The present study tested the hypothesis that chronic prenatal
ethanol exposure causes long-lasting changes in
glucocorticoid signalling in postnatal offspring. Pregnant guinea pigs were treated with
ethanol (4 g/kg maternal
body weight/day), isocaloric-
sucrose/pair-feeding or water throughout gestation, and maternal saliva
cortisol concentration was determined 2 h
after treatment at different stages of gestation. Electrically-stimulated release of
glutamate and
GABA, in the presence or absence of
dexamethasone, as well as
glucocorticoid and
mineralocorticoid receptor mRNA expression, was determined in the hippocampus and prefrontal cortex of adult offspring of treated pregnant guinea pigs. Maternal saliva
cortisol concentration increased throughout pregnancy, which was associated with increased foetal plasma and amniotic fluid
cortisol concentration.
Ethanol administration to pregnant guinea pigs increased maternal saliva
cortisol concentration during early and mid-gestation. In late gestation,
ethanol administration did not increase saliva
cortisol concentration above that induced by pregnancy. Chronic prenatal
ethanol exposure had no effect on stimulated
glutamate or
GABA release, but selectively prevented
dexamethasone-mediated suppression of stimulated
glutamate release, and decreased expression of
mineralocorticoid, but not
glucocorticoid, receptor mRNA in the hippocampus of adult offspring. These data indicate that maternal
ethanol administration leads to excessively increased maternal
cortisol concentration that can impact negatively the developing foetal brain, leading to persistent postnatal deficits in
glucocorticoid regulation of
glutamate signalling in the adult hippocampus.