Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3065667 | Journal of Neuroimmunology | 2007 | 6 Pages |
Abstract
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.
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Authors
Karine Palin, Rose-Marie Bluthé, Robert H. McCusker, Françoise Moos, Robert Dantzer, Keith W. Kelley,