Regulation Of BK Channel On Intracellular Ca~ (2+) Level And Neuronal Cells Apoptosis After Focal Cerebral Ischemia Injury In Rats

objectives: To investigate the regulation of BK channel on intracelullar free calcium concentration [Ca²⁺]i and apoptosis in neuronal cells in the rat brain following focalcerebral ischemia injury.Methods: Seventy-two SD rats were randomly assigned to sham group (n=36), ischemic reperfusion group (n=36), IBTX group (n=36). The focal cerebral ischemia model was produced by occluding middle cerebral artery occlusion (MCAO) for 90min and reperfusing 6h(n=12), 12h(n=12), 24h (n=12) respectively. Compared neurological function defect and infarct size of different groups at the same reperfusing time. Laser scanning confocal microscope imaging of the calcium fluorescent indicator dye Fluo3/ AM was used to determine the changes of [Ca²⁺] in neurons, the expression of BK tunnel was investigated by immunohistochemistry and neuronal cells apoptosis were measured by TUNEL.Results: The neurological deficit scores in IBTX group at each time point were obviously higher than in sham group and ischemic reperfusion group(P<0.05). The brain infarct volume was larger than sham group and ischemic reperfusion group(P<0.05). The [Ca²⁺]i and the cell apoptosis rate of IBTX group had significant difference at the corresponding time point compared with other two groups (P<0.05). The results of immunohistochemistry indicate that the expression of BK channel in ischemic reperfusion group decreased,but the defference between three groups was not different significantly.Conclusion: BK channels could inhibit significantly the ascension of [Ca²⁺]i and decrease neurons apotosis.