Mice lacking sodium channel beta1 subunits display defects in neuronal excitability, sodium channel expression, and nodal architecture.

doi:10.1523/JNEUROSCI.4139-03.2004

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Article

Mice lacking sodium channel beta1 subunits display defects in neuronal excitability, sodium channel expression, and nodal architecture.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 21 Apr 2004

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

Abstract excerpt

Sodium channel beta1 subunits modulate alpha subunit gating and cell surface expression and participate in cell adhesive interactions in vitro. beta1-/- 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 Na(v)1.6, contactin, caspr 1, and K(v)1 channels are...

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PMID: 15102918
DOI: 10.1523/JNEUROSCI.4139-03.2004
PMCID: PMC6729427

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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