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 that utilize excitatory and inhibitory amino acids as transmitters and astroglial 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 thus lead to idiopathic sexual precocity. According to this notion, such a premature activation of LHRH neuronal function would be neither associated with structural damage of the neuroendocrine brain system, nor related to a generalized activation of the neuronal-glial mechanisms underlying the onset of puberty. On the contrary, localized activation of discrete cellular subsets functionally connected to LHRH neurons would suffice to promote an increase in LHRH release of sufficient magnitude and duration to initiate the pubertal process.