  The outer hair cell (OHC) of the organ of Corti underlies a mechanically
based process that enhances hearing, termed cochlear amplification. The cell
possesses a unique motor protein, prestin, which senses voltage and
consequently changes conformation to cause large cell length changes, termed
electromotility (eM). In OHCs studied in vitro, the prestin voltage sensor
generates a capacitance that is both voltage and frequency dependent, peaking
in magnitude at a characteristic membrane voltage (Vh), which can be greater
than the linear capacitance of the cell. Consequently, the OHC membrane time
constant is multifarious depending upon resting potential and frequency of AC
evaluation. After precisely correcting for this influence on the whole-cell
voltage clamp time constant, we find that OHC eM is low pass in nature,
substantially attenuating in magnitude within the frequency bandwidth of human
speech. The frequency response is slowest at Vh, with a cut-off near 1.5 kHz,
but increases up to six-fold in a U shaped manner as holding voltage deviates
from Vh. NLC measures follow this pattern. Viscous drag alone cannot account
for such eM behavior; nor can it arise from viscous drag in combination with a
sigmoidal voltage-dependent OHC stiffness. However, viscous drag combined with
kinetics of prestin, likely corresponding to its bell-shaped conformational
gating compliance (Iwasa, 2000), is in line with our observations. How OHC eM
influences cochlear amplification at higher frequencies needs reconsideration.
