Asphyxia-induced decrease in endocochlear potential is triggered by the activation of L-type Ca²⁺ channel

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 this study, we examined the effect of the intracellular Ca²⁺ concentration ([Ca]_i) in the endolymphatic surface cells on EP by using conventional and Ca²⁺-sensitive microelectrodes. 1) A large increase in the Ca²⁺ concentration in the endolymph up to 10⁻³ M with a decrease in EP from +70 mV to +20 mV was induced by transient asphyxia (100 sec). 2) The application of 300 μM EGTA-tetraacetoxymethyl ester (EGTA-AM) with 10 mM EGTA-containing solution or 3 μM nifedipine to the endolymph produced a slight increase in EP and suppressed significantly an initial decrease in EP induced by transient asphyxia. 3) The administration of 10 μM Bay K 8644, an activator of L-type Ca²⁺ channels, to the endolymph produced a gradual decrease in EP. 4) Perilymphatic administration of 1 mM EGTA-AM or 30 μM nifedipine caused no significant suppression of the asphyxia-induced decrease in EP. These results suggest that transient asphyxia-induced decrease in the EP is triggered by an increase in [Ca]_i with the activation of L-type Ca²⁺ channel in endolymphatic surface cells. [J Physiol Sci. 2006;56 Suppl:S186]