Role of brain monoaminergic systems in the increased ethanol drinking caused by REM-sleep deprivation.

: The central monoaminergic neuronal effects of REM-sleep deprivation, and the effect of different monoamine uptake blocking agents on the REM-sleep deprivation-induced increase in ethanol intake were studied. The levels of 5-HT and 5-HIAA in the hypothalamus were increased both in the REM-sleep deprived rats and the stressed control rats, but the hypothalamic level of MHPG was decreased only in the REM-sleep deprived animals. Two daily injections (5-20 mg/kg/d) of citalopram or GBR-12909 (uptake blocking agents for 5-HT and dopamine, respectively) did not modify the increased level of ethanol intake. The noradrenaline uptake blocking agent, talsupram (5-10 mg/kg/d), however, decreased ethanol intake to the levels seen prior to deprivation. This effect of talsupram could be antagonized by blocking alpha-1-adrenoreceptors with prazosin (1 mg/kg/d).