Inflammation-associated depression: from serotonin to kynurenine.
Inflammation-associated depression: from serotonin to kynurenine.
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DOI：
10.1016/j.psyneuen.2010.09.012
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发表时间：
2011-04
影响因子：
3.7
通讯作者：
Kelley, Keith W.
中科院分区：
文献类型：
--
作者：
Dantzer, Robert;O'Connor, Jason C.;Lawson, Marcus A.;Kelley, Keith W.
关键词：
在抑郁症领域，炎症相关性抑郁症是一个例外，因为它的原因很明显，而且很容易在动物模型中模拟。此外，准实验研究可以在长期接受重组细胞因子治疗的患者中进行，因为这些患者可以在刺激免疫系统之前、期间和之后进行纵向研究。这些临床研究表明，抑郁症是一种晚期现象，是在早期出现疾病的背景下发展起来的。在炎症相关性抑郁症的动物模型中结合这一特征，可以证明大脑5-羟色胺能神经传递的改变在发病机制中不起主要作用。这与色氨酸降解酶吲哚-2，3-双加氧酶的激活形成对比，该酶产生潜在的神经毒性犬尿氨酸代谢物，如3-羟基犬尿氨酸和喹啉酸。尽管外周和中枢产生的犬尿氨酸的相对重要性以及这种化合物的细胞来源仍有待确定，但这些发现为炎症性抑郁的治疗提供了新的靶点，可以通过激活神经免疫机制将其扩展到其他精神疾病。
In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptotphan degrading enzyme indoleamine 2,3 dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms.
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