ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Nicotinic acetylcholine receptor stability at the NMJ deficient in α-syntrophin in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Abnormalities in the genioglossus muscle and its neuromuscular synapse in leptin-deficient male mice.Skeletal muscle · 2025Article
- Regulation of miR-206 in denervated and dystrophic muscles, and its effect on acetylcholine receptor clustering.Journal of cell science · 2024Article
- Distinct roles of the dystrophin-glycoprotein complex: α-dystrobrevin and α-syntrophin in the maintenance of the postsynaptic apparatus of the neuromuscular synapse.Human molecular genetics · 2022Article
- The Metabolic Stability of the Nicotinic Acetylcholine Receptor at the Neuromuscular Junction.Cells · 2021Review
- The disassembly of the neuromuscular synapse in high-fat diet-induced obese male mice.Molecular metabolism · 2020Article
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- An improved method for culturing myotubes on laminins for the robust clustering of postsynaptic machinery.Scientific reports · 2020Article
- Spatial distribution and molecular dynamics of dystrophin glycoprotein components at the neuromuscular junctionJournal of cell science · 2017Article
- The knockdown of αkap alters the postsynaptic apparatus of neuromuscular junctions in living mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- LRP4 is critical for neuromuscular junction maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Degeneration of neuromuscular junction in age and dystrophy.Frontiers in aging neuroscience · 2014Review
- Article
- A role for the calmodulin kinase II-related anchoring protein (αkap) in maintaining the stability of nicotinic acetylcholine receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Participation of myosin Va and Pka type I in the regeneration of neuromuscular junctions.PloS one · 2012Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
α-Syntrophin (α-syn), a scaffold protein, links signaling molecules to the dystrophin-glycoprotein complex. Absence of α-syn from the DGC is known to lead to structurally aberrant neuromuscular junctions (NMJs) with few acetylcholine receptors (AChRs) clustered at synaptic sites. Using α-syn knock-out mice, we show that during the first postnatal week, α-syn is not required for synapse formation. However, at postnatal day 6 (P6)-P7, the structural integrity of the postsynaptic apparatus is altered, the turnover rate of AChRs increases significantly, and the number/density of AChRs is impaired. At the adult α-syn(-/-) NMJ, the turnover rate of AChRs is ∼ 4 times faster than wild-type synapses, and most removed receptors are targeted to degradation as few AChRs recycled to synaptic sites. Biochemical analyses show that in muscle cells of adult knock-out α-syn mice, total AChRs and scaffold protein rapsyn are significantly reduced, the 89 kDa and 75 kDa isoforms of tyrosine phosphorylated α-dystrobrevin (α-dbn) 1 (which are required for the maintenance and stability of AChR in α-dbn(-/-) synapses) are barely detectable. Electroporation of GFP-α-dbn1 in α-syn(-/-) muscle cells partially restored receptor density, turnover rate, and the structural integrity of the postsynaptic apparatus, whereas expression of rapsyn-GFP failed to rescue the α-syn(-/-) synaptic phenotype. These results demonstrate that α-syn is required for the maturation and stability of the postsynaptic apparatus and suggest that α-syn may act via α-dbn1.
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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.