Involvement of dopamine D2 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 isolated animals used as the control. dl-alpha-Methyl- p-tyrosine methyl ester HCl (250 mg/kg, IP) decreased the swimming activity in REMs-deprived mice, whereas neither disulfiram (400 mg/kg, SC), a noradrenaline synthesis inhibitor, nor dl-p-chlorophenylalanine methyl ester HCl (300 mg/kg, IP) changed it. (+)-SCH23390 HCl (30 and 100 micrograms/kg, IP), a selective dopamine D1 antagonist, did not affect the activity in REMs-deprived mice. (+/-)-Sulpiride (12.5 and 25 mg/kg, IP), a selective dopamine D2 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 deprivation treatment-induced increase in swimming activity is mainly due to the functional changes in the dopaminergic system rather than the noradrenergic or serotonergic system, and that dopamine D2 but not D1 receptor mechanism is involved in the increase in swimming activity in REMs-deprived animals.