Evidence map›Paper›PMID 19805741›Full record

ArticleThe Journal of physiology2009

Extracellular ATP inhibits chloride channels in mature mammalian skeletal muscle by activating P2Y1 receptors.

Andrew A Voss

Abstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Influence of neuromuscular transmission and NaJournal of muscle research and cell motility · 2025
    Article
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  3. Review
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  6. Depressed Synaptic Transmission and Reduced Vesicle Release Sites in Huntington's Disease Neuromuscular Junctions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  7. Article
  8. Article
  9. Neuronal involvement in muscular atrophy.Frontiers in cellular neuroscience · 2014
    Review
  10. Review
  11. Article
  12. De novo expression of connexin hemichannels in denervated fast skeletal muscles leads to atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  13. Review
  14. Article
  15. Article
  16. Article
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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

1 author.

Andrew A VossCalifornia State Polytechnic University, Pomona, Biological Sciences, 3801 West Temple Avenue, Pomona, CA 91768-4032, USA. aavoss@csupomona.edu

Funding

Electrogenic glucose sensor of neuromuscular junctionF32DK072818 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VOSS, ANDREW ALVIN · 2006 to 2008
$145k
NIDDK NIH HHS DK072818NIDDK NIH HHS F32 DK072818
6 · The paper itself

Abstract

ATP is released from skeletal muscle during exercise, a discovery dating back to 1969. Surprisingly, few studies have examined the effects of extracellular ATP on mature mammalian skeletal muscle. This electrophysiological study examined the effects of extracellular ATP on fully innervated rat levator auris longus using two intracellular microelectrodes. The effects of ATP were determined by measuring the relative changes of miniature endplate potentials (mEPPs) and voltage responses to step current pulses in individual muscle fibres. Exposure to ATP (20 microm) prolonged the mEPP falling phase by 31 +/- 7.5% (values +/- s.d., n = 3 fibres). Concurrently, the input resistance increased by 31 +/- 2.0% and the time course of the voltage responses increased by 59 +/- 3.0%. Analogous effects were observed using 2 and 5 microm ATP, and on regions distal from the neuromuscular junction, indicating that physiologically relevant levels of ATP enhanced electrical signalling over the entire muscle fibre. The effects of extracellular ATP were blocked by 200 microm anthracene-9-carboxylic acid, a chloride channel inhibitor, and reduced concentrations of extracellular chloride, indicating that ATP inhibited chloride channels. A high affinity agonist for P2Y receptors, 2-methylthioadenosine-5-O-diphosphate (2MeSADP), induced similar effects to ATP with an EC(50) of 160 +/- 30 nm. The effects of 250 nm2MeSADP were blocked by 500 nmMRS2179, a specific P2Y(1) receptor inhibitor, suggesting that ATP acts on P2Y(1) receptors to inhibit chloride channels. The inhibition of chloride channels by extracellular ATP has implications for muscle excitability and fatigue, and the pathophysiology of myotonias.

Indexed as

Purinergic P2 Receptor AgonistsAdenosine TriphosphateAnimalsChloride ChannelsData Interpretation, StatisticalDose-Response Relationship, DrugElectric StimulationElectrophysiologyIn Vitro TechniquesMembrane PotentialsMuscle Fibers, SkeletalMuscle, SkeletalNeuromuscular JunctionPatch-Clamp TechniquesRana pipiensRatsAdenosine TriphosphateChloride ChannelsP2ry1 protein, ratPurinergic P2 Receptor AgonistsReceptors, Purinergic P2Receptors, Purinergic P2Y1

Identifiers

PMID19805741
PMCPMC2805382

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.