Auditory periphery: cochlear processing.

For over 50 years now, the propagation of travelling waves on the basilar membrane of the cochlea has been known to underlie the generation of the auditory sensation (von Békésy, 1960). To date, physiology textbooks give a graphical representation of this phenomenon stressing solely action potential generation on the afferent acoustic nerve fibres contacting inner hair cells. These produce a receptor potential upon displacement of their stereocilia bundle: a process called forward transduction. Stereocilia deflection is caused by the shearing motion of the tectorial membrane relative to the organ of Corti, which rides on the basilar membrane as the wave pushes it up and down. In this type of representation the organ of Corti has no internal degrees of freedom. Besides, the fact that the more numerous outer hair cells are prevalently contacted by efferent innervation (Spoendlin, 1978) is completely overlooked. At the beginning of the eighties crucial experiments performed on the guinea pig basilar membrane showed that travelling wave amplitudes are several orders of magnitude larger in vivo than post-mortem, or even post-trauma (Sellick et al., 1982, 1983; Johnstone et al., 1986). The wave amplitude profiles are also rather different in a properly functioning cochlea, being much more peaked and terminating abruptly after reaching their maximum. When the wave amplitude is plotted against stimulus frequency at a fixed site on the basilar membrane, the slope on the falling high-frequency skirt is hundreds of dB/octave for near threshold acoustic inputs. Davis (1983) called "cochlear amplifier" the physiologically vulnerable process that underlies travelling wave amplification. A cochlea with amplification is said to be active, in contrast with the passive one typical of von Békésy's description. Here we shall discuss some key results concerning the mechanisms of travelling wave amplification in an active cochlea.