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Received June 4, 2004
Revised July 8, 2004
Accepted after revision August 16, 2004
1 Northwestern University
2 St. Jude Children's Research Hospital
* To whom correspondence should be addressed. E-mail: m-cheatham{at}northwestern.edu.
Summary Gross-potential recordings in mice lacking the Prestin gene indicate that compound action potential (CAP) thresholds are shifted by ~45 dB at 5 kHz and by ~60 dB at 33 kHz. However, in order to conclude that outer hair cell (OHC) electromotility is associated with the cochlear amplifier, frequency selectivity must be evaluated and the integrity of the OHC's forward transducer ascertained. The present report demonstrates no frequency selectivity in CAP tuning curves recorded in homozygotes. In addition, CAP input-output functions indicate that responses in knockouts approach those in controls at high levels where the amplifier has little influence. Although the CM in knockouts remains ~12 dB below that in wildtype mice even at the highest levels, this deficit is thought to reflect hair cell losses in mice lacking prestin. A change in OHC forward transduction is not implied because knockout mice display nonlinear responses similar to those in controls. For example, homozygotes exhibit a bipolar summating potential with positive responses at high frequencies; negative responses at low frequencies. Measurement of intermodulation distortion also shows that the cubic difference tone, 2f1-f2, is ~20 dB down from the primaries in both homozygotes and their controls. Because OHCs are the sole generators of the negative SP and because 2f1-f2 is also thought to originate in OHC transduction, these data support the idea that forward transduction is not degraded in OHCs lacking prestin. Finally, application of AM1-43, which initially enters hair cells through their transducer channels, produces fluorescence in wildtype and knockout mice indicating transducer channel activity in both inner and outer hair cells.
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