Augmented memory loss in aging mice after one embryonic exposure to alcohol.
Prenatal exposure to alcohol can produce behavioral and cognitive deficits even in the absence of dysmorphic facial features. In a mouse model, we tested whether embryonic exposure to alcohol could exacerbate functional loss as animals age. Normal-appearing offspring were selected from litters produced by C57Bl/6J mice that had been gavaged with one teratogenic dose (5.8 g/kg) of ethyl alcohol during organogenesis on the 9th day of gestation. In adulthood, the offspring suffered a deficit in long-term retention, but not acquisition, of a place learning task. Although barely detectable in young adults, the retention deficit was severe in aging mice. These findings demonstrate that the functional deficits resulting from embryonic exposure to alcohol can interact with those of aging.
Dumas
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RM
New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314.
Rabe
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D000375:Aging / Q000523:psychology; D000818:Animals; D004195:Disease Models, Animal; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D008297:Male; D008431:Maternal-Fetal Exchange; D018782:Maze Learning / Q000187:drug effects; D008568:Memory / Q000187:drug effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
D000431:Ethanol