The Neurobiology of Anhedonia and Other Reward-Related Deficits
By Andre Der-Avakian, A. Markou. Trends in Neurosciences, 2011
1,015 citations recorded by the source corpus.
Anhedonia, or markedly diminished interest or pleasure, is a hallmark symptom of major depression, schizophrenia, and other neuropsychiatric disorders. Over the past three decades, the clinical definition of anhedonia has remained relatively unchanged, although cognitive psychology and behavioral neuroscience have expanded our understanding of other reward-related processes. Here, we review the neural bases of the construct of anhedonia that reflects deficits in hedonic capacity, and is also closely linked to the constructs of reward valuation, decision-making, anticipation, and motivation. The neural circuits subserving these reward-related processes include the ventral striatum, prefrontal cortical regions, and afferent and efferent projections. Understanding anhedonia and other reward-related constructs will facilitate diagnosis and treatment of disorders that include reward deficits as key symptoms.
Subfields: Cardiology and Cardiovascular Medicine, Cellular and Molecular Neuroscience, Pharmacology
View Paper: https://www.semanticscholar.org/paper/457ba6b4e9756c5127004a401ab7c4b970763108
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In Cellular and Molecular Neuroscience
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Citations in the corpus
- The Clinical Assessment Interview for Negative Symptoms (CAINS): Final Development and Validation (2013, background): “Research that seeks to delineate the neurobiological and behavioral processes that undergird these symptoms, processes that are also a current focus of the Research Domain Criteria (5, 6, 39), will further help to focus the development of treatments for the motivation/pleasure and expression domains”
- Dopamine System Dysregulation in Major Depressive Disorders (2017, background): “It should be noted that molecular deficits as well as disruptions in specific neural circuits underlying different reward-related processes have been reviewed in detail in (Der-Avakian and Markou, 2012) and (Nestler and Carlezon, 2006).”