Impaired nerve fiber regeneration in axotomized peripheral nerves in streptozotocin-diabetic rats.
OBJECTIVE
Impaired nerve fiber regeneration is a salient feature of diabetic neuropathy. Its pathogenesis is still unclear. We attempted to characterize the structure of regenerated myelinated fibers after transection in streptozotocin-diabetic rats.


METHODS
Streptozotocin-diabetic rats underwent transection of the sciatic nerve. Two and 4 weeks post-axotomy, regenerated myelinated fibers of the cut end and fibers at its proximal site were morphometrically examined. Non-diabetic control rats with axotomy were also examined for comparison.


RESULTS
At 4 weeks post-axotomy, diabetic rats showed an increased myelinated fiber density and total fiber number with a trend toward reduced fiber size at the cut end compared with those in control rats. The average number of myelin lamellae relative to axonal size in regenerated fibers at the cut end was significantly reduced in diabetic rats compared with that in control rats. The proximal site showed a reduced size of fibers and axons in both diabetic and control rats to a similar extent compared with those in a non-axotomized state. At 2 weeks post-axotomy, these findings were less apparent.


CONCLUSIONS
The nerves of diabetic rats when axotomized undergo impaired regeneration characterized by increased fiber density with hypomyelination.
Department of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan ; Department of Legal Medicine Graduate School of Medicine and Pharmaceutical Sciences University of Toyama Toyama Japan.
Naoki
N
Nishida
Department of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan.
Shin-Ichiro
S
Yamagishi
Department of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan.
Hiroki
H
Mizukami
Department of Pathology and Molecular Medicine Hirosaki University Graduate School of Medicine Hirosaki Japan.
Soroku
S
Yagihashi
Fiber atrophy; Myelination; Nerve regeneration