Exposure to alcohol on E9 raises poststress corticosterone in mature but not old mice.

Prenatal exposure to alcohol alters postnatal function of the hypothalamic-pituitary-adrenal axis. Hyperresponsiveness to stress, or increased secretion of corticosterone, is a commonly studied effect in offspring of rats exposed to alcohol during a substantial period of gestation. No studies have reported on stress hormone secretion following alcohol exposure on a single day during embryonic development even though exposure at this time may damage the hypothalamus and pituitary. To explore the effect of an acute exposure, we used the offspring of C57BL/6J mice exposed to alcohol or saline on embryonic day (E) 9 (2.9 g/kg administered twice, 4h apart). At 7.5 or 22 months of age these mice were subjected to a 12-h restraint stress, or merely kept in the same environment without restraint. After the 12-h period, a blood sample was obtained from the retro-orbital plexus, and analyzed for the amount of corticosterone. The 7.5-month old group of alcohol-treated offspring were indeed hyperresponsive to restraint stress, but the 22-month old mice were not. Whether the normal-appearing corticosterone response of the old alcohol-exposed mice indicated adaptation to restraint, an aging-associated ceiling effect in corticosterone secretion, or an expression of pathology, cannot be decided on the basis of present data.