Amylin mRNA in the rat brain: induction of its expression in the preoptic area of rat dams

Abstract

Event Abstract Back to Event Amylin mRNA in the rat brain: induction of its expression in the preoptic area of rat dams Arpad Dobolyi1* 1 Hungarian Academy of Sciences and Semmelweis University, Department of Anatomy, Hungary Postpartum behavioral and neuroendocrine changes in females are critically important parts of mammalian reproduction and are expected to be associated with gene expressional alterations. The preoptic area of the hypothalamus plays a central role in postpartum regulations as concluded from the absence of maternal behaviors following preoptic lesions in rats. In the present study, a microarray experiment was performed to investigate gene expressional regulations in rat dams. Preoptic mRNA levels of 4 lactating dams and 4 mothers whose pups were removed on the day of delivery were compared 9 days after parturition. We found 95 genes whose expression increased and 96 genes whose expression decreased significantly. The gene whose expression level demonstrated the largest change, a 25.7 times increase, was amylin, or islet amyloid polypeptide. Subsequently, quantitative real-time RT-PCR measurements were performed using mRNA from the preoptic area of 12 lactating dams and 12 mothers whose pups were removed. A 24.1 times, highly significant increase in the mRNA level of amylin validated the induction of its expression found by the microarray experiment. In situ hybridization histochemistry for amylin demonstrated its expression in the medial preoptic nucleus and parts of the lateral preoptic area but nowhere else in the rat brain. Amylin is a 37 aa peptide previously described only in the pancreas. In this study, we first revealed its expression in the central nervous system and also showed that the level of amylin expression is very low in control female rats and in mothers deprived of their pups but is dramatically induced in normal mothers. The results suggest a role for amylin in the control of physiological and behavioral alterations in mother rats. Support was provided by the Hungarian Science Foundation NKTH-OTKA K67646 grant. Arpád Dobolyi is grantee of the Bolyai János Scholarship. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Homeostatic regulatory mechanisms Citation: Dobolyi A (2009). Amylin mRNA in the rat brain: induction of its expression in the preoptic area of rat dams. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.008 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: 25 Feb 2009; Published Online: 25 Feb 2009. * Correspondence: Arpad Dobolyi, Hungarian Academy of Sciences and Semmelweis University, Department of Anatomy, Budapest, Hungary, dobolyi@ana.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 Arpad Dobolyi Google Arpad Dobolyi Google Scholar Arpad Dobolyi PubMed Arpad Dobolyi 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.