Subiculum–entorhinal cortex interactions during in vitro ictogenesis. (September 2015)

• Record Type: Journal Article
• Authors: Herrington, Rochelle; Lévesque, Maxime; Avoli, Massimo
• Is Part Of: Seizure. Volume 31(2015)
• Page Start: 33
• Page End: 40
• Publication Date: 2015-09
• Subjects: 4-Aminopyridine -- Sudden onset -- Low-voltage fast onset -- Entorhinal cortex -- Subiculum; Epilepsy -- Periodicals; Epilepsy -- Periodicals; Seizures -- Periodicals; Épilepsie -- Périodiques; Electronic journals; Electronic journals; 616.853
• DOI: 10.1016/j.seizure.2015.07.002
• Languages: English
• ISSNs: 1059-1311

Abstract

Highlights: In intact horizontal brain slices, sudden onset ictal events often onset in the entorhinal cortex. In intact horizontal brain slices, LVF onset ictal events predominantly initiated from the subiculum. Severing connections between EC and subiculum abolished ictal discharge occurrence in subiculum. CPP blocked ictal events in the EC and fast trains of spikes in the isolated subiculum after cut. CPP disrupted the rhythmicity of fast polyspike interictal discharges in the EC following cut. Abstract: Purpose: Our aim was to establish the contribution of neuronal networks located in the entorhinal cortex (EC) and subiculum to the generation of interictal and ictal onset patterns recorded in vitro . Methods: We employed field potential recordings of epileptiform activity in rat brain slices induced with the application of the K + channel blocker 4-aminopyridine. Local connections between the EC and subiculum were severed to understand how EC–subicular circuits contribute to patterns of epileptiform synchronization. Results: First, we found that ictal discharges occurred synchronously in these two structures, initiating from either the EC or subiculum, and were characterized by low voltage fast (LVF) or sudden onsets. Second, sudden onset ictal events initiated more frequently in the EC, whereas LVF onset ictal discharges appeared more likely to initiate in the subiculum ( P < 0.001). In both structures, polyspike interictal discharges occurred in brain slices generating sudden onset ictal events while isolated slow interictal discharges were recorded in experiments characterized by LVF onset ictal activity. Third, severing the connections between subiculum and EC desynchronized both interictal and ictal discharges occurring in these two regions, leading to a significant decrease in ictal duration (regardless of the onset type) along with blockade of polyspike interictal activity in subiculum. Conclusions: These findings highlight the contribution of EC–subicular interactions to epileptiform synchronization and, specifically, to ictogenesis in this in vitro model.