Depression: Perspectives from Affective Neuroscience
Abstract
Depression is a disorder of the representation and regulation of mood and emotion. The circuitry underlying the representation and regulation of normal emotion and mood is reviewed, including studies at the animal level, human lesion studies, and human brain imaging studies. This corpus of data is used to construct a model of the ways in which affect can become disordered in depression. Research on the prefrontal cortex, anterior cingulate, hippocampus, and amygdala is reviewed and abnormalities in the structure and function of these different regions in depression is considered. The review concludes with proposals for the specific types of processing abnormalities that result from dysfunctions in different parts of this circuitry and offers suggestions for the major themes upon which future research in this area should be focused.
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Heightened amygdala activity has been associated with deficient prefrontal cognitive control over limbic emotion processing, evidenced by diminished frontal regulatory activity and weaker amygdala-frontal connectivity during emotion processing in depression.
“This increased amygdala activity has been linked to impaired cognitive control exerted by specific regions of the prefrontal cortex (Davidson, Pizzagalli, Nitschke, Putnam, 2002;Holmes & Pizzagalli, 2008) onto limbic emotion processing”
From Understanding depressive rumination from a cognitive science perspective: The impaired disengagement hypothesis (2011) · cites this paper as Davidson et al., 2002
Depression involves reduced activation in cortical areas that support attentional control, and this reduction may relate to impaired emotion regulation.
“Depression is associated with hypoactivation in cortical structures involved in attentional control which can be related to impaired emotion regulation.”
From Understanding depressive rumination from a cognitive science perspective: The impaired disengagement hypothesis (2011) · cites this paper as Davidson et al., 2002
When connectivity is normal, the DLPFC can engage emotion regulation and inhibit the amygdala through links with other frontal areas, including the orbitofrontal cortex.
“In the case of normal connectivity, the DLPFC can initiate emotion regulation, inhibiting the amygdala (Davidson et al., 2002) via connections with other frontal regions such as the orbitofrontal (OFC) cortex (Taylor & Fragopaganos, 2005).”
From Understanding depressive rumination from a cognitive science perspective: The impaired disengagement hypothesis (2011) · cites this paper as Davidson et al., 2002
Changes in affective state and cognitive effects associated with depression alter mechanisms involved in speech production.
“It was proven that changes in affective state and cognitive effects associated with depression have altered the mechanisms involved in speech production [57,58].”
From Human-centred artificial intelligence for mobile health sensing: challenges and opportunities (2023) · cites this paper as [58]
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“…4 February 2009 Accepted 3 March 2009 Available online 17 March 2009 Keywords: Depression Ventromedial prefrontal cortex Dorsolateral prefrontal cortex a b s t r a c t A primary aim in the neuroscientific study of depression is to identify the brain areas involved in the pathogenesis of symptoms.”
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- Authors
- Davidson, R. J., Pizzagalli, D., Nitschke, J. B., & Putnam, K.
- Affiliations
- University of Wisconsin–Madison (US)
- Venue
- Annual Review of Psychology
- Publisher
- Annual Reviews
- Published
- 2002-02
- Volume
- 53
- Issue
- 1
- Pages
- 545-574
- ISSN
- 0066-4308 (ISSN-L)
- 1545-2085
- OpenAlex
- W2143380734
- Cited by
- 1,138
- References
- 178
- Citations by year
- 2026: 16 · 2025: 19 · 2024: 25 · 2023: 27 · 2022: 29 · 2021: 32 · 2020: 40 · 2019: 50 · 2018: 46 · 2017: 49 · 2016: 64 · 2015: 54 · 2014: 62 · 2013: 77 · 2012: 59
- FWCI
- 4.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Psychology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Research Foundation
- National Institutes of Health (5r01mh040747-14, 5k05mh000875-10)
- National Institute of Mental Health (P50 MH61083, P50MH061083, T32MH18931, P50-MH 52354, P50MH052354, MH40747, MH 43454, K05-MH 00875, T32MH018931)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- depression, emotion regulation, mood regulation, affective neuroscience, prefrontal cortex, anterior cingulate cortex, hippocampus, amygdala, brain lesions, neuroimaging
- MeSH terms
- Affect, Amygdala, Brain, Depressive Disorder, Gyrus Cinguli, Hippocampus, Humans, Neurosciences, Prefrontal Cortex, Mood Disorders
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