ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Paralytic zebrafish lacking acetylcholine receptors fail to localize rapsyn clusters to the synapse.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 123 citations in OpenAlex.
- CaOpen biology · 2025Article
- Normal locomotion in zebrafish lacking the sodium channel NaV1.4 suggests that the need for muscle action potentials is not universal.PLoS biology · 2025Article
- Spatially ordered recruitment of fast muscles in accordance with movement strengths in larval zebrafish.Zoological letters · 2025Article
- Article
- Neuropeptidergic regulation of neuromuscular signaling in larval zebrafish alters swimming behavior and synaptic transmission.iScience · 2024Article
- Context-dependent hyperactivity inFrontiers in molecular neuroscience · 2024Article
- A forward genetic screen identifies Dolk as a regulator of startle magnitude through the potassium channel subunit Kv1.1.PLoS genetics · 2021Article
- Primary and secondary motoneurons use different calcium channel types to control escape and swimming behaviors in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Synaptic silencing of fast muscle is compensated by rewired innervation of slow muscle.Science advances · 2020Article
- αM-Conotoxin MIIIJ Blocks Nicotinic Acetylcholine Receptors at Neuromuscular Junctions of Frog and Fish.Toxins · 2020Article
- Zebrafish neuromuscular junction: The power of N.Neuroscience letters · 2019Review
- The synaptic receptor Lrp4 promotes peripheral nerve regeneration.Nature communications · 2018Article
- The beta-adrenergic agonist salbutamol modulates neuromuscular junction formation in zebrafish models of human myasthenic syndromes.Human molecular genetics · 2018Article
- Expressing acetylcholine receptors after innervation suppresses spontaneous vesicle release and causes muscle fatigue.Scientific reports · 2017Article
- Cone signals in monostratified and bistratified amacrine cells of adult zebrafish retina.The Journal of comparative neurology · 2017Article
- A Gradient in Synaptic Strength and Plasticity among Motoneurons Provides a Peripheral Mechanism for Locomotor Control.Current biology : CB · 2017Article
- Zebrafish: A Model for the Study of Toxicants Affecting Muscle Development and Function.International journal of molecular sciences · 2016Review
- Fatigue in Rapsyn-Deficient Zebrafish Reflects Defective Transmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- A circuit motif in the zebrafish hindbrain for a two alternative behavioral choice to turn left or right.eLife · 2016Article
- Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Physiological analysis of two lines of paralytic mutant zebrafish, relaxed and sofa potato, reveals defects in distinct types of receptors in skeletal muscle. In sofa potato the paralysis results from failed synaptic transmission because of the absence of acetylcholine receptors, whereas relaxed mutants lack dihydropyridine receptor-mediated release of internal calcium in response to the muscle action potential. Synaptic structure and function appear normal in relaxed, showing that muscle paralysis per se does not impede proper synapse development. However, sofa potato mutants show incomplete development of the postsynaptic complex. Specifically, in the absence of ACh receptors, clusters of the receptor-aggregating protein rapsyn form in the extrasynaptic membrane but generally fail to localize to the subsynaptic region. Our results indicate that, although rapsyn molecules are capable of self-aggregation, interaction with ACh receptors is required for proper subsynaptic localization.
Indexed as
Identifiers
11466415PMC6762670W1943218535What 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.