Differential control over cocaine-seeking behavior by nucleus accumbens core and shell
Differential control over cocaine-seeking behavior by nucleus accumbens core and shell
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DOI：
10.1038/nn1217
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发表时间：
2004-04-01
影响因子：
25
通讯作者：
Everitt, BJ
中科院分区：
文献类型：
--
作者：
Ito, R;Robbins, TW;Everitt, BJ
伏核(NAC)多巴胺广泛参与药物滥用强化效应的调节。然而，国家药品监督管理局本身在药物自我管理中的确切作用一直难以确定。在这里，我们展示了一种神经双重分离的行为过程，在大鼠的可卡因自我管理。尽管NAC核心的选择性兴奋毒性损伤对在标准的持续强化程序下获得对可卡因的反应只有很小的影响，但这些损害深刻地损害了由药物相关的条件增强程序维持的药物寻找行为的获得，并使用二级可卡因加强程序进行评估。相反，选择性兴奋毒性损毁NAC壳并不损害药物的自我给药或寻求可卡因的获得，但它们确实减弱了可卡因的精神刺激作用。这些结果进一步加深了我们对南汽如何控制寻毒和吸毒行为的理解。
Nucleus accumbens (NAc) dopamine is widely implicated in mediating the reinforcing effects of drugs of abuse. However, the precise function of the NAc itself in drug self-administration has been difficult to establish. Here we show a neural double-dissociation of the behavioral processes that underlie cocaine self-administration in rats. Whereas selective excitotoxic lesions of the NAc core had only a minor effect on the acquisition of responding for cocaine under a standard schedule of continuous reinforcement, these lesions profoundly impaired the acquisition of drug-seeking behavior that was maintained by drug-associated conditioned reinforcers and assessed using a second-order schedule of cocaine reinforcement. In contrast, selective excitotoxic lesions of the NAc shell did not impair drug self-administration or the acquisition of cocaine-seeking, but they did attenuate the psychostimulant effects of cocaine. These results further our understanding of how the NAc controls drug-seeking and drug-taking behavior.