ArticleCell reports2022
Synaptic hyperexcitability of cytomegalic pyramidal neurons contributes to epileptogenesis in tuberous sclerosis complex.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Anti-seizure potential of J4, an equilibrative nucleoside transporter 1 inhibitor, in a mouse model of tuberous sclerosis complex in response to pentylenetetrazol.Cell & bioscience · 2026Article
- Alterations in dopaminergic innervation and receptors in focal cortical dysplasia.Brain : a journal of neurology · 2025Article
- Effects of ATF2/TSC1 on epilepsy by modulating the microphages polarization of microglia.Scientific reports · 2025Article
- Article
- Synaptic and cognitive impairment associated with L444P heterozygous glucocerebrosidase mutation.Brain : a journal of neurology · 2025Article
- Altered cortical excitability in tuberous sclerosis and the effect of mTOR inhibitors: An intracranial electrical stimulation study.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2025Article
- Influenza A virus during pregnancy disrupts maternal intestinal immunity and fetal cortical development in a dose- and time-dependent manner.Molecular psychiatry · 2025Article
- Multiparameter quantitative analyses of diagnostic cells in brain tissues from tuberous sclerosis complex.Cytometry. Part B, Clinical cytometry · 2025Article
- Cytoplasmic vacuolization and ectopic formation of perineuronal nets are characteristic pathologies of cytomegalic neurons in tuberous sclerosis.Journal of neuropathology and experimental neurology · 2024Article
- Cannabinoids and Genetic Epilepsy Models: A Review with Focus on CDKL5 Deficiency Disorder.International journal of molecular sciences · 2024Review
- Seizures exacerbate excitatory: inhibitory imbalance in Alzheimer's disease and 5XFAD mice.Brain : a journal of neurology · 2024Article
- The Neurovascular Unit Dysfunction in the Molecular Mechanisms of Epileptogenesis and Targeted Therapy.Neuroscience bulletin · 2024Review
- The mTOR pathway geneseLife · 2024Article
- The mTOR pathway genesbioRxiv : the preprint server for biology · 2024Article
- Between neurons and networks: investigating mesoscale brain connectivity in neurological and psychiatric disorders.Frontiers in neuroscience · 2024Review
- Glycosphingolipids are linked to elevated neurotransmission and neurodegeneration in a Drosophila model of Niemann Pick type C.Disease models & mechanisms · 2023Article
- Epileptogenesis in tuberous sclerosis complex-related developmental and epileptic encephalopathy.Brain : a journal of neurology · 2023Review
- Review
- More is Different in mTORopathies.Epilepsy currentsArticle
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Tuberous sclerosis complex (TSC) is a developmental disorder associated with epilepsy, autism, and cognitive impairment. Despite inactivating mutations in the TSC1 or TSC2 genes and hyperactive mechanistic target of rapamycin (mTOR) signaling, the mechanisms underlying TSC-associated neurological symptoms remain incompletely understood. Here we generate a Tsc1 conditional knockout (CKO) mouse model in which Tsc1 inactivation in late embryonic radial glia causes social and cognitive impairment and spontaneous seizures. Tsc1 depletion occurs in a subset of layer 2/3 cortical pyramidal neurons, leading to development of cytomegalic pyramidal neurons (CPNs) that mimic dysplastic neurons in human TSC, featuring abnormal dendritic and axonal overgrowth, enhanced glutamatergic synaptic transmission, and increased susceptibility to seizure-like activities. We provide evidence that enhanced synaptic excitation in CPNs contributes to cortical hyperexcitability and epileptogenesis. In contrast, astrocytic regulation of synapse formation and synaptic transmission remains unchanged after late embryonic radial glial Tsc1 inactivation, and astrogliosis evolves secondary to seizures.
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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.