Cited by 1,608Neural and Behavioral Psychology StudiesNeurotransmitter Receptor Influence on BehaviorMemory and Neural Mechanisms

The DOI matches its Crossref record; 375 of the 379 references it cites were found in a registry or an index; 36 of the 262 sources its claims cite were checked for support.

Neurocircuitry of Mood Disorders

Open access
Price, Joseph L, Drevets, Wayne C·2010·Neuropsychopharmacology

Abstract

This review begins with a brief historical overview of attempts in the first half of the 20th century to discern brain systems that underlie emotion and emotional behavior. These early studies identified the amygdala, hippocampus, and other parts of what was termed the 'limbic' system as central parts of the emotional brain. Detailed connectional data on this system began to be obtained in the 1970s and 1980s, as more effective neuroanatomical techniques based on axonal transport became available. In the last 15 years these methods have been applied extensively to the limbic system and prefrontal cortex of monkeys, and much more specific circuits have been defined. In particular, a system has been described that links the medial prefrontal cortex and a few related cortical areas to the amygdala, the ventral striatum and pallidum, the medial thalamus, the hypothalamus, and the periaqueductal gray and other parts of the brainstem. A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in mood disorders.

Overview

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Written from the paper’s full text.

TL;DR

This review synthesizes anatomical and clinical evidence that mood disorders arise from dysfunction in an extended medial prefrontal–limbic–striatal–pallidal–thalamic circuit. It argues that the medial prefrontal network and amygdala are central to emotional, autonomic, endocrine, and reward-related disturbances in major depression and bipolar disorder.

Key findings

  • The paper describes two main prefrontal networks: an orbital network tied to sensory integration and value assessment, and a medial network tied to limbic structures, visceral control, and mood regulation. The medial network connects with the amygdala, ventral striatum, mediodorsal thalamus, hypothalamus, periaqueductal gray, and brainstem.
  • In mood disorders, the most consistently reported structural abnormality is reduced gray matter in the left subgenual anterior cingulate cortex ventral to the corpus callosum genu. Reductions are also reported in orbitofrontal cortex, ventrolateral prefrontal cortex, frontal polar/dorsolateral prefrontal cortex, parahippocampal gyrus, and temporopolar cortex.
  • Hippocampal volume reductions in major depression are reported at 8–19% in some studies, but other studies do not replicate this. Amygdala volume findings are mixed: smaller in unmedicated bipolar disorder in one high-resolution study, but larger in bipolar subjects receiving mood-stabilizing treatments.
  • Postmortem and spectroscopy findings include reduced glia, especially oligodendrocytes, reduced synapses or synaptic proteins, reduced neuronal size, and reduced GABA and Glx levels in prefrontal regions. The review links these to stress-related dendritic atrophy and elevated glutamatergic/glucocorticoid activity.

Methods

  • Narrative review, not a primary study. It integrates historical models of the limbic system with modern axonal tracing studies in macaque monkeys, human lesion and neuroimaging data, postmortem neuropathology, magnetic resonance spectroscopy, and rodent chronic stress models.
  • The anatomical synthesis focuses on connectional networks of the orbital and medial prefrontal cortex, amygdala, striatum, pallidum, mediodorsal and midline thalamic nuclei, hypothalamus, and brainstem.
  • Clinical synthesis reviews structural MRI, functional imaging, neuropathological, and treatment studies in major depressive disorder and bipolar disorder, then proposes a circuit-based model of depression.

Limitations

  • The paper states that understanding remains at an early stage and that later generations may view current misconceptions with bemusement. It also states that translating monkey findings to humans is difficult, that the human cortex is not simply an enlarged monkey brain, and that new architectonic maps of human cortex are needed.
  • The paper states that current DSM-based nosology is insufficient for discovering disease mechanisms and that a circuit-based nosology is needed.
  • Evident from the text: as a narrative review, it does not use a systematic search or quantitative meta-analysis; it reports inconsistent findings across studies, including discrepant hippocampal and amygdala volumes and conflicting subgenual cingulate metabolism results, which the authors partly attribute to partial volume effects and clinical heterogeneity.

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Integrity signals

Registry

Crossref · 10.1038/npp.2009.104

Cites

375 of 375 references verified0 citation errors · 0 not checkable

Statistics

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Verification

Claims the paper makes

36 of 262 cited sources checked · 11 supported · 1 flagged · accuracy not yet measured

Show all 177 claims

  • It may state two separate claims as one. 46
  • Probably not a substantial claim. 28
64 of 64
  • The paper relies on this without support.

