Abstract
Using electrophysiological and immunohistochemical methods, we investigated the role of L-type Ca2+ channel in the regulation of endocochlear potential (EP) in the stria vascularis. 1) Administration of 1 μg/ml nifedipine into endolymph, which produced a gradual increase in EP, inhibits significantly transient asphyxia induced decrease (TAID) in the EP. TAID in EP was inhibited by endolymphatic perfusion with nifedipine (0.001-10 μg/ml) in dose dependent manner. Administration of 30 μg/ml nifedipine via vertebral artery suppressed significantly TAID in EP, whereas it produced the gradual decrease in EP at a control level. These results suggested that L-type Ca2+ channel in marginal cells or intermediate cells may participated in the regulation of both control level and TAID in EP. 2) A positive staining for L-type Ca2+ channel was presented in the luminal and basolateral membrane in marginal cells. 3) Administration of (-)-Bay K 8644, a L-type Ca2+ channel activator, into the endolymph caused the large decrease in EP, whereas administration of (+)-Bay K 8644, a L-type Ca2+ channel blocker, produced the increase in EP and suppressed the TAID in EP. These findings support the view that L-type Ca2+ channel in the marginal cells regulates the EP in both control and asphyxia conditions. [J Physiol Sci. 2007;57 Suppl:S231]
