The time course of the expression of Dp116, talin, vinculin and vimentin in rat sciatic nerve was investigated after experimental transection. Dp116 was still found at 5 days after experiment in some degenerating myelinated fibers of both proximal and distal stumps. The findings are consistent with the known preservation of electrical excitability of the distal nerve in the first days after injury. Some regenerating nerve fibers into the neuroma also expressed Dp116 at 25 and 40 days after nerve transection. Talin and vinculin markedly and diffusely immunostained the neuroma. Talin in the distal stump and vimentin in both proximal and distal stumps were found decreased during the time course of the experiment. Vinculin binding increased in the distal stump, due to a real overexpression or simply to a cross-reaction to degeneration products.

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Background: Nuclear Factor‐kB (NF‐kB) is a transcription factor expressed ubiquitously, that plays an important role in immune and inflammatory responses by regulating the expression of different genes. Furthermore many studies have shown its involvement in the apoptosis of neurodegenerative disorders. Objective: The aim of the study was to evaluate the expression of this factor in inflammatory demyelinating and axonal neuropathies as well as in non‐inflammatory neuropathies. Materials and Methods: We studied the expression of NF‐kB by immunocytochemistry and Western Blot of nuclear extract proteins in sural nerve biopsies of 11 patients with peripheral neuropathies of different origin: 3 with CIDP, 2 with chronic axonal inflammatory neuropathy, 2 with vasculitis, 2 with CMT1 and 2 with CMT2. Three normal nerves served as controls. Immunohistochemistry for macrophages, B, CD4 and CD8 cell subsets was also performed. Results: NF‐kB expression was found in some endoneurial vessel walls, many cell nuclei and in the outermost layer of myelin sheath of some nerve fibers in inflammatory axonal and demyelinating neuropathies. Few positive cells were found in hereditary neuropathies whereas no immunoreactivity was detected in normal controls. Western blot analysis confirmed such findings. Conclusion: Our findings underline the role of NF‐kB in the immune response of inflammatory neuropathies. NF‐kB reactivity in hereditary neuropathies may be related to the apoptotic mechanism.