Oestrogen‐Dependent Stimulation of Luteinising Hormone Release by Galanin‐Like Peptide in Female Rats
Oestrogen‐Dependent Stimulation of Luteinising Hormone Release by Galanin‐Like Peptide in Female Rats
复制标题
DOI：
10.1111/j.1365-2826.2008.01703.x
复制
发表时间：
2008-05
影响因子：
3.2
通讯作者：
Y. Uenoyama;H. Tsukamura;M. Kinoshita;S. Yamada;K. Iwata;V. Pheng;S. Sajapitak;M. Sakakibara;T. Ohtaki;H. Matsumoto;K. Maeda
中科院分区：
文献类型：
--
作者：
Y. Uenoyama;H. Tsukamura;M. Kinoshita;S. Yamada;K. Iwata;V. Pheng;S. Sajapitak;M. Sakakibara;T. Ohtaki;H. Matsumoto;K. Maeda
甘丙素样肽(GALP)是三种甘丙素受体的配基，据报道在雄性啮齿动物和灵长类动物中具有调节黄体生成素(LH)释放的作用，但它在雌性啮齿动物黄体生成素释放中的作用仍存在争议。本研究旨在探讨GALP对雌性大鼠促黄体生成素分泌的刺激作用。I.C.V.的效果。在Wistar-Imamichi系雌性大鼠和瘦肥胖的Zucker大鼠上，观察了GALP(5nmoL)对雌性大鼠搏动性黄体生成素释放的影响。雌性Wistar-Imamichi雌性大鼠腹腔注射17-雌二醇(β，雌二醇组)。注射GALP后的前1.5小时，黄体生成素释放逐渐增加，随后1.5小时的黄体生成素脉冲频率增加，导致整个采样期的平均黄体生成素浓度和基础水平以及后半期的黄体生成素脉冲频率显著高于使用赋形剂的对照组。GALP的刺激作用是雌激素依赖的，因为相同的GALP处理不影响去卵巢大鼠在没有雌激素的情况下的黄体生成素的释放。在精瘦的Zucker大鼠中，雌激素刺激的OVX个体中发现有促黄体生成素脉冲，中央注射GALP增加了后半期的平均促黄体生成素浓度。相比之下，据报道下丘脑GALP表达较低的雌性OVX肥胖Zucker大鼠很少有促黄体生成素脉冲。中心注射GALP导致黄体生成素释放明显但短暂的增加，导致在采样周期的前半部分，与赋形剂处理的对照组相比，黄体生成素脉冲的所有脉冲参数都显著增加。这些结果提示，下丘脑GALP可能参与刺激雌性大鼠促性腺激素释放激素/黄体生成素的释放，并且GALP对黄体生成素的刺激作用具有雌激素依赖性。
Galanin‐like peptide (GALP), a ligand for three types of galanin receptor, is reported to have a role in regulating luteinising hormone (LH) release in male rodents and primates, but its role in LH release in female rodents remains controversial. The present study was conducted to test whether GALP has a stimulatory role in regulating LH secretion in female rats. The effect of i.c.v. infusion of GALP (5 nmol) on pulsatile LH release was investigated in Wistar‐Imamichi strain female rats, or lean and obese Zucker rats. In oestradiol‐17β (oestradiol)‐primed ovariectomised (OVX) Wistar‐Imamichi female rats, i.c.v. infusion of GALP caused a gradual increase in LH release for the first 1.5 h after the infusion followed by an increased LH pulse frequency during the next 1.5 h, resulting in a significant increase in the mean LH concentrations and baseline levels of LH pulses throughout the sampling period and in the frequency of LH pulses at the last half of the period compared to vehicle‐treated controls. The stimulatory effect of GALP was oestrogen‐dependent because the same GALP treatment did not affect LH release in OVX rats in the absence of oestradiol. In lean Zucker rats, LH pulses were found in oestradiol‐primed OVX individuals and central GALP infusion increased mean LH concentrations in the last half of the period. By contrast, few LH pulses were found in oestradiol‐primed OVX obese Zucker rats reportedly with lower hypothalamic GALP expression. Central GALP infusion caused an apparent but transient increase in LH release, resulting in the significant increase in all pulse parameters of LH pulses compared to vehicle‐treated controls in the first half of the sampling period. These results suggest that hypothalamic GALP is likely involved in stimulating GnRH/LH release, and that the stimulatory effect of GALP on LH release is oestrogen‐dependent in female rats.