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Cited by 109Parkinson's Disease Mechanisms and TreatmentsNerve injury and regenerationNuclear Receptors and Signaling

BDNF receptor blockade hinders the beneficial effects of exercise in a rat model of Parkinson s disease

Real, C.C., Ferreira, A.F.B., Chaves-Kirsten, G.P., Torrão, A.S., Pires, R.S., Britto, L.R.G.·2013·Neuroscience
DOI 10.1016/j.neuroscience.2013.01.060
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Abstract

Physical exercise is known to produce beneficial effects to the nervous system. In most cases, brain-derived neurotrophic factor (BDNF) is involved in such effects. However, little is known on the role of BDNF in exercise-related effects on Parkinson's disease (PD). The aim of this study was to investigate the effects of intermittent treadmill exercise-induced behavioral and histological/neurochemical changes in a rat model of unilateral PD induced by striatal injection of 6-hydroxydopamine (6-OHDA), and the role of BDNF in the exercise effects. Adult male Wistar rats were divided into two main groups: (1) injection of K252a (a blocker of BDNF receptors), and (2) without BDNF receptor blockade. These groups were then subdivided into four groups: control (CLT), sedentary (SED, non-exercised with induction of PD), exercised 3×/week during four weeks before and four weeks after the induction of PD (EXB+EXA), and exercised 3×/week during four weeks after the induction of PD (EXA). One month after 6-OHDA injections, the animals were subjected to rotational behavioral test induced by apomorphine and the brains were collected for immunohistochemistry and immunoblotting assays, in which we measured BDNF and tyrosine hydroxylase (TH) in the substantia nigra pars compacta (SNc) and the striatum (caudate-putamen, CPu). Our results showed a significant reduction of rotational asymmetry induced by apomorphine in the exercised parkinsonian rats. BDNF decreased in the SNc of the SED group, and exercise was able to revert that effect. Exercised groups exhibited reduced damage to the dopaminergic system, detected as a decreased drop of TH levels in SNc and CPu. On the other hand, BDNF blockade was capable of substantially reducing TH expression postlesion, implying enhanced dopaminergic cell loss. Our data revealed that physical exercise is capable of reducing the damage induced by 6-OHDA, and that BDNF receptors are involved in that effect.

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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 [128]

  • Use of the BDNF receptor inhibitor K252a reversed the protective effect of exercise on rotational bias.

    “Additionally, the use of BDNF receptor inhibitor K252a reversed the protective effect of exercise on rotational bias [128].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [128]

  • 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 [128]

  • 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 [128]

  • Dopamine depletion in the striatum induces hyper-excitability in the indirect pathway in response to alterations in glutamatergic expression and underlies critical aspects of motor impairment in Parkinson's disease.

    “DA depletion in the striatum induces hyper-excitability in the indirect pathway in response to alterations in glutamatergic expression (receptors and neurotransmitter release) and underlies critical aspects of motor impairment in PD 84.”

    From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [84]

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Authors
Real, C. C., Ferreira, A. F. B., Chaves-Kirsten, G. P., Torrão, A. S., Pires, R. S., & Britto, L. R. G.
Affiliations
Universidade de São Paulo (BR)
Corresponding author
Real, C.C.
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2013-05
Volume
237
Pages
118-129
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2013.01.060
OpenAlex
W2083783300
Cited by
109
References
52
Citations by year
2026: 3 · 2025: 3 · 2024: 7 · 2023: 9 · 2022: 7 · 2021: 6 · 2020: 13 · 2019: 11 · 2018: 11 · 2017: 12 · 2016: 9 · 2015: 8 · 2014: 5 · 2013: 5
FWCI
5.71
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • Scopus (Elsevier) (submittedVersion)
Funders
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
Parkinson's disease, brain-derived neurotrophic factor, K252a, treadmill exercise, 6-hydroxydopamine lesion, dopaminergic neuron loss, tyrosine hydroxylase, substantia nigra pars compacta, striatum, apomorphine-induced rotation, neuroprotection
MeSH terms
Analysis of Variance, Animals, Apomorphine, Carbazoles, Corpus Striatum, Disease Models, Animal, Enzyme Inhibitors, Exercise Test, Exercise Therapy, Gene Expression Regulation, Male, Parkinson Disease, Putamen, Stereotyped Behavior, Time Factors, Tyrosine 3-Monooxygenase, Oxidopamine, Rats, Wistar, Receptor, trkB, Indole Alkaloids, Rats

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