Testosterone and Estradiol Potentiate the Serum Gonadotropin Response to Gonadotropin-Releasing Hormone in Goldfish1

Abstract

The effects of gonadal steroids on gonadosomatic index (GSI; gonad wt/total body wt x 100), pituitary gonadotropin (GTH) content, and serum GTH response to [D-Ala6,Pro9-Net]-luteinizing hormone-releasing hormone (LHRH-A) were investigated throughout the seasonal reproductive cycle of the goldfish. Gonad-intact female fish were implanted i.p. for 5 days with silastic pellets containing no steroid (blank), testosterone (T; 100 micrograms/g), or estradiol (E2; 100 micrograms/g). The serum GTH response at 6 h following i.p. injection of saline or 0.1 microgram/g LHRH-A was assessed. In blank-implanted, saline-injected animals, seasonal variations in GSI, pituitary GTH content, and serum GTH levels were evident; maximal and minimal levels were noted in the spring and summer months, respectively. In blank-implanted fish, LHRH-A effectively stimulated GTH release in females undergoing gonadal recrudescence (late autumn and winter) and in sexually mature (spring) females, but not in sexually regressed (summer and early autumn) females. Implantation of T or E2 raised serum steroid levels to those found during ovulation in goldfish. Steroid treatments did not affect unstimulated serum GTH levels at any time of the year. Testosterone effectively potentiated the serum GTH response to LHRH-A during the entire reproductive cycle, whereas the positive effects of E2 were evident in sexually regressed and post-spawning females only. Both T and E2 potentiated the GTH response to LHRH-A in male fish. To examine the involvement of T aromatization in mediating its actions on induced GTH secretion, male and female fish were implanted with T or the nonaromatizable androgens 5 alpha-dihydroxytestosterone (DHT; 100 micrograms/g) and 11-keto-testosterone (11-KT; 250 micrograms/animal). Testosterone potentiated the GTH response to LHRH-A in both males and females whereas DHT and 11-KT were without effect. Furthermore, the positive action of T on induced GTH secretion was blocked by 2-day pretreatment with the aromatase inhibitor 1,4,6-androstatrien-3,17-dione (100 or 300 micrograms/g). Multiple i.p. injections of hCG (0.2 microgram/g every 3 days for 39 days), probably through stimulation of endogenous T secretion, resulted in potentiation of the GTH response to LHRH-A in mature male goldfish. These results clearly demonstrate that T, through aromatization to E2, can increase pituitary responsiveness to exogenous LHRH-A in gonad-intact male and female goldfish.

Profiling neuroendocrine gene expression changes following fadrozole-induced estrogen decline in the female goldfish

“…In goldfish, serum E2 levels exhibit a distinct seasonal profile with an increase around April and May, corresponding to the prespawning period (55). Accordingly, a similar seasonal profile for aromatase activity (42) and AroB expression (71) has been observed in the neuroendocrine brain Tel and Hyp.…”

Endocrine disruptors in the environment (IUPAC Technical Report)

“…In female rainbow trout, the concentration of vitellogenin in plasma increases million-fold during this period and can reach levels of tens of milligrams per liter. In adult male fish (e.g., rainbow trout), circulating levels of endogenous estradiol are nearly undetectable, but there is some evidence that other teleost male fish do synthesize small amounts of estradiol, and that the hormone may regulate the production of the male androgens 11-ketotestosterone and testosterone [38,39]. Although the vitellogenin gene is also present in male fish, no remarkable concentrations of vitellogenin can be detected, presumably due to the very low concentration of plasma estradiol.…”

Estradiol Stimulates Growth Hormone Production in Female Goldfish

“…Female goldfish at the end of the spawning season were implanted for 5 days with silastic pellets containing E 2 (100 µg/g) or no steroid (control) as previously described (Trudeau et al, 1991). This treatment raises serum E 2 levels to 5-10 ng/ml, approximating the concentrations of E 2 observed during natural ovulation.…”