ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
A single mutation in the acetylcholine receptor δ-subunit causes distinct effects in two types of neuromuscular synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 18 citations in OpenAlex.
- CaOpen biology · 2025Article
- Palisade Endings Have an Exocytotic Machinery But Lack Acetylcholine Receptors and Distinct Acetylcholinesterase Activity.Investigative ophthalmology & visual science · 2020Article
- Synaptic silencing of fast muscle is compensated by rewired innervation of slow muscle.Science advances · 2020Article
- Early Exposure to THC Alters M-Cell Development in Zebrafish Embryos.Biomedicines · 2020Article
- Expressing acetylcholine receptors after innervation suppresses spontaneous vesicle release and causes muscle fatigue.Scientific reports · 2017Article
- Zebrafish mutants of the neuromuscular junction: swimming in the gene pool.The journal of physiological sciences : JPS · 2015Review
- "Slow" skeletal muscles across vertebrate species.Cell & bioscience · 2015Review
- Inherited disorders of the neuromuscular junction: an update.Journal of neurology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in AChR subunits, expressed as pentamers in neuromuscular junctions (NMJs), cause various types of congenital myasthenic syndromes. In AChR pentamers, the adult ε subunit gradually replaces the embryonic γ subunit as the animal develops. Because of this switch in subunit composition, mutations in specific subunits result in synaptic phenotypes that change with developmental age. However, a mutation in any AChR subunit is considered to affect the NMJs of all muscle fibers equally. Here, we report a zebrafish mutant of the AChR δ subunit that exhibits two distinct NMJ phenotypes specific to two muscle fiber types: slow or fast. Homozygous fish harboring a point mutation in the δ subunit form functional AChRs in slow muscles, whereas receptors in fast muscles are nonfunctional. To test the hypothesis that different subunit compositions in slow and fast muscles underlie distinct phenotypes, we examined the presence of ε/γ subunits in NMJs using specific antibodies. Both wild-type and mutant larvae lacked ε/γ subunits in slow muscle synapses. These findings in zebrafish suggest that some mutations in human congenital myasthenic syndromes may affect slow and fast muscle fibers differently.
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Registered trials
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