Swerdlow N R, Hauger R, Irwin M, Koob G F, Britton K T, Pulvirenti L
Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla 92093.
Neuropsychopharmacology. 1991 Aug;5(1):23-31.
In humans who chronically abuse amphetamine (AMPH), sudden abstinence often precipitates an organic mood disorder that mimics many symptoms of major depression. We report that AMPH exposure and withdrawal in rats modifies hypothalamic-pituitary-adrenal axis endocrine responses, peripheral immune functions, and regional brain catecholamine levels. Compared to vehicle-treated animals, rats treated with AMPH for 10 days exhibit significantly decreased physostigmine-induced release of adrenocorticotropin hormone (ACTH). During AMPH withdrawal, these animals show a loss of the normal correlation between levels of plasma ACTH and corticosterone. Chronic AMPH treatment in rats causes a significant increase in natural killer cell activity. Brain dopamine levels in these animals are decreased in the caudate nucleus but are increased in the nucleus accumbens. AMPH withdrawal in rats may be a useful model for studying the physiologic and neural substrates of human AMPH withdrawal states.
在长期滥用苯丙胺（AMPH）的人类中，突然戒断常常会引发一种器质性情绪障碍，该障碍模仿了重度抑郁症的许多症状。我们报告称，大鼠接触AMPH及戒断会改变下丘脑-垂体-肾上腺轴的内分泌反应、外周免疫功能以及脑区的儿茶酚胺水平。与用赋形剂处理的动物相比，用AMPH处理10天的大鼠毒扁豆碱诱导的促肾上腺皮质激素（ACTH）释放显著减少。在AMPH戒断期间，这些动物血浆ACTH水平与皮质酮水平之间的正常相关性丧失。大鼠长期接受AMPH处理会导致自然杀伤细胞活性显著增加。这些动物脑内尾状核中的多巴胺水平降低，但伏隔核中的多巴胺水平升高。大鼠AMPH戒断可能是研究人类AMPH戒断状态的生理和神经基础的有用模型。
