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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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Citing This Article：

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).