Development of sensory neuropathy in streptozotocin-induced diabetic mice
Article first published online: 23 DEC 2012
© 2012 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Brain and Behavior
Volume 3, Issue 1, pages 35–41, January 2013
How to Cite
Brain and Behavior 2013; 3(1):35–41.
- Issue published online: 9 JAN 2013
- Article first published online: 23 DEC 2012
- Manuscript Accepted: 17 NOV 2012
- Manuscript Revised: 14 NOV 2012
- Manuscript Received: 23 OCT 2012
- Kawasaki Medical School. Grant Numbers: 22-A19, 23-13, 24-2
- KAKENHI. Grant Number: 23591260
- Diabetic sensory neuropathy;
- impaired maturation;
- sensory conduction velocity;
- STZ-induced diabetic mice;
- unmyelinated fiber atrophy
Diabetic polyneuropathy is a major complication of diabetes and the most common cause of peripheral neuropathy. Sensory-dominant neuropathy is the most common type. We previously used streptozotocin (STZ)-induced diabetic ddY mice with sensory neuropathy to evaluate the therapeutic effects of vascular endothelial growth factor and placental growth factor isoforms. In this study, to characterize the development of diabetic sensory neuropathy, electrophysiological, behavioral, and histopathological studies were performed in these diabetic mice. A significant difference in sensory conduction velocity in the tail nerve was observed between healthy and diabetic mice at 1 week after STZ injection. Diabetic mice developed hypoalgesia at 5 weeks after STZ injection. Axon area and myelin thickness of the myelinated fibers were increased in 17-week-old healthy mice compared with those in 8-week-old healthy mice. However, these increases were retarded in 17-week-old diabetic mice. In unmyelinated fibers, axon area was significantly reduced in 17-week-old diabetic mice compared with 8- and 17-week-old healthy mice. These findings suggest that both impaired maturation of myelinated fibers and atrophy of unmyelinated fibers simultaneously occur in the early stage of diabetes in these mice. Our mouse model may be useful for studying the pathogenesis of and therapies for diabetic sensory neuropathy.