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目的:研究可卡因导致细胞环素依赖激酶5(CDK5)过度表达与细胞骨架蛋白阿尔采末病样过度磷酸化的关系。方法:大鼠腹腔注射可卡因(20mg·kg(?)·d~_(-1)),采用免疫印迹技术检测tau蛋白和神经细丝的过度磷酸化。结果:腹腔注射可卡因8天和16天后,大鼠海马、皮质和尾壳核的tau蛋白在PHF-1位点的磷酸化和神经细丝磷酸化水平显著增加。在4天未见细胞骨架蛋白磷酸程度的改变。另外,在同样的脑区和相同的时相点,tau蛋白在Tau-1位点的非磷酸化和神经细丝的非磷酸化水平显著降低。然而,未在实验中发现CDK5和p35的过度表达。结论:腹腔注射可卡因可导致大鼠大脑tau和神经细丝的阿尔采末病样过度磷酸化,但这种变化可能与CDK5的过度激活和表达无关。
AIM: To investigate the relationship between cocaine-induced over-expression of CDK5 and Alzheimer’s disease-like hyperphosphorylation of cytoskeleton proteins. METHODS: Cocaine (20 mg · kg · d-1) was intraperitoneally injected into rats. The tau phosphorylation and nerve filaments were examined by immunoblotting. Results: At day 8 and day 16 post cocaine injection, tau protein phosphorylation and neurofilament phosphorylation in hippocampus, cortex and caudate putamen were significantly increased. No changes in cytosolic protein phosphorylation were observed at 4 days. In addition, non-phosphorylation of tau protein at Tau-1 site and non-phosphorylation of nerve filaments were significantly reduced in the same brain regions and at the same time phase. However, no overexpression of CDK5 and p35 was found in experiments. Conclusion: Intraperitoneal injection of cocaine can cause Alzheimer’s disease-like hyperphosphorylation of rat brain tau and nerve filaments, but this change may not be related to the over-activation and expression of CDK5.