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Previous Article | Next Article
The Journal of Neuroscience, August 1, 2002, 22(15):6507-6514
A Myelin Galactolipid, Sulfatide, Is Essential for Maintenance of Ion Channels on Myelinated Axon But Not Essential for Initial Cluster Formation
Tomoko Ishibashi1, 2, 3, Jeffrey L. Dupree4, Kazuhiro Ikenaka1, 3, Yukie Hirahara5, Koichi Honke6, Elior Peles7, Brian Popko8, Kinuko Suzuki9, Hitoo Nishino10, and Hiroko Baba2 1 Department of Physiological Sciences, The Graduate University for Advanced Studies, Okazaki 444-8585, Japan, 2 Department of Molecular Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Science, Hachioji 192-0392, Japan, 3 Laboratory of Neural Information, National Institute for Physiological Sciences, Okazaki National Research Institutes, Okazaki 444-8585, Japan, 4 Department of Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, Virginia 23507, 5 Research Institute, Osaka Medical Center for Maternal and Child Health, Izumi 594-1101, Japan, 6 Department of Biochemistry, Osaka University Graduate School of Medicine, Suita 565-0871, Japan, 7 Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel, 8 Neuroscience Center, Department of Biochemistry and Biophysics, Program in Molecular Biology and Biotechnology and 9 Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, and 10 Department of Physiology, Nagoya City University Medical School, Nagoya 467-8601, Japan
Myelinated axons are divided into four distinct regions: the node of Ranvier, paranode, juxtaparanode, and internode, each of which is characterized by a specific set of axonal proteins. Voltage-gated Na+ channels are clustered at high densities at the nodes, whereas shaker-type K+ channels are concentrated at juxtaparanodal regions. These channels are separated by the paranodal regions, where septate-like junctions are formed between the axon and the myelinating glial cells. Although oligodendrocytes and myelin sheaths are believed to play an instructive role in the local differentiation of the axon to distinct domains, the molecular mechanisms involved are poorly understood. In the present study, we have examined the distribution of axonal components in mice incapable of synthesizing sulfatide by disruption of the galactosylceramide sulfotransferase gene. These mice displayed abnormal paranodal junctions in the CNS and PNS, whereas their compact myelin was preserved. Immunohistochemical analysis demonstrated a decrease in Na+ and K+ channel clusters, altered nodal length, abnormal localization of K+ channel clusters appearing primarily in the presumptive paranodal regions, and diffuse distribution of contactin-associated protein along the internode. Similar abnormalities have been reported previously in mice lacking both galactocerebroside and sulfatide. Interestingly, although no demyelination was observed, these channel clusters decreased markedly with age. The initial timing and the number of Na+ channel clusters formed were normal during development. These results indicate a critical role for sulfatide in proper localization and maintenance of ion channels clusters, whereas they do not appear to be essential for initial cluster formation of Na+ channels.
Key words: sulfatide; paranodal junction; myelin; node of Ranvier; Na+ channel; K+ channel
Copyright © 2002 Society for Neuroscience 0270-6474/02/22156507-08$05.00/0
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