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 accessAbstract
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
AI snapshot
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.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
36 of 262 cited sources checked · 11 supported · 1 flagged · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Conversely, lesions of the mPFC enhance behavioral, sympathetic, and endocrine responses to stressors or fearconditioned stimuli in rats (Morgan and LeDoux, 1995;Sullivan and Gratton, 1999).”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
What the sources say
- Not checked — no full text of the sourcecites Morgan and LeDoux, 1995 source
- Disputedcites Sullivan and Gratton, 1999 sourceExperimental — accuracy not yet measured
The Discussion reports that right or bilateral mPFC lesions suppressed corticosterone responses and reduced stress-ulcer pathology, contrary to the claimed enhancement of endocrine and autonomic responses. Left-sided lesions increased restraint-induced defecation, but that isolated finding does not support the broad claim; this study did not test fear-conditioned stimuli. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, lesions of the orbital cortex produce a deficit in the ability to use reward as a guide to behavior (Rudebeck and Murray, 2008)”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
What the sources say
- Partly supportedcites Rudebeck and Murray, 2008 sourceExperimental — accuracy not yet measured
The Discussion reports that monkeys with orbitofrontal cortex lesions were impaired at using reward information to guide subsequent choices. The claim omits an important limit: this deficit was observed after a reversal, while initial discrimination learning was unaffected. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and recent fMRI studies have shown that activity in the medial prefrontal cortex correlates with visceral activation in response to emotional (Critchley et al, 2000;Williams et al, 2000) or even non-emotional (Teves et al, 2004) stimuli.”
§ Neurocircuitry of Mood Disorders > CORTICAL PROJECTIONS TO HYPOTHALAMUS AND BRAINSTEM
What the sources say
- Not checked — no full text of the sourcecites Critchley et al, 2000 source
- Not checked — no full text of the sourcecites Williams et al, 2000 source
- Partly supportedcites Teves et al, 2004 sourceExperimental — accuracy not yet measured
The paper’s opening section reports medial prefrontal cortex activation during autonomic responses to hypoglycemia, without cognitive or emotional stress, supporting the non-emotional-stimulus portion attributed to Teves et al. But it explicitly says the study used positron emission tomography (PET), not fMRI. (LLM, conf=0.90)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Imaging studies show that a circuit including the medial prefrontal cortex and the periaqueductal gray area is activated by acute hypoglycemia (Teves et al, 2004)”
§ Neurocircuitry of Mood Disorders > Midline 'Intralaminar' Nuclei of Thalamus
What the sources say
- Partly supportedcites Teves et al, 2004 sourceExperimental — accuracy not yet measured
The Results report statistically significant activation of the medial prefrontal cortex during hypoglycemia. The Discussion reports evidence for periaqueductal gray activation, but says it did not meet the prespecified criteria for statistical significance. The claim omits that qualification for one component of the proposed circuit. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The striatal projection from the LPFC as a whole is directed to the central and dorsal part of the striatum (Calzavara et al, 2007).”
§ Neurocircuitry of Mood Disorders > Prefrontal Projections to the Striatum
What the sources say
- Supportedcites Calzavara et al, 2007 source
The Results (pages not provided) place the focal projections from areas 9 and 46 in central and dorsal regions of the caudate nucleus and describe their combined projections as occupying a large portion of the dorsocentral striatum at rostral levels. The paper also reports more widely distributed diffuse fibres, so the claim describes the main projection pattern rather than every terminal. (LLM, conf=0.86)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Many of the hypothalamic and brainstem inputs to the PVT utilize specific transmitters, including corticosteroid releasing hormone, orexin, serotonin, and norepinephrine (Hsu and Price, 2009).”
§ Neurocircuitry of Mood Disorders > Midline 'Intralaminar' Nuclei of Thalamus
What the sources say
- Supportedcites Hsu and Price, 2009 source
The Functional Considerations section says Pa receives inputs involving 5-HT, CRH, orexin, and norepinephrinergic fibers. The Discussion identifies hypothalamic orexin input and serotonin input from brainstem raphe nuclei. The paper calls CRH “corticotropin-releasing hormone,” rather than the citing sentence’s “corticosteroid releasing hormone.” (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
What the sources say
- Supportedcites Dewar et al, 2003 source
The Excitotoxicity section states that glutamate is toxic to oligodendrocytes through AMPA and kainate receptor activation and describes glutamate receptor overactivation as an important mechanism of their injury. The supplied passages do not give a page number. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Matute et al, 1997 source
- Not checked — no full text of the sourcecites McDonald et al, 1998 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
What the sources say
- Supportedcites Dewar et al, 2003 source
The Excitotoxicity section states that oligodendrocytes in adult rodent brain express AMPA/kainate receptor subunits. It also describes AMPA and kainate receptor expression in oligodendrocyte progenitor cells. Page numbers are not supplied in the excerpts. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Matute et al, 1997 source
- Not checked — no full text of the sourcecites McDonald et al, 1998 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Nevertheless, a longitudinal study also has shown progression of the abnormality in subjects with psychotic mood disorders (Koo et al, 2008).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Supportedcites Koo et al, 2008 source
The Comment’s Longitudinal Findings section states that gray matter volume deficits progressed in the subgenual cingulate in patients with first-episode affective psychosis compared with healthy controls. The Methods’ Participants section identifies this group as predominantly patients with bipolar disorder, supporting the reference to psychotic mood disorders. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Elevated glutamatergic transmission within discrete anatomical circuits also may explain the targeted nature of gray matter changes within mood disorders (eg, affecting left more than right sgACC) (McEwen and Magarinos, 2001;Drevets and Price, 2005a;Shansky et al, 2009).”
§ Neurocircuitry of Mood Disorders > Correlations with Rodent Models of Chronic and Repeated Stress
What the sources say
- Not checked — no full text of the sourcecites McEwen and Magarinos, 2001 source
- Not checked — no full text of the sourcecites Drevets and Price, 2005a source
- Partly supportedcites Shansky et al, 2009 sourceExperimental — accuracy not yet measured
The Abstract reports circuit-specific dendritic remodeling after stress in rats, and the Functional Implications section suggests that a spared pathway might receive increased input and become overstimulated (page numbers not supplied). The paper does not establish elevated glutamatergic transmission as the cause of targeted gray-matter changes in mood disorders, nor does it address left–right differences in the sgACC. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 46
- Probably not a substantial claim. 28
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The perigenual prefrontal cortex is also connected to both the same ventromedial part of the striatum (Haber et al, 1995;Ferry et al, 2000b), and the same region of MD (Russchen et al, 1987;Ray and Price, 1992).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Supportedcites Haber et al, 1995 source
Haber et al. is cited for the striatal connection, not the mediodorsal thalamic connection, which has separate citations. The Discussion reports that medial prefrontal areas 25 and 32 project to the medial ventral striatum, where orbitofrontal areas 13a and 13b also project. Page numbers are unavailable in our copy. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites Ferry et al, 2000b source
- Not checked — no full text of the sourcecites Russchen et al, 1987 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, many neurons appear to code for the presence or expectation of reward (Schultz et al, 1997), and for the relative value of stimuli (Padoa-Schioppa and Assad, 2006).”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
What the sources say
- Partly supportedcites Schultz et al, 1997 sourceExperimental — accuracy not yet measured
The citation to Schultz et al. is attached to the presence-or-expectation-of-reward clause, not the relative-value clause. In “Information Encoded in Dopaminergic Activity” (p. 2), the paper reports responses to unpredicted rewards and reward-predicting cues, but identifies the neurons as dopaminergic neurons of the VTA and substantia nigra, not orbital neurons. It also characterizes their signal more specifically as a reward-prediction error, rather than a general code for reward presence or expectation. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Padoa-Schioppa and Assad, 2006 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In addition to its role in control of saccadic eye movements, the caudal system may be part of the dorsal attention system (Corbetta et al, 2002).”
