Genetic reconstruction of dopamine D1 receptor signaling in the nucleus accumbens facilitates natural and drug reward responses.
Genetic reconstruction of dopamine D1 receptor signaling in the nucleus accumbens facilitates natural and drug reward responses.
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DOI：
10.1523/jneurosci.5532-12.2013
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发表时间：
2013-05-15
期刊：
影响因子：
--
通讯作者：
Zweifel LS
中科院分区：
文献类型：
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作者：
Gore BB;Zweifel LS
多巴胺D1受体（D1R）促进奖励获取，其改变导致深刻的学习缺陷。然而，其最低功能电路要求是未知的。在D1R基因敲除小鼠中使用功能性D1R信号传导的条件重建，我们定义了特定奖励维度的D1R亚区（NAc）的不同要求。我们证明D1R的表达选择性的核心区域的NAc（NAcCore），而不是外壳（NAcShell），增强了一种独特的形式的巴甫洛夫条件的方法和介导D1R依赖的可卡因致敏。然而，在NAcCore或NAcShell中的D1R表达改善了对奖励的工具性反应。相比之下，无论是NAcCore还是NAcShell D1R都不足以促进在渐进比率任务或运动学习中为奖励而工作的动机。这些结果突出了多巴胺依赖性行为的D1R的解离电路要求。
The dopamine D1 receptor (D1R) facilitates reward acquisition, and its alteration leads to profound learning deficits. However, its minimal functional circuit requirement is unknown. Using conditional reconstruction of functional D1R signaling in D1R knockout mice, we define distinct requirements of D1R in subregions of the nucleus accumbens (NAc) for specific dimensions of reward. We demonstrate D1R expression selectively in the core region of the NAc (NAcCore), but not the shell (NAcShell), enhances a unique form of Pavlovian conditioned approach and mediates D1R-dependent cocaine sensitization. However, D1R expression in either the NAcCore or the NAcShell improves instrumental responding for reward. In contrast, neither NAcCore nor NAcShell D1R is sufficient to promote motivation to work for reward in a progressive ratio task or for motor learning. These results highlight dissociated circuit requirements of D1R for dopamine-dependent behaviors.