Peripheral neuropathy in mouse hereditary diabetes mellitus. II. Ultrastructural correlates of degenerative and regenerative changes.
The fine structural changes in some peripheral nerves and sensory ganglia from mice (C57BL/KsJ, db/db) with an hereditary diabetic syndrome, similar to human maturity-onset diabetes mellitus, were studied during development of the mild peripheral neuropathy. The abnormalities observed included axonal degeneration, disruption of myelin, accumulation of electro-dense material in axons, satellite cells and Schwann cells, increased frequency of pi granules of Reich in Schwann cells, enlarged mitochondria, and proliferated and thickened Schwann cell basal laminae. Distal hind limb nerves were most affected. Sensory ganglion neurons were normal except for occasional chromatolytic cells, so that nerve cell loss was not present in this peripheral neuropathy. Morphological indications of Schwann cell hyperplasia, hypertrophy, and axonal sprouting supported the contention that a continuous cycle of axonal degeneration and regeneration was occurring. The ultrastructural changes and accumulation of electron-opaque, lipid material suggested that a defect in lipid metabolism, secondary to the diabetic condition, could be an important factor in the peripheral neuropathy in the diabetic mouse.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000235:genetics*; D003929:Diabetic Neuropathies / Q000473:pathology*; D005727:Ganglia, Spinal / Q000648:ultrastructure*; D051379:Mice; D008810:Mice, Inbred C57BL; D008854:Microscopy, Electron; D009410:Nerve Degeneration; D009416:Nerve Regeneration; D010525:Peripheral Nerves / Q000648:ultrastructure*; D012583:Schwann Cells / Q000648:ultrastructure; D013126:Spinal Nerve Roots / Q000648:ultrastructure; D012668:Trigeminal Ganglion / Q000648:ultrastructure