ArticleEpilepsia2025
Absence seizures and sleep-wake abnormalities in a rat model of GRIN2B neurodevelopmental disorder.
Article in Epilepsia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- A mouse model of GRIN2D developmental and epileptic encephalopathy recapitulates the human disease.Brain : a journal of neurology · 2026Article
- Absence seizures and sleep-wake abnormalities in a rat model of GRIN2B neurodevelopmental disorder.Epilepsia · 2025Article
- Traditional Chinese medicine on epilepsy: focus on N-methyl-D-aspartate receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors.Medical review (2021) · 2025Review
- Assessing oligodendrocyte and myelin alterations following absence seizures in a rat model ofBrain and neuroscience advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
objectivePathogenic mutations in GRIN2B are an important cause of severe neurodevelopmental disorders resulting in epilepsy, autism, and intellectual disability. GRIN2B encodes the GluN2B subunit of N-methyl-d-aspartate receptors (NMDARs), which are ionotropic glutamate receptors critical for normal development of the nervous system and synaptic plasticity. Here, we characterized a novel Grin2b heterozygous knockout rat model with electroencephalography (EEG) and pharmacological interventions to block spontaneous seizures.
methodsThrough western blot analysis we assessed the extent of GluN2B protein knockdown in knockout (Grin2b
resultsCompared to wild-type rats, Grin2b SIGNIFICANCE: Our data show that the new rat Grin2b haploinsufficiency model exhibits clinically relevant phenotypes and highlights two potential therapeutic options for GRIN2B-related epilepsy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.