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The Journal of Neuroscience, October 29, 2003, 23(30):9888-9896
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Cellular/Molecular
Different Mechanisms Promote Astrocyte Ca2+ Waves and Spreading Depression in the Mouse Neocortex
Oliver Peters,1 Carola G. Schipke,1 Yoshinori Hashimoto,2 andHelmut Kettenmann1 1Max-Delbrück Center for Molecular Medicine, Cellular Neuroscience, D-13092 Berlin, Germany, and 2Laboratory of Cellular Neurobiology, Tokyo University of Pharmacy & Life Science, Hachioji, Tokyo 192-0392, Japan
Cortical spreading depression (CSD) is thought to play an important role in different pathological conditions of the human brain. Here we investigated the interaction between CSD and Ca2+ waves within the astrocyte population in slices from mouse neocortex (postnatal days 10–14). After local KCl ejection as a trigger for CSD, we recorded the propagation of Ca2+ increases within a large population of identified astrocytes in synchrony with CSD measured as intrinsic optical signal (IOS) or negative DC-potential shift. The two events spread with 39.2 ± 3.3 µm/sec until the IOS and negative DC-potential shift decayed after
1 mm. However, the astrocyte Ca2+ wave continued to propagate for up to another 500µm but with a reduced speed of 18.3 ± 2.5µm/sec that is also typical for glial Ca2+ waves in white matter or culture. While blocking CSD using MK-801 (40 µM), an NMDA-receptor antagonist, the astrocyte Ca2+ wave persisted with a reduced speed (13.2 ± 1.5µm/sec). The specific gap junction blocker carbenoxolon (100µM) did not prevent CSD but decelerated the speed (2.9 ± 0.9µm/sec) of the astrocyte Ca2+ wave in the periphery of CSD. We also found that interfering with intracellular astrocytic Ca2+ signaling by depletion of internal Ca2+ stores does not affect the spread of the IOS. We conclude that CSD determines the velocity of an accompanying astrocytic Ca2+ response, but the astrocyte Ca2+ wave penetrates a larger territory and by this represents a self-reliant phenomenon with a different mechanism of propagation.
Key words: glia; neocortex; gap junctions; intrinsic optical signals; migraine; stroke
Received July 17, 2003; revised September 5, 2003; accepted September 5, 2003.
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