糖皮质激素引起哺乳类神经元超极化反应的离子机制  

IONIC MECHANISM OF HYPERPOLARIZATION INDUCED BY GLUCOCORTICOID IN MAMMALIAN NEUR0NS

作　　者：汪文[1] 邢宝仁[1] 陈宜张[1] 

机构地区：[1]第二军医大学生理学教研室

出　　处：《生理学报》1997年第5期537-544,共8页Acta Physiologica Sinica

基　　金：国家自然科学基金!39330100

摘　　要：在豚鼠腹腔神经节上对383个神经元作细胞内记录，给予1μmol／L半琥珀酸皮质醇灌流，38个神经元膜电位发生超极化反应，幅度变化为2～12mV（6．3±0.1mV），伴有膜电阻的降低，反应呈剂量效应关系。9个神经元呈去极化反应，其余336个神经元不反应。用单电极间断电压箝方法记录43个神经元在糖皮质激素作用下膜电流的变化，其中5个神经元出现外向电流，膜电导增加；1个神经元为内向电流。用低钙高镁液阻断突触传递和蛋白质合成抑制剂放线菌素D后，超极化反应仍然存在。皮质醇超极化反应的翻转电位为-79.0±4.3mV（n=5）。皮质醇超极化反应和GABA去极化反应可在同一神经元上出现，印防己毒素可拮抗GABA的去极化反应，但不能拮抗皮质醇的超极化反应。钾离子通道阻断剂四乙基铵（TEA）和4-氨基吡啶（4-AP）能拮抗皮质醇的超极化反应。我们推断皮质醇的超极化反应是细胞膜钾离子通道介导的。The rapid membrane actions of glucocorticoid were investigated by intracellular electrical recording from 383 coeliac ganglion neurons of gUinea-pig in vitro. Thirty-eight neurons were hyperpolarizaed by 2 ~ 12 mV when perfused with 1 μmol/L hydrocortisone 21-hemisuccinate (F-suc ), associated with a decrease in input membrane resistance. The hyperpolarizati0n was dose-dependent. Nine neurons were depolarized, and the other 336neurons were unresponsive. The memhrane current was also observed with discontinuous single-electrode v0ltage clamp technique under perfusion of F-suc in another 43 neurons.In five neurons the current was found outward, but it was inward in one neuron. The hyperpolarization persisted after the elimination of synaptic input by low Ca2+ high Mgl+Perfusion and the suppression of protein synthesis by antinomycin D. The reversal potential of F-suc hyperp0larization is - 79 4. 3 mV (n = 5) .F-suc induced hyperpolarization and GABA induced depolarization could occur in same neuron. The later action c0uld be blocked by picrotoxin. F-suc induced hyperpolarization could be inhibited by TEA and 4-AP, but not picrotoxin. It is suggested that the F-suc' S hrperpoalrization is mediated by potassium channel rather than Cl-channel in the sympathetic ganglion neurons.

关 键 词：糖皮质激素 神经元 超极化反应 

分 类 号：R338[医药卫生—人体生理学]