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新生大鼠大脑闭合性低温损伤后皮质板的修复与重建

Repair and reconstruction of the cortical plate following closed cryogenic injury to the neonatal rat cerebrum.

作者信息

Suzuki M, Choi B H

机构信息

Department of Pathology, University of California, Irvine 92717.

出版信息

Acta Neuropathol. 1991;82(2):93-101. doi: 10.1007/BF00293950.

Abstract

A cryogenic lesion was induced in the parietal cortex of neonatal rats at postnatal day 2, and the chronological sequence of cellular events during repair and reconstruction of the cortical plate examined. Serial sections of cerebra obtained at varying intervals ranging from 1 to 60 days postinjury were studied by light and electron microscopy and by immunocytochemistry for fibronectin, laminin, type IV collagen, vimentin and glial fibrillary acidic protein. In addition, localization of heavily labeled neurons (generated on embryonic day 20) in the cerebral cortical plate was examined by [3H]thymidine radioautography. Repair of a well-defined coagulative lesion was accomplished with little or no mesenchymal cell proliferation in either the necrotic zone or the leptomeninges. Eventually, fusion of the adjacent cortical plates took place with the formation of a microsulcus. Migration of neurons continued to take place along the outer margins of the lesion, and postmigratory neurons accumulated within the upper cortical layers. Around the microsulcus, heavily labeled neurons aligned themselves with layers II-III of the adjacent normal cortical plate. Irregular clusters of neurons closely abutting the leptomeningeal surface were frequently noted when repair took place without an intervening molecular layer and/or a well-defined pial-glial barrier. Supplementing intrinsic information inherent in migrating neurons, local environmental signals provided by the radial glia, glia limitans, basal lamina and pial-glial barrier appear to influence the polarity and final positioning of postmigratory neurons within the cortical plate. The necrotic zone within the deeper layers of the cortex eventually healed with a cell-sparse gliotic layer. The end result was a histological pattern that, in many respects, resembled that of human micropolygyria.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在出生后第2天对新生大鼠的顶叶皮质造成低温损伤,并检查皮质板修复和重建过程中细胞事件的时间顺序。通过光镜、电镜以及针对纤连蛋白、层粘连蛋白、IV型胶原、波形蛋白和胶质纤维酸性蛋白的免疫细胞化学方法,研究了在损伤后1至60天不同时间间隔获取的大脑连续切片。此外,通过[3H]胸腺嘧啶放射自显影检查了大脑皮质板中标记强烈的神经元(在胚胎第20天产生)的定位。明确的凝固性损伤的修复过程中,坏死区或软脑膜中几乎没有间充质细胞增殖。最终,相邻的皮质板融合形成微沟。神经元继续沿着损伤的外缘迁移,迁移后的神经元聚集在上层皮质内。在微沟周围,标记强烈的神经元与相邻正常皮质板的II-III层对齐。当修复过程中没有中间分子层和/或明确的软膜-胶质屏障时,经常会注意到紧邻软脑膜表面的不规则神经元簇。除了迁移神经元固有的内在信息外,由放射状胶质细胞、胶质界膜、基膜和软膜-胶质屏障提供的局部环境信号似乎会影响迁移后神经元在皮质板内的极性和最终定位。皮质深层的坏死区最终愈合形成细胞稀疏的胶质化层。最终的组织学模式在许多方面类似于人类微小多脑回。(摘要截断于250字)

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