Kõks S, Soosaar A, Võikar V, Volke V, Ustav M, Männistö P T, Bourin M, Vasar E
Department of Physiology, University of Tartu, Estonia.
Neuropeptides. 1998 Jun;32(3):235-40. doi: 10.1016/s0143-4179(98)90042-7.
This study investigated the interplay of cholecystokinin (CCK) and endogenous opioid peptides in the regulation of anxiety. The acute administration of non-selective CCK agonist caerulein (1 and 5 microg/kg) and a selective CCK(B) receptor agonist BOC-CCK-4 (1, 10 and 50 microg/kg) induced a dose-dependent anxiogenic-like action in the plus-maze model of anxiety. BOC-CCK-4 displayed a similar efficacy with caerulein, indicating that the described effect was mediated via CCK(B) receptor subtype. The opioid antagonist naloxone itself (0.5 mg/kg) did not change the exploratory activity of rats in the plus-maze. However, the combination of naloxone with the sub-effective doses of caerulein (1 microg/kg) and BOC-CCK-4 (1 microg/kg) induced a significant inhibition of exploratory behaviour in rats. Accordingly, CCK and endogenous opioid peptides have an antagonistic role in the exploratory model of anxiety in rats.
本研究调查了胆囊收缩素（CCK）与内源性阿片肽在焦虑调节中的相互作用。急性给予非选择性CCK激动剂雨蛙素（1和5μg/kg）和选择性CCK（B）受体激动剂BOC-CCK-4（1、10和50μg/kg）在焦虑加迷宫模型中诱导出剂量依赖性的焦虑样作用。BOC-CCK-4与雨蛙素表现出相似的效力，表明所述作用是通过CCK（B）受体亚型介导的。阿片拮抗剂纳洛酮本身（0.5mg/kg）并未改变大鼠在加迷宫中的探索活动。然而，纳洛酮与亚有效剂量的雨蛙素（1μg/kg）和BOC-CCK-4（1μg/kg）联合使用可显著抑制大鼠的探索行为。因此，CCK和内源性阿片肽在大鼠焦虑探索模型中具有拮抗作用。
