Fadda F, Argiolas A, Melis M R, Serra G
Boll Soc Ital Biol Sper. 1980 Dec 30;56(24):2553-8.
A single oral administration of 3.2 g/kg ethanol to normal rats increased 3,4-dihydroxyphenylacetic acid (DOPAC) content and DOPA formation in the caudate nucleus but had no effect in frontal cortex and substantia nigra and did not modify dopamine (DA) levels in any of the brain regions analyzed. Complete tolerance to the stimulant effect on DOPA formation developed after chronic ethanol-treatment (3.2 g/kg daily for 60 days). However ethanol administration to ethanol dependent rats produces a marked DA depletion and increases DOPAC concentration in the brain areas studied. The present results show that acute and chronic ethanol release DA stores, but only in the acute conditions DA depletion is compensated by enhanced synthesis.
给正常大鼠单次口服3.2克/千克乙醇，可增加尾状核中3,4 - 二羟基苯乙酸（DOPAC）含量和多巴胺（DOPA）生成，但对额叶皮质和黑质无影响，且未改变所分析的任何脑区中的多巴胺（DA）水平。慢性乙醇处理（每日3.2克/千克，持续60天）后，对DOPA生成的刺激作用产生了完全耐受性。然而，给乙醇依赖大鼠施用乙醇会导致所研究脑区中DA明显耗竭，并增加DOPAC浓度。目前的结果表明，急性和慢性乙醇都会释放DA储备，但只有在急性情况下，DA耗竭会通过增强合成来补偿。
