Mu opioid receptors (MOR) are common targets of opiate analgesics. Potentially functional genetic variation is present within the human MOR gene (OPRM1). For instance, several single-nucleotide polymorphisms are present within both coding and noncoding regions1-3. The most common functional polymorphism occurs at position 118 in exon 12-3. The mutation results in an exchange from asparagine (N) to aspartate (D) at position 40 (N40D) on the extracellular N-terminal domain. The asparagine residue is one of five putative glycosylation sites on the MOR. Several clinical studies have reported that the A118G polymorphism may play a role in opiate effectiveness in the treatment of acute and chronic pain4-13, susceptibility to drug addiction14-18, stress19, and suicide20. Findings from in vitro studies have suggested that this polymorphism affects receptor binding characteristics21, messenger RNA expression levels22, and ion channel activation1. However, under some experimental conditions this polymorphism showed no effect on function23 or expression levels24.
