Research ArticleNeuroscience

Extracellular Ca2+ Acts as a Mediator of Communication from Neurons to Glia

Science Signaling  24 Jan 2012:
Vol. 5, Issue 208, pp. ra8
DOI: 10.1126/scisignal.2002160

You are currently viewing the editor's summary.

View Full Text

Log in

Calcium Signals Outside the Cell

Excitatory glutamatergic signaling is accompanied by calcium influx into neurons through voltage-dependent calcium channels and ionotropic glutamate receptors. The crucial role of calcium as an intracellular second messenger makes it easy to overlook the consequences of a localized decrease in extracellular calcium. Here, Torres et al. explored the functional consequences of a localized decrease in extracellular calcium in hippocampal slices. They found that a localized decrease in extracellular calcium—elicited either directly through activation of a photosensitive calcium buffer or secondary to glutamate-stimulated calcium influx in neurons—evoked astrocytic release of ATP, as did high-frequency stimulation, which elicited a comparable decrease in extracellular calcium. Moreover, decreased extracellular calcium increased the activity of inhibitory interneurons bearing purinergic receptors, suggesting that, under conditions of high-intensity glutamatergic signaling, a local decline in extracellular calcium could, by stimulating astrocyte calcium signals and ATP release, activate a compensatory increase in synaptic inhibition.