Effect of clonidine on motoneuron excitability in spinalized rats.
In a dose of 0.1 mg/kg clonidine, an alpha-2 receptor agonist, depressed the spontaneous EMG activity of the biceps and quadriceps femoris in chronically-spinalized rats. It also antagonized in a dose-dependent manner the stimulating effect of 5-hydroxytryptophan (5-HTP, 100 mg/kg). Doses of more than 0.1 mg/kg were less potent in antagonizing the effect of 5-HTP. Clonidine reduced the tonic activity of the hindlimb muscles but allowed walking movements. The depressant effect of clonidine in animals pretreated with 5-HTP was prevented by yohimbine (1.25 mg/kg), while the depressant action of the serotonin antagonist, cyproheptadine was not. In chronically-spinalized rats, clonidine (0.1 mg/kg) increased the threshold of electrically-induced flexor and extensor reflexes and decreased their amplitude. No significant modification of reflexes was seen with this dose 24 hr after spinalization. Thus, clonidine in doses of 0.1 mg/kg or less reduced directly or indirectly the excitability of motoneurons. Clonidine may prove to be a useful therapeutic adjunct in the treatment of spasticity.
D000818:Animals; D000870:Anterior Horn Cells / Q000187:drug effects*; D003000:Clonidine / Q000494:pharmacology*; D003655:Decerebrate State / Q000503:physiopathology; D003864:Depression, Chemical; D004525:Efferent Pathways / Q000502:physiology; D004576:Electromyography; D005260:Female; D009046:Motor Neurons / Q000187:drug effects*; D009638:Norepinephrine / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex / Q000187:drug effects; D009435:Synaptic Transmission
D003000:Clonidine; D009638:Norepinephrine