Category: Translational

Symposium

Anhedonia: Reduced reward signaling, or enhanced noise in appetitive systems?

Friday, November 17
12:00 PM - 1:30 PM
Location: Sapphire Ballroom M & N, Level 4, Sapphire Level

Keywords: Depression | Motivation | Translational Research
Presentation Type: Symposium

Background: Anhedonia is a core diagnostic criterion for mood disorders, as well as being present more widely within a variety of psychiatric conditions. In addition, high levels of anhedonia represent an impediment to treatment for unipolar depression. However, establishing objective neural and behavior measures of the construct has not always been straightforward. Across several studies, we assess areas of reward-related neural activation which are clearly intact, as well as those which are not.


Methods: The first study included medicated unipolar (n=37) and bipolar (n=23) depression, healthy controls (n=40); the second, unmedicated unipolar depressed individuals (n=148) and healthy controls (n=31); the third, distressed (n=48) and healthy (n=52) young adults. All studies employed a card-guessing paradigm which was administered during an fMRI scan, although the paradigm design was altered for the final study.


Results: Across all studies, a robust measure of reward-related function, reward prediction error in the ventral striatum, was insensitive to the presence of depressive symptoms. However, in the first two studies, an inverse relationship between reward expectancy and prediction error was altered in depressed cohorts, and in particular, to higher levels of anhedonia (p=0.004). In the third study, reward expectancy related activations were reduced by increasing levels of depression severity (t=3.35, p=0.001). This study also employed a novel behavioral measure, which revealed a trend towards more variable decision making performance in distressed individuals (t=1.72, p=0.088).


Conclusions: Together, these data will be considered in light of a proposal that appetitive neural systems (including the ventral striatum and medial prefrontal cortex) are corrupted by noise in individuals who are high in anhedonia, rather than that the systems are simply less active. A theme across these studies is that a computational approach provides clarification of behavioral and neural phenomena, including neural and behavioral variability, that might otherwise be difficult to identify. The implications of this reconceptualization for treatment of anhedonic syndromes will be discussed. 

Henry W. Chase

Research Assistant Professor
University of Pittsburgh

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