Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson's disease
Abstract
Exercise is thought to improve motor function and emotional well-being in patients with Parkinson's disease (PD). However, it is not clear if the improvements are due to neurochemical alterations within the affected nigrostriatal region or result from a more general effect of exercise on affect and motivation. In this study we show that motorized treadmill running improves the neurochemical and behavioral outcomes in two rodent models of PD: the unilateral 6-hydroxydopamine (6-OHDA) rat model and bilateral 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model in aged C57bl mice. Exposure to the dopamine (DA) toxins 6-OHDA or MPTP resulted in permanent behavioral and neurochemical loss. In contrast, when lesioned animals were exposed to treadmill activity two times a day for the first 10 days post-lesion they displayed no behavioral deficits across testing days and had significant sparing of striatal DA, its metabolites, tyrosine hydroxylase, vesicular monoamine transporter, and DA transporter levels compared to lesion sedentary animals. These results demonstrate that exercise following nigrostriatal damage ameliorates related motor symptoms and neurochemical deficits in rodent models of PD.
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In these toxin models, neuroprotection has been principally attributed to an exercise-induced increase of neurotrophic factors such as brain-derived neurotrophic factor or glial-derived neurotrophic factor.
“In these toxin models, neuroprotection has been principally attributed to an exercise-induced increase of neurotrophic factors such as brain-derived neurotrophic factor (BDNF) or glial-derived neurotrophic factor (GDNF) 78–81.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [78]
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- Authors
- Tillerson, J. L., Caudle, W. M., Reverón, M. E., & Miller, G. W.
- Affiliations
- The University of Texas at Austin (US)
- Emory University (US)
- Corresponding author
- Miller, G.W
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2003-07
- Volume
- 119
- Issue
- 3
- Pages
- 899-911
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2042936248
- Cited by
- 399
- References
- 70
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 12 · 2023: 5 · 2022: 11 · 2021: 5 · 2020: 19 · 2019: 23 · 2018: 18 · 2017: 17 · 2016: 21 · 2015: 26 · 2014: 13 · 2013: 32 · 2012: 24
- FWCI
- 8.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS-37031, R01NS037031)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, physical activity, treadmill running, 6-hydroxydopamine lesion, MPTP, nigrostriatal pathway, dopamine, striatum, tyrosine hydroxylase, vesicular monoamine transporter, dopamine transporter, motor recovery, behavioral recovery, aged mice
- MeSH terms
- Animals, Behavior, Animal, Disease Models, Animal, Dopamine, Exercise Test, Exercise Therapy, Functional Laterality, Male, Membrane Glycoproteins, Motor Activity, Neural Pathways, Neuropeptides, Physical Conditioning, Animal, Rats, Inbred F344, Reaction Time, Substantia Nigra, Tyrosine 3-Monooxygenase, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Up-Regulation, Oxidopamine, Neostriatum, Recovery of Function, Parkinsonian Disorders, Membrane Transport Proteins, Vesicular Biogenic Amine Transport Proteins, Vesicular Monoamine Transport Proteins, Mice, Rats
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