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In this study, the effects of stress, GCs, and NMDA receptors on lipopolysaccharide (LPS)-induced activation of NF-\u03baB in the brain were investigated. One day after chronic unpredictable stress (CUS), nonstressed and CUS rats were treated with saline or LPS and killed 2 h later. CUS potentiated the increase in LPS-induced activation of NF-\u03baB in frontal cortex and hippocampus but not in the hypothalamus. This stress effect was blocked by pretreatment of rats with RU-486, an antagonist of the GC receptor. MK-801 [(+)-5-methyl-10,11-dihydro-5<jats:italic>H<\/jats:italic>-dibenzo [a,d] cyclohepten-5,10-imine maleate], an NMDA receptor antagonist, also reduced the effect of LPS in all three brain regions. However, the combined antagonism of both GC and NMDA receptors produced no further reduction in NF-\u03baB activation when compared with the effect of each treatment alone. Our results indicate that stress, via GC secretion, can increase LPS-induced NF-\u03baB activation in the frontal cortex and hippocampus, agreeing with a growing literature demonstrating proinflammatory effects of GCs.<\/jats:p>","DOI":"10.1523\/jneurosci.4398-05.2006","type":"journal-article","created":{"date-parts":[[2006,4,6]],"date-time":"2006-04-06T12:53:28Z","timestamp":1144328008000},"page":"3813-3820","source":"Crossref","is-referenced-by-count":254,"title":["Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-\u03baB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion"],"prefix":"10.1523","volume":"26","author":[{"given":"Carolina Demarchi","family":"Munhoz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucilia B.","family":"Lepsch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisa 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