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

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.

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 2754-2769 ◽  
Author(s):  
E. Ron de Kloet

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.


Endocrinology ◽  
2009 ◽  
Vol 150 (2) ◽  
pp. 749-761 ◽  
Author(s):  
Marc S. Weinberg ◽  
Aadra P. Bhatt ◽  
Milena Girotti ◽  
Cher V. Masini ◽  
Heidi E. W. Day ◽  
...  

Repeated exposure to a moderately intense stressor typically produces attenuation of the hypothalamic-pituitary-adrenal (HPA) axis response (habituation) on re-presentation of the same stressor; however, if a novel stressor is presented to the same animals, the HPA axis response may be augmented (sensitization). The extent to which this adaptation is also evident within neural activity patterns is unknown. This study tested whether repeated ferret odor (FO) exposure, a moderately intense psychological stressor for rats, leads to both same-stressor habituation and novel-stressor sensitization of the HPA axis response and neuronal activity as determined by immediate early gene induction (c-fos mRNA). Rats were presented with FO in their home cages for 30 min a day for up to 2 wk and subsequently challenged with FO or restraint. Rats displayed HPA axis activity habituation and widespread habituation of c-fos mRNA expression (in situ hybridization) throughout the brain in as few as three repeated presentations of FO. However, repeated FO exposure led to a more gradual development of sensitized HPA-axis and c-fos mRNA responses to restraint that were not fully evident until after 14 d of prior FO exposure. The sensitized response was evident in many of the same brain regions that displayed habituation, including primary sensory cortices and the prefrontal cortex. The shared spatial expression but distinct temporal development of habituation and sensitization neural response patterns suggests two independent processes with opposing influences across overlapping brain systems. Repeated exposure of rats to ferret odor leads to rapid development of stimulus-specific habituation and slower development of novel-stressor sensitization of forebrain and hypothalamic-pituitary-adrenal axis activity.


1983 ◽  
Vol 76 (6) ◽  
pp. 452-457 ◽  
Author(s):  
M A Byron ◽  
J Jackson ◽  
B M Ansell

Linear growth was recorded in 36 children with juvenile chronic arthritis. In 20, the hypothalamic-pituitary-adrenal axis (HPA axis) was assessed by insulin-induced hypoglycaemia, the results of which correlated well with resting Cortisol levels. Three groups were identified according to type of corticosteroid regimen administered. Group 1 (6 children), receiving daily corticosteroid therapy, were clearly suppressed and failing to grow. Group 2 (13 children) had received an alternate-day regimen from the initiation of corticosteroid therapy; they were not suppressed and growth was satisfactory in 11. Group 3 (17 children) were receiving alternate-day therapy, but had had daily corticosteroid in the past; they showed no clear pattern of suppression or growth. Factors influencing the recovery of the HPA axis and resumption of growth were assessed. No difference was found in the individual growth of 7 children who commenced alternate-day therapy before the age of 5, compared with matched controls. It is suggested that daily divided doses of corticosteroid should not be used. Ideally, a single morning dose (up to 2 mg/kg) alternate-day regimen should be employed, as this regimen has minimal effects on HPA function and growth, even in young children. For very severe systemic features, it may be necessary to add a small single dose on the alternate day.


2012 ◽  
Vol 1 (4) ◽  
pp. 199-207 ◽  
Author(s):  
Femke Rutters ◽  
Susanne La Fleur ◽  
Sofie Lemmens ◽  
Jurriaan Born ◽  
Mieke Martens ◽  
...  

1994 ◽  
Vol 130 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Hiroo Imura ◽  
Jun-ichi Fukata

Imura H, Fukata J. Endocrine–paracrine interaction in communication between the immune and endocrine systems. Activation of the hypothalamic-pituitary-adrenal axis in inflammation. Eur J Endocrinol 1994;130:32–7. ISSN 0804–4643 There are bidirectional communications between the immune and endocrine systems. Cytokines produced in inflammatory foci cause changes in the endocrine system, including activation of the hypothalamic-pituitary-adrenal (HPA) axis. Hormones produced in the endocrine system, especially glucocorticoids, affect the immune system to modulate its function. This is an important endocrine system for the defence mechanism. In addition, bacterial lipopolysaccharide produces cytokines in the brain and endocrine organs which are considered to act through the paracrine mechanism to regulate the HPA axis. Endocrine–paracrine interaction is important for the defence mechanism of the organism. Hiroo Imura, Kyoto University School of Medicine, Yoshida Honmachi Sakyo-ku, Kyoto 606-01, Japan


1994 ◽  
Vol 141 (3) ◽  
pp. 467-472 ◽  
Author(s):  
B R Walker ◽  
B C Williams ◽  
C R W Edwards

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


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