ArticleThe Journal of physiology2001
Presynaptic M(2) muscarinic receptors are involved in controlling the kinetics of ACh release at the frog neuromuscular junction.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Nonlinear high-activity neuronal excitation enhances odor discrimination.Current biology : CB · 2025Article
- Article
- Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions.Biomedicines · 2022Review
- Balanced modulation of neuromuscular synaptic transmission via M1 and M2 muscarinic receptors during inhibition of cholinesterases.Scientific reports · 2022Article
- Gestational exposures to organophosphorus insecticides: From acute poisoning to developmental neurotoxicity.Neuropharmacology · 2020Review
- Autoregulation of Acetylcholine Release and Micro-Pharmacodynamic Mechanisms at Neuromuscular Junction: Selective Acetylcholinesterase Inhibitors for Therapy of Myasthenic Syndromes.Frontiers in pharmacology · 2018Review
- Adenosine Receptors in Developing and Adult Mouse Neuromuscular Junctions and Functional Links With Other Metabotropic Receptor Pathways.Frontiers in pharmacology · 2018Article
- Effects of presynaptic muscarinic cholinoreceptor blockade on neuromuscular transmission as assessed by the train-of-four and the tetanic fade response to rocuronium.Clinical and experimental pharmacology & physiology · 2017Article
- Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- 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
- Endocannabinoids mediate muscarine-induced synaptic depression at the vertebrate neuromuscular junction.The European journal of neuroscience · 2007Article
- Release of neurotransmitter induced by Ca2+-uncaging: reexamination of the ca-voltage hypothesis for release.Journal of computational neuroscience · 2005Article
- Cholinergic regulation of the evoked quantal release at frog neuromuscular junction.The Journal of physiology · 2004Article
- Nitric oxide, cAMP and the biphasic muscarinic modulation of ACh release at the lizard neuromuscular junction.The Journal of physiology · 2004Article
- Chronic acetylcholinesterase overexpression induces multilevelled aberrations in mouse neuromuscular physiology.The Journal of physiology · 2003Article
- Can the Ca2+ hypothesis and the Ca2+-voltage hypothesis for neurotransmitter release be reconciled?Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Ca2+-independent feedback inhibition of acetylcholine release in frog neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Macropatch recording was used to study release of acetylcholine in the frog neuromuscular junction evoked by either direct local depolarization or by an action potential. 2. The quantal content was established by directly counting the released quanta. The time course of release was obtained by constructing synaptic delay histograms. 3. Perfusion of the neuromuscular junction with methoctramine, a selective M(2)/M(4) muscarinic antagonist, increased the quantal content and slowed the exponential decay of the synaptic delay histograms. Addition of the agonist muscarine reversed these effects. 4. Addition of acetylcholinesterase prolonged the decay of the delay histogram, and muscarine reversed this effect. 5. Methoctramine slowed the rise time of the postsynaptic current produced by axon stimulation without affecting either the excitatory nerve terminal current or the presynaptic Ca(2+) current. 6. These results show that presynaptic M(2) muscarinic receptors are involved in the process which terminates evoked ACh release.
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