    The anatomical and functional organization of the emotion-related circuits described in monkeys and other animals is sufficiently similar to that in humans to inform conclusions about human mood disorders.

    “In the last 15 years these methods have been applied extensively to the limbic system and prefrontal cortex of monkeys, and much more specific circuits have been defined.”
    “A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in mood disorders.”
  • The paper relies on this without support.

    MDD and BD are not associated with gross brain pathology or with clear animal models for spontaneous recurrent mood episodes.

    “As these conditions are not associated with gross brain pathology, or with clear animal models for spontaneous recurrent mood episodes, the development of tools that allowed noninvasive assessment of human brain structure and function has proven critical to elucidating their neurobiology.”
  • The paper relies on this without support.

    Findings from animal models of stress and lesions can be generalized to humans to understand mood disorders.

    “It is likely that the role of the PVT is general across many types of stressors.”
  • The paper relies on this without support.

    Neuroimaging abnormalities in mood disorders reflect the underlying neural circuitry rather than epiphenomenal changes.

    “The neuroimaging abnormalities found in MDD and BD generally have corroborated hypotheses regarding the neural circuitry underlying depression that initially were based on observations from the behavioral effects of lesions experimentally placed in experimental animals (see 'Cortico-Striatal-Thalamic Circuits Related to the OMPFC' above)”
  • The paper relies on this without support.

    MRS spectra reflect combined intracellular and extracellular pools of glutamate-glutamine and GABA but are dominated overwhelmingly by the intracellular pools.

    “Although these spectra reflect the combined intracellular and extracellular pools of glutamate-glutamine and GABA, they are dominated overwhelmingly by the intracellular pools.”
  • The paper relies on this without support.

    The majority of the GABA pool exists within GABAergic neurons.

    “The majority of the GABA pool exists within GABAergic neurons, so the reduction in GABA in the dorsal anterolateral PFC is compatible with the report of reduced GABAergic neurons in this region (BA9) in MDD (Rajkowska et al, 2007).”
  • The paper relies on this without support.

    The Glx measure reflects the intracellular glutamate and glutamine pools.

    “As the Glx measure reflects the intracellular glutamate and glutamine pools this abnormality appears compatible with the reductions in glial cells found postmortem in the same regions in MDD.”
  • The paper relies on this without support.

    Perineuronal oligodendroglia and astroglia play roles in glutamate-glutamine cycling.

    “Both perineuronal oligodendroglia and astroglia play roles in glutamate-glutamine cycling.”
  • The paper relies on this without support.

    Neuropil occupies most of the gray matter volume.

    “Dendritic atrophy presumably would be reflected by a decrease in the volume of the neuropil, which occupies most of the gray matter volume.”
  • The paper relies on this without support.

    The ACC receives extensive dopaminergic innervation from the VTA and sends projections to the VTA that regulate phasic dopamine release.

    “The ACC receives extensive dopaminergic innervation from the VTA and sends projections to the VTA that regulate phasic dopamine (DA) release.”
  • The paper relies on this without support.

    Stimulation of projections from the amygdala to the ventral striatum interrupts the maintenance of cortically driven response patterns.

    “Stimulation of projections from the amygdala to the ventral striatum interrupts the maintenance of these cortically driven response patterns, providing an adaptive over-ride that interrupts goal-directed thought or behavior in response to threat or novelty.”
  • The paper relies on this without support.

    Antidepressant drugs impact serotonergic, dopaminergic, noradrenergic, cholinergic, glutamatergic, GABAergic, glucocorticoid, and peptidergic systems through either primary or secondary pharmacological actions.

    “Antidepressant drugs (AD) impact these systems through either primary or secondary pharmacological actions.”
  • The paper relies on this without support.

    The medial and orbital prefrontal networks connect to separate but parallel cortico-striato-pallido-thalamic loops that use adjacent cortical, mediodorsal thalamic, striatal, and pallidal regions.

    “Note that the two networks are related to parallel but distinct loops that involve adjacent parts of the cortex MD thalamus striatum and pallidum.”
  • The paper relies on this without support.

    The amygdala and hippocampus, as limbic structures, are mainly associated with the medial network.

    “Limbic structures such as the amygdala and hippocampus are primarily related to the medial network.”
  • The paper relies on this without support.

    The dorsal midline paraventricular nucleus of the thalamus connects with frontal cortex, striatum, hypothalamus, amygdala, and dorsal midbrain regions.

