title: Anhedonia and altered cardiac atrial natriuretic peptide following chronic stressor and endotoxin treatment in mice.
abstract: Chronic stressors and inflammatory immune activation may contribute to pathophysiological alterations associated with both major depression and cardiovascular disease. The present study, conducted in mice, assessed whether a chronic stressor of moderate severity that induced an anhedonic effect, when coupled with a bacterial endotoxin, lipopolysaccharide (LPS), additively or interactively provoked circulating and heart atrial natriuretic peptide (ANP), a potentially useful diagnostic and prognostic tool in cardiac diseases. As well, given the potential role of inflammatory processes in both depression and cardiovascular disease, we assessed pro-inflammatory mRNA expression in heart in response to the stressor and the LPS treatments. Male CD-1 mice that had been exposed to a chronic, variable stressor over 4 weeks displayed reduced sucrose consumption, possibly reflecting the anhedonic effects of the stressor. Treatment with LPS (10mug) provoked increased circulating corticosterone levels in both chronically stressed and non-stressed mice. Moreover, ANP concentrations in plasma and in the left ventricle were increased by both the stressor and the LPS treatments, as were left atrial and ventricular cytokine (interleukin-1beta; tumor necrosis factor-alpha) mRNA expression. Further, these treatments synergistically influenced the rise of plasma ANP. A link may exist between stressor-provoked depressive features (anhedonia) and immune activation, with elevated levels of ANP, a potential marker of cardiovascular disturbance. These findings are consistent with the view that chronic stressors and inflammatory immune activation may represent a common denominator subserving the frequent comorbidity between these illnesses.
authors: Institute of Neuroscience, Department of Psychology, Carleton University, Ottawa, Ontario, Canada K1S5B6. wannpasto@gmail.com
authors: Boubacar Pasto
authors: BP
authors: Wann
authors: Marie-Claude
authors: MC
authors: Audet
authors: Julie
authors: J
authors: Gibb
authors: Hymie
authors: H
authors: Anisman
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood; D003863:Depression / Q000209:etiology* / Q000378:metabolism; D019422:Dietary Sucrose / Q000494:pharmacology; D004435:Eating / Q000502:physiology; D004731:Endotoxins / Q000494:pharmacology*; D005518:Food Preferences / Q000502:physiology; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D013315:Stress, Psychological / Q000097:blood / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D019422:Dietary Sucrose; D004731:Endotoxins; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009320:Atrial Natriuretic Factor; D003345:Corticosterone