The combined effects of the thalamic feed-forward inhibition and feed-back inhibition in controlling absence seizures

Absence seizures usually occur in dysfunctional neural networks. Thalamic feed-forward inhibition and feed-back inhibition are the two most critical microcircuits, which can be detected in multiple brain regions such as the thalamus and the neocortex. To theoretically explore whether these two inhibition microcircuits have combined effects on absence seizures, we improve corticothalamic mean-field network model through introducing GABA(B)-mediated inhibitory interneurons in the cerebral cortex (Ctx). On the one hand, we certify that thalamic feed-forward inhibition, i.e., the neurons of the thalamic reticular nucleus (TRN), receive excitatory signals from Ctx and transmit GABA(A) and GABA(B)-mediated inhibitory signals to the thalamic relay nucleus (SRN), which plays critical roles in preventing absence seizures. On the other hand, we demonstrate that feed-back inhibition in thalamus, i.e., the neurons of SRN, send excitatory signals to TRN and receive GABA(B) and GABA(A)-mediated inhibitory signals from the TRN and also participates in the suppression of absence seizures. Finally, we mainly consider the combined effects of two microcircuits involved in the feed-forward inhibited CTX-TRN pathway and the feed-back inhibited SRN-TRN pathway on absence seizures. Our results show that the two microcircuits play combination roles in eliminating absence seizures. Importantly, feed-back inhibition of thalamus is stronger than feed-forward inhibition in suppressing absence seizures. These results highlight the important significance of two kinds of microcircuit motifs on absence seizures and might provide theoretical guidance for the treatment of epilepsy.

Automated summary

This study investigates the combined effects of thalamic feed-forward inhibition and feed-back inhibition on absence seizures. The results show that these two microcircuits play critical roles in eliminating absence seizures, with the feed-back inhibition of thalamus being stronger than the feed-forward inhibition.