Time dependent alterations of co-localization of S100β and GFAP in the MPTP-treated mice

Abstract
S100β is a calcium-binding peptide produced by astrocytes. This protein is expressed at high levels in brain and is known as a marker of brain damage. However, little is known about the role of S100β protein during neuronal damage caused by MPTP. To determine exactly changes of expression of S100β protein in relation to changes of glial cells, we investigated immunohistochemically the expression of S100β protein using MPTP-treated mice. The present study showed that tyrosine hydroxylase (TH) immunoreactivity was decreased in the striatum and substantia nigra from 5 h and 1 day after MPTP treatment, respectively. Thereafter, a severe reduction in TH immunoreactivity was observed in the striatum and substantia nigra 1, 3 and 7 days after MPTP treatment. In our double-labeled immunostaining, the number of S100-positive/GFAP-negative cells decreased from 1 day up to 7 days after MPTP treatment. In contrast, the number of double-labeled S100/GFAP-immnoreactive cells increased from 1 day up to 7 days after MPTP treatment. The number of S100β-positive/GFAP-negative cells also decreased 3 and 7 days after MPTP treatment. In contrast, the number of double-labeled S100β/GFAP-immunoreactive cells increased from 1 day up to 7 days after MPTP treatment. The present study demonstrates that S100β/GFAP-positive cells may play some role in the pathogenesis of MPTP-induced dopaminergic neurodegeneration in the striatum. The present results also suggest the presence of the S100β protein in a subpopulation of GFAP-negative astrocytes in the striatum after MPTP treatment. These results suggest that the modulation of astrocytic activation may offer a novel therapeutic strategy of Parkinson’s disease.

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