Failure of parturition in mice lacking the prostaglandin F receptor

Y Sugimoto, A Yamasaki, E Segi, K Tsuboi, Y Aze… - Science, 1997 - science.org
Y Sugimoto, A Yamasaki, E Segi, K Tsuboi, Y Aze, T Nishimura, H Oida, N Yoshida…
Science, 1997science.org
Mice lacking the gene encoding the receptor for prostaglandin F2α (FP) developed normally
but were unable to deliver normal fetuses at term. Although these FP-deficient mice showed
no abnormality in the estrous cycle, ovulation, fertilization, or implantation, they did not
respond to exogenous oxytocin because of the lack of induction of oxytocin receptor (a
proposed triggering event in parturition), and they did not show the normal decline of serum
progesterone concentrations that precedes parturition. Ovariectomy at day 19 of pregnancy …
Mice lacking the gene encoding the receptor for prostaglandin F (FP) developed normally but were unable to deliver normal fetuses at term. Although these FP-deficient mice showed no abnormality in the estrous cycle, ovulation, fertilization, or implantation, they did not respond to exogenous oxytocin because of the lack of induction of oxytocin receptor (a proposed triggering event in parturition), and they did not show the normal decline of serum progesterone concentrations that precedes parturition. Ovariectomy at day 19 of pregnancy restored induction of the oxytocin receptor and permitted successful delivery in the FP-deficient mice. These results indicate that parturition is initiated when prostaglandin F interacts with FP in ovarian luteal cells of the pregnant mice to induce luteolysis.
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