ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Acetylcholine receptors in innervated muscles of dystrophic mdx mice degrade as after denervation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 71 citations in OpenAlex.
- Early postsynaptic instability and acetylcholine receptor compartmentalization precede neuromuscular synapse dismantling.Communications biology · 2026Article
- Neuromuscular junction dysfunction in Lafora disease.Disease models & mechanisms · 2024Article
- Respiratory characterization of a humanized Duchenne muscular dystrophy mouse model.Respiratory physiology & neurobiology · 2024Article
- Dystrophin S3059 phosphorylation partially attenuates denervation atrophy in mouse tibialis anterior muscles.Physiological reports · 2024Article
- Plum modulates Myoglianin and regulates synaptic function inOpen biology · 2023Article
- Breathing in Duchenne muscular dystrophy: translation to therapy.The Journal of physiology · 2022Review
- Lithium causes differential effects on postsynaptic stability in normal and denervated neuromuscular synapses.Scientific reports · 2021Article
- The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021Review
- Motor function recovery: deciphering a regenerative niche at the neuromuscular synapse.Biological reviews of the Cambridge Philosophical Society · 2021Review
- Regulatory Function of Sympathetic Innervation on the Endo/Lysosomal Trafficking of Acetylcholine Receptor.Frontiers in physiology · 2021Article
- Alterations of neuromuscular junctions in Duchenne muscular dystrophy.Neuroscience letters · 2020Review
- Article
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- What is Normal? Neuromuscular junction reinnervation after nerve injury.Muscle & nerve · 2019Article
- A 3D culture model of innervated human skeletal muscle enables studies of the adult neuromuscular junction.eLife · 2019Article
- Motor Endplate-Anatomical, Functional, and Molecular Concepts in the Historical Perspective.Cells · 2019Article
- Article
- Turnover of acetylcholine receptors at the endplate revisited: novel insights into nerve-dependent behavior.Journal of muscle research and cell motility · 2015Article
- Alterations of cAMP-dependent signaling in dystrophic skeletal muscle.Frontiers in physiology · 2013Review
- Effects of in vivo injury on the neuromuscular junction in healthy and dystrophic muscles.The Journal of physiology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acetylcholine receptors (AChRs) are present at the top of the postsynaptic membrane of the neuromuscular junction (NMJ) at very high density, possibly anchored to cytoskeletal elements. The present study investigated whether AChR degradation is affected in animals lacking dystrophin, a protein that is an integral part of the cytoskeletal complex and is missing in Duchenne muscular dystrophy. The animal model for Duchenne muscular dystrophy, the mutant mdx mouse, was used to determine whether disruption of the cytoskeleton, caused by the absence of dystrophin, affects AChR degradation. Of the two populations of junctional AChRs, Rs (expressed in innervated adult muscles) and Rr (expressed in embryonic or denervated muscles), only Rs are affected in mdx animals. In innervated mdx soleus, diaphragm, and sternomastoid muscles, the AChRs have an accelerated degradation rate (t1/2 of approximately 3-5 d), similar to that acquired by Rs in control muscles after denervation. The Rs in mdx NMJs do not accelerate further when the muscles are denervated. The absence of dystrophin does not affect the degradation rate of the Rr AChRs (t1/2 of 1 d), which are expressed after denervation in mdx as in control muscles. These results suggest that dystrophin or an intact cytoskeletal complex may be required for neuronal stabilization of Rs receptors at the adult neuromuscular junctions.
Indexed as
Identifiers
9334395PMC6573762W2132764921What OpenQuestion holds
Registered trials
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.