Initially, the majority of studies investigating alcohol’s actions on VTA activity used high concentrations of ethanol. More recently, there have been efforts to identify effects at low and medium concentrations. These studies have found that very low concentrations of acute ethanol (1- 10 mM) increase excitatory synaptic currents and decreased inhibitory activity. Direct effects on DA neuron excitability have been observed at slightly higher concentrations (20 mM) and this sensitivity shifts to lower concentrations based on alcohol experience. GABAergic neurons in the VTA also appear to be inhibited by acute alcohol. A summary of the data reported would suggest that acute alcohol in this more relevant dose range likely affects VTA activity by directly modulating voltage-gated ion channels on DA neurons and by shifting activity from ligand-gated ion channels towards excitatory activity. The increase in activity of DA neurons following alcohol would therefore be expected to alter the activity of several downstream regions including the prefrontal cortex, amygdala, thalamic structures, and ventral striatum (nucleus accumbens), among other projection targets of the VTA [26]. The network including the VTA is thought
