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Reproduction (endocrinology)
Articles on the role of kisspeptin on modulation of the HPG axis.
Environmental factors such as photoperiod play a regulatory role in the HPG axis via regulation of GnRH production (Porkka-Heiskanen et al., 1997). In view of its major role in the regulation of the GnRH neuron, kisspeptin neurons were hypothesised to relay photoperiod effects on GnRH neurons in seasonally breeding species.
In the AVPV of rats, females have 12-fold higher KiSS-1 expression than males, probably in order to produce a synchronised LH surge. This elevation appears to be due to steroid exposure during neonatal life.
It has been known for many years that the HPG axis is under the control of steroid hormone feedback from the gonads. Steroid hormone levels fluctuate across the cycle in females (Almond and Dial, 1990; Gill et al., 2002; Karsch and Evans, 1996; Moenter et al., 2003). However, the mediator of steroid hormone feedback has remained elusive for many years, as GnRH neurons only possess estrogen receptor β (ERβ) which does not play a role in feedback (Herbison and Pape, 2001). Therefore, neurons upstream of the GnRH neuron, which possess estrogen receptor α (ERα), progesterone receptor (PR) and androgen receptor (AR) have been sought as possible mediators of steroid effects on GnRH release.
It has been known for many years that the HPG axis is under the control of steroid hormone feedback from the gonads. Steroid hormone levels fluctuate across the cycle in females (Almond and Dial, 1990; Gill et al., 2002; Karsch and Evans, 1996; Moenter et al., 2003). However, the mediator of steroid hormone feedback has remained elusive for many years, as GnRH neurons only possess estrogen receptor β (ERβ) which does not play a role in feedback (Herbison and Pape, 2001). Therefore, neurons upstream of the GnRH neuron, which possess estrogen receptor α (ERα), progesterone receptor (PR) and androgen receptor (AR) have been sought as possible mediators of steroid effects on GnRH release.
KiSS-1 mRNA and protein have been localised in the ARC and the AVPV of the rodent hypothalamus, with a small group of neurons also being identified in the periventricular nucleus (PeN) (Clarkson and Herbison, 2006; Gottsch et al., 2004; Kauffman et al., 2007a).
Acute injection of kisspeptin stimulates LH release and repeated injections produce LH pulses (Tovar et al., 2006).
The expression of both kisspeptin and its receptor in the hypothalamus and pituitary respectively, and their crucial role in puberty suggests that kisspeptins may also be key regulators of the HPG axis in adults. In gpr-54 -/- and KiSS-1 -/- mice, LH levels were found to be significantly lower than in wild type (WT) mice even though GnRH receptor levels were normal and GnRH could elicit a robust LH stimulation.
The realisation of the pivotal role of the KiSS-1/gpr-54 system stimulated further research in the quest to elucidate the mechanistic details. KiSS-1 and possibly gpr-54 hypothalamic mRNA levels increase with pubertal maturation in mice (Han et al., 2005), rats (Sun et al., 2007) and primates (Keen et al., 2008; Shahab et al., 2005).
At the same time as gpr-54 mutations were being found to cause iHH in humans, a gpr-54 knockout mouse had been produced with similar findings to those from the patients described above. Gpr-54 -/- male mice had small testes, delayed puberty and reduced sexual behaviour and females had small ovaries and uteri, delayed vaginal opening, no maturation of follicles in the ovary and reduced sexual behaviour.
As well as inactivating mutations of the gpr-54 receptor, a mutation, R386P, apparently caused prolonged signalling of the receptor leading to precocious puberty in a 8-year old girl (Teles et al., 2008).
KiSS-1 was first shown to play a role in the reproductive axis in 2003, when two groups discovered that mutations in the gpr-54 receptor led to idiopathic hypogonadotropic hypogonadism (iHH)