Effects of Treadmill Exercise on the Recovery of Dopaminergic Neuron Loss and Muscle Atrophy in the 6-OHDA Lesioned Parkinson's Disease Rat Model.
10.4196/kjpp.2012.16.5.305
- Author:
Myoung Ae CHOE
1
;
Byung Soo KOO
;
Gyeong Ju AN
;
Songhee JEON
Author Information
1. College of Nursing, Seoul National University, Seoul 110-744, Korea.
- Publication Type:Original Article
- Keywords:
ERK;
Exercise;
GSK3beta;
Muscle atrophy;
Parkinson's disease
- MeSH:
Animals;
Atrophy;
Cell Death;
Dopaminergic Neurons;
Glycogen Synthase Kinase 3;
Muscle, Skeletal;
Muscles;
Muscular Atrophy;
Myosin Heavy Chains;
Neurons;
Neuroprotective Agents;
Oxidopamine;
Parkinson Disease;
Phosphorylation;
Rats;
Substantia Nigra;
Tyrosine 3-Monooxygenase
- From:The Korean Journal of Physiology and Pharmacology
2012;16(5):305-312
- CountryRepublic of Korea
- Language:English
-
Abstract:
This study was to determine the effect of exercise on the recovery of dopaminergic neuron loss and muscle atrophy in 6-OHDA-induced hemi Parkinson's disease model. Exercise was loaded twice per day for 30 minutes each time, at 5 days after 6-OHDA lesioning and continued for 16 days using a treadmill. Exercise significantly increased the number of tyrosine hydroxylase positive neuron in the lesioned substantia nigra and the expression level of tyrosine hydroxylase in the striatum compared with the control group. To examine which signaling pathways may be involved in the exercise, the phosphorylation of GSK3beta and ERK were observed in the striatum. In the control group, basal level of GSK3beta phosphorylation was less than in both striatum, but exercise increased it. ERK phosphorylation decreased in the lesioned striatum, but exercise recovered it. These findings suggest that exercise inactivates GSK3beta by phosphorylation which may be involved in the neuroprotective effect of exercise on the 6-OHDA-induced cell death. In the exercise group, weight, and Type I and II fiber cross-sectional area of the contralateral soleus significantly recovered and expression of myosin heavy chain and Akt and ERK phosphorylation significantly increased by exercise. These results suggest that exercise recovers Parkinson's disease induced dopaminergic neuron loss and contralateral soleus muscle atrophy.
