Neurocircuitry of Mood Disorders

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).”

What the sources say

• ?Not checked — no full text of the sourcecites Morgan and LeDoux, 1995 source
• Disputed

  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.

  cites Sullivan and Gratton, 1999 sourceExperimental — accuracy not yet measured

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)”

What the sources say

• Partly supported

  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)

  cites Rudebeck and Murray, 2008 sourceExperimental — accuracy not yet measured

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.”

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 supported

  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)

  cites Teves et al, 2004 sourceExperimental — accuracy not yet measured

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)”

What the sources say

• Partly supported

  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)

  cites Teves et al, 2004 sourceExperimental — accuracy not yet measured

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).”

What the sources say

• Supported

  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)

  cites Calzavara et al, 2007 source

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).”

What the sources say

• Supported

  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)

  cites Hsu and Price, 2009 source

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).”

What the sources say

• Supported

  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)

  cites Dewar et al, 2003 source
• ?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

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).”

What the sources say

• Supported

  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)

  cites Dewar et al, 2003 source
• ?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

In the paper

“Nevertheless, a longitudinal study also has shown progression of the abnormality in subjects with psychotic mood disorders (Koo et al, 2008).”

What the sources say

• Supported

  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)

  cites Koo et al, 2008 source

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).”

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 supported

  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)

  cites Shansky et al, 2009 sourceExperimental — accuracy not yet measured

In the paper

“In rats the stressinduced dendritic atrophy in the medial PFC was associated with impaired modulation of behavioral responses to fearconditioned stimuli (Izquierdo et al, 2006), suggesting that this process can alter emotional behavior.”

What the sources say

• Partly supported

  The Discussion reports that the same stressor caused medial PFC dendritic retraction and fear-extinction deficits, supporting the association with altered responses to conditioned fear. But this study tested mice, not rats; its mention of rat studies concerns morphological changes, not this combined finding. Page numbers are not available in our copy. (LLM, conf=0.91)

  cites Izquierdo et al, 2006 sourceExperimental — accuracy not yet measured

In the paper

“Notably, repeated stress results in hyperexcitability in the BLA in rodents (Shekhar et al, 2005;Vyas et al, 2006) suggesting a mechanism that might produce pathological amygdala activity in depression.”

What the sources say

• Partly supported

  In “Proposed intrinsic BLA circuit regulating anxiety responses” (page unavailable), the paper proposes that repeated activation during chronic stress could reduce inhibition in the BLA, making it more responsive. “Internal circuitry of BLA” (page unavailable) reports lasting facilitation after repeated experimental disruption of BLA inhibition, but does not establish that repeated stress itself results in BLA hyperexcitability in rodents. The proposed link to depression is the citing authors’ inference, not a finding attributed to this source. (LLM, conf=0.84)

  cites Shekhar et al, 2005 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Vyas et al, 2006 source

In the paper

“In the basolateral amygdala (BLA) chronic unpredictable stress also produced dendritic atrophy but chronic immobilization stress instead increased dendritic branching (Banasr and Duman, 2007;Vyas et al, 2002Vyas et al, , 2003)).”

What the sources say

• ?Not checked — no full text of the sourcecites Banasr and Duman, 2007 source
• Supported

  In the section “Effects of chronic immobilization stress on dendritic morphology of amygdala neurons,” the paper reports more branch points in CIS-treated BLA pyramidal neurons than in controls. This supports the claim that chronic immobilization stress increases dendritic branching in the BLA. (LLM, conf=0.94)

  cites Vyas et al, 2002 source
• ?Not checked — no full text of the sourcecites Vyas et al, 2003 source

In the paper

“In rats, stimulation of the amygdala inhibits neuronal ensemble activity in the mPFC, and stimulation of the mPFC to the amygdala excites intra-amygdaloid GABAergic cells that inhibit neuronal activity in the central amygdaloid nucleus (ACe) (Likhtik et al, 2005;Perez-Jaranay and Vives, 1991).”

What the sources say

• Partly supported

  In “Extinction and the mPFC-amygdala circuit” (page unavailable), the authors hypothesize that mPFC activity inhibits central amygdala neurons by activating GABAergic cells, including intercalated cells. The claim presents that proposed mechanism as established in rats, whereas the paper’s experiments used adult cats (“Materials and Methods,” page unavailable) and did not directly demonstrate the proposed GABAergic pathway. (LLM, conf=0.88)

  cites Likhtik et al, 2005 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Perez-Jaranay and Vives, 1991 source

In the paper

“In rats the stressinduced dendritic atrophy in the medial PFC was associated with impaired modulation of behavioral responses to fearconditioned stimuli (Izquierdo et al, 2006), suggesting that this process can alter emotional behavior.”

What the sources say

• Partly supported

  The Discussion (page not provided) reports that stress-induced changes in infralimbic neuronal morphology were associated with impaired fear extinction, supporting the suggestion that the process may alter emotional behavior. The study was conducted in mice, not rats as the citing sentence states; it also describes the morphological and behavioral effects as potentially, rather than demonstrably, functionally linked. (LLM, conf=0.88)

  cites Izquierdo et al, 2006 sourceExperimental — accuracy not yet measured

In the paper

“The abnormally increased CBF and metabolism in the VLPFC, OFC, sgACC, pgACC, amygdala, ventral striatum, and medial thalamus evident in depression (Table 1; Figure 8) implicate a limbic-cortical-striato-pallido-thalamic circuit involving these structures (Drevets et al, 1992) (Figure 6).”

What the sources say

• Supported

  In “Anatomical circuits related to depression” (page unavailable), Drevets et al. say their blood-flow findings suggest two interconnected circuits involving the amygdala, prefrontal cortex, medial thalamus, striatum, and ventral pallidum. This supports the cited implication that these regions participate in a limbic-cortical-striatal-pallidal-thalamic circuit. (LLM, conf=0.91)

  cites Drevets et al, 1992 source

In the paper

“Conversely, the glucocorticoid response to stress is inhibited by stimulation of glucocorticoid receptors in the ventral ACC, such that lesions in this cortex in rats increase ACTH and CORT secretion during stress (Diorio et al, 1993).”

