Domino E F, Mathews B N, Tait S K, Ortiz A
Arch Int Pharmacodyn Ther. 1983 Sep;265(1):49-54.
Oral phosphatidylcholine (PC) in a dose of 250 mg/kg choline equivalent, was given 1, 2, 4, 8, 12, and 24 hr prior to brain assay to groups of fasted mice. The animals were then killed by focused microwave irradiation to the head and brain choline (Ch) and acetylcholine (ACh) assayed by chemical demethylation using gas chromatography-nitrogen phosphorous (GC-NP) detection. Mouse brain Ch levels increased significantly at 4 (P less than .001) and 8 (P less than .01) hr after PC administration. However, there was no change in mouse brain ACh. When this experiment was repeated in a second series of animals at 1, 3, 6, and 12 hr pretreatment with PC, only the 6 hr pretreatment showed a significant increase in brain Ch (P less than .01). The effects of PC administration to alter the known ACh depleting effects of scopolamine were also determined by giving PC orally 4 hr before and scopolamine, 0.1, 0.32, and 1 mg/kg, one hr before microwave irradiation. The known depleting effects of scopolamine pretreatment on brain ACh were confirmed (P less than .001). A large dose (1 mg/kg) of scopolamine also caused a decrease in brain Ch (P less than .001). Pretreatment with PC reversed the depletion of brain Ch induced by scopolamine but had no effect on depleted brain ACh. The results indicate that, although mouse brain Ch can be increased by oral PC, there is no effect on mouse brain ACh.
将剂量为250毫克/千克胆碱当量的口服磷脂酰胆碱(PC),在进行脑分析前1、2、4、8、12和24小时给予禁食小鼠组。然后通过对头进行聚焦微波照射处死动物,并使用气相色谱 - 氮磷(GC - NP)检测通过化学脱甲基法测定脑胆碱(Ch)和乙酰胆碱(ACh)。给予PC后4小时(P小于0.001)和8小时(P小于0.01),小鼠脑Ch水平显著升高。然而,小鼠脑ACh没有变化。当在第二组动物中在给予PC预处理1、3、6和12小时后重复此实验时,只有6小时预处理显示脑Ch有显著增加(P小于0.01)。还通过在微波照射前4小时口服PC和在照射前1小时给予0.1、0.32和1毫克/千克的东莨菪碱,来确定PC给药改变东莨菪碱已知的ACh耗竭作用的效果。东莨菪碱预处理对脑ACh的已知耗竭作用得到证实(P小于0.001)。大剂量(1毫克/千克)的东莨菪碱也导致脑Ch减少(P小于0.001)。PC预处理逆转了东莨菪碱诱导的脑Ch耗竭,但对耗竭的脑ACh没有影响。结果表明,虽然口服PC可增加小鼠脑Ch,但对小鼠脑ACh没有影响。