ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Ca2+-independent feedback inhibition of acetylcholine release in frog neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- G Protein-Coupled Receptors Regulated by Membrane Potential.International journal of molecular sciences · 2022Review
- Loading a Calcium Dye into Frog Nerve Endings Through the Nerve Stump: Calcium Transient Registration in the Frog Neuromuscular Junction.Journal of visualized experiments : JoVE · 2017Article
- A novel fast mechanism for GPCR-mediated signal transduction--control of neurotransmitter release.The Journal of cell biology · 2011Article
- Control of neurotransmitter release: From Ca2+ to voltage dependent G-protein coupled receptors.Pflugers Archiv : European journal of physiology · 2010Review
- Molecular mechanisms that control initiation and termination of physiological depolarization-evoked transmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Release of neurotransmitter induced by Ca2+-uncaging: reexamination of the ca-voltage hypothesis for release.Journal of computational neuroscience · 2005Article
- Decreased entry of calcium into motor nerve endings upon activation of presynaptic cholinergic receptors.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of membrane potential on feedback inhibition of acetylcholine (ACh) release was studied using the frog neuromuscular junction. It was found that membrane potential affects the functional affinity (K(i)) of the presynaptic M2 muscarinic receptor. The K(i) for muscarine shifts from approximately 0.23 microm (at resting potential) to approximately 8 microm (at a high depolarization). Measurements of Ca2+ currents in axon terminals showed that the depolarization-mediated shift in K(i) does not stem from depolarization-dependent changes in Ca2+ influx. Pretreatments with pertussis toxin (PTX) abolished the depolarization-dependent shift in K(i); at all depolarizations K(i) was the same and higher (approximately 32 microm) than before PTX treatment. The inhibitory effect of muscarine on ACh release is produced by two independent mechanisms: a slow, PTX-sensitive process, which prevails at low to medium depolarizations and operates already at low muscarine concentrations, and a fast, PTX-insensitive and voltage-independent process, which requires higher muscarine concentrations. Neither of the two processes involves a reduction in Ca2+ influx.
Indexed as
Identifiers
11978819PMC6758345W1494403004What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.