In many species, the timing of puberty is different in males and females. This does not simply reflect differences in the time course of activation of the testes and ovaries. Rather, sex differences in pubertal onset reside within brain mechanisms controlling GnRH secretion, as exemplified by studies conducted in sheep. Exposure of sheep fetuses to testicular steroids alters the timing of puberty, principally by reducing photoperiod responsiveness. This is manifest as an early increase in LH secretion in males or in females exposed experimentally to testosterone before birth. Steroids also act on non-photoperiodic mechanisms to abolish the preovulatory gonadotrophin surge. In view of these multiple organizational actions of steroids to control postnatal gonadotrophin secretion, it is becoming clear that there are many critical periods of brain development for organizing the GnRH neurosecretory system, and that these may be sensitive to different testosterone metabolites. Although GnRH neurones are not sexually dimorphic with respect to number, distribution or gross morphology, fundamental questions remain as to how steroids exert their effects at the cell through actions on GnRH afferents. Teleologically, these early sex-specific changes in mechanisms timing puberty maximize the chance that reproductive activity will ultimately be successful in each sex.