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

M. Charles Liberman, Jiangang Gao, David Z. Z. He, Xudong Wu, Shuping Jia and Jian Zuo ()
Additional contact information
M. Charles Liberman: Massachusetts Eye & Ear Infirmary
Jiangang Gao: St Jude Children's Research Hospital
David Z. Z. He: Boys Town National Research Hospital
Xudong Wu: St Jude Children's Research Hospital
Shuping Jia: Boys Town National Research Hospital
Jian Zuo: St Jude Children's Research Hospital

Nature, 2002, vol. 419, issue 6904, 300-304

Abstract: Abstract 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 cells1,2,3,4. 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 vitro5,6,7. This electromotility is thought to arise through voltage-gated conformational changes in a membrane protein8,9, and prestin has been proposed as this molecular motor10,11,12. 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.

Date: 2002
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DOI: 10.1038/nature01059

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