Changes in local cerebral glucose utilization associated with Parkinson's syndrome induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the primate

The quantitative 2-14C]deoxyglucose autoradiographic method was used to map the pattern of alterations in local cerebral glucose utilization associated with the Parkinsonian syndrome induced by the administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), to rhesus monkeys. Monkeys treated with the neurotoxin exhibited both behavioral symptoms (e.g. akinesia, rigidity, flexed posture, and eyelid closure) and neuropathological changes (degeneration of the cells of the substantia nigra pars compacta) that closely paralleled those in human Parkinson's disease. Glucose utilization was significantly reduced in the pars compacta of the substantia nigra and in the subthalamus, and increased in the external segment of the globus pallidus. Outside the basal ganglia reductions in glucose utilization were limited to the mediodorsal nucleus of the thalamus, frontal eye fields, and ventral tegmental area. The results of these studies indicate that the profound functional and behavioral deficits in MPTP-induced Parkinson's syndrome are the consequences of highly selective functional changes in a few cerebral structures, mainly within the basal ganglia.