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

Neurodevelopmental defects in Dravet syndrome Scn1a+/− mice: Targeting GABA-switch rescues behavioral dysfunctions but not seizures and mortality

26 Feb 2025

Abstract excerpt

1.1 expression. We thus reveal that neurodevelopmental components in DS, in particular GABA switch, underlie some cognitive/behavioral defects, but not seizures. Our work provides further evidence that seizures and neuropsychiatric dysfunctions in DEEs can be uncoupled and can have differential pathological mechanisms. They could be treated separately with targeted pharmacological strategies.

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 Genetics and Neurodevelopmental Disorders
Share to Neuroscience and Neuropharmacology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 40021096
DOI: 10.1016/j.nbd.2025.106853

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

Neurodevelopmental defects in Dravet syndrome Scn1a+/− mice: Targeting GABA-switch rescues behavioral dysfunctions but not seizures and mortalityPMID 40021096Read ↗

Neurodevelopmental defects in Dravet syndrome <i>Scn1a</i> <sup>+/-</sup> mice: targeting GABA-switch rescues behavioral dysfunctions but not seizures and mortalitySemantic proximity Read ↗

Sexual dimorphism in epilepsy and comorbidities in Dravet syndrome mice carrying a targeted deletion of exon 1 of the <i>Scn1a</i> geneSemantic proximity Read ↗

Hippocampal circuit-specific enhancement of GABA-inhibition caused by discrete gene regions in a Down syndrome modelSemantic proximity Read ↗

Life-span characterization of epilepsy and comorbidities in Dravet syndrome mice carrying a targeted deletion of exon 1 of the Scn1a geneSemantic proximity Read ↗

Dravet Syndrome: Past, Present, and Future.Semantic proximity Read ↗

Clinical and Genetic Features of Dravet Syndrome: A Prime Example of the Role of Precision Medicine in Genetic EpilepsySemantic proximity Read ↗

Exogenous Na <sub>V</sub> 1.1 activity in excitatory and inhibitory neurons reverts Dravet syndrome comorbidities when delivered post-symptom onset in mice with DravetSemantic proximity Read ↗

Preictal dysfunctions of inhibitory interneurons paradoxically lead to their rebound hyperactivity and to Low-Voltage-Fast onset seizures in Dravet syndromeSemantic proximity Read ↗

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

A novel rat model of Dravet syndrome recapitulates clinical hallmarksSemantic proximity Read ↗

Dravet syndrome and its mimics: Beyond SCN1A.Semantic proximity Read ↗

SCN1A mutations in Dravet syndrome: impact of interneuron dysfunction on neural networks and cognitive outcome.Semantic proximity Read ↗

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