Anhedonia is a core symptom of major depressive disorder (MDD), the neurobiological
mechanisms of which remain poorly understood. Despite decades of speculation regarding
the role of dopamine (DA) in anhedonic symptoms, empirical evidence has remained elusive,
with frequent reports of contradictory findings. In the present review, we argue that
this has resulted from an underspecified definition of anhedonia, which has failed
to dissociate between consummatory and motivational aspects of reward behavior. Given
substantial preclinical evidence that DA is involved primarily in motivational aspects
of reward, we suggest that a refined definition of anhedonia that distinguishes between
deficits in pleasure and motivation is essential for the purposes of identifying its
neurobiological substrates. Moreover, bridging the gap between preclinical and clinical
models of anhedonia may require moving away from the conceptualization of anhedonia
as a steady-state, mood-like phenomena. Consequently, we introduce the term "decisional
anhedonia" to address the influence of anhedonia on reward decision-making. These
proposed modifications to the theoretical definition of anhedonia have implications
for research, assessment and treatment of MDD.
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