Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8686370 | Neurobiology of Disease | 2018 | 9 Pages |
Abstract
Ictal discharges induced by 4-aminopyridine in the in vitro rodent entorhinal cortex present with either low-voltage fast or sudden onset patterns. The role of interneurons in initiating low-voltage fast onset ictal discharges is well established but the processes leading to sudden onset ictal discharges remain unclear. We analysed here the participation of interneurons (nâ¯=â¯75) and principal cells (nâ¯=â¯13) in the sudden onset pattern by employing in vitro tetrode wire recordings in the entorhinal cortex of brain slices from Sprague-Dawley rats. Ictal discharges emerged from a background of frequently occurring interictal spikes that were associated to a specific interneuron/principal cell interplay. High rates of interneuron firing occurred 12â¯ms before interictal spike onset while principal cells fired later during low interneuron firing. In contrast, the onset of sudden ictal discharges was characterized by increased firing from principal cells 627â¯ms before ictal onset whereas interneurons increased their firing rates 161â¯ms before ictal onset. Our data show that sudden onset ictogenesis is associated with frequently occurring interictal spikes resting on the interplay between interneurons and principal cells while ictal discharges stem from enhanced principal cell firing leading to increased interneuron activity. These findings indicate that specific patterns of interactions between interneurons and principal cells shape interictal and ictal discharges with sudden onset in the rodent entorhinal cortex. We propose that specific neuronal interactions lead to the generation of distinct onset patterns in focal epileptic disorders.
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Authors
Maxime Lévesque, Li-Yuan Chen, Shabnam Hamidi, Massimo Avoli,