Wilson D B, Wyatt D P
Department of Surgery, School of Medicine, University of California, San Diego 92093.
J Neuropathol Exp Neurol. 1988 Nov;47(6):609-17. doi: 10.1097/00005072-198811000-00004.
Closure of the posterior neuropore was analyzed by means of ultrastructural cytochemistry in ten-day dysraphic mouse embryos homozygous for the mutant gene vl, and comparisons were made with normal embryos in terms of convergence, apposition and fusion of the apices of the neural folds. In abnormal embryos, regional differences in the distribution of the surface coat were comparable to those in normal embryos. However, there was an abnormally acute medial bending of the neural folds, as well as a delay in closure of the posterior neuropore. In closed areas of the abnormal embryos the dorsum also showed an erratic knot of disorganized cells. Thus, the pathogenetic mechanism in this mutant appears to involve not only a failure in apposition in open areas, as well as an inappropriate association of cells in areas which do fuse, but possibly also a failure of proper alignment of neural fold apices prior to apposition and fusion.
通过超微结构细胞化学方法，对纯合突变基因vl的10日龄脊柱裂小鼠胚胎的后神经孔闭合情况进行了分析，并就神经褶顶端的汇聚、并置和融合情况与正常胚胎进行了比较。在异常胚胎中，表面被膜分布的区域差异与正常胚胎相当。然而，神经褶出现了异常尖锐的内侧弯曲，后神经孔的闭合也延迟。在异常胚胎的闭合区域，背部还出现了一团杂乱无章的细胞。因此，该突变体的发病机制似乎不仅涉及开放区域的并置失败，以及融合区域细胞的不适当结合，还可能涉及并置和融合之前神经褶顶端的正确排列失败。
