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Is astrocyte calcium signaling relevant for synaptic plasticity?

Published online by Cambridge University Press:  02 December 2010

Sarrah Ben Achour
Affiliation:
Ecole Normale Supérieure, Institut de Biologie de l'ENS, IBENS, Paris, France Inserm, U1024, Paris, France CNRS, UMR 8197, Paris, France
Lorena Pont-Lezica
Affiliation:
Ecole Normale Supérieure, Institut de Biologie de l'ENS, IBENS, Paris, France Inserm, U1024, Paris, France CNRS, UMR 8197, Paris, France
Catherine Béchade
Affiliation:
Ecole Normale Supérieure, Institut de Biologie de l'ENS, IBENS, Paris, France Inserm, U1024, Paris, France CNRS, UMR 8197, Paris, France
Olivier Pascual*
Affiliation:
Ecole Normale Supérieure, Institut de Biologie de l'ENS, IBENS, Paris, France Inserm, U1024, Paris, France CNRS, UMR 8197, Paris, France
*
Correspondence should be addressed to: Olivier Pascual, Ecole Normale Supérieure, 46 rue d'Ulm, 75005Paris email: olivier.pascual@biologie.ens.fr

Abstract

Astrocytes constitute a major group of glial cells which were long regarded as passive elements, fulfilling nutritive and structural functions for neurons. Calcium rise in astrocytes propagating to neurons was the first demonstration of direct interaction between the two cell types. Since then, calcium has been widely used, not only as an indicator of astrocytic activity but also as a stimulator switch to control astrocyte physiology. As a result, astrocytes have been elevated from auxiliaries to neurons, to cells involved in processing synaptic information. Curiously, while there is evidence that astrocytes play an important role in synaptic plasticity, the data relating to calcium's pivotal role are inconsistent. In this review, we will detail the various mechanisms of calcium flux in astrocytes, then briefly present the calcium-dependent mechanisms of gliotransmitter release. Finally, we will discuss the role of calcium in plasticity and present alternative explanations that could reconcile the conflicting results published recently.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2010

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Footnotes

*

These authors contributed equally to this work.

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