What the sources say

• Partly supported

  The Results report higher ACTH and CORT in rats with medial prefrontal/cingulate lesions after restraint stress. The increase occurred after restraint, not at peak levels during it, and lesions had no effect after ether stress. Histology also shows that the lesions extended into the infralimbic region, so they were not confined to the ventral ACC. (LLM, conf=0.88)

  cites Diorio et al, 1993 sourceExperimental — accuracy not yet measured

In the paper

“In rats, stimulation of the amygdala inhibits neuronal ensemble activity in the mPFC, and stimulation of the mPFC to the amygdala excites intra-amygdaloid GABAergic cells that inhibit neuronal activity in the central amygdaloid nucleus (ACe) (Likhtik et al, 2005;Perez-Jaranay and Vives, 1991).”

What the sources say

• ?Could not verify

  The Discussion and ‘Extinction and the mPFC-amygdala circuit’ section describe the effect of mPFC stimulation on amygdala neurons, not the effect of amygdala stimulation on mPFC neuronal ensembles. Searches for amygdala stimulation and suppression of prefrontal neurons found no passage addressing the claimed direction of effect. Page numbers were not available in our copy. (LLM, conf=0.76)

  cites Likhtik et al, 2005 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Perez-Jaranay and Vives, 1991 source

In the paper

“In the basolateral amygdala (BLA) chronic unpredictable stress also produced dendritic atrophy but chronic immobilization stress instead increased dendritic branching (Banasr and Duman, 2007;Vyas et al, 2002Vyas et al, , 2003)).”

What the sources say

• ?Not checked — no full text of the sourcecites Banasr and Duman, 2007 source
• Partly supported

  The Results section, “Effects of chronic unpredictable stress on dendritic morphology of amygdala neurons” (page not provided), reports dendritic atrophy in the BLA after chronic unpredictable stress. The effect was limited to bipolar/bitufted neurons; the paper reports no effect on BLA pyramidal or stellate neurons, a qualification the claim omits. (LLM, conf=0.88)

  cites Vyas et al, 2002 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Vyas et al, 2003 source

In the paper

“Notably, repeated stress results in hyperexcitability in the BLA in rodents (Shekhar et al, 2005;Vyas et al, 2006)”

What the sources say

• Partly supported

  In “Proposed intrinsic BLA circuit regulating anxiety responses” (page not available), the paper says chronic stress could reduce inhibition in BLA circuitry after repeated activation. “Internal circuitry of BLA” reports long-term synaptic facilitation after repeated disruption of BLA inhibition, including evidence from rats. These passages support increased BLA excitability as a plausible mechanism, but do not establish that repeated stress itself reliably produces hyperexcitability in rodents. (LLM, conf=0.86)

  cites Shekhar et al, 2005 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Vyas et al, 2006 source

In the paper

“Conversely, the glucocorticoid response to stress is inhibited by stimulation of glucocorticoid receptors in the ventral ACC, such that lesions in this cortex in rats increase ACTH and CORT secretion during stress (Diorio et al, 1993).”

What the sources say

• Partly supported

  The Results and Discussion report that corticosterone implants in the rat medial prefrontal cortex (cingulate gyrus) reduced ACTH and CORT responses to restraint stress, while lesions increased both hormones after restraint. The paper suggests glucocorticoid receptors are involved, but does not demonstrate selective receptor stimulation or identify the site as the ventral ACC. Neither manipulation had the reported effect with ether stress, so the claim is too broad about stress generally. (LLM, conf=0.86)

  cites Diorio et al, 1993 sourceExperimental — accuracy not yet measured

In the paper

“deep brain stimulation applied via electrodes situated in the accumbens area/ventral internal capsule improves depressive symptoms in treatmentrefractory depression (Malone et al, 2009;Schlaepfer et al, 2008).”

What the sources say

• Supported

  The Methods report bilateral electrode implantation in the ventral capsule/ventral striatum (VC/VS) region in 15 patients with highly refractory depression. The Discussion reports significant, sustained improvement in depression measures following stimulation. (LLM, conf=0.94)

  cites Malone et al, 2009 source
• Supported

  The Introduction reports bilateral electrodes with contacts in the nucleus accumbens and ventral internal capsule in three patients with severe treatment-resistant depression. The Discussion reports immediate improvements in depression ratings with bilateral DBS. The DBS Method specifies that stimulation used the two contacts in the nucleus accumbens. (LLM, conf=0.91)

  cites Schlaepfer et al, 2008 source

In the paper

“In rats, stimulation of these ventral ACC areas elicits burst-firing patterns in the VTA-DA neurons whereas inactivation of the ventral ACC converts burstfiring patterns to pacemaker-like firing activity (Drevets et al, 1998;Murase et al, 1993;Taber and Fibiger, 1993;Gariano and Groves, 1988).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 1998
• ?Not checked — no full text of the sourcecites Murase et al, 1993 source
• ?Could not verify

  The Results report increased striatal dopamine after medial prefrontal cortex stimulation in rats. The Discussion mentions a possible projection to the ventral tegmental area, but neither passage reports whether stimulation of ventral ACC areas elicits burst firing in VTA dopamine neurons. Searches for burst firing and pacemaker activity found no passage addressing that outcome. (LLM, conf=0.75)

  cites Taber and Fibiger, 1993 sourceExperimental — accuracy not yet measured

In the paper

“based upon evidence that DA depletion caused by degeneration of DA neurons (in Parkinson's Disease) or drugs (reserpine a-methyl-para-tyrosine) induced depressive syndromes in vulnerable individuals (Santamaria et al, 1986;Hasler et al, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Santamaria et al, 1986 source
• Partly supported

  The Results (page unavailable) report that AMPT-induced catecholamine depletion caused depressive symptoms, especially in people with remitted major depressive disorder. The paper does not isolate dopamine depletion from norepinephrine depletion as the cause, and it does not establish that degeneration of dopamine neurons or reserpine caused depressive syndromes. (LLM, conf=0.86)

  cites Hasler et al, 2008 sourceExperimental — accuracy not yet measured

In the paper

“In rats, stimulation of these ventral ACC areas elicits burst-firing patterns in the VTA-DA neurons whereas inactivation of the ventral ACC converts burstfiring patterns to pacemaker-like firing activity (Drevets et al, 1998;Murase et al, 1993;Taber and Fibiger, 1993;Gariano and Groves, 1988).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 1998
• ?Not checked — no full text of the sourcecites Murase et al, 1993 source
• ?Could not verify

