兴奋毒性
NMDA受体
神经科学
冲程(发动机)
缺血性中风
谷氨酸受体
变构调节
神经保护
医学
化学
药理学
缺血
生物
受体
内科学
机械工程
工程类
作者
Hongyu Zhu,Xin Chen,Lu Zhang,Xuequan Liu,Ji Chen,Han‐Ting Zhang,Mingxin Dong
出处
期刊:RSC medicinal chemistry
[The Royal Society of Chemistry]
日期:2024-01-01
卷期号:15 (4): 1307-1319
摘要
Excitotoxicity due to excessive activation of NMDARs is one of the main mechanisms of neuronal death during ischemic stroke. Previous studies have suggested that activation of either synaptic or extrasynaptic GluN2B-containing NMDARs results in neuronal damage, whereas activation of GluN2A-containing NMDARs promotes neuronal survival against ischemic insults. This study applied a systematic
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