title: Stress-induced increases in hypothalamic IL-1: a systematic analysis of multiple stressor paradigms.
abstract: Exposure to stressors such as footshock, tailshock, and immobilization have been shown to induce hypothalamic IL-1 production, while other stressors such as restraint, maternal separation, social isolation, and predator exposure have no effect on hypothalamic IL-1 levels. This disparity of findings has led to considerable controversy regarding the ability of stressors to induce hypothalamic IL-1 expression. Thus, the goal of the following experiments was to examine hypothalamic IL-1 responses in adult male Sprague-Dawley rats following exposure to a diverse set of stressors. Our data indicate that exposure to 2h of restraint in a Plexiglas tube, glucoprivic challenge induced by administration of 2-deoxyglucose (2-DG), or insulin-induced hypoglycemia all fail to alter hypothalamic IL-1 levels despite robust activation of the pituitary-adrenal response. However, when restraint was administered on an orbital shaker or in combination with insulin-induced hypoglycemia, robust increases in hypothalamic IL-1 were observed. No effects of glucoprivic (2-DG) challenge were observed when combined with restraint, indicating some specificity in the hypothalamic IL-1 response to stress. We also provide a preliminary validation of the ELISA detection method for IL-1, showing that (a) Western blot analyses confirmed strong immunopositive banding at the apparent molecular weight of both mature IL-1beta and the IL-1beta prohormone, and (b) footshock led to a two-fold increase in mRNA for IL-1 in the hypothalamus as detected by RT-PCR. These data provide novel insight into the characteristics of a stressor that may be necessary for the observation of stress-induced increases in hypothalamic IL-1.
authors.affiliation: Behavioral Neuroscience Program, Department of Psychology, State University of New York at Binghamton, Vestal Parkway East, Binghamton, NY 13902-6000, USA. tdeak@binghamton.edu
authors.forename: Terrence
authors.initials: T
authors.lastname: Deak
authors.forename: Kelly A
authors.initials: KA
authors.lastname: Bordner
authors.forename: Nevin K
authors.initials: NK
authors.lastname: McElderry
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Barnum
authors.forename: Peter
authors.initials: P
authors.lastname: Blandino
authors.forename: Molly M
authors.initials: MM
authors.lastname: Deak
authors.forename: Steven P
authors.initials: SP
authors.lastname: Tammariello
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000963:Antimetabolites / Q000633:toxicity; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western / Q000379:methods; D003345:Corticosterone / Q000097:blood; D003847:Deoxyglucose / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D004597:Electroshock / Q000009:adverse effects; D005508:Food Deprivation; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D007031:Hypothalamus / Q000378:metabolism*; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D012149:Restraint, Physical / Q000379:methods; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013154:Spleen / Q000378:metabolism; D013312:Stress, Physiological / Q000209:etiology / Q000378:metabolism*; D013997:Time Factors
chemical_list: D000963:Antimetabolites; D001786:Blood Glucose; D007375:Interleukin-1; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D003847:Deoxyglucose; D003345:Corticosterone