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Cited by 206Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

Running exercise protects the substantia nigra dopaminergic neurons against inflammation-induced degeneration via the activation of BDNF signaling pathway

Wu, Shih-Ying, Wang, Tzu-Feng, Yu, Lung, Jen, Chauying J., Chuang, Jih-Ing, Wu, Fong-Sen, Wu, Chih-Wei, Kuo, Yu-Min·2011·Brain Behavior and Immunity
DOI 10.1016/j.bbi.2010.09.006
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Abstract

Parkinson's disease (PD) is characterized by a progressive and selective loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although the etiology of PD remains unclear, neuroinflammation has been implicated in the development of PD. Running exercise (Ex) promotes neuronal survival and facilitates the recovery of brain functions after injury. Therefore, we hypothesize that Ex protects the DA neurons against inflammation-induced injury in the SN. An intraperitoneal lipopolysaccharide (LPS, 1 mg/kg) injection induced microglia activation in the SN within hours, followed by a reduction in the number of DA neurons. LPS reduced the level of dopamine in the striatum and impaired the performance of motor coordination. Furthermore, the levels of the brain-derived neurotrophic factor (BDNF) were reduced in the SN by the LPS treatment. Four weeks of Ex before LPS treatment completely prevented the LPS-induced loss of DA neurons, reduction of dopamine levels and dysfunction of motor movement. Ex did not change the LPS-induced status of microglia activation or the levels of cytokines/chemokines, but restored the levels of LPS-reduced BDNF-TrkB signaling molecules. Blocking the action of BDNF, through its receptor TrkB antagonist, abolished the Ex-induced protection against LPS-induced DA neuron loss. Intrastriatal perfusion of BDNF alone was sufficient to counteract the LPS-induced DA neuron loss. Altogether, our results show that Ex protects DA neurons against inflammation-induced insults. The neuroprotective effects of Ex are not due to the modulation of inflammation status, but rather to the activation of the BDNF-TrkB signaling pathway.

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Crossref · 10.1016/j.bbi.2010.09.006

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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 [129]

  • Exercise increased TrkB content in substantia nigra.

    “In another study, it was shown that exercise increased TrkB content in SN [129]; however, in yet another study, TrkB content was significantly decreased in ST even below the level in the sedentary PD mice [131].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [129]

  • Long-term endurance training increases TH expression in structures involved in extrapyramidal movement regulation, i.e., the ST and midbrain.

    “Animal studies have shown that long-term endurance training increased both TrkB receptor and TH expression in structures involved in extrapyramidal movement regulation, i.e., in the ST and midbrain [128,129,179,183,184,185].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [129]

  • Long-term endurance training increases TrkB receptor expression in structures involved in extrapyramidal movement regulation, i.e., the ST and midbrain.

    “Animal studies have shown that long-term endurance training increased both TrkB receptor and TH expression in structures involved in extrapyramidal movement regulation, i.e., in the ST and midbrain [128,129,179,183,184,185].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [129]

  • Studies in the MPTP mouse model have demonstrated that intensive exercise can restore aspects of glutamate receptor expression, including the AMPA receptor subtype.

    “Studies in the MPTP mouse model have demonstrated that intensive exercise can restore aspects of glutamate receptor expression, including the glutamate receptor subtype AMPA 85.”

    From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [85]

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Authors
Wu, S.-Y., Wang, T.-F., Yu, L., Jen, C. J., Chuang, J.-I., Wu, F.-S., Wu, C.-W., & Kuo, Y.-M.
Affiliations
National Cheng Kung University (TW)
ORCID
Venue
Brain Behavior and Immunity
Publisher
Elsevier BV
Published
2011-01
Volume
25
Issue
1
Pages
135-146
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2010.09.006
OpenAlex
W1984965817
Cited by
206
References
77
Citations by year
2026: 9 · 2025: 8 · 2024: 14 · 2023: 6 · 2022: 13 · 2021: 10 · 2020: 14 · 2019: 16 · 2018: 20 · 2017: 10 · 2016: 11 · 2015: 16 · 2014: 16 · 2013: 13 · 2012: 15
FWCI
8.19
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Cheng Kung University
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
running, Parkinson's disease, substantia nigra, dopaminergic neurons, neuroinflammation, lipopolysaccharide, microglial activation, brain-derived neurotrophic factor, TrkB signaling, neuroprotection, dopamine, motor coordination, striatum
MeSH terms
Animals, Carbazoles, Cell Count, Cell Survival, Corpus Striatum, Dopamine, Immunohistochemistry, Inflammation, Injections, Intraventricular, Male, Mice, Inbred C57BL, Motor Activity, Nerve Degeneration, Neurons, Physical Conditioning, Animal, Psychomotor Performance, Running, Substantia Nigra, Signal Transduction, Cytokines, Microglia, Chemokines, Brain-Derived Neurotrophic Factor, Indole Alkaloids, Mice

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