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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Calmodulin and Munc13 form a Ca2+ sensor/effector complex that controls short-term synaptic plasticity. Junge, H.J., Rhee, J.S., Jahn, O., Varoqueaux, F., Spiess, J., Waxham, M.N., Rosenmund, C., Brose, N. Cell (2004) [Pubmed]
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