Tanaka M
Department of Pharmacology, Kurume University School of Medicine, Japan.
Nihon Arukoru Yakubutsu Igakkai Zasshi. 1998 Feb;33(1):31-43.
Research on the interaction of ethanol and stress with experimental animals are briefly reviewed. There might be the two aspects of the interaction of stress and ethanol, i.e., how stress affects ethanol ingestion and response to ethanol, and how ethanol modifies stress response. In general, stress increases ingestion of ethanol in animals exposed to various stresses including electric shock, immobilization and psychological or emotional stresses, wherein the psychological or emotional factors were predominantly involved. However, in most cases, ethanol ingestion is increased after release from stress not during exposure to stress. A variety of stressful stimuli caused marked increases in the neurotransmitter release in many brain regions. Immobilization stress increased noradrenaline release in the extended brain regions in rats. These increases were significantly attenuated by pretreatment with ethanol in the rat amygdala and locus coeruleus, but not in the hypothalamus, although ethanol by itself increased noradrenaline release in the hypothalamus. Further, psychological stress, wherein the rats were given no electrical shock, but exposed to the emotional responses such as struggling, vocalization, jumping and defecation shown by the other electrically-shocked rats, increased noradrenaline release preferentially in the hypothalamus, amygdala and locus coeruleus. Among the former two regions, stress-induced increases in noradrenaline release were significantly attenuated by ethanol in the amygdala, but not in the hypothalamus. Together with the finding that increases, in noradrenaline release are closely related to the provocation of anxiety and/or fear, ethanol, in part, reduced tension, as mentioned in the tension reduction hypothesis, by attenuating stress-induced increases in noradrenaline release in the amygdala and locus coeruleus. Moreover, ethanol, administered i.p. and directly through the microdialysis probe, increased dopamine release in the nucleus accumbens assessed by in vivo microdialysis, similarly as addictive drugs such as amphetamine did. This might be, in part, neurochemical basis for motivation of repeated drinking of ethanol.
本文简要综述了关于乙醇与应激相互作用的实验动物研究。应激与乙醇的相互作用可能存在两个方面，即应激如何影响乙醇摄入及对乙醇的反应，以及乙醇如何改变应激反应。一般来说，应激会增加暴露于各种应激（包括电击、固定和心理或情绪应激）下的动物的乙醇摄入量，其中心理或情绪因素起主要作用。然而，在大多数情况下，乙醇摄入在应激解除后增加，而非在应激暴露期间增加。多种应激刺激导致许多脑区神经递质释放显著增加。固定应激增加了大鼠扩展脑区的去甲肾上腺素释放。在大鼠杏仁核和蓝斑中，乙醇预处理可显著减弱这些增加，但在下丘脑中则不然，尽管乙醇本身会增加下丘脑中去甲肾上腺素的释放。此外，心理应激（即不给大鼠电击，但让其暴露于其他受电击大鼠表现出的挣扎、发声、跳跃和排便等情绪反应）优先增加下丘脑、杏仁核和蓝斑中的去甲肾上腺素释放。在前两个区域中，应激诱导的去甲肾上腺素释放增加在杏仁核中被乙醇显著减弱，但在下丘脑中则未减弱。与去甲肾上腺素释放增加与焦虑和/或恐惧激发密切相关的发现一致，乙醇部分地通过减弱应激诱导的杏仁核和蓝斑中去甲肾上腺素释放增加，如紧张减轻假说中所述，降低了紧张感。此外，腹腔注射乙醇并通过微透析探针直接给药，与苯丙胺等成瘾药物类似，通过体内微透析评估发现其增加了伏隔核中的多巴胺释放。这可能部分是反复饮用乙醇动机的神经化学基础。
