The lack of synaptic GluA1-containing AMPARs in the absence of CNIH-2/-3 expression may be explained by either a selective loss in total GluA1 protein expression or a specific involvement of CNIH proteins in the forward trafficking of GluA1-containing AMPARs to synapses. To examine potential effects of CNIH-2 on synaptic protein expression, Cnih2fl/fl mice were crossed to the Nex-CRE mouse line to create NexCnih2−/− mice. CRE expression in these mice includes pyramidal neurons of the neocortex and hippocampus as well as mossy and granule cells in the dentate gyrus (Goebbels et al., 2006).
