Male offspring of mothers stressed during pregnancy show feminized and demasculinized patterns of sexual behavior in adulthood. This so called Prenatal Stress Syndrome has been demonstrated in rats and mice, and may provide insight into intersexed behaviors shown by humans. The several objectives of the present research program include characterizing more completely in prenatally stressed male rats various sexual (e.g. ejaculation, lordosis) and nonsexual (e.g. adolescent play) behaviors known to be organized by exposure to androgens during perinatal life. Secondly, two aspects of the potential mechanism(s) mediating this syndrome will be investigated. The first will utilize radioimmunoassay to determine whether stressed males fail to experience the surge in plasma testosterone during the first hours of birth known to occur in controls. If they do not, critical neonatal factors will have to be considered as playing a causal role in this syndrome which currently is believed to result entirely from an abnormal hormonal milieu during fetal life. The possible involvement of endogenous opiates in the mediation of the Prenatal Stress Syndrome will be assessed by injecting stressed and control mothers with the opiate receptor blocker maltrexone. If stress-induced opiate release is involved then the abnormal adult behavioral and fetal testicular enzyme pattern(s) characteristic of prenatally stressed males should be prevented by pretreating mothers with naltrexone before administering gestational stress. An additional series of studies will investigate the extent to which prepuberal social factors interact with prenatal stress to determine adult sexual behavior potentials and will probe possible physiological mechanisms by which this interaction might be achieved. Finally, an attempt will be made to extend the Prenatal Stress Syndrome to the guinea pig, a laboratory species in which, like man but unlike the rat, sexual differentiation is completed during fetal ontogeny.
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