Corticosteroid status influences the volume of the rat cingulate cortex – a magnetic resonance imaging study

Cerqueira, João José; Catania, Caterina; Sotiropoulos, Ioannis; Schubert, Mirjam; Kalisch, Raffaël; Almeida, Osborne F. X.; Auer, Dorothee P.; Sousa, Nuno

doi:10.1016/j.jpsychires.2005.01.003

Cited by 105 publications

(74 citation statements)

References 53 publications

(56 reference statements)

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“…In line with this hypothesis, a study of ACC volume in adults has shown an inverse correlation with number of stressful or traumatic adverse childhood events (50). There is also a mechanism in place to explain how environmental stressors may alter ACC anatomy; stress induces the release of glucocorticoids, which have been shown to mediate structural alterations of the medial prefrontal cortex (51)(52)(53). It is possible that these structural changes reflect a shift in the activity of neural systems that acts to favor increased vigilance and heightened reactivity to negative emotional stimuli.…”

Section: Discussionmentioning

confidence: 94%

Rostral Anterior Cingulate Cortex Volume Correlates with Depressed Mood in Normal Healthy Children

Boes¹,

McCormick²,

Coryell³

et al. 2008

Biological Psychiatry

134

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BACKGROUND-The rostral anterior cingulate cortex (rACC) has been implicated as a structural neural correlate of familial major depressive disorder, raising the possibility that the structure of this region may act as a biologic marker of depression vulnerability. The aim of the current study was to determine whether children and adolescents with depressive symptoms have lower rACC volume relative to those without symptoms and examine how a positive family history of depression affects this relationship.

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Section: Discussionmentioning

confidence: 94%

Rostral Anterior Cingulate Cortex Volume Correlates with Depressed Mood in Normal Healthy Children

Boes¹,

McCormick²,

Coryell³

et al. 2008

Biological Psychiatry

134

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“…Both stress and GC can induce neurodegenerative changes in the hippocampus and PFC. 23,[40][41][42][43][44][45] These brain regions express GRs; 46 they are important for cognition and are affected early in the development of AD. 47 Clinical reports of hypercortisolism in a significant number of AD patients 18,19 suggest a causal role for GC in AD, a view supported by studies in laboratory rodents that have shown that GC participate in the regulation of APP levels.…”

Section: Discussionmentioning

confidence: 99%

The amyloidogenic potential and behavioral correlates of stress

et al. 2007

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Observations of elevated basal cortisol levels in Alzheimer's disease (AD) patients prompted the hypothesis that stress and glucocorticoids (GC) may contribute to the development and/or maintenance of AD. Consistent with that hypothesis, we show that stress and GC provoke misprocessing of amyloid precursor peptide in the rat hippocampus and prefrontal cortex, resulting in increased levels of the peptide C-terminal fragment 99 (C99), whose further proteolytic cleavage results in the generation of amyloid-b (Ab). We also show that exogenous Ab can reproduce the effects of stress and GC on C99 production and that a history of stress strikingly potentiates the C99-inducing effects of Ab and GC. Previous work has indicated a role for Ab in disruption of synaptic function and cognitive behaviors, and AD patients reportedly show signs of heightened anxiety. Here, behavioral analysis revealed that like stress and GC, Ab administration causes spatial memory deficits that are exacerbated by stress and GC; additionally, Ab, stress and GC induced a state of hyperanxiety. Given that the intrinsic properties of C99 and Ab include neuroendangerment and behavioral impairment, our findings suggest a causal role for stress and GC in the etiopathogenesis of AD, and demonstrate that stressful life events and GC therapy can have a cumulative impact on the course of AD development and progression.

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“…Please note that during the production process errorsmaybe discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Cerqueira et al, 2005a, Cerqueira et al, 2005b. …”

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confidence: 99%

“…dexamethasone (DEX) reduces anterior cingulate cortex volume through dendritic atrophy (Cerqueira et al, 2005a, Cerqueira et al, 2005b.…”

mentioning

confidence: 99%

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex

Sandau

Handa

2007

Neuroscience

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Neonatal administration of the synthetic glucocorticoid, dexamethasone (DEX) retards brain growth, alters adult behaviors and induces cell death in the rat brain, thereby implicating glucocorticoids as developmentally neuroendangering compounds. Glucocorticoids also increase expression of proapoptotic Bcl-2 family members and exacerbate expression of hypoxic responsive genes. Bnip3 is a pro-apoptotic Bcl-2 family member that is upregulated in response to hypoxia. In these studies, we investigated the interactions of glucocorticoid receptor and hypoxia in the regulation of Bnip3 mRNA in cortical neurons. Using quantitative real time RT-PCR, we found that DEX treatment of postnatal day 4-6 rat pups caused a significant increase in Bnip3 mRNA expression compared to vehicle controls. A significant increase in Bnip3 mRNA was also measured in primary cortical neurons 72 hours after treatment with RU28362, a glucocorticoid receptor selective agonist. In primary cortical neurons, hypoxia increased Bnip3 mRNA expression and this was exacerbated with RU28362 treatment. To elucidate the mechanism of glucocorticoid and hypoxia mediated regulation of Bnip3 transcription, a Bnip3 promoter -luciferase reporter construct was utilized in primary cortical neurons. Upregulation of the Bnip3 promoter was mediated by a single glucocorticoid response element and a hypoxic response element. Bnip3 overexpression in primary cortical neurons significantly increased cell death, which is dependent on the Bnip3 transmembrane domain. However, despite the increased expression of Bnip3 following glucocorticoid and hypoxia treatment, corresponding decreases in cell survival were minimal. These studies identify a novel pathway in the developing cortex through which glucocorticoids may enhance a metabolic insult, such as hypoxia. KeywordsBcl-2; glucocorticoid receptor; dexamethasone; primary cortical neurons; postnatal; apoptosis Corticosterone, the endogenous glucocorticoid secreted by the rat adrenal gland, binds with high affinity to two different receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) (Reagan and McEwen, 1997). MR activation is associated with a neuroprotective phenotype (Almeida et al., 2000), whereas GR activation is implicated in the induction of an endangered neural phenotype (Sapolsky et al., 1986, Reagan andMcEwen, 1997). For example, in the adult, GR activation by the synthetic glucocorticoid Name and address of corresponding author: Robert J. Handa, Colorado State University, Department of Biomedical Sciences, W103 Anatomy, 1617 Campus Delivery, Fort Collins, CO 80523-1617, Phone: (970) Facsimile: (970) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process er...

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Corticosteroid status influences the volume of the rat cingulate cortex – a magnetic resonance imaging study

Cited by 105 publications

References 53 publications

Rostral Anterior Cingulate Cortex Volume Correlates with Depressed Mood in Normal Healthy Children

Rostral Anterior Cingulate Cortex Volume Correlates with Depressed Mood in Normal Healthy Children

The amyloidogenic potential and behavioral correlates of stress

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex

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