Basal μ-opioid receptor availability in the amygdala predicts the inhibition of pain-related brain activity during heterotopic noxious counter-stimulation

The aim of this study was to investigate the association between the magnitude of anti-nociceptive effects induced by heterotopic noxious counter-stimulation (HNCS) and the basal mu-opioid receptor availability in the amygdala. In 8 healthy volunteers (4 females and 4 males), transcutaneous electrical stimulation was applied to the right sural nerve to produce the nociceptive flexion reflex (RIII-reflex), moderate pain, and scalp somatosensory evoked potentials (SEPs). Immersion of the left hand in cold water for 20 min was used as HNCS. In a separate session, basal mu-opioid receptor availability was measured using positron emission tomography with the radiotracer [C-11]carfentanil. HNCS produced a reduction of the P260 amplitude (p < 0.05), a late component of SEP that reflects activity in the anterior cingulate cortex. This reduction was associated with higher basal mu-opioid receptor availability in the amygdala on the right (R-2 = 0.55, p = 0.03) with a similar trend on the left (R-2 = 0.24, p = 0.22). Besides, HNCS did not induce significant changes in pain and RIII-reflex amplitude (p > 0.05). These results suggest that activation of mu-opioid receptors in the amygdala may contribute to the anti-nociceptive effects of HNCS. The lack of RIII-reflex modulation further suggests that mu-opioid receptor activation in the amygdala contributes to decrease pain-related brain activity through a cerebral mechanism independent of descending modulation. (C) 2014 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.