ArticleProgress in neurobiology2021
mTOR-driven neural circuit changes initiate an epileptogenic cascade.
Article in Progress in neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 29 citations in OpenAlex.
- A patient-derived mouse model reproduces molecular, neurological, and sleep symptoms of SHINE syndrome.Human molecular genetics · 2026Article
- Targeted interneuron ablation in an mTORopathy model: Testing a two-hit mechanism of epileptogenesis.Progress in neurobiology · 2026Article
- Scaling of Neuronal Growth and Excitability Through Separable mTORC1 and mTORC2 Pathways.bioRxiv : the preprint server for biology · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.Molecular and cellular neurosciences · 2026Article
- Chronic sleep deprivation promotes drug-resistant epilepsy via the BMAL1-mTOR-P-gp axis.Epilepsia open · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.bioRxiv : the preprint server for biology · 2026Article
- Altered PI3K/mTOR Signaling within the Forebrain Leads to Respiratory Deficits in a Mouse Model of Epilepsy.eNeuro · 2025Article
- Sex-specific proteomic analysis of epileptic brain tissues from Pten knockout mice and human refractory epilepsy.Experimental neurology · 2025Article
- DEPDC5 regulates the strength of excitatory synaptic transmission by interacting with ubiquitin-specific protease 46.Neurobiology of disease · 2025Article
- Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025Article
- PTEN deletion in the adult dentate gyrus induces epilepsy.Neurobiology of disease · 2024Article
- Variants of TSC1 are associated with developmental and epileptic encephalopathy and focal epilepsy without tuberous sclerosis : For the China Epilepsy Gene 1.0 Project.Acta epileptologica · 2024Article
- Developmental trajectory and sex differences in auditory processing in a PTEN-deletion model of autism spectrum disorders.Neurobiology of disease · 2024Article
- PTEN DELETION IN THE ADULT DENTATE GYRUS INDUCES EPILEPSY.bioRxiv : the preprint server for biology · 2024Article
- Molecular Genetics of Acquired Temporal Lobe Epilepsy.Biomolecules · 2024Review
- mTOR and neuroinflammation in epilepsy: implications for disease progression and treatment.Nature reviews. Neuroscience · 2024Review
- Transient Seizure Clusters and Epileptiform Activity Following Widespread Bilateral Hippocampal Interneuron Ablation.eNeuro · 2024Article
- Unraveling the Neural Circuits: Techniques, Opportunities and Challenges in Epilepsy Research.Cellular and molecular neurobiology · 2024Review
- Somatostatin interneuron fate-mapping and structure in a Pten knockout model of epilepsy.Frontiers in cellular neuroscience · 2024Article
- Advances in the mTOR signaling pathway and its inhibitor rapamycin in epilepsy.Brain and behavior · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Mutations in genes regulating mTOR pathway signaling are now recognized as a significant cause of epilepsy. Interestingly, these mTORopathies are often caused by somatic mutations, affecting variable numbers of neurons. To better understand how this variability affects disease phenotype, we developed a mouse model in which the mTOR pathway inhibitor Pten can be deleted from 0 to 40 % of hippocampal granule cells. In vivo, low numbers of knockout cells caused focal seizures, while higher numbers led to generalized seizures. Generalized seizures coincided with the loss of local circuit interneurons. In hippocampal slices, low knockout cell loads produced abrupt reductions in population spike threshold, while spontaneous excitatory postsynaptic currents and circuit level recurrent activity increased gradually with rising knockout cell load. Findings demonstrate that knockout cells load is a critical variable regulating disease phenotype, progressing from subclinical circuit abnormalities to electrobehavioral seizures with secondary involvement of downstream neuronal populations.
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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.