Contribution of Ca²⁺-permeable channels to the regulation of endocochlear potential in guinea pigs

Abstract

A large positive potential in the endolymph, named the endocochlear potential (EP) has been considered to occur at cochlear stria vascularis and this DC potential is essential for the transduction of sound by hair cells. In the previous paper, we examined the regulation of EP by studying the L-type Ca²⁺ channels in the basolateral membrane of marginal cells in the stria vascularis (JPS, 2007). In this study, we examined the contribution of TRP channels to the regulation of EP, measuring the transient asphyxia- or furosemide-induced decrease in the EP (TAIDEP or FUIDEP) with or without inhibitors of Ca²⁺-permeable channels. 1) Endolymphatic administration of 100 μM SKF96365, an inhibitor of both L-type Ca²⁺ and TRPC channels, inhibited almost completely the TAIDEP and the FUIDEP. 2) Administration of 1 μg/ml (3 μM) nifedipine, a specific inhibitor of L-type Ca²⁺ channels, into the endolymph significantly inhibits the TAIDEP, but slightly the FUIDEP. 3) The administration of 300 μM EGTA-tetraacetoxymethyl ester (EGTA-AM), a membrane-permeable Ca²⁺ chelator, to the endolymph significantly but partially suppressed the TAIDEP or almost completely the FUIDEP. These findings suggest that both the TRPC channels and the L-type Ca²⁺ channels play an important role in the regulation of the EP by affecting the cytosolic Ca²⁺ concentration of the endolymphatic surface cells (marginal cells) in the stria vascularis. [J Physiol Sci. 2008;58 Suppl:S170]