scholarly journals Plasma Transcortin Influences Endocrine and Behavioral Stress Responses in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 649-659 ◽  
Author(s):  
Elodie M. Richard ◽  
Jean-Christophe Helbling ◽  
Claudine Tridon ◽  
Aline Desmedt ◽  
Amandine M. Minni ◽  
...  
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Learned Helplessness ◽  
Critical Role ◽  
Adaptive Responses ◽  
Adrenal Axis ◽  
Response To Stress ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Deficient Mice ◽  
Pituitary Adrenal Axis

Glucocorticoids are released after hypothalamus-pituitary-adrenal axis stimulation by stress and act both in the periphery and in the brain to bring about adaptive responses that are essential for life. Dysregulation of the stress response can precipitate psychiatric diseases, in particular depression. Recent genetic studies have suggested that the glucocorticoid carrier transcortin, also called corticosteroid-binding globulin (CBG), may have an important role in stress response. We have investigated the effect of partial or total transcortin deficiency using transcortin knockout mice on hypothalamus-pituitary-adrenal axis functioning and regulation as well as on behaviors linked to anxiety and depression traits in animals. We show that CBG deficiency in mice results in markedly reduced total circulating corticosterone at rest and in response to stress. Interestingly, free corticosterone concentrations are normal at rest but present a reduced surge after stress in transcortin-deficient mice. No differences were detected between transcortin-deficient mice for anxiety-related traits. However, transcortin-deficient mice display increased immobility in the forced-swimming test and markedly enhanced learned helplessness after prolonged uncontrollable stress. The latter is associated with an approximately 30% decrease in circulating levels of free corticosterone as well as reduced Egr-1 mRNA expression in hippocampus in CBG-deficient mice. Additionally, transcortin-deficient mice show no sensitization to cocaine-induced locomotor responses, a well described corticosterone-dependent test. Thus, transcortin deficiency leads to insufficient glucocorticoid signaling and altered behavioral responses after stress. These findings uncover the critical role of plasma transcortin in providing an adequate endocrine and behavioral response to stress.

scholarly journals Regulation of Pituitary Corticotropin-Releasing Hormone-Binding Protein Messenger Ribonucleic Acid Levels by Restraint Stress and Adrenalectomy**This work is supported by National Institutes of Health Grant DK-42730 (to A.F.S) and by a Young Investigator Award (to A.F.S.) from the National Alliance for Research on Schizophrenia and Depression.

Endocrinology ◽  
1998 ◽  
Vol 139 (11) ◽  
pp. 4435-4441 ◽  
Author(s):  
Shanna J. McClennen ◽  
Daniel N. Cortright ◽  
Audrey F. Seasholtz
Keyword(s):  
Steady State ◽  
Stress Response ◽  
Messenger Rna ◽  
Restraint Stress ◽  
Adrenal Axis ◽  
Acute Restraint Stress ◽  
Steady State Levels ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis ◽  
Acth Release

Abstract CRH is the primary hypothalamic regulator of the stress response in higher organisms, where it acts as the key mediator of ACTH release in the hypothalamus-pituitary-adrenal axis. The 37-kDa CRH-binding protein (CRH-BP) is known to bind CRH and antagonize CRH-induced ACTH release in vitro. The expression of this protein in anterior pituitary corticotrophs suggests a role for CRH-BP in modulation of the stress response. To investigate the in vivo role of rat CRH-BP, the regulation of pituitary CRH-BP gene expression by acute restraint stress and/or adrenalectomy was examined using ribonuclease protection assays. After restraint stress, steady-state levels of CRH-BP transcripts increase two to three times over basal level and remain significantly higher than basal levels for 120 min after the start of restraint. Adrenalectomy decreases CRH-BP messenger RNA steady-state levels to 8% of control levels. These results demonstrate that pituitary CRH-BP messenger RNA levels are increased in response to acute restraint stress and that glucocorticoids play a significant role in this positive regulation. These data also suggest that increased CRH-BP levels, in response to stress, may modulate the endocrine stress response by providing an additional feedback mechanism to maintain homeostasis of the hypothalamus-pituitary-adrenal axis.

scholarly journals Limbic response to stress linking life trauma and hypothalamus-pituitary-adrenal axis function

2019 ◽  
Vol 99 ◽  
pp. 38-46 ◽  
Author(s):  
Dongju Seo ◽  
Arielle G. Rabinowitz ◽  
Ryan J. Douglas ◽  
Rajita Sinha
Keyword(s):  
Adrenal Axis ◽  
Response To Stress ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

scholarly journals Maternal Dietary Fat Determines Metabolic Profile and the Magnitude of Endocannabinoid Inhibition of the Stress Response in Neonatal Rat Offspring

