Prenatal exposure to alcohol alters short-term plasticity in hippocampus.
Paired-pulse potentiation was studied in the CA1 region of rats exposed prenatally to alcohol. Pregnant rats were fed a liquid diet containing 35% ethanol-derived calories on days 3 to 21 of gestation. Control animals were fed liquid diets without ethanol. When the pups of both groups were 40 to 60 days old, hippocampal slices were prepared and maintained in vitro. Paired-pulse potentiation was examined at intervals from 5 to 400 ms. Recordings made from these slices showed that the response inhibition typically seen at short interpulse intervals was minimal or absent in the animals with prenatal exposure to alcohol. Potentiation of population spike amplitude was enhanced at intervals to 100 ms.
D000818:Animals; D000431:Ethanol / Q000494:pharmacology*; D005071:Evoked Potentials; D005260:Female; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D013569:Synapses / Q000502:physiology
D000431:Ethanol