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Genetic analysis of synaptotagmin 2 in spontaneous and Ca2+-triggered neurotransmitter release.

Synaptotagmin 2 resembles synaptotagmin 1, the Ca2+ sensor for fast neurotransmitter release in forebrain synapses, but little is known about synaptotagmin 2 function. Here, we describe a severely ataxic mouse strain that harbors a single, destabilizing amino-acid substitution (I377N) in synaptotagmin 2. In Calyx of Held synapses, this mutation causes a delay and a decrease in Ca2+-induced but not in hypertonic sucrose-induced release, suggesting that synaptotagmin 2 mediates Ca2+ triggering of evoked release in brainstem synapses. Unexpectedly, we additionally observed in synaptotagmin 2 mutant synapses a dramatic increase in spontaneous release. Synaptotagmin 1-deficient excitatory and inhibitory cortical synapses also displayed a large increase in spontaneous release, demonstrating that this effect was shared among synaptotagmins 1 and 2. Our data suggest that synaptotagmin 1 and 2 perform equivalent functions in the Ca2+ triggering of action potential-induced release and in the restriction of spontaneous release, consistent with a general role of synaptotagmins in controlling 'release slots' for synaptic vesicles at the active zone.

Pubmed ID: 16642042


  • Pang ZP
  • Sun J
  • Rizo J
  • Maximov A
  • S├╝dhof TC


The EMBO journal

Publication Data

May 17, 2006

Associated Grants


Mesh Terms

  • Action Potentials
  • Amino Acid Sequence
  • Animals
  • Ataxia
  • Brain
  • Calcium
  • In Vitro Techniques
  • Mice
  • Molecular Sequence Data
  • Neurons
  • Neurotransmitter Agents
  • Patch-Clamp Techniques
  • Point Mutation
  • Protein Denaturation
  • Protein Structure, Tertiary
  • Sequence Alignment
  • Synapses
  • Synaptic Transmission
  • Synaptotagmin I
  • Synaptotagmin II