Submitted to: Midwestern Section of the American Society of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: 11/2/2010
Publication Date: 9/1/2011
Citation: Lents, C.A. 2011. Advancement in understanding the central pathways that underlie the effects of exteroceptive signals on the gonadotropic axis of the female for initiation of puberty and maintenance of normal reproductive cycles [abstract]. Journal of Animal Science. 89 (E-Supplement 2):139 (Abstract #275).
Technical Abstract: Neural circuits within the brain regulate the proper temporal release of GnRH from hypothalamic neurons for the initiation of puberty and maintenance of normal reproductive cycles in the female. This process involves feedback from gonadal steroids and is metabolically gated. Full understanding of how these mechanisms are controlled, and the ability to manipulate them in domestic animals, remains elusive. Recent studies have demonstrated that RFamide peptides, such as kisspeptin and gonadotropin-inhibitory hormone (GnIH) play a critical role in this progression. Kisspeptin is a potent stimulator of LH secretion due to its direct action on GnRH cells. Kisspeptin neurons express estrogen receptor, and expression of kisspeptin mRNA in the hypothalamus changes with pubertal development and stage of the reproductive cycle. Gonadotropin-inhibitory hormone acts at the hypothalamus and pituitary gland to suppress secretion of LH. It has been implicated in control of the ovulatory surge of LH but the role of GnIH in pubertal development is not well established. Expression of GnIH is observed in areas of the hypothalamus that have important roles in regulating feeding behavior. Kisspeptin is a target for leptin signaling and may integrate metabolism with reproductive function. The recently identified adipocyte factor nesfatin-1 regulates feed intake and may additionally link metabolic state with the gonadotropic axis for the initiation of puberty through its effects at the hypothalamus. Advancing our understanding of how these central pathways function to control puberty is expected to lead to new strategies to increase gonadotropin secretion and minimize the number of replacement females that fail to reach puberty within acceptable production cycles.