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Publication : Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier.

First Author  Liberman MC Year  2002
Journal  Nature Volume  419
Issue  6904 Pages  300-4
PubMed ID  12239568 Mgi Jnum  J:79029
Mgi Id  MGI:2386840 Doi  10.1038/nature01059
Citation  Liberman MC, et al. (2002) Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier. Nature 419(6904):300-4
abstractText  Hearing sensitivity in mammals is enhanced by more than 40 dB (that is, 100-fold) by mechanical amplification thought to be generated by one class of cochlear sensory cells, the outer hair cells. In addition to the mechano-electrical transduction required for auditory sensation, mammalian outer hair cells also perform electromechanical transduction, whereby transmembrane voltage drives cellular length changes at audio frequencies in vitro. This electromotility is thought to arise through voltage-gated conformational changes in a membrane protein, and prestin has been proposed as this molecular motor. Here we show that targeted deletion of prestin in mice results in loss of outer hair cell electromotility in vitro and a 40-60 dB loss of cochlear sensitivity in vivo, without disruption of mechano-electrical transduction in outer hair cells. In heterozygotes, electromotility is halved and there is a twofold (about 6 dB) increase in cochlear thresholds. These results suggest that prestin is indeed the motor protein, that there is a simple and direct coupling between electromotility and cochlear amplification, and that there is no need to invoke additional active processes to explain cochlear sensitivity in the mammalian ear.
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