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DEADLINE FEBRUARY 1, 2017 ICCE18 Abstract Submission Form please upload after completion at https://regonline.ca/ICCE18. Each registered person is allowed to submit one abstracts as presenting author. There is no limit on the number of abstracts submitted as co-author. The presenting author will be notified of the acceptance of the abstract. PLEASE NOTE: Presenting author must be registered for the ICCE18 and pay the registration fee before abstracts are considered. Full Name Address E-mail Select the topic relevant to your abstract (X) ____ Endocrine Disruption in Aquatic Vertebrates - Lessons Learned and Future Prospects. A Tribute to Professor Louis J. Guillette, Jr. ____ Steroid Receptor Actions and Their Signaling: Nongenomic vs. Genomic ____ Fish sexual development ____ Kisspeptins: mandatory or optional for reproduction ____ The Hormonal Control of Osmoregulation in Vertebrates ____ Early Life Adversity and the Stress Response/Stress coping mechanisms ____ Old questions, new technological approaches in thyroid hormone signaling/Thyroid ____ Neurochemical Regulation of Instinctive Behavior ____ Biological Rhythms, circadian clock ____ Environmental Regulation of Reproductive Processes' ____ Eco-Evo-Devo: The Physiology of Phenotypic Variation ____ Symposium on Growth ____Integrating factors of appetite, energy balance and growth ____ Insulin and insulin-like peptides, vertebrate and invertebrate ____ Invertebrate sex steroids: facts and misconceptions ____ Plasticity in the neuroendocrine system (sponsored symposium, Medicine and Alberta Children’s Hospital) ____ Recent Progress in Cartilaginous Fish Endocrinology (NASCE President’s Symposium) ____ Neuroendocrinology of invertebrate deuterostomes - a crucial link between protostomes and vertebrates ____ ISAREN: Environmental and genetic influences on amphibian and reptilian endocrine systems ____ Signaling and Neuroendocrine Control ____ Tackling Endocrine Mysteries in Domestic Animals (sponsored symposium University of Calgary-University of Saskatchewan School of Veterinary Medicine) ____ Other topics Select one category ____ Invited speaker ____ Contributed abstract For the contributed abstract, do you want to be considered for oral presentation? ____ Yes ____ No Do you wish to be considered for the best poster award? ____ Yes ____ No Have you already registered? ____ Yes ____ No Please copy and paste the abstract below, using the format shown in the example provided in the website. Please do not exceed character limit since additional characters will not be printed. Title is limited to 200 characters and the abstract is limited to 2000 characters (excluding space). Replace the example provided below: THE PROTEIN KINASE C AND EXTRACELLULAR SIGNAL-REGULATED KINASE PATHWAYS ARE DIFFERENTIALLY INVOLVED IN BASAL AND GONADOTROPIN-RELEASING HORMONE-INDUCED GONADOTROPIN SUBUNIT GENE EXPRESSION IN GOLDFISH PITUITARY CELLS. Klausen C(1), Chang JP(3), Habibi HR(1,2) (1) Departments of Biological Sciences and (2) Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada, (3) Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada The goldfish brain and pituitary contains two forms of gonadotropin (GtH)-releasing hormone (GnRH): salmon (s)GnRH and chicken (c)GnRH-II. The involvement of protein kinase C (PKC) in GnRH-induced GtH secretion is well established in goldfish. In contrast, little information is available on the post-receptor mechanisms mediating GnRH-stimulated GtH subunit gene expression. In this study, we investigated the involvement of PKC and the extracellular signal-regulated kinase (ERK) pathway in GnRH-induced changes in GtH subunit mRNA levels. Western blot analysis with antibodies directed against various PKC types revealed the presence of immunoreactive isoforms of conventional (a), novel (d and q) and atypical (z) classes of PKC. Using primary cultures of dispersed goldfish pituitary cells, we examined the effects of PKC inhibition and activation on GnRH-induced GtH subunit mRNA levels. Treatment with PKC inhibitors, calphostin C and GF109203X, revealed a basal repression of GtH subunit mRNA levels by PKC. GtH mRNA levels were also increased by the PKC activators, phorbol-12-myristate-13-acetate and 1,2-dioctanoyl-sn-glycerol. In general, sGnRH- and cGnRH-II-induced responses were not reduced by pretreatment with PKC inhibitors and were additive to those induced by PKC activation. In contrast, increases in GtH subunit mRNA levels induced by GnRH were significantly reduced in the presence of the ERK kinase inhibitor, PD98059. Together these results support the hypothesis that GnRHinduced increases in GtH subunit mRNA are mediated by the ERK pathway and are not likely to involve conventional and novel PKCs. These findings suggest that GnRH signals in a function-specific manner to regulate GtH secretion and gene expression in the goldfish pituitary. Acknowledgements: Supported by: NSERC Canada operating grants to JPC and HRH. CK was the recipient of an AHFMR studentship