Physiological Role of L-Type Ca²⁺ Channel in Marginal Cells in the Stria Vascularis of Guinea Pigs

Abstract

Using immunohistochemical and electrophysiological methods, we investigated the role of L-type Ca²⁺ channel in the regulation of the endocochlear potential (EP) of the endolymphatic surface cells (ESC) of the guinea pig stria vascularis. The following findings were made: (1) Administration of 30 µg/ml nifedipine via a vertebral artery suppressed significantly the transient asphyxia-induced decrease in the EP (TAID) and the transient asphyxia-induced increase in the Ca²⁺ concentration in the endolymph ([Ca]_e), referred to as TAIICa. (2) Endolymphatic administration of 1 µg/ml nifedipine inhibited significantly the TAID as well as the TAIICa. Endolymphatic administration of nifedipine (0.001–10 µg/ml) inhibited the TAID in a dose-dependent manner. (3) Endolymphatic administration of (+)-Bay K8644, a L-type Ca²⁺ channel closer, inhibited significantly the TAID; whereas (–)-Bay K8644, an L-type Ca²⁺ channel opener, caused a large decrease in the EP from ∼+75 mV to ∼+20 mV at 10 min after the endolymphatic administration. (4) By immunohistochemistry, a positive staining reaction for L-type Ca²⁺ channels was detected in the marginal cells in the stria vascularis. (5) Under the high [Ca]_e condition, we examined the mechanism of the TAIICa and hypothesized that the TIICa might have been caused by the decrease in the EP through a shunt pathway in the ESC. (6) The administration of nifedipine to the endolymph significantly inhibited the Ba²⁺-induced decrease in the EP. These findings support the view that L-type Ca²⁺ channels in the marginal cells regulate the EP, but not directly the TAIICa.