Journal
NATURE NEUROSCIENCE
Volume 17, Issue 12, Pages 1664-1672Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3859
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Funding
- US National Institutes of Health [NS044916, NS069688, NS49119]
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- CURE (Citizens United for Research on Epilepsy)
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The scaffolding protein ankyrin-G is required for Na+ channel clustering at axon initial segments. It is also considered essential for Na+ channel clustering at nodes of Ranvier to facilitate fast and efficient action potential propagation. However, notwithstanding these widely accepted roles, we show here that ankyrin-G is dispensable for nodal Na+ channel clustering in vivo. Unexpectedly, in the absence of ankyrin-G, erythrocyte ankyrin (ankyrin-R) and its binding partner beta I spectrin substitute for and rescue nodal Na+ channel clustering. In addition, channel clustering is also rescued after loss of nodal beta IV spectrin by beta I spectrin and ankyrin-R. In mice lacking both ankyrin-G and ankyrin-R, Na+ channels fail to cluster at nodes. Thus, ankyrin R-beta I spectrin protein complexes function as secondary reserve Na+ channel clustering machinery, and two independent ankyrin-spectrin protein complexes exist in myelinated axons to cluster Na+ channels at nodes of Ranvier.
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