Within the dorsomedial (associative) and dorsolateral (sensorimotor) striatum effects of acute ethanol exposure on both glutamatergic and GABAergic synaptic transmission have been characterized within the last decade. It has long been known that ethanol acutely inhibits the function of NMDA-type ionotropic glutamate receptors (Hoffman, Rabe et al. 1989, Lovinger, White et al. 1989) (Woodward and Gonzales 1990), and this inhibition is also observed at synapses in the dorsal striatum (Yin, Park et al. 2007) (Wang, Lanfranco et al. 2010). This inhibitory action likely contributes to a decreased ability to induce long-term potentiation (LTP) of glutamatergic synapses in striatum (Yin, Park et al. 2007). As LTD is thought to contribute to learning and memory, suppression of NMDAR function likely underlies cognitive deficits associated with acute intoxication. Within the dorsomedial striatum, the inhibition observed in the presence of ethanol gives way to facilitation of NMDAR-mediated transmission upon cessation of a single exposure to acute ethanol (Wang, Carnicella et al. 2007). This rebound long-term facilitation (LTF) seems to set the stage for gradual induction of LTP at glutamatergic striatal synapses (Wang, Ben Hamida
