ArticleEpilepsia2011
Inhibition of the mammalian target of rapamycin blocks epilepsy progression in NS-Pten conditional knockout mice.
Article in Epilepsia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 122 citations in OpenAlex.
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.Molecular and cellular neurosciences · 2026Article
- Cell-Intrinsic Regulation of Epilepsy-Associated Pathology by mTORC1 and mTORC2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Repurposing drugs for treating the neurobehavioral manifestations of PTEN hamartoma tumor syndrome.iScience · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.bioRxiv : the preprint server for biology · 2026Article
- Sex-specific proteomic analysis of epileptic brain tissues from Pten knockout mice and human refractory epilepsy.Experimental neurology · 2025Article
- Glial changes in the dentate gyrus of neuronal-specific PTEN knockout mice correlate with changes in cell proliferation.Journal of neuroimmunology · 2025Article
- Somatic mosaicism and interneuron involvement in mTORopathies.Trends in neurosciences · 2025Review
- Seizures in brain tumors: pathogenesis, risk factors and management (Review).International journal of molecular medicine · 2025Review
- Article
- PTEN deletion in the adult dentate gyrus induces epilepsy.Neurobiology of disease · 2024Article
- NS-Pten knockout mice exhibit sex and hippocampal subregion-specific increases in microglia/macrophage density.Epilepsy research · 2024Article
- PTEN DELETION IN THE ADULT DENTATE GYRUS INDUCES EPILEPSY.bioRxiv : the preprint server for biology · 2024Article
- Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss.eLife · 2024Article
- Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss.bioRxiv : the preprint server for biology · 2024Article
- Rapamycin improves social and stereotypic behavior abnormalities induced by pre-mitotic neuronal subset specific Pten deletion.Genes, brain, and behavior · 2023Article
- mTORC2 Inhibition Improves Morphological Effects of PTEN Loss, But Does Not Correct Synaptic Dysfunction or Prevent Seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Seizures and epilepsy in patients with ischaemic stroke.Neurological research and practice · 2021Review
- A vitamin D enriched diet attenuates sex-specific behavioral deficits, increases the lifespan, but does not rescue bone abnormalities in a mouse model of cortical dysplasia.Epilepsy & behavior : E&B · 2021Article
- Rapamycin, but not minocycline, significantly alters ultrasonic vocalization behavior in C57BL/6J pups in a flurothyl seizure model.Behavioural brain research · 2021Article
- PI3K isoform-selective inhibition in neuron-specific PTEN-deficient mice rescues molecular defects and reduces epilepsy-associated phenotypes.Neurobiology of disease · 2020Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
purposeIncreased activity of mTOR Complex 1 (mTORC1) has been demonstrated in cortical dysplasia and tuberous sclerosis complex, as well as in animal models of epilepsy. Recent studies in such models revealed that inhibiting mTORC1 with rapamycin effectively suppressed seizure activity. However, seizures can recur after treatment cessation, and continuous rapamycin exposure can adversely affect animal growth and health. Here, we evaluated the efficacy of an intermittent rapamycin treatment protocol on epilepsy progression using neuron subset-specific-Pten (NS-Pten) conditional knockout mice.
methodsNS-Pten knockouts were treated with a single course of rapamycin during postnatal weeks 4 and 5, or intermittently over a period of 5 months. Epileptiform activity was monitored using video-electroencephalography (EEG) recordings, and mossy fiber sprouting was evaluated using Timm staining. Survival and body weight were assessed in parallel. KEY
findingsNS-Pten knockouts treated with a single course of rapamycin had recurrence of epilepsy 4-7 weeks after treatment ended. In contrast, epileptiform activity remained suppressed, and survival increased if knockout mice received additional rapamycin during weeks 10-11 and 16-17. Aberrant mossy fiber sprouting, present by 4 weeks of age and progressing in parallel with epileptiform activity, was also blocked by rapamycin. SIGNIFICANCE: These findings demonstrate that a single course of rapamycin treatment suppresses epileptiform activity and mossy fiber sprouting for several weeks before epilepsy recurs. However, additional intermittent treatments with rapamycin prevented this recurrence and enhanced survival without compromising growth. Therefore, these studies add to the growing body of evidence implicating an important role for mTORC1 signaling in epilepsy.
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