Regulation of the HPA Axis by Acute and Chronic Stress

2010 ◽  
pp. 149-153 ◽  
Author(s):  
J.P. Herman
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Acute And Chronic Stress

scholarly journals Facilitation of the HPA Axis to a Novel Acute Stress Following Chronic Stress Exposure Modulates Histone Acetylation and the ERK/MAPK Pathway in the Dentate Gyrus of Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 2942-2952 ◽  
Author(s):  
Chantelle L. Ferland ◽  
Erin P. Harris ◽  
Mai Lam ◽  
Laura A. Schrader
Keyword(s):  
Dentate Gyrus ◽  
Histone Acetylation ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Acute Stress ◽  
Male Rats ◽  
Stress Exposure ◽  
Erk Activation ◽  
Acute And Chronic Stress ◽  
Acute Stressor

Evidence suggests that when presented with novel acute stress, animals previously exposed to chronic homotypic or heterotypic stressors exhibit normal or enhanced hypothalamic-pituitary-adrenal (HPA) response compared with animals exposed solely to that acute stressor. The molecular mechanisms involved in this effect remain unknown. The extracellular signal-regulated kinase (ERK) is one of the key pathways regulated in the hippocampus in both acute and chronic stress. The aim of this study was to examine the interaction of prior chronic stress, using the chronic variable stress model (CVS), with exposure to a novel acute stressor (2,5-dihydro-2,4,5-trimethyl thiazoline; TMT) on ERK activation, expression of the downstream protein BCL-2, and the glucocorticoid receptor co-chaperone BAG-1 in control and chronically stressed male rats. TMT exposure after chronic stress resulted in a significant interaction of chronic and acute stress in all 3 hippocampus subregions on ERK activation and BCL-2 expression. Significantly, acute stress increased ERK activation, BCL-2 and BAG-1 protein expression in the dentate gyrus (DG) of CVS-treated rats compared with control, CVS-treated alone, and TMT-only animals. Furthermore, CVS significantly increased ERK activation in medial prefrontal cortex, but acute stress had no significant effect. Inhibition of corticosterone synthesis with metyrapone had no significant effect on ERK activation in the hippocampus; therefore, glucocorticoids alone do not mediate the molecular effects. Finally, because post-translational modifications of histones are believed to play an important role in the stress response, we examined changes in histone acetylation. We found that, in general, chronic stress decreased K12H4 acetylation, whereas acute stress increased acetylation. These results indicate a molecular mechanism by which chronic stress-induced HPA axis plasticity can lead to neurochemical alterations in the hippocampus that influence reactivity to subsequent stress exposure. This may represent an important site of dysfunction that contributes to stress-induced pathology such as depression, anxiety disorders, and posttraumatic stress disorder.

scholarly journals The Anteroventral Bed Nucleus of the Stria Terminalis Differentially Regulates Hypothalamic-Pituitary-Adrenocortical Axis Responses to Acute and Chronic Stress

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 818-826 ◽  
Author(s):  
Dennis C. Choi ◽  
Nathan K. Evanson ◽  
Amy R. Furay ◽  
Yvonne M. Ulrich-Lai ◽  
Michelle M. Ostrander ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Restraint Stress ◽  
Body Weight Gain ◽  
Stria Terminalis ◽  
Thymic Involution ◽  
Bed Nucleus ◽  
Acute And Chronic Stress

The anteroventral region of the bed nucleus of the stria terminalis (BST) stimulates hypothalamic-pituitary-adrenocortical (HPA) axis responses to acute stress. However, the role of the anterior BST nuclei in chronic drive of the HPA axis has yet to be established. Therefore, this study tests the role of the anteroventral BST in physiological responses to chronic drive, using a chronic variable stress (CVS) model. Male Sprague-Dawley rats received either bilateral ibotenate lesions, targeting the anteroventral BST, or vehicle injection into the same region. Half of the lesion and control rats were exposed to a 14-d CVS paradigm consisting of twice-daily exposure to unpredictable, alternating stressors. The remaining rats were nonhandled control animals that remained in home cages. On the morning after the end of CVS exposure, all rats were exposed to a novel restraint stress challenge. CVS induced attenuated body weight gain, adrenal hypertrophy, thymic involution, and enhanced CRH mRNA in hypophysiotrophic neurons of the hypothalamic paraventricular nucleus, none of which were affected by anteroventral BST lesions. In the absence of CVS, lesions attenuated the plasma corticosterone and paraventricular nucleus c-fos mRNA responses to the acute restraint stress. In contrast, lesions of the anteroventral BST elevated plasma ACTH and corticosterone responses to novel restraint in the rats previously exposed to CVS. These data suggest that the anterior BST plays very different roles in integrating acute stimulation and chronic drive of the HPA axis, perhaps mediated by chronic stress-induced recruitment of distinct BST cell groups or functional reorganization of stress-integrative circuits.

