Disruption of GnRH pulses by anti-GnRH serum and phentolamine obliterates pulsatile LH but not FSH secretion in ovariectomized rabbits.
Disruption of GnRH pulses by anti-GnRH serum and phentolamine obliterates pulsatile LH but not FSH secretion in ovariectomized rabbits.
复制标题
抗 GnRH 血清和酚妥拉明对 GnRH 脉冲的干扰会消除去卵巢兔子的搏动性 LH 分泌，但不会消除 FSH 分泌。
DOI：
10.1159/000125745
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发表时间：
1991
影响因子：
4.1
通讯作者：
Spies,HG
中科院分区：
文献类型：
--
作者：
Pau,KY;Gliessman,PM;Oyama,T;Spies,HG
据推测，促性腺激素（即促黄体生成素（LH）和促卵泡激素（FSH））的分泌是由同步神经网络（“脉冲发生器”）驱动的。该网络部分受α-肾上腺素能活性调节，最终产生下丘脑促性腺激素释放激素（GnRH）释放的爆发。在这项研究中，我们使用的推拉（PP）灌注技术在卵巢切除兔调查（“GnRH/促性腺激素脉冲发生器”）的假设的三个方面。目的是确定：（1）如果血浆LH和FSH脉冲与下丘脑中基底（MBH-）GnRH脉冲同时发生，（2）当MBH GnRH脉冲信号被GnRH局部免疫中和或静脉输注α-肾上腺素能拮抗剂酚妥拉明阻断时，LH和FSH脉冲分泌模式的变化（PHEN，4 mg/kg BW）和（3）第三脑室（3VT-）GnRH模式是否反映MBH的神经元GnRH释放。我们发现，虽然血浆LH和FSH模式都是脉动的，但MBH GnRH脉冲仅与LH脉冲显著耦合（94%符合率）。MBH GnRH脉冲的局部免疫中和和PHEN诱导的MBH GnRH脉冲的抑制都消除了LH的脉冲式分泌，但不是FSH。MBH GnRH或血浆LH或血浆FSH脉冲均不与3VTGnRH脉冲同时发生。然而，3VT的PP灌注似乎改变了MBH GnRH和垂体LH的脉动释放。结果支持了以下假设：在没有卵巢信号的情况下，“脉冲发生器”由紧张性α-肾上腺素能输入维持，MBH GnRH释放（GnRH脉冲）的“细胞统一性”驱动促性腺激素细胞以脉冲形式分泌LH。与此相反，FSH的脉冲式释放似乎涉及额外的非卵巢调节事件，以控制LH分泌。
It has been hypothesized that the secretion of gonadotropins, i.e. luteinizing hormone (LH) and follicle-stimulating hormone (FSH), is driven by a synchronized neural network (‘pulse generator’). This network, regulated in part by α-adrenergic activity, ultimately generates bursts of hypothalamic gonadotropin-releasing hormone (GnRH) release. In this study, we used the push-pull (PP) perfusion technique in ovariectomized rabbits to investigate three aspects of the (‘GnRH/gonadotropin pulse generator’) hypothesis. The objectives were to determine: (1) if plasma LH and FSH pulses occur concomitantly with mediobasal hypothalamic (MBH-) GnRH pulses, (2) changes in the patterns of pulsatile LH and FSH secretion when pulsatile MBH GnRH signals are interrupted by eitherlocalimmunoneutralization of GnRH or intravenous infusion of the α-adrenergic antagonist phentolamine (PHEN, 4 mg/kg BW), and (3) whether third cerebroventricular (3VT-) GnRH patterns reflect neuronal GnRH release from the MBH. We found that while both plasma LH and FSH patterns were pulsatile, MBH GnRH pulses were significantly coupled only with LH pulses (94% coincidence). Both the local immunoneutralization of MBH GnRH pulses and the PHEN-induced suppression of MBH GnRH pulses obliterated the pulsatile secretion of LH, but not FSH. Neither MBH GnRH nor plasma LH or plasma FSH pulses were concurrent with 3VTGnRH pulses. However, the PP perfusion of the 3VT appeared to alter the pulsatile release of MBH GnRH and pituitary LH. The results support the hypothesis that in the absence of ovarian signals, the ‘pulse generator’ is maintained by tonic α-adrenergic input and that a ‘cellular unity’ of MBH GnRH release (GnRH pulses) drives the gonadotrophs to secrete LH in pulses. In contrast, the pulsatile release of FSH appears to involve additional nonovarian regulatory events to those controlling LH secretion.