SCOOSIE

STIMULATION CONTROLLED RESTORATION OF SUBNET INTERACTION IN EPILEPSY


Relevant for Research Area

A - Foundations


Summary

In SCOOSIE we aim to understand the mechanisms leading to the initiation of epileptic activity and develop neurotechnological tools to reduce seizures probability in an animal model of mesial temporal lobe epilepsy, one of the most prevalent forms of epilepsy. While some neurotechnological approaches to stop seizures undergo clinical trials, none of these provides satisfactory solutions, in part because they react only when seizures have already started; they do not prevent seizures. In SCOOSIE, we investigate persistent signatures of epilepsy in field potential recordings in periods between seizures to define indicators of momentary seizure susceptibility to control closed-loop interventions. We use implanted wires and silicon probes with multiple electrodes to identify epileptic foci and use computational neuronal network models to identify potential stimulation paradigms.

Meanwhile SCOOSIE is prolonged under a new project title: ACCESS


Research Status

In mesial temporal lobe epilepsy inhibitory neurons in the dentate gyrus (DG) and other hippocampal neurons degenerate, which predicts excessive excitability of the remaining granule cells. Counterintuitively, however, number, size and strength of synapses between the medial entorhinal cortex and the DG increase, suggesting stronger input [1]. Nonetheless, coupling of rhythmic theta-activity between entorhinal cortex and DG weakens, indicating a mismatch that could affect network stability [2].

[1] Janz P, Savanthrapadian S, Häussler U, Kilias A, Nestel S, Kretz O, Kirsch M, Bartos M, Egert U, Haas CA (2017) Synaptic remodeling of entorhinal input contributes to an aberrant hippocampal network in temporal lobe epilepsy. Cereb Cortex, 27(3).

[2] Froriep UP, Kumar A, Cosandier-Rimélé D, Häussler U, Kilias A, Haas CA, Egert U (2012) Altered theta coupling between medial entorhinal cortex and dentate gyrus in temporal lobe epilepsy. Epilepsia, volume: 53, pp. 1937–47.