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一种甾体信息素和产卵刺激通过不同的神经内分泌机制,增加雄性金鱼(Carassius auratus)的促性腺激素和精液量。

A steroidal pheromone and spawning stimuli act via different neuroendocrine mechanisms to increase gonadotropin and milt volume in male goldfish Carassius auratus.

作者信息

Zheng W, Stacey N E

机构信息

Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada.

出版信息

Gen Comp Endocrinol. 1997 Feb;105(2):228-38. doi: 10.1006/gcen.1996.6825.

DOI:10.1006/gcen.1996.6825
PMID:9038255
Abstract

In goldfish (Carassius auratus), pheromonal 17alpha, 20beta-dihydroxy-4-pregnen-3-one (17,20beta-P) and spawning stimuli (interaction with a sexually active female releasing prostaglandin pheromone) both increase gonadotropin-II (GtH-II) and milt volume. In the goldfish pituitary, GtH-II release is stimulated by gonadotropin-releasing hormone (GnRH) and inhibited by dopamine (DA). In this study, we investigated the possibility that 17,20beta-P and spawning stimuli act via separate neuroendocrine mechanisms by determining whether their effects on GtH-II could be selectively disrupted by injection of DA type-2 receptor (D-2) agonists (bromocryptine and LY171555) or a goldfish GnRH antagonist, [Ac-Delta3-Pro1, 4FD-Phe2, d-Trp3,6]-mGnRH (analog E). D-2 agonists blocked 17,20beta-P-induced increases in GtH-II and milt volume but did not affect spawning-induced responses. GnRH antagonist blocked 17,20beta-P-induced increases in GtH-II and milt volume, and spawning-induced GtH-II increase, but did not affect spawning-induced increase in milt volume. These results suggest that (1) pheromonal 17,20beta-P and spawning stimuli increase GtH-II increase via distinct neuroendocrine mechanisms, (2) the effect of pheromonal 17,20beta-P on increasing milt volume is GtH-II-dependent, and (3) the effect of spawning stimuli on increasing milt volume is GtH-II-independent.

摘要

在金鱼(Carassius auratus)中,信息素17α,20β - 二羟基 - 4 - 孕烯 - 3 - 酮(17,20β - P)和产卵刺激(与释放前列腺素信息素的性活跃雌鱼相互作用)均会增加促性腺激素 - II(GtH - II)和精液量。在金鱼垂体中,促性腺激素释放激素(GnRH)刺激GtH - II释放,而多巴胺(DA)则抑制其释放。在本研究中,我们通过确定注射DA 2型受体(D - 2)激动剂(溴隐亭和LY171555)或金鱼GnRH拮抗剂[Ac - Delta3 - Pro1, 4FD - Phe2, d - Trp3,6] - mGnRH(类似物E)是否能选择性地破坏它们对GtH - II的影响,来研究17,20β - P和产卵刺激是否通过不同的神经内分泌机制起作用。D - 2激动剂阻断了17,20β - P诱导的GtH - II和精液量增加,但不影响产卵诱导的反应。GnRH拮抗剂阻断了17,20β - P诱导的GtH - II和精液量增加以及产卵诱导的GtH - II增加,但不影响产卵诱导的精液量增加。这些结果表明:(1)信息素17,20β - P和产卵刺激通过不同的神经内分泌机制增加GtH - II;(2)信息素17,20β - P对增加精液量的作用依赖于GtH - II;(3)产卵刺激对增加精液量的作用不依赖于GtH - II。

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