Hyde J F, Keller B K
Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington 40536-0084.
Endocrinology. 1991 Feb;128(2):917-22. doi: 10.1210/endo-128-2-917.
Lactotrophs, somatotrophs, and thyrotrophs have been shown to contain immunoreactive galanin. Furthermore, estrogen stimulates galanin mRNA and peptide levels in the rat anterior pituitary, particularly within lactotrophs. To determine whether galanin is released from the anterior pituitary in a regulated manner, we used cultured pituitary cells from male and ovariectomized Fischer 344 rats implanted with estrogen-containing capsules. Anterior pituitary cells (5 x 10(5) cells/well) were challenged (0.5-3 h) with hypothalamic factors known to regulate anterior pituitary hormone secretion, and medium galanin levels were measured by RIA. In female pituitary cells, galanin secretion was inhibited by dopamine (10 and 100 nM) and stimulated by TRH (20 and 100 nM). Although galanin release was significantly lower in male pituitary cells, dopamine and TRH inhibited and stimulated galanin secretion, respectively. Medium galanin levels were also significantly reduced by somatostatin (5 nM) in both female and male cells. The pattern of PRL release in response to dopamine, TRH, and somatostatin was similar to that observed for galanin, regardless of the sex of the pituitary donor. Although galanin has been localized in somatotrophs, 5 nM GH-releasing hormone (GRF) failed to alter galanin release in male as well as female pituitary cells; GH secretion was significantly increased by GRF. LHRH (5 nM) and CRF (5 nM) failed to alter galanin release in vitro. We conclude that in estrogen-exposed pituitary cells obtained from male and ovariectomized Fischer 344 rats: 1) galanin secretion is inhibited by dopamine and somatostatin, and stimulated by TRH; 2) GRF, LHRH, and CRF do not regulate galanin release in these cells; and 3) the profile of the regulated pathway for galanin release suggests that the primary location of galanin is the lactotroph, probably within secretory granules.
已证实催乳素细胞、生长激素细胞和促甲状腺激素细胞含有免疫反应性甘丙肽。此外,雌激素可刺激大鼠垂体前叶中甘丙肽的信使核糖核酸(mRNA)和肽水平,尤其是在催乳素细胞内。为了确定甘丙肽是否以前调节的方式从垂体前叶释放,我们使用了来自植入含雌激素胶囊的雄性和去卵巢Fischer 344大鼠的培养垂体细胞。垂体前叶细胞(5×10⁵个细胞/孔)用已知调节垂体前叶激素分泌的下丘脑因子进行刺激(0.5 - 3小时),并通过放射免疫分析(RIA)测量培养基中甘丙肽水平。在雌性垂体细胞中,多巴胺(10和100 nM)抑制甘丙肽分泌,促甲状腺激素释放激素(TRH,20和100 nM)刺激其分泌。尽管雄性垂体细胞中的甘丙肽释放明显较低,但多巴胺和TRH分别抑制和刺激甘丙肽分泌。生长抑素(5 nM)在雌性和雄性细胞中也显著降低培养基中甘丙肽水平。无论垂体供体的性别如何,催乳素(PRL)对多巴胺、TRH和生长抑素的释放模式与甘丙肽的相似。尽管甘丙肽已定位在生长激素细胞中,但5 nM生长激素释放激素(GRF)未能改变雄性和雌性垂体细胞中甘丙肽的释放;GRF显著增加生长激素分泌。促黄体生成素释放激素(LHRH,5 nM)和促肾上腺皮质激素释放因子(CRF,5 nM)在体外未能改变甘丙肽释放。我们得出结论,在从雄性和去卵巢Fischer 344大鼠获得的暴露于雌激素的垂体细胞中:1)甘丙肽分泌受多巴胺和生长抑素抑制,受TRH刺激;2)GRF、LHRH和CRF在这些细胞中不调节甘丙肽释放;3)甘丙肽释放调节途径的特征表明甘丙肽的主要位置是催乳素细胞,可能在分泌颗粒内。