Cited by 471Stress Responses and CortisolNeuroinflammation and Neurodegeneration MechanismsNeuropeptides and Animal Physiology

Type 1 interleukin‐1 receptor in the rat brain: Distribution, regulation, and relationship to sites of IL‐1–induced cellular activation

Ericsson, A., Liu, C., Hart, R. P., Sawchenko, P. E.·1995·Journal of Comparative Neurology

Abstract

Systemic interleukin‐1 (IL‐1) activates the hypothalamo‐pituitary‐adrenal (HPA) axis, an effect exerted through increased synthesis and secretion of corticotropin‐releasing factor (CRF) by parvicellular neurosecretory neurons. The site(s) and mechanism(s) through which circulat ing IL‐1 may access central systems governing HPA axis output remain obscure. To identify potential cellular targets for blood‐borne IL‐1, we analyzed the distribution of mRNA encoding the rat type 1 IL‐1 receptor (IL‐1R1) in rat brain. Regional ribonuclease protection assays detected a single protected fragment corresponding to the membrane‐bound form of the IL‐1R1 mRNA in all areas analyzed. In situ hybridization revealed labeling predominantly over barrier‐related cells, including the leptomeninges, non‐tanycytic portions of the ependyma, the choroid plexus, and vascular endothelium. Low to moderate levels of the IL‐1111 mRNA were detected in just a few neuronal cell groups, including the basolateral nucleus of the amygdala, the arcuate nucleus of the hypothalamus, the trigeminal and hypoglossal motor nuclei, and the area postrema. No specific labeling for IL‐1R1 mRNA was detected over neurons that respond to intravenous IL‐1β; by induction of transcription factor Fos, including hypophysiotropic CRF cells and brainstem catecholamine neurons. Injection of IL‐1β did, however, provoke induction of mRNA encoding the immediate‐early gene, NGFI‐B, but not c‐fos, in two major loci of IL‐1R1 expression, vascular endothelial cells, and the area postrema. Intravenous inection of IL‐1β acutely down‐regulated IL‐1R1 mRNA in perivascular cells, but not in neuronal cell groups. These results suggest the parenchymal sites of IL‐1R1 expression in rat to be distinct from those reported previously in mouse. The common expression in both species of an IL‐1R in non‐neuronal elements highlights the possibility that IL‐1‐mediated activation of CRF neurons may result from cytokine‐receptor interaction at vascular, and/or other barrier‐related, sites to trigger release of secondary signalling molecules in a position to interact with components of HPA control circuitry. © 1995 Wiley‐Liss, Inc.

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Crossref · 10.1002/cne.903610410

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  • BBB endothelial cells express key cytokine receptors (IL-1R1, IL-6, TNF receptor), and binding of these receptors leads to transport or secretion of additional proinflammatory cytokines and secondary mediators (prostaglandins) that propagate inflammatory signaling into the CNS.

    “For instance, BBB endothelial cells express key cytokine receptors (IL-1R1, IL-6, TNF receptor), and binding of these receptors leads to transport or secretion of additional proinflammatory cytokines and secondary mediators (prostaglandins) that propagate inflammatory signaling into the CNS (Bebo and Linthicum, 1995;Ericsson et al, 1995;Vallieres and Rivest, 1999).”

    From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Ericsson et al, 1995

  • CVOs and other CNS barrier tissues can respond to various inflammatory stimuli through expression of cytokine receptors, Toll-like receptors (TLRs), and CD14.

    “CVOs and other CNS barrier tissues can, in turn, respond to various inflammatory stimuli through expression of cytokine receptors (103), Toll-like receptors (TLRs) (104), and CD14 (105).”

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Authors
Ericsson, A., Liu, C., Hart, R. P., & Sawchenko, P. E.
Affiliations
  • Salk Institute for Biological Studies (US)
  • Rutgers, The State University of New Jersey (US)
Corresponding author
Sawchenko, P. E.
Venue
Journal of Comparative Neurology
Publisher
Wiley
Published
1995-10-30
Volume
361
Issue
4
Pages
681-698
ISSN
  • 0021-9967 (ISSN-L)
  • 1096-9861
OpenAlex
W2037280691
Cited by
471
References
94
Citations by year
2026: 2 · 2025: 2 · 2024: 5 · 2023: 4 · 2022: 7 · 2021: 8 · 2020: 8 · 2019: 12 · 2018: 11 · 2017: 11 · 2016: 14 · 2015: 13 · 2014: 13 · 2013: 13 · 2012: 12
FWCI
11.93
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Comparative Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5k02mh000855-02, 5r01mh051564-03)
  • National Institute of Mental Health (MH51564, MH-00855)
  • Fogarty International Center
  • National Institute of Neurological Disorders and Stroke (NS21182)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
IL1R1, IL-1β, hypothalamic-pituitary-adrenal axis, corticotropin-releasing factor, area postrema, choroid plexus, vascular endothelium, leptomeninges, ependyma, Nur77, c-fos, receptor down-regulation, blood-brain barrier, rat brain
MeSH terms
Animals, Brain, Hypothalamo-Hypophyseal System, Immunohistochemistry, Interleukin-1, Male, Pituitary-Adrenal System, RNA, Messenger, Rats, Sprague-Dawley, In Situ Hybridization, Receptors, Interleukin-1, Rats

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