mean of 38 and 75 intermediate cells. By contrast, albino littermates also given BrdU averaged only 23 and 42 labeled intermediate cells in the same 2 and 4 day experiments. The mean number of proliferating cells/mm of stria per 24 h was 1.54 in the pigmented animals and 0.88 in the albinos. Both the total number and density of labeled intermediate cells were significantly smaller in the albino than the pigmented guinea pigs. These results demonstrate that the melanocytes in the stria vascularis undergo continuous baseline mitosis, and at a rate comparable to the melanocytes of the skin. This surprising similarity promotes the speculation that the proliferative rate of the strial melanocytes may be influenced by some of the same factors known to affect replication and pigment production in the skin. C1 UNIV UTAH,SCH MED,DEPT NEUROBIOL & ANAT,SALT LAKE CITY,UT 84132. RP CONLEE, JW (reprint author), VET AFFAIRS MED CTR,SALT LAKE CITY,UT 84148, USA. 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L., 1970, CONT RES METHODS NEU, P252 STEEL KP, 1989, DEVELOPMENT, V107, P453 STERKERS O, 1988, PHYSIOL REV, V68, P1083 SUGIHARA H, 1986, HISTOCHEMISTRY, V85, P193, DOI 10.1007/BF00494803 TASAKI I, 1959, J NEUROPHYSIOL, V22, P149 Wolff D, 1931, ARCHIV OTOLARYNGOL, V14, P195 WRIGHT CG, 1989, ACTA OTO-LARYNGOL, V108, P190, DOI 10.3109/00016488909125518 NR 42 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 1994 VL 79 IS 1-2 BP 115 EP 122 DI 10.1016/0378-5955(94)90133-3 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900012 PM 7806474 ER PT J AU GLEICH, O DOOLING, RJ MANLEY, GA AF GLEICH, O DOOLING, RJ MANLEY, GA TI INNER-EAR ABNORMALITIES AND THEIR FUNCTIONAL CONSEQUENCES IN BELGIAN WATERSLAGER CANARIES (SERINUS-CANARIUS) SO HEARING RESEARCH LA English DT Article DE BIRD; CANARY; COCHLEA; HAIR-CELL; PATHOLOGY; DEAFNESS ID BUDGERIGARS MELOPSITTACUS-UNDULATUS; FINCHES POEPHILA-GUTTATA; HAIR CELL REGENERATION; CHICK BASILAR PAPILLA; ACOUSTIC TRAUMA; STEREOCILIARY BUNDLES; AUDITORY-THRESHOLDS; COCHLEA; OTOTOXICITY; AFFERENTS AB Recent reports of elevated auditory thresholds in canaries of the Belgian Waterslager strain have shown that this strain has an inherited auditory deficit in which absolute auditory thresholds at high frequencies (i.e. above 2.0 kHz) are as much as 40 dB less sensitive than the thresholds of mixed-breed canaries and those of other strains. The measurement of CAP audiograms showed that the hearing deficit is already present at the level of the auditory nerve (Gleich and Dooling, 1992). Here we show gross abnormalities in the anatomy of the basilar papilla of Belgian Waterslager canaries at the level of the hair cell. The extent of these abnormalities was correlated with the amount of hearing deficit as measured behaviorally. C1 TECH UNIV MUNICH,INST ZOOL,D-85747 GARCHING,GERMANY. UNIV MARYLAND,DEPT PSYCHOL,COLLEGE PK,MD 20742. CR BROWN SD, 1993, J NEUROBIOL, V24 CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 COTANCHE DA, 1987, HEARING RES, V30, P181, DOI 10.1016/0378-5955(87)90135-3 COTANCHE DA, 1991, HEARING RES, V52, P379, DOI 10.1016/0378-5955(91)90027-7 COUSILLAS H, 1988, HEARING RES, V32, P117, DOI 10.1016/0378-5955(88)90083-4 DOOLING RJ, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P545 FISCHER FP, 1988, HEARING RES, V34, P87, DOI 10.1016/0378-5955(88)90053-6 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 GIROD DA, 1991, LARYNGOSCOPE, V101, P1139 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, 1992, RHYTHMOGENESIS NEURO, P207 GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 GLEICH O, 1994, J MORPHOL, V221, P1, DOI 10.1002/jmor.1052210102 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 GUTTINGER HR, 1985, BEHAVIOUR, V92, P255 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 KOPPL C, 1993, J COMP PHYSIOL A, V171, P695, DOI 10.1007/BF00213066 MANLEY GA, 1992, EVOLUTIONARY BIOLOGY OF HEARING, P561 MANLEY GA, 1986, AUDITORY FREQUENCY S, P63 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MARLER P, 1977, J COMP PHYSIOL PSYCH, V91, P8, DOI 10.1037/h0077303 Miller E. H., 1982, ACOUSTIC COMMUNICATI, V2, P95 NOTTEBOHM F, 1981, SCIENCE, V214, P1368, DOI 10.1126/science.7313697 OKANOYA K, 1987, J COMP PSYCHOL, V101, P213, DOI 10.1037/0735-7036.101.2.213 OKANOYA K, 1990, HEARING RES, V50, P185, DOI 10.1016/0378-5955(90)90044-P OKANOYA K, 1990, HEARING RES, V46, P271, DOI 10.1016/0378-5955(90)90008-D OKANOYA K, 1990, HEARING RES, V50, P175, DOI 10.1016/0378-5955(90)90043-O OKANOYA K, 1985, J ACOUST SOC AM, V78, P1170, DOI 10.1121/1.392885 PATUZZI RB, 1991, HEARING RES, V53, P57, DOI 10.1016/0378-5955(91)90214-T PICKLES JO, 1991, HEARING RES, V55, P244, DOI 10.1016/0378-5955(91)90109-M SAUNDERS JC, 1992, EXP NEUROL, V115, P13, DOI 10.1016/0014-4886(92)90213-A STEEL KP, 1991, ANN NY ACAD SCI, V630, P68, DOI 10.1111/j.1749-6632.1991.tb19576.x STEEL KP, 1983, AUDITORY PSYCHOBIOLO, P341 Stresemann E., 1923, Ornithologische Monatsberichte, V31, P103 TILNEY MS, 1987, HEARING RES, V25, P141, DOI 10.1016/0378-5955(87)90087-6 WASER MS, 1977, J COMP PHYSIOL PSYCH, V91, P1, DOI 10.1037/h0077299 NR 40 TC 20 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 1994 VL 79 IS 1-2 BP 123 EP 136 DI 10.1016/0378-5955(94)90134-1 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900013 PM 7806475 ER PT J AU PEDROZO, HA WIEDERHOLD, ML AF PEDROZO, HA WIEDERHOLD, ML TI EFFECTS OF HYPERGRAVITY ON STATOCYST DEVELOPMENT IN EMBRYONIC APLYSIA-CALIFORNICA SO HEARING RESEARCH LA English DT Article DE STATOCYST; STATOLITH; MINERALIZATION; GRAVITY; APLYSIA CALIFORNICA ID MICROGRAVITY; OTOCONIA AB Aplysia californica is a marine gastropod mollusc with bilaterally paired statocysts as gravity-receptor organs. Data from three experiments in which embryonic Aplysia californica were exposed to 2 X g are discussed. The experimental groups were exposed to excess gravity until hatching (9-12 day), whereas control groups were maintained at normal gravity. Body diameter was measured before exposure to 2 X g. Statocyst, statolith and body diameter were each determined for samples of 20 embryos from each group on successive days. Exposure to excess gravity led to an increase in body size. Statocyst size was not affected by exposure to 2 X g. Statolith size decreased with treatment as indicated by smaller statolith-to-body ratios observed in the 2 X g group in all three experiments. Mean statolith diameter was significantly smaller for the 2 x g group in Experiment 1 but not in Experiments 2 and 3. Defective statocysts, characterized by very small or no statoliths, were found in the 2 X g group in Experiments 1 and 2. RP PEDROZO, HA (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 137 EP 146 DI 10.1016/0378-5955(94)90135-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900014 PM 7806476 ER PT J AU ZHOU, SL PICKLES, JO AF ZHOU, SL PICKLES, JO TI EARLY HAIR-CELL DEGENERATION IN THE EXTREME APEX OF THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; HAIR CELLS; STEREOCILIA; PATHOLOGY; DEGENERATION; DEVELOPMENT; AGE ID BASILAR PAPILLA; GANGLION-CELL; STEREOCILIA; DENSITY; GERBILS AB Guinea pigs, aged from 3 weeks before term to 31 weeks after birth, were prepared for scanning electron microscopy. Examination of the extreme apex of the cochlea showed apparently pathological hair cells, even 3 weeks before term. The pathologies included loss and fusion of stereocilia, and the formation of giant stereocilia. The pathologies were most prevalent on row 3 of outer hair cells, declining to outer hair cell rows 2 and 1, with the inner hair cells being least affected. The abnormalities increased with time, increasing rapidly over the first few weeks of life, and more slowly thereafter. It is suggested that early degeneration in the extreme cochlear apex forms a novel model for spontaneous hair cell degeneration, with applicability to other types of spontaneous hair cell degeneration. C1 UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,BRISBANE,QLD 4072,AUSTRALIA. 