scholarly journals The regulatory effect of Xiaoyao San on glucocorticoid receptors under the condition of chronic stress

2018 ◽  
Vol 64 (6) ◽  
pp. 103 ◽  
Author(s):  
Jiandong Lu ◽  
Lijun Fu ◽  
Guozhong Qin ◽  
Pengliang Shi ◽  
Wenjun Fu
Keyword(s):  
Chronic Stress ◽  
Glucocorticoid Receptors ◽  
Regulatory Effect

scholarly journals Chronic restraint stress impairs cognition via modulating HDAC2 expression

2021 ◽  
Vol 12 (1) ◽  
pp. 154-163
Author(s):  
Jie Wu ◽  
Cui Liu ◽  
Ling Zhang ◽  
Bing He ◽  
Wei-Ping Shi ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hippocampal Neurons ◽  
Restraint Stress ◽  
Glucocorticoid Receptors ◽  
Chronic Restraint Stress ◽  
Akt Signaling Pathway ◽  
Object Recognition Test ◽  
Protein Levels ◽  
Synaptic Functions ◽  
Plus Maze

Abstract Background To investigate the effects of chronic restraint stress on cognition and the probable molecular mechanism in mice. Methods In the current work, a restraining tube was used as a way to induce chronic stress in mice. The protein levels were determined with ELISA and western blot. A series of behavior tests, including the Morris water maze, elevated plus maze, open field test, and novel object recognition test, were also performed to examine the anxiety and the ability of learning and memory. Moreover, murine neuroblastoma N2a cells were used to confirm the findings from mice under chronic stress. Results Decreased synaptic functions were impaired in chronic stress with the downregulation of PSD95, GluR-1, the neurotrophic factor BDNF, and immediate-onset genes Arc and Egr. Chronic restraint decreased the histone acetylation level in hippocampal neurons while HDAC2 was increased and was co-localized with glucocorticoid receptors. Moreover, chronic stress inhibited the PI3K/AKT signaling pathway and induced energy metabolism dysfunctions. Conclusion This work examining the elevated levels of HDAC2 in the hippocampus may provide new insights and targets for drug development for treating many neurodegenerative diseases.

scholarly journals Neuroendocrine Function After Hypothalamic Depletion of Glucocorticoid Receptors in Male and Female Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (8) ◽  
pp. 2843-2853 ◽  
Author(s):  
Matia B. Solomon ◽  
Matthew Loftspring ◽  
Annette D. de Kloet ◽  
Sriparna Ghosal ◽  
Ryan Jankord ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Glucocorticoid Receptors ◽  
Acute Stress ◽  
Feedback Inhibition ◽  
Forced Swim Test ◽  
Feedback Regulation ◽  
Signaling Mechanism ◽  
Cell Groups ◽  
Neuroendocrine Responses

Abstract Glucocorticoids act rapidly at the paraventricular nucleus (PVN) to inhibit stress-excitatory neurons and limit excessive glucocorticoid secretion. The signaling mechanism underlying rapid feedback inhibition remains to be determined. The present study was designed to test the hypothesis that the canonical glucocorticoid receptors (GRs) is required for appropriate hypothalamic-pituitary-adrenal (HPA) axis regulation. Local PVN GR knockdown (KD) was achieved by breeding homozygous floxed GR mice with Sim1-cre recombinase transgenic mice. This genetic approach created mice with a KD of GR primarily confined to hypothalamic cell groups, including the PVN, sparing GR expression in other HPA axis limbic regulatory regions, and the pituitary. There were no differences in circadian nadir and peak corticosterone concentrations between male PVN GR KD mice and male littermate controls. However, reduction of PVN GR increased ACTH and corticosterone responses to acute, but not chronic stress, indicating that PVN GR is critical for limiting neuroendocrine responses to acute stress in males. Loss of PVN GR induced an opposite neuroendocrine phenotype in females, characterized by increased circadian nadir corticosterone levels and suppressed ACTH responses to acute restraint stress, without a concomitant change in corticosterone responses under acute or chronic stress conditions. PVN GR deletion had no effect on depression-like behavior in either sex in the forced swim test. Overall, these findings reveal pronounced sex differences in the PVN GR dependence of acute stress feedback regulation of HPA axis function. In addition, these data further indicate that glucocorticoid control of HPA axis responses after chronic stress operates via a PVN-independent mechanism.

