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Exposure to chronic pregnancy stress reverses peripartum-associated adaptations: implications for postpartum anxiety and mood disorders.

机译:暴露于慢性妊娠应激会逆转与产期相关的适应:对产后焦虑和情绪障碍的影响。

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Maternal adaptations, such as decreased anxiety and attenuated stress responsiveness, are necessary to enable successful postnatal development of the offspring. However, there is growing evidence that they are also required to protect the mental health of the mother and that exposure to chronic stress during pregnancy may prevent such adaptations. Overcrowding stress (24 h) and restraint stress (2 x 1 h) were employed on alternate days between pregnancy d 4-16 to examine the impact of chronic pregnancy stress on relevant behavioral, neuroendocrine, and neuronal peripartum adaptations. To determine whether the chronic stress-induced alterations were specific to the peripartum period, we included virgins as controls. Validating the stress procedure, we demonstrated decreased body-weight gain and increased adrenal weight in stressed dams, relative to their nonstressed controls. Chronic stress prevented a number of peripartum adaptations, including basal plasma hypercorticosterone levels, increased oxytocin mRNA expression in the hypothalamic paraventricular nucleus, and anxiolysis. However, chronic stress did not prevent the peripartum-associated decrease in CRH mRNA expression or attenuate corticosterone response to an acute stressor, nor did it affect hypothalamic vasopressin mRNA expression. Illustrating the specificity of these stress-induced changes to the peripartum period, none of these parameters were affected in stressed virgins. Although chronic stress did not alter depression-related behavior, it reversed the response to acute imipramine treatment and increased active maternal behavior in lactation. Thus, prevention of the peripartum-associated increases in basal corticosterone and oxytocin system activity by pregnancy stress reveal two alterations that may increase the risk of postpartum psychiatric disorders, particularly anxiety.
机译:产妇的适应性,例如焦虑的减轻和应激反应的减弱,是使后代成功发育的必要条件。但是,越来越多的证据表明,也需要它们来保护母亲的心理健康,并且在怀孕期间暴露于慢性压力下可能会阻止这种适应。在妊娠第4-16天之间的交替日使用过度拥挤压力(24 h)和束缚压力(2 x 1 h),以检查长期妊娠压力对相关行为,神经内分泌和神经元围产期适应的影响。为了确定慢性应激诱发的改变是否对围产期具有特异性,我们将处女作为对照。验证压力程序,我们证明了相对于未受压的对照组,受压的大坝的体重增加减少且肾上腺重量增加。慢性应激阻止了许多围产期适应,包括基础血浆高皮质酮水平,下丘脑室旁核中催产素mRNA表达的增加以及抗焦虑作用。但是,慢性应激不能阻止围产期相关的CRH mRNA表达下降或减弱对急性应激源的皮质酮反应,也不会影响下丘脑血管加压素mRNA表达。说明了这些压力诱发的围产期变化的特异性,这些参数在处女处均未受到影响。尽管慢性应激并没有改变与抑郁症相关的行为,但它逆转了对急性丙咪嗪治疗的反应,并增加了哺乳期母亲的活跃行为。因此,通过妊娠应激来预防与围产期相关的基础皮质酮和催产素系统活性的增加显示出两种改变,这些改变可能会增加产后精神病,特别是焦虑症的风险。

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