Gap junctions are highly conductive channels that allow the direct transfer of intracellular messengers such as Ca 2 � and inositol triphosphate (IP 3) between interconnected cells. In brain, astrocytes are coupled extensively by gap junctions. We found here that gap junctions among astrocytes in acutely prepared brain slices as well as in culture remained open during ischemic conditions. Uncoupling first occurred after the termi-When local cerebral blood flow declines to �15–20 % of normal, anoxic depolarization ensues (Astrup et al., 1977). Within minutes both neurons and astrocytes are depleted of cellular energy metabolites and lose their ability to regulate transmembrane ion gradients (Hansen, 1985). Ionic homeostasis is lost, and all cell types are killed during the resultant ischemic infarction (Siesjo, 1992; Ginsberg, 1995). Several lines of evidence indicate that the evolving infarct gradually expands: cells in the ischemic core lose viability first, whereas more peripherally located, better perfused regions are recruited to the infarct only at a later stage (Hossmann, 1996). It has been estimated that an ischemic lesion achieves its final size 4–8 hr after arterial occlusion in rodents but that the same process lasts several days in human brain (Ginsberg, 1995). It is possible to limit the extent of infarction without changing either the duration or degree of ischemia. A variety of interventions may control an ischemic lesion, including blocking NMDA receptor-linked calcium channels (Park, 1988; Siesjo, 1992), increasing cellular calcium buffers (Tymianski et al., 1993), lowering brain temperature (Dietrich et al., 1996), reducing freeradical formation (Pelligrini-Giampietro et al., 1990; Chan, 1994), and decreasing the frequency of spontaneous waves of spreadin
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