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 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.

scholarly journals Vasopressin in mechanisms of stress reactions and modulation of emotion

2018 ◽  
Vol 16 (3) ◽  
pp. 5-12
Author(s):  
Svetlana G. Belokoskova ◽  
Sergey G. Tsikunov
Keyword(s):  
Chronic Stress ◽  
Depressive Disorders ◽  
Stress Reactions ◽  
Acute And Chronic Stress ◽  
Adrenal System ◽  
Vasopressin Receptors ◽  
Response To Stress

The review presents modern conceptions about the role of the vasopressinergic system in regulating reactions to stress and modulation of emotions in animals and humans. The contribution of vasopressin to activation of the hypothalamic-pituitary-adrenal system in conditions of acute and chronic stress is reflected in the work. It is noted that the activation of vasopressin receptors of type 1 enhances the response to stress, which contributes to the development of psychopathology. It is emphasized that the role of vasopressin receptors of type 2 in the regulation of emotions has been studied little. At the same time, there is evidence that the activation of vasopressin receptors of type 2 in patients with depressive disorders after a stroke is accompanied by effects that are opposite in direction to the effects of activation of vasopressin receptors of type 1. The review examines promising areas of further studies of the involvement of vasopressin receptors of type 2 in modulating stress reactions and emotions. The use of receptor antagonist’s vasopressin of type 1 and receptor agonists of type 2 in the treatment of depressive and anxiety disorders are discussed.

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.

Role of the basolateral amygdala in mediating the effects of the fatty acid amide hydrolase inhibitor URB597 on HPA axis response to stress

2014 ◽  
Vol 24 (9) ◽  
pp. 1511-1523 ◽  
Author(s):  
Gaurav Bedse ◽  
Roberto Colangeli ◽  
Angelo M. Lavecchia ◽  
Adele Romano ◽  
Fabio Altieri ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Hpa Axis ◽  
Basolateral Amygdala ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Response To Stress ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

Hair cortisol and its potential value as a physiological measure of stress response in human and non-human animals

2017 ◽  
Vol 57 (3) ◽  
pp. 401 ◽  
Author(s):  
C. Burnard ◽  
C. Ralph ◽  
P. Hynd ◽  
J. Hocking Edwards ◽  
A. Tilbrook
Keyword(s):  
Chronic Stress ◽  
Stress Responses ◽  
Sampling Site ◽  
Future Research ◽  
Hair Cortisol ◽  
Hair Sampling ◽  
Acute And Chronic Stress ◽  
Lack Of Information ◽  
Technical Validation ◽  
Response To Stress

There is considerable interest in the potential for measuring cortisol in hair as a means of quantifying stress responses in human and non-human animals. This review updates the rapid advancement in our knowledge of hair cortisol, methods for its measurement, its relationship to acute and chronic stress, and its repeatability and heritability. The advantages of measuring cortisol in hair compared with other matrices such as blood, saliva and excreta and the current theories of the mechanisms of cortisol incorporation into the fibre are described. Hair cortisol as a measure of the physiological response to stress in a variety of species is presented, including correlations with other sample matrices, the relationship between hair cortisol and psychosocial stress and the repeatability and heritability of hair cortisol concentrations. Current standards for the quantification of hair cortisol are critically reviewed in detail for the first time and gaps in technical validation of these methods highlighted. The known effects of a variety of sources of hair cortisol variation are also reviewed, including hair sampling site, sex, age and adiposity. There is currently insufficient evidence to conclude that cortisol concentration in hair accurately reflects long-term blood cortisol concentrations. Similarly, there is a lack of information surrounding the mechanisms of cortisol incorporation into the hair. This review highlights several directions for future research to more fully validate the use of hair cortisol as an indicator of chronic stress.

Chronic stress and epigenetics. Relation between academic sciences and theology

2012 ◽  
Vol 153 (14) ◽  
pp. 525-530
Author(s):  
Kornél Simon
Keyword(s):  
Chronic Stress ◽  
Mental Status ◽  
Causative Role ◽  
Short Account ◽  
Stress Theory ◽  
Therapeutic Consequences ◽  
Acute And Chronic Stress ◽  
Somatic Alterations ◽  
Enzymatic Mechanisms

The author gives a short account on the principles of Selye’s stress theory, and discusses similarities and dissimilarities of acute and chronic stress. Both the external, and the internal environment, as well as the psycho-mental status are involved in the notion of the environment. Basic principles of epigenetics are reviewed: interaction between environment and genes, neuroendocrine and enzymatic mechanisms involved in silencing and activation of genes, notions of phenotypic plasticity, and epigenetic reprogramming are discussed. Epigenetic mechanisms of interrelation between pathological clinical states (diseases) and the characteristic phenotypes, causative role of psycho-mental status in evoking pathological somatic alterations, and the potential therapeutic consequences are briefly discussed. The etiological role of chronic, civilization stress in producing the worldwide increment of cardiovascular morbidity is cited, argumentation and criticism of the current therapeutical practice is discussed. The author concludes that recent advances in epigenetic knowledge seem to solve the controversy between the academic and theological sciences. Orv. Hetil., 2012, 153, 525–530.

Abnormalities in neuroendocrine stress response in psychosis: the role of endocannabinoids

2015 ◽  
Vol 46 (1) ◽  
pp. 27-45 ◽  
Author(s):  
E. Appiah-Kusi ◽  
E. Leyden ◽  
S. Parmar ◽  
V. Mondelli ◽  
P. McGuire ◽  
...  
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Psychotic Disorders ◽  
Endocannabinoid System ◽  
Current Evidence ◽  
Response To Stress ◽  
Health And Disease ◽  
Stress Response System ◽  
Precise Role

The aim of this article is to summarize current evidence regarding alterations in the neuroendocrine stress response system and endocannabinoid system and their relationship in psychotic disorders such as schizophrenia. Exposure to stress is linked to the development of a number of psychiatric disorders including psychosis. However, the precise role of stress in the development of psychosis and the possible mechanisms that might underlie this are not well understood. Recently the cannabinoid hypothesis of schizophrenia has emerged as a potential line of enquiry. Endocannabinoid levels are increased in patients with psychosis compared with healthy volunteers; furthermore, they increase in response to stress, which suggests another potential mechanism for how stress might be a causal factor in the development of psychosis. However, research regarding the links between stress and the endocannabinoid system is in its infancy. Evidence summarized here points to an alteration in the baseline tone and reactivity of the hypothalamic–pituitary–adrenal (HPA) axis as well as in various components of the endocannabinoid system in patients with psychosis. Moreover, the precise nature of the inter-relationship between these two systems is unclear in man, especially their biological relevance in the context of psychosis. Future studies need to simultaneously investigate HPA axis and endocannabinoid alterations both at baseline and following experimental perturbation in healthy individuals and those with psychosis to understand how they interact with each other in health and disease and obtain mechanistic insight as to their relevance to the pathophysiology of schizophrenia.

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