Aversive emotional reactions to real or imagined social harms infuse moral judgment and motivate prosocial behavior. Here, we show that the neurotransmitter serotonin directly alters both moral judgment and behavior through increasing subjects’ aversion to personally harming others. We enhanced serotonin in healthy volunteers with citalopram (a selective serotonin reuptake inhibitor) and contrasted its effects with both a pharmacological control treatment and a placebo on tests of moral judgment and behavior. We measured the drugs' effects on moral judgment in a set of moral 'dilemmas' pitting utilitarian outcomes (e.g., saving five lives) against highly aversive harmful actions (e.g., killing an innocent person). Enhancing serotonin made subjects more likely to judge harmful actions as forbidden, but only in cases where harms were emotionally salient. This harm-avoidant bias after citalopram was also evident in behavior during the ultimatum game, in which subjects decide to accept or reject fair or unfair monetary offers from another player. Rejecting unfair offers enforces a fairness norm but also harms the other player financially. Enhancing serotonin made subjects less likely to reject unfair offers. Furthermore, the prosocial effects of citalopram varied as a function of trait empathy. Individuals high in trait empathy showed stronger effects of citalopram on moral judgment and behavior than individuals low in trait empathy. Together, these findings provide unique evidence that serotonin could promote prosocial behavior by enhancing harm aversion, a prosocial sentiment that directly affects both moral judgment and moral behavior.A commentary by Tost and Meyer-Lindgerg notes:
In a broader context, the work by Crockett et al. supports a number of interesting conclusions. It extends prior evidence suggesting that there are at least two major pharmacological routes that modulate human social behavior: a direct route (“bottom-up”) involving prosocial neuropeptides such as oxytocin and vasopressin, which promote prosocial behaviors such as attachment, empathy, and generosity, and an indirect route (“top-down”) involving serotonin, which delimits antisocial behaviors by reducing negative affect and enhancing the aversiveness of harming others (see figure below). If this is true, functional interactions between these transmitter systems are likely. Consistent with this, Crockett et al. report a pronounced impact of serotonin augmentation on social decision making in subjects with high trait empathy, a finding suggestive of additive prosocial effects of both routes. The study also demonstrates that the effects of serotonin on prosocial behavior are relatively specific and are absent under norepinephrine augmentation with atomoxetine.
Figure - Regulatory circuits of social-emotional information processing in humans. “Top-down” control of the amygdala (AMY) arises from the anterior cingulate cortex (ACG) and ventral medial prefrontal cortex (vmPFC), with the latter being particularly important for the regulation of moral behaviors. “Bottom-up” modulation arises from neurons in the hypothalamus (HYP) expressing the neuropeptides oxytocin and vasopressin, which target distinct neuronal populations in the central amygdala. Projections from the amygdala to the brainstem, via the hypothalamus, regulate the expression of autonomic reactions to social signals. PFC, prefrontal cortex.