Subiculum-entorhinal cortex interactions during in vitro ictogenesis

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.

Keywords: 4-Aminopyridine; Entorhinal cortex; Low-voltage fast onset; Subiculum; Sudden onset.