We previously showed that the absence of FGF2 did not significantly alter OP amplification in response to acute cuprizone demyelination (12) . A robust OP proliferative response occurred after 5 weeks of cuprizone in FGF2 null and wild-type mice that was similar to the previously mentioned data for C57Bl/6 mice (Fig. 3) . However, the OP population was depleted during chronic demyelination in contrast to the amplified OP response to acute demyelination in C57Bl/6 ( Fig. 3) . Therefore, we examined the effect of FGF2 genotype on the density of OP cells and cycling cells in the corpus callosum after chronic demyelination. FGF2 genotype did not appear to alter the OP population dynamics of chronically demyelinated mice or age-matched nonlesioned mice (Fig. 7) . The density of OP cells, identified by in situ hybridization for PDGF>R mRNA, was similar in FGF2 +/+ mice and FGF2 j/j mice (Fig. 7A) . Somewhat unexpectedly, mice of both FGF2 null and wild-type genotypes, which are on a 129 Sv-Ev:Black Swiss genetic background, exhibited an increase in OP cell density after 12 weeks of cuprizone that was not observed in C57Bl/6 mice (Fig. 3A ). This strain difference in OP accumulation after chronic demyelination corresponded with fewer oligodendrocytes observed during the recovery period in FGF2 +/+ mice (Fig. 6 ) as compared with C57Bl/6 mice (Fig. 2) . Therefore, the FGF2 background appears to be even less favorable than the C57Bl/6 background for OP differentiation and oligodendrocyte regeneration, yet the detrimental effects of the chronic lesion environment can still be overcome in the FGF2 j/j mice.