| Abstract: |
| Absence epilepsy is the most typical generalized epilepsy. As the electrophysiological hallmark, the spike-wave discharges (SWDs) with frequency 2-4 Hz can be observed in the EEG recordings during absence seizures. Using computational models based on neural-filed theory, we identified that strengthening the thalamic feedforward inhibition (TFFI) can inhibits the seizure activities. In this pathway, strong GABAB inhibition tends to suppress SWDs, while GABAA inhibition mainly dominates the frequency of seizure dynamics. Furthermore, we also found that the basal ganglia (BG) might multiply control absence seizures via three inhibition pathways sending to thalamus and cerebral cortex. The SWD suppression induced by the inhibitory pathway projecting from the substantia nigra pars reticulate (SNr) to thalamic specific relay nuclei (SRN) is due to the GABAB weakening, while the SWD suppression induced by the SNr-TRN (thalamic reticular nucleus) pathway is because of the collision in TRN. Owing to the competition between these two pathways, we observed that the bidirectional control of absence seizures by the BG. Further investigations demonstrated that the GABAergic pallido-cotrical pathway might can also directly inhibit the typical 2-4 Hz SWDs generated in our model. These findings highlight the functional significance of TFFI and BG in controlling and modulating absence seizures. |
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