§ Neurocircuitry of Mood Disorders > Caudal Prefrontal System
What the sources say
- Could not verifycites Corbetta et al, 2002 sourceExperimental — accuracy not yet measured
The Conclusions (page unavailable) identify the intraparietal and superior frontal cortex as a dorsal attention network. The section on the dorsal frontal-parietal network also discusses the frontal eye field, but our copy does not identify a ‘caudal system’ or place one in that network. Searches for ‘caudal system’ and ‘caudal’ did not resolve that link. (LLM, conf=0.72)
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The extant data suggest this volumetric reduction exists early in illness and in young adults at high familial risk for MDD (Botteron et al, 2002;Hirayasu et al, 1999;Drevets et al, 2004b;Boes et al, 2008).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Not checked — no full text of the sourcecites Botteron et al, 2002 source
- Partly supportedcites Hirayasu et al, 1999 sourceExperimental — accuracy not yet measured
The Discussion reports reduced left subgenual cingulate volume at first hospitalization, supporting the early-illness part of the claim. The Method describes a young first-episode affective-disorder group, predominantly with bipolar disorder, and the comparison is based on family history of affective disorder—not specifically young adults at high familial risk for MDD. (LLM, conf=0.88)
- Not matchedcites Drevets et al, 2004b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“One study showed that the mean sgACC gray matter volume was reduced significantly vs controls in subjects with psychotic affective illness who also had mood-disordered first-degree relatives but not in subjects without mood-disordered first-degree relatives (Hirayasu et al, 1999).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Partly supportedcites Hirayasu et al, 1999 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It has also been reported that the left perigenulate ACC volume was smaller in boys with subclinical depressive symptoms, and that the negative correlation between left sgACC volume and depression symptoms was particularly robust in boys with a family history of depression (Boes et al, 2008).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Partly supportedcites Boes et al, 2008 sourceExperimental — accuracy not yet measured
The Results (Tables 2 and 3; page unavailable) show smaller left rostral ACC (rACC) volume in boys with depressive symptoms and a stronger negative correlation in boys with a positive nuclear family history of depression. The study measured rACC, which includes the subgenual region, but did not establish these findings specifically for left subgenual ACC or an isolated perigenual region. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The volumetric deficit applies to males (Hastings et al, 2004;Boes et al, 2008) and females (Botteron et al, 2002), to psychotic unipolar and bipolar depression (Hirayasu et al, 1999;Coryell et al, 2005;Adler et al, 2007), and to bipolar-spectrum illness (Haznedar et al, 2005).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Not checked — no full text of the sourcecites Hastings et al, 2004 source
- Supportedcites Boes et al, 2008 source
Boes et al. is cited for the male portion of the sentence, not for females or the specified diagnoses. The Results report significantly smaller rACC volume in boys with depressive symptoms than in boys without them. These were healthy children without a psychiatric diagnosis, so the finding should not be read as evidence about diagnosed depression. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites Botteron et al, 2002 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The burst-firing patterns increase DA release in the accumbens, which may encode information about reward prediction in monkeys (Schultz et al, 1997).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
- Partly supportedcites Schultz et al, 1997 sourceExperimental — accuracy not yet measured
The ‘Information Encoded in Dopaminergic Activity’ section (p. 2) says dopamine-neuron output in monkeys appears to encode errors in reward prediction. It identifies the nucleus accumbens as a target of these neurons, but does not establish that burst-firing increases dopamine release there or that release there carries the prediction signal. (LLM, conf=0.84)
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In spite of this the initial framework was adequate to indicate that the system included the hippocampus and amygdala, the anterior and medial thalamus, the cingulate gyrus, and related visceral control areas in the hypothalamus and brainstem.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Remarkably, although recording studies have indeed indicated that neurons in the orbital network areas respond to multi-modal stimuli (eg, the sight, flavor, and texture of food stimuli) the responses reflect affective as well as sensory qualities of the stimuli.”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Recently a projection from the amygdala has been identified to the posterior cingulate cortex (Buckwalter et al, 2008).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Buckwalter et al, 2008 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Subsequently, the hippocampus has been shown to be more involved in memory processing, and the amygdala to be more related to emotion (Zola- Morgan et al, 1991)”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Zola- Morgan et al, 1991 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These early studies identified the amygdala, hippocampus, and other parts of what was termed the 'limbic' system as central parts of the emotional brain.”
§ Neurocircuitry of Mood Disorders > Abstract
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Emotions are obviously linked to visceral function, and visceral reactions provide the means of emotional expression and possibly even the basis for the emotions themselves, as James W (1884) argued.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not matchedcites James W (1884)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As discussed in later parts of this chapter, these circuits form the core of the neural system that has been implicated in mood disorders.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
- Rests on an assumption: 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.
None of the sources cited for this claim have been checked yet.
In the paper
“Work by Gaskell, Langley, Cannon and others in the late nineteenth and early twentieth century established that many visceral functions are controlled by the autonomic nervous system, which is itself controlled and coordinated by the hypothalamus, the so-called 'head ganglion of the autonomic nervous system'.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“These striatal areas in turn project to the ventral and rostral pallidum, which itself sends GABAergic axons to the mediodorsal thalamic nucleus (MD, Russchen et al, 1987).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Russchen et al, 1987 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Papez and MacLean proposed that the 'Limbic System,' including the hippocampal formation, cingulate gyrus, and anterior thalamus, elaborates emotion and, through its interaction with the hypothalamus, is involved in emotional expression (Figure 1).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The orbital network therefore appears to function both as a system for integration of multi-modal stimuli, and as a system for assessment of the value of those stimuli.”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Observations on decorticate cats by Bard (1928) and others suggested that the hypothalamus was involved in the production of sham rage, and was responsible for the experience as well as the expression of emotion.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Bard (1928) source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Subsequently, however, many observations indicated that the structures in the cerebral hemispheres are responsible for the generation and experience of emotion, although the hypothalamus and other visceral control structures are responsible for many aspects of emotional expression.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As with the medial network, there are outputs from dorsal areas to the hypothalamus and PAG, so this system can also modulate visceral functions.”
§ Neurocircuitry of Mood Disorders > Dorsal Prefrontal System
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“To account for such deficits, Damasio and his colleagues have proposed the 'somatic marker hypothesis,' which supposes that the visceral or bodily reaction that normally accompanies emotion (the somatic marker) serves as a subconscious warning or guide, indicating some behaviors are disadvantageous and should be avoided (Damasio, 1994).”
§ Neurocircuitry of Mood Disorders > CORTICAL PROJECTIONS TO HYPOTHALAMUS AND BRAINSTEM
What the sources say
- Not checked — no full text of the sourcecites Damasio, 1994 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this case, however, the brainstem areas do not project directly to the cortex, so lateral MD serves as a relay of information to cortex, possibly as well as modulating thalamo-corticothalamic interactions.”
§ Neurocircuitry of Mood Disorders > Lateral Segment of Mediodorsal Thalamic Nucleus
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Although the organization of the thalamocortical interconnections are complex, the OMPFC is generally related to medial MD (MDm), whereas the LPFC is related to more lateral parts of MD (Ray and Price, 1993).”
§ Neurocircuitry of Mood Disorders > CORTICO-STRIATAL-THALAMIC CIRCUITS RELATED TO OMPFC
What the sources say
- Not checked — no full text of the sourcecites Ray and Price, 1993 source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is possible that this region represents a multi-modal cortex that also connected to circuits responsible for emotion.”
§ Neurocircuitry of Mood Disorders > Area 45a
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A similar deficit in subjects with mood disorders might be the difficulty of 'letting go' of a negative mood or mind-set long after the resolution of any traumatic events that might have justified it.”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: 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.
None of the sources cited for this claim have been checked yet.
In the paper
“Indeed, in most cases the projection to the cortex involves more neurons than that to MD, suggesting that the non-thalamic input to cortex carries more detailed information (Russchen et al, 1987;Carmichael et al, 1994;Price, 2003).”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
What the sources say
- Not checked — no full text of the sourcecites Russchen et al, 1987 source
- Not matchedcites Carmichael et al, 1994
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Price, 2003
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The prefrontal cortex as a whole is reciprocally connected to the mediodorsal thalamic nucleus (MD), with different prefrontal regions related to different portions of MD (Figure 6).”
§ Neurocircuitry of Mood Disorders > CORTICO-STRIATAL-THALAMIC CIRCUITS RELATED TO OMPFC
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The major difference with the orbital network is that there do not appear to be olfactory or taste inputs to the ventral system; it is possible that it functions in the assessment of non-food sensory objects.”
§ Neurocircuitry of Mood Disorders > Ventral Prefrontal System
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It can be suggested that these convergent but antagonistic inputs would interact to modulate the reciprocal thalamocortical interactions between the OMPFC and MDm.”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“For example, the medial network is primarily connected with the anterior and posterior parts of the cingulate cortex, whereas the orbital network connects primarily to the middle portion of the cingulate (Miller et al, 2008).”
§ Neurocircuitry of Mood Disorders > Medial Prefrontal Network
What the sources say
- Not matchedcites Miller et al, 2008
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the limbic inputs are dominant, ongoing patterns of thalamo-cortical and cortico-thalamic activity would be maintained, allowing for consistent behavior.When pallidal inputs become more prominent, ongoing patterns would be interrupted, allowing a switch from one behavior to another.”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“It consists of areas on the ventromedial surface of the frontal cortex, rostral and ventral to the genu, areas along the medial edge of the orbital cortex, and a small caudolateral orbital region at the rostral end of the insula (Carmichael and Price, 1996; Figure 3).”
