Expression and modulation of K+ currents in oligodendrocytes: possible role in myelinogenesis.
Expression and modulation of K+ currents in oligodendrocytes: possible role in myelinogenesis.
复制标题
少突胶质细胞中 K 电流的表达和调节：在髓鞘形成中的可能作用。
DOI：
10.1159/000111893
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发表时间：
1989
影响因子：
2.9
通讯作者：
Nelson,DJ
中科院分区：
文献类型：
--
作者：
Soliven,B;Szuchet,S;Arnason,BG;Nelson,DJ
我们采用全细胞和单通道记录技术研究了培养的绵羊少突胶质细胞（OLG）的电生理特性。我们的研究得出以下结论。(1)培养的成熟OLG表达各种电压依赖性K+电导，包括外向电流，包括瞬态分量和稳态分量，以及内向整流K+电流。(2)这些电导被顺序地表示为文化发展的函数。内向整流钾离子电流的出现晚于外向电流。(3)虽然过程延伸可能会影响离子通道的表达，但大多数K+通道位于OLG的索马中，可能集中在基底质膜中。(4)最后，OLG中K+通道的激活可以被两种不同的第二信使抑制，cAMP通过蛋白激酶A起作用，甘油二酯通过蛋白激酶C起作用，其作用可能集中在一个共同的磷酸化酶或调节蛋白的水平。cAMP和甘油二酯都被认为是控制与OLG基质附着相关的髓鞘生成代谢诱导的重要因素。因此，膜离子通道可能提供了一个重要的中间步骤，连接细胞基质附着的髓鞘形成的最终诱导。
We have used whole-cell and single-channel recording techniques to investigate the electrophysiological properties of cultured ovine oligodendrocytes (OLGs). Our studies have led to the following conclusions. (1) Cultured mature OLGs express a variety of voltage-dependent K+conductances including an outward current that consists of a transient component and a steady-state component, as well as an inwardly rectifying K+current. (2) These conductances are expressed sequentially as a function of development in culture. The inwardly rectifying K+current appears later than the outward current. (3) Although process extension may influence the expression of the ion channels, the majority of the K+channels are located in the soma of OLGs, probably concentrated in the basal plasma membrane. (4) Finally, the activation of K+channels in OLGs can be inhibited by two distinct second messengers, cAMP acting through protein kinase A and diacylglycerol acting through protein kinase C, the effects of which perhaps converge at the level of a common phosphorylated enzyme or regulatory protein. Both cAMP and diacylglycerol have been implicated as factors important in controlling the induction of a myelinogenic metabolism associated with OLG substratum attachment. Thus, membrane ion channels may provide an important intermediate step linking cellular substratum attachment to the eventual induction of myelinogenesis.