G118 allele-carriers found decreased agonist-induced receptor signaling efficacy in tissue from secondary somatosensory cortex, but not thalamus. However, there were no alterations in receptor expression or binding affinity (Oertel et al., 2009). Together, studies demonstrating that the G118 variant results in significantly reduced levels of MOPR expression and/or signaling suggest a loss-of-function of the mutation, while others reporting an increase in affinity and signaling suggest a gain-of-function.
