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.
Original language | English (US) |
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Pages (from-to) | 55-60 |
Number of pages | 6 |
Journal | Journal of Neuroimmunology |
Volume | 187 |
Issue number | 1-2 |
DOIs | |
State | Published - Jul 2007 |
Externally published | Yes |
Keywords
- Central nervous system
- Gene deficiency
- IGF-I
- Sickness behavior
- TNF receptor
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology