中文摘要：

尽管锂拥有 neuropro-tective 功能，位于它的行动下面的分子的机制充分没被阐明。在现在的纸，在尖锐地从老鼠马头鱼尾的怪兽孤立的 CAl 金字塔形的神经原的电压依赖者钾水流上的氯化锂的效果用整个房间的补丁夹钳技术被学习。Depolarizingtest 脉搏激活外面的钾水流的二个部件：一个很快激活并且使失去活性的部件， I_A 和一个推迟的部件， I_k。结果证明那氯化锂以一种集中依赖者方式增加了 I_A 的振幅。半改进集中(EC_(50 )) 是 22.80 +- 5.45 亩摩尔中心点 L~(25 亩摩尔中心的 -1), 氯化锂 dotL~(-1) 转移了不变的激活曲线并且在到更否定的潜力的 I_A 的激活曲线，但是主要影响了激活动力学。振幅和 I_K 的激活过程没被氯化锂影响。钾隧道上的氯化锂的效果看起来由 Ca~(2+)-lowing 效果拥有 neuroprotective 性质由在老鼠激活 I_A 调制 neuronalexcitability 海马趾的神经原。

英文摘要：

Although lithium possesses neuroprotective functions, the molecular mechanism underlying its actions has not been fully elucidated. In the present paper, the effects of lithium chloride on voltage-dependent potassium currents in the CA1 pyramidal neurons acutely isolated from rat hippocampus were studied using the whole-cell patch-clamp technique. Depolarizing test pulses activated two components of outward potassium currents： a rapidly activating and inactivating component, /A and a delayed component, /K. Results showed that lithium chloride increased the amplitude of /A in a concentration-dependent manner. Half enhancement concentration （EC50） was 22.80 ± 5.45 μmol·L^-1. Lithium chloride of 25 μmol·L^-1 shifted the steady-state activation curve and inactivation curve of /A to more negative potentials, but mainly affected the activation kinetics. The amplitude and the activation processes of/Kwere not affected by lithium chloride. The effects of lithium chloride on potassium channel appear to possess neuroprotective properties by Ca^2＋-Iowing effects modulate neuronal excitability by activating /A in rat hippocampal neurons.