basis for learning and memory, is also found to be severely reduced in hippocampal neurons from GluA1 KO mice (Zamanillo et al., 1999). We, therefore, examined LTP in neurons lacking CNIH-2/-3. If GluA1-containing AMPARs are removed from synapses in the absence of CNIH-2/-3, LTP should be compromised. Indeed, when compared to uninfected neurons, LTP was markedly reduced in Cnih2/3fl/fl neurons infected with CRE (Figure 2K). Thus, knocking out CNIH-2/-3 appeared to phenocopy knocking out GluA1 in three key parameters. Previous studies in HEK cells (Kato et al., 2010a) suggested that the absence of CNIH proteins in neurons should result in AMPAR resensitization and alterations in cyclothiazide potentiation of kainate-induced currents. However, neither of these effects were observed (Figure S3C and D).
