Kosofsky B E, Wilkins A S, Gressens P, Evrard P
Laboratory of Molecular and Developmental Neuroscience, Massachusetts General Hospital, Charlestown 02129.
J Child Neurol. 1994 Jul;9(3):234-41. doi: 10.1177/088307389400900303.
Between 10% and 15% of infants born in urban America today have been exposed to cocaine in utero. Clinical studies have suggested that impairment of brain growth is the single best marker of significant prenatal cocaine exposure, and postnatal developmental compromise seen in a subset of affected children as a consequence of that exposure. We have developed an animal model, in mice, of prenatal cocaine exposure that has allowed us to dissociate the direct effects of cocaine in altering fetal development from the indirect effects associated with cocaine-induced malnutrition. We find that transplacental cocaine exposure independently impairs fetal brain and body growth and results in behavioral deficits and permanent alterations in neocortical cytoarchitecture in exposed offspring.
如今在美国城市出生的婴儿中，有10%至15%在子宫内接触过可卡因。临床研究表明，脑生长受损是产前大量接触可卡因的最佳单一指标，并且在一部分受影响的儿童中会出现因这种接触而导致的产后发育受损。我们已经在小鼠中建立了一种产前接触可卡因的动物模型，这使我们能够区分可卡因改变胎儿发育的直接作用和与可卡因诱导的营养不良相关的间接作用。我们发现，经胎盘接触可卡因会独立损害胎儿的脑和身体生长，并导致暴露后代出现行为缺陷和新皮质细胞结构的永久性改变。
