The secretion of LHRH from the median eminence, into hypophyseal portalblood provides a signal whereby the central nervous system interfaces with the endocrine system. The pulsatile nature of this system originates from phasic neural signals and, except in extreme cases where pulses are elimnated by the pituitary action of steroids, pulse frequency is determined by LHRH secretion. Steroidal feedback and other extrinsic influences that affect pulse frequency act via neural afferents to the LHRH neurons. Amplitude regulation may be by way of steroidal influence at the level of the pituitary gland, or indirectly via changes in LHRH pulse frequency. In this chapter, we have attempted to outline our current knowledge of factors regulating LHRH pulsatility and how this is transmitted into pulsatile gonadotrophin secretion. Regarding PRL secretion, we have outlined evidence that pulsatility is inherent in the lactotrophs, requiring no hypothalamic input. The possible roles of PRL releasing factors in circumstances like suckling and stress and of PRL inhibiting factors have been discussed with reference to the pulsatile nature of PRL secretion.