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Cytokine mediation of experimental heart failure-induced anhedonia
Journal article   Peer reviewed

Cytokine mediation of experimental heart failure-induced anhedonia

Angela J Grippo, Joseph Francis, Robert M Weiss, Robert B Felder and Alan Kim Johnson
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.284(3), pp.R666-R673
03/2003
DOI: 10.1152/ajpregu.00430.2002
PMID: 12611391

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Abstract

Immune system dysfunction is hypothesized to influence several disease states, including cardiovascular disease and psychological depression. The comorbidity of depression and coronary artery disease may be influenced by immune system-brain interactions involving proinflammatory cytokines. The present studies evaluated an index of depression in a rodent model of heart failure by measuring responses to rewarding electrical brain stimulation, which provides an experimental procedure to operationally define anhedonia in rats. Heart failure led to a rightward shift in the current-response relationship in the brain stimulation paradigm, indicative of reduced rewarding properties of the brain stimulation (i.e., anhedonia). Acute treatment with a tumor necrosis factor antagonist, etanercept, reduced circulating tumor necrosis factor- levels in rats with heart failure and restored responding for electrical brain stimulation. The current findings have implications for the study of pathophysiological mechanisms underlying the association of cardiovascular disease and depression.
Tumor Necrosis Factor-alpha - metabolism Depression - physiopathology Electric Stimulation Brain - physiopathology Rats Behavior, Animal - physiology Male Rats, Sprague-Dawley Depression - etiology Animals Etanercept Receptors, Tumor Necrosis Factor Immunoglobulin G - pharmacology Behavior, Animal - drug effects Reward Heart Failure - psychology Immunosuppressive Agents - pharmacology Tumor Necrosis Factor-alpha - antagonists & inhibitors

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