TRPC Channels Activated by G Protein-Coupled Receptors Drive Ca²⁺ Dysregulation Leading to Secondary Brain Injury in the Mouse Model.

ABSTRACT: Canonical transient receptor potential (TRPC) non-selective cation channels, particularly those assembled with TRPC3, TRPC6, and TRPC7 subunits, are coupled to G_αq-type G protein-coupled receptors for the major classes of excitatory neurotransmitters. Sustained activation of this TRPC channel-based pathophysiological signaling hub in neurons and glia likely contributes to prodigious excitotoxicity-driven secondary brain injury expansion. This was investigated in mouse models with selective Trpc gene knockout (KO). In adult cerebellar brain slices, application of glutamate and the class I metabotropic glutamate receptor agonist (S)-3,5-dihydroxyphenylglycine to Purkinje neurons expressing the GCaMP5g Ca²⁺ reporter demonstrated that the majority of the Ca²⁺ l

SUBMITTER: Parmar J 

PROVIDER: S-EPMC11226524 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature