• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Inputs from the basolateral amygdala to the nucleus accumbens shell control opiate reward magnitude via differential dopamine D1 or D2 receptor transmission.
【24h】

Inputs from the basolateral amygdala to the nucleus accumbens shell control opiate reward magnitude via differential dopamine D1 or D2 receptor transmission.

机译：从基底外侧杏仁核到伏隔核壳的输入通过差分多巴胺D1或D2受体的传递来控制鸦片的奖励幅度。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The basolateral amygdala (BLA), ventral tegmental area and nucleus accumbens (NAc) form a functionally connected neural circuit involved in the processing of opiate-related reward and memory. Dopamine (DA) projections from the ventral tegmental area to the BLA modulate associative plasticity mechanisms within the BLA. However, the role of DA receptor signaling in the BLA and its functional outputs to the NAc during opiate reward processing is not currently understood. Using an unbiased place conditioning procedure, we measured the rewarding effects of morphine following intra-BLA microinfusions of specific DA D1 or D2 receptor agonists in either opiate-naive or opiate-dependent/withdrawn rats. Activation of intra-BLA D1 receptors strongly potentiated the behaviorally rewarding effects of opiates, only in the opiate-naive state. However, once opiate dependence and withdrawal occurred, the intra-BLA DA-mediated potentiation of opiate reward salience switched to a D2 receptor-dependent substrate. We next performed single-unit, in-vivo extracellular neuronal recordings in the NAc shell (NA shell), to determine if intra-BLA D1/D2 receptor activation may modulate the NA shell neuronal response patterns to morphine. Consistent with our behavioral results, intra-BLA D1 or D2 receptor activation potentiated NAc 'shell' (NA shell) neuronal responses to sub-reward threshold opiate administration, following the same functional boundary between the opiate-naive and opiate-dependent/withdrawn states. Finally, blockade of N-methyl-d-aspartate transmission within the NA shell blocked intra-BLA DA D1 or D2 receptor-mediated opiate reward potentiation. Our findings demonstrate a novel and functional DA D1/D2 receptor-mediated opiate reward memory switch within the BLA→NA shell circuit that controls opiate reward magnitude as a function of opiate exposure state.
机译：基底外侧杏仁核（BLA），腹侧被盖区和伏伏核（NAc）形成功能连接的神经回路，参与鸦片相关奖励和记忆的处理。从腹侧被盖区到BLA的多巴胺（DA）投影可调节BLA内的相关可塑性机制。但是，目前尚不了解在鸦片制剂奖励过程中DA受体信号在BLA中的作用及其向NAc的功能输出。使用无偏位调节程序，我们测量了在鸦片幼稚或鸦片依赖性/戒断大鼠中特定DA D1或D2受体激动剂的BLA内微输注后吗啡的奖励作用。仅在未使用鸦片的状态下，BLA D1内受体的激活强烈增强了鸦片的行为奖励作用。但是，一旦发生鸦片依赖和戒断，BLA DA介导的鸦片奖励显着性增强就会转变为D2受体依赖性底物。接下来，我们在NAc外壳（NA外壳）中进行了单个单位的体内细胞外神经元录音，以确定BLA D1 / D2受体内的激活是否可以调节NA外壳神经元对吗啡的反应方式。与我们的行为结果一致，BLA D1或D2受体内激活增强了对鸦片亚给药阈值亚奖励阈值的NAc“壳”（NA壳）神经元的反应，这取决于鸦片幼稚和鸦片依赖/戒断状态之间的相同功能边界。最终，NA壳内N-甲基-d-天冬氨酸的传递受阻，阻断了BLA内DA D1或D2受体介导的阿片样物质奖赏增强。我们的发现表明，BLA→NA壳电路内有一种新颖且功能强大的DA D1 / D2受体介导的鸦片奖励记忆开关，该开关控制鸦片奖励的水平与鸦片暴露状态有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号