Maternal Care, Hippocampal Glucocorticoid Receptors, and Hypothalamic–Pituitary–Adrenal Responses to Stress

2002 ◽  
Keyword(s):  
Maternal Care ◽  
Glucocorticoid Receptors ◽  
Hypothalamic Pituitary Adrenal

scholarly journals Dream Recall/Affect and the Hypothalamic–Pituitary–Adrenal Axis

2021 ◽  
Vol 3 (3) ◽  
pp. 403-408
Author(s):  
Athanasios Tselebis ◽  
Emmanouil Zoumakis ◽  
Ioannis Ilias
Keyword(s):  
Hpa Axis ◽  
Glucocorticoid Receptors ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Free Form ◽  
Dream Recall ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Concise Review ◽  
Pathological Conditions ◽  
Pituitary Adrenal Axis

In this concise review, we present an overview of research on dream recall/affect and of the hypothalamic–pituitary–adrenal (HPA) axis, discussing caveats regarding the action of hormones of the HPA axis (mainly cortisol and its free form, cortisol-binding globulin and glucocorticoid receptors). We present results of studies regarding dream recall/affect and the HPA axis under physiological (such as waking) or pathological conditions (such as in Cushing’s syndrome or stressful situations). Finally, we try to integrate the effect of the current COVID-19 situation with dream recall/affect vis-à-vis the HPA axis.

scholarly journals From Receptor Balance to Rational Glucocorticoid Therapy

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 2754-2769 ◽  
Author(s):  
E. Ron de Kloet
Keyword(s):  
Glucocorticoid Receptors ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Memory Storage ◽  
Glucocorticoid Therapy ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Stress Experience ◽  
Stressful Experience ◽  
Appraisal Processes ◽  
Pituitary Adrenal Axis

Corticosteroids secreted as end product of the hypothalamic-pituitary-adrenal axis act like a double-edged sword in the brain. The hormones coordinate appraisal processes and decision making during the initial phase of a stressful experience and promote subsequently cognitive performance underlying the management of stress adaptation. This action exerted by the steroids on the initiation and termination of the stress response is mediated by 2 related receptor systems: mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs). The receptor types are unevenly distributed but colocalized in abundance in neurons of the limbic brain to enable these complementary hormone actions. This contribution starts from a historical perspective with the observation that phasic occupancy of GR during ultradian rhythmicity is needed to maintain responsiveness to corticosteroids. Then, during stress, initially MR activation enhances excitability of limbic networks that are engaged in appraisal and emotion regulation. Next, the rising hormone concentration occupies GR, resulting in reallocation of energy to limbic-cortical circuits with a role in behavioral adaptation and memory storage. Upon MR:GR imbalance, dysregulation of the hypothalamic-pituitary-adrenal axis occurs, which can enhance an individual's vulnerability. Imbalance is characteristic for chronic stress experience and depression but also occurs during exposure to synthetic glucocorticoids. Hence, glucocorticoid psychopathology may develop in susceptible individuals because of suppression of ultradian/circadian rhythmicity and depletion of endogenous corticosterone from brain MR. This knowledge generated from testing the balance hypothesis can be translated to a rational glucocorticoid therapy.

scholarly journals Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

2004 ◽  
Vol 181 (2) ◽  
pp. 207-221 ◽  
Author(s):  
JI Webster ◽  
EM Sternberg
Keyword(s):  
Mortality Rate ◽  
Hpa Axis ◽  
Glucocorticoid Receptors ◽  
Viral Infections ◽  
Lethal Effects ◽  
Hypothalamic Pituitary Adrenal ◽  
Glucocorticoid Response ◽  
Pituitary Adrenal Axis ◽  
Synthetic Glucocorticoid

