The effect of generalized absence seizures on the progression of kindling in the rat

The involvement of the thalamus in limbic epileptogenesis has recently drawn attention to the connectivity between the nuclei of the thalamus and limbic structures. Thalamo-limbic circuits are thought to regulate limbic seizure activity whereas thalamocortical circuits are involved in the expression and generation of spike-and-wave discharges (SWDs) in the absence epilepsy models. Genetic Absence Epilepsy Rats From Strasbourg (GAERS) and WAG/Rij (Wistar Albino Glaxo from Rijswijk) are well-defined genetic animal models of absence epilepsy. We aimed to examine the duration of behavioral changes in the kindling process and the relation of SWD activity to the kindling progress in the GAERS and WAG/Rij animals. Electrodes were stereotaxically implanted into the basolateral amygdala and the cortex of rats for stimulation and recording. The animals were stimulated at the threshold for producing afterdischarges. EEG was recorded to analyze SWDs and afterdischarge durations. The seizure severity was evaluated using Racine's 5-stage scale. None of the GAERS animals reached stage 3, 4, or 5 after application of 30 stimulations. The WAG/Rij animals showed different rate of kindling, therefore they were further categorized into the kindling-resistant, slow-kindled, and rapid-kindled groups. The kindling-resistant animals demonstrated a significantly longer duration of SWDs on the first day of the experiment before kindling stimulation and shorter duration of afterdischarge than did the kindled WAG/Rij animals. Behavioral durations at stage 2 were longer in kindled Wistar and WAG/Rij animals compared to kindling-resistant WAG/Rij and GAERS. These results suggest that mechanisms involved in the generation of SWDs act as a counterbalance to the excitability induced by kindling

Proteome Profile of Extratemporal Structures in Amygdala Kindling Mesial Temporal Lobe Epilepsy Rat Model: A Preliminary Study

WOS: 000392741600003Background: Mesial temporal lobe epilepsy is the most prevalent type of human epilepsy and its pathogenesis still remains unknown. Structures outside the temporal lobe may also play critical roles in the disease's progress. Objective: The aim of this study was to investigate proteome alterations and to identify differentially expressed proteins in frontoparietal cortex and thalamus regions of 6-month-old amygdala-kindled WAG/Rij rats as a mesial temporal lobe epilepsy model by using bottom-up proteomics approach. Method: Protein extraction from the tissues was followed by two-dimensional gel electrophoresis. Proteins were identified by peptide mass fingerprinting analysis using MALDI-TOF MS followed by MASCOT database search. Results: 58 and 47 proteins were identified in frontoparietal cortex and thalamus, respectively. Differentially expressed proteins in frontoparietal cortex were all up-regulated in the kindled groups compared to kindled-resistant group (p<0.05). These proteins were; Fabp4, Gamma-enolase, Annexin AT, Rab-15, RAB6-interacting golgin, PGAM1, DAB-2 and Fructose-bisphosphate aldolase C. In thalamus, BDNF (in spot 13), TRAPPC2L, Ras-related protein Rab-2A, GTP-binding protein REM 2 and Calcyclin-binding protein were up-regulated (p<0.05); and BDNF (in spot 9), kif3a, Parvalbumin alpha were down-regulated in the kindled groups compared to the kindled-resistant group (p<0,05). Conclusion: In this study, we identified proteins that might have roles in enabling or complicating mesial temporal lobe epilepsy progress. The potential of these proteins as biomarkers needs further research.TUBITAK (Scientific and Technological Research Council of Turkey) [108S196]This study was funded by TUBITAK (Scientific and Technological Research Council of Turkey) (Grant number: 108S196)