THE EFFECTS OF GONADAL DEVELOPMENT AND SEX STEROIDS ON GROWTH-HORMONESECRETION IN THE MALE TILAPIA HYBRID (OREOCHROMIS-NILOTICUS X OREOCHROMIS-AUREUS)

Profiles of plasma growth hormone (GH) in male tilapia hybrid (Oreochr omis niloticus x O. aureus) were measured and compared at different ti mes of the year. The profiles did not appear to be repetitive, however , differences in their nature were observed at the different seasons; the most erratic profiles were seen in the height of the reproductive season (July), while the peaks were more subdued in the spring and dis appeared in the autumn. Peaks in male fish were more prominent than in the females when measured in July. Perifused pituitary fragments from fish with a high GSI responded to salmon gonadotropin-releasing hormo ne (sGnRH) analog (10 nM-1 mu M), while those from fish with a low GSI barely responded to even the highest dose. Exposure of perifused pitu itary fragments from sexually-regressed fish to carp growth hormone-re leasing hormone (cGHRH; 0.1 mu M) or sGnRH (1 mu M) stimulated GH rele ase only after injection of the fish with methyl testosterone (MT; 3 i njections of 0.4 mg kg-l). The same MT pretreatment did not alter the response to dopamine (DA; 1 or 10 mu M). GH pituitary content in MT-tr eated fish was lower than in control fish, which may be explained by t he higher circulating GH levels in these fish, but does not account fo r the increased response to the releasing hormones. Castration abolish ed the response of cultured pituitary cells to sGnRH (1 fM-100 nM) wit hout altering either their basal rate of secretion or circulating GH l evels. Addition of steroids to the culture medium (MT or estradiol at 10 nM for 2 days) enabled a GH response to sGnRH stimulation in cells from sexually regressed fish. Pituitary cells which had not been expos ed to steroids failed to respond to sGnRH, although their response to forskolin or TPA was similar to that of steroid-exposed cells. It woul d appear, therefore, that at least one of the effects of the sex stero ids on the response to GnRH is exerted proximally to the formation of cAMP, or PKC, presumably at the level of the receptor. An increase in the number of receptors to the GH-releasing hormones, following steroi d exposure, would explain also the changing nature of the GH secretory profile in different stages of the reproductive season.