title: Corticosterone changes in response to stressors, acute and protracted actions of tumor necrosis factor-alpha, and lipopolysaccharide treatments in mice lacking the tumor necrosis factor-alpha p55 receptor gene.
abstract: Systemic administration of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has acute as well as sensitizing effects on behavioral and neurochemical functioning.
  
  
  OBJECTIVE
  As many of the central consequences of TNF-alpha are mediated by its p55 receptor, the present investigation determined the role of this receptor on the plasma corticosterone increase associated with the acute TNF-alpha treatment and the sensitized response evident upon reexposure to the cytokine. Moreover, the role of p55 in the provocation of corticosterone release engendered by lipopolysaccharide (LPS) and psychogenic stressors (noise or restraint) was also determined.
  
  
  METHODS
  Plasma corticosterone levels were determined in wild-type and p55-deficient mice that received systemic treatments with TNF-alpha and LPS, as well as exposure to auditory and restraint stressors.
  
  
  RESULTS
  Mice deficient for p55 displayed a greatly attenuated plasma corticosterone response to TNF-alpha irrespective of whether they had been previously exposed to the cytokine. In contrast, p55 deletion did not affect corticosterone responses elicited by LPS and by stressors.
  
  
  CONCLUSIONS
  It appears that although p55 modulates the corticosterone-inducing effects of TNF-alpha, the receptor does not play a critical role in the activation of the HPA axis by 'traditional' psychogenic stressors (noise, restraint) or systemic endotoxin challenge.
authors.affiliation: Institute of Neuroscience, Carleton University, Ottawa, Ont., Canada. shawnhayley@sympatico.ca
authors.forename: Shawn
authors.initials: S
authors.lastname: Hayley
authors.forename: Owen
authors.initials: O
authors.lastname: Kelly
authors.forename: Hymie
authors.initials: H
authors.lastname: Anisman
mesh_terms: D000208:Acute Disease; D000818:Animals; D015703:Antigens, CD / Q000235:genetics*; D003345:Corticosterone / Q000097:blood*; D004305:Dose-Response Relationship, Drug; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010913:Pituitary-Adrenal System / Q000276:immunology; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics*; D047888:Receptors, Tumor Necrosis Factor, Type I; D013312:Stress, Physiological / Q000097:blood / Q000276:immunology / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism* / Q000494:pharmacology
chemical_list: D015703:Antigens, CD; D008070:Lipopolysaccharides; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha; D003345:Corticosterone