Jiang Qiying, Hu Yanqiu, Wu Ping, Cheng Xiangshu, Li Mingshan, Yu Dongming, Deng Jinbo
Institute of Neurobiology, Henan University, Jinming Campus of Henan University, Kaifeng 475004, Henan Province, P. R. China.
Alcohol Alcohol. 2007 Jul-Aug;42(4):285-90. doi: 10.1093/alcalc/agm032. Epub 2007 May 30.
The prenatal ethanol exposure induced neuroapoptosis and neuron loss in visual cortex would be investigated in mice at P0, P7 and P14.
Intubating pregnant mice ethanol daily began on E5 and continued through the pup's birth. The neuroapoptosis in visual cortex was visualized by the caspase 3 immunocytochemistry, and the neuron loss was observed with Nissl method as well.
With prenatal ethanol exposure, the dose-dependent neuroapoptosis and neuron loss in visual cortex could be found at P0 and even at P7 and P14 as well.
The prenatal ethanol exposure induced neuroapoptosis and neuron loss will persist into postnatal stage, and the long-term effect of neuroapoptosis might be one of the causes of postnatal neurobehavioural disturbances associated with fetal alcohol syndrome.
研究孕期乙醇暴露对出生后0天、7天和14天小鼠视觉皮层神经细胞凋亡及神经元丢失的影响。
从胚胎第5天开始，每天给怀孕小鼠插管灌胃乙醇，持续至幼崽出生。采用半胱天冬酶3免疫细胞化学法观察视觉皮层神经细胞凋亡情况，同时用尼氏染色法观察神经元丢失情况。
孕期乙醇暴露可导致出生后0天、7天及14天小鼠视觉皮层出现剂量依赖性神经细胞凋亡及神经元丢失。
孕期乙醇暴露所致的神经细胞凋亡及神经元丢失可持续至出生后阶段，神经细胞凋亡的长期影响可能是胎儿酒精综合征相关出生后神经行为障碍的原因之一。