Navigating Alzheimer’s Disease via Chronic Stress: The Role of Glucocorticoids

2020 ◽  
Vol 21 (5) ◽  
pp. 433-444 ◽  
Author(s):  
Vivek Kumar Sharma ◽  
Thakur Gurjeet Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Chronic Stress ◽  
Glucocorticoid Receptors ◽  
Molecular Mechanisms ◽  
Senile Plaques ◽  
Symptomatic Relief ◽  
Therapeutic Interventions ◽  
Physiological Status

Alzheimer’s disease (AD) is a chronic intensifying incurable progressive disease leading to neurological deterioration manifested as impairment of memory and executive brain functioning affecting the physical ability like intellectual brilliance, common sense in patients. The recent therapeutic approach in Alzheimer's disease is only the symptomatic relief further emerging the need for therapeutic strategies to be targeted in managing the underlying silent killing progression of dreaded pathology. Therefore, the current research direction is focused on identifying the molecular mechanisms leading to the evolution of the understanding of the neuropathology of Alzheimer's disease. The resultant saturation in the area of current targets (amyloid β, τ Protein, oxidative stress etc.) has led the scientific community to rethink of the mechanistic neurodegenerative pathways and reprogram the current research directions. Although, the role of stress has been recognized for many years and contributing to the development of cognitive impairment, the area of stress has got the much-needed impetus recently and is being recognized as a modifiable menace for AD. Stress is an unavoidable human experience that can be resolved and normalized but chronic activation of stress pathways unsettle the physiological status. Chronic stress mediated activation of neuroendocrine stimulation is generally linked to a high risk of developing AD. Chronic stress-driven physiological dysregulation and hypercortisolemia intermingle at the neuronal level and leads to functional (hypometabolism, excitotoxicity, inflammation) and anatomical remodeling of the brain architecture (senile plaques, τ tangles, hippocampal atrophy, retraction of spines) ending with severe cognitive deterioration. The present review is an effort to collect the most pertinent evidence that support chronic stress as a realistic and modifiable therapeutic earmark for AD and to advocate glucocorticoid receptors as therapeutic interventions.

Glucocorticoids and the Genesis of Depressive Illness a Psychobiological Model

1994 ◽  
Vol 164 (3) ◽  
pp. 365-371 ◽  
Author(s):  
Timothy G. Dinan
Keyword(s):  
Growth Hormone ◽  
Chronic Stress ◽  
Glucocorticoid Receptors ◽  
Depressive Illness ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Prolactin Release ◽  
Central Neurons ◽  
High Level ◽  
Pituitary Adrenal Axis

Abnormalities in the hypothalamic–pituitary–adrenal axis (HPA) have been the most consistently demonstrated biological markers in depressive illness. Numerous other neuroendocrine disturbances have also been described, including blunted clonidine-induced growth hormone release and blunted fenfluramine-induced prolactin release. These disturbances are generally interpreted in terms of monoaminergic receptor dysfunction. The theory presented here suggests that chronic stress which activates the HPA will in certain susceptible people produce changes in central monoamines. The high level of glucocorticoid receptors on such central neurons is postulated as mediating the alterations. Thus monoamine abnormalities, rather than being a core aetiological feature of depression, are seen as secondary to HPA overdrive.

Cortisol-mediated regulation of uterine artery contractility: effect of chronic hypoxia

2004 ◽  
Vol 286 (2) ◽  
pp. H716-H722 ◽  
Author(s):  
DaLiao Xiao ◽  
XiaoHui Huang ◽  
Soochan Bae ◽  
Charles A. Ducsay ◽  
Lawrence D. Longo ◽  
...  
Keyword(s):  
Blood Flow ◽  
High Altitude ◽  
Chronic Stress ◽  
Uterine Artery ◽  
Vascular Tone ◽  
Glucocorticoid Receptors ◽  
Chronic Hypoxia ◽  
Hydroxysteroid Dehydrogenase ◽  
Uterine Arteries ◽  
Normoxic Control

We previously demonstrated that cortisol regulated α1-adrenoceptor-mediated contractions differentially in nonpregnant and pregnant uterine arteries. Given that chronic hypoxia during pregnancy has profound effects on maternal uterine artery reactivity, the present study investigated the effects of chronic hypoxia on cortisol-mediated regulation of uterine artery contractions. Pregnant ( day 30) and nonpregnant ewes were divided between normoxic control and chronically hypoxic [maintained at high altitude (3,820 m), arterial Po2: 60 mmHg for 110 days] groups. Uterine arteries were isolated and contractions measured. In hypoxic animals, cortisol (10 ng/ml for 24 h) increased norepinephrine-induced contractions in pregnant, but not in nonpregnant, uterine arteries. The 11β-hydroxysteroid dehydrogenase inhibitor carbenoxolone did not change cortisol effects in nonpregnant uterine arteries, but abolished it in pregnant uterine arteries by increasing norepinephrine pD2 (–log EC50) in control tissues. The dissociation constant of norepinephrine-α1-adrenoceptors was not changed by cortisol in nonpregnant, but decreased in pregnant uterine arteries. There were no differences in the density of glucocorticoid receptors between normoxic and hypoxic tissues. Cortisol inhibited the norepinephrine-induced increase in Ca2+ concentrations in nonpregnant arteries, but potentiated it in pregnant arteries. In addition, cortisol attenuated phorbol 12,13-dibutyrate-induced contractions in normoxic nonpregnant and pregnant uterine arteries, but had no effect on the contractions in hypoxic arteries. The results suggest that cortisol differentially regulates α1-adrenoceptor- and PKC-mediated contractions in uterine arteries. Chronic hypoxia suppresses uterine artery sensitivity to cortisol, which may play an important role in the adaptation of uterine vascular tone and blood flow in response to chronic stress of hypoxia during pregnancy.

