Cytosolic Ca^<2+> Mobilization during In Vitro Ischemia in Mouse Hippocampal Neurons

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Cell calcium is thought to play a role in mediating ischemic neuronal damage. However, pathways of cytosolic Ca^<2+> increase in hippocampal neurons under the ischemic conditions are well unknown, although there are reports on the contribution of Ca^<2+> influx through ionotropic glutamate receptors (GluR). In this study, we monitored cytosolic Ca^<2+> concentrations during in vitro ischemia in hippocampal slice or single CAl neurons isolated from hippocampus of mice using fluorescence measurements of a Ca^<2+> -sensitive dye fura-2. In vitro ischemia (O_2/glucose deprivation) induced a cytosolic Ca^<2+> increase in the hippocampal slice of mice, especially CAl region. The isohemia-induced Ca^<2+> response was depressed by dantrolene, a blocker^<2+> release of Ca from calcium stores, or by depletion of Ca^<2+> in the stores with cyclopiazonic acid, but not by ionotropic GluR antagonists, MK-801 and CNQX. The ischemia-induced Ca^<2+> response was also observed in single CAl neurons isolated from hippocampus. These results suggest that the Ca^<2+> increase in the hippocampal neurons may be caused by Ca^<2+> release from calcium stores but not by Ca^<2+> influx through GluR channels during an early state of ischemia.
日本組織細胞化学会の論文