ArticlePflugers Archiv : European journal of physiology1996
On the possible origin of giant or slow-rising miniature end-plate potentials at the neuromuscular junction.
Article in Pflugers Archiv : European journal of physiology, 1996. 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, 29 citations in OpenAlex.
- Increased Frequency of Giant Miniature End-Plate Potentials at the Neuromuscular Junction in Diabetic Rats.Biomedicines · 2023Article
- Ablation of All Synaptobrevin vSNAREs Blocks Evoked But Not Spontaneous Neurotransmitter Release at Neuromuscular Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- PLAA Mutations Cause a Lethal Infantile Epileptic Encephalopathy by Disrupting Ubiquitin-Mediated Endolysosomal Degradation of Synaptic Proteins.American journal of human genetics · 2017Article
- A rare type of fibrillation-like EMG activity.Clinical neurophysiology practice · 2017Article
- Article
- Early changes of neuromuscular transmission in the SOD1(G93A) mice model of ALS start long before motor symptoms onset.PloS one · 2013Article
- Regulation of quantal shape by Rab3A: evidence for a fusion pore-dependent mechanism.The Journal of physiology · 2008Article
- Modulation of Ca(2+)-dependent and Ca(2+)-independent miniature endplate potentials by phorbol ester and adenosine in frog.British journal of pharmacology · 2005Article
- 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
- Subcellular localization of tetanus neurotoxin-insensitive vesicle-associated membrane protein (VAMP)/VAMP7 in neuronal cells: evidence for a novel membrane compartment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Caffeine- and ryanodine-induced changes in the spectrum of spontaneously secreted quanta of the mediator in the neuromuscular synapse of mice.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Giant or slow-rising miniature end-plate potentials (GMEPPs) caused by vesicular release of acetylcholine (ACh) occur at any time in about 50% of mouse diaphragm neuro muscular junctions, but generally at frequencies less than 0.03 s-1. Their frequency is, unlike that of miniature end-plate potentials (MEPPs), not affected by nerve terminal depolarization. Unlike MEPPs and stimulus-evoked end-plate potentials, GMEPPs have a prolonged time-to-peak and show an increase in time-to-peak with amplitude. By using these differences in amplitude and time course, GMEPPs can be separated from MEPPs. In contrast to MEPPs, GMEPPs are not blocked by botulinum neurotoxin type A. GMEPPs have a greater temperature sensitivity than MEPPs, disappearing at temperatures below 15 degrees C. Long-term paralysis by botulinum toxin and certain drugs which inhibit protein kinase C or affect actin filament polymerization (cytochalasins) enhance the frequency of GMEPPs. End-plate current recordings show that similar postsynaptic ACh receptors are activated by MEPPs and GMEPPs. It is suggested that GMEPPs are not caused by mechanisms involved in regulated neurotransmitter release but are generated by constitutive secretion.
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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.