Regulation of gonadotropin releasing hormone release by neuropeptide Y at the median eminence during the preovulatory period in ewes
Regulation of gonadotropin releasing hormone release by neuropeptide Y at the median eminence during the preovulatory period in ewes
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DOI：
10.1159/000070280
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发表时间：
2003-04-01
影响因子：
4.1
通讯作者：
Conover, CA
中科院分区：
文献类型：
--
作者：
Advis, JP;Klein, J;Conover, CA
下丘脑的中隆起（ME）是一个重要的大脑部位，在这里，刺激和抑制信号可能会影响到下丘脑的神经元末梢，从而调节促垂体释放。由于神经肽Y （NPY）在排卵前促黄体生成素（LH）释放中的作用已被提出，我们假设NPY可能在ME中起作用，控制排卵前促性腺激素释放激素（GnRH）的释放，从而控制排卵前促黄体生成素的激增。为了检验这种可能性，我们使用母羊作为动物模型来确定：(a) GnRH和NPY在母羊ME中的免疫细胞化学分布；(b)外侧内部和外部层横向变化,NPY和GnRH-containing过程被发现,因此proin激性腺素释放素使用我体内释放NPY和推挽式套管(PPC)灌流液样本,以及血浆LH,在黄体,同步发情周期卵泡和排卵期前的阶段,我和(c)影响灌注NPY或Y1-NPY拮抗剂,或在体内释放ME-GnRH NPY抗血清和血浆LH在卵泡期同步。免疫定位显示弓形核及其附近、垂体柄和栅栏内有密集的含gnrh的束状神经突。相反，含有npy的密集神经丛出现在内层，偶尔在ME的中间和外侧外区发现纤维。在为含有NPY-和gnrh的神经元之间的突触和/或旁分泌相互作用提供机会之间的区域。激素分析表明，通过连续植入和移除硅酮包裹的雌二醇（E2）或孕酮（P4）植入，可在2小时内引起同步的促排卵前LH激增。在这种情况下，在同步LH激增之前，NPY和GnRH的ME释放平行增加。这种同步LH激增的发生被外源性NPY的ME灌注提前，而被NPY拮抗剂的ME灌注延迟和减弱（两者都通过PPC探针灌注2小时，在LH激增的预期发生前2-3小时开始）。此外，NPY在ME中的灌注增加，而Y1-NPY拮抗剂或NPY抗血清的灌注降低了早期卵泡母羊ME- ppc GnRH含量和血浆LH水平。最后，在持续的LH激增期间灌注NPY抗血清破坏了LH的释放。这些结果表明，NPY和GnRH神经元之间的相互作用在控制排卵前LH激增的时间、幅度和维持方面很重要。
The median eminence (ME) of the hypothalamus is known to be an important brain site where hypophysiotropic release might be regulated by excitatory and inhibitory signals impinging on their neuronal terminals. Since a role for neuropeptide Y (NPY) on preovulatory luteinizing hormone (LH) release has been suggested, we hypothesized that NPY might act at the ME to control preovulatory gonadotropin-releasing hormone (GnRH) release and thus the onset of the preovulatory surge of LH. To examine this possibility, we used the ewe as an animal model to determine: (a) immunocytochemical distribution of GnRH and NPY in the ewe ME; (b) changes the lateral internal and lateral external layers, both NPY and GnRH-containing processes were found, thus proin in vivo release of NPY and GnRH using ME push-pull cannula (PPC) perfusate samples, as well as in plasma LH, during the luteal, follicular and preovulatory phases of a synchronized estrous cycle, and (c) effects of ME perfusion of NPY or a Y1-NPY antagonist, or an NPY antiserum on in vivo release of ME-GnRH and plasma LH during a synchronized follicular phase. Immunolocalization reveals a dense plexus of beaded GnRH-containing neurites in the arcuate nucleus and in its vicinity, the pituitary stalk and the palisade. In contrast, a dense plexus of NPY-containing neurites occurs in the internal layer, with occasional fibers found in the intermediate and lateral external zone of the ME. In the area between viding opportunities for synaptic and/or paracrine interactions between NPY- and GnRH-containing neurons. Hormonal analysis indicated that a synchronized preovulatory surge of LH is elicited within a 2-hour window by the sequential implantation and removal of silastic-encased estradiol (E2) or progesterone (P4) implants. In this paradigm, there was a parallel increase in ME release of both NPY and GnRH preceding the synchronized LH surge. The onset of this synchronized LH surge was advanced by ME perfusion of exogenous NPY and was both delayed and blunted by ME perfusion with the NPY antagonist (both were perfused through the PPC probe for 2 h, starting 2-3 h before the expected onset of the LH surge). In addition, NPY perfusion in the ME increases, while perfusion of the Y1-NPY antagonist or of the NPY antiserum decreases ME-PPC GnRH content and plasma levels of LH in early follicular ewes. Finally, perfusion of NPY antiserum during an ongoing LH surge disrupted LH release. These results suggest that interactions between NPY and GnRH neurons are important in controlling the timing, magnitude and maintenance of the preovulatory LH surge.