Abstract. Glucocorticoids have heterogeneous effects on reproductive function. We used a gonadotropin-primed, immature rat model to study the influence of dexamethasone (1 mg/kg), given during the latter stages of follicular development, on litter size, the number of oocytes released, and pituitary hormone levels. Dexamethasone-treated females released a larger number of oocytes at ovulation and gave birth to larger litters indicating the oocytes were viable. Survival to weaning age was not affected but average weight at weaning was lower for pups born to DEXtreated females. Serum FSH and LH were assayed at 12, 24 and 48 h following eCG and did not differ between dexamethasone-treated and control animals, but prolactin showed a prolonged pattern of elevation in DEX-treated females. Prolactin, which normally exhibits an elevation on proestrous, may modulate follicular development. Dexamethasone enhances fertility and fecundity possible through an effect of prolactin on follicle development, or by other direct effects on the ovary. These results may improve our understanding of the usefulness of DEX in assisted reproductive therapies for women. Key words: Fecundity, Glucocorticoids, Ovary (J. Reprod. Dev. 55: [247][248][249][250][251] 2009) eproductive function is often suppressed by the elevation of endogenous, or administration of exogenous, glucocorticoids. Anovulation and menstrual or estrous cycle disruptions can occur in conditions marked by adrenal hyperactivity (e.g. Cushing's Syndrome), or when women or animals experience chronic stimulation of the hypothalamic-pituitary-adrenal axis [1]. Glucocorticoidrelated reproductive suppression may involve disruption of central [1][2][3][4][5] and peripheral [6][7][8][9][10] functions of the reproductive axis as demonstrated by work in multiple species including rats [11][12][13], mice [14], sheep [15][16][17], humans [18,19] and other primates [7,20].The suppressive effect of glucocorticoids, however, is not universal. Synthetic corticoids variably stimulate the release of pituitary hormones, follicle stimulating hormone (FSH), luteinizing hormone (LH) and prolactin (PRL) [21], enhance FSH action in the follicular phase of the cycle [10], and may accelerate the timing of ovulation and increase the number of oocytes released [22][23][24][25]. In addition, acute exposure to stressful stimuli (e.g. restraint), presumably activating the endogenous hypothalamic-pituitary-adrenal axis, can enhance ovulation and increase fertility [26]. These stimulatory effects have been reported in rodent models, especially the rat, usually following treatment with dexamethasone (DEX) but triamcinolone acetonide, corticosterone and cortisol have also been used and some of these compounds give similar results [23,27]. Prior studies did not assess whether DEX-enhanced reproductive function also impacted fertility or offspring quality. The immature, gonadotropin-primed rat model is commonly used to assess follicular development, ovarian steroidogenesis, and ovulation. Because these ani...