Researchers report a link between potassium channels in the brain and the tendency for binge drinking in mice. Ion channels called G protein-gated inwardly rectifying potassium (GIRK) channels regulate neuronal excitability. Such channels can be activated by ethanol, but the role of the activation in the behavioral effects of ethanol consumption is unclear. Candice Contet and colleagues found that the absence of GIRK3, a subunit of GIRK channels, promotes binge drinking in mice by blocking activation of a neural pathway that controls reward seeking. Mice that were genetically engineered to lack GIRK3 consumed more ethanol than their wild-type counterparts. However, the absence of GIRK3 had no effect on ethanol metabolism or the effects of intoxication. Ethanol activates neurons in a brain region called the Ventral Tegmental Area (VTA), triggering a neural pathway called the mesolimbic dopaminergic pathway, which confers incentive properties on reward-associated cues and thereby facilitates reward seeking. In the engineered mice, no such activation was observed. When GIRK3 was reintroduced to the VTA of the engineered mice, ethanol consumption returned to normal levels. Wild-type mice that received similar treatment also showed reduced ethanol consumption. Because previous research has shown that loss of GIRK3 has little effect on behavior, other than in response to addictive drugs, the authors suggest that selective targeting of GIRK3-containing channels might help reduce binge drinking with minimal side effects.