Cox N M, Britt J H
J Anim Sci. 1982 Oct;55(4):901-8. doi: 10.2527/jas1982.554901x.
Two experiments were conducted to measure pituitary gonadotropins, hypothalamic-gonadotropin releasing hormone (GnRH) and pituitary response to GnRH during periods when serum luteinizing hormone (LH) was suppressed by estradiol-17 beta (e2) in ovariectomized pigs. In the first experiment, 10 ovariectomized gilts were assigned to two groups of five each according to time of slaughter (24 or 36 h after injection). Within each group, gilts were given corn oil (n = 2) or 400 micrograms E2 (n = 3). Neither serum nor anterior pituitary (AP) concentrations of follicle-stimulating hormone (FSH) were affected by E2. Serum LH was suppressed from 12 to 26 h after E2. Concentrations of LH in AP were unchanged at 24 h, but increased at 36 h after E2 injection. Concentrations of GnRH in medial basal hypothalamus (MBH), stalk-median eminence (SME) and hypophyseal portal area (HPA) were lower at 24 h after E2 than in oil-treated gilts. At 36 h after E2, suppressive effects of E2 on LH in serum had subsided and concentrations of LH in AP and GnRH in MBH and SME were greater than in oil-treated controls. The observation that E2 suppressed LH in serum without a detectable suppression of LH in AP led to the hypothesis that E2 had caused the suppression of serum LH by suppression of GnRH release. In a second experiment, 12 ovariectomized gilts were assigned to receive corn oil (n = 4), 400 micrograms E2 (n = 4) or 400 micrograms E2 plus GnRH (1.5 micrograms/h; n = 4). Patterns of LH in sera of E2-treated animals were similar to those in the first experiment, with serum LH in E2-treated gilts suppressed from 4 to 32 h after treatment. However, in gilts receiving GnRH in addition to E2, serum LH concentrations during 20 to 32 h after treatment were intermediate between gilts receiving E2 alone and controls. Thus the pituitary of the pig is capable of responding to GnRH when LH is normally suppressed by E2. These experiments provide two lines of evidence that suppression of serum LH by E2 is due at least in part to suppression of GnRH. These experiments also establish the hypothalamus as a site for negative feedback of E2 in the female pig.
进行了两项实验，以测量去卵巢猪在血清促黄体生成素（LH）被17β-雌二醇（E2）抑制期间的垂体促性腺激素、下丘脑促性腺激素释放激素（GnRH）以及垂体对GnRH的反应。在第一个实验中，根据屠宰时间（注射后24或36小时）将10头去卵巢小母猪分为两组，每组5头。在每组中，给小母猪注射玉米油（n = 2）或400微克E2（n = 3）。E2对血清和垂体前叶（AP）中促卵泡生成素（FSH）的浓度均无影响。E2注射后12至26小时血清LH被抑制。E2注射后24小时，AP中LH的浓度未发生变化，但在36小时时升高。E2注射后24小时，内侧基底部下丘脑（MBH）、垂体柄-正中隆起（SME）和垂体门脉区（HPA）中GnRH的浓度低于注射玉米油的小母猪。E2注射后36小时，E2对血清中LH的抑制作用减弱，AP中LH的浓度以及MBH和SME中GnRH的浓度高于注射玉米油的对照组。E2抑制血清LH但未检测到对AP中LH的抑制这一观察结果导致了这样的假设，即E2通过抑制GnRH释放导致血清LH受到抑制。在第二个实验中，将12头去卵巢小母猪分为三组，分别接受玉米油（n = 4）、400微克E2（n = 4）或400微克E2加GnRH（1.5微克/小时；n = 4）。E2处理组动物血清中LH的变化模式与第一个实验相似，E2处理的小母猪血清LH在处理后4至32小时被抑制。然而，在除E2外还接受GnRH的小母猪中，处理后20至32小时血清LH浓度介于单独接受E2的小母猪和对照组之间。因此，当LH正常情况下被E2抑制时，猪的垂体能够对GnRH作出反应。这些实验提供了两条证据，表明E2对血清LH的抑制至少部分是由于对GnRH的抑制。这些实验还确定下丘脑是雌性猪中E2负反馈的位点。
