An α7 nicotinic and GABA_B receptor-mediated pathway controls acetylcholine release in the tripartite neuromuscular junction.

ABSTRACT: Terminal Schwann cells (TSCs) are capable of regulating acetylcholine (ACh) release at the neuromuscular junction (NMJ). We have identified GABA as a gliotransmitter at mouse NMJs. When ACh activates α7 nicotinic ACh receptor (nAChRs) on TSCs, GABA is released and activates GABA_B receptors on the nerve terminal that subsequently reduce ACh release. Indeed, specific deletion of the α7 nAChR in TSCs or inhibition of the metabotropic GABA_B receptor prevents the reduction in the quantal content of the end-plate potential induced by cholinesterase inhibitors. The α7/GABA_B receptor-mediated pathway is activated when ACh that escapes from collagen Q (ColQ) anchored AChE in the synaptic cleft and from PRiMA-anchored butyrylcholinesterase on the TSC activates α7 nAC

SUBMITTER: Petrov K 

PROVIDER: S-EPMC11737540 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature