胆囊收缩素8对大鼠大脑皮质细胞钙调素和蛋白激酶C活性的影响

 为阐明中枢神经系统中胆囊收缩素 8(CCK8)受体的信号传递机制 ,以分离的大鼠大脑皮质神经细胞为材料 ,观察了CCK8对细胞内钙调素 (CaM)、3′ ,5′ 环腺苷酸 (cAMP)、蛋白激酶C(PKC)活性的影响 研究结果表明 ,CCK8可刺激大脑皮质细胞CaM、PKC活性的增加 ,并有剂量依赖关系 但CCK8在 10 -12 ～ 10 -6mol L范围内 ,细胞内cAMP含量无显著变化 利用受体亚型L 364,718和L 365,2 60的研究表明 ,两种拮抗剂均可抑制CCK8引起的CaM和PKC活性变化 ,但两者IC50 不同 对于CaM ,CCKB 受体拮抗剂L 365,2 60的IC50 比CCKA 受体拮抗剂L 364,718低 4 0倍 ;而对于PKC ,L 365,2 60的IC50 比L 364,718低 60倍 因此认为 ,CCK8主要是通过CCKB 受体介导了CaM和PKC活性的变化

The Effects Cholecystokinin Octapeptide on CaM and PKC Activities in Rat Cerebral Cortex Neurocytes

To investigate the effects of cholecystokinin octapeptide(CCK 8)on camodulin(CaM),protein kinase C(PKC)and 3′,5′ cyclic AMP,the rat cerebral cortex neurocytes were used as model.No cAMP accmulations could be observed,except for a high concentration(10 -5 mol/L).On the other hand,evidence of CCK 8 induced CaM and PKC activiation was found in a dose dependent manner.The CCK B selective antagonist L 365,260 and the CCK A selective receptor antagonist L 364,718 were able to block a maximal effect of CCK 8 induced CaM and PKC activation.But the IC 50 were different.The effect of L 364,718 was evidently weaker than that of L 365,260.All these results suggest that CCK 8 may regulate signal transduction in rat cerebral cortex through CCK B receptor.