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Neurosci Res. 2014 Apr-May;81-82:78-84. doi: 10.1016/j.neures.2014.02.006. Epub 2014 Feb 27.

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

Author information

1
Department of Chiropractic, Université du Québec à Trois-Rivières, Canada; Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
2
Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
3
Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
4
Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. Electronic address: hhotta@tmig.or.jp.

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.

KEYWORDS:

Amygdala; Carfentanil; Conditioned pain modulation; Diffuse noxious inhibitory controls; Pain; μ-Opioid receptors

PMID:
24583336
DOI:
10.1016/j.neures.2014.02.006
[Indexed for MEDLINE]
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