The KA-R agonist ATPA has been shown to increase synaptic strength in BLA principal neurons via an unknown, calcium-dependent mechanism (Li et al., 2001). However, in the CA1 region of the hippocampus, long-term ATPA application led to an enduring increase in the number of glutamatergic synapses in that region (Vesikansa et al., 2007). Using 5μM ATPA, a concentration that does not affect AMPA receptors (Stensbol et al., 1999), we were able to replicate the ATPA-induced synaptic plasticity in the current work. We have recently shown that this facilitation can be blocked by GluR5 antagonist UBP 296 and by acute ethanol (Lack et al., 2008). In the present study, both CIE and WD occluded ATPA-induced synaptic plasticity in the BLA. This was an unexpected finding considering the function of the KA-Rs was elevated in CIE neurons and went back to baseline during WD. One possible explanation is that extrasynaptic KAR, and not the synaptic receptors measured in Figure 1, are responsible for ATPA-induced plasticity. However, the initiation of synaptic plasticity at EC-BLA synapses by low-frequency electrical stimulation is dependent on synaptic
