ArticleNature communications2024
Net synaptic drive of fast-spiking interneurons is inverted towards inhibition in human FCD I epilepsy.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Conserved Kir channel mechanisms governing intrinsic excitability in human and rodent parvalbumin neurons.Communications biology · 2026Article
- High-frequency, high-intensity electrical stimulation selectively activates human fast-spiking interneurons.Frontiers in synaptic neuroscience · 2026Article
- Microstructural spine alterations increase neuronal excitability in focal cortical dysplasia Type I.Frontiers in computational neuroscience · 2026Article
- Regulation of input excitability in human and mouse parvalbumin interneurons by Kir potassium channels.bioRxiv : the preprint server for biology · 2025Article
- Critical contributions of neuronal subtypes to pediatric drug-resistant focal dysplasia.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
9 authors.
Funding
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Abstract
Focal cortical dysplasia type I (FCD I) is the most common cause of pharmaco-resistant epilepsy with the poorest prognosis. To understand the epileptogenic mechanisms of FCD I, we obtained tissue resected from patients with FCD I epilepsy, and from tumor patients as control. Using whole-cell patch clamp in acute human brain slices, we investigated the cellular properties of fast-spiking interneurons (FSINs) and pyramidal neurons (PNs) within the ictal onset zone. In FCD I epilepsy, FSINs exhibited lower firing rates from slower repolarization and action potential broadening, while PNs had increased firing. Importantly, excitatory synaptic drive of FSINs increased progressively with the scale of cortical activation as a general property across species, but this relationship was inverted towards net inhibition in FCD I epilepsy. Further comparison with intracranial electroencephalography (iEEG) from the same patients revealed that the spatial extent of pathological high-frequency oscillations (pHFO) was associated with synaptic events at FSINs.
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