we would argue that native surface GluA1A2 receptors could have up to 2 CNIH associated with the GluA1 subunits, but that, if present, they exert no effect on gating kinetics due to γ-8’s prevention of a functional CNIH association with the GluA2 subunit (Figure 8C). If this is the case, CNIH expression in the absence of γ-8 should slow the gating kinetics of surface AMPARs in neurons. Indeed, when CNIH-2 is expressed in pyramidal neurons from γ-8 KO mice the gating kinetics of surface AMPARs at synapses are markedly slowed (Figure 7B).
