Structural abnormalities do not explain the early functional abnormalities in the peripheral nerves of the streptozotocin diabetic rat Academic Article Article uri icon


MeSH Major

  • Cornea
  • Diabetes Mellitus, Type 1
  • Diabetes Mellitus, Type 2
  • Diabetic Neuropathies
  • Microscopy, Confocal


  • The streptozotocin (STZ)-diabetic rat, the most commonly employed model of experimental diabetic neuropathy, is characterised by a reduction in nerve conduction velocity, pain threshold and blood flow. Whether or not structural abnormalities underlie these functional abnormalities is unclear. 10 adult male Sprague-Dawley STZ-diabetic rats (diabetes duration 27 d) and 10 age-matched (23 wk) control animals were studied. Motor nerve conduction velocity (m s(-1)) was significantly reduced in diabetic (41.31 +/- 0.8) compared with control (46.15 +/- 1.5) animals (P < 0.001). The concentration of sciatic nerve glucose (P < 0.001), fructose (P < 0.001) and sorbitol (P < 0.001) was elevated, and myoinositol (P < 0.001) was reduced in diabetic compared with control animals. Detailed morphometric studies demonstrated no significant difference in fascicular area, myelinated fibre density, fibre and axon areas as well as unmyelinated fibre density and diameter. Endoneurial capillary density, basement membrane area and endothelial cell profile number did not differ between diabetic and control animals. However, luminal area (P < 0.03) was increased and endothelial cell area (P < 0.08) was decreased in the diabetic rats. We conclude there is no detectable structural basis for the reduction in nerve conduction velocity, pain threshold or blood flow, observed in the streptozotocin diabetic rat.

publication date

  • October 1999



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1017/S002187829900549X

PubMed ID

  • 10580857

Additional Document Info

start page

  • 419

end page

  • 27


  • 195


  • 3