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The role of Synaptobrevin1/VAMP1 in Ca 2+ ‐triggered neurotransmitter release at the mouse neuromuscular junction
Author(s) -
Liu Yun,
Sugiura Yoshie,
Lin Weichun
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.201939
Subject(s) - neuromuscular junction , neurotransmission , synaptic vesicle , neurotransmitter , neuromuscular transmission , neuroscience , microbiology and biotechnology , biology , synaptobrevin , synaptic cleft , motor nerve , vesicle , endocrinology , central nervous system , biochemistry , membrane , receptor
Non‐technical summary The neuromuscular junction (NMJ) is the synaptic connection between the nerve and the muscle. The neuromuscular synaptic transmission is highly reliable, as each nerve impulse results in the release of more neurotransmitter than is required for evoking an action potential in the muscle. This feature, often referred as the ‘safety factor’, ensures that a muscle contraction will occur in response to each nerve impulse under normal physiological conditions. Here we show that a small, integral membrane protein of synaptic vesicles, named synaptobrevin (Syb)/vesicle‐associated membrane protein (VAMP), is required for optimum synaptic transmission at the NMJ. A genetic mutation in Syb1/VAMP1 in mice causes marked reduction of neurotransmitter release at the NMJ, suggesting an important role for Syb1/VAMP1 in maintaining the ‘safety factor’ of the NMJ.