...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Cooperative activation of dopamine D1 and D2 receptors increases spike firing of nucleus accumbens neurons via G-protein betagamma subunits.
【24h】

Cooperative activation of dopamine D1 and D2 receptors increases spike firing of nucleus accumbens neurons via G-protein betagamma subunits.

机译：多巴胺D1和D2受体的协同激活通过G蛋白betagamma亚基增加伏伏核神经元的突波发射。

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

Dopamine in the nucleus accumbens modulates both motivational and addictive behaviors. Dopamine D1 and D2 receptors are generally considered to exert opposite effects at the cellular level, but many behavioral studies find an apparent cooperative effect of D1 and D2 receptors in the nucleus accumbens. Here, we show that a dopamine-induced enhancement of spike firing in nucleus accumbens neurons in brain slices required both D1 and D2 receptors. One intracellular mechanism that might underlie cooperativity of D1 and D2 receptors is activation of specific subtypes of adenylyl cyclases by G-protein betagamma subunits (Gbetagamma) released from the Gi/o-linked D2 receptor in combination with Galpha(s)-like subunits from the D1 receptor. In this regard, dopaminergic enhancement of spike firing was prevented by inhibitors of protein kinase A or Gbetagamma. Furthermore, intracellular perfusion with Gbetagamma enabled D1 receptor activation but not D2 receptor activation to enhance spike firing. Finally, our data suggest that these pathways may increase spike firing by inhibition of a slow A-type potassium current. These results provide evidence for a novel cellular mechanism through which cooperative action of D1 and D2 receptors in the nucleus accumbens could mediate dopamine-dependent behaviors.
机译：伏隔核中的多巴胺调节动机和成瘾行为。多巴胺D1和D2受体通常被认为在细胞水平上具有相反的作用，但是许多行为研究发现伏隔核中D1和D2受体具有明显的协同作用。在这里，我们表明，多巴胺诱导的伏安核中神经元在脑切片中的尖峰放电增强需要D1和D2受体。一种可能与D1和D2受体协同作用的细胞内机制是通过从Gi / o-连接的D2受体释放的G蛋白betagamma亚基（Gbetagamma）与来自G1 / D2受体的Galpha-like亚基的结合激活腺苷酸环化酶的特定亚型D1受体。在这方面，蛋白激酶A或Gbetagamma的抑制剂阻止了多巴胺能增强尖峰发射。此外，用Gbetagamma进行的细胞内灌注能够激活D1受体，但不能激活D2受体，以增强突波发射。最后，我们的数据表明，这些途径可能会通过抑制慢速A型钾电流来增加尖峰放电。这些结果提供了一种新颖的细胞机制的证据，通过该机制，伏伏核中D1和D2受体的协同作用可以介导多巴胺依赖性行为。

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