In rodent OPCs delayed outwardly rectifying K+ (I K) channels and A‐type K+ (I A) channels largely contribute to sustained and transient outward membrane currents, respectively, and are downregulated upon differentiation to oligodendrocytes 24, 25. Analysis of the expression of I K‐mediated currents (Fig. 4A, 4B) in OPCs and oligodendrocytes derived from the ES line revealed that there was a greater than 50‐fold reduction in I K‐channel current density in week 3 O4+‐oligodendrocytes compared with the levels seen in week 1 PDGFRα+‐OPCs (Fig. 4C). I A‐channel activity (Fig. 4D, 4E) was also reduced as cells differentiated from PDGFRα+‐OPCs to O4+‐oligodendrocytes (Fig. 4F). This strong downregulation in week 3 O4+‐oligodendrocytes of I K (1.9 ± 0.8% of the value seen in week 1 PDGFRα+‐OPCs) and I A (7.6 ± 1.9%) seen in the ES line was recapitulated in the two iPS lines (For I K; iPS1, 2.9 ± 1.2%, iPS2, 7.0 ± 1.1%, n = 4–6, N = 2, and for I A; iPS1, 0.8 ± 0.4%, iPS2, 5.0 ± 0.5%, n = 3–9, N = 2–9, p<0.001 in all cases,
