circuitry. Therefore, characterization of MOR N40D in other neuronal cell types will be addressed in future studies. This work identifies neurophysiological differences in the human neuronal response to alcohol that is influenced by common variation in human OPRM1. Our findings may help explain differential alcohol sensitivities and/or dependence in humans. This model provides a platform to understand alcohol’s physiological impact on human neurons and allows researchers to dissect drugs of abuse in relation to addiction-associated SNPs. Ultimately, the use of human stem cells to understand the interplay of alcohol and MOR gene variants may provide the necessary information required to develop patient-specific, therapeutic interventions for subjects with AUDs.
