FN Thomson Reuters Web of Science™ VR 1.0 PT J AU EGGERMONT, JJ AF EGGERMONT, JJ TI MATURATIONAL ASPECTS OF PERIODICITY CODING IN CAT PRIMARY AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE CAT; AUDITORY CORTEX; SINGLE UNIT; MATURATION; CLICK-TRAIN STIMULI; MODULATION TRANSFER FUNCTIONS; ENTRAINMENT; VECTOR STRENGTH ID ANTEROVENTRAL COCHLEAR NUCLEUS; POSTNATAL-DEVELOPMENT; NEURONS; FREQUENCY; RESPONSES; MIDBRAIN; SENSITIVITY; INTENSITY; GRASSFROG; NEOCORTEX AB The click-following responses for single units in the primary auditory cortex of the cat were explored as a function of age. Recordings were obtained in kittens from 9-53 days of age and assembled in four age groups; 10- 15 days, 16-21 days, 22-27 days and 30-60 days. Age group means were compared to results obtained in adult cats. The stimulus consisted of one second long click trains presented every three seconds with click rates ranging from 1-32 clicks per second. The response was characterized by entrainment, rate Modulation Transfer Function (rMTF), vector strength (VS) and temporal Modulation Transfer Function (tMTF). Maturational effects on periodicity coding comprised changes in overall responsiveness as well as click-rate dependent changes. The number of spikes elicited by single stimuli increased on average 3-fold between the second post-natal week and adulthood, probably as a result of more efficient synapses in the central auditory pathway and some improvement in thresholds. Adaptation became less pronounced with age; neurons started to respond to the later clicks in the 8/s and 16/s click trains from the third post natal week on. By the end of the first post-natal month the click following responses resembled the adult ones qualitatively, however, increased firing rates and spontaneous rates together with rebound responses continued to produce quantitative differences between the 30-60 day olds and the adults. Limiting rates for the tMTF (50% of the response at 1/s) increased from 6 Hz in the 10-15 day old to 12 Hz in adults. The decrease in the duration of the post-activation suppression coupled with the increased response with age to trains with higher click rates suggested that the maturation of inhibitory processes in the cortex play a major role in this rate dependence. RP EGGERMONT, JJ (reprint author), UNIV CALGARY,DEPT PSYCHOL,BEHAV NEUROSCI RES GRP,2500 UNIV DR NW,CALGARY T2N 1N4,ALBERTA,CANADA. 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PD DEC PY 1991 VL 57 IS 1 BP 45 EP 56 DI 10.1016/0378-5955(91)90073-I PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500006 PM 1774211 ER PT J AU YATES, GK AF YATES, GK TI AUDITORY-NERVE SPONTANEOUS RATES VARY PREDICTABLY WITH THRESHOLD SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS RATE; AUDITORY THRESHOLD; RATE-INTENSITY FUNCTIONS; INNER HAIR CELL; SYNAPSE ID RATE-INTENSITY FUNCTIONS; SHORT-TERM ADAPTATION; COCHLEAR HAIR-CELLS; BASILAR-MEMBRANE; LEVEL FUNCTIONS; FIBERS; RESPONSES; PATTERNS; INNER; MODEL AB The variation of spontaneous rate with auditory nerve thresholds is compared with predictions from a simple assumption: that spontaneous and driven activity are basically similar, both being evoked by inner hair cell transmembrane potential. Under this view, spontaneous activity is seen as a response to a standing current within the hair cell and should therefore vary with threshold in a manner predictable from measured rate-intensity functions. A method for comparing spontaneous rates of fibres with differing thresholds is developed and applied to previously-collected data. The results show that spontaneous rates are quite consistent with the hypothesis, indicating no need for more complicated theories of spontaneous activity. RP YATES, GK (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. 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Res. PD DEC PY 1991 VL 57 IS 1 BP 57 EP 62 DI 10.1016/0378-5955(91)90074-J PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500007 PM 1774212 ER PT J AU MULLER, M ROBERTSON, D AF MULLER, M ROBERTSON, D TI RELATIONSHIP BETWEEN TONE BURST DISCHARGE PATTERN AND SPONTANEOUS FIRING RATE OF AUDITORY-NERVE FIBERS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE FIBER; GUINEA PIG; ONSET RESPONSE; PSTH; SPONTANEOUS FIRING RATE ID RATE-INTENSITY FUNCTIONS; RAPID ADAPTATION; LEVEL FUNCTIONS; FIBERS; CATS AB A detailed investigation was carried out of the response of single auditory nerve fibres in the guinea pig to tone bursts. Comparisons were made between the shapes of peri-stimulus-time histograms (PSTHs) of low and high characteristic frequency (CF) fibres grouped according to their spontaneous firing rates (SR). Both low and high CF fibres of high spontaneous rate ( > 18 spikes/s) exhibited marked rapid adaptation in their PSTH's which became most pronounced at high stimulus intensities. The ratio of onset-to-adapted firing estimated from PSTH data in these fibres increased monotonically as a function of adapted firing rate. The behaviour of fibres with the lowest spontaneous rates (< 0.5 spikes/s) was markedly different, particularly in fibres from low CF regions. In general, these low-SR fibres showed slower adaptation than high-SR fibres, and a less pronounced onset peak. This was most striking in low CF fibres. Furthermore, the ratio of onset-to-adapted firing rate tended to decrease with increasing stimulus intensity in both low and high CF fibres with low spontaneous firing rates. Low-SR fibres also showed the highest maximum discharge rates to tone burst stimuli. Fibres with medium spontaneous rates between 0.5 and 18 spikes/s displayed intermediate characteristics in their PSTH's. Recent data in the chinchilla (Relkin and Doucet, 1991), suggest that these differences may arise in part from differences in inter-stimulus recovery processes in the different spontaneous rate groups. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. RP ROBERTSON, D (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR ALDER VA, 1978, J ACOUST SOC AM, V64, P684, DOI 10.1121/1.381993 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, 1990, J COMP NEUROL, V301, P4443 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIBERMAN MC, 1990, HEARING RES, V49, P209, DOI 10.1016/0378-5955(90)90105-X MEDDIS R, 1986, HEARING RES, V23, P287, DOI 10.1016/0378-5955(86)90118-8 MULLER M, 1991, HEAR RES, V57 PALMER AR, 1980, HEARING RES, V2, P319, DOI 10.1016/0378-5955(80)90065-9 RELKIN EM, 1991, ABSTR ASS RES OT CLE, P127 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 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 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YATES GK, 1985, HEARING RES, V17, P1, DOI 10.1016/0378-5955(85)90124-8 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 YATES GK, 1986, HEARING RES, V23, P288 YATES GK, 1991, HEAR RES, V57 NR 19 TC 24 Z9 24 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1991 VL 57 IS 1 BP 63 EP 70 DI 10.1016/0378-5955(91)90075-K PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500008 PM 1774213 ER PT J AU MULLER, M ROBERTSON, D AF MULLER, M ROBERTSON, D TI SHAPES OF RATE-VERSUS-LEVEL FUNCTIONS OF PRIMARY AUDITORY-NERVE FIBERS - TEST OF THE BASILAR-MEMBRANE MECHANICAL HYPOTHESIS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE FIBER; RATE-VERSUS-LEVEL FUNCTION; BASILAR MEMBRANE NONLINEARITY ID RATE-INTENSITY FUNCTIONS; FIBERS; CATS AB Rate-versus level functions (RI functions) for characteristic frequency (CF) stimulation were measured from primary auditory nerve fibres from different spontaneous rate categories in the guinea pig cochlea. Attention was focussed on those fibres that showed clear breakpoints in their RI functions (sloping-saturation fibres). A statistical curve fitting procedure to an empirical equation was used to provide a quantitative estimate of the breakpoint position in individual fibres. It was found that, within the limits of reliability of the curve fitting procedure, the breakpoint position was the same in fibres from the same CF regions in any given animal. This result is consistent with the notion that the breakpoint position is determined by global basilar membrane mechanics and not by processes private to each nerve fibre. However, a subgroup of fibres not easily classifiable as sloping-saturation, showed features of their RI functions suggesting that factors other than basilar membrane mechanics could lead to fibre-to-fibre differences in rate-versus-level behaviour C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. RP ROBERTSON, D (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR ALDER VA, 1978, J ACOUST SOC AM, V64, P684, DOI 10.1121/1.381993 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 MULLER M, 1991, HEARING RES, V55, P50, DOI 10.1016/0378-5955(91)90091-M PALMER AR, 1980, HEARING RES, V2, P319, DOI 10.1016/0378-5955(80)90065-9 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBERTSON D, 1991, HEARING RES, V51, P29, DOI 10.1016/0378-5955(91)90004-S ROBERTSON D, 1990, INFORMATION PROCESSI, P661 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 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 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M YATES GK, 1991, HEAR RES, V57 NR 17 TC 17 Z9 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1991 VL 57 IS 1 BP 71 EP 78 DI 10.1016/0378-5955(91)90076-L PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500009 PM 1774214 ER PT J AU PTOK, M NAIR, TS ALTSCHULER, RA SCHACHT, J CAREY, TE AF PTOK, M NAIR, TS ALTSCHULER, RA SCHACHT, J CAREY, TE TI MONOCLONAL-ANTIBODIES TO INNER-EAR ANTIGENS .2. ANTIGENS EXPRESSED IN SENSORY CELL STEREOCILIA SO HEARING RESEARCH LA English DT Article DE COCHLEA; MONOCLONAL ANTIBODIES; HAIR CELLS; STEREOCILIA ID OUTER HAIR-CELLS; GUINEA-PIG ORGAN; SUPPORTING CELLS; ACTIN-FILAMENTS; LOCALIZATION; CORTI; IMMUNOREACTIVITY; IDENTIFICATION; IMMUNIZATION; COCHLEA AB To develop biological reagents for investigating structure-function relationships in the organ of Corti, we have raised monoclonal antibodies, (MAb) to inner ear tissues. Our first series of antibodies prepared after intrasplenic immunization of mice with guinea pig tissues, identified antigens restricted to supporting cell structures, but no hair cell specific antibodies were developed [Zajic et al., Hear. Res. 52, 59-72, 1991]. In this report we describe the isolation, binding specificity and initial characterization of the stereocilia-binding monoclonal antibodies, KHRI-4, and KHRI-5. Mice were immunized with avian, amphibian and mammalian sensory hair cell-containing tissues and antibodies were screened for selective binding to cochlear extracts in ELISA. In the inner ear, KHRI-4 and KHRI-5 bind specifically to stereocilia in both avian and mammalian cochlear and vestibular tissue preparations using immunofluorescence and immunoperoxidase assays. In other tissues only certain cells of mesothelial origin, such as smooth muscle in gut and the arteriolar vasculature, were stained by KHRI-4 indicating that the antigenic structure defined by this antibody has limited distribution. KHRI-5 binding could be detected in other tissues only at high antibody concentrations suggesting that the gene product identified by this antibody is also weakly expressed in other cell lineages. Western blot analysis showed that KHRI-4 and -5 detect different protein complexes, KHRI-4 identifies an antigenic structure common to gut, cochlea, vestibular tissue and cultured fibroblasts consisting of a approximately 195 and a 230 kDa heterodimer designated p195/230. KHRI-5 binds to a prominent approximately 200-210 kDa band in Western blots of cochlear tissues, gut and fibroblasts. In immunoprecipitation experiments, KHRI-5 precipitated three proteins of M(r) approximately 200-210, 230 and 260 kDa indicating that the approximately 200-210 kDa protein carrying the epitope for this antibody is a member of a heterotrimer complex. Our results show that these protein complexes are structural components of stereocilia and that the same proteins are arrayed in conjunction with the actin stress fibers of cultured mesothelial cells. Thus, they are likely to be important for maintaining the actin structure of stereocilia essential to transduction in sensory hair cells. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. RP CAREY, TE (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR ALTSCHULER RA, 1985, HEARING RES, V17, P249, DOI 10.1016/0378-5955(85)90069-3 ALTSCHULER RA, 1985, BRAIN RES, V327, P379, DOI 10.1016/0006-8993(85)91541-0 BENNETT V, 1989, BIOCHIM BIOPHYS ACTA, V988, P1407 Burridge K, 1987, J Cell Sci Suppl, V8, P211 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 EGELMAN E, 1981, NATURE, V294, P674, DOI 10.1038/294674a0 FEX J, 1985, HEARING RES, V17, P101, DOI 10.1016/0378-5955(85)90014-0 FEX J, 1986, HEARING RES, V22, P249, DOI 10.1016/0378-5955(86)90102-4 FEX J, 1981, P NATL ACAD SCI-BIOL, V78, P1255, DOI 10.1073/pnas.78.2.1255 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 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 JOHNSON D, 1983, J EXP MED, V159, P1751 KIMMEL KA, 1986, CANCER RES, V46, P2614 KOHLER G, 1975, NATURE, V256, P495, DOI 10.1038/256495a0 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 MACARTNEY JC, 1980, NATURE, V288, P491, DOI 10.1038/288491a0 OROZCO CR, 1990, LARYNGOSCOPE, V100, P941 RICHARDSON GP, 1988, INNER EAR BIOL WORKS RICHARDSON GP, 1990, J CELL BIOL, V110, P1055, DOI 10.1083/jcb.110.4.1055 SANS A, 1989, HEARING RES, V40, P117, DOI 10.1016/0378-5955(89)90105-6 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SLEPECKY N, 1986, CELL TISSUE RES, V245, P229 SOBIN A, 1981, ACTA OTOLARYNGOL STO, V911, P247 SOBIN A, 1983, ACTA OTO-LARYNGOL, V96, P407, DOI 10.3109/00016488309132726 SPITZ M, 1984, J IMMUNOL METHODS, V70, P39, DOI 10.1016/0022-1759(84)90387-9 SPITZ M, 1986, METHOD ENZYMOL, V121, P33 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 TILNEY MS, 1989, J CELL BIOL, V109, P1711, DOI 10.1083/jcb.109.4.1711 TOWBIN H, 1979, P NATL ACAD SCI USA, V73, P2599 ZAJIC C, 1991, HEARING RES, V52, P59 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1986, NEUROBIOLOGY HEARING, P1 NR 38 TC 13 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1991 VL 57 IS 1 BP 79 EP 90 DI 10.1016/0378-5955(91)90077-M PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500010 PM 1774215 ER PT J AU CAIRD, DM PALMER, AR REES, A AF CAIRD, DM PALMER, AR REES, A TI BINAURAL MASKING LEVEL DIFFERENCE EFFECTS IN SINGLE UNITS OF THE GUINEA-PIG INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE GUINEA-PIG; INFERIOR COLLICULUS; SINGLE CELL RECORDING; INTERAURAL DELAYS; BINAURAL MASKING ID LOW-FREQUENCY NEURONS; INTERAURAL TIME DELAYS; SPATIAL RECEPTIVE-FIELDS; NOISE STIMULI; AUDITORY-NERVE; RESPONSE PROPERTIES; CHANGING FREQUENCY; CENTRAL NUCLEUS; COMBINED TONE; CAT AB We have studied the masking effects of a binaurally presented noise on the responses to binaural signals recorded from low-frequency cells in the inferior colliculus of the guinea pig. The spike rates to the masker and signal + masker were compared to quantify masking at different interaural time delays of the noise. The signal was a 50-ms tone burst at best frequency or a 50-ms segment of a synthetic vowel, presented at the best interaural delay of the unit tested. At each noise masker delay, the noise level was adjusted to obtain a criterion spike difference. In most cases, the level required was lowest at the best delay for the noise. The mean difference between maximum and minimum masked thresholds across the cell population was very similar to the human psychophysical masking level difference under the same signal and masker conditions. In another series of tests, we measured the effect of the noise masker on the temporal pattern of the discharge to the signal. The signal used was a 500-ms segment of the synthetic vowel. In virtually all cases the addition of a continuous noise masker reduced the discharge rate synchronized to the fundamental frequency of the vowel. The degree of this reduction was dependent on the interaural time delay of the noise masker. For most units, maximum reduction was seen when the vowel and noise had the same interaural time delay. The similarity between the masking which we have shown physiologically and that reported in a variety of human psychophysical experiments suggests that the processing at levels up to and including the inferior colliculus contributes to the psychophysical BMLD. C1 UNIV NOTTINGHAM,MRC,INST HEARING RES,UNIV PK,NOTTINGHAM NG7 2RD,ENGLAND. ZENTRUM PHYSIOL,FRANKFURT,GERMANY. MED SCH NEWCASTLE UPON TYNE,DEPT PHYSIOL SCI,NEWCASTLE TYNE,ENGLAND. RP PALMER, AR (reprint author), UNIV NOTTINGHAM,MRC,INST HEARING RES,UNIV PK,NOTTINGHAM NG7 2RD,ENGLAND. 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Res. PD DEC PY 1991 VL 57 IS 1 BP 91 EP 106 DI 10.1016/0378-5955(91)90078-N PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500011 PM 1774216 ER PT J AU NIEDZIELSKI, AS SCHACHT, J AF NIEDZIELSKI, AS SCHACHT, J TI PHOSPHOLIPID-METABOLISM IN THE COCHLEA - DIFFERENCES BETWEEN BASE AND APEX SO HEARING RESEARCH LA English DT Article DE COCHLEA; ORGAN OF CORTI; STRIA VASCULARIS; PHOSPHATIDYLCHOLINE; PHOSPHATIDYLINOSITOL; 2ND MESSENGERS ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; INNER-EAR; ADENYLATE-CYCLASE; STRIA VASCULARIS; RAT COCHLEA; NEOMYCIN; BINDING; POLYPHOSPHOINOSITIDES; BREAKDOWN AB Phospholipid-derived second messenger systems are one of the primary means for the transduction of extracellular signals to intracellular effector sites. We have investigated the longitudinal distribution of phospholipid metabolism in the guinea pig cochlea because of increasing evidence that the apex and base process auditory signals differently. Phospholipid metabolism was assayed by measuring the incorporation of radioactive phosphate (P-32(i)) into lipids of the organ of Corti and the lateral wall tissues (stria vascularis and spiral ligament P-32-labeling of total phospholipids was higher in the apex than the base, and individual phospholipids exhibited a tissue-specific base/apex distribution. Phosphatidylinositol was the most abundant of the labeled lipids in all tissues except the basal lateral wall, where phosphatidylinositol and phosphatidylcholine were labeled to a similar extent. Experiments on the availability of [P-32]-ATP and other non-lipid substrates (inositol, choline, and cytidine) suggested that the base/apex distribution of phospholipid metabolism is based on differences in enzymatic activities. Additional evidence for this is an increased hydrolysis of phosphoinositides in the apex. The base/apex distribution of lipid metabolism suggests that physiological and pathological mechanisms involving phospholipids differ between the turns of the cochlea. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. RP SCHACHT, J (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR AHLSTROM P, 1975, LARYNGOSCOPE, V85, P1241, DOI 10.1288/00005537-197507000-00016 Ansell GB, 1982, PHOSPHOLIPIDS, P1 AXELROD J, 1988, TRENDS NEUROSCI, V11, P117, DOI 10.1016/0166-2236(88)90157-9 BANDURSKI RS, 1951, J BIOL CHEM, V193, P405 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 CARTER JR, 1966, J LIPID RES, V7, P678 DEAN NM, 1989, ANAL BIOCHEM, V183, P199, DOI 10.1016/0003-2697(89)90468-5 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 GODFREY DA, 1985, ANN OTO RHINOL LARYN, V94, P409 GUIRAMAND J, 1990, BIOCHEM PHARMACOL, V39, P1913, DOI 10.1016/0006-2952(90)90609-O HALLCHER LM, 1980, J BIOL CHEM, V255, P896 HAWKINS JE, 1977, ACTA OTOLARYNGOL, V86, P110 IMAI A, 1987, NATURE, V325, P726, DOI 10.1038/325726a0 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 LISANTI MP, 1990, J MEMBRANE BIOL, V117, P1, DOI 10.1007/BF01871561 NIEDZIELSKI A, 1991, ABSTR ASS RES OT, V14, P135 OFFNER FF, 1987, HEARING RES, V29, P117, DOI 10.1016/0378-5955(87)90160-2 ONO T, 1989, NEUROCHEM INT, V14, P327, DOI 10.1016/0197-0186(89)90058-2 ORSULAKOVA A, 1976, J NEUROCHEM, V26, P285, DOI 10.1111/j.1471-4159.1976.tb04478.x PELECH SL, 1989, TRENDS BIOCHEM SCI, V14, P28, DOI 10.1016/0968-0004(89)90086-8 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SCHACHT J, 1976, J NEUROCHEM, V27, P1119, DOI 10.1111/j.1471-4159.1976.tb00318.x SCHACHT J, 1985, HEARING RES, V20, P9, DOI 10.1016/0378-5955(85)90053-X SCHACHT J, 1978, J LIPID RES, V19, P1063 SPOENDLIN H, 1985, AM J OTOLARYNG, V6, P453, DOI 10.1016/S0196-0709(85)80026-0 STERKERS O, 1985, AUDIOLOGY BIOCH, P473 VANROOIJEN LAA, 1983, BIOCHEM BIOPH RES CO, V112, P919, DOI 10.1016/0006-291X(83)91705-9 WANG SC, 1990, HEARING RES, V47, P53, DOI 10.1016/0378-5955(90)90166-M WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 Ylikoski J, 1974, Acta Otolaryngol Suppl, V326, P5 NR 31 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1991 VL 57 IS 1 BP 107 EP 112 DI 10.1016/0378-5955(91)90079-O PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500012 PM 1663501 ER PT J AU COLING, DE SCHACHT, J AF COLING, DE SCHACHT, J TI PROTEIN-PHOSPHORYLATION IN THE ORGAN OF CORTI - DIFFERENTIAL REGULATION BY 2ND MESSENGERS BETWEEN BASE AND APEX SO HEARING RESEARCH LA English DT Article DE INNER EAR; ORGAN OF CORTI; PROTEIN KINASES; PROTEIN PHOSPHATASES; PHOSPHORYLATION; 2ND MESSENGERS; CALMODULIN; AMP, CYCLIC; GMP, CYCLIC; CALCIUM; LIPIDS ID ELONGATION FACTOR-II; GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; INNER-EAR; ADENYLATE-CYCLASE; CONTRACTILE PROTEINS; KINASE-ACTIVITY; CALMODULIN; MOUSE; IDENTIFICATION AB Major aspects of cellular physiology are regulated by the phosphorylation state of proteins through the action of protein kinases and protein phosphatases. Phosphorylation of proteins by endogenous protein kinase activity was assayed in homogenates from guinea pig inner ear tissues with [gamma-P-32] ATP. Phosphoproteins showed distinct distributions in organ of Corti, lateral wall and spiral ganglion. In the organ of Corti, several protein kinase activities were distinguished by their activation by appropriate agonists: protein kinase C, calmodulin-dependent protein kinases and cyclic nucleotide-dependent protein kinases. Twelve putative substrates for these kinases were identified in organ of Corti on the basis of increased P-32-incorporation with addition of lipids, calmodulin, and cyclic nucleotides, respectively. In addition, differences in phosphorylation were observed between the base and apex of the organ of Corti. P-32-incorporation into proteins of molecular weights between 45 and 100 kDa was significantly higher in apical tissue than in tissue from the base. In contrast, phosphate incorporation into proteins of around 29 kDa was much lower in apical tissues than in basal tissues. Furthermore, labeling of both the high and low molecular weight proteins from the apex but not the base markedly increased in response to calcium. These data indicate the presence of differential modes of regulation that may underlie structural and functional gradients along the sensory epithelium. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. RP SCHACHT, J (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 1991 VL 57 IS 1 BP 113 EP 120 DI 10.1016/0378-5955(91)90080-S PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500013 PM 1774202 ER PT J AU LEVINE, RA DAVIS, PJ AF LEVINE, RA DAVIS, PJ TI ORIGIN OF THE CLICK-EVOKED BINAURAL INTERACTION POTENTIAL, BETA, OF HUMANS SO HEARING RESEARCH LA English DT Article DE BRAIN-STEM AUDITORY EVOKED POTENTIALS; BINAURAL INTERACTION; DERIVED POTENTIALS; MASKING; CLICK POLARITY ID SUPERIOR OLIVARY COMPLEX; INTERAURAL TIME; CAT; LATERALIZATION; SENSITIVITY; COMPONENT; POLARITY; STIMULI AB The human click-evoked binaural difference waveform has as its most prominent feature the peak, beta, which has been shown to be related to binaural perception. In normal human subjects, we investigated the effect upon beta of (1) delivering the clicks in the presence of high passed masking noise (4000 Hz cut-off) and (2) reversing click polarity. In the presence of the masker, little activity occurs at the time the click-evoked-beta would be expected. No significant change in beta-latency occurs when the click polarity is inverted. We conclude that beta is principally due to the high-frequency components of the broad band click, so that it is through the activity in high characteristic frequency auditory nerve fibers that click-evoked-beta is generated. Because the medial superior olive is the major nucleus of the human superior olivary complex, our results suggest that beta is possibly generated by the high-frequency cells of the medial superior olive. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP LEVINE, RA (reprint author), MASSACHUSETTS EYE & EAR HOSP,DEPT OTOLARYNGOL,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114, USA. 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Res. PD DEC PY 1991 VL 57 IS 1 BP 121 EP 128 DI 10.1016/0378-5955(91)90081-J PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500014 PM 1774203 ER PT J AU PUJOL, R ZAJIC, G DULON, D RAPHAEL, Y ALTSCHULER, RA SCHACHT, J AF PUJOL, R ZAJIC, G DULON, D RAPHAEL, Y ALTSCHULER, RA SCHACHT, J TI 1ST APPEARANCE AND DEVELOPMENT OF MOTILE PROPERTIES IN OUTER HAIR-CELLS ISOLATED FROM GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEAR DEVELOPMENT; OUTER HAIR CELL MOTILITIES; OUTER HAIR CELL ULTRASTRUCTURE ID FREQUENCY-SELECTIVITY; ORGAN; CORTI; ACTIN; CONTRACTIONS; PHYSIOLOGY; EPITHELIUM; MECHANISM; EMISSIONS; MEMBRANE AB Cochleae from fetal guinea-pigs (37 to 64 gestation days, gd) were used to correlate the appearance of motile properties of isolated outer hair cells (OHCs) with the development of specific morphological features. Both the 'fast' electrically-driven and the 'slow' calcium-induced motilities appeared first in OHCs from basal turn of 52 gd fetuses. At 56 gd, most of basal and some apical OHCs responded positively to both types of stimulation. All tested cells were positive at 64 gd. It is noteworthy that this period closely corresponds to the onset and maturation of the gross cochlear potentials. Some structural changes in the organ of Corti may be correlated with the development of OHC motile properties: the acquisition of an adult-like cylindrical shape by the OHC, its lateral detachment from neighboring Deiters cells, and its surrounding by fluid spaces. At the ultrastructural level, the formation of a first layer of laminated cisternae regularly aligned along the OHC plasma membrane from the cuticular plate down to the nuclear level, temporally coincided with the onset of in vitro motility (52 gd). The following days, pillars and a sub-membrane lattice were clearly noticed between the outermost cisternal membrane and the plasma membrane. The results support the ideas that: motile properties observed in vitro reflect the in vivo active mechanisms, and that one single layer of laminated cisternae and its associated sub-plasma membrane material may be needed for OHC motility. C1 HOP PELLEGRIN,INSERM,U229,F-33076 BORDEAUX,FRANCE. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP PUJOL, R (reprint author), HOP ST CHARLES,INSERM,U254,F-34059 MONTPELLIER,FRANCE. CR ARNOLD W, 1990, ACTA OTO-LARYNGOL, V109, P213, DOI 10.3109/00016489009107436 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Bannister L H, 1988, Prog Brain Res, V74, P213 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BROWNELL WE, 1984, SCANNING ELECTRON MI, V3, P1401 CARLIER E, 1979, HEARING RES, V1, P197, DOI 10.1016/0378-5955(79)90013-3 DALLOS P, 1991, NATURE, V350, P155, DOI 10.1038/350155a0 DIELER R, 1991, IN PRESS J NEUROCYTO DODSON HC, 1982, ACTA OTO-LARYNGOL, V94, P193, DOI 10.3109/00016488209128905 Draper RL, 1920, ANAT REC, V18, P369, DOI 10.1002/ar.1090180408 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1989, INT J RADIAT BIOL, V55, P1007, DOI 10.1080/09553008914551031 DULON D, 1990, J NEUROSCI, V10, P1388 DULON D, 1991, HEARING RES, V52, P225, DOI 10.1016/0378-5955(91)90202-K Engström H, 1967, J Laryngol Otol, V81, P687, DOI 10.1017/S0022215100067657 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 FORGE A, 1991, IN PRESS CELL TISS R GULLEY RL, 1977, ANAT REC, V189, P109, DOI 10.1002/ar.1091890108 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLLEY MC, 1988, NATURE, V335, P635, DOI 10.1038/335635a0 HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 LENOIR M, 1987, ANAT EMBRYOL, V175, P477, DOI 10.1007/BF00309683 LENOIR M, 1987, HEARING RES, V29, P265, DOI 10.1016/0378-5955(87)90173-0 LIM DJ, 1989, ACTA OTO-LARYNGOL, V107, P398, DOI 10.3109/00016488909127529 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PUEL JL, 1987, DEV BRAIN RES, V37, P179, DOI 10.1016/0165-3806(87)90239-2 PUJOL R, 1973, ACTA OTO-LARYNGOL, V76, P1, DOI 10.3109/00016487309121476 Pujol R., 1986, BIOL CHANGE OTOLARYN, P47 PUJOL R, 1990, ABSTR ASS RES OT STP, P247 PUJOL R, 1980, HEARING RES, V2, P423, DOI 10.1016/0378-5955(80)90078-7 PUJOL R, 1989, ARCH INT PHYSIOL BIO, V97, pA51, DOI 10.3109/13813458909105536 PUJOL R, 1990, 27TH WORKSH INN EAR RAPHAEL Y, 1991, IN PRESS J COMP NEUR RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x RAPHAEL Y, 1991, CELL MOTIL CYTOSKELE, V18 RAPHAEL Y, 1986, J SUBMICR CYTOL PATH, V18, P731 ROMAND R, 1971, J PHYSIOL-PARIS, V63, P763 ROMAND R, 1971, J PHYSIOL-PARIS, V63, pA280 SAITO K, 1983, CELL TISSUE RES, V229, P467 SANTOSSACCHI J, 1988, PHYSL EAR, P271 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SPOENDIN H, 1966, ADV OTOLRHINOLARYNGO, V13 SPOENDLIN H, 1970, AUDITORY VESTIBULAR, P173 THORN L, 1975, ADV ANAT EMBRYOL CEL, V51, P1 THORNE PR, 1987, HEARING RES, V30, P253, DOI 10.1016/0378-5955(87)90141-9 ULFENDAHL M, 1988, J SUBMICR CYTOL PATH, V20, P47 VATER M, 1991, IN PRESS J COMP NEUR VONLUBIT DKJ, 1981, CELL TISSUE RES, V230, P787 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V149, P304, DOI 10.1016/0006-291X(87)91639-1 ZENNER HP, 1986, HEARING RES, V22, P1 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 57 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 DEC PY 1991 VL 57 IS 1 BP 129 EP 141 DI 10.1016/0378-5955(91)90082-K PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500015 PM 1774204 ER PT J AU PROSEN, CA MOODY, DB AF PROSEN, CA MOODY, DB TI LOW-FREQUENCY DETECTION AND DISCRIMINATION FOLLOWING APICAL HAIR CELL DESTRUCTION SO HEARING RESEARCH LA English DT Article DE COCHLEAR APEX; LOW-FREQUENCY HEARING; FREQUENCY DISCRIMINATION; FREQUENCY SELECTIVITY; HIGH-PASS MASKING ID PSYCHOPHYSICAL TUNING CURVES; HEARING-IMPAIRED LISTENERS; SIGNAL LEVEL; PATAS MONKEY; CHINCHILLA; PERCEPTION; MASKING; MODEL; NOISE; SELECTIVITY AB This study assessed the effects of apical hair cell destruction on the detection and discrimination of low-frequency stimuli. Monauralized chinchillas were trained using operant conditioning and positive reinforcement to respond to pure-tone stimuli in the absence and the presence of a high-pass noise masker. Following the collection of the baseline absolute thresholds, psychophysical tuning curves (PTCs) also were determined at low and high frequencies. Apical hair cells in the experimental ear of each subject then were destroyed by applying a liquid-nitrogen-cooled miniature cryoprobe to the bony wall of the cochlea. Post-cryosurgery, unmasked and masked absolute thresholds and psychophysical tuning curves were re-evaluated. Following cryosurgery, low-frequency absolute thresholds increased by 30-50 dB. High-pass masking data suggested that receptors that were unaffected by the masking noise were responsible for the remaining low-frequency hearing. Low-frequency tuning, monitored by assessing changes in PTCs, was significantly altered following apical receptor cell loss, with the most effective maskers located several octaves above the test tone frequency. Following these determinations, one control and two experimental subjects then participated in a third experiment assessing low-frequency discrimination acuity. Some discrimination ability was retained after the cryosurgery; however, these post-lesion difference limens increased when a high-pass noise masker was added to the test environment. At the termination of the behavioral experiment, subjects were euthanized and their cochleae dissected to correlate behavioral and histopathological data. The data suggest that receptors located in frequency regions of the cochlea normally responsive to middle and high frequencies may be responsible for detection and discrimination of low-frequency stimuli in apically damaged cochleae. These data are consistent with other reports which indicate that redundant mechanisms are available for the detection of low-frequency stimuli, and they provide new information regarding how low-frequency stimuli are discriminated throughout the cochlea. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,SCH MED,ANN ARBOR,MI 48109. RP MOODY, DB (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,SCH MED,ANN ARBOR,MI 48109, USA. CR BROWN JN, 1987, HEARING RES, V26, P301, DOI 10.1016/0378-5955(87)90065-7 BUTLER RA, 1956, ARCH OTOLARYNGOL, V56, P411 CLARK WW, 1986, SENSORINEURAL HEARIN, P59 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 FLORENTINE M, 1983, J ACOUST SOC AM, V73, P961, DOI 10.1121/1.389021 GOLDSTEIN R, 1983, J SPEECH HEAR DISORD, V48, P70 GREEN DM, 1981, J ACOUST SOC AM, V69, P1758, DOI 10.1121/1.385911 HAWKINS JE, 1977, ACTA OTO-LARYNGOL, V83, P123, DOI 10.3109/00016487709128821 HORST JW, 1987, J ACOUST SOC AM, V82, P874, DOI 10.1121/1.395286 KIANG NYS, 1974, J ACOUST SOC AM, V55, P620, DOI 10.1121/1.1914572 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KLEIN JO, 1983, PEDIATRICS, V71, P639 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LONG GR, 1984, J ACOUST SOC AM, V75, P1184, DOI 10.1121/1.390768 LONG GR, 1988, J SPEECH HEAR RES, V31, P659 NELSON DA, 1982, J ACOUST SOC AM, V71, P660, DOI 10.1121/1.387541 NELSON DA, 1978, J ACOUST SOC AM, V64, P114, DOI 10.1121/1.381977 NELSON DA, 1984, J ACOUST SOC AM, V75, P1570, DOI 10.1121/1.390866 PROSEN CA, 1990, J ACOUST SOC AM, V88, P2152, DOI 10.1121/1.400112 PROSEN CA, 1989, ABSTR ASS RES OT, V222 PROSEN CA, 1990, HEARING RES, V44, P179, DOI 10.1016/0378-5955(90)90079-5 PROSEN CA, 1989, J ACOUST SOC AM, V85, P1302, DOI 10.1121/1.397461 SMALL AM, 1959, J ACOUST SOC AM, V31, P1619, DOI 10.1121/1.1907670 SMITH DW, 1987, HEARING RES, V29, P125, DOI 10.1016/0378-5955(87)90161-4 SMITH DW, 1987, J ACOUST SOC AM, V82, P63, DOI 10.1121/1.395438 SMITH DW, 1987, HEARING RES, V26, P311, DOI 10.1016/0378-5955(87)90066-9 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 THORNTON AR, 1980, J ACOUST SOC AM, V67, P638, DOI 10.1121/1.383888 TURNER C, 1983, J ACOUST SOC AM, V73, P966, DOI 10.1121/1.389022 TURNER CW, 1982, J SPEECH HEAR RES, V25, P34 TYLER RS, 1983, J ACOUST SOC AM, V74, P1190, DOI 10.1121/1.390043 WAKEFIELD GH, 1985, J ACOUST SOC AM, V77, P613, DOI 10.1121/1.391879 ZUREK PM, 1981, J SPEECH HEAR RES, V46, P108 Zwicker E., 1974, FACTS MODELS HEARING, P132 NR 35 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1991 VL 57 IS 1 BP 142 EP 152 DI 10.1016/0378-5955(91)90083-L PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500016 PM 1774205 ER PT J AU MULLER, M AF MULLER, M TI DEVELOPMENTAL-CHANGES OF FREQUENCY REPRESENTATION IN THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE RAT; COCHLEA; DEVELOPMENT; PLACE-FREQUENCY MAP; HRP ID TONOTOPIC ORGANIZATION; INFERIOR COLLICULUS; GERBIL COCHLEA; CHICK COCHLEA; MAP; SHIFT; BAT; STEREOCILIA; PATHOLOGY; HEARING AB The place-frequency map of the developing rat cochlea was measured by iontophoretic HRP-injections into the ventral cochlear nucleus at electrophysiologically characterized positions. Distribution of retrograde HRP transport in cochlear spiral ganglion cells was analysed by means of a three dimensional reconstruction of the cochlea. Cochlear place-frequency maps were derived in rats of two ages groups: 13 to 22 days, and 36/37 day old animals. These maps were compared with the place-frequency map of adult rats (Muller, 1991). No systematic difference in the place-frequency map between 36/37 day old and adult rats was observed. In animals of the younger age group the place-frequency map (for frequencies above 4 kHz) was shifted towards lower frequencies for a given place along the basilar membrane. The morphological and physiological basis for this frequency shift during development is discussed. C1 UNIV FRANKFURT,INST ZOOL,W-6000 FRANKFURT,GERMANY. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 BLATCHLEY BJ, 1987, DEV BRAIN RES, V32, P75, DOI 10.1016/0165-3806(87)90140-4 BRUGGE JF, 1983, DEV AUDITORY VESTIBU, P89 BURDA H, 1985, HEARING RES, V17, P201, DOI 10.1016/0378-5955(85)90064-4 COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 CROWLEY DE, 1966, J COMP PHYSIOL PSYCH, V62, P427, DOI 10.1037/h0023953 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KRAUS HJ, 1982, VERH DTSCH ZOOL GES, V279 KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 LENOIR M, 1987, ANAT EMBRYOL, V175, P477, DOI 10.1007/BF00309683 LIBERMAN MC, 1984, HEARING RES, V16, P33, DOI 10.1016/0378-5955(84)90023-6 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 LIPPE WR, 1987, HEARING RES, V25, P205, DOI 10.1016/0378-5955(87)90092-X MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MULLER M, 1991, IN PRESS HEAR RES MULLER M, 1990, EXP BRAIN RES, V81, P140 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NORTON SJ, 1991, HEARING RES, V51, P73, DOI 10.1016/0378-5955(91)90008-W PATUZZI R, 1988, PHYSIOL REV, V68, P1005 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PUEL JL, 1987, DEV BRAIN RES, V37, P179, DOI 10.1016/0165-3806(87)90239-2 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 Romand R., 1983, DEV AUDITORY VESTIBU, P47 ROMAND R, 1990, DEV BRAIN RES, V54, P221, DOI 10.1016/0165-3806(90)90145-O Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEL EW, 1984, ANN OTO RHINOL LARYN, V93, P609 RUBSAMEN R, 1989, J COMP PHYSIOL A, V165, P755, DOI 10.1007/BF00610874 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SANES DH, 1988, PHYSL EAR, P431 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 TILNEY MS, 1987, HEARING RES, V25, P141, DOI 10.1016/0378-5955(87)90087-6 VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 Wada T., 1923, American Anatomical Memoir, Vno. 10, P1 WOOLF NK, 1988, HEARING RES, V35, P131, DOI 10.1016/0378-5955(88)90112-8 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 41 TC 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 NOV PY 1991 VL 56 IS 1-2 BP 1 EP 7 DI 10.1016/0378-5955(91)90147-2 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300001 PM 1769905 ER PT J AU YOST, WA AF YOST, WA TI AUDITORY IMAGE PERCEPTION AND ANALYSIS - THE BASIS FOR HEARING SO HEARING RESEARCH LA English DT Article DE AUDITORY IMAGES; SOUND SOURCES; HEARING; CODING; AUDITORY PERCEPTION ID AMPLITUDE-MODULATION; INHIBITION; SIGNALS; MODEL; PITCH AB The premise of this paper is that the auditory system's primary function is its ability to determine the sources of sound. Auditory image perception and analysis are defined as the basis for sound source determination. Few studies in the literature have focused on understanding these abilities and the paper argues that more attention should be paid to auditory image perception and analysis. Four questions are posed for understanding auditory image formation and seven physical variables are described which might be used for auditory image perception. The paper relates auditory image perception and analysis to a number of other topics in the hearing sciences in order to reinforce the argument that auditory image perception and analysis are the basis of hearing. RP YOST, WA (reprint author), LOYOLA UNIV,PARMLY HEARING INST,6525 N SHERIDAN RD,CHICAGO,IL 60626, USA. CR BERG BG, 1990, J ACOUST SOC AM, V88, P149, DOI 10.1121/1.399962 Boring E. 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M., 1982, AUDITORY PERCEPTION WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 Yost W., 1987, DIRECTIONAL HEARING Yost W. A., 1987, AUDITORY PROCESSING YOST WA, 1989, J ACOUST SOC AM, V86, P2138, DOI 10.1121/1.398474 YOST WA, 1990, J ACOUST SOC AM, V87, P897, DOI 10.1121/1.398899 YOST WA, 1989, CHABA100 NAT AC SCI YOST WA, 1982, J ACOUST SOC AM, V72, P416, DOI 10.1121/1.388094 NR 50 TC 84 Z9 85 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 8 EP 18 DI 10.1016/0378-5955(91)90148-3 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300002 PM 1769927 ER PT J AU DING, JP SALVI, RJ SACHS, F AF DING, JP SALVI, RJ SACHS, F TI STRETCH-ACTIVATED ION CHANNELS IN GUINEA-PIG OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELL; STRETCH-ACTIVATED ION CHANNEL; ACOUSTIC STIMULATION; COCHLEA; TUNING; MOTILITY ID ELECTRICAL RESONANCE; MECHANICAL RESPONSES; INDUCED MOTILITY; BULL-FROG; TRANSDUCTION; CURRENTS; COCHLEA; ACTIN; CHICK AB Two types of stretch-activated (SA) ion channels have been found in the lateral wall of isolated outer hair cells (OHC) from the guinea pig cochlea. One type had a reversal potential of -12 mV and was non-selective to cations, passing Ca2+ as well as monovalent ions. The channel had a conductance of 38-50 pS and the amplitude of the current through the open SA channel was independent of suction. The probability of the channel being open increased with applied suction and was voltage dependent with the maximum probability occurring at pipette potentials of -40 to -60 mV. The second type of SA channel had a conductance of approximately 150 pS and a reversal potential of approximately -50 mV. The ionic selectivity of this channel has not yet been determined, but it is probably K+ selective. OHCs have been shown to undergo a slow change in length in response to acoustic stimulation directed at the lateral wall of the OHC. The SA channels reported here could affect the motile response by altering the membrane potential or by allowing the entry of free Ca2+ which could lead to a change in OHC length through the interaction of actin and myosin. SA channels could also play an important role in regulating the osmotic pressure of OHC thereby influencing its electro-mechanical response. C1 SUNY BUFFALO,DEPT BIOPHYS SCI,118 CARY HALL,BUFFALO,NY 14214. SUNY BUFFALO,DEPT COMMUNICAT DISORDERS & SCI,BUFFALO,NY 14260. CR ART JJ, 1986, HEARING RES, V22, P31, DOI 10.1016/0378-5955(86)90073-0 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 ASHMORE JF, 1989, COCHLEAR MECH STRUCT, P109 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BROWNELL WE, 1990, ABSTR ASS RES OTOLAR, V228 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 CODY AR, 1986, BASIC APPL ASPECTS N, P149 COREY DP, 1979, NATURE, V281, P675, DOI 10.1038/281675a0 COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 DALLOS P, 1985, J NEUROSCI, V5, P1609 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 HAMILL OP, 1981, PFLUG ARCH EUR J PHY, V391, P85, DOI 10.1007/BF00656997 HOLLEY MC, 1990, J CELL SCI, V96, P283 HOLTON T, 1986, J PHYSIOL-LONDON, V375, P195 HOWARD J, 1988, ANNU REV BIOPHYS BIO, V17, P99 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P275 HUDSPETH AJ, 1977, P NATL ACAD SCI USA, V74, P2407, DOI 10.1073/pnas.74.6.2407 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 LI M, 1990, INT C BIOPHYS, V359 OHMORI H, 1984, P NATL ACAD SCI-BIOL, V81, P1888, DOI 10.1073/pnas.81.6.1888 OHMORI H, 1985, J PHYSIOL-LONDON, V359, P189 OSTERLE EC, 1989, J ACOUST SOC AM, V68, P1013 SACHS F, 1984, ANNU REV BIOPHYS BIO, V13, P269 SACHS F, 1988, CRIT REV BIOMED ENG, V16, P141 SANTOS-SACCHI J, 1989, Society for Neuroscience Abstracts, V15, P208 SANTOSSACCHI J, 1989, ABSTR ASS RES OT, P81 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SLEPECKY N, 1988, BASIC ISSUES HEARING, P49 ULFENDAHL M, 1987, ACTA PHYSIOL SCAND, V130, P521, DOI 10.1111/j.1748-1716.1987.tb08171.x YANG XC, 1989, SCIENCE, V243, P1068, DOI 10.1126/science.2466333 ZENNER HP, 1980, ARCH OTORHINOLARYNGO, V230, P82 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 39 TC 52 Z9 55 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 19 EP 28 DI 10.1016/0378-5955(91)90149-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300003 PM 1722801 ER PT J AU SALT, AN OHYAMA, K THALMANN, R AF SALT, AN OHYAMA, K THALMANN, R TI RADIAL COMMUNICATION BETWEEN THE PERILYMPHATIC SCALAE OF THE COCHLEA .1. ESTIMATION BY TRACER PERFUSION SO HEARING RESEARCH LA English DT Article DE SPIRAL LIGAMENT; COCHLEA; PERILYMPH; ION-SELECTIVE ELECTRODES ID GUINEA-PIG COCHLEA; TRANSPORT AB The degree to which radial exchange between scala tympani (ST) and scala vestibuli (SV) can occur has not previously been quantified. We have measured the amount of cross-communication in the third turn of the guinea pig cochlea using an ionic tracer, trimethylphenylammonium (TMPA). TMPA was perfused through one scala while TMPA concentrations were measured simultaneously in the perfused and non-perfused scalae. On the basis of the time course of TMPA increase recorded in the non-perfused scala, we were able to calculate rate constants for cross-leak and clearance. Cross-leak in the third turn occurred remarkably rapidly with a rate constant from ST to SV of 0.049 min-1 and from SV to ST of 0.031 min-1. These correspond to transfer half times of 14.2 and 22.4 min respectively. This result demonstrates that ST and SV in the third turn cannot be regarded as independent compartments. C1 TOHOKU UNIV,DEPT OTOLARYNGOL,SENDAI,MIYAGI 980,JAPAN. RP SALT, AN (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID,ST LOUIS,MO 63110, USA. CR Axelsson A, 1988, PHYSL EAR, P295 DUVALL AJ, 1972, ANN OTO RHINOL LARYN, V81, P705 FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 INAMURA N, 1989, J ACOUST SOC AM, V85, pS68 KONISHI T, 1978, ACTA OTO-LARYNGOL, V86, P22, DOI 10.3109/00016487809124717 LANGE G, 1981, MENIERES DIS PATHOGE, P208 OHYAMA K, 1988, HEARING RES, V35, P119, DOI 10.1016/0378-5955(88)90111-6 SAIJO S, 1984, ACTA OTO-LARYNGOL, V97, P593, DOI 10.3109/00016488409132937 SALT AN, 1991, IN PRESS J NEUROSCI SALT AN, 1991, HEAR RES, V56 SALT AN, 1991, IN PRESS ACTA OTOLAR SCHUKNECHT HF, 1959, ACTA OTOLRYNGOL S, V132, P5 STRELIOF.D, 1973, J ACOUST SOC AM, V54, P620, DOI 10.1121/1.1913642 TONNDORF J, 1962, ANN OTO RHINOL LARYN, V71, P801 NR 14 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 NOV PY 1991 VL 56 IS 1-2 BP 29 EP 36 DI 10.1016/0378-5955(91)90150-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300004 PM 1769922 ER PT J AU SALT, AN OHYAMA, K THALMANN, R AF SALT, AN OHYAMA, K THALMANN, R TI RADIAL COMMUNICATION BETWEEN THE PERILYMPHATIC SCALAE OF THE COCHLEA .2. ESTIMATION BY BOLUS INJECTION OF TRACER INTO THE SEALED COCHLEA SO HEARING RESEARCH LA English DT Article DE PERILYMPH; SPIRAL LIGAMENT; COCHLEA; ION-SELECTIVE ELECTRODES ID GUINEA-PIG COCHLEA; INNER-EAR; FLOW-RATE; ENDOLYMPH; GRADIENTS AB Radial communication between ST and SV was measured in the sealed cochlea by monitoring the dispersal of an ionic tracer, trimethylphenylammonium (TMPA) injected in the form of a minute bolus. Tracer movements were recorded by a pair of ion-selective electrodes scaled into the injected and non-injected scalae close to the injection site. Measurements were made in the basal or third turn of the guinea pig cochlea. In the third turn, radial communication occurred rapidly with a ST half time from ST to SV of 25 min and from SV to ST of 26 min. In the basal turn the communication was markedly slower, with a ST half time from ST to SV of 170 min and from SV to ST of 240 min. However. The difference between the basal and third turns can be shown to arise almost totally from differences in cross-sectional area of the perilymphatic scalae. When normalized with respect to scala cross-section, the process of tracer movement across the spiral ligament is similar in the basal and third turns. These results demonstrate that radial communication between scala tympani and scala vestibuli is an important route which must be considered in studies involving perilymph. C1 TOHOKU UNIV,DEPT OTOLARYNGOL,SENDAI,MIYAGI 980,JAPAN. RP SALT, AN (reprint author), WASHINGTON UNIV,SCH MED,DEPT OTOLARYNGOL,517 S EUCLID,ST LOUIS,MO 63110, USA. CR FERNANDEZ C, 1952, J ACOUST SOC AM, V24, P519 JAHNKE K, 1989, MENIERES DISEASE PAT, P427 LANGE G, 1981, MENIERES DIS PATHOGE, P208 OHYAMA K, 1988, HEARING RES, V35, P119, DOI 10.1016/0378-5955(88)90111-6 SAIJO S, 1984, ACTA OTO-LARYNGOL, V97, P593, DOI 10.3109/00016488409132937 SALT AN, 1986, HEARING RES, V23, P141, DOI 10.1016/0378-5955(86)90011-0 Salt AN, 1989, MENIERES DIS, P69 SALT AN, 1989, AM J OTOLARYNG, V10, P371, DOI 10.1016/0196-0709(89)90030-6 SALT AN, 1991, HEAR RES, V56 SALT AN, 1988, PHYSL EAR, P341 SCHUKNECHT HF, 1959, ACTA OTOLRYNGOL S, V132, P5 STERKERS O, 1984, AM J PHYSIOL, V247, pF602 NR 12 TC 34 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 37 EP 43 DI 10.1016/0378-5955(91)90151-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300005 PM 1769923 ER PT J AU JACOBSON, GP AHMAD, BK MORAN, J NEWMAN, CW TEPLEY, N WHARTON, J AF JACOBSON, GP AHMAD, BK MORAN, J NEWMAN, CW TEPLEY, N WHARTON, J TI AUDITORY EVOKED CORTICAL MAGNETIC-FIELD (M100-M200) MEASUREMENTS IN TINNITUS AND NORMAL GROUPS SO HEARING RESEARCH LA English DT Article DE NEUROMAGNETISM; AUDITORY EVOKED FIELDS; TINNITUS ID POTENTIALS AB Recently, Hoke et al. (1989) and Pantev et al. (1989) demonstrated that the auditory evoked cortical magnetic field (AECMF) M100 component was larger, and M200 was smaller and occurred later in subjects with unilateral tinnitus compared with normal subjects. These group amplitude differences resulted in an M200/M100 amplitude ratio that was smaller for the subjects with tinnitus. The purposes of the present investigation were to: 1) extend the observations of Hoke et al. (1989), and, 2) determine whether contralateral AECMF differences existed following stimulation of the non-tinnitus and tinnitus ears of patients with tinnitus. Neuromagnetic AECMF recordings were recorded from 25 young normal hearing and 14 patients with unilateral tinnitus and hearing loss. The results failed to support the findings of Hoke et al. (1989). Specifically, there is no evidence suggesting that the M100 amplitude is larger, the M200 latency later, or, the M200/M100 amplitude ratios smaller, when the two samples are compared. Additionally, there were no differences in the amplitudes or latencies of M100 or M200 when results from stimulation of the tinnitus and non-tinnitus ears of tinnitus subjects were compared. C1 HENRY FORD HOSP,DEPT NEUROL,NEUROMAGNETISM LAB,DETROIT,MI 48202. OAKLAND UNIV,DEPT PHYS,ROCHESTER,MI 48063. RP JACOBSON, GP (reprint author), HENRY FORD HOSP,DEPT OTOLARYNGOL,DIV AUDIOL,2799 W GRAND BLVD,DETROIT,MI 48202, USA. CR FISCH U, 1970, ADV OTO-RHINO-LARYNG, V17, P203 HOKE M, 1989, HEARING RES, V37, P281, DOI 10.1016/0378-5955(89)90028-2 MARTIN FW, 1980, CLIN OTOLARYNGOL, V5, P3, DOI 10.1111/j.1365-2273.1980.tb01622.x McFadden D, 1982, TINNITUS FACTS THEOR MCILWAIN JC, 1987, J LARYNGOL OTOL, V101, P552, DOI 10.1017/S0022215100102221 METZ O, 1952, AMA ARCH OTOLARYNGOL, V55, P536 MOLLER MB, 1987, 3 P INT TINN SEM, P340 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 Pantev C, 1986, Acta Otolaryngol Suppl, V432, P21 PANTEV C, 1986, AUDIOLOGY, V25, P263 PANTEV C, 1989, HEARING RES, V40, P261, DOI 10.1016/0378-5955(89)90167-6 PANTEV C, 1986, AUDIOLOGY, V25, P54 PICTON TW, 1978, ELECTROEN CLIN NEURO, V45, P186, DOI 10.1016/0013-4694(78)90003-2 PULEC JL, 1984, AM J OTOL, V5, P479 1968, VITAL HLTH STATIS 11, V32 1981, CIBA F S, V85 NR 16 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 NOV PY 1991 VL 56 IS 1-2 BP 44 EP 52 DI 10.1016/0378-5955(91)90152-Y PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300006 PM 1769924 ER PT J AU SPICER, SS SCHULTE, BA AF SPICER, SS SCHULTE, BA TI DIFFERENTIATION OF INNER-EAR FIBROCYTES ACCORDING TO THEIR ION-TRANSPORT RELATED ACTIVITY SO HEARING RESEARCH LA English DT Article DE ATPASE-NA, K; CARBONIC ANHYDRASE; CREATINE KINASE; FIBROCYTES; COCHLEA; VESTIBULAR SYSTEM; GERBIL ID AUDITORY-NERVE FIBERS; CARBONIC-ANHYDRASE; CREATINE-PHOSPHOKINASE; IMMUNOCYTOCHEMICAL LOCALIZATION; SARCOPLASMIC-RETICULUM; SPIRAL LIGAMENT; GUINEA-PIG; GERBIL; NA+,K+-ATPASE; ACETAZOLAMIDE AB Fibrocytes in the lateral wall and limbus of the gerbil cochlea evidenced a capacity for ion transport activity by immunostaining for transport mediating enzymes including Na,K-ATPase, carbonic anhydrase (CA) and creatine kinase (CK). Fibrocytes of the spiral ligament unlike those in the suprastrial region and limbus decreased in abundance from base to apex. Spiral ligament fibrocytes at a given position along the cochlea varied in content of transport related enzymes, and on the basis of immunostaining, location and orientation, were classified into four types. Type I fibrocytes under the stria vascularis stained for CA isozymes II and III and CK isozyme BB. Type II fibrocytes under the outer sulcus and spiral prominence epithelium were found to contain only Na,K-ATPase. Type III fibrocytes lying adjacent to bone in the inferior region of the spiral ligament contained CA II and III and CK isozymes BB and MM. Type IV fibrocytes located more superficially in the inferior part of the spiral ligament stained variably for all the enzymes. Superficial fibrocytes in the suprastrial area disclosed Na,K-ATPase whereas the underlying fibrocytes stained for CA and CK. Limbal fibrocytes reacted with antisera to all the enzymes except CA III. Most fibrocytes in stromal plates beneath the vestibular system's neurosensory epithelium contained Na,K-ATPase and CA II but not CA III. These findings point to cooperativity in fluid and ion transport between epithelial cells and neighboring fibrocytes and demonstrate functional diversity of fibrocytes of the inner ear providing a basis for classifying those in the spiral ligament. RP SPICER, SS (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR ADAMS JC, 1987, J COMP NEUROL, V262, P375, DOI 10.1002/cne.902620305 BASKIN RJ, 1970, J BIOL CHEM, V245, P1345 BESSMAN SP, 1985, ANNU REV BIOCHEM, V54, P831, DOI 10.1146/annurev.biochem.54.1.831 DRESCHER DG, 1977, P NATL ACAD SCI USA, V74, P892, DOI 10.1073/pnas.74.3.892 ERULKAR SD, 1961, NATURE, V189, P459, DOI 10.1038/189459a0 HAMILTON DW, 1967, ANAT REC, V157, P627, DOI 10.1002/ar.1091570409 HENSON MM, 1988, HEARING RES, V35, P237, DOI 10.1016/0378-5955(88)90121-9 Hsu C J, 1985, Acta Otolaryngol Suppl, V418, P1 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P1349 IKEDA K, 1987, HEARING RES, V31, P211, DOI 10.1016/0378-5955(87)90189-4 IWANO T, 1989, J HISTOCHEM CYTOCHEM, V37, P353 JACOBUS WE, 1974, CIRCULATION S3, V49, P180 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 LEVITSKY DO, 1978, MEMBRANE BIOCHEM, V2, P81, DOI 10.3109/09687687809063859 LIM DJ, 1983, AM J OTOLARYNG, V4, P33, DOI 10.1016/S0196-0709(83)80005-2 MARCUS DC, 1986, NEUROBIOLOGY HEARING, P123 MASON TE, 1969, J HISTOCHEM CYTOCHEM, V17, P563 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 Morera C, 1980, Rev Laryngol Otol Rhinol (Bord), V101, P73 Nakai Y, 1968, Acta Otolaryngol, V66, P120, DOI 10.3109/00016486809126280 PRAZMA J, 1978, AM J PHYSIOL, V235, pF317 REALE E, 1975, J ULTRA MOL STRUCT R, V53, P284, DOI 10.1016/S0022-5320(75)80030-X SAKS VA, 1977, BIOCHIM BIOPHYS ACTA, V465, P550, DOI 10.1016/0005-2736(77)90272-3 SALT AN, 1988, PHYSL EAR, P341 SANTI PA, 1988, PHYSL EAR, P173 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1987, NEUR ABSTR, V13, P1260 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 SIEGEL GJ, 1984, J HISTOCHEM CYTOCHEM, V32, P1309 SPICER SS, 1979, J HISTOCHEM CYTOCHEM, V27, P820 SPICER SS, 1987, LAB INVEST, V57, P535 SPICER SS, 1990, HEARING RES, V43, P205, DOI 10.1016/0378-5955(90)90229-I SPICER SS, 1992, IN PRESS J HISTOCHEM SPICER SS, 1984, NY ACAD SCI, V249, P382 STERKERS O, 1984, AM J PHYSIOL, V246, pF47 TAKAHASHI T, 1970, Acta Oto-Laryngologica, V69, P46, DOI 10.3109/00016487009123335 TURNER DC, 1973, P NATL ACAD SCI USA, V70, P702, DOI 10.1073/pnas.70.3.702 WATANABE K, 1984, ANN OTO RHINOL LARYN, V93, P262 WOLD L E, 1981, American Journal of Clinical Pathology, V75, P327 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 NR 42 TC 169 Z9 175 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 1991 VL 56 IS 1-2 BP 53 EP 64 DI 10.1016/0378-5955(91)90153-Z PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300007 PM 1663106 ER PT J AU SUBRAMANIAM, M CAMPO, P HENDERSON, D AF SUBRAMANIAM, M CAMPO, P HENDERSON, D TI DEVELOPMENT OF RESISTANCE TO HEARING-LOSS FROM HIGH-FREQUENCY NOISE SO HEARING RESEARCH LA English DT Article DE TOUGHENING; RESISTANCE; FREQUENCY OF EXPOSURE ID AUDIBILITY CURVE; EXPOSURE; CHINCHILLA AB The effect of interrupted exposure on the development of progressive resistance to hearing loss from exposure to high frequency noise was studied using monaural chinchillas. The animals were exposed to an octave band noise centered at 4 kHz at 85 dB SPL for 6 h a day for ten consecutive days. Hearing thresholds were measured using evoked potential recording before and after each exposure. Results indicated a reduction in threshold shift with repeated exposures. This reduction in threshold shift or 'toughening' was more rapid for the high frequency exposures than the 'toughening' from similar low frequency exposures. C1 SUNY BUFFALO,DEPT COMMUNICAT DISORDERS & SCI,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214. INST NATL RECH & SECUR,VANDOEUVRE NANCY,FRANCE. CR ALTSCHULER RA, 1991, IN PRESS EFFECTS NOI BOHNE BA, 1987, HEARING RES, V29, P251, DOI 10.1016/0378-5955(87)90172-9 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 CLARK WW, 1991, IN PRESS EFFECTS NOI FIORINO F, 1989, VALSALVA S1, V65, P36 HENDERSON D, 1991, IN PRESS EFFECTS NOI HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 MILLS JH, 1973, J SPEECH HEAR RES, V16, P426 SAUNDERS JC, 1977, J ACOUST SOC AM, V61, P558, DOI 10.1121/1.381298 SUBRAMANIAM M, 1991, HEARING RES, V52, P181, DOI 10.1016/0378-5955(91)90197-H NR 12 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 NOV PY 1991 VL 56 IS 1-2 BP 65 EP 68 DI 10.1016/0378-5955(91)90154-2 PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300008 PM 1769925 ER PT J AU GUTH, PS AUBERT, A RICCI, AJ NORRIS, CH AF GUTH, PS AUBERT, A RICCI, AJ NORRIS, CH TI DIFFERENTIAL MODULATION OF SPONTANEOUS AND EVOKED NEUROTRANSMITTER RELEASE FROM HAIR-CELLS - SOME NOVEL HYPOTHESES SO HEARING RESEARCH LA English DT Article DE HAIR CELL; NEUROTRANSMITTER; OCTAVOLATERALIS; SEMICIRCULAR CANAL; GLUTAMATE; CALCIUM ID GUINEA-PIG COCHLEA; AMINO-ACID AGONISTS; LATERAL-LINE ORGAN; XENOPUS-LAEVIS; GLUTAMATE; FROG; RECEPTORS; TRANSDUCTION; POTENTIALS; CALCIUM AB It has been generally accepted that even in the absence of mechanical stimulation of the transductional elements, a resting depolarizing current exists which is ultimately responsible for the spontaneous release of neurotransmitter. Movement of the transductional elements modulates this resting current and thereby the evoked release of neurotransmitter occurs. Recent data from our laboratory and others have led us to question whether the relationship between spontaneous and evoked neurotransmitter release is as simple as stated. Indeed, a variety of experimental manipulations appear to influence the two modes of release differently. Examination of our results and the results of others has led us to four hypotheses: 1. the two modes of neurotransmitter release are processed differently by the hair cells: 2. cyclic AMP is involved in spontaneous but not evoked neurotransmitter release; 3. there is a positive feedback step involving an excitatory amino acid and its receptor on the hair cell in evoked neurotransmitter release and; 4. different pools of calcium are involved according to the mode of release. Accordingly, there may be several biochemical steps between the transductional movement of the stereocilia at the apex of the hair cells and the ultimate release of the neurotransmitter at the base of these cells. Some of these biochemical steps are different depending on whether the mode of release is spontaneous or evoked. These biochemical steps may amplify or at least interact with the biophysical processes previously described in the hair cells. C1 TULANE UNIV,SCH MED,DEPT OTOLARYNGOL,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,NEUROSCI PROGRAM,NEW ORLEANS,LA 70112. RP GUTH, PS (reprint author), TULANE UNIV,SCH MED,DEPT PHARMACOL,1430 TULANE AVE,NEW ORLEANS,LA 70112, USA. 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PD NOV PY 1991 VL 56 IS 1-2 BP 69 EP 78 DI 10.1016/0378-5955(91)90155-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300009 PM 1685158 ER PT J AU HUFFMAN, RF HENSON, OW AF HUFFMAN, RF HENSON, OW TI COCHLEAR AND CNS TONOTOPY - NORMAL PHYSIOLOGICAL SHIFTS IN THE MOUSTACHED BAT SO HEARING RESEARCH LA English DT Article DE COCHLEA; TONOTOPY; BAT; COCHLEAR RESONANCE; COCHLEAR NUCLEUS; INFERIOR COLLICULUS ID SPONTANEOUS OTOACOUSTIC EMISSIONS; BASILAR-MEMBRANE MOTION; PRIMARY AUDITORY FIBERS; INFERIOR COLLICULUS; PTERONOTUS-PARNELLII; TEMPERATURE-DEPENDENCE; RESPONSE PROPERTIES; FREQUENCY REPRESENTATION; ASCENDING PROJECTIONS; CAIMAN-CROCODILUS AB The ear of the mustached bat (Pteronotus parnellii) shows marked cochlear resonance near 60 kHz and many sharply tuned neurons throughout the brain have best frequencies (BF) near the cochlear resonance frequency (CRF). Controlled changes in the normal physiological range of body temperature (approx 37-42-degrees-C) were used to change the CRF and to study the tuning properties of neurons in the cochlear nucleus (CN) and inferior colliculus (IC). In all cases there were concomitant shifts in the CRF and the BFs. Results were the same for single and multi-units, and for CN and IC units. Although the BF reliably changed with shifts in the CRF, the majority of the units showed no change in minimum threshold or the sharpness (Q10 dB) of tuning. The temperature-induced effects on cochlear tuning were similar to those previously described in nonmammalian vertebrates. The physiological data reveal that, within a narrow frequency band, cochlear and CNS tonotopy are labile in the mustached bat. The lability of tuning is further substantiated by adaptations of biosonar emission behavior with shifts in CRF (Henson et al., 1990). C1 UNIV N CAROLINA,CURRICULUM NEUROBIOL,CHAPEL HILL,NC 27514. 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PD NOV PY 1991 VL 56 IS 1-2 BP 79 EP 85 DI 10.1016/0378-5955(91)90156-4 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300010 PM 1769926 ER PT J AU ZUMGOTTESBERGE, AMM GAGELMANN, M FORSSMANN, WG AF ZUMGOTTESBERGE, AMM GAGELMANN, M FORSSMANN, WG TI ATRIAL NATRIURETIC PEPTIDE-LIKE IMMUNOREACTIVE CELLS IN THE GUINEA-PIG INNER-EAR SO HEARING RESEARCH LA English DT Article DE ATRIAL NATRIURETIC PEPTIDES; CARDIODILATIN; HORMONAL REGULATION; COCHLEAR DUCT; VESTIBULAR ORGAN; OUTER HAIR CELLS ID ENDOLYMPHATIC SAC; ADENYLATE-CYCLASE; ENDOCRINE; RELEASE; HEART; BIOCHEMISTRY; INVITRO; SYSTEM AB Using specific antibodies against cardiodilatin/atrial natriuretic peptide (CDD/ANP) in a conventional immuno-histochemical method (PAP) we located ANP/CDD-like immuno-reactive cells related to the secretory area, to the sensory and to the neuronal area in the compartments of the inner ear (cochlea, utricle/ampulla, and endolymphatic sac). Immunoreactive cells were unevenly distributed in the different compartments as well as within the cochlear space. Our findings suggest that ANP/CDD may play a role in the local control of fluid and electrolyte homeostasis of the inner ear. ANP/CDD-binding sites and ANP/CDD-like immunoreactivity in the inner ear may also indicate that the peptide has an additional paracrine and/or autocrine function in the organ. C1 UNIV HEIDELBERG,INST ANAT & ZELLBIOL,W-6900 HEIDELBERG,GERMANY. NIEDERSACHS INST PEPTID FORSCH GMBH,HANNOVER,GERMANY. RP ZUMGOTTESBERGE, AMM (reprint author), UNIV DUSSELDORF,HNO KLIN,FORSCHUNGSLAB,MOORENSTR 5,W-4000 DUSSELDORF 1,GERMANY. CR BRENNER BM, 1990, PHYSIOL REV, V70, P665 Brownell W. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 86 EP 92 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300011 ER PT J AU VOSSIECK, T SCHERMULY, L KLINKE, R AF VOSSIECK, T SCHERMULY, L KLINKE, R TI THE INFLUENCE OF DC-POLARIZATION OF THE ENDOCOCHLEAR POTENTIAL ON SINGLE FIBER ACTIVITY IN THE PIGEON COCHLEAR NERVE SO HEARING RESEARCH LA English DT Article DE PIGEON; ENDOCOCHLEAR POTENTIAL; CURRENT INJECTION; AFFERENT ACTIVITY ID INNER HAIR-CELLS; INFRASOUND SENSITIVE NEURONS; BASILAR-MEMBRANE MOTION; AUDITORY-NERVE; RECEPTOR POTENTIALS; GUINEA-PIG; MOSSBAUER TECHNIQUE; TRANSIENT ASPHYXIA; TURTLE; FIBERS AB The endocochlear potential (EP) in the pigeon ear was altered by injecting current into the scala media. Simultaneous recordings from different fibres in the cochlear ganglion were performed. The mean rate of spontaneous activity was little affected by current injection and the consequent shifts in EP. In contrast to this lack of effect, the preferred intervals seen in some fibres in birds were accentuated by positive current injection and reduced or in some cases suppressed by negative current injection. The threshold of the tuning curve was raised by injection of negative current but the characteristic frequency showed little change. Sharpness of tuning decreased. Analysis of the results shows that current injection in the scala media produces significant changes in the filter characteristics of the cochlea. as well as altering the driving force for the transduction process (difference between EP and hair cell membrane potential). C1 UNIV FRANKFURT KLINIKUM,ZENTRUM PHYSIOL,THEODOR STERN KAI 7,W-6000 FRANKFURT 70,GERMANY. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 93 EP 100 DI 10.1016/0378-5955(91)90158-6 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300012 PM 1769928 ER PT J AU BOBBIN, RP FALLON, M KUJAWA, SG AF BOBBIN, RP FALLON, M KUJAWA, SG TI MAGNITUDE OF THE NEGATIVE SUMMATING POTENTIAL VARIES WITH PERILYMPH CALCIUM LEVELS SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELL; NIMODIPINE; ION CHANNELS ID SACCULAR HAIR-CELLS; GUINEA-PIG COCHLEA; LATERAL-LINE ORGAN; DIVALENT-CATIONS; RANA-CATESBEIANA; NEURAL ACTIVITY; AUDITORY-NERVE; XENOPUS-LAEVIS; BULL-FROG; FREQUENCY AB Previous results demonstrated that nimodipine, an L-type of Ca2+ channel antagonist, abolished the negative summating potential (SP) recorded from anesthetized guinea pigs (Bobbin el al., 1990). suggesting that Ca2+ is involved in generation of the negative SP. Therefore we examined the effect of changing concentrations of perilymph Ca2+ on this cochlear potential. Perilymph spaces of guinea pig cochleae were perfused with artificial perilymph solutions containing zero mM Ca2+, zero mM Ca2+ with 2 mM EGTA, 30 mM Mg2+ and increasing levels of Ca2+ (2, 4, 8, 16 mM) at a rate of 2.5-mu-l/min for 10 min. Immediately after each period of perfusion the compound action potential of the auditory nerve (CAP), cochlear microphonics (CM) and the negative SP evoked by 10 kHz tone bursts of varying intensities were recorded from a wire inserted in the basal turn scala vestibuli. Decreasing the level of Ca2+ decreased the magnitude of the negative SP, whereas increasing the level of Ca2+ progressively increased the magnitude of the negative SP. Mg2+ (30 mM) suppressed the CAP to the same extent as zero mM Ca2+ with 2 mM EGTA, but only slightly increased the magnitude of the negative SP. These results support the hypothesis that Ca2+ and L-type Ca2+ channels are involved in the function of the hair cells and the generation of the negative SP. Mg2+ appears to be a selective antagonist of the Ca2+ channel involved in transmitter release. C1 LOUISIANA STATE UNIV,MED CTR,SCH MED,KRESGE HEARING RES LAB S,DEPT OTORHINOLARYNGOL & BIOCOMMUN,NEW ORLEANS,LA 70112. UNIV ARIZONA,DEPT SPEECH & HEARING SCI,TUCSON,AZ 85721. CR ARTS HA, 1990, ABSTR ASS RES OT, P194 ASSAD JA, 1989, P NATL ACAD SCI USA, V86, P2918, DOI 10.1073/pnas.86.8.2918 BLEDSOE SC, 1988, PHYSL EAR, pA406 BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BOBBIN RP, 1987, HEARING RES, V25, P77, DOI 10.1016/0378-5955(87)90081-5 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DILGER JP, 1988, PHYSL EAR, P487 DRESCHER DG, 1987, LIFE SCI, V40, P1371, DOI 10.1016/0024-3205(87)90327-4 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 DULON D, 1990, J NEUROSCI, V10, P1388 FEX J, 1966, J ACOUST SOC AM, V41, P666 FEX J, 1967, NATURE, V213, P1233, DOI 10.1038/2131233a0 GUTH SL, 1990, BRAIN RES, V508, P76, DOI 10.1016/0006-8993(90)91120-6 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P275 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 HUDSPETH AJ, 1986, HEARING RES, V22, P21, DOI 10.1016/0378-5955(86)90070-5 JASTREBOFF PJ, 1988, ANN NY ACAD SCI, V522, P716, DOI 10.1111/j.1749-6632.1988.tb33419.x JASTREBOFF PJ, 1987, 3 P INT TINN SEM MUE, P95 JENISON GL, 1986, COMP BIOCHEM PHYS C, V84, P385, DOI 10.1016/0742-8413(86)90110-6 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x JOHNSTONE BM, 1989, J PHYSIOL-LONDON, V408, P77 KONISHI T, 1970, J ACOUST SOC AM, V47, P1055, DOI 10.1121/1.1912005 LEPAGE EL, 1989, HEARING RES, V38, P177, DOI 10.1016/0378-5955(89)90064-6 LITTMAN T, 1989, HEARING RES, V40, P45, DOI 10.1016/0378-5955(89)90098-1 MOSCOVIT.DH, 1966, J ACOUST SOC AM, V40, P583, DOI 10.1121/1.1910122 POU AM, 1991, HEARING RES, V52, P305, DOI 10.1016/0378-5955(91)90020-A PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 ROBERTS WM, 1988, ANNU REV CELL BIOL, V4, P63, DOI 10.1146/annurev.cb.04.110188.000431 ROBERTS WM, 1990, J NEUROSCI, V10, P3664 ROBERTSON D, 1979, PFLUG ARCH EUR J PHY, V380, P7, DOI 10.1007/BF00582605 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOSSACCHI J, 1988, PHYSL EAR, P271 SATO Y, 1989, ACTA OTO-LARYNGOL, V108, P76, DOI 10.3109/00016488909107395 SIEGEL JH, 1987, HEARING RES, V28, P131, DOI 10.1016/0378-5955(87)90044-X TAKADA A, 1982, HEARING RES, V8, P179, DOI 10.1016/0378-5955(82)90073-9 TSIEN RW, 1988, TRENDS NEUROSCI, V11, P431, DOI 10.1016/0166-2236(88)90194-4 ZENNER HP, 1986, NEUROBIOLOGY HEARING, P1 NR 39 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 101 EP 110 DI 10.1016/0378-5955(91)90159-7 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300013 PM 1663103 ER PT J AU OHYAMA, K WADA, H KOBAYASHI, T TAKASAKA, T AF OHYAMA, K WADA, H KOBAYASHI, T TAKASAKA, T TI SPONTANEOUS OTOACOUSTIC EMISSIONS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSION; GUINEA PIG; COCHLEAR MICROMECHANICS; COCHLEA ID OTO-ACOUSTIC EMISSIONS; NONHUMAN PRIMATE; COCHLEAR BIOMECHANICS; DISTORTION; EAR; SUPPRESSION; RESPONSES; FREQUENCY AB Measurement of spontaneous otoacoustic emission (SOAE) in a large number of animals was conducted in the guinea pig. A remarkably high incidence of SOAE (51 ears out of 248 ears; 20.6%) was observed in the animals that were raised under unexceptional conditions. The frequencies of SOAE were distributed between 0.7 kHz and 2.3 kHz (average: 1.16 kHz). The emission signals disappeared with hypoxia and with furosemide injection, and recovered after certain periods with some frequency fluctuations. Their electrical correlates that behaved in exactly the same manner as SOAE were clearly distinguished by FFT analysis of the AC potential from the cochlear surface. The signals could be divided into 4 types: (1) emission with pure and stable frequency spectrum and steady level, (2) emission with stable frequency and fluctuating level, (3) emission alternating between two closely situated frequency points, (4) emission having an irregular, wide spectrum band. Light microscopy revealed no abnormalities in the organ of Corti that have been widely accepted to be SOAE-related, i.e., patchy lesions of the organ of Corti and/or irregularities in hair cell arrangement. This suggests that the spontaneous oscillation within the guinea pig cochlea can be generated by some minor, functional, and probably reversible disturbances of the active cochlear transduction mechanism, without major structural derangement of the organ of Corti. C1 TOHOKU UNIV,DEPT MECH ENGN,SENDAI,MIYAGI 980,JAPAN. RP OHYAMA, K (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 AVAN P, 1990, HEARING RES, V44, P151, DOI 10.1016/0378-5955(90)90077-3 BIALEK W, 1984, PHYS LETT A, V104, P173, DOI 10.1016/0375-9601(84)90371-2 BROWN AM, 1988, INNER EAR BIOL WORKS BROWN AM, 1987, HEARING RES, V31, P25, DOI 10.1016/0378-5955(87)90211-5 BURNS EM, 1984, HEARING RES, V16, P271, DOI 10.1016/0378-5955(84)90116-3 CLARK WW, 1984, HEARING RES, V16, P299, DOI 10.1016/0378-5955(84)90119-9 COMIS SD, 1980, NEUROPHARMACOLOGY, V20, P405 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 Engstrom H, 1966, STRUCTURAL PATTERN O EVANS EF, 1981, TINNITUS, P108 FRITZE W, 1985, ARCH OTO-RHINO-LARYN, V242, P43, DOI 10.1007/BF00464404 KEMP DT, 1981, TINNITUS, P54 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 KOSSL M, 1985, HEARING RES, V19, P157, DOI 10.1016/0378-5955(85)90120-0 LONSBURYMARTIN BL, 1990, ANN OTO RHINOL LARYN, V99, P15 LONSBURYMARTIN BL, 1988, HEARING RES, V33, P69, DOI 10.1016/0378-5955(88)90021-4 MARTIN GK, 1988, HEARING RES, V33, P49, DOI 10.1016/0378-5955(88)90020-2 MARTIN GK, 1985, HEARING RES, V20, P91, DOI 10.1016/0378-5955(85)90062-0 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NEELY ST, 1983, HEARING RES, V15, P103 Neely ST, 1983, MECH HEARING, P111 NORTON SJ, 1989, HEARING RES, V38, P243, DOI 10.1016/0378-5955(89)90069-5 Palmer AR, 1982, J PHYSL, V324, P66 Probst R, 1990, Adv Otorhinolaryngol, V44, P1 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 RUGGERO MA, 1984, HEARING RES, V13, P293, DOI 10.1016/0378-5955(84)90083-2 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SCHLOTH E, 1983, ACUSTICA, V53, P250 SCHMIEDT RA, 1981, HEARING RES, V5, P295, DOI 10.1016/0378-5955(81)90053-8 STRICKLAND AE, 1984, J ACOUST SOC AM S1, V75, pS82 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 SUGASAWA T, 1990, 37TH M JAP ASS BAS O, V154 VANDIJK P, 1989, HEARING RES, V42, P273, DOI 10.1016/0378-5955(89)90151-2 WHITEHEAD ML, 1986, AUDITORY FREQUENCY S, P39 Wilson JP, 1981, TINNITUS, P82 WIT HP, 1990, C MECHANICS BIOPHYSI, P205 WRIGHT A, 1984, HEARING RES, V13, P89, DOI 10.1016/0378-5955(84)90099-6 ZUREK PM, 1981, J ACOUST SOC AM, V70, P446, DOI 10.1121/1.386787 ZWICKER E, 1986, PERIPHERAL AUDITORY, P250 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 43 TC 31 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 111 EP 121 DI 10.1016/0378-5955(91)90160-B PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300014 PM 1769906 ER PT J AU HENSON, MM HENSON, OW AF HENSON, MM HENSON, OW TI SPECIALIZATIONS FOR SHARP TUNING IN THE MOUSTACHED BAT - THE TECTORIAL MEMBRANE AND SPIRAL LIMBUS SO HEARING RESEARCH LA English DT Article DE TECTORIAL MEMBRANE; SPIRAL LIMBUS; COCHLEA; MOUSTACHED BAT; PTERONOTUS ID DOPPLER-SHIFTED ECHOES; PTERONOTUS-PARNELLII; INFERIOR COLLICULUS; COCHLEAR MECHANICS; FREQUENCY REPRESENTATION; BASILAR-MEMBRANE; AUDITORY-SYSTEM; SOUND ANALYSIS; SINGLE UNITS; INNER-EAR AB The sense of hearing in the mustached bat, Pteronotus parnellii, is specialized for fine frequency analysis in three narrow bands that correspond to approx 30, 60 and 90 kHz constant frequency harmonics in the biosonar signals used for Doppler-shift compensation and acoustic imaging of the environment. Previous studies have identified anatomical specializations in and around the area of the cochlea that processes the dominant second harmonic component. but similar features have not been found in areas related to sharp tuning and high sensitivity for the first or third harmonics. In this report we call attention to the large size of the tectorial membrane and spiral limbus in all three areas that appear to process the harmonically related constant frequency components. These structures are especially pronounced in the regions of the cochlea that respond to the approx 61 kHz, second harmonic and 91.5 kHz, third harmonic bands: they correspond specifically to areas where the density of afferent nerve fibers is high and where verv sharply tuned neurons occur. These data for cochleae with multiple specializations lend strong support to the idea that the mass of the tectorial membrane can be an important factor in establishing the response properties of the cochlea. C1 UNIV N CAROLINA,DEPT CELL BIOL & ANAT,TAYLOR BLDG,CB 7090,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27514. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 122 EP 132 DI 10.1016/0378-5955(91)90161-2 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300015 PM 1769907 ER PT J AU MATSUSHIMA, JI SHEPHERD, RK SELDON, HL XU, SA CLARK, GM AF MATSUSHIMA, JI SHEPHERD, RK SELDON, HL XU, SA CLARK, GM TI ELECTRICAL-STIMULATION OF THE AUDITORY-NERVE IN DEAF KITTENS - EFFECTS ON COCHLEAR NUCLEUS MORPHOLOGY SO HEARING RESEARCH LA English DT Article DE AUDITORY DEPRIVATION; ELECTRICAL STIMULATION; SOMA SIZE; COCHLEAR NUCLEI; COCHLEAR IMPLANTS ID SENSORINEURAL HEARING-LOSS; BRAIN-STEM; INFERIOR COLLICULUS; AFFERENT INFLUENCES; PROTEIN-SYNTHESIS; NEURONS; PROJECTIONS; DEPRIVATION; CHICKEN; REMOVAL AB The present study examines the effects of long-term electrical stimulation of the auditory nerve on the morphology of neurons in the cochlear nucleus in young, sensorineural deaf animals. Kittens, systemically deafened using kanamycin and ethacrynic acid, received bilateral cochlear implants and were stimulated unilaterally for periods of up to four months. After sacrifice, cross-sectional areas of neuron somata were measured with an image-analysis system and compared using nonparametric statistics. The areas of cell somata within the anteroventral cochlear nucleus (AVCN) on the stimulated side were significantly larger than those of corresponding somata on the control, unstimulated side (P < 0.001). However, there was no statistically significant difference among dorsal cochlear nucleus (DCN) neurons. These results indicate that long-term electrical stimulation of the auditory nerve can at least partially negate some effects of early postnatal auditory deprivation at the level of the cochlear nucleus. C1 UNIV MELBOURNE,DEPT OTOLARYNGOL,32 GISBORNE ST,MELBOURNE,VIC 3002,AUSTRALIA. HOKKAIDO UNIV,SCH MED,DEPT OTOLARYNGOL,SAPPORO,HOKKAIDO 060,JAPAN. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 133 EP 142 DI 10.1016/0378-5955(91)90162-3 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300016 PM 1769908 ER PT J AU SAITO, T MOATAZ, R DULON, D AF SAITO, T MOATAZ, R DULON, D TI CISPLATIN BLOCKS DEPOLARIZATION-INDUCED CALCIUM ENTRY IN ISOLATED COCHLEAR OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE COCHLEA; OUTER HAIR CELL; OTOTOXICITY; CISPLATIN; ANTITUMOR DRUG; CALCIUM CHANNEL; INDO-1 ID GUINEA-PIG; OTOTOXICITY; DNA; MECHANISM; MOTILITY AB The effects of the ototoxic molecule cisplatin (cis-DDP) were tested on the physiology of isolated cochlear outer hair cells. Cis-DDP, even at a high concentration of 1 mM, did not affect the viability of the OHCs maintained in short-term culture in vitro (6 h following cell dissociation was the longest time tested). Also, the presence of cis-CDP (1 mM) did not inhibit the contractile responses of the OHCs stimulated by the external application of the calcium ionophore, ionomycin. However, cis-DDP was able to block calcium entry evoked by [K+]-depolarization and a dose-inhibition curve indicated an IC50 of 45 +/- 30-mu-M. These results suggest that one of the acute actions of cis-DDP on OHCs physiology might be situated at the level of the plasma membrane where it acts as a Ca2+-channel blocker. C1 UNIV BORDEAUX 2,HOP PELLEGRIN,AUDIOL EXPTL LAB,INSERM,U229,F-33076 BORDEAUX,FRANCE. CR ASHMORE JF, 1990, J PHYSIOL-LONDON, V428, P109 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1991, NEUROREPORT, V2, P69, DOI 10.1097/00001756-199102000-00001 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 DULON D, 1990, J NEUROSCI, V10, P1388 EASTMAN A, 1986, BIOCHEMISTRY-US, V25, P3912, DOI 10.1021/bi00361a026 ESTREM SA, 1981, OTOLARYNG HEAD NECK, V89, P638 GEMBA M, 1987, TOXICOL LETT, V38, P291, DOI 10.1016/0378-4274(87)90011-7 HAMEL B, 1990, CANCER BIOCHEM BIOPH, V11, P155 JOHNSON NP, 1985, J AM CHEM SOC, V107, P6376, DOI 10.1021/ja00308a036 KONISHI T, 1983, AM J OTOLARYNG, V4, P18, DOI 10.1016/S0196-0709(83)80003-9 MCALPINE D, 1990, HEARING RES, V47, P191, DOI 10.1016/0378-5955(90)90151-E MURRAY D, 1985, CANCER RES, V45, P6446 NAKAI Y, 1982, ACTA OTO-LARYNGOL, V93, P227, DOI 10.3109/00016488209130876 OHTANI I, 1989, PRACTICA OTOL KYOT S, V32, P49 SCHAEFER SD, 1985, CANCER, V56, P1934, DOI 10.1002/1097-0142(19851015)56:8<1934::AID-CNCR2820560807>3.0.CO;2-F SIMPKINS H, 1988, BIOCHIM BIOPHYS ACTA, V972, P25 NR 18 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 NOV PY 1991 VL 56 IS 1-2 BP 143 EP 147 DI 10.1016/0378-5955(91)90163-4 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300017 PM 1663104 ER PT J AU RYAN, AF WATTS, AG SIMMONS, DM AF RYAN, AF WATTS, AG SIMMONS, DM TI PRESERVATION OF MESSENGER-RNA DURING INSITU HYBRIDIZATION IN THE COCHLEA SO HEARING RESEARCH LA English DT Article DE INNER EAR; GENE EXPRESSION; MESSENGER-RNA; HYBRIDIZATION; INSITU ID GENE-EXPRESSION; MESSENGER-RNAS; PROBES AB Specific nucleic acid sequences can be identified within cells using in situ hybridization. Hybridization for mRNA can document the distribution and amount of specific gene transcripts. Decalcification protocols used for immunohistochemistry in the cochlea were evaluated for use with in situ mRNA hybridization. No loss of mRNA was detected following the use of decalcification solutions at 4-degrees-C when paraformaldehyde was added to the EDTA solution. The primary determinant of mRNA preservation was paraformaldehyde. C1 VET ADM MED CTR,SAN DIEGO,CA 92161. SALK INST BIOL STUDIES,NEURAL SYST LAB,LA JOLLA,CA 92037. UNIV CALIF SAN DIEGO,SCH MED,DEPT SURG OTOLARYNGOL,LA JOLLA,CA 92093. UNIV SO CALIF,DEPT NEUROSCI,LOS ANGELES,CA 90089. UNIV CALIF SAN DIEGO,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. CR COX KH, 1984, DEV BIOL, V101, P485, DOI 10.1016/0012-1606(84)90162-3 CRENSHAW EB, 1991, J NEUROSCI, V11, P1524 DOUGLASS J, 1984, ANNU REV BIOCHEM, V53, P665 HE X, 1989, Nature (London), V340, P35, DOI 10.1038/340035a0 JONES P S, 1986, Journal of Histotechnology, V9, P181 Kawasaki ES, 1990, PCR PROTOCOLS GUIDE, P21 Lewin B, 1990, GENES RYAN A F, 1991, Molecular and Cellular Neuroscience, V2, P179, DOI 10.1016/1044-7431(91)90011-C RYAN AF, 1991, IN PRESS P NY ACAD S RYAN AF, 1991, IN PRESS NEUR ABSTR SAIKI RK, 1988, SCIENCE, V239, P487, DOI 10.1126/science.2448875 SIMMONS DM, 1989, J HISTOTECHNOL, V12, P169 WACKYM PA, 1990, OTOLARYNG HEAD NECK, V103, P519 WATTS AG, 1991, IN PRESS PNAS WHITE BA, 1982, J BIOL CHEM, V257, P8569 NR 15 TC 27 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 148 EP 152 DI 10.1016/0378-5955(91)90164-5 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300018 PM 1769909 ER PT J AU EGGERMONT, JJ AF EGGERMONT, JJ TI RATE AND SYNCHRONIZATION MEASURES OF PERIODICITY CODING IN CAT PRIMARY AUDITORY-CORTEX SO HEARING RESEARCH LA English DT Article DE PRIMARY AUDITORY CORTEX; RESPONSE TO CLICK TRAINS; PERIODICITY CODING; VECTOR STRENGTH; ENTRAINMENT; MODULATION TRANSFER FUNCTION; SUPPRESSION ID INFERIOR COLLICULUS; AMPLITUDE-MODULATION; DYNAMIC PROPERTIES; COCHLEAR NUCLEUS; TEMPORAL CHARACTERISTICS; SINGLE NEURONS; RESPONSES; MIDBRAIN; REPRESENTATION; GRASSFROG AB Periodicity coding was studied in primary auditory cortex of the ketamine anesthetized cat by simultaneously recording with two electrodes from up to 6 neural units in response to one second long click trains presented once per 3 s. Trains with click rates of 1, 2, 4, 8, 16 and 32/s were used and the responses of the single units were quantified by both rate measures (entrainment and rate modulation transfer function, rMTF) and synchronization measures (vector strength VS and temporal modulation transfer functions, tMTF). The rate measures resulted in low-pass functions of click rate and the synchrony measures resulted in band-pass functions of click rate. Limiting rates (-6 dB point of maximum response) were in the range of 3-24 Hz depending on the measure used. Best modulating frequencies were in the range of 5-8 Hz again depending on the synchrony measure used. It appeared that especially the VS was highly sensitive to spontaneous firing rate. duration of the post click suppression and the size of the rebound response after the suppression. These factors were dominantly responsible for the band-pass character of the VS-rate function and the peak VS frequency was nearly identical to the inverse of the suppression period. It is concluded that the use of the VS and to a lesser extent also the tMTF as the sole measure for the characterization of periodicity coding is not recommended in cases where there is a strong suppression of spontaneous activity. The combination of entrainment and tMTF appeared to characterize the periodicity coding in an unambiguous way. RP EGGERMONT, JJ (reprint author), UNIV CALGARY,DEPT PSYCHOL,BEHAV NEUROSCI RES GRP,2500 UNIV DR NW,CALGARY T2N 1N4,ALBERTA,CANADA. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 153 EP 167 DI 10.1016/0378-5955(91)90165-6 PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300019 PM 1769910 ER PT J AU SAKAGAMI, M FUKAZAWA, K MATSUNAGA, T FUJITA, H MORI, N TAKUMI, T OHKUBO, H NAKANISHI, S AF SAKAGAMI, M FUKAZAWA, K MATSUNAGA, T FUJITA, H MORI, N TAKUMI, T OHKUBO, H NAKANISHI, S TI CELLULAR-LOCALIZATION OF RAT ISK PROTEIN IN THE STRIA VASCULARIS BY IMMUNOHISTOCHEMICAL OBSERVATION SO HEARING RESEARCH LA English DT Article DE RAT ISK PROTEIN; POTASSIUM CHANNEL; MARGINAL CELL; STRIA VASCULARIS; IMMUNOHISTOCHEMISTRY ID PARA-NITROPHENYLPHOSPHATASE ACTIVITY; GUINEA-PIG; MEMBRANE-PROTEIN; INNER-EAR; OUABAIN; MECHANISMS; ATPASE; CELLS AB A novel rat membrane protein, termed I(sk) protein, that exhibits a voltage-dependent potassium channel activity was first reported through molecular cloning combined with an electrophysiological assay (Takumi et al., 1988). In the present study, we made an attempt to identify the cellular localization of the rat I(sk) protein in the stria vascularis using two types of antibodies that specifically react with the distinct parts of the rat I(sk) protein. Immunohistochemical analysis showed that the rat I(sk) protein was present only on the endolymphatic surface of the marginal cell. The possibility that the I(sk) protein is involved in potassium permeation in the luminal membrane of the marginal cell will be also discussed. C1 OSAKA UNIV,SCH MED,DEPT ANAT,OSAKA,JAPAN. KAGAWA MED SCH,DEPT OTOLARYNGOL,KAGAWA,JAPAN. KYOTO UNIV,FAC MED,INST IMMUNOL,KYOTO 606,JAPAN. RP SAKAGAMI, M (reprint author), OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,1-1-50 FUKUSHIMA,OSAKA 553,JAPAN. CR BOSHER SK, 1980, ACTA OTO-LARYNGOL, V90, P219, DOI 10.3109/00016488009131718 GITTER AH, 1988, ABSTR ASS RES OT, V11, P79 IINUMA T, 1967, LARYNGOSCOPE, V77, P141 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 KOBAYASHI T, 1987, J HISTOCHEM CYTOCHEM, V35, P601 KOBAYASHI T, 1985, ANAT ANZEIGER, V160, P101 KUIJPERS W, 1967, SCIENCE, V157, P949, DOI 10.1126/science.157.3791.949 KUIJPERS W, 1969, BIOCHIM BIOPHYS ACTA, V173, P477, DOI 10.1016/0005-2736(69)90012-1 KUSAKARI J, 1978, LARYNGOSCOPE, V88, P12 MARCUS DC, 1985, HEARING RES, V17, P79, DOI 10.1016/0378-5955(85)90133-9 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 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 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SEGUCHI H, 1983, ACTA HISTOCHEM CYTOC, V16, P610 SELLICK PM, 1974, PFLUG ARCH EUR J PHY, V352, P339, DOI 10.1007/BF00585686 SUGIMOTO T, 1990, J MEMBRANE BIOL, V113, P39, DOI 10.1007/BF01869604 TAKUMI T, 1988, SCIENCE, V242, P1042, DOI 10.1126/science.3194754 YOSHIHARA T, 1987, ACTA OTO-LARYNGOL, V103, P161, DOI 10.3109/00016488709107779 NR 20 TC 75 Z9 77 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 168 EP 172 DI 10.1016/0378-5955(91)90166-7 PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300020 PM 1663105 ER PT J AU SHONE, G ALTSCHULER, RA MILLER, JM NUTTALL, AL AF SHONE, G ALTSCHULER, RA MILLER, JM NUTTALL, AL TI THE EFFECT OF NOISE EXPOSURE ON THE AGING EAR SO HEARING RESEARCH LA English DT Article DE MICE; NOISE-INDUCED HEARING LOSS; AGING; PRESBYCUSIS ID AGE-RELATED-CHANGES; PIGMENTED GUINEA-PIGS; BRAIN-STEM RESPONSE; HEARING-LOSS; AUDITORY-THRESHOLDS; ACOUSTIC TRAUMA; MICE; MOUSE; PRESBYCUSIS; POTENTIALS AB The effect of noise exposure on auditory sensitivity and inner ear morphology was compared in aged and young mature mice. Hearing thresholds were obtained by auditory evoked brain stem responses (ABR) before and after noise exposure, and hair cell loss was quantified. The study was done in two parts: first to assess the effect of noise exposure on subjects with presbycusis, and second to assess its effect on aged subjects without measurable presbycusis. In the first experiment C57BL/6 mice, with an age-related hearing loss, were used as a model for presbycusis. C57BL/6 mice exhibiting presbycusis were more susceptible to noise injury than age-matched CBA/Ca mice. In the second experiment CBA/Ca mice were used. These mice retain normal hearing even with advancing age. The aged CBA/Ca mice had the same susceptibility to noise injury as young CBA/Ca mice. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. CR BENNETT CL, 1983, BEHAV NEUROSCI, V97, P602, DOI 10.1037//0735-7044.97.4.602 CHOLE RA, 1983, AUDIOLOGY, V22, P384 CHURCH MW, 1986, AUDIOLOGY, V25, P363 CROWLEY DE, 1972, ANN OTO RHINOL LARYN, V81, P739 DUM N, 1980, ARCH OTO-RHINO-LARYN, V228, P249, DOI 10.1007/BF00660737 DUM N, 1980, ARCH OTO-RHINO-LARYN, V229, P191, DOI 10.1007/BF02565521 HAWKINS JE, 1985, BEHAV PATHOLOGY AGIN, P137 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1983, PSYCHOBIOLOGY MOUSE, P470 HENRY KR, 1983, AUDIOLOGY, V22, P372 HENRY KR, 1982, J GERONTOL, V37, P275 HENRY KR, 1978, ACTA OTO-LARYNGOL, V86, P366, DOI 10.3109/00016487809107515 HENRY KR, 1982, BEHAV GENET, V12, P563, DOI 10.1007/BF01070410 HENRY KR, 1982, HEARING RES, V8, P285, DOI 10.1016/0378-5955(82)90020-X HUMES LE, 1984, J ACOUST SOC AM, V76, P1318, DOI 10.1121/1.391447 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 LUTOVAC M, 1969, Srpski Arkhiv za Tselokupno Lekarstvo, V97, P869 MCGINN MD, 1991, HEAR RES MCRAE JH, 1971, AUDIOLOGY, V10, P323 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 Novotný Z, 1975, Cesk Otolaryngol, V24, P5 Novotný Z, 1975, Cesk Otolaryngol, V24, P151 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SHNERSON A, 1981, DEV BRAIN RES, V2, P65, DOI 10.1016/0165-3806(81)90059-6 WELLESCHIK B, 1978, LARYNG RHINOL OTOL V, V57, P1037 WENNGREN BI, 1988, ACTA OTO-LARYNGOL, V106, P238, DOI 10.3109/00016488809106431 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 NR 28 TC 53 Z9 53 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 173 EP 178 DI 10.1016/0378-5955(91)90167-8 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300021 PM 1769911 ER PT J AU ROUILLER, EM WELKER, E AF ROUILLER, EM WELKER, E TI MORPHOLOGY OF CORTICOTHALAMIC TERMINALS ARISING FROM THE AUDITORY-CORTEX OF THE RAT - A PHASEOLUS VULGARIS-LEUKOAGGLUTININ (PHA-L) TRACING STUDY SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; AUDITORY THALAMUS; MEDIAL GENICULATE BODY; CORTICOTHALAMIC PROJECTION; PHASEOLUS VULGARIS-LEUKOAGGLUTININ; RAT ID MEDIAL GENICULATE-BODY; THALAMIC RETICULAR NUCLEUS; TONOTOPIC ORGANIZATION; HORSERADISH-PEROXIDASE; FUNCTIONAL-ORGANIZATION; RESPONSE PROPERTIES; VENTRAL DIVISION; DEFINED REGIONS; BARREL CORTEX; ALBINO-RAT AB Phaseolus vulgaris-leucoagglutinin (PHA-L) injection in the auditory cortex of the rat labeled anterogradely corticothalamic axons whose trajectory, morphology of terminals and their distribution were analyzed in light microscopy. From the primary auditory cortex, corticofugal axons ran in a rostral direction in the white matter (external capsule), and reached the internal capsule by crossing the caudate putamen. Then, they turned caudally, crossed the reticular nucleus (RE) of the thalamus, where some of them were seen to give off collaterals, ramifying in the 'auditory sector' of RE. From RE, the parent corticofugal axons continued in a caudal and medial direction to enter in the medial geniculate body (MGB). Corticofugal axons from the auditory cortex gave rise to 2 distinct types of terminals in the thalamus. First, small boutons (about 1-mu-m in diameter) were observed in the ventral division of the MGB (v-MGB; the main auditory relay nucleus in the thalamus), in RE, in the lateral part of the posterior thalamic nucleus, in the dorsal division of the MGB (d-MGB), as well as occasionally in the medial division of the MGB. Giant terminals (5-10-mu-m in diameter) formed the second type of cortical terminals, only present in a restricted zone of the ventral portion of d-MGB. Both types of terminals were observed as boutons 'terminaux' and 'en passant'. The zone of termination in v-MGB and RE varied as a function of the site of cortical injection. The similarity in the morphology and distribution of the terminals of corticothalamic axons arising from the primary auditory cortex with those of the primary somatosensory cortex of the mouse is striking and points to the existence of a basic pattern of connectivity used in corticothalamic processing of sensory information in rodents. C1 UNIV LAUSANNE,FAC MED,INST PHYSIOL,CH-1000 LAUSANNE 17,SWITZERLAND. UNIV LAUSANNE,FAC MED,INST ANAT,CH-1000 LAUSANNE 17,SWITZERLAND. RP ROUILLER, EM (reprint author), UNIV FRIBOURG,INST PHYSIOL,CH-1700 FRIBOURG,SWITZERLAND. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 179 EP 190 DI 10.1016/0378-5955(91)90168-9 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300022 PM 1769912 ER PT J AU MULLER, M OTT, H BRUNS, V AF MULLER, M OTT, H BRUNS, V TI FREQUENCY REPRESENTATION AND SPIRAL GANGLION-CELL DENSITY IN THE COCHLEA OF THE GERBIL PACHYUROMYS-DUPRASI SO HEARING RESEARCH LA English DT Article DE COCHLEA; PLACE-FREQUENCY MAP; INNERVATION; GERBIL; HRP ID HEARING RANGE; MAP; CAT; BAT AB The tonotopic map of the cochlea in the gerbil Pachyuromys duprasi was analysed by local iontophoretic HRP-application into physiologically defined regions of the cochlear nucleus and mapping of subsequent HRP transport patterns in cochlear spiral ganglion cells. Furthermore the spiral ganglion cell density along the cochlear duct was determined. The cochlear tonotopic map was established in the frequency range between 0.6 and 17.5 kHz. These frequencies corresponded to locations between 86 and 3% basilar membrane length (0% = cochlear base). It was found that the slope of the place-frequency map varied with frequency, the maximum slope being found between 1 and 4 kHz. This frequency range corresponds to the frequency range of highest auditory sensitivity as determined from cochlear microphonic recordings (Plassmann et al., 1987). The density of spiral ganglion cells also varied along the cochlear duct. A pronounced maximum (1927 cells/mm) was located at around 70% basilar membrane length, compared to values of 800 cells per mm near the cochlear apex and base. This region of high ganglion cell density also corresponds to the frequency range of highest auditory sensitivity. RP MULLER, M (reprint author), UNIV FRANKFURT,INST ZOOL,SIESMAYERSTR 70,W-6000 FRANKFURT,GERMANY. CR ALLEN JB, 1988, PHYSL EAR, P243 Bekesy G., 1960, EXPT HEARING BRUNS V, 1988, HEARING RES, V33, P1, DOI 10.1016/0378-5955(88)90017-2 BURDA H, 1989, J MORPHOL, V198, P269 FAY RR, 1988, HEARIZNG VERTEBRATES HEFFNER RS, 1990, HEARING RES, V46, P239, DOI 10.1016/0378-5955(90)90005-A HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 KIANG NYS, 1982, SCIENCE, V217, P175, DOI 10.1126/science.7089553 Konigsmark BW, 1970, CONT RES METHODS NEU, P315 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KRAUS HJ, 1982, VERH DTSCH ZOOL GES, V279 LAY DOUGLAS, 1972, J MORPHOL, V138, P41, DOI 10.1002/jmor.1051380103 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 MULLER M, 1989, NATURWISSENSCHAFTEN, V76, P134, DOI 10.1007/BF00366611 MULLER M, 1990, EXP BRAIN RES, V81, P140 MULLER M, 1991, HEARING RES, V51, P247, DOI 10.1016/0378-5955(91)90041-7 PATTUZI R, 1988, PHYSIOL REV, V68, P1009 PLASSMANN W, 1987, BRAIN BEHAV EVOLUT, V30, P82, DOI 10.1159/000118639 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X SPOENDLIN H, 1979, ACTA OTO-LARYNGOL, V87, P381, DOI 10.3109/00016487909126437 VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 Webster D.B., 1984, CONTRIBUTIONS TO SENSORY PHYSIOLOGY, V8, P161 NR 22 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 NOV PY 1991 VL 56 IS 1-2 BP 191 EP 196 DI 10.1016/0378-5955(91)90169-A PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300023 PM 1769913 ER PT J AU HENRY, KR AF HENRY, KR TI FREQUENCY-SPECIFIC ENHANCEMENT OF THE COCHLEAR COMPOUND ACTION-POTENTIAL - INFLUENCE OF THE FORWARD MASKER SO HEARING RESEARCH LA English DT Article DE ENHANCEMENT; ADAPTATION; MASKING; GERBIL; COMPOUND ACTION POTENTIAL; COCHLEA; 2 TONE SUPPRESSION ID AUDITORY-NERVE FIBERS; MASKING; THRESHOLDS; ADAPTATION; RESPONSES; DURATION; EARS; AP AB Under restricted frequency and intensity conditions, forward masking can result in the amplitude of the CAP being increased above its unmasked value (Henry, 1991). The present study provides a quantitative analysis of this enhancement effect. In response to forward maskers having the same frequency as the probe stimulus, central frequency (CF) enhancement varies as a function of the level of the forward masker: the lowest masker level at which it can reliably be detected is often well below the visual detection threshold of the CAP generated by the unmasked probe stimulus; the highest masker level at which it can reliably be detected corresponds to approximately 10 dB above the probe stimulus CAP threshold. A second low frequency (LF) enhancement region also exists, encompassing a narrow range of more intense maskers. CF enhancement can double the amplitude of the CAP, whereas LF enhancement is less pronounced. The magnitude of CF enhancement varies as a function of the duration of the forward masker, with longer durations generally increasing the magnitude of the effect. This duration effect, however, interacts with the level of the stimulus. Decreasing the interval between the end of the forward masker and the beginning of the probe increases the magnitude of CF enhancement. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR ABBAS PJ, 1981, J ACOUST SOC AM, V69, P492, DOI 10.1121/1.385477 CACACE AT, 1986, HEARING RES, V23, P223, DOI 10.1016/0378-5955(86)90111-5 CARLYON RP, 1989, HEARING RES, V41, P223, DOI 10.1016/0378-5955(89)90014-2 CARLYON RP, 1988, HEARING RES, V32, P65, DOI 10.1016/0378-5955(88)90147-5 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DOLAN DF, 1983, J ACOUST SOC AM, V73, P580, DOI 10.1121/1.389005 EGGERMONT JJ, 1975, BIOL CYBERN, V19, P181, DOI 10.1007/BF00334437 EHMER RH, 1969, J ACOUST SOC AM, V46, P1445, DOI 10.1121/1.1911883 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HENRY KR, 1991, ENHANCEMENT COCHLEAR, V56 JESTEADT W, 1982, J ACOUST SOC AM, V71, P950, DOI 10.1121/1.387576 KEMP DT, 1978, J ACOUST SOC AM, V64, P1384 KIDD G, 1982, J ACOUST SOC AM, V72, P1384, DOI 10.1121/1.388443 Kim D.O., 1985, P241 MARTIN GK, 1990, EAR HEARING, V11, P106 MOORE TJ, 1968, J ACOUST SOC AM, V44, P1390, DOI 10.1121/1.1911274 RELKIN EM, 1988, J ACOUST SOC AM, V84, P584, DOI 10.1121/1.396836 ROSENBLITH RA, 1950, SCIENCE, V111, P569 RUBIN H, 1960, J ACOUST SOC AM, V32, P670, DOI 10.1121/1.1908177 SMITH RL, 1979, J ACOUST SOC AM, V65, P166, DOI 10.1121/1.382260 ZWICKER E, 1984, J ACOUST SOC AM, V75, P219, DOI 10.1121/1.390398 ZWISLOCKI J, 1959, J ACOUST SOC AM, V31, P9, DOI 10.1121/1.1907619 NR 26 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 197 EP 202 DI 10.1016/0378-5955(91)90170-E PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300024 PM 1769914 ER PT J AU LIPPE, WR WESTBROOK, EW RYALS, BM AF LIPPE, WR WESTBROOK, EW RYALS, BM TI HAIR CELL REGENERATION IN THE CHICKEN COCHLEA FOLLOWING AMINOGLYCOSIDE TOXICITY SO HEARING RESEARCH LA English DT Article DE GENTAMICIN; BIRD; HEARING; AUDITORY SYSTEM; BASILAR PAPILLA; COCHLEAR NUCLEUS ID BASILAR PAPILLA; ACOUSTIC TRAUMA; AVIAN COCHLEA; STEREOCILIARY BUNDLES; INTENSE SOUND; INNERVATION; EXPOSURE AB Hair cell loss in the avian cochlea partially recovers following both acoustic trauma and aminoglycoside intoxication. DNA labeling with tritiated thymidine has shown that the restoration of cell number following acoustic trauma results from the production of new hair cells by mitotic division. The purpose of the present study was to determine if mitosis also contributes to the recovery of hair cell number which occurs following aminoglycoside intoxication. Chickens received daily injections of either gentamicin sulfate or distilled water for 10 consecutive days. During the latter 7 days of this period, all birds were also injected with [H-3]thymidine. Following postinjection survival periods of 3 or 6 days, one papilla from each bird was processed for autoradiography and the other for scanning electron microscopy (SEM). Incorporation of [H-3]thymidine was seen over hair cells and support cells in experimental papillae in regions of hair cell loss. No labeling was seen outside of damaged regions or in the papillae of control birds. SEM showed that damaged regions in experimental birds contained cells similar in appearance to developing auditory hair cells in avian embryos. These results show that the restoration of hair cell number following aminoglycoside toxicity results from the production of new cells by mitosis. C1 DEPT VET AFFAIRS MED CTR,SEATTLE,WA. DEPT VET AFFAIRS MED CTR,RICHMOND,VA. RP LIPPE, WR (reprint author), UNIV WASHINGTON,SCH MED,DEPT OTOLARYNGOL,RL-30,SEATTLE,WA 98195, USA. CR BALAK KJ, 1990, J NEUROSCI, V10, P2502 COHEN GM, 1978, ACTA OTO-LARYNGOL, V86, P342, DOI 10.3109/00016487809107513 CORWIN JT, 1988, SCIENCE, V240, P1771 COTANCHE DA, 1987, HEARING RES, V28, P35, DOI 10.1016/0378-5955(87)90151-1 Cotanche D. A., 1986, ASS RES OT ABSTR, V9, P14 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 COUSILLAS H, 1988, HEARING RES, V32, P117, DOI 10.1016/0378-5955(88)90083-4 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 FIRBAS W, 1983, HEARING RES, V10, P109, DOI 10.1016/0378-5955(83)90021-7 GIROD DA, 1990, ASS RES OT ABSTR, V13, P320 GIROD DA, 1989, HEARING RES, V42, P175, DOI 10.1016/0378-5955(89)90143-3 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 HIROKAWA N, 1978, J COMP NEUROL, V181, P361, DOI 10.1002/cne.901810208 JOHNS ME, 1980, ASS RES OT ABSTR, V3, P58 LIPPE WR, 1991, HEARING RES, V51, P193, DOI 10.1016/0378-5955(91)90036-9 LIPPE WR, 1988, ASS RES OT ABSTR, V11, P42 MARSH RR, 1990, HEARING RES, V46, P229, DOI 10.1016/0378-5955(90)90004-9 REBILLARD M, 1983, ACTA OTO-LARYNGOL, V96, P379, DOI 10.3109/00016488309132723 RYALS BM, 1990, HEARING RES, V50, P87, DOI 10.1016/0378-5955(90)90035-N RYALS BM, 1985, HEARING RES, V19, P73, DOI 10.1016/0378-5955(85)90099-1 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 WESTBROOK EW, 1988, ASS RES OT ABSTR, V11, P41 NR 24 TC 82 Z9 87 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 203 EP 210 DI 10.1016/0378-5955(91)90171-5 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300025 PM 1769915 ER PT J AU MANLEY, GA HAESELER, C BRIX, J AF MANLEY, GA HAESELER, C BRIX, J TI INNERVATION PATTERNS AND SPONTANEOUS ACTIVITY OF AFFERENT-FIBERS TO THE LAGENAR MACULA AND APICAL BASILAR PAPILLA OF THE CHICKS COCHLEA SO HEARING RESEARCH LA English DT Article DE CHICK; COCHLEA; LAGENA; AFFERENT FIBERS ID PRIMARY AUDITORY NEURONS; INFRASOUND SENSITIVE NEURONS; SEMICIRCULAR CANALS; VESTIBULAR NERVE; SQUIRREL-MONKEY; PREFERRED INTERVALS; DISCHARGE PATTERNS; SINGLE FIBERS; PIGEON; GANGLION AB To investigate the origin of non-auditory fibres in the apical area of the avian cochlear ganglion, we recorded from nerve fibres in the young chick (87% of animals were aged between 5 and 10 days post-hatching). After characterization of their spontaneous activity patterns and, if present, their responses to sound, some fibres were stained with cobalt-ion injections and traced to their peripheral terminals. All stained fibres which were traced to the lagenar macula (N = 13) were non-auditory. They did not increase firing rate or phase-couple to sound stimuli. Their spontaneous activity was either regular (12 cases) or irregular (1 case). Regularly-firing cells all innervated several to very many hair cells, whereby there was no great difference in the pattern of spontaneous activity between those making calyx endings on relatively few hair cells in the striola region and those making small bouton endings on up to 80 hair cells outside the striola. All fibres that responded in any way to sound were irregularly spontaneously active. Three fibres, two of which only responded to sound with phase-coupling, innervated several hair celts in the apical, abneural region of the basilar papilla. Two other fibres traced to the basilar papilla are of previously undescribed types. RP MANLEY, GA (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,W-8046 GARCHING,GERMANY. 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Foren, V133, P121 JORGENSEN J M, 1973, Acta Zoologica (Stockholm), V54, P121 KOPPL C, 1988, HEARING RES, V32, P111, DOI 10.1016/0378-5955(88)90082-2 KREITHEN ML, 1979, J COMP PHYSIOL, V129, P1 LAVIGNEREBILLARD M, 1985, J COMP NEUROL, V238, P340, DOI 10.1002/cne.902380308 LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LOWENSTEIN O, 1950, J PHYSIOL, V110, P392 MacNAUGHTAN I P J, 1946, J Laryngol Otol, V61, P204, DOI 10.1017/S0022215100007842 MANLEY GA, 1979, NATURWISSENSCHAFTEN, V66, P582, DOI 10.1007/BF00368823 MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1984, NATURWISSENSCHAFTEN, V71, P592, DOI 10.1007/BF01189191 MANLEY GA, 1977, INNER EAR BIOL, P127 MANLEY GA, 1981, PROGR SENSORY PHYSL, V2, P49 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 NARINS PM, 1975, BIOL BULL, V149, P438 OECKINGHAUS H, 1985, J COMP PHYSIOL A, V157, P643, DOI 10.1007/BF01351358 POPPER AN, 1973, J ACOUST SOC AM, V53, P1515, DOI 10.1121/1.1913496 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X ROSENHAL.U, 1970, ARCH KLIN EXP OHR, V197, P154, DOI 10.1007/BF00306164 RYALS BM, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 SACHS MB, 1974, BRAIN RES, V70, P431, DOI 10.1016/0006-8993(74)90253-4 SAIDEL WM, 1990, HEARING RES, V47, P139, DOI 10.1016/0378-5955(90)90171-K SAIDEL WM, 1983, J MORPHOL, V177, P301, DOI 10.1002/jmor.1051770307 SCHERMULY L, 1990, HEARING RES, V48, P69, DOI 10.1016/0378-5955(90)90199-Y SCHERMULY L, 1990, J COMP PHYSIOL A, V166, P355 SCHWARTZKOPFF J, 1963, J PHYSIOL-PARIS, V55, P495 SMITH CA, 1985, FORM FUNCTIONS BIRDS, V3, P273 TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 TEMCHIN AN, 1988, J COMP PHYSIOL A, V163, P99, DOI 10.1007/BF00612001 WALSH BT, 1972, INT J NEUROSCI, V3, P221, DOI 10.3109/00207457209147026 WARCHOL ME, 1989, MIDWINTER M ASS RES, P125 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 NR 51 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 NOV PY 1991 VL 56 IS 1-2 BP 211 EP 226 DI 10.1016/0378-5955(91)90172-6 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300026 PM 1685157 ER PT J AU RUNHAAR, G SCHEDLER, J MANLEY, GA AF RUNHAAR, G SCHEDLER, J MANLEY, GA TI THE POTASSIUM CONCENTRATION IN THE COCHLEAR FLUIDS OF THE EMBRYONIC AND POSTHATCHING CHICK SO HEARING RESEARCH LA English DT Article DE CHICK; ENDOLYMPH; PERILYMPH; ENDOLYMPHATIC POTENTIAL; POTASSIUM CONCENTRATION; ONTOGENY ID TECTORIAL MEMBRANE; TEGMENTUM VASCULOSUM; ENDOLYMPHATIC SPACE; ION CONCENTRATIONS; GUINEA-PIG; INNER-EAR; MATURATION; PERILYMPH; CELLS AB The potassium concentration was measured in the perilymphatic and endolymphatic spaces of the chick's cochlea using ion-specific microelectrodes. The mean values in post-hatching chicks were 8.1 and 161 mM/l, respectively and are thus the same as in mammals. The high potassium concentration is reached at the latest at stage E42, and thus before the tegmentum vasculosum is fully developed. The endocochlear potential of chicks was maximally +13 mV and thus somewhat below the published values for birds. Positive potentials in the endolymphatic space of 5 mV or more were already present in animals of age E41 and E42 and the developmental process is complete at the latest one day after hatching. C1 TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,W-8046 GARCHING,GERMANY. 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A., 1990, PERIPHERAL HEARING M MANLEY GA, 1985, J COMP PHYSIOL A, V157, P161, DOI 10.1007/BF01350025 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 MANLEY GA, 1980, PSYCHOPHYSICAL PHYSL MANLEY GA, 1987, SCIENCE, V237, P655, DOI 10.1126/science.3603046 MORGENSTERN C, 1982, AM J OTOLARYNG, V3, P323, DOI 10.1016/S0196-0709(82)80004-5 NECKER R, 1970, Z VERGL PHYSIOL, V69, P367, DOI 10.1007/BF00333768 PETERSON SK, 1978, J COMP PHYSIOL, V126, P1 RAUCH S, 1974, HDB SENSORY PHYSL, V5, P663 ROSS MD, 1974, AM J ANAT, V139, P449, DOI 10.1002/aja.1001390402 RUNHAAR G, 1989, HEARING RES, V37, P179, DOI 10.1016/0378-5955(89)90039-7 RUNHAAR G, 1987, HEARING RES, V29, P93, DOI 10.1016/0378-5955(87)90207-3 RUSSELL IJ, 1976, J PHYSIOL-LONDON, V257, P245 SAITO N, 1980, STRUCTURE FUNCTION A, P241 SALT AN, 1987, LARYNGOSCOPE, V97, P984 SANTI PA, 1987, HEARING RES, V27, P47, DOI 10.1016/0378-5955(87)90025-6 SCHEIBE F, 1985, HEARING RES, V17, P61, DOI 10.1016/0378-5955(85)90131-5 SCHERMULY L, 1990, HEARING RES, V50, P295, DOI 10.1016/0378-5955(90)90053-R SCHMIDT RS, 1963, COMP BIOCHEM PHYSIOL, V10, P83, DOI 10.1016/0010-406X(63)90105-1 SCHMIDT RS, 1963, J EXP ZOOL, V153, P227, DOI 10.1002/jez.1401530305 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, 1963, J PHYSIOL-PARIS, V55, P495 SELLICK PM, 1974, PFLUG ARCH EUR J PHY, V352, P351, DOI 10.1007/BF00585687 SELLICK PM, 1972, PFLUG ARCH EUR J PHY, V336, P21, DOI 10.1007/BF00589138 SMITH CA, 1954, LARYNGOSCOPE, V64, P141 SMITH CA, 1985, FORM FUNCTIONS BIRDS, V3, P273 STERKERS O, 1982, AM J PHYSIOL, V243, P173 WOOLF NK, 1986, AM J PHYSIOL, V250, pR493 YOSHIHARA T, 1987, ARCH OTO-RHINO-LARYN, V243, P401, DOI 10.1007/BF00464651 NR 61 TC 12 Z9 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 227 EP 238 DI 10.1016/0378-5955(91)90173-7 PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300027 PM 1769916 ER PT J AU HENRY, KR AF HENRY, KR TI ENHANCEMENT OF THE COCHLEAR NERVE COMPOUND ACTION-POTENTIAL - SHARPLY DEFINED FREQUENCY-INTENSITY DOMAINS BORDERING THE TUNING CURVE SO HEARING RESEARCH LA English DT Article DE ENHANCEMENT; ADAPTATION; MASKING; GERBIL; COMPOUND ACTION POTENTIAL; COCHLEA ID AUDITORY BRAIN-STEM; MASKING; THRESHOLDS; RESPONSES; MICE; AP AB Forward masking can either decrease or increase the response to a subsequent stimulus. In the gerbil, frequency-intensity domains of the maskers that decrease the amplitude of the compound action potential (CAP) can be plotted as the sharply defined CAP tuning curve (TC). Regions were also found over which masking increases (enhances) the amplitude of the CAP. Center-frequency (CF) enhancement domains were found in approximately 2/3 of the animals tested, in response to maskers having frequencies very near that of the probe stimulus. at levels ranging from below the CAP detection threshold to just below the tip threshold of the TC. Approximately 2/3 of the animals showing CF enhancement also displayed low-frequency (LF) enhancement, in response to a domain which borders the low-frequency tail of the TC. RP HENRY, KR (reprint author), UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616, USA. CR ABBAS PJ, 1984, J ACOUST SOC AM, V75, P1541, DOI 10.1121/1.390825 ANANTHANARAYAN AK, 1987, ELECTROEN CLIN NEURO, V66, P427 ANANTHANARAYAN AK, 1983, ELECTROEN CLIN NEURO, V55, P223, DOI 10.1016/0013-4694(83)90191-8 CACACE AT, 1986, HEARING RES, V23, P223, DOI 10.1016/0378-5955(86)90111-5 CARLYON RP, 1989, HEARING RES, V41, P223, DOI 10.1016/0378-5955(89)90014-2 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DOLAN DF, 1983, J ACOUST SOC AM, V73, P580, DOI 10.1121/1.389005 GERKEN GM, 1973, ELECTROEN CLIN NEURO, V34, P509, DOI 10.1016/0013-4694(73)90068-0 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HENRY KR, 1989, AUDIOLOGY, V28, P19 HENRY KR, 1991, HEARING RES, V56, P197, DOI 10.1016/0378-5955(91)90170-E HENRY KR, 1985, HEARING RES, V19, P115, DOI 10.1016/0378-5955(85)90115-7 HENRY KR, 1973, J COMP PHYSIOL PSYCH, V84, P430, DOI 10.1037/h0035264 HUGHES JR, 1954, J ACOUST SOC AM, V26, P1064, DOI 10.1121/1.1907450 HUGHES JR, 1957, J ACOUST SOC AM, V29, P275, DOI 10.1121/1.1908854 Kiang N. Y.-S., 1965, MIT RES MONOGRAPH, V35 MOORE TJ, 1970, J ACOUST SOC AM, V47, P534, DOI 10.1121/1.1911925 PIERSON MG, 1982, HEARING RES, V6, P61, DOI 10.1016/0378-5955(82)90007-7 ROSENBLITH RA, 1950, SCIENCE, V111, P569 ROSENBLITH WA, 1950, J ACOUST SOC AM, V22, P792, DOI 10.1121/1.1906691 RUBIN H, 1960, J ACOUST SOC AM, V32, P670, DOI 10.1121/1.1908177 SALVI RJ, 1990, HEARING RES, V50, P245, DOI 10.1016/0378-5955(90)90049-U SAUNDERS JC, 1972, EXP NEUROL, V37, P388, DOI 10.1016/0014-4886(72)90082-9 SIEGEL JH, 1987, HEARING RES, V29, P169, DOI 10.1016/0378-5955(87)90165-1 ZWISLOCKI J, 1959, J ACOUST SOC AM, V31, P9, DOI 10.1121/1.1907619 ZWISLOCK.JJ, 1974, PERCEPT PSYCHOPHYS, V16, P87 NR 27 TC 11 Z9 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 239 EP 245 DI 10.1016/0378-5955(91)90174-8 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300028 PM 1769917 ER PT J AU SNYDER, RL REBSCHER, SJ LEAKE, PA KELLY, K CAO, K AF SNYDER, RL REBSCHER, SJ LEAKE, PA KELLY, K CAO, K TI CHRONIC INTRACOCHLEAR ELECTRICAL-STIMULATION IN THE NEONATALLY DEAFENED CAT .2. TEMPORAL PROPERTIES OF NEURONS IN THE INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE ELECTRICAL STIMULATION; COCHLEAR PROSTHESIS; PLASTICITY; AUDITORY DEVELOPMENT; INFERIOR COLLICULUS ID BINAURAL RESPONSE PROPERTIES; SPATIAL EXCITATION PATTERNS; SINGLE FIBER RECORDINGS; AUDITORY-NERVE FIBERS; UNIT RESPONSES; FREQUENCY NEURONS; COCHLEAR NUCLEUS; RABBIT AB The major focus of this study was to define the effects of chronic intracochlear electrical stimulation (ICES) on single unit responses in the inferior colliculus from three experimental groups: 1) normal adults 2) neonatally-deafened/unstimulated adults; and 3) neonatally-deafened/chronically stimulated adults. The major findings include: 1) IC neurons in normal adults showed a diversity of perstimulus responses to ICES which were qualitatively similar to those evoked by acoustic stimuli. They responded with: an onset burst, a sustained discharge, a decrease in their spontaneous activity, or a strong post-stimulus response. The excitatory responses showed either a monotonic or a nonmonotonic increase in activity with increasing stimulus intensity. Response latencies ranged from 5 to over 40 ms. 2) Responses to ICES in normal and deafened/unstimulated animals were virtually indistinguishable from one another. 3) In contrast, responses to ICES in neonatally deafened stimulated animals were different from normal and from deafened, unstimulated animals. Their perstimulus response latencies were significantly shorter, their late response latencies were significantly longer, and the frequency of occurrence of inhibitory and late responses were significantly higher. From these results we conclude that the responses to intracochlear electrical stimulation are directly comparable to those observed following normal acoustic stimulation: that development of cochleotopic organization of the inferior colliculus is not affected by the almost complete lack of normal acoustic input experienced by neonatally deafened animals; and that the basic response properties of IC units are likewise unaffected by neonatal deafening. Moreover, the results suggest that. although the limited regime of electrical stimulation employed in these studies produced no major qualitative distortions in the perstimulus response patterns of IC neurons, it did result in some quantitative changes in those responses. RP SNYDER, RL (reprint author), UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,COLEMAN & EPSTEIN LAB,871 HSE,SAN FRANCISCO,CA 94143, USA. CR BATRA R, 1989, J NEUROPHYSIOL, V61, P257 BRUGGE JF, 1984, J ACOUST SOC AM, V75, P1548, DOI 10.1121/1.390826 CLOPTON BM, 1984, HEARING RES, V14, P1, DOI 10.1016/0378-5955(84)90063-7 GLASS I, 1983, HEARING RES, V12, P223, DOI 10.1016/0378-5955(83)90108-9 HARTMANN R, 1984, ADV AUDIOL, V1, P18 HARTMANN R, 1987, ANN OTO RHINOL LARYN, V96, P30 HARTMANN R, 1984, HEARING RES, V13, P42 HARTMANN R, 1989, COCHLEAR IMPLANTS MO, P135 HULTCRANTZ M, 1991, HEARING RES, V54, P272, DOI 10.1016/0378-5955(91)90121-O IRVINE DRF, 1990, J NEUROPHYSIOL, V63, P570 JAVEL E, 1989, COCHLEAR IMPLANTS MO, P247 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 KIANG NYS, 1972, ANN OTO RHINOL LARYN, V81, P714 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 KUWADA S, 1989, J NEUROPHYSIOL, V61, P269 LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1982, HEARING RES, V7, P281 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X LEAKE PA, 1990, ARO MIDWINTER RES M, V13, P328 MERZENICH MM, 1973, ANN OTOL, V83, P486 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MOXON ED, 1971, NEURAL MECHANICAL RE PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 REBSCHER S, 1988, 3RD Q PROGR REP Rebscher S. J., 1985, COCHLEAR IMPLANTS, P74 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 ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 SCHMIDT JT, 1985, CELL MOL NEUROBIOL, V5, P5, DOI 10.1007/BF00711083 SCHMIDT JT, 1989, COMMENTS DEV NEUROBI, V1, P1 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SEMPLE MN, 1985, J NEUROPHYSIOL, V53, P1467 SNYDER RL, 1990, ASS RES OTOLARYNGOL, V13, P329 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S 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 VUREK LS, 1981, ANN OTO RHINOL LARYN, V90, P21 WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 NR 40 TC 59 Z9 60 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD NOV PY 1991 VL 56 IS 1-2 BP 246 EP 264 DI 10.1016/0378-5955(91)90175-9 PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300029 PM 1769918 ER PT J AU HATCH, M TSAI, M LAROUERE, MJ NUTTALL, AL MILLER, JM AF HATCH, M TSAI, M LAROUERE, MJ NUTTALL, AL MILLER, JM TI THE EFFECTS OF CARBOGEN, CARBON-DIOXIDE, AND OXYGEN ON NOISE-INDUCED HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; AUDITORY BRAIN-STEM RESPONSE; TEMPORARY THRESHOLD SHIFT; TEMPERATURE ID COCHLEAR BLOOD-FLOW; LASER DOPPLER MEASUREMENTS; INNER-EAR; EXPOSURE; SOUND AB An investigation into the effect of Carbogen (95% O2/5% CO2), 5% CO2/air, and 100% oxygen on cochlear threshold shifts caused by noise was undertaken. Five groups of eight pigmented guinea pigs were exposed to 105 dB broad band noise for 6 h per day for five consecutive days with each group receiving the various gaseous mixtures either during noise exposure or for 1 h immediately after noise exposure. A control group received the same noise exposure but respired air. Auditory threshold shifts, as measured by the auditory evoked brainstem response, were measured at 2,4,8,12,16, 20 and 24 kHz. Recordings were taken pre-exposure and at Day 1, 3, 5, and Weeks 2 and 3 after noise exposure. Carbogen, given during noise exposure, resulted in a trend toward less post noise exposure threshold shift (as compared to controls) which reached statistical significance by Week 3 at all frequencies except 2 and 20 kHz. Subjects given Carbogen after exposure also showed a general trend toward decreased noise induced threshold shifts, as compared to controls, but this was not statistically significant. The mixture of 5% CO2/air given during noise exposure yielded no difference in threshold shifts as compared to controls. When 100% oxygen was administered during noise exposure, a marked decrease in noise induced threshold shifts could be seen as compared to controls, with differences reaching statistical significance by day 5 at most frequencies. These results indicate that oxygen (i.e. cochlear-oxygenation) is a more important factor than CO2 (i.e., as a vasodilator) in protection of the cochlea from noise induced damage. C1 UNIV MICHIGAN,SCH MED,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. CR AXELSSON A, 1982, NEW PERSPECTIVES NOI, P49 BERNDT H, 1981, ARCH OTO-RHINO-LARYN, V232, P199, DOI 10.1007/BF00505038 BROWN JJ, 1985, ACTA OTO-LARYNGOL, V100, P218, DOI 10.3109/00016488509104784 BROWN JJ, 1982, ACTA OTO-LARYNGOL, V93, P319, DOI 10.3109/00016488209130889 FISCH V, 1976, ACTA OTOLARYNGOL STO, V81, P278 HAWKINS JE, 1972, LARYNGOSCOPE, V82, P1901 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HULCRANTZ E, 1987, AM J OTOLARYNG, V8, P16 HULTCRANTZ E, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P271 HULTCRANTZ E, 1980, ARCH OTO-RHINO-LARYN, V228, P211, DOI 10.1007/BF00454230 JOGLEKAR SS, 1977, ARCH OTOLARYNGOL, V103 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P364 KALLINEN J, 1991, HEARING RES, V55, P255, DOI 10.1016/0378-5955(91)90110-U Kellerhals B, 1972, Adv Otorhinolaryngol, V18, P91 LIPSCOMB DM, 1977, ACTA OTO-LARYNGOL, V84, P44, DOI 10.3109/00016487709123941 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 MISRAHY GA, 1958, J ACOUST SOC AM, V30, P701, DOI 10.1121/1.1909734 PRAZMA J, 1983, ARCH OTOLARYNGOL, V109, P611 PRAZMA J, 1978, ANN OTOLARYNGOL, V84, P622 QUIRK WS, 1990, NOISE INDUCED CHANGE QUIRK WS, 1991, INFLUENCE LOUD SOUND QUIRK WS, 1988, HEARING RES, V36, P175, DOI 10.1016/0378-5955(88)90059-7 RYAN AF, 1982, BRAIN RES, V234, P213, DOI 10.1016/0006-8993(82)90863-0 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 THORNE PR, 1989, ACTA OTO-LARYNGOL, V107, P71, DOI 10.3109/00016488909127481 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 VERTES D, 1979, ARCH OTO-RHINO-LARYN, V224, P97, DOI 10.1007/BF00455230 Witter H L, 1980, Am J Otol, V1, P227 WRIGHT JW, 1981, J ACOUST SOC AM, V70, P1353, DOI 10.1121/1.387124 NR 29 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 NOV PY 1991 VL 56 IS 1-2 BP 265 EP 272 DI 10.1016/0378-5955(91)90176-A PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300030 PM 1769919 ER PT J AU KELLY, JB GLENN, SL BEAVER, CJ AF KELLY, JB GLENN, SL BEAVER, CJ TI SOUND FREQUENCY AND BINAURAL RESPONSE PROPERTIES OF SINGLE NEURONS IN RAT INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE AUDITORY MIDBRAIN; INFERIOR COLLICULUS; FREQUENCY RESPONSE; TUNING CURVE; BINAURAL INTERACTION ID INTERAURAL INTENSITY DIFFERENCES; SUPERIOR OLIVARY COMPLEX; MOUSE MUS-MUSCULUS; AUDITORY-CORTEX; ALBINO-RAT; CENTRAL NUCLEUS; TONOTOPIC ORGANIZATION; PRESSURE LEVEL; UNIT RESPONSES; CAT AB Sound frequency and binaural response properties were determined for single neurons in the rat's inferior colliculus. Nerve cell responses in the central nucleus of the inferior colliculus were narrowly tuned and had clearly defined characteristic frequencies (CF). The central nucleus was tonotopically organized with low frequencies represented dorsolaterally and high frequencies ventromedially from 0.87 to 45 kHz. Sharpness of tuning, as indicated by Q10, covered a wide range of values for neurons with the same CF, but the maximum Q10 at each frequency increased monotonically with CF. Maximum Q10s were larger than previously reported for auditory cortex at the same CF. Binaural responses were classified as either suppression, summation or mixed. Most of the units encountered exhibited binaural suppression but there were substantial numbers of both summation and mixed responses. Each major binaural response type was distributed broadly across sound frequencies within the rat's hearing range. Binaural suppression responses were most numerous at high frequencies and summation responses at low frequencies. The binaural response types, their relative proportions and their distribution by CF were similar for neurons in the central nucleus of inferior colliculus and primary auditory cortex of the albino rat. RP KELLY, JB (reprint author), CARLETON UNIV,DEPT PSYCHOL,SENSORY NEUROSCI LAB,OTTAWA K1S 5B6,ONTARIO,CANADA. 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Res. PD NOV PY 1991 VL 56 IS 1-2 BP 273 EP 280 DI 10.1016/0378-5955(91)90177-B PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GR403 UT WOS:A1991GR40300031 PM 1769920 ER PT J AU GUMMER, AW AF GUMMER, AW TI 1ST ORDER TEMPORAL PROPERTIES OF SPONTANEOUS AND TONE-EVOKED ACTIVITY OF AUDITORY AFFERENT NEURONS IN THE COCHLEAR GANGLION OF THE PIGEON SO HEARING RESEARCH LA English DT Article DE QUASI-PERIODIC SPONTANEOUS ACTIVITY; SYNCHRONIZATION INDEX; SPIKE-GENERATOR FUNCTION; ENTROPY; PIGEON; COCHLEAR GANGLION ID NERVE-FIBER RESPONSES; VERTEBRATE HAIR-CELLS; SINGLE-OSSICLE EAR; DISCHARGE PATTERNS; GUINEA-PIG; PTERONOTUS-PARNELLII; PHASE-LOCKING; MUSTACHE BAT; MECHANOELECTRICAL TRANSDUCTION; CHARACTERISTIC FREQUENCY AB Spontaneous and tone-evoked single-unit activity was recorded from afferent neurones in the cochlear ganglion of the anaesthetized pigeon, and the data analysed in a way that allowed the physics of underlying mechanisms to be described. The periodicity of neural activity was quantified by Fourier analysis of the histogram of successive spike intervals. Spontaneous activity was quasiperiodic for 57% of neurones (average rate: 74 s-1); it was irregular for the remainder of neurones (average rate: 55 s-1). The preferred frequency (PF) of the quasiperiodic spontaneous activity was, on average, equal to the characteristic frequency (CF) of the neurone (70% of cases) or CF/2 (30%). This observation can be explained by supposing that preferred intervals of spontaneous activity are generated by noise passing through a filter tuned to the CF of the neurone; in most cases (70%) discharge was synchronized to CF, but in the others the neurone fired to every second cycle of the filtered signal. Consistent with this interpretation, for 79% of neurones, the modal interval of spontaneous activity was, on average, directly proportional to the CF-period, irrespective of whether preferred intervals were detected. The synchronization index at the PF was inversely related to the PF, and was quantified by the amplitude response of a first-order low-pass filter with cutoff frequency of 48 +/- 18 Hz. The spontaneous activity of 9% of neurones exhibited a second-harmonic component of the PF. For both tone-evoked and spontaneous activity, the observed synchronization indices of harmonics of the stimulus frequency or of the PF were consistent with an underlying exponential spike-generator function. If such a function does indeed govern spike generation, then it implies that the Shannon entropy of the probability density function of the instantaneous firing rate is near its maximum value and suggests that the system is close to statistical equilibrium. Single-tone rate-suppression was detected for 53% of those neurones that exhibited multiple preferred intervals of spontaneous activity. It is conjectured that the phenomena of quasiperiodic spontaneous activity and single-tone rate-suppression are different aspects of a single presynaptic process. According to this model, we would expect to find these two phenomena in animals that have auditory fibres innervating electrically tuned hair cells, and that have stereocilia firmly coupled to a tectorial membrane. RP GUMMER, AW (reprint author), AUSTRALIAN NATL UNIV,RES SCH BIOL SCI,DEV NEUROBIOL GRP,CANBERRA,ACT 2601,AUSTRALIA. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 143 EP 166 DI 10.1016/0378-5955(91)90100-N PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200001 PM 1757283 ER PT J AU HILL, KG PALMER, AR AF HILL, KG PALMER, AR TI TIME COURSE OF RATE RESPONSES TO 2-TONE STIMULI IN AUDITORY-NERVE FIBERS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; 2-TONE SUPPRESSION; GUINEA PIG ID BASILAR-MEMBRANE NONLINEARITY; COCHLEAR-NERVE; DISCHARGE PATTERNS; FIBER RESPONSES; RATE-INTENSITY; SUPPRESSION; NOISE; ADAPTATION; SATURATION; BOUNDARIES AB Peri-stimulus time histograms (PSTHs) were constructed from responses of auditory nerve fibres in anaesthetized guinea pigs. Acoustic stimuli consisted of pure tones, presented either as tone bursts, or in two-tone combinations in which a gated test tone was superimposed on a continuous excitatory tone at characteristic frequency (CF). The majority of the sample of fibres displayed two-tone rate suppression (2TRS). The suppression was either a monotonic or a non-monotonic function of the level of the superimposed test tone. Monotonic suppression of CF-driven rate occurred only for test tones at frequencies higher than CF, presented at levels up to the maximum available (approx. 100 dB SPL). For test tones below CF, 2TRS initially increased, then reverted towards excitation for higher levels of the test tone. Three levels were identified in non-monotonic, two-tone rate functions; (1) the threshold for rate suppression, (2) the maximally suppressing level and (3) the level (referred to as the balance point) at which average firing rate was restored to the background, CF-driven rate. PSTHs for two-tone responses obtained for test tone levels between the maximally-suppressing level and the balance point typically showed brief decrements (notches) in spike rate, at the onset and following the offset of the test tone. The latency, depth and duration of notches, however, depended on the level of the test tone, in a different manner for onset and offset. In some cases, without overt rate excitation above the probe-driven rate, the offset notch became more pronounced and of extended duration with increased level of the test tone, suggestive of adaptation to the test tone. Two-tone responses, in which rate exceeded the background, CF-driven rate, in general were preceded by a reduced onset notch and were followed by a longer-lasting depression of the background spike rate, typical of post-excitatory depression. Relative to responses obtained to the test tones presented alone, excitatory two-tone responses were of lower rate and were delayed by the onset notch. Onset notches sometimes preceded rate excitation in responses to single tones. Some features of the time course of rate suppression and excitation displayed in PSTHs for responses to one and two-tone stimuli seem inconsistent with current models of 2TRS. C1 UNIV NOTTINGHAM,MRC,INST HEARING RES,NOTTINGHAM NG7 2RD,ENGLAND. RP HILL, KG (reprint author), AUSTRALIAN NATL UNIV,RES SCH BIOL SCI,DEV NEUROBIOL GRP,GPO BOX 475,CANBERRA,ACT 2601,AUSTRALIA. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 167 EP 176 DI 10.1016/0378-5955(91)90101-E PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200002 PM 1757284 ER PT J AU FAY, RR AF FAY, RR TI MASKING AND SUPPRESSION IN AUDITORY-NERVE FIBERS OF THE GOLDFISH, CARASSIUS-AURATUS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; GOLDFISH; MASKING; SUPPRESSION ID RESPONSES; PATTERNS; NOISE; ADAPTATION AB The responses of single fibers of the auditory nerve of the goldfish (Carassius auratus) were recorded in response to two tones of different duration (20 ms 'signals' and 200 ms 'maskers') presented simultaneously or non-simultaneously. A single tone may produce excitation, adaptation, and suppression in auditory nerve fibers. For fibers with characteristic frequencies (CF) in the 200 to 400 Hz range, frequencies well above CF tend to produce suppression. If the net response to the masker tone is excitation, an added excitatory signal tone tends to increment the response in a way predictable from the rate-level function for the masker. A masker can attenuate the response to a signal as a result of a compressive and saturating response to the masker, and as a result of low signal-to-masker ratio. If the net response to a masker tone is suppression, it effectively subtracts from signal excitation, causing 'suppressive masking.' In non-spontaneous fibers, suppression, additive excitatory effects, and adaptation can be revealed by responses to the signal in the absence of spike responses to the masker. In general, the ability of one tone (the masker) to reduce the response to a second tone (the signal) is greater in non-spontaneous fibers than in spontaneous fibers. These results also show that estimates of the frequency selectivity of many goldfish auditory nerve fibers will depend on whether the response of the fiber is defined by excitation, suppression, or both. The response of many fibers with CF in the 200-400 Hz region, as defined by excitation, can be masked or suppressed by a broad range of frequencies covering the effective hearing range of the goldfish. C1 LOYOLA UNIV,DEPT PSYCHOL,CHICAGO,IL 60626. RP FAY, RR (reprint author), LOYOLA UNIV,PARMLY HEARING INST,6525 N SHERIDAN RD,CHICAGO,IL 60626, USA. CR ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 COOMBS S, 1989, J ACOUST SOC AM, V86, P925, DOI 10.1121/1.398727 Fay R. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 177 EP 187 DI 10.1016/0378-5955(91)90102-F PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200003 PM 1757285 ER PT J AU HENNING, GB AF HENNING, GB TI BINAURAL AMPLITUDE DISCRIMINATION AND THE BINAURAL MASKING-LEVEL DIFFERENCE SO HEARING RESEARCH LA English DT Article DE FREQUENCY CODING; BINAURAL MASKING; AMPLITUDE DISCRIMINATION ID AUDITORY-NERVE FIBERS; INTERAURAL PHASE; FREQUENCY DISCRIMINATION; MODEL; RESPONSES; TONES; NOISE AB Under certain conditions, amplitude discrimination is not a monotonic increasing function of signal-to-noise ratio. The non-monotonicity arises when the tones to be discriminated are presented 180-degrees out-of-phase at the observer's ears and just above their detection 'threshold' in noise that is in-phase at the observer's ears, and with 2-6-dB differences in amplitude. RP HENNING, GB (reprint author), DEPT EXPTL PSYCHOL,S PK RD,OXFORD OX1 3UD,ENGLAND. CR CARNEY LH, 1988, J NEUROPHYSIOL, V60, P1653 Durlach N.I., 1972, F MODERN AUDITORY TH, P371 ERELL A, 1988, J ACOUST SOC AM, V84, P204, DOI 10.1121/1.396966 Goldstein J.L., 1977, PSYCHOPHYSICS PHYSL, P337 HENNING GB, 1990, HEARING RES, V48, P195, DOI 10.1016/0378-5955(90)90059-X HENNING GB, 1990, HEARING RES, V48, P201, DOI 10.1016/0378-5955(90)90060-3 HENNING GB, 1973, J ACOUST SOC AM, V54, P1160, DOI 10.1121/1.1914363 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 Jeffress L.A., 1972, F MODERN AUDITORY TH, VII, P349 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 LIM JS, 1978, J ACOUST SOC AM, V63, P1233, DOI 10.1121/1.381937 LIM JS, 1977, J ACOUST SOC AM, V62, P1256, DOI 10.1121/1.381641 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 VONHELMHOLTZ H, 1863, SENSATIONS TONE ZWICKER E, 1985, HEARING RES, V19, P29, DOI 10.1016/0378-5955(85)90096-6 Zwicker E., 1967, OHR ALS NACHRICHTENE ZWICKER E, 1991, HEARING RES, V50, P141 NR 17 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 OCT PY 1991 VL 55 IS 2 BP 188 EP 194 DI 10.1016/0378-5955(91)90103-G PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200004 PM 1757286 ER PT J AU CAMPO, P SUBRAMANIAM, M HENDERSON, D AF CAMPO, P SUBRAMANIAM, M HENDERSON, D TI THE EFFECT OF CONDITIONING EXPOSURES ON HEARING-LOSS FROM TRAUMATIC EXPOSURE SO HEARING RESEARCH LA English DT Article DE CONDITIONING; SUSCEPTIBILITY; THRESHOLD SHIFT ID AUDIBILITY CURVE; CHINCHILLA; NOISE AB The role of 'conditioning' exposures as moderators of hearing loss produced by exposure to a higher level noise was explored using chinchillas. Monaural chinchillas were exposed to an octave band of noise centered at 0.5 KHz at 95 dB for six hours/day for ten days. The subjects were allowed to recover to pre-exposure sensitivity and at five days after the last exposure they were re-exposed to the same noise at 106 dB. Thresholds recorded at various time intervals following the second exposure were compared with those recorded in a control group exposed only to the higher level noise. The experimental animals were found to have less threshold shift at all stages of recovery. Results are discussed in the light of results of other related studies and possible mechanisms involved are hypothesized. C1 SUNY BUFFALO,DEPT COMMUN DISORDERS & SCI,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214. INST NATL RECH & SECUR,F-54501 VANDOEUVRE NANCY,FRANCE. CR BYRNE C, 1991, UNPUB J ACOUST SOC A CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CHUNG D, 1982, SALVI NEW PERSPECTIV CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 FIORINO F, 1989, VALSALVA S1, V65, P36 HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 KRYTER KD, 1966, J ACOUST SOC AM, V39, P451, DOI 10.1121/1.1909912 LIBERMAN MC, 1990, FEB ASS RES OT ST PE Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 PUEL JL, 1988, HEARING RES, V37, P65, DOI 10.1016/0378-5955(88)90078-0 RAJAN R, 1983, HEARING RES, V9, P279, DOI 10.1016/0378-5955(83)90032-1 Ward W D, 1965, J Occup Med, V7, P595, DOI 10.1097/00043764-196512000-00001 WENTHOLD RJ, 1990, 4 INT C EFF NOIS AUD NR 14 TC 71 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 OCT PY 1991 VL 55 IS 2 BP 195 EP 200 DI 10.1016/0378-5955(91)90104-H PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200005 PM 1757287 ER PT J AU MURATA, K MORIYAMA, T HOSOKAWA, Y MINAMI, S AF MURATA, K MORIYAMA, T HOSOKAWA, Y MINAMI, S TI ALTERNATING-CURRENT INDUCED OTOACOUSTIC EMISSIONS IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE OTOACOUSTIC EMISSION; AC INDUCED OAE; OCB EFFECT ON OAE; FUROSEMIDE; ANOXIA; CARDIAC ARREST ID OUTER HAIR-CELLS; CROSSED OLIVOCOCHLEAR BUNDLE; STIMULATED ACOUSTIC EMISSIONS; COCHLEAR MECHANICS; ELECTRIC STIMULATION; CONTRALATERAL EAR; NERVE-FIBERS; RESPONSES; CAT; FREQUENCY AB Injection of alternating current (AC) into the scala media of the guinea pig cochlea induced otoacoustic emissions (OAEs) at the frequency of the AC fundamental, together with harmonic and intermodulation distortion products. Although the waveform of the injected ACs was distorted, probably due to nonlinear polarization of the metal electrodes, and was composed of the fundamental plus distortion products of every order, only a few of the lowest order distortion products were selectively emitted with the fundamental. AC injection at a basal site extended the high frequency limit of OAEs. Electrical stimulation of the crossed olivocochlear bundle inhibited the sideband emissions with little change in the fundamental. OAE was reduced reversibly by temporary impairment of the cochlea due to exposure to fatiguing sound, by intravenous application of furosemide and by temporary anoxia. Irreversible reduction resulted from intracochlear perfusion with excess K+ solution, acoustic trauma and cardiac arrest. These facts imply that AC-induced OAE is not an artifact generated electrically; rather, such emissions originate in the cochlea and normal metabolic activity in the cochlea is essential. A proposed mechanism of generation includes two components: 1) electromechanical transduction from AC to mechanical vibration in the cochlea and 2) a distortion-producing process; the contribution of each component to the receptor mechanism is discussed. RP MURATA, K (reprint author), TOKYO MED & DENT UNIV,INST MED RES,DEPT NEUROPHYSIOL,2-3-10 KANDASURUGADAI,CHIYODA KU,TOKYO 101,JAPAN. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 201 EP 214 DI 10.1016/0378-5955(91)90105-I PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200006 PM 1757288 ER PT J AU RELKIN, EM DOUCET, JR AF RELKIN, EM DOUCET, JR TI RECOVERY FROM PRIOR STIMULATION .1. RELATIONSHIP TO SPONTANEOUS FIRING RATES OF PRIMARY AUDITORY NEURONS SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; FORWARD MASKING; SPONTANEOUS RATE; ADAPTATION ID COCHLEAR NERVE-FIBERS; MASKING; LEVEL; TONES; CATS; DISCRIMINATION; POPULATION; THRESHOLDS; FREQUENCY AB Recovery of neural thresholds following a forward masker was measured for auditory neurons in anesthetized chinchillas. We find that recovery of forward-masked thresholds is slower for low spontaneous-rate neurons compared to high spontaneous-rate neurons. In addition, we studied the dependence of the shape of PST histograms on the time between repetitions of a tone-burst. We find that for low spontaneous-rate neurons, peak onset responses increase in magnitude over a longer range of interstimulus intervals compared to high spontaneous-rate neurons. Both results are consistent with the conclusion that low spontaneous-rate neurons take longer to recover from prior stimulation compared to high spontaneous-rate neurons. We suggest applications of this finding in psychophysical experiments to investigate the role of low spontaneous-rate neurons in intensity coding. C1 SYRACUSE UNIV,DEPT BIOENGN,SYRACUSE,NY 13210. RP RELKIN, EM (reprint author), SYRACUSE UNIV,INST SENSORY RES,MERRILL LANE,SYRACUSE,NY 13244, USA. CR EVANS EF, 1980, EXP BRAIN RES, V40, P115 FLORENTINE M, 1987, J ACOUST SOC AM, V81, P1528, DOI 10.1121/1.394505 GREENBERG S, 1986, AUDITORY FREQUENCY S, P241 JESTEADT W, 1982, J ACOUST SOC AM, V71, P950, DOI 10.1121/1.387576 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KIM DO, 1990, J ACOUST SOC AM, V87, P1648, DOI 10.1121/1.399412 KIM DO, 1979, J NEUROPHYSIOL, V42, P16 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 RELKIN EM, 1988, J ACOUST SOC AM, V84, P584, DOI 10.1121/1.396836 RELKIN EM, 1991, HEARING RES, V53, P131, DOI 10.1016/0378-5955(91)90220-4 RELKIN EM, 1987, J ACOUST SOC AM, V82, P1679, DOI 10.1121/1.395159 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 SACHS MB, 1988, J PHONETICS, V16, P37 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 Salvi R., 1982, NEW PERSPECTIVES NOI, P165 SALVI RJ, 1986, BASIC APPL ASPECTS N, P179 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 TAYLOR MM, 1967, J ACOUST SOC AM, V41, P782, DOI 10.1121/1.1910407 WIDIN GP, 1986, J ACOUST SOC AM, V80, P108, DOI 10.1121/1.394170 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YOUNG E, 1973, J ACOUST SOC AM, V54, P1535, DOI 10.1121/1.1914451 ZENG FG, 1991, HEARING RES, V55, P223, DOI 10.1016/0378-5955(91)90107-K NR 24 TC 85 Z9 88 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD OCT PY 1991 VL 55 IS 2 BP 215 EP 222 DI 10.1016/0378-5955(91)90106-J PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200007 PM 1757289 ER PT J AU ZENG, FG TURNER, CW RELKIN, EM AF ZENG, FG TURNER, CW RELKIN, EM TI RECOVERY FROM PRIOR STIMULATION .2. EFFECTS UPON INTENSITY DISCRIMINATION SO HEARING RESEARCH LA English DT Article DE INTENSITY DISCRIMINATION; FORWARD-MASKING; AUDITORY NEURONS; SPONTANEOUS RATE ID MODEL INCORPORATING REFRACTORINESS; AUDITORY-NERVE; SIMULTANEOUS MASKING; NOISE; LOUDNESS; FREQUENCY; EXCITATION; SPREAD; LEVEL; TONES AB We obtained just-noticeable differences (jnds) for the intensity of pure tones following a forward masker. The masker was a 100-ms burst of narrow-band noise centered at 1000 Hz presented at 90 dB SPL; the pure-tone signal was at 1000 Hz and was 25 ms in duration. The masker-signal delay was 100 ms. Under these conditions, there is no threshold shift for the detection of the pure-tone signal following the forward masker. In contrast with the absence of a forward-masker effect upon detection thresholds, unusually large midlevel (40-60 dB SPL) jnds were observed. These large midlevel jnds were measured as a function of signal delay, revealing that they are not completely recovered to the normal (unmasked) values by 400 ms. We interpret these data as a consequence of the slower recovery of low-spontaneous rate, high-threshold neurons following prior stimulation (Relkin and Doucet, 1990). These experiments may therefore provide psychophysical evidence that the low-spontaneous rate, high-threshold neurons are a necessary physiological component in the coding of the large dynamic range for intensity. In addition, the present data provide evidence that the assumption that the effect of forward masking is limited to 100-200 ms is inappropriate, as this recovery time does not necessarily apply to suprathreshold tasks. C1 SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 223 EP 230 DI 10.1016/0378-5955(91)90107-K PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200008 PM 1757290 ER PT J AU GUMMER, AW AF GUMMER, AW TI POSTSYNAPTIC INHIBITION CAN EXPLAIN THE CONCENTRATION OF SHORT INTER-SPIKE-INTERVALS IN AVIAN AUDITORY-NERVE FIBERS SO HEARING RESEARCH LA English DT Article DE QUASI-PERIODIC SPONTANEOUS ACTIVITY; POSTSYNAPTIC INHIBITION; PHASE-LOCKING; RECIPROCAL SYNAPSES; PIGEON; COCHLEAR GANGLION ID OUTER HAIR-CELLS; RECIPROCAL SYNAPSES; COCHLEAR NERVE; ORGAN; CORTI; PATTERNS; FIBERS; NOISE; TRAIN AB Spontaneous and sound-evoked single-unit activity was recorded from afferent neurones in the cochlear ganglion of the anaesthetized pigeon. The histogram of successive intervals of spontaneous activity of 51% of neurones exhibited more short intervals than expected from a Poisson point-process description of spike times; for another 43% of neurones the point-process was Poisson. A model of spike generation was developed to account for the concentration of short spike-intervals. The proposed model contains inhibitory postsynaptic potentials at the afferent dendrite, in addition to the excitatory postsynaptic potentials. Not only does the model reproduce the first-order interval statistics of neural activity, but it provides a mechanism for improving phase-locking to the fundamental frequency of a sinusoid, and also offers an explanation for the presence of reciprocal synapses in the human cochlea. RP GUMMER, AW (reprint author), AUSTRALIAN NATL UNIV,RES SCH BIOL SCI,NEUROBIOL GRP,CANBERRA,ACT 2601,AUSTRALIA. CR Abramowitz M., 1965, HDB MATH FUNCTIONS Bailey N. T. 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PD OCT PY 1991 VL 55 IS 2 BP 231 EP 243 DI 10.1016/0378-5955(91)90108-L PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200009 PM 1757291 ER PT J AU PICKLES, JO ROUSE, GW AF PICKLES, JO ROUSE, GW TI EFFECTS OF STREPTOMYCIN ON DEVELOPMENT OF THE APICAL STRUCTURES OF HAIR-CELLS IN THE CHICK BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE HAIR CELL; STREPTOMYCIN; DEVELOPMENT; STEREOCILIA; AMINOGLYCOSIDE ANTIBIOTICS; CRITICAL PERIOD; CHICK ID AUDITORY EVOKED-RESPONSES; GUINEA-PIG; ACTIN-FILAMENTS; BIRD COCHLEA; RAT COCHLEA; OTOTOXICITY; KANAMYCIN; STEREOCILIA; TRANSDUCTION; ANTIBIOTICS AB A single dose of streptomycin (166 mg/kg egg weight) was given to chick embryos 7-15 days after the beginning of incubation. Embryos were fixed 4-12 days later, and the hair cells examined by scanning and transmission electron microscopy. The highest proportion of abnormalities was produced by injections on or before the 11th day of incubation, later injections affecting a substantially smaller proportion of embryos. This suggests the possibility of a critical period for streptomycin ototoxicity in the chick. In addition to the normal signs of cellular degeneration, the most striking abnormality was a massive expansion in the apical surface, sometimes by a factor of 20, in area. The organisation of stereocilia was also commonly affected. The stereocilia could be broken up into multiple small separate bundles, and often there was a wide separation between the kinocilium and the stereocilia. Stereocilia tended to be reduced in number, fused, and either of abnormally large, small, or irregular diameters. Structures with the appearance of stereociliar cores often lay horizontally within the surface of the cuticular plate, sometimes running for 15-mu-m or more. Sometimes abnormal 'stereocilia' were expressed around the extreme margins of the cuticular plate. In addition, adjacent hair cells could show very different developmental stages, as though the development of some cells had been arrested. With all these changes, the short hair cells in the centre of a papillar cross-section tended to be the most affected, with the tall hair cells and the short hair cells on the extreme inferior (i.e. abneural) edge being least affected. It is suggested that the streptomycin alters the balance of the different aspects of development of the hair cells. It might therefore be possible to use ototoxicity as a way of analysing hair-cell development. C1 UNIV QUEENSLAND,UIS TOUCH & HEARING RES CTR,DEPT PHYSIOL & PHARMACOL,ST LUCIA,QLD 4067,AUSTRALIA. RP PICKLES, JO (reprint author), UNIV BIRMINGHAM,SCH MED,SCH BASIC MED SCI,DEPT PHYSIOL,BIRMINGHAM B15 2TJ,W MIDLANDS,ENGLAND. RI Rouse, Greg/F-2611-2010 CR BARTOLAMI S, 1990, HEARING RES, V47, P229, DOI 10.1016/0378-5955(90)90154-H BERNARD PA, 1981, LARYNGOSCOPE, V91, P1985 CARLIER E, 1980, ARCH OTO-RHINO-LARYN, V226, P129, DOI 10.1007/BF00455127 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DUCKERT LG, 1990, HEARING RES, V48, P161, DOI 10.1016/0378-5955(90)90206-5 DUMAS G, 1982, ACTA OTO-LARYNGOL, V94, P203, DOI 10.3109/00016488209128906 FERMIN CD, 1983, AM J OTOLARYNG, V4, P174, DOI 10.1016/S0196-0709(83)80040-4 HAMBURGER V, 1951, J MORPHOL, V88, P49, DOI 10.1002/jmor.1050880104 HASH JH, 1972, ANNU REV PHARMACOLOG, V12, P35, DOI 10.1146/annurev.pa.12.040172.000343 HENRY KR, 1981, ARCH OTOLARYNGOL, V107, P92 JANMEY PA, 1989, J BIOL CHEM, V264, P4825 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LASSING I, 1985, NATURE, V314, P472, DOI 10.1038/314472a0 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 OSAKO S, 1979, ACTA OTO-LARYNGOL, V88, P359, DOI 10.3109/00016487909137180 PARK JC, 1984, AM J OTOLARYNG, V5, P387, DOI 10.1016/S0196-0709(84)80053-8 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 RAPHAEL Y, 1983, ARCH OTO-RHINO-LARYN, V238, P45, DOI 10.1007/BF00453740 SANDERS WE, 1979, ANNU REV PHARMACOL, V19, P53, DOI 10.1146/annurev.pa.19.040179.000413 SAUNDERS JC, 1973, BRAIN RES, V63, P59, DOI 10.1016/0006-8993(73)90076-0 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X Smith C.A., 1971, Contributions sens Physiol, V5, P129 SOMEYA A, 1979, J ANTIBIOT, V32, P156 STOCKHORST E, 1977, ACTA OTO-LARYNGOL, V83, P401, DOI 10.3109/00016487709128864 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 UZIEL A, 1979, HEARING RES, V1, P203, DOI 10.1016/0378-5955(79)90014-5 WHITEHEAD MC, 1985, NEUROSCIENCE, V14, P255, DOI 10.1016/0306-4522(85)90177-0 YU FX, 1990, SCIENCE, V250, P1413, DOI 10.1126/science.2255912 NR 30 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 1991 VL 55 IS 2 BP 244 EP 254 DI 10.1016/0378-5955(91)90109-M PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200010 PM 1757292 ER PT J AU KALLINEN, J DIDIER, A MILLER, JM NUTTALL, A GRENMAN, R AF KALLINEN, J DIDIER, A MILLER, JM NUTTALL, A GRENMAN, R TI THE EFFECT OF CO2-GAS AND O2-GAS MIXTURES ON LASER DOPPLER MEASURED COCHLEAR AND SKIN BLOOD-FLOW IN GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE CO2; O2; COCHLEA BLOOD FLOW; SKIN BLOOD FLOW; BLOOD GASES; GUINEA PIG ID CARBON-DIOXIDE; SUDDEN DEAFNESS; TENSION; CO2; HYPERCAPNIA; RESPONSES; FLOWMETRY; RATS AB The effects of carbogen (5% CO2:95% O2) 10% CO2-in-air and 100% O2 on cochlear blood flow (CBF), skin blood flow (SBP), blood pressure (BP) and arterial blood gases were investigated in the anesthetized, respired or self-respiring guinea pig. In respired animals, CBF and SBF were increased with carbogen and 10% CO2-in-air and decreased with O2. BP was elevated with each gas. In freely bearing animals, only 10% CO2-in-air caused a small increse in CBF; both carbogen and O2 caused CBF to decrease. SPF changes were similar in form, but larger than those seen in respirated subjects. No consistant change in BP was seen during breathing of these mixtures. Arterial PO2 was increased by carbogen and 10% CO2-in-air for both groups. PCO2 increased for both CO2 gas mixtures during forced respiration; but in free-breathing animals PCO2 only increased for 10% CO2-in-air (normal PCO2 values were maintained with carbogen thorough increased breathing rate). The observed changes in CBF were consistant with a balance between a combined vasoconstrictive effect of PO2 and vasodilation effect of PCO2 on cochlear vessels. Analysis of cochlear vascular conductivity (CBF/BP) indicated that vasodilation was significant only with 10% CO2-in-air in respirated animals. In all other conditions the increased CBF apparently reflects the increase profusion pressure associated with respiration of each gas. For clinical purposes, while carbogen does not appear to directly cause vasodilation of cochlear vessels it does lead to an increased oxygenation of the cochlea blood and would appear to avoid the cochlear vasoconstriction caused by 100% O2. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. UNIV TURKU,CENT HOSP,DEPT OTOLARYNGOL,SF-20500 TURKU 50,FINLAND. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 255 EP 262 DI 10.1016/0378-5955(91)90110-U PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200011 PM 1757293 ER PT J AU SUGIYAMA, S SPICER, SS MUNYER, PD SCHULTE, BA AF SUGIYAMA, S SPICER, SS MUNYER, PD SCHULTE, BA TI HISTOCHEMICAL ANALYSIS OF GLYCOCONJUGATES IN GELATINOUS MEMBRANES OF THE GERBILS INNER-EAR SO HEARING RESEARCH LA English DT Article DE COCHLEA; EAR; GERBIL; TECTORIAL MEMBRANE; CUPULA; OTOLITHIC MEMBRANE; LECTIN HISTOCHEMISTRY ID WHEAT-GERM-AGGLUTININ; LIGHT MICROSCOPIC DETECTION; ANIONIC SULFATE GROUPS; COCHLEAR HAIR-CELLS; VICIA-VILLOSA SEEDS; TECTORIAL MEMBRANE; CARBOHYDRATE-BINDING; STRUCTURAL DETERMINANTS; DOLICHOS-BIFLORUS; COMBINING SITES AB The gelatnous membranes of the gerbil inner ear were analyzed histochemically for glycoconjugates with a battery of twenty horseradish peroxidase-conjugated lectins. Glycoconjugates with mannose (Man) and/or glucose (Glc), galactose (Gal), fucose (Fuc), N-acetylglucosamine (GlcNAc), N-acetylgalactosamine (GalNAc) and N-acetylneuraminic acid (NeuAc) were detected in the tectorial and otolithic membranes and cupula. Differences in lectin reactivity were observed between tectorial and vestibular membranes and also among zones and between the medial and lateral regions of the middle zone of the tectorial membrane. The distribution of staining differed markedly for several lectins that bind specifically to GalNAc or to GlcNAc but vary in affinity for oligosaccharides containing these sugars in different sequences or linkages. The findings suggest presence of the terminal disaccharides GalNAc-alpha-1,3Gal in tectrial membrane and Gal-beta-1,3GalNAc in vestibular membranes. Lectin binding profiles provided evidence that the limbal zone's fibrous and attachment layers contain mainly O-glycosidically linked oligosaccharides whereas the middle zone's medial fibrous layer contains both O- and N-linked chains. The remaining regions of the tectorial membrane contain mainly N-linked oligosaccharides with bisected biantennary type chains predominating. Additionally, the marginal band and the middle zone's basal layer contain abundant N-linked oligosaccharides with a triantennary structure. RP SUGIYAMA, S (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. 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Res. PD OCT PY 1991 VL 55 IS 2 BP 263 EP 272 DI 10.1016/0378-5955(91)90111-L PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GK072 UT WOS:A1991GK07200012 PM 1757294 ER PT J AU MCLAREN, GM COLEMAN, JKM QUIRK, WS DENGERINK, HA WRIGHT, JW AF MCLAREN, GM COLEMAN, JKM QUIRK, WS DENGERINK, HA WRIGHT, JW TI THE INFLUENCE OF INTRAARTERIAL INFUSION OF ARGININE VASOPRESSIN ON COCHLEAR BLOOD-FLOW IN THE RAT SO HEARING RESEARCH LA English DT Article DE COCHLEAR BLOOD FLOW; COCHLEA; BLOOD PRESSURE; ARGININE VASOPRESSIN; AUTOREGULATION; LASER DOPPLER FLOWMETER ID LASER DOPPLER; AUTO-REGULATION; ADRENERGIC-INNERVATION; GUINEA-PIG; ANGIOTENSIN; SYSTEM AB Intra-arterially infused arginine vasopressin (AVP) elevated systemic blood pressure (BP) in the Sprague-Dawley rat according to a dose-response pattern while cochlear blood flow (CoBF), as measured by laser Doppler flowmetry, was elevated only at the highest dose. Skin blood flow (SBF) decreased significantly with AVP infusion. The local infusion of AVP into the anterior inferior cerebellar artery (AICA), which supplies the common cochlear artery, produced significant dose-dependent reductions in CoBF with no changes in systemic blood pressure. Pretreatment of the local cochlear supplying vessels with an AVP-specific V1 receptor antagonist attenuated subsequent AVP-induced decreases in CoBF, thereby demonstrating specificity of the response. These results suggest that CoBF is reasonably stable in response to systemic AVP infusion until blood pressure exceeds an elevation from base level of approximately +60 mm Hg. One of the mechanisms responsible for this autoregulatory response may be vasoconstriction mediated by the interaction of vasoactive peptides such as AVP and its receptors located in the vasculature of the inner ear or in the more peripheral vessels directly supplying the cochlea. C1 WASHINGTON STATE UNIV,DEPT PSYCHOL,PULLMAN,WA 99164. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR Axelsson A, 1988, PHYSL EAR, P295 AXELSSON A, 1978, ACTA OTO-LARYNGOL, V85, P198, DOI 10.3109/00016487809111927 BAUMBACH GL, 1985, ANN BIOMED ENG, V13, P303, DOI 10.1007/BF02584248 Bayliss WM, 1902, J PHYSIOL-LONDON, V28, P220 BONJOUR J, 1976, AM J PHYSIOL, V218, P1555 BRECHTELSBAUER PB, 1990, ASS RES OT ABSTR, V13, P359 CARLISLE L, 1990, HEARING RES, V43, P107, DOI 10.1016/0378-5955(90)90219-F COLEMAN JKM, 1991, UNPUB SAR1 ILE8 AII COOK VI, 1991, UNPUB PERINATAL COMP DENGERINK HA, 1986, BASIC APPLIED ASPECT, P559 DENGERINK HA, 1985, HEARING RES, V20, P31, DOI 10.1016/0378-5955(85)90056-5 DENGERINK HA, 1987, ACTA OTO-LARYNGOL, V104, P113, DOI 10.3109/00016488709109055 DENSERT O, 1974, ACTA OTO-LARYNGOL, V77, P185, DOI 10.3109/00016487409124616 DENSERT O, 1974, ACTA OTO-LARYNGOL, V78, P345, DOI 10.3109/00016487409126365 FLYNN AJ, 1988, HEARING RES, V34, P201, DOI 10.1016/0378-5955(88)90108-6 GOODWIN PC, 1984, ACTA OTO-LARYNGOL, V98, P403, DOI 10.3109/00016488409107581 HULTCRANTZ E, 1982, ARCH OTO-RHINO-LARYN, V234, P151, DOI 10.1007/BF00453622 JOHNSON PC, 1986, CIRC RES, V59, P483 KEIL LC, 1984, BRAIN RES, V297, P329, DOI 10.1016/0006-8993(84)90574-2 KRUZYNSKI M, 1980, J MED CHEM, V23, P364 LAROUERE MJ, 1989, OTOLARYNG HEAD NECK, V101, P375 LAWRENCE M, 1977, ACTA OTO-LARYNGOL, V83, P146, DOI 10.3109/00016487709128825 Lorente de No R., 1937, LARYNGOSCOPE, V47, P373 MATSUYAMA T, 1986, BRAIN BLOOD PRESSURE, P427 Miller J M, 1986, Scand Audiol Suppl, V26, P11 MILLER JM, 1988, AM J OTOLARYNG, V9, P302, DOI 10.1016/S0196-0709(88)80038-3 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 MILLER JM, 1984, ARCH OTOLARYNGOL, V110, P305 PHILLIPS MI, 1979, FED PROC, V38, P2260 PHILLIPS MI, 1987, ANNU REV PHYSIOL, V49, P413, DOI 10.1146/annurev.physiol.49.1.413 PRAZMA J, 1990, FEB ARO MIDW M PET QUIRK WS, 1989, HEARING RES, V41, P53, DOI 10.1016/0378-5955(89)90178-0 QUIRK WS, 1988, HEARING RES, V32, P129 RYAN AF, 1988, PHYSL EAR, P317 RYAN AF, 1988, ACTA OTO-LARYNGOL, V105, P232, DOI 10.3109/00016488809097003 SHORT SO, 1985, OTOLARYNG HEAD NECK, V93, P786 SLADECK CD, 1979, ENDOCRINOLOGY, V41, P148 SMITH CA, 1951, LARYNGOSCOPE, V61, P1073 SNOW JB, 1971, ARCH OTOLARYNGOL, V97, P365 Spoendlin H, 1966, Acta Otolaryngol, V61, P423 WRIGHT JW, 1985, HEARING RES, V17, P41, DOI 10.1016/0378-5955(85)90128-5 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 SEP PY 1991 VL 55 IS 1 BP 1 EP 8 DI 10.1016/0378-5955(91)90086-O PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900001 PM 1752789 ER PT J AU MOLLER, AR JHO, HD AF MOLLER, AR JHO, HD TI EFFECT OF HIGH-FREQUENCY HEARING-LOSS ON COMPOUND ACTION-POTENTIALS RECORDED FROM THE INTRACRANIAL PORTION OF THE HUMAN 8TH NERVE SO HEARING RESEARCH LA English DT Article DE HUMAN AUDITORY NERVE; COMPOUND ACTION POTENTIALS; INTRAOPERATIVE RECORDINGS; ACTIVE COCHLEAR PROCESSES ID HUMAN AUDITORY-NERVE; STEM EVOKED-POTENTIALS; BRAIN-STEM; 8TH NERVE; MICROVASCULAR DECOMPRESSION; RESPONSES AB Compound action potentials (CAP) were recorded from the exposed intracranial portion of the eighth nerve to stimulation with click sounds in patients with sensorineural high-frequency hearing loss who underwent microvascular decompression (MVD) operations to treat trigeminal neuralgia (TN). In patients with normal hearing the CAP recorded in that way is characterized by a negative peak, preceded by a small positivity and followed by a positivity and sometimes a second negative peak. In patients with high-frequency hearing loss the CAP also usually had an initial sharp negative peak in response to clicks of high intensity (105 to 110 dB Pe SPL), similar to findings in patients with normal hearing, but in patients with high-frequency hearing loss the initial negative peak was often followed by a slow negative deflection. The latency of the initial negative peak in the CAP in patients with high-frequency hearing loss was longer than the latency of this peak in patients with normal hearing, but the difference in latencies of this peak to condensation and rarefaction clicks was small. When the stimulus intensity was lowered the amplitude of the initial peak decreased, and the CAP became dominated by a broad negative peak with a latency of 6 to 8 ms. In 11 of 15 patients with severe high-frequency hearing loss, a series of quasiperiodic waves was superimposed on the CAP. The frequency of these waves varied between 500 and 1200 Hz, and the waves could be detected between 6 and 16 ms after presentation of the click stimulus. These waves were usually present in the response to stimuli in the intensity range from 75 to 110 dB Pe SPL. Only 4 of 17 patients with normal hearing had similar waves. C1 UNIV PITTSBURGH,SCH MED,DEPT NEUROL SURG,PITTSBURGH,PA 15261. CR Blackman R.B., 1959, MEASUREMENT POWER SP COATS AC, 1977, ARCH OTOLARYNGOL, V103, P605 ELBERLING C, 1974, SCAND AUDIOL, V3, P13, DOI 10.3109/01050397409044959 Goldstein M.H. Jr., 1960, Information and Control, V3, DOI 10.1016/S0019-9958(60)90212-6 HASHIMOTO I, 1981, BRAIN, V104, P841, DOI 10.1093/brain/104.4.841 HAWKINS JE, 1976, EFFECTS NOISE HEARIN, P91 JANNETTA PJ, 1981, CRANIAL NERVES, P1 Jannetta PJ, 1981, CRANIAL NERVES, P331 JANNETTA PJ, 1977, NEUROCHIRURGIA, V20, P145 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 Lang J., 1983, CLIN ANATOMY HEAD NE LANG J, 1981, CRANIAL NERVES, P363 LAZORTHES G, 1961, PRESSE MED, V69, P1067 MOLLER AR, 1983, HEARING RES, V11, P267, DOI 10.1016/0378-5955(83)90062-X MOLLER AR, 1989, NEUROSURGERY, V24, P257 MOLLER AR, 1988, ELECTROEN CLIN NEURO, V71, P198, DOI 10.1016/0168-5597(88)90005-6 MOLLER AR, 1975, J NEUROPHYSIOL, V38, P812 MOLLER AR, 1988, HEARING RES, V37, P47, DOI 10.1016/0378-5955(88)90076-7 MOLLER AR, 1981, ELECTROEN CLIN NEURO, V52, P18, DOI 10.1016/0013-4694(81)90184-X MOLLER AR, 1989, HEARING RES, V42, P237, DOI 10.1016/0378-5955(89)90148-2 MOLLER AR, 1988, EVOKED POTENTIALS IN MOLLER AR, 1981, ANN OTO RHINOL LARYN, V90, P591 MOLLER AR, 1989, HEARING RES, V38, P163, DOI 10.1016/0378-5955(89)90137-8 MOLLER AR, 1983, J NEUROSURG, V59, P493, DOI 10.3171/jns.1983.59.3.0493 MOLLER AR, 1990, HEARING RES, V45, P75, DOI 10.1016/0378-5955(90)90184-Q MOLLER AR, 1991, IN PRESS AUDIOLOGY MOLLER AR, 1991, IN PRESS ANN OTOLRHI MOLLER MB, 1985, AUDIOLOGY, V24, P396 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 TEAS DONALD C, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1438, DOI 10.1121/1.1918366 NR 30 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 9 EP 23 DI 10.1016/0378-5955(91)90087-P PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900002 PM 1752798 ER PT J AU KIPKE, DR CLOPTON, BM ANDERSON, DJ AF KIPKE, DR CLOPTON, BM ANDERSON, DJ TI SHARED-STIMULUS DRIVING AND CONNECTIVITY IN GROUPS OF NEURONS IN THE DORSAL COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE MULTIUNIT RECORDING; DCN; THIN-FILM ELECTRODE; NEURAL NETWORKS; NOISE CHARACTERIZATION ID CROSS-CORRELATION ANALYSIS; RESPONSE PROPERTIES; INHIBITORY INTERACTIONS; SPIKE TRAINS; CAT; REPRESENTATION; UNITS; CELLS; IDENTIFICATION; DISTRIBUTIONS AB Extracellular spike discharges were recorded from ensembles of up to five neurons simultaneously in the DCN of guinea pig using solid-state, thin-film, multichannel electrodes having up to five recording sites spanning up to 600 microns. Responses from 73 unit pairs were collected of which 54 had both units responding to pseudorandom wideband noise stimulation. Shared-stimulus driving was present in 78% (42/54) of the unit pairs and could be attributed to an overlap in their spectral sensitivities. Effective connectivity was indicated for 87% (47/54) of the unit pairs. Wideband noise proved more useful than tonebursts for investigating shared-stimulus driving and connectivity because it evoked widespread, but not overly synchronous, responses in the ensembles. C1 UNIV MICHIGAN,GRAD PROGRAM BIOENGN,ANN ARBOR,MI 48109. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT ELECT ENGN & COMP SCI,ANN ARBOR,MI 48109. CR ABELES M, 1982, J NEUROSCI METH, V5, P317, DOI 10.1016/0165-0270(82)90002-4 AERTSEN AMHJ, 1989, J NEUROPHYSIOL, V61, P900 BACKOFF PM, 1991, HEARING RES, V53, P28, DOI 10.1016/0378-5955(91)90211-Q BEMENT SL, 1986, IEEE T BIO-MED ENG, V33, P230, DOI 10.1109/TBME.1986.325895 BI Q, 1989, J ACOUST SOC AM, V85, P2504, DOI 10.1121/1.397745 Bourk TR, 1976, THESIS MIT CAMBRIDGE BOURK TR, 1981, HEARING RES, V4, P215, DOI 10.1016/0378-5955(81)90008-3 BRILLINGER DR, 1988, BIOL CYBERN, V59, P189, DOI 10.1007/BF00318010 CHORNOBOY ES, 1988, BIOL CYBERN, V59, P265, DOI 10.1007/BF00332915 CLOPTON BM, 1991, HEARING RES, V52, P329, DOI 10.1016/0378-5955(91)90023-3 COHEN L, 1989, P IEEE, V77, P941, DOI 10.1109/5.30749 DRAKE KL, 1988, IEEE T BIO-MED ENG, V35, P719, DOI 10.1109/10.7273 EDWARDS B, 1991, UNPUB CONFIDENCE INT EDWARDS BW, 1990, BIOL CYBERN, V64, P145, DOI 10.1007/BF02331344 EGGERMONT JJ, 1983, Q REV BIOPHYS, V16, P341 EGGERMONT JJ, 1990, J ACOUST SOC AM, V87, P246, DOI 10.1121/1.399291 EPPING WJM, 1987, J NEUROPHYSIOL, V57, P1464 EVANS EF, 1973, EXP BRAIN RES, V17, P428 GERSTEIN GL, 1985, J NEUROPHYSIOL, V54, P1513 GERSTEIN GL, 1972, BIOPHYS J, V12, P453 GERSTEIN GL, 1989, IEEE T BIO-MED ENG, V36, P4, DOI 10.1109/10.16444 GOCHIN PM, 1989, BRAIN RES, V497, P1, DOI 10.1016/0006-8993(89)90963-3 HACKNEY CM, 1990, ANAT EMBRYOL, V182, P123 JOHNSON DH, 1983, J ACOUST SOC AM, V74, P493, DOI 10.1121/1.389815 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S MELSSEN WJ, 1987, BIOL CYBERN, V57, P403, DOI 10.1007/BF00354985 MOORE JK, 1986, NEUROBIOLOGY HEARING, P283 MOORE JK, 1989, UNPUB J COMP NEUROL NAJAFI K, 1990, IEEE T BIO-MED ENG, V37, P1, DOI 10.1109/10.43605 NAJAFI K, 1985, IEEE T ELECTRON DEV, V32, P1206, DOI 10.1109/T-ED.1985.22102 NAJAFI K, 1990, IN PRESS IEEE T BIOM PALM G, 1988, BIOL CYBERN, V59, P1, DOI 10.1007/BF00336885 PERKEL DH, 1967, BIOPHYS J, V7, P419 PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 RHODE WS, 1983, J COMP NEUROL, V213, P426, DOI 10.1002/cne.902130407 RIHACZEK AW, 1968, IEEE T INFORM THEORY, V14, P369, DOI 10.1109/TIT.1968.1054157 RYAN AF, 1988, HEARING RES, V36, P181, DOI 10.1016/0378-5955(88)90060-3 SCHNEIDER J, 1983, BIOL CYBERN, V46, P129, DOI 10.1007/BF00339981 SMITH PH, 1985, J COMP NEUROL, V237, P127, DOI 10.1002/cne.902370110 VOIGT HF, 1988, J NEUROPHYSIOL, V59, P1014 VOIGT HF, 1980, J NEUROPHYSIOL, V44, P76 VOIGT HF, 1990, J NEUROPHYSIOL, V64, P1590 WISE KD, 1990, PASSIVE MULTICHANNEL YOUNG ED, 1982, HEARING RES, V6, P153, DOI 10.1016/0378-5955(82)90051-X YOUNG ED, 1988, AUDITORY FUNCTION YOUNG ED, 1984, HEARING SCI YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 YOUNG ED, 1980, BRAIN RES, V200, P23, DOI 10.1016/0006-8993(80)91091-4 NR 48 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 24 EP 38 DI 10.1016/0378-5955(91)90088-Q PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900003 PM 1752791 ER PT J AU KELLY, JB PHILLIPS, DP AF KELLY, JB PHILLIPS, DP TI CODING OF INTERAURAL TIME DIFFERENCES OF TRANSIENTS IN AUDITORY-CORTEX OF RATTUS-NORVEGICUS - IMPLICATIONS FOR THE EVOLUTION OF MAMMALIAN SOUND LOCALIZATION SO HEARING RESEARCH LA English DT Article DE SOUND LOCALIZATION; AUDITORY CORTEX; RAT; EVOLUTION; INTERAURAL TIME DIFFERENCE ID INFERIOR COLLICULUS; ALBINO-RAT; BINAURAL STIMULATION; NEURONS; CAT; FREQUENCY; RESPONSES; INTENSITY; NEUROPHYSIOLOGY; ORGANIZATION AB We obtained quantitative evidence on the coding of interaural time differences (ITDs) of click stimuli by 40 single neurons in the auditory cortex of anesthetized albino rats. Most of the neurons (31/40) received an excitatory input from the contralateral ear, and an inhibitory input from the ipsilateral ear (EI cells). These neurons expressed their sensitivity to ITDs in a sigmoidal relation between spike count and ITD, with maximal responses associated with contralateral-leading ITDs. The mean ITD dynamic range was 590-mu-s. The dynamic ranges typically encompassed at least part of the behaviorally-relevant range (about +/- 130-mu-s). Variations in ITD from 130-mu-s favoring one ear to 130-mu-s favoring the other ear caused spike response rate changes, on average, of 29.5%. These data are similar to those previously presented for the central auditory systems of larger mammals, whose auditory localization acuity is significantly better than that of the rat. We argue, therefore, that the sound localization mechanisms based on transient ITDs have not evolved in a fashion that covaries with interaural distance, and that there exists a mismatch between the ITDs the rat will encounter in the free field, and the ITDs which are encoded by its nervous system. This may be one reason why sound localization acuity has a roughly inverse relation to interaural distance. C1 DALHOUSIE UNIV,DEPT PSYCHOL,HALIFAX B3H 4J1,NS,CANADA. DALHOUSIE UNIV,DEPT OTOLARYNGOL,HALIFAX B3H 4J1,NS,CANADA. CARLETON UNIV,DEPT PSYCHOL,OTTAWA K1S 5B6,ONTARIO,CANADA. RI Phillips, Dennis/A-6496-2011 CR BENSON DA, 1976, BRAIN RES, V103, P313, DOI 10.1016/0006-8993(76)90801-5 BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 CAIRD D, 1987, EXP BRAIN RES, V68, P379 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 HEFFNER HE, 1985, HEARING RES, V19, P151, DOI 10.1016/0378-5955(85)90119-4 HEFFNER RS, 1988, J COMP PSYCHOL, V102, P66, DOI 10.1037/0735-7036.102.1.66 HEFFNER RS, 1982, J COMP PHYSIOL PSYCH, V96, P926, DOI 10.1037/0735-7036.96.6.926 HEFFNER RS, 1988, HEARING RES, V36, P221, DOI 10.1016/0378-5955(88)90064-0 KAVANAGH GL, 1986, BEHAV NEUROSCI, V100, P200, DOI 10.1037//0735-7044.100.2.200 KELLY JB, 1980, J NEUROPHYSIOL, V44, P1161 KELLY JB, 1988, J NEUROPHYSIOL, V59, P1756 KITZES LM, 1980, J COMP NEUROL, V192, P455, DOI 10.1002/cne.901920306 KITZES LM, 1978, J NEUROPHYSIOL, V41, P1165 MARTIN RL, 1987, HEARING RES, V30, P239, DOI 10.1016/0378-5955(87)90140-7 MIDDLEBROOKS JC, 1990, J ACOUST SOC AM, V87, P2149, DOI 10.1121/1.399183 Mills A. W., 1972, FOUNDATIONS MODERN A, V2, P303 PHILLIPS DP, 1987, J ACOUST SOC AM, V82, P1, DOI 10.1121/1.395547 PHILLIPS DP, 1985, ANNU REV PSYCHOL, V36, P245 PHILLIPS DP, 1990, J ACOUST SOC AM, V88, P1403, DOI 10.1121/1.399718 PHILLIPS DP, 1989, HEARING RES, V37, P269, DOI 10.1016/0378-5955(89)90027-0 POLLAK GD, 1988, HEARING RES, V36, P107, DOI 10.1016/0378-5955(88)90054-8 ROTH GL, 1980, J ACOUST SOC AM, V68, P1643, DOI 10.1121/1.385196 SALLY SL, 1988, J NEUROPHYSIOL, V59, P1627 STILLMAN RD, 1971, EXP NEUROL, V32, P404, DOI 10.1016/0014-4886(71)90007-0 YIN TCT, 1983, J NEUROPHYSIOL, V50, P1020 NR 25 TC 32 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 39 EP 44 DI 10.1016/0378-5955(91)90089-R PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900004 PM 1752792 ER PT J AU HENLEY, CM AF HENLEY, CM TI POSTNATAL DEVELOPMENTAL-CHANGES IN INNER-EAR ORNITHINE DECARBOXYLASE (ODC) SO HEARING RESEARCH LA English DT Article DE ORNITHINE DECARBOXYLASE; INNER EAR; COCHLEA; DEVELOPMENT; RAT ID ALPHA-DIFLUOROMETHYLORNITHINE; HEARING-LOSS; POLYAMINES; INHIBITOR AB Ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine synthesis, is important in cellular growth, differentiation and development. Although ODC has been quantitated in cochlear tissues of the adult rat, it has not been assessed quantitatively in developing inner-ear tissues. The purpose of the present study was to quantitate ODC in cochlear tissues of the rat during the period of development of hearing. Cochlear ODC was significantly elevated throughout the period of cochlear maturation in that it increased rapidly during the first 10 days, peaked on day 10 and then declined thereafter. ODC in the lateral wall/organ of Corti tissues was significantly higher than in the cochlear nerve in developing, but not in adult rats. Further examination of separate cochlear tissues from 10-day old rats revealed that ODC activity was higher in the organ of Corti than in the lateral wall or cochlear nerve. Postnatal changes in ODC paralleled functional maturation of hearing and the hypersensitive period for aminoglycoside ototoxicity in the rat. Since aminoglycosides have been shown to inhibit ODC in vitro, aminoglycoside inhibition of polyamine synthesis may mediate the hypersensitivity of developing animals to the effects of these drugs. RP HENLEY, CM (reprint author), BAYLOR COLL MED,DEPT OTORHINOLARYNGOL & COMMUN SCI,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. CR ABELOFF MD, 1986, CANCER TREAT REP, V70, P843 ABELOFF MD, 1984, J CLIN ONCOL, V2, P124 BARTOLOME J, 1980, SCIENCE, V210, P798 HENLEY C, 1990, J CELL BIOCH F S, V14, P22 HENLEY CM, 1987, BRAIN RES BULL, V19, P695, DOI 10.1016/0361-9230(87)90056-6 JANSEN C, 1989, ARCH OTOLARYNGOL, V115, P1234 PEGG AE, 1988, ISI ATLAS-BIOCHEM, P11 PEGG AE, 1986, BIOCHEM J, V234, P249 PEGG AE, 1982, AM J PHYSIOL, V243, pC212 PEGG AE, 1988, CANCER RES, V48, P751 PUJOL R, 1986, ACTA OTOLARYNGOL, V249, P29 RUSSELL D, 1968, P NATL ACAD SCI USA, V60, P1420, DOI 10.1073/pnas.60.4.1420 RUSSELL DH, 1985, DRUG METAB REV, V16, P1, DOI 10.3109/03602538508991430 SALZER SJ, 1990, HEARING RES, V46, P101, DOI 10.1016/0378-5955(90)90143-D SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SCHWEITZER L, 1986, BRAIN RES BULL, V16, P215, DOI 10.1016/0361-9230(86)90035-3 SJOERDSMA A, 1984, T ASSOC AM PHYSICIAN, V97, P70 SLOTKIN TA, 1986, BRAIN RES BULL, V17, P307, DOI 10.1016/0361-9230(86)90236-4 Slotkin T A, 1983, Int J Dev Neurosci, V1, P7, DOI 10.1016/0736-5748(83)90004-7 SLOTKIN TA, 1979, LIFE SCI, V24, P1623, DOI 10.1016/0024-3205(79)90244-3 Uziel A, 1986, Acta Otolaryngol Suppl, V429, P23 NR 21 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 45 EP 49 DI 10.1016/0378-5955(91)90090-V PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900005 PM 1752793 ER PT J AU MULLER, M ROBERTSON, D YATES, GK AF MULLER, M ROBERTSON, D YATES, GK TI RATE-VERSUS-LEVEL FUNCTIONS OF PRIMARY AUDITORY-NERVE FIBERS - EVIDENCE FOR SQUARE LAW BEHAVIOR OF ALL FIBER CATEGORIES IN THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE AUDITORY NERVE; RATE-INTENSITY FUNCTION; THRESHOLD ID RATE-INTENSITY FUNCTIONS; INPUT-OUTPUT FUNCTIONS; BASILAR-MEMBRANE; FIBERS; RESPONSES; COCHLEA; CATS AB Detailed measurements of rate-versus-level (RI) functions close to threshold were made from single primary auditory nerve fibres in the guinea pig cochlea. For all fibres, a simple square law provided the best statistical fit to the data near threshold, regardless of spontaneous firing rate of the fibre. In no case was a better fit obtained with an exponent greater than 2. We conclude that a simple square law is an accurate description of the underlying synaptic drive to all primary auditory nerve fibres. For fibres with very low spontaneous firing rates the best square law fit near threshold frequently led to the formal mathematical estimate of a negative firing rate as the asymptotic value of the spontaneous firing rate. The 'negative spontaneous rate' of low spontaneous rate fibres derived from curve fitting can be conceptualized by postulating that for sound pressures well below threshold in these fibres the underlying synaptic drive lies below a threshold value at a site determining action potential generation. C1 UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR ALDER VA, 1978, J ACOUST SOC AM, V64, P684, DOI 10.1121/1.381993 ENGEBRET.AM, 1968, J ACOUST SOC AM, V44, P548, DOI 10.1121/1.1911119 GEISLER CD, 1990, HEARING RES, V44, P1, DOI 10.1016/0378-5955(90)90017-J GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 HARRIS DM, 1979, J NEUROPHYSIOL, V42, P1083 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 PATUZZI R, 1983, J ACOUST SOC AM, V74, P1734, DOI 10.1121/1.390282 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBERTSON D, 1991, HEARING RES, V51, P29, DOI 10.1016/0378-5955(91)90004-S ROBERTSON D, 1990, INFORMATION PROCESSI, P61 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 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 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SILINSKY EM, 1985, PHARMACOL REV, V37, P81 SMITH SJ, 1988, TRENDS NEUROSCI, V11, P458, DOI 10.1016/0166-2236(88)90199-3 SNYDER SH, 1985, ANNU REV NEUROSCI, V8, P103 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 YATES GK, 1990, HEARING RES, V50, P145, DOI 10.1016/0378-5955(90)90041-M NR 22 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 1991 VL 55 IS 1 BP 50 EP 56 DI 10.1016/0378-5955(91)90091-M PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900006 PM 1752794 ER PT J AU CONLEE, JW JENSEN, RP PARKS, TN CREEL, DJ AF CONLEE, JW JENSEN, RP PARKS, TN CREEL, DJ TI TURN-SPECIFIC AND PIGMENT-DEPENDENT DIFFERENCES IN THE STRIA VASCULARIS OF NORMAL AND GENTAMICIN-TREATED ALBINO AND PIGMENTED GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE ALBINISM; AMINOGLYCOSIDES; GENTAMICIN; INNER EAR; MELANIN PIGMENTATION ID INNER-EAR TISSUES; OTOTOXICITY; KANAMYCIN; RAT; CELLS; MELANOCYTES; MELANIN; KIDNEY AB The aims of the present study were to determine which structures in the stria vascularis (SV) may depend upon the presence of pigmented melanocytes both for normal morphology and for the expression of gentamicin ototoxicity in the inner ear. These pigment-dependent influences were inferred through comparisons of the SV in pigmented guinea pigs and in albinos containing nonpigmented melanocytes. Results were obtained from 6 albino and 8 pigmented guinea pigs given gentamicin, and from 3 albino and 3 pigmented control animals not receiving the drug. One-month old animals received gentamicin daily (100 mg/kg) for 14 days and recovered for an additional 14 days before being prepared for electron microscopy. The SV from each of the 4 cochlear turns was analyzed using stereological point counting procedures. In control animals, differences were found in the higher cochlear turns, where volume density for the marginal cells in albinos was abnormally large (turns 3 and 4), while the volume density for intermediate cells (melanocytes) was abnormally small (turn 3). Cell volume estimates for the intermediate cells were significantly smaller in the albino than pigmented control animals in the higher cochlear turns, indicating that functional abnormalities may be found in the albino cochlea. In animals exposed to gentamicin, marginal cell volume density was reduced significantly in turn 4 of albinos, but not in any region of the pigmented inner ears. Radial area of SV and estimates of the absolute volumes for marginal cells in albinos given gentamicin also were significantly reduced in turn 1 compared to their controls; such differences were not observed in the pigmented animals. The results indicate that marginal cell size is significantly reduced in albino but not pigmented animals 14 days after gentamicin exposure, and further suggest a role of pigmented melanocytes in ameliorating gentamicin-induced cochlear damage. C1 VET AFFAIRS MED CTR,SALT LAKE CITY,UT. RP CONLEE, JW (reprint author), UNIV UTAH,SCH MED,DEPT ANAT,SALT LAKE CITY,UT 84132, USA. CR ANNIKO M, 1976, ACTA OTO-LARYNGOL, V82, P70, DOI 10.3109/00016487609120864 BARZA M, 1976, ANTIMICROB AGENTS CH, V10, P569 Bonaccorsi P, 1965, Ann Laringol Otol Rinol Faringol, V64, P725 BRUMMETT RE, 1972, ARCHIV OTOLARYNGOL, V96, P505 COMIS SD, 1980, HEARING RES, V3, P249, DOI 10.1016/0378-5955(80)90051-9 CONLEE JW, 1989, HEARING RES, V41, P43, DOI 10.1016/0378-5955(89)90177-9 CONLEE JW, 1989, ACTA OTO-LARYNGOL, V107, P48, DOI 10.3109/00016488909127478 Crovetto M A, 1988, Rev Laryngol Otol Rhinol (Bord), V109, P453 DEOL MS, 1970, PROC R SOC SER B-BIO, V175, P201, DOI 10.1098/rspb.1970.0019 DEOL MS, 1970, J EMBRYOL EXP MORPH, V23, P773 ECHANDIA EL, 1965, Z ZELLFORSCH MIK ANA, V67, P600, DOI 10.1007/BF00340327 FORGE A, 1987, HEARING RES, V31, P253, DOI 10.1016/0378-5955(87)90195-X FORGE A, 1985, HEARING RES, V20, P233, DOI 10.1016/0378-5955(85)90028-0 GRATACAP B, 1985, ACTA OTO-LARYNGOL, V99, P339, DOI 10.3109/00016488509108920 HARPUR ES, 1976, EXPERIENTIA, V32, P1562, DOI 10.1007/BF01924454 HARPUR ES, 1975, EXPERIENTIA, V31, P1323, DOI 10.1007/BF01945807 Hawkins J E Jr, 1973, Adv Otorhinolaryngol, V20, P125 HILDING DA, 1977, ACTA OTO-LARYNGOL, V84, P24, DOI 10.3109/00016487709123939 HUY PTB, 1983, ANTIMICROB AGENTS CH, V23, P344 HUY PTB, 1986, J CLIN INVEST, V77, P1492 LEFERRIERE K, 1974, ANN OTOL RHINO LARYN, V83, P685 LINDQUIST NG, 1973, ACTA RADIOL STOCKH S, V325 LOHUIS PJFM, 1990, HEARING RES, V47, P95, DOI 10.1016/0378-5955(90)90169-P LYTTKENS L, 1979, ACTA OTO-LARYNGOL, V88, P61, DOI 10.3109/00016487909137141 NAKAMURA F, 1957, Ann Otol Rhinol Laryngol, V66, P1080 SANTI PA, 1983, HEARING RES, V11, P7, DOI 10.1016/0378-5955(83)90041-2 SCHACHT J, 1976, J ACOUST SOC AM, V59, P940, DOI 10.1121/1.380929 SCHACHT J, 1979, ARCH OTO-RHINO-LARYN, V224, P129, DOI 10.1007/BF00455236 SHADDOCK LC, 1984, AM J OTOLARYNG, V5, P99, DOI 10.1016/S0196-0709(84)80028-9 SULLIVAN MJ, 1987, HEARING RES, V31, P161, DOI 10.1016/0378-5955(87)90122-5 TACHIBANA M, 1983, ACTA OTO-LARYNGOL, V96, P31, DOI 10.3109/00016488309132872 TOU JS, 1972, ARCH BIOCHEM BIOPHYS, V149, P146, DOI 10.1016/0003-9861(72)90308-6 WASTERSTROM SA, 1986, AM J OTOL, V7, P11 WASTERSTROM SA, 1986, AM J OTOL, V7, P19 WASTERSTROM SA, 1984, SCAND AUDIOL S, V23 Weibel E. R., 1979, STEREOLOGICAL METHOD, V1 WHITE FH, 1982, ARCH DERMATOL RES, V273, P307, DOI 10.1007/BF00409260 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 Witkop Jr CJ, 1983, METABOLIC BASIS INHE, P301 YLIKOSKI J, 1974, ACTA OTOLARYNGOL S S, V326 NR 40 TC 23 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 57 EP 69 DI 10.1016/0378-5955(91)90092-N PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900007 PM 1752795 ER PT J AU WEBSTER, WR MARTIN, RL AF WEBSTER, WR MARTIN, RL TI THE DEVELOPMENT OF FREQUENCY REPRESENTATION IN THE INFERIOR COLLICULUS OF THE KITTEN SO HEARING RESEARCH LA English DT Article DE KITTEN; INFERIOR COLLICULUS; AUDITORY SYSTEM; FREQUENCY REPRESENTATION; DEVELOPMENT ID AUDITORY-NERVE FIBERS; TONOTOPIC ORGANIZATION; PLACE PRINCIPLE; POSTNATAL-DEVELOPMENT; C-14 2-DEOXYGLUCOSE; GERBIL COCHLEA; ONTOGENY; MAP; RESPONSES; CHICKEN AB While morphologically the kitten's cochlea matures first at the basal or high-frequency region, behavioural and physiological evidence suggests that it responds first to low-frequency sound. Explanations of this paradox include the suggestion that the spatial representation of frequency within the cochlea changes as a function of age. We have used the [C-14]-2-deoxyglucose technique to study the development of frequency representation in the central auditory system of the kitten. We report here that while the locations within the inferior colliculus (IC) where high- and mid-frequency sounds are represented shift markedly between 10 and 35 days of age, the location where low-frequency sound is represented does not alter. The IC representation of low frequencies is adult-like by 10 days of age but that of higher frequencies continues to mature until as many as 35 days. Despite its morphological immaturity with respect to other regions, the apex of the cochlea appears to be the first region to become tuned to those frequencies to which it is tuned in the adult. We found little labelling at 5 and 7 days of age to 75-80 dB stimuli, but it is quite possible that the high-frequency region might respond to very intense low frequencies before 10 days of age. RP WEBSTER, WR (reprint author), MONASH UNIV,DEPT PSYCHOL,WELLINGTON RD,CLAYTON,VIC 3168,AUSTRALIA. CR ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 DOLAN DF, 1985, J ACOUST SOC AM, V78, P544, DOI 10.1121/1.392421 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 EHRET G, 1981, J COMP PHYSIOL PSYCH, V95, P304, DOI 10.1037/h0077770 FOSS I, 1974, ACTA OTO-LARYNGOL, V77, P202, DOI 10.3109/00016487409124618 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 HUANG C, 1986, EXP BRAIN RES, V61, P506 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 LIPPE W, 1985, J COMP NEUROL, V237, P273, DOI 10.1002/cne.902370211 MARTIN RL, 1988, HEARING RES, V33, P245, DOI 10.1016/0378-5955(88)90155-4 NUDO RJ, 1984, CONTRIBUTIONS SENSOR, V8, P79 ROMAND R, 1982, J COMP NEUROL, V204, P1, DOI 10.1002/cne.902040102 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, 1976, J COMP NEUROL, V166, P469, DOI 10.1002/cne.901660408 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SOKOLOFF L, 1981, J CEREBR BLOOD F MET, V1, P7 WALSH EJ, 1987, HEARING RES, V28, P97, DOI 10.1016/0378-5955(87)90157-2 WEBSTER WR, 1984, EXP BRAIN RES, V56, P427 NR 23 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 1991 VL 55 IS 1 BP 70 EP 80 DI 10.1016/0378-5955(91)90093-O PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900008 PM 1752796 ER PT J AU SIMMONS, DD MANSONGIESEKE, L HENDRIX, TW MORRIS, K WILLIAMS, SJ AF SIMMONS, DD MANSONGIESEKE, L HENDRIX, TW MORRIS, K WILLIAMS, SJ TI POSTNATAL MATURATION OF SPIRAL GANGLION NEURONS - A HORSERADISH-PEROXIDASE STUDY SO HEARING RESEARCH LA English DT Article DE DEVELOPMENT; COCHLEA; ORGAN OF CORTI; NEURONAL MORPHOLOGY; BRANCHING PATTERNS ID HAIR-CELL INNERVATION; GUINEA-PIG COCHLEA; ADULT CATS; AFFERENT INNERVATION; MICROSCOPIC ANALYSIS; EFFERENT FIBERS; GOLGI METHOD; RAT; MORPHOLOGY; ELIMINATION AB Using an in vitro cochlear preparation from postnatal hamsters, spiral ganglion cells (SGCs) were labeled retrogradely following extracellular injections of HRP into the cochlear nerve. In 24 cochleae from hamsters between postnatal days (P) 0 and 10, the neuronal morphology of 201 SGCs and their peripheral axons were analyzed. From P 0 to 3, labeled SGCs had few distinguishable features. Although SGCs could be traced separately to inner hair cells (IHCs) and outer hair cells (OHCs), they all had roughly bipolar-shaped cell bodies. Approximately half of the labeled SGCs had peripheral axons that spiraled some distance before entering radial fiber bundles. From P 3 to 7, SGCs increased in size by nearly 30% and the number of SGCs with spiraling peripheral axons decreased to near zero. At P 10, the central axon diameter to peripheral axon diameter ratios distinguished two populations of SGCs. The hair-cell innervation patterns of SGCs also changed morphologically as a function of postnatal age. At P 0, radial fiber (RF) terminals of peripheral axons contacted as many as 8 IHCs; by P 3, RFs contacted typically one or two IHCs. The terminal portions of peripheral axons contacting OHCs did not show any appreciable spiral until P 2. By P 5, individual outer spiral fibers (OSFs) had greater spiral lengths underneath row-3 OHCs and the number of OHC contacts was also greatest for row-3 OSFs. These data suggest that SGCs undergo a systematic maturational process. Furthermore, the morphological differentiation of SGCs occurs after they have established separate inner and outer hair cell innervations. C1 UNIV CALIF LOS ANGELES,INST BRAIN RES,LOS ANGELES,CA 90024. PEPPERDINE UNIV,DIV NAT SCI,MALIBU,CA 90265. RP SIMMONS, DD (reprint author), UNIV CALIF LOS ANGELES,DEPT BIOL,405 HILGARD AVE,LOS ANGELES,CA 90024, USA. 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Res. PD SEP PY 1991 VL 55 IS 1 BP 81 EP 91 DI 10.1016/0378-5955(91)90094-P PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900009 PM 1752797 ER PT J AU SOHMER, H FREEMAN, S AF SOHMER, H FREEMAN, S TI HYPOXIA INDUCED HEARING-LOSS IN ANIMAL-MODELS OF THE FETUS INUTERO SO HEARING RESEARCH LA English DT Article DE ENDOCOCHLEAR POTENTIAL; AUDITORY NERVE BRAIN-STEM EVOKED RESPONSE; NEONATE; FETUS; HYPOXIA; HEMATOCRIT; DEVELOPMENT ID BRAIN-STEM RESPONSE; EVOKED-POTENTIALS; GUINEA-PIGS; THRESHOLD; HYPOXEMIA; INFANTS; ORIGIN; ONSET AB The human fetus in-utero has low arterial oxygen tension. It has, therefore, been suggested that at greater than 28 weeks gestational age, the fetus may have a sensori-neural hearing loss comparable to that seen in adult cats exposed to similar degrees of hypoxia. This is due to hypoxia induced depression of the endocochlear potential. However, fetal blood is provided with compensatory mechanisms (elevated hematocrit and hemoglobin and special fetal hemoglobin) which enable pick up and transport of more oxygen from the placenta than adult blood under the same physiological conditions. Therefore, the hypothesis of a fetal sensori-neural hearing loss due to oxygen lack was tested in the following animal models: a) Adult cats to which feline red blood cells were infused thus causing a polycythemia similar to fetal conditions; b) Adult rats acclimated to altitude in a hypobaric chamber, inducing erythropoiesis with elevated hematocrit and hemoglobin; c) Neonatal guinea pigs and goats studied when they were less than 12 hours old so that the fetal compensatory mechanisms were still present. In each model, hypoxia (PaO2 20-30 mmHg) induced an ABR threshold elevation resembling that obtained in the uncompensated adult animal. Thus these experiments seem to have confirmed the hypothesis of a fetal, hypoxic induced sensori-neural hearing loss even though such experiments have not been conducted directly on fetal animals. RP SOHMER, H (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PHYSIOL,POB 1172,IL-91010 JERUSALEM,ISRAEL. 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Res. PD SEP PY 1991 VL 55 IS 1 BP 92 EP 97 DI 10.1016/0378-5955(91)90095-Q PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900010 PM 1752799 ER PT J AU WILSON, JL HENSON, MM HENSON, OW AF WILSON, JL HENSON, MM HENSON, OW TI COURSE AND DISTRIBUTION OF EFFERENT FIBERS IN THE COCHLEA OF THE MOUSE SO HEARING RESEARCH LA English DT Article DE OLIVOCOCHLEAR; EFFERENT; INNER EAR; COCHLEA; PHA-L; MOUSE ID GUINEA-PIG COCHLEA; OUTER HAIR-CELLS; SUPERIOR OLIVARY COMPLEX; CROSSED OLIVOCOCHLEAR BUNDLE; BRAIN-STEM; FLUORESCENT TRACERS; MEDIAL ZONES; PHA-L; NEURONS; PROJECTIONS AB The course, distribution and termination of single efferent fibers to the cochlea has been described in only a few animals and relatively few fibers have been studied with knowledge of their ipsilateral or contralateral origin. In order to examine the efferent fibers in the mouse, the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was iontophoretically injected into one side of the brain stem near the location of known efferent nuclei. Examination of surface preparations of the cochlea revealed detailed information for both the lateral olivocochlear (LOC) and medial olivocochlear (MOC) systems. Many, but not all, fibers entered the cochlea within the intraganglionic spiral bundle (IGSB). The LOC fibers were restricted to the ipsilateral cochlea and rarely branched within the IGSB and osseous spiral lamina (OSL). In the organ of Corti, they traveled either basally or apically in the region of the inner hair cells (IHCs), spanning lengths up to 130-mu-m (basally) and 890-mu-m (apically). Terminal swellings of these fibers were ca 3.0-mu-m in diameter. Numerous en passant swellings were present where the fibers formed a plexus in the area of the IHCs. The MOC fibers followed a similar course in the IGSB and OSL, and within the OSL the fibers had few branches. Within the organ of Corti they traveled apically (up to 70-mu-m) in the nerve bundles located in the IHC area before they crossed the tunnel of Corti. In the region of the OHCs, 9% of the traceable fibers branched to innervate two to three OHCs while 91% appeared to innervate only one OHC. There was no discernible difference in the distribution of contralateral and ipsilateral MOC projections in terms of cochlear region or outer hair cell rows. C1 UNIV N CAROLINA,DEPT CELL BIOL & ANAT,108 TAYLOR HALL,CB 7090,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27514. 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B., 1986, NEUROBIOLOGY HEARING, P333 WARR WB, 1975, J COMP NEUROL, V161, P159, DOI 10.1002/cne.901610203 WARR WB, 1979, BRAIN RES, V173, P152, DOI 10.1016/0006-8993(79)91104-1 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WHITLON DS, 1989, J NEUROCYTOL, V18, P505, DOI 10.1007/BF01474546 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 WRIGHT CG, 1976, ACTA OTO-LARYNGOL, V82, P41, DOI 10.3109/00016487609120861 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 68 TC 27 Z9 27 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 98 EP 108 DI 10.1016/0378-5955(91)90096-R PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900011 PM 1752800 ER PT J AU HOOD, LJ BERLIN, CI HEFFNER, RS MOREHOUSE, CR SMITH, EG BARLOW, EK AF HOOD, LJ BERLIN, CI HEFFNER, RS MOREHOUSE, CR SMITH, EG BARLOW, EK TI OBJECTIVE AUDITORY THRESHOLD ESTIMATION USING SINE-WAVE DERIVED RESPONSES SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; ACTION POTENTIAL; THRESHOLD; TONEBURSTS; SINUSOIDS; GUINEA PIG; CHINCHILLA; POCKET GOPHER; ANIMAL HEARING ID GUINEA-PIG; POTENTIALS; HEARING; NOISE AB A derived response method of acquiring frequency specific auditory evoked potentials that utilizes a pure tone in combination with a toneburst is applied to the measurement of hearing sensitivity in guinea pigs, chinchillas and pocket gophers. Two experiments which demonstrate that thresholds acquired via tone-derived responses are 10 to 15 dB more sensitive than thresholds to solitary tonebursts are described. The derived potentials approximate behaviorally acquired thresholds at frequencies of 0.5 kHz and above. This technique may provide a more rapid means of assessing hearing sensitivity in laboratory animals than by behavioral means. C1 UNIV TOLEDO,DEPT PSYCHOL,COMPART HEARING LAB,TOLEDO,OH 43606. LOUISIANA STATE UNIV,MED CTR,SCH ALLIED HLTH PROFESSIONS,DEPT COMMUN DISORDERS,NEW ORLEANS,LA 70112. NICOLET BIOMED INSTRUMENTS,MADISON,WI. AMER AUDIOL ASSOCIATES,RIVERDALE,GA. 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, 1991, HEARING RES, V52, P271, DOI 10.1016/0378-5955(91)90017-4 DAVIS H, 1984, AUDIOLOGY, V23, P59 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 DON M, 1979, ANN OTOLRHINOLLA S57, V88 GORGA MP, 1988, J SPEECH HEAR RES, V31, P87 HEFFNER R, 1971, J ACOUST SOC AM, V49, P1888, DOI 10.1121/1.1912596 HEFFNER RS, 1990, HEARING RES, V46, P239, DOI 10.1016/0378-5955(90)90005-A HEFFNER RS, 1991, HEARING RES, V52, P13, DOI 10.1016/0378-5955(91)90183-A MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 PICTON TW, 1979, J OTOLARYNGOL, V8, P289 PROSEN CA, 1978, J ACOUST SOC AM, V63, P559, DOI 10.1121/1.381754 SALT AN, 1990, AUDIOLOGY, V29, P135 STAPELLS DR, 1985, AUDITORY BRAINSTEM R NR 13 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 109 EP 116 DI 10.1016/0378-5955(91)90097-S PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900012 PM 1752790 ER PT J AU ZRULL, MC COLEMAN, JR AF ZRULL, MC COLEMAN, JR TI STRUCTURAL FEATURES OF NEURONS IN WHOLE GRAFTS OF THE RAT INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; TECTUM; TRANSPLANTATION; RAPID GOLGI; MORPHOLOGY ID DORSAL COCHLEAR NUCLEUS; TONOTOPIC ORGANIZATION; TECTAL TRANSPLANTS; AUDITORY PATHWAY; NEURAL IMPLANTS; STRIATAL GRAFTS; GOLGI ANALYSIS; NEWBORN RATS; ALBINO-RAT; ADULT AB The inferior colliculus (IC) is a midbrain structure that receives ascending auditory input from brainstem nuclei via the lateral lemniscus, sends efferent fibers to the medial geniculate body of thalamus and receives descending projections from auditory cortex. In the rat, the IC consists of dorsal and external cortices surrounding the central nucleus of IC (CNIC) which is populated by discoid and stellate neurons; the CNIC has a laminar appearance arising from organization of lemniscal fibers and processes of discoid cells. The IC of adult rats was chosen for implantation of whole grafts of E16-17 caudal tectum into unilateral lesion sites. Dendritic and somal architecture of graft neurons was examined 1 to 4.5 months following implantation using rapid Golgi, HRP and Nissl methods. The CNIC of rat is dominated by principal neurons with relatively flattened dendritic fields. In grafts of caudal tectum the most common neuron class observed possesses flattened dendritic arbors which often parallel one another. These neurons also resemble CNIC neurons of host tissue adjacent to the graft border. Spine formations appear on both proximal and distal dendrites of this neural type in both normal and implanted tissues. In addition, comparable somal features of graft neurons include ovoid or fusiform shapes with regular nuclear membranes as found in the normal colliculus. In Golgi stained material fewer stellate class neurons appear as in the normal CNIC, although stellate cell classes are more abundant in the pericentral areas of normal tissue. Both neuron populations are retrogradely labelled in graft and normal IC after HRP injection into the medial geniculate body. These features suggest that the graft core typically consists of prototypic CNIC cells. Other features of neuron and glial cell density vary in graft material which also shows a complex network of vasculature. These results demonstrate that whole grafts of caudal tectum placed into the inferior colliculus can form organized neural architecture similar to the normal CNIC. The somal, dendritic and spine features of these neurons form a potential substrate for connectional and functional properties which establish this preparation as suitable for further investigation as a model for development and recovery of function in the central auditory system. C1 UNIV S CAROLINA,DEPT PSYCHOL,COLUMBIA,SC 29208. UNIV S CAROLINA,DEPT PHYSIOL,COLUMBIA,SC 29208. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ALTMAN J, 1981, EXP BRAIN RES, V42, P411 BJORKLUND A, 1987, TRENDS NEUROSCI, V10, P509, DOI 10.1016/0166-2236(87)90131-7 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 CLERICI WJ, 1990, J COMP NEUROL, V296, P1 CLERICI WJ, 1986, DEV BRAIN RES, V27, P127, DOI 10.1016/0165-3806(86)90239-7 COLEMAN JR, 1990, 13TH ANN MIDW M COLEMAN JR, 1991, IN PRESS EXP NEUROL COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 COLEMAN JR, 1982, OTOLARYNG HEAD NECK, V90, P795 DARDENNES R, 1984, DEV BRAIN RES, V16, P159, DOI 10.1016/0165-3806(84)90022-1 DASZUTA A, 1989, BRAIN RES, V498, P323, DOI 10.1016/0006-8993(89)91111-6 DIFIGLIA M, 1988, J NEUROSCI, V8, P1112 DYSON SE, 1988, J NEUROSCI, V8, P1822 EYERLY M R, 1989, Society for Neuroscience Abstracts, V15, P747 FAINGOLD CL, 1989, BRAIN RES, V500, P302, DOI 10.1016/0006-8993(89)90326-0 FAYELUND H, 1986, ANAT EMBRYOL, V175, P35, DOI 10.1007/BF00315454 FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 FAYELUND H, 1985, ANAT EMBRYOL, V173, P53, DOI 10.1007/BF00707304 FROTSCHER M, 1987, J COMP NEUROL, V259, P266, DOI 10.1002/cne.902590207 GAGE FH, 1986, J NEUROSCI, V6, P2837 Geniec P, 1971, Acta Otolaryngol Suppl, V295, P1 GOLDEN GT, 1989, BRAIN RES BULL, V22, P461, DOI 10.1016/0361-9230(89)90073-7 HARVEY AR, 1986, ANAT EMBRYOL, V174, P361, DOI 10.1007/BF00698786 HARVEY AR, 1982, EXP BRAIN RES, V47, P437 HUANG C, 1986, EXP BRAIN RES, V61, P506 JAEGER CB, 1981, J COMP NEUROL, V200, P213, DOI 10.1002/cne.902000204 KROMER LF, 1983, J COMP NEUROL, V218, P433, DOI 10.1002/cne.902180408 LEVIN BE, 1987, BRAIN RES BULL, V19, P723, DOI 10.1016/0361-9230(87)90060-8 LINDVALL O, 1990, SCIENCE, V247, P574, DOI 10.1126/science.2105529 MCLOON SC, 1983, J COMP NEUROL, V217, P376, DOI 10.1002/cne.902170403 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 NEAFSEY EJ, 1989, BRAIN RES, V493, P33, DOI 10.1016/0006-8993(89)90997-9 OLIVER DL, 1984, J COMP NEUROL, V222, P237, DOI 10.1002/cne.902220207 OLIVER DL, 1984, J COMP NEUROL, V224, P155, DOI 10.1002/cne.902240202 OLIVER DL, 1984, NEUROSCIENCE, V11, P409, DOI 10.1016/0306-4522(84)90033-2 PERRY VH, 1985, J COMP NEUROL, V231, P353, DOI 10.1002/cne.902310306 PINTOLORD MC, 1979, J COMP NEUROL, V187, P49 ROBERTS RC, 1987, J NEUROCYTOL, V16, P333, DOI 10.1007/BF01611345 RYAN AF, 1982, J COMP NEUROL, V207, P369, DOI 10.1002/cne.902070408 RYUGO DK, 1985, J COMP NEUROL, V242, P381, DOI 10.1002/cne.902420307 TONDER N, 1989, EXP BRAIN RES, V74, P512 ZRULL M C, 1989, Society for Neuroscience Abstracts, V15, P747 ZRULL M C, 1990, Society for Neuroscience Abstracts, V16, P722 ZRULL MC, 1990, HEARING RES, V45, P237, DOI 10.1016/0378-5955(90)90123-7 NR 45 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 1991 VL 55 IS 1 BP 117 EP 132 DI 10.1016/0378-5955(91)90098-T PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900013 PM 1721616 ER PT J AU SAHLEY, TL KALISH, RB MUSIEK, FE HOFFMAN, DW AF SAHLEY, TL KALISH, RB MUSIEK, FE HOFFMAN, DW TI EFFECTS OF OPIOID BE DRUGS ON AUDITORY EVOKED-POTENTIALS SUGGEST A ROLE OF LATERAL OLIVOCOCHLEAR DYNORPHINS IN AUDITORY FUNCTION SO HEARING RESEARCH LA English DT Article DE OPIOID; OPIOID PEPTIDES; DYNORPHIN; OLIVOCOCHLEAR EFFERENT BUNDLE; COCHLEA; AUDITORY EVOKED POTENTIAL; PENTAZOCINE; U50-488 ID ENKEPHALIN-LIKE IMMUNOREACTIVITY; ANESTHETIZED GUINEA-PIGS; STEM RESPONSES ABRS; BRAIN-STEM; OPIATE RECEPTOR; CEREBRAL-CORTEX; SERIAL SECTIONS; MET-ENKEPHALIN; CAT COCHLEA; RAT AB Multiple gene products of opioid peptide families (e.g., enkephalins, dynorphins) with differing opioid receptor specificities are present within olivocochlear efferent terminals. Enkephalins activate mu- and delta-opioid receptors, and are generally inhibitory in the nervous system, and dynorphins are kappa-receptor agonists, which may be excitatory to postsynaptic neurons. We have examined the effects of intravenously administered opioid agonists and antagonists on click-evoked N1 and N2 amplitudes and latencies of the compound action potential in the chinchilla recorded at the round window. Parenteral administration of the opioid receptor antagonist naloxone or the potent mu-receptor agonist fentanyl did not alter N1 and N2 amplitudes or latencies. The kappa-receptor agonist, mu-receptor antagonist pentazocine caused marked increases in N1 and N2 amplitudes over baseline values at threshold intensities. These effects were not abolished by naloxone. No effects were seen on the cochlear microphonic, supporting a site of action of these effects at the lateral olivocochlear efferent terminals on auditory nerve dendrites under inner hair cells. Similar results were obtained when far field auditory evoked responses were recorded. Results were obtained under ketamine/pentobarbital anesthesia, which provided stable recording baselines in contrast to tiletamine/zolezepam/pentobarbital, with which an upward drift in auditory potentials was observed. This stimulatory action of kappa-agonists on auditory-evoked potential amplitudes appears to represent a physiological role of the lateral olivocochlear efferent innervation. The different neurotransmitters of the olivocochlear efferents (e.g. enkephalins, dynorphins, acetylcholine) may have antagonistic actions on auditory potentials, as may the lateral and medial systems themselves. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PSYCHIAT,NEUROCHEM LAB,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PHARMACOL,NEUROCHEM LAB,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT SURG,DIV AUDIOL,HANOVER,NH 03756. UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,SAN FRANCISCO,CA 94143. 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B., 1986, NEUROBIOLOGY HEARING, P333 WATSON SJ, 1984, OPIOIDS PAST PRESENT, P145 WATSON SJ, 1982, SCIENCE, V218, P1134, DOI 10.1126/science.6128790 WIEDERHOLD ML, 1986, NEUROBIOLOGY HEARING, P349 WILBER LA, 1988, J ACOUST SOC AM, V83, P669, DOI 10.1121/1.396162 ZAKRISSON JE, 1975, ACTA OTO-LARYNGOL, V79, P228, DOI 10.3109/00016487509124678 NR 66 TC 25 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD SEP PY 1991 VL 55 IS 1 BP 133 EP 142 DI 10.1016/0378-5955(91)90099-U PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GG569 UT WOS:A1991GG56900014 PM 1684359 ER PT J AU PICKLES, JO VONPERGER, M ROUSE, GW BRIX, J AF PICKLES, JO VONPERGER, M ROUSE, GW BRIX, J TI THE DEVELOPMENT OF LINKS BETWEEN STEREOCILIA IN HAIR-CELLS OF THE CHICK BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE CHICK; PAPILLA; HAIR CELL; STEREOCILIA; LINK; TIP LINK; DEVELOPMENT ID GUINEA-PIG COCHLEA; FISH INNER-EAR; ACTIN-FILAMENTS; BIRD COCHLEA; TIP LINKS; INTERCONNECTIONS; TRANSDUCTION; LIZARD; ORGANIZATION; STEREOVILLI AB Auditory papillae of chicks (embryonic age 6-21 days) were examined by scanning and transmission electron microscopy, in order to trace the development of the tip links between the stereocilia, and in order to trace the development of the spatial organisation of the tip links. In the most immature bundles, stereocilia were not graded in height, while strands of tenuous material interconnected adjacent stereocilia, this material being concentrated in a band near the tips of the stereocilia. The material joined the stereocilia in all directions, with no preferential direction for the interconnecting material being visible. Similarly, no columnar organisation of the stereocilia was visible. As soon as a gradation in height of the stereocilia began to appear, material could be seen running upwards from the shorter stereocilia to the adjacent lengthening stereocilia. There was a continuum in appearance between (i) the material running laterally between short immature stereocilia, (ii) the material running upwards between stereocilia which were developing a gradation in height, and (iii) the tip links seen in more mature bundles. It is suggested that tip links are a specialisation of the links which join immature stereocilia laterally near their tips. It is also suggested that the orientation of tip links, parallel to the hair cell axis of bilateral symmetry, is produced by the gradient in growth of the stereocilia. C1 UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VIS TOUCH & HEARING RES CTR,ST LUCIA,QLD 4067,AUSTRALIA. TECH UNIV MUNICH,INST ZOOL,W-8046 GARCHING,GERMANY. RP PICKLES, JO (reprint author), UNIV BIRMINGHAM,SCH MED,DEPT PHYSIOL,BIRMINGHAM B15 2TJ,W MIDLANDS,ENGLAND. 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Res. PD AUG PY 1991 VL 54 IS 2 BP 153 EP 163 DI 10.1016/0378-5955(91)90116-Q PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200001 PM 1938624 ER PT J AU SCARFONE, E ULFENDAHL, M FIGUEROA, L FLOCK, A AF SCARFONE, E ULFENDAHL, M FIGUEROA, L FLOCK, A TI ANESTHETICS MAY CHANGE THE SHAPE OF ISOLATED TYPE-I HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE VESTIBULAR; TYPE-I HAIR CELL; ANESTHETICS; BARBITURATE; KETAMINE; ISOLATED CELLS ID GLUTAMATE AB Type I hair cells isolated from animals anaesthetised with barbiturates or ether were found to be shorter and to lack a prominent 'neck' region when compared to cells isolated from non-anaesthetised animals. Ketamine did not have this effect. The changes observed could have important implications for the physiology of inner ear receptors. These findings infer that care should be taken in the choice of anaesthetics used in studies on cells from the inner ear. C1 KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. RP SCARFONE, E (reprint author), UNIV MONTPELLIER 2,NEUROPHYS SENSORIELLE LAB,INSERM,U254,CP089 PL E BATAILLON,F-34095 MONTPELLIER 5,FRANCE. CR ANDINE P, 1988, NEUROSCI LETT, V90, P208, DOI 10.1016/0304-3940(88)90813-0 ANIS NA, 1983, BRIT J PHARMACOL, V79, P565 BENDIXEN HH, 1965, CLIN PHARMACOL THER, V6, P510 CLARK GD, 1987, NEUROSCIENCE, V21, P665, DOI 10.1016/0306-4522(87)90027-3 DEMEMES D, 1990, HEARING RES, V46, P261, DOI 10.1016/0378-5955(90)90007-C DIVE C, 1988, MOL CELL PROBE, V2, P131, DOI 10.1016/0890-8508(88)90035-7 FAVRE D, 1983, MICRON MICROSC ACTA, V14, P319, DOI 10.1016/0047-7206(83)90003-1 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 MARSHALL BE, 1972, ANESTHESIOLOGY, V37, P128 RAYMOND J, 1988, PROG BRAIN RES, V76, P29 ROTHMAN SM, 1986, ANN NEUROL, V19, P105, DOI 10.1002/ana.410190202 SCARFONE E, 1991, IN PRESS CELL TISSUE SCARFONE E, 1988, J NEUROSCI, V8, P4640 STOHR M, 1980, FLOW CYTOMETRY, V4, P96 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 AUG PY 1991 VL 54 IS 2 BP 247 EP 250 DI 10.1016/0378-5955(91)90119-T PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200004 PM 1938627 ER PT J AU LEAKE, PA HRADEK, GT REBSCHER, SJ SNYDER, RL AF LEAKE, PA HRADEK, GT REBSCHER, SJ SNYDER, RL TI CHRONIC INTRACOCHLEAR ELECTRICAL-STIMULATION INDUCES SELECTIVE SURVIVAL OF SPIRAL GANGLION NEURONS 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; BRAIN-STEM; INFERIOR COLLICULUS; COCHLEAR NUCLEUS; ACOUSTIC DEPRIVATION; PROJECTIONS; PERIOD; RAT AB Ten newborn kittens were deafened by systemic administration of neomycin sulfate. Profound hearing losses were documented by ABR and FFR (500 Hz) testing. At 9-17 weeks of age, the young deafened cats were unilaterally implanted with a multichannel scala tympani electrode. Six of the animals were chronically stimulated at 6 dB above electrically evoked ABR thresholds for 1 h/day for periods of 1 month or 3 months. Stimuli were charge-balanced biphasic pulses (200-mu-s/phase, 30 pps.) The remaining 4 cats underwent identical deafening and implantation schedules but were not stimulated. Results indicate that administration of neomycin in neonatal cats induced degeneration of hair cells and spiral ganglion cell loss that was bilaterally symmetrical between the two cochleas of each individual animal, although there was variation between animals in the severity of the ototoxic drug effect. In animals receiving passive (unstimulated) implants, morphometric analysis of spiral ganglion cell density showed no significant difference in ganglion cell survival between the implanted cochleas and the contralateral control ears. In contrast, animals that were chronically stimulated for 3 months showed significantly better neuronal survival in implanted and stimulated cochleas as compared to contralateral deafened control ears. The induced conservation of spiral ganglion neurons was observed consistently within the basal cochlear region near the stimulating electrodes. In more apical regions there was no significant difference between the stimulated and control cochleas. The mechanisms underlying this selective conservation of spiral ganglion neurons induced by chronic intracochlear electrical stimulation are uncertain. Since no comparable chronic stimulation studies have been conducted in adults, it is not known whether similar conservation effects could be induced in mature animals. C1 UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,COLEMAN LAB,SAN FRANCISCO,CA 94143. RP LEAKE, PA (reprint author), UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,EPSTEIN LAB,HSE 871,SAN FRANCISCO,CA 94143, USA. CR [Anonymous], 1988, SAS STAT USERS GUIDE BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 COLEMAN J R, 1979, Experimental Neurology, V64, P533 Eggermont J.J., 1986, ACTA OTOLARYNGOL S, V429, P1 EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 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 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 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, 1990, NEURAL PROSTHESES FU, P253 LEAKEJONES PA, 1979, SEM1979III SEM INC LEAKEJONES PA, 1980, SEM1980III SEM INC LEAKEJONES PA, 1982, HEARING RES, V8, P225, DOI 10.1016/0378-5955(82)90076-4 LOUSTEAU RJ, 1987, LARYNGOSCOPE, V97, P836 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 Nadol JJ, 1981, AMINOGLYCOSIDE OTOTO, P409 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 OTTE J, 1978, LARYNGOSCOPE, V88, P1231 Rebscher S. J., 1985, COCHLEAR IMPLANTS, P74 Rubel E.W., 1985, P109 RUBEN RJ, 1980, ANN OTO RHINOL LARYN, V89, P303 Ruben R J, 1986, Acta Otolaryngol Suppl, V429, P61 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 SNYDER RL, 1991, IN PRESS HEAR RES 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 WALSH EJ, 1986, NEUROBIOLOGY HEARING, P247 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WEBSTER DB, 1983, HEARING RES, V12, P145, DOI 10.1016/0378-5955(83)90123-5 Weibel E. R., 1979, STEREOLOGICAL METHOD, V1 YLIKOSKI J, 1974, ACTA OTOLARYNGOL, V79, P266 NR 38 TC 139 Z9 141 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1991 VL 54 IS 2 BP 251 EP 271 DI 10.1016/0378-5955(91)90120-X PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200005 PM 1938628 ER PT J AU HULTCRANTZ, M SNYDER, R REBSCHER, S LEAKE, P AF HULTCRANTZ, M SNYDER, R REBSCHER, S LEAKE, P TI EFFECTS OF NEONATAL DEAFENING AND CHRONIC INTRACOCHLEAR ELECTRICAL-STIMULATION ON THE COCHLEAR NUCLEUS IN CATS SO HEARING RESEARCH LA English DT Article DE CHRONIC ELECTRICAL STIMULATION; CATS; COCHLEAR NUCLEUS; NEONATAL DEAFNESS; AUDITORY DEPRIVATION ID CONDUCTIVE HEARING-LOSS; STEM AUDITORY NUCLEI; BRAIN-STEM; INFERIOR COLLICULUS; ACOUSTIC DEPRIVATION; PROJECTIONS; RAT; NEURONS; PERIOD; MICE AB Four newborn kittens were deafened by daily intramuscular injections of neomycin sulfate, beginning the day after birth and continuing for 14-16 days. At 10-16 weeks of age the deaf kittens were implanted unilaterally with a four wire intracochlear electrode array. The animals were stimulated daily (starting at 13-18 weeks of age), for a period of one hour, at 6 dB above the electrically evoked auditory brainstem response threshold. After 3 months of chronic intracochlear electrical stimulation, animals were studied in acute electrophysiological experiments and euthanized for histological studies. This study compares the stimulated and control cochlear nuclei (CN) of these deafened animals to the CN of four normal adult cats. Statistical comparisons of spherical cell densities in the anteroventral cochlear nucleus (AVCN), cross-sectional spherical cell areas, and volumes of the cochlear nucleus subdivisions were included in the analysis. The results indicate that, by all of these measures, the cochlear nuclei in neonatally deafened animals were significantly different from the cochlear nuclei of control animals. As a result of deafening, the density of spherical cells was decreased by 30%, the cross-sectional areas of spherical cells were reduced by 20%, and the volume of the cochlear nucleus was reduced by 25%. These changes were observed in both cochlear nuclei (ipsilateral to both stimulated and unstimulated cars) of the deafened animals. With the measures employed, no significant difference was demonstrated in comparisons between the deafened/unstimulated and the deafened/stimulated cochlear nuclei. That is, no reversal of the profound effects of deafening was observed in the cochlear nuclei as a consequence of chronic intracochlear electrical stimulation which was begun 11 to 16 weeks after deafening. C1 UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,COLEMAN LAB,SAN FRANCISCO,CA 94143. CR BLATCHLEY BJ, 1983, EXP NEUROL, V80, P81, DOI 10.1016/0014-4886(83)90008-0 CHOUARD CH, 1983, ACTA OTO-LARYNGOL, V95, P639, DOI 10.3109/00016488309139456 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 COLEMAN J R, 1979, Experimental Neurology, V64, P533 CURTISS J, 1989, COCHLEAR IMPLANTS YO, P293 EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 FENG AS, 1980, BRAIN RES, V189, P530, DOI 10.1016/0006-8993(80)90112-2 HOLM VA, 1969, PEDIATRICS, V43, P833 JEANBAPTIST M, 1975, J COMP NEUROL, V161, P111 Larsen S A, 1984, Acta Otolaryngol Suppl, V417, P1 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1991, HEARING RES, V54, P251, DOI 10.1016/0378-5955(91)90120-X MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 OWENS E, 1989, COCHLEAR IMPLANTS YO, P315 POWELL TPS, 1962, J ANAT, V96, P249 Rebscher S. J., 1985, COCHLEAR IMPLANTS, P74 RUBEL EW, 1984, HEARING SCI, P109 Ruben R J, 1986, Acta Otolaryngol Suppl, V429, P61 SNYDER RL, 1990, HEARING RES, V50, P7, DOI 10.1016/0378-5955(90)90030-S TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 WEBSTER DB, 1977, ARCH OTOLARYNGOL, V103, P392 WEBSTER DB, 1983, INT J PEDIATR OTORHI, V6, P107 WEBSTER DB, 1988, HEARING RES, V32, P185, DOI 10.1016/0378-5955(88)90090-1 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 WEBSTER DB, 1983, HEARING RES, V12, P145, DOI 10.1016/0378-5955(83)90123-5 NR 28 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 AUG PY 1991 VL 54 IS 2 BP 272 EP 280 DI 10.1016/0378-5955(91)90121-O PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200006 PM 1938629 ER PT J AU CODE, RA CHURCHILL, L AF CODE, RA CHURCHILL, L TI GABA-A RECEPTORS IN AUDITORY BRAIN-STEM NUCLEI OF THE CHICK DURING DEVELOPMENT AND AFTER COCHLEA REMOVAL SO HEARING RESEARCH LA English DT Article DE NUCLEUS MAGNOCELLULARIS; NUCLEUS LAMINARIS; SUPERIOR OLIVE; IMMUNOCYTOCHEMISTRY; RECEPTOR AUTORADIOGRAPHY ID IMMUNOCYTOCHEMICAL LOCALIZATION; AUTORADIOGRAPHIC LOCALIZATION; BENZODIAZEPINE RECEPTORS; GABAERGIC NEURONS; CHANNEL COMPLEX; RAT-BRAIN; STEM; IMMUNOREACTIVITY; SYSTEM; TERMINALS AB The presence of GABA(A) receptors (GABARs) in auditory brainstem nuclei of the chick was determined by immunocytochemical (ICC) and receptor autoradiographic techniques. A monoclonal antibody to the GABAR/benzodiazepine/chloride channel complex and radiolabeled ligand binding using [H-3]-muscimol, a GABA agonist, revealed labeling in nucleus magnocellularis (NM), nucleus laminaris (NL), nucleus angularis (NA), and the superior olive (SO) in both posthatch and embryonic chicks. GABAR-immunoreactivity (GABAR-I), as well as [H-3]-muscimol binding, appear homogeneous throughout these nuclei at all ages studied. During development, GABAR-I is first observed in these nuclei around embryonic day 13 (E13). GABAR-I, which appears heavier in embryos than in posthatch chicks, becomes less intense with age in all 4 nuclei. Levels of receptor binding are also greater in embryos compared to posthatch chicks. [H-3]-Muscimol binding is consistently greatest in SO followed by that in NL. NM and NA exhibit the least amount of binding at all ages studied. [H-3]-Muscimol binding decreases in auditory brainstem nuclei as a function of age. Two days after unilateral cochlea removal, there is an apparent increase in GABAR-I in the ipsilateral NM compared to controls. This, however, may be the result of a decrease in the cross-sectional area of NM neurons as a result of de-afferentation (Born and Rubel, 1985). In contrast, there is a 28% decrease in [H-3]-muscimol binding in the ipsilateral NM compared to controls probably reflecting the 30% reduction in the number of NM neurons due to cochlea removal (Born and Rubel, 1985). Fourteen days after cochlea removal, there is still a small, but not significant, decrease in [H-3]-muscimol binding in the ipsilateral NM. In the contralateral NM, GABAR-I is less intense compared to that in the ipsilateral NM and controls. Additionally, there is a slight but insignificant decrease in [H-3]-muscimol binding compared to that in controls 2 days after cochlea removal. After 14 days survival, however, the average binding is similar to that in controls. Thus, cochlea removal appears to transiently decrease the number of GABARs in the ipsilateral NM and may have a similar, but not as dramatic, effect in the contralateral NM. These GABARs are most likely to be postsynaptic, that is, located on NM neurons. C1 UNIV WASHINGTON,SCH MED,HEARING DEV LABS,SEATTLE,WA 98195. WASHINGTON STATE UNIV,DEPT VET & COMPARAT ANAT PHYSIOL & PHARMACOL,PULLMAN,WA 99164. CR ADAMS JC, 1987, J COMP NEUROL, V262, P375, DOI 10.1002/cne.902620305 BORN DE, 1985, J COMP NEUROL, V231, P435, DOI 10.1002/cne.902310403 CARR CE, 1989, J COMP NEUROL, V286, P190, DOI 10.1002/cne.902860205 CASPARY DM, 1984, HEARING RES, V13, P113, DOI 10.1016/0378-5955(84)90102-3 CHANGEUX JP, 1976, NATURE, V264, P705, DOI 10.1038/264705a0 CHURCHILL L, 1989, BRAIN RES, V511, P41 CODE RA, 1990, J COMP NEUROL, V301, P643, DOI 10.1002/cne.903010411 CODE RA, 1989, J COMP NEUROL, V284, P504, DOI 10.1002/cne.902840403 CODE RA, 1988, EFFECTS UNILATERAL R, P43 DEBLAS AL, 1988, J NEUROSCI, V8, P602 DIETL MM, 1988, BRAIN RES, V439, P366, DOI 10.1016/0006-8993(88)91496-5 GLENDENNING KK, 1988, J COMP NEUROL, V275, P288, DOI 10.1002/cne.902750210 HENDRY SHC, 1990, J NEUROSCI, V10, P2438 HERKENHAM M, 1986, QUANTITATIVE RECEPTO, P137 HERKENHAM M, 1987, NEUROSCIENCE, V23, P1, DOI 10.1016/0306-4522(87)90268-5 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 ISEN RW, 1981, MOL PHARMACOL, V19, P217 KUHAR MJ, 1985, TRENDS NEUROSCI, V8, P190, DOI 10.1016/0166-2236(85)90076-1 MALOTEAUX JM, 1987, EUR J PHARMACOL, V144, P173, DOI 10.1016/0014-2999(87)90517-6 MCCABE RT, 1986, LIFE SCI, V39, P1937 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 MUGNAINI E, 1985, J COMP NEUROL, V235, P61, DOI 10.1002/cne.902350106 MULLER CM, 1987, BRAIN RES, V414, P376, DOI 10.1016/0006-8993(87)90019-9 MULLER CM, 1987, NEUROSCI LETT, V77, P272, DOI 10.1016/0304-3940(87)90511-8 OLSEN RW, 1983, J NEUROCHEM, V41, P1653, DOI 10.1111/j.1471-4159.1983.tb00877.x PALACIOS JM, 1979, BRAIN RES, V179, P390, DOI 10.1016/0006-8993(79)90456-6 PALACIOS JM, 1981, BRAIN RES, V222, P285, DOI 10.1016/0006-8993(81)91034-9 PAN HS, 1983, J NEUROSCI, V3, P1189 PENNEY JB, 1981, SCIENCE, V214, P1036, DOI 10.1126/science.6272394 PEYRET D, 1986, HEARING RES, V23, P115, DOI 10.1016/0378-5955(86)90008-0 RIOS H, 1987, INT J DEV NEUROSCI, V5, P319, DOI 10.1016/0736-5748(87)90007-4 Roberts E., 1976, GABA NERVOUS SYSTEM ROBERTS EUGENE, 1968, BRAIN RES, V8, P1, DOI 10.1016/0006-8993(68)90170-4 ROBERTS RC, 1987, J COMP NEUROL, V258, P267, DOI 10.1002/cne.902580207 RUBEL EW, 1990, J NEUROBIOL, V21, P169, DOI 10.1002/neu.480210112 STRAUS W, 1982, J HISTOCHEM CYTOCHEM, V30, P491 TALLMAN JF, 1985, ANNU REV NEUROSCI, V8, P21 THOMPSON GC, 1985, BRAIN RES, V339, P119, DOI 10.1016/0006-8993(85)90628-6 VITORICA J, 1988, J NEUROSCI, V8, P615 WADDINGTON JL, 1978, NATURE, V276, P618, DOI 10.1038/276618a0 WENTHOLD RJ, 1986, BRAIN RES, V380, P7, DOI 10.1016/0006-8993(86)91423-X YAZULLA S, 1989, J COMP NEUROL, V280, P15, DOI 10.1002/cne.902800103 NR 42 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 1991 VL 54 IS 2 BP 281 EP 295 DI 10.1016/0378-5955(91)90122-P PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200007 PM 1657849 ER PT J AU GAO, WY DING, DL ZHENG, XY RUAN, FM AF GAO, WY DING, DL ZHENG, XY RUAN, FM TI CHANGES IN THE STEREOCILIA AND NONMONOTONIC PATTERN OF THRESHOLD SHIFT AFTER EXPOSURE TO IMPULSE NOISE SO HEARING RESEARCH LA English DT Article DE IMPULSE NOISE; STEREOCILIA; THRESHOLD SHIFT; TECTORIAL MEMBRANE ID GUINEA-PIG COCHLEA; ACOUSTIC TRAUMA; DAMAGE AB The recovery pattern of threshold shift (TS) and 'dynamic' changes in the stereocilia after exposure to high-level impulse noise in guinea pigs were investigated. 