  The Results and Discussion (page numbers unavailable) describe increased striatal dopamine release during medial prefrontal cortex stimulation in rats. A search for ventral ACC inactivation and burst-to-pacemaker firing found no passage addressing the claimed change in VTA dopamine-neuron activity. (LLM, conf=0.75)

  cites Taber and Fibiger, 1993 sourceExperimental — accuracy not yet measured

In the paper

“positive t-values in a sagittal section located 17 mm left of midline (X ¼ À17) show areas where CBF is increased in depressives vs controls in the amygdala and medial (MED) orbital cortex”

What the sources say

• Partly supported

  The Discussion reports increased blood flow in the left amygdala and left prefrontal cortex in depressed subjects with familial pure depressive disease compared with controls. However, the Other regions section identifies the medial prefrontal component as pregenual anterior cingulate, while Previous studies says the assessed region included part of the lateral orbital cortex. Our copy does not identify an increase specifically in the medial orbital cortex. (LLM, conf=0.86)

  cites Drevets et al, 1992 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Drevets et al, 1997a source
• ?Not checked — no full text of the sourcecites Price et al, 1996 source

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).”

What the sources say

• Partly supported

  In “Information Encoded in Dopaminergic Activity” (p. 2), the paper describes bursts of dopamine-neuron impulses in monkeys and identifies the nucleus accumbens as a projection target. “Summary and Future Questions” (p. 6) discusses changes in dopamine delivery to target regions, but our copy does not establish that burst firing increases dopamine release specifically in the accumbens. (LLM, conf=0.84)

  cites Schultz et al, 1997 sourceExperimental — accuracy not yet measured

In the paper

“The medial network in the OMPFC is probably still more significant for mood disorders.”

In the paper

“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.”

In the paper

“In addition to confirming the earlier findings, these studies both provided more detail about the cortical areas that received amygdaloid inputs and showed that the fibers, especially from the central and medial amygdaloid nuclei, extend to a variety of visceral control areas from the hypothalamus to the reticular formation and vagal nuclei of the lower medulla.”

In the paper

“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.”

In the paper

“Outputs to hypothalamic and brainstem areas involved directly in visceral control were also found, including not just the medial and lateral hypothalamus, but also the periaqueductal gray and the parabrachial nuclei.”

In the paper

“These include primary olfactory and gustatory cortex, visual areas in the inferior temporal cortex (TEa), and the ventral bank of the superior temporal sulcus, somatic sensory areas in the dysgranular insula (Id) and the frontal operculum (Carmichael and Price, 1995b;Saleem et al, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Carmichael and Price, 1995b source
• ?Not checked — no full text of the sourcecites Saleem et al, 2008 source

In the paper

“The only sensory modality that apparently lacks an input to the orbital network is audition.”

In the paper

“This means that there are overlapping and interconnected medial prefrontal cortico-striato-pallidothalamic and amygdalo-striato-pallido-thalamic loops (Figure 2, left).”

In the paper

“The orbital network consists of areas in the central and caudal part of the orbital cortex and the adjacent anterior agranular insular cortex (Figure 3); it does not include areas along the medial edge of the orbital cortex, and two areas in the caudolateral orbital cortex.”

In the paper

“Since 1995, a series of axonal tracing experiments in macaque monkeys have more completely defined the cortical and subcortical circuits related to the medial prefrontal cortex and amygdala.”

In the paper

“In addition, there are substantial amygdaloid projections to the medial, caudal, and lateral edges of the orbital cortex (leaving the central orbital cortex relatively free), to the rostroventral insula, and to the temporal pole and inferior temporal cortex, extending caudally to the primary visual cortex (V1) (Figure 2, right).”

In the paper

“The most prominent amygdaloid and other limbic connections are with areas of the medial network (Carmichael and Price, 1995a;Kondo et al, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Carmichael and Price, 1995a source
• ?Not checked — no full text of the sourcecites Kondo et al, 2005 source

In the paper

“There are also amygdaloid interactions with the entorhinal and perirhinal cortex and the hippocampus (subiculum) (Amaral et al, 1992).”

What the sources say

• ?Not checked — no full text of the sourcecites Amaral et al, 1992 source

In the paper

“In the striatum, an extensive major amygdaloid projection was shown to the nucleus accumbens, and adjacent medial caudate nucleus and ventral putamen (Russchen et al, 1985).”

What the sources say

• ?Not checked — no full text of the sourcecites Russchen et al, 1985 source

In the paper

“In 1961, Nauta showed in monkeys that the amygdala projects strongly to the hypothalamus, preoptic area, basal forebrain, and the mediodorsal thalamic nucleus.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Nauta 1961

In the paper

“Other experiments (Nauta, 1962;Cowan et al, 1965) indicated that there are also connections between the medial thalamus, orbital cortex, striatum, and hypothalamus, providing the outlines of an interconnected circuit that relates these structures to each other and to the amygdala.”

What the sources say

• ?Not checked — no full text of the sourcecites Nauta, 1962 source
• ?Not checked — no full text of the sourcecites Cowan et al, 1965 source

In the paper

“Based on local cortico-cortical connections, two connectional systems or networks were recognized within the OMPFC, which have been referred to as the 'orbital' and 'medial prefrontal networks'.”

What the sources say

• ?Not checked — no full text of the sourcecites Carmichael and Price, 1996 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites O ¨ngu ¨r and Price, 2000
• ?Not checked — no full text of the sourcecites Saleem et al, 2008 source

In the paper

“The cortical projections of the amygdala are widespread, but the strongest connections are with the medial prefrontal cortex rostral and ventral to the genu of the corpus callosum.”

