Cited by 143Stress Responses and CortisolTryptophan and brain disordersNeuroinflammation and Neurodegeneration Mechanisms

Timecourse and corticosterone sensitivity of the brain, pituitary, and serum interleukin-1β protein response to acute stress

Nguyen, Kien T., Deak, Terrence, Will, Matthew J., Hansen, M.K., Hunsaker, Bradley N., Fleshner, Monika, Watkins, Linda R., Maier, Steven F.·2000·Brain Research

Abstract

Activation of peripheral immune cells leads to increases of interleukin-1beta (IL-1beta) mRNA, immunoreactivity, and protein levels in brain and pituitary. Furthermore, IL-1beta in brain plays a role in mediating many of the behavioral, physiological, and endocrine adjustments induced by immune activation. A similarity between the consequences of immune activation and exposure to stressors has often been noted, but the potential relationship between stress and brain IL-1beta has received very little attention. A prior report indicated that exposure to inescapable tailshocks (IS) raised levels of brain IL-1beta protein 2 h after IS, but only in adrenalectomized (and basal corticosterone replaced) subjects. The studies reported here explore this issue in more detail. A more careful examination revealed that IL-1beta protein levels in hypothalamus were elevated by IS in intact subjects, although adrenalectomy, ADX (with basal corticosterone replacement) exaggerated this effect. IL-1beta protein increases were already present immediately after the stress session, both in the hypothalamus and in other brain regions in adrenalectomized subjects, and no longer present 24 h later. Furthermore, IS elevated levels of IL-1beta protein in the pituitary, and did so in both intact and adrenalectomized subjects. IS also produced increased blood levels of IL-1beta, but only in adrenalectomized subjects. Finally, the administration of corticosterone in an amount that led to blood levels in adrenalectomized subjects that match those produced by IS, inhibited the IS-induced rise in IL-1beta in hypothalamus and pituitary, but not in other brain regions or blood.

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Crossref · 10.1016/s0006-8993(99)02443-9

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Authors
Nguyen, K. T., Deak, T., Will, M. J., Hansen, M. K., Hunsaker, B. N., Fleshner, M., Watkins, L. R., & Maier, S. F.
Affiliations
University of Colorado Boulder (US)
Corresponding author
Maier, Steven F.
Venue
Brain Research
Publisher
Elsevier BV
Published
2000-03
Volume
859
Issue
2
Pages
193-201
ISSN
0006-8993 (ISSN-L)
OpenAlex
W2104012185
Cited by
143
References
45
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 6 · 2019: 6 · 2018: 4 · 2017: 6 · 2016: 4 · 2015: 8 · 2014: 6 · 2013: 9 · 2012: 6
FWCI
2.30
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01mh045045-12)
  • National Institute of Mental Health (MH-00314, MH 50479, MH-45045)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
IL-1β, acute stress, corticosterone, adrenalectomy, hypothalamus, pituitary gland, brain cytokines, stress-immune interaction, corticosteroid feedback
MeSH terms
Adrenalectomy, Animals, Brain, Corticosterone, Interleukin-1, Male, Pituitary Gland, Stress, Physiological, Time Factors, Rats, Sprague-Dawley, Rats

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