Toward an objective characterization of an anhedonic phenotype: a signal-detection approach.

By Diego A. Pizzagalli, Allison L. Jahn, James P. O'Shea. Biological Psychiatry, 2005

733 citations recorded by the source corpus.

BACKGROUND Difficulties in defining and characterizing phenotypes has hindered progress in psychiatric genetics and clinical neuroscience. Decreased approach-related behavior and anhedonia (lack of responsiveness to pleasure) are considered cardinal features of depression, but few studies have used laboratory-based measures to objectively characterize these constructs. METHODS To assess hedonic capacity in relation to depressive, particularly anhedonic, symptoms, 62 participants completed a signal-detection task based on a differential reinforcement schedule. Anhedonia was operationalized as decreased reward responsiveness. RESULTS Unequal frequency of reward between two correct responses produced a response bias (i.e., a systematic preference to identify the stimulus paired with the more frequent reward). Subjects with elevated depressive symptoms (Beck Depression Inventory scores >/= 16) failed to show a response bias. Impaired reward responsiveness predicted higher anhedonic symptoms 1 month later, after controlling for general negative affectivity. CONCLUSIONS Impaired tendency to modulate behavior as a function of prior reinforcement might underline diminished hedonic capacity in depression. When applied to a clinical population, objective assessments of participants' propensity to modulate behavior as a function of reward might provide a powerful tool for improving the phenotypic definition of depression and thus offer a reliable behavioral screening approach for neuroscience studies of depression.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Pharmacology

View Paper: https://www.semanticscholar.org/paper/892af8b71652db9abe310135818774e25fc6f4fb

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Citations in the corpus

The role of the nucleus accumbens and rostral anterior cingulate cortex in anhedonia: Integration of resting EEG, fMRI, and volumetric techniques (2009, background): “Consistent with this view, anhedonia is currently considered a promising endophenotype of MDD, because it is a cardinal symptom of the disorder but is considerably more homogeneous, more easily quantified, and tied to dysfunction in the neural circuitry of reward, which is increasingly well-understo”
Reconsidering Anhedonia in Depression: Lessons from Translational Neuroscience (2010, background): “One well-replicated finding has been that individuals with depression fail to develop a response bias towards rewarded stimuli (Henriques et al., 1994; Pizzagalli et al., 2008; Pizzagalli et al., 2005).”
Reduced Caudate and Nucleus Accumbens Response to Rewards in Unmedicated Subjects with Major Depressive Disorder (2009, background): “This relationship provides impetus for continued investigation of depressive endophenotypes (1, 2), because it is unclear whether reduced caudate volume predisposes individuals to anhedonic or more severe depression or instead represents a state-related correlate of these symptoms.”
Worth the ‘EEfRT’? The Effort Expenditure for Rewards Task as an Objective Measure of Motivation and Anhedonia (2009, methodology): “In recent years, investigators have focused on the objective characterization of anhedonic symptoms using quantitative behavioral and biological markers (e.g., Pizzagalli et al., 2005) [8].”
The origins and current status of behavioral activation treatments for depression. (2011, background): “…that depressed individuals are less responsive to reward than nondepressed individuals, and that such differences are correlated with hypoactivation of brain regions indicative of a deficit in approach-related behavior (Henriques & Davidson 1991, Henriques et al. 1994, Pizzagalli et al. 2005).”
Bonsai Trees in Your Head: How the Pavlovian System Sculpts Goal-Directed Choices by Pruning Decision Trees (2012, result): “We also expected to replicate prior findings whereby the reward sensitivity parameter b should be negatively correlated with BDI and NEO neuroticism [21–24].”
Mental Activity as the Bridge between Neural Biomarkers and Symptoms of Psychiatric Illness (2022, methodology): “In our exper-iment, we ran a dimension-discovery analysis on the individual items of these assessments using prior research for validation: independent groups have found separable symptom dimensions within the HAM-D and the BDI-II.”