Deficiency in mouse oxytocin prevents milk ejection, but not fertility or parturition

W. Scott Young, Emily Shepard, Janet Amico, Lothar Hennighausen, Kay Uwe Wagner, Mary E. Lamarca, Cindy McKinney, Edward I. Ginns

Research output: Contribution to journalArticlepeer-review

268 Scopus citations


Oxytocin is a nonapeptide hormone that participates in the regulation of parturition and lactation. It has also been implicated in various behaviors, such as mating and maternal, and memory. To investigate whether or not oxytocin (OT) is essential for any of these functions, we eliminated, by homologous recombination, most of the first intron and the last two exons of the OT gene in mice. Those exons encode the neurophysin portion of the oxytocin preprohormone which is hypothesized to help in the packaging and transport of OT. The homozygous mutant mice have no detectable neurophysin or processed oxytocin in the paraventricular nucleus, supraoptic nucleus or posterior pituitary. Interestingly, homozygous mutant males and females are fertile and the homozygous mutant females are able to deliver their litters. However, the pups do not successfully suckle and die within 24 h without milk in their stomachs. OT injection into the dams restores the milk ejection in response to suckling. These results indicate an absolute requirement for oxytocin for successful milk ejection, but not for mating, parturition and milk production, in mice.

Original languageEnglish (US)
Pages (from-to)847-853
Number of pages7
JournalJournal of Neuroendocrinology
Issue number11
StatePublished - 1996
Externally publishedYes


  • Homologous recombination
  • Lactation
  • Mammary gland
  • Reproduction paraventricular
  • Supraoptic

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience


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