Role of amygdala kisspeptin in pubertal timing in female rats.

Role of amygdala kisspeptin in pubertal timing in female rats.
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杏仁核亲吻肽在雌性大鼠青春期时机中的作用。

DOI:
10.1371/journal.pone.0183596
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发表时间:
2017
期刊:
影响因子:
3.7
通讯作者:
O'Byrne KT
O'Byrne KT
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Adekunbi DA;Li XF;Li S;Adegoke OA;Iranloye BO;Morakinyo AO;Lightman SL;Taylor PD;Poston L;O'Byrne KT

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为了研究母体肥胖破坏后代生殖功能的机制,我们研究了青春期前和年轻成年后代下丘脑弓状核(ARC)和前腹侧室周核(AVPV)以及背内侧杏仁核(MePD)中Kiss 1的表达。Sprague-Dawley大鼠在交配前以及整个妊娠期和哺乳期喂食标准或能量密集饮食6周。雄性和雌性后代在出生后第21天断奶,开始正常饮食。在pnd 30或100收集脑用于qRT-PCR以确定Kiss 1 mRNA水平。母亲肥胖增加Kiss 1 mRNA的表达在MePD的青春期前的男性和女性后代,而Kiss 1的表达在ARC或AVPV在这个年龄没有受到影响。母亲肥胖减少Kiss 1表达在所有三个大脑区域的3个月大的女性后代,但只有在MePD的男性。MePD kisspeptin对青春期、动情周期和排卵前LH峰的作用在一组单独的断奶后和年轻成年雌性大鼠中直接评估,这些大鼠在其整个生命过程中暴露于正常饮食。在pnd 21或100时,长期植入连接至渗透微型泵的双侧MePD内插管,用于递送kisspeptin受体拮抗剂(肽234,持续14天)。MePD kisspeptin的拮抗作用延迟了青春期的开始,破坏了发情周期,降低了LH峰的发生率。这些数据表明MePD在青春期时间和排卵中起着关键作用,并且母体肥胖可能通过杏仁核kisspeptin信号传导影响后代的生殖功能。
To investigate the mechanism by which maternal obesity disrupts reproductive function in offspring, we examined Kiss1 expression in the hypothalamic arcuate (ARC) and anteroventral periventricular (AVPV) nuclei, and posterodorsal medial amygdala (MePD) of pre-pubertal and young adult offspring. Sprague-Dawley rats were fed either a standard or energy-dense diet for six weeks prior to mating and throughout pregnancy and lactation. Male and female offspring were weaned onto normal diet on postnatal day (pnd) 21. Brains were collected on pnd 30 or 100 for qRT-PCR to determine Kiss1 mRNA levels. Maternal obesity increased Kiss1 mRNA expression in the MePD of pre-pubertal male and female offspring, whereas Kiss1 expression was not affected in the ARC or AVPV at this age. Maternal obesity reduced Kiss1 expression in all three brain regions of 3 month old female offspring, but only in MePD of males. The role of MePD kisspeptin on puberty, estrous cyclicity and preovulatory LH surges was assessed directly in a separate group of post-weanling and young adult female rats exposed to a normal diet throughout their life course. Bilateral intra-MePD cannulae connected to osmotic mini-pumps for delivery of kisspeptin receptor antagonist (Peptide 234 for 14 days) were chronically implanted on pnd 21 or 100. Antagonism of MePD kisspeptin delayed puberty onset, disrupted estrous cyclicity and reduced the incidence of LH surges. These data show that the MePD plays a key role in pubertal timing and ovulation and that maternal obesity may act via amygdala kisspeptin signaling to influence reproductive function in the offspring.
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