Glutamate excitotoxicity during ischemia triggers an intracellular signaling avalanche leading to cell death, yet blocking NMDA receptors directly in human stroke trials failed. In this issue of Neuron, Zong et al. (2022) disrupt downstream NMDAR-TRPM2 coupling to improve stroke outcomes, supporting intracellular NMDAR signaling as an alternate therapeutic target.

中文翻译：

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中风模拟肽的另一个胜利：TRPM2-NMDAR 信号的中断

缺血期间的谷氨酸兴奋性毒性触发细胞内信号雪崩导致细胞死亡，但在人类中风试验中直接阻断 NMDA 受体失败。在本期《神经元》中，Zong 等人。(2022) 破坏下游 N​​MDAR-TRPM2 耦合以改善中风结果，支持细胞内 NMDAR 信号作为替代治疗靶点。