Adrenergic and muscarinic control of cochlear endolymph production.

摘要

The transduction of sound into nerve impulses in the cochlea is dependent on the stria vascularis. It is a multilayered epithelium, which is part of the epithelial barrier between endolymph and perilymph. The current model designed to explain the generation of the endocochlear potential assumes that the molecular mechanism for the generation of the endocochlear potential is the K(IR)4.1 K+ channel localized in the intermediate cells and that strial marginal cells play an indirect role in the generation of the endocochlear potential. This role is limited to the maintenance of a low K+ concentration in the intrastrial space by absorbing K+ from this space and secreting it into the endolymph. The molecular mechanisms for K+ secretion by strial marginal cells are well established. Strial marginal cells absorb K+ from the intrastrial space via the Na+-K+-ATPase and the Na+2Cl-K+ cotransporter and secrete it across the apical membrane via the IsK/KvLQT1 K+ channel. K+ secretion by strial marginal cells is not only required for the maintenance of the endocochlear potential and to provide the charge carrier for the transduction mechanism, but also to maintain a constant volume of endolymph. Thus, the presence of multiple control mechanisms regulating the rate of K+ secretion is likely. Recent observations suggest that the rate of K+ secretion in strial marginal cells is stimulated by beta1-adrenergic receptors and inhibited by M3 and/or M4 muscarinic receptors.