Axon-Glia Interactions and the Domain Organization of Myelinated Axons Requires Neurexin IV/Caspr/Paranodin
| Autor: | Manzoor A. Bhat, Jose C. Rios, German P. Garcia-Fresco, Yue Lu, Jingjun Li, Jack Rosenbluth, Mary St. Martin, Steven Einheber, William Ching, Mitchell Chesler, James L. Salzer, Hugo J. Bellen |
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| Jazyk: | angličtina |
| Předmět: |
Male
Aging Heterozygote Potassium Channels Neuroscience(all) NFASC Cell Adhesion Molecules Neuronal Restriction Mapping Neurexin Nerve Tissue Proteins Receptors Cell Surface Biology Nerve Fibers Myelinated Nerve conduction velocity 03 medical and health sciences Mice 0302 clinical medicine Paranodal junction medicine Animals Drosophila Proteins Humans Axon Cloning Molecular 030304 developmental biology Mice Knockout 0303 health sciences Genomic Library Node of Ranvier Membrane Glycoproteins General Neuroscience Saltatory conduction Homozygote Neuropeptides Membrane Proteins Optic Nerve Sciatic Nerve Axons medicine.anatomical_structure nervous system Contactins Drosophila Female Neuroscience Neuroglia 030217 neurology & neurosurgery |
| Zdroj: | Neuron. (2):369-383 |
| ISSN: | 0896-6273 |
| DOI: | 10.1016/S0896-6273(01)00294-X |
| Popis: | Myelinated fibers are organized into distinct domains that are necessary for saltatory conduction. These domains include the nodes of Ranvier and the flanking paranodal regions where glial cells closely appose and form specialized septate-like junctions with axons. These junctions contain a Drosophila Neurexin IV-related protein, Caspr/Paranodin (NCP1). Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis. In the absence of NCP1, normal paranodal junctions fail to form, and the organization of the paranodal loops is disrupted. Contactin is undetectable in the paranodes, and K + channels are displaced from the juxtaparanodal into the paranodal domains. Loss of NCP1 also results in a severe decrease in peripheral nerve conduction velocity. These results show a critical role for NCP1 in the delineation of specific axonal domains and the axon-glia interactions required for normal saltatory conduction. |
| Databáze: | OpenAIRE |
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