§ Neurocircuitry of Mood Disorders > Medial Prefrontal Network
What the sources say
- Not checked — no full text of the sourcecites Carmichael and Price, 1996 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The ventral system of the LPFC consists of areas ventral to the principal sulcus, including area 46v, 12r, and 45b (area 45a is a special case, section 45a see below) (Figure 3).”
§ Neurocircuitry of Mood Disorders > Ventral Prefrontal System
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“There is some degree of organization within this system, such that the subgenual cortex provides the heaviest projection, which terminates in both the medial and lateral hypothalamus, and in both dorsolateral and ventrolateral columns of the PAG, while the fibers from the lateral part of the medical network (areas Iai, and 47/12s) are restricted to the lateral hypothalamus, and the ventrolateral P”
§ Neurocircuitry of Mood Disorders > CORTICAL PROJECTIONS TO HYPOTHALAMUS AND BRAINSTEM
What the sources say
- Not matchedcites O ¨ngu ¨r et al, 1998a, b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites An et al, 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This analysis has indicated that large parts of the LPFC are closely related to the medial and orbital prefrontal networks, and may have similar functional roles.”
§ Neurocircuitry of Mood Disorders > LATERAL PREFRONTAL CORTEX (LPFC)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As with the orbital network, the areas of the medial network are preferentially interconnected with each other, and the network is also characterized by outputs to visceral control areas in the hypothalamus and periaqueductal gray.”
§ Neurocircuitry of Mood Disorders > Medial Prefrontal Network
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The specific projections from the dorsal, ventral, and caudal parts of the LPFC that were described above have not been clearly defined.”
§ Neurocircuitry of Mood Disorders > Prefrontal Projections to the Striatum
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“They are specifically and reciprocally connected to the medial prefrontal network areas, with little connection to the orbital network.”
§ Neurocircuitry of Mood Disorders > Midline 'Intralaminar' Nuclei of Thalamus
What the sources say
- Not matchedcites Hsu andPrice, 2007, 2009
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The dorsal system is interconnected with the medial prefrontal network, and shares most of its other connections (Figure 5).”
§ Neurocircuitry of Mood Disorders > Dorsal Prefrontal System
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These studies have implicated subgenual PFC regions of the infralimbic cortex (BA 25) (eg, Coryell et al, 2005) and the adjacent sgACC corresponding to BA 24sg (eg, O ¨ngu ¨r et al, 1998a, b, 2003;Drevets et al, 1997a) (Figure 9).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because the amount of GFAP varies with the functional state of astrocytes, and GFAP staining often does not demonstrate all astrocytes, it is unclear whether these results indicate changes in astrocyte number or function.”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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)”
§ Neurocircuitry of Mood Disorders > Neuroimaging Abnormalities in Mood Disorders
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“elevated glucocorticoid concentrations and repeated stress decrease the proliferation of oligoden-drocyte precursors (Alonso, 2000;Banasr and Duman, 2007).”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
What the sources say
- Not checked yetcites Alonso, 2000
- Not checked — no full text of the sourcecites Banasr and Duman, 2007 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Notably, the short allele of the serotonin transporter promoter region length polymorphism (5HTT-PRL) has been identified as a genetic factor that is associated with both an increased vulnerability for developing MDD within the context of stress (Caspi et al, 2003) and a reduction in sgACC gray matter volume (Pezawas et al, 2005).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, the same domains are implicated in depression and mania, although the characteristic disturbance in emotional behavior within these syndromes appears opposite with respect to emotional valence.”
§ Neurocircuitry of Mood Disorders > Neuroimaging Abnormalities in Mood Disorders
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In BD, episodes of depression occur alternately with manic or hypomanic episodes during which the mood becomes euphoric and labile, the capacity for deriving pleasure increases, behaviors aimed at deriving pleasure increase, and energy psychomotor activity, libido, and self esteem become elevated.”
§ Neurocircuitry of Mood Disorders > Neuroimaging Abnormalities in Mood Disorders
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Extant neural models of depression posit that dysfunction within the medial network and related limbic structures underlie the disturbances in emotional behavior and other cognitive aspects of the major depressive syndrome.”
§ Neurocircuitry of Mood Disorders > RECENT OBSERVATIONS IN HUMANS WITH MOOD DISORDERS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The neuropathological changes evident in the mPFC and amygdala in mood disorders may impair their roles in modulating visceral responses to stressors and emotional stimuli.”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Rats exposed to fear-conditioned stimuli show reduced mPFC neuronal firing activity, the magnitude of which correlates inversely with the corresponding increase in amygdala neuron activity and fear behavior (Garcia et al, 1999).”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
What the sources say
- Not checked — no full text of the sourcecites Garcia et al, 1999 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Such reciprocal relationships between the medial prefrontal network and amygdala may be related to the observations that in MDD depression severity correlates positively with amygdala and sgACC activity, but negatively with activity in the left VLPFC/lateral OFC (approximately BA 45a and 47s) (Drevets et al, 2004a).”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
What the sources say
- Not matchedcites Drevets et al, 2004a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“The results from MRS studies of MDD show reductions in cerebral GABA levels and in the 'Glx' peak, which reflects the combined concentrations of glutamate plus glutamine, that appear compatible with the postmortem findings of cellular reductions.”
§ Neurocircuitry of Mood Disorders > Magnetic Resonance Spectroscopy (MRS) Imaging of Glutamate and GABA
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Dendritic atrophy presumably would be reflected by a decrease in the volume of the neuropil, which occupies most of the gray matter volume.”
§ Neurocircuitry of Mood Disorders > Correlations with Rodent Models of Chronic and Repeated Stress
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
- Rests on an assumption: Neuropil occupies most of the gray matter volume.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One neural model that could account for the neuroendocrine autonomic neurotransmitter attention and rewardseeking abnormalities associated with MDE suggests that impairment of medial prefrontal network and BLA function disinhibits the efferent transmission from the ACe and BNST to the hypothalamus and brainstem (Figure 10).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Severe depression is associated with hypersecretion of cortisol during the circadian nadir, pituitary and adrenal gland enlargement, and CSF-CRF levels that are increased to an extent that is inappropriate to the plasma cortisol concentrations”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If the neuropathological changes extant within the ACC in mood disorders interfere with the cortical drive on VTA-DA neuronal burst-firing activity, they may impair perception or learning of reward, and potentially interfere with behavioral engagement in pleasurable or positively reinforcing activities.”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The autonomic imbalance associated with depression also could reflect medial network dysfunction coupled with excessive amygdala activity.”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“although this has not been found in primates (An et al, 1998;Freedman et al, 2000), it may be expected that multisynaptic pathways would serve a similar function.”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
- Not matchedcites An et al, 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites Freedman et al, 2000
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, depressed subjects showed abnormal reductions in the CSF and jugular vein plasma levels of the DA metabolite homovanillic acid (Willner, 1995;Lambert et al, 2000), striatal DA transporter binding (Meyer et al, 2001), [ 11 C]L-DOPA uptake across the blood-brain barrier (A ˚gren et al, 1993), and striatal dopamine D 1 receptor binding (Cannon et al, 2009).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Preliminary reports indicate that chronic SSRI treatment or deep brain stimulation of the anterior capsule also reduces the abnormally elevated metabolism in the accumbens area in depression (Drevets et al, 2006) or in depression associated with obsessive-compulsive disorder (Van Laere et al, 2006)”
§ Neurocircuitry of Mood Disorders > Antidepressant Treatment Effects
What the sources say
- Not matchedcites Drevets et al, 2006
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Van Laere et al, 2006
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
In the paper
“The mesolimbic DA projections from the VTA to the nucleus accumbens shell and the mPFC thus have major roles in learning associations between operant behaviors, or sensory stimuli and reward, and in mediating the reinforcing properties of natural rewards such as food and sex (Nestler and Carlezon, 2006).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
- Not checked — no full text of the sourcecites Nestler and Carlezon, 2006 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“both deficits in negative feedback systems and excessive central stimulation of the secretion of CRF and/or other ACTH secretagogues are implicated in mood disorders (Gold and Chrousos, 2002;Drevets et al, 2004a;Swaab et al, 2005;Carroll et al, 2007).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Antidepressant therapies may compensate for this dysfunction by modulating the pathological limbic activity that putatively mediates depressive symptoms (Drevets et al, 2002a), or by enhancing the expression of neurotrophic factors that protect medial network function from the effects of repeated stress (Manji et al, 2001).”
