Event Abstract Back to Event Mechanism of the persistent sodium current activator veratridine-evoked Ca2+ elevation: implication for epilepsy Tibor Zelles1*, Adám Fekete1, Laura Franklin1, Takeshi Ikemoto1, Balázs Rózsa1, Balázs Lendvai1 and Sylvester E. Vizi1 1 HAS, Institute of Experimental Medicine, Hungary Although the role of Na+ in several aspects of Ca2+ regulation has already been shown, the exact mechanism of intracellular Ca2+ concentration ([Ca2+]i) increase resulting from an enhancement in the persistent, non-inactivating Na+ current (INa,P), a decisive factor in certain forms of epilepsy, has yet to be resolved. Persistent Na+ current, evoked by veratridine, induced bursts of action potentials and sustained membrane depolarization with monophasic intracellular Na+ concentration ([Na+]i) and biphasic [Ca2+]i increase in CA1 pyramidal cells in acute hippocampal slices. The Ca2+ response was tetrodotoxin- and extracellular Ca2+ -dependent and ionotropic glutamate receptor-independent. The first phase of Ca2+ rise was the net result of Ca2+ influx through voltage-gated Ca2+ channels and mitochondrial Ca2+ sequestration. The robust second phase in addition involved reverse operation of the Na+-Ca2+ exchanger and mitochondrial Ca2+ release. We excluded contribution of the endoplasmic reticulum. These results demonstrate a complex interaction between persistent, non-inactivating Na+ current and Ca2+ regulation in CA1 pyramidal cells. The described cellular mechanisms are most likely part of the pathomechanism of certain forms of epilepsy that are associated with INa,P. Describing the magnitude, temporal pattern and sources of Ca2+ increase induced by INa,P may provide novel targets for antiepileptic drug therapy. Conference: IBRO International Workshop 2010, Pécs, Hungary, 21 Jan - 23 Jan, 2010. Presentation Type: Poster Presentation Topic: Disorders of the nervous system Citation: Zelles T, Fekete A, Franklin L, Ikemoto T, Rózsa B, Lendvai B and Vizi SE (2010). Mechanism of the persistent sodium current activator veratridine-evoked Ca2+ elevation: implication for epilepsy. Front. Neurosci. Conference Abstract: IBRO International Workshop 2010. doi: 10.3389/conf.fnins.2010.10.00072 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: 21 Apr 2010; Published Online: 21 Apr 2010. * Correspondence: Tibor Zelles, HAS, Institute of Experimental Medicine, Budapest, Hungary, zelles@koki.hu 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 Tibor Zelles Adám Fekete Laura Franklin Takeshi Ikemoto Balázs Rózsa Balázs Lendvai Sylvester E Vizi Google Tibor Zelles Adám Fekete Laura Franklin Takeshi Ikemoto Balázs Rózsa Balázs Lendvai Sylvester E Vizi Google Scholar Tibor Zelles Adám Fekete Laura Franklin Takeshi Ikemoto Balázs Rózsa Balázs Lendvai Sylvester E Vizi PubMed Tibor Zelles Adám Fekete Laura Franklin Takeshi Ikemoto Balázs Rózsa Balázs Lendvai Sylvester E Vizi 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.