TNFalpha-induced sickness behavior in mice with functional 55 kD TNF receptors is blocked by central IGF-I.
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.
Palin
Karine
K
Department of Animal Sciences, Integrative Immunology and Behavior Program, Laboratory of Integrative Immunophysiology, University of Illinois at Urbana--Champaign, IL, USA.
Bluthé
Rose-Marie
RM
McCusker
Robert H
RH
Moos
Françoise
F
Dantzer
Robert
R
Kelley
Keith W
KW
D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D004333:Drug Administration Routes; D004347:Drug Interactions; D046352:Freezing Reaction, Cataleptic / Q000187:drug effects; D007334:Insulin-Like Growth Factor I / Q000008:administration & dosage*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008970:Molecular Weight; D018124:Receptors, Tumor Necrosis Factor / Q000172:deficiency / Q000378:metabolism*; D012803:Sick Role; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I