INVOLVEMENT OF DOPAMINE D-2 RECEPTOR MECHANISM IN THE REM-SLEEP DEPRIVATION-INDUCED INCREASE IN SWIMMING ACTIVITY IN THE FORCED SWIMMING TEST

Effects of monoamine synthesis inhibitors and dopamine antagonists on rapid eye movement sleep (REMs) deprivation treatment-induced increase in swimming activity were examined. Mice were deprived of REMs for 48 h by a small pedestal method. Swimming activity in REMs-deprived mice was significantly higher than those in group-housed or socially isola ted animals used as the control. dl-alpha-Methyl-p-tyrosine methyl est er HCl (250 mg/kg, IP) decreased the swimming activity in REMs-deprive d mice, whereas neither disulfiram (400 mg/kg, SC), a noradrenaline sy nthesis inhibitor, nor dl-p-chlorophenylalanine methyl ester HCl (300 mg/kg, IP) changed it. (+)-SCH23390 HCl (30 and 100 mu g/kg, IP), a se lective dopamine D-1 antagonist, did not affect the activity in REMs-d eprived mice. (+/-)-Sulpiride (12.5 and 25 mg/kg, IP), a selective dop amine D-2 antagonist, dose-dependently decreased swimming activity in REMs-deprived mice, while it did not significantly change the swimming activity in the control animals. These results suggest that REMs depr ivation treatment-induced increase in swimming activity is mainly due to the functional changes in the dopaminergic system rather than the n oradrenergic or serotonergic system, and that dopamine D-2 but not D-1 receptor mechanism is involved in the increase in swimming activity i n REMs-deprived animals.