in inhibition of AMPAR‐mediated currents by NASPM, an antagonist which blocks AMPARs that do not contain GluA2(R) subunits. While these data indicate AMPARs predominantly expressed in OPCs are GluA2(R)‐lacking and oligodendrocytes are GluA2(R)‐containing, our data suggest that small populations of AMPARs that possess GluA2(R)‐containing subunits in OPCs and a population of GluA2(R)‐lacking AMPARs in oligodendrocytes. Consistent with this notion is the finding that native rodent OPCs that have been shown to express both GluA2(R)‐lacking and GluA2(R)‐containing AMPARs, and in which their relative proportions are influenced in an activity‐dependent manner 57. Our data are consistent with numerous studies reporting an increase in functional expression of the GluA2(R) subunit in AMPARs expressed in rodent oligodendrocytes upon differentiation and maturation from OPCs 55, 58, 59. This developmental variability in AMPAR composition (and Ca2+‐permeability) is disease‐relevant and confers sensitivity of immature oligodendroglial cells to excitotoxic conditions 60. Adult human mature oligodendrocytes obtained from white matter post mortem samples however have been reported to express AMPARs at a low level and do not appear to express the GluA2 subunit mRNA 34. In this regard, AMPAR data in this study, therefore, are in direct contrast to human data, but are in good agreement with rodent AMPAR
