Cochlear amplification, outer hair cells and prestin

Abstract

Mechanical amplification of acoustic signals is apparently a common feature of vertebrate auditory organs. In non-mammalian vertebrates amplification is produced by stereociliary processes, related to the mechanotransducer channel complex and probably to the phenomenon of fast adaptation. The extended frequency range of the mammalian cochlea has probably co-evolved with a novel hair cell type, the outer hair cell and its constituent membrane protein, prestin. Cylindrical outer hair cells are motile and their somatic length changes are voltage driven and powered by prestin. One of the central outstanding problems in mammalian cochlear neurobiology is the relation between the two amplification processes.

Figure 1

A schematic cross-section of the organ of Corti is shown. BM: basilar membrane, TM: tectorial membrane, IHC: inner hair cell, OHC: outer hair cell. The two putative mechanisms of the amplification process are shown in the inserts. On the left, the OHC membrane is shown with the incorporated motor (prestin) molecular complex, possible a tetramer, in two conformational states. On the right, stereocilia and the mechanotranducer channel are shown in cartoon form. Deflection toward the taller stereocilium opens the channel via the tip link, cations (K⁺ and Ca²⁺) enter, driven principally by an electrical gradient of some 160 mV, due to the summing of the positive endocochlear potential and the cell’s negative resting potential. Potassium current dominates the transducer current and it produces the cell’s receptor potential. The voltage change facilitates neurotransmitter release from IHCs and drives prestin motors in OHCs. Calcium current regulates slow and fast adaptation, probably through different mechanisms. Fast adaptation is thought to relate to amplification by controlling channel open probability and thereby producing ciliary deflection.