Analysis of the mechanism underlying the pathway formation using mutant animals.

我们主要用形态学技术研究了正常动物和突变动物的脑发育。最近获得的发现如下：1)Calbindin D-28k是一种钙结合蛋白，定位于从大鼠新生的犁鼻器迁移到大脑的神经元(Toba等人，2001年)。N-Syndecan是一种肝素硫酸盐蛋白多糖，表达于大鼠嗅觉定位的迁移途径(Toba等人，2002)。2)在缺乏转录因子BRN-2、Nkx2.1和Pax-6的动物中发现下丘脑神经分泌神经元发育和途径形成缺陷(Kawano等人，2002)。3)在缺乏BRN-1和BRN-2的双基因敲除小鼠中观察到大脑新皮质发育异常(Sugitani等人，2002)。4)在Pax-6突变大鼠中，延髓小脑前脑神经元表现出延迟迁移和异常迁移途径(Horie et al.5)缺乏Nkx2.1基因敲除小鼠的中脑多巴胺能轴突异常地越过中线(Kawano等人，2003)。6)缺乏细胞识别分子NB3的小鼠的运动功能异常(Takeda等人，2003)。

We have examined the brain development in both normal and mutant animals by chiefly using the morphological technique. Recent findings obtained are as follows.1) Calbindin D-28k, a calsium-binding protein, is localized in neurons migrating from the nascent vomeronasal organ to the brain in rats (Toba et al., 2001). N-syndecan, a heparansulfate proteoglycan, is expressed in the migratory route from the rat olfactory placode (Toba et al., 2002).2) Defects of the development and pathway formation of hypothalamic neurosecretory neurons were found in animals lacking transcription factors Brn-2, Nkx2.1 and Pax-6 (Kawano et al., 2002).3) The abnormal development of cerebral neocortex is observed in double-knockout mice lacking both Brn-1 and Brn-2 (Sugitani et al., 2002).4) InPax-6 mutant rats, precerebellar neurons of the medulla oblongata exhibit a delayed migration and aberrant migratory route (Horie et al., 2003).5) Ascending dopaminergic axons of the mesencephalon abnormally cross the midline in knochout mice lacking Nkx2.1 (Kawano et al., 2003).6) The motor function of mice lackingNB3, a cell recognition molecule, is abnormal (Takeda et al., 2003).