Basic fibroblast growth factor potentiates myelin repair following induction of experimental demyelination in adult mouse optic chiasm and nerves.

Induction of demyelination in the central nervous system induce the oligodendrocyte progenitors to proliferate, migrate, and differentiate for restoring new myelin sheathes around demyelinated axons. Factors which increase the response of endogenous progenitor cells could be used to improve remyelination. In the current study, the effect of bFGF on lysolecithin-induced demyelination and remyelination processes in mouse optic chiasm and nerves was investigated. Lysolecithin was injected into the optic chiasm of Balb/C mice. Two groups of animals received doses of bFGF (1 or 5 ng/kg i.p.) just before and every 3 days after lysolecithin injection. Delay and amplitude of visual evoked potential (VEP) waves were recorded as indices of axonal demyelination at 7th, 13th, and 28th days post-lesion. Myelin basic protein (MBP) and Olig2 gene expressions were studied as indices of myelination and oligodendrocyte precursors' recruitment into the lesion. Lysolecithin elongated delay of P1 wave and declined the amplitude of P1-N1 wave. Lysolecithin decreased MBP and increased Olig2 expression in different days post-lesion. Lysolecithin-induced changes in VEPs were partially ameliorated by endogenous repair. bFGF reduced the increased delay, increased the reduced amplitude of P1-N1 wave, increased MBP gene expression, and accelerated the increasing pattern of Olig2. bFGF seems to be able to potentiate the endogenous repair mechanisms of myelin. Its effect on demyelination and remyelination processes seems to be mediated by oligodendrocyte progenitor cells and their differentiation to myelinating cells.