title: Social defeat promotes specific cytokine variations within the prefrontal cortex upon subsequent aggressive or endotoxin challenges.
abstract: Stressful experiences typically have short-lived neuroendocrine and neurochemical effects, but the processes leading to these biological alterations may be sensitized so that later challenges promote exaggerated responses. As stressors and immunogenic insults have both been associated with inflammatory immune variations within the brain, we assessed whether a social defeat stressor would result in augmented corticosterone release and mRNA expression of pro-inflammatory cytokines within the prefrontal cortex (PFC) upon later social defeat (sensitization) or endotoxin (lipopolysaccharide: LPS) challenges (cross-sensitization). In the absence of a prior stressor experience, the social defeat challenge did not affect prefrontal interleukin (IL)-1β or tumor necrosis factor (TNF)-α mRNA expression, but increased that of IL-6, whereas LPS increased the expression of each cytokine. Among mice that had initially been repeatedly defeated, IL-1β and TNF-α expression was enhanced after the social defeat challenge, whereas this was not evident in response to the LPS challenge. In contrast, the initial social defeat stressor had protracted effects in that increase of IL-6 expression was limited upon subsequent challenge with either social defeat or LPS. Previous social stressor experiences also limited the corticosterone rise ordinarily elicited by either social defeat or LPS treatment. It seems that a powerful stressor, such as social defeat, may have persistent effects on later corticosterone and cytokine responses to different types of stressful insults (social versus systemic challenges), but the nature of the effects varies with the specific process assessed.
authors: Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada K1S 5B6. mcaudet@connect.carleton.ca
authors: Marie-Claude
authors: MC
authors: Audet
authors: Shlomit
authors: S
authors: Jacobson-Pick
authors: Boubacar Pasto
authors: BP
authors: Wann
authors: Hymie
authors: H
authors: Anisman
mesh_terms: D000378:Agonistic Behavior / Q000502:physiology*; D000818:Animals; D003345:Corticosterone / Q000097:blood / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D004731:Endotoxins / Q000633:toxicity*; D005786:Gene Expression Regulation; D007249:Inflammation; D053583:Interleukin-1beta / Q000096:biosynthesis* / Q000235:genetics; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D051379:Mice; D010538:Peritonitis / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology; D017397:Prefrontal Cortex / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D017472:Receptors, Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D019947:Receptors, Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012930:Social Dominance; D013315:Stress, Psychological / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D013731:Territoriality; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D016207:Cytokines; D004731:Endotoxins; D053583:Interleukin-1beta; D015850:Interleukin-6; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D019947:Receptors, Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; C044101:endotoxin, Escherichia coli; D003345:Corticosterone