Neuromelanin, Reinforcement Learning, and Anhedonia: Identifying Associations, Antecedents, and Consequences

Reward processing plays a transdiagnostic role in the etiopathogenesis of psychopathology. Reinforcement learning deficits, driven by dopamine dysregulation, are hypothesized to explain key aspects of such abnormalities. Therefore, this project examines whether dopamine, assessed using neuromelanin-sensitive magnetic resonance imaging (NM-MRI), a novel imaging technique for assessing long-term midbrain dopamine function in the Substantia Nigra (SN) and Ventral Tegmental Area (VTA), contributes to reinforcement learning performance. Additionally, the relationship between dopamine dysfunction and anhedonia is investigated. Finally, due to evidence suggesting that life stress may interrupt dopaminergic and learning processes, the influence of prospective measures of early childhood adversity (ECA) and chronic life stress on reinforcement learning and dopamine dysfunction are examined. Importantly, each of these questions have bearing on the construct validity of NM-MRI as an individual-difference measure of dopamine function.

Participants (N = 81) were recruited from the Stony Brook Temperament Study (SBTS), an ongoing longitudinal study, shortly after their 18th birthday to complete NM-MRI imaging, a behavioral reinforcement learning task, and anhedonia questionnaires. Associations were examined between NM-MRI-assessed dopamine, multiple measures of reinforcement learning performance, multiple assessments of anhedonia, and ECA and chronic life stress. Results from the current investigation indicate that NM-MRI-assessed dopamine was significantly associated with certain measures of reinforcement learning, but not others. Additionally, other measures of impaired reinforcement learning were related to increased concurrent anhedonic symptoms. Finally, higher levels of chronic life stress, but not ECA, were associated with impairments in reinforcement learning performance. Taken together, there are links between dopaminergic function, reinforcement learning, life stress, and anhedonia, but these associations vary across measures. Future work should continue to elucidate potentially important etiological processes in the development of reinforcement learning and anhedonia.