TNFalpha-induced sickness behavior in mice with functional 55 kD TNF receptors is blocked by central IGF-I

J Neuroimmunol. 2007 Jul;187(1-2):55-60. doi: 10.1016/j.jneuroim.2007.04.011. Epub 2007 May 18.


A variety of pathogenic insults cause synthesis of tumor necrosis factor (TNF)alpha in the brain, resulting in sickness behavior. Here we used TNF-receptor (TNF-R)2-deficient and wild-type mice to demonstrate that the reduction in social exploration of a novel juvenile, the increase in immobility and the loss of body weight caused by central TNFalpha (i.c.v., 50 ng/mouse) are blocked by central pre-treatment with the multifunctional peptide, insulin-like growth factor (IGF-I; i.c.v., 300 ng/mouse). These results establish that sickness behavior induced by central TNFalpha via the TNF-R1 (p55) is directly opposed by IGF-I in the brain.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Analysis of Variance
  • Animals
  • Behavior, Animal / drug effects*
  • Body Weight / drug effects
  • Drug Administration Routes
  • Drug Interactions
  • Freezing Reaction, Cataleptic / drug effects
  • Insulin-Like Growth Factor I / administration & dosage*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Molecular Weight
  • Receptors, Tumor Necrosis Factor / deficiency
  • Receptors, Tumor Necrosis Factor / metabolism*
  • Sick Role*
  • Tumor Necrosis Factor-alpha / pharmacology*


  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Insulin-Like Growth Factor I