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首页> 外文期刊>The European Journal of Neuroscience >Molecular and electrophysiological evidence for the expression of BK channels in oligodendroglial precursor cells.
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Molecular and electrophysiological evidence for the expression of BK channels in oligodendroglial precursor cells.

机译：BK通道在少突胶质前体细胞中表达的分子和电生理证据。

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摘要

Changes in intracellular Ca(2+) play a key role in regulating gene expression and developmental changes in oligodendroglial precursor cells (OPCs). However, the mechanisms by which Ca(2+) influx in OPCs is controlled remains incompletely understood. Although there are several mechanisms that modulate Ca(2+) influx, in many systems the large-conductance, voltage- and Ca(2+) -activated K(+) channel (BK channel) plays an important role in regulating both membrane excitability and intracellular Ca(2+) levels. To date, the role of the BK channel in the regulation of intracellular Ca(2+) in oligodendroglial lineage cells is unknown. Here we investigated whether cells of the oligodendroglial lineage express BK channels and what potential role they play in regulation of Ca(2+) influx in these cells. In oligodendrocytes derived from differentiated adult neural precursor cells (NPCs, obtained from C57bl6 mice) we observed outward currents that were sensitive to the BK channel blocker iberiotoxin (IbTx). Further confirmation of the expression of the BK channel was obtained utilizing other blockers of the BK channel and by confocal immunofluoresence labelling of the BK channel on oligodendroglia. Using Fura-2AM to monitor intracellular Ca(2+) , it was observed that inhibition of the BK channel during glutamate-induced depolarization led to an additive increase in intracellular Ca(2+) levels. Electrophysiological difference currents demonstrated that the expression levels of the BK channel decrease with developmental age. This latter finding was further corroborated via RT-PCR and Western blot analysis. We conclude that the BK channel is involved in regulating Ca(2+) influx in OPCs, and may potentially play a role during differentiation of oligodendroglial lineage cells.
机译：细胞内Ca（2+）的变化在调节基因表达和少突胶质前体细胞（OPCs）的发育变化中起关键作用。但是，尚不完全了解控制OPC中Ca（2+）流入的机制。尽管有几种机制可以调节Ca（2+）的流入，但是在许多系统中，大电导，电压和Ca（2+）激活的K（+）通道（BK通道）在调节两种膜的兴奋性中都起着重要作用。和细胞内Ca（2+）水平。迄今为止，BK通道在少突胶质细胞系细胞内细胞内Ca（2+）调控中的作用尚不清楚。在这里，我们调查了少突神经胶质谱系的细胞是否表达BK通道，以及它们在调节Ca（2+）流入这些细胞中起什么潜在作用。在来自分化的成年神经前体细胞（从C57bl6小鼠获得的NPC）衍生的少突胶质细胞中，我们观察到了对BK通道阻滞剂埃博毒素（IbTx）敏感的外向电流。利用BK通道的其他阻滞剂并通过共聚焦免疫荧光标记少突枝菌上的BK通道，进一步证实了BK通道的表达。使用Fura-2AM监视细胞内Ca（2+），已观察到在谷氨酸诱导的去极化过程中BK通道的抑制导致细胞内Ca（2+）水平的累加增加。电生理差异电流表明，BK通道的表达水平随着年龄的增长而降低。通过RT-PCR和Western blot分析进一步证实了后者的发现。我们得出的结论是，BK通道参与调节OPC中的Ca（2+）流入，并可能在少突胶质细胞系分化过程中发挥作用。

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