PubMed2002
Sexual development after birth in rodents, nonhuman primates, and humans is driven by the gonadotropin-releasing hormone (GnRH) pulse generator. During the neonatal period in primates, pulsatile GnRH discharge from the medial basal hypothalamus drives an active period of pituitary gonadotropin and gonadal hormone secretion. During the transition from the neonatal to the juvenile period, however, the activity of the GnRH pulse generator is restrained or arrested and gonadotropin and gonadal hormone secretion enters a quiescent period that continues until the onset of puberty. As puberty approaches the GnRH pulse generator is reactivated, resulting in enhanced gonadotropin secretion, accelerated growth, maturation of the gonads, and the achievement of sexual competence. Rodents do not appear to exhibit a developmental phase analogous to the quiescent juvenile period in primates when the GnRH pulse generator is held in check. Instead, progressive maturational changes in the pattern of GnRH pulsatility appear to drive sexual development in rodents. The role that leptin plays in sexual development has not been fully defined, but the balance of current evidence appears to support the idea that, in both rodents and primates, leptin plays a permissive rather than a causal role in timing this process. When body energy reserves rise above a critical level, blood leptin increases to a threshold concentration signaling to the central nervous system that the body can support sexual function. Puberty can apparently occur over a wide range of concentrations above this critical leptin threshold. Leptin does not appear to act as a trigger to time the initiation of puberty but, instead, once leptin reaches this threshold pubertal development may proceed if, and only if, other critical control mechanisms are operational.