K+ cycling and its regulation in the cochlea and the vestibular labyrinth

Abstract

Potassium (K+) plays a very important role in the cochlea. K+is the major cation in endolymph and the charge carrier for sensory transduction and the generation of the endocochlear potential. The importance of K+handling in the cochlea is marked by the discovery of several forms of hereditary deafness that are due to mutations of K+channels. Deafness results from mutations of KCNQ4, a K+channel in the sensory hair cells, as well as from mutations of the gap junction proteins GJB2, GJB3 and GJB6 that may facilitate cell-to-cell movements of K+. Deafness results also from mutations of KCNQ1 or KCNE1, subunits of a K+channel that carries K+from strial marginal cells and vestibular dark cells into endolymph. Further, deafness results from mutations of KCNJ10, a K+channel that generates the endocochlear potential in conjunction with the high K+concentration in strial intermediate cells and the low K+concentration in the intrastrial fluid spaces. This review details recent advances in the understanding of K+transport and its regulation in the cochlea and the vestibular labyrinth. Copyright © 2002 S. Karger AG, Basel.