Tuon T, Valvassori S S, Dal Pont G C, Paganini C S, Pozzi B G, Luciano T F, Souza P S, Quevedo J, Souza C T, Pinho R A
Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina 88806-000, Brazil.
Laboratory of Neurosciences, National Institute for Translational Medicine (INCT-TM), Center of Excellence in Applied Neurosciences of Santa Catarina (NENASC), Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina 88806-000, Brazil.
Brain Res Bull. 2014 Sep;108:106-12. doi: 10.1016/j.brainresbull.2014.09.006. Epub 2014 Sep 28.
Depression is a neuropsychiatric disorder that is commonly found in patients with Parkinson's disease (PD). Many studies have suggested that physical exercise can have an antidepressant effect by increasing the levels of brain-derived neurotrophic factor (BDNF), and may also prevent neurodegenerative disease. However, different forms of training may promote different changes in the brain. The aim of this study was to investigate the effects of two types of physical training on depressive-like behavior, and on the levels of proBDNF, BDNF, and its receptor, TrkB, in a mouse model of PD. C57BL/6 mice were subjected to 60 days of exercise: either running on a treadmill or performing a strength exercise. PD was induced by striatal administration of 6-OHDA 24h after the last physical exercise session. Seven days after 6-OHDA injection, depressive-like behavior and apomorphine-induced rotational behavior were evaluated. The levels of proBDNF, BDNF, and TRKB were measured in the striatum and the hippocampus of mice by immunoblotting assay. The 6-OHDA-treated animals showed a significant increase in immobility time and rotational behavior compared with the control group. In addition, significant decreases in the levels of proBDNF, BDNF, and its receptor, TrkB were observed in the 6-OHDA group. Both types of physical exercise prevented depressive-like behavior and restored the levels of proBDNF, BDNF, and TrkB in the striatum and hippocampus of mice administered 6-OHDA. Our results demonstrate that exercise training was effective for neuroprotection in the striatum and the hippocampus in an experimental model of PD.
抑郁症是一种常见于帕金森病（PD）患者的神经精神障碍。许多研究表明，体育锻炼可通过提高脑源性神经营养因子（BDNF）水平产生抗抑郁作用，还可能预防神经退行性疾病。然而，不同形式的训练可能会促进大脑发生不同的变化。本研究的目的是在PD小鼠模型中，研究两种体育训练方式对抑郁样行为以及前体BDNF、BDNF及其受体TrkB水平的影响。将C57BL/6小鼠进行60天的运动：要么在跑步机上跑步，要么进行力量训练。在最后一次体育锻炼24小时后，通过纹状体内注射6-羟基多巴胺（6-OHDA）诱导PD。在注射6-OHDA七天后，评估抑郁样行为和阿扑吗啡诱导的旋转行为。通过免疫印迹法测定小鼠纹状体和海马中前体BDNF、BDNF和TRKB的水平。与对照组相比，6-OHDA处理的动物静止时间和旋转行为显著增加。此外，在6-OHDA组中观察到前体BDNF、BDNF及其受体TrkB水平显著降低。两种体育锻炼方式均能预防6-OHDA处理小鼠的抑郁样行为，并恢复其纹状体和海马中前体BDNF、BDNF和TrkB的水平。我们的结果表明，在PD实验模型中，运动训练对纹状体和海马具有神经保护作用。
