TY - JOUR
T1 - Trimethyltin ototoxicity
T2 - evidence for a cochlear site of injury
AU - Fechter, Laurence D.
AU - Young, John S.
AU - Nuttall, Alfred L.
N1 - Funding Information:
Supported in part by NIH grant nos. ES 02852 and NS 11731.L .F. is supported by RCDA no. ES 00125. The authors express their gratitude to Blair Miller, A. Gail Lee, Michelle Griffiths and J. Nadine Brown for their expert technical assistance. to Susan Pierson, Jane Rogers and Janet Mello for their patient and efficient typing, and to Dr. P. Thorne for comments on an earlier version of this manuscript.
PY - 1986
Y1 - 1986
N2 - The environmental contaminant, trimethyltin (TMT), produces a profound elevation in tone intensity necessary to inhibit the acoustic startle reflex in laboratory animals which recovers over a prolonged period except at very high frequencies. The recovery that is observed does not begin until 3 to 5 weeks after a single acute administration depending upon dosage. As opposed to the very temporary threshold shifts by the salicylates and loop diuretics or the permanent and progressive ototoxicity resulting from aminoglycoside antibiotics the time course for recovery of acoustic startle reflex inhibition after TMT appears to be an anomaly for a chemical ototoxicant. In terms of the duration of loss only, this pattern appears similar to that sometimes observed after noise exposure. The current investigation replicates the finding that recovery of acoustic startle reflex inhibition after TMT is frequency related in that only the highest frequency impairment appears to be permanent. While this frequency dependence suggests a cochlear locus of injury, both the known neurotoxic effects of TMT and the time course of the behavioral impairment suggest a more central locus of injury. Compound action potential and cochlear microphonic recordings made from the round window in the current study confirm a preferential high frequency effect of TMT and demonstrate a significant cochlear component to the ototoxic effects of this agent. ototoxicity, peripheral auditory damage, trimethyltin, reflex modification audiometry, compound action potential, cochlear microphonic.
AB - The environmental contaminant, trimethyltin (TMT), produces a profound elevation in tone intensity necessary to inhibit the acoustic startle reflex in laboratory animals which recovers over a prolonged period except at very high frequencies. The recovery that is observed does not begin until 3 to 5 weeks after a single acute administration depending upon dosage. As opposed to the very temporary threshold shifts by the salicylates and loop diuretics or the permanent and progressive ototoxicity resulting from aminoglycoside antibiotics the time course for recovery of acoustic startle reflex inhibition after TMT appears to be an anomaly for a chemical ototoxicant. In terms of the duration of loss only, this pattern appears similar to that sometimes observed after noise exposure. The current investigation replicates the finding that recovery of acoustic startle reflex inhibition after TMT is frequency related in that only the highest frequency impairment appears to be permanent. While this frequency dependence suggests a cochlear locus of injury, both the known neurotoxic effects of TMT and the time course of the behavioral impairment suggest a more central locus of injury. Compound action potential and cochlear microphonic recordings made from the round window in the current study confirm a preferential high frequency effect of TMT and demonstrate a significant cochlear component to the ototoxic effects of this agent. ototoxicity, peripheral auditory damage, trimethyltin, reflex modification audiometry, compound action potential, cochlear microphonic.
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U2 - 10.1016/0378-5955(86)90116-4
DO - 10.1016/0378-5955(86)90116-4
M3 - Article
C2 - 3745026
AN - SCOPUS:0022485217
SN - 0378-5955
VL - 23
SP - 275
EP - 282
JO - Hearing Research
JF - Hearing Research
IS - 3
ER -