Prenatal ethanol exposure reduces the effects of excitatory amino acids in the rat hippocampus.
Prenatal ethanol exposure reduces the effects of excitatory amino acids in the rat hippocampus.
复制标题
产前乙醇暴露会降低大鼠海马中兴奋性氨基酸的影响。
DOI：
10.1016/0024-3205(89)90173-2
复制
发表时间：
1989
期刊：
影响因子：
6.1
通讯作者：
Ritchie,T
中科院分区：
文献类型：
--
作者：
Noble,EP;Ritchie,T
怀孕期间长期摄入酒精会导致胎儿酒精综合征（FAS），这是一种以学习障碍为特征的疾病。通过将妊娠Sprague-Dawley大鼠引入含有35%乙醇衍生卡路里的液体饮食（E）来使用FAS大鼠模型，而第二组成对喂食不含乙醇的等热量液体饮食（P）。第三组妊娠母鼠自由采食实验室饲料（C）。分娩时，E组和P组的幼仔由C组母亲交叉饲养，所有组均接受实验室食物。在成年期，雄性后代被处死，海马和前额叶皮质切片预先标记的[3 H]肌醇。磷酸肌醇（PI）水解通过测量在LiCl存在下响应于各种兴奋性氨基酸（EAA）受体的激活的[3 H]肌醇磷酸的积累来确定。在海马切片中，鹅膏蕈氨酸和使君子酸诱导的PI水解减少E相比，P和C动物。此外，N-甲基-D-天冬氨酸（NMDA）对卡巴胆碱诱导的PI水解的抑制作用，在P和C动物中明显，在E动物的海马中完全消除。相比之下，在大脑前额叶皮层，NMDA的这种抑制作用甚至在E组动物中也普遍存在。有证据表明，产前乙醇暴露改变了海马第二信使中EAA受体的活性。
Chronic alcohol ingestion during pregnancy can lead to the Fetal Alcohol Syndrome (FAS), a disorder marked by learning disabilities. A rat model of FAS was used by introducing pregnant Sprague-Dawley rats to a liquid diet containing 35% ethanol-derived calories (E), while a second group was pair-fed an isocaloric liquid diet without ethanol (P). A third group of pregnant dams received ad libitum lab chow (C). At parturition, pups from the E and P groups were cross-fostered by C mothers and all groups received lab chow. During adulthood, male offspring were sacrificed and hippocampal and prefrontal cortical slices were prelabeled with [3H] inositol. Phosphoinositide (PI) hydrolysis was determined by measuring the accumulation of [3H] inositol phosphates in the presence of LiCl in response to activation of various excitatory amino acid (EAA) receptors. In hippocampal slices, ibotenate-and quisqualate-induced PI hydrolysis was reduced in E compared to P and C animals. Moreover, the inhibitory effect of N-methyl-D-aspartate (NMDA) on carbachol-induced PI hydrolysis, evident in P and C animals, was completely abolished in the hippocampus of E animals. In contrast, in the prefrontal cerebral cortex, this inhibitory effect of NMDA prevailed even in the E animals. The evidence suggests that prenatal ethanol exposure alters the activity of EAA receptors in the hippocampal generation of 2nd messengers.