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Early environmental exposure to methanol as a sensitization factor for Parkinson's disease: a closer look into the etiology of PD
Author(s) -
Mackey Veronica Renee,
Charlton Clivel G.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.715.4
Subject(s) - mptp , substantia nigra , striatum , parkinson's disease , dopaminergic , basal ganglia , medicine , tyrosine hydroxylase , endocrinology , sensitization , dopamine , neuroscience , disease , psychology , chemistry , central nervous system
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive loss of substantia nigra (SN) dopaminergic neurons that project to the striatum. The etiology of PD is unknown; there is the possibility of early exposure to toxicants creating a vulnerability stage for PD to occur later in life. Here, we investigate whether methanol (MeOH) exposure in early life causes sensitization of the basal ganglia to challenges, such as 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) that precipitates the symptoms of PD. C57/bl6 mice were exposed to sub‐chronic levels of MeOH in utero. At 12 wks of age, the offspring were treated with MPTP for seven days. Tyrosine hydroxylase (TH) protein was analyzed in the midbrain and striatum. MPTP increases the expression of TH in the midbrain and reduces it in the striatum, suggesting that the increase of TH in the midbrain may be due to impairment of its transport from cell bodies in the SN to the terminals in the striatum. Lastly, the fetal MeOH sensitized the mice to MPTP reducing effects, suggesting that fetal exposure to MeOH may be a pre‐disposing factor for PD. This project was supported, in part by NIH Grant 1R21 NS 049623‐01A1