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The Journal of Neuroscience, July 27, 2005, 25(30):7004-7013; doi:10.1523/JNEUROSCI.0288-05.2005

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Development/Plasticity/Repair
Region-Specific Myelin Pathology in Mice Lacking the Golli Products of the Myelin Basic Protein Gene

Erin C. Jacobs,¹ Thomas M. Pribyl,¹ Kathy Kampf,¹ Celia Campagnoni,¹ Christopher S. Colwell,¹ Samuel D. Reyes,¹ Melanie Martin,² Vance Handley,¹ Timothy D. Hiltner,² Carol Readhead,² Russell E. Jacobs,² Albee Messing,³ Robin S. Fisher,¹ and Anthony T. Campagnoni¹

¹Neuropsychiatric Institute, University of California Los Angeles School of Medicine, Los Angeles, California 90024, ²Biological Imaging Center, Beckman Institute, California Institute of Technology, Pasadena, California 91125, and ³Waisman Center and Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53705

The myelin basic protein (MBP) gene encodes two families of proteins, the classic MBP constituents of myelin and the golli-MBPs, the function of which is less well understood. In this study, targeted ablation of the golli-MBPs, but not the classic MBPs, resulted in a distinct phenotype unlike that of knock-outs (KOs) of the classic MBPs or other myelin proteins. Although the golli KO animals did not display an overt dysmyelinating phenotype, they did exhibit delayed and/or hypomyelination in selected areas of the brain, such as the visual cortex and the optic nerve, as determined by Northern and Western blots and immunohistochemical analysis with myelin protein markers. Hypomyelination in some areas, such as the visual cortex, persisted into adulthood. Ultrastructural analysis of the KOs confirmed both the delay and hypomyelination and revealed abnormalities in myelin structure and in some oligodendrocytes. Abnormal visual-evoked potentials indicated that the hypomyelination in the visual cortex had functional consequences in the golli KO brain. Evidence that the abnormal myelination in these animals was a consequence of intrinsic problems with the oligodendrocyte was indicated by an impaired ability of oligodendrocytes to form myelin sheets in culture and by the presence of abnormal Ca²⁺ transients in purified cortical oligodendrocytes studied in vitro. The Ca²⁺ results reported in this study complement previous results implicating golli proteins in modulating intracellular signaling in T-cells. Together, all these findings suggest a role for golli proteins in oligodendrocyte differentiation, migration, and/or myelin elaboration in the brain.

Key words: oligodendrocytes; calcium imaging; dysmyelination; visual cortex; optic nerve; ablation

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Received Jan 20, 2005; revised June 7, 2005; accepted June 9, 2005.

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