Effects of lithium chloride on outward potassium currents in acutely isolated hippocampal CA1 pyramidal neurons

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, I _A and a delayed component, I _K. Results showed that lithium chloride increased the amplitude of I _A in a concentration-dependent manner. Half enhancement concentration (EC ₅₀) 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 I _A to more negative potentials, but mainly affected the activation kinetics. The amplitude and the activation processes of I _K were not affected by lithium chloride. The effects of lithium chloride on potassium channel appear to possess neuroprotective properties by Ca²⁺-lowing effects modulate neuronal excitability by activating I _A in rat hippocampal neurons.