【摘要】 大鼠双侧杏仁核内注射CCK-81 ng(1μl),能明显降低皮下注射4 mg/kg吗啡产生的镇痛作用,并在0.1—1ng范围内呈量效关系。分别向双侧杏仁校注射CCK-A受体拮抗剂Devazepide50 ng能部分翻转,200 ng则完全翻转CCK-8的抗吗啡镇痛作用,10 ng无效;而CCK-B受体拮抗剂L-365,260在5—8 ns时即可完全翻转CCK-8的抗吗啡镇痛作用。杏仁核注射200 ng的De-vazepide和8 ng的L-365,260均不影响基础痛阈,但均能加强度下注射吗啡产生的镇痛作用。上述实验结果提示:(1)杏仁核是CCK-8发挥抗阿片镇痛作用的有效部位之一;(2)CCK-8在杏仁核可能通过CCK-B受体拮抗吗啡的镇痛作用。更多还原

【Abstract】 CCK--8 administered bilaterally to the amygdala at 0.1--1.0 ng dose--dependentlyantagonized the analgesia induced by morphine (4 mg/kg, s.c.) as measured by thechanges in tail flick latency (TFL). This effect of CCK--8 could be reversed by De-vazepide, a CCK--A receptor antagonist dose--dependently at 50 ng and 200 ng, and byL--365, 260, a CCK--B receptor antugonist at 5 ng and 8 ng administered to the samesite. 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 secondshowed no significant influence on basal TFL. The results indicate that amygdala is astrategic site where CCK--8 exerts an antiopioid activity. Since the effect of L--365, 260was 25 times more potent than Devazepide, it suggests that the anti--opiod effect of CCKin amygdala is mediated by CCK--B receptors.更多还原