THE EFFECTS OF ALPHA-2-ADRENOCEPTOR STIMULATION ON NEOCORTICAL EEG ACTIVITY IN CONTROL AND 6-HYDROXYDOPAMINE DORSAL NORADRENERGIC BUNDLE-LESIONED RATS

The present study investigated the effects of a alpha2-adrenoceptor ag onist, D-medetomidine (0.3, 3.0, 30.0 and 300.0 mug/kg, s.c.), on neoc ortical EEG activity in control and 6-hydroxydopamine dorsal noradrene rgic bundle-lesioned rats. D-Medetomidine at 0.3, 3.0 and 30.0 mug/kg dose dependently increased waking-immobility-related high-voltage spik e and wave spindles. Movement and waking-immobility-related slow wave activity was increased at doses of 3.0, 30.0 and 300.0 mug/kg. D-Medet omidine at 300.0 mug/kg produced continuous 1-2 Hz slow wave activity and the animals were markedly sedated. In rats injected with D-medetom idine at 0.3, 3.0 and 30.0, mug/kg EEG activity could be desynchronize d (block of high-voltage spindles and slow waves) by pinching the tail . However, rats injected with D-medetomidine at 300.0 mug/kg showed no change in EEG activity or behavior following tail pinching. D-Medetom idine induced similar EEG activity (high-voltage spindles and slow wav es) and behavioral changes (sedation) in 6-hydroxydopamine dorsal nora drenergic bundle-lesioned rats. Atipamezole, an alpha2-adrenoceptor an tagonist, blocked D-medetomidine-induced EEG and behavioral changes in control and 6-hydroxydopamine dorsal noradrenergic bundle-lesioned ra ts. Based on the present results we suggest that stimulation of presyn aptic noradrenergic fibers is not a prerequisite for the increase of h igh-voltage spindle and slow wave activity induced by an alpha2-adreno ceptor agonist and that the magnitude of EEG slowing induced by D-mede tomidine correlates with the decreased behavioral response to sensory stimulation.