Non-human primate research has been invaluable in the study of human disease and behavior. A conserved SNP, in which a cystine is replaced by a guanine at position 77 (C77G) resulting in a substitution of arginine with proline (R26P), occurs in the N-terminal arm of the monkey orthologue OPRM1 and has been suggested to be comparable to the A118G SNP (Miller et al., 2004). In this initial characterization of 32 male and female macaques, 44% were homozygous for the C77-allele, 50% heterozygous, and 6% homozygous for the G77 allele. It was demonstrated that monkeys possessing the minor allele (G77), had lower CORT levels both at baseline and following dexamethasone suppression and subsequent ACTH challenge. In addition to lower CORT levels, the G77 allele was associated with an increase in aggression threat, which is the early communicative aspect of aggression occurring prior to actual physical actions. By expressing these receptor-coding regions in HEK-293, the authors were able to identify an elevated affinity of the G77 allele for β-endorphin (~3.5 fold), but not exogenous ligands, similarly to original in vitro work in
