Mice with altered myelin proteolipid protein gene expression display cognitive deficits accompanied by abnormal neuron-glia interactions and decreased conduction velocities

Hisataka Tanaka, Jianmei Ma, Kenji F. Tanaka, Keizo Takao, Munekazu Komada, Koichi Tanda, Ayaka Suzuki, Tomoko Ishibashi, Hiroko Baba, Tadashi Isa, Ryuichi Shigemoto, Katsuhiko Ono, Tsuyoshi Miyakawa, Kazuhiro Ikenaka

研究成果: Article

52 引用 (Scopus)

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Conduction velocity (CV) of myelinated axons has been shown to be regulated by oligodendrocytes even after myelination has been completed. However, how myelinating oligodendrocytes regulate CV, and what the significance of this regulation is for normal brain function remain unknown. To address these questions, we analyzed a transgenic mouse line harboring extra copies of the myelin proteolipid protein 1 (plp1) gene (plp1tg/- mice) at 2 months of age. At this stage, the plp1tg/- mice have an unaffected myelin structure with a normally appearing ion channel distribution, but the CV in all axonal tracts tested in the CNS is greatly reduced. We also found decreased axonal diameters and slightly abnormal paranodal structures, both of which can be a cause for the reduced CV. Interestingly the plp1tg/- mice showed altered anxiety-like behaviors, reduced prepulse inhibitions, spatial learning deficits and working memory deficit, all of which are schizophrenia-related behaviors. Our results implicate that abnormalities in the neuron-glia interactions at the paranodal junctions can result in reduced CV in the CNS, which then induces behavioral abnormalities related to schizophrenia.

元の言語English
ページ(範囲)8363-8371
ページ数9
ジャーナルJournal of Neuroscience
29
発行部数26
DOI
出版物ステータスPublished - 01-07-2009

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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    Tanaka, H., Ma, J., Tanaka, K. F., Takao, K., Komada, M., Tanda, K., Suzuki, A., Ishibashi, T., Baba, H., Isa, T., Shigemoto, R., Ono, K., Miyakawa, T., & Ikenaka, K. (2009). Mice with altered myelin proteolipid protein gene expression display cognitive deficits accompanied by abnormal neuron-glia interactions and decreased conduction velocities. Journal of Neuroscience, 29(26), 8363-8371. https://doi.org/10.1523/JNEUROSCI.3216-08.2009