Impact of social reward on stress circuit function and regulation: Path differences between value affirmation and emotional support

Background

As two typical types of social rewards, both value affirmation and emotional support could alleviate acute stress response, but it is not clear whether they can impact stress circuit function and regulation through different neural pathways.

Method

Sixty-two participants were randomly assigned to the value affirmation, emotional support, and non-reward conditions, then administered an adapted version of the ScanSTRESS paradigm. Participants’ subjective reports of uncontrollability and social evaluative threat were measured to explore the mitigation of stress by social rewards at the behavioral level. Meanwhile, their acute salivary cortisol response to stress was compared among different social reward conditions. Furthermore, we computed linear contrasts for performance (vs relaxation) and reward (vs non-reward) and used psychophysiological interaction (PPI) analysis to explore the impact of social reward on stress circuit function and regulation.

Results

Both value affirmation and emotional support conditions reduced subjective reports of uncontrollability and social evaluation threat, but not cortisol response to stress. Furthermore, value affirmation reduced uncontrollability by enhancing putamen activation, whereas emotional support reduced social evaluation threat by enhancing putamen activation. More importantly, during stress, value affirmation enhanced the functional connectivity of the putamen-hippocampus and putamen-angular gyrus (AG), whereas emotional support enhanced the functional connectivity of the putamen-ventrolateral prefrontal cortex (vlPFC) and putamen-temporal pole mid, compared to the non-reward condition.

Conclusion

Value affirmation and emotional support alleviated acute stress response in different neural pathways. These findings suggested a precise categorization of social reward in intervention of a range of adverse psychological and physiological responses caused by stress.