Ultrastructural and biochemical characterization of autonomic neuropathy in rats with chronic streptozotocin diabetes

Alterations in the extrinsic innervation of the alimentary tract and in various sympathetic autonomic ganglia were examined using quantitative ultrastructural and biochemical methods in streptozotocin diabetic rats maintained without treatment for 9–15 months. Heal mesenteric nerves of 13–15 month diabetics showed the characteristic alterations of neuroaxonal dystrophy qualitatively similar to changes seen in this system in animals which were diabetic for shorter durations. Dystrophie axonopathy was not accompanied by significant axonal loss or atrophy. Dystrophie axons, presumably involving presynaptic elements, also were increased in frequency in the superior mesenteric ganglia, but not in the superior cervical ganglia, of animals diabetic for various durations. In addition, the superior mesenteric ganglia of diabetic animals contained an increased number of postsynaptic dendritic processes which were dilated by unusual tubular profiles. These ganglionic alterations were not accompanied by changes in the activity of the presynaptic cholinergic marker enzyme, choline acetyltransferase. The activity of the noradrenergic marker enzyme, dopa-mine-beta-hydroxylase, was unaltered in diabetic superior mesenteric ganglia compared to controls, but showed a 30–40% decrease in diabetic superior cervical ganglia, in which site it was unaccompanied by neuronal loss, atrophy, or ultrastructural alterations.