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Basic fibroblast growth factor treatment partially protects from visual deficits but does not increase retinal ganglion cell survival following controlled optic nerve crush


Lack of trophic support after axonal injury leads to the degeneration of neurons. To study whether the application of trophic factor can improve functional recovery and retinal ganglion cell (RGC) survival after unilateral controlled optic nerve crush injury, we have now treated adult rats intraocularly (i.o.) with basic fibroblast growth factor (bFGF). To monitor visual deficits, rats were trained in a two-choice pattern discrimination test. Immediately after the crush, and on postoperative days 3 and 6, either 1.1 µg recombinant bFGF or phosphate buffered saline (PBS) was injected i.o. Sham-operated controls received intraocular injection of PBS or bFGF. Within the first few days after the crush, all animals showed a loss of discrimination ability which was followed by a significant recovery within 2–3 weeks. Animals treated with bFGF had a significantly smaller initial deficit and thus recovered earlier compared to PBS controls. Retrograde RGC death was evaluated using retrograde HRP-tracing technique, but bFGF-treatment had no neuroprotective effect. Thus, the behavioral effects of bFGF could not be related to neuroprotection of RGCs and therefore other mechanisms may have to be considered.