EFFECTS OF SELECTIVE INNER HAIR CELL LOSS ON AUDITORY-NERVE FIBER THRESHOLD, TUNING AND SPONTANEOUS AND DRIVEN DISCHARGE RATE

Citation
J. Wang et al., EFFECTS OF SELECTIVE INNER HAIR CELL LOSS ON AUDITORY-NERVE FIBER THRESHOLD, TUNING AND SPONTANEOUS AND DRIVEN DISCHARGE RATE, Hearing research, 107(1-2), 1997, pp. 67-82
Citations number
42
Categorie Soggetti
Neurosciences,Acoustics
Journal title
ISSN journal
03785955
Volume
107
Issue
1-2
Year of publication
1997
Pages
67 - 82
Database
ISI
SICI code
0378-5955(1997)107:1-2<67:EOSIHC>2.0.ZU;2-B
Abstract
Current theories assume that the outer hair cells (OHC) are responsibl e for the sharp tuning and exquisite sensitivity of the ear whereas in ner hair cells (IHC) are mainly responsible for transmitting acoustic information to the central nervous system. To further evaluate this mo del, we used a single (38 mg/kg) or double dose (38 mg/kg, 2 times) of carboplatin to produce a moderate (20-28%) or severe (60-95%) IHC los s while sparing a large proportion of the OHCs. The surviving OHCs wer e functionally intact as indicated by normal cochlear microphonic (CM) potentials and distortion product otoacoustic emissions (DPOAE). Sing le-unit responses were recorded from auditory nerve fibers to determin e the effects of the moderate or severe IHC loss on the output of the surviving IHCs. Most neurons that responded to sound in the single-dos e group had normal or near-normal thresholds and normal tuning. Relati vely few neurons in the double-dose group responded to sound because o f the severe IHC loss. The neurons that did respond to sound had narro w tuning curves. Some neurons in the double-dose group also had thresh olds that were within the normal range, but most had thresholds that w ere elevated a mild-to-moderate degree. These results indicate that in tact IHCs can retain relatively normal sensitivity and tuning despite massive IHC loss in surrounding regions of the cochlea. However, the s pontaneous and driven discharge rates of neurons in the carboplatin-tr eated animals were significantly lower than normal. These changes coul d conceivably be due to sublethal damage to surviving IHCs or to posts ynaptic dysfunction in the auditory nerve.