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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Intra-accumbal orexin-1 receptor inhibition prevents the anxiolytic-like effect of ethanol and leads to increases in orexin-A content and receptor expression
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Intra-accumbal orexin-1 receptor inhibition prevents the anxiolytic-like effect of ethanol and leads to increases in orexin-A content and receptor expression

机译：宫内orexin-1受体抑制阻止乙醇的抗焦力样效果，并导致orexin-a含量和受体表达的增加

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摘要

Alcohol use is frequently associated with mood disorders. Similarly, individuals suffering from these disorders have a higher risk of developing alcoholism. Several reports have implicated orexin signaling in different behaviors related to alcohol consumption, whereas antagonists block these actions. However, the involvement of orexin-1-receptor (Orx(1)R) in ethanol-induced anxiolysis remains relatively unexplored. The purpose of this study was to investigate whether intra-accumbal inhibition of Orx(1)R blocks the anxiolytic-like effect of ethanol and to determine if ethanol administration modifies orexin-A content and Orx(1)R expression in the nucleus accumbens (NAc). The elevated-plus-maze test (EPM-test) was used to measure anxiety; orexin-A content and Orx(1)R expression were determined by enzyme-immunoassay and western blot, respectively. The results showed that the pretreatment with a selective antagonist of Orx(1)R, SB-334867 (SB, 3 mu g/side), prevents the anxiolytic-like behavior induced by acute ethanol (2.5 g/kg). SB-334867 per se had no effect on anxiety levels. Pretreatment with SB-334867 followed by ethanol (SB + Et) increased orexin-A content and Orx(1)R levels in the NAc in comparison to the groups that only received ethanol (V + Et) or SB-334867 (SB + S). Ethanol treatment significantly augmented Orx(1)R expression but not the peptide content. The increase in orexin-A observed in SB + Et animals could be due in part to the inhibition of Orx(1)R, since SB-334867 prevents the binding of orexin-A to the receptor. This increase in orexin-A may, in turn, induce an up-regulation of receptor.
机译：酒精使用经常与情绪障碍有关。类似地，患有这些疾病的个体具有更高的发育酗酒风险。几份报告在与酒精消费相关的不同行为中涉及orexin信号传导，而拮抗剂阻止这些行为。然而，orexin-1-受体（ORX（1）r）在乙醇诱导的焦炭中的参与仍然是较为未探索的。本研究的目的是研究ORX（1）R的内骨内抑制是否阻断乙醇的抗焦力样效果，并确定乙醇给药是否在核心宫内改变乙醇蛋白 - 一种含量和ORX（1）r表达（ NAC）。升高的加迷宫试验（EPM-Test）用于测量焦虑; orexin-含含量和ORX（1）r表达分别通过酶 - 免疫测定和蛋白质印迹测定。结果表明，使用Orx（1）R，Sb-334867（Sb，3μg/侧）的选择性拮抗剂的预处理可防止急性乙醇（2.5g / kg）诱导的抗焦虑状行为。 SB-334867本身对焦虑水平没有影响。与仅接受乙醇（V + ET）或SB-334867（SB + S的组（SB + S ）。乙醇治疗显着增强ORX（1）r表达但不是肽含量。在Sb +等动物中观察到的orexin-a的增加可以部分地归因于ORX（1）R的抑制，因为Sb-334867防止orexin-a与受体的结合。反过来，orexin-a的这种增加促使受体的上调。

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