Abstract
The clinical trials with neural transplantation in patients with Parkinson’s disease are based on 15 years of grafting studies in animal models of this disorder. In these models, the mesostriatal dopamine system is destroyed by a neurotoxin (6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)), which leads to a severe depletion of striatal dopamine levels. It has been shown both in rats and in monkeys that fetal neural grafts, rich in dopamine neurons, taken from the ventral mesencephalon and implanted into the dopamine-denervated striatum, can reinnervate the host striatum, form morphologically normal synaptic contacts with host neurons, release dopamine and improve motor and sensorimotor deficits, including the cardinal symptoms of Parkinson’s disease: tremor, rigidity and hypokinesia (Dunnett, 1991; Freed, 1991). Also human fetal dopamine neurons implanted into the rat parkinson model reinnervate the striatum, release dopamine and improve motor deficits. However, this symptomatic recovery is not complete — all deficits in animals are not reversed by neural grafts.
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