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大鼠实验性无脑畸形和脊髓裂

Experimental exencephaly and myeloschisis in rats.

作者信息

Hong S K, Chi J G, Sim B S

机构信息

Department of Neurosurgery, Seoul Red Cross Hospital.

出版信息

J Korean Med Sci. 1989 Mar;4(1):35-50. doi: 10.3346/jkms.1989.4.1.35.

DOI:10.3346/jkms.1989.4.1.35
PMID:2789737
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3053682/
Abstract

To elucidate the early sequential morphogenetic progress of exencephaly and myeloschisis, rat embryos whose mothers had been treated with hypervitaminosis A were studied at 1-day interval from gestation day 10.5 to 15.5. In exposed animals sequential change was found in both exencephaly and myeloschisis as the embryos grew up. The 10.5-day old exencephalic embryos had still widely open cephalic neural tubes. Exencephalic embryos older than 13.5 days of gestation showed strikingly severe eversion and overgrowth of the cephalic neuroepithelium, thus failed in forming normal primitive brain. The convex dorsal surface of the exencephaly was covered with ependyma, which was connected directly with surrounding surface eqithelium at the periphery. The earliest morphologically recognized myeloschisis was in the 13.5-day old embryos. In myeloschisis, divergence at the roof plate and eversion of the spinal neural tube, disorganized overgrowth of the neuroepithelium, malformed and misplaced spinal ganglia and nerve roots, and absence of the neural arch and dermal covering were characteristic. It is suggested that exencephaly results from failure of the cephalic neural tube closure which is followed by eversion and overgrowth of the neuroepithelium. And failure in closure of the posterior neuropore and disturbance in the development of the tail bud probably play major role in the morphogenesis of myeloschisis.

摘要

为阐明无脑儿和脊柱裂早期连续的形态发生过程,对其母亲患有维生素A过多症的大鼠胚胎从妊娠第10.5天至15.5天每隔1天进行研究。在暴露的动物中,随着胚胎的生长,无脑儿和脊柱裂均出现了连续变化。妊娠10.5天的无脑儿胚胎的头端神经管仍广泛开放。妊娠13.5天以上的无脑儿胚胎显示出头端神经上皮显著严重的外翻和过度生长,因此未能形成正常的原始脑。无脑儿的凸背表面覆盖有室管膜,其在周边直接与周围的表面上皮相连。最早在形态学上识别出的脊柱裂见于妊娠13.5天的胚胎。在脊柱裂中,顶板处的分离和脊髓神经管的外翻、神经上皮的无序过度生长、脊髓神经节和神经根的畸形和错位以及神经弓和皮肤覆盖物的缺失是其特征。提示无脑儿是由于头端神经管闭合失败,随后神经上皮外翻和过度生长所致。而后神经孔闭合失败和尾芽发育障碍可能在脊柱裂的形态发生中起主要作用。

相似文献

1
Experimental exencephaly and myeloschisis in rats.大鼠实验性无脑畸形和脊髓裂
J Korean Med Sci. 1989 Mar;4(1):35-50. doi: 10.3346/jkms.1989.4.1.35.
2
The morphogenesis of myeloschisis in the rat.大鼠脊髓裂的形态发生
Proc Natl Sci Counc Repub China B. 1988 Jul;12(3):124-8.
3
Identical embryopathogenesis for exencephaly and myeloschisis: an experimental study.
J Neurosurg. 1990 Mar;72(3):450-7. doi: 10.3171/jns.1990.72.3.0450.
4
Methanol-induced neural tube defects in mice: pathogenesis during neurulation.甲醇诱导的小鼠神经管缺陷:神经胚形成过程中的发病机制。
Teratology. 1994 Jun;49(6):497-517. doi: 10.1002/tera.1420490610.
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[Overgrowth and DNA synthesis of neuroepithelium in embryonic stages of induced Long-Evans rat myeloschisis].[诱导的Long-Evans大鼠脊髓裂胚胎期神经上皮的过度生长和DNA合成]
Hokkaido Igaku Zasshi. 1993 Jan;68(1):8-17.
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The morphogenesis of hindbrain crowding associated with lumbosacral myeloschisis.
Neurol Med Chir (Tokyo). 1989 Nov;29(11):981-8. doi: 10.2176/nmc.29.981.
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Concanavalin-A-induced open neural tube defects in chick embryos.
Neurol Med Chir (Tokyo). 1996 Oct;36(10):691-6; discussion 696-7. doi: 10.2176/nmc.36.691.
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Histogenesis of experimental open neural defects in the early chick embryo.
Anat Anz. 1979;146(2):171-87.
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Retinoic acid-induced lumbosacral neural tube defects: myeloschisis and hamartoma.维甲酸诱导的腰骶部神经管缺陷:脊髓裂和错构瘤。
Childs Nerv Syst. 2007 May;23(5):549-54. doi: 10.1007/s00381-006-0289-y. Epub 2007 Jan 25.
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Aberrant differentiation of the axially condensed tail bud mesenchyme in human embryos with lumbosacral myeloschisis.腰骶部脊髓脊膜膨出的人类胚胎中轴浓缩尾芽间充质的异常分化。
Anat Rec (Hoboken). 2007 Mar;290(3):251-8. doi: 10.1002/ar.20426.

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