The development of kindling was examined in adult rats exposed to ethanol prenatally. Pregnant Wistar rats were fed a liquid diet containing either 6.7% ethanol or pair fed an isocaloric equivalent. At birth, the litters were cross fostered to surrogate mothers. At 80 days of age, a bipolar electrode was placed either in the right basolateral amygdala or the right angular bundle of entorhinal cortex. Kindling stimulations were administered three times a day until each rat had exhibited three class 5 kindled motor seizures. The total number of kindling stimulations required to exhibit class 1 through class 5 motor seizures was significantly greater in the rats exposed to ethanol prenatally. Further, the retardation in kindling development was due to a slower progression from class 0 to class 1 kindled motor seizures. Progression between other stages was not different between the two groups. Similar results were obtained in both amygdala and angular bundle kindling experiments. Kindling is retarded in a similar fashion by partial destruction of the dentate granule cells of the hippocampal formation. Further, the pattern of dentate granule cell axonal projections to hippocampal CA3 pyramidal neurons is altered in rats exposed to ethanol prenatally. Taken together, these data suggest the possibility that a defect in the neuronal circuitry within the hippocampal formation of fetal alcohol rats may underlie a retardation in their kindling progression. This proposed defect may have functional implications related to learning deficiencies in rats and children exposed to ethanol prenatally.