Depression Symptoms Correlate with Attenuated Emotional Processing Signals in the Caudate During Reward Feedback

Introduction: Depression is one of the most prevalent psychiatric disorders worldwide, and anhedonia, characterized by reward insensitivity, is a core feature. Additionally, ​​depressed patients have been shown to experience negative affective biases as well as reduced activation in the caudate, amygdala, and hippocampus when responding to emotional versus neutral stimuli. These findings could indicate a decreased capacity for striato-limbic emotional arousal and regulation in depression. We have previously shown that caudate alpha-beta power increases following reward feedback and that this increase negatively correlates with depression symptom severity. However, the neurophysiological relationship between reward signaling and emotional processing in depression remains unknown. We investigated how emotional valence of reward stimuli and depression symptoms interact to modulate reward-related caudate alpha-beta power.

Methods: Twenty movement disorder patients undergoing awake deep brain stimulation surgery with electrode trajectories traversing the caudate participated in this study. Subjects completed an emotional verbal 2-back working memory task, which sequentially presented words characterized by negative, neutral, or positive emotional qualities. For correct responses, the word presented turned green to serve as visual reward feedback. Subjects completed the Beck Depression Inventory-II preoperatively, for which scores ≥14 designated clinically significant depression symptoms. We then performed repeated-measures ANOVAs to assess how stimuli emotional valence affects alpha-beta power during reward feedback in depressed and non-depressed patients.

Results: In non-depressed patients, we found a significant main effect of emotional valence of the presented word on reward-related caudate alpha-beta power (p=0.0099), with positive valence stimuli evoking significantly higher power compared to negative stimuli (p=0.012). In depressed patients, emotional valence did not modulate reward-related alpha-beta power (p=0.15).

Conclusion : These results suggest that caudate alpha-beta power response to reward is enhanced by positive emotional stimuli. However, depression symptoms dampen the effect of emotional stimuli on caudate reward signaling. These findings support caudate alpha-beta power as a potential biomarker for how emotion and anhedonia interact in depression and could inform adaptive neuromodulation strategies for these symptoms in treatment-resistant depression.