ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Extrasynaptic muscarinic acetylcholine receptors on neuronal cell bodies regulate presynaptic function in Caenorhabditis elegans.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Pharmacological Profiling of a Brugia malayi Muscarinic Acetylcholine Receptor as a Putative Antiparasitic Target.Antimicrobial agents and chemotherapy · 2023Article
- Article
- Extrasynaptic acetylcholine signaling through a muscarinic receptor regulates cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Novel actions of arecoline in themicroPublication biology · 2020Article
- Article
- Neurotransmitter signaling through heterotrimeric G proteins: insights from studies in C. elegans.WormBook : the online review of C. elegans biology · 2018Review
- Acute Effects of Drugs onG3 (Bethesda, Md.) · 2018Article
- Novel Mutations in Synaptic Transmission Genes Suppress Neuronal Hyperexcitation inG3 (Bethesda, Md.) · 2017Article
- The Multilayer Connectome of Caenorhabditis elegans.PLoS computational biology · 2016Article
- Chemical activation of a food deprivation signal extends lifespan.Aging cell · 2016Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Acetylcholine (ACh) is a potent neuromodulator in the brain, and its effects on cognition and memory formation are largely performed through muscarinic acetylcholine receptors (mAChRs). mAChRs are often preferentially distributed on specialized membrane regions in neurons, but the significance of mAChR localization in modulating neuronal function is not known. Here we show that the Caenorhabditis elegans homolog of the M1/M3/M5 family of mAChRs, gar-3, is expressed in cholinergic motor neurons, and GAR-3-GFP fusion proteins localize to cell bodies where they are enriched at extrasynaptic regions that are in contact with the basal lamina. The GAR-3 N-terminal extracellular domain is necessary and sufficient for this asymmetric distribution, and mutation of a predicted N-linked glycosylation site within the N-terminus disrupts GAR-3-GFP localization. In transgenic animals expressing GAR-3 variants that are no longer asymmetrically localized, synaptic transmission at neuromuscular junctions is impaired and there is a reduction in the abundance of the presynaptic protein sphingosine kinase at release sites. Finally, GAR-3 can be activated by endogenously produced ACh released from neurons that do not directly contact cholinergic motor neurons. Together, our results suggest that humoral activation of asymmetrically localized mAChRs by ACh is an evolutionarily conserved mechanism by which ACh modulates neuronal function.
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