Research ReportRole of fibroblast growth factor 8 in neurite outgrowth from spiral ganglion neurons in vitro

- We report that FGF8a and FGF8b promote spiral ganglion neurons (SGN) neurite growth in vitro.
- This action is mediated by FGF receptors.
- FGF8b competitively interferes with the action of FGF8a.
- The NFκB signaling pathway is required for SGN neurite outgrowth.
- The DCX antibody reveals the distal neurites of cultured SGN.

Many neurons degenerate after injuries resulting from overstimulation, drugs, genetic mutations, and aging. Although several growth factors and neurotrophins delay degeneration and promote regrowth of neural processes, the role of fibroblast growth factor 8 (FGF8) in mammalian spiral ganglion neurons (SGN) neurite outgrowth has not been examined. This study develops and uses SGN cell cultures suitable for experimental analysis, it investigates whether FGF8a and FGF8b isoforms affect the neurite outgrowth from SGN cultured in vitro. We found that both FGF8a and FGF8b promoted the outgrowth of neurites from cultured SGN. This response is mediated by FGF receptors and involves the activation of IκBα-mediated NFκB signaling pathway. These findings suggest that, besides its morphogenetic role during development, FGF8 may have trophic functions in the adult which are relevant to regeneration.