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 significant interaction between variables (F=3.48, P<0.0001). Comparing these data from the baseline region (first 10 min) and the last 10min of washout (Fig. 2C), ATPA increased fEPSP slope in CON slices (406.3%±29.11%) but was significantly less effective in slices from both CIE (177.5%±21.33%, P<0.05, One-way ANOVA with Bonferroni’s posttest) and WD animals (207.4%±32.11%, n=10, P<0.05). These data indicate that ATPA-induced synaptic plasticity at EC-BLA glutamatergic synapses is partially occluded by CIE and WD. Since KA-R synaptic function is up-regulated in CIE slices (relative to control, Fig. 1), these data also suggest that the mechanisms involved with the expression of kainate receptor-dependent increases in synaptic function might be affected by these treatments.
