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This Article Full Text Full Text (PDF) All Versions of this Article: 99/4/1607    most recent 01216.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Drexl, M. Articles by Russell, I. J. PubMed PubMed Citation Articles by Drexl, M. Articles by Russell, I. J.

The Role of Prestin in the Generation of Electrically Evoked Otoacoustic Emissions in Mice

¹School of Life Sciences, University of Sussex, Brighton, United Kingdom; and ²Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee

Submitted 31 October 2007; accepted in final form 30 January 2008

Electrically evoked otoacoustic emissions are sounds emitted from the inner ear when alternating current is injected into the cochlea. Their temporal structure consists of short- and long-delay components and they have been attributed to the motile responses of the sensory-motor outer hair cells of the cochlea. The nature of these motile responses is unresolved and may depend on either somatic motility, hair bundle motility, or both. The short-delay component persists after almost complete elimination of outer hair cells. Outer hair cells are thus not the sole generators of electrically evoked otoacoustic emissions. We used prestin knockout mice, in which the motor protein prestin is absent from the lateral walls of outer hair cells, and Tecta^ENT/ENT mice, in which the tectorial membrane, a structure with which the hair bundles of outer hair cells normally interact, is vestigial and completely detached from the organ of Corti. The amplitudes and delay spectra of electrically evoked otoacoustic emissions from Tecta^ENT/ENT and Tecta^+/+ mice are very similar. In comparison with prestin^+/+ mice, however, the short-delay component of the emission in prestin^–/– mice is dramatically reduced and the long-delay component is completely absent. Emissions are completely suppressed in wild-type and Tecta^ENT/ENT mice at low stimulus levels, when prestin-based motility is blocked by salicylate. We conclude that near threshold, the emissions are generated by prestin-based somatic motility.