BDNF and Activity-Dependent Synaptic Modulation: Figure 1.
Open accessAbstract
It is widely accepted that neuronal activity plays a pivotal role in synaptic plasticity. Neurotrophins have emerged recently as potent factors for synaptic modulation. The relationship between the activity and neurotrophic regulation of synapse development and plasticity, however, remains unclear. A prevailing hypothesis is that activity-dependent synaptic modulation is mediated by neurotrophins. An important but unresolved issue is how diffusible molecules such as neurotrophins achieve local and synapse-specific modulation. In this review, I discuss several potential mechanisms with which neuronal activity could control the synapse-specificity of neurotrophin regulation, with particular emphasis on BDNF. Data accumulated in recent years suggest that neuronal activity regulates the transcription of BDNF gene, the transport of BDNF mRNA and protein into dendrites, and the secretion of BDNF protein. There is also evidence for activity-dependent regulation of the trafficking of the BDNF receptor, TrkB, including its cell surface expression and ligand-induced endocytosis. Further study of these mechanisms will help us better understand how neurotrophins could mediate activity-dependent plasticity in a local and synapse-specific manner.
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BDNF is involved in multiple levels of neuroplasticity like synaptic modulation, adult neurogenesis, and dendritic growth.
“BDNF is involved in multiple levels of neuroplasticity like synaptic modulation, adult neurogenesis, and dendritic growth (29–32).”
From Psychedelics and Neuroplasticity: A Systematic Review Unraveling the Biological Underpinnings of Psychedelics. (2021) · cites this paper as [30]
The Abstract discusses synaptic modulation and dendritic growth, and the section ‘Possible Mechanisms for Local and Synapse-Specific Modulation by Neurotrophins’ specifically describes BDNF’s regulation of dendritic arborization. Our copy does not establish a role for BDNF in adult neurogenesis, so that part of the attributed claim is unsupported. (LLM, conf=0.86)
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- Authors
- Lu, B.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Lu, Bai
- ORCID
- Lu, Bai
- Venue
- Learning & Memory
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2003-03-01
- Volume
- 10
- Issue
- 2
- Pages
- 86-98
- ISSN
- 1072-0502 (ISSN-L)
- 1549-5485
- PMC
- PMC5479144
- OpenAlex
- W1987615735
- Cited by
- 945
- References
- 197
- Citations by year
- 2026: 22 · 2025: 32 · 2024: 31 · 2023: 28 · 2022: 29 · 2021: 41 · 2020: 34 · 2019: 37 · 2018: 40 · 2017: 47 · 2016: 42 · 2015: 39 · 2014: 59 · 2013: 56 · 2012: 49
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Learning & Memory (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- brain-derived neurotrophic factor, synaptic plasticity, neurotrophins, TrkB receptor, dendritic transport, BDNF secretion, receptor internalization
- MeSH terms
- Animals, Brain, Gene Expression Regulation, Humans, Synaptic Transmission, Neuronal Plasticity, Neurons, Signal Transduction, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Brain-Derived Neurotrophic Factor, Receptor, trkB
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