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目的 :研究两种钙离子通道 :NMDA受体型和L 型电压门控钙通道 (L VGCC)在短暂全脑缺血复灌后海马c Jun表达中的作用。方法 :采用SD大鼠四动脉结扎全脑缺血模型 ,取缺血复灌不同时间 (0 ,1,3,6 ,12 ,2 4和72h)以及对照组SD大鼠的海马 ,应用免疫印迹的方法来研究c Jun的表达并观察几种钙通道拮抗剂对c Jun表达的影响。 结果 :c Jun在假手术以及复灌的各个时间点均有表达 ,并在复灌 6h达到高峰。氯胺酮 (一种非竞争性NMDA受体拮抗剂 )和硝苯吡啶 (一种L VGCC阻滞剂 )抑制c Jun表达的增加。而DNQX(一种AMPA/KA受体拮抗剂 )则无抑制作用 (数据未显示 )。 结论 :缺血复灌后 ,c Jun的表达增加了 ,这种增加与NMDA受体和L VGCC这两种钙离子通道的开放有关。
AIM: To investigate the role of NMDA receptor and L-type voltage-gated calcium channels (L VGCC) in the expression of c Jun protein in hippocampus after transient global cerebral ischemia and reperfusion in two calcium channels. Methods: The model of global cerebral ischemia was induced by four-artery occlusion of SD rats. The hippocampus of SD rats at different time points (0, 1, 3, 6, 12, 24 and 72 h) To investigate the expression of c Jun and observe the effect of several calcium channel antagonists on c Jun expression. Results: c Jun was expressed at all time points after sham operation and reperfusion, and peaked at 6 hours after reperfusion. Ketamine, a noncompetitive NMDA receptor antagonist, and nifedipine, an L VGCC blocker, inhibit the increase of c Jun expression. However, DNQX, an AMPA / KA receptor antagonist, showed no inhibitory effect (data not shown). CONCLUSION: The expression of c Jun increases after ischemia and reperfusion, and this increase is associated with the opening of two calcium channels, NMDA receptor and L VGCC.