Wei Suli, Xu Zhiqiang, Gao Junying, Ding Jiong, Xiao Ming
Department of Anatomy, Wuxi Higher Health Vocational Technology School, Wuxi, Nanjing Medical University, Nanjing, Jiangsu, PR China.
Neuroreport. 2013 Mar 6;24(4):196-201. doi: 10.1097/WNR.0b013e32835e3258.
Genetic factors are involved in variation in fetal alcohol spectrum disorders (FASD), which is also observed among various inbred mouse strains. The CD1 mouse strain is often used in toxicological and genetic experiments. However, there is little literature using this strain to study long-term neurologic abnormalities of FASD. In the present study, we addressed the effect of prenatal ethanol exposure on neurological alterations in adult CD1 mice. The female CD1 mice received exposure to ethanol solution (10 vol%) starting from 2 weeks before mating up to pups born (postnatal day 1). At 24 weeks after the birth, the prenatal ethanol-exposed mice and control mice showed no difference in spatial learning and memory performance in a Morris water maze. Consistently, pathological changes, such as increased neuronal apoptosis, decreased synaptic protein synaptophysin expression, synaptic loss and reactive astrogliosis, were not observed in the hippocampus of mice prenatally exposed to ethanol. These results suggest that CD1 mice are highly resistant to prenatal alcohol exposure and may serve as genetic modification models of FASD.
遗传因素参与胎儿酒精谱系障碍（FASD）的变异，这种变异在各种近交系小鼠中也有观察到。CD1小鼠品系常用于毒理学和遗传学实验。然而，很少有文献使用该品系研究FASD的长期神经学异常。在本研究中，我们探讨了产前乙醇暴露对成年CD1小鼠神经学改变的影响。雌性CD1小鼠从交配前2周开始直至幼崽出生（出生后第1天）接受乙醇溶液（10%体积分数）暴露。出生后24周，产前乙醇暴露小鼠和对照小鼠在Morris水迷宫中的空间学习和记忆表现没有差异。同样，在产前暴露于乙醇的小鼠海马体中未观察到神经元凋亡增加、突触蛋白突触素表达降低、突触丢失和反应性星形胶质细胞增生等病理变化。这些结果表明，CD1小鼠对产前酒精暴露具有高度抗性，可作为FASD的基因修饰模型。
