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Articles in PresS, published online ahead of print November 7, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00430.2002
Submitted on July 18, 2002
Accepted on November 1, 2002
1 Department of Psychology, University of Iowa, Iowa City, IA, USA; Cardiovascular Center, University of Iowa, Iowa City, IA, USA
2 Internal Medicine, University of Iowa, Iowa City, IA, USA; Cardiovascular Center, University of Iowa, Iowa City, IA, USA
3 Internal Medicine, University of Iowa, Iowa City, IA, USA; Cardiovascular Center, University of Iowa, Iowa City, IA, USA; Veteran's Affairs Medical Center, Iowa City, IA, USA
4 Department of Psychology, University of Iowa, Iowa City, IA, USA; Pharmacology, University of Iowa, Iowa City, IA, USA; Exercise Science, University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: alan-johnson{at}uiowa.edu.
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.
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