Evidence map›Paper›PMID 28724748›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

Depressed Synaptic Transmission and Reduced Vesicle Release Sites in Huntington's Disease Neuromuscular Junctions.

Ahmad Khedraki, Eric J Reed, Shannon H Romer, Qingbo Wang, William Romine, Mark M Rich, Robert J Talmadge, Andrew A Voss

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Huntingtin regulates calcium fluxes in skeletal muscle.The Journal of general physiology · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Mechanisms of exercise as a preventative measure to muscle wasting.American journal of physiology. Cell physiology · 2021
    Review
  11. Article
  12. Molecular Mechanisms Underlying Muscle Wasting in Huntington's Disease.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

8 authors at 2 institutions in 1 country.

Ahmad KhedrakiDepartments of Biological Sciences and.ORCID 0000-0003-1843-5558
Eric J ReedDepartments of Biological Sciences and.
Shannon H RomerDepartments of Biological Sciences and.
Qingbo WangNeuroscience, Cell Biology & Physiology, Wright State University, Dayton, Ohio 45435, and.
William RomineDepartments of Biological Sciences and.
Mark M RichNeuroscience, Cell Biology & Physiology, Wright State University, Dayton, Ohio 45435, and.
Robert J TalmadgeCalifornia State Polytechnic University, Pomona, Department of Biological Sciences, Pomona, California 91768.
Andrew A VossDepartments of Biological Sciences and andrew.voss@wright.edu.ORCID 0000-0001-7530-6272
Wright State University · USCalifornia State Polytechnic University · US

Funding

Mechanism and function of a novel purinergic signaling cascade in skeletal muscleSC3GM096945 · NIGMS · CALIFORNIA STATE POLY U POMONA · PI VOSS, ANDREW ALVIN · 2012 to 2014
$322k
NIGMS NIH HHS SC3 GM096945
6 · The paper itself

Abstract

Huntington's disease (HD) is a progressive and fatal degenerative disorder that results in debilitating cognitive and motor dysfunction. Most HD studies have focused on degeneration of the CNS. We previously discovered that skeletal muscle from transgenic R6/2 HD mice is hyperexcitable due to decreased chloride and potassium conductances. The progressive and early onset of these defects suggest a primary myopathy in HD. In this study, we examined the relationship between neuromuscular transmission and skeletal muscle hyperexcitability. We used an

Indexed as

AnimalsFemaleHuntington DiseaseMaleMiceMice, TransgenicMotor EndplateMuscle, SkeletalNeuromuscular JunctionOrgan Culture TechniquesRandom AllocationSynaptic TransmissionSynaptic VesicleselectrophysiologyHuntington's diseaseneuromuscular transmissionsynaptic transmissiontrinucleotide repeat disorder

Identifiers

PMID28724748
PMCPMC5566863
OpenAlexW2736640744

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.