ArticleNature communications2025
Neuronal hyperactivity in neurons derived from individuals with gray matter heterotopia.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- Defective EV-mediated transport of SHH alters neural fate specification in EPM1 epilepsy.Science advances · 2026Article
- Research on the role and mechanism of FAT4 in the development and progression of tumor and non-tumor diseases.Discover oncology · 2026Review
- Brain Organoids: Emerging Platforms for Modern Neuroscience.Brain sciences · 2026Review
- Advances in the pathophysiological study of brain development: application of cerebral organoid combined with Spatial omics technology.Stem cell research & therapy · 2026Review
- A novel homozygousFrontiers in pediatrics · 2026Article
- Integrative multi-omics and machine learning analysis identifies candidate biomarkers associated with mitochondrial quality control in major depressive disorder.Frontiers in psychiatry · 2026Article
- A pediatric patient with Warsaw breakage syndrome presenting with epilepsy: a case report and literature review.Frontiers in neuroscience · 2026Article
- Comparison of ectopic versus normal gray matter via quantitative magnetic resonance imaging: a cross-sectional study.Quantitative imaging in medicine and surgery · 2025Article
- DCHS1 Modulates Forebrain Proportions in Modern Humans via a Glycosylation Change.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Periventricular heterotopia (PH), a common form of gray matter heterotopia associated with developmental delay and drug-resistant seizures, poses a challenge in understanding its neurophysiological basis. Human cerebral organoids (hCOs) derived from patients with causative mutations in FAT4 or DCHS1 mimic PH features. However, neuronal activity in these 3D models has not yet been investigated. Here we show that silicon probe recordings reveal exaggerated spontaneous spike activity in FAT4 and DCHS1 hCOs, suggesting functional changes in neuronal networks. Transcriptome and proteome analyses identify changes in neuronal morphology and synaptic function. Furthermore, patch-clamp recordings reveal a decreased spike threshold specifically in DCHS1 neurons, likely due to increased somatic voltage-gated sodium channels. Additional analyses reveal increased morphological complexity of PH neurons and synaptic alterations contributing to hyperactivity, with rescue observed in DCHS1 neurons by wild-type DCHS1 expression. Overall, we provide new comprehensive insights into the cellular changes underlying symptoms of gray matter heterotopia.
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Registered trials
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