ArticleNature communications2017
Munc13-1 and Munc18-1 together prevent NSF-dependent de-priming of synaptic vesicles.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed.
- Reorganization of synchronous and asynchronous release in developing hippocampal autaptic neurons of mice.Physiological reports · 2026Article
- NSF is required for diverse endocytic modes by promoting fusion and fission pore closure in secretory cells.iScience · 2026Article
- SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.Cell reports · 2026Article
- Initial Distance-Dependent Mean Force Drives Synaptic Vesicle Motion Toward Fusion Sites in Stimulated Hippocampal Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Pathogenic UNC13A variants cause a neurodevelopmental syndrome by impairing synaptic function.Nature genetics · 2025Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
- Complexin gains effective access to the assembling SNAREs via its membrane-binding C-terminal domain.The Journal of physiology · 2025Article
- RIM and MUNC13 membrane-binding domains are essential for neuropeptide secretion.The Journal of cell biology · 2025Article
- Beyond the MUN domain, Munc13 controls priming and depriming of synaptic vesicles.Cell reports · 2024Article
- Differential SNARE chaperoning by Munc13-1 and Munc18-1 dictates fusion pore fate at the release site.Nature communications · 2024Article
- Interpretation of presynaptic phenotypes of synaptic plasticity in terms of a two-step priming process.The Journal of general physiology · 2024Article
- Expression and function of Caenorhabditis elegans UNCP-18, a paralog of the SM protein UNC-18.Genetics · 2023Article
- Fully-primed slowly-recovering vesicles mediate presynaptic LTP at neocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Altered synaptic connectivity in an in vitro human model of STXBP1 encephalopathy.Brain : a journal of neurology · 2023Article
- Article
- Optogenetics and electron tomography for structure-function analysis of cochlear ribbon synapses.eLife · 2022Article
- Listeria monocytogenes Co-Opts the Host Exocyst Complex To Promote Internalin A-Mediated Entry.Infection and immunity · 2022Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic transmission requires a stable pool of release-ready (primed) vesicles. Here we show that two molecules involved in SNARE-complex assembly, Munc13-1 and Munc18-1, together stabilize release-ready vesicles by preventing de-priming. Replacing neuronal Munc18-1 by a non-neuronal isoform Munc18-2 (Munc18-1/2SWAP) supports activity-dependent priming, but primed vesicles fall back into a non-releasable state (de-prime) within seconds. Munc13-1 deficiency produces a similar defect. Inhibitors of N-ethylmaleimide sensitive factor (NSF), N-ethylmaleimide (NEM) or interfering peptides, prevent de-priming in munc18-1/2SWAP or munc13-1 null synapses, but not in CAPS-1/2 null, another priming-deficient mutant. NEM rescues synaptic transmission in munc13-1 null and munc18-1/2SWAP synapses, in acute munc13-1 null slices and even partially in munc13-1/2 double null synapses. Together these data indicate that Munc13-1 and Munc18-1, but not CAPS-1/2, stabilize primed synaptic vesicles by preventing NSF-dependent de-priming.
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