Sensitization associated with stressors and cytokine treatments

Hymie Anisman, Zul Merali, Shawn Hayley

Research output: Contribution to journalShort surveypeer-review

76 Citations (Scopus)

Abstract

Like stressors, interleukin-1β and tumor necrosis factor-α (TNF-α) increase hypothalamic-pituitary-adrenal (HPA) activity and monoamine turnover at hypothalamic and extrahypothalamic sites. These effects can be re-elicited more readily upon reintroduction of these challenges (sensitization), depending on their time of re-exposure and the particular system being assessed. Following TNF-α administration, the co-expression of corticotropin releasing hormone (CRH) and arginine vasopressin increased within the median eminence, peaking 7-14 days after treatment, and was associated with an early corticosterone sensitization. However, the re-elicitation of sickness symptoms and corticosterone release was most pronounced at lengthy re-exposure intervals (28 days), possibly reflecting histamine release from mast cells. In addition, the cytokine engendered the sensitization of norepinephrine and serotonin utilization, and CRH immunoreactivity at mesocorticolimbic sites, but these effects were most prominent at brief re-exposure intervals (1-7 days). Cytokines may independently prime multiple regulatory systems, and by virtue of the neurochemical changes imparted, have both immediate and proactive influences on the evolution of psychopathology.

Original languageEnglish
Pages (from-to)86-93
Number of pages8
JournalBrain, Behavior, and Immunity
Volume17
Issue number2
DOIs
Publication statusPublished - Apr 2003
Externally publishedYes

Keywords

  • CRH
  • Corticosterone
  • Cytokine
  • Depression
  • Interleukin
  • Neuroendocrine
  • Norepinephrine
  • Sensitization
  • Serotonin
  • Tumor necrosis factor

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