Effects of prenatal restraint stress on hypothalamic-pituitary-adrenocortical and sympatho-adrenomedullary axis in neonatal pigs

2001 ◽  
Vol 73 (2) ◽  
pp. 279-287 ◽  
Author(s):  
W. Often ◽  
E. Kanitz ◽  
M. Tuchscherer ◽  
G. Nürnberg

AbstractStudies in rodents and primates strongly indicate that prenatal stress affects the survival, behaviour and physiology of the offspring. Stressful stimuli during gestation may have a direct or hormone mediated effect on the development of stress systems in the foetal organism, resulting in an altered coping during stressful situations. The present study was conducted to elucidate prenatal stress effects in domestic pigs on the responses of the hypothalamicpituitary- adrenocortical (HPA) axis and the sympatho-adrenomedullary (SAM) system as well as on morbidity, mortality and growth of the offspring. Pregnant sows were subjected to a restraint stress for five minutes daily during the last five weeks of gestation. Endocrine reactions of the piglets were tested at 3, 7, 21 and 35 days of age using an immobilization test and an ACTH challenge test. Prenatally stressed piglets showed lower basal plasma cortisol and increased corticosteroid binding globulin (CBG) concentrations at 3 days of age, indicating decreased free cortisol concentrations after birth. Cortisol levels after ACTH stimulation and catecholamine levels after immobilization were not affected by the stress treatment of the sows. Piglets from stressed sows tended to have lower noradrenaline : adrenaline ratios at three days of age compared with the control piglets. In addition, stressed sows tended to have lower litter weights after birth. The morbidity and mortality during the suckling period was higher in the prenatally stressed litters, as shown by a higher frequency of diseased and perished piglets per litter. We suppose that prenatal stress during late gestation in pigs alters the development of the HPA system and impairs the vitality of the offspring.

2017 ◽  
Vol 11 ◽  
pp. 117906951770466 ◽  
Author(s):  
Nombuso Valencia Pearl Mkhize ◽  
Lihle Qulu ◽  
Musa Vuyisile Mabandla

Febrile seizures are childhood convulsions resulting from an infection that leads to an inflammatory response and subsequent convulsions. Prenatal stress has been shown to heighten the progression and intensity of febrile seizures. Current medications are costly and have adverse effects associated with prolonged use. Quercetin flavonoid exhibits anti-inflammatory, anti-convulsant, and anti-stress effects. This study was aimed to investigate the therapeutic effect of quercetin in a prenatally stressed rat model of febrile seizures. We hypothesized that quercetin will alleviate the effects of prenatal stress in a febrile seizure rat model. On gestational day 13, Sprague-Dawley rat dams were subjected to restraint stress for 1 hour/d for 7 days. Febrile seizures were induced on postnatal day 14 on rat pups by intraperitoneally injecting lipopolysaccharide followed by kainic acid and quercetin on seizure onset. Hippocampal tissue was harvested to profile cytokine concentrations. Our results show that quercetin suppresses prenatal stress–induced pro-inflammatory marker (interleukin 1 beta) levels, subsequently attenuating febrile seizures. This shows that quercetin can be therapeutic for febrile seizures in prenatally stressed individuals.


2013 ◽  
Vol 280 (1753) ◽  
pp. 20122368 ◽  
Author(s):  
Floriane Guibert ◽  
Sophie Lumineau ◽  
Kurt Kotrschal ◽  
Erich Möstl ◽  
Marie-Annick Richard-Yris ◽  
...  

