Study summary · research use only
Kisspeptin and puberty in mammals
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses kisspeptin and its receptor (G-protein coupled receptor 54) in relation to puberty in mammals (species not specified). The authors propose a hypothesis that arcuate nucleus (ARC) kisspeptin neurons are critical for puberty because they are an integral component of the hypothalamic GnRH pulse-generating mechanism that drives intermittent release of the decapeptide, an increase in GnRH being obligatory for the onset of puberty, rather than ARC kisspeptin neurons playing a direct "regulatory" role in the timing of puberty. The review characterizes ARC kisspeptin neurons as part of the neural network responsible for GnRH pulse generation, subserving upstream regulatory mechanisms responsible for the timing of puberty.
Abstract
Since the discovery of the G-protein coupled receptor 54 (kisspeptin receptor) and its ligand, kisspeptin, our understanding of the neurobiological mechanisms that govern the pituitary-gonadal axis has evolved dramatically. In this chapter, we have reviewed progress regarding the relationship between kisspeptin and puberty, and have proposed a novel hypothesis for the role of kisspeptin signaling in the onset of this crucial developmental event. According to this hypothesis, although kisspeptin neurons in the arcuate nucleus (ARC) are critical for puberty, this is simply because these cells are an integral component of the hypothalamic GnRH pulse generating mechanism that drives intermittent release of the decapeptide, as an increase in GnRH is obligatory for the onset of puberty. In our model, ARC kisspeptin neurons play no "regulatory" role in controlling the timing of puberty. Rather, as a component of the neural network responsible for GnRH pulse generation, they subserve upstream regulatory mechanisms that are responsible for the timing of puberty.
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