ArticleThe Journal of physiology2004
Cholinergic regulation of the evoked quantal release at frog neuromuscular junction.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- From Frog Muscle to Brain Neurons: Joys and Sorrows in Neuroscience.Physiological research · 2024Review
- Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions.Biomedicines · 2022Review
- Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing CaInternational journal of molecular sciences · 2021Article
- Acetylcholine-Induced Inhibition of Presynaptic Calcium Signals and Transmitter Release in the Frog Neuromuscular Junction.Frontiers in physiology · 2016Article
- Bayesian analysis of the kinetics of quantal transmitter secretion at the neuromuscular junction.Journal of computational neuroscience · 2015Article
- Identification of the muscarinic receptor subtypes involved in autoregulation of acetylcholine quantal release from frog motor nerve endings.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2015Article
- α-Conotoxin M1 (CTx) blocks αδ binding sites of adult nicotinic receptors while ACh binding at αε sites elicits only small and short quantal synaptic currents.Physiological reports · 2014Article
- 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
- Revealing of T-type low-voltage activated calcium channels (CaV3) in frog neuromuscular junctions.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2013Article
- Mechanisms of the inhibition of endplate acetylcholine receptors by antiseptic chlorhexidine (experiments and models).Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Participation of different types of voltage-dependent calcium channels in evoked quantal transmitter release in frog neuromuscular junctions.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
- 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
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The effects of cholinergic drugs on the quantal contents of the nerve-evoked endplate currents (EPCs) and the parameters of the time course of quantal release (minimal synaptic latency, main modal value of latency histogram and variability of synaptic latencies) were studied at proximal, central and distal regions of the frog neuromuscular synapse. Acetylcholine (ACh, 5 x 10(-4) M), carbachol (CCh, 1 x 10(-5) M) or nicotine (5 x 10(-6) M) increased the numbers of EPCs with long release latencies mainly in the distal region of the endplate (90-120 microm from the last node of Ranvier), where the synchronization of transmitter release was the most pronounced. The parameters of focally recorded motor nerve action potentials were not changed by either ACh or CCh. The effects of CCh and nicotine on quantal dispersion were reduced substantially by 5 x 10(-7) M (+)tubocurarine (TC). The muscarinic agonists, oxotremorine and the propargyl ester of arecaidine, as well as antagonists such as pirenzepine, AF-DX 116 and methoctramine, alone or in combination, did not affect the dispersion of the release. Muscarinic antagonists did not block the dispersion action of CCh. Cholinergic drugs either decreased the quantal content m(o) (muscarinic agonist, oxotremorine M, and nicotinic antagonist, TC), or decreased m(o) and dispersed the release (ACh, CCh and nicotine). The effects on m(o) were not related either to the endplate region or to the initial level of release dispersion. It follows that the mechanisms regulating the amount and the time course of transmitter release are different and that, among other factors, they are altered by presynaptic nicotinic receptors.
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