§ Neurocircuitry of Mood Disorders > FUTURE DIRECTIONS
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
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.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Brain-imaging studies of depressed patients provide strong and consistent evidence of decreased volume of cortical and limbic brain regions— such as the prefrontal cortex (PFC) and the hippocampus—that control emotion, mood, and cognition, suggestive of neuronal atrophy that is related to length of illness and time of treatment (8, 9).”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [9]
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
“Two independent seed ROIs placed in the pregenual anterior cingulate cortex (pgACC) and the dorsal anterior cingulated cortex (dACC) were chosen based on previous reports on their involvement in meditation and affective disorders such as depression [55].”
From State and training effects of mindfulness meditation on brain networks reflect neuronal mechanisms of its antidepressant effect (2016) · cites this paper as [55]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Both these accounts of depression are supported by the involvement of agranular visceromotor cortices in the pathophysiology of depression (e.g. [89]).”
From Active interoceptive inference and the emotional brain (2016) · cites this paper as [89]
The cited source says what the claim attributes to it.
In the citing paper
“Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas.”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“Research on mood disorder pathophysiology has implicated abnormalities in glutamatergic transmission, along with disrupted function and structure in neural circuits involved in mood regulation (4), findings that led to further investigation of glutamatergic N-methyl-D-aspartate (NMDA) receptor modulators in treating depression (5,6).”
In the citing paper
“Similar reductions have been found in proteins such as CREB and its upstream effectors ERK and PKC172-174.”
From Dysregulation of adult hippocampal neuroplasticity in major depression: Pathogenesis and therapeutic implications (2022) · cites this paper as [174]
In the citing paper
“It has been proposed that major depressive symptoms are associated with the dysregulation of a distributed neuronal network encompassing cortical and limbic regions rather than with the (functional) breakdown of a single discrete brain region (Mayberg, 1997(Mayberg, , 2003;;Davidson et al., 2002;Drevets, 2003;Phillips et al., 2003;Seminowicz et al., 2004;Drevets et al., 2008;Price and Drevets, 201”
From Identifying major depression using whole-brain functional connectivity: a multivariate pattern analysis (2012) · cites this paper as Price and Drevets, 2010
In the citing paper
“These vmPFC-subcortical pathways are thought to constitute a ‘visceromotor’ system whose functions are to coordinate several aspects of autonomic activity [11].”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“However, the major subdivisions of the vmPFC are interconnected with each other and with subcortical nuclei in several interlocked functional systems [11], prompting a number of researchers to characterize the region’s broad functional roles with terms such as ‘affect’ [14], ‘regulation’ [3], ‘valuation’ [7,15], ‘self-projection’ [5], ‘self-reference’ [8], ‘mentalizing’ [9], ‘somatic markers’ [16]”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“Conversely, dysfunction of the vmPFC is thought to be critical in a number of brain disorders, most notably post-traumatic stress disorder (PTSD) [10], depression [11] and dysregulation related to chronic stress [12] and pain [13].”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“The vmPFC is also directly connected with memory-related circuits in hippocampus and medial temporal lobe [11] that can subserve both memory and future projection[5].”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“What is suggested is that a potential mechanism of action of rTMS to dmPFC is increased influence of cognitive control networks over thalamic and striatal regions, possibly linked with improved facilitation of goal-directed behavior (Corbetta and Shulman, 2002; Price and Drevets, 2010; Sheline et al, 2010).”
From Resting-state cortico-thalamic-striatal connectivity predicts response to dorsomedial prefrontal rTMS in major depressive disorder (2014) · cites this paper as Price and Drevets, 2010
In the citing paper
“an area that also has strong projections to medial prefrontal cortical regions associated with the regulation of emotions and visceral reactions (Price and Drevets, 2010).”
From Phasic and sustained fear in humans elicits distinct patterns of brain activity (2011) · cites this paper as Price and Drevets, 2010
In the citing paper
“Subgenual anterior cingulate cortex (sACC) is central to the medial prefrontal network that has been associated with mood and anxiety dysregulation, and has been implicated in the regulation of visceral responses during stress and anxiety (Price and Drevets, 2010).”
From Phasic and sustained fear in humans elicits distinct patterns of brain activity (2011) · cites this paper as Price and Drevets, 2010
In the citing paper
“Numerous studies suggest that depression and anxiety in humans result in part from hypo–activation and reduced volume of frontal cortical and hipppocampal regions that control subcortical structures such as nucleus accumbens (NAc) and amygdala, although hyper–activation of certain PFC regions (e.g., subgenual area of anterior cingulate cortex) is also involved58–61.”
From Neurobiology of resilience (2012) · cites this paper as [58]
In the citing paper
“The amygdala has strong, bidirectional connections to medial prefrontal regions along the anterior cingulate cortex surrounding the corpus callosum, extending from ventral regions (subgenual cingulate cortex) to rostral (pregenual cingulate) and dorsal (supragenual cingulate) regions (Fig. 2).”
From Neural Substrates of Childhood Anxiety Disorders (2012) · cites this paper as [36]
In the citing paper
“Among these findings, abnormal activity in the ventromedial prefrontal cortex (vmPFC) is probably the most widely reported (1–4).”
From Functional anatomy of ventromedial prefrontal cortex: implications for mood and anxiety disorders (2012) · cites this paper as [4]
In the citing paper
“IL/25 projects directly to a number of autonomic regions which have been found to enhance sympathetic activity, including the perifornical area, dorsomedial hypothalamus, dorsolateral periaqueductal gray, lateral parabrachial nucleus, cuneiform nucleus, and lateral septum, among other regions (4, 33, 35–37, 39, 47, 82, 97, 98).”
From Functional anatomy of ventromedial prefrontal cortex: implications for mood and anxiety disorders (2012) · cites this paper as [4]
In the citing paper
“of the mPFC as a modulatory region interconnected with limbic structures8 and involved in emotion regulation.9”
From Altered resting-state amygdala functional connectivity in men with posttraumatic stress disorder (2012) · cites this paper as [8]
In the citing paper
“Studies utilizing brain-imaging methods have shown that cortical and limbic region atrophy, including decreased volumes in the prefrontal cortex (PFC) and hippocampus, is associated with the duration of illness and treatment.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [9]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Two 1978 references start on the same journal page
MinorThe two differently titled papers are both listed as beginning on page 225 of volume 178 of the same journal, although their stated ending pages differ.
“142. Krettek JE, Price JL (1978a). Amygdaloid projections to subcortical structures within the basal forebrain and brainstem in the rat and cat. J Comp Neurol 178: 225-254.”
“143. Krettek JE, Price JL (1978b). A description of the amygdaloid complex in the rat and cat with observations on intra-amygdaloid axonal connections. J Comp Neurol 178: 225-280.”
Two 1977 references have identical journal pages
MinorThe bibliography assigns the same journal, volume, and complete page range to two differently titled papers by the same authors.
“145. Krettek JE, Price JL (1977b). An autoradiographic study of projections from the amygdaloid complex to the thalamus and cerebral cortex. J Comp Neurol 172: 723-752.”
“146. 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.”
Citations
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Research works printed but not linked: 7
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Items 601–700 of 1,608
Opel, N., Zwanzger, P., Redlich, R., Grotegerd, D., Dohm, K., Arolt, V., Heindel, W. L., Kugel, H., & Dannlowski, U. (2015) · Psychological Medicine · doi:10.1017/s0033291715001683 · Cited by 47
“…are apparent in subjects at high familial risk but also in subjects exposed to early environmental stress (Drevets et al. 1997; Baaré et al. 2010; Price & Drevets, 2010; Rao et al. 2010; Amico et al. 2011; Dannlowski et al. 2012; Chaney et al. 2014; Dager et al. 2015; Hibar et al. 2015; Knowles…”
BackgroundResultAnatomical brain difference of subthreshold depression in young and middle-aged individuals
Li, J., Wang, Z., Hwang, J., Zhao, B., Yang, X., Xin, S., Wang, Y., Jiang, H., Shi, P., Zhang, Y., et al. (2017) · NeuroImage Clinical · doi:10.1016/j.nicl.2017.02.022 · Cited by 48
“It is involved in the mediating of motivation, emotional drive, and planning of goal-directed behavior (Haber and Calzavara, 2009; Taber et al., 2004) and is regarded as one of the centrally disrupted regions in mood disorders (Li et al., 2014; Price and Drevets, 2010).”
