Ueda S, Saitoh Y, Koibuchi N, Ishizuya-Oka A
Department of Histology and Neurobiology, Dokkyo University School of Medicine, Mibu, Tochigi 321-02, Japan.
Cell Tissue Res. 1997 Sep;289(3):547-51. doi: 10.1007/s004410050900.
Homozygotes of a mouse strain with genetic polydactyly (Pdn) show disrupted cortical lamination and a significant decrease of S-100beta-immunoreactive elements in a particular area of the brain. In order to understand the abnormal cortical formation at the cellular level, the migration of cortical neurons and the development of glial cells were studied using bromodeoxyuridine (BrdU), S-100beta, and glial fibrillary acidic protein (GFAP) immunohistochemistry. Homozygous mice (Pdn/Pdn) displayed a variable pattern of abnormalities. Irregular GFAP-positive radial glial cells and disturbance of neuronal migration were found in a circumscribed area of the caudo-dorsal cortex of newborn Pdn mouse. The number of S-100beta-positive cells was reduced in this area. The present results suggest that abnormal cortical lamination closely correlates with disturbance of neuronal migration and abnormalities of glial cells, especially a significant decrease of S-100beta-immunoreactive cells.
具有遗传性多指（Pdn）的小鼠品系的纯合子表现出皮质分层紊乱，并且在大脑的特定区域中S-100β免疫反应性元件显著减少。为了在细胞水平上理解异常的皮质形成，使用溴脱氧尿苷（BrdU）、S-100β和胶质纤维酸性蛋白（GFAP）免疫组织化学研究了皮质神经元的迁移和胶质细胞的发育。纯合子小鼠（Pdn/Pdn）表现出可变的异常模式。在新生Pdn小鼠尾背皮质的一个限定区域中发现了不规则的GFAP阳性放射状胶质细胞和神经元迁移紊乱。该区域中S-100β阳性细胞的数量减少。目前的结果表明，异常的皮质分层与神经元迁移紊乱和胶质细胞异常密切相关，尤其是S-100β免疫反应性细胞的显著减少。
