We chose to analyze an SNP at position 118 (A118G or 118A>G) of the gene for the OPMR1 receptor, since this has been shown in earlier studies to alter the response to opioids [10]. The 118A>G mutation changes the base adenine to guanine, with the consequence that the amino acid asparagine is changed to aspartic acid at position 40 of the OPMR1 amino acid sequence. As this change occurs on the extracellular part of the receptor, it results in an additional net charge with loss of a putative glucosylation site in the area of the ligand-receptor interaction. This can result in differences in opioid sensitivity, clinically manifested as altered analgesic requirements [15-17], variations in pain sensitivity [18], or altered propensity for opioid addiction [10]. The major allele is AA and, in this study, the minor allele was defined as the joint AG/GG allele, because of the low frequency of the homozygous minor allele GG.
