Subacute combined degeneration and induction of ornithine decarboxylase in spinal cords of totally gastrectomized rats.

Totally gastrectomized rats have been used to induce a spongy demyelination in the white matter of the spinal cord (SC) which is strongly reminiscent of that observed in subacute combined degeneration of human SC. Totally gastrectomized rats are deprived of intrinsic factor and thereafter become deficient in cobalamin. Morphologically, the spongy demyelination of the white matter of the rat SC, was evident 2 months after total gastrectomy. Biochemically, we investigated the hypothesis that polyamine biosynthesis might be deranged in the rat SC with experimental subacute combined degeneration, since polyamines are well known to be bound to myelin in the mammalian central nervous system. We measured the levels of both the polyamine biosynthetic decarboxylases, L-ornithine decarboxylase (ODC) and S-adenosyl-L-methionine decarboxylase, the key points in the polyamine biosynthetic pathway, in these SC. There was a sharp increase in ODC activity in SC 2 months after total gastrectomy, without significant changes in S-adenosyl-L-methionine decarboxylase activity. The increase in ODC activity seems to be organ-specific and was not due to a proliferation of neuroglial cells. Interestingly enough, the same morphologic and biochemical features found in SC of 2-month-totally-gastrectomized rats were present also in SC of newborn rats, which indeed showed incomplete myelination, vacuolated appearance, and an ODC activity level higher than that of adult SC. Therefore, total gastrectomy seems to induce a type of regression in the SC of totally gastrectomized rats toward neonatal life, at least in terms of the degree of myelination and of ODC activity level. Biochemically, no changes in ODC activity were observed in SC of rats fed a cobalamin-deficient diet for 3 months. Morphologically, only a proliferation of neuroglial cells with a moderate demyelination was observed in SC of these rats maintained on a cobalamin-deficient diet for 3 months.