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首页> 外文期刊>The European Journal of Neuroscience >Suppressed oxytocin neuron responses to immune challenge in late pregnant rats: a role for endogenous opioids.
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Suppressed oxytocin neuron responses to immune challenge in late pregnant rats: a role for endogenous opioids.

机译：催产素神经元对晚期妊娠大鼠免疫挑战的抑制作用：内源性阿片类药物的作用。

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Abstract Cytokine challenge (mimicking infection) with systemic interleukin-1beta (IL-1beta) stimulates oxytocin neurons via a noradrenergic brainstem pathway similar to that involved in parturition. As the responses of oxytocin neurons to several stimuli are reduced in late pregnancy, we have investigated whether responses to IL-1beta are also suppressed. In virgin Sprague-Dawley rats, IL-1beta (500 ng/kg i.v.) rapidly increased oxytocin secretion (3.2-fold), via a central action as the firing rate of oxytocin neurons in the supraoptic nucleus was increased. In contrast, IL-1beta had no significant effect on the electrical or secretory activity of oxytocin neurons in late pregnant rats. In pregnancy activation of a central inhibitory opioid mechanism restrains oxytocin neuron responses to various stimuli. Accordingly, we tested the effects of the opioid antagonist, naloxone, on oxytocin neuron responses to IL-1beta in pregnancy. Naloxone (5 mg/kg i.v.) did not affect the oxytocin secretory response toIL-1beta in virgin rats, whereas in late pregnant rats naloxone revealed a greater oxytocin secretory response to IL-1beta (3.5-fold) than in virgin rats. In virgin rats, naloxone decreased oxytocin neuron firing rate after IL-1beta, however, in pregnant rats naloxone increased the firing rate response to IL-1beta to the level seen in virgin rats. Thus, systemic IL-1beta acts centrally to increase oxytocin secretion. In pregnancy this response is suppressed by endogenous opioids, thus preserving neurohypophysial oxytocin stores for parturition and minimizing the risk of preterm labour. The exaggerated oxytocin secretory response to IL-1beta in pregnancy after naloxone reflects increased oxytocin stores and/or increased efficiency of excitation-secretion coupling at the posterior pituitary.
机译：摘要系统性白介素-1β（IL-1beta）引起的细胞因子攻击（模仿感染）通过去甲肾上腺素能的脑干途径刺激催产素神经元，类似于分娩。催产素神经元对几种刺激的反应在妊娠晚期降低了，因此我们研究了对IL-1β的反应是否也被抑制。在处女的Sprague-Dawley大鼠中，IL-1beta（500 ng / kg静脉内）通过催产素提高了视上核中神经元的放电速度，从而迅速增加了催产素的分泌（3.2倍）。相反，IL-1β对晚期妊娠大鼠催产素神经元的电或分泌活性没有明显影响。在妊娠期，中枢抑制性阿片样物质机制的激活会抑制催产素神经元对各种刺激的反应。因此，我们测试了阿片类药物拮抗剂纳洛酮对孕妇催产素神经元对IL-1β的反应的影响。纳洛酮（5 mg / kg静脉内）不会影响原始大鼠的催产素对IL-1beta的催产素分泌反应，而纳洛酮在晚期妊娠大鼠中显示出的催产素对IL-1beta的催产素分泌反应要比原始大鼠更大（3.5倍）。在处女大鼠中，纳洛酮降低了IL-1beta后催产素神经元的放电速度，但是，在孕鼠中，纳洛酮使对IL-1beta的放电速率反应增加到了处女大鼠中的水平。因此，全身性IL-1β集中作用以增加催产素的分泌。在怀孕期间，这种反应会被内源性阿片类药物抑制，从而保留了神经垂体催产素储存以进行分娩，并最大程度地减少了早产的风险。纳洛酮后妊娠中对IL-1β的催产素分泌反应过度，反映出催产素储存增加和/或垂体后叶兴奋性分泌分泌耦合效率增加。

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