Synergistic effects of interleukin-1β, interleukin-6, and tumor necrosis factor-α: Central monoamine, corticosterone, and behavioral variations

Karen Brebner, Shawn Hayley, Robert Zacharko, Znl Merali, Hymie Anisman

Research output: Contribution to journalArticlepeer-review

190 Citations (Scopus)

Abstract

The proinflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) influence neuroendocrine activity, promote central neurotransmitter alterations, and induce a constellation of symptoms collectively referred to as sickness behaviors. These cytokines may also elicit anxiety and anhedonia, and have been associated with psychological disturbances in humans. In the present investigation, systemic IL-1β and TNF-α dose-dependently and synergistically disrupted consumption of a highly palatable food source (chocolate milk), possibly reflecting anorexia or anhedonia engendered by the treatments. As well, these cytokines synergistically increased plasma corticosterone levels. Although IL-1β and TNF-α provoked variations of amine turnover in the hypothalamus, locus coeruleus, and central amygdala, synergistic effects were not evident in this respect. Nevertheless, in view of the central amine variations induced by the cytokines, it is suggested that immune activation may come to influence complex behavioral processes, as well as affective state. Copyright (C) 2000 American College of Neuropsychopharmacology.

Original languageEnglish
Pages (from-to)566-580
Number of pages15
JournalNeuropsychopharmacology
Volume22
Issue number6
DOIs
Publication statusPublished - Jun 2000
Externally publishedYes

Keywords

  • Corticosterone
  • Cytokines
  • Dopamine
  • IL-1
  • IL-6
  • Monoamines
  • Neurochemical
  • Norepinephrine
  • Serotonin
  • Synergism
  • TNF-α

Fingerprint

Dive into the research topics of 'Synergistic effects of interleukin-1β, interleukin-6, and tumor necrosis factor-α: Central monoamine, corticosterone, and behavioral variations'. Together they form a unique fingerprint.

Cite this