Impaired acquisition in the water maze and hippocampal long-term potentiation after chronic prenatal ethanol exposure in the guinea-pig

In the hippocampus, the CA1 region is selectively vulnerable to the effects of chronic prenatal ethanol exposure. In the guinea‐pig, the number of CA1 pyramidal cells is decreased after chronic prenatal ethanol exposure. We tested the hypotheses that chronic prenatal ethanol exposure (through maternal ethanol ingestion) results in impairments in spatial learning and short‐ and long‐term plasticity in the CA1 region of the postnatal guinea‐pig hippocampus. Timed, pregnant guinea‐pigs were treated with ethanol (4 g/kg maternal body weight/day), isocaloric sucrose/pair‐feeding, or water throughout gestation. Offspring were studied between postnatal days 40 and 80. In the Morris water maze, animals exposed to ethanol prenatally showed slower acquisition of an escape response to a hidden platform over 5 days of training. The amplitude of the field excitatory postsynaptic potential in the CA1 region in response to contralateral CA3 stimulation was decreased in offspring exposed to ethanol prenatally. Two forms of short‐term plasticity (paired‐pulse and frequency facilitation) were unaffected by chronic prenatal ethanol exposure. Long‐term potentiation (LTP) in response to high‐frequency CA3 stimulation was induced reliably and maintained over 60 min in isocaloric‐sucrose and water control animals. However, LTP failed to be induced in the CA1 area of the hippocampus in prenatal ethanol‐exposed offspring. These data show that chronic prenatal ethanol exposure, through maternal ethanol administration, impairs spatial performance and LTP in CA1 neurons. Hippocampal dysfunction could contribute importantly to the cognitive and behavioural deficits resulting from chronic prenatal ethanol exposure.