两类钙通道拮抗剂对缺氧大鼠海马脑片Ca^(2+)/CaM PKⅡ活性的影响

Effect of two types of Ca^(2+) channels antagonist on Ca^(2+) /CaM PKⅡin anoxic rat hippocampal slices

用离体孵育的大鼠海马脑片模型，研究了两类钙通道拮抗剂对缺氧海马脑片Ca2+/CaM PKⅡ活性的影响。结果如下：(1)缺氧30min导致大鼠海马脑片Ca2+/CaM PKⅡ活性降至对照组的16.4%；(2)100μmol/L氯胺酮可部分拮抗缺氧导致的酶活性下降，使之恢复至对照组的40.6%；(3)10μmol/L苄丙咯可使缺氧导致的酶活性下降恢复至对照组的35.8%；(4)15μmol/L苄丙咯和50μmol/L氯胺酮联合用药可产生协同作用，使缺氧导致的酶活性下降恢复至对照组的63.8%。由此得出结论：缺氧对海马脑片Ca2+/CaM PKⅡ活性的抑制作用与NMDA受体门控的钙通道和Na+/Ca2+交换通道异常开放有关。

Effect of two types of Ca2+ channels antagonist on anoxia-induced inhibition of Ca2+/CaM PKⅡ activity were studied in vitro in a model of rat hippocampal slices. The results were as follows: 1)Ca 2+/CaM PKⅡ activity values of rat hippocampal slices decreased to 16.4% of co ntrol at 30min of anoxia. 2)Inhibition of Ca2+/CaM PKⅡ activity of the sl ices induced by 30min of anoxia was partly antagonized by NMDA receptor antagoni st Ketamine and Na+/Ca2+ exchanger antagonist Bepridil, and Ca2+/C aM PKⅡ activity values changed from 16.4% of control to 40.6% of control (100μ mol/L Ketamine) and to 35.8% of control(10μmol/L Bepridil). 3)Combination of 50 μmol/L Ketamine with 15μmol/L Bepridil synergetically antagonized Inhibition o f Ca2+/CaM PKⅡ activity, and Ca2+/CaM PKⅡ activity values changed from 16.4% of control to 63.8% of control. According to our results, we suggeste d that NMDA receptor and Na+Ca2+ exchanger be involved in anoxia-induce d Inhibition of Ca2+/CaM PKⅡ activity in rat hippocampal slices.