Comparable to the period of pubertal transition, sleep also exerts profound effects on episodic gonadotropin secretion in adult women. During the early follicular phase of the menstrual cycle, a sleep-induced slowing of luteinizing hormone (LH) secretion occurs concurrently with a rise in LH pulse amplitude. A selective increase in opioidergic, but not in dopaminergic or serotoninergic activity may account for this decline in LH pulsatility. In addition, sleep-reversal studies have confirmed that the presence of sleep is essential for the expression of this neuroendocrine function. Since pituitary gonadotropin responsiveness to gonadotropin-releasing hormone (GnRH) is virtually unchanged during sleep, the reasons for the enhanced LH pulse amplitude remain unresolved. This sleep-associated increase in opioidergic activity may be restricted to a hypothalamic site, since opiate blockade does not modify the gonadotropin response to GnRH stimulation. In addition, circadian variability is shown in terms of gonadotropin secretion in regularly cycling women; this may again represent sleep-associated effects on gonadotropin release. Although the physiological importance of sleep-associated neuroendocrine phenomena remains basically unexplained, the observed changes in LH secretory profiles during sleep in adult women suggest close functional links between the endocrine secretion and the rest-activity cycle of the brain.