Decreased postnatal testosterone and corticosterone concentrations in rats following acute intermittent prenatal hypoxia without alterations in adult male sex behavior.

The prenatal and postnatal testosterone surges in the male rat are associated with neurobehavioral sexual differentiation of the brain. Both surges can be attenuated by maternal stress or other environmental factors that activate the maternal and/or fetal hypothalamic/pituitary/adrenal (HPA) axis during the last week of gestation. Since hypoxia is known to activate the HPA axis, we studied its effect during gestation on sexual differentiation in the male rat. We examined the influence of intermittent hypoxic exposure during gestation with respect to the postnatal testosterone surge and corticosterone levels, and subsequent development of adult reproductive and nonreproductive sexually dimorphic behaviors. Plasma testosterone and corticosterone concentrations of male neonates were measured after maternal exposure to acute, intermittent, prenatal hypoxia (9% O2 6 h/day from Day 15 to 21 of gestation). Relative to normoxic controls, acute, intermittent, prenatal hypoxia significantly attenuated the postnatal testosterone surge. Postpartum plasma corticosterone levels in these animals were also suppressed. In adulthood, prenatally hypoxic animals exhibited normal masculine sex behavior. Lordosis behavior in response to estrogen and progesterone priming was not significantly different between treatment groups. Saccharin preference, a nonreproductive, sexually dimorphic behavior, was not significantly influenced by prenatal hypoxic exposure. These results demonstrate that in the male acute intermittent prenatal hypoxia attenuates the postnatal testosterone surge. However, this reduction failed to result in significant alterations in the expression of sex related behaviors in adulthood.