ArticleEpilepsia2026
Synaptic ultrastructural alterations in human focal cortical dysplasia: Insights from volume electron microscopy.
Article in Epilepsia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Neurocentric No More? Oligodendrocyte Dysfunction Supports Epileptogenesis.Epilepsy currents · 2026Article
- Focal cortical dysplasias: modeling pediatric drug-resistant epilepsy using human brain organoids.Frontiers in cellular neuroscience · 2026Review
- Microstructural spine alterations increase neuronal excitability in focal cortical dysplasia Type I.Frontiers in computational neuroscience · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
objectiveFocal cortical dysplasia (FCD) is a developmental malformation of the cerebral cortex and a leading cause of drug-resistant epilepsy in children and young adults. Disruption of the excitation-inhibition (E-I) balance is a hallmark of neuronal hyperexcitability in FCD, yet the underlying synaptic ultrastructural changes remain poorly understood. This study aimed to investigate synaptic architecture and associated organelle alterations in epileptogenic cortex affected by FCD.
methodsUsing volume electron microscopy, we performed a detailed morphological assessment of synaptic density, size, and organelle distribution within synapses in the temporal cortical layer III of a patient with FCD. Comparative analyses were conducted between dysplastic and nondysplastic cortical regions.
resultsThe dysplastic cortex exhibited a lower density of excitatory synapses but contained unusually large excitatory synapses with an increased number of synaptic vesicles. Inhibitory synapses were positioned farther from the nearest excitatory synapses along distal dendrites, potentially reducing the effectiveness of shunting inhibition in the dysplastic area. Presynaptic boutons in the dysplastic region showed increased mitochondrial density and abnormal mitochondrial morphology, whereas the proportion of postsynaptic protrusions containing a spine apparatus was reduced. These changes suggest potential deficits in intracellular calcium handling, metabolic homeostasis, and synaptic plasticity in the epileptogenic cortex. Additionally, maladaptive myelination was a prominent feature in the dysplastic region. SIGNIFICANCE: This study identifies distinct synaptic and subcellular structural abnormalities in FCD that may contribute to E-I imbalance and neuronal hyperexcitability. These findings provide novel ultrastructural insights into the pathophysiology of FCD and may inform future therapeutic strategies targeting synaptic and metabolic dysfunction.
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