ArticleExperimental neurobiology2019
Distinct Topographical Patterns of Spike-Wave Discharge in Transgenic and Pharmacologically Induced Absence Seizure Models.
Article in Experimental neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 24 citations in OpenAlex.
- Beyond seizure control: Identifying deficits in cognitive networks in absence epilepsy.Science advances · 2026Article
- Absence seizures: Update on signaling mechanisms and networks.Epilepsia open · 2025Article
- Parvalbumin neurons in the anterior nucleus of thalamus control absence seizures.Epilepsia open · 2023Article
- Modulation of pacemaker channel function in a model of thalamocortical hyperexcitability by demyelination and cytokines.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Nine-day continuous recording of EEG and 2-hour of high-density EEG under chronic sleep restriction in mice.Scientific data · 2022Article
- Deletion of Phospholipase C β1 in the Thalamic Reticular Nucleus Induces Absence Seizures.Experimental neurobiology · 2022Article
- Neuronal excitatory-to-inhibitory balance is altered in cerebral organoid models of genetic neurological diseases.Molecular brain · 2021Article
- From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research.Frontiers in neurology · 2021Review
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
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Authors and funding
4 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Absence seizures (AS) are generalized non-convulsive seizures characterized by a brief loss of consciousness and spike-and-wave discharges (SWD) in an electroencephalogram (EEG). A number of animal models have been developed to explain the mechanisms of AS, and thalamo-cortical networks are considered to be involved. However, the cortical foci have not been well described in mouse models of AS. This study aims to use a high density EEG in pathophysiologically different AS models to compare the spatiotemporal patterns of SWDs. We used two AS models: a pharmacologically induced model (gamma-hydroxybutyric acid, GHB model) and a transgenic model (phospholipase beta4 knock-out, PLCβ4 model). The occurrences of SWDs were confirmed by thalamic recordings. The topographical analysis of SWDs showed that the onset and propagation patterns were markedly distinguishable between the two models. In the PLCβ4 model, the foci were located within the somatosensory cortex followed by propagation to the frontal cortex, whereas in the GHB model, a majority of SWDs was initiated in the prefrontal cortex followed by propagation to the posterior cortex. In addition, in the GHB model, foci were also observed in other cortical areas. This observation indicates that different cortical networks are involved in the generation of SWDs across the two models.
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