Roles of the nucleus accumbens and amygdala in the acquisition and expression of ethanol-conditioned behavior in mice

Roles of the nucleus accumbens and amygdala in the acquisition and expression of ethanol-conditioned behavior in mice
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DOI:
10.1523/jneurosci.4520-07.2008
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发表时间:
2008-01-30
影响因子:
5.3
通讯作者:
Cunningham, Christopher L.
Cunningham, Christopher L.
中科院分区:
医学1区
文献类型:
--
作者:
Gremel, Christina M.;Cunningham, Christopher L.

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尽管在确定乙醇的主要强化效应的神经区方面取得了进展,但很少有研究研究乙醇诱导的条件性效应的神经区。先前使用条件性位置偏爱(CPP)过程的工作涉及腹侧被盖区(VTA)(Bechtholt和Cunningham,2005),但调节乙醇的条件性奖赏效应的下游神经区尚未确定。虽然伏隔核(ACB)和杏仁核(AMY)都接受来自VTA的多巴胺神经支配,但这些区域在乙醇条件行为中所起的作用尚不清楚。在目前的一系列实验中,我们使用CPP程序和选择性电解损伤来检查乙醇条件性行为获得和表达的神经区域。在习得实验中,雄性DBA/2J小鼠在CPP训练前接受双侧ACB或AMY损毁。在表达实验中,小鼠在训练后但测试前接受双侧ACB、ACB壳、ACB核心和AMY的损伤,或单侧的AMY损伤。训练前ACB和AMY的损伤干扰了乙醇CPP的获得和表达。然而,当在训练后给予时,只有AMY的损伤破坏了表达,而ACB核心的损伤促进了乙醇CPP的反应的丧失。这些结果首次证明了ACB和AMY在乙醇诱导的条件性奖赏的获得和表达中的作用。
Although progress has been made identifying the neural areas underlying the primary reinforcing effects of ethanol, few studies have examined the neural areas mediating ethanol-induced conditioned effects. Previous work using the conditioned place preference (CPP) procedure implicates the ventral tegmental area (VTA) (Bechtholt and Cunningham, 2005), but the downstream neural areas modulating the conditioned rewarding effects of ethanol have not been identified. Although the nucleus accumbens (Acb) and the amygdala (Amy), which both receive dopamine innervation from the VTA, have been implicated in the primary reinforcing effects of ethanol, the roles these areas play in ethanol-conditioned behaviors are unknown. In the present set of experiments, we use the CPP procedure along with selective electrolytic lesions to examine the neural areas underlying the acquisition and expression of ethanol conditioned behavior. In the acquisition experiment, male DBA/2J mice received bilateral lesions of the Acb or Amy before CPP training. In the expression experiments, mice received bilateral lesions of the Acb, Acb shell, Acb core, and Amy, or unilateral lesions of the Amy after training but before testing. Lesions of the Acb and Amy before training disrupted acquisition and expression of ethanol CPP. However, when given after training, only lesions of the Amy disrupted expression, whereas lesions of the Acb core facilitated loss of responding, of ethanol CPP. For the first time, these results demonstrate the role of the Acb and Amy in the acquisition and expression of ethanol-induced conditioned reward.