Recently, mutations in the alpha -synuclein (PARK1) and parkin (PARK2) genes have been identified from patients with the familial Parkinson's disease and parkinsonism, respectively. Systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is known to damage the nigrostriatal dopaminergic system in C57BL/6 mice, in this study, we have investigated changes of immunoreactivities for alpha -synuclein, parkin and tyrosine hydroxylase (TH) in MPTP-treated C57BL/6N mouse brains. Immunoreactivities for alpha -synuclein, parkin and TH were differentially distributed in the mouse brain. MPTP treatment caused significant decrease of the number of TH-, alpha -synuclein- and parkin-immunopositive neurons in the substantia nigra, although these immunoreactivities were not markedly changed in the striatum. These results suggest that alpha -synuclein and parkin may participate in MPTP-induced dopaminergic neurodegeneration in the substantia nigra.