Abstract

The sulfation of peripheral nerve glycolipids was examined at 35 days after both crush injury or permanent transection of the adult rat sciatic nerve by in vitro incorporation of [35S]sulfate into endoneurial slices. These experimental models of neuropathy are characterized by the presence and absence of both axonal regeneration and subsequent myelin assembly. Although the sulfo-glucuronosyl glycosphingolipids (SGGLs) were not detected by alpha-napthol reagent after HPTLC separation of the total acidic lipid extract, fluorographic analysis after sulfate incorporation revealed a 4.7-fold increase in [35S]sulfate in the sulfo-glucuronosyl paragloboside (SGPG) and a 3.5-fold increase in the sulfo-glucuronosyl-lactosaminosyl paragloboside (SGLPG) after the crush injury compared to permanent transection. These [35S]sulfate-labeled lipids were identified by comigration after HPTLC separation by immunostaining with specific IgM monoclonal antibodies from a patient with demyelinating neuropathy and plasma cell dyscrasia. Enhanced incorporation of sulfate in the crushed nerves was also observed in the sulfatides and in several unknown lipids migrating between GM2 and GM3, between GM1, and GM2, slightly above the origin, and at the origin. Since previous studies (Yao and Poduslo: J Neurochem 50:630-638, 1988) have shown [35S]sulfate incorporation, but not [3H]Gal or [3H]Glc, into sulfatides at 35 days after transection, it is possible that the sulfation observed in the present studies does not represent de novo biosynthesis but rather sulfation of an endogenous pool of glycolipids that results from the nerve injury.(ABSTRACT TRUNCATED AT 250 WORDS)

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