ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Reactive astrogliosis causes the development of spontaneous seizures.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers.
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169 citing papers in PubMed, 282 citations in OpenAlex.
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- Temporal profiling of hippocampal astrocyte reactivity reveals persistent GFAP cleavage and complement C3 association after status epilepticus.Brain structure & function · 2026Article
- Astrocytes in Genetic Epilepsies: Supporting Actor or Key Player?Journal of neuroscience research · 2026Review
- GATOR1 signaling defects promote astrocytic metabolic rewiring and excitatory neurotransmitter cycling.EMBO reports · 2026Article
- Light- and temperature-sensitive seizures are regulated by spatially distinct cortex glial populations in the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Tumor-suppressive role of CNTNAP2 in glioma: Dual regulation of the NDN-ERK axis and M2 macrophage polarization.Cancer gene therapy · 2026Article
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- Calponin-3 is associated with epilepsy through the regulation of astrocyte activity.Brain pathology (Zurich, Switzerland) · 2026Article
- Plasma KCC2, NKCC1, and GABA as peripheral biomarkers in autism spectrum disorder: a combined ROC analysis.Metabolic brain disease · 2026Article
- Subicular Astrocytes Govern Seizure-Impaired Fear Memory.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The spatial architecture of neuroimmune interactions in epilepsy.Frontiers in immunology · 2026Review
- Analysis of cortical dysplasias using b-tensor encoding diffusion MRI in an animal model.PloS one · 2026Article
- Identification of epileptic hippocampal sclerosis related genes through bulk and single-nucleus RNA sequencing datasets.Cellular and molecular life sciences : CMLS · 2025Article
- Plasma proteomics identifies proteins and pathways associated with incident epilepsy.Cell reports. Medicine · 2025Article
- Aberrant neural activity in the peritumoral cortex underlies the progression of tumor-associated seizures.Nature communications · 2025Article
- Abnormal glycosylation changes in brain tissue of kainic acid-induced epileptic rats.Scientific reports · 2025Article
- Tcf4 Deficiency causes recurrent seizures in mice.Progress in neurobiology · 2025Article
- Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
109 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Epilepsy is one of the most common chronic neurologic diseases, yet approximately one-third of affected patients do not respond to anticonvulsive drugs that target neurons or neuronal circuits. Reactive astrocytes are commonly found in putative epileptic foci and have been hypothesized to be disease contributors because they lose essential homeostatic capabilities. However, since brain pathology induces astrocytes to become reactive, it is difficult to distinguish whether astrogliosis is a cause or a consequence of epileptogenesis. We now present a mouse model of genetically induced, widespread chronic astrogliosis after conditional deletion of β1-integrin (Itgβ1). In these mice, astrogliosis occurs in the absence of other pathologies and without BBB breach or significant inflammation. Electroencephalography with simultaneous video recording revealed that these mice develop spontaneous seizures during the first six postnatal weeks of life and brain slices show neuronal hyperexcitability. This was not observed in mice with neuronal-targeted β1-integrin deletion, supporting the hypothesis that astrogliosis is sufficient to induce epileptic seizures. Whole-cell patch-clamp recordings from astrocytes further suggest that the heightened excitability was associated with impaired astrocytic glutamate uptake. Moreover, the relative expression of the cation-chloride cotransporters (CCC) NKCC1 (Slc12a2) and KCC2 (Slc12a5), which are responsible for establishing the neuronal Cl(-) gradient that governs GABAergic inhibition were altered and the NKCC1 inhibitor bumetanide eliminated seizures in a subgroup of mice. These data suggest that a shift in the relative expression of neuronal NKCC1 and KCC2, similar to that observed in immature neurons during development, may contribute to astrogliosis-associated seizures.
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