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Dexamethasone reverses the ethanol-induced anxiolytic effect in rats.

机译:地塞米松逆转了乙醇诱导的大鼠抗焦虑作用。

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The effects of intraperitoneal and intrahippocampal administration of the glucocorticoid dexamethasone were assessed regarding ethanol-induced anxiolysis in the elevated plus-maze in rats. Animals pretreated with systemic injections of dexamethasone (0.5, 1. 0, or 2.0 mg/kg, IP) 15 min before ethanol (1.2 g/kg, 14% w/v, IP) administration showed a significant dose-dependent attenuation of the increased percentage of frequency and time spent on open arms of the maze. However, IP dexamethasone treatment 4 h before the test had no effect. Unilateral intrahippocampal injection of dexamethasone (2 and 20 nmol in 0.5 microl) also significantly attenuated the increased exploration of the open arms induced by ethanol. The results are interpreted in terms of the modulation of the anxiolytic effects of ethanol by glucocorticoids and the possible involvement of hippocampus in this response. The rapid blockade of ethanol induced anxiolysis by dexamethasone strengthens the suggestion that a nongenomic mechanism may underlie this response.
机译:关于乙醇诱导的高迷宫迷迭香中乙醇诱导的抗焦虑作用,评估了腹膜内和海马内给予糖皮质激素地塞米松的效果。在乙醇(1.2 g / kg,14%w / v,IP)给药前15分钟,以系统注射地塞米松(0.5、1。0或2.0 mg / kg,IP)进行预处理的动物表现出明显的剂量依赖性衰减。增加了迷宫张开双臂的频率和时间所占的百分比。但是,在测试前4小时IP地塞米松治疗无效。海马侧向注射地塞米松(0.5微升中分别加入2和20 nmol)也显着减弱了乙醇诱导的张开双臂的探索性增加。根据糖皮质激素对乙醇的抗焦虑作用的调节以及海马可能参与该反应来解释该结果。地塞米松对乙醇诱导的抗焦虑作用的快速阻断,加强了这种反应可能是非基因组机制的提示。

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