    “Diagram of connections between the dorsal midline paraventricular nucleus of the thalamus (PVT) with areas of the frontal cortex striatum hypothalamus amygdala and dorsal midbrain.”
  • The paper relies on this without support.

    Within the amygdala, connections link the basal and lateral nuclei to the central and medial nuclei and to the bed nucleus of the stria terminalis.

    “Intra-amygdaloid connections link the basal and lateral amygdaloid nuclei to the central and medial nuclei of the amygdala and the bed nucleus of the stria terminalis (BNST).”
  • The paper relies on this without support.

    The amygdala and medial prefrontal network interact with a shared cortico-striatal-pallidal-thalamic loop via strong connections to the accumbens nucleus, medial caudate, and mediodorsal and paraventricular thalamic nuclei; this interaction may control and limit stress responses.

    “In addition, the amygdala and medial prefrontal network interact with the same cortico-striatal-pallidal-thalamic loop, through prominent connections both with the accumbens nucleus and medial caudate, and with the mediodorsal and paraventricular thalamic nuclei, which may function to control and limit responses to stress.”
  • The paper relies on this without support.

    The medial prefrontal network serves as a central node in the cortical default system, which seems to support self-referential functions like mood.

    “Finally, the medial prefrontal network is a central node in the cortical 'default system' that appears to support self-referential functions such as mood.”
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Citations

Cites

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Show all 379 references

4 of the 379 references couldn’t be matched to a known paper.

Research works printed but not linked: 7

  1. Drevets WC, Gautier C, Lowry T, Bogers W, Greer P, Kupfer DJ (2001). Abnormal hemodynamic responses to facially expressed emotion in major depression. Soc Neurosci Abstr 27: 785.1.
  2. Drevets WC, Ryan N, Bogers W, Birmaher B, Axelson D, Dahl R (2004b). Subgenual prefrontal cortex volume decreased in healthy humans at high familial risk for mood disorders. Soc Neurosci Abs 799: 18.
  3. Horovitz Z (1966). The amygdala and depression. In: Garattini S, Dukes M (eds). Antidepressant Drugs. Excerpta Medica: Amsterdam. pp 121–129.
  4. Krettek JE, Price JL (1977c). The connections of the amygdaloid complex and related olfactory cortical areas with the entorhinal cortex and the hippocampus. J Comp Neurol 172: 723–752. · DOI
  5. Martin-Soelch C, Szczepanik J, Fromm S, Barhaghi K, Wang H, Drevets W (2008). Catecholamine depletion Affects Amygdala Response to Reward: An fMRI-study. Program No. 520.10. Neuroscience Meeting Planner. Society for Neuroscience: Washington, DC (online).
  6. Miller B, Saleem KS, Price JL (2008). Cingulate Cortex Connections with Prefrontal Cortex Circuits in Monkeys. Program No. 465.11. Neuroscience Meeting Planner. Society for Neuroscience: Washington, DC (online).
  7. Öngür D, An X, Price JL (1998a). Prefrontal cortical projections to the hypothalamus in macaque monkeys. J Comp Neurol 401: 480–505. · DOI · Paper page

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Metadata

Authors
Price, J. L., & Drevets, W. C.
Affiliations
  • Washington University in St. Louis (US)
  • National Institutes of Health (US)
Corresponding author
Price, Joseph L
Venue
Neuropsychopharmacology
Published
2009-08-19
Volume
35
Issue
1
Pages
192-216
ISSN
  • 0893-133X (ISSN-L)
  • 1740-634X
OpenAlex
W2122384242
Cited by
1,606
References
379
Citations by year
2026: 50 · 2025: 75 · 2024: 71 · 2023: 57 · 2022: 89 · 2021: 122 · 2020: 102 · 2019: 110 · 2018: 83 · 2017: 101 · 2016: 105 · 2015: 119 · 2014: 127 · 2013: 124 · 2012: 113
FWCI
6.57
Type
journal article
Language
en
Open access
Locations
  • Neuropsychopharmacology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Public Health Service
  • National Institute of Mental Health (R01MH070941)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
mood disorders, neurocircuitry, limbic system, amygdala, medial prefrontal cortex, ventral striatum, globus pallidus, medial thalamus, hypothalamus, periaqueductal gray, brainstem, emotional behavior, history of emotion research, monkeys, human brain imaging
MeSH terms
Animals, Brain, Humans, Models, Neurological, Neural Pathways, Mood Disorders

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