33 albino guinea pigs were exposed to 10 impulse noises at the rate of 1/min. The noise had peak level of 166 dB SPL and a duration of 0.1 ms. Thirteen of the exposed animals were used to systematically measure threshold shifts at regular intervals from 0.5 h to 30 days post-exposure by click auditory cortex evoked response (AC-ER). Twelve of the animals who had typical TS at the same intervals were killed for scanning electron microscopic examination. The recovery pattern of threshold shifts was non-monotonic, which was different from that seen with continuous noise. There was an increase in TS after the exposure and the maximum level of TS was found at 8 h post-exposure. Morphological analysis also showed delayed changes in the stereocilia after exposure. The severity of changes in the stereocilia reached a peak at 8 h, at which time complete fusion of hair bundles took place. The tectorial material found on the tips of the stereocilia may be responsible for the sequence of the changes. C1 CHANG ZHENG HOSP,DEPT OTOLARYNGOL,SHANGHAI,PEOPLES R CHINA. RENJI HOSP,DEPT OTOLARYNGOL,SHANGHAI,PEOPLES R CHINA. CR BOHNE BA, 1983, HEARING RES, V11, P41, DOI 10.1016/0378-5955(83)90044-8 CODY AR, 1983, HEARING RES, V9, P55, DOI 10.1016/0378-5955(83)90134-X ENGSTROM B, 1983, HEARING RES, V12, P251, DOI 10.1016/0378-5955(83)90110-7 FREDELIUS L, 1988, ACTA OTO-LARYNGOL, V106, P81, DOI 10.3109/00016488809107374 GAO WY, 1990, NAVY MED J CHIN PLA, V1, P6 GAO WY, 1989, J ACOUST SOC AM S1, V86, pS72, DOI 10.1121/1.2027629 HAMERNIK RP, 1987, J ACOUST SOC AM, V81, P1118, DOI 10.1121/1.394632 HENDERSON D, 1986, J ACOUST SOC AM, V80, P569, DOI 10.1121/1.394052 KONISHI T, 1979, HEARING RES, V1, P325, DOI 10.1016/0378-5955(79)90004-2 LENOIR M, 1987, HEARING RES, V26, P199, DOI 10.1016/0378-5955(87)90112-2 LIBERMAN MC, 1987, HEARING RES, V26, P45, DOI 10.1016/0378-5955(87)90035-9 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 LUZ GA, 1970, J ACOUST SOC AM, V48, pA96 LUZ GA, 1971, J ACOUST SOC AM, V49, P1770, DOI 10.1121/1.1912580 POPELAR J, 1987, HEARING RES, V26, P239, DOI 10.1016/0378-5955(87)90060-8 ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 SLEPECKY N, 1982, ACTA OTO-LARYNGOL, V93, P329, DOI 10.3109/00016488209130890 THORNE PR, 1986, HEARING RES, V21, P41, DOI 10.1016/0378-5955(86)90044-4 WARD WD, 1959, J ACOUST SOC AM, V31, P522, DOI 10.1121/1.1907746 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 AUG PY 1991 VL 54 IS 2 BP 296 EP 304 PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200008 PM 1938630 ER PT J AU DECRAEMER, WF KHANNA, SM FUNNELL, WRJ AF DECRAEMER, WF KHANNA, SM FUNNELL, WRJ TI MALLEUS VIBRATION MODE-CHANGES WITH FREQUENCY SO HEARING RESEARCH LA English DT Article DE MANUBRIUM; VIBRATION MODE; ROTATION AXIS; INTERFEROMETER ID HETERODYNE INTERFEROMETER; CAT; EAR AB The mode of vibration of the cat manubrium is investigated by measuring its vibration in response to sound stimulus at four locations between the umbo and the processus lateralis with a heterodyne interferometer. The determination of mode requires high precision in measurement because amplitude differences between the points are small (about 20% at low audio-frequencies). Changes in the frequency response with time have been reported in an earlier paper. The nature and magnitude of this time change is analysed in detail: over a period of 1 h the average change in amplitude is about 5% and in phase 5-degrees. The malleus vibration at some frequencies is purely translational, it is rotational at others and mixed at most frequencies. When the motion is rotational the position of the axis of rotation shifts with frequency, the shifts are so large that the axis can lie near the umbo so that amplitudes at the processus lateralis are larger than at the umbo. The classical concept of the malleus rotating around a fixed axis running from the anterior mallar to the posterior incudal ligament fits our measurements only at low frequencies. C1 COLUMBIA UNIV,DEPT OTOLARYNGOL,NEW YORK,NY 10027. MCGILL UNIV,DEPT BIOMED ENGN,MONTREAL H3A 2T5,QUEBEC,CANADA. MCGILL UNIV,DEPT OTOLARYNGOL,MONTREAL H3A 2T5,QUEBEC,CANADA. RP DECRAEMER, WF (reprint author), ANTWERP STATE UNIV CTR,BIOMED PHYS LAB,171 GROENENBORGERLAAN,B-2020 ANTWERP,BELGIUM. RI Funnell, Robert/B-4488-2013 CR BARANY E, 1938, ACTA OTOLARYNGOL S S, V26 DECRAEMER WF, 1989, HEARING RES, V38, P1, DOI 10.1016/0378-5955(89)90123-8 DECRAEMER WF, 1990, HEARING RES, V47, P205, DOI 10.1016/0378-5955(90)90152-F GUINAN JJ, 1967, J ACOUST SOC AM, V41, P1237, DOI 10.1121/1.1910465 GUNDERSEN T, 1976, ACTA OTO-LARYNGOL, V82, P16, DOI 10.3109/00016487609120858 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 KHANNA SM, 1970, HOLOGRAPHIC STUDY TY MOLLER AR, 1963, J ACOUST SOC AM, V35, P1526, DOI 10.1121/1.1918742 VLAMING MSM, 1987, THESIS TECHNICAL U D von Bekesy G., 1960, EXPT HEARING, P745 Wever EG, 1954, PHYSL ACOUSTICS WILLEMIN JF, 1988, J ACOUST SOC AM, V83, P787, DOI 10.1121/1.396122 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 NR 13 TC 46 Z9 46 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD AUG PY 1991 VL 54 IS 2 BP 305 EP 318 DI 10.1016/0378-5955(91)90124-R PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GC652 UT WOS:A1991GC65200009 PM 1938631 ER PT J AU SMITH, DI MILLS, JH AF SMITH, DI MILLS, JH TI LOW-FREQUENCY COMPONENT OF THE GERBIL BRAIN-STEM RESPONSE - RESPONSE CHARACTERISTICS AND ANESTHESIA EFFECTS SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM RESPONSE; AUDITORY EVOKED POTENTIAL; LOW-FREQUENCY POTENTIAL; SLOW-WAVE; ANESTHESIA; KETAMINE; GERBIL ID AUDITORY EVOKED-POTENTIALS; MIDDLE LATENCY RESPONSE; STEM RESPONSE; SLOW; CAT; STIMULI; SCALP AB The auditory brainstem response (ABR) was recorded with epidural electrodes in awake and anesthetized gerbils. Low- and high-frequency components of the ABR were separated by analog filters and compared as functions of stimulus intensity, frequency, repetition rate, and effects of anesthesia. In response to 0.5 kHz tone bursts, thresholds of the low-frequency component (LF-ABR) were significantly lower than that of the most prominent peak of the high-frequency components (wave P4). At both 2 and 4 kHz, thresholds of the LF-ABR and wave P4 were not significantly different. Changes in stimulus intensity over a 70 dB range produced similar changes in peak amplitudes and latencies for the LF-ABR and P4, However, while the amplitude of the LF-ABR was inversely related to stimulus frequency, the amplitude of P4 was reduced at 0.5 kHz, as compared to 2 and 4 kHz. Increases in stimulus rate from 7 to 100 bursts/s produced little change in the amplitude of the LF-ABR. At rates of 80 and 100 bursts/s, the LF-ABR was sinusoidal in appearance due to the proximity of successively generated potentials. In contrast, the amplitude of P4 varied inversely with stimulus rate between 20 and 100 bursts/s. Administration of ketamine and xylazine produced minor changes in the amplitudes and latencies of both the LF-ABR and wave P4. The response characteristics of the gerbil LF-ABR are similar to those of the low-frequency component of the ABR in humans and cats. The LF-ABR provides an estimate of hearing threshold at low frequencies (0.5 kHz) as well as higher frequencies (2-4 kHz). A major advantage to the LF-ABR is that it can be recorded at high stimulation rates in awake and anesthetized animals, thus providing an efficient measure of auditory function. C1 MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,CHARLESTON,SC 29425. 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Res. PD JUL PY 1991 VL 54 IS 1 BP 1 EP 10 DI 10.1016/0378-5955(91)90130-2 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800001 PM 1917708 ER PT J AU HARRISON, RV NAGASAWA, A SMITH, DW STANTON, S MOUNT, RJ AF HARRISON, RV NAGASAWA, A SMITH, DW STANTON, S MOUNT, RJ TI REORGANIZATION OF AUDITORY-CORTEX AFTER NEONATAL HIGH-FREQUENCY COCHLEAR HEARING-LOSS SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; COCHLEAR HEARING LOSS ID GUINEA-PIGS; CAT; ORGANIZATION; ADULT; REPRESENTATION; RESPONSES; COLUMNS; MAMMALS AB Cochleotopic representation in cortex (AI) is extensively reorganized in cats having neonatal, bilateral high frequency cochlear hearing loss. Anterior areas of AI, normally devoted to high frequencies, contain neurons which are almost all tuned to one lower frequency. This frequency corresponds, at the level of the cochlea, to the border between normal and damaged haircell regions. C1 UNIV TORONTO,DEPT OTOLARYNGOL,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT PHYSIOL,TORONTO M5S 1A1,ONTARIO,CANADA. RP HARRISON, RV (reprint author), HOSP SICK CHILDREN,RES INST,DEPT OTOLARYNGOL,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. CR DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 EVANS EF, 1975, AUDIOLOGY, V14, P419 Harrison R V, 1979, SCAND AUDIOL S, P83 HARRISON RV, 1984, HEARING RES, V14, P79, DOI 10.1016/0378-5955(84)90070-4 HARRISON RV, 1981, J ACOUST SOC AM, V70, P1036, DOI 10.1121/1.386954 HUBEL DH, 1965, J NEUROPHYSIOL, V28, P1041 IMIG TJ, 1977, BRAIN RES, V138, P241, DOI 10.1016/0006-8993(77)90743-0 ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 KAAS JH, 1983, ANNU REV NEUROSCI, V6, P325, DOI 10.1146/annurev.ne.06.030183.001545 KAAS JH, 1990, SCIENCE, V248, P229, DOI 10.1126/science.2326637 Kiang N Y, 1970, Ciba Found Symp, P241 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 MERZENICH MM, 1982, TRENDS NEUROSCI, V5, P434, DOI 10.1016/0166-2236(82)90235-1 MERZENICH MM, 1983, NEUROSCIENCE, V8, P33, DOI 10.1016/0306-4522(83)90024-6 MERZENIC.MM, 1973, BRAIN RES, V50, P275, DOI 10.1016/0006-8993(73)90731-2 MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MOVSHON JA, 1981, ANNU REV PSYCHOL, V32, P477, DOI 10.1146/annurev.ps.32.020181.002401 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 ROSE JE, 1949, J COMP NEUROL, V91, P409, DOI 10.1002/cne.900910305 SCHREINER CE, 1984, J NEUROPHYSIOL, V51, P1284 WAITE PME, 1978, NATURE, V274, P600, DOI 10.1038/274600a0 WIESEL TN, 1963, J NEUROPHYSIOL, V26, P1003 WIESEL TN, 1974, J COMP NEUROL, V158, P307, DOI 10.1002/cne.901580306 Woolsey C. N., 1942, J HOPKINS HOSP B, V71, P315 NR 25 TC 100 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 JUL PY 1991 VL 54 IS 1 BP 11 EP 19 DI 10.1016/0378-5955(91)90131-R PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800002 PM 1917710 ER PT J AU BANCROFT, BR BOETTCHER, FA SALVI, RJ WU, JH AF BANCROFT, BR BOETTCHER, FA SALVI, RJ WU, JH TI EFFECTS OF NOISE AND SALICYLATE ON AUDITORY EVOKED-RESPONSE THRESHOLDS IN THE CHINCHILLA SO HEARING RESEARCH LA English DT Article DE ASPIRIN; HEARING LOSS, CHEMICAL-INDUCED; CHINCHILLA; HEARING LOSS, NOISE-INDUCED; SALICYLATE; THRESHOLD SHIFT ID HEARING-LOSS; SODIUM-SALICYLATE; AUDIBILITY CURVE; ASPIRIN; KANAMYCIN; EXPOSURE AB The combined effects of noise and sodium salicylate on auditory sensitivity were examined in the chinchilla. Sensitivity was monitored by recording the evoked response recorded with an electrode implanted in the inferior colliculus. Sodium salicylate (300 mg/kg/day), an octave band of noise centered at 500 Hz (80 or 105 dB SPL), or both of these agents were delivered for 15 days. Threshold testing was performed at 7 frequencies before, during, and after exposure to the ototraumatic agent(s). The salicylate alone caused an average temporary threshold shift of less than 10 dB and essentially no permanent shift. Animals exposed to noise alone had temporary and permanent threshold shifts which were not significantly different from those observed in animals exposed to noise plus salicylate. The data suggest that a single daily injection of sodium salicylate, resulting in peak serum salicylate concentrations of 28 to 34 mg% 2 to 4 hours after delivery, does not exacerbate the temporary or permanent threshold shifts induced by 15-day, 24-hour-per day exposure to either a moderate- or high-level, low-frequency noise. A second series of experiments utilizing a higher dose of salicylate (450 mg/kg/day) was not completed due to a high mortality rate among subjects that received salicylate and were exposed to noise. This result was consistent with other recent examinations of the interaction of these agents. C1 SUNY BUFFALO,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14260. CR BERGER EH, 1987, SOUND VIBRATION, V21, P40 BOETTCHER FA, 1990, ARCH OTOLARYNGOL, V116, P681 BOETTCHER FA, 1989, HEARING RES, V42, P129, DOI 10.1016/0378-5955(89)90139-1 BOETTCHER FA, 1987, EAR HEARING, V8, P192, DOI 10.1097/00003446-198708000-00003 BRENNAN JF, 1989, EXPERIENTIA, V45, P731, DOI 10.1007/BF01974571 BROWN JJ, 1980, ARCH OTOLARYNGOL, V106, P744 CARSON SS, 1989, ARCH OTOLARYNGOL, V115, P1070 DAY RO, 1989, BRIT J CLIN PHARMACO, V28, P695 EDDY LB, 1976, ISA T, V15, P103 FECHTER LD, 1988, HEARING RES, V34, P39, DOI 10.1016/0378-5955(88)90049-4 GRATTON MA, 1990, HEARING RES, V50, P211, DOI 10.1016/0378-5955(90)90046-R HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 JARDINI L, 1978, RHEUMATOL REHABIL, V17, P233, DOI 10.1093/rheumatology/17.4.233 LAMBERT PR, 1986, ARCH OTOLARYNGOL, V112, P1043 LINDGREN F, 1987, SCAND AUDIOL, V16, P41 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, 1983, HEARING RES, V9, P295, DOI 10.1016/0378-5955(83)90033-3 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 MITCHELL C, 1974, J ACOUST SOC AM, V55, pS2 MORATA TC, 1989, SCAND AUDIOL, V18, P53, DOI 10.3109/01050398909070723 MYERS EN, 1965, ARCHIV OTOLARYNGOL, V82, P483 PEDERSEN CB, 1974, AUDIOLOGY, V13, P311 Rainsford KD, 1984, ASPIRIN SALICYLATES RYAN AF, 1982, AM J OTOLARYNG, V3, P264, DOI 10.1016/S0196-0709(82)80065-3 SALVI RJ, 1982, AM J OTOLARYNG, V3, P408, DOI 10.1016/S0196-0709(82)80018-5 SPONGR V, 1990, EFFECTS SALICYLATE N, P372 TRINDER P, 1954, BIOCHEM J, V57, P301 WOODFORD CM, 1978, ANN OTO RHINOL LARYN, V87, P117 NR 29 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 20 EP 28 DI 10.1016/0378-5955(91)90132-S PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800003 PM 1917714 ER PT J AU DRENCKHAHN, D MERTE, C VONDURING, M SMOLDERS, J KLINKE, R AF DRENCKHAHN, D MERTE, C VONDURING, M SMOLDERS, J KLINKE, R TI ACTIN, MYOSIN AND ALPHA-ACTININ CONTAINING FILAMENT BUNDLES IN HYALINE CELLS OF THE CAIMAN COCHLEA SO HEARING RESEARCH LA English DT Article DE HYALINE CELLS; BASILAR MEMBRANE; CONTRACTILE PROTEINS; CAIMAN ID HAIR-CELLS; BASILAR-MEMBRANE; NERVE-FIBERS; TEMPERATURE; MICROSCOPE; CROCODILUS; MATRIX AB Hyaline cells of the auditory organ of the spectacled caiman contain smooth muscle-like filament bundles within their basal cell pole. These bundles were heavily labeled with antibodies to actin, myosin and alpha-actinin (muscular Z-line protein). Since hyaline cells are firmly attached to the basilar membrane these cells may actively modify the stiffness of the basilar membrane. A contractile mechanism in hyaline cells might affect frequency tuning of primary auditory afferents. This frequency tuning has been shown to be a temperature-dependent process in caimans and other submammalian species. The presence of synaptic contacts between efferent nerve fibres and hyaline cells suggests neural control of hyaline cell activity. C1 RUHR UNIV BOCHUM,INST ANAT,W-4630 BOCHUM,GERMANY. UNIV FRANKFURT,ZENTRUM PHYSIOL,W-6000 FRANKFURT,GERMANY. RP DRENCKHAHN, D (reprint author), UNIV WURZBURG,INST ANAT,DEPT ANAT,W-8700 WURZBURG,GERMANY. CR DRENCKHAHN D, 1986, J CELL BIOL, V102, P1738, DOI 10.1083/jcb.102.5.1738 DRENCKHAHN D, 1980, J CELL BIOL, V86, P475, DOI 10.1083/jcb.86.2.475 DRENCKHAHN D, 1988, J CELL BIOL, V107, P1037, DOI 10.1083/jcb.107.3.1037 DRENCKHAHN D, 1982, NATURE, V300, P531, DOI 10.1038/300531a0 DRENCKHAHN D, 1987, EUR J CELL BIOL, V45, P107 DRENCKHAHN D, 1985, AUDITORY BIOCH, P317 EATOCK RA, 1981, J COMP PHYSIOL, V142, P219 EATOCK RA, 1976, J ACOUST SOC AM, V60, pS80, DOI 10.1121/1.2003544 EVANS E F, 1974, Journal of Physiology (Cambridge), V242, p129P EVANS EF, 1974, J PHYSL, V238, P65 EVANS EF, 1982, J PHYSIOL-LONDON, V331, P385 FETTIPLACE R, 1987, TRENDS NEUROSCI, V10, P421, DOI 10.1016/0166-2236(87)90013-0 FUCHS PA, 1988, J NEUROSCI, V8, P2460 FUCHS PA, 1988, J COMP PHYSIOL A, V164, P151, DOI 10.1007/BF00603947 GUMMER AW, 1983, HEARING RES, V12, P367, DOI 10.1016/0378-5955(83)90006-0 GUMMER AW, 1987, HEARING RES, V29, P63, DOI 10.1016/0378-5955(87)90206-1 HELD H, 1926, HDB NORMALEN PATHOLO, V11, P467 HENSON MM, 1988, HEARING RES, V35, P237, DOI 10.1016/0378-5955(88)90121-9 KLINKE R, 1977, PSYCHOPHYSICS PHYSL, P109 MOFFAT AJM, 1976, J ACOUST SOC AM, V60, pS80, DOI 10.1121/1.2003543 SCHERMULY L, 1985, J COMP PHYSIOL A, V156, P209, DOI 10.1007/BF00610863 SMOLDERS JWT, 1984, J COMP PHYSIOL, V155, P19, DOI 10.1007/BF00610927 STIEBLER IB, 1991, IN PRESS HEAR RES TAKASAKA T, 1971, J ULTRA MOL STRUCT R, V35, P20, DOI 10.1016/S0022-5320(71)80141-7 VANDIJK P, 1991, IN PRESS HEAR RES VONBEKESY G, 1960, EXP HEARING, P500 von Düring M, 1974, Z Anat Entwicklungsgesch, V145, P41 WILSON JP, 1985, HEARING RES, V18, P1, DOI 10.1016/0378-5955(85)90105-4 NR 28 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 1991 VL 54 IS 1 BP 29 EP 38 DI 10.1016/0378-5955(91)90133-T PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800004 PM 1717422 ER PT J AU HOEFFDING, V FECHTER, LD AF HOEFFDING, V FECHTER, LD TI UNUSUAL MORPHOLOGY OF THE STRIA VASCULARIS IN PIGMENTED STRAIN-2/NCR GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE COCHLEA; STRIA VASCULARIS; MELANIN; STRAIN DIFFERENCE; GUINEA PIG ID NORWAY RATS; ALBINO; DIFFERENCE AB This paper reports an abnormality in the morphology of the apical stria vascularis of inbred 2/NCR guinea pigs as compared to outbred animals. Cochleas were embedded in plastic, sectioned, and examined in the light and electron microscopes. In the 2/NCR animals, the apical stria vascularis consisted of a cuboidal epithelium composed of a monolayer of poorly differentiated cells. Few or no capillaries were associated with this epithelium. No melanin pigment was present in the abnormal region of the stria in these animals, although pigmentation appeared normal in lower turns of the cochlea. Measurements of compound action potential thresholds between 2 and 40 kHz revealed no differences in auditory function between the two strains. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT ENVIRONM HLTH SCI,DIV TOXICOL SCI,ROOM 7033,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,BALTIMORE,MD 21205. 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PD JUL PY 1991 VL 54 IS 1 BP 39 EP 44 DI 10.1016/0378-5955(91)90134-U PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800005 PM 1917715 ER PT J AU PATUZZI, RB THOMPSON, ML AF PATUZZI, RB THOMPSON, ML TI COCHLEAR EFFERENT NEURONS AND PROTECTION AGAINST ACOUSTIC TRAUMA - PROTECTION OF OUTER HAIR CELL-RECEPTOR CURRENT AND INTERANIMAL VARIABILITY SO HEARING RESEARCH LA English DT Article DE EFFERENTS; ACOUSTIC TRAUMA; PROTECTION; OUTER HAIR CELLS; SUSCEPTIBILITY ID CROSSED OLIVOCOCHLEAR BUNDLE; BRAIN-STEM ANOMALIES; GUINEA-PIG COCHLEA; TEMPORARY THRESHOLD SHIFTS; ELECTRICAL-STIMULATION; FLUORESCENT TRACERS; ALBINO CATS; PROJECTIONS; SENSITIVITY; EXPOSURES AB We have measured the changes in neural and microphonic sensitivity in the basal turn of the guinea-pig cochlea produced by intense acoustic overstimulation (10 kHz, 115 dB SPL for 60 s and 150 s). As reported previously, the drop in neural and microphonic sensitivities observed after overstimulation were highly correlated [Patuzzi et al. (1989) Hear. Res. 39, 189-202]. Presentation of a non-traumatizing pure-tone to the contralateral ear (10 kHz, 80 dB SPL) during acoustic overstimulation reduced the amount of acoustic trauma measured using the neural response or the microphonic response. Transection of the medial olivo-cochlear system of efferent fibres at the floor of the fourth ventricle abolished this protective effect of contralateral sound and dramatically reduced the variability in the data. Since the low-frequency microphonic is a simple measure of the receptor current through the outer hair cells, and this current probably plays a part in enhancing the mechanical sensitivity of the cochlea, the protection of the microphonic we have observed suggests that the efferent system protects neural sensitivity by protecting the mechano-electrical transduction of outer hair cells. The drop in variability after sectioning the efferents also suggests that inter-animal variations in susceptibility to noise trauma may be a consequence of differing tonic activity of the efferents, and/or a variation in the sensitivity of the efferent pathway. RP PATUZZI, RB (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. 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Res. PD JUL PY 1991 VL 54 IS 1 BP 45 EP 58 DI 10.1016/0378-5955(91)90135-V PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800006 PM 1917716 ER PT J AU PRIETO, JJ RUEDA, J RUBIO, ME MERCHAN, JA AF PRIETO, JJ RUEDA, J RUBIO, ME MERCHAN, JA TI PILOCARPINE ELICITS THE INTERDENTAL CELL SECRETORY ACTIVITY OF THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE INNER EAR; INTERDENTAL CELLS; TECTORIAL MEMBRANE; ENDOLYMPH; PILOCARPINE; SECRETION ID TANNIC-ACID; TECTORIAL MEMBRANE; FIXATION; ACTIN; RAT AB Subcutaneous injection of pilocarpine in guinea pigs resulted in the following ultrastructural changes: 1) the apical cavities of the interdental cells were filled with a substance indistinguishable from the overlying amorphous layer of the TM; 2) a great number of spherical structures appeared over the limbal portion of the tectorial membrane. In TEM photomicrographs these structures displayed the same appearance as the amorphous layer of the TM and were usually continuous to it; 3) the number of holes that decorate the upper surface of the limbal portion of the TM was dramatically increased and it was found that they connect the endolymphatic space to the apical cavities of the interdental cells; 4) there was an increase in the number of the small extracellular vesicles found in the clear spaces of the tectorial membrane. These facts suggest that pilocarpine stimulates the secretion of the interdental cells, confirming the existence of the secretory processes previously described (Prieto et al., 1990). These findings can be related to the turnover of the TM in the adult animal and, perhaps, to the secretion of some organic compound to the endolymph. We postulate that the actions of pilocarpine on the interdental cells are most probably mediated by the activation of muscarinic acetylcholine receptors in these cells. C1 UNIV ALICANTE,INST NEUROSCI,E-03080 ALICANTE,SPAIN. RP PRIETO, JJ (reprint author), UNIV ALICANTE,DEPT HISTOL,APDO 374,E-03080 ALICANTE,SPAIN. CR BEBBINGTON A., 1965, ADVANCE DRUG RES, V2, P143 BELANGER LF, 1953, SCIENCE, V118, P520, DOI 10.1126/science.118.3070.520 BIREMBAUT P, 1982, J HISTOCHEM CYTOCHEM, V30, P75 FUTAESAKU Y, 1972, P INT C HISTOCHEM CY, V4, P155 ISHIYAMA E, 1970, PRACT-OTO-RHINO-LARY, V32, P321 IURATO S, 1962, Z ZELLFORSCH MIK ANA, V56, P40, DOI 10.1007/BF00326848 KHALKHALIELLIS Z, 1987, HEARING RES, V25, P185, DOI 10.1016/0378-5955(87)90090-6 Kuijpers W, 1986, Acta Otolaryngol Suppl, V429, P35 LAFOUNTAIN JR, 1977, J ULTRA MOL STRUCT R, V58, P78, DOI 10.1016/S0022-5320(77)80009-9 LIDOW MS, 1984, J ULTRA MOL STRUCT R, V86, P18, DOI 10.1016/S0022-5320(84)90092-3 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 LIM D J, 1970, Journal of Laryngology and Otology, V84, P1241, DOI 10.1017/S0022215100072984 Lim D J, 1969, Acta Otolaryngol Suppl, V255, P1 MANNI JJ, 1987, HEARING RES, V26, P229, DOI 10.1016/0378-5955(87)90059-1 MAUPIN P, 1983, J CELL BIOL, V96, P51, DOI 10.1083/jcb.96.1.51 NATHANSON NM, 1987, ANNU REV NEUROSCI, V10, P195 PRIETO J, 1986, HEARING RES, V21, P277, DOI 10.1016/0378-5955(86)90225-X PRIETO JJ, 1990, HEARING RES, V45, P51, DOI 10.1016/0378-5955(90)90182-O RICHARDSON GP, 1987, HEARING RES, V25, P45, DOI 10.1016/0378-5955(87)90078-5 RODEWALD R, 1974, J CELL BIOL, V60, P423, DOI 10.1083/jcb.60.2.423 SIMIONESCU N, 1976, J CELL BIOL, V70, P608, DOI 10.1083/jcb.70.3.608 SINGLEY CT, 1980, HISTOCHEMISTRY, V65, P93, DOI 10.1007/BF00493158 STEEL KP, 1983, HEARING RES, V12, P265, DOI 10.1016/0378-5955(83)90111-9 THORN L, 1979, ANAT EMBRYOL, V155, P303, DOI 10.1007/BF00317643 VANDEURS B, 1975, J ULTRA MOL STRUCT R, V50, P185, DOI 10.1016/S0022-5320(75)80049-9 Voldrich L, 1967, Acta Otolaryngol, V63, P503 WILSMAN NJ, 1982, AM J ANAT, V164, P343, DOI 10.1002/aja.1001640405 NR 27 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 59 EP 66 DI 10.1016/0378-5955(91)90136-W PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800007 PM 1917717 ER PT J AU JIANG, ZD ZHENG, MS SUN, DK LIU, XY AF JIANG, ZD ZHENG, MS SUN, DK LIU, XY TI BRAIN-STEM AUDITORY EVOKED-RESPONSES FROM BIRTH TO ADULTHOOD - NORMATIVE DATA OF LATENCY AND INTERVAL SO HEARING RESEARCH LA English DT Article DE BRAIN-STEM AUDITORY EVOKED RESPONSES; DEVELOPMENT; AUDITORY; BRAIN-STEM; NORMATIVE STUDY; CHILDREN ID STEM RESPONSE; AUDIOMETRY; POTENTIALS; INFANTS; VARIABILITY; MATURATION; DIAGNOSIS; TERM AB Development of wave latency and interpeak interval (IPI) in brainstem auditory evoked responses (BAER) from birth to adulthood was examined. Adult equivalence was reached for most wave latencies and IPIs between the ages of 9 months and 3 years. The observation of the III-V/I-III interval ratio suggests that after term date the I-III IPI decreases more than the III-V IPI. I-III, III-V and I-V IPIs shortened from the 1-month old group to the 4-6 year old group by 22%, 15% and 19% respectively. The III-V/I-III interval ratio may be a useful BAER measure. Normative data of various BAER measures at different ages are presented. The slope of the L-I function for wave V was slightly steeper in younger groups than in older groups (40-mu-s/dB in the 1-month old group; 32-mu-s/dB in the adult group). This change which was accompanied by an age-related difference in the absolute wave latency. It is suggested that age-dependent norms should be used in evaluation of the L-I function. C1 SHANGHAI MED UNIV,CHILDRENS HOSP,DEPT CHILD HLTH,SHANGHAI,PEOPLES R CHINA. CR CHABOT RJ, 1986, HDB ELECTROENCEPHALO, V2, P263 CHIAPPA KH, 1979, ARCH NEUROL-CHICAGO, V36, P81 CLEMIS JD, 1979, LARYNGOSCOPE, V89, P31 COX LC, 1981, INT J PEDIATR OTORHI, V3, P213, DOI 10.1016/0165-5876(81)90005-7 DESPLAND PA, 1980, PEDIATR RES, V14, P154, DOI 10.1203/00006450-198002000-00018 GALAMBOS R, 1978, OTOLARYNG CLIN N AM, V11, P709 GOLDSTEIN PJ, 1979, AM J OBSTET GYNECOL, V135, P622 HECOX K, 1982, ANN NY ACAD SCI, V388, P538, DOI 10.1111/j.1749-6632.1982.tb50815.x HECOX K, 1974, ARCH OTOLARYNGOL, V99, P30 JACOBSON JT, 1982, EAR HEARING, V3, P263, DOI 10.1097/00003446-198209000-00006 JACOBSON S, 1963, J COMP NEUROL, V121, P5, DOI 10.1002/cne.901210103 JIANG ZD, 1991, IN PRESS ACTA PAEDIA JIANG ZD, 1990, DEV MED CHILD NEUROL, V32, P473 JIANG ZD, 1991, SCAND AUDIOL, V20, P41, DOI 10.3109/01050399109070789 JIANG ZD, 1990, EARLY HUM DEV, V23, P41, DOI 10.1016/0378-3782(90)90127-5 JIANG ZD, 1991, ELECTROEN CLIN NEURO, V80, P60, DOI 10.1016/0168-5597(91)90044-X KENDROR A, 1987, ELECTROEN CLIN NEURO, V68, P209, DOI 10.1016/0168-5597(87)90028-1 KRUMHOLZ A, 1985, ELECTROEN CLIN NEURO, V62, P124, DOI 10.1016/0168-5597(85)90024-3 LIU XY, 1991, IN PRESS ACTA OTOLAR LYNN GE, 1985, AUDITORY BRAINSTEM R, P203 Musiek F.E., 1985, AUDITORY BRAINSTEM R, P181 PICTON TW, 1978, OTOLARYNG CLIN N AM, V11, P263 PRATT H, 1976, ARCH OTO-RHINO-LARYN, V212, P85, DOI 10.1007/BF00454268 ROSENHAMER HJ, 1980, SCAND AUDIOL, V9, P93, DOI 10.3109/01050398009076342 ROWE MJ, 1978, ELECTROEN CLIN NEURO, V44, P459, DOI 10.1016/0013-4694(78)90030-5 SALAMY A, 1976, ELECTROEN CLIN NEURO, V40, P418, DOI 10.1016/0013-4694(76)90193-0 SALAMY A, 1982, EARLY HUM DEV, V6, P331, DOI 10.1016/0378-3782(82)90071-8 SCHULMANGALAMBOS C, 1975, J SPEECH HEAR RES, V18, P456 STOCKARD JE, 1983, EAR HEARING, V4, P11, DOI 10.1097/00003446-198301000-00005 NR 29 TC 22 Z9 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 67 EP 74 DI 10.1016/0378-5955(91)90137-X PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800008 PM 1917718 ER PT J AU ELBARBARY, A AF ELBARBARY, A TI AUDITORY-NERVE OF THE NORMAL AND JAUNDICED RAT .1. SPONTANEOUS DISCHARGE RATE AND COCHLEAR NERVE HISTOLOGY SO HEARING RESEARCH LA English DT Article DE HYPERBILIRUBINEMIA; AUDITORY NERVE FIBER; SPONTANEOUS DISCHARGE ACTIVITY; GUNN RAT; COCHLEAR NERVE HISTOLOGY ID BRAIN-STEM RESPONSES; BIRTH-WEIGHT INFANTS; GUINEA-PIG COCHLEA; HAIR CELL LESIONS; SERUM BILIRUBIN; GUNN-RATS; HYPER-BILITRUBINEMIA; TUNING CURVES; KERNICTERUS; DEAFNESS AB Hyperbilirubinemia is a major problem in neonatal intensive care. Hearing impairment is one of its sequelae. Although lesions of the central auditory pathways are known to be associated with this disorder in both humans and homozygous Gunn rats, the presence of cochlear pathology is still controversial. The purpose of this study was to examine the functional integrity of the peripheral auditory system in the Gunn rat. The Gunn rat is a mutant of the Wistar strain with congenital deficiency of the liver enzyme uridine diphosphoglucuronyl transferase which is essential for bilirubin conjugation. This deficiency is inherited as an autosomal recessive trait, with the homozygous animals (jj) showing evidence of bilirubin encephalopathy. The heterozygotes (Jj) have 50% enzyme deficiency and are not jaundiced. The Long-Evans rat served as a control. The approach was to study the discharge characteristics of single auditory nerve fibers using standard procedures in a closed and calibrated sound system. Various response measurements which would reveal pathological processes in the cochlea were analyzed. In this study, spontaneous discharge rate distribution and interspike interval statistics derived from Gunn rat auditory nerve recording were found to be within the normal range, and cochlear nerve histology showed no evidence of neuropathy. C1 UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,MADISON,WI 53706. UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. CR ANNIKO M, 1988, ARCH OTO-RHINO-LARYN, V245, P155, DOI 10.1007/BF00464018 BELAL A, 1975, J LARYNGOL OTOL, V89, P259, DOI 10.1017/S002221510008035X BENGTSSO.B, 1974, ACTA PAEDIATR SCAND, V63, P70, DOI 10.1111/j.1651-2227.1974.tb04351.x BEYERS RK, 1955, PEDIATRICS, V15, P248 BLAKELEY RW, 1959, J SPEECH HEAR RES, V2, P5 BLANC WA, 1959, J NEUROPATH EXP NEUR, V18, P165, DOI 10.1097/00005072-195901000-00011 BOORD RL, 1958, ANAT REC, V130, P394 BRUGGE JF, 1986, CONDITIONS COCHLEAR CASHORE WJ, 1982, PEDIATR CLIN N AM, V29, P1191 CASHORE WJ, 1982, PEDIATRICS, V69, P481 CHISIN R, 1979, ANN OTO RHINOL LARYN, V88, P352 CLAIREAUX AE, 1953, LANCET, V2, P1226 Cohen P., 1975, APPLIED MULTIPLE REG Comis S D, 1981, Scand Audiol Suppl, V14 Suppl, P85 COOK RD, 1973, BRAIN RES, V61, P191, DOI 10.1016/0006-8993(73)90527-1 CRABTREE N, 1950, J Laryngol Otol, V64, P482, DOI 10.1017/S0022215100012329 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 DEVRIES LS, 1985, PEDIATRICS, V76, P351 DUBLIN WB, 1951, AM J CLIN PATHOL, V21, P935 ELBARBARY A, 1991, HEARING RES, V54, P91 Evans EF, 1976, J PHYSIOL-LONDON, V256, P43 FLOTTORP G, 1957, Acta Otolaryngol, V48, P404, DOI 10.3109/00016485709126901 GACEK RR, 1961, ANAT REC, V139, P455, DOI 10.1002/ar.1091390402 GARTNER LM, 1970, PEDIATRICS, V45, P906 GOLDBERG JM, 1966, J NEUROPHYSIOL, V29, P72 GOLDBERG JM, 1964, J NEUROPHYSIOL, V27, P706 GOLDBERG JM, 1984, J NEUROPHYSIOL, V51, P1236 GOODHILL V, 1950, T AM ACAD OPHTHALMOL, V44, P671 GOODHILL V, 1956, J SPEECH HEAR DISORD, V21, P407 GOZDZIKZ.T, 1969, ACTA OTO-LARYNGOL, V68, P85, DOI 10.3109/00016486909121546 Gunn CH, 1938, J HERED, V29, P137 HANSEN TWR, 1980, ACTA PEDIATR SCAND, V75, P513 Harrison R V, 1979, SCAND AUDIOL S, P83 HARRISON RV, 1984, HEARING RES, V14, P79, DOI 10.1016/0378-5955(84)90070-4 HOEFFDING V, 1988, BRAIN RES, V449, P104, DOI 10.1016/0006-8993(88)91029-3 HOLLANDER H, 1968, Brain Research, V10, P120, DOI 10.1016/0006-8993(68)90117-0 HYMAN CB, 1969, AM J DIS CHILD, V117, P395 ISCHII T, 1978, T AM OTOL SOC, V65, P154 JEW JY, 1979, ARCH NEUROL-CHICAGO, V36, P149 JEW JY, 1977, J ANAT, V124, P599 JOHNSON L, 1959, AMA J DIS CHILD, V97, P591 KAGA K, 1979, INT J PEDIATR OTORHI, V1, P255, DOI 10.1016/0165-5876(79)90020-X KARP WB, 1979, PEDIATRICS, V64, P361 KEASTER J, 1969, AM J DIS CHILD, V117, P406 Kiang N Y, 1970, Ciba Found Symp, P241 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 KOCHHAR RK, 1989, CELL ANAL PACKAGE DO KOCHHAR RK, 1984, CELL ANAL PACKAGE DO KOSSACK C, 1975, INTRODUCTION STATIST LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LENHARDT ML, 1984, J PEDIATR-US, V104, P281, DOI 10.1016/S0022-3476(84)81013-6 LEVI G, 1981, ARCH OTO-RHINO-LARYN, V232, P139, DOI 10.1007/BF00505033 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LIBERMAN MC, 1979, ACTA OTO-LARYNGOL, V88, P161, DOI 10.3109/00016487909137156 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 LIBERMAN MC, 1984, HEARING RES, V16, P43, DOI 10.1016/0378-5955(84)90024-8 Malloy HT, 1937, J BIOL CHEM, V119, P481 MANLEY GA, 1976, J PHYSIOL-LONDON, V258, P323 MATKIN ND, 1966, ARCH OTOLARYNGOL, V64, P502 MERCHAN MA, 1988, J NEUROCYTOL, V17, P711, DOI 10.1007/BF01260998 Odell GB, 1985, CEREBRAL ENERGY META, P229 ODELL GB, 1980, MONOGRAPHS NEONATOLO, P143 ODELL GB, 1970, J PEDIATR-US, V76, P12, DOI 10.1016/S0022-3476(70)80124-X PERLMAN M, 1983, PEDIATRICS, V72, P658 PERLSTEIN M, 1950, AM J DIS CHILD, V79, P605 Perlstein MA., 1960, PEDIATR CLIN N AM, V7, P665 PLEDGER DR, 1982, BIOL NEONATE, V41, P38 POLLACK W, 1978, PERINATAL CARE, V2, P8 PORTMANN M, 1971, ACTA OTO-LARYNGOL, V71, P253, DOI 10.3109/00016487109125360 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBERTSON D, 1980, HEARING RES, V3, P167, DOI 10.1016/0378-5955(80)90044-1 ROBERTSON D, 1981, J ACOUST SOC AM, V69, P1096, DOI 10.1121/1.385689 ROSEN J, 1956, J SPEECH HEAR DISORD, V21, P418 ROSS MD, 1971, AM J ANAT, V130, P73, DOI 10.1002/aja.1001300106 SCHMID R, 1958, J CLIN INVEST, V37, P1123, DOI 10.1172/JCI103702 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1390 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 SCHUTTA H, 1969, THESIS U PENNSYLVANI SHAPIRO SM, 1986, ANN NEUROL, V20, P395 SHAPIRO SM, 1988, DEV BRAIN RES, V41, P147, DOI 10.1016/0165-3806(88)90178-2 SPOENDLIN H, 1989, HEARING RES, V43, P25, DOI 10.1016/0378-5955(89)90056-7 TAKAGISHI Y, 1989, BRAIN RES, V492, P116, DOI 10.1016/0006-8993(89)90894-9 TOWNSEND JJ, 1978, J NEUROPATH EXP NEUR, V37, P255, DOI 10.1097/00005072-197805000-00003 TSUCHITANI C, 1984, J ACOUST SOC AM, V77, P1484 UZIEL A, 1983, ACTA OTO-LARYNGOL, V95, P651, DOI 10.3109/00016488309139458 VOLPE JJ, 1981, NEUROLOGY NEWBORN, P336 WALSH BT, 1972, INT J NEUROSCI, V3, P221, DOI 10.3109/00207457209147026 YLIKOSKI J, 1984, ACTA OTO-LARYNGOL, V98, P418, DOI 10.3109/00016488409107583 YLIKOSKI JS, 1981, J LARYNGOL OTOL, V95, P631, DOI 10.1017/S0022215100091209 NR 91 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 JUL PY 1991 VL 54 IS 1 BP 75 EP 90 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800009 PM 1917719 ER PT J AU ELBARBARY, A AF ELBARBARY, A TI AUDITORY-NERVE OF THE NORMAL AND JAUNDICED RAT .2. FREQUENCY-SELECTIVITY AND 2-TONE RATE SUPPRESSION SO HEARING RESEARCH LA English DT Article DE HYPERBILIRUBINEMIA; AUDITORY NERVE FIBER; FREQUENCY THRESHOLD TUNING; 2-TONE RATE SUPPRESSION; COCHLEAR NONLINEARITIES; GUNN RAT ID COCHLEAR-NERVE; GUINEA-PIG; TUNING CURVES; SINGLE FIBERS; RESPONSES; CAT; THRESHOLDS; INHIBITION; INTENSITY; NEURONS AB This study is the continuation of the functional probing of the auditory periphery in the normal and jaundiced rat. Threshold tuning curves from normal rat auditory nerve fibers were comparable to those reported in other mammals. Life-long unconjugated hyperbilirubinemia does not appear to have a widespread, demonstrable effect on cochlear frequency selectivity and sensitivity as measured by the shapes of FTCs of single auditory nerve fibers. Most fibers from the jj Gunn rats had threshold tuning curves as sharp as those from control animals (Jj Gunn and Long-Evans). Any difference seems to lie in a greater threshold variability, particularly for the high-SR fibers, for the Gunn rat strain. Two-tone rate suppression, particularly above CF, was detected in most fibers from the three groups of rats. The optimal suppression frequency (SF) as a function of CF displayed the same progression. Suppression thresholds at any given CF were generally higher for high-SR fibers than for low-SR fibers for all three groups of animals. C1 UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,MADISON,WI 53706. UNIV WISCONSIN,DEPT NEUROPHYSIOL,MADISON,WI 53706. CR ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BORG E, 1982, HEARING RES, V8, P101, DOI 10.1016/0378-5955(82)90069-7 Comis S D, 1981, Scand Audiol Suppl, V14 Suppl, P85 COSTALUPES JA, 1987, HEARING RES, V26, P155, DOI 10.1016/0378-5955(87)90107-9 DALLOS P, 1980, PSYCHOPHYSICAL PHYSL, P24 DALLOS P, 1978, J NEUROPHYSIOL, V41, P365 ELBARBARY A, 1991, HEARING RES, V54, P75 EVANS EF, 1972, J PHYSIOL-LONDON, V226, P263 Evans EF, 1976, J PHYSIOL-LONDON, V256, P43 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 GOUREVIT.G, 1966, J COMP PHYSIOL PSYCH, V62, P289, DOI 10.1037/h0023669 GREENWOOD DD, 1976, J ACOUST SOC AM, V59, P607, DOI 10.1121/1.380906 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 Harrison R V, 1979, SCAND AUDIOL S, P83 HARRISON RV, 1984, HEARING RES, V14, P79, DOI 10.1016/0378-5955(84)90070-4 HARRISON R V, 1977, INSERM (Institut National de la Sante et de la Recherche Medicale) Colloque, V68, P105 HIND JE, 1967, J NEUROPHYSIOL, V30, P794 HOLTON T, 1980, HEARING RES, V2, P21, DOI 10.1016/0378-5955(80)90014-3 JAVEL E, 1983, J ACOUST SOC AM, V74, P801, DOI 10.1121/1.389867 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 NOMOTO M, 1964, J NEUROPHYSIOL, V27, P768 PICKLES JO, 1984, HEARING RES, V14, P245, DOI 10.1016/0378-5955(84)90053-4 PICKLES JO, 1976, J ACOUST SOC AM, V60, P1151, DOI 10.1121/1.381217 PRIJS VF, 1989, HEARING RES, V42, P73, DOI 10.1016/0378-5955(89)90118-4 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBERTSON D, 1976, NATURE, V259, P477, DOI 10.1038/259477a0 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 ROBERTSON D, 1981, J ACOUST SOC AM, V69, P1096, DOI 10.1121/1.385689 ROBERTSON D, 1982, HEARING RES, V7, P55, DOI 10.1016/0378-5955(82)90081-8 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1969, J ACOUST SOC AM, V45, P1025, DOI 10.1121/1.1911493 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1980, J NEUROPHYSIOL, V43, P1367 NR 43 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 1991 VL 54 IS 1 BP 91 EP 104 PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800010 PM 1917720 ER PT J AU GEISLER, CD AF GEISLER, CD TI A COCHLEAR MODEL USING FEEDBACK FROM MOTILE OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE COCHLEAR VIBRATION; OUTER HAIR CELL; FEEDBACK; MODEL ID OTOACOUSTIC EMISSIONS; TUNING CURVES; MECHANICS; VIBRATIONS; SATURATION; AMPLIFIER; HEARING; PHASES; FORCE AB A model of cochlear vibrations based upon motile outer hair cells (OHCs) has been developed using physiologically demonstrated phenomena. Rapid longitudinally directed OHC forces are connected in such a way as to form a negative-feedback system. The responses at the higher frequencies (> 1 kHZ) are quite realistic: they have properly shaped amplitude curves with large tip-to-tail ratios (30-50 dB), Q10's of 2-6, and 'shoulders' at frequencies an octave below the resonant frequency. The phases are also quite realistic, though asymptoting at somewhat lower values (about -6-pi radians) than observed physiologically. The responses in the apical section are not so realistic. The form of the OHC force is physically unrealizable, but realizable forms are discussed. RP GEISLER, CD (reprint author), UNIV WISCONSIN,DEPT ELECT & COMP ENGN,DEPT NEUROPHYSIOL,MADISON,WI 53706, USA. CR ALLEN JB, 1980, J ACOUST SOC AM, V68, P1660, DOI 10.1121/1.385198 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 Brundin L, 1989, Acta Otolaryngol Suppl, V467, P229 ENGEBRET.AM, 1968, J ACOUST SOC AM, V44, P548, DOI 10.1121/1.1911119 FRIEDMAN DH, 1990, MECHANICS BIOPHYSICS, P372 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GEISLER CD, 1982, J ACOUST SOC AM, V71, P1201, DOI 10.1121/1.387768 GEISLER CD, 1985, J ACOUST SOC AM, V78, P257, DOI 10.1121/1.392568 GEISLER CD, 1986, HEARING RES, V24, P125, DOI 10.1016/0378-5955(86)90056-0 GEISLER CD, 1990, MECHANICS BIOPHYSICS, P86 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 KEMP DT, 1986, HEARING RES, V22, P95, DOI 10.1016/0378-5955(86)90087-0 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P151 Kiang NY-s, 1965, DISCHARGE PATTERNS S Kim DO, 1979, SCAND AUDIOL S, V63-81 KOLSTON PJ, 1990, J ACOUST SOC AM, V88, P1794, DOI 10.1121/1.400200 LIBERMAN MC, 1982, J ACOUST SOC AM, V72, P1441, DOI 10.1121/1.388677 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LONG GR, 1988, HEARING RES, V36, P125, DOI 10.1016/0378-5955(88)90055-X MASON SJ, 1960, ELECT CIRCUITS SIGNA, pCH9 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 Mountain DC, 1983, MECHANICS HEARING, P119 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SHAN X, 1988, THESIS U WISCONSIN M STRELIOFF D, 1984, HEARING RES, V15, P19, DOI 10.1016/0378-5955(84)90221-1 WICKESBERG RE, 1985, PERIPHERAL AUDITORY, P113 Wit HP, 1986, PERIPHERAL AUDITORY, P221 YATES GK, 1989, COCHLEAR MECHANISMS, P177 ZWEIG G, 1990, MECHANICS BIOPHYSICS, P362 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 ZWICKER E, 1986, J ACOUST SOC AM, V80, P146, DOI 10.1121/1.394175 ZWISLOCKI JJ, 1980, J ACOUST SOC AM, V67, P1679 NR 36 TC 42 Z9 44 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 105 EP 117 DI 10.1016/0378-5955(91)90140-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800011 PM 1917709 ER PT J AU IKEDA, K MORIZONO, T AF IKEDA, K MORIZONO, T TI THE IONIC AND ELECTRIC ENVIRONMENT IN THE ENDOLYMPHATIC SAC OF THE CHINCHILLA - RELEVANCE TO THE LONGITUDINAL FLOW SO HEARING RESEARCH LA English DT Article DE ENDOLYMPHATIC SAC; IONIC ACTIVITY; DC POTENTIAL; LONGITUDINAL FLOW ID GUINEA-PIG; COCHLEAR ENDOLYMPH; TRANSPORT; MODEL; SPACE AB The ionic composition of the endolymph in the endolymphatic sac (ES) of the chinchilla was measured using double-barreled ion-selective micro-electrodes. The DC potential of the ES was 9.3 +/- 1.8 mV (N = 18). The K+, Na+, and Cl- concentrations of the ES were 13.3 +/- 4.7 mM (N = 6), 129.0 +/- 8.8 mM (N = 6), and 124.3 +/- 16.6 mM (N = 6), respectively. In light of the chemical potentials of the cochlear endolymph previously reported [Ikeda and Morizono (1989), Hear. Res., 39, 279-286] the pressure gradient of the endolymph between the cochlea and ES was calculated to be 71.5 mmHg at 38-degrees-C. The contribution of the osmotic and hydrostatic pressure gradients of the endolymph to the longitudinal flow is discussed. C1 UNIV MINNESOTA,SCH MED,DEPT OTOLARYNGOL,MINNEAPOLIS,MN 55455. RP IKEDA, K (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. CR AMANO H, 1983, ARCH OTO-RHINO-LARYN, V237, P273, DOI 10.1007/BF00453732 ANGELBORG C, 1975, ACTA OTO-LARYNGOL, V79, P81, DOI 10.3109/00016487509124658 Guild SR, 1927, AM J ANAT, V39, P57, DOI 10.1002/aja.1000390103 GUYTON AC, 1971, TXB MED PHYSL, P236 IKEDA K, 1987, HEARING RES, V26, P117, DOI 10.1016/0378-5955(87)90040-2 IKEDA K, 1988, HEARING RES, V32, P103, DOI 10.1016/0378-5955(88)90081-0 IKEDA K, 1989, HEARING RES, V39, P279, DOI 10.1016/0378-5955(89)90047-6 KIMURA RS, 1967, ANN OTO RHINOL LARYN, V76, P664 LONG CH, 1987, OTOLARYNG HEAD NECK, V96, P83 LUNDQUIST PG, 1965, ACTA OTOLARYNGOL S, V201, P100 MAKIMOTO K, 1978, ARCH OHREN NASEN KEH, V220, P259, DOI 10.1007/BF00455361 MANNI JJ, 1987, HEARING RES, V26, P229, DOI 10.1016/0378-5955(87)90059-1 MIYAMOTO H, 1979, ARCH OHREN NASEN KEH, V222, P77, DOI 10.1007/BF00456341 MORGENSTERN C, 1982, AM J OTOLARYNG, V3, P323, DOI 10.1016/S0196-0709(82)80004-5 MORI N, 1987, ARCH OTO-RHINO-LARYN, V244, P61, DOI 10.1007/BF00453493 NINOYU O, 1986, ORL J OTO-RHINO-LARY, V48, P199 RASKANDERSEN H, 1981, ANN NY ACAD SCI, V374, P11, DOI 10.1111/j.1749-6632.1981.tb30855.x RASKANDERSEN H, 1981, MENIERES DIS PATHOGE, P99 SALT AN, 1986, HEARING RES, V23, P141, DOI 10.1016/0378-5955(86)90011-0 SALT AN, 1989, 2 S MEN DIS AMST, P69 SILVERST.H, 1966, LARYNGOSCOPE, V76, P498 NR 21 TC 11 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 118 EP 122 DI 10.1016/0378-5955(91)90141-U PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800012 PM 1917711 ER PT J AU TARNOWSKI, BI SCHMIEDT, RA HELLSTROM, LI LEE, FS ADAMS, JC AF TARNOWSKI, BI SCHMIEDT, RA HELLSTROM, LI LEE, FS ADAMS, JC TI AGE-RELATED-CHANGES IN COCHLEAS OF MONGOLIAN GERBILS SO HEARING RESEARCH LA English DT Article DE COCHLEA; AGING; HAIR CELL; COMPOUND ACTION POTENTIAL; PRESBYCUSIS; HEARING LOSS; MONGOLIAN GERBIL ID HAIR CELL LOSS; AUDITORY-NERVE FIBERS; GUINEA-PIG; ACOUSTIC TRAUMA; INNER-EAR; THRESHOLDS; MOUSE; SUPPRESSION; CHINCHILLA; NOISE AB The effects of aging on the gerbil cochlea were studied in 16 animals raised in a quiet environment. Animals were tested at ages ranging from 33 to 36 months, the approximate average lifespan of gerbils in our colony. Hearing sensitivity was assessed by measures of whole-nerve compound action potential (CAP) thresholds and surface preparations of the organ of Corti were subsequently examined by light microscopy for losses of sensory hair cells. These quiet-aged animals showed a wide range of hair-cell losses and threshold shifts. Outer hair cells often showed significant losses while inner hair cells were rarely absent. All animals had some threshold shift, especially at frequencies above 4 kHz. These shifts ranged from 1 to 68 dB. At high frequencies, threshold shifts often occurred without hair-cell losses at corresponding cochlear locations. At low frequencies, threshold shifts seldom reflected the losses of hair cells commonly found in the cochlear apex. Thus, the correlation of specific hair-cell losses and CAP threshold shifts at corresponding frequencies was poor. On the other hand, the total number of missing hair cells, irrespective of location, was a good, general indicator of the hearing capacity in a given ear. It appears that the factor or factors that makes cochleas susceptible to hair-cell loss with increasing age also affects other cochlear mechanisms that are necessary for normal functioning of the ear. C1 MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,CHARLESTON,SC 29425. 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P., 1957, LARYNGOSCOPE, V67, P118 CROWLEY DE, 1972, LARYNGOSCOPE, V82, P2079, DOI 10.1288/00005537-197211000-00009 CROWLEY DE, 1972, ANN OTO RHINOL LARYN, V81, P739 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 Dayal V S, 1975, Laryngoscope, V85, P1 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FEDERSPI.P, 1972, ARCH KLIN EXP OHR, V201, P283, DOI 10.1007/BF00571666 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 HARRISON RV, 1981, J ACOUST SOC AM, V70, P1036, DOI 10.1121/1.386954 HENRY KR, 1980, AUDIOLOGY, V19, P369 HENRY KR, 1983, AUDIOLOGY, V22, P372 JOHNSSON LG, 1972, ANN OTO RHINOL LARYN, V81, P179 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KERR TP, 1982, AM J OTOLARYNG, V3, P332, DOI 10.1016/S0196-0709(82)80006-9 KIANG N. Y., 1960, ANN OTOL RHINOL AND LARYNGOL, V69, P448 KOEPPEN BM, 1985, REGULATION DEV MEMBR, P90 Liberman M C, 1978, Acta Otolaryngol Suppl, V358, P1 Liberman MC, 1982, NEW PERSPECTIVES NOI, P105 LIBERMAN MC, 1987, HEARING RES, V26, P65, DOI 10.1016/0378-5955(87)90036-0 MEES K, 1983, ACTA OTO-LARYNGOL, V95, P277, DOI 10.3109/00016488309130944 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 MIZUKOSHI O., 1957, ANN OTOL RHINOL AND LARYNGOL, V66, P106 ROBERTSON D, 1980, J ACOUST SOC AM, V67, P1295, DOI 10.1121/1.384182 SALVI RJ, 1979, ARCH OTO-RHINO-LARYN, V224, P111, DOI 10.1007/BF00455233 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 Schuknecht H. F., 1974, PATHOLOGY EAR SCHUKNECHT HF, 1964, ARCHIV OTOLARYNGOL, V80, P369 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P127 SCHULTE BA, 1989, DEGENERATION STRIA V, P47 SMITH DW, 1987, HEARING RES, V26, P311, DOI 10.1016/0378-5955(87)90066-9 SOKOLICH WG, 1976, J ACOUST SOC AM, V59, P963, DOI 10.1121/1.380955 Spoendlin H, 1976, EFFECTS NOISE HEARIN, P69 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 SPOENDLIN H, 1977, ACTA OTO-LARYNGOL, V83, P130, DOI 10.3109/00016487709128822 TACHIBANA M, 1984, ACTA OTO-LARYNGOL, V97, P257, DOI 10.3109/00016488409130987 ULEHLOVA L, 1973, ARCH KLIN EXP OHR, V204, P321, DOI 10.1007/BF00303740 WARD WD, 1971, ANN OTO RHINOL LARYN, V80, P881 WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 NR 55 TC 68 Z9 70 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 123 EP 134 DI 10.1016/0378-5955(91)90142-V PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800013 PM 1917712 ER PT J AU BOBBIN, RP CEASAR, G FALLON, M AF BOBBIN, RP CEASAR, G FALLON, M TI CHANGING CATION LEVELS (MG2+, CA2+, NA+) ALTERS THE RELEASE OF GLUTAMATE, GABA AND OTHER SUBSTANCES FROM THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE AMINO ACID; UPTAKE; NEUROTRANSMITTER; HAIR CELL ID POTASSIUM-INDUCED RELEASE; ACID-TRANSPORT-SYSTEMS; GAMMA-AMINOBUTYRIC ACID; LATERAL-LINE ORGAN; AMINO-ACIDS; XENOPUS-LAEVIS; EXTRACELLULAR CALCIUM; SOUND STIMULATION; TAURINE RELEASE; CEREBRAL-CORTEX AB We examined the effects of changes in cation levels (increased Mg2+ concentration combined with low Ca2+ concentration, and two low concentrations of Na+) on the perilymph levels of gamma-aminobutyric acid (GABA), glutamate (Glu), aspartate (Asp) and other substances. Artificial perilymph solutions containing normal (5 mM) and high (50 mM) levels of K+ were perfused through the perilymphatic compartment of the guinea pig cochlea to examine basal release (5 mM K-) and depolarization-induced release (50 mM K+). Each of the two K+ concentrations were contained in four different solutions: [1] normal artificial perilymph (NARP; NaCl, 137 mM; CaCl2, 2 mM; MgCl2, 1 mM;); [II] high Mg2+ (20 mM)/low Ca2+ (0.1 mM) (HMgLCa); [III) low Na+ (117 mM; LNa), and [IV] very low Na+ (NaCl, 0 mM; VLNa). The effluent was collected and assayed for eighteen primary amines by HPLC. Compared with NARP, the HMgLCa group had an increase in the high K+-induced release of Asp and Glu with no change in GABA. VLNa increased the normal K+ levels of Asp, Glu and GABA up to those observed with high K+ in NARP. VLNa increased the high K+ levels of Asp and Glu over fivefold compared with the high K+ levels in NARP, but decreased GABA. We ascribe the results to an interference with either a Na+-dependent uptake processes or a Na/Ca2+ exchange carrier. RP BOBBIN, RP (reprint author), LOUISIANA STATE UNIV,MED CTR,KRESGE HEARING RES LAB S,DEPT OTORHINOLARYNGOL & BIOCOMMUN,NEW ORLEANS,LA 70112, USA. CR ALTSCHULER RA, 1986, NEUROBIOLOGY HEARING, P383 ARTS HA, 1990, INFLUENCE PERILYMPHA, P194 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BLEDSOE SC, 1980, EXP BRAIN RES, V40, P97 BLEDSOE SC, 1989, BRAIN RES, V493, P113, DOI 10.1016/0006-8993(89)91005-6 BOBBIN RP, 1990, HEARING RES, V46, P83, DOI 10.1016/0378-5955(90)90141-B BOBBIN RP, 1991, 4TH INT C EFF NOIS A BOBBIN RP, 1990, HEARING RES, V46, P277, DOI 10.1016/0378-5955(90)90009-E BOBBIN RP, 1990, NEUR ABSTR, V16, P872 BRADFORD HF, 1987, NEUROSCI LETT, V81, P296, DOI 10.1016/0304-3940(87)90399-5 COUTINHO OP, 1984, BRAIN RES, V290, P261, DOI 10.1016/0006-8993(84)90943-0 DAVIES LP, 1976, J NEUROCHEM, V26, P1007, DOI 10.1111/j.1471-4159.1976.tb06485.x DIXON WJ, 1969, INTRO STAT ANAL, P330 DRESCHER DG, 1987, LIFE SCI, V40, P1371, DOI 10.1016/0024-3205(87)90327-4 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 DRESCHER DG, 1985, AUDITORY BIOCH, P50 DRESCHER MJ, 1987, BRAIN RES, V417, P39, DOI 10.1016/0006-8993(87)90177-6 DRESCHER MJ, 1983, J NEUROCHEM, V41, P309, DOI 10.1111/j.1471-4159.1983.tb04745.x ERECINSKA M, 1987, BIOCHEM PHARMACOL, V36, P3547, DOI 10.1016/0006-2952(87)90001-3 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 EYBALIN M, 1983, NEUROSCIENCE, V9, P863, DOI 10.1016/0306-4522(83)90274-9 FERKANY J, 1986, J NEUROSCI RES, V16, P491, DOI 10.1002/jnr.490160305 FEX J, 1984, HEARING RES, V15, P123, DOI 10.1016/0378-5955(84)90043-1 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 GULLEY RL, 1979, ACTA OTO-LARYNGOL, V88, P177, DOI 10.3109/00016487909137157 HERTZ L, 1979, PROG NEUROBIOL, V13, P277, DOI 10.1016/0301-0082(79)90018-2 HOELTZLI SD, 1990, AM J PHYSIOL, V259, pC47 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x JOHNSTON GA, 1974, J NEUROCHEM, V22, P101, DOI 10.1111/j.1471-4159.1974.tb12184.x KACZOROWSKI GJ, 1989, BIOCHIM BIOPHYS ACTA, V988, P287, DOI 10.1016/0304-4157(89)90022-1 LEHMANN A, 1989, J NEUROCHEM, V53, P525, DOI 10.1111/j.1471-4159.1989.tb07365.x LITTMAN T, 1989, HEARING RES, V40, P45, DOI 10.1016/0378-5955(89)90098-1 MARTIN DL, 1990, J NEUROSCI, V10, P571 MARTIN DL, 1989, J NEUROSCI RES, V23, P191, DOI 10.1002/jnr.490230209 MARTIN DL, 1972, J NEUROCHEM, V19, P841, DOI 10.1111/j.1471-4159.1972.tb01398.x MEDINA JE, 1981, NEUROSCIENCE, V6, P505, DOI 10.1016/0306-4522(81)90142-1 MELAMED B, 1982, HEARING RES, V7, P13, DOI 10.1016/0378-5955(82)90079-X MINCHIN MCW, 1975, J NEUROCHEM, V24, P571, DOI 10.1111/j.1471-4159.1975.tb07676.x PETERSON NA, 1974, BIOCHEM PHARMACOL, V23, P2491, DOI 10.1016/0006-2952(74)90249-4 PITKANEN RI, 1985, BRAIN RES, V326, P384, DOI 10.1016/0006-8993(85)90051-4 POTASHNER SJ, 1978, J NEUROCHEM, V31, P187, DOI 10.1111/j.1471-4159.1978.tb12447.x RUBIN RP, 1970, PHARMACOL REV, V22, P389 SARANTIS M, 1990, BRAIN RES, V516, P322, DOI 10.1016/0006-8993(90)90935-5 SATO Y, 1989, ACTA OTO-LARYNGOL, V108, P76, DOI 10.3109/00016488909107395 SCHWARTZ IR, 1990, J ELECTRON MICR TECH, V15, P225, DOI 10.1002/jemt.1060150304 SEWELL WF, 1978, SCIENCE, V202, P910, DOI 10.1126/science.30998 SILINSKY EM, 1985, PHARMACOL REV, V37, P81 STALLCUP WB, 1979, J NEUROCHEM, V32, P57, DOI 10.1111/j.1471-4159.1979.tb04509.x THOMPSON GC, 1986, BRAIN RES, V372, P72, DOI 10.1016/0006-8993(86)91459-9 VIZI ES, 1984, NEUROCHEM INT, V6, P435, DOI 10.1016/0197-0186(84)90112-8 WESTERINK BHC, 1988, N-S ARCH PHARMACOL, V337, P373 NR 51 TC 14 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUL PY 1991 VL 54 IS 1 BP 135 EP 144 DI 10.1016/0378-5955(91)90143-W PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800014 PM 1680843 ER PT J AU DOYLE, WJ WEBSTER, DB AF DOYLE, WJ WEBSTER, DB TI NEONATAL CONDUCTIVE HEARING-LOSS DOES NOT COMPROMISE BRAIN-STEM AUDITORY FUNCTION AND STRUCTURE IN RHESUS-MONKEYS SO HEARING RESEARCH LA English DT Article DE ABRS; COCHLEAR NUCLEI; CONDUCTIVE LOSS; DEVELOPMENT; EAM ATRESIAS; MONKEY ID STEM RESPONSES; OTITIS-MEDIA; POTENTIALS; COCHLEAR; NUCLEI; DEPRIVATION; PLASTICITY; EFFUSION; MICE; LIFE AB The effect of conductive hearing loss on the maturation of the auditory pathway was evaluated using the auditory brainstem response (ABR) in rhesus monkeys. Ten newborn rhesus monkeys were assigned to control (N = 4), unilateral hearing loss (N = 3), or bilateral hearing loss (N = 3) groups. Hearing loss was created by surgically excising a 3 mm section of the external auditory canal and suturing the canal. Auditory brainstem responses to click stimuli were recorded prior to and after the surgical procedure and bi-monthly or monthly for a 14 month follow-up period. Results showed that after surgery all ears developed an estimated 30-50 dB conductive hearing loss which was retained throughout the follow-up period. Contrary to expectations, the latencies of the ABR component waves decreased with age in all ears. When adjusted for hearing level, there were no differences between ears in maturation of the component waves of the ABR. These data suggest that, in primates, a conductive hearing loss does not affect the maturation of those aspects of the auditory pathway reflected in the ABR. Furthermore, the conductive losses were not accompanied by any discernible change in the neuronal sizes of brainstem auditory neurons or the volume of the cochlear nuclei. C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES LAB,2020 GRAVIER ST,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,DEPT ANAT,NEW ORLEANS,LA 70112. UNIV PITTSBURGH,SCH MED,DEPT OTOLARYNGOL,PITTSBURGH,PA 15261. CHILDRENS HOSP PITTSBURGH,PITTSBURGH,PA. CR ANTEBY I, 1986, INT J PEDIATR OTORHI, V12, P1, DOI 10.1016/S0165-5876(86)80051-9 COATS AC, 1978, ARCH OTOLARYNGOL, V104, P709 COLEMAN J, 1982, DEV BRAIN RES, V4, P119, DOI 10.1016/0165-3806(82)90104-3 DOYLE WJ, 1983, ELECTROEN CLIN NEURO, V56, P210, DOI 10.1016/0013-4694(83)90075-5 EGGERMONT JJ, 1983, AUDITORY DEV INFANCY EVANS WJ, 1983, HEARING RES, V10, P269, DOI 10.1016/0378-5955(83)90092-8 FOLSOM RC, 1983, ANN OTO RHINOL LARYN, V92, P249 FRIA TJ, 1985, EAR HEARING, V5, P361 FRIA TJ, 1985, ARCH OTOLARYNGOL, V111, P1 FRIA TJ, 1982, OTOLARYNG HEAD NECK, V90, P824 OGRA PL, 1989, ANN OTOL RHINOL S139, V98, P23 PAPARELLA MM, 1984, ANN OTO RHINOL LARYN, V93, P623 PARADISE JL, 1981, PEDIATRICS, V68, P869 RUBEN RJ, 1989, ANN OTO RHINOL LARYN, V98, P46 RUBEN RJ, 1980, ANN OTO RHINOL LARYN, V89, P303 SALAMY A, 1976, ELECTROEN CLIN NEURO, V40, P418, DOI 10.1016/0013-4694(76)90193-0 SHAH SN, 1978, EXP NEUROL, V58, P111, DOI 10.1016/0014-4886(78)90126-7 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 TRUNE DR, 1988, HEARING RES, V33, P141, DOI 10.1016/0378-5955(88)90027-5 TUCCI DL, 1985, J COMP NEUROL, V238, P371, DOI 10.1002/cne.902380402 TUCCI DL, 1987, ANN OTO RHINOL LARYN, V96, P343 WEBSTER DB, 1983, CENTRAL AUDITORY PRO, P185 WEBSTER DB, 1989, NEUR ABSTR 1, P743 WEBSTER DB, 1983, INT J PEDIATR OTORHI, V6, P107 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 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 1991 VL 54 IS 1 BP 145 EP 151 DI 10.1016/0378-5955(91)90144-X PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FX328 UT WOS:A1991FX32800015 PM 1917713 ER PT J AU COLLINGE, C SCHWEITZER, L AF COLLINGE, C SCHWEITZER, L TI DETAILS OF THE CENTRAL PROJECTIONS OF THE COCHLEAR NERVE IN THE HAMSTER REVEALED BY THE FLUORESCENT TRACER DII SO HEARING RESEARCH LA English DT Article DE COCHLEAR NERVE; COCHLEAR NUCLEUS; DII; TONOTOPIC; OLIVOCOCHLEAR ID HORSERADISH-PEROXIDASE HRP; GUINEA-PIG COCHLEA; AFFERENT-FIBERS; SPIRAL GANGLION; NUCLEI; RAT; CATS; ACETYLCHOLINESTERASE; MORPHOLOGY; BRANCHES AB A new fluorescent tracer, DiI, may be used postmortem in perfused animals making placement in small structures such as the cochlea much less difficult. We have mapped cochlear nerve terminations in the cochlear nucleus with DiI and, using three-dimensional reconstructions, have demonstrated the topography and geometry of the cochlear input. By placing DiI in two regions of the cochlea, we have demonstrated that terminations from the cochlea form stacked sheets of inputs. If enough closely situated ganglion cells were labeled in the cochlea, a well-delineated stripe of label could be found in each section of the cochlear nucleus up to the superficial granule cell region. Here a small extension of label, separate from the stripe may represent the medial olivocochlear axons. When fewer axons were labelled in the cochlear nerve, the sheets were absent and discontinuous patches of label were found. These patches apposed rostrocaudally to form bands of label that run orthogonal to the tonotopic organization. C1 UNIV LOUISVILLE,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. CR BENSON TE, 1990, J COMP NEUROL, V295, P52, DOI 10.1002/cne.902950106 BROWN MC, 1987, J COMP NEUROL, V260, P605, DOI 10.1002/cne.902600412 BROWN MC, 1988, J COMP NEUROL, V278, P591, DOI 10.1002/cne.902780410 BROWN MC, 1990, HEARING RES, V49, P103 BROWN MC, 1987, J COMP NEUROL, V260, P591, DOI 10.1002/cne.902600411 BROWN MC, 1990, IN PRESS J COMP NEUR BROWN MC, 1988, J COMP NEUROL, V278, P581, DOI 10.1002/cne.902780409 De Nó R L, 1976, Ann Otol Rhinol Laryngol, V85, P1 FEKETE DM, 1984, J COMP NEUROL, V229, P432, DOI 10.1002/cne.902290311 FELDMAN ML, 1969, J COMP NEUROL, V137, P267, DOI 10.1002/cne.901370303 GODEMENT P, 1987, DEVELOPMENT, V101, P697 HARRISON JM, 1966, J COMP NEUROL, V126, P391, DOI 10.1002/cne.901260303 HONIG MG, 1989, TRENDS NEUROSCI, V12, P333, DOI 10.1016/0166-2236(89)90040-4 LEAKE PA, 1989, J COMP NEUROL, V281, P612, DOI 10.1002/cne.902810410 Lorente de No R, 1933, LARYNGOSCOPE, V43, P327 MARTIN MR, 1981, J COMP NEUROL, V197, P153, DOI 10.1002/cne.901970112 MERCHAN MA, 1986, J ANAT, V144, P71 MERCHAN MA, 1985, J ANAT, V141, P121 OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 OSEN KK, 1970, ARCH ITAL BIOL, V108, P21 POWELL TPS, 1962, J ANAT, V96, P269 Sando I, 1965, ACTA OTOLARYNG STOCK, V59, P417, DOI 10.3109/00016486509124577 SCHWEITZER L, 1984, J COMP NEUROL, V225, P228, DOI 10.1002/cne.902250208 THANOS S, 1987, J COMP NEUROL, V261, P155, DOI 10.1002/cne.902610114 TICKLE DR, 1976, THESIS HAMPSHIRE COL, P1 VANNOORT J, 1969, PSYCHIAT NEUROL NEUR, V72, P109 VIDALSANZ M, 1988, EXP NEUROL, V102, P92, DOI 10.1016/0014-4886(88)90081-7 VONBARTHELD CS, 1990, J HISTOCHEM CYTOCHEM, V38, P725 WEBSTER DB, 1971, J COMP NEUROL, V143, P323, DOI 10.1002/cne.901430305 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 WICKESBERG RE, 1988, J COMP NEUROL, V268, P389, DOI 10.1002/cne.902680308 WINTER IM, 1989, J COMP NEUROL, V280, P143, DOI 10.1002/cne.902800110 NR 32 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1991 VL 53 IS 2 BP 159 EP 172 DI 10.1016/0378-5955(91)90051-A PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900001 PM 1652583 ER PT J AU RAPHAEL, Y AF RAPHAEL, Y TI PURE-TONE OVERSTIMULATION PROTECTS SURVIVING AVIAN HAIR-CELLS FROM ACOUSTIC TRAUMA SO HEARING RESEARCH LA English DT Article DE CHICK; ACOUSTIC TRAUMA; HAIR CELL; TECTORIAL MEMBRANE; PROTECTION; ACTIN ID INTENSE SOUND EXPOSURE; CHICK COCHLEA; TECTORIAL MEMBRANE; REGENERATION; STEREOCILIA AB It was found that intense pure-tones which damage hair cells in chicks, also result in damage to the tectorial membrane (TM). This study was designed to elucidate the effects of a second pure-tone insult on hair cells which surived a priming pure-tone exposure. Chicks were exposed to a pure-tone of 1.5 kHz at 124 dB SPL. Lesion was found in both TM and hair cells, but the area of damage to the TM was much larger than that to the hair cells. Following this exposure, chicks were exposed to a second intense pure-tone at 2.2 kHz 124 dB SPL. The frequency of the second exposure corresponded to a region where the TM did, but hair cells did not appear to be injured by the first exposure. The second exposure caused significantly less hair cell damage in chicks already exposed to the 1.5 kHz pure-tone than in controls which were not primed with the first exposure. This findings suggests that the first exposure provides a degree of protection for the surviving hair cells, perhaps by uncoupling them from the TM. RP RAPHAEL, Y (reprint author), UNIV MICHIGAN,SCH MED,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR BORG E, 1984, ACOUSTIC REFLEX, P413 CANLON B, 1987, HEARING RES, V30, P127, DOI 10.1016/0378-5955(87)90130-4 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 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 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 MCFADDEN EA, 1989, HEARING RES, V41, P205, DOI 10.1016/0378-5955(89)90012-9 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 RAPHAEL Y, 1991, HEARING RES, V51, P173, DOI 10.1016/0378-5955(91)90034-7 RAPHAEL Y, 1989, 26 WORKSH INN EAR BI SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 TILNEY LG, 1988, HEARING RES, V37, P71, DOI 10.1016/0378-5955(88)90079-2 TILNEY LG, 1982, HEARING RES, V7, P181, DOI 10.1016/0378-5955(82)90013-2 NR 13 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 JUN PY 1991 VL 53 IS 2 BP 173 EP 184 DI 10.1016/0378-5955(91)90052-B PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900002 PM 1880073 ER PT J AU FRANKLIN, DJ LONSBURYMARTIN, BL STAGNER, BB MARTIN, GK AF FRANKLIN, DJ LONSBURYMARTIN, BL STAGNER, BB MARTIN, GK TI ALTERED SUSCEPTIBILITY OF 2F1-F2 ACOUSTIC-DISTORTION PRODUCTS TO THE EFFECTS OF REPEATED NOISE EXPOSURE IN RABBITS SO HEARING RESEARCH LA English DT Article DE BEHAVIORAL THRESHOLDS; 2F1-F2 DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS; NOISE EXPOSURE; SUSCEPTIBILITY RESISTANCE; RABBIT ID CROSSED OLIVOCOCHLEAR BUNDLE; COCHLEAR MECHANICS; THRESHOLD SHIFT; PERIODIC REST; STIMULATION; DAMAGE; TRAUMA; REGENERATION; PROTECTION; EMISSIONS AB Hearing sensitivity and the generation of acoustic-distortion products at 2f1 - f2 were examined systematically in behaviorally trained rabbits, before, during, and following regular exposure to a 95-dB SPL octave band of noise, centered at 1 kHz. During the exposure period, the octave-band noise was interrupted once every 24 h in order to monitor the progressive loss in auditory function using tests of behavioral threshold and distortion-product otoacoustic emissions (DPOAEs). When low-frequency DPOAEs from 1-4 kHz diminished to noise-floor levels, i.e., when their amplitudes were reduced by about 20-30 dB, the exposure was terminated. Subsequent recovery of behavioral thresholds and DPOAE amplitudes and detection 'thresholds' was evaluated at regular intervals over a 3-week post-exposure period. Following the recovery period, the rabbits again received the identical exposure/recovery treatment until a permanent 10 dB or greater loss in DPOAE amplitudes was achieved for any point of measurement between 2-10 kHz. The primary result was that the number of days of overstimulation required for rabbits to reach the criterion loss in DPOAE amplitudes increased for each successive exposure session. In addition, DPOAEs accurately tracked the frequency pattern described by the behavioral threshold shifts during both the development and recovery stages of exposure. C1 BAYLOR UNIV,DEPT OTORHINOLARYNGOL & COMMUN SCI,HOUSTON,TX 77030. CR BOHNE BA, 1985, ANN OTO RHINOL LARYN, V94, P122 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 CLARK WW, 1978, ANN OTOL RHINOL LA S, V51, P1 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 FRANKLIN DJ, 1988, J ACOUST SOC AM, V83, pS115, DOI 10.1121/1.2025165 Fried M P, 1976, Trans Sect Otolaryngol Am Acad Ophthalmol Otolaryngol, V82, P285 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LONSBURYMARTIN BL, 1988, SOC NEUR ABSTR, V18, P1099 LONSBURYMARTIN BL, 1990, EAR HEARING, V11, P144 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 LONSBURYMARTIN BL, 1989, 2 INT S MEN DIS PATH, P337 MARTIN GK, 1980, HEARING RES, V2, P65, DOI 10.1016/0378-5955(80)90017-9 MARTIN GK, 1989, 2ND INT S MEN DIS PA, P205 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MARTIN GK, 1983, HEARING RES, V12, P65, DOI 10.1016/0378-5955(83)90119-3 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 RAJAN R, 1988, BRAIN RES, V459, P241, DOI 10.1016/0006-8993(88)90640-3 RAJAN R, 1989, HEARING RES, V39, P263, DOI 10.1016/0378-5955(89)90046-4 RYALS BM, 1988, SCIENCE, V240, P1774, DOI 10.1126/science.3381101 SATALOFF J, 1983, ANN OTO RHINOL LARYN, V92, P623 SAUNDERS JC, 1986, HEARING RES, V23, P233, DOI 10.1016/0378-5955(86)90112-7 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 WARD WD, 1970, J ACOUST SOC AM, V48, P561, DOI 10.1121/1.1912172 ZUREK PM, 1982, J ACOUST SOC AM, V72, P774, DOI 10.1121/1.388258 NR 28 TC 43 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 JUN PY 1991 VL 53 IS 2 BP 185 EP 208 DI 10.1016/0378-5955(91)90053-C PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900003 PM 1880074 ER PT J AU MEURICE, JC PAQUEREAU, J MARILLAUD, A AF MEURICE, JC PAQUEREAU, J MARILLAUD, A TI SAME LOCATION OF THE SOURCE OF P1 OF BAEPS AND N1 OF CAP IN GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; LESION; BRAIN-STEM AUDITORY EVOKED POTENTIALS; COMPOUND ACTION POTENTIAL; COCHLEAR NERVE; GENERATORS ID AUDITORY-EVOKED-POTENTIALS; BRAIN-STEM RESPONSES; TRAPEZOID BODY; CEREBELLOPONTINE ANGLE; COCHLEAR NERVE; LESIONS; GENERATION; ABRS; ABNORMALITIES AB The purpose of this study was to point out the location of N1 and N2 of the compound action potential (CAP) and the first waves of the brainstem auditory evoked potentials (BAEPs) by the mean of the section of the eight nerve at the porus acousticus in guinea pigs. Our results agree with most of the studies in the literature. In the absence of lesion of the internal auditory artery, the section of the cochlear nerve induced the persistence, alone, of the P1 of BAEPs in which latency was similar to initial P1 before section, and the subsequent waves disappeared. Simultaneously, a monophasic negative potential (N1) of the auditory nerve remained without N2. When the section included the internal auditory artery all BAEPs and CAP components disappeared simultaneously and very suddenly just after the section. These results definitively excluded a proximal contribution of the cochlear nerve in the N1 of CAP and P1 of BAEPs. The N2 of CAP and P2 of BAEPs are not generated, even in part, in the intracochlear or intrapetrous portion of the cochlear nerve. C1 FAC MED POITIERS,PHYSIOL GEN LAB,CNRS,UA 290,34 RUE JARDIN PLANTES,F-86034 POITIERS,FRANCE. CR ACHOR LJ, 1980, ELECTROEN CLIN NEURO, V48, P174, DOI 10.1016/0013-4694(80)90302-8 ACHOR LJ, 1980, ELECTROEN CLIN NEURO, V48, P154, DOI 10.1016/0013-4694(80)90301-6 BUCHWALD JS, 1975, SCIENCE, V189, P382, DOI 10.1126/science.1145206 BUCHWALD JS, 1980, BASES AUDITORY BRAIN, P157 DAIGNEAU.EA, 1974, ACTA OTO-LARYNGOL, V77, P405, DOI 10.3109/00016487409124642 DAVIS H, 1958, AM J PHYSIOL, V195, P251 DEUPREE DL, 1988, ELECTROEN CLIN NEURO, V70, P355, DOI 10.1016/0013-4694(88)90054-5 GERSDORFF MCH, 1982, ARCH OTO-RHINO-LARYN, V234, P15, DOI 10.1007/BF00453533 HASHIMOTO I, 1981, BRAIN, V104, P841, DOI 10.1093/brain/104.4.841 HASHIMOTO I, 1979, ARCH NEUROL-CHICAGO, V36, P161 HENRY KR, 1979, J AM AUDITORY SOC, V4, P173 JEWETT DL, 1987, ELECTROEN CLIN NEURO, V68, P323, DOI 10.1016/0168-5597(87)90012-8 JEWETT DL, 1970, ELECTROEN CLIN NEURO, V28, P609, DOI 10.1016/0013-4694(70)90203-8 LEGOUIX JP, 1974, J ACOUST SOC AM, V56, P1222, DOI 10.1121/1.1903411 MAURER K, 1983, ELECTROEN CLIN NEURO, V55, P586, DOI 10.1016/0013-4694(83)90170-0 MOLLER AR, 1988, ELECTROEN CLIN NEURO, V71, P198, DOI 10.1016/0168-5597(88)90005-6 MOLLER AR, 1983, EXP NEUROL, V80, P633, DOI 10.1016/0014-4886(83)90313-8 Moller AR, 1981, J EXP NEUROL, V74, P862 MOLLER AR, 1983, J NEUROSURG, V59, P1013, DOI 10.3171/jns.1983.59.6.1013 PAQUEREAU J, 1988, AUDIOLOGY, V27, P291 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 PRATT H, 1984, ELECTROEN CLIN NEURO, V58, P83, DOI 10.1016/0013-4694(84)90204-9 SCHERG M, 1985, ELECTROEN CLIN NEURO, V62, P290, DOI 10.1016/0168-5597(85)90006-1 SEKIYA T, 1988, ACTA NEUROCHIR, V90, P45, DOI 10.1007/BF01541266 SEKIYA T, 1987, J NEUROSURG, V67, P244, DOI 10.3171/jns.1987.67.2.0244 SOHMER H, 1974, ELECTROEN CLIN NEURO, V37, P663, DOI 10.1016/0013-4694(74)90081-9 STOCKARD JJ, 1977, NEUROLOGY, V27, P316 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P352, DOI 10.1016/0013-4694(83)90261-4 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P326, DOI 10.1016/0013-4694(83)90259-6 WADA SI, 1983, ELECTROEN CLIN NEURO, V56, P340, DOI 10.1016/0013-4694(83)90260-2 NR 30 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1991 VL 53 IS 2 BP 209 EP 216 DI 10.1016/0378-5955(91)90054-D PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900004 PM 1880075 ER PT J AU HELLSTROM, LI SCHMIEDT, RA AF HELLSTROM, LI SCHMIEDT, RA TI RATE LEVEL FUNCTIONS OF AUDITORY-NERVE FIBERS IN YOUNG AND QUIET-AGED GERBILS SO HEARING RESEARCH LA English DT Article DE RATE LEVEL FUNCTION; AUDITORY NERVE; GERBIL; AGING; COMPOUND ACTION POTENTIAL; PRESBYACUSIS ID NORMATIVE DATA; BRAIN-STEM; SUPPRESSION; POTENTIALS; AP AB Steady-state rate/level functions of single auditory-nerve fibers to characteristic frequency (CF) tone bursts were measured in quiet-aged (35-37 months) and young control (4-7 months) gerbils. Rate/level functions of aged gerbils are different from those of young controls in that the thresholds are shifted to higher sound levels, but otherwise the shapes of the aged and young rate/level functions are similar. Specifically, there is little difference in the slope of the dynamic range portion of the rate/level functions when comparing aged gerbils to young controls. This is in contrast to whole-nerve input/output (I/O) functions of aged gerbils, which exhibit slopes that are less steep than those of the young controls (Hellstrom and Schmiedt, 1990b). Thus, it is likely that the deterioration of the CAP I/O function in aged animals is not due to a deterioration of rate/level functions in single units, but rather to other factors such as spiral ganglion cell degeneration or a loss of synchrony. RP HELLSTROM, LI (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUN SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR ANTOLICANDELA F, 1978, EVOKED ELECTRICAL AC, P165 CHAMBERLAIN SC, 1977, J COMP NEUROL, V171, P193, DOI 10.1002/cne.901710205 Derbyshire AJ, 1935, AM J PHYSIOL, V113, P476 DOLAN TG, 1985, HEARING RES, V18, P203, DOI 10.1016/0378-5955(85)90038-3 DOLAN TG, 1985, HEARING RES, V17, P259, DOI 10.1016/0378-5955(85)90070-X HELLSTROM LI, 1990, HEARING RES, V50, P163, DOI 10.1016/0378-5955(90)90042-N HELLSTROM LI, 1990, ASS RES OTOLARYNGOL, V13, P149 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KEITHLEY EM, 1990, NEUR ABSTR, V20, P796 LEVINE MS, 1988, CENTRAL DETERMINANTS, P314 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 OZDAMAR O, 1976, J ACOUST SOC AM, V59, P143 ROGERS J, 1988, CENTRAL DETERMINANTS, P251 SACHS MB, 1974, J ACOUST SOC AM, V56, P1835, DOI 10.1121/1.1903521 SCHMIEDT RA, 1982, J ACOUST SOC AM, V72, P142, DOI 10.1121/1.387998 SCHMIEDT RA, 1991, ASS RES OTOLARYNGOLO, V14, P80 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SOKOLICH WG, 1976, J ACOUST SOC AM, V59, P963, DOI 10.1121/1.380955 NR 19 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1991 VL 53 IS 2 BP 217 EP 222 DI 10.1016/0378-5955(91)90055-E PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900005 PM 1880076 ER PT J AU KHAN, KM HATFIELD, JS DRESCHER, DG AF KHAN, KM HATFIELD, JS DRESCHER, DG TI CARBOHYDRATES ASSOCIATED WITH THE CELL COAT SURROUNDING CELLS OF THE RAINBOW-TROUT SACCULAR MACULA AS REVEALED BY LECTIN PROBES SO HEARING RESEARCH LA English DT Article DE CELL COAT; LECTIN BINDING; SACCULAR MACULA; SALMO-GAIRDNERI ID COCHLEAR HAIR-CELLS; SUPPORTING CELLS; RUTHENIUM RED; TANNIC-ACID; INNER-EAR; ORGAN; INTERCONNECTIONS; GLYCOPROTEINS; GLYCOCALYX; MEMBRANE AB The luminal surface of the saccular macula in the rainbow trout is covered with a glycoconjugate-rich cell coat. The aim of this study was to identify specific carbohydrate moieties present in this coat, using biotinylated lectins as probes. Saccular tissues were fixed in Karnovsky's fixative for 2 h at 1-2-degrees-C, followed by incubation with biotinylated lectins for 12-16 h at 25-degrees-C. Lectin binding was visualized by performing avidin-biotin-peroxidase reactions. As controls, specimens were reacted with solutions of lectins preincubated with their specific inhibitory sugars. Staining was observed that was consistent with the presence of glucose, galactose, fucose, mannose, N-acetylglucosamine, N-acetylneuraminic acid, and N-acetylgalactosamine in the cell coat. The variability in the intensity of staining associated with the lectin-carbohydrate complexes suggests quantitative differences among the various carbohydrate moieties detected. The presence of these carbohydrates in the cell coat of the trout saccular macula also suggests biochemical similarities between cell coats in teleost and mammalian inner ear structures. C1 WAYNE STATE UNIV,SCH MED,DEPT OTOLARYNGOL,BIOOTOL LAB,540 E CANFIELD AVE,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT BIOCHEM,DETROIT,MI 48201. VET ADM MED CTR,ELECTRON MICROSCOPY LAB,ALLEN PK,MI 48101. CR BOURRILLON R, 1989, INT REV CYTOL, V116, P257, DOI 10.1016/S0074-7696(08)60642-7 CASTELLS MT, 1990, HISTOCHEM J, V22, P24, DOI 10.1007/BF01962876 FLOCK A, 1977, ACTA OTO-LARYNGOL, V83, P85, DOI 10.3109/00016487709128817 GILLOYZAGA P, 1985, HEARING RES, V20, P1 GILLOYZAGA P, 1985, HEARING RES, V18, P269, DOI 10.1016/0378-5955(85)90043-7 GILLOYZAGA P, 1988, HEARING RES, V34, P149, DOI 10.1016/0378-5955(88)90102-5 HOWARD J, 1987, SENSORY TRANSDUCTION, P138 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 KARNOVSK.MJ, 1965, J CELL BIOL, V27, pA137 KHAN KM, 1990, ABSTR SOC NEUROSCI, V16, P1079 KHAN KM, 1990, J HISTOCHEM CYTOCHEM, V38, P1615 LIM DJ, 1986, HEARING RES, V22, P117, DOI 10.1016/0378-5955(86)90089-4 LIS H, 1986, ANNU REV BIOCHEM, V55, P35, DOI 10.1146/annurev.bi.55.070186.000343 NEUGEBAUER DC, 1986, NATURWISSENSCHAFTEN, V73, P508, DOI 10.1007/BF00367202 NEUGEBAUER DC, 1986, ORL J OTO-RHINO-LARY, V48, P87 PICKLES JO, 1988, COCHLEAR MECHANISMS, P37 PICKLES JO, 1987, HEARING RES, V29, P237, DOI 10.1016/0378-5955(87)90170-5 PRIETO JJ, 1986, HEARING RES, V24, P237, DOI 10.1016/0378-5955(86)90022-5 Reuter G, 1988, Acta Histochem Suppl, V36, P51 RUSSELL P, 1986, EXP EYE RES, V42, P95, DOI 10.1016/0014-4835(86)90034-5 SANTI PA, 1987, HEARING RES, V27, P47, DOI 10.1016/0378-5955(87)90025-6 SCHULTE BA, 1985, J HISTOCHEM CYTOCHEM, V33, P427 SHARON N, 1982, MOL CELL BIOCHEM, V42, P167, DOI 10.1007/BF00238511 SHARON N, 1989, SCIENCE, V246, P227, DOI 10.1126/science.2552581 SLEPECKY N, 1985, HEARING RES, V17, P281, DOI 10.1016/0378-5955(85)90072-3 TAKUMIDA M, 1988, ACTA OTO-LARYNGOL, V106, P130, DOI 10.3109/00016488809107380 TAKUMIDA M, 1989, HEARING RES, V37, P163, DOI 10.1016/0378-5955(89)90037-3 TAKUMIDA M, 1989, ARCH OTO-RHINO-LARYN, V246, P26, DOI 10.1007/BF00454130 NR 28 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JUN PY 1991 VL 53 IS 2 BP 223 EP 229 DI 10.1016/0378-5955(91)90056-F PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900006 PM 1715341 ER PT J AU MARKS, SC MATTOX, DE CASERO, RA AF MARKS, SC MATTOX, DE CASERO, RA TI THE EFFECTS OF DFMO ON POLYAMINE METABOLISM IN THE INNER-EAR SO HEARING RESEARCH LA English DT Article DE DIFLUOROMETHYLORNITHINE; POLYAMINE METABOLISM; HEARING LOSS; ORNITHINE DECARBOXYLASE; GUINEA PIGS ID COLON CARCINOMA-CELLS; ALPHA-DIFLUOROMETHYLORNITHINE; ORNITHINE DECARBOXYLASE; IRREVERSIBLE INHIBITION; GROWTH; DEPLETION; HEARING AB Difluoromethylornithine (DFMO) is a novel antineoplastic agent that was associated with an unexpected hearing loss in Phase II clinical trials. DFMO interferes with polyamine synthesis by inhibition of the enzyme ornithine decarboxylase (ODC). The objective of the current study was to establish a methodology to determine the effect of DFMO on polyamine levels and ODC activity in the cochlea. Guinea pigs received DFMO in their drinking water and were tested for auditory brainstem response threshold shifts. The organ of Corti, the lateral wall, and the acoustic nerve were assayed for both ODC activity and polyamine levels. In DFMO treated animals there was an inhibition of ODC activity in cochlear tissues as well as in intestinal mucosa. In addition, a significant depletion of cochlear polyamines was observed in the treatment animals. This study suggests that systematically administered DFMO inhibits ODC activity and interferes with polyamine synthesis in the cochlea. C1 JOHNS HOPKINS UNIV HOSP,DEPT OTOLARYNGOL HEAD & NECK SURG,600 N WOLFE ST,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD 21205. CR ABELOFF MD, 1986, CANCER TREAT REP, V70, P843 ABELOFF MD, 1984, CANCER TREAT REP, V70, P124 BICHLER E, 1982, ARCH OTO-RHINO-LARYN, V234, P175, DOI 10.1007/BF00453626 BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999 BROOKES GB, 1985, AM J OTOL, V6, P102 CASERO RA, 1987, CANCER RES, V47, P3964 CASERO RA, 1984, J CELL PHYSIOL, V121, P476, DOI 10.1002/jcp.1041210305 CELANO P, 1989, J BIOL CHEM, V264, P8922 CELANO P, 1988, J BIOL CHEM, V263, P5491 GILL GV, 1982, J NEUROL NEUROSUR PS, V45, P861, DOI 10.1136/jnnp.45.10.861 HENLEY CM, 1987, BRAIN RES BULL, V19, P695, DOI 10.1016/0361-9230(87)90056-6 JANSEN C, 1989, ARCH OTOLARYNGOL, V115, P1234 KABRA PM, 1986, J CHROMATOGR, V380, P19, DOI 10.1016/S0378-4347(00)83621-X MAMONT PS, 1978, BIOCHEM BIOPH RES CO, V81, P58, DOI 10.1016/0006-291X(78)91630-3 METCALF BW, 1978, J AM CHEM SOC, V100, P2551, DOI 10.1021/ja00476a050 PEGG AE, 1983, METHOD ENZYMOL, V94, P158 PEGG AE, 1968, BIOCHEM J, V108, P533 PEGG AE, 1986, BIOCHEM J, V234, P249 RUSSELL DH, 1985, DRUG METAB REV, V16, P1, DOI 10.3109/03602538508991430 SALZER SJ, 1991, HEARING RES, V46, P101 SCHWEITZER L, 1986, BRAIN RES BULL, V16, P215, DOI 10.1016/0361-9230(86)90035-3 SJOERDSMA A, 1984, CLIN PHARMACOL THER, V35, P287 SWEET RJ, 1988, AUDIOLOGY, V27, P305 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 JUN PY 1991 VL 53 IS 2 BP 230 EP 236 DI 10.1016/0378-5955(91)90057-G PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900007 PM 1880077 ER PT J AU PRATT, H ZAAROOR, M BLEICH, N STARR, A AF PRATT, H ZAAROOR, M BLEICH, N STARR, A TI EFFECTS OF MYELIN OR CELL BODY BRAIN-STEM LESIONS ON 3-CHANNEL LISSAJOUS TRAJECTORIES OF FELINE AUDITORY BRAIN-STEM EVOKED-POTENTIALS SO HEARING RESEARCH LA English DT Article DE AUDITORY BRAIN-STEM EVOKED POTENTIALS; 3CLT; MYELIN LESIONS; NEURONAL LESIONS; COCHLEAR NUCLEUS; SUPERIOR OLIVARY COMPLEX; TRAPEZOID BODY ID STEM RESPONSES ABRS; LYSOPHOSPHATIDYL CHOLINE; DIGITAL-FILTERS; TRAPEZOID BODY; GUINEA-PIGS; CAT; NERVE; INJECTION; MONKEY; SCALP AB Auditory brainstem evoked potentials (ABEP) were recorded from 16 awake cats to obtain 3-Channel Lissajous' Trajectories (3CLTs) using three orthogonal differential electrode configurations (nasion - midline nuchal ridge, left - right mastoids, vertex - midline under the mandible). Potentials, evoked by monaural 80 dBnHL (re. human threshold) clicks, were studied before, and up to 7 weeks after inducing neuronal lesions localized to the cochlear nucleus (CN) or the superior olivary complex (SOC), or myelin lesions localized to the fibers of the trapezoid body connecting these two structures. Neuronal lesions were induced by injection of kainic acid (KA), while myelin lesions were induced by injection of L-alpha-lysophosphatidylcholine (LPC). With CN neuronal lesions the major changes in 3CLT were in the time domain of 'b', 'c' and 'd' (components P2, P3 and P4 of single-channel ABEP). With SOC neuronal lesions the major changes were in 'c' and 'd' of 3CLT (P3 and P4 of ABEP). With trapezoid body lesions the major changes was in 'c' (P3 of ABEP). The results are compatible with the peripheral generation of the first ABEP components (P1a and P1b). The second component (P2) is generated by ipsilateral CN neurones and their outputs. The third component (P3) is generated primarily by ipsilateral SOC neurones and their outputs, with the ipsilateral CN providing input. The fourth component (P4) is generated bilaterally by the SOC neurones and their outputs, receiving their inputs from ipsilateral CN. The fifth ABEP component (P5) is generated by structures central to the SOCs and their immediate outputs. Neither focal neuronal nor myelin lesions were sufficient to produce obliteration of any component, consistent with a set of generators for each of the ABEP components, consisting of both cell bodies and their output fibers, that is distributed spatially in the brainstem. C1 UNIV CALIF IRVINE,DEPT NEUROL,IRVINE,CA 92717. RP PRATT, H (reprint author), TECHNION ISRAEL INST TECHNOL,EVOKED POTENTIALS LAB,IL-32000 HAIFA,ISRAEL. 