Contribution of Sex and Cellular Context in the Regulation of Brain Corticosteroid Receptors following Restraint Stress

2000 ◽  
Vol 71 (6) ◽  
pp. 343-353 ◽  
Author(s):  
Despoina Karandrea ◽  
Christos Kittas ◽  
Efthimia Kitraki
Keyword(s):  
Restraint Stress ◽  
Corticosteroid Receptors ◽  
Cellular Context

scholarly journals Vitamin A regulates hypothalamic–pituitary–adrenal axis status in LOU/C rats

2013 ◽  
Vol 219 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Nathalie Marissal-Arvy ◽  
Rachel Hamiani ◽  
Emmanuel Richard ◽  
Marie-Pierre Moisan ◽  
Véronique Pallet
Keyword(s):  
Vitamin A ◽  
Hpa Axis ◽  
Restraint Stress ◽  
Vitamin A Deficiency ◽  
Plasma Corticosterone ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosteroid Receptors ◽  
Vitamin A Status ◽  
Corticosterone Response ◽  
Hpa Axis Activity

The aim of this study was to explore the involvement of retinoids in the hypoactivity and hyporeactivity to stress of the hypothalamic–pituitary–adrenal (HPA) axis in LOU/C rats. We measured the effects of vitamin A deficiency administered or not with retinoic acid (RA) on plasma corticosterone in standard conditions and in response to restraint stress and on hypothalamic and hippocampal expression of corticosteroid receptors, corticotropin-releasing hormone and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in LOU/C rats. Interestingly, under control conditions, we measured a higher plasma concentration of retinol in LOU/C than in Wistar rats, which could contribute to the lower basal activity of the HPA axis in LOU/C rats. Vitamin A deficiency induced an increased HPA axis activity in LOU/C rats, normalized by RA administration. Compared with LOU/C control rats, vitamin A-deficient rats showed a delayed and heightened corticosterone response to restraint stress. The expression of corticosteroid receptors was strongly decreased by vitamin A deficiency in the hippocampus, which could contribute to a less efficient feedback by corticosterone on HPA axis tone. The expression of 11β-HSD1 was increased by vitamin A deficiency in the hypothalamus (+62.5%) as in the hippocampus (+104.7%), which could lead to a higher production of corticosterone locally and contribute to alteration of the hippocampus. RA supplementation treatment restored corticosterone concentrations and 11β-HSD1 expression to control levels. The high vitamin A status of LOU/C rats could contribute to their low HPA axis activity/reactivity and to a protective effect against 11β-HSD1-mediated deleterious action on cognitive performances during ageing.

Acute restraint stress has a similar effect on visceral sensitivity in different types of maternal deprivation in rats

2001 ◽  
Vol 120 (5) ◽  
pp. A715-A715
Author(s):  
A ROSZTOCZY ◽  
S BRADESI ◽  
C BEAUFRAND ◽  
J FIORAMONTI ◽  
T WITTMANN ◽  
...  
Keyword(s):  
Restraint Stress ◽  
Maternal Deprivation ◽  
Visceral Sensitivity ◽  
Acute Restraint Stress ◽  
Different Types

Restraint stress of male mice triggers apoptosis in spermatozoa and spermatogenic cells via activating the TNF-α system

Zygote ◽  
2020 ◽  
Vol 28 (2) ◽  
pp. 160-169 ◽  
Author(s):  
Jie Zhang ◽  
De-Ling Kong ◽  
Bin Xiao ◽  
Hong-Jie Yuan ◽  
Qiao-Qiao Kong ◽  
...  
Keyword(s):  
Psychological Stress ◽  
Restraint Stress ◽  
Semen Quality ◽  
Sperm Quality ◽  
Fertilization Rate ◽  
Seminiferous Tubules ◽  
Spermatogenic Cells ◽  
Male Mice ◽  
Testicular Cells ◽  
Tnf Α

SummaryStudies have indicated that psychological stress impairs human fertility and that various stressors can induce apoptosis of testicular cells. However, the mechanisms by which psychological stress on males reduces semen quality and stressors induce apoptosis in testicular cells are largely unclear. Using a psychological (restraint) stress mouse model, we tested whether male psychological stress triggers apoptosis of spermatozoa and spermatogenic cells through activating tumour necrosis factor (TNF)-α signalling. Wild-type or TNF-α−/− male mice were restrained for 48 h before examination for apoptosis and expression of TNF-α and TNF receptor 1 (TNFR1) in spermatozoa, epididymis, seminiferous tubules and spermatogenic cells. The results showed that male restraint significantly decreased fertilization rate and mitochondrial membrane potential, while increasing levels of malondialdehyde, active caspase-3, TNF-α and TNFR1 in spermatozoa. Male restraint also increased apoptosis and expression of TNF-α and TNFR1 in caudae epididymides, seminiferous tubules and spermatogenic cells. Sperm quality was also significantly impaired when spermatozoa were recovered 35 days after male restraint. The restraint-induced damage to spermatozoa, epididymis and seminiferous tubules was significantly ameliorated in TNF-α−/− mice. Furthermore, incubation with soluble TNF-α significantly reduced sperm motility and fertilizing potential. Taken together, the results demonstrated that male psychological stress induces apoptosis in spermatozoa and spermatogenic cells through activating the TNF-α system and that the stress-induced apoptosis in spermatogenic cells can be translated into impaired quality in future spermatozoa.

Restraint stress exacerbates cell degeneration induced by acute binge ethanol in the adolescent, but not in the adult or middle-aged, brain

2019 ◽  
Vol 364 ◽  
pp. 317-327 ◽  
Author(s):  
Macarena Soledad Fernández ◽  
Soledad de Olmos ◽  
Michael E. Nizhnikov ◽  
Ricardo Marcos Pautassi
Keyword(s):  
Restraint Stress ◽  
Middle Aged ◽  
Cell Degeneration ◽  
Aged Brain ◽  
Binge Ethanol
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