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J., 1967, ACTA OTO-LARYNGOL, V220, P1 RYALS BM, 1988, HEARING RES, V36, P1, DOI 10.1016/0378-5955(88)90133-5 SCHULTE BA, 1992, HEARING RES, V61, P35, DOI 10.1016/0378-5955(92)90034-K SMOORENBURG GF, 1992, NOISE INDUCED HEARIN, P313 SPEIDEL CC, 1948, AM J ANAT, V82, P277, DOI 10.1002/aja.1000820205 SWANSON GJ, 1990, DEV BIOL, V137, P243, DOI 10.1016/0012-1606(90)90251-D TARNOWSKI BI, 1991, HEARING RES, V54, P123, DOI 10.1016/0378-5955(91)90142-V Van De Water T., 1976, ANN OTOL RHINOL S33, V85, P1 NR 32 TC 7 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1994 VL 79 IS 1-2 BP 147 EP 160 DI 10.1016/0378-5955(94)90136-8 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900015 PM 7806477 ER PT J AU SPICER, SS SCHULTE, BA AF SPICER, SS SCHULTE, BA TI DIFFERENCES ALONG THE PLACE-FREQUENCY MAP IN THE STRUCTURE OF SUPPORTING CELLS IN THE GERBIL COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; DEITERS CELLS; GERBIL; ION TRANSPORT; MICROTUBULES; MORPHOLOGY; SUPPORTING CELLS ID TUBULOCISTERNAL ENDOPLASMIC-RETICULUM; AGE-RELATED-CHANGES; GUINEA-PIG; LATERAL WALL; INNER-EAR; ORGAN; CORTI; POTENTIALS; JUNCTIONS; NA+,K+-ATPASE AB The function of supporting cells was investigated by comparing their morphologic adaptations at six different places in the gerbil cochlea. The volume of Deiters cells and tectal (cover) cells increased whereas that of Boettcher and Claudius cells decreased from base to apex. Deiters cells in the basal region tuned between 40 and 20 kHz lacked the unique rosette complex seen in regions encoding frequencies at or below 10 kHz. Deiters cells in high frequency regions differed from those at lower frequency places in several other ways: they possessed more apical microtubules, a larger basal microtubule stalk, mitochondria in the basal compartment, apical mitochondria that were unassociated with plasmalemma and more symmetric, and a less elaborately folded apicomedial plasmalemma enveloping fewer nerves. The tectal cells covering the outer tunnel appeared unlike Hensen cells in location and structure and differed further in exhibiting more variability with position in the cochlea. These covering cells in regions encoding high frequencies (20 and 40 kHz) extended a thin process medially that formed the roof of the outer tunnel and connected with the phalanx of the third Deiters cell. The tectal cells exclusively in places at 10 kHz or below projected numerous fimbriae into the outer tunnel. Hensen cells lateral to the cover cells also differed with frequency in showing abundant apical microvilli and mitochondria and basal juxtaposition to Boettcher cells only in the 40 to 20 kHz region. The observed structural differences provide evidence for functional variability along the place-frequency map. They attest to greater ion resorption from the outer tunnel by Deiters and tectal cells in low to mid frequency regions, and for greater ion exchange between endolymph and perilymph by Hensen, Boettcher and outer sulcus cells in regions of the cochlea encoding high frequencies. Amplification of the Deiters cells' microtubule system in the base of the cochlea possibly imparts increased stiffness to these cells and enhances transmission of mechanical energy at high frequency. RP SPICER, SS (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 161 EP 177 DI 10.1016/0378-5955(94)90137-6 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900016 PM 7806478 ER PT J AU GILLOYZAGA, P VICENTETORRES, MA FERNANDEZMATEOS, P ARCE, A ESQUIFINO, A AF GILLOYZAGA, P VICENTETORRES, MA FERNANDEZMATEOS, P ARCE, A ESQUIFINO, A TI PIRIBEDIL AFFECTS DOPAMINE TURNOVER IN COCHLEAS STIMULATED BY WHITE-NOISE SO HEARING RESEARCH LA English DT Article DE DOPAMINE RELEASE; WHITE NOISE; HPLC; D-2 AGONIST; PIRIBEDIL; OLIVOCOCHLEAR EFFERENT SYSTEM; COCHLEA ID GUINEA-PIG COCHLEA; PRESYNAPTIC AUTORECEPTORS; INVIVO RELEASE; BRAIN; NOREPINEPHRINE; MODULATION; NEURONS; ACETYLCHOLINE; INNERVATION; RECEPTORS AB The presence of dopamine (DA) within the cochlea has been previously reported, indicating that its turnover increases under noise stimulation. In the present report, piribedil, a dopaminergic D-2 agonist, was used in order to provide evidence of the activity of D-2 receptors in the turnover of DA under noise stimulation. Long-Evans rats were intraperitoneally injected with distilled water or with a solution of piribedil one hour previously to either noise or silence exposure. Noise stimulation was performed in an anechoic chamber at 70, 90 or 110 dB SPL for one hour. The animals were then sacrificed and the cochlear contents of DA and its metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were quantified by HPLC with electrochemical detection. The administration of piribedil to animals kept in silence did not modify the cochlear DA, DOPAC and HVA content. Noise stimulation resulted in a decrease of the cochlear DA content and an increase of the cochlear DOPAC and HVA contents in vehicle treated animals. The administration of piribedil resulted in a blockade of this noise induced cochlear DA turnover. These results suggest that piribedil stimulates cochlear D-2 receptors controlling the cochlear DA release. Piribedil action on D-2 receptors could explain the improvement observed in some cochleo-vestibular diseases signs after piribedil treatment. C1 UNIV COMPLUTENSE MADRID,FAC MED,DEPT BIOQUIM,MADRID,SPAIN. RP GILLOYZAGA, P (reprint author), UNIV COMPLUTENSE MADRID,FAC MED,DEPT CIENCIAS MORFOL,NEUROBIOL SENSORIAL & AUDIOL LAB,E-28080 MADRID,SPAIN. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 178 EP 182 DI 10.1016/0378-5955(94)90138-4 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900017 PM 7806480 ER PT J AU LEWIS, ER HENRY, KR AF LEWIS, ER HENRY, KR TI DYNAMIC CHANGES IN TUNING IN THE GERBIL COCHLEA SO HEARING RESEARCH LA English DT Article DE REVERSE CORRELATION; TUNING; COCHLEA ID SYSTEMS; WIENER AB Afferent axons of the gerbil cochlear nerve were studied with reverse correlation analyses carried out with movable time windows and with noise that was modulated with a 10-Hz trapezoidal envelope that switched the noise amplitude between two levels, 20 dB apart. At the time of switching, the attributes of the axonal tuning curves derived in this manner switched very rapidly (e.g., within 10 ms) from those characteristic of lower-level stimuli to those characteristic of higher-level stimuli and vice versa. As previous investigators have shown, the attributes of tuning curves at higher levels include broader bandwidth and an accentuated low-frequency hump. Characteristic frequencies (CFs) of gerbil axons used in this study ranged from approximately 500 Hz to approximately 5 kHz. Over this range, the low-frequency hump was most pronounced in our studies for units with higher CFs, each of which showed a sharp high-frequency peak and a distinctly separate, broad low-frequency hump (reminiscent of the tip and tail of a conventional frequency-threshold tuning curve). The amplitude of the peak relative to that of the hump, and the breadth of the peak, both changed rapidly and reversibly following sudden change of noise level. Observation of such rapid changes of tuning would be difficult to achieve with conventional frequency-threshold tuning curves, derived from tonal stimuli. C1 UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616. RP LEWIS, ER (reprint author), UNIV CALIF BERKELEY,DEPT EECS,BERKELEY,CA 94720, USA. CR ALLEN JB, 1993, BIOPHYSICS HAIR CELL, P296 BROWN AM, 1993, BIOPHYSICS HAIR CELL, P72 CARNEY LH, 1988, J NEUROPHYSIOL, V60, P653 DEBOER E, 1978, J ACOUST SOC AM, V63, P115, DOI 10.1121/1.381704 DEBOER E, 1968, IEEE T BME, V15, P115 EGGERMONT JJ, 1983, Q REV BIOPHYS, V16, P341 EGGERMONT JJ, 1993, HEARING RES, V66, P177, DOI 10.1016/0378-5955(93)90139-R Evans EF, 1977, PSYCHOPHYSICS PHYSL, P185 LEWIS ER, 1990, MECHANICS BIOPHYSICS, P129 LEWIS ER, 1989, HEARING RES, V39, P209, DOI 10.1016/0378-5955(89)90092-0 MARMARELIS VZ, 1991, ANN BIOMED ENG, V19, P345, DOI 10.1007/BF02584316 MOLLER AR, 1979, ACUSTICA, V41, P258 MOLLER AR, 1977, J ACOUST SOC AM, V62, P136 MOLLER AR, 1986, COMPUT MATH APPL-A, V12, P803, DOI 10.1016/0898-1221(86)90065-9 MOLLER AR, 1978, ACTA PHYSIOL SCAND, V104, P24, DOI 10.1111/j.1748-1716.1978.tb06247.x NEELY ST, 1993, BIOPHYSICS HAIR CELL, P64 NR 16 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 SEP PY 1994 VL 79 IS 1-2 BP 183 EP 189 DI 10.1016/0378-5955(94)90139-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900018 PM 7806481 ER PT J AU HENRY, KR PRICE, JM AF HENRY, KR PRICE, JM TI AMPLITUDE ENHANCEMENT IS SEEN IN THE COCHLEAR NERVE BUT NOT AT, OR BEFORE, THE AFFERENT SYNAPSE SO HEARING RESEARCH LA English DT Article DE ENHANCEMENT; COMPOUND ACTION POTENTIAL; AUDITORY BRAIN-STEM RESPONSE; INFERIOR COLLICULUS; COCHLEA; THRESHOLD; ROUND WINDOW; TETRODOTOXIN; STRYCHNINE; KAINIC ACID ID BRAIN-STEM RESPONSE; TUNING CURVES; EVOKED-RESPONSE; AUDITORY-NERVE; KAINIC ACID; MASKING; POTENTIALS; CELLS AB The amplitude of the cochlear nerve compound action potential (CAP) produced by a moderate intensity tonal stimulus (S-2) can be enhanced when S-2 is preceded by a low intensity S-1 of the same frequency. The presence of S-1 had no observable influence on the threshold of the CAP to S-2. Enhancement was not observed in the cochlear microphonics or summating potentials. Deactivation of the contralateral olivocochlear bundle did not influence enhancement. Tetrodotoxin (TTX) was applied to the round window to block cochlear nerve spike activity, resulting in a residual EPSP-like potential, as described in the guinea pig by Dolan et al. (1989). Kainic acid, in turn, eliminated this EPSP-like response. Even though some differences were found in the responses of the gerbil and their guinea pig preparation to TTX and kainic acid, enhancement was not observed in this residual potential. When enhancement was observed at the level of the CAP, it was also observed at brainstem levels. It is suggested that enhancement originates within the cochlear nerve axons. