Hippocampal mechanisms in the initiation and perpetuation of epileptiform network synchronisation

Abstract

Event Abstract Back to Event Hippocampal mechanisms in the initiation and perpetuation of epileptiform network synchronisation Gleb Barmashenko1*, Rika Bajorat1 and Rüdiger Köhling1 1 University of Rostock, Institute of Physiology, Germany This project is characterised by joint experimental approaches which contribute to the development of new network models of one of the most common neurological diseases - epilepsy. Hypersynchronisation is a key factor in ictal epileptic activity, and there is evidence that abnormal synchronising effects of interneuronal GABAergic transmission play an important role in the initiation of epileptic activity and the generation of ictal discharges. However, a concise characterisation of the role of different types of interneurones and of their function in the exact spatio-temporal organisation of the epileptogenic network has yet to be determined.Electrophysiological measurements in slices from acute animal models of focal epilepsy, both in normal and chronically epileptic tissue, started to determine the role of different types of interneurones with respect to initiation of epilepsy and interictal-ictal transitions. There is growing evidence that functional alterations in the epileptiform hippocampus critically depends on GABAergic mechanisms and cation-chloride cotransporters. To understand the cellular basis of specific morphological and functional alterations in the epileptic hippocampus we studied the physiological characteristics and transmembrane currents of neurones in hippocampal slices from epileptic and control rats using whole-cell and gramicidin perforated patch-clamp recordings. Whereas the resting membrane potential, input resistance, time constant, rheobase and chronaxy were not significantly different between control and epileptic tissue, the reversal potential of the GABAAR mediated currents (EGABA) was significantly shifted to more positive values in the epileptic rats, which can contribute to hyperexcitability and abnormal synchronisation within the epileptic hippocampus. Pharmacological experiments showed that the observed changes in the epileptic tissue were due to a combined upregulation of the main Cl- uptake transporter (Na+-K+-2Cl- cotransporter, NKCC1) and downregulation of the main Cl- extrusion transporter (K+-Cl- cotransporter, KCC2).For paired recordings commonly juvenile animals (P16-P25) are taken. Therefore we currently establish a model for chronic epilepsy in young rats verified by EEG recordings. In the further course of the project, a detailed analysis of interneurone-principal neurone interactions will be undertaken. These biophysical parameters will serve to establish realistic models of computational behaviour of neurones and neuronal networks. This in turn will allow to establish models with increasing complexity and to predict both functional and dysfunctional synchronisation patterns. These predictions will then be tested experimentally in order to validate the models (in cooperation with Bernstein Center for Computational Neuroscience, Freiburg). Conference: Bernstein Conference on Computational Neuroscience, Frankfurt am Main, Germany, 30 Sep - 2 Oct, 2009. Presentation Type: Poster Presentation Topic: Learning and plasticity Citation: Barmashenko G, Bajorat R and Köhling R (2009). Hippocampal mechanisms in the initiation and perpetuation of epileptiform network synchronisation. Front. Comput. Neurosci. Conference Abstract: Bernstein Conference on Computational Neuroscience. doi: 10.3389/conf.neuro.10.2009.14.089 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Aug 2009; Published Online: 26 Aug 2009. * Correspondence: Gleb Barmashenko, University of Rostock, Institute of Physiology, Rostock, Germany, gleb.barmashenko@uni-rostock.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Gleb Barmashenko Rika Bajorat Rüdiger Köhling Google Gleb Barmashenko Rika Bajorat Rüdiger Köhling Google Scholar Gleb Barmashenko Rika Bajorat Rüdiger Köhling PubMed Gleb Barmashenko Rika Bajorat Rüdiger Köhling Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.