Studies in the late 1970s first reported that transplantation of fetal ventral mesencephalic tissue into the striatum could improve motor function in the 6-hydroxy dopamine (6-OHDA) lesioned rat model of PD (Bjorklund and Stenevi, 1971; Perlow et al., 1979). Autopsy studies in these animals showed that transplantation was associated with significant increases in striatal tyrosine hydroxylase (TH) immunoreactive staining and dopamine levels (Nikkhah et al., 1994). Motor improvement in this model was proportional to the number of transplanted fetal ventral mesen-cephalic cells (Brundin et al., 1986). Transplantation of dopamine neurons into the SNc failed to produce similar benefits unless axons extended to the striatum, illustrating the importance of striatal dopamine innervation for motor function (Dunnett et al., 1983; Collier et al., 2002). Implanted cells have been shown to manufacture and release dopamine, to form normal appearing synapses, to have normal electrical firing patterns, and to be capable of autoregulation (Wuerthele et al., 1981; Schmidt et al., 1982; Brundin et al., 1988). The specificity of the transplant procedure is illustrated by the observation that benefits are not detected if the right tissue (fetal mesen-cephalon) is implanted into the wrong part of the brain (cerebellum), or if the wrong tissue (non-dopaminergic cells) is implanted into the right place (striatum) (Dunnett et al., 1988). Importantly, numerous studies have demonstrated motor benefits following transplantation of fetal nigral dopamine cells into the striatum of both the 6-OHDA lesioned rodent and the MPTP-lesioned primate (Dunnett and Annett, 1991; Olanow et al., 1996).
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