There is a growing body of evidence from rodent studies that demonstrates an important role of alternatively spliced forms of OPRM1 in mediating opiate analgesia (32–34). The synergistic activities of these splice variants have been proposed to explain the complex pharmacology of μ-opioids (35). Still, it is unclear whether the findings from rodent studies are applicable to human opioid responses because of a striking discrepancy between the genomic organizations of the mouse and human OPRM1. According to the NCBI database, the mouse OPRM1 gene consists of 20 exons and codes for 39 alternative-spliced forms. In contrast, the human OPRM1 gene consists of only nine exons and codes for only 19 alternative-spliced forms (Unigene database).
