Caudle W Michael, Tillerson Jennifer L, Reverón María E, Miller Gary W
Center for Neurodegenerative Disease, Emory University, Atlanta, GA 30322, USA.
Neurosci Lett. 2007 May 18;418(3):213-6. doi: 10.1016/j.neulet.2006.03.045. Epub 2006 Apr 17.
Early in Parkinson's disease (PD) physical activity becomes difficult resulting in a more sedentary lifestyle. Clinical and experimental studies have found that increased activity following striatal dopamine loss leads to increased motor function. Decreased physical activity early in PD along with findings that increased physical activity results in functional improvement suggested to us that decreased physical activity during the period of nigrostriatal degeneration may not only be a symptom of the injury, but may also act to potentiate the degeneration. Using the bilateral MPTP mouse model of PD, we restricted use of one forelimb for the first 7 days post-injection. This transient behavioral manipulation during the period of dopamine degeneration resulted in a long-lasting deficit of the restricted forelimb. This was manifested as sustained asymmetrical use of the forelimbs during wall exploration, as well as a neurochemical imbalance between striatal hemispheres measured by immunoreactivity of the dopamine terminal markers, DAT, VMAT2 and TH. These results show a significant interaction between behavior and neurochemistry and suggest that a reduction in activity level may further exacerbate degeneration.
在帕金森病(PD)早期,身体活动变得困难,导致生活方式更加久坐不动。临床和实验研究发现,纹状体多巴胺丧失后活动增加会导致运动功能增强。PD早期身体活动减少,以及增加身体活动会导致功能改善的研究结果表明,在黑质纹状体变性期间身体活动减少不仅可能是损伤的症状,还可能起到加剧变性的作用。使用双侧MPTP小鼠PD模型,我们在注射后前7天限制一只前肢的使用。在多巴胺变性期间这种短暂的行为操纵导致受限前肢出现长期缺陷。这表现为在墙壁探索期间前肢持续不对称使用,以及通过多巴胺终端标记物DAT、VMAT2和TH的免疫反应性测量的纹状体半球之间的神经化学失衡。这些结果显示了行为与神经化学之间的显著相互作用,并表明活动水平降低可能会进一步加剧变性。