[The role of dopamine neurotransmission on the development of ethanol dependence and course of abstinence syndrome].

This paper evaluates the influence of acute and chronic ethanol intoxication and withdrawal syndrome in rats and humans on central dopaminergic neurotransmission. Acute, low dose of ethanol (1.0 g/kg), produced a significant increase of dopamine level in rat's central nervous system (CNS) and decreased prolactin (PRL) level in blood serum. In chronic experiment rats were given the following dopaminergic agents: SKF 38393, PPHT, SCH 23393, Pimozide. Ethanol potentiated D1 agonist features, whereas has no influence on D1 antagonist action in CNS, which reveals that chronic ethanol produced hypersensitivity of D1 receptors. Chronic ethanol potentiated pimozide action in behavioral tests. Chronic ethanol produced a decrease of compensatory augmentation of dopamine in rat's CNS after pimozide administration. PPHT, a potent D2 agonist normalized withdrawal symptoms in alcohol dependent rats. In the clinical part of experiment 21 alcohol dependent male individuals were examined for ethanol withdrawal syndrome, using DSM-III/R criteria, alcohol dependence index (WGU), and presence of dependence scale symptoms (WWO). The intensity of withdrawal symptoms was examined using Sandowal-Wang scale. The level of blood serum PRL was also measured, twice a day (8 a.m. and 8 p.m.) on the 1st, 3rd, 7th, 14th, 21st day of experiment. It was established that WGU as well as WWO and DSM-III-R criteria did separate similar groups of patients with the same depth of dependence, clinical symptoms and prognosis. This study reveals a negative correlation between intensity of withdrawal symptoms and PRL levels in blood serum on the 1st day of abstinence. PRL levels were increased from 3rd to 21st day of study. Ethanol withdrawal symptoms intensity index was positively correlated with WGU.