HPA-axis multilocus genetic variation moderates associations between environmental stress and depressive symptoms among adolescents

2018 ◽  
Vol 31 (04) ◽  
pp. 1339-1352 ◽  
Author(s):  
Lisa R. Starr ◽  
Meghan Huang
Keyword(s):  
Genetic Variation ◽  
Depressive Symptoms ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Acute Stress ◽  
Childhood Adversity ◽  
Genetic Profile ◽  
Acute And Chronic Stress ◽  
Adolescent Depressive Symptoms ◽  
Gene Environment

AbstractResearch suggests that genetic variants linked to hypothalamic-pituitary-adrenal (HPA)-axis functioning moderate the association between environmental stressors and depression, but examining gene–environment interactions with single polymorphisms limits power. The current study used a multilocus genetic profile score (MGPS) approach to measuring HPA-axis–related genetic variation and examined interactions with acute stress, chronic stress, and childhood adversity (assessed using contextual threat interview methods) with depressive symptoms as outcomes in an adolescent sample (ages 14–17, N = 241; White subsample n = 192). Additive MGPSs were calculated using 10 single nucleotide polymorphisms within HPA-axis genes (CRHR1, NR3C2, NR3C1, FKBP5). Higher MGPS directly correlated with adolescent depressive symptoms. Moreover, MGPS predicted stronger associations between acute and chronic stress and adolescent depressive symptoms and also moderated the effect of interpersonal, but not noninterpersonal, childhood adversity. Gene–environment interactions individually accounted for 5%–8% of depressive symptom variation. All results were retained following multiple test correction and stratification by race. Results suggest that using MGPSs provides substantial power to examine gene–environmental interactions linked to affective outcomes among adolescents.

scholarly journals Steroid Receptor Coactivator-1-Deficient Mice Exhibit Altered Hypothalamic-Pituitary-Adrenal Axis Function

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1322-1332 ◽  
Author(s):  
Jonathon N. Winnay ◽  
Jianming Xu ◽  
Bert W. O’Malley ◽  
Gary D. Hammer
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Feedback Inhibition ◽  
Steroid Receptor ◽  
Serum Glucose ◽  
Compensatory Mechanism ◽  
Hypothalamic Pituitary Adrenal ◽  
Steroid Receptor Coactivator ◽  
Acute And Chronic Stress

Steroidogenic factor-1 (SF-1), has emerged as a critical nuclear receptor regulating development and differentiation at several levels of the hypothalamic-pituitary-steroidogenic axis. Although many coregulatory factors have been shown to physically and functionally interact with SF-1, the relative importance of these interactions in SF-1 target tissues has not been thoroughly established. In this study we assessed roles of steroid receptor coactivator-1 (SRC-1) in hypothalamic-pituitary-adrenal (HPA) axis function using SRC-1-deficient (SRC-1−/−) mice in the absence or presence of SF-1 haploinsufficiency. Surprisingly, SRC-1 deficiency did not alter baseline HPA axis function or the acute rise in corticosterone after ACTH administration and failed to exacerbate adrenocortical dysfunction in SF-1+/− mice. However, after exposure to paradigms of acute and chronic stress, SRC-1−/− mice exhibited an elevation in serum corticosterone despite normal (nonsuppressed) ACTH, suggesting an increase in adrenal sensitivity as well as a concomitant defect in glucocorticoid-mediated feedback inhibition of the HPA axis. An examination of potential compensatory mechanism(s) revealed an increase in adrenal weight, selective elevation of melanocortin 2 receptor mRNA, and a coincident increase in SRC-2 and SRC-3 expression in SRC-1−/− adrenals. A reduction in blood glucose was observed in SRC-1−/− mice after chronic stress, consistent with a generalized state of glucocorticoid resistance. Dexamethasone suppression tests confirmed a weakened ability of glucocorticoids to 1) elevate serum glucose levels and induce hepatic phosphoenolpyruvate carboxykinase transcription and 2) suppress pituitary proopiomelanocortin transcript levels in SRC-1−/− animals. Collectively, these data are consistent with an indispensable role for SRC-1 in mediating actions of glucocorticoids in pituitary and liver.

