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The μ-opioid receptor (OPRM1) is the principal receptor target for both endogenous and exogenous opioid analgesics. There are substantial individual differences in human responses to painful stimuli and to opiate drugs that are attributed to genetic variations in  OPRM1 . In searching for new functional variants, we employed comparative genome analysis and obtained evidence for the existence of an expanded human  OPRM1  gene locus with new promoters, alternative exons and regulatory elements. Examination of polymorphisms within the human  OPRM1  gene locus identified strong association between single nucleotide polymorphism (SNP) rs563649 and individual variations in pain perception. SNP rs563649 is located within a structurally conserved internal ribosome entry site (IRES) in the 5′-UTR of a novel exon 13-containing OPRM1 isoforms (MOR-1K) and affects both mRNA levels and translation efficiency of these variants. Furthermore, rs563649 exhibits very strong linkage disequilibrium throughout the entire  OPRM1  gene locus and thus affects the functional contribution of the corresponding haplotype that includes other functional  OPRM1  SNPs. Our results provide evidence for an essential role for MOR-1K isoforms in nociceptive signaling and suggest that genetic variations in alternative  OPRM1  isoforms may contribute to individual differences in opiate responses.

Expansion of the human μ-opioid receptor gene architecture: novel functional variants