Abstract
BackgroundResearch suggests that the COMT Val158Met, BDNF Val66Met and OPRM1 A118G polymorphisms moderate the experience of pain. In order to obtain experimental confirmation and extension of findings, cortical processing of experimentally-induced pain was used.MethodA sample of 78 individuals with chronic low back pain complaints and 37 healthy controls underwent EEG registration. Event-Related Potentials were measured in response to electrical nociceptive stimuli and moderation by COMT Val158Met, BDNF Val66Met and OPRM1 A118G polymorphisms was assessed.ResultsGenetic variation did not have a direct effect on cortical processing of experimental pain. However, genetic effects (COMT Val158Met and BDNF Val66Met) on experimental pain were moderated by the presence of chronic pain. In the presence of chronic pain, the COMT Met allele and the BDNF Met allele augmented cortical pain processing, whilst reducing pain processing in pain-free controls. No significant effects were found concerning the OPRM1 A118G polymorphism.ConclusionsThe current study suggests that chronic experience of pain enhances genetic sensitivity to experimentally induced mildly painful stimuli, possibly through a process of epigenetic modification.
Highlights
The experience of pain is subject to individual differences resulting from psychological factors, behavioral factors and biological factors [1,2,3,4]
Genetic effects (COMT Val158Met and Brain Derived Neurotrophic Factor (BDNF) Val66Met) on experimental pain were moderated by the presence of chronic pain
Crosstabs revealed no significant difference in allelic distribution between the healthy control group and chronic pain group (COMT Met allele: p = 0.167, BDNF Met allele: p = 0.910 and OPRM1 G allele: p = 0.815)
Summary
The experience of pain is subject to individual differences resulting from psychological factors, behavioral factors and biological factors [1,2,3,4]. Three single nucleotide polymorphisms (SNPs) have been proposed to impact on pain perception; COMT Val158Met (rs4680), BDNF Val66Met (rs6265) and the OPRM1 A118G (rs1799971) [7,8,9]. The val158met polymorphism alters the in-vivo activity of the COMT enzyme; Val/Val homozygotes have higher levels of the COMT enzyme and correspondingly lower levels of D2 receptor neurotransmission leading to a higher level of activation of the m-opioid system [11,12]. Met/Met homozygotes have lower levels of the COMT enzyme activity, resulting in increased dopaminergic neurotransmission. Met/Met homozygotes have decreased m-opioid system activation in response to pain [15]. Research suggests that the COMT Val158Met, BDNF Val66Met and OPRM1 A118G polymorphisms moderate the experience of pain. In order to obtain experimental confirmation and extension of findings, cortical processing of experimentally-induced pain was used
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