Robust OP proliferation in response to acute demyelination appears to be required for spontaneous remyelination (29) . During acute demyelination, the OP pool is dramatically amplified so that efficient differentiation into mature oligodendrocytes may not be required for extensive remyelination. PDGF-AA ligand, acting through PDGF>R activation, is an important mitogen for this OP amplification in response to acute cuprizone demyelination (11, 30) . In PDGF>R heterozygous mice, amplification of the OP pool in response to acute cuprizone demyelination is compromised and the corresponding generation of oligodendrocytes is reduced (11) . Crossing these PDGF>R heterozygous mice to FGF2 j/j mice actually increased oligodendroglial repopulation of lesions after acute cuprizone demyelination (11) . Therefore, in both acute and chronic lesion environments, FGF2 removal may promote the generation of oligodendrocytes from OP cells during remyelination.