The HPA and immune axes in stress: the involvement of the serotonergic system

2005 ◽  
Vol 20 (S3) ◽  
pp. S302-S306 ◽  
Author(s):  
B.E. Leonard
Keyword(s):  
Stress Response ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Feedback Inhibition ◽  
Critical Role ◽  
Serotonergic System ◽  
Anxiety And Depression ◽  
Acute And Chronic Stress ◽  
The Impact ◽  
The Brain

AbstractThe impact of acute and chronic stress on the hypothalamic-pituitary-adrenal (HPA) axis is reviewed and evidence presented that corticotrophin releasing factor (CRF) is the stress neurotransmitter which plays an important role in the activation of the central sympathetic and serotonergic systems. The activity of CRF is expressed through specific receptors (CRF 1 and 2) that are antagonistic in their actions and widely distributed in the limbic regions of the brain, as well as in the hypothalamus, and on immune cells.The mechanism whereby chronic stress, via the CRF induced activation of the dorsal raphe nucleus, can induce a change in the serotonergic system, involves an increase in the 5HT2A and a decrease in the 5HT1A receptor mediated function. Such changes contribute to the onset of anxiety and depression. In addition, the hypersecretion of glucocorticoids that is associated with chronic stress and depression desensitises the central glucocorticoid receptors to the negative feedback inhibition of the HPA axis. This indirectly results in the further activation of the HPA axis.The rise in pro-inflammatory cytokines that usually accompanies the chronic stress response results in a further stimulation of the HPA axis thereby adding to the stress response. While CRF would appear to play a pivotal role, evidence is provided that simultaneous changes in the serotonergic and noradrenergic systems, combined with the activation of peripheral and central macrophages that increase the pro-inflammatory cytokine concentrations in the brain and blood, also play a critical role in predisposing to anxiety and depression. Neurodegenerative changes in the brain that frequently occur in the elderly patient with major depression, could result from the activation of indoleaminedioxygenase (IDO), a widely distributed enzyme that converts tryptophan via the kynenine pathway to for the neurotoxic end product quinolinic acid.

scholarly journals Influences of Stress and Sex on the Paraventricular Thalamus: Implications for Motivated Behavior

2021 ◽  
Vol 15 ◽  
Author(s):  
Sydney A. Rowson ◽  
Kristen E. Pleil
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Reciprocal Relationship ◽  
Stress Exposure ◽  
Acute And Chronic Stress ◽  
Motivated Behavior ◽  
Neuroendocrine Response ◽  
Response To Stress ◽  
Motivated Behaviors

The paraventricular nucleus of the thalamus (PVT) is a critical neural hub for the regulation of a variety of motivated behaviors, integrating stress and reward information from environmental stimuli to guide discrete behaviors via several limbic projections. Neurons in the PVT are activated by acute and chronic stressors, however several roles of the PVT in behavior modulation emerge only following repeated stress exposure, pointing to a role for hypothalamic pituitary adrenal (HPA) axis modulation of PVT function. Further, there may be a reciprocal relationship between the PVT and HPA axis in which chronic stress-induced recruitment of the PVT elicits an additional role for the PVT to regulate motivated behavior by modulating HPA physiology and thus the neuroendocrine response to stress itself. This complex interaction may make the PVT and its role in influencing motivated behavior particularly susceptible to chronic stress-induced plasticity in the PVT, especially in females who display increased susceptibility to stress-induced maladaptive behaviors associated with neuropsychiatric diseases. Though literature is describing the sex-specific effects of acute and chronic stress exposure on HPA axis activation and motivated behaviors, the impact of sex on the role of the PVT in modulating the behavioral and neuroendocrine response to stress is less well established. Here, we review what is currently known regarding the acute and chronic stress-induced activation and behavioral role of the PVT in male and female rodents. We further explore stress hormone and neuropeptide signaling mechanisms by which the HPA axis and PVT interact and discuss the implications for sex-dependent effects of chronic stress on the PVT’s role in motivated behaviors.