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Res. PD JUN PY 1991 VL 53 IS 2 BP 237 EP 252 DI 10.1016/0378-5955(91)90058-H PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900008 PM 1880078 ER PT J AU DANNHOF, BJ BRUNS, V AF DANNHOF, BJ BRUNS, V TI THE ORGAN OF CORTI IN THE BAT HIPPOSIDEROS-BICOLOR SO HEARING RESEARCH LA English DT Article DE COCHLEA; MORPHOMETRY; BAT; HIPPOSIDEROS ID OUTER HAIR-CELLS; GREATER HORSESHOE BAT; COCHLEAR MECHANICS; BASILAR-MEMBRANE; GUINEA-PIG; PTERONOTUS-PARNELLII; INNER-EAR; FREQUENCY; MICROMECHANICS; ADAPTATIONS AB The bat Hipposideros bicolor (Hipposideridae, Microchiroptera) is the mammalian species with the highest upper limit of hearing in which the structure of the organ of Corti has been studied. H. bicolor emits pure tone echo-locating signals of 153 kHz, compensates for Doppler shifts in the echo and hears ultrasonic frequencies up to 200 kHz (Neuweiler et al., 1984). The organ of Corti was investigated qualitatively and quantitatively using the technique of semi-thin sectioning. Some complementary ultra-thin sections were also examined. Length, width and cross-sectional area of the basilar membrane, the tectorial membrane, the hair cells with their stereocilia and the organ of Corti were measured at equi-distant positions on the basilar membrane. The organ of Corti of H. bicolor is composed of elements similar to those found in the cochleae of other eutherian mammals studied. However, in H. bicolor some of these elements show species-specific differences when compared to auditorily unspecialized mammals. The most basal region of the cochlea is characterized by miniaturization and re-inforcement of macro- and micro-mechanically important elements. This is interpreted as an adaptation for hearing extremely high frequencies. Specialized structures as well as local maxima of 'normal' elements in the basal and middle cochlear region are associated with evaluation of the echos of emitted pure tones. Besides the basal specializations, Hipposideros also shows specializations in the apical, low frequency, region which can be correlated with passive acoustic orientation. C1 JW GOETHE UNIV,INST ZOOL,SIESMAYERSTR 70,W-6000 FRANKFURT 11,GERMANY. 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PD JUN PY 1991 VL 53 IS 2 BP 253 EP 268 DI 10.1016/0378-5955(91)90059-I PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900009 PM 1880079 ER PT J AU WHITEHEAD, ML AF WHITEHEAD, ML TI SLOW VARIATIONS OF THE AMPLITUDE AND FREQUENCY OF SPONTANEOUS OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE SPONTANEOUS OTOACOUSTIC EMISSIONS; FREQUENCY VARIATIONS; AMPLITUDE VARIATIONS; CONTRALATERAL EAR ID ACTIVE MICROMECHANICAL PROPERTIES; OTO-ACOUSTIC EMISSIONS; COCHLEAR MECHANICS; FINE-STRUCTURE; STIMULATION; NONLINEARITY; THRESHOLD; INFANTS AB Systematic, slow variations of the amplitude and frequency of spontaneous otoacoustic emissions in human ears, occurring over the first 20-30 min of recording, are described. Experimental observations suggest that these variations may arise from a centrally mediated, bilateral influence on the mechanics of the ear. C1 UNIV KEELE,DEPT COMMUN & NEUROSCI,KEELE ST5 5BG,STAFFS,ENGLAND. CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 BARGONES JY, 1988, J ACOUST SOC AM, V83, P1809, DOI 10.1121/1.396515 BROWN AM, 1988, HEARING RES, V34, P27, DOI 10.1016/0378-5955(88)90048-2 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E EVANS EF, 1981, TINNITUS, P108 FRICK LR, 1988, EAR HEARING, V9, P190, DOI 10.1097/00003446-198808000-00004 FRITZE W, 1983, ARCH OTO-RHINO-LARYN, V238, P189, DOI 10.1007/BF00454312 Fritze W, 1986, Scand Audiol Suppl, V25, P129 FROEHLICH P, 1990, BRAIN RES, V508, P286, DOI 10.1016/0006-8993(90)90408-4 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 KEMP DT, 1979, ARCH OTO-RHINO-LARYN, V224, P37, DOI 10.1007/BF00455222 KEMP DT, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 KEMP DT, 1981, TINNITUS, P54 Kemp DT, 1980, PSYCHOPHYSICAL PHYSL, P34 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Puel J.L., 1989, COCHLEAR MECHANISMS, P315 PUEL JL, 1988, BRAIN RES, V447, P380, DOI 10.1016/0006-8993(88)91144-4 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 RABINOWITZ WM, 1984, J ACOUST SOC AM, V76, P1713, DOI 10.1121/1.391618 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SCHLOTH E, 1983, ACUSTICA, V53, P250 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 STRICKLAND E, 1984, J ACOUST SOC AM S1, V75, pS82, DOI 10.1121/1.2021637 STRICKLAND EA, 1985, J ACOUST SOC AM, V78, P931, DOI 10.1121/1.392924 WHITEHEAD ML, 1991, HEARING RES, V51, P55, DOI 10.1016/0378-5955(91)90007-V WHITEHEAD ML, 1991, HEARING RES, V51, P293, DOI 10.1016/0378-5955(91)90045-B WHITEHEAD ML, 1989, THESIS U KEELE STAFF WHITEHEAD ML, 1988, BR J AUDIOL, V23, P149 WILSON JP, 1980, J PHYSIOL-LONDON, V298, pP8 Wilson JP, 1981, TINNITUS, P82 WILSON JP, 1981, PERIPHERAL AUDITORY, P82 WILSON JP, 1986, PERIPHERAL AUDITORY, P266 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X WIT HP, 1985, HEARING RES, V18, P197, DOI 10.1016/0378-5955(85)90012-7 ZUREK PM, 1981, J ACOUST SOC AM, V69, P514, DOI 10.1121/1.385481 NR 36 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 JUN PY 1991 VL 53 IS 2 BP 269 EP 280 DI 10.1016/0378-5955(91)90060-M PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900010 PM 1880080 ER PT J AU FISCHER, FP BRIX, J SINGER, I MILTZ, C AF FISCHER, FP BRIX, J SINGER, I MILTZ, C TI CONTACTS BETWEEN HAIR-CELLS IN THE AVIAN COCHLEA SO HEARING RESEARCH LA English DT Article DE BIRD; COCHLEA; HAIR CELL; CELL CONTACT ID BASILAR PAPILLA; TONOTOPIC ORGANIZATION; CHICK COCHLEA; RESPONSES; INNERVATION; PATTERN; BUNDLE AB In the avian papilla basilaris, contacts between hair cells are a common feature. With few exceptions, they only occur between tall hair cells (THC), and they are more frequent in the apical half of the papilla. In this quantitative study, four types of contacts are defined: Protrusion contacts, touch contacts, fusion contacts and multiple contacts. 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Res. PD JUN PY 1991 VL 53 IS 2 BP 281 EP 292 DI 10.1016/0378-5955(91)90061-D PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900011 PM 1880081 ER PT J AU RICHARDSON, GP RUSSELL, IJ AF RICHARDSON, GP RUSSELL, IJ TI COCHLEAR CULTURES AS A MODEL SYSTEM FOR STUDYING AMINOGLYCOSIDE INDUCED OTOTOXICITY SO HEARING RESEARCH LA English DT Article DE COCHLEAR CULTURES; AMINOGLYCOSIDE ANTIBIOTICS; OTOTOXICITY ID INDUCED HEARING-LOSS; HAIR-CELLS; ORGANOTYPIC CULTURES; MOUSE COCHLEA; ANTIBIOTICS; KANAMYCIN; MORPHOLOGY; NEOMYCIN; INVITRO; RAT AB Light and electron microscopy have been used to evaluate the effects of treating mouse cochlear cultures with the ototoxic aminoglycoside antibiotic neomycin sulphate at concentrations of 0.2 mM and greater for periods of up to 1 hour. Neomycin rapidly induces the formation of numerous, membrane filled blisters on the apical surfaces of the sensory hair cells. Such morphological damage is restricted to the hair cells, and is not observed on the surfaces of supporting cells within the organ of Corti. Hair cells in apical-coil cultures are less sensitive than those in basal-coil cultures, and, at any given point along the cochlea, outer hair cells appear to be more extensively damaged by neomycin than inner hair cells. These morphological effects of neomycin are considerably more severe when the drug is applied in calcium/magnesium free saline, and can be blocked by elevating the saline concentration of either calcium or magnesium. The effects can also be blocked by lowering the temperature to 4-degrees-C, but not by either K+ depolarization or the lectin Concanavalin A. The potential value of this culture system as a model for studying aminoglycoside induced ototoxicity is discussed. RP RICHARDSON, GP (reprint author), UNIV SUSSEX,SCH BIOL SCI,BRIGHTON BN1 9QG,E SUSSEX,ENGLAND. 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PD JUN PY 1991 VL 53 IS 2 BP 293 EP 311 DI 10.1016/0378-5955(91)90062-E PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FT009 UT WOS:A1991FT00900012 PM 1880082 ER PT J AU PEAKE, WT ROSOWSKI, JJ AF PEAKE, WT ROSOWSKI, JJ TI IMPEDANCE MATCHING, OPTIMUM VELOCITY, AND IDEAL MIDDLE EARS SO HEARING RESEARCH LA English DT Article DE IDEAL EARS; IMPEDANCE MATCHING ID EXTERNAL EAR; MECHANICS; PRESSURE AB One way to assess an ear's performance as a receiver of acoustic power is to consider impedance matching at the tympanic membrane. Assumptions about some of the impedances involved have lead to the idea of an optimum velocity magnitude (per unit pressure), which has been used as a test of middle-ear performance. We show that this approach is not a realistic way to assess effectiveness of power absorption at the tympanic membrane. More generally, we suggest that, if the performance of the combined external-and-middle ear in collecting acoustic power and delivering it to the inner ear is considered, the external- and middle-ear power-transfer efficiencies, as well as impedance matching, are involved in relating performance to an ideal. C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OTOLARYNGOL,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114. RP PEAKE, WT (reprint author), MIT,ELECTR RES LAB,ROOM 36-825,77 MASSACHUSETTS AVE,CAMBRIDGE,MA 02139, USA. CR DALLOS P, 1984, HDB PHYSL 1 2, V3, P595 Dallos P, 1973, AUDITORY PERIPHERY Dear S., 1987, THESIS U PENNSYLVANI Desoer C. 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PD MAY PY 1991 VL 53 IS 1 BP 1 EP 6 DI 10.1016/0378-5955(91)90208-Q PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200001 PM 2066277 ER PT J AU CANLON, B BRUNDIN, L AF CANLON, B BRUNDIN, L TI MECHANICALLY INDUCED LENGTH CHANGES OF ISOLATED OUTER HAIR-CELLS ARE METABOLICALLY DEPENDENT SO HEARING RESEARCH LA English DT Article DE COCHLEA; MOTILITY; METABOLISM; OUTER HAIR CELLS ID POLYCATIONS; RESPONSES; MOTILITY; PH AB Isolated outer hair cells from the organ of Corti of the guinea pig have been shown to change length in response to a mechanical stimulus in the form of a tone burst at a fixed frequency of 200 Hz (Canlon et al., 1988). In the present study, the threshold of movement for individual outer hair cells is related to the original length of the cell such that long cells are more sensitive than short cells for all cochlear locations studied. Length changes could be elicited when the stimulus was projected at any site along the longitudinal axis of the plasma membrane. Length changes were not elicited when the stereocilia were stimulated directly. These mechanically-induced length changes were found to be metabolically dependent. In the presence of either sodium cyanide or 2,4-dinitrophenol, the motile response of outer hair cells was completely blocked within 30 min. When the extracellular pH was altered in a graded fashion, the motile response decreased gradually. Furthermore, 3-mu-M poly-L-lysine or poly-D-lysine of different molecular weights were also effective in blocking the motile response, whereas the negatively charged polyaminoacid, poly-L-aspartate, was not effective. Fluorescently-labelled poly-lysine demonstrated that the plasma membrane, stereocilia, and nucleus were the most intensely stained structures of the outer hair cells. It is suggested that the passive influx of poly-lysine is responsible for the inhibition of the motile response. Finally, the finding that the bidirectional motile response of isolated outer hair cells induced by mechanical stimulation is dependent on the metabolic state of the cell distinguishes this type of motility from the electrically induced outer hair cell shape changes. RP CANLON, B (reprint author), KAROLINSKA INST, DEPT PHYSIOL 2, S-10401 STOCKHOLM 60, SWEDEN. CR AHLSTROM P, 1975, LARYNGOSCOPE, V85, P1241, DOI 10.1288/00005537-197507000-00016 ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CANLON B, 1988, P NATL ACAD SCI USA, V85, P7033, DOI 10.1073/pnas.85.18.7033 DALLOS P, 1972, ACTA OTO-LARYNGOL, P1 DAVIS H, 1958, AM J PHYSIOL, V195, P251 DING JP, 1990, STRETCH ACTIVATED IO DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1991, IN PRESS J NEUROSCI EVANS EF, 1976, EFFECTS NOISE HEARIN, P199 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GOLD T, 1948, PROC R SOC SER B-BIO, V135, P492, DOI 10.1098/rspb.1948.0025 GUHARAY F, 1985, J PHYSIOL-LONDON, V363, P119 Guild SR, 1937, LARYNGOSCOPE, V47, P365, DOI 10.1288/00005537-193706000-00001 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 MADSHUS IH, 1988, BIOCHEM J, V250, P1 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 OKU N, 1986, J BIOCHEM-TOKYO, V100, P935 SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SEILER MW, 1975, SCIENCE, V189, P390, DOI 10.1126/science.1145209 TAKADA A, 1982, J PHARM SCI, V71, P1410, DOI 10.1002/jps.2600711226 Wever EG, 1930, P NATL ACAD SCI USA, V16, P344, DOI 10.1073/pnas.16.5.344 ZENNER HP, 1986, NEUROBIOLOGY HEARING ZENNER HP, 1980, ARCH OTORHINOLARYNGO, V230, P82 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 26 TC 19 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 7 EP 16 DI 10.1016/0378-5955(91)90209-R PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200002 PM 2066289 ER PT J AU PHILLIPS, DP SARK, SA AF PHILLIPS, DP SARK, SA TI SEPARATE MECHANISMS CONTROL SPIKE NUMBERS AND INTER-SPIKE INTERVALS IN TRANSIENT RESPONSES OF CAT AUDITORY-CORTEX NEURONS SO HEARING RESEARCH LA English DT Article DE AUDITORY CORTEX; SINGLE NEURON; TRANSIENT RESPONSE; SPIKE TIMING; INTER-SPIKE INTERVAL ID VENTRAL COCHLEAR NUCLEUS; BINAURAL STIMULATION; REPRESENTATION; LATENCY; MONKEY; DORSAL; CELLS; TIME AB In the anesthetized cat, some cortical auditory neurons discharge a train of up to 5 spikes in response to the onset of a characteristic frequency tone pulse. This report provides the first description of the inter-spike intervals (ISIs) in these responses. The ISIs were typically close to 2.0 ms in length, and, as indexed by the standard deviation of the interval length, were very regular. Except at threshold levels of stimulation, mean ISIs were relatively insensitive to both tone amplitude and repitition rate. This was true even over ranges of those variables that exerted dramatic effects on spike numbers and first spike latency. These data suggest that the relative timing of discharges within the spike burst is controlled by a mechanism which is separable from that which determines the number of spikes in them. The brevity of the ISIs suggest that they may be a means of enhancing the salience of the transient response against a background of spontaneous discharges. C1 DALHOUSIE UNIV,DEPT OTOLARYNGOL,HALIFAX B3H 4J1,NS,CANADA. RP PHILLIPS, DP (reprint author), DALHOUSIE UNIV,DEPT PSYCHOL,HALIFAX B3H 4J1,NS,CANADA. RI Phillips, Dennis/A-6496-2011 CR BRUGGE JF, 1973, J NEUROPHYSIOL, V36, P1138 BRUGGE JF, 1969, J NEUROPHYSIOL, V32, P1005 GOLDBERG JM, 1966, J NEUROPHYSIOL, V29, P72 Kiang N.Y.S., 1965, MIT RES MONOGRAPH, V35 KITZES LM, 1980, J COMP NEUROL, V192, P455, DOI 10.1002/cne.901920306 KITZES LM, 1978, J NEUROPHYSIOL, V41, P1165 PFEIFFER RR, 1965, BIOPHYS J, V5, P301 PHILLIPS DP, 1988, J NEUROPHYSIOL, V59, P1524 PHILLIPS DP, 1988, PHYSL EAR, P407 PHILLIPS DP, 1990, BEHAV BRAIN RES, V37, P197, DOI 10.1016/0166-4328(90)90132-X PHILLIPS DP, 1990, J ACOUST SOC AM, V88, P1403, DOI 10.1121/1.399718 PHILLIPS DP, 1989, J ACOUST SOC AM, V85, P1524 PHILLIPS DP, 1990, BEHAV BRAIN RES, V40, P85, DOI 10.1016/0166-4328(90)90001-U RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RHODE WS, 1987, J NEUROPHYSIOL, V57, P414 RHODE WS, 1986, J NEUROPHYSIOL, V56, P261 RHODE WS, 1983, J COMP NEUROL, V213, P448, DOI 10.1002/cne.902130408 STEINSCHNEIDER M, 1980, BRAIN RES, V198, P75, DOI 10.1016/0006-8993(80)90345-5 STEINSCHNEIDER M, 1982, BRAIN RES, V252, P353, DOI 10.1016/0006-8993(82)90403-6 YOUNG ED, 1988, J NEUROPHYSIOL, V60, P1 NR 20 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 MAY PY 1991 VL 53 IS 1 BP 17 EP 27 DI 10.1016/0378-5955(91)90210-Z PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200003 PM 2066284 ER PT J AU BACKOFF, PM CLOPTON, BM AF BACKOFF, PM CLOPTON, BM TI A SPECTROTEMPORAL ANALYSIS OF DCN SINGLE UNIT RESPONSES TO WIDE-BAND NOISE IN GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE SPECTROTEMPORAL ANALYSIS; RECEPTIVE FIELD; DORSAL COCHLEAR NUCLEUS; NOISE; GUINEA PIG ID DORSAL COCHLEAR NUCLEUS; AUDITORY-NERVE FIBERS; SPECTRO-TEMPORAL CHARACTERISTICS; NEURONS; CAT; TONES; REPRESENTATION; DISTRIBUTIONS; MIDBRAIN AB Spectrotemporal receptive fields (STRFs) were estimated for chopper and pauser units recorded in guinea pig dorsal cochlear nucleus (DCN). Sixteen wideband, periodic noise stimuli, represented as time-frequency surfaces of energy density, were crosscorrelated in time with the unit's corresponding period histograms to determine if specific energy patterns tended to precede spike occurrence. The STRFs obtained were unique to the DCN, as compared to the ventral cochlear nucleus (VCN) [Clopton and Backoff, spectral complexity. Certain unit response types, classified from their peristimulus-time histograms (PSTHs) to tonebursts, were associated with distinctive patterns in the STRFs. All STRFs had at least one region of elevated energy density (peak region) closely preceding spike occurrence, which may reflect a short-pathway, primary excitatory input (or inputs) to the neuron. In addition, some units displayed low-energy regions (troughs) with greater temporal precedences on their STRFs, particularly when higher stimulus intensities were used. This analysis approach appears to have potential for investigating functional neural connectivity and predicting responses to novel complex stimuli, although specific implementations of the technique impose limitations on the interpretation of results. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP BACKOFF, PM (reprint author), SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,POB 19230,SPRINGFIELD,IL 62794, USA. CR BACKOFF PM, 1989, TIME FREQUENCY SURFA, P57 CASPARY DM, 1985, AUDITORY BIOCH, P198 CASPARY DM, 1987, BRAIN RES, V417, P273, DOI 10.1016/0006-8993(87)90452-5 CHOI HI, 1989, IEEE T ACOUST SPEECH, V37, P862, DOI 10.1109/ASSP.1989.28057 CLOPTON BM, 1991, HEARING RES, V52, P329, DOI 10.1016/0378-5955(91)90023-3 CLOPTON BM, 1989, ESTIMATION TIME FREQ, P56 COHEN L, 1989, P IEEE, V77, P941, DOI 10.1109/5.30749 DEBOER E, 1978, J ACOUST SOC AM, V63, P115, DOI 10.1121/1.381704 EGGERMONT JJ, 1981, HEARING RES, V5, P109, DOI 10.1016/0378-5955(81)90030-7 EGGERMONT JJ, 1983, Q REV BIOPHYS, V16, P341 EGGERMONT JJ, 1990, J ACOUST SOC AM, V87, P246, DOI 10.1121/1.399291 EPPING WJM, 1985, HEARING RES, V19, P15, DOI 10.1016/0378-5955(85)90095-4 EVANS EF, 1973, EXP BRAIN RES, V17, P428 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 HERMES DJ, 1981, HEARING RES, V5, P147, DOI 10.1016/0378-5955(81)90043-5 JOHANNESMA P, 1981, HEARING RES, V5, P123, DOI 10.1016/0378-5955(81)90042-3 Johannesma PIM, 1972, P IPO S HEARING THEO, P58 JOHNSON DH, 1980, J ACOUST SOC AM, V68, P1115, DOI 10.1121/1.384982 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIANG NYS, 1965, ANN OTO RHINOL LARYN, V74, P463 KIM DO, 1990, HEARING RES, V45, P95, DOI 10.1016/0378-5955(90)90186-S KIPKE DR, 1991, UNPUB HEAR RES PFEIFFER RR, 1966, EXP BRAIN RES, V1, P220 RHODE WS, 1986, J NEUROPHYSIOL, V56, P287 RIHACZEK AW, 1968, IEEE T INFORM THEORY, V14, P369, DOI 10.1109/TIT.1968.1054157 RUGGERO MA, 1973, J NEUROPHYSIOL, V36, P569 VOIGT HF, 1980, J NEUROPHYSIOL, V44, P76 Young E. D., 1988, AUDITORY FUNCTION NE, P277 YOUNG ED, 1982, HEARING RES, V6, P153, DOI 10.1016/0378-5955(82)90051-X YOUNG ED, 1976, J NEUROPHYSIOL, V39, P282 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 MAY PY 1991 VL 53 IS 1 BP 28 EP 40 DI 10.1016/0378-5955(91)90211-Q PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200004 PM 2066285 ER PT J AU SHAPIRO, SM AF SHAPIRO, SM TI BINAURAL EFFECTS IN BRAIN-STEM AUDITORY EVOKED-POTENTIALS OF JAUNDICED GUNN-RATS SO HEARING RESEARCH LA English DT Article DE BILIRUBIN; BINAURAL; BRAIN-STEM; EVOKED POTENTIALS, AUDITORY; GUNN RAT; JAUNDICE ID BILIRUBIN ENCEPHALOPATHY; HEADPHONE SIMULATION; STEM RESPONSES; HYPERBILIRUBINEMIA; LOCALIZATION; INFANTS; SOUND; NERVE AB Bilirubin toxicity causes encephalopathy associated with lesions of the central auditory nervous system. Abnormal brainstem auditory evoked potentials (BAEPs) in jaundiced Gunn rats made acutely bilirubin toxic suggest abnormal input into the superior olivary complex, which might result in abnormal binaural interaction. Binaural difference waves (BDWs), obtained by subtracting the sum of two monaural BAEPs from a binaural BAEP, were obtained in 16- to 20-day-old jaundiced Gunn rats before and after injection of sulfadimethoxine, which produces bilirubin neurotoxicity by promoting net transfer of bilirubin out of the circulation into brain tissue. Reliable BDWs were recorded with onset 4.5 ms after the stimulus, followed by a large, often bimodal, positive peak occurring at about 6 ms. Following injection of sulfadimethoxine to produce bilirubin neurotoxicity, there was loss of BDW amplitude (21% +/- 14% of baseline, P < 0.0001) and increase in latency (0.62 +/- 0.42 ms, P = 0.03) in bilirubin-toxic jaundiced rats compared to baseline, but no significant changes in nonjaundiced controls treated similarly. This documents abnormal BDWs in acute bilirubin encephalopathy suggesting that abnormalities of functions dependent on binaural processing of auditory information may be found as neurologic sequelae to bilirubin toxicity. BAEP BDWs may be a sensitive method for detecting neurophysiological abnormalities due to bilirubin toxicity. C1 UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,DEPT NEUROL,MADISON,WI 53706. UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,DEPT PEDIAT,MADISON,WI 53706. CR AHDABBARMADA M, 1984, J NEUROPATH EXP NEUR, V43, P45, DOI 10.1097/00005072-198401000-00004 AINSLIE PJ, 1980, ELECTROEN CLIN NEURO, V49, P291, DOI 10.1016/0013-4694(80)90223-0 BLANC WA, 1959, J NEUROPATH EXP NEUR, V18, P165, DOI 10.1097/00005072-195901000-00011 Blauert J., 1983, SPATIAL HEARING BRUGGE JF, 1987, COCHLEAR NUCLEI HYPE BUTLER RA, 1977, J ACOUST SOC AM, V61, P1264, DOI 10.1121/1.381427 BUTLER RA, 1975, INFLUENCE EXTERNAL M BUTLER RA, 1976, PERCEPT PSYCHOPHYS, V19, P103, DOI 10.3758/BF03199393 DIAMOND I, 1966, CLIN INVEST, V45, P678 DOBIE RA, 1979, ARCH OTOLARYNGOL, V105, P391 DOBIE RA, 1980, ELECTROEN CLIN NEURO, V49, P303, DOI 10.1016/0013-4694(80)90224-2 FISHER H G, 1968, Journal of Auditory Research, V8, P15 HOSFORDDUNN H, 1981, AUDIOLOGY, V20, P394 JEW JY, 1977, J ANAT, V124, P599 JOHNSON L, 1959, AMA J DIS CHILD, V97, P591 LENHARDT ML, 1984, J PEDIATR-US, V104, P281, DOI 10.1016/S0022-3476(84)81013-6 MATKIN ND, 1966, ARCHIV OTOLARYNGOL, V84, P502 MOLLER AR, 1981, ANN OTO RHINOL LARYN, V90, P591 NAKAMURA H, 1985, PEDIATRICS, V75, P703 NWAESEI CG, 1984, PEDIATRICS, V74, P800 ODELL GB, 1959, J PEDIATR-US, V55, P268, DOI 10.1016/S0022-3476(59)80223-7 PERLMAN M, 1983, PEDIATRICS, V72, P658 ROSE AL, 1979, J NEUROPATH EXP NEUR, V38, P152, DOI 10.1097/00005072-197903000-00006 SCHUTTA HS, 1969, J PEDIATR, V75, P1070, DOI 10.1016/S0022-3476(69)80351-3 SHAPIRO SM, 1988, PEDIATR RES, V23, P306, DOI 10.1203/00006450-198803000-00015 SHAPIRO SM, 1989, ANN OTO RHINOL LARYN, V98, P308 SHAPIRO SM, 1988, DEV BRAIN RES, V41, P147, DOI 10.1016/0165-3806(88)90178-2 STREBEL L, 1971, PEDIATR RES, V5, P548, DOI 10.1203/00006450-197110000-00007 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P858, DOI 10.1121/1.397557 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P868, DOI 10.1121/1.397558 WREGE KS, 1981, ARCH NEUROL-CHICAGO, V38, P572 NR 31 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 41 EP 48 DI 10.1016/0378-5955(91)90212-R PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200005 PM 2066286 ER PT J AU SCHERMULY, L TOPP, G KLINKE, R AF SCHERMULY, L TOPP, G KLINKE, R TI A PREVIOUSLY UNKNOWN HAIR CELL EPITHELIUM IN THE PIGEON COCHLEA - THE PAPILLA-CHAOTICA SO HEARING RESEARCH LA English DT Article DE PIGEON; HAIR CELL; HEARING; EQUILIBRIUM ID INFRASOUND SENSITIVE NEURONS; BASILAR PAPILLA; DIFFERENTIATION AB A previously unknown sensory epithelium can be found on the medial wall of the apical part of the pigeon cochlear duct. It comprises about 200 hair cells. These are not arranged in any regular pattern, shape and orientation of the ciliary bundles even differ in neighbouring hair cells. We therefore propose the term papilla chaotica. C1 ZENTRUM PHYSIOL,THEODOR STERN KAI 7,W-6000 FRANKFURT 70,GERMANY. CR GLEICH O, 1988, HEARING RES, V34, P69, DOI 10.1016/0378-5955(88)90052-4 Jorgensen J. M., 1970, Vidensk. Meddr dansk. naturh. Foren, V133, P121 KREITHEN ML, 1979, J COMP PHYSIOL, V129, P1 LAVIGNEREBILLARD M, 1985, J COMP NEUROL, V238, P340, DOI 10.1002/cne.902380308 MANLEY GA, 1989, J COMP PHYSIOL A, V164, P289, DOI 10.1007/BF00612989 ROSENHAL.U, 1970, ARCH KLIN EXP OHR, V197, P154, DOI 10.1007/BF00306164 SCHERMULY L, 1990, HEARING RES, V48, P69, DOI 10.1016/0378-5955(90)90199-Y SCHERMULY L, 1990, J COMP PHYSIOL A, V166, P355 SCHWARTZKOPFF J., 1960, BIOL ZENTRALBL, V79, P607 TILNEY LG, 1986, DEV BIOL, V116, P100, DOI 10.1016/0012-1606(86)90047-3 NR 10 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 49 EP 56 DI 10.1016/0378-5955(91)90213-S PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200006 PM 2066287 ER PT J AU PATUZZI, RB BULL, CL AF PATUZZI, RB BULL, CL TI ELECTRICAL RESPONSES FROM THE CHICKEN BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE CHICKEN; BASILAR PAPILLA; HAIR CELL; TUNING ID COCHLEAR HAIR-CELLS; PRIMARY AUDITORY AFFERENTS; ALLIGATOR LIZARD COCHLEA; NERVE-FIBERS; INNER-EAR; CHARACTERISTIC FREQUENCY; PREFERRED INTERVALS; MOSSBAUER TECHNIQUE; DISCHARGE PATTERNS; MEMBRANE MOTION AB A surgical approach to the basilar papilla of the chicken cochlea has been developed which allows recordings from within the hair cells and supporting cells in vivo. The frequency tuning curves for the AC receptor potentials measured in extracellular space immediately outside hair cells, within the hair cells and in adjacent supporting cells were similar, with best frequencies ranging from 600 Hz to 2000 Hz, and Q10 dB values between 0.6 and 2.5. In cells classified as hair cells there was no evidence of spontaneous oscillations in the membrane potentials, nor of ringing of the membrane potential in response to injected current pulses. Moreover, displacement of the papilla with the microelectrodes could modulate the hair cell membrane potential over the range 0 to -90 mV, suggesting that the current-voltage relationship in these cells was essentially linear. This view was supported by preliminary investigations of cell properties with current injection. We interpret these observations as evidence that the hair cells impaled were not electrically tuned under our experimental conditions, unlike the hair cells of the turtle cochlea. These observations, taken together with the electrode angles used, fluorescent dye-marking and previous measurements of chicken hair cells in vitro [Fuchs, P.A., Nagai, T. and Evans, M.G. (1988) J. Neuro. Sci. 8, 2460-2467], suggest that the hair cells we have impaled were the short hair cells of the papilla, and that the tuning of the AC receptor potentials we have observed was due solely to a tuned mechanical drive to their hair bundles. RP PATUZZI, RB (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. 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Res. PD MAY PY 1991 VL 53 IS 1 BP 57 EP 77 DI 10.1016/0378-5955(91)90214-T PG 21 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200007 PM 2066288 ER PT J AU WILLOTT, JF PARHAM, K HUNTER, KP AF WILLOTT, JF PARHAM, K HUNTER, KP TI COMPARISON OF THE AUDITORY-SENSITIVITY OF NEURONS IN THE COCHLEAR NUCLEUS AND INFERIOR COLLICULUS OF YOUNG AND AGING C57BL/6J AND CBA/J MICE SO HEARING RESEARCH LA English DT Article DE AGE-RELATED HEARING LOSS; COCHLEAR NUCLEUS; MICE; PRESBYCUSIS; TUNING CURVES ID BRAIN-STEM; RESPONSE PROPERTIES; NERVE FIBERS; HEARING-LOSS; MOUSE; PRESBYCUSIS; DORSAL; PROJECTIONS; CAT AB Thresholds of neurons to sounds were compared as a function of central auditory structure [ventral cochlear nucleus (VCN), dorsal cochlear nucleus (DCN), and inferior colliculus (IC)] in young and middle-aged C57BL/6J mice (multiple- and single-unit recordings) and in young and old CBA/J mice (single-unit recordings). Middle-aged C57 mice show progressive loss of sensitivity to high frequencies and noise due to cochlear pathology; CBA mice show little loss of sensitivity through most of their lifespan. Multiple-unit threshold curves (MTCs) for tones indicated that neurons in the C57 VCN suffered a greater degree of age-related loss of sensitivity than neurons in the IC (from an earlier study). Furthermore, whereas the low frequency portions of MTCs in IC neurons in high frequency tonotopic regions typically become 'sensitized' in middle-aged C57 mice (i.e., lower thresholds than young mice), such was not the case for VCN neurons. In contrast to VCN neurons, MTCs of the population of DCN neurons studied were statistically indistinguishable from those of the IC. Measurements of single-unit response areas in C57 mice corroborated the MTCs. In CBA mice, little effect of age was found in comparing single-unit response areas of young and old mice. The findings indicate that sensorineural impairment in middle-aged C57 mice is accompanied by threshold changes that are more severe in the VCN than in the IC or DCN. Because the VCN and DCN are believed to play different roles in hearing, the functions they support should, likewise, be affected to different extents by age-related hearing loss. RP WILLOTT, JF (reprint author), NO ILLINOIS UNIV,DEPT PSYCHOL,DE KALB,IL 60115, USA. CR Aitkin L, 1984, HDB PHYSL 1, P675 BRUGGE JF, 1978, ANNU REV NEUROSCI, V1, P363, DOI 10.1146/annurev.ne.01.030178.002051 CANT NB, 1984, HEARING SCI RECENT A, P371 CODY AR, 1980, HEARING RES, V3, P3, DOI 10.1016/0378-5955(80)90004-0 EVANS EF, 1973, EXP BRAIN RES, V17, P428 FEKETE DM, 1984, J COMP NEUROL, V229, P432, DOI 10.1002/cne.902290311 GOLDBERG JM, 1973, BRAIN RES, V64, P35, DOI 10.1016/0006-8993(73)90169-8 Henry K. R., 1983, AUDITORY PSYCHOBIOLO, P470 HENRY KR, 1980, AUDIOLOGY, V19, P369 HIRSCH JA, 1988, J PHYSIOL-LONDON, V396, P535 HUNTER KP, 1987, HEARING RES, V30, P207, DOI 10.1016/0378-5955(87)90137-7 Irvine D. R. F., 1986, PROGR SENSORY PHYSL, V7 KIANG NYS, 1976, ANN OTO RHINOL LARYN, V85, P752 KOERBER KC, 1966, EXP NEUROL, V16, P119, DOI 10.1016/0014-4886(66)90091-4 MIKAELIAN DO, 1979, LARYNGOSCOPE, V89, P1 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 OERTEL D, 1983, J NEUROSCI, V3, P2043 OERTEL D, 1989, J COMP NEUROL, V283, P283 POWELL TPS, 1962, J ANAT, V96, P249 SALVI RJ, 1983, HEARING RES, V10, P37, DOI 10.1016/0378-5955(83)90017-5 WICKESBERG RE, 1990, J NEUROSCI, V10, P1762 Willard FH, 1983, AUDITORY PSYCHOBIOLO, P201 WILLOTT JF, 1988, HEARING RES, V37, P15, DOI 10.1016/0378-5955(88)90074-3 WILLOTT JF, 1988, HEARING RES, V37, P1, DOI 10.1016/0378-5955(88)90073-1 WILLOTT JF, 1986, J NEUROPHYSIOL, V56, P391 WILLOTT JF, 1987, J COMP NEUROL, V260, P472, DOI 10.1002/cne.902600312 WILLOTT JF, 1991, AGE RELATED COCHLEAR Young E.D, 1984, HEARING SCI, P423 NR 28 TC 66 Z9 68 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 78 EP 94 DI 10.1016/0378-5955(91)90215-U PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200008 PM 2066290 ER PT J AU KARLSSON, KK ULFENDAHL, M KHANNA, SM FLOCK, A AF KARLSSON, KK ULFENDAHL, M KHANNA, SM FLOCK, A TI THE EFFECTS OF QUININE ON THE COCHLEAR MECHANICS IN THE ISOLATED TEMPORAL BONE PREPARATION SO HEARING RESEARCH LA English DT Article DE HEARING LOSS; COCHLEAR MECHANICS; OUTER HAIR CELLS; QUININE; CONTRACTION ID TETRACAINE; EAR AB Quinine is known to induce a reversible hearing loss and to evoke motile responses of isolated outer hair cells. To study the effect of quinine, mechanical tuning curves of the Hensen's cells were measured in the isolated cochlea preparation in response to acoustical stimuli applied to the ear before and after application of the drug. It was shown that 0.5-4 mM quinine increased the vibration amplitude at the peak of the mechanical resonance curves and increased the sharpness of tuning. The time course of the event depended on whether the scala media was opened or not. The results show that quinine alters the micromechanical tuning of the organ of Corti. C1 KAROLINSKA INST,DEPT PHYSIOL 2,S-10401 STOCKHOLM 60,SWEDEN. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. RP KARLSSON, KK (reprint author), HUDDINGE UNIV HOSP,DEPT AUDIOL,B53,S-14186 HUDDINGE,SWEDEN. CR ALVAN G, 1989, LIFE SCI, V45, P751, DOI 10.1016/0024-3205(89)90095-7 ALVAN G, 1991, IN PRESS BR J CLIN P Aly S, 1975, J Egypt Med Assoc, V58, P144 DAIGNEAU.EA, 1970, TOXICOL APPL PHARM, V17, P223, DOI 10.1016/0041-008X(70)90146-8 DENCKER L, 1975, ARCH OTOLARYNGOL, V101, P185 HAWKINS JE, 1972, LARYNGOSCOPE, V82, P1091, DOI 10.1288/00005537-197207000-00001 HENNEBERT D, 1959, ARCHIV OTOLARYNGOL, V70, P321 ISAACSON A, 1970, J PHARMACOL EXP THER, V171, P26 KARLSSON KK, 1990, T ROY SOC TROP MED H, V84, P765, DOI 10.1016/0035-9203(90)90069-Q KARLSSON KK, 1990, NEUROSCI LETT, V116, P101, DOI 10.1016/0304-3940(90)90393-N Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P183 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P139 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P189 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P163 Khanna S M, 1989, Acta Otolaryngol Suppl, V467, P151 Koester C J, 1989, Acta Otolaryngol Suppl, V467, P27 Lund D T, 1989, Acta Otolaryngol Suppl, V467, P77 MELIER F, 1843, MEM ACAD MED PARIS, V10, P722 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SOKOLICH WG, 1977, J ACOUST SOC AM, V56, pS12 STINSON MR, 1989, J ACOUST SOC AM, V85, P2481, DOI 10.1121/1.397743 SUAREZKU.G, 1973, J PHARMACOL EXP THER, V186, P562 ULFENDAHL M, 1989, HEARING RES, V40, P55, DOI 10.1016/0378-5955(89)90099-3 Ulfendahl M, 1989, Acta Otolaryngol Suppl, V467, P145 Ulfendahl M, 1989, Acta Otolaryngol Suppl, V467, P91 Ulfendahl M, 1989, Acta Otolaryngol Suppl, V467, P221 Willemin J F, 1989, Acta Otolaryngol Suppl, V467, P35 NR 27 TC 19 Z9 19 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 95 EP 100 DI 10.1016/0378-5955(91)90216-V PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200009 PM 2066291 ER PT J AU GERKEN, GM SOLECKI, JM BOETTCHER, FA AF GERKEN, GM SOLECKI, JM BOETTCHER, FA TI TEMPORAL INTEGRATION OF ELECTRICAL-STIMULATION OF AUDITORY NUCLEI IN NORMAL-HEARING AND HEARING-IMPAIRED CAT SO HEARING RESEARCH LA English DT Article DE TEMPORAL INTEGRATION; SOUND-INDUCED HEARING LOSS; ELECTRICAL STIMULATION; INFERIOR COLLICULUS; COCHLEAR NUCLEUS; CAT ID SUMMATION; SYSTEM AB Temporal integration functions were measured, before and after a sound-induced hearing loss, in 5 cats using trains of electrical pulses applied to auditory nuclei in the brainstem. The 8 stimuli ranged from 1 pulse (0.25 ms duration) to 16 pulses (0.25 ms pulses spaced over 240 ms). The stimuli were applied to inferior colliculus or cochlear nucleus via permanently implanted electrodes. One electrode was tested extensively in each animal to obtain 10 sets of behaviorally-measured electrical detection thresholds counterbalanced across stimuli. The animal was then exposed to a 110 dB SPL, 2 kHz tone for 48 h and pre- and post-exposure audiograms were measured. The mean permanent threshold shift for acoustic stimuli was 48.5 dB. Another 10 thresholds for each of the 8 electrical stimuli were then measured. In the normal hearing animals, the mean slope of the temporal integration function for electrical stimulation was - 7.6 dB per factor of 10 pulses. Alternatively, the mean time constant was 139 ms. In the hearing impaired animals, the slope was reduced to - 1.5 dB per factor of 10 pulses, which corresponded to a mean time constant of 17 ms. In addition, the hearing impaired animals showed a decreased threshold for the electrical stimuli (stimulation hypersensitivity) as well as reduced variability across electrical stimulation thresholds. The results suggest that a major contribution to temporal integration occurs in inferior colliculus or higher. In addition, the results suggest that the reduction in temporal integration that follows hearing impairment is a peripherally-induced, central effect. C1 UNIV TEXAS,SW MED CTR,DEPT OTORHINOLARYNGOL,DALLAS,TX 75230. BUFFALO HEARING & SPEECH CTR,BUFFALO,NY. SUNY BUFFALO,HEARING RES LAB,BUFFALO,NY 14260. RP GERKEN, GM (reprint author), UNIV TEXAS,CALLIER CTR COMMUN DISORDERS,1966 INWOOD RD,DALLAS,TX 75235, USA. CR Algom D., 1984, CONTRIBUTIONS SENSOR, P131 DALLOS PJ, 1964, J ACOUST SOC AM, V36, P743, DOI 10.1121/1.1919059 FLORENTINE M, 1988, J ACOUST SOC AM, V84, P195, DOI 10.1121/1.396964 GENGEL RW, 1971, J SPEECH HEAR DISORD, V36, P213 GERKEN GM, 1990, J ACOUST SOC AM, V88, P767, DOI 10.1121/1.399726 GERKEN GM, 1970, BRAIN RES, V17, P483, DOI 10.1016/0006-8993(70)90255-6 GERKEN GM, 1991, ELECTROEN CLIN NEURO, V80, P73, DOI 10.1016/0168-5597(91)90046-Z GERKEN GM, 1984, HEARING RES, V13, P249, DOI 10.1016/0378-5955(84)90078-9 GERKEN GM, 1979, J ACOUST SOC AM, V66, P728, DOI 10.1121/1.383223 GERKEN GM, 1991, IN PRESS EFFECTS NOI HATTLER KW, 1970, J AUD RES, V10, P72 JERGER J, 1959, ARCHIV OTOLARYNGOL, V69, P200 KITZES LM, 1978, J NEUROPHYSIOL, V41, P1165 LEVITT H, 1971, J ACOUST SOC AM, V49, P467, DOI 10.1121/1.1912375 MARTIN FN, 1970, J AUD RES, V10, P82 MOREST DK, 1982, NEW PERSPECTIVES NOI, P87 OERTEL D, 1985, J ACOUST SOC AM, V78, P328, DOI 10.1121/1.392494 PEDERSEN CB, 1972, ACTA OTO-LARYNGOL, V74, P398, DOI 10.3109/00016487209128469 PENNER MJ, 1978, J ACOUST SOC AM, V63, P195, DOI 10.1121/1.381712 PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 RANCK JB, 1975, BRAIN RES, V98, P417, DOI 10.1016/0006-8993(75)90364-9 SOLECKI JM, 1990, J ACOUST SOC AM, V88, P779, DOI 10.1121/1.399727 STEVENS SS, 1962, AM PSYCHOL, V17, P29, DOI 10.1037/h0045795 WATSON CS, 1969, J ACOUST SOC AM, V46, P989, DOI 10.1121/1.1911819 ZWISLOCKI J, 1960, J ACOUST SOC AM, V32, P1046, DOI 10.1121/1.1908276 NR 25 TC 28 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 101 EP 112 DI 10.1016/0378-5955(91)90217-W PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200010 PM 2066278 ER PT J AU RYDMARKER, S HORNER, KC AF RYDMARKER, S HORNER, KC TI ATROPHY OF OUTER HAIR CELL STEREOCILIA AND HEARING-LOSS IN HYDROPIC COCHLEAE SO HEARING RESEARCH LA English DT Article DE HEARING LOSS; HYDROPS; MENIERES DISEASE; MORPHOLOGY; SCANNING ELECTRON MICROSCOPY; STEREOCILIA ID ENDOLYMPHATIC HYDROPS; TECTORIAL MEMBRANE; GUINEA-PIG; MORPHOLOGICAL-CHANGES AB We have earlier described selective atrophy of short and middle stereocilia on outer hair cells of the three upper cochlear turns in hydropic cochleae of guinea pigs. The present study describes sequential early stages of stereocilia degeneration leading to this specific atrophy. Comparison of the morpho-pathology with the ultimate CAP audiograms taken before sacrifice indicated a close association between the low frequency hearing loss and this atrophy of stereocilia. The atrophy appeared to be associated first with the short and then the middle stereocilia of the 2nd and 3rd rows of outer hair cells between 0.5 kHz and 2 kHz and with time included the 1st row of all outer hair cells of the upper cochlear turns down to the 8 kHz region. C1 UNIV BORDEAUX 2,HOP PELLEGRIN,INSERM,U229,AUDIOL EXPTL LAB,F-33076 BORDEAUX,FRANCE. CR ALBERS FWJ, 1987, ANN OTO RHINOL LARYN, V96, P282 ARAN JM, 1984, ACTA OTO-LARYNGOL, V97, P547, DOI 10.3109/00016488409132933 Beal D D, 1968, Acta Otolaryngol, V66, P333, DOI 10.3109/00016486809126300 BOHMER A, 1989, 2 INT S MEN DIS, P221 ELDREDGE DH, 1974, HDB SENSORY PHYSL, V5, P549 Hallpike C. 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Res. PD MAY PY 1991 VL 53 IS 1 BP 113 EP 122 DI 10.1016/0378-5955(91)90218-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200011 PM 2066279 ER PT J AU PLINKERT, PK ZENNER, HP HEILBRONN, E AF PLINKERT, PK ZENNER, HP HEILBRONN, E TI A NICOTINIC ACETYLCHOLINE RECEPTOR-LIKE ALPHA-BUNGAROTOXIN-BINDING SITE ON OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE INNER EAR; EFFERENT INNERVATION; HEARING; COCHLEA; MOTILITY; CYTOSKELETON ID GUINEA-PIG COCHLEA; SKELETAL-MUSCLE; INOSITOL 1,4,5-TRISPHOSPHATE; MONOCLONAL-ANTIBODIES; OLIVOCOCHLEAR BUNDLE; TORPEDO-CALIFORNICA; SUBUNIT PRECURSOR; ACTIN-FILAMENTS; INNER-EAR; CDNA AB Acetylcholine (ACh) appears to be the major neurotransmitter liberated from olivocochlear efferents terminating on outer hair cells (OHC). Recently, cholinergic receptor epitopes were visualized at the basal pole of the OHCs. To evaluate the ACh receptor type at OHC we performed binding studies with [I-125]-labelled alpha-bungarotoxin (alpha-bgtx), a close to irreversibly acting blocker of the nicotinic acetylcholine receptor (nAChR) of skeletal muscle and of electrocytes of Torpedo and Electrophorus. An irreversible and saturable binding (80 nM) of the radiolabelled compound to OHCs was observed. The number of alpha-bgtx sensitive binding sites present on each OHC was calculated to be about 2 x 10(-17) mol/OHC, which would amount to about 10(7) binding sites/cell. Preincubation with the reversibly acting cholinergic ligands, carbamylcholine (1 mM), nicotine (0.1 mM) and d-tubocurarine (1-100-mu-M) was found to inhibit alpha-bgtx binding to a varying degree. Atropine (0.05 mM), a muscarinic antagonist, had no influence on the binding of alpha-bgtx to OHCs. [H-3]-QNB, a specific marker and antagonist for muscarinic AChR, and [I-125]-kappa-toxin, known to react with neuronal and ganglionic nAChR, showed no specific binding to OHCs. The data indicate that a peripheral type nAChR is present on OHCs mediating ACh-induced modulation of the biomechanics of the cochlea by influencing OHC motility. C1 UNIV STOCKHOLM,NEUROCHEM & NEUROTOXICOL UNIT,S-10691 STOCKHOLM,SWEDEN. RP PLINKERT, PK (reprint author), UNIV TUBINGEN,DEPT OTOLARYNGOL,SILCHERSTR 5,W-7400 TUBINGEN 1,GERMANY. 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B., 1986, NEUROBIOLOGY HEARING, P333 ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V149, P304, DOI 10.1016/0006-291X(87)91639-1 ZENNER HP, 1989, MECHANISMS HEARING, P933 ZENNER HP, 1981, ARCH OTO-RHINO-LARYN, V230, P81, DOI 10.1007/BF00665383 ZENNER HP, 1985, LARYNGO RHINO OTOL, V64, P642, DOI 10.1055/s-2007-1008225 ZENNER HP, 1986, NEUROBIOLOGY HEARING, P1 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 73 TC 29 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 123 EP 130 DI 10.1016/0378-5955(91)90219-Y PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200012 PM 2066280 ER PT J AU RELKIN, EM SMITH, RL AF RELKIN, EM SMITH, RL TI FORWARD MASKING OF THE COMPOUND ACTION-POTENTIAL - THRESHOLDS FOR THE DETECTION OF THE N1 PEAK SO HEARING RESEARCH LA English DT Article DE COMPOUND ACTION POTENTIAL; AUDITORY NERVE; FORWARD MASKING; DETECTION; THRESHOLD ID AUDITORY-NERVE; RESPONSES; NOISE AB A two-interval forced-choice method was developed that provides a rapid and objective computerized measurement of the threshold for detection of the N1 peak of the compound action potential (CAP) recorded in response to a probe tone. The CAP was recorded at the round window of anesthetized chinchillas and several gerbils. An adaptive threshold-tracking procedure was verified by comparing measured thresholds to those obtained from neurometric functions, which plot the proportion of correct detections of the probe as a function of probe intensity. The adaptive procedure was applied in a forward masking paradigm to study the growth of masking of the CAP as a function of masker intensity. Results indicate that growth of masking of the CAP more closely corresponds to that observed psychophysically, than does forward masking observed in the response of a single neuron. Implications for neural encoding mechanisms are discussed. C1 SYRACUSE UNIV,DEPT BIOENGN,SYRACUSE,NY 13244. RP RELKIN, EM (reprint author), SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244, USA. 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Res. PD MAY PY 1991 VL 53 IS 1 BP 131 EP 140 DI 10.1016/0378-5955(91)90220-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200013 PM 2066281 ER PT J AU ZWICKER, E HENNING, GB AF ZWICKER, E HENNING, GB TI ON THE EFFECT OF INTERAURAL PHASE DIFFERENCES ON LOUDNESS SO HEARING RESEARCH LA English DT Article DE BINAURAL LOUDNESS; PARTIAL MASKING; INTERAURAL PHASE DIFFERENCE ID INTENSITY PERCEPTION; FREQUENCY; DISCRIMINATION AB The loudness of four monaurally presented Gaussian shaped, 60-ms tone bursts was matched to that of four similar pulses presented binaurally. The stimuli to be matched were all presented in continuous binaural noise of three levels and, in different experiments, either the monaural or the binaural stimuli were adjusted by the observer. With 250- and 710-Hz tone bursts, there are large differences in loudness that, at low signal-to-noise ratios, depend on the interaural phase conditions in a manner consistent with the changes in masked threshold produced by the phase manipulation; there is little, if any, effect of interaural phase on loudness for 2-kHz signals. The effect of interaural phase on loudness decreases with increasing level but, at 250 Hz, remains measurable some 30-40 dB above masked threshold. The matching function for signals out-of-phase grows in proportion to the level to be matched over the entire range from masked threshold to the highest level used. In contrast, for the in-phase condition, the observers show a step at a level that depends both on frequency and on the observer from proportional growth near thresholds to parallel proportional growth some 6 to 12 dB higher. C1 TECH UNIV MUNICH,INST ELECTROACOUST,W-8000 MUNICH 2,GERMANY. CR ALGOM D, 1989, PERCEPT PSYCHOPHYS, V46, P155, DOI 10.3758/BF03204975 ALGOM D, 1988, J ACOUST SOC AM, V84, P1302, DOI 10.1121/1.396629 DOLAN TR, 1968, J ACOUST SOC AM, V44, P1507, DOI 10.1121/1.1911289 Durlach N.I., 1972, F MODERN AUDITORY TH, P371 EGAN JP, 1948, J ACOUST SOC AM, V20, P58, DOI 10.1121/1.1906348 HENNING GB, 1990, HEARING RES, V48, P195, DOI 10.1016/0378-5955(90)90059-X HENNING GB, 1973, J ACOUST SOC AM, V54, P1160, DOI 10.1121/1.1914363 HIRSH IJ, 1948, J ACOUST SOC AM, V20, P761, DOI 10.1121/1.1906434 HOUTSMA AJM, 1980, J ACOUST SOC AM, V68, P807, DOI 10.1121/1.384819 LIM JS, 1978, J ACOUST SOC AM, V63, P1233, DOI 10.1121/1.381937 LIM JS, 1977, J ACOUST SOC AM, V62, P1256, DOI 10.1121/1.381641 RABINOWITZ WM, 1976, J ACOUST SOC AM, V59, P1506, DOI 10.1121/1.381000 RIESZ RR, 1933, J ACOUST SOC AM, V5, P211 SRULOVICZ P, 1983, J ACOUST SOC AM, V73, P1266, DOI 10.1121/1.389275 Zwicker E., 1982, PSYCHOAKUSTIK ZWICKER E, 1985, HEARING RES, V19, P29, DOI 10.1016/0378-5955(85)90096-6 Zwicker E., 1967, OHR ALS NACHRICHTENE NR 17 TC 4 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAY PY 1991 VL 53 IS 1 BP 141 EP 152 DI 10.1016/0378-5955(91)90221-T PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FN282 UT WOS:A1991FN28200014 PM 2066282 ER PT J AU BERLIN, CI HOOD, LJ BARLOW, EK MOREHOUSE, CR SMITH, EG AF BERLIN, CI HOOD, LJ BARLOW, EK MOREHOUSE, CR SMITH, EG TI DERIVED GUINEA-PIG COMPOUND 8TH-NERVE ACTION-POTENTIALS TO CONTINUOUS PURE-TONES SO HEARING RESEARCH LA English DT Article DE DERIVED POTENTIALS; SINUSOIDS; PURE TONE; GUINEA PIG FAR-FIELD COMPOUND ACTION POTENTIALS; SUBTRACTION ID BRAIN-STEM RESPONSES; MASKING PROFILES; MECHANICS; NOISE AB A technique is described which verifies neural activity to a very faint continuous sine wave through subtraction of two different far-field whole nerve action potentials from one another. A brief transient is presented to an animal in order to elicit a supra-threshold action potential. The technique is then repeated, but on the second trial a near-threshold sine wave is mixed with the transient and another action potential is collected. The resultant evoked response is then subtracted from the evoked potential generated by the transient alone and a small but persistent difference potential is acquired that presumably represents the unit activity occupied by the continuous sine wave. Four experiments are presented to show the validity of this technique, along with a surprising stability of the derived-response latency despite a 30 dB range of the probes. The technique may have promise in predicting behavioral responses to sinusoids acquired from individual animals. C1 AMER AUDIOL ASSOCIATES,RIVERDALE,GA. NICOLET BIOMED INSTRUMENTS,MADISON,WI. RP BERLIN, CI (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL,KRESGE HEARING RES LAB,2020 GRAVIER ST,NEW ORLEANS,LA 70112, USA. CR BERLIN CI, 1987, ABSTR ASS RES OT, P172 Berlin C I, 1981, Ciba Found Symp, V85, P139 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 Davis H, 1976, Ann Otol Rhinol Laryngol, V85 SUPPL 28, P1 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 Don M., 1979, ANN OTOL RHINOL LA S, V57, P1 DON M, 1978, J ACOUST SOC AM, V63, P1084, DOI 10.1121/1.381816 FOLSOM RC, 1984, J ACOUST SOC AM, V75, P919, DOI 10.1121/1.390538 FOLSOM RC, 1985, J ACOUST SOC AM, V78, P555, DOI 10.1121/1.392422 HOOD LJ, 1988, ABSTR ASS RES OT, P10 HOOD LJ, 1987, ABSTR ASS RES OT, P173 KLEIN AJ, 1981, J ACOUST SOC AM, V70, P1045, DOI 10.1121/1.386955 PANTEV C, 1985, AUDIOLOGY, V24, P275 PATUZZI RB, 1987, HEARING RES, V30, P73, DOI 10.1016/0378-5955(87)90185-7 PICTON TW, 1979, J OTOLARYNGOL, V8, P289 PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 SALT AN, 1990, AUDIOLOGY, V29, P135 TEAS DONALD C, 1962, JOUR ACOUSTICAL SOC AMER, V34, P1438, DOI 10.1121/1.1918366 NR 18 TC 10 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1991 VL 52 IS 2 BP 271 EP 280 DI 10.1016/0378-5955(91)90017-4 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500001 PM 2061218 ER PT J AU SCHNEIDER, I GRAY, L AF SCHNEIDER, I GRAY, L TI RAPID DEVELOPMENT OF A SENSORY ATTRIBUTE IN YOUNG CHICKENS SO HEARING RESEARCH LA English DT Article DE HEARING; CHICKEN; DEVELOPMENT; EXPERIENCE; FREQUENCY; SCALING ID RESPONSIVENESS; RESPONSES; FREQUENCY; ONTOGENY AB Development of a consistent pattern in responses to frequency changes is revealed with individual differences scaling. Newborn chicks respond to changes in a background tone to which they have become habituated with momentary delays in their otherwise regular peeping. Durations of these delays are used as measures of perceived difference between all possible pairs of five frequencies between 500 and 608 Hz. Coordinates of five points are calculated to create a map of these frequencies such that distances between points are maximally correlated with delays. A steeply sloped s-shaped curve describes the rapid emergence, from the beginning to the middle of the first postnatal day, of maps that explain significantly more of the input data than expected by chance. This implies that over a few hours birds come to reliably rank different frequencies along a consistent scale. Controlled rearing conditions of decreased external stimulation or early exposure to frequency changes have no effect on this development. In conclusion, scaling is a replicable way to evaluate the development of consistent responses to frequency changes. Similar processes are likely important in other aspects of perceptual development, learning, and memory. C1 UNIV TEXAS,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,HOUSTON,TX 77030. 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W., 1978, DEV SENSORY SYSTEMS, P135 SCHNEIDE.B, 1972, PERCEPT PSYCHOPHYS, V12, P373, DOI 10.3758/BF03207224 SEVERNS M, 1985, PHYSIOL BEHAV, V34, P843, DOI 10.1016/0031-9384(85)90388-9 SHEPARD RN, 1972, MULTIDIMENSIONAL SCA, P1 SPEAR NE, 1987, PERINATAL DEV PSYCHO, P83 Stevens S. S., 1975, PSYCHOPHYSICS INTRO NR 26 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1991 VL 52 IS 2 BP 281 EP 287 DI 10.1016/0378-5955(91)90018-5 PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500002 PM 2061219 ER PT J AU EVANS, BN HALLWORTH, R DALLOS, P AF EVANS, BN HALLWORTH, R DALLOS, P TI OUTER HAIR CELL ELECTROMOTILITY - THE SENSITIVITY AND VULNERABILITY OF THE DC COMPONENT SO HEARING RESEARCH LA English DT Article DE HAIR CELL, OUTER; MOTILITY; NONLINEARITY ID GUINEA-PIG COCHLEA; INDUCED HEARING-LOSS; RECEPTOR CURRENT; RESPONSES; ORGAN; CORTI; INNER AB A technique was devised in order to study the fast electromechanical length changes of outer hair cells at low stimulus levels. Solitary outer hair cells were drawn into a glass microchamber. Length changes were evoked by the application of transcellular potentials and were detected with a photodiode. The method is non-invasive to the cell and offers superior sensitivity and stability for the recording of cell length changes. The function relating command voltage and cell length (V-delta-L) change was determined. A nonlinearity, consisting of a DC component superimposed on the AC response, was shown to be present at the lowest stimulus levels measured. The nonlinearity was sensitive to imposed electrical bias as well as vulnerable to overstimulation. The observations are interpreted in reference to the V-delta-L function. A parallel is suggested between the nonlinearity seen in the mechanical response and that observed in the responses of the intact cochlea. C1 NORTHWESTERN UNIV,DEPT NEUROBIOL & PHYSIOL,EVANSTON,IL 60201. RP EVANS, BN (reprint author), NORTHWESTERN UNIV,HUGH KNOWLES CTR,AUDITORY PHYSIOL LAB,2299 SHERIDAN RD,EVANSTON,IL 60208, USA. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 Ashmore J F, 1988, Prog Brain Res, V74, P3 ASHMORE JF, 1986, NATURE, V322, P368, DOI 10.1038/322368a0 BAYLOR DA, 1979, J PHYSIOL-LONDON, V288, P589 CLARK BA, 1990, PFLUG ARCH EUR J PHY, V415, P490, DOI 10.1007/BF00373629 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 CODY AR, 1988, HEARING RES, V35, P59, DOI 10.1016/0378-5955(88)90040-8 CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 COREY DP, 1983, J NEUROSCI, V3, P962 CRAWFORD AC, 1989, J PHYSIOL-LONDON, V419, P405 DALLOS P, 1969, SCIENCE, V164, P449, DOI 10.1126/science.164.3878.449 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1983, HEARING RES, V12, P89, DOI 10.1016/0378-5955(83)90120-X DALLOS P, IN PRESS NATURE DURRANT JD, 1974, J ACOUST SOC AM, V56, P562, DOI 10.1121/1.1903291 DURRANT JD, 1972, J ACOUST SOC AM, V52, P542, DOI 10.1121/1.1913143 EVANS BN, 1989, MECHANICS HEARING, P205 EVANS BN, 1990, HEARING RES, V45, P265, DOI 10.1016/0378-5955(90)90126-A EVANS BN, 1988, THESIS U TEXAS HLTH GITTER A H, 1988, Pfluegers Archiv European Journal of Physiology, V412, pR75 HALLWORTH R, 1990, Society for Neuroscience Abstracts, V16, P1078 HOLLEY MC, 1988, PROC R SOC SER B-BIO, V232, P413, DOI 10.1098/rspb.1988.0004 HONRUBIA V, 1969, J ACOUST SOC AM, V47, P498 HOOKE R, 1961, J ACM, V8, P212, DOI 10.1145/321062.321069 HUDSPETH AJ, 1989, NATURE, V341, P397, DOI 10.1038/341397a0 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 KLIS JFL, 1985, HEARING RES, V20, P1523 KLIS JFL, 1988, HEARING RES, V36, P163, DOI 10.1016/0378-5955(88)90058-5 MOUNTAIN DC, 1989, HEARING RES, V42, P195, DOI 10.1016/0378-5955(89)90144-5 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 RHODE WS, 1978, J ACOUST SOC AM, V64, P158, DOI 10.1121/1.381981 ROBERTSON D, 1974, SCI WASH, V186, P623 RUSSELL IJ, 1983, HEARING RES, V11, P373, DOI 10.1016/0378-5955(83)90068-0 SALVI RJ, 1983, HEARING RES, V10, P37, DOI 10.1016/0378-5955(83)90017-5 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SEWELL WF, 1984, HEARING RES, V14, P305, DOI 10.1016/0378-5955(84)90057-1 NR 37 TC 83 Z9 85 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1991 VL 52 IS 2 BP 288 EP 304 DI 10.1016/0378-5955(91)90019-6 PG 17 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500003 PM 2061220 ER PT J AU POU, AM FALLON, M WINBERY, S BOBBIN, RP AF POU, AM FALLON, M WINBERY, S BOBBIN, RP TI LOWERING EXTRACELLULAR CALCIUM DECREASES THE LENGTH OF ISOLATED OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE HAIR CELLS, OUTER; CALCIUM; MOTILITY; CONTRACTILE MECHANISM ID SMOOTH-MUSCLE; MECHANICAL RESPONSES; INDUCED MOTILITY; DEPOLARIZATION; CONTRACTION; ACTIN AB Transduction by the inner hair cells is hypothesized to be modulated through a change in the length of the outer hair cells (OHC). It has been suggested that the slow change occurring in OHC length is mediated by an actin-myosin system requiring Ca2+ and ATP. This study was designed to systematically examine the effects of lowering extracellular Ca2+ on OHC length. OHCs were isolated from guinea pig cochlea, mechanically dissociated and dispersed, and placed in a Hank's balanced salt solution (HBS). Exposing the cells to a Ca2+-free HBS and Ca2+-free HBS supplemented with 200-mu-m EDTA produced a shortening in OHC length with a concomitant increase in cell width. The shortening was reversed successfully by bathing the cells in 8 mM Ca2+. We speculate that the decrease in length due to lowering extracellular Ca2+ may be caused by a relaxation of a circumferential contractile mechanism which is thought to cause elongation of intact OHCs (Slepecky, 1989; Dulon et al., 1990). C1 LOUISIANA STATE UNIV,MED CTR,DEPT OTORHINOLARYNGOL & BIOCOMMUN,KRESGE HEARING RES LABS,NEW ORLEANS,LA 70112. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BOBBIN RP, 1990, HEARING RES, V47, P39, DOI 10.1016/0378-5955(90)90165-L BROWNELL WE, 1990, EAR HEARING, V11, P82, DOI 10.1097/00003446-199004000-00003 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 BROWNELL WE, 1990, BIOMECHANICS ACTIVE, P493 BRUNDIN L, 1989, NATURE, V342, P814, DOI 10.1038/342814a0 DALLOS P, 1988, AUDITORY FUNCTION NE, P153 DEFEO TT, 1985, J PHYSIOL-LONDON, V369, P269 DRESCHER DG, 1987, COMP BIOCHEM PHYS A, V87, P305, DOI 10.1016/0300-9629(87)90126-5 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1989, ABSTR ASS RES O 0205, P197 DULON D, 1987, ARCH OTO-RHINO-LARYN, V244, P104, DOI 10.1007/BF00458558 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1986, HEARING RES, V22, P80, DOI 10.1016/0378-5955(86)90079-1 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 GUTH SL, 1990, BRAIN RES, V508, P76, DOI 10.1016/0006-8993(90)91120-6 HIMPENS B, 1988, J PHYSIOL-LONDON, V395, P507 KACHAR B, 1986, NATURE, V322, P365, DOI 10.1038/322365a0 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X SCHACHT J, 1987, HEARING RES, V31, P155, DOI 10.1016/0378-5955(87)90121-3 SLEPECKY N, 1988, HEARING RES, V32, P11, DOI 10.1016/0378-5955(88)90143-8 SLEPECKY N, 1989, CELL TISSUE RES, V257, P69 SOMLYO AP, 1989, FASEB J, V3, P2266 SUMIMOTO K, 1986, PFLUG ARCH EUR J PHY, V406, P173, DOI 10.1007/BF00586679 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 ZENNER HP, 1988, ACTA OTO-LARYNGOL, V105, P39, DOI 10.3109/00016488809119443 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 31 TC 15 Z9 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1991 VL 52 IS 2 BP 305 EP 311 DI 10.1016/0378-5955(91)90020-A PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500004 PM 2061221 ER PT J AU BOOTH, JC CRAMB, DA AF BOOTH, JC CRAMB, DA TI THRESHOLD INTEGRATION OF BI-AMPLITUDE SIGNALS SO HEARING RESEARCH LA English DT Article DE TEMPORAL INTEGRATION; DIVERTED-INPUT HYPOTHESIS; MINIMUM INTENSITY LEVEL; INTENSITY INTEGRATION; BI-AMPLITUDE ID TEMPORAL INTEGRATION; MASKING; HEARING AB This study examined the pattern of intensity integration at threshold. The stimuli studied are unique in that they have a compound peak-to-peak amplitude envelope. This waveform was partitioned into two segments, each having a different peak-to-peak magnitude (bi-amplitude). All signals in the bi-amplitude series were the same duration (100 ms). Therefore, threshold differences between these signals are due solely to the integration of intensity in the amplitude dimension. A prediction of the pattern of thresholds, based on the diverted-input hypothesis, suggested that little or no integration would occur when the amplitude difference between segments is greater than a specific magnitude. Our results indicate that there are similarities in the integration process found with variable duration signals and with bi-amplitude signals. We conclude that previous estimates of the minimum intensity level based on temporal integration data underestimates the intensity levels that can contribute to threshold. Our results suggest that there are no apparent constraints on the intensity levels that can be integrated near threshold. The auditory system integrates distributed stimulus intensity in both the time and amplitude dimensions. Temporal integration in the auditory system can be viewed as a signal process, where an enhanced internal representation is given low-level stimuli. C1 CENTENARY HOSP,DEPT SPEECH LANGUAGE PATHOL & AUDIOL,SCARBOROUGH,ONTARIO,CANADA. RP BOOTH, JC (reprint author), UNIV WESTERN ONTARIO,ELBORN COLL,DEPT COMMUN DISORDERS,LONDON N6G 1H1,ONTARIO,CANADA. CR BROADBENT DE, 1970, SENSORINEURAL HEARIN, P157 DALLOS PJ, 1964, J ACOUST SOC AM, V36, P743, DOI 10.1121/1.1919059 FLORENTINE M, 1988, J ACOUST SOC AM, V84, P195, DOI 10.1121/1.396964 GARNER WR, 1947, J EXP PSYCHOL, V37, P293, DOI 10.1037/h0055734 GOLDSTEIN R, 1960, J SPEECH HEAR RES, V3, P249 GREEN DM, 1957, J ACOUST SOC AM, V29, P523, DOI 10.1121/1.1908951 GREEN DM, 1966, SIGNAL DETECTION THE GROEN J J, 1964, Acta Otolaryngol, V57, P224, DOI 10.3109/00016486409137078 HAMILTON PM, 1957, J ACOUST SOC AM, V29, P506, DOI 10.1121/1.1908942 HEMPSTOCK TI, 1964, J SOUND VIB, V4, P365 HUGHES JW, 1946, PROC R SOC SER B-BIO, V133, P486, DOI 10.1098/rspb.1946.0026 KIDD G, 1984, J ACOUST SOC AM, V75, P937, DOI 10.1121/1.390558 LOCKLIDER JCR, 1951, HDB EXPT PSYCHOL, P985 MARTIN FN, 1970, J AUD RES, V10, P82 MISKOLCZYFODOR F, 1959, J ACOUST SOC AM, V31, P1128, DOI 10.1121/1.1907839 OLSEN W O, 1987, Ear and Hearing, V8, p13S, DOI 10.1097/00003446-198708001-00005 OLSEN WO, 1966, J ACOUST SOC AM, V40, P591, DOI 10.1121/1.1910123 PEDERSEN CB, 1972, ACTA OTO-LARYNGOL, V74, P398, DOI 10.3109/00016487209128469 PLOMP R, 1959, J ACOUST SOC AM, V31, P749, DOI 10.1121/1.1907781 PULEO JS, 1980, J ACOUST SOC AM, V67, P947, DOI 10.1121/1.383973 SANDERS JW, 1967, ARCHIV OTOLARYNGOL, V85, P640 SORKIN RD, 1965, J ACOUST SOC AM, V38, P207, DOI 10.1121/1.1909635 TAYLOR MM, 1971, J ACOUST SOC AM, V50, P1151, DOI 10.1121/1.1912748 TAYLOR MM, 1967, J ACOUST SOC AM, V41, P782, DOI 10.1121/1.1910407 ZWISLOCKI J, 1960, J ACOUST SOC AM, V32, P1046, DOI 10.1121/1.1908276 1969, ANSI S361969 AM NATL NR 26 TC 1 Z9 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1991 VL 52 IS 2 BP 312 EP 320 DI 10.1016/0378-5955(91)90021-Z PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500005 PM 2061222 ER PT J AU HILLERDAL, M ANDERSSON, SE AF HILLERDAL, M ANDERSSON, SE TI THE EFFECTS OF CALCITONIN GENE-RELATED PEPTIDE (CGRP) ON COCHLEAR AND MUCOSAL BLOOD-FLOW IN THE ALBINO RABBIT SO HEARING RESEARCH LA English DT Article DE COCHLEA; MUCOSA; UPPER RESPIRATORY TRACT; MIDDLE EAR; BLOOD FLOW; MICROSPHERE METHOD; CGRP; RABBIT ID MICROSPHERE METHOD; RESPIRATORY-TRACT; MIDDLE-EAR; RAT; LOCALIZATION; ORGAN; CORTI; CAT AB The effects of intravenously infused calcitonin gene-related peptide (CGRP) on the regional blood flow of the cochlea, the middle ear and the upper respiratory tract were studied. Two series of experiments were performed without pretreatment on either conscious or pentobarbital anaesthetized animals; in one series the cervical sympathetic chain was severed on one side; in another series anaesthetized animals were subjected to ganglionic blockade with hexamethonium bromide in order to abolish reflexes involving the autonomic nervous system. In still another series conscious animals were pretreated with indomethacin in order to reduce the formation of prostaglandins. In all groups of animals where sympathetic influence was diminished cochlear blood flow increased during the infusion of CGRP. In the mucosa of middle ear and the upper airways, the blood flow increased in all groups. The results indicate that CGRP at these doses causes vasorelaxation in the mucosa of the middle ear and upper airways and does so also in the cochlea if the sympathetic influence is abolished. C1 UNIV UPPSALA,DEPT OTORHINOLARYNGOL,S-75105 UPPSALA,SWEDEN. UNIV UPPSALA,DEPT PHYSIOL & MED BIOPHYS,S-75105 UPPSALA,SWEDEN. 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Res. PD APR PY 1991 VL 52 IS 2 BP 321 EP 328 DI 10.1016/0378-5955(91)90022-2 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500006 PM 2061223 ER PT J AU CLOPTON, BM BACKOFF, PM AF CLOPTON, BM BACKOFF, PM TI SPECTROTEMPORAL RECEPTIVE-FIELDS OF NEURONS IN COCHLEAR NUCLEUS OF GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE STRF; COCHLEAR NUCLEUS; NOISE CHARACTERIZATION ID SPECTRO-TEMPORAL CHARACTERISTICS; SINGLE UNIT-ACTIVITY; AUDITORY MIDBRAIN; DORSAL; CAT; FREQUENCY; NOISE; GRASSFROG; TIME; REPRESENTATION AB Spectrotemporal receptive fields (STRFs) [Hermes et al., Hear. Res. 5, 147-178, 1981] for neurons in the cochlear nuclei (CN) of guinea pig were estimated. Sixteen periodic segments of bandlimited, synthesized noise evoked replicable, distinctive period histograms for spike discharges. All driven units in the major divisions of the CN having their characteristic frequency (CF) within the noise bandlimits had unique STRFs for a given intensity of noise stimulation. The STRF maximum corresponded to the unit's CF, and details of the STRF patterns differed over CN divisions and response classes derived from tonebursts. The sizes of features in STRFs from this mammal appeared significantly smaller in their temporal and spectral extents than those reported in the torus semicircularis of an amphibian and were roughly comparable to the few units reported from cat ventral CN [Eggermont et al., Quart. Rev. Biophys. 16, 341-414, 1983]. STRFs, as they are presently obtained, provide useful insight into some aspects of afferent processing and perhaps connectivity, but their interpretation is specific to the level of stimulation and limited by the need to choose a specific energy distribution to represent the stimulus. RP CLOPTON, BM (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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PD APR PY 1991 VL 52 IS 2 BP 329 EP 344 DI 10.1016/0378-5955(91)90023-3 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500007 PM 2061224 ER PT J AU PIRVOLA, U LEHTONEN, E YLIKOSKI, J AF PIRVOLA, U LEHTONEN, E YLIKOSKI, J TI SPATIOTEMPORAL DEVELOPMENT OF COCHLEAR INNERVATION AND HAIR CELL-DIFFERENTIATION IN THE RAT SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELLS; DIFFERENTIATION; ACTIN; FODRIN; INNERVATION ID ACTIN-FILAMENTS; SENSORY EPITHELIUM; CUTICULAR PLATE; CHICK-EMBRYO; BIRD COCHLEA; STEREOCILIA; MOUSE; SYNAPTOGENESIS; GANGLION; PROTEINS AB The apical cytoskeleton of cochlear hair cells is largely comprised of actin microfilaments and actin-associated proteins, of which fodrin is one of the most prominent. We studied the development of this mechanosensory apical portion of cochlear hair cells of the rat by fluorescence microscopy using rhodamine conjugated phalloidin to detect F-actin and an antibody against alpha-fodrin. An antibody against the 160 kDa neurofilament polypeptide was used for tracing nerve fibers. The first sign of differentiation of the mechanosensory region, actin-containing stereocilia, was observed on the 19th gestational day in the inner hair cells of the basal coil. The appearance of expression of cytoskeletal actin in the cochlear hair cells proceeded gradientally from basal to apical coil and from inner to outer hair cells. Corresponding maturation sequences were observed in the development of fodrin immunoreactivity in the cuticular plates, but the first evidence of this reactivity was found one day later than the appearance of stereocilia in the hair cells at the same location. Also the penetration of neurofilament-positive neurites into the sensory epithelium followed the same kind of longitudinal and radial maturation gradients throughout the cochlea. Fibers were revealed beneath the sensory cells shortly before the first appearance of differentiation of their mechanosensory region. The results suggest that ingrowing nerve fibers may influence the timing of the apical cytoskeleton differentiation in cochlear hair cells or that both these processes could be controlled by the same external signals that are gradientally expressed throughout the cochlea. C1 UNIV HELSINKI,DEPT OTOLARYNGOL,SF-00290 HELSINKI 29,FINLAND. RP PIRVOLA, U (reprint author), UNIV HELSINKI,DEPT PATHOL,HAARTMANINKATU 3,SF-00290 HELSINKI 29,FINLAND. CR ANNIKO M, 1983, ANAT EMBRYOL, V166, P355, DOI 10.1007/BF00305923 ANNIKO M, 1983, AM J OTOLARYNG, V4, P375, DOI 10.1016/S0196-0709(83)80043-X ARD MD, 1985, NEUROSCIENCE, V16, P151, DOI 10.1016/0306-4522(85)90053-3 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 COCHARD P, 1984, J NEUROSCI, V4, P2080 DRENCKHAHN D, 1985, AUDITORY BIOCH, P312 FLOCK A, 1982, HEARING RES, V6, P75 FLOCK A, 1977, J CELL BIOL, V75, P339, DOI 10.1083/jcb.75.2.339 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 GILLLOYZAGA P, 1987, ABSTR ASS RES O 0201, P223 GINZBERG RD, 1979, DEV BIOL, V68, P110, DOI 10.1016/0012-1606(79)90247-1 GINZBERG RD, 1980, J NEUROCYTOL, V9, P405, DOI 10.1007/BF01181545 HAFIDI A, 1989, DEV BRAIN RES, V48, P143, DOI 10.1016/0165-3806(89)90098-9 HIROKAWA N, 1983, CELL, V32, P953, DOI 10.1016/0092-8674(83)90080-6 HIROKAWA N, 1978, J NEUROCYTOL, V7, P283, DOI 10.1007/BF01176994 HOLLEY MC, 1990, J CELL SCI, V96, P283 LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0 LEHTONEN E, 1985, DEV BIOL, V108, P481, DOI 10.1016/0012-1606(85)90051-X MBIENE JP, 1988, ANAT EMBRYOL, V177, P331, DOI 10.1007/BF00315841 MBIENE JP, 1989, CELL TISSUE RES, V255, P81 RAYMOND J, 1987, HEARING RES, V28, P45, DOI 10.1016/0378-5955(87)90152-3 Romand R., 1983, DEV AUDITORY VESTIBU, P47 ROMAND R, 1987, HEARING RES, V28, P1, DOI 10.1016/0378-5955(87)90148-1 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 Ruben R. 