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 cells1-4. 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 vitro5-7. This electromotility is thought to arise through voltage-gated conformational changes in a membrane protein8,9, and prestin has been proposed as this molecular motor10-12. 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.
| Original language | English |
|---|---|
| Pages (from-to) | 300-304 |
| Number of pages | 5 |
| Journal | Nature |
| Volume | 419 |
| Issue number | 6904 |
| DOIs | |
| State | Published - Sep 19 2002 |
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All Science Journal Classification (ASJC) codes
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Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier. / Liberman, M. Charles; Gao, Jiangang; He, David Z.; Wu, Xudong; Jia, Shuping; Zuo, Jian.
In: Nature, Vol. 419, No. 6904, 19.09.2002, p. 300-304.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier
AU - Liberman, M. Charles
AU - Gao, Jiangang
AU - He, David Z.
AU - Wu, Xudong
AU - Jia, Shuping
AU - Zuo, Jian
PY - 2002/9/19
Y1 - 2002/9/19
N2 - 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 cells1-4. 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 vitro5-7. This electromotility is thought to arise through voltage-gated conformational changes in a membrane protein8,9, and prestin has been proposed as this molecular motor10-12. 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.
AB - 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 cells1-4. 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 vitro5-7. This electromotility is thought to arise through voltage-gated conformational changes in a membrane protein8,9, and prestin has been proposed as this molecular motor10-12. 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.
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U2 - 10.1038/nature01059
DO - 10.1038/nature01059
M3 - Article
VL - 419
SP - 300
EP - 304
JO - Nature
JF - Nature
SN - 0028-0836
IS - 6904
ER -