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 190 EP 196 DI 10.1016/0378-5955(94)90140-6 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900019 PM 7806482 ER PT J AU FREEMAN, DM COTANCHE, DA EHSANI, F WEISS, TF AF FREEMAN, DM COTANCHE, DA EHSANI, F WEISS, TF TI THE OSMOTIC RESPONSE OF THE ISOLATED TECTORIAL MEMBRANE OF THE CHICK TO ISOSMOTIC SOLUTIONS - EFFECT OF NA+, K+, AND CA2+ CONCENTRATION SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; LYMPH COMPOSITION; CHICK ID MECHANICAL-PROPERTIES; CHONDROITIN SULFATE; CORNEAL STROMA; GUINEA-PIG; INNER-EAR; BINDING; CALCIUM; INVITRO; GLYCOSAMINOGLYCANS; ORGANIZATION AB Changes in the size, shape, and structure of the isolated tectorial membrane of the chick were measured in response to isosmotic changes in the ionic composition of the perfusion solution. Substitution of artificial perilymph (AP) for artificial endolymph (AE) caused a small (similar to 15%), slow (time constants tau similar to 12 min) shrinkage of the thickness of the tectorial membrane that was largely reversed on return to AE. Substitution of AP for AE alters not only the predominate cation (from K+ to Na+) but also the Ca2+ concentration(from < 7 mu mol/l to 2 mmol/l). Additional experiments were performed to separate effects of each of these changes. When a high-Na+, low-Ca2+ solution was substituted for a high-K+, low-Ca2+ solution (AE), the tectorial membrane swelled significantly, often to more than twice its original thickness (the largest swelling was 337%), with a slow time course (tau similar to 23 min). Addition of Ca2+ to either high-K+ or high-Na+ solutions caused rapid shrinkage of the tectorial membrane (tau similar to 2-3 min). Addition of the Ca2+ chelator EGTA caused rapid swelling (tau similar to 4 min). Large osmotic responses were only partially reversible and caused long-lasting changes. For example, long-duration solution changes that produced large, rapid osmotic responses early in an experiment tended to produce smaller and slower responses later in the experiment. In contrast, the small osmotic responses to short-duration solution changes were repeatable for tens of hours. Changes in ionic composition of the bath affected not only the thickness of the tectorial membrane but also its other dimensions. Responses were not generally isotropic; both the size and shape of the tectorial membrane generally changed. Consistent changes in microstructure accompanied the osmotic changes. C1 MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,BOSTON,MA 02118. RP FREEMAN, DM (reprint author), MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139, USA. 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Res. PD SEP PY 1994 VL 79 IS 1-2 BP 197 EP 215 DI 10.1016/0378-5955(94)90141-4 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PG269 UT WOS:A1994PG26900020 PM 7806483 ER PT J AU MCFADDEN, SL WILLOTT, JF AF MCFADDEN, SL WILLOTT, JF TI RESPONSES OF INFERIOR COLLICULUS NEURONS IN C57BL/6J MICE WITH AND WITHOUT SENSORINEURAL HEARING-LOSS - EFFECTS OF CHANGING THE AZIMUTHAL LOCATION OF AN UNMASKED PURE-TONE STIMULUS SO HEARING RESEARCH LA English DT Article DE DIRECTIONAL HEARING; EXTRACELLULAR RECORDING; INBRED MICE; PRESBYCUSIS; SOUND LOCALIZATION ID SOUND PRESSURE LEVEL; INTERAURAL INTENSITY DIFFERENCES; FREQUENCY NEURONS; CAT; MOUSE; REPRESENTATION; LOCALIZATION; OWL; PRESBYCUSIS; SENSITIVITY AB Azimuth functions (discharge rates evoked by tone bursts as a function of stimulus azimuth) were obtained from neurons in the inferior colliculus (IC) of C57 mice aged 2, 7 and 12 months. Because of a gene that affects the cochlea, C57 mice exhibit high-frequency sensorineural hearing loss at 7 and 12 months. Azimuth functions were examined for differences that might be related to the decline in localization acuity that accompanies hearing loss in this strain. Irrespective of age group, nearly all neurons in the central area of the IC were sensitive to the azimuth of a best frequency (BF) stimulus, as revealed by azimuth functions in which firing rates varied by more than 50% from maximum to minimum at one or more intensities. The age groups were similar in many respects (e.g., there were no significant differences in the proportion of functions meeting the criterion for direction sensitivity, the proportion of neurons with direction sensitive functions over a range of intensities, azimuth function shapes, the locations or stability of 'borders' separating angles evoking high versus low discharge rates). However, in 7- and 12-month-olds: the proportion of IC neurons in which the strongest excitatory driving was evoked by ipsilateral stimulation was significantly larger; azimuth function borders were more likely to be 'reversed' (i.e., the high rates being evoked by the more ipsilateral angle); and a greater proportion of azimuth functions met the criterion for direction sensitivity only minimally. The findings suggest that binaural excitatory-inhibitory interactions are altered in IC neurons of hearing-impaired mice. C1 NO ILLINOIS UNIV,DEPT PSYCHOL,DE KALB,IL 60115. 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F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1981, J NEUROPHYSIOL, V45, P35 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 NR 45 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 AUG PY 1994 VL 78 IS 2 BP 115 EP 131 DI 10.1016/0378-5955(94)90018-3 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100001 PM 7982806 ER PT J AU MCFADDEN, SL WILLOTT, JF AF MCFADDEN, SL WILLOTT, JF TI RESPONSES OF INFERIOR COLLICULUS NEURONS IN C57BL/6J MICE WITH AND WITHOUT SENSORINEURAL HEARING-LOSS - EFFECTS OF CHANGING THE AZIMUTHAL LOCATION OF A CONTINUOUS NOISE MASKER ON RESPONSES TO CONTRALATERAL TONES SO HEARING RESEARCH LA English DT Article DE BINAURAL MASKING; DIRECTIONAL HEARING; EXTRACELLULAR RECORDING; INBRED MICE; PRESBYCUSIS ID AUDITORY-NERVE; SINGLE UNITS; IMPAIRED LISTENERS; COCHLEAR NUCLEI; WIDEBAND NOISE; HOUSE MOUSE; STIMULI; MASKING; CAT; INTELLIGIBILITY AB Extracellular recordings were obtained from inferior colliculus neurons of young adult (2-month-old) C57 mice with normal hearing and middle-aged (6-month-old) C57 mice with sensorineural hearing loss as they responded to best frequency (BF) tones (signal) in the presence of a continuous background noise (masker). Rate/level functions were obtained for the signal alone, noise bursts alone, and the signal in continuous noise as a function of masker location. For both groups of mice, thresholds for BF tones were significantly elevated in the presence of noise at all three noise locations. Separating the signal and masker sources significantly improved masked tone thresholds of 2-month-old mice but not hearing-impaired mice. The decreased ability of middle-aged mice to benefit from separation of the signal and masker sources may reflect alterations in binaural processing as a result of sensorineural hearing loss. C1 NO ILLINOIS UNIV,DEPT PSYCHOL,DE KALB,IL 60115. 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F., 1991, AGING AUDITORY SYSTE WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1981, J NEUROPHYSIOL, V45, P35 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 WILLOTT JF, 1984, EXP NEUROL, V83, P495, DOI 10.1016/0014-4886(84)90118-3 WILSON RH, 1985, AUDIOLOGY, V24, P15 YIN TCT, 1986, J NEUROPHYSIOL, V55, P280 Yost WA, 1991, NEUROBIOLOGY HEARING, P389 ZWICKER E, 1975, HDB SENSORY PHYSL, V2, P401 1978, ANSI321 AM NAT STAND NR 59 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 AUG PY 1994 VL 78 IS 2 BP 132 EP 148 DI 10.1016/0378-5955(94)90019-1 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100002 PM 7982807 ER PT J AU SCHROTTFISCHER, A EGG, G KONG, WJ RENARD, N EYBALIN, M AF SCHROTTFISCHER, A EGG, G KONG, WJ RENARD, N EYBALIN, M TI IMMUNOCYTOCHEMICAL DETECTION OF CHOLINE-ACETYLTRANSFERASE IN THE HUMAN ORGAN OF CORTI SO HEARING RESEARCH LA English DT Article DE ACETYLCHOLINE; CHOLINE ACETYLTRANSFERASE (CHAT); IMMUNOHISTOCHEMISTRY; HUMAN TEMPORAL BONE; INNER EAR; IMMUNOELECTRONMICROSCOPY ID OLIVOCOCHLEAR NEURONS; GUINEA-PIG; ENKEPHALIN-LIKE; BRAIN-STEM; LOCALIZATION; COCHLEA; ACETYLCHOLINESTERASE; IMMUNOREACTIVITY; CELLS; RAT AB In the mammalian cochlea acetylcholine has been considered a major neurotransmitter of the lateral and medial efferent fibers. The aims of the present study were to investigate the expression of ChAT in the human cochlea and to develop a new method for immunohistochemical investigations in the human cochlea both at the light and electronmicroscopic level. We thus examined the ChAT-like immunoreactivity in the human inner ear using light and electron microscopy with a pre-embedding technique. Our present results agree with the previously published data acquired in rodent species. The ChAT-like immunostaining could be found in the inner spiral fibers, the inner spiral bundle, tunnel crossing fibers and at the base of the outer hair cells. No staining was noted in the negative controls experiments, while rat cochleas used as positive controls showed the usual ChAT-like immunostaining as described above. The main difference between human and rat cochleas was that the efferent nerve supply seems to be less pronounced in the human cochleas. C1 UNIV MONTPELLIER 1, HOP ST CHARLES, INSERM, U254, NEUROBIOL AUDIT LAB, F-34295 MONTPELLIER 5, FRANCE. RP SCHROTTFISCHER, A (reprint author), UNIV INNSBRUCK, DEPT OTOLARYNGOL, ANICHSTR 35, A-6020 INNSBRUCK, AUSTRIA. 