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Res. PD APR PY 1991 VL 52 IS 2 BP 345 EP 355 DI 10.1016/0378-5955(91)90024-4 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500008 PM 1905709 ER PT J AU HASHINO, E TANAKA, Y SOKABE, M AF HASHINO, E TANAKA, Y SOKABE, M TI HAIR CELL-DAMAGE AND RECOVERY FOLLOWING CHRONIC APPLICATION OF KANAMYCIN IN THE CHICK COCHLEA SO HEARING RESEARCH LA English DT Article DE HAIR CELL; REGENERATION; KANAMYCIN; OTOTOXICITY; CHICK ID ACOUSTIC TRAUMA; BASILAR PAPILLA; INNER-EAR; REGENERATION; STEREOCILIA; OTOTOXICITY AB Three-day old chicks were given kanamycin at a dose of 200 mg/kg/day for 10 days and their cochleae were processed for scanning electron microscopy at 1, 3, 7 and 14 days following the last injection. Both hair cells and supporting cells were damaged by kanamycin in the basal 35% of the basilar papilla. By 14 days post-treatment, however, most of the damaged region had been replaced with regenerating hair cells and supporting cells. The base-to-apex gradient of morphological development along the cochlea was observed in the process of regeneration. Kinocilium and microvilli were observed on the apical surfaces of the regenerating hair cells. C1 TOKYO WOMENS CHRISTIAN UNIV,DEPT COMMUN,TOKYO,JAPAN. DOKKYO UNIV,KOSHIGAYA HOSP,SCH MED,DEPT OTOLARYNGOL,SAITAMA,JAPAN. NAGOYA UNIV,SCH MED,DEPT PHYSIOL,NAGOYA,AICHI 466,JAPAN. 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Res. PD APR PY 1991 VL 52 IS 2 BP 356 EP 368 DI 10.1016/0378-5955(91)90025-5 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500009 PM 2061225 ER PT J AU MUNYER, PD SCHULTE, BA AF MUNYER, PD SCHULTE, BA TI IMMUNOHISTOCHEMICAL IDENTIFICATION OF PROTEOGLYCANS IN GELATINOUS MEMBRANES OF CAT AND GERBIL INNER-EAR SO HEARING RESEARCH LA English DT Article DE INNER EAR; COCHLEA; VESTIBULAR SYSTEM; PROTEOGLYCANS; IMMUNOHISTOCHEMISTRY; CAT; GERBIL ID TECTORIAL MEMBRANE; MONOCLONAL-ANTIBODY; CARTILAGE PROTEOGLYCAN; LOCALIZATION; SUPRASTRUCTURE; NA+,K+-ATPASE; ORGANIZATION; SULFATE; MACULA AB Proteoglycans have been identified in gelatinous membranes of adult cat and gerbil inner ears using highly specific histochemical techniques. The tectorial and otoconial membranes and cupula of both species stained strongly with high iron diamine which is specific for sulfate esters and with monoclonal antibody against keratan sulfate proteoglycan (KSPG). The cat tectorial membrane also showed strong immunoreactivity with monoclonal antibody against chondroitin sulfate proteoglycan (CSPG) but the gerbil tectorial membrane reacted only weakly with this antibody. Otoconial membranes and the cupula of both species showed little if any immunostaining with antibodies against CSPG. Supporting cells in the vestibular neurosensory epithelium and planum semilunatum cells in the ampullae of the cat stained strongly with anti-KSPG, demonstrating the origin of KSPG in the cat. These cell types failed to stain in the gerbil, however, suggesting a different mechanism of secretion or a slower rate of turnover of membraneous KSPG in the gerbil. Interdental cells of both species failed to react with either antibody, leaving the origin of tectorial membrane proteoglycans in question. The approach used here provides a highly sensitive and reliable means of assessing the contribution of specific proteoglycans to inner ear structure and function. RP MUNYER, PD (reprint author), MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425, USA. 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Res. PD APR PY 1991 VL 52 IS 2 BP 369 EP 378 DI 10.1016/0378-5955(91)90026-6 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500010 PM 2061226 ER PT J AU COTANCHE, DA CORWIN, JT AF COTANCHE, DA CORWIN, JT TI STEREOCILIARY BUNDLES REORIENT DURING HAIR CELL-DEVELOPMENT AND REGENERATION IN THE CHICK COCHLEA SO HEARING RESEARCH LA English DT Article DE HEARING; AUDITORY; EAR; POLARITY; TRANSDUCTION ID SEVERE ACOUSTIC TRAUMA; ACTIN-FILAMENTS; BIRD COCHLEA; TECTORIAL MEMBRANE; BASILAR PAPILLA; INNER-EAR; DIFFERENTIATION; SENSITIVITY; RESPONSES; ANATOMY AB We have examined changes in the orientation of stereociliary bundles of hair cells in the cochlear sensory epithelium that occur during normal embryonic development and during the regeneration of hair cells that follows acoustic trauma. At the time when hair cell surfaces become recognizable in the embryonic cochlea, the bundles of stereocilia exhibit a range of orientations, as indicated by the position of the kinocilium and later, by the location of the tallest row of stereocilia. With time, the orientations of bundles on neighboring hair cells become more uniform, a condition that is maintained in the adult. Changes in stereocilia orientation are also observed during the regeneration of hair cells after acoustic trauma. When new hair cells first differentiate at sites of trauma in the recovering sensory epithelium, their stereociliary bundles are not uniformly oriented. Then as the cells mature over a period of days, the bundles become aligned both with the neighboring bundles in the region of the previous lesion and with the pre-existing bundles that surround the site of regeneration. We conclude that the stereociliary bundles of hair cells are reorienting as the cells differentiate. A common mechanism may guide reorientation both during embryonic development and during regeneration. Observations in living cochleae indicate that differentiating stereociliary bundles establish asymmetric linkages to the extracellular matrix of the developing tectorial membrane. During the growth of the tectorial membrane, its progressive extension across the surface of the sensory epithelium may exert traction forces through those asymmetric linkages that pull the bundles of the hair cells into uniform alignment. C1 UNIV VIRGINIA,MED CTR,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,CHARLOTTESVILLE,VA 22901. UNIV VIRGINIA,MED CTR,SCH MED,DEPT NEUROSCI,CHARLOTTESVILLE,VA 22901. RP COTANCHE, DA (reprint author), BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,80 E CONCORD ST,BOSTON,MA 02118, USA. 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Res. PD APR PY 1991 VL 52 IS 2 BP 379 EP 402 DI 10.1016/0378-5955(91)90027-7 PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FH335 UT WOS:A1991FH33500011 PM 2061227 ER PT J AU KLUMP, GM OKANOYA, K AF KLUMP, GM OKANOYA, K TI TEMPORAL-MODULATION TRANSFER-FUNCTIONS IN THE EUROPEAN STARLING (STURNUS-VULGARIS) .1. PSYCHOPHYSICAL MODULATION DETECTION THRESHOLDS SO HEARING RESEARCH LA English DT Article DE TEMPORAL MODULATION TRANSFER FUNCTION; AMPLITUDE MODULATION; ENVELOPE; STARLING; BIRD ID AUDITORY-NERVE FIBERS; GAP DETECTION; TONOTOPIC ORGANIZATION; INFERIOR COLLICULUS; BROAD-BAND; NOISE; FOREBRAIN; HEARING; SYSTEM; RESOLUTION AB Temporal modulation transfer functions (TMTF) were obtained from four European starlings (Sturnus vulgaris) using a psychophysical Go/NoGo procedure combined with the method of constant stimuli. The TMTF for a continuous, broad-band noise of 55 dB SPL had a low-pass characteristic with a cut-off frequency of 123 Hz. For an 800 ms gated stimulus of the same sound-pressure level, the TMTF had the shape of a band-pass filter with the most sensitive modulation frequency at around 20 Hz. At 75 dB the band-pass shape of the TMTF was preserved, whereas at 35 dB SPL the TMTF had a low-pass characteristic. The cut-off frequency of the TMTF for continuous noise depends on which part of the spectrum carries the information on the envelope fluctuations. If only sound energy below 1 or 1.5 kHz is modulated, then the cut-off frequencies are 40 and 38 Hz, respectively. If only sound above 3 kHz carries the information on the modulation, then the cut-off frequency is 125 Hz and the shape of the TMTF is similar to that found for broadband noise. The results are discussed with respect to the coding of sinusoidal amplitude modulations by the auditory system and to different measure of time, frequency and intensity resolution in the starling. RP KLUMP, GM (reprint author), TECH UNIV MUNICH,INST ZOOL,LICHTENBERGSTR 4,W-8046 GARCHING,GERMANY. RI Okanoya, Kazuo/F-8528-2010 CR BACON SP, 1985, AUDIOLOGY, V24, P117 BIGALKEKUNZ B, 1987, J COMP PHYSIOL A, V161, P255, DOI 10.1007/BF00615245 BUCHFELLNER E, 1989, J COMP PHYSIOL A, V164, P539, DOI 10.1007/BF00610447 COOMBS S, 1985, HEARING RES, V19, P57, DOI 10.1016/0378-5955(85)90098-X COSTALUPES JA, 1984, J NEUROPHYSIOL, V51, P1326 DOOLING RJ, 1981, J COMP PHYSIOL, V143, P383 DUNIA R, 1989, J ACOUST SOC AM, V85, P1630, DOI 10.1121/1.397951 EVANS E, 1974, FACTS MODELS HEARING FAY RR, 1980, J NEUROPHYSIOL, V44, P312 FORMBY C, 1988, J ACOUST SOC AM, V84, P545, DOI 10.1121/1.396831 FORREST TG, 1987, J ACOUST SOC AM, V82, P1933, DOI 10.1121/1.395689 GLEICH O, 1988, HEARING RES, V32, P81, DOI 10.1016/0378-5955(88)90148-7 Greenewalt CH, 1968, BIRD SONG ACOUSTICS HENDERSON D, 1984, J ACOUST SOC AM, V75, P1177, DOI 10.1121/1.390767 HOSE B, 1987, BRAIN RES, V422, P367, DOI 10.1016/0006-8993(87)90946-2 KLUMP GM, 1989, J COMP PHYSIOL A, V164, P531, DOI 10.1007/BF00610446 KLUMP GM, 1990, J COMP PSYCHOL, V104, P94, DOI 10.1037/0735-7036.104.1.94 KLUMP GM, 1990, IN PRESS NATURWISS KLUMP GM, UNPUB GAP DETECTION, V3 KNIPSCHILD M, 1986, THESIS RUHR U BOCHUM LANGNER G, 1983, EXP BRAIN RES, V52, P333 LANGNER G, 1987, HEARING RES, V31, P197, DOI 10.1016/0378-5955(87)90127-4 MAIER EH, 1990, J ACOUST SOC AM, V88, P616, DOI 10.1121/1.399765 MILLER GA, 1947, J ACOUST SOC AM, V19, P609, DOI 10.1121/1.1916528 MULLER CM, 1985, EXP BRAIN RES, V59, P587 NARINS PM, 1987, HEARING RES, V26, P145, DOI 10.1016/0378-5955(87)90106-7 OKANOYA Y, 1991, IN PRESS HEAR RES REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 REES A, 1987, HEARING RES, V27, P192 Rodenburg M., 1977, PSYCHOPHYSICS PHYSL, P429 ROSE GJ, 1985, J NEUROPHYSIOL, V53, P446 SALVI RJ, 1982, J ACOUST SOC AM, V71, P424, DOI 10.1121/1.387445 SHAILER MJ, 1983, J ACOUST SOC AM, V74, P467, DOI 10.1121/1.389812 Swets J.A., 1964, SIGNAL DETECTION REC TAKAHASHI T, 1984, J NEUROSCI, V4, P1782 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 ZHANG W, 1990, HEARING RES, V46, P181, DOI 10.1016/0378-5955(90)90001-6 NR 37 TC 17 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 1 EP 11 DI 10.1016/0378-5955(91)90182-9 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500001 PM 2061200 ER PT J AU HEFFNER, RS HEFFNER, HE AF HEFFNER, RS HEFFNER, HE TI BEHAVIORAL HEARING RANGE OF THE CHINCHILLA SO HEARING RESEARCH LA English DT Article DE RODENT; HUMAN; PSYCHOPHYSICS; METHOD; AUDIOGRAM; THRESHOLD ID THRESHOLD SHIFT; NOISE AB The audiograms of three chinchillas were determined using pure tones ranging from 32 Hz to 45 kHz. The animals were tested with a conditioned avoidance procedure in which their heads were fixed within the sound field by requiring them to place their mouths on a water spout. At a level of 60 dB SPL the average hearing range extended from 50 Hz to 33 kHz with none of the animals able to hear 45 kHz at 89 dB. Overall, the audiogram of the chinchilla appears to resemble the human audiogram more closely than do other rodent audiograms. An analysis of ten published chinchilla audiograms indicates that those procedures which do not fix an animal within the sound field may overestimate their sensitivity. RP HEFFNER, RS (reprint author), UNIV TOLEDO,DEPT PSYCHOL,2801 BANCROFT ST,TOLEDO,OH 43606, USA. CR ADES HW, 1974, ACTA OTO-LARYNGOL, V78, P192, DOI 10.3109/00016487409126345 BLAKESLEE EA, 1978, J ACOUST SOC AM, V63, P876, DOI 10.1121/1.381767 CLARK WW, 1978, ANN OTOL RHINOL S51, V51 CLARK WW, 1974, J ACOUST SOC AM, V56, P1202, DOI 10.1121/1.1903409 DALLOS P, 1978, J ACOUST SOC AM, V64, P151, DOI 10.1121/1.381980 DAVIS R I, 1983, Journal of Auditory Research, V23, P281 HEFFNER HE, 1985, J COMP PSYCHOL, V99, P275, DOI 10.1037//0735-7036.99.3.275 HEFFNER RS, 1985, HEARING RES, V19, P85, DOI 10.1016/0378-5955(85)90100-5 MILLER JD, 1970, J ACOUST SOC AM, V48, P5513 SALVI RJ, 1983, HEARING RES, V10, P37, DOI 10.1016/0378-5955(83)90017-5 SAUNDERS JC, 1977, J ACOUST SOC AM, V61, P558, DOI 10.1121/1.381298 SAUNDERS SS, 1987, J ACOUST SOC AM, V82, P1604, DOI 10.1121/1.395150 NR 12 TC 59 Z9 61 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 13 EP 16 DI 10.1016/0378-5955(91)90183-A PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500002 PM 2061202 ER PT J AU GONZALEZHERNANDEZ, TH GALINDOMIRELES, D CASTANEYRAPERDOMO, A FERRESTORRES, R AF GONZALEZHERNANDEZ, TH GALINDOMIRELES, D CASTANEYRAPERDOMO, A FERRESTORRES, R TI DIVERGENT PROJECTIONS OF PROJECTING NEURONS OF THE INFERIOR COLLICULUS TO THE MEDIAL GENICULATE-BODY AND THE CONTRALATERAL INFERIOR COLLICULUS IN THE RAT SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; DIVERGENT PROJECTIONS; DOUBLE LABELING; FLUORESCENT TRACERS; RAT ID CENTRAL NUCLEUS; AUDITORY-SYSTEM; ORGANIZATION; CAT; CONNECTIONS; AFFERENTS AB The present paper shows, by means of the combination of two fluorescent tracers, that a significant number of neurons of the three divisions of the inferior colliculus in the rat project to the contralateral inferior colliculus and the ipsilateral medial geniculate body. The topographic distribution of double-labeled cells depends on the location of injections in each case. According to the soma size and the dendritic stem, different neuron types may be distinguished. Our results suggest that the inputs that converge in individual neurons of the inferior colliculus can diverge again. RP GONZALEZHERNANDEZ, TH (reprint author), UNIV LA LAGUNA,FAC MED,DEPT ANAT,LA LAGUNA,SPAIN. CR ADAMS JC, 1979, J COMP NEUROL, V183, P519, DOI 10.1002/cne.901830305 ADAMS JC, 1980, NEUROSCI LETT, V19, P1, DOI 10.1016/0304-3940(80)90246-3 AITKIN LM, 1984, NEUROSCI LETT, V44, P259, DOI 10.1016/0304-3940(84)90032-6 BEYERL BD, 1978, BRAIN RES, V145, P209, DOI 10.1016/0006-8993(78)90858-2 BRUNSOBECHTOLD JK, 1981, J COMP NEUROL, V197, P705, DOI 10.1002/cne.901970410 COLEMAN JR, 1987, J COMP NEUROL, V262, P215, DOI 10.1002/cne.902620204 FAYELUND H, 1985, ANAT EMBRYOL, V171, P1, DOI 10.1007/BF00319050 GONZALEZHERNANDEZ TH, 1987, J HIRNFORSCH, V28, P315 González Hernández T H, 1986, Brain Res, V368, P268, DOI 10.1016/0006-8993(86)90571-8 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 KUYPERS HGJM, 1980, EXP BRAIN RES, V40, P383 MOORE DR, 1983, DEV AUDITORY VESTIBU, P121 OLIVER DL, 1984, NEUROSCIENCE, V11, P409, DOI 10.1016/0306-4522(84)90033-2 Paxinos G, 1986, RAT BRAIN STEREOTAXI, V2nd SCHWEIZER H, 1981, J COMP NEUROL, V201, P25, DOI 10.1002/cne.902010104 TOKUNAGA A, 1984, J HIRNFORSCH, V25, P461 WENSTRUP JJ, 1985, HEARING RES, V17, P191, DOI 10.1016/0378-5955(85)90021-8 WILLARD FH, 1984, BRAIN RES, V303, P171, DOI 10.1016/0006-8993(84)90225-7 NR 18 TC 14 Z9 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 17 EP 21 DI 10.1016/0378-5955(91)90184-B PG 5 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500003 PM 2061205 ER PT J AU STARR, PA SEWELL, WF AF STARR, PA SEWELL, WF TI NEUROTRANSMITTER RELEASE FROM HAIR-CELLS AND ITS BLOCKADE BY GLUTAMATE-RECEPTOR ANTAGONISTS SO HEARING RESEARCH LA English DT Article DE AUDITORY; GLUTAMATE; NEUROTRANSMITTER; COBALT; QUANTAL; SYNAPSE; GOLDFISH ID POST-SYNAPTIC POTENTIALS; ION-DEPENDENT CONDUCTANCES; AFFERENT NERVE-FIBERS; INNER-EAR; MICROPHONIC POTENTIALS; GOLDFISH SACCULUS; AUDITORY FIBERS; FROG; TRANSMISSION; SYNAPSES AB To assess the mechanism by which glutamate-receptor antagonist block afferent discharge at the hair cell synapse, we examined the effects of these and other agents on sound-evoked excitatory post-synaptic potentials (EPSPs) and on spontaneous miniature post-synaptic potentials (MEPSPs) in auditory-nerve fibers of the goldfish (Carassius auratus) saccule. A quantal analysis of synaptic transmission under conditions in which the probability of transmitter release was reduced by cobalt, an agent that can block transmitter release, supports Furukawa's (Jpn. J. Physiol. 36, 1059-1077, 1986) conclusion that transmitter release at this synapse is quantal. Cobalt reduced the rate of occurrence of spontaneous MEPSPs without reducing their amplitude. The glutamate-receptor antagonists, gamma-D-glutamyl glycine (DGG) and 5-aminophosphonovaleric acid (APV) both reduced the amplitude of sound-evoked EPSPs much more than that of the spontaneous MEPSPs. The glutamate-receptor agonists, L-glutamate, kainate, and quisqualate, produced a depolarization of the afferent nerve fiber, a decrease in the amplitude of the EPSP and an increased tendency for an EPSP to generate an action potential. C1 MASSACHUSETTS EYE & EAR HOSP,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 23 EP 41 DI 10.1016/0378-5955(91)90185-C PG 19 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500004 PM 1676396 ER PT J AU CZIBULKA, A SCHWARTZ, IR AF CZIBULKA, A SCHWARTZ, IR TI NEURONAL POPULATIONS IN THE GERBIL PVCN - EFFECTS OF AGE, HEARING STATUS AND MICROCYSTS SO HEARING RESEARCH LA English DT Article DE PVCN; COCHLEAR NUCLEUS; GERBIL; NEURONAL CELL TYPES; MICROCYSTS; AGING ID MONGOLIAN GERBIL AB This study was designed to test the hypothesis that microcysts in the gerbil auditory system are formed from neuronal somata. Six neuronal types (octopus, multipolar, bushy, elongate, miscellaneous and small) were distinguished counted and measured along with the microcysts in the posteroventral cochlear nuclei (PVCNs) of 3, 12 and 36 month old gerbils. No decrease was observed in the numbers of neurons in any neuronal class, or in the neuronal population as a whole, in the PVCN of the gerbil as a function of age. Neither was any change observed in the PVCN area occupied by non-neuronal, non-microcyst elements. Neuronal sizes were unchanged between 3 and 12 months, but multipolar and bushy cells, as well as the total neuronal population decreased significantly in size between 12 and 36 months. The number and size of microcysts increased significantly between 3 and 12 months of age and accounts for increases in PVCN volume. The number and size of microcysts decreased significantly between 12 and 36 months. Thus, the appearance of microcysts can not result from the selective loss of any single class of neurons. Hearing was assessed in five 36 month old animals with suditory brainstem responses (ABR) and number and size of microcysts were found to correlate with hearing status, being largest and most numerous in animals with the best hearing, and smallest and fewest in the deaf animal. It is concluded that microcysts cannot represent a neurodegenerative disease of neuronal somata. Microcyst formation appears to be a dynamic process related to the degree of auditory stimulation. C1 YALE UNIV,SCH MED,DEPT SURG,OTOLARYNGOL SECT,333 CEDAR ST,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,NEUROANAT SECT,NEW HAVEN,CT 06510. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 43 EP 57 DI 10.1016/0378-5955(91)90186-D PG 15 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500005 PM 2061213 ER PT J AU ZAJIC, G NAIR, TS PTOK, M VANWAES, C ALTSCHULER, RA SCHACHT, J CAREY, TE AF ZAJIC, G NAIR, TS PTOK, M VANWAES, C ALTSCHULER, RA SCHACHT, J CAREY, TE TI MONOCLONAL-ANTIBODIES TO INNER-EAR ANTIGENS .1. ANTIGENS EXPRESSED BY SUPPORTING CELLS OF THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; MONOCLONAL ANTIBODIES; SUPPORTING CELLS ID RICIN A-CHAIN; T-CELLS; IMMUNOTOXINS; PROTEINS AB Murine monoclonal antibodies against guinea pig cochlear epithelium were generated with the goal of identifying cochlea-specific antigens and elucidating their function. To compensate for the limited amount of cochlear tissue, intrasplenic immunization was used. Hybridoma supernatants were screened by ELSIA for antibody production and for binding to homogenates from cochlea, liver, lung, kidney and brain. Hybrids producing antibody to cochlea were subcloned and tested immunocytochemically against frozen sections and surface preparations of paraformaldehyde-fixed cochlear tissue. KHRI-1, a low titer IgM antibody stained only Hensen cells. KHRI-2, also an IgM antibody, stained tectorial membrane, cells of the spiral limbus, cells bordering the space of Nuel, Hensen cells and the root cells of the spiral prominence. KHRI-3, an IgG1 antibody, stained the phalangeal processes of outer pillar cells and the apical portion of phalangeal processes of Deiters' cells in a distinctive wine goblet pattern on surface preparations. KHRI-3 antibody also reacted with peripheral nerves and pia mater of brain in unfixed frozen sections but the antigenic site was not stable to fixation in contrast to the epitope detected in the cochlea. In Western blots of detergent extracts from cochlea KHRI-3 stained a broad tissue-specific band of Mr 70-75 kDa; a narrower band of Mr 68-70 kDa was identified by KHRI-3 in extracts of tongue and brain. KHRI-1 and KHRI-2 did not detect any proteins in Western blots. The monoclonal antibodies KHRI-1, -2, and -3 which define epitopes expressed by discrete populations of supporting cells in the inner ear should be useful in characterizing the nature and function of cellular structures in the cochlea. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109. 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PD MAR PY 1991 VL 52 IS 1 BP 59 EP 71 DI 10.1016/0378-5955(91)90187-E PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500006 PM 2061214 ER PT J AU EHRENBERGER, K FELIX, D AF EHRENBERGER, K FELIX, D TI GLUTAMATE RECEPTORS IN AFFERENT COCHLEAR NEUROTRANSMISSION IN GUINEA-PIGS SO HEARING RESEARCH LA English DT Article DE INNER HAIR CELL; AFFERENTS; NEUROTRANSMITTERS; GLUTAMATE; RECEPTORS; MICROIONTOPHORESIS ID EXCITATORY AMINO-ACIDS; METHYL-D-ASPARTATE; OUTER HAIR-CELLS; LONG-TERM POTENTIATION; NMDA-RECEPTORS; SYNAPTIC TRANSMISSION; GLYCINE; SUBSTANCES; ANTAGONIST; NEURONS AB With the aid of microiontophoretic techniques we tested the action of the transmitter candidate glutamate (Glu) at the afferent synapses of inner hair cells (IHC) in guinea pigs. In order to determine the various types of glutamate receptors, further agonistic excitatory amino acids (EAA) as well as competitive EAA-antagonists were used. Applied perisynaptically, Glu, aspartate, N-methyl-D-aspartate (NMDA), quisqualate (Q) and kaniate (K) active the subsynaptic, phasic firing activity of the afferent dendrites. The NMDA-induced activation is augumented by simultaneous application of glycine. The firing rate induced by Glu and NMDA is blocked by the specific NMDA-antagonist D-2-amino-7-phosphonoheptanoate (AP-7). Furthermore, activity induced by Glu and Q decreases under the influence of the selective Q-antagonist glutamic acid diethylester (GDEE). These results are consistent with the hypothesis that Glu acts as a possible afferent neurotransmitter of the IHC. This neurotransmission is mediated by postsynaptic EAA-receptor subpopulations which are sensitive to NMDA, Q and K. The activity of the NMDA-receptors depends, however, on the amount of glycine available. Our data suggest that the afferent synapses of the IHC possess functional properties which are equivalent to the properties of glutamatergic NMDA-sensitive and NMDA-non-sensitive synapses in the central nervous system. C1 UNIV BERN,INST ZOOL,DIV NEUROBIOL,CH-3000 BERN,SWITZERLAND. RP EHRENBERGER, K (reprint author), UNIV VIENNA,DEPT EARS NOSE & THROAT 1,LAZARETTGASSE 14,A-1090 VIENNA,AUSTRIA. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 73 EP 80 DI 10.1016/0378-5955(91)90188-F PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500007 PM 1648061 ER PT J AU DECORY, L HIEL, H ARAN, JM AF DECORY, L HIEL, H ARAN, JM TI INVIVO NOISE EXPOSURE ALTERS THE INVITRO MOTILITY AND VIABILITY OF OUTER HAIR-CELLS SO HEARING RESEARCH LA English DT Article DE ISOLATED HAIR CELL; MOTILITY; VIABILITY; NOISE EXPOSURE; GUINEA PIG ID GUINEA-PIG COCHLEA; ACOUSTIC STIMULATION; OLIVOCOCHLEAR BUNDLE; THRESHOLD SHIFT; AUDITORY-SYSTEM; TRAUMA; STEREOCILIA; RESPONSES; ORGAN AB The in vitro motility and viability of outer cells isolated from cochleae of normal control guinea pigs have been compared to that of guinea pigs exposed, just before sacrifice, to low-frequency high-intensity noise inducing acute 30 dB thresholds shifts at all frequencies below 10kHz. The results indicate that the cells' viability is shortened, their contractile response to Ca2+/ATP reduced, while their electrically-induced motility is not modified. These experiments demonstrate that in vivo cochlear dysfunction can correlate with changes in in vitro outer hair cell's properties. Thus the morphological and "functional" investigation of hair cells in vitro can be a valuable approach to the study of cochlea physiopathology. Here the acoustic overstimulation seems to have modified the outer hair cells Ca2+/ATP dependent slow contractile apparatus in a way which could modify in turn their mechanical excitation by the noise. C1 HOP PELLEGRIN,AUDIOL EXPTL LAB,INSERM,U299,F-33076 BORDEAUX,FRANCE. INST FRANCO ALLEMAN ST LOUIS,ST LOUIS,FRANCE. UNIV BORDEAUX 2,AUDOL EXPTL LAB,INSERM,U229,F-33076 BORDEAUX,FRANCE. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 81 EP 88 DI 10.1016/0378-5955(91)90189-G PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500008 PM 2061215 ER PT J AU SANTOS-SACCHI, J AF SANTOS-SACCHI, J TI ISOLATED SUPPORTING CELLS FROM THE ORGAN OF CORTI - SOME WHOLE CELL ELECTRICAL CHARACTERISTICS AND ESTIMATES OF GAP JUNCTIONAL CONDUCTANCE SO HEARING RESEARCH LA English DT Article DE VOLTAGE CLAMP; ORGAN OF CORTI; SUPPORTING CELLS; GAP JUNCTIONS; CELL COUPLING ID OUTER HAIR-CELLS; INTRACELLULAR-RECORDINGS; COMMUNICATION; COCHLEA AB Whole cell voltage clamp studies were performed upon isolated and small groups of supporting cells from the guinea pig organ of Corti in order to evaluate junctional and non-junctional membrane characteristics. Single Hensen cells have an average input resistance and capacitance of 1.03 G-OMEGA and 24.9 pF, respectively. I-V functions indicate an outward K+ rectification, which is blocked by external TEA, intracellular Cs, or photo-irradiation of intracellularly injected fluorescent dye. Voltage clamping of pairs of small groups of cells indicates that supporting cells 'share' K+ channels within the syncitium. The input impedance of coupled cells was studied during uncoupling with CO2 or octanol media. As expected, coupled cells showed an increase in input capacitance and a decrease in input resistance over single cell values. Input capacitance is a more sensitive indicator of cell coupling than dc input resistance. During uncoupling, input capacitance values drop to single cell levels prior to an increase of dc input resistance to single cell levels. Modeling the results indicates that Hensen cells are well-coupled under normal conditions and may have junctional resistances with values less than 0.1% of the non-junctional resistance. The sensitivity of the supporting cell syncitium's input impedance to small changes in junctional resistance markedly influences the syncitium's RC filter characteristics, and thus may control the frequency response of sound evoked electrical activity measurable in supporting cells in vivo. RP SANTOS-SACCHI, J (reprint author), UNIV MED & DENT NEW JERSEY, NEW JERSEY MED SCH, OTORHINOLARYNGOL LAB, MSB H518, NEWARK, NJ 07103 USA. CR BENNETT MVL, 1966, ANN NY ACAD SCI, V137, P509, DOI 10.1111/j.1749-6632.1966.tb50178.x COLE KS, 1971, BIOPHYSICS PHYSL EXC DALLOS P, 1982, SCIENCE, V218, P582, DOI 10.1126/science.7123260 Fricke H, 1925, J GEN PHYSIOL, V9, P137, DOI 10.1085/jgp.9.2.137 GOLDSTEI.AJ, 1967, ANN OTO RHINOL LARYN, V76, P414 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 GULLEY RL, 1976, J NEUROCYTOL, V5, P479, DOI 10.1007/BF01181652 HAMA K, 1977, J NEUROCYTOL, V6, P1, DOI 10.1007/BF01175410 IURATO S, 1976, ACTA OTO-LARYNGOL, V82, P57, DOI 10.3109/00016487609120863 JAHNKE K, 1975, ACTA OTO-LARYNGOL, P336 JOHNSTON M, NATURE, V286, P498 Marty A, 1983, SINGLE CHANNEL RECOR, P107 MARUYAMA Y, 1983, NATURE, V305, P228, DOI 10.1038/305228a0 OESTERLE E, 1988, J ACOUST SOC AM S1, V83, pS97 OESTERLE E, 1986, HEARING RES, V22, P229, DOI 10.1016/0378-5955(86)90099-7 OESTERLE EC, 1989, J ACOUST SOC AM, V86, P1013, DOI 10.1121/1.398092 OGEN DC, 1987, MICROELECTRODE TECHN, P63 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 PETERSEN OH, 1985, GAP JUNCTIONS, P315 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 SANTOS-SACCHI J, 1983, HEARING RES, V9, P317, DOI 10.1016/0378-5955(83)90034-5 SANTOSSACCHI J, 1984, FEB ASS RES OT CLEAR SANTOSSACCHI J, 1988, FEB ASS RES OT CLEAR SANTOS-SACCHI J, 1986, HEARING RES, V21, P205, DOI 10.1016/0378-5955(86)90219-4 SANTOSSACCHI J, 1987, ASS RES OTOLARYNGOL SANTOS-SACCHI J, 1984, HEARING RES, V14, P203, DOI 10.1016/0378-5955(84)90019-4 SANTOS-SACCHI J, 1987, HEARING RES, V25, P227, DOI 10.1016/0378-5955(87)90094-3 SANTOSSACCHI J, 1988, 4TH INT C CELL BIOL SANTOS-SACCHI J, 1985, HEARING RES, V19, P207, DOI 10.1016/0378-5955(85)90140-6 SANTOS-SACCHI J, 1989, J NEUROSCI, V9, P2954 SANTOS-SACCHI J, 1986, CELL TISSUE RES, V245, P525 SOMJEN GG, 1979, ANNU REV PHYSIOL, V41, P151 TURIN L, 1977, NATURE, V270, P56, DOI 10.1038/270056a0 ZENNER HP, 1985, HEARING RES, V18, P127, DOI 10.1016/0378-5955(85)90004-8 NR 34 TC 60 Z9 64 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 89 EP 98 DI 10.1016/0378-5955(91)90190-K PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500009 PM 2061216 ER PT J AU AVAN, P BONFILS, P LOTH, D NARCY, P TROTOUX, J AF AVAN, P BONFILS, P LOTH, D NARCY, P TROTOUX, J TI QUANTITATIVE ASSESSMENT OF HUMAN COCHLEAR FUNCTION BY EVOKED OTOACOUSTIC EMISSIONS SO HEARING RESEARCH LA English DT Article DE CLICK EVOKED OTOACOUSTIC EMISSIONS; STIMULUS FREQUENCY EMISSIONS; ACTIVE MECHANISMS; EOE THRESHOLD; PURE TONE AUDIOMETRY; EVALUATION ID STIMULATED ACOUSTIC EMISSIONS; AUDITORY-SYSTEM; HEARING-LOSS; HUMAN EAR; MODEL AB The amplitudes of evoked otoacoustic emissions (EOE) and their detection threshold were measured in 44 normal young adults and 118 patients with two categories of cochlear dysfunction, acoustic trauma and presbycusis. A different method was used for each category: detection of click EOE or of stimulus frequency emissions. A partial correlation and multivariate analysis was performed for both groups of results to investigate the relations between EOE threshold and pure tone audiometric thresholds (250 to 8000 Hz). Only one significant correlation was found, linearly relating EOE threshold and hearing threshold at 2 kHz (P < 0.001), independently of the origin of cochlear dysfunction. It suggests that EOE threshold is not frequency-specific since the frequency of EOE at threshold was nearly always close to 1 kHz. A simple model is proposed, based on the assumption that EOE amplitudes and threshold are proportional to the total number of residual active sites in the organ of Corti, i.e. to the total length of active basilar membrane. It is shown that this model accounts for the results disclosed by the statistical analysis and fits the experimental data. It can be used for quantitatively predicting the residual cochlear activity of a patient. However, the EOE threshold is only sensitive to already important cochlear alterations and this parameter does not seem to allow a follow-up of early stages of cochlear dysfunction. C1 UNIV PARIS 07,LARIBOISIERE ST LOUIS,FAC MED,CENT SERV BIOPHYS & NUCL MED,F-75221 PARIS 05,FRANCE. UNIV PARIS 05,BOUCICAUT HOSP,FAC MED NECKER ENFANTS MALADES,EAR NOSE THROAT SERV,F-75270 PARIS 06,FRANCE. UNIV PARIS 07,R DEBRE HOSP,FAC MED BICHAT,EAR NOSE THROAT SERV,F-75221 PARIS 05,FRANCE. CR RUGGERO MA, 1983, HEARING RES, V10, P283, DOI 10.1016/0378-5955(83)90094-1 AVAN P, 1990, HEARING RES, V44, P151, DOI 10.1016/0378-5955(90)90077-3 BONFILS P, 1988, J OTOLARYNGOL, V17, P207 BONFILS P, 1988, ARCH OTO-RHINO-LARYN, V245, P53, DOI 10.1007/BF00463550 BONFILS P, 1988, AUDIOLOGY, V27, P27 BONFILS P, 1990, LARYNGOSCOPE, V100, P186 COLLET L, 1989, ARCH OTOLARYNGOL, V115, P1060 DANCER A, 1988, PHYSL COCHLEE, P27 DAVIS H, 1983, HEARING RES, V9, P79, DOI 10.1016/0378-5955(83)90136-3 DIXON WJ, 1985, BMDP STATISTICAL SOF DRESCHLER WA, 1985, AUDIOLOGY, V24, P387 FURST M, 1988, J ACOUST SOC AM, V84, P222, DOI 10.1121/1.396969 GRENNER J, 1990, ACTA OTO-LARYNGOL, V109, P41, DOI 10.3109/00016489009107413 JOHNSEN NJ, 1988, SCAND AUDIOL, V17, P27, DOI 10.3109/01050398809042177 KEMP DT, 1980, HEARING RES, V2, P213, DOI 10.1016/0378-5955(80)90059-3 Kemp D T, 1986, Scand Audiol Suppl, V25, P71 KEMP DT, 1978, J ACOUST SOC AM, V64, P1386, DOI 10.1121/1.382104 KEMP DT, 1990, IN PRESS EAR HEAR 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 MANLEY G, 1983, JMECHANISMS HEARING, P36 MONTGOMERY D, 1982, INTRO LINEAR REGRESS, P275 NORTON SJ, 1987, J ACOUST SOC AM, V81, P1860, DOI 10.1121/1.394750 PROBST R, 1987, AM J OTOLARYNG, V8, P73, DOI 10.1016/S0196-0709(87)80027-3 PROBST R, 1986, HEARING RES, V21, P261, DOI 10.1016/0378-5955(86)90224-8 Schuknecht H. F., 1974, PATHOLOGY EAR STRUBE HW, 1989, HEARING RES, V38, P35, DOI 10.1016/0378-5955(89)90126-3 Sutton GJ, 1983, MECHANICS HEARING, P83 WILSON JP, 1980, PSYCHOPHYSICAL PHYSL, P72 WILSON JP, 1980, HEARING RES, V2, P233, DOI 10.1016/0378-5955(80)90060-X WIT HP, 1980, HEARING RES, V2, P253, DOI 10.1016/0378-5955(80)90061-1 ZWICKER E, 1984, J ACOUST SOC AM, V75, P1148, DOI 10.1121/1.390763 ZWICKER E, 1986, J ACOUST SOC AM, V80, P154, DOI 10.1121/1.394176 NR 33 TC 66 Z9 66 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 99 EP 112 DI 10.1016/0378-5955(91)90191-B PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500010 PM 2061217 ER PT J AU VANSTOKKUM, IHM MELSSEN, WJ AF VANSTOKKUM, IHM MELSSEN, WJ TI MEASURING AND MODELING THE RESPONSE OF AUDITORY MIDBRAIN NEURONS IN THE GRASSFROG TO TEMPORALLY STRUCTURED BINAURAL STIMULI SO HEARING RESEARCH LA English DT Article DE ANURAN; BINAURAL HEARING; NEURAL MODELING; TEMPORAL SELECTIVITY; TORUS SEMICIRCULARIS ID AMPLITUDE-MODULATED SOUNDS; DORSAL MEDULLARY NUCLEUS; DIRECTIONAL HEARING; RANA-TEMPORARIA; NERVE FIBERS; INFERIOR COLLICULUS; HAIR-CELLS; FROG; SENSITIVITY; ANURANS AB The combined selectivity for amplitude modulation frequency (AMF) and interaural time difference (ITD) was investigated for single units in the auditory midbrain of the grassfrog. Stimuli were presented by means of a closed sound system. A large number of units was found to be selective for AMF (95%) or ITD (85%) and mostly, these selectivities were intricately coupled. At zero ITD most units showed a band-pass (54%) or bimodal (24%) AMF-rate histogram. At an AMF of 36 Hz, which is equal to the pulse repetition rate of the mating call, 70% of the units possessed an asymmetrical ITD-rate histogram, whereas about 15% showed a symmetrically peaked histogram. With binaural stimulation more units appeared to be selective for AMF (95%) as was the case with monaural stimulation (85%). A large fraction of the units appeared to be most selective for ITD at AMFs of 36 and 72 Hz, whereas units seldomly exhibited ITD selectivity with unmodulated tones. Based upon previous papers (Melssen et al., 1990; Van Stokkum, 1990) a binaural model is proposed to explain these findings. An auditory midbrain neuron is modelled as a third order neuron which receives excitatory input from second order neurons. Furthermore the model neuron receives inputs from the other ear, which may be either excitatory or inhibitory. Spatiotemporal integration of inputs from both ears, followed by action potential generation, produces a combined selectivity for AMF and ITD. In particular the responses of an experimentally observed EI neuron to a set of stimuli are reproduced well by the model. C1 CATHOLIC UNIV NIJMEGEN,DEPT MED PHYS & BIOPHYS,NIJMEGEN,NETHERLANDS. RI van Stokkum, Ivo/E-7175-2015 OI van Stokkum, Ivo/0000-0002-6143-2021 CR AERTSEN AMHJ, 1986, HEARING RES, V21, P17, DOI 10.1016/0378-5955(86)90043-2 BATRA R, 1989, J NEUROPHYSIOL, V61, P257 Bibikov N. G., 1978, AKUST ZH, V24, P816 BIBIKOV NG, 1977, AKUST ZH, V23, P346 BIBIKOV NG, 1981, NEUROPHYSIOLOGY, V12, P185, DOI 10.1007/BF01068051 BRZOSKA J, 1984, ZOOL JAHRB ALLG ZOOL, V88, P179 BRZOSKA J, 1977, J COMP PHYSIOL, V118, P173 CAPRANIC.RR, 1966, J ACOUST SOC AM, V40, P1131, DOI 10.1121/1.1910198 CARNEY LH, 1989, J NEUROPHYSIOL, V62, P144 Cox D., 1980, POINT PROCESSES CRAWFORD AC, 1981, J PHYSIOL-LONDON, V315, P317 CRAWFORD AC, 1980, J PHYSIOL-LONDON, V306, P79 DERIBAUPIERRE F, 1980, HEARING RES, V3, P65, DOI 10.1016/0378-5955(80)90008-8 DUNIA R, 1989, J ACOUST SOC AM, V85, P1630, DOI 10.1121/1.397951 EGGERMONT JJ, 1990, HEARING RES, V43, P181, DOI 10.1016/0378-5955(90)90227-G EGGERMONT JJ, 1985, HEARING RES, V18, P57, DOI 10.1016/0378-5955(85)90110-8 EPPING WJM, 1986, HEARING RES, V24, P55, DOI 10.1016/0378-5955(86)90005-5 EPPING WJM, 1985, HEARING RES, V18, P223, DOI 10.1016/0378-5955(85)90040-1 EPPING WJM, 1987, J NEUROPHYSIOL, V57, P1464 EPPING WJM, 1986, HEARING RES, V24, P37, DOI 10.1016/0378-5955(86)90004-3 EPPING WJM, 1985, HEARING RES, V19, P15, DOI 10.1016/0378-5955(85)90095-4 FENG AS, 1978, J NEUROPHYSIOL, V41, P43 FENG AS, 1981, HEARING RES, V5, P201, DOI 10.1016/0378-5955(81)90046-0 FENG AS, 1982, HEARING RES, V6, P241, DOI 10.1016/0378-5955(82)90057-0 FENG AS, 1976, J NEUROPHYSIOL, V39, P871 FLEISS JL, 1988, ENCY STATISTICAL SCI, V9, P33 GERHARDT HC, 1988, J COMP PHYSIOL A, V162, P261, DOI 10.1007/BF00606090 GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 HALL JC, 1988, HEARING RES, V36, P261, DOI 10.1016/0378-5955(88)90067-6 Itoh K., 1984, Transactions of the Institute of Electronics and Communication Engineers of Japan, Section E (English), VE67 JOHANNESMA PIM, 1985, ACTA APPL MATH, V4, P201, DOI 10.1007/BF00052461 MARDIA KV, 1972, STATISTICS DIRECTION MELSSEN WJ, 1990, HEARING RES, V44, P35, DOI 10.1016/0378-5955(90)90020-P MELSSEN WJ, 1990, HEARING RES, V47, P235, DOI 10.1016/0378-5955(90)90155-I MELSSEN WJ, 1988, BASIC ISSUES HEARING, P279 MELSSEN WJ, 1987, BIOL CYBERN, V57, P403, DOI 10.1007/BF00354985 MICHELSEN A, 1986, NATURWISSENSCHAFTEN, V73, P682, DOI 10.1007/BF00366697 PERKEL DH, 1967, BIOPHYS J, V7, P419 PINDER AC, 1983, PROC R SOC SER B-BIO, V219, P371, DOI 10.1098/rspb.1983.0079 Press W. H., 1986, NUMERICAL RECIPES ROSE GJ, 1984, J COMP PHYSIOL, V154, P211, DOI 10.1007/BF00604986 ROSE GJ, 1985, J NEUROPHYSIOL, V53, P446 SCHNEIDERLOWITZ B, 1983, THESIS BONN VANSTOKKUM IHM, 1990, HEARING RES, V43, P231, DOI 10.1016/0378-5955(90)90231-D VANSTOKKUM IHM, 1987, HEARING RES, V29, P223, DOI 10.1016/0378-5955(87)90169-9 VANGELDER JJ, 1978, J ANIM ECOL, V47, P667 VANSTOKKUM IHM, 1989, HEARING RES, V41, P71, DOI 10.1016/0378-5955(89)90180-9 VLAMING MSMG, 1984, HEARING RES, V14, P191, DOI 10.1016/0378-5955(84)90018-2 Walkowiak W., 1988, P275 WALKOWIAK W, 1982, BEHAV ECOL SOCIOBIOL, V11, P247, DOI 10.1007/BF00299301 NR 50 TC 6 Z9 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 113 EP 132 DI 10.1016/0378-5955(91)90192-C PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500011 PM 2061201 ER PT J AU KUIJPERS, W TONNAER, ELGM PETERS, TA RAMAEKERS, FCS AF KUIJPERS, W TONNAER, ELGM PETERS, TA RAMAEKERS, FCS TI EXPRESSION OF INTERMEDIATE FILAMENT PROTEINS IN THE MATURE INNER-EAR OF THE RAT AND GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE INTERMEDIATE FILAMENT PROTEINS; RAT; GUINEA PIG; INNER EAR; ADULT ID MONOCLONAL-ANTIBODY; CYTOKERATIN POLYPEPTIDES; EPITHELIA; CELLS; KERATINS; TUMORS; DIFFERENTIATION; IDENTIFICATION; LOCALIZATION; DIVERSITY AB The expression of intermediate filament proteins was studied in the mature inner ear of the rat and guinea pig, using a panel of polyclonal and monoclonal antibodies directed against cytokeratins, desmin, neurofilament proteins and glial fibrillary acidic protein (GFAP). The epithelial lining of the endolymphatic space displayed a complex expression pattern of cytokeratin filament proteins, suggesting greater cell diversity than was known sofar from morphological studies. The cytokeratin antibodies when applied to the inner ear tissues revealed the presence of only cytokeratin polypeptides which are typical of simple epithelia (i.e. nos. 7, 8, 18, and 19). Profound differences in cytokeratin expression patterns were, however, found in the various cell types of both the cochlear and vestibular partition. Remarkably, the sensory cells appeared to be devoid of both cytokeratins and neurofilament proteins. Staining with a 200 kDa neurofilament antibody displayed the presence of different populations of ganglion cells in the spiral ganglion and the vestibular ganglion. There was no reaction with antibodies directed against desmin and GFAP. The great resemblance of the intermediate filament protein expression patterns in the inner ear of the rat and guinea pig indicates a close similarity between the different epitopes. C1 UNIV HOSP NIJMEGEN,DEPT OTORHINOLARYNGOL,NIJMEGEN,NETHERLANDS. CR AEBI U, 1986, NATURE, V323, P560, DOI 10.1038/323560a0 ANNIKO M, 1989, ACTA OTO-LARYNGOL, V107, P191, DOI 10.3109/00016488909127498 ANNIKO M, 1989, ACTA OTO-LARYNGOL, V108, P206, DOI 10.3109/00016488909125520 ANNIKO M, 1986, ORL J OTO-RHINO-LARY, V48, P98 ANNIKO M, 1987, ACTA OTOLARYNGOL S S, V437, P1 ANNIKO M, 1989, ACTA OTO-LARYNGOL, V108, P385, DOI 10.3109/00016488909125544 ARNOLD W, 1989, ORL J OTO-RHINO-LARY, V51, P339 BOSHER SK, 1971, J PHYSIOL-LONDON, V212, P739 FEITZ WFJ, 1986, J UROLOGY, V136, P922 FRANKE WW, 1981, J MOL BIOL, V153, P933, DOI 10.1016/0022-2836(81)90460-5 FRANKE WW, 1987, EXP CELL RES, V173, P17, DOI 10.1016/0014-4827(87)90328-4 HAFIDI A, 1989, HEARING RES, V42, P203, DOI 10.1016/0378-5955(89)90145-7 HERMAN CJ, 1985, AM J PATHOL, V120, P419 JONSSON R, 1986, J IMMUNOL METHODS, V88, P109, DOI 10.1016/0022-1759(86)90058-X KASPER M, 1987, ARCH OTO-RHINO-LARYN, V244, P66, DOI 10.1007/BF00453494 KIMURA RS, 1969, ANN OTO RHINOL LARYN, V78, P542 KUIJPERS W, 1969, THESIS U NIJMEGEN NE LANE EB, 1985, ANN NY ACAD SCI, V455, P241, DOI 10.1111/j.1749-6632.1985.tb50415.x MANNI JJ, 1987, HEARING RES, V26, P229, DOI 10.1016/0378-5955(87)90059-1 MCLEAN IW, 1974, J HISTOCHEM CYTOCHEM, V22, P1077 MOLENGRAFT V, 1986, VIRCHOWS ARCH B, V51, P285 MOLL R, 1982, CELL, V31, P11, DOI 10.1016/0092-8674(82)90400-7 MUIJEN GNP, 1986, EXP CELL RES, V162, P97 OSBORN M, 1984, ANN NY ACAD SCI, V455, P669 PURKIS PE, 1990, IN PRESS J CELL SCI QUINLAN RA, 1985, ANN NY ACAD SCI, V455, P282, DOI 10.1111/j.1749-6632.1985.tb50418.x RAMAEKERS F, 1983, LAB INVEST, V49, P353 RAMAEKERS F, 1987, EXP CELL RES, V170, P235, DOI 10.1016/0014-4827(87)90133-9 Ramaekers FCS, 1987, APPLICATION MONOCLON, P65 RAMAEKERS FCS, 1989, PROSTATE, V14, P323, DOI 10.1002/pros.2990140405 RAMAEKERS FCS, 1983, HISTOCHEM J, V15, P691, DOI 10.1007/BF01002988 RAPHAEL Y, 1987, DIFFERENTIATION, V35, P151, DOI 10.1111/j.1432-0436.1987.tb00163.x ROMAND R, 1988, BRAIN RES, V462, P167, DOI 10.1016/0006-8993(88)90601-4 ROSENBLUTH J, 1962, J CELL BIOL, V12, P329, DOI 10.1083/jcb.12.2.329 SCHAAFSMA HE, 1989, HISTOCHEMISTRY, V91, P151, DOI 10.1007/BF00492389 SCHMIDT RS, 1963, J EXP ZOOL, V153, P227, DOI 10.1002/jez.1401530305 SCHROTT A, 1988, ARCH OTO-RHINO-LARYN, V245, P250, DOI 10.1007/BF00463937 SCHULTE BA, 1989, J HISTOCHEM CYTOCHEM, V37, P1787 Schwartz A. M, 1986, NEUROBIOLOGY HEARING, P271 SPASSOVA I, 1982, J HIRNFORSCH, V23, P652 SUN TT, 1985, ANN NY ACAD SCI, V455, P307, DOI 10.1111/j.1749-6632.1985.tb50419.x TONNAER EL, 1990, J HISTOCHEM CYTOCHEM, V38, P1223 Traub P., 1985, INTERMEDIATE FILAMEN TSENG SCG, 1982, CELL, V30, P361, DOI 10.1016/0092-8674(82)90234-3 VERHAGEN APM, 1988, PROSTATE, V13, P25, DOI 10.1002/pros.2990130104 VOLLRATH M, 1985, DIFFERENTIATION, V29, P243, DOI 10.1111/j.1432-0436.1985.tb00323.x WIKSTROM SO, 1988, ACTA OTO-LARYNGOL, V106, P71, DOI 10.3109/00016488809107373 NR 47 TC 36 Z9 37 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 133 EP 146 DI 10.1016/0378-5955(91)90193-D PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500012 PM 1712009 ER PT J AU HORNER, KC AF HORNER, KC TI OLD THEME AND NEW REFLECTIONS - HEARING IMPAIRMENT ASSOCIATED WITH ENDOLYMPHATIC HYDROPS SO HEARING RESEARCH LA English DT Article DE ENDOLYMPHATIC HYDROPS; HYDROPS; MENIERES DISEASE; PERILYMPH; ENDOLYMPH; HEARING; COCHLEA ID GUINEA-PIG COCHLEA; HAIR-CELLS; FLOW-RATE; PRESSURE; FLUID; STEREOCILIA; PERILYMPH; AQUEDUCT AB The cause(s) of the hearing impairment associated with Menieres's disease are not understood but are undoubtedly associated with the inner ear endolymphatic hydrops. Two major hypotheses have been proposed and widely received: endolymphatic overpressure followed by leaky membranes and subsequently the mixing of high K+ endolymph with perilymph. Our recent data on an experimental model of endolymphatic hydrops have provided grounds for renewed reflections on the pathology. Indeed our data might be interpreted without involving either of the above hypotheses and suggests that the symptoms of Meniere's disease might be accounted for by a flow of perilymph from scala vestibuli towards scala tympani with the mixing of the two perilymphs which are similar but not identical in composition. The higher K+ concentration arriving from the scala vestibuli into the scala tympani at the apex of the cochlea via the helicotrema is likely to be toxic to hair cell and auditory nerve fiber function. The mixing of the two perilymphs could result in deterioration of low frequency sensitivity, provoke low frequency tinnitus and in the long term cause spiral ganglion cell degeneration at the apex of the cochlea. The feeling of fullness in the ear might be the result of the decreasing perilymph volume in the scala vestibuli which could give rise to inner ear conductive losses. The patency of the cochlear aqueduct might play a role in determining the high risk group of individuals likely to manifest the symptoms of endolymphatic hydrops. RP HORNER, KC (reprint author), HOP PELLEGRIN,AUDIOL EXPTL LAB,INSERM,U229,PL AMELIE RABA LEON,F-33076 BORDEAUX,FRANCE. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 147 EP 156 DI 10.1016/0378-5955(91)90194-E PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500013 PM 2061203 ER PT J AU DESPRES, G HAFIDI, A ROMAND, R AF DESPRES, G HAFIDI, A ROMAND, R TI IMMUNOHISTOCHEMICAL LOCALIZATION OF NERVE GROWTH-FACTOR RECEPTOR IN THE COCHLEA AND IN THE BRAIN-STEM OF THE PERINATAL RAT SO HEARING RESEARCH LA English DT Article DE NGF; NGF-RECEPTOR; COCHLEA; BRAIN-STEM; DEVELOPMENT; IMMUNOHISTOCHEMISTRY ID RETROGRADE AXONAL-TRANSPORT; EMBRYONIC OTIC VESICLE; HIGH-AFFINITY; VESTIBULAR GANGLION; CHOLINERGIC NEURONS; PERIPHERAL-NERVE; BASAL FOREBRAIN; BINDING-SITES; NGF-RECEPTOR; SYSTEM AB Nerve growth factor receptor (NGF-R) localization was studied immunohistochemically in the cochlea and in the brainstem of the perinatal rat, using a specific monoclonal antibody directed against the rat NGF-R. In the cochlea, NGF-R immunoreactivity is positive during the whole perinatal period studied, and is located at the hair cell level, in fibers that reach the organ of Corti, in the intraganglionic spiral bundle and in some small bundles of fibers in the auditory nerve. In the brainstem, NGF-R is detected in auditory structures such as the ventral cochlear nucleus, the superior olivary complex, the nuclei of the trapezoid body and the trapezoid body. Many auditory structures labelled by the NGF-R antibody are implicated in the efferent cochlear innervation. These results suggest that NGF could be implicated in interactions between auditory receptors and efferent innervation of the developing cochlea. This coincides with findings on the immunohistochemical localization of NGF-like protein in the organ of Corti of the developing rat. Moreover, these observations could be related to an early prenatal development of auditory efferent innervation. C1 UNIV CLERMONT FERRAND,NEUROBIOL LAB,F-63177 CLERMONT FERRAND,FRANCE. CR ALTSCHULER RA, 1984, J HISTOCHEM CYTOCHEM, V32, P839 BERND P, 1989, DEV BIOL, V134, P11, DOI 10.1016/0012-1606(89)90073-0 BERND P, 1984, J BIOL CHEM, V259, P5509 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BUCK CR, 1987, P NATL ACAD SCI USA, V84, P3060, DOI 10.1073/pnas.84.9.3060 CHANDLER CE, 1984, J BIOL CHEM, V259, P6882 CHAO MV, 1986, SCIENCE, V232, P518, DOI 10.1126/science.3008331 DAVIES AM, 1987, NATURE, V326, P353, DOI 10.1038/326353a0 ECKENSTEIN F, 1988, BRAIN RES, V446, P149, DOI 10.1016/0006-8993(88)91305-4 FINN PJ, 1987, J NEUROCYTOL, V16, P639, DOI 10.1007/BF01637656 GNAHN H, 1983, DEV BRAIN RES, V9, P45, DOI 10.1016/0165-3806(83)90107-4 Godfrey D.A., 1985, P163 GREEN SH, 1986, J BIOL CHEM, V261, P5316 GREENE LA, 1980, ANNU REV NEUROSCI, V3, P353, DOI 10.1146/annurev.ne.03.030180.002033 HEFTI F, 1986, NEUROSCI LETT, V69, P37, DOI 10.1016/0304-3940(86)90410-6 HEFTI F, 1985, NEUROSCIENCE, V14, P55, DOI 10.1016/0306-4522(85)90163-0 HENDRY IA, 1974, BRAIN RES, V68, P103, DOI 10.1016/0006-8993(74)90536-8 HONEGGER P, 1982, DEV BRAIN RES, V3, P229, DOI 10.1016/0165-3806(82)90023-2 HSU SM, 1981, J HISTOCHEM CYTOCHEM, V29, P577 JOHNSON EM, 1987, J NEUROSCI, V7, P923 JOHNSON EM, 1988, TRENDS NEUROSCI, V11, P299, DOI 10.1016/0166-2236(88)90090-2 KORSCHING S, 1986, TRENDS NEUROSCI, V9, P570, DOI 10.1016/0166-2236(86)90179-7 KORSCHING S, 1983, NEUROSCI LETT, V39, P1, DOI 10.1016/0304-3940(83)90155-6 LEFEBVRE PP, 1990, BRAIN RES, V507, P254, DOI 10.1016/0006-8993(90)90279-K LEVIMONT.R, 1968, PHYSIOL REV, V48, P534 OSEN KK, 1984, ARCH ITAL BIOL, V122, P169 RAIVICH G, 1987, NEUROSCIENCE, V20, P23, DOI 10.1016/0306-4522(87)90003-0 RASMUSSEN GL, 1953, J COMP NEUROL, V99, P61, DOI 10.1002/cne.900990105 Rasmussen G.L, 1942, ANAT REC, V82, P441 REPRESA J, 1989, DEV BIOL, V134, P21, DOI 10.1016/0012-1606(89)90074-2 RICHARDSON PM, 1986, J NEUROSCI, V6, P2312 RICHARDSON PM, 1982, BRAIN RES, V246, P57, DOI 10.1016/0006-8993(82)90141-X RIOPELLE RJ, 1981, NEUROSCI LETT, V25, P311, DOI 10.1016/0304-3940(81)90410-9 Romand R, 1984, ULTRASTRUCTURAL ATLA, P165 SHNEIDERMAN A, 1985, HEARING RES, V19, P199, DOI 10.1016/0378-5955(85)90139-X SPRINGER JE, 1988, EXP NEUROL, V102, P354, DOI 10.1016/0014-4886(88)90231-2 SPRINGER JE, 1987, J NEUROSCI RES, V17, P111, DOI 10.1002/jnr.490170204 STACH RW, 1987, J NEUROSCI RES, V17, P1, DOI 10.1002/jnr.490170102 STEEL KP, 1983, HEARING RES, V9, P327, DOI 10.1016/0378-5955(83)90035-7 SUTTER A, 1979, J BIOL CHEM, V254, P5972 TANIUCHI M, 1985, J CELL BIOL, V101, P1100, DOI 10.1083/jcb.101.3.1100 THOENEN H, 1980, PHYSIOL REV, V60, P1284 THOENEN H, 1987, REV PHYSIOL BIOCH P, V109, P145, DOI 10.1007/BFb0031026 Warr W. B., 1982, CONTRIB SENS PHYSIOL, V7, P1 WHITE JS, 1983, J COMP NEUROL, V219, P203, DOI 10.1002/cne.902190206 YAN Q, 1988, J NEUROSCI, V8, P3481 NR 46 TC 28 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 157 EP 165 DI 10.1016/0378-5955(91)90195-F PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500014 PM 1648058 ER PT J AU KIM, DO PARHAM, K AF KIM, DO PARHAM, K TI AUDITORY-NERVE SPATIAL ENCODING OF HIGH-FREQUENCY PURE-TONES - POPULATION RESPONSE PROFILES DERIVED FROM D' MEASURE ASSOCIATED WITH NEARBY PLACES ALONG THE COCHLEA SO HEARING RESEARCH LA English DT Article DE FREQUENCY DISCRIMINATION; AUDITORY NERVE; POPULATION RESPONSE; SIGNAL DETECTION THEORY ID DISCHARGE RATE; SINGLE TONES; FIBERS; REPRESENTATION; NOISE; CATS; THRESHOLDS; DURATION AB We examined a measure of discriminability in auditory nerve (AN) population responses that may underlie behavioral frequency discrimination of high-frequency pure tones in the cat. Population responses of high- (> = 15 spikes/s) and low- (< 15 spikes/s) spontaneous rate (SR) AN fibers in unanesthetized decerebrate cats to 5 kHz pure tones were measured in the form of mean, mu, and standard deviation, sigma, of spike counts for 0.2 s tone bursts. The AN responses were analyzed in terms of a d'(e)(x, DELTA-x) associated with adjoining cochlear places as defined in the manner of signal detection theory. We also examined sigma-d'(e)(x, DELTA-x), a spatial summation of the discriminability measure. The major findings are: (1) the d'(e)(x, DELTA-x) function conveys information about 5 kHz pure tone frequency over a region of +/- 0.5 to 1.0 octave, or +/- 1.67 to 3.33 mm, around the characteristic place (CP), with the region being narrower at lower stimulus levels; (2) at 30 dB SPL, the integrated d'(e)(x, DELTA-x) discriminability scores are similar for the apical and basal regions surrounding the CP whereas, at 70 dB SPL, the scores are higher for the apical region than for the basal region; and (3) at 50 and 70 dB SPL, the integrated d'(e)(x, DELTA-x) discriminability scores of low-SR fibers were higher than those of high-SR fibers although, at 30 dB SPL, the latter were higher than the former. By using the cat cochlear frequency-place relationship and the inner hair cell (IHC) spacing, we interpret that the cat's frequency difference limen, DELTA-f/f = 0.0088 at 4 kHz [Elliott et al., 1960, J. Acoust. Soc. Am. 32, 380-384], corresponds to a shift of cochlear excitation profile by 4.5 IHCs. From the present analysis of AN responses, we conclude that, for high-frequency pure tones, the d'(e)(x, DELTA-x) code, an example of rate-place code, of frequency provides sufficient information to support the cat's behavioral frequency discrimination. C1 UNIV CONNECTICUT,CTR HLTH,SURG RES CTR,FARMINGTON,CT 06032. UNIV CONNECTICUT,CTR HLTH,CTR NEUROL SCI,FARMINGTON,CT 06032. RP KIM, DO (reprint author), UNIV CONNECTICUT,CTR HLTH,DEPT SURG,DIV OTORHINOLARYNGOL,ROOM L-1071,FARMINGTON,CT 06032, USA. 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S., 1938, HEARING ITS PSYCHOL TEICH MC, 1985, J ACOUST SOC AM, V77, P1110, DOI 10.1121/1.392176 VERSCHUURE J, 1980, HEARING RES, V2, P397, DOI 10.1016/0378-5955(80)90074-X VIEMEISTER NF, 1988, HEARING RES, V34, P267, DOI 10.1016/0378-5955(88)90007-X WEVER EG, 1977, J ACOUST SOC AM, V61, P178 Wright A, 1987, Acta Otolaryngol Suppl, V444, P1 YOUNG ED, 1979, J ACOUST SOC AM, V66, P470 YOUNG ED, 1986, J ACOUST SOC AM, V79, P426, DOI 10.1121/1.393530 Zwicker E., 1970, FREQUENCY ANAL PERIO, P376 NR 45 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 167 EP 179 DI 10.1016/0378-5955(91)90196-G PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500015 PM 2061204 ER PT J AU SUBRAMANIAM, M CAMPO, P HENDERSON, D AF SUBRAMANIAM, M CAMPO, P HENDERSON, D TI THE EFFECT OF EXPOSURE LEVEL ON THE DEVELOPMENT OF PROGRESSIVE RESISTANCE TO NOISE SO HEARING RESEARCH LA English DT Article DE THRESHOLD SHIFT; EXPOSURE LEVEL; TOUGHENING ID AUDIBILITY CURVE; PERIODIC REST; CHINCHILLA AB The effect of exposure level on the development of progressive resistance to temporary threshold shift caused by exposures to an octave band of noise centered at 0.5 kHz was explored using chinchillas. The animals were exposed to either 85,95 or 100 dB SPL for six hours a day for ten days. Hearing thresholds were recorded electrophysiologically, prior to and after each daily exposure. A trend toward decreasing threshold shift with increase in the number of exposures was seen at all the levels. The amount of threshold shift appeared to depend upon the level as well as the test frequency. The findings are discussed in the light of results of previous studies and possible mechanisms involved in the process of 'toughening' are hypothesized. C1 SUNY BUFFALO,DEPT COMMUNICAT DISORDERS & SCI,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214. INST NATL RECH & SECUR,VANDOEUVRE NANCY,FRANCE. CR BYRNE C, 1991, IN PRESS J ACOUST SO CANLON B, 1988, HEARING RES, V34, P197, DOI 10.1016/0378-5955(88)90107-4 CARDER H M, 1971, Transactions of the American Academy of Ophthalmology and Oto-Laryngology, V75, P1346 CLARK WW, 1987, J ACOUST SOC AM, V82, P1253, DOI 10.1121/1.395261 ELDRED KM, 1955, CRITERIA SHORT TIME, P55 FIORINO F, 1991, IN PRESS 2ND P INT S GIRAUDIPERRY DM, 1982, J ACOUST SOC AM, V72, P1387, DOI 10.1121/1.388444 HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 LIBERMAN MC, 1990, 1990 ASS RES OT ST P Miller J. D., 1963, ACTA OTO-LARYNGOL, V176, P1 MILLER JD, 1970, J ACOUST SOC AM, V48, P513, DOI 10.1121/1.1912166 MILLS JH, 1990, 1990 ASS RES OT ST P SINEX DG, 1987, J ACOUST SOC AM, V82, P1265, DOI 10.1121/1.395829 NR 13 TC 41 Z9 42 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 181 EP 187 DI 10.1016/0378-5955(91)90197-H PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500016 PM 2061206 ER PT J AU BERNSTEIN, LR AF BERNSTEIN, LR TI MEASUREMENT AND SPECIFICATION OF THE ENVELOPE CORRELATION BETWEEN 2 NARROW BANDS OF NOISE SO HEARING RESEARCH LA English DT Article DE CORRELATION; ENVELOPE; NARROW-BAND NOISE ID COMODULATION MASKING RELEASE; INTER-AURAL CORRELATION; CORRELATION DISCRIMINATION; CORRELATION PERCEPTION; LEVEL; BANDWIDTH; MASKER AB Empirical measurements show that when two independent, narrow-band, Gaussian noises are 'mixed' or combined according to the method specified by Licklider and Dzendolet (1948) [Science, 107, 121-124], the correlation coefficient between the envelopes (r(Exy)) of the two resulting narrow-band noises is approximately equal to the square of the correlation between the waveforms (r(xy)). This relation also holds for waveform correlations produced by de-correlating two perfectly correlated noises by the addition of a sinusoid (at the center frequency) that is phase-reversed (N0S-pi). This is true so long as the signal-to-noise ratio is small. A method is detailed whereby any desired r(Exy) may be achieved with reasonable accuracy between two noises of the same or different center-frequency. This method may prove particularly useful in the study of listeners' sensitivities to dissimilarities in the envelope fluctuation of bands of noise occupying discrete spectral loci, a topic currently of interest. It is hoped that the empirical relations between r(xy) and r(Exy) may stimulate efforts to derive or locate analytic expressions that relate the two. C1 UNIV CONNECTICUT,CTR HLTH,DEPT SURG OTOLARYNGOL,FARMINGTON,CT 06032. RP BERNSTEIN, LR (reprint author), UNIV CONNECTICUT,CTR HLTH,SURG RES CTR,CTR NEUROL SCI,FARMINGTON,CT 06032, USA. CR COHEN MF, 1987, J ACOUST SOC AM, V81, P452, DOI 10.1121/1.394910 DURLACH NI, 1986, J ACOUST SOC AM, V79, P1548, DOI 10.1121/1.393681 GABRIEL KJ, 1981, J ACOUST SOC AM, V69, P1394, DOI 10.1121/1.385821 GRANTHAM DW, 1979, J ACOUST SOC AM, V65, P1509, DOI 10.1121/1.382915 HALL JW, 1984, J ACOUST SOC AM, V76, P50, DOI 10.1121/1.391005 HALL JW, 1990, J ACOUST SOC AM, V87, P269, DOI 10.1121/1.399294 JEFFRESS LA, 1962, J ACOUST SOC AM, V34, P1658, DOI 10.1121/1.1909077 LANGFORD TL, 1964, J ACOUST SOC AM, V36, P1455, DOI 10.1121/1.1919224 LICKLIDER JCR, 1948, SCIENCE, V107, P121, DOI 10.1126/science.107.2770.121-a MCFADDEN D, 1986, J ACOUST SOC AM, V80, P1658, DOI 10.1121/1.394277 MCNEMAR Q, 1969, PSYCHOL STATISTICS MOORE BCJ, 1990, J ACOUST SOC AM, V87, P2628, DOI 10.1121/1.399055 MOORE BCJ, 1990, J ACOUST SOC AM, V88, P725, DOI 10.1121/1.399775 POLLACK I, 1959, J ACOUST SOC AM, V31, P1250, DOI 10.1121/1.1907852 POLLACK I, 1959, J ACOUST SOC AM, V31, P1616, DOI 10.1121/1.1907669 RICHARDS VM, 1987, J ACOUST SOC AM, V82, P1621, DOI 10.1121/1.395153 RICHARDS VM, 1988, HEARING RES, V35, P47, DOI 10.1016/0378-5955(88)90039-1 ROBINSON DE, 1963, J ACOUST SOC AM, V35, P1947, DOI 10.1121/1.1918864 SCHOONEVELDT GP, 1987, J ACOUST SOC AM, V82, P1944, DOI 10.1121/1.395639 NR 19 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 189 EP 194 DI 10.1016/0378-5955(91)90198-I PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500017 PM 2061207 ER PT J AU ZHOU, N PARKS, TN AF ZHOU, N PARKS, TN TI PHARMACOLOGY OF EXCITATORY AMINO-ACID NEUROTRANSMISSION IN NUCLEUS LAMINARIS OF THE CHICK SO HEARING RESEARCH LA English DT Article DE KAINIC ACID; AMPA; KYNURENIC ACID; QUINOXALINEDIONES; AUDITORY SYSTEM ID AVIAN COCHLEAR NUCLEUS; D-ASPARTATE RECEPTORS; SYNAPTIC TRANSMISSION; KAINATE RECEPTORS; AUDITORY-NERVE; ANTAGONISTS; SYSTEM; AXON AB The receptors mediating excitatory neurotransmission from the cochlear nucleus (nuc. magnocellularis, NM) to third-order auditory neurons in nucleus laminaris (NL) of the chicken were studied using in vitro brain slices, bath application of drugs, and electrophysiological recording of postsynaptic field potentials. Postsynaptic responses in NL were blocked completely, in a concentration-dependent and reversible fashion, by bath application of the broad-spectrum excitatory amino acid (EAA) antagonist kynurenic acid, the 'non-NMDA' EAA receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), and the EAA agonists domoic acid, kainic acid, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and quisqualic acid. The selective NMDA receptor antagonists 3-((-)-2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP) and dibenzocycloheptenimine (MK-801) had no effect. The results demonstrate that excitatory input from the cochlear nucleus to NL is mediated by non-NMDA (G2) EAA receptors which exhibit some of the pharmacologic features typical of the AMPA receptors defined by binding studies. C1 UNIV UTAH, SCH MED, DEPT ANAT, SALT LAKE CITY, UT 84132 USA. CR AGRAWAL SG, 1986, BRIT J PHARMACOL, V87, P345 BOULTER J, 1990, SCIENCE, V249, P1033, DOI 10.1126/science.2168579 COLLINGRIDGE GL, 1989, PHARMACOL REV, V41, P143 COLLINS GGS, 1989, NEUROPHARMACOLOGY, V28, P1123, DOI 10.1016/0028-3908(89)90127-5 HACKETT JT, 1982, NEUROSCIENCE, V7, P1455, DOI 10.1016/0306-4522(82)90257-3 HENLEY J M, 1989, New Biologist, V1, P153 HONORE T, 1988, SCIENCE, V241, P701, DOI 10.1126/science.2899909 HONORE T, 1989, MED RES REV, V9, P1, DOI 10.1002/med.2610090102 JACKSON H, 1985, NEUROSCIENCE, V16, P171, DOI 10.1016/0306-4522(85)90054-5 JACKSON H, 1982, J NEUROSCI, V2, P1736 KEINANEN K, 1990, SCIENCE, V249, P556, DOI 10.1126/science.2166337 Konishi M, 1988, AUDITORY FUNCTION NE, P721 LAMBOLEZ B, 1990, NATURE, V347, P26, DOI 10.1038/347026b0 LODGE D, 1990, TRENDS PHARMACOL SCI, V11, P81, DOI 10.1016/0165-6147(90)90323-Z MARTIN MR, 1985, HEARING RES, V17, P153, DOI 10.1016/0378-5955(85)90018-8 MONAGHAN DT, 1989, ANNU REV PHARMACOL, V29, P365 NEMETH EF, 1983, NEUROSCI LETT, V40, P39, DOI 10.1016/0304-3940(83)90089-7 NEMETH EF, 1985, NEUROSCI LETT, V59, P297, DOI 10.1016/0304-3940(85)90148-X OBRIEN RJ, 1986, J NEUROSCI, V6, P3275 PARKS TN, 1987, CURR TOP DEV BIOL, V21, P309 PARKS TN, 1983, J COMP NEUROL, V214, P32, DOI 10.1002/cne.902140104 PERQUANSKY M, 1989, J NEUROSCI, V9, P70 REPRESA A, 1987, NEUROSCIENCE, V20, P739, DOI 10.1016/0306-4522(87)90237-5 Rubel EW, 1988, AUDITORY FUNCTION NE, P3 VERDOORN TA, 1989, MOL PHARMACOL, V35, P360 WATKINS JC, 1990, TRENDS PHARMACOL SCI, V11, P25, DOI 10.1016/0165-6147(90)90038-A WATKINS JC, 1989, NMDA RECEPTOR WICKESBERG RE, 1989, BRAIN RES, V486, P39, DOI 10.1016/0006-8993(89)91275-4 NR 28 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 MAR PY 1991 VL 52 IS 1 BP 195 EP 200 DI 10.1016/0378-5955(91)90199-J PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500018 PM 1648059 ER PT J AU FAINGOLD, CL BOERSMA, CA ANDERSON CASPARY, DM AF FAINGOLD, CL BOERSMA, CA ANDERSON CASPARY, DM TI INVOLVEMENT OF GABA IN ACOUSTICALLY-EVOKED INHIBITION IN INFERIOR COLLICULUS NEURONS SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; GABA; INTENSITY-INDUCED INHIBITION; BICUCULLINE; NIPECOTIC ACID; BINAURAL INHIBITION; RATE-INTENSITY FUNCTION; NONMONOTONIC ID EPILEPSY-PRONE RAT; SUPERIOR OLIVARY NEURONS; GAMMA-AMINOBUTYRIC ACID; STEM AUDITORY NUCLEI; BRAIN-STEM; RESPONSE PROPERTIES; LATERAL LEMNISCUS; GABAERGIC NEURONS; DORSAL NUCLEUS; GUINEA-PIG AB Most criteria for establishing GABA as an inhibitory neurotransmitter in the central nucleus of inferior colliculus (ICc) have been satisfied, but the role of GABA in acoustic coding in ICc is not established. The present study examined this issue by evaluating the effects of iontophoretic application of agents that alter activity at GABA receptors on potential forms of acoustically-evoked inhibition in ICc neurons. Application of the GABA(A) antagonist, bicuculline, selectively blocked the firing reduction at high intensities observed during non-monotonic rate-intensity functions in ICc neurons. Binaural inhibition was selectively blocked by bicuculline and increased by nipecotic acid. Application of GABA, nipecotic acid (GABA uptake inhibitor) and a benzodiazepine (flurazepam), which enhances the action of GABA, increased the duration and intensity of ipsilateral inhibition and response pause, while bicuculline blocked these acoustically-evoked inhibitory events. Offset inhibition was increased by nipecotic acid application and reduced by bicuculline with the appearance of an offset peak. The present data support an important role for GABA as a neurotransmitter, mediating, in part, non-monotonicity, binaural inhibition, response pause and offset inhibition in ICc neurons. Alterations of these GABA-mediated inhibitory phenomena may occur in auditory dysfunctions observed with aging and audiogenic seizures. RP FAINGOLD, CL (reprint author), SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,POB 19230,SPRINGFIELD,IL 62794, USA. 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L., 1987, NEUROTRANSMITTERS EP, P215 FAINGOLD CL, 1986, EXP NEUROL, V93, P145, DOI 10.1016/0014-4886(86)90154-8 FAINGOLD C L, 1988, Society for Neuroscience Abstracts, V14, P253 FAINGOLD CL, 1991, NEUROBIOLOGY HEARING, V2 FAINGOLD CL, 1989, HEARING RES, V40, P127, DOI 10.1016/0378-5955(89)90106-8 FAINGOLD CL, 1989, BRAIN RES, V500, P302, DOI 10.1016/0006-8993(89)90326-0 FAINGOLD CL, 1990, ASS RES OTOLARYNGOL, P58 FINAGOLD CL, 1990, EXP NEUROL, V108, P55 FINLAYSON PG, 1989, HEARING RES, V38, P221, DOI 10.1016/0378-5955(89)90067-1 FISHER SK, 1976, J NEUROCHEM, V27, P1145, DOI 10.1111/j.1471-4159.1976.tb00321.x FLAMMINO F, 1975, J ACOUST SOC AM, V57, P692, DOI 10.1121/1.380494 GONSALVES SF, 1988, J PHARMACOL EXP THER, V244, P79 HAVEY DC, 1980, ELECTROEN CLIN NEURO, V48, P249, DOI 10.1016/0013-4694(80)90313-2 HERMAN GE, 1977, J GERONTOL, V32, P187 KUWADA S, 1980, PSYCHOPHYSICAL PHYSL, P401 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 LOPEZCOLOME AM, 1978, NEUROSCIENCE, V3, P1069, DOI 10.1016/0306-4522(78)90124-0 MAURER JF, 1979, HEARING AGING, P33 MEHTA AK, 1988, J PHARMACOL EXP THER, V246, P558 MOISEFF A, 1985, Society for Neuroscience Abstracts, V11, P735 MOORE JK, 1987, J COMP NEUROL, V260, P157, DOI 10.1002/cne.902600202 MOORE MJ, 1983, J NEUROSCI, V3, P237 NAGAI T, 1985, J COMP NEUROL, V231, P260, DOI 10.1002/cne.902310213 NELSON PG, 1963, J NEUROPHYSIOL, V26, P908 OLIVER DL, 1989, J NEUROSCI, V9, P967 Olsen R W, 1986, Adv Neurol, V44, P365 Ottersen O. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 201 EP 216 DI 10.1016/0378-5955(91)90200-S PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500019 PM 2061208 ER PT J AU QUIRK, WS SHAPIRO, BD MILLER, JM NUTTALL, AL AF QUIRK, WS SHAPIRO, BD MILLER, JM NUTTALL, AL TI NOISE-INDUCED CHANGES IN RED-BLOOD-CELL VELOCITY IN LATERAL WALL VESSELS OF THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE NOISE; RED BLOOD CELL VELOCITY; STRIA VASCULARIS; VASOCONSTRICTION; HOMEOSTASIS ID GUINEA-PIG; FLOW; EXPOSURE AB The effects of loud sound on the microvasculature of the cochlea are not well characterized or understood. Morphological changes in the stria vascularis and changes in blood flow are known to occur during or following sound stimulation, however the effects on cochlear blood flow appear to be complex. Studies have shown that noise exposure may produce increases in blood flow, decreases in blood flow, or no measureable change in blood flow. These inconsistent results probably reflect the various noise exposure parameters, the animal model used, and could be a function of the specific procedures utilized to assess blood flow changes. The purpose of the current study was to investigate the effects of one specific class of sound exposure (high intensity noise) on red blood cell velocity in the capillaries of the second turn of the rat cochlea using intravital microscopy. This class of sound exposure was selected in order to attempt a confirmation of previous findings of increased blood flow (Perlman and Kimura, 1962) using the quantitative technique of red blood cell velocity measurement. Following determination of pre-exposure red blood cell velocities in capillaries of the rat cochlea second turn, animals were exposed to 133 dB or 110 dB broad-band noise for ten minutes. The red blood cell velocity was recorded continuously during the exposure. Exposure to both sound intensities disrupted stable and orderly baseline flow patterns and resulted in overall intensity-dependent increases in red blood cell velocity. Qualitatively, we observed aggregations of red blood cells, local vasoconstriction and directional reversals of red blood cell flow during noise exposure at both intensities. These results may represent the interaction of several mechanisms that participate in the control of blood flow in the cochlea during noise exposure. RP QUIRK, WS (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR Angelborg C, 1979, Adv Otorhinolaryngol, V25, P41 AXELSSON A, 1990, ACTA OTO-LARYNGOL, V109, P263, DOI 10.3109/00016489009107442 AXELSSON A, 1981, ACTA OTO-LARYNGOL, V91, P237, DOI 10.3109/00016488109138504 AXELSSON A, 1982, NEW PERSPECTIVES NOI, P49 Bohne B.A., 1976, EFFECTS NOISE HEARIN, P41 DENGERINK H, 1985, ACTA OTO-LARYNGOL, V100, P19, DOI 10.3109/00016488509108582 DUVALL AJ, 1974, ANN OTO RHINOL LARYN, V83, P498 FRUHSTORFER B, 1988, INT J NEUROSCI, V39, P197, DOI 10.3109/00207458808985704 GRANGER HJ, 1988, AM J OTOLARYNG, V9, P264, DOI 10.1016/S0196-0709(88)80035-8 HAWKINS JE, 1971, ANN OTO RHINOL LARYN, V80, P903 HILLERDAL M, 1987, ACTA OTO-LARYNGOL, V104, P270, DOI 10.3109/00016488709107328 MCLAREN GM, UNPUB EFFECTS ARGINI MILES FP, 1989, HEARING RES, V33, P191 MORIMITS.T, 1965, ANN OTO RHINOL LARYN, V74, P22 NUTTALL AL, 1981, HEARING RES, V5, P285, DOI 10.1016/0378-5955(81)90052-6 NUTTALL AL, 1987, HEARING RES, V27, P111, DOI 10.1016/0378-5955(87)90012-8 PERLMAN H B, 1962, Acta Otolaryngol, V54, P99, DOI 10.3109/00016486209126927 PRAZMA J, 1983, ARCH OTOLARYNGOL, V109, P611 PRAZMA J, 1987, ARCH OTOLARYNGOL, V113, P36 RYAN AF, 1988, ACTA OTO-LARYNGOL, V105, P232, DOI 10.3109/00016488809097003 SCHEIBE F, 1990, EUR ARCH OTO-RHINO-L, V247, P84 THORNE PR, 1987, HEARING RES, V27, P1, DOI 10.1016/0378-5955(87)90021-9 WRIGHT JW, 1981, J ACOUST SOC AM, V70, P1353, DOI 10.1121/1.387124 NR 23 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 MAR PY 1991 VL 52 IS 1 BP 217 EP 223 DI 10.1016/0378-5955(91)90201-J PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500020 PM 2061209 ER PT J AU DULON, D ZAJIC, G SCHACHT, J AF DULON, D ZAJIC, G SCHACHT, J TI DIFFERENTIAL MOTILE RESPONSE OF ISOLATED INNER AND OUTER HAIR-CELLS TO STIMULATION BY POTASSIUM AND CALCIUM-IONS SO HEARING RESEARCH LA English DT Article DE OUTER HAIR CELLS; INNER HAIR CELLS; MOTILITY; POTASSIUM DEPOLARIZATION; CALCIUM ID MECHANICAL RESPONSES AB Inner and outer hair cells were mechanically isolated from the guinea pig cochlea and subjected to stimuli known to induce shape changes in outer hair cells. Depolarization by 70 mM KCl which causes osmotic swelling of outer hair cells also swelled inner hair cells by approximately 8% of their volume. The application of the calcium ionophore ionomycin which induces cortical contractions and elongation of outer hair cells, did not affect the shape of inner hair cells. Since ionomycin increased free intracellular calcium levels in both inner and outer hair cells, the results demonstrate that inner hair cells do not possess the mechanisms necessary for a contractile response to calcium. Thus, calcium is a specific regulator of outer hair cell motility making this mechanism a likely physiological modulator of a transduction feedback process. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. CR ASHMORE JF, 1987, J PHYSIOL-LONDON, V388, P323 BROWNELL WE, 1985, SCIENCE, V227, P194, DOI 10.1126/science.3966153 CODY AR, 1985, NATURE, V315, P662, DOI 10.1038/315662a0 DULON D, 1989, J NEUROSCI RES, V24, P338, DOI 10.1002/jnr.490240226 DULON D, 1988, HEARING RES, V32, P123, DOI 10.1016/0378-5955(88)90084-6 DULON D, 1990, J NEUROSCI, V10, P1388 FLOCK A, 1986, ARCH OTO-RHINO-LARYN, V243, P83, DOI 10.1007/BF00453755 KAO JPY, 1989, J BIOL CHEM, V264, P8179 LIM DJ, 1980, J ACOUST SOC AM, V67, P1686, DOI 10.1121/1.384295 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 SAITO K, 1983, CELL TISSUE RES, V220, P787 SANTOS-SACCHI J, 1988, HEARING RES, V35, P143, DOI 10.1016/0378-5955(88)90113-X ULFENDAHL M, 1988, ARCH OTO-RHINO-LARYN, V245, P237, DOI 10.1007/BF00463935 YAMASHITA T, 1990, ACTA OTO-LARYNGOL, V109, P256, DOI 10.3109/00016489009107441 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1987, BIOCHEM BIOPH RES CO, V149, P304, DOI 10.1016/0006-291X(87)91639-1 ZENNER HP, 1986, HEARING RES, V22, P83, DOI 10.1016/0378-5955(86)90082-1 NR 17 TC 24 Z9 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD MAR PY 1991 VL 52 IS 1 BP 225 EP 231 DI 10.1016/0378-5955(91)90202-K PG 7 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500021 PM 2061210 ER PT J AU ZAKARAUSKAS, P CYNADER, MS AF ZAKARAUSKAS, P CYNADER, MS TI AURAL INTENSITY FOR A MOVING SOURCE SO HEARING RESEARCH LA English DT Article DE MOVING SOUND; TRAJECTORY; AURAL INTENSITY; SOURCE DETECTION; MATHEMATICAL EQUATION ID AUDIBLE MOVEMENT ANGLE; SOUND SOURCE; HORIZONTAL PLANE; DISCRIMINATION; DIRECTION; VELOCITY; NEURONS; MOTION AB Considerable, highly specific information is available to the auditory system concerning the trajectory of a moving sound source. This paper delineates the set of stimuli that motion-sensitive systems might use. General expressions for the sound intensity, the interaural intensity difference, and their first time derivatives, are derived for a source moving along an arbitrary trajectory. The general expressions are then made explicit for three special cases of motion of an omnidirectional constant level source: a source moving directly away from or toward the obsever, a source moving around the observer's head, and a source moving in a straight line across the auditory field of the observer. The later special case combine characteristics of the two first ones. The functions are plotted and their characteristics compared. The combination of all four functions provides a unique signature for each source trajectory. The first time derivative of the monaural spectrum level function is found to be directly proportional to the velocity scaled by the distance of the source for omnidirectional sources of constant intensity. This makes the first time derivative of the spectrum level especially attractive as a component of a specialized source detection system in the brain. C1 UNIV BRITISH COLUMBIA,DEPT PSYCHOL,VANCOUVER V6T 1W5,BC,CANADA. UNIV BRITISH COLUMBIA,DEPT OPHTALMOL,VANCOUVER V6T 1W5,BC,CANADA. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 233 EP 244 DI 10.1016/0378-5955(91)90203-L PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500022 PM 2061211 ER PT J AU SCHROTT, A PUEL, JL REBILLARD, G AF SCHROTT, A PUEL, JL REBILLARD, G TI COCHLEAR ORIGIN OF 2F1-F2 DISTORTION PRODUCTS ASSESSED BY USING 2-TYPES OF MUTANT MICE SO HEARING RESEARCH LA English DT Article DE MUTANT MICE; DISTORTION PRODUCT EMISSIONS; COCHLEAR NONLINEARITY ID HEREDITARY DEAFNESS; MECHANICS; HEARING; MOUSE; CAT AB Mutant mice with a particular type of cochlear pathology are excellent models to study the functional role of various structures in the cochlea. In order to assess the contribution of inner and outer hair cells to the generation of distortion product emissions (DPEs) we have recorded the 2f1-f2 DPE in a control group of CBA mice, which have normal numbers of inner and outer hair cells and two different types of mutant mice: the Bronx-waltzer mice and the W(v)/W(v) mice. In the Bronx waltzer mutant mice, 70% of inner hair cells are missing whereas the outer hair cells are present in normal number. The distortion product emissions 2f1-f2 is clearly recordable with a 10-20 dB lower magnitude as compared to normal CBA control mice. The homozygous W(v)/W(v) mutant mice on the other hand present a selective outer hair cell loss as a constant defect with no progressive degeneration of the organ of Corti and an essentially normal inner hair cell population. The cubic distortion products 2f1-f2 could not be detected in all but one animal. Therefore, the present study strongly suggests, that the outer hair cells are critically involved in the production of DPEs. C1 INSERM,U254,NEUROBIOL AUDIT LAB,F-34100 MONTPELLIER,FRANCE. RP SCHROTT, A (reprint author), UNIV INNSBRUCK,DEPT OTOLARYNGOL,KLIN HALS NASEN OHRENHEILKUNDE,ANICHSTR 35,A-6020 INNSBRUCK,AUSTRIA. