Voluntary exercise induces a BDNF-mediated mechanism that promotes neuroplasticity
Abstract
We have investigated potential mechanisms by which exercise can promote changes in neuronal plasticity via modulation of neurotrophins. Rodents were exposed to voluntary wheel running for 3 or 7 days, and their lumbar spinal cord and soleus muscle were assessed for changes in brain-derived neurotrophic factor (BDNF), its signal transduction receptor (trkB), and downstream effectors for the action of BDNF on synaptic plasticity. Exercise increased the expression of BDNF and its receptor, synapsin I (mRNA and phosphorylated protein), growth-associated protein (GAP-43) mRNA, and cyclic AMP response element-binding (CREB) mRNA in the lumbar spinal cord. Synapsin I, a synaptic mediator for the action of BDNF on neurotransmitter release, increased in proportion to GAP-43 and trkB mRNA levels. CREB mRNA levels increased in proportion to BDNF mRNA levels. In separate experiments, the soleus muscle was paralyzed unilaterally via intramuscular botulinum toxin type A (BTX-A) injection to determine the effects of reducing the neuromechanical output of a single muscle on the neurotrophin response to motor activity. In sedentary BTX-A-treated rats, BDNF and synapsin I mRNAs were reduced below control levels in the spinal cord and soleus muscle. Exercise did not change the BDNF mRNA levels in the spinal cord of BTX-A-treated rats but further reduced the BDNF mRNA levels in the paralyzed soleus relative to the levels in sedentary BTX-A-treated rats. Exercise also restored synapsin I to near control levels in the spinal cord. These results indicate that basal levels of neuromuscular activity are required to maintain normal levels of BDNF in the neuromuscular system and the potential for neuroplasticity.
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Motor training is an effective paradigm for increasing plasticity.
“Motor training is also an effective paradigm for increasing plasticity (Cotman et al., 2007;Ding et al., 2006;Gómez-Pinilla et al., 2002;Neeper et al., 1995;van Praag et al., 1999).”
From The hyaluronan and proteoglycan link proteins: Organizers of the brain extracellular matrix and key molecules for neuronal function and plasticity (2015) · cites this paper as Gómez-Pinilla et al., 2002
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- Authors
- Gómez-Pinilla, F., Ying, Z., Roy, R. R., Molteni, R., & Edgerton, V. R.
- Affiliations
- Department of Physiological Science,
- Department of Physiological Sciences (RU)
- Brain Research Institute, Los Angeles, California 90095
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 2002-11-01
- Volume
- 88
- Issue
- 5
- Pages
- 2187-2195
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- OpenAlex
- W1995800438
- Cited by
- 724
- References
- 30
- Citations by year
- 2026: 14 · 2025: 30 · 2024: 27 · 2023: 30 · 2022: 16 · 2021: 33 · 2020: 33 · 2019: 27 · 2018: 26 · 2017: 27 · 2016: 41 · 2015: 49 · 2014: 43 · 2013: 50 · 2012: 39
- FWCI
- 6.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns038978-03)
- National Institute of Neurological Disorders and Stroke (NS 39522, NS-38978, R01NS039522)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- voluntary wheel running, physical activity, brain-derived neurotrophic factor, TrkB receptor, neuroplasticity, synapsin I, GAP-43, CREB, lumbar spinal cord, soleus muscle, botulinum toxin type A, neuromuscular activity, synaptic plasticity, neuromuscular system
- MeSH terms
- Adaptation, Physiological, Animals, Physical Exertion, Hindlimb, Immunoassay, Immunohistochemistry, Male, Muscle Proteins, Neuromuscular Agents, Neuronal Plasticity, RNA, Messenger, Running, Spinal Cord, Synapses, Synapsins, Rats, Sprague-Dawley, Muscle, Skeletal, Brain-Derived Neurotrophic Factor, Botulinum Toxins, Type A, Reverse Transcriptase Polymerase Chain Reaction, Receptor, trkB, Rats
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