...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neuron >Molecular substrates for retrieval and reconsolidation of cocaine-associated contextual memory.
【24h】

Molecular substrates for retrieval and reconsolidation of cocaine-associated contextual memory.

机译：可卡因相关情境记忆的检索和重组的分子底物。

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

Relapse into drug taking among addicts often depends on learned associations between drug-paired cues and the rewarding effects of these drugs, such as cocaine (COC). Memory for drug-paired cues resists extinction and contributes to the high rate of relapse; however, the molecular mechanisms underlying these associations are not understood. We show that COC-conditioned place preference (CPP) activates ERK, CREB, Elk-1, and Fos in the nucleus accumbens core (AcbC) but not shell. Intra-AcbC infusions of U0126, an inhibitor of the ERK kinase MEK, prevent both the activation of ERK, CREB, Elk-1, and Fos and retrieval of COC-CPP. When tested again 24 hr or 14 days after intra-AcbC infusions of U0126 or another MEK inhibitor, PD98059, CPP retrieval and concomitant protein activation were significantly attenuated. Together, these findings indicate the necessity of the AcbC ERK signaling pathway for drug-paired contextual cue memories and suggest that these strong memories can become susceptible to disruption by therapeutic agents.
机译：成瘾者中吸毒的复发通常取决于配对药物的线索与这些药物（例如可卡因（COC））的奖励作用之间的学习关联。药物配对线索的记忆可抵抗灭绝并有助于高复发率。然而，尚不清楚这些关联的分子机制。我们表明，COC条件的位置偏好（CPP）激活伏伏核核心（AcbC）中的ERK，CREB，Elk-1和Fos，但不激活外壳。 U0126（ERK激酶MEK的抑制剂）的Ac0C内输注可防止ERK，CREB，Elk-1和Fos的激活以及COC-CPP的恢复。当在U0126或另一种MEK抑制剂的AcbC内输注后24小时或14天再次测试时，PD98059，CPP恢复和伴随的蛋白质活化被大大减弱。在一起，这些发现表明药物配对上下文提示记忆的AcbC ERK信号通路的必要性，并表明这些强大的记忆可能变得容易受到治疗剂的破坏。

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