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.
Department of Molecular Neurobiology, Max-Planck-Institute for Experimental Medicine, Hermann-Rein-Strasse 3, D-37077 Göttingen, Germany.
Harald J
HJ
Junge
Jeong-Seop
JS
Rhee
Olaf
O
Jahn
Frederique
F
Varoqueaux
Joachim
J
Spiess
M Neal
MN
Waxham
Christian
C
Rosenmund
Nils
N
Brose
D000818:Animals; D001665:Binding Sites; D002118:Calcium / Q000378:metabolism*; D002147:Calmodulin / Q000378:metabolism*; D047908:Intracellular Signaling Peptides and Proteins; D051379:Mice; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*
D002147:Calmodulin; D047908:Intracellular Signaling Peptides and Proteins; D009419:Nerve Tissue Proteins; C485549:Unc13b protein, mouse; D002118:Calcium