ArticleFrontiers in computational neuroscience2017
Control of Absence Seizures by the Thalamic Feed-Forward Inhibition.
Article in Frontiers in computational neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Analysis of Epilepsy Treatment Strategies Based on an Astrocyte-Neuron-Coupled Network Model.Brain sciences · 2025Article
- A novel mouse model of mitochondrial disease exhibits juvenile-onset severe neurological impairment due to parvalbumin cell mitochondrial dysfunction.Communications biology · 2023Article
- Suppression of seizure in childhood absence epilepsy using robust control of deep brain stimulation: a simulation study.Scientific reports · 2023Article
- The cerebellum and epilepsy.Epilepsy & behavior : E&B · 2021Review
- Outgrowing seizures in Childhood Absence Epilepsy: time delays and bistability.Journal of computational neuroscience · 2019Article
- Analytically determining frequency and amplitude of spontaneous alpha oscillation in Jansen's neural mass model using the describing function method.Chinese physics B = Zhongguo wu li B · 2018Article
- Combined Effects of Feedforward Inhibition and Excitation in Thalamocortical Circuit on the Transitions of Epileptic Seizures.Frontiers in computational neuroscience · 2017Article
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Authors and funding
4 authors.
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Abstract
As a subtype of idiopathic generalized epilepsies, absence epilepsy is believed to be caused by pathological interactions within the corticothalamic (CT) system. Using a biophysical mean-field model of the CT system, we demonstrate here that the feed-forward inhibition (FFI) in thalamus, i.e., the pathway from the cerebral cortex (Ctx) to the thalamic reticular nucleus (TRN) and then to the specific relay nuclei (SRN) of thalamus that are also directly driven by the Ctx, may participate in controlling absence seizures. In particular, we show that increasing the excitatory Ctx-TRN coupling strength can significantly suppress typical electrical activities during absence seizures. Further, investigation demonstrates that the GABA
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