In addition to regional specificity, others have also suggested that adolescent ethanol exposure via behavioral drinking paradigms in rodents may potentiate the effects of physiologically relevant ethanol concentrations in slice preparations. Previous work showed that chronic intermittent ethanol exposure during adolescence enhanced GABA-A mediated tonic inhibition and decreased phasic GABAA-gated current in adult rat dentate granule cells upon application of 30mM ethanol [31]. All of these studies discussed above utilize rodent models to study the effects of physiologically relevant ethanol concentrations in humans. However, Ariwodola et al. used 40mM ethanol application in brain slices to perform a direct comparison between rodent and primate dentate granule cell response to low ethanol concentrations (Ariwodola et al., 2003). They found that bath application of ethanol significantly enhanced the area of GABA-A receptor-mediated IPSCs in both the rat and primate (Macaca fascicularis) hippocampal slices [33]. Importantly, while there was variability among individual dentate granule cells in each species, there was no difference between species in the efficacy or potency of 40mM ethanol to enhance GABA-A receptor-mediated IPSCs [33]. This finding reinforces the translational potential of results from studies of the effects of these ethanol concentrations in rodent models.