ArticleJCI insight2021
Reactive astrocyte-driven epileptogenesis is induced by microglia initially activated following status epilepticus.
Article in JCI insight, 2021. 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, 125 citations in OpenAlex.
- Deletion of Astrocytic TNFR1 Attenuates Hyperexcitability and Initiation of Epileptogenesis.Glia · 2026Article
- Temporal profiling of hippocampal astrocyte reactivity reveals persistent GFAP cleavage and complement C3 association after status epilepticus.Brain structure & function · 2026Article
- Article
- Inhibition of endocannabinoid degradation in astrocytes reprograms glial reactivity and prevents seizure sequelae.Journal of neuroinflammation · 2026Article
- Targeting MEF2A suppresses microglial hyperactivation and synaptic phagocytosis to attenuate epilepsy pathogenesis.Cell death & disease · 2026Article
- Microfluidic co-culture system for synaptically segregated neural networks to explore astrocyte-driven neural pathology.Microsystems & nanoengineering · 2026Article
- Review
- Reblastatin as a neuroprotective agent in temporal lobe epilepsy and excitotoxic conditions of Alzheimer's disease and Parkinson's disease.Acta pharmaceutica Sinica. B · 2026Article
- Single-Nucleus Transcriptomics Reveals Cell Type-Specific Remodeling and Epilepsy-Associated Microglia.bioRxiv : the preprint server for biology · 2026Article
- Single-Nucleus Transcriptomic Sequencing Revealed Cellular and Molecular Changes in a Pilocarpine-Induced Epilepsy Rat Model.Neuroscience bulletin · 2026Article
- Exploring the Role of TSPO-PET Imaging Among MRI-Negative Patients with Temporal Lobe Epilepsy: From the Perspective of Heterogeneity.Brain sciences · 2026Article
- Targeting necroptosis protects against astrocyte death and hippocampal sclerosis in experimental temporal lobe epilepsy.The Journal of physiology · 2026Article
- C1q neutralization during epileptogenesis attenuates complement-mediated synaptic elimination and epileptiform activity.Epilepsia · 2026Article
- Single-Cell Dissection of the SPP1-CD44 Axis Reveals Microglia-Astrocyte Crosstalk Driving Neuroinflammation in Temporal Lobe Epilepsy.Molecular neurobiology · 2026Article
- Spatiotemporal transcriptomic mapping reveals region-specific glial activation and astrocyte shifts in epileptogenesis beyond the hippocampus.Acta neuropathologica communications · 2026Article
- Astrocytic Igfbp2 Promotes Spontaneous Seizures in a Mouse Model of Mesial Temporal Lobe Epilepsy.Glia · 2026Article
- Microglial pathological synaptic pruning in epilepsy: pathophysiology and therapeutic potential.Frontiers in immunology · 2026Review
- Time-resolved phenotyping of seizure evolution in developmental and epileptic encephalopathy: insights and gaps from the CYFIP2 Arg87Cys mouse model.Frontiers in synaptic neuroscience · 2026Review
- The spatial architecture of neuroimmune interactions in epilepsy.Frontiers in immunology · 2026Review
- Explainable machine learning identifies immune-inflammatory biomarkers and therapeutic candidates in drug-resistant epilepsy.Scientific reports · 2025Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive activation of glial cells during a latent period has been well documented in various animal models of epilepsy. However, it remains unclear whether activated glial cells contribute to epileptogenesis, i.e., the chronically persistent process leading to epilepsy. Particularly, it is not clear whether interglial communication between different types of glial cells contributes to epileptogenesis, because past literature has mainly focused on one type of glial cell. Here, we show that temporally distinct activation profiles of microglia and astrocytes collaboratively contributed to epileptogenesis in a drug-induced status epilepticus model. We found that reactive microglia appeared first, followed by reactive astrocytes and increased susceptibility to seizures. Reactive astrocytes exhibited larger Ca2+ signals mediated by IP3R2, whereas deletion of this type of Ca2+ signaling reduced seizure susceptibility after status epilepticus. Immediate, but not late, pharmacological inhibition of microglial activation prevented subsequent reactive astrocytes, aberrant astrocyte Ca2+ signaling, and the enhanced seizure susceptibility. These findings indicate that the sequential activation of glial cells constituted a cause of epileptogenesis after status epilepticus. Thus, our findings suggest that the therapeutic target to prevent epilepsy after status epilepticus should be shifted from microglia (early phase) to astrocytes (late phase).
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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.