Dopaminergic Fibers In Striatum Research Articles

Complement 3-deficient mice are not protected against MPTP-induced dopaminergic neurotoxicity

Recent studies have invoked inflammation as a major contributor to the pathogenesis of Parkinson's disease (PD). Emerging evidence indicated that components of complement system may be involved in such disorder and contribute to its development. We thus observed the influence of deficiency of complement 3 (C3), the key component of complement system, on the death of dopaminergic neurons in substantia nigra pars compacta (SNpc) and the loss of dopaminergic fibers in striatum induced by acute or chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Immunohistochemical staining of dopaminergic neurons in SNpc and neurochemical analysis of dopamine and its metabolites in striata revealed that there was no significant difference between the two genotypes. Longer survival time also indicated that C3 might not mediate the spontaneous recovery of dopaminergic fibers in mouse striatum acutely challenged by MPTP. We conclude that, despite growing evidence indicating the involvement of complement system in the pathogenesis of PD, our data do not support a role for C3 in this established model of PD, as indicated by results from HPLC analysis and immunohistochemical staining.

Chapter 69 Recovery of dopaminergic fibers in striatum of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mouse is enhanced by grafts of adrenal medulla

Publisher Summary This chapter discusses the suitability of the l-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridin (MPTP)-treated mouse as a rodent model for grafting in Parkinson's disease, after the adult mouse adrenal medulla is grafted into the striatum of MPTP-treated mice. The chapter also describes the effects of these homografts were studied by following catecholaminergic phenotypic markers in the host brain, and in the graft itself. As adrenal medullary cells synthesize dopamine and have the potential for growing neuronal-like processes when placed in vitro and in oculo, they are considered possible replacements for dopamine neurons, which are lost in Parkinson's disease. However, studies of grafted adrenal cells in rodent models of Parkinson's disease suggest that these cells survive poorly after grafting to the brain, although survival is improved by nerve growth factor. Thus, the mechanisms responsible for the dramatic recovery of dopaminergic fibers in the striatum, and the source of cells elaborating these processes remain to be elucidated.