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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 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


  • Reim K
  • Mansour M
  • Varoqueaux F
  • McMahon HT
  • S├╝dhof TC
  • Brose N
  • Rosenmund C



Publication Data

January 12, 2001

Associated Grants


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