Secretion of gonadotropin releasing hormone (GnRH) and gonadotropins rises at puberty, but the neurochemical basis for this is unclear. Kisspeptin is a stimulator of GnRH secretion that is essential for puberty. Neurokinin B (NKB) and Dynorphin (DYN) co-localize to kisspeptin expressing cells in the arcuate nucleus (ARC) and are respective positive and negative regulators of kisspeptin secretion. Gonadotropin inhibitory hormone (GnIH) negatively regulates GnRH cells and may play a role in the pubertal transition. We aimed to determine gene expression for these neuropeptides across puberty in sheep.
Brains were harvested from male and female sheep (n=4/group) prior to (20 weeks) and following puberty (32 weeks) and gene expression was quantified by in situ hybridization. Kisspeptin cell number increased (P<0.05) during puberty in females but was reduced (P<0.05) in males in caudal ARC. Kisspeptin (Kiss1) gene expression was increased (P<0.05) by castration after puberty in males. Expression of NKB was unchanged across puberty, with no effect of castration. DYN cell number was higher (P<0.05) after puberty, but was reduced (P<0.05) by castration in males. GnIH mRNA expression decreased (P<0.05) after puberty in females but increased (P<0.01) in males and was reduced (P<0.01) by castration in males.
These data provide no definitive evidence for post-pubertal upregulation of either kisspeptin gene expression in ARC or NKB, the putative stimulator of kisspeptin secretion. Changes across puberty in DYN expression do not explain the rise in GnRH/gonadotropin secretion that occurs at this time. The reduction in GnIH expression across puberty in females is consistent with activation of reproductive function at puberty, but this is not seen in males. Castration effects in early post-pubertal animal differ from those recorded in adult animals. We conclude that changes in the expression of the genes examined in this study do not explain the pubertal process in sheep.