pS (n = 14, N = 4) to 2.9 ± 0.1 pS in week 3 O4+‐oligodendrocytes (n = 4, N = 2, p<0.001, unpaired t tests, Fig. 6H). Equivalent data were also obtained from iPSC‐derived oligodendrocyte‐lineage cells (Fig. 6H). The data are consistent with the notion that GluR2(R) subunits are functionally upregulated in AMPARs expressed by oligodendrocytes. Supporting the idea that OPCs express a greater proportion of AMPARs that lack edited GluA2 subunits and oligodendrocytes AMPARs contain edited GluA2 subunits is the fact that the GluA2(R)‐lacking AMPAR antagonist polyamine, 1‐naphthyl acetyl spermine (NASPM, 36) caused substantial inhibition of AMPAR‐mediated currents in PDGFRα+‐OPCs (Fig. 6I), but not week 3 O4+‐oligodendrocytes (Fig. 6J, 6K).
