Publication: Estrogen increases striatal GDNF immunoreactivity with no effect on striatal FGF-2 immunoreactivity of MPTP-treated mice
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0
Issued Date
2015
Resource Type
File Type
application/pdf
ISSN
1252208
Other identifier(s)
2-s2.0-84957619639
Rights Holder(s)
มหาวิทยาลัยศรีนครินทรวิโรฒ
Bibliographic Citation
Journal of the Medical Association of Thailand. Vol 98, (2015), p.S16-S22
Suggested Citation
Tripanichkul W., Jaroensuppaperch E.O. Estrogen increases striatal GDNF immunoreactivity with no effect on striatal FGF-2 immunoreactivity of MPTP-treated mice. Journal of the Medical Association of Thailand. Vol 98, (2015), p.S16-S22. Retrieved from: https://hdl.handle.net/20.500.14740/6077
Author(s)
Abstract
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. © 2015, Medical Association of Thailand. All rights reserved.
Subject(s)
1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
Estradiol
Fibroblast growth factor 2
Glial cell line derived neurotrophic factor
Tyrosine 3 monooxygenase
1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
Dopamine
Estradiol
Estrogen
Fibroblast growth factor 2
Glial cell line derived neurotrophic factor
Neuroprotective agent
Tyrosine 3 monooxygenase
Adult
Animal experiment
Animal model
Animal tissue
Article
Controlled study
Dopaminergic nerve cell
Immunohistochemistry
Immunoreactivity
Innervation
Male
Mouse
Nerve fiber
Nigroneostriatal system
Nonhuman
Optical density
Protein expression
Animal
C57BL mouse
Corpus striatum
Immunology
Metabolism
Substantia nigra
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Animals
Corpus Striatum
Dopamine
Estradiol
Estrogens
Fibroblast Growth Factor 2
Glial Cell Line-Derived Neurotrophic Factor
Male
Mice
Mice, Inbred C57BL
Neuroprotective Agents
Substantia Nigra
Tyrosine 3-Monooxygenase
Estradiol
Fibroblast growth factor 2
Glial cell line derived neurotrophic factor
Tyrosine 3 monooxygenase
1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
Dopamine
Estradiol
Estrogen
Fibroblast growth factor 2
Glial cell line derived neurotrophic factor
Neuroprotective agent
Tyrosine 3 monooxygenase
Adult
Animal experiment
Animal model
Animal tissue
Article
Controlled study
Dopaminergic nerve cell
Immunohistochemistry
Immunoreactivity
Innervation
Male
Mouse
Nerve fiber
Nigroneostriatal system
Nonhuman
Optical density
Protein expression
Animal
C57BL mouse
Corpus striatum
Immunology
Metabolism
Substantia nigra
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Animals
Corpus Striatum
Dopamine
Estradiol
Estrogens
Fibroblast Growth Factor 2
Glial Cell Line-Derived Neurotrophic Factor
Male
Mice
Mice, Inbred C57BL
Neuroprotective Agents
Substantia Nigra
Tyrosine 3-Monooxygenase