[4][5] This is because the resonant frequency of the membrane depends on its own width and stiffness, not on the diameter of the cochlea at each point.

Sound-driven vibrations travel as waves along this membrane, along which, in humans, lie about 3,500 inner hair cells spaced in a single row.

When the vibration of the membrane rocks the triangular frames, the hairs on the cells are repeatedly displaced, and that produces streams of corresponding pulses in the nerve fibers, which are transmitted to the auditory pathway.

[9] The outer hair cells feed back energy to amplify the traveling wave, by up to 65 dB at some locations.

Consequently, the inner hair cells get more displacement of their cilia and move a little bit more and get more information than they would in a passive cochlea.

This can cause opening and closing of the mechanically gated potassium channels on the cilia of the hair cell.

Depolarization will open the voltage gated calcium channel, releasing neurotransmitter (glutamate) at the nerve ending, acting on the spiral ganglion cell, the primary auditory neurons, making them more likely to spike.

Hyperpolarization causes less calcium influx, thus less neurotransmitter release, and a reduced probability of spiral ganglion cell spiking.