scholarly journals The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

Diabetologia ◽  
1986 ◽  
Vol 29 (3) ◽  
pp. 168-174 ◽  
Author(s):  
N. E. Cameron ◽  
M. B. Leonard ◽  
I. S. Ross ◽  
P. H. Whiting
1999 ◽  
Vol 195 (3) ◽  
pp. 419-427
Author(s):  
DAVID WALKER ◽  
ANNE CARRINGTON ◽  
SUSAN A. CANNAN ◽  
DIANE SAWICKI ◽  
JANET SREDY ◽  
...  

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.


2006 ◽  
Vol 16 (5) ◽  
pp. 207-213 ◽  
Author(s):  
Yoshihisa Fujino ◽  
Xiaojuan Guo ◽  
Kiyoyumi Shirane ◽  
Jun Liu ◽  
Kegong Wu ◽  
...  

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S107-S107
Author(s):  
Stacy A Hussong ◽  
Veronica Galvan

Abstract With age, peripheral nerves undergo demyelination along with overall decrease in peripheral nerve conduction velocity in both sensory and motor nerves. Loss of innervation in muscles is thought to be a major factor in causing age-related sarcopenia including a decrease in muscle function. Dietary restriction attenuates the detrimental effects of aging in mice. Reduction of mTOR signaling is hypothesized to have overlapping mechanisms with dietary restriction. Furthermore, inhibition of mTOR via rapamycin treatment is known to extend lifespan in mice as well as improve peripheral nerve myelination. Therefore, I hypothesized that reducing mTORC1 signaling in neurons would be able to ameliorate the deleterious effects of aging in peripheral nerves. An overall decrease in nerve conduction velocity was observed in both tail sensory and sural nerves with age (15 vs. 30 months). In neuronal mTORC1 KD animals, there was an age-related preservation of both sural and sciatic nerve conduction. Rapamycin treatment produced similar effects with a trend towards increased sciatic nerve conduction velocity in rapamycin-treated wild-type mice at 19 months. The preserve sciatic nerve conduction velocity could be partially explained by preserved myelination. Neuronal mTORC1 knockdown animals had more myelin in the sciatic nerve at 30 mo. as compared to age-matched controls. Overall, these data indicate that mTORC1 signaling plays a role in the age-related decline in peripheral nerve myelination as well as nerve conduction velocity. Future therapeutics could utilize rapamycin or other rapalogs to combat the decline in peripheral nerve function associated with age and other diseases as well.


Neurology ◽  
1981 ◽  
Vol 31 (3) ◽  
pp. 327-327 ◽  
Author(s):  
R. O. Robinson ◽  
W. C. Robertson

1993 ◽  
Vol 62 (1) ◽  
pp. 148-154 ◽  
Author(s):  
K. Teramoto ◽  
F. Wakitani ◽  
S. Horiguchi ◽  
T. Jo ◽  
T. Yamamoto ◽  
...  

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