able to induce a greater response at a lower concentration when compared to the common μ receptor. Using different methods, a study by Kroslak et al [71] found no changes in β-endorphin signaling at the rs1799971 μ receptor, and also determined that the binding affinities for exogenous agonists (morphine, methadone, and DAMGO) were not different. The potential variation in β-endorphin’s binding capacity in these two studies [71, 73] may be attributable to the distinct methodologies that were used, however the overall findings imply that the altered binding affinity and pathway activation of the rs1799971 μ opioid receptor may impact a subject’s vulnerability to opioid dependence due to the involvement of β-endorphin in limbic signaling [75] and the stress response pathway [73]. This conclusion is supportive of the role that the rs1799971 SNP has in the pathophysiology of opioid dependence.
