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

Tanaka H, Ma J, Tanaka K, 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.

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Tanaka, Hisataka; Ma, Jianmei; Tanaka, Kenji F; Takao, Keizo; Komada, Munekazu; Tanda, Koichi; Suzuki, Ayaka; Ishibashi, Tomoko; Baba, Hiroko; Isa, Tadashi; Shigemoto, RyuichiISTA ; Ono, Katsuhiko
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Abstract
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.
Publishing Year
Date Published
2009-07-01
Journal Title
Journal of Neuroscience
Volume
29
Issue
26
Page
8363 - 8371
IST-REx-ID

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Tanaka H, Ma J, Tanaka K, et al. Mice with altered myelin proteolipid protein gene expression display cognitive deficits accompanied by abnormal neuron-glia interactions and decreased conduction velocities. Journal of Neuroscience. 2009;29(26):8363-8371. doi:10.1523/JNEUROSCI.3216-08.2009
Tanaka, H., Ma, J., Tanaka, K., Takao, K., Komada, M., Tanda, K., … 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. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.3216-08.2009
Tanaka, Hisataka, Jianmei Ma, Kenji Tanaka, Keizo Takao, Munekazu Komada, Koichi Tanda, Ayaka Suzuki, et al. “Mice with Altered Myelin Proteolipid Protein Gene Expression Display Cognitive Deficits Accompanied by Abnormal Neuron-Glia Interactions and Decreased Conduction Velocities.” Journal of Neuroscience. Society for Neuroscience, 2009. https://doi.org/10.1523/JNEUROSCI.3216-08.2009.
H. Tanaka et al., “Mice with altered myelin proteolipid protein gene expression display cognitive deficits accompanied by abnormal neuron-glia interactions and decreased conduction velocities,” Journal of Neuroscience, vol. 29, no. 26. Society for Neuroscience, pp. 8363–8371, 2009.
Tanaka H, Ma J, Tanaka K, 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.
Tanaka, Hisataka, et al. “Mice with Altered Myelin Proteolipid Protein Gene Expression Display Cognitive Deficits Accompanied by Abnormal Neuron-Glia Interactions and Decreased Conduction Velocities.” Journal of Neuroscience, vol. 29, no. 26, Society for Neuroscience, 2009, pp. 8363–71, doi:10.1523/JNEUROSCI.3216-08.2009.

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