Gonadotropin releasing hormone is produced by cells in the medial-basal hypothalamus and delivered to the portal circulation via the GnRH-tuberoin-fundibular tract. The arcuate nucleus is the central site of action, releasing GnRH into the portal circulation in a pulsatile fashion. Normal gonadotropin secretion requires pulsatile GnRH discharge within a critical range in frequency and amplitude (Knobil 1980). This critical range of GnRH pulsatile secretion is rather narrow, and increased GnRH pulse frequency or dose will eliminate gonadotropin secretion. Decreasing the pulse frequency decreases luteinizing hormone (LH) secretion but increases follicle stimulating hormone (FSH) secretion. Elegant studies by Filicori showed that GnRH pulse frequencies were at every 94, 71, 103, and 216 min in the early follicular, late follicular, early luteal, and late luteal phases of the menstrual cycle (Filicori et al. 1986) respectively. GnRH secretion is regulated by norepinephrine (facilitory) and dopamine (inhibitory). In turn, the catecholamine system can be influenced by endorphins. Furthermore, serotonin and melatonin are also instrumental in this regulation. Since GnRH neurons lack estrogen receptors, estrogen control of GnRH secretion is modulated through neurotransmitters.