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Amplitude enhancement is seen in the cochlear nerve but not at, or before, the afferent synapse.

作者信息

Henry K R, Price J M

机构信息

Department of Psychology, University of California, Davis 95616.

出版信息

Hear Res. 1994 Sep;79(1-2):190-6. doi: 10.1016/0378-5955(94)90140-6.

DOI:10.1016/0378-5955(94)90140-6
PMID:7806482
Abstract

The amplitude of the cochlear nerve compound action potential (CAP) produced by a moderate intensity tonal stimulus (S2) can be enhanced when S2 is preceded by a low intensity S1 of the same frequency. The presence of S1 had no observable influence on the threshold of the CAP to S2. Enhancement was not observed in the cochlear microphonics or summating potentials. Deactivation of the contralateral olivocochlear bundle did not influence enhancement. Tetrodotoxin (TTX) was applied to the round window to block cochlear nerve spike activity, resulting in a residual EPSP-like potential, as described in the guinea pig by Dolan et al. (1989). Kainic acid, in turn, eliminated this EPSP-like response. Even though some differences were found in the responses of the gerbil and their guinea pig preparation to TTX and kainic acid, enhancement was not observed in this residual potential. When enhancement was observed at the level of the CAP, it was observed at brainstem levels. It is suggested that enhancement originates within the cochlear nerve axons.

摘要

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1
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