The effect of oestradiol and progesterone on hypoglycaemic stress-induced suppression of pulsatile luteinizing hormone release and on corticotropin-releasing hormone mRNA expression in the rat
The effect of oestradiol and progesterone on hypoglycaemic stress-induced suppression of pulsatile luteinizing hormone release and on corticotropin-releasing hormone mRNA expression in the rat
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DOI：
10.1046/j.1365-2826.2003.01014.x
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发表时间：
2003-05-01
影响因子：
3.2
通讯作者：
O'Byrne, KT
中科院分区：
文献类型：
--
作者：
Li, XF;Mitchell, JC;O'Byrne, KT
促肾上腺皮质激素释放激素（CRH）与各种应激刺激对促黄体生成激素（LH）脉冲分泌的抑制有关; 17 β-雌二醇（E-2）已被证明可调节这种抑制反应。本研究在卵巢切除（OVX）大鼠中进行，旨在研究E-2和孕酮（P-4）对低血糖应激诱导的LH脉动分泌变化以及下丘脑-垂体-肾上腺轴中枢和外周成分相关变化的影响。E-2增强了低血糖应激诱导的LH脉冲抑制;除E-2外，P-4进一步增强了抑制反应。胰岛素诱导的低血糖（IIH）后血浆皮质酮的升高在E-2+P-4组中最高。然而，当通过给予皮质酮达到这样的水平时，LH脉冲的发生完全不受影响，与卵巢类固醇环境无关。E-2和E-2+P-4上调室旁核（PVN）的基础CRH mRNA表达，通过原位杂交测定;该信号也增加了内侧视前核（MPN）后E-2。IIH导致CRH mRNA在PVN中升高，但在MPN中不升高;这种升高可能反映了PVN在本背景下的更重要作用。神经肽mRNA表达的变化可能是神经元活动变化的信号;然而，在IIH后OVX、E-2和E-2+P-4大鼠LH脉冲抑制的显著差异并没有反映在PVN CRH mRNA的同时变化中。结果表明，虽然皮质酮对LH脉冲在大鼠中没有急性影响，但卵巢类固醇激素上调PVN和/或MPN中的基础CRH mRNA可能有助于这些脉冲在应激反应中的中枢调节。
Corticotropin-releasing hormone (CRH) is implicated in the suppression of pulsatile luteinizing hormone (LH) secretion by a variety of stressful stimuli; 17beta-oestradiol (E-2) has been shown to modulate this inhibitory response. The present study in ovariectomized (OVX) rats was designed to investigate the effect of E-2 and progesterone (P-4) on hypoglycaemic stress-induced changes in pulsatile LH secretion and on the associated changes in both central and peripheral components of the hypothalamic-pituitary-adrenal axis. E-2 enhanced the hypoglycaemic stress-induced suppression of LH pulses; P-4 in addition to E-2 further potentiated the inhibitory response. The rise in plasma corticosterone following insulin-induced hypoglycaemia (IIH) was highest in the E-2+P-4 group. Nevertheless, when such levels were achieved by administration of corticosterone, the occurrence of LH pulses was completely unaffected, irrespective of ovarian steroid milieu. E-2 and E-2+P-4 up-regulated basal CRH mRNA expression in the paraventricular nucleus (PVN) as measured by in situ hybridization; this signal was also increased in the medial preoptic nucleus (MPN) following E-2. IIH resulted in a rise in CRH mRNA in the PVN, but not in the MPN; this rise may reflect a more significant role for the PVN in the present context. Changes in neuropeptide mRNA expression may signal changes in neuronal activity; nevertheless, the profound differences in LH pulse suppression in OVX, E-2 and E-2+P-4 rats following IIH were not reflected in the concurrent changes in CRH mRNA in the PVN. The results suggest that while corticosterone has no acute effect on LH pulses in the rat, the up-regulation by ovarian steroids of basal CRH mRNA in the PVN and/or MPN may contribute to the central regulation of these pulses in response to stress.