Cochlea function

Cochlea hair cells lose their kinocilia during development and the tips of their tallest stereocilia are embedded in the overlying tectorial membrane, a matrix of proteins and mucopoly-saccharides. The oscillations of basilar membrane in response to a sound stimulus cause it to shear with respect to the tectorial membrane, bending the stereocilia first in one way and then other. This outcome in periodic hyperpolarization and depolarization of hair cells, generating cyclical modifications in the tonic secretion of glutamate. The transduction method for hair cells is like that of vestibular hair cells.

A sound stimulus causes a traveling wave (like that produced by twitching the free end of a rope fixed at its other end) to spread along the basilar membrane from base to the apex. High frequencies cause vibration at the basal end while low frequencies cause vibration towards the apex. This frequency sorting is an outcome of the continuous variation in the mass, width, and stiffness of the basilar membrane along its length. The basilar membrane is narrow (50 µm) and stiff at the base, wider (500 µm) and less firm at the apex. The relationship between frequency and length is logarithmic. At a given frequency, increasing the SPL increases the amplitude of the vibration and the length of basilar membrane responding.

The outer hair cells (OHCs) contract in a voltage-dependent manner. Depolarization causes them to short. The speed with which they change length is so rapid that they are capable to follow the high frequency voltage changes generated by sound stimuli. This means OHCs augment the vibrations of the basilar membrane, a procedure known as cochlear amplification. It possibly contributes to the high sensitivity and fine tuning to frequency displayed by the basilar membrane, as these features are lost whenever OHCs are selectively damaged by aminoglycoside antibiotics like streptomycin. The Cochlear amplification causes vibrations of perilymph which are transmitted to the oval window across the middle ear in the “wrong” direction to the tympanic membrane that now acts as a loudspeaker generating inaudible otoacoustic emissions. These are not essential for normal audition but provide insights into ear function.