Otero Losada M E, Rubio M C
Naunyn Schmiedebergs Arch Pharmacol. 1986 Feb;332(2):169-72. doi: 10.1007/BF00511408.
The acute (1 h, i.p.) and chronic (14 days, p.o.) effects of LiCl treatment upon GABA-ergic neurons were studied in the rat corpus striatum and frontal cerebral cortex. One hour after a single injection of LiCl the activity of glutamic acid decarboxylase (GAD) was reduced by 29% in the striatum (2 meq/kg LiCl) and by 38% in the cerebral cortex (10 meq/kg LiCl). In contrast, striatal GAD was activated by 34% 1 h after the injection of 10 meq/kg of LiCl; this dose also reduced the endogenous striatal GABA level by 24%. After 14 days of oral LiCl administration (2 meq/kg/day): a) cortical GAD activity was enhanced by 50% and GABA concentration was decreased by 28%; b) no changes were observed in the striatum. These findings suggest that: LiCl administration stimulates GABA-ergic function in specific areas (depending on the dose and length of treatment) increasing both GAD activity and probably GABA release. This occurs in the striatum after acute treatment only with a high dose, and in the frontal cerebral cortex after chronic treatment with a low dose.
在大鼠纹状体和额叶皮质中研究了氯化锂处理对γ-氨基丁酸（GABA）能神经元的急性（腹腔注射1小时）和慢性（口服14天）影响。单次注射氯化锂1小时后，纹状体（2毫当量/千克氯化锂）中谷氨酸脱羧酶（GAD）的活性降低了29%，在大脑皮质（10毫当量/千克氯化锂）中降低了38%。相反，注射10毫当量/千克氯化锂1小时后，纹状体GAD活性增加了34%；该剂量还使纹状体内源性GABA水平降低了24%。口服氯化锂14天（2毫当量/千克/天）后：a）皮质GAD活性增强了50%，GABA浓度降低了28%；b）纹状体未观察到变化。这些发现表明：给予氯化锂可刺激特定区域的GABA能功能（取决于剂量和治疗时长），增加GAD活性并可能增加GABA释放。这仅在急性高剂量处理后的纹状体以及慢性低剂量处理后的额叶皮质中出现。
