大敌当前。钙离子通过瞬时受体电位阳离子通道M7（TRPM7）进入细胞与缺氧性神经元死亡。
The enemy at the gates. Ca2+ entry through TRPM7 channels and anoxic neuronal death.
作者信息
Nicotera Pierluigi, Bano Daniele
机构信息
MRC Toxicology Unit, University of Leicester, Lancaster Road, LE1 9HN Leicester, UK.
出版信息
Cell. 2003 Dec 26;115(7):768-70. doi: 10.1016/s0092-8674(03)01019-5.
Abstract
In brain ischemia, gating of postsynaptic glutamate receptors is thought to initiate Ca2+ overload leading to excitotoxic neuronal death. In this issue, Aarts and colleagues describe a novel mechanism, whereby gating of TRPM7, a Ca2+-permeable nonselective cation channel, mediates Ca2+ overload and demise of anoxic neurons.
摘要
在脑缺血中，突触后谷氨酸受体的门控被认为会引发钙离子超载，导致兴奋性毒性神经元死亡。在本期杂志中，阿尔茨及其同事描述了一种新机制，即TRPM7（一种钙离子可通透的非选择性阳离子通道）的门控介导了缺氧神经元的钙离子超载和死亡。
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