Kir potassium channel subunit expression in retinal glial cells: Implications for spatial potassium buffering
Kir potassium channel subunit expression in retinal glial cells: Implications for spatial potassium buffering
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DOI：
10.1002/glia.10112
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发表时间：
2002-09-01
期刊：
影响因子：
6.2
通讯作者：
Reichenbach, A
中科院分区：
文献类型：
--
作者：
Kofuji, P;Biedermann, B;Reichenbach, A
为了了解不同K+通道亚型在胶质细胞介导的细胞外K+空间缓冲中的作用，在小鼠视网膜中进行了向内整流K+通道亚基（Kir2.1、Kir2.2、Kir2.3、Kir4.1和Kir5.1）的免疫组织化学定位。弱内向整流钾离子通道亚基Kir4.1和强内向整流钾离子通道亚基Kir2.1均存在双链结构。Kir4.1蛋白的最突出的标记被发现在Muller神经胶质细胞面对玻璃体和周围的视网膜血管的端足膜。在视网膜各层和外界膜处观察到离散点状标记。相反，Kir2.1免疫反应性主要位于与视网膜神经元接触的米勒细胞的膜区域，即，沿着两个茎突，在索马上，以及在延伸到突触层的侧支中。结果表明，神经胶质细胞介导的细胞外K+从兴奋的神经元的运输是由不同的Kir通道亚型的合作介导的模型。弱整流Kir通道（Kir4.1）主要在膜结构域中表达，其中K+电流离开神经胶质细胞并进入细胞外“汇”，而K+从神经元“源”流入神经胶质细胞主要由强整流Kir通道（Kir 2.1）介导。强整流Kir通道沿着“电缆”的空间缓冲电流的表达可以防止不必要的K+向外泄漏，从而避免神经元信息处理的干扰。
To understand the role of different K+ channel subtypes in glial cell-mediated spatial buffering of extracellular K+, immunohistochemical localization of inwardly rectifying K+ channel subunits (Kir2.1, Kir2.2, Kir2.3, Kir4.1, and Kir5.1) was performed in the retina of the mouse. Stainings were found for the weakly inward-rectifying K+ channel subunit Kir4.1 and for the strongly inward-rectifying K+ channel subunit Kir2.1. The most prominent labeling of the Kir4.1 protein was found in the endfoot membranes of Muller glial cells facing the vitreous body and surrounding retinal blood vessels. Discrete punctate label was observed throughout all retinal layers and at the outer limiting membrane. By contrast, Kir2.1 immunoreactivity was located predominantly in the membrane domains of Miller cells that contact retinal neurons, i.e., along the two stem processes, over the soma, and in the side branches extending into the synaptic layers. The results suggest a model in which the glial cell-mediated transport of extracellular K+ away from excited neurons is mediated by the cooperation of different Kir channel subtypes. Weakly rectifying Kir channels (Kir4.1) are expressed predominantly in membrane domains where K+ currents leave the glial cells and enter extracellular "sinks," whereas K+ influxes from neuronal "sources" into glial cells are mediated mainly by strongly rectifying Kir channels (Kir 2.1). The expression of strongly rectifying Kir channels along the "cables" for spatial buffering currents may prevent an unwarranted outward leak of K+, and, thus, avoid disturbances of neuronal information processing.