Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 9 March 2010
Vol. 3, Issue 112, p. ec76
[DOI: 10.1126/scisignal.3112ec76]


Neuroscience Reexamining Glial Function

Peter R. Stern

Science, AAAS, Cambridge CB2 1LQ, UK

In the past 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. (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 did not affect synaptic transmission or short- and long-term synaptic plasticity.

C. Agulhon, T. A. Fiacco, K. D. McCarthy, Hippocampal short- and long-term plasticity are not modulated by astrocyte Ca2+ signaling. Science 327, 1250–1254 (2010). [Abstract] [Full Text]

F. Kirchhoff, Questionable calcium. Science 327, 1212–1213 (2010). [Summary] [Full Text]

Citation: P. R. Stern, Reexamining Glial Function. Sci. Signal. 3, ec76 (2010).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882