纳洛酮等药物在大鼠杏仁核点燃模型中的作用  

THE EFFECTS OF NALOXONE AND OTHER AGENTS ON AMYGDALA KINDLING MODEL IN RATS

作　　者：张芳[1] 张婷[2] 王蕾[1] 岳旺[1] 

机构地区：[1]青岛大学医学院药理教研室,青岛266021 [2]青岛大学医学院松山医院内科,青岛266021

出　　处：《中国药物依赖性杂志》2005年第4期258-261,共4页Chinese Journal of Drug Dependence

摘　　要：目的:观察纳洛酮等药物在点燃模型中的作用,探讨成瘾性药物的戒断症状与点燃模型的内在联系。方法:观察纳洛酮、可乐定、东莨菪碱、MK-801和尼卡地平对杏仁核点燃大鼠的影响,并测定点燃大鼠伏隔核(NAc)脑区的DA及其代谢产物的含量。结果:纳洛酮可易化杏仁核点燃,可乐定、东莨菪碱、MK-801和尼卡地平则可抑制杏仁核点燃发作(P<0·05)。点燃大鼠NAc区DA及其代谢产物升高(P<0·05)。结论:杏仁核点燃模型对纳洛酮等药物的反应及NAc脑区DA及其代谢产物的变化都与戒断反应的表现一致。Objective： To observe the effects of naloxone and other agents on amygdala kindling model in rats, and investigate the underlying relationship between the mechanism of withdrawal syndrome of addictive substances and kindling model. Method： The effects of naloxone, clonidine, scopolamine, MK-801 and nicardipine on amygdala kindling model were observed, and the content of dopamine （DA） and its metabolites were determined in NAc in kindled rats. Results： Naloxone facilitated, while clonidine, scopolamine, MK-801 and nicardipine inhibited amygdala kindling（P〈0.05）. The content of DA and its metabolites in NAc in kindled rats increased significantly compared with those of the control group（P〈0.05）. Conclusion ： The response of amygdala kindling model to naloxone and other agents and the change of the content of DA and its metabolites are consistent with withdrawal syndromes.

关 键 词：点燃模型 戒断反应 戒毒药 杏仁核点燃模型 成瘾性药物 纳洛酮 大鼠 MK-801 代谢产物 东莨菪碱 

分 类 号：R971.6[医药卫生—药品] R971[医药卫生—药学]