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Nat Neurosci. 2014 Dec;17(12):1664-72. doi: 10.1038/nn.3859. Epub 2014 Nov 2.

A hierarchy of ankyrin-spectrin complexes clusters sodium channels at nodes of Ranvier.

Author information

1
Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA.
2
Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA.
3
Department of Neurology, Baylor College of Medicine, Houston, Texas, USA.
4
1] Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA. [2] Department of Neurology, Baylor College of Medicine, Houston, Texas, USA.
5
Department of Pathology, Yale University, New Haven, Connecticut, USA.
6
Department of Cell Biology, Duke University, Durham, North Carolina, USA.
7
1] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA. [2] Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA.

Abstract

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 βI spectrin substitute for and rescue nodal Na(+) channel clustering. In addition, channel clustering is also rescued after loss of nodal βIV spectrin by βI spectrin and ankyrin-R. In mice lacking both ankyrin-G and ankyrin-R, Na(+) channels fail to cluster at nodes. Thus, ankyrin R-βI 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.

PMID:
25362473
PMCID:
PMC4271271
DOI:
10.1038/nn.3859
[Indexed for MEDLINE]
Free PMC Article
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