Dept. of Behavioral and Molecular Neurobiology, University of Regensburg, 93053 Regensburg, Germany.
Endocrinology. 2011 Oct;152(10):3930-40. doi: 10.1210/en.2011-1091. Epub 2011 Aug 16.
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 × 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.
母体适应,如焦虑减少和应激反应减弱,对于成功的后代产后发育是必要的。然而,越来越多的证据表明,它们也需要保护母亲的心理健康,并且怀孕期间暴露于慢性应激可能会阻止这种适应。在妊娠第 4-16 天期间,每隔一天使用拥挤应激(24 小时)和束缚应激(2×1 小时)来检查慢性妊娠应激对相关行为、神经内分泌和围产期神经元适应的影响。为了确定慢性应激引起的改变是否仅限于围产期,我们将处女作为对照组。通过验证应激程序,我们证明了应激母鼠体重增加减少,肾上腺重量增加,相对于非应激对照组。慢性应激阻止了许多围产期适应,包括基础血浆皮质酮水平升高、下丘脑室旁核催产素 mRNA 表达增加以及焦虑缓解。然而,慢性应激并没有阻止围产期相关的 CRH mRNA 表达减少或减弱皮质酮对急性应激源的反应,也没有影响下丘脑血管加压素 mRNA 表达。这些应激引起的变化对围产期的特异性表明,处女应激鼠没有受到这些参数的影响。尽管慢性应激没有改变与抑郁相关的行为,但它逆转了对急性丙咪嗪治疗的反应,并增加了哺乳期的主动母性行为。因此,妊娠应激对基础皮质酮和催产素系统活性的围产期相关增加的预防揭示了两种可能增加产后精神障碍风险的改变,特别是焦虑。