GPR39 regulated spinal glycinergic inhibition and mechanical inflammatory pain.

ABSTRACT: G protein-coupled receptor 39 (GPR39) senses the change of extracellular divalent zinc ion and signals through multiple G proteins to a broad spectrum of downstream effectors. Here, we found that GPR39 was prevalent at inhibitory synapses of spinal cord somatostatin-positive (SOM⁺) interneurons, a mechanosensitive subpopulation that is critical for the conveyance of mechanical pain. GPR39 complexed specifically with inhibitory glycine receptors (GlyRs) and helped maintain glycinergic transmission in a manner independent of G protein signalings. Targeted knockdown of GPR39 in SOM⁺ interneurons reduced the glycinergic inhibition and facilitated the excitatory output from SOM⁺ interneurons to spinoparabrachial neurons that engaged superspinal neural circuits e

SUBMITTER: Bai HH 

PROVIDER: S-EPMC10836721 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature