Oxytocin secretion from the posterior pituitary gland is increased during parturition, stimulated by the uterine contractions that forcefully expel the fetuses. Since oxytocin stimulates further contractions of the uterus, which is exquisitely sensitive to oxytocin at the end of pregnancy, a positive feedback loop is activated. The neural pathway that drives oxytocin neurons via a brainstem relay has been partially characterised, and involves A2 noradrenergic cells in the brainstem. Until close to term the responsiveness of oxytocin neurons is restrained by neuroactive steroid metabolites of progesterone that potentiate GABA inhibitory mechanisms. As parturition approaches, and this inhibition fades as progesterone secretion collapses, a central opioid inhibitory mechanism is activated that restrains the excitation of oxytocin cells by brainstem inputs. This opioid restraint is the predominant damper of oxytocin cells before and during parturition, limiting stimulation by extraneous stimuli, and perhaps facilitating optimal spacing of births and economical use of the store of oxytocin accumulated during pregnancy. During parturition, oxytocin cells increase their basal activity, and hence oxytocin secretion increases. In addition, the oxytocin cells discharge a burst of action potentials as each fetus passes through the birth canal. Each burst causes the secretion of a pulse of oxytocin, which sharply increases uterine tone; these bursts depend upon auto-stimulation by oxytocin released from the dendrites of the magnocellular neurons in the supraoptic and paraventricular nuclei. With the exception of the opioid mechanism that emerges to restrain oxytocin cell responsiveness, the behavior of oxytocin cells and their inputs in pregnancy and parturition is explicable from the effects of hormones of pregnancy (relaxin, estrogen, progesterone) on pre-existing mechanisms, leading through relative quiescence at term inter alia to net increase in oxytocin storage, and reduced auto-inhibition by nitric oxide generation. Cyto-architectonic changes in parturition, involving evident retraction of glial processes between oxytocin cells so they get closer together, are probably a response to oxytocin neuron activation rather than being essential for their patterns of firing in parturition.

中文翻译：

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大细胞催产素系统，母性之源：妊娠适应

在分娩过程中，在子宫收缩的刺激下，脑垂体后叶的催产素分泌增加，子宫收缩有力地将胎儿排出体外。由于催产素会刺激子宫进一步收缩，而子宫在怀孕末期对催产素非常敏感，因此会激活正反馈回路。通过脑干中继驱动催产素神经元的神经通路已被部分表征，涉及脑干中的 A2 去甲肾上腺素能细胞。直到接近术语，催产素神经元的反应性受到黄体酮的神经活性类固醇代谢物的抑制，从而增强 GABA 抑制机制。随着分娩的临近，这种抑制会随着孕激素分泌的减少而消失，中枢阿片类抑制机制被激活，抑制脑干输入对催产素细胞的激发。这种阿片类药物抑制是分娩前和分娩期间催产素细胞的主要抑制因素，限制了外来刺激的刺激，并可能促进最佳生育间隔和妊娠期间积累的催产素储存的经济使用。在分娩过程中，催产素细胞增加其基础活性，因此催产素分泌增加。此外，当每个胎儿通过产道时，催产素细胞会释放出一阵动作电位。每次爆发都会引起催产素脉冲的分泌，从而使子宫张力急剧增加；这些爆发依赖于从视上核和室旁核中的大细胞神经元的树突释放的催产素的自动刺激。除了出现抑制催产素细胞反应的阿片类药物机制外，催产素细胞的行为及其在妊娠和分娩中的输入可以从妊娠激素（松弛素、雌激素、孕激素）对预先存在的机制的影响中得到解释，导致通过相对静止期，尤其是催产素储存的净增加，以及由一氧化氮生成引起的自动抑制减少。分娩中的细胞结构变化，包括催产素细胞之间的神经胶质过程明显收缩，使它们更靠近，这可能是对催产素神经元激活的一种反应，而不是它们在分娩时的放电模式所必需的。催产素细胞的行为及其在妊娠和分娩中的输入可以从妊娠激素（松弛素、雌激素、黄体酮）对预先存在的机制的影响来解释，导致在足月期间的相对静止，尤其是催产素储存的净增加，以及通过产生一氧化氮减少自动抑制。分娩中的细胞结构变化，包括催产素细胞之间的神经胶质过程明显收缩，使它们更接近，可能是对催产素神经元激活的反应，而不是它们在分娩时的放电模式所必需的。催产素细胞的行为及其在妊娠和分娩中的输入可以从妊娠激素（松弛素、雌激素、黄体酮）对预先存在的机制的影响来解释，导致在足月期间的相对静止，尤其是催产素储存的净增加，以及通过产生一氧化氮减少自动抑制。分娩中的细胞结构变化，包括催产素细胞之间的神经胶质过程明显收缩，使它们更接近，可能是对催产素神经元激活的反应，而不是它们在分娩时的放电模式所必需的。并减少由一氧化氮生成引起的自动抑制。分娩中的细胞结构变化，包括催产素细胞之间的神经胶质过程明显收缩，使它们更接近，可能是对催产素神经元激活的反应，而不是它们在分娩时的放电模式所必需的。并减少由一氧化氮生成引起的自动抑制。分娩中的细胞结构变化，包括催产素细胞之间的神经胶质过程明显收缩，使它们更接近，可能是对催产素神经元激活的反应，而不是它们在分娩时的放电模式所必需的。