TRANSPLACENTAL COCAINE EXPOSURE - A MOUSE MODEL DEMONSTRATING NEUROANATOMICAL AND BEHAVIORAL ABNORMALITIES
TRANSPLACENTAL COCAINE EXPOSURE - A MOUSE MODEL DEMONSTRATING NEUROANATOMICAL AND BEHAVIORAL ABNORMALITIES
复制标题
DOI：
10.1177/088307389400900303
复制
发表时间：
1994-07-01
影响因子：
1.9
通讯作者：
EVRARD, P
中科院分区：
文献类型：
--
作者：
KOSOFSKY, BE;WILKINS, AS;EVRARD, P
如今，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，大脑发育受损是产前严重接触可卡因的唯一最佳标志，而在部分受影响的儿童中，由于接触可卡因，会出现产后发育受损。我们开发了一种产前可卡因暴露的小鼠动物模型，使我们能够将可卡因改变胎儿发育的直接影响与可卡因引起的营养不良相关的间接影响区分开来。我们发现，经胎盘接触可卡因会独立损害胎儿大脑和身体生长，并导致接触可卡因的后代出现行为缺陷和新皮质细胞结构的永久性改变。
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 compromised 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 behavioural deficits and permanent alterations in neocortical cytoarchitecture in exposed offspring.