The Regulation of Gonadotropin-Releasing Hormone and Gonadotropin II by Sex Steroids in the Protandrous Black Porgy,Acanthopagrus schlegeli

Autor: Yu-shu shih, 石昱書
Rok vydání: 2001
Druh dokumentu: 學位論文 ; thesis
Popis: 89
The objectives were to investigate the in vivo and in vitro regulation of gonadotropin-releasing hormone (GnRH) and gonadotropin II (GTH II) using sex steroids in the protandrous black porgy, Acanthopagrus schlegeli. Estradiol-17b (E2) significantly stimulated plasma GTH II levels after 4 hour injection, and the stimulation could last for 9 days, whereas testosterone (T), 11-ketotestosterone (11-KT) and 5a-dihydrotestosterone had no effects. LHRH antagonist blocked E2-stimulatory effects in the stimulation of plasma GTH II levels. It is suggested that the stimulation of E2 on plasma GTH II levels is mediated through GnRH receptor. In vivo injection of sex steroids stimulated the levels of sbGnRH in the brain. T took 5 hours to increase brain sbGnRH levels, while E2 and 11-KT needed 2 days. During the spawning season, all sex steroids stimulated brain sGnRH and cGnRH-II levels; in non-spawning season, the stimulation in brain sGnRH levels was significantly occurred in midbrain, and E2 only increased brain cGnRH-II levels. Brain primary cell culture (in vitro) was developed in black porgy to further study GnRH regulation. Different doses of E2, T, and 11-KT were tested in brain cell culture. E2 stimulated the release of sbGnRH in 6 hours after treatment, while T and 11-KT only took one hour. The stimulation of sbGnRH occurred after 3 hours of cortisol treatment, but cholesterol had no effect. In the long-term experiment, the stimulation of 10-10 M E2 was the most significant group, both 10-10 and 10-8 M T had notable effects. 11-KT stimulated the release of sbGnRH one day after treatment, and the effect was lasted for 6 days. It is concluded that all sex steroids can increase brain GnRH levels both in vivo and in vitro. The mechanism of E2-stimulation in plasma GTH II levels may be due to the induced release of sbGnRH. It is not clear why T and 11-KT stimulated the increased GnRH levels but failed to induce the increased levels in plasma GTH II.
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