Abstract
Summary points
An individual’s response to opioids is influenced by a complex combination of genetic, molecular and phenotypic factors. Intra- and inter-individual variations in response to mu opioids have led to the suggestion that mu-opioid receptor subtypes exist. Scientists have now proven that mu-opioid receptor subtypes exist and that they occur through a mechanism promoting protein diversity, called alternative splicing. The ability of mu opioids to differentially activate splice variants may explain some of the clinical differences observed between mu opioids. This article examines how differential activation of splice variants by mu opioids occurs through alternative mu-opioid receptor binding, through differential receptor activation, and as a result of the distinct distribution of variants located regionally and at the cellular level.
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