Abnormal migration of the motor trigeminal, facial, and ambiguus nuclei neurons of the SRK rat

Reeler小鼠是一种常染色体隐性遗传突变小鼠，以步态共济失调和震颤为特征。自从D 'Arcangelo等（Nature 374：719-723，1995）发现了引起reeler突变的基因reelin以来，在该领域已经取得了许多进展。reelin基因编码一种细胞外蛋白，对神经元迁移至关重要。在胚胎发育过程中，reelin在大脑皮层的Cajal-Retzius细胞和小脑皮层的外颗粒细胞中表达。虽然非层状结构，如面神经核，下橄榄复合体，背侧耳蜗核也cytoarchtectually在这种突变的错乱，只有少数研究已经做了澄清，在这些非层状结构的详细异常。本文主要对reeler小鼠面神经核的细胞构筑异常进行综述。面神经核内的鳃裂神经元位于第四脑室底的室区， 关于我们 腹外侧进食，最后在后脑腹面附近定居。正常小鼠和reeler小鼠面部运动神经元的产生、轴突形成和迁移的时间表相似，但在神经元迁移结束时，reeler表型变得可识别。虽然Reeler小鼠面神经核的细胞结构异常的原因，如此长的迁移的面运动神经元似乎更容易在Reeler小鼠比在正常对照。尽管存在细胞结构异常，但逆行辣根过氧化物酶（HRP）研究证实，在reeler小鼠的面神经核内仍然保留了肌肉定位排列，这表明神经元的迁移/重排和靶点识别是独立调节的。其中，yotari和scrambler小鼠是由mdab 1突变引起的，mdab 1是一种与果蝇基因残疾（dab）相关的小鼠基因。10多年前，一种常染色体隐性突变的大鼠，摇晃大鼠川崎（SRK），已被描述为表现出与reeler相同的表型，但负责这种大鼠突变的基因仍然未知。非常有趣的是，与正常的对应物相比，yotari和SRK的面神经核在细胞结构上更加混乱。yotari在层状结构中表现出与reeler相同的表型，而在非层状结构如面核中表现出与reeler不同的表型的原因仍然不清楚，这表明mDab 1和Reelin蛋白质在非层状结构和层状结构之间以不同的方式作为信号分子发挥作用。少

Reeler mouse is an autosomal recessive mutant mouse, and characterized by ataxic gait and tremor. Since reelin, the gene responsible for the reeler mutation is discovered by D'Arcangelo et al. (Nature 374 : 719-723, 1995), much progresses have occurred in this field. The reelin gene encodes an extracellular protein that is crucial for neuronal migration. During the embryogenesis, reelin is expressed in the cerebral cortex in Cajal-Retzius cells and in the cerebellar cortex in outer granule cells. Although non-laminated structures such as facial nucleus, inferior olivary complex, and dorsal cochlear nucleus are also cytoarchtectually deranged in this mutant, only a few studies have been done to clarify the detailed abnormalities in these non-laminated structures. In this review, we focused the cytoarchitectonic abnormality in the facial nucleus of the reeler mouse. The branchiomotor neurons in the facial nucleus are born in the ventricular zone of the floor of the fourth ventricle, migr … More ate ventrolaterally, and finally settle near by the ventral surface of the hindbrain. Time schedules for the generation, axon formation and migration of facial motoneurons are similar both in normal and reeler mouse, but the reeler phenotype becomes identifiable at the end of neuronal migration. Although the reason why the facial nucleus is cytoarchitecually abnormal in the reeler mouse, such a long migration of the facial motoneurons seems to be more susceptible to Reelin in the reeler mouse than in the normal control. In spite of cytoarcitectual abnormality, retrograde horseradish peroxidase (HRP) study confirmed that musculotopic arrangements within the facial nucleus of the reeler mouse are still preserved, suggesting neuronal migration/rearrangement and target recognition are independently regulated.More recently, other kinds of reeler-like mutants have been known (yotari, scrambler, SRK). Among these, yotari and scrambler mice arises from mutations in mdab1, a mouse gene related to the Drosophila gene disabled (dab). More than 10 years ago, an autosomal recessive rat mutant, shaking rat Kawasaki (SRK), has been described that exhibits a phenotype identical to reeler, but the gene responsible for this rat mutation has remained unknown. Very interestingly, the facial nucleus is cytoarchitectually more deranged in yotari and SRK compared to the normal counterparts. The reason why yotari exhibits a phenotype identical to reeler in the laminated structures but not in non-laminates structures such as the facial nucleus has remained obscure, suggesting mDab1 and Reelin proteins function as signaling molecules in a different way between non-laminated and laminated structures. Less