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

内淋巴中的一种大的正电位，称为耳蜗内电位(EP)，被认为发生在耳蜗纹。在以前的研究中，我们报道了一过性窒息引起的EP的下降是由于边缘细胞基侧膜上L类钙通道的激活导致细胞内钙离子增加所致。在本研究中，我们证明了内淋巴给予钙离子螯合剂、L类钙通道阻滞剂、C激酶(PKC)抑制剂或磷脂酶C(PLC)抑制剂，可抑制一过性窒息引起的EP下降。因此，窒息引起的EP减少是由于血管纹细胞内钙离子的增加，通过激活由PLC激活所产生的蛋白激酶C而介导的L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.