Calmodulin and Munc13 form a Ca2+ sensor/effector complex that controls short-term synaptic plasticity

Cell. 2004 Aug 6;118(3):389-401. doi: 10.1016/j.cell.2004.06.029.


The efficacy of synaptic transmission between neurons can be altered transiently during neuronal network activity. This phenomenon of short-term plasticity is a key determinant of network properties; is involved in many physiological processes such as motor control, sound localization, or sensory adaptation; and is critically dependent on cytosolic [Ca2+]. However, the underlying molecular mechanisms and the identity of the Ca2+ sensor/effector complexes involved are unclear. We now identify a conserved calmodulin binding site in UNC-13/Munc13s, which are essential regulators of synaptic vesicle priming and synaptic efficacy. Ca2+ sensor/effector complexes consisting of calmodulin and Munc13s regulate synaptic vesicle priming and synaptic efficacy in response to a residual [Ca2+] signal and thus shape short-term plasticity characteristics during periods of sustained synaptic activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Binding Sites
  • Calcium / metabolism*
  • Calmodulin / metabolism*
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*


  • Calmodulin
  • Intracellular Signaling Peptides and Proteins
  • Nerve Tissue Proteins
  • Unc13b protein, mouse
  • Calcium