八肽胆囊收缩素对大鼠大脑皮质蛋白激酶C活性的影响

目的　探讨胆囊收缩素受体 (CCK receptor)在中枢神经系统的信号传递机制。方法　采用分离的大鼠大脑皮质神经细胞 ,观察 CCK8、CCKA 受体拮抗剂 L- 36 4,718和 CCKB受体拮抗剂 L- 36 5 ,2 6 0对大鼠大脑皮质蛋白激酶 C(PKC)活性的影响。结果　 CCK8在 10 - 1 1 ～ 10 - 6 mol/L范围内可刺激 PKC活性的增加 ,超过 10 - 6mol/L后 ,逐渐趋于饱和。 CCKA受体拮抗剂 L - 36 4,718、CCKB受体拮抗剂 L - 36 5 ,2 6 0均可根据剂量的大小不同程度地抑制 CCK8引起的 PKC活性改变 ,但两者 IC50 相差 6 0倍 ,L - 36 5 ,2 6 0在较低浓度时即能明显拮抗 CCK8引起的 PKC活性变化。结论　本研究结果提示 ,CCK8可能通过 CCKB受体引起 PKC活性变化 ,而 PKC可能是 CCKB受体的重要信号传递机制之一

The Effects of Cholecystokinin Octapeptide on PKC Activity in Rat Cerebral Cortex Neurocytes

Objective To investigate the effects of CCK 8 on protein kinase C activity in rat cerebral cortex.Methods The cerebral cortex neurocytes were isolated and used as a model. The effects of CCK 8, L 364,718 and L 365,260 on PKC activities were detected by using a non radioactive method. Results CCK 8 caused a detectable increase in PKC activity at 10 -11 mol/L, and a peak increase of PKC activity was observed at 10 -5 mol/L (about 4 5 U/ mg protein). PKC activity was increased in dose dependent manner by CCK 8(10 -11 10 -6 mol/L). The CCK B selective receptor antagonist L 365,260 with a higher efficiency,and the CCK A selective receptor antagonist L 364,718 with a lower efficiancy were able to block a maximal effect of CCK 8 induced PKC activation. Conclusions CCK 8 may regulate PKC activities in rat cerebral cortex through CCK B receptor.