Treadway Michael T
Curr Top Behav Neurosci. 2016;27:337-55. doi: 10.1007/7854_2015_400.
Anhedonia has long been recognized as a central feature of major depression, yet its neurobiological underpinnings remain poorly understood. While clinical definitions of anhedonia have historically emphasized reductions in pleasure and positive emotionality, there has been growing evidence that motivation may be substantially impaired as well. Here, we review recent evidence suggesting that motivational deficits may reflect an important dimension of symptomatology that is discrete from traditional definitions of anhedonia in terms of both behavior and pathophysiology. In summarizing this work, we highlight two candidate neurobiological mechanisms--elevated inflammation and reduced synaptic plasticity--that may underlie observed reductions in motivation and reinforcement learning in depression.
长期以来，快感缺失一直被视为重度抑郁症的核心特征，但其神经生物学基础仍知之甚少。虽然快感缺失的临床定义在历史上一直强调愉悦感和积极情绪的减少，但越来越多的证据表明动机也可能受到严重损害。在此，我们回顾了近期的证据，这些证据表明动机缺陷可能反映了症状学的一个重要维度，在行为和病理生理学方面都与快感缺失的传统定义不同。在总结这项工作时，我们强调了两种候选神经生物学机制——炎症升高和突触可塑性降低——它们可能是抑郁症中观察到的动机和强化学习减少的基础。
