Hakim A M, Cooper B A, Rosenblatt D S, Pappius H M
J Neurochem. 1983 Apr;40(4):1155-60. doi: 10.1111/j.1471-4159.1983.tb08107.x.
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.
通过2-脱氧-D-[1-¹⁴C]葡萄糖技术测量的局部脑葡萄糖利用（LCGU）反映了局部脑功能活动。为了阐明与维生素B₁₂缺乏相关的脑病机制，在最近描述的两种有效的B₁₂缺乏模型中测定了LCGU：将大鼠暴露于亚麻醉剂量的氧化亚氮（N₂O）和/或给予1-氨基环戊烷-1-羧酸（环亮氨酸）。我们的结果表明，成年大鼠暴露于N₂O会选择性地抑制皮质、听觉和边缘结构中的LCGU，同时维生素B₁₂依赖性甲基四氢叶酸-同型半胱氨酸甲基转移酶（EC 2.1.1.13，甲硫氨酸合成酶）的全脑活性也会受到抑制。环亮氨酸对成年大鼠的LCGU没有明显影响，也不会改变甲硫氨酸合成酶的脑活性。
