Differential effects of limbic versus striatal dopamine loss on motoric function.
Bilateral 6-hydroxydopamine injections into either the ventral tegmental area, or the substantia nigra pars compacta in rats, produced severe losses of dopamine in the nucleus accumbens-olfactory tubercle and striatum respectively. After 1 and 3 months postoperation, the depletion of limbic dopamine was associated with reduced spontaneous locomotor activity, which was enhanced by apomorphine (0.125 mg/kg), but not amphetamine (1.0 mg/kg). The severe loss of striatal dopamine had no persistent effect on spontaneous or D-amphetamine-induced locomotor activity, but did produce a persistent augmentation of rigidity. Although there was considerable recovery, both lesions chronically increased catalepsy scores. The results of this study suggested that limbic dopamine deficits may be important in initiation of movement; whereas, striatal dopamine deficits may contribute more to the rigidity aspects of Parkinsonism.
D000818:Animals; D002375:Catalepsy / Q000503:physiopathology; D003342:Corpus Striatum / Q000502:physiology*; D003913:Dextroamphetamine / Q000494:pharmacology; D004298:Dopamine / Q000502:physiology*; D006801:Humans; D006892:Hydroxydopamines / Q000494:pharmacology; D008032:Limbic System / Q000502:physiology*; D008124:Locomotion; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009127:Muscle Rigidity / Q000503:physiopathology; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains
D006892:Hydroxydopamines; D016627:Oxidopamine; D003913:Dextroamphetamine; D004298:Dopamine