In the present study, we examined the longitudinal effects of prenatal etha
nol exposure on the electrophysiological characteristics of CAL neurons in
hippocampal slices. Hippocampal slices were obtained from young (25-32-day
old) and adult (63-77-day old) male offspring of rats given one of four tre
atments during gestation. Three groups of pregnant rats were orally intubat
ed with 0, 4, or 6 g/kg ethanol on gestational days 8-20. Caloric intake fo
r the 0- (nutritional control) and 4-g/kg groups was yoked to that of the 6
g/kg group. A fourth group (untreated control) was not intubated, and was
given ad lib access to food. Long-term potentiation and paired-pulse inhibi
tion were unaffected by prenatal ethanol exposure in young and adult rats;
however, slices taken from the young 6 g/kg ethanol group displayed a signi
ficantly lower maximal CA1 population spike amplitude evoked by Schaffer co
llateral stimulation as compared to young controls. This difference was not
observed in adult animals. These data suggest that some aspects of hippoca
mpal physiology are negatively affected in young rats as a result of prenat
al ethanol exposure, but this effect reverses as the animal matures. (C) 19
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