Involvement of dopamine D 2 receptor mechanism in the REM sleep deprivation-induced increase in swimming activity in the forced swimming test

Abstract

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- α-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 gmg/kg, IP), a selective dopamine D 1 antagonist, did not affect the activity in REMs-deprived mice. (±)-Sulpiride (12.5 and 25 mg/kg, IP), a selective dopamine 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 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 D 2 but not D 1 receptor mechanism is involved in the increase in swimming activity in REMs-deprived animals.