This brief review has highlighted some of the major advances in the last decade or so in understanding the central control of puberty. These include the discovery that GnRH-I neurons develop in the olfactory placode and migrate into the forebrain, the recognition that puberty is a reactivation of GnRH secretion, the identification of leptin as a metabolic signal which may permit puberty to occur, unraveling the molecular basis of the circadian clock which underlies photoperiodic control of puberty in seasonal species, the identification of the structure of pheromones in urine, and the discovery of other populations of GnRH neurons in mammals expressing the GnRH-II gene. Such advances generate further questions: what regulates the migratory pathways of GnRH neurons, and what controls axon outgrowth and targeting to the median eminence? What is the mechanism which causes GnRH secretion to decline between the neonatal and pubertal phase of development? How do leptin and other sensory inputs finally communicate to the GnRH neuron? How do GnRH neurons communicate with each other such that co-ordinated pulsatile release of GnRH occurs? What is the function of GnRH-II? Some of these issues may be better addressed using the transgenic technologies which allow the identification and thus the recording, sampling and observation of GnRH neurons in living tissue, but in order to understand how internal and external cues influence puberty it will also be important to study a variety of other mammalian models in which the relative importance of such inputs differs.