In the paper

“For example, responses to food stimuli change with the hunger or satiety of the animal (Rolls, 2000;Pritchard et al, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Rolls, 2000 source
• ?Not checked — no full text of the sourcecites Pritchard et al, 2008 source

In the paper

“Using eight different staining methods, 22 areas were recognized, which provided the basis for a relatively high-resolution analysis of cortical organization.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Carmichael and Price, 1994

In the paper

“In the 1970s Krettek andPrice (1977a, b, c, 1978a, b) used the anterograde transport of 3H-leucine in cats and rats to define projections from the basal and lateral amygdala to the orbital and medial prefrontal, insular, and temporal cortical areas, the mediodorsal thalamic nucleus, and the medial and lateral hypothalamus.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Krettek andPrice (1977a, b, c, 1978a, b)

In the paper

“Older reports indicate that electrical stimulation of the medial network areas produces disturbances in functions such as heart rate and respiration (Kaada, 1960)”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Kaada, 1960

In the paper

“Rats subjected to stressors show an acute response, which then habituates when the stressor continues to become chronic.”

In the paper

“Although they are relatively small, the midline nuclei have remarkably extensive connections (Hsu andPrice, 2007, 2009) (Figure 7).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Hsu andPrice, 2007, 2009

In the paper

“The PVT are connected to the perigenual areas just ventral and rostral to the genu of the corpus callosum.”

In the paper

“In addition, the medial network is connected to a very specific set of other cortical regions, particularly the rostral part of the superior temporal gyrus (STGr) and dorsal bank of the superior temporal sulcus (STSd), the anterior and posterior cingulate cortex, and the entorhinal and parahippocampal cortex (Figures 4 and 5; Saleem et al., 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Saleem et al., 2008 source

In the paper

“These nuclei also have important connections with the amygdala, hypothalamus, and brainstem areas, including the periaqueductal gray.”

In the paper

“Furthermore, the midline nuclei also have a very substantial projection to the same areas of the ventromedial striatum that receives input from the medial network areas.”

In the paper

“These striatal regions, in turn, project to the ventral pallidum.”

In the paper

“For example, acute footshock in rats activates paraventricular neurons that project to the medial prefrontal cortex, accumbens nucleus, and the amygdala (Bubser and Deutch, 1999)”

What the sources say

• ?Not checked — no full text of the sourcecites Bubser and Deutch, 1999 source

In the paper

“In humans, there is a similar habituation to the neuroendocrine stress response caused by chronic hypoglycemia (Cryer, 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Cryer, 2004 source

In the paper

“Lesions of the PVT block the habituation to the chronic stress (Bhatnagar et al, 2002)”

What the sources say

• ?Not checked — no full text of the sourcecites Bhatnagar et al, 2002 source

In the paper

“The origin of this projection extends beyond the medial prefrontal network to include the STGr and STSd, and area 9 in the dorsal prefrontal cortex, both of which are strongly connected to the medial network.”

In the paper

“Area 25, in the subgenual part of the medial PFC, projects specially to the 'shell' of the nucleus accumbens.”

In the paper

“MDm receives substantial subcortical inputs from the amygdala, olfactory cortex and other limbic areas (Russchen et al, 1987).”

What the sources say

• ?Not checked — no full text of the sourcecites Russchen et al, 1987 source

In the paper

“In support of this hypothesis, lesions of the ventral striatum and pallidum, MD, or the OMPFC have been shown to cause perseverative deficits in stimulus-reward reversal tasks in rats and monkeys, such that the animals have difficulty switching away from previously rewarded, but now unrewarded stimuli (Roberts et al, 1990;McBride and Slotnick, 1997;Ferry et al, 2000a;Kazama and Bachevalier, 2009).”

What the sources say

• ?Not checked — no full text of the sourcecites Roberts et al, 1990 source
• ?Not checked — no full text of the sourcecites McBride and Slotnick, 1997 source
• ?Not checked — no full text of the sourcecites Ferry et al, 2000a source

In the paper

“In addition, lateral MD receives GABAergic, pallidal-like fibers from the pars reticulata of the substantia nigra (Ilinsky et al, 1985;Kuroda and Price, 1991b).”

What the sources say

• ?Not checked — no full text of the sourcecites Ilinsky et al, 1985 source
• ?Not checked — no full text of the sourcecites Kuroda and Price, 1991b source

In the paper

“When the orbital network is to some extent a sensory-related system, therefore, the medial network is more an output system that can modulate visceral function in relation to emotion or other factors.”

In the paper

“In addition to the prefrontal connections with MD, there are also important connections with the midline nuclei of the thalamus.These include the paraventricular thalamic nucleus (PVT), as well as other nuclei that extend ventrally on the midline between the anterior and mediodorsal thalamic nuclei.”

In the paper

“The principal cortico-cortical connections of this system are with the dorsal premotor cortex, the posterior part of the dorsal STS (area TPT), and areas LIP and 7a in the posterior parietal cortex (Figure 5).”

In the paper

“In addition to these inputs from limbic structures, which are excitatory and probably glutamatergic, MDm also receives GABAergic inputs from the ventral pallidum and rostral globus pallidus (Kuroda and Price, 1991a;Churchill et al, 1996), which is part of the cortico-striato-pallido-thalamic loop involving the OMPFC (Figure 6).”

What the sources say

• ?Not checked — no full text of the sourcecites Kuroda and Price, 1991a source
• ?Not checked — no full text of the sourcecites Churchill et al, 1996 source

In the paper

“The orbital network areas connect to a relatively central region that spans the internal capsule, and includes parts of both the caudate nucleus and the putamen.”

In the paper

“The PVT and other midline thalamic nuclei are therefore situated to relay information about visceral function to both the medial prefrontal network, and the cortico-striato-pallido-thalamic loop that interacts with it.”

In the paper

“Furthermore, it appears that the role of the PVT may be to control the response to chronic stress.”

In the paper

“but that the chronic stage is specifically associated with activity in the midline thalamus (Arbelaez et al, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Arbelaez et al, 2008 source

In the paper

“and lesions of the PVT increase the activation of the central amygdaloid nuclei by an acute stressor (Spencer et al, 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Spencer et al, 2004 source

In the paper

“As mentioned above, there are substantial outputs from the medial prefrontal network to the hypothalamus, the periaqueductal gray, and other visceral control centers.(O ¨ngu ¨r et al, 1998a, b;An et al, 1998;Rempel-Clower and Barbas 1998;Freedman et al, 2000;Barbas et al, 2003).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites O ¨ngu ¨r et al, 1998a, b
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites An et al, 1998
• ?Not checked — no full text of the sourcecites Rempel-Clower and Barbas 1998 source

In the paper

“In addition to the amygdala, the primary olfactory cortex, the entorhinal, perirhinal, and parahippocampal cortex, and the subiculum all send axonal projections both to the OMPFC Carmichael et al, 1994;Carmichael and Price, 1995a;Kondo et al, 2005), and to medial MD (Russchen et al, 1987).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Carmichael et al, 1994
• ?Not checked — no full text of the sourcecites Carmichael and Price, 1995a source
• ?Not checked — no full text of the sourcecites Kondo et al, 2005 source

In the paper

“The more lateral parts of MD receive most of their subcortical input from the brainstem, including the superior colliculus and vestibular nuclei, as well as the portions of the reticular formation (Russchen et al, 1987).”

