ReviewNeuron2013
Neurotransmitter release: the last millisecond in the life of a synaptic vesicle.
Review in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 690 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
690 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,207 citations in OpenAlex.
- Mass Spectrometry as a Quantitative Proteomic Analysis Tool for the Search for Temporal Lobe Epilepsy Biomarkers: A Systematic Review.International journal of molecular sciences · 2023Pooled it
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- Synapse-like specializations at dopamine release sites orchestrate efficient and precise neuromodulatory signaling.Science advances · 2026Article
- Astrocyte-Derived Extracellular Vesicles and the Evolution of Neural Complexity: Perspectives on Vesicle-Mediated Neuron-Glia Communication.Molecular neurobiology · 2026Review
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- Chromogranin A mediates glucocorticoid-induced enhancement of vesicular dopamine storage and secretion in PC12 cells.The Journal of biological chemistry · 2026Article
- Multimodal Imaging Reveals Rapid Catecholamine Uptake and Release by Neutrophils.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- The Synaptic Vesicle Priming Protein Munc13 Mediates Evoked Somatodendritic Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Resolving endogenous protein organization in cells with nanometer resolution.Nature communications · 2026Article
- Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons.Nature communications · 2026Article
- Prenatal cannabis exposure affects human fetal neurodevelopment: an integrated multi-omics study.bioRxiv : the preprint server for biology · 2026Article
- Article
- Genetic mutations and synaptic dysfunctions in social interaction disorders: insights from invertebrate models to humans.Metabolic brain disease · 2026Review
- Grain-Size-Controlled Resistive Switching Memories Enabling Domain-Specific Functionality for Real-Time Video Signal Processing.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
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- Signaling Connectomics: A Brain-wide Framework for Intercellular Communication.Experimental neurobiology · 2026Article
- A primordial synaptotagmin-independent function of complexin in regulated exocytosis.Nature communications · 2026Article
- Article
630 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
During an action potential, Ca(2+) entering a presynaptic terminal triggers synaptic vesicle exocytosis and neurotransmitter release in less than a millisecond. How does Ca(2+) stimulate release so rapidly and precisely? Work over the last decades revealed that Ca(2+) binding to synaptotagmin triggers release by stimulating synaptotagmin binding to a core fusion machinery composed of SNARE and SM proteins that mediates membrane fusion during exocytosis. Complexin adaptor proteins assist synaptotagmin by activating and clamping this core fusion machinery. Synaptic vesicles containing synaptotagmin are positioned at the active zone, the site of vesicle fusion, by a protein complex containing RIM proteins. RIM proteins activate docking and priming of synaptic vesicles and simultaneously recruit Ca(2+) channels to active zones, thereby connecting in a single complex primed synaptic vesicles to Ca(2+) channels. This architecture allows direct flow of Ca(2+) ions from Ca(2+) channels to synaptotagmin, which then triggers fusion, thus mediating tight millisecond coupling of an action potential to neurotransmitter release.
Indexed as
Identifiers
What OpenQuestion holds
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.