Stimulatory effect of RFRP-3 on the gonadotrophic axis in the male Syrian hamster: the exception proves the rule.

In seasonal mammals, a distinct photoneuroendocrine circuit that involves the pineal hormone melatonin tightly synchronizes reproduction with seasons. In the Syrian hamster, a seasonal model in which sexual activity is inhibited by short days, we have previously shown that the potent GnRH stimulator, kisspeptin, is crucial to convey melatonin's message; however, the precise mechanisms through which melatonin affects kisspeptin remain unclear. Interestingly, rfrp gene expression in the neurons of the dorsomedial hypothalamic nucleus, a brain region in which melatonin receptors are present in the Syrian hamster, is strongly down-regulated by melatonin in short days.

Early metabolic programming of puberty onset: impact of changes in postnatal feeding and rearing conditions on the timing of puberty and development of the hypothalamic kisspeptin system.

Kiss1 neurons have recently emerged as a putative conduit for the metabolic gating of reproduction, with leptin being a regulator of hypothalamic Kiss1 expression. Early perturbations of the nutritional status are known to predispose to different metabolic disorders later in life and to alter the timing of puberty; however, the potential underlying mechanisms remain poorly defined. Here we report how changes in the pattern of postnatal feeding affect the onset of puberty and evaluate key hormonal and neuropeptide [Kiss1/kisspeptin (Kp)] alterations linked to these early nutritional manipulations.

Kisspeptins: bridging energy homeostasis and reproduction.

Body energy reserves and metabolic state are relevant modifiers of puberty onset and fertility; forms of metabolic stress ranging from persistent energy insufficiency to morbid obesity are frequently linked to reproductive disorders. The mechanisms for such a close connection between energy balance and reproduction have been the subject of considerable attention; however, our understanding of the neurobiological basis for this phenomenon is still incomplete. In mid 1990s, the adipose-hormone, leptin, was proven as an essential signal for transmitting metabolic information onto the centers governing puberty and reproduction; yet, the ultimate mode of action of leptin on GnRH neurons has remained contentious for years.

Maturation of kisspeptinergic neurons coincides with puberty onset in male rats.

Kisspeptins, derived from the Kiss1 gene play a central role in activation of the hypothalamo-pituitary gonadal (HPG) axis via stimulation of GnRH neurons. Both Kiss1 and Kiss1R (receptor) mRNA levels are found to be low in pre-pubertal rats, but whether an increase in kisspeptin and/or its receptor is the primary component in the initiation of puberty and where in the hypothalamus regulation of the kisspeptin/Kiss1R system occurs is unresolved. Using immunohistochemistry and in situ hybridization, we analyzed the level of Kiss1 mRNA and kisspeptin-immunoreactivity in the anteroventral periventricular nucleus (AVPV) and the arcuate nucleus of male rats along pubertal development.

Comparison of the effects of peripherally administered kisspeptins.

Kisspeptins are structurally closely related peptides derived from the Kiss1 gene that have been demonstrated to stimulate the hypothalamo-pituitary gonadal axis. The natural peptide products derived from post-translational processing of the kisspeptin precursor have not been elucidated. We examined the acute effect on serum levels of free testosterone in the adult male mouse after systemic administration of kisspeptins with different lengths of both human and mouse origin.