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

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...

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Bibliographic Details
Published in:Cell 2001-01, Vol.104 (1), p.71-81
Main Authors: Reim, K, Mansour, M, Varoqueaux, F, McMahon, H T, Südhof, T C, Brose, N, Rosenmund, C
Format: Article
Language:English
Subjects:
Adaptor Proteins, Vesicular Transport
Animals
Calcimycin - pharmacology
Calcium - metabolism
Cells, Cultured
Excitatory Postsynaptic Potentials - drug effects
Excitatory Postsynaptic Potentials - physiology
Gene Deletion
Hippocampus - cytology
Ionophores - pharmacology
Mice
Mice, Mutant Strains
Microscopy, Electron
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Neuronal Plasticity - physiology
Neurons - physiology
Neurons - ultrastructure
Neurotransmitter Agents - metabolism
Patch-Clamp Techniques
Synaptic Transmission - drug effects
Synaptic Transmission - physiology
Synaptic Vesicles - physiology
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Summary: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.
ISSN:0092-8674
DOI:10.1016/S0092-8674(01)00192-1