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

Karine Palin, Rose Marie Bluthé, Robert H. McCusker, Françoise Moos, Robert Dantzer, Keith W. Kelley

Research output: Contribution to journalArticle

42 Scopus citations


A variety of pathogenic insults cause synthesis of tumor necrosis factor (TNF)α 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 TNFα (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 TNFα via the TNF-R1 (p55) is directly opposed by IGF-I in the brain.

Original languageEnglish (US)
Pages (from-to)55-60
Number of pages6
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Jul 1 2007



  • Central nervous system
  • Gene deficiency
  • IGF-I
  • Sickness behavior
  • TNF receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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