The effects of non-genomic glucocorticoid mechanisms on bodily functions and the central neural system. A critical evaluation of findings

Haller, József; Mikics, Éva; Makara, Gábor B.

doi:10.1016/j.yfrne.2007.10.004

Cited by 185 publications

(119 citation statements)

References 185 publications

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“…Although the classically recognized mode of action of glucocorticoids is to alter gene transcription via direct translocation of ligand-receptor dimer complexes into the nucleus (27), such genomic effects do not seem to account for the rapid onset of corticosterone effects on PKA activity (21). Findings of several studies suggest that some behavioral and physiological effects of glucocorticoids occur too rapidly to be mediated by alterations in gene transcription (28). Emerging evidence indicates that these nongenomic effects of glucocorticoids occur through the activation of G protein-coupled receptors or membrane-associated cytosolic steroid receptors (29)(30)(31).…”

Section: Activation Of a Membrane Steroid Receptor In The Mpfc Impairsmentioning

confidence: 99%

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Barsegyan

Mackenzie

Kurose

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

232

169

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It is well established that acute administration of adrenocortical hormones enhances the consolidation of memories of emotional experiences and, concurrently, impairs working memory. These different glucocorticoid effects on these two memory functions have generally been considered to be independently regulated processes. Here we report that a glucocorticoid receptor agonist administered into the medial prefrontal cortex (mPFC) of male Sprague-Dawley rats both enhances memory consolidation and impairs working memory. Both memory effects are mediated by activation of a membrane-bound steroid receptor and depend on noradrenergic activity within the mPFC to increase levels of cAMPdependent protein kinase. These findings provide direct evidence that glucocorticoid effects on both memory consolidation and working memory share a common neural influence within the mPFC.

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Section: Activation Of a Membrane Steroid Receptor In The Mpfc Impairsmentioning

confidence: 99%

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Barsegyan

Mackenzie

Kurose

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

232

169

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“…Nonetheless, the rapid secretion of cortisol in response to any type of stressor is not in line with the late effects mediated via the genomic signaling pathway (1,5). Several clinical effects of glucocorticoids occur within a few minutes (5), and these observations have led to an increasing number of studies that elucidate rapid glucocorticoid signaling mediated by non-genomic mechanisms (6,7). Non-genomic steroid effects occur within a few minutes, and may be mediated by specific receptors, transporters, other known (non-steroid) membrane receptors, or classical steroid receptor isoforms in non-nuclear locations (8).…”

Section: Introductionmentioning

confidence: 99%

Acute effects of hydrocortisone on the metabolic response to a glucose load: increase in the first-phase insulin secretion

Vila¹,

Krebs²,

Riedl³

et al. 2010

European Journal of Endocrinology

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Background and aim: Several basic science studies support the existence of non-genomic glucocorticoid signaling in pancreas, liver, and adipocytes, but its clinical relevance has not yet been elucidated. This study aimed at investigating the rapid effects of hydrocortisone on the human metabolic response to glucose. Subjects and methods: In a randomized placebo-controlled crossover study, ten healthy men received an i.v. bolus of 0.6 mg/kg hydrocortisone once and placebo once 4 min before the administration of 330 mg/kg glucose. Cortisol, glucose, insulin, C-peptide, ghrelin, and peptide YY (PYY) levels were measured during the following 3 h. Minimal model analysis was performed for evaluating the metabolic response. Results: Hydrocortisone attenuated the rise in plasma glucose during the initial 15 min following glucose administration (PZ0.039), and it led to lower glucose levels during the first 2 h (PZ0.017). This was accompanied by enhanced circulating insulin (PZ0.02) and C-peptide (PZ0.03) levels during the initial 15 min, and a 35% increase in the first-phase b-cell function (PZ0.003). Hydrocortisone decreased PYY concentrations during the initial 30 min (PZ0.014), but it did not affect the ghrelin response to glucose. Conclusion: One i.v. bolus of hydrocortisone induces rapid effects on carbohydrate metabolism increasing the first-phase b-cell function. The modulation of PYY plasma levels suggests the possible non-genomic effects of glucocorticoids on appetite-regulatory hormones.

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“…Finally, glucocorticoids may also act via mechanisms that do not involve transcriptional regulation. These so-called non-genomic effects are still poorly understood (reviewed in [86]). …”

Section: Rhythms Of Glucocorticoidsmentioning

confidence: 99%

Glucocorticoids and circadian clock control of cell proliferation: At the interface between three dynamic systems

Dickmeis

Foulkes

2011

Molecular and Cellular Endocrinology

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The circadian clock, an endogenous timekeeper that regulates daily rhythms of physiology, also influences the dynamic release of glucocorticoids. The release of glucocorticoids is characteristically pulsatile and is further modulated in a circadian fashion. A circadian pacemaker in the brain regulates daily rhythms of hypothalamicpituitary-adrenal axis and autonomic nervous system activity that both influence glucocorticoid release from the adrenal gland. This systemic regulation interacts with rhythms in the adrenal gland itself that are driven by its own circadian clock. One function of glucocorticoids is the regulation of cell proliferation. Depending on the tissue, this can involve both negative and positive regulation of a variety of processes, including cell differentiation and cell death. Cell proliferation is also under circadian control, and recent evidence suggests that this regulation may involve glucocorticoid signalling. Here, we review the dynamic processes participating in the interplay between the circadian clock, glucocorticoids and cell proliferation, and we discuss the potential implications for therapy.

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The effects of non-genomic glucocorticoid mechanisms on bodily functions and the central neural system. A critical evaluation of findings

Cited by 185 publications

References 185 publications

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Acute effects of hydrocortisone on the metabolic response to a glucose load: increase in the first-phase insulin secretion

Glucocorticoids and circadian clock control of cell proliferation: At the interface between three dynamic systems

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