FGF-2 modulates expression and distribution of GAP-43 in frog retinal ganglion cells after optic nerve injury

✍ Scribed by Ileana Soto; Bruno Marie; Deborah J. Baro; Rosa E. Blanco

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 490 KB
• Volume: 73
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.10673

✦ Synopsis

Abstract

Basic fibroblast growth factor (bFGF or FGF‐2) has been implicated as a trophic factor that promotes survival and neurite outgrowth of neurons. We found previously that application of FGF‐2 to the proximal stump of the injured axon increases retinal ganglion cell (RGC) survival. We determine here the effect of FGF‐2 on expression of the axonal growth‐associated phosphoprotein (GAP)‐43 in retinal ganglion cells and tectum of Rana pipiens during regeneration of the optic nerve. In control retinas, GAP‐43 protein was found in the optic fiber layer and in optic nerve; mRNA levels were low. After axotomy, mRNA levels increased sevenfold and GAP‐43 protein was significantly increased. GAP‐43 was localized in retinal axons and in a subset of RGC cell bodies and dendrites. This upregulation of GAP‐43 was sustained through the period in which retinal axons reconnect with their target in the tectum. FGF‐2 application to the injured nerve, but not to the eyeball, increased GAP‐43 mRNA in the retina but decreased GAP‐43 protein levels and decreased the number of immunopositive cell bodies. In the tectum, no treatment affected GAP‐43 mRNA but FGF‐2 application to the axotomized optic nerve increased GAP‐43 protein in regenerating retinal projections. We conclude that FGF‐2 upregulates the synthesis and alters the distribution of the axonal growth‐promoting protein GAP‐43, suggesting that it may enhance axonal regrowth. © 2003 Wiley‐Liss, Inc.