repeated cycles of unregulated EtOH consumption altered neurotransmission in the dorsomedial striatum, evident as strengthening of glutamatergic transmission in direct pathway neurons [91]. In addition, months of EtOH consumption leads to opposing effects on synaptic transmission in the dorsomedial versus dorsolateral striatum, with increased transmission in the dorsomedial striatum and reduced transmission in the dorsolateral striatum [92, 93]. Furthermore, the increased synaptic transmission observed after months of EtOH consumption in the dorsomedial striatum is not restored by abstinence, indicating that the effects are long-lasting [93]. Taken together, these studies demonstrate that the effects of EtOH (acute and in vivo) and washout/withdrawal from EtOH on synaptic transmission and synaptic plasticity in the dorsal striatum are multifaceted, and particularly the dorsomedial striatum is bidirectional [82, 87].
