Ca2+ regulation of endocochlear potential in marginal cells
Ca2+ regulation of endocochlear potential in marginal cells
复制标题
DOI：
10.1007/s12576-009-0043-9
复制
发表时间：
2009-09-01
影响因子：
2.3
通讯作者：
Kubota, Takahiro
中科院分区：
文献类型：
--
作者：
Mori, Yoshiaki;Watanabe, Masahito;Kubota, Takahiro
我们通过在短暂窒息或静脉注射速尿期间用或不用 Ca2+ 螯合剂或 Ca2+ 通透通道抑制剂或 Ca2+ 泵灌注内淋巴，检查了边缘细胞中胞质 Ca2+ 浓度 ([Ca2+](c)) 对窒息或速尿诱导的耳蜗内电位 (EP) 降低的影响。我们得到了以下结果。 (1) 内淋巴给药 SKF96365（TRPC 和 L 型 Ca2+ 通道抑制剂）或 EGTA-乙酰氧基甲酯 (EGTA-AM) 显着抑制短暂性窒息引起的 EP 下降 (TAID) 和呋塞米引起的 EP 下降 (FUID)。 (2)硝苯地平内淋巴灌注显着抑制TAID，但不抑制FUID。 (3) 通过用 EGTA-AM、硝苯地平或 SKF96365 灌注内淋巴，显着抑制 FUID 的恢复。 (4)毒胡萝卜素内淋巴给药抑制FUID和TAID。 (5)FUID的回收率比TAID慢得多，表明呋塞米可能抑制Ca2+泵。 (6)边缘细胞管腔膜和基底外侧膜TRPC通道免疫组化染色呈强烈反应。 (7)边缘细胞管腔膜和基底外侧膜可见上皮Na+通道γ亚基阳性染色反应。 (8)通过用10μM阿米洛利或10μM非那米进行内淋巴灌注，阳性EP向0mV减小。综上所述，这些发现表明边缘细胞中内质 Ca2+ 泵和 Ca2+ 通透通道调节的 [Ca2+](c) 可能调节正 EP，其部分是由 Na+ 穿过边缘细胞基底外侧膜的扩散电位产生的。
We examined the effect of the cytosolic Ca2+ concentration ([Ca2+](c)) in marginal cells on the asphyxia- or furosemide-induced decrease in the endocochlear potential (EP) by perfusing the endolymph with or without a Ca2+ chelator or inhibitors of Ca2+-permeable channels or Ca2+-pump during transient asphyxia or intravenous administration of furosemide. We obtained the following results. (1) Endolymphatic administration of SKF96365 (an inhibitor of TRPC and L-type Ca2+ channels) or EGTA-acetoxymethyl ester (EGTA-AM) significantly inhibited both the transient asphyxia-induced decrease in EP (TAID) and the furosemide-induced decrease in EP (FUID). (2) Endolymphatic perfusion with nifedipine significantly inhibited the TAID but not the FUID. (3) The recovery from the FUID was significantly suppressed by perfusing the endolymph with EGTA-AM, nifedipine, or SKF96365. (4) Endolymphatic administration of thapsigargin inhibited both the FUID and TAID. (5) The recovery rate from the FUID was much slower than that from the TAID, indicating that furosemide may inhibit the Ca2+-pump. (6) A strong reaction in immunohistochemical staining for TRPC channels was observed in the luminal and basolateral membranes of marginal cells. (7) A positive staining reaction for the gamma subunit of epithelial Na+ channels was observed in the luminal and basolateral membranes of marginal cells. (8) Positive EP was diminished toward 0 mV by the endolymphatic perfusion with 10 mu M amiloride or 10 mu M phenamil. Taken together, these findings suggest that [Ca2+](c) regulated by endoplasmic Ca2+-pump and Ca2+-permeable channels in marginal cells may regulate the positive EP, which is partly produced by the diffusion potential of Na+ across the basolateral membrane in marginal cells.