In vivo and in vitro sex steroids stimulate seabream gonadotropin-releasing hormone content and release in the protandrous black porgy, Acanthopagrus schlegeli.

The objective of the present study was to investigate the regulation of seabream gonadotropin-releasing hormone (sbGnRH) release using in vivo and in vitro approaches in the protandrous black porgy, Acanthopagrus schlegeli. Estradiol-17beta (E2), testosterone (T), and 11-ketotestosterone (11-KT) were found to significantly stimulate the increase of sbGnRH levels in pituitary of black porgy after 5-96 h of injection. An in vitro culture system using dispersed brain neurons was also developed to investigate the effects of various steroids on sbGnRH release. Different doses (10(-6) - 10(-12) M) of E2, T, 11-KT, and cortisol were applied during 6 h experiment. KCl stimulated sbGnRH release at a dose- and time-dependent manner. The concentration of sbGnRH increased 2-fold in the highest dose of KCl treatment compared to the control. Treatments with E2, T, 11-KT and cortisol significantly stimulated the release of sbGnRH from the cultured brain neurons. The concentration of sbGnRH in medium was increased by 2-, 1.9-, 2.1-, and 4.9-fold when treated with E2, T, 11-KT, and cortisol, respectively, as compared to the respective control. Cholesterol did not have any stimulatory effects in the release of sbGnRH. The results showed that sex steroids and cortisol had direct effect on brain neuronal cells stimulating the release of sbGnRH.

Aromatase inhibitors block natural sex change and induce male function in the protandrous black porgy, Acanthopagrus schlegeli Bleeker: possible mechanism of natural sex change.

The objectives of the present study were to investigate the effects of oral administration of aromatase inhibitors on sex change, milt volume, 11-ketotestosterone (11-KT), and LH in plasma; aromatase activity in gonad, pituitary, and brain in the protandrous fish, black porgy (Acanthopagus schlegeli Bleeker). Two-year-old functional male black porgy were divided into two groups; one was fed a control diet and the other was fed a diet mixed with aromatase inhibitors (AIs; fadrozole and 1,4,6-androstatriene-3,17-dione, each 10 mg/kg feed) for 8.5 mo. A significantly higher gonadosomatic index was observed in the AI group. Fish treated with AIs showed complete suppression of natural sex change. Significantly higher levels of plasma 11-KT, LH, and milt volume were shown in the AI group than the controls. Lower aromatase activity in the gonad, pituitary, forebrain, midbrain, and hindbrain in concordance with the suppression of sex change was observed in the AI group. The data show that aromatase is directly involved in the mechanism of natural sex change of protandrous black porgy. AIs also enhanced male function in concordance with the elevated plasma levels of 11-KT and spermiation in milt volume.

Cold-stress induced the modulation of catecholamines, cortisol, immunoglobulin M, and leukocyte phagocytosis in tilapia.

The concentrations of norepinephrine in hypothalamus and norepinephrine and epinephrine in head kidney were significantly decreased in treated tilapia (Oreochromis aureus) during the time course of cold exposure (12 degrees) as compared to the control (25 degrees). The elevation of norepinephrine and epinephrine in plasma was detected earlier than that of cortisol in cold-treated tilapia. Phagocytic activity of leukocytes and the levels of plasma immunoglobulin M (IgM) were depressed in cold-treated tilapia as compared to the control group. Handling stress in the control (25 degrees) also resulted in increased plasma cortisol and decreased plasma IgM levels but not phagocytic activity. In vitro cortisol suppressed leukocyte phagocytosis in a dose (10(-12) to 10(-4) M)-dependent manner. Adrenergic agonist (phenylephrine and isoproterenol) had a significant suppression of phagocytosis only at the highest dose (10(-4) M). No effect on phagocytosis was detected in the treatment with norepinephrine and epinephrine. A combination of cortisol and isoproterenol (0.1 mM) had an additive effect in the suppression of phagocytosis. It is concluded that the cold stress modulated the changes of catecholamines and cortisol and further depressed phagocytic activity and antibody levels in tilapia. Cortisol could play a main and important role in the down-regulation of phagocytic activity. Adrenergic agonists also could interact with cortisol to further suppress immunity in tilapia.

Estradiol-17beta triggers luteinizing hormone release in the protandrous black porgy (Acanthopagrus schlegeli Bleeker) through multiple interactions with gonadotropin-releasing hormone control.

We investigated the mechanism of estradiol-17beta (E2) action on stimulation of LH (=gonadotropin II) release in the black porgy fish (Acanthopagrus schlegeli Bleeker) using an in vivo approach and primary cultures of dispersed pituitary cells in vitro. In vivo, E2 but not androgens (testosterone [T] and 11-ketotestosterone [11-KT]) significantly stimulated plasma LH in a dose-dependent manner. Estradiol-17beta also increased brain content of seabream GnRH. GnRH antagonist prevented E2 stimulation of LH release in vivo, indicating that the effect of E2 on LH was mediated by GnRH. In vitro, sex steroids (E2, T, 11-KT) alone had no effect on basal LH release in the cultured pituitary cells, but GnRH significantly stimulated LH release. Estradiol-17beta potentiated GnRH stimulation of LH release, an effect that was inhibited by GnRH antagonist, and 11-KT, but not T, also potentiated GnRH stimulation of LH release. The potentiating effect of 11-KT on GnRH-induced LH release in vitro was stronger than that of E2. These data suggest that E2 triggers LH release in vivo by acting both on GnRH production at the hypothalamus and on GnRH action at the pituitary. In contrast, 11-KT may only stimulate GnRH action at the pituitary. The E2) induction of LH release, through multiple interactions with GnRH control, supports a possible central role of E2in the sex change observed in the protandrous black porgy.