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Parkinson’s Disease
Volume 2015, Article ID 564095, 8 pages
http://dx.doi.org/10.1155/2015/564095
Research Article

The Neuroprotective Mechanism of Low-Frequency rTMS on Nigral Dopaminergic Neurons of Parkinson’s Disease Model Mice

1Fifth Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua Western Road, Cangzhou, Hebei 061000, China
2Hebei Province Key Laboratory of Brain Aging and Cognitive Neuroscience, No. 16 Xinhua Western Road, Cangzhou, Hebei 061000, China
3Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua Western Road, Cangzhou, Hebei 061000, China

Received 27 October 2014; Revised 24 January 2015; Accepted 24 January 2015

Academic Editor: Antonio Pisani

Copyright © 2015 Qiaoyun Dong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Parkinson’s disease is a neurodegenerative disease in elder people, pathophysiologic basis of which is the severe deficiency of dopamine in the striatum. The purpose of the present study was to evaluate the neuroprotective effect of low-frequency rTMS on Parkinson’s disease in model mice. Methods. The effects of low-frequency rTMS on the motor function, cortex excitability, neurochemistry, and neurohistopathology of MPTP-induced Parkinson’s disease mice were investigated through behavioral detection, electrophysiologic technique, high performance liquid chromatography-electrochemical detection, immunohistochemical staining, and western blot. Results. Low-frequency rTMS could improve the motor coordination impairment of Parkinson’s disease mice: the resting motor threshold significantly decreased in the Parkinson’s disease mice; the degeneration of nigral dopaminergic neuron and the expression of tyrosine hydroxylase were significantly improved by low-frequency rTMS; moreover, the expressions of brain derived neurotrophic factor and glial cell line derived neurotrophic factor were also improved by low-frequency rTMS. Conclusions. Low-frequency rTMS had a neuroprotective effect on the nigral dopaminergic neuron which might be due to the improved expressions of brain derived neurotrophic factor and glial cell line-derived neurotrophic factor. The present study provided a theoretical basis for the application of low-frequency rTMS in the clinical treatment and recovery of Parkinson’s disease.