The effect of restraint stress in early pregnancy in mice

Wiebold, J. L.; Stanfield, P H; Becker, W. C.; Hillers, J.K.

doi:10.1530/jrf.0.0780185

Cited by 88 publications

(68 citation statements)

References 26 publications

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“…Embryonic implantation was not affected by restraint stress at any of the gestational stages, in contrast to the implantation failure induced by 5-h stress on GD1-6 in SW/B6D2F1 mice [39]. This shows a strain difference.…”

Section: Discussionmentioning

confidence: 63%

“…Unexpectedly, the 4-day repeated stress did not induce implantation failure and costal malformations, but it did enhance the incidence of cleft palate, post-implantation loss and sternal abnormalities, in addition to growth retardation. In spite of the somewhat different aspects of fetal abnormalities observed by previous investigations [9,14,21,28,39], it should be emphasized that different outcomes in embryo-fetal toxicity were obtained by maternal stress at each gestational stage, pre-and peri-implantation, early and late organogenesis, and fetal development. A more detailed study using a highly susceptible mouse strain under a longer duration of stress might clarify the hypothetical hormonal mechanism involved in embryo-fetal toxicity.…”

Section: Discussionmentioning

confidence: 77%

“…In comparison, it is known that restraint in the peri-implantation period leads to implantation failure, and that stress at appropriate times in organogenesis produces cleft palate, costal abnormalities and resorption of fetuses in mice [9,14,21,28,39]. Furthermore, some factors including type and duration of restraint, position and strain of mice, and lights are believed to be closely related to the incidence of maternal and fetal toxicities [15].…”

Section: Discussionmentioning

confidence: 99%

“…Although the mechanism behind this result remains to be clarified, it has been proposed that environmental imprinting factors such as hormonal imbalance might affect the fertilized ova, causing delayed embryonic resorptions, malformations and growth [39]. Restraint stress only on GD9-12 induced cleft palate of fetuses, indicative of the disturbing effect of glucocorticoids induced by the stress on the development of the palatine process.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Maternal Restraint Stress on Fetal Development of ICR Mice

et al. 2008

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of Maternal Restraint Stress on Fetal Development of ICR Mice

et al. 2008

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“…Although Soede et al (2007) failed to observe any difference in fertilization rate and embryonic development in sows, data in rodents showed that stress during early gestation can lead to abortions (Wiebold et al, 1986). In species with multiple foetuses like pigs, maternal stress is suspected to reduce the number of youngs born alive, suggesting an increased foetal mortality (von Borell et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Behavioural, endocrine and immune responses to repeated social stress in pregnant gilts

Couret

Otten

Puppe

et al. 2009

Animal

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Pregnant sows are exposed to various stressors in intensive pig husbandry that may have negative consequences on their health, reproductive performances and welfare. Social stress is one of these challenges, because gestating sows have to be housed in groups according to EU guidelines (2001/88/CE). The purpose of this study was to determine the consequences of repeated social stress in pregnant female pigs on their behavioural, endocrine and immunological responses and on pregnancy outcome. Pregnant gilts were submitted to a repeated social stress procedure induced by housing unfamiliar gilts in pairs changed twice a week between days 77 and 105 of gestation (S group, n 5 18). Control gilts were housed in stable pairs during the same period (C group, n 5 18). Agonistic behaviour was observed during the first 3 h after each grouping. Skin lesions were numbered 2 h after each grouping. Salivary cortisol was measured before and repeatedly during the 4 weeks of grouping. Gilts were immunized against keyhole limpet haemocyanin (KLH) on days 81 and 95 of gestation. Immunoglobulins G against KLH, proliferative responses to concanavalin A, lipopolysaccharide, pokeweed mitogen and KLH and peripheral blood leukocyte numbers were evaluated 1 week before the first grouping and 3 days after the last one. Agonistic interactions and skin lesions were observed in S gilts at each grouping, although there was a decline between the first and the last grouping ( P , 0.05). The repeated social stress induced a sustained endocrine response as shown by elevated salivary cortisol levels from 1 to 48 h after grouping in S gilts compared to C gilts. The cellular as well as the humoral immunity and the leukocyte numbers were not influenced by social stress. Gestation length tended to be shorter in S gilts ( P 5 0.09), but litter size, piglet weight or mortality at birth were not affected. Variability of the response of S gilts to groupings was partly explained by their average success value determined according to the outcome (defeat or win) of all the groupings. In conclusion, our study demonstrates that the application of repeated social stress to pregnant gilts during the last third of their gestation repeatedly activates their hypothalamo-pituitary-adrenal axis but does not impair their immune function and pregnancy outcome.

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Refinement of inducible gene deletion in embryos of pregnant mice

Savery¹,

Maniou²,

Culshaw³

et al. 2019

Birth Defects Research

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CreERT2‐mediated gene recombination is widely applied in developmental biology research. Activation of CreERT2 is typically achieved by injection of tamoxifen in an oily vehicle into the peritoneal cavity of mid‐gestation pregnant mice. This can be technically challenging and adversely impacts welfare. Here we characterize three refinements to this technique: Pipette feeding (not gavage) of tamoxifen, ex vivo CreERT2 activation in whole embryo culture and injection of cell‐permeable TAT‐Cre into Cre‐negative cultured embryos. We demonstrate that pipette feeding of tamoxifen solution to the mother on various days of gestation reliably activates embryonic CreERT2, illustrated here using β‐Actin CreERT2, Sox2 CreERT2, T CreERT2, and Nkx1.2 CreERT2. Pipette feeding of tamoxifen induces dose‐dependent recombination of Rosa26 mTmG reporters when administered at E8.5. Activation of two neuromesodermal progenitor‐targeting Cre drivers, T CreERT2, and Nkx1.2 CreERT2, produces comparable neuroepithelial lineage tracing. Dose‐dependent CreERT2 activation can also be achieved by brief exposure to 4OH‐tamoxifen in whole embryo culture, allowing temporal control of gene deletion and eliminating the need to treat pregnant mice. Rosa26 mTmG reporter recombination can also be achieved regionally by injecting TAT‐Cre into embryonic tissues at the start of culture. This allows greater spatial control over Cre activation than can typically be achieved with endogenous CreERT2, for example by injecting TAT‐Cre on one side of the midline. We hope that our description and application of these techniques will stimulate refinement of experimental methods involving CreERT2 activation for gene deletion and lineage tracing studies. Improved temporal (ex vivo treatment) and spatial (TAT‐Cre injection) control of recombination will also allow previously intractable questions to be addressed.

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The effect of restraint stress in early pregnancy in mice

Cited by 88 publications

References 26 publications

Effect of Maternal Restraint Stress on Fetal Development of ICR Mice

Effect of Maternal Restraint Stress on Fetal Development of ICR Mice

Behavioural, endocrine and immune responses to repeated social stress in pregnant gilts

Refinement of inducible gene deletion in embryos of pregnant mice

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