ArticleThe Journal of physiology2002
Vesicle size and transmitter release at the frog neuromuscular junction when quantal acetylcholine content is increased or decreased.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 34 citations in OpenAlex.
- Microelectrode-based approaches for studying cholinergic neuromuscular transmission.Biophysical reviews · 2025Review
- Molecular, Structural, Functional, and Pharmacological Sites for Vesicular Glutamate Transporter Regulation.Molecular neurobiology · 2020Review
- Ultrafast and Slow Cholinergic Transmission. Different Involvement of Acetylcholinesterase Molecular Forms.Molecules (Basel, Switzerland) · 2017Review
- Article
- Article
- Dynamic regulation of synaptic GABA release by the glutamate-glutamine cycle in hippocampal area CA1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Structural insights into substrate traffic and inhibition in acetylcholinesterase.The EMBO journal · 2006Article
- Homeostatic scaling of vesicular glutamate and GABA transporter expression in rat neocortical circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Galphao2 regulates vesicular glutamate transporter activity by changing its chloride dependence.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Normal biogenesis and cycling of empty synaptic vesicles in dopamine neurons of vesicular monoamine transporter 2 knockout mice.Molecular biology of the cell · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
We investigated whether the synaptic vesicles at the neuromuscular junction change size when their acetylcholine (ACh) content is altered. The size of the miniature endplate potential (MEPP) increased 3- or 4-fold in preparations pre-treated in a hypertonic solution in which the anion was gluconate. We measured the dimensions of synaptic vesicles in such preparations and in controls. The size of the vesicles and size distribution were indistinguishable. Quanta contained about half of the usual amount of ACh in preparations stimulated in the presence of hemicholinium-3, an inhibitor of choline uptake, or in NH(4)(+), which diminishes the proton gradient for ACh uptake into the vesicles. Neither treatment changed the size of the synaptic vesicles. ACh content and vesicle size were both decreased in preparations stimulated in (-)-vesamicol, an inhibitor of ACh uptake in vesicles. Since the other inhibitors decreased ACh content by a similar amount without altering vesicle size, (-)-vesamicol may decrease vesicle size by acting on another target. We also found that a hypertonic solution in which the anion was aspartate increased quantal size similar to gluconate. Both anions have high hydration energy and a large volume. When these treatments increased quantal size the mean 20-80 % rise time of MEPPs recorded with an extracellular electrode was 170 micros. In the controls it was 97 micros. Perhaps some of the added ACh is bound within the vesicles, which slows the rise. Our major conclusion is that ACh content can change notably without any change in the size of the synaptic vesicles.
Indexed as
Identifiers
What 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.