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Changes in axon size and slow axonal transport are related in experimental diabetic neuropathy

From the Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.

In the sciatic system of rats with streptozocin (SZ)-induced diabetes, delay of axonal transport of neurofilament (NF) proteins, tubulin, and other proteins is associated with a change in axonal caliber, which increases by 40% in lumbar motor roots and decreases by 36% in tibial nerves. Since in large myelinated axons caliber is a function of the number of NF, which, in turn, is regulated by axonal transport, we studied the correlation of the number of NF and microtubules (MT) with axonal cross-sectional area in the sciatic system of SZ-treated rats to investigate whether the changes in caliber could be attributed to the impairment of transport. Despite the changes in cross-sectional area, diabetic axons in both proximal motor roots and distal tibial nerves maintained the ratios of number of NF and MT to cross-sectional area found in controls. Our findings suggest that, in rats with SZ-induced diabetes, the proximal and distal alterations of axonal caliber are an adjustment to the change in number of NF and/or MT that results from the impairment of the slow axonal transport.

Address correspondence and reprint requests to Dr. Gambetti, Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106.

Supported by the Juvenile Diabetes Foundation International grant # 18656 and by NIH grants NS 14509 and AG 00795.

Received April 7, 1987. Accepted for publication in final form July 28, 1987.

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