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Neuron:线粒体分裂和可卡因成瘾关系

2017-12-21 海北 MedSci原创

已有的研究表明,在可卡因成瘾过程中,脑内能量平衡的改变是大脑中发生的一个关键适应过程。但是至今为止,可卡因对线粒体,能量的根本来源,的影响还是未知的。

已有的研究表明,在可卡因成瘾过程中,脑内能量平衡的改变是大脑中发生的一个关键适应过程。但是至今为止,可卡因对线粒体,能量的根本来源,的影响还是未知的。

近日,来自马里兰大学医学院的研究人员发现,在重复可卡因暴露后,以及可卡因依赖的个体中,伏隔核(NAc)中的dynamin相关蛋白-1Drp1)有所增加,其可以介导线粒体的分裂。

Mdivi-1是一种已被证实的线粒体分裂抑制剂,其可以阻止对可卡因的找寻以及运动过敏,同时其可以阻断含有NAc中型棘状神经元(MSNs)的多巴胺受体-1D1)的c-Fos诱导和兴奋性输入。在D1-MSNs中,研究人员发现Drp1和裂变促进Drp1有所增加,这与在重复的可卡因暴露之后,D1-MSN树突中较小线粒体的增加一致。在D1-MSNs中,Drp1的敲除阻止了可卡因自我注射后的药物寻求。如果增加裂变促进Drp1,在长期禁食可卡因之后会增强对药物的寻求。

因此,研究人员证明在早期可卡因戒断期间,NAc中改变的线粒体分裂的作用,提供了一条可能的可卡因成瘾治疗途径。


原始出处:

Ramesh Chandra et al. Drp1 Mitochondrial Fission in D1 Neurons Mediates Behavioral and Cellular Plasticity during Early Cocaine AbstinenceNeuron, 2017; 96 (6): 1327 DOI: 10.1016/j.neuron.2017.11.037


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