Alcohol intake, ethanol-induced narcosis and intoxication in rats following neonatal 6-hydroxydopamine or 5, 7-dihydroxytryptamine treatment.

Newborn rats were treated with 5,7-dihydroxytryptamine (5,7-HT; 2 x 100 mg/kg s.c., 24 h interval) after pretreatment with desipramine (20 mg/kg s.c.) for depletion of brain 5-hydroxytryptamine (5-HT) or with 6-hydroxydopamine (6-OHDA; 3 x 100 mg/kg s.c., 24 h interval) for selective reduction of brain noradrenaline (NA). The 5,7-HT treatment resulted in a 53% reduction in endogenous 5-HT in the cerebral cortex and a 60% increase in the pons-medulla when determined in adult rats. The 5-HT content in the midbrain was not affected. Endogenous NA in the 6-OHDA treated animals was selectively reduced by 100% in the cerebral cortex, 35% in the midbrain and increased by 117% in the pons-medulla. No difference was found between the voluntary ethanol selection of these groups and that of the controls when measured at the age of 3 months. In a tilting-plane test, ethanol (2 g/kg i.p.) impaired the performance of the 6-OHDA treated rats significantly more than that of the controls. Moreover ethanol (4 g/kg e.p.) produced significantly longer narcosis in these rats. In contrast, the 5,7-HT treated rats were not affected significantly more than the controls in these tests. These results suggest that catecholamine neuronal systems interact with the expression of alcohol intoxication.