New thoughts on female precocious puberty

Much effort has been devoted in recent years to unravel the neuroendocrine mechanisms responsible for the initiation of mammalian puberty. The concept that has emerged is that puberty results from the unfolding of a centrally originated process involving the concerted influence of neuronal systems t hat utilize excitatory and inhibitory amino acids as transmitters and astro glial networks: that produce growth factors able to affect LHRH secretion. We discuss the idea that an isolated alteration of each of these components may result in the precocious activation of pulsatile LHRH release, and thu s lead to idiopathic sexual precocity. According to this notion, such a pre mature activation of LHRH neuronal function would be neither associated wit h structural damage of the neuroendocrine brain system, nor related to a ge neralized activation of the neuronal-glial mechanisms underlying the onset of puberty. On the contrary, localized activation of discrete cellular subs ets functionally connected to LHRH neurons would suffice to promote an incr ease in LHRH release of sufficient magnitude and duration to initiate the p ubertal process.