The problem of diabetic neuropathy has not been studied experimentally to the same extent as have other manifestations of diabetes mellitus. One reason may be that neurological symptoms have not been apparent in animals that have been made diabetic. Lukens (2) stated in his review of al-loxan diabetes that nervous system lesions had not been observed. Pancreatectomized animals have been prepared in large numbers, but no men-tion has been made of neurological complications. Minor neurological deficit, particularly of the sensory functions, could easily have been over-looked (3). The data presented below demonstrate a de-crease in conduction velocity under in vitro con-ditions in the peripheral nerves from alloxanized rats but only if these rats also become diabetic. Because of the toxic effects of alloxan, a group of pancreatectomized rats was also prepared and showed essentially the same slowing of conduction. Treatment with insulin of the animals before the experiment or addition of insulin in vitro did not restore conduction velocity to normal values. Methods Sprague-Dawley rats 1 were used. The rats weighed between 300 and 450 g and were over 5 months old. The animals were injected with alloxan monohydrate in citrate buffer in amounts of 40 to 50 mg per kg (4). Litter mates were used as controls. Intravenous in-jection method was used, and injections were given after 18 hours of starvation. Some of the injected animals did not become diabetic. These animals were used a
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