This research was initiated to assess the turnover rates (TORs) of dopamine (DA), norepinephrine (NA), serotonin (5-HT), aspartate, glutamate, and GABA in brain regions during rodent ethanol/sucrose (EtOH) and sucrose (SUC) drinking and in animals with a history of EtOH or SUC drinking to further characterize the neuronal systems that underlie compulsive consumption. Groups of five male rats were used, with two trained to drink EtOH solutions, two to drink SUC and one to serve as a non-drinking control. When stable drinking patterns were obtained, rats were pulse labeled intravenously and killed 60 or 90 min later and the TORs of DA, norepinephrine, 5-HT, aspartate, glutamate, and GABA determined in brain regions. Changes in the TOR of 5-HT, DA, and NA were detected specific to EtOH drinking, SUC drinking or a history of EtOH or SUC drinking. An acute EtOH deprivation effect was detected that was mostly reversed with EtOH drinking. These results suggest that binge-like drinking of moderate amounts of EtOH produces a deficit in neuronal function that could set the stage for the alleviation of anhedonic stimuli with further EtOH intake that strengthen EtOH seeking behaviors which may contribute to increased EtOH use in at risk individuals.

译文

:本研究旨在评估啮齿动物乙醇/蔗糖(EtOH)和蔗糖在大脑区域中多巴胺(DA),去甲肾上腺素(NA),5-羟色胺(5-HT),天冬氨酸,谷氨酸和GABA的转化率(TORs) (SUC)饮酒和具有EtOH或SUC饮酒史的动物,以进一步表征强迫性饮酒的神经系统。使用五只雄性大鼠的组,其中两只受过训练可以喝EtOH溶液,两只可以喝SUC,另一只可以作为非饮酒对照。当获得稳定的饮酒方式时,对大鼠进行静脉脉冲标记并在60或90分钟后处死,并在大脑区域确定DA,去甲肾上腺素,5-HT,天冬氨酸,谷氨酸和GABA的TOR。检测到5-HT,DA和NA的TOR的变化特定于EtOH饮用,SUC饮用或EtOH或SUC饮用的历史。检测到急性的EtOH剥夺作用,多数情况下通过饮用EtOH可以逆转。这些结果表明,像暴饮般饮适量的EtOH会导致神经元功能的缺陷,这可能为进一步减少EtOH摄入而减轻麻痹性刺激提供了条件,从而加强了EtOH的寻求行为,这可能会增加高危人群中EtOH的使用。

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