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Oxytocin induces embryonic diapause.

Jessica L Minder1,2,3,4,5,6,7, Sarah B Winokur1,2,3,4,5,6,7, Janaye Stephens2,4

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Oxytocin triggers embryonic diapause, a temporary halt in development, in mice. This finding reveals a key hormone coordinating pregnancy timing with maternal conditions for reproductive success.

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Area of Science:

  • Reproductive biology
  • Developmental biology
  • Endocrinology

Background:

  • Embryonic diapause, a temporary developmental arrest before implantation, occurs in various species.
  • Facultative diapause is linked to maternal metabolic stress, such as during nursing.
  • The natural inducing factor for embryonic diapause remained unidentified.

Purpose of the Study:

  • To identify a natural inducing factor for embryonic diapause.
  • To investigate the role of oxytocin in regulating embryonic diapause in mice.

Main Methods:

  • Induction of gestational delays via nursing or optogenetic stimulation of oxytocin neurons.
  • Analysis of oxytocin receptor expression in mouse blastocysts.
  • In vitro culture of embryos with oxytocin to observe developmental effects.
  • Assessment of embryo survival rates in oxytocin receptor-knockout models.

Main Results:

  • Oxytocin administration or stimulation of oxytocin neurons triggered gestational delays mimicking diapause.
  • Mouse blastocysts were found to express oxytocin receptors.
  • Oxytocin exposure induced delayed implantation-like dispersion in cultured mouse embryos.
  • Embryos lacking oxytocin receptors exhibited reduced survival rates during diapause.

Conclusions:

  • Oxytocin is identified as a natural inducer of embryonic diapause in mice.
  • Oxytocin plays a crucial role in coordinating embryonic development with uterine conditions during pregnancy.
  • This mechanism represents an evolutionarily conserved strategy for ensuring reproductive success.