Abstract
Puberty is an important developmental milestone. It can be considered as a complex sequence of biological events leading to progressive maturation of sexual characteristics ultimately leading to attainment of full reproductive capacity. The decline in age at puberty in the general population has been paralleled by an increase in the number of girls referred for evaluation of precocious puberty (PP). The recent pubertal trends have resulted in a concomitant lowering of the lower limit of normality of the pubertal onset. However, evidence suggests that age at the gonadotropin and sex steroid surges have not changed. Thus, it looks as if an increasing proportion of contemporary early pubertal girls may experience isolated gonadotropinindependent thelarche rather than central PP, which may not be discernible on pubertal examination alone. Thus, the population-based limits of normality srapid progressive PP as well as intracranial and other underlying pathology. The initiation of mammalian puberty requires an increased pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. This increase is brought about by changes in transsynaptic and glial-neuronal communication. Coordination of these cellular interactions likely requires the participation of sets of genes hierarchically arranged within functionally connected networks. The role of kisspeptins in the control of GnRH neurons and the transmission of the regulatory actions of key signals, such as sex steroids, metabolic hormones and environmental cues, has been recently studied, point out that the Kiss1 system is an indispensable player of the brain sexual differentiation during early periods of maturation and the timing of puberty onset.
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