Sexual Dimorphism of the Human Stress Response May Be Due to Estradiol-Mediated Stimulation of Hypothalamic Corticotropin-Releasing Hormone Synthesis

1997 ◽  
Vol 82 (3) ◽  
pp. 982-984 ◽  
Author(s):  
D. J. Torpy
Keyword(s):  
Sexual Dimorphism ◽  
Stress Response ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Hormone Synthesis ◽  
Human Stress ◽  
Stimulation Of

scholarly journals Sexual dimorphism of stress response and immune/ inflammatory reaction: the corticotropin releasing hormone perspective

1995 ◽  
Vol 4 (3) ◽  
pp. 163-174 ◽  
Author(s):  
Nicholas V. Vamvakopoulos
Keyword(s):  
Gene Expression ◽  
Sexual Dimorphism ◽  
Stress Response ◽  
Inflammatory Reaction ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
New Concepts ◽  
Glucocorticoid Administration ◽  
Regulatory Potential ◽  
Key Aspects

This review higlghts key aspects of corticotropin releasing hormone (CRH) biology of potential relevance to the sexual dimorphism of the stress response and immune/inflammatory reaction, and introduces two important new concepts based on the regulatory potential of the human (h) CRH gene: (1) a proposed mechanism to account for the tissue-specific antithetical responses of hCRH gene expression to glucocorticolds, that may also explain the frequently observed antithetical effects of chronic glucocorticoid administration in clinical practice and (2) a heuristic diagram to illustrate the proposed modulation of the stress response and immune/ inflammatory reaction by steroid hormones, from the perspective of the CRH system.

Is the acute psychobiological stress response in healthy pregnant women associated with amniotic fluid corticotropin-releasing hormone?

2015 ◽  
Vol 61 ◽  
pp. 12
Author(s):  
Pearl La Marca-Ghaemmaghami ◽  
Sara M. Dainese ◽  
Roberto La Marca ◽  
Roland Zimmermann ◽  
Ulrike Ehlert
Keyword(s):  
Stress Response ◽  
Amniotic Fluid ◽  
Pregnant Women ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Brain oxytocin receptors mediate corticotropin-releasing hormone-induced anorexia

1991 ◽  
Vol 260 (2) ◽  
pp. R448-R452 ◽  
Author(s):  
B. R. Olson ◽  
M. D. Drutarosky ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Food Intake ◽  
Adrenocorticotropic Hormone ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Oxytocin Receptors ◽  
Artificial Cerebrospinal Fluid ◽  
Pituitary Secretion ◽  
Inhibit Food Intake ◽  
Stimulation Of

Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.

scholarly journals 0306 Corticotropin-Releasing Hormone Receptor 1 Gene Polymorphism Modulates Cognitive Flexibility Following Acute Stress and Total Sleep Deprivation

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A115-A116
Author(s):  
B C Satterfield ◽  
I Anlap ◽  
S L Esbit ◽  
W D Killgore
Keyword(s):  
Stress Response ◽  
Sleep Deprivation ◽  
Cognitive Flexibility ◽  
Acute Stress ◽  
Relevant Information ◽  
Corticotropin Releasing Hormone ◽  
Reversal Performance ◽  
Releasing Hormone ◽  
Total Sleep Deprivation ◽  
Stimulus Response

Abstract Introduction Dynamic decision processes requiring flexible updating of information are impaired by stress and sleep loss, both of which activate the hypothalamic-pituitary-adrenal (HPA) stress response. Corticotropin-releasing hormone (CRH) initiates the HPA pathway. The CRH receptor (CRHR1) gene contains a single nucleotide polymorphism that modulates this response. We investigated whether cognitive flexibility is affected by CRHR1 polymorphism following a night of acute stress and total sleep deprivation (TSD). Methods N=46 healthy, young adults (21.8±3.4y; 21 females) participated in an in-laboratory 31h sleep deprivation study. Beginning at 19:30 until 07:30, the Maastricht Acute Stress Test (MAST) was administered every 4h. The MAST alternates a cold pressor task with an oral subtraction task five times in a single bout. At 29h wakefulness, subjects performed a novel go/no-go reversal learning task. Stimulus-response rules were presented at the beginning of the task, and subjects were asked to either respond or withhold a response to the presented stimuli while receiving accuracy feedback. Halfway through the task, the stimulus-response rules were reversed. Performance was assessed by discriminability index (d’), hit rate (HR), and false alarm rate (FAR). Saliva samples were collected immediately prior, immediately after, and 30min after each MAST and assayed for cortisol. One saliva sample from each subject was assayed for CRHR1 genotype. Results CRHR1 genotypes were in Hardy-Weinberg equilibrium (χ 2=2.97, p=0.08). Mixed effects ANOVA with fixed effects of CRHR1 genotype, pre/post-reversal, and their interaction found a significant CRHR1 by reversal interaction for d’ (F2,319=3.88, p=0.022) and HR (F2,319=3.16, p=0.044) following a night of stress and TSD. No such interaction was found at well-rested baseline (d’: F2,319=2.51, p=0.083; HR: F2,319=1.55, p=0.213). Subjects homozygous for the T allele had higher mean post-MAST cortisol levels (0.40±0.06 µg/dL) with better pre-reversal performance, but worse post-reversal performance compared to heterozygous and homozygous G allele carriers. Conclusion CRHR1 genotype modulates dynamic decision making following a night of acute stress and TSD. A higher cortisol stress response (T/T genotype) is beneficial to maintaining task relevant information (stability), but significantly impairs the ability to update task-relevant information following a change in situational demands (flexibility). Support CDMRP grant W81XWH-17-C-0088

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