ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Complexin controls spontaneous and evoked neurotransmitter release by regulating the timing and properties of synaptotagmin activity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 136 citations in OpenAlex.
- Beyond the structure-function paradigm: A comprehensive review of intrinsically disordered proteins.Biochemistry and biophysics reports · 2026Review
- Postsynaptic Complexin Mediates Constitutive Exocytosis of Nicotinic Acetylcholine Receptor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Disease-causing mutations in Synaptotagmin can act via dominant-negative, gain-of-function or haploinsufficient mechanisms.bioRxiv : the preprint server for biology · 2026Article
- Article
- Presynaptic quantal size enhancement counteracts post-tetanic release depression.The Journal of physiology · 2025Article
- Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Using multiscale molecular dynamics simulations to explore the fusion machinery underlying neurotransmitter release.Quarterly reviews of biophysics · 2025Review
- The exocytosis regulator complexin controls spontaneous synaptic vesicle release in a CAPS-dependent manner at C. elegans excitatory synapses.PLoS biology · 2025Article
- Molecular Dynamics Simulations of the SNARE Complex Interacting with Synaptotagmin, Complexin, and Lipid Bilayers.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Complexin regulation of synaptic vesicle release: mechanisms in the central nervous system and specialized retinal ribbon synapses.Cell communication and signaling : CCS · 2024Review
- Article
- Dynamic formation of the protein-lipid prefusion complex.Biophysical journal · 2024Article
- Mutations of Single Residues in the Complexin N-terminus Exhibit Distinct Phenotypes in Synaptic Vesicle Fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Dynamic Formation of the Protein-Lipid Pre-fusion Complex.bioRxiv : the preprint server for biology · 2024Article
- Frequency of Spontaneous Neurotransmission at Individual Boutons Corresponds to the Size of the Readily Releasable Pool of Vesicles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release.Cell reports · 2023Article
- Loss of the extracellular matrix protein Perlecan disrupts axonal and synaptic stability duringeLife · 2023Article
- Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release.bioRxiv : the preprint server for biology · 2023Article
- Review
- Molecular Logic of Synaptic Diversity BetweenbioRxiv : the preprint server for biology · 2023Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Neurotransmitter release following synaptic vesicle (SV) fusion is the fundamental mechanism for neuronal communication. Synaptic exocytosis is a specialized form of intercellular communication that shares a common SNARE-mediated fusion mechanism with other membrane trafficking pathways. The regulation of synaptic vesicle fusion kinetics and short-term plasticity is critical for rapid encoding and transmission of signals across synapses. Several families of SNARE-binding proteins have evolved to regulate synaptic exocytosis, including Synaptotagmin (SYT) and Complexin (CPX). Here, we demonstrate that Drosophila CPX controls evoked fusion occurring via the synchronous and asynchronous pathways. cpx(-/-) mutants show increased asynchronous release, while CPX overexpression largely eliminates the asynchronous component of fusion. We also find that SYT and CPX coregulate the kinetics and Ca(2+) co-operativity of neurotransmitter release. CPX functions as a positive regulator of release in part by coupling the Ca(2+) sensor SYT to the fusion machinery and synchronizing its activity to speed fusion. In contrast, syt(-/-); cpx(-/-) double mutants completely abolish the enhanced spontaneous release observe in cpx(-/-) mutants alone, indicating CPX acts as a fusion clamp to block premature exocytosis in part by preventing inappropriate activation of the SNARE machinery by SYT. CPX levels also control the size of synaptic vesicle pools, including the immediate releasable pool and the ready releasable pool-key elements of short-term plasticity that define the ability of synapses to sustain responses during burst firing. These observations indicate CPX regulates both spontaneous and evoked fusion by modulating the timing and properties of SYT activation during the synaptic vesicle cycle.
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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.