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A dual-Ca2+-sensor model for neurotransmitter release in a central synapse.

Ca2+-triggered synchronous neurotransmitter release is well described, but asynchronous release-in fact, its very existence-remains enigmatic. Here we report a quantitative description of asynchronous neurotransmitter release in calyx-of-Held synapses. We show that deletion of synaptotagmin 2 (Syt2) in mice selectively abolishes synchronous release, allowing us to study pure asynchronous release in isolation. Using photolysis experiments of caged Ca2+, we demonstrate that asynchronous release displays a Ca2+ cooperativity of approximately 2 with a Ca2+ affinity of approximately 44 microM, in contrast to synchronous release, which exhibits a Ca2+ cooperativity of approximately 5 with a Ca2+ affinity of approximately 38 muM. Our results reveal that release triggered in wild-type synapses at low Ca2+ concentrations is physiologically asynchronous, and that asynchronous release completely empties the readily releasable pool of vesicles during sustained elevations of Ca2+. We propose a dual-Ca2+-sensor model of release that quantitatively describes the contributions of synchronous and asynchronous release under conditions of different presynaptic Ca2+ dynamics.

Pubmed ID: 18046404


  • Sun J
  • Pang ZP
  • Qin D
  • Fahim AT
  • Adachi R
  • S├╝dhof TC



Publication Data

November 29, 2007

Associated Grants

  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Action Potentials
  • Animals
  • Calcium
  • Kinetics
  • Mice
  • Mice, Knockout
  • Neurotransmitter Agents
  • Photolysis
  • Presynaptic Terminals
  • Synapses
  • Synaptic Transmission
  • Synaptotagmin II