Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome. - Wikidata - awgldk - TriplyDB

Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome.

Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome.

http://www.wikidata.org/entity/Q36221618

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Altered cardiac electrophysiology and SUDEP in a model of Dravet syndrome Characterization of a de novo SCN8A mutation in a patient with epileptic encephalopathy Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders Sudden unexpected death in epilepsy: fatal post-ictal respiratory and arousal mechanisms Dissecting the phenotypes of Dravet syndrome by gene deletion Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies Genetic background modulates impaired excitability of inhibitory neurons in a mouse model of Dravet syndrome Mechanisms of sudden unexplained death in epilepsy Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain FOXG1-Dependent Dysregulation of GABA/Glutamate Neuron Differentiation in Autism Spectrum Disorders Prioritizing the development of mouse models for childhood brain disorders Sudden unexpected death in a mouse model of Dravet syndrome.CaV 2.1 ablation in cortical interneurons selectively impairs fast-spiking basket cells and causes generalized seizures.Mapping genetic modifiers of survival in a mouse model of Dravet syndrome.Correlations in timing of sodium channel expression, epilepsy, and sudden death in Dravet syndrome.Large-scale structural alteration of brain in epileptic children with SCN1A mutation Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome WONOEP appraisal: new genetic approaches to study epilepsy ABHD6 blockade exerts antiepileptic activity in PTZ-induced seizures and in spontaneous seizures in R6/2 mice.High-resolution molecular genomic autopsy reveals complex sudden unexpected death in epilepsy risk profile.Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction.Characterization of a subpopulation of developing cortical interneurons from human iPSCs within serum-free embryoid bodies GABAB receptors in maintenance of neocortical circuit function.Sleep impairment and reduced interneuron excitability in a mouse model of Dravet Syndrome.Disruption of Fgf13 causes synaptic excitatory-inhibitory imbalance and genetic epilepsy and febrile seizures plus Pharmacotherapy for Dravet Syndrome.Clemizole and modulators of serotonin signalling suppress seizures in Dravet syndrome.From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.Unaltered Network Activity and Interneuronal Firing During Spontaneous Cortical Dynamics In Vivo in a Mouse Model of Severe Myoclonic Epilepsy of Infancy.Analysis of endocannabinoid signaling elements and related proteins in lymphocytes of patients with Dravet syndrome Model systems for studying cellular mechanisms of SCN1A-related epilepsy.Synergistic GABA-enhancing therapy against seizures in a mouse model of Dravet syndrome.Peripheral nerve injury is accompanied by chronic transcriptome-wide changes in the mouse prefrontal cortex.A human Dravet syndrome model from patient induced pluripotent stem cells.2014 Epilepsy Benchmarks Area II: Prevent Epilepsy and Its Progression.A deleterious Nav1.1 mutation selectively impairs telencephalic inhibitory neurons derived from Dravet Syndrome patients.Upregulation of Haploinsufficient Gene Expression in the Brain by Targeting a Long Non-coding RNA Improves Seizure Phenotype in a Model of Dravet Syndrome.Dravet syndrome patient-derived neurons suggest a novel epilepsy mechanism.Sudden unexpected death in epilepsy genetics: Molecular diagnostics and prevention Nav1.1 haploinsufficiency in excitatory neurons ameliorates seizure-associated sudden death in a mouse model of Dravet syndrome.

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Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome.

http://www.wikidata.org/entity/Q36221618

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Christine S Cheah

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Frank H Yu

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Gregory B Potter

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P2860

De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy

From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels

Sodium channel beta subunits: anything but auxiliary

Modification of seizure activity by electrical stimulation. II. Motor seizure

Mice lacking Dlx1 show subtype-specific loss of interneurons, reduced inhibition and epilepsy

Reduced sodium current in Purkinje neurons from Nav1.1 mutant mice: implications for ataxia in severe myoclonic epilepsy in infancy

Reduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancy

Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation

The VGL-Chanome: A Protein Superfamily Specialized for Electrical Signaling and Ionic Homeostasis

The origin and specification of cortical interneurons

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