TRPing into excitotoxic neuronal death

Matthew V Green; Anne E West

doi:10.1016/j.ceca.2020.102331

TRPing into excitotoxic neuronal death

Cell Calcium. 2021 Jan:93:102331. doi: 10.1016/j.ceca.2020.102331. Epub 2020 Dec 8.

Authors

Matthew V Green¹, Anne E West²

Affiliations

¹ Duke University, Department of Neurobiology, 311 Research Drive, Durham, NC, 27710, USA.
² Duke University, Department of Neurobiology, 311 Research Drive, Durham, NC, 27710, USA. Electronic address: west@neuro.duke.edu.

PMID: 33341523
DOI: 10.1016/j.ceca.2020.102331

Abstract

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.

Keywords: Excitotoxicity; Ischemia; NMDA-type glutamate receptors; Neuronal cell; TRPM4.

Publication types

Comment

MeSH terms

Cell Death / drug effects
Cells, Cultured
Neuroprotective Agents* / pharmacology
Receptors, N-Methyl-D-Aspartate* / metabolism
Signal Transduction / drug effects

Substances

Neuroprotective Agents
Receptors, N-Methyl-D-Aspartate