Reversible diabetic nerve dysfunction: structural correlates to electrophysiological abnormalities.
Structural alterations of the nodal and paranodal areas were examined in the posterior tibial nerve in insulin-depleted and insulin-treated diabetic BB rats. The early metabolic phase of the distal symmetrical polyneuropathy was characterized by paranodal axonal swellings and nodal bulgings of the axon. These alterations correlate with intraaxonal sodium accumulation and decreased sodium equilibrium potentials which account for the early nerve conduction defect. Both the structural and electrophysiological abnormalities were completely normalized after vigorous insulin therapy. In the chronic diabetic polyneuropathy the paranodal area showed loss of paranodal axoglial junctions and paranodal myelin retraction. These changes may be partially responsible for the impaired electrical activity at the node as exemplified by irreversibly impaired sodium permeability and nerve conduction.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D003929:Diabetic Neuropathies / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D004594:Electrophysiology; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D009412:Nerve Fibers / Q000473:pathology; D009431:Neural Conduction; D011901:Ranvier's Nodes / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D013979:Tibial Nerve / Q000473:pathology
D007328:Insulin