THE EMBRYONIC-DEVELOPMENT OF THE CEREBELLUM IN NORMAL AND REELER MUTANT MICE
THE EMBRYONIC-DEVELOPMENT OF THE CEREBELLUM IN NORMAL AND REELER MUTANT MICE
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DOI：
10.1007/bf00305400
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发表时间：
1983-01-01
期刊：
影响因子：
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通讯作者：
GOFFINET, AM
中科院分区：
文献类型：
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作者：
GOFFINET, AM
在正常和reeler小鼠中研究了小脑的发育，从胚胎第14天开始，即，从这个器官开始形态发生到出生。两种基因型的小脑核按照相似的顺序发育。它们的神经元迁移到小脑芽的吻侧区，在那里它们凝聚成圆形的团块，在E14中清晰可见。从E17开始，这种细胞特遣队横向扩展，3-roof核变得清晰。在reeler突变体，似乎有一个异常的发展的架构外侧核。浦肯野细胞迁移到皮质在同一时间在两种基因型。在正常动物中，从E14开始，浦肯野细胞浓缩在一个明确定义的板中，其中它们呈现放射状组织。突变的浦肯野细胞不是排列在一个板，但分散在周边的皮质。外颗粒层的神经元在两种基因型中是相同的。放射状胶质纤维和早期高尔基上皮细胞似乎正常存在于卷轴胚胎中。在正常胚胎中，小脑皮质的叶状开始于E17。从这一阶段开始，叶片在卷叶突变体中越来越缺乏。显然，在正常的小脑发育中，一种特定的、遗传决定的机制负责迁移后神经元的组织和稳定，这种机制受到reeler突变的影响。
Development of the cerebellum was studied in normal and reeler mice, from embryonic day [E] 14, i.e., when morphogenesis begins in this organ, to birth. The cerebellar nuclei develop according to a similar sequence in both genotypes. Their neurons migrate into the rostral field of the cerebellar bud where they condense in a rounded mass, well defined in E14. From E17, this cell contingent spreads transversally and the 3-roof nuclei become clearly defined. In reeler mutants, there seems to be an abnormal development of the architectonics of the lateral nucleus. The Purkinje cells migrate into the cortex at the same time in both genotypes. In the normal animal, from E14 onward, Purkinje cells are condensed in a clearly defined plate, wher they assume a radial organization. The mutant Purkinje cells are not arranged in a plate but are scattered in the periphery of the cortex. The neurons of the external granular layer are identical in both genotypes. Radial glial fibers and early Golgi epithelial cells appear to be normally present in the reeler embryo. The foliation of the cerebellar cortex begins at E17 in the normal embryo. From this stage onward, foliation is increasingly deficient in reeler mutants. Apparently, in normal cerebellar development, a specific, genetically determined mechanism is responsible for the organization and the stabilization of postmigratory neurons and this mechanism is affected by the reeler mutation.