The term "Cochlear Amplifier" was coined by Hallowell Davies for "an active process" which "somehow provides additional energy that enhances the vibration of a narrow segment of the basilar membrane near the apical foot of the familiar, travelling wave envelope". Currently there are two putative candidates for the cochlear amplifier. These are voltage-dependent, somatic, motility mediated by the unique outer hair cell motor protein prestin and calcium-mediated, hair-bundle, motility, which is a ubiquitous feature of hair cells. We have attempted to distinguish between these possibilities by measuring basilar membrane displacements from Tecta mice in response to acoustic and electrical stimulation. At low stimulus levels basilar membrane displacements at and around the peak of the travelling wave are dominated by electromechanical amplification from the outer hair cells. In response to acoustic stimulation this amplification is mediated through sensory transduction caused by displacements of the outer hair cell hair-bundles through their interaction with the tectorial membrane, to which they are attached. Electrical stimulation of the cochlea bypasses sensory transduction and drives directly both outer hair cell somatic and hair-bundle motility. We measured basilar membrane displacements in response to acoustic and electrical stimulation in wild type Tecta^+/+ mice, which have a tectorial membrane that will permit electrically elicited hair-bundle movements to interact with it. This opportunity is precluded to the hair bundles of Tecta^DENT/DENT mice where the residual tectorial membrane is detached from the organ of Corti. Basilar membrane frequency tuning measured from Tecta^+/+ mice in response to acoustic stimulation and from Tecta^+/+ and Tecta^DENT/DENT mice in response to electrical stimulation are very similar at threshold when OHC activity dominates the electromechanical properties of the cochlea. At low stimulus levels, electrically elicited hair-bundle motility cannot amplify basilar membrane responses of Tecta^DENT/DENT mice since OHC sensory bundles cannot react against the tectorial membrane, a prerequisite for exerting forces on the basilar membrane. Thus, amplification and compression of basilar membrane responses of Tecta^DENT/DENT mice in response to near-threshold electrical stimulation (similar to near-threshold acoustically and electrically elicited responses from Tecta^+/+ mice) cannot be due to hair-bundle motility.

If time permits, evidence will be presented for a role for prestin in the frequency tuning of cochlear mechanical responses and their transmission to neural excitation.