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Cell. 2004 Aug 6;118(3):389-401.

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

Author information

1
Department of Molecular Neurobiology, Max-Planck-Institute for Experimental Medicine, Hermann-Rein-Strasse 3, D-37077 Göttingen, Germany.

Abstract

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.

PMID:
15294163
DOI:
10.1016/j.cell.2004.06.029
[Indexed for MEDLINE]
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