| 大鼠杏仁核内注射八肽胆囊收缩素（CCK—8）拮抗吗啡镇痛的研究 |
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| 引用本文： | 朴素芬,韩济生.大鼠杏仁核内注射八肽胆囊收缩素（CCK—8）拮抗吗啡镇痛的研究[J].生理学报,1993,45(5):470-478. |
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| 作者姓名： | 朴素芬 韩济生 |
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| 作者单位： | 北京医科大学生理教研室，北京医科大学生理教研室 北京 100083，北京 100083 |
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| 基金项目： | 中国自然科学基金委员会资助(No.938900705)，美国国立药物成瘾研究所科研基金(No.DA03983) |
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| 摘 要： | 大鼠双侧杏仁核内注射ＣＣＫ－８１ｎｇ（１μｌ），能明显降低皮下注射４ｍｇ／ｋｇ吗啡产生的镇痛作用，并在０．１－１ｎｇ范围内呈量效关系。分别向双侧仁核注射ＣＣＫ－Ａ受体拮抗剂Ｄｅｖａｚｅｐｉｄｅ５０ｎｇ能部分翻转，２００ｎｇ则完全翻转ＣＣＫ－８的抗吗啡镇痛作用，１０ｎｇ无效；而ＣＣＫ－Ｂ受体拮抗剂Ｌ－３６５，２６０在５－８ｎｇ时即可完全番转ＣＣＫ－８的抗吗啡镇痛作用。杏仁核注射２００ｎｇ的Ｄｅｖａｚ
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| 关 键 词： | 八肽 胆囊收缩素 杏仁核 吗啡 止痛 |
CHOLECYSTOKININ OCTAPEPTIDE (CCK--8) ANTAGONIZES MORPHINE ANALGESIA IN AMYGDALA OF THE RAT |
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| PU SU-FEN,HAN JI SHENG.CHOLECYSTOKININ OCTAPEPTIDE (CCK--8) ANTAGONIZES MORPHINE ANALGESIA IN AMYGDALA OF THE RAT[J].Acta Physiologica Sinica,1993,45(5):470-478. |
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| Authors: | PU SU-FEN HAN JI SHENG |
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| Affiliation: | PU SU-FEN,HAN JI SHENG Department of Physiology,Beijing Medical University,Beijing 100083 |
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| 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. |
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| Keywords: | morphine analgesia cholecystokinin (CCK) amygdala L-365 260 CCK receptor Devazepide (formly L-346 718 MK-369) |
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