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Using transgenic mice over\u2010expressing FGF\u20102 (TgFGF\u20102), we addressed the importance of endogenously generated FGF\u20102 on sensory neuron loss and sciatic nerve regeneration. After sciatic nerve transection, wild\u2010type and transgenic mice showed the same degree of cell death in L5 spinal ganglia. Also, the number of chromatolytic, eccentric, and pyknotic sensory neurons was not changed under elevated levels of FGF\u20102. Morphometric evaluation of intact nerves from TgFGF\u20102 mice revealed no difference in number and size of myelinated fibers compared to wild\u2010type mice. One week after crush injury, the number of regenerated axons was doubled and the myelin thickness was significantly smaller in transgenic mice. After 2 and 4 weeks, morphometric analysis and functional tests revealed no differences in recovery of sensory and motor nerve fibers. To study the role of FGF\u20102 over\u2010expression on Schwann cell proliferation during the early regeneration process, we used BrdU\u2010labeling to mark dividing cells. In transgenic mice, the number of proliferating cells was significantly increased distal to the crush site compared to wild\u2010types. We propose that endogenously synthesized FGF\u20102 influences early peripheral nerve regeneration by regulating Schwann cell proliferation, axonal regrowth, and remyelination. \u00a9 2006 Wiley Periodicals, Inc. 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