Department of Neurobiology, Xuzhou Medical College, Xuzhou, Jiangsu, China.
Mol Neurobiol. 2013 Feb;47(1):117-22. doi: 10.1007/s12035-012-8332-3. Epub 2012 Aug 25.
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.
钙结合蛋白-28k（CaBP-28k）的过表达可诱导多巴胺能神经元细胞的突起生长，并可能为帕金森病中的多巴胺能神经元提供一些保护。生成了过表达 CaBP-28k 的转基因小鼠和 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的小鼠模型，并评估了中脑多巴胺神经元在行为学上的影响。计数酪氨酸羟化酶（TH）免疫反应性神经元，并测量四个动物模型纹状体的总蛋白和多巴胺（DA）浓度。结果表明，MPTP 诱导的转基因小鼠中的阳性 TH 细胞、DA 含量和行为学能力明显高于 MPTP 诱导的野生型小鼠。这些发现表明，CaBP-28k 的过表达可以为 DA 神经元提供免受神经退行性变的保护。这为帕金森病的治疗提供了一种潜在策略。
