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Reconsidering anhedonia in depression: Lessons from translational neuroscience
Open accessAbstract
Anhedonia is a core symptom of major depressive disorder (MDD), the neurobiological mechanisms of which remain poorly understood. Despite decades of speculation regarding the role of dopamine (DA) in anhedonic symptoms, empirical evidence has remained elusive, with frequent reports of contradictory findings. In the present review, we argue that this has resulted from an underspecified definition of anhedonia, which has failed to dissociate between consummatory and motivational aspects of reward behavior. Given substantial preclinical evidence that DA is involved primarily in motivational aspects of reward, we suggest that a refined definition of anhedonia that distinguishes between deficits in pleasure and motivation is essential for the purposes of identifying its neurobiological substrates. Moreover, bridging the gap between preclinical and clinical models of anhedonia may require moving away from the conceptualization of anhedonia as a steady-state, mood-like phenomena. Consequently, we introduce the term "decisional anhedonia" to address the influence of anhedonia on reward decision-making. These proposed modifications to the theoretical definition of anhedonia have implications for research, assessment and treatment of MDD.
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“Anhedonia and impaired reward circuit pathways are associated with a poorer prognosis and suboptimal treatment response (Buckner et al., 2008;Uher et al., 2012;Treadway and Zald, 2011).”
From Effectiveness of Vortioxetine on Emotional Blunting in Patients with Major Depressive Disorder with inadequate response to SSRI/SNRI treatment (2021) · cites this paper as Treadway and Zald, 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“co-morbid traits, such as depression, anxiety, or inattention/hyperactivity, are often associated with ASD [212], and are known to affect general reward processing [213,214] and intervention response [215].”
From Social “wanting” dysfunction in autism: neurobiological underpinnings and treatment implications (2012) · cites this paper as [213]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“studies of the neurobiology of reward processing have highlighted the variety of distinct pathways involved in its different aspects resulting in the recognition of separate subtypes of anhedonia, including consummatory, anticipatory, motivational and decisional [20,21].”
From Prefrontal cortex and depression (2022) · cites this paper as [20]
Experimental — accuracy not yet measuredIn the citing paper
“Anhedonia is a broad construct that includes deficits in anticipation of, motivation toward, and responsiveness to reward, as well as deficits in reward learning (ability to recall and make decisions based on past rewarding experiences) (Treadway and Zald, 2011) and is estimated to be 46% heritable in studies of monozygotic twins (Bogdan and Pizzagalli, 2009).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Treadway and Zald, 2011
In the citing paper
“hyposensitivity to reward and hypersensitivity to punishment have been a consistent finding in depression”
From Cognitive neuropsychological theory of antidepressant action: a modern-day approach to depression and its treatment (2021) · cites this paper as Treadway and Zald 2011
In the citing paper
“Dysregulation of dopamine release in motivating responses to rewarding and aversive stimuli, as well as cognitive demand, is a plausible mechanistic cause that can explain a range of depression symptoms [24][25][26][27][28][29].”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [25]
In the citing paper
“Particularly relevant in the present context are previous reports [290,296,297] that although both DA and non-DA agents can be used to effectively treat mood disorders, DA agents generally have superior effects on symptoms of anhedonia, specifically when compared with non-DA agents [19,298-300].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [19]
In the citing paper
“The mesolimbic DA system represents only one component of a very complex and integrated set of circuits, and although DA is clearly a crucial neurotransmitter in the reward-processing system, non-DA systems clearly also modulate reward responsibility [19,735].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [19]
In the citing paper
“Additionally, multiple non-DA compounds have shown efficacy in improving reward responses, such as agents that affect glutamate circuits involved in regulating monoamine systems [19].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [19]
In the citing paper
“However, recent studies suggest that many patients with schizophrenia or Parkinson’s, and possibly some with major depression, are not actually anhedonic after all: they report normal sensory pleasure ratings of ice cream or other sensory reward in the moment, even though they attach little value to any sensory, social or other pleasant reward in life.”
From Evolving Concepts of Emotion and Motivation (2018) · cites this paper as Treadway and Zald, 2011
In the citing paper
“Some investigators therefore have suggested their deficit really reflects a selective loss of incentive motivation or ‘wanting,’ rather than loss of pleasure ‘liking’ (Sienkiewicz-Jarosz et al., 2005; Dowd and Barch, 2010; Treadway and Zald, 2011; Barch et al., 2014).”
From Evolving Concepts of Emotion and Motivation (2018) · cites this paper as Treadway and Zald, 2011
In the citing paper
“Anhedonia typically does not respond to first-line pharmacotherapies [5, 7, 8]”
From Chronic unpredictable stress induces depression-related behaviors by suppressing AgRP neuron activity (2021) · cites this paper as [5]
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Metadata
- Authors
- Treadway, M. T., & Zald, D. H.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Treadway, Michael T.
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 35
- Issue
- 3
- Pages
- 537-555
- ISSN
- 0149-7634 (ISSN-L)
- PMC
- PMC3005986
- OpenAlex
- W2049882268
- Cited by
- 1,579
- References
- 357
- Citations by year
- 2026: 154 · 2025: 141 · 2024: 107 · 2023: 120 · 2022: 93 · 2021: 109 · 2020: 158 · 2019: 107 · 2018: 118 · 2017: 95 · 2016: 93 · 2015: 92 · 2014: 74 · 2013: 51 · 2012: 48
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (F31MH087015)
- National Institute on Drug Abuse (R01DA019670)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- anhedonia, major depressive disorder, dopamine, reward motivation, translational neuroscience
- MeSH terms
- Animals, Depression, Dopamine, Humans, Motivation, Neurosciences, Reward, Translational Research, Biomedical
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