Abstract
Acute exposure of the nicotinic acetylcholine receptor (AchR) to hydrocortisone (HC) induced a dose-dependent reduction in the channel open time and burst duration and an increase in the closed time, with no changes in channel amplitude. Similar effects were observed with 11-desoxycortisone, thus suggesting that the oxygen atom at position 11 is not required for channel modification. The changes were observed when HC was added to either face of the membrane, but the concentration dependence of the effect differed, indicating a certain sidedness of the corticoid action. The results are consistent with the corticoids acting either at a site on the AChR which can be reached via a membrane pathway or at the lipid annulus immediately surrounding the AChR, i.e. at the lipid-protein interface.
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