What the sources say

• ?Not checked — no full text of the sourcecites Russchen et al, 1987 source

In the paper

“The OMPFC projects principally to the rostral, ventromedial part of the striatum.”

In the paper

“There is a considerable amount of evidence that links the PVT to the stress response.”

In the paper

“Lesions of the ventromedial prefrontal cortex in humans abolish the normal, automatic visceral response to emotive stimuli (Damasio et al, 1990;Bechara et al, 2000).”

What the sources say

• ?Not checked — no full text of the sourcecites Damasio et al, 1990 source
• ?Not checked — no full text of the sourcecites Bechara et al, 2000 source

In the paper

“Of more significance for mood disorders, however, the medial network areas project to the nucleus accumbens, and the adjacent medial edge of the caudate nucleus bordering the lateral ventricle (Ferry et al, 2000b).”

What the sources say

• ?Not checked — no full text of the sourcecites Ferry et al, 2000b source

In the paper

“via a mechanism that involves corticosterone action in the PVT (Jaferi and Bhatnagar, 2006).”

What the sources say

• ?Not checked — no full text of the sourcecites Jaferi and Bhatnagar, 2006 source

In the paper

“The amygdala input to the striatum is essentially coextensive with that of the medial network.”

In the paper

“From the viewpoint of mood disorders, over-activation of this system (eg, due to excessive activity in the subgenual cortex, see Neurophysiological Imaging in Major Depressive and Bipolar Disorders below) could produce the chronic sense of 'unease' that is a frequent component of depression.”

In the paper

“Because of the direct cortical projections, information from the limbic structures does not require a thalamic relay to reach the cortex.”

In the paper

“In MDm, the GABAergic terminals of afferent pallidal fibers synapse on the same dendrites, and occasionally even on the same dendritic spines as the excitatory terminals from the amygdala and other limbic structures (Kuroda and Price, 1991a).”

What the sources say

• ?Not checked — no full text of the sourcecites Kuroda and Price, 1991a source

In the paper

“Patients with mood disorders manifest abnormalities of morphology or morphometry in several medial prefrontal network and limbic structures (Drevets and Price, 2005a).”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets and Price, 2005a source

In the paper

“the expression of genes related to myelinating oligodendrocyte function was decreased in the middle temporal gyrus in MDD subjects relative to controls (Aston et al, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Aston et al, 2005 source

In the paper

“Clinical studies of individuals with mood disorders have implicated the networks formed by the OMPFC and anatomically related areas of the striatum, thalamus, temporal cortex, and limbic system reviewed above in the pathophysiology of depression, based upon converging evidence from neuroimaging, neuropathological, and lesion analysis studies.”

In the paper

“The glial cell type implicated most consistently in mood disorders has been the oligodendrocyte (eg, Uranova et al, 2004;Hamidi et al, 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Uranova et al, 2004 source
• ?Not checked — no full text of the sourcecites Hamidi et al, 2004 source

In the paper

“These hypotheses are compatible with treatments for depression, involving pharmacological, neurosurgical, and deep brain stimulation methods, that appear to suppress pathological activity within components of extended medial prefrontal network such as the subgenual anterior cingulate cortex (sgACC), ventromedial frontal polar cortex, ventromedial striatum, and amygdala (Drevets et al, 2002a;Mayber”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 2002a source
• ?Not checked — no full text of the sourcecites Mayberg et al, 2005 source
• ?Not checked — no full text of the sourcecites Drevets and Price, 2005 source

In the paper

“These data implicated the limbic-cortico-striato-pallido-thalamic circuits related to the medial and orbital prefrontal networks (Figure 6).”

In the paper

“at least one study that used the astrocyte-specific protein S100b to identify these cells in the amygdala did not find a reduction in astrocytes in MDD cases (Hamidi et al, 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Hamidi et al, 2004 source

In the paper

“Glucocorticoids affect both glia and neurons (Cheng and de Vellis, 2000)”

What the sources say

• ?Not checked — no full text of the sourcecites Cheng and de Vellis, 2000 source

In the paper

“For example early-onset nonpsychotic MDD and BD cases also consistently show volumetric abnormalities that appear localized to structures within the extended medial prefrontal network (Table 1).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Table 1

In the paper

“In several reports, the deficits in glia in the cerebral cortex depended upon laminar analysis with the greatest effects in layers III, V, and VI (Cotter et al, 2001a(Cotter et al, , 2002;;Rajkowska et al, 1999Rajkowska et al, , 2001;;Uranova et al, 2004;Vostrikov et al, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Cotter et al, 2001a source
• ?Not checked — no full text of the sourcecites Rajkowska et al, 1999 source
• ?Not checked — no full text of the sourcecites Uranova et al, 2004 source

In the paper

“In contrast, elderly MDD subjects with late-onset depression show a higher prevalence of neuroimaging correlates of cerebrovascular disease relative both to age-matched healthy controls and to elderly depressives with an early age at depression-onset (reviewed in Drevets et al, 2004a).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 2004a

In the paper

“As the medial network and limbic system exert forebrain modulation over visceral responses mediated via the hypothalamus and brainstem, dysfunction within these circuits also may account for the disturbances in autonomic and neuroendocrine function that have been associated with mood disorders.”

