Smith M T, Wood L R, Honig S R
Neurology. 1982 Sep;32(9):992-9. doi: 10.1212/wnl.32.9.992.
The scanning electronmicroscope was used to study the development of anencephaly in an experimental model. Anencephaly was produced consistently, using vitamin A as the teratogen. Embryos destined to become anencephalic displayed failure of opposing sides of the rostral neural tube to fuse. Subsequently, the neural folds of the experimental embryos progressively curved laterally away from the midline, whereas the neutral folds of the control embryos fused in the midline by day 12. The anlage of the choroid plexus could be identified on the surface of the everting brain folds as early as gestational day 13. Thus, the abnormal eversion of the neural tube occurred before development of the choroid plexus. This study supports the view that anencephaly ultimately results from neural tube nonclosure.
利用扫描电子显微镜研究实验模型中无脑儿的发育情况。以维生素A作为致畸剂，能持续诱导出无脑儿。注定会成为无脑儿的胚胎显示出，其头侧神经管的相对两侧未能融合。随后，实验胚胎的神经褶逐渐向外侧弯曲，远离中线，而对照胚胎的神经褶在第12天时在中线融合。早在妊娠第13天，脉络丛原基就能在外翻的脑褶表面被识别出来。因此，神经管的异常外翻发生在脉络丛发育之前。这项研究支持了无脑儿最终是由神经管未闭合导致的这一观点。
