Referenced in: none

Automatically associated channels: Kir2.3

Title: [Ionic mechanism of hyperpolarization induced by glucocorticoid in mammalian neurons]

Authors: W Wang, B R Xing, Y Z Chen

Journal, date & volume: , 1997 Oct , 49, 537-44

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/9813493

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 mumol/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 membrane 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 Ca2+ high Mg2+ 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. The later action could 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 hyperpoalrization is mediated by potassium channel rather than Cl- channel in the sympathetic ganglion neurons.