On the Origin of Interictal Activity in Human Temporal Lobe Epilepsy in Vitro

TLDR

The origin and mechanisms of human interictal epileptic discharges remain unclear. The study describes spontaneous, rhythmic activity initiated in the subiculum of slices from temporal lobe epilepsy patients. Synchronous events resembling patient interictal discharges were observed, suppressed by glutamatergic or GABAergic antagonists, and involved subicular interneurons and pyramidal cells with depolarizing GABAergic responses downstream of sclerotic CA1, contributing to interictal activity.

Abstract

The origin and mechanisms of human interictal epileptic discharges remain unclear. Here, we describe a spontaneous, rhythmic activity initiated in the subiculum of slices from patients with temporal lobe epilepsy. Synchronous events were similar to interictal discharges of patient electroencephalograms. They were suppressed by antagonists of either glutamatergic or γ-aminobutyric acid (GABA)–ergic signaling. The network of neurons discharging during population events comprises both subicular interneurons and a subgroup of pyramidal cells. In these pyramidal cells, GABAergic synaptic events reversed at depolarized potentials. Depolarizing GABAergic responses in neurons downstream to the sclerotic CA1 region contribute to human interictal activity.