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Stress, Inflammation and Reward Processing: Implications for Major Depressive Disorder

  • Author(s): Boyle, Chloe Cassandra
  • Advisor(s): Bower, Julienne E
  • et al.
Abstract

Anhedonia, or pervasive diminished interest or pleasure, is a core diagnostic symptom of depression that predicts poor treatment response and may also play a role in depression etiology. Anhedonia is increasingly recognized as multidimensional, reflecting decreased reward motivation, reward sensitivity, and/or reward-learning. The mechanisms that give rise to dysregulation in these dimensions of reward have yet to be characterized. Compelling evidence and theory suggest two processes may play a central role: stress and elevated inflammation. Both stress and inflammation induce anhedonic behavior, and Social Signal Transduction Theory posits that inflammation is a central mechanism linking stress to depression more broadly. However, studies have yet to test whether stress-induced inflammation alters specific dimensions of reward. Thus, the current study experimentally evaluated the effects of stress-induced inflammation on multiple dimensions of reward. Fifty-four female young adults were randomized to undergo an acute psychosocial laboratory stressor or a no-stress active control, and completed three behavioral tasks for assessment of reward motivation (Effort Expenditure for Rewards Task; EEfRT), learning (Probabilistic Reward Task; PRT) and sensitivity (positive faces on an emotional dot probe task, EEfRT, PRT). To test inflammation as a mediator of effects of stress on reward, the tasks were administered before and 90 minutes post stress to coincide with the peak of the inflammatory response to stress. Participants provided blood samples for assessment of the pro-inflammatory cytokine interleukin-6 at study entry and 90 and 120 minutes post stress. Consistent with hypotheses, stress-induced inflammation decreased sensitivity to social reward, operationalized as decreased attentional bias towards positive faces. Contrary to hypotheses, stress-induced inflammation increased sensitivity and motivation for monetary reward. These associations were not moderated by depressive symptoms or early life stress. Together, findings demonstrate that stress-induced inflammation does indeed alter multiple dimensions of reward, though effects were not always in the hypothesized direction. Most notably, stress-induced inflammation was associated with increases in reward motivation and sensitivity for monetary reward, but decreased sensitivity to social reward. This study contributes to a growing literature characterizing the relationship between inflammation and dimensions of reward processing, which will ultimately promote targeted and effective treatment for anhedonia and depression.

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