BackgroundMethodInfluentialJiang, X., Dai, X., Edmiston, E. K., Zhou, Q., Xu, K., Zhou, Y., Wu, F., Kong, L., Wei, S., Zhou, Y., et al. (2017) · Journal of Affective Disorders · doi:10.1016/j.jad.2017.05.025 · Cited by 47
Structural and resting state functional connectivity beyond the cortex
Harrison, O. K., Guell, X., Klein-Flügge, M. C., & Barry, R. L. (2021) · NeuroImage · doi:10.1016/j.neuroimage.2021.118379 · Cited by 47
“Amygdala connections become weaker n more anterior dysgranular and granular OFC and MFC regions Aggleton et al., 2015 ; Amaral et al., 1992 ; Ghashghaei et al., 2007 ; rice and Drevets, 2010 ).”
BackgroundDevelopmental Risk I: Depression and the Developing Brain
Weir, J. M., Zakama, A. K., & Rao, U. (2012) · Child and Adolescent Psychiatric Clinics of North America · doi:10.1016/j.chc.2012.01.004 · Cited by 54
“These mental processes are inextricably linked and represented in dynamic neural networks composed of interconnected prefrontal and limbic brain structures.(48,49,51) During dolescence, social relationships take on a new importance and adolescents become dept at reading social and emotional cues and modulating their a…”
BackgroundHoman, P., Neumeister, A., Nugent, A. C., Charney, D. S., Drevets, W. C., & Hasler, G. (2015) · Translational Psychiatry · doi:10.1038/tp.2015.25 · Cited by 46
Self-citationBenson, B. E., Willis, M. W., Ketter, T. A., Speer, A., Kimbrell, T. A., Herscovitch, P., George, M. S., & Post, R. M. (2014) · Journal of Affective Disorders · doi:10.1016/j.jad.2014.05.045 · Cited by 47
“Amygdalar and hippocampal dysfunction is thought to play a major role in these symptoms, often figuring predominately in models of affective disorders (Krishnan and Nestler, 2010; Price and Drevets, 2010; Strakowski et al., 2005).”
BackgroundBlossom, V., Ullal, S. D., D’Souza, M. M., Ranade, A. V., Kumar, N. A., & Rai, R. (2025) · 3 Biotech · doi:10.1007/s13205-025-04468-2 · Cited by 57
“Both human and animal studies, as shown in Tables 2, 3 & 4, have demonstrated solid involvement of the medial prefrontal cortex (mPFC), ventral hippocampus, and amygdala in the development of anxiety, depression, and associated behavioural regulation (Russo and Nestler 2013; Price and Drevets 2010).”
Cortico-limbic network abnormalities in individuals with current and past major depressive disorder
Klauser, P., Fornito, A., Lorenzetti, V., Davey, C. G., Dwyer, D., Allen, N. B., & Yücel, M. (2014) · Journal of Affective Disorders · doi:10.1016/j.jad.2014.10.041 · Cited by 49
“This medial prefrontal network encompasses the medial part of the orbito-frontal cortex, also known as ventromedial prefrontal cortex (vmPFC), and can also be extended to limbic structures as well as to basal ganglia and thalamus to form an extended medial prefrontal network (Price and Drevets, 2010).”
BackgroundHippocampal subfields differentially correlate with chronic pain in older adults
Ezzati, A., Zimmerman, M. E., Katz, M. J., Sundermann, E. E., Smith, J. L., Lipton, M. L., & Lipton, R. B. (2014) · Brain Research · doi:10.1016/j.brainres.2014.05.025 · Cited by 45
“P A A uthor M anuscript The hippocampus plays an important role in a variety of physiological processes including memory, mood and stress (Price and Drevets, 2010; Zimmerman et al., 2008).”
BackgroundDepressive Symptoms and Mild Cognitive Impairment in the Elderly: An Ominous Combination
Steffens, D. C. (2012) · Biological Psychiatry · doi:10.1016/j.biopsych.2012.02.002 · Cited by 46
“(7), which focuses on dorsal and ventral ystems, and is also informed by more recent work by Price and revets (8).”
Li, P., Hsiao, I., Liu, C.-Y., Chen, C., Huang, S., Yen, T., Wu, K.-Y., & Lin, K. (2017) · EJNMMI Research · doi:10.1186/s13550-017-0273-4 · Cited by 48
“connect with the prefrontal network known to be related to depressive disorder [31].”
BackgroundLiu, C., Pu, W., Wu, G., Zhao, J., & Xue, Z. (2019) · BMC Neuroscience · doi:10.1186/s12868-019-0508-6 · Cited by 48
“Taken together, these evidence suggest that the neuropathology of depression involves dysfunctions within a neuroanatomical circuit including the frontal cortex and limbic structures [23, 24], but the specific pattern of neural changes are different between unipolar and bipolar depression in this circuit.”
BackgroundTozzi, L., Staveland, B. R., Holt-Gosselin, B., Chesnut, M., Chang, S. E., Choi, D., Shiner, M., Wu, H., Lerma‐Usabiaga, G., Sporns, O., et al. (2020) · NeuroImage · doi:10.1016/j.neuroimage.2020.116715 · Cited by 48
“Altered activation and connectivity of these regions has been consistently observed across multiple diagnostic categories of disordered emotional states, including depression, generalized anxiety, social phobia, specific phobia, and panic (Fonzo et al., 2015; Jaworska et al., 2015; Killgore et al., 2014; Phillips et a…”
Causal Interactions in Human Amygdala Cortical Networks across the Lifespan
Jiang, Y., Tian, Y., & Wang, Z. (2019) · Scientific Reports · doi:10.1038/s41598-019-42361-0 · Cited by 45
Multi-Level Processes and Retina–Brain Pathways of Photic Regulation of Mood
Maruani, J., & Geoffroy, P. A. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11020448 · Cited by 52
Ji, C., Patil, K. R., Yeo, B. T. T., & Eickhoff, S. B. (2022) · Biological Psychiatry · doi:10.1016/j.biopsych.2022.07.025 · Cited by 43
Zhang, C. H., Sha, Z., Mundahl, J., Liu, S., Lu, Y., Henry, T. R., & He, B. (2015) · NeuroImage Clinical · doi:10.1016/j.nicl.2015.07.014 · Cited by 45
“In fact, the specific cortical projections of mediodorsal nucleus to the frontal cortex has long been reported in rodents andmonkeys (Krettek and Price, 1977; Leonard, 1969; Price and Drevets, 2010).”
InfluentialHyde, L. W. (2015) · Development and Psychopathology · doi:10.1017/s0954579415000188 · Cited by 48
“Similarly, elevated amygdala reactivity to threat has been correlated with internalizing outcomes (Price & Drevets, 2010), whereas low amygdala reactivity has been correlated with psychopathy (Blair, 2013).”
BackgroundInfluentialAltered directed functional connectivity of the right amygdala in depression: high-density EEG study
Damborská, A., Honzírková, E., Barteček, R., Hořínková, J., Fedorová, S., Ondruš, Š., Michel, C. M., & Rubega, M. (2020) · Scientific Reports · doi:10.1038/s41598-020-61264-z · Cited by 48
Corticolimbic connectivity as a possible biomarker for bipolar disorder
Vai, B., Bollettini, I., & Benedetti, F. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2014.915744 · Cited by 44
“Compromised WM integrity in cortical and subcortical structures of the anterior limbic network [62] and anterior prefrontal network [107] is consistent with the concept of disrupted neurocircuitry involved in impulse control and emotional regulation, which are core features of BD (see a comprehensive review in [108]).”
BackgroundClinical and Neurobiological Perspectives of Empowering Pediatric Cancer Patients Using Videogames
Govender, M., Bowen, R. C., German, M. L., Bulaj, G. W., & Bruggers, C. S. (2015) · Games for Health Journal · doi:10.1089/g4h.2015.0014 · Cited by 50
Kappa Opioids, Salvinorin A and Major Depressive Disorder
Taylor, G. T., & Manzella, F. M. (2016) · Current Neuropharmacology · doi:10.2174/1570159x13666150727220944 · Cited by 44
“The caudate nucleus and putamen that comprise the striatum are involved in motor movement as well as mood [59].”
BackgroundHippocampal Volume as an Amplifier of the Effect of Social Context on Adolescent Depression
Schriber, R. A., Anbari, Z., Robins, R. W., Conger, R. D., Hastings, P. D., & Guyer, A. E. (2017) · Clinical Psychological Science · doi:10.1177/2167702617699277 · Cited by 46
“…to such self-reflective and often social acts as self-projection (Spreng et al., 2008) and rumination (Mandell et al., 2014), including via connectivity of the hippocampus within the default mode network (Greicius, Supekar, Menon, & Dougherty, 2009; Price & Drevets, 2009; Sambataro et al., 2014).”
