Molecular dissection of inwardly rectifying KィイD1+ィエD1 channel, Kir4.1/KィイD2abィエD2-2, of glial cells.

（3） Kir4.1被描述为科切利亚恒河的卫星细胞。因为Kir4.1 prominently located in myelin sheaths of satellite cell， Kir4.1可以参与Kyi D1+ Kyi D1空间缓冲行动，我们发现了一个不受限制的potassium channel， Kir4.1/Kyi D2 ab Kyi D2-2，被描述为glial cell。为了进一步研究Kir4.1的分布和功能，我们审查了各种问题，并获得了以下的结果。（1）使用免疫电子显微镜技术，我们找到了Kir4.1协同本地化与水通道（AQP 4）的膜，在视网膜Muller发光细胞的附件中，与基础膜相对应。Previously， water transport has been considered to couple ky D1+ y D1 transport。Thus，Kir 401和AQP 4可以调节神经质的水含量。（2） Kir4.1 was found in retinal pigment epithelial cells， suggesting Kir4.1 participates in extracellular Ky D1+ Ky D1 homeostasis of rod outer segments。（4） Kir4.1 was expressed in gastric parietal cells。BaイイD12+aイイD1， an inhibitor of inwardly rectifying KイD1+イエD1 channel， suppressed acid secretion of isolated rat parietal cells， but inhibitors of voltage sensitive and CaイD12+イエD1-activated KイD1+イエD1 channels did not。Immunoelectron microscopic examination indicated that Kir4.1 localized in apical membranes but not in tubulovesicles and basolateral membranes of parietal cells。这些结果表明Kir4.1可能参与酸盐的秘密。Kir4. 1 may export K-D1 + Y-D1 ions into gastric lumen which are imported into parietal cells by H-D1 + Y-D1。KイD1+イエD1-ATPase。

(3) Kir4.1 was expressed in satellite cells of cochlea ganglia. Because Kir4.1 prominently localized in myelin sheaths of satellite cells, Kir4.1 may participate in KィイD1+ィエD1 spatial buffering action of cochlea ganglia.We found that inwardly rectifying potassium channel, Kir4.1/KィイD2abィエD2-2, was expressed in glial cell. To investigate further the distribution and function of Kir4.1, we examined various tissues and obtained following results.(1) Using immunoelectron microscopic technique, we found that Kir4.1 co-localized with water channel, AQP4, in the membranes of retinal Muller glial cells adjacent to basal membranes. Previously, water transport has been considered to couple KィイD1+ィエD1 transport. Thus, Kir401 and AQP4 may regulate water content of neural tissues.(2) Kir4.1 was found in retinal pigment epithelial cells, suggesting Kir4.1 participates in extracellular KィイD1+ィエD1 homeostasis of rod outer segments.(4) Kir4.1 was expressed in gastric parietal cells. BaィイD12+aィエD1, an inhibitor of inwardly rectifying KィイD1+ィエD1 channel, suppressed acid secretion of isolated rat parietal cells, but inhibitors of voltage sensitive and CaィイD12+ィエD1-activated KィイD1+ィエD1 channels did not. Immunoelectron microscopic examination indicated that Kir4.1 localized in apical membranes but not in tubulovesicles and basolateral membranes of parietal cells. These results indicated that Kir4.1 may participate in acid secretion of stomach. Kir4.1 may export KィイD1+ィエD1 ions into gastric lumen which are imported into parietal cells by HィイD1+ィエD1. KィイD1+ィエD1-ATPase.