The A112G mouse model, similarly to the C77G non-human primate model, possesses analogous phenotypes as those reported in human studies and identifies new behaviors that have not been investigated. The A112G mouse model seems to replicate the loss-of-function phenotypes (e.g., decreased expression, reduced morphine-mediated antinociception, decreased hedonic reward), though it should be noted that decreases are not present in all morphine-mediated behaviors, suggesting that the alterations are dependent on other factors, including brain region, other neurotransmitter systems, and sex. Future work will investigate the effects of the A112G SNP on alcohol consumption and stress responsivity to evaluate whether or not these animals display any gain-of-function phenotypes as suggested by human studies.
