Behavioral, Reproductive & Neuroendocrine Consequences of Prenatal Stress

雌性哺乳动物，特别是啮齿动物，由于暴露在产前压力下，表现出许多生殖缺陷。其中最严重的是对生育力和繁殖力的影响。到目前为止，还没有一个系统的分析，描述了那些因素负责生殖生理缺陷和可能的行为在产前压力的女性。在目前的建议中，生殖缺陷存在于产前应激的女性将重点研究生理，即内分泌/神经内分泌，行为过程和女性的行为状态和她的生理反应之间的相互作用。在初步的研究中，发现怀孕压力大的雌性大鼠的繁殖成功率下降，多达80%的雌性大鼠不能怀孕到足月，只有10%的雌性交配大鼠能在哺乳期的第一周产下一窝。此外，产前应激的雌性对幼崽的行为反应较差，成年后的内分泌反应也较差。由于大鼠的妊娠维持和母性行为的诱导都受到内分泌（激素）的控制，因此妊娠维持、哺乳期表现和母性行为的缺陷可能是由于雌性分泌激素能力的共同潜在缺陷造成的，这种缺陷是由子宫内暴露于压力造成的。在目前的研究中。罗伯特·布里奇斯（Robert Bridges）和克雷格·金斯利（Craig Kinsley）正在研究导致生殖生理和行为下降的潜在共同潜在生理机制。这项工作将重点关注妊娠、哺乳和行为方面的危害是否由产前应激经历带来的激素（催乳素）调节和作用的变化引起的。这些研究的结果将有助于确定那些负责正常维持妊娠和哺乳的因素，并将为评估包括人类在内的其他哺乳动物的类似内分泌和行为缺陷提供数据基础。

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.