4.5 Article

Physical training prevents depressive symptoms and a decrease in brain-derived neurotrophic factor in Parkinson's disease

期刊

BRAIN RESEARCH BULLETIN
卷 108, 期 -, 页码 106-112

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2014.09.006

关键词

Parkinson's disease; 6-Hydroxydopamine; Depression; Physical exercise; Neurotrophins

资金

  1. UNESC
  2. CNPq
  3. FAPESC
  4. NENASC projects (PRONEX program CNPq/FAPESC) (Brazil)

向作者/读者索取更多资源

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 24 h 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. (C) 2014 Elsevier Inc. All rights reserved.

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