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糖皮质激素引起哺乳类神经元超极化反应的离子机制

汪文, 邢宝仁, 陈宜张

第二军医大学生理学教研室、神经科学研究所. 上海 200433

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。作者推断皮质醇的超极化反应是细胞膜钾离子通道介导的。

关键词： 糖皮质激素; 腹腔神经节; 钾离子通道; 超极化反应; 电压箝; 非基因组机制

Ionic mechanism of hyperpolarization induced by glucocorticoid in mammalian neurons

Wang Wen, Xing Baoren, Chen Yizhang

Department of Physiology, Institute of Neuroscience, Second Military Medical University. Shanghai 200433, China

Abstract

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 #mu#mol/L hydrocortisone 21-hemisuccinate (F-suc), associated with a decrease in input membrane resistance. The hyperpolarization was dose-dependent. Nine neurons were depolarized, and the other 336 neurons were unresponsive. The memhrane current was also observed with discontinuous single-electrode voltage 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 Ca~(2+) high Mg~(2+) perfusion and the suppression of protein synthesis by antinomycin D. The reversal potential of F-suc hyperpolarization is -79+-4.3 mV (n=5). F-suc induced hyperpolarization and GABA induced depolarization could occur in same neuron.

Key words: Glucocorticoid;coeliac ganglion;Potassium channel;Hrperpolarization;Voltage clamp;Non-genomic mechanism

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引用本文：

汪文, 邢宝仁, 陈宜张. 糖皮质激素引起哺乳类神经元超极化反应的离子机制 [J]. 生理学报 1997; 49 (5): .

Wang Wen, Xing Baoren, Chen Yizhang. Ionic mechanism of hyperpolarization induced by glucocorticoid in mammalian neurons. Acta Physiol Sin 1997; 49 (5): (in Chinese with English abstract).