Basic Fibroblast Growth Factor (bFGF or FGF-2) is a well established and multifunctional neurotrophic factor for peripheral as well as central neurons.

Previous studies have shown that in embryonic chick ciliary ganglion neurons bFGF promotes neuronal survival through the activation of the PI3K pathway only. On the other hand, the three main signaling cascades activated downstream of the high affinity tyrosine kinase receptor FGFR1, the PI3K, MAPK and PLCgamma pathways, all converge on the regulation of neurite growth.

The aim of the present study has been to analyze the calcium dependence of bFGF-promoted neurite growth, together with the specific calcium entry pathways potentially involved.

Experiments conducted on ciliary ganglion neurons with the intracellular calcium chelator BAPTA-AM point to a specific involvement of calcium signals in this bFGF-mediated neurotrophic effect. Furthermore, inhibitors of L- and N-type voltage dependent calcium channels, but not of voltage dependent sodium channels, significantly decreased neurite growth sustained by the factor. These results lead to hypothesize that activation of voltage-independent cationic channels (such as TRP channels) may lead to depolarization thus allowing the recruitment of voltage dependent calcium channels.

In parallel, calcium imaging experiments have shown that bFGF induced signals both at the level of cell soma and growth cones.