Does EMX2 directly interfere with glutamatergic versus GABAergic phenotype decision?

Abstract

Event Abstract Back to Event Does EMX2 directly interfere with glutamatergic versus GABAergic phenotype decision? Nóra Hádinger1*, B. Varga1, K. Barabas1 and Emilia Madarasz1 1 IEM-HAS, Hungary For proper development of the mammalian cerebral cortex, region-specific transcription factors should be activated on schedule. EMX2 is expressed early (8th day) in mouse embryos, in the anterior neural plate. At the time of anterior tube closure, Emx2 is expressed in the dorsal part of the forebrain vesicles with increasing intensity to caudo-medial direction. Lack of EMX2 results in a rearrangement of the anterior cortical areas, and impairs the development of the whole dorsal forebrain. The target genes of EMX2 transcription factor are not known. In healthy developing mice, Emx2 is uniformly expressed in the ventricular zone of the entire dorsal forebrain, which is the birthplace of cortical glutamatergic neurons. Its expression, however, is maintained in the subventricular zone of adult mice. In the present work, the effects of EMX2 on neuronal cell fate decision and on the choice of neurotransmitter phenotype were investigated by comparing wild type and EMX2 overexpressing neural stem cells and differentiated progenies. The results demonstrated that continuous expression of EMX2 did not inhibit the in vitro differentiation of neural stem cells. Moreover, the expression of EMX2 was not sufficient to suppress some GABAergic features (VGAT1) in stem cell derived post-mitotic neurons or to increase markedly the proportion of neurons with VGLUT2 immunoreactivity. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Developmental neurobiology and subcortical functions Citation: Hádinger N, Varga B, Barabas K and Madarasz E (2009). Does EMX2 directly interfere with glutamatergic versus GABAergic phenotype decision?. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.235 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: 13 Mar 2009; Published Online: 13 Mar 2009. * Correspondence: Nóra Hádinger, IEM-HAS, Budapest, Hungary, hadinger@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 Nóra Hádinger B. Varga K. Barabas Emilia Madarasz Google Nóra Hádinger B. Varga K. Barabas Emilia Madarasz Google Scholar Nóra Hádinger B. Varga K. Barabas Emilia Madarasz PubMed Nóra Hádinger B. Varga K. Barabas Emilia Madarasz 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.