Work by many groups demonstrate links between peripheral markers of inflammation and symptoms of depression. Here, Nusslock and colleagues present an update to their neuroimmune network model to incorporate a developmental lens. They propose that specific neural circuits may be responsible for causing heightened inflammation. One principal circuit includes the amygdala and prefrontal cortex and is proposed to be involved in threat detection. Thus, heightened threat sensitivity resulting from early life stress is suggested to cause increases in inflammatory signaling. Second, the authors suggest that reward circuits, including the striatum, may be targets of increased inflammation leading to symptoms of anhedonia. In this commentary, I add context to the model proposed by Nusslock et al., suggesting that taking a learning perspective and considering additional circuits, including the hippocampus and midline structures may be necessary to more fully account for the phenomena described by the authors.

中文翻译：

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添加到神经免疫网络模型：Nusslock 等人的评论。 (2024)

许多小组的工作证明了炎症外周标志物与抑郁症状之间的联系。在这里，努斯洛克和同事展示了他们的神经免疫网络模型的更新，以纳入发育透镜。他们提出，特定的神经回路可能是导致炎症加剧的原因。一个主要回路包括杏仁核和前额皮质，提议参与威胁检测。因此，早期生活压力导致的威胁敏感性升高被认为会导致炎症信号的增加。其次，作者认为，包括纹状体在内的奖励回路可能是炎症增加的目标，导致快感缺乏症状。在这篇评论中，我为 Nusslock 等人提出的模型添加了上下文，建议采取学习的角度并考虑其他回路，包括海马体和中线结构，可能有必要更全面地解释作者描述的现象。