Cited by 607Neurogenesis and neuroplasticity mechanismsStress Responses and CortisolTryptophan and brain disorders

Nuclear factor-κB is a critical mediator of stress-impaired neurogenesis and depressive behavior

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Koo, Ja Wook, Russo, Scott J., Ferguson, Deveroux, Nestler, Eric J., Duman, Ronald S.·2010·Proceedings of the National Academy of Sciences

Abstract

Proinflammatory cytokines, such as IL-1β, have been implicated in the cellular and behavioral effects of stress and in mood disorders, although the downstream signaling pathways underlying these effects have not been determined. In the present study, we demonstrate a critical role for NF-κB signaling in the actions of IL-1β and stress. Stress inhibition of neurogenesis in the adult hippocampus, which has been implicated in the prodepressive effects of stress, is blocked by administration of an inhibitor of NF-κB. Further analysis reveals that stress activates NF-κB signaling and decreases proliferation of neural stem-like cells but not early neural progenitor cells in the adult hippocampus. We also find that depressive-like behaviors caused by exposure to chronic stress are mediated by NF-κB signaling. Together, these data identify NF-κB signaling as a critical mediator of the antineurogenic and behavioral actions of stress and suggest previously undescribed therapeutical targets for depression.

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Crossref · 10.1073/pnas.0910658107

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  • Social defeat stress induces downstream inflammatory signaling pathways, such as NFkB, and increases monocyte trafficking throughout a number of CNS structures known to control depression and anxiety behavior.

    “Our results are interesting in light of recent studies showing that social defeat stress induces downstream inflammatory signaling pathways, such as NFkB (26, 35 -37), and increases monocyte trafficking (29) throughout a number of CNS structures known to control depression and anxiety behavior.”

    From Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress (2014) · cites this paper as [36]

    The Results (p. 3) show that acute immobilization stress increased NFκB activation in hippocampal neural stem-like cells, and the Discussion (p. 4) describes stress-activated IL-1β/NFκB signaling. The paper does not test social defeat stress specifically, so it supports the NFκB point but not that stress-model qualifier. Monocyte trafficking is attached to a different citation (29) and is not assessed here. (LLM, conf=0.86)

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Authors
Koo, J. W., Russo, S. J., Ferguson, D., Nestler, E. J., & Duman, R. S.
Affiliations
  • Yale University (US)
  • Icahn School of Medicine at Mount Sinai (US)
Venue
Proceedings of the National Academy of Sciences
Published
2010-01-26
Volume
107
Issue
6
Pages
2669-2674
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2001997781
Cited by
607
References
13
Citations by year
2026: 20 · 2025: 28 · 2024: 34 · 2023: 40 · 2022: 38 · 2021: 53 · 2020: 46 · 2019: 27 · 2018: 40 · 2017: 46 · 2016: 36 · 2015: 45 · 2014: 29 · 2013: 39 · 2012: 42
FWCI
12.36
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Mental Health (2-PO1-MH25642, MH-45481, R01 MH-51399, R01MH051399, R37MH045481, P01MH025642, R01MH045481)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
NF-κB signaling, chronic stress, neurogenesis, hippocampus, depression, IL-1β, inflammatory cytokines, neural progenitor cells, neurogenesis inhibition, depression-like behavior, mood disorders
MeSH terms
Animals, Cells, Cultured, Depressive Disorder, Female, Hippocampus, Male, Mice, Transgenic, Neurons, Phenylenediamines, Restraint, Physical, Stem Cells, Stress, Psychological, Thiophenes, Signal Transduction, NF-kappa B, Rats, Sprague-Dawley, Cell Proliferation, Mice, Rats, Interleukin-1beta, Neurogenesis

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