Further evidence for a decrease in MOPR expression was demonstrated by studies showing a reduction in Bmax, indicative of a lower receptor number, following [3H]-DAMGO binding using both transient and stable expression of MOPR in AV-12 and HEK293 cells (Kroslak et al., 2007). Additionally, there was a decrease in agonist-mediated cAMP signaling for morphine, methadone, and DAMGO, but not β-endorphin, using stable expression in the two lines; this alteration in cAMP signaling was not seen in cell lines transiently expressing the receptor (Kroslak et al., 2007). Another study using HEK293 cells stably expressing the hMOPR also found a decrease in Bmax using DAMGO binding in the G118 variant, though they did not find alterations in binding affinity or signal transduction (Beyer et al., 2004). Conversely, a recent study investigating MOPR expression, binding, and signaling in post mortem human tissue from 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
