Ethanol also inhibited up-states evoked by brief electrical stimulation of the VTA designed to mimic the in vivo bursting pattern of DA neurons upon presentation of rewarding stimuli (Schultz, 1986; Bayer et al., 2007). As compared to spontaneous up-states, there was less inhibition of VTA-stimulated persistent activity and this difference was eliminated when the D1 receptor antagonist SCH23390 was included in the bath solution. These results suggest that the phasic release of dopamine induced by DA neuron bursting can partially offset the inhibitory actions of ethanol on prefrontal neuron function. The mechanism underlying this effect is not known but may involve potentiation of NMDA receptors that are an important component of up-states. In a follow-up study, we examined the effects of acute ethanol on pharmacologically isolated synaptic currents in deep-layer pyramidal neurons of rat prefrontal cortex (Weitlauf and Woodward, 2008). Ethanol, at concentrations up to 88mM (~0.4% blood ethanol concentration), had no significant effect on evoked or spontaneous AMPA-mediated EPSCs (Fig. 4). Inhibitory currents mediated by the synaptic release of GABA were also largely insensitive to high concentrations of ethanol
