ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 55 citations in OpenAlex.
- Age-dependent reduction in voltage-gated inward sodium current and Scn8a gene expression in murine stellate ganglia.Annals of the New York Academy of Sciences · 2025Article
- Review
- Trafficking mechanisms underlying NaChannels (Austin, Tex.) · 2020Review
- Rapid evolution of a voltage-gated sodium channel gene in a lineage of electric fish leads to a persistent sodium current.PLoS biology · 2018Article
- Current injection and receptor-mediated excitation produce similar maximal firing rates in hypoglossal motoneurons.Journal of neurophysiology · 2016Article
- Prioritizing the development of mouse models for childhood brain disorders.Neuropharmacology · 2016Review
- Developing electrical properties of postnatal mouse lumbar motoneurons.Frontiers in cellular neuroscience · 2015Article
- Two Nedd4-binding motifs underlie modulation of sodium channel Nav1.6 by p38 MAPK.The Journal of biological chemistry · 2010Article
- Analysis of the mouse mutant Cloth-ears shows a role for the voltage-gated sodium channel Scn8a in peripheral neural hearing loss.Genes, brain, and behavior · 2009Article
- Review
- The contribution of resurgent sodium current to high-frequency firing in Purkinje neurons: an experimental and modeling study.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Molecular determinants of emerging excitability in rat embryonic motoneurons.The Journal of physiology · 2002Article
- Transcriptional channelopathies: an emerging class of disorders.Nature reviews. Neuroscience · 2001Review
- Channelopathies: ion channel defects linked to heritable clinical disorders.Journal of medical genetics · 2000Review
- Neuronal death and perinatal lethality in voltage-gated sodium channel alpha(II)-deficient mice.Biophysical journal · 2000Article
- Functional analysis of the mouse Scn8a sodium channel.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Sodium currents were recorded from motoneurons that were isolated from mice at postnatal days 0-8 (P0-P8) and maintained in culture for 12-24 hr. Motoneurons from normal mice exhibited a more than threefold increase in peak sodium current density from P0 to P8. For mice lacking a functional Scn8a sodium channel gene, motoneuronal sodium current density was comparable at P0 to that of normal mice but failed to increase from P0 to P8. The absence of Scn8a sodium channels is associated with the phenotype "motor end plate disease," which is characterized by a progressive neuromuscular failure and is fatal by 3-4 postnatal weeks. Thus, it appears that the development and function of mature motoneurons depends on the postnatal induction of Scn8a expression.
Indexed as
Identifiers
9651206PMC6793491W1921512660What OpenQuestion holds
Registered trials
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.