Translating neuronal activity at the synapse: presynaptic calcium sensors in short-term plasticity.
The complex manner in which patterns of presynaptic neural activity are translated into short-term plasticity (STP) suggests the existence of multiple presynaptic calcium (Ca(2+)) sensors, which regulate the amplitude and time-course of STP and are the focus of this review. We describe two canonical Ca(2+)-binding protein domains (C2 domains and EF-hands) and define criteria that need to be met for a protein to qualify as a Ca(2+) sensor mediating STP. With these criteria in mind, we discuss various forms of STP and identify established and putative Ca(2+) sensors. We find that despite the multitude of proposed sensors, only three are well established in STP: Munc13, protein kinase C (PKC) and synaptotagmin-7. For putative sensors, we pinpoint open questions and potential pitfalls. Finally, we discuss how the molecular properties and modes of action of Ca(2+) sensors can explain their differential involvement in STP and shape net synaptic output.
Department of Neurobiology, Harvard Medical School Boston, MA, USA.
Arthur P H
AP
de Jong
Department of Neurobiology, Physiology and Behavior, Center for Neuroscience, University of California Davis Davis, CA, USA.
Diasynou
D
Fioravante
C2 domain; Munc13; calmodulin; post-tetanic potentiation; protein kinase C; residual calcium; short-term plasticity; synaptotagmin