ArticleCurrent biology : CB2021
Circuit Mechanisms Underlying Epileptogenesis in a Mouse Model of Focal Cortical Malformation.
Article in Current biology : CB, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- CX3CL1/CX3CR1 axis dysregulation contributes to epileptogenic mechanisms in focal cortical dysplasia.Acta neuropathologica communications · 2026Article
- Microstructural spine alterations increase neuronal excitability in focal cortical dysplasia Type I.Frontiers in computational neuroscience · 2026Article
- Layer-specific changes in sensory cortex across the lifespan in mice and humans.Nature neuroscience · 2025Article
- Modulation of cortical representations of sensory and contextual information underlies aversive associative learning.Cell reports · 2024Article
- Unraveling the Neural Circuits: Techniques, Opportunities and Challenges in Epilepsy Research.Cellular and molecular neurobiology · 2024Review
- The alteration of cortical microstructure similarity in drug-resistant epilepsy correlated with mTOR pathway genes.EBioMedicine · 2023Article
- Excitatory somatostatin interneurons in the dentate gyrus drive a widespread seizure network in cortical dysplasia.Signal transduction and targeted therapy · 2023Article
- Spatial Distribution of Inhibitory Innervations of Excitatory Pyramidal Cells by Major Interneuron Subtypes in the Auditory Cortex.Bioengineering (Basel, Switzerland) · 2023Article
- Seizing After Freezing: Layer-, Site-, and Cell-Type-Specific Rewiring Mediates Epileptogenesis Following Cortical Freeze Lesion in Mouse.Epilepsy currentsArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The way in which aberrant neural circuits contribute to epilepsy remains unclear. To elucidate this question, we dissected the circuit mechanisms underlying epileptogenesis using a mouse model of focal cortical malformation with spontaneous epileptiform discharges. We found that spontaneous spike-wave discharges and optogenetically induced hyperexcitable bursts in vivo were present in a cortical region distal to (>0.7 mm) freeze-lesion-induced microgyrus, instead of near the microgyrus. ChR2-assisted circuit mapping revealed ectopic inter-laminar excitatory input from infragranular layers to layers 2/3 pyramidal neurons as the key component of hyperexcitable circuitry. This hyperactivity disrupted the balance between excitation and inhibition and was more prominent in the cortical region distal to the microgyrus. Consistently, the inhibition from both parvalbumin-positive interneurons (PV) and somatostatin-positive interneurons (SOM) to pyramidal neurons were altered in a layer- and site-specific fashion. Finally, closed-loop optogenetic stimulation of SOM, but not PV, terminated spontaneous spike-wave discharges. Together, these results demonstrate the occurrence of highly site- and cell-type-specific synaptic reorganization underlying epileptic cortical circuits and provide new insights into potential treatment strategies.
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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.