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 and PSD-95 in drug abusers represent an induction of synaptic GluA1 that leads to strengthening of synaptic connectivity and increased responsiveness of the amygdala during, for example, relapse.
