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Complexins regulate a late step in Ca2+-dependent neurotransmitter release.

Cell | Jan 12, 2001

http://www.ncbi.nlm.nih.gov/pubmed/11163241

Synaptic vesicle fusion at synapses is triggered by increases in cytosolic Ca2+ levels. However, the identity of the Ca2+ sensor and the transduction mechanism of the Ca2+ trigger are unknown. We show that Complexins, stoichiometric components of the exocytotic core complex, are important regulators of transmitter release at a step immediately preceding vesicle fusion. Neurons lacking Complexins show a dramatically reduced transmitter release efficiency due to decreased Ca2+ sensitivity of the synaptic secretion process. Analyses of mutant neurons demonstrate that Complexins are acting at or following the Ca2+-triggering step of fast synchronous transmitter release by regulating the exocytotic Ca2+ sensor, its interaction with the core complex fusion machinery, or the efficiency of the fusion apparatus itself.

Pubmed ID: 11163241 RIS Download

Mesh terms: Adaptor Proteins, Vesicular Transport | Animals | Calcimycin | Calcium | Cells, Cultured | Excitatory Postsynaptic Potentials | Gene Deletion | Hippocampus | Ionophores | Mice | Mice, Mutant Strains | Microscopy, Electron | Nerve Tissue Proteins | Neuronal Plasticity | Neurons | Neurotransmitter Agents | Patch-Clamp Techniques | Synaptic Transmission | Synaptic Vesicles

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