Structural abnormalities do not explain the early functional abnormalitiesin the peripheral nerves of the streptozotocin diabetic rat

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 structur al abnormalities underlie these functional abnormalities is unclear. 10 adu lt male Sprague-Dawley STZ-diabetic rats (diabetes duration 27 d) and 10 ag e-matched (23 wk) control animals were studied. Motor nerve conduction velo city (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 sciat ic 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 signif icant difference in fascicular area, myelinated fibre density, fibre and ax on areas as well as unmyelinated fibre density and diameter. Endoneurial ca pillary 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 decrease d in the diabetic rats. We conclude there is no detectable structural basis for the reduction in nerve conduction velocity, pain threshold or blood fl ow, observed in the streptozotocin diabetic rat.