Gorell J M, Navarro C P, Schwendner S P
J Neurochem. 1981 Jan;36(1):321-4. doi: 10.1111/j.1471-4159.1981.tb02415.x.
During insulin stupor in mice, acetylcholine levels in cerebral cortex, cerebellum, brainstem, striatum, and hippocampus were unchanged from control values despite brain glucose concentrations 3-10% of normal, whereas choline levels rose 2.4-3.6-fold in all five CNS regions. Brain acetylcholine and choline levels did not change during recovery following glucose injection. The data suggest that, in hypoglycemic stupor, (1) overall rates of acetylcholine synthesis and degradation remain balanced within each of the CNS regions studied; (2) the biochemical mechanism that elevates brain choline levels is unlikely to be related only to cholinergic synaptic processes; and (3) brain choline levels need not rise for stupor to occur.
在小鼠胰岛素昏迷期间,尽管脑葡萄糖浓度仅为正常水平的3%-10%,但大脑皮层、小脑、脑干、纹状体和海马体中的乙酰胆碱水平与对照值相比并无变化,而在所有这五个中枢神经系统区域中,胆碱水平却升高了2.4-3.6倍。在注射葡萄糖后的恢复过程中,脑内乙酰胆碱和胆碱水平并未改变。这些数据表明,在低血糖昏迷中,(1) 在每个所研究的中枢神经系统区域内,乙酰胆碱的合成和降解总体速率保持平衡;(2) 提高脑胆碱水平的生化机制不太可能仅与胆碱能突触过程有关;(3) 昏迷的发生并不一定需要脑胆碱水平升高。