【摘 要】
：
目的单针吗啡诱导的行为敏化是研究阿片类药物成瘾神经可塑性变化的重要动物模型。目前认为隔核是脑内与奖赏、学习和记忆等关系较为密切的核团之一。因此,本研究将探讨隔核在单针吗啡诱导的行为敏化中的作用,并初步解析其作用机制。方法和结果通过旷场实验发现,单针吗啡(第1天：3～-30 mg·kg-1,sc)预处理的大鼠在吗啡(第8天：3 mg·kg-1,sc)激发时表现出高活动性,也就是行为敏化反应；在敏化实
【机 构】
：
北京大学中国药物依赖性研究所,北京 100191 Department of Pharmacolo
【出 处】
：
第十五届中国神经精神药理学学术会议
论文部分内容阅读
目的单针吗啡诱导的行为敏化是研究阿片类药物成瘾神经可塑性变化的重要动物模型。目前认为隔核是脑内与奖赏、学习和记忆等关系较为密切的核团之一。因此,本研究将探讨隔核在单针吗啡诱导的行为敏化中的作用,并初步解析其作用机制。方法和结果通过旷场实验发现,单针吗啡(第1天：3～-30 mg·kg-1,sc)预处理的大鼠在吗啡(第8天：3 mg·kg-1,sc)激发时表现出高活动性,也就是行为敏化反应；在敏化实验前进行双侧隔核电损毁手术,发现大鼠对吗啡的行为敏化反应消失,但对吗啡的急性反应不受影响；而在单针吗啡预处理之后立即进行双侧隔核电损毁,发现7d后大鼠在吗啡激发时仍表现出行为敏化；此外,通过条件性位置偏爱实验和甩尾实验,分别评价了吗啡在隔核损毁大鼠中的奖赏与镇痛作用；为了进一步明确隔核参与行为敏化的过程,按照侧隔核与中隔核的分区,分别通过核团内微量注射吗啡的方法建立行为敏化。发现预处理时在侧隔核或中隔核给于吗啡(30 μg/rat)能使大鼠在激发后(3mg·kg-1,sc)出现行为敏化；预处理前,在侧隔核或中隔核内给与利多卡因(10μg,/rat)或mu受体拮抗剂β-FNA(2μg/tat)能抑制行为敏化的建立。结论 在吗啡预处理前,隔核损毁或者阻断隔核内阿片受体能抑制行为敏化的建立,说明隔核是参与单针吗啡诱导行为敏化形成期的关键性核团,并且侧隔核与中隔核的mu受体可能是这一过程的作用靶点。
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