Lau Y S, Fung Y K
Brain Res. 1986 Mar 26;369(1-2):311-5. doi: 10.1016/0006-8993(86)90541-x.
In mice, chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces an increase in the maximum number of [3H]spiperone binding sites in the striatum. The sensitivity of striatal protein phosphorylation to calcium plus calmodulin is also potentiated in MPTP-treated mice. These observations are associated with an enhancement of apomorphine-induced climbing behavior in the drug-treated animals. The results of this study suggest that in an animal model for Parkinson's disease, MPTP interrupts the dopamine (DA) transmission by chemically denervating the nigrostriatal neurons and through a compensatory mechanism, it increases the number of DA receptors as well as the sensitivity of protein phosphorylation to calcium plus calmodulin in mouse striatum. The latter two events may contribute to the development of DA receptor supersensitivity.
在小鼠中，长期给予1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）会使纹状体中[3H]司来吉兰结合位点的最大数量增加。在MPTP处理的小鼠中，纹状体蛋白磷酸化对钙加钙调蛋白的敏感性也增强。这些观察结果与药物处理动物中阿扑吗啡诱导的攀爬行为增强有关。本研究结果表明，在帕金森病动物模型中，MPTP通过化学去神经支配黑质纹状体神经元中断多巴胺（DA）传递，并且通过一种补偿机制，增加了小鼠纹状体中DA受体的数量以及蛋白磷酸化对钙加钙调蛋白的敏感性。后两个事件可能促成了DA受体超敏反应的发展。