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1685-1694 ◽  
Author(s):  
Esterina D'Asti ◽  
Hong Long ◽  
Jennifer Tremblay-Mercier ◽  
Magdalena Grajzer ◽  
Stephen C. Cunnane ◽  
...  
Keyword(s):  
Stress Responses ◽  
Dietary Fat ◽  
Maternal Diet ◽  
Neonatal Rat ◽  
Pregnant Rats ◽  
Metabolic Hormones ◽  
Adrenal Axis ◽  
Corticosterone Secretion ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

Endocannabinoids (eCBs) are products of phospholipid (PL)-derived arachidonic acid (AA) that regulate hypothalamus-pituitary-adrenal axis activity. We hypothesized that differences in the quality and quantity of maternal dietary fat would modulate the PL AA content in the neonatal brain affecting stress responsiveness via differences in eCB production and activity in stress-activated brain areas. Pregnant rats were fed a 5% [control (C)] or 30% fat [high fat (HF)] diet rich in either n-6 (HF-n-6) or n-3 (HF-n-3) fat during the last week of gestation and lactation. Postnatal d 10 offspring were tested for metabolic hormones, AA (n-6) and eCB brain content, and hormonal effects of eCB receptor antagonism (AM251, 1 or 3 mg/kg ip) on stress responses. Like maternal diet, milk from HF-n-3 mothers had a reduced n-6/n-3 fat ratio compared with that of C and HF-n-6 mothers. Hypothalamic and hippocampal levels of PL AA were diet specific, reflecting the maternal milk and dietary n-6/n-3 ratio, with HF-n-3 offspring displaying reduced AA content relative to C and HF-n-6 offspring. Plasma corticosterone and insulin were elevated in HF-fed pups, whereas leptin was increased only in HF-n-6 pups. Basal eCB concentrations were also diet and brain region specific. In C pups, eCB receptor antagonist pretreatment increased stress-induced ACTH secretion, but not in the HF groups. Stress-induced corticosterone secretion was not sensitive to AM251 treatment in HF-n-3 pups. Thus, the nature of preweaning dietary fat differentially influences neonatal metabolic hormones, brain PL AA levels, and eCB, with functional consequences on hypothalamus-pituitary-adrenal axis modulation in developing rat pups.

Deciphering the Association Between Hypothalamus‐Pituitary‐Adrenal Axis Activity and Obesity: A Meta‐Analysis

Obesity ◽  
2021 ◽  
Author(s):  
Giada Ostinelli ◽  
Anaïs Scovronec ◽  
Sylvain Iceta ◽  
Anne‐Sophie Ouellette ◽  
Simone Lemieux ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Adrenal Axis ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

Contribution of Growth Arrest-Specific 5/miR-674 to the Hypothalamus Pituitary Adrenal Axis Regulation Effect by Electroacupuncture following Trauma

2021 ◽  
pp. 1-13
Author(s):  
Jing Zhu ◽  
Chunxia Guo ◽  
Pingping Lu ◽  
Shuijin Shao ◽  
Bing Tu
Keyword(s):  
Hpa Axis ◽  
Interleukin 1 ◽  
Growth Arrest ◽  
Luciferase Assay ◽  
Function Evaluation ◽  
Protein Levels ◽  
Adrenal Axis ◽  
Post Surgery ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

<b><i>Background:</i></b> Electroacupuncture (EA) can improve trauma-induced hypothalamus pituitary adrenal axis (HPA) hyperactivity. However, the mechanism underlying the EA effect has not been fully understood. <b><i>Methods and Study Design:</i></b> This study was undertaken to explore the role of hypothalamic growth arrest-specific 5 (Gas5) in the regulation of EA on HPA axis function post-surgery. Paraventricular nuclear Gas5 levels were upregulated in rats using an intracerebroventricular injection of pAAV-Gas5. Primary hypothalamic neurons and 293T cells were cultured for miRNA and siRNAs detection. Radioimmunoassay, PCR, Western blot, and immunohistochemistry were used for HPA axis function evaluation. <b><i>Results:</i></b> The overexpression of Gas5 abolished the effect of EA on the regulation of trauma-induced HPA axis hyperactivity. Using a bioinformatics analysis and dual luciferase assay, we determined that miRNA-674 was a target of Gas5. Additionally, miRNA-674 levels were found to have decreased in trauma rats, and this effect was reversed after EA intervention. TargetScan analysis showed that serum and glucocorticoid inducible kinase 1 (SGK1) were targets of miR-674. Moreover, we found that SGK1 protein levels increased in trauma rats and SGK1 expression inhibition alleviated HPA axis abnormality post-surgery. EA could improve the number of hypothalamus iba-1 positive cells and hypothalamic interleukin 1 beta protein expression. <b><i>Conclusions:</i></b> Our study demonstrated the involvement of the hypothalamic Gas5/miRNA-674/SGK1 signaling pathway in EA regulation of HPA axis function after trauma.

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