POLYNEUROPATHY DUE TO COBALAMIN DEFICIENCY IN THE RAT

In the present study, we investigated the peripheral nervous system (P NS) (both in terms of its ultrastructure and in terms of its function) of rats made cobalamin (Cbl)-deficient either through total gastrecto my or through prolonged feeding on a Cbl-deficient diet. In both these types of Cbl-deficient neuropathies we found: (a) ultrastructurally, intramyelin and endoneural edema, with no or minimal axonal damage in the PNS, in dorsal root ganglia, and the ventral and dorsal rootlets o f the spinal cord; (b) electrophysiologically, a significant reduction in the nerve conduction velocity, consistent with that reported in (a ); (c) morphometrically, a significant reduction in the density of mye linated fibers both in the sciatic nerve and in the peroneal nerve. Al l these pathological changes were reversed by chronic postoperative ad ministration of Cbl into totally gastrectomized (TGX)-rats, hinting at the specificity of the damage itself in relation to the permanent Cbl -deficient status of the TGX-rats. No signs of segmental demyelination or remyelination were found. We also observed a turning of type I fib ers into type II fibers in the soleus muscle of all our Cbl-deficient rats, however the Cbl deficiency had been induced. This muscular chang e was still present in TGX- and Cbl-treated rats, and it cannot be rel ated to a malnutrition status, since it has been observed also in rats fed a Cbl-deficient diet. All these results demonstrate that Cbl defi ciency strongly affects rat PNS within different parameters. (C) 1998 Elsevier Science B.V.