Control of absence epilepsy seizures in specific relay nuclei of thalamus

In this paper, we used a classic basal ganglia-corticothalamic model(BGCT) to study the onset and control mechanism of absence epilepsy in specific relay nuclei (SRN) of thalamus. It was found that the seizure state may appear in SRN by turning the coupling strength -v_sr and signal transmission delay τ on the route "Thalamic reticular nuclei (TRN) of thalamus ⟶ SRN". With increasing of -v_sr, the seizure state appeared two times, and its onset mechanism has not been discussed in previous studies. The seizure activity can be well controlled by adjusting the activation level of the substantia nigra pars reticulata (SNr) in basal ganglia, which is a main output tissue to the corticothalamic system through two direct inhibitory pathways "SNr ⟶ SRN" and "SNr ⟶ TRN" in our model. We found that the interesting bidirectional regulation phenomenon appeared as considering the single pathway "SNr ⟶ SRN" and "SNr ⟶ TRN", or when they coexisted in one network, the mechanism of which is also different from some previous theoretical studies. At last, we pointed out that the mechanism obtained above can also explain the onset and control of the poly-spikes slow wave appeared in SRN by turning τ to large enough. Therefore, the results in the paper will further deepen our understanding of the generation and control mechanism of epilepsy disease.