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首页> 外文期刊>Frontiers in neuroendocrinology >The magnocellular oxytocin system, the fount of maternity: adaptations in pregnancy.
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The magnocellular oxytocin system, the fount of maternity: adaptations in pregnancy.

机译：孕产妇的源头是大细胞催产素系统：妊娠适应症。

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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.
机译：在分娩时，垂体后叶催产素的分泌增加，这是由于子宫收缩迫使胎儿排出而引起的。由于催产素刺激子宫的进一步收缩，子宫在妊娠结束时对催产素非常敏感，因此激活了积极的反馈回路。通过脑干继电器驱动催产素神经元的神经通路已被部分表征，并涉及脑干中的A2去甲肾上腺素能细胞。直到近期，催产素神经元的反应能力仍受孕激素增强GABA抑制机制的激素性类固醇代谢产物的抑制。随着分娩的临近，随着黄体酮分泌的减弱，这种抑制作用逐渐减弱，激活了一种中央阿片样物质抑制机制，该机制抑制了脑干输入对催产素细胞的刺激。这种阿片样物质抑制作用是分娩之前和分娩过程中催产素细胞的主要阻尼器，限制了外部刺激的刺激，并可能促进了最佳的分娩间隔，并有利于经济使用怀孕期间积累的催产素。在分娩期间，催产素细胞增加其基础活性，因此催产素的分泌增加。另外，催产素细胞在每个胎儿通过产道时释放出一系列动作电位。每次爆发都会引起催产素脉冲的分泌，从而急剧增加子宫的张力。这些爆发取决于从视上和脑室旁核中大细胞神经元树突释放的催产素的自动刺激。除了可以抑制催产素细胞反应性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通过妊娠激素（松弛素，雌激素，孕酮）对既有机制的影响来解释，从而导致通过长期保持相对静止来使催产素的储存净增加，并减少一氧化氮产生的自抑制作用。细胞结构的分娩改变，包括催产素细胞之间神经胶质过程的明显收缩，使它们彼此靠近，可能是对催产素神经元激活的反应，而不是其在分娩过程中的放电模式所必需。

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