ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Voltage-gated sodium channels and ankyrinG occupy a different postsynaptic domain from acetylcholine receptors from an early stage of neuromuscular junction maturation in rats.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- MuSK Regulates Neuromuscular Junction Nav1.4 Localization and Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Nerve-independent formation of membrane infoldings at topologically complex postsynaptic apparatus by caveolin-3.Science advances · 2023Article
- Ankyrin-dependent NaCurrent biology : CB · 2021Article
- New Challenges Resulting From the Loss of Function of NaFrontiers in pharmacology · 2021Review
- Microutrophin expression in dystrophic mice displays myofiber type differences in therapeutic effects.PLoS genetics · 2020Article
- Ankyrins: Roles in synaptic biology and pathology.Molecular and cellular neurosciences · 2018Review
- The Structure of Human Neuromuscular Junctions: Some Unanswered Molecular Questions.International journal of molecular sciences · 2017Review
- Neuromuscular junctions are pathological but not denervated in two mouse models of spinal bulbar muscular atrophy.Human molecular genetics · 2016Article
- A system for studying mechanisms of neuromuscular junction development and maintenance.Development (Cambridge, England) · 2016Article
- A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis.Neurology · 2016Article
- Membrane domains based on ankyrin and spectrin associated with cell-cell interactions.Cold Spring Harbor perspectives in biology · 2009Review
- Truncated dystrophins can influence neuromuscular synapse structure.Molecular and cellular neurosciences · 2009Article
- Na+/K+ ATPase regulates the expression and localization of acetylcholine receptors in a pump activity-independent manner.Molecular and cellular neurosciences · 2008Article
- Ion channels and ion transporters of the transverse tubular system of skeletal muscle.Journal of muscle research and cell motility · 2006Review
- A selective role for MRF4 in innervated adult skeletal muscle: Na(V) 1.4 Na+ channel expression is reduced in MRF4-null mice.Gene expression · 2005Article
- Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the surface of cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Basic helix-loop-helix factors recruit nuclear factor I to enhance expression of the NaV 1.4 Na+ channel gene.Biochimica et biophysica actaArticle
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Authors and funding
5 authors.
Funding
Abstract
Spatial segregation of membrane proteins is a feature of many excitable cells. In skeletal muscle, clusters of acetylcholine receptors (AChRs) and voltage-gated sodium channels (Na(V)1s) occupy distinct domains at the neuromuscular junction (NMJ). We used quantitative immunolabeling of developing rat soleus muscles to study the mechanism of ion channel segregation and Na(V)1 clustering at NMJs. When Na(V)1s can first be detected, at birth, they already occupy a postsynaptic domain that is distinct from that occupied by AChRs. At this time, Na(V)1s are expressed only in a diffuse area that extends 50-100 microm from the immature NMJ. However, in the region of the high-density AChR cluster at NMJ itself, Na(V)1s are actually present in lower density than in the immediately surrounding membrane. These distinctive features of the Na(V)1 distribution at birth are closely correlated with the distribution of ankyrinG immunolabeling. This suggests that an interaction with ankyrinG plays a role in the initial segregation of Na(V)1s from AChRs. Both Na(V)1 and ankyrinG become clustered at the NMJ itself 1-2 weeks after birth, coincident with the formation of postsynaptic folds. Syntrophin immunolabeling codistributes with AChRs and never resembles that for Na(V)1 or ankyrinG. Therefore, syntrophin is unlikely to play an important part in the initial accumulation of Na(V)1 at the NMJ. These findings suggest that the segregation of Na(V)1 from AChRs begins early in NMJ formation and occurs as a result of the physical exclusion of Na(V)1 and ankyrinG from the region of nerve-muscle contact rather than by a process of active clustering.
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12657669PMC6742006What OpenQuestion holds
Registered trials
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