Evidence map›Paper›PMID 23109110›Full record

ArticleThe Journal of physiology2013

Effects of in vivo injury on the neuromuscular junction in healthy and dystrophic muscles.

Stephen J P Pratt, Sameer B Shah, Christopher W Ward, Mario P Inacio, Joseph P Stains, Richard M Lovering

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

78 citing papers in PubMed, 108 citations in OpenAlex.

  1. Eccentric Exercise and Muscle Damage: An Introductory Guide.Journal of functional morphology and kinesiology · 2026
    Review
  2. Article
  3. CORP: In vivo muscle strength-perspectives on the design and interpretation of preclinical animal studies.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Review
  4. Article
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Mechanisms of weakness in Mdx muscle following in vivo eccentric contractions.Journal of muscle research and cell motility · 2022
    Article
  16. Alteration of skeletal and cardiac muscles function inIntractable & rare diseases research · 2021
    Article
  17. Lysine methyltransferase 2D regulates muscle fiber size and muscle cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  18. Article
  19. Article
  20. The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021
    Review

18 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Stephen J P PrattDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Sameer B Shah
Christopher W Ward
Mario P Inacio
Joseph P Stains
Richard M Lovering
University of Maryland, Baltimore · USUniversity of California, San Diego · US

Funding

Spatial Control of Bone Remodeling by Gap Junction-Communicated cAMPR01AR063631 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI STAINS, JOSEPH P. · 2013 to 2024
$3.3M
Mechanisms of Force Loss in Injured and Dystrophic Skeletal MuscleR01AR059179 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI LOVERING, RICHARD M · 2010 to 2014
$1.4M
Intercellular Signaling in BoneR01AR052719 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI STAINS, JOSEPH P. · 2006 to 2010
$1.3M
The Role of Intermediate Filaments in Skeletal Muscle Injury and DiseaseK01AR053235 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI LOVERING, RICHARD M · 2007 to 2011
$654k
NIAMS NIH HHS 1R01AR059179NIAMS NIH HHS K01 AR053235NIAMS NIH HHS K01AR053235NIAMS NIH HHS R01 AR052719NIAMS NIH HHS R01 AR059179NIAMS NIH HHS R01 AR063631
6 · The paper itself

Abstract

The most common and severe form of muscular dystrophy is Duchenne muscular dystrophy (DMD), a disorder caused by the absence of dystrophin, a structural protein found on the cytoplasmic surface of the sarcolemma of striated muscle fibres. Considerable attention has been dedicated to studying myofibre damage and muscle plasticity, but there is little information to determine if damage from contraction-induced injury occurs at or near the nerve terminal axon. We used α-bungarotoxin to compare neuromuscular junction (NMJ) morphology in healthy (wild-type, WT) and dystrophic (mdx) mouse quadriceps muscles and evaluated transcript levels of the post-synaptic muscle-specific kinase signalling complex. Our focus was to study changes in NMJs after injury induced with an established in vivo animal injury model. Neuromuscular transmission, electromyography (EMG), and NMJ morphology were assessed 24 h after injury. In non-injured muscle, muscle-specific kinase expression was significantly decreased in mdx compared to WT. Injury resulted in a significant loss of maximal torque in WT (39 ± 6%) and mdx (76 ± 8%) quadriceps, but significant changes in NMJ morphology, neuromuscular transmission and EMG data were found only in mdx following injury. Compared with WT mice, motor end-plates of mdx mice demonstrated less continuous morphology, more disperse acetylcholine receptor aggregates and increased number of individual acetylcholine receptor clusters, an effect that was exacerbated following injury. Neuromuscular transmission failure increased and the EMG measures decreased after injury in mdx mice only. The data show that eccentric contraction-induced injury causes morphological and functional changes to the NMJs in mdx skeletal muscle, which may play a role in excitation-contraction coupling failure and progression of the dystrophic process.

Indexed as

Isometric ContractionAnimalsAxonsBungarotoxinsDystrophinGene ExpressionMiceMice, Inbred C57BLMotor EndplateMuscle, SkeletalMuscular Dystrophy, DuchenneNeuromuscular JunctionReceptor Protein-Tyrosine KinasesReceptors, CholinergicRNA, MessengerTorqueBungarotoxinsDystrophinMuSK protein, mouseReceptor Protein-Tyrosine KinasesReceptors, CholinergicRNA, Messenger

Identifiers

PMID23109110
PMCPMC3577526
OpenAlexW1549340072

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.