ArticleThe Journal of physiology2001
Repetitive nerve stimulation decreases the acetylcholine content of quanta 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 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Presynaptic compensation sustains neuromuscular transmission in the mouse diaphragm at a late stage of aging.Biogerontology · 2026Article
- Cyclic extranasal neurostimulation for dry eye disease: a 4-week stimulation and 6-week intermission regimen based on neural adaptation dynamics.Eye and vision (London, England) · 2025Article
- Article
- A Novel Striated Muscle-Specific Myosin-Blocking Drug for the Study of Neuromuscular Physiology.Frontiers in cellular neuroscience · 2016Article
- Presynaptic clathrin levels are a limiting factor for synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Depolarization-induced Ca2+ entry preferentially evokes release of large quanta in the developing Xenopus neuromuscular junction.Journal of neurophysiology · 2010Article
- TGF-beta2 alters the characteristics of the neuromuscular junction by regulating presynaptic quantal size.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Quantal release of acetylcholine in mice with reduced levels of the vesicular acetylcholine transporter.Journal of neurochemistry · 2010Article
- The vesicle cycle in motor nerve endings of the mouse diaphragm.Neuroscience and behavioral physiology · 2009Article
- Trafficking of vesicular neurotransmitter transporters.Traffic (Copenhagen, Denmark) · 2008Review
- Modeling study of mecamylamine block of muscle type acetylcholine receptors.European biophysics journal : EBJ · 2008Article
- Activity-dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals.The Journal of physiology · 2003Article
- Effects of 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one on synaptic vesicle cycling at the frog neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Vesicle size and transmitter release at the frog neuromuscular junction when quantal acetylcholine content is increased or decreased.The Journal of physiology · 2002Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We investigated how elevated quantal release produced by motor nerve stimulation affects the size of the quanta. The motor nerve was stimulated at 10 Hz in preparations in which excitation-contraction coupling was disrupted. Two hundred stimuli reduced the size of the time integrals of the miniature endplate currents ([integral]MEPCs), measured at the same junction immediately after stimulation, by 16 %. Three thousand stimuli reduced size by 23 %. When the solution contained 10 microM neostigmine (NEO) 3000 stimuli reduced [integral]MEPCs by 60 %, because with acetylcholinesterase (AChE) inhibited, [integral]MEPC size is more sensitive to changes in acetylcholine (ACh) content. Similar decreases in miniature endplate potential size ([integral]MEPP) followed repetitive stimulation of contracting preparations. The depolarization produced by iontophoretic pulses of ACh was scarcely changed by 3000 nerve stimuli at 10 Hz, suggesting that the decreases in miniature sizes are largely due to less ACh released per quantum. Following 3000 stimuli at 10 Hz the sizes of the [integral]MEPCs increased back to pre-stimulus values with a half-time of 8-10 min. Recovery was blocked by (-)-vesamicol (VES), by hemicholinium-3 (HC3) and by nicotinic cholinergic agonists - all of which inhibit ACh loading into synaptic vesicles. The number of quanta in the total store was estimated by releasing them with carbonyl cyanide m-chlorophenylhydrazone (CCCP). CCCP releases fewer quanta after stimulation than from unstimulated controls. After resting for hours following stimulation, the releasable number increased, even when ACh loading inhibitors were present. We conclude that the inhibitors do not block a significant fraction of the ACh loading into reformed reserve vesicles and propose that ACh can be loaded in a series of steps.
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