[HTML][HTML] Calmodulin and Munc13 form a Ca2+ sensor/effector complex that controls short-term synaptic plasticity
Cell, 2004•cell.com
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 [Ca 2+].
However, the underlying molecular mechanisms and the identity of the Ca 2+ sensor/effector
complexes involved are unclear. We now identify a conserved calmodulin binding site in …
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 [Ca 2+].
However, the underlying molecular mechanisms and the identity of the Ca 2+ sensor/effector
complexes involved are unclear. We now identify a conserved calmodulin binding site in …
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.
cell.com