Vacher Coralie, Ferrière François, Marmignon Marie-Hélène, Pellegrini Elisabeth, Saligaut Christian
Endocrinologie Moléculaire de la Reproduction, UMR CNRS 6026, Campus de Beaulieu, 35042 Rennes Cedex, France.
Gen Comp Endocrinol. 2002 Jun 15;127(2):198-206. doi: 10.1016/s0016-6480(02)00046-1.
The role of sexual steroids in the modulation of a dopaminergic inhibitory tone on FSH and LH release was studied in the rainbow trout. The experiments were performed on previtellogenic trout, implanted or not with estradiol (E(2)), and vitellogenic trout. E(2) implant increased the circulating levels of LH and decreased the circulating levels of FSH in previtellogenic fish. The catecholamine inhibitor alphaMPT increased the circulating levels of LH, implanted or not with E(2). AlphaMPT increased circulating levels of LH in vitellogenic fish. This increase could be prevented by the dopaminergic agonist bromocryptine. The dopaminergic drugs had no effect on the circulating levels of FSH in all groups. E(2) decreased mRNA levels of sGnRH1 and sGnRH2 in the telencephalon of previtellogenic fish. The dopaminergic treatments had no effect on mRNA levels of both forms of sGnRH in previtellogenic and vitellogenic fish. Primary cultures of pituitary cells were primed for three days with steroids (E(2) or 17alpha-hydroxy, 20beta-dihydroprogesterone (17alpha20betaP)) before treatment with increasing doses of bromocryptine, associated or not with sGnRH. E(2), but not 17alpha20betaP, potentiated the sGnRH-induced release of LH. Bromocryptine induced a slight dose-dependent decrease of sGnRH-induced release of LH. This decrease was potentiated by 17alpha20betaP. E(2) and 17alpha20betaP had no effect on the release of FSH, but bromocryptine decreased the 10(-8)M sGnRH-induced release of FSH. In conclusion, the development of the dopaminergic inhibitory tone on gonadotropin release, at the onset of vitellogenesis, requires factors other than estradiol. E(2) should contribute in part to decrease the release of FSH. At the end of the reproductive cycle, 17alpha20betaP should reinforce the dopaminergic inhibitory tone.
在虹鳟鱼中研究了性类固醇在调节多巴胺能对促卵泡激素(FSH)和促黄体生成素(LH)释放的抑制性调节作用中的角色。实验在未成熟卵母细胞期的虹鳟鱼上进行,这些鱼被植入或未植入雌二醇(E₂),同时也对卵黄生成期的虹鳟鱼进行了实验。在未成熟卵母细胞期的鱼中,植入E₂会增加LH的循环水平,并降低FSH的循环水平。儿茶酚胺抑制剂α-甲基对酪氨酸(alphaMPT)会增加LH的循环水平,无论是否植入E₂。alphaMPT会增加卵黄生成期鱼中LH的循环水平。这种增加可被多巴胺能激动剂溴隐亭阻止。多巴胺能药物对所有组中FSH的循环水平均无影响。E₂会降低未成熟卵母细胞期鱼端脑中促性腺激素释放激素1(sGnRH1)和促性腺激素释放激素2(sGnRH2)的mRNA水平。多巴胺能处理对未成熟卵母细胞期和卵黄生成期鱼中两种形式的sGnRH的mRNA水平均无影响。垂体细胞原代培养物在用类固醇(E₂或17α-羟基-20β-二氢孕酮(17α20βP))预处理三天后,再用递增剂量的溴隐亭处理,同时添加或不添加促性腺激素释放激素(sGnRH)。E₂而非17α20βP会增强sGnRH诱导的LH释放。溴隐亭会导致sGnRH诱导的LH释放出现轻微的剂量依赖性降低。这种降低会被17α20βP增强。E₂和17α20βP对FSH的释放均无影响,但溴隐亭会降低10⁻⁸M sGnRH诱导的FSH释放。总之,在卵黄生成开始时,多巴胺能对促性腺激素释放的抑制性调节作用的发展需要除雌二醇之外的其他因素。E₂应部分有助于降低FSH的释放。在生殖周期结束时,17α20βP应增强多巴胺能的抑制性调节作用。