ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Alpha-latrotoxin stimulates a novel pathway of Ca2+-dependent synaptic exocytosis independent of the classical synaptic fusion machinery.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 53 citations in OpenAlex.
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- Alternative splicing controls teneurin-latrophilin interaction and synapse specificity by a shape-shifting mechanism.Nature communications · 2020Article
- Ablation of All Synaptobrevin vSNAREs Blocks Evoked But Not Spontaneous Neurotransmitter Release at Neuromuscular Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Alternative Transcription at Venom Genes and Its Role as a Complementary Mechanism for the Generation of Venom Complexity in the Common House Spider.Frontiers in ecology and evolution · 2019Article
- Teneurins and latrophilins: two giants meet at the synapse.Current opinion in structural biology · 2019Review
- Catching Latrophilin With Lasso: A Universal Mechanism for Axonal Attraction and Synapse Formation.Frontiers in neuroscience · 2019Review
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- Function Suggests Nano-Structure: Quantitative Structural Support for SNARE-Mediated Pore Formation.Neurotoxicity research · 2016Article
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- Structural Basis of Latrophilin-FLRT-UNC5 Interaction in Cell Adhesion.Structure (London, England : 1993) · 2015Article
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Alpha-latrotoxin induces neurotransmitter release by stimulating synaptic vesicle exocytosis via two mechanisms: (1) A Ca(2+)-dependent mechanism with neurexins as receptors, in which alpha-latrotoxin acts like a Ca(2+) ionophore, and (2) a Ca(2+)-independent mechanism with CIRL/latrophilins as receptors, in which alpha-latrotoxin directly stimulates the transmitter release machinery. Here, we show that the Ca(2+)-independent release mechanism by alpha-latrotoxin requires the synaptic SNARE-proteins synaptobrevin/VAMP and SNAP-25, and, at least partly, the synaptic active-zone protein Munc13-1. In contrast, the Ca(2+)-dependent release mechanism induced by alpha-latrotoxin does not require any of these components of the classical synaptic release machinery. Nevertheless, this type of exocytotic neurotransmitter release appears to fully operate at synapses, and to stimulate exocytosis of the same synaptic vesicles that participate in physiological action potential-triggered release. Thus, synapses contain two parallel and independent pathways of Ca(2+)-triggered exocytosis, a classical, physiological pathway that operates at the active zone, and a novel reserve pathway that is recruited only when Ca(2+) floods the synaptic terminal.
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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.