The molecular mechanism of synaptic activity‐induced astrocytic volume transient
The molecular mechanism of synaptic activity‐induced astrocytic volume transient
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DOI：
10.1113/jp279741
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发表时间：
2020-07
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通讯作者：
Junsung Woo;M. Jang;Jaekwang Lee;Wuhyun Koh;K. Mikoshiba;C. J. Lee
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文献类型：
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作者：
Junsung Woo;M. Jang;Jaekwang Lee;Wuhyun Koh;K. Mikoshiba;C. J. Lee
神经元活动通过含有双孔域钾通道的 TREK-1 摄取 K+，导致星形胶质细胞体积变化。 Cl− 通过 Ca2+ 激活的阴离子通道 BEST1 流出，终止体积瞬变。打开 BEST1 所需的 Ca2+ 来源似乎是拉伸激活的 TRPA1 通道。强烈的神经元活动通过体积瞬变与星形胶质细胞的物理变化发生突触耦合。
Neuronal activity causes astrocytic volume change via K+ uptake through TREK‐1 containing two‐pore domain potassium channels. The volume transient is terminated by Cl− efflux through the Ca2+‐activated anion channel BEST1. The source of the Ca2+ required to open BEST1 appears to be the stretch‐activated TRPA1 channel. Intense neuronal activity is synaptically coupled with a physical change in astrocytes via volume transients.