ArticleCerebral cortex (New York, N.Y. : 1991)2021
Impaired State-Dependent Potentiation of GABAergic Synaptic Currents Triggers Seizures in a Genetic Generalized Epilepsy Model.
Article in Cerebral cortex (New York, N.Y. : 1991), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 9 citations in OpenAlex.
- Preoptic area influences sleep-related seizures in a genetic epilepsy mouse model.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Sleep slow-wave oscillations trigger seizures in a genetic epilepsy model of Dravet syndrome.Brain communications · 2023Article
- A comprehensive atlas of fetal splicing patterns in the brain of adult myotonic dystrophy type 1 patients.NAR genomics and bioinformatics · 2022Article
- Artificial sleep-like up/down-states induce synaptic plasticity in cortical neurons from mouse brain slices.Frontiers in cellular neuroscience · 2022Article
- You Snooze You Seize: GABAergic Potentiation of Genetic Generalized Seizures During NREM.Epilepsy currentsArticle
- Slow Down and Seize: Seizures Triggered by Slow Wave Oscillations in a GABAergic Model of Dravet Syndrome.Epilepsy currentsArticle
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7 authors at 1 institution in 1 country.
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Abstract
Epileptic activity in genetic generalized epilepsy (GGE) patients preferentially appears during sleep and its mechanism remains unknown. Here, we found that sleep-like slow-wave oscillations (0.5 Hz SWOs) potentiated excitatory and inhibitory synaptic currents in layer V cortical pyramidal neurons from wild-type (wt) mouse brain slices. In contrast, SWOs potentiated excitatory, but not inhibitory, currents in cortical neurons from a heterozygous (het) knock-in (KI) Gabrg2+Q/390X model of Dravet epilepsy syndrome. This created an imbalance between evoked excitatory and inhibitory currents to effectively prompt neuronal action potential firings. Similarly, physiologically similar up-/down-state induction (present during slow-wave sleep) in cortical neurons also potentiated excitatory synaptic currents within brain slices from wt and het KI mice. Moreover, this state-dependent potentiation of excitatory synaptic currents entailed some signaling pathways of homeostatic synaptic plasticity. Consequently, in het KI mice, in vivo SWO induction (using optogenetic methods) triggered generalized epileptic spike-wave discharges (SWDs), being accompanied by sudden immobility, facial myoclonus, and vibrissa twitching. In contrast, in wt littermates, SWO induction did not cause epileptic SWDs and motor behaviors. To our knowledge, this is the first mechanism to explain why epileptic SWDs preferentially happen during non rapid eye-movement sleep and quiet-wakefulness in human GGE patients.
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