TRPing into excitotoxic neuronal death Comment

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.

Automated summary

The activation of NMDA-type glutamate receptors (NMDARs) can both promote neuronal survival and induce excitotoxic cell death. A recent study reveals that a novel interaction between NMDARs and TRPM4 is required for NMDAR-induced neuronal death. Disrupting this interaction reduces excitotoxicity without blocking physiological NMDAR signaling.