Cytoarchitecture of the olfactory bulb in the laggard mutant mouse
Cytoarchitecture of the olfactory bulb in the laggard mutant mouse
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DOI：
10.1016/j.neuroscience.2014.06.011
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发表时间：
2014-09
期刊：
影响因子：
3.3
通讯作者：
J. Yunus;T. Setsu;S. Kikkawa;T. Sakisaka;T. Terashima
中科院分区：
文献类型：
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作者：
J. Yunus;T. Setsu;S. Kikkawa;T. Sakisaka;T. Terashima
迟滞（lag）突变小鼠是由kif14基因突变引起的一种自发发生的突变小鼠，其特征是髓鞘发育低下和小脑性共济失调。在这只突变小鼠中，层压结构如大脑和小脑皮层以及齿状回在细胞结构上异常。从宏观上看，突变小鼠的嗅球比正常的嗅球更小，更透明。苏木精-伊红染色显示突变体嗅球层积正常，但详细分析发现嗅球茎周围细胞和颗粒细胞数量减少。在突变体中，嗅肾小球的细胞结构紊乱，二尖瓣细胞排列在多个细胞层中，而不是单层。突变体的吻侧迁移流在出生后的早期逐渐变薄或消失。一些二尖瓣细胞和肾小球周围细胞是多核的，提示kif14突变导致细胞分裂异常。在突变体中，侧脑室下区末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）阳性细胞数量增加，特别是在围产儿年龄，表明突变体小鼠颗粒细胞数量减少是由凋亡细胞死亡增加引起的。嗅觉输入似乎是完整的，通过向嗅觉粘膜注射小麦胚芽凝集素-辣根过氧化物酶（WGA-HRP）来顺行标记嗅觉神经。综上所述，突变小鼠的嗅球在细胞结构上受到了影响，这表明突变的致病基因，即Kif14，除了髓磷脂的形成外，还对中枢神经系统层状结构的发育有多重影响。
Thelaggard(lag) mutant mouse, characterized by hypomyelination and cerebellar ataxia, is a spontaneously occurring mutant mouse caused by mutation in theKif14gene. In this mutant mouse, the laminated structures such as the cerebral and cerebellar cortices and the dentate gyrus are cytoarchitecturally abnormal. Macroscopically, the olfactory bulb of thelagmutant mouse is smaller in size and more transparent than the normal counterpart. Hematoxylin–eosin staining reveals that the mutant olfactory bulb has normal lamination in general, but detailed analysis has demonstrated that olfactory periglomerular cells and granule cells are reduced in number. In the mutant, olfactory glomeruli are cytoarchitecturally disorganized and mitral cells are arranged in multiple cell layers instead of being arranged in a single layer. The rostral migratory stream in the mutant becomes gradually thinner or obliterated during early postnatal days. Some of mitral cells and periglomerular cells are multinucleated, suggesting thatKif14mutation leads to an abnormal cell division. In the mutant, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the subventricular zone of the lateral ventricle are increased in number, especially at perinatal age, suggesting that the decreased population of granule cells in thelagmutant mouse is caused by the increased apoptotic cell death. The olfactory input appears to be intact, as indicated by anterograde labeling of olfactory nerves with an injection of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the olfactory mucosa. In conclusion, the olfactory bulb of thelagmutant mouse is cytoarchitecturally affected, suggesting that the causal gene forlagmutation, i.e.,Kif14, has multiple effects on the development of laminated structures in the central nervous system in addition to the myelin formation.