Role of the hippocampus in Nav1.6 (Scn8a) mediated seizure resistance.

No abstract is available for this paper.

• Publication year

  2014

• Venue

  Neurobiology of Disease

• Publication date

  2014-08-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.nbd.2014.03.014PMID 24704313PMCID PMC4077284
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Fisher's Exact Test.

  2016cited by this paper
• Glyoxalase 1 and its substrate methylglyoxal are novel regulators of seizure susceptibility

  2013cited by this paper
• Altered sleep regulation in a mouse model of SCN1A‐derived genetic epilepsy with febrile seizures plus (GEFS+)

  2013cited by this paper
• Aberrant sodium channel activity in the complex seizure disorder of Celf4 mutant mice

  2013cited by this paper
• Preferential inactivation of Scn1a in parvalbumin interneurons increases seizure susceptibility.

  2013cited by this paper
• De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP.

  2012influential reference
• Neuronal voltage-gated ion channels are genetic modifiers of generalized epilepsy with febrile seizures plus.

  2011cited by this paper
• Molecular correlates of age-dependent seizures in an inherited neonatal-infantile epilepsy.

  2010cited by this paper
• Altered Function of the SCN1A Voltage-gated Sodium Channel Leads to γ-Aminobutyric Acid-ergic (GABAergic) Interneuron Abnormalities*

  2010influential reference
• Molecular Identity of Dendritic Voltage-Gated Sodium Channels

  2010cited by this paper
• Axonal sodium channel distribution shapes the depolarized action potential threshold of dentate granule neurons

  2009influential reference
• Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in mice

  2009cited by this paper
• Role of hippocampal sodium channel Nav1.6 in kindling epileptogenesis

  2009influential reference
• Exaggerated emotional behavior in mice heterozygous null for the sodium channel Scn8a (Nav1.6)

  2008cited by this paper
• Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons.

  2008cited by this paper
• Reduced expression of Na(v)1.6 sodium channels and compensation by Na(v)1.2 channels in mice heterozygous for a null mutation in Scn8a.

  2008cited by this paper
• The dentate gyrus as a filter or gate: a look back and a look ahead.

  2007cited by this paper
• The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancy.

  2007influential reference
• Hippocampus-specific deletion of BDNF in adult mice impairs spatial memory and extinction of aversive memories

  2007influential reference
• Heterozygosity for a protein truncation mutation of sodium channel SCN8A in a patient with cerebellar atrophy, ataxia, and mental retardation

  2005cited by this paper
• Genes and mutations in human idiopathic epilepsy.

  2004cited by this paper
• Use-dependent potentiation of the Nav1.6 sodium channel.

  2004cited by this paper
• Floxed allele for conditional inactivation of the voltage‐gated sodium channel Scn8a (Nav1.6)

  2004influential reference
• Exploring New Gene Discoveries in Idiopathic Generalized Epilepsy

  2003cited by this paper
• Molecular and pathological effects of a modifier gene on deficiency of the sodium channel Scn8a (Na(v)1.6).

  2002cited by this paper
• Comparative distribution of voltage-gated sodium channel proteins in human brain.

  2001cited by this paper
• Delivery of the Cre recombinase by a self-deleting lentiviral vector: Efficient gene targeting in vivo

  2001cited by this paper
• De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy.

  2001cited by this paper
• Pharmacological characterization of the 6 Hz psychomotor seizure model of partial epilepsy

  2001cited by this paper
• Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2

  2000cited by this paper
• Type I and type II Na+ channel α‐subunit polypeptides exhibit distinct spatial and temporal patterning, and association with auxiliary subunits in rat brain

  1999cited by this paper
• Development of a Self-Inactivating Lentivirus Vector

  1998cited by this paper
• Altered subthreshold sodium currents and disrupted firing patterns in Purkinje neurons of Scn8a mutant mice.

  1997cited by this paper
• Alternative Splicing of the Sodium Channel SCN8A Predicts a Truncated Two-domain Protein in Fetal Brain and Non-neuronal Cells*

  1997cited by this paper
• Mutation Detection in the med and medJ Alleles of the Sodium Channel Scn8a

  1996cited by this paper
• Mutation of a new sodium channel gene, Scn8a, in the mouse mutant ‘motor endplate disease’

  1995cited by this paper
• MYELINATION IN RAT BRAIN: CHANGES IN MYELIN COMPOSITION DURING BRAIN MATURATION 1

  1973cited by this paper
• Properties and Alterations of Electrically‐Induced Seizures in Mice 1

  1953cited by this paper

• A research roadmap for SCN8A-related disorders: addressing knowledge gaps and aligning research priorities across stakeholders

  2025cites this paper
• Age at onset of genetic disease and genetic dependent stage: evidence from cases with SCN1A variants.

  2025cites this paper
• Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.

  2025cites this paper
• Classification of Current Experimental Models of Epilepsy

  2024cites this paper
• Exosomal TNF-α mediates voltage-gated Na+ channel 1.6 overexpression and contributes to brain tumor–induced neuronal hyperexcitability

  2024cites this paper
• Development and application of a multiple reaction monitoring method for the simultaneous quantification of sodium channels Nav 1.1, Nav 1.2, and Nav 1.6 in solubilized membrane proteins from stable HEK293 cell lines, rodents, and human brain tissues.

