Prenatal ethanol exposure decreases hippocampal 3H-glutamate binding in 45-day-old rats.

The effect of prenatal ethanol exposure on putative glutamate receptor binding sites in rat brain was studied using radiohistochemical techniques. Pregnant Sprague-Dawley rats were fed a liquid diet containing either 3% or 6% (vol./vol.) ethanol throughout gestation. Pair-fed dams received isocalorically matched liquid diets and a lab chow ad lib group served as control for paired feeding. At 45 days of age, the offspring were sacrificed and their brains analyzed by in vitro 3H-glutamate autoradiography. Compared to pair-fed controls, specific 3H-glutamate binding was reduced by 49-53% in regions of the dorsal hippocampal formation of 45-day-old rats whose mothers consumed either 3% or 6% ethanol diets. Specific 3H-glutamate binding was decreased also in the ventral hippocampal formation, entorhinal and posterior neocortex, but to a less consistent degree and magnitude than in dorsal hippocampal formation of fetal alcohol rats. The reduction in hippocampal 3H-glutamate binding 45 days after prenatal ethanol exposure suggests a long-lasting net decrease in glutamate-mediated excitatory neurotransmission within the hippocampal formation of fetal alcohol rats. This glutamate receptor binding site alteration may be one factor contributing to a decrease in long-term potentiation of hippocampal CA1 pyramidal neurons in fetal alcohol rats. In addition, this alteration may underlie learning and other behavioral deficits associated with functional defects of the hippocampal formation.