Electrophysiological features were studied longitudinally in the spontaneously diabetic insulin-dependent, BB-Wistar rat. These were correlated in time with the state of the patency of the protective barriers in peripheral nerves. Motor nerve conduction velocity was significantly slowed only 3 weeks after the onset of the diabetes. When ultrastructural changes began, the maximal conduction velocity was further diminished. The amplitudes of evoked muscle potentials and distal latencies were significantly altered in diabetic rats. No change in the permeability of the blood-nerve barrier could be demonstrated before, during or after the onset of the nerve conduction defect. The possible pathogenetic mechanisms are discussed and a possible mechanism is suggested, namely a reduced availability of energy to axons in diabetes.
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