Rouzaire-Dubois B, Gérard V, Dubois J M
Laboratoire de Physiologie Comparée, URA CNRS 1121, Orsay, France.
Pflugers Arch. 1991 Nov;419(5):467-71. doi: 10.1007/BF00370790.
The effects of fatty acids on voltage-dependent potassium (K+) channels in neuroblastoma cells were studied using the whole-cell current recording technique. At a concentration of 5 microM, unsaturated and medium chain length (C10-C14) saturated fatty acids accelerated the apparent inactivation of the K+ current. This effect was reversed by albumin. In the absence of exogenous fatty acids, albumin slowed the inactivation of the K+ current. The acceleration of the K+ current inactivation induced by unsaturated fatty acids was associated with an increase in the sensitivity of K+ channels to 4-amino-pyridine. It is concluded that kinetic and pharmacological properties of K+ channels are, in part, controlled by membrane fatty acids which, in this way, should contribute to an apparent diversity of K+ channels and the modulation of cell excitability.
利用全细胞电流记录技术研究了脂肪酸对神经母细胞瘤细胞中电压依赖性钾(K+)通道的影响。在5微摩尔浓度下,不饱和脂肪酸和中链长度(C10 - C14)的饱和脂肪酸加速了K+电流的表观失活。这种作用可被白蛋白逆转。在没有外源性脂肪酸的情况下,白蛋白会减缓K+电流的失活。不饱和脂肪酸诱导的K+电流失活加速与K+通道对4 - 氨基吡啶敏感性的增加有关。得出的结论是,K+通道的动力学和药理学特性部分受膜脂肪酸控制,膜脂肪酸应以这种方式促成K+通道的明显多样性以及细胞兴奋性的调节。