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新生期经雌激素处理的雄性大鼠促黄体生成素分泌改变的机制

Mechanisms of altered LH secretion in neonatally oestrogenized male rats.

作者信息

Pinilla L, Tena-Sempere M, Gonzalez D, Aguilar E

机构信息

Department of Physiology, Faculty of Medicine, University of Córdoba, Spain.

出版信息

J Endocrinol. 1995 Oct;147(1):43-50. doi: 10.1677/joe.0.1470043.

Abstract

It is well known that the control of LH secretion depends on the steroid milieu during the postnatal period. In this study LH secretion was analysed in adult male rats injected neonatally with 500 micrograms oestradiol benzoate (1) after orchidectomy, (2) after selective elimination of androgens by destruction of Leydig cells with ethylene dimethane sulphonate (EDS), and (3) after removal in orchidectomized animals of Silastic capsules containing testosterone. In addition, (4) in vivo and in vitro LH secretion in response to LHRH agonist and antagonists, (5) the hypothalamic LHRH content, (6) the basal and stimulated in vitro LHRH release, and (7) the LH responses after administration of naloxone (2 mg/kg), alpha-methyl-p-tyrosine (alpha-MPT; 250 mg/kg), N-methyl-D-aspartic acid (NMDA, 15 mg/kg) or kainic acid (KA; 15 mg/kg) were also examined. Our data indicated that (1) the LH response after orchidectomy, after EDS administration and after removal of Silastic capsules containing testosterone was diminished in oestrogenized male rats, (2) the pituitaries from oestrogenized males retained responsiveness to LHRH, (3) hypothalamic LHRH content was reduced in oestrogenized males, but the hypothalamus from oestrogenized males released more LHRH than those of control groups both under basal conditions or after depolarization, (4) alpha-MPT decreased LH secretion only in oestrogenized males, and (5) NMDA and KA stimulated LH only in oestrogenized males. We conclude that in oestrogenized male rates the loss of sensitivity to the negative feedback action of testosterone on LH secretion was not due to decreased pituitary responsiveness to LHRH stimulation or to the inherent damage of LHRH neurones.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

众所周知,产后时期促黄体生成素(LH)分泌的调控取决于类固醇环境。在本研究中,对成年雄性大鼠进行了如下实验并分析LH分泌情况:(1)在睾丸切除术后,(2)在用乙烯二甲磺酸酯(EDS)破坏睾丸间质细胞选择性去除雄激素后,以及(3)在切除含睾酮的硅橡胶胶囊后,给新生期注射过500微克苯甲酸雌二醇的成年雄性大鼠进行上述处理。此外,还检测了:(4)体内和体外对促性腺激素释放激素(LHRH)激动剂和拮抗剂的LH分泌反应,(5)下丘脑LHRH含量,(6)基础状态及刺激后的体外LHRH释放,以及(7)注射纳洛酮(2毫克/千克)、α-甲基对酪氨酸(α-MPT;250毫克/千克)、N-甲基-D-天冬氨酸(NMDA,15毫克/千克)或 kainic 酸(KA;15毫克/千克)后的LH反应。我们的数据表明:(1)雌激素化雄性大鼠在睾丸切除术后、给予EDS后以及去除含睾酮的硅橡胶胶囊后的LH反应减弱;(2)雌激素化雄性大鼠的垂体对LHRH仍保持反应性;(3)雌激素化雄性大鼠下丘脑LHRH含量降低,但在基础状态或去极化后,雌激素化雄性大鼠下丘脑释放的LHRH比对照组更多;(4)α-MPT仅降低雌激素化雄性大鼠的LH分泌;(5)NMDA和KA仅刺激雌激素化雄性大鼠的LH分泌。我们得出结论,在雌激素化雄性大鼠中,对睾酮对LH分泌的负反馈作用敏感性丧失并非由于垂体对LHRH刺激的反应性降低或LHRH神经元的内在损伤。(摘要截短至250字)

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