Anhedonia is associated with reduced incentive cue related activation in the basal ganglia.


Journal Article

Research has shown that reward incentives improve cognitive control in motivationally salient situations. Much previous work in this domain has focused on incentive cue-related activity in a number of brain regions, including the dorsolateral prefrontal cortex (DLPFC) and striatum. However, the more sustained changes in functional brain activity during task contexts with incentives have been relatively less explored. Here, we examined both the cue-related and sustained effects of rewards (i.e., monetary incentives) on cognitive control, with a particular focus on the roles of the DLPFC and striatum, using a mixed state-item design. We investigated whether variability in a reward-related trait (i.e., anhedonia) would modulate the sustained and/or the cue-related transient aspects of motivated cognitive control. Twenty-seven healthy individuals performed a modified response conflict task (Padmala & Pessoa, Journal of Cognitive Neuroscience, 23, 3419-3432, 2011) during scanning, in which participants were asked to categorize images as either houses or buildings with either congruent or incongruent overlaid words. Participants performed a baseline condition without knowledge of monetary incentives, followed by reward blocks with monetary incentives on some cued trials (reward cues) for fast and correct responses. We replicated previous work by showing increases in both sustained activity during reward versus baseline blocks and transient. cue-related activity in bilateral DLPFC and the basal ganglia. Importantly, healthy individuals with higher anhedonia showed less of an increase in trial-by-trial activity as a function of reward in the lateral globus pallidus. Together, our results suggest that reduced hedonic experience may be related to abnormality of reward cue-related activity in the basal ganglia.

Full Text

Duke Authors

Cited Authors

  • Chung, YS; Barch, D

Published Date

  • December 2015

Published In

Volume / Issue

  • 15 / 4

Start / End Page

  • 749 - 767

PubMed ID

  • 26105776

Pubmed Central ID

  • 26105776

Electronic International Standard Serial Number (EISSN)

  • 1531-135X

International Standard Serial Number (ISSN)

  • 1530-7026

Digital Object Identifier (DOI)

  • 10.3758/s13415-015-0366-3


  • eng