ArticleNeurobiology of disease2014
Strain- and age-dependent hippocampal neuron sodium currents correlate with epilepsy severity in Dravet syndrome mice.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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110 citing papers in PubMed, 191 citations in OpenAlex.
- Article
- Compensatory rearrangement of parvalbumin interneuron voltage-gated sodium channel subunits in a mouse model of Dravet syndrome.Epilepsia · 2026Article
- AAV9-mediated targeting of natural antisense transcript as a novel treatment for Dravet syndrome.Molecular therapy. Nucleic acids · 2026Article
- Ameliorating Seizures in Dravet Syndrome: A Review of Newly Approved and Investigational Drugs, RNA and Gene-Based Therapies.CNS drugs · 2026Review
- The impact of seizures on REM sleep and the cholinergic pedunculopontine nucleus in a mouse model of Dravet Syndrome.bioRxiv : the preprint server for biology · 2026Article
- Dravet Syndrome Patient-Derived Neural Cells Present Altered Levels of Potassium, Copper, and Zinc.ACS chemical neuroscience · 2026Article
- Medial septum parvalbumin-expressing inhibitory neurons are impaired in a mouse model of Dravet syndrome.Epilepsia · 2025Article
- Article
- Gene therapies alleviate absence epilepsy associated withbioRxiv : the preprint server for biology · 2025Article
- Spotlight on mechanism of sudden unexpected death in epilepsy in Dravet syndrome.Translational psychiatry · 2025Review
- Advances in AAV-mediated gene replacement therapy for pediatric monogenic neurological disorders.Molecular therapy. Methods & clinical development · 2024Review
- Voltage-gated sodium channels in genetic epilepsy: up and down of excitability.Journal of neurochemistry · 2024Review
- Review
- Voltage-Gated Ion Channel Compensatory Effect in DEE: Implications for Future Therapies.Cells · 2024Review
- Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability.Translational psychiatry · 2024Article
- Ndnf Interneuron Excitability Is Spared in a Mouse Model of Dravet Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Antisense oligonucleotides restore excitability, GABA signalling and sodium current density in a Dravet syndrome model.Brain : a journal of neurology · 2024Article
- Temporal manipulation of the Scn1a gene reveals its essential role in adult brain function.Brain : a journal of neurology · 2024Article
- Hyperexcitability and translational phenotypes in a preclinical mouse model ofResearch square · 2024Article
- SCN1A-deficient excitatory neuronal networks display mutation-specific phenotypes.Brain : a journal of neurology · 2023Article
50 more citing papers are in PubMed but not listed here.
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6 authors at 1 institution in 1 country.
Funding
Abstract
Heterozygous loss-of-function SCN1A mutations cause Dravet syndrome, an epileptic encephalopathy of infancy that exhibits variable clinical severity. We utilized a heterozygous Scn1a knockout (Scn1a(+/-)) mouse model of Dravet syndrome to investigate the basis for phenotype variability. These animals exhibit strain-dependent seizure severity and survival. Scn1a(+/-) mice on strain 129S6/SvEvTac (129.Scn1a(+/-)) have no overt phenotype and normal survival compared with Scn1a(+/-) mice bred to C57BL/6J (F1.Scn1a(+/-)) that have severe epilepsy and premature lethality. We tested the hypothesis that strain differences in sodium current (INa) density in hippocampal neurons contribute to these divergent phenotypes. Whole-cell voltage-clamp recording was performed on acutely-dissociated hippocampal neurons from postnatal days 21-24 (P21-24) 129.Scn1a(+/-) or F1.Scn1a(+/-) mice and wild-type littermates. INa density was lower in GABAergic interneurons from F1.Scn1a(+/-) mice compared to wild-type littermates, while on the 129 strain there was no difference in GABAergic interneuron INa density between 129.Scn1a(+/-) mice and wild-type littermate controls. By contrast, INa density was elevated in pyramidal neurons from both 129.Scn1a(+/-) and F1.Scn1a(+/-) mice, and was correlated with more frequent spontaneous action potential firing in these neurons, as well as more sustained firing in F1.Scn1a(+/-) neurons. We also observed age-dependent differences in pyramidal neuron INa density between wild-type and Scn1a(+/-) animals. We conclude that preserved INa density in GABAergic interneurons contributes to the milder phenotype of 129.Scn1a(+/-) mice. Furthermore, elevated INa density in excitatory pyramidal neurons at P21-24 correlates with age-dependent onset of lethality in F1.Scn1a(+/-) mice. Our findings illustrate differences in hippocampal neurons that may underlie strain- and age-dependent phenotype severity in a Dravet syndrome mouse model, and emphasize a contribution of pyramidal neuron excitability.
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