BackgroundA multiscale cerebral neurochemical connectome of the rat brain
Noori, H. R., Schöttler, J., Ercsey-Ravasz, M., Cosa‐Linan, A., Varga, M., Toroczkai, Z., & Spanagel, R. (2017) · PLoS Biology · doi:10.1371/journal.pbio.2002612 · Cited by 46
Witkin, J. M., Knutson, D. E., Rodriguez, G. J., & Shi, S. X.-Y. (2018) · Current Pharmaceutical Design · doi:10.2174/1381612824666180730104707 · Cited by 45
Rakesh, D., Allen, N. B., & Whittle, S. (2020) · Developmental Cognitive Neuroscience · doi:10.1016/j.dcn.2020.100775 · Cited by 44
“…circuits underlying emotion regulation (which could be related to the genetic and environment factors outlined above) may represent a common risk mechanism for both depressive and substance use disorders (Bonelli and Cummings, 2007; Kober, 2014; Koob and Volkow, 2009; Price and Drevets, 2009).”
Dournes, C., Beeské, S., Belzung, C., & Griebel, G. (2012) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2012.07.019 · Cited by 47
Osoba, A., Hänggi, J., Li, M., Horn, D. I., Metzger, C. D., Eckert, U., Kaufmann, J., Zierhut, K. C., Steiner, J. H., Schiltz, K., et al. (2013) · Journal of Affective Disorders · doi:10.1016/j.jad.2012.12.026 · Cited by 44
“One potential explanation would be that the observed change in functional connectivity is not paralleled by effects in direct connections but mediated by indirect routes (Price and Drevets, 2010).”
BackgroundGadea, M., Espert, R., Salvador, A., & Martí‐Bonmatí, L. (2011) · Brain and Cognition · doi:10.1016/j.bandc.2011.03.003 · Cited by 42
“The emotional network also includes as a central key some cortical areas (e.g. prefrontal cortex, parietal cortex ) linked to emotional processing, with the connection of both the subcortical and cortical systems being object of an actual and extensive research (Price & Drevets, 2010).”
Witkin, J. M., Mitchell, S. N., Wafford, K. A., Carter, G., Gilmour, G., Li, J., Eastwood, B. J., Overshiner, C. D., Li, X., Rorick‐Kehn, L. M., et al. (2017) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.116.238121 · Cited by 42
“, 2016a), a brain area known to regulate hedonic valuation and regulate a neurotransmitter system well characterized for its control of mood (Price and Drevets, 2010).”
BackgroundFrom symptoms of psychopathology to the explanation of clinical phenomena
Ward, T. J., & Clack, S. (2019) · New Ideas in Psychology · doi:10.1016/j.newideapsych.2019.01.004 · Cited by 43
Neurons in the monkey orbitofrontal cortex mediate reward value computation and decision-making
Setogawa, T., Mizuhiki, T., Matsumoto, N., Akizawa, F., Kuboki, R., Richmond, B. J., & Shidara, M. (2019) · Communications Biology · doi:10.1038/s42003-019-0363-0 · Cited by 41
Duan, G., He, Q., Pang, Y., Chen, W., Liao, H., Liu, H., Tan, L., Liu, Y., Tao, J., Zhang, J., et al. (2019) · Brain Imaging and Behavior · doi:10.1007/s11682-019-00178-5 · Cited by 43
Moral Motivation and the Basal Forebrain
Zahn, R., de Oliveira‐Souza, R., & Moll, J. (2019) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2019.10.022 · Cited by 45
Human amygdala compared to orbitofrontal cortex connectivity, and emotion
Rolls, E. T., Deco, G., Huang, C., & Feng, J. (2022) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2022.102385 · Cited by 44
“In non-human primates, connections are found between the amygdala and the medial orbitofrontal cortex (including pOFC), both directly and via the mediodorsal nucleus of the thalamus pars magnocellularis (Freese and Amaral, 2009; Price and Drevets, 2010; Timbie et al., 2020).”
Huang, X., Huang, P., Li, D., Zhang, Y., Wang, T., Mu, J., Li, Q., & Xie, P. (2014) · International Journal of Psychophysiology · doi:10.1016/j.ijpsycho.2014.10.011 · Cited by 43
Pudhiyidath, A., Morton, N. W., Duran, R. V., Schapiro, A. C., Momennejad, I., Hinojosa-Rowland, D. M., Molitor, R. J., & Preston, A. R. (2022) · Journal of Cognitive Neuroscience · doi:10.1162/jocn_a_01864 · Cited by 46
“An mPFC ROI was manually drawn on the MNI ICBM 152 Non-Linear 6th Generation Asymmetric (MNI152NLin6Asym) template based on published definitions of anatomical mPFC (Price & Drevets, 2009; Öngür, Ferry, & Price, 2003).”
Philp, D. J., Korgaonkar, M. S., & Grieve, S. M. (2014) · NeuroImage · doi:10.1016/j.neuroimage.2013.12.057 · Cited by 44
“, 2012), and cognitive theories (Price and Drevets, 2010) both involve the thalamus as part of the dysfunctional circuit.”
BackgroundSensorimotor Modulation of Mood and Depression: In Search of an Optimal Mode of Stimulation
Canbeyli, R. (2013) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2013.00428 · Cited by 42
“In addition to the evidence presented in Section “Neuroanatomical Basis of Sensorimotor Stimulation” above, a multitude of studies provide support for amygdalar involvement in the cortical and cognitive factors involved in regulation of mood (Price and Drevets, 2010).”
BackgroundNugent, A. C., Robinson, S. E., Coppola, R., & Zarate, C. A. (2016) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2016.06.006 · Cited by 42
“Similar to the sgACC findings, abnormalities in the structure and function of the amygdala have been documented extensively in individuals with MDD (Price and Drevets, 2010).”
Depressive disorders: Processes leading to neurogeneration and potential novel treatments
Brown, G. M., McIntyre, R. S., Rosenblat, J. D., & Hardeland, R. (2017) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2017.04.023 · Cited by 44
“Evidence implicates that they form part of a functional circuit for emotions in humans; hence it is theorized that these changes result in abnormal functioning in MDD(Delvecchio et al., 2012; Price and Drevets, 2010).”
BackgroundSönmez, İ., Köşger, F., & Aykan, Ü. (2015) · Nöro Psikiyatri Arşivi · doi:10.5152/npa.2015.10115 · Cited by 45
“In vivo structural and functional imaging studies, as well as postmortem investigations of adults, suggest that the frontal-striatal-thalamic and limbic-thalamic-frontal neural circuits have an important role in the pathogenesis of depression (2).”
BackgroundEngaging homeostatic plasticity to treat depression
Workman, E. R., Niere, F., & Raab‐Graham, K. F. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.225 · Cited by 43
Cortico-limbic connectivity as a possible biomarker for bipolar disorder: where are we now?
Vai, B., Bertocchi, C., & Benedetti, F. (2019) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2019.1562338 · Cited by 41
“tional regulation, which are core features of BD [65].”
BackgroundJiang, N., Xu, J., Li, X., Wang, Y., Zhuang, L., & Qin, S. (2020) · Biological Psychiatry · doi:10.1016/j.biopsych.2020.08.002 · Cited by 41
“Dysconnectivity of the amygdala and prefrontal circ uitry has been consistently reported among individuals with depression and anxi ety symptoms (31, 32).”
BackgroundHuang, J., Shen, C., Ye, R., Shi, Y., & Li, W. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2021.539299 · Cited by 42
Olesen, P. J., Gustafson, D. R., Simoni, M., Pantoni, L., Östling, S., Guo, X., & Skoog, I. (2010) · Neuropsychopharmacology · doi:10.1038/npp.2010.176 · Cited by 42
Stan, A. D., Schirda, C. V., Bertocci, M. A., Bebko, G. M., Kronhaus, D. M., Aslam, H. A., LaBarbara, E. J., Tanase, C., Lockovich, J. C., Pollock, M. H., et al. (2014) · Psychiatry Research: Neuroimaging · doi:10.1016/j.pscychresns.2014.05.016 · Cited by 35
“…of the ACC1/subgenual cingulate cortex localization is consistent with the robust human literature documenting processing of negative emotions in the subgenual anterior cingulate cortex (Kross et al., 2009; Liotti et al., 2000; Mayberg et al., 1999; Price and Drevets, 2010; Smith et al., 2011).”
BackgroundIntermediate phenotypes and biomarkers of treatment outcome in major depressive disorder
Leuchter, A. F., Hunter, A. M., Krantz, D. E., & Cook, I. A. (2014) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2014.16.4/aleuchter · Cited by 42
Wang, T., Huang, X., Huang, P., Li, D., Lv, F., Zhang, Y., Zhou, L., Yang, D., & Xie, P. (2013) · PLoS ONE · doi:10.1371/journal.pone.0063081 · Cited by 40
“The mPFC network is connected to the medial thalamus, and this system is involved in modulating visceral function in animal models and human mood disorders [42].”
