Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Selective targeting of Scn8a prevents seizure development in a mouse model of mesial temporal lobe epilepsy.

Scientific reports - 9 Jan 2018

Wong Jennifer C, Makinson Christopher D, Lamar Tyra, Cheng Qi, Wingard Jeffrey C, Terwilliger Ernest F, Escayg Andrew

Abstract excerpt

We previously found that genetic mutants with reduced expression or activity of Scn8a are resistant to induced seizures and that co-segregation of a mutant Scn8a allele can increase survival and seizure resistance of Scn1a mutant mice. In contrast, Scn8a expression is increased in the hippocampus following status epilepticus and amygdala kindling. These findings point to Scn8a as a promising therapeutic target...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Electroencephalography
Share to Epilepsy, Temporal Lobe

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Knockdown Techniques

Share to Hippocampus

Share to Immunohistochemistry

Share to NAV1.6 Voltage-Gated Sodium Channel

Share to RNA, Small Interfering

Share to Seizures

Source

Open in PubMed Open full text

Identifiers

PMID: 29317669
DOI: 10.1038/s41598-017-17786-0
PMCID: PMC5760706

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Selective targeting of Scn8a prevents seizure development in a mouse model of mesial temporal lobe epilepsy.PMID 29317669Read ↗

Role of the hippocampus in Nav1.6 (Scn8a) mediated seizure resistance.Semantic proximity Read ↗

The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancy.Semantic proximity Read ↗

An Scn1a epilepsy mutation in Scn8a alters seizure susceptibility and behavior.Semantic proximity Read ↗

Autistic-like behavior, spontaneous seizures, and increased neuronal excitability in a Scn8a mouse model.Semantic proximity Read ↗

Dentate gyrus granule cells are a locus of pathology in Scn8a developmental encephalopathy.Semantic proximity Read ↗

Antisense oligonucleotide therapy for SCN2A gain-of-function epilepsySemantic proximity Read ↗

Spontaneous seizures and elevated seizure susceptibility in response to somatic mutation of sodium channel Scn8a in the mouse.Semantic proximity Read ↗

Gene therapies alleviate absence epilepsy associated with <i>Scn2a</i> deficiency in DBA/2J miceSemantic proximity Read ↗

Antisense oligonucleotide therapy reduces seizures and extends life span in an SCN2A gain-of-function epilepsy model.Semantic proximity Read ↗

A gain-of-function mutation in the sodium channel gene Scn2a results in seizures and behavioral abnormalities.Semantic proximity Read ↗

Deletion of the Na-K-2Cl cotransporter NKCC1 results in a more severe epileptic phenotype in the intrahippocampal kainate mouse model of temporal lobe epilepsy.Semantic proximity Read ↗

Distinct neuronal mechanisms for motor impairment and seizures in a novel mouse model of SCN8A epileptic encephalopathy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.