In the paper

“Compatible with these data myelin staining was decreased in the deep white matter of the dorsolateral PFC in MDD and BD subjects (Regenold et al, 2007)”

What the sources say

• ?Not checked — no full text of the sourcecites Regenold et al, 2007 source

In the paper

“the white matter volume of the genual and splenial portions of the corpus callosum were abnormally reduced in MDD and BD (eg, Brambilla et al, 2004;Martinez et al, 2002).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Brambilla et al, 2004
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Martinez et al, 2002

In the paper

“In particular, it had been observed that degenerative basal ganglia diseases, and lesions of the striatum and OMPFC, increased the risk of developing MDE (Folstein et al, 1985).”

What the sources say

• ?Not checked — no full text of the sourcecites Folstein et al, 1985 source

In the paper

“Factors that may contribute to a loss of oligodendroglia include the elevated glucocorticoid secretion and glutamatergic transmission evident during depression (see below).”

In the paper

“Satellite oligodendrocytes are immunohistochemically reactive for glutamine synthetase, suggesting they function like astrocytes to take up synaptically released glutamate for conversion to glutamine and cycling back into neurons (D' Amelio et al, 1990).”

What the sources say

• ?Not checked — no full text of the sourcecites D' Amelio et al, 1990 source

In the paper

“Nevertheless, such cases have been differentiated from relevant control groups on the basis of lesions or gray matter loss within the OMPFC (MacFall et al, 2001;Coryell et al, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites MacFall et al, 2001 source
• ?Not checked — no full text of the sourcecites Coryell et al, 2005 source

In the paper

“Reductions in astroglia or astroglial markers have also been observed in postmortem studies of mood disorders.”

In the paper

“Notably, myelin-basic protein concentration was decreased in the frontal polar cortex (BA 10) (Honer et al, 1999)”

What the sources say

• ?Not checked — no full text of the sourcecites Honer et al, 1999 source

In the paper

“Similarly, McDonald et al (2004) showed that reduced volume of the right 'perigenual' ACC region (including both the sgACC and the 'pregenual' ACC (pgACC) anterior to the corpus callosum); was associated with increasing genetic risk for BD (based upon numbers of affected relatives).”

What the sources say

• ?Not checked — no full text of the sourcecites McDonald et al (2004) source

In the paper

“The abnormal reduction in sgACC volume primarily has been identified in mood-disordered subjects with evidence for familial aggregation of illness.”

In the paper

“It is likely that the role of the PVT is general across many types of stressors.”

In the paper

“Most of these used glial fibrillary acidic protein (GFAP) as a marker for astrocytes, and reported that GFAP, or GFAPpositive cells were decreased in mood-disordered subjects relative to controls (Johnston-Wilson et al, 2000;Si et al, 2004;Rajkowska and Miguel-Hidalgo, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Johnston-Wilson et al, 2000 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Si et al, 2004
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Rajkowska and Miguel-Hidalgo, 2007

In the paper

“The clinical phenomenology of MDE implicates brain systems involved in the regulation of mood, anxiety, fear (eg, phobias, panic attacks, and post-traumatic stress syndromes commonly occur comorbidly with depression), reward processing, attention, motivation, stress responses, social cognition, and neurovegetative function (ie, sleep, appetite, energy, libido) (APA, 1994;Kessler et al, 2005).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites APA, 1994
• ?Not checked — no full text of the sourcecites Kessler et al, 2005 source

In the paper

“In MDD the reduction in sgACC volume persists despite successful treatment with antidepressant drugs (Drevets et al, 1997a).”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 1997a source

In the paper

“Satellite oligodendrocytes are immunohistochemically reactive for glutamine synthetase, suggesting they function like astrocytes to take up synaptically released glutamate for conversion to glutamine and cycling back into neurons (D' Amelio et al, 1990).”

What the sources say

• ?Not checked — no full text of the sourcecites D' Amelio et al, 1990 source

In the paper

“Furthermore, other studies did not find abnormalities in the number of GFAP-stained cells or GFAP levels in MDD or BD cases (Webster et al, 2001;Cotter et al, 2001b)”

What the sources say

• ?Not checked — no full text of the sourcecites Webster et al, 2001 source
• ?Not checked — no full text of the sourcecites Cotter et al, 2001b source

In the paper

“Similarly, MDD and BD cases that have either delusions or late-life illness-onset show nonspecific signs of atrophy, such as lateral ventricle enlargement, that are absent in early-onset non-psychotic MDD cases.”

In the paper

“The magnitude or prevalence of these abnormalities depends to some extent on clinical characteristics such as age-at illness-onset, capacity for developing mania or psychosis, and evidence for familial aggregation of illness.”

In the paper

“In mood disorder subjects, the medial prefrontal network and related regions have been shown to contain alterations in gray matter volume, cellular elements, neurophysiological activity, receptor pharmacology, and gene expression.”

In the paper

“Satellite (perineuronal) oligodendrocytes also were implicated in mood disorders by an electron microscopic study of the PFC in BD, which revealed decreased nuclear size clumping of chromatin and indications of both apoptotic and necrotic degeneration in these cells (Uranova et al, 2001;Vostrikov et al, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Uranova et al, 2001 source
• ?Not checked — no full text of the sourcecites Vostrikov et al, 2007 source

In the paper

“The anatomical specificity of these findings is attested to by the lack of difference in whole brain volume between samples with early-onset mood disorders and age-matched healthy control samples.”

In the paper

“Thus the clinical manifestations of mood disorders would appear to implicate the cognitive, emotional and visceral functions subserved by the orbital and medial prefrontal networks.”

In the paper

“Because these neurological disorders affect synaptic transmission through the cortico-striato-pallidothalamic circuitry in diverse ways it appears that dysfunction that alters transmission through these circuits in a variety of ways can produce the pathological emotional symptoms encompassed by the MDE criteria (Drevets et al, 2004a).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 2004a

In the paper

“The most prominent volumetric abnormality reported to date in MDD and BD has been a reduction in gray matter in the left anterior cingulate cortex (ACC) ventral to the corpus callosum genu (ie, 'subgenual'; Figure 8) (Botteron et al, 2002;Coryell et al, 2005;Drevets et al, 1997;Hirayasu et al, 1999;Koo et al, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Botteron et al, 2002 source
• ?Not checked — no full text of the sourcecites Coryell et al, 2005 source
• ?Not checked — no full text of the sourcecites Drevets et al, 1997 source

In the paper

“The finding that reductions in cortex volume and/or histopathological changes appear to occur specifically in regions that show hypermetabolism during depression such as the medial and orbital PFC, amygdala, ventral striatum, and cingulate cortex raises the possibility that excitatory amino acid transmission has a role in the neuropathology of mood disorders.”