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 245 EP 253 DI 10.1016/0378-5955(91)90204-M PG 9 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500023 PM 2061212 ER PT J AU SHORE, SE HELFERT, RH BLEDSOE, SC ALTSCHULER, RA GODFREY, DA AF SHORE, SE HELFERT, RH BLEDSOE, SC ALTSCHULER, RA GODFREY, DA TI DESCENDING PROJECTIONS TO THE DORSAL AND VENTRAL DIVISIONS OF THE COCHLEAR NUCLEUS IN GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE HORSERADISH PEROXIDASE; VENTRAL COCHLEAR NUCLEUS; DORSAL COCHLEAR NUCLEUS; SUPERIOR OLIVARY NUCLEI; INFERIOR COLLICULUS ID SUPERIOR OLIVARY COMPLEX; IMMUNOCYTOCHEMICAL LOCALIZATION; HORSERADISH-PEROXIDASE; SYNAPTIC RESPONSES; CAT; CELLS; ORGANIZATION; NEURONS; FIBERS; INPUTS AB The origins of extrinsic projections to the guinea pig dorsal and ventral cochlear nuclei were identified by examining the retrograde transport of horseradish peroxidase conjugated to wheatgerm agglutin following its injection into each of these divisions. Major projections originated in periolivary regions of the superior olivary complex, the contralateral cochlear nucleus and the inferior colliculus. There was no contribution from the nuclei of the lateral lemniscus to these pathways. The heaviest projection from the periolivary regions to both divisions of the cochlear nucleus arose bilaterally in the ventral nucleus of the trapezoid body. The ipsilateral lateral nucleus of the trapezoid body also projected heavily to dorsal and ventral cochlear nucleus. In addition, the ventral cochlear nucleus received a substantial projection from the dorsal aspect of the ipsilateral dorsomedial periolivary nucleus. Projections originating bilaterally in the central nucleus of the inferior colliculus terminated in the deep layers of dorsal cochlear nucleus. These projections appear to be more strongly ipsilateral and specific than those reported in the cat. C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. RP SHORE, SE (reprint author), MED COLL OHIO,DEPT OTOLARYNGOL,TOLEDO,OH 43699, USA. CR ADAMS JC, 1983, J COMP NEUROL, V215, P275, DOI 10.1002/cne.902150304 ADAMS J C, 1985, Society for Neuroscience Abstracts, V11, P32 ADAMS JC, 1976, J COMP NEUROL, V170, P107, DOI 10.1002/cne.901700108 ADAMS J C, 1989, Society for Neuroscience Abstracts, V15, P1114 ALTSCHULER RA, 1986, BRAIN RES, V369, P316, DOI 10.1016/0006-8993(86)90542-1 BENSON CG, 1990, J COMP NEUROL, V296, P415, DOI 10.1002/cne.902960307 BORG, 1973, ACTA MORPHOL NEERL S, V11, P49 Bourk TR, 1976, THESIS MIT CAMBRIDGE BROWN KA, 1976, EXP NEUROL, V53, P663, DOI 10.1016/0014-4886(76)90146-1 BROWN MC, 1988, J COMP NEUROL, V278, P591, DOI 10.1002/cne.902780410 BROWNELL WE, 1975, BRAIN RES, V94, P413, DOI 10.1016/0006-8993(75)90226-7 CAJAL SR, 1909, HISTOLOGIE SYSTEME N, V1, P774 CANT NB, 1982, J COMP NEUROL, V212, P313, DOI 10.1002/cne.902120308 CANT NB, 1978, NEUROSCIENCE, V3, P1003, DOI 10.1016/0306-4522(78)90120-3 CANT NB, 1979, NEUROSCIENCE, V4, P1925, DOI 10.1016/0306-4522(79)90066-6 CANT NB, 1984, HEARING SCI RECENT A, P371 Caspary D.M., 1986, NEUROBIOLOGY HEARING, P303 COMIS SD, 1969, J NEUROCHEM, V16, P423, DOI 10.1111/j.1471-4159.1969.tb10383.x COMIS SD, 1968, J NEUROPHYSIOL, V31, P62 COMIS SD, 1970, J PHYSIOL-LONDON, V210, P751 COVEY E, 1984, J COMP NEUROL, V226, P289, DOI 10.1002/cne.902260212 ELVERLAND HM, 1977, EXP BRAIN RES, V27, P389 EVANS EF, 1973, EXP BRAIN RES, V17, P428 FAYELUND H, 1986, ANAT EMBRYOL, V175, P35, DOI 10.1007/BF00315454 FRISINA R, 1983, IRSS23 I SENS RES SP Godfrey DA, 1988, AUDITORY PATHWAY, P107 GODFREY DA, 1975, J COMP NEUROL, V162, P247, DOI 10.1002/cne.901620206 GODFREY DA, 1987, HEARING RES, V28, P237, DOI 10.1016/0378-5955(87)90052-9 HASHIKAWA T, 1983, J COMP NEUROL, V219, P241, DOI 10.1002/cne.902190209 HELFERT RH, 1989, BRAIN RES, V501, P269, DOI 10.1016/0006-8993(89)90644-6 ITOH K, 1987, BRAIN RES, V400, P145, DOI 10.1016/0006-8993(87)90662-7 JOSEPH MP, 1985, J COMP NEUROL, V232, P43, DOI 10.1002/cne.902320105 JUIZ JM, 1989, IN PRESS BRAIN RES KANE ES, 1979, J COMP NEUROL, V187, P759, DOI 10.1002/cne.901870408 KANE ES, 1977, NEUROSCIENCE, V2, P897, DOI 10.1016/0306-4522(77)90113-0 Kiang NY, 1973, BASIC MECHANISMS HEA, P455 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 MOREST D. 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Res. PD MAR PY 1991 VL 52 IS 1 BP 255 EP 268 DI 10.1016/0378-5955(91)90205-N PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA FE825 UT WOS:A1991FE82500024 PM 1648060 ER PT J AU RAPHAEL, Y ALTSCHULER, RA AF RAPHAEL, Y ALTSCHULER, RA TI SCAR FORMATION AFTER DRUG-INDUCED COCHLEAR INSULT SO HEARING RESEARCH LA English DT Article DE OTOTOXICITY; PHALANGEAL SCAR; ACTIN; CYTOKERATINS ID SENSORY HAIR-CELLS; RETICULAR LAMINA; ACOUSTIC TRAUMA; ORGAN; CORTI; REGENERATION; EPITHELIUM; FILAMENTS; JUNCTIONS; ACTIN AB Structural and molecular changes in the guinea pig organ of Corti were studied using histochemistry and electron microscopy in the course of drug-induced hair cell degeneration. Actin filaments disappear from the cuticular plate and the stereocilia. An actin-rich bridge appears in the apical region of dying hair cells. Two supporting cells form a scar for a given hair cell. The supporting cells expand and invade the spaces of Nuel and then the region previously occupied by the hair cell. The scar region becomes cytokeratin-labeled. In this study, the apical domain of the hair cell is the last part of the cell to degenerate. Hair cell degeneration coincides temporally with scar formation. We define the resulting scar as a 'type I' scar. The results provide preliminary information about the molecular composition of the type I scar and suggest a structural basis for the dynamics of scar formation. RP RAPHAEL, Y (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,SCH MED,1301 E ANN ST,ANN ARBOR,MI 48109, USA. 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Res. PD FEB PY 1991 VL 51 IS 2 BP 173 EP 183 DI 10.1016/0378-5955(91)90034-7 PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900001 PM 1709631 ER PT J AU IKEDA, K MORIZONO, T AF IKEDA, K MORIZONO, T TI IONIC ACTIVITIES OF THE INNER-EAR FLUID AND IONIC PERMEABILITIES OF THE COCHLEAR DUCT IN ENDOLYMPHATIC HYDROPS OF THE GUINEA-PIG SO HEARING RESEARCH LA English DT Article DE ENDOLYMPHATIC HYDROPS; INNER EAR FLUID; ION CONCENTRATION; ION PERMEABILITY; ANOXIA; ENDOCOCHLEAR POTENTIAL ID CALCIUM-TRANSPORT MECHANISM; STRIA VASCULARIS; PERILYMPH; POTENTIALS; PARTITION; BARRIER; CA-2+; MODEL AB Ionic activities (K+, Na+, and Cl-) of the perilymph and endolymph of the basal turn were measured using ion-selective microelectrodes in experimentally induced endolymphatic hydrops of the guinea pig. Three months following the obstruction of the endolymphatic duct and sac, the endocochlear potential (EP) of hydroptic ears was measured at 59.7 +/- 9.6 mV (N = 12) which was significantly lower than the EP of the contralateral control ears (84.4 +/- 2.8 mV, N = 12). A paired t-test (P > 0.05) showed no significant differences of ion concentrations of the inner ear fluid between the hydroptic and contralateral ears. Ion permeabilities of the cochlear duct following anoxia were calculated according to the Nernst-Planck equation. Comparing hydroptic and normal ears following anoxia, a statistically decrease was observed in the permeability coefficients for K+. Similarly, K+ conductance was significantly lower in the hydroptic ears than in the normal ears. Total conductance of the cochlear duct, defined as the sum of each ion conductance, was 0.560 siemens in the normal ears and 0.217 siemens in the hydroptic ears. On the basis of the Goldman-Hodgkin-Katz equation, preexisting negative EP in the normal state was calculated to be -24.5 mV in normal ears and -21.4 mV in hydroptic ears. Therefore, the positive component of the EP was 108.9 mV in normal ears and 81.1 mV in hydroptic ears. These findings suggest that the pathophysiology of hydrops involves changes in K+ permeability and the inhibition of the electrogenic transport processes. C1 UNIV MINNESOTA,SCH MED,MINNEAPOLIS,MN 55455. RP IKEDA, K (reprint author), TOHOKU UNIV,SCH MED,DEPT OTOLARYNGOL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. CR ALBERS FWJ, 1987, ACTA OTO-LARYNGOL, V104, P202, DOI 10.3109/00016488709107319 ALVAREZLEEFMANS FJ, 1981, J PHYSIOL-LONDON, V315, P531 COHEN J, 1984, ACTA OTO-LARYNGOL, V98, P398, DOI 10.3109/00016488409107580 GIEBEL W, 1979, 16TH WORKSH INN EAR Hallpike C. 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PD FEB PY 1991 VL 51 IS 2 BP 185 EP 192 DI 10.1016/0378-5955(91)90035-8 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900002 PM 2032956 ER PT J AU LIPPE, WR AF LIPPE, WR TI REDUCTION AND RECOVERY OF NEURONAL SIZE IN THE COCHLEAR NUCLEUS OF THE CHICKEN FOLLOWING AMINOGLYCOSIDE INTOXICATION SO HEARING RESEARCH LA English DT Article DE NUCLEUS MAGNOCELLULARIS; REGENERATION; HAIR CELL; AMINOGLYCOSIDE; COCHLEAR NUCLEUS; NEURON AREA ID STEM AUDITORY NUCLEI; LATERAL GENICULATE-NUCLEUS; HAIR CELL REGENERATION; BASILAR PAPILLA; AFFERENT INFLUENCES; N-MAGNOCELLULARIS; SOUND DEPRIVATION; ACOUSTIC TRAUMA; GUINEA-PIG; ORGANIZATION AB The effect of aminoglycoside intoxication on the cross-sectional area of neurons in nucleus magnocellularis (NM) was studied in neonatal chickens. Birds received daily injections of 100 mg/kg body weight of gentamicin for 10 consecutive days. Cell area was measured at five different tonotopic regions along the posterior-to-anterior dimension of NM (low-to-high frequency) after post-treatment survival times of 8, 23 and 40 days. Gentamicin caused a reversible reduction of cell area that varied as a function of location and survival time. Significant decreases of cell area occurred only in the rostral half of the nucleus. Cell area was reduced at 8 and 23 days survival and recovered to near control values by 40 days post-treatment. Body weight, brain weight and the cross-sectional area of cerebellar Purkinje neurons were also reduced but did not recover. The present results show that aminoglycoside toxicity can affect auditory neurons in the brain. 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Res. PD FEB PY 1991 VL 51 IS 2 BP 193 EP 202 DI 10.1016/0378-5955(91)90036-9 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900003 PM 2032957 ER PT J AU NUTTALL, AL DOLAN, DF AVINASH, G AF NUTTALL, AL DOLAN, DF AVINASH, G TI LASER DOPPLER VELOCIMETRY OF BASILAR-MEMBRANE VIBRATION SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; TUNING CURVES; LASER DOPPLER VIBROMETRY; MICROSCOPY ID AUDITORY-NERVE FIBERS; COCHLEAR HAIR-CELLS; GUINEA-PIG; CAPACITIVE PROBE; MOSSBAUER EXPERIMENTS; MAMMALIAN COCHLEA; TUNING PROPERTIES; INNER-EAR; RESPONSES; MOTION AB A method is described for the measurement of basilar membrane (BM) vibration using a commercially made laser Doppler velocimeter (LDV). The instrumentation was coupled to a compound microscope which served to visualize reflective glass microbeads placed on the BM. The laser beam of the LDV was focused in the microscope object plane and positioned over the reflective bead. We show examples of frequency tuning curves and displacement input/output intensity functions obtained with the technique. RP NUTTALL, AL (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,SCH MED,ANN ARBOR,MI 48109, USA. CR BORN GVR, 1978, BIORHEOLOGY, V15, P163 BROWN MC, 1984, J PHYSIOL-LONDON, V354, P625 BROWN MC, 1983, SCIENCE, V222, P69, DOI 10.1126/science.6623058 BROWN MC, 1983, HEARING RES, V10, P345, DOI 10.1016/0378-5955(83)90097-7 DALLOS P, 1985, J NEUROSCI, V5, P1591 EINAV S, 1975, BIORHEOLOGY, V12, P203 EVANS EF, 1979, AUDITORY INVESTIGATI GEISLER CD, 1974, J NEUROPHYSIOL, V37, P1156 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 GREATED C. 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Res. PD FEB PY 1991 VL 51 IS 2 BP 203 EP 213 DI 10.1016/0378-5955(91)90037-A PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900004 PM 1827786 ER PT J AU RUGGERO, MA RICH, NC AF RUGGERO, MA RICH, NC TI APPLICATION OF A COMMERCIALLY-MANUFACTURED DOPPLER-SHIFT LASER VELOCIMETER TO THE MEASUREMENT OF BASILAR-MEMBRANE VIBRATION SO HEARING RESEARCH LA English DT Article DE LASER DOPPLER-SHIFT VELOCIMETRY; LASER VIBROMETRY; LASER HETERODYNE INTERFEROMETRY; BASILAR MEMBRANE; COCHLEAR MECHANICS ID LOW-FREQUENCY TONES; INPUT-OUTPUT FUNCTIONS; AUDITORY-NERVE FIBERS; GUINEA-PIG COCHLEA; MAMMALIAN COCHLEA; INNER-EAR; HETERODYNE INTERFEROMETER; MOSSBAUER TECHNIQUE; CHINCHILLA COCHLEA; SQUIRREL-MONKEY AB A commercially-available laser Doppler-shift velocimeter has been coupled to a compound microscope equipped with ultra-long-working-distance objectives for the purpose of measuring basilar membrane vibrations in the chinchilla. The animal preparation is nearly identical to that used in our laboratory for similar measurements using the Mossbauer technique. The vibrometer head is mounted on the third tube of the microscope's trinocular head and its laser beam is focused on high-refractive-index glass microbeads (10-30 mu-m) previously dropped, through the perilymph of scala tympani, on the basilar membrane. For equal sampling times, overall sensitivity of the laser velocimetry system is at least one order of magnitude greater than usually attained using the Mossbauer technique. However, the most important advantage of laser velocimetry vis-a-vis the Mossbauer technique is its linearity, which permits undistorted recording of signals over a wide velocity range. Thus, for example, we have measured basilar-membrane responses to clicks whose waveforms have dynamic ranges exceeding 60 dB. RP RUGGERO, MA (reprint author), UNIV MINNESOTA,DEPT OTOLARYNGOL,2630 UNIV AVE SE,MINNEAPOLIS,MN 55414, USA. 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Res. PD FEB PY 1991 VL 51 IS 2 BP 215 EP 230 DI 10.1016/0378-5955(91)90038-B PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900005 PM 1827787 ER PT J AU BOBBIN, RP FALLON, M LI, L BERLIN, CI AF BOBBIN, RP FALLON, M LI, L BERLIN, CI TI GUINEA-PIGS SHOW POSTNATAL STABILITY IN FREQUENCY MAPPING AT THE BASAL TURN SO HEARING RESEARCH LA English DT Article DE COCHLEA; DEVELOPMENT; COCHLEAR MICROPHONIC; GUINEA PIG ID MONGOLIAN GERBIL; TONOTOPIC ORGANIZATION; AUDITORY FUNCTION; PLACE PRINCIPLE; COCHLEA; ONTOGENY; SYSTEM; EAR AB Others have shown that in animals born with immature cochleae the basal turn undergoes changes in function during the early days of postnatal life. We examined whether similar changes could be detected in the guinea pig, an animal born with a functionally mature cochlea. 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Res. PD FEB PY 1991 VL 51 IS 2 BP 231 EP 234 DI 10.1016/0378-5955(91)90039-C PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900006 PM 2032958 ER PT J AU NUTTALL, AL DOLAN, DF AF NUTTALL, AL DOLAN, DF TI COCHLEAR MICROPHONIC ENHANCEMENT IN 2 TONE INTERACTIONS SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; 2 TONE SUPPRESSION; ACTIVE PROCESS; PHYSIOLOGICAL VULNERABILITY; PHASE EFFECTS; VECTOR CANCELLATION ID HAIR CELL RESPONSES; GUINEA-PIG AB Two tone interaction functions of the cochlear microphonic (CM) were obtained from pigmented guinea pigs. First (basal) cochlear turn recording locations show optimally enhanced levels of CM when the interfering tone (F2) was positioned about 4 kHz above probe tones (F1) of 12 kHz and 20 kHz. Maximum enhancement occurred for equal level tones. No enhancement was seen for a probe tone of 4 kHz. When basal turn cochlear sensitivity was compromised, CM enhancement caused by the interfering tone was altered and only CM reduction was then seen. The CM reduction was the typical characteristic described by many earlier studies. Guinea pigs with various changes in cochlear sensitivity were studied, providing evidence in support of earlier reports that CM interference (both reductions and enhancements) depends on far field vector summation of the outputs of hair cells from a restricted area of the basilar membrane. No CM enhancement was seen in micropipette recordings from within the organ of Corti. RP NUTTALL, AL (reprint author), UNIV MICHIGAN,KRESGE HEARING RES INST,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR Black LJ, 1936, P SOC EXP BIOL MED, V33, P509 Bray CW, 1942, J COMP PSYCHOL, V33, P279, DOI 10.1037/h0057655 BROWN MC, 1984, J PHYSIOL-LONDON, V354, P625 BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 CHEATHAM MA, 1982, HEARING RES, V8, P29, DOI 10.1016/0378-5955(82)90032-6 Covell WP, 1936, AM J PHYSIOL, V116, P524 DALLOS P, 1974, J ACOUST SOC AM, V55, P597, DOI 10.1121/1.1914570 Dallos P., 1973, AUDITORY PERIPHERY B GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 KHANNA SM, 1982, SCIENCE, V215, P305, DOI 10.1126/science.7053580 LEGOUIX JP, 1977, 15 WORKSH INN EAR BI, P93 LEGOUIX JP, 1976, HEARING DAVIS ESSAYS, P53 LEGOUIX JP, 1973, J ACOUST SOC AM, V53, P409, DOI 10.1121/1.1913337 NIEDER P, 1968, J ACOUST SOC AM, V44, P1409, DOI 10.1121/1.1911276 NIEDER P, 1968, J ACOUST SOC AM, V43, P1092, DOI 10.1121/1.1910944 PATUZZI RB, 1989, HEARING RES, V42, P47, DOI 10.1016/0378-5955(89)90117-2 PATUZZI RB, 1989, HEARING RES, V39, P177, DOI 10.1016/0378-5955(89)90089-0 ROBERTSON D, 1979, J ACOUST SOC AM, V66, P466, DOI 10.1121/1.383097 SHORE SE, 1985, J ACOUST SOC AM, V77, P590, DOI 10.1121/1.391877 Wever EG, 1941, J EXP PSYCHOL, V29, P283, DOI 10.1037/h0056919 Wever EG, 1940, J ACOUST SOC AM, V12, P268, DOI 10.1121/1.1916102 NR 21 TC 5 Z9 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 1991 VL 51 IS 2 BP 235 EP 245 DI 10.1016/0378-5955(91)90040-G PG 11 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900007 PM 2032959 ER PT J AU MULLER, M AF MULLER, M TI FREQUENCY REPRESENTATION IN THE RAT COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; PLACE-FREQUENCY MAP; RAT; HRP ID PTERONOTUS-PARNELLII; INFERIOR COLLICULUS; MUSTACHE BAT; MAP; ORGANIZATION; CONNECTIONS; SENSITIVITY; AFFERENT; NUCLEUS; FIBERS AB In order to determine the place-frequency map of the rat cochlea, iontophoretic HRP-injections were made into the cochlear nucleus at electrophysiologically characterized positions. Distribution of retrograde HRP transport in cochlear spiral ganglion cells was analysed by means of a three dimensional reconstruction of the cochlea. The map was established for frequencies between 1.2 and 54 kHz, corresponding to positions between 96.5 to 2% of basilar membrane length (base = 0%). At apex of the cochlea the slope of the place-frequency map was below 0.25 mm/octave. The slope increased to a value of 2.1 mm/octave at 34% basilar membrane length, and remained almost constant towards the cochlear base. The close relationship between frequency range of highest sensitivity and maximum receptor- and innervation-density in the rat cochlea is discussed. C1 UNIV FRANKFURT,INST ZOOL,W-6000 FRANKFURT 1,GERMANY. CR ADAM JC, 1977, NEUROSCIENCE, V2, P142 Bekesy G., 1960, EXPT HEARING BORG E, 1982, HEARING RES, V8, P101, DOI 10.1016/0378-5955(82)90069-7 BURDA H, 1989, J MORPHOL, V198, P269 CLOPTON BM, 1973, BRAIN RES, V56, P355, DOI 10.1016/0006-8993(73)90352-1 EHRET G, 1979, J COMP NEUROL, V183, P73, DOI 10.1002/cne.901830107 FENG AS, 1985, J COMP NEUROL, V235, P529, DOI 10.1002/cne.902350410 KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 KOSSL M, 1985, J COMP PHYSIOL A, V157, P687, DOI 10.1007/BF01351362 KOSSL M, 1990, J COMP PHYSIOL A, V166, P695 KRAUS HJ, 1982, VERH DTSCH ZOOL GES, V279 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 MACHMERT H, 1974, ACOUSTICA, V34, P81 MESULAM MM, 1978, J HISTOCHEM CYTOCHEM, V26, P106 MULLER M, 1990, EXP BRAIN RES, V81, P140 ROBERTSON D, 1990, INFORMATION PROCESSI, P61 ROBERTSON D, 1984, HEARING RES, V15, P113, DOI 10.1016/0378-5955(84)90042-X RYAN AF, 1988, HEARING RES, V36, P181, DOI 10.1016/0378-5955(88)90060-3 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 UHL B, 1986, POSTNATALE ENTWICKLU VATER M, 1985, J COMP PHYSIOL A, V157, P671, DOI 10.1007/BF01351361 VONBEKESY G, 1944, AKUST Z, V9, P3 WALTHER Y, 1987, QUANTITATIVE MORPHOL ZOOK JM, 1989, J COMP NEUROL, V290, P243, DOI 10.1002/cne.902900206 NR 25 TC 136 Z9 136 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 1991 VL 51 IS 2 BP 247 EP 254 DI 10.1016/0378-5955(91)90041-7 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900008 PM 2032960 ER PT J AU PUEL, JL LADRECH, S CHABERT, R PUJOL, R EYBALIN, M AF PUEL, JL LADRECH, S CHABERT, R PUJOL, R EYBALIN, M TI ELECTROPHYSIOLOGICAL EVIDENCE FOR THE PRESENCE OF NMDA RECEPTORS IN THE GUINEA-PIG COCHLEA SO HEARING RESEARCH LA English DT Article DE N-METHYL-D-ASPARTATE; 2-AMINO-5-PHOSPHONOVALERATE; HAIR CELL TRANSMISSION; GLUTAMATERGIC RECEPTORS; COCHLEAR POTENTIALS; GUINEA PIG ID METHYL-D-ASPARTATE; AUDITORY-NERVE; KAINIC ACID; HAIR-CELLS; SYNAPTIC TRANSMISSION; AFFERENT TRANSMITTER; AMINO-ACIDS; NEURONS; HIPPOCAMPUS; QUISQUALATE AB An excitatory amino acid, possibly L-glutamate, most probably acts as a neurotransmitter at the inner hair cell-afferent fiber synapses in the cochlea. In the present study, we have used an electrophysiological approach to investigate at this level the presence of a major type of excitatory amino acid receptor, namely the glutamatergic receptor for which N-methyl-D-aspartate is a selective agonist. Our results show that, when N-methyl-D-aspartate and the antagonist 2-amino-5-phosphonovalerate are perfused through the perilymphatic scalae, they induced, by different mechanisms, a significant reduction of the amplitude of the compound action potential and an increase of the N1 latency, both predominant at high intensity tone burst stimulations. No significant difference was found in the presence or absence of Mg2+ in the artificial perilymph used as a vehicle. A further slight N-methyl-D-aspartate-induced decrease of the amplitude of the compound action potential, although non significant, was observed when the Mg2+-free perilymph contained 100 or 1000-mu-M glycine. In all the experimental conditions, no effect was observed on the cochlear microphonic potential. This observation is consistent with an action of N-methyl-D-aspartate and 2-amino-5-phosphonovalerate at receptors located on the auditory nerve dendrites contacting the inner hair cells. In conclusion, our results suggest the presence of N-methyl-D-aspartate receptors in the cochlea. RP PUEL, JL (reprint author), CHR HOP ST CHARLES,INSERM,U254,NEUROBIOL AUDIT LAB,F-34059 MONTPELLIER 1,FRANCE. CR ALTSCHULER RA, 1989, HEARING RES, V42, P167, DOI 10.1016/0378-5955(89)90142-1 BERTOLINO M, 1988, NEUROSCI LETT, V84, P351, DOI 10.1016/0304-3940(88)90534-4 BLEDSOE SC, 1981, HEARING RES, V4, P109, DOI 10.1016/0378-5955(81)90040-X BOBBIN GP, 1990, HEARING RES, V46, P83 BOBBIN RP, 1984, HEARING SCI RECENT A, P159 BOBBIN RP, 1978, ANN OTO RHINOL LARYN, V87, P185 BOBBIN RP, 1981, PHARM HEARING, P19 BOBBIN RP, 1979, EXP BRAIN RES, V34, P389 BOBBIN RP, 1981, ASS RES OTOLARYNGOL, V4, P27 BOBBIN RP, 1987, HEARING RES, V25, P77, DOI 10.1016/0378-5955(87)90081-5 COLLINGRIDGE GL, 1988, J PHYSIOL-LONDON, V399, P301 COMIS SD, 1979, EXP BRAIN RES, V36, P119 COUSILLAS H, 1988, HEARING RES, V36, P213, DOI 10.1016/0378-5955(88)90063-9 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X Dallos P., 1973, AUDITORY PERIPHERY B EYBALIN M, 1990, EUR U NEUROSCI S, V3, P118 EYBALIN M, 1983, NEUROSCIENCE, V9, P863, DOI 10.1016/0306-4522(83)90274-9 FELIX D, 1989, INNER EAR BIOL, V29, P19 FEX J, 1980, NEUROPHARMACOLOGY, V19, P809, DOI 10.1016/0028-3908(80)90076-3 FLETCHER EJ, 1989, EUR J NEUROSCI, V1, P196, DOI 10.1111/j.1460-9568.1989.tb00788.x GILLOYZAGA P, 1990, ARCH OTORHINOLARYNGO, V248, P40 HERRON CE, 1986, NATURE, V322, P265, DOI 10.1038/322265a0 JENISON GL, 1986, COMP BIOCHEM PHYS C, V84, P385, DOI 10.1016/0742-8413(86)90110-6 JENISON GL, 1985, HEARING RES, V20, P261, DOI 10.1016/0378-5955(85)90030-9 JENISON GL, 1985, J NEUROCHEM, V44, P1845, DOI 10.1111/j.1471-4159.1985.tb07178.x JOHNSON JW, 1987, NATURE, V325, P529, DOI 10.1038/325529a0 JUIZ JM, 1989, HEARING RES, V40, P65, DOI 10.1016/0378-5955(89)90100-7 KEITH R A, 1988, Society for Neuroscience Abstracts, V14, P792 KLINKE R, 1977, EXP BRAIN RES, V30, P145 KUSAKARI J, 1984, LARYNGOSCOPE, V94, P1365 LITTMAN T, 1989, HEARING RES, V40, P45, DOI 10.1016/0378-5955(89)90098-1 LLANO I, 1988, P NATL ACAD SCI USA, V85, P3221, DOI 10.1073/pnas.85.9.3221 LODGE D, 1990, TRENDS PHARMACOL SCI, V11, P81, DOI 10.1016/0165-6147(90)90323-Z MEDINA JE, 1981, NEUROSCIENCE, V6, P505, DOI 10.1016/0306-4522(81)90142-1 NOWAK L, 1984, NATURE, V307, P462, DOI 10.1038/307462a0 PATEL J, 1990, J NEUROCHEM, V54, P849, DOI 10.1111/j.1471-4159.1990.tb02329.x PUEL JL, 1988, HEARING RES, V37, P53, DOI 10.1016/0378-5955(88)90077-9 PUEL JL, 1989, COMP BIOCHEM PHYS C, V93, P73, DOI 10.1016/0742-8413(89)90013-3 PUEL JL, 1989, BRAIN RES, V487, P9, DOI 10.1016/0006-8993(89)90934-7 PUEL JL, 1990, EUR J NEUROSCI, V3, P152 PUEL JL, 1988, HEARING RES, V37, P83, DOI 10.1016/0378-5955(88)90080-9 PUEL JL, 1990, INNER EAR BIOL, V27, P49 PUJOL R, 1985, HEARING RES, V18, P145, DOI 10.1016/0378-5955(85)90006-1 RYAN AF, 1984, BRAIN RES, V290, P376, DOI 10.1016/0006-8993(84)90960-0 SIEGEL JH, 1987, HEARING RES, V28, P131, DOI 10.1016/0378-5955(87)90044-X WATKINS JC, 1990, TRENDS PHARMACOL SCI, V11, P25, DOI 10.1016/0165-6147(90)90038-A YOUNG AB, 1990, TRENDS PHARMACOL SCI, V11, P126, DOI 10.1016/0165-6147(90)90199-I NR 47 TC 78 Z9 79 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 1991 VL 51 IS 2 BP 255 EP 264 DI 10.1016/0378-5955(91)90042-8 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900009 PM 1674507 ER PT J AU CARLILE, S AF CARLILE, S TI THE AUDITORY PERIPHERY OF THE FERRET - POSTNATAL-DEVELOPMENT OF ACOUSTIC PROPERTIES SO HEARING RESEARCH LA English DT Article DE EXTERNAL EAR; PINNA; ACOUSTICS; DEVELOPMENT; SOUND LOCALIZATION; FERRET ID PIG SUPERIOR COLLICULUS; CAT INFERIOR COLLICULUS; GUINEA-PIG; HUMAN EAR; MONAURAL LOCALIZATION; SOUND-PRESSURE; RESPONSE PROPERTIES; DISCHARGE PATTERNS; HORIZONTAL PLANE; COCHLEAR NUCLEUS AB The development of the acoustics of the auditory periphery of the ferret was examined by measuring the spectral transfer functions (STFs) and the directional characteristics of the outer ears of animals ranging in age from postnatal day 32 (P32) to P54. Using an impulse response technique the STFs were obtained from up to 250 locations throughout free space. The directional responses were calculated for frequencies between 1 kHz and 30 kHz. The low frequency roll-off of the STF decreased with increasing age from around 15 kHz at P32 to an adult value of around 8 kHz by P51. The directional responses of the outer ear of the immature ferrets differed significantly from adult animals in a fashion that was consistent with the smaller size of the auditory periphery. However, by P51 the responses were generally within the normal adult range. The implications of the relatively rapid development of the acoustics of the auditory periphery are discussed in terms of the development of mechanisms subserving sound localization. RP CARLILE, S (reprint author), UNIV OXFORD,PHYSIOL LAB,PARKS RD,OXFORD OX1 3PT,ENGLAND. CR BELENDIUK K, 1975, J ACOUST SOC AM, V58, P701, DOI 10.1121/1.380717 BLAUERT J, 1969, ACUSTICA, V22, P205 BRUGGE JF, 1988, AUDITORY FUNCTION NE, P113 BRUGGE JF, 1978, J NEUROPHYSIOL, V41, P1557 BUTLER RA, 1977, J ACOUST SOC AM, V61, P1264, DOI 10.1121/1.381427 BUTLER RA, 1980, PERCEPT PSYCHOPHYS, V28, P449, DOI 10.3758/BF03204889 CALFORD MB, 1984, HEARING RES, V14, P13, DOI 10.1016/0378-5955(84)90064-9 CARLILE S, 1990, J ACOUST SOC AM, V88, P2180, DOI 10.1121/1.400115 CARLILE S, 1987, HEARING RES, V31, P123, DOI 10.1016/0378-5955(87)90118-3 CARLILE S, 1987, HEARING RES, V31, P111, DOI 10.1016/0378-5955(87)90117-1 CARLILE S, 1990, J ACOUST SOC AM, V88, P2196, DOI 10.1121/1.400116 CARLILE S, 1990, BR J ADUIOL, V24, P192 Freedman S. J., 1968, NEUROPSYCHOLOGY SPAT, P135 GARDNER MB, 1973, J ACOUST SOC AM, V53, P400, DOI 10.1121/1.1913336 HORNER KC, 1987, HEARING RES, V26, P327, DOI 10.1016/0378-5955(87)90068-2 INGLIS JK, 1980, INTRO LABORATORY ANI JONGKEES L B W, 1946, J Laryngol Otol, V61, P494, DOI 10.1017/S002221510000832X KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 KING AJ, 1987, J NEUROPHYSIOL, V57, P596 KING A J, 1987, Society for Neuroscience Abstracts, V13, P80 KING AJ, 1983, J PHYSIOL-LONDON, V342, P361 KING AJ, 1989, NEUR SOC ABST, V15, P746 Maling D.H., 1973, COORDINATE SYSTEMS M MEHRGARDT S, 1977, J ACOUST SOC AM, V61, P1567, DOI 10.1121/1.381470 MIDDLEBROOKS JC, 1989, J ACOUST SOC AM, V86, P89, DOI 10.1121/1.398224 MIDDLEBROOKS JC, 1984, J NEUROSCI, V4, P2621 MOORE DR, 1979, BRAIN RES, V163, P49, DOI 10.1016/0006-8993(79)90150-1 MOORE DR, 1988, FETAL NEONATAL DEV, P203 MOORE DR, 1983, DEV AUDITORY VESTIBU, P121 MOORE DR, 1984, HEARING RES, V13, P159, DOI 10.1016/0378-5955(84)90106-0 Moore D R, 1985, Acta Otolaryngol Suppl, V421, P19 MOORE DR, 1982, BRAIN RES, V253, P309, DOI 10.1016/0006-8993(82)90698-9 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 MOREY AL, 1990, DEV BRAIN RES, V53, P279 MUSICANT AD, 1984, HEARING RES, V14, P185, DOI 10.1016/0378-5955(84)90017-0 OLDFIELD SR, 1984, PERCEPTION, V13, P601, DOI 10.1068/p130601 PALMER AR, 1982, NATURE, V299, P248, DOI 10.1038/299248a0 PALMER AR, 1985, HEARING RES, V17, P267, DOI 10.1016/0378-5955(85)90071-1 RABBITT RD, 1988, J ACOUST SOC AM, V83, P1064, DOI 10.1121/1.396051 SANES DH, 1988, J NEUROSCI, V8, P682 SEARLE CL, 1975, J ACOUST SOC AM, V57, P448, DOI 10.1121/1.380442 Shaw BAG, 1974, HDB SENSORY PHYSL, VV/1, P455 SHAW EAG, 1968, J ACOUST SOC AM, V44, P240, DOI 10.1121/1.1911059 SHIPLEY C, 1980, BRAIN RES, V182, P313, DOI 10.1016/0006-8993(80)91191-9 SINYOR A, 1973, J ACOUST SOC AM, V54, P916, DOI 10.1121/1.1914346 STINSON MR, 1982, J ACOUST SOC AM, V72, P766, DOI 10.1121/1.388257 STINSON MR, 1985, J ACOUST SOC AM, V78, P1596, DOI 10.1121/1.392797 STINSON MR, 1989, J ACOUST SOC AM, V85, P2492, DOI 10.1121/1.397744 TERANISH.R, 1968, J ACOUST SOC AM, V44, P257, DOI 10.1121/1.1911061 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P867 WIGHTMAN FL, 1989, J ACOUST SOC AM, V85, P858, DOI 10.1121/1.397557 WITHINGTONWRAY DJ, 1990, DEV BRAIN RES, V51, P225, DOI 10.1016/0165-3806(90)90279-8 WOOLF NK, 1985, DEV BRAIN RES, V17, P131, DOI 10.1016/0165-3806(85)90138-5 1987, UNIRAS GEOPAK INTERP NR 54 TC 23 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 1991 VL 51 IS 2 BP 265 EP 277 DI 10.1016/0378-5955(91)90043-9 PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900010 PM 2032961 ER PT J AU RENNIE, KJ ASHMORE, JF AF RENNIE, KJ ASHMORE, JF TI IONIC CURRENTS IN ISOLATED VESTIBULAR HAIR-CELLS FROM THE GUINEA-PIG CRISTA-AMPULLARIS SO HEARING RESEARCH LA English DT Article DE HAIR CELL; VESTIBULAR SYSTEM; PATCH CLAMP; POTASSIUM CURRENTS ID DEPENDENT CONDUCTANCES; ELECTRICAL RESONANCE; MEMBRANE-PROPERTIES; POTASSIUM CURRENT; RANA-CATESBEIANA; SENSORY NEURONS; VOLTAGE CLAMP; ADULT PIGEON; BULL-FROG; CHANNELS AB Ionic currents have been recorded under whole cell patch clamp in cells isolated from the guinea-pig vestibular system. Type I and type II cells were separately identified. Type II cells were further classified as short (< 15-mu-m in length) or tall (> 15-mu-m). Under whole cell voltage clamp, cells showed an outward current which activated at potentials above about -50 mV, and tail currents which reversed near the potassium equilibrium potential. The outward current was reduced in the presence of external 10 mM tetraethylammonium or cadmium ions and when calcium was removed from the external medium. A small cadmium-sensitive transient inward current, a putative calcium current, was observed in cells loaded with caesium from the patch pipette. In 27 out of 64 cells a component of the recorded outward current inactivated. Such current components were most common in tall type II cells. This inactivating component was blocked by 4-aminopyridine and removed by depolarizing prepulses consistent with it being an A-type potassium current. Type I cells, on the other hand, showed mainly a non-inactivating outward current which slowly relaxed on repolarization to resting potentials. When membrane potentials were measured under current clamp, injections of less than 100 pA produced a single, highly damped transient followed by a plateau in Type II cells. No such transient was present in Type I cells. There is thus little evidence for an electrical resonance in these cells. C1 SCH MED SCI,DEPT PHYSIOL,UNIV WALK,BRISTOL BS8 1TD,ENGLAND. CR ART JJ, 1987, J PHYSIOL-LONDON, V385, P207 ASHMORE JF, 1983, NATURE, V304, P536, DOI 10.1038/304536a0 BAGGERSJOBACK D, 1988, ACTA OTO-LARYNGOL, V106, P393, DOI 10.3109/00016488809122262 BAIRD RA, 1988, J NEUROPHYSIOL, V60, P182 CARBONE E, 1984, NATURE, V310, P501, DOI 10.1038/310501a0 CONNOR JA, 1971, J PHYSIOL-LONDON, V213, P1 CORREIA MJ, 1989, J NEUROPHYSIOL, V62, P924 CRAWFORD A, 1989, J PHYSIOL-LONDON, V40, pP90 CRAWFORD AC, 1981, J PHYSIOL-LONDON, V312, P377 CURTHOYS IS, 1982, EXP BRAIN RES, V47, P286 DIDIER A, 1990, CELL TISSUE RES, V260, P415, DOI 10.1007/BF00318645 EVANS MG, 1987, BIOPHYS J, V52, P649 FOX AP, 1987, J PHYSIOL-LONDON, V394, P149 FUCHS PA, 1986, J PHYSIOL-LONDON, V371, pP71 GOLDBERG JM, 1987, J NEUROPHYSIOL, V58, P700 GOLDBERG JM, 1990, J NEUROPHYSIOL, V63, P791 GULLEY RL, 1979, J NEUROCYTOL, V8, P591, DOI 10.1007/BF01208511 HAGIWARA S, 1981, ANNU REV NEUROSCI, V4, P69, DOI 10.1146/annurev.ne.04.030181.000441 HAMILTON DW, 1968, J ULTRA MOL STRUCT R, V23, P98, DOI 10.1016/S0022-5320(68)80034-6 HOUSLEY GD, 1989, HEARING RES, V38, P259, DOI 10.1016/0378-5955(89)90070-1 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P275 HUDSPETH AJ, 1988, J PHYSIOL-LONDON, V400, P237 KROS CJ, 1990, J PHYSIOL-LONDON, V421, P263 LANG DG, 1989, J NEUROPHYSIOL, V62, P935 LATTORE R, 1989, ANNU REV PHYSIOL, V51, P385 LEWIS RS, 1983, NATURE, V304, P538, DOI 10.1038/304538a0 LIM DJ, 1971, ARCHIV OTOLARYNGOL, V94, P69 LINDEMAN HH, 1981, ACTA OTO-LARYNGOL, V92, P315, DOI 10.3109/00016488109133267 Lindeman H H, 1969, Ergeb Anat Entwicklungsgesch, V42, P1 MARCHETTI C, 1988, J GEN PHYSIOL, V91, P255, DOI 10.1085/jgp.91.2.255 Marty A, 1983, SINGLE CHANNEL RECOR, P107 MEECH RW, 1975, J PHYSIOL-LONDON, V249, P211 NAKAJIMA Y, 1986, P NATL ACAD SCI USA, V83, P3022, DOI 10.1073/pnas.83.9.3022 NARAHASHI T, 1987, J PHYSIOL-LONDON, V383, P231 OHMORI H, 1984, J PHYSIOL-LONDON, V350, P561 PITCHFORD S, 1987, HEARING RES, V27, P75, DOI 10.1016/0378-5955(87)90027-X RUDY B, 1988, NEUROSCIENCE, V25, P729, DOI 10.1016/0306-4522(88)90033-4 SCARFONE E, 1988, J NEUROSCI, V8, P4640 SCHESSEL DA, 1981, ANN NY ACAD SCI, V374, P210, DOI 10.1111/j.1749-6632.1981.tb30871.x SUGIHARA I, 1989, J NEUROPHYSIOL, V62, P1330 THOMPSON SH, 1977, J PHYSIOL-LONDON, V265, P465 VALAT J, 1989, HEARING RES, V40, P255, DOI 10.1016/0378-5955(89)90166-4 WERSALL J, 1956, Acta Otolaryngol Suppl, V126, P1 YAMASHITA M, 1990, EXP BRAIN RES, V80, P475 NR 44 TC 71 Z9 71 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD FEB PY 1991 VL 51 IS 2 BP 279 EP 291 DI 10.1016/0378-5955(91)90044-A PG 13 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EZ929 UT WOS:A1991EZ92900011 PM 2032962 ER PT J AU CHAMBERS, RD GRIFFITHS, SK AF CHAMBERS, RD GRIFFITHS, SK TI EFFECTS OF AGE ON THE ADULT AUDITORY MIDDLE LATENCY RESPONSE SO HEARING RESEARCH LA English DT Article DE AUDITORY EVOKED RESPONSE; MIDDLE LATENCY RESPONSE; AGE-RELATED ID AVERAGED ELECTROENCEPHALIC RESPONSE; CONSTANT LEVEL CLICKS; EVOKED-POTENTIALS; EARLY COMPONENTS; SLEEP AB The middle latency components of the auditory evoked response were obtained from a group of normal-hearing, healthy female subjects from 22 to 68 years of age. Recordings were made at several intensity levels to assess the level-dependence of any age-related effects. Cross-sectional analyses revealed that the amplitude of component Pa grows linearly with age, becoming significantly larger in older (50-68 years of age) compared to younger (22-37 years) subjects. The amplitude-intensity function is steeper in the older subjects by a factor of two. Correlational analyses suggested that at higher intensity levels age accounts for about 20% of the variance in the amplitude of Pa. A positive shift in response baseline was observed in the older subjects, and could contribute to the age-related increase in the absolute amplitude of Pa. However, a similar increase in the peak-to-peak and area measures of Pa suggests that some of the increase in the magnitude of Pa is independent of baseline shift. A confounding of age and hearing sensitivity in this study makes it difficult to interpret the age-related effects as strictly central in nature. RP CHAMBERS, RD (reprint author), UNIV ILLINOIS,DEPT SPEECH & HEARING SCI,901 S 6TH ST,CHAMPAIGN,IL 61820, USA. 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M., 1985, ADV PSYCHOPHYSIOLOGY, V1, P301 FORD JM, 1980, AGING 1980S PSYCHOL, P115, DOI 10.1037/10050-008 HEFFLEY E, 1985, NEUROBEH TOXICOL TER, V7, P399 JERGER J, 1988, Seminars in Hearing, V9, P75, DOI 10.1055/s-0028-1085653 KLEIN AJ, 1983, ARCH OTOLARYNGOL, V109, P6 LUDERS H, 1970, ELECTROEN CLIN NEURO, V29, P450, DOI 10.1016/0013-4694(70)90062-3 MENDEL MI, 1974, AUDIOLOGY, V13, P23 MENDEL MI, 1971, J SPEECH HEAR RES, V14, P829 PFEFFERBAUM A, 1979, ELECTROEN CLIN NEURO, V46, P81, DOI 10.1016/0013-4694(79)90052-X PFEFFERBAUM A, 1980, ELECTROEN CLIN NEURO, V49, P266, DOI 10.1016/0013-4694(80)90221-7 PICTON TW, 1974, ELECTROEN CLIN NEURO, V36, P179, DOI 10.1016/0013-4694(74)90155-2 Smith D.B.D., 1980, AGING 80S, P135, DOI 10.1037/10050-010 SMITH DBD, 1978, 11TH INT C GER STRAUMANIS JJ, 1965, J GERONTOL, V20, P498 WOODS DL, 1986, ELECTROEN CLIN NEURO, V65, P297, DOI 10.1016/0168-5597(86)90008-0 NR 21 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 JAN PY 1991 VL 51 IS 1 BP 1 EP 10 DI 10.1016/0378-5955(91)90002-Q PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300001 PM 2013537 ER PT J AU SAINTMARIE, RL BENSON, CG OSTAPOFF, EM MOREST, DK AF SAINTMARIE, RL BENSON, CG OSTAPOFF, EM MOREST, DK TI GLYCINE IMMUNOREACTIVE PROJECTIONS FROM THE DORSAL TO THE ANTEROVENTRAL COCHLEAR NUCLEUS SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS; GLYCINE; GABA; IMMUNOCYTOCHEMISTRY; GUINEA PIG; AUDITORY PATHWAYS; HORSERADISH PEROXIDASE ID CENTRAL NERVOUS-SYSTEM; AUDITORY BRAIN-STEM; GUINEA-PIG; IMMUNOCYTOCHEMICAL LOCALIZATION; HORSERADISH-PEROXIDASE; GABA IMMUNOREACTIVITY; RESPONSE PROPERTIES; GOLGI IMPREGNATION; REACTION-PRODUCT; CAT AB The aim of the present study was to investigate whether projections from the dorsal cochlear nucleus (DCN) to the anteroventral cochlear nucleus (AVCN) use either of two inhibitory transmitters, glycine or GABA. Retrograde HRP labeling of DCN-to-AVCN projection neurons was combined with postembedding immunocytochemistry in the DCN of guinea pigs. Following injections of HRP in the anterior or posterior divisions of AVCN, large numbers of neurons were labeled in the DCN. All of these were located in the deep layer, except for a few granule cells. Nearly all (96%) of the projection neurons were immunoreactive for glycine and most had dendritic and somatic morphologies corresponding to those of elongate neurons (so-called 'corn' cells); only a few resembled small stellate neurons. Few (3%) retrogradely labeled neurons were immunoreactive for GABA. The results suggest that projections from the deep DCN to the AVCN are formed primarily by glycinergic elongate neurons. These projections could have a substantial inhibitory influence on the output of neurons in the AVCN. C1 UNIV CONNECTICUT,CTR HLTH,CTR NEUROL SCI,FARMINGTON,CT 06030. RP SAINTMARIE, RL (reprint author), UNIV CONNECTICUT,CTR HLTH,DEPT ANAT,FARMINGTON,CT 06030, USA. 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Res. PD JAN PY 1991 VL 51 IS 1 BP 11 EP 28 DI 10.1016/0378-5955(91)90003-R PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300002 PM 1672865 ER PT J AU ROBERTSON, D WILSON, SA AF ROBERTSON, D WILSON, SA TI CHANGES IN COCHLEAR SENSITIVITY DO NOT ALTER RELATIVE THRESHOLDS OF DIFFERENT SPONTANEOUS RATE CATEGORIES OF PRIMARY AUDITORY-NERVE FIBERS SO HEARING RESEARCH LA English DT Article DE SINGLE UNIT; CF THRESHOLD; CAP THRESHOLD; SPONTANEOUS RATE; PATHOLOGY ID STEREOCILIA DAMAGE; LEVEL FUNCTIONS; TUNING CURVES; FIBERS; MODEL; PATHOLOGY; PATTERNS; CATS AB The CF thresholds of three different spontaneous firing rate categories of single auditory nerve fibres were measured in guinea pigs with widely differing cochlear sensitivities. The CF thresholds for all fibres were compared to the CAP thresholds at the same frequencies. The relationship between single fibre CF threshold and CAP threshold for the three different fibre categories remained unchanged despite the very wide range of absolute CAP thresholds. The widely ranging CAP thresholds in these animals were probably due to the varying degrees of outer hair cell pathology and these data therefore support the notion that in normal animals, the origin of differences in threshold between fibres with different spontaneous rates, lies in the properties of the inner hair cells and/or their synapses with afferent dendrites. RP ROBERTSON, D (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,AUDITORY LAB,NEDLANDS,WA 6009,AUSTRALIA. CR BORG E, 1988, HEARING RES, V36, P191, DOI 10.1016/0378-5955(88)90061-5 EVANS EF, 1980, EXP BRAIN RES, V40, P115 GEISLER CD, 1981, BRAIN RES, V212, P198, DOI 10.1016/0006-8993(81)90051-2 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 JOHNSTONE JR, 1979, J ACOUST SOC AM, V65, P254, DOI 10.1121/1.382244 LIBERMAN MC, 1988, HEARING RES, V34, P179, DOI 10.1016/0378-5955(88)90105-0 LIBERMAN MC, 1984, HEARING RES, V16, P55, DOI 10.1016/0378-5955(84)90025-X LIBERMAN MC, 1982, SCIENCE, V216, P1239, DOI 10.1126/science.7079757 LIBERMAN MC, 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 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 RHODE WS, 1985, HEARING RES, V18, P159, DOI 10.1016/0378-5955(85)90008-5 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 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 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 NR 20 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 29 EP 32 DI 10.1016/0378-5955(91)90004-S PG 4 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300003 PM 2013543 ER PT J AU HAFNER, H PRATT, H JOACHIMS, Z FEINSOD, M BLAZER, S AF HAFNER, H PRATT, H JOACHIMS, Z FEINSOD, M BLAZER, S TI DEVELOPMENT OF AUDITORY BRAIN-STEM EVOKED-POTENTIALS IN NEWBORN-INFANTS - A 3-CHANNEL LISSAJOUS TRAJECTORY STUDY SO HEARING RESEARCH LA English DT Article DE NEWBORNS; AUDITORY BRAIN-STEM EVOKED POTENTIALS; 3CLT ID INTENSIVE-CARE UNIT; STEM RESPONSE; NEUROLOGICAL LESIONS; MATURATION; CAT; ABNORMALITIES; SYSTEM; TERM AB Auditory brainstem evoked potentials (ABEP) were recorded from 50 newborns (35-43 weeks gestational age), using three orthogonal differential electrode pairs, in addition to the widely used vertex-mastoid derivation. Potentials were evoked by alternating polarity, 75 dBnHL clicks presented monaurally at a rate of 10/s. From the records of the three orthogonal electrode pairs (nasion-inion; vertex-spinous cervical process VII; left-right mastoids), Three-channel Lissajous' trajectories (3CLT) were derived and analyzed. 3CLT point-by-point, as well as segmental descriptors were compared with peak latencies of the vertex-mastoid derivation. Point-by-point 3CLT descriptors included apex amplitude, latency and orientation. Segmental descriptors included planar segment beginning latencies, duration and orientation. The interpretation of these results in relation to development aspects of the auditory system, as well as to the question of ABEP generators, is enhanced by using 3CLT descriptors of ABEP, which are more comprehensive than their single-channel counterparts. 3CLT apices correlated well with the Vertex-Mastoid defined peaks. Both peak and apex latency changes indicate that at the developmental stages surveyed in this study, development takes place in the more central portions of the pathway, whereas the peripheral portion is already relatively mature. The results also indicate a maturational change in the relative contributions of constituent generators of ABEP components. C1 TECHNION ISRAEL INST TECHNOL,EVOKED POTENTIALS LAB,GUTWIRTH BLDG,IL-32000 HAIFA,ISRAEL. RAMBAM MED CTR,OTORHINOLARYNGOL UNIT,HAIFA,ISRAEL. RAMBAM MED CTR,NEUROSURG UNIT,HAIFA,ISRAEL. TECHNION ISRAEL INST TECHNOL,NEONATAL INTENS CARE UNIT,IL-32000 HAIFA,ISRAEL. 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I., 1967, REGIONAL DEV BRAIN E, P3 NR 38 TC 9 Z9 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 33 EP 48 DI 10.1016/0378-5955(91)90005-T PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300004 PM 2013544 ER PT J AU HILDESHEIMER, M SHARON, R MUCHNIK, C SAHARTOV, E RUBINSTEIN, M AF HILDESHEIMER, M SHARON, R MUCHNIK, C SAHARTOV, E RUBINSTEIN, M TI THE EFFECT OF BILATERAL SYMPATHECTOMY ON NOISE INDUCED TEMPORARY THRESHOLD SHIFT SO HEARING RESEARCH LA English DT Article DE TEMPORARY THRESHOLD SHIFT; SYMPATHETIC INNERVATION; NOISE ID COCHLEAR BLOOD-FLOW AB The cochlea is innervated by sympathetic nerves originating or passing the superior cervical ganglion. The termination of one type (the vascular independent) is in the habenular region close to the auditory nerve fibers, and the other, the perivascular type, is associated with blood vessels, particularly in the spiral vessel of the tympanic lip. Suggested functions have so far received partial evidence in the literature. Borg (1982) suggested the protective value of sympathectomy of the ear in noise. Our experiments further elaborate this protective value, as it was seen that bilateral cervical sympathectomy diminished the temporary threshold shift in awake, sound exposed GP. RP HILDESHEIMER, M (reprint author), TEL AVIV UNIV,CHAIM SHEBA MED CTR,SACKLER SCH MED,IL-52621 TEL HASHOMER,ISRAEL. 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Res. PD JAN PY 1991 VL 51 IS 1 BP 49 EP 54 DI 10.1016/0378-5955(91)90006-U PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300005 PM 2013545 ER PT J AU WHITEHEAD, ML MARTIN, GK LONSBURYMARTIN, BL AF WHITEHEAD, ML MARTIN, GK LONSBURYMARTIN, BL TI EFFECTS OF THE CROSSED ACOUSTIC REFLEX ON DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN AWAKE RABBITS SO HEARING RESEARCH LA English DT Article DE DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS; CONTRALATERAL ACOUSTIC STIMULI; OLIVOCOCHLEAR EFFERENTS; CROSSED ACOUSTIC MIDDLE-EAR REFLEX ID AUDITORY-NERVE RESPONSES; OLIVOCOCHLEAR BUNDLE; CONTRALATERAL SOUND; ELECTRICAL-STIMULATION; COCHLEAR MECHANICS; ACTION-POTENTIALS; EAR; SUPPRESSION; FEATURES; FIBERS AB Recent studies in anesthetized cats suggest that contralateral-sound stimulation acts to suppress ipsilateral neural responses via the medial olivocochlear-efferent system. Activation of this descending efferent pathway presumably influences ipsilateral outer hair cell motility and, thus, cochlear micromechanics, resulting in reduced input to auditory-nerve fibers. The principal aim of the present study was to determine if contralateral-sound stimuli influence the generation of ipsilateral distortion-product otoacoustic emissions, in the ears of the awake rabbits. The results showed no effects of contralateral stimuli on these emissions that could not be attributed to the crossed acoustic middle-ear reflex. The findings further indicate that distortion-product otoacoustic emission amplitudes over a wide range of frequencies can be dramatically reduced when the middle-ear reflex is activated. RP WHITEHEAD, ML (reprint author), BAYLOR UNIV,DEPT OTORHINOLARYNGOL & COMMUNICAT SCI,ONE BAYLOR PL,HOUSTON,TX 77030, USA. CR BORG E, 1972, ACTA PHYSIOL SCAND, V85, P374, DOI 10.1111/j.1748-1716.1972.tb05272.x Borg E, 1968, Acta Otolaryngol, V65, P575, DOI 10.3109/00016486809121001 BORG E, 1975, ACTA PHYSIOL SCAND, V94, P327, DOI 10.1111/j.1748-1716.1975.tb05893.x BORG E, 1988, HEARING RES, V36, P191, DOI 10.1016/0378-5955(88)90061-5 BORG E, 1971, EXP NEUROL, V31, P301, DOI 10.1016/0014-4886(71)90234-2 Borg E, 1972, Acta Otolaryngol Suppl, V304, P1 BORG E, 1971, ACTA PHYSL SCAND, V86, P175 BROWN AM, 1984, HEARING RES, V13, P29, DOI 10.1016/0378-5955(84)90092-3 COLLET L, 1990, HEARING RES, V43, P251, DOI 10.1016/0378-5955(90)90232-E COUNTER SA, 1989, AUDIOLOGY, V28, P135 FOLSOM RC, 1987, ACTA OTO-LARYNGOL, V103, P262, DOI 10.3109/00016488709107792 GUINAN JJ, 1988, HEARING RES, V33, P97, DOI 10.1016/0378-5955(88)90023-8 Guinan J J Jr, 1986, Scand Audiol Suppl, V25, P53 KEMP DT, 1988, HEARING RES, V34, P49, DOI 10.1016/0378-5955(88)90050-0 KEMP DT, 1981, TINNITUS, P54 Kiang NY-s, 1965, DISCHARGE PATTERNS S KIM DO, 1986, HEARING RES, V22, P105, DOI 10.1016/0378-5955(86)90088-2 LIBERMAN MC, 1989, HEARING RES, V38, P47, DOI 10.1016/0378-5955(89)90127-5 LONSBURYMARTIN BL, 1987, HEARING RES, V28, P173, DOI 10.1016/0378-5955(87)90048-7 MARTIN GK, 1987, HEARING RES, V28, P191, DOI 10.1016/0378-5955(87)90049-9 MOLLER A R, 1965, Acta Otolaryngol, V60, P129, DOI 10.3109/00016486509126996 MOTT JB, 1989, HEARING RES, V38, P229, DOI 10.1016/0378-5955(89)90068-3 MOUNTAIN DC, 1980, SCIENCE, V210, P71, DOI 10.1126/science.7414321 Pang X-D, 1986, PERIPHERAL AUDITORY, P36 PRICE GR, 1966, J AUD RES, V6, P175 PUEL JL, 1990, J ACOUST SOC AM, V87, P1630, DOI 10.1121/1.399410 ROSSI G, 1965, ACTA ANAT, V60, P362 SCHLOTH E, 1983, HEARING RES, V11, P285, DOI 10.1016/0378-5955(83)90063-1 SIEGEL JH, 1982, HEARING RES, V6, P171, DOI 10.1016/0378-5955(82)90052-1 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 WIEDERHO.ML, 1970, J ACOUST SOC AM, V48, P950, DOI 10.1121/1.1912234 WINSLOW RL, 1987, J NEUROPHYSIOL, V57, P1002 NR 33 TC 44 Z9 46 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 55 EP 72 DI 10.1016/0378-5955(91)90007-V PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300006 PM 2013546 ER PT J AU NORTON, SJ BARGONES, JY RUBEL, EW AF NORTON, SJ BARGONES, JY RUBEL, EW TI DEVELOPMENT OF OTOACOUSTIC EMISSIONS IN GERBIL - EVIDENCE FOR MICROMECHANICAL CHANGES UNDERLYING DEVELOPMENT OF THE PLACE CODE SO HEARING RESEARCH LA English DT Article DE ACOUSTIC DISTORTION PRODUCTS; AUDITORY DEVELOPMENT; PLACE CODE; COCHLEAR MECHANICS; GERBIL ID STIMULATED ACOUSTIC EMISSIONS; CHRONIC COCHLEAR PATHOLOGY; STEM AUDITORY NUCLEI; OUTER HAIR-CELLS; TONOTOPIC ORGANIZATION; MONGOLIAN GERBIL; TUNING CURVES; CHARACTERISTIC FREQUENCY; DISTORTION PRODUCTS; ONTOGENETIC CHANGES AB The development of the acoustic distortion product (ADP) 2f1-f2 was studied in gerbils, beginning 12 days after birth (P12). ADPs were measured as a function of stimulus frequency region (1.0 to 13.0 kHz) and level (10 to 80 dB SPL). There was an orderly progression in the appearance and maturation of the emissions, with responses to high-frequency stimuli (f2 = 13.0 kHz) appearing first, at P13-14. Responses to mid and high frequencies (f2 = 3.9 to 13.0 kHz) matured earlier than responses to lower frequencies. Responses to low-frequency stimuli (f2 = 1.3 KHz) did not appear until P18-19 and were not mature until after one month of age. The first emissions to develop in a given frequency region had elevated thresholds, were reduced in amplitude, and displayed monotonic input-output functions. As the auditory system matured, emission growth functions became non-monotonic displaying saturation, but initially retained a reduced dynamic range. Data from the developing gerbil suggest that initially its cochlear mechanics are passive and that active elements associated with normal outer hair cell function mature first in the basal turn and last near the apex. Furthermore, the development of active nonlinear elements underlying ADP generation is consistent with the development of frequency selectivity and developmental shifts in the place code which have been demonstrated in the gerbil. C1 UNIV WASHINGTON,HEARING DEV LABS,SEATTLE,WA 98195. RP NORTON, SJ (reprint author), UNIV KANSAS,MED CTR,DEPT HEARING & SPEECH,39TH & RAINBOW BLVD,KANSAS CITY,KS 66103, USA. 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Res. PD JAN PY 1991 VL 51 IS 1 BP 73 EP 92 DI 10.1016/0378-5955(91)90008-W PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300007 PM 2013547 ER PT J AU DIRCKX, JJJ DECRAEMER, WF AF DIRCKX, JJJ DECRAEMER, WF TI HUMAN TYMPANIC MEMBRANE DEFORMATION UNDER STATIC PRESSURE SO HEARING RESEARCH LA English DT Article DE EARDRUM; HUMAN; STATIC PRESSURE ID MIDDLE-EAR; MORNING PRESSURE AB The effects of static pressures in the range of plus and minus 1.6 kPa on the shape of the tympanic membrane is measured using a non-contacting optical technique on a fresh human temporal bone. Full field data of the deformation are presented as well as cross-sections along two major directions. Strong asymmetry between medial and lateral movements is demonstrated. The displacement of the umbo is compared to other work. The rotation angle of the manubrium in function of pressure is calculated and also compared to other work. It is demonstrated that the rotation angels can not account for the measured movement of the umbo, which leads to the conclusion that for static high pressure levels the classical hypothesis of rotation around a fixed axis has to be abandoned. The comparison with data of TM displacement under dynamic stimuli is discussed. C1 UNIV ANTWERP,BIOMED PHYS LAB,ANTWERP,BELGIUM. CR ARS B, 1987, AM J OTOL, V8, P148 ARS B, 1989, CLIN OTOLARYNGOL, V14, P471, DOI 10.1111/j.1365-2273.1989.tb00406.x ARS B, 1989, 3RD P INT C CHOL MAT Dahmann H, 1929, Z HALS NASEN OHRENH, V24, P462 DECRAEMER WF, 1991, HEARING RES, V51, P107, DOI 10.1016/0378-5955(91)90010-7 DIRCKX JJJ, 1989, REV SCI INSTRUM, V60, P3698, DOI 10.1063/1.1140477 DIRCKX JJJ, 1988, APPL OPTICS, V27, P1164, DOI 10.1364/AO.27.001164 ELNER A, 1971, Acta Oto-Laryngologica, V72, P397, DOI 10.3109/00016487109122499 FLISBERG K, 1963, Acta Otolaryngol Suppl, V182, P43 GRAHAM MD, 1978, ANN OTO RHINOL LARYN, V87, P426 GRONTVED A, 1989, ACTA OTO-LARYNGOL, V108, P101, DOI 10.3109/00016488909107399 GUELKE R, 1952, J PHYSIOL-LONDON, V116, P175 GUNDERSE.T, 1972, ARCHIV OTOLARYNGOL, V96, P416 GUNDERSEN T, 1975, ACTA OTOLARYNGOLS TO, V82, P16 HELMHOLT ZH, 1868, PFLUGERS ARCH, V1, P1 Helmholtz H, 1868, PFLUGERS ARCH, V1, P1, DOI 10.1007/BF01640310 HERGILS L, 1985, ARCH OTOLARYNGOL, V111, P86 HUTTENBRINK KN, 1989, ACTA OTO-LARYNGOL, V451, P1 Kobrak HG, 1959, MIDDLE EAR KOBRAK HG, 1948, J ACOUST SOC AM, V20, P125, DOI 10.1121/1.1906353 KRINGLEBOTN M, 1985, J ACOUST SOC AM, V77, P159, DOI 10.1121/1.392280 LOCH WE, 1942, ANN OTO RHINOL LARYN, V51, P396 Loch WE, 1942, ANN OTO RHINOL LARYN, V51, P995 MACH E, 1872, SITZUNGSBER AKAD MN3, V66, P337 METZ O, 1946, ACTA OTOLARYNGOL S, V63 MUELLER J, 1840, HDB PHYSL MENSCHEN, V2 RASMUSSEN HELMER, 1946, ACTA OTO LARYNGOL [STOCKHOLM], V34, P415, DOI 10.3109/00016484609119536 Shinkawa H, 1987, Acta Otolaryngol Suppl, V435, P107 TONNDORF J, 1972, J ACOUST SOC AM, V52, P1221, DOI 10.1121/1.1913236 Tonndorf J, 1966, Arch Klin Exp Ohren Nasen Kehlkopfheilkd, V187, P431, DOI 10.1007/BF02470486 VLAMING MSMG, 1986, CLIN OTOLARYNGOL, V11, P353, DOI 10.1111/j.1365-2273.1986.tb00137.x von Bekesy G., 1941, AKUST Z, V6, P1 von Bekesy G, 1929, PHYS Z, V30, P115 NR 33 TC 29 Z9 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 93 EP 106 DI 10.1016/0378-5955(91)90009-X PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300008 PM 2013548 ER PT J AU DECRAEMER, WF DIRCKX, JJJ FUNNELL, WRJ AF DECRAEMER, WF DIRCKX, JJJ FUNNELL, WRJ TI SHAPE AND DERIVED GEOMETRICAL PARAMETERS OF THE ADULT, HUMAN TYMPANIC MEMBRANE MEASURED WITH A PHASE-SHIFT MOIRE INTERFEROMETER SO HEARING RESEARCH LA English DT Article DE TYMPANIC MEMBRANE; HUMAN; SHAPE; MOIRE INTERFEROMETER ID FINITE-ELEMENT MODEL; CAT EARDRUM; FREQUENCIES; FRINGES AB The shape of the tympanic membrane is fairly complex and seems to be a significant importance in the coupling of the acoustic sound pressure in the external ear canal to the motion of the middle ear ossicles. A moire shift interferometer was used to measure with great precision the shape of the external surface of human tympanic membrane. The dense matrix of z(x,y) values thus obtained is used to calculate different geometrical parameters (area, curvature,..). We show further how the same data can be used to specify exactly the shape of the tympanic membrane in a mathematical finite-element model of the middle ear. C1 UNIV ANTWERP,BIOMED PHYS LAB,ANTWERP,BELGIUM. MCGILL UNIV,DEPT BIOMED ENGN,MONTREAL H3A 2T5,QUEBEC,CANADA. MCGILL UNIV,DEPT OTOLARYNGOL,MONTREAL H3A 2T5,QUEBEC,CANADA. RI Funnell, Robert/B-4488-2013 CR ARS B, 1987, AM J OTOL, V8, P148 DECRAEMER WF, 1982, SPIE P, V370, P116 DIRCKX JJJ, 1989, REV SCI INSTRUM, V60, P3698, DOI 10.1063/1.1140477 DIRCKX JJJ, 1990, APPL OPTICS, V29, P1474, DOI 10.1364/AO.29.001474 DIRCKX JJJ, 1988, APPL OPTICS, V27, P1164, DOI 10.1364/AO.27.001164 DIRCKX JJJ, 1991, HEARING RES, V51, P93, DOI 10.1016/0378-5955(91)90009-X FUNNELL WRJ, 1979, J ACOUST SOC AM, V65, pS9, DOI 10.1121/1.2017551 FUNNELL WRJ, 1978, J ACOUST SOC AM, V63, P1461, DOI 10.1121/1.381892 FUNNELL WRJ, 1983, J ACOUST SOC AM, V73, P1657, DOI 10.1121/1.389386 FUNNELL WRJ, 1981, APPL OPTICS, V20, P3245, DOI 10.1364/AO.20.003245 FUNNELL WRJ, 1987, J ACOUST SOC AM, V81, P1851, DOI 10.1121/1.394749 Goursat E., 1959, COURSE MATH ANAL, VI GRAHAM MD, 1978, ANN OTO RHINOL LARYN, V87, P426 Helmholtz H, 1868, PFLUGERS ARCH, V1, P1, DOI 10.1007/BF01640310 JANSSENS JL, 1985, OPTIK, V71, P45 KHANNA SM, 1975, J ACOUST SOC AM, V57, pS72, DOI 10.1121/1.1995400 KHANNA SM, 1975, J ACOUST SOC AM, V58, pS88, DOI 10.1121/1.2002370 KHANNA SM, 1985, J ACOUST SOC AM, V77, P577, DOI 10.1121/1.391876 Kirikae I., 1960, STRUCTURE FUNCTION M KOJO Y, 1954, J O R L SOC JPN, V57, P115 MARQUET J, 1973, ARCH OTOLARYNGOL, V87, P58 NR 21 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 JAN PY 1991 VL 51 IS 1 BP 107 EP 122 DI 10.1016/0378-5955(91)90010-7 PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300009 PM 2013538 ER PT J AU ABBAS, PJ BROWN, CJ AF ABBAS, PJ BROWN, CJ TI ELECTRICALLY EVOKED AUDITORY BRAIN-STEM RESPONSE - GROWTH OF RESPONSE WITH CURRENT LEVEL SO HEARING RESEARCH LA English DT Article DE ELECTRICAL STIMULATION; COCHLEAR IMPLANT; EABR ID NERVE SURVIVAL; STEM RESPONSE; STIMULATION; COCHLEA; POTENTIALS AB The electrically evoked brainstem response (EABR) was measured in cochlear implant users who had received either the Ineraid multichannel implant or the Nucleus multichannel implant. Although both implants use a multi-electrode array, they are different in a number of ways. In the Ineraid system the electrodes can be accessed directly through a percutaneous plug and stimulation is generally on four different intracochlear electrodes relative to a common ground outside the cochlea. In the Nucleus implant stimulation is accomplished via an internal coil and stimulation is bipolar between pairs along the 22 electrode array. The ABR waveforms were similar for both groups of subjects, consisting of a series of 3 or 4 positive peaks at the highest levels of stimulation. Using the normal stimulation mode (bipolar for Nucleus and monopolar for Ineraid), users of both devices demonstrated an increase in response amplitude and a decrease in response latency with increases in current level. The threshold of response tended to be higher and growth of the response with level tended to be more gradual for Nucleus users than for Ineraid users. However, with bipolar stimulation for both implant types, when the stimulating electrodes were closely spaced the threshold of response was higher and the growth of amplitude with level was more gradual than the case where the electrodes were separated further. When bipolar stimulation and similar electrode spacing was used, the response growth and threshold were similar for both implant types. Results from neither device showed a strong correlation with performance on word recognition tests. RP ABBAS, PJ (reprint author), UNIV IOWA,DEPT SPEECH PATHOL & AUDIOL,IOWA CITY,IA 52242, USA. CR ABBAS PJ, 1988, HEARING RES, V36, P153, DOI 10.1016/0378-5955(88)90057-3 BLACK FO, 1987, ANN OTO RHINOL LARYN, V96, P96 BLACK RC, 1980, J ACOUST SOC AM, V67, P868, DOI 10.1121/1.383966 COLUMBO J, 1987, HEARING RES, V31, P287 CROSBY PA, 1985, Patent No. 14532930 EDDINGTON DK, 1990, 2ND IN COCHL IMPL S, P20 GAME CJA, 1987, ANN OTO RHINOL LARYN, V96, P94 GANTZ BJ, 1988, LARYNGOSCOPE, V98, P1100 GARDI JN, 1985, COCHLEAR IMPLANTS, P351 HALL RD, 1990, ABSTR ASS RES OT ST HERMANN B, 1990, 2ND INT COCHL IMPL S LUSTED HS, 1984, LARYNGOSCOPE, V94, P878 MARSH RR, 1981, OTOLARYNG HEAD NECK, V89, P125 Meyer B, 1984, Acta Otolaryngol Suppl, V411, P168 MIYAMOTO RT, 1987, OTOLARYNG HEAD NECK, V96, P34 OLEARY SJ, 1985, HEARING RES, V18, P273, DOI 10.1016/0378-5955(85)90044-9 SCHINDLER RA, 1977, ARCH OTOLARYNGOL, V103, P691 SHALLOP JK, 1990, 2ND INT COCHL IMPL S, P57 SHALLOP JK, 1990, EAR HEARING, V11, P5, DOI 10.1097/00003446-199002000-00004 SIMMONS FB, 1984, ANN OTO RHINOL LARYN, V93, P97 SMITH L, 1983, ANN OTO RHINOL LARYN, V92, P19 STARR A, 1979, ANN OTO RHINOL LARYN, V88, P550 Tyler R. S., 1983, IOWA COCHLEAR IMPLAN TYLER RS, 1986, IOWA LASER VIDEODISC VANDENHONERT C, 1986, HEARING RES, V21, P109, DOI 10.1016/0378-5955(86)90033-X VANDENHONERT C, 1987, HEARING RES, V29, P195, DOI 10.1016/0378-5955(87)90167-5 NR 26 TC 64 Z9 65 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 123 EP 138 DI 10.1016/0378-5955(91)90011-W PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300010 PM 2013539 ER PT J AU ABBAS, PJ BROWN, CJ AF ABBAS, PJ BROWN, CJ TI ELECTRICALLY EVOKED AUDITORY BRAIN-STEM RESPONSE - REFRACTORY PROPERTIES AND STRENGTH-DURATION FUNCTIONS SO HEARING RESEARCH LA English DT Article DE EABR; REFRACTION; CHRONAXIE ID PHYSIOLOGICAL-PROPERTIES; STIMULATION; NERVE; RECORDINGS AB The electrically evoked auditory brainstem potential (EABR) was recorded in users of both the Nucleus cochlear implant and the Ineraid cochlear implant. The refractory properties of the EABR were evaluated by measuring the response amplitude to a two-pulse stimulus where the interpulse interval was varied. The threshold of response for a single pulse stimulus was also measured as a function of the duration of the biphasic pulse. These strength-duration functions were then used to calculate an EABR chronaxie measure. Both of these measures showed a similar range for the monopolar stimulation used with the Ineraid implant and the bipolar stimulation used with the Nucleus implant. Neither for these two measures of the temporal response properties showed any clear relationship to the ability of individual subjects to perform on a speech perception task. RP ABBAS, PJ (reprint author), UNIV IOWA,DEPT SPEECH PATHOL & AUDIOL,IOWA CITY,IA 52242, USA. CR ABBAS PJ, 1991, HEARING RES, V51, P123, DOI 10.1016/0378-5955(91)90011-W ABBAS PJ, 1988, HEARING RES, V36, P153, DOI 10.1016/0378-5955(88)90057-3 BROWN CJ, 1990, IN PRESS J ACOUST SO COLUMBO J, 1987, HEARING RES, P287 LOEB GE, 1983, ANN NY ACAD SCI, V405, P123, DOI 10.1111/j.1749-6632.1983.tb31625.x PARKINS CW, 1987, HEARING RES, V31, P267, DOI 10.1016/0378-5955(87)90196-1 SHANNON RV, 1983, HEARING RES, V11, P157, DOI 10.1016/0378-5955(83)90077-1 STYPULKOWSKI PH, 1984, HEARING RES, V14, P205, DOI 10.1016/0378-5955(84)90051-0 Tyler R. S., 1983, IOWA COCHLEAR IMPLAN TYLER RS, 1986, IOWA VIDEODISC TESTS VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 NR 11 TC 28 Z9 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 139 EP 148 DI 10.1016/0378-5955(91)90012-X PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300011 PM 2013540 ER PT J AU KALTENBACH, JA LAZOR, J AF KALTENBACH, JA LAZOR, J TI TONOTOPIC MAPS OBTAINED FROM THE SURFACE OF THE DORSAL COCHLEAR NUCLEUS OF THE HAMSTER AND RAT SO HEARING RESEARCH LA English DT Article DE TONOTOPIC MAPPING; RAT; HAMSTER; DORSAL COCHLEAR NUCLEUS; COMPARATIVE STUDY; DEVELOPMENT ID AUDITORY-CORTEX; MONGOLIAN GERBIL; REPRESENTATION; ORGANIZATION; FREQUENCY; 2-DEOXYGLUCOSE; CAT AB Tonotopic organization was mapped over the surface of the dorsal cochlear nucleus (DCN) on the Syrian golden hamster and albino rat. The purpose of this study was to describe comparative similarities and differences in fine map features that exist between these two species, and to differentiate features which show a high degree of constancy from those which show significant variations across individuals of the same species. In general, the tonotopic organization seen in both species was characterized by a mediolateral gradient in which high CFs were located medially and low CFs laterally. Maps within each species displayed a high degree of constancy both in the slopes of the gradient as well as in the preferred rostrocaudal orientation of isofrequency contours. However, between species significant differences were seen in the slope of the CF gradient. In the rat, CFs declined toward the lateral extremity at a rate which was nearly twice that seen in the hamster, despite the fact that there were no apparent differences in the width of the DCN in these two species. The precise configuration of areas subtending selected frequency ranges also showed considerable individual variation and defined a 'microstructure' of tonotopic organization that was unique for each animal. The implications of these findings on concepts of DCN development and modes of innervation by the auditory nerve are discussed. C1 LOYOLA UNIV,SCH MED,CHICAGO,IL 60611. RP KALTENBACH, JA (reprint author), WAYNE STATE UNIV,SCH MED,DEPT AUDIOL,4201 ST ANTOINE,DETROIT,MI 48201, USA. CR BOCK GR, 1978, AUDIOLOGY, V17, P193 BOCK GR, 1977, SCIENCE, V197, P396, DOI 10.1126/science.877565 EVANS EF, 1978, AUDIOLOGY, V17, P369 Fay R. R., 1988, HEARING VERTEBRATES ROBERTSON D, 1989, J COMP NEUROL, V282, P456, DOI 10.1002/cne.902820311 JENKINS WM, 1990, J NEUROPHYSIOL, V63, P82 KALTENBACH JA, 1987, EXP NEUROL, V96, P406, DOI 10.1016/0014-4886(87)90058-6 KALTENBACH JM, 1985, THESIS U MICROFILMS KELLY JB, 1977, J COMP PHYSIOL PSYCH, V91, P930, DOI 10.1037/h0077356 Lorente de No R, 1981, PRIMARY ACOUSTIC NUC MERZENICH MM, 1975, J NEUROPHYSIOL, V38, P231 MERZENICH MM, 1987, J COMP NEUROL, V258, P281, DOI 10.1002/cne.902580208 MOREST DK, 1983, HEARING RES, V9, P145, DOI 10.1016/0378-5955(83)90024-2 Mountcastle V B, 1979, NEUROSCIENCES 4TH ST, P21 OSEN KK, 1969, J COMP NEUROL, V136, P453, DOI 10.1002/cne.901360407 RAKIC P, 1988, SCIENCE, V241, P170, DOI 10.1126/science.3291116 REALE RA, 1980, J COMP NEUROL, V192, P265, DOI 10.1002/cne.901920207 ROSE JE, 1959, B JOHNS HOPKINS HOSP, V104, P211 RYAN AF, 1982, EXP BRAIN RES, V47, P428 RYAN AF, 1988, HEARING RES, V36, P181, DOI 10.1016/0378-5955(88)90060-3 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 RYAN AF, 1988, ABSTR ASS RES OTOLAR, V11, P197 SCHWEITZER L, 1984, J COMP NEUROL, V225, P228, DOI 10.1002/cne.902250208 SPERRY RW, 1963, P NATL ACAD SCI USA, V50, P703, DOI 10.1073/pnas.50.4.703 SUGA N, 1987, J NEUROPHYSIOL, V58, P643 SZENTAGOTHAI J, 1983, REV PHYSIOL BIOCH P, V98, P11, DOI 10.1007/BFb0033866 UDIN SB, 1988, ANNU REV NEUROSCI, V11, P289, DOI 10.1146/annurev.neuro.11.1.289 WEBSTER DB, 1971, J COMP NEUROL, V143, P323, DOI 10.1002/cne.901430305 WILLOTT JF, 1983, AUDITORY PSYCHOBIOLO, P305 YAJIMA Y, 1989, EXP BRAIN RES, V75, P381 NR 30 TC 45 Z9 45 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD JAN PY 1991 VL 51 IS 1 BP 149 EP 160 DI 10.1016/0378-5955(91)90013-Y PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300012 PM 2013541 ER PT J AU HILDESHEIMER, M HENKIN, Y MUCHNIK, C ANAFI, R SAHARTOV, E RUBINSTEIN, M AF HILDESHEIMER, M HENKIN, Y MUCHNIK, C ANAFI, R SAHARTOV, E RUBINSTEIN, M TI SEDATION EFFECT ON TEMPORARY THRESHOLD SHIFT INDUCED BY ACOUSTIC OVERSTIMULATION SO HEARING RESEARCH LA English DT Article DE SEDATION; TEMPERATURE; TEMPORARY THRESHOLD SHIFT ID COCHLEAR ELECTRICAL-ACTIVITY; GUINEA-PIGS; NOISE; TEMPERATURE; RESPONSES; SUSCEPTIBILITY; HYPOTHERMIA; BARBITURATE; EAR AB The mechanism by which noise damages the inner ear has not as yet been fully elucidated. Experiments were done to study the influence of the sedation in temporary threshold shift (TS) induced by acoustic overstimulation, as barbiturates were found to improve the brain's tolerance to ischemia. Four groups of guinea pigs (GP) were used. The temporary TS was decreased with the reduction of the temperature in awake, as well as sedated, sound-exposed GP. However, the temporary TS in the sedated, but normothermic GP was as great as in the awake, normothermic group. The high temperature counteracts the protection effect of the sedation in noise-induced hearing loss. RP HILDESHEIMER, M (reprint author), TEL AVIV UNIV,CHAIM SHEBA MED CTR,SACKLER FAC MED,SCH HLTH PROFESS,IL-52621 TEL HASHOMER,ISRAEL. CR BERNDT H, 1979, ARCH OTO-RHINO-LARYN, V224, P125, DOI 10.1007/BF00455235 BERNDT H, 1981, ARCH OTO-RHINO-LARYN, V232, P199, DOI 10.1007/BF00505038 BORG E, 1984, ACOUSTIC REFLEX, P413 BORG E, 1982, ACTA PHYSIOL SCAND, V115, P281, DOI 10.1111/j.1748-1716.1982.tb07077.x BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 CONLEE JW, 1986, HEARING RES, V23, P81, DOI 10.1016/0378-5955(86)90177-2 DENGERINK HA, 1984, AUDIOLOGY, V23, P401 DRESCHER DG, 1976, J ACOUST SOC AM, V59, P401, DOI 10.1121/1.380877 HENRY KR, 1980, AUDIOLOGY, V19, P44 HENRY KR, 1984, HEARING RES, V16, P225, DOI 10.1016/0378-5955(84)90111-4 HILDESHEIMER M, 1979, ACTA OTO-LARYNGOL, V88, P37, DOI 10.3109/00016487909137137 HILDESHEIMER M, 1990, HEARING RES, V43, P263, DOI 10.1016/0378-5955(90)90233-F HILDESHEIMER M, 1990, IN PRESS EUR ARCH OT HO IK, 1981, ANNU REV PHARMACOL, V21, P83, DOI 10.1146/annurev.pa.21.040181.000503 ISING H, 1982, ARCH OTO-RHINO-LARYN, V236, P139, DOI 10.1007/BF00454034 LINDGREN F, 1988, SCAND AUDIOL, V17, P11, DOI 10.3109/01050398809042175 MICHENFELDER JD, 1976, ARCH NEUROL-CHICAGO, V33, P345 MICHENFELDER JD, 1975, STROKE, V6, P405 MICHENFELDER JD, 1989, ARCH NEUROL-CHICAGO, V244, P1 NUSSMEIER NA, 1986, ANESTHESIOLOGY, V64, P171 RUBINSTEIN M, 1976, ANN OTO RHINOL LARYN, V85, P276 RYAN AF, 1982, BRAIN RES, V234, P213, DOI 10.1016/0006-8993(82)90863-0 SIMMONS FB, 1960, ANN OTO RHINOL LARYN, V69, P1063 SPOENDLI.H, 1971, ACTA OTO-LARYNGOL, V71, P166, DOI 10.3109/00016487109125346 Ward W D, 1968, Contrib Sens Physiol, V3, P191 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 1991 VL 51 IS 1 BP 161 EP 166 DI 10.1016/0378-5955(91)90014-Z PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EW973 UT WOS:A1991EW97300013 PM 2013542 ER PT J AU HARRIS, DM ROTCHE, R FREEDOM, T AF HARRIS, DM ROTCHE, R FREEDOM, T TI POSTNATAL-GROWTH OF COCHLEAR SPIRAL IN MONGOLIAN GERBIL SO HEARING RESEARCH LA English DT Article DE AUDITORY GROWTH AND DEVELOPMENT; GERBIL; COCHLEA; OTIC CAPSULE; MIDDLE EAR; INFERIOR COLLICULUS ID TONOTOPIC ORGANIZATION; ACOUSTIC TRAUMA; PLACE PRINCIPLE; FREQUENCY; HEARING; MAP; EAR AB Measurements were made of cochlear dimensions in an age-graded series of Mongolian gerbils. The radii of the cochlear spiral at five locations and the length of the modiolus were determined from in situ photographs of mid-modiolar sections. The anterior to posterior dimensions of the auditory bulla and of the inferior colluculus were also measured to provide a general context for inner ear growth functions. At birth in this species, the cochlear capsule is still growing, and, although the basal turn is closer to the final adult proportion than more apical turns, all radii approach adult dimensions together at 9-10 days after birth (DAB). Comparison of the morphological development of gerbil otic capsule with the change in cochlear tonotopic mapping observed during physiological development shows that growth is complete before the onset of measurable electrical responses at 12-14 DAB. C1 UNIV ILLINOIS,COLL MED,DEPT OTOLARYNGOL HEAD & NECK SURG,CHICAGO,IL 60680. CR ANSON BJ, 1973, SURGICAL ANATOMY TEM ARJMAND E, 1988, HEARING RES, V32, P93, DOI 10.1016/0378-5955(88)90149-9 COTANCHE DA, 1987, HEARING RES, V25, P267, DOI 10.1016/0378-5955(87)90098-0 COUSILLAS H, 1985, HEARING RES, V19, P217, DOI 10.1016/0378-5955(85)90141-8 ECHTELER SM, 1989, NATURE, V341, P147, DOI 10.1038/341147a0 FINCK A, 1972, J COMP PHYSIOL PSYCH, V78, P375, DOI 10.1037/h0032373 GANS D, 1989, BRAIN RES BULL, V22, P475, DOI 10.1016/0361-9230(89)90075-0 HARRIS DM, 1986, ABSTR ASS RES OTOLAR, V9, P88 HARRIS DM, 1984, SCIENCE, V225, P741, DOI 10.1126/science.6463651 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 KRAUS HJ, 1981, HEARING RES, V4, P89, DOI 10.1016/0378-5955(81)90038-1 LIPPE W, 1983, SCIENCE, V219, P514, DOI 10.1126/science.6823550 LIPPE WR, 1987, HEARING RES, V25, P205, DOI 10.1016/0378-5955(87)90092-X OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 ROMAND R, 1987, HEARING RES, V28, P117, DOI 10.1016/0378-5955(87)90158-4 Rubel E.W., 1978, HDB SENSORY PHYSL, V9, P135 RUBEL EW, 1983, SCIENCE, V219, P512, DOI 10.1126/science.6823549 RUBEL EW, 1976, J COMP NEUROL, V166, P469, DOI 10.1002/cne.901660408 RYALS BM, 1984, ACTA OTO-LARYNGOL, V98, P93, DOI 10.3109/00016488409107539 Ryan A F, 1988, Brain Res, V469, P61 SANES DH, 1989, J COMP NEUROL, V279, P436, DOI 10.1002/cne.902790308 SCHMIEDT RA, 1987, ABSTR ASS RES OT, V10, P67 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 Sher A E, 1971, Acta Otolaryngol Suppl, V285, P1 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 YANCEY C, 1985, HEARING RES, V18, P189, DOI 10.1016/0378-5955(85)90011-5 NR 28 TC 28 Z9 28 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 1 EP 6 DI 10.1016/0378-5955(90)90029-O PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300001 PM 2076965 ER PT J AU SNYDER, RL REBSCHER, SJ CAO, K LEAKE, PA KELLY, K AF SNYDER, RL REBSCHER, SJ CAO, K LEAKE, PA KELLY, K TI CHRONIC INTRACOCHLEAR ELECTRICAL-STIMULATION IN THE NEONATALLY DEAFENED CAT .1. EXPANSION OF CENTRAL REPRESENTATION SO HEARING RESEARCH LA English DT Article DE ELECTRICAL STIMULATION; COCHLEAR PROSTHESIS; PLASTICITY; AUDITORY DEVELOPMENT; INFERIOR COLLICULUS ID UNILATERAL COCHLEAR ABLATION; CONDUCTIVE HEARING-LOSS; AUDITORY-NERVE FIBERS; INFERIOR COLLICULUS; BRAIN-STEM; BINAURAL INTERACTION; SOUND DEPRIVATION; SENSITIVE PERIOD; BARN OWL; NUCLEUS AB Intracochlear electrical stimulation via cochlear prostheses has been employed as a means of providing some hearing to deaf children. Since chronically restricted stimuli are known to have profound effects on central nervous system development, it is important to examine the effects of chronic intracochlear electrical stimulation in a neonatally deafened animal model. In this study neonatally deafened cats were implanted with a scala tympani electrode consisting of two pairs of electrodes. Chronic electrical stimulation was delivered using one electrode pair and consisted of charge-balanced biphasic pulses (200-mu-s/phase, 30 pps) at 2 dB above the electrically evoked auditory brain response (EABR) threshold for 4 h/day or at 6 dB 1 h/day, 5 days/week, for up to 3 months. The second electrode pair was unstimulated and served as an internal control. Following chronic stimulation, acute mapping experiments were performed in the central nucleus of the inferior colliculus (ICC) using single unit and multi-unit recording techniques and activating each electrode pair separately. In addition to these chronically stimulated animals, 2 other groups of experimental animals were studied: A normal group consisting of prior normal adult cats that were acutely implanted; and an unstimulated control group consisting of neonatally deafened adult cats that were either acutely implanted or implanted at 8-10 weeks of age but not chronically stimulated. Among the major findings of this study are: Electrical stimulation of the intracochlear bipolar electrode consistently produces activation of a reproducibly limited sector of the ICC. The location of this activated sector was found to be consistent with the known cochleotopic organization of the ICC and the intracochlear location of the stimulating electrodes. No major differences in the spatial representation of activated electrodes were found between prior normal cats and neonatally deafened unstimulated cats. The locations, shapes and widths of these spatial representations were virtually indistinguishable indicating that ICC cochleotopic organizations were equivalent in these two experimental groups. In contrast, the ICC representation of chronically stimulated electrode pairs were found to be significantly different. The average area activated by chronically stimulated electrode pairs at 6 dB above minimum threshold was approximately twice that of unstimulated deafened animals and prior normal animals; and it was larger, but not significantly so, than the average of the unstimulated electrode pair in the same experimental group. These results indicate that: 1) One of the fundamental features of the central auditory organization, the orderly topographic representation of cochlear place, is unaltered (at least to the level of the midbrain) by the lack of normal acoustic input during development. 