Evidence map›Paper›PMID 29326174›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Muscle Nicotinic Acetylcholine Receptors May Mediate Trans-Synaptic Signaling at the Mouse Neuromuscular Junction.

Xueyong Wang, J Michael McIntosh, Mark M Rich

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Positive allosteric modulator selective for adult muscle nicotinic acetylcholine receptor.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Robust PHP in Adult Hippocampus: Essential Assay Optimizations.bioRxiv : the preprint server for biology · 2026
    Article
  4. Nonionic signaling rapidly remodels postsynaptic DLG to induce retrograde homeostatic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Postsynaptic receptors regulate presynaptic transmitter stability through transsynaptic bridges.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Glial Sphingosine-Mediated Epigenetic Regulation Stabilizes Synaptic Function inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. Article
  12. Article
  13. ACh Transfers: Homeostatic Plasticity of Cholinergic Synapses.Cellular and molecular neurobiology · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Xueyong WangDepartment of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435.ORCID 0000-0002-6219-9129
J Michael McIntoshGeorge E. Wahlen Veterans Affairs Medical Center, Salt Lake City, UT 84108, and.
Mark M RichDepartment of Neuroscience, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, mark.rich@wright.edu.ORCID 0000-0002-6956-5531
Wright State University · USUniversity of Utah · US

Funding

Synaptic Function: Effects of the Nerve Injury, Repair, and Altered ActivityP01NS057228 · NINDS · WRIGHT STATE UNIVERSITY · PI COPE, TIMOTHY C · 2007 to 2017
$9.1M
Novel nAChR-Targeted PeptidesR01GM103801 · NIGMS · UNIVERSITY OF UTAH · PI MCINTOSH, J MICHAEL · 2012 to 2019
$2.4M
NIGMS NIH HHS R01 GM103801NINDS NIH HHS P01 NS057228
6 · The paper itself

Abstract

Block of neurotransmitter receptors at the neuromuscular junction (NMJ) has been shown to trigger upregulation of the number of synaptic vesicles released (quantal content, QC), a response termed homeostatic synaptic plasticity. The mechanism underlying this plasticity is not known. Here, we used selective toxins to demonstrate that block of α1-containing nicotinic acetylcholine receptors (nAChRs) at the NMJ of male and female mice triggers the upregulation of QC. Reduction of current flow through nAChRs, induced by drugs with antagonist activity, demonstrated that reduction in synaptic current

Indexed as

AnimalsFemaleKineticsMaleMiceMuscle, SkeletalNeuromuscular JunctionNeurotoxinsNicotinic AntagonistsReceptors, NicotinicSignal TransductionSynapsesSynaptic PotentialsSynaptic TransmissionSynaptic VesiclesCHRNA1 protein, mouseNeurotoxinsNicotinic AntagonistsReceptors, Nicotinicendplatehomeostaticneurotransmitterplasticitysynaptictransmission

Identifiers

PMID29326174
PMCPMC5815454
OpenAlexW2782666026

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.