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. In compartmentalized cultures, 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, when applied either on the somatic compartment or at the growth cone. Moreover, a TRPC channel blocker reduced neurite growth to a similar extent, providing evidence that these channels are involved in the growth of neuritic processes promoted by bFGF. In calcium imaging experiments, simultaneous recordings of bFGF-elicited signals at the soma and at the growth cone showed distinct time courses.