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Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH, UK

Correspondence to Baljit S. Khakh: bkhakh{at}mednet.ucla.edu

Brain astrocytes signal to each other and neurons. They use changes in their intracellular calcium levels to trigger release of transmitters into the extracellular space. These can then activate receptors on other nearby astrocytes and trigger a propagated calcium wave that can travel several hundred micrometers over a timescale of seconds. A role for endogenous ATP in calcium wave propagation in hippocampal astrocytes has been suggested, but the mechanisms remain incompletely understood. Here we explored how calcium waves arise and directly tested whether endogenously released ATP contributes to astrocyte calcium wave propagation in hippocampal astrocytes. We find that vesicular ATP is the major, if not the sole, determinant of astrocyte calcium wave propagation over distances between 100 and 250 µm, and 15 s from the point of wave initiation. These actions of ATP are mediated by P2Y1 receptors. In contrast, metabotropic glutamate receptors and gap junctions do not contribute significantly to calcium wave propagation. Our data suggest that endogenous extracellular astrocytic ATP can signal over broad spatiotemporal scales.

B.S. Khakh's present address is Department of Physiology, David Geffen School of Medicine, UCLA, 10833 Le Conte Ave., Los Angeles, CA 90095-1751.

Abbreviations used in this paper: CBX, carbenoxolone; FFA, flufenamic acid; FWHM, full width at half maximal height; MS, mechanical stimulation.

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