Vs. Tantuwaya et al., PERIPHERAL-NERVE REGENERATION THROUGH SILICONE CHAMBERS IN STREPTOZOCIN-INDUCED DIABETIC RATS, Brain research, 759(1), 1997, pp. 58-66
The silicone chamber model was used to evaluate peripheral nerve regen
eration (PNR) in streptozocin (STZ)-induced diabetic rats. Diabetic an
d control animals underwent sciatic nerve transection and silicone cha
mber implantation establishing gaps of various lengths between the tra
nsected nerve ends. In animals with 5 and 10 mm gaps, diabetes was ind
uced in experimental rats I week before surgery, and the animals were
sacrificed 3 weeks after surgery. In animals with 8 mm gaps, diabetes
induction occurred 3 days after surgery, and they were sacrificed afte
r 7 weeks. Diabetic rats with 10 mm gaps demonstrated an impaired abil
ity to form bridging cables, the initial step of regeneration through
chambers. Morphometric studies of bridging cables between transected n
erve ends demonstrated a significant reduction in the mean endoneurial
area in diabetic animals with 5 and 8 mm gaps compared to controls. T
he number of regenerated myelinated axons in the chamber was significa
ntly decreased in diabetic rats with 8 and 10 mm gaps, The mean myelin
ated fiber area in the regenerated cables of the diabetic group was si
gnificantly decreased with 5 mm gaps and significantly increased with
8 mm gaps compared to controls, Size-frequency histograms of regenerat
ed myelinated fiber areas suggest a delay in the maturation of small c
aliber axons, Schwann cell migration across 5 mm gaps was examined wit
h S-100 immunohistochemistry. The total distance of Schwann eel migrat
ion into cables from bath proximal and distal ends was significantly r
educed in diabetic animals. Characterization of PNR across gaps throug
h silicone chambers in diabetic rats showed impairment in multiple asp
ects of the regenerative process, including cable formation, Schwann c
ell migration, and axonal regeneration.