焦亚硫酸钠对大鼠海马CA1区神经元钠电流的影响

目的：探讨SO2 及其体内衍生物（亚硫酸盐和亚硫酸氢盐）对中枢神经元钠通道的影响。 方法: 采用全细胞膜片钳技术研究了焦亚硫酸钠（SMB）对大鼠海马CA1区神经元钠电流的影响及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)及谷胱甘肽过氧化物酶(GPx)相应的保护作用。 结果： ① 焦亚硫酸钠可剂量依赖性地增大全细胞钠电流，剂量为2 μmol/L和20 μmol/L时，钠电流分别增大（22.36±3.28）% 和（65.05±5.75）%（n=10）。② 10　μmol/L的焦亚硫酸钠不影响钠电流的激活过程，却非常显著地影响其失活过程，使失活曲线显著右移，作用前后的半数失活电压分别为（-82.38±0.54）mV和（-69.39±0.41）mV (n=10, P<0.01), 但失活曲线的斜率因子未见改变。③ SOD(1×106 U/L)、CAT(2×106 U/L) 及GPx (1×104 U/L) 均可使SMB（10 μmol/L）增大的钠电流部分恢复。 结论： SMB增大钠电流并抑制其失活过程，从而影响神经细胞的兴奋性，这一效应可能与硫中心或氧中心自由基的损伤作用有关。

Effects of sodium metabisulfite on sodium current in acutely isolated rat hippocampal CA1 neurons

AIM: To study the effects of sodium metabisulfite (SMB), sulfur dioxide (SO2) and its derivatives in vivo, sodium bisulfite and sulfite, on Na+ currents. The effects of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) against SMB were also studied in freshly dissociated hippocampal CA1 neurons in rats. METHODS: The whole-cell patch-clamp techniques were used in the experiments. RESULTS: ① SMB increased the voltage-activated Na+ currents in a concentration-and voltage-dependent manner. The amplitudes of Na+ currents was increased (22.36±3.28) % and (65.05±5.75)% (n=10) by SMB at 2 μmol/L and 20 μmol/L, respectively. ② SMB (10 μmol/L) did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 μmol/L SMB, the half-inactivation voltage was (-82.38±0.54) mV and (-69.39±0.41) mV (n=10, P<0.01). However, the slope factor remained unchanged. ③ SOD, CAT and GPx partly inhibited the incremental effect of SMB on Na+ currents. CONCLUSION: SMB increases Na+ currents and inhibits the steady-state inactivation, which contributes to the increase in the excitibility of neuronal cells. Its mechanism may involve oxidative damage caused by sulfur-and oxygen-centered free radicals in the rat hippocampal CA1 neurons.