2012), but concluded that CNIH-2 remained bound to AMPARs on the surface of neurons (Gill et al., 2011; Harmel et al., 2012; Kato et al., 2010a). Furthermore, it was proposed that CNIH-2 displaced γ-8, the primary TARP expressed in the hippocampus, thus reducing TARP stoichiometry (Gill et al., 2011; Gill et al., 2012; Kato et al., 2010a), which challenged previous work suggesting that all possible γ-8 binding sites on native AMPARs were occupied (Shi et al., 2009).
