Audition Promenade round Cochlea autour Cochlée oreille ear organ of Corti oreille ear CRIC Montpellier Remy Pujol U254

	Outer Hair Cells (OHCs)
	Overview / Coupling / Membrane / Synapses / Active mechanism / Oto-acoustic emissions
	Upgrade 2003, by G. Rebillard. Drawings: S. Blatrix

The cochlear amplifier

In the early eighties, cochlear physiology was still poorly understood. On one side, neurophysiologists were describing a remarkable sensitivity and frequency selectivity of the single unit auditory nerve fibres (see Kiang et al.) attributed to a "magic" second filter. On the other side, Békésy's travelling wave theory meant that the cochlea had to be thought of as a passive and very poorly tuned organ. Nobody remembered that in 1945 Gold (ref. e11), in a premonitory paper, had told of "active mechanical processes" which "should be there"! Two types of research, roughly simultaneously, delivered the proof that Gold's prediction was right, and that the living cochlea was far removed from the post-mortem models of Békésy. The discovery of oto-acoustic emissions (see refs.) revealed an active mechanism, and precise measurements on living cochleas demonstrated that the tuning of the basilar membrane was as good as that of the single unit auditory fibres.

Schematic representation of the OHC active mechanism

For a pure tone of 10 kHz, the vibration of the basilar membrane is shown above as a diagram along the spiral of a guinea-pig cochlea.

The OHC active mechanism shifts by about half an octave the maximum site of vibration, which is amplified by about 50 dB and remarkably tuned. Thus the vibration acting on IHC stereocilia is far removed from the passive Békésy wave.

From the discovery of OHC electromotility to the current concept
Electromotility was discovered on isolated OHCs in 1985 (ref. e12). It has been demonstrated that this unique mechanism, capable of occurring at high frequencies (at least up to 20-30 kHz), independent of Ca2+ and ATP, depends on specific properties of the OHC lateral plasma membrane coupled with a very specific cytoskeleton network. OHC contraction is the sum of contraction of motors located within the OHC lateral plasma membrane (ref. e19). Then, because of the arrangement of this protein on the membrane, and because of its connection with a cytoskeletal spring, shortening of the OHC length is induced. In turn, the OHC coupling with support cells allows transfer of this energy into the basilar and tectorial membrane, giving the organ of Corti its exquisite properties of sensitivity and frequency selectivity. The current concept is that K+-mediated OHC membrane depolarisation changes the conformation of the motor protein PRESTIN (see animated drawing), which is now clearly identified (refs. e22, e 23).
	Schematic representation of the OHC electromotility. OHC depolarisation extracts anions (most probably chloride) from their prestin binding sites. This induces a shortening of the prestin molecule and a contraction of the plasma membrane. When the OHC repolarizes anions bind to prestin again, which elongates.
	Scheme: G. Rebillard, drawing and animation: S. Blatrix
Note. - OHC electromotility is the basis of the cochlear active mechanism. However, for feeding energy back into the the cochlear partition a strong mechanical coupling is needed. This is mainly realised by the OHC-Deiters' cell-basilar membrane junctions, and by the firm embedding of the tips of the tallest OHC stereocilia into the tectorial membrane (see coupling). - Such a mechanical coupling is much stronger at the base than at the apex of the cochlea. This explains why OHC active mechanisms are more potent for high than low frequencies.
- Beside electromotility, other motile properties of isolated OHCs have been described. For example, a slow Ca2+-dependent motility (refs. e15, e16), driven by the medial efferent system (ref. e20) modulates (reduces) OHC electromotility.