ABSTRACT
In 1996, the century-old thesis that OT was required for parturition was falsified by the surprisingly normal delivery of OT (–/–) null mice.2,3 Although homozygote OT null mice die postpartum, due to the inability of the mother to lactate, delivery of viable pups occurs unhindered on the normal day of parturition. Thus, in mice, OT is critical for the milk ejection reflex but not parturition. Although difficult to reconcile with the wealth of data supporting a role for OT in the timing of parturition, subsequent analysis of the OT null mouse in conjunction with other transgenic mice has revealed far more about the role of OT in mouse parturition than was previously described. Perhaps the most important implication of the OT null mouse is the interrelationship of OT with PG.
