Nicotera Pierluigi, Bano Daniele
MRC Toxicology Unit, University of Leicester, Lancaster Road, LE1 9HN Leicester, UK.
Cell. 2003 Dec 26;115(7):768-70. doi: 10.1016/s0092-8674(03)01019-5.
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.
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。
