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Cytokines and sickness behavior

R Dantzer1, R M Bluthé, S Layé

  • 1Neurobiologie Intégrative, INSERM, Bordeaux, France. robert.dantzer@bordeaux.inserm.fr

Annals of the New York Academy of Sciences
|June 18, 1998
PubMed
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The vagus nerve transmits sickness signals from the periphery to the brain, influencing behavior. Vagotomy blocks these effects, indicating neural afferents are key for immune-to-brain communication.

Area of Science:

  • Neuroimmunology
  • Behavioral Neuroscience

Background:

  • Interleukin-1 (IL-1) and lipopolysaccharide (LPS) trigger brain inflammation and behavioral changes.
  • The vagus nerve's role in mediating these central effects is not fully understood.

Purpose of the Study:

  • To investigate the role of vagal afferents in transmitting peripheral immune signals to the brain.
  • To elucidate the neural pathways involved in cytokine-induced behavioral alterations.

Main Methods:

  • Vagotomy in rats and mice to assess behavioral responses to peripheral IL-1 and LPS.
  • Measurement of peripheral cytokine levels.
  • Administration of IL-1 via different routes (intraperitoneal, intravenous, subcutaneous, intracerebroventricular).
  • Pharmacological interventions targeting substance P and cholecystokinin pathways.

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Main Results:

  • Vagotomy abrogated the behavioral effects of intraperitoneally administered IL-1 and LPS.
  • Vagotomy did not affect peripheral cytokine levels.
  • Vagotomized animals still responded to IL-1 administered intravenously, subcutaneously, or intracerebroventricularly.
  • Capsaicin or CCK receptor antagonists did not alter LPS/IL-1-induced behavioral changes.

Conclusions:

  • Vagal afferents are crucial for transmitting peripheral immune-derived sickness signals to the brain.
  • The transmission pathway is specific to the route of cytokine administration.
  • Substance P and cholecystokinin are unlikely to be the primary mediators of this immune-to-brain communication.