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

实验J.研究了Ihara‘s遗传性癫痫大鼠海马区微发育不良的结构特征。2月龄、12月龄雌性和雌性大鼠在前背侧海马CA1区放射层(St.rad)均可见异位神经元团。CA1区也可见锥体神经元排列紊乱或锥体细胞层有小的中断灶，CA3区有时也可见。在任何年龄和性别的对照组大鼠中，没有发现海马结构中的这些微发育不良。本研究证明异位神经元簇和锥体神经元的排列紊乱是一种遗传性损伤，即程序性神经元微发育不良。实验II和实验III。BrdU标记方法追踪了Iger海马神经元的迁移。CA1区脑室层(VL)的标记神经元迁移到浅层中间带(IMZ)，然后到达可能的锥体层。在ED16，第3次注射后1小时，IER和对照海马室下区均有大量标记细胞，IMZ内有少量标记细胞。在ED17，IGER组IMZ的标记细胞数明显多于对照组。在ED20和ED21，大部分标记细胞位于假定锥体层和St.rad。对照组的海马体。相反，在IER的IMZ，标记细胞明显增多。这些结果表明，在IER中，原始神经元从SVZ迁移到IMZ的时间较早，而在IMZ中的迁移时间较长。有人认为，在胚胎发育阶段负责调节神经元迁移的基因表达失败可能导致MDG。

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