Acute Stress Reduces Reward Responsiveness: Implications for Depression

Department of Psychology, Harvard University, 33 Kirkland Street, Cambridge, MA 02138, USA.
Biological Psychiatry (Impact Factor: 10.26). 12/2006; 60(10):1147-54. DOI: 10.1016/j.biopsych.2006.03.037
Source: PubMed


Stress, one of the strongest risk factors for depression, has been linked to "anhedonic" behavior and dysfunctional reward-related neural circuitry in preclinical models.
To test if acute stress reduces reward responsiveness (i.e., the ability to modulate behavior as a function of past reward), a signal-detection task coupled with a differential reinforcement schedule was utilized. Eighty female participants completed the task under both a stress condition, either threat-of-shock (n = 38) or negative performance feedback (n = 42), and a no-stress condition.
Stress increased negative affect and anxiety. As hypothesized based on preclinical findings, stress, particularly the threat-of-shock condition, impaired reward responsiveness. Regression analyses indicate that self-report measures of anhedonia predicted stress-induced hedonic deficits even after controlling for anxiety symptoms.
These findings indicate that acute stress reduces reward responsiveness, particularly in individuals with anhedonic symptoms. Stress-induced hedonic deficit is a promising candidate mechanism linking stressful experiences to depression.

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Available from: Ryan Bogdan
    • "Trials with reaction times more than 3 SD away from the mean, or premature/no response trials, were excluded (3.59%). Reward response bias (or simply reward bias, Log b) and discriminability (Log d) were computed using the method described in previous studies (Bogdan and Pizzagalli, 2006; Pizzagalli et al., 2005). Reward bias (towards the'rich', i.e. more frequently rewarded, stimulus ) was our main behavioural outcome measure, while discriminability acted as a control measure for overall task performance . "
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    ABSTRACT: Background: Anhedonia is a cardinal feature of major depression and is hypothesized to be driven by low motivation, in particular blunted reward sensitivity. It has been suggested to be a marker that represents a genetic predisposition to this disorder. However, little is known about the mechanisms underlying this heightened risk in unaffected first-degree relatives of patients with major depression. We previously demonstrated abnormal reward biases in acutely depressed patients. The present study aimed to examine the development of reward bias in first-degree relatives of patients with major depression. Methods: Forty-seven first-degree relatives of patients with major depression (26 females, age 18-52) and 60 healthy controls with no family history of depression (34 females, age 21-48) were recruited. A probabilistically rewarded difficult visual discrimination task, in which participants were instructed about the contingencies, was used to assess blunted reward sensitivity. A response bias towards the more frequently rewarded stimulus (termed "reward bias") was the primary outcome variable in this study. Participants also completed self-reported measures of anhedonia and depressive symptoms. Results: Compared with the control group, relatives of patients with major depression with sub-clinical depressive symptoms displayed a blunted reward bias. Relatives without symptoms displayed largely intact motivational processing on both self-report and experimental measures. The degree of anhedonia was associated with attenuated reward bias in first-degree relatives of patients with major depression, especially in those with sub-clinical symptoms. Limitations: The study did not include a depressed patient group, which restricted our ability to interpret the observed group differences. Conclusions: Blunted reward sensitivity may be largely manifested in a subgroup of relatives with high levels of depressive symptoms.
    No preview · Article · Nov 2015 · Journal of Affective Disorders
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    • ") and adults (Bogdan and Pizzagalli, 2006; Pizzagalli et al., 2008) exhibit reward dysfunction, which may be a promising phenotype of depression. Converging evidence from neuroimaging studies characterizing the neuropathology of these reward deficits has highlighted dysfunction within the anterior cingulate cortex (Steele et al., 2007) and striatum (Pizzagalli et al., 2009). "
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    ABSTRACT: Background: Adolescent depression and suicide are pressing public health concerns, and identifying key differences among suicide ideators and attempters is critical. The goal of the current study is to test whether depressed adolescent suicide attempters report greater anhedonia severity and exhibit aberrant effort–cost computations in the face of uncertainty. Methods: Depressed adolescents (n ¼ 101) ages 13–19 years were administered structured clinical interviews to assess current mental health disorders and a history of suicidality (suicide ideators¼55, suicide attempters¼46). Then, participants completed self-report instruments assessing symptoms of suicidal ideation, depression, anhedonia, and anxiety as well as a computerized effort–cost computation task. Results: Compared with depressed adolescent suicide ideators, attempters report greater anhedonia severity, even after concurrently controlling for symptoms of suicidal ideation, depression, and anxiety. Additionally, when completing the effort–cost computation task, suicide attempters are less likely to pursue the difficult, high value option when outcomes are uncertain. Follow-up, trial-level analyses of effort–cost computations suggest that receipt of reward does not influence future decision-making among suicide attempters, however, suicide ideators exhibit a win–stay approach when receiving rewards on previous trials. Limitations: Findings should be considered in light of limitations including a modest sample size, which limits generalizability, and the cross-sectional design. Conclusions: Depressed adolescent suicide attempters are characterized by greater anhedonia severity, which may impair the ability to integrate previous rewarding experiences to inform future decisions. Taken together, this may generate a feeling of powerlessness that contributes to increased suicidality and a needless loss of life.
    Full-text · Article · Aug 2015 · Journal of Affective Disorders
    • "The notions of environmental reinforcement and biological reward responsiveness have been linked in a study by Bogdan and Pizzagalli (2006) who found that acute stress (a response to stressful environments) reduces reward responsiveness, particularly in individuals with anhedonic symptoms. Since stress is one of the strongest risk factors for depression, the hypothesis of a stress-induced hedonic deficit is a promising candidate mechanism linking stressful experiences to depression, via deficient accessing of reinforcing events. "
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