ArticleProceedings of the National Academy of Sciences of the United States of America2013
Abnormal neuronal patterning occurs during early postnatal brain development of Scn1b-null mice and precedes hyperexcitability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 75 citations in OpenAlex.
- Article
- A Novel Mouse Model for Developmental and Epileptic Encephalopathy by Purkinje Cell-Specific Deletion ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Diverse species of animal models in epilepsy research: Progress and perspectives.Zoological research · 2025Review
- Ataxia and cerebellar hypoexcitability in a mouse model of SCN1B-linked Dravet syndrome.JCI insight · 2025Article
- Article
- 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
- A dynamic gradient architecture generates brain activity states.NeuroImage · 2022Article
- Impact of In Utero Exposure to Antiepileptic Drugs on Neonatal Brain Function.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.JCI insight · 2022Article
- Epilepsy Combined With Multiple Gene Heterozygous Mutation.Frontiers in pediatrics · 2022Article
- Individual differences in stereotypy and neuron subtype translatome with TrkB deletion.Molecular psychiatry · 2021Article
- Homozygous SCN1B variants causing early infantile epileptic encephalopathy 52 affect voltage-gated sodium channel function.Epilepsia · 2021Article
- Sodium channel β1 subunits participate in regulated intramembrane proteolysis-excitation coupling.JCI insight · 2021Article
- Channelopathy of Dravet Syndrome and Potential Neuroprotective Effects of Cannabidiol.Journal of central nervous system disease · 2021Review
- Excitatory and inhibitory neuron defects in a mouse model of Scn1b-linked EIEE52.Annals of clinical and translational neurology · 2020Article
- Sodium channel β1 subunits are post-translationally modified by tyrosine phosphorylation,The Journal of biological chemistry · 2020Article
- Ion Channel Functions in Early Brain Development.Trends in neurosciences · 2020Review
- From Neural Tube Formation Through the Differentiation of Spinal Cord Neurons: Ion Channels in Action During Neural Development.Frontiers in molecular neuroscience · 2020Article
- SCN1B-linked early infantile developmental and epileptic encephalopathy.Annals of clinical and translational neurology · 2019Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-gated Na(+) channel (VGSC) β1 subunits, encoded by SCN1B, are multifunctional channel modulators and cell adhesion molecules (CAMs). Mutations in SCN1B are associated with the genetic epilepsy with febrile seizures plus (GEFS+) spectrum disorders in humans, and Scn1b-null mice display severe spontaneous seizures and ataxia from postnatal day (P)10. The goal of this study was to determine changes in neuronal pathfinding during early postnatal brain development of Scn1b-null mice to test the hypothesis that these CAM-mediated roles of Scn1b may contribute to the development of hyperexcitability. c-Fos, a protein induced in response to seizure activity, was up-regulated in the Scn1b-null brain at P16 but not at P5. Consistent with this, epileptiform activity was observed in hippocampal and cortical slices prepared from the P16 but not from the P5-P7 Scn1b-null brain. On the basis of these results, we investigated neuronal pathfinding at P5. We observed disrupted fasciculation of parallel fibers in the P5 null cerebellum. Further, P5 null mice showed reduced neuron density in the dentate gyrus granule cell layer, increased proliferation of granule cell precursors in the hilus, and defective axonal extension and misorientation of somata and processes of inhibitory neurons in the dentate gyrus and CA1. Thus, Scn1b is critical for neuronal proliferation, migration, and pathfinding during the critical postnatal period of brain development. We propose that defective neuronal proliferation, migration, and pathfinding in response to Scn1b deletion may contribute to the development of hyperexcitability.
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