Properties of isolated nerve fibres from alloxanized rats.

Rat sciatic nerve fibres do not conduct nerve impulses at a normal rate after the rat has been injected with alloxan (Eliasson, 1964). The dose given to the rat must be large enough to cause clinically detectable diabetes. The conduction rate slows to levels of 30 to 50% of the original within the first 10 days after the injection; possibly this is due to a direct toxic effect of the alloxan on the neural structures. Nerves from rats which have been diabetic for six weeks or longer have less conduction impairment. Sensory and motor fibres are involved at both time intervals, but no change has been noted in the autonomic nerves. The conduction velocity changeisnot reversedby insulin, but hypophysectomy may result in a return of normal conduction velocity (Mayher, Mimbs, and Allen, 1967). Different pathological findings found in toxic neuropathies could be used to account for the decrease in the conduction velocity in the alloxanized, diabetic animal. Paranodal demyelination is the lesion seen in chronic alcoholism (Mayer, 1966), lead neuropathy (Lampert and Schochet, 1968), and diphtheric neuropathy (Waksman, Adams, and Mansmann, 1957), whereas acrylamide intoxication results in axonal degeneration (Fullerton and Barnes, 1966). Neither of these findings has been noted in chronic alloxanized animals, but focal Schwann cell damage was observed to occur in acute alloxan intoxication by Preston (1967). Loss of nerve fibre with a change in fibre spectrum and conduction was observed in isoniazid intoxication by Cavanagh (1967). Data from our animals as seen in Table I did not substantiate any such change in the composition of the nerve for alloxanized animals. It therefore remained to explore the possibility that the conduction velocity changes described in the diabetic animal were due to changes in the insulating properties of the internodal segments and/or the nodal membranes themselves.