한빛사논문
Yongjeon Cheong, PhD,1 Seonkyoung Lee, PhD,1 Hidehiko Okazawa, MD, PhD,2,3 Hirotaka Kosaka, MD, PhD2,3,4* and Minyoung Jung, PhD1*
1Cognitive Science Research Group, Korea Brain Research Institute, Daegu, Republic of Korea
2Research Centre for Child Mental Development, University of Fukui, Eiheiji, Fukui, Japan
3Division of Developmental Higher Brain Functions, Department of Child Development, United Graduate School of Child Development, University of Fukui, Fukui, Japan
4Department of Neuropsychiatry, University of Fukui, Fukui, Japan
*Correspondence: Hirotaka Kosaka, Minyoung Jung
Abstract
Aim
Pain is reconstructed by brain activities and its subjectivity comes from an interplay of multiple factors. The current study aims to understand the contribution of genetic factors to the neural processing of pain. Focusing on the single-nucleotide polymorphism (SNP) of opioid receptor mu 1 (OPRM1) A118G (rs1799971) and catechol-O-methyltransferase (COMT) val158met (rs4680), we investigated how the two pain genes affect pain processing.
Method
We integrated a genetic approach with functional neuroimaging. We extracted genomic DNA information from saliva samples to genotype the SNP of OPRM1 and COMT. We used a percept-related model, in which two different levels of perceived pain intensities (“low pain: mildly painful” vs “high pain: severely painful”) were employed as experimental stimuli.
Results
Low pain involves a broader network relative to high pain. The distinct effects of pain genes were observed depending on the perceived pain intensity. The effects of low pain were found in supramarginal gyrus, angular gyrus, and anterior cingulate cortex (ACC) for OPRM1 and in middle temporal gyrus for COMT. For high pain, OPRM1 affected the insula and cerebellum, while COMT affected the middle occipital gyrus and ACC.
Conclusion
OPRM1 primarily affects sensory and cognitive components of pain processing, while COMT mainly influences emotional aspects of pain processing. The interaction of the two pain genes was associated with neural patterns coding for high pain and neural activation in the ACC in response to pain. The proteins encoded by the OPRM1 and COMT may contribute to the firing of pain-related neurons in the human ACC, a critical center for subjective pain experience.
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