Abstract
In myelinated axons, K+ channels are concealed under the myelin sheath in the juxtaparanodal region, where they are associated with Caspr2, a member of the neurexin superfamily. Deletion of Caspr2 in mice by gene targeting revealed that it is required to maintain K+ channels at this location. Furthermore, we show that the localization of Caspr2 and clustering of K+ channels at the juxtaparanodal region depends on the presence of TAG-1, an immunoglobulin-like cell adhesion molecule that binds Caspr2. These results demonstrate that Caspr2 and TAG-1 form a scaffold that is necessary to maintain K+ channels at the juxtaparanodal region, suggesting that axon-glia interactions mediated by these proteins allow myelinating glial cells to organize ion channels in the underlying axonal membrane.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Axons / metabolism*
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Axons / ultrastructure
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Cell Adhesion Molecules, Neuronal / metabolism*
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Cell Communication / genetics
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Contactin 2
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Gene Targeting
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Membrane Proteins*
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Mice
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Mice, Knockout
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Microscopy, Electron
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Mutation / genetics
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Nerve Fibers, Myelinated / metabolism*
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Nerve Fibers, Myelinated / ultrastructure
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Nerve Tissue Proteins / deficiency*
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Nerve Tissue Proteins / genetics
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Neural Conduction / genetics
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Neuroglia / metabolism
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Neuroglia / ultrastructure
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Potassium Channels / genetics
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Potassium Channels / metabolism*
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Ranvier's Nodes / metabolism*
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Ranvier's Nodes / ultrastructure
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Shaker Superfamily of Potassium Channels
Substances
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CNTN2 protein, human
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CNTNAP2 protein, human
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Cell Adhesion Molecules, Neuronal
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Cntn2 protein, mouse
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Contactin 2
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Membrane Proteins
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Nerve Tissue Proteins
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Potassium Channels
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Shaker Superfamily of Potassium Channels