Psychopharmacological modulation of event-related potentials suggests that first-hand pain and empathy for pain rely on similar opioidergic processes.

Accumulating evidence suggests that empathy for pain recruits similar neural processes as the first-hand experience of pain. The pain-related P2, an event-related potential component, has been suggested as a reliable indicator of neural processes associated with first-hand pain. Recent evidence indicates that placebo analgesia modulates this component for both first-hand pain and empathy for pain. Moreover, a psychopharmacological study showed that administration of an opioid antagonist blocked the effects of placebo analgesia on self-report of both first-hand pain and empathy for pain. Together, these findings suggest that the opioid system plays a similar role during first-hand pain and empathy for pain. However, such a conclusion requires evidence showing that neural activity during both experiences is similarly affected by psychopharmacological blockage of opioid receptors. Here, we measured pain-related P2 amplitudes and self-report in a group of participants who first underwent a placebo analgesia induction procedure. Then, they received an opioid receptor antagonist known to block the previously induced analgesic effects. Self-report showed that blocking opioid receptors after the induction of placebo analgesia increased both first-hand pain and empathy for pain, replicating previous findings. Importantly, P2 amplitudes were also increased during both experiences. Thus, the present findings extend models proposing that empathy for pain is partially grounded in first-hand pain by suggesting that this also applies to the underlying opioidergic neurochemical processes.