| Autor: |
Chen, Chunling, Westenbroek, Ruth E., Xu, Xiaorong, Edwards, Chris A., Sorenson, Dorothy R., Chen, Yuan, McEwen, Dyke P., O'Malley, Heather A., Bharucha, Vandana, Meadows, Laurence S., Knudsen, Gabriel A., Vilaythong, Alex, Noebels, Jeffrey L., Saunders, Thomas L., Scheuer, Todd, Shrager, Peter, Catterall, William A., Isom, Lori L. |
| Předmět: |
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| Zdroj: |
Journal of Neuroscience; 4/21/2004, Vol. 24 Issue 16, p4030-4042, 13p, 8 Diagrams, 3 Charts, 3 Graphs |
| Abstrakt: |
Sodium channel β1 subunits modulate α subunit gating and cell surface expression and participate in cell adhesive interactions in vitro. β1 (-/-) mice appear ataxic and display spontaneous generalized seizures. In the optic nerve, the fastest components of the compound action potential are slowed and the number of mature nodes of Ranvier is reduced, but Nav 1.6, contactin, caspr 1, and Kv 1 channels are all localized normally at nodes. At the ultrastructural level, the paranodal septate-like junctions immediately adjacent to the node are missing in a subset of axons, suggesting that β1 may participate in axo-glial communication at the periphery of the nodal gap. Sodium currents in dissociated hippocampal neurons are normal, but Nav 1.1 expression is reduced and Nav1.3 expression is increased in a subset of pyramidal neurons in the CA2/CA3 region, suggesting a basis for the epileptic phenotype. Our results show that β1 subunits play important roles in the regulation of sodium channel density and localization, are involved in axo-glial communication at nodes of Ranvier, and are required for normal action potential conduction and control of excitability in vivo. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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