Meeting Abstract
In mammals, the neuropeptide kisspeptin stimulates the release of gonadotropin releasing hormone (GnRH) and thereby regulates sexual maturation and reproduction. Increasing evidence indicates that kisspeptin homologues may play a similar role in teleosts. In medaka, as in other teleosts, multiple homologues of kisspeptin are expressed. Previous research has shown that the gene endoding the Kiss1 homologue is expressed throughout medaka embryonic development, but its function in embryogenesis is unknown. Based on the known relationship between kisspeptin and GnRH in other vertebrates, we hypothesized that Kiss1 plays a role in the development of GnRH neural network in embryonic medaka. We tested this hypothesis by exposing medaka embryos to Kiss1 or a Kiss receptor blocker and examining the effects on GnRH neuron development and gnrh expression throughout embryogenesis. To test whether Kiss1 affects GnRH neuronal proliferation and migration, we treated GnRH-1 promoter:GFP transgenic embryos, collected them at 2-8 days post fertilization, then mapped and quantified GFP-labeled neurons. In preliminary analysis of 4-day embryos, neuron number varied from 19 ± 6.8 (mean ± SD) in controls, to 22 ± 6.9 in Kiss1-treated embryos and 16 ± 4.6 in blocker-treated embryos (n=6). These differences were not significant, however, (ANOVA; p = 0.3) indicating that Kiss1 signaling does not regulate GnRH-1 neuron proliferation or differentiation at this stage. To examine the effects of Kiss1 on gnrh-1 and gnrh-3 expression, we collected control, Kiss-1, and blocker treated wild-type embryos throughout embryogenesis and are quantifying gnrh expression with qPCR.
