Endogenous FGF2 has been predicted to contribute to proliferation of neonatal and adult OPs, especially when present in combination with PDGF-AA, based on in vitro studies (31Y33). In our current analysis, the densities of OP cells and Ki-67-immunolabeled cells were similar between FGF2 wild-type and null genotypes. These results are consistent with our previous BrdU incorporation studies indicating that endogenous FGF2 is not a predominant mitogen for OPs in the acute cuprizone model (11) . However, subtle changes in the proliferation rate among an asymmetrically dividing OP pool could be relatively difficult to detect in a small population of cells over a prolonged disease and recovery course. FGF2 is also predicted to stimulate neural stem cells in the subventricular zone (SVZ) to contribute to repopulation of corpus callosum lesions (34) . During the prolonged demyelination period of the current study, the contribution of cells derived from the SVZ should have been evident in the dynamics of the OP pool in the corpus callosum. The lack of a detrimental effect of FGF2 absence on the OP pool may indicate that FGF2 effects on the SVZ cells may not be a significant contribution to the remyelination of the overlying corpus callosum. However, more direct analysis of the response of cells in the SVZ is required to make this determination. In addition, endogenous elevation of FGF2 in lesions may elicit specific effects that are not replicated with in vivo methods of elevating exogenous FGF2 levels (34Y37).