The hypothalamic-pituitary-adrenal (HPA) axis is activated during many bacterial and viral infections, resulting in an increase in circulating glucocorticoid levels. This HPA axis activation and glucocorticoid response are critical for the survival of the host, as demonstrated by the fact that removal of the HPA axis (by adrenalectomy or hypophysectomy) or glucocorticoid receptor (GR) blockade enhances the severity of the infection and in some cases enhances the mortality rate. Replacement with a synthetic glucocorticoid reverses these effects by reducing the severity of the infection and provides protection against lethal effects. In addition, some bacteria and viral infections have been shown to affect the GR directly. These have been described and the implications of such an effect discussed.

scholarly journals Future therapeutic targets in mood disorders: the glucocorticoid receptor

2000 ◽  
Vol 177 (5) ◽  
pp. 390-395 ◽  
Author(s):  
Richard McQuade ◽  
Allan H. Young
Keyword(s):  
Glucocorticoid Receptor ◽  
Mood Disorders ◽  
Hpa Axis ◽  
Negative Feedback ◽  
Clinical Studies ◽  
Glucocorticoid Receptors ◽  
Therapeutic Targets ◽  
Feedback Mechanism ◽  
Hypothalamic Pituitary Adrenal ◽  
Negative Feedback Mechanism

BackgroundThe hypercortisolaemia and dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis associated with mood disorders have been attributed to a breakdown in the glucocorticoid-receptor-mediated negative feedback mechanism regulating HPA activity. Reinstating normal feedback may be therapeutic in mood disorders.AimsTo review the evidence for the involvement of the glucocorticoid receptor in the pathogenesis and treatment of mood disorders.MethodMedline and hand searches were carried out, selecting literature relevant to psychiatrists and psychopharmacologists.ResultsA dysfunction in glucocorticoid receptors is integral to the HPA abnormalities of mood disorders. Antidepressant and mood-stabilising drugs can up-regulate glucocorticoid receptors, restoring glucocorticoid function. Preliminary clinical studies targeting the glucocorticoid receptor are encouraging.ConclusionsDrugs designed specifically to up-regulate glucocorticoid receptors may be integral to future strategies in treating mood disorders.

Regulation of 11β-hydroxysteroid dehydrogenase activity by the hypothalamic-pituitary-adrenal axis in the rat

1994 ◽  
Vol 141 (3) ◽  
pp. 467-472 ◽  
Author(s):  
B R Walker ◽  
B C Williams ◽  
C R W Edwards
Keyword(s):  
Enzyme Activity ◽  
Glucocorticoid Receptors ◽  
Renal Cortex ◽  
Hydroxysteroid Dehydrogenase ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
High Dose ◽  
Rat Tissues ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Pituitary Adrenal Axis

Abstract 11β-Hydroxysteroid dehydrogenase (11β-OHSD) inactivates glucocorticoids and thereby modulates their access to both mineralocorticoid and glucocorticoid receptors. Since 11β-OHSD activity influences the biological responses of the hypothalamic-pituitary-adrenal axis, it might be regulated by components of this axis. We examined 11β-OHSD activity in adrenalectomized rats treated for 9 days with dexamethasone and with or without ACTH. Adrenalectomy and low-dose (2 μg/day) dexamethasone had no effect on 11β-OHSD activity in renal cortex, hippocampus or heart, and reduced enzyme activity in aorta. High-dose dexamethasone (50 μg/day) had no effect in renal cortex but increased enzyme activity by at least 50% in all other sites. This effect of dexamethasone was unaffected by the co-administration of ACTH. We also examined the metabolism of dexamethasone by 11β-OHSD in homogenized rat tissues. Only in kidney, in the presence of NAD rather than NADP, was dexamethasone converted to a more polar metabolite previously identified as 11-dehydrodexamethasone. We conclude that: dexamethasone induction of 11β-OHSD is tissue-specific, and includes vascular tissues and hippocampus but not kidney; this tissue-specificity may be explained by contrasting metabolism of dexamethasone by the isoforms of 11β-OHSD; fluctuations of glucocorticoid levels within the physiological range may not have a biologically significant effect on 11β-OHSD activity; and the inhibitory effect of ACTH, observed previously in humans, is likely to depend on the presence of intact adrenal glands. Journal of Endocrinology (1994) 141, 467–472

scholarly journals Deprivation of maternal care has long-lasting consequences for the hypothalamic–pituitary–adrenal axis of zebra finches

