NMDA AND DOPAMINE D1 RECEPTORS WITHIN NAc-SHELL REGULATE IEG PROTEINS EXPRESSION IN REWARD CIRCUIT DURING COCAINE MEMORY RECONSOLIDATION
NMDA AND DOPAMINE D1 RECEPTORS WITHIN NAc-SHELL REGULATE IEG PROTEINS EXPRESSION IN REWARD CIRCUIT DURING COCAINE MEMORY RECONSOLIDATION
复制标题
NAc-壳内的 NMDA 和多巴胺 D-1 受体在可卡因记忆重建过程中调节奖赏回路中的 IEG 蛋白表达
DOI：
10.1016/j.neuroscience.2015.11.063
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发表时间：
2016-02-19
期刊：
影响因子：
3.3
通讯作者：
Wang, X.
中科院分区：
文献类型：
--
作者：
Li, Y.;Ge, S.;Wang, X.
巩固记忆的重新激活启动了记忆的重新巩固过程，在此过程中，重新激活的记忆易于加强，削弱或更新。因此，有效地干预记忆再巩固过程有望成为药物成瘾的重要治疗手段。神经核（NAc）已被公认为是一种可以防止药物复发的通路成分，尽管对这种功能的机制知之甚少。我们的目的是澄清的调节作用的NAc在可卡因的记忆再巩固过程中，通过检查应用不同的药物干预NAc的Zif 268和Fos B的表达在整个奖励电路可卡因记忆再激活后的效果。通过可卡因诱导的条件性位置偏爱（CPP）模型，应用免疫组织化学和荧光染色技术，观察可卡因记忆再激活后激活的脑核团中Zif 268和Fos B的变化。结果表明，Zif 268和Fos B在内侧前额叶皮质（mPFC）、边缘下皮质（IL）、NAc-core、NAcshell、海马中的表达普遍增加，（CA 1，CA 2和CA 3亚区），杏仁核，腹侧被盖区（VTA）和乳头体上核（SuM）的记忆再巩固后，并且通常观察到Zif 268/Fos B共表达（对于Zif 268：51-68%;对于Fos B：52-66%）。此外，在成瘾性记忆再巩固之前，双侧NAC壳输注MK 801和SCH 23390，而不是雷氯必利或普萘洛尔，降低了除杏仁核外整个奖赏回路中的Zif 268和Fos B表达，并有效地干扰了随后的CPP相关行为。总之，N-甲基-o-天冬氨酸（NMDA）和多巴胺D1受体，但不是多巴胺D2或β肾上腺素能受体，在NAC壳内，可以调节Zif 268和Fos B的表达在大多数大脑核的奖励电路后，可卡因的记忆再激活。这些结果表明，NAc通过影响整个成瘾记忆网络的功能，在调节成瘾记忆再巩固过程中发挥关键作用。(C)2015由Elsevier Ltd.代表！兄弟
Reactivation of consolidated memory initiates a memory reconsolidation process, during which the reactivated memory is susceptible to strengthening, weakening or updating. Therefore, effective interference with the memory reconsolidation process is expected to be an important treatment for drug addiction. The nucleus accumbens (NAc) has been well recognized as a pathway component that can prevent drug relapse, although the mechanism underlying this function is poorly understood. We aimed to clarify the regulatory role of the NAc in the cocaine memory reconsolidation process, by examining the effect of applying different pharmacological interventions to the NAc on Zif 268 and Fos B expression in the entire reward circuit after cocaine memory reactivation. Through the cocaineinduced conditioned place preference (CPP) model, immunohistochemical and immunofluorescence staining for Zif 268 and Fos B were used to explore the functional activated brain nuclei after cocaine memory reactivation. Our results showed that the expression of Zif 268 and Fos B was commonly increased in the medial prefrontal cortex (mPFC), the infralimbic cortex (IL), the NAc-core, the NAcshell, the hippocampus (CA1, CA2, and CA3 subregions), the amygdala, the ventral tegmental area (VTA), and the supramammillary nucleus (SuM) following memory reconsolidation, and Zif 268/Fos B co-expression was commonly observed (for Zif 268: 51-68%; for Fos B: 52-66%). Further, bilateral NAc-shell infusion of MK 801 and SCH 23390, but not raclopride or propranolol, prior to addictive memory reconsolidation, decreased Zif 268 and Fos B expression in the entire reward circuit, except for the amygdala, and effectively disturbed subsequent CPP-related behavior. In summary, N-methyl-o-aspartate (NMDA) and dopamine D1 receptors, but not dopamine D2 or beta adrenergic receptors, within the NAc-shell, may regulate Zif 268 and Fos B expression in most brain nuclei of the reward circuit after cocaine memory reactivation. These findings indicated that the NAc played a key role in regulating addictive memory reconsolidation by influencing the function of the entire addictive memory network. (C) 2015 Published by Elsevier Ltd. on behalf of !BRO.