scholarly journals Lateral Hypothalamus Corticotropin Releasing Hormone Receptor-1 Inhibition Modulates Stress- Induced Anxiety Behavior

2021 ◽  
Author(s):  
Masoumeh Eghtesad ◽  
◽  
Mahmoud Elahdadi Salmani ◽  
Taghi Lashkarbolouki ◽  
Iran Goudarzi1 ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Acute Stress ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Area ◽  
Releasing Hormone ◽  
Male Wistar Rats ◽  
Induced Changes ◽  
Crh Receptor Type 1

Stress is a reaction to unwanted events disturbing body homeostasis which influences its pathways and target areas. Stress affects the brain through the lateral hypothalamic area (LHA) orexinergic system that mediates the effect of corticotropin-releasing hormone (CRH) through CRH receptor type 1 (CRHr1). Therefore, this study explores the outcome of stress exposure on anxiety development and the involvement of the LHA through LHA-CRHr1. Male Wistar rats (220-250g) implanted with a cannula in either side of the LHA received acute or chronic stress. Subsequently, exploratory behavior and anxiety was examined using the open field (OF) and elevated plus maze (EPM), respectively. Prior to sacrifice, the cerebrospinal fluid (CSF) and the blood were sampled. Nissl stain was performed on fixed brain tissues. Acute stress resulted in a decrease of exploration in the OF and an increase of anxiety in the EPM. LHA-CRHr1 inhibition reversed the variables to increase the exploration and decrease the anxiety. In contrast, chronic stress did not show any effect on the anxiety-related behaviors. Chronic stress decreased the cell population in the LHA, which was prevented by the CRHr1 inhibition. However, the CRHr1 inhibition was unable to reverse the chronic stress increase of the CSF orexin level. Furthermore, both acute and chronic stresses increased the plasma corticosterone level and only the CRHr1 inhibition impeded the effect. Our results recognize LHA-CRHr1 as a capable candidate modulating acute stress-induced anxiety development and chronic stress-induced changes in the cellular population of the region.

Dehydration-induced drinking decreases Fos expression in hypothalamic paraventricular neurons expressing vasopressin but not corticotropin-releasing hormone

2007 ◽  
Vol 292 (3) ◽  
pp. R1349-R1358 ◽  
Author(s):  
Cheryl Wotus ◽  
Michelle M. Arnhold ◽  
William C. Engeland
Keyword(s):  
Acute Stress ◽  
Plasma Osmolality ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Corticotropin Releasing Hormone ◽  
Plasma Acth ◽  
Releasing Hormone ◽  
Parvocellular Neurons ◽  
Fos Expression ◽  
Receiving Water

Water-restricted (WR) rats exhibit a rapid suppression of plasma corticosterone following drinking. The present study monitored Fos-like immunoreactivity (Fos) to assess the effect of WR-induced drinking on the activity of vasopressin (VP)-positive magnocellular and parvocellular neurons and corticotropin-releasing hormone (CRH)-positive parvocellular neurons in the paraventricular nucleus of the hypothalamus. Adult male rats received water for 30 min (WR) in the post meridiem (PM) each day for 6 days and were killed without receiving water or at 1 h after receiving water for 15 min. In WR rats, Fos increased in VP magnocellular and parvocellular neurons but not CRH neurons. After drinking, Fos was reduced in VP magnocellular and parvocellular neurons but did not change in CRH neurons. To assess the severity of osmotic stress, rats were sampled throughout the final day of WR. Plasma osmolality, hematocrit and plasma VP were increased throughout the day before PM rehydration, and plasma ACTH and corticosterone were elevated at 1230 and 1430, respectively, showing that WR activates hypothalamic-pituitary-adrenal activity during the early PM before the time of rehydration. To determine the effects of WR-induced drinking on CRH neurons activated by acute stress, WR rats underwent restraint. Restraint increased plasma ACTH and corticosterone and Fos in CRH neurons; although rehydration reduced plasma ACTH and Fos expression in VP neurons, Fos in CRH neurons was not affected. These results suggest that inhibition of VP magnocellular and parvocellular neurons, but not CRH parvocellular neurons, contributes to the suppression of corticosterone after WR-induced drinking.

Differential regulation of hypothalamic pituitary corticotropin releasing hormone receptors during development of adjuvant-induced arthritis in the rat

1997 ◽  
Vol 153 (2) ◽  
pp. 185-191 ◽  
Author(s):  
G Aguilera ◽  
D S Jessop ◽  
M S Harbuz ◽  
A Kiss ◽  
S L Lightman
Keyword(s):  
Chronic Stress ◽  
Anterior Pituitary ◽  
Hormone Receptors ◽  
Acute Stress ◽  
Feedback Regulation ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Adjuvant Induced Arthritis

Abstract The expression of corticotropin releasing hormone (CRH) in the hypothalamic paraventricular nucleus (PVN) and CRH receptor mRNA in the PVN and anterior pituitary was studied during development of adjuvant-induced arthritis in Piebald–Viral–Glaxo rats, using in situ hybridization techniques. As previously shown with i.p. hypertonic saline injection, basal and immobilization stress-stimulated CRH mRNA levels in the PVN were significantly lower than in controls 14 days after adjuvant injection. However, 7 days after injection, preceding the onset of inflammation, the increase of CRH mRNA following immobilization was significantly higher than in control rats. In contrast to other chronic stress paradigms, inflammation stress failed to induce type-1 CRH receptor (CRH-R1) mRNA in the PVN, either at 7 days, or at 14 days after adjuvant injection, when inflammation is present. The ability of acute immobilization to induce CRH-R1 mRNA in the PVN was not affected 14 days after adjuvant injection but parallel to the CRH peptide mRNA response it was markedly potentiated at 7 days. Pro-opiomelanocorpin (POMC) mRNA levels in the anterior pituitary increased significantly 14 days after adjuvant injection, and they were unaffected by 1 h immobilization. While CRH binding in the pituitary decreased significantly 14 days after adjuvant injection, CRH-Rl mRNA was unchanged. This study shows biphasic hypothalamic responses to acute stress during development of adjuvant-induced arthritis, with enhanced CRH peptide and CRH-Rl mRNAs responses at 7 days, preceding the onset of inflammation, and blunted CRH mRNA responses at 14 days at the height of the inflammatory response. The lack of CRH receptor expression in the PVN in this model of chronic inflammation stress associated to low hypothalamic CRH peptide levels supports the view that positive feedback regulation by CRH is necessary to maintain enhanced CRH expression during chronic stress. Journal of Endocrinology (1997) 153, 185–191

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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