Dendritic BDNF Synthesis Is Required for Late-Phase Spine Maturation and Recovery of Cortical Responses Following Sensory Deprivation
Open accessAbstract
Sensory experience in early postnatal life shapes neuronal connections in the brain. Here we report that the local synthesis of brain-derived neurotrophic factor (BDNF) in dendrites plays an important role in this process. We found that dendritic spines of layer 2/3 pyramidal neurons of the visual cortex in mutant mice lacking dendritic Bdnf mRNA and thus local BDNF synthesis were normal at 3 weeks of age, but thinner, longer, and more closely spaced (morphological features of immaturity) at 4 months of age than in wild-type (WT) littermates. Layer 2/3 of the visual cortex in these mutant animals also had fewer GABAergic presynaptic terminals at both ages. The overall size and shape of dendritic arbors were, however, similar in mutant and WT mice at both ages. By using optical imaging of intrinsic signals and single-unit recordings, we found that mutant animals failed to recover cortical responsiveness following monocular deprivation (MD) during the critical period, although they displayed normally the competitive loss of responsiveness to an eye briefly deprived of vision. Furthermore, MD still induced a loss of responsiveness to the closed eye in adult mutant mice, but not in adult WT mice. These results indicate that dendritic BDNF synthesis is required for spine pruning, late-phase spine maturation, and recovery of cortical responsiveness following sensory deprivation. They also suggest that maturation of dendritic spines is required for the maintenance of cortical responsiveness following sensory deprivation in adulthood.
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BDNF plays critical roles in both pattern separation and dendritic spine development.
“Since brain-derived neurotrophic factor (BDNF) plays critical roles in both pattern separation [47] and dendritic spine development [48], [49]”
From Arf4 Determines Dentate Gyrus-Mediated Pattern Separation by Regulating Dendritic Spine Development (2012) · cites this paper as [49]
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- Authors
- Kaneko, M., Xie, Y., An, J. J., Stryker, M. P., & Xu, B.
- Affiliations
- University of California, San Francisco (US)
- Georgetown University Medical Center (US)
- Corresponding author
- Stryker, Michael P.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-04-04
- Volume
- 32
- Issue
- 14
- Pages
- 4790-4802
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3356781
- OpenAlex
- W2054970745
- Cited by
- 55
- References
- 7
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 3 · 2014: 10 · 2013: 7 · 2012: 7
- FWCI
- 3.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (EY02874)
- National Institute of Mental Health (P50MH077972)
- National Eye Institute (R01EY002874)
- National Institute of Neurological Disorders and Stroke (R56NS050596, R01NS050596, R01NS073930)
- 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
- brain-derived neurotrophic factor, dendritic spines, spine maturation, sensory deprivation, monocular deprivation, critical period, visual cortex, layer 2/3 pyramidal neurons, postnatal development, adult plasticity
- MeSH terms
- Animals, Dendrites, Female, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Sensory Deprivation, Visual Cortex, Mice, Knockout, Brain-Derived Neurotrophic Factor, Dendritic Spines, Mice
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