In the dorsal striatum, local GABAergic connections include synapses between FSIs and MSNs, as well as collateral MSN-MSN connections (Wilson, 2007). Effects of both acute and chronic ethanol on these GABAergic synapses have been characterized in rodents (Patton et al., 2016; Wilcox et al., 2014) (Figure 2V) and non-human primates (Cuzon Carlson et al., 2011). One theme that has emerged from these studies is that ethanol has opposing actions on GABAergic synapses in two subregions of the striatum. In the “associative” or DMS, ethanol potentiates GABAergic transmission via a presynaptic mechanism, while ethanol inhibits GABAergic transmission in the “sensorimotor” or dorsolateral striatum, with the aforementioned opiate receptor-dependent presynaptic mechanism implicated in this action (Wilcox et al., 2014). Ethanol also inhibits MSN-MSN synapses via a mechanism that is not as well characterized (Patton et al., 2016). Thus, the net effect of acute ethanol is to inhibit MSN output from associative striatum while disinhibiting output from sensorimotor striatum. These striatal subregions are part of larger circuits that control goal-directed, conscious actions (the associative circuit) and habitual, unconscious actions (the sensorimotor circuit). The
