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Mol Neurobiol ; 47(1): 117-22, 2013 Feb.
Article in English | MEDLINE | ID: mdl-22923348

ABSTRACT

Overexpression of calbindin-D(28k) (CaBP-28 k) induces neurite outgrowth in dopaminergic neuronal cells and could provide some protection to dopaminergic neurons against the pathological process in Parkinson's disease. Transgenic mice CaBP-28 k overexpression and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse models were generated, and the effect of midbrain dopamine neurons in ethology was also assessed. Tyrosine hydroxylase (TH)-immunoreactive neurons were counted, and the concentration of total protein and dopamine (DA) of striatum corpora was measured in four animal models. Results showed that the positive TH cells, content of DA, and ability of ethology in MPTP-induced transgenic mice were significantly higher than that in MPTP-induced wild-type mice. The findings demonstrate that overexpression of CaBP-28 k could provide protection for DA neurons from neurodegeneration. It would provide a potential strategy in the treatment of Parkinson's diseases.


Subject(s)
Neuroprotective Agents/metabolism , Parkinson Disease/metabolism , Parkinson Disease/pathology , S100 Calcium Binding Protein G/metabolism , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine , Animals , Behavior, Animal , Blotting, Western , Calbindins , Caspase 3/metabolism , Corpus Striatum/metabolism , Corpus Striatum/pathology , Disease Models, Animal , Dopaminergic Neurons/metabolism , Dopaminergic Neurons/pathology , Mice , Mice, Inbred C57BL , Mice, Transgenic , Parkinson Disease/enzymology , Proto-Oncogene Proteins c-bcl-2/metabolism , Substantia Nigra/enzymology , Substantia Nigra/metabolism , Substantia Nigra/pathology , Tyrosine 3-Monooxygenase/metabolism
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