Treadmill training improves motor deficits and mitochondrial function in the unilateral 6-hydroxydopamine rat model of Parkinson’s disease

• Main Authors: Chieh-Sen Chuang, 莊介森
• Other Authors: Hong-Lin Su
• Format: Others
• Language: en_US
• Published: 2017
• Online Access: http://ndltd.ncl.edu.tw/handle/30921026821759244353

博士 === 國立中興大學 === 生命科學系所 === 105 === Parkinson’s disease (PD) is a progressive degenerative central nervous system disorder that particularly impairs motor function. As PD advances, gait disorders become more pronounced and are often difficult to treat with current pharmacological therapies. Physical activity improves mobility in and activities of daily living of patients with PD. Mitochondrial alterations and oxidative stress contribute to PD progression. The association between mitochondria and exercise in PD remains unclear. In this study, we developed a unilateral 6-hydroxydopamine rat model of PD and executed 4 weeks of treadmill training. Motor behaviour was evaluated through gait changes analysis (the CatWalk method) and a rotational test. The viability of dopaminergic neurons, mitochondrial function, and oxidative stress in the substantia nigra and striatum were investigated through Western blot and immunohistochemical staining. Treadmill training improved the performance of gait parameters in the max area, swing speed, stride length, and stance phase and reduced methamphetamine induced rotation. This training not only improved dopaminergic neuron viability but also recovered mitochondrial function and attenuated oxidative stress in PD rats. The mechanism may be associated with the facilitation of mitochondrial turnover, including that of mitochondrial fusion, fission, and clearance accompanying an increased mitochondrial amount. Consequently, mitochondrial function was improved in PD rats.