  2023cites this paper
• Long-Term Downregulation of the Sodium Channel Gene Scn8a Is Therapeutic in Mouse Models of SCN8A Epilepsy

  2023cites this paper
• Relationship between right‐to‐left shunt, hypoxia, and epilepsy

  2023cites this paper
• CaMKII Inhibition Attenuates Distinct Gain-of-Function Effects Produced by Mutant Nav1.6 Channels and Reduces Neuronal Excitability

  2022cites this paper
• Overexpression of NaV1.6 in the rostral ventrolateral medulla in rats mediates stress-induced hypertension via glutamate regulation

  2022cites this paper
• Autistic-like behavior, spontaneous seizures, and increased neuronal excitability in a Scn8a mouse model

  2021cites this paper
• Pathogenic in-Frame Variants in SCN8A: Expanding the Genetic Landscape of SCN8A-Associated Disease

  2021cites this paper
• Distinctive Properties and Powerful Neuromodulation of Nav1.6 Sodium Channels Regulates Neuronal Excitability

  2021cites this paper
• Dendritic Integration Dysfunction in Neurodevelopmental Disorders

  2021cites this paper
• Sodium channelopathies in neurodevelopmental disorders

  2021cites this paper
• Comparison of the toxicokinetics of the convulsants picrotoxinin and tetramethylenedisulfotetramine (TETS) in mice

  2020cites this paper
• Perspective: Is Cortical Hyperexcitability the Only Path to Generalized Absence Epilepsy?

  2020cites this paper
• Removal of KCNQ2 from Parvalbumin-expressing Interneurons Improves Anti-Seizure Efficacy of Retigabine

  2020cites this paper
• Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Nav1.6 sodium channels

  2020cites this paper
• Preferential Pharmacological Inhibition of Nav1.6, but not Nav1.1, Abolishes Epileptiform Activity Induced by 4-AP in Mouse Cortical Slices

  2020cites this paper
• Distinct functional alterations in SCN8A epilepsy mutant channels

  2019cites this paper
• Prominent role of forebrain excitatory neurons in SCN8A encephalopathy

  2019cites this paper
• On the feasibility of quantifying sodium channel Nav 1.6 protein in mouse brain using targeted ultra-high-performance/electrospray ionization multiple reaction monitoring mass spectrometry.

  2019cites this paper
• Modified age-dependent expression of NaV1.6 in an ALS model correlates with motor cortex excitability alterations.

  2019cites this paper
• SiRNA-mediated ankyrin-G silence modulates the expression of voltage-gated Na channels in murine hippocampal HT22 cells

  2019cites this paper
• PRRT2 frameshift mutation reduces its mRNA stability resulting loss of function in paroxysmal kinesigenic dyskinesia.

  2019cites this paper
• Identification of CNS-Penetrant Aryl Sulfonamides as Isoform-Selective NaV1.6 Inhibitors with Efficacy in Mouse Models of Epilepsy.

  2019cites this paper
• The NaV1.7 Channel Subtype as an Antinociceptive Target for Spider Toxins in Adult Dorsal Root Ganglia Neurons

  2018cites this paper
• Differential roles of NaV1.2 and NaV1.6 in regulating neuronal excitability at febrile temperature and distinct contributions to febrile seizures

  2018cites this paper
• Selective targeting of Scn8a prevents seizure development in a mouse model of mesial temporal lobe epilepsy

  2018cites this paper
• Regulation of Thalamic and Cortical Network Synchrony by Scn8a.

  2017influential citation
• Unexpected Efficacy of a Novel Sodium Channel Modulator in Dravet Syndrome

  2017cites this paper
• Altered gene expression profile in a mouse model of SCN8A encephalopathy

  2017cites this paper
• Neuronal hyperexcitability in a mouse model of SCN8A epileptic encephalopathy

  2017cites this paper
• SCN3A deficiency associated with increased seizure susceptibility.

  2017cites this paper
• De novo and inherited SCN8A epilepsy mutations detected by gene panel analysis.

  2017cites this paper
• Models for discovery of targeted therapy in genetic epileptic encephalopathies

  2017cites this paper
• Pro-excitatory alterations in sodium channel activity facilitate subiculum neuron hyperexcitability in temporal lobe epilepsy.

  2017cites this paper
• Understanding Network Connections Connects Genotype to Epilepsy Phenotype

  2017cites this paper
• An Scn1a epilepsy mutation in Scn8a alters seizure susceptibility and behavior.

  2016influential citation
• SCN8A encephalopathy: Research progress and prospects

  2016cites this paper
• β1-C121W Is Down But Not Out: Epilepsy-Associated Scn1b-C121W Results in a Deleterious Gain-of-Function

  2016cites this paper
• Remarkable alterations of Nav1.6 in reactive astrogliosis during epileptogenesis

  2016cites this paper
• Mutant huntingtin downregulates myelin regulatory factor-mediated myelin gene expression and affects mature oligodendrocytes.

  2015cites this paper