FAILURE OF PARTURITION IN MICE LACKING THE PROSTAGLANDIN-F RECEPTOR

Mice lacking the gene encoding the receptor for prostaglandin F-2 alph a (FP) developed normally but were unable to deliver normal fetuses at term. Although these FP-deficient mice showed no abnormality in the e strous cycle, ovulation, fertilization, or implantation, they did not respond to exogenous oxytocin because of the lack of induction of oxyt ocin receptor (a proposed triggering event in parturition), and they d id not show the normal decline of serum progesterone concentrations th at precedes parturition. Ovariectomy at day 19 of pregnancy restored i nduction of the oxytocin receptor and permitted successful delivery in the FP-deficient mice. These results indicate that parturition is ini tiated when prostaglandin F-2 alpha interacts with FP in ovarian lutea l cells of the pregnant mice to induce luteolysis.