<p>A series of experimental findings provide compelling evidence that GABAergic interneurons (TIN) in the thalamus play a potential role in the generation of absence seizures. Recently, we establish a thalamocortical model to investigate the epilepsy mechanism with a primary focus on such interneurons. The proposed model produces epileptic discharges driven by inhibition projections from TIN population, which matches the basic experimental observations. Also, pyramidal (PY) population has excitatory projection to TIN and constructs the feed-forward inhibition circuit PY-TIN-TC which can also result in transition behaviors from background to seizure state. Notably, we explain the seizure production and transition to unveiling intrinsic mechanisms through bifurcation analysis. As an important intervention in epilepsy treatment, the electromagnetic effect on epileptic activity is further explored. It shows the significant role of electromagnetic induction <i>k</i><sub>0</sub> in controlling generalized seizures, which is strengthened by the feedback gain from populations to magnetic flux <i>k</i><sub>1</sub> and weakened by the self-feedback gain of magnetic flux <i>k</i><sub>2</sub>. For the weak electromagnetic induction (<i>k</i><sub>0</sub> &lt; 0.1), the seizure rate is still up to 50%, and we apply external electromagnetic radiation to further regulate. It is observed that the external electromagnetic radiation has a remarkable modulation of absence seizures with optimal stimulus parameters. Overall, this work not only reveals the mechanism of thalamus interneurons in seizures, but, more importantly, provides a theoretical basis for electromagnetic therapy in epilepsy regulation.</p>

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Insights into the role of thalamus interneurons in regulating seizure-like discharges under electromagnetic internal induction and external radiation

  • Luyao Yan,
  • Honghui Zhang,
  • Zhongkui Sun

摘要

A series of experimental findings provide compelling evidence that GABAergic interneurons (TIN) in the thalamus play a potential role in the generation of absence seizures. Recently, we establish a thalamocortical model to investigate the epilepsy mechanism with a primary focus on such interneurons. The proposed model produces epileptic discharges driven by inhibition projections from TIN population, which matches the basic experimental observations. Also, pyramidal (PY) population has excitatory projection to TIN and constructs the feed-forward inhibition circuit PY-TIN-TC which can also result in transition behaviors from background to seizure state. Notably, we explain the seizure production and transition to unveiling intrinsic mechanisms through bifurcation analysis. As an important intervention in epilepsy treatment, the electromagnetic effect on epileptic activity is further explored. It shows the significant role of electromagnetic induction k0 in controlling generalized seizures, which is strengthened by the feedback gain from populations to magnetic flux k1 and weakened by the self-feedback gain of magnetic flux k2. For the weak electromagnetic induction (k0 < 0.1), the seizure rate is still up to 50%, and we apply external electromagnetic radiation to further regulate. It is observed that the external electromagnetic radiation has a remarkable modulation of absence seizures with optimal stimulus parameters. Overall, this work not only reveals the mechanism of thalamus interneurons in seizures, but, more importantly, provides a theoretical basis for electromagnetic therapy in epilepsy regulation.