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胚胎中期酒精暴露诱导大鼠视皮层胼胝体投射神经元发育异常 ,出生前酒精暴露造成很多中枢神经系统发育性缺陷。新近许多研究进一步揭示了各种浓度的酒精对神经系统从行为到分子机制各个过程都有严重的毒性作用。胼胝体是联系两侧大脑半球功能的重要结构。然而 ,酒精对胼胝体投射神经元发育的影响报道甚少。本文利用胃饲法大鼠胚胎中期酒精暴露模型 ,观察酒精对大脑视皮层胼胝体投射神经元树突发育的影响。在胚胎第 11～ 2 0d ,给予妊娠鼠 1.5～ 6 .0 g/kg酒精 (2 0 %乙醇 )灌胃。对照组包括正常鼠和食物控制对照。将仔鼠分别于出生当天、G2 6 (以妊娠第一天为G1)、G2 9,4%多聚甲醛灌定。置DiI于胼胝体的中矢状切面的纤维束中。共聚焦激光扫描显微镜收集 10 0 μm厚脑片图像。图像分析系统测量标记神经元树突第一级分支数量和最长分支长度。结果指出 :酒精暴露组树突一级分支数量和长度都较对照组有不同程度的增加 ,并呈剂量依赖关系。出生后一周内可见这种趋势 ,随年龄增加而表现逐渐明显。这种酒精出生前暴露所引起的增加已有一些报道如胼胝体投射神经元轴突数目增加等。本文的结果可能是由于在胚胎中期酒精致使大量的胼胝体投射神经元产生减少 ,而引起的可塑性代偿反应。继续观察较大年龄组的发育状况
Mid-term alcohol exposure in embryos induces aberrant neuronal development of the corpus callosum in the visual cortex of the rat, leading to many central nervous system developmental defects during prenatal exposure to alcohol. Many recent studies have further revealed that various concentrations of alcohol have serious toxic effects on various processes of the nervous system from behavior to molecular mechanisms. The corpus callosum is an important structure that links the functions of the cerebral hemispheres on both sides. However, the effects of alcohol on the development of the corpus callosum neurons are poorly documented. In this paper, we use the medium-dose alcohol exposure rat embryo model of alcohol exposure to observe the visual cortex of the corpus callosum neurons projecting dendrites development. On the 11th ~ 20th day of embryo, 1.5 ~ 6.0 g / kg alcohol (20% ethanol) was given intragastrically to the pregnant rats. Control groups included normal mice and food control controls. The pups were infused on the day of their birth with G2 6 (G1 on the first day of gestation) and G2 9,4% paraformaldehyde. DiI was placed in the midsagittal section of the corpus callosum. Confocal Laser Scanning Microscope Images of 10 μm thick slices were collected. The image analysis system measures the number of first-level branches and the longest branch length of dendrites labeled with neurons. The results showed that: alcohol exposure group dendrites a branch of the number and length of the control group increased to varying degrees, and in a dose-dependent manner. This trend can be seen within a week after birth, with the aging of the performance gradually apparent. There have been some reports of this increase in prenatal exposure to alcohol, such as an increase in the number of neurons projecting into the corpus callosum. Our results may be due to the plastic compensatory response caused by the reduced production of large numbers of corpus callosum neurons in the mid-embryonic stage of alcohol administration. Continue to observe the development of older age groups