Ethanol-induced anxiolysis and neuronal activation in the amygdala and bed nucleus of the stria terminalis.
Ethanol-induced anxiolysis and neuronal activation in the amygdala and bed nucleus of the stria terminalis.
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DOI：
10.1016/j.alcohol.2015.11.001
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发表时间：
2016-02
期刊：
影响因子：
--
通讯作者：
Wilson MA
中科院分区：
文献类型：
--
作者：
Sharko AC;Kaigler KF;Fadel JR;Wilson MA
焦虑症和酒精使用障碍的高并发率表明这些疾病之间存在因果关系。先前的研究表明，近交系 Long-Evans 大鼠的基础焦虑水平与自愿乙醇消耗的差异相关，并且杏仁核神经肽 Y (NPY) 系统可能在这种关系中发挥作用。目前的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不同的乙醇自我给药的可能性，并研究了中枢和外周 NPY 在介导这种关系中的潜在作用。首先将动物暴露于高架十字迷宫 (EPM)，以评估焦虑样行为以及循环 NPY 和皮质酮 (CORT) 水平的个体差异。然后在急性乙醇治疗（1 g/kg；腹膜内[i.p.]）后在明暗盒（LD盒）中测试大鼠的焦虑样行为，并使用Fos免疫组织化学评估杏仁核和终纹床核（BNST）中的神经元激活。 EPM 暴露增加血浆 CORT 水平，但不改变血浆 NPY 水平。急性乙醇治疗显着增加了明暗转变和重新进入光场的潜伏期，但在高焦虑组和低焦虑组之间没有发现差异，并且在 EPM 和 LD 盒中的焦虑样行为之间没有发现相关性。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。尽管乙醇暴露后 NPY 神经元没有显着激活，但在盐水处理的动物中，LD 盒中较低水平的焦虑样行为（更多的时间在光场和更多的转换）与中央杏仁核中较高的 NPY 阳性细胞密度相关。我们的结果表明，CeA 和 BNST 的激活参与了乙醇诱导的抗焦虑作用的行为表达，并且基础焦虑状态的差异可能与扩展杏仁核中的 NPY 系统相关。
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 g/kg; intraperitoneally [i.p.]), 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.