Effect of α2-adrenergic drugs on REM sleep deprivation-induced increase in swimming activity

Abstract

Effects of α 2-adrenergic agents on rapid eye movement sleep (REMs) deprivation-induced anti-immobility effect in the forced swimming test (FST) were investigated. Mice were deprived of REMs for 24–72 h by a small pedestal method. Animals that were either group housed or socially isolated during the same period as REMs deprivation were used as the control groups. REMs deprivation for 48 and 72 but not 24 h significantly increased swimming activity without increasing locomotor activity. Clonidine HCl (30–300 μg/kg, IP), an α 2-adrenoceptor agonist, dose-dependently increased swimming activity in group-housed, isolated, and REMs-deprived mice, but the effective doses of clonidine in REMs-deprived mice were lower than those in group-housed or isolated animals. Yohimbine HCl (5 mg/kg, IP), an α 2-adrenoceptor antagonist, blocked the clonidine (300 μg/kg)- but not the REMs deprivation-induced increase in swimming activity. These results suggest that REMs deprivation enhances the sensitivity of the α 2-adrenoceptor and that the increase in swimming activity by REMs deprivation may be mediated by other neuronal mechanisms rather than the α 2-adrenoceptor.