Because our ATPA-fEPSP data suggested that the mechanisms responsible for the expression of synaptic plasticity were engaged by CIE and WD, we examined whether there was any treatment-specific alteration in presynaptic release of glutamate. This hypothesis was supported by our previous data that showed an increase in glutamate release from ‘local’ glutamatergic synapses during CIE and WD (Lack et al., 2007). However, unlike at local glutamatergic synapses, we found no evidence of an increase in presynaptic probability of glutamate release at EC/BLA synapses following CIE and WD. The EC-BLA synapses contain cortical inputs for many divergent brain regions including insular cortices (McDonald and Mascagni, 1996), the neighboring entorhinal cortex (McDonald and Mascagni, 1997), and executive-control areas like the anterior cingulate (McDonald and Mascagni, 1996). The ‘local stimulus’ approach used in the Lack et al. 2007 study would have engaged these inputs as well as glutamatergic synapses arising from thalamus (LeDoux et al., 1991), hippocampus (Kishi et al., 2006), limbic and parietal cortex (McDonald and Mascagni, 1996), and intra-amygdala projections (Savander et al., 1995). The contrasting results found in the current