scholarly journals Analysis of cortisol in dog hair - a potential biomarker of chronic stress: a review

2017 ◽  
Vol 62 (No. 7) ◽  
pp. 363-376 ◽  
Author(s):  
L. Mesarcova ◽  
J. Kottferova ◽  
L. Skurkova ◽  
L. Leskova ◽  
N. Kmecova
Keyword(s):  
Chronic Stress ◽  
Stress Responses ◽  
Glucocorticoid Receptors ◽  
Stress Disorder ◽  
Acute Stress ◽  
Stress Hormones ◽  
Cortisol Concentration ◽  
Non Invasive ◽  
Potential Biomarker ◽  
Different Types

Cortisol, which is produced in the adrenal glands, is an endogenous glucocorticoid hormone that delivers its hormonal message to cells by acting on glucocorticoid receptors. It is one of the main stress hormones responsible for stress responses in animals and humans, and its overproduction is characteristic of certain diseases. While acute stress disorder can be evaluated by means of measuring the cortisol concentration in blood and urine, chronic stress disorder can be detected by monitoring the cortisol concentration in fur or hair. Hair collection is simple, inexpensive and non-invasive, and can be performed easily and rapidly; thus, it appears to be a suitable method for determining the level of stress in dogs from shelters, abused dogs or dogs involved in different types of animal interactions. Since it is a relatively new method, monitoring cortisol in hair or fur requires further research in order to definitively prove its efficacy, and possibly to determine reference range values for different breeds of dogs.

scholarly journals Chronic blockade of hindbrain glucocorticoid receptors reduces blood pressure responses to novel stress and attenuates adaptation to repeated stress

2009 ◽  
Vol 296 (5) ◽  
pp. R1445-R1454 ◽  
Author(s):  
Andrea G. Bechtold ◽  
Gina Patel ◽  
Guenther Hochhaus ◽  
Deborah A. Scheuer
Keyword(s):  
Arterial Pressure ◽  
Chronic Stress ◽  
Restraint Stress ◽  
Glucocorticoid Receptors ◽  
Acute Stress ◽  
Cardiovascular Responses ◽  
Pressure Response ◽  
Repeated Restraint Stress ◽  
Response To Stress ◽  
Corticosterone Response

Exogenous glucocorticoids act within the hindbrain to enhance the arterial pressure response to acute novel stress. Here we tested the hypothesis that endogenous glucocorticoids act at hindbrain glucocorticoid receptors (GR) to augment cardiovascular responses to restraint stress in a model of stress hyperreactivity, the borderline hypertensive rat (BHR). A 3- to 4-mg pellet of the GR antagonist mifepristone (Mif) was implanted over the dorsal hindbrain (DHB) in Wistar-Kyoto (WKY) and BHRs. Control pellets consisted of either sham DHB or subcutaneous Mif pellets. Rats were either subjected to repeated restraint stress (chronic stress) or only handled (acute stress) for 3–4 wk, then all rats were stressed on the final day of the experiment. BHR showed limited adaptation of the arterial pressure response to restraint, and DHB Mif significantly ( P ≤ 0.05) attenuated the arterial pressure response to restraint in both acutely and chronically stressed BHR. In contrast, WKY exhibited a substantial adaptation of the pressure response to repeated restraint that was significantly reversed by DHB Mif. DHB Mif and chronic stress each significantly increased baseline plasma corticosterone concentration and adrenal weight and reduced the corticosterone response to stress in all rats. We conclude that endogenous corticosterone acts via hindbrain GR to enhance the arterial pressure response to stress in BHR, but to promote the adaptation of the arterial pressure response to stress in normotensive rats. Endogenous corticosterone also acts in the hindbrain to restrain corticosterone at rest but to maintain the corticosterone response to stress in both BHR and WKY rats.

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