Abstract

It has been widely assumed that the function of the OHC is to increase the sensitivity and frequency selectivity of the cochlea via a phasic OHC voltage, which controls the soma length. This action is called the cochlear amplifier. According to this view the length of the OHC is assumed to follow the stimulus to the upper frequency limit of hearing, in a phasic manner (cycle by cycle), adding power at the signal frequency. We propose an alternative view that the OHC controls the dynamic range in a parametric, or tonic manner, via the cells axial stiffness. In this case the change in gain seen by the IHC does not require a phasic response at high frequencies. The OHC could mediate a fast acting gain control, via impedance changes, that follows the OHC membrane tonic voltage envelope. Given a level-dependent change in dynamic range (i.e., dynamic range compression), the tuning and sensitivity would necessarily change. Our analysis and conclusions are based upon a re-interpretation of existing mammalian outer hair cell (OHC) studies using a generalized admittance matrix formulation of the OHC, that relates the plasma membrane voltage and current to the soma axial force and velocity.

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