兴奋毒性
受体
谷氨酸受体
神经科学
程序性细胞死亡
生物
NMDA受体
细胞凋亡
生物化学
作者
Matthew Green,Anne West
标识
DOI:10.1016/j.ceca.2020.102331
摘要
It is a striking paradox that the activation of NMDA-type glutamate receptors (NMDARs) can both promote neuronal survival and induce excitotoxic cell death. Yet the molecular mechanisms that distinguish these cellular consequences have remained obscure. A recent study by Yan et al. (2020) reveals a novel interaction between NMDARs and TRPM4 that is required for NMDAR-induced neuronal death. Small molecule disruption of this interaction reduces excitotoxicity in stroke without blocking physiological NMDAR signaling.
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