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 was expressed in satellite cells of cochlea ganglia. Because Kir4.1 prominently localizedmyelin sheaths of satellite cells，Kir4.1 may participate in K - D1 spatial buffering action of cochlea ganglia.We found thatinwardly rectifying potassium channel, Kir4.1/ kii - D2ab -2，expressed in glial cell. To investigate further the distribution and function of Kir4.1，(1)使用免疫系统微生物学（immunoelectron microscopic）technique, we found that Kir4.1 co-localized with water channel, AQP4in the membranes of retinal Muller glial cells adjacent to basal membranes.前，water transport has been considered to couple K transport. Thus，Kir401和AQP4 may regulate water content of neural tissues.(2) Kir4.1 was found in retinal pigmentepithelial cells,suggesting Kir4.1 participates in extracellular K - D1+ homeostasis of rod outer segments.(4)Kir4.1 was expressed in gastric parietal cells. Ba - D12+a - D1inhibitor of inwardly rectifying K - i - D1+ i - D1 channel，suppressed acid secretion of isolated rat parietal cells，but inhibitors of voltage sensitive and Ca i D12+ i D1-activated K i D1+ i D1 channels did not.Immunoelectron microscopic examination indicated that Kir4.1 localized in apical membranes but notin tubulovesicles and basolateral membranes of parietal cells.这些results indicated that Kir4.1may participate in acid secretion of stomach. Kir4.1 may export ions into gastric lumenwhich are imported into parietal cells by H - D1+ K - D1+ d - 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.