[The ionic mechanism of hyperpolarization induced by glucocorticoid and its modulatory effects in mammalian neurons].
This is the first report to investigate the rapid hyperpolarization by glucocorticoid in coeliac ganglion neurons of guinea pig in vitro. Hydrocortisone 21-hemisuccinate (F-suc) caused rapidly hyperpolarization in neurons; hyperpolarization persisted after the elimination of synaptic inputs and after suppression of protein synthesis with actinomycin D; F-suc also induced hyperpolarization when picrotoxin or Ca(2+)-free in perfusion solution; TEA and 4-AP can inhibit the hyperpolarization of F-suc. These results provided evidence that F-suc's hyperpolarization may be mediated by potassium channel in the membrane. Also F-suc suppressed the discharges of neurons; and modulated rapidly effects of neurons to excitatory or inhibitory amino acids (P < 0.05).
Wang
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W
Department of Physiology, Second Military Medical University, Shanghai.
D000818:Animals; D005728:Ganglia, Sympathetic / Q000187:drug effects*; D006168:Guinea Pigs; D006854:Hydrocortisone / Q000031:analogs & derivatives* / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D015221:Potassium Channels
D015221:Potassium Channels; C007133:hydrocortisone hemisuccinate; D006854:Hydrocortisone