Objective The aim of this project is to study the possible pathogenesis involved in the formation of neural tube defect (NTD).Methods NTD was induced in chick embryos by injecting 0.01-0.02mg/kg methotrexate (MTX) into fertilized eggs on the 4 th and 5 th day of incubation.Sixty-six hatched chicks with NTD were studied.Nitric oxide synthase (NOS) was immuno-stained with nicotinamide adenine dinucleotide phosphate-dependent dependent diaphorase(NADPH-d).Utrastructure of mitochondria was studied with electro-microscopy.Results NOS positive neurons were found in the spinal cord of abnormal neural tube.The total number of neurons decrease.Electromicroscopy showed that mitochondria were swollen and had decreased folds.Conclusions No is produced in NTD.NO is neurotoxic and leads to impaired nitochondrial oxidative metabolism.%目的 鸡胚内注射甲氨喋呤(MTX),制作鸡胚神经管缺陷动物模型.利用该模型,进一步研究观察病变脊髓的病理变化及组织化学改变.方法 选用上海农科院"莱杭"鸡受精蛋66枚,在孵化期第4、5天,注射MTX,计量为:0.01 mg/kg及0.02 mg/kg.孵化3周后,选取病变鸡,采用NADPH-黄递酶组织化学染色,测定病变脊髓神经元NOS含昔;电镜观察病变脊髓神经元内线粒体结构变化.结果 NADPH-黄递酶组织化学染色显示神经管缺陷病变脊髓出现NOS阳性染色神经元,神经元数量减少,形态发育差.电镜观察,病变脊髓线粒体肿胀,嵴减少.结论 神经管缺陷病变脊髓有NO产生,NO对神经细胞有毒性作用,使线粒体功能受损,能量代谢障碍.
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