| Abstrak/Abstract |
Background The laggard (lag) mutant mouse, characterized by hypomyelination and cerebellar ataxia, is a spontaneously occurring mutant mouse caused by mutation in the Kif14 gene. In this mutant mouse, the laminated structures such as the cerebral and cerebellar cortices and the dentate gyrus are cytoarchitecturally abnormal. Methods We studied the cytoarchitecture of the lag mutant olfactory bulb on the basis of hematoxylin-eosin staining and immunohistochemistry in the mouse pups at various pre- and postnatal ages. Results Macroscopically, the olfactory bulb of the lag mutant mouse was smaller in size and more transparent than the normal counterpart. Hematoxylin-eosin staining revealed that the mutant olfactory bulb had normal lamination in general, but detailed analysis had demonstrated that olfactory periglomerular cells and granule cells were reduced in number. In the mutant, olfactory glomeruli were cytoarchitecturally disorganized and mitral cells were arranged in multiple cell layers instead of being arranged in a single layer. The rostral migratory stream in the mutant became gradually thinner or obliterated during early postnatal days. Some of mitral cells and periglomerular cells were multinucleated, suggesting that Kif14 mutation led to an abnormal cell division. In the mutant, TUNEL-positive cells in the subventricular zone of the lateral ventricle were increased in number, especially at perinatal age, suggesting that the decreased population of granule cells in the lag mutant mouse was caused by the increased apoptotic cell death. The olfactory input appeared to be intact, as indicated by anterograde labeling of olfactory nerves with an injection of WGA-HRP into the olfactory mucosa. Conclusions The olfactory bulb of the lag mutant mouse is cytoarchitecturally affected, suggesting that the causal gene for lag mutation, i.e., Kif14, has multiple effects on the development of laminated structures in the central nervous system in addition to the myelin formation. |
