Anhedonia is a core symptom of major depressive disorder (MDD), but its neurobiological mechanisms remain poorly understood. Despite decades of research, empirical evidence on dopamine (DA) involvement in anhedonic symptoms has been inconsistent. This review argues that this inconsistency arises from an underspecified definition of anhedonia, which fails to distinguish between motivational and consummatory aspects of reward behavior. The authors propose a refined definition of anhedonia that differentiates between deficits in pleasure (consummatory anhedonia) and motivation (motivational anhedonia). They introduce the term "decisional anhedonia" to address the influence of anhedonia on reward decision-making. These modifications are essential for identifying the neurobiological substrates of anhedonia and improving research, assessment, and treatment of MDD. Anhedonia is defined in the DSM-IV-TR as a diminished interest or pleasure in previously rewarding stimuli. However, current assessments focus heavily on pleasure, neglecting motivational aspects. This may obscure important associations related to specific symptoms. The review highlights the importance of distinguishing between hedonic (pleasure) and motivational (wanting) aspects of reward processing. Preclinical studies suggest that DA is primarily involved in motivational aspects of reward, not pleasure. This has implications for understanding the neurobiological basis of anhedonia in MDD. The review discusses the neurobiological bases of motivational and consummatory anhedonia, emphasizing the role of DA in the striatum and other brain regions. DA is involved in reward motivation and reinforcement, with evidence from animal studies showing that DA dysfunction contributes to anhedonia in MDD. Human studies also support the role of DA in MDD, with findings on DA turnover, receptor availability, and imaging studies indicating reduced DA function in MDD. These findings suggest that DA dysfunction is a key factor in the pathophysiology of MDD. The review also addresses the heterogeneity in MDD, including diagnostic, etiological, and symptom heterogeneity. These factors complicate the interpretation of neurobiological findings. The authors argue that a more nuanced understanding of anhedonia, including its motivational and consummatory aspects, is necessary for accurate diagnosis and treatment. They emphasize the need for refined assessment tools that reflect the multi-faceted nature of reward deficits in MDD. The review concludes that DA dysfunction is a critical component of MDD, and further research is needed to clarify its role in the disorder.Anhedonia is a core symptom of major depressive disorder (MDD), but its neurobiological mechanisms remain poorly understood. Despite decades of research, empirical evidence on dopamine (DA) involvement in anhedonic symptoms has been inconsistent. This review argues that this inconsistency arises from an underspecified definition of anhedonia, which fails to distinguish between motivational and consummatory aspects of reward behavior. The authors propose a refined definition of anhedonia that differentiates between deficits in pleasure (consummatory anhedonia) and motivation (motivational anhedonia). They introduce the term "decisional anhedonia" to address the influence of anhedonia on reward decision-making. These modifications are essential for identifying the neurobiological substrates of anhedonia and improving research, assessment, and treatment of MDD. Anhedonia is defined in the DSM-IV-TR as a diminished interest or pleasure in previously rewarding stimuli. However, current assessments focus heavily on pleasure, neglecting motivational aspects. This may obscure important associations related to specific symptoms. The review highlights the importance of distinguishing between hedonic (pleasure) and motivational (wanting) aspects of reward processing. Preclinical studies suggest that DA is primarily involved in motivational aspects of reward, not pleasure. This has implications for understanding the neurobiological basis of anhedonia in MDD. The review discusses the neurobiological bases of motivational and consummatory anhedonia, emphasizing the role of DA in the striatum and other brain regions. DA is involved in reward motivation and reinforcement, with evidence from animal studies showing that DA dysfunction contributes to anhedonia in MDD. Human studies also support the role of DA in MDD, with findings on DA turnover, receptor availability, and imaging studies indicating reduced DA function in MDD. These findings suggest that DA dysfunction is a key factor in the pathophysiology of MDD. The review also addresses the heterogeneity in MDD, including diagnostic, etiological, and symptom heterogeneity. These factors complicate the interpretation of neurobiological findings. The authors argue that a more nuanced understanding of anhedonia, including its motivational and consummatory aspects, is necessary for accurate diagnosis and treatment. They emphasize the need for refined assessment tools that reflect the multi-faceted nature of reward deficits in MDD. The review concludes that DA dysfunction is a critical component of MDD, and further research is needed to clarify its role in the disorder.