NYU Dataset
Oxytocin Induces Embryonic Diapause in Mice
Part of: Oxytocin U19 BRAIN Initiative |
UID: 10742
- Description
- Through multiple experiments, this study demonstrated that oxytocin induces diapause, a temporary developmental delay, in pre-implantation mouse embryos to help ensure their survival. To assess whether oxytocin receptor (OXTR) signaling might influence this gestational delay, heterozygous (OXTR+/−) dams which retain sufficient OXTR function for apparently normal parturition and nursing, were bred. After the second breeding, these animals were found to experience a prolonged gestational delay and fewer OXTR knockout (KO) pups were born in litters that experienced diapause. The investigators also observed the effect of temporal patterns of oxytocin release and patterned optogenetic stimulation on the induction of diapause. To examine examining embryonic oxytocin receptor expression in blastocysts, nondiapaused blastocysts were harvested at E3.5 and probed for the presence of OXTRs. In vitro, oxytocin-treated blastocysts were found to exhibit diapause-like delayed implantation. Embryonic survival following ovariectomy-induced diapause was mediated by OXTR signaling; OXTR KO embryos had lower survival rates after diapause induction compared to wild-type embryos.
C57BL/6 mice
Ai9 mice
OXTR−/− mice
OXT-Cre mice
OXTR+/− mice
CD-1 mice
Associated Publications
Data Type
Equipment Used
Software Used
Dataset Format(s)
Microsoft Excel
Access
- Restrictions
-
Free to All
- Instructions
- All data needed to evaluate the conclusions in the paper are present in the paper on PubMed Central (PMC) under Supplementary Materials. The dataset includes source data and statistical analysis for figures in the associated publication.
- Grant Support
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Edward Mallinckrodt Jr. Foundation/Edward Mallinckrodt Jr. FoundationBarnard College Summer Research Institute/Golden Family Foundation Endowment Fund
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