Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson's disease

被引:310
作者
Tillerson, JL
Caudle, WM
Reverón, ME
Miller, GW [1 ]
机构
[1] Univ Texas, Inst Neurosci, Austin, TX 78712 USA
[2] Emory Univ, Sch Publ Hlth, Ctr Neurodegenerat Disorders, Dept Environm & Occupat Hlth, Atlanta, GA 30322 USA
[3] Univ Texas, Div Pharmacol & Toxicol, Austin, TX 78712 USA
关键词
Parkinson's disease; treadmill running; dopamine; plasticity; dopamine transporter; vesicular monoamine transporter;
D O I
10.1016/S0306-4522(03)00096-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Exercise is thought to improve motor function and emotional well-being in patients with Parkinson's disease (PD). However, it is not clear if the improvements are due to neurochemical alterations within the affected nigrostriatal region or result from a more general effect of exercise on affect and motivation. In this study we show that motorized treadmill running improves the neurochemical and behavioral outcomes in two rodent models of PD: the unilateral 6-hydroxydopamine (6-OHDA) rat model and bilateral 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model in aged C57bl mice. Exposure to the dopamine (DA) toxins 6-OHDA or MPTP resulted in permanent behavioral and neurochemical loss. In contrast, when lesioned animals were exposed to treadmill activity two times a day for the first 10 days post-lesion they displayed no behavioral deficits across testing days and had significant sparing of striatal DA, its metabolites, tyrosine hydroxylase, vesicular monoamine transporter, and DA transporter levels compared to lesion sedentary animals. These results demonstrate that exercise following nigrostriatal damage ameliorates related motor symptoms and neurochemical deficits in rodent models of PD. (C) 2003 IBRO. Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:899 / 911
页数:13
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