Although the endogenous populations did not efficiently remyelinate after chronic cuprizone demyelination in C57Bl/6 mice (Fig. 1) , transplantation of OP cells has shown that the axons remain viable for remyelination (16) . Therefore, we used this chronic demyelination model in FGF2 FIGURE 6 . Oligodendroglial repopulation of the corpus callosum after chronic demyelination was dramatically improved in FGF2 j/j mice as compared with FGF2 +/+ mice. (A) Quantification of the density of oligodendrocytes in the corpus callosum of FGF2 mice. In situ hybridization for PLP mRNA, which identified premyelinating and myelinating oligodendrocytes, was quantified using unbiased stereology with at least three sections per mouse and at least four mice per condition. The oligodendrocyte density after 12 weeks of continuous cuprizone was significantly below nonlesioned values (noted by asterisks [*]; p G 0.01 for FGF2 +/+ ; p G 0.05 for FGF2 j/j mice; n = 4 for each condition). After 12 weeks of cuprizone and a subsequent 3-and 6-week period for recovery on normal chow, oligodendrocyte densities in FGF2 j/j mice were no longer significantly different as compared with nonlesion values (p > 0.05 at 3 weeks and at 6 weeks; n = 4 for each condition). Comparison of the FGF2 +/+ values with the matching conditions in FGF2 j/j mice demonstrated a significant effect of genotype (p = 0.0196). knockout mice to test whether repair from the endogenous OP population might be improved by removing endogenous FGF2 from the lesion environment. The extent of demyelination after 12 weeks of cuprizone ingestion was similar in C57Bl/6 mice and mice of both FGF2 wild-type (FGF2 +/+ ) and null (FGF2 j/j ) genotypes (Figs. 1, 5) . The percentage of the corpus callosum area with myelin immunolabeling was 45.8 T 14.1% in C57Bl/6 mice, 50.05 T 7.8% in FGF2 +/+ mice, and 46.9 T 4.3% in FGF2 j/j mice. After the chronic demyelination, only in FGF2 j/j mice did myelin immunostaining in the corpus callosum significantly increase during the recovery period (Fig. 5) . Surprisingly, the myelin immunostaining recovered to approximately nonlesion levels by 6 weeks after removal of cuprizone from the diet of FGF2 j/j mice. In contrast, in C57Bl/6 mice (Fig. 1) or FGF2 +/+ mice (Fig. 5) , the myelinated proportion of corpus callosum area did not significantly increase during the recovery period.