The purpose of the present study was to extend this investigation in order to determine the pharmacological profile of two clinically relevant MOR ligands not examined in the original study, morphine and fentanyl, on the MOR-stimulated coupling to voltage-gated Ca2+ channels in sensory neurons. These ion channels play a crucial role in nociceptive signaling26. Of particular relevance, studies of spontaneous nociception indicate the minor 118G allele to be a gain-of-function variant27. However, studies of morphine analgesia suggest functional consequences of the mutation to be just the opposite, with requirement of higher post-operative morphine doses2.
