蛙类促性腺激素释放激素的研究

蛙类促性腺激素释放激素的研究李远友林浩然（中山大学生物系广州５１０２７５）关键词促性腺激素释放激素特性作用蛙促性腺激素释放激素（ＧｎＲＨ）是脊椎动物脑垂体促性激素（ＧｔＨ）合成和释放的主要调节者,在生殖功能神经激素调控中起关键作用。近年来,哺乳类和...     

促性腺激素释放激素的种类,作用及调节

促性腺激素释放激素的种类、作用及调节禹龙香李远友（湖南农业大学医院,长沙４１０１２８）（中山大学生物系,广州５１０２７５）促性腺激素释放激素（ＧｎＲＨ）是由脊椎动物的脑（主要是视前—下丘脑）产生的一类十肽激素,它在脑垂体促性腺激素（ＧｔＨ）的合成和分...     

大鼠颌下腺促性腺激素释放激素及其mRNA的免疫组织化学与原位杂交研究

用免疫组织化学及原位杂交法,研究了促性腺激素释放激素及其ｍＲＮＡ在大鼠颌下腺的分布。结果显示,大鼠颌下腺的浆液性腺泡的上皮细胞,各级导管的上皮细胞及副交感神经节细胞均呈促性腺激素释放激素免疫反应阳性,阳性反应物质分布在胞质,胞核呈阴性反应。颌下腺的浆液性腺泡上皮细胞,各级导管上皮细胞同样被检测到很强的促性腺激素释放激素ｍＲＮＡ杂交信号。以上结果提示,大鼠颌下腺能自身合成促性腺激素释放激素,促性腺激素释放激素对消化功能可能有重要调节作用。     

根田鼠下丘脑促性腺激素释放激素的放射免疫学测定

利用大鼠促性腺激素释放激素放射免疫学测定试剂检测了根田鼠下丘脑促性腺激素释放激素水平．测定线性范围为2.5 Pg至160pg/管,批内和批间差为1.7％ (n=10)和7.8%（n=4),样品平均标准回收率为108.2±8.4％。根田鼠下丘脑促性腺激素释放激素测定为0.28±0.04 ng/mg湿重组织。从根田鼠下丘脑提取物稀释曲线与大鼠(人工合成)促性腺激素释放激素有较好的平行关系判断, 可以推知根田鼠下丘脑促性腺激素释放激素结构活性类似于大鼠(人工合成)的活性。     

促性腺激素释放激素受体的结构及其生物学功能

促性腺激素释放激素受体(GnRHR)属于类视紫红质G-蛋白结合受体(GPCRs)家族的成员.当促性腺激素释放激素(GnRH)与GnRHR结合后,一系列细胞内信号通路被激活从而调节和表达各种生物学功能.本文对GnRHR的基因结构、分子结构、信号调节及生物学功能等进行了综述.     

大鳍Hu促性腺激素分泌调控的研究

用非洲鲶鱼促性腺激素放射免疫测定方法测定了Ｃｈａｎｇ科鱼类样品中的促性腺激素含量。用这种方法和鲤鱼促性腺激素β－亚基放射免疫测定法测定大鳍Ｈｕ同一批血清样品结果也相当吻合。通过注射促黄体素释放激素类似物和／或多巴胺的Ｄ２受体拮抗剂地欧酮后,定时取样测定血清促性腺激素含量,证明大鳍Ｈｕ促性腺激素的释放同时受到下丘脑分泌的促性腺激素释放激素和多巴胺的双重调节。但是,多巴胺只能抑制由促性腺激素释放激素诱     

大鳍促性腺激素分泌调控的研究

用非洲鲶鱼促性腺激素放射免疫测定方法测定了科鱼类样品中的促性腺激素含量。用这种方法和鲤鱼促性腺激素β亚基放射免疫测定法测定大鳍同一批血清样品结果也相当吻合。通过注射促黄体素释放激素类似物和／或多巴胺的Ｄ２受体拮抗剂地欧酮后,定时取样测定血清促性腺激素含量,证明大鳍促性腺激素的释放同时受到下丘脑分泌的促性腺激素释放激素和多巴胺的双重调节。但是,多巴胺只能抑制由促性腺激素释放激素诱导的促性腺激素分泌,而不能直接抑制基础的促性腺激素分泌,这与非洲鲶鱼相似而与金鱼和鲤鱼等鲤科鱼类明显不同。     

外源激素对雄性黄鳝性类固醇激素分泌的影响

硬骨鱼类促性腺激素(GTH)的分泌受到双重调控,即促性腺激素释放激素(GnRH)的刺激和促性腺激素释放抑制因子(GRIF)的抑制1.       

鱼类生殖内分泌学研究的进展及其在渔业生产中的应用

鱼类生殖活动的整个调节过程包括:感觉器官把外界环境的刺激(如温度、光照、降雨等)传送到脑,使下丘脑产生促性腺激素释放激素(GnRH)和促性腺激素释放的抑制因素(GRIF),激发或抑制脑垂体合成和释放促性腺激素(GtH);促性腺激素作用于性腺并促使它分泌     

外源激素对雌性黄鳝血清类固醇激素的影响

本文研究了几种外源激素对不同季节的雌性黄鳝血清性类固醇激素的影响。结果表明:鲤鱼垂体匀浆和人绒毛膜促性腺激素均显著蹭加血清类固醇水平,多巴胺拮抗剂domperidone降低血清类固醇水平,鲑鱼促性腺激素释放激素类似物增加血清类固醇水平。这些结果提示:雌鳝促性腺激素分泌亦受促性腺激素释放激素刺激,但多巴胺是否也起促性腺激素释放抑制因子的作用尚不清楚。垂体-性腺轴对外源激素的反应有明显的季节性差异,繁殖季节性腺成熟系数高的鱼反应性最强,繁殖前性腺未成熟期较繁殖后恢复发育期反应快.     

Plasma levels of gonadotropin releasing hormone during menstrual cycle ofMacaca radiata

A sensitive radioimmunoassay for gonadotropin releasing hormone has been developed. The assay has been validated for its specificity by testing various analogues of gonadotropin releasing hormone. Analysis of plasma samples during the menstrual cycle of 4 female bonnet monkeys showed a significant increase in the immunoreactive gonadotropin releasing hormone levels during preovulatory period of the menstrual cycle.     

长臀（鱼危）脑垂体和血清中促性腺激素的生殖周期变化

鲇形目鱼类在世界养殖鱼类中占有重要的位置.     

神经内分泌因子调控鱼类生殖和生长的相互作用

脊椎动物的生长与生殖活动有着密切的联系并相互作用。许多调节生长和代谢活动的内分泌因子对青春期或者性腺的发育产生影响。同样,调节生殖活动的许多激素亦同时对生长和代谢产生影响。近年来,我们和其他学者对鱼类生长和生殖的神经内分泌调节的相互作用进行了研究,主要的进展是：①在促进性腺的激素影响生长方面,发现促性腺激素释放激素（ＧｎＲＨ）和多巴胺都能和脑垂体生长激素细胞的特异性受体结合而刺激生长激素释放,并能     

Gonadotropin releasing hormone in first trimester human placenta: Isolation,partial characterisation andin vitro biosynthesis

Using a specific radioimmunoassay for gonadotropin releasing hormone, the presence of gonadotropin releasing hormone like material in the first trimester human placenta has been demonstrated. The material has been partially characterized using carboxy methyl cellulose chromatography, high pressure gel permeation chromatography and reverse phase C18 high pressure liquid chromatographic analysis. Analysis for bioactivity revealed that placental gonadotropin releasing hormone is much more active than synthetic gonadotropin releasing hormone inin vitro rat pituitary lutinising hormone release assay.In vitro biosynthetic studies using labelled precursors and immunoaffinity chromatography indicated that first trimester human placenta synthesizes gonadotropin releasing hormone like material.     

Cation-dependent gonadotropin releasing hormone activation of guanylate cyclase

Summary Gonadotropin releasing hormone enhanced guanylate cyclase [E.C.4.6.1.2] two- to threefold in pituitary, testis, liver and kidney. Dose response relationships revealed that at a concentration of 1 nanomolar, gonadotropin releasing hormone caused a maximal augmentation of guanylate cyclase activity and that increasing its concentration to the millimolar range caused no further enhancement of this enzyme. There was an absolute cation requirement for gonadotropin releasing hormone's enhancement of guanylate cyclase activity as there was no increase without any cation present. Gonadotropin releasing hormone could increase guanylate cyclase activity with either calcium or manganese in the incubation medium but more augmentation was observed with manganese. The data in this investigation suggest that guanylate cyclase may play a role in the mechanism of action of gonadotropin releasing hormone.     

Ovarian follicular differentiation with prepubertal gonadotropin surges and gonadotropin priming in mice

Preantral follicles were mechanically isolated from the ovaries of 1.5 to 8 week old mice and cultured in vitro for 4 days in the presence or absence of either activin A or FSH. Plasma gonadotropin, estradiol and immunoreactive (IR) inhibin levels were measured. Cultured follicles showed stepwise changes in response to recombinant human (rh) FSH, with no response until 11 days, a gradual increase from 2 weeks, culminating in a strong response to rhFSH at 8 weeks. The response to activin A was vice versa. It enhanced the effect of rhFSH on preantral follicular growth of up to 4-week-old mice, but inhibited the effect of rhFSH in 8-week-old mice. The peak of the prepubertal gonadotropin surge was observed on day 11. Seven-day-old mice were treated with either luteinizing hormone releasing hormone (LHRH) or rhFSH or human chorionic gonadotropin (hCG) for 3 consecutive days from day 7, and follicles were collected on day 11. Those follicles showed enhanced response to rhFSH, no response to activin A, and an enhanced response to the combination of rhFSH and activin A, suggesting that the chronological changes in follicular response are a result of the prepubertal gonadotropin surge.     

腹腔镜联合促性腺激素释放激素激动剂治疗子宫内膜异位症伴不孕症的疗效观察

目的:探讨腹腔镜联合促性腺激素释放激素激动剂治疗子宫内膜异位症伴不孕症的疗效。方法:将我院2013年2月~2014年2月收治的200例子宫内膜异位症伴不孕症患者随机分为2组各100例,对照组采用曲普瑞林治疗,观察组采用腹腔镜联合曲普瑞林治疗,检测患者治疗前后血清雌二醇(E2)、癌胚抗原125(CA125)及基质金属蛋白酶-1(MMP-1)水平,对比两组治疗后疼痛视觉评分(VAS)、盆腔包块和用药停止后月经恢复情况、随访1年记录两组复发率及妊娠率。结果:治疗后观察组VAS评分、盆腔包块和月经恢复情况均明显优于对照组,差异有统计学意义(P0.05);两组患者血清CA125、E2及MMP-1水平均显著下降,且观察组下降更明显,差异有统计学意义(P0.05);随访1年后,观察组妊娠率明显高于对照组,复发率明显低于对照组,差异有统计学意义(P0.05)。结论:腹腔镜联合促性腺激素释放激素激动剂治疗子宫内膜异位症的疗效显著,能有效降低复发率、提高妊娠率,值得临床推广应用。     

Desensitization of testicular ornithine decarboxylase to gonadotropin releasing hormone and gonadotropic hormones

Prior exposure of the testis to gonadotropin releasing hormone, luteinizing hormone or follicle stimulating hormone caused the testis refractory to these hormones in terms of ornithine decarboxylase activity at 24 h. Luteinizing hormone caused desensitization in the Leydig cells while the levels of ornithine decarboxylase in the seminiferous tubules were unaltered. In gonadotropin releasing hormone desensitized testis all the other treated compounds namely, luteinizing hormone, follicle stimulating hormone, prostaglandin F2 alpha, norepinephrine and cyclic AMP caused stimulation of ornithine decarboxylase activity. The testis desensitized with LH responded to cyclic AMP and norepinephrine whereas prostaglandin E2 or gonadotropin releasing hormone caused less stimulation of ornithine decarboxylase activity. These results indicate that testicular desensitization to gonadotropin releasing hormone and luteinizing hormone is not due to a post cyclic AMP block.     

A regulator of G Protein signaling, RGS3, inhibits gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) secretion

Background  

Luteinizing hormone secreted by the anterior pituitary gland regulates gonadal function. Luteinizing hormone secretion is regulated both by alterations in gonadotrope responsiveness to hypothalamic gonadotropin releasing hormone and by alterations in gonadotropin releasing hormone secretion. The mechanisms that determine gonadotrope responsiveness are unknown but may involve regulators of G protein signaling (RGSs). These proteins act by antagonizing or abbreviating interaction of Gα proteins with effectors such as phospholipase Cβ. Previously, we reported that gonadotropin releasing hormone-stimulated second messenger inositol trisphosphate production was inhibited when RGS3 and gonadotropin releasing hormone receptor cDNAs were co-transfected into the COS cell line. Here, we present evidence for RGS3 inhibition of gonadotropin releasing hormone-induced luteinizing hormone secretion from cultured rat pituitary cells.