ArticleProceedings of the National Academy of Sciences of the United States of America2010
Functional reciprocity between Na+ channel Nav1.6 and beta1 subunits in the coordinated regulation of excitability and neurite outgrowth.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 148 citations in OpenAlex.
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- FGF14 Peptide Derivative Differentially Regulates Nav1.2 and NaLife (Basel, Switzerland) · 2025Article
- Saxitoxin potentiates human neuronal cell death induced by Zika virus while sparing neural progenitors and astrocytes.Scientific reports · 2024Article
- Conotoxins Targeting Voltage-Gated Sodium Ion Channels.Pharmacological reviews · 2024Review
- Antisense oligonucleotides restore excitability, GABA signalling and sodium current density in a Dravet syndrome model.Brain : a journal of neurology · 2024Article
- Complex Synaptic and Intrinsic Interactions Disrupt Input/Output Functions in the Hippocampus ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Sodium channels and the ionic microenvironment of breast tumours.The Journal of physiology · 2023Article
- Cryo-EM structure of human voltage-gated sodium channel NaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The volatile anesthetic isoflurane differentially inhibits voltage-gated sodium channel currents between pyramidal and parvalbumin neurons in the prefrontal cortex.Frontiers in neural circuits · 2023Article
- Therapeutic Potential of Targeting Regulated Intramembrane Proteolysis Mechanisms of Voltage-Gated Ion Channel Subunits and Cell Adhesion Molecules.Pharmacological reviews · 2022Review
- The voltage-gated KPlatelets · 2022Article
- iPSCs and DRGs: stepping stones to new pain therapies.Trends in molecular medicine · 2022Review
- Resurgent NaNature communications · 2021Article
- Therapeutically leveraging GABAExperimental biology and medicine (Maywood, N.J.) · 2021Review
- A novel gain-of-function sodium channel β2 subunit mutation in idiopathic small fiber neuropathy.Journal of neurophysiology · 2021Article
- Review
- Sodium channel β1 subunits participate in regulated intramembrane proteolysis-excitation coupling.JCI insight · 2021Article
- Sodium channel β1 subunits are post-translationally modified by tyrosine phosphorylation,The Journal of biological chemistry · 2020Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Voltage-gated Na(+) channel (VGSC) beta1 subunits regulate cell-cell adhesion and channel activity in vitro. We previously showed that beta1 promotes neurite outgrowth in cerebellar granule neurons (CGNs) via homophilic cell adhesion, fyn kinase, and contactin. Here we demonstrate that beta1-mediated neurite outgrowth requires Na(+) current (I(Na)) mediated by Na(v)1.6. In addition, beta1 is required for high-frequency action potential firing. Transient I(Na) is unchanged in Scn1b (beta1) null CGNs; however, the resurgent I(Na), thought to underlie high-frequency firing in Na(v)1.6-expressing cerebellar neurons, is reduced. The proportion of axon initial segments (AIS) expressing Na(v)1.6 is reduced in Scn1b null cerebellar neurons. In place of Na(v)1.6 at the AIS, we observed an increase in Na(v)1.1, whereas Na(v)1.2 was unchanged. This indicates that beta1 is required for normal localization of Na(v)1.6 at the AIS during the postnatal developmental switch to Na(v)1.6-mediated high-frequency firing. In agreement with this, beta1 is normally expressed with alpha subunits at the AIS of P14 CGNs. We propose reciprocity of function between beta1 and Na(v)1.6 such that beta1-mediated neurite outgrowth requires Na(v)1.6-mediated I(Na), and Na(v)1.6 localization and consequent high-frequency firing require beta1. We conclude that VGSC subunits function in macromolecular signaling complexes regulating both neuronal excitability and migration during cerebellar development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.