VanDongen A M, VanErp M G, Voskuyl R A
Epilepsia. 1986 May-Jun;27(3):177-82. doi: 10.1111/j.1528-1157.1986.tb03525.x.
Effects of the antiepileptic drug valproate on sodium and potassium currents in the nodal membrane of peripheral nerve fibers of Xenopus laevis were determined by voltage- and current-clamp experiments. Under voltage-clamp conditions, a reduction of both sodium and potassium conductance (in a ratio of 2:1) was observed. Typically, 2.4 mM (400 mg/L) valproate reduced the sodium current 54% and the potassium current 26%, at a membrane potential of 5 mV. Valproate did not affect the leakage conductance. The reduction of potassium conductance was voltage dependent, being more pronounced at more positive membrane potentials. For the sodium system, a voltage dependency of the blockage could not be established. Under current-clamp conditions, valproate caused a reduction of excitability of nerve membrane: amplitude of the action potential and maximum rate of rise were decreased, whereas threshold potential was increased. The ability to follow high-frequency stimulation was impaired.
通过电压钳和电流钳实验，测定了抗癫痫药物丙戊酸盐对非洲爪蟾外周神经纤维结膜中钠电流和钾电流的影响。在电压钳条件下，观察到钠电导和钾电导均降低（比例为2:1）。通常，在膜电位为5 mV时，2.4 mM（400 mg/L）丙戊酸盐可使钠电流降低54%，钾电流降低26%。丙戊酸盐不影响漏电导。钾电导的降低与电压有关，在更正的膜电位下更为明显。对于钠系统，无法确定阻断的电压依赖性。在电流钳条件下，丙戊酸盐导致神经膜兴奋性降低：动作电位幅度和最大上升速率降低，而阈电位升高。跟随高频刺激的能力受损。
