ArticleThe Journal of physiology2011
The role of synaptobrevin1/VAMP1 in Ca2+-triggered neurotransmitter release at the mouse neuromuscular junction.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
- Structural and Molecular Features of Human Extraocular Muscle Spindles Suggest a Unique Role in Proprioception.Investigative ophthalmology & visual science · 2026Article
- Presynaptic Congenital Myasthenic Syndromes.Muscle & nerve · 2026Review
- In Vivo Positron Emission Tomography Imaging of Presynaptic Density Reveals Stress-Associated Synaptic Deficits Related to Behavioral and Molecular Alterations in Rats.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2026Article
- HSAInternational journal of molecular sciences · 2025Article
- Bltp1 Is Required for Survival and Normal Development and Function of the Neuromuscular Junction in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Beyond the Genotype: A Multi-Omic Analysis of APOEe4's Role in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Chronic variable mild stress alters the transcriptome and signaling properties of the anterodorsal bed nucleus of the stria terminalis in a sex-dependent manner.Journal of neuroendocrinology · 2025Article
- Expanding the genetic and phenotypic spectrum of congenital myasthenic syndrome: new homozygous VAMP1 splicing variants in 2 novel individuals.Journal of human genetics · 2024Article
- Morphological and functional alterations of neuromuscular synapses in a mouse model of ACTA1 congenital myopathy.Human molecular genetics · 2024Article
- Fast, precise and cloning-free knock-in of reporter sequences in vivo with high efficiency.Development (Cambridge, England) · 2023Article
- Presynaptic Congenital Myasthenic Syndromes: Understanding Clinical Phenotypes through In vivo Models.Journal of neuromuscular diseases · 2023Review
- Similarity and Diversity of Presynaptic Molecules at Neuromuscular Junctions and Central Synapses.Biomolecules · 2022Review
- The function of VAMP2 in mediating membrane fusion: An overview.Frontiers in molecular neuroscience · 2022Review
- Proteomic and Bioinformatic Analysis of Decellularized Pancreatic Extracellular Matrices.Molecules (Basel, Switzerland) · 2021Article
- Palisade Endings Have an Exocytotic Machinery But Lack Acetylcholine Receptors and Distinct Acetylcholinesterase Activity.Investigative ophthalmology & visual science · 2020Article
- Tetanus insensitive VAMP2 differentially restores synaptic and dense core vesicle fusion in tetanus neurotoxin treated neurons.Scientific reports · 2020Article
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- Ablation of All Synaptobrevin vSNAREs Blocks Evoked But Not Spontaneous Neurotransmitter Release at Neuromuscular Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Mutations in the Neuronal Vesicular SNARE VAMP2 Affect Synaptic Membrane Fusion and Impair Human Neurodevelopment.American journal of human genetics · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Synaptobrevin (Syb)/vesicle-associated membrane protein (VAMP) is a small, integral membrane protein of synaptic vesicles. Two homologous isoforms of synaptobrevin, Syb1/VAMP1 and Syb2/VAMP2, exhibit distinct but partially overlapping patterns of expression in adult mammalian neurons: Syb1 is predominantly expressed in the spinal cord, especially in motor neurons and motor nerve terminals of the neuromuscular junction (NMJ), whereas Syb2 is primarily expressed in central synapses in the brain. Whereas many studies have focused on the function of Syb2 in the brain, few studies have examined the role of Syb1. Here we report that Syb1 plays a critical role in neuromuscular synaptic transmission. A null mutation of Syb1 resulting from a spontaneous, nonsense mutation in mice significantly impairs the function, but not the structure, of the NMJ. In particular, both spontaneous and evoked synaptic activities in Syb1 mutant mice are reduced significantly relative to control mice. Short-term synaptic plasticity in Syb1-deficient NMJs is markedly altered: paired-pulse facilitation is significantly enhanced, suggesting a reduction in the initial release probability of synaptic vesicles. Furthermore, Syb1-deficient NMJs display a pronounced asynchrony in neurotransmitter release. These impairments are not due to an alteration of the size of the readily releasable pool of vesicles, but are attributable to reduced sensitivity and cooperativity to calcium (Ca2+) due to the absence of Syb1. Our findings demonstrate that Syb1 plays an essential, non-redundant role in Ca2+-triggered vesicle exocytosis at the mouse NMJ.
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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.