Ionic mechanism of hyperpolarization induced by glucocorticoid in mammalian neurons

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.