title: Basal μ-opioid receptor availability in the amygdala predicts the inhibition of pain-related brain activity during heterotopic noxious counter-stimulation.
abstract: 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 μ-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 20min was used as HNCS. In a separate session, basal μ-opioid receptor availability was measured using positron emission tomography with the radiotracer [(11)C]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 μ-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 μ-opioid receptors in the amygdala may contribute to the anti-nociceptive effects of HNCS. The lack of RIII-reflex modulation further suggests that μ-opioid receptor activation in the amygdala contributes to decrease pain-related brain activity through a cerebral mechanism independent of descending modulation.
authors.affiliation: Department of Chiropractic, Université du Québec à Trois-Rivières, Canada; Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Mathieu
authors.initials: M
authors.lastname: Piché
authors.affiliation: Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Watanabe
authors.affiliation: Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Muneyuki
authors.initials: M
authors.lastname: Sakata
authors.affiliation: Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Oda
authors.affiliation: Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Jun
authors.initials: J
authors.lastname: Toyohara
authors.affiliation: Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Kenji
authors.initials: K
authors.lastname: Ishii
authors.affiliation: Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Kiichi
authors.initials: K
authors.lastname: Ishiwata
authors.affiliation: Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. Electronic address: hhotta@tmig.or.jp.
authors.forename: Harumi
authors.initials: H
authors.lastname: Hotta
mesh_terms: D000679:Amygdala / Q000378:metabolism*; D000698:Analgesia; D001921:Brain / Q000502:physiology*; D003080:Cold Temperature; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory; D005260:Female; D006801:Humans; D008297:Male; D009433:Neural Inhibition; D010146:Pain / Q000378:metabolism* / Q000503:physiopathology; D010147:Pain Measurement; D017450:Receptors, Opioid, mu / Q000378:metabolism*; D012018:Reflex / Q000502:physiology
chemical_list: D017450:Receptors, Opioid, mu
keywords: Amygdala; Carfentanil; Conditioned pain modulation; Diffuse noxious inhibitory controls; Pain; μ-Opioid receptors