Inactivation of the Cerebral NF¿B Pathway Inhibits Interleukin-1ß-Induced Sickness Behavior and c-Fos Expression in Various Brain Nuclei
Neuropsychopharmacol. 2005-05-18; 30(8): 1492-1499
DOI: 10.1038/sj.npp.1300755
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https://www.bordeaux-neurocampus.fr/12511
Nadjar A(1), Bluthé RM, May MJ, Dantzer R, Parnet P.
Author information:
(1)UMR INRA I 244-CNRS-Université Victor Segalen Bordeaux II, Institut François
Magendie, rue Léo Saignat Bordeaux, Cedex, France.
The behavioral effects of peripherally administered interleukin-1beta (IL-1beta)
are mediated by the production of cytokines and other proinflammatory mediators
at the level of the blood-brain interface and by activation of neural pathway.
To assess whether this action is mediated by NFkappaB activation, rats were
injected into the lateral ventricle of the brain with a specific inhibitor of
NFkappaB activation, the NEMO Binding Domain (NBD) peptide that has been shown
previously to abolish completely IL-1beta-induced NFkappaB activation and Cox-2
synthesis in the brain microvasculature. NFkappaB pathway inactivation
significantly blocked the behavioral effects of intraperitoneally administered
IL-1beta in the form of social withdrawal and decreased food intake, and
dramatically reduced IL-1beta-induced c-Fos expression in various brain regions
as paraventricular nucleus, supraoptic nucleus, and lateral part of the central
amygdala. These findings strongly support the hypothesis that IL-1beta-induced
NFkappaB activation at the blood-brain interface is a crucial step in the
transmission of immune signals from the periphery to the brain that underlies
further events responsible of sickness behavior.
DOI: 10.1038/sj.npp.1300755
PMID: 15900319 [Indexed for MEDLINE]