Abstract:
Kisspeptin, a product of the Kiss1 gene is considered a potent stimulator of gonadotropin release, by interacting with its receptor, the G protein-coupled receptor 54. Kiss1 neurons are known to mediate the positive and negative feedback effects of oestradiol on GnRH neurons that control the pulsatile and surge secretion of GnRH. While in spontaneously ovulating mammals the GnRH/LH surge is initiated by a rise in ovarian oestradiol secreted from maturing follicles, in induced ovulators, the primary trigger is the mating stimulus. Damaraland mole rats (Fukomys damarensis) are cooperatively breeding, subterranean rodents that exhibit induced ovulation. We have previously described in this species the distribution and differential expression pattern of Kiss1-expressing neurons in the hypothalamus of males and females. Here we examine whether oestradiol (E2) regulates the hypothalamic Kiss1 expression in a similar way as described for spontaneously ovulating rodent species. By means of in situ hybridisation, we measured Kiss1 mRNA among groups of ovary-intact, ovariectomized (OVX) and OVX females treated with E2 (OVX + E2). In the arcuate nucleus (ARC), Kiss1 expression increased after ovariectomy and decreased with E2 treatment. In the preoptic region, Kiss1 expression after gonadectomy was similar to the level of wild-caught gonad-intact controls, but was dramatically upregulated with E2 treatment. The data suggest that, similar to other species, Kiss1 neurons in the ARC, which are inhibited by E2, play a role in the negative feedback control on GnRH release. The exact role of the Kiss1 neuron population in the preoptic region, which is stimulated by E2, remains to be determined.
