ArticleEpilepsia open2025
Deficiency of nNOS in adult-born dentate granule cells causes epilepsy.
Article in Epilepsia open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Deficiency of nNOS in adult-born dentate granule cells causes epilepsy.Epilepsia open · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
objectiveThis study aimed to elucidate the molecular role of neuronal nitric oxide synthase (nNOS, encoded by Nos1) in adult-born dentate granule cells (DGCs) during temporal lobe epilepsy (TLE).
methodsWe used GFP-expressing retrovirus (RV) to analyze morphological changes in DGCs. Nos1 knockout (Nos1
resultsWe found seizures induced ectopic location, hilar basal dendrites, and dendritic hypertrophy in DGCs. While nNOS deficiency did not induce abnormal MFS or affect neurogenesis, it caused a significant increase in somatic size, branch points, dendritic length, and spine density in adult-born DGCs. A notable increase in mushroom spine density was observed in the middle and outer 1/3 of the molecular layer. Selective deletion of Nos1 in adult-born DGCs induced epileptic spikes and spontaneous recurrent seizures. Single-nucleus RNA-seq analysis confirmed that newborn neurons in the TLE hippocampus showed reduced nNOS expression and distinct gene expression profiles, likely contributing to abnormal synaptic and dendritic development, as well as increased hippocampal excitability. Single-nucleus RNA-seq analysis further confirmed that newborn neurons in the TLE hippocampus exhibited reduced nNOS expression and distinct gene expression profiles, likely contributing to abnormal synaptic and dendritic development, as well as increased hippocampal excitability. SIGNIFICANCE: Our findings suggest that selective Nos1 knockout in adult-born DGCs contributes to epileptogenesis, and regulating nNOS expression may offer a novel therapeutic approach for treating TLE. PLAIN LANGUAGE SUMMARY: Epilepsy is a brain disorder where nerve cells become overly active. We found that deleting a gene called Nos1 in adult-born DGCs of mice led to seizures. These cells also showed abnormal shapes and gene activity. Our results suggest that Nos1 helps maintain normal brain circuits and could be a new target to treat 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.