[Cholecystokinin octapeptide (CCK-8) antagonizes morphine analgesia in amygdala of the rat].

CCK-8 administered bilaterally to the amygdala at 0.1-1.0 ng dose-dependently antagonized the analgesia induced by morphine (4 mg/kg, s. c.) as measured by the changes in tail flick latency (TFL). This effect of CCK-8 could be reversed by Devazepide, a CCK-A receptor antagonist dose-dependently at 50 ng and 200 ng, and by L-365, 260, a CCK-B receptor antagonist at 5 ng and 8 ng administered to the same site. The effect of morphine analgesia was potentiated by 200 ng Devazepide or 8 ng L-365, 260 administered bilaterally to amygdala. Devazepide and L-365, 260 per second showed no significant influence on basal TFL. The results indicate that amygdala is a strategic site where CCK-8 exerts an antiopioid activity. Since the effect of L-365, 260 was 25 times more potent than Devazepide, it suggests that the anti-opiod effect of CCK in amygdala is mediated by CCK-B receptors.