Anhedonia, a core symptom of Major Depressive Disorder (MDD), remains poorly understood neurobiologically. The authors argue that the lack of empirical evidence regarding the role of dopamine (DA) in anhedonic symptoms is due to an underspecified definition of anhedonia, which fails to distinguish between consummatory and motivational aspects of reward behavior. They propose a refined definition of anhedonia that distinguishes between deficits in pleasure and motivation, suggesting that a behavioral model emphasizing the influence of anhedonia on decision-making may be more appropriate. The introduction of the term "decisional anhedonia" is proposed to address the impact of anhedonia on reward decision-making. The review highlights the importance of refining symptom definitions and assessment tools to better reflect the multifaceted nature of reward deficits in MDD. The neurobiological bases of motivational and consummatory anhedonia are discussed, focusing on the role of DA and striatal circuitry. Studies showing altered DA function in MDD and the antidepressant effects of DA-related interventions are reviewed. The authors conclude that a better understanding of the neurobiological substrates of anhedonia is crucial for improving the diagnosis and treatment of MDD.Anhedonia, a core symptom of Major Depressive Disorder (MDD), remains poorly understood neurobiologically. The authors argue that the lack of empirical evidence regarding the role of dopamine (DA) in anhedonic symptoms is due to an underspecified definition of anhedonia, which fails to distinguish between consummatory and motivational aspects of reward behavior. They propose a refined definition of anhedonia that distinguishes between deficits in pleasure and motivation, suggesting that a behavioral model emphasizing the influence of anhedonia on decision-making may be more appropriate. The introduction of the term "decisional anhedonia" is proposed to address the impact of anhedonia on reward decision-making. The review highlights the importance of refining symptom definitions and assessment tools to better reflect the multifaceted nature of reward deficits in MDD. The neurobiological bases of motivational and consummatory anhedonia are discussed, focusing on the role of DA and striatal circuitry. Studies showing altered DA function in MDD and the antidepressant effects of DA-related interventions are reviewed. The authors conclude that a better understanding of the neurobiological substrates of anhedonia is crucial for improving the diagnosis and treatment of MDD.