25-Hydroxyvitamin D depletion does not exacerbate MPTP-induced dopamine neuron damage in mice.

Dean ED, Mexas LM, Cápiro NL, McKeon JE, DeLong MR, Pennell KD, Doorn JA, Tangpricha V, Miller GW, Evatt ML
PLoS One. 2012 7 (7): e39227

PMID: 22768297 · PMCID: PMC3388077 · DOI:10.1371/journal.pone.0039227

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.

MeSH Terms (13)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Animals Corpus Striatum Dopamine Plasma Membrane Transport Proteins Dopaminergic Neurons Male Mice MPTP Poisoning Nerve Tissue Proteins Neurotoxins Substantia Nigra Tyrosine 3-Monooxygenase Vitamin D

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