ArticleCommunications biology2023
The release of inhibition model reproduces kinetics and plasticity of neurotransmitter release in central synapses.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.Cell reports · 2026Article
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- Bacterial zinc metalloproteases as facilitators of pathogenic success: a review.Archives of microbiology · 2026Review
- Phosphorylation of SNAP-25 at Ser187 is enhanced following its cleavage by Botulinum Neurotoxin Serotype A, promoting the dominant-negative effect of the resulting fragment.PLoS pathogens · 2025Article
- Magnetic Cell-Mimetic Droplet Microrobots with Division and Exocytosis Capabilities.Research (Washington, D.C.) · 2025Article
- Minimal presynaptic protein machinery governing diverse kinetics of calcium-evoked neurotransmitter release.Nature communications · 2024Article
- Redefining Roles: A Paradigm Shift in Tryptophan-Kynurenine Metabolism for Innovative Clinical Applications.International journal of molecular sciences · 2024Review
- Synaptotagmins 3 and 7 mediate the majority of asynchronous release from synapses in the cerebellum and hippocampus.Cell reports · 2024Article
- A minimal presynaptic protein machinery mediating synchronous and asynchronous exocytosis and short-term plasticity.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Calcium-evoked release of neurotransmitters from synaptic vesicles (SVs) is catalysed by SNARE proteins. The predominant view is that, at rest, complete assembly of SNARE complexes is inhibited ('clamped') by synaptotagmin and complexin molecules. Calcium binding by synaptotagmins releases this fusion clamp and triggers fast SV exocytosis. However, this model has not been quantitatively tested over physiological timescales. Here we describe an experimentally constrained computational modelling framework to quantitatively assess how the molecular architecture of the fusion clamp affects SV exocytosis. Our results argue that the 'release-of-inhibition' model can indeed account for fast calcium-activated SV fusion, and that dual binding of synaptotagmin-1 and synaptotagmin-7 to the same SNARE complex enables synergistic regulation of the kinetics and plasticity of neurotransmitter release. The developed framework provides a powerful and adaptable tool to link the molecular biochemistry of presynaptic proteins to physiological data and efficiently test the plausibility of calcium-activated neurotransmitter release models.
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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.