Female mammals, particularly rodents, exhibit a number of reproductive deficits as a consequence of exposure to prenatal stress. Among the most serious are the effects upon fertility and fecundity. To date, there has not been a systematic analysis that has delineated those factors responsible for the deficits on reproductive physiology and possibly behavior in prenatally stressed females. In the present proposal the reproductive deficits present in the prenatally-stressed female will be studied with focus upon physiological, i.e. endocrine/neuroendocrine, and behavioral processes and the interactions between the behavioral state of the female and her physiological responses. In preliminary studies, decrements in reproductive success in prenatally-stressed female rats were found with as many as 80% of these females failing to carry their pregnancies to term and only 10% of the mated females raising a litter through the first week of lactation. In addition, prenatally-stressed females were behaviorally less responsive to their young, and prenatally-stressed females showed diminished endocrine responses as adults. Since both pregnancy maintenance as well as the induction of maternal behavior in the rat are under endocrine (hormonal) control, it is possible that the deficits in pregnancy maintenance, lactational performance, and maternal behavior in the prenatally-stressed female, may result from a common underlying deficiency in the female's ability to secrete hormones, a deficiency brought about by exposure to stress in utero. In the current research, Drs. Robert Bridges and Craig Kinsley are studying the potential common underlying physiological mechanisms that contribute to both the decrements in reproductive physiology and behavior. The work will focus on whether the detriments in pregnancy, lactation and behavior result from changes in hormone (prolactin) regulation and action brought about by the prenatal stress experience. The results of these studies will help to define those factors responsible for the normal maintenance of pregnancy and lactation, and will provide a data base for evaluating analogous endocrine and behavioral deficits in other mammals, including humans.
