Previous studies have shown dramatic increases in glutamatergic function at local BLA synapses after CIE and WD (Lack et al., 2007). This suggests that CIE and WD might occlude ATPA-induced plasticity by engaging expression-associated mechanisms at EC-BLA synapses. To test this, we measured stimulus-response relationships for fEPSPs in BLA slices from CON-, CIE-, and WD- treated rats. We electrically stimulated the external capsule using a range of intensities, from 5μA to 40μA at intervals of 5μA (Fig. 3 A & B). fEPSP slope in CIE and WD slices significantly differed from CON at most stimuli >15μA (Fig. 3A) with two-way ANOVA indicating significant main effects of treatment (F=28.8, P<0.0001) and stimulation intensity (F=19.5, P<0.0001) but no interaction between these factors. These results are complementary to previous findings showing that there is increased AMPA-type glutamate receptor function in the BLA in response to chronic intermittent ethanol treatment and 24 hours of withdrawal (Lack et al., 2007). Importantly, the findings suggest that the occlusion of ATPA-induced plasticity is related to the increased synaptic responses in CIE and WD slices. These ethanol/withdrawal-dependent effects closely parallel the cellular responses that characterize activity-dependent synaptic plasticity in this brain region.
