Villarroel A
Howard Hughes Medical Institute, Department of Neurobiology and Behavior, SUNY at Stony Brook 11794-5230.
FEBS Lett. 1993 Dec 6;335(2):184-8. doi: 10.1016/0014-5793(93)80726-b.
The effect of arachidonic acid on the A current (IA) has been studied in dissociated bullfrog neurons under whole-cell voltage-clamp conditions. Arachidonic acid reduced IA in a dose-dependent and reversible manner without a shift in the prepulse inactivation voltage-current relation. 1.75 microM inhibited IA by 50%, and higher concentrations caused a total suppression. In addition, arachidonic acid increased the M-current (IM), a different potassium current that does not inactivate. Neither indomethacin nor nordihydroguaiaretic acid, cyclooxygenase and lipoxygenase inhibitors respectively, prevented IA reduction. In contrast, nordihydroguaiaretic acid prevented IM enhancement. Eicosatetraynoic acid, an arachidonic acid analog that cannot be metabolized, also reduced IA. These results suggest that arachidonic acid metabolism is not required to suppress IA.
在全细胞电压钳制条件下,研究了花生四烯酸对离体牛蛙神经元A电流(IA)的影响。花生四烯酸以剂量依赖性和可逆的方式降低IA,且预脉冲失活电压-电流关系无偏移。1.75微摩尔抑制IA达50%,更高浓度则导致完全抑制。此外,花生四烯酸增加M电流(IM),这是一种不同的非失活钾电流。消炎痛和去甲二氢愈创木酸分别作为环氧化酶和脂氧合酶抑制剂,均不能阻止IA降低。相反,去甲二氢愈创木酸阻止IM增强。不能被代谢的花生四烯酸类似物二十碳四炔酸也降低IA。这些结果表明,抑制IA不需要花生四烯酸代谢。