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

W. Scott Young, III, Emily Shepard, Janet AmicoÝ, Lothar Hennighausen§, Kay-Uwe Wagner§, Mary E. LaMarca*, Cindy McKinney*, Edward I. Ginns*

Laboratory of Cell Biology1 and *Clinical Neuroscience Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-4068; §Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases; and ÝDivision of Endocrinology and Metabolism, University of Pittsburgh, School of Medicine and VA Medical Center, Pittsburgh, PA 15261

J. Neuroendocrinol. 8: 847-853, 1996. 

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 (see 21K figure). 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 hours 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.

See also short article on oxytocin, reproduction and behavior.