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Diabetes does not accelerate neuronal loss following nerve injury
Author(s) -
Severinsen Kaare,
Jakobsen Johannes
Publication year - 2007
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/j.1529-8027.2007.00147.x
Subject(s) - medicine , chromatolysis , diabetes mellitus , dorsal root ganglion , streptozotocin , nerve injury , sciatic nerve , endocrinology , anesthesia , spinal cord , psychiatry
To determine the resistance of neuronal dorsal root ganglion (DRG) cells in experimental diabetes, we studied the neuronal cell loss after severe axonal injury in streptozotocin (STZ) diabetic rats with unilateral transection of the L5 spinal nerve for 12 weeks. Fifty 18‐week‐old inbred male Wistar rats were randomly allocated to three study groups. In study group 1 without spinal nerve injury, STZ diabetes was induced in 9 and 10 rats were kept as nondiabetic controls. In study group 2, spinal nerve injury was performed in 10 diabetic rats and in 10 nondiabetic controls. In study group 3, six nondiabetic control rats at 18 weeks and five nondiabetic control rats at 30 weeks were included to determine whether DRG cell changes occur without nerve injury during the study period. In group 1, the stereologically determined number of all neuronal DRG cells was unchanged after 12 weeks of diabetes. The mean perikaryal volume of neuronal DRG cells of the A and B subtypes was reduced by 10% each (p < 0.05). In group 2, spinal nerve injury led to neuronal cell loss, chromatolysis, and perikaryal shrinkage but without any acceleration of cell loss after 12 weeks of diabetes. In group 3, there were no changes indicating that the reduction of perikaryal volume in diabetic rats without nerve injury represents shrinkage. We conclude that neuronal DRG cells in rats are resistant to diabetes per se and that addition of diabetes for 12 weeks to spinal nerve injury does not further accelerate the cell loss.