It has been suggested that in mammals, glucocorticoids, beside their stress-related inhibitory effects on reproductive function, may also play a stimulatory role at the onset of puberty. Using the juvenile female eel as a model, we investigated the potential stimulatory role of cortisol (F) on pituitary gonadotropin (GtH-II). GtH-II levels were measured by RIA, and messenger RNA (mRNA) levels for alpha- and GtH-II beta-subunits were determined by dot blot using homologous probes. F treatment increased eel pituitary GtH-II content in vivo and in vitro. Using a long term, serum-free primary culture of pituitary cells, we studied the direct effect of F on GtH-II production. F increased the GtH-II cellular content in vitro in a dose- and time-dependent manner. The relative potencies of various corticosteroids on GtH-II were: triamcinolone acetonide > dexamethasone > F >> cortisone and aldosterone, indicating a glucocorticoid-specific receptor (GR). F stimulated GtH-II production through a selective increase in mRNA levels for GtH-II beta-subunit; no significant effect was observed on alpha-subunit mRNA levels. This stimulatory effect of F on GtH-II beta, played out directly at the pituitary cell level, recalls that of F on FSHbeta in the rat. The present study, performed in a primitive teleost at the juvenile stage, suggests that the role of F in the positive regulation of gonadotropins at puberty may have arisen early in vertebrate evolution.