Ethanol produces its acute actions through low-affinity interactions with a variety of molecular targets (Howard, Slesinger et al. 2011, Lovinger and Roberto 2013). In the brain, concentrations ranging from 5–100 mM produce intoxication, increased sedation and ultimately coma and death. While there are many neuronal molecules and functions that are relatively unchanged by ethanol even at the high end of this concentration range, the drug still lacks the molecular specificity exhibited by other drugs of abuse (e.g. heroin), with no single molecule accounting for all acute actions of the drug. To understand the initial effects of ethanol on a given circuit it is important to determine what molecular and cellular targets are sensitive to ethanol in the neurons and synapses that make up that circuit. Information regarding alcohol effects on one circuit or brain region will not necessarily explain the alcohol effects on another circuit, given the diverse molecular composition of neuronal subtypes in different brain regions. Within the C-BG-C circuits this is a daunting task, given the large number of neuronal subtypes within the each subregion. Still, a great
