Publication
25-Hydroxyvitamin D Depletion Does Not Exacerbate MPTP-Induced Dopamine Neuron Damage in Mice
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- Last modified
- 02/20/2025
- Type of Material
- Authors
- Language
- English
- Date
- 2012-07-02
- Publisher
- Public Library of Science
- Publication Version
- Copyright Statement
- This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
- License
- Final Published Version (URL)
- Title of Journal or Parent Work
- ISSN
- 1932-6203
- Volume
- 7
- Issue
- 7
- Start Page
- e39227
- End Page
- e39227
- Grant/Funding Information
- This material is the result of work supported with resources and the use of facilities at the Atlanta Veterans Affairs Medical Center.
- Dr. Tangpricha is supported by grant K23 AR054334 from the National Institutes of Health.
- This study was funded by grants from the National Institutes of Health (P01 ES 016731 and T32 ES 012870).
- Abstract
- Recent clinical evidence supports a link between 25-hydroxyvitamin D insufficiency (serum 25-hydroxyvitamin D [25(OH)D] levels <30 ng/mL) and Parkinson’s disease. To investigate the effect of 25(OH)D depletion on neuronal susceptibility to toxic insult, we induced a state of 25(OH)D deficiency in mice and then challenged them with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP). We found there was no significant difference between control and 25(OH)D-deficient animals in striatal dopamine levels or dopamine transporter and tyrosine hydroxylase expression after lesioning with MPTP. Additionally, we found no difference in tyrosine hydroxylase expression in the substantia nigra pars compacta. Our data suggest that reducing 25(OH)D serum levels in mice has no effect on the vulnerability of nigral dopaminergic neurons in vivo in this model system of parkinsonism.
- Author Notes
- Research Categories
- Health Sciences, Public Health
- Health Sciences, Pharmacology
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