The Effect of Kisspeptin 1 on Gonadotropin Releasing Hormone Neurons in Embryonic Medaka (Oryzias Latipes)

Location

Old Dominion University, Learning Commons at Perry Library, West Foyer

Start Date

4-8-2017 8:30 AM

End Date

4-8-2017 10:00 AM

Description

In adult vertebrates, the neuropeptide kisspeptin1 stimulates the release of gonadotropin releasing hormone (GnRH) thereby regulating sexual maturation and reproduction. In the model teleost medaka, Kiss1 is expressed throughout embryonic development, where its function is unknown. We hypothesized that Kiss1 plays a role in the development of GnRH neural network in embryonic medaka. We exposed either GnRH-1promoter:GFP transgenic or wild-type medaka embryos to Kiss1 or a Kiss receptor blocker and examined the effects on GnRH. We quantified GFP-labeled neurons in the 4 dpf transgenic embryos. Neuron number varied from 19 ± 6.8 (mean ± SD) in controls, to 22 ± 6.9 in Kiss1 embryos and 16 ± 4.6 in blocker embryos (n=6). These differences were not significant, however, (ANOVA; p = 0.3) indicating that Kiss1 signaling doesn’t regulate GnRH-1 neuron proliferation or differentiation during embryogenesis. To examine the effects of Kiss1 on gnrh-1 and gnrh-3 expression, we collected treated wild-type embryos throughout embryogenesis and are quantifying expression with qPCR.

Presentation Type

Poster

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Apr 8th, 8:30 AM Apr 8th, 10:00 AM

The Effect of Kisspeptin 1 on Gonadotropin Releasing Hormone Neurons in Embryonic Medaka (Oryzias Latipes)

Old Dominion University, Learning Commons at Perry Library, West Foyer

In adult vertebrates, the neuropeptide kisspeptin1 stimulates the release of gonadotropin releasing hormone (GnRH) thereby regulating sexual maturation and reproduction. In the model teleost medaka, Kiss1 is expressed throughout embryonic development, where its function is unknown. We hypothesized that Kiss1 plays a role in the development of GnRH neural network in embryonic medaka. We exposed either GnRH-1promoter:GFP transgenic or wild-type medaka embryos to Kiss1 or a Kiss receptor blocker and examined the effects on GnRH. We quantified GFP-labeled neurons in the 4 dpf transgenic embryos. Neuron number varied from 19 ± 6.8 (mean ± SD) in controls, to 22 ± 6.9 in Kiss1 embryos and 16 ± 4.6 in blocker embryos (n=6). These differences were not significant, however, (ANOVA; p = 0.3) indicating that Kiss1 signaling doesn’t regulate GnRH-1 neuron proliferation or differentiation during embryogenesis. To examine the effects of Kiss1 on gnrh-1 and gnrh-3 expression, we collected treated wild-type embryos throughout embryogenesis and are quantifying expression with qPCR.