Recently, mutations in the alpha -synuclein (PARK1) and parkin (PARK2) gene
s have been identified from patients with the familial Parkinson's disease
and parkinsonism, respectively. Systemic administration of 1-methyl-4-pheny
l-1,2,3,6-tetrahydropyridine (MPTP) is known to damage the nigrostriatal do
paminergic system in C57BL/6 mice, in this study, we have investigated chan
ges of immunoreactivities for alpha -synuclein, parkin and tyrosine hydroxy
lase (TH) in MPTP-treated C57BL/6N mouse brains. Immunoreactivities for alp
ha -synuclein, parkin and TH were differentially distributed in the mouse b
rain. MPTP treatment caused significant decrease of the number of TH-, alph
a -synuclein- and parkin-immunopositive neurons in the substantia nigra, al
though these immunoreactivities were not markedly changed in the striatum.
These results suggest that alpha -synuclein and parkin may participate in M
PTP-induced dopaminergic neurodegeneration in the substantia nigra.