𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Impaired retrograde axonal transport from a nerve crush in streptozotocin diabetic rats

✍ Scribed by P. Sidenius; J. Jakobsen


Publisher
Springer
Year
1980
Tongue
English
Weight
673 KB
Volume
19
Category
Article
ISSN
0012-186X

No coin nor oath required. For personal study only.

✦ Synopsis


The axonal transport of proteins in crushed nerves of streptozotocin (40 mg/kg) diabetic rats was investigated 4 weeks after induction of diabetes. 35S-methionine was used as a marker for protein and 3H-fucose as a marker for glycoprotein. The precursors were injected into the fifth lumbar spinal ganglion and the accumulation of TCA-insoluble activity proximal and distal to a sciatic nerve ligature was measured at different time intervals after application of a crush. The start of accumulation distal to the ligature was delayed by 1 hour for proteins as well as for glycoproteins. Furthermore, the total amount of accumulated protein after 19 h was decreased by 18% while the decrease was 21% for glycoprotein. By insulin treatment the differences could both be prevented and reversed after 3 days of normoglycaemia. These findings demonstrate an impaired response to a nerve crush and might be the explanation for the regenerative abnormalities of peripheral nerves in diabetes.


πŸ“œ SIMILAR VOLUMES


Impaired induction of ornithine decarbox
✍ W. G. McLean; J. E. Chapman; N. A. Cullum πŸ“‚ Article πŸ“… 1987 πŸ› Springer 🌐 English βš– 297 KB

Ornithine decarboxylase activity was measured in the dorsal root ganglia from crushed and uncrushed contralateral sciatic nerve of control and streptozotocin-diabetic rats. A further group of diabetic rats was treated with insulin throughout the experiment. Ornithine decarboxylase activity in gangli

Prevention of defects of axonal transpor
✍ J. H. Mayer; D. R. Tomlinson πŸ“‚ Article πŸ“… 1983 πŸ› Springer 🌐 English βš– 759 KB

The effects of orally-administered myo-inositol have been compared with those of an aldose reductase inhibitor on acute neurological defects in experimentally diabetic rats. Three groups of streptozotocin-treated diabetic rats (50 mg/kg, IP) together with three groups of age-matched controls (saline