Reches A, Benalal D, Weissman B A, Bachrach U, Lindner H R, Salomon Y
Clin Neuropharmacol. 1982 Dec;5(4):395-404. doi: 10.1097/00002826-198212000-00007.
Exposure of neuroblastoma X glioma hybrid cells to LiCl (Li+) for 48 h significantly reduces prostaglandin E1 (PGE1)-dependent cyclic adenosine monophosphate (AMP) accumulation. When applied simultaneously with morphine for the same period, Li+ inhibits the excessive accumulation of cyclic AMP in response to PGE1 characteristically exhibited by these cells upon opiate withdrawal. Likewise, Li+ inhibits, in vitro, PGE1-dependent cyclic AMP accumulation in tissue slices from rat corpus striatum. Prophylactic administration of Li+ in the diet attenuates the withdrawal symptoms in morphine-addicted rats. These findings support clinical reports that suggest that prophylactic treatment with Li+ attenuates the severity of the opiate withdrawal syndrome.
将神经母细胞瘤X胶质瘤杂交细胞暴露于氯化锂（Li +）48小时可显著降低前列腺素E1（PGE1）依赖性环磷酸腺苷（AMP）的积累。当与吗啡同时应用相同时间时，Li +抑制了这些细胞在阿片类药物戒断时特有的对PGE1产生的环AMP过度积累。同样，Li +在体外抑制大鼠纹状体组织切片中PGE1依赖性环AMP的积累。在饮食中预防性给予Li +可减轻吗啡成瘾大鼠的戒断症状。这些发现支持了临床报告，即Li +的预防性治疗可减轻阿片类药物戒断综合征的严重程度。
