Stress-Induced Depressive Behaviors Require a Functional NLRP3 Inflammasome
Stress-Induced Depressive Behaviors Require a Functional NLRP3 Inflammasome
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DOI：
10.1007/s12035-015-9408-7
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发表时间：
2016-09-01
影响因子：
5.1
通讯作者：
Cordero, Mario D.
中科院分区：
文献类型：
--
作者：
Alcocer-Gomez, Elisabet;Ulecia-Moron, Cristina;Cordero, Mario D.
抑郁症是现代社会的一个主要公共卫生问题，但人们对这种疾病与神经炎症之间的分子联系知之甚少。炎性小体复合体最近被证明与抑郁症有关。本研究显示NLRP 3炎性体在应激诱导的抑郁症动物模型中的意义。因此，我们在这里表明，在没有NLRP 3炎性体的情况下，长期的应激不会引起小鼠的抑郁行为或小胶质细胞活化，也不会抑制海马神经发生。事实上，NLRP 3缺失或抑制小胶质细胞活化会损害与抑郁症相关的应激诱导的改变。根据动物模型中的这些发现，炎性小体可能是预防患者抑郁症的新治疗干预的靶点。
Depression is a major public health concern in modern society, yet little is known about the molecular link between this condition and neuroinflammation. The inflammasome complex was recently shown to be implicated in depression. The present study shows the implication of NLRP3 inflammasome in animal model of stress-induced depression. Accordingly, we show here that in the absence of a NLRP3 inflammasome, prolonged stress does not provoke depressive behaviors or microglial activation in mice or dampen hippocampal neurogenesis. Indeed, NLRP3 deletion or inhibition of microglial activation impairs the stress-induced alterations associated with depression. According to these findings in animal model, the inflammasome could be a target for new therapeutic interventions to prevent depression in patients.