Oestrogen-dependent suppression of pulsatile luteinising hormone secretion and kissl mRNA expression in the arcuate nucleus during late lactation in rats.
Oestrogen-dependent suppression of pulsatile luteinising hormone secretion and kissl mRNA expression in the arcuate nucleus during late lactation in rats.
复制标题
雌激素依赖性抑制大鼠哺乳后期弓状核中的脉动黄体生成激素分泌和 Kissl mRNA 表达。
DOI：
10.1111/j.1365-2826.2012.02330.x
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发表时间：
2012
影响因子：
3.2
通讯作者：
山田俊児
中科院分区：
文献类型：
--
作者：
Tomikawa J;Uenoyama Y;Ozawa M;Fukanuma T;Takase K;Goto T;Abe H;Ieda N;Minabe S;Deura C;Inoue N;Sanbo M;Tomita K;Hirabayashi M;Tanaka S;Imamura T;Okamura H;Maeda K-I;Tsukamura H.;榊原基嗣;山田俊児
哺乳动物在哺乳期间，通过对促性腺激素分泌的深度抑制，卵泡发育和排卵受到强烈抑制。本研究旨在探讨雌激素反馈作用在抑制黄体生成素（LH）分泌和下丘脑kisspeptin表达在哺乳后期的作用。在完整和雌激素替代的卵巢切除（OVX）泌乳大鼠中，血浆LH浓度在整个泌乳期保持在低水平，而在泌乳OVX大鼠中，血浆LH浓度从产后第10天开始逐渐升高。OVX泌乳大鼠表现出频繁的LH脉冲在哺乳后期，虽然LH脉冲显着抑制雌激素替代，这是不太有效的LH释放在非哺乳大鼠。在哺乳期OVX大鼠中，雌激素替代显著减少了哺乳后期弓状核（ARC）中Kiss 1 mRNA表达细胞的数量，尽管相同的雌激素治疗对非哺乳对照组中Kiss 1表达细胞的数量没有影响。在产后第16天，将外源性kisspeptin（0.2 nmol）注入第三脑室显著增加了OVX哺乳期大鼠、OVX哺乳期大鼠+皮下17β-雌二醇和完整哺乳期大鼠的LH分泌。 这些结果表明，泌乳后期LH脉冲抑制可能是ARC kisspeptin表达增强的雌激素依赖性抑制的结果。
Follicular development and ovulation are strongly suppressed during lactation in mammals via a profound suppression of gonadotrophin secretion. The present study aimed to examine the role of oestrogen feedback action in suppressing luteinising hormone (LH) secretion and hypothalamic kisspeptin expression during the latter half of lactation. Plasma LH concentrations kept at low levels throughout the lactating period in intact and oestrogen‐replaced ovariectomised (OVX) lactating rats, whereas plasma LH concentrations gradually elevated from day 10 postpartum in lactating OVX rats. OVX lactating rats showed frequent LH pulses at late lactation, although the LH pulses were significantly inhibited by an oestrogen replacement, which is much less effective on LH release in nonlactating rats. Oestrogen replacement in lactating OVX rats significantly reduced the number ofKiss1mRNA‐expressing cells in the arcuate nucleus (ARC) at late lactation, although the same oestrogen treatment did not affect the number ofKiss1‐expressing cells in nonlactating controls. Exogenous kisspeptin challenge (0.2 nmol) into the third cerebroventricle significantly increased LH secretion in lactating OVX, lactating OVX + subcutaneous 17β‐oestradiol and intact lactating rats at day 16 postpartum. These results suggest that LH pulse suppression during late lactation could be a result of the enhanced oestrogen‐dependent suppression of ARC kisspeptin expression.