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.