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 GABAA- and GABAB-mediated inhibitions in the TRN-SRN pathway perform combination roles in the regulation of absence seizures. Overall, these results may provide an insightful mechanistic understanding of how the thalamic FFI serves as an intrinsic regulator contributing to the control of absence seizures.
Highlights
Absence epilepsy is a common subtype of idiopathic generalized epilepsies and mainly occurs in the childhood years (Durón et al, 2005; Tolaymat et al, 2015)
The thalamic reticular nucleus (TRN)-specific relay nuclei (SRN) inhibitions mediated by GABAA and GABAB receptors effectively shape SRN firing at different instants
Most of spike and wave discharges (SWDs) oscillation region is contained in the typical 2–4 Hz frequency range, which can be comparable with EEG signals of real patients during absence seizures
Summary
Absence epilepsy is a common subtype of idiopathic generalized epilepsies and mainly occurs in the childhood years (Durón et al, 2005; Tolaymat et al, 2015). We find that both the excitatory Ctx-TRN coupling strength and the relative strength between the GABAB- and GABAA-mediated inhibitions in the TRN-SRN pathway play critical roles in preventing pathological 2–4 Hz SWDs generated by the CT system.
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