Cochlear amplification

An alternative view of the source of cochlear amplification is that it arises in the OHC s bundles of stereocilia. The stereocilia bundle is composed of many actin filaments, and the kinocilium containing mainly axonemal microtubules. At least three types of actin-dependent molecular motor proteins are expressed in the stereocilia and are involved in adaptation of the hair cell MET channels myosin 15A (Rzadzinska et al., 2004), myosin 7A (Kros et al., 2002), and myosin 1C (Gillespie and Cyr, 2004). Many studies have shown that fast adaptation of MET channels can amplify the oscillation of hair bundles in the nonmammalian auditory... 

However, new support for the somatic electromotility model of cochlear amplification has been provided by Jia and He (2005), who demonstrated, using a coil preparation of the gerbil cochlea, that active hair bundle movement depends on the developmental onset of somatic electromotility. At postnatal day 4 (P4), when hair bundle MET channels are functional but the OHCs are not yet electromotile, no hair bundle motility could be detected from the apical turn of the coil in response to a sinusoidal voltage command (Jia and He, 2005). The hair bundle movement appeared when somatic electromotility developed. This observation is supported by findings from studies of the cochlea of prestin knockout mice, in which active movement of the hair bundle is not detected despite the presence of functional MET channels (Jia and He, 2005). In addition, the amphtude of the motility-associated hair bundle movement is 20 dB greater than that of the transduction-charmel-based hair bundle motion. They propose that somatic motility in conjunction with bundle motion is responsible for the cochlear amplifier (Jia and He, 2005). 

Kennedy HI, Crawford AC, Fettiplace R. 2005. Force generation by mammalian hair bundles supports a role in cochlear amplification. Nature 433 880-883. 

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