SOUND PREPROCESSING BY AC AND DC MOVEMENTS OF COCHLEAR OUTER HAIR-CELLS

In inner and outer hair cells, a sound event results mechano-electrically in a receptor potential from the hair cells by the functioning of apical and lateral K+-channels. However, after this point, the signal transfer is divided. Inner hair cells (IHC) release an unknown afferent transmitter. By contrast, outer hair cells (OHC) are proposed to produce mechanical ac and dc responses. In our model, the ac components of the sound signal, the carrier frequencies, determine the response of the OHC. Usually, they respond by ac and dc movements. The rapid ac movements of OHC, for which the underlying mechanism is unknown, may respond cycle-by-cycle to and interfere with the carrier frequency of the traveling wave. Near hearing threshold, they could drastically amplify the traveling wave thus contributing to the postulated cochlear amplifier. Active dc movements of the cytoskeleton of the cell body, as well as of the cuticular plate with the sensory hairs, are proposed to respond to millisecond changes of the sound stimulus over time. Such changes could be a modulation of the amplitude (AM), i.e., an increase or decrease of the sound pressure level (SPL), which is reflected in the envelope of the traveling wave. The active mechanical dc response of OHC to the amplitude (AM) and frequency modulation (FM) pattern is then expected to result in dc position changes of the reticular lamina (RL). These should control the operation point of the stereocilia, thus influencing their transfer function and sensitivity. In addition, experimental data suggest that there are modulations of the compliance of the organ of Corti (OC) and changes of its geometry. This dc modulation of micromechanical properties and geometry of the OC by active force generation of OHCs might contribute to automatic gain control, adaptation, TTS, as well as to the homeostasis of the basilar membrane location. In particular, the motile mechanism may protect the vulnerable cochlear partition against high sound pressure levels. Moreover, according to this model, changes of the sound signal with time are expected to be encoded in the actively produced dc movements of the RL. As the signal changes may carry important information (e.g., complex sound signal modulations such as formant transitions in speech), this is extracted and mechanically encoded by the proposed active dc mechanism. It cannot be excluded that the information-carrying dc signal is transferred to inner hair cells contributing to their adequate stimulus. If this is true, then information due to sound signal changes would appear subsequently in the cochlea as active mechanical low-frequency events even at high-carrier frequencies. This would allow the cochlea to adapt parts of its information encoding to the limited frequency of the afferent transmitter release from IHC whose cycle-by-cycle encoding is known to be restricted to low frequencies (phase locking).