Abstract

The objective of the present study was to investigate the nature of the gonadotrophic stimulation of estradiol (E 2) secretion by the ovary of a teleost fish in vitro. Spontaneous output of E 2 decreased to a low baseline after 3 hr of superfusion and increased to a maximal level 2–3 hr after the introduction of homologous pituitary extract (T-PE) or human chorionic gonadotrophin into the superfusion system. Addition of the phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX, 0.5 m M), into a closed-system incubation resulted in an augmented response of the ovary to either dibutyryl cyclic AMP or to T-PE. It is concluded that the gonadotrophic stimulation of E 2 secretion from the ovary of Sarotherodon aureus is mediated by cyclic AMP as a second messenger. Purified carp GTH or ovine LH stimulated E 2 secretion in vitro in a dose-dependent manner in the range 3–300 ng/ml. In order to examine the effect of ovarian stage on E 2 secretion rate in response to a gonadotrophic stimulation, fish with regressed ovaries were transferred to 30° for 29 days. Five fish were bled every 4 days and their ovaries were incubated individually with and without T-PE. A sevenfold increase in plasma E 2 occurred 4 days after the transfer to 30°, whereas the first significant increase in the gonadosomatic index (GSI) could be noted only on Day 12. Both the spontaneous secretion rate of E 2 in vitro ( E 2 basal ) and the secretion rate in response to T-PE ( E 2 max ) increased together with the GSI throughout the experiment. However, the ratio E 2 max E 2 basal , which reflects the capacity of the ovary to respond to the gonadotrophic stimulation, reached a peak on Day 16, when GSI was about 1. The ratio then declined and remained low until the end of the experiment. The early increase in plasma E 2 can be explained by the elevated sensitivity of the ovary to GTH during the initial phase of the temperature-induced ovarian recrudescence. The high level of plasma E 2 maintained from Day 16 on may be due to a spontaneous synthesis and secretion of the steroid, not necessarily controlled by GTH.

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