Additionally, by changing the Ca2+ permeability of AMPARs, Ca2+ signaling via AMPA and colocalized NMDA channels might be disturbed, thereby impairing memory formation. Other forms of plasticity [77,78] induced by Ca2+-permeable AMPARs might play a prevalent role in olfactory memory. Alternatively, long-term stabilization might involve GluR-B phosphorylation similar to cerebellar long-term depression [79] and thus be selectively impaired by GluR-B depletion. Physiological experiments to assess these hypotheses will ideally make use of even more restricted genetic modifications with completely undisturbed input structures. One possibility would be Cre-mediated GluR-B depletion and GluR-B(Q) expression in piriform cortex as suggested above.