Embryopathegenesis of cerebral dysgenesis and involvement of NGF in the neuronal maturation

在我们以前的实验室实验中，已经对呼吸不全状态的胚胎发育进行了广泛的研究。在神经闭合不全的动物模型中，尤其是在“鸡胚胎脊髓劈裂或脑外畸形模型”中，最引人注目的发现是神经胎盘的过度成熟。我们提出了一种新的神经营养不良发病机制假说，即“过度生长再开放”疗法，旨在分析神经生长因子(NGF)的发育过程以及伴随着“过度生长”而紊乱的神经元成熟过程。将免疫组织化学技术应用于正常小鼠和脑外小鼠模型。神经生长因子家族中的一种(成纤维细胞生长因子：基本成纤维细胞生长因子)在出生后即刻出现在海马区(这一时期是人类胎儿生命的晚期)。进一步的调查目前正在进行中，以比较来自失写模型的数据。

The embryopathegenesis of dysraphic state has been extensive investigated in our previous laboratory experiments. The most striking findings revealed in the animal models of dysraphism, especially in "chick embryo myeloschisis or exencephaly models were the overmaturation of the neural placode. We have proposed a new hypothesis of pathogenesis of dysraphic state, namely "Overgrowth & Reopening" therapy.The purpose of the research project in this period is to analyze the developmental process of nerve growth factor (NGF) along with the disturbed neuronal maturation process with "overgrowth" . The immunohistochemical technique was applied in the normal mouse and exencephalic mouse model. One of the NGF family (fibroblast growth factor : basic FGF) appeared in the hippocampus immediately after birth (This period is in the third trimester of the fetal life in human. The further investigation is now ongoing to compare the data from the dysraphic models.