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B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WARR WB, 1992, ANATOMY MAMMALIAN AU, V1, P410 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 NR 29 TC 16 Z9 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1994 VL 78 IS 2 BP 149 EP 157 DI 10.1016/0378-5955(94)90020-5 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100003 PM 7527018 ER PT J AU SYKA, J RYBALKO, N POPELAR, J AF SYKA, J RYBALKO, N POPELAR, J TI ENHANCEMENT OF THE AUDITORY-CORTEX EVOKED-RESPONSES IS AWAKE GUINEA-PIGS AFTER NOISE EXPOSURE SO HEARING RESEARCH LA English DT Article DE AMPLITUDE ENHANCEMENT; AUDITORY CORTEX; EVOKED RESPONSES; NOISE EXPOSURE; GUINEA PIG ID HEARING-LOSS AB In a previous paper [Popelar et al., Hear. Res. 26, 239-247 (1987)] we have shown that amplitudes of the auditory cortex evoked responses (AC-ER) in awake guinea pigs were enhanced for several hours after 1 h of noise exposure whereas amplitudes of the compound potential of the auditory nerve (CAP) and of the inferior colliculus evoked responses (IC-ER) declined. The present study demonstrates that the duration of the AC-ER amplitude increase is related to the intensity of the noise exposure (white noise, for 30 min or 1 h, intensity range 105-125 dB). The AC-ER amplitude as well as the threshold shift increased linearly with increasing intensity of the noise. The maximum AC-ER increase occurred when clicks served as stimuli; amplitude enhancement was smaller for 1 kHz tone pips and was absent when 20 kHz tone pips were used. The amplitude enhancement was specific for the auditory cortex since the amplitude of visually evoked responses, recorded in the occipital cortex, was unchanged after noise exposure. It is suggested that the postexposure amplitude enhancement of the AC-ER is produced by temporary exhaustion of inhibitory processes in the auditory cortex. RP SYKA, J (reprint author), ACAD SCI CZECH REPUBL,INST EXPTL MED,PRAGUE,CZECH REPUBLIC. RI Rybalko, Natalia/H-2629-2014; Popelar, Jiri/H-2558-2014; Syka, Josef/H-3103-2014 CR AVAN P, 1992, HEARING RES, V59, P59, DOI 10.1016/0378-5955(92)90102-S BABIGHIAN G, 1975, AUDIOLOGY, V14, P72 Bock G R, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P338 Borg E, 1968, Acta Otolaryngol, V66, P461, DOI 10.3109/00016486809126311 Borg E, 1981, Acta Otolaryngol Suppl, V381, P1 CHALOUPK.Z, 1968, ACTIV NERV SUPER, V10, P207 EGGERMONT JJ, 1977, ANN OTO RHINOL LARYN, V86, P138 GERKEN GM, 1973, ELECTROEN CLIN NEURO, V34, P509, DOI 10.1016/0013-4694(73)90068-0 GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 GERKEN GM, 1993, J ACOUST SOC AM, V93, P2038, DOI 10.1121/1.406690 GUMNIT RJ, 1961, AM J PHYSIOL, V200, P1219 LONSBURYMARTIN BL, 1981, J NEUROPHYSIOL, V46, P563 POPELAR J, 1982, HEARING RES, V8, P273, DOI 10.1016/0378-5955(82)90019-3 POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 POWERS NL, 1989, ABSTR ASS RES OT, P223 RYAN AF, 1992, HEARING RES, V61, P24, DOI 10.1016/0378-5955(92)90032-I SALVI B, 1975, SCIENCE, V190, P486 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SYKA J, 1982, HEARING RES, V8, P263, DOI 10.1016/0378-5955(82)90018-1 Syka J, 1989, PROGR SENSORY PHYSL, V9, P97 WILLOTT JF, 1982, SCIENCE, V216, P1331, DOI 10.1126/science.7079767 WREE A, 1981, ANAT EMBRYOL, V162, P81, DOI 10.1007/BF00318096 NR 22 TC 42 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 AUG PY 1994 VL 78 IS 2 BP 158 EP 168 DI 10.1016/0378-5955(94)90021-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100004 PM 7982808 ER PT J AU WU, CY STAPELLS, DR AF WU, CY STAPELLS, DR TI PURE-TONE MASKING PROFILES FOR HUMAN AUDITORY BRAIN-STEM AND MIDDLE LATENCY RESPONSES TO 500-HZ TONES SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; MIDDLE LATENCY RESPONSE; FREQUENCY SELECTIVITY; HUMAN ID EVOKED-POTENTIALS; FREQUENCY SPECIFICITY; STEM RESPONSES; NORMAL-HEARING; TUNING CURVES; CHILDREN; INFANTS; SELECTIVITY; THRESHOLDS; LESIONS AB A simultaneous masking paradigm was used to determine the frequency selectivity of human auditory brainstem (ABR) and middle latency (MLR) responses to 60 dB pe SPL 500-Hz probe tones in 12 normal adults. Masking profiles for simultaneous recordings of the ABR and MLR were obtained in the presence of pure-tone maskers presented at 60- and 70-dB SPL. Results show sharp amplitude profiles with maximum reduction in amplitude seen using the 500-Hz maskers. There were no significant differences in the masking profiles for the ABR and MLR waves to the 500-Hz probe tones. An additional measure of frequency selectivity, bandwidth at 50% reduction in amplitude (W50), also demonstrated no significant difference between the ABR and MLR waves. In summary, the results of this study and those of an earlier study (Mackersie et al., 1993) suggest no significant difference in the frequency selectivity of the ABR and MLR to low-intensity (60 dB pe SPL) 500- and 2000-Hz tones. C1 ALBERT EINSTEIN COLL MED,ROSE F KENNEDY CTR,DEPT OTOLARYNGOL,AUDITORY EVOKED POTENTIAL LABS,BRONX,NY 10467. CR BROWN CJ, 1987, HEARING RES, V25, P193, DOI 10.1016/0378-5955(87)90091-8 BURROWS DL, 1990, J ACOUST SOC AM, V88, P180, DOI 10.1121/1.399938 Davis H, 1976, ANN OTOL RHINOL S28, V85, P5 Davis H, 1983, Adv Otorhinolaryngol, V31, P208 DOLAN TG, 1985, HEARING RES, V18, P203, DOI 10.1016/0378-5955(85)90038-3 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 GREENHOUSE SW, 1959, PSYCHOMETRIKA, V24, P95, DOI 10.1007/BF02289823 KAVANAGH KT, 1984, ANN OTOL RHINOL LA S, V108, P2 KILENY P, 1986, J SPEECH HEAR RES, V29, P20 KILENY P, 1987, ELECTROEN CLIN NEURO, V66, P108, DOI 10.1016/0013-4694(87)90180-5 KILENY PR, 1987, ARCH OTOLARYNGOL, V113, P1072 KILENY PR, 1987, EAR HEARING, V8, P217, DOI 10.1097/00003446-198708000-00005 KLEIN AJ, 1983, ARCH OTOLARYNGOL, V109, P74 KLEIN AJ, 1981, J ACOUST SOC AM, V69, P760, DOI 10.1121/1.385576 KLEIN SK, 1994, IN PRESS ELECTROPHYS 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, 1989, EAR HEARING, V10, P339, DOI 10.1097/00003446-198912000-00004 LEGATT AD, 1988, NEUROL CLIN, V6, P681 MACKERSIE C, 1993, HEARING RES, V65, P61, DOI 10.1016/0378-5955(93)90201-B MITCHELL C, 1980, J ACOUST SOC AM, V68, P896, DOI 10.1121/1.384829 NUTTALL AH, 1981, IEEE T ACOUST SPEECH, V29, P84, DOI 10.1109/TASSP.1981.1163506 OZDAMAR O, 1983, AUDIOLOGY, V22, P34 OZDAMAR O, 1982, ELECTROEN CLIN NEURO, V53, P224, DOI 10.1016/0013-4694(82)90027-X PICTON T. W., 1990, CURRENT PRACTICE CLI, P625 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 PORTMANN M, 1983, ACTA OTO-LARYNGOL, V95, P657, DOI 10.3109/00016488309139459 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 STAPEKKS DR, 1993, ARO ABSTR, V16, P59 Stapells D. R., 1994, PRINCIPLES APPL AUDI, P251 STAPELLS DR, 1981, EAR HEARING, V2, P20 STAPELLS DR, 1994, IN PRESS AM J AUDIOL STAPELLS DR, 1988, ELECTROEN CLIN NEURO, V71, P289, DOI 10.1016/0168-5597(88)90029-9 STAPELLS DR, 1990, AUDIOLOGY, V29, P262 Suzuki J. I., 1984, SENSORY EVOKED POTEN, P85 WEBER B A, 1987, Ear and Hearing, V8, p49S, DOI 10.1097/00003446-198708001-00010 WOODS DL, 1987, ELECTROEN CLIN NEURO, V68, P132, DOI 10.1016/0168-5597(87)90040-2 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 AUG PY 1994 VL 78 IS 2 BP 169 EP 174 DI 10.1016/0378-5955(94)90022-1 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100005 PM 7982809 ER PT J AU FURUTA, H MORI, N SATO, CB HOSHIKAWA, H SAKAI, S IWAKURA, S DOI, K AF FURUTA, H MORI, N SATO, CB HOSHIKAWA, H SAKAI, S IWAKURA, S DOI, K TI MINERALOCORTICOID TYPE-I RECEPTOR IN THE RAT COCHLEA - MESSENGER-RNA IDENTIFICATION BY POLYMERASE CHAIN-REACTION (PCR) AND IN-SITU HYBRIDIZATION SO HEARING RESEARCH LA English DT Article DE ALDOSTERONE; MINERALOCORTICOID RECEPTOR; PCR; IN SITU HYBRIDIZATION; RAT; STRIA VASCULARIS ID MAMMALIAN INNER-EAR; ADENOSINE-TRIPHOSPHATASE; ENZYMATIC AMPLIFICATION; ALDOSTERONE BINDING; RABBIT TUBULES; ADRENOCORTICOSTEROIDS; NA+,K+-ATPASE; MODULATION; SEQUENCE; ABSENCE AB Expression of mineralocorticoid type I receptor (MR) gene in the rat cochlea was determined using molecular biological techniques. We synthesized complementary DNA (cDNA) from rat cochlear total RNA and then amplified MR cDNA fragments by polymerase chain reaction (PCR). The amplified cDNA fragments were subcloned into an expression vector and the nucleotide sequence was analyzed to confirm the expression of mRNA encoding MR in the cochlea. We then synthesized digoxigenin-labeled riboprobes with this cloned DNA template and examined the localization of MR mRNA in the cochlea by in situ hybridization. The amino acid sequence of MR cDNA expressed in the cochlea was identical to that of the MR first cloned in the rat hippocampus. In situ hybridization showed the expression of MR mRNA in marginal cells of the stria vascularis, suggesting that aldosterone may regulate microhomeostasis of the endolymph, presumably by modulating Na, K-ATPase activity. Intense MR signal was also identified in spiral ganglion cells, the function of which remains to be determined. C1 KAGAWA MED SCH,DEPT BIOL,KAGAWA 76107,JAPAN. OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,OSAKA 553,JAPAN. RP FURUTA, H (reprint author), KAGAWA MED SCH,DEPT OTOLARYNGOL,1750-1 MIKI CHO,KAGAWA 76107,JAPAN. CR DOUCET A, 1981, AM J PHYSIOL, V241, pF605 ENCIO IJ, 1991, J BIOL CHEM, V266, P7182 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P352 KROZOWSKI ZS, 1989, ENDOCRINOLOGY, V125, P192 LOHUIS PJFM, 1990, ACTA OTO-LARYNGOL, V110, P348, DOI 10.3109/00016489009107454 MUJAIS SK, 1985, J CLIN INVEST, V76, P170, DOI 10.1172/JCI111942 MULLIS K, 1986, COLD SPRING HARB SYM, V51, P263 NOMURA S, 1988, J CELL BIOL, V106, P441, DOI 10.1083/jcb.106.2.441 NUDEL U, 1983, NUCLEIC ACIDS RES, V11, P1759, DOI 10.1093/nar/11.6.1759 PATEL PD, 1989, MOL ENDOCRINOL, V3, P1877 PITOVSKI DZ, 1993, BRAIN RES, V601, P273, DOI 10.1016/0006-8993(93)91720-D