Abstract
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 CA 3 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have