Date of Award
2011
Degree Type
Thesis
Degree Name
Master of Science
Program
Anatomy and Cell Biology
Supervisor
Dr. Michael Lehman
Abstract
Neurokinin B (NKB) acting via the neurokinin-3-receptor (NK3R) plays a critical role in neuroendocrine control of mammalian reproductioa In prenatal testosterone (T) treated sheep, a model of polycystic ovarian syndrome (PCOS), decreased NKB in the hypothalamic arcuate nucleus (ARC) may underlie reproductive neuroendocrine defects. We hypothesized that, in addition to NKB, its receptor, NK3R would also be decreased in prenatal T-treated sheep. NK3R-positive cells were observed in multiple hypothalamic nuclei, but prenatal T decreased NK3R only in the ARC. Dual-label immunocytochemistry revealed the decrease to be due, in part, to decreased colocalization within ARC kisspeptin cells that relay hormonal signals to GnRH cells. In addition, we found NK3R localized in presynaptie terminals contacting GnRH neurons, suggesting that NKB may regulate GnRH secretion by presynaptie actions. Based on our findings, we speculate that decreased NK3R contributes to the neuroendocrine defects seen in this animal model of PCOS
Recommended Citation
Ahn, TaeEun, "Prenatal Testosterone Excess Decreases Neurokinin 3 Receptor (NK3R) and Its Colocalization with Kisspeptin in the Ovine Arcuate Nucleus: Impact of Changes in Receptor Expression in an Animal Model of Polycystic ovarian syndrome (PCOS)" (2011). Digitized Theses. 3693.
https://ir.lib.uwo.ca/digitizedtheses/3693