NG2 glial cells integrate synaptic input in global and dendritic calcium signals
NG2 glial cells integrate synaptic input in global and dendritic calcium signals
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DOI：
10.7554/elife.16262
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发表时间：
2016-09-19
期刊：
影响因子：
7.7
通讯作者：
Dietrich, Dirk
中科院分区：
文献类型：
--
作者：
Sun, Wenjing;Matthews, Elizabeth A.;Dietrich, Dirk
向表达NG2的少突胶质细胞前体细胞（NG2细胞）的突触信号传导可能是使轴突髓鞘形成依赖于神经元活动的关键，但仍不清楚NG2胶质细胞是否整合并响应突触输入。在这里，我们表明，NG2细胞进行线性整合的神经元突触输入和响应增加树突状细胞钙离子浓度升高。在电压门控性A型K+通道的严格抑制控制下，突触活动诱导由低电压激活的Ca 2+通道介导的快速Ca 2+信号。Ca2+信号可以是全局性的，并且起源于整个细胞。然而，电压门控通道也存在于细树突中，其充当区室化处理单元并产生局部钙瞬变。总之，A型通道对Ca 2+信号的活性依赖性控制以及全局与局部信号结构域使NG2细胞中的细胞内Ca 2+成为将神经递质释放转化为活性依赖性髓鞘形成的主要信号分子。
Synaptic signaling to NG2-expressing oligodendrocyte precursor cells (NG2 cells) could be key to rendering myelination of axons dependent on neuronal activity, but it has remained unclear whether NG2 glial cells integrate and respond to synaptic input. Here we show that NG2 cells perform linear integration of glutamatergic synaptic inputs and respond with increasing dendritic calcium elevations. Synaptic activity induces rapid Ca2+ signals mediated by low-voltage activated Ca2+ channels under strict inhibitory control of voltage-gated A-type K+ channels. Ca2+ signals can be global and originate throughout the cell. However, voltage-gated channels are also found in thin dendrites which act as compartmentalized processing units and generate local calcium transients. Taken together, the activity-dependent control of Ca2+ signals by A-type channels and the global versus local signaling domains make intracellular Ca2+ in NG2 cells a prime signaling molecule to transform neurotransmitter release into activity-dependent myelination.