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Am J Physiol Regul Integr Comp Physiol 284: R666-R673, 2003. First published November 7, 2002; doi:10.1152/ajpregu.00430.2002
0363-6119/03 $5.00
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Vol. 284, Issue 3, R666-R673, March 2003

Cytokine mediation of experimental heart failure-induced anhedonia

Angela J. Grippo1,2, Joseph Francis2,3, Robert M. Weiss2,3,4, Robert B. Felder2,3,4, and Alan Kim Johnson1,2,5

Departments of 1 Psychology, 5 Pharmacology, 3 Internal Medicine, and the 2 Cardiovascular Center, The University of Iowa and 4 Veterans Affairs Medical Center, Iowa City, Iowa 52242

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-alpha 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.

cardiovascular disease; depression; etanercept; immune system; tumor necrosis factor-alpha


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