A.C. and D.C. motility of mammalian auditory sensory cells--a new concept in hearing physiology

Abstract

Transduction of sound events results mechano-electrically in a.c. and d.c. movements of the auditory sensory cells based on de- and repolarization steps through the opening of apical and lateral K(+)--conductive ion channels. During transduction, apical ionic channels are thought to allow an influx of K+ resulting in a depolarization of the outer cell membrane. This is followed by a K(+)--efflux through basolateral K(+)--channels, inducing a re- or hyperpolarization phase. Different hypotheses expect the apical transduction channels to be located either in the cell membrane of the stereocilia and/or in the cell membrane of the cuticular plate (CP). Patch-clamp techniques revealed the presence of an unspecific CP-channel adjacent to the insertion of the stereocilia. In the basolateral cell membrane of outer hair cells (OHC) from the mammalian cochlea, the prevailing channel type, a rectifying high-conductance K(+)--channel, has been characterized as C-channel. After depolarization of the auditory sensory cells, however, the signal transfer divides at this point. The depolarization of inner hair cells (IHC) leads to the release of afferent transmitters for which glutamate is a good candidate. By contracts in OHCs the stimulation induces active mechanical responses of the sensory cells. Slow d.c. movements of the cylindrical hair cell body as well as of the cuticular plate with the sensory hairs are thought to control the operation point of the stereocilia. The mechanical characteristics of the cochlear partition during adaptation, TTS as well as the homeostasis of the basilar membrane location could be modulated by the OHCs. In particular, the slow d.c. movements may protect the vulnerable cochlear partition against high sound pressure levels. Rapid d.c. movements of which the underlying mechanisms is unknown, may interfere cycle-by-cycle with the travelling wave. Thus, near hearing threshold, they could drastically amplify and tune the travelling wave. This could explain otoacoustic emissions, the high sensitivity and the frequency selectivity of the ear at low sound pressures. Moreover, it cannot be excluded that the actomyosin skeleton significantly helps to amplify the travelling wave by intermittent stimulations of a resonance system.