NF-κB/Rel Regulates Inhibitory and Excitatory Neuronal Function and Synaptic Plasticity
Open accessAbstract
Changes in synaptic plasticity required for memory formation are dynamically regulated through opposing excitatory and inhibitory neurotransmissions. To explore the potential contribution of NF-kappaB/Rel to these processes, we generated transgenic mice conditionally expressing a potent NF-kappaB/Rel inhibitor termed IkappaBalpha superrepressor (IkappaBalpha-SR). Using the prion promoter-enhancer, IkappaBalpha-SR is robustly expressed in inhibitory GABAergic interneurons and, at lower levels, in excitatory neurons but not in glia. This neuronal pattern of IkappaBalpha-SR expression leads to decreased expression of glutamate decarboxylase 65 (GAD65), the enzyme required for synthesis of the major inhibitory neurotransmitter, gamma-aminobutyric acid (GABA) in GABAergic interneurons. IkappaBalpha-SR expression also results in diminished basal GluR1 levels and impaired synaptic strength (input/output function), both of which are fully restored following activity-based task learning. Consistent with diminished GAD65-derived inhibitory tone and enhanced excitatory firing, IkappaBalpha-SR+ mice exhibit increased late-phase long-term potentiation, hyperactivity, seizures, increased exploratory activity, and enhanced spatial learning and memory. IkappaBalpha-SR+ neurons also express higher levels of the activity-regulated, cytoskeleton-associated (Arc) protein, consistent with neuronal hyperexcitability. These findings suggest that NF-kappaB/Rel transcription factors act as pivotal regulators of activity-dependent inhibitory and excitatory neuronal function regulating synaptic plasticity and memory.
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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 O’Mahony et al, 2006
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 O’Mahony et al, 2006
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- Authors
- O'Mahony, A., Raber, J., Montano, M., Foehr, E., Han, V., Lu, S.-M., Kwon, H., LeFevour, A., Chakraborty-Sett, S., & Greene, W. C.
- Affiliations
- Gladstone Institute of Virology and Immunology
- Oregon National Primate Research Center (US)
- Gladstone Institutes (US)
- Department of Neurology, Center for Aging and Developmental Biology
- Departments of Behavioral Neuroscience
- Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York 14642
- Corresponding author
- Greene, Warner C.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2006-10-01
- Volume
- 26
- Issue
- 19
- Pages
- 7283-7298
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC1592877
- OpenAlex
- W2116207236
- Cited by
- 110
- References
- 82
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 6 · 2022: 4 · 2021: 7 · 2020: 8 · 2019: 2 · 2018: 1 · 2017: 4 · 2016: 2 · 2015: 6 · 2014: 8 · 2013: 7 · 2012: 12
- FWCI
- 2.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Johns Hopkins University
- Gladstone Institutes
- National Institutes of Health (1c06rr018928-01)
- University of California, San Francisco
- National Institute on Aging (R01AG020904, AG20904)
- National Center for Research Resources (C06-RR-018928)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- synaptic plasticity, inhibitory interneurons, GABAergic neurons, glutamate decarboxylase 65, GABA synthesis, GluR1, long-term potentiation, hyperactivity, seizures, spatial learning and memory, Arc protein, neuronal excitability, activity-dependent gene expression
- MeSH terms
- NF-KappaB Inhibitor alpha, Animals, Behavior, Animal, Cognition, gamma-Aminobutyric Acid, Glutamate Decarboxylase, Hippocampus, Isoenzymes, Memory, Mice, Transgenic, Synaptic Transmission, Neuronal Plasticity, Neurons, RNA, Messenger, Synapses, Gene Expression Regulation, Enzymologic, Long-Term Potentiation, Receptors, AMPA, Glutamic Acid, I-kappa B Proteins, Mice, Transcription Factor RelA
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