title: Neither acute nor chronic exposure to a naturalistic (predator) stressor influences the interleukin-1beta system, tumor necrosis factor-alpha, transforming growth factor-beta1, and neuropeptide mRNAs in specific brain regions.
abstract: Physical (neurogenic) stressors may influence immune functioning and interleukin-1beta (IL-1beta) mRNA levels within several brain regions. The present study assessed the effects of an acute or repeated naturalistic, psychogenic stressor (predator exposure) on brain cytokine and neuropeptide mRNAs. Acute predator (ferret) exposure induced stress-like behavioral effects, including elicitation of a startle response and reduced exploratory behaviors; these responses diminished after 30 sessions. Moreover, acute and repeated predator exposure, like acute restraint stress, increased plasma corticosterone levels measured 5 min later, but not 2 h after stressor exposure. In contrast, none of the stressors used influenced IL-1beta, IL-1 receptor antagonist, IL-1 receptor type I, IL-1 receptor accessory proteins I and II, or tumor necrosis factor-alpha mRNA levels in the prefrontal cortex, amygdala, hippocampus, or hypothalamus. Likewise, there were no stressor effects on transforming growth factor-beta1, neuropeptide Y, glycoprotein 130, or leptin receptor mRNAs in brain regions. Thus, the naturalistic/psychogenic stressor used does not affect any of the brain cytokine component mRNAs studied. It is suggested that this type of stressor activates homeostatic mechanisms (e.g., glucocorticoid release), which act to preclude brain cytokine alterations that would otherwise favor neuroinflammatory/neuroimmunological responses and the consequent increase of brain sensitivity to neurotoxic and neurodegenerative processes.
authors.affiliation: Molecular Biology, School of Life and Health Sciences, University of Delaware, Newark 19716-2590, USA. crps@udel.edu
authors.forename: C R
authors.initials: CR
authors.lastname: Plata-Salamán
authors.forename: S E
authors.initials: SE
authors.lastname: Ilyin
authors.forename: N P
authors.initials: NP
authors.lastname: Turrin
authors.forename: D
authors.initials: D
authors.lastname: Gayle
authors.forename: M C
authors.initials: MC
authors.lastname: Flynn
authors.forename: T
authors.initials: T
authors.lastname: Bedard
authors.forename: Z
authors.initials: Z
authors.lastname: Merali
authors.forename: H
authors.initials: H
authors.lastname: Anisman
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism*; D008297:Male; D009025:Morpholines / Q000378:metabolism; D009478:Neuropeptide Y / Q000235:genetics / Q000378:metabolism; D009479:Neuropeptides / Q000235:genetics / Q000378:metabolism*; D011333:Pro-Opiomelanocortin / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D013315:Stress, Psychological / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
chemical_list: D002352:Carrier Proteins; D007375:Interleukin-1; D009025:Morpholines; D009478:Neuropeptide Y; D009479:Neuropeptides; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; C005759:2-phenyl-5,5-dimethyltetrahydro-1,4-oxazine; D011333:Pro-Opiomelanocortin