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Neuron. 2008 May 8;58(3):333-9. doi: 10.1016/j.neuron.2008.02.028.

Prestin-based outer hair cell motility is necessary for mammalian cochlear amplification.

Author information

1
Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208, USA. p-dallos@northwestern.edu

Abstract

It is a central tenet of cochlear neurobiology that mammalian ears rely on a local, mechanical amplification process for their high sensitivity and sharp frequency selectivity. While it is generally agreed that outer hair cells provide the amplification, two mechanisms have been proposed: stereociliary motility and somatic motility. The latter is driven by the motor protein prestin. Electrophysiological phenotyping of a prestin knockout mouse intimated that somatic motility is the amplifier. However, outer hair cells of knockout mice have significantly altered mechanical properties, making this mouse model unsatisfactory. Here, we study a mouse model without alteration to outer hair cell and organ of Corti mechanics or to mechanoelectric transduction, but with diminished prestin function. These animals have knockout-like behavior, demonstrating that prestin-based electromotility is required for cochlear amplification.

PMID:
18466744
PMCID:
PMC2435065
DOI:
10.1016/j.neuron.2008.02.028
[Indexed for MEDLINE]
Free PMC Article

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