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

Parvalbumin interneuron impairment causes synaptic transmission deficits and seizures in SCN8A developmental and epileptic encephalopathy

22 Oct 2024

Abstract excerpt

SCN8A developmental and epileptic encephalopathy (DEE) is a severe epilepsy syndrome resulting from mutations in the voltage-gated sodium channel Nav1.6, encoded by the gene SCN8A. Nav1.6 is expressed in excitatory and inhibitory neurons, yet previous studies primarily focus on how SCN8A mutations affect excitatory neurons, with limited studies on the importance of inhibitory interneurons. Parvalbumin (PV)...

Read the complete abstract on PubMed

Topics

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

Share to Epilepsy research and treatment
Share to Ion channel regulation and function
Share to Neuroscience and Neuropharmacology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 39435659
DOI: 10.1172/jci.insight.181005

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Parvalbumin interneuron impairment causes synaptic transmission deficits and seizures in SCN8A developmental and epileptic encephalopathyPMID 39435659Read ↗

Parvalbumin Interneuron Impairment Leads to Synaptic Transmission Deficits and Seizures in <i>SCN8A</i> Epileptic EncephalopathySemantic proximity Read ↗

Developmentally regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of Dravet syndromeSemantic proximity Read ↗

Developmentally-regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of Dravet syndromeSemantic proximity Read ↗

Heterozygous expression of a <i>Kcnt1</i> gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neuronsSemantic proximity Read ↗

A Transient Developmental Window of Fast-Spiking Interneuron Dysfunction in a Mouse Model of Dravet SyndromeSemantic proximity Read ↗

Neuronal hyperexcitability in a mouse model of SCN8A epileptic encephalopathy.Semantic proximity Read ↗

Nav1.1 haploinsufficiency in excitatory neurons ameliorates seizure-associated sudden death in a mouse model of Dravet syndrome.Semantic proximity Read ↗

Attenuated ectopic action potential firing in parvalbumin expressing interneurons in a mouse model of Dravet SyndromeSemantic proximity Read ↗

Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndromeSemantic proximity Read ↗

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

Sodium channels and the neurobiology of epilepsy.Semantic proximity Read ↗

SCN8A encephalopathy: Mechanisms and models.Semantic proximity Read ↗

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