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In Non-Breeding Ewes the Kisspeptin Analog C6 Triggers

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In Non-Breeding Ewes the Kisspeptin Analog C6 Triggers In non-breeding ewes the kisspeptin analog c6 triggers ovulation without progestogen priming Massimiliano Beltramo, Caroline Decourt, Vincent Robert, Didier Lomet, Vincent Aucagne To cite this version: Massimiliano Beltramo, Caroline Decourt, Vincent Robert, Didier Lomet, Vincent Aucagne. In non- breeding ewes the kisspeptin analog c6 triggers ovulation without progestogen priming. 9. Inter- national Congress of Neuroendocrinology. ICN2018, Jul 2018, Toronto, Canada. 2018, The 9th International Congress of Neuroendocrinology. Abstract book. hal-02735160 HAL Id: hal-02735160 https://hal.inrae.fr/hal-02735160 Submitted on 2 Jun 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Follow us @ICN_2018 Join the conversation #ICN2018 Abstract Book 22nd Annual Meeting of the Society for Behavioral Neuroendocrinology | British Society for Neuroendocrinology | Société de Neuroendocrinologie | Hypothalamic Neuroscience and Neuroendocrinology Australasia | ICN2018.ORG Pan American Neuroendocrine Society | Japan Neuroendocrine Society Table of Contents Plenary Presentations ................................................................................................................................... 3 Plenary Presentations – Saturday, July 14, 2018 ...................................................................................... 4 Plenary Presentations – Sunday, July 15, 2018 ......................................................................................... 4 Plenary Presentations – Monday, July 16, 2018 ....................................................................................... 6 Plenary Presentations – Tuesday, July 17, 2018 ....................................................................................... 7 Plenary Presentations – Wednesday, July 18, 2018 ................................................................................. 9 Young Ambassadors Keynote Lecture ........................................................................................................ 10 Young Ambassadors Keynote Lecture – Wednesday, July 18, 2018 ....................................................... 11 Symposia Presentations .............................................................................................................................. 12 Symposia Presentations – Sunday, July 15, 2018 ................................................................................... 13 Symposia Presentations – Monday, July 16, 2018 .................................................................................. 24 Symposia Presentations – Tuesday, July 17, 2018 .................................................................................. 36 Symposia Presentations – Wednesday, July 18, 2018 ............................................................................ 49 Award Presentations .................................................................................................................................. 61 Award Presentations – Sunday, July 15, 2018 ........................................................................................ 62 Award Presentations – Wednesday, July 18, 2018 ................................................................................. 64 Trainee Award Presentations ..................................................................................................................... 67 Oral Presentations ....................................................................................................................................... 70 Oral Presentations – Sunday, July 15, 2018 ............................................................................................ 71 Oral Presentations – Tuesday, July 17, 2018 .......................................................................................... 82 Poster Presentations ................................................................................................................................... 99 Poster Session 1 – Sunday, July 15 to Monday, July 16, 2018.............................................................. 100 Poster Session 2 – Tuesday, July 17 to Wednesday, July 18, 2018 ............................................................ 230 Author Index ............................................................................................................................................ 358 2 ICN2018 3OHQDU\3UHVHQWDWLRQV Plenary Presentations – Saturday, July 14, 2018 PL01.001 THE NEUROGENOMIC ARCHITECTURE OF STRESS SUSCEPTIBILITY Michael Meaney McGill University, Montreal, QC, Canada Stress is a well-established ‘trigger’ for multiple forms of chronic illness including mental disorders. Despite the compelling epidemiological evidence, most individuals exposed to chronic, severe stress during development or adulthood are largely unaffected. These findings reflect the remarkable individual variation in susceptibility to stress. Animal models of differential susceptibility have identified transcriptional pathways and neural circuits associated with susceptibility. In the studies reported here we attempted to integrate this knowledge into an analysis of the genetic architecture of stress susceptibility in humans using a publicly- available genome-wide association study of addictions in individuals who were or were not exposed to stressful conditions known to predict an increased risk for chronic illness, including addictions. We developed a genomic profile score for stress susceptibility (Gypsums) by comparing stress-exposed individuals with (susceptible) or without (resilient) a history of addiction. The resulting Gypsums predicted stress-related mental disorders in an independent sample of individuals exposed to childhood abuse. We also found highly significant overlap between the genes that comprised our Gypsums and differentially expressed genes in a rodent model of stress susceptibility (chronic social defeat) using Ranse data from the ventral hippocampus. The overlapping genes are highly enriched for mithqal’s, suggesting epigenetic mediation through DNA methylation. Informatic analyses of both human and rodent data sets implicate estrogen- and glucocorticoid-signaling pathways. Direct manipulation of ESR1 expression resulted in significant alterations in stress susceptibility in the murine chronic social defeat model. These findings suggest a role for brain region- specific, steroid-sensitive transcriptional signaling in defining individual differences in susceptibility to stress. Plenary Presentations – Sunday, July 15, 2018 PL02.001 A NEURAL CIRCUIT THAT RESPONDS TO THREATS AND CONTROLS APPETITE Richard Palmiter University of Washington, Seattle, United States of America Both visceral and somatosensory neuronal information is relayed to higher brain regions by glutamatergic neurons that reside in the parabrachial nucleus (PBN) that express calcitonin gene-related peptide (CGRP) and several other neuropeptides. Activation of these CGRP- expressing neurons either by photo-activation of channel rhodopsin (ChR2) or CNO activation of 4 hM3Dq DREADD receptors inhibits feeding and chronic activation of these neurons would lead to starvation. Additional experiments demonstrate that a relevant output of these CGRP- expressing neurons that mediates anorexia is a projection to the lateral capsule region of the central nucleus of the amygdala onto neurons that express the receptor for CGRP. Pairing artificial activation of CGRP-expressing neurons with either a novel taste or a novel tone/context is sufficient to establish conditioned taste aversion or fear behaviors (freezing), respectively. Inactivation of CGRP neurons ameliorates taste or fear conditioning, indicating that they transmit the classical unconditioned stimulus for both learning paradigms. Calcium imaging reveals that virtually CGRP neurons are activated by all threats that have been examined; thus, they serve as a general alarm system. These neurons respond to potential threats and cues that have been associated with harm in the past. Different threats are presumably distinguished by the intensity of the stimulations and where conditioned stimuli (sensory cues) and unconditioned stimuli (pain) converge in the brain. PL03.001 HYPOTHALAMIC PULSE GENERATION FOR FERTILITY Allan E. Herbison Centre For Neuroendocrinology and The Department of Physiology, Otago School of Medical Sciences, University of Otago, Dunedin, New Zealand Several hypothalamic circuits can generate a pulsatile pattern of hormone secretion. The gonadotropin-releasing hormone (GnRH) neuronal network is one such circuitry that releases GnRH in an episodic manner to drive pulsatile gonadotropin hormone secretion. The GnRH neurons migrate from the nose into the brain during development and have many peculiar properties including a scattered distribution and the projection of a blended dendrite/axon (“dendron”) to the median eminence secretory zone. Studies in a variety of genetic mouse models using tract-tracing, brain slice and in vivooptogenetic approaches have been
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