Event Abstract Back to Event PEPTIDERGIC SIGNALING CASCADES IN THE REGULATION OF INSECT ECDYSIS Michael E. Adams1*, Do-Hyoung Kim1, Young-Joon Kim1 and Dusan Zitnan2 1 University of California, Riverside, Entomology, United States 2 Slovak Academy of Sciences, Institute of Zoology, Slovakia Molting and ecdysis are among the most distinctive and characteristic features of arthropod physiology and are vital for growth and metamorphosis from juvenile to the winged, reproductive adult. These events are by precisely timed release of steroid and peptide hormones. We are interested in how hormones initiate and schedule the ecdysis sequence, a series of innate behaviors that allows escape from the old cuticle to terminate the molt. These behaviors are initiated and scheduled by ecdysis triggering hormones (ETHs) that regulate neuropeptide signaling cascades in the central nervous system (CNS). Ecdysteroids signal onset of the molt and program expression of genes encoding ecdysis signaling molecules. In moths (Bombyx mori, Manduca sexta) and flies (Drosophila melanogaster), we have identified primary neuronal targets of ETH in the CNS by detecting expression of ETH receptor (ETHR) transcripts. We monitor activities of ETHR neurons by electrophysiology and calcium imaging. ETHRs are expressed predominantly in “peptidergic ensembles”, groups of central neurons that release FMRFamides, eclosion hormone, kinins, CCAP, MIPs, and bursicon into the CNS to schedule activation of central pattern generators that drive pre-ecdysis, ecdysis, and post-ecdysis. We are examining the roles played by these neurons in behavioral scheduling using genetics and physiological manipulations. Our findings offer insights into how neural substrates for behaviors are assembled and regulated. Supported by NIH grant GM 067310 Acknowledgements Supported by NIH grant GM 067310 Keywords: Behavior, Calcium, Electrophysiology, imaging, Innate, peptide, steroid Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Invited Symposium Topic: Developmental endocrinology Citation: Adams ME, Kim D, Kim Y and Zitnan D (2011). PEPTIDERGIC SIGNALING CASCADES IN THE REGULATION OF INSECT ECDYSIS. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00101 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 Aug 2011; Published Online: 09 Aug 2011. * Correspondence: Prof. Michael E Adams, University of California, Riverside, Entomology, Riverside, CA, 92521, United States, adams@ucr.edu 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 Michael E Adams Do-Hyoung Kim Young-Joon Kim Dusan Zitnan Google Michael E Adams Do-Hyoung Kim Young-Joon Kim Dusan Zitnan Google Scholar Michael E Adams Do-Hyoung Kim Young-Joon Kim Dusan Zitnan PubMed Michael E Adams Do-Hyoung Kim Young-Joon Kim Dusan Zitnan 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.
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