BackgroundStructural covariance of the neostriatum with regional gray matter volumes
Soriano‐Mas, C., Harrison, B. J., Pujol, J., López‐Solà, M., Hernández‐Ribas, R., Alonso, P., Contreras‐Rodríguez, O., Giménez, M., Blanco‐Hinojo, L., Ortiz, H., et al. (2012) · Brain Structure and Function · doi:10.1007/s00429-012-0422-5 · Cited by 43
“, anterior insular cortex/frontal operculum) of the ventral-lateral prefrontal system (Price and Drevets 2010).”
BackgroundResultVictor, T. A., Furey, M. L., Fromm, S. J., Bellgowan, P. S. F., Öhman, A., & Drevets, W. C. (2012) · PLoS ONE · doi:10.1371/journal.pone.0046439 · Cited by 43
“In contrast, the regions that showed hemodynamic responses that were opposite in direction to those seen in the amygdala, namely the left pregenual anterior cingulate cortex, left anterior OFC (BA 10o) and bilateral areas of the rSTG form part of the extended medial prefrontal, or ‘‘visceromotor’’, network [21,49].”
BackgroundResultSelf-citationWesley, M. J., Lile, J. A., Hanlon, C. A., & Porrino, L. J. (2015) · Psychopharmacology · doi:10.1007/s00213-015-4180-y · Cited by 44
“*p < 0.05 ventral striatum, and amygdala, where more somatic and limbic-based affective signals may arise (Drevets et al. 2008; Price and Drevets 2010).”
InfluentialKhalid, A., Kim, B. S., Seo, B. A., Lee, S., Jung, K., Chu, K., Lee, S. K., & Jeon, D. (2016) · BMC Neuroscience · doi:10.1186/s12868-016-0239-x · Cited by 41
Klimes‐Dougan, B., Eberly, L. E., Schreiner, M. W., Kurkiewicz, P., Houri, A. K., Schlesinger, A., Thomas, K. M., Mueller, B. A., Lim, K. O., & Cullen, K. R. (2014) · Development and Psychopathology · doi:10.1017/s0954579414001059 · Cited by 43
“1321 There are several existing models that highlight the challenges of threat processing for those struggling with depression (Drevets, 1999; Ghashghaei & Barbas, 2002; Mayberg, 1997; Nestler et al., 2002; Phillips, Drevets, Rauch, & Lane 2003; Price & Drevets, 2010).”
BackgroundYu, H., Chen, L., Li, H., Xin, H., Zhang, J., Wei, Z., & Peng, D. (2019) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s191441 · Cited by 42
Depressive symptom severity is associated with increased cortical thickness in older adults
Szymkowicz, S. M., McLaren, M. E., Kirton, J. W., O’Shea, A. M., Woods, A. J., Manini, T. M., Anton, S. D., & Dotson, V. M. (2015) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.4324 · Cited by 44
Neonatal amygdala lesions alter responsiveness to objects in juvenile macaques
Bliss-Moreau, E., Toscano, J. E., Bauman, M. D., Mason, W. A., & Amaral, D. G. (2011) · Neuroscience · doi:10.1016/j.neuroscience.2010.12.038 · Cited by 40
“Research in both humans and nonhuman animals attests to the amygdala’s broad role in emotion (for reviews: LeDoux, 000; Phelps, 2006; Murray, 2007; Seymour and Dolan, 008; Pessoa and Adolphs, 2010; Price and Drevets, 2010; alzman and Fusi, 2010).”
BackgroundMenculini, G., Chipi, E., Paoletti, F. P., Gaetani, L., Nigro, P., Simoni, S., Mancini, A., Tambasco, N., Filippo, M. D., Tortorella, A. A. V., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22094440 · Cited by 44
Keller, M., Mendoza-Quiñones, R., Muñoz, A. C., Iglesias-Fuster, J., Virués, A. V., Zvyagintsev, M., Edgar, J., Zweerings, J., & Mathiak, K. (2021) · BMC Psychiatry · doi:10.1186/s12888-022-03780-y · Cited by 36
Lipsman, N., Mendelsohn, D. A., Taira, T., et al. (2011) · Stereotactic and Functional Neurosurgery · doi:10.1159/000323545 · Cited by 40
“DBS and functional neuroimaging offer opportunities to probe the mechanisms of aberrant circuitry that underlie much of abnormal human behaviour [8].”
BackgroundStubberud, J., Langenbahn, D. M., Levine, B., Stanghelle, J. K., & Schanke, A. (2014) · Rehabilitation Psychology · doi:10.1037/rep0000018 · Cited by 40
Clinical neuroprediction: Amygdala reactivity predicts depressive symptoms 2 years later
Mattson, W. I., Hyde, L. W., Shaw, D. S., Forbes, E. E., & Monk, C. S. (2016) · Social Cognitive and Affective Neuroscience · doi:10.1093/scan/nsw018 · Cited by 40
Samara, Z., Evers, E. A. T., Peeters, F., Uylings, H. B. M., Rajkowska, G., Ramaekers, J. G., & Stiers, P. (2018) · Biological Psychiatry: Cognitive Neuroscience and Neuroimaging · doi:10.1016/j.bpsc.2018.01.004 · Cited by 40
Poletti, S., Melloni, E. M. T., Aggio, V., Colombo, C., Valtorta, F., Benedetti, F., & Comai, S. (2019) · Journal of Affective Disorders · doi:10.1016/j.jad.2019.08.034 · Cited by 38
Lama, A., Pirozzi, C., Annunziata, C., Morgese, M. G., Senzacqua, M., Severi, I., Calignano, A., Trabace, L., Giordano, A., Meli, R., et al. (2020) · British Journal of Pharmacology · doi:10.1111/bph.15071 · Cited by 45
Executive functioning and psychological adjustment in children and youth with spina bifida
Kelly, N. C., Ammerman, R. T., Rausch, J. R., Ris, M. D., Yeates, K. O., Oppenheimer, S. G., & Enrile, B. G. (2011) · Child Neuropsychology · doi:10.1080/09297049.2011.613814 · Cited by 42
“Functional and structural imaging work suggests that these systems are implicated in mood disorders (Price & Drevets, 2010).”
BackgroundBordukalo-Nikšić, T., Mokrović, G., Štefulj, J., Živin, M., Jernej, B., & Čičin‐Šain, L. (2010) · Behavioural Brain Research · doi:10.1016/j.bbr.2010.05.002 · Cited by 41
Sugama, S., Takenouchi, T., Sekiyama, K., Kitani, H., & Hashimoto, M. (2011) · Neuroscience · doi:10.1016/j.neuroscience.2011.06.051 · Cited by 40
Association of central serotonin transporter availability and body mass index in healthy Europeans
Hesse, S., van de Giessen, E., Zientek, F., et al. (2014) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2014.05.005 · Cited by 40
“Interestingly, this part of the thalamus is responsible for the control response to chronic stress mediated by the serotonergic system and consequently the expression of SERT may play a role (reviewed by Price and Drevets (2010)).”
BackgroundConway, C. R., Chibnall, J. T., Gangwani, S., Mintun, M. A., Price, J. L., Hershey, T. G., Giuffra, L. A., Bucholz, R. D., Christensen, J. J., & Sheline, Y. I. (2012) · Journal of Affective Disorders · doi:10.1016/j.jad.2012.02.007 · Cited by 41
“…VNS TRMD neuroimaging studies (Bohning et al., 2001; Conway et al., 2006, 2011; Kosel et al., 2011; Lomarev et al., 2002; Mu et al., 2004; Nahas et al., 2007; Pardo et al., 2008; Zobel et al., 2005), and are established regions in depression models (Mayberg, 1997b, 2003; Price and Drevets, 2010).”
BackgroundInfluentialSelf-citationLeWinn, K. Z., Strigo, I. A., Connolly, C. G., Ho, T. C., Tymofiyeva, O., Sacchet, M. D., Weng, H. Y., Blom, E. H., Simmons, A. N., & Yang, T. T. (2018) · Journal of Affective Disorders · doi:10.1016/j.jad.2018.07.020 · Cited by 38
“Studies of emotion processing in general suggest that depressed adults show alterations in corticolimbic circuitry and altered function in those cognitive control regions involved in top-down regulation of emotion, such as the dlPFC, as well as in limbic regions like the amygdala and insula which are associated with b…”
BackgroundResultHomer, B., Judd, J., Dehcheshmeh, M. M., Ebrahimie, E., & Trott, D. J. (2023) · Animals · doi:10.3390/ani13091458 · Cited by 39
“The hippocampus and prefrontal cortex are the main areas of the brain affected by most mood disorders such as anxiety [98,99].”
