Cited by 399Parkinson's Disease Mechanisms and TreatmentsNeurological disorders and treatmentsNuclear Receptors and Signaling

Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson's disease

Tillerson, J.L, Caudle, W.M, Reverón, M.E, Miller, G.W·2003·Neuroscience

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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Crossref · 10.1016/s0306-4522(03)00096-4

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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.”

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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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