为了探讨胆囊收缩素(CCK)受体在中枢神经系统中的信号传递机制,观察了CCK8和CCKA受体拮抗剂L-364,718、CCKB受体拮抗剂L-365,260对大鼠大脑皮质钙调素(CaM)活性的影响.结果表明:a.CCK8对CaM活性的影响具有时间依赖性,15 min达到最高点后逐渐下降;b.CCK8在10-12~10-7 mol/L范围内可刺激CaM活性的增加,超过10-7 mol/L后,逐渐趋于饱和.c.CCKA受体拮抗剂L-364,718、CCKB受体拮抗剂L-365,260均可抑制10-7 mol/L CCK8引起的CaM活性的增加,但两者IC50相差40倍,L-365,260在较低浓度时即能明显拮抗CCK8引起的CaM活性变化.研究结果提示CCK8可能通过CCKB受体引起CaM活性变化,而CaM可能是CCKB受体的重要信号传递机制之一.
In order to investigate the effects of cholecystokinin octapeptide(CCK8) on calmodulin activity in rat cerebral cortex,the cerebral cortex neurocytes was used as a model. CCK8 stimulated the activation of CaM in a time-dependent manner. After 15 minutes of treatment of 1 μmol/L CCK8,the CaM activity reached the maximum increase. CaM activity was increased in a dose-dependent manner by CCK8 (10-12~10-7 mol/L). The CCKB-specific receptor antagonist L-365,260 and with a weaker efficiency,the CCKA-specific receptor antagonist L-364,718,were able to block a maximal effect of CCK8-induced CaM activation,suggesting that CCKB receptor may regulate CaM activity in cerebral cortex.
项鹏,陈曼玲,吴兆锋.八肽胆囊收缩素对大鼠大脑皮质细胞钙调素活性的影响[J].生物化学与生物物理进展,2000,27(5):533-536
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