Evidence map›Paper›PMID 15647477›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Activity-dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo.

Xueyong Wang, Yingjie Li, Kathrin L Engisch, Stan T Nakanishi, Sara E Dodson, Gary W Miller, Timothy C Cope, Martin J Pinter, Mark M Rich

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Muscle Nicotinic Acetylcholine Receptors May Mediate Trans-Synaptic Signaling at the Mouse Neuromuscular Junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  6. Review
  7. Article
  8. Synaptic Deficits at Neuromuscular Junctions in Two Mouse Models of Charcot-Marie-Tooth Type 2d.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  9. Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  10. Review
  11. Article
  12. Article
  13. Skeletal muscle IP3R1 receptors amplify physiological and pathological synaptic calcium signals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  14. Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy.American journal of physiology. Regulatory, integrative and comparative physiology · 2011
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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 · 2010
    Article
  20. Neuromuscular adaptations to respiratory muscle inactivity.Respiratory physiology & neurobiology · 2009
    Review
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

9 authors.

Xueyong WangCenter for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Yingjie Li
Kathrin L Engisch
Stan T Nakanishi
Sara E Dodson
Gary W Miller
Timothy C Cope
Martin J Pinter
Mark M Rich

Funding

PERIPHERAL NERVE INJURY AND RECOVERY OF FUNCTIONP01NS040405 · NINDS · EMORY UNIVERSITY · PI NICHOLS, RICHARD · 2000 to 2004
$6.7M
NINDS NIH HHS P01 NS040405NINDS NIH HHS P01 NS 40405
6 · The paper itself

Abstract

Changes in synaptic activity alter quantal size, but the relative roles of presynaptic and postsynaptic cells in these changes are only beginning to be understood. We examined the mechanism underlying increased quantal size after block of synaptic activity at the mammalian neuromuscular junction in vivo. We found that changes in neither acetylcholinesterase activity nor acetylcholine receptor density could account for the increase. By elimination, it appears likely that the site of increased quantal size after chronic block of activity is presynaptic and involves increased release of acetylcholine. We used mice with muscle hyperexcitability caused by mutation of the ClC-1 muscle chloride channel to examine the role of postsynaptic activity in controlling quantal size. Surprisingly, quantal size was increased in ClC mice before block of synaptic activity. We examined the mechanism underlying increased quantal size in ClC mice and found that it also appeared to be located presynaptically. When presynaptic activity was completely blocked in both control and ClC mice, quantal size was large in both groups despite the higher level of postsynaptic activity in ClC mice. This suggests that postsynaptic activity does not regulate quantal size at the neuromuscular junction. We propose that presynaptic activity modulates quantal size at the neuromuscular junction by modulating the amount of acetylcholine released from vesicles.

Indexed as

AcetylcholinesteraseAnimalsChloride ChannelsElectromyographyElectrophysiologyIn Vitro TechniquesMiceMice, KnockoutMotor ActivityMotor EndplateMuscle ProteinsNeuromuscular JunctionPatch-Clamp TechniquesPresynaptic TerminalsReceptors, CholinergicSynaptic VesiclesAcetylcholinesteraseChloride ChannelsCLC-1 channelMuscle ProteinsReceptors, Cholinergic

Identifiers

PMID15647477
PMCPMC6725499

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.