ArticleAnnals of clinical and translational neurology2020
Excitatory and inhibitory neuron defects in a mouse model of Scn1b-linked EIEE52.
Article in Annals of clinical and translational neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Interpretable Machine Learning Identifies an Emergent Absence Seizure Mechanism.bioRxiv : the preprint server for biology · 2026Article
- Compensatory rearrangement of parvalbumin interneuron voltage-gated sodium channel subunits in a mouse model of Dravet syndrome.Epilepsia · 2026Article
- Multimodal evidence for a mechanistic model of working memory deficits in schizophrenia.medRxiv : the preprint server for health sciences · 2026Article
- 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
- Altered cardiac excitability and arrhythmia in models of SCN1B-linked developmental and epileptic encephalopathy.JCI insight · 2025Article
- Ataxia and cerebellar hypoexcitability in a mouse model of SCN1B-linked Dravet syndrome.JCI insight · 2025Article
- Neuromodulation of voltage-gated sodium channels by Gβ1γ2 subunits: Implications for GNB1-linked encephalopathy.Neurobiology of disease · 2025Article
- A spatial single-cell atlas of the claustro-insular region uncovers key regulators of neuronal identity and excitability.Nature communications · 2025Article
- Article
- Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism.eLife · 2025Article
- Voltage-gated sodium channels in genetic epilepsy: up and down of excitability.Journal of neurochemistry · 2024Review
- Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism.bioRxiv : the preprint server for biology · 2024Article
- 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
- Heterogeneity of voltage gated sodium current density between neurons decorrelates spiking and suppresses network synchronization in Scn1b null mouse models.Scientific reports · 2023Article
- Developmental and epileptic encephalopathies: from genetic heterogeneity to phenotypic continuum.Physiological reviews · 2023Review
- Epilepsy and sudden unexpected death in epilepsy in a mouse model of humanBrain communications · 2023Article
- SCN1B Genetic Variants: A Review of the Spectrum of Clinical Phenotypes and a Report of Early Myoclonic Encephalopathy.Children (Basel, Switzerland) · 2022Review
- Sodium channel β1 subunits participate in regulated intramembrane proteolysis-excitation coupling.JCI insight · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveHuman variants in voltage-gated sodium channel (VGSC) α and β subunit genes are linked to developmental and epileptic encephalopathies (DEEs). Inherited, biallelic, loss-of-function variants in SCN1B, encoding the β1/β1B subunits, are linked to early infantile DEE (EIEE52). De novo, monoallelic variants in SCN1A (Nav1.1), SCN2A (Nav1.2), SCN3A (Nav1.3), and SCN8A (Nav1.6) are also linked to DEEs. While these VGSC-linked DEEs have similar presentations, they have diverse mechanisms of altered neuronal excitability. Mouse models have suggested that Scn2a-, Scn3a-, and Scn8a-linked DEE variants are, in general, gain of function, resulting in increased persistent or resurgent sodium current (I
methodsWe investigated excitability defects in pyramidal and parvalbumin-positive (PV +) interneurons in the Scn1b
resultsScn1b
interpretationThis work suggests that SCN1B-linked DEE variants impact both excitatory and inhibitory neurons, leading to the increased severity of EIEE52 relative to other DEEs.
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Registered trials
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