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应激与药物成瘾的啮齿动物模型:腹侧被盖区-伏隔核-前额叶皮质-杏仁核回路的作用

Stress and Rodent Models of Drug Addiction: Role of VTA-Accumbens-PFC-Amygdala Circuit.

作者信息

Yap Jasmine J, Miczek Klaus A

机构信息

Department of Psychology, Tufts University, 530 Boston Ave., Medford, MA 02155.

出版信息

Drug Discov Today Dis Models. 2008 Winter;5(4):259-270. doi: 10.1016/j.ddmod.2009.03.010.

Abstract

Stress can trigger, intensify, and prolong drug consumption, as well as reinstate previously extinguished drug-taking behavior by directly impacting a neural circuit often referred to as a reward pathways. Animal models of drug abuse have been used to understand these neural circuits mediating stress-induced drug intake and relapse through examination of cellular and subcellular molecular mechanisms. Several types of intermittent stressors have been shown to induce cross-sensitization to psychomotor stimulants, enhance conditioned place preference under most conditions, increase self-administration of cocaine and amphetamine and induce reinstatement of heroin and cocaine seeking via activation of the mesocorticolimbic dopamine system.

摘要

压力可触发、加剧并延长药物使用,还能通过直接影响通常被称为奖赏通路的神经回路,使先前已消退的药物摄取行为恢复。药物滥用的动物模型已被用于通过研究细胞和亚细胞分子机制来理解这些介导压力诱导的药物摄入和复发的神经回路。几种类型的间歇性应激源已被证明可诱导对精神运动兴奋剂的交叉致敏,在大多数情况下增强条件性位置偏爱,增加可卡因和苯丙胺的自我给药,并通过激活中脑皮质边缘多巴胺系统诱导海洛因和可卡因觅药行为的恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d8f/2794209/63620ac2fb1a/nihms107522f1.jpg

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