Chronic binge-like moderate ethanol drinking in rats results in widespread decreases in brain serotonin, dopamine, and norepinephrine turnover rates reversed by ethanol intake.
Chronic binge-like moderate ethanol drinking in rats results in widespread decreases in brain serotonin, dopamine, and norepinephrine turnover rates reversed by ethanol intake.
复制标题
大鼠慢性暴食式适度饮酒会导致大脑血清素、多巴胺和去甲肾上腺素周转率普遍下降，而乙醇摄入却逆转了这一现象。
DOI：
10.1111/j.1471-4159.2008.05296.x
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发表时间：
2008
影响因子：
4.7
通讯作者：
Cunningham,CarolC
中科院分区：
文献类型：
--
作者：
Smith,JamesE;Co,Conchita;McIntosh,Scott;Cunningham,CarolC
这项研究的目的是评估啮齿类动物饮用乙醇/蔗糖 (EtOH) 和蔗糖 (SUC) 期间以及有饮用乙醇/蔗糖 (SUC) 史的动物脑区多巴胺 (DA)、去甲肾上腺素 (NA)、血清素 (5-HT)、天冬氨酸、谷氨酸和 GABA 的周转率 (TOR)，以进一步表征强迫性消费背后的神经系统。使用五只雄性大鼠为一组，其中两只经过训练喝 EtOH 溶液，两只训练喝 SUC，一只作为不饮酒对照。当获得稳定的饮酒模式时，对大鼠进行静脉内脉冲标记，并在 60 或 90 分钟后处死大鼠，并测定大脑区域中 DA、去甲肾上腺素、5-HT、天冬氨酸、谷氨酸和 GABA 的 TOR。检测到 EtOH 饮用、SUC 饮用或 EtOH 或 SUC 饮用史特异的 5-HT、DA 和 NA TOR 变化。检测到急性乙醇剥夺效应，该效应大部分可通过饮用乙醇而逆转。这些结果表明，狂饮适量乙醇会导致神经元功能缺陷，这可能会为缓解快感缺乏刺激奠定基础，进一步摄入乙醇会加强乙醇寻找行为，这可能会导致高危人群中乙醇的使用增加。
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.