PITOVSKI DZ, 1993, HEARING RES, V69, P10, DOI 10.1016/0378-5955(93)90088-I RAREY KE, 1989, ARCH OTOLARYNGOL, V115, P817 RAREY KE, 1989, HEARING RES, V41, P217, DOI 10.1016/0378-5955(89)90013-0 SAIKI RK, 1985, SCIENCE, V230, P1350, DOI 10.1126/science.2999980 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 STERKERS O, 1988, PHYSIOL REV, V68, P1083 NR 17 TC 27 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1994 VL 78 IS 2 BP 175 EP 180 DI 10.1016/0378-5955(94)90023-X PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100006 PM 7982810 ER PT J AU KUJAWA, SG FALLON, M BOBBIN, RP AF KUJAWA, SG FALLON, M BOBBIN, RP TI ATP ANTAGONISTS CIBACRON BLUE, BASILEN BLUE AND SURAMIN ALTER SOUND-EVOKED RESPONSES OF THE COCHLEA AND AUDITORY-NERVE SO HEARING RESEARCH LA English DT Article DE ATP ANTAGONISTS; COCHLEA; PURINOCEPTORS ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; PHEOCHROMOCYTOMA CELLS; EXTRACELLULAR ATP; REACTIVE BLUE-2; P2-PURINOCEPTORS; TRANSMISSION; NUCLEOTIDES; STIMULATION; RECEPTORS AB The P-2-purinergic receptor antagonists suramin, cibacron blue and basilen blue, the latter two being isomers of reactive blue 2, were studied for their effects on sound-evoked responses from the cochlea (cochlear microphonic, CM; summating potential, SP; distortion product otoacoustic emissions, DPOAE) and auditory nerve (compound action potential, CAP). Local application of these compounds (10-1000 mu M) into the cochlear perilymph was associated with concentration-dependent response alterations. Effects of suramin on cochlear responses were minimal: High-intensity SP was reduced slightly at concentrations greater than or equal to 330 mu M without significant alterations in CM or DPOAEs. The amplitude of the auditory nerve CAP was suppressed and its latency increased at drug concentrations > 100 mu M, Cibacron blue and basilen blue were of greater potency in their effects on cochlear and auditory nerve responses. DPOAEs were generally reduced, low-intensity SP was reduced and high-intensity SP was increased and CM was little affected at drug concentrations 100-1000 mu M. The CAP was suppressed and its latency increased at concentrations 133 mu M. Effects of suramin were largely reversible; those associated with cibacron blue and basilen blue generally were not. To the extent that these drugs acted selectively as antagonists of ATP receptor-mediated activity, results support the hypothesis that endogenous ATP exerts profound actions at the level of the cochlea and the auditory nerve. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUNICAT,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 AUBERT A, 1994, IN PRESS NEUROSCIENC BEAN BP, 1992, TRENDS PHARMACOL SCI, V13, P87, DOI 10.1016/0165-6147(92)90032-2 BOBBIN RP, 1992, NOISE INDUCED HEARIN, P38 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1981, PHARM HEARING, P19 BURNSTOCK G, 1987, BRIT J PHARMACOL, V90, P383 DUBYAK GR, 1993, AM J PHYSIOL, V265, pC577 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 DUNN PM, 1988, BRIT J PHARMACOL, V93, P243 EVANS RJ, 1992, NATURE, V357, P503, DOI 10.1038/357503a0 HOUSLEY GD, 1992, P ROY SOC B-BIOL SCI, V249, P265, DOI 10.1098/rspb.1992.0113 HOYLE CHV, 1990, BRIT J PHARMACOL, V99, P617 KENNEDY C, 1990, ARCH INT PHARMACOD T, V303, P30 KUJAWA SG, 1994, HEARING RES, V76, P87, DOI 10.1016/0378-5955(94)90091-4 LEFF P, 1990, BRIT J PHARMACOL, V101, P645 Lin Xi, 1993, Journal of Neurophysiology (Bethesda), V70, P1593 MURRIN RJA, 1992, MOL PHARMACOL, V41, P561 NAKAGAWA T, 1990, J NEUROPHYSIOL, V63, P1068 NAKAZAWA K, 1991, PFLUG ARCH EUR J PHY, V418, P214, DOI 10.1007/BF00370517 NAKAZAWA K, 1990, BRIT J PHARMACOL, V101, P224 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 REILLY WM, 1987, EUR J PHARMACOL, V140, P47 SANTOSSACCHI J, 1988, PHYSL EAR, P271 SILINSKY EM, 1993, J PHYSIOL-LONDON, V464, P197 NR 27 TC 41 Z9 41 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1994 VL 78 IS 2 BP 181 EP 188 DI 10.1016/0378-5955(94)90024-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100007 PM 7982811 ER PT J AU FECHTER, LD LIU, Y AF FECHTER, LD LIU, Y TI TRIMETHYLTIN DISRUPTS N-1 SENSITIVITY, BUT HAS LIMITED EFFECTS ON THE SUMMATING POTENTIAL AND COCHLEAR MICROPHONIC SO HEARING RESEARCH LA English DT Article DE TRIMETHYLTIN; OTOTOXICITY; COMPOUND ACTION POTENTIAL; SUMMATING POTENTIAL ID GUINEA-PIG; TRANSMITTER; OTOTOXICITY; EXPOSURE; INJURY AB Trimethyltin (TMT), a model neurotoxicant, has previously been demonstrated to disrupt auditory thresholds in laboratory subjects. In this experiment we characterized the potency of this ototoxicant by means of a dose response study and then evaluated the functional effects of TMT administration when tone-bursts were presented at supra-threshold levels. Guinea pigs were anaesthetized and prepared for electrophysiological measurement of the compound action potential (CAP) and cochlear microphonic (CM). Subsequently averaged wave forms generated by tone-bursts of 0-80 dB SPL were evaluated in order to calculate both a N-1 and a summating potential (SP) input-output function. We show that TMT at doses as low as 0.2 mg/kg produce elevations in N-1, but not in the CM isopotential curve. Using exposures to 0.5 mg/kg TMT we show a profound reduction in the slope of the N, input-output curve, but no shift in the SP. The results are consistent with the hypothesis that TMT disrupts function at the synapse between the inner hair cell and the Type 1 spiral ganglion cell. RP FECHTER, LD (reprint author), UNIV OKLAHOMA,HLTH SCI CTR,COLL PHARM,TOXICOL PROGRAM,OKLAHOMA CITY,OK 73190, USA. CR Aldridge W. 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Res. PD AUG PY 1994 VL 78 IS 2 BP 189 EP 196 DI 10.1016/0378-5955(94)90025-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100008 PM 7982812 ER PT J AU PFINGST, BE HOLLOWAY, LA POOPAT, N SUBRAMANYA, AR WARREN, MF ZWOLAN, TA AF PFINGST, BE HOLLOWAY, LA POOPAT, N SUBRAMANYA, AR WARREN, MF ZWOLAN, TA TI EFFECTS OF STIMULUS LEVEL ON NONSPECTRAL FREQUENCY DISCRIMINATION BY HUMAN-SUBJECTS SO HEARING RESEARCH LA English DT Article DE AUDITORY PROSTHESIS; COCHLEAR IMPLANT; ELECTRICAL STIMULATION; RATE DISCRIMINATION; HUMANS; NONSPECTRAL FREQUENCY DISCRIMINATION; PSYCHOPHYSICS ID MODULATION TRANSFER-FUNCTIONS; COCHLEAR IMPLANTS; ELECTRICAL-STIMULATION; CONSONANT RECOGNITION; DIFFERENCE LIMENS; HEARING; SENSITIVITY; THRESHOLDS; CUES AB Frequency difference limens were determined as a function of reference-stimulus level for pulsatile electrical stimuli in 5 postlingually deaf human subjects with Nucleus-22 cochlear implants and for sinusoidally amplitude-modulated acoustic white noise stimuli in 4 normal-hearing humans. Subjects were tested at levels throughout the dynamic range and extending to the lowest detectable levels. Response stability was measured over the course of 10 sessions. For electrical stimulation in the deaf ears, difference limens decreased as; a function of level throughout much or all of the dynamic range of hearing. This result contrasts with the case for nonspectral acoustic stimulation of normal-hearing subjects, where nonspectral frequency difference limens were strongly affected by level only near the detection threshold. These data suggest differences in the acoustic and electrical response spaces that must be considered in the design of auditory prosthesis processors. RP PFINGST, BE (reprint author), UNIV MICHIGAN,CTR MED,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,ANN ARBOR,MI 48109, USA. CR [Anonymous], 1979, ETHICAL PRINCIPLES G BARRETTO RL, 1992, HEARING RES, V62, P245, DOI 10.1016/0378-5955(92)90191-O Clark G., 1987, ADV OTORHINOLARYNGOL, V38, P1 EDWARDS BW, 1988, J ACOUST SOC AM S1, V83, pS17, DOI 10.1121/1.2025236 FEINMAN GR, 1990, 2ND INT COCH IMPL S, P43 FORMBY C, 1985, J ACOUST SOC AM, V78, P70, DOI 10.1121/1.392456 HINOJOSA R, 1983, ANN NY ACAD SCI, V405, P459, DOI 10.1111/j.1749-6632.1983.tb31662.x Hochmair-Desoyer I. 