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Adolescent Depression: Stress and Reward Dysfunction
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LEARNING OBJECTIVES: After participating in this educational activity, the physician should be better able to 1. Evaluate the relationship between reward processes, stress, and depression. 2. Assess the characteristics of the three etiological models of stress and reward processes. 3. Identify the biological basis for stress and reward processes. Adolescence is a peak period for the onset of depression, and it is also a time marked by substantial stress as well as neural development within the brain reward circuitry. In this review, we provide a selective overview of current animal and human research investigating the relationship among reward processes, stress, and depression. Three separate, but related, etiological models examine the differential roles that stress may play in relation to reward dysfunction and adolescent depression. First, the reward mediation model suggests that both acute and chronic stress contribute to reward deficits, which, in turn, potentiate depressive symptoms or increase the risk for depression. Second, in line with the stress generation perspective, it is plausible that premorbid reward-related dysfunction generates stress--in particular, interpersonal stress--which then leads to the manifestation of depressive symptoms. Third, consistent with a diathesis-stress model, the interaction between stress and premorbid reward dysfunction may contribute to the onset of depression. Given the equifinal nature of depression, these models could shed important light on different etiological pathways during adolescence, particularly as they may relate to understanding the heterogeneity of depression. To highlight the translational potential of these insights, a hypothetical case study is provided as a means of demonstrating the importance of targeting reward dysfunction in both assessment and treatment of adolescent depression.
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“Both acute and chronic stress also appears to increase reward deficits, which, in turn, raises the risk for depression (47).”
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“Although alterations in anticipatory and consummatory reward processing may underlie risk for NSSI, divergent associations between mental disorders and reward responsiveness (e.g., MDD (91) vs. ADHD (94)) may influence this effect.”
From Neural correlates associated with suicide and nonsuicidal self-injury in youth (2021) · cites this paper as [91]
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“The neurobiology of MDD may be similar (91), but the antecedent trigger may differ.”
From Neural correlates associated with suicide and nonsuicidal self-injury in youth (2021) · cites this paper as [91]
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Metadata
- Authors
- Auerbach, R. P., Admon, R., & Pizzagalli, D. A.
- Affiliations
- Harvard University (US)
- Corresponding author
- Auerbach, Randy P.
- Venue
- Harvard Review of Psychiatry
- Published
- 2014-05
- Volume
- 22
- Issue
- 3
- Pages
- 139-148
- ISSN
- 1067-3229 (ISSN-L)
- PMC
- PMC4016104
- OpenAlex
- W2323072403
- Cited by
- 104
- References
- 98
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 7 · 2023: 14 · 2022: 15 · 2021: 14 · 2020: 6 · 2019: 11 · 2018: 6 · 2017: 6 · 2016: 4 · 2015: 6
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Harvard Review of Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R01MH101521, R01MH095809, R01MH068376, K23MH097786, R01 MH68376)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Keywords
- adolescent depression, stress, diathesis-stress model, brain reward system, interpersonal stress, equifinality, depression heterogeneity, depression treatment
- MeSH terms
- Adolescent, Adolescent Behavior, Animals, Major Depressive Disorder, Humans, Reward, Stress, Psychological
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