The administration of the opioid buprenorphine decreases motivational error signals.

While opioid addiction has reached pandemic proportions, we still lack a good understanding of how the administration of opioids interacts with cognitive functions. Error processing - the ability to detect erroneous actions and correct one's behaviour afterwards - is one such cognitive function that might be susceptible to opioidergic influences. Errors are hypothesised to induce aversive negative arousal, while opioids have been suggested to reduce aversive arousal induced by unpleasant and stressful stimuli. Thus, this study investigated whether the acute administration of an opioid would affect error processing. In a double-blind between-subject study, 42 male volunteers were recruited and received either 0.2 mg buprenorphine (a partial µ-opioid receptor agonist and κ-opioid receptor antagonist) or a placebo pill before they performed a stimulus-response task provoking errors. Electroencephalograms (EEG) were recorded while participants performed the task. We observed no group differences in terms of reaction times, error rates, and affective state ratings during the task between buprenorphine and control participants. Additional measures of adaptive control, however, showed interfering effects of buprenorphine administration. On the neural level, decreased Pe (Error Positivity) amplitudes were found in buprenorphine compared to control participants following error commission. Further, frontal delta oscillations were decreased in the buprenorphine group after all responses. Our neural results jointly demonstrate a general reduction in error processing in those participants who received an opioid before task completion, thereby suggesting that opioids might have indeed the potential to dampen motivational error signals. Importantly, the effects of the opioid were evident in more elaborate error processing stages, thereby impacting on processes of conscious error appraisal and evidence accumulation.

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.