In the paper

“in particular, in schizophrenia a reduction of oligodendrocytes has also been reported in the frontal cortex (Hof et al, 2002(Hof et al, , 2003)).”

What the sources say

• ?Not checked — no full text of the sourcecites Hof et al, 2002 source
• ?Not checked — no full text of the sourcecites Hof et al, 2003 source

In the paper

“Depressed MDD subjects show abnormally reduced GABA levels in the dorsomedial/dorsal anterolateral PFC and occipital cortex (Sanacora et al, 1999;Hasler et al, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Sanacora et al, 1999 source
• ?Not checked — no full text of the sourcecites Hasler et al, 2007 source

In the paper

“As reviewed above, the BLA, medial prefrontal network and MD are interconnected by excitatory, glutamatergic projections (Amaral and Price, 1984;Amaral and Insausti, 1992;Bacon et al, 1996;Kuroda and Price, 1991a;Jackson and Moghaddam, 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites Amaral and Price, 1984 source
• ?Not checked — no full text of the sourcecites Amaral and Insausti, 1992 source
• ?Not checked — no full text of the sourcecites Bacon et al, 1996 source

In the paper

“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).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Rajkowska et al, 2007

In the paper

“Cerebral glucose metabolism largely reflects the energetic requirements associated with glutamatergic transmission (Shulman et al, 2004).”

What the sources say

• ?Not checked — no full text of the sourcecites Shulman et al, 2004 source

In the paper

“The amygdala mediates the stressed component of glucocorticoid hormone secretion by disinhibiting CRF release from the hypothalamic paraventricular nucleus (Herman and Cullinan, 1997).”

What the sources say

• ?Not checked — no full text of the sourcecites Herman and Cullinan, 1997 source

In the paper

“After effective antidepressant treatment, there is evidence that metabolic activity decreases in these regions (Table 1; reviewed in Drevets et al, 2002aDrevets et al, , 2004a)), and there is desensitization of NMDA receptors in the PFC (Paul and Skolnick, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites Paul and Skolnick, 2003 source

In the paper

“In regions that appear homologous to the areas where gray matter reductions are evident in depressed humans (ie, medial PFC, hippocampus) repeated stress results in dendritic atrophy and reductions in glial cell counts in rodents (Banasr and Duman, 2007;Czeh et al, 2006;McEwen and Magarinos, 2001;Wellman, 2001;Radley et al, 2008).”

What the sources say

• ?Not checked — no full text of the sourcecites Banasr and Duman, 2007 source
• ?Not checked — no full text of the sourcecites Czeh et al, 2006 source
• ?Not checked — no full text of the sourcecites McEwen and Magarinos, 2001 source

In the paper

“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.”

In the paper

“The abnormally increased CBF and metabolism in the VLPFC, OFC, sgACC, pgACC, amygdala, ventral striatum, and medial thalamus evident in depression (Table 1; Figure 8) implicate a limbic-cortical-striato-pallido-thalamic circuit involving these structures (Drevets et al, 1992) (Figure 6).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Table 1
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Figure 8

In the paper

“The dendritic remodeling associated with repeated stress depends on interactions between the increased N-methyl-Daspartate (NMDA) receptor stimulation and glucocorticoid secretion (McEwen and Magarinos, 2001).”

What the sources say

• ?Not checked — no full text of the sourcecites McEwen and Magarinos, 2001 source

In the paper

“Finally, decreases in oligodendrocyte density are probably not specific to mood disorders; in particular, in schizophrenia a reduction of oligodendrocytes has also been reported in the frontal cortex (Hof et al, 2002(Hof et al, , 2003)).”

What the sources say

• ?Not checked — no full text of the sourcecites Hof et al, 2002 source
• ?Not checked — no full text of the sourcecites Hof et al, 2003 source

In the paper

“The abnormalities of structure and function evident within the extended visceromotor network may impair this network's modulation of endocrine, autonomic, emotional, and behavioral responses to aversive and reward-related stimuli or contexts (O ¨ngu ¨r et al, 2003), potentially accounting for the disturbances within these domains in mood disorders.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites O ¨ngu ¨r et al, 2003

In the paper

“Thus, the increased activity seen within some medial prefrontal network areas during depressive episodes may reflect a compensatory response that modulates depressive symptoms.”

In the paper

“The limbic-cortical-striato-pallido-thalamic circuit constitutes a disinhibitory side loop between the amygdala or PFC and the MD.”

In the paper

“After effective antidepressant treatment, there is evidence that metabolic activity decreases in these regions (Table 1; reviewed in Drevets et al, 2002aDrevets et al, , 2004a)), and there is desensitization of NMDA receptors in the PFC (Paul and Skolnick, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 2002a source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 2004a

In the paper

“The anatomical projections from the amygdala and mPFC to the hypothalamus, PAG, locus ceruleus, raphe, and autonomic-related brainstem nuclei play major roles in organizing the endocrine, autonomic, and behavioral responses to stressors and emotional stimuli (Figure 10) (Davis and Shi, 1999;LeDoux, 2003;O ¨ngu ¨r et al, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites Davis and Shi, 1999 source
• ?Not checked — no full text of the sourcecites LeDoux, 2003 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites O ¨ngu ¨r et al, 2003

In the paper

“In agreement with the neuroimaging evidence of elevated activity in this circuit, post mortem studies of the NMDA receptor complex in suicide victims found evidence that glutamatergic transmission had been increased in the PFC antemortem in depression (Paul and Skolnick, 2003).”

