Local cerebral glucose utilization in two models of B12 deficiency.
Local cerebral glucose utilization (LCGU), as measured by the 2-deoxy-D-[1-14C]glucose technique, reflects local cerebral functional activity. In an effort to elucidate mechanisms of the encephalopathy associated with deficiency of vitamin B12, LCGU was determined in two recently described models of effective B12 deficiency: exposure of rats to subanesthetic doses of nitrous oxide (N2O) and/or administration of 1-amino-cyclopentane-1-carboxylic acid (cycloleucine). Our results show that exposure of adult rats to N2O depresses LCGU selectively in cortical, auditory, and limbic structures, in association with a depression in whole-brain activities of the vitamin B12-dependent methyltetrahydrofolate-homocysteine methyl-transferase (EC 2.1.1.13, methionine synthetase). Cycloleucine has no discernible effect on LCGU in the adult rat and does not change the cerebral activity of methionine synthetase.
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002250:Carbon Radioisotopes; D003837:Deoxy Sugars / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009609:Nitrous Oxide / Q000494:pharmacology; D009928:Organ Specificity; D051381:Rats; D011919:Rats, Inbred Strains; D014806:Vitamin B 12 Deficiency / Q000378:metabolism*
D002250:Carbon Radioisotopes; D003837:Deoxy Sugars; D003847:Deoxyglucose; D009609:Nitrous Oxide