The prenatal environment is a source of phenotypic variability influencing the animal's characteristics. Prenatal stress affects not only the development of offspring, but also that of the following generation. Such effects have been best documented in mammals but can also be observed in birds, suggesting common processes across phylogenetic orders. We found previously that Japanese quail females stressed during laying produced offspring with higher fearfulness, probably related to modulation of testosterone levels in their eggs. Here, we evaluated long-term effects of prenatal stress by analysing reproductive traits of these F 1 offspring and, then, the development of their subsequent (F 2 ) offspring. The sexual behaviour of F 1 prenatally stressed (F1PS) males was impaired. F1PS females' eggs contained less yolk and more albumen, and higher yolk testosterone and progesterone levels than did F 1 prenatal control females. The fearfulness of F 2 prenatally stressed quail was greater than that of F 2 prenatal control quail. These F 2 behavioural differences paralleled those evidenced by their parents, suggesting trans-generational transmission of prenatal stress effects, probably mediated by egg compositions of F1PS females.


1995 ◽  
Vol 146 (1) ◽  
pp. 121-130 ◽  
Author(s):  
E T M Berdusco ◽  
K Yang ◽  
G L Hammond ◽  
J R G Challis

Abstract Plasma cortisol levels increase in fetal sheep during late gestation and this is associated with an increase in plasma corticosteroid-binding globulin (CBG) concentrations. However, the relative tissue sources of plasma CBG, the ontogeny of its biosynthesis and glycoform composition have not been established in the ovine fetus. Therefore we examined whether changes in plasma corticosteroid binding capacity (CBC) in fetal sheep during late gestation were associated with different patterns of glycosylation and reflected changes in tissue CBG expression. Since free cortisol is considered the bioactive fraction, we measured changes in the percent and absolute free cortisol in fetal plasma during late gestation. In order to examine whether CBG alters cortisol negative feedback at the level of the fetal pituitary, we also examined the effect of exogenous CBG in mediating the glucocorticoid-induced suppression of basal and corticotrophin-releasing hormone (CRH)-stimulated ACTH release from fetal pituitary cells in culture. The mean free cortisol concentration in plasma was not different between days 15 and 20 prior to parturition, and between 5 and 10 days prepartum, although it did rise between these times. Plasma CBC in chronically catheterized fetuses rose from 23·3 ± 4·6 ng/ml at day 115 to 86·5 ± 20·8 ng/ml at term and then decreased rapidly after birth. Between day 125 and day 140 of pregnancy approximately 10% of fetal plasma CBG was retarded by Concanavalin-A chromatography. This proportion increased at birth and attained adult values of >70% by one month of age. By Northern blotting the relative levels of CBG mRNA in the fetal liver did not change between days 100 and 125, then increased significantly at day 140, but declined at term and in newborn lambs. CBG mRNA was undetectable in total RNA from lung, kidney, hypothalamus and placentomes, but was present in the fetal pituitary at days 125 and 140. Reverse transcription-PCR was used to confirm the presence of CBG mRNA in pituitary tissue from term fetuses. In cultures of term fetal pituitary cells, added CBG attenuated the cortisol- but not the dexamethasone-mediated suppression of basal and CRH-stimulated ACTH release. We conclude that in fetal sheep there is an increase in the corticosteroid binding capacity of plasma during late pregnancy which regulates, in part, free cortisol levels in the circulation. The liver is the major site of CBG biosynthesis in the fetus and at least until day 140 of gestation the rise in plasma CBC is associated with an increase in hepatic CBG mRNA levels. The fetal pituitary was also established as a site of CBG production. Output of ACTH by cultured pituitary cells was inhibited by cortisol and this effect was diminished in the presence of added CBG. This study supports a role for systemic CBG in modulating the availability of cortisol to the fetal pituitary and suggests an additional way of modifying feedback effects of cortisol at the pituitary through its own production of CBG. Journal of Endocrinology (1995) 146, 121–130


Stress ◽  
2021 ◽  
pp. 1-12
Author(s):  
Daniele J. Feriani ◽  
Andressa S. Sousa ◽  
Maria Andreia Delbin ◽  
Olívia M. Ruberti ◽  
Carlos C. Crestani ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Livio Provenzi ◽  
Fabiana Mambretti ◽  
Marco Villa ◽  
Serena Grumi ◽  
Andrea Citterio ◽  
...  

