OPTIC-NERVE INJURY ALTERS BASIC FIBROBLAST GROWTH-FACTOR LOCALIZATIONIN THE RETINA AND OPTIC TRACT

Basic fibroblast growth factor (bFGF) is thought to be a trophic facto r for several classes of neurons. Its distribution changes in response to cortical neural injury. We have determined the effect of injury to the optic nerve on localization of bFGF in the rodent retina and visu al pathways. Our observations were confirmed by using different antise ra and monoclonal antibodies. While photoreceptors normally contain vi rtually no bFGF, crushing the optic nerve causes a striking increase, over a period of several weeks, in the amount of bFGF in retinal photo receptors. Since photoreceptors do not synapse directly upon the injur ed ganglion cells, intermediary cells must participate in the cascade of events that results in the elevated bFGF. In light of the observati on that exogenous bFGF protects photoreceptors from photodamage (Fakto rovich et al., 1992), this increase in bFGF in photoreceptors may expl ain, in part, why crushing the optic nerve protects photoreceptors aga inst photodamage (Bush and Williams, 1991). Whereas bFGF is constituti vely found in glia in the optic nerve, little bFGF is found in glia in the optic tract. However, damage to the optic nerve increases bFGF in astrocytes in the optic tract. This change occurs within days, sugges ting that a relatively direct signal may intervene between the injured axon and the adjacent glial cells. Thus, despite the fact that the op tic nerve and optic tract are contiguous structures through which axon s of retinal ganglion cells project, the glial elements in these struc tures express distinct properties, because of differences in either gl ial subclasses or microenvironment. We suggest that changes in neurona l and glial bFGF expression are part of a coordinated injury response that involves a dynamic interaction between neural cells and trophic f actors. These changes may contribute to either a beneficial regenerati ve response or a pathological change that inhibits regeneration.