Based on the results in Figure 6Ai, one might expect the kinetics of the AMPAR EPSC to be slow in pyramidal neurons from GluA2 KO mice, because most receptors are composed of GluA1 homomers (Lu et al., 2009), presumably bound to CNIH-2/-3. This, however, is not the case (Lu et al., 2009). Surprisingly, we find a marked enhancement in the total expression and association of γ-2 with GluA1-containing receptors when GluA2 expression is reduced (Figure S8A–C). γ-2 has been shown to reverse the kinetic effects of CNIH-2/-3 on GluA1 homomers (Gill et al., 2012 and Figure S8C). Indeed, in neurons from stargazer mice (a γ-2 deficient mouse line), GluA2 KD leads to slowing of AMPA mEPSC decay kinetics as expected (Figure S8D–E). See Figure S8 for more details.
