Exercise exerts neuroprotective effects on Parkinson's disease model of rats
Abstract
Recent studies demonstrate that rehabilitation ameliorates physical and cognitive impairments of patients with stroke, spinal cord injury, and other neurological diseases and that rehabilitation also has potencies to modulate brain plasticity. Here we examined the effects of compulsive exercise on Parkinson's disease model of rats. Before 6-hydroxydopamine (6-OHDA, 20 microg) lesion into the right striatum of female SD rats, bromodeoxyuridine (BrdU) was injected to label the proliferating cells. Subsequently, at 24 h after the lesion, the rats were forced to run on the treadmill (5 days/week, 30 min/day, 11 m/min). As behavioral evaluations, cylinder test was performed at 1, 2, 3, and 4 weeks and amphetamine-induced rotational test was performed at 2 and 4 weeks with consequent euthanasia for immunohistochemical investigations. The exercise group showed better behavioral recovery in cylinder test and significant decrease in the number of amphetamine-induced rotations, compared to the non-exercise group. Correspondingly, significant preservation of tyrosine hydroxylase (TH)-positive fibers in the striatum and TH-positive neurons in the substantia nigra pars compacta (SNc) was demonstrated, compared to the non-exercise group. Additionally, the number of migrated BrdU- and Doublecortin-positive cells toward the lesioned striatum was increased in the exercise group. Furthermore, brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor increased in the striatum by exercise. The results suggest that exercise exerts neuroprotective effects or enhances the neuronal differentiation in Parkinson's disease model of rats with subsequent improvement in deteriorated motor function.
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BDNF upregulation due to exercise was observed in midbrain, substantia nigra, striatum, hippocampus, and cortex.
“BDNF upregulation was observed in midbrain [125], SN [126,128,129], ST [127,129,131,133], hippocampus [133], and cortex [132,133].”
From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [127]
In rodent models, BDNF, insulin-like growth factor 1, mitogen-activated protein kinase phosphatase-1, and glial-derived neurotrophic factor are elevated by exercise.
“in rodent models, BDNF, insulin– like growth factor 1 (IGF-1), mitogen-activated protein kinase phosphatase-1 (MKP-1), and glial-derived neurotrophic factor (GDNP) are elevated by exercise [1, 53, 179]”
From The neuropathology of sport (2014) · cites this paper as [179]
Pathways involving the basal ganglia in PD may be capable of plasticity, and their activity patterns may be partly corrected with appropriate intensive training.
“In fact, it has been shown that pathways involving the basal ganglia in PD may be capable of plasticity, and their activity patterns may be partly corrected with appropriate intensive training [5–7].”
From A wearable system for gait training in subjects with Parkinson's disease (2014) · cites this paper as [7]
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- Authors
- Tajiri, N., Yasuhara, T., Shingo, T., Kondo, A., Yuan, W., Kadota, T., Wang, F., Baba, T., Tayra, J. T., Morimoto, T., Jing, M., Kikuchi, Y., Kuramoto, S., Agari, T., Miyoshi, Y., Fujino, H., Obata, F., Takeda, I., Furuta, T., & Date, I.
- Affiliations
- Okayama University (JP)
- Kobe University (JP)
- Kibi International University (JP)
- Himeji Dokkyo University (JP)
- Corresponding author
- Yasuhara, Takao
- ORCID
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 1310
- Pages
- 200-207
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W1993088678
- Cited by
- 308
- References
- 37
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 14 · 2023: 9 · 2022: 22 · 2021: 11 · 2020: 22 · 2019: 27 · 2018: 22 · 2017: 22 · 2016: 18 · 2015: 29 · 2014: 21 · 2013: 26 · 2012: 22
- FWCI
- 8.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- physical activity, Parkinson's disease, neuroprotection, treadmill running, 6-hydroxydopamine lesion, striatum, substantia nigra pars compacta, tyrosine hydroxylase, neuronal migration, doublecortin, brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, motor recovery, neuroplasticity
- MeSH terms
- Doublecortin Domain Proteins, Doublecortin Protein, Amphetamine, Animals, Ascorbic Acid, Behavior, Animal, Bromodeoxyuridine, Corpus Striatum, Disease Models, Animal, Exercise Test, Female, Microtubule-Associated Proteins, Movement, Neuropeptides, Parkinson Disease, Secondary, Physical Conditioning, Animal, Rotation, Substantia Nigra, Time Factors, Tyrosine 3-Monooxygenase, Oxidopamine, Rats, Sprague-Dawley, Brain-Derived Neurotrophic Factor, Cell Proliferation, Glial Cell Line-Derived Neurotrophic Factors, Rats
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