2) Electrical stimulation of very limited duration and intensity delivered to a restricted sector of the cochlear spiral can expand the central representation of that sector and alter cochleotopic representations in the auditory CNS. RP SNYDER, RL (reprint author), UNIV CALIF SAN FRANCISCO,DEPT OTOLARYNGOL,COLEMAN & EPSTEIN LABS,871 HSE,SAN FRANCISCO,CA 94143, USA. CR AITKIN LM, 1975, J NEUROPHYSIOL, V38, P1196 BLACK RC, 1983, ANN NY ACAD SCI, V405, P137, DOI 10.1111/j.1749-6632.1983.tb31626.x BRUGGE JF, 1985, HEARING RES, V20, P275, DOI 10.1016/0378-5955(85)90032-2 BRUGGE JF, 1984, J ACOUST SOC AM, V75, P1548, DOI 10.1121/1.390826 BRUMMER SB, 1983, ANN NY ACAD SCI, V405, P159, DOI 10.1111/j.1749-6632.1983.tb31628.x CLARK SA, 1988, NATURE, V332, P444, DOI 10.1038/332444a0 CLOPTON BM, 1986, DEV NEUROPSYCHOBIOLO CLOPTON BM, 1983, ANN NY ACAD SCI, V405, P146, DOI 10.1111/j.1749-6632.1983.tb31627.x 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 DORMAN MF, 1990, IN PRESS EAR HEAR DUBIN MW, 1986, J NEUROSCI, V6, P1021 FENG AS, 1980, BRAIN RES, V189, P530, DOI 10.1016/0006-8993(80)90112-2 HARTMANN R, 1984, ADV AUDIOL, V1, P18 HARTMANN R, 1987, ANN OTO RHINOL LARYN, V96, P30 HARTMANN R, 1989, COCHLEAR IMPLANTS MO, P135 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 KAAS JH, 1988, NEUROBIOLOGY NEOCORT, P101 KITZES LM, 1985, J NEUROPHYSIOL, V53, P1483 KNUDSEN EI, 1984, J NEUROSCI, V4, P1001 KNUDSEN EI, 1985, J NEUROSCI, V5, P3094 KNUDSEN EI, 1984, J NEUROSCI, V4, P10012 LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 LEAKE PA, 1988, HEARING RES, V33, P11, DOI 10.1016/0378-5955(88)90018-4 LEAKE PA, 1982, HEARING RES, V7, P281 LEAKE PA, 1990, ASS RES OTOLARYNGOL, V13 LUXFORD WM, 1985, COCHLEAR IMPLANTS, P1 MERZENICH MM, 1973, ANN OTOL, V83, P486 MERZENICH MM, 1977, FUNCTIONAL ELECT STI, P321 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 Merzenich M.M., 1988, NEUROBIOLOGY NEOCORT, P41 Mitchell DE, 1984, HDB PHYSL 1 1, V3, P507 MOORE DR, 1989, J NEUROSCI, V9, P1213 MOORE DR, 1988, J COMP NEUROL, V272, P503, DOI 10.1002/cne.902720405 MOORE DR, 1985, J COMP NEUROL, V240, P180, DOI 10.1002/cne.902400208 MOORE DR, 1981, BRAIN RES, V208, P198, DOI 10.1016/0006-8993(81)90632-6 MOVSHON JA, 1981, ANNU REV PSYCHOL, V32, P477, DOI 10.1146/annurev.ps.32.020181.002401 MOXON ED, 1971, NEURAL MECHANICAL RE NICOLL RA, 1988, NEURON, V1, P97, DOI 10.1016/0896-6273(88)90193-6 NORDEEN KW, 1983, J COMP NEUROL, V214, P144, DOI 10.1002/cne.902140204 NUDO RJ, 1990, IN PRESS REPETITIVE OWENS E, 1989, COCHLEAR IMPLANTS YO, P352 PARKINS CW, 1989, HEARING RES, V41, P137, DOI 10.1016/0378-5955(89)90007-5 POWELL TPS, 1962, J ANAT, V96, P249 REBSCHER S, 1988, 3RD Q PROGR REP Rebscher S. J., 1985, COCHLEAR IMPLANTS, P74 RECANZONE G, 1990, IN PRESS BRAIN RES ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 ROTH GL, 1978, J COMP NEUROL, V182, P661, DOI 10.1002/cne.901820407 Rubel E.W., 1985, P109 SCHINDLER RA, 1989, AM J OTOL, V10, P79 SCHREINER CE, 1988, J NEUROPHYSIOL, V60, P1823 SILVERMAN MS, 1977, J NEUROPHYSIOL, V40, P1266 Simmons F. B., 1966, ARCH OTOLARYNGOL, V84, P24 SNYDER RL, 1990, IN PRESS EFFECTS CHR SNYDER RL, 1990, ASS RES OTOLARYNGOL, V13 STRYKER MP, 1986, J NEUROSCI, V6, P2117 STRYKER MP, 1984, ARVO SPR TRUNE DR, 1982, J COMP NEUROL, V209, P425, DOI 10.1002/cne.902090411 TRUNE DR, 1982, J COMP NEUROL, V209, P409, DOI 10.1002/cne.902090410 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 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 WIESEL TN, 1963, J NEUROPHYSIOL, V26, P978 WIESEL TN, 1965, J NEUROPHYSIOL, V28, P1029 NR 69 TC 129 Z9 131 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 1990 VL 50 IS 1-2 BP 7 EP 34 DI 10.1016/0378-5955(90)90030-S PG 28 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300002 PM 2076984 ER PT J AU DEGROOT, JCMJ MEEUWSEN, F RUIZENDAAL, WE VELDMAN, JE AF DEGROOT, JCMJ MEEUWSEN, F RUIZENDAAL, WE VELDMAN, JE TI ULTRASTRUCTURAL-LOCALIZATION OF GENTAMICIN IN THE COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEA; AMINOGLYCOSIDE COCHLEOTOXICITY; GENTAMICIN; IMMUNOELECTRON MICROSCOPY ID INNER-EAR; HAIR-CELLS; AMINOGLYCOSIDE OTOTOXICITY; IMMUNOGOLD; TISSUES; DRUGS; RAT AB The ultrastructural distribution of gentamicin in the cochlea was investigated immunocytochemically. Specific labeling was restricted to the organ of Corti, in particular to the outer and inner hair cells, the Deiters' cells, Hensen's cells and the tympanic layer cells of the basilar membrane. Other cochlear tissues did not demonstrate any labeling. At the subcellular level, gentamicin was found in lysosomes, multivesicular bodies and small tubules and vesicles. A model is proposed in which it is hypothesized that gentamicin is internalized by endocytotic vesicles and is transferred to the lysosomal compartment as well as to the endoplasmic reticulum and Golgi complex. RP DEGROOT, JCMJ (reprint author), UNIV HOSP UTRECHT,DEPT OTORHINOLARYNGOL,HISTOPHYSIOL & EXPTL PATHOL LAB,ROOM G02531,3584 CX UTRECHT,NETHERLANDS. CR AUBERTTULKENS G, 1979, LAB INVEST, V40, P481 BONVENTRE P F, 1970, Infection and Immunity, V2, P89 DEGROOT JCM, 1988, GLYCOCONJUGATES MED, P324 DEGROOT JCMJ, 1988, HEARING RES, V35, P39, DOI 10.1016/0378-5955(88)90038-X DUVALL AJ, 1983, AM J OTOLARYNG, V4, P400, DOI 10.1016/S0196-0709(83)80046-5 FORGE A, 1989, HEARING RES, V37, P129, DOI 10.1016/0378-5955(89)90035-X FORGE A, 1981, AUDIOLOGY, V20, P274 GRIFFITHS G, 1984, J ULTRA MOL STRUCT R, V89, P65, DOI 10.1016/S0022-5320(84)80024-6 GRIFFIN J P, 1988, British Journal of Audiology, V22, P195, DOI 10.3109/03005368809076453 HAYASHIDA T, 1989, ARCH OTO-RHINO-LARYN, V246, P161, DOI 10.1007/BF00456659 HAYASHIDA T, 1985, ARCH OTO-RHINO-LARYN, V242, P257, DOI 10.1007/BF00453548 HUDSPETH AJ, 1983, J PHYSL, V346, pP66 HUY PTB, 1986, J CLIN INVEST, V77, P1492 IINUMA T, 1967, LARYNGOSCOPE, V77, P159 JUST M, 1977, N-S ARCH PHARMACOL, V300, P57, DOI 10.1007/BF00505080 KALOYANIDES GJ, 1980, KIDNEY INT, V18, P571, DOI 10.1038/ki.1980.175 KROESE ABA, 1989, HEARING RES, V37, P203, DOI 10.1016/0378-5955(89)90023-3 LEAKE PA, 1987, HEARING RES, V25, P153, DOI 10.1016/0378-5955(87)90088-8 LIM DJ, 1986, AM J OTOLARYNG, V7, P73, DOI 10.1016/S0196-0709(86)80037-0 MORRIN JP, 1982, AMINOGLYCOSIDES MICR, P303 NEWMAN GR, 1984, MED LAB SCI, V41, P238 PORTMANN M, 1974, ARCH OTOLARYNGOL, V100, P473 RYBAK LP, 1986, ANNU REV PHARMACOL, V26, P79 SCHACHT J, 1986, HEARING RES, V22, P297, DOI 10.1016/0378-5955(86)90105-X SCHACHT J, 1986, BIOCHEM PHARMACOL, V35, P2843, DOI 10.1016/0006-2952(86)90203-0 SIEGEL JH, 1986, J NEUROCYTOL, V15, P311, DOI 10.1007/BF01611434 SILVERBLATT FJ, 1982, AMINOGLYCOSIDES MICR, P223 SLOT JW, 1984, IMMUNOLABELLING ELEC, P129 SOKABE M, 1982, P JPN ACAD B-PHYS, V58, P177, DOI 10.2183/pjab.58.177 TACHIBANA M, 1984, P JAPAN ACAD B, V69, P318 TAKADA A, 1985, HEARING RES, V19, P245, DOI 10.1016/0378-5955(85)90144-3 TAMMELA MN, 1986, ACTA OTO-LARYNGOL, V101, P247, DOI 10.3109/00016488609132834 TIMMS BG, 1986, AM J ANAT, V175, P267, DOI 10.1002/aja.1001750211 HUY PTB, 1988, ACTA OTO-LARYNGOL, V105, P511, DOI 10.3109/00016488809119511 VELDMAN JE, 1987, LARYNGOSCOPE, V97, P413 Veldman J E, 1985, Acta Otolaryngol Suppl, V423, P29 von Ilberg C, 1971, Acta Otolaryngol, V71, P159, DOI 10.3109/00016487109125345 WILLIAMS SE, 1987, HEARING RES, V30, P11, DOI 10.1016/0378-5955(87)90177-8 Yamane H, 1988, Acta Otolaryngol Suppl, V447, P28 YAMANE H, 1987, ANN OTO RHINOL LARYN, V96, P411 NR 40 TC 56 Z9 56 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 35 EP 42 DI 10.1016/0378-5955(90)90031-J PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300003 PM 2076981 ER PT J AU PFINGST, BE RAI, DT AF PFINGST, BE RAI, DT TI EFFECTS OF LEVEL ON NONSPECTRAL FREQUENCY DIFFERENCE LIMENS FOR ELECTRICAL AND ACOUSTIC STIMULI SO HEARING RESEARCH LA English DT Article DE FREQUENCY DISCRIMINATION; LEVEL; AMPLITUDE MODULATION; AUDITORY PROSTHESIS; ELECTRICAL STIMULATION; SAM NOISE; PSYCHOPHYSICS; NONHUMAN PRIMATE ID MODULATION TRANSFER-FUNCTIONS; COCHLEAR NUCLEUS UNITS; AUDITORY-NERVE FIBERS; AMPLITUDE-MODULATION; INFERIOR COLLICULUS; IMPLANTS; HEARING; DISCRIMINATION; PITCH; CAT AB The purpose of this experiment was to study the effects of stimulus level on discrimination of frequency as represented in the temporal waveforms of acoustic and electrical signals. The subjects were four nonhuman primates in which one ear had been deafened and implanted with an electrode array and the other ear was untreated. Frequency difference limens for 100 Hz electrical sinusoidal stimulation via a cochlear implant in the deafened ear were compared to those for 100 Hz sinusoidally amplitude-modulated white noise (SAM noise) acoustic stimuli to the normal-hearing contralateral ear. To correct for loudness cues, levels of the test stimuli were varied relative to the reference-stimulus level. The test-stimulus levels at which the percent responses were minimum were determined. These levels were used to measure the frequency difference limens. Frequency difference limens for the electrical stimuli decreased as a function of reference-stimulus level through most of the dynamic range, while those for the acoustic stimuli reached a minimum at 20 dB to 40 dB above threshold. For the electrical stimuli the slopes and relative positions of the frequency difference limen vs. level functions varied from subject to subject, and with changes in electrode configuration within a subject. These differences were related to threshold level and dynamic range. At higher levels of stimulation, frequency difference limens for acoustic and electrical stimuli fell in the same range. The slopes and relative positions of the frequency difference limen vs. level functions for electrical stimuli did not parallel those of level difference limen vs. level functions collected simultaneously from the same ears. The data suggest that nonspectral frequency discrimination may depend on the number of nerve fibers stimulated. With prostheses in cochleas with less than a full complement of auditory nerve fibers, the data suggest that stimulation level is an important variable influencing discriminability. RP PFINGST, BE (reprint author), UNIV MICHIGAN,MED CTR,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,1301 E ANN ST,ANN ARBOR,MI 48109, USA. CR BACON SP, 1985, AUDIOLOGY, V24, P117 BILGER RC, 1977, ANN OTOL RHINOL LA S, V38, P92 BURNS EM, 1981, J ACOUST SOC AM, V70, P1655, DOI 10.1121/1.387220 BURNS EM, 1976, J ACOUST SOC AM, V60, P863, DOI 10.1121/1.381166 CLARK GM, 1986, OTOLARYNG CLIN N AM, V19, P329 EDDINGTON DK, 1980, J ACOUST SOC AM, V68, P885, DOI 10.1121/1.384827 EMMERICH DS, 1989, J ACOUST SOC AM, V85, P1653, DOI 10.1121/1.397953 FORMBY C, 1985, J ACOUST SOC AM, V78, P70, DOI 10.1121/1.392456 FOURCIN A, 1984, ARCH OTOLARYNGOL, V110, P145 GLASS I, 1984, EXP BRAIN RES, V55, P386 GLASS I, 1983, HEARING RES, V12, P223, DOI 10.1016/0378-5955(83)90108-9 HARTMANN R, 1984, HEARING RES, V13, P47, DOI 10.1016/0378-5955(84)90094-7 HENNING GB, 1966, J ACOUST SOC AM, V39, P336, DOI 10.1121/1.1909894 HERNDON MK, 1981, G9065 STANF U TECHN HOUSE WF, 1982, ANN OTO RHINOL LARYN, V91, P104 JAVEL E, 1980, J ACOUST SOC AM, V68, P133, DOI 10.1121/1.384639 LANGNER G, 1988, J NEUROPHYSIOL, V60, P1799 MERZENIC.MM, 1973, ANN OTO RHINOL LARYN, V82, P486 MOLLER AR, 1972, ACTA PHYSIOL SCAND, V86, P223, DOI 10.1111/j.1748-1716.1972.tb05328.x MOODY DB, 1970, ANIMAL PSYCHOPHYSICS, P277 MULLER C, 1981, J ACOUST SOC AM, V70, pS52 PALMER AR, 1982, ARCH OTO-RHINO-LARYN, V236, P197, DOI 10.1007/BF00454039 PARKIN JL, 1988, LARYNGOSCOPE, V98, P262 PFINGST BE, 1984, 7 MIDW RES M ASS RES, P10 PFINGST BE, 1987, ANN OTO RHINOL LARYN, V96, P34 PFINGST BE, 1983, ANN NY ACAD SCI, V405, P224, DOI 10.1111/j.1749-6632.1983.tb31635.x PFINGST BE, 1975, J ACOUST SOC AM, V57, P421, DOI 10.1121/1.380465 PFINGST BE, 1985, COCHLEAR IMPLANTS, P305 PFINGST BE, 1979, ANN OTO RHINOL LARYN, V88, P613 PFINGST BE, 1988, HEARING RES, V34, P243, DOI 10.1016/0378-5955(88)90005-6 PFINGST BE, 1984, ARCH OTOLARYNGOL, V110, P140 PFINGST BE, 1989, J NEUROSCI METH, V29, P207, DOI 10.1016/0165-0270(89)90145-3 PFINGST BE, 1985, SEMIN HEAR, V6, P7, DOI 10.1055/s-0028-1091989 PIERCE JR, 1975, BIOSCI COMMUN, V1, P111 REES A, 1987, HEARING RES, V27, P129, DOI 10.1016/0378-5955(87)90014-1 SCHREINER CE, 1986, HEARING RES, V21, P227, DOI 10.1016/0378-5955(86)90221-2 SHANNON RV, 1986, SENSORINEURAL HEARIN, P349 Simmons F. B., 1966, ARCH OTOLARYNGOL, V84, P24 SMITH RL, 1980, HEARING RES, V2, P123, DOI 10.1016/0378-5955(80)90034-9 SPELMAN FA, 1978, P SAN DIEGO BIOMED S, V17, P1 TONG YC, 1989, 2ND Q PROGR REP VANDENHONERT C, 1987, HEARING RES, V29, P207, DOI 10.1016/0378-5955(87)90168-7 VANDENHONERT C, 1984, HEARING RES, V14, P225, DOI 10.1016/0378-5955(84)90052-2 VIEMEISTER NF, 1979, J ACOUST SOC AM, V66, P1364, DOI 10.1121/1.383531 VIEMEISTER NF, 1985, 8TH MIDW RES M ASS R, P170 XUE XL, 1989, J NEUROSCI METH, V28, P189, DOI 10.1016/0165-0270(89)90035-6 YATES GK, 1987, HEARING RES, V27, P221, DOI 10.1016/0378-5955(87)90003-7 NR 47 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 1990 VL 50 IS 1-2 BP 43 EP 56 DI 10.1016/0378-5955(90)90032-K PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300004 PM 2076982 ER PT J AU RYAN, AF MILLER, JM WANG, ZX WOOLF, NK AF RYAN, AF MILLER, JM WANG, ZX WOOLF, NK TI SPATIAL-DISTRIBUTION OF NEURAL ACTIVITY EVOKED BY ELECTRICAL-STIMULATION OF THE COCHLEA SO HEARING RESEARCH LA English DT Article DE COCHLEAR PROSTHESIS; CENTRAL AUDITORY SYSTEM; 2-DEOXYGLUCOSE; GERBIL; EAR, INNER ID CENTRAL AUDITORY-SYSTEM; MONGOLIAN GERBIL; TONOTOPIC ORGANIZATION; INFERIOR COLLICULUS; C-14 2-DEOXYGLUCOSE; NERVE; CAT; LOCALIZATION; METABOLISM; TISSUE AB Activity in the central auditory system was mapped with 2-deoxyglucose (2-DG) autoradiography, using either pure tones or electrical stimulation of the normal cochlea. Electrical stimulation with both monopolar (distant reference electrode) and bipolar prostheses near threshold increased 2-DG uptake in auditory nuclei in a manner similar to that seen with a pure tone: increased 2-DG uptake was restricted to a small frequency region of brainstem and mid-brain auditory nuclei. The position of this area was related to the cochlear location of the prosthesis. At higher current amplitudes only the bipolar prosthesis retained spatial restriction of evoked neural activity, while stimulation through a monopolar prosthesis produced evoked activity in all frequency regions of auditory nuclei, and in non-auditory nuclei. Activation of non-auditory structures was consistent with spread of current through the brainstem, rather than activation of peripheral nerves. At all current amplitudes, a monopolar prosthesis evoked higher levels of 2-DG uptake than a bipolar prosthesis. The results suggest that while a bipolar prosthesis provides greater spatial restriction of evoked neural activity and a greater dynamic range, a monopolar prosthesis produces higher levels of evoked activity. evoked activity. C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. VET ADM MED CTR,LA JOLLA,CA. UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. INST HYG,DEPT EXPTL PATHOL,TIANJIN,PEOPLES R CHINA. RP RYAN, AF (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT SURG OTOLARYNGOL,LA JOLLA,CA 92093, USA. CR ACKERMANN RF, 1984, J NEUROSCI, V4, P251 CLOPTON BM, 1983, ANN NY ACAD SCI, V405, P146, DOI 10.1111/j.1749-6632.1983.tb31627.x DURHAM D, 1981, J NEUROSCI, V1, P519 EVANS DA, 1990, LARYNGOSCOPE, V100, P128 GLASS I, 1983, HEARING RES, V12, P223, DOI 10.1016/0378-5955(83)90108-9 HUANG C, 1986, EXP BRAIN RES, V61, P506 HUNGERBUHLER JP, 1981, EXP NEUROL, V71, P104, DOI 10.1016/0014-4886(81)90074-1 JAVEL E, 1987, ANN OTO RHINOL LARYN, V96, P26 MERZENICH MM, 1977, BIOMED ENG INSTRUM, V3, P321 NUDO RJ, 1986, J COMP NEUROL, V245, P553, DOI 10.1002/cne.902450410 OLEARY SJ, 1985, HEARING RES, V18, P273, DOI 10.1016/0378-5955(85)90044-9 OSTAPOFF EM, 1989, HEARING RES, V37, P141, DOI 10.1016/0378-5955(89)90036-1 PFINGST BE, 1984, 10TH ANN C COCHL IMP ROSE JE, 1963, J NEUROPHYSIOL, V26, P294 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 RYAN AF, 1982, BRAIN RES, V252, P177, DOI 10.1016/0006-8993(82)90994-5 RYAN AF, 1982, J COMP NEUROL, V207, P369, DOI 10.1002/cne.902070408 RYAN AF, 1988, DEV BRAIN RES, V41, P61, DOI 10.1016/0165-3806(88)90169-1 RYAN AF, 1988, BRAIN RES, V483, P293 SCHEICH H, 1986, NEUR ABSTR, V12, P1274 SCHMEIDT RA, 1977, THESIS SYRACUSE U SERVIERE J, 1984, J COMP NEUROL, V228, P463, DOI 10.1002/cne.902280403 SHARP FR, 1981, BRAIN RES, V230, P87, DOI 10.1016/0006-8993(81)90393-0 SHARP FR, 1983, BRAIN RES, V263, P97, DOI 10.1016/0006-8993(83)91204-0 SOKOLOFF L, 1977, J NEUROCHEM, V29, P13, DOI 10.1111/j.1471-4159.1977.tb03919.x SPELMAN FA, 1982, ANN OTO RHINOL LARYN, V91, P3 THEURICH M, 1984, BRAIN RES, V322, P157, DOI 10.1016/0006-8993(84)91197-1 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 WANG ZX, 1987, HEARING RES, V27, P145 WEBSTER WR, 1978, NEUROSCI LETT, V10, P43, DOI 10.1016/0304-3940(78)90009-5 NR 31 TC 34 Z9 34 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 57 EP 70 DI 10.1016/0378-5955(90)90033-L PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300005 PM 2076983 ER PT J AU PALMER, AR REES, A CAIRD, D AF PALMER, AR REES, A CAIRD, D TI INTERAURAL DELAY SENSITIVITY TO TONES AND BROAD-BAND SIGNALS IN THE GUINEA-PIG INFERIOR COLLICULUS SO HEARING RESEARCH LA English DT Article DE GUINEA PIG; INFERIOR COLLICULUS; INTERAURAL TIME DELAYS; SINGLE UNIT RECORDING ID LOW-FREQUENCY NEURONS; BINAURAL INTERACTION; NOISE STIMULI; TIME DELAYS; CHANGING FREQUENCY; COCHLEAR NERVE; PHASE-LOCKING; CAT; RESPONSES; CELLS AB We have measured the sensitivity of 243 low-frequency cells in the central nucleus of the guinea pig to the interaural time delay of best frequency (BF) tones, wideband noise and synthetic vowels. The highest rate of firing for the majority of cells occurred when the stimulus to the contralateral ear arrived 100-400-mu-s before that to the ipsilateral ear. The best delays for tones and noise measured in the same cell were highly correlated. In contrast to the tone delay functions, the majority of the delay functions obtained in response to wideband signals did not cycle, but were characterized by a single dominant peak or trough. The response frequency calculated from the delay functions to the vowel often did not correspond to the unit's BF, suggesting that the unit was responding to a component close to the first formant frequency (730 Hz) of the vowel. Phase-locked responses, on the other hand, only occurred to the fundamental frequency of the vowel (100 Hz) and not to higher frequency components. The responses to delayed tone and noise signals in the guinea pig are very like those obtained in the cat and other mammals. The similarity of the range of best delays for the guinea-pig with those reported for the cat, despite the difference in head size in these two species, suggests that the sensitivity to interaural delays reflects the properties of the binaural pathways rather than an adaptation to the delays normally experienced by the animal. C1 UNIV NEWCASTLE UPON TYNE,SCH MED,DEPT PHYSIOL SCI,NEWCASTLE TYNE NE1 7RU,TYNE & WEAR,ENGLAND. ZENTRUM PHYSIOL,FRANKFURT,GERMANY. RP PALMER, AR (reprint author), UNIV NOTTINGHAM,CNRS,INST HEARING,UNIV PK,NOTTINGHAM NG7 2RD,ENGLAND. RI Rees, Adrian/H-2200-2012 CR AITKIN LM, 1985, J NEUROPHYSIOL, V53, P43 AITKIN LM, 1972, BRAIN RES, V47, P91, DOI 10.1016/0006-8993(72)90254-5 BULLOCK DC, 1988, MED BIOL ENG COMPUT, V26, P669, DOI 10.1007/BF02447511 CAIRD D, 1983, EXP BRAIN RES, V52, P385 CAIRD D, 1987, EXP BRAIN RES, V68, P379 CHAN JCK, 1987, J NEUROPHYSIOL, V58, P543 CROW G, 1978, J ACOUST SOC AM, V64, P493, DOI 10.1121/1.381999 EVANS EF, 1979, ARCH OTOLARYNGOL, V105, P185 FLECKNELL PA, 1987, LABORATORY ANIMAL AN GOLDBERG JM, 1969, J NEUROPHYSIOL, V32, P613 JEFFRESS LA, 1948, J COMP PHYSIOL PSYCH, V41, P35, DOI 10.1037/h0061495 KLATT DH, 1980, J ACOUST SOC AM, V67, P971, DOI 10.1121/1.383940 KUWADA S, 1983, J NEUROPHYSIOL, V50, P981 KUWADA S, 1987, J NEUROPHYSIOL, V57, P1338 KUWADA S, 1984, J NEUROPHYSIOL, V51, P1306 MCFADDEN D, 1973, J ACOUST SOC AM, V54, P528, DOI 10.1121/1.1913611 MERRILL EG, 1972, MED BIOL ENG, V10, P662, DOI 10.1007/BF02476084 MOISEFF A, 1981, J NEUROSCI, V1, P40 MOREST DK, 1984, J COMP NEUROL, V222, P209, DOI 10.1002/cne.902220206 MOUSHEGIAN G, 1971, PHYSL AUDITORY SYSTE PALMER AR, 1986, HEARING RES, V24, P1, DOI 10.1016/0378-5955(86)90002-X PALMER AR, 1986, J ACOUST SOC AM, V79, P100, DOI 10.1121/1.393633 POPELAR J, 1988, 25 INN EAR BIOL WORK, P94 REES A, 1987, HEARING RES, V27, P129, DOI 10.1016/0378-5955(87)90014-1 REES A, 1983, HEARING RES, V10, P301, DOI 10.1016/0378-5955(83)90095-3 REES A, 1989, J ACOUST SOC AM, V85, P1978, DOI 10.1121/1.397851 ROSE JE, 1966, J NEUROPHYSIOL, V29, P288 ROTH GL, 1980, J ACOUST SOC AM, V68, P1643, DOI 10.1121/1.385196 STILLMAN RD, 1971, EXP NEUROL, V32, P404, DOI 10.1016/0014-4886(71)90007-0 TAKAHASHI T, 1986, J NEUROSCI, V6, P3413 TEAS DC, 1975, J ACOUST SOC AM, V58, P1066, DOI 10.1121/1.380766 WITHINGTONWRAY DJ, 1990, DEV BRAIN RES, V51, P225, DOI 10.1016/0165-3806(90)90279-8 Woodworth R. S., 1938, EXPT PSYCHOL YIN TCT, 1988, AUDITORY FUNCTION NE YIN TCT, 1983, J NEUROPHYSIOL, V50, P1020 YIN TCT, 1986, J NEUROPHYSIOL, V55, P280 YIN TCT, 1984, J ACOUST SOC AM, V76, P1401, DOI 10.1121/1.391457 YIN TCT, 1987, J NEUROPHYSIOL, V58, P562 NR 38 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 DEC PY 1990 VL 50 IS 1-2 BP 71 EP 86 DI 10.1016/0378-5955(90)90034-M PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300006 PM 2076985 ER PT J AU RYALS, BM WESTBROOK, EW AF RYALS, BM WESTBROOK, EW TI HAIR CELL REGENERATION IN SENESCENT QUAIL SO HEARING RESEARCH LA English DT Article DE HAIR CELLS; REGENERATION; AGE ID ACOUSTIC TRAUMA; COTURNIX QUAIL; INNER-EAR; AGE; COCHLEA; EXPOSURE; PAPILLA; MICE AB Hair cell regeneration was studied following exposure to an intense pure tone stimulus in young adult and senescent Coturnix quail. Three, 3-month old and four, 3-year old quail were continuously exposed to a 1500 Hz pure tone at 115 dB SPL for 12 h. Four quail were not noise exposed and were used as age-matched controls. Control and experimental birds received injections of [H-3]thymidine daily for 10 days after noise exposure. Ten days after noise exposure birds were killed and their cochleae embedded, sectioned serially and processed through standard methods of autoradiography. Hair cell counts showed a discreet area of hair cell loss for both age groups in the proximal half of the papilla. Incorporation of [H-3]thymidine was clearly seen over the nuclei of hair cells and support cells in the region of hair cell loss in both age groups. Incorporation of [H-3]thymidine was also seen over the nuclei of hair cells and support cells in a very small area in two of the non-exposed control birds. These results demonstrate that the potential for hair cell regeneration is maintained throughout life in Coturnix quail. Further, they suggest that there may be some very low level of hair cell production in the normal adult quail ear which is activated in the absence of massive trauma. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT OTOLARYNGOL,RICHMOND,VA 23298. VET ADM MED CTR,RICHMOND,VA 23249. CR BHATTACHARYYA TK, 1985, ANN OTO RHINOL LARYN, V94, P75 BURD GD, 1985, J COMP NEUROL, V240, P143, DOI 10.1002/cne.902400204 CHOLE RA, 1983, AUDIOLOGY, V22, P384 COLEMAN JW, 1976, ACTA OTO-LARYNGOL, V82, P33, DOI 10.3109/00016487609120860 CORWIN JT, 1988, SCIENCE, V240, P1772, DOI 10.1126/science.3381100 CORWIN JT, 1987, ABSTR ASS RES OT, V10, P204 CRUZ RM, 1987, ARCH OTOLARYNGOL, V113, P1058 DAYAL VS, 1986, ANN OTO RHINOL LARYN, V95, P510 HENRY WJ, 1988, OTOLARYNG HEAD NECK, V98, P607 HUBEL SB, 1989, HEARING RES, V37, P171, DOI 10.1016/0378-5955(89)90038-5 Ishii T, 1967, Acta Otolaryngol, V64, P17, DOI 10.3109/00016486709139088 JORGENSEN JM, 1988, NATURWISSENSCHAFTEN, V75, P319, DOI 10.1007/BF00367330 KATAYAMA A, 1989, J COMP NEUROL, V281, P129, DOI 10.1002/cne.902810110 KEITHLEY EM, 1982, HEARING RES, V8, P249, DOI 10.1016/0378-5955(82)90017-X RUBEL EW, 1982, ACTA OTO-LARYNGOL, V93, P31, DOI 10.3109/00016488209130849 Ruben R. J., 1967, ACTA OTO-LARYNGOL, V220, P1 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. C., 1982, NEW PERSPECTIVES NOI, P229 SEIDMAN DA, 1989, ABSTR ASS RES OTOLAR, V12, P135 TANAKA K, 1978, AM J ANAT, V153, P251, DOI 10.1002/aja.1001530206 NR 21 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 DEC PY 1990 VL 50 IS 1-2 BP 87 EP 96 DI 10.1016/0378-5955(90)90035-N PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300007 PM 1963886 ER PT J AU AITKIN, L MARTIN, R AF AITKIN, L MARTIN, R TI NEURONS IN THE INFERIOR COLLICULUS OF CATS SENSITIVE TO SOUND-SOURCE ELEVATION SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; SINGLE UNIT; ELEVATION; FREE-FIELD; SOUND LOCALIZATION ID OWL TYTO-ALBA; SPATIAL RECEPTIVE-FIELDS; SUPERIOR COLLICULUS; MEDIAN PLANE; STIMULUS AZIMUTH; CENTRAL NUCLEUS; DOMESTIC CAT; LOCALIZATION; FREQUENCY; REPRESENTATION AB The sensitivity to variations in sound-source elevation was studied in 48 units, previously examined as to their azimuthal sensitivity, of the inferior colliculi of cats. Of these units, 36 were directionally-sensitive (firing rate varied by more than 50% across the range of positions studied) to both azimuthal and elevational changes. Elevation sensitivity was common to noise stimuli (19/25 units) and pure tones in excess of 6 kHz (17/17 units). Not one of the 8 azimuth-sensitive units with CFs below 6 kHz was directionally-sensitive to the elevation of CF stimuli. The 4 units omnidirectional to azimuthal variation were similarly insensitive to elevation. The shapes of functions relating sound-source elevation to spike count (elevation functions) varied across an apparent continuum, with some very sharply-peaked functions being observed. Peak spike counts almost invariably occurred at stimulus elevations above the horizontal plane. Comparisons of the widths of elevation and azimuth functions at the same sound pressure level were made for 36 units. The relative sharpness of elevation and azimuthal tuning varied across the population. The common association of sensitivity to both azimuth and elevation suggests that elevation sensitivity may be mediated partly by binaural comparisons. RP AITKIN, L (reprint author), MONASH UNIV,DEPT PHYSIOL,CLAYTON,VIC 3168,AUSTRALIA. CR AITKIN LM, 1985, J NEUROPHYSIOL, V53, P43 AITKIN LM, 1987, J NEUROPHYSIOL, V57, P1185 AITKIN LM, 1984, J NEUROPHYSIOL, V52, P1 CALFORD MB, 1984, HEARING RES, V14, P13, DOI 10.1016/0378-5955(84)90064-9 CASSEDAY JH, 1973, J ACOUST SOC AM, V54, P365, DOI 10.1121/1.1913586 COLES RB, 1988, J COMP PHYSIOL A, V163, P117, DOI 10.1007/BF00612002 GARDNER MB, 1973, J ACOUST SOC AM, V53, P400, DOI 10.1121/1.1913336 HEBRANK J, 1974, J ACOUST SOC AM, V56, P935, DOI 10.1121/1.1903351 HEBRANK J, 1974, J ACOUST SOC AM, V56, P1829, DOI 10.1121/1.1903520 HEFFNER RS, 1988, HEARING RES, V36, P221, DOI 10.1016/0378-5955(88)90064-0 IVARSSON C, 1980, HEARING RES, V3, P241, DOI 10.1016/0378-5955(80)90050-7 JENKINS WM, 1982, J NEUROPHYSIOL, V47, P987 KING AJ, 1983, J PHYSIOL-LONDON, V342, P361 KNUDSEN EI, 1979, J COMP PHYSIOL, V133, P1 KNUDSEN EI, 1977, SCIENCE, V198, P1278, DOI 10.1126/science.929202 KNUDSEN EI, 1978, J NEUROPHYSIOL, V41, P870 KNUDSEN EI, 1979, J COMP PHYSIOL, V133, P13 MARTIN RL, 1989, HEARING RES, V38, P289, DOI 10.1016/0378-5955(89)90072-5 MARTIN RL, 1987, HEARING RES, V30, P239, DOI 10.1016/0378-5955(87)90140-7 MERZENIC.MM, 1974, BRAIN RES, V77, P397, DOI 10.1016/0006-8993(74)90630-1 MIDDLEBROOKS JC, 1984, J NEUROSCI, V4, P2621 MIDDLEBROOKS JC, 1981, J NEUROSCI, V1, P107 MIDDLEBROOKS JC, 1987, J NEUROPHYSIOL, V57, P672 MILLS AW, 1958, J ACOUST SOC AM, V30, P237, DOI 10.1121/1.1909553 MOORE DR, 1984, HEARING RES, V13, P175, DOI 10.1016/0378-5955(84)90107-2 PHILLIPS DP, 1982, HEARING RES, V8, P13, DOI 10.1016/0378-5955(82)90031-4 ROFFLER SK, 1968, J ACOUST SOC AM, V43, P1255, DOI 10.1121/1.1910976 SEMPLE MN, 1983, HEARING RES, V10, P203, DOI 10.1016/0378-5955(83)90054-0 Shaw BAG, 1974, HDB SENSORY PHYSL, VV/1, P455 NR 29 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 DEC PY 1990 VL 50 IS 1-2 BP 97 EP 106 DI 10.1016/0378-5955(90)90036-O PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300008 PM 2076986 ER PT J AU FUKUSHIMA, N WHITE, P HARRISON, RV AF FUKUSHIMA, N WHITE, P HARRISON, RV TI INFLUENCE OF ACOUSTIC DEPRIVATION ON RECOVERY OF HAIR-CELLS AFTER ACOUSTIC TRAUMA SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELL; ACOUSTIC TRAUMA; ACOUSTIC DEPRIVATION; OSSICULECTOMY ID GUINEA-PIG COCHLEA; STEM AUDITORY NUCLEI; BRAIN-STEM; THRESHOLD SHIFT; TUNING CURVES; HEARING-LOSS; NOISE; STEREOCILIA; DAMAGE; EXPOSURE AB The purpose of this study was to investigate how the recovery of the cochlea, after acoustic trauma, might be influenced by acoustic stimulation or deprivation. In anaesthetized adult chinchillas, both ears were simultaneously exposed to a traumatizing acoustic stimulus (2 kHz tone, at 117 dB SPL for 15 min). Probe microphones positioned in both bullae were used to ensure identical exposure to the two ears; this was important because the experiment relies on within-animal controls. Cochlear action potential thresholds across frequency (CAP audiograms) were used to verify the similarity of threshold shifts to the two ears. Immediately following, a unilateral ossiculectomy was performed which resulted in one cochlea being acoustically deprived during the recovery period, whilst the other was not. In groups of animals with recovery periods of 1, 3, 6, and 12 weeks, both the acoustically deprived and the normally stimulated cochleas were examined with scanning electron microscopy. To quantify hair cell damage, we used a damage scale based on stereociliar integrity; for each cochlea, a standard region 5.5-8.5 mm from the apex was studied in detail. We found that after acoustic trauma, hair cell damage to the cochlea which is deprived of sound during the recovery period, is significantly greater compared with that in the normally stimulated, contra-lateral cochlea. Our results suggest that mechanical activation of the inner ear acts to inhibit long-term degenerative processes, or influence repair of partially damaged hair cells. C1 HOSP SICK CHILDREN,RES INST,DEPT OTOLARYNGOL,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. HIROSHIMA UNIV,DEPT OTOLARYNGOL,HIROSHIMA 730,JAPAN. UNIV TORONTO,DEPT OTOLARYNGOL,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT PHYSIOL,TORONTO M5S 1A1,ONTARIO,CANADA. 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C., 1982, NEW PERSPECTIVES NOI, P229 SAUNDERS JC, 1985, J ACOUST SOC AM, V78, P833, DOI 10.1121/1.392915 SAUNDERS JC, 1986, HEARING RES, V24, P217, DOI 10.1016/0378-5955(86)90020-1 SCHMIEDT RA, 1984, J ACOUST SOC AM, V76, P1293, DOI 10.1121/1.391446 STOPP PE, 1983, HEARING RES, V11, P55, DOI 10.1016/0378-5955(83)90045-X TUCCI DL, 1985, J COMP NEUROL, V238, P371, DOI 10.1002/cne.902380402 WEBSTER DB, 1983, INT J PEDIATR OTORHI, V6 WEBSTER DB, 1979, ANN OTO RHINOL LARYN, V88, P684 NR 39 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 DEC PY 1990 VL 50 IS 1-2 BP 107 EP 118 DI 10.1016/0378-5955(90)90037-P PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300009 PM 2076966 ER PT J AU FLYNN, AJ DENGERINK, HA WRIGHT, JW AF FLYNN, AJ DENGERINK, HA WRIGHT, JW TI ANDROGENIC EFFECTS ON ANGIOTENSIN-II-INDUCED BLOOD-PRESSURE AND COCHLEAR BLOOD-FLOW CHANGES IN RATS SO HEARING RESEARCH LA English DT Article DE ANDROGENS; ANGIOTENSIN-II; BLOOD PRESSURE; COCHLEAR BLOOD FLOW; RAT ID LASER DOPPLER MEASURES; AUTO-REGULATION; PROGESTERONE; TESTOSTERONE; RECEPTORS AB Ovariectomized, castrated, and sham-castrated rats pretreated with oil or testosterone were intra-arterially infused with saline and three doses of angiotensin II while blood pressure and cochlear blood flow were measured. The results indicated a positive dose-response relationship for blood pressure and cochlear blood flow. Sham-castrated males had higher mean blood pressure responses than castrated males, followed by ovariectomized females. Cochlear blood flow responses were higher in the sham-castrated males than the ovariectomized females, followed by the castrated males. In comparison to the male groups, the ovariectomized females evidenced the lowest, middle, and highest cochlear blood flow responses to the three increasing doses of angiotensin II. Testosterone pretreatment facilitated angiotensin-induced cochlear blood flow elevations in all three angiotensin doses. These results suggest that endogenous and exogenous androgens may alter blood pressure and/or cochlear blood flow responses to angiotensin II via different mechanisms. C1 WASHINGTON STATE UNIV,DEPT PSYCHOL,1812 E MCLOUGHLIN BLVD,PULLMAN,WA 99163. CR BAUMBACH GL, 1985, ANN BIOMED ENG, V13, P303, DOI 10.1007/BF02584248 Bayliss WM, 1902, J PHYSIOL-LONDON, V28, P220 BUKHARI AR, 1981, STEROIDS, V38, P1, DOI 10.1016/0039-128X(81)90016-7 CARLBORG BIR, 1983, ANN OTOLOGY RHINOL S, V104, P2 CARROLL JE, 1984, SCIENCE, V224, P1009, DOI 10.1126/science.6326265 COYLE P, 1986, HYPERTENSION S2, V8, P1167 DENGERINK HA, 1985, HEARING RES, V20, P31, DOI 10.1016/0378-5955(85)90056-5 FLYNN AJ, 1989, HEARING RES, V41, P249, DOI 10.1016/0378-5955(89)90016-6 GOODWIN PC, 1984, ACTA OTO-LARYNGOL, V98, P403, DOI 10.3109/00016488409107581 HALL CE, 1982, J LAB CLIN MED, V100, P641 LAUGEL GR, 1987, HEARING RES, V31, P245, DOI 10.1016/0378-5955(87)90194-8 LAUGEL GR, 1988, ACTA OTO-LARYNGOL, V106, P34, DOI 10.3109/00016488809107368 MILLER JM, 1983, HEARING RES, V11, P385, DOI 10.1016/0378-5955(83)90069-2 MILLER JM, 1984, ARCH OTOLARYNGOL, V110, P305 Murad F, 1985, PHARMACOL BASIS THER, P1440 Murad F, 1985, PHARMACOL BASIS THER, P1412 NARUSE K, 1986, ENDOCRINOLOGY, V118, P2470 PARVIZI N, 1975, NATURE, V256, P59, DOI 10.1038/256059a0 QUIRK WS, 1989, HEARING RES, V38, P119, DOI 10.1016/0378-5955(89)90133-0 QUIRK WS, 1989, HEARING RES, V41, P53, DOI 10.1016/0378-5955(89)90178-0 QUIRK WS, 1988, HEARING RES, V33, P129, DOI 10.1016/0378-5955(88)90025-1 SCHIFFRIN EL, 1984, AM J PHYSIOL, V246, pH608 SNOW JB, 1972, VASCULAR DISORDERS H, P167 SPOENDLIN H, 1972, VASCULAR DISORDERS H, P93 SUGA F, 1969, ANN OTO RHINOL LARYN, V78, P358 VALIQUETTE G, 1982, ACTA ENDOCRINOL-COP, V99, P493 VOIGT J, 1980, EUR J BIOCHEM, V110, P57, DOI 10.1111/j.1432-1033.1980.tb04840.x WILLIAMS LT, 1978, RECEPTOR BINDING STU WRIGHT JW, 1985, HEARING RES, V17, P41, DOI 10.1016/0378-5955(85)90128-5 ZARROW MX, 1964, EXP ENDOCRINOL NR 30 TC 3 Z9 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 119 EP 126 DI 10.1016/0378-5955(90)90038-Q PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300010 PM 2076967 ER PT J AU SEWELL, WF MROZ, EA AF SEWELL, WF MROZ, EA TI PURIFICATION OF A LOW-MOLECULAR-WEIGHT EXCITATORY SUBSTANCE FROM THE INNER EARS OF GOLDFISH SO HEARING RESEARCH LA English DT Article DE NEUROTRANSMITTER; EXCITATORY AMINO ACIDS; HEARING; HAIR CELLS; CHROMATOGRAPHY ID GENE-RELATED PEPTIDE; GUINEA-PIG ORGAN; CORTI; RAT; IMMUNOREACTIVITY; LOCALIZATION; MICROSCOPY; GLUTAMATE; NEURONS; COCHLEA AB The neurotransmitter released by the hair cell has not been identified; little is known about other neuroactive substances that may be important in hair-cell organ function. To identify neuroactive substances in hair cell tissue, we have examined substances in extracts of the inner ears of goldfish that can excite afferent fibers innervating hair cells. The extracts contain an unidentified low-molecular-weight (LMW) excitatory substance that is a candidate to be the hair-cell neurotransmitter. The LMW excitatory substance has been highly purified by a sequential combination of (1) treatment with cation-exchange resin; (2) gel-permeation chromatography; (3) gradient-elution cation-exchange chromatography; (4) isocratic-elution cation-exchange chromatography; and (5) high-performance anion-exchange chromatography. Based upon its separation behavior in these purification steps, the LMW excitatory substance may be a small, zwitterionic compound with titratable anionic and cationic groups. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RP SEWELL, WF (reprint author), MASSACHUSETTS EYE & EAR HOSP,EATON PEABODY LAB AUDITORY PHYSIOL,243 CHARLES ST,BOSTON,MA 02114, USA. CR ADAMS JC, 1987, BRAIN RES, V419, P347, DOI 10.1016/0006-8993(87)90606-8 Bledsoe Jr S.C., 1988, PHYSL HEARING, P385 BLEDSOE SC, 1983, COMP BIOCHEM PHYS C, V75, P119 DRESCHER MJ, 1981, ANAL BIOCHEM, V116, P280, DOI 10.1016/0003-2697(81)90357-2 EYBALIN M, 1988, NEUROSCIENCE, V24, P29, DOI 10.1016/0306-4522(88)90308-9 FEX J, 1984, HEARING RES, V15, P123, DOI 10.1016/0378-5955(84)90043-1 FEX J, 1986, BRAIN RES, V366, P106, DOI 10.1016/0006-8993(86)91285-0 GUTH P, 1981, PHARM HEARING, P99 GUTH PS, 1988, HEARING RES, V33, P223, DOI 10.1016/0378-5955(88)90152-9 GUTH PS, 1976, PHARMACOL REV, V28, P95 KITAJIRI M, 1985, BRAIN RES, V358, P394, DOI 10.1016/0006-8993(85)90992-8 KLINKE R, 1986, HEARING RES, V22, P235, DOI 10.1016/0378-5955(86)90100-0 LU SM, 1987, HEARING RES, V31, P137, DOI 10.1016/0378-5955(87)90119-5 MEZA G, 1985, AUDITORY BIOCH, P80 MROZ EA, 1989, HEARING RES, V38, P141, DOI 10.1016/0378-5955(89)90136-6 SEWELL WF, 1987, J NEUROSCI, V7, P2465 SLIWINSKAKOWALSKA M, 1989, HEARING RES, V42, P83, DOI 10.1016/0378-5955(89)90119-6 STARR PA, 1988, SOC NEUR ABSTR, V14, P331 TAKEDA N, 1987, ACTA OTO-LARYNGOL, V103, P567 TAKEDA N, 1986, EXP BRAIN RES, V61, P575 TANAKA M, 1989, BRAIN RES, V504, P31, DOI 10.1016/0006-8993(89)91593-X THALMANN R, 1982, LARYNGOSCOPE, V92, P321 VETTER D E, 1986, Society for Neuroscience Abstracts, V12, P779 NR 23 TC 8 Z9 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 127 EP 138 DI 10.1016/0378-5955(90)90039-R PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300011 PM 1981769 ER PT J AU PICKLES, JO BRIX, J MANLEY, GA AF PICKLES, JO BRIX, J MANLEY, GA TI INFLUENCE OF COLLAGENASE ON TIP LINKS IN HAIR-CELLS OF THE CHICK BASILAR PAPILLA SO HEARING RESEARCH LA English DT Article DE STEREOCILIA; CHICK; TIP LINK; COLLAGENASE; HYALURONIDASE; TRANSDUCTION ID STEREOCILIA; TRANSDUCTION; ORGANIZATION; MORPHOLOGY; ORGAN AB Chick basilar papillae were incubated in collagenase, using concentrations previously employed for the isolation of viable hair cells. When assessed by scanning electron microscopy, the hair bundles had a normal conformation, with no loss of tip links compared with control incubations. The results suggest that collagenase does not destroy the integrity of structures on the apical surface of hair cells, and that tip links are not composed of collagen. The results are in agreement with the hypothesis that tip links are involved in mechanotransduction. C1 UNIV BIRMINGHAM,SCH MED,DEPT PHYSIOL,BIRMINGHAM B15 2TT,W MIDLANDS,ENGLAND. TECH UNIV MUNICH,INST ZOOL,W-8046 GARCHING,GERMANY. RP PICKLES, JO (reprint author), UNIV QUEENSLAND,DEPT PHYSIOL & PHARMACOL,VISION TOUCH & HEARING RES CTR,ST LUCIA,QLD 4067,AUSTRALIA. CR ASHMORE JF, 1983, NATURE, V304, P536, DOI 10.1038/304536a0 Gosline JM, 1984, EXTRACELLULAR MATRIX, P191 GOTTE L, 1974, J ULTRA MOL STRUCT R, V46, P23, DOI 10.1016/S0022-5320(74)80019-5 HOWARD J, 1988, NEURON, V1, P189, DOI 10.1016/0896-6273(88)90139-0 HUDSPETH AJ, 1979, P NATL ACAD SCI USA, V76, P1506, DOI 10.1073/pnas.76.3.1506 KISHINO A, 1988, NATURE, V334, P74, DOI 10.1038/334074a0 LIM DJ, 1985, ACTA OTO-LARYNGOL, V99, P478, DOI 10.3109/00016488509108941 MANDL I, 1953, J CLIN INVEST, V32, P1323, DOI 10.1172/JCI102861 NEUGEBAUER DC, 1987, CELL TISSUE RES, V249, P199, DOI 10.1007/BF00215434 OSBORNE MP, 1984, CELL TISSUE RES, V237, P43 OSBORNE MP, 1988, HEARING RES, V35, P99, DOI 10.1016/0378-5955(88)90044-5 PICKLES JO, 1985, PROG NEUROBIOL, V24, P1, DOI 10.1016/0301-0082(85)90014-0 PICKLES JO, 1984, HEARING RES, V15, P103, DOI 10.1016/0378-5955(84)90041-8 PICKLES JO, 1989, HEARING RES, V41, P31, DOI 10.1016/0378-5955(89)90176-7 ZAJIC G, 1987, HEARING RES, V26, P249, DOI 10.1016/0378-5955(87)90061-X ZENNER HP, 1988, HEARING RES, V34, P233, DOI 10.1016/0378-5955(88)90003-2 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 DEC PY 1990 VL 50 IS 1-2 BP 139 EP 144 DI 10.1016/0378-5955(90)90040-V PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300012 PM 1963885 ER PT J AU YATES, GK AF YATES, GK TI BASILAR-MEMBRANE NONLINEARITY AND ITS INFLUENCE ON AUDITORY-NERVE RATE-INTENSITY FUNCTIONS SO HEARING RESEARCH LA English DT Article DE DYNAMIC RANGE; RATE-INTENSITY FUNCTION; OUTER HAIR CELLS; BASILAR MEMBRANE NONLINEARITY ID 2-TONE RATE SUPPRESSION; INPUT-OUTPUT FUNCTIONS; RATE-LEVEL FUNCTIONS; GUINEA-PIG COCHLEA; MOSSBAUER TECHNIQUE; MAMMALIAN COCHLEA; ACTIVE ELEMENTS; HAIR-CELLS; MODEL; FIBERS AB Previous papers have shown that the shapes of rate-intensity functions of auditory nerve fibres vary with spontaneous rate (Sachs and Abbas 1974; Sachs et al. 1989; Winter et al. 1990; Yates et al. 1990), and that the variation is due to the nonlinear properties of the basilar membrane. This paper examines the basilar membrane nonlinearity and provides a semi-quantitative explanation for it in terms of previous models (Zwicker 1979; Patuzzi et al. 1989) and an analogue model. It thereby provides explanations for the shapes of the basilar membrane input-output curves and for the way in which they vary with trauma. The shapes of the neural rate-intensity functions are quantified and shown to be consistent with the low-threshold data of Geisler et al. (1985). Several nonlinear properties of the cochlea, such as recruitment, are also interpreted. RP YATES, GK (reprint author), UNIV WESTERN AUSTRALIA,DEPT PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA. CR ABBAS PJ, 1978, J ACOUST SOC AM, V63, P1878, DOI 10.1121/1.381929 ARTHUR RM, 1971, J PHYSIOL-LONDON, V212, P593 BROPHY JJ, 1983, BASIC ELECTRONICS SC CODY AR, 1987, J PHYSIOL-LONDON, V383, P551 COSTALUPES JA, 1987, HEARING RES, V26, P155, DOI 10.1016/0378-5955(87)90107-9 DIEPENDAAL RJ, 1986, J ACOUST SOC AM, V80, P124, DOI 10.1121/1.394460 Fowler EP, 1936, ARCHIV OTOLARYNGOL, V24, P731 GEISLER CD, 1990, HEARING RES, V44, P1, DOI 10.1016/0378-5955(90)90017-J GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GEISLER CD, 1985, J ACOUST SOC AM, V77, P1102, DOI 10.1121/1.392228 GOODMAN DA, 1982, HEARING RES, V7, P161, DOI 10.1016/0378-5955(82)90012-0 JOHNSTONE BM, 1986, HEARING RES, V22, P147, DOI 10.1016/0378-5955(86)90090-0 LIBERMAN MC, 1978, J ACOUST SOC AM, V63, P442, DOI 10.1121/1.381736 MOORE BCJ, 1985, J ACOUST SOC AM, V77, P1505, DOI 10.1121/1.392045 Mountain DC, 1983, MECHANICS HEARING, P119 NEELY ST, 1986, J ACOUST SOC AM, V79, P1472, DOI 10.1121/1.393674 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 PALMER AR, 1980, HEARING RES, V2, P319, DOI 10.1016/0378-5955(80)90065-9 PATUZZI R, 1983, J ACOUST SOC AM, V74, P1734, DOI 10.1121/1.390282 PATUZZI R, 1988, PHYSIOL REV, V68, P1009 PATUZZI RB, 1989, HEARING RES, V39, P189, DOI 10.1016/0378-5955(89)90090-7 POHLMAN AG, 1924, P SOC EXP BIOL MED, V20, P335 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 RUSSELL IJ, 1978, J PHYSIOL-LONDON, V284, P261 SACHS MB, 1968, J ACOUST SOC AM, V43, P1120, DOI 10.1121/1.1910947 SACHS MB, 1969, J ACOUST SOC AM, V45, P1025, DOI 10.1121/1.1911493 SACHS MB, 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 SCHALK TB, 1980, J ACOUST SOC AM, V67, P903, DOI 10.1121/1.383970 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SOKOLOWSKI BHA, 1989, HEARING RES, V41, P115, DOI 10.1016/0378-5955(89)90005-1 TEICH MC, 1985, J ACOUST SOC AM, V77, P1110, DOI 10.1121/1.392176 WINTER IM, 1990, HEARING RES, V45, P191, DOI 10.1016/0378-5955(90)90120-E YATES GK, 1990, HEARING RES, V45, P203, DOI 10.1016/0378-5955(90)90121-5 ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 ZWICKER E, 1986, J ACOUST SOC AM, V80, P146, DOI 10.1121/1.394175 NR 38 TC 132 Z9 133 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 1990 VL 50 IS 1-2 BP 145 EP 162 DI 10.1016/0378-5955(90)90041-M PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300013 PM 2076968 ER PT J AU HELLSTROM, LI SCHMIEDT, RA AF HELLSTROM, LI SCHMIEDT, RA TI COMPOUND ACTION-POTENTIAL INPUT-OUTPUT FUNCTIONS IN YOUNG AND QUIET-AGED GERBILS SO HEARING RESEARCH LA English DT Article DE COMPOUND ACTION POTENTIAL; AUDITORY NERVE; AGING; GERBIL; PRESBYACUSIS; COCHLEAR MICROPHONIC ID WHOLE-NERVE AP; MONGOLIAN GERBIL; TUNING CURVES; NORMATIVE DATA; BRAIN-STEM; INNER-EAR; THRESHOLDS; SUPPRESSION; DISTORTION; NEURONS AB Auditory-nerve compound action potentials (CAP) and cochlear microphonic (CM) potentials were measured with round window electrodes in two sets of quiet-reared gerbils: young (N = 9 ears, 4-7 months) and aged (N = 11 ears, 35-37 months). CAP thresholds, measured at probe frequencies from 0.5 to 25.6 kHz, are plotted as audibility curves. Input/output (I/O) functions were derived from CAP and CM amplitude measurements at six frequencies. When compared to young controls, CAP audibility curves from aged animals all show some degree of threshold shift, ranging from minimal to severe, as well as increased variability. Our data suggest that some of the variability in the aged-animal audibility curves can be attributed to variations in individual genetic factors. Maximum CAP amplitudes for the aged animals average significantly less than those of the young controls at all frequencies tested. Young control I/O functions are generally steeper than those of the aged gerbils. Differences in the CM amplitudes of the young and aged gerbils are not as clear cut as the differences in the CAP. Possible mechanisms explaining the decrease in amplitudes and slopes of the CAP I/O functions in aged animals include changes in numbers or thresholds of primary ganglion cells, or a decrease in synchrony in discharges of auditory-nerve fibers. RP HELLSTROM, LI (reprint author), MED UNIV S CAROLINA,DEPT OTOLARYNGOL & COMMUNICATIVE SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. CR ADAMS JC, 1989, ABSTR ASS RES OTOLAR, P46 ARRINGTO.LR, 1973, LAB ANIM SCI, V23, P262 CHAMBERLAIN SC, 1977, J COMP NEUROL, V171, P193, DOI 10.1002/cne.901710205 DALLOS P, 1976, J ACOUST SOC AM, V59, P591, DOI 10.1121/1.380903 DALLOS P, 1971, J ACOUST SOC AM, V49, P1144, DOI 10.1121/1.1912476 DOLAN TG, 1985, HEARING RES, V18, P203, DOI 10.1016/0378-5955(85)90038-3 DOLAN TG, 1985, HEARING RES, V17, P259, DOI 10.1016/0378-5955(85)90070-X DOLAN TG, 1989, HEARING RES, V37, P193, DOI 10.1016/0378-5955(89)90022-1 Eldredge D H, 1973, Adv Otorhinolaryngol, V20, P64 HAMERNIK RP, 1989, HEARING RES, V38, P199, DOI 10.1016/0378-5955(89)90065-8 HARRIS DM, 1979, HEARING RES, V1, P133, DOI 10.1016/0378-5955(79)90024-8 HELLSTROM LI, 1989, ABSTR ASS RES OT, P149 HELLSTROM LI, 1991, UNPUB HEAR RES HOOD LJ, 1986, NEUROBIOLOGY HEARING, P397 KEITHLEY EM, 1989, HEARING RES, V38, P125, DOI 10.1016/0378-5955(89)90134-2 MILLS JH, 1990, HEARING RES, V46, P201, DOI 10.1016/0378-5955(90)90002-7 OZDAMAR O, 1976, J ACOUST SOC AM, V59, P143 ROBERTSON D, 1980, HEARING RES, V2, P39, DOI 10.1016/0378-5955(80)90015-5 RONKEN DA, 1981, J ACOUST SOC AM, V70, P410, DOI 10.1121/1.386784 RYAN A, 1976, J ACOUST SOC AM, V59, P1222, DOI 10.1121/1.380961 RYAN AF, 1983, HEARING RES, V9, P173, DOI 10.1016/0378-5955(83)90026-6 RYAN AF, 1982, J COMP NEUROL, V207, P369, DOI 10.1002/cne.902070408 SCHMIEDT RA, 1982, HEARING RES, V7, P335, DOI 10.1016/0378-5955(82)90044-2 SCHMIEDT RA, 1977, J ACOUST SOC AM, V61, P133, DOI 10.1121/1.381283 SCHMIEDT RA, 1989, HEARING RES, V42, P23, DOI 10.1016/0378-5955(89)90115-9 SCHMIEDT RA, 1989, ABSTR ASS RES OT, P41 SCHMIEDT RA, 1986, J ACOUST SOC AM, V79, P1481, DOI 10.1121/1.393675 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 Schuknecht H. F., 1974, PATHOLOGY EAR SMITH RL, 1977, J NEUROPHYSIOL, V40, P1098 SOKOLICH WG, 1976, J ACOUST SOC AM, V59, P963, DOI 10.1121/1.380955 SOKOLOCH WG, 1977, ISRS15 SYR U I SENS TARNOWSKI BI, 1991, UNPUB HEAR RES NR 33 TC 60 Z9 62 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 163 EP 174 DI 10.1016/0378-5955(90)90042-N PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300014 PM 2076969 ER PT J AU OKANOYA, K DOOLING, RJ AF OKANOYA, K DOOLING, RJ TI DETECTION OF AUDITORY SINUSOIDS OF FIXED AND UNCERTAIN FREQUENCY BY BUDGERIGARS (MELOPSITTACUS-UNDULATUS) AND ZEBRA FINCHES (POEPHILA-GUTTATA) SO HEARING RESEARCH LA English DT Article DE FREQUENCY UNCERTAINTY; CRITICAL RATIOS; BIRDS ID AGELAIUS-PHOENICEUS; CRITICAL RATIOS; MOLOTHRUS-ATER; THRESHOLDS; HEARING; ABSOLUTE AB Three budgerigars and three zebra finches were tested for their ability to detect sinusoidal stimuli in the presence of broadband noise. Masked thresholds for 1, 2, and 4 KHz pure tones were measured with a fixed frequency condition, in which only one test frequency was presented in a session, and with an uncertain frequency condition, in which three signal frequencies were presented in random order in one session. The critical signal/noise ratios obtained in the fixed frequency condition were similar to those reported in a previous study (Okanoya and Dooling, 1987) for both species. When tested in the uncertain frequency condition, critical ratios for zebra finches increased for 1.5 dB at 1 KHz signal but remained unchanged 2 and 4 kHz. The critical ratios for budgerigars showed no difference at any frequency in the uncertain frequency condition. These results suggest that (1) budgerigars and zebra finches are similar in the degree to which attention factors are involved in the detection of signals in noise, and (2) the unusual shape of the budgerigar critical ratio function is not the result of central attentional processes. C1 UNIV MARYLAND,DEPT PSYCHOL,COLLEGE PK,MD 20742. RI Okanoya, Kazuo/F-8528-2010 CR DOOLING RJ, 1980, HEARING RES, V3, P279, DOI 10.1016/0378-5955(80)90023-4 DOOLING RJ, 1975, J COMP PHYSIOL PSYCH, V88, P1, DOI 10.1037/h0076226 DOOLING RJ, 1986, EXPT BIOL, P195 Ehret G, 1987, CATEGORICAL PERCEPTI, P301 FAY RR, 1988, HEARING VETEBRATES P GRAY R, 1988, ABSTR ASS RES OT, P232 GREEN DM, 1966, SIGNAL DETECTION THE GREEN DM, 1961, J ACOUST SOC AM, V33, P897, DOI 10.1121/1.1908839 HASHINO E, 1989, J ACOUST SOC AM, V85, P289, DOI 10.1121/1.397736 HIENZ RD, 1987, J COMP PSYCHOL, V101, P16, DOI 10.1037/0735-7036.101.1.16 HIENZ RD, 1977, J COMP PHYSIOL PSYCH, V91, P1365, DOI 10.1037/h0077403 KUHN A, 1980, J ACOUST SOC AM, V68, P1892, DOI 10.1121/1.385182 Miller E. H., 1982, ACOUSTIC COMMUNICATI, V2, P95 OKANOYA K, 1987, J COMP PSYCHOL, V101, P7, DOI 10.1037//0735-7036.101.1.7 SAUNDERS JC, 1979, HEARING RES, V1, P303, DOI 10.1016/0378-5955(79)90003-0 SINNOTT JM, 1980, J COMP PHYSL PSYCHOL, V94 SWETS JA, 1984, VARIETY ATTENTION WILSON WB, 1979, BIRDS READINGS SCI A ZANN R, 1984, Z TIERPSYCHOL, V66, P328 NR 19 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 175 EP 184 DI 10.1016/0378-5955(90)90043-O PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300015 PM 2076970 ER PT J AU OKANOYA, K DOOLING, RJ AF OKANOYA, K DOOLING, RJ TI DETECTION OF GAPS IN NOISE BY BUDGERIGARS (MELOPSITTACUS-UNDULATUS) AND ZEBRA FINCHES (POEPHILA-GUTTATA) SO HEARING RESEARCH LA English DT Article DE GAP DETECTION; TEMPORAL ACUITY; BIRD HEARING; SPECTRAL-TEMPORAL TRADE-OFF ID STARLING STURNUS-VULGARIS; FREQUENCY-SELECTIVITY; CRITICAL RATIOS; CONTACT CALLS; THRESHOLDS; HEARING; VOCALIZATIONS; CHINCHILLAS; BANDWIDTH; ABSOLUTE AB Temporal gap detection thresholds were obtained for two species of birds, budgerigars and zebra finches, which are known to have different auditory filter bandwidths. Both species showed gap detection thresholds of about 2.5 msec for broadband noise stimuli. Comparing octave bands of noise centered at 1, 3, and 5 kHz, zebra finches showed the smallest gap thresholds for the noise band centered at 5 kHz whereas budgerigars showed the smallest gap detection thresholds for the noise band centered at 3 kHz. The results from zebra finches are generally consistent with filter theories of auditory spectro-temporal perception whereas the result from budgerigars are not. In aggregate, these comparative data suggest the relation between spectral and temporal resolving power in these two species may involve different mechanisms. C1 UNIV MARYLAND,DEPT PSYCHOL,COLLEGE PK,MD 20742. RI Okanoya, Kazuo/F-8528-2010 CR Becker P. H., 1982, ACOUSTIC COMMUNICATI, P214 BROWN SD, 1988, J COMP PSYCHOL, V102, P236, DOI 10.1037/0735-7036.102.3.236 BUCHFELLNER E, 1989, J COMP PHYSIOL A, V164, P539, DOI 10.1007/BF00610447 Buus S, 1985, TIME RESOLUTION AUDI, P159 DOOLING RJ, 1975, J COMP PHYSIOL PSYCH, V88, P1, DOI 10.1037/h0076226 DOOLING RJ, 1978, J COMP PHYSIOL PSYCH, V92, P867, DOI 10.1037/h0077529 DOOLING RJ, 1978, J ACOUST SOC AM, V63, P1640, DOI 10.1121/1.381865 DUIFHUIS H, 1973, J ACOUST SOC AM, V54, P1471, DOI 10.1121/1.1914446 FAY RR, 1988, HEAIRNG VERTEBRATES FAY RR, 1985, J ACOUST SOC AM, V78, P1296, DOI 10.1121/1.392899 FITZGIBBONS PJ, 1983, J ACOUST SOC AM, V74, P67, DOI 10.1121/1.389619 FORMBY C, 1988, J ACOUST SOC AM, V84, P545, DOI 10.1121/1.396831 GIRAUDIPERRY DM, 1982, J ACOUST SOC AM, V72, P1387, DOI 10.1121/1.388444 GRAY R, 1988, ABSTR ASS RES OT, V232 GROSS JH, 1985, BASIC ISSUES HEARING Hashino E., 1989, Journal of the Acoustical Society of Japan (E), V10 HIENZ RD, 1987, J COMP PSYCHOL, V101, P16, DOI 10.1037/0735-7036.101.1.16 ISON JR, 1982, J COMP PHYSIOL PSYCH, V96, P945, DOI 10.1037/0735-7036.96.6.945 KLUMP GM, 1989, J COMP PHYSIOL A, V164, P531, DOI 10.1007/BF00610446 Marler P., 1984, BIOL LEARNING, P289 Moore B. C., 1986, AUDITORY FREQUENCY S Moore B.C.J., 1986, FREQUENCY SELECTIVIT OKANOYA K, 1990, HEARING RES, P175 OKANOYA K, 1987, J COMP PSYCHOL, V101, P7, DOI 10.1037//0735-7036.101.1.7 PARK TJ, 1985, J COMP PSYCHOL, V99, P391, DOI 10.1037/0735-7036.99.4.391 PENNER MJ, 1977, J ACOUST SOC AM, V61, P552, DOI 10.1121/1.381297 SALVI RJ, 1985, J ACOUST SOC AM, V77, P1173, DOI 10.1121/1.392181 SAUNDERS JC, 1979, HEARING RES, V1, P303, DOI 10.1016/0378-5955(79)90003-0 SHAILER MJ, 1983, J ACOUST SOC AM, V74, P467, DOI 10.1121/1.389812 NR 29 TC 32 Z9 33 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 185 EP 192 DI 10.1016/0378-5955(90)90044-P PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300016 PM 2076971 ER PT J AU CHEATHAM, MA DALLOS, P AF CHEATHAM, MA DALLOS, P TI COMPARISON OF LOW-SIDE AND HIGH-SIDE 2-TONE SUPPRESSION IN INNER HAIR CELL AND ORGAN OF CORTI RESPONSES SO HEARING RESEARCH LA English DT Article DE COCHLEA; HAIR CELL; NONLINEARITY; 2-TONE SUPPRESSION ID AUDITORY-NERVE FIBERS; BASILAR-MEMBRANE; COCHLEAR POTENTIALS; MOSSBAUER TECHNIQUE; MODEL; NONLINEARITIES; FREQUENCY; INTENSITY; VIBRATION; MECHANICS AB Two-tone interactions were measured from inner hair cells and from the organ of Corti fluid space in the third turn of the guinea pig cochlea. At relatively low stimulus levels, a low-side suppressor caused frequency response functions to become broader. Phase changes exhibited a lag/lead transition around the characteristic frequency in harmony with the change in magnitude. These patterns are similar to those previously documented for a high-side suppressor (Cheatham and Dallos 1989) and suggest that suppression is not simply an attenuation phenomenon since level reductions for single-tone inputs produce response patterns which are mirror images of those obtained for the two-tone conditions. In contrast to the low-level results, data measured at moderately high stimulus levels indicate that the magnitude changes produced by both low- and high-side suppressors are qualitatively similar to changes generated by reducing the input sound level. In other words, ac frequency response functions become narrower, partially reversing the broadening of these functions which occurs as sound level increases. Companion phase measures, however, demonstrate that low- and high-side suppressors, in spite of producing similar changes in filter shape, do not produce similar changes in response phase. In fact, neither of the two-tone conditions produce response patterns similar to the one associated with reducing the input sound level. RP CHEATHAM, MA (reprint author), NORTHWESTERN UNIV,HUGH KNOWLES CTR,AUDITORY PHYSIOL LAB,EVANSTON,IL 60208, USA. CR ALLEN JB, 1983, J ACOUST SOC AM, V73, P2071, DOI 10.1121/1.389575 ANDERSON DJ, 1971, J ACOUST SOC AM, V49, P1131, DOI 10.1121/1.1912474 Bode H. W., 1945, NETWORK ANAL FEEDBAC BROWN MC, 1983, J ACOUST SOC AM, V73, P1662, DOI 10.1121/1.389387 CHEATHAM MA, 1989, HEARING RES, V40, P187, DOI 10.1016/0378-5955(89)90159-7 CHEATHAM MA, 1990, HEARING RES, V43, P135, DOI 10.1016/0378-5955(90)90222-B COSTALUPES JA, 1987, HEARING RES, V26, P155, DOI 10.1016/0378-5955(87)90107-9 DALLOS P, 1985, J NEUROSCI, V5, P1591 DALLOS P, 1986, HEARING RES, V22, P185, DOI 10.1016/0378-5955(86)90095-X DALLOS P, 1983, MECHANISMS HEARING, P11 DALLOS P, 1974, FACTS MODELS HEARING, P312 DALLOS P, 1974, J ACOUST SOC AM, V55, P597, DOI 10.1121/1.1914570 DALLOS P, 1976, J ACOUST SOC AM, V60, P510, DOI 10.1121/1.381086 Dallos P, 1973, BASIC MECHANISMS HEA, P335 Dallos P, 1980, PSYCHOPHYSICAL PHYSL, P242 DELGUTTE B, 1990, J ACOUST SOC AM, V87, P791, DOI 10.1121/1.398891 DELGUTTE B, 1989, J ACOUST SOC AM, V85, pS14, DOI 10.1121/1.2026806 EVANS EF, 1983, HEARING PHYSL BASES, P140 Evans EF, 1977, PSYCHOPHYSICS PHYSL, P185 GEISLER CD, 1986, J ACOUST SOC AM, V80, P1359, DOI 10.1121/1.394388 GEISLER CD, 1990, HEARING RES, V44, P241, DOI 10.1016/0378-5955(90)90084-3 GEISLER CD, 1982, J ACOUST SOC AM, V71, P1201, DOI 10.1121/1.387768 GEISLER CD, 1986, HEARING RES, V24, P125, DOI 10.1016/0378-5955(86)90056-0 GREENBERG S, 1986, J ACOUST SOC AM, V79, P1010, DOI 10.1121/1.393373 GREENWOOD DD, 1977, PSYCHOPHYSICS PHYSL, P43 HALL JL, 1980, HEARING RES, V2, P455, DOI 10.1016/0378-5955(80)90082-9 HALL JL, 1980, J ACOUST SOC AM, V68, P480, DOI 10.1121/1.384746 JARVILEHTO M, 1986, J NEUROSCI METH, V17, P327, DOI 10.1016/0165-0270(86)90134-2 JAVEL E, 1981, J ACOUST SOC AM, V69, P1735, DOI 10.1121/1.385953 JAVEL E, 1978, J ACOUST SOC AM, V63, P1093, DOI 10.1121/1.381817 KIM DO, 1986, PERIPHERAL AUDITORY, P239 MOUNTAIN DC, 1986, NEUROBIOLOGY HEARING, P77 NEELY ST, 1983, HEARING RES, V9, P123, DOI 10.1016/0378-5955(83)90022-9 Neely ST, 1983, MECH HEARING, P111 Patuzzi R. B., 1989, COCHLEAR MECHANISMS, P169 PFEIFFER RR, 1975, J ACOUST SOC AM, V58, P867, DOI 10.1121/1.380735 RHODE WS, 1974, J ACOUST SOC AM, V55, P588, DOI 10.1121/1.1914569 Rhode WS., 1977, PSYCHOPHYSICS PHYSL, P27 RHODE WS, 1971, J ACOUST SOC AM, V49, P1218, DOI 10.1121/1.1912485 ROBLES L, 1989, COCHLEAR MECH STRUCT, P369 ROBLES L, 1986, J ACOUST SOC AM, V80, P1364, DOI 10.1121/1.394389 SACHS MB, 1980, J ACOUST SOC AM, V68, P858, DOI 10.1121/1.384825 SACHS MB, 1976, J ACOUST SOC AM, V60, P1157, DOI 10.1121/1.381218 SCHMIEDT RA, 1990, HEARING RES, V45, P221, DOI 10.1016/0378-5955(90)90122-6 SELLICK PM, 1979, HEARING RES, V1, P227, DOI 10.1016/0378-5955(79)90016-9 SELLICK PM, 1982, J ACOUST SOC AM, V72, P131, DOI 10.1121/1.387996 SHAMMA SA, 1987, J ACOUST SOC AM, V81, P1486, DOI 10.1121/1.394501 TASAKI I, 1952, J ACOUST SOC AM, V24, P502, DOI 10.1121/1.1906928 WILSON JP, 1980, MECHANISMS HEARING, P30 WILSON JP, 1975, J ACOUST SOC AM, V57, P705, DOI 10.1121/1.380472 YATES GK, 1989, COCHLEAR MECHANISMS, P177 ZWEIG G, 1988, MECHANICS HEARING CU ZWICKER E, 1979, BIOL CYBERN, V35, P243, DOI 10.1007/BF00344207 NR 53 TC 20 Z9 20 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 193 EP 210 DI 10.1016/0378-5955(90)90045-Q PG 18 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300017 PM 2076972 ER PT J AU GRATTON, MA SALVI, RJ KAMEN, BA SAUNDERS, SS AF GRATTON, MA SALVI, RJ KAMEN, BA SAUNDERS, SS TI INTERACTION OF CISPLATIN AND NOISE ON THE PERIPHERAL AUDITORY-SYSTEM SO HEARING RESEARCH LA English DT Article DE CISPLATIN; OTOTOXICITY; NOISE/DRUG INTERACTION; EVOKED RESPONSE; HAIR CELL LOSS; HEARING LOSS ID CIS-PLATINUM OTOTOXICITY; GUINEA-PIG; BEHAVIORAL THRESHOLDS; CHINCHILLA; DIAMMINEDICHLOROPLATINUM; KANAMYCIN; COCHLEAS; ANIMALS; CANCER AB The potentiation of cisplatin otoxicity by noise expolored in the chinchilla. The effects of exposure to cisplatin alone, noise alone or concurrent exposure to both agents were compared in terms of the threshold shift of the auditory evoked potential and the amount of hair cell loss. The combination of cisplatin plus noise produced significantly more hair cell loss and hearing loss at the high frequencies than did either the noise or cisplatin alone when the noise level was 85 dB SPL or higher; no interaction was seen when the noise level was 70 dB SPL. The amount of the interaction, when present, was constant regardless of the noise level. These results indicate that moderate to high levels of noise can exacerbate cisplatin ototoxicity. C1 UNIV TEXAS,TEXAS MED CTR,DEPT PEDIAT,HOUSTON,TX 77025. UNIV TEXAS,TEXAS MED CTR,DEPT PHARMACOL,HOUSTON,TX 77025. SUNY BUFFALO,DEPT COMMUN DISORDERS & SCI,HEARING RES LAB,BUFFALO,NY 14260. CR AGUILARMARKULIS NV, 1981, J SURG ONCOL, V16, P111, DOI 10.1002/jso.2930160203 BARANAK CC, 1988, J NEURO-ONCOL, V6, P261, DOI 10.1007/BF00163711 BLAKESLEE EA, 1978, J ACOUST SOC AM, V63, P876, DOI 10.1121/1.381767 BOHNE BA, 1986, J ACOUST SOC AM, V80, P1729, DOI 10.1121/1.394285 BOHNE BA, 1979, J ACOUST SOC AM, V66, P411, DOI 10.1121/1.383092 Borch R.F., 1987, METABOLISM ACTION AN, P163 BROWN JJ, 1978, ACTA OTO-LARYNGOL, V86, P394, DOI 10.3109/00016487809107518 BRUMETT RE, 1988, M ASS RES OTOLARYNGO, V12, P255 Brummett R E, 1981, Scand Audiol Suppl, V14 Suppl, P215 DAVIS RI, 1984, EAR HEARING, V5, P153, DOI 10.1097/00003446-198405000-00006 ELDREDGE DH, 1981, J ACOUST SOC AM, V69, P1091, DOI 10.1121/1.385688 Engstrom H, 1966, STRUCTURAL PATTERN O FAUSTI SA, 1984, CANCER, V53, P224, DOI 10.1002/1097-0142(19840115)53:2<224::AID-CNCR2820530207>3.0.CO;2-D FLEISCHMAN RW, 1975, TOXICOL APPL PHARM, V33, P320, DOI 10.1016/0041-008X(75)90098-8 FLEMING S, 1985, AM J CLIN ONCOL-CANC, V8, P302, DOI 10.1097/00000421-198508000-00005 Granowetter L, 1983, J Neurooncol, V1, P293, DOI 10.1007/BF00165711 HAWKINS JE, 1975, J ACOUST SOC AM S, V1, pS89 HELSON L, 1978, CLIN TOXICOL, V13, P469 HENDERSON D, 1983, AUDIOLOGY, V22, P172 HENDERSO.D, 1973, J ACOUST SOC AM, V54, P1099, DOI 10.1121/1.1914321 HOLLEB A, 1986, AM CANCER SOC BOOK P KOMUNE S, 1981, ARCH OTOLARYNGOL, V101, P66 KOVACH JS, 1973, CANCER CHEMOTH REP 1, V57, P357 LAURELL G, 1986, ACTA OTO-LARYNGOL, V101, P66, DOI 10.3109/00016488609108609 LITTERST CL, 1979, CANCER TREAT REP, V63, P1485 LITTERST CL, 1984, CANCER CHEMOTH PHARM, V12, P46 REDDEL RR, 1982, CANCER TREAT REP, V66, P19 RYAN AF, 1982, AM J OTOLARYNG, V3, P264, DOI 10.1016/S0196-0709(82)80065-3 SALVI RJ, 1982, AM J OTOLARYNG, V3, P408, DOI 10.1016/S0196-0709(82)80018-5 SCHWEITZER VG, 1984, OTOLARYNG HEAD NECK, V92, P38 SHARMA RP, 1984, BIOCHEM PHARMACOL, V32, P2665 STRAUSS M, 1983, LARYNGOSCOPE, V93, P1554, DOI 10.1288/00005537-198312000-00007 VERMORKEN JB, 1983, EUR J CANCER CLIN ON, V19, P53, DOI 10.1016/0277-5379(83)90398-X NR 33 TC 49 Z9 50 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1990 VL 50 IS 1-2 BP 211 EP 224 DI 10.1016/0378-5955(90)90046-R PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300018 PM 2076973 ER PT J AU PFINGST, BE AF PFINGST, BE TI CHANGES OVER TIME IN THRESHOLDS FOR ELECTRICAL-STIMULATION OF THE COCHLEA SO HEARING RESEARCH LA English DT Article DE AUDITORY PROSTHESIS; ELECTRICAL STIMULATION; NONHUMAN PRIMATE; PSYCHOPHYSICS; THRESHOLD ID AUDITORY-NERVE; REVERSIBLE DAMAGE; IMPLANTS; MODEL; HISTOPATHOLOGY; MONKEYS AB The purpose of this paper is to better characterize changes over time that occurred in psychophysical detection thresholds for electrical stimulation of the cochlea. Threshold changes observed in nonhuman primates implanted with cochlear electrode arrays can be divided into at least three types based on the patterns of change over time. Short-term increases and subsequent decreases in threshold were commonly observed during the first months after implantation and were often followed by periods of long-term threshold stability. Long-term slow increases in thresholds and more rapid increases after a period of threshold stability have also been observed. The threshold changes may be divided into at least two classes based on their dependence on the waveforms used for the threshold measurements. Some changes occurred primarily in thresholds for long phase-duration signals while other changes were equal in magnitude (in decibels) for all tested stimuli. This suggests that at least two mechanisms underlay these threshold changes. The observed changes in thresholds have implications for experimental studies of electrical stimulation and for clinical application of auditory prostheses. RP PFINGST, BE (reprint author), UNIV MICHIGAN,MED CTR,KRESGE HEARING RES INST,DEPT OTOLARYNGOL,1301 E ANN ST,BOX 0506,ANN ARBOR,MI 48109, USA. 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Res. PD DEC PY 1990 VL 50 IS 1-2 BP 225 EP 236 DI 10.1016/0378-5955(90)90047-S PG 12 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300019 PM 2076974 ER PT J AU YANO, J SUGAI, T SUGITANI, M OOYAMA, H AF YANO, J SUGAI, T SUGITANI, M OOYAMA, H TI OBSERVATIONS OF THE SENSING AND THE TECTORIAL MEMBRANE IN BULLFROG AMPHIBIAN PAPILLA - THEIR POSSIBLE FUNCTIONAL ROLES SO HEARING RESEARCH LA English DT Article DE AMPHIBIAN PAPILLA; TONOTOPIC ORGANIZATION; SENSING MEMBRANE; TECTORIAL MEMBRANE; FROG ID TONOTOPIC ORGANIZATION; ALLIGATOR LIZARD; BASILAR PAPILLA; AUDITORY ORGAN; INNER-EAR; MORPHOLOGY; EVOLUTION; FIBERS; FROG AB Three dimensional reconstructions of the amphibian papilla were performed with light microscopic observations, mainly for the sensing membrane (SM). In horizontal sections of the papilla, the anteromedial end of the SM, which makes contact with the massive anterior portion of the tectorial membrane (TM), is several times thicker than the posterolateral end close to the column of the innervating nerves. This gradient of thickness is observed in all the sections from the dorsal portion attached to the TM to the ventral floor of the papilla. The SM connects to the TM in a topological manner; the anteromedial portion of the TM relates to the anterior end of the SM and the anterolateral and the middle portions of the TM correspond to the sites shifting posteriorly on the SM. The morphology of the SM and its manner of connection to the TM suggest that the SM plays important roles in the occurrence of frequency selectivity and of tonotopic organization of the amphibian papilla. RP YANO, J (reprint author), KANAZAWA MED UNIV,DEPT PHYSIOL,KAHOKU,ISHIKAWA 92002,JAPAN. 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Res. PD DEC PY 1990 VL 50 IS 1-2 BP 237 EP 244 DI 10.1016/0378-5955(90)90048-T PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300020 PM 2076975 ER PT J AU SALVI, RJ SAUNDERS, SS GRATTON, MA AREHOLE, S POWERS, N AF SALVI, RJ SAUNDERS, SS GRATTON, MA AREHOLE, S POWERS, N TI ENHANCED EVOKED-RESPONSE AMPLITUDES IN THE INFERIOR COLLICULUS OF THE CHINCHILLA FOLLOWING ACOUSTIC TRAUMA SO HEARING RESEARCH LA English DT Article DE INFERIOR COLLICULUS; EVOKED RESPONSE; ACOUSTIC TRAUMA; HEARING LOSS ID PSYCHOPHYSICAL TUNING CURVES; COCHLEAR NERVE-FIBERS; SENSORY-MOTOR CORTEX; THRESHOLD SHIFT; HEARING-LOSS; SOMATOSENSORY CORTEX; AUDIOGENIC SEIZURES; NOISE EXPOSURE; BALB/C MICE; PATTERNS AB Evoked response amplitude-level functions were measured from electrodes in the inferior colliculus of the chinchilla before and after exposure to a 2 kHz pure tone of 105 dB SPL. The exposure produced approximately 20-30 dB of permanent threshold shift from 2 to 8 kHz, but little or no hearing loss at higher or lower frequencies. Generally less than 60% of the outer hair cells were missing in the region of hearing loss. The amplitude-level functions measured at 4 and 8 kHz generally showed a loss in sensitivity at low sound levels, a reduction in the maximum amplitude and sometimes steeper than normal slopes. The amplitude-level functions measured at 2 kHz also showed a loss in sensitivity; however, the maximum amplitude was often greater than normal. Even though there was no loss in sensitivity at 0.5 kHz, the amplitude-level function was steeper than normal and the maximum amplitude of the evoked response was almost always substantially larger than normal. The enhancement of the evoked response amplitude from the inferior colliculus does not appear to originate in the cochlea, but may reflect a reorganization of neural activity in the central auditory pathway. RP SALVI, RJ (reprint author), SUNY BUFFALO,HEARING RES LAB,215 PARKER HALL,BUFFALO,NY 14214, USA. 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Res. PD DEC PY 1990 VL 50 IS 1-2 BP 245 EP 258 DI 10.1016/0378-5955(90)90049-U PG 14 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300021 PM 2076976 ER PT J AU HENSON, OW KOPLAS, PA KEATING, AW HUFFMAN, RF HENSON, MM AF HENSON, OW KOPLAS, PA KEATING, AW HUFFMAN, RF HENSON, MM TI COCHLEAR RESONANCE IN THE MOUSTACHED BAT - BEHAVIORAL ADAPTATIONS SO HEARING RESEARCH LA English DT Article DE COCHLEAR POTENTIALS; BATS; COCHLEAR RESONANCE; COCHLEAR EMISSIONS; ECHOLOCATION ID PTERONOTUS-P-PARNELLII; STIMULATED ACOUSTIC EMISSIONS; PERIPHERAL AUDITORY-SYSTEM; DOPPLER-SHIFTED ECHOES; CF-FM BAT; SPIRAL LIGAMENT; EAR; TENSION AB Mustached bats, Pteronotus p. parnellii, use complex, multiharmonic biosonar signals with prominent approx. 60 kHz (CF) components. The sense of hearing is especially acute to sounds near 60 kHz and the cochlea shows a number of specializations in the 60 kHz region. Foremost is a remarkable degree of cochlear resonance. In this study it is shown that: 1) any sounds near the resonance frequency elicit a pronounced resonance that continues after the stimulus terminates; 2) Doppler-shifted echoes of the bat's own cries may cause resonance; 3) continuous resonance can be produced by stimulating the ear with broadband noise but such resonance does not interfere with the bat's ability to Doppler-shift compensate during simulated flight; 4) significant changes in the resonance frequency of the cochlea occur during and after flight; 5) the changes in resonance can be dependent or independent of body temperature changes; and 6) mustached bats continuously adjust the CF component of their pulses to keep the second harmonic echoes in a constant frequency band near the resonance frequency. Thus, mustached bats not only compensate for Doppler-shifts imposed by their movements relative to that of a target, but they cochlear resonance compensate to deal with small changes in the micromechanical properties of the cochlea. C1 UNIV N CAROLINA,CURRICULUM NEUROBIOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT SURG,DIV OTOLARYNGOL HEAD & NECK SURG,CHAPEL HILL,NC 27599. RP HENSON, OW (reprint author), UNIV N CAROLINA,DEPT CELL BIOL & ANAT,TAYLOR BLDG,CB 7090,CHAPEL HILL,NC 27599, USA. 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Res. PD DEC PY 1990 VL 50 IS 1-2 BP 259 EP 274 DI 10.1016/0378-5955(90)90050-Y PG 16 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA EP803 UT WOS:A1990EP80300022 PM 2076977 ER PT J AU STATLER, KD CHAMBERLAIN, SC SLEPECKY, NB SMITH, RL AF STATLER, KD CHAMBERLAIN, SC SLEPECKY, NB SMITH, RL TI DEVELOPMENT OF MATURE MICROCYSTIC LESIONS IN THE COCHLEAR NUCLEI OF THE MONGOLIAN GERBIL, MERIONES-UNGUICULATUS SO HEARING RESEARCH LA English DT Article DE COCHLEAR NUCLEUS; GERBIL; MICROCYSTIC LESION; AGING ID CENTRAL AUDITORY PATHWAY; INNER-EAR; PHYSIOLOGY; ANATOMY AB Microcystic lesions are a persistent final stage in a neurodegenerative disorder characteristic of the cochlear nuclei of gerbils. When gerbils of various ages raised under known acoustic conditions were examined, the volume density and number of lesions increased with age, however, the affected region was restricted to the posteroventral cochlear nucleus and adjacent portions of the dorsal cochlear nucleus, interstitial nucleus, and posterior anteroventral cochlear nucleus. Lesions were also noted in a separate locus in the auditory nerve trunk associated with the acoustic nerve nucleus. The fusiform and molecular layers of the dorsal cochlear necleus were spared at all ages observed. The spherical cell region of the anteroventral cochlear nucleus was also largely spared. A good correlation was observed between the cumulative input from the auditory nerve fibers caused by the ambient acoustic environment acting over the life of the animal and the number of lesions in tonotopic subdivisions of the cochlear nuclei. The earliest microcysts formed in regions receiving auditory nerve fibers most strongly stimulated by the ambinet noise. Thereafter, short exposures to higher levels of input or long exposures to lower levels of input were quantitatively equivalent in producing microcystic lesions. C1 SYRACUSE UNIV,DEPT BIOENGN,SYRACUSE,NY 13244. RP STATLER, KD (reprint author), SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244, USA. 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