Abstract
David Kemp’s discovery of otoacoustic emissions signalled a new era in cochlear modelling and neurobiology. After Bekesy, the emphasis on cochlear processing had centered on the physics of frequency selectivity with any underlying physiological or cellular contributions taking a back seat. Since then, many lines of evidence have revealed that the (at the time) enigmatic population of outer hair cells (OHCs) within the cochlea plays a central role in modifying the basilar membrane mechanics: OHCs act as fast actuators up to at least 80 kHz in order to cancel fluid damping of the partition. The active mechanical feedback due to OHCs appears to be delicately poised so that small variations from section to section provides a substrate for the inhomogeneities required for OAEs. Metabolically labile, the intrinsic non-linearities of the system can be traced to the hair cell mechano-electrical transduction step itself. Mammalian OHC “motor” function has an identified molecular basis, and only recently have structural studies partially clarified how it this molecule (“prestin”/SLC26A5) works. A further contemporary concern is whether the mammalian cochlea employs the same, but scaled, mechanism of sound amplification for high as well as for low frequencies and this issue will be discussed.
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