BackgroundZhao, K., Liu, H., Yan, R., Hua, L., Chen, Y., Shi, J., Yao, Z., & Lü, Q. (2016) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2016.12.001 · Cited by 39
The Hippocampus and Memory Integration: Building Knowledge to Navigate Future Decisions
Schlichting, M. L., & Preston, A. R. (2017) · Springer eBooks · doi:10.1007/978-3-319-50406-3_13 · Cited by 48
“Anatomical features of MPFC may make it especially well suited to form such complex representations of goals or task rules, as it receives a broad range of input from sensory and limbic regions (Price and Drevets 2009).”
BackgroundNoninvasive neuromodulation of the prefrontal cortex in mental health disorders
Regenold, W. T., Deng, Z., & Lisanby, S. H. (2021) · Neuropsychopharmacology · doi:10.1038/s41386-021-01094-3 · Cited by 38
Whole-brain morphological alterations associated with trigeminal neuralgia
Mo, J., Zhang, J., Hu, W., Luo, F., & Zhang, K. (2021) · The Journal of Headache and Pain · doi:10.1186/s10194-021-01308-5 · Cited by 38
Sawaya, H., Johnson, K. A., Schmidt, M., Arana, A. B., Chahine, G., Atoui, M., Pincus, D., George, M. S., Panksepp, J., & Nahas, Z. H. (2015) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyu112 · Cited by 45
“The subgenual ACC (Brodmann area 25), with its extensive connections to cortical and subcortical regions (Price and Drevets, 2010), was proposed as a critical node in the DMN of depressed and at-risk individuals.”
BackgroundLi, R., Ma, Z., Yu, J., Yong He, A., & Li, J. (2014) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2014.02.013 · Cited by 40
Imaging genetics studies on monoaminergic genes in major depressive disorder
Won, E., & Ham, B. (2015) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2015.03.014 · Cited by 42
Suzuki, H., Botteron, K. N., Luby, J. L., Belden, A. C., Gaffrey, M. S., Babb, C. M., Nishino, T., Miller, M. I., Ratnanather, J. T., & Barch, D. M. (2012) · Cognitive Affective & Behavioral Neuroscience · doi:10.3758/s13415-012-0121-y · Cited by 42
“…basal ganglia (Fu et al., 2004), while it has also been postulated that the hippocampus structurally interacts with the amygdala, medial PFC, cingulate cortex, and basal ganglia (Botteron, 2001; Drevets et al., 2008; Price & Drevets, 2010; Small et al., 2011) within emotional processing network.”
BackgroundSynaptic alterations associated with depression and schizophrenia: potential as a therapeutic target
Calabrese, F., Riva, M. A., & Molteni, R. (2016) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2016.1188080 · Cited by 38
“hippocampus in the brain of depressed patients [11,12].”
BackgroundHopkins, S. C., Ogirala, A., Loebel, A. D., & Koblan, K. S. (2017) · Schizophrenia Bulletin · doi:10.1093/schbul/sbx101 · Cited by 38
Dissociable components of the reward circuit are involved in appraisal versus choice
Shenhav, A., & Karmarkar, U. R. (2019) · Scientific Reports · doi:10.1038/s41598-019-38927-7 · Cited by 34
“Functional and structural distinctions have been documented between more dorsal and more ventral regions of vmPFC, and similarly for the posterior midline (Price and Drevets, 2010; Smith et al., 2010; Roy et al., 2012; Wallis, 2012; Clithero and Rangel, 2013; Córcoles-Parada et al., 2017).”
BackgroundChoi, J., Kim, J., Kim, T.-K., Park, J. Y., Lee, J. E., Kim, H., Lee, E. H., & Han, P. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2015.03.030 · Cited by 38
“…(Orsini et al., 2011; Sierra-Mercado et al., 2011), the hippocampus (Orsini et al., 2011; Felix-Ortiz and Tye, 2014; Sotres-Bayon et al., 2012), and the nucleus accumbens (Price and Drevets, 2010), it centers in the middle of the neuronal circuit that regulates stress-induced depressive states.”
BackgroundOpen‐Space Forced Swim Model of Depression for Mice
Stone, E. A., & Lin, Y. (2011) · Current Protocols in Neuroscience · doi:10.1002/0471142301.ns0936s54 · Cited by 38
“Similar results have been found in the Morris water maze with rats during extinction of a previously learned spatial memory response (Schulz et al., 2007).”
ResultZhong, Q., Yu, H. M., Huang, C., Zhong, J., Wang, H., Xu, J., & Cheng, Y. (2018) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2018.10.017 · Cited by 37
Distinct neural mechanisms of emotional processing in prolonged grief disorder
Bryant, R. A., Andrew, E., & Korgaonkar, M. S. (2021) · Psychological Medicine · doi:10.1017/s0033291719003507 · Cited by 39
Takahashi, K., Murasawa, H., Yamaguchi, K., Yamada, M., Nakatani, A., Yoshida, M., Iwai, T., Inagaki, M., Yamada, M., & Saitoh, A. (2010) · Behavioural Brain Research · doi:10.1016/j.bbr.2010.07.002 · Cited by 37
Oscillatory serotonin function in depression
Salomon, R. M., & Cowan, R. L. (2013) · Synapse · doi:10.1002/syn.21675 · Cited by 36
Pereira, V. S., Suavinha, A. C. D. R., Wegener, G., & Joca, S. R. L. (2015) · Psychopharmacology · doi:10.1007/s00213-014-3853-2 · Cited by 37
The neuropsychiatry of tinnitus: a circuit-based approach to the causes and treatments available
Minen, M. T., Camprodon, J. A., Nehme, R., & Chemali, Z. N. (2014) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2013-307339 · Cited by 36
Brendel, M., Initiative, A. D. N., Sauerbeck, J., Greven, S., Kotz, S., Scheiwein, F., Blautzik, J., Delker, A., Pogarell, O. M., Ishii, K., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170387 · Cited by 37
“The most significantly spared VOIs included regions implicated in AD (temporal gyri) but were predominantly found in mood-related brain networks (e.g., orbitofrontal and anterior cingulate gyri) [43, 44].”
Cognitive emotional processing across mood disorders
Panchal, P., Kaltenboeck, A., & Harmer, C. J. (2019) · CNS Spectrums · doi:10.1017/s109285291800130x · Cited by 37
“As well as being involved in emotional processing and executive functions such as attention—linking the two together— disruptions in these regions and circuits are also thought to increase the risk of developing the disorder.(63) Other researchers have also reported increased activation in limbic areas, such as the hi…”
Marques, R. C., Vieira, L., Marques, D., & Cantilino, A. (2019) · Brazilian Journal of Psychiatry · doi:10.1590/1516-4446-2019-0344 · Cited by 42
In vivo human brain expression of histone deacetylases in bipolar disorder
Tseng, C.-E. J., Gilbert, T. M., Catanese, M. C., Hightower, B. G., Peters, A. T., Parmar, A. J., Kim, M., Wang, C., Roffman, J. L., Brown, H. E., et al. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-00911-5 · Cited by 39
Jiang, X., Wang, X., Jia, L., Sun, T., Kang, J., Zhou, Y., Wei, S., Wu, F., Kong, L., Wang, F., et al. (2020) · Journal of Affective Disorders · doi:10.1016/j.jad.2020.09.133 · Cited by 36
Chiuccariello, L., Cooke, R. G., Miler, L., Levitan, R. D., Baker, G. B., Kish, S. J., Kolla, N. J., Rusjan, P., Houle, S., Wilson, A. A., et al. (2015) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyv078 · Cited by 36
“…cingulate cortex, but additional regions with high MAO-A density and/or functional relevance to mood disorder symptoms were also included: the hippocampus, ventral striatum, dorsal putamen, thalamus, and midbrain (Saura et al., 1992, 1996; Ressler and Mayberg, 2007; Price and Drevets, 2010).”
BackgroundRodrigues, N. B., Mithani, K., Meng, Y., Lipsman, N., & Hamani, C. (2018) · Brain Sciences · doi:10.3390/brainsci8020023 · Cited by 40
“Many reviews focus on targetable brain regions that may play a role in depression mentioning the role of white matter in passing [62].”
Background
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
- ORCID
- Drevets, Wayne C
- Venue
- Neuropsychopharmacology
- Published
- 2009-08-19
- Volume
- 35
- Issue
- 1
- Pages
- 192-216
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3055427
- 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
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- 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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