GONADOTROPIN RELEASING MECHANISM VIA RECEPTORS OF PITUITARY CELLS IN POULTRY

(1)在母鸡垂体细胞中发现了具有高亲和力和低容量的促性腺激素释放激素受体。受体的平衡解离常数和每毫克膜蛋白的结合位点的最大数量在产蛋鸡比在nonlaying母鸡。单一肌内注射孕酮、雌二醇-17 β或5 α-双氢睾酮可引起非产蛋母鸡的Kd和Bmax值增加。在一个排卵周期中，Kd值和Bmax值在排卵前16 ~ 14 h和8 ~ 6 h呈下降趋势。单次静脉注射鸡LHRH-1引起的Kd和Bmax值在注射后2分钟内下降。这表明，母鸡垂体促性腺激素释放激素受体结合的卵巢类固醇激素的影响，在排卵周期中的变化可能与释放的促性腺激素从垂体。(2)孕酮受体的量在母鸡的垂体细胞的胞质部分被发现增加时，与雌二醇-17 β孵育1-4小时，但不孵育时，放线菌酮，放线菌素-D，或α-鹅膏蕈碱的存在。提示雌激素通过蛋白质合成途径增强鸡垂体细胞孕酮受体结合。(3)垂体细胞经17 β-雌二醇预孵育2 h后再与孕酮孵育4 h，细胞内黄体生成素含量增加。孕酮引起的细胞LH增加呈剂量依赖性。蛋白质合成抑制剂（放线菌酮，放线菌素-D，和α-鹅膏蕈碱）阻断细胞对孕酮的反应。提示孕酮通过蛋白质合成途径刺激雌激素致敏的母鸡垂体细胞LH的产生。

(1) Gonadotropin-releasing hormone receptors having a high affinity and low capacity have been found in the hen pituitary cells. The equilibrium dissociation constant of the receptor and the maximum number of binding sites per milligram of membrane protein were greater in laying hens than in nonlaying hens. A single i.m. injection of progesterone, estradiol-17beta, or 5alpha-dihydrotestosterone into nonlaying hens caused an increase in Kd and Bmax values. During an ovulatory cycle of the laying hen, Kd and Bmax values decreased from 16 to 14 h and 8 to 6 h before ovulation. A single i.v. injection of chicken LHRH-1 caused a decrease in the Kd and Bmax values within 2 min after the injection. It is suggested that the hen pituitary gonadotropin-releasing hormone receptor bindings are affected by ovarian steroid hormones and that their changes during the ovulatory cycle may relate to the release of a gonadotropin from the pituitary. (2) The amount of progesterone receptor in the cytosolic fraction of the pituitary cells of the hen was found to increase when incubated with estradiol-17beta for 1-4 h, but not when incubated with the presence of cycloheximide, actinomycin-D, or alpha-amanitin. It is suggested that the cytosolic progesterone receptor binding of the hen pituitary cells was enhanced by the action of estrogen through a protein synthesizing pathway. (3) The cellular content of Luteinizing hormone was found to increase when the pituitary cells were preincubated with estradiol-17beta for 2 h and then incubated with progesterone for 4 h. The increase in the cellular LH in response to progesterone was dose dependent. Protein synthesis inhibitors (cycloheximide, actinomycin-D, and alpha-amanitin) blocked the response of the cells to progesterone. It is suggested that LH production in estrogen-primed pituitary cells of the hen was stimulated by progesterone through a protein-synthesizing pathway.