Abstract
According to expression studies and functional analyses in mutant mice and in rats, FGF-2 appears to be specifically involved during development of peripheral nerves and in de-/re-generating processes at the lesion site and in spinal ganglia. In the absence of FGF receptor (FGFR)3, axonal and myelin diameters of peripheral nerves are significantly reduced, suggesting that FGFR3 physiologically regulates axonal development. The normally occurring neuronal cell death in spinal ganglia after peripheral nerve axotomy does not take place in FGF-2 and FGFR3-deleted mice, respectively, suggesting that injury-induced apoptosis is mediated via FGF-2 binding to FGFR3. According to a bimodal function of FGF-2, lesion-induced neuron death in rat spinal ganglia can be prevented by application of FGF-2 to the proximal nerve stump, which could be mediated via FGFR1/2. At the lesion site, FGF-2 appears to be involved in stimulating Schwann cell proliferation, promoting neurite outgrowth, especially of sensory nerve fibers, and regulating remyelination.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
