By identifying the correlation between GIRK2 expression levels and altered GIRK2-mediated function, we predict that neuronal excitability will be affected by KCNJ6 variants and alcohol exposure. While GIRK channels play relatively small role in maintaining neuronal homeostasis, modulating GIRK activity to alter cell excitability is predicted to play a critical role. Additionally, downstream effectors of the G protein-mediated signaling pathways presumably regulate neuronal function indirectly [14, 15, 17, 19]. GIRK channels are implicated in several other disorders with abnormal neuronal excitability, including epilepsy, suggesting that they have therapeutic potential [19–21, 60–63].
