Effect of progesterone on the activation of neurones of the supraoptic nucleus during parturition.
Effect of progesterone on the activation of neurones of the supraoptic nucleus during parturition.
复制标题
DOI：
10.1530/jrf.0.1200367
复制
发表时间：
2000-11
期刊：
影响因子：
--
通讯作者：
I. Antonijevic;J. Russell;R. Bicknell;G. Leng;A. Douglas
中科院分区：
文献类型：
--
作者：
I. Antonijevic;J. Russell;R. Bicknell;G. Leng;A. Douglas
分娩是由催产素分泌的脉动模式驱动的，这是由视上催产素神经元的突发放电活动引起的，并通过诱导Fos表达来反映。大鼠注射孕激素在怀孕的第20天，以调查的作用，减少孕激素：雌激素的比例，这之前交付，视上神经元的激活。与溶剂（对照）相比，黄体酮使分娩开始延迟28小时，并延长了分娩持续时间，但脉冲式注射催产素可以克服这一点，这表明缓慢的分娩可能反映了催产素分泌受损。孕激素预处理的临产大鼠在视上核的Fos免疫反应阳性细胞核比预处理的车辆。催产素注射后Fos免疫反应核的数量没有恢复，表明催产素神经元的适当激活受到孕酮的损害，并且缺乏刺激性传入驱动。Fos的表达增加在孤束核在分娩过程中的车辆或孕激素预处理的大鼠，但不是在大鼠已被孕激素预处理和催产素诱导，表明这种输入被抑制。内源性阿片抑制催产素神经元在晚期妊娠和阿片受体拮抗剂，纳洛酮，增加Fos的表达在视上核阻止抑制。然而，孕激素衰减纳洛酮诱导的Fos表达在视上核在妊娠晚期和纳洛酮在分娩期间给药并没有加速孕激素给药延迟分娩的持续时间，表明孕激素不起作用的内源性阿片紧张度的超活化。孕激素受体拮抗剂RU486在妊娠晚期增强视上神经元Fos表达，表明孕激素受体介导的作用。因此，孕激素戒断是必要的适当激活视上和孤束神经元在分娩过程中。
Parturition is driven by a pulsatile pattern of oxytocin secretion, resulting from burst firing activity of supraoptic oxytocin neurones and reflected by induction of Fos expression. Rats were injected with progesterone on day 20 of pregnancy to investigate the role of the decreasing progesterone:ratio oestrogen ratio, which precedes delivery, in the activation of supraoptic neurones. Progesterone delayed the onset of birth by 28 h compared with vehicle (control) and prolonged the duration of delivery, which was overcome by pulsatile injections of oxytocin, indicating that the slow delivery may reflect impaired oxytocin secretion. Parturient rats pretreated with progesterone had fewer Fos immunoreactive nuclei in the supraoptic nucleus than did parturient rats pretreated with vehicle. The number of Fos immunoreactive nuclei was not restored after oxytocin injection, indicating that appropriate activation of oxytocin neurones is impaired by progesterone and also that there is a lack of stimulatory afferent drive. Fos expression increased in the nucleus of the tractus solitarius during parturition in rats pretreated with either vehicle or progesterone, but not in rats that had been pretreated with progesterone and induced with oxytocin, indicating that this input was inhibited. Endogenous opioids inhibit oxytocin neurones in late pregnancy and the opioid antagonist, naloxone, increases Fos expression in supraoptic nuclei by preventing inhibition. However, progesterone attenuated naloxone-induced Fos expression in the supraoptic nucleus in late pregnancy and naloxone administered during parturition did not accelerate the duration of births delayed by progesterone administration, indicating that progesterone does not act by hyperactivation of endogenous opioid tone. RU486, a progesterone receptor antagonist, enhanced supraoptic neurone Fos expression in late pregnancy, indicating progesterone receptor-mediated actions. Thus, progesterone withdrawal is necessary for appropriate activation of supraoptic and tractus solitarius neurones during parturition.