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Related Experiment Videos

Systemic capsaicin pretreatment fails to block the decrease in food-motivated behavior induced by lipopolysaccharide

J L Bret-Dibat1, C Creminon, J Y Couraud

  • 1INSERM U394, Bordeaux, France.

Brain Research Bulletin
|January 1, 1997
PubMed
Summary

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Proinflammatory cytokines and LPS trigger sickness behaviors by acting centrally. Capsaicin treatment, which destroys C-fiber afferents, did not block these sickness behaviors, suggesting other nerve fibers are involved.

Area of Science:

  • Neuroscience
  • Immunology
  • Physiology

Background:

  • Systemic administration of proinflammatory cytokines (e.g., interleukin-1, IL-6, tumor necrosis factor-alpha) or lipopolysaccharide (LPS) reproduces infection-induced physiological and behavioral disturbances.
  • These molecules act centrally, but the mechanisms of their central access remain unclear.
  • Previous research suggested cytokines act on peripheral afferent neuron terminations to signal the central nervous system.

Purpose of the Study:

  • To investigate the role of capsaicin-sensitive C-fiber afferents in mediating the central effects of peripheral proinflammatory cytokines and LPS.
  • To determine if selective destruction of C-fibers blocks sickness behaviors induced by IL-1beta and LPS.

Main Methods:

  • Adult rats and mice were treated with capsaicin to selectively destroy C-fiber afferents.

Related Experiment Videos

  • The effects of capsaicin treatment on visceral chemosensory function, pain sensitivity, and substance P levels were assessed.
  • The ability of capsaicin treatment to block the decrease in food-motivated behavior induced by IL-1beta and LPS was evaluated.

    • Main Results:

    • Capsaicin treatment altered visceral chemosensory function, corneal and pain sensitivity, and depleted substance P levels.
    • However, capsaicin treatment was completely ineffective in blocking the decrease in food-motivated behavior induced by IL-1beta and LPS.
    • This indicates that capsaicin-sensitive C-fibers are not the primary mediators of these sickness behaviors.

    Conclusions:

    • The findings suggest that afferent nerve fibers other than capsaicin-sensitive C-fibers are involved in the transduction of cytokine and LPS effects.
    • These results challenge the proposed mechanism involving solely C-fiber activation for cytokine-mediated sickness responses.
    • Further research is needed to identify the specific peripheral afferent pathways mediating these central effects during inflammation and infection.