Table of Contents
ISRN Neurology
Volume 2011, Article ID 919043, 7 pages
Review Article

Ca2+/Calmodulin and Presynaptic Short-Term Plasticity

Department of Physiology, Tokyo Medical University, 1-1 Shinjuku-6-chome, Shinjuku-ku, Tokyo 160-8402, Japan

Received 22 March 2011; Accepted 18 April 2011

Academic Editors: L. Srivastava and F. G. Wouterlood

Copyright © 2011 Sumiko Mochida. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Synaptic efficacy is remodeled by neuronal firing activity at the presynaptic terminal. Presynaptic activity-dependent changes in transmitter release induce postsynaptic plasticity, including morphological change in spine, gene transcription, and protein synthesis and trafficking. The presynaptic transmitter release is triggered and regulated by Ca2+, which enters through voltage-gated Ca2+ (CaV) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca2+ is sensed by Ca2+-binding proteins, among other potential actions, it mediates time- and space-dependent synaptic facilitation and depression via effects on CaV2 channel gating and vesicle replenishment in the readily releasable pool (RRP). Calmodulin, a Ca2+-sensor protein with an EF-hand motif that binds Ca2+, interacts with CaV2 channels and autoreceptors in modulation of SNARE-mediated exocytosis.