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Ethanol-induced anxiolysis and neuronal activation in the amygdala and bed nucleus of the stria terminalis

机译:乙醇诱导纹状体杏仁核和床核中的抗焦虑和神经元活化

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High rates of comorbidity for anxiety and alcohol-use disorders suggest a causal relationship between these conditions. Previous work demonstrates basal anxiety levels in outbred Long-Evans rats correlate with differences in voluntary ethanol consumption and that amygdalar Neuropeptide Y (NPY) systems may play a role in this relationship. The present work explores the possibility that differences in sensitivity to ethanol's anxiolytic effects contribute to differential ethanol self-administration in these animals and examines the potential role of central and peripheral NPY in mediating this relationship. Animals were first exposed to the elevated plus maze (EPM) to assess individual differences in anxiety like behaviors and levels of circulating NPY and corticosterone (CORT). Rats were then tested for anxiety like behavior in the light dark box (LD box) following acute ethanol treatment (1 glkg; intraperitoneally li.p.1), and neuronal activation in the amygdala and bed nucleus of the stria terminalis (BNST) was assessed using Fos immunohistochemistry. EPM exposure increased plasma CORT levels without altering plasma NPY levels. Acute ethanol treatment significantly increased light dark transitions and latency to re-enter the light arena, but no differences were seen between high-and low-anxiety groups and no correlations were found between anxiety-like behaviors in the EPM and LD box. Acute ethanol treatment significantly increased Fos immunoreactivity in the BNST and the central amygdala. Although NPY neurons were not significantly activated following ethanol exposure, in saline-treated animals lower levels of anxiety-like behavior in the LD box (more time in the light arena and more transitions) were correlated with higher NPY-positive cell density in the central amygdala. Our results suggest that activation of the CeA and BNST are involved in the behavioral expression of ethanol-induced anxiolysis, and that differences in basal anxiety state may be correlated with NPY systems in the extended amygdala. (C) 2016 Elsevier Inc. All rights reserved.
机译:焦虑症和酒精使用障碍合并症的发生率很高,表明这些病症之间存在因果关系。先前的研究表明,远交长Evans大鼠的基础焦虑水平与自愿饮酒的差异有关,并且杏仁核神经肽Y(NPY)系统可能在这种关系中起作用。本工作探讨了对乙醇抗焦虑作用的敏感性差异导致这些动物体内乙醇自我施用差异的可能性,并研究了中央和周边NPY在介导这种关系中的潜在作用。首先将动物暴露于高架迷宫(EPM)中,以评估焦虑的个体差异,如行为和循环NPY和皮质酮水平(CORT)。然后,在急性乙醇治疗(1千克/公斤;腹膜内li.p.1)之后,在浅色暗箱(LD箱)中测试大鼠的焦虑样行为,并在杏仁核和纹状体终末床核(BNST)中激活神经元。使用Fos免疫组织化学评估。 EPM暴露可增加血浆CORT水平,而不会改变血浆NPY水平。急性乙醇治疗显着增加了光暗过渡和重新进入光明竞技场的潜伏期,但在高和低焦虑组之间未见差异,在EPM和LD盒中的焦虑样行为之间未发现相关性。急性乙醇治疗显着增加了BNST和中央杏仁核的Fos免疫反应性。尽管暴露于乙醇后NPY神经元并未被显着激活,但在盐水处理的动物中,LD箱中较低水平的焦虑样行为(光舞台上的时间更长,过渡次数更多)与中部较高的NPY阳性细胞密度相关。杏仁核。我们的研究结果表明CeA和BNST的激活与乙醇诱导的抗焦虑行为的表达有关,而基础焦虑状态的差异可能与杏仁核中的NPY系统有关。 (C)2016 Elsevier Inc.保留所有权利。

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