SUBCELLULAR HETEROGENEITY OF VOLTAGE-GATED CA2+ CHANNELS IN CELLS OF THE OLIGODENDROCYTE LINEAGE
SUBCELLULAR HETEROGENEITY OF VOLTAGE-GATED CA2+ CHANNELS IN CELLS OF THE OLIGODENDROCYTE LINEAGE
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DOI：
10.1002/glia.440130102
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发表时间：
1995-01-01
期刊：
影响因子：
6.2
通讯作者：
KETTENMANN, H
中科院分区：
文献类型：
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作者：
KIRISCHUK, S;SCHERER, J;KETTENMANN, H
我们研究了电压门控性钙通道的分布在视网膜和皮质培养的少突胶质细胞系的细胞。通过电压门控通道的Ca 2+内流被膜去极化激活，细胞外K+浓度升高（[K+]（e）），局部亚细胞内游离Ca 2+浓度增加（[Ca 2 +]（i）n）可以用连接到激光扫描共聚焦显微镜的荧光系统监测。在视网膜和皮质的神经胶质前体细胞中，小的去极化（用10或20 mM K+）激活过程中的Ca 2+瞬变，表明存在低电压激活的Ca 2+通道。较大的去极化（50 mM K+）额外激活了索马体中的高电压激活的Ca 2+通道。在成熟的少突胶质细胞中也观察到Ca 2+通道的不均匀分布;过程中的Ca 2+瞬变相当大。电压诱导的内流后的Ca 2+水平的恢复是通过质膜Ca 2+泵的活性来实现的，而线粒体在通过电压操作通道内流后恢复Ca 2+水平方面发挥了次要作用。在白色物质束的发育过程中，少突胶质细胞谱系的细胞接触轴突以形成髓鞘。神经元活动伴随着[K+]（e）的增加;这可能导致过程中的Ca 2+变化，Ca 2+增加可能是神经胶质前体细胞开始髓鞘形成的信号。(C)1995 Wiley-Liss，Inc.
We studied the distribution of voltage-gated Ca2+ channels in cells of the oligodendrocyte lineage from retinal and cortical cultures. Influx of Ca2+ via voltage-gated channels was activated by membrane depolarization with elevated extracellular K+ concentration ([K+](e)) and local, subcellular increases in cytosolic free Ca2+ concentration ([Ca2+](i)n) could be monitored with a fluometric system connected to a laser scanning confocal microscope. In glial precursor cells from both retina and cortex, small depolarizations (with 10 or 20 mM K+) activated Ca2+ transients in processes indicating the presence of low-voltage-activated Ca2+ channels. Larger depolarizations (with 50 mM K+) additionally activated high-voltage-activated Ca2+ channels in the soma. An uneven distribution of Ca2+ channels was also observed in the mature oligodendrocytes; Ca2+ transients in processes were considerably larger. Recovery of Ca2+ levels after the voltage-induced influx was achieved by the activity of the plasmalemmal Ca2+ pump, while mitochondria played a minor role to restore Ca2+ levels after an influx through voltage-operated channels. During the development of white matter tracts, cells of the oligodendrocyte lineage contact axons to form myelin. Neuronal activity is accompanied by increases in [K+](e); this may lead to Ca2+ changes in the processes and the Ca2+ increase might be a signal for the glial precursor cell to start myelin formation. (C) 1995 Wiley-Liss, Inc.