What the sources say

• ?Not checked — no full text of the sourcecites Paul and Skolnick, 2003 source

In the paper

“As the pallidal neurons have relatively high spontaneous firing rates (DeLong, 1972)”

What the sources say

• ?Not checked — no full text of the sourcecites DeLong, 1972 source

In the paper

“Notably, the depressive subgroups (eg, BD FPDD) that show reductions in regional gray matter volume also show evidence of having elevated glutamatergic transmission and cortisol secretion (Drevets et al, 2002b).”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 2002b source

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).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 2004a

In the paper

“The abnormalities of structure and function evident within the extended visceromotor network may impair this network's modulation of endocrine, autonomic, emotional, and behavioral responses to aversive and reward-related stimuli or contexts (O ¨ngu ¨r et al, 2003), potentially accounting for the disturbances within these domains in mood disorders.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites O ¨ngu ¨r et al, 2003

In the paper

“activity in the PFC or amygdala that activates the striatum and in turn inhibits the ventral pallidum may release the MD from the inhibitory pallidal influence (Figure 6; Russchen et al, 1985;Graybiel, 1990;Kuroda and Price, 1991a, b).”

What the sources say

• ?Not checked — no full text of the sourcecites Russchen et al, 1985 source
• ?Not checked — no full text of the sourcecites Graybiel, 1990 source
• ?Not checked — no full text of the sourcecites Kuroda and Price, 1991a, b source

In the paper

“Depressed subjects also show abnormally reduced Glx levels in the dorsomedial/dorsal anterolateral and ventromedial PFC (Hasler et al, 2007).”

What the sources say

• ?Not checked — no full text of the sourcecites Hasler et al, 2007 source

In the paper

“Stimulation of the projections from the ACe and BNST in rats increases sympathetic autonomic arousal in rodents, presumably via projections to the lateral hypothalamus, PAG, locus ceruleus, and ponto-medullary reticular formation (Le-Doux, 2003;Gold and Chrousos, 2002).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Le-Doux, 2003
• ?Not checked — no full text of the sourcecites Gold and Chrousos, 2002 source

In the paper

“Activity in the broader limbic-thalamo-cortical circuitry also decreases during effective treatment with antidepressant drugs or electroconvulsive therapy (Drevets et al, 2002a(Drevets et al, , 2004a)).”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 2002a source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Drevets et al, 2004a

In the paper

“Convergent results from studies conducted using neuroimaging lesion analysis, and postmortem techniques support models in which the signs and symptoms of depression emanate from dysfunction within an extended visceromotor network that interferes with this system's modulation of emotional behavior (Figure 10).”

In the paper

“For example, neurophysiological activity in the amygdala decreases in rats, monkeys, and/or humans during several antidepressant treatments, including drugs, vagal nerve stimulation, or deep brain stimulation of the anterior capsule, potentially reducing efferent transmission via the ACe (Drevets et al, 2002a;Sheline et al, 2001;Fu et al, 2004;Van Laere et al, 2006;Gerber et al, 1983;Henry et al,”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 2002a source
• ?Not checked — no full text of the sourcecites Sheline et al, 2001 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Fu et al, 2004

In the paper

“In addition, data support the importance of modulating activity within the limbic-cortical-striato-pallido-thalamic circuitry in the treatment of depression.”

In the paper

“We propose more specifically that impaired function within the circuits formed by the medial prefrontal network and anatomically related limbic structures can account for the disturbances of emotional processing, cognitive performance, neurotransmission, autonomic regulation, and neuroendocrine responses associated with mood disorders.”

In the paper

“Notably, in rats Horovitz (1966) observed that injection of antidepressant drugs into the amygdala produced identical effects as lesions of the ACe in animal models used to predict antidepressant drug efficacy.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Horovitz, 1966

In the paper

“Depressed subjects also show exaggerated cortisol responses to stress (Drevets et al, 1999(Drevets et al, , 2002b) )”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 1999 source
• ?Not checked — no full text of the sourcecites Drevets et al, 2002b source

In the paper

“In rats there is a direct projection from the sgACC to the autonomic nuclei in the medulla (Terreberry and Neafsey, 1987);”

What the sources say

• ?Not checked — no full text of the sourcecites Terreberry and Neafsey, 1987 source

In the paper

“Stimulation of the projections from the ACe and BNST in rats increases sympathetic autonomic arousal in rodents, presumably via projections to the lateral hypothalamus, PAG, locus ceruleus, and ponto-medullary reticular formation (Le-Doux, 2003;Gold and Chrousos, 2002).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Le-Doux, 2003
• ?Not checked — no full text of the sourcecites Gold and Chrousos, 2002 source

In the paper

“Mood disorders have been associated with abnormalities of serotonergic, dopaminergic, noradrenergic, cholinergic, glutamatergic, GABAergic, glucocorticoid, and peptidergic function (Drevets et al, 2007;Nestler and Carlezon, 2006;Krystal et al, 2002;Gold et al, 2002).”

What the sources say

• ?Not checked — no full text of the sourcecites Drevets et al, 2007 source
• ?Not checked — no full text of the sourcecites Nestler and Carlezon, 2006 source
• ?Not checked — no full text of the sourcecites Krystal et al, 2002 source

In the paper

“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.”

In the paper

“For example interpersonal psychotherapy can reduce depressive symptoms in MDD, and has been shown to enhance activity in the intrasulcal portion of BA 47 (Brody et al, 2001)”

What the sources say

• ?Not checked — no full text of the sourcecites Brody et al, 2001 source

In the paper

“Finally, the cognitive and behavioral response patterns supporting goal-or reward-directed activity are thought to depend upon PFC inputs to the ventral striatum, which are maintained or 'gated' by projections from the hippocampus (subiculum) to the ventral striatum (Goto and Grace, 2005).”

What the sources say

• ?Not checked — no full text of the sourcecites Goto and Grace, 2005 source

In the paper

“Functional imaging studies in depressed humans indicate that metabolism and blood flow decrease in the sgACC/ ventromedial PFC in response to chronic treatment with antidepressant drugs, vagus nerve stimulation, or deep brain stimulation of the sgACC or anterior capsule (Mayberg et al, 1999(Mayberg et al, , 2005;;Drevets et al, 2002a;Van Laere et al, 2006;Nahas et al, 2007;Conway et al, 2006).”

What the sources say

• ?Not checked — no full text of the sourcecites Mayberg et al, 1999 source
• ?Not checked — no full text of the sourcecites Mayberg et al, 2005 source
• ?Not checked — no full text of the sourcecites Drevets et al, 2002a source

In the paper

“Pathologically elevated amygdala activity during MDE could interfere with cognitive performance and goal-directed behavior to an extent that is maladaptive.”

In the paper