AbstractThe COVID-19 pandemic represents a collective trauma that may have enduring stress effects during sensitive periods, such as pregnancy. Prenatal stress may result in epigenetic signatures of stress-related genes (e.g., the serotonin transporter gene, SLC6A4) that may in turn influence infants’ behavioral development. In April 2020, we launched a longitudinal cohort study to assess the behavioral and epigenetic vestiges of COVID-19-related prenatal stress exposure in mothers and infants. COVID-19-related prenatal stress was retrospectively assessed at birth. SLC6A4 methylation was assessed in thirteen CpG sites in mothers and infants’ buccal cells. Infants’ temperament was assessed at 3-month-age. Complete data were available from 108 mother-infant dyads. Greater COVID-19-related prenatal stress was significantly associated with higher infants’ SLC6A4 methylation in seven CpG sites. SLC6A4 methylation at these sites predicted infants’ temperament at 3 months.


Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3640
Author(s):  
Kyung-A. Hwang ◽  
Hye-Jeong Hwang ◽  
Yu Jin Hwang ◽  
Young Jun Kim

Mustard leaf (Brassica juncea var. crispifolia L. H. Bailey) has been reported to have psychological properties such as anti-depressant activities. However, studies on chronic stress and depression caused by restraint have not been conducted. Therefore, this study aimed to evaluate the effects of a mustard leaf (ML) extract on chronic restraint stress (CRS) in mice. Male mice were subjected to a CRS protocol for a period of four weeks to induce stress. The results showed that the ML extract (100 and 500 mg/kg/perorally administered for four weeks) significantly decreased corticosterone levels and increased neurotransmitters levels in stressed mice. Apoptosis by CRS exposure was induced by Bcl-2 and Bax expression regulation and was suppressed by reducing caspase-3 and poly (ADP-ribose) polymerase expression after treatment with the ML extract. Our results confirmed that apoptosis was regulated by increased expression of brain-derived neurotrophic factor (BDNF). Additionally, cytokine levels were regulated by the ML extract. In conclusion, our results showed that the ML extract relieved stress effects by regulating hormones and neurotransmitters in CRS mice, BDNF expression, and apoptosis in the brain. Thus, it can be suggested that the studied ML extract is an agonist that can help relieve stress and depression.


1991 ◽  
Vol 24 (5) ◽  
pp. 361-372 ◽  
Author(s):  
T. Szuran ◽  
E. Zimmerman ◽  
V. Pliska ◽  
H. P. Pfister ◽  
H. Welzl

2007 ◽  
Vol 292 (2) ◽  
pp. E615-E620 ◽  
Author(s):  
Ben A. Weissman ◽  
Chantal M. Sottas ◽  
Ping Zhou ◽  
Costantino Iadecola ◽  
Matthew P. Hardy

Immobilization stress (IMO) induces a rapid increase in glucocorticoid secretion [in rodents, corticosterone CORT)] and this is associated with decreased circulating testosterone (T) levels. Nitric oxide (NO), a reactive free radical and neurotransmitter, has been reported to be produced at higher rates in tissues such as brain during stress. The biosynthesis of T is also known to be dramatically suppressed by NO. Specifically, the inducible isoform of nitric oxide synthase (iNOS) was directly implicated in this suppression. To assess the respective roles of CORT and NO in stress-mediated inhibition of T production, adult wild-type (WT) and inducible nitric oxide synthase knockout (iNOS−/−) male mice were evaluated. Animals of each genotype were assigned to either basal control or 3-h IMO groups. Basal plasma and testicular T levels were equivalent in both genotypes, whereas testicular weights of mutant mice were significantly higher compared with WT animals. Exposure to 3-h IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. Testicular T levels were also affected by stress in WT and mutant males, being sharply reduced in both genotypes. However, the concentrations of nitrite and nitrate, the stable metabolites of NO measured in testicular extracts, did not differ between control and stressed WT and iNOS−/− mice. These results support the hypothesis that CORT, but not NO, is a plausible candidate to mediate rapid stress-induced suppression of Leydig cell steroidogenesis.


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