from KCNJ6 variant AUD-affected individuals demonstrated initial transcriptomic and morpho-physiological differences, mostly affecting excitability of the cells, which were paralleled by differences in GIRK2 expression levels. Ethanol exposure, conversely, induced GIRK2 expression, ameliorating differences in excitability. Moreover, by overexpressing KCNJ6 we replicated effects of ethanol on neuronal excitability. The results promote a better understanding of the association between genetic variants and brain-wide changes affecting AUD risk and can potentially be used for development of personalized interventions.
