Hippocampal Short- and Long-Term Plasticity Are Not Modulated by Astrocyte Ca 2+ Signaling

Author:

Agulhon Cendra1,Fiacco Todd A.2,McCarthy Ken D.1

Affiliation:

1. Department of Pharmacology, University of North Carolina at Chapel Hill, Genetic Medicine Building, CB 7365, Chapel Hill, NC 27599, USA.

2. Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, CA 92521, USA.

Abstract

Reexamining Glial Function In the last 20 years glial cells have been elevated from being considered as passive elements during neuronal transmission. By eliciting astroglial calcium rises, so-called gliotransmitters such as glutamate, ATP, or d -serine can be released and the activity of neighboring neurons modulated. However, this emerging picture has been challenged. Agulhon et al. (p. 1250 ; see the Perspective by Kirchhoff ) reexamined these questions using two previously characterized mouse models. Calcium elevations induced selectively in astrocytes caused no change in multiple measures of synaptic activity. Furthermore, in mutant mice unable to elevate intracellular calcium, all synaptic measures were at wild-type levels. Astrocytic calcium signaling activity was thus not tied to the release of gliotransmitters and didn't affect synaptic transmission, short and long-term synaptic plasticity.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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