In the absence of MPP+, the treatment of FGF9-neutralizing antibody-induced DA neuronal apoptosis whereas FGF9 protein reduced it indicating that endogenous FGF9 is a survival factor for DA neurons. We conclude that MPP+ down-regulates FGF9 expression to cause DA neuron death and that the prevention of FGF9 down-regulation is involved in melatonin-provided neuroprotection.;Simultaneous treatment with FGF9 and MPP+ prevented MPP+-induced neuron death and H2O2 overproduction but did not affect the FGF9-increased a-GCS and HO-1 protein expression.[...] These results indicate that FGF9 upregulates a-GCS and HO-1 expression to protect cortical and dopaminergic neurons from MPP+-induced oxidative insult.;Expression of each FGFR and effects of the preferred ligand for FGFR-3, FGF9, upon RGC survival and neurite outgrowth were examined in primary retinal cell cultures: whereas there was no stimulation of neuritogenesis, RGC survival was promoted in a dose-dependent manner (ED50 500 pg/ml, mean maximal increase of 60%) and could be completely blocked by addition of FGF9 neutralising antibody.