title: Exposure to forced swim stress does not alter central production of IL-1.
abstract: In recent years, there has been increasing recognition that pro-inflammatory cytokines play a role in behavioral and physiological alterations produced by exposure to psychological stressors. Indeed, increases in central IL-1 production have been observed following stressors such as inescapable tailshock and social isolation, while no changes in IL-1 have been observed following other stressors (e.g., exposure to a predator). The goal of the following work was to establish whether exposure to the forced swim test (FST), a commonly used animal model of behavioral despair/depression, leads to an increase in central or peripheral production of IL-1. Briefly, adult male Sprague-Dawley rats (n=8 per group) were forced to swim for 15-30 min (25 degrees C) and killed at various intervals (ranging from immediately to 24 h) following stressor termination. Brains (hippocampus, hypothalamus, posterior cortex) and multiple peripheral tissues (pituitary, adrenals, spleen, plasma) were then dissected and frozen for subsequent measurement of IL-1 using a commercially available enzyme-linked immunosorbent assay. No observable increases in IL-1 were found in rats that were forced to swim acutely, or in rats that were re-exposed to the forced swim stressor 24 h later. These data suggest that exposure to forced swim does not lead to an increase in central production of IL-1, suggesting that the central IL-1 system is unlikely to play a role in mediating behavioral consequences of this stressor. However, these data do not exclude the possibility that other pro-inflammatory cytokines (such as IL-6 and TNF-alpha) might be produced in response to forced swim exposure.
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: Cherie
authors.initials: C
authors.lastname: Bellamy
authors.forename: Leah G
authors.initials: LG
authors.lastname: D'Agostino
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D001522:Behavior, Animal; D001921:Brain / Q000378:metabolism*; D001923:Brain Chemistry / Q000502:physiology; D003345:Corticosterone / Q000378:metabolism; D003463:Cues; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004597:Electroshock / Q000379:methods; D007375:Interleukin-1 / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D010902:Pituitary Gland / Q000378:metabolism; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000378:metabolism; D013312:Stress, Physiological / Q000378:metabolism*; D013550:Swimming; D013997:Time Factors
chemical_list: D007375:Interleukin-1; D008070:Lipopolysaccharides; D003345:Corticosterone