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

在我们以前的实验室实验中，对书写障碍状态的胚胎病理发生进行了广泛的研究。在脊髓闭合不全的动物模型，特别是鸡胚脊髓劈裂或露脑畸形模型中，最引人注目的发现是神经基板的过度成熟。我们提出了一个新的书写障碍的发病机制假说，即“过度生长&重新开放”疗法，本课题的研究目的是分析神经生长因子（NGF）沿着“过度生长”扰乱神经元成熟过程的发育过程。应用免疫组化技术对正常小鼠和裸脑小鼠模型进行研究。神经生长因子家族中的一种（成纤维细胞生长因子：碱性成纤维细胞生长因子）在出生后立即出现在海马中（这一时期是人类胎儿生命的第三个三月。目前正在进行进一步的调查，以比较来自书写障碍模型的数据。

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.