Vertical displacements of the basilar membrane cause deflection of the stereocilia (hair) of the hair cells, themselves situated on the membrane (on the organ of Corti - Davis 1958). The mechanical motion of the basilar membrane is thus converted to a probability of spike occurrence in the post-synaptic auditory nerve. This conversion is performed by the inner hair cells on the basilar membrane, and is explained briefly below using the Meddis I model. A more detailed account of the model is given later in this document (see CRL reference).
The Meddis 86 inner hair cell (IHC) model assumes that the spike activity of the post-synaptic auditory nerve is linearly related to the amount of transmitter in the synaptic cleft between the inner hair cell and its corresponding auditory nerve. Transmitter substance is released into the cleft from the hair cell in amounts that depend upon the permeability, which is modulated by the driving signal amplitude. The model decomposes the hair cell operation into four distinct stages: (i) a factory wherein transmitter is manufactured and transferred to the (ii) free transmitter pool. Transmitter is then released into the (iii) synaptic cleft at a rate dependent upon the hair cell membrane permeability, some of which is taken up by the synapse. Some transmitter is lost from the cleft, however, while the remainder is passed back though the hair cell membrane to a (iv) reprocessing store, which ultimately passes reprocessed transmitter substance back to the free transmitter pool (see (ii)).
This completes the physiological description of the auditory periphery which is pertinent to the present release of the CRL. As mentioned before, further research will produce additional physiological models as more of the auditory system's secrets are laid bare.