ArticleeNeuro2025
Characterizing the Diversity of Layer 2/3 Human Neocortical Neurons in Pediatric Epilepsy.
Article in eNeuro, 2025. 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.
- Single cell protein profiling of focal cortical dysplasia in a patient requiring multiple resections.Acta neuropathologica communications · 2026Article
- Mapping spatially organized molecular and genetic signatures of schizophrenia across multiple scales in human prefrontal cortex.bioRxiv : the preprint server for biology · 2026Article
- Processing and sectioning of organ donor spinal cord tissue for electrophysiology on acute human spinal cord slices.Brain communications · 2026Article
- 4-Aminopyridine induced hyperpolarizing oscillations in pediatric human epileptic tissue are network-driven potassium currents that are abolished by activation of KCNQ2-5 (Kv7.2-Kv7.5) channels.Neurobiology of disease · 2026Article
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Authors and funding
11 authors.
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Abstract
Childhood epilepsy is a common and devastating condition, for which many children still do not have adequate treatment. Some children with drug-resistant epilepsy require surgical excision of epileptogenic brain tissue for seizure control, affording the opportunity to study this tissue ex vivo to interrogate human epileptic neurons for potentially hyperexcitable perturbations in intrinsic electrophysiological properties. In this study, we characterized the diversity of layer L2/3 (L2/3) pyramidal neurons (PNs) in ex vivo brain slices from pediatric patients with epilepsy. We found a remarkable diversity in the firing properties of epileptic L2/3 PNs: five distinct subpopulations were identified. Additionally, we investigated whether the etiology of epilepsy influenced the intrinsic neuronal properties of L2/3 PNs when comparing tissue from patients with epilepsy due to malformations of cortical development (MCDs), other forms of epilepsy (OEs), or with deep-seated tumors. When comparing epileptic with control L2/3 PNs, we observed a decrease in voltage sag and lower maximum firing rates. Moreover, we found that MCD and OE L2/3 PNs were mostly similar indicating that epilepsy etiology may not outweigh the influences of epileptiform activity on L2/3 PN physiology. Lastly, we show that the proconvulsant drug, 4-aminopyridine (4-AP), leads to increased AP half-width, reduced firing rate accommodation, and slower AHPs. These changes imply that 4-AP induces an increase in [K
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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 Socratic graph.