Event Abstract Back to Event Cyclophilin D Deficiency Attenuates Swelling of Neuronal Mitocohondria During Excitotoxic Glutamate Stimulation Judit Doczi1*, Vera Adam-Vizi1 and Christos Chinopoulos1 1 Department of Medical Biochemistry , Semmelweis University, Hungary Excitotoxic neuronal injury is involved in acute, as well as in chronic neurodegenenerative diseases. Opening of the mitochondrial permeability transition pore (mPTP) leading to bioenergetic crisis has been shown to promote excitotoxicity and neuronal cell death. The aim of this study was to determine whether lack of cyclophilin D, a putative mPTP modulator, is protective against opening of the mPTP in neurons upon excitotoxic glutamate stimulation. Mitochondrial swelling is an indicator of the opening of the mPTP and this was measured here with a novel quantitative in situ single cell assay in primary cultures of wild type or cyclophilin D knockout neurons. In wild type neurons excitotoxic glutamate exposure always triggered biphasic mitochondrial swelling and the late onset, secondary mitochondrial swelling was correlated temporally to the start of the irreversible rise of [Ca2+]i termed delayed calcium deregulation (DCD). In contrast, in 38 % of cyclophilin D knockout neurons examined, secondary mitocohondrial swelling was not detected during DCD. Our results demonstrate, that lack of cyclophilin D is protective against mitochondrial swelling triggered in glutamate excitotoxicity, but these results also predict the existence of a cyclophilin D independent pathway of the opening of the mPTP leading to delayed calcium deregulation and cell death. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Pathophysiology and neurology - degenerative disorders Citation: Doczi J, Adam-Vizi V and Chinopoulos C (2009). Cyclophilin D Deficiency Attenuates Swelling of Neuronal Mitocohondria During Excitotoxic Glutamate Stimulation. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.147 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: 05 Mar 2009; Published Online: 05 Mar 2009. * Correspondence: Judit Doczi, Department of Medical Biochemistry , Semmelweis University, Budapest, Hungary, judit.doczi@eok.sote.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 Judit Doczi Vera Adam-Vizi Christos Chinopoulos Google Judit Doczi Vera Adam-Vizi Christos Chinopoulos Google Scholar Judit Doczi Vera Adam-Vizi Christos Chinopoulos PubMed Judit Doczi Vera Adam-Vizi Christos Chinopoulos 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.