关键词: 抑郁, 快感缺失, 金钱奖赏, 社会奖赏, 伏隔核

Abstract: Monetary and social rewards (e.g., praise) are common incentives that drive motivation and reinforce behaviors linked to future gains. Individuals with depression often confront social dysfunction and anhedonia, a diminished interest in pleasurable activities, raising questions about potential differences in the neural mechanisms that process these rewards. This review summarizes the neural processes involved in the processing of monetary and social rewards at two critical stages: anticipation and consumption. It first examines how these rewards activate neural systems in healthy individuals, before exploring the alterations in reward processing observed in those with subclinical depression and depressive disorders. Lastly, the review identifies unresolved questions in this field and aims to inspire future research that will deepen our understanding and inform clinical strategies for treating anhedonia symptoms.
Neuroimaging evidence using the broadly applied incentive delay tasks has connected reward processing to brain reward circuits, particularly the ventral striatum. Specifically, studies in healthy populations demonstrate that compared to non-reward cues, anticipating monetary and social rewards elicited heightened activations in the reward and action preparation brain networks, including the nucleus accumbens, caudate, and supplementary motor area. Social rewards additionally engage the mentalizing system for social signal evaluation, involving areas such as the temporoparietal junction and precuneus. EEG studies indicate that components such as cue-P3, contingent negative variation (CNV), and stimulus-preceding negativity (SPN) elicited by reward cues serve as markers of anticipatory responses, with more desirable rewards yielding larger amplitudes. During reward consumption, enhanced activation is observed in the orbitofrontal cortex (OFC)/ventromedial prefrontal cortex (VMPFC), brain regions involved in encoding the value of either monetary or social reward feedback. Notably, there is limited evidence suggesting neural differences in processing monetary vs. social rewards: monetary rewards predominantly activate the thalamus, whereas social rewards engage emotional brain regions like the amygdala. Moreover, EEG findings suggest that reward-related positivity (RewP) and feedback-P3 are crucial markers of reward consumption, with more favored rewards showing larger amplitudes.
Anhedonia in individuals with depression may stem from abnormalities in either or both stages of reward anticipation and consumption, though conclusive evidence remains elusive. Research shows that depressed individuals exhibit deficits in anticipatory pleasure for both monetary and social rewards, characterized primarily by attenuated ventral striatal activation, reduced functional connectivity between the dorsolateral prefrontal cortex (DLPFC) and striatum/putamen, and altered activation in the anterior cingulate cortex. Notably, the impaired anticipation of social rewards is more pronounced than that of monetary rewards, marked by insufficient activation in areas such as the dorsomedial prefrontal cortex and reduced CNV amplitudes. Intriguingly, depression does not seem to affect individuals’ anticipation of social rewards from humanoid robots, suggesting significant potential for artificial intelligence devices to restore social functions among depressed individuals. Concerning consumption anhedonia, deficits in social reward processing are particularly prominent in depressed populations, as evidenced by altered feedback-related negativity (FRN) and feedback-P3 amplitudes, as well as aberrant activity in the striatum and insula.
Several critical avenues warrant further exploration. First, research on neuromodulation aimed at rectifying aberrant pleasure processing is limited. While existing studies have shown that excitatory brain stimulation over the DLPFC via transcranial magnetic stimulation (TMS) can enhance anticipation for monetary rewards in patients with major depressive disorder, its effects on consumption pleasure remain largely unexplored. Investigating neuromodulation or neurofeedback targeting value-encoding regions, such as the OFC/VMPFC could provide insights into alleviating consumption anhedonia. Additionally, transferring intervention strategies from monetary to social reward processing and assessing the efficacy in targeting the social brain require further examination. Second, comparative studies should rigorously control for the levels of “wanting” and “liking” associated with monetary and social rewards. Research in healthy populations indicates that reaction times differ between social and monetary incentive paradigms but converge when these levels are accounted for. Similarly, while studies reveal no significant group differences in reward anticipation between healthy and depressed individuals, healthy participants exhibit greater effort and faster responses with increasing reward levels, a pattern not seen in the depressed group. Furthermore, a critical review of comparative studies on monetary and social rewards highlights differences in dimensions such as timing, familiarity, processing priority, and certainty. Future research should carefully control for these potential factors and further investigate the effects of reward types on processing. Third, exploring the feasibility of using artificial intelligence devices to assist depressed individuals in restoring social reward processing and other social functions holds great promise. Studies suggest that interactions with intelligent robots can improve emotional connections and alleviate depressive symptoms, suggesting the therapeutic potential of artificial intelligence devices. Future research should explore these possibilities to offer novel insights and improve treatment outcomes and quality of life for individuals with depression and anhedonia.

Key words: depression, anhedonia, monetary reward, social reward, nucleus accumbens