Journal
NEUROTOXICITY RESEARCH
Volume 22, Issue 4, Pages 274-279Publisher
SPRINGER
DOI: 10.1007/s12640-012-9309-8
Keywords
Nifedipine; Iron; L-type Ca2+ channel; Dopamine neuron
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Funding
- Natural Science Foundation of China [30800353, 30930036]
- Outstanding Young Scientist Research Fund of Shandong Province [BS2011YY002]
- Bureau of Science and Technology of Qingdao [09-1-3-80-jch, 10-3-3-1-3-nsh]
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The mechanisms of iron accumulation in substantia nigra (SN) of Parkinson's diseases remain unclear. The objective of this study was to investigate effects of nifedipine on iron-overload-induced iron accumulation and neurodegeneration in SN of rats. By high performance liquid chromatography-electrochemical detection, tyrosine hydroxylase (TH) immunohistochemistry, and iron content array, we first quantified iron content and the number of dopamine neurons in SN of experimental rats treated with iron dextran. We further assessed effects of treatment with nifedipine. Our results showed that nifedipine treatment prevents iron dextran-induced dopamine depletion in the striatum. Consistently, we found that nifedipine restores the number of TH-positive neurons reduced by iron dextran overload and prevents increase of iron content in the SN. These results suggested that nifedipine may suppress iron toxicity in dopamine neurons and prevent neurodegeneration.
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