RT Journal Article SR Electronic T1 Mice with Altered Myelin Proteolipid Protein Gene Expression Display Cognitive Deficits Accompanied by Abnormal Neuron–Glia Interactions and Decreased Conduction Velocities JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 8363 OP 8371 DO 10.1523/JNEUROSCI.3216-08.2009 VO 29 IS 26 A1 Hisataka Tanaka A1 Jianmei Ma A1 Kenji F. Tanaka A1 Keizo Takao A1 Munekazu Komada A1 Koichi Tanda A1 Ayaka Suzuki A1 Tomoko Ishibashi A1 Hiroko Baba A1 Tadashi Isa A1 Ryuichi Shigemoto A1 Katsuhiko Ono A1 Tsuyoshi Miyakawa A1 Kazuhiro Ikenaka YR 2009 UL http://www.jneurosci.org/content/29/26/8363.abstract AB 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 (plp1 tg/− mice) at 2 months of age. At this stage, the plp1 tg/− 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 plp1 tg/− 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.