The distribution of voltage sensitive sodium channels on axons in the dorsal and ventral spinal roots of the dystrophic mouse 129/ReJ-Lama2dy was determined using immunocytochemistry. In these nerves there are regions in which Schwann cells fail to proliferate and myelinate axons in a normal fashion, leaving bundles of closely packed large diameter amyelinated axons. We have identified discrete and focal concentrations of sodium channel immunoreactivity on these axons by confocal immunofluorescence, immunoelectron microscopy and Intermediate Voltage Electron Microscopy (IVEM) using a peptide-derived polyclonal antibody. In addition, simultaneous labeling with an antibody recognizing neuronal-specific ankyrinG revealed a distinct colocalization with the sodium channels on both normal and amyelinated axons. The presence of patches of sodium channels along with their anchoring protein on amyelinated axons in the absence of intervening Schwann cells demonstrates that axons can independently form and maintain these initial aggregations. This confirms that direct contact between Schwann cell and axon is not required for the formation of sodium channel patches of nodal dimensions and density. Furthermore, this strongly suggests that local transfer of sodium channels from Schwann cells to axons is not required for this process. This work was published in the Journal of Neuroscience (Deerinck et al., J. Neurosci., 17: 5080-5088, 1997).
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