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

Published online by Cambridge University Press:  01 October 1999

DAVID WALKER
Affiliation:
Department of Medicine, Manchester Royal Infirmary, UK
ANNE CARRINGTON
Affiliation:
The Institute for Diabetes Discovery, Branford, Connecticut, USA
SUSAN A. CANNAN
Affiliation:
The Institute for Diabetes Discovery, Branford, Connecticut, USA
DIANE SAWICKI
Affiliation:
The Institute for Diabetes Discovery, Branford, Connecticut, USA
JANET SREDY
Affiliation:
The Institute for Diabetes Discovery, Branford, Connecticut, USA
ANDREW J. M. BOULTON
Affiliation:
Department of Medicine, Manchester Royal Infirmary, UK
RAYAZ A. MALIK
Affiliation:
Department of Medicine, Manchester Royal Infirmary, UK
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Abstract

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.

Type
Research Article
Copyright
© Anatomical Society of Great Britain and Ireland 1999

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