certain neurotransmitters such as dopamine or GABA. This may induce an LTD in the corticostriatal afferents. Conversely, if the stimulating electrode is located dorsally to the dorsomedial striatum on the cortical side, LTP is easily induced. This minimal current spread into the striatum is believed to minimize the release of large dopamine transients that bias toward LTD [27, 36]. Taken together, the varied and distinct forms of synaptic plasticity in the dorsal striatum and its modulation by EtOH (discussed in the later sections) may therefore be important for understanding the cellular mechanisms underlying the behavioral deficits seen in alcoholics and AUDs [2].
