Calcium Signaling in Dendritic Spines

  1. Bernardo L. Sabatini2
  1. 1Department of Neurobiology, Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale School of Medicine, New Haven, Connecticut 06520
  2. 2Howard Hughes Medical Institute, Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115
  1. Correspondence: bsabatini{at}hms.harvard.edu

Abstract

Calcium (Ca2+) is a ubiquitous signaling molecule that accumulates in the cytoplasm in response to diverse classes of stimuli and, in turn, regulates many aspects of cell function. In neurons, Ca2+ influx in response to action potentials or synaptic stimulation triggers neurotransmitter release, modulates ion channels, induces synaptic plasticity, and activates transcription. In this article, we discuss the factors that regulate Ca2+ signaling in mammalian neurons with a particular focus on Ca2+ signaling within dendritic spines. This includes consideration of the routes of entry and exit of Ca2+, the cellular mechanisms that establish the temporal and spatial profile of Ca2+ signaling, and the biophysical criteria that determine which downstream signals are activated when Ca2+ accumulates in a spine. Furthermore, we also briefly discuss the technical advances that made possible the quantitative study of Ca2+ signaling in dendritic spines.



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      1. Cold Spring Harb. Perspect. Biol. 4: a005686 Copyright © 2012 Cold Spring Harbor Laboratory Press; all rights reserved

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