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Res. PD AUG PY 1994 VL 78 IS 2 BP 197 EP 209 DI 10.1016/0378-5955(94)90026-4 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100009 PM 7982813 ER PT J AU UPPENKAMP, S KOLLMEIER, B AF UPPENKAMP, S KOLLMEIER, B TI NARROW-BAND STIMULATION AND SYNCHRONIZATION OF OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; EVOKED OTOACOUSTIC EMISSIONS; COCHLEAR MODELS ID ACOUSTIC EMISSIONS; AUDITORY-SYSTEM; HUMAN EAR; SUPPRESSION; OSCILLATORS; RESPONSES AB Tone-burst-evoked otoacoustic emissions were obtained for several normal listeners with and without spontaneous otoacoustic emission using an optimized tone burst. The dependence of the response amplitude on stimulation level shows a linear increase below a certain value close to the threshold in quiet and levels off at higher levels exhibiting only small differences between non-linear and linear averaging modus. In addition, the latency of the response tends to decrease and the sharpness of the resonance decreases with increasing stimulation level. Synchronization tuning- curves were obtained using a fixed tone burst to elicit an evoked otoacoustic emission and a probe tone at different frequencies for synchronizing the SOAE. These synchronization tuning curves exhibit relatively sharp resonance characteristics (Q(3) varying between 3 and 8) for subjects with spontaneous otoacoustic emissions and less sharp tuning (Q(3) varying between 1 and 3) for subjects without spontaneous otoacoustic emissions. These experimental results could be reproduced very well with a model of a single non-linear Van-der-Pol-oscillator with the appropriate parameters. The results indicate that spontaneous otoacoustic emissions and narrow-band-evoked otoacoustic emissions are generated by the same mechanism which can be modelled as a self-sustained oscillator. C1 UNIV GOTTINGEN,DRITTES PHYS INST,W-3400 GOTTINGEN,GERMANY. CR BIALEK W, 1984, PHYS LETT A, V104, P173, DOI 10.1016/0375-9601(84)90371-2 BRAY P, 1987, British Journal of Audiology, V21, P191, DOI 10.3109/03005368709076405 EVANS BN, 1991, HEARING RES, V52, P288, DOI 10.1016/0378-5955(91)90019-6 Johannesma PIM, 1980, PSYCHOPHYSICAL PHYSL, P62 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, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 KOSHIGOE S, 1983, MECH HEARING, P153 LONG GR, 1988, J ACOUST SOC AM, V84, P1343, DOI 10.1121/1.396633 LONG GR, 1991, J ACOUST SOC AM, V89, P1201, DOI 10.1121/1.400651 Moore B.C.J., 1986, FREQUENCY SELECTIVIT NEELY ST, 1988, J ACOUST SOC AM, V83, P652, DOI 10.1121/1.396542 NEUMANN J, 1994, IN PRESS HEAR RES NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 PALMER AR, 1981, J PHYSL, V324, pP66 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 OTOLAR, V14, P66 STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 TALMADGE CL, 1990, LECT NOTES BIOMATH, V87, P235 TALMADGE CL, 1991, J ACOUST SOC AM, V89, P2391, DOI 10.1121/1.400958 UPPENKAMP S, 1992, THESIS U GOTTINGEN 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, 1988, BASIC ISSUES HEARING, P101 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X WILSON JP, 1990, ADV AUDIOL, P47 WIT HP, 1981, J ACOUST SOC AM, V70, P437, DOI 10.1121/1.386786 WIT HP, 1990, LECT NOTES BIOMATH, V87, P259 WIT HP, 1979, J ACOUST SOC AM, V66, P911, DOI 10.1121/1.383202 WIT HP, 1990, ADV AUDIOL, V7, P110 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 ZWICKER E, 1985, FORTSCHRITTE AKUSTIK, P29 ZWICKER E, 1983, HEARING RES, V11, P359, DOI 10.1016/0378-5955(83)90067-9 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 AUG PY 1994 VL 78 IS 2 BP 210 EP 220 DI 10.1016/0378-5955(94)90027-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100010 PM 7982814 ER PT J AU COOPER, NP YATES, GK AF COOPER, NP YATES, GK TI NONLINEAR INPUT-OUTPUT FUNCTIONS DERIVED FROM THE RESPONSES OF GUINEA-PIG COCHLEAR NERVE-FIBERS - VARIATIONS WITH CHARACTERISTIC FREQUENCY SO HEARING RESEARCH LA English DT Article DE COCHLEAR NERVE FIBER; NONLINEARITY; COCHLEAR MECHANICS ID RATE-INTENSITY FUNCTIONS; BASILAR-MEMBRANE NONLINEARITY; AUDITORY-NERVE; MAMMALIAN COCHLEA; MOSSBAUER TECHNIQUE; LEVEL FUNCTIONS; FIBERS; CAT; STIMULI; NEURONS AB Rate-versus-level functions (RLFs) were recorded from individual cochlear nerve fibres in anaesthetised guinea-pigs. Variations in the shapes of these functions with frequency were used to derive input-output (IO) relationships for the mechanical preprocessing mechanisms in the cochlea. It was assumed that these preprocessing mechanisms operated linearly at frequencies well below each fibre's characteristic frequency (CF). The IO functions derived at each fibre's CF provided strong evidence of compressively nonlinear preprocessing in most regions of the cochlea. However, the apparent degree of compression depended on the fibre's CF, and hence on the presumed site of cochlear innervation. For fibres with CFs of between 1.5 and 3.6 kHz, the CF derived 10 functions grew at rates of around 0.5 dB/dB. For fibres with CFs above 4 kHz, the IO functions were more compressive, with high-intensity asymptotic slopes of around 0.13 dB/dB. In the highest (greater than or equal to 10 kHz) CF fibres, the degree of compression depended on the physiological condition of the cochlea; the derived IO functions becoming more linear as the cochlea became less sensitive. The derived IO technique was not well suited to analyse responses evoked by very low frequency (e.g., < 500 Hz) tones. Nonetheless, the CF RLFs from fibres with CFs lower than similar to 1 KHz provided little evidence of mechanical nonlinearity near the apex of the cochlea. These findings imply a longitudinal variation in the mechanisms of cochlear preprocessing, and provide important new tests for functional models of the cochlea. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. CR ALDER VA, 1978, J ACOUST SOC AM, V64, P684, DOI 10.1121/1.381993 Bekesy G., 1960, EXPT HEARING BUUNEN TJF, 1981, J ACOUST SOC AM, V69, P744, DOI 10.1121/1.385574 Cooper N. P., 1993, BIOPHYSICS HAIR CELL, P249 COOPER NP, 1989, THESIS KEELE U STAFF DE de Boer E, 1969, INT AUDIOL, V8, P547, DOI 10.3109/05384916909070224 Evans E. F., 1974, FACTS MODELS HEARING, P118 EVANS EF, 1989, COCHLEAR MECH STRUCT, P241 Evans EF, 1977, PSYCHOPHYSICS PHYSL, P185 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 GEISLER CD, 1974, J NEUROPHYSIOL, V37, P1156 HARRISON RV, 1982, HEARING RES, V6, P303, DOI 10.1016/0378-5955(82)90062-4 HARRISON RV, 1980, J ACOUST SOC AM, V70, P1036 HIND JE, 1971, PHYSL AUDITORY SYSTE, P101 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 Kiang N. Y.-s., 1965, DISCHARGE PATTERNS S, P1 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 MOLLER AR, 1977, J ACOUST SOC AM, V62, P135 MULLER M, 1992, HEARING RES, V57, P71 OHLEMILLER KK, 1992, J ACOUST SOC AM, V90, P274 PALMER AR, 1980, HEARING RES, V2, P319, DOI 10.1016/0378-5955(80)90065-9 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 RAJAN R, 1991, HEARING RES, V53, P153, DOI 10.1016/0378-5955(91)90222-U RELKIN EM, 1991, HEARING RES, V55, P215, DOI 10.1016/0378-5955(91)90106-J Rhode W. S., 1973, BASIC MECHANISMS HEA, P49 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 ROBERTSON D, 1976, BRAIN RES, V109, P487, DOI 10.1016/0006-8993(76)90029-9 Ruggero M A, 1992, Curr Opin Neurobiol, V2, P449, DOI 10.1016/0959-4388(92)90179-O 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 SCHROEDE.MR, 1974, J ACOUST SOC AM, V55, P1055, DOI 10.1121/1.1914647 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 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, 1992, TRENDS NEUROSCI, V15, P57, DOI 10.1016/0166-2236(92)90027-6 YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M ZWISLOCKI JJ, 1972, KYBERNETIK, V12, P169 1989, ACTA OTOLARYNGOL S, V467 NR 44 TC 74 Z9 75 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1994 VL 78 IS 2 BP 221 EP 234 DI 10.1016/0378-5955(94)90028-0 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100011 PM 7982815 ER PT J AU LI, HS NIEDZIELSKI, AS BEISEL, KW HIEL, H WENTHOLD, RJ MORLEY, BJ AF LI, HS NIEDZIELSKI, AS BEISEL, KW HIEL, H WENTHOLD, RJ MORLEY, BJ TI IDENTIFICATION OF A GLUTAMATE/ASPARTATE TRANSPORTER IN THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE GLUTAMATE TRANSPORTER; COCHLEA; CDNA; POLYMERASE CHAIN REACTION ID GUINEA-PIG COCHLEA; POTASSIUM-INDUCED RELEASE; SPIRAL GANGLION NEURONS; RECEPTOR MESSENGER-RNAS; AMINO-ACID CONTENT; KAINIC ACID; AUDITORY-NERVE; HAIR-CELLS; GLUTAMATE TRANSPORTER; SOUND STIMULATION AB The neurotransmitter at the synapses between hair cells and spiral ganglion cells in the cochlea is probably L-glutamate or a similar excitatory amino acid. Glutamate uptake by nerve terminals and glial cells is an important component of neurotransmission at glutamatergic synapses of the central nervous system, for providing a reservoir of transmitter or transmitter precursors and the termination of the released glutamate. Hair cell synapses are not surrounded by glial cells, therefore, the uptake mechanism for glutamate in the cochlea may be unique, cDNA was synthesized from total RNA isolated separately from the rat organ of Corti, spiral ganglia, and lateral wall tissues. The expression of a glutamate/aspartate transporter (GLAST) was detected by DNA amplification with the polymerase chain reaction. The other two members of glutamate transporters in this family were not detected by this method. A partial cDNA encoding to GLAST was identified by sequence analysis in a rat cochlear cDNA library. Data concerning the expression and the molecular structure of the glutamate transporter GLAST in the cochlea may provide important information regarding the neurotransmission process at the hair cell-afferent synapses. C1 BOYS TOWN NATL RES HOSP,OMAHA,NE 68131. NATL INST DEAFNESS & COMMUN DISORDERS,NEUROCHEM LAB,BETHESDA,MD. 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Res. PD AUG PY 1994 VL 78 IS 2 BP 235 EP 242 DI 10.1016/0378-5955(94)90029-9 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100012 PM 7527019 ER PT J AU HUANG, JM BERLIN, CI CULLEN, JK WICKREMASINGHE, AR AF HUANG, JM BERLIN, CI CULLEN, JK WICKREMASINGHE, AR TI DEVELOPMENT OF CONTRALATERAL SUPPRESSION OF THE VIIITH NERVE COMPOUND ACTION-POTENTIAL (CAP) IN THE MONGOLIAN GERBIL SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; VIIITH NERVE CAP; AUDITORY EFFERENT SYSTEM; CONTRALATERAL SUPPRESSION; GERBIL ID SUPERIOR OLIVARY COMPLEX; OLIVOCOCHLEAR PROJECTIONS; EFFERENT INNERVATION; RESPONSE PROPERTIES; COCHLEAR EFFERENTS; MEDIAL ZONES; GUINEA-PIG; BRAIN-STEM; FREQUENCY; NEURONS AB We studied whether same-frequency contralateral tones of 65 dB pSPL (peak Sound Pressure Level) suppress the VIIIth nerve compound action potential (CAP) evoked by 40-45 dB pSPL tone pips in the Mongolian gerbil from 22 to 92 days after birth (DAB). The primary stimuli were tone pips of 1, 2, 4, 8, and 10 kHz; only the 1 kHz CAP amplitude was suppressed significantly by tones of the same frequency. The suppression was seen at 22 DAB, and underwent little relative change with development. