Impaired retrograde axonal transport from a nerve crush in streptozotocin diabetic rats.
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.
D000818:Animals; D001370:Axonal Transport; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000503:physiopathology*; D005643:Fucose / Q000378:metabolism; D005727:Ganglia, Spinal / Q000503:physiopathology*; D006023:Glycoproteins / Q000378:metabolism; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008715:Methionine / Q000378:metabolism; D011506:Proteins / Q000378:metabolism*; D051381:Rats
D006023:Glycoproteins; D007328:Insulin; D011506:Proteins; D005643:Fucose; D008715:Methionine