Membrane Receptor-Mediated Electrophysiological Effects of Glucocorticoid on Mammalian Neurons*

The results strongly suggest that glucocorticoid can act nongenomically through its neuronal membrane receptor and that steroid-induced hyperpolarization of membrane potential decreased or eliminated the discharges in neurons with spontaneous discharges.

Abstract

The nongenomic membrane receptor-mediated mechanism is an important but not fully explored facet in the action of steroid hormones. In the present study the action of glucocorticoid on nerve cell membrane was studied using isolated and superfused coeliac ganglion preparations by an intracellular electrophysiological technique. Glucocorticoid hyperpolarized the membrane potential of guinea pig ganglion neurons in vitro with a latency of less than 2 min. The effect persisted under low Ca2+/high Mg2+ superfusion conditions and could be abolished by RU38486, a competitive antagonist of glucocorticoid cytosolic receptor. Bovine albumin glucocorticoid conjugant exhibited the same effect. In neurons with spontaneous discharges the glucocorticoid-caused hyperpolarization of membrane potential decreased or eliminated the discharges. The results strongly suggest that glucocorticoid can act nongenomically through its neuronal membrane receptor. The steroid-induced hyperpolarization was accompanied by a change in the input resistance of the cell, indicating an involvement of some kind(s) of ion channel(s) in the action of glucocorticoid.