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PubMed · 9482786

Cochlear electrically evoked emissions modulated by mechanical transduction channels.

Abstract

Cochlear outer hair cells are capable of both mechanical-to-electrical and electrical-to-mechanical transduction. Vibration of their stereocilia by sound is believed to stimulate somatic motility via a receptor potential developed across the basolateral membrane, thereby enhancing the mechanical vibration and increasing the sensitivity and frequency selectivity of the ear. Extrinsic electrical currents, applied at the tops of the cells, also appear to activate motility in vivo, presumably after entering the cell. Earlier experiments suggested such currents might enter through the transduction channels themselves, but an alternative shunt pathway through the membrane capacitance seems more likely on physical grounds. We therefore recorded electrically evoked oto-acoustic emissions while modulating the transduction channels by driving them with low-frequency sound. Recordings of the low-frequency cochlear microphonic provided a measure of the mean electrical conductance through the channels during sound stimulation. Emissions increased during displacement of the basilar membrane toward scala vestibuli, when the channels were biased open, and decreased on the opposite phase, and the modulation of the emission was in direct proportion to the cochlear microphonic. The results are the strongest evidence yet that electrically evoked emissions are generated directly by mechanisms related to cochlear transduction and lead to the surprising conclusion that, for frequencies up to at least 12 kHz, extrinsic electrical currents enter the hair cell predominantly by the resistive pathway through the transduction channels. Alternatively, the results might be consistent with direct modulation of a motility source driven by capacitive currents but whose output depends on the state of the channels.

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BibTeXRIS

G K Yates, D L Kirk. 1998-03-15. Cochlear electrically evoked emissions modulated by mechanical transduction channels.. https://pubmed.ncbi.nlm.nih.gov/9482786/

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