Fibroblast growth factor receptor 3 signaling regulates injury-related effects in the peripheral nervous system.

Fibroblast growth factor receptor (FGFR) signaling is crucial for neural development and regeneration. Here we investigated the L5 spinal ganglion and the sciatic nerve of intact Fgfr3-deficient mice after nerve injury. Quantification of sensory neurons in the L5 spinal ganglion revealed no significant differences between wild-type and Fgfr3-deficient mice. Seven days after nerve lesion, the normally occurring neuron loss in wild-type mice was not found in Fgfr3-deficient animals, suggesting that FGFR3 signaling is involved in the cell death process. Morphometric analysis of the sciatic nerve showed similar numbers of myelinated axons, but the axonal and myelin diameter was significantly smaller in Fgfr3-deficient mice compared to the wild types. Evaluation of regenerating myelinated axons of the sciatic nerve revealed no differences between both mouse strains 7 days after crush injury. Our results suggest that FGFR3 signaling seems to be involved in processes of damage-induced neuron death and axonal development.