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

Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability.

Translational psychiatry - 2 Oct 2024

Fenton Timothy A, Haouchine Olivia Y, Hallam Elizabeth B, Smith Emily M, Jackson Kiya C, Rahbarian Darlene, Canales Cesar P, Adhikari Anna, Nord Alex S, Ben-Shalom Roy, Silverman Jill L

Abstract excerpt

Disruption of SYNGAP1 directly causes a genetically identifiable neurodevelopmental disorder (NDD) called SYNGAP1-related intellectual disability (SRID). Without functional SynGAP1 protein, individuals are developmentally delayed and have prominent features of intellectual disability (ID), motor impairments, and epilepsy. Over the past two decades, there have been numerous discoveries indicating the critical role...

Read the complete abstract on PubMed

Topics

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

Share to Behavior, Animal
Share to Disease Models, Animal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Electroencephalography

Share to Intellectual Disability

Share to Neurons

Share to Phenotype

Share to ras GTPase-Activating Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 39358332
DOI: 10.1038/s41398-024-03077-6
PMCID: PMC11447000

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

Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability.PMID 39358332Read ↗

Hyperexcitability and translational phenotypes in a preclinical model of <i>SYNGAP1</i> mutationsSemantic proximity Read ↗

Hyperexcitability and translational phenotypes in a preclinical model of SYNGAP1 mutationsSemantic proximity Read ↗

Low-dose Perampanel rescues cortical gamma dysregulation associated with parvalbumin interneuron GluA2 upregulation in epileptic <i>Syngap1</i> <sup>+/-</sup> miceSemantic proximity Read ↗

Abnormal brain state distribution and network connectivity in a <i>SYNGAP1</i> rat modelSemantic proximity Read ↗

Re-expression of SynGAP Protein in Adulthood Improves Translatable Measures of Brain Function and Behavior in a Model of Neurodevelopmental DisordersSemantic proximity Read ↗

Dissociation of SYNGAP1 Enzymatic and Structural Roles: Intrinsic Excitability and Seizure SusceptibilitySemantic proximity Read ↗

Translatable electrophysiological and behavioral abnormalities in a humanized model of <i>SYNGAP1</i> -disorderSemantic proximity Read ↗

GABAergic signaling promotes early-life seizures in epileptic SYNGAP1 <sup>+/-</sup> miceSemantic proximity Read ↗

Human <i>SYNGAP1</i> Regulates the Development of Neuronal Activity by Controlling Dendritic and Synaptic MaturationSemantic proximity Read ↗

Phenotypic characterization of individuals with SYNGAP1 pathogenic variants reveals a potential correlation between posterior dominant rhythm and developmental progressionSemantic proximity Read ↗

SYNGAP1-related disorder: pathophysiology, epilepsy, cognitive and behavioral phenotypes, and precision therapeutic approaches.Semantic proximity Read ↗

Sensory processing dysregulations as reliable translational biomarkers in <i>SYNGAP1</i> haploinsufficiencySemantic proximity Read ↗

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