Parsing Anhedonia: Translational Models of Reward-Processing Deficits in Psychopathology

Abstract

The term anhedonia has long been used in the psychiatric literature to describe reward-processing dysfunction in psychopathology, especially depression and schizophrenia. Although anhedonia literally describes a lack of pleasurable experiences in everyday life, recent advances in both the basic science and clinical literatures indicate that reward deficits in these disorders are much broader than hedonic responses. In this article, we summarize some of the recent theoretical and empirical advances in understanding deficits in reward processing and their neurobehavioral mechanisms, with a particular focus on the neural underpinnings of motivation and effort-based decision making. We also highlight the potential of translational neuroscience to enhance diagnostic clarity by defining clinical symptoms in terms of underlying pathophysiology.

Keywords: anhedonia; depression; dopamine; motivation; nosology; schizophrenia.

Conflict of interest statement

Declaration of Conflicting Interests

The authors declared that they had no conflicts of interest with respect to their authorship or the publication of this article.

Figures

Figure

Associations among dopamine (DA), depression, and the Effort-Expenditure for Rewards Task. (A) Amphetamine increases the percentage of high effort choices (Wardle, Treadway, Mayo, Zald, & de Wit, 2011). PL = Placebo. Error bars represent the standard deviation. *p < .05. (B) Positron emission tomography imaging shows that individual differences in the percentage of high effort choices are positively associated with the magnitude of amphetamine-induced DA release in striatum and are (C) negatively associated with DA release in the insula (Treadway, Buckholtz, et al., 2012). (D) Patients with major depressive disorder (MDD) chose fewer high effort choices than matched controls (Treadway, Bossaller, Shelton, & Zald, 2012). Error bars represent the standard error of the mean. *p < .05.