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运动可诱导帕金森病啮齿动物模型的行为恢复并减轻神经化学缺陷。

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

作者信息

Tillerson J L, Caudle W M, Reverón M E, Miller G W

机构信息

Institute for Neuroscience, University of Texas at Austin, Austin, TX, 78712, USA.

出版信息

Neuroscience. 2003;119(3):899-911. doi: 10.1016/s0306-4522(03)00096-4.

DOI:10.1016/s0306-4522(03)00096-4
PMID:12809709
Abstract

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.

摘要

运动被认为可改善帕金森病(PD)患者的运动功能和情绪健康。然而,尚不清楚这些改善是由于受影响的黑质纹状体区域内的神经化学改变,还是运动对情感和动机的更普遍影响所致。在本研究中,我们表明电动跑步机跑步可改善两种PD啮齿动物模型的神经化学和行为结果:单侧6-羟基多巴胺(6-OHDA)大鼠模型和老年C57bl小鼠的双侧1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)模型。暴露于多巴胺(DA)毒素6-OHDA或MPTP会导致永久性的行为和神经化学损失。相比之下,当损伤动物在损伤后的前10天每天两次暴露于跑步机活动时,它们在整个测试期间均未表现出行为缺陷,并且与损伤后久坐不动的动物相比,纹状体DA、其代谢产物、酪氨酸羟化酶、囊泡单胺转运体和DA转运体水平有显著保留。这些结果表明,黑质纹状体损伤后的运动可改善PD啮齿动物模型中的相关运动症状和神经化学缺陷。

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