scholarly journals Predictive modeling of the hypothalamic-pituitary-adrenal (HPA) axis response to acute and chronic stress

2011 ◽  
Vol 58 (10) ◽  
pp. 889-904 ◽  
Author(s):  
Vladimir M. Markovic ◽  
Zeljko Cupic ◽  
Vladana Vukojevic ◽  
Ljiljana Kolar-Anic
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Predictive Modeling ◽  
Hypothalamic Pituitary Adrenal ◽  
Acute And Chronic Stress

scholarly journals The Role of the Forebrain Glucocorticoid Receptor in Acute and Chronic Stress

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5482-5490 ◽  
Author(s):  
Amy R. Furay ◽  
Amy E. Bruestle ◽  
James P. Herman
Keyword(s):  
Glucocorticoid Receptor ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Negative Feedback ◽  
Basolateral Amygdala ◽  
Feedback Regulation ◽  
Negative Feedback Regulation ◽  
Acute And Chronic Stress ◽  
Corticosterone Secretion

Previous work has implicated the forebrain glucocorticoid receptor (GR) in feedback regulation of the hypothalamic-pituitary-adrenocortical (HPA) axis. The present series of experiments used male mice with a targeted forebrain-specific GR knockout (in which forebrain includes the prefrontal cortex, hippocampus, and basolateral amygdala) to determine the role of forebrain GR in HPA axis regulation after stress. The data indicate that the forebrain GR is necessary for maintaining basal regulation of corticosterone secretion in the morning, confirming its role in HPA axis regulation. Our data further indicate that the forebrain GR is necessary for negative feedback after both mild and robust acute psychogenic stressors but not hypoxia, a systemic stressor. In contrast, forebrain-specific GR knockout and control mice exhibit equivalent HPA axis hyperactivity and facilitation after chronic variable stress, suggesting that changes in forebrain GR are not essential for chronic stress-induced pathology. These studies provide novel and definitive evidence that the forebrain GR selectively contributes negative feedback regulation of HPA axis responses to psychogenic stressors. Moreover, the data indicate that chronic stress-induced alterations in HPA axis function are mediated by mechanisms independent of the forebrain GR. Overall, the data are consistent with an essential role of the forebrain GR in coordinating endocrine responses to stimuli of a psychological origin.

An intervention study on the effectiveness of an anti-stress-app on psychophysiological acute and chronic stress (Preprint)

2018 ◽  
Author(s):  
Franziska Lautenbach
Keyword(s):  
Chronic Stress ◽  
Acute Stress ◽  
Physiological Stress ◽  
Stress Test ◽  
Experimental Studies ◽  
Trier Social Stress Test ◽  
Control Group ◽  
Subjective Perception ◽  
Face To Face ◽  
Acute And Chronic Stress

BACKGROUND Dealing with stress is of central importance. Lately, smartphone applications (apps) are deployed in stress interventions as they offer maximal flexibility for users. First results of experimental studies show that anti-stress apps effect subjective perception of stress positively (Ly et al., 2014). However, current literature lacks studies on physiological stress reactions (e.g., cortisol), although they are of special interest to health issues. OBJECTIVE Therefore, the aim of this study was to investigate the effectiveness of an anti-stress app in chronic and acute stress reduction on a physiological (cortisol) and psychological level (subjective perception of stress) in comparison to a face-to-face and a control group in a pre-post design, for the first time. METHODS Sixty-two participants took part in the pretesting procedure (drop-out of 53 %). Based on age, gender, physical activity and subjectively perceived acute stress due to the Trier Social Stress Test for groups (TSST-G; von Dawans et al., 2011) as well as based on subjectively chronic stress assessed during the pretest, participants were parallelized in three groups (anti-stress-app: n = 10, face-to-face: n = 11, control group: n = 9). RESULTS After six weeks of the cognitive-based resource-oriented intervention, participants were exposed to the TSST-G for post testing. Results did not show a change of cortisol secretion or cognitive appraisal of the acute stressor. Further, no changes were detected in the chronic physiological stress reaction. CONCLUSIONS Possible causes are discussed extensively. CLINICALTRIAL no

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