Exercise differentially regulates synaptic proteins associated to the function of BDNF
Abstract
We explored the capacity of exercise to impact select events comprising synaptic transmission under the direction of brain-derived neurotrophic factor (BDNF), which may be central to the events by which exercise potentiates synaptic function. We used a specific immunoadhesin chimera (TrkB-IgG) that mimics the BDNF receptor, TrkB, to selectively block BDNF in the hippocampus during 3 days of voluntary wheel running. We measured resultant synapsin I, synaptophysin, and syntaxin levels involved in vesicular pool formation, endocytosis, and exocytosis, respectively. Synapsin I is involved in vesicle pool formation and neurotransmitter release, synaptophysin, in the biogenesis of synaptic vesicles and budding, and syntaxin, in vesicle docking and fusion. Exercise preferentially increased synapsin I and synaptophysin levels, without affecting syntaxin. There was a positive correlation between synapsin I and synaptophysin in exercising rats and synapsin I with the amount of exercise. Blocking BDNF abrogated the exercise-induced increases in synapsin I and synatophysin, revealing that exercise regulates select properties of synaptic transmission under the direction of BDNF.
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When exercise conditions were supplemented with antibodies blocking TrkB, mice had attenuated learning capabilities involving the hippocampus and lacked synaptic-specific proteins in the hippocampus.
“When the exercise conditions were supplemented with antibodies blocking TrkB, however, the mice had attenuated learning capabilities involving the hippocampus. Furthermore, these mice also lacked synaptic-specific proteins in the hippocampus, thereby demonstrating that BDNF signaling is necessary to allow the benefits of exercise to manifest (Vaynman et al., 2004, 2006).”
From Exercise-Mediated Neurogenesis in the Hippocampus via BDNF (2018) · cites this paper as Vaynman et al., 2006
BDNF signaling is necessary to allow the benefits of exercise to manifest.
“When the exercise conditions were supplemented with antibodies blocking TrkB, however, the mice had attenuated learning capabilities involving the hippocampus. Furthermore, these mice also lacked synaptic-specific proteins in the hippocampus, thereby demonstrating that BDNF signaling is necessary to allow the benefits of exercise to manifest (Vaynman et al., 2004, 2006).”
From Exercise-Mediated Neurogenesis in the Hippocampus via BDNF (2018) · cites this paper as Vaynman et al., 2006
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References 41 · Cited by 248
- Authors
- Vaynman, S. S., Ying, Z., Yin, D., & Gomez-Pinilla, F.
- Affiliations
- University of California, Los Angeles (US)
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2006-01
- Volume
- 1070
- Issue
- 1
- Pages
- 124-130
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2038145816
- Cited by
- 248
- References
- 41
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 9 · 2023: 6 · 2022: 15 · 2021: 10 · 2020: 15 · 2019: 16 · 2018: 10 · 2017: 24 · 2016: 9 · 2015: 20 · 2014: 12 · 2013: 11 · 2012: 17
- FWCI
- 5.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS 39522, R01NS045804, NS 045804, R01NS039522)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- physical activity, brain-derived neurotrophic factor, TrkB receptor, synaptic proteins, synapsin I, synaptophysin, syntaxin, synaptic vesicle formation, neurotransmitter release, hippocampus, voluntary wheel running, synaptic transmission
- MeSH terms
- Animals, Hippocampus, Immunoglobulin G, Male, Motor Activity, Nerve Tissue Proteins, Synaptic Transmission, Recombinant Fusion Proteins, Synapses, Synaptic Vesicles, Synapsins, Synaptophysin, Rats, Sprague-Dawley, Brain-Derived Neurotrophic Factor, Receptor, trkB, Rats
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