Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease

Physical training confers protection to dopaminergic neurons in rodent models of parkinsonism produced by neurotoxins. The sparing effect of physical training on dopaminergic neurons can be tested with training applied during chronic MPTP treatment, while the neurorestorative effect when training is...

Full description

Saved in:
Bibliographic Details
Main Authors: Ewelina Palasz, Wiktor Niewiadomski, Anna Gasiorowska, Anna Mietelska-Porowska, Grazyna Niewiadomska
Format: Article
Language:English
Published: Wiley 2019-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2019/8215017
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832564699843002368
author Ewelina Palasz
Wiktor Niewiadomski
Anna Gasiorowska
Anna Mietelska-Porowska
Grazyna Niewiadomska
author_facet Ewelina Palasz
Wiktor Niewiadomski
Anna Gasiorowska
Anna Mietelska-Porowska
Grazyna Niewiadomska
author_sort Ewelina Palasz
collection DOAJ
description Physical training confers protection to dopaminergic neurons in rodent models of parkinsonism produced by neurotoxins. The sparing effect of physical training on dopaminergic neurons can be tested with training applied during chronic MPTP treatment, while the neurorestorative effect when training is applied after completing such treatment. In this study, the effect of the onset of training respective to chronic MPTP treatment was specifically addressed. Three groups of mice were injected with 10 doses of MPTP (12.5 mg/kg/injection) over 5 weeks. The first group remained sedentary; the second one underwent early onset training, which started 1 week before commencing MPTP treatment, continued throughout 5 weeks of treatment and 4 weeks thereafter; the third group underwent late-onset training of the same length and intensity as the former group, except that it started immediately after the end of MPTP treatment. Two groups served as controls: a saline-injected group that remained sedentary and saline-injected group, which underwent the same training as the early and late-onset training groups. Both early and late-onset physical training saved almost all nigral and VTA dopaminergic neurons, prevented inflammatory response, and increased the BDNF and GDNF levels to a similar extent. From these results one may conclude that early and late-onset training schedules were equipotent in their neuroprotective effect and that the mechanism of neuroprotection was similar. The sparing effect of early onset training may be satisfactorily explained by assuming that the increased level of BDNF and GDNF prevented the degeneration of dopaminergic neurons. To explain a similar number of dopaminergic neurons detected at the end of the early and late-onset training, one should additionally assume that the former training schedule induced neurogenesis. Results of this study support the view that physical activity may be neuroprotective even at a more advanced stage of PD and justify starting physical activity at any point of the disease.
format Article
id doaj-art-a37ad5cae2934e52a8aab957ab0fb071
institution Kabale University
issn 2090-5904
1687-5443
language English
publishDate 2019-01-01
publisher Wiley
record_format Article
series Neural Plasticity
spelling doaj-art-a37ad5cae2934e52a8aab957ab0fb0712025-02-03T01:10:26ZengWileyNeural Plasticity2090-59041687-54432019-01-01201910.1155/2019/82150178215017Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s DiseaseEwelina Palasz0Wiktor Niewiadomski1Anna Gasiorowska2Anna Mietelska-Porowska3Grazyna Niewiadomska4Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, PolandMossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, PolandNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, PolandNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, PolandNencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, PolandPhysical training confers protection to dopaminergic neurons in rodent models of parkinsonism produced by neurotoxins. The sparing effect of physical training on dopaminergic neurons can be tested with training applied during chronic MPTP treatment, while the neurorestorative effect when training is applied after completing such treatment. In this study, the effect of the onset of training respective to chronic MPTP treatment was specifically addressed. Three groups of mice were injected with 10 doses of MPTP (12.5 mg/kg/injection) over 5 weeks. The first group remained sedentary; the second one underwent early onset training, which started 1 week before commencing MPTP treatment, continued throughout 5 weeks of treatment and 4 weeks thereafter; the third group underwent late-onset training of the same length and intensity as the former group, except that it started immediately after the end of MPTP treatment. Two groups served as controls: a saline-injected group that remained sedentary and saline-injected group, which underwent the same training as the early and late-onset training groups. Both early and late-onset physical training saved almost all nigral and VTA dopaminergic neurons, prevented inflammatory response, and increased the BDNF and GDNF levels to a similar extent. From these results one may conclude that early and late-onset training schedules were equipotent in their neuroprotective effect and that the mechanism of neuroprotection was similar. The sparing effect of early onset training may be satisfactorily explained by assuming that the increased level of BDNF and GDNF prevented the degeneration of dopaminergic neurons. To explain a similar number of dopaminergic neurons detected at the end of the early and late-onset training, one should additionally assume that the former training schedule induced neurogenesis. Results of this study support the view that physical activity may be neuroprotective even at a more advanced stage of PD and justify starting physical activity at any point of the disease.http://dx.doi.org/10.1155/2019/8215017
spellingShingle Ewelina Palasz
Wiktor Niewiadomski
Anna Gasiorowska
Anna Mietelska-Porowska
Grazyna Niewiadomska
Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease
Neural Plasticity
title Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease
title_full Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease
title_fullStr Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease
title_full_unstemmed Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease
title_short Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease
title_sort neuroplasticity and neuroprotective effect of treadmill training in the chronic mouse model of parkinson s disease
url http://dx.doi.org/10.1155/2019/8215017
work_keys_str_mv AT ewelinapalasz neuroplasticityandneuroprotectiveeffectoftreadmilltraininginthechronicmousemodelofparkinsonsdisease
AT wiktorniewiadomski neuroplasticityandneuroprotectiveeffectoftreadmilltraininginthechronicmousemodelofparkinsonsdisease
AT annagasiorowska neuroplasticityandneuroprotectiveeffectoftreadmilltraininginthechronicmousemodelofparkinsonsdisease
AT annamietelskaporowska neuroplasticityandneuroprotectiveeffectoftreadmilltraininginthechronicmousemodelofparkinsonsdisease
AT grazynaniewiadomska neuroplasticityandneuroprotectiveeffectoftreadmilltraininginthechronicmousemodelofparkinsonsdisease