Recent research indicates that alcohol and/or drugs of abuse have a profound developmental effect on the PSD as well174,177,178; such that, similar to earlier reports on the vulnerability of the adolescent hippocampus to alcohol and/or drug exposure,175,176 there is a differential effect of binge-like ethanol exposure between adolescent and adult rats. Risher et al.177 reported that adolescent intermittent ethanol (AIE) exposure in rats reduced PSD-95 expression levels in the hippocampus, leading to the retention of immature-like dendritic spine phenotypes into adulthood. There was also a reduction in the number of VGlut1/PSD-95 and VGlut1/SAP102 (another MAGUK) colocalized synaptic puncta and these effects were driven by decreases in PSD-95 and SAP102 density with no effect on presynaptic VGlut1 expression levels.177 In contrast, chronic intermittent ethanol (CIE) during adulthood178 did not alter PSD-95 expression in the hippocampus as a whole. However, these authors indicated that adult CIE could alter dendritic complexity in a subregion-specific manner, with a partial return to basal levels after protracted abstinence.178 Taken together these studies suggest that the PSD-95, and glutamate activity, may be more vulnerable to ethanol-induced changes
