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An ultrastructural study of the dorsal sympathetic ganglia, chain, and myenteric plexus is described in the streptozotocin diabetic rat after intermittent insulin treatment. The observations described cover the first two weeks following induction of diabetes in which insulin was administered subcutaneously twice daily. Significant regenerative changes were seen with marked axonal sprouting noted at three days. Degenerative changes were seen to be less severe than those in untreated animals. It is concluded that the improvement in the neuropathic changes with insulin treatment supports a transient primary role of the streptozotocin in causing the neuropathy — but that the subsequent improvement seems to be related to the partial control of the diabetes.
An ultrastructural study of the sympathetic ganglia, dorsal sympathetic chain, and Auerbach's plexus is described in the streptozotocin diabetic rat. The observations cover the first six weeks following induction of diabetes. Degenerative changes began to appear in the axonal plasma membranes and axoplasm of unmyelinated fibers at 24 hours and were widespread by two weeks. Axonal sprouting and regenerating axons began to appear and increase in number through the 6th week. Chromatolysis in ganglion cells in sympathetic ganglia became apparent by two weeks as did degenerative changes in axons of Auerbach's plexus. This somewhat later appearance of changes in ganglion cells and Auerbach's plexus suggested the primary changes occurred in the postganglionic fibers. The cycle of change from degeneration to regeneration in the areas examined suggests either a possible toxic effect of strepiozotocin or a combination of metabolic disturbances as a cause of this neuropathy.
The results are reported of single muscle fiber uptake of tritiated leucine in muscle biopsy material from Duchenne dystrophy and Charcot-Marie Tooth disease. The uptake in the two conditions is compared and suggests that the previously reported increase in synthesis of cytoplasmic proteins in muscular dystrophy are probably related to regenerative efforts by the muscle fibers.
In previous studies, the incorporation of 3H(G)L-leucine into muscles of patients with Charcot-Marie-Tooth (CMT) disease was shown to he increased in comparison with that observed in motor neuron disease (MND). To determine the cause of the increased uptake in CMT, studies of single fiber leucine incorporation have been undertaken. The results of this study indicate that the increased incorporation is into those muscle fibers which are undergoing
regeneration following reinnervation. These results do not support the thesis that there is an associated myopathic
process in CMT.
The autoradiographic findings using tritiated leucine are described in muscle biopsy material from five patients with progressive muscular dystrophy (P.M.D.), three with motor neuron disease (M.N.D.) and four with Charcot-Marie-Tooth disease (C.M.T.). In progressive muscular dystrophy there is a marked increase in uptake of leucine into cytoplasmic proteins and precursors, and reduced incorporation into structural protein. In Charcot-Marie Tooth disease muscle there is a significantly increased uptake into cytoplasmic elements and a normal uptake into structural protein. In motor neuron disease the uptake into cytoplasmic elements appears normal but is reduced into structural proteins.
The abnormal uptake in C.M.T. could be explained as a product of regenerative efforts associated with reinnervation. However, the abnormal uptake may represent the primary effects of gene action in the muscle, as seems probable in progressive muscular dystrophy.
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