C1q deletion exacerbates stress-induced learned helplessness behavior and induces neuroinflammation in mice.
C1q deletion exacerbates stress-induced learned helplessness behavior and induces neuroinflammation in mice.
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DOI：
10.1038/s41398-022-01794-4
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发表时间：
2022-02-01
影响因子：
6.8
通讯作者：
Pillai A
中科院分区：
文献类型：
--
作者：
Madeshiya AK;Whitehead C;Tripathi A;Pillai A
据报道，抑郁症患者死后脑样本和血液中促炎细胞因子水平升高。然而，导致抑郁样症状的炎症途径尚不清楚。使用抑郁症的习得性无助 (LH) 模型，我们研究了 C1q（经典补体途径的启动子）在介导小鼠应激诱发的抑郁样行为中的作用。我们观察到野生型 (WT) 和 C1q 敲除 (KO) 小鼠的社交行为、绝望行为、空间记忆和攻击行为没有显着变化。然而，C1q 缺失加剧了小鼠不可避免的电足电击引起的习得性无助行为。我们发现，与幼稚小鼠相比，WT 无助小鼠的前额皮质 (PFC) 中 C1q mRNA 水平显着降低。 C1q KO 小鼠的 PFC 中促炎细胞因子水平升高。这些发现表明，经典补体途径介导的习得性无助行为在压力条件下伴随着神经炎症变化。
Increased levels of pro-inflammatory cytokines have been reported in postmortem brain samples and in the blood of depressed subjects. However, the inflammatory pathways that lead to depressive-like symptoms are not well understood. Using the learned helplessness (LH) model of depression, we examined the role of C1q, the initiator of classical complement pathway in mediating stress-induced depressive-like behavior in mice. We observed no significant changes in social behavior, despair behavior, spatial memory, and aggressive behavior between the wild type (WT) and C1q knockout (KO) mice. However, C1q deletion exacerbated the inescapable electric foot shock-induced learned helplessness behavior in mice. We found significant reductions in C1q mRNA levels in the prefrontal cortex (PFC) of WT helpless mice as compared to the naïve mice. Increased levels of pro-inflammatory cytokines were found in the PFC of C1q KO mice. These findings suggest that classical complement pathway-mediated learned helplessness behavior is accompanied by neuroinflammatory changes under stressful conditions.
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