Prenatal ethanol exposure has been associated with long-lasting intellectual impairments in children. Previous studies using animal models of fetal ethanol exposure suggest that these deficits are, at least in part, linked to neurochemical abnormalities in the hippocampal formation. We explored whether prenatal exposure to moderate quantities of ethanol produced functional deficits at the entorhinal cortical perforant path-dentate granule cell connection by examining some electrophysiological properties, including the induction of long-term potentiation (LTP). Rat dams consumed one of three diets throughout gestation: 1) a BioServ liquid diet containing 5% (v/v) ethanol (26% ethanol-derived calories), which produces a maternal peak blood ethanol concentration of 83 mg/dl; 2) pair-fed an isocalorically equivalent amount of 0% ethanol liquid diet; or 3) Purina rat chow ad libitum. Adult offspring (120-150 days of age) from each experimental diet group were anesthetized with urethane and field excitatory postsynaptic potentials (EPSPs) and population spikes were measured in the dentate gyrus in response to ipsilateral perforant path stimulation. We examined input-output functions using a wide range of single pulse stimulation intensities and induction of LTP using high-frequency stimulation. In the 50-500 microA range of single pulse intensities, there were no significant differences among the diet groups in dentate gyrus evoked potentials. In response to high-frequency stimulation, prenatal ethanol-exposed rats showed a smaller increase in field EPSPs and population spikes compared with rats from either of the two control groups. Thus, prenatal exposure to moderate ethanol levels can produce a long-lasting deficit in synaptic enhancement in a neural pathway believed to be critical in certain forms of learning and memory. This deficit in hippocampal synaptic plasticity may, in part, account for cognitive impairments seen in children whose mothers consumed ethanol during pregnancy.