产后抑郁症（PPD）是分娩的一种重大心理并发症，影响了高达20％的母亲，然而，它仍然研究不足。线粒体是细胞稳态和能量产生的关键器官，与PPD病理学的许多提出机制存在联系。大脑线粒体功能受到压力的影响，压力是发展PPD的一个重要风险因素，并与焦虑样和社交行为有关。考虑到线粒体在调节脑功能和行为中的重要性，我们假设线粒体功能失调与慢性应激诱导的PPD大鼠模型中的行为改变相关。我们使用在晚期妊娠期间经过验证和具有翻译参考价值的慢性轻度不可预测应激模式诱导成年产后Wistar大鼠中的PPD相关行为。在产后中期，我们使用高分辨率呼吸法测量了前额叶皮层（PFC）和伏隔核（NAc）中的线粒体功能。然后，我们测量了PFC和血浆中线粒体复合物蛋白和4-羟基壬酸醛（氧化应激标志物）的蛋白表达，以及Th1 / Th2细胞因子水平。我们报道了一个新发现，即妊娠应激降低了产后母鼠PFC中的线粒体功能，但没有影响NAc。然而，对于单独控制应激或胎次效应的组，与无产鼠对照组相比，两个脑区的线粒体呼吸测量结果没有差异。受应激的产鼠PFC线粒体功能下降伴随着产后负面行为后果、特定于复合物-I的蛋白表达缺陷以及血浆和PFC中肿瘤坏死因子α细胞因子水平的增加。总体而言，我们报道了PFC线粒体呼吸率、PPD相关行为和妊娠应激后炎症之间的相互关系，突显了线粒体功能在产后健康中的潜在作用。

Postpartum depression (PPD) is a major psychiatric complication of childbirth, affecting up to 20% of mothers, yet remains understudied. Mitochondria, dynamic organelles crucial for cell homeostasis and energy production, share links with many of the proposed mechanisms underlying PPD pathology. Brain mitochondrial function is affected by stress, a major risk factor for development of PPD, and is linked to anxiety-like and social behaviors. Considering the importance of mitochondria in regulating brain function and behavior, we hypothesized that mitochondrial dysfunction is associated with behavioral alterations in a chronic stress-induced rat model of PPD. Using a validated and translationally relevant chronic mild unpredictable stress paradigm during late gestation, we induced PPD-relevant behaviors in adult postpartum Wistar rats. In the mid-postpartum, we measured mitochondrial function in the prefrontal cortex (PFC) and nucleus accumbens (NAc) using high-resolution respirometry. We then measured protein expression of mitochondrial complex proteins and 4-hydroxynonenal (a marker of oxidative stress), and Th1/Th2 cytokine levels in PFC and plasma. We report novel findings that gestational stress decreased mitochondrial function in the PFC, but not the NAc of postpartum dams. However, in groups controlling for the effects of either stress or parity alone, no differences in mitochondrial respiration measured in either brain regions were observed compared to nulliparous controls. This decrease in PFC mitochondrial function in stressed dams was accompanied by negative behavioral consequences in the postpartum, complex-I specific deficits in protein expression, and increased Tumor Necrosis Factor alpha cytokine levels in plasma and PFC. Overall, we report an association between PFC mitochondrial respiration, PPD-relevant behaviors, and inflammation following gestational stress, highlighting a potential role for mitochondrial function in postpartum health.