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J Neurophysiol (January 30, 2008). doi:10.1152/jn.01216.2007
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Submitted on October 31, 2007
Accepted on January 30, 2008

THE ROLE OF PRESTIN IN THE GENERATION OF ELECTRICALLY EVOKED OTOACOUSTIC EMISSIONS IN MICE

Markus Drexl1, Marcia Maria Mellado Lagarde2, Jian Zuo3, AN Lukashkin1, and I. J. Russell1*

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

* To whom correspondence should be addressed. E-mail: i.j.russell{at}sussex.ac.uk.

Electrically evoked otoacoustic emissions are sounds emitted from the inner ear when alternating current is injected into the cochlea. Their temporal structure consists of a short- and a long-delay component 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 either on 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 TectaΔENT/ΔENT 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+/+ mice, TectaΔENT/ΔENT 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 TectaΔENT/ΔENT mice at low stimulus levels, when prestin-based motility is suppressed by salicylate. We conclude that near threshold, the emissions are generated by prestin-based somatic motility.







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