Corticosteroids and the Control of Function in the Hypothalamo‐Pituitary‐Adrenal (HPA) Axisa

Dallman, Mary F.; Akana, Susan F.; Levin, Nancy; Walker, C.‐D.; Bradbury, Margaret J.; Suemaru, Shuso; Scribner, K S

doi:10.1111/j.1749-6632.1994.tb39206.x

Cited by 180 publications

(80 citation statements)

References 18 publications

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“…GR is known to repress its own synthesis in a hormone-dependent manner (Webster and Cidlowski, 1999). Negative feedback at the level of the pituitary gland to block synthesis and secretion of ACTH by the corticotroph cells occurs by directly inhibiting synthesis of Pomc mRNA (Dallman et al, 1994). No such effect was found in pituitary glands of CGG mice in this study.…”

Section: Discussioncontrasting

confidence: 54%

Altered hypothalamus–pituitary–adrenal gland axis regulation in the expanded CGG-repeat mouse model for fragile X-associated tremor/ataxia syndrome

Brouwer

Severijnen

Jong

et al. 2008

Psychoneuroendocrinology

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The human FMR1 gene contains an unstable CGG-repeat in its 5′ untranslated region. The repeat length in the normal population is polymorphic (5-54 CGG-repeats). Individuals carrying lengths beyond 200 CGGs (i.e. the full mutation) show hypermethylation and as a consequence gene silencing of the FMR1 gene. The absence of the gene product FMRP causes the fragile X syndrome, the most common inherited form of mental retardation. Elderly carriers of the premutation (PM), which is defined as a repeat length between 55-200 CGGs, can develop a progressive neurodegenerative syndrome: fragile X-associated tremor/ataxia syndrome (FXTAS). The high FMR1 mRNA levels observed in cells from PM carriers have led to the hypothesis that FXTAS is caused by a pathogenic RNA gain-of-function mechanism. Apart from tremor/ataxia, specific psychiatric symptoms have been described in PM carriers with or without FXTAS. Since these symptoms could arise from elevated stress hormone levels, we investigated hypothalamicpituitary-adrenal (HPA) axis regulation using a knock-in mouse model with an expanded CGGrepeat in the PM range (>98 repeats) in the Fmr1 gene, which shows repeat instability, and displays biochemical, phenotypic and neuropathological characteristics of FXTAS. We show elevated levels of corticosterone in serum and ubiquitin-positive inclusions in both the pituitary and adrenal gland of 100-week old animals. In addition, we demonstrate ubiquitin-positive © 2008 Elsevier Ltd. All rights reserved. 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 errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Financial disclosuresWe declare no conflict of interest. HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript inclusions in the amygdala from aged expanded CGG-repeat mice. We hypothesize that altered regulation of the HPA axis and the amygdala and higher stress hormone levels in the mouse model for FXTAS may explain associated psychological symptoms in humans.

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Section: Discussioncontrasting

confidence: 54%

Altered hypothalamus–pituitary–adrenal gland axis regulation in the expanded CGG-repeat mouse model for fragile X-associated tremor/ataxia syndrome

Brouwer

Severijnen

Jong

et al. 2008

Psychoneuroendocrinology

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“…Hippocampal lesions likewise increase the duration and peak levels of stress-induced HPA-axis activation and impair negative feedback determined by glucocorticoid administration in rodents (24)(25)(26). Impaired glucocorticoid feedback occurs in stress-related psychiatric disorders (27,28), but evidence for hippocampal regulation of the HPA-axis in humans (29,30) and monkeys (31) is limited to studies previously conducted at baseline in stress-free conditions.…”

Section: Discussionmentioning

confidence: 98%

Preliminary Evidence That Hippocampal Volumes in Monkeys Predict Stress Levels of Adrenocorticotropic Hormone

Lyons

Parker

Zeitzer

et al. 2007

Biological Psychiatry

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“…For example, rapid effects in the hypothalamus are long lasting (Di et al 2003) and thus HPA-axis feedback will be inhibited over a long period of time. Indeed, dexamethasone infusions in the PVN exert both rapid and delayed negative feedback actions on the HPA-axis activity (Dallman et al 1994, Dallman 2005. Similarly, the increased excitability in the BLA starts as a non-genomic MR-dependent phenomenon and eventually evolves into a genomic phenomenon that also requires the GR (Karst et al 2010).…”

Section: Integration Of Non-genomic and Genomic Effectsmentioning

confidence: 99%

Rapid non-genomic effects of corticosteroids and their role in the central stress response

Groeneweg¹,

Karst²,

Kloet³

et al. 2011

Journal of Endocrinology

361

269

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In response to a stressful encounter, the brain activates a comprehensive stress system that engages the organism in an adaptive response to the threatening situation. This stress system acts on multiple peripheral tissues and feeds back to the brain; one of its key players is the family of corticosteroid hormones. Corticosteroids affect brain functioning through both delayed, genomic and rapid, non-genomic mechanisms. The latter mode of action has long been known, but it is only in recent years that the physiological basis in the brain is beginning to be unravelled. We now know that corticosteroids exert rapid, non-genomic effects on the excitability and activation of neurons in (amongst others) the hypothalamus, hippocampus, amygdala and prefrontal cortex. In addition, corticosteroids affect cognition, adaptive behaviour and neuroendocrine output within minutes. Knowledge on the identity of the receptors and secondary pathways mediating the non-genomic effects of corticosteroids on a cellular level is accumulating. Interestingly, in many cases, an essential role for the 'classical' mineralocorticoid and glucocorticoid receptors in a novel membrane-associated mechanism is found. Here, we systematically review the recent literature on non-genomic actions of corticosteroids on neuronal activity and functioning in selected limbic brain targets. Further, we discuss the relevance of these permissive effects for cognition and neuroendocrine control, and the integration of this novel mode of action into the complex balanced pattern of stress effects in the brain.

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Corticosteroids and the Control of Function in the Hypothalamo‐Pituitary‐Adrenal (HPA) Axisa

Cited by 180 publications

References 18 publications

Altered hypothalamus–pituitary–adrenal gland axis regulation in the expanded CGG-repeat mouse model for fragile X-associated tremor/ataxia syndrome

Altered hypothalamus–pituitary–adrenal gland axis regulation in the expanded CGG-repeat mouse model for fragile X-associated tremor/ataxia syndrome

Preliminary Evidence That Hippocampal Volumes in Monkeys Predict Stress Levels of Adrenocorticotropic Hormone

Rapid non-genomic effects of corticosteroids and their role in the central stress response

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