Neuroprotective Effect of Voluntary Wheel Running Exercise on GDNF levels of Cerebellum in Parkinsonian Rats

Document Type : original article

Abstract


Introduction: Parkinson's disease is caused by disorder in control centers of body and leads to vibration at rest, bradykinesia, tremor, muscular rigidity and postural imbalance. The disease occures due to the loss of midbrain dopaminergic cells. Glial cell line-derived neurotrophic factor in the midbrain dopaminergic neurons has been identified as a nerotrophic factor of dopaminergic neurons in midbrain. The purpose of this study was to investigate the protective effects of 12 weeks of voluntary exercise on a running wheel on the GDNF levels of cerebellum against 6-hydroxydopamine lesions in Parkinsonian rats.
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Methods: In this experimental study, twenty one rats were divided into three groups: healthy, Parkinson control and Training-Parkinson (initially had training and then received a solution of 6 hydroxy-dopamine). Parkinson and control groups have been kept in special cages until the end of the study. Training- Parkinson group was housed in individual cages geared with running wheels. After 12 weeks, 250) Micrograms of 6-hydroxydopamine (6-OHDA) were administered to the right ventricle (ICV) in Parkinson controls and training - Parkinson. Finally, five days after intraventricular injection, GDNF levels in the cerebellum were measured by ELISA method. Data was analyzed using one-way Analysis of Variance (ANOVA) and Tukey post-hoc tests. Significance level was considered to be P<.05.
Findings: Results showed that GDNF levels in cerebellum of Parkinsonian rats in training group had significant difference with healthy and Parkinson groups (P=.001).
Conclusion: Pre-treatment with voluntary exercise prevented the decrease in increased GDNF levels of cerebellum and its levels compared with base levels. Thus, it seems that Voluntary exercise have protective role against 6-hydroxydopamine lesions in cerebellum of Parkinsonian rats.

Keywords

References

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History

  • Receive Date: 01 June 2015
  • Revise Date: 18 June 2024
  • Accept Date: 31 December 2020
  • First Publish Date: 31 December 2020
  • Publish Date: 22 September 2012

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