Most of the information garnered to date about amygdala dysfunction of synaptic plasticity derive from studies of fear conditioning that is widely used to examine associative emotional memory formation (37), which is of critical importance in the etiology of addiction. As such, similar neurobiological mechanisms are likely to play a significant role in both fear conditioning and the development of addiction disorders (38, 39). It is well documented that fear conditioning induces strengthening of excitatory synapses within the lateral and basal amygdala nuclei and requires trafficking of GluA1 into synapses (40–42). Increased GluA1 in the plasma membrane has been reported following fear conditioning although the total amount of GluA1 mRNA and protein levels are unchanged (43). The GluA1 and PSD-95 correlation observed in our study was also not accompanied by alteration in the total GluA1 or PSD-95 mRNA or protein levels. It is therefore possible that functional rearrangement of GluA1 subunits is masked when measuring total levels of GluA1 similar to that observed in morphine-exposed rats (44). It would therefore be tempting to speculate that the strong coupling between GluA1
