A Requirement for Nuclear Factor-κB in Developmental and Plasticity-Associated Synaptogenesis
Open accessAbstract
Structural plasticity of dendritic spines and synapses is a fundamental mechanism governing neuronal circuits and may form an enduring basis for information storage in the brain. We find that the p65 subunit of the nuclear factor-κB (NF-κB) transcription factor, which is required for learning and memory, controls excitatory synapse and dendritic spine formation and morphology in murine hippocampal neurons. Endogenous NF-κB activity is elevated by excitatory transmission during periods of rapid spine and synapse development. During in vitro synaptogenesis, NF-κB enhances dendritic spine and excitatory synapse density and loss of endogenous p65 decreases spine density and spine head volume. Cell-autonomous function of NF-κB within the postsynaptic neuron is sufficient to regulate the formation of both presynaptic and postsynaptic elements. During synapse development in vivo, loss of NF-κB similarly reduces spine density and also diminishes the amplitude of synaptic responses. In contrast, after developmental synaptogenesis has plateaued, endogenous NF-κB activity is low and p65 deficiency no longer attenuates basal spine density. Instead, NF-κB in mature neurons is activated by stimuli that induce demand for new synapses, including estrogen and short-term bicuculline, and is essential for upregulating spine density in response to these stimuli. p65 is enriched in dendritic spines making local protein–protein interactions possible; however, the effects of NF-κB on spine density require transcription and the NF-κB-dependent regulation of PSD-95, a critical postsynaptic component. Collectively, our data define a distinct role for NF-κB in imparting transcriptional regulation required for the induction of changes to, but not maintenance of, excitatory synapse and spine density.
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NF-kB plays neuron-specific roles in learning and memory.
“Intriguingly, the inflammatory transcription factor NF‐kB also plays neuron‐specific roles in learning and memory.”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Boersma et al, 2011
Inhibition of NF-kB signaling specifically in neurons impairs synaptic plasticity and synaptogenesis.
“Inhibition of NF‐kB signaling specifically in neurons impairs synaptic plasticity and synaptogenesis (O’Mahony et al, 2006; Boersma et al, 2011).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Boersma et al, 2011
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- Authors
- Boersma, M. C. H., Dresselhaus, E. C., De Biase, L. M., Mihalas, A. B., Bergles, D. E., & Meffert, M. K.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Meffert, Mollie K.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-04-06
- Volume
- 31
- Issue
- 14
- Pages
- 5414-5425
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3113725
- OpenAlex
- W1999744197
- Cited by
- 168
- References
- 62
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 6 · 2023: 9 · 2022: 11 · 2021: 12 · 2020: 17 · 2019: 7 · 2018: 9 · 2017: 11 · 2016: 14 · 2015: 10 · 2014: 12 · 2013: 16 · 2012: 17
- FWCI
- 6.36
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (R01MH080740, P50MH084020, MH-084020)
- National Eye Institute (T32EY017203)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- NF-κB, p65 subunit, synaptogenesis, dendritic spines, excitatory synapses, hippocampal neurons, synaptic plasticity, PSD-95, spine density, estrogen, bicuculline, synaptic transmission, transcriptional regulation, learning and memory
- MeSH terms
- Disks Large Homolog 4 Protein, Potassium Channels, Sodium-Activated, Animals, Animals, Newborn, Bacterial Proteins, Bicuculline, Cells, Cultured, Dendrites, Female, Hippocampus, Humans, Luminescent Proteins, Male, Membrane Proteins, Mutation, Nerve Tissue Proteins, Neuronal Plasticity, Synapses, Time Factors, Transfection, Valine, Potassium Channels, NF-kappa B, Pyramidal Cells, Patch-Clamp Techniques, Gene Expression Regulation, Developmental, Excitatory Amino Acid Antagonists, Computational Biology, Excitatory Postsynaptic Potentials, Intracellular Signaling Peptides and Proteins, Dendritic Spines, Green Fluorescent Proteins, Vesicular Inhibitory Amino Acid Transport Proteins, Mice, Guanylate Kinases, Neurogenesis, GABA-A Receptor Antagonists
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