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Morphogenesis of neuronal microdysgenesis in hippocampal formation of Ihara's genetically epileptic rat (IGER)

伊原遗传性癫痫大鼠（IGER）海马形成中神经元微发育障碍的形态发生

基本信息

批准号：
10670202
负责人：
AMANO Shigeru
金额：
$ 2.05万
依托单位：
KYOTO UNIVERSITY (1999)Shiga University of Medical Science (1998)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10670202/
关键词：
Thara's genetically epileptic rat hipocampus neuronal microdysgenesisi Morphogenesis epileptic foci mutant 発理発生

项目摘要

Experiment J. Structural property of microdysgenesis in IGER(Ihara's genetically epileptic rat) hippocampus was investigated. In both two and twelve month-old IGERs and in both sexes, the ectopic neuronal clusters were found in the region of stratum radiatum (St. rad) in the CA1 of the anterior dorsal hippocampus. The disarrangement of pyramidal neurons or small foci of interruption in the pyramidal cell layer were also found in the CA1 and sometimes in the CA3 regions. In control rats in any age and in both sexes, those microdysgenesis in the hippocampal formation was not found. This study demonstrates that the ectopic neuronal clusters and the disarrangement of the pyramidal neurons are the hereditary lesion, i. e. programmed neuronal microdysgenesis.Experiment II and III. BrdU labeling method traced neuronal migration in the hippocampal neurons of IGER. Labeled neurons in the ventricular layer (VL) of CA1region migrated into the superficial portion, the intermediate zone (IMZ), and then reached to the presumptive pyramidal layer. On ED16, one hour after the third injection, labeled cells abounded in the subventricular zone and a few were located in IMZ in both IER and control hippocampus. On ED17, there were significant more labeled cells in IMZ of IGER than that of control. On ED20 and ED21, greater part of labeled cells was located in presumptive pyramidal layer and St. rad. of control hippocampus. On the contrary, significant more labeled cells were located in IMZ of IER. These results indicated that in IER, primitive neurons migrate earlier from SVZ to IMZ, then remained longer in IMZ than those of control, respectively. It was suggested that a failure of gene expression, not yet defined, responsible for regulation of neuronal migration in embryonal developing phase might cause MDG in

实验J.研究了IGER（Ihara's genetically epileptic rat）海马微小发育不全的结构特征。在两个和十二个月大的IGER和在两种性别，异位神经元簇被发现在该地区的辐射层（圣拉德）在前背海马CA1区。锥体细胞层内锥体神经元排列紊乱或小的中断灶也见于CA 1区，有时也见于CA 3区。在对照组大鼠中，无论男女，均未发现上述海马结构的微小发育异常。本研究表明，异位神经元簇和锥体神经元排列紊乱是一种遗传性病变，即海马结构的异常。e.程序性神经元发育不全。实验二和三。BrdU标记法追踪IGER海马神经元的迁移。标记的CA1区室层（VL）神经元迁移到浅层、中间带（IMZ），然后到达假定的锥体层。在ED 16，即第三次注射后1h，IER和对照海马的室管膜下区有大量标记细胞，IMZ区也有少量标记细胞。ED17时IGER组IMZ区标记细胞数明显多于对照组。在ED 20和ED 21，标记细胞主要位于假定锥体层和St. rad。海马体的控制。相反，IER的IMZ中有更多的标记细胞。这些结果表明，在IER中，原始神经元从SVZ到IMZ的迁移时间比对照组更早，然后在IMZ中停留的时间更长。这表明，在胚胎发育阶段负责调节神经元迁移的基因表达的失败（尚未确定）可能导致MDG。