ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Dysfunction of synaptic inhibition in epilepsy associated with focal cortical dysplasia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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81 citing papers in PubMed, 184 citations in OpenAlex.
- Increased Cannabinoid Receptor 1-Immunopositive Perisomatic Input of Principal Cells in Human Epileptic Patients in Focal Cortical Dysplasia Type IIB.International journal of molecular sciences · 2026Article
- Interictal and seizure-onset scalp electroencephalographic patterns in malformations of cortical development.Epilepsia · 2026Article
- Synaptic ultrastructural alterations in human focal cortical dysplasia: Insights from volume electron microscopy.Epilepsia · 2026Article
- Microstructural spine alterations increase neuronal excitability in focal cortical dysplasia Type I.Frontiers in computational neuroscience · 2026Article
- Late-onset epileptic spasms: presentation, aetiology and outcome.Brain communications · 2026Article
- MeCP2 regulates telencephalic development in human cerebral organoids.Cell reports · 2025Article
- Seizure occurrence in FCD type II is predicted by lesion position and linked to cytoarchitectural alterations.Acta neuropathologica communications · 2025Article
- No association between histopathology and neurophysiology in surgical specimens from pediatric focal epilepsy patients.Epilepsia · 2025Article
- Localization of the Epileptogenic Zone Using Neural Spatial Volatility in Epilepsy Surgery.Neurology · 2025Observational
- Characterizing the Diversity of Layer 2/3 Human Neocortical Neurons in Pediatric Epilepsy.eNeuro · 2025Article
- Chloride deregulation and GABA depolarization in MTOR-related malformations of cortical development.Brain : a journal of neurology · 2025Article
- Normative high-frequency oscillation phase-amplitude coupling and effective connectivity under sevoflurane.Brain communications · 2025Article
- Critical contributions of neuronal subtypes to pediatric drug-resistant focal dysplasia.Frontiers in cell and developmental biology · 2025Article
- Architecture and cellular composition of focal cortical dysplasia type II: qualitative review of histological studies.Frontiers in cellular neuroscience · 2025Review
- Localization of the epileptogenic network from scalp EEG using a patient-specific whole-brain model.Network neuroscience (Cambridge, Mass.) · 2025Article
- WONOEP appraisal: The role of glial cells in focal malformations associated with early onset epilepsies.Epilepsia · 2024Review
- Net synaptic drive of fast-spiking interneurons is inverted towards inhibition in human FCD I epilepsy.Nature communications · 2024Article
- Targeting pathological cells with senolytic drugs reduces seizures in neurodevelopmental mTOR-related epilepsy.Nature neuroscience · 2024Article
- Article
- The mTOR pathway geneseLife · 2024Article
21 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
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Abstract
Focal cortical dysplasia (FCD) is a common and important cause of medically intractable epilepsy. In patients with temporal lobe epilepsy and in several animal models, compromised neuronal inhibition, mediated by GABA, contributes to seizure genesis. Although reduction in GABAergic interneuron density has been reported in FCD tissue samples, there is little available information on the resulting physiological changes in synaptic inhibition and the potential contribution of these changes to epileptogenesis in the dysplastic human brain. Using visualized whole-cell patch-clamp recordings from identified neurons in tissue slices obtained from patients with FCD, we demonstrate that GABAA-receptor-mediated inhibition is substantially altered in regions of dysplasia. These alterations include a significant reduction in IPSC frequency and a potentially compensatory decrease in transporter-mediated GABA reuptake function; the latter is marked by a significant increase in the decay-time constant for evoked and spontaneous IPSCs and a lack of effect of the GABA transport-inhibitor 1-[2([(diphenylmethylene)imino]oxy)ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride on IPSC kinetics. Immunohistochemical staining revealed a scattering of GABAergic interneurons across dysplastic cortex and striking reductions in GABA transporter expression. Together, these results suggest that profound alterations in GABA-mediated synaptic inhibition play an essential role in the process of epileptogenesis in patients with FCD.
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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.