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES LAB S,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,DEPT COMMUN SCI & DISORDERS,BATON ROUGE,LA 70803. LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 ARNESEN AR, 1984, ACTA OTO-LARYNGOL, V98, P501, DOI 10.3109/00016488409107591 ASCHOFF A, 1988, EXP BRAIN RES, V71, P252 ASCHOFF A, 1987, J COMP NEUROL, V264, P56, DOI 10.1002/cne.902640106 BACON CK, 1992, 15TH MIDW RES M ASS, P99 BERLIN CI, 1990, 13TH MIDW RES M ASS, P220 BLEDSOE SC, 1981, HEARING RES, V4, P109, DOI 10.1016/0378-5955(81)90040-X BROWN MC, 1989, HEARING RES, V40, P93, DOI 10.1016/0378-5955(89)90103-2 BRUNS V, 1980, HEARING RES, V3, P27, DOI 10.1016/0378-5955(80)90006-4 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 DESMEDT JE, 1961, NATURE, V192, P1263, DOI 10.1038/1921263a0 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FEX J, 1965, ACTA PHYSIOL SCAND, V64, P43, DOI 10.1111/j.1748-1716.1965.tb04152.x FEX J, 1962, ACTA PHYSIOL SCAND, V55, P1 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 FOLSOM RC, 1987, ACTA OTO-LARYNGOL, V103, P262, DOI 10.3109/00016488709107792 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 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 KLINKE R, 1969, PFLUG ARCH EUR J PHY, V306, P165, DOI 10.1007/BF00586883 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 MCGUIRT JP, 1992, ABSTR ASS RES OTOLAR, P106 MURATA K, 1978, J ACOUST SOC AM S136, V64 MURATA K, 1980, NEUROSCI LETT, V18, P289, DOI 10.1016/0304-3940(80)90299-2 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PURIA S, 1993, ABSTR ASS RES OT, P145 RASMUSSEN GL, 1946, J COMP NEUROL, V84, P141, DOI 10.1002/cne.900840204 SCHWARTZ IR, 1986, J COMP NEUROL, V246, P500, DOI 10.1002/cne.902460407 SMITH DI, 1987, HEARING RES, V27, P157, DOI 10.1016/0378-5955(87)90016-5 THOMPSON GC, 1986, J COMP NEUROL, V254, P246, DOI 10.1002/cne.902540208 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 WINER BJ, 1971, STAT PRINCIPLES EXPT, P359 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 40 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 1994 VL 78 IS 2 BP 243 EP 248 DI 10.1016/0378-5955(94)90030-2 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100013 PM 7982816 ER PT J AU MCEVOY, L MAKELA, JP HAMALAINEN, M HARI, R AF MCEVOY, L MAKELA, JP HAMALAINEN, M HARI, R TI EFFECT OF INTERAURAL TIME DIFFERENCES ON MIDDLE-LATENCY AND LATE AUDITORY-EVOKED MAGNETIC-FIELDS SO HEARING RESEARCH LA English DT Article DE MAGNETOENCEPHALOGRAPHY; EVOKED RESPONSES; MIDDLE-LATENCY RESPONSES; AUDITORY CORTEX; INTERAURAL TIME DIFFERENCE; SOUND LATERALIZATION; HUMANS ID MASKING LEVEL DIFFERENCE; SOUND LATERALIZATION; CORTICAL MECHANISMS; CORTEX; FREQUENCY; NEURONS; LOCATION; BRAIN AB To determine if interaural time differences (ITDs) in binaural stimuli affect the middle-latency auditory evoked fields (AEFs) in the same manner as they affect the N100m deflection, neuromagnetic responses were recorded over the whole head using a IM-channel SQUID magnetometer. Binaural stimuli were lateralized to three positions, left, midline, and right, on the basis of ITDs. The N100m was significantly larger to stimuli with contralaterally-leading ITDs than to stimuli with no, or with ipsilaterally-leading ITDs. Neither the P30m nor the P50m deflections of the middle-latency response were significantly affected by ITD, although the P30m showed a tendency, similar to but smaller than that of N100m, to be larger to stimuli with contralaterally-leading ITDs. In some subjects, the source location of the P50m was anterior and inferior to the sources of the P30m and N100m, which are generated in the superior surface of the temporal lobe. Sound-related muscular artifacts were seen in the posterior recording channels of one subject, and the contribution of this activity to the signals over the temporal area was determined. C1 HELSINKI UNIV TECHNOL,LOW TEMP LAB,SF-02150 ESPOO,FINLAND. HELSINKI UNIV TECHNOL,NEUROMAG LTD,SF-02150 ESPOO,FINLAND. RI Hamalainen, Matti/C-8507-2013; Hari, Riitta/J-1880-2012 OI Hari, Riitta/0000-0002-3142-2703 CR AHISSAR M, 1992, J NEUROPHYSIOL, V67, P203 AHONEN AI, 1993, PHYS SCRIPTA, VT49A, P198, DOI 10.1088/0031-8949/1993/T49A/033 BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BICKFORD RG, 1964, ANN NY ACAD SCI, V112, P204, DOI 10.1111/j.1749-6632.1964.tb26749.x BOMANS M, 1990, IEEE T MED IMAGING, V9, P177, DOI 10.1109/42.56342 CODY DTR, 1969, LARYNGOSCOPE, V79, P400, DOI 10.1288/00005537-196903000-00007 DON M, 1993, J ACOUST SOC AM, V94, P2135, DOI 10.1121/1.407485 FOWLER CG, 1992, ELECTROEN CLIN NEURO, V84, P157, DOI 10.1016/0168-5597(92)90020-C HAMALAINEN M, 1993, REV MOD PHYS, V65, P413, DOI 10.1103/RevModPhys.65.413 KAUKORANTA E, 1986, EXP BRAIN RES, V63, P60 KEVANISHVILI Z, 1987, SCAND AUDIOL, V16, P3, DOI 10.3109/01050398709042149 MAKELA JP, IN PRESS ELECTROENCE MCEVOY L, 1993, HEARING RES, V67, P98, DOI 10.1016/0378-5955(93)90237-U MCEVOY LK, 1991, EAR HEARING, V12, P389, DOI 10.1097/00003446-199112000-00003 MCGEE T, 1988, AUDIOLOGY, V27, P119 NAATANEN R, 1988, ELECTROEN CLIN NEURO, V69, P523, DOI 10.1016/0013-4694(88)90164-2 PELIZZONE M, 1987, NEUROSCI LETT, V82, P303, DOI 10.1016/0304-3940(87)90273-4 PICTON T. W., 1990, CURRENT PRACTICE CLI, P625 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 RAJAN R, 1990, J NEUROPHYSIOL, V64, P888 REALE RA, 1990, J NEUROPHYSIOL, V64, P1247 SAMS M, 1993, HEARING RES, V67, P89, DOI 10.1016/0378-5955(93)90236-T Scherg M., 1989, ADV BIOMAGNETISM, P97 TISSARI SO, 1993, 9TH INT C BIOM VIENN WOODS DL, 1993, HEARING RES, V66, P46, DOI 10.1016/0378-5955(93)90258-3 NR 25 TC 34 Z9 35 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1994 VL 78 IS 2 BP 249 EP 257 DI 10.1016/0378-5955(94)90031-0 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA PB851 UT WOS:A1994PB85100014 PM 7982817 ER PT J AU HENSELMAN, LW HENDERSON, D SUBRAMANIAM, M SALLUSTIO, V AF HENSELMAN, LW HENDERSON, D SUBRAMANIAM, M SALLUSTIO, V TI THE EFFECT OF CONDITIONING EXPOSURES ON HEARING-LOSS FROM IMPULSE NOISE SO HEARING RESEARCH LA English DT Article DE IMPULSE NOISE; TOUGHENING; THRESHOLD SHIFT ID TRAUMATIC EXPOSURE; PERIODIC REST; PROTECTION; RESISTANCE; RECOVERY; DAMAGE; LEVEL AB Research has shown that prior noise exposures or 'conditioning' can moderate the amount of permanent threshold shift (PTS) from subsequent high intensity noise exposures. The aim of this experiment was to study the effect of 'conditioning' on subsequent exposure to high intensity impulse noise. The subjects were seven experimental and 14 control monaural chinchillas. Evoked potential (EVP) thresholds were measured before and after the noise exposures. Experimental animals received 10 days of exposure to an octave band noise (OBN) centered at 0.5 kHz OBN at 95 dB SPL (6 h on/18 h off) and allowed to recover for 5 days. The subjects were then exposed to an impulse noise at 150 dB SPL. The temporal spacing of the impulses consisted of a series of 50 pairs of impulses presented 50 ms apart with 1000 ms between the onset of each pair. The total duration of exposure was approximately 1 min. Control animals received only the impulse noise exposure. PTS was measured after 4 weeks. The threshold shift (TS) patterns during the 'conditioning' phase were consistent with previous research, with the greatest amount of TS occurring on the second day and decreasing with continued exposures. Four weeks after recovery from the impulse noise, the experimental animals showed significantly less PTS than the control animals. In addition, histological examination revealed significantly less hair cell loss in the experimental than in the control subjects. The results are discussed in the context of previous studies on 'toughening' and on the effects of impulse noise. RP HENSELMAN, LW (reprint author), SUNY BUFFALO,DEPT COMMUN DISORDERS & SCI,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214, USA. CR 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, P486 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 DANIELSON R, 1991, J ACOUST SOC AM, V90, P209, DOI 10.1121/1.402361 HAMERNIK RP, 1984, HEARING RES, V13, P229, DOI 10.1016/0378-5955(84)90077-7 HAMERNIK RP, 1988, J ACOUST SOC AM, V84, P941, DOI 10.1121/1.396663 HENDERSON D, 1993, IN PRESS HEAR RES HENDERSON D, 1994, UNPUB LONGEVITY PROT HENDERSON D, 1973, J ACOUST SOC AM, V55, P1099 HENDERSON D, 1992, NOISE INDUCED HEARIN, P476 LIM DJ, 1994, 17TH ANN MIDW RES M, P3 LUZ GA, 1970, J ACOUST SOC AM, V48, P96, DOI 10.1121/1.1975463 LUZ GA, 1971, J ACOUST SOC AM, V49, P1770, DOI 10.1121/1.1912580 Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 PRICE GR, 1983, J ACOUST SOC AM, V73, P556, DOI 10.1121/1.389001 RAJAN R, 1988, HEARING RES, V36, P53, DOI 10.1016/0378-5955(88)90137-2 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 SUBRAMANIAM M, 1993, J ACOUST SOC AM, V93, P952, DOI 10.1121/1.405455 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 SUBRAMANIAM M, 1992, HEARING RES, V58, P57, DOI 10.1016/0378-5955(92)90008-B SUBRAMANIAM M, 1993, HEARING RES, V65, P234, DOI 10.1016/0378-5955(93)90216-N NR 24 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 JUL PY 1994 VL 78 IS 1 BP 1 EP 10 DI 10.1016/0378-5955(94)90038-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800001 PM 7961172 ER PT J AU MILLER, CA ABBAS, PJ ROBINSON, BK AF MILLER, CA ABBAS, PJ ROBINSON, BK TI THE USE OF LONG-DURATION CURRENT PULSES TO ASSESS NERVE SURVIVAL SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; ELECTRICAL STIMULATION; COCHLEAR IMPLANT; EVOKED POTENTIALS ID STIMULATED AUDITORY-NERVE; BRAIN-STEM RESPONSE; ELECTRICAL-STIMULATION; PHYSIOLOGICAL-PROPERTIES; COCHLEAR PROSTHESIS; ACTION-POTENTIALS; GUINEA-PIG; FIBERS; EXCITATION; THRESHOLDS AB This study investigated the usefulness of long-duration current pulses in assessing the status of the auditory nerve in ears with various degrees of retrograde neural degeneration. Guinea pigs were deafened with aminoglycosides prior to acute implantation of the cochlea and collection of electrically evoked auditory brainstem responses (EABRs). Analysis of wave I evoked with long-duration current pulses suggests that this evoked response is sensitive to degeneration of the peripheral processes of the auditory nerve. Correlations with spiral ganglion cell density show that EABR measures obtained with long-duration pulses are comparable to those previously established for estimating nerve survival. Further analysis indicates that this measure may provide unique information about the degenerative state of the nerve. Threshold EABR measures using long-duration pulses are evidently more place-specific than other measures. Also, results suggest that long-duration pulses may be sensitive to two phases of the degenerative process: degradation of the peripheral processes and subsequent degeneration of neural processes central to the spiral ganglion. 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 ALLEN RC, 1982, WIDE ANGLE, V5, P4 Bevington P. R., 1969, DATA REDUCTION ERROR Black R C, 1983, Acta Otolaryngol Suppl, V399, P5 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P59 BOSTOCK H, 1983, J PHYSIOL-LONDON, V341, P41 BRISMAR T, 1981, ACTA PHYSIOL SCAND, V113, P161, DOI 10.1111/j.1748-1716.1981.tb06877.x BROWN CJ, 1990, J ACOUST SOC AM, V88, P2205, DOI 10.1121/1.400117 BROWN CJ, 1990, J ACOUST SOC AM, V88, P1385, DOI 10.1121/1.399716 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BRYANT GM, 1984, HEARING RES, V15, P173, DOI 10.1016/0378-5955(84)90048-0 CHIU SY, 1981, J PHYSIOL-LONDON, V313, P415 CLOPTON BM, 1984, HEARING RES, V14, P1, DOI 10.1016/0378-5955(84)90063-7 COLOMBO J, 1987, HEARING RES, V31, P287, DOI 10.1016/0378-5955(87)90197-3 Finley C. C., 1990, COCHLEAR IMPLANTS MO, P55 FLECKNELL PA, 1987, LABORATORY ANIMAL AN FRANK K, 1956, J PHYSIOL-LONDON, V134, P451 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 HALL RD, 1990, HEARING RES, V45, P123, DOI 10.1016/0378-5955(90)90188-U Hill AV, 1936, PROC R SOC SER B-BIO, V119, P305, DOI 10.1098/rspb.1936.0012 JAVEL E, 1987, ANN OTOL RHINOL LA S, V128, P26 KIANG NYS, 1983, ANN NY ACAD SCI, V405, P114, DOI 10.1111/j.1749-6632.1983.tb31623.x LAFONTAINE S, 1982, J PHYSIOL-LONDON, V323, P287 Lapicque L, 1907, J PHYSIOL-PARIS, V9, P622 Lathi BP, 1968, COMMUNICATION SYSTEM LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1987, ANN OTOL LARYNGOL S, V128, P48 LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LOEB GE, 1983, ANN NY ACAD SCI, V405, P123, DOI 10.1111/j.1749-6632.1983.tb31625.x MARSH RR, 1981, OTOLARYNG HEAD NECK, V89, P125 MILLER CA, 1992, HEARING RES, V69, P35 MILLER JM, 1983, ANN OTO RHINOL LARYN, V92, P599 Moxon E.C., 1971, THESIS MIT PFINGST BE, 1991, J ACOUST SOC AM, V90, P1857, DOI 10.1121/1.401665 PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1979, ANN OTO RHINOL LARYN, V88, P613 PFINGST BE, 1990, HEARING RES, V50, P225, DOI 10.1016/0378-5955(90)90047-S RATTAY F, 1989, IEEE T BIO-MED ENG, V36, P676, DOI 10.1109/10.32099 RANCK JB, 1975, BRAIN RES, V98, P417, DOI 10.1016/0006-8993(75)90364-9 RATTAY F, 1987, J THEOR BIOL, V125, P339, DOI 10.1016/S0022-5193(87)80066-8 ROBERTS WJ, 1973, ACTA PHYSIOL SCAND, V89, P384, DOI 10.1111/j.1748-1716.1973.tb05533.x SCHINDLER RA, 1977, ARCH OTOLARYNGOL, V103, P691 SIMMONS FB, 1979, ANN OTO RHINOL LARYN, V88, P533 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 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 SPURR AR, 1969, J ULTRA MOL STRUCT R, V26, P31, DOI 10.1016/S0022-5320(69)90033-1 STYPULKOWSKI PH, 1986, OTOLARYNG CLIN N AM, V19, P249 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 Weibel E. R., 1979, STEREOLOGICAL METHOD, V1 Weiss G, 1901, ARCH ITAL BIOL, V35, P413 YAMANE H, 1981, OTOLARYNG HEAD NECK, V89, P117 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P23 YLIKOSKI J, 1974, ACTA OTOLARYNGOL, V79, P266 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 JUL PY 1994 VL 78 IS 1 BP 11 EP 26 DI 10.1016/0378-5955(94)90039-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800002 PM 7961173 ER PT J AU CORTOPASSI, G HUTCHIN, T AF CORTOPASSI, G HUTCHIN, T TI A MOLECULAR AND CELLULAR HYPOTHESIS FOR AMINOGLYCOSIDE-INDUCED DEAFNESS SO HEARING RESEARCH LA English DT Article DE OTOTOXICITY; HAIR CELLS; AMINOGLYCOSIDE; MOLECULAR MECHANISM; MITOCHONDRIA; RIBOSOME ID MITOCHONDRIAL-DNA DAMAGE; RIBOSOMAL-RNA; ANTIBIOTICS; INHERITANCE; MUTATION; DISEASE; BINDING; SITES; GENE AB The ototoxic effects of aminoglycoside antibiotics are well known. However, a molecular and cellular mechanism for the death of cochlear hair cells has remained difficult to prove. Human genetic studies have shown that a rare trait for hypersensitivity to aminoglycosides is conferred by mitochondrial genetic variation. Recently, a gene involved has been identified as the mitochondrial small ribosomal RNA gene, consistent with the known mechanism of aminoglycoside action against bacteria. We used the existing data as a basis for our hypothesis of a molecular and cellular model for aminoglycoside ototoxicity that is described in this paper. RP CORTOPASSI, G (reprint author), UNIV SO CALIF,SCH PHARM,DEPT MOLEC PHARMACOL & TOXICOL,INST TOXICOL,1985 ZONAL AVE,LOS ANGELES,CA 90033, USA. 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Res. PD JUL PY 1994 VL 78 IS 1 BP 27 EP 30 DI 10.1016/0378-5955(94)90040-X PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800003 PM 7961174 ER PT J AU SUPIN, AY POPOV, VV MILEKHINA, ON TARAKANOV, MB AF SUPIN, AY POPOV, VV MILEKHINA, ON TARAKANOV, MB TI FREQUENCY RESOLVING POWER MEASURED BY RIPPLED NOISE SO HEARING RESEARCH LA English DT Article DE FREQUENCY RESOLVING POWER; RIPPLED NOISE; AUDITORY FILTERS; HUMAN ID PSYCHOPHYSICAL TUNING CURVES; AUDITORY FILTER SHAPES; SPEECH-PERCEPTION; HEARING-LOSS; MASKING; SELECTIVITY; LISTENERS; THRESHOLD; PITCH AB Frequency resolving power (FRP) was measured in normal humans using rippled noise with a phase-reversal test. The principle of the test was to find the highest ripple density at which an interchange of mutual peak and trough position (the phase reversal) in the rippled spectrum is detectable. In the frequency range below 0.5 kHz FRP was found to be about 21 ripples per kHz when tested by both broad-band and narrow-band rippled noise. In the frequency range above 2 kHz, FRP measured by the narrow-band rippled noise was 22 to 23 relative units (relation of the noise central frequency to the ripple frequency spacing). RP SUPIN, AY (reprint author), RUSSIAN ACAD SCI,INST ANIM EVOLUT MORPHOL & ECOL,LENINSKY PROSPECT 33,MOSCOW 117071,RUSSIA. 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Res. PD JUL PY 1994 VL 78 IS 1 BP 31 EP 40 DI 10.1016/0378-5955(94)90041-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA NW528 UT WOS:A1994NW52800004 PM 7961175 ER PT J AU MIZUNO, C SCHWARTZ, JL CAZALS, Y AF MIZUNO, C SCHWARTZ, JL CAZALS, Y TI PERIODICITY OF LONG-TERM CONTEXT CAN INFLUENCE GAP DETECTION SO HEARING RESEARCH LA English DT Article DE GAP DETECTION; PERIODIC VERSUS APERIODIC; AMPLITUDE-MODULATED NOISE ID HEARING-IMPAIRED LISTENERS; TEMPORAL GAP; BAND SIGNALS; NOISE-BAND; FREQUENCY; BANDWIDTH; MODULATION; DURATION; THRESHOLDS; PERCEPTION AB Temporal gap detection in bands of noise is a basic paradigm to investigate auditory temporal resolution. This study further examined the role of the long-term temporal organization for gap detection. Our experiments aimed at determining whether a gap superimposed on an amplitude-modulated noise was easier to detect when the amplitude modulation was regular - or periodic - than when it was not. Care was taken to ensure that the stimulus portion, where the gap was inserted, was exactly the same for both periodic and aperiodic conditions. Results show that gap detection in periodically modulated white noise (125 Hz fundamental frequency, or 8 ms duration from peak to peak) is easier (with a threshold 4.7 ms lower) than in an aperiodically modulated noise (modulation randomly varied from 5 to 18 ms). This effect is observed for variations of the modulation frequency from 125 to 1000 Hz. These results indicate that the regularity of long-term temporal organization of amplitude modulations in noise can improve the detection of a gap. C1 UNIV BORDEAUX 2,INSERM,U229,AUDIOL EXPTL LAB,F-33076 BORDEAUX,FRANCE. 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