Melatonin inhibits the gonadotropin-releasing hormone (GnRH)-stimulated secretion of luteinizing hormone and follicle-stimulating hormone from the pars distalis region of the neonatal rat pituitary gland. Over the initial weeks of postnatal life, this response to melatonin declines in parallel with a loss of iodo-melatonin binding sites. Although neonatal gonadotrophs have since been extensively used to study melatonin receptor signalling pathways, the mechanisms driving this phenomenon, together with its physiological significance, remain unknown. Melatonin receptors are expressed in the foetal pars distalis before activation of the GnRH system. Furthermore, the MT1 melatonin receptor promoter contains response elements for transcription factors involved in both pituitary differentiation and gonadotroph regulation. These data, coupled with the known ability of melatonin to regulate rhythmical gene expression in adult pars tuberalis cells, leads us to propose that melatonin acts in the developing animal as a regulator of internal synchrony between tissues.