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Published on: December 8, 2018
Dynamics of directional coupling underlying spike-wave discharges
M V Sysoeva1, A Lüttjohann2, G van Luijtelaar3
1Yuri Gagarin State Technical University of Saratov, Saratov, Russia; Saratov Branch of Kotel'nikov Institute of Radio Engineering and Electronics of RAS, Saratov, Russia.
Spike and wave discharges (SWDs) in absence epilepsy initiate with increased cortical and thalamic coupling. Seizure termination involves a surge in network interactions, potentially acting as an endogenous brake.
Area of Science:
- Neuroscience
- Epileptology
- Computational Neuroscience
Background:
- Spike and wave discharges (SWDs) are the hallmark of absence epilepsy.
- Understanding the dynamic interactions within cortico-thalamic networks is crucial for elucidating SWD mechanisms.
Purpose of the Study:
- To investigate the initiation, maintenance, and termination mechanisms of SWDs.
- To analyze the dynamics and directionality of interactions between the neocortex and thalamic nuclei during SWDs.
Main Methods:
- Local-field potential recordings were obtained from WAG/Rij rats.
- Electrodes targeted the somatosensory cortex and specific thalamic nuclei (rRTN, cRTN, VPM, ATN, PO).
- Time-variant adapted nonlinear Granger causality was employed to analyze neural interactions.
Main Results:
- Cortico-cortical coupling increased pre-SWD onset.
- Cortico-thalamic and thalamo-cortical coupling evolved from unidirectional to bidirectional.
- Seizure onset involved a transient decrease in coupling, with cortex-cRTN maintaining influence; SWD maintenance showed minimal changes except for cortex-cRTN unidirectional coupling.
- SWD termination was associated with a gradual increase in bidirectional coupling.
Conclusions:
- SWD initiation involves progressive intracortical coupling followed by selective cortico-thalamic and intrathalamic coupling.
- During SWD maintenance, cortical influence on the cRTN persists despite decreased coupling in other pairs.
- SWD termination appears to be mediated by a strengthening of network coupling, possibly an endogenous braking mechanism.
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