• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Addiction biology >The role of amygdaloid brain-derived neurotrophic factor, activity-regulated cytoskeleton-associated protein and dendritic spines in anxiety and alcoholism.
【24h】

The role of amygdaloid brain-derived neurotrophic factor, activity-regulated cytoskeleton-associated protein and dendritic spines in anxiety and alcoholism.

机译：杏仁状脑源性神经营养因子，活性调节的细胞骨架相关蛋白和树突棘在焦虑和酒精中毒中的作用。

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

Innate anxiety appears to be a robust factor in the promotion of alcohol intake, possibly due to the anxiolytic effects of self-medication with alcohol. Brain-derived neurotrophic factor (BDNF) and its downstream target, activity-regulated cytoskeleton-associated (Arc) protein, play a role in the regulation of synaptic function and structure. In order to examine the role of the BDNF-Arc system and associated dendritic spines in the anxiolytic effects of ethanol, we investigated the effects of acute ethanol exposure on anxiety-like behaviors of alcohol-preferring (P) and -nonpreferring (NP) rats. We also examined changes in the expression of BDNF and Arc, and dendritic spine density (DSD), in amygdaloid brain regions of P and NP rats with or without ethanol exposure. It was found that in comparison with NP rats, P rats displayed innate anxiety-like behaviors, and had lower mRNA and protein levels of both BDNF and Arc, and also had lower DSD in the central amygdala (CeA) and medial amygdala (MeA), but not in the basolateral amygdala (BLA). Acute ethanol treatment had an anxiolytic effect in P, but not in NP rats, and was associated with an increase in mRNA and protein levels of BDNF and Arc, and in DSD in the CeA and MeA, but not BLA. These results suggest that innate deficits in BDNF-Arc levels, and DSD, in the CeA and MeA may be involved in the anxiety-like and excessive alcohol-drinking behaviors of P rats, as ethanol increased these amygdaloid synaptic markers and produced anxiolytic effects in P rats, but not NP rats.
机译：先天性焦虑似乎是促进酒精摄入的重要因素，这可能是由于自我用酒精进行药物的抗焦虑作用所致。脑源性神经营养因子（BDNF）及其下游靶标，活性调节的细胞骨架相关（Arc）蛋白在突触功能和结构调节中发挥作用。为了检查BDNF-Arc系统和相关的树突棘在乙醇抗焦虑作用中的作用，我们研究了急性乙醇暴露对嗜酒精（P）和非嗜酒精（NP）大鼠焦虑样行为的影响。 。我们还检查了在有或没有乙醇暴露的P和NP大鼠的杏仁体大脑区域中BDNF和Arc的表达以及树突棘密度（DSD）的变化。结果发现，与NP大鼠相比，P大鼠表现出先天性的焦虑样行为，BDNF和Arc的mRNA和蛋白水平较低，中央杏仁核（CeA）和内侧杏仁核（MeA）的DSD也较低，但不在基底外侧杏仁核（BLA）中。急性乙醇治疗对P有抗焦虑作用，但对NP大鼠无抗焦虑作用，并且与BDNF和Arc的mRNA和蛋白质水平以及CeA和MeA的DSD的mRNA和蛋白质水平增加相关，而与BLA无关。这些结果表明，CeA和MeA中BDNF-Arc水平和DSD的先天缺陷可能与P大鼠的焦虑样和过度饮酒行为有关，因为乙醇会增加这些杏仁状突触标记物并在小鼠体内产生抗焦虑作用。 P大鼠，但不包括NP大鼠。

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