ArticleCNS neuroscience & therapeutics2024
Spike-and-wave discharges of absence seizures in a sleep waves-constrained corticothalamic model.
Article in CNS neuroscience & therapeutics, 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, 4 citations in OpenAlex.
- Awake alpha bursting emerges as the dynamic working state in a lateral geniculate thalamocortical cell model.PLoS computational biology · 2026Article
- Molecular Mechanisms of Seizure Gating in Sleep-Related Epilepsy: Genes, Channels, Sleep Stages and Circadian Rhythm.Current issues in molecular biology · 2026Review
- Spontaneous spike-and-wave discharges during sleep in mice: circadian distribution and impact on sleep quality.Frontiers in neurology · 2025Article
- A Comprehensive Overview of the Current Status and Advancements in Various Treatment Strategies against Epilepsy.ACS pharmacology & translational science · 2024Review
- Spike-and-wave discharges of absence seizures in a sleep waves-constrained corticothalamic model.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
aimsRecurrent network activity in corticothalamic circuits generates physiological and pathological EEG waves. Many computer models have simulated spike-and-wave discharges (SWDs), the EEG hallmark of absence seizures (ASs). However, these models either provided detailed simulated activity only in a selected territory (i.e., cortical or thalamic) or did not test whether their corticothalamic networks could reproduce the physiological activities that are generated by these circuits.
methodsUsing a biophysical large-scale corticothalamic model that reproduces the full extent of EEG sleep waves, including sleep spindles, delta, and slow (<1 Hz) waves, here we investigated how single abnormalities in voltage- or transmitter-gated channels in the neocortex or thalamus led to SWDs.
resultsWe found that a selective increase in the tonic γ-aminobutyric acid type A receptor (GABA-A) inhibition of first-order thalamocortical (TC) neurons or a selective decrease in cortical phasic GABA-A inhibition is sufficient to generate ~4 Hz SWDs (as in humans) that invariably start in neocortical territories. Decreasing the leak conductance of higher-order TC neurons leads to ~7 Hz SWDs (as in rodent models) while maintaining sleep spindles at 7-14 Hz.
conclusionBy challenging key features of current mechanistic views, this simulated ictal corticothalamic activity provides novel understanding of ASs and makes key testable predictions.
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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.