Author:
Miyazaki Haruko,Nishioka Saki,Yamanaka Tomoyuki,Abe Manabu,Imamura Yukio,Miyasaka Tomohiro,Kakuda Nobuto,Oohashi Toshitaka,Shimogori Tomomi,Yamakawa Kazuhiro,Ikawa Masahito,Nukina Nobuyuki
Abstract
AbstractGolli–myelin basic proteins, encoded by the myelin basic protein gene, are widely expressed in neurons and oligodendrocytes in the central nervous system. Further, prior research has shown that Golli–myelin basic protein is necessary for myelination and neuronal maturation during central nervous system development. In this study, we established Golli–myelin basic protein-floxed mice to elucidate the cell-type-specific effects of Golli–myelin basic protein knockout through the generation of conditional knockout mice (Golli–myelin basic proteinsfl/fl; E3CreN), in which Golli–myelin basic proteins were specifically deleted in cerebellar granule neurons, where Golli–myelin basic proteins are expressed abundantly in wild-type mice. To investigate the role of Golli–myelin basic proteins in cerebellar granule neurons, we further performed histopathological analyses of these mice, with results indicating no morphological changes or degeneration of the major cellular components of the cerebellum. Furthermore, behavioral analysis showed that Golli–myelin basic proteinsfl/fl; E3CreN mice were healthy and did not display any abnormal behavior. These results suggest that the loss of Golli–myelin basic proteins in cerebellar granule neurons does not lead to cerebellar perturbations or behavioral abnormalities. This mouse model could therefore be employed to analyze the effect of Golli–myelin basic protein deletion in specific cell types of the central nervous system, such as other neuronal cells and oligodendrocytes, or in lymphocytes of the immune system.
Funder
Grants-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan
The Center for Baby Science, Doshisha University
Takeda Science Foundation
Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care
AMED
Okayama University
Publisher
Springer Science and Business Media LLC