Event Abstract Back to Event Hypothalamic CRH expression in fractalkine receptor (CX3CR1) deficient mouse Andrea Molnár1* and Krisztina J. Kovacs1 1 Institute of Experimental Medicine, Hungary There is a bidirectional communication between immune system and neuroendocrine sytem, e.g. cytokines activate to hypothalamic-pituitary-adrenal axis. In the central nervous system (CNS), microglia act as immune competent cells. Fractalkine, secreted by neurons, affect microglial activation.Recently CX3CR1 deficient mice became available. In these animals, cx3cr1 gene was replaced by a GFP reporter gene. In both homozygote (CX3CR1GFP/GFP) and heterozygote (CX3CR1+/GFP) mice microglial cells can be revealed by GFP, but the CX3CR1GFP/GFP mice have complete absence of fractalkine receptor. The phenotype of CX3CR1+/GFP mice corresponds with wild type C57Bl6 mouse strain. To reveal the role of fractalkine receptor in mediation of immune signals to the hypothalamus, CX3CR1 trangenic animals were exposed to chronic variable stress paradigm and corticotropin-releasing hormone (CRH) expression has been evaluated.Under baseline conditions, in homozygote animals CRH mRNA levels are increased in the paraventricular nucleus (PVN), but sex difference in CRH expression remained. After chronic stress, in heterozygote males the CRF expression increased, while in the heterozygote females this increase is not significant. The increase is also not significant in the homozygote males. However, in the homozygote females the CRF expression are significantly decreased. This data suggests as role of microglial fractalkine receptor in regulation of hypothalamic stress related gene expression. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Homeostatic regulatory mechanisms Citation: Molnár A and Kovacs KJ (2009). Hypothalamic CRH expression in fractalkine receptor (CX3CR1) deficient mouse. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.115 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: 04 Mar 2009; Published Online: 04 Mar 2009. * Correspondence: Andrea Molnár, Institute of Experimental Medicine, Budapest, Hungary, molnara@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 Andrea Molnár Krisztina J Kovacs Google Andrea Molnár Krisztina J Kovacs Google Scholar Andrea Molnár Krisztina J Kovacs PubMed Andrea Molnár Krisztina J Kovacs 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.