Alteration in hypothalamic neuropeptide Y (NPY) secretion may underlie female reproductive ageing: induction of steroid-induced luteinising hormone surge by NPY in ovariectomised aged rats.
Alteration in hypothalamic neuropeptide Y (NPY) secretion may underlie female reproductive ageing: induction of steroid-induced luteinising hormone surge by NPY in ovariectomised aged rats.
复制标题
下丘脑神经肽 Y (NPY) 分泌的改变可能是雌性生殖衰老的基础：在卵巢切除的老年大鼠中，NPY 诱导类固醇诱导的黄体生成素激增。
DOI：
10.1111/j.1365-2826.2006.01449.x
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Sahu,A
中科院分区：
文献类型：
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作者：
Sahu,A
大量证据表明，下丘脑功能缺陷可能是雌性大鼠生殖衰老的主要原因。我们先前已经证明，促黄体生成素(LH)峰相关的下丘脑神经肽Y(NPY)基因表达和正中隆起(ME)NPY水平的变化在幼年大鼠中不会发生在中年(MA)大鼠中。本研究探讨了去卵巢(OVX)MA大鼠激素诱导的促黄体生成素(LH)高峰期间下丘脑NPY释放是否发生改变，以及外源性NPY是否启动去卵巢老年大鼠激素诱导的促黄体生成素(LH)高峰。在第一项研究中，在雌激素(E_2)诱导的去卵巢幼鼠(2-3 月大鼠)孕酮诱导的促黄体生成素高峰之前和期间，用推拉插管技术评估的从ME弓状核释放的神经肽Y显著增加。幼鼠体内神经肽Y释放的这种先期增加在11-13 龄的MA大鼠中并不明显，与延迟和减弱的黄体生成素峰有关。在第二项研究中，黄体酮不能诱导去卵巢老年大鼠(23-25 月龄)的黄体生成素高峰，而脑室注射神经肽Y(0.1-0.5 微克)1100、1200和13.00 h可引起去卵巢老年大鼠黄体生成素高峰的诱导，而雌二醇孕酮诱导的去卵巢老年大鼠则有促黄体生成素高峰。由于下丘脑NPY合成和释放增加是幼年大鼠排卵前促黄体生成素释放的必需因素，本研究结果提示，中脑弓状核NPY释放的改变是MA大鼠黄体生成素高峰延迟和减少的原因之一，也可能是老年大鼠黄体生成素高峰消失的原因之一。
A large body of evidence suggests that a defect in the hypothalamic function may be the primary cause of reproductive ageing in female rats. We have previously shown that luteinising hormone (LH)‐surge associated changes in hypothalamic neuropeptide Y (NPY) gene expression and median eminence (ME) NPY levels seen in young rats do not occur in middle‐aged (MA) rats. The present study examined whether hypothalamic NPY release is altered during the steroid‐induced LH surge in ovariectomised (OVX) MA rats, and whether exogenous NPY initiates steroid‐induced LH surge in OVX old rats. In the first study, NPY release from the ME‐arcuate nucleus, as assessed by the push–pull cannula technique, was significantly increased before and during the progesterone‐induced LH surge in oestrogen (E2)‐primed ovariectomised young rats (2–3 months old). This antecedent increase in NPY release seen in young rats was not apparent in MA rats (11–13 months old) in association with a delayed and attenuated LH surge. In the second study, whereas progesterone failed to induce LH surges in E2‐primed ovariectomised old rats (23–25 months old), intracerebroventricular NPY (0.1–0.5 µg) injections at 1100, 1200 and 13.00 h resulted in LH surge induction in E2+ progesterone‐primed ovariectomised old rats. Because increased hypothalamic NPY synthesis and release is obligatory for the preovulatory LH discharge in young rats, the present findings suggest that alteration in NPY release from the ME‐arcuate nucleus contributes to the delayed and reduced LH surges in MA rats and may be involved in the subsequent loss of the LH surges in old rats.