Primary demyelination induced by exposure to tellurium alters Schwann cell gene expression: a model for intracellular targeting of NGF receptor

摘要: Exposure of developing rats to tellurium results in a highly synchronous segmental demyelination peripheral nerves with sparing axons; this is followed closely by period rapid remyelination. Demyelination occurs subsequent tellurium-induced block the synthesis cholesterol, major myelin lipid. We utilized techniques Northern blotting, situ hybridization, and immunocytochemistry examine temporal alterations Schwann cell gene expression related Tellurium- induced associated downregulation protein corresponding upregulation NGF receptor (NGF-R) glial fibrillary acidic (GFAP) expression. Steady- state mRNA levels (expressed on “per nerve” basis) for P0, protein, were decreased about 50% after 5 d exposure, while NGF-R GFAP markedly increased (about 15-fold). In hybridization teased fibers suggested that increase steady-state was primarily demyelinated internodes not adjacent unaffected internodes. Although P0 message almost totally absent from demyelinating internodes, it also reduced normal-appearing as well. This suggests limiting supply required membrane component (cholesterol) may lead partial all myelinating cells. partially immunofluorescence appeared largely confined regions. specific targeting these proteins local areas where there loss. These demonstrate reversion affected cells precursor phenotype. Because axons remain intact, our suggest changes do require input degenerating axon, but instead depend whether concerted occurring.