Taken together, the different forms of synaptic plasticity, namely LTP and LTD are thought to contribute significantly to learning and memory, and involve long lasting changes in the efficacy of glutamatergic synaptic activity. The potential role of these forms of plasticity in addiction has been reviewed extensively [18–20]. The remainder of the review will briefly focus on the cellular mechanisms of synaptic plasticity in dorsal striatal, neocortical, as well as hippocampal synapses based on several electrophysiological studies, and will discuss the effect of ethanol (EtOH) on synaptic plasticity in these brain regions. We restricted our focus on these three regions of the brain, as they are proposed to be significantly involved in the binge/intoxication (dorsal striatum) and preoccupation/anticipation (neocortex and hippocampus) stages of AUD [21].
