目的:研究氧化还原药物对三叉神经节细胞离子通道的调节作用。方法:采用全细胞膜片钳电生理方法,记录氧化还原药物对三叉神经节细胞大电导钙激活钾通道(BKca)的影响。结果:蛋氨酸特异性氧化剂chloramine-T(Ch—T)1mmol/L可轻微增加通道电流幅值,但该作用不能被半胱氨酸还原剂1,4-dithio-DL-threitol(DTT)所逆转。相反,半胱氨酸特异性氧化剂5,5’-dithio-bis(2-nitribenzoic acid)(DTNB)500μmol/L降低BKCa的电流幅值,此作用可被DTT 2mmol/L所逆转。结论:ROS通过氧化调节BKCa通道而参与三叉神经节细胞的功能调节,BKCa通道在氧化应激相关性生理、病理状态下起重要的调节作用。
To observe redox modulation of ion channel in trigeminal ganglion neurons by oxidants and reducing agents. Methods: The effects of oxidants and reducing agents on maxi-conductance calcium-activated potassium channel in cultured rat trigeminal ganglion neurons by using whole-cell patch-clamp technique. Results: Methionine-specific oxidant chloramine-T (Ch-T) 1 mmol/L slightly increased the current amplitude and this enhancement did not antagonized by DTT. In contrast, cysteine-specific reagent 5, 5'-dithiobis(2-nitrobenzoic acid) (DTNB) 500μmol/L significantly decreased current amplitude of BKCa channels. The effect was reversed by the reducing agent 2 mmol/L 1, 4-dithio-DL-threitol (DTT). Conclusion: Reactive oxygen species were definitely involved in regulation of native neuronal function via redox modulation of BKca channels, which are suggested to play compensatory roles under oxidative stress-related conditions.