Evidence suggesting that the potentiating action of neuropeptide Y on luteinizing hormone (LH)-releasing hormone-induced LH release remains unaltered in aged female rats.
Evidence suggesting that the potentiating action of neuropeptide Y on luteinizing hormone (LH)-releasing hormone-induced LH release remains unaltered in aged female rats.
复制标题
有证据表明，神经肽 Y 对黄体生成素 (LH) 释放激素诱导的 LH 释放的增强作用在老年雌性大鼠中保持不变。
DOI：
10.1046/j.1365-2826.2000.00480.x
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发表时间：
2000
影响因子：
3.2
通讯作者：
Sahu,A
中科院分区：
文献类型：
--
作者：
Sahu,A
多项证据表明，下丘脑神经肽 Y 在幼鼠排卵前黄体生成素 (LH) 释放中发挥重要作用的机制之一是增强 LH 释放激素 (LHRH) 对垂体水平 LH 释放的作用。本研究探讨了神经肽 Y 对 LHRH 诱导的 LH 释放的增强作用的改变是否可能导致女性生殖衰老过程中 LH 激增的减弱或消失。对切除卵巢 7 天的定期循环的年轻大鼠（2-3 个月大）和持续发情的老年大鼠（19-20 个月大）用雌二醇-17β 填充的硅橡胶胶囊进行预激发。两天后，大鼠接受皮下注射。 09点时注射黄体酮，然后腹腔注射。 13.30 时使用生理盐水或戊巴比妥。戊巴比妥治疗的大鼠接受静脉注射神经肽 Y、LHRH、神经肽 Y 和 LHRH 的组合或盐水脉冲，从 14 点到 18 点每 30 分钟通过颈静脉插管进行一次。每小时 11 点至 21 点之间采集血样。在老年大鼠中，与年轻大鼠相比，黄体酮引起的 LH 激增显着减弱和延迟。戊巴比妥注射完全阻断了 LH 激增。单独的神经肽 Y 脉冲对 LH 释放没有显着影响。相比之下，LHRH 脉冲增加了两个年龄组的 LH 释放，尽管老年大鼠的反应显着降低。虽然与单独使用 LHRH 相比，神经肽 Y 和 LHRH 的组合脉冲显着增加了年轻和老年大鼠的 LH 释放，但神经肽 Y 对 LHRH 诱导的 LH 释放的增强作用在两个年龄组之间保持不变。这些结果，加上我们最近在中年发情大鼠中下丘脑神经肽 Y 神经元活动改变的证明，表明下丘脑中神经肽 Y 分泌和作用的缺陷，而不是垂体对神经肽 Y 反应性的降低，可能部分原因是老年大鼠没有出现 LH 激增。
Several lines of evidence suggest that one of the mechanisms by which the hypothalamic neuropeptide Y plays an obligatory role in the preovulatory luteinizing hormone (LH) discharge in young rats is to potentiate the action of LH‐releasing hormone (LHRH) on LH release at the level of the pituitary. This study examined whether an alteration in the potentiating action of neuropeptide Y on LHRH‐induced LH release may contribute to the attenuation or absence of LH surges during female reproductive ageing. Young regularly cycling (2–3‐month‐old) and old constant oestrous (19–20‐month‐old) rats ovariectomized for 7 days were primed with oestradiol‐17β‐filled Silastic capsules. Two days later, rats received s.c. progesterone at 09.00 h and then were injected i.p. with either saline or pentobarbital at 13.30 hours. Pentobarbital‐treated rats received i.v. pulses of neuropeptide Y, LHRH, a combination of neuropeptide Y and LHRH, or saline, every 30 min from 14.00 to 18.00 h via a jugular cannula. Hourly blood samples were collected between 11.00 and 21.00 h. In old rats, the progesterone‐induced LH surge was significantly attenuated and delayed as compared to that of young rats. Pentobarbital injection completely blocked the LH surge. Neuropeptide Y pulses alone had no significant effect on LH release. In contrast, LHRH pulses increased LH release in both age groups, although the response was significantly reduced in older rats. While combined pulses of neuropeptide Y and LHRH significantly increased LH release in both young and old rats as compared to that of LHRH alone, the potentiating action of neuropeptide Y on LHRH‐induced LH release remained unchanged between the two age groups. These results, together with our recent demonstration of altered hypothalamic neuropeptide Y neuronal activity in middle‐aged pro‐oestrous rats, suggest that a deficit in neuropeptide Y secretion and action in the hypothalamus, rather than a decrease in pituitary responsiveness to neuropeptide Y, may partially be responsible for the absence of LH surges in old rats.