Role of calcium-permeable channels in marginal cells on the regulation of endocochlear potential.

在耳蜗血管纹处，内淋巴有一个大的正电位，被称为耳蜗内电位（EP）。在之前的研究中，我们报道了短暂性窒息导致EP下降是由于边缘细胞基底外膜l型钙通道激活导致细胞内钙离子增加所致。在本研究中，我们证明了钙螯合剂、l型钙通道抑制剂、C激酶（PKC）抑制剂或内淋巴磷脂酶C （PLC）抑制剂可以抑制短暂性窒息引起的EP下降。因此，窒息导致的EP下降是由血管纹细胞中钙离子的增加引起的，通过PLC激活引起的PKC激活介导的l型钙通道的激活。

A large positive potential in the endolymph, named the endocochlear potential (EP) has been considered to occur at cochlear stria vascularis. In the previous study, we reported that the decrease in EP induced by transient asphyxia was result from the increase in intracellular calcium ion induced by the activation of L-type calcium channels in the basolateral membrane of the marginal cells. In the present study, we demonstrated that a fall in the EP induced by transient asphyxia was suppressed by the administration of calcium-chelator, L-type calcium channel inhibitor, C kinase (PKC) inhibitors, or phospholipase C (PLC) inhibitors to the endolymph. Thus, asphyxia induced decrease in the EP was induced by the increase in calcium ion in the cells of stria vascularis, through the activation of L-type calcium channels mediated by the PKC activation result from the PLC activation.