Estrogen Increases Striatal GDNF Immunoreactivity with no Effect on Striatal FGF-2 Immunoreactivity of MPTP-Treated Mice
Wanida Tripanichkul PhD*, Em-orn Jaroensuppaperch MSc*
Affiliation : * Department of Anatomy, Faculty of Medicine, Srinakharinwirot University, Bangkok, Thailand
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 of GDNF and FGF-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 processed for tyrosine hydroxylase (TH), GDNF,
and FGF-2 immunohistochemistry. Extent of DA 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 of the MPTP-intoxicated animals.
Conclusion : One possible mechanism by which E2 protects nigrostriatal DA axons against MPTP is through upregulation
of striatal GDNF.
Keywords : GDNF, FGF-2, Estrogen, MPTP, Nigrostriatal dopaminergic axon
