Download SUBMISSION PROCEDURES Please register using the

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?
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____ No
Do you wish to be considered for the best poster award?
____ Yes
____ No
Have you already registered?
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____ 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