PURPOSE OF REVIEW: Normal cochlear function depends on maintaining the correct ionic environment for the sensory hair cells. Here we review recent literature on the cellular distribution of potassium transport-related molecules in the cochlea. RECENT FINDINGS: Transgenic animal models have identified novel molecules essential for normal hearing and support the idea that potassium is recycled in the cochlea. The findings indicate that extracellular potassium released by outer hair cells into the space of Nuel is taken up by supporting cells, that the gap junction system in the organ of Corti is involved in potassium handling in the cochlea, that the gap junction system in stria vascularis is essential for the generation of the endocochlear potential, and that computational models can assist in the interpretation of the systems biology of hearing and integrate the molecular, electrical, and mechanical networks of the cochlear partition. Such models suggest that outer hair cell electromotility can amplify over a much broader frequency range than expected from isolated cell studies. SUMMARY: These new findings clarify the role of endolymphatic potassium in normal cochlear function. They also help current understanding of the mechanisms of certain forms of hereditary hearing loss.

Normal hearing depends on sound amplification within the mammalian cochlea. The amplification, without which the auditory system is effectively deaf, can be traced to the correct functioning of a group of motile sensory hair cells, the outer hair cells of the cochlea. Acting like motor cells, outer hair cells produce forces that are driven by graded changes in membrane potential. The forces depend on the presence of a motor protein in the lateral membrane of the cells. This protein, known as prestin, is a member of a transporter superfamily SLC26. The functional and structural properties of prestin are described in this review. Whether outer hair cell motility might account for sound amplification at all frequencies is also a critical question and is reviewed here.

Understanding how the cochlea works as a system has become increasingly important. We need to know this before integrating new information from genetic, physiological and clinical sources. This chapter will show how the cochlea should be seen as a device for carrying out a frequency analysis built from cells that have been adapted for specialist purposes. Sensory hair cells convert mechanical displacements into the neural code. The transducer channel remains to be identified. The biomechanics of the cochlear duct depends on an energy-dependent feedback from the sensory outer hair cells. The molecular basis for outer hair cell feedback depends on a protein that has recently been identified. The auditory signal encoded by the cochlea is further modified by membrane properties of the hair cells and cochlear supporting cells. The interplay between techniques of genetics, molecular biology and cell physiology has started to reveal which ion channels and transporters in the cochlea are mutated in certain forms of deafness. The interpretation of these mutations requires the cell physiology of the cochlear partition to be better characterised in the future.