一项刊登在PNAS上的研究发现，不可预测的长期压力可能减少一种基因的表达，这种基因帮助防止涉及情绪障碍的一种大脑细胞萎缩。神经可塑性是指大脑细胞对新的体验做出响应而重新组织的能力，许多研究已经把大脑海马区的可塑性减少与长期压力联系了起来。
Ronald Duman及其同事研究了一种维持可塑性且被抗抑郁药物上调的基因“neuritin”的表达水平的减少是否会导致抑郁症状。这组作者使用一个大鼠模型发现了不可预测的长期压力减少了neuritin在海马区的表达，而抗抑郁药物的治疗逆转了这种效应。此外，这组作者证明了增加neuritin的表达直接防止了情绪障碍以及抑郁和焦虑相关行为的典型的大脑细胞萎缩。
这组作者报告说，相反，在实验中降低了neuritin水平的大鼠表现出了类似于长期不可预测的压力引发的抑郁样行为。把这些结合起来，这些发现提示随着时间推移，重复的压力可能产生导致海马区神经元萎缩的neuritin缺乏，因此也就增加了对焦虑和情绪障碍的易感性。（生物谷Bioon.com）
doi:10.1073/pnas.1201191109
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Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress
Hyeon Sona,b,1, Mounira Banasra, Miyeon Choib, Seung Yeon Chaeb, Pawel Licznerskia, Boyoung Leea, Bhavya Voletia, Nanxin Lia, Ashley Lepacka, Neil M. Fourniera, Ka Rim Leeb, In Young Leeb, Juhyun Kimc, Joung-Hun Kimc, Yong Ho Kimd, Sung Jun Junge, and Ronald S. Dumana,1
Decreased neuronal dendrite branching and plasticity of the hippocampus, a limbic structure implicated in mood disorders, is thought to contribute to the symptoms of depression. However, the mechanisms underlying this effect, as well as the actions of antidepressant treatment, remain poorly characterized. Here, we show that hippocampal expression of neuritin, an activity-dependent gene that regulates neuronal plasticity, is decreased by chronic unpredictable stress (CUS) and that antidepressant treatment reverses this effect. We also show that viral-mediated expression of neuritin in the hippocampus produces antidepressant actions and prevents the atrophy of dendrites and spines, as well as depressive and anxiety behaviors caused by CUS. Conversely, neuritin knockdown produces depressive-like behaviors, similar to CUS exposure. The ability of neuritin to increase neuroplasticity is confirmed in models of learning and memory. Our results reveal a unique action of neuritin in models of stress and depression, and demonstrate a role for neuroplasticity in antidepressant treatment response and related behaviors.
