BLA KA-Rs have been shown to mediate a form of glutamatergic synaptic plasticity in principal neurons, potentially through recruitment of additional excitatory synapses (Li and Rogawski, 1998). We have recently shown that this synaptic plasticity, induced by the selective agonist ATPA, can be inhibited by both acute application of ethanol and the GluR5 competitive antagonist, UBP 296 ((RS)-1-(2-Amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione; (Lack et al., 2008)). Given that CIE, but not WD, increased KA-R synaptic function, we hypothesized that ATPA-induced plasticity would be more readily established in CIE slices relative to both CON and WD. Following a 10min baseline, we applied 5μM ATPA for 15min, followed with a 40 min washout period with drug-free aCSF. ATPA exposure caused a slowly developing increase in the fEPSP slope in CON slices (n=10, Fig. 2A & B). This is consistent with previous findings (Lack et al., 2008; Li et al., 2001). Surprisingly, this time-dependent, ATPA-induced plasticity (Fig. 2B) was significantly attenuated in slices from both CIE (n=8) and WD (n=10) with significant main effects of treatment (F=45.94, P<0.0001, two-way ANOVA) and time (F= 11.73, P<0.0001) with a
