Evidence map›Paper›PMID 12042346›Full record

ArticleThe Journal of physiology2002

Vesicle size and transmitter release at the frog neuromuscular junction when quantal acetylcholine content is increased or decreased.

William Van der Kloot, Jordi Molgó, Roger Cameron, Cesare Colasante

Open access · greenAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 28% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. 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 · 2006
    Article
  7. Article
  8. 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 · 2005
    Article
  9. Galphao2 regulates vesicular glutamate transporter activity by changing its chloride dependence.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

William Van der KlootDepartment of Physiology and Biophysics, SUNY at Stony Brook, Stony Brook, NY 11794-8661, USA. wvanderkloot@post.harvard.edu
Jordi Molgó
Roger Cameron
Cesare Colasante
Instituto de Cardiología y Cirugía Cardiovascular · CULaboratoire de Neurobiologie Cellulaire et Moléculaire · FRStony Brook School · US

Funding

TRANSMITTER RELEASE BY NERVE TERMINALSR01NS010320 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI VAN DER KLOOT, WILLIAM G · 1985 to 1998
–
NINDS NIH HHS NS10320
6 · The paper itself

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

AcetylcholineAlgorithmsAnimalsAspartic AcidChemical PhenomenaChemistry, PhysicalElectrodesElectrophysiologyGluconatesHypertonic SolutionsIn Vitro TechniquesMembrane PotentialsMicroscopy, ElectronMotor EndplateNeuromuscular JunctionNeurotransmitter AgentsAcetylcholineAspartic AcidGluconatesHypertonic SolutionsNeurotransmitter Agents

Identifiers

PMID12042346
PMCPMC2290324
OpenAlexW1487926525

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.