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Estrogen Increases Striatal GDNF Immunoreactivity with no Effect on Striatal FGF-2 Immunoreactivity of MPTP-Treated
Background:
Glial derived neurotrophic factor (GDNF) and basic fibroblast growth factor (FGF-2) protect nigrostriatal dopaminergic (DA) neurons and their projections in animal models of Parkinson's disease (PD). Recent data indicate neuroprotective effects of estrogen in PD animal models through its anti-inflammatory and anti-oxidative effects, yet the hormonal effects on GDNF and FGF-2 expression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice remain uninvestigated.
Objective:
To determine the effects of 17 beta-estradiol (E2) on DA innervation and the expression ofGDNFandFGF-2 in the striatum of MPTP-treated mice.
Material And Method:
Adult male mice were treated with E2 or vehicle for 11 days during which they were injected with MPTP or saline on the sixth day. The striatum was collected on day 11 and processedfor tyrosine hydroxylase (TH), GDNF and FGF-2 immunohistochemistry. Extent ofDA innervation and the expression of GDNF and FGF-2 in the striatum were assessed by measuring optical density of TH, GDNF and FGF-2 immunoreactivity, respectively.
Results:
MPTP induced loss of DA axons and upregulation of FGF-2 expression, but did not alter GDNF level. E2 alleviated loss of DA axons, increased GDNF level, yet caused no change in FGF-2 level ofthe MPTP-intoxicated animals.
Conclusion:
One possible mechanism by which E2 protects nigrostriatal DA axons against MPTP is through upregulation ofstriatal GDNF.