2011 ◽  
Vol 279 (1729) ◽  
pp. 759-766 ◽  
Author(s):  
Sunayana B. Banerjee ◽  
Adam S. Arterbery ◽  
Daniel J. Fergus ◽  
Elizabeth Adkins-Regan
Keyword(s):  
Maternal Care ◽  
Life Stress ◽  
Paternal Care ◽  
Mammalian Species ◽  
Early Life Stress ◽  
Mrna Levels ◽  
Hypothalamic Pituitary Adrenal ◽  
Stress Responsiveness ◽  
Pituitary Adrenal Axis ◽  
Hpa Function

Early-life stress caused by the deprivation of maternal care has been shown to have long-lasting effects on the hypothalamic–pituitary–adrenal (HPA) axis in offspring of uniparental mammalian species. We asked if deprivation of maternal care in biparental species alters stress responsiveness of offspring, using a biparental avian species—the zebra finch, Taeniopygia guttata . In our experiment, one group of birds was raised by both male and female parents (control), and another was raised by males alone (maternally deprived). During adulthood, offspring of both groups were subjected to two stressors (restraint and isolation), and corticosterone concentrations were measured. Additionally, we measured baseline levels of the two corticosteroid receptors—glucocorticoid receptor (GR) and mineralocorticoid receptor (MR)—in the hippocampus, hypothalamus and cerebellum. Our results suggest that maternally deprived offspring are hyper-responsive to isolation in comparison with controls. Furthermore, mRNA levels of both GR and MR receptors are altered in maternally deprived offspring in comparison with controls. Thus, absence of maternal care has lasting consequences for HPA function in a biparental species where paternal care is available.

scholarly journals HIV-1 Tat Dysregulates the Hypothalamic-Pituitary-Adrenal Stress Axis and Potentiates Oxycodone-Mediated Psychomotor and Anxiety-Like Behavior of Male Mice

2020 ◽  
Vol 21 (21) ◽  
pp. 8212
Author(s):  
Mohammed F. Salahuddin ◽  
Fakhri Mahdi ◽  
Jason J. Paris
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Glucocorticoid Receptors ◽  
Regulatory Protein ◽  
Stress Axis ◽  
Male Mice ◽  
Hiv Patients ◽  
Hypothalamic Pituitary Adrenal ◽  
Pharmacological Blockade ◽  
Hiv 1

Human immunodeficiency virus (HIV) is associated with co-morbid affective and stress-sensitive neuropsychiatric disorders that may be related to dysfunction of the hypothalamic-pituitary-adrenal (HPA) stress axis. The HPA axis is perturbed in up to 46% of HIV patients, but the mechanisms are not known. The neurotoxic HIV-1 regulatory protein, trans-activator of transcription (Tat), may contribute. We hypothesized that HPA dysregulation may contribute to Tat-mediated interactions with oxycodone, a clinically-used opioid often prescribed to HIV patients. In transgenic male mice, Tat expression produced significantly higher basal corticosterone levels with adrenal insufficiency in response to a natural stressor or pharmacological blockade of HPA feedback, recapitulating the clinical phenotype. On acute exposure, HIV-1 Tat interacted with oxycodone to potentiate psychomotor and anxiety like-behavior in an open field and light-dark transition tasks, whereas repeated exposure sensitized stress-related psychomotor behavior and the HPA stress response. Pharmacological blockade of glucocorticoid receptors (GR) partially-restored the stress response and decreased oxycodone-mediated psychomotor behavior in Tat-expressing mice, implicating GR in these effects. Blocking corticotrophin-releasing factor (CRF) receptors reduced anxiety-like behavior in mice that were exposed to oxycodone. Together, these effects support the notion that Tat exposure can dysregulate the HPA axis, potentially raising vulnerability to stress-related substance use and affective disorders.

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