Stimulation of salmon calcitonin on secretion of 17β-estradiol by the ovarian follicles of common carp, Cyprinus carpio

The effects of salmon calcitonin (sCT) on the secretion of 17b-estradiol (E2) were examined in female common carp, Cyprinus carpio. Vitellogenic stage fish adapted to high-Ca water were i.p. injected with vehicle, sCT, human chorionic gonadotropin (hCG), or hCG plus sCT. To determine whether ovarian follicles are equipped with CT receptors, a CT binding assay was conducted. In the in vitro experiments, vitellogenic follicles were incubated with stimulators and inhibitors. Administration of sCT increased the basal and hCG-stimulated E2 release in vivo and in vitro. Binding characteristics of [ 125 I]sCT to plasma membrane preparation of carp ovarian follicles showed saturability with high-affinity (KdZ48.48 pmol/l and BmaxZ1.2 pmol/mg protein). To clarify the mechanism of E2 production by sCT, in vitro effect of sCT and hCG on aromatase activity (conversion of testosterone to E2) and cytochrome P450 aromatase (P450arom) gene expression in carp ovarian follicles were investigated. Salmon CT-stimulated both aromatase activity and P450arom gene expression in ovarian follicles of carp. sCT-stimulated E2 release by the ovarian follicles in vitro was augmented in the presence of dibutyryl cAMP. Inhibitor of protein kinase A (PKA), SQ 22536 inhibited sCT-stimulated steroid production in a dose-dependent manner. Specific inhibitor of protein kinase C (PKC), NPC-15437 dihydrochloride had no inhibitory effects on sCT-induced E2 release. The present study indicates that sCT binds specifically to carp ovary and stimulates E2 production by increasing the activity of cytochrome P450 aromatase and P450arom gene expression. The results further suggest that stimulatory action of sCTon E2 production is mediated through cAMP pathway.