REPEATED STIMULATION OF D-1 DOPAMINE-RECEPTORS ENHANCES (-)-11-HYDROXY-DELTA-8-TETRAHYDROCANNABINOL-DIMETHYLHEPTYL-INDUCED CATALEPSY IN MALE-RATS

DOPAMINERGIC and cannabinoid receptors are localized in the outflow nuclei of the basal ganglia. We have investigated the possible interrelation of these receptors in the regulation of motor activity in male rats. To this end we have first studied the behavioural effects of the highly potent cannabinoid receptor agonist (-)11-hydroxy-Delta(8)-tetrahydrocannabinol-dimethylheptyl (HU-210, 20 mu g kg(-1)) after chronic stimulation of dopamine D-1 and D-2 receptors. The catalepsy induced by the synthetic cannabinoid, measured as the descent latency in the bar test, was enhanced in male rats chronically treated with the dopamine D-1 receptor agonist SKF38393 (8 mg kg(-1), twice a day during 21 days). However, animals exposed to the dopamine D-2 agonist quinpirole (1 mg kg(-1) daily during 21 days) displayed the same degree of catalepsy as those exposed to HU-210 alone. Although a possible involvement of D-2 receptors cannot be excluded, this finding suggests a predominant role for dopamine D-1 receptors in the regulation of the cataleptic response to cannabinoids. The possible cross-talk between dopamine D-1 and cannabinoid receptors is further supported by the decreased responsiveness to the acute behavioural effects of SKF38393 (8 mg kg(-1)) observed in animals chronically exposed to HU-210 (20 mu g kg(-1) daily during 14 days).