Monoamine depletion attenuates the REM sleep deprivation-induced increase in clonidine response in the forced swimming test

Abstract

Effect of monoamine depletion on the REM sleep (REMs) deprivation-induced increase in clonidine response in the forced swimming test was investigated. Mice were deprived of REMs by the small pedestal method. Clonidine HCl (10–1000 μm/kg, IP), an α 2-adrenoceptor agonist, dose dependently increased swimming activities in group-housed and socially isolated mice used as the control groups. The dose-response relationship shifted to the left following REMs deprivation (ED 50 values in the group-housed, isolated, and REMs-deprived mice were 250, 200, and 27 μg/kg, respectively). Monoamine depletion, induced by reserpine (5 mg/kg, IP) plus α-methyl- p-tyrosine (250 mg/kg, IP), did not produce any changes in the effects of clonidine in the control groups. However, in REMs-deprived mice, monoamine depletion significantly decreased the effect of 100 μg/kg clonidine, but not that of 300 μg/kg clonidine on swimming activity. These results indicate that clonidine-induced increase in swimming activity in the forced swimming test is mainly mediated by postsynaptic α 2-adrenoceptor, and that endogenous noradrenaline in the brain plays an important role in the increase of clonidine response following REMs deprivation treatment. The neuronal mechanism of the increase in clonidine response is discussed.