GTH I and GTH II secretion profiles during the reproductive cycle in female rainbow trout: Relationship with pituitary responsiveness to GnRH-A stimulation
GTH I and GTH II secretion profiles during the reproductive cycle in female rainbow trout: Relationship with pituitary responsiveness to GnRH-A stimulation
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DOI：
10.1006/gcen.1998.7088
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发表时间：
1998-07-01
影响因子：
2.7
通讯作者：
Mikolajczyk, T
中科院分区：
文献类型：
--
作者：
Breton, B;Govoroun, M;Mikolajczyk, T
最近对硬骨鱼中的两种促性腺激素Gth I和Gth II进行了纯化，并利用针对其β亚基的抗体建立了它们的特异性放射免疫分析方法，这表明早期对Gth II的分析也测定了Gth I。因此，大多数关于鱼类促性腺激素对繁殖的控制的结果必须用每种促性腺激素的特定分析来重新研究。外源卵黄发生开始时，GTH-I水平显著升高，从7.83+/-3.37 ng/ml升至16.87+/-4.52 ng/ml，GTH-I一直维持在很低的水平，直到卵黄发生结束。两种激素在围排卵期的变化最显著，GTH II水平在成熟当天达到峰值，但呈双相上升，第一个峰值出现在成熟前4天，在此之前，GTH I水平从成熟前8天的5.83+/-2.17 ng/ml开始逐渐显著上升，并在成熟当天增加到10 ng/ml以上。因此，GTH II成熟高峰并不是排卵前唯一的促性腺激素信号。排卵前GTH I升高的作用尚不清楚。排卵后，这两种激素的分泌情况取决于体腔中是否有排卵卵。在排卵和卵子剥离后4天，GTH-I水平开始显著升高，达到25 ng/ml以上，反之，GTH-II水平逐渐下降。在将卵保存在体腔内的鱼中，这一进程被逆转；成熟后8天，GTH II增加到与成熟前相似的水平；卵的存在阻止了GTH I的增加。这似乎表明GTH I和GTH II分泌的排泄后调节可能涉及以拮抗方式作用的卵巢因素。在卵子存在的情况下防止GTH I水平的增加表明，只要卵子存在于体腔中，就不可能发展出新的配子发生周期，因为GTH I是主要参与控制这一现象的促性腺激素。GnRH在配子发生的任何阶段都不能显著刺激GTH I的分泌，即使排卵后GnRH水平升高，也涉及其他拮抗GnRH的因素。已知的多巴胺对GnRH刺激的GTH II分泌的拮抗作用未被涉及，因为多巴胺拮抗剂Pimozide不能诱导GnRH对GTH I分泌的刺激作用。虽然GnRH能刺激卵黄发生中期GTH-II的分泌，但对GnRH的反应与血中GTH-II无相关性。这些结果表明，GTH I和GTH II的分泌受到不同的机制和不同的因素的调节。(C)1998年学术出版社。
The recent purification of two gonadotropins, GTH I and GTH II, in teleost fish and the development of their specific radioimmunoassays using antibodies directed against their beta subunits have demonstrated that earlier assays for GTH II also measured GTH I. Most of the results on the gonadotropic control of reproduction in fish must thus be reinvestigated using specific assays for each gonadotropin, The present investigation examines changes in blood plasma levels of GTH I and GTH II during the annual reproductive cycle of rainbow trout in relation to the ability of gonadotropin-releasing hormone (GnRH) to stimulate in vivo GTH I and GTH II secretion, with focus on the periovulatory period. GTH I was detected from immature to postovulatory stages, with a significant increase at the onset of exogenous vitellogenesis, with GTH I levels rising from 7.83 +/- 3.37 to 16.87 +/- 4.52 ng/ml. GTH II remained very low until the end of the vitellogenesis. For both hormones, the most significant variations were measured during the periovulatory period, GTH II levels peaked on the day of maturation, but the increase was biphasic with a first peak arising 4 days prior to maturation, This elevation of GTH II was preceded by a progressive and significant rise of GTH I levels starting from 5.83 +/- 2.17 ng/ml 8 days before maturation and increasing to more than 10 ng/ml on the day of maturation. Thus, the GTH II maturation surge is not the only gonadotropic signal occurring before ovulation. The role of the preovulatory GTH I increase remains unknown. After ovulation the secretory profiles of the two hormones depended on the presence or absence of ovulated eggs in the body cavity. There was a major increase in GTH I levels starting 4 days after ovulation and egg stripping, reaching more than 25 ng/ml. Conversely, in these fish the GTH II levels gradually decreased. In the fish which kept their eggs in the body cavity the progress was reversed; 8 days after maturation, GTH II increased to levels similar to those measured prior to maturation; the presence of the eggs prevented an increase in GTH I. This seems to indicate that postovulatory regulation of GTH I and GTH II secretion might involve ovarian factors that act in an antagonistic fashion. The prevention of the increase in GTH I levels in the presence of eggs suggests that as long as eggs are present in the body cavity, the development of a new cycle of gametogenesis is not possible, since GTH I is the gonadotropin mainly involved in controlling this phenomena. GnRH cannot significantly stimulate GTH I secretion at any stage of gametogenesis, even when its levels increased after ovulation, Other factors antagonizing GnRH are involved. The well-known antagonistic effect of dopamine on the GnRH stimulated GTH II secretion in fish is not involved since the dopamine antagonist, pimozide, was ineffective in inducing a stimulatory action of GnRH on GTH I secretion. Although GnRH can stimulate GTH II secretion from mid-vitellogenesis, the response to GnRH was not correlated with GTH II in blood. These results suggest that GTH I and GTH II secretions are regulated by different mechanisms and different factors. (C) 1998 Academic Press.