Role of Kisspeptin and Neurokinin B in Puberty in Female Non-Human Primates. Review

Abstract

Pubertal onset and subsequently reproduction result from the awakening of a complex neuroendocrine machinery leading to the acceleration of the gonadotropin-releasing hormone (GnRH) secretion by the hypothalamus. Several neuronal, glial or peripheral factors have been identified as playing a major role in the onset of puberty1. This paper reviews data obtained in non-human primates illustrating the crucial role played by kisspeptin and neurokinin B (NKB) in this pubertal activation of GnRH secretion. Both kisspeptin and NKB signaling appear to contribute to the pubertal increase in GnRH release independently or in concert in females while there seems to have no interaction between kisspeptin and NKB in sexually immature females. The contribution of direct NKB signaling to GnRH release, however, may be secondary, as NKB signaling to GnRH release does not change across puberty, whereas NKB signaling to kisspeptin release greatly increases. Thus, in females, kisspeptin signaling appears to be the main force driving the pubertal GnRH release increases. The role of NKB in the pubertal increase in GnRH release, however, requires further experiments. In females, reciprocal signaling pathways between kisspeptin and NKB neurons could provide the necessary efficiency and flexibility for the stimulation of GnRH